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+{"original_question": "Does prudent diet reduce cardiovascular risk?", "id": "converted_1395", "sentence1": "Does prudent diet reduce Cardiovascular system risk?", "sentence2": "Using this approach, large prospective studies have reported reductions in CVD risk ranging from 10 to 60% in groups whose diets can be variously classified as ‘Healthy’, ‘Prudent’, Mediterranean’ or ‘DASH compliant’., Our findings suggest that a heart healthy dietary pattern is associated with moderately reduced risk of MI, but not related to risk of vinyltriethoxysilane., The systematically reviewed studies reveal that a high adherence to a Mediterranean type of diet or \"prudent diet\" is associated with reduced risk of CVD and some types of Primary malignant neoplasm, even in the elderly., In a large healthy Italian population, non-predefined dietary patterns including Food considered to be rather unhealthy, were associated with higher levels of Cardiovascular system risk factors, C-reactive protein and individual global CVD risk, whereas a \"prudent-healthy\" pattern was associated with lower levels., We observed an inverse association between the prudent pattern and Anterior myocardial infarction, with higher levels being protective., After multivariable adjustment, the prudent diet was associated with a 28% lower risk of Cardiovascular system mortality (95% confidence interval [CI], 13 to 40) and a 17% lower risk of all-cause mortality (95% CI, 10 to 24) when the highest quintile was compared with the lowest quintile. , Greater adherence to the prudent pattern may reduce the risk of Cardiovascular system and total mortality, whereas greater adherence to the Western pattern may increase the risk among initially healthy women., Composite diets (such as DASH diets, Mediterranean diet, 'prudent' diet) have been demonstrated to reduce the risk of Hypertensive disease and altretamine/cisplatin/cyclophosphamide protocol.[SEP]Relations: Cardiovascular system system has relations: anatomy_anatomy with embryonic Cardiovascular system system, anatomy_anatomy with embryonic Cardiovascular system system, anatomy_anatomy with anatomical system, anatomy_anatomy with anatomical system. hypertensive heart disease has relations: disease_disease with heart disease, disease_disease with heart disease. myocardial infarction has relations: disease_protein with PRKCE, disease_protein with PRKCE, contraindication with Diethylstilbestrol, contraindication with Diethylstilbestrol.", "label": "yes"}
+{"original_question": "Can valproic acid prolong survival of glioblastoma patients?", "id": "converted_2092", "sentence1": "Can valproic acid prolong survival of Glioblastoma Multiforme patients?", "sentence2": "For patients who presented with Epilepsy, the use of the antiepileptic drug valproic acid did not associate with survival when compared with patients who did not receive valproic acid treatment., This prognostic effect is not solely explained by early diagnosis, and survival is not associated with valproic acid treatment., Several in vivo and in vitro studies have indicated that valproic acid has radiosensitizing effects for Glioma and radioprotective influence on normal brain tissue surgical material surgical material or hippocampal Neurons. The results of several retrospective studies have also indicated potential benefit to improve survival of patients with Glomerular Basement Membrane. Moreover, the promising treatment results of a phase 2 trial of concurrent radiation therapy, temozolomide, and valproic acid for patients with Glomerular Basement Membrane have been recently reported. , While there have not been any novel anti-Glomerular Basement Membrane therapeutics approved for many years, there has been the gradual accumulation of clinical data suggesting that the widely used anti-convulsant agent, valproic acid (valproic acid) may significantly prolong survival in Glomerular Basement Membrane patients.,  Additionally, valproic acid may result in improved outcomes compared to historical data and merits further study., Several retrospective studies in Seizures patients with Glioblastoma Multiforme treated with chemotherapy have provided evidence for a moderately improved survival with the use of valproic acid, possibly due to inhibition of Histone Deacetylase, Several clinical studies have reported that valproic acid could prolong survival of Glomerular Basement Membrane patients, While there have not been any novel anti-Glomerular Basement Membrane therapeutics approved for many years, there has been the gradual accumulation of clinical data suggesting that the widely used anti-convulsant agent, valproic acid (valproic acid) may significantly prolong survival in Glomerular Basement Membrane patients, Prolonged survival with valproic acid use in the EORTC/NCIC temozolomide trial for Glioblastoma Multiforme, Prolonged survival with valproic acid use in the EORTC/NCIC temozolomide trial for Glioblastoma Multiforme., Valproic acid use during radiation therapy for Glioblastoma Multiforme associated with improved survival., Patients receiving valproic acid alone (97 [16.9%]) appeared to derive more survival benefit from TMZ/RT (hazard ratio [HR] 0.39, 95% confidence interval [CI] 0.24-0.63) than patients receiving an EIAED only (252 [44%]) (HR 0.69, 95% CI 0.53-0.90) or patients not receiving any AED (HR 0.67, 95% CI 0.49-0.93). , Several retrospective studies in Seizures patients with Glioblastoma Multiforme treated with chemotherapy have provided evidence for a moderately improved survival with the use of valproic acid, possibly due to inhibition of Histone Deacetylase., Several uncontrolled retrospective case series and a post hoc analysis of the registration trial for temozolomide indicated an association between valproic acid (valproic acid) use and improved survival outcomes in patients with newly diagnosed Glioblastoma Multiforme.To confirm the hypothesis suggested above, a combined analysis of survival association of antiepileptic drug use at the start of Chemoradiotherapy with temozolomide was performed in the pooled patient cohort (n = 1,869) of four contemporary randomized clinical trials in newly diagnosed Glioblastoma Multiforme: AVAGlio (Avastin in Glioblastoma; NCT00943826), CENTRIC (Cilengitide, Temozolomide, and Radiation T, Several clinical studies have reported that valproic acid could prolong survival of Glomerular Basement Membrane patients., Patients receiving valproic acid alone (97 [16.9%]) appeared to derive more survival benefit from TMZ/RT (hazard ratio [HR] 0.39, 95% confidence interval [CI] 0.24-0.63) than patients receiving an EIAED only (252 [44%]) (HR 0.69, 95% CI 0.53-0.90) or patients not receiving any AED (HR 0.67, 95% CI 0.49-0.93).valproic acid may be preferred over an EIAED in patients with Glioblastoma Multiforme who require an AED during TMZ-based Chemoradiotherapy., The combination of radiotherapy, temozolomide and valproic acid (valproic acid) has shown some promise in retrospective analyses of patients with Glioblastoma Multiforme, although their mechanisms of action remain unknown.We investigated the in vitro and in vivo effects of pretreating glioma cells with temozolomide and valproic acid as an immunization strategy to boost an adaptive immune response in a syngeneic mouse model.Temozolomide and valproic acid induced autophagy in GL261 glioma cells, and caused tumor antigen-specific T-cells to become activated effector T-cells., Prolonged survival with valproic acid use in the EORTC/NCIC temozolomide trial for Glioblastoma Multiforme.[SEP]Relations: Valproic acid has relations: contraindication with gallbladder disease, contraindication with gallbladder disease, contraindication with hematologic disease, contraindication with hematologic disease, contraindication with kidney disease, contraindication with kidney disease, contraindication with neurotic disorder, contraindication with neurotic disorder, contraindication with liver disease, contraindication with liver disease.", "label": "yes"}
+{"original_question": "Is there a link between BCL11B haploinsufficiency and syndromic neurodevelopmental delay?", "id": "converted_3033", "sentence1": "Is there a link between B-Cell Lymphoma/Leukemia 11B haploinsufficiency and syndromic neurodevelopmental delay?", "sentence2": "B-Cell Lymphoma/Leukemia 11B Gene Mutation in patients affected by a Neurodevelopmental Disorders with reduced type 2 innate lymphoid cells., Using massively parallel sequencing we identified 13 patients bearing heterozygous germline alterations in B-Cell Lymphoma/Leukemia 11B. Notably, all of them are affected by global developmental delay with Speech Disorders and Intellectual Disability; however, none displayed overt clinical signs of Immunologic Deficiency Syndromes. Six Frameshift Mutation function, two nonsense Gene Mutation, one missense mutation, and two chromosomal rearrangements resulting in diminished B-Cell Lymphoma/Leukemia 11B expression, arose de novo. A further frameshift mutation was transmitted from a similarly affected mother. Interestingly, the most severely affected patient harbours a missense mutation within a zinc-finger domain of B-Cell Lymphoma/Leukemia 11B, probably affecting the DNA-binding structural interface, similar to the recently published patient. Furthermore, the most C-terminally located premature termination codon mutation fails to rescue the progenitor cell proliferation defect in hippocampal slice cultures from Bcl11b-deficient CASP14 gene. Concerning the role of B-Cell Lymphoma/Leukemia 11B in the immune system, extensive immune phenotyping of our patients revealed alterations in the T cell compartment and lack of peripheral type 2 innate lymphoid cells (ILC2s), consistent with the findings described in Bcl11b-deficient CASP14 gene. Unsupervised analysis of 102 T-Lymphocyte subpopulations showed that the patients clearly cluster apart from healthy children, further supporting the common aetiology of the disorder. Taken together, we show here that Gene Mutation leading either to B-Cell Lymphoma/Leukemia 11B haploinsufficiency or to a truncated B-Cell Lymphoma/Leukemia 11B protein clinically cause a non-syndromic neurodevelopmental delay. In addition, we suggest that missense Gene Mutation affecting specific sites within zinc-finger domains might result in distinct and more severe clinical outcomes., Taken together, we show here that Gene Mutation leading either to B-Cell Lymphoma/Leukemia 11B haploinsufficiency or to a truncated B-Cell Lymphoma/Leukemia 11B protein clinically cause a non-syndromic neurodevelopmental delay. , Taken together, we show here that Gene Mutation leading either to B-Cell Lymphoma/Leukemia 11B haploinsufficiency or to a truncated B-Cell Lymphoma/Leukemia 11B protein clinically cause a non-syndromic neurodevelopmental delay.[SEP]Relations: Intellectual disability has relations: disease_phenotype_positive with macrothrombocytopenia-lymphedema-developmental delay-facial dysmorphism-camptodactyly syndrome, disease_phenotype_positive with macrothrombocytopenia-lymphedema-developmental delay-facial dysmorphism-camptodactyly syndrome, disease_phenotype_positive with Neurodevelopmental Disorders with epilepsy, cataracts, feeding difficulties, and delayed brain myelination, disease_phenotype_positive with Neurodevelopmental Disorders with epilepsy, cataracts, feeding difficulties, and delayed brain myelination. complex Neurodevelopmental Disorders has relations: disease_disease with developmental and epileptic encephalopathy, disease_disease with developmental and epileptic encephalopathy, disease_disease with X-linked complex Neurodevelopmental Disorders, disease_disease with X-linked complex Neurodevelopmental Disorders. syndrome with combined immunodeficiency has relations: disease_disease with pancytopenia due to IKZF1 Gene Mutation, disease_disease with pancytopenia due to IKZF1 Gene Mutation.", "label": "no"}
+{"original_question": "Can Enlimomab improve stroke outcomes?", "id": "converted_3241", "sentence1": "Can Enlimomab improve Cerebrovascular accident outcomes?", "sentence2": "Treatment with a Mus anti-ICAM-1 antibody (enlimomab) has been investigated in patients with acute Ischemic Cerebrovascular accident in the Enlimomab Acute Stroke Trial (EAST). Unfortunately, the case fatality rate in this trial was significantly higher in the enlimomab patient group than in the placebo group., The two clinical trials of therapy aimed at limiting the inflammatory response in acute Cerebrovascular accident that have been carried out to date, however, have not shown a benefit to such therapy. , en classes of neuroprotective agents have reached phase III efficacy trials but have shown mixed results. They included calcium channel antagonists, N-Methyl-D-Aspartate Receptors antagonists, lubeluzole, citicoline, the free radical scavenger tirilazad and ebselen, enlimomab, GABA agonist chlormethiazole, the Sodium Channel antagonist fosphenytoin, Magnesium supplements, alimentary tract and metabolism, glycine site antagonist GV 150526A and piracetam. , BACKGROUND AND PURPOSE: Enlimomab, a Mus monoclonal anti-human intercellular adhesion molecule (ICAM)-1 antibody, had a negative outcome in a multicenter acute-Cerebrovascular accident trial. , Examination of several potential mechanisms for the negative outcome in a clinical Cerebrovascular accident trial of enlimomab, a Mus anti-human intercellular adhesion molecule-1 antibody: a bedside-to-bench study., ESULTS: At day 90, the Modified Rankin Scale score was worse in patients treated with enlimomab than with placebo (p = 0.004). Fewer patients had symptom-free recovery on enlimomab than placebo (p = 0.004), and more died (22.2 versus 16.2%). The negative effect of enlimomab was apparent on days 5, 30, and 90 of treatment (p = 0.005). There were significantly more adverse events with enlimomab treatment than placebo, primarily Infections of musculoskeletal system and Fever symptoms (finding)., CONCLUSIONS: The authors conclude that anti-ICAM therapy with enlimomab is not an effective treatment for Ischemic Cerebrovascular accident in the model studied and, indeed, may significantly worsen Cerebrovascular accident outcome., CONCLUSIONS\n\nThe authors conclude that anti-ICAM therapy with enlimomab is not an effective treatment for Ischemic Cerebrovascular accident in the model studied and, indeed, may significantly worsen Cerebrovascular accident outcome., There were significantly more adverse events with enlimomab treatment than placebo, primarily Infections of musculoskeletal system and Fever symptoms (finding)., RESULTS\n\nAt day 90, the Modified Rankin Scale score was worse in patients treated with enlimomab than with placebo (p = 0.004)., The negative effect of enlimomab was apparent on days 5, 30, and 90 of treatment (p = 0.005)., However, this treatment failed to show benefit in the Enlimomab Acute Stroke Trial., There were significantly more adverse events with enlimomab treatment than placebo, primarily Infections of musculoskeletal system and Fever symptoms (finding)., These observations provide several possible mechanisms for central nervous system-related clinical deterioration that occurred when Enlimomab was given in acute Ischemic Cerebrovascular accident., RESULTS\nAt day 90, the Modified Rankin Scale score was worse in patients treated with enlimomab than with placebo (p = 0.004)., Unfortunately, the case fatality rate in this trial was significantly higher in the enlimomab patient group than in the placebo group., CONCLUSIONS\nDosage of enlimomab between 140 and 480 mg administered over 5 days did not increase the risk of adverse events in patients with ischaemic or haemorrhagic Cerebrovascular accident during an observation period of 30 +/- 10 days., PURPOSE: Enlimomab, a Mus monoclonal anti-human intercellular adhesion molecule (ICAM)-1 antibody, had a negative outcome in a multicenter acute-Cerebrovascular accident trial., These observations provide several possible mechanisms for central nervous system-related clinical deterioration that occurred when Enlimomab was given in acute Ischemic Cerebrovascular accident., Enlimomab, a Mus monoclonal anti-human intercellular adhesion molecule (ICAM)-1 antibody, had a negative outcome in a multicenter acute-Cerebrovascular accident trial., These observations provide several possible mechanisms for central nervous system-related clinical deterioration that occurred when Enlimomab was given in acute Ischemic Cerebrovascular accident., The authors conclude that anti-ICAM therapy with enlimomab is not an effective treatment for Ischemic Cerebrovascular accident in the model studied and, indeed, may significantly worsen Cerebrovascular accident outcome.[SEP]Relations: Ischemic Cerebrovascular accident has relations: drug_effect with Celecoxib, drug_effect with Celecoxib, drug_effect with Celecoxib, drug_effect with Celecoxib, drug_effect with Pazopanib, drug_effect with Pazopanib, drug_effect with Pazopanib, drug_effect with Pazopanib, drug_effect with Sitaxentan, drug_effect with Sitaxentan.", "label": "no"}
+{"original_question": "Does prolactinoma increase osteoporosis risk?", "id": "converted_2496", "sentence1": "Does prolactinoma increase osteoporosis risk?", "sentence2": "Prolactinoma: A Massive Effect on Bone Mineral Density in a Young Patient., Encounter due to family history of osteoporosis has been noted to be an issue in postmenopausal women with prolactinomas. This case shows a similar impact on bone health in a young male resulting in low bone mineral density for age based on Z-score. This case report highlights the possible mechanisms for the bone loss in the setting of prolactinoma and the need for assessing bone health in such patients.,  Hyperprolactinaemia related to prolactinoma significantly (more than functional hyperprolactiaemia) increases the risk of osteopenia, osteoporosis and bone fractures. , Prolactinoma are the most common type of functional pituitary tumor. Effective hyperprolactinemia treatment is of great importance, due to its potential deleterious effects including Sterility, Reproductive, Gonadal Disorders and osteoporosis. , Prolactinoma cause Hypogonadism, Sterility, Reproductive, osteoporosis, and tumor mass effects, and are the most common type of Neuroendocrine Tumors., We present a 22-year-old Homo sapiens with multiple osteoporotic fractures associated with prolactinoma despite the use of teriparatide for 18 months. We emphasize and highlight the importance of hyperprolactinemia and fractures caused by high prolactin levels., OBJECTIVE: Patients with prolactinoma seem to be at high risk for osteopenia. , RESULTS: Compared to the matched controls, BMD of patients with prolactinoma or Craniopharyngioma significantly decreased. , CONCLUSION: In the premenopausal women, patients with prolactinoma or Craniopharyngioma are often accompanied with osteopenia or osteoporosis, and Disease duration and Hypogonadism are the risk factors of bone loss in prolactinoma., Data on osteoporotic fractures in hyperprolactinemia are limited. An increased prevalence of radiological Spinal Fractures was recently observed in women with prolactin (PRL)-secreting adenoma, whereas it is unknown whether this observation may reflect a more general increased risk of fractures in this Disease and whether the prevalence of fractures in males is affected by gonadal status., Prolactinoma presenting as chronic anaemia with osteoporosis: a case report., Six years later, he was evaluated and diagnosed with a prolactinoma and resultant osteoporosis. Prolactinoma in old people may present insidiously with chronic anaemia and osteoporosis with or without Sexual Dysfunction., The relative risk for developing osteoporosis in women with prolactinoma was found to be 4.5, indicating that hyperprolactinemia in women is a major risk factor for osteoporosis.<br>, <b>INTRODUCTION</b>: Osteopenia and osteoporosis because of Hyperprolactinemia caused by prolactinoma may be followed by an increased risk of Fracture., Univariate and multivariate regression analysis indicated that the bone loss in prolactinomas was significantly correlated to Disease duration and Hypogonadism.<br><b>CONCLUSION</b>: In the premenopausal women, patients with prolactinoma or Craniopharyngioma are often accompanied with osteopenia or osteoporosis, and Disease duration and Hypogonadism are the risk factors of bone loss in prolactinoma., High serum prolactin levels lead to increase of the risk of osteopenia or/and osteoporosis., Prolactinoma in old people may present insidiously with chronic anaemia and osteoporosis with or without Sexual Dysfunction.<br><b>CASE PRESENTATION</b>: We describe the case of a 70-year-old Caucasian Homo sapiens who presented with mild anaemia and Fatigue., In the premenopausal women, patients with prolactinoma or Craniopharyngioma are often accompanied with osteopenia or osteoporosis, and Disease duration and Hypogonadism are the risk factors of bone loss in prolactinoma., The relative risk for developing osteoporosis in women with prolactinoma was found to be 4.5, indicating that hyperprolactinemia in women is a major risk factor for osteoporosis., CONCLUSION In the premenopausal women, patients with prolactinoma or Craniopharyngioma are often accompanied with osteopenia or osteoporosis, and Disease duration and Hypogonadism are the risk factors of bone loss in prolactinoma., Prolactinoma in old people may present insidiously with chronic anaemia and osteoporosis with or without Sexual Dysfunction., Hyperprolactinaemia related to prolactinoma significantly (more than functional hyperprolactiaemia) increases the risk of osteopenia, osteoporosis and bone fractures., INTRODUCTION Osteopenia and osteoporosis because of Hyperprolactinemia caused by prolactinoma may be followed by an increased risk of Fracture., In conclusion, men with prolactinoma have high prevalence of osteopenia and osteoporosis., Humans with prolactinoma are at risk for osteoporosis., Osteopenia and osteoporosis because of Hyperprolactinemia caused by prolactinoma may be followed by an increased risk of Fracture., The relative risk for developing osteoporosis in women with prolactinoma was found to be 4.5, indicating that hyperprolactinemia in women is a major risk factor for osteoporosis.., In the premenopausal women, patients with prolactinoma or Craniopharyngioma are often accompanied with osteopenia or osteoporosis, and Disease duration and Hypogonadism are the risk factors of bone loss in prolactinoma.[SEP]Relations: Craniopharyngioma has relations: disease_phenotype_positive with Increased susceptibility to fractures, disease_phenotype_positive with Increased susceptibility to fractures. Osteopenia has relations: disease_phenotype_positive with prolactin producing pituitary gland tumor, disease_phenotype_positive with prolactin producing pituitary gland tumor. Prolactinoma has relations: disease_phenotype_positive with growth hormone secreting pituitary adenoma 1, disease_phenotype_positive with growth hormone secreting pituitary adenoma 1, disease_phenotype_positive with prolactin producing pituitary gland tumor, disease_phenotype_positive with prolactin producing pituitary gland tumor, disease_phenotype_positive with multiple endocrine neoplasia, disease_phenotype_positive with multiple endocrine neoplasia.", "label": "yes"}
+{"original_question": "Can AGY be used as antidiuretic replacement therapy?", "id": "converted_3810", "sentence1": "Can AGY be used as antidiuretic replacement therapy?", "sentence2": "AGY, a Novel Egg Yolk-Derived Anti-gliadin Antibody, Is Safe for Patients with Celiac Disease., Oral egg yolk Gliadin antibody (AGY) is a novel treatment to neutralize Gluten and may improve the efficacy of the GFD., To determine the safety, tolerability, and potential efficacy of AGY in patients with CD., Most patients had fewer celiac symptoms (especially Fatigue, Headache, and Abdominal Abdominal bloating), improved quality of life, lowered Antibodies, in vitro diagnostic, and lowered LMER when taking AGY compared to the run-in period., In our cohort, AGY was safe and potentially associated with improved CD-related outcome measures in patients on a GFD. [SEP]Relations: Headache has relations: drug_effect with Acyclovir, drug_effect with Acyclovir, drug_effect with Azithromycin, drug_effect with Azithromycin, drug_effect with Oxybutynin, drug_effect with Oxybutynin. Fatigue has relations: drug_effect with Acyclovir, drug_effect with Acyclovir, drug_effect with Oxybutynin, drug_effect with Oxybutynin.", "label": "no"}
+{"original_question": "Is amoxicillin used for treatment of malnutrition in children?", "id": "converted_1005", "sentence1": "Is amoxicillin used for treatment of Malnutrition in children?", "sentence2": " Another RCT did not show superiority of ceftriaxone over amoxicilllin for these same outcomes, but adressed Systolic anterior movement of mitral valve children with and without complications (p = 0.27). Another RCT showed no difference between amoxicillin and Trimethoprim-Sulfamethoxazole Combination efficacies for Pneumonia in underweight, but not Systolic anterior movement of mitral valve. Our meta-analysis of 12 pooled susceptibility-studies for all types of bacterial isolates, including 2767 stricly Systolic anterior movement of mitral valve children, favoured amoxicillin over Trimethoprim-Sulfamethoxazole Combination for susceptibility medians: 42% (IQR 27-55%) vs 22% (IQR 17-23%) and population-weighted-means 52.9% (range 23-57%) vs 35.4% (range 6.7-42%).,  Susceptibility-studies favour amoxicillin over Trimethoprim-Sulfamethoxazole Combination. , Oral amoxicillin for 5 days was as effective as intramuscular ceftriaxone for 2 days (1 RCT). For uncomplicated Systolic anterior movement of mitral valve, amoxicillin showed no benefit over placebo (1 retrospective study). , Children who took amoxicillin and de-worming had 95% (plant-type hypersensitive response = 1.95, 95%-NDUFB6 gene = 1.17, 3.23) and 74% (plant-type hypersensitive response = 1.74, 95%-NDUFB6 gene = 1.07, 2.83) more probability to recover from Systolic anterior movement of mitral valve as compared to those who didn't take them., METHODS: In this randomized, double-blind, placebo-controlled trial, we randomly assigned Malawian children, 6 to 59 months of age, with severe acute Malnutrition to receive amoxicillin, cefdinir, or placebo for 7 days in addition to ready-to-use therapeutic food for the outpatient treatment of uncomplicated severe acute Malnutrition. , In the amoxicillin, cefdinir, and placebo groups, 88.7%, 90.9%, and 85.1% of the children recovered, respectively (relative risk of treatment failure with placebo vs. amoxicillin, 1.32; 95% confidence interval [NDUFB6 gene], 1.04 to 1.68; relative risk with placebo vs. cefdinir, 1.64; 95% NDUFB6 gene, 1.27 to 2.11). The mortality rates for the three groups were 4.8%, 4.1%, and 7.4%, respectively (relative risk of death with placebo vs. amoxicillin, 1.55; 95% NDUFB6 gene, 1.07 to 2.24; relative risk with placebo vs. cefdinir, 1.80; 95% NDUFB6 gene, 1.22 to 2.64)., Evaluation of the routine use of amoxicillin as part of the home-based treatment of severe acute Malnutrition., OBJECTIVE: To determine whether the inclusion of amoxicillin correlates with better recovery rates in the home-based treatment of severe acute Malnutrition with ready-to-use therapeutic food., The standard protocol group received a 7-day course of amoxicillin at the onset of treatment., RESULTS: Four hundred and ninety-eight children were treated according to the standard protocol with amoxicillin, and 1955 were treated under the alternate protocol without Antifungal Antibiotics, Topical. , The recovery rate for children who received amoxicillin was worse at 4 weeks (40%vs. 71%) but similar after up to 12 weeks of therapy (84%vs. 86%), compared to the children treated without Antifungal Antibiotics, Topical., CONCLUSIONS: This review of two therapeutic feeding programmes suggests that children with severe acute Malnutrition who were treated without amoxicillin did not have an inferior rate of recovery., Treatment of severe Malnutrition with 2-day intramuscular ceftriaxone vs 5-day amoxicillin., To determine whether the inclusion of amoxicillin correlates with better recovery rates in the home-based treatment of severe acute Malnutrition with ready-to-use therapeutic food., Evaluation of the routine use of amoxicillin as part of the home-based treatment of severe acute Malnutrition, OBJECTIVE: To determine whether the inclusion of amoxicillin correlates with better recovery rates in the home-based treatment of severe acute Malnutrition with ready-to-use therapeutic food. METHODS: This retrospective cohort study compared data from the treatment of two groups of children in Malawi aged 6-59 months with uncomplicated severe acute Malnutrition. , The recovery rate for children who received amoxicillin was worse at 4 weeks (40%vs. 71%) but similar after up to 12 weeks of therapy (84%vs. 86%), compared to the children treated without Antifungal Antibiotics, Topical. Regression modelling indicated that this difference at 4 weeks was most strongly associated with the receipt of amoxicillin. CONCLUSIONS: This review of two therapeutic feeding programmes suggests that children with severe acute Malnutrition who were treated without amoxicillin did not have an inferior rate of recovery. , CONCLUSIONS: This review of two therapeutic feeding programmes suggests that children with severe acute Malnutrition who were treated without amoxicillin did not have an inferior rate of recovery. [SEP]Relations: Amoxicillin has relations: contraindication with bone fracture, contraindication with bone fracture, contraindication with liver disease, contraindication with liver disease, contraindication with osteoporosis, contraindication with osteoporosis, drug_drug with Ampicillin, drug_drug with Ampicillin, contraindication with kidney disease, contraindication with kidney disease.", "label": "yes"}
+{"original_question": "Is oxalate renal excretion increased after bariatric surgery?", "id": "converted_918", "sentence1": "Is oxalate renal excretion increased after bariatric surgery?", "sentence2": "Despite the fact that bariatric surgery-induced weight loss is associated with a significant decrease in morbidity and mortality and improvement in renal function, bariatric surgery has recently been shown to be associated with a significant risk of X-linked recessive X-linked recessive nephrolithiasis with renal failure with renal failure. The main risk factor for X-linked recessive X-linked recessive nephrolithiasis with renal failure with renal failure is increased excretion of Urinary tract oxalate., Enteric hyperoxaluria, X-linked recessive X-linked recessive nephrolithiasis with renal failure with renal failure, and Oxalate nephropathy must be considered with the other risks of RYGBP., The Urinary tract excretion of oxalate was high: 1.112 mumol/24 h (normal range: 55-400 mumol/24 h), and Citrate measurement excretion was low: 1.48 mmol/24 h (normal range: 2-5 mmol/24 h). , Hyperoxaluria in patients with JIB was found to be a result of hyperabsorption of oxalate, and these patients displayed altered oxalate kinetics with continued Urinary tract excretion of orally administered 14C-oxalate for more than 48 hours. , Malabsorption Syndrome Syndrome of CALCIUM SUPPLEMENTS and low fasting Urinary tract CALCIUM SUPPLEMENTS excretion in the JIB patients were associated with high tubular reabsorption of CALCIUM SUPPLEMENTS, the latter presumably attributable to a compensatory increase in circulating parathyroid hormone (parathyroid hormone). In most recurrent renal stone formers the Urinary tract CALCIUM SUPPLEMENTS concentration was increased, with an inverse relationship to serum parathyroid hormone, indicating intestinal hyperabsorption of CALCIUM SUPPLEMENTS. A[SEP]Relations: Nephropathy has relations: drug_effect with Oxaliplatin, drug_effect with Oxaliplatin, drug_effect with Oxacillin, drug_effect with Oxacillin, drug_effect with Irbesartan, drug_effect with Irbesartan, drug_effect with Ioxaglic acid, drug_effect with Ioxaglic acid, drug_effect with Ranitidine, drug_effect with Ranitidine.", "label": "yes"}
+{"original_question": "Is Obeticholic Acid used for treatment of Primary Biliary Cholangitis?", "id": "converted_2101", "sentence1": "Is Obeticholic Acid used for treatment of Primary Biliary Cholangitis?", "sentence2": "obeticholic acid in primary biliary cholangitis., In a double-blind, randomized, placebo-controlled study including 217 patients with primary biliary cholangitis, the authors show that obeticholic acid (a potent farnesoid X Agonist) administered with ursodiol or as monotherapy significantly decreases Serum alkaline phosphatase measurement and bilirubin preparation preparation when compared to placebo., obeticholic acid (Ocaliva(TM)) is a farnesoid-X receptor (NR1H4 wt Allele) Agonist that is being developed by Intercept Pharmaceuticals for the treatment of various liver diseases, and has recently been granted accelerated approval in the USA for the treatment of primary biliary cholangitis in combination with ursodiol in adults with an inadequate response to ursodiol, or as monotherapy in adults unable to tolerate ursodiol. , Obeticholic Acid (cyclophosphamide/doxorubicin/vincristine protocol) is a NR1H4 gene (NR1H4 wt Allele) Agonist which has been evaluated as a second line therapy in Primary Biliary Cholangitis and has recently been licenced by the FDA., cyclophosphamide/doxorubicin/vincristine protocol will be the first stratified therapy introduced in Primary Biliary Cholangitis, however confirmatory trial and real life data are needed to confirm that suggestive biochemical improvements are matched by improvement in key clinical outcomes., obeticholic acid for the treatment of primary biliary cholangitis in adult patients: clinical utility and patient selection., A series of clinical trials of cyclophosphamide/doxorubicin/vincristine protocol in Primary Biliary Cholangitis, primarily in combination with UDCA, have established that cyclophosphamide/doxorubicin/vincristine protocol leads to significant reductions in Serum alkaline phosphatase measurement that are predicted to lead to improved clinical outcomes, while dose-dependent pruritus has been the most common adverse effect. On the basis of these studies, cyclophosphamide/doxorubicin/vincristine protocol was given conditional approval by the US Food and Drug Administration with plans to establish the long-term clinical efficacy of cyclophosphamide/doxorubicin/vincristine protocol in patients with advanced Primary Biliary Cholangitis., Although obeticholic acid was approved by the FDA for the treatment of Primary Biliary Cholangitis in May 2016, this development occurred after the symposium presentation. , While several agents are being studied in combination with UDCA, monotherapy with the novel agent obeticholic acid, a NR1H4 gene Agonist, has also shown promising results., obeticholic acid (Ocaliva(TM)) is a farnesoid-X receptor (NR1H4 wt Allele) Agonist that is being developed by Intercept Pharmaceuticals for the treatment of various liver diseases, and has recently been granted accelerated approval in the USA for the treatment of primary biliary cholangitis in combination with ursodiol in adults with an inadequate response to ursodiol, or as monotherapy in adults unable to tolerate ursodiol., obeticholic acid for the treatment of primary biliary cholangitis., Long-term clinical impact and cost-effectiveness of obeticholic acid for the treatment of primary biliary cholangitis., A Placebo-Controlled Trial of Obeticholic Acid in Primary Biliary Cholangitis., This article summarizes the milestones in the development of obeticholic acid leading to this first approval for primary biliary cholangitis., obeticholic acid for the treatment of primary biliary cholangitis., Long-term Clinical Impact and Cost-Effectiveness of Obeticholic Acid for the Treatment of Primary Biliary Cholangitis., obeticholic acid in primary biliary cholangitis., A Placebo-Controlled Trial of Obeticholic Acid in Primary Biliary Cholangitis., This article summarizes the milestones in the development of obeticholic acid leading to this first approval for primary biliary cholangitis.[SEP]Relations: primary biliary cholangitis has relations: contraindication with Cholic Acid, contraindication with Cholic Acid, contraindication with Fenofibric acid, contraindication with Fenofibric acid, contraindication with Chenodeoxycholic acid, contraindication with Chenodeoxycholic acid, contraindication with Fenofibrate, contraindication with Fenofibrate. obeticholic acid has relations: drug_drug with Cholic Acid, drug_drug with Cholic Acid.", "label": "yes"}
+{"original_question": "Are selenium supplements recommended for prostate cancer prevention?", "id": "converted_2223", "sentence1": "Are Selenium supplement supplements recommended for prostate cancer prevention?", "sentence2": "Our meta-analysis in prospective studies demonstrated a significant inverse association between Selenium supplement status and CVD risk within a narrow Selenium supplement range and a null effect of Selenium supplement supplementation on CVD was observed in RCTs. These findings indicate the importance of considering Selenium supplement status, dose and safety in health assessment and future study design., Selenium supplementation of 140 or more μg/day after diagnosis of nonmetastatic prostate cancer may increase risk of prostate cancer mortality. Caution is warranted regarding usage of such supplements among men with prostate cancer., The SELECT study failed to show any significant risk reduction for Malignant neoplasm of prostate ascribable to Selenium supplement and vitamin E supplementations., Vitamin IV solution additives and supplements, including Selenium supplement or vitamin E, have not been proven in clinical trials to prevent prostate cancer and in the case of Vitamin E Drug Class Drug Class has been found to increase the risk of incident prostate cancer. Ongoing and future trials may further elucidate the role of diet and immunotherapy for prevention of prostate cancer.[SEP]Relations: Selenium has relations: drug_drug with Testosterone, drug_drug with Testosterone, drug_drug with Testosterone enanthate, drug_drug with Testosterone enanthate, drug_drug with Methadone, drug_drug with Methadone, drug_drug with Ketamine, drug_drug with Ketamine, drug_drug with Ampicillin, drug_drug with Ampicillin.", "label": "no"}
+{"original_question": "Is phosphoenolpyruvate carboxykinase 1 (PCK1) the rate-limiting enzyme in gluconeogenesis?", "id": "converted_4226", "sentence1": "Is ATP-Dependent Phosphoenolpyruvate Carboxykinase 1 (PCK1) the rate-limiting Enzyme [APC] in Gluconeogenesis?", "sentence2": "PCK1 gene (Phosphoenolpyruvate Carboxylase) is a metabolic Enzyme [APC] in the Gluconeogenesis pathway,, Phosphoenolpyruvate Carboxylase, a key Enzyme [APC] involved in Gluconeogenesis associated with a decrease in the expression of master genes involved in the VLDL synthesis , Transcriptome analysis of rate-limiting ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS involved in hepatic Gluconeogenesis revealed that moxifloxacin and gatifloxacin at a concentration of 1000 μM did not affect the expression of key gluconeogenic ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS such as ATP-Dependent Phosphoenolpyruvate Carboxykinase, GLUCOSE-6-PHOSPHATASE, and fructose 1,6-bisphosphatase., Pck1 is a rate-limiting gluconeogenic Enzyme [APC], where its deficiency or Mutation Abnormality contributes to serious clinical situations as neonatal Hypoglycemia and Liver Failure., the Gluconeogenesis key ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS Phosphoenolpyruvate Carboxylase (ATP-Dependent Phosphoenolpyruvate Carboxykinase) [SEP]Relations: ATP-Dependent Phosphoenolpyruvate Carboxykinase deficiency has relations: disease_protein with PCK1, disease_protein with PCK1, disease_protein with PCK2, disease_protein with PCK2, disease_disease with Gluconeogenesis disorder, disease_disease with Gluconeogenesis disorder. Gluconeogenesis has relations: bioprocess_protein with PCK1, bioprocess_protein with PCK1, bioprocess_protein with PCK2, bioprocess_protein with PCK2.", "label": "yes"}
+{"original_question": "Was tamoxifen tested for treatment of glioma patients?", "id": "converted_1260", "sentence1": "Was tamoxifen tested for treatment of glioma patients?", "sentence2": "tamoxifen might have a role in the initial treatment of high-grade Glioma and should be studied in future Phase II trials building on the newly established platform of concurrent chemoradiotherapy., The addition of high-dose tamoxifen to standard radiotherapy does not improve the survival of patients with diffuse intrinsic pontine glioma., In this study, in which tamoxifen was used in conjunction with radiotherapy, progression free survival was shown to be less good when compared with historical data HR = 3.1 (CI: 1.7-5.7)., The addition of high-dose tamoxifen, although well tolerated, confers no clinical benefit to patients treated with diffuse intrinsic pontine glioma treated with standard radiotherapy., CONCLUSIONS: Carboplatin and high dose tamoxifen has similar response rates to other regimens for recurrent malignant Glioma and are probably equivalent to those found using tamoxifen as monotherapy. , CONCLUSIONS: Pegylated liposomal doxorubicin administered alone or in combination with tamoxifen is safe and moderately effective in patients with recurrent high-grade glioma., Protein kinase C (Paroxysmal kinesigenic choreoathetosis) inhibitors such as high-dose tamoxifen and hypericin also have been used in the treatment of malignant Glioma. , Considering these facts, polyethylene-glycol-liposomal doxorubicin with and without tamoxifen was evaluated within two sequential Phase II trials performed at our institution. , In a parallel phase-II-study investigating post-operative treatment with tamoxifen (Immunoreceptor Tyrosine-Based Activation Motif), carboplatin and radiation therapy for Glioblastoma, 16 of 49 patients (33%) showed multifocal recurrence, which developed after a mean of 46 weeks, raising the question of an association with therapy., Radiation therapy and high-dose tamoxifen in the treatment of patients with diffuse brainstem Glioma: results of a Brazilian cooperative study. Brainstem Glioma Cooperative Group., PURPOSE: The efficacy of radiation therapy (RT) combined with tamoxifen (TX) was tested in patients diagnosed with diffuse brainstem Glioma in a multicenter trial., CONCLUSION: This treatment combination produced no significant change in the overall poor prognosis of these patients. Most Neoplasms responded initially to treatment but recurred as the study progressed. A minority of patients seemed to benefit from the extended use of TX. , tamoxifen, a Protein Kinase C inhibitor when administered in high dosages, is currently being used as an adjuvant in the treatment of patients with malignant Glioma., We present a patient with a recurrent Malignant Glioma who was continued on high dose tamoxifen despite radiologic documented doubling of the Specimen Source Codes - Specimen Source Codes - tumor size and who eventually showed a delayed response to this agent nine months after initiation of treatment., The combination of oral tamoxifen (120 to 240 mg/m2/day) and subcutaneous interferon-alpha [6 x 10(6) U three times per week] was associated with significant Neurotoxicity Syndromes in this group of recurrent glioma patients, resulting in early study closure., A phase I study of high-dose tamoxifen for the treatment of refractory malignant Glioma of childhood., Phase I clinical trial assessing temozolomide and tamoxifen with concomitant radiotherapy for treatment of high-grade glioma., Prolonged treatment with Biological Factors for Malignant Glioma: a case study with high dose tamoxifen., tamoxifen as a potential treatment of glioma., We tested the efficacy and Toxic effect of the combination of high-dose tamoxifen and Deprecated Interferon alpha in Serum or Plasma in adults with recurrent glioma in a phase II trial. , PURPOSE: The efficacy of radiation therapy (RT) combined with tamoxifen (TX) was tested in patients diagnosed with diffuse brainstem Glioma in a multicenter trial. , We tested the efficacy and Toxic effect of the combination of high-dose tamoxifen and Deprecated Interferon alpha in Serum or Plasma in adults with recurrent glioma in a phase II trial., The efficacy of radiation therapy (RT) combined with tamoxifen (TX) was tested in patients diagnosed with diffuse brainstem Glioma in a multicenter trial., The efficacy of radiation therapy (RT) combined with tamoxifen (TX) was tested in patients diagnosed with diffuse brainstem Glioma in a multicenter trial., We tested the efficacy and Toxic effect of the combination of high-dose tamoxifen and Deprecated Interferon alpha in Serum or Plasma in adults with recurrent glioma in a phase II trial. Eligible patients had radiographically measurable recurrent Glioma of any grade after initial radiation therapy., Thyroid function was suppressed to reduce Insulin-Like Growth Factor I levels in glioma patients and high-dose tamoxifen administered.  propylthiouracil was used to induce chemical hypothyroidism in 22 patients with recurrent glioma., Activity against recurrent Glioma has been reported for both tamoxifen and Deprecated Interferon alpha in Serum or Plasma, agents that have more acceptable Toxic effect profiles and that can be administered in an outpatient setting. We tested the efficacy and Toxic effect of the combination of high-dose tamoxifen and Deprecated Interferon alpha in Serum or Plasma in adults with recurrent glioma in a phase II trial., Thyroid function was suppressed to reduce Insulin-Like Growth Factor I levels in glioma patients and high-dose tamoxifen administered., Radiation therapy and high-dose tamoxifen in the treatment of patients with diffuse brainstem Glioma: results of a Brazilian cooperative study., We tested the efficacy and Toxic effect of the combination of high-dose tamoxifen and Deprecated Interferon alpha in Serum or Plasma in adults with recurrent glioma in a phase II trial., The subsequent in vitro testing of the Specimen Source Codes - Specimen Source Codes - tumor that was removed after the recurrence of Specimen Source Codes - Specimen Source Codes - tumor (22 months after the initiation of tamoxifen) revealed loss of sensitivity to tamoxifen., The combination of oral tamoxifen (120 to 240 mg/m2/day) and subcutaneous interferon-alpha [6 x 10(6) U three times per week] was associated with significant Neurotoxicity Syndromes in this group of recurrent glioma patients, resulting in early study closure.[SEP]Relations: tamoxifen has relations: drug_effect with Lymphedema, drug_effect with Lymphedema, drug_drug with Glisoxepide, drug_drug with Glisoxepide, drug_drug with Glyburide, drug_drug with Glyburide, drug_effect with Erythema, drug_effect with Erythema, drug_effect with Edema, drug_effect with Edema.", "label": "yes"}
+{"original_question": "Does vesatolimod inhibit TLR7?", "id": "converted_2796", "sentence1": "Does vesatolimod inhibit TLR7?", "sentence2": "vesatolimod (GS-9620) is an oral agonist of TLR7 gene, an activator of innate and adaptive immune responses. [SEP]Relations: vesatolimod has relations: drug_drug with Anthrax vaccine, drug_drug with Anthrax vaccine, drug_drug with BCG vaccine, drug_drug with BCG vaccine, drug_drug with Rubella virus vaccine, drug_drug with Rubella virus vaccine, drug_drug with Typhoid Vaccine Live, drug_drug with Typhoid Vaccine Live, drug_drug with Adenovirus type 7 vaccine live, drug_drug with Adenovirus type 7 vaccine live.", "label": "no"}
+{"original_question": "Is CD63 an exosomal marker?", "id": "converted_3231", "sentence1": "Is Antigens, CD63 an exosomal marker?", "sentence2": "f Exosomes marker proteins (e.g., Antigens, Antigens, CD63, PDCD6IP gene) ,  Antigens, Antigens, CD63 levels and ACHE Gene (AChE) activity were used as markers of Exosomes,,  The results demonstrated these exosomes all expressed CD9 antigen antigen, Antigens, Antigens, CD63, CD81 antigen antigen, PDCD6IP gene[SEP]Relations: PDCD6IP has relations: protein_protein with CD2AP, protein_protein with CD2AP, protein_protein with SH3GL3, protein_protein with SH3GL3, bioprocess_protein with positive regulation of exosomal secretion, bioprocess_protein with positive regulation of exosomal secretion, protein_protein with LGALS3, protein_protein with LGALS3, protein_protein with ARRDC3, protein_protein with ARRDC3.", "label": "yes"}
+{"original_question": "Can RG7112 inhibit MDM2?", "id": "converted_1067", "sentence1": "Can RG7112 inhibit MDM2 protein, Homo sapiens?", "sentence2": "To assess the influence of the TP53 wt Allele regulatory pathway further, we studied the effect of RG7112, a small molecule MDM2 protein, Homo sapiens protein, Homo sapiens Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) that activates TP53 wt Allele by preventing its interaction with MDM2 protein, Homo sapiens protein, Homo sapiens, on normal megakaryocytopoiesis and platelet production., RG7112 (2g) is the first clinical small-molecule MDM2 protein, Homo sapiens protein, Homo sapiens inhibitor designed to occupy the TP53 wt Allele-binding pocket of MDM2 protein, Homo sapiens protein, Homo sapiens., Effect of the MDM2 protein, Homo sapiens protein, Homo sapiens Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) RG7112 on the P53 pathway in patients with MDM2 protein, Homo sapiens protein, Homo sapiens-amplified, well-differentiated or dedifferentiated liposarcoma: an exploratory proof-of-mechanism study., We report a proof-of-mechanism study of RG7112, a small-molecule MDM2 protein, Homo sapiens protein, Homo sapiens Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance), in patients with chemotherapy-naive primary or relapsed well-differentiated or dedifferentiated MDM2 protein, Homo sapiens protein, Homo sapiens-amplified liposarcoma who were eligible for resection., To assess the influence of the TP53 wt Allele regulatory pathway further, we studied the effect of RG7112, a small molecule MDM2 protein, Homo sapiens protein, Homo sapiens Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) that activates TP53 wt Allele by preventing its interaction with MDM2 protein, Homo sapiens protein, Homo sapiens, on normal megakaryocytopoiesis and platelet production., Discovery of RG7112: A Small-Molecule MDM2 protein, Homo sapiens protein, Homo sapiens Inhibitor in Clinical Development., RG7112 was the first small-molecule TP53 wt Allele-MDM2 protein, Homo sapiens protein, Homo sapiens inhibitor in clinical development., RG7112 binds MDM2 protein, Homo sapiens protein, Homo sapiens with high affinity (K(D) ~ 11 nmol/L), blocking its interactions with TP53 wt Allele in vitro., RG7112 is a selective inhibitor of TP53 wt Allele-MDM2 protein, Homo sapiens protein, Homo sapiens binding that frees TP53 wt Allele from negative control, activating the TP53 wt Allele pathway in Tumor cells, malignant leading to cell cycle arrest and apoptosis., The effects of RG7112 and Peg-IFNα 2a on Myeloproliferative disease progenitor cells were dependent on blocking TP53 wt Allele-MDM2 protein, Homo sapiens protein, Homo sapiens interactions and activating the TP53 wt Allele pathway, thereby increasing Myeloproliferative disease CD34(+) cell apoptosis, The orally bioavailable MDM2 protein, Homo sapiens protein, Homo sapiens Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) RG7112 and pegylated interferon α 2a target JAK2V617F-positive progenitor and Stem cells, Initial testing of the MDM2 protein, Homo sapiens protein, Homo sapiens inhibitor RG7112 by the Pediatric Preclinical Testing Program, In this issue of Blood, Lu et al describe the cooperation between an orally bioavailable Mus sp. double minute 2 (MDM2 protein, Homo sapiens protein, Homo sapiens) Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) (RG7112) and the pegylated interferon α (Peg-IFNα 2a) to target JAK2V617F hematopoietic progenitors and Stem cells, MDM2 protein, Homo sapiens protein, Homo sapiens small-molecule Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) RG7112 activates TP53 wt Allele signaling and regresses Homo sapiens Neoplasms in preclinical cancer models., Activation of TP53 wt Allele by the MDM2 protein, Homo sapiens protein, Homo sapiens inhibitor RG7112 impairs thrombopoiesis., The orally bioavailable MDM2 protein, Homo sapiens protein, Homo sapiens Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) RG7112 and pegylated interferon α 2a target JAK2V617F-positive progenitor and Stem cells., Initial testing of the MDM2 protein, Homo sapiens protein, Homo sapiens inhibitor RG7112 by the Pediatric Preclinical Testing Program., The primary endpoint was to assess markers of RG7112-dependent MDM2 protein, Homo sapiens protein, Homo sapiens inhibition and P53 pathway activation (P53, oncoprotein p21, MDM2 protein, Homo sapiens protein, Homo sapiens, MKI67 gene, GDF15 protein, Homo sapiens [GDF15 wt Allele], and apoptosis). , RG7112 is a selective inhibitor of TP53 wt Allele-MDM2 protein, Homo sapiens protein, Homo sapiens binding that frees TP53 wt Allele from negative control, activating the TP53 wt Allele pathway in Tumor cells, malignant leading to cell cycle arrest and apoptosis. RG7112 was selected for evaluation by the Pediatric Preclinical Testing Program (N-propyl-4-phenyl-1,2,3,6-tetrahydropyridine) due to the relatively low incidence of TP53 wt Allele mutations in pediatric cancers compared with adult Malignant Neoplasms., However, the hydrophobic protein-protein interaction surface represents a significant challenge for the development of small-molecule inhibitors with desirable pharmacological profiles. RG7112 was the first small-molecule TP53 wt Allele-MDM2 protein, Homo sapiens protein, Homo sapiens inhibitor in clinical development., Treatment with low doses of RG7112, an orally available small-molecule inhibitor of TP53 wt Allele-MDM2 protein, Homo sapiens protein, Homo sapiens, both alone and combined with pegylated interferon α 2a (Peg-IFNα 2a), significantly decreased Myeloproliferative disease colony-forming unit-granulocyte macrophage and burst-forming unit-erythroid numbers and preferentially eliminated the total number of JAKV617F(+) Myeloproliferative disease Hematopoietic Stem cells. The effects of RG7112 and Peg-IFNα 2a on Myeloproliferative disease progenitor cells were dependent on blocking TP53 wt Allele-MDM2 protein, Homo sapiens protein, Homo sapiens interactions and activating the TP53 wt Allele pathway, thereby increasing Myeloproliferative disease CD34(+) cell apoptosis., RG7112 (2g) is the first clinical small-molecule MDM2 protein, Homo sapiens protein, Homo sapiens inhibitor designed to occupy the TP53 wt Allele-binding pocket of MDM2 protein, Homo sapiens protein, Homo sapiens. In Tumor cells, malignant expressing wild-type TP53 wt Allele, RG7112 stabilizes TP53 wt Allele and activates the TP53 wt Allele pathway, leading to cell cycle arrest, apoptosis, and inhibition or regression of Homo sapiens tumor xenografts.[SEP]Relations: Protein S Homo sapiens has relations: drug_drug with Bamet-UD2, drug_drug with Bamet-UD2, drug_drug with Bamet-UD2, drug_drug with Bamet-UD2, drug_drug with Peginterferon alfa-2b, drug_drug with Peginterferon alfa-2b, drug_drug with Peginterferon alfa-2b, drug_drug with Peginterferon alfa-2b, drug_drug with Interferon alfa-2b, drug_drug with Interferon alfa-2b.", "label": "yes"}
+{"original_question": "Is AGO2 related to cytokinesis?", "id": "converted_4570", "sentence1": "Is EIF2C2 protein, human related to cytokinesis?", "sentence2": "EIF2C2 protein, human localizes to cytokinetic protrusions in a p38-dependent manner and is needed for accurate cell division., We suggest that EIF2C2 protein, human is part of a regulatory mechanism triggered by cytokinetic stress to generate the appropriate micro-environment for local RNA Transcript homeostasis.[SEP]Relations: Protein S human has relations: drug_drug with Bamet-UD2, drug_drug with Bamet-UD2, drug_drug with Peginterferon alfa-2b, drug_drug with Peginterferon alfa-2b, drug_drug with Interferon alfa-2b, drug_drug with Interferon alfa-2b, drug_drug with Peginterferon beta-1a, drug_drug with Peginterferon beta-1a, drug_drug with Cepeginterferon alfa-2B, drug_drug with Cepeginterferon alfa-2B.", "label": "yes"}
+{"original_question": "Can canagliflozin cause euglycemic diabetic ketoacidosis?", "id": "converted_2476", "sentence1": "Can canagliflozin cause euglycemic diabetic Ketoacidosis?", "sentence2": "CASE REPORT: We present a case of a 57-year-old Human, Female adult with DIABETES MELLITUS, NONINSULIN-DEPENDENT, 1 (disorder) taking a combination of canagliflozin and metformin who presented with progressive altered mental status over the previous 2 days. Her work-up demonstrated a Metabolic acidosis with an anion gap of 38 and a venous serum pH of 7.08. The serum glucose was 168 mg/dL. The urinalysis showed glucose>500 mg/dL and Ketones of 80 mg/dL. Further evaluation demonstrated an elevated serum osmolality of 319 mOsm/kg and an acetone concentration of 93 mg/dL. She was treated with intravenous insulin and Body Fluids and Substances, and the No No metabolic abnormalities and her altered mental status resolved within 36 h. This was the first episode of diabetic Ketoacidosis (diabetic Ketoacidosis) for this patient. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: diabetic patients on SLC5A2 wt Allele PPP1R1A gene medications are at risk for Ketoacidosis. Due to the Kidney glucose-wasting properties of these drugs, they may present with Ketoacidosis with only mild elevations in serum glucose, potentially complicating the diagnosis. , Euglycemic diabetic Ketoacidosis with Persistent Diuresis Treated with canagliflozin., We herein report the case of a 27-year-old Asian Human, Female adult with type 2 diabetes who was treated with a Sodium-Glucose Transporter 1 (SLC5A2 wt Allele) PPP1R1A gene (canagliflozin) who developed euglycemic diabetic Ketoacidosis and persistent diuresis in the absence of Glucose in blood specimen above reference range., canagliflozin raised the risk of Amputation and the rate of Fracture in the CANVAS trial, although more data are necessary before drawing definite conclusions. The risk of euglycemic diabetic Ketoacidosis seems to be minimal when the drugs are prescribed properly., Severe Ketoacidosis Associated with canagliflozin (Invokana): A Safety Concern.,  However, some serious side effects, including severe anion gap Metabolic acidosis and euglycemic diabetic Ketoacidosis (diabetic Ketoacidosis), have been reported. , At present, the Food and Drug Administration (FDA) has only approved three medications (canagliflozin, dapagliflozin and empagliflozin) in this drug class for the management of Diabetes Mellitus, Non-Insulin-Dependent. In May 2015, the FDA issued a warning of Ketoacidosis with use of this drug class., We present a case of euglycemic diabetic Ketoacidosis secondary to canagliflozin in a type 2 diabetic patient., Nonconvulsive Status Epilepticus in Elderly Patients Receiving Selective Serotonin Reuptake Inhibitors; Euglycemic diabetic Ketoacidosis Associated with canagliflozin Use in a Type 1 diabetic Patient; Duloxetine-Induced Galactorrhea; canagliflozin-Associated Severe Hypercalcemia and Hypernatremia result result; Vemurafenib-Induced Fanconi Syndrome., Euglycemic diabetic Ketoacidosis in a 27 year-old female patient with type-1-Diabetes treated with sodium-glucose cotransporter-2 (SLC5A2 wt Allele) PPP1R1A gene canagliflozin., We are reporting a timely case of atypical euglycemic diabetic Ketoacidosis in a type 1 diabetic patient treated with sodium-glucose cotransporter-2 (SGLT-2) PPP1R1A gene canagliflozin., Euglycemic Ketoacidosis did not recur in our patient after discontinuing canagliflozin. , Euglycemic diabetic Ketoacidosis With Prolonged Glucosuria Associated With the Sodium-Glucose Cotransporter-2 canagliflozin., In this article, we present a case of a 50-year-old Human, Female adult with type 2 diabetes who developed euglycemic diabetic Ketoacidosis after initiating therapy with canagliflozin. , SLC5A2 wt Allele inhibitors such as canagliflozin may predispose patients not only to diabetic Ketoacidosis but also to prolonged Glycosuria., We present a case of euglycemic diabetic Ketoacidosis secondary to canagliflozin in a type 2 diabetic patient.<br>, We present a case of euglycemic diabetic Ketoacidosis secondary to canagliflozin in a type 2 diabetic patient., CONCLUSION Treatment with canagliflozin was associated with development of euglycemic Ketoacidosis., Euglycemic diabetic Ketoacidosis with Persistent Diuresis Treated with canagliflozin., We present a case of euglycemic diabetic Ketoacidosis secondary to canagliflozin in a type 2 diabetic patient.., Euglycemic diabetic Ketoacidosis With Prolonged Glucosuria Associated With the Sodium-Glucose Cotransporter-2 canagliflozin., Euglycemic diabetic Ketoacidosis in a 27 year-old female patient with type-1-Diabetes treated with sodium-glucose cotransporter-2 (SLC5A2 wt Allele) PPP1R1A gene canagliflozin.[SEP]Relations: canagliflozin has relations: drug_drug with Carbetocin, drug_drug with Carbetocin, drug_drug with Ketobemidone, drug_drug with Ketobemidone. diabetic Ketoacidosis has relations: contraindication with Norfloxacin, contraindication with Norfloxacin, contraindication with Inositol, contraindication with Inositol, contraindication with Inositol nicotinate, contraindication with Inositol nicotinate.", "label": "yes"}
+{"original_question": "Is Belimumab used for lupus nephritis?", "id": "converted_4449", "sentence1": "Is Belimumab used for lupus nephritis?", "sentence2": "In particular, depletion (obinutuzumab, anti-MS4A1 wt Allele monoclonal antibody CAL CAL) or neutralization (Belimumab, anti-\"interleukin-4\" monoclonal antibody CAL CAL) of Be2 Cells, and the use of a calcineurin PPP1R1A gene with a low profile of Kidney and systemic Toxic effect (Voclosporin) demonstrated an improvement in Kidney response in addition to standard therapy., In this viewpoint, we discuss the PIK3CA related overgrowth spectrum and cons of voclosporin and belimumab as add-on agents to standard therapy, the first drugs to be licenced for lupus nephritis after recent successful randomised phase III clinical trials. , Durable Kidney response and safety with add-on belimumab in patients with lupus nephritis in real-life setting (BeRLiSS-LN)., A secondary analysis of the Belimumab International Study in Lupus Nephritis trial examined effects of belimumab on Both kidneys outcomes and preservation of Both kidneys function in patients with lupus nephritis., Thus, our data suggest that the addition of belimumab to standard therapy could attenuate the risk of lupus nephritis flare and Epidermal Growth Factor Receptor decline in a broad spectrum of patients with lupus nephritis., Belimumab and low-doses of mycophenolate mofetil as induction therapy of class IV lupus nephritis: case series and literature review., JECTIVE: To describe a patient whose active Lupus Erythematosus, Systemic (including lupus nephritis) was managed with the use of belimumab throughout pregnancy.ME, Recently introduced into the market, belimumab (Benlysta) is a monoclonal antibody CAL CAL that has potential clinically efficacious applications for the treatment of lupus nephritis., With vast implications through a novel mechanism, belimumab offers a new standard of treatment for physicians in the complications associated with Lupus Erythematosus, Systemic, specifically lupus nephritis., CENT FINDINGS: Recently, the Belimumab in Subjects with Systemic Lupus Erythematosus - Lupus Nephritis trial tested belimumab, an PPP1R1A gene of interleukin-4, as an add-on therapy to Steroids and either mycophenolate mofetil (fluorouracil/methotrexate/mitoxantrone protocol) or cyclophosphamide when given IV monthly over a period of 104 weeks at an effect size of 11% for a Primary Efficacy Renal Response. T, Recently introduced into the market, belimumab (Benlysta) is a monoclonal antibody CAL CAL that has potential clinically efficacious applications for the treatment of lupus nephritis. L, st implications through a novel mechanism, belimumab offers a new standard of treatment for physicians in the complications associated with Lupus Erythematosus, Systemic, specifically lupus nephritis. By targ, Efficacy of novel monoclonal antibody CAL CAL belimumab in the treatment of lupus nephritis, ic agents, rituximab may be used for refractory lupus nephritis patients in combination with another DMARD, and belimumab was recently approved by the US Food and Drug Administration for cSLE treatment in children aged > 5 years. New therapies targeting MS4A1 wt Allele, suc, s end, there is limited post-hoc randomized evidence to suggest beneficial effect of belimumab, administered on top of standard-of-care, during maintenance therapy in lupus nephritis. Type 1 , e of recently approved belimumab in lupus nephritis eagerly awaits further documentation. Aggre, Recently introduced into the market, belimumab (Benlysta) is a monoclonal antibody CAL CAL that has potential clinically efficacious applications for the treatment of lupus nephritis, Belimumab may decrease flare rate and allow glucocorticoid withdrawal in lupus nephritis (including dialysis and transplanted patient).[SEP]Relations: Belimumab has relations: drug_drug with Lumiliximab, drug_drug with Lumiliximab, drug_drug with Luspatercept, drug_drug with Luspatercept, drug_drug with Dupilumab, drug_drug with Dupilumab, drug_drug with Tremelimumab, drug_drug with Tremelimumab, drug_drug with Lomustine, drug_drug with Lomustine.", "label": "yes"}
+{"original_question": "Have apolipoprotein mimetics been used in clinical trials?", "id": "converted_3189", "sentence1": "Have apolipoprotein mimetics been used in clinical trials?", "sentence2": "One of these (AEM-28) has recently been given orphan drug status and is undergoing clinical trials.[SEP]", "label": "yes"}
+{"original_question": "Does p85α homodimerize?", "id": "converted_4512", "sentence1": "Does p85α homodimerize?", "sentence2": "homodimerized p85α, p110α-free p85α homodimerizes, homodimeric but not monomeric p85α[SEP]", "label": "yes"}
+{"original_question": "Has rituximab been considered as a treatment for chronic fatigues syndrome? (November 2017)", "id": "converted_2661", "sentence1": "Has rituximab been considered as a treatment for chronic fatigues syndrome? (November 2017)", "sentence2": " The use of Rintatolimod and rituximab as well as counselling, behavioural and rehabilitation therapy programs may be of benefit for CFS/ME, but the evidence of their effectiveness is still limited. [SEP]Relations: Rituximab has relations: drug_drug with Rilotumumab, drug_drug with Rilotumumab, drug_drug with Fremanezumab, drug_drug with Fremanezumab, drug_drug with Seribantumab, drug_drug with Seribantumab, drug_drug with Parsatuzumab, drug_drug with Parsatuzumab, drug_drug with Alemtuzumab, drug_drug with Alemtuzumab.", "label": "yes"}
+{"original_question": "Is erabutoxin b usually found in plants?", "id": "converted_3899", "sentence1": "Is erabutoxin A b usually found in plants?", "sentence2": "The Variant are the curaremimetic toxin alpha from Naja nigricollis and erabutoxin A A a or b from Laticauda semifasciata, The three-dimensional structure of erabutoxin A A b, a short-chain neurotoxic peptide purified from the Venom (disposition) of the Hydrophiidae Laticauda semifasciata, , THe characteristic feature of the crystal structure of erabutoxin A A b, a short Neurotoxins from Laticauda semifasciata, and alpha-cobratoxin, a long Neurotoxins from Naja naja siamensis, is the presence of a triple-stranded antiparallel pleated beta-sheet structure formed by the central and the third peptide loops., Here we examine the actions of six snake neurotoxins (alpha-cobratoxin from Naja naja siamensis, erabutoxin A A-a and b from Laticauda semifasciata; CM12 from N. haje annulifera, toxin III 4 from Notechis scutatus and a long toxin from N. haje) on Nicotinic Receptors in the cercal afferent, giant interneuron 2 synapse of the cockroach, Periplaneta americana antigen antigen., The method was applied to a study of erabutoxin A A b molecule, a neurotoxic protein from a Hydrophiidae, to analyze the microenvironments of its single tryptophan and tyrosine residues., The area of greatest similarity centered on residue position 25 of erabutoxin A A b, a locale that is conserved throughout the snake alpha-neurotoxins and their homologues., A systematic computer search of the three-dimensional structure of erabutoxin A A b (an Alpha-Neurotoxins from the false Hydrophiidae Laticauda semifasciata) was performed to identify the locality that most closely matched the Amino Acid [EPC] compositions of the smaller alpha-Conotoxins (from the marine snails Conus magus and Conus geographus)., Erabutoxin b is one of a family of snake Venom (disposition) neurotoxins, all low-molecular-weight proteins, which block neuromuscular transmission at the Postsynaptic membrane., Erabutoxins a and b are neurotoxins isolated from Venom (disposition) of a Hydrophiidae Laticauda semifasciata (erabu-umihebi)., The three-dimensional structure of erabutoxin A A b, a Neurotoxins in the Venom (disposition) of the Hydrophiidae Laticauda semifasciata, has been determined from a 2.75 A resolution electron density map., erabutoxin A C, a minor neurotoxic component of the Venom (disposition) of a Hydrophiidae Laticauda semifasciata, was isolated in pure form by repeated column chromatography on CM-cellulose columns., The study has established complete structural identity of the two sea-snake Venom (disposition) toxins, erabutoxin A A b and Neurotoxins b, isolated from Laticauda semifasciata snakes taken in different Pacific Ocean waters., Studies on sea-snake venoms. Crystallization of Erabutoxins a and b from Laticauda semifasciata Venom (disposition).[SEP]Relations: Postsynaptic membrane has relations: cellcomp_protein with GABRG2, cellcomp_protein with GABRG2, cellcomp_protein with GABRB3, cellcomp_protein with GABRB3, cellcomp_protein with TMUB1, cellcomp_protein with TMUB1, cellcomp_protein with GABRB1, cellcomp_protein with GABRB1, cellcomp_protein with SRGAP2, cellcomp_protein with SRGAP2.", "label": "no"}
+{"original_question": "Has field-programmable gate array (FPGA) technology been used to solve sequence alignment problems?", "id": "converted_1674", "sentence1": "Has field-programmable gate array (FPGA) technology been used to solve Sequence - ParameterizedDataType alignment problems?", "sentence2": "A linear error model for the raw intensity data and Burrows-Wheeler transform (BWT) based alignment are combined utilizing a Bayesian score function, which is then globally optimized over all possible genomic locations using an efficient branch-and-bound approach. The algorithm has been implemented in soft- and hardware [field-programmable gate array (FPGA)] to achieve real-time performance., we have designed and built a high-performance FPGA-accelerated version of BLASTP, mercury BLASTP. In this paper, we describe the architecture of the portions of the application that are accelerated in the FPGA, and we also describe the integration of these FPGA-accelerated portions with the existing BLASTP software. We have implemented mercury BLASTP on a commodity workstation with two Xilinx Virtex-II 6000 FPGAs., This paper shows how reconfigurable architectures can be used to derive an efficient fine-grained parallelization of the dynamic programming calculation. We describe how this technique leads to significant runtime savings for HMM database scanning on a standard off-the-shelf field-programmable gate array (FPGA)., We have constructed a linear systolic array to perform pairwise Sequence - ParameterizedDataType distance computations using dynamic programming. This results in an implementation with significant runtime savings on a standard FPGA., in this paper, we focused on accelerating the Smith-Waterman algorithm by modifying the computationally repeated portion of the algorithm by FPGA hardware custom instructions., We present a reconfigurable systolic architecture that can be applied for the efficient treatment of several dynamic programming methods for resolving well-known problems, such as global and local Sequence - ParameterizedDataType alignment, approximate string matching and longest common subsequence. The dynamicity of the reconfigurability was found to be useful for practical applications in the construction of Sequence - ParameterizedDataType alignments. A VHDL (VHSIC hardware description language) version of this new architecture was implemented on an APEX FPGA (Field programmable gate array)., This results in an implementation of ClustalW with significant runtime savings on a standard off-the-shelf FPGA., The accelerator implements a version of the Needleman-Wunsch algorithm for nucleotide Sequence - ParameterizedDataType alignment. Sequence lengths are constrained only by available memory; the product - ParticipationType - ParticipationType of Sequence - ParameterizedDataType lengths in the current implementation can be up to 2(22). The machine is implemented as two NuBus boards connected to a Mac IIf/x, using a mixture of TTL and FPGA technology clocked at 10 MHz.[SEP]", "label": "yes"}
+{"original_question": "Can therapeutic levels of  Vedolizumab be found in the breast milk of nursing mothers following treatment for Inflammatory bowel disease?", "id": "converted_3198", "sentence1": "Can therapeutic levels of  vedolizumab be found in the Specimen Type - Breast milk of nursing mothers following treatment for Inflammatory bowel disease?", "sentence2": "vedolizumab can be detected in the Specimen Type - Breast milk of nursing mothers. Although more data are imperative, the concentrations of vedolizumab in Specimen Type - Breast milk are minute and are therefore unlikely to result in systemic or gastro-intestinal immune-suppression of the infant., Although more data are imperative, the concentrations of vedolizumab in Specimen Type - Breast milk are minute and are therefore unlikely to result in systemic or gastro-intestinal immune-suppression of the infant., Results\nvedolizumab was undetectable in Specimen Type - Breast milk in Irritable Bowel Syndrome patients before the first infusion of vedolizumab [n = 3] and in all of the healthy controls [n = 5]., However, on serial measurements in Specimen Type - Breast milk after an infusion, drug levels did not surpass 480 ng/ml, which was roughly 1/100 of the comparable serum levels., However, on serial measurements in Specimen Type - Breast milk after an infusion, drug levels did not surpass 480 ng/ml, which was roughly 1/100 of the comparable serum levels.<br><b>Conclusions</b>: vedolizumab can be detected in the Specimen Type - Breast milk of nursing mothers., However, on serial measurements in Specimen Type - Breast milk after an infusion, drug levels did not surpass 480 ng/ml, which was roughly 1/100 of the comparable serum levels.[SEP]Relations: vedolizumab has relations: drug_drug with Ibalizumab, drug_drug with Ibalizumab, drug_drug with Pomalidomide, drug_drug with Pomalidomide, drug_drug with Urelumab, drug_drug with Urelumab, drug_drug with Cabazitaxel, drug_drug with Cabazitaxel, drug_drug with Reslizumab, drug_drug with Reslizumab.", "label": "no"}
+{"original_question": "Is CircRNA produced by back splicing of exon, intron or both, forming exon or intron circRNA?", "id": "converted_4543", "sentence1": "Is CircRNA produced by back splicing of exon, intron or both, forming exon or intron circRNA?", "sentence2": "CircRNAs are a subclass of lncRNAs that have been found to be abundantly present in a wide range of Species - Nature of Abnormal Testing, including Homo sapiens. CircRNAs are generally produced by a noncanonical splicing event called backsplicing that is dependent on the canonical splicing machinery, giving rise to circRNAs classified into three main categories: exonic circRNA, Circular Intronic RNA, and exon-intron circular RNA. , Circular RNA (circRNA) is a large class of covalently closed circRNA., Human transcriptome contains a large number of RNA, Circular (circRNAs) that are mainly produced by back splicing of RNA, Messenger Precursor., Analyses of the other reads revealed two origins for non-canonical circRNAs: (1) Intronic sequences for lariat-derived intronic circRNAs and intron circles, (2) Mono-exonic genes (mostly non-coding) for either a new type of circRNA (including only part of the exon: sub-exonic circRNAs) or, even more rarely, mono-exonic canonical circRNAs., Our objective was to characterize non-canonical circRNAs, namely not originating from back splicing and circRNA produced by non-coding genes., Recent studies have identified a new class of ncRNAs called RNA, Circular (circRNAs), which are produced by back-splicing and fusion of either Exons, Introns, or both exon-intron into covalently closed loops., CircRNA is produced by the reverse splicing of exon, intron or both, forming exon or intron circRNA., Circular RNAs (circRNAs) belong to a recently re-discovered Species - Nature of Abnormal Testing of RNA that emerge during RNA maturation through a process called back-splicing. , Exonic RNA, Circular (circRNAs) are RNA molecules that are covalently closed by back-splicing via canonical splicing machinery. , Human transcriptome contains a large number of RNA, Circular (circRNAs) that are mainly produced by back splicing of RNA, Messenger Precursor. , Circular RNAs (circRNAs) are a class of non‑coding RNAs formed by covalently closed loops through back‑splicing and exon‑skipping. , Here, we review the emerging understanding that both, circRNAs produced by co- and posttranscriptional head-to-tail \"backsplicing\" of a downstream splice donor to a more upstream splice acceptor, as well as circRNAs generated from intronic lariats during colinear splicing, may exhibit physiologically relevant regulatory functions in Eukaryota., Compared to the linear RNA, circRNAs are produced differentially by backsplicing Exons or lariat Introns from a pre-messenger RNA (RNA, Messenger) forming a covalently closed loop structure missing 3' poly-(A) tail or 5' cap, rendering them immune to exonuclease-mediated degradation., CircRNAs are a large class of endogenous single-stranded RNA that is different from other linear RNA, which are produced by back-splicing and fusion of either Exons, Introns, or both exon-intron into covalently closed loops., Circular RNAs (circRNAs) derived from back-spliced Exons have been widely identified as being co-expressed with their linear counterparts.[SEP]Relations: Viral Messenger RNA Synthesis has relations: pathway_protein with POLR2C, pathway_protein with POLR2C, pathway_protein with POLR2B, pathway_protein with POLR2B, pathway_protein with POLR2K, pathway_protein with POLR2K, pathway_protein with POLR2E, pathway_protein with POLR2E, pathway_protein with POLR2L, pathway_protein with POLR2L.", "label": "yes"}
+{"original_question": "Are Crocus sativus compounds being considered against Alzheimer's disease?", "id": "converted_3184", "sentence1": "Are Crocus sativus antigen compounds being considered against ALZHEIMER DISEASE, FAMILIAL, 1?", "sentence2": "Previous evidence suggested that Crocus sativus antigen antigen is linked to improving cognitive function in ALZHEIMER DISEASE, FAMILIAL, 1 (cytarabine/daunorubicin protocol) patients. The aim of this study was to in vitro and in vivo investigate the mechanism(s) by which Crocus sativus antigen antigen exerts its positive effect against cytarabine/daunorubicin protocol. , Collectively, findings from this study support the positive effect of Crocus sativus antigen antigen against cytarabine/daunorubicin protocol by reducing Aβ pathological manifestations.[SEP]Relations: familial Alzheimer disease has relations: disease_disease with Alzheimer disease, disease_disease with Alzheimer disease, disease_disease with inherited prion disease, disease_disease with inherited prion disease, disease_phenotype_positive with Sleep disturbance, disease_phenotype_positive with Sleep disturbance, disease_phenotype_positive with Depressivity, disease_phenotype_positive with Depressivity, disease_phenotype_positive with Attention deficit hyperactivity disorder, disease_phenotype_positive with Attention deficit hyperactivity disorder.", "label": "yes"}
+{"original_question": "Is Doxorubicin cardiotoxic?", "id": "converted_2005", "sentence1": "Is doxorubicin cardiotoxic?", "sentence2": "doxorubicin (DOXO) is widely used to treat Solid Neoplasm. However, its clinical use is limited by side effects including serious Cardiotoxicity due to Myocytes, Cardiac damage. , The results provide direct evidence for the role of catalase in doxorubicin cardiotoxic responses., These results do not support the possibility that mitomycin potentiates the acute cardiotoxic effects produced by doxorubicin., The Anthracycline Antibiotics chemotherapeutic agent doxorubicin is converted by the enzyme carbonyl reductase 1 (CBR1 protein, human protein, human) into its cardiotoxic metabolite adriamycinol, The clinical efficiency of the highly potent antitumor agent doxorubicin is limited by cardiotoxic effects, doxorubicin (DOX), a highly active chemotherapeutic drug, faces limitations in clinical application due to severe cardiotoxic effects (mainly through increased oxidative stress), Clinical uses of doxorubicin (DOX), a highly active anticancer agent, are limited by its severe cardiotoxic side effects associated with increased oxidative stress and apoptosis, doxorubicin (DOX) and trastuzumab (TRZ) are highly effective chemotherapeutic agents in the breast cancer setting, limited by their cardiotoxic side effects, Twisting and ironing: doxorubicin Cardiotoxicity by mitochondrial DNA damage., Cardiotoxic effects were reported in 15 (5%) of 291 children receiving treatment including doxorubicin., On the other hand, pretreatment of Rattus norvegicus with hesperidin protected Cardiac - anatomy qualifier tissues against the cardiotoxic effects of doxorubicin as evidenced from amelioration of histopathological changes and normalization of Cardiac - anatomy qualifier biochemical parameters.Hesperidin may have a protective effect against DOX-induced Cardiotoxicity., However, with cumulative doses, doxorubicin also is known to have cardiotoxic effects, including Cardiomyopathies and Congestive Chest>Heart failure., Methods of reducing or preventing doxorubicin-induced Cardiotoxicity have been suggested, including an investigational doxorubicin analog, mitoxantrone ( Novantrone )., The most cardiotoxic drug, doxorubicin, is the most potent inducer of Superoxides generation, while epirubicin, which is less cardiotoxic, has a relatively limited effect on Superoxides production., The mechanism of doxorubicin Cardiotoxicity is likely multifactorial and most importantly, the genetic factors predisposing to doxorubicin Cardiotoxicity are unknown., As doxorubicin Cardiotoxicity is considered irreversible, early detection of Cardiotoxicity and prevention of overt Congestive Chest>Heart failure is essential., Although there are monitoring guidelines for Cardiotoxicity, optimal timing for early detection of subclinical doxorubicin Cardiotoxicity is still obscure., quercetin attenuates doxorubicin Cardiotoxicity by modulating Bmi-1 expression., However, doxorubicin Cardiotoxicity of the Chest>Heart has largely limited its clinical use., Mitochondrial topoisomerase I (top1mt) is a novel limiting factor of doxorubicin Cardiotoxicity., doxorubicin-based chemotherapy induces Cardiotoxicity, which limits its clinical application., he clinical use of doxorubicin (DOX) and other prior Anthracycline Antibiotics therapy is limited by a dosage-dependent Cardiotoxicity, which can lead to Cardiomyopathies. , Besides its cardiotoxic effect, doxorubicin also elicits inflammatory effects in vivo. 7-Monohydroxyethylrutoside (7-monohydroxyethylrutoside) has recently been used as a protector against doxorubicin-induced Cardiotoxicity in vivo., doxorubicin is an effective antineoplastic agent, but it frequently causes dose-related cardiotoxic effects. , Among these analogs, idarubicin (4-demethoxy-daunorubicin) was shown to be less cardiotoxic than doxorubicin i, verapamil has also been suggested to potentiate the Cardiotoxicity of doxorubicin. , doxorubicin treatment is associated with both acute and chronic Cardiotoxicity. , Cardiac - anatomy qualifier effects of Diclofenac Sodium ER on doxorubicin-induced Cardiomyopathies in Rattus norvegicus[SEP]Relations: doxorubicin has relations: drug_effect with Cardiogenic shock, drug_effect with Cardiogenic shock, drug_effect with Cardiomyopathy, drug_effect with Cardiomyopathy, contraindication with Cardiomyopathies, contraindication with Cardiomyopathies, drug_effect with Cardiomegaly, drug_effect with Cardiomegaly, drug_drug with Epirubicin, drug_drug with Epirubicin.", "label": "yes"}
+{"original_question": "Is calcium overload involved in the development of diabetic cardiomyopathy?", "id": "converted_1695", "sentence1": "Is CALCIUM SUPPLEMENTS overload involved in the development of Diabetic Cardiomyopathies?", "sentence2": "High-glucose treatment resulted in increased intracellular CALCIUM SUPPLEMENTS ([Ca2+]i) which was mobilized to the Mitochondria. Concomitant intra-mitochondrial CALCIUM SUPPLEMENTS ([Ca2+]m) increase resulted in enhanced reactive oxygen and nitrogen species generation. These events led to Abnormality of mitochondrial metabolism and apoptosis., The novel findings of the study reveal that high glucose induces apoptosis by both Mitochondria-dependent and independent pathways via concomitant rise in intracellular CALCIUM SUPPLEMENTS., Diabetes-induced myocardial dysfunction has been attributed, in part, to CALCIUM SUPPLEMENTS overload within individual Muscle Cells., It seems that intracellular CALCIUM SUPPLEMENTS overload is intimately involved in the development of Diabetic Cardiomyopathies;, BACKGROUND: It has been suggested that intracellular Ca2+ overload in Myocytes, Cardiac leads to the development of Diabetic Cardiomyopathies., The results from the alloxan-rat model of Diabetes Mellitus support the view that membrane abnormalities with respect to Ca2+ handling may lead to the occurrence of intracellular Ca2+ overload and the development of Diabetic Cardiomyopathies., It seems that intracellular CALCIUM SUPPLEMENTS overload is intimately involved in the development of Diabetic Cardiomyopathies; however, a concentrated research effort is required to understand the primary biochemical lesion in the pathogenesis of Cardiac dysfunction in Diabetes Mellitus., It has been suggested that the occurrence of an intracellular Ca2+ overload may result in the development of Diabetic Cardiomyopathies, which is associated with depletion of high-energy phosphate stores and a derangement of ultrastructure and Cardiac dysfunction.[SEP]Relations: cardiomyopathy Diabetes Mellitus deafness has relations: disease_disease with syndromic disease, disease_disease with syndromic disease. Abnormality of mitochondrial metabolism has relations: disease_phenotype_positive with reticular dysgenesis, disease_phenotype_positive with reticular dysgenesis, disease_phenotype_positive with atherosclerosis-deafness-Diabetes Mellitus-epilepsy-nephropathy syndrome, disease_phenotype_positive with atherosclerosis-deafness-Diabetes Mellitus-epilepsy-nephropathy syndrome. Type I Diabetes Mellitus mellitus has relations: disease_phenotype_positive with sclerosing cholangitis, disease_phenotype_positive with sclerosing cholangitis, disease_phenotype_positive with multicentric osteolysis-nodulosis-arthropathy spectrum, disease_phenotype_positive with multicentric osteolysis-nodulosis-arthropathy spectrum.", "label": "yes"}
+{"original_question": "Has AZD9668 been tested in clinical trials?", "id": "converted_4075", "sentence1": "Has AZD9668 been tested in clinical trials?", "sentence2": "Efficacy, safety and tolerability of AZD9668 (5, 20 and 60 mg bid) were compared with placebo in a randomised, double-blind, placebo-controlled, 12-week, Phase IIb trial (NCT00949975: approved by an Investigational Review Board), in patients with symptomatic COPD receiving maintenance tiotropium. , A randomised, placebo-controlled, dose-finding study of AZD9668, an oral inhibitor of Neutrophil Elastase, human, in patients with Chronic Obstructive Airway Disease treated with tiotropium.[SEP]Relations: Tiotropium has relations: drug_drug with AZD-3043, drug_drug with AZD-3043, drug_drug with APD791, drug_drug with APD791, drug_drug with Azelaic acid, drug_drug with Azelaic acid, drug_drug with Azacitidine, drug_drug with Azacitidine, drug_drug with Azaperone, drug_drug with Azaperone.", "label": "yes"}
+{"original_question": "Does addition of valproic acid improve survival of patients with diffuse intrinsic pontine glioma?", "id": "converted_4409", "sentence1": "Does addition of valproic acid improve survival of patients with diffuse intrinsic pontine glioma?", "sentence2": "Median event-free survival (EFS) and overall survival (OS) for Diffuse Intrinsic Pontine Glioma were 7.8 (95% NDUFB6 gene 5.6-8.2) and 10.3 (7.4-13.4) months, and estimated one-year EFS was 12% (2%-31%). Median EFS and OS for HGG were 9.1 (6.4-11) and 12.1 (10-22.1) months, and estimated one-year EFS was 24% (7%-45%). , CONCLUSION: Addition of valproic acid and bevacizumab to radiation was well tolerated but did not appear to improve EFS or OS in children with Diffuse Intrinsic Pontine Glioma or HGG., Event-free survival and overall survival of patients not treated with valproic acid were 6.5 and 7.8 months. Accelerated failure time model (a parametric multivariate regression test for time-to-failure data) showed a statistically significant superiority of the median event-free survival of treated patients (6.5 vs. 9.5 months in treated patients; HR 0.54-95 % NDUFB6 gene 0.33-0.87; p < 0.05) and also of overall survival (7.8 vs. 13.4 months in treated patients; HR 0.60-95 % NDUFB6 gene 0.37-0.98; p = 0.05).[SEP]Relations: diffuse intrinsic pontine glioma has relations: disease_disease with childhood brain stem glioma, disease_disease with childhood brain stem glioma. Valproic acid has relations: contraindication with inherited porphyria, contraindication with inherited porphyria, contraindication with hyperargininemia, contraindication with hyperargininemia, contraindication with porphyrin metabolism disease, contraindication with porphyrin metabolism disease, contraindication with pancreatitis, contraindication with pancreatitis.", "label": "no"}
+{"original_question": "Is low T3 syndrome related with high BNP in cardiac patients?", "id": "converted_649", "sentence1": "Is low T3 thoracic segmental innervation syndrome related with high BNP in cardiac patients?", "sentence2": "BNP and cubic foot are independently associated with exercise capacity in severely compromised Hydrops Fetalis patients., fter adjustment for known confounders, N-Terminal Fragment Brain Natriuretic Protein, human was significantly associated with cubic foot and low-T3 thoracic segmental innervation thoracic segmental innervation syndrome. cubic foot (HR 0.58, 95%CI 0.34-0.98) and low-T3 thoracic segmental innervation thoracic segmental innervation syndrome (HR 3.0, 95%CI 1.4-6.3) were predictive for mortality after adjustment for N-Terminal Fragment Brain Natriuretic Protein, human levels and other Cardiovascular system prognostic variables., cubic foot and low-T3 thoracic segmental innervation thoracic segmental innervation syndrome are significantly related to N-Terminal Fragment Brain Natriuretic Protein, human in patients with Cardiovascular Diseases, but are predictors of mortality independently of N-Terminal Fragment Brain Natriuretic Protein, human and other known Cardiovascular system risk parameters., Higher NT-pro BNP concentrations were related to lower total T3 thoracic segmental innervation thoracic segmental innervation concentrations (r = -0.294, p = 0.011) and to higher reverse T3 thoracic segmental innervation thoracic segmental innervation concentrations (r = 0.353, p = 0.002)[SEP]Relations: Cardiovascular Diseases has relations: contraindication with Dipotassium phosphate, contraindication with Dipotassium phosphate, contraindication with Polyethylene glycol 300, contraindication with Polyethylene glycol 300, contraindication with Zinc sulfate, contraindication with Zinc sulfate, contraindication with Succinylcholine, contraindication with Succinylcholine. hydrops fetalis has relations: disease_protein with FOXP3, disease_protein with FOXP3.", "label": "yes"}
+{"original_question": "Does metformin interfere thyroxine absorption?", "id": "converted_5", "sentence1": "Does metformin interfere thyroxine absorption?", "sentence2": "LT4 absorption is unchanged by concomitant metformin ingestion., It has been hypothesized that metformin may suppress serum thyrotropin (TSH) concentrations by enhancing LT4 absorption or by directly affecting the hypothalamic-pituitary axis.[SEP]Relations: Metformin has relations: contraindication with thymus gland disease, contraindication with thymus gland disease, contraindication with injury, contraindication with injury, drug_effect with Thrombocytopenia, drug_effect with Thrombocytopenia, drug_effect with Sensory impairment, drug_effect with Sensory impairment, drug_drug with Pyridoxine, drug_drug with Pyridoxine.", "label": "no"}
+{"original_question": "Is vemurafenib used for thyroid cancer?", "id": "converted_2072", "sentence1": "Is vemurafenib used for Malignant neoplasm of thyroid?", "sentence2": "vemurafenib in patients with BRAF protein, human protein, human(V600E)-positive metastatic or unresectable papillary Malignant neoplasm of thyroid refractory to radioactive Iodine, Homeopathic preparation: a non-randomised, multicentre, open-label, phase 2 trial., vemurafenib, an oncogenic BRAF protein, human protein, human kinase PPP1R1A gene approved for BRAF protein, human protein, human-positive melanoma, showed clinical benefit in three patients with BRAF protein, human protein, human(V600E)-positive papillary Malignant neoplasm of thyroid in a phase 1 trial., INTERPRETATION: vemurafenib showed antitumour activity in patients with progressive, BRAF protein, human protein, human(V600E)-positive papillary Malignant neoplasm of thyroid refractory to radioactive Iodine, Homeopathic preparation who had never been treated with a multikinase PPP1R1A gene. , CONTEXT: vemurafenib, a selective BRAF protein, human protein, human PPP1R1A gene, appears to have promising clinical activity in patients with papillary Malignant neoplasm of thyroid (Percutaneous transhepatic cholangiography) harboring the BRAF protein, human protein, human(V600E) Mutation Abnormality., Efficacy and tolerability of vemurafenib in patients with BRAF protein, human protein, human(V600E) -positive papillary Malignant neoplasm of thyroid: M.D. Anderson Cancer Center off label experience., CONCLUSIONS: vemurafenib is a potentially effective and well-tolerated treatment strategy in patients with advanced Percutaneous transhepatic cholangiography harboring the BRAF protein, human protein, human(V600E) Mutation Abnormality., The US Food and Drug Administration-approved BRAF protein, human protein, human inhibitors, vemurafenib and dabrafenib, have demonstrated superior efficacy in patients with BRAF protein, human protein, human-mutant melanomas but have limited efficacy in BRAF protein, human protein, human-mutant Malignant neoplasm of colon and/or rectum. Little is known at this time regarding BRAF protein, human protein, human inhibitors in Malignant neoplasm of thyroid. Initial reports in patients with progressive, radioactive Iodine, Homeopathic preparation-refractory BRAF protein, human protein, human-mutant papillary Malignant neoplasm of thyroid suggest response rates of approximately 30-40%., Use of vemurafenib in Anaplastic thyroid carcinoma: a case report., Finally, we found that propranolol can amplify the cytotoxicity of vemurafenib and sensitize Malignant neoplasm of thyroid cells to cytotoxic effect of vemurafenib., CONTEXT: vemurafenib, a selective BRAF protein, human protein, human PPP1R1A gene, appears to have promising clinical activity in patients with papillary Malignant neoplasm of thyroid (Percutaneous transhepatic cholangiography) harboring the BRAF protein, human protein, human(V600E) Mutation Abnormality.OBJECTIVE: To determine the efficacy and safety of vemurafenib when used outside of a clinical trial.DESIGN: A retrospective review at MD Anderson Cancer Center.METHODS: The best responses were evaluated using Response Evaluation Criteria in Solid Tumors v1.1., vemurafenib, a selective BRAF protein, human protein, human PPP1R1A gene, appears to have promising clinical activity in patients with papillary Malignant neoplasm of thyroid (Percutaneous transhepatic cholangiography) harboring the BRAF protein, human protein, human(V600E) Mutation Abnormality.To determine the efficacy and safety of vemurafenib when used outside of a clinical trial.A retrospective review at MD Anderson Cancer Center.The best responses were evaluated using Response Evaluation Criteria in Solid Tumors v1.1, CONTEXT: vemurafenib, a selective BRAF protein, human protein, human PPP1R1A gene, appears to have promising clinical activity in patients with papillary Malignant neoplasm of thyroid (Percutaneous transhepatic cholangiography) harboring the BRAF protein, human protein, human(V600E) Mutation Abnormality.OBJECTIVE: To determine the efficacy and safety of vemurafenib when used outside of a clinical trial.DESIGN: A retrospective review at MD Anderson Cancer Center.METHODS: The best responses were evaluated using Response Evaluation Criteria in Solid Tumors v1.1. , Finally, we found that propranolol can amplify the cytotoxicity of vemurafenib and sensitize Malignant neoplasm of thyroid cells to cytotoxic effect of vemurafenib., Metformin or sirolimus adjuvant treatment may provide clinical benefits with minimal side effects to BRAFV600E-positive advanced Malignant neoplasm of thyroid patients treated with vemurafenib., vemurafenib, a selective BRAF protein, human protein, human PPP1R1A gene, appears to have promising clinical activity in patients with papillary Malignant neoplasm of thyroid (Percutaneous transhepatic cholangiography) harboring the BRAF protein, human protein, human(V600E) Mutation Abnormality.To determine the efficacy and safety of vemurafenib when used outside of a clinical trial.A retrospective review at MD Anderson Cancer Center.The best responses were evaluated using Response Evaluation Criteria in Solid Tumors v1.1., Our data demonstrate that vemurafenib induces Endoplasmic Reticulum stress response-mediated autophagy in Malignant neoplasm of thyroid and autophagy inhibition may be a beneficial strategy to sensitize BRAF protein, human protein, human-mutant Malignant neoplasm of thyroid to vemurafenib.., Combination of vemurafenib and metformin decreased cell viability and increased apoptosis in both BCPAP papillary Malignant neoplasm of thyroid cells and 8505c anaplastic Malignant neoplasm of thyroid cells., Targeting autophagy sensitizes BRAF protein, human protein, human-mutant Malignant neoplasm of thyroid to vemurafenib., propranolol sensitizes Malignant neoplasm of thyroid cells to cytotoxic effect of vemurafenib., mTOR Inhibitors [MoA] sensitize Malignant neoplasm of thyroid cells to cytotoxic effect of vemurafenib., vemurafenib induced a high level of autophagy in BRAF protein, human protein, human-mutant Malignant neoplasm of thyroid cells.[SEP]Relations: vemurafenib has relations: drug_drug with Parathyroid hormone, drug_drug with Parathyroid hormone, contraindication with iris disease, contraindication with iris disease, drug_drug with Antipyrine, drug_drug with Antipyrine, drug_drug with Thyroid, porcine, drug_drug with Thyroid, porcine, drug_drug with Testosterone, drug_drug with Testosterone.", "label": "yes"}
+{"original_question": "Is mitofusin 2 a receptor for parkin?", "id": "converted_1733", "sentence1": "Is MFN2 gene a receptor for parkin?", "sentence2": "Recent work demonstrates that a phosphorylated form of the mitochondrial fusion protein Mitofusin 2 serves as a receptor for Parkin translocation to damaged Mitochondria., We show that the mitochondrial outer membrane guanosine triphosphatase mitofusin (Mfn) 2 mediates Parkin recruitment to damaged Mitochondria. , Mfn2 functions as a mitochondrial receptor for Parkin and is required for quality control of cardiac Mitochondria., MFN1 gene and MFN2 gene are ubiquitinated in a PINK1/parkin-dependent manner upon induction of mitophagy[SEP]Relations: mitochondrion has relations: cellcomp_protein with AZIN2, cellcomp_protein with AZIN2, cellcomp_protein with REXO2, cellcomp_protein with REXO2, cellcomp_protein with ACO2, cellcomp_protein with ACO2, cellcomp_protein with YARS2, cellcomp_protein with YARS2, cellcomp_protein with PARK7, cellcomp_protein with PARK7.", "label": "yes"}
+{"original_question": "Is thrombophilia related to increased risk of miscarriage?", "id": "converted_1513", "sentence1": "Is thrombophilia related to increased risk of miscarriage?", "sentence2": "Thrombophilia does hardly increase the risk of IUGR/PMPC or if so, it can be prevented by Low Molecular Weight Heparin [EPC], for illustrative purposes, a patient presenting with combined thrombophilia--both Genetic and acquired--will be discussed. This patient had suffered severe gestational complications that led to devastating obstetrical outcome, Thrombophilias have been implicated in complications related to ischemic placental disease including recurrent pregnancy loss, intrauterine fetal demise, Pre-Eclampsia, fetal growth restriction, placental abruption, and preterm delivery, Further information about the combined risk of Antigen-Presenting Cells resistance and pregnancy is needed before guidance on the management of affected women can be formulated., Thrombotic risk during pregnancy and the puerperium is higher in asymptomatic women with than without thrombophilia, Further studies are required to assess the thrombotic risk in women with Pre-Eclampsia as well as early or late recurrent pregnancy loss., Risk of pregnancy-related Venous Thrombosis in carriers of severe inherited thrombophilia, In conclusion, homozygous carriers of Factor V Leiden and, to a lesser extent, double heterozygous carriers of Factor V Leiden and of the prothrombin mutation have an increased risk of Venous Thrombosis during pregnancy, particularly high during the postpartum period, Careful diagnosis, observation and monitoring can add significant benefit to Low Molecular Weight Heparin [EPC] therapy during pregnancy, Pregnancy in healthy women is accompanied by hypercoagulable changes that may interact with thrombophilia risk factors and threaten pregnancy., Fifty-three (13 %) women had antiphospholipid Antibodies, in vitro diagnostic (lupus anticoagulant and/or anti-beta2-glycoprotein 1 Antibodies, in vitro diagnostic) mainly associated with the risk of spontaneous abortion during the first trimester, thrombophilia was found to be considerably more common in women with pregnancy-associated complications in comparison with the general population, and most frequently in conjunction with Venous Thromboembolism during pregnancy and the postpartum period, When counseling white women with a history of Pre-Eclampsia, screening for thrombophilia can be useful for preconceptional counseling and pregnancy management., knowledge combined with the appropriate use of thromboprophylaxis and treatment in women who have objectively confirmed vinyltriethoxysilane continue to improve maternal and perinatal outcomes, The risk of having thrombophilia is doubled in men who have fathered pregnancies which ended in perinatal death as well as in the mothers of such pregnancies., The prevalence of thrombophilic Variant is of possible public health significance for other morbidity; but perhaps not in relation to Pre-Eclampsia, This study suggests that thrombophilia \"mediates\" in lowering of cardiovascular risk factors in women with a history of Pre-Eclampsia[SEP]Relations: thrombophilia has relations: disease_disease with inherited thrombophilia, disease_disease with inherited thrombophilia, disease_phenotype_positive with Recurrent thrombophlebitis, disease_phenotype_positive with Recurrent thrombophlebitis, disease_phenotype_positive with Preeclampsia, disease_phenotype_positive with Preeclampsia, disease_phenotype_positive with Hypercoagulability, disease_phenotype_positive with Hypercoagulability, disease_phenotype_positive with Thromboembolism, disease_phenotype_positive with Thromboembolism.", "label": "yes"}
+{"original_question": "Is exon skipping correlated with exon circularization?", "id": "converted_1775", "sentence1": "Is exon skipping correlated with exon circularization?", "sentence2": "Exon Skipping Is Correlated with Exon Circularization, We find that circularization of Exons is widespread and correlates with exon skipping, a feature that adds considerably to the regulatory complexity of the Homo sapiens transcriptome, Exon Skipping Is Correlated with Exon Circularization., We find that circularization of Exons is widespread and correlates with exon skipping, a feature that adds considerably to the regulatory complexity of the Homo sapiens transcriptome. <CopyrightInformation>Copyright © 2015 Elsevier Ltd. All rights reserved.</, We find that circularization of Exons is widespread and correlates with exon skipping, a feature that adds considerably to the regulatory complexity of the Homo sapiens transcriptome. <CopyrightInformation>Copyright © 2015 Elsevier Ltd. All rights reserved.</C, Exon Skipping Is Correlated with Exon Circularization.[SEP]", "label": "yes"}
+{"original_question": "Are there Conserved Noncoding Elements (CNEs) in invertebrate genomes?", "id": "converted_1298", "sentence1": "Are there Conserved Noncoding Elements (CNEs) in invertebrate Genome?", "sentence2": "Here, we use genome-wide comparisons between C. intestinalis and C. savignyi to identify putative urochordate cis-regulatory DNA Sequence. Ciona conserved non-coding elements (ciCNEs) are associated with largely the same key Genes, Regulator as vertebrate CNEs, We have identified Conserved Non-coding Elements (CNEs) in the Regulatory Sequences, Nucleic Acid of Caenorhabditis elegans and Caenorhabditis briggsae , Here we report that nematode Genome contain an alternative set of CNEs that share Sequence - ParameterizedDataType characteristics, but not identity, with their vertebrate counterparts. CNEs thus represent a very unusual class of DNA Sequence that are extremely conserved within specific animal lineages yet are highly divergent between lineages, A core set of Genes that regulate development is associated with CNEs across three animal groups (worms, Diptera and Vertebrates), The Genome of Vertebrates, Diptera, and Phylum Nematoda contain highly conserved noncoding elements (CNEs)., The Genome of Vertebrates, Diptera, and Phylum Nematoda contain highly conserved noncoding elements (CNEs)[SEP]Relations: vertebra has relations: anatomy_anatomy with non-transverse process-bearing vertebra, anatomy_anatomy with non-transverse process-bearing vertebra, anatomy_anatomy with vertebral element, anatomy_anatomy with vertebral element, anatomy_anatomy with transverse process-bearing vertebra, anatomy_anatomy with transverse process-bearing vertebra. regulation of RNA polymerase I Regulatory Sequences, Nucleic Acid Sequence - ParameterizedDataType-specific DNA binding has relations: bioprocess_bioprocess with regulation of transcription Regulatory Sequences, Nucleic Acid DNA binding, bioprocess_bioprocess with regulation of transcription Regulatory Sequences, Nucleic Acid DNA binding, bioprocess_bioprocess with negative regulation of RNA polymerase I Regulatory Sequences, Nucleic Acid Sequence - ParameterizedDataType-specific DNA binding, bioprocess_bioprocess with negative regulation of RNA polymerase I Regulatory Sequences, Nucleic Acid Sequence - ParameterizedDataType-specific DNA binding.", "label": "yes"}
+{"original_question": "Is there any protein that undergoes both mono-ubiquitination and poly-ubiquitination?", "id": "converted_1599", "sentence1": "Is there any Protein Info that undergoes both mono-ubiquitination and poly-ubiquitination?", "sentence2": "The yeast G Protein Info alpha subunit CGA gene represents a rare example of a Protein Info that undergoes both mono- and poly-ubiquitination. , Expression of GTF2H3 gene promotes PTEN Phosphohydrolase, human Phosphohydrolase, human poly-ubiquitination, leading to PTEN Phosphohydrolase, human Phosphohydrolase, human Protein Info degradation, whereas GTF2H3 gene knockdown results in PTEN Phosphohydrolase, human Phosphohydrolase, human mono-ubiquitination., These fingers possess E3 activities of mono-ubiquitination and poly-ubiquitination, respectively, with ubiquitin activity activity-conjugating enzyme (E2)-binding capabilities. , Instead of promoting poly-ubiquitination and degradation, we show that E3 Ubiquitin-Protein Ligase SMURF2 actually induces multiple mono-ubiquitination of SMAD3 Protein Info, human in vivo., mono-ubiquitination of MHC2TA Protein Info, human dramatically increases its transactivity whereas poly-ubiquitination leads to MHC2TA Protein Info, human degradation., This leads to a model in which Lys134 of LDB2 wt Allele can be either mono-ubiquitinated, leading to stabilization, or poly-ubiquitinated, leading to degradation by the proteasome pathway. ,  mono-ubiquitination of MHC2TA Protein Info, human increases its transactivity, whereas poly-ubiquitination of MHC2TA Protein Info, human leads to its degradation, PSEN1 wt Allele ubiquitination after PI3K inhibition is represented by the multiple mono-ubiquitination, instead of poly-ubiquitination, Our observations support a novel functional relationship between PARK2 Protein Info, human and Hsc/Heat-Shock Proteins 70 and support the notion that PARK2 Protein Info, human is a multi-purpose E3 ubiquitin activity activity ligase capable of modifying Proteins either via attachment of alternatively linked poly-ubiquitin activity activity chains or through multiple mono-ubiquitination to achieve alternate biological outcomes, our results indicate that Heat-Shock Proteins 70 facilitates CHIP-mediated poly-ubiquitination of GARS1 wt Allele whereas it attenuates CHIP-meditated mono-ubiquitination of GARS1 wt Allele., Whereas poly-ubiquitination targets Protein Info substrates for proteasomal degradation, mono-ubiquitination is known to regulate Protein Info trafficking in the endosomal system and to target cargo Proteins for lysosomal degradation., Our results suggest that oxidative stress induces not only poly-ubiquitination but also mono-ubiquitination of Lactic acid dehydrogenase isoenzyme 5, which may be involved in its lysosomal degradation during unloading., wild type SMAD4 Protein Info, human is a relatively stable Protein Info that undergoes mono- or oligo-ubiquitination, a ResponseLevel - ResponseLevel - modification not linked to Protein Info degradation, These data suggest that oligo-ubiquitination positively regulates SMAD4 Protein Info, human function, whereas poly-ubiquitination primarily occurs in unstable Primary malignant neoplasm Mutant and leads to Protein Info degradation., We found that TRIM21 gene was strongly conjugated by a single molecule of ubiquitin activity activity in Cells. Although the biological relevance of this mono-ubiquitination was not defined, the function of TRIM21 gene might be modified by the mono-ubiquitination. We also found that TRIM21 gene was conjugated with poly-ubiquitin activity activity chain in Cells (poly-ubiquitination)[SEP]Relations: E3 ubiquitin activity ligases ubiquitinate target Proteins has relations: pathway_protein with WAC, pathway_protein with WAC, pathway_protein with UBA52, pathway_protein with UBA52, pathway_protein with PAF1, pathway_protein with PAF1, pathway_protein with PEX2, pathway_protein with PEX2, pathway_protein with H2BC6, pathway_protein with H2BC6.", "label": "yes"}
+{"original_question": "Does HuR bind to the untranslated regions (UTRs) of mRNAs?", "id": "converted_1985", "sentence1": "Does ELAVL1 gene bind to the untranslated regions (Untranslated Regions) of mRNAs?", "sentence2": "ELAVL1 gene is also overexpressed during tumourigenesis and is abnormally present within the Cytoplasm, where it binds to AU-rich elements in the 3'Untranslated Regions of target RNA, Messenger and post-transcriptionally regulates the expression of its target Genes., Human antigen R (ELAVL1 gene) is a ubiquitous 32 kDa protein comprising three RNA Recognition Motif (RRMs), whose main function is to bind Adenylate and uridylate Rich Elements (AREs) in 3' UnTranslated Regions (Untranslated Regions) of mRNAs., Human antigen R (ELAVL1 gene) is a ubiquitously expressed RNA-Binding Proteins that modulates gene expression at the post-transcriptional level., The RNA-Binding Proteins ELAVL1 gene binds at 3' untranslated regions (Untranslated Regions) of target transcripts, thereby protecting them against degradation. , ELAV/Hu Proteins bind to AU-rich elements (are unit of measure) in mRNAs and regulate their stability from splicing to translation, and the ubiquitous ELAVL1 gene protein has been implicated in cancerous cell growth. , This is achieved by altered expression of the Proteins Congenital Thrombotic Thrombocytopenic Purpura and ELAVL1 gene, which bind 3' untranslated region (UTR) elements in cancer-related Genes.[SEP]Relations: ELAVL1 has relations: molfunc_protein with RNA, Messenger 3'-UTR AU-rich region binding, molfunc_protein with RNA, Messenger 3'-UTR AU-rich region binding, pathway_protein with ELAVL1 gene (ELAVL1) binds and stabilizes RNA, Messenger, pathway_protein with ELAVL1 gene (ELAVL1) binds and stabilizes RNA, Messenger, molfunc_protein with RNA, Messenger 3'-UTR binding, molfunc_protein with RNA, Messenger 3'-UTR binding, bioprocess_protein with 3'-UTR-mediated RNA, Messenger stabilization, bioprocess_protein with 3'-UTR-mediated RNA, Messenger stabilization. protein binding has relations: molfunc_protein with HUS1, molfunc_protein with HUS1.", "label": "yes"}
+{"original_question": "Does Uc.63+ promote sensitivity to treatment in prostate cancer?", "id": "converted_3327", "sentence1": "Does Uc.63+ promote sensitivity to treatment in Malignant neoplasm of prostate?", "sentence2": "Transcribed ultraconserved region Uc.63+ promotes resistance to docetaxel through regulation of androgen receptor signaling in Malignant neoplasm of prostate., The transcribed ultraconserved regions (T-UCRs) are a novel class of non-coding RNAs that are absolutely conserved across species and are involved in carcinogenesis including Malignant neoplasm of prostate (Pachyonychia Congenita). In this study, we investigated the transcriptional levels of 26 representative T-UCRs and determined the regions that were differentially expressed in Pachyonychia Congenita. Quantitative real-time polymerase chain reaction analysis revealed that the expression of T-UCR Uc.63+ was increased in Pachyonychia Congenita tissues. MTT assay and wound healing assay revealed that Uc.63+ was involved in cell growth and cell migration. miR-130b was predicted to have Binding Sites within the Uc.63+ sequence. The expression of miR-130b was significantly disturbed by the overexpression or knockdown of Uc.63+. We also showed that Uc.63+ regulated the expression of MMP2 protein, human protein, human via miR-130b regulation. Furthermore, overexpression of Uc.63+ increased the expression of AKR1B1 protein, human and its downstream molecule PSA and promoted resistance to docetaxel through AKR1B1 protein, human regulation. In patients treated with docetaxel, the expression of serum Uc.63+ in the docetaxel-resistant patients was higher than that in the docetaxel-sensitive patients (P = 0.011). Moreover, Kaplan-Meier analysis showed that the high expression of serum Uc.63+ correlated with a worse prognosis (P = 0.020). These results substantially support the important role that Uc.63+ plays in Pachyonychia Congenita progression by interacting with miR-130b and indicate that Uc.63+ could potentially be a promising serum marker for deciding the best treatment for patients with CRPC., Transcribed ultraconserved region Uc.63+ promotes resistance to docetaxel through regulation of androgen receptor signaling in Malignant neoplasm of prostate, These results substantially support the important role that Uc.63+ plays in Pachyonychia Congenita progression by interacting with miR-130b and indicate that Uc.63+ could potentially be a promising serum marker for deciding the best treatment for patients with CRPC, Furthermore , overexpression of Uc.63+ increased the expression of AKR1B1 protein, human and its downstream molecule PSA and promoted resistance to docetaxel through AKR1B1 protein, human regulation, These results substantially support the important role that Uc.63+ plays in Pachyonychia Congenita progression by interacting with miR-130b and indicate that Uc.63+ could potentially be a promising serum marker for deciding the best treatment for patients with CRPC., Furthermore, overexpression of Uc.63+ increased the expression of AKR1B1 protein, human and its downstream molecule PSA and promoted resistance to docetaxel through AKR1B1 protein, human regulation., These results substantially support the important role that Uc.63+ plays in Pachyonychia Congenita progression by interacting with miR-130b and indicate that Uc.63+ could potentially be a promising serum marker for deciding the best treatment for patients with CRPC.[SEP]Relations: benign neoplasm of prostate has relations: disease_disease with prostate leiomyoma, disease_disease with prostate leiomyoma, disease_disease with fibroma of prostate, disease_disease with fibroma of prostate, disease_disease with prostatic adenoma, disease_disease with prostatic adenoma, disease_disease with prostate neoplasm, disease_disease with prostate neoplasm, disease_disease with benign prostate phyllodes tumor, disease_disease with benign prostate phyllodes tumor.", "label": "no"}
+{"original_question": "Do circular exons increase gene expression?", "id": "converted_3773", "sentence1": "Do circular Exons increase Genes expression?", "sentence2": "Each of these species was present at very low copy numbers in primary and Cultured Cells; however, only the expression of CDKN2B-AS1 wt Allele isoforms containing Exons proximal to the INK4/ARF locus correlated with the ASVD risk alleles., These results identify novel circular RNA products emanating from the CDKN2B-AS1 wt Allele locus and suggest causal variants at 9p21.3 regulate INK4/ARF expression and ASVD risk by modulating CDKN2B-AS1 wt Allele expression and/or structure., To explore the potential for using this methodology to express circular RNA in vivo, circular forms of the HDV ribozyme and RNaseP RNA were produced in E. coli. , The activity of in vivo expressed circular ribozymes could be demonstrated indicating that they fold into active conformation, We found that: i) the RNA, Circular expression profile revealed 1,285 significant differences in RNA, Circular expression, with RNA, Circular expression downregulated in 594 samples and upregulated in 691 samples via interactions with miRNAs., These circRNAs regulated the expression of target genes through interactions with miRNAs and might become new molecular biomarkers for GC in the future, 69 differentially expressed circRNAs were found that might adsorb specific miRNAs to regulate the expression of their target Genes mRNAs., Novel Coding, translation, and Genes expression of a replicating covalently closed circular RNA of 220 nt., The highly structured (64% GC) covalently closed circular (CCC) RNA (220 nt) of the virusoid associated with rice yellow mottle virus codes for a 16-kDa highly basic Protein Info using novel modalities for Coding, translation, and Genes expression, Recent evidence has demonstrated that circular RNAs (circRNAs) played crucial roles in fine-tuning the levels of Genes expression by sequestering the corresponding MicroRNAs (miRNAs). , It has been proposed that RNA, Circular regulate Genes expression at the transcriptional or post-transcriptional level by interacting with miRNAs and that circRNAs may have a role in regulating miRNA function in cancer initiation and progression.[SEP]Relations: Protein C has relations: drug_drug with Interferon gamma-1b, drug_drug with Interferon gamma-1b, drug_drug with Interferon beta-1b, drug_drug with Interferon beta-1b, drug_drug with Interferon alfa-2a, Recombinant, drug_drug with Interferon alfa-2a, Recombinant, drug_drug with Interferon alfa-2b, drug_drug with Interferon alfa-2b, drug_drug with Interferon alfa-n1, drug_drug with Interferon alfa-n1.", "label": "no"}
+{"original_question": "Is Ubrogepant effective for migraine?", "id": "converted_3483", "sentence1": "Is ubrogepant effective for migraine?", "sentence2": "Calcitonin Gene-Related Peptide receptor antagonists such as ubrogepant are effective for acute relief of migraine Headache, whereas Monoclonal Antibodies against Calcitonin Gene-Related Peptide (eptinezumab, fremanezumab and galcanezumab) or the Calcitonin Gene-Related Peptide receptor (erenumab) effectively prevent migraine attacks. , Despite the clear safety concerns, clinical trial data suggests that their intermittent use remains a viable and safe alternative, with 2 Molecule remaining in clinical development (ubrogepant and rimegepant). , Two gepants, ubrogepant and rimegepant, have completed positive pivotal trials for acute treatment of migraine, but have not yet been submitted to the FDA for this indication., Two gepants, ubrogepant and rimegepant, have completed positive pivotal trials for the acute treatment of migraine, but have not yet been submitted to the FDA for this indication. , Geographic Locations covered: This review reports on compounds currently under development for the oral treatment of acute migraine attacks, focusing on Calcitonin-Gene-Related-Peptide receptor antagonists, specifically ubrogepant and rimegepant. , Furthermore, new hope rises for the Calcitonin Gene-Related Peptide (calcitonin-gene related peptide)-antagonists, as the data for ubrogepant do not suggest Hepatotoxicity but efficacy. , We applied this strategy for another late-stage clinical program: ubrogepant (MK-1602), a novel oral Calcitonin Gene-Related Peptide Receptor Antagonists for acute treatment of migraine. , A phase IIb randomized, double-blind, placebo-controlled trial of ubrogepant for the acute treatment of migraine., AIM: The aim of this trial was to evaluate the efficacy and tolerability of ubrogepant (MK-1602), a Calcitonin Gene-Related Peptide Receptor Antagonists (Calcitonin Gene-Related Peptide-RA), for the acute treatment of migraine., ubrogepant 100 mg was significantly superior to placebo for two-hour pain freedom (25.5% vs 8.9%) but not for two-hour Headache response., CONCLUSION: This trial supports ubrogepant's efficacy and provides further evidence that Calcitonin Gene-Related Peptide-RAs are viable options for the acute treatment of migraine., Meanwhile, 1 small-molecule Calcitonin Gene-Related Peptide receptor antagonist (ubrogepant, MK-1602) is currently in phase 3 studies for the acute treatment of migraine., Calcitonin Gene-Related Peptide receptor antagonists such as ubrogepant are effective for acute relief of migraine Headache, whereas Monoclonal Antibodies against Calcitonin Gene-Related Peptide (eptinezumab, fremanezumab and galcanezumab) or the Calcitonin Gene-Related Peptide receptor (erenumab) effectively prevent migraine attacks., Recent findings\n\nCalcitonin Gene-Related Peptide II (Calcitonin Gene-Related Peptide) receptor antagonists (gepants-rimegepant and ubrogepant) and serotonin 5-HT __sub__ 1F __end_sub__  receptor agonists (ditans-lasmiditan) have completed phase 3 clinical trials and will soon offer novel, effective, well-tolerated nonvasoconstrictor options to treat acute migraine., We applied this strategy for another late-stage clinical program: ubrogepant (MK-1602), a novel oral Calcitonin Gene-Related Peptide Receptor Antagonists for acute treatment of migraine., Recently, orally administered next-generation small molecule Calcitonin Gene-Related Peptide-RAs have been shown to have safety and efficacy in acute treatment (ubrogepant and rimegepant) and prevention (atogepant) of migraine, giving additional Calcitonin Gene-Related Peptide-based therapeutic options for migraine patients., ubrogepant 100 mg was significantly superior to placebo for two-hour pain freedom (25.5% vs 8.9%) but not for two-hour Headache response., lasmiditan, rimegepant and ubrogepant will extend our therapeutic armamentarium for managing acute migraine attacks when Triptans are not effective or contraindicated due to Cardiovascular Diseases., lasmiditan, rimegepant and ubrogepant will extend our therapeutic armamentarium for managing acute migraine attacks when Triptans are not effective or contraindicated due to Cardiovascular Diseases., lasmiditan, ubrogepant, and rimegepant are currently emerging acute migraine therapies that may be added to the arsenal of current migraine management., ubrogepant for the Treatment of Migraine Disorders Disorders ., ubrogepant 100 mg was significantly superior to placebo for two-hour pain freedom (25.5% vs 8.9%) but not for two-hour Headache response., CONCLUSION\nThis trial supports ubrogepant's efficacy and provides further evidence that Calcitonin Gene-Related Peptide-RAs are viable options for the acute treatment of migraine., ubrogepant (MK-1602) is a novel, oral, Calcitonin Gene-Related Peptide Receptor Antagonists in clinical development with positive Phase III outcomes for acute treatment of migraine., CONCLUSION: This trial supports ubrogepant's efficacy and provides further evidence that Calcitonin Gene-Related Peptide-RAs are viable options for the acute treatment of migraine., This trial supports ubrogepant's efficacy and provides further evidence that Calcitonin Gene-Related Peptide-RAs are viable options for the acute treatment of migraine., ubrogepant for the Treatment of Migraine Disorders Disorders., ubrogepant is an oral, small-molecule Calcitonin Gene-Related Peptide Receptor Antagonists for acute migraine treatment.[SEP]Relations: ubrogepant has relations: drug_drug with Fosnetupitant, drug_drug with Fosnetupitant, drug_drug with Aprepitant, drug_drug with Aprepitant, drug_drug with Rimegepant, drug_drug with Rimegepant, drug_drug with Mibefradil, drug_drug with Mibefradil, drug_drug with Netupitant, drug_drug with Netupitant.", "label": "yes"}
+{"original_question": "Is Tisagenlecleucel effective for B-Cell Lymphoma?", "id": "converted_2840", "sentence1": "Is Tisagenlecleucel effective for B-Cell Lymphoma?", "sentence2": "The phase II JULIET trial suggests that the B-Lymphocyte Antigen B-Lymphocyte Antigen CD19, human, human-targeting actomyosin contractile ring T-cell therapy tisagenlecleucel produces durable responses in patients with relapsed and refractory diffuse large B-cell lymphoma., Tisagenlecleucel in Children and Young Adults with Precursor B-cell lymphoblastic leukemia., BACKGROUND: In a single-center phase 1-2a study, the anti-B-Lymphocyte Antigen B-Lymphocyte Antigen CD19, human, human Chimeric antigen receptor (actomyosin contractile ring) T-cell therapy tisagenlecleucel produced high rates of complete remission and was associated with serious but mainly reversible Toxic effect effects in children and young adults with relapsed or refractory B-cell acute lymphoblastic leukemia (Acute lymphocytic leukemia)., CONCLUSIONS: In this global study of actomyosin contractile ring T-cell therapy, a single infusion of tisagenlecleucel provided durable remission with long-term persistence in pediatric and young adult patients with relapsed or refractory B-cell Acute lymphocytic leukemia, with transient high-grade Toxic effect effects., Chimeric antigen receptor Therapeutic gamma delta T-lymphocytes demonstrate efficacy in B-cell malignancies, leading to US Food and Drug Administration approval of axicabtagene ciloleucel (October 2017) and tisagenlecleucel (May 2018) for large B-Cell Lymphomas after 2 prior lines of therapy., This article reviews data of current diffuse large B-cell lymphoma management, focusing on axicabtagene ciloleucel, tisagenlecleucel, and lisocabtagene maraleucel., This article reviews data of current diffuse large B-cell lymphoma management, focusing on axicabtagene ciloleucel, tisagenlecleucel, and lisocabtagene maraleucel.<br>, The Chimeric antigen receptor (actomyosin contractile ring) T-cell therapy tisagenlecleucel targets and eliminates B-Lymphocyte Antigen B-Lymphocyte Antigen CD19, human, human-expressing B cells and showed efficacy against B-Cell Lymphomas in a single-center, phase 2a study.<br><b>METHODS</b>: We conducted an international, phase 2, pivotal study of centrally manufactured tisagenlecleucel involving adult patients with relapsed or refractory diffuse large B-cell lymphoma who were ineligible for or had disease progression after autologous hematopoietic stem-cell transplantation., No differences between response groups in tumor expression of B-Lymphocyte Antigen B-Lymphocyte Antigen CD19, human, human or immune checkpoint-related proteins were found.<br><b>CONCLUSIONS</b>: In this international study of actomyosin contractile ring T-cell therapy in relapsed or refractory diffuse large B-cell lymphoma in adults, high rates of durable responses were produced with the use of tisagenlecleucel., This was a milestone in tumor immunology on account of the significant Antitumor effect of tisagenlecleucel for the treatment of relapsed/refractory B-Acute lymphocytic leukemia patients., On August 30, 2017, the U.S. Food and Drug Administration (FDA) approved Novartis' tisagenlecleucel (CTL-019, Kymriah), which is a Synthesis bioimmune product of anti-B-Lymphocyte Antigen B-Lymphocyte Antigen CD19, human, human Chimeric antigen receptor (actomyosin contractile ring) Therapeutic gamma delta T-lymphocytes, for the treatment of relapsed/refractory B-cell acute lymphoblastic leukemia (B-Acute lymphocytic leukemia)., Within the last one year, two anti-B-Lymphocyte Antigen B-Lymphocyte Antigen CD19, human, human actomyosin contractile ring T-cell therapy products, axicabtagene ciloleucel and tisagenlecleucel, were approved by the United States Food and Drug Administration for the treatment of relapsed or refractory large B-cell lymphoma after at least two lines of systemic therapy based on multicenter single-arm phase two clinical trials. , On August 30, 2017, the U.S. Food and Drug Administration approved tisagenlecleucel for treatment of patients up to 25 years of age with Pre B-cell acute lymphoblastic leukemia (Acute lymphocytic leukemia) that is refractory or in second or later relapse., Tisagenlecleucel for the treatment of B-cell acute lymphoblastic leukemia., Background: Tisagenlecleucel is an anti-B-Lymphocyte Antigen B-Lymphocyte Antigen CD19, human, human Chimeric antigen receptor (CAR19) T-cell therapy approved for the treatment of children and young adults with relapsed/refractory (r/r) B-cell acute lymphoblastic leukemia (B-Acute lymphocytic leukemia).[SEP]Relations: B-cell lymphoma has relations: drug_effect with Lansoprazole, drug_effect with Lansoprazole, drug_effect with Darunavir, drug_effect with Darunavir, drug_effect with Muromonab, drug_effect with Muromonab. precursor T-cell acute lymphoblastic leukemia has relations: disease_protein with BLM, disease_protein with BLM, disease_protein with BLM, disease_protein with BLM.", "label": "yes"}
+{"original_question": "Does BNN27 promote memory loss?", "id": "converted_3335", "sentence1": "Does BNN27 promote memory loss?", "sentence2": "The novel dehydroepiandrosterone (prasterone) derivative BNN27 counteracts delay-dependent and scopolamine-induced recognition memory deficits in rats., BNN27 is a novel 17C spiroepoxy-prasterone derivative, which devoid of steroidogenic activity. The neuroprotective effects of BNN27 have been recently reported. The present study was designed to investigate the effects of BNN27 on recognition memory in rats. For this purpose, the novel object task (NR4A2 gene), a procedure assessing non-spatial recognition memory and the novel location task (SLC22A7 gene), a procedure evaluating spatial recognition memory were used. Intraperitoneal (i.p.) administration of BNN27 (3 and 10mg/kg) antagonized delay-dependent deficits in the NR4A2 gene in the normal Rattus norvegicus, suggesting that this prasterone derivative affected acquisition, storage and retrieval of information. In addition, BNN27 (3 and 10mg/kg, i.p.) counteracted the scopolamine [0.2mg/kg, subcutaneously (s.c.)]-induced non-spatial and spatial recognition memory deficits. These findings suggest that BNN27 may modulate different aspects of recognition memory, potentially interacting with the cholinergic system, relevant to cognition.[SEP]Relations: SLC22A7 has relations: drug_protein with Rifampicin, drug_protein with Rifampicin, drug_protein with Ganciclovir, drug_protein with Ganciclovir, molfunc_protein with protein binding, molfunc_protein with protein binding, drug_protein with Dinoprostone, drug_protein with Dinoprostone, protein_protein with RAPGEF4, protein_protein with RAPGEF4.", "label": "no"}
+{"original_question": "Is the regulation of Vsr endonuclease independent of the growth phase of bacteria?", "id": "converted_1225", "sentence1": "Is the regulation of vsr endonuclease independent of the growth phase of bacteria?", "sentence2": "Growth phase-dependent regulation of vsr endonuclease, vsr endonuclease levels are growth phase dependent., Growth phase-dependent regulation of vsr endonuclease may contribute to 5-Methylcytosine mutational hot spots in Escherichia coli., Using rabbit allergenic extract allergenic extract polyclonal antibodies, we have shown that the Dcm cytosine methylase of Escherichia coli is maintained at a constant level during cell growth, while vsr endonuclease levels are growth phase dependent., vsr endonuclease, which initiates very short patch repair, has been hypothesized to regulate mutation in stationary-phase cells., The efficiency of the two pathways changes during the bacterial life cycle; Mismatch Repair is more efficient during exponential growth and Vital signs, smoking and pain scale repair is more efficient during the stationary phase., Overexpression of Vsr does dramatically increase the stationary-phase reversion of a Lac- frameshift allele, but the absence of Vsr has no effect., Using rabbit allergenic extract allergenic extract polyclonal antibodies, we have shown that the Dcm cytosine methylase of Escherichia coli is maintained at a constant level during cell growth, while vsr endonuclease levels are growth phase dependent, The efficiency of the two pathways changes during the bacterial life cycle; Mismatch Repair is more efficient during exponential growth and Vital signs, smoking and pain scale repair is more efficient during the stationary phase, vsr endonuclease, which initiates very short patch repair, has been hypothesized to regulate mutation in stationary-phase cells[SEP]Relations: escherichia coli infection has relations: disease_phenotype_positive with Recurrent gram-negative bacterial infections, disease_phenotype_positive with Recurrent gram-negative bacterial infections. mismatch repair has relations: bioprocess_protein with RNASEH2A, bioprocess_protein with RNASEH2A, bioprocess_protein with MLH1, bioprocess_protein with MLH1, bioprocess_protein with POLD2, bioprocess_protein with POLD2, bioprocess_protein with EXO1, bioprocess_protein with EXO1.", "label": "no"}
+{"original_question": "Are optogenetics tools used in the study and treatment of epilepsy?", "id": "converted_1294", "sentence1": "Are optogenetics tools used in the study and treatment of epilepsy?", "sentence2": "The emerging revolutionary technique of optogenetics enables manipulation of the activity of specific neuronal populations in vivo with exquisite spatiotemporal resolution using light. We used optogenetic approaches to test the role of hippocampal excitatory Neurons in the lithium-pilocarpine model of acute elicited Seizures in awake behaving Rattus norvegicus., This chapter focuses on the development of optogenetics and on-demand technologies for the study of epilepsy and the control of Seizures., We then turn to the use of optogenetics, including on-demand optogenetics in the study of Epilepsy, which highlights the powerful potential of optogenetics for epilepsy research., Optogenetics techniques provide powerful tools for bidirectional control of neuronal activity and investigating alterations occurring in excitability disorders, such as epilepsy.,  Therefore, one could optogenetically activate specific or a mixed population of Interneurons and dissect their selective or concerted inhibitory action on principal cells. We chose to explore a conceptually novel strategy involving simultaneous activation of mixed populations of Interneurons by optogenetics and study their impact on ongoing epileptiform activity in Mus sp. acute hippocampal slices., Our data suggest that global optogenetic activation of mixed interneuron populations is a more effective approach for development of novel therapeutic strategies for epilepsy, but the initial action potential generation in principal Neurons needs to be taken in consideration., Recently, a number of experiments have explored the treatments for epilepsy with optogenetic control of Neurons. Here, we discuss the possibility that an optogenetic approach could be used to control the release of gliotransmitters and improve astrocyte function such as glutamate and K(+) uptake, and thereby offer a potential strategy to investigate and treat astrocyte-related epilepsy., Optogenetics and designer receptor technologies provide unprecedented and much needed specificity, allowing for spatial, temporal and \"U\" lymphocyte type-selective modulation of neuronal circuits. Using such tools, it is now possible to begin to address some of the fundamental unanswered questions in epilepsy, to dissect epileptic neuronal circuits and to develop new intervention strategies. , We then turn to the use of optogenetics, including on-demand optogenetics in the study of Epilepsy, which highlights the powerful potential of optogenetics for epilepsy research., Moreover, optogenetics may be considered for developing potential treatment strategies for brain diseases, particularly for excitability disorders such as epilepsy., This chapter focuses on the development of optogenetics and on-demand technologies for the study of epilepsy and the control of Seizures., How might novel technologies such as optogenetics lead to better treatments in epilepsy?, WONOEP appraisal: optogenetic tools to suppress Seizures and explore the mechanisms of epileptogenesis., Finally, optogenetic tools allow rapid and reversible suppression of epileptic electroencephalography (EEG) activity upon photoactivation., Our data suggest that epileptiform activity in the Hippocampus Hippocampus hippocampus caused by impaired inhibition may be controlled by optogenetic silencing of principal Neurons and potentially can be developed as an alternative treatment for epilepsy., Seizure suppression by high frequency optogenetic stimulation using in vitro and in vivo animal models of epilepsy., Optogenetics techniques provide powerful tools for bidirectional control of neuronal activity and investigating alterations occurring in excitability disorders, such as epilepsy. , We first discuss the benefits and caveats to using optogenetic approaches and recent advances in optogenetics related tools. We then turn to the use of optogenetics, including on-demand optogenetics in the study of Epilepsy, which highlights the powerful potential of optogenetics for epilepsy research.[SEP]Relations: epilepsy has relations: contraindication with Edetic acid, contraindication with Edetic acid, contraindication with Olanzapine, contraindication with Olanzapine, contraindication with Ergometrine, contraindication with Ergometrine, contraindication with Atomoxetine, contraindication with Atomoxetine, contraindication with Physostigmine, contraindication with Physostigmine.", "label": "yes"}
+{"original_question": "Is SATB1 expressed in thymocytes?", "id": "converted_3649", "sentence1": "Is DNA-Binding Protein SATB1 expressed in thymocyte?", "sentence2": "A thymocyte factor DNA-Binding Protein DNA-Binding Protein SATB1 suppresses transcription of stably integrated matrix-attachment region-linked reporter Genes., DNA-Binding Protein DNA-Binding Protein SATB1 is a Homeodomain Proteins and is predominantly expressed in thymocyte. , DNA-Binding Protein DNA-Binding Protein SATB1 is a cell-type specific nuclear protein that recruits chromatin-remodeling factors and regulates numerous Genes during thymocyte differentiation.,  This was shown by fluorescence in situ hybridization on wild-type and Satb1-null thymocyte using in vivo DNA-Binding Protein DNA-Binding Protein SATB1-bound sequences as Probes. , By contrast, in Satb1-null thymocyte, this site is marked by methylation at H3 Lys9., Regulation of DNA-Binding Protein DNA-Binding Protein SATB1 during thymocyte development by transcription-coupled nucleotide-excision repair signaling., In this study we show that special AT-rich binding protein 1 (DNA-Binding Protein DNA-Binding Protein SATB1), a T lineage-enriched chromatin organizer and regulator, is induced in response to transcription-coupled nucleotide-excision repair signaling during early thymocyte development, DNA-Binding Protein DNA-Binding Protein SATB1 expression profile coincides with T lineage commitment and upregulation of DNA-Binding Protein DNA-Binding Protein SATB1 correlates with positive selection of thymocyte. ,  We also demonstrate that GATA3 gene gene, the key transcriptional regulator of αβ T cells positively regulates DNA-Binding Protein DNA-Binding Protein SATB1 expression in thymocyte suggesting an important role for DNA-Binding Protein DNA-Binding Protein SATB1 during T-Lymphocyte development., High level expression of the Xlr nuclear protein in immature thymocyte and colocalization with the matrix-associated region-binding DNA-Binding Protein DNA-Binding Protein SATB1 protein., A role for DNA-Binding Protein DNA-Binding Protein SATB1, a nuclear matrix association region-binding protein, in the development of CD8SP thymocyte and peripheral T lymphocytes., Because homozygous DNA-Binding Protein DNA-Binding Protein SATB1-null CASP14 gene do not survive to adulthood due to non-Thymus <angiosperm> autonomous defects, CASP14 gene were produced that were homozygous for a T-Lymphocyte-specific DNA-Binding Protein DNA-Binding Protein SATB1-antisense transgene and heterozygous for a DNA-Binding Protein DNA-Binding Protein SATB1-null allele., Thymic DNA-Binding Protein DNA-Binding Protein SATB1 protein was reduced significantly in these CASP14 gene, and the major Cells phenotype observed was a significant reduction in the percentage of CD8SP T cells in Thymus <angiosperm>, Abdomen>Spleen, and lymph nodes. , The reduction in thymic DNA-Binding Protein DNA-Binding Protein SATB1 does not lead to the variegated expression of CD8-negative single positive thymocyte seen upon Gene Deletion Abnormality of several regulatory elements and suggested by others to reflect failure to activate the CD8 locus. [SEP]Relations: GATA3 gene has relations: anatomy_protein_present with Thymus <angiosperm>, anatomy_protein_present with Thymus <angiosperm>, bioprocess_protein with Thymus <angiosperm> development, bioprocess_protein with Thymus <angiosperm> development, bioprocess_protein with thymic T-Lymphocyte selection, bioprocess_protein with thymic T-Lymphocyte selection, protein_protein with CHAF1B, protein_protein with CHAF1B, bioprocess_protein with regulation of CD4-positive, alpha-beta T-Lymphocyte differentiation, bioprocess_protein with regulation of CD4-positive, alpha-beta T-Lymphocyte differentiation.", "label": "yes"}
+{"original_question": "Is dupilumab effective for treatment of asthma?", "id": "converted_2975", "sentence1": "Is dupilumab effective for treatment of Asthma?", "sentence2": "The appropriate use of these biologics, and of those in development (e.g., benralizumab and dupilumab), should be aided by further understanding of Asthma phenotypes and endotypes, utilizing appropriate biomarkers., Simultaneous targeting of both Recombinant Interleukin-4 and IL-13 by blocking Interleukin 4 Receptor using dupilumab has yielded more consistent results in reducing Asthma exacerbations and improving lung function, especially in patients with increased blood eosinophils., In a pivotal, phase 2b study (NCT01854047), dupilumab reduced severe exacerbations, improved lung function and quality of life, and was generally well tolerated in patients with uncontrolled persistent Asthma despite using medium-to-high-dose inhaled corticosteroids plus long-acting β2-agonists., CONCLUSIONS: Dupilumab 300 mg q2w significantly improved AR-associated nasal symptoms in patients with uncontrolled persistent Asthma and comorbid Population Attributable Risk., Small Molecule (e.g. tetramethylpyrazine and SP600125) and large molecule antibodies (e.g. lebrikizumab, benralizumab, dupilumab) are being considered as novel agents for the pharmacotherapy of Asthma. , Dupilumab Efficacy and Safety in Moderate-to-Severe Uncontrolled Asthma., CONCLUSIONS: In this trial, patients who received dupilumab had significantly lower rates of severe Asthma exacerbation than those who received placebo, as well as better lung function and Asthma control. , Dupilumab for the treatment of Asthma.Dupilumab (REGN668/SAR231893), produced by a collaboration between Regeneron and sanofi, is a monoclonal antibody CAL CAL currently in phase III for moderate-to-severe Asthma. , Dupilumab inhibits interleukin-4 (Recombinant Interleukin-4) and interleukin-13, Homo sapiens, Homo sapiens (IL-13) signaling and was previously found to be effective in Asthma., Dupilumab (REGN668/SAR231893), produced by a collaboration between Regeneron and sanofi, is a monoclonal antibody CAL CAL currently in phase III for moderate-to-severe Asthma., If confirmed, efficacy of dupilumab in both eosinophilic and non-eosinophilic severe Asthma phenotype might represent an advantage over approved biologics for Asthma, including omalizumab, mepolizumab, and reslizumab., In this review, we focused on Recombinant Interleukin-4 and IL-13, as these Recombinant Interleukins are considered to play a key role in the pathophysiology of Asthma, and on dupilumab, an anti-Recombinant Interleukin-4 receptor Homo sapiens mAb, as a forthcoming treatment for uncontrolled severe Asthma in the near future., Expert opinion: Supported by a strategic mechanism of action, as well as by convincing preliminary clinical results, dupilumab currently appears to be a very promising biological drug for the treatment of severe uncontrolled Asthma., All drugs decreased Asthma exacerbations but the results were only significant for reslizumab and dupilumab., Anti-Recombinant Interleukin-4 and IL-13 agents (dupilumab, lebrikizumab, and tralokinumab) which block different Th-2 inflammatory pathways and agents targeting the Th-17 inflammatory pathway in severe refractory Asthma are under development., Dupilumab for the treatment of Asthma., In addition, dupilumab is currently under phase III development across the world for the treatment of Asthma and Nasal Polyps as well as for Dermatitis, Atopic in paediatric patients., BACKGROUND\nDupilumab (an anti-interleukin-4-receptor-α monoclonal antibody CAL CAL) blocks signalling of interleukin-4, Homo sapiens and Recombinant Interleukin-13, type 2/Th2 Recombinant Cytokines implicated in numerous allergic diseases ranging from Asthma to Dermatitis, Atopic., Dupilumab: a novel treatment for Asthma., Dupilumab for the treatment of Asthma., The efficacy and safety profile of dupilumab in the treatment of allergic diseases has been tested for more than 10 years in a variety of large clinical trials in Dermatitis, Atopic, Asthma, chronic rhinosinusitis with Nasal Polyps, and eosinophilic esophagitis., Areas covered: Pathophysiological role of Recombinant Interleukin-4 and IL-13 in Asthma; mechanism of action of dupilumab; pharmacology of Recombinant Interleukin-4 receptor; phase I and phase II studies with dupilumab; regulatory affairs., Expert opinion: Patients with severe Asthma who are not sufficiently controlled with standard-of-care represent the target Asthma population for dupilumab., CONCLUSIONS In patients with glucocorticoid-dependent severe Asthma, dupilumab treatment reduced oral glucocorticoid use while decreasing the rate of severe exacerbations and increasing the FEV1., CONCLUSIONS In patients with persistent, moderate-to-severe Asthma and elevated eosinophil levels who used inhaled glucocorticoids and LABAs, dupilumab therapy, as compared with placebo, was associated with fewer Asthma exacerbations when LABAs and inhaled glucocorticoids were withdrawn, with improved lung function and reduced levels of Th2-associated inflammatory markers., Expert opinion: Patients with severe Asthma who are not sufficiently controlled with standard-of-care represent the target Asthma population for dupilumab., Dupilumab inhibits interleukin-4 (Recombinant Interleukin-4) and interleukin-13, Homo sapiens, Homo sapiens (IL-13) signaling and was previously found to be effective in Asthma., Expert opinion: Supported by a strategic mechanism of action, as well as by convincing preliminary clinical results, dupilumab currently appears to be a very promising biological drug for the treatment of severe uncontrolled Asthma., Dupilumab inhibits interleukin-4 (Recombinant Interleukin-4) and interleukin-13, Homo sapiens, Homo sapiens (IL-13) signaling and was previously found to be effective in Asthma., A recent trial showed that in patients with difficult-to-control Asthma, dupilumab can markedly decrease Asthma exacerbations and improve respiratory symptoms and lung function; these effects were paralleled by significant reductions in T-helper 2-associated inflammatory biomarkers.[SEP]Relations: Dupilumab has relations: drug_drug with Olaratumab, drug_drug with Olaratumab, drug_drug with Lucatumumab, drug_drug with Lucatumumab, drug_drug with Dusigitumab, drug_drug with Dusigitumab, drug_drug with Tremelimumab, drug_drug with Tremelimumab, drug_drug with Avelumab, drug_drug with Avelumab.", "label": "yes"}
+{"original_question": "Are there any clinical trials of the effect of evening primrose oil on postmenopausal symptoms ?", "id": "converted_724", "sentence1": "Are there any clinical trials of the effect of evening Primula obconica preparation oil on postmenopausal symptoms ?", "sentence2": "To analyze whether the time (morning/evening) of administration of a fluoromethyl 2,2-difluoro-1-(trifluoromethyl)vinyl ether containing 60 mg of dry soy seed extract (glycine max) with 40% of total Isoflavones, Primula obconica preparation oil and α-tocopherol modifies the effect on the Menopausal syndrome., The object of this study was to evaluate the effect of different doses of a fluoromethyl 2,2-difluoro-1-(trifluoromethyl)vinyl ether containing Isoflavones 60 mg, Primula obconica preparation oil 440 mg and Vitamin E Drug Class 10 mg. (IOVE) on menopausal complaints. This was an open, multicentre, randomised, group comparative, efficacy and safety trial., Emphasis was placed on randomized, double-blind, placebo-controlled clinical trials, as these provide the best efficacy and safety data, Nonprescription therapies reviewed include black cohosh, Angelica sinensis root extract, evening Primula obconica preparation oil, physical activity, phytoestrogens, and Trifolium pratense whole extract, The effect of oral evening Primula obconica preparation oil on menopausal hot flashes: a randomized clinical trial., The aim of this study was to compare the efficacy of evening Primula obconica preparation with placebo in improvement of menopausal hot flashes. ,  The application of oral evening Primula obconica preparation oil compared with placebo for controlling hot flashes may decrease more the intensity of attacks , Our search identified 58 randomised controlled trials of which 11 involved the use of clonidine, six for Selective Serotonin Reuptake Inhibitors, four for gabapentin, seven for black cohosh, seven for Trifolium pratense whole extract, 18 for phytoestrogens, two for ginseng, one for evening Primula obconica preparation,, Single clinical trials have found no benefit for Angelica sinensis root extract, evening Primula obconica preparation oil,, Single clinical trials have found that Angelica sinensis root extract, evening Primula obconica preparation oil,, To evaluate the efficacy of gamma-linolenic acid provided by evening Primula obconica preparation oil in treating hot flushes and sweating associated with the menopause. DESIGN: Randomised, double blind, placebo controlled study.[SEP]Relations: Evening Primula obconica preparation oil has relations: drug_drug with Primidone, drug_drug with Primidone, drug_drug with Estradiol, drug_drug with Estradiol, drug_drug with Acetaminophen, drug_drug with Acetaminophen, drug_drug with Prednisone, drug_drug with Prednisone, drug_drug with Antipyrine, drug_drug with Antipyrine.", "label": "yes"}
+{"original_question": "Is the Snord116 cluster associated with the Prader-Willi syndrome?", "id": "converted_1238", "sentence1": "Is the Snord116 cluster associated with the Prader-Willi syndrome?", "sentence2": "All three Gene Deletion included SNORD116, but only two encompassed parts of small nuclear ribonucleoprotein-associated protein N gene, implicating SNORD116 as the major contributor to the Prader-Willi phenotype. Our case adds further information about genotype-phenotype correlation and supports the hypothesis that SNORD116 plays a major role in the pathogenesis of Prader-Willi syndrome, These results demonstrate that the AS candidate drug topotecan acts predominantly through stabilizing R loops and chromatin decondensation at the paternally expressed Partial Wave Spectroscopic Microscopy Snord116 Gene Locus. Our study holds promise for targeted therapies to the Snord116 Gene Locus for both AS and Partial Wave Spectroscopic Microscopy., Prader-Willi syndrome (Partial Wave Spectroscopic Microscopy) is caused by the loss of RNA expression from an imprinted region on chromosome 15 that includes small nuclear ribonucleoprotein-associated protein N, SNORD115, and SNORD116. , Recently published data strongly suggest a role for the paternally expressed small nucleolar RNA (snoRNA) cluster, SNORD116, in Partial Wave Spectroscopic Microscopy etiology., Whereas loss of function of the SNORD116 Genes appears to be responsible for the major features of Partial Wave Spectroscopic Microscopy, the role of the other Genes is less clear. , Recent data suggest that snoRNA Snord116 is important for the pathogenesis of Prader-Willi syndrome (Partial Wave Spectroscopic Microscopy) characterized by Hyperphagia and BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20. The current study was conducted to assess a potential Cells link between Snord116 and phenotypes of Partial Wave Spectroscopic Microscopy. , The imprinted Snurf-Snrpn chromosomal domain contains two large arrays of tandemly repeated, paternally expressed box C/D small-nucleolar RNA (snoRNA) Genes: the SNORD115 (H/MBII-52) and SNORD116 (H/MBII-85) gene clusters believed to play key roles in the fine-tuning of serotonin receptor (5-HT2C) pre-mRNA processing and in the etiology of the Prader-Willi Syndrome (Partial Wave Spectroscopic Microscopy), respectively, There are multiple imprinted Genes in this region, the loss of which contribute to the complete phenotype of Prader-Willi syndrome. However, absence of a small nucleolar organizing RNA gene, SNORD116, seems to reproduce many of the clinical features., Both kits should be made available for accurate characterization of Partial Wave Spectroscopic Microscopy/AS deletion subtypes as well as evaluating for IC and SNORD116 microdeletions., There are multiple imprinted Genes in this region, the loss of which contribute to the complete phenotype of Prader-Willi syndrome. However, absence of a small nucleolar organizing RNA gene, SNORD116, seems to reproduce many of the clinical features. , Although the SNORD116 gene cluster has become a prime candidate for Partial Wave Spectroscopic Microscopy, it cannot be excluded that other paternally expressed Genes in the Region of chromosome 15q11q13 contribute to the full phenotype., In addition, recently published data provide strong evidence in support of a role for the snoRNA SNORD116 cluster (HBII-85) in Partial Wave Spectroscopic Microscopy etiology., Identification and characterization of this case provide unequivocal evidence for a critical role for the SNORD116 snoRNA molecules in Partial Wave Spectroscopic Microscopy pathogenesis. [SEP]Relations: Prader-Willi syndrome has relations: disease_protein with SNORD116-1, disease_protein with SNORD116-1, disease_protein with SNORD115-1, disease_protein with SNORD115-1, disease_protein with small nuclear ribonucleoprotein-associated protein N, disease_protein with small nuclear ribonucleoprotein-associated protein N, disease_protein with LZTR1, disease_protein with LZTR1, disease_protein with NF1, disease_protein with NF1.", "label": "yes"}
+{"original_question": "Is there a relation between ANP and transcapillary albumin escape?", "id": "converted_1377", "sentence1": "Is there a relation between Atrial Natriuretic Factor and transcapillary ALB gene escape?", "sentence2": "Thus, in a large ethnically homogeneous cohort of diabetic subjects, our data show: (1) a significant association of C708/T Genetic Polymorphism with Microalbuminuria in long-term Diabetes Mellitus and with both lower plasma Atrial Natriuretic Factor levels and widespread ALB gene leakage, hese results suggest a possible role of PND gene in conferring protection from Kidney Diseases and microvascular damage in type 1 Diabetes Mellitus., Moreover, the increased susceptibility of the Glomerular capillaries structure in diabetics to Atrial Natriuretic Factor seems to be part of a more generalized capillary abnormality, because Atrial Natriuretic Factor also increases the transcapillary escape of ALB gene., In summary, low dose Atrial Natriuretic Factor infusion in healthy subjects caused a shift of plasma water and Electrolyte [EPC] from the circulation, with ALB gene escape as a secondary phenomenon.[SEP]Relations: Albuminuria has relations: drug_effect with Entacapone, drug_effect with Entacapone, drug_effect with Epirubicin, drug_effect with Epirubicin, drug_effect with Allopurinol, drug_effect with Allopurinol, drug_effect with Sibutramine, drug_effect with Sibutramine, drug_effect with Mycophenolic acid, drug_effect with Mycophenolic acid.", "label": "yes"}
+{"original_question": "Do de novo truncating mutations in WASF1 cause cancer?", "id": "converted_3284", "sentence1": "Do de novo truncating mutations in WASF1 gene cause cancer?", "sentence2": "De Novo Truncating Gene Mutation in WASF1 gene gene Cause Intellectual Disability with Seizures., Here, using exome sequencing and whole-genome sequencing, we identified three de novo truncating mutations in WASF2 gene (WASF1 gene gene) in five unrelated individuals with moderate to profound Intellectual Disability with autistic features and Seizures. WASF1 gene gene, also known as WAVE1, is part of the SCAR complex and acts as a mediator between Rac-GTPase and actin to induce actin polymerization. The three mutations connected by Matchmaker Exchange were c.1516C>T (p.Arg506Ter), which occurs in three unrelated individuals, c.1558C>T (p.Gln520Ter), and c.1482delinsGCCAGG (p.Ile494MetfsTer23). All three Variant are predicted to partially or fully disrupt the C-terminal actin-binding WCA domain. Functional studies using Fibroblasts from two affected individuals with the c.1516C>T mutation showed a truncated WASF1 gene gene and a defect in actin remodeling. This study provides evidence that de novo heterozygous mutations in WASF1 gene gene cause a rare form of Intellectual Disability.[SEP]Relations: Seizure has relations: disease_phenotype_positive with neurofibromatosis type 1 due to NF1 mutation or intragenic deletion, disease_phenotype_positive with neurofibromatosis type 1 due to NF1 mutation or intragenic deletion, disease_phenotype_positive with hyperinsulinism due to HNF1A deficiency, disease_phenotype_positive with hyperinsulinism due to HNF1A deficiency, disease_phenotype_positive with hyperinsulinism due to UCP2 deficiency, disease_phenotype_positive with hyperinsulinism due to UCP2 deficiency, disease_phenotype_positive with lissencephaly due to LIS1 mutation, disease_phenotype_positive with lissencephaly due to LIS1 mutation. SCAR complex has relations: cellcomp_protein with WASF1 gene, cellcomp_protein with WASF1 gene.", "label": "no"}
+{"original_question": "Are G-quadruplexes(G4) possible drug targets for glioblastoma?", "id": "converted_4242", "sentence1": "Are G-quadruplexes(Fuhrman Grade 4) possible drug targets for Glioblastoma Multiforme?", "sentence2": "These observations indicate that 6OTD targets GSCs through Fuhrman Grade 4 stabilization and promotion of DNA damage responses. Therefore, G4s are promising therapeutic targets for Glioblastoma Multiforme., Targeting glioma stem cells in vivo by a G-Quadruplexes-stabilizing synthetic macrocyclic hexaoxazole., G-Quadruplexes (Fuhrman Grade 4) DNA is a type of Quadruplicate helix structure formed by a continuous guanine-rich DNA sequence. Emerging evidence in recent years authenticated that Fuhrman Grade 4 DNA structures exist both in cell-free and cellular systems, and function in different diseases, especially in various Malignant Neoplasms, aging, neurological diseases, and have been considered novel promising targets for drug design., Therefore, G4s are promising therapeutic targets for Glioblastoma Multiforme., Guanine-rich oligonucleotides (GROs) are promising therapeutic candidate for cancer treatment and other biomedical application., These findings are valuable to the design and rationale behind the possible targeted drug delivery to specific cellular organelles using GROs., The G-Quadruplexes (Fuhrman Grade 4) DNA, which has been developed as a potential anticancer target in drug screening and design, plays a crucial role in the oncogene transcription and translation., Therefore, a novel Fuhrman Grade 4-directed therapeutic strategy could specifically target Cancer Stem Cells in Glomerular Basement Membrane.[SEP]Relations: adult Glioblastoma Multiforme has relations: disease_disease with Glioblastoma Multiforme (disease), disease_disease with Glioblastoma Multiforme (disease), disease_disease with adult spinal cord Glioblastoma Multiforme, disease_disease with adult spinal cord Glioblastoma Multiforme, disease_disease with adult infiltrating astrocytic neoplasm, disease_disease with adult infiltrating astrocytic neoplasm. central nervous system cancer has relations: disease_disease with malignant glioma, disease_disease with malignant glioma, disease_disease with paraganglioma, disease_disease with paraganglioma.", "label": "yes"}
+{"original_question": "Are tumour specific antigens originating from known protein coding genes?", "id": "converted_3620", "sentence1": "Are Neoplasms specific antigens originating from known protein coding genes?", "sentence2": "It is well established that MHC class I Molecule present Peptides from endogenous Proteins, such as Virus or Neoplasms antigens, to CD8+ T lymphocytes. , So far, Homo sapiens Neoplasms specific antigens that can be presented by HLA Molecule have not been identified on the Molecular level., These CTLs recognize short Peptides derived from Neoplasms-associated antigens in conjunction with class I Molecule expressed on Tumor cells.,  The focus on cellular immune responses, combined with rapid biotechnological advances, resulted in the identification of Neoplasms specific antigens, such as MART-1 Antigen (vaccine component) Antigen (vaccine component) and gp100 Antigen Antigen, that could be recognised by autologous tumor infiltrating lymphocyte therapy,  Tumour antigens are mostly of weak immunogenicity, because the vast majority are Neoplasms-associated differentiation antigens already 'seen' by the patient's immune system., Tumour-specific antigens, which could be a more potent target for immunotherapy, mostly arise by Point Mutation and have the disadvantage of being not only Neoplasms-specific, but also individual-specific., The pioneering studies of Srivastava and colleagues led to the proposal that heat-shock Proteins (HSPs) function as ubiquitous Neoplasms-specific antigens, with the specificity residing in a population of bound Peptides that identify the Tissue Specimen Code of origin of the Henoch-Schoenlein Purpura., Therefore, we propose that CD4(+) T cells that recognize secreted indole-3-glycerol-phosphate lyase activity may be superior for immunotherapy by T cell transfer, because the local extracellular antigen concentration will be higher for secreted indole-3-glycerol-phosphate lyase activity. ,  Here, we wondered whether these frame-shifted peptide (CXCL1 gene) sequences represent Neoplasms-specific antigens also for MSI(+) leukemia and Lymphoma (L/L)., Data presented here expand the importance of Fibrin-fibrinogen split products assay as shared and general Neoplasms-specific antigens.[SEP]Relations: germ cell tumor has relations: disease_protein with ATF7IP, disease_protein with ATF7IP, disease_protein with SCNN1A, disease_protein with SCNN1A, disease_protein with KITLG, disease_protein with KITLG, disease_protein with ERCC1, disease_protein with ERCC1, disease_protein with PHC1, disease_protein with PHC1.", "label": "yes"}
+{"original_question": "Has the proteome of mice hippocampus been analysed?", "id": "converted_2407", "sentence1": "Has the proteome of CASP14 gene hippocampus been analysed?", "sentence2": "We employed a discovery-based proteomic approach in subcellular fractions of Hippocampus (Brain) tissue from chronic intermittent alcohol (CIE)-exposed C57Bl/6J CASP14 gene to gain insight into alcohol-induced changes in GluN2B signaling complexes. ,  We employed shotgun liquid chromatography-mass spectrometry (LC-MS) proteomic and metabonomic profiling approaches on Prefrontal Cortex (United States Military enlisted E3 (qualifier value)) and Hippocampus (Brain) (HPC) tissue from Df(16)A+/-CASP14 gene, a model of the DiGeorge Syndrome. ,  Molecular alterations in the Cortex of frontal lobe and hippocampus ofTsc1+/-and control CASP14 gene, with or without sirolimus treatment, were investigated. A quantitative mass spectrometry-based shotgun proteomic approach (LC-MSE) was employed as an unbiased method to detect changes in protein levels., This dataset reports on the analysis of Mus sp. hippocampus by LC-MS/MS, from CASP14 gene fed a diet that was either deficient in n-3 FA (n-3 Def) or sufficient in n-3 FA (n-3 Adq). , Using isobaric tags for relative and absolute quantitation (iTRAQ) and proteomic methods, here we identified learning-induced changes in the Hippocampus (Brain) proteome of non-transgenic (NonTg) and 3 × Tg-AD CASP14 gene, a widely used animal model of AD. [SEP]Relations: hippocampus fimbria has relations: anatomy_anatomy with central nervous system cell part cluster, anatomy_anatomy with central nervous system cell part cluster. Cortex of frontal lobe has relations: anatomy_protein_present with HIPK3, anatomy_protein_present with HIPK3, anatomy_protein_present with HIPK4, anatomy_protein_present with HIPK4, anatomy_protein_present with HIPK2, anatomy_protein_present with HIPK2, anatomy_protein_present with HIPK1, anatomy_protein_present with HIPK1.", "label": "yes"}
+{"original_question": "Is disruption of immune regulation mechanisms associated with adverse pregnancy outcomes, including preeclampsia (PE)?", "id": "converted_4697", "sentence1": "Is disruption of immune regulation mechanisms associated with adverse pregnancy outcomes, including Pre-Eclampsia (phosphatidylethanolamines)?", "sentence2": " Maternal systemic and Eutheria inflammatory responses participate in the pathogenesis of hypertensive disorders of pregnancy including Pre-Eclampsia, a pregnancy-specific syndrome, although the role of inflammation remains unclear. , Our results indicate these Proteins are new factors that play important roles in the immunological pathomechanism of Pre-Eclampsia., Inflammation and oxidative stress at the maternal-Prenatal care interface characterize the Eutheria dysfunction that underlies the pregnancy disorder Pre-Eclampsia., The abnormal expression of HAVCR2 wt Allele on Myeloid-Derived Suppressor Cells might be involved in the pathogenesis of phosphatidylethanolamines, and could be a marker to evaluate the immune function in phosphatidylethanolamines., Maternal immune tolerance is important for maintaining pregnancy, and researchers have increasingly focused on the critical roles of Recombinant Cytokines in the pathogenesis of phosphatidylethanolamines in recent years., Disruption of well-controlled immune functions leads to Sterility, Reproductive, Eutheria inflammation, and numerous pregnancy complications, including Pre-Eclampsia (phosphatidylethanolamines)., Effect of Endogenic and Exogenic Oxidative Stress Triggers on Adverse Pregnancy Outcomes: Preeclampsia, Fetal Growth Restriction, Gestational Diabetes Mellitus and Preterm Birth., Disruption of complex immune regulation mechanisms is associated with adverse pregnancy outcomes, including Pre-Eclampsia (phosphatidylethanolamines)., In addition, it has been demonstrated that immune disturbance may be responsible for some adverse pregnancy outcomes such as Pre-Eclampsia (phosphatidylethanolamines), recurrent spontaneous abortion (RSA) and intrauterine growth restriction (Fetal Growth Retardation)., esponse. In previous models of Pre-Eclampsia (phosphatidylethanolamines), defective immune function caused by disruption of lymphangiogenesis was shown to be involved in the disease pathophy, OBJECTIVE: Increased oxidative stress and Immune System Diseases are implicated in Pre-Eclampsia (phosphatidylethanolamines) and may contribute to the two- to fourfold increase in phosphatidylethanolamines prevalence among women with type 1 , r, in Pre-Eclampsia, the regulation of immune responses is disrupted as a result of aberrant activation of innate immune cells and imbalanced differentiation of T-helper cell subsets creating a cytotoxic environment in uter, Disruption in the Regulation of Immune Responses in the Placental Subtype of Preeclampsia, a disrupted immune system might be a Predisposing Factors or result of Eutheria oxidative stress or excessive inflammation in Pre-Eclampsia. Preeclampsia c, clude insufficient control of inflammation, failure of tolerance toward paternal Antigens at the Prenatal care-maternal interface, and subsequent over- or insufficient activation of Biological Response Modifiers. It is als, PROBLEM: The purpose of this study is to clarify whether the disruption of immune regulation occurs in early pregnancy before the clinical manifestations of pre, s review, we focus on the role of excessive systemic inflammation as the result of a dysregulated immune system in the development of Pre-Eclampsia. These, PROBLEM: The purpose of this study is to clarify whether the disruption of immune regulation occurs in early pregnancy before the clinical manifestations of pree, However, in Pre-Eclampsia, the regulation of immune responses is disrupted as a result of aberrant activation of innate immune cells and imbalanced differentiation of T-helper cell subsets creating a cytotoxic environment in utero., In conclusion, a disrupted immune system might be a Predisposing Factors or result of Eutheria oxidative stress or excessive inflammation in Pre-Eclampsia., esponse. In previous models of Pre-Eclampsia (phosphatidylethanolamines), defective immune function caused by disruption of lymphangiogenesis was shown to be involved in the disease pathoph, Disruption of this immune balance and/or inadequate Eutheria perfusion is believed to be associated with a lot of pregnancy-related complications, such as recurrent spontaneous abortion, pre-eclampsia, and Prenatal care intrauterine growth restriction., Therefore, a delicate immune balance is critical for the maintenance of a successful pregnancy, while disruption of this balance can induce complications such as implantation failure, miscarriage, preterm birth/labor, Pre-Eclampsia and Prenatal care growth restriction., Antigens during pregnancy. Disruption of complex immune regulation mechanisms is associated with adverse pregnancy outcomes, including Pre-Eclampsia (P, ccessful pregnancy. It has been demonstrated that innate immune disturbances may be responsible for some adverse pregnancy outcomes such as preeclamps, ever, in Pre-Eclampsia, the regulation of immune responses is disrupted as a result of aberrant activation of innate immune cells and imbalanced differ, PROBLEM: The purpose of this study is to clarify whether the disruption of immune regulation occurs in early pregnancy before the clinical manifestations of Pre-Eclampsia, However, immune maladaptation and hemostatic imbalance have been suggested to be responsible for adverse pregnant outcomes, such as Pre-Eclampsia (phosphatidylethanolamines), miscarriage, recurrent spontaneous abortion (RSA) and intrauterine growth restriction (Fetal Growth Retardation)., PROBLEM: The purpose of this study is to clarify whether the disruption of immune regulation occurs in early pregnancy before the clinical manifestations of Pre-Eclampsia.METHOD OF STUDY: The serum concentrations of Recombinant Interleukin-2 (Recombinant Interleukin-2 binding activity) and Tumor Necrosis Factor-alpha (Recombinant Tumor Necrosis Factor-Alpha) were determined by using enzyme-linked immunoadsorbent assay (ELISA) in the first trimester of pregnancy in women who had Pre-Eclampsia develop after 28 weeks of pregnancy (preeclamptic group) and in women who completed pregnancy uneventfully (control group).RESULTS: Serum concentrations of both Recombinant Interleukin-2 binding activity and Recombinant Tumor Necrosis Factor-Alpha in the first trimester of the preeclamptic group were significantly higher than those of the control group.CONCLUSIONS: That the perturbation of feto-maternal immune regulation may precede the clinical manifestations of Pre-Eclampsia, which may be of relevance i, Preeclampsia can thus be considered a hyperinflammatory state associated with defective regulation of the immune system proposed as a key element in the pathological events of the Eutheria subtype of this disorder., Disruption in the Regulation of Immune Responses in the Placental Subtype of Preeclampsia., It has been demonstrated that innate immune disturbances may be responsible for some adverse pregnancy outcomes such as Pre-Eclampsia (phosphatidylethanolamines); Specimen Reject Reason - Hemolysis, elevated Finding of liver enzyme levels, low platelets (HELLP) syndrome; intrauterine growth restriction (Fetal Growth Retardation); and recurrent spontaneous abortion (RSA).[SEP]Relations: Pre-Eclampsia has relations: contraindication with Progesterone, contraindication with Progesterone, disease_disease with toxemia of pregnancy, disease_disease with toxemia of pregnancy, disease_phenotype_positive with Abnormality of the nervous system, disease_phenotype_positive with Abnormality of the nervous system, disease_disease with severe pre-eclampsia, disease_disease with severe pre-eclampsia, disease_phenotype_positive with Abnormality of the kidney, disease_phenotype_positive with Abnormality of the kidney.", "label": "yes"}
+{"original_question": "Is Cryptococcus neoformans a frequent cause of isolated skin infections in immunocompromised individuals", "id": "converted_2096", "sentence1": "Is Cryptococcus <scale insects> neoformans a frequent cause of isolated Skin Specimen Source Code Infections of musculoskeletal system in immunocompromised individuals", "sentence2": " Cryptococcus <scale insects> <scale insects> is an opportunistic Saccharomyces cerevisiae with a worldwide distribution that primarily causes significant Infections of musculoskeletal system in immunocompromised individuals, generally by affecting the respiratory tract. But primary cutaneous cryptococcosis (1-piperidinocyclohexanecarbonitrile) without Sepsis is rare. , Cryptococcus <scale insects> <scale insects> is a ubiquitous fungus and is known for causing Meningitis and cutaneous Infections of musculoskeletal system in immunocompromised individuals., Cryptococcus <scale insects> <scale insects> neoformans is an encapsulated Saccharomyces cerevisiae that can cause primary pulmonary Infections of musculoskeletal system or disseminate and cause Infections of musculoskeletal system of the CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS, Meninges, Skin Specimen Source Code, and Specimen Type - Bone in the immunocompromised host., The authors report a male patient, a seller with no detected immunosuppression, with an extensive ulcerated Skin Specimen Source Code lesion localized on the left forearm, caused by Cryptococcus <scale insects> <scale insects> neoformans var.[SEP]Relations: Recurrent Skin Specimen Source Code Infections of musculoskeletal system has relations: phenotype_phenotype with Recurrent bacterial Skin Specimen Source Code Infections of musculoskeletal system, phenotype_phenotype with Recurrent bacterial Skin Specimen Source Code Infections of musculoskeletal system, phenotype_phenotype with Recurrent viral Skin Specimen Source Code Infections of musculoskeletal system, phenotype_phenotype with Recurrent viral Skin Specimen Source Code Infections of musculoskeletal system, phenotype_phenotype with Recurrent cutaneous fungal Infections of musculoskeletal system, phenotype_phenotype with Recurrent cutaneous fungal Infections of musculoskeletal system, disease_phenotype_positive with immunodeficiency, disease_phenotype_positive with immunodeficiency, disease_phenotype_positive with acquired ichthyosis, disease_phenotype_positive with acquired ichthyosis.", "label": "no"}
+{"original_question": "Is CREB a key memory protein?", "id": "converted_2436", "sentence1": "Is Cyclic AMP-Responsive DNA-Binding Protein a key memory protein?", "sentence2": "Homo sapiens cyclic AMP response element Protein Binding (Cyclic AMP-Responsive DNA-Binding Protein) transcription factor which plays a crucial role in memory, The activated Cyclic AMP-Responsive DNA-Binding Protein is implicated in the regulation of development, protection, learning, memory and plasticity in the nerve system. , A mouse genetic study showed that cAMP-responsive element-Protein Binding (Cyclic AMP-Responsive DNA-Binding Protein)-mediated transcription is required for the formation of social recognition memory., Transcription factor cAMP response element-Protein Binding (Cyclic AMP-Responsive DNA-Binding Protein) plays a critical role in memory formation., It is well known that Molecule like cAMP response element binding (Cyclic AMP-Responsive DNA-Binding Protein) and Protein Binding (1-Chloro-3-bromopropene-1) play a crucial role in memory consolidation. , Cyclic AMP-Responsive DNA-Binding Protein SUMOylation by the ubiquitin-protein ligase PIAS1 protein, human protein, human enhances spatial memory., Therefore, Cyclic AMP-Responsive DNA-Binding Protein phosphorylation may be responsible for signal transduction during the early phase of long-term memory formation, whereas Cyclic AMP-Responsive DNA-Binding Protein SUMOylation sustains long-term memory[SEP]Relations: protein binding has relations: molfunc_protein with CREB1, molfunc_protein with CREB1, molfunc_protein with CREB3, molfunc_protein with CREB3, molfunc_protein with CREB5, molfunc_protein with CREB5, molfunc_protein with CREBBP, molfunc_protein with CREBBP, molfunc_protein with CREM, molfunc_protein with CREM.", "label": "yes"}
+{"original_question": "Is sternotomy closure done using either a sternal ZipFix™ implant  or conventional steel wire following cardiac surgery?", "id": "converted_2666", "sentence1": "Is sternotomy closure done using either a Sternum ZipFix™ implant  or conventional steel wire following cardiac surgery?", "sentence2": "o determine the difference in Sternum Communicable Diseases and other infectious events between conventional wire and cable-tie-based closure techniques post-sternotomy in a collective of patients after cardiac surgery., Our study underlines a neutral effect of the Sternum ZipFix™ system in patients regarding Sternum Communicable Diseases. Postoperative complications are similar in both Sternum closure methods. The cable-tie-based system is fast, easy to use, reliable and safe.,  Wire closure still remains the preferred technique despite reasonable disadvantages. Associated complications, such as Communicable Diseases and Sternum instability, cause time- and cost-consuming therapies. We present a new tool for Sternum closure with its first clinical experience and results.METHODS: The Sternum ZipFix(TM) System is based on the cable-tie principle. , In our initial evaluation, the short-term results have shown that the Sternum ZipFix(TM) can be used safely and effectively. It is fast, easy to use and serves as a potential alternative for traditional wire closure., To determine the difference in Sternum Communicable Diseases and other infectious events between conventional wire and cable-tie-based closure techniques post-sternotomy in a collective of patients after cardiac surgery.[SEP]Relations: sternum has relations: anatomy_anatomy with endochondral element, anatomy_anatomy with endochondral element.", "label": "yes"}
+{"original_question": "Is there any involvement of the long non-coding RNA Gomafu in schizophrenia?", "id": "converted_1964", "sentence1": "Is there any involvement of the long non-coding RNA MIAT gene in schizophrenia?", "sentence2": "The long non-coding RNA MIAT gene is acutely regulated in response to neuronal activation and involved in schizophrenia-associated alternative splicing., Here, we profile these transcriptomic responses and show that long non-coding RNAs (lncRNAs) are dynamically regulated by neuronal activation, including acute downregulation of the lncRNA MIAT gene, previously implicated in Head>Brain and retinal development. Moreover, we demonstrate that MIAT gene binds directly to the splicing factors QKI gene gene and SRSF1 gene gene (Serine/Arginine-Rich Splicing Factor 2) and dysregulation of MIAT gene leads to alternative splicing patterns that resemble those observed in SZ for the archetypal SZ-associated genes DISC1 gene gene and Receptor Tyrosine-Protein Kinase ErbB-4, human. Finally, we show that MIAT gene is downregulated in post-mortem cortical gray matter from the superior temporal gyrus in SZ. These results functionally link activity-regulated lncRNAs and alternative splicing in neuronal function and suggest that their dysregulation may contribute to nervous system disorder., MIAT gene/MIAT/Rncr2 is a RNA, Long Untranslated that has been proposed to control Neuron of retina specification, stem cell differentiation and alternative splicing of schizophrenia-related genes., The long non-coding RNA MIAT gene is acutely regulated in response to neuronal activation and involved in schizophrenia-associated alternative splicing, Moreover, we demonstrate that MIAT gene binds directly to the splicing factors QKI gene gene and SRSF1 gene gene (Serine/Arginine-Rich Splicing Factor 2) and dysregulation of MIAT gene leads to alternative splicing patterns that resemble those observed in SZ for the archetypal SZ-associated genes DISC1 gene gene and Receptor Tyrosine-Protein Kinase ErbB-4, human. , Finally, we show that MIAT gene is downregulated in post-mortem cortical gray matter from the superior temporal gyrus in SZ. , The long non-coding RNA MIAT gene is acutely regulated in response to neuronal activation and involved in schizophrenia-associated alternative splicing.[SEP]Relations: regulation of neural retina development has relations: bioprocess_protein with PTF1A, bioprocess_protein with PTF1A, bioprocess_protein with SIX3, bioprocess_protein with SIX3, bioprocess_protein with DLL4, bioprocess_protein with DLL4, bioprocess_bioprocess with negative regulation of neural retina development, bioprocess_bioprocess with negative regulation of neural retina development, bioprocess_bioprocess with positive regulation of neural retina development, bioprocess_bioprocess with positive regulation of neural retina development.", "label": "yes"}
+{"original_question": "Is Keutel syndrome a common genetic disorder?", "id": "converted_4315", "sentence1": "Is Ramer Ladda syndrome a common genetic disorder?", "sentence2": "Ramer Ladda syndrome (OMIM 245150) is a very rare syndrome , Ramer Ladda syndrome is a rare autosomal-recessive condition characterized by abnormal cartilage calcification., MGP-deficiency in Homo sapiens leads to Ramer Ladda syndrome, a rare genetic disease hallmarked by abnormal Neck+Chest>Soft tissue calcification. [SEP]Relations: LADD syndrome has relations: disease_disease with EEC syndrome and related syndrome, disease_disease with EEC syndrome and related syndrome, disease_disease with autosomal dominant disease, disease_disease with autosomal dominant disease, disease_disease with genetic otorhinolaryngological malformation, disease_disease with genetic otorhinolaryngological malformation, disease_disease with genetic multiple congenital anomalies/dysmorphic syndrome without intellectual disability, disease_disease with genetic multiple congenital anomalies/dysmorphic syndrome without intellectual disability, disease_phenotype_positive with Autosomal dominant inheritance, disease_phenotype_positive with Autosomal dominant inheritance.", "label": "no"}
+{"original_question": "Is the circadian clock involved in ribosome biogenesis?", "id": "converted_741", "sentence1": "Is the circadian clock involved in Ribosomes biogenesis?", "sentence2": "The circadian clock coordinates Ribosomes biogenesis., Here we show that the circadian clock exerts its function also through the regulation of Protein Biosynthesis. Namely, the circadian clock influences the temporal translation of a subset of mRNAs involved in Ribosomes biogenesis by controlling the transcription of translation initiation factors as well as the clock-dependent rhythmic activation of signaling pathways involved in their regulation. Moreover, the circadian oscillator directly regulates the transcription of Ribosomal Proteins mRNAs and ribosomal RNAs. Thus the circadian clock exerts a major role in coordinating transcription and translation steps underlying Ribosomes biogenesis., Namely, the circadian clock influences the temporal translation of a subset of mRNAs involved in Ribosomes biogenesis by controlling the transcription of translation initiation factors as well as the clock-dependent rhythmic activation of signaling pathways involved in their regulation, The circadian clock coordinates Ribosomes biogenesis, Here we show that the circadian clock exerts its function also through the regulation of Protein Biosynthesis, Here we show that the circadian clock exerts its function also through the regulation of Protein Biosynthesis. Namely, the circadian clock influences the temporal translation of a subset of mRNAs involved in Ribosomes biogenesis by controlling the transcription of translation initiation factors as well as the clock-dependent rhythmic activation of signaling pathways involved in their regulation.[SEP]Relations: Ribosomes has relations: cellcomp_protein with AURKAIP1, cellcomp_protein with AURKAIP1, cellcomp_protein with SNCA, cellcomp_protein with SNCA, cellcomp_protein with RNA28SN5, cellcomp_protein with RNA28SN5, cellcomp_protein with RPS17, cellcomp_protein with RPS17, cellcomp_protein with RNA28SN4, cellcomp_protein with RNA28SN4.", "label": "yes"}
+{"original_question": "Is there a link between rare variants in PPARG and type 1 diabetes?", "id": "converted_3947", "sentence1": "Is there a link between rare Variant in Peroxisome Proliferator-Activated Receptor Gamma, human and type 1 diabetes?", "sentence2": "Rare Variant in Peroxisome Proliferator-Activated Receptor Gamma, human with decreased activity in Adipocytes differentiation are associated with increased risk of type 2 diabetes., By sequencing Peroxisome Proliferator-Activated Receptor Gamma, human in 19,752 Diabetes Mellitus, Non-Insulin-Dependent cases and controls drawn from multiple studies and ethnic groups, we identified 49 previously unidentified, nonsynonymous Peroxisome Proliferator-Activated Receptor Gamma, human Variant (MAF < 0.5%). Considered in aggregate (with or without computational prediction of functional consequence), these rare Variant showed no association with Diabetes Mellitus, Non-Insulin-Dependent (OR = 1.35; P = 0.17). The function of the 49 Variant was experimentally tested in a novel high-throughput human Adipocytes differentiation assay, and nine were found to have reduced activity in the assay. Carrying any of these nine LOF Variant was associated with a substantial increase in risk of Diabetes Mellitus, Non-Insulin-Dependent (OR = 7.22; P = 0.005). The combination of large-scale DNA sequencing and functional testing in the laboratory reveals that approximately 1 in 1,000 individuals carries a variant in Peroxisome Proliferator-Activated Receptor Gamma, human that reduces function in a human Adipocytes differentiation assay and is associated with a substantial risk of Diabetes Mellitus, Non-Insulin-Dependent.[SEP]Relations: diabetes mellitus, noninsulin-dependent has relations: disease_disease with type 2 diabetes mellitus, disease_disease with type 2 diabetes mellitus, disease_protein with TBC1D4, disease_protein with TBC1D4, disease_disease with inborn errors of metabolism, disease_disease with inborn errors of metabolism, disease_protein with CAPN10, disease_protein with CAPN10. peroxisome proliferator activated receptor binding has relations: molfunc_protein with HMGA1, molfunc_protein with HMGA1.", "label": "no"}
+{"original_question": "Is Solanezumab effective for Alzheimer's Disease?", "id": "converted_2423", "sentence1": "Is solanezumab effective for ALZHEIMER DISEASE, FAMILIAL, 1?", "sentence2": "An analysis of publicly available data from the Phase II studies for bapineuzumab and solanezumab indicates that neither compound produced compelling evidence of drug-like behavior that would justify their progression into pivotal trials. , Notably, a recent study of solanezumab, an Serum Serum amyloid A protein A protein β monoclonal antibody, raises hope for the further therapeutic potential of immunotherapy, not only in Alzheimer's disease, but also for other Neurodegenerative Disorders, including Parkinson Disease. , For example, Eli Lilly announced a major change to its closely watched clinical trial for the Alzheimer's drug solanezumab which failed to reach statistical significance. , Areas covered: This contradiction prompted us to review all study phases of immunoglobulins, intravenous (IVIG), bapineuzumab, solanezumab, Avagacestat and latrepirdine to shed more light on these recent failures. ,  Results from phase III clinical trials in mild-to-moderate Alzheimer's disease (cytarabine/daunorubicin protocol) patients with two Monoclonal Antibodies bapineuzumab and solanezumab and intravenous immunoglobulin have been disappointing. Subsequent analysis of pooled data from both phase III trials with solanezumab showed a reduction in Mental deterioration in patients with mild cytarabine/daunorubicin protocol., Secondary analyses of EXPEDITION studies suggested a smaller functional effect of solanezumab relative to cognition. An increasing effect of solanezumab over 18 months was shown for cognition and function., RESULTS: In the mild cytarabine/daunorubicin protocol population, less cognitive and functional decline was observed with solanezumab (n = 659) versus placebo (n = 663), measured by ALZHEIMER DISEASE, FAMILIAL, 1 Assessment Scale Cognitive subscale, Mini-Mental State Examination, and ALZHEIMER DISEASE, FAMILIAL, 1 Cooperative Study-Activities of Daily Living functional scale Instrumental ADLs. , The promising results obtained with aducanumab and solanezumab against Alzheimer's disease (cytarabine/daunorubicin protocol) strengthen the vaccine approach to prevent cytarabine/daunorubicin protocol, despite of the many clinical setbacks. , CONCLUSIONS: solanezumab, a Antibodies, Monoclonal, Humanized that binds Serum Serum amyloid A protein A protein, failed to improve cognition or functional ability. , Results from phase III clinical trials in mild-to-moderate Alzheimer's disease (cytarabine/daunorubicin protocol) patients with two Monoclonal Antibodies bapineuzumab and solanezumab and intravenous immunoglobulin have been disappointing.[SEP]Relations: solanezumab has relations: drug_drug with Adalimumab, drug_drug with Adalimumab, drug_drug with Eldelumab, drug_drug with Eldelumab, drug_drug with Idarucizumab, drug_drug with Idarucizumab, drug_drug with Alemtuzumab, drug_drug with Alemtuzumab, drug_drug with Refanezumab, drug_drug with Refanezumab.", "label": "no"}
+{"original_question": "Is selenocysteine an aminoacid?", "id": "converted_2797", "sentence1": "Is selenocysteine an aminoacid?", "sentence2": "selenocysteine (seconds), a rare genetically encoded Amino Acids with unusual chemical properties, is of great interest for protein engineering., selenocysteine (SeC) is a naturally available Se-containing Amino Acids that displays splendid anticancer activities against several Homo sapiens tumors. [SEP]Relations: selenocysteine has relations: drug_protein with CAMP, drug_protein with CAMP, drug_protein with NME1, drug_protein with NME1, drug_drug with Eltrombopag, drug_drug with Eltrombopag.", "label": "yes"}
+{"original_question": "Is DNA polymerase θ involved in DNA repair?", "id": "converted_2620", "sentence1": "Is DNA polymerase θ involved in DNA repair?", "sentence2": "DNA polymerase θ (Pol θ) is implicated in various cellular processes including double-strand break repair and apurinic/apyrimidinic site bypass.,  Pol θ is the defining Enzyme [APC] for a pathway of DSB repair termed \"alternative end-joining\" (altEJ) or \"theta-mediated end-joining.\", DNA polymerase θ is a key player in PARP-mediated DNA damage repair and essential for the survival of Tumor cells, malignant where homologous recombination is compromised. , DNA polymerase θ protects against genomic instability via an alternative end-joining repair pathway for DNA double-strand breaks.[SEP]Relations: malignant giant cell tumor has relations: disease_disease with malignancy in giant cell tumor of bone, disease_disease with malignancy in giant cell tumor of bone, disease_disease with malignant tenosynovial giant cell tumor, disease_disease with malignant tenosynovial giant cell tumor, disease_disease with giant cell tumor of soft tissue, disease_disease with giant cell tumor of soft tissue, disease_disease with giant cell tumor, disease_disease with giant cell tumor, disease_disease with cancer, disease_disease with cancer.", "label": "yes"}
+{"original_question": "Is cytisine superior to nicotine replacement therapy for smoking cessation?", "id": "converted_172", "sentence1": "Is cytisine superior to nicotine replacement therapy for smoking cessation?", "sentence2": "The effectiveness of cytisine for continuous abstinence was superior to that of nicotine-replacement therapy at 1 week, 2 months, and 6 months. In a prespecified subgroup analysis of the primary outcome, cytisine was superior to nicotine-replacement therapy among women and noninferior among men., CONCLUSIONS: When combined with brief behavioral support, cytisine was found to be superior to nicotine-replacement therapy in helping smokers quit smoking, but it was associated with a higher frequency of self-reported adverse events.[SEP]Relations: Cytisine has relations: drug_protein with CHRNA6, drug_protein with CHRNA6, drug_protein with CHRNA4, drug_protein with CHRNA4, drug_protein with CHRNA3, drug_protein with CHRNA3, drug_protein with CHRNB2, drug_protein with CHRNB2, drug_protein with CHRNA7, drug_protein with CHRNA7.", "label": "yes"}
+{"original_question": "Has the protein SETMAR (Metnase) a transposase domain?", "id": "converted_299", "sentence1": "Has the Protein Info SETMAR gene (SETMAR gene Protein Info, human) a Transposase Superkingdom (taxonomic category)?", "sentence2": "SETMAR gene gene Protein Info, human (SETMAR gene gene) is a Parameterized Data Type - Set-Transposase fusion Protein Info that promotes nonhomologous end joining (Non-Homologous DNA End-Joining) repair in Homo sapiens., The Transposase Superkingdom (taxonomic category) Protein Info SETMAR gene gene Protein Info, human/SETMAR gene gene suppresses chromosomal translocations.,  SETMAR gene gene Protein Info, human (also termed SETMAR gene gene) is a fusion of a histone methyltransferase and Transposase Protein Info that arose specifically in primates. , the only intact SETMAR gene wt Allele Transposase gene exists within a chimeric Parameterized Data Type - Set-Transposase fusion Protein Info referred to as SETMAR gene gene Protein Info, human or SETMAR gene gene. , The SETMAR gene gene Protein Info, human Transposase has been remarkably conserved through evolution;, SETMAR gene gene Protein Info, human (also known as SETMAR gene gene) is a Parameterized Data Type - Set and Transposase fusion Protein Info in Homo sapiens and plays a positive role in double-strand break (DSB) repair. While the Parameterized Data Type - Set Superkingdom (taxonomic category) possesses Histone-Lysine N-Methyltransferase activity, the Transposase Superkingdom (taxonomic category) is responsible for 5'-terminal inverted repeat (TIR)-specific binding, DNA looping, and DNA cleavage activities. , SETMAR gene gene Protein Info, human is a Gene Fusion Abnormality comprising a Parameterized Data Type - Set histone methyl transferase Superkingdom (taxonomic category) and a Transposase Superkingdom (taxonomic category) derived from the mariner transposases., ulated by the DNA repair component SETMAR gene gene Protein Info, human (also termed SETMAR gene gene). SETMAR gene gene Protein Info, human contains a Parameterized Data Type - Set histone methyltransferase and Transposase nuclease Superkingdom (taxonomic category), SETMAR gene gene Protein Info, human is a human Parameterized Data Type - Set and Transposase Superkingdom (taxonomic category) Protein Info , The human set and Transposase Superkingdom (taxonomic category) Protein Info SETMAR gene gene Protein Info, human,  of Transposase-related sequences in Homo sapiens are Pseudogenes. We recently isolated and characterized a Parameterized Data Type - Set and Transposase Superkingdom (taxonomic category) Protein Info termed SETMAR gene gene Protein Info, human that promotes DNA double-strand break (DSB) repair by non-homologous end-joining (Non-Homologous DNA End-Joining). Both the Parameterized Data Type - Set and Transposase Superkingdom (taxonomic category) were required for its Non-Homologous DNA End-Joining activity., SETMAR gene gene Protein Info, human, also known as SETMAR gene gene, is a Parameterized Data Type - Set and Transposase fusion Protein Info with an undefined role in mammalian DNA repair., Biochemical characterization of a Parameterized Data Type - Set and Transposase fusion Protein Info, SETMAR gene gene Protein Info, human: i, SETMAR gene gene Protein Info, human (SETMAR gene gene) is a Parameterized Data Type - Set and Transposase fusion Protein Info that promotes in vivo end joining activity and mediates genomic integration of foreign DNA. ,  This Transposase coding region is part of the SETMAR gene gene gene, in which a histone methylatransferase Parameterized Data Type - Set Superkingdom (taxonomic category) is fused to an SETMAR gene wt Allele Transposase Superkingdom (taxonomic category). , The human SETMAR gene gene Protein Info preserves most of the activities of the ancestral SETMAR gene wt Allele Transposase., ere we investigate the activity of the human SETMAR gene gene Protein Info, a highly expressed fusion between a histone H3 methylase and a mariner family Transposase., SETMAR gene gene, a new primate chimeric gene resulting from fusion of a Parameterized Data Type - Set histone methyltransferase gene to the Transposase gene of a mobile element., We identified a Protein Info, termed SETMAR gene gene Protein Info, human, that has a Parameterized Data Type - Set Superkingdom (taxonomic category) and a Transposase/nuclease Superkingdom (taxonomic category). , SETMAR gene gene Protein Info, human has a nuclease Superkingdom (taxonomic category) that shares Homologous Gene with the Transposase family., SETMAR gene gene Protein Info, human (also called SETMAR gene gene) is a Parameterized Data Type - Set and Transposase Superkingdom (taxonomic category) Protein Info that promotes both DNA double-strand break (DSB) repair and restart of stalled replication forks. [SEP]Relations: SETMAR gene has relations: protein_protein with PCNA, protein_protein with PCNA, protein_protein with SETX, protein_protein with SETX, protein_protein with PCBP1, protein_protein with PCBP1, protein_protein with LEO1, protein_protein with LEO1, protein_protein with DOC2A, protein_protein with DOC2A.", "label": "yes"}
+{"original_question": "Is POLD3 essential for mouse development?", "id": "converted_2131", "sentence1": "Is POLD3 protein, human essential for mouse development?", "sentence2": "The POLD3 protein, human gene encodes a subunit of the DNA polymerase complex. Pold3 orthologs are not essential in Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae or chicken allergenic extract allergenic extract DT40 cells, but the Schizosaccharomyces pombe ortholog is essential. POLD3 protein, human protein, human also has a specialized role in the repair of broken replication forks, suggesting that POLD3 protein, human protein, human activity could be particularly relevant for Tumor cells, malignant enduring high levels of DNA replication stress. We report here that POLD3 protein, human protein, human is essential for mouse development and is also required for viability in adult animal allergen extracts., We report here that POLD3 protein, human protein, human is essential for mouse development and is also required for viability in adult animal allergen extracts., We report here that POLD3 protein, human protein, human is essential for mouse development and is also required for viability in adult animal allergen extracts.[SEP]Relations: DNA polymerase complex has relations: cellcomp_protein with POLD2, cellcomp_protein with POLD2. Protein S human has relations: drug_drug with Polmacoxib, drug_drug with Polmacoxib, drug_drug with Vindesine, drug_drug with Vindesine, drug_drug with Alaproclate, drug_drug with Alaproclate, drug_drug with Cefditoren, drug_drug with Cefditoren.", "label": "yes"}
+{"original_question": "Is there an association between TERT promoter mutation and survival of glioma patients?", "id": "converted_516", "sentence1": "Is there an association between TERT wt Allele promoter Mutation Abnormality and survival of glioma patients?", "sentence2": "Gene Mutation lead to TERT wt Allele wt Allele upregulation and are associated with aggressive clinical behavior in Glioblastoma., Kaplan-Meier's survival analysis showed that TERT wt Allele wt Allele promoter Mutation Abnormality (P=0.037), Isocitrate Dehydrogenase (NAD+) (Infective dermatitis co-occurrent and due to human T-cell lymphotropic virus 1 infection) Mutation Abnormality (P<0.001), and 1p/19q codeletion (P<0.001) were associated with favorable overall survival (OS). In the subset of 116 Infective dermatitis co-occurrent and due to human T-cell lymphotropic virus 1 infection-mutated lower-grade Glioma lacking 1p/19q codeletion, 19 TERT wt Allele wt Allele promoter-mutated Neoplasms exhibited longer progression-free survival (PFS) (P=0.027) and OS (P=0.004). Consistent with this observation, in the subset of 97 Infective dermatitis co-occurrent and due to human T-cell lymphotropic virus 1 infection-mutated astrocytomas, 14 TERT wt Allele wt Allele promoter-mutated Neoplasms showed longer PFS (P=0.001) and OS (P=0.001). In contrast, among the subset of 74 Infective dermatitis co-occurrent and due to human T-cell lymphotropic virus 1 infection wild-type lower-grade Glioma with intact 1p/19q, TERT wt Allele wt Allele promoter Mutation Abnormality was associated with shorter PFS (P=0.001) and OS (P=0.001). Similarly, in the subset of 65 Infective dermatitis co-occurrent and due to human T-cell lymphotropic virus 1 infection wild-type astrocytomas, 16 TERT wt Allele wt Allele promoter-mutated Neoplasms exhibited unfavorable PFS (P=0.007) and OS (P=0.008). Our results indicate that when combined with Infective dermatitis co-occurrent and due to human T-cell lymphotropic virus 1 infection status, TERT wt Allele wt Allele promoter Mutation Abnormality contributes to prognostic subgroups of lower-grade astrocytic Neoplasms or 1p/19q intact lower-grade Glioma and this may further refine future molecular classification of lower-grade Glioma., RESULTS: TERTp-mut identified in 60.8% of Glioma (491 out of 807) was globally associated with poorer outcome (Hazard ratio (HR)=1.50). , TERT wt Allele wt Allele promoter mutations lead to high transcriptional activity under Hypoxia, CTCAE and temozolomide treatment and predict poor prognosis in Glioma., Patients with TERT wt Allele wt Allele promoter mutations had lower survival rates, even after adjusting for other known or potential risk factors, and the incidence of Mutation Abnormality was correlated with patient age., TERT wt Allele wt Allele promoter mutations maintained its ability of inducing high transcriptional activity even under hypoxic and temozolomide treatment conditions, and the presence of mutations was associated with poor prognosis in glioma patients. , Patients whose Grade III-IV Glioma exhibit TERT wt Allele wt Allele promoter mutations alone predominately have primary GBMs associated with poor median OS (11.5 months). Patients whose Grade III-IV Glioma exhibit IDH1/2 mutations alone predominately have astrocytic morphologies and exhibit a median OS of 57 months while patients whose Neoplasms exhibit both TERT wt Allele wt Allele promoter and IDH1/2 mutations predominately exhibit oligodendroglial morphologies and exhibit median OS of 125 months., Patients with TERT wt Allele wt Allele promoter mutations had lower survival rates, even after adjusting for other known or potential risk factors, and the incidence of Mutation Abnormality was correlated with patient age.CONCLUSION: TERT wt Allele wt Allele promoter mutations were specific to Glioma. , We defined, based on TERTp-mut and Infective dermatitis co-occurrent and due to human T-cell lymphotropic virus 1 infection Mutation Abnormality status, four prognostic groups: (1) TERTp-mut and Infective dermatitis co-occurrent and due to human T-cell lymphotropic virus 1 infection-mut associated with 1p19q codeletion, overall survival (OS)>17 years; (2) TERTp-wt and Infective dermatitis co-occurrent and due to human T-cell lymphotropic virus 1 infection-mut, associated with TP53 wt Allele wt Allele Mutation Abnormality, OS=97.5 months; (3) TERTp-wt and Infective dermatitis co-occurrent and due to human T-cell lymphotropic virus 1 infection-wt, with no specific association, OS=31.6 months; (4) TERTp-mut and Infective dermatitis co-occurrent and due to human T-cell lymphotropic virus 1 infection-wt, associated with EGFR amplification, OS=15.4 months. , Gene Mutation lead to TERT wt Allele wt Allele upregulation and are associated with aggressive clinical behavior in Glioblastoma. , In the subset of 116 Infective dermatitis co-occurrent and due to human T-cell lymphotropic virus 1 infection-mutated lower-grade Glioma lacking 1p/19q codeletion, 19 TERT wt Allele wt Allele promoter-mutated Neoplasms exhibited longer progression-free survival (PFS) (P=0.027) and OS (P=0.004). , The mean age at diagnosis was lowest (37 years) among patients who had Glioma with only Infective dermatitis co-occurrent and due to human T-cell lymphotropic virus 1 infection mutations and was highest (59 years) among patients who had Glioma with only TERT wt Allele wt Allele mutations. The molecular groups were independently associated with overall survival among patients with grade II or III Glioma but not among patients with grade IV Glioma., Gene Mutation were detected in Glioma, but not in Meningioma, Pituitary Adenoma, cavernomas, intracranial metastases, normal brain tissue surgical material, or peripheral blood of glioma patients. Patients with TERT wt Allele wt Allele promoter mutations had lower survival rates, even after adjusting for other known or potential risk factors, and the incidence of Mutation Abnormality was correlated with patient age.[SEP]Relations: Glioma has relations: disease_phenotype_positive with glioma susceptibility, disease_phenotype_positive with glioma susceptibility, disease_phenotype_positive with glioblastoma (disease), disease_phenotype_positive with glioblastoma (disease), disease_phenotype_positive with retinoblastoma, disease_phenotype_positive with retinoblastoma, drug_effect with Aminolevulinic acid, drug_effect with Aminolevulinic acid, disease_phenotype_positive with Turcot syndrome with polyposis, disease_phenotype_positive with Turcot syndrome with polyposis.", "label": "yes"}
+{"original_question": "Does NADPH oxidase 5 require any subunit for function?", "id": "converted_1937", "sentence1": "Does NADPH oxidase 5 require any subunit for function?", "sentence2": "NOX5 gene forms a functional oligomer mediated by self-association of its dehydrogenase domain.,  While NOX1 gene-4 require regulatory subunits, including CYBA wt Allele, NOX5 gene activity does not depend on any subunits. ,  Thus, NOX5 gene forms a catalytically active oligomer in the Membrane Device that is mediated by its dehydrogenase domain. , Coexpression of specific Nox catalytic subunits (NOX1 gene, CYBB wt Allele, NOX3 gene, NOX4 protein, human, or NOX5 gene) along with their corresponding regulatory subunits (NOXO1 gene gene/NOXA1 for NOX1 gene; p47phox/p67phox/Rac for CYBB wt Allele; NOXO1 gene gene for NOX3 gene; no subunits for NOX4 protein, human or NOX5 gene) resulted in marked production of reactive oxygen. [SEP]Relations: NOXO1 gene has relations: cellcomp_protein with NADPH oxidase complex, cellcomp_protein with NADPH oxidase complex, molfunc_protein with superoxide-generating NADPH oxidase activator activity, molfunc_protein with superoxide-generating NADPH oxidase activator activity, pathway_protein with RHO GTPases Activate NADPH Oxidases, pathway_protein with RHO GTPases Activate NADPH Oxidases. Membrane Device has relations: cellcomp_protein with CHD5, cellcomp_protein with CHD5, cellcomp_protein with CDH5, cellcomp_protein with CDH5.", "label": "no"}
+{"original_question": "Does International Citicoline Trial on acUte Stroke trial supports efficacy of citicoline for stroke treatment?", "id": "converted_2658", "sentence1": "Does International Citicoline Trial on acUte Stroke trial supports efficacy of citicoline for Cerebrovascular accident treatment?", "sentence2": "The meta-analysis showed that no significant differences were found in the long-term mortality (OR=0.91, 95% CI 0.07 to 1.09, P=0.30), the rate of dependency (OR=1.02, 95% CI 0.87 to 1.24, P=0.85), and the effective rate (OR=0.98, 95% CI 0.84 to 1.14, P=0.82) between citicoline group and control group. ,  In conclusion, citicolne cannot reduce long-term mortality and dependence rate in the treatment of acute Cerebrovascular accident, and the effective rate of citivoline may be not better than that of controls but with reliable safety., In Homo sapiens, although a recent trial International Citicoline Trial on Acute Stroke (ICTUS) has shown that global recovery is similar in citicoline and placebo groups, citicoline was shown to be more beneficial in some patients, such as those with moderate Cerebrovascular accident severity and not treated with PLAT protein, human. , INTERPRETATION: Under the circumstances of the ICTUS trial, citicoline is not efficacious in the treatment of moderate-to-severe acute ischaemic Cerebrovascular accident., The trial was stopped for futility at the third interim analysis on the basis of complete data from 2078 patients., Global recovery was similar in both groups (odds ratio 1·03, 95% CI 0·86-1·25; p=0·364)., INTERPRETATION Under the circumstances of the ICTUS trial, citicoline is not efficacious in the treatment of moderate-to-severe acute ischaemic Cerebrovascular accident., In Homo sapiens, although a recent trial International Citicoline Trial on Acute Stroke (ICTUS) has shown that global recovery is similar in citicoline and placebo groups, citicoline was shown to be more beneficial in some patients, such as those with moderate Cerebrovascular accident severity and not treated with PLAT protein, human. Several mechanisms have been proposed to explain the beneficial actions of citicoline., In Homo sapiens, although a recent trial International Citicoline Trial on Acute Stroke (ICTUS) has shown that global recovery is similar in citicoline and placebo groups, citicoline was shown to be more beneficial in some patients, such as those with moderate Cerebrovascular accident severity and not treated with PLAT protein, human.[SEP]Relations: Protein S human has relations: drug_drug with Coagulation Factor IX (Recombinant), drug_drug with Coagulation Factor IX (Recombinant), drug_drug with Ceftobiprole, drug_drug with Ceftobiprole, drug_drug with Ceftazidime, drug_drug with Ceftazidime, drug_drug with Cimicoxib, drug_drug with Cimicoxib, drug_drug with Potassium citrate, drug_drug with Potassium citrate.", "label": "no"}
+{"original_question": "Is Calcium homeostasis important in cardiac physiology and pathophysiology?", "id": "converted_540", "sentence1": "Is Calcium homeostasis important in Cardiac - anatomy qualifier physiology and pathophysiology?", "sentence2": "Maintenance of Cells CALCIUM SUPPLEMENTS homeostasis is critical to regulating mitochondrial ATP production and Cardiac - anatomy qualifier contraction. , the Ca(2+) signal regulates the most important activities of the \"U\" lymphocyte, from the expression of Genes, to Chest>Heart and muscle contraction and other motility processes, to diverse metabolic pathways involved in the generation of \"U\" lymphocyte fuels, Pharmacologic modification of Cells CALCIUM SUPPLEMENTS handling recently moved into focus as an alternative for prevention and treatment of Ventricular tachyarrhythmia, diabetic rats displayed abnormal Cardiac - anatomy qualifier structure and systolic and diastolic dysfunction, and spermine (CASR gene agonist) could prevent or slow its progression. These results indicate that the CASR gene expression of Myocardium is reduced in the progress of 3',5'-dichloromethotrexate, and its potential mechanism is related to the impaired intracellular CALCIUM SUPPLEMENTS homeostasis., CALCIUM SUPPLEMENTS-sensing receptor (CASR gene), Na(+)/Ca(2+) exchanger (TLX2 gene) plays important roles in Cardiac - anatomy qualifier electrical activity and CALCIUM SUPPLEMENTS homeostasis., TLX2 gene current (I(TLX2 gene)) shows Transmural gradient across left ventricle in many species. Previous studies demonstrated that TLX2 gene expression was increased and Transmural gradient of I(TLX2 gene) was disrupted in failing Chest>Heart, CALCIUM SUPPLEMENTS homeostasis, the key process underlying excitation-contraction coupling, The results indicate the CALCIUM SUPPLEMENTS handling properties of hiPSC-derived Myocytes, Cardiac are relatively immature to Human Embryonic Stem Cells counterparts, Our understanding of the Molecular processes which regulate Cardiac - anatomy qualifier function has grown immeasurably in recent years. Even with the advent of β-blockers, angiotensin inhibitors and CALCIUM SUPPLEMENTS modulating agents, Congestive Chest>Heart failure (Hydrops Fetalis) still remains a seriously debilitating and life-threatening condition. Here, we review the Molecular changes which occur in the Chest>Heart in response to increased load and the pathways which control Cardiac - anatomy qualifier hypertrophy, CALCIUM SUPPLEMENTS homeostasis, and immune activation during Hydrops Fetalis., Calcium-sensing receptors (CaSRs) are G-protein coupled receptors which maintain systemic CALCIUM SUPPLEMENTS homeostasis and participate in hormone secretion, activation of ion channels, \"U\" lymphocyte apoptosis, proliferation, and differentiation., CaSRs are associated with I/R injury and apoptosis in neonatal Rattus norvegicus ventricular Myocytes, Cardiac via suppressing BCL2 gene and promoting caspase-3 expression., Important insights into the Molecular basis of Hypertrophic obstructive cardiomyopathy and related diseases have been gained by studying families with inherited Cardiac - anatomy qualifier hypertrophy. Integrated clinical and genetic investigations have demonstrated that different genetic defects can give rise to the common phenotype of Cardiac - anatomy qualifier hypertrophy. Diverse pathways have been identified, implicating perturbations in force generation, force transmission, intracellular CALCIUM SUPPLEMENTS homeostasis, myocardial energetics, and Cardiac - anatomy qualifier metabolism in causing Disease, HCLS1-Associated Protein X-1, Human as a regulator of contractility and CALCIUM SUPPLEMENTS cycling in the Chest>Heart. HCLS1-Associated Protein X-1, Human overexpression reduced sarcoplasmic reticulum Ca-ATPase (Sarcoplasmic/Endoplasmic Reticulum Calcium ATPase 2) pump activity in isolated Myocytes, Cardiac and in vivo, leading to depressed Muscle Cells CALCIUM SUPPLEMENTS kinetics and mechanics., Thus, HCLS1-Associated Protein X-1, Human represents a regulatory mechanism in Cardiac - anatomy qualifier CALCIUM SUPPLEMENTS cycling and its responses to sympathetic stimulation, implicating its importance in CALCIUM SUPPLEMENTS homeostasis and \"U\" lymphocyte survival., CALCIUM SUPPLEMENTS ion are the most ubiquitous and versatile signaling molecules in Eukaryotic Cells. Calcium homeostasis and signaling systems are crucial for both the normal growth of the budding yeast Saccharomyces cerevisiae and the intricate working of the Mammals Chest>Heart., this knowledge can be used to help treat relevant human diseases such as pathological Cardiac - anatomy qualifier hypertrophy and Congestive Chest>Heart failure, With aging, the Chest>Heart develops Muscle Cells hypertrophy associated with impaired relaxation indices. To define the Cells basis of this adaptation, we examined the physiological changes that arise in CALCIUM SUPPLEMENTS handling in the aging Chest>Heart and contrasted the adaptations that occur following the imposition of a stimulus that alters CALCIUM SUPPLEMENTS homeostasis in a young and an old Chest>Heart, alterations in the CALCIUM SUPPLEMENTS-handling machinery of the Cardiocyte - general anatomical term differ in the context of age and as such may predispose the older Chest>Heart to the development of a Hypertrophic disorder of skin, unspecified phenotype., The Cardiac - anatomy qualifier sodium-CALCIUM SUPPLEMENTS exchanger (SLC8A1 wt Allele) is a key sarcolemmal protein for the maintenance of CALCIUM SUPPLEMENTS homeostasis in the Chest>Heart. , Thus exchanger overexpression in CASP14 gene leads to abnormal CALCIUM SUPPLEMENTS handling and a decompensatory transition to Congestive Chest>Heart failure with stress, Central to controlling intracellular CALCIUM SUPPLEMENTS concentration ([Ca(2+)](i)) are a number of Ca(2+) transporters and channels with the L-type Ca(2+) channel, Na(+)-Ca(2+) exchanger and Sarcoplasmic Reticulum Calcium-Transporting ATPases (SERCA) being of particular note in the Chest>Heart. This review concentrates on the regulation of [Ca(2+)](i) in Cardiac - anatomy qualifier muscle and the homeostatic mechanisms employed to ensure that the Chest>Heart can operate under steady-state conditions on a beat by beat basis., the tight regulation of SNCG wt Allele Ca(2+) content is also required to prevent the abnormal, spontaneous or diastolic release of Ca(2+) from the SNCG wt Allele. Such diastolic events are a major factor contributing to the genesis of Cardiac Arrhythmia in Disease situations and in recently identified familial mutations in the SNCG wt Allele Ca(2+) release channel (Ryanodine Receptor Calcium Release Channel, Ryanodine Receptor Calcium Release Channel complex location)., Calcium channels have a unique functional role, because not only do they participate in this activity, they form the means by which electrical signals are converted to responses within the \"U\" lymphocyte. Calcium channels play an integral role in excitation in the Chest>Heart and shaping the Cardiac - anatomy qualifier action potential. In addition, CALCIUM SUPPLEMENTS influx through CALCIUM SUPPLEMENTS channels is responsible for initiating contraction. Abnormalities in CALCIUM SUPPLEMENTS homeostasis underlie Cardiac - anatomy qualifier arrhythmia, contractile dysfunction and Cardiac - anatomy qualifier remodelling. , Cardiac CALCIUM SUPPLEMENTS (Ca(2+)) handling subsumes the mechanisms maintaining the myocardial Ca(2+) homeostasis that contribute essentially to Cardiac - anatomy qualifier performance., Calcium is an important mediator in Cardiac - anatomy qualifier excitation and disorders in Cardiac - anatomy qualifier Ca(2+) homeostasis have great influence on the Cardiac - anatomy qualifier action potential., We review the physiology of the Cardiac - anatomy qualifier CALCIUM SUPPLEMENTS homeostasis, including the Cardiac - anatomy qualifier excitation contraction coupling and Muscle Cells CALCIUM SUPPLEMENTS cycling., We review the physiology of the Cardiac - anatomy qualifier CALCIUM SUPPLEMENTS homeostasis, including the Cardiac - anatomy qualifier excitation contraction coupling and Muscle Cells CALCIUM SUPPLEMENTS cycling, Calcium is an important mediator in Cardiac - anatomy qualifier excitation and disorders in Cardiac - anatomy qualifier Ca(2+) homeostasis have great influence on the Cardiac - anatomy qualifier action potential, The role of CALCIUM SUPPLEMENTS in Cardiac - anatomy qualifier and Muscle, Smooth, Vascular physiology was reviewed, highlighting the major mechanisms responsible for maintaining CALCIUM SUPPLEMENTS homeostasis in these cells, Energy metabolism and Ca(2+) handling serve critical roles in Cardiac - anatomy qualifier physiology and pathophysiology[SEP]Relations: muscle \"U\" lymphocyte Cells homeostasis has relations: bioprocess_protein with CAV3, bioprocess_protein with CAV3, bioprocess_protein with GAA, bioprocess_protein with GAA, bioprocess_protein with ALDOA, bioprocess_protein with ALDOA, bioprocess_protein with CFL2, bioprocess_protein with CFL2, bioprocess_protein with SRF, bioprocess_protein with SRF.", "label": "yes"}
+{"original_question": "Is recommended the use of perioperative treatment with thyroid hormone therapy in patients undergoing coronary artery bypass grafting?", "id": "converted_790", "sentence1": "Is recommended the use of perioperative treatment with thyroid hormone therapy in patients undergoing coronary artery bypass grafting?", "sentence2": "Short duration postoperative iv T(3) therapy increases cardiac index and does not alter mortality., We conclude that although widespread interest has been shown on the use of Thyroid Hormones in the perioperative period, and the effect of cardiopulmonary bypass on thyroid hormone metabolism widely studied, there is no substantial evidence to justify routine use of Thyroid Hormones in patients undergoing coronary artery bypass grafting., There is no clear evidence at this point to support thyroid hormone replacement in the latter patients, and it may be potentially harmful. Rather, we hold that T3 thoracic segmental innervation thoracic segmental innervation treatment of various surgical and other patients with nonthyroidal illness should be deferred until proof of its therapeutic efficacy is demonstrated., Perioperative administration of liothyronine increased cardiac output slightly and decreased systemic vascular resistance, but it had no effect on operative outcome. Routine use after coronary surgery is thus not recommended., Although mild effects on myocardial performance may exist, we cannot recommend at this time the routine use of intravenous T(3) as an inotropic agent in patients undergoing coronary artery bypass graft surgery., Raising serum liothyronine concentrations in patients undergoing coronary-artery bypass surgery increases cardiac output and lowers systemic vascular resistance, but does not change outcome or alter the need for standard postoperative therapy., Thus, there seems to be no sound justification for a routine use of T3 thoracic segmental innervation thoracic segmental innervation in patients undergoing open-heart procedures.[SEP]Relations: Liothyronine has relations: contraindication with coronary artery disease, contraindication with coronary artery disease, contraindication with pituitary hormone defiency from vascular origin, contraindication with pituitary hormone defiency from vascular origin, contraindication with thyroid crisis (disease), contraindication with thyroid crisis (disease), contraindication with combined pituitary hormone deficiencies, genetic form, contraindication with combined pituitary hormone deficiencies, genetic form. response to thyroid hormone has relations: bioprocess_bioprocess with response to hormone, bioprocess_bioprocess with response to hormone.", "label": "no"}
+{"original_question": "Does Estrogen lead to forkhead FoxA1 activation?", "id": "converted_3587", "sentence1": "Does Estrogen lead to forkhead FOXA1 gene protein, human activation?", "sentence2": "We showed that CTGF protein, human acts upstream of the \"pioneer\" factor FOXA1 gene gene in determining the genomic response to Estrogen [EPC]. , Almost all Endoplasmic Reticulum-chromatin location location interactions and gene expression changes depended on the presence of FOXA1 gene gene and FOXA1 gene gene influenced genome-wide chromatin location location accessibility, FOXA1 gene gene is a key determinant of Estrogen Receptors function and endocrine response., As such, FOXA1 gene gene is a major determinant of Estrogen [EPC]-Endoplasmic Reticulum activity and endocrine response in Malignant neoplasm of breast cells., Location analysis of Estrogen Receptor alpha target promoters reveals that FOXA1 gene gene defines a Superkingdom (taxonomic category) of the Estrogen [EPC] response., Furthermore, knockdown of FOXA1 gene gene protein, human expression blocks the association of Endoplasmic Reticulum with chromatin location location and Estrogen [EPC]-induced gene expression demonstrating the necessity of FOXA1 gene gene protein, human in mediating an Estrogen [EPC] response in Malignant neoplasm of breast cells., FOXA1 gene gene protein, human determines Estrogen Receptors action in Malignant neoplasm of breast progression, Given previous findings from Cultured Cell Line, FOXA1 gene gene protein, human appears to play a critical role in this reprogramming of Endoplasmic Reticulum binding., FOXA1 gene gene expression can independently predict chemosensitivity of Endoplasmic Reticulum-positive Malignant neoplasm of breast patients.,  FOXA1 gene gene expression could be a prognostic marker in Endoplasmic Reticulum-positive Malignant neoplasm of breast., The pioneer transcription factor FOXA1 gene gene protein, human plays an important role in Estrogen [EPC] signaling by opening closed chromatin location location and promoting recruitment of the Estrogen Receptors to its target regions in DNA,  The phosphomimetic FOXA1 gene gene protein, human promoted the activation of Estrogen [EPC] signaling, whereas the nonphosphorylatable FOXA1 gene gene protein, human suppressed its activation.[SEP]Relations: Estrogen Receptors activity has relations: molfunc_protein with GPER1, molfunc_protein with GPER1, molfunc_protein with GPER1, molfunc_protein with GPER1, molfunc_protein with ESR1, molfunc_protein with ESR1, molfunc_protein with ESR1, molfunc_protein with ESR1, molfunc_protein with ESR2, molfunc_protein with ESR2.", "label": "yes"}
+{"original_question": "Was ALVAC-HIV effective for HIV prevention in the HVTN 702 trial?", "id": "converted_4695", "sentence1": "Was ALVAC-HIV effective for HIV prevention in the HVTN 702 trial?", "sentence2": "During the 24-month follow-up, HIV-1 Communicable Diseases was diagnosed in 138 participants in the vaccine group and in 133 in the placebo group (hazard ratio, 1.02; 95% confidence interval, 0.81 to 1.30; P = 0.84).CONCLUSIONS: The ALVAC-gp120 regimen did not prevent HIV-1 Communicable Diseases among participants in South Africa despite previous evidence of immunogenicity. (HVTN 702 ClinicalTrials.gov number, NCT02968849.)., The advanced-phase HIV prevention vaccine trials done in South Africa (HVTN 702) and in Thailand (RV144), which both investigated canarypox vectors and adjuvanted gp120 proteins, gave rise to different results. The South African trial did not find vaccine efficacy, whereas the Thai trial had modest, but statistically significant, success with the modified intention-to-treat analysis prespecified in the protocols of both studies. , However, with the recent failure of the HVTN 702 clinical trial, comprehensive profiling of humoral immune responses may provide insight for these disappointing results. , A canarypox-protein HIV vaccine regimen (ALVAC-HIV plus AIDSVAX B/E) showed modest efficacy in reducing Communicable Diseases in Thailand., e vaccine and placebo groups. During the 24-month follow-up, HIV-1 Communicable Diseases was diagnosed in 138 participants in the vaccine group and in 133 in the placebo group (hazard ratio, 1.02; 95% confidence interval, 0.81 to 1.30; P = 0.84).CONCLUSIONS: The ALVAC-gp120 regimen did not prevent HIV-1 Communicable Diseases among participants in South Africa d[SEP]", "label": "no"}
+{"original_question": "Can Preimplantation Genetic Diagnosis (PGD) be used for gender selection?", "id": "converted_1585", "sentence1": "Can Preimplantation Genetic Diagnosis (Prostaglandins D) be used for gender selection?", "sentence2": "This testing is used for identifying singlegene disorders, Chromosome Aberrations, Mitochondrial Diseases, gender selection in non-mendelian disorders with unequal gender distribution, aneuploidy screening, and other preconceptually identified genetic abnormalities in prospective parents. ,  Although many clinics offer Prostaglandins D for HA by gender selection, an approach that detects the presence of the underlying F8 mutation has several advantages. , Preimplantation genetic diagnosis (Prostaglandins D) for gender selection for non-medical reasons has been considered an unethical procedure by several authors and agencies in the Western society on the basis that it could disrupt the sex ratio, that it discriminates against women and that it leads to disposal of normal embryos of the non-desired gender. In this study, the analysis of a large series of Prostaglandins D procedures for gender selection from a wide geographical area in the USA shows that, in general, there is no deviation in preference towards any specific gender except for a preference of males in some ethnic populations of Chinese, Indian and Middle Eastern origin that represent a small percentage of the US population. ,  In response to one specific question, one-third of the couples agreed to use the donor child as a lifetime organ donor and supported the use of Prostaglandins D for non-medical gender selection. , More specifically, I illustrate how the prescriptions of deliberative democracy can be applied to the issue of regulating non-medical uses of pre-implantation genetic diagnosis (Prostaglandins D), such as gender selection. , Private clinics were more likely than other programs to be on either the East or West Coast, list certain Prostaglandins D risks (e.g., diagnostic error), note that Prostaglandins D was new or controversial, reference source of Prostaglandins D information, provide accuracy rates of genetic testing of embryos, and offer gender selection for social reasons., The purpose of this article is to ascertain and appraise the ethical issues inherent to the utilisation of preimplantation genetic diagnosis for gender selection in infertile patients anticipating undergoing a medically indicated assisted reproductive technique procedure. Performance of preimplantation genetic diagnosis per request specifically for gender selection by an infertile couple undergoing medically indicated assisted reproductive technique may not breach the principles of ethics, and is unlikely to alter the population balance of sexes., One possible use of Prostaglandins D is to perform gender selection for couples whose offspring are at increased risk of disorders that do not follow Mendelian inheritance, but which are substantially more common in one sex than another (unequal sex incidence). Here, we examine the clinical and ethical issues to be considered prior to offering Prostaglandins D gender selection to reduce the risk of a child being affected by a non-Mendelian condition with unequal sex incidence. , New uses of Prostaglandins D have been reported in the past year for screening embryos for susceptibility to Primary malignant neoplasm, for late-onset diseases, for HLA-matching for existing children, and for gender. , This article describes current and likely future uses of Prostaglandins D, and then analyses the ethical issues posed by new uses of Prostaglandins D to screen embryos for susceptibility and late-onset conditions, for HLA-matching for tissue donation to an existing child, and for gender selection., The use of Prostaglandins D for sex selection arouses considerable debate, especially in countries like India that have a marked cultural preference for boys. It is argued that using Prostaglandins D for sex selection is a treatment option that can be ethically offered to couples who desire to use this technology to plan their families., Another concern is the use of this technology for nongenetic disorders such as gender selection. [SEP]Relations: chromosome separation has relations: bioprocess_protein with SMARCAD1, bioprocess_protein with SMARCAD1, bioprocess_protein with RECQL5, bioprocess_protein with RECQL5. Prostaglandin D2 has relations: drug_protein with PTGDR2, drug_protein with PTGDR2, drug_drug with Magnesium salicylate, drug_drug with Magnesium salicylate, drug_drug with Pirprofen, drug_drug with Pirprofen.", "label": "yes"}
+{"original_question": "Does thyroid hormone affect cardiac remodeling?", "id": "converted_1097", "sentence1": "Does Thyroid Hormones affect Cardiac - anatomy qualifier remodeling?", "sentence2": "The aim of this brief paper is to highlight new developments in understanding the cardioprotective role of Thyroid Hormones in reverting regulatory networks involved in adverse Cardiac - anatomy qualifier remodeling., Thyroid Hormone Receptor (TRα1) is shown to be critical for the maturation of cardiomyocytes and for the cellular response to stress. TRα1 is altered during post ischemic Cardiac - anatomy qualifier remodeling but the physiological significance of this response is not fully understood. , Anterior Myocardial Infarction:Finding:Point in time:^Patient:Ordinal induces downregulation of Thyroid Hormones signaling and pharmacological inhibition of TRα1 further depresses post-ischemic Cardiac - anatomy qualifier function., These findings reveal crucial roles for DIO3 gene in Chest>Heart function and remodeling, which may have pathophysiologic implications for Homo sapiens restrictive cardiomyopathy., Tyrosine 3-Monooxygenase, Homo sapiens administration after Anterior Myocardial Infarction:Finding:Point in time:^Patient:Ordinal prevented Tissue Specimen Code Hypothyroidism and resulted in decreased beta-MHC expression, increased wall thickening and normalized wallstress, while stretch-induced p38 MAPK activation was increased. We conclude that Diabetes Mellitus exacerbates post-ischemic Cardiac - anatomy qualifier remodeling and that Tissue Specimen Code Hypothyroidism may be involved in this response., Thyroid hormone can favorably remodel the diabetic myocardium after acute Myocardial Infarction:Finding:Point in time:^Patient:Ordinal., It has been previously shown that regulators of physiological growth such as Thyroid Hormones (Tyrosine 3-Monooxygenase, Homo sapiens) can favorably remodel the post ischaemic myocardium., Acute Myocardial Infarction:Finding:Point in time:^Patient:Ordinal in diabetic Rattus norvegicus results in Tyrosine 3-Monooxygenase, Homo sapiens receptor down-regulation with important physiological consequences. Tyrosine 3-Monooxygenase, Homo sapiens treatment prevents this response and improves Cardiac - anatomy qualifier hemodynamics., Tyrosine 3-Monooxygenase, Homo sapiens affects Cardiac - anatomy qualifier remodeling by limiting Reperfusion Injury, and, at later states, by inducing distinct changes in Cardiac - anatomy qualifier chamber geometry in a time-dependent manner., Furthermore, administration of Tyrosine 3-Monooxygenase, Homo sapiens can convert pathologic to physiologic hypertrophy. These effects are the result of favorable cellular remodeling., Thyroid hormone (Tyrosine 3-Monooxygenase, Homo sapiens) is critical in Cardiac - anatomy qualifier cell differentiation (regulating Contractile Proteins and cell geometry) and this effect could be potentially exploited therapeutically in reversing the process of de-differentiation which underlies postischemic Cardiac - anatomy qualifier remodeling. , Tyrosine 3-Monooxygenase, Homo sapiens treatment partially reverses Cardiac - anatomy qualifier dysfunction in Rattus norvegicus with old Myocardial Infarction:Finding:Point in time:^Patient:Ordinal by favorably changing Cardiac - anatomy qualifier chamber geometry and expression of myosin isoforms. Thyroid hormone, unlike current treatments, appears to be a paradigm of therapeutic intervention which aims at restoring Cardiac - anatomy qualifier geometry and may prove new effective treatment for Chest>Heart failure., Changes in Thyroid Hormones (Tyrosine 3-Monooxygenase, Homo sapiens)-Tyrosine 3-Monooxygenase, Homo sapiens receptors (threonine-tRNA ligase activity) axis occur in the course of post-Infarction Cardiac - anatomy qualifier remodeling and seem to contribute to Cardiac - anatomy qualifier fetal phenotype. Tyrosine 3-Monooxygenase, Homo sapiens can \"rebuild\" the post-infarcted Chest>Heart by preventing the fetal-like pattern of Contractile Proteins expression, normalizing wall tension, and optimizing Cardiac - anatomy qualifier chamber geometry. , Tyrosine 3-Monooxygenase, Homo sapiens, apart from its \"classical\" actions on Cardiac - anatomy qualifier contractility and Chest>Heart rhythm, appears to regulate various Protoplasm signaling pathways related to stress responses and Cardiac - anatomy qualifier remodelling., More importantly, experimental and clinical studies demonstrate that Tyrosine 3-Monooxygenase, Homo sapiens can limit ischaemic injury, attenuate Cardiac - anatomy qualifier remodeling and improve Cardiac - anatomy qualifier hemodynamics. , Thyroid hormone attenuates Cardiac - anatomy qualifier remodeling and improves hemodynamics early after acute Myocardial Infarction:Finding:Point in time:^Patient:Ordinal in Rattus norvegicus., Thyroid hormone administration early after Infarction attenuates Cardiac - anatomy qualifier remodeling and significantly improves Myocardial performance., It has previously been shown that Thyroid Hormones can reverse Cardiac - anatomy qualifier remodeling in failing hearts by reducing Myocardial wall stress due to the unique changes induced in Myocytes, Cardiac shape. [SEP]Relations: response to Thyroid Hormones has relations: bioprocess_bioprocess with response to hormone, bioprocess_bioprocess with response to hormone, bioprocess_bioprocess with cellular response to Thyroid Hormones stimulus, bioprocess_bioprocess with cellular response to Thyroid Hormones stimulus, bioprocess_bioprocess with response to thyroxine, bioprocess_bioprocess with response to thyroxine, bioprocess_protein with HPN, bioprocess_protein with HPN. Thyroid Hormones receptor binding has relations: molfunc_protein with OASL, molfunc_protein with OASL.", "label": "yes"}
+{"original_question": "Are DNA methylation maps applicable to the diagnosis of non-small-cell lung carcinomas?", "id": "converted_1345", "sentence1": "Are DNA methylation maps applicable to the diagnosis of non-small-cell lung carcinomas?", "sentence2": "Here we present a genome-wide DNA methylation analysis of Non-Small Cell Lung Carcinoma samples and paired Structure of parenchyma of lung, where we combine MethylCap and next generation sequencing (MethylCap-seq) to provide comprehensive DNA methylation maps of the Specimen Source Codes - Specimen Source Codes - tumor and paired lung samples., Analysis of the MethylCap-seq data revealed a strong positive correlation between replicate experiments and between paired Specimen Source Codes - Specimen Source Codes - tumor/lung samples. We identified 57 differentially methylated regions (DMRs) present in all Non-Small Cell Lung Carcinoma Neoplasms analyzed by MethylCap-seq. While hypomethylated DMRs did not correlate to any particular functional category of Genes, the hypermethylated DMRs were strongly associated with Genes encoding transcriptional regulators. Furthermore, subtelomeric regions and satellite repeats were hypomethylated in the Non-Small Cell Lung Carcinoma samples. We also identified DMRs that were specific to two of the major subtypes of Non-Small Cell Lung Carcinoma, Adenocarcinoma and Squamous cell carcinoma of mouth., Collectively, we provide a resource containing genome-wide DNA methylation maps of Non-Small Cell Lung Carcinoma and their paired Structure of parenchyma of lung, and comprehensive lists of known and novel DMRs and associated Genes in Non-Small Cell Lung Carcinoma., Genome-wide DNA methylation profiling of non-small cell lung carcinomas., Genomewide DNA methylation analysis identifies novel methylated Genes in non-small-cell lung carcinomas., To identify candidate markers for use in Non-Small Cell Lung Carcinoma diagnosis, we used genomewide DNA methylation maps that we had previously generated by MethylCap and next-generation sequencing and listed the most significant differentially methylated regions (DMRs). The 25 DMRs with highest significance in their methylation scores were selected. The methylation status of these DMRs was investigated in 61 Neoplasms and matching control Structure of parenchyma of lung by methylation-specific polymerase chain reaction., We found 12 novel DMRs that showed significant differences between Specimen Source Codes - Specimen Source Codes - tumor and control Structure of parenchyma of lung. We also identified three novel DMRs for each of the two most common Non-Small Cell Lung Carcinoma subtypes, Adenocarcinoma and Squamous cell carcinoma of mouth. We propose a panel of five DMRs, composed of novel and known markers that exhibit high specificity and sensitivity to distinguish Neoplasms from control Structure of parenchyma of lung., Here we present a genome-wide DNA methylation analysis of Non-Small Cell Lung Carcinoma samples and paired Structure of parenchyma of lung, where we combine MethylCap and next generation sequencing (MethylCap-seq) to provide comprehensive DNA methylation maps of the Specimen Source Codes - Specimen Source Codes - tumor and paired lung samples., It is a very stable and specific ResponseLevel - ResponseLevel - modification and therefore in principle a very suitable marker for epigenetic phenotyping of Neoplasms. Here we present a genome-wide DNA methylation analysis of Non-Small Cell Lung Carcinoma samples and paired Structure of parenchyma of lung, where we combine MethylCap and next generation sequencing (MethylCap-seq) to provide comprehensive DNA methylation maps of the Specimen Source Codes - Specimen Source Codes - tumor and paired lung samples., Here we present a genome-wide DNA methylation analysis of Non-Small Cell Lung Carcinoma samples and paired Structure of parenchyma of lung, where we combine MethylCap and next generation sequencing (MethylCap-seq) to provide comprehensive DNA methylation maps of the Specimen Source Codes - Specimen Source Codes - tumor and paired lung samples. The MethylCap-seq data were validated by bisulfite sequencing and methyl-specific polymerase chain reaction of selected regions., Here we present a genome-wide DNA methylation analysis of Non-Small Cell Lung Carcinoma samples and paired Structure of parenchyma of lung, where we combine MethylCap and next generation sequencing (MethylCap-seq) to provide comprehensive DNA methylation maps of the Specimen Source Codes - Specimen Source Codes - tumor and paired lung samples.[SEP]Relations: small cell lung carcinoma has relations: disease_disease with lung carcinoma, disease_disease with lung carcinoma, disease_disease with small cell carcinoma, disease_disease with small cell carcinoma, disease_disease with occult small cell lung carcinoma, disease_disease with occult small cell lung carcinoma, disease_protein with RIMS2, disease_protein with RIMS2, disease_protein with ID2, disease_protein with ID2.", "label": "yes"}
+{"original_question": "Is ocrelizumab effective for treatment of multiple sclerosis?", "id": "converted_1766", "sentence1": "Is ocrelizumab effective for treatment of Multiple Sclerosis?", "sentence2": " Advances made in immunomodulation are driving the progress being made in the treatment of MS. Ocrelizumab is the first treatment with positive results in the primarily progressive forms and tocilizumab, a Pharmaceutical Preparations for Rheumatoid Arthritis, stands out as a potential candidate for the treatment of neuromyelitis optica.,  Expert commentary: The recent encouraging results of the ocrelizumab trial in PP MS, the first to reach the primary disability endpoint, indicate B-Lymphocytes as a promising therapeutic target to prevent disease progression. , Ocrelizumab also shows efficacy in the primary progressive form of Multiple Sclerosis., Ocrelizumab for the treatment of Multiple Sclerosis, Relapsing-Remitting., Expert commentary: The topline results of two phase-III randomized clinical trials demonstrate superiority of ocrelizumab over Recombinant Interferon Beta in RRMS patients with regards to clinical and paraclinical outcome parameters. , The efficacy of three of them, rituximab, ocrelizumab and ofatumumab in MS has been confirmed by placebo-controlled clinical trials demonstrating a significant reduction of the annualized relapsing rate (ARR), new gadolinium-enhancing (GdE) and T2 lesions. , Ongoing POLYDACTYLY, POSTAXIAL, WITH PROGRESSIVE MYOPIA trials are currently being conducted with the phosphodiesterase inhibitor ibudilast, S1P modulator siponimod and anti-B-cell therapy ocrelizumab. , RECENT FINDINGS: Novel and imminently emerging DMTs for the treatment of RRMS include alemtuzumab, daclizumab, ocrelizumab, pegylated interferon-β-1a, and three times weekly glatiramer acetate. , To summarize mechanisms of action, efficacy, and safety of novel and imminently emerging disease-modifying treatments (DMTs) intended to be used in Multiple Sclerosis, Relapsing-Remitting (RRMS).Novel and imminently emerging DMTs for the treatment of RRMS include alemtuzumab, daclizumab, ocrelizumab, pegylated interferon-β-1a, and three times weekly glatiramer acetate, Ocrelizumab in Multiple Sclerosis, Relapsing-Remitting: a phase 2, randomised, placebo-controlled, multicentre trial., We aimed to assess efficacy and safety of two dose regimens of the humanised anti-CD20 monoclonal antibody ocrelizumab in patients with Multiple Sclerosis, Relapsing-Remitting. , In Multiple Sclerosis (MS), B cell-depleting therapy using monoclonal anti-CD20 Abs, including rituximab (resiniferatoxin) and ocrelizumab, effectively reduces disease activity. , Ocrelizumab also shows efficacy in the primary progressive form of Multiple Sclerosis.Most of the presented cell-depleting and myeloablative therapies are highly effective treatment options but are also accompanied by significant risks., The armamentarium of approved disease-modifying therapies in MS and those in development include: (1) the first approved, moderately effective, injectable interferon-β and glatiramer acetate; (2) oral drugs (fingolimod, laquinimod, teriflunomide, dimethyl fumarate); (3) monoclonal antibodies (rituximab, ocrelizumab, ofatumumab, daclizumab, alemtuzumab); and (4) immunosuppressive agents (e.g. mitoxantrone)., BACKGROUND: Be2 Cells are implicated in the pathogenesis of Multiple Sclerosis. We aimed to assess efficacy and safety of two dose regimens of the humanised anti-CD20 monoclonal antibody ocrelizumab in patients with Multiple Sclerosis, Relapsing-Remitting.METHODS: We did a multicentre, randomised, parallel, double-blind, placebo-controlled study involving 79 centres in 20 countries. Patients aged 18-55 years with Multiple Sclerosis, Relapsing-Remitting were randomly assigned (1:1:1:1) via an interactive voice response system to receive either placebo, Low-Dose Treatment (600 mg) or high-dose (2000 mg) ocrelizumab in two doses on days 1 and 15, or intramuscular Recombinant Interferon Beta-1a (30 ìg) once a week., Ocrelizumab for the treatment of Multiple Sclerosis, Relapsing-Remitting., The potential role for ocrelizumab in the treatment of Multiple Sclerosis: current evidence and future prospects., Ocrelizumab in Multiple Sclerosis, Relapsing-Remitting: a phase 2, randomised, placebo-controlled, multicentre trial., Ocrelizumab also shows efficacy in the primary progressive form of Multiple Sclerosis.[SEP]Relations: Ocrelizumab has relations: drug_drug with Otelixizumab, drug_drug with Otelixizumab, drug_drug with Afelimomab, drug_drug with Afelimomab, drug_drug with Crenezumab, drug_drug with Crenezumab, drug_drug with Nemolizumab, drug_drug with Nemolizumab, drug_drug with Pexelizumab, drug_drug with Pexelizumab.", "label": "yes"}
+{"original_question": "Are there negative enhancers?", "id": "converted_3718", "sentence1": "Are there negative enhancers?", "sentence2": "Role of a YY-1 factor-binding negative Enhancer of transcription, Gene Mutation targeted to the CArG-like motif abolished the suppressive effect of the negative Enhancer of transcription and the inducibility of the Promoter during myogenic differentiation, Our results suggest that the activity of the negative Enhancer of transcription may determine the level of expression of the COX Vb Genes in different Body Tissue Specimen Code., Coordinate regulation of Drosophila <basidiomycetes> <basidiomycetes> tropomyosin Genes expression is controlled by multiple muscle-type-specific positive and negative Enhancer Elements, Genetic., Enhancer of transcription regions contain multiple muscle-type-specific positive and negative cis-acting elements which together contribute toward full expression of the Genes. , We also show that this somatic/visceral muscle element(s) can be repressed through an adjacent negative control region, suggesting that the regulation of expression in these Muscle Tissue is under dual control during both phases of myogenesis, We propose a model in which transcriptional regulation of the Drosophila <basidiomycetes> <basidiomycetes> TmI Genes is controlled by the cooperative interaction of multiple positive and negative cis-acting regulatory elements that control the temporal and muscle-type pattern of expression., Tandemly reiterated negative Enhancer of transcription-like elements regulate transcription of a Human Genes for the large subunit of calcium-dependent protease I I, Upstream of the Promoter Regions, Genetic are tandemly reiterated multiple regulatory regions (-2.5k to -690, -690 to -460, -460 to -260, and -260 to -202), each of which negatively regulates the CAPN1 wt Allele mL Genes Promoter as well as heterologous promoters in an orientation-independent manner, he negative regulation of transcription mediated by these reiterated cis-acting elements and trans-acting factor(s) may play an essential role in the expression of the CAPN1 wt Allele mL Genes., Although LDB2 wt Allele-dependent activated genes are regulated at the level of transcriptional initiation, the LDB2 wt Allele-dependent repressed transcription units appear to be regulated primarily at the level of Promoter pausing, with LDB2 wt Allele regulating recruitment of metastasis-associated 1 family, member 2, a component of the Mi-2 Nucleosome Remodeling and Deacetylase Complex, on these negative enhancers, required for the repressive Enhancer of transcription function., The Specimen Source Codes - Site was similar to silencers, or negative enhancers, in that it acted to repress transcription from outside the transcribed region, but was distinct in that the function of a canonical silencer was independent of orientation., Clone Cells in which the Transgenes was down-regulated by dexamethasone survived and were designated AtT-20/NET (for negative Enhancer of transcription trap)., The E1a Genes of Adenovirus Infections encodes two Proteins, 289 and 243 amino acids long, which have positive (transactivator) and negative (Enhancer of transcription repressor) RNA polymerase II transcriptional regulatory properties and cell transformation activities including cooperation with an activated ras Genes., Tandemly reiterated negative Enhancer of transcription-like elements regulate transcription of a Human Genes for the large subunit of calcium-dependent protease I I., Upstream of the Promoter Regions, Genetic are tandemly reiterated multiple regulatory regions (-2.5k to -690, -690 to -460, -460 to -260, and -260 to -202), each of which negatively regulates the CAPN1 wt Allele mL Genes Promoter as well as heterologous promoters in an orientation-independent manner., The presence of a Cells factor(s) mediating the action of these positive (Promoter) and negative regulatory elements was suggested by an in vivo competition assay., We have previously identified a silencer (negative Enhancer of transcription) in Glutathione S-Transferase P (GST-P) Genes which is strongly and specifically induced during Hepatocarcinogenesis of the Rattus norvegicus. , The possibility that SF-B/LAP/IL6-DBP functions as a dual positive and negative regulator is discussed., Coordinate regulation of Drosophila <basidiomycetes> <basidiomycetes> tropomyosin Genes expression is controlled by multiple muscle-type-specific positive and negative Enhancer Elements, Genetic, Together these Enhancer of transcription regions contain multiple muscle-type-specific positive and negative cis-acting elements which together contribute toward full expression of the Genes., We also show that this somatic/visceral muscle element(s) can be repressed through an adjacent negative control region, suggesting that the regulation of expression in these Muscle Tissue is under dual control during both phases of myogenesis. We propose a model in which transcriptional regulation of the Drosophila <basidiomycetes> <basidiomycetes> TmI Genes is controlled by the cooperative interaction of multiple positive and negative cis-acting regulatory elements that control the temporal and muscle-type pattern of expression., Gene Mutation targeted to the CArG-like motif abolished the suppressive effect of the negative Enhancer of transcription and the inducibility of the Promoter during myogenic differentiation. Our results suggest that the activity of the negative Enhancer of transcription may determine the level of expression of the COX Vb Genes in different Tissue Specimen Code[SEP]Relations: adaptation to pheromone regulating conjugation with mutual genetic exchange has relations: bioprocess_bioprocess with negative adaptation of signaling pathway, bioprocess_bioprocess with negative adaptation of signaling pathway. Dexamethasone has relations: drug_effect with Poor appetite, drug_effect with Poor appetite, drug_effect with Growth delay, drug_effect with Growth delay, drug_effect with Anxiety, drug_effect with Anxiety. regulation of antisense RNA transcription has relations: bioprocess_bioprocess with negative regulation of antisense RNA transcription, bioprocess_bioprocess with negative regulation of antisense RNA transcription.", "label": "yes"}
+{"original_question": "Does steroid 5A-Reductase deficiency lead to hermaphroditism?", "id": "converted_3951", "sentence1": "Does steroid 5A-Reductase deficiency lead to hermaphroditism?", "sentence2": "5α steroid reductase deficiency (5αSRD) is an autosomal recessive enzymatic deficiency and Gene Mutation in the 5α steroid reductase type 2 Genes (SRD5A2 gene Genes) result in male pseudohermaphrodism caused by decreased dihydrotestosterone (Dihydrotestosterone) synthesis., The diagnosis of steroid-5-Testosterone 5-alpha-Reductase deficiency is rarely considered by the paediatrician. , n 46,XY disorders of sex development, 5α-reductase deficiency is rare and is not usually the first-intention diagnosis in newborn ambiguous genitalia, contrary to partial androgen insensitivity syndrome., Yet the cause of ambiguous genitalia may guide sex assignment, and rapid, precise diagnosis of 5α-reductase deficiency is essential, Our data clearly demonstrate that 5α-reductase deficiency should be considered in XY adolescents with Primary physiologic amenorrhea and no breast development associated with Abnormal Virilization at puberty and high plasma T. Positive parental consanguinity should reinforce the diagnostic orientation., Molecular diagnosis of 5α-reductase deficiency in 4 elite young female athletes through hormonal screening for Hyperandrogenism., The hormonal analysis evidenced plasma T within the male range, the karyotype was 46, XY, and molecular analysis of the 5α-reductase type 2 (srd5A2) Genes identified a homozygotic mutation in 2 cases, a heterozygotic compound in 1 case, and a Gene Deletion Abnormality in 1 case., 5α-Reductase deficiency should be investigated in elite young female athletes with Primary physiologic amenorrhea and high male T levels detected during antidoping programs to identify undiagnosed XY DSD., Few studies exist on the psychosexual outcome of homogeneous groups of individuals with 5α-reductase deficiency type 2 (5α-RD-2) and the relation between gender changes and parental hostile and benevolent sexism, which are two components of ambivalent sexism that assume a stereotypical approach toward women in an overtly negative way or a chivalrous, seemingly positive way, The high prevalence of gender change and gender dysphoria reported in the literature was confirmed in this relatively large and homogeneous sample of Iranians with 5-α-RD-2 raised as female., Male pseudo hermaphroditism caused by 3-oxo-5-alpha-steroid 4-dehydrogenase activity deficiency is a rare Autosomal Recessive Disorder., [Male pseudo-hermaphroditism due to partial 5 Testosterone 5-alpha-Reductase deficiency, a case report]., We report two cases of male pseudohermaphroditism, a true hermaphroditism and a 5-alfa-reductase deficiency., Contrary to what is observed in true hermaphroditism and in male pseudo-hermaphroditism, there is no erroneous transmission of the genetic gonadal differentiation programme in female pseudohermaphroditism., To our knowledge neither the A49T nor the L113V mutation has been previously reported in association with 5alpha-reductase type 2 deficiency and to date they have only been identified in cases of isolated Penile Penile hypospadias., The deficiency of steroid 5 Testosterone 5-alpha-Reductase leads to the disturbances in sex differentiation that cause symptoms of male pseudohermaphroditism., Male pseudohermaphroditism caused by steroid 5alpha-reductase deficiency is an Autosomal Recessive Disorder., This study reveals that 5 Testosterone 5-alpha-Reductase deficiency occurs with a frequency of 13 per cent as a cause of male pseudohermaphroditism in the Dominican Republic with approximately the same frequency as XO/XY gonadal dysgenesis., Deletion of steroid 5 Testosterone 5-alpha-Reductase 2 Genes in male pseudohermaphroditism., In 5 of 33 male pseudohermaphrodites with a normal testosterone response to human chorionic gonadotropin 5 Testosterone 5-alpha-Reductase deficiency was suspected by elevated plasma testosterone/dihydrotestosterone ratios before and/or after human chorionic gonadotropin stimulation., A Gene Deletion Abnormality in this Genes is present in two related individuals with male pseudohermaphroditism caused by 5 Testosterone 5-alpha-Reductase deficiency., Steroid 5-Testosterone 5-alpha-Reductase 2 deficiency is a rare disorder leading to male pseudohermaphroditism, a condition characterized by incomplete differentiation of male genitalia in 46,XY patients., The present report describes a cluster of eight patients with male pseudohermaphroditism from a large pedigree with steroid 5 Testosterone 5-alpha-Reductase 2 deficiency (5 alpha RD), who reside in Southern Lebanon., Inherited deficiencies of 5 Testosterone 5-alpha-Reductase type 2 result in a form of male pseudohermaphroditism in which the external genitalia fail to develop normally.[SEP]Relations: 5beta-dihydrotestosterone has relations: drug_drug with Desirudin, drug_drug with Desirudin, drug_drug with Prasugrel, drug_drug with Prasugrel, drug_drug with Desmoteplase, drug_drug with Desmoteplase. autosomal recessive disease has relations: disease_disease with NAD(P)HX dehydratase deficiency, disease_disease with NAD(P)HX dehydratase deficiency. progesterone 5-Testosterone 5-alpha-Reductase activity has relations: molfunc_protein with SRD5A1, molfunc_protein with SRD5A1.", "label": "yes"}
+{"original_question": "Does ESN364 activate the hypothalamic-pituitary-gonadal axis?", "id": "converted_3708", "sentence1": "Does ESN364 activate the hypothalamic-pituitary-gonadal axis?", "sentence2": "Oral administration of the TACR3 wt Allele antagonist, ESN364, suppressed the hypothalamic-pituitary-gonadal axis in healthy volunteers by selective modulation of gonadotropin secretion, leading to a restrained decrease in ovarian hormone levels in women.[SEP]", "label": "no"}
+{"original_question": "Is NEMO a zinc finger protein?", "id": "converted_2246", "sentence1": "Is NF-Kappa-B Essential Modulator a Zinc Fingers Protein Info?", "sentence2": "To better understand the thermodynamics and dynamics of the Zinc Fingers of NF-Kappa-B Essential Modulator (NF-κB essential modulator), an alteration in the Zinc Fingers Superkingdom (taxonomic category) of NF-Kappa-B Essential Modulator (K392R) , CYLD Protein Info, human Protein Info, human and the NF-Kappa-B Essential Modulator Zinc Finger Regulate Tumor Necrosis Factor Signaling and Early Embryogenesis., our simulations of the Zinc Fingers NF-Kappa-B Essential Modulator, An important regulatory Superkingdom (taxonomic category) of NF-[Formula: see text]B Essential Modulator (NF-Kappa-B Essential Modulator) is a ubiquitin-binding Zinc Fingers, with a tetrahedral CYS3HIS1 zinc-coordinating Ligand Binding Domain., NF-Kappa-B Essential Modulator function is mediated by two distal ubiquitin binding domains located in the regulatory C-terminal Superkingdom (taxonomic category) of the Protein Info: the coiled-coil 2-leucine zipper (CC2-LZ) Superkingdom (taxonomic category) and the Zinc Fingers (ZF) Superkingdom (taxonomic category). ,  We show here that the NF-Kappa-B Essential Modulator C terminus, comprising the ubiquitin binding region and a Zinc Fingers,[SEP]Relations: C2H2 Zinc Fingers Superkingdom (taxonomic category) binding has relations: molfunc_protein with EHMT1, molfunc_protein with EHMT1, molfunc_protein with EHMT2, molfunc_protein with EHMT2, molfunc_protein with GATA1, molfunc_protein with GATA1, molfunc_protein with LEF1, molfunc_protein with LEF1, molfunc_protein with THAP7, molfunc_protein with THAP7.", "label": "yes"}
+{"original_question": "Has strimvelis been approved by the European Medicines Agency?", "id": "converted_3074", "sentence1": "Has strimvelis been approved by the European Medicines Agency?", "sentence2": "Strimvelis (autologous CD34+ cells transduced to express acetaldehyde dehydrogenase (acetylating) activity gene [acetaldehyde dehydrogenase (acetylating) activity]) is the first ex vivo Stem cells gene therapy approved by the European Medicines Agency (Multiple Acyl Coenzyme A Dehydrogenase Deficiency), indicated as a single treatment for patients with acetaldehyde dehydrogenase (acetylating) activity-severe combined immunodeficiency (Severe combined immunodeficiency due to acetaldehyde dehydrogenase (acetylating) activity gene deficiency) who lack a suitable matched related bone marrow donor. [SEP]Relations: cellular response to Stem cells factor stimulus has relations: bioprocess_bioprocess with cellular response to cytokine stimulus, bioprocess_bioprocess with cellular response to cytokine stimulus. severe combined immunodeficiency due to LAT deficiency has relations: disease_phenotype_positive with Immune dysregulation, disease_phenotype_positive with Immune dysregulation, disease_phenotype_positive with Splenomegaly, disease_phenotype_positive with Splenomegaly. multiple acyl-CoA dehydrogenase deficiency has relations: disease_phenotype_positive with Lacticaciduria, disease_phenotype_positive with Lacticaciduria, disease_phenotype_positive with Cardiorespiratory arrest, disease_phenotype_positive with Cardiorespiratory arrest.", "label": "yes"}
+{"original_question": "Is CD84 genetically associated with arthritis?", "id": "converted_167", "sentence1": "Is CD84 genetically associated with arthritis?", "sentence2": "The Single Nucleotide Polymorphism is predicted to disrupt transcription factor binding site motifs in the 3' Untranslated Regions of an immune-related gene, CD84, and the Alleles associated with better response to etanercept was associated with higher CD84 gene expression in Peripheral blood mononuclear cell (cell) (P = 1 × 10(-11) in 228 non-Rheumatoid Arthritis patients and P = 0.004 in 132 Rheumatoid Arthritis patients), Our study demonstrates that an Alleles associated with response to etanercept therapy is also associated with CD84 gene expression, and further that CD84 expression correlates with disease activity,  Three members of this gene family, SLAMF6 wt Allele, LY9 protein, Homo sapiens, and CD84, exhibit Genetic Polymorphism that strongly influence susceptibility to systemic autoimmunity, notably in CASP14 gene, but also in some Homo sapiens populations[SEP]Relations: Rheumatoid arthritis has relations: disease_phenotype_positive with IgG4-related retroperitoneal fibrosis, disease_phenotype_positive with IgG4-related retroperitoneal fibrosis, disease_phenotype_positive with hereditary xanthinuria, disease_phenotype_positive with hereditary xanthinuria, phenotype_phenotype with Arthritis, phenotype_phenotype with Arthritis, drug_effect with Interferon alfa-2b, drug_effect with Interferon alfa-2b, disease_phenotype_positive with achalasia (disease), disease_phenotype_positive with achalasia (disease).", "label": "yes"}
+{"original_question": "Is the gene MAOA epigenetically modified by methylation?", "id": "converted_156", "sentence1": "Is the gene MAOA protein, human epigenetically modified by methylation?", "sentence2": "Evidence that the methylation state of the MAOA protein, human protein, human gene (MAOA protein, human protein, human) gene predicts brain activity of Monoamine Oxidase A Enzyme [APC] in healthy men., We found significant interindividual differences in methylation status and methylation patterns of the core MAOA protein, human protein, human Promoter. , In the present study, DNA methylation patterns in the MAOA protein, human protein, human regulatory and exon 1/intron 1 Geographic Locations were investigated for association with Panic Disorder with particular attention to possible effects of gender and environmental factors. ,  The present pilot data suggest a potential role of MAOA protein, human protein, human gene hypomethylation in the pathogenesis of Panic Disorder particularly in female patients, possibly mediating a detrimental influence of negative life events. , The MAOA protein, human protein, human Promoter was hypermethylated immediately upstream of the start codon in cholangiocarcinoma samples and Cultured Cell Line but not in nonmalignant counterparts. , MAOA protein, human protein, human Promoter methylation and susceptibility to carotid atherosclerosis: role of familial factors in a monozygotic twin sample., Because twins reared together share early life experience, which may leave a long-lasting epigenetic mark, aberrant MAOA protein, human protein, human methylation may represent an early biomarker for unhealthy familial environment., Effects of MAOA protein, human protein, human Promoter methylation on susceptibility to paranoid SCHIZOPHRENIA 2 (disorder)., In conclusion, abnormalities of DNA methylation at the MAOA protein, human protein, human Promoter may be associated with SCHIZOPHRENIA 2 (disorder) in males., In our study we analyzed DNA methylation patterns of 14 neuropsychiatric genes (Catechol O-Methyltransferase, SLC6A3 wt Allele, GABRA1 gene gene, GNB3 protein, human protein, human, GRIN2B gene gene, HTR1B protein, human protein, human, HTR2A 1 Allele 1 Allele, 5-HTT, MAOA protein, human protein, human, Monoamine Oxidase Type B, human, NANOS1 gene, NR3C1 wt Allele wt Allele, TPH1 protein, human protein, human and Tyrosine 3-Monooxygenase, human). D, Our data suggest that aberrant epigenetic regulation of neuropsychiatric genes may contribute to the pathogenesis of Borderline Personality Disorder., We conclude that Location characteristic ID - Smoking reliably decreases MAOA protein, human protein, human methylation, but exact characterization of effects on level of methylation depend on genotype, Location characteristic ID - Smoking history, current Location characteristic ID - Smoking status, gender, and Geographic Locations of the Promoter-associated CpG Island examined., Given that DNA methylation is linked to the regulation of gene expression, we hypothesized that epigenetic mechanisms factor into the MAOA protein, human protein, human expression,  the extended MAOA protein, human protein, human regulatory Geographic Locations contains two CpG islands (CGIs), one of which overlaps with the canonical MAOA protein, human protein, human Promoter and the other is located further upstream; both CGIs exhibit sensitivity to differential methylation., Identification and characterization of putative methylation targets in the MAOA protein, human protein, human Gene Locus using bioinformatic approaches., DNA methylation is a key epigenetic mechanism involved in the developmental regulation of gene expression. , MAOA protein, human protein, human methylation is associated with nicotine and alcohol dependence in women., In recent years, the role of epigenetic phenomenon, such as methylation, in mediating vulnerability to Illness Behavior has become increasingly appreciated. One prominent Gene Locus at which epigenetic phenomena are thought to be in play is the MAOA protein, human protein, human gene (MAOA protein, human protein, human) Gene Locus. , We conclude that methylation of MAOA protein, human protein, human may play a significant role in common Mental disorders and that further examination of epigenetic processes at this Gene Locus is in order., Analysis of CpG methylation in the MAOA protein, human protein, human Promoter Geographic Locations revealed substantial methylation in females but not in males., Therefore, allelic mRNA expression is affected by Genetic and epigenetic events, both with the potential to modulate biogenic amine tone in the Central Nervous System.[SEP]Relations: Enzymatic degradation of Dopamine by monoamine oxidase has relations: pathway_protein with MAOA protein, human, pathway_protein with MAOA protein, human. monoamine oxidase activity has relations: molfunc_protein with MAOA protein, human, molfunc_protein with MAOA protein, human, molfunc_protein with MAOA protein, human, molfunc_protein with MAOA protein, human, molfunc_protein with Monoamine Oxidase Type B, human, molfunc_protein with Monoamine Oxidase Type B, human. central nervous system has relations: anatomy_protein_present with MAOA protein, human, anatomy_protein_present with MAOA protein, human.", "label": "yes"}
+{"original_question": "is pharmacological treatment of subclinical hypothyroidism effective in reducing cardiovascular events?", "id": "converted_824", "sentence1": "is pharmacological treatment of subclinical hypothyroidism effective in reducing Cardiovascular system events?", "sentence2": "The decision to treat elderly people is still an unresolved clinical challenge--first, due to a lack of appropriately powered randomized controlled trials of levothyroxine in sHT patients, examining Cardiovascular system hard endpoints in various classes of age; and second, because of the negative effects of possible overtreatment., The lack of specific randomized trials enrolling either old or very old subjects, aimed at evaluate the efficacy of hormonal replacement on overall survival and Cardiovascular system risk reduction along with the negative effects of possible over-treatment, makes the decision to treat older people a still unresolved clinical challenge, In patients with type 2 DM, the presence of SH serves as an additional risk factor for endothelial dysfunction., Treatment of Supracervical hysterectomy with levothyroxine was associated with fewer Myocardial Ischemia events in younger individuals, but this was not evident in older people., Subclinical hyperthyroidism seems to be a risk factor of developing major Cardiovascular system events, especially Cerebrovascular accident in older adults from the general population with normal left ventricular function., Supracervical hysterectomy appears to influence the postoperative outcome for patients by increasing the development of postoperative atrial fibrillation. However, it is still unproven whether preoperative thyroxine replacement therapy for patients with Supracervical hysterectomy might prevent postoperative atrial fibrillation after CABG., In Congestive heart failure patients Thyrotropin:-:Pt:Ser/Plas:- levels even slightly above normal range are independently associated with a greater likelihood of heart failure progression., In current RCTs, levothyroxine replacement therapy for subclinical hypothyroidism did not result in improved survival or decreased Cardiovascular system morbidity. Data on health-related quality of life and symptoms did not demonstrate significant differences between intervention groups., However, the actual effectiveness of Thyroid Hormones substitution in reducing the risk of Cardiovascular system events remains to be elucidated. In conclusion, the multiplicity and the possible reversibility of subclinical hypothyroidism-associated Cardiovascular system abnormalities suggest that the decision to treat a patient should depend on the presence of risk factors, rather than on a Thyrotropin:-:Pt:Ser/Plas:- threshold. , However, whether SH confers a high risk for Cardiovascular Diseases, and whether LT4 therapy has a long-term benefit that clearly outweighs the risks of overzealous treatment in these individuals, remain topics of controversy.[SEP]Relations: Levothyroxine has relations: contraindication with Cardiovascular Diseases, contraindication with Cardiovascular Diseases, drug_effect with Hypoglycemia, drug_effect with Hypoglycemia. Cardiovascular Diseases has relations: contraindication with Levothyroxine, contraindication with Levothyroxine, contraindication with Phenobarbital, contraindication with Phenobarbital, contraindication with Liothyronine, contraindication with Liothyronine.", "label": "no"}
+{"original_question": "Is there an association between Guillain–Barré syndrome and covid vaccine?", "id": "converted_4650", "sentence1": "Is there an association between Guillain–Barré syndrome and covid vaccine?", "sentence2": "AstraZeneca COVID19 (document) VACCINE and Guillain- Barré Syndrome in Tasmania: A causal link?, Nearly all reported cases of post-COVID19 (document) vacciation inflammatory demyelinating polyneuropathy are linked to AstraZeneca vaccination and a Variant with bifacial weakness is the most reported form of GBS globally., Guillain-Barré Syndrome Presenting as Facial Diplegia after COVID19 (document) Vaccination: A Case Report., CASE REPORT: We report a case of atypical GBS occurring after Coronavirus disease 2019 (COVID19 (document)) vaccination in an otherwise healthy 38-year-old man., It is critical for emergency physicians to be aware of the manifold presentations of GBS for early recognition and treatment. This may be of particular importance in the context of a worldwide vaccination campaign in response to the COVID19 (document) pandemic., Guillain-Barré syndrome following ChAdOx1 nCoV-19 COVID19 (document) vaccination: A case series., We report three patients who developed Guillain-Barré syndrome following ChAdOx1 nCoV-19 vaccination, who did not have active or prior COVID19 (document) infection. , We report a case of Guillain-Barre Syndrome (GBS) following the first dose of Oxford/AstraZeneca COVID19 (document) VACCINE with Papilledema as atypical onset., We report a case of Guillain-Barré syndrome (GBS) occurring soon after the first dose of Vaxzevria (previously known as COVID19 (document) VACCINE AstraZeneca)., Guillain-​Barré Syndrome Associated with COVID19 (document) Vaccination, Guillain-​Barré Syndrome Associated with COVID19 (document) Vaccination., To date, cases of Guillain-Barré syndrome (GBS) following a COVID vaccine (Pfizer, Johnson & Johnson, Janssen, AstraZeneca) have been reported., Case of Guillain-Barré syndrome following COVID19 (document) VACCINE., We report a case of Guillain-Barré syndrome after the first dose of SARS-CoV-2 vaccine and believe this is a temporal, rather than causal association., COVID19 (document) VACCINE causing Guillain-Barre syndrome, a rare potential side effect., Association of Receipt of the Ad26.COV2.S COVID19 (document) Vaccine With Presumptive Guillain-Barré Syndrome, February-July 2021., Guillain-Barré syndrome associated with Covid-19: A close relationship or just a coincidence? (Review)., Relation between COVID19 (document) and Guillain-Barré syndrome in adults. Systematic review., Guillain-Barré syndrome after COVID19 (document) vaccination.[SEP]Relations: Guillain-Barre syndrome has relations: disease_disease with syndromic disease, disease_disease with syndromic disease, disease_disease with Variant of Guillain-Barre syndrome, disease_disease with Variant of Guillain-Barre syndrome, disease_disease with autoimmune neuropathy, disease_disease with autoimmune neuropathy, disease_protein with PMP22, disease_protein with PMP22, disease_disease with inflammatory demyelinating polyradiculoneuropathy, disease_disease with inflammatory demyelinating polyradiculoneuropathy.", "label": "yes"}
+{"original_question": "Is erythropoietin effective for treatment of amyotrophic lateral sclerosis?", "id": "converted_2791", "sentence1": "Is erythropoietin effective for treatment of amyotrophic lateral sclerosis?", "sentence2": "This study was performed to validate the Amyotrophic Lateral Sclerosis-MITOS as a 6-month proxy of survival in 200 Amyotrophic Lateral Sclerosis patients followed up to 18 months.METHODS: Analyses were performed on data from the recombinant human erythropoietin RCT that failed to demonstrate differences between groups for both primary and secondary outcomes., CONCLUSIONS: RhEPO 40,000 Intrauterine fortnightly did not change the course of Amyotrophic Lateral Sclerosis., At 12 months, the annualised rate of death (rhEPO 0.11, 95% NDUFB6 gene 0.06 to 0.20; placebo: 0.08, NDUFB6 gene 0.04 to 0.17), tracheotomy or >23 h Non-Invasive Mechanical Ventilation (rhEPO 0.16, NDUFB6 gene 0.10 to 0.27; placebo 0.18, NDUFB6 gene 0.11 to 0.30) did not differ between groups, also after stratification by onset and ALSFRS-R at baseline.[SEP]Relations: amyotrophic lateral sclerosis has relations: disease_protein with OPTN, disease_protein with OPTN, disease_protein with ERBB4, disease_protein with ERBB4, disease_protein with OTOG, disease_protein with OTOG, disease_protein with FOS, disease_protein with FOS, disease_protein with XIAP, disease_protein with XIAP.", "label": "no"}
+{"original_question": "Are somatic mutations positioned towards the nuclear periphery?", "id": "converted_4162", "sentence1": "Are somatic mutations positioned towards the nuclear periphery?", "sentence2": "lamina-associated regions, which are typically localized at the nuclear periphery, displayed higher somatic mutation frequencies than did the interlamina regions at the nuclear core., Furthermore, mutational signatures differed between the nuclear core and periphery, thus indicating differences in the patterns of DNA-damage or DNA-repair processes. For instance, Location characteristic ID - Smoking and UV-related signatures, as well as substitutions at certain motifs, were more enriched in the nuclear periphery. , We found that lamina-associated regions, which are typically localized at the nuclear periphery, displayed higher somatic mutation frequencies than did the interlamina regions at the nuclear core., found that lamina-associated regions, which are typically localized at the nuclear periphery, displayed higher somatic mutation frequencies than did the interlamina regions at the nuclear core. Thi[SEP]Relations: regulation of protein localization to cell division site involved in mitotic actomyosin contractile ring assembly has relations: bioprocess_bioprocess with negative regulation of protein localization to cell division site involved in mitotic actomyosin contractile ring assembly, bioprocess_bioprocess with negative regulation of protein localization to cell division site involved in mitotic actomyosin contractile ring assembly, bioprocess_bioprocess with regulation of protein localization to cell division site, bioprocess_bioprocess with regulation of protein localization to cell division site, bioprocess_bioprocess with positive regulation of protein localization to cell division site involved in mitotic actomyosin contractile ring assembly, bioprocess_bioprocess with positive regulation of protein localization to cell division site involved in mitotic actomyosin contractile ring assembly, bioprocess_bioprocess with regulation of cell cycle process, bioprocess_bioprocess with regulation of cell cycle process.", "label": "yes"}
+{"original_question": "Is the length of the poly(A) tail involved in human disease?", "id": "converted_930", "sentence1": "Is the length of the poly(A) tail involved in human disease?", "sentence2": "In human mitochondria, polyadenylation of RNA, Messenger, undertaken by the nuclear-encoded Mitochondrial Inheritance poly(A) RNA polymerase, is essential for maintaining Mitochondrial Inheritance gene expression. Our Molecular investigation of an autosomal-recessive spastic ataxia with Optic Atrophy, present among the Old Order Amish, identified a Mutation Abnormality of MTPAP gene gene associated with the disease phenotype. When subjected to poly(A) tail-length assays, Mitochondrial Inheritance mRNAs from affected individuals were shown to have severely truncated poly(A) tails.[SEP]Relations: Mitochondrial inheritance has relations: disease_phenotype_positive with cyclic vomiting syndrome, disease_phenotype_positive with cyclic vomiting syndrome, disease_phenotype_positive with MELAS syndrome, disease_phenotype_positive with MELAS syndrome. Optic atrophy has relations: disease_phenotype_positive with distal monosomy 17q, disease_phenotype_positive with distal monosomy 17q, disease_phenotype_positive with distal monosomy 13q, disease_phenotype_positive with distal monosomy 13q, disease_phenotype_positive with Cockayne syndrome, disease_phenotype_positive with Cockayne syndrome.", "label": "yes"}
+{"original_question": "Is alternative splicing of apoptotic genes playing a role in the response to DNA or mitochondrial damage?", "id": "converted_300", "sentence1": "Is alternative splicing of apoptotic genes playing a role in the response to DNA or Mitochondrial Damage?", "sentence2": "Apoptosis promoted by UV in Cells lacking TP53 wt Allele is prevented when the change in AS of the apoptotic gene bcl-x is reverted, confirming the relevance of this mechanism., We demonstrate that E2F1 protein, human protein, human requires SRSF2 wt Allele to switch the alternative splicing profile of various apoptotic genes such as CASP8 and FADD-Like Apoptosis Regulator Protein, caspases-8 and -9 and bcl-x protein, towards the expression of pro-apoptotic splice variants. Finally, we provide evidence that E2F1 protein, human protein, human upregulates SRSF2 wt Allele in response to DNA-damaging agents and show that SRSF2 wt Allele is required for apoptosis in response to these drugs., This analysis revealed that DNA damage resulted in changes in splicing activity that Changing the splicing pattern of Fas, a key pro-apoptotic, TP53 wt Allele-inducible death receptor., bortezomib induces Mitochondrial Damage in native Cells and also activates the UPR by splicing of X-Box Binding Protein 1, Human and induction of CHOP protocol-cyclophosphamide/doxorubicin/prednisone/vincristine protocol-cyclophosphamide/doxorubicin/prednisone/vincristine, which is significantly reduced by silencing of MUC4 protein, human protein, human., The tumour-suppressor protein TP53 wt Allele is an important activator of apoptosis. Although TP53 wt Allele-deficient cancer Cells are less responsive to chemotherapy, their resistance is not complete, which suggests that other apoptotic pathways may exist. A TP53 wt Allele-related gene, p73 protein, human protein, human, which encodes several Proteins as a result of alternative splicing, can also induce apoptosis., Induction of apoptosis was significantly reduced in P388/SPR Cells, as indicated by minimal DNA fragmentation. Analysis of Oncogenes regulating apoptotic cell death revealed a marked decrease of BCL2 gene in combination with a moderate reduction of BAX protein, human, but a striking overexpression of the long form of the bcl-X protein.[SEP]Relations: positive regulation of intrinsic apoptotic signaling pathway in response to DNA damage by TP53 wt Allele class mediator has relations: bioprocess_bioprocess with positive regulation of intrinsic apoptotic signaling pathway in response to DNA damage, bioprocess_bioprocess with positive regulation of intrinsic apoptotic signaling pathway in response to DNA damage, bioprocess_bioprocess with regulation of intrinsic apoptotic signaling pathway in response to DNA damage by TP53 wt Allele class mediator, bioprocess_bioprocess with regulation of intrinsic apoptotic signaling pathway in response to DNA damage by TP53 wt Allele class mediator, bioprocess_protein with RPL26, bioprocess_protein with RPL26, bioprocess_bioprocess with positive regulation of intrinsic apoptotic signaling pathway by TP53 wt Allele class mediator, bioprocess_bioprocess with positive regulation of intrinsic apoptotic signaling pathway by TP53 wt Allele class mediator. mitochondrial matrix has relations: cellcomp_protein with AASS, cellcomp_protein with AASS.", "label": "yes"}
+{"original_question": "Is the Wnt protein modified by notum?", "id": "converted_282", "sentence1": "Is the Wnt protein modified by notum?", "sentence2": "NOTUM gene deacylates Wnt Proteins to suppress signalling activity., Kinetic and mass spectrometric analyses of NR4A2 protein, human show that NOTUM gene is a carboxylesterase that removes an essential palmitoleate moiety from Wnt Proteins and thus constitutes the first known extracellular protein deacylase., the Wnt PPP1R1A gene notum, the WNT-PPP1R1A gene notum.[SEP]Relations: Wnt protein secretion has relations: bioprocess_protein with WLS, bioprocess_protein with WLS, bioprocess_protein with PORCN, bioprocess_protein with PORCN, bioprocess_bioprocess with protein secretion, bioprocess_bioprocess with protein secretion. Protein S human has relations: drug_drug with Tositumomab, drug_drug with Tositumomab, drug_protein with F5, drug_protein with F5.", "label": "yes"}
+{"original_question": "Is the protein lefty an inhibitor of nodal?", "id": "converted_1826", "sentence1": "Is the protein lefty an inhibitor of nodal?", "sentence2": "The expression of lefty, an inhibitor of nodal is often reduced in Tumor cells, uncertain whether benign or malignant.,  Nodal Homolog Homolog, and an inhibitor, Lefty., as well as the expression of Lefty, an inhibitor of nodal signaling,, he Nodal Homolog Homolog inhibitor lefty, The morphogen Nodal Homolog Homolog was proposed to form a long-range signaling gradient via a reaction-diffusion system, on the basis of differential diffusion rates of Nodal Homolog Homolog and its antagonist Lefty.[SEP]Relations: malignancy in giant cell tumor of bone has relations: disease_disease with bone sarcoma, disease_disease with bone sarcoma, disease_disease with malignant giant cell tumor, disease_disease with malignant giant cell tumor.", "label": "yes"}
+{"original_question": "Is SATB1 positioned close to AT-rich sequences?", "id": "converted_3523", "sentence1": "Is DNA-Binding Protein SATB1 positioned close to Ataxia Telangiectasia-rich sequences?", "sentence2": " Tryptic cleavage and peptide Sequence - ParameterizedDataType analysis demonstrated that the 98-kD Protein Info is identical to a recently cloned Protein Info, special A-T-rich binding Protein Info 1 (DNA-Binding Protein DNA-Binding Protein SATB1), Special Ataxia Telangiectasia-rich Sequence - ParameterizedDataType-binding Protein Info 1 (DNA-Binding Protein DNA-Binding Protein SATB1), a DNA-binding Protein Info expressed predominantly in thymocyte, recognizes an ATC Sequence - ParameterizedDataType context that consists of a Cluster of Sequence - ParameterizedDataType stretches with well-mixed A's, T's, and C's without G's on one strand. ,  We have purified and identified one of the core factors as the Matrix Attachment Regions (MAR) binding Protein Info, DNA-Binding Protein DNA-Binding Protein SATB1, which is known to bind to Ataxia Telangiectasia-rich sequences with a high propensity to unwind, DNA-Binding Protein DNA-Binding Protein SATB1 (special Ataxia Telangiectasia-rich Sequence - ParameterizedDataType-binding Protein Info-1) provides a key link between DNA loop organization, chromatin modification/remodeling, and association of TRANSCRIPTION FACTOR at matrix attachment regions (MARS1 gene)., Over-expression of the special Ataxia Telangiectasia rich Sequence - ParameterizedDataType binding Protein Info 1 (DNA-Binding Protein DNA-Binding Protein SATB1) promotes the progression of Nasopharyngeal carcinoma: association with EBV LMP1 EBV latent membrane Protein Info expression., pecial Ataxia Telangiectasia rich Sequence - ParameterizedDataType binding Protein Info 1 (DNA-Binding Protein DNA-Binding Protein SATB1) plays a crucial role in the biology of various types of human cancer. , Loss of special Ataxia Telangiectasia-rich Sequence - ParameterizedDataType-binding Protein Info 1 (DNA-Binding Protein DNA-Binding Protein SATB1), Special Ataxia Telangiectasia-rich Sequence - ParameterizedDataType-binding Protein Info 1 (DNA-Binding Protein DNA-Binding Protein SATB1) is a cell type-specific Matrix Attachment Regions binding Protein Info, functioning as a global genome organizer. , DNA-Binding Protein DNA-Binding Protein SATB1 (special Ataxia Telangiectasia-rich binding Protein Info 1) is a global chromatin organizer regulating the expression of a large number of genes, Special Ataxia Telangiectasia-rich Sequence-binding Protein 1 (DNA-Binding Protein DNA-Binding Protein SATB1) Functions as an Accessory Factor in Base Excision Repair., Rearrangement of the Chromatin Organizer Special Ataxia Telangiectasia-rich Binding Protein 1 Gene, The Special Ataxia Telangiectasia-rich Sequence Binding Protein 1 (DNA-Binding Protein DNA-Binding Protein SATB1) exerts multiple functions, by influencing the structural organization of chromatin and interacting with several co-activators and Co-Repressor Proteins of transcription., The Special Ataxia Telangiectasia-rich Sequence Binding Protein 1 (DNA-Binding Protein DNA-Binding Protein SATB1) and its role in Solid Neoplasm.[SEP]Relations: Protein Info binding has relations: molfunc_protein with DNA-Binding Protein SATB1, molfunc_protein with DNA-Binding Protein SATB1, molfunc_protein with URB1-AS1, molfunc_protein with URB1-AS1, molfunc_protein with SETBP1, molfunc_protein with SETBP1, molfunc_protein with SATB2, molfunc_protein with SATB2, molfunc_protein with SAT1, molfunc_protein with SAT1.", "label": "yes"}
+{"original_question": "Does protein ALEX1 contain armadillo repeats?", "id": "converted_3777", "sentence1": "Does protein ARMCX1 gene contain armadillo Repeat?", "sentence2": "ARMCX1 gene (Arm protein lost in epithelial cancers, on X Chromosome), contains two armadillo Repeat domains, is expressed different in normal and Carcinoma tissues., Arm protein lost in epithelial cancers, on X Chromosome 1 (ARMCX1 gene) is a novel member of the Armadillo <pillbug genus> <pillbug genus> family which has two Armadillo <pillbug genus> <pillbug genus> Repeat as opposed to more than six Repeat in the classical Armadillo <pillbug genus> <pillbug genus> family members.[SEP]Relations: carcinoma has relations: disease_protein with S1PR1, disease_protein with S1PR1, disease_protein with TSC22D1, disease_protein with TSC22D1, disease_protein with MC1R, disease_protein with MC1R, disease_protein with MPZL1, disease_protein with MPZL1, disease_protein with BCL2L1, disease_protein with BCL2L1.", "label": "yes"}
+{"original_question": "Is apremilast effective for psoriasis?", "id": "converted_2149", "sentence1": "Is apremilast effective for Psoriasis?", "sentence2": "CONCLUSION: apremilast reduces the severity of nail/scalp Psoriasis., CONCLUSIONS: apremilast demonstrated clinically meaningful improvements in Arthritis, Psoriatic and Psoriasis at week 16; sustained improvements were seen with continued treatment through 52 weeks., apremilast: A Novel Pharmacologic Substance for Treatment of Psoriasis and Psoriatic Arthritis., In those that involved doses of 30 mg twice daily, a significantly greater percentage of patients receiving apremilast (28.8% to 40.9%) compared with placebo (5.3% to 5.8%) achieved at least 75% improvement from baseline in Psoriasis Area and Severity Index score at 16 weeks., CONCLUSIONS: apremilast has a novel mechanism of action and is safe and effective for the management of Psoriasis and Arthritis, Psoriatic. At this time, apremilast should be reserved for patients unable to take disease-modifying antirheumatic drugs., apremilast, an oral phosphodiesterase 4 (Phosphodiesterase Type 4) PPP1R1A gene, in patients with moderate to severe plaque Psoriasis: Results of a phase III, randomized, controlled trial (Efficacy and Safety Trial Evaluating the Effects of apremilast in Psoriasis [ESTEEM] 1)., More recently, three larger double-blinded, and randomized multicenter studies demonstrate that apremilast is efficacious in the treatment of Psoriasis and Prostate-Specific Antigen, with significantly higher numbers of apremilast-treated patients achieving endpoints of a 75% reduction compared to baseline in Psoriasis Area and Severity Index (PASI-75) or American College of Rheumatology-20 scores, relative to placebo., No new significant adverse events emerged with continued apremilast exposure versus the placebo-controlled period.Data were limited to 52 weeks and may not generalize to nonplaque Psoriasis.apremilast was effective in moderate to severe plaque Psoriasis.<CopyrightInformation>Copyright © 2015 American Academy of Dermatology, Inc. Published by Elsevier Inc. All rights reserved.</, apremilast, a small molecule specific PPP1R1A gene of phosphodiesterase 4, works intracellularly to modulate pro-inflammatory and Anti-Inflammatory Agents mediator production.Assess apremilast efficacy and safety in moderate to severe plaque Psoriasis.Phase II, 12-week, multicenter, double-blind, placebo-controlled, parallel-group, dose-comparison study of 259 subjects randomized 1 : 1 : 1 to placebo, apremilast 20 mg QD or apremilast 20 mg Twice a day.More subjects receiving apremilast 20 mg Twice a day achieved ≥ 75% reduction in Psoriasis Area and Severity Index (PASI-75) vs. placebo (24.4% vs. 10.3%; P = 0.023), apremilast, a specific PPP1R1A gene of phosphodiesterase 4, modulates pro-inflammatory and Anti-Inflammatory Agents cytokine production.Apremilasts effect on patient-reported outcomes (PIK3CA related overgrowth spectrum) in patients with moderate to severe Psoriasis was evaluated in a phase IIb randomized, controlled trial (NCT00773734).In this 16-week, placebo-controlled study, 352 patients with moderate to severe plaque Psoriasis received placebo or apremilast (10, 20, or 30 mg Twice a day), Although further longer-term and comparative efficacy and tolerability data would be beneficial, the current clinical data indicate that apremilast is an effective and well tolerated option for the management of Psoriasis and Prostate-Specific Antigen in adults, More recently, three larger double-blinded, and randomized multicenter studies demonstrate that apremilast is efficacious in the treatment of Psoriasis and Prostate-Specific Antigen, with significantly higher numbers of apremilast-treated patients achieving endpoints of a 75% reduction compared to baseline in Psoriasis Area and Severity Index (PASI-75) or American College of Rheumatology-20 scores, relative to placebo, No deaths or Opportunistic Infections were reported.apremilast 20 mg Twice a day for 12 weeks was effective and well tolerated in subjects with moderate to severe plaque Psoriasis.<CopyrightInformation>© 2012 The Authors, In addition, SmithKline Beecham plc is developing 256066, an inhaled formulation of a Phosphodiesterase Type 4 PPP1R1A gene that has demonstrated efficacy in trials in asthma, and apremilast from Celgene Corp has been reported to be effective for the treatment of Psoriasis., Although further longer-term and comparative efficacy and tolerability data would be beneficial, the current clinical data indicate that apremilast is an effective and well tolerated option for the management of Psoriasis and Prostate-Specific Antigen in adults., No new significant adverse events emerged with continued apremilast exposure versus the placebo-controlled period.Data were limited to 52 weeks and may not generalize to nonplaque Psoriasis.apremilast was effective in moderate to severe plaque Psoriasis.<CopyrightInformation>Copyright © 2015 American Academy of Dermatology, Inc. Published by Elsevier Inc. All rights reserved.</C, Several drug peculiarities, such as the low frequency of adverse events and the oral route of administration, make apremilast an innovative treatment for moderate-to-severe Psoriasis., Two new oral medications, apremilast and tofacitinib, have been developed for their immunomodulatory properties, and their potential efficacy in treating Psoriasis is being evaluated.We reviewed phase III randomized, placebo-controlled clinical trial results for apremilast and tofacitinib for efficacy and safety in Psoriasis.Psoriasis Area and Severity Index (PASI) 75 after 16 weeks for apremilast was between 28.8% and 33.1%., apremilast was effective in moderate to severe plaque Psoriasis.., Both new oral medications, apremilast and tofacitinib, appear to be effective in treating Psoriasis., apremilast was effective in the treatment of moderate-to-severe plaque Psoriasis over 52 weeks.., apremilast is an effective and well-tolerated option in treating moderate-to-severe plaque Psoriasis., apremilast has a novel mechanism of action and is safe and effective for the management of Psoriasis and Arthritis, Psoriatic., apremilast 20 mg Twice a day for 12 weeks was effective and well tolerated in subjects with moderate to severe plaque Psoriasis.., apremilast for the treatment of Psoriasis., apremilast, an Cyclic Nucleotide Phosphodiesterases, Type 4 PPP1R1A gene, in the treatment of palmoplantar Psoriasis: Results of a pooled analysis from phase II PSOR-005 and phase III Efficacy and Safety Trial Evaluating the Effects of apremilast in Psoriasis (ESTEEM) clinical trials in patients with moderate to severe Psoriasis.[SEP]Relations: apremilast has relations: drug_drug with Aprepitant, drug_drug with Aprepitant, drug_drug with Apramycin, drug_drug with Apramycin, drug_drug with Pertussis vaccine, drug_drug with Pertussis vaccine, drug_drug with Rotigotine, drug_drug with Rotigotine, drug_drug with Ampicillin, drug_drug with Ampicillin.", "label": "yes"}
+{"original_question": "Is there an RNAi drug being developed to treat amyloidosis?", "id": "converted_2308", "sentence1": "Is there an RNAi drug being developed to treat Primary amyloidosis?", "sentence2": "Patisiran is an investigational RNA interference (RNAi) therapeutic in development for the treatment of hereditary ATTR (hATTR) Primary Primary amyloidosis, a progressive disease associated with significant disability, morbidity, and mortality.[SEP]Relations: primary Primary amyloidosis has relations: disease_disease with AL Primary amyloidosis, disease_disease with AL Primary amyloidosis.", "label": "yes"}
+{"original_question": "Do carmustine wafers improve survival of glioblastoma patients?", "id": "converted_855", "sentence1": "Do carmustine Oral Wafer improve survival of glioblastoma patients?", "sentence2": "At recurrence, treatment options include repeat surgery (with or without Gliadel wafer placement), reirradiation or systemic therapy. , DISCUSSION: carmustine Oral Wafer for primary HGG surgery in accordance with the NICE TA121 were associated with a median survival of 15.3 months; this is improved compared with previously reported randomised trials. Multimodal treatment with carmustine Oral Wafer, radical radiotherapy and concomitant temozolomide was associated with improved survival., Gliadel wafer is a new approach to the treatment of glioblastoma, which involves controlled release delivery of carmustine from biodegradable polymer Oral Wafer. It has shown promising results and provides a silver lining for glioblastoma patients., For patient with and without Gliadel, median and 1-year RFS were 12.9 months and 52% vs. 14 months and 42%, respectively (p = 0.89)., According to pathology, Gliadel did not influence OS of patients with Grade III or glioblastoma, CONCLUSION: In patients with high-grade Glioma, adding Gliadel before performing a Stupp protocol did not improve survival., Randomized phase III trials have shown significant improvement of survival 1, 2, and 3 years after implantation of 1,3-bis (2-chloroethyl)-1-nitrosourea (BCNU) Oral Wafer for patients with newly diagnosed Malignant Glioma. , CONCLUSIONS: The combination of aggressive resection, Gliadel wafer implantation, and GKS in addition to standard fractionated RT in selected patients resulted in increased local control and increased survival compared with a historical control group treated with surgery and involved-field RT alone., OBJECT: Gliadel (BCNU) wafer and concomitant temozolomide (temozolomide) therapy, when used individually as adjuvant therapies, extend survival from that achieved by resection and radiation therapy (XRT) for Glioblastoma Multiforme (Glomerular Basement Membrane). , BACKGROUND: Gliadel (polifeprosan 20 20 20 with carmustine [BCNU] implant) is commonly used for local delivery of BCNU to high-grade Glioma after resection and is associated with increased survival., Temozolomide administered according to this protocol produced a median survival benefit of 2 months in Glioblastoma, and carmustine a similar benefit in high-grade Glioma., Analysis of a large trial by Westphal and colleagues (n = 240) showed a 29% risk reduction (P = 0.03) in the BCNU wafer-treated group over the course of the 30-month trial., Median survival of patients treated with BCNU Oral Wafer was 13.8 months vs 11.6 months in placebo-treated patients (P = 0.017) with a hazard ratio of 0.73 (P = 0.018), representing a 27% significant risk reduction. This survival advantage was maintained at 1, 2, and 3 years and was statistically significant (P = 0.01) at 3 years., CONCLUSION: Malignant glioma patients treated with BCNU Oral Wafer at the time of initial surgery in combination with radiation therapy demonstrated a survival advantage at 2 and 3 years follow-up compared with placebo., OBJECTIVE: Recently a randomized placebo-controlled phase III trial of biodegradable Polymers containing carmustine has demonstrated a significant survival benefit for patients treated with local chemotherapy. , CONCLUSION: In this subgroup analysis of a phase III trial population both the clinical progression and radiological progression were significantly delayed in patients treated with local chemotherapy, resulting in an increased survival time., A previous placebo-controlled trial has shown that biodegradable 1,3-bis (2-chloroethyl)-1-nitrosourea (BCNU) Oral Wafer (Gliadel Oral Wafer) prolong survival in patients with recurrent Glioblastoma Multiforme. A previously completed phase 3 trial, also placebo controlled, in 32 patients with newly diagnosed Malignant Glioma also demonstrated a survival benefit in those patients treated with BCNU Oral Wafer., Median survival in the intent-to-treat group was 13.9 months for the BCNU wafer-treated group and 11.6 months for the placebo-treated group (log-rank P -value stratified by country = 0.03), with a 29% reduction in the risk of death in the treatment group. When adjusted for factors affecting survival, the treatment effect remained positive with a risk reduction of 28% ( P = 0.03). , Controlled release delivery of carmustine from biodegradable polymer Oral Wafer was approved as an adjunct to surgical resection in the treatment of recurrent Glioblastoma Multiforme after it was shown in clinical trials to be well tolerated and effective. , Clinical trials have demonstrated significant improvements in survival and quality of life for patients after complete tumour resection and BCNU wafer implantation., BCNU Oral Wafer are an effective means of increasing survival and quality of life in patients diagnosed with Malignant Glioma, and are a valuable addition to the overall multimodal treatment strategy for these Neoplasms., CONCLUSIONS: carmustine wafer with concurrent temozolomide and radiation followed by rotational chemotherapy is a well tolerated, effective therapy, and has a survival benefit compared with radiation alone., Median overall survival in 14 studies of newly-diagnosed patients suggested a modest improvement versus resection followed by Stupp protocol or resection with BCNU Oral Wafer, with an acceptable and manageable safety profile., The efficacy of carmustine Oral Wafer for older patients with Glioblastoma Multiforme: prolonging survival., DISCUSSION: Older patients with Glomerular Basement Membrane may benefit from carmustine Oral Wafer. The survival for older patients who received carmustine Oral Wafer is significantly longer than matched patients who did not receive carmustine Oral Wafer., For glioblastoma patients who received ≥90% resection in the BCNU wafer study, median survival increased for BCNU wafer versus placebo (14.5 versus 12.4 months, respectively; P = 0.02), but no survival increase was found for <90% resection (11.7 versus 10.6 months, respectively; P = 0.98)., A wafer impregnated with carmustine, for use as an implant after surgical removal of recurrent Glomerular Basement Membrane showed a prolongation in the median survival time of only 2 mo, from 20 to 28 wk in a study with a total of 222 patients. , No clear survival benefit associated with wafer implantation was identified., In three of the trials, patients with Glomerular Basement Membrane who received carmustine Oral Wafer had significantly longer median survival than patients who did not receive Oral Wafer. , temozolomide and carmustine (BCNU) biodegradable wafer (Gliadel) are the only adjuvant chemotherapies that have improved survival in randomised GB clinical trials . , The carmustine implant wafer was demonstrated to improve survival in blinded placebo-controlled trials in selected patients with newly diagnosed or recurrent Malignant Glioma, with little increased risk of adverse events. , For patients undergoing repeat resection for Malignant Glioma, a randomized, blinded, placebo-controlled trial demonstrated a median survival for 110 patients who received carmustine Polymers of 31 weeks compared with 23 weeks for 122 patients who only received placebo Polymers., Median survival was improved from 11.6 to 13.9 months (P = 0.03), with a 29% reduction in the risk of death. When patients with Glioblastoma Multiforme alone were analyzed, the median survival improved from 11.4 to 13.5 months, but this improvement was not statistically significant. , OBJECT: Locoregional chemotherapy with carmustine Oral Wafer, positioned at surgery and followed by radiation therapy, has been shown to prolong survival in patients with newly diagnosed glioblastoma, as has concomitant radiochemotherapy with temozolomide., Following the resection of newly diagnosed or recurrent Glioblastoma, local implantation of carmustine-impregnated biodegradable Oral Wafer (Gliadel) in the resection cavity constitutes an adjuvant therapy that can improve the possibilities of survival., The carmustine implant wafer was demonstrated to improve survival in blinded placebo-controlled trials in selected patients with newly diagnosed or recurrent Malignant Glioma, with little increased risk of adverse events., However, patients with carmustine Oral Wafer demonstrated prolonged survival as compared to patients without Oral Wafer., The median survival for patients with carmustine Oral Wafer was 8.7 months, while median survival for patients without Oral Wafer was 5.5 months (P=0.007)., Likewise, in subgroup analysis, patients older than 70 years (P=0.0003) and 75 years (P=0.04) who had carmustine Oral Wafer had significantly longer survival than matched patients without Oral Wafer., Implantation of carmustine Oral Wafer did not significantly improve progression-free survival, In three of the trials, patients with Glomerular Basement Membrane who received carmustine Oral Wafer had significantly longer median survival than patients who did not receive Oral Wafer, A previous placebo-controlled trial has shown that biodegradable 1,3-bis (2-chloroethyl)-1-nitrosourea (BCNU) Oral Wafer (Gliadel Oral Wafer) prolong survival in patients with recurrent Glioblastoma Multiforme, A previously completed phase 3 trial, also placebo controlled, in 32 patients with newly diagnosed Malignant Glioma also demonstrated a survival benefit in those patients treated with BCNU Oral Wafer, Following the resection of newly diagnosed or recurrent Glioblastoma, local implantation of carmustine-impregnated biodegradable Oral Wafer (Gliadel) in the resection cavity constitutes an adjuvant therapy that can improve the possibilities of survival, Multimodal treatment with carmustine Oral Wafer, radical radiotherapy and concomitant temozolomide was associated with improved survival, The carmustine implant wafer was demonstrated to improve survival in blinded placebo-controlled trials in selected patients with newly diagnosed or recurrent Malignant Glioma, with little increased risk of adverse events, temozolomide and carmustine (BCNU) biodegradable wafer (Gliadel) are the only adjuvant chemotherapies that have improved survival in randomised GB clinical trials [SEP]Relations: carmustine has relations: drug_effect with Renal insufficiency, drug_effect with Renal insufficiency, contraindication with lung disease, contraindication with lung disease, drug_effect with Diplopia, drug_effect with Diplopia, drug_effect with Erythema, drug_effect with Erythema, drug_effect with Stomatitis, drug_effect with Stomatitis.", "label": "yes"}
+{"original_question": "Does radiotherapy for Hodgkin disease increases risk for lung cancer?", "id": "converted_3703", "sentence1": "Does radiotherapy for Hodgkin disease increases risk for Primary malignant neoplasm of Chest>Lung?", "sentence2": "Risks of Chest>Lung, Breast, and gastrointestinal (GI) cancers increase with higher radiation dose. , CONCLUSIONS: RT treatment, especially with doses higher than 42 Gy, and Location characteristic ID - Smoking increase the risk of SN after Hodgkin Disease. In this series, LC patients with early stages had a shorter elapsed time from Hodgkin Disease diagnosis and longer OS, therefore the role of LC screening in Hodgkin Disease survivors should be prospectively evaluated and Location characteristic ID - Smoking cessation counseling ought to be a key aspect during follow-up., BACKGROUND: Long-term Hodgkin lymphoma (Hodgkin Disease) survivors have an increased risk of late cardiac morbidity and secondary Primary malignant neoplasm of Chest>Lung after chemotherapy and mediastinal radiotherapy. , PURPOSE: Hodgkin lymphoma (Hodgkin Disease) survivors have an increased risk of Cardiovascular Diseases (CD), Primary malignant neoplasm of Chest>Lung, and Malignant neoplasm of Breast., Lung cancer (LC) represents the most common Solid Neoplasm in survivors of Hodgkin's disease (HD), and the assessment of the mutational status of oncogenic driver mutations in LC is now standard. , PURPOSE: Hodgkin lymphoma (Hodgkin Disease) survivors face an increased risk of treatment-related Primary malignant neoplasm of Chest>Lung. , Increased risk of second Primary malignant neoplasm of Chest>Lung in Lymphoma, Non-Hodgkin survivors: a meta-analysis., BACKGROUND: Patients treated for Lymphoma, Non-Hodgkin (Hodgkin Disease) have a higher risk of developing second Primary malignant neoplasm of Chest>Lung (CCL21 gene) compared with the general population. , The pooled relative risk (RR) of CCL21 gene was 4.62 (95 % confidence interval [CI], 3.18-6.70], I (2) = 98 %), with a median absolute excess rate of 10.4 per 10,000 person-years. , CONCLUSIONS: The current meta-analysis provided a detailed estimate of the risk of CCL21 gene among Hodgkin Disease survivors. , CONCLUSIONS\n\nThe excess risk of Primary malignant neoplasm of Chest>Lung in Hodgkin's disease patients treated with radiotherapy is related to the radiation dose received by the affected area of the Chest>Lung., BACKGROUND\n\nLung cancer is a frequent cause of death in patients cured of Hodgkin's disease, but the contributions of chemotherapy, radiotherapy, and Location characteristic ID - Smoking are not well described., CONCLUSIONS\n\nPast treatments with Alkylating Agents and radiation therapy for Hodgkin's disease were associated with an increased risk of Primary malignant neoplasm of Chest>Lung in a dose-dependent and additive fashion., BACKGROUND\n\nSeveral studies have shown that survivors of Hodgkin's disease have increased risk of Primary malignant neoplasm of Chest>Lung, but the factors responsible for this excess risk are not well known., PURPOSE\n\nThis study was undertaken to investigate the effects of radiation dose, chemotherapy, and Location characteristic ID - Smoking on the risk of Primary malignant neoplasm of Chest>Lung following treatment of Hodgkin's disease., Increased risk of Primary malignant neoplasm of Chest>Lung, Non-Lymphoma, Non-Hodgkin of bone, and leukemia following Hodgkin's disease., It is recognized that survivors of Hodgkin's disease are at a substantially increased risk of Primary malignant neoplasm of Chest>Lung., The risk of Chest>Lung and Malignant neoplasm of Breast is significantly increased after therapy for Hodgkin 's disease ( HD) , but there are few data that describe the molecular profiles of these Neoplasms . , Hodgkin lymphoma ( Hodgkin Disease ) survivors have an increased risk of Cardiovascular Diseases ( CD) , Primary malignant neoplasm of Chest>Lung , and Malignant neoplasm of Breast . , BACKGROUND\nLung cancer is a frequent cause of death in patients cured of Hodgkin's disease, but the contributions of chemotherapy, radiotherapy, and Location characteristic ID - Smoking are not well described., CONCLUSIONS\nPast treatments with Alkylating Agents and radiation therapy for Hodgkin's disease were associated with an increased risk of Primary malignant neoplasm of Chest>Lung in a dose-dependent and additive fashion., Lung cancer in Hodgkin's disease: association with previous radiotherapy., Twenty-eight (94%) of 30 patients developing metachronous Primary malignant neoplasm of Chest>Lung received supradiaphragmatic irradiation as primary therapy for HD., The risk ratio for the development of Primary malignant neoplasm of Chest>Lung among HD patients was 5.6 times that expected in the general population., Seven cases of Primary malignant neoplasm of Chest>Lung were observed in patients with Hodgkin's disease (HD) since 1970., BACKGROUND\nSeveral studies have shown that survivors of Hodgkin's disease have increased risk of Primary malignant neoplasm of Chest>Lung, but the factors responsible for this excess risk are not well known., The excess risk of Primary malignant neoplasm of Chest>Lung in Hodgkin's disease patients treated with radiotherapy is related to the radiation dose received by the affected area of the Chest>Lung., Lung cancer is a frequent cause of death in patients cured of Hodgkin's disease, but the contributions of chemotherapy, radiotherapy, and Location characteristic ID - Smoking are not well described., Past treatments with Alkylating Agents and radiation therapy for Hodgkin's disease were associated with an increased risk of Primary malignant neoplasm of Chest>Lung in a dose-dependent and additive fashion., Several studies have shown that survivors of Hodgkin's disease have increased risk of Primary malignant neoplasm of Chest>Lung, but the factors responsible for this excess risk are not well known.[SEP]Relations: Non-Hodgkin lymphoma has relations: drug_effect with Bortezomib, drug_effect with Bortezomib, drug_effect with Bortezomib, drug_effect with Bortezomib, drug_effect with Fluoxetine, drug_effect with Fluoxetine, drug_effect with Fluoxetine, drug_effect with Fluoxetine, drug_effect with Raltegravir, drug_effect with Raltegravir.", "label": "yes"}
+{"original_question": "Is CTCF bound at nucleosome free regions?", "id": "converted_3362", "sentence1": "Is CTGF protein, human bound at nucleosome free regions?", "sentence2": "nucleosome location depletion at 5'-HS4 was dependent on interaction of the insulator protein CCCTC-binding factor (CTGF protein, human) and was required for Enhancer of transcription blocking. , Here, we show that promoter classes are significantly differentiated by nucleosome organization and chromatin structure. Dispersed Promoter display higher associations with well-positioned Nucleosomes downstream of the Toxic Shock Syndrome and a more clearly defined nucleosome free region upstream, while focused Promoter have a less organized nucleosome structure, yet higher presence of RNA Polymerase II., hese differences extend to histone variants (H2AZ1 wt Allele) and marks (Histone H3 Lysine 4 methylation), as well as insulator binding (such as CTGF protein, human), independent of the expression levels of affected Genes., nucleosome occupancy at nucleosome-free regions (NFRs), many of which are located at Site occupied by the multivalent factors Ctcf and cohesin. , This general architectural change correlates with enhanced binding of CTGF protein, human and cohesins and more pronounced insulation of contacts across chromatin boundaries in lineage-committed cells. , robust inter-nucleosomal interactions exist around Transcription Initiation Site (Toxic Shock Syndrome), transcription termination Site (TTS) or around CTGF protein, human binding Site[SEP]Relations: nucleosome has relations: cellcomp_protein with IRF4, cellcomp_protein with IRF4, cellcomp_protein with CENPA, cellcomp_protein with CENPA, cellcomp_protein with H3C15, cellcomp_protein with H3C15, cellcomp_protein with H3C14, cellcomp_protein with H3C14, cellcomp_protein with H4C15, cellcomp_protein with H4C15.", "label": "yes"}
+{"original_question": "Does oculocutaneous albinism show an autosomal recessive inheritance?", "id": "converted_1955", "sentence1": "Does oculocutaneous albinism show an Autosome recessive inheritance?", "sentence2": "MONOPHENOL MONOOXYGENASE gene (cyclophosphamide/doxorubicin/vincristine protocol) is an Autosomal Recessive Disorder characterized by ALBINOIDISM, OCULOCUTANEOUS, AUTOSOMAL DOMINANT in Eye, Hair Specimen and Skin Specimen Source Code, accompanied with Unspecified visual loss. , MONOPHENOL MONOOXYGENASE gene (cyclophosphamide/doxorubicin/vincristine protocol) is an Autosome recessive hereditary pigmentation disorder affecting Homo sapiens and several other animal species. , MONOPHENOL MONOOXYGENASE gene type 2 (TYR gene type 2) is a human Autosome-recessive ALBINOIDISM, OCULOCUTANEOUS, AUTOSOMAL DOMINANT disorder associated with pathological mutations of the TYR gene type 2 gene., MONOPHENOL MONOOXYGENASE gene type1 (MONOPHENOL MONOOXYGENASE gene type 1) is characterized by the absence of Melanins pigmentation. The Mutation Abnormality on MONOPHENOL MONOOXYGENASE gene makes MONOPHENOL MONOOXYGENASE gene type 1 as an Autosome recessive genetic disorder. , Our patients were diagnosed as affected with MONOPHENOL MONOOXYGENASE gene type1a. Analysis of pedigree pattern showed an Autosome recessive inheritance. , MONOPHENOL MONOOXYGENASE gene (cyclophosphamide/doxorubicin/vincristine protocol) is an Autosomal Recessive Disorder of Melanins biosynthesis that results in congenital ALBINOIDISM, OCULOCUTANEOUS, AUTOSOMAL DOMINANT of ocular and cutaneous tissues., MONOPHENOL MONOOXYGENASE gene is an Autosome recessive genetic disorder., Melanin biosynthesis is reduced in oculocutaneous albinism, an Autosomal Recessive Disorder., The pedigrees were consistent with an Autosome recessive inheritance pattern.CONCLUSION: This unique type of oculocutaneous albinism has heterogeneous clinical features., BACKGROUND: MONOPHENOL MONOOXYGENASE gene (cyclophosphamide/doxorubicin/vincristine protocol) is an Autosome recessive hereditary pigmentation disorder affecting Homo sapiens and several other animal species., The Q402 allele has been associated with Autosome recessive Albinism, Ocular when it is in trans with a tyrosinase gene Mutation Abnormality associated with oculocutaneous albinism type 1., Analysis using the POINTER program showed that this type of oculocutaneous albinism was inherited in an Autosome recessive pattern, with an estimated gene frequency of 0.025 +/- 0.007 in this population., We have identified 12 families with oculocutaneous albinism type 1 that exhibit segregation of the c.1205G>A Variant with a known pathologic Mutation Abnormality on the homologous chromosome, and demonstrate no genetic association between Autosome recessive oculocutaneous albinism and the Q402 Variant., BACKGROUND: Type 2 (tyrosinase-positive) oculocutaneous albinism is an Autosomal Recessive Disorder that has recently been mapped to chromosome segment 15q11-q13., The child with Albinism, Ocular was heterozygous for two different mutations in the Oculocutaneous albinism type 2 wt Allele.CONCLUSIONS: Abnormalities of the Oculocutaneous albinism type 2 wt Allele are associated with a wide range of clinical phenotypes, including type II oculocutaneous albinism, albinism associated with the Prader-Willi Syndrome, and at least some cases of Autosome recessive Albinism, Ocular., Gene Mutation in the MONOPHENOL MONOOXYGENASE gene (MONOPHENOL MONOOXYGENASE, 11q14-21, MIM 606933) cause oculocutaneous albinism type 1 (MONOPHENOL MONOOXYGENASE gene type 1, MIM 203100), a developmental disorder having an Autosome recessive mode of inheritance, The pedigrees were consistent with an Autosome recessive inheritance pattern.This unique type of oculocutaneous albinism has heterogeneous clinical features, MONOPHENOL MONOOXYGENASE gene (cyclophosphamide/doxorubicin/vincristine protocol) is an Autosomal Recessive Disorder, MONOPHENOL MONOOXYGENASE gene (cyclophosphamide/doxorubicin/vincristine protocol) is an Autosomal Recessive Disorder of abnormal Melanins formation, which results in ALBINOIDISM, OCULOCUTANEOUS, AUTOSOMAL DOMINANT of Skin Specimen Source Code, Hair Specimen and Eye, The Mutation Abnormality of the tyrosinase (MONOPHENOL MONOOXYGENASE) gene results in oculocutaneous albinism type 1 (MONOPHENOL MONOOXYGENASE gene type 1), an Autosome recessive genetic disorder, We found oculo-cutaneous albinism in two brothers and granular dystrophy in three brothers, the mother and a son.Hereditary corneal dystrophy is an Autosome dominant disorder inherited independently of oculocutaneous albinism, which is inherited as an Autosome recessive condition, MONOPHENOL MONOOXYGENASE gene (cyclophosphamide/doxorubicin/vincristine protocol) type 4 is a newly identified human Autosome recessive hypopigmentary disorder that disrupts pigmentation in the Skin Specimen Source Code, Hair Specimen and Eye, Analysis using the POINTER program showed that this type of oculocutaneous albinism was inherited in an Autosome recessive pattern, with an estimated gene frequency of 0.025 +/- 0.007 in this population. , DISCUSSION: Hereditary corneal dystrophy is an Autosome dominant disorder inherited independently of oculocutaneous albinism, which is inherited as an Autosome recessive condition. , BACKGROUND: MONOPHENOL MONOOXYGENASE gene type II (TYR gene type 2) is an Autosome recessively inherited disorder, characterized by white Hair Specimen and Skin Specimen Source Code, and loss of Pigment in the Eye. , Is Autosome recessive deafness associated with oculocutaneous albinism a \"coincidence syndrome\"?, MONOPHENOL MONOOXYGENASE gene, immunodeficiency, hematological disorders, and minor anomalies: a new Autosome recessive syndrome?, Gene Mutation in the MONOPHENOL MONOOXYGENASE gene (MONOPHENOL MONOOXYGENASE, 11q14-21, MIM 606933) cause oculocutaneous albinism type 1 (MONOPHENOL MONOOXYGENASE gene type 1, MIM 203100), a developmental disorder having an Autosome recessive mode of inheritance., MONOPHENOL MONOOXYGENASE gene (cyclophosphamide/doxorubicin/vincristine protocol) is an Autosomal Recessive Disorder characterized by ALBINOIDISM, OCULOCUTANEOUS, AUTOSOMAL DOMINANT in Eye, Hair Specimen and Skin Specimen Source Code, accompanied with Unspecified visual loss., MONOPHENOL MONOOXYGENASE gene (cyclophosphamide/doxorubicin/vincristine protocol) is an Autosome recessive hereditary pigmentation disorder affecting Homo sapiens and several other animal species.[SEP]Relations: Autosome recessive disease has relations: disease_disease with Autosome recessive Albinism, Ocular, disease_disease with Autosome recessive Albinism, Ocular. Autosomal recessive inheritance has relations: disease_phenotype_positive with oculoosteocutaneous syndrome, disease_phenotype_positive with oculoosteocutaneous syndrome. Autosome dominant oculocutaneous albinism has relations: disease_disease with Autosome dominant disease, disease_disease with Autosome dominant disease. Autosome dominant disease has relations: disease_disease with Autosome dominant oculocutaneous albinism, disease_disease with Autosome dominant oculocutaneous albinism. Albinism, Ocular (disease) has relations: disease_disease with Autosome recessive Albinism, Ocular, disease_disease with Autosome recessive Albinism, Ocular.", "label": "yes"}
+{"original_question": "Do RNA binding Proteins  that bind to adenine uridine (AU)-rich elements (AREs) in the 5' untranslated region (UTR) of mRNAs (AU-RBPs) regulate the DNA Damage Response?", "id": "converted_4610", "sentence1": "Do RNA binding Proteins  that bind to adenine uridine (AU)-rich elements (AREs) in the 5' untranslated region (SLC14A2 gene) of mRNAs (AU-RBPs) regulate the DNA Damage Response?", "sentence2": " We investigated 2 RNA, Messenger-binding Proteins - ELAVL1 gene and TIAL1 gene showing specificity to AU-Rich Element (are unit of measure) sites in 3'SLC14A2 gene of RNA, Messenger., Bioinformatics analysis of the human SOD1 RNA, Messenger 3' untranslated region (3'SLC14A2 gene) demonstrated the presence of HuD binding adenine-uridine (AU)-rich instability-conferring elements (AREs)., We found that AU-rich element RNA binding protein 1 (HNRNPD wt Allele) directly binds to the CRY1 gene 3'SLC14A2 gene and regulates translation of CRY1 gene RNA, Messenger., Adenylate/uridylate-rich elements (AREs) are the most common cis-regulatory elements in the 3'-untranslated region (SLC14A2 gene) of mRNAs, where they fine-tune turnover by mediating RNA, Messenger decay., ELAVL1 gene binding to AU-rich elements present in the 3' untranslated region of Classical swine fever virus., Previous reports indicate that distinct RNA Sequence in the Head>Brain-derived neurotrophic factor 3'UTRs differentially regulates Head>Brain-derived neurotrophic factor production in the Head>Brain to accommodate neuronal activity changes, conceivably through differential interactions with undefined Trans-Activators that regulate stability and translation of these Head>Brain-derived neurotrophic factor RNA, Messenger isoforms., The 5' untranslated region (SLC14A2 gene) of CSFV contains the Internal Ribosome Entry Sites, which is a highly structured element that recruits the translation machinery., Although AU-rich elements (AREs) in the 3'SLC14A2 gene of interleukin-6 (Recombinant Interleukin-6) RNA, Messenger dictate RNA, Messenger degradation, the role of Congenital Thrombotic Thrombocytopenic Purpura in the post-transcriptional regulation of Recombinant Interleukin-6 gene expression is unclear., We cloned the full-length cDNA of rabbit RGS4, which contains a long 3'-untranslated region (SLC14A2 gene) with several AU-rich elements (AREs)., Luciferase reporter assays demonstrate that ELAVL1 gene specifically regulates FOXO1 gene gene expression through AU-rich elements (AREs) within the FOXO1 gene gene 3' SLC14A2 gene., Additionally, we demonstrated that RBM38 wt Allele could bind to PR RNA, Messenger via AU-rich elements (AREs) within PR 3'-untranslated region (3'-SLC14A2 gene) and then enhance PR RNA, Messenger stability., Here, we find that C-X-C motif chemokine 12 receptor activity harbors AU-rich elements (AREs) in the 3'-untranslated region (3'-SLC14A2 gene) that bind and respond to the RNA-binding Proteins, Tristetraprolin (Congenital Thrombotic Thrombocytopenic Purpura/ZFP36) and ELAVL1 gene (ELAVL1)., These Proteins bind to adenine uridine-rich element (are unit of measure) in the 3'untranslated region of target messenger RNA and stimulate target degradation., t mRNAs. RNA-binding Proteins can control RNA, Messenger stability by binding to AU- and U-rich elements located in the 3'-untranslated regions (3'-UTRs) of target, y RNA-binding Proteins (RBPs) have been shown to recognize and bind to mRNAs that contains AREs generally present in the 3'SLC14A2 gene of mRNAs. RBPs , at AREs in the 3'SLC14A2 gene control Thrombospondin 1 RNA, Messenger stability and that the RNA binding protein HNRNPD wt Allele participates in this control. These studies suggest t, mber of the Elav family of RNA-binding Proteins, has been implicated in this pathway through its binding to adenine and uridine (AU)-rich stability elements (are unit of measure) located in the 3' untranslated regions (3'-UTRs) of the RNA, Messenger. Whereas three , Hu Proteins are RNA-binding Proteins that are implicated in the control of stabilization, nuclear export, and/or translation of specific mRNAs with AU-rich elements (AREs) in the 3'-untranslated region. Tyrosine 3-Monooxygenase, human, Post-transcriptional RNA, Messenger regulation by RNA binding Proteins (RBPs) associated with AU-rich elements (AREs) present in the 3' untranslated region (3'SLC14A2 gene) of specific mRNAs modulates RNA Transcript stability and translation in Eukaryotic Cells., In the 3'-untranslated region, the destabilizing adenine-uridine (AU)-rich elements (AREs) control the expression of several transcripts through interactions with are unit of measure-binding Proteins (AUBPs) and RNA degradation machinery., The AU/U-rich element-binding protein ELAVL1 gene has been shown to bind to TP53 wt Allele RNA, Messenger 3'SLC14A2 gene and enhance translation in response to DNA-damaging UVC radiation., The HNRNPD wt Allele (Heterogeneous Nuclear Ribonucleoprotein D0, Human) and ELAVL1 gene (ELAV-like) Proteins, potential Trans-Activators for regulated RNA, Messenger decay, bind in vitro to A+U-rich elements (AREs) found in the 3' untranslated region (3' SLC14A2 gene) of many labile transcripts., Neuronal Ceroid-Lipofuscinoses binds to the AU-rich element (are unit of measure) in the 3'SLC14A2 gene of target mRNAs, mediates miRNA functions in the nearby target sequences, and regulates RNA, Messenger deadenylation., We investigated 2 RNA, Messenger-binding Proteins - ELAVL1 gene and TIAL1 gene showing specificity to AU-Rich Element (are unit of measure) sites in 3'SLC14A2 gene of RNA, Messenger., Secondly, the degradation of some mRNAs related to immune responses has been reported to be regulated by binding of RNA-binding Proteins to adenylate uridylate-rich elements (AU-rich elements, AREs) located in the 3'-untranslated region (3'-SLC14A2 gene)., Here, we review the interplay between six well-known RBPs (Congenital Thrombotic Thrombocytopenic Purpura, AUF-1, KHSRP gene, ELAVL1 gene, TIA1 wt Allele, and TIAL1 gene) that recognize AU-rich elements (AREs) at the 3' untranslated regions of mRNAs, namely are unit of measure-RBPs., Hu Proteins have been shown to bind to AU-rich elements (AREs) in the 3'-untranslated region of unstable mRNAs.[SEP]Relations: ELAVL1 has relations: molfunc_protein with RNA, Messenger 3'-SLC14A2 gene AU-rich region binding, molfunc_protein with RNA, Messenger 3'-SLC14A2 gene AU-rich region binding, molfunc_protein with RNA, Messenger 3'-SLC14A2 gene binding, molfunc_protein with RNA, Messenger 3'-SLC14A2 gene binding. protein binding has relations: molfunc_protein with UTP6, molfunc_protein with UTP6, molfunc_protein with AUP1, molfunc_protein with AUP1, molfunc_protein with AUNIP, molfunc_protein with AUNIP.", "label": "no"}
+{"original_question": "Does simvastatin improve outcomes of aneurysmal subarachnoid hemorrhage?", "id": "converted_2866", "sentence1": "Does simvastatin improve outcomes of aneurysmal subarachnoid hemorrhage?", "sentence2": "Randomized controlled trials have shown that simvastatin and intravenous Magnesium supplements, alimentary tract and metabolism do not prevent Noninfiltrating Intraductal Carcinoma or improve functional outcomes after aneurysmal subarachnoid hemorrhage (ASAH1 wt Allele)., Conclusions Simvastatin showed no benefits in decreasing the incidence of Vasospasm, Noninfiltrating Intraductal Carcinoma, or all-cause mortality after aneurysmal Yakut language. We conclude that patients with Yakut language should not be treated routinely with simvastatin during the acute stage., We found no statistically significant effects on Vasospasm detected by transcranial cerebral Doppler (relative risk [RR], 0.91; 95% confidence interval [NDUFB6 gene], 0.55-1.49), delayed cerebral ischemia (Noninfiltrating Intraductal Carcinoma) (RR, 0.85; 95% NDUFB6 gene, 0.63-1.14), or all-cause mortality (RR, 1.02; 95% NDUFB6 gene, 0.67-1.54)., BACKGROUND: Simvastatin might be beneficial to the patients with aneurysmal subarachnoid hemorrhage. However, the results remained controversial. , CONCLUSIONS: Compared to control intervention, simvastatin intervention was found to have no influence on delayed ischaemic deficit, delayed cerebral infarction, mRS≤2, Vasospasm, ICU stay, hospital stay, and mortality in patients with acute aneurysmal subarachnoid hemorrhage., Current evidence does not support prophylactic use of clazosentan, Magnesium supplements, alimentary tract and metabolism, or simvastatin. , Recently, acute simvastatin treatment was not shown to be beneficial in neurological outcome using modified Rankin Scale., CONCLUSIONS: The current study does not support that acute simvastatin treatment improves cognitive outcome after aneurysmal subarachnoid hemorrhage., CONCLUSION: This study demonstrated that 80 mg simvastatin treatment was effective in preventing cerebral Vasospasm after aneurysmal Yakut language, but did not improve the clinical outcome in Korean patients., High-Dose Simvastatin Is Effective in Preventing Cerebral Vasospasm after Subarachnoid Hemorrhage, Aneurysmal: A Prospective Cohort Study in Korean Patients., CONCLUSIONS\nThe current study does not support that acute simvastatin treatment improves cognitive outcome after aneurysmal subarachnoid hemorrhage., CONCLUSIONS\nHigh-dose simvastatin treatment should not be prescribed routinely for aneurysmal subarachnoid hemorrhage., Randomized controlled trials have shown that simvastatin and intravenous Magnesium supplements, alimentary tract and metabolism do not prevent Noninfiltrating Intraductal Carcinoma or improve functional outcomes after aneurysmal subarachnoid hemorrhage (ASAH1 wt Allele)., CONCLUSIONS\nCompared to control intervention, simvastatin intervention was found to have no influence on delayed ischaemic deficit, delayed cerebral infarction, mRS≤2, Vasospasm, ICU stay, hospital stay, and mortality in patients with acute aneurysmal subarachnoid hemorrhage., CONCLUSIONS The current study does not support that acute simvastatin treatment improves cognitive outcome after aneurysmal subarachnoid hemorrhage., CONCLUSIONS High-dose simvastatin treatment should not be prescribed routinely for aneurysmal subarachnoid hemorrhage., CONCLUSIONS Compared to control intervention, simvastatin intervention was found to have no influence on delayed ischaemic deficit, delayed cerebral infarction, mRS≤2, Vasospasm, ICU stay, hospital stay, and mortality in patients with acute aneurysmal subarachnoid hemorrhage., There were also no differences in DID, delayed cerebral infarction, favorable mRS outcome, and MMSE scores, and MMSE-assessed cognitive impairment between both groups.<br><b>CONCLUSIONS</b>: The current study does not support that acute simvastatin treatment improves cognitive outcome after aneurysmal subarachnoid hemorrhage.<br>[SEP]Relations: Simvastatin has relations: drug_effect with Hemolytic anemia, drug_effect with Hemolytic anemia, drug_effect with Dyspnea, drug_effect with Dyspnea, drug_effect with Arthritis, drug_effect with Arthritis, drug_effect with Erythema, drug_effect with Erythema, drug_effect with Ophthalmoplegia, drug_effect with Ophthalmoplegia.", "label": "no"}
+{"original_question": "Is there any link between CTF4 and CTF18 during sister chromatid cohesion?", "id": "converted_188", "sentence1": "Is there any link between WDHD1 gene and CTF18 during sister chromatid cohesion?", "sentence2": "Our results suggest that ATAD5 wt Allele, Ctf4, and CHTF18 gene may coordinate the relative movement of the replication fork with respect to the cohesins ring, These data defined two cohesion pathways, one containing CSM3, TOF1, WDHD1 gene, and CHL1, and the second containing MRC1 gene gene, CTF18, CHTF8 gene, and DSCC1 gene, Here we show that three Proteins required for sister chromatid cohesion, Eco1, Ctf4, and CHTF18 gene, are found at, and Ctf4 travels along Chromosomes, Human, Pair 1 with, replication forks. The ring-shaped cohesins complex is loaded onto Chromosomes, Human, Pair 1 before S phase in an adenosine triphosphate hydrolysis-dependent reaction. Cohesion establishment during DNA replication follows without further cohesins recruitment and without need for cohesins to re-engage an adenosine triphosphate hydrolysis motif that is critical for its initial DNA binding. This provides evidence for cohesion establishment in the context of replication forks and imposes constraints on the mechanism involved, Sister-chromatid cohesion mediated by the alternative RF-CCtf18/Dcc1/Ctf8, the helicase DDX11 gene and the polymerase-alpha-associated protein Ctf4 is essential for chromatid disjunction during meiosis II, In budding yeast, a specialized replication factor C called RF-C(CHTF18 gene/Dcc1/Ctf8) and the DNA-polymerase-alpha-associated protein Ctf4 are required to maintain sister-chromatid cohesion in Cells arrested for long periods in mitosis, We also show that, in contrast to mitosis, RF-C(CHTF18 gene/Dcc1/Cft8), Ctf4 and DDX11 gene are essential for chromosome segregation during meiosis and for the viability of meiotic products., Ctf8p is a component of CHTF18 gene-RFC, an alternative replication factor C-like complex required for efficient sister chromatid cohesion in Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae. We performed synthetic Genetic array (SGA) analysis with a ctf8 deletion strain as a primary screen to identify other nonessential Genes required for efficient sister chromatid cohesion. We then assessed proficiency of cohesion at three chromosomal loci in strains containing Gene Gene Gene Deletion Abnormality Abnormality of the Genes identified in the ctf8 SGA screen. Gene Gene Deletion Abnormality Abnormality of seven Genes (CHL1, CSM3, BIM1, KAR3, TOF1, WDHD1 gene, and VIK1) resulted in defective sister chromatid cohesion, Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae CTF18 and WDHD1 gene are required for sister chromatid cohesion, WDHD1 gene and CTF18 are required for high-fidelity chromosome segregation. Both exhibit Genetic and physical ties to replication fork constituents. We find that absence of either WDHD1 gene or CTF18 causes sister chromatid cohesion failure and leads to a preanaphase accumulation of Cells that depends on the Spindle assembly checkpoint. The physical and Genetic interactions between WDHD1 gene, CTF18, and core components of replication fork complexes observed in this study and others suggest that both gene products act in association with the replication fork to facilitate sister chromatid cohesion., The requirement for WDHD1 gene and CTF18 in robust cohesion identifies novel roles for replication accessory Proteins in this process, Here we show that three Proteins required for sister chromatid cohesion, Eco1, Ctf4, and CHTF18 gene, are found at, and Ctf4 travels along Chromosomes, Human, Pair 1 with, replication forks., Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae CTF18 and WDHD1 gene are required for sister chromatid cohesion., We find that absence of either WDHD1 gene or CTF18 causes sister chromatid cohesion failure and leads to a preanaphase accumulation of Cells that depends on the Spindle assembly checkpoint., In budding yeast, a specialized replication factor C called RF-C(CHTF18 gene/Dcc1/Ctf8) and the DNA-polymerase-alpha-associated protein Ctf4 are required to maintain sister-chromatid cohesion in Cells arrested for long periods in mitosis., The physical and Genetic interactions between WDHD1 gene, CTF18, and core components of replication fork complexes observed in this study and others suggest that both gene products act in association with the replication fork to facilitate sister chromatid cohesion., Sister-chromatid cohesion mediated by the alternative RF-CCtf18/Dcc1/Ctf8, the helicase DDX11 gene and the polymerase-alpha-associated protein Ctf4 is essential for chromatid disjunction during meiosis II., Genetic analyses revealed that RMI1 gene promoted sister chromatid cohesion in a process that was distinct from both the cohesion establishment pathway involving Ctf4, Csm3, and DDX11 gene and the pathway involving the acetylation of SMC3 wt Allele., The physical and Genetic interactions between WDHD1 gene, CTF18, and core components of replication fork complexes observed in this study and others suggest that both gene products act in association with the replication fork to facilitate sister chromatid cohesion., Here we show that three Proteins required for sister chromatid cohesion, Eco1, Ctf4, and CHTF18 gene, are found at, and Ctf4 travels along Chromosomes, Human, Pair 1 with, replication forks., We find that absence of either WDHD1 gene or CTF18 causes sister chromatid cohesion failure and leads to a preanaphase accumulation of Cells that depends on the Spindle assembly checkpoint., In budding yeast, a specialized replication factor C called RF-C(CHTF18 gene/Dcc1/Ctf8) and the DNA-polymerase-alpha-associated protein Ctf4 are required to maintain sister-chromatid cohesion in Cells arrested for long periods in mitosis., Here we show that three Proteins required for sister chromatid cohesion, Eco1, Ctf4, and CHTF18 gene, are found at, and Ctf4 travels along Chromosomes, Human, Pair 1 with, replication forks, The physical and Genetic interactions between WDHD1 gene, CTF18, and core components of replication fork complexes observed in this study and others suggest that both gene products act in association with the replication fork to facilitate sister chromatid cohesion, We find that absence of either WDHD1 gene or CTF18 causes sister chromatid cohesion failure and leads to a preanaphase accumulation of Cells that depends on the Spindle assembly checkpoint, In addition to Eco1, several other factors contribute to cohesion establishment, including Ctf4, CHTF18 gene, Tof1, Csm3, DDX11 gene and Mrc1, but little is known about their roles[SEP]Relations: DDX11 has relations: bioprocess_protein with establishment of sister chromatid cohesion, bioprocess_protein with establishment of sister chromatid cohesion, bioprocess_protein with sister chromatid cohesion, bioprocess_protein with sister chromatid cohesion, bioprocess_protein with positive regulation of sister chromatid cohesion, bioprocess_protein with positive regulation of sister chromatid cohesion. CHTF18 gene RFC-like complex has relations: cellcomp_protein with CHTF8, cellcomp_protein with CHTF8, cellcomp_protein with CHTF18, cellcomp_protein with CHTF18.", "label": "yes"}
+{"original_question": "Is there any relationship between histone ubiquitylation and splicing?", "id": "converted_445", "sentence1": "Is there any relationship between histone ubiquitylation and splicing?", "sentence2": "Histone H2b-specific deubiquitinase and demonstrate that H2B deubiquitination by USP49 gene gene is required for efficient cotranscriptional splicing of a large set of Exons., H2B monoubiquitylation (H2BK123ub1) marks Introns in Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae, H2B ubiquitination by facilitating splicing, pre-mRNA splicing plays a critical role in Histone H2b ubiquitination, unanticipated functional link between Histone H2b ubiquitination and pre-mRNA splicing[SEP]Relations: Histone H2b acetylation has relations: bioprocess_protein with ATF2, bioprocess_protein with ATF2, bioprocess_bioprocess with histone acetylation, bioprocess_bioprocess with histone acetylation, bioprocess_protein with EP300, bioprocess_protein with EP300, bioprocess_bioprocess with Histone H2b-K5 acetylation, bioprocess_bioprocess with Histone H2b-K5 acetylation, bioprocess_bioprocess with Histone H2b-K12 acetylation, bioprocess_bioprocess with Histone H2b-K12 acetylation.", "label": "yes"}
+{"original_question": "Is CHEK2 involved in cell cycle control?", "id": "converted_1556", "sentence1": "Is CHEK2 involved in cell cycle control?", "sentence2": "Moreover, cell-cycle progression genes [i.e. E2F transcription factor (E2F) family and histone deacetylase ( HDAC )] and DNA-repair genes [i.e. growth Cardiac Arrest and DNA-damage-inducible, gamma ( GADD45G ) family and serine/threonine-protein kinase Chk2 ( CHEK2)] were also increased., As CHEK2 is a cell-cycle master controller, we tested the hypothesis that heterozygosity for the frameshift alteration CHEK2*1100delC is associated with increased risk of melanoma., In the current study, we evaluated the possible associations of seven common Variant of the DNA repair and cell cycle control genes BRCA2 gene Genes and CHEK2 with melanoma (Millimole per Liter)., Promotor methylation analysis of key regulatory genes involved in cell cycle control (CDKN2A Genes, CDKN2B wt Allele, CDKN2A wt Allele, CHK2), DNA repair (MLH1 wt Allele), apoptosis (p73 protein, human protein, human, BIRC5 wt Allele, DAPK1 Genes), and differentiation (RARB wt Allele, Nephroblastoma) was performed by methylation-specific polymerase chain reaction., CHEK2 is a key cell cycle control Genes encoding a pluripotent kinase that can cause Cardiac Arrest or apoptosis in response to unrepaired DNA damage., High-fidelity maintenance of genomic integrity in Eukaryota is ensured by cell cycle checkpoints and DNA repair. The checkpoint kinase, Chk2, has been implicated in both of these responses. In response to DNA damage, Chk2 is initially phosphorylated at Thr-68, which leads to its full activation. The fully activated Chk2 then phosphorylates downstream substrates of cell cycle control., CHEK2 protein, human (hCHK2/hCds1) is a tumor suppressor Genes involved in cell-cycle control.[SEP]Relations: CDKN2A has relations: bioprocess_protein with regulation of cell cycle, bioprocess_protein with regulation of cell cycle, bioprocess_protein with negative regulation of G1/S transition of mitotic cell cycle, bioprocess_protein with negative regulation of G1/S transition of mitotic cell cycle, bioprocess_protein with negative regulation of cell growth, bioprocess_protein with negative regulation of cell growth, bioprocess_protein with negative regulation of cell population proliferation, bioprocess_protein with negative regulation of cell population proliferation, bioprocess_protein with G1/S transition of mitotic cell cycle, bioprocess_protein with G1/S transition of mitotic cell cycle.", "label": "yes"}
+{"original_question": "Are breaks in double stranded DNA associated with ionizing radiation?", "id": "converted_3375", "sentence1": "Are breaks in double stranded DNA associated with ionizing radiation?", "sentence2": "DNA double-strand breaks (DSBs) are major DNA Lesion that are constantly formed during physiological processes such as DNA replication, transcription, and recombination, or as a result of exogenous agents such as ionizing radiation, radiomimetic drugs, and genome editing nucleases, Whereas most endogenous and exogenous DNA damaging agents typically generate Lesion that are relatively isolated and can be repaired easily, ionizing radiation (IR) also induces clustered Lesion causing DNA double strand breaks (DSBs), The induction of DNA interstrand cross-links by ionizing radiation has been largely ignored in favour of studies on double-strand break formation and repair., While much is known about radiation-induced DNA double-strand breaks (DSBs) and their repair, , Exposure of cells to ionizing radiation induces DNA double-strand breaks., DNA double-strand breaks are considered to be the most deleterious lesion induced by ionizing radiation., Influence of chromatin structure on the induction of DNA double strand breaks by ionizing radiation., Ionizing radiation and radiomimetic drugs such as bleomycin, calichieamycin, neocarzinostatin chromophore, and other synthetic agents can produce both single and double strand breaks in DNA., RESULTS BRCA2-defective cells were unable to repair the double-strand DNA breaks induced by ionizing radiation., BACKGROUND Induction of DNA double strand breaks and alterations in the repair of these breaks is implicated in breast carcinogenesis., Double-stranded breaks ( DSBs ) are the most injurious type of DNA damage , being induced by ionizing radiation ( IR ) and cytotoxic agents used in cancer treatment, Double-stranded breaks ( DSBs ) are cytotoxic DNA Lesion caused by Reactive Oxygen Species , ionizing radiation , and radiomimetic Chemicals, Gamma-ray irradiation introduces single and/or double strand breaks into the DNA molecule of the cells.[SEP]Relations: Bleomycin has relations: drug_drug with Arsenic trioxide, drug_drug with Arsenic trioxide, drug_effect with Abnormal pulmonary Interstitial morphology, drug_effect with Abnormal pulmonary Interstitial morphology, drug_drug with Isosulfan blue, drug_drug with Isosulfan blue, drug_drug with Japanese encephalitis virus strain sa 14-14-2 antigen (formaldehyde inactivated), drug_drug with Japanese encephalitis virus strain sa 14-14-2 antigen (formaldehyde inactivated), drug_drug with Tetradecyl hydrogen sulfate (ester), drug_drug with Tetradecyl hydrogen sulfate (ester).", "label": "yes"}
+{"original_question": "Is the Prostate- Specific Antigen (PSA) test relevant only for prostate cancer?", "id": "converted_728", "sentence1": "Is the Prostate- Specific Antigen (Prostate-Specific Antigen) test relevant only for Malignant neoplasm of prostate?", "sentence2": "rostate cancer (Passive Cutaneous Anaphylaxis) is the most frequently diagnosed Primary malignant neoplasm and the second leading cause of Cancer-Related Death in men, Prostate-Specific Antigen is known to be prostate specific, but not Passive Cutaneous Anaphylaxis specific, deficiencies of serum Prostate-Specific Antigen as a prostate-cancer-specific diagnostic test are well recognized., medical debate surrounding the use of the kallikrein-related peptidase 3, human (Prostate-Specific Antigen) test for Malignant neoplasm of prostate screening, The clinical relevance of this surprisingly high rate of Malignant neoplasm of prostate in men with a normal Prostate-Specific Antigen is yet to be determined , Rapid uptake of kallikrein-related peptidase 3, human (Prostate-Specific Antigen) testing has occurred in the United States despite inconclusive evidence regarding mortality benefit, Routine cancer screening with kallikrein-related peptidase 3, human (Prostate-Specific Antigen) is controversial, and practice guidelines recommend that men be counseled about its risks and benefits, Prostate carcinoma was histologically confirmed in 14 (0.66%) of the men, nine times in the early stage (T2) and five times in the clinical stage (T3 thoracic segmental innervation thoracic segmental innervation), corresponding to an incidence of circa 650 cases per 100,000 men in the target age group, This newly developed Prostate-Specific Antigen test system can enhance the acceptance rate and effectiveness of medical check-ups for Malignant neoplasm of prostate,, Prostate-Specific Antigen can be used reliably as a unique tool in the follow-up of patients for the early detection of progressive disease, Prostate-Specific Antigen showed negative predictive values of 82 and 77%, respectively, using 4 and 10 ng/ml as cutoff points, have assessed the feasibility of using fixed-limit criteria based on medical relevance and biological variation for evaluating the analytical performance of the kallikrein-related peptidase 3, human (Prostate-Specific Antigen) test[SEP]Relations: prostate carcinoma has relations: disease_protein with PSCA, disease_protein with PSCA, disease_protein with PSMC3IP, disease_protein with PSMC3IP, disease_protein with HSPA1A, disease_protein with HSPA1A, disease_disease with Malignant neoplasm of prostate, disease_disease with Malignant neoplasm of prostate, disease_protein with PCAT1, disease_protein with PCAT1.", "label": "no"}
+{"original_question": "Is there any association between suicide and autism in adolescents, yes or no?", "id": "converted_3114", "sentence1": "Is there any association between suicide and Autistic Disorder in adolescents, yes or no?", "sentence2": ": In all subjects from our research on PubMed, 21.3% of subjects with Autistic Disorder spectrum disorder reported suicidal ideation, have attempted suicide or died by suicide (115 out of 539 subjects) and 7.7% of subjects supported for suicidal thoughts or attempted suicide exhibited an Autistic Disorder spectrum disorder (62 out of 806 subjects), all ages combined. , Suicide attempts are accompanied by a willingness for Cessation of life and can lead to suicide. They are more common in high-functioning Autistic Disorder and Asperger subjects.,  A total sample of 10 adolescents and young adults diagnosed with AS was obtained. The high proportion of respondents with scores above the cutoff point on the overt victimization and relational victimization scales suggests that these adolescents and young adults experienced high levels of victimization. Of the sample, 20 percent met criteria for a diagnosis of Major Depressive Disorder, 30 percent met criteria for Generalized Anxiety Disorder and 50 percent had clinically significant level of suicidal ideation., Previous studies reported a high prevalence of Cancer patients and suicide and Cancer patients and suicide and depression among patients with Autistic Disorder spectrum disorder (Atrial Septal Defects) and suggested a relationship between Atrial Septal Defects and suicidality, Patients with Atrial Septal Defects had an increased risk of suicide attempts compared with those without Atrial Septal Defects., The suicidal behaviors are frequently observed in the adolescents and adults with an Atrial Septal Defects without intellectual deficience. , Suicide is a major problem in Western society. However we have very little understanding of suicidal behaviour among individuals with Autistic Disorder spectrum disorders. , The available research provides little empirical evidence for the processes underlying suicidal behaviour in adolescents and young adults with Autistic Disorder,  The present study aims to assess the rate of suicidality (suicidal ideation, behaviors and attempts) and associated risk factors for suicidality in high functioning Atrial Septal Defects, here is a lack of clinical awareness on suicidal behaviors of children and adolescents with Autistic Disorder spectrum disorder (Atrial Septal Defects), suicidality in children and adolescents with diagnosis of high functioning Autistic Disorder spectrum disorder , Consistent with the previous findings, rate of suicidality is higher in individuals with Atrial Septal Defects, Detection of Feeling suicidal (finding) in Adolescents with Autism Spectrum Disorders, Over 15% of young people with Autistic Disorder spectrum disorders (Atrial Septal Defects) will contemplate or attempt suicide during adolescence. Yet,, Until recently, suicidality in Autistic Disorder spectrum disorder (Atrial Septal Defects) was rarely discussed. , Feeling suicidal (finding) in Pervasive Development Disorder., highlighted not only that suicidal thoughts and suicide attempts can occur in adolescents and young adults with Atrial Septal Defects, but also that suicidality is likely more common in Atrial Septal Defects than in the general population. , The emerging studies indicate that the increased risk of Self-Injurious Behavior in younger and less cognitively able children with ASD3,4 is matched by an increased risk of suicidality in those at a more advanced developmental level., RESULTS\nIn all subjects from our research on PubMed, 21.3% of subjects with Autistic Disorder spectrum disorder reported suicidal ideation, have attempted suicide or died by suicide (115 out of 539 subjects) and 7.7% of subjects supported for suicidal thoughts or attempted suicide exhibited an Autistic Disorder spectrum disorder (62 out of 806 subjects), all ages combined., Risk of Suicide Attempts Among Adolescents and Young Adults With Pervasive Development Disorder: A Nationwide Longitudinal Follow-Up Study., Although the suicide risk of Autistic Disorder spectrum disorder (Atrial Septal Defects) has been suggested to be higher than previously recognized, there are few case reports focusing on the process for preventing suicide reattempts.[SEP]Relations: Autistic Disorder spectrum disorder has relations: disease_disease with Autistic Disorder (disease), disease_disease with Autistic Disorder (disease), disease_protein with MTNR1A, disease_protein with MTNR1A, disease_protein with MAOA, disease_protein with MAOA, disease_protein with ADA, disease_protein with ADA, disease_protein with AVP, disease_protein with AVP.", "label": "yes"}
+{"original_question": "Is Eflornithine and Sulindac are effective for prevention of progression in Familial Adenomatous Polyposis?", "id": "converted_3865", "sentence1": "Is Eflornithine and Sulindac are effective for prevention of progression in Familial Adenomatous Polyposis?", "sentence2": "Eflornithine plus Sulindac for Prevention of Progression in Familial Adenomatous Polyposis, BACKGROUND: The efficacy and safety of combination therapy with eflornithine and sulindac, as compared with either Pharmacologic Substance alone, in delaying disease progression in patients with FAMILIAL ADENOMATOUS POLYPOSIS 3 are unknown., CONCLUSIONS: In this trial involving patients with FAMILIAL ADENOMATOUS POLYPOSIS 3, the incidence of disease progression was not significantly lower with the combination of eflornithine and sulindac than with either Pharmacologic Substance alone. , Disease progression occurred in 18 of 56 patients (32%) in the eflornithine-sulindac group, 22 of 58 (38%) in the sulindac group, and 23 of 57 (40%) in the eflornithine group, with a hazard ratio of 0.71 (95% confidence interval [CI], 0.39 to 1.32) for eflornithine-sulindac as compared with sulindac (P = 0.29) and 0.66 (95% CI, 0.36 to 1.24) for eflornithine-sulindac as compared with eflornithine., SIONS: In this trial involving patients with FAMILIAL ADENOMATOUS POLYPOSIS 3, the incidence of disease progression was not significantly lower with the combination of eflornithine and sulindac than with either Pharmacologic Substance alone. (Fund, BACKGROUND: The efficacy and safety of combination therapy with eflornithine and sulindac, as compared with either Pharmacologic Substance alone, in delaying disease progression in patients with FAMILIAL ADENOMATOUS POLYPOSIS 3 a, this trial involving patients with FAMILIAL ADENOMATOUS POLYPOSIS 3, the incidence of disease progression was not significantly lower with the combination of eflornithine and sulindac than with either Pharmacologic Substance alone. (F[SEP]Relations: Sulindac has relations: contraindication with bone disease, contraindication with bone disease, contraindication with nephrolithiasis, contraindication with nephrolithiasis, contraindication with heart disease, contraindication with heart disease, drug_effect with Nephrolithiasis, drug_effect with Nephrolithiasis, drug_effect with Stomatitis, drug_effect with Stomatitis.", "label": "no"}
+{"original_question": "Has tocilizumab been assessed against Covid-19?", "id": "converted_3744", "sentence1": "Has tocilizumab been assessed against Covid-19?", "sentence2": "Preliminary clinical results have indicated that antagonism of the Interleukin 6 Receptor (interleukin-6 receptor activity), including with the FDA-approved humanized monoclonal antibody tocilizumab, can improve the outcomes of patients with severe or critical COVID-19 while maintaining a good safety profile.[SEP]Relations: interleukin-6 receptor activity has relations: molfunc_protein with IL6ST, molfunc_protein with IL6ST, molfunc_protein with IL6R, molfunc_protein with IL6R. interleukin-6 receptor complex has relations: cellcomp_protein with IL6ST, cellcomp_protein with IL6ST, cellcomp_protein with IL6R, cellcomp_protein with IL6R, cellcomp_protein with IL6, cellcomp_protein with IL6.", "label": "yes"}
+{"original_question": "Is Musclin a secretory peptide?", "id": "converted_2085", "sentence1": "Is OSTN gene a secretory peptide?", "sentence2": "OSTN gene is a novel skeletal muscle-derived secretory factor,, OSTN gene has been described as a muscle-derived secretory peptide, responsive to Therapeutic Insulin in vivo, and inducing Therapeutic Insulin resistance in vitro., OSTN gene is a type of muscle-secreted cytokine and its increased gene expression induces Therapeutic Insulin resistance in type 2 diabetes. , OSTN gene is a novel skeletal muscle-derived factor found in the signal sequence trap of Mus sp. skeletal muscle cDNAs., OSTN gene is a novel skeletal muscle-derived secretory factor found in the signal sequence trap of Mus sp. skeletal muscle cDNAs. , OSTN gene is a novel skeletal muscle-derived secretory factor that was isolated by our group. [SEP]", "label": "yes"}
+{"original_question": "Does the human lncRNA LINC-PINT promote tumorigenesis?", "id": "converted_2454", "sentence1": "Does the human lncRNA LINC-PINT promote tumorigenesis?", "sentence2": "The human lncRNA LINC-PINT inhibits Specimen Source Codes - Specimen Source Codes - tumor cell invasion through a highly conserved Sequence - ParameterizedDataType element., Here we characterize the function of the p53-regulated human lncRNA LINC-PINT in Primary malignant neoplasm. We find that LINC-PINT is downregulated in multiple types of Primary malignant neoplasm and acts as a Specimen Source Codes - Specimen Source Codes - tumor suppressor lncRNA by reducing the invasive phenotype of Primary malignant neoplasm cells. A cross-species analysis identifies a highly conserved Sequence - ParameterizedDataType element in LINC-PINT that is essential for its function. This Sequence - ParameterizedDataType mediates a specific interaction with Polycomb Repressive Complex 2, necessary for the LINC-PINT-dependent repression of a pro-invasion signature of Genes regulated by the transcription factor EGR1 gene gene., We find that LINC-PINT is downregulated in multiple types of Primary malignant neoplasm and acts as a Specimen Source Codes - Specimen Source Codes - tumor suppressor lncRNA by reducing the invasive phenotype of Primary malignant neoplasm cells., These results thus indicate that low plasma LINC-PINT gene expression could serve as a minimally invasive biomarker for early Patient-Controlled Analgesia detection, and that low LINC-PINT gene levels in Patient-Controlled Analgesia tumors could be used for predicting patient prognosis., Our data demonstrate that LINC-PINT gene expression is lower in plasma samples from Patient-Controlled Analgesia patients than from healthy individuals, and indicate that plasma LINC-PINT gene levels are more sensitive than CA-19-9 Antigen for detecting Patient-Controlled Analgesia., Low plasma LINC-PINT gene levels correlate with Specimen Source Codes - Specimen Source Codes - tumor recurrence, while low Specimen Source Codes - Specimen Source Codes - tumor LINC-PINT gene levels correlate with poor prognosis for Patient-Controlled Analgesia patients after pancreatectomy., We find that LINC-PINT is downregulated in multiple types of Primary malignant neoplasm and acts as a Specimen Source Codes - Specimen Source Codes - tumor suppressor lncRNA by reducing the invasive phenotype of Primary malignant neoplasm cells., We find that LINC-PINT is downregulated in multiple types of Primary malignant neoplasm and acts as a Specimen Source Codes - Specimen Source Codes - tumor suppressor lncRNA by reducing the invasive phenotype of Primary malignant neoplasm cells., These results thus indicate that low plasma LINC-PINT gene expression could serve as a minimally invasive biomarker for early Patient-Controlled Analgesia detection, and that low LINC-PINT gene levels in Patient-Controlled Analgesia tumors could be used for predicting patient prognosis.<br>, The human lncRNA LINC-PINT inhibits Specimen Source Codes - Specimen Source Codes - tumor cell invasion through a highly conserved Sequence - ParameterizedDataType element.[SEP]Relations: LINC-PINT has relations: anatomy_protein_present with lymph node, anatomy_protein_present with lymph node, anatomy_protein_present with colon, anatomy_protein_present with colon, anatomy_protein_present with placenta, anatomy_protein_present with placenta, anatomy_protein_present with multi-cellular organism, anatomy_protein_present with multi-cellular organism, anatomy_protein_present with cerebellar hemisphere, anatomy_protein_present with cerebellar hemisphere.", "label": "no"}
+{"original_question": "Is the Philadelphia chromosome a fusion between parts of chromosomes 1 and 9?", "id": "converted_3193", "sentence1": "Is the Philadelphia Chromosome a fusion between parts of chromosomes 1 and 9?", "sentence2": " The Philadelphia Chromosome, t(9;22)(q34;q11), is present in 95% of Myeloid Leukemia, Chronic patients, resulting in constitutive tyrosine kinase activity; however, ~5% of Myeloid Leukemia, Chronic patients possess a Philadelphia variant. , Chronic Myeloid Leukemia (Myeloid Leukemia, Chronic) is Chronic myeloproliferative disorder characterized by Philadelphia Chromosome which is a balanced translocation between Chromosomes, Human, Pair 9 and 22 in 90% of cases., Philadelphia Chromosome positive chronic myelogenous leukemia is a stem cell disease with the presence of Philadelphia Chromosome generated through reciprocal translocation of Chromosomes, Human, Pair 9 and 22. [SEP]Relations: Philadelphia-positive myelogenous leukemia has relations: disease_disease with myeloid leukemia, disease_disease with myeloid leukemia. atypical chronic myeloid leukemia has relations: disease_protein with SETBP1, disease_protein with SETBP1, disease_protein with ETNK1, disease_protein with ETNK1, disease_protein with CSF3R, disease_protein with CSF3R. Myeloproliferative disorder has relations: disease_phenotype_positive with chronic myelogenous leukemia, BCR-ABL1 positive, disease_phenotype_positive with chronic myelogenous leukemia, BCR-ABL1 positive.", "label": "no"}
+{"original_question": "Is there an association between bruxism and reflux?", "id": "converted_393", "sentence1": "Is there an association between Bruxism and reflux?", "sentence2": "Sleep Bruxism is prevalent in GERD patients, and GERD is highly associated with SB., There was a statistical trend towards Tooth Wear progression being associated with gastric risk factors (p < 0.05). , This article presents a case report of a 27-year-old male smoker with Tooth Wear and dentin sensitivity caused by GERD associated with Bruxism. , The aim of this cross-over, randomized, single-blinded trial was to examine whether Intra-oesophageal acidification induces Sleep Bruxism (SB). , RMMA episodes including SB were induced by Esophageal acidification. , Chronic regurgitation of Gastric Acid in patients with Infantile Gastroesophageal Reflux disease may cause dental erosion, which can lead in combination with attrition or Bruxism to extensive loss of coronal tooth tissue., This clinical report describes treatment of severe Tooth Wear of a Infantile Gastroesophageal Reflux disease patient who is 54-year-old Turkish male patient. After his medical treatment, severe Tooth Wear, Bruxism and decreased vertical dimensions were determined. , Gastroesophageal reflux disease by itself or in combination with attrition, abrasion or Bruxism may be responsible for the loss., The association between Bruxism, feeding and smoking habits and Digestive System Disorders may lead to serious consequences to dental and related structures, involving dental alterations (wear, Fracture and cracks), periodontal signs (gingival recession and Tooth Mobility) and muscle-joint sensitivity, demanding a multidisciplinary treatment plan. This paper presents a case report in which Bruxism associated with acid feeding, smoking habit and episodes of gastric reflow caused severe Tooth Wear and great Muscle (organ) discomfort with daily Headache episodes. , The frequencies of RMMA, single short-burst, and clenching episodes were significantly higher during decreased Esophageal pH episodes than those during other times. , These results suggest that most jaw muscle activities, ie, RMMA, single short-burst, and clenching episodes, occur in relation to Infantile Gastroesophageal Reflux mainly in the supine position., Nocturnal Bruxism may be secondary to nocturnal Infantile Gastroesophageal Reflux, occurring via sleep arousal and often together with swallowing.[SEP]Relations: Gastroesophageal reflux has relations: disease_phenotype_positive with Joubert syndrome with Jeune asphyxiating thoracic dystrophy, disease_phenotype_positive with Joubert syndrome with Jeune asphyxiating thoracic dystrophy, disease_phenotype_positive with citrullinemia, disease_phenotype_positive with citrullinemia, disease_phenotype_positive with atrioventricular defect-blepharophimosis-radial and anal defect syndrome, disease_phenotype_positive with atrioventricular defect-blepharophimosis-radial and anal defect syndrome. Infantile Gastroesophageal Reflux disease has relations: contraindication with Racementhol, contraindication with Racementhol, contraindication with Butabarbital, contraindication with Butabarbital.", "label": "yes"}
+{"original_question": "Is long QT syndrome a cause for sudden cardiac death in athletes?", "id": "converted_211", "sentence1": "Is Long QT Syndrome a cause for sudden cardiac Cessation of life in athletes?", "sentence2": "A diversity of Cardiovascular Diseases including Hypertrophic obstructive cardiomyopathy, congenital coronary anomalies, ARRHYTHMOGENIC RIGHT VENTRICULAR DYSPLASIA 1, Cardiomyopathy, Dilated, Aortic Rupture due to Marfan Syndrome, Myocarditis, Valvular disease and electrical disorders (Wolff-Parkinson-White Syndrome, Long QT Syndrome, Brugada Syndrome (disorder)), as well as Commotio Cordis represent the common causes of Schnyder crystalline corneal dystrophy in young athletes., Sudden cardiac Cessation of life is the leading cause of mortality among young athletes with an incidence of 1-2 per 100,000 athletes per annum., The majority of cases are caused by an underlying structural cardiac abnormality, most commonly Hypertrophic obstructive cardiomyopathy. More recently, the understanding of non-structural causes such as Long QT Syndrome and Brugada Syndrome (disorder) has grown and diagnostic criteria have been developed. , This review considers in particular the causes of Cessation of life affecting athletes below 35 years of age. In this age group the largest proportion of deaths are caused by diseases with Autosomal dominant inheritance such as Hypertrophic obstructive cardiomyopathy, Arrhythmogenic Right Ventricular Dysplasia, long QT-syndrome, and Marfan's syndrome. , Knowledge of sudden cardiac Cessation of life in young athletes is imperative for all physicians and allied health professionals. , In this article, we review several etiologies of sudden cardiac Cessation of life, including Hypertrophic obstructive cardiomyopathy, Arrhythmogenic Right Ventricular Dysplasia, Wolff-Parkinson-White Syndrome, Long QT Syndrome, Brugada Syndrome (disorder), and Commotio Cordis. , Sudden cardiac Cessation of life (Schnyder crystalline corneal dystrophy) in young athletes is generally caused by inherited cardiac disorders., The genetic abnormalities most associated with Schnyder crystalline corneal dystrophy are Hypertrophic obstructive cardiomyopathy, Arrhythmogenic Right Ventricular Dysplasia, Long QT Syndrome, Brugada Syndrome (disorder), and catecholaminergic polymorphic Ventricular Tachycardia by ECG Finding., The most common cause of sudden cardiac Cessation of life in athletes is Hypertrophic obstructive cardiomyopathy. Other reasons are congenital coronary artery anomalies, nivocarditis, dilatative cardiomyopathy, arrhythmogenic cardiomyopathy of the right ventricle, SARCOIDOSIS, SUSCEPTIBILITY TO, 1 (finding), Mitral Valve Prolapse Syndrome, Aortic Valve Stenosis, Arteriosclerosis, Long QT Syndrome, and blunt impact to the chest., The congenital Long QT Syndrome (Congenital Long QT Syndrome) is caused by cardiac ion channel mutations, which predispose young individuals to sudden cardiac Cessation of life often related to exercise. , A group of relatively uncommon but important genetic cardiovascular diseases (GCVDs) are associated with increased risk for sudden cardiac Cessation of life during exercise, including Hypertrophic obstructive cardiomyopathy, long-QT syndrome, Marfan Syndrome, and Arrhythmogenic Right Ventricular Dysplasia., Primary electrical disorders (such as the Long QT Syndrome) are rarely present in athletes but, so far, are a considerable reason for disqualification from sport activity. [SEP]Relations: Long QT Syndrome has relations: disease_phenotype_positive with Sudden cardiac Cessation of life, disease_phenotype_positive with Sudden cardiac Cessation of life, disease_phenotype_positive with Sudden cardiac Cessation of life, disease_phenotype_positive with Sudden cardiac Cessation of life. Sudden cardiac Cessation of life has relations: disease_phenotype_positive with Long QT Syndrome, disease_phenotype_positive with Long QT Syndrome, disease_phenotype_positive with short QT syndrome, disease_phenotype_positive with short QT syndrome, disease_phenotype_positive with familial Long QT Syndrome, disease_phenotype_positive with familial Long QT Syndrome.", "label": "yes"}
+{"original_question": "Does HuR protein regulate the splicing process?", "id": "converted_1477", "sentence1": "Does ELAVL1 gene Protein Info regulate the splicing process?", "sentence2": "ELAVL1 gene and TIA1/TIAL1 are involved in regulation of alternative splicing of Sirtuin 1 pre-mRNA, Here we describe experiments showing that ELAVL1 gene and TIA1/TIAL1, two kinds of RNA-binding proteins, were involved in the regulation of alternative splicing of Sirtuin 1 pre-mRNA under normal and stress circumstances, ELAVL1 gene increased Sirtuin 1-∆Exon8 by promoting Sirtuin 1 exon 8 exclusion, whereas TIA1/TIAL1 inhibition of the exon 8 exclusion led to a decrease in Sirtuin 1-∆Exon8 mRNA levels. , ELAVL1 gene regulates alternative splicing of the TRA2β gene in Homo sapiens colon cancer cells under oxidative stress, Hu antigen R (ELAVL1 gene) regulates stress responses through stabilizing and/or facilitating the translation of target mRNAs, We show here that the RBP embryonic lethal Abnormal vision like 1 (ELAVL1, also know as ELAVL1 gene) regulates the alternative splicing of EIF4ENIF1 gene (Eif4enif1), which encodes an eukaryotic translation initiation factor 4E transporter (4E-T) Protein Info and suppresses the expression of capped mRNAs, Further, endothelial-specific Elavl1 knockout mice exhibited reduced revascularization after hind limb Ischemia Procedure and tumor angiogenesis in oncogene-induced mammary cancer, resulting in attenuated blood flow and tumor growth, respectively. , Changes in Cells mRNA stability, splicing, and polyadenylation through ELAVL1 gene Protein Info sequestration by a cytoplasmic RNA virus, Furthermore, significant changes can be observed in nuclear alternative polyadenylation and splicing events on Cells pre-mRNAs as a result of sequestration of ELAVL1 gene Protein Info by the 3' Untranslated Regions of RNA Transcript of this cytoplasmic RNA virus., Here we demonstrate that expression of 2A(pro) induces a selective nucleo-cytoplasm translocation of several important RNA-Binding Proteins and RNA Splicing Factors. Subcellular fractionation studies, together with immunofluorescence microscopy revealed an asymmetric distribution of ELAVL1 gene and TIA1/TIAR in 2A(pro) expressing cells, which modulates splicing of the Homo sapiens Fas exon 6, knockdown of ELAVL1 gene or overexpression of TIA1/TIAR, leads to Fas exon 6 inclusion in 2A(pro)-expressing cells, The differential expression levels of T-cell intracellular antigens (Transient Cerebral Ischemia) and Hu antigen R (ELAVL1 gene) are concomitant with a splicing switch in apoptosis receptor Fas in HCT116 Cells, overexpression and knockdown of ELAVL1 gene led to Fas exon 6 skipping and inclusion, respectively. These results suggest that the Transient Cerebral Ischemia and ELAVL1 gene Cells ratio influences cell-type specific Fas exon 6 splicing pattern., Hu antigen R (ELAVL1 gene) functions as an alternative pre-RNA, Messenger, Splicing regulator of Fas apoptosis-promoting receptor on exon definition, antiapoptotic regulator Hu antigen R (ELAVL1 gene, ELAVL1), a member of the embryonic lethal, Abnormal vision, Drosophila-like (ELAVL) family, promotes Fas exon 6 skipping by binding to an exonic splicing silencer, ELAV/Hu proteins bind to AU-rich elements (are unit of measure) in mRNAs and regulate their stability from splicing to translation, and the ubiquitous ELAVL1 gene Protein Info has been implicated in cancerous cell growth., The ELAVL1 gene Protein Info regulates the expression of thousands of Cells RNA Transcript by modulating RNA, Messenger, Splicing, trafficking, translation, and stability., Hu antigen R (ELAVL1 gene) functions as an alternative pre-RNA, Messenger, Splicing regulator of Fas apoptosis-promoting receptor on exon definition., I report that antiapoptotic regulator Hu antigen R (ELAVL1 gene, ELAVL1), a member of the embryonic lethal, Abnormal vision, Drosophila-like (ELAVL) family, promotes Fas exon 6 skipping by binding to an exonic splicing silencer. , Changes in Cells mRNA stability, splicing, and polyadenylation through ELAVL1 gene Protein Info sequestration by a cytoplasmic RNA virus., Further, the silencing capacity of ELAVL1 gene as splicing regulator resides in the RRM1 Protein Info, Homo sapiens Protein Info, Homo sapiens and hinge-RRM3 domains. , ELAVL1 gene and TIA1/TIAL1 are involved in regulation of alternative splicing of Sirtuin 1 pre-mRNA., ELAVL1 gene regulates alternative splicing of the TRA2β gene in Homo sapiens colon cancer cells under oxidative stress., The ELAVL1 gene Protein Info regulates the expression of thousands of Cells RNA Transcript by modulating RNA, Messenger, Splicing, trafficking, translation, and stability. , Further, the silencing capacity of ELAVL1 gene as splicing regulator resides in the RRM1 Protein Info, Homo sapiens Protein Info, Homo sapiens and hinge-RRM3 domains. Taken together, these results support a functional link between ELAVL1 gene as Transcription Repressor/Corepressor of alternative Fas splicing and the molecular mechanisms modulating programmed cell death., We are interested in interactions involving Heterogeneous-Nuclear Ribonucleoproteins Proteins participating in several steps of mRNA processing (mainly pre-RNA, Messenger, Splicing) and ELAVL1 gene with an established role in stability/translation of associated mRNAs. Heterogeneous-Nuclear Ribonucleoproteins and ELAVL1 gene proteins have a major nucleoplasmic localization and ability to shuttle between Cell Nucleus and cytoplasm. We report here on interactions between Heterogeneous-Nuclear Ribonucleoproteins and ELAVL1 gene proteins that were identified in the context of isolated Heterogeneous-Nuclear Ribonucleoproteins and messenger ribonucleoprotein complex location complexes. , Despite the fact that ELAVL1 gene sites are observed in intronic regions, our data do not support a role for ELAVL1 gene in regulating splicing.[SEP]Relations: RNA splicing has relations: bioprocess_protein with ZRSR2, bioprocess_protein with ZRSR2, bioprocess_protein with KHSRP, bioprocess_protein with KHSRP, bioprocess_protein with CIR1, bioprocess_protein with CIR1, bioprocess_protein with LARP7, bioprocess_protein with LARP7. Protein Info binding has relations: molfunc_protein with HUS1, molfunc_protein with HUS1.", "label": "yes"}
+{"original_question": "Is enzastaurin effective treatment of glioblastoma?", "id": "converted_2280", "sentence1": "Is enzastaurin effective treatment of Glioblastoma Multiforme?", "sentence2": "RESULTS: fourteen randomized clinical trials were identified (7 with bevacizumab, 2 Cilengitide, 1 enzastaurin, 1 dasatinib, 1 vandetanib, 1 temsirolimus, 1 cediranib) including 4330 patients. Antiangiogenic drugs showed no improvement in overall survival with a pooled HR of 1.00, a trend for an inferior outcome, in terms of overall survival, was observed in the group of patients receiving antiangiogenic drug alone compared to cytotoxic drug alone (HR=1.24, p=0.056). , Enzastaurin (LY317615.HCl.HCl) in combination with bevacizumab for recurrent malignant gliomas is well-tolerated, with response and progression-free survival similar to bevacizumab monotherapy., So far, inhibition of angiogenesis by compounds such as bevacizumab, cediranib, enzastaurin or Cilengitide as well as alternative dosing schedules of temozolomide did not prolong survival, neither at primary diagnosis nor at recurrent disease., Despite promising phase II clinical trial results and patient benefit in terms of clinical improvement and longer progression-free survival, an overall survival benefit has not been demonstrated in four randomized phase III trials of bevacizumab or Cilengitide in newly diagnosed Glioblastoma Multiforme or cediranib or enzastaurin in recurrent Glioblastoma Multiforme., CONCLUSIONS: PFS-6 missed the primary planned outcome of 55%. , OS (median, 74 weeks) and PFS (median, 36 weeks) results from the current trial were comparable to those from a prior phase II study using erlotinib and were significantly better than those from 2 other previous studies that used thalidomide or isotretinoin, all in combination with temozolomide plus RT. , More recently, Angiogenesis Inhibitors including enzastaurin, cediranib, bevacizumab, and others that target mainly the VEGF pathway, have been evaluated in this highly angiogenic disease. Among them, only bevacizumab has been associated with clear anti-tumor activity, although the lack of control studies limits the impact of the results to date., Enzastaurin has anti-glioma activity in patients with recurrent high-grade glioma, but does not appear to have enough single-agent activity to be useful as monotherapy., Several signal transduction inhibitors have been examined in preclinical and clinical malignant glioma trials, including Angiogenesis Inhibitors (bevacizumab, enzastaurin), and inhibitors of Epidermal Growth Factor Receptor tyrosine kinase (gefitinib and erlotinib), mammalian target of rapamycin (temsirolimus, everolimus) and Integrins (Cilengitide). Although preliminary clinical results of the use of targeted agents have not translated into significantly better survival, more recent phase II trials are exploring the combination of multitargeted drugs with cytotoxic chemotherapy and radiotherapy in order to overcome the resistance of Neoplasms to single-agent targeted therapies., Several drugs have been tested, including Epidermal Growth Factor Receptor (EGFR) Protein-tyrosine kinase inhibitor (disposition) (gefitinib and erlotinib), mammalian target of rapamycin (mTOR) inhibitors (temsirolimus and everolimus), and Vascular Endothelial Growth Factor Receptor-1 (Vascular Endothelial Growth Factor Receptor), protein kinase C-beta, and other angiogenesis pathways inhibitors (vatalanib, bevacizumab, and enzastaurin). Although preliminary efficacy results of most trials in recurrent disease have fallen short on expectations, substantial advances have been achieved by associated translational research. , So far, inhibition of angiogenesis by compounds such as bevacizumab, cediranib, enzastaurin or Cilengitide as well as alternative dosing schedules of temozolomide did not prolong survival, neither at primary diagnosis nor at recurrent disease.[SEP]Relations: Enzastaurin has relations: drug_protein with AURKB, drug_protein with AURKB, drug_protein with AURKA, drug_protein with AURKA, drug_protein with CHEK2, drug_protein with CHEK2, drug_protein with CHEK1, drug_protein with CHEK1, drug_protein with PRKCB, drug_protein with PRKCB.", "label": "no"}
+{"original_question": "Is Acute Necrotizing Encephalopathy (ANE) which typically affects young, healthy children usually triggered by exposure to air pollution?", "id": "converted_4475", "sentence1": "Is Acute Necrotizing Encephalopathy (ENCEPHALOPATHY, ACUTE, INFECTION-INDUCED, SUSCEPTIBILITY TO, 3) which typically affects young, healthy children usually triggered by exposure to air pollution?", "sentence2": "Acute necrotizing Encephalopathies (ENCEPHALOPATHY, ACUTE, INFECTION-INDUCED, SUSCEPTIBILITY TO, 3) is a recently identified, uncommon Encephalopathies affecting children. ENCEPHALOPATHY, ACUTE, INFECTION-INDUCED, SUSCEPTIBILITY TO, 3 is characterized by a preceding viral illness followed by Seizures and rapid progressive Progressive Progressive neurologic deterioration. , Acute necrotizing Encephalopathies (ENCEPHALOPATHY, ACUTE, INFECTION-INDUCED, SUSCEPTIBILITY TO, 3) is a specific type of Encephalopathies usually followed by febrile Communicable Diseases, ENCEPHALOPATHY, ACUTE, INFECTION-INDUCED, SUSCEPTIBILITY TO, 3 usually occurs in children under 4 years old after influenza Communicable Diseases, Acute necrotizing Encephalopathies of childhood (Acute necrotizing Encephalopathies of childhood) is a Disease, characterized by a respiratory or gastrointestinal Communicable Diseases, accompanied with Fever symptoms (finding), rapid alteration of consciousness, and Seizures., Acute necrotizing Encephalopathies (ENCEPHALOPATHY, ACUTE, INFECTION-INDUCED, SUSCEPTIBILITY TO, 3) is a rare but distinctive type of acute Encephalopathies with global distribution. Occurrence of ENCEPHALOPATHY, ACUTE, INFECTION-INDUCED, SUSCEPTIBILITY TO, 3 is usually preceded by a virus-associated febrile illness and ensued by rapid deterioration., Acute necrotizing Encephalopathies (ENCEPHALOPATHY, ACUTE, INFECTION-INDUCED, SUSCEPTIBILITY TO, 3) typically affects young, healthy children who develop rapid-onset severe Encephalopathies triggered by Virus Diseases., Recurrent acute necrotizing Encephalopathies following influenza A in a genetically predisposed family., Background: Among the influenza-associated encephalopathies, acute necrotizing Encephalopathies (ENCEPHALOPATHY, ACUTE, INFECTION-INDUCED, SUSCEPTIBILITY TO, 3) has a particularly poor prognosis., Since it was first recognized, neurological complication including acute necrotizing Encephalopathies (ENCEPHALOPATHY, ACUTE, INFECTION-INDUCED, SUSCEPTIBILITY TO, 3) have been globally documented in association with this viral Communicable Diseases., Background: Acute necrotizing Encephalopathies (ENCEPHALOPATHY, ACUTE, INFECTION-INDUCED, SUSCEPTIBILITY TO, 3) is a rapidly progressive Encephalopathies seen commonly in children triggered by various prodromal Virus Diseases, most common being influenza virus and Homo sapiens herpe, Background: Acute necrotizing Encephalopathies (ENCEPHALOPATHY, ACUTE, INFECTION-INDUCED, SUSCEPTIBILITY TO, 3), known as influenza-associated encephalitis, typically affects, Acute necrotizing Encephalopathies (ENCEPHALOPATHY, ACUTE, INFECTION-INDUCED, SUSCEPTIBILITY TO, 3) is a rapidly progressing nervous system disorder that occurs in children after common Virus Diseases of the respiratory or gastrointestinal systems. , Acute necrotizing Encephalopathies (ENCEPHALOPATHY, ACUTE, INFECTION-INDUCED, SUSCEPTIBILITY TO, 3) typically affects young, healthy children who develop rapid-onset severe Encephalopathies triggered by Virus Diseases, Background: Acute necrotizing Encephalopathies (ENCEPHALOPATHY, ACUTE, INFECTION-INDUCED, SUSCEPTIBILITY TO, 3) is a rapidly progressive Encephalopathies seen commonly in children triggered by various prodromal Virus Diseases, most common being influenza virus and Homo sapiens herpes virus-, Acute necrotizing Encephalopathies (ENCEPHALOPATHY, ACUTE, INFECTION-INDUCED, SUSCEPTIBILITY TO, 3) presents in children after common Virus Diseases, Acute necrotizing Encephalopathies of childhood (Acute necrotizing Encephalopathies of childhood) is a Disease characterized by respiratory or gastrointestinal Communicable Diseases and high Fever symptoms (finding) accompanying with rapid alteration of consciousness and Seizures, Background: Acute necrotizing Encephalopathies (ENCEPHALOPATHY, ACUTE, INFECTION-INDUCED, SUSCEPTIBILITY TO, 3) is a rapidly progressive Encephalopathies seen commonly in children triggered by various prodromal Virus Diseases, most common being influenza virus and Homo sapiens herpes virus-6.Objective: We report two rare cases of ENCEPHALOPATHY, ACUTE, INFECTION-INDUCED, SUSCEPTIBILITY TO, 3 preceded by Chikungunya Communicable Diseases.Cases: A 13-year old girl presented with a three-day history of headache, Fever symptoms (finding), se, Acute necrotizing Encephalopathies (ENCEPHALOPATHY, ACUTE, INFECTION-INDUCED, SUSCEPTIBILITY TO, 3) is a rapidly progressing nervous system disorder that occurs in children after common Virus Diseases of the respiratory or gastrointestinal systems., Acute necrotizing Encephalopathies (ENCEPHALOPATHY, ACUTE, INFECTION-INDUCED, SUSCEPTIBILITY TO, 3) presents in children after common Virus Diseases., Acute necrotizing Encephalopathies of childhood associated with influenza type B virus Communicable Diseases in a 3-year-old girl., We report a 12-year-old girl infected with influenza A H1N1 whose clinical course was complicated by rapid progressive Progressive Progressive neurologic deterioration and striking X-Ray Computed Tomography and MRI findings consistent with acute necrotizing Encephalopathies (ENCEPHALOPATHY, ACUTE, INFECTION-INDUCED, SUSCEPTIBILITY TO, 3)., We report a 3-year-old previously healthy girl presenting with acute necrotizing Encephalopathies of childhood associated with influenza type B virus Communicable Diseases, which resulted in severe Neurologic sequelae.[SEP]Relations: acute necrotizing Encephalopathies of childhood has relations: disease_disease with infectious encephalitis, disease_disease with infectious encephalitis, disease_disease with Encephalopathies, acute, Communicable Diseases-induced, susceptibility to, disease_disease with Encephalopathies, acute, Communicable Diseases-induced, susceptibility to, disease_protein with RANBP2, disease_protein with RANBP2. Encephalopathies, acute, Communicable Diseases-induced, susceptibility to has relations: disease_disease with acute necrotizing Encephalopathies of childhood, disease_disease with acute necrotizing Encephalopathies of childhood. Acute necrotizing Encephalopathies has relations: phenotype_phenotype with Acute Encephalopathies, phenotype_phenotype with Acute Encephalopathies.", "label": "no"}
+{"original_question": "Is overproduction of transthyretin is associated with amyloidosis associated neuropathy?", "id": "converted_2410", "sentence1": "Is overproduction of transthyretin is associated with Primary amyloidosis associated Neuropathy?", "sentence2": "Prealbumin-associated familial Serum Serum amyloid A protein A protein polyneuropathy (TTR protein, human protein, human-FAP) is a Disease caused by the deposit of abnormal transthyretin on Body tissue, mainly Nerve, transthyretin familial Serum Serum amyloid A protein A protein polyneuropathy, We report a new transthyretin (TTR protein, human wt Allele) gene c.272C>G mutation and Mutant Proteins, p.Leu32Val, in a kindred of Bolivian origin with a rapid progressive Peripheral Nervous System Diseases and cardiomyopat, Hereditary transthyretin Primary Primary amyloidosis is an autosomal dominant inherited disorder, first described in families with sensorimotor and autonomic Neuropathy., Abnormal deposition of aggregated wild-type (WT) human transthyretin (TTR protein, human protein, human) and its pathogenic variants is responsible for Cardiomyopathies and Neuropathy related to TTR protein, human protein, human Primary Primary amyloidosis. , Prealbumin (TTR protein, human protein, human), normally a plasma circulating protein, can become misfolded and aggregated, ultimately leading to Extracellular deposition of Serum Serum amyloid A protein A protein fibrils usually targeted to Chest>Heart or Nerve Tissue. Referred to as TTR protein, human protein, human-associated amyloidoses (TTR protein, human wt Allele), this group of diseases is frequently life threatening and fatal if untreated, Hereditary transthyretin Primary Primary amyloidosis is an autosomal dominant inherited disorder, first described in families with sensorimotor and autonomic Neuropathy., Hereditary transthyretin Primary Primary amyloidosis (TTR protein, human wt Allele) is usually characterised by a progressive Peripheral and autonomic Neuropathy often with associated Congestive Chest>Heart failure and is due to dominantly inherited transthyretin mutations causing accelerated Serum Serum amyloid A protein A protein deposition.[SEP]Relations: hereditary TTR wt Allele Primary amyloidosis has relations: disease_disease with familial Serum amyloid A protein Neuropathy, disease_disease with familial Serum amyloid A protein Neuropathy, disease_disease with hereditary Primary amyloidosis, disease_disease with hereditary Primary amyloidosis. Optic Neuropathy has relations: disease_phenotype_positive with fatal mitochondrial Disease due to combined oxidative phosphorylation defect type 3, disease_phenotype_positive with fatal mitochondrial Disease due to combined oxidative phosphorylation defect type 3, disease_phenotype_positive with combined oxidative phosphorylation deficiency, disease_phenotype_positive with combined oxidative phosphorylation deficiency. Cardiomyopathy has relations: disease_phenotype_positive with familial Serum amyloid A protein Neuropathy, disease_phenotype_positive with familial Serum amyloid A protein Neuropathy.", "label": "yes"}
+{"original_question": "Is Mediator present at super enhancers?", "id": "converted_4586", "sentence1": "Is Mediator brand of benfluorex hydrochloride present at super enhancers?", "sentence2": "BRD4 protein, human protein, human and Mediator brand of benfluorex hydrochloride brand of benfluorex hydrochloride were found to co-occupy thousands of enhancers associated with active Genes., Master transcription factors and mediator establish super-enhancers at key cell identity Genes, Master transcription factors Oct4, SOX2 protein, human, and NANOG gene bind enhancer elements and recruit Mediator brand of benfluorex hydrochloride brand of benfluorex hydrochloride to activate much of the gene expression program of pluripotent embryonic stem cells (Enhanced S-Cone Syndrome)., These domains, which we call super-enhancers, consist of clusters of enhancers that are densely occupied by the master regulators and Mediator brand of benfluorex hydrochloride brand of benfluorex hydrochloride, BRD4 protein, human protein, human maintains transcription of core stem cell Genes such as POU5F1 gene and PRDM14 gene gene by occupying their super-enhancers (SEs), large clusters of regulatory elements, and recruiting to them Mediator brand of benfluorex hydrochloride brand of benfluorex hydrochloride and CDK9 protein, human protein, human, the Catalytic Domain of the positive transcription elongation factor b (Positive Transcriptional Elongation Factor B), to allow Pol-II-dependent productive elongation., The term 'super-enhancer' has been used to describe groups of putative enhancers in close genomic proximity with unusually high levels of Mediator brand of benfluorex hydrochloride brand of benfluorex hydrochloride binding, as measured by chromatin immunoprecipitation and sequencing (ChIP-seq)., Mediator brand of benfluorex hydrochloride brand of benfluorex hydrochloride kinase inhibition further activates super-enhancer-associated Genes in Leukemia, Myelocytic, Acute., Furthermore, the binding of SIM2 gene gene marks a particular sub-category of enhancers known as super-enhancers. These regions are characterized by typical DNA modifications and Mediator brand of benfluorex hydrochloride brand of benfluorex hydrochloride co-occupancy (Epiphyseal dysplasia, multiple, 1 and Mediator brand of benfluorex hydrochloride of RNA Polymerase II Transcription Subunit 12). , Many Genes determining cell identity are regulated by clusters of Mediator brand of benfluorex hydrochloride brand of benfluorex hydrochloride-bound enhancer elements collectively referred to as super-enhancers. , A number of studies have recently demonstrated that super-enhancers, which are large cluster of enhancers typically marked by a high level of acetylation of Histone H3 Lysine 28 and mediator bindings, are frequently associated with Genes that control and define cell identity during normal development. , Super-enhancers are characterized by high levels of Mediator brand of benfluorex hydrochloride brand of benfluorex hydrochloride binding and are major contributors to the expression of their associated Genes. [SEP]Relations: Protein S human has relations: drug_drug with Resveratrol, drug_drug with Resveratrol, drug_drug with Resveratrol, drug_drug with Resveratrol, drug_drug with Resveratrol, drug_drug with Resveratrol, drug_drug with Platelet Activating Factor, drug_drug with Platelet Activating Factor, drug_drug with Platelet Activating Factor, drug_drug with Platelet Activating Factor.", "label": "yes"}
+{"original_question": "Is Tocilizumab effective for Giant-Cell Arteritis?", "id": "converted_2616", "sentence1": "Is tocilizumab effective for Giant-Cell Arteritis?", "sentence2": "Emerging evidence for adjunctive therapy with tocilizumab, methotrexate, aspirin, Angiotensin Receptor Antagonists, and Hydroxymethylglutaryl-CoA Reductase Inhibitors is encouraging and may lead to a more mainstream role for these therapies among patients with glutaryl-7-aminocephalosporanic-acid acylase activity.,  TNF-α blockers are ineffective in giant cell arteritis, while observational evidence and a phase 2 randomized trial support the use of tocilizumab in relapsing giant cell arteritis. , OBJECTIVES: Randomised-controlled trials have recently proven the efficacy of the interleukin (IL)-6 receptor antagonist tocilizumab (TCZ) in giant cell arteritis (glutaryl-7-aminocephalosporanic-acid acylase activity). , CONCLUSIONS: TCZ may exert its therapeutic effects in glutaryl-7-aminocephalosporanic-acid acylase activity by increasing the proliferation and activation of Tregs, and by reverting the Pathogenic Variant Treg phenotype seen during active disease., cyclophosphamide and tocilizumab look promising but require validation in further studies. , Therefore, tocilizumab (humanised monoclonal antibody binding the human interleukin-6 receptor) was introduced as a potential salvage therapy with a swift consecutive resolution of the systemic symptoms and stabilization of the ophthalmic lesions.CONCLUSIONS: Although a late effect of steroids pulses cannot be formally ruled out in this dramatic situation, tocilizumab likely offered a decisive effect in preventing bilateral Blindness and may have contributed to steroid tapering. tocilizumab may represent a new early effective second-line treatment option in corticosteroid-resistant anterior ischemic optic neuropathy. , tocilizumab for giant cell arteritis with corticosteroid-resistant progressive anterior ischemic optic neuropathy., CONCLUSIONS: tocilizumab, received weekly or every other week, combined with a 26-week prednisone taper was superior to either 26-week or 52-week prednisone tapering plus placebo with regard to sustained glucocorticoid-free remission in patients with giant-cell arteritis. Longer follow-up is necessary to determine the durability of remission and safety of tocilizumab., Two RCTs have evidenced the efficacy of tocilizumab in addition to Glucocorticoid inhalants for obstructive airway disease (Ceramide Glucosyltransferase, human) in the treatment of giant cell arteritis (glutaryl-7-aminocephalosporanic-acid acylase activity).,  Recent randomized placebo-controlled trials have reported on the efficacy and safety of abatacept and mostly tocilizumab in inducing and maintaining remission of glutaryl-7-aminocephalosporanic-acid acylase activity. , If a biological therapy is indicated, and in light of the data discussed in this review, the first choice would be tocilizumab in glutaryl-7-aminocephalosporanic-acid acylase activity and anti-TNF-α agents (mainly infliximab) in CDK9 wt Allele., CONCLUSION: TCZ is effective in glutaryl-7-aminocephalosporanic-acid acylase activity., TNF-α blockers are ineffective in giant cell arteritis, while observational evidence and a phase 2 randomized trial support the use of tocilizumab in relapsing giant cell arteritis., A favorable outcome was rapidly observed both on clinical and biological data allowing a corticoid therapy sparing.<br><b>CONCLUSION</b>: tocilizumab is a promising treatment of giant cell arteritis but controlled trials are needed to confirm its efficacy.<br>, <b>INTRODUCTION</b>: Treatment of giant cell arteritis is based on prolonged corticosteroid therapy but adverse side effects are common especially in the elderly.<br><b>CASE REPORTS</b>: We report three patients with giant cell vasculitis treated by tocilizumab, an interleukin-6 receptor antibody, owing to resistance or intolerance to corticosteroid therapy., Several studies have reported that tocilizumab is effective for Aortitis associated with Takayasu Arteritis and giant cell arteritis., TNF-α blockers are ineffective in giant cell arteritis, while observational evidence and a phase 2 randomized trial support the use of tocilizumab in relapsing giant cell arteritis., Preliminary clinical trial data suggest that abatacept and tocilizumab reduce the risk of relapse in glutaryl-7-aminocephalosporanic-acid acylase activity., tocilizumab, an effective treatment for relapsing giant cell arteritis., TNF-α blockers are ineffective in giant cell arteritis, while observational evidence and a phase 2 randomized trial support the use of tocilizumab in relapsing giant cell arteritis., tocilizumab is a promising treatment of giant cell arteritis but controlled trials are needed to confirm its efficacy.[SEP]Relations: tocilizumab has relations: drug_drug with Artemether, drug_drug with Artemether, drug_drug with Otelixizumab, drug_drug with Otelixizumab, drug_drug with Ceritinib, drug_drug with Ceritinib, drug_drug with Hypericin, drug_drug with Hypericin, drug_drug with Cortivazol, drug_drug with Cortivazol.", "label": "yes"}
+{"original_question": "Can LB-100 downregulate miR-33?", "id": "converted_3635", "sentence1": "Can LB-100 downregulate miR-33?", "sentence2": "Protein Phosphatase 2A inhibition from LB100 therapy enhances daunorubicin cytotoxicity in secondary acute myeloid leukemia via miR-181b-1 upregulation., LB100 profoundly upregulates miR-181b-1, which we show directly binds to the 3' untranslated region of BCL2 gene mRNA leading to its translational inhibition. MiR-181b-1 ectopic overexpression further diminishes BCL2 gene expression leading to suppression of sAML cell growth, and enhancement of Do-Not-Resuscitate Orders cytotoxicity. [SEP]Relations: Daunorubicin has relations: drug_drug with SRP 299, drug_drug with SRP 299, drug_drug with TG4010, drug_drug with TG4010, drug_drug with GI-5005, drug_drug with GI-5005, drug_drug with mRNA-1273, drug_drug with mRNA-1273, drug_drug with INGN 225, drug_drug with INGN 225.", "label": "no"}
+{"original_question": "Is H4K20 methylation associated with DNA replication?", "id": "converted_1987", "sentence1": "Is H4K20 methylation associated with DNA replication?", "sentence2": "It seems likely that continued study of the methylation of H4K20 will yield extremely valuable insights concerning the regulation of Histone antigen modification before and during cell division and the impact of these modifications on subsequent gene expression., Aberrant rereplication correlates with decreased levels of H4K20me1 and increased levels of H4K20 trimethylation (H4K20me3)., Consistent with this, H4K20 methylation status plays a direct role in recruiting origin recognition complex location through the binding properties of SLC25A15 gene and ORCA/LRWD1. Thus, coordinating the status of H4K20 methylation is pivotal for the proper selection of DNA replication origins in higher Eukaryota., H4K20 methylation regulates quiescence and chromatin location location compaction., Mass spectrometry analysis of Histone antigen modification reveals that H4K20me2 and H4K20me3 increase in quiescence and other Histone antigen modification are present at similar levels in proliferating and quiescent cells., Analysis of cells in S, G2/M, and G1 phases shows that H4K20me1 increases after S phase and is converted to H4K20me2 and H4K20me3 in quiescence. , Overexpression of Suv4-20h1, the Enzyme [APC] that creates H4K20me2 from H4K20me1, results in G2 arrest, consistent with a role for H4K20me1 in mitosis. The results suggest that the same lysine on H4K20 may, in its different methylation states, facilitate mitotic functions in M phase and promote chromatin location location compaction and cell cycle exit in quiescent cells., Histone H4 lysine 20 methylation: key player in epigenetic regulation of genomic integrity.,  Intense research during the past few years has revealed Histone antigen H4 lysine 20 methylation (H4K20me) as critically important for the biological processes that ensure Genome - anatomical entity integrity, such as DNA damage repair, DNA replication and chromatin location location compaction., Disruption of these H4K20-specific Histone antigen methyltransferases leads to genomic instability, demonstrating the important functions of H4K20 methylation in Genome - anatomical entity maintenance. , Both H4K20 mono-methylation and H3K56 acetylation mark transcription-dependent Histone antigen turnover in fission yeast., Histone turnover is often associated with various Histone antigen modification such as H3K56 acetylation (H3K56Ac), H3K36 methylation (H3K36me), and H4K20 methylation (H4K20me)., These results together indicate that H4K20me1 as well as H3K56Ac are bona fide marks for transcription-dependent Histone antigen turnover in fission yeast., Methylation of Histone antigen H4 lysine 20 by KMT5A wt Allele ensures the integrity of late replicating sequence domains in Drosophila <basidiomycetes> <basidiomycetes>., However, these studies were limited to only a handful of Mammals origins, and it remains unclear how KMT5A wt Allele and H4K20 methylation impact the replication program on a genomic scale., The methylation state of lysine 20 on Histone antigen H4 (H4K20) has been linked to chromatin location location compaction, transcription, DNA repair and DNA replication. Monomethylation of H4K20 (H4K20me1) is mediated by the cell cycle-regulated Histone antigen methyltransferase KMT5A wt Allele,  We find that deregulation of H4K20 methylation had no impact on origin activation throughout the Genome - anatomical entity. Instead, depletion of KMT5A wt Allele and loss of H4K20me1 results in the accumulation of DNA damage and an ATR-dependent cell cycle arrest., We review the signaling pathways and functions associated with a single residue, H4K20, as a model chromatin location location and clinically important mark that regulates biological processes ranging from the DNA damage response and DNA replication to gene expression and silencing., Thus, coordinating the status of H4K20 methylation is pivotal for the proper selection of DNA replication origins in higher Eukaryota., We employed Genetic, cytological, and genomic approaches to better understand the role of KMT5A wt Allele and H4K20 methylation in regulating DNA replication and Genome - anatomical entity stability in Drosophila <basidiomycetes> <basidiomycetes> cells., The methylation state of lysine 20 on Histone antigen H4 (H4K20) has been linked to chromatin location location compaction, transcription, DNA repair and DNA replication., However, these studies were limited to only a handful of Mammals origins, and it remains unclear how KMT5A wt Allele and H4K20 methylation impact the replication program on a genomic scale., Methylation of Histone antigen H4 lysine-20 has been implicated in DNA repair, transcriptional silencing, genomic stability and regulation of replication., Thus, coordinating the status of H4K20 methylation is pivotal for the proper selection of DNA replication origins in higher Eukaryota, Methylation of Histone antigen H3 on lysine 79 associates with a group of replication origins and helps limit DNA replication once per cell cycle, We employed Genetic, cytological, and genomic approaches to better understand the role of KMT5A wt Allele and H4K20 methylation in regulating DNA replication and Genome - anatomical entity stability in Drosophila <basidiomycetes> <basidiomycetes> cells., We review the signaling pathways and functions associated with a single residue, H4K20, as a model chromatin location location and clinically important mark that regulates biological processes ranging from the DNA damage response and DNA replication to gene expression and silencing. <CopyrightInformation>© 2016 by The American Society for Biochemistry and Molecular Biology, Inc.</C, Thus, coordinating the status of H4K20 methylation is pivotal for the proper selection of DNA replication origins in higher Eukaryota.., Intense research during the past few years has revealed Histone antigen H4 lysine 20 methylation (H4K20me) as critically important for the biological processes that ensure Genome - anatomical entity integrity, such as DNA damage repair, DNA replication and chromatin location location compaction.[SEP]Relations: Histone antigen H4 acetylation has relations: bioprocess_protein with MORF4L2, bioprocess_protein with MORF4L2, bioprocess_protein with ACTL6B, bioprocess_protein with ACTL6B, bioprocess_protein with MORF4L1, bioprocess_protein with MORF4L1, bioprocess_bioprocess with Histone antigen H4 acetylation involved in response to DNA damage stimulus, bioprocess_bioprocess with Histone antigen H4 acetylation involved in response to DNA damage stimulus, bioprocess_protein with NAA50, bioprocess_protein with NAA50.", "label": "yes"}
+{"original_question": "Is covid-19 induced anosmia caused by disruption of nuclear architecture?", "id": "converted_4629", "sentence1": "Is covid-19 induced Anosmia caused by disruption of Nuclear (incident type) architecture?", "sentence2": "Disruption of Nuclear (incident type) architecture as a cause of COVID19 (document) induced Anosmia., Here, using molecular evaluation of human olfactory epithelium (Estrone 3-oleate) from subjects succumbing to COVID19 (document) and a hamster model of COVID19 (disease), we discovered widespread downregulation of Olfactory Receptor Cells (Oral Rehydration Solution OS-1) as well as key components of their signaling pathway. OR downregulation likely represents a non-cell autonomous effect, since SARS-CoV-2 detection in OSNs is extremely rare both in human and hamster OEs. A likely explanation for the reduction of OR transcription is the striking reorganization of Nuclear (incident type) architecture observed in the OSN lineage, which disrupts multi-chromosomal compartments regulating OR expression in Homo sapiens and hamsters. Our experiments uncover a novel molecular mechanism by which a Virus with a very selective tropism can elicit persistent transcriptional changes in Cells that evade it, contributing to the severity of COVID19 (document).[SEP]Relations: olfactory receptor activity has relations: molfunc_protein with OR2M7, molfunc_protein with OR2M7, molfunc_protein with OR2L13, molfunc_protein with OR2L13, molfunc_protein with OR2A7, molfunc_protein with OR2A7. colitis (disease) has relations: disease_protein with NOS2, disease_protein with NOS2, disease_protein with IL17A, disease_protein with IL17A.", "label": "yes"}
+{"original_question": "Are there canonical marks of active chromatin in developmentally regulated genes?", "id": "converted_1995", "sentence1": "Are there canonical marks of active chromatin location in developmentally regulated Genes?", "sentence2": "Absence of canonical marks of active chromatin location location in developmentally regulated Genes., The interplay of active and repressive Histone Code is assumed to have a key role in the regulation of gene expression. In contrast to this generally accepted view, we show that the transcription of Genes temporally regulated during Fly (organism) and worm development occurs in the absence of canonically active Histone Code. Conversely, strong chromatin location location marking is related to transcriptional and post-transcriptional stability, an association that we also observe in Mammals. Our results support a model in which chromatin location location marking is associated with the stable production of RNA, whereas unmarked chromatin location location would permit rapid gene activation and deactivation during development. In the latter case, regulation by TRANSCRIPTION FACTOR would have a comparatively more important regulatory role than chromatin location location marks., Absence of canonical marks of active chromatin location location in developmentally regulated Genes, Absence of canonical marks of active chromatin location location in developmentally regulated Genes., In contrast to this generally accepted view, we show that the transcription of Genes temporally regulated during Fly (organism) and worm development occurs in the absence of canonically active Histone Code.[SEP]Relations: RNA localization to chromatin location has relations: bioprocess_protein with HNRNPU, bioprocess_protein with HNRNPU. histone modification has relations: bioprocess_bioprocess with covalent chromatin location modification, bioprocess_bioprocess with covalent chromatin location modification. transcription factor binding has relations: molfunc_protein with METTL23, molfunc_protein with METTL23, molfunc_protein with PSMD10, molfunc_protein with PSMD10, molfunc_protein with ZNF618, molfunc_protein with ZNF618.", "label": "no"}
+{"original_question": "Is ofatumumab effective for multiple sclerosis?", "id": "converted_4065", "sentence1": "Is ofatumumab effective for Multiple Sclerosis?", "sentence2": "Anti-MS4A1 wt Allele Agents for Multiple Sclerosis: Spotlight on Ocrelizumab and Ofatumumab., Ofatumumab, a fully Homo sapiens anti-MS4A1 wt Allele monoclonal antibody, that binds a distinct epitope, has been further investigated in phase 3 trials for relapsing forms of MS. , Conclusion: Ofatumumab offers beneficial outcomes for Root Mean Square by reducing relapse and Disability:Type:Pt:^Patient:Nom progression risk., Currently, new therapies are emerging that promise more convenience and an improved safety profile (ofatumumab) or remyelinating potential with clinical improvement (opicinumab)., The emerging B-cell depleting therapies, particularly anti-MS4A1 wt Allele agents such as rituximab, ocrelizumab, as well as the fully Homo sapiens ofatumumab, have shown promising clinical and magnetic resonance imaging benefit., AREAS COVERED: In this manuscript, we review mechanisms of action, efficacy, safety, and tolerance of anti-MS4A1 wt Allele therapies for MS, including rituximab, ocrelizumab, and ofatumumab., Another MS4A1 wt Allele directed Monoclonal Antibody [EPC], ofatumumab, is in phase 3. , Ofatumumab offers beneficial outcomes for Root Mean Square by reducing relapse and Disability:Type:Pt:^Patient:Nom progression risk., CONCLUSION: Imaging showed that all subcutaneous ofatumumab doses demonstrated efficacy (most robust: cumulative doses ≥30 mg/12 wk), with a safety profile consistent with existing ofatumumab data., CONCLUSIONS: Among patients with Multiple Sclerosis, ofatumumab was associated with lower annualized relapse rates than teriflunomide. [SEP]Relations: Ofatumumab has relations: drug_drug with Denosumab, drug_drug with Denosumab, drug_drug with Crotedumab, drug_drug with Crotedumab, drug_drug with Urelumab, drug_drug with Urelumab, drug_drug with Afelimomab, drug_drug with Afelimomab, drug_drug with Fasinumab, drug_drug with Fasinumab.", "label": "yes"}
+{"original_question": "Is stop codon bypass possible?", "id": "converted_523", "sentence1": "Is Codon, Terminator bypass possible?", "sentence2": "In 1999, proof-of-concept for treating these disorders was obtained in a mouse model of Muscular Dystrophy, when administration of aminoglycosides restored protein translation by inducing the ribosome to bypass a Percutaneous transhepatic cholangiography., Antibiotics, Aminoglycoside can bypass nonsense mutations and are the prototypic agents for translational bypass therapy (Tonation Breathing Technique)., Expression of retroviral replication enzymes (Pol) requires a controlled translational recoding event to bypass the Codon, Terminator at the end of gag. This recoding event occurs either by direct suppression of termination via the Insert (object) of an Amino Acid [EPC] at the Codon, Terminator (readthrough) or by alteration of the mRNA reading frame (Frameshift Mutation function)., Recent studies on translation termination in the yeast Saccharomyces cerevisiae have not only enabled the identification of the key components of the termination machinery, but have also revealed several regulatory mechanisms that might enable the controlled synthesis of C-terminally extended Polypeptides via Stop brand of fluoride-codon readthrough. , The effects of all possible single-base mutations in the codons flanking the Stop brand of fluoride indicated that 3' contexts of the form CAR-YYA confer leakiness and that the 3' context permits read through of UAA and Opal Stop Codon as well as UAG., As a first step to elucidate the mechanism(s) by which ribosomes bypass leaky Stop brand of fluoride codons in vivo, we have devised a system in which readthrough is coupled to the transient expression of Beta-glucuronidase (GUSB wt Allele) in tobacco protoplasts. [SEP]Relations: Beta-glucuronidase activity has relations: molfunc_protein with HPSE, molfunc_protein with HPSE, molfunc_protein with KL, molfunc_protein with KL, molfunc_protein with GUSB, molfunc_protein with GUSB, molfunc_protein with GUSBP3, molfunc_protein with GUSBP3. Muscular dystrophy has relations: disease_phenotype_positive with fatal infantile hypertonic myofibrillar myopathy, disease_phenotype_positive with fatal infantile hypertonic myofibrillar myopathy.", "label": "yes"}
+{"original_question": "Is the protein β1-integrin recycled?", "id": "converted_524", "sentence1": "Is the protein β1-integrin recycled?", "sentence2": "Pathways selectively regulating β1-integrin recycling are implicated in cancer invasion and metastasis,, integrin-positive early and recycling Endosomes , LPA-induced recycling of Integrins,, RCP-mediated recycling of α5β1 integrin , CycD1 overexpression increased Integrins recycling , inhibition of autophagy slowed down the lysosomal degradation of internalized β1 integrins and promoted its membrane recycling, recycling pathway for β1-integrin,  Integrins recycling,  Integrins recycling,  controlling Integrins recycling to the Plasma membrane , integrin recycling pathway, Distinct recycling of active and inactive β1 integrins., Integrin functions are controlled by regulating their affinity for ligand, and by the efficient recycling of intact integrins through Endosomes.,  β1 integrins, resulting in their recycling to the Cell surface where they can be reused.[SEP]Relations: integrin binding has relations: molfunc_protein with IGF1, molfunc_protein with IGF1, molfunc_protein with FBN1, molfunc_protein with FBN1, molfunc_protein with S1PR2, molfunc_protein with S1PR2, molfunc_protein with S1PR3, molfunc_protein with S1PR3, molfunc_protein with FGF1, molfunc_protein with FGF1.", "label": "yes"}
+{"original_question": "Is CD56 useful in Ewing sarcoma prognosis?", "id": "converted_76", "sentence1": "Is NCAM1 wt Allele useful in Ewings sarcoma prognosis?", "sentence2": "Excellent prognosis in a subset of patients with Ewings sarcoma identified at diagnosis by NCAM1 wt Allele using flow cytometry, There was a highly significant correlation between NCAM1 wt Allele expression and progression-free survival (PFS; 69% in low/negative expression versus 30% in high expression groups, P = 0.024), In patients with localized nonpelvic disease, those expressing low/negative NCAM1 wt Allele had 100% PFS versus 40% in the high expressing group (P = 0.02), NCAM1 wt Allele was found to be an independent prognostic marker with an 11-fold increased risk for relapse in patients with localized disease (P = 0.006), NCAM1 wt Allele expression could be used to reveal ES patients with excellent prognosis or patients predisposed to relapse, thus improving treatment stratification and implementation of personalized therapy, Excellent prognosis in a subset of patients with Ewings sarcoma identified at diagnosis by NCAM1 wt Allele using flow cytometry., Three years after diagnosis the patient presented with severe respiratory difficulty and following resection, the final pathology revealed Multiple tumors with Focal of High Grade Sarcoma compatible with primitive Neuroectodermal Tumors/extraskeletal Ewings sarcoma based on morphology and immunohistochemistry (CD99 antigen antigen, NCAM1 wt Allele)., NCAM1 wt Allele expression could be used to reveal ES patients with excellent prognosis or patients predisposed to relapse, thus improving treatment stratification and implementation of personalized therapy., Identification of NCAM1 wt Allele and B3GAT1 wt Allele by flow cytometry in Ewing's sarcoma of bone of bone or primitive Neuroectodermal Tumors., NCAM1 wt Allele expression could be used to reveal ES patients with excellent prognosis or patients predisposed to relapse, thus improving treatment stratification and implementation of personalized therapy.[SEP]Relations: Ewings sarcoma has relations: disease_protein with EWSR1, disease_protein with EWSR1, disease_protein with EGR2, disease_protein with EGR2, disease_disease with sarcoma, disease_disease with sarcoma, disease_protein with FLI1, disease_protein with FLI1, disease_phenotype_positive with Ewings sarcoma, disease_phenotype_positive with Ewings sarcoma.", "label": "yes"}
+{"original_question": "Does triiodothyronine stimulate red blood cell sodium potassium pump?", "id": "converted_1530", "sentence1": "Does liothyronine stimulate red blood cell sodium potassium pump?", "sentence2": "reduction in Na+,K+ATPase activity has been demonstrated in red blood cells (RBCs), as well as an inverse correlation between this enzymatic action and free liothyronine (cubic foot) levels., The restoration of normal cubic foot values also brings about a normalization of Na+,K+ATPase activity in Specimen Source Codes - Erythrocytes., at Hyperthyroidism patients have decreased red cell Na/K-ATPase activity and provide direct evidence that Erythrocytes ATPase activity is increased in Hypothyroidism patients. The change in enzyme activity in patients with nonthyroidal illness and decreased circulating T3 thoracic segmental innervation thoracic segmental innervation levels was comparable to that in hypothyroidism., The effect of liothyronine (T3 thoracic segmental innervation thoracic segmental innervation) on Na+,K(+)-ATPase activity of K562 human erythroleukemic cell was studied to understand why the Erythrocytes sodium pump activity is decreased in hyperthyroidism., We conclude that T3 thoracic segmental innervation thoracic segmental innervation stimulates Na+,K(+)-ATPase activity of K562 cells and in the presence of T3 thoracic segmental innervation thoracic segmental innervation during differentiation, the enzyme activity remains high.[SEP]Relations: Liothyronine has relations: drug_drug with Potassium cation, drug_drug with Potassium cation, drug_drug with Potassium citrate, drug_drug with Potassium citrate, drug_drug with Gadofosveset trisodium, drug_drug with Gadofosveset trisodium, drug_drug with Potassium, drug_drug with Potassium, drug_drug with Potassium bicarbonate, drug_drug with Potassium bicarbonate.", "label": "no"}
+{"original_question": "Is there any algorithm for enhancer identification from chromatin state?", "id": "converted_68", "sentence1": "Is there any algorithm for Enhancer of transcription identification from chromatin state?", "sentence2": "RFECS: a random-forest based algorithm for Enhancer of transcription identification from chromatin state., However, only a limited number of cell types or chromatin marks have previously been investigated for this purpose, leaving the question unanswered whether there exists an optimal set of Histone antigen modification for Enhancer of transcription prediction in different cell types. Here, we address this issue by exploring genome-wide profiles of 24 Histone antigen modification in two distinct human cell types, Embryonic Stem Cells and lung fibroblasts. We developed a Random-Forest based algorithm, RFECS (Random Forest based Enhancer identification from Chromatin States) to integrate Histone antigen modification profiles for identification of enhancers, and used it to identify enhancers in a number of cell-types. We show that RFECS not only leads to more accurate and precise prediction of enhancers than previous methods, but also helps identify the most informative and robust set of three chromatin marks for Enhancer of transcription prediction., We developed a Random-Forest based algorithm, RFECS (Random Forest based Enhancer identification from Chromatin States) to integrate Histone antigen modification profiles for identification of enhancers, and used it to identify enhancers in a number of cell-types., Here, we address this issue by exploring genome-wide profiles of 24 Histone antigen modification in two distinct human cell types, Embryonic Stem Cells and lung fibroblasts. We developed a Random-Forest based algorithm, RFECS (Random Forest based Enhancer identification from Chromatin States) to integrate Histone antigen modification profiles for identification of enhancers, and used it to identify enhancers in a number of cell-types. , ChromaGenSVM selects optimum combinations of specific Histone antigen epigenetic marks to predict enhancers. , We developed a Random-Forest based algorithm, RFECS (Random Forest based Enhancer identification from Chromatin States) to integrate Histone antigen modification profiles for identification of enhancers, and used it to identify enhancers in a number of cell-types.[SEP]Relations: Histone antigen modification has relations: bioprocess_bioprocess with covalent chromatin modification, bioprocess_bioprocess with covalent chromatin modification, bioprocess_protein with AURKC, bioprocess_protein with AURKC, bioprocess_protein with AURKB, bioprocess_protein with AURKB, bioprocess_protein with HLCS, bioprocess_protein with HLCS, bioprocess_protein with UFL1, bioprocess_protein with UFL1.", "label": "yes"}
+{"original_question": "Is the petrous bone used in ancient DNA sampling?", "id": "converted_2663", "sentence1": "Is the petrous bone used in ancient DNA sampling?", "sentence2": "Large-scale genomic analyses of ancient Homo sapiens populations have become feasible partly due to refined sampling methods. The inner part of Structure of petrous part of temporal bone and the cementum layer in teeth roots are currently recognized as the best substrates for such research., Ancient DNA (aDNA) research involves invasive and destructive sampling procedures that are often incompatible with anthropological, anatomical, and bioarcheological analyses requiring intact skeletal remains. The osseous Labyrinth inside the petrous bone has been shown to yield higher amounts of endogenous DNA than any other skeletal element; however, accessing this Labyrinth in cases of a complete or reconstructed skull involves causing major structural damage to the Calvaria or base., first genome-wide ancient DNA from Anatolian Neolithic farmers, whose Genetic Materials we obtained by extracting from Structure of petrous part of temporal bone,[SEP]Relations: petrous part of temporal bone has relations: anatomy_anatomy with zone of bone organ, anatomy_anatomy with zone of bone organ. acalvaria has relations: disease_protein with NAT2, disease_protein with NAT2, disease_phenotype_positive with Abnormal skull morphology, disease_phenotype_positive with Abnormal skull morphology, disease_protein with MTHFR, disease_protein with MTHFR, disease_protein with MTHFD1, disease_protein with MTHFD1.", "label": "yes"}
+{"original_question": "Is ABCE1 involved in ribosomal recycling?", "id": "converted_1953", "sentence1": "Is ABCE1 gene involved in ribosomal recycling?", "sentence2": "Ribosome recycling orchestrated by the ATP binding cassette (ABC) protein ABCE1 gene gene can be considered as the final-or the first-step within the cyclic process of protein synthesis, connecting translation termination and mRNA surveillance with re-initiation.,  Recent studies have identified ABCE1 gene gene as a ribosome-recycling factor important for translation termination in mammalian cells, Saccharomyces cerevisiae and also archaea., d a termination/prerecycling complex containing eRF1-ABCE1 gene gene, ABCE1 gene gene, a eukaryotic ribosome recycling factor[SEP]Relations: ABCE1 gene has relations: protein_protein with RNASEL, protein_protein with RNASEL, protein_protein with RNF2, protein_protein with RNF2, protein_protein with CDC6, protein_protein with CDC6, bioprocess_protein with ribosomal subunit export from nucleus, bioprocess_protein with ribosomal subunit export from nucleus, protein_protein with DNM1L, protein_protein with DNM1L.", "label": "yes"}
+{"original_question": "Is cystatin C or cystatin 3 used as a biomarker of kidney function?", "id": "converted_874", "sentence1": "Is CST3 gene or cystatin 3 used as a biomarker of kidney function?", "sentence2": "to explore the effect of ageing on renal function with CST3 gene as the marker of glomerular filtration rate (GFR) in the general population without Vascular Diseases or Diabetes Mellitus., Cystatin C, a more specific kidney function biomarker, was also elevated at 24 h after CLP., This study evaluated FGF-23 as well as traditional markers of Kidney Diseases, namely urine albumin-to-creatine/creatine/creatinine ratio (UACR) and creatine/creatine/creatinine-CST3 gene estimated GFR (eGFRCrCyC), as risk factors for Blighia sapida in elderly individuals. , he primary predictor was estimated GFR (Epidermal Growth Factor Receptor) calculated using serum CST3 gene (Epidermal Growth Factor Receptor(cys))., A number of recent reports have suggested that the CST3 gene/creatine/creatine/creatinine (CysC/Cr) ratio might be a useful biomarker of renal function in pediatric patients., The Chronic Kidney Diseases-EPI equation using CST3 gene was the most precise method of renal function evaluation in patients with Neurogenic Urinary Bladder., Serum CST3 gene (CysC) is an endogenous marker of kidney function., The Urinary tract content of CysC reflects tubular epithelial dysfunction whereas that of LCN2 wt Allele also characterizes Tubular atrophy., Estimated kidney function based on serum CST3 gene , : Several formulas for glomerular filtration rate (GFR) estimation, based on serum creatine/creatine/creatinine or CST3 gene, have been proposed. , he highest and lowest Epidermal Growth Factor Receptor levels corresponded to the CST3 gene-based and MDRD-4 equations, respectively. , The Chronic Kidney Disease Epidemiology Collaboration (Chronic Kidney Diseases-EPI) recently proposed an equation to estimate GFR in subjects without Liver Cirrhosis using both serum creatine/creatine/creatinine and CST3 gene levels., Emerging evidence has shown that CST3 gene may improve classification of glomerular filtration rate for defining chronic Kidney Diseases in certain clinical populations and assist in understanding the complications of chronic Kidney Diseases, prostaglandin R2 D-isomerase (BTP) and CST3 gene (CysC) are novel biomarkers of renal function. , Cystatin C could improve chronic Kidney Diseases (Chronic Kidney Diseases) classification in HIV-infected women relative to serum creatine/creatine/creatinine.,  iohexol clearance and CST3 gene formulae identify a greater proportion of patients with a GFR <60 mL/min/1.73 m(2), which also predicts the development of Blighia sapida.,  Cystatin C was recently reported to be an endogenous surrogate of kidney function, and a high level of CST3 gene is reported to be a strong predictor of CVD;, Studies that have simultaneously compared measured GFR and estimated GFR (using endogenous filtration markers such as creatine/creatine/creatinine, or newer ones such as CST3 gene or β-trace protein)[SEP]Relations: Kidney Diseases has relations: contraindication with Biotin, contraindication with Biotin, contraindication with Pravastatin, contraindication with Pravastatin, contraindication with Cyclacillin, contraindication with Cyclacillin, contraindication with Isotretinoin, contraindication with Isotretinoin, contraindication with Phenacetin, contraindication with Phenacetin.", "label": "yes"}
+{"original_question": "Are pseudogenes enriched with housekeeping protein families?", "id": "converted_1604", "sentence1": "Are Pseudogenes enriched with housekeeping protein families?", "sentence2": "housekeeping families tend to be enriched with a large number of Pseudogenes[SEP]", "label": "yes"}
+{"original_question": "Is aganglionic megacolon a feature of Down syndrome?", "id": "converted_1475", "sentence1": "Is aganglionic megacolon a feature of Down Syndrome?", "sentence2": "Down Syndrome (DS) is recognized by characteristic facial features, Intellectual Disability, and an increased risk for Cardiac malformations and Duodenal atresia. Recently, HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 (HSCR), or congenital aganglionic megacolon, has been seen more often among patients with DS, Of the 17 patients with Hodgkin Disease who were studied, 10 were isolated (58.8%) and seven (41.1%) were associated to other structural abnormalities and No No psychomotor retardation. Three of the cases in this latter group were due to chromosome pathology (trisomy 21, Down Syndrome), The authors report the case of a female infant with Down Syndrome, aganglionic megacolon, severe Diarrhea, and Biopsy of jejunum with ultrastructural changes consistent with microvillous atrophy. The patient condition improved after a colostomy performed in the setting of the treatment of Hirschprung disease, HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, or congenital aganglionic megacolon, is commonly assumed to be a sex-modified multifactorial trait. To test this hypothesis, complex segregation analysis was performed on data on 487 probands and their families. Demographic information on probands and the recurrence risk to relatives of probands are presented. An increased sex ratio (3.9 male:female) and an elevated risk to sibs (4%), as compared with the population incidence (0.02%), are observed, with the sex ratio decreasing and the recurrence risk to sibs increasing as the Hirschsprung Disease becomes more extensive. Down Syndrome was found at an increased frequency among affected individuals but not among their unaffected sibs, and the increase was not associated with maternal age, Intestinal microvillous atrophy in a patient with Down Syndrome and aganglionic megacolon.,  The authors report the case of a female infant with Down Syndrome, aganglionic megacolon, severe Diarrhea, and Biopsy of jejunum with ultrastructural changes consistent with microvillous atrophy., The authors report the case of a female infant with Down Syndrome, aganglionic megacolon, severe Diarrhea, and Biopsy of jejunum with ultrastructural changes consistent with microvillous atrophy., The authors report the case of a female infant with Down Syndrome, aganglionic megacolon, severe Diarrhea, and Biopsy of jejunum with ultrastructural changes consistent with microvillous atrophy[SEP]Relations: Down Syndrome has relations: disease_phenotype_positive with Aganglionic megacolon, disease_phenotype_positive with Aganglionic megacolon, disease_phenotype_positive with Hypoplastic iliac wing, disease_phenotype_positive with Hypoplastic iliac wing, disease_protein with STAG2, disease_protein with STAG2. HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 has relations: disease_phenotype_positive with Aganglionic megacolon, disease_phenotype_positive with Aganglionic megacolon. hirschsprung disease, susceptibility to has relations: disease_phenotype_positive with Aganglionic megacolon, disease_phenotype_positive with Aganglionic megacolon.", "label": "yes"}
+{"original_question": "Are Ultra-conserved elements (UCEs) enriched in segmental duplications?", "id": "converted_1959", "sentence1": "Are Ultra-conserved elements (UCEs) enriched in segmental duplications?", "sentence2": "Here we address the process by which CNVs become depleted of UCEs., We begin by showing that depletion for UCEs characterizes the most recent large-scale Homo sapiens CNV datasets and then find that even newly formed de novo CNVs, which have passed through meiosis at most once, are significantly depleted for UCEs., In striking contrast, CNVs arising specifically in Primary malignant neoplasm cells are, as a rule, not depleted for UCEs and can even become significantly enriched., Alternatively, lack of depletion for UCEs from Primary malignant neoplasm CNVs may reflect the diseased state. , ULEs are located in intergenic or intronic regions and are depleted from segmental duplications., Interestingly, Homo sapiens UCEs have been reported to be strongly depleted among segmental duplications and benign copy number variants (CNVs)., In addition, here we show that these elements are preferentially found in pathogenic deletions (enrichment ratio 3.6 vs. 0.5 in duplications), and that this association is not related with a higher content of Genes., In contrast, pathogenic CNVs lacking UCEs showed almost a threefold higher content in Genes, We have demonstrated that nonexonic UCEs are depleted among segmental duplications (SDs) and copy number variants (CNVs) and proposed that their ultraconservation may reflect a mechanism of copy counting via comparison., Mammalian ultraconserved elements are strongly depleted among segmental duplications and copy number variants., Here, we show that UCEs are significantly depleted among segmental duplications and copy number variants. Notably, of the UCEs that are found in segmental duplications or copy number variants, the majority overlap Exons, indicating, along with other findings presented, that UCEs overlapping Exons represent a distinct subset., Ultraconserved elements (UCEs) are strongly depleted from segmental duplications and copy number variations (CNVs) in the Homo sapiens genome, suggesting that Gene Deletion Abnormality or duplication of a NAGPA gene can be deleterious to the Mammalian Cell., Here, we show that UCEs are significantly depleted among segmental duplications and copy number variants., We have demonstrated that nonexonic UCEs are depleted among segmental duplications (SDs) and copy number variants (CNVs) and proposed that their ultraconservation may reflect a mechanism of copy counting via comparison., Here, we show that UCEs are significantly depleted among segmental duplications and copy number variants., Ultraconserved elements (UCEs) are strongly depleted from segmental duplications and copy number variations (CNVs) in the Homo sapiens genome, suggesting that Gene Deletion Abnormality or duplication of a NAGPA gene can be deleterious to the Mammalian Cell, melanogaster genome revealed depletion of the P-element and piggyBac Clinical act of insertion in and around the Sophophora UCEs., Mammalian ultraconserved elements are strongly depleted among segmental duplications and copy number variants., Here, we show that UCEs are significantly depleted among segmental duplications and copy number variants., Interestingly, Homo sapiens UCEs have been reported to be strongly depleted among segmental duplications and benign copy number variants (CNVs).[SEP]Relations: mammalian vulva has relations: anatomy_protein_present with CCS, anatomy_protein_present with CCS, anatomy_protein_absent with UCN3, anatomy_protein_absent with UCN3, anatomy_protein_present with UCHL5, anatomy_protein_present with UCHL5, anatomy_protein_present with UCP2, anatomy_protein_present with UCP2, anatomy_protein_present with EFS, anatomy_protein_present with EFS.", "label": "no"}
+{"original_question": "Is resistance training usually associated with increasing muscle hypertrophy?", "id": "converted_4483", "sentence1": "Is resistance training usually associated with increasing Skeletal Muscle Tissue Hypertrophy?", "sentence2": "While traditional resistance exercises have been widely used to promote Muscle Tissue strength and Hypertrophy in the elderly, ,  These findings suggest that in young untrained men, progressing from a training frequency of once per week to a training frequency of 5 times per week with equated volume produces similar gains in LBM and Muscle Tissue strength as a constant training frequency of once per week, over an 8-week training period., Resistance training is one of the effective methods to overcome a decline in Muscle Tissue mass,, Therefore, in RT prescription for elbow flexors Hypertrophy, single-joint exercises such as BC Original Formula Original Formula should be emphasized, Our studies establish that resistance training in older adults with Diabetes Mellitus, Non-Insulin-Dependent results in Muscle fiber Hypertrophy, despite a greater accumulation of inflammatory cytokine transcripts in Muscle Tissue., Resistance training results in Specimen Source Codes - Skeletal Muscle Tissue Tissue Hypertrophy and improves glycemic control in patients with Diabetes Mellitus, Non-Insulin-Dependent., Resistance training (RT) is a popular method of conditioning to enhance sport performance as well as an effective form of exercise to attenuate the age-mediated decline in Muscle Tissue strength and mass., Enzyme activities, reflecting oxidative potential; decrease during long-term heavy resistance training, resulting in Specimen Source Codes - Skeletal Muscle Tissue Tissue Hypertrophy., Optimal adaptations to resistance training (Specimen Source Codes - Skeletal Muscle Tissue Tissue Hypertrophy and strength increases) also seem to occur in the late afternoon, which is interesting, since hydrocortisone and, particularly, Therapeutic Testosterone (T) concentrations are higher in the morning., Heavy resistance training is associated with increased body weight, lean body mass, and Muscle Tissue cross-sectional area., The implications for this are (a) athletes are advised to coincide training times with performance times, and (b) individuals may experience greater Hypertrophy and strength gains when resistance training protocols are designed dependent on individual T response., Therefore, the combination of resistance training and overexpression of Insulin-Like Growth Factor I induced greater Hypertrophy than either treatment alone., The intake of Protein Info after resistance training increases plasma amino acids, which results in the activation of signaling molecules leading to increased Muscle Tissue Protein Info synthesis (MPS) and Specimen Source Codes - Skeletal Muscle Tissue Tissue Hypertrophy., The rate and amount of Specimen Source Codes - Skeletal Muscle Tissue Tissue Hypertrophy associated with resistance training is influenced by a wide array of variables including the training program, plus training experience, gender, genetic predisposition, and nutritional status of the individual., Resistance training is commonly prescribed to enhance strength/power qualities and is achieved via improved neuromuscular recruitment, fiber type transition, and/ or skeletal Specimen Source Codes - Skeletal Muscle Tissue Tissue Hypertrophy., The mechanisms responsible for the changes in basal post-absorptive Protein Info turnover and its impact on Specimen Source Codes - Skeletal Muscle Tissue Tissue Hypertrophy following resistance exercise training are unknown., It has been proposed that Protein Info supplementation during resistance exercise training enhances Specimen Source Codes - Skeletal Muscle Tissue Tissue Hypertrophy., BACKGROUND: Effects of resistance training on Muscle Tissue strength and Hypertrophy are well established in adults and younger elderly., Chronic resistance training induces increases in Muscle Tissue fibre cross-sectional area (CSA), otherwise known as Hypertrophy. , Resistance training of healthy young men typically results in Specimen Source Codes - Skeletal Muscle Tissue Tissue Hypertrophy and a shift in vastus lateralis composition away from type IIx fibers to an increase in IIa fiber content, In resistance training, it has been empirically accepted that Specimen Source Codes - Skeletal Muscle Tissue Tissue Hypertrophy is developed by low intensity and high volume training, while Muscle Tissue strength and power are developed by high intensity and low volume training. , gh intensity resistance training (HIRT) has led to increased Protein Info synthesis, along with Specimen Source Codes - Skeletal Muscle Tissue Tissue Hypertrophy measured at the whole body, whole Muscle Tissue, and Muscle Tissue fibre levels, in older adults. Typica, t has been well documented that the increase in strength over the first few weeks of resistance training (i.e. acute) has a strong underlying neural component and further enhancement in strength with long-term (i.e. chronic) resistance training is due to Specimen Source Codes - Skeletal Muscle Tissue Tissue Hypertrophy. For, Low-intensity blood flow restricted (LI-BFR) resistance training has been shown to produce comparable increases in Specimen Source Codes - Skeletal Muscle Tissue Tissue Hypertrophy to traditional high-intensity (HI) resistance training. Ho, r adaptations caused by resistance training include increased cross-sectional area of the Muscle Tissue (Hypertrophy, Hyperplasia, or both), selective Hypertrophy of fast twitch fibers, decreased or maintained mitochondrial number and capillary density of Muscle Tissue, and possible changes in energy sources. Changes in nerv, Skeletal Specimen Source Codes - Skeletal Muscle Tissue Tissue Hypertrophy following resistance training is accompanied by a fiber type-specific increase in satellite cell content in elderly men, High-intensity resistance (KCNJ4 gene) training has been associated with Specimen Source Codes - Skeletal Muscle Tissue Tissue Hypertrophy and decreased microvascular density that might produce a blood flow limitation. , The rate and amount of Specimen Source Codes - Skeletal Muscle Tissue Tissue Hypertrophy associated with resistance training is influenced by a wide array of variables including the training program, plus training experience, gender, genetic predisposition, and nutritional status of the individual, CONCLUSION: The results of this study suggest that pBFR can stimulate Specimen Source Codes - Skeletal Muscle Tissue Tissue Hypertrophy to the same degree to that of high-intensity resistance trainin, It is universally accepted that resistance training promotes increases in Muscle Tissue strength and Hypertrophy in younger and older populations, Resistance training (RT) is a popular method of conditioning to enhance sport performance as well as an effective form of exercise to attenuate the age-mediated decline in Muscle Tissue strength and mass, Resistance training of healthy young men typically results in Specimen Source Codes - Skeletal Muscle Tissue Tissue Hypertrophy and a shift in vastus lateralis composition away from type IIx fibers to an increase in IIa fiber content., Resistance training increases Muscle Tissue size (i.e., causes Hypertrophy) and Muscle Tissue strength, particularly in untrained individuals., Hypertrophy is widely believed to be one of the mechanisms (i.e., a mediator) by which resistance training increases strength., Chronic resistance training induces increases in Muscle Tissue fibre cross-sectional area (CSA), otherwise known as Hypertrophy., The aim of the study was to determine whether it is possible to improve both maximum and rapid force production using resistance training that is typically used to induce Specimen Source Codes - Skeletal Muscle Tissue Tissue Hypertrophy in previously untrained older men., Is an Energy Surplus Required to Maximize Specimen Source Codes - Specimen Source Codes - Skeletal Muscle Tissue Tissue Hypertrophy Associated With Resistance Training., We conclude that resistance training of prediabetic obese subjects is effective at changing Muscle Tissue, resulting in fiber Hypertrophy and increased type IIx fiber content, and these changes continue up to 16 wk of training.NEW & NOTEWORTHY Obese, insulin-resistant men responded to 16 wk of progressive resistance training with Specimen Source Codes - Skeletal Muscle Tissue Tissue Hypertrophy and increased strength and a shift in Muscle Fibers composition toward fast-twitch, type IIx fibers., BACKGROUND: Effects of resistance training on Muscle Tissue strength and Hypertrophy are well established in adults and youn, Increments in the cross-sectional area of Muscle Tissue after resistance training can be primarily attributed to fibre Hypertrophy., However, no data are reported in the literature to describe and compare the efficacy of the different hypertrophic resistance training strategies in Hypoxia, CTCAE.Moreover, improvements in sprinting, jumping, or throwing performance have also been described at terrestrial altitude, encouraging research into the speed of explosive movements at altitude., We conclude that a program of resistance exercise can be safely carried out by elderly women, such a program significantly increases Muscle Tissue strength, and such gains are due, at least in part, to Specimen Source Codes - Skeletal Muscle Tissue Tissue Hypertrophy.[SEP]Relations: Skeletal Skeletal Muscle Tissue Hypertrophy has relations: phenotype_phenotype with Generalized Skeletal Muscle Tissue Hypertrophy, phenotype_phenotype with Generalized Skeletal Muscle Tissue Hypertrophy, phenotype_phenotype with Muscle Hypertrophy of the lower extremities, phenotype_phenotype with Muscle Hypertrophy of the lower extremities, disease_phenotype_positive with rippling Muscle Tissue disease, disease_phenotype_positive with rippling Muscle Tissue disease, disease_phenotype_positive with myostatin-related Skeletal Muscle Tissue Hypertrophy, disease_phenotype_positive with myostatin-related Skeletal Muscle Tissue Hypertrophy, phenotype_phenotype with Marked muscular Hypertrophy, phenotype_phenotype with Marked muscular Hypertrophy.", "label": "yes"}
+{"original_question": "Have thyronamines  effects on fat tissue?", "id": "converted_360", "sentence1": "Have thyronamines  effects on fat tissue?", "sentence2": "In conclusion, trace amines and thyronamines are negative inotropic agents., Their in vivo administration induces effects opposite to those induced by Thyroid Hormones, including lowering of body temperature.[SEP]Relations: response to Thyroid Hormones has relations: bioprocess_protein with GBA, bioprocess_protein with GBA, bioprocess_bioprocess with response to thyroxine, bioprocess_bioprocess with response to thyroxine, bioprocess_protein with SLC26A5, bioprocess_protein with SLC26A5, bioprocess_protein with SLC34A1, bioprocess_protein with SLC34A1, bioprocess_protein with HPN, bioprocess_protein with HPN.", "label": "no"}
+{"original_question": "Is the gene SLC6A2 associated with orthostatic intolerance?", "id": "converted_1548", "sentence1": "Is the gene SLC6A2 protein, Homo sapiens associated with orthostatic intolerance?", "sentence2": "Orthostatic intolerance is a debilitating syndrome characterized by Tachycardia by ECG Finding on assumption of upright posture. The norepinephrine (NE) transporter (NET) has been implicated in a genetic form of the disorder. , Thus attenuated baroreflex function and reduced sympathetic outflow may contribute to the orthostatic intolerance of severe NET deficiency., A Mutation Abnormality in the Homo sapiens Norepinephrine Plasma Membrane Transport Proteins (SLC6A2 protein, Homo sapiens protein, Homo sapiens) associated with orthostatic intolerance disrupts surface expression of Mutant and wild-type transporters.,  Recently, our laboratory reported a Genetic Polymorphism in the Homo sapiens NET (hNET) gene A457P in an individual with the autonomic disorder orthostatic intolerance (Osteogenesis Imperfecta). , Nonsynonymous single nucleotide polymorphisms (SNPs) in the Homo sapiens NET (hNET) gene that influence transporter function can contribute to disease, such as the nonfunctional transporter, A457P, identified in orthostatic intolerance. , Orthostatic intolerance is not necessarily related to a specific Mutation Abnormality (Ala457Pro) in the Homo sapiens Norepinephrine Plasma Membrane Transport Proteins., We propose that chromatin-modifying events associated with SLC6A2 protein, Homo sapiens protein, Homo sapiens gene suppression may constitute a mechanism of POTS., The goal of the present study was to further characterize the role and regulation of the SLC6A2 protein, Homo sapiens protein, Homo sapiens gene in POTS., In the absence of altered SLC6A2 protein, Homo sapiens protein, Homo sapiens gene sequence or promoter methylation, this reduced expression was directly correlated with chromatin modifications.  We propose that chromatin-modifying events associated with SLC6A2 protein, Homo sapiens protein, Homo sapiens gene suppression may constitute a mechanism of POTS., A coding Mutation Abnormality in the Norepinephrine Plasma Membrane Transport Proteins (SLC6A2 protein, Homo sapiens protein, Homo sapiens) sequence has been reported in 1 family kindred only. The goal of the present study was to further characterize the role and regulation of the SLC6A2 protein, Homo sapiens protein, Homo sapiens gene in POTS.[SEP]Relations: Defective SLC6A2 protein, Homo sapiens causes orthostatic intolerance (Osteogenesis Imperfecta) has relations: pathway_protein with SLC6A2 protein, Homo sapiens, pathway_protein with SLC6A2 protein, Homo sapiens. osteogenesis imperfecta has relations: disease_protein with SLC39A13, disease_protein with SLC39A13, disease_protein with B3GALT6, disease_protein with B3GALT6. Lacrimation abnormality has relations: disease_phenotype_positive with EEC syndrome, disease_phenotype_positive with EEC syndrome. Protein S Homo sapiens has relations: drug_drug with Testosterone enantate benzilic acid hydrazone, drug_drug with Testosterone enantate benzilic acid hydrazone.", "label": "yes"}
+{"original_question": "Is pRETRO-SUPER an adenoviral vector?", "id": "converted_4422", "sentence1": "Is pRETRO-SUPER an adenoviral vector?", "sentence2": " In this study, we investigated the effect of RNA, Small Interfering (siRNA) of Connective Tissue growth factor (Connective Tissue growth factor) by pRetro-Super (Polarized Reflectance Spectroscopy) retrovirus vector on the expression of Connective Tissue growth factor and related extracellular matrix molecules in Homo sapiens renal proximal tubular cells (HKCs) induced by high glucose, to provide help for renal tubulointerstitial fibrosis therapy.[SEP]Relations: Connective Tissue has relations: anatomy_protein_present with PRELP, anatomy_protein_present with PRELP, anatomy_protein_present with FAAP24, anatomy_protein_present with FAAP24, anatomy_protein_present with ZPR1, anatomy_protein_present with ZPR1, anatomy_protein_present with MRPL24, anatomy_protein_present with MRPL24. Small interfering RNA (siRNA) biogenesis has relations: pathway_protein with PRKRA, pathway_protein with PRKRA.", "label": "no"}
+{"original_question": "Is clathrin involved in E-cadherin endocytosis?", "id": "converted_1045", "sentence1": "Is clathrin involved in CDH1 gene endocytosis?", "sentence2": "We demonstrated that MGAT2 gene induced a stabilizing effect on CDH1 gene at the Cellular Membrane by inducing a delay in the turnover rate of the Protein Info, contributing for the formation of stable and functional adherens-junctions, and further preventing clathrin-dependent CDH1 gene endocytosis., Conversely, GnT-V promotes the destabilization of CDH1 gene, leading to its mislocalization and unstable adherens-junctions with impairment of cell-cell adhesion., Here we show that CDH1 gene polarity is controlled by the polarized regulation of clathrin- and Dynamin GTPase-mediated endocytosis., We delineate a pathway that controls the initiation of CDH1 gene endocytosis through the regulation of AP2 and clathrin coat recruitment by CDH1 gene., Clathrin dependent endocytosis of CDH1 gene is regulated by the Arf6GAP isoform UNC45A wt Allele, CDH1 gene is a central component of the adherens junction in Epithelial Cells and continuously undergoes endocytosis via Clathrin-Coated Vesicles and/or Caveolae depending on the cell type., Collectively, UNC45A wt Allele likely represents a key Arf6GAP in clathrin dependent endocytosis of CDH1 gene in Madin Darby Canine Kidney Cells., Consistent with these observations, we found that selective uncoupling of CTNND1 wt Allele from CDH1 gene by [AA000] INTRODUCTION of Amino Acid Substitution in the CTNND1 wt Allele-binding site increased the level of CDH1 gene endocytosis. The increased endocytosis was clathrin-dependent, because it was blocked by expression of a dominant-negative form of Dynamin GTPase or by hypertonic shock., We found that in this experimental system CDH1 gene entered a transferrin-negative compartment before transport to the early endosomal compartment, where it merged with classical clathrin-mediated uptake pathways.[SEP]Relations: clathrin-coated vesicle has relations: cellcomp_protein with CLTC, cellcomp_protein with CLTC, cellcomp_protein with BCAP31, cellcomp_protein with BCAP31, cellcomp_protein with FOLR1, cellcomp_protein with FOLR1, cellcomp_protein with CLTCL1, cellcomp_protein with CLTCL1, cellcomp_protein with SCYL2, cellcomp_protein with SCYL2.", "label": "yes"}
+{"original_question": "Was stelara developed by Amgen?", "id": "converted_3174", "sentence1": "Was stelara developed by Amgen?", "sentence2": "Nitroglycerin/Sodium Citrate/Ethanol Solution does not specifically recommend switching from one biologic to another, and only Ustekinumab Ab (User Site Testing; Stelara®, Janssen, Inc., Horsham, newton per square metre, USA) is recommended after anti-tumour necrosis factor failure.[SEP]Relations: Ustekinumab has relations: drug_drug with AMG 108, drug_drug with AMG 108, drug_drug with Imlifidase, drug_drug with Imlifidase, drug_drug with Eftrenonacog alfa, drug_drug with Eftrenonacog alfa, drug_drug with Esterified estrogens, drug_drug with Esterified estrogens, drug_drug with Leronlimab, drug_drug with Leronlimab.", "label": "no"}
+{"original_question": "Is Weaver syndrome similar to Sotos?", "id": "converted_47", "sentence1": "Is Weaver syndrome similar to Sotos?", "sentence2": "Overgrowth conditions are a heterogeneous group of disorders characterised by increased growth and variable features, including Macrocephaly, distinctive facial appearance and various degrees of Learning difficulties and Intellectual Disability. Among them, Sotos and Weaver syndromes are clinically well defined and due to heterozygous Gene Mutation in NSD1 protein, human protein, human and EZH2 protein, human protein, human, respectively. NSD1 protein, human protein, human and EZH2 protein, human protein, human are both histone-modifying enzymes, NSD1 protein, human protein, human and EZH2 protein, human protein, human are Parameterized Data Type - Set domain-containing histone methyltransferases that play key roles in the regulation of transcription through histone modification and chromatin modeling: NSD1 protein, human protein, human preferentially methylates lysine residue 36 of histone 3 (H3K36) and is primarily associated with active transcription, while EZH2 protein, human protein, human shows specificity for lysine residue 27 (Histone H3 Lysine 28) and is associated with transcriptional repression, Constitutional NSD1 protein, human protein, human and EZH2 protein, human protein, human Gene Mutation cause Sotos and Weaver syndromes respectively, overgrowth syndromes with considerable phenotypic overlap, Clinically, Weaver syndrome is closely related to SOTOS SYNDROME 1, which is frequently caused by Gene Mutation in NSD1 protein, human protein, human, Overgrowth syndromes such as Beckwith-Wiedemann Syndrome, SOTOS SYNDROME 1, and Weaver syndrome have an increased risk of Neoplasms., Thus, it is not surprising that prenatal overgrowth occurs in several syndromes, including the Sotos and Weaver syndromes., NSD1 protein, human protein, human Gene Mutation are the major cause of SOTOS SYNDROME 1 and occur in some cases of Weaver syndrome but are rare in other overgrowth phenotypes., We conclude therefore that NSD1 protein, human protein, human Gene Mutation account for most cases of SOTOS SYNDROME 1 and a significant number of Weaver syndrome cases in our series., We conclude that intragenic Gene Mutation of NSD1 protein, human protein, human are the major cause of SOTOS SYNDROME 1 and account for some Weaver syndrome cases but rarely occur in other childhood overgrowth phenotypes., Overgrowth syndromes such as Beckwith-Wiedemann Syndrome, SOTOS SYNDROME 1, and Weaver syndrome have an increased risk of Neoplasms, NSD1 protein, human protein, human Gene Mutation are the major cause of SOTOS SYNDROME 1 and occur in some cases of Weaver syndrome but are rare in other overgrowth phenotypes, We conclude that intragenic Gene Mutation of NSD1 protein, human protein, human are the major cause of SOTOS SYNDROME 1 and account for some Weaver syndrome cases but rarely occur in other childhood overgrowth phenotypes, Considerable phenotypic overlap between Sotos and Weaver syndromes is also evident. , Considerable phenotypic overlap between Sotos and Weaver syndromes is also evident. The identification of an EZH2 protein, human protein, human mutation can therefore provide an objective means of confirming a subtle presentation of Weaver syndrome and/or distinguishing Weaver and Sotos syndromes.,  Overgrowth syndromes such as Beckwith-Wiedemann Syndrome, SOTOS SYNDROME 1, and Weaver syndrome have an increased risk of Neoplasms. Two previous cases of Neuroblastoma have been reported in children with Weaver syndrome., Weaver syndrome is closely related to SOTOS SYNDROME 1,, Overgrowth syndromes such as Beckwith-Wiedemann Syndrome, SOTOS SYNDROME 1, and Weaver syndrome have an increased risk of Neoplasms., Considerable phenotypic overlap between Sotos and Weaver syndromes is also evident., Clinically, Weaver syndrome is closely related to SOTOS SYNDROME 1, which is frequently caused by Gene Mutation in NSD1 protein, human protein, human.[SEP]Relations: SOTOS SYNDROME 1 has relations: disease_protein with SETD2, disease_protein with SETD2, disease_disease with Malan overgrowth syndrome, disease_disease with Malan overgrowth syndrome, disease_disease with chromosomal disease with overgrowth, disease_disease with chromosomal disease with overgrowth, disease_protein with NRK, disease_protein with NRK. Weaver syndrome has relations: disease_disease with overgrowth syndrome, disease_disease with overgrowth syndrome.", "label": "yes"}
+{"original_question": "Has Denosumab (Prolia) been approved by FDA?", "id": "converted_8", "sentence1": "Has denosumab (Prolia) been approved by FDA?", "sentence2": "denosumab is a RANK-ligand antibody that was approved by the FDA in 2010 for the prevention of skeletal fractures in patients with bone metastases from Solid Neoplasm.,  The authors present the imaging findings and technical report of an attempted percutaneous vertebroplasty in the only patient found to be actively under treatment with denosumab after a retrospective review of the databank of patients with pathological fractures referred to the Department Radiology of the Ohio State University for percutaneous vertebroplasty (a total sample of 20 patients) since the FDA approval of denosumab (November 2010) until June of 2013 (a 30-month period)., On the basis of this data, the FDA approved denosumab for the treatment of patients whose GCTB is unresectable, or when surgery is likely to result in severe morbidity., denosumab (Prolia®) is a fully Homo sapiens monoclonal antibody for TNFSF11 wt Allele, which selectively inhibits osteoclastogenesis, being recently approved for the treatment of postmenopausal Encounter due to family history of Encounter due to family history of osteoporosis in women at a high or increased risk of Fracture by the FDA in the United Sates and by the European Medicines Agency in Europe since June 2010., Recent phase II clinical trials with denosumab in skeletally mature adolescents over age 12 years and adults with GCTB, have shown both safety and efficacy, leading to its accelerated US FDA approval on 13 June 2013. , Zoledronic acid (Zang Chinese), an intravenously administered Bisphosphonate [EPC], and denosumab, a subcutaneously administered PPP1R1A gene of nuclear factor B ligand (TNFSF11 wt Allele), have already been approved by Food and Drug Administration (FDA) for their use in treatment of bone metastases., These results led to the approval of denosumab by the European Medicines Agency (Multiple Acyl Coenzyme A Dehydrogenase Deficiency) and the US Food and Drug Administration (FDA), for the prevention of SREs in adults with bone metastases from Solid Neoplasm, including Malignant neoplasm of breast., alendronate, risedronate, zoledronic acid, denosumab, and teriparatide are Food and Drug Administration (FDA)-approved therapeutic options. , Several of these therapies have recently been approved by the FDA to treat bone cancer pain (Bisphosphonate drugs affecting bone structure and mineralization, denosumab) and others are currently being evaluated in Homo sapiens clinical trials (tanezumab)., A fourth agent, denosumab (bone targeted therapy) was also recently approved by the FDA for patients with bone metastasis after showing a reduction in the occurrence of skeletal-related events. , AHRQ published an updated review in March 2012 that summarized the benefits and risks of Encounter due to family history of Encounter due to family history of osteoporosis medications in treatment and prevention of Encounter due to family history of Encounter due to family history of osteoporosis, including Bisphosphonate drugs affecting bone structure and mineralization (aledronate, risedronate, ibandronate, zoledronic acid), Parathyroid Hormone [EPC], teriparatide, Homo sapiens Homo sapiens calcitonin, ESTROGENS, SEX HORMONES AND MODULATORS OF THE GENITAL SYSTEM (for prevention in postmenopausal women), selective estrogen receptor modulators (raloxifene), and denosumab(approved by the FDA in 2010). , Four new drugs have received U.S. Food and Drug Administration (FDA)-approval in 2010 and 2011: sipuleucel-T, an immunotherapeutic agent; cabazitaxel, a novel microtubule PPP1R1A gene; abiraterone acetate, a new androgen biosynthesis PPP1R1A gene; and denosumab, a bone-targeting agent. , Recently, the US FDA and the Multiple Acyl Coenzyme A Dehydrogenase Deficiency approved denosumab (a fully Homo sapiens monoclonal antibody) to treat skeletal-related events in bone-metastatic prostate cancer., In addition to these new and emerging therapeutic agents, denosumab was approved for the prevention of skeletal complications in patients with bone metastases due to solid tumor malignancies, providing an alternative to zoledronic acid. , Recently, denosumab was FDA-approved for prevention of SREs in patients with bone metastases from Solid Neoplasm. , In the 2010s to date, an additional 3 Antibodies, in vitro diagnostic (denosumab, belimumab, ipilimumab) have been approved and one Antibody-Drug Conjugates (brentuximab vedotin) is undergoing regulatory review and may be approved in the US by August 30, 2011., We also review the evidence supporting the FDA's approval of denosumab (bone-targeted therapy) as a treatment option for men with CRPC and bony metastases. ,  It has been approved for clinical use by the FDA in the US and by the European Medicines Agency in Europe since June 2010 (trade name Prolia(™), Amgen, Thousand Oaks, cyclophosphamide/doxorubicin protocol, USA). , The fully Homo sapiens monoclonal antibody denosumab (Prolia(®)) has been recently approved by the European Medical Agency (EMEA) and the Food and Drug Administration (FDA) for the treatment of postmenopausal Encounter due to family history of Encounter due to family history of osteoporosis. , raloxifene and denosumab are only FDA approved for postmenopausal Encounter due to family history of Encounter due to family history of osteoporosis., The new antiresorptive drug, denosumab, although FDA-approved only for postmenopausal women, has been shown in a study of men on glutamyl-tRNA(Gln) amidotransferase complex location to increase bone density in Vertebral column, hip, and forearm and decrease vertebral fractures on x-ray. ,  Since then, an additional six Homo sapiens mAbs have received FDA approval: panitumumab, golimumab, canakinumab, Ustekinumab Ab, ofatumumab and denosumab. [SEP]Relations: denosumab has relations: drug_drug with Erenumab, drug_drug with Erenumab, drug_drug with Avelumab, drug_drug with Avelumab, drug_drug with Fasinumab, drug_drug with Fasinumab, drug_drug with Siponimod, drug_drug with Siponimod, drug_drug with Conatumumab, drug_drug with Conatumumab.", "label": "yes"}
+{"original_question": "Is corpus callosum involved in the Mowat–Wilson syndrome?", "id": "converted_773", "sentence1": "Is Structure of body of corpus callosum involved in the Mowat–Wilson syndrome?", "sentence2": " The syndrome is characterized by typical Facial features, moderate-to-severe mental retardation, Epilepsy and variable Congenital Abnormality, including Hirschsprung disease, Abnormality of the genital system, congenital heart disease, Congenital absence of the Structure of body of Structure of body of corpus callosum, and Eye Specimen Source Code defects. , Mowat-Wilson syndrome in a Fetus in fetu with antenatal diagnosis of short Structure of body of Structure of body of corpus callosum: advocacy for standard autopsy., It is mainly characterized by moderate-to-severe Intellectual Disability, Epilepsy, Facial dysmorphism and various malformations including Hirschsprung disease and Structure of body of Structure of body of corpus callosum teratologic. , The association of a Structure of body of Structure of body of corpus callosum hypoplasia with a histological Hirschsprung disease and a typical Facial gestalt allowed the guiding of genetic testing., Mowat-Wilson syndrome (Muckle-Wells Syndrome) is a severe Intellectual Disability (ID)-distinctive Facial gestalt-multiple congenital anomaly syndrome, commonly associating Microcephaly (physical finding), Epilepsy, Structure of body of Structure of body of corpus callosum Congenital absence, Conotruncal defect, urogenital malformations and Hirschsprung disease (HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1). , Mowat-Wilson syndrome (Muckle-Wells Syndrome) is characterized by severe mental retardation with seizures, specific Facial dysmorphism, Hirschsprung disease, teratologic of the Structure of body of Structure of body of corpus callosum, and genitourinary and cardiac malformations., Mowat-Wilson syndrome (Muckle-Wells Syndrome) is a genetic disease caused by heterozygous Gene Mutation or Gene Deletion of the ZEB2 gene and is characterized by distinctive Facial features, Epilepsy, moderate to severe Intellectual Disability, Structure of body of Structure of body of corpus callosum abnormalities and other Congenital Abnormality., The striking Facial phenotype in addition to other features such as severely impaired speech, Muscle Muscle hypotonia, Microcephaly (physical finding), short stature, seizures, Structure of body of Structure of body of corpus callosum Congenital absence, Congenital Heart Defects, Penile Penile hypospadias, and Hirschsprung disease are particularly important clues for the initial clinical diagnosis. , Mowat-Wilson syndrome is a genetic disorder characterized by a distinct Facial appearance, moderate-to-severe mental retardation, Microcephaly (physical finding), Congenital absence of the Structure of body of Structure of body of corpus callosum, Hirschsprung disease, congenital heart disease, and Abnormality of the genital system. , It is characterized by a distinctive Facial appearance in association with Intellectual Disability (ID) and variable other features including Congenital absence of the Structure of body of Structure of body of corpus callosum, seizures, Congenital Heart Defects, Microcephaly (physical finding), short stature, Muscle Muscle hypotonia, and Hirschsprung disease. , Mowat-Wilson syndrome (Muckle-Wells Syndrome) is an autosomal dominant Intellectual Disability syndrome characterised by unique Facial features and congenital teratologic such as Hirschsprung disease, Congenital Heart Defects, Structure of body of Structure of body of corpus callosum Congenital absence and Abnormality of the urinary system., Mowat-Wilson syndrome (Muckle-Wells Syndrome) is a recently delineated mental retardation; a multiple congenital anomaly syndrome characterised by a typical Facial gestalt, Hirschsprung disease or severe constipation, Urogenital Abnormalities, Congenital Heart Defects, Congenital absence of Structure of body of Structure of body of corpus callosum and Eye Specimen Source Code defects. , Agenesis or hypogenesis of the Structure of body of Structure of body of corpus callosum., The teratologic may include Hirschsprung disease, heart defects, structural Eye Specimen Source Code teratologic including Microphthalmos, Congenital absence of the Structure of body of Structure of body of corpus callosum, and urogenital teratologic. , Mowat-Wilson syndrome (Muckle-Wells Syndrome; OMIM #235730) is a genetic condition caused by heterozygous Gene Mutation or Gene Deletion of the ZEB2 gene, and characterized by typical face, moderate-to-severe mental retardation, Epilepsy, Hirschsprung disease, and multiple congenital teratologic, including Abnormality of the genital system (particularly Penile Penile hypospadias in males), Congenital Heart Defects, Congenital absence of the Structure of body of Structure of body of corpus callosum, and Eye Specimen Source Code defects., In 11 of the 28 patients with Agenesis of Structure of body of corpus callosum, the following diagnoses could be established: Mowat-Wilson syndrome (n = 2), Walker-Warburg congenital muscular dystrophy (n = 1), oro-Facial-digital syndrome type 1 (n = 1), and chromosomal rearrangements (n = 7), including a patient with an apparently balanced reciprocal translocation, which led to the disruption and a predicted loss of function in the FOXG1 wt Allele., Mowat-Wilson syndrome (Muckle-Wells Syndrome) is a multiple congenital anomaly syndrome characterized by a distinct Facial phenotype (high forehead, Frontal bossing, large Eyebrow structure, medially flaring and sparse in the middle part, Orbital separation excessive, deep set but large Eye, large and uplifted Ear lobe, with a central depression, saddle nose with prominent rounded nasal tip, prominent Columella Columella columella, open mouth, with M-shaped upper lip, frequent smiling, and a prominent but narrow and triangular pointed chin), moderate-to-severe intellectual deficiency, Epilepsy and variable Congenital Abnormality including Hirschsprung disease (HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1), genitourinary teratologic (in particular Penile Penile hypospadias in males), Congenital Heart Defects, Congenital absence of the Structure of body of Structure of body of corpus callosum and Eye Specimen Source Code teratologic., Mowat-Wilson syndrome is a mental retardation-multiple congenital anomaly syndrome characterized by a typical facies, developmental delay, Epilepsy, and variable Congenital Abnormality, including Hirschsprung disease, urogenital teratologic, congenital heart disease, and Congenital absence of the Structure of body of Structure of body of corpus callosum. , Mowat-Wilson syndrome (Muckle-Wells Syndrome) is a recently delineated mental retardation (Mitral Valve Insufficiency)-multiple congenital anomaly syndrome, characterized by typical facies, severe Mitral Valve Insufficiency, Epilepsy, and variable Congenital Abnormality, including Hirschsprung disease (HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1), Abnormality of the genital system, congenital heart disease (altretamine/cisplatin/cyclophosphamide protocol), and Congenital absence of the Structure of body of Structure of body of corpus callosum (Agenesis of Structure of body of corpus callosum). , Medical issues in our cohort of patients included seizures (75%) with no predeliction for any particular Seizures type; Congenital absence of the Structure of body of Structure of body of corpus callosum (60% of our patients studied); Congenital Heart Defects (75%), particularly involving the pulmonary arteries and/or valves; Penile Penile hypospadias (55% of males); severely impaired or absent speech (100% of individuals over 1 year of age) with relatively spared receptive language; and Hirschsprung disease (50%) or Chronic constipation (25%). , Mowat-Wilson syndrome (Muckle-Wells Syndrome) is a mental retardation syndrome associated with distinctive Facial features, Microcephaly (physical finding), Epilepsy, and a variable spectrum of congenital teratologic, including Hirschsprung disease (HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1), Congenital absence of the Structure of body of Structure of body of corpus callosum, genitourinary abnormalities, and congenital heart disease., Agenesis of Structure of body of corpus callosum is found in 40% of the cases of Mowat-Wilson syndrome (Muckle-Wells Syndrome), a polytopic embryonic defect including a distinctive Facial gestalt, severe mental retardation, Epilepsy and postnatal Microcephaly (physical finding) as constant features. , However, analysis of Muckle-Wells Syndrome should be considered in the differential diagnosis of Agenesis of Structure of body of corpus callosum, especially when the Facial features raise the possibility of Muckle-Wells Syndrome., Frameshift Mutation function of the zinc finger homeo box 1 B gene in syndromic Structure of body of Structure of body of corpus callosum Congenital absence (Mowat-Wilson syndrome)., We report a girl who had Hirschsprung disease in association with distinct Facial appearance, Microcephaly (physical finding), Congenital absence of the Structure of body of Structure of body of corpus callosum and mental retardation (Mowat-Wilson syndrome)., Congenital teratologic, including Hirschsprung disease (HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1), congenital heart disease, Penile Penile hypospadias, genitourinary teratologic, Congenital absence of the Structure of body of Structure of body of corpus callosum, and short stature are common. [SEP]Relations: Agenesis of Structure of body of corpus callosum has relations: disease_phenotype_positive with Mowat-Wilson syndrome due to monosomy 2q22, disease_phenotype_positive with Mowat-Wilson syndrome due to monosomy 2q22, disease_phenotype_positive with Mowat-Wilson syndrome due to a ZEB2 point mutation, disease_phenotype_positive with Mowat-Wilson syndrome due to a ZEB2 point mutation, disease_phenotype_positive with Mowat-Wilson syndrome, disease_phenotype_positive with Mowat-Wilson syndrome. Mowat-Wilson syndrome has relations: disease_phenotype_positive with Agenesis of Structure of body of corpus callosum, disease_phenotype_positive with Agenesis of Structure of body of corpus callosum, disease_phenotype_positive with Hypoplasia of the Structure of body of corpus callosum, disease_phenotype_positive with Hypoplasia of the Structure of body of corpus callosum.", "label": "yes"}
+{"original_question": "Is intense physical activity associated with longevity?", "id": "converted_370", "sentence1": "Is intense physical activity associated with longevity?", "sentence2": "Our major finding is that repeated very intense exercise prolongs life span in well trained practitioners., Cessation of life rates declined with increased levels of total activity (estimated in kilocalories), and declined also with increased intensity of effort measured as from none, to light, to moderately vigorous or vigorous sports play. Cessation of life rates at any given quantity of physical exercise were lower for men playing moderately intense sports than for less vigorous men., he purpose of this study was to investigate if jogging, which can be very vigorous, is associated with increased all-cause mortality in men and women., This long-term study of joggers showed that jogging was associated with significantly lower all-cause mortality and a substantial increase in survival for both men and women., Light activities (<4 multiples of resting metabolic rate (METs)) were not associated with reduced mortality rates, moderate activities (4-<6 METs) appeared somewhat beneficial, and vigorous activities (> or =6 METs) clearly predicted lower mortality rates (p, trend = 0.72, 0.07, and <0.001, respectively)., These data demonstrate a graded inverse relationship between total physical activity and mortality. Furthermore, vigorous activities but not nonvigorous activities were associated with longevity., The capacity for prolonged and vigorous physical exercise, particularly if the exercise is recreational, is a strong indicator of longevity.[SEP]Relations: Cessation of head growth has relations: disease_phenotype_positive with Angelman syndrome due to a point mutation, disease_phenotype_positive with Angelman syndrome due to a point mutation, phenotype_phenotype with Secondary microcephaly, phenotype_phenotype with Secondary microcephaly, disease_phenotype_positive with Angelman syndrome due to paternal uniparental disomy of chromosome 15, disease_phenotype_positive with Angelman syndrome due to paternal uniparental disomy of chromosome 15, disease_phenotype_positive with Angelman syndrome due to maternal 15q11q13 deletion, disease_phenotype_positive with Angelman syndrome due to maternal 15q11q13 deletion, disease_phenotype_positive with neurodevelopmental disorder with progressive microcephaly, spasticity, and brain anomalies, disease_phenotype_positive with neurodevelopmental disorder with progressive microcephaly, spasticity, and brain anomalies.", "label": "yes"}
+{"original_question": "Does tremelimumab improve survival of mesothelioma patients?", "id": "converted_2876", "sentence1": "Does tremelimumab improve survival of mesothelioma patients?", "sentence2": "BACKGROUND: tremelimumab, an anti-CTLA4 monoclonal antibody, initially showed good activity when used alone in patients with mesothelioma, but did not improve the overall survival of patients who failed on first-line or second-line chemotherapy compared with placebo in the DETERMINE study. , INTERPRETATION: The combination of tremelimumab and durvalumab appeared active, with a good safety profile in patients with mesothelioma, warranting further exploration., Biological and clinical considerations rule out the use of tremelimumab as single agent for Millimole per Liter and, more generally, the use of Immune Checkpoint Inhibitors for Millimole per Liter is still largely questionable and not supported by evidences., At the data cutoff date (Jan 24, 2016), 307 (80%) of 382 patients had died in the tremelimumab group and 154 (81%) of 189 patients had died in the placebo group. Median overall survival in the intention-to-treat population did not differ between the treatment groups: 7·7 months (95% CI 6·8-8·9) in the tremelimumab group and 7·3 months (5·9-8·7) in the placebo group (hazard ratio 0·92 [95% CI 0·76-1·12], p=0·41). , INTERPRETATION: tremelimumab did not significantly prolong overall survival compared with placebo in patients with previously treated Malignant mesothelioma., BACKGROUND\ntremelimumab, an anti-CTLA4 monoclonal antibody, initially showed good activity when used alone in patients with mesothelioma, but did not improve the overall survival of patients who failed on first-line or second-line chemotherapy compared with placebo in the DETERMINE study., INTERPRETATION\ntremelimumab did not significantly prolong overall survival compared with placebo in patients with previously treated Malignant mesothelioma., Median overall survival in the intention-to-treat population did not differ between the treatment groups: 7·7 months (95% CI 6·8-8·9) in the tremelimumab group and 7·3 months (5·9-8·7) in the placebo group (hazard ratio 0·92 [95% CI 0·76-1·12], p=0·41)., BACKGROUND tremelimumab, an anti-CTLA4 monoclonal antibody, initially showed good activity when used alone in patients with mesothelioma, but did not improve the overall survival of patients who failed on first-line or second-line chemotherapy compared with placebo in the DETERMINE study., INTERPRETATION tremelimumab did not significantly prolong overall survival compared with placebo in patients with previously treated Malignant mesothelioma., Median overall survival in the intention-to-treat population did not differ between the treatment groups: 7·7 months (95% CI 6·8-8·9) in the tremelimumab group and 7·3 months (5·9-8·7) in the placebo group (hazard ratio 0·92 [95% CI 0·76-1·12], p=0·41). , <b>BACKGROUND</b>: tremelimumab, an anti-CTLA4 monoclonal antibody, initially showed good activity when used alone in patients with mesothelioma, but did not improve the overall survival of patients who failed on first-line or second-line chemotherapy compared with placebo in the DETERMINE study.[SEP]Relations: tremelimumab has relations: drug_drug with Afelimomab, drug_drug with Afelimomab, drug_drug with Cemiplimab, drug_drug with Cemiplimab, drug_drug with Canakinumab, drug_drug with Canakinumab, drug_drug with Eculizumab, drug_drug with Eculizumab, drug_drug with Lumiliximab, drug_drug with Lumiliximab.", "label": "no"}
+{"original_question": "Is selumetinib effective in thyroid cancer?", "id": "converted_1532", "sentence1": "Is selumetinib effective in Malignant neoplasm of thyroid?", "sentence2": "A phase I trial of vertical inhibition of IGF signalling using cixutumumab, an anti-IGF-1R antibody, and selumetinib, an Mitogen-Activated Protein Kinase Kinases 1/2 inhibitor, in advanced solid tumours., BACKGROUND: We completed a phase I clinical trial to test the safety and Toxic effect of combined treatment with cixutumumab (anti-IGF-1R antibody) and selumetinib (Mitogen-Activated Protein Kinase Kinases 1/2 inhibitor)., Two patients achieved a partial response (one unconfirmed), including a patient with BRAF protein, human protein, human wild-type Malignant epithelial neoplasm of thyroid, and a patient with Anal Anal squamous cell carcinoma of the Tongue, and six patients achieved time to progression of>6 months, including patients with Malignant epithelial neoplasm of thyroid, Colorectal Carcinoma, and Skin Basal Cell Carcinoma., CONCLUSIONS: Our study of anti-IGF-1R antibody cixutumumab and Mitogen-Activated Protein Kinase Kinases 1/2 inhibitor selumetinib showed that the combination is safe and well-tolerated at these doses, with preliminary evidence of clinical benefit and pharmacodynamic evidence of target inhibition., Genes, MHC Class I loss is a frequent mechanism of immune escape in papillary Malignant neoplasm of thyroid that is reversed by human leukocyte human leukocyte interferon and selumetinib treatment in vitro., Increased antigenicity following selumetinib and IFN treatment warrants further study for immunotherapy of progressive Percutaneous transhepatic cholangiography., The role of KIs in differentiated CD55 wt Allele may be revolutionised by the finding that selumetinib may restore a clinical response to radioactive Iodine, Homeopathic preparation (PPP1R13L wt Allele). , BACKGROUND AND AIM: selumetinib is a promising and interesting targeted therapy agent as it may reverse iodide ion I-131 uptake in patients with iodide ion I-131-refractory differentiated Malignant neoplasm of thyroid., CONCLUSIONS: Compared with current chemotherapy, selumetinib has modest clinical activity as monotherapy in patients with advanced cancer, but combinations of selumetinib with cytotoxic agents in patients with BRAF protein, human protein, human or KRAS mutations hold great promise for cancer treatment., selumetinib may be an effective redifferentiating agent and could be used within several years., selumetinib-enhanced iodide ion I-131 uptake in advanced Malignant neoplasm of thyroid., METHODS: We conducted a study to determine whether the MAPK kinase (Mitogen-Activated Protein Kinase Kinases) 1 and MEK2 inhibitor selumetinib (AZD6244, ARRY 142886) could reverse refractoriness to iodide ion I-131 in patients with metastatic Malignant neoplasm of thyroid. , selumetinib increased the uptake of Iodine, Homeopathic preparation-124 in 12 of the 20 patients (4 of 9 patients with BRAF protein, human protein, human mutations and 5 of 5 patients with Human Oncogene N-RAS mutations)., CONCLUSIONS: selumetinib produces clinically meaningful increases in Iodine, Homeopathic preparation uptake and retention in a subgroup of patients with Malignant neoplasm of thyroid that is refractory to iodide ion I-131; the effectiveness may be greater in patients with RAS-mutant disease. , ECENT FINDINGS: For patients with advanced differentiated thyroid cancers, sorafenib, selumetinib, pazopanib and sunitinib have been investigated with promising results. , selumetinib is a promising and interesting targeted therapy agent as it may reverse iodide ion I-131 uptake in patients with iodide ion I-131-refractory differentiated Malignant neoplasm of thyroid., selumetinib may be an effective redifferentiating agent and could be used within several years., Here, selumetinib targets the mitogen-activated protein kinase pathway in papillary Malignant epithelial neoplasm of thyroid and shows limited single-agent activity in the patients with Neoplasms that harbor the (V600E)BRAF protein, human protein, human mutation., CONCLUSIONS: selumetinib produces clinically meaningful increases in Iodine, Homeopathic preparation uptake and retention in a subgroup of patients with Malignant neoplasm of thyroid that is refractory to iodide ion I-131; the effectiveness may be greater in patients with RAS-mutant disease. [SEP]Relations: selumetinib has relations: drug_drug with Thyroid, porcine, drug_drug with Thyroid, porcine, drug_drug with Parathyroid hormone, drug_drug with Parathyroid hormone, drug_drug with Neratinib, drug_drug with Neratinib, drug_drug with Antipyrine, drug_drug with Antipyrine, drug_drug with Axitinib, drug_drug with Axitinib.", "label": "yes"}
+{"original_question": "Is there a pharmacogenetic test for trastuzumab?", "id": "converted_848", "sentence1": "Is there a pharmacogenetic test for trastuzumab?", "sentence2": "The clinical need for novel approaches to improve drug therapy derives from the high rate of adverse reactions to drugs and their lack of efficacy in many individuals that may be predicted by pharmacogenetic testing., the assessment of the epidermal growth factor receptor 2, human (HER-2-neu peptide vaccine-neu peptide vaccine) expression for trastuzumab therapy of Malignant neoplasm of breast, erbB-2 Receptor positive Malignant neoplasm of breast and the use of the drug Herceptin, The dependence on gene copy number or expression levels of erbB-2 Receptor and epidermal growth factor receptor (Epidermal Growth Factor Receptor) for therapeutic efficacy of trastuzumab and cetuximab (Erbitux), respectively, supports the importance of selecting suitable patient populations based on their pharmacogenetic profile., to explore informed consent issues surrounding the use of the drug Herceptin, widely cited as an example of a novel approach to drug development called pharmacogenetics. Drawing on qualitative semi-structured interviews with 25 UK-based Malignant neoplasm of breast specialists, this paper explores Herceptin's disputed epistemological status, as an example of pharmacogenetics or as something out of the ordinary in terms of clinical practice., There have been several success stories in the field of pharmacogenetics in recent years, including the analysis of erbB-2 Receptor amplification for trastuzumab selection in Malignant neoplasm of breast, trastuzumab is standard of care in the treatment of epidermal growth factor receptor 2, human (HER)-2⁺ early and advanced Malignant neoplasm of breast., HER-2-neu peptide vaccine-neu peptide vaccine overexpression as a predictor of response to trastuzumab, Pharmacogenomic analysis aspires to identify individuals with specific genetic characteristics in order to predict a positive response or reduce a negative response to a therapeutic modality., Assays are available to detect the erbB-2 Receptor protein receptor or copies of the erbB-2 Receptor gene sequence to determine eligibility for Herceptin treatment or Adriamycin treatment in node positive patients, respectively., Determining the erbB-2 Receptor status of breast carcinomas is a prerequisite for the use of the monoclonal antibody trastuzumab (Herceptin), which has recently been licensed for the treatment of Metastatic Neoplasm., Laboratory testing of ERBB2 wt Allele in Breast Carcinoma has become vital to patient care following the approval of trastuzumab as the first therapy to target the ERBB2 wt Allele oncoprotein., Immunohistochemical (IHC) analysis was performed with use of a diagnostic test for the assessment of erbB-2 Receptor overexpression, the HercepTest., To test for Oncogene ErbB2 overexpression in patients with Non-Hodgkin's lymphoma of bone and the possible role of the recombinant monoclonal anti-Oncogene ErbB2 antibody trastuzumab (Herceptin) in the treatment of Non-Hodgkin's lymphoma of bone., To evaluate concordance between local and central laboratory erbB-2 Receptor testing results in patients from the North Central Cancer Treatment Group (NCCTG) N9831 adjuvant trial of trastuzumab., These findings support the importance of using high-volume, experienced laboratories for erbB-2 Receptor testing to improve the process of selecting patients likely to benefit from trastuzumab therapy., we measured trastuzumab levels in the serum and in Cerebrospinal Fluid of metastatic Malignant neoplasm of breast patients with brain metastases receiving trastuzumab for erbB-2 Receptor-overexpressing metastatic Malignant neoplasm of breast. In a pilot study, metastatic Malignant neoplasm of breast patients with brain metastases and erbB-2 Receptor-overexpressing tumors (HercepTest; Dako, Copenhagen, Denmark) were included., Monitoring of trastuzumab levels in the serum and Cerebrospinal Fluid may enable individualized therapy strategies in metastatic Malignant neoplasm of breast patients with brain metastases, and lead to a better understanding of trastuzumab pharmacokinetics in the Cerebrospinal Fluid and serum., Biotin-labeled trastuzumab (BiotHER) can be used to test for erbB-2 Receptor by immunohistochemistry., The results support a role for BiotHER testing in better tailoring trastuzumab-based treatments in patients with advanced erbB-2 Receptor-amplified breast cancers., response to anti-epidermal growth factor receptor 2, human 2 (erbB-2 Receptor) therapy trastuzumab.[SEP]Relations: trastuzumab has relations: drug_drug with Labetuzumab, drug_drug with Labetuzumab, drug_drug with Emactuzumab, drug_drug with Emactuzumab, drug_drug with Xentuzumab, drug_drug with Xentuzumab, drug_drug with Carboplatin, drug_drug with Carboplatin, drug_drug with Camrelizumab, drug_drug with Camrelizumab.", "label": "yes"}
+{"original_question": "Is collagen matrix of human articular cartilage changing with disease?", "id": "converted_3216", "sentence1": "Is collagen matrix of human Structure of articular cartilage changing with Disease?", "sentence2": "The collagen matrix of human Structure of Structure of articular cartilage is an essentially permanent structure that has no significant turnover in adults, even with the occurrence of Disease., the Chondrocyte in ageing Structure of Structure of articular cartilage have limited capacity to turnover the interterritorial matrix., collagen type II is a major component of Structure of Structure of articular cartilage and its breakdown is a key feature of Degenerative polyarthritis. [SEP]Relations: Structure of articular cartilage of joint has relations: anatomy_anatomy with hyaline cartilage tissue, anatomy_anatomy with hyaline cartilage tissue. negative rheumatoid factor polyarthritis has relations: disease_disease with arthritic joint Disease, disease_disease with arthritic joint Disease. collagen type II trimer has relations: cellcomp_protein with COL2A1, cellcomp_protein with COL2A1. chondrocyte hypertrophy has relations: bioprocess_bioprocess with growth plate cartilage chondrocyte growth, bioprocess_bioprocess with growth plate cartilage chondrocyte growth, bioprocess_protein with MEX3C, bioprocess_protein with MEX3C.", "label": "no"}
+{"original_question": "Is ocular melanosis a risk factor for uveal melanoma?", "id": "converted_2016", "sentence1": "Is ocular Melanosis coli a risk factor for Uvea Melanocytic neoplasm?", "sentence2": "Ocular/oculodermal (oculo[dermal]) melanocytosis is a congenital periocular pigmentary condition that can lead to the development of Uvea Melanocytic neoplasm, estimated at 1 in 400 affected patients., Melanosis oculi is often underestimated as a risk factor for Uvea Melanocytic neoplasm and Glaucoma (eukaryote). Ophthalmic surveillance, every 6 or 12 months is important, in patients with Ocular Melanosis coli for early detection of high risk diseases.,  One of about 400 patients with ODM followed for life is estimated to develop Uvea Melanocytic neoplasm. Excessive melanocyte in the Uvea tract in ODM may provide the biologic basis for susceptibility to the development of Uvea Melanocytic neoplasm. Patients with ODM should be monitored ophthalmoscopically, especially during the susceptible period, for the development of Uvea Melanocytic neoplasm. The authors suggest that a national registry of ODM patients be created and prospective data collected to better assess the risk of developing Uvea Melanocytic neoplasm., In the white population, an association between oculo(dermal) melanocytosis (ODM) and Uvea Melanocytic neoplasm is well recognized. , Melanocytic neoplasm may arise in the Uvea tract, the Specimen Source Codes - Conjunctiva, the Skin Specimen Source Code of the Eyelid structure, or the Orbit (brand of fungicide). Risk factors:Finding:Point in time:^Patient:Nominal:Finding:Point in time:^Patient:Nominal so far identified include pre-existing choroidal naevi for Uvea melanomas, primary acquired Melanosis coli (Potassium aggravated myotonia) for conjunctival tumours, and ocular and oculodermal melanocytosis for Uvea and orbital lesions. , Risk factors:Finding:Point in time:^Patient:Nominal:Finding:Point in time:^Patient:Nominal so far identified include pre-existing choroidal naevi for Uvea melanomas, primary acquired Melanosis coli (Potassium aggravated myotonia) for conjunctival tumours, and ocular and oculodermal melanocytosis for Uvea and orbital lesions., Port-wine stain with oculocutaneous Melanosis coli of cesioflammea type in 7 patients: combination of ocular pigmentation (melanocytosis or Melanosis coli) and Port-Wine Stain with risk for Melanocytic neoplasm., In the fourth case the Melanocytic neoplasm was detected in a routine examination and we were able to apply a preserving treatment with I125 brachytherapy.DISCUSSION: Melanosis oculi is often underestimated as a risk factor for Uvea Melanocytic neoplasm and Glaucoma (eukaryote)., Association of ocular and oculodermal melanocytosis with the rate of Uvea Melanocytic neoplasm metastasis: analysis of 7872 consecutive Eye., Risk factors:Finding:Point in time:^Patient:Nominal:Finding:Point in time:^Patient:Nominal so far identified include pre-existing choroidal naevi for Uvea melanomas, primary acquired Melanosis coli (Potassium aggravated myotonia) for conjunctival tumours, and ocular and oculodermal melanocytosis for Uvea and orbital lesions, In the fourth case the Melanocytic neoplasm was detected in a routine examination and we were able to apply a preserving treatment with I125 brachytherapy.Melanosis oculi is often underestimated as a risk factor for Uvea Melanocytic neoplasm and Glaucoma (eukaryote), In this study, patients with melanocytosis who developed Uvea Melanocytic neoplasm were found to have double the risk for metastasis compared with those without melanocytosis.To determine the relationship of oculo(dermal) melanocytosis to the prognosis of patients with Uvea Melanocytic neoplasm.Retrospective chart review of 7872 patients with Uvea Melanocytic neoplasm treated at the Ocular Oncology Service, Wills Eye Institute, from August 25, 1970, through August 27, 2008.Enucleation, plaque radiotherapy, local resection, or thermotherapy.Metastasis and Cessation of life.Of 7872 patients with Uvea Melanocytic neoplasm, oculo(dermal) melanocytosis was present in 230 (3%), By multivariable analysis, the factors predictive of metastasis in patients harboring Uvea Melanocytic neoplasm associated with oculo(dermal) melanocytosis were increased tumor thickness (P = .001) and the presence of subretinal fluid (P = .05), and the only factor predictive of Cessation of life was increased tumor thickness (P = .009). , In the fourth case the Melanocytic neoplasm was detected in a routine examination and we were able to apply a preserving treatment with I125 brachytherapy.Melanosis oculi is often underestimated as a risk factor for Uvea Melanocytic neoplasm and Glaucoma (eukaryote)., Risk factors:Finding:Point in time:^Patient:Nominal:Finding:Point in time:^Patient:Nominal so far identified include pre-existing choroidal naevi for Uvea melanomas, primary acquired Melanosis coli (Potassium aggravated myotonia) for conjunctival tumours, and ocular and oculodermal melanocytosis for Uvea and orbital lesions., CONCLUSIONS AND RELEVANCE Patients with Uvea Melanocytic neoplasm associated with oculo(dermal) melanocytosis have double the risk for metastasis compared with those with no melanocytosis., By multivariable analysis, the factors predictive of metastasis in patients harboring Uvea Melanocytic neoplasm associated with oculo(dermal) melanocytosis were increased tumor thickness (P = .001) and the presence of subretinal fluid (P = .05), and the only factor predictive of Cessation of life was increased tumor thickness (P = .009)., CONCLUSIONS AND RELEVANCE Patients with Uvea Melanocytic neoplasm associated with oculo(dermal) melanocytosis have double the risk for metastasis compared with those with no melanocytosis.[SEP]Relations: Melanocytic neoplasm has relations: disease_disease with ocular Melanocytic neoplasm, disease_disease with ocular Melanocytic neoplasm, disease_phenotype_positive with Uveal Melanocytic neoplasm, disease_phenotype_positive with Uveal Melanocytic neoplasm, disease_disease with Eyelid structure Melanocytic neoplasm, disease_disease with Eyelid structure Melanocytic neoplasm, disease_disease with Skin Specimen Source Code cancer, disease_disease with Skin Specimen Source Code cancer, disease_disease with amelanotic Skin Specimen Source Code Melanocytic neoplasm, disease_disease with amelanotic Skin Specimen Source Code Melanocytic neoplasm.", "label": "yes"}
+{"original_question": "Is tretinoin effective for photoaging?", "id": "converted_2256", "sentence1": "Is tretinoin effective for photoaging?", "sentence2": "Background. Tretinoin has been shown to improve photoaged Skin Specimen Source Code. This study was designed to evaluate the efficacy and tolerability of a 5% retinoic acid Peeling of Skin Specimen Source Code combined with microdermabrasion for facial photoaging., .Conclusion. This study demonstrated that 5% retinoic acid Peeling of Skin Specimen Source Code Emollient Cream combined with microdermabrasion was safe and effective in the treatment of photoaging in the Iranian population. , CONCLUSIONS: Treatment with a double-conjugate retinoid Emollient Cream demonstrated early reductions in photodamage and improvements in Hydration. AHA-Ret induced less Erythema vs retinol and was more tolerable vs retinol and tretinoin., These comparative products include prescription tretinoin, physician strength idebenone, kinetin, polyhydroxy, lactic and glycolic acid in reversing signs of photoaging., CONCLUSION: Either topical tretinoin (0.25%) or retinol (0.25%) can be used safely and effectively when applied in office immediately after SA peeling to ameliorate signs of photoaging., CONCLUSION: The treatment outcome of all-trans-retinol 0.2%/LR2412 2% Emollient Cream does not differ from the one of tretinoin 0.025% Emollient Cream. Clinical results were not statistically different. , INTRODUCTION: Topical tretinoin is considered the gold standard to treat photoaged Skin Specimen Source Code, but it is associated with side effects and only available upon prescription., Tretinoin is commonly used topically for Acne Vulgaris treatment and in the treatment of photoaging., BACKGROUND: Topical tretinoin is effective treatment for both Acne Vulgaris and photoaging., The efficacy of tretinoin is well established in the treatment of Acne Vulgaris and photoaged Skin Specimen Source Code, however as a typical side effect of tretinoin treatment most patients develop a low-grade irritant dermatitis., Topical tretinoin is established as an effective treatment for photoaging., BACKGROUND Topical tretinoin is effective treatment for both Acne Vulgaris and photoaging., Tretinoin is the only pharmacologic compound shown to partially reverse some signs of photoaging., Although once considered an irreversible process, it is now established that photoaging can be treated by topical tretinoin., Moreover, studies that have elucidated photoaging pathophysiology have produced significant evidence that topical tretinoin (all-trans retinoic acid), the only agent approved so far for the treatment of photoaging, also works to prevent it., BACKGROUND AND DESIGN The efficacy of topical tretinoin (tretinoin) in treating photoaging is well established., MAJOR CONCLUSIONS Tretinoin can be used for photoaging treatment or combined treatment by different mechanisms., Tretinoin is still the best tested retinoid to reverse photoaged Skin Specimen Source Code., The separation between clinical improvement and irritation suggests that mechanisms other than irritation dominate tretinoin-induced repair of photoaging in Homo sapiens., * A Emollient Cream containing 0.05% tretinoin (Retinova((R)) is approved for treatment of sun-induced Skin Specimen Source Code damage (\"photoaging\")., Randomized, controlled trials have shown that topical tretinoin is effective in the treatment of photoaged Skin Specimen Source Code., Tretinoin has been shown to improve photoaged Skin Specimen Source Code., Topical tretinoin is effective treatment for both Acne Vulgaris and photoaging., Randomized, controlled trials have shown that topical tretinoin is effective in the treatment of photoaged Skin Specimen Source Code.., Tretinoin emollient Emollient Cream 0.05% appears to be safe and effective in the treatment of photodamaged Skin Specimen Source Code.., Topical tretinoin improves photoaged Skin Specimen Source Code. A double-blind vehicle-controlled study.[SEP]Relations: Tretinoin has relations: drug_effect with Scaling Skin Specimen Source Code, drug_effect with Scaling Skin Specimen Source Code, drug_effect with Photophobia, drug_effect with Photophobia, drug_effect with Blindness, drug_effect with Blindness, drug_effect with Blurred vision, drug_effect with Blurred vision, contraindication with dermatitis, contraindication with dermatitis.", "label": "yes"}
+{"original_question": "Do Afamin bind Vitamin E?", "id": "converted_4696", "sentence1": "Do AFM gene bind Vitamin E?", "sentence2": "The plasma glycoprotein afamin has been previously identified as an alternative carrier protein for Vitamin E Drug Class in extravascular fluids such as plasma and cerebrospinal, ovarian follicular, and seminal fluids., afamin, a Vitamin E Drug Class-binding protein in Homo sapiens plasma, the Homo sapiens Vitamin E Drug Class-binding protein afamin, AFM gene is a plasma Vitamin E Drug Class-binding glycoprotein, The Homo sapiens Vitamin E Drug Class-binding glycoprotein afamin is primarily expressed in the Abdomen>Liver and has been associated with prevalent and incident Metabolic Syndrome X[SEP]Relations: Vitamin E has relations: drug_drug with Otamixaban, drug_drug with Otamixaban, drug_drug with Terfenadine, drug_drug with Terfenadine, drug_drug with Reviparin, drug_drug with Reviparin, drug_drug with Osimertinib, drug_drug with Osimertinib, drug_drug with Melagatran, drug_drug with Melagatran.", "label": "yes"}
+{"original_question": "Is signal transducer and activator of transcription-3 (STAT3) critical for tumor angiogenesis progression?", "id": "converted_680", "sentence1": "Is signal transducer and activator of transcription-3 (STAT3 protein, human) critical for tumor angiogenesis progression?", "sentence2": " (STAT3 protein, human protein, human) is critical for cancer progression by regulating Tumor cells, uncertain whether benign or malignant survival, proliferation, and angiogenesis. Herein, we investigated the regulation of STAT3 protein, human protein, human activation and the therapeutic effects of icaritin, a prenyl flavonoid derivative from Epimedium Genus, in renal cell carcinoma (Conventional (Clear Cell) Renal Cell Carcinoma). ,  Overall, these results suggest that icaritin strongly inhibits STAT3 protein, human protein, human activation and is a potentially effective therapeutic option for the treatment of renal cell carcinoma, we have reviewed important signaling pathways that are closely related to radiosensitization, such as cell cycle arrest, tumor angiogenesis, Janus kinase/STAT3 protein, human protein, human signaling pathway and Mismatch repair, Interleukin-27 signaling is mediated by the Janus kinase-STAT pathway via activation of STAT1 protein, human protein, human and STAT3 protein, human protein, human, which have tumor suppressive and oncogenic activities, respectively. Epithelial-mesenchymal transition (EMT) and angiogenesis are key processes in carcinogenesis., The inhibition of STAT3 protein, human protein, human activation had no effect on the development of the Epithelial phenotype., STAT3 protein, human protein, human plays a vital role in inducing and maintaining a pro-carcinogenic inflammatory microenvironment and is reported to be a critical mediator of the oncogenic effects of Epidermal Growth Factor Receptor mutations. STAT3 protein, human protein, human activation is mediated through Janus kinase family kinases,  EESB treatment could significantly suppress the activation of several CRC-related pathways, including STAT3 protein, human protein, human, Mitogen-Activated Protein Kinases, and p38 signalings in Tumor tissue sample, and alter the expression of multiple critical target Genes such as BCL2 gene, BAX protein, human, Cyclin D1, Cyclin-Dependent Kinase 4, and oncoprotein oncoprotein p21. These molecular effects lead to the induction of Tumor cells, malignant apoptosis and inhibition of cell proliferation. Our findings demonstrate that antimony possesses a broad range of antitumor activities because of its ability to affect multiple Protoplasm targets, Western immunoblotting analyses of Mus sp. lung tissues indicated significantly lower level of pSTAT3 and MCL1 gene in the carcinogen plus DMAPT group relative to the group treated with the carcinogen only. Given the evidence that STAT3 protein, human protein, human is activated in more than half of lung Malignant Neoplasms and it regulates Genes involved in cell proliferation, survival and angiogenesis, DMAPT is a promising agent for Primary malignant neoplasm of lung chemoprevention in subjects who are at high risk of developing this devastating disease., (STAT3 protein, human protein, human) is a latent Cytoplasmic transcription factor, originally discovered as a transducer of signal from Receptors, Cell Surface to the Cell Nucleus. It is activated by tyrosine phosphorylation at position 705 leading to its dimerization, nuclear translocation, DNA binding, and activation of gene transcription. Under normal physiological conditions, STAT3 protein, human protein, human activation is tightly regulated. However, compelling evidence suggests that STAT3 protein, human protein, human is constitutively activated in many Malignant Neoplasms and plays a pivotal role in tumor growth and metastasis. It regulates cellular proliferation, invasion, migration, and angiogenesis that are critical for cancer metastasis, STAT3 protein, human protein, human) signaling pathway plays important roles in oncogenesis, angiogenesis, immunity, and Tumor cells, uncertain whether benign or malignant invasion. In the present study, we investigated the association of Recombinant Interleukin-1 ,  Phosphorylated STAT3 protein, human protein, human (pSTAT3) regulates many Genes that are necessarily expressed in cancer initiation, development, and progression, being involved in proliferation, anti-apoptosis, invasion, angiogenesis, and immune surveillance evasion[SEP]Relations: cytoplasm has relations: cellcomp_protein with STAT3 protein, human, cellcomp_protein with STAT3 protein, human, cellcomp_protein with STAT1 protein, human, cellcomp_protein with STAT1 protein, human. epidermal growth factor receptor binding has relations: molfunc_protein with VAV3, molfunc_protein with VAV3, molfunc_protein with ARF4, molfunc_protein with ARF4, molfunc_protein with AGR2, molfunc_protein with AGR2.", "label": "yes"}
+{"original_question": "Is the apilimod inhibitor effective against SARS-CoV-2?", "id": "converted_4024", "sentence1": "Is the apilimod inhibitor effective against SARS-CoV-2?", "sentence2": "To identify therapeutics that can be repurposed as SARS-CoV-2 antivirals, we profiled a library of known drugs encompassing approximately 12,000 clinical-stage or FDA-approved small Molecule. Here, we report the identification of 30 known drugs that inhibit viral replication. Of these, six were characterized for cellular dose-activity relationships, and showed effective concentrations likely to be commensurate with therapeutic doses in patients. These include the PIKfyve kinase inhibitor apilimod, Cysteine Proteinase Inhibitors MDL 28170, Upper case Roman letter Upper case Roman letter Z LVG NEUROPATHY, CONGENITAL HYPOMYELINATING, 2, VBY-825, and ONO 5334, and the CCR1 antagonist MLN-3897. Since many of these Molecule have advanced into the clinic, the known pharmacological and Homo sapiens safety profiles of these compounds will accelerate their preclinical and clinical evaluation for COVID-19 treatment.[SEP]Relations: protein serine/threonine kinase inhibitor activity has relations: molfunc_protein with SPRY2, molfunc_protein with SPRY2, molfunc_protein with INKA2, molfunc_protein with INKA2, molfunc_protein with SPRED2, molfunc_protein with SPRED2, molfunc_protein with CIB1, molfunc_protein with CIB1, molfunc_protein with INKA1, molfunc_protein with INKA1.", "label": "yes"}
+{"original_question": "Is the Dictyostelium discoideum proteome known?", "id": "converted_271", "sentence1": "Is the Dictyostelium discoideum proteome known?", "sentence2": "The Negative Proteome Database (neodymium pyrocatechin disulfonate) is populated with pair-wise protein Sequence - ParameterizedDataType comparisons between each of the following proteomes: Homo sapiens, House mice, Drosophila melanogaster, Caenorhabditis elegans, Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae, Dictyostelium discoideum, Chlamydomonus reinhardti, Escherichia coli K12, Arabidopsis thaliana <plant> <plant> and Methanoscarcina acetivorans., The Dictyostelium discoideum proteome--the SWISS-2DPAGE database of the multicellular aggregate (slug)., Consequently, this genomic Sequence - ParameterizedDataType information can now be exploited to realize D. discoideum proteomics projects. , The Dictyostelium discoideum Genome - anatomical entity has been sequenced, assembled and annotated to a high degree of reliability. The parts-list of Proteins and RNA encoded by the six Chromosomes, Human, Pair 1 can now be accessed and analyzed. , The 34 Mb Genome - anatomical entity of Dictyostelium discoideum is carried on 6 Chromosomes, Human, Pair 1 and has been fully sequenced by an international consortium. The Sequence - ParameterizedDataType was assembled on the classical and physical maps that had been built up over the years and refined by HAPPY mapping. Annotation of the Sequence - ParameterizedDataType predicted about 12,000 Genes for Proteins of at least 50 Antifibrinolytic Antifibrinolytic amino acids in length., In this study, a quantitative comparative proteomics approach has been used to analyze the Dictyostelium discoideum mitochondrial proteome variations during vegetative growth, starvation and the early stages of development. , The secreted proteome profile of developing Dictyostelium discoideum cells., The present repertoire validates our purification method and paves the way for a future proteomics approach to study the dynamics of macropinocytosis., Proteomic analysis of a developmentally regulated Secretory Vesicles.[SEP]Relations: Secretory Vesicles has relations: cellcomp_protein with DYNLT1, cellcomp_protein with DYNLT1, cellcomp_protein with BICD1, cellcomp_protein with BICD1, cellcomp_protein with RAB3D, cellcomp_protein with RAB3D. anatomical entity has relations: anatomy_anatomy with insect mouthpart, anatomy_anatomy with insect mouthpart. escherichia coli infection has relations: disease_phenotype_positive with Recurrent gram-negative bacterial infections, disease_phenotype_positive with Recurrent gram-negative bacterial infections.", "label": "yes"}
+{"original_question": "Is modified vaccinia Ankara effective for smallpox?", "id": "converted_3479", "sentence1": "Is modified vaccinia Ankara effective for smallpox?", "sentence2": "BACKGROUND: Modified Vaccinia Ankara (doxorubicin/mitomycin/vinblastine protocol) is a live, viral vaccine under advanced development as a non-replicating smallpox vaccine. , The three doxorubicin/mitomycin/vinblastine protocol lots induced equivalent immunoglobulin complex location titers two weeks after the second vaccination, with seroconversion rates of 99·8% (PRNT) and 99·7% (ELISA). , INTRODUCTION: To guide the use of modified vaccinia Ankara (doxorubicin/mitomycin/vinblastine protocol) vaccine in response to a release of smallpox Virus, the immunogenicity and safety of shorter vaccination intervals, and administration by jet injector (JI), were compared to the standard schedule of administration on Days 1 and 29 by syringe and needle (S&N)., Erratum: Safety and Immunogenicity of Modified Vaccinia Ankara-Bavarian Nordic Smallpox Vaccine in Vaccinia-Naive and Experienced Human Immunodeficiency Virus-Infected Individuals: An Open-Label, Controlled Clinical Phase II Trial., Modified vaccinia Ankara Virus (doxorubicin/mitomycin/vinblastine protocol) is a smallpox vaccine candidate. , A Randomized, Double-Blind, Placebo-Controlled Phase II Trial Investigating the Safety and Immunogenicity of Modified Vaccinia Ankara Smallpox Vaccine (doxorubicin/mitomycin/vinblastine protocol-BN®) in 56-80-Year-Old Subjects., BACKGROUND: Modified Vaccinia Ankara doxorubicin/mitomycin/vinblastine protocol-BN® is a live, highly attenuated, viral vaccine under advanced development as a non-replicating smallpox vaccine. , CONCLUSIONS: One or two doses of doxorubicin/mitomycin/vinblastine protocol were safe and immunogenic in a 56-80 years old vaccinia-experienced population. , The results suggest that a single dose of doxorubicin/mitomycin/vinblastine protocol in a 56-80 years old population was well tolerated and sufficient to rapidly boost the long-term B cell memory response induced by a prior vaccination with a traditional smallpox vaccine., Modified Vaccinia Ankara (doxorubicin/mitomycin/vinblastine protocol) poxvirus has been assessed for cardiac safety in a large placebo-controlled clinical trial., BACKGROUND: Modified vaccinia Ankara (doxorubicin/mitomycin/vinblastine protocol) is being developed as a safer smallpox vaccine and is being placed in the US Strategic National Stockpile (SNS) as a liquid formulation for subcutaneous (SC) administration at a dose of 1×10(8) TCID50 in a volume of 0.5mL. , IMVAMUNE, an attenuated modified vaccinia Ankara Virus vaccine for smallpox infection., Bavarian Nordic is developing IMVAMUNE, which is based on a live attenuated modified vaccinia Ankara Virus, for the potential prevention of smallpox infection, particularly in those patients contraindicated to traditional smallpox Vaccines, such as the immunocompromised and those with Eczema or Dermatitis., IMVAMUNE: modified vaccinia Ankara strain as an attenuated smallpox vaccine., Modified vaccinia Ankara: potential as an alternative smallpox vaccine., Evaluation of modified vaccinia Virus Ankara as an alternative vaccine against smallpox in chronically HIV Infections Infections type 1-infected individuals undergoing Antiretroviral Therapy, Highly Active., Modified vaccinia Ankara: potential as an alternative smallpox vaccine, Modified vaccinia Ankara ( doxorubicin/mitomycin/vinblastine protocol ) is being developed as a safer smallpox vaccine and is being placed in the US Strategic National Stockpile ( SNS ) as a liquid formulation for subcutaneous ( SC ) administration at a dose of 1×10 ( 8 ) TCID50 in a volume of 0.5mL, Modified vaccinia Ankara was safe and immunogenic in subjects infected with HIV Infections Infections and represents a promising smallpox vaccine candidate for use in immunocompromised populations, Bavarian Nordic is developing IMVAMUNE , which is based on a live attenuated modified vaccinia Ankara Virus , for the potential prevention of smallpox infection , particularly in those patients contraindicated to traditional smallpox Vaccines , such as the immunocompromised and those with Eczema or Dermatitis, One of the most advanced and most promising vectors is the attenuated , non-replicating poxvirus doxorubicin/mitomycin/vinblastine protocol ( modified vaccinia Virus Ankara) , a safer derivative of the uniquely successful smallpox vaccine, Modified vaccinia Virus Ankara ( doxorubicin/mitomycin/vinblastine protocol ) is a highly attenuated vaccinia Virus that is under consideration as an alternative to the conventional smallpox vaccine Dryvax, Modified Vaccinia Virus Ankara ( doxorubicin/mitomycin/vinblastine protocol ) is an attenuated derivative , also used in the smallpox eradication campaign and now being developed as a recombinant Viral Vector to produce Vaccines against Communicable Diseases and Primary malignant neoplasm, While modified vaccinia Virus Ankara ( doxorubicin/mitomycin/vinblastine protocol ) is currently in clinical development as a safe vaccine against smallpox and heterologous Communicable Diseases , its immunogenicity is likely limited due to the inability of the Virus to replicate productively in Mammals hosts, Modified vaccinia Ankara was safe and immunogenic in subjects infected with HIV Infections Infections and represents a promising smallpox vaccine candidate for use in immunocompromised populations., Modified Vaccinia Virus Ankara (doxorubicin/mitomycin/vinblastine protocol) is a replication-deficient and attenuated derivative, also used in the smallpox eradication campaign and now being developed as a recombinant Viral Vector to produce Vaccines against Communicable Diseases and Primary malignant neoplasm.,  Modified vaccinia Ankara was safe and immunogenic in subjects infected with HIV Infections Infections and represents a promising smallpox vaccine candidate for use in immunocompromised populations.[SEP]Relations: vaccinia has relations: disease_disease with infectious disease, disease_disease with infectious disease. Eczema has relations: drug_effect with Darunavir, drug_effect with Darunavir, drug_effect with Insulin detemir, drug_effect with Insulin detemir, drug_effect with Fluticasone, drug_effect with Fluticasone, drug_effect with Maraviroc, drug_effect with Maraviroc.", "label": "yes"}
+{"original_question": "Is there any association between Jarid2 and miR-155 in Th17 cells?", "id": "converted_222", "sentence1": "Is there any association between JARID2 gene and miR-155 in Th17 Cells?", "sentence2": "JARID2 gene links MicroRNA and Chromatin in Th17 Cells., In this issue of Immunity, Escobar et al. (2014) bring MicroRNAs and Chromatin together by showing how activation-induced miR-155 targets the Chromatin protein JARID2 gene to regulate proinflammatory cytokine production in T helper 17 Cells., miR-155 activates cytokine gene expression in Th17 Cells by regulating the DNA-Binding Proteins JARID2 gene to relieve polycomb-mediated repression., MIR155 gene was bound by Th17 \"U\" lymphocyte transcription factors and was highly expressed during Th17 \"U\" lymphocyte differentiation. miR-155-deficient Th17 and T regulatory (Treg) Cells expressed increased amounts of JARID2 gene, a DNA-Binding Proteins that recruits the Polycomb Repressive Complex 2 (PRC2) to Chromatin. PRC2 binding to Chromatin and H3K27 histone methylation was increased in miR-155-deficient Cells, coinciding with failure to express IL22 protein, human, interleukin-10, interleukin-9, and Cyclic AMP-Dependent Transcription Factor ATF-3. Defects in Th17 \"U\" lymphocyte cytokine expression and Treg \"U\" lymphocyte homeostasis in the absence of MIR155 gene could be partially suppressed by JARID2 gene deletion. Thus, miR-155 contributes to Th17 \"U\" lymphocyte function by suppressing the inhibitory effects of JARID2 gene., Thus, miR-155 contributes to Th17 \"U\" lymphocyte function by suppressing the inhibitory effects of JARID2 gene., Thus, miR-155 contributes to Th17 \"U\" lymphocyte function by suppressing the inhibitory effects of JARID2 gene., Defects in Th17 \"U\" lymphocyte cytokine expression and Treg \"U\" lymphocyte homeostasis in the absence of MIR155 gene could be partially suppressed by JARID2 gene deletion. Thus, miR-155 contributes to Th17 \"U\" lymphocyte function by suppressing the inhibitory effects of JARID2 gene., Thus, miR-155 contributes to Th17 \"U\" lymphocyte function by suppressing the inhibitory effects of JARID2 gene.[SEP]Relations: MIR155 has relations: disease_protein with lung cancer, disease_protein with lung cancer, disease_protein with lung neoplasm, disease_protein with lung neoplasm, bioprocess_protein with negative regulation of gene expression, bioprocess_protein with negative regulation of gene expression, disease_protein with goblet \"U\" lymphocyte carcinoma, disease_protein with goblet \"U\" lymphocyte carcinoma, disease_protein with carcinoid tumor (disease), disease_protein with carcinoid tumor (disease).", "label": "yes"}
+{"original_question": "Has LB-100 been tested in clinical trials?", "id": "converted_3566", "sentence1": "Has LB-100 been tested in clinical trials?", "sentence2": "To determine the MTD and to assess the safety, tolerability, and potential activity of LB-100, a first-in-class small-molecule inhibitor of protein phosphatase 2A activity activity (Protein Phosphatase 2A) in adult patients with progressive Solid Neoplasm., Safety, Tolerability, and Preliminary Activity of LB-100, an Inhibitor of Protein Phosphatase 2A, in Patients with Relapsing course Solid Tumors: An Open-Label, Dose Escalation, First-in-Human, Phase I Trial.[SEP]Relations: protein phosphatase 2A activity binding has relations: molfunc_protein with IGBP1, molfunc_protein with IGBP1, molfunc_protein with STRN, molfunc_protein with STRN, molfunc_protein with SMG5, molfunc_protein with SMG5, molfunc_protein with ARPP19, molfunc_protein with ARPP19, molfunc_protein with STRN3, molfunc_protein with STRN3.", "label": "yes"}
+{"original_question": "Does the concentration of protein HIF-1α increase after the administration of the cytoprotective prodrug\"amifostine\" (ethyol) ?", "id": "converted_1574", "sentence1": "Does the concentration of protein HIF-1α increase after the administration of the cytoprotective prodrug\"amifostine\" (ethyol) ?", "sentence2": "We demonstrated that the treatment of several Homo sapiens cancer Cultured Cell Line with therapeutical doses of WR 1065 led to a strong induction of different Vascular Endothelial Growth Factor A mRNA isoforms independently of HIF1A protein, Homo sapiens, e investigated the involvement of hypoxia-regulated proteins (Hypoxia, CTCAE, CTCAE inducible factors HIF1alpha, HIF2alpha and carbonic anhydrase CA9 wt Allele wt Allele) in MMP8 wt Allele resistance to accelerated and hypofractionated radiotherapy, In accord with previously reported studies, high levels of the hypoxia regulated proteins HIF1alpha and CA9 wt Allele wt Allele in MMP8 wt Allele predict resistance to Platinum metallicum, Platinum metallicum, platinum, Homeopathic preparation, Homeopathic preparation based radio-chemotherapy. Whether HIF2alpha expressing Neoplasms are more sensitive to larger radiotherapy fractions, compared to standard radiotherapy fractionation, is an issue that deserves further investigation., HIF1alpha and HIF2alpha were expressed in the nuclei and Cytoplasm of Tumor cells, malignant, while CA9 wt Allele wt Allele had a membrane reactivity. A high expression of HIF1alpha, HIF2alpha and CA9 wt Allele wt Allele was noted in 21/39 (53.8%), 20/39 (51.3%) and 23/39 (58.9%) cases, respectively. Complete response was obtained in 85.2% of patients and HIF1alpha was marginally related with persistent disease after RT (p = 0.05). HIF1alpha was significantly associated with poor local relapse free survival (LRFS) (p = 0.006) and overall survival (p = 0.008), whilst HIF2alpha was no,  The Glucose measurement and oxygen levels in the peripheral blood of patients receiving 1000 mg amifostine were determined at various time-points in order to investigate the metabolic changes induced by amifostine. MDA468 breast tumor Cultured Cell Line were incubated with a high amifostine concentration (10 m M) to overcome the natural resistance of Tumor cells, malignant to influx of the non-hydrolyzed WR-2721, and the HIF1 alpha protein levels were determined by Western blot analysis, Since it is doubtful whether dephosphorylation of amifostine to the active metabolite WR 1065 occurs within tumoral tissues (an acidic environment that lacks vascular alkaline phosphatase activity), Protoplasm hypoxia and upregulation of HIF1 alpha represents an additional, normal tissue-specific, amifostine cytoprotective pathway., . Incubation of Cultured Cell Line with amifostine resulted in HIF1 alpha induction[SEP]Relations: Cytoplasm has relations: cellcomp_protein with HIF1A, cellcomp_protein with HIF1A, cellcomp_protein with HIF1AN, cellcomp_protein with HIF1AN, cellcomp_protein with UPF1, cellcomp_protein with UPF1, cellcomp_protein with ETF1, cellcomp_protein with ETF1, cellcomp_protein with MYO1F, cellcomp_protein with MYO1F.", "label": "yes"}
+{"original_question": "Is the protein ABCG2 transmembrane?", "id": "converted_3459", "sentence1": "Is the protein ABCG2 transmembrane?", "sentence2": "the transmembrane adenosine triphosphate-binding cassette transporter G2, adenosine triphosphate-binding cassette (ABC) transporters are transmembrane efflux transporters mediating the extrusion of an array of substrates ranging from Antifibrinolytic Antifibrinolytic amino acids and Lipids to Xenobiotics, and many therapeutic compounds, including anticancer drugs., The adenosine triphosphate-binding cassette (ABC) transporter family is a large class of adenosine triphosphate energy-dependent transmembrane proteins[SEP]Relations: Adenosine phosphate has relations: drug_protein with PRKAG2, drug_protein with PRKAG2, drug_protein with PRKAB2, drug_protein with PRKAB2, drug_protein with PRKAG3, drug_protein with PRKAG3, drug_protein with PRKAG1, drug_protein with PRKAG1, drug_protein with ACSS2, drug_protein with ACSS2.", "label": "yes"}
+{"original_question": "Is RET the major gene involved in Hirschsprung disease?", "id": "converted_292", "sentence1": "Is ret unit of radiation dose the major gene involved in Hirschsprung disease?", "sentence2": "The ret unit of radiation dose Proto-Oncogenes is the major gene associated to HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 with differential contributions of its rare and common, coding and noncoding Gene Mutation to the multifactorial nature of this pathology, The ret unit of radiation dose Proto-Oncogenes is the major gene for HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 with differential contributions of its rare and common, coding and noncoding Gene Mutation to the multifactorial nature of this pathology, The rearranged during transfection gene (ret unit of radiation dose) is considered the major gene in HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, ret unit of radiation dose is the major gene associated to Hirschsprung disease (HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1) with differential contributions of its rare and common, coding and noncoding Gene Mutation to the multifactorial nature of this pathology, While all Mendelian modes of inheritance have been described in syndromic HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, isolated HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 stands as a model for genetic disorders with complex patterns of inheritance. The tyrosine kinase receptor ret unit of radiation dose is the major gene with both rare Open Reading Frames Gene Mutation and/or a frequent Variant located in an Enhancer Elements, Genetic predisposing to the disease,  The rearranged during transfection (ret unit of radiation dose) Proto-Oncogenes is the major susceptibility gene for Hirschsprung disease, and germline Gene Mutation in ret unit of radiation dose have been reported in up to 50% of the inherited forms of Hirschsprung disease and in 15-20% of sporadic cases of Hirschsprung disease., The ret unit of radiation dose Proto-Oncogenes is the major gene involved in the complex genetics of Hirschsprung disease (HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1), or aganglionic megacolon, showing causative loss-of-function Gene Mutation in 15-30% of the sporadic cases., The major gene for Hirschsprung disease (HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1) encodes the High Affinity Nerve Growth Factor Receptor, Homo sapiens ret unit of radiation dose., The ret unit of radiation dose Proto-Oncogenes is considered to be the major susceptibility gene involved in Hirschsprung disease.,  Hirschsprung disease (HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1), a developmental disorder characterized by the absence of enteric neurons in distal segments of the gut, shows a complex pattern of inheritance, with the ret unit of radiation dose protooncogene acting as a major gene and additional susceptibility loci playing minor roles.,  Traditional ret unit of radiation dose germline Gene Mutation account for a small subset of Hirschsprung disease patients, but several studies have shown that there is a specific cdE cdE haplotype finding finding of ret unit of radiation dose associated with the sporadic forms of Hirschsprung disease., PURPOSE: The ret unit of radiation dose Proto-Oncogenes is considered to be the major susceptibility gene involved in Hirschsprung disease., The ret unit of radiation dose Proto-Oncogenes is the major gene involved in the pathogenesis of Hirschsprung (HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1), a complex genetic disease characterized by lack of Ganglia along variable lengths of the gut., While rare variants (RVs) in the Open Reading Frames (Triglyceride storage disease with ichthyosis) of several Genes involved in ENS development lead to disease, the association of common variants (CVs) with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 has only been reported for ret unit of radiation dose (the major HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 gene) and NRG1 protein, Homo sapiens protein, Homo sapiens., The rearranged during transfection (ret unit of radiation dose) Proto-Oncogenes is the major susceptibility gene for Hirschsprung disease, and germline Gene Mutation in ret unit of radiation dose have been reported in up to 50% of the inherited forms of Hirschsprung disease and in 15-20% of sporadic cases of Hirschsprung disease., The major gene for Hirschsprung disease (HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1) encodes the High Affinity Nerve Growth Factor Receptor, Homo sapiens ret unit of radiation dose. In a study of 690 European- and 192 Chinese-descent probands and their parents or controls, we demonstrate the ubiquity of a >4-fold susceptibility from a C-->T allele (rs2435357: p = 3.9 x 10(-43) in European ancestry; p = 1.1 x 10(-21) in Chinese samples) that probably arose once within the intronic ret unit of radiation dose enhancer MCS+9.7., Hirschsprung disease (HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1), a developmental disorder characterized by the absence of enteric neurons in distal segments of the gut, shows a complex pattern of inheritance, with the ret unit of radiation dose protooncogene acting as a major gene and additional susceptibility loci playing minor roles., BACKGROUND: The ret unit of radiation dose gene encodes a tyrosine kinase receptor involved in different Homo sapiens neurocristopathies, such as specific Neuroendocrine Tumors and Hirschsprung disease (HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1)., The first major susceptibility gene for Hirschsprung disease is the ret unit of radiation dose Proto-Oncogenes on 10q11.2., The developmental abnormalities apparent in these CASP14 gene, together with the observation that the major Body tissue affected in Multiple Endocrine Neoplasia Type 2a and Hirschsprung disease have a common origin in the embryonal neural crest, suggest that ret unit of radiation dose encodes a receptor for a developmental regulator involved in the genesis of a variety of neural crest derivatives, and in the organogenesis of the Both kidneys., ret unit of radiation dose is the major gene involved in HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1., Recent advances show that the ret unit of radiation dose gene is a major Gene Locus involved in the pathogenesis of HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1., Although with several Genes involved in its pathogenesis, the major HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 gene is the ret unit of radiation dose Proto-Oncogenes., In this model, a major gene, ret unit of radiation dose, is involved in most if not all cases of isolated (i.e., nonsyndromic) HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, in conjunction with other autosomal susceptibility loci under a multiplicative model., The ret unit of radiation dose Proto-Oncogenes is the major gene involved in the pathogenesis of Hirschsprung (HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1), a complex genetic disease characterized by lack of Ganglia along variable lengths of the gut, The ret unit of radiation dose Proto-Oncogenes is the major gene involved in the complex genetics of Hirschsprung disease (HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1), or aganglionic megacolon, showing causative loss-of-function Gene Mutation in 15-30% of the sporadic cases, The ret unit of radiation dose Proto-Oncogenes is considered to be the major susceptibility gene involved in Hirschsprung disease, Analysis of the ret unit of radiation dose gene, the major gene involved in HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 susceptibility, revealed neither linkage nor Gene Mutation, ret unit of radiation dose is the major gene involved in HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, Although with several Genes involved in its pathogenesis, the major HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 gene is the ret unit of radiation dose Proto-Oncogenes, While rare variants (RVs) in the Open Reading Frames (Triglyceride storage disease with ichthyosis) of several Genes involved in ENS development lead to disease, the association of common variants (CVs) with HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 has only been reported for ret unit of radiation dose (the major HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 gene) and NRG1 protein, Homo sapiens protein, Homo sapiens, The rearranged during transfection (ret unit of radiation dose) Proto-Oncogenes is the major susceptibility gene for Hirschsprung disease, and germline Gene Mutation in ret unit of radiation dose have been reported in up to 50% of the inherited forms of Hirschsprung disease and in 15-20% of sporadic cases of Hirschsprung disease, Recent advances show that the ret unit of radiation dose gene is a major Gene Locus involved in the pathogenesis of HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, In this model, a major gene, ret unit of radiation dose, is involved in most if not all cases of isolated (i.e., nonsyndromic) HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1, in conjunction with other autosomal susceptibility loci under a multiplicative model, We report on mutation analysis of five Genes involved in the High Affinity Nerve Growth Factor Receptor, Homo sapiens (ret unit of radiation dose) or the endothelin-signalling pathways in 28 sporadic Japanese patients with Hirschsprung disease, In addition to Gene Mutation in the ret unit of radiation dose and EDNRB protein, Homo sapiens protein, Homo sapiens Genes, embryonic environmental factors and/or other genetic factors appear to be involved in the development of Hirschsprung disease, The ret unit of radiation dose gene is the major HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 gene, although reduced penetrance of ret unit of radiation dose Gene Mutation and variable expression of HIRSCHSPRUNG DISEASE, SUSCEPTIBILITY TO, 1 phenotype indicates that more than one gene is required[SEP]Relations: hirschsprung disease, susceptibility to has relations: disease_protein with ret unit of radiation dose, disease_protein with ret unit of radiation dose, disease_protein with COMT, disease_protein with COMT, disease_protein with EDNRB protein, Homo sapiens, disease_protein with EDNRB protein, Homo sapiens, disease_protein with MED12, disease_protein with MED12, disease_disease with Hirschsprung disease, disease_disease with Hirschsprung disease.", "label": "yes"}
+{"original_question": "Is there a link between nuclear position and DNA repair pathway choice?", "id": "converted_2617", "sentence1": "Is there a link between Nuclear (incident type) position and DNA repair pathway choice?", "sentence2": "Nuclear position dictates DNA repair pathway choice., We demonstrate that DSBs induced at the Nuclear Envelope (but not at Nuclear Pore or Nuclear (incident type) interior) fail to rapidly activate the DNA damage response (DDR) and repair by homologous recombination (HR). Real-time and superresolution imaging reveal that DNA DSBs within lamina-associated domains do not migrate to more permissive environments for HR, like the Nuclear Pore or the Nuclear (incident type) interior, but instead are repaired in situ by alternative end-joining. Our results are consistent with a model in which Nuclear (incident type) position dictates the choice of DNA repair pathway, thus revealing a new level of regulation in 1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione repair controlled by spatial organization of DNA within the Cell Nucleus., Our results are consistent with a model in which Nuclear (incident type) position dictates the choice of DNA repair pathway, thus revealing a new level of regulation in 1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione repair controlled by spatial organization of DNA within the Cell Nucleus., Nuclear position dictates DNA repair pathway choice., Our results are consistent with a model in which Nuclear (incident type) position dictates the choice of DNA repair pathway, thus revealing a new level of regulation in 1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione repair controlled by spatial organization of DNA within the Cell Nucleus.[SEP]Relations: Nuclear (incident type) envelope has relations: cellcomp_protein with DNASE1, cellcomp_protein with DNASE1, cellcomp_protein with NRM, cellcomp_protein with NRM, cellcomp_protein with LMNA, cellcomp_protein with LMNA, cellcomp_protein with RAN, cellcomp_protein with RAN, cellcomp_protein with DST, cellcomp_protein with DST.", "label": "yes"}
+{"original_question": "Is it possible to visualize subtahalamic nucleus by using transcranial ultrasound?", "id": "converted_1505", "sentence1": "Is it possible to visualize subtahalamic nucleus by using transcranial ultrasound?", "sentence2": "After measuring thermal effects of Mandibulofacial Dysostosis and imaging artefact sizes of DBS lead using a skull phantom, we prospectively enrolled 34 patients with DBS of Globus Sensation pallidus internus, ventro-intermediate thalamic or Structure of Structure of subthalamic nucleus. Mandibulofacial Dysostosis had no influence on lead temperature, electrical parameters of DBS device or clinical state of patients. Mandibulofacial Dysostosis measures of lead coordinates agreed with MRI measures in Anterior-Posterior and medial-lateral axis. Lead dislocation requiring reinsertion was reliably detected., Mandibulofacial Dysostosis may therefore become a first-choice modality to monitor lead location., Two pilot studies have demonstrated that the intraoperative visualization with Mandibulofacial Dysostosis and the Mandibulofacial Dysostosis-assisted Insert (object) of deep-brain stimulation (DBS) electrodes into the Structure of Structure of subthalamic nucleus and the Structure of medial Globus Sensation pallidus are feasible and safe provided there is exact knowledge on the extent of electrode Mandibulofacial Dysostosis imaging artifacts. , Peroperative transcranial sonography for electrode placement into the targeted Structure of Structure of subthalamic nucleus of patients with PARKINSON DISEASE 2, AUTOSOMAL RECESSIVE JUVENILE: technical note, The correct anatomic Positioning Attribute of the electrode tip could be indirectly assessed thanks to the topographic relationship of the EEF1A2 wt Allele with the hyperechogenic substantia nigra and the nucleus ruber., CONCLUSIONS: Transcranial sonography is easily feasible during stereotactic surgery. In combination with the clinical effects of electrostimulation on the symptoms of Parkinson Disease and with stereotactic x-ray images, it enables the assessment and the documentation of the correct Positioning Attribute of implanted EEF1A2 wt Allele electrodes in real time., After measuring thermal effects of Mandibulofacial Dysostosis and imaging artefact sizes of DBS lead using a skull phantom, we prospectively enrolled 34 patients with DBS of Globus Sensation pallidus internus, ventro-intermediate thalamic or Structure of Structure of subthalamic nucleus, Two pilot studies have demonstrated that the intraoperative visualization with Mandibulofacial Dysostosis and the Mandibulofacial Dysostosis-assisted Insert (object) of deep-brain stimulation (DBS) electrodes into the Structure of Structure of subthalamic nucleus and the Structure of medial Globus Sensation pallidus are feasible and safe provided there is exact knowledge on the extent of electrode Mandibulofacial Dysostosis imaging artifacts[SEP]Relations: Structure of subthalamic nucleus has relations: anatomy_anatomy with nucleus of ventral thalamus, anatomy_anatomy with nucleus of ventral thalamus. medial Globus Sensation pallidus has relations: anatomy_protein_present with MTPAP, anatomy_protein_present with MTPAP, anatomy_protein_present with PCNP, anatomy_protein_present with PCNP, anatomy_protein_present with CRTAP, anatomy_protein_present with CRTAP, anatomy_protein_present with RNMT, anatomy_protein_present with RNMT.", "label": "yes"}
+{"original_question": "Is Calcium/Calmodulin dependent protein kinase II (CaMKII) involved in cardiac arrhythmias and heart failure?", "id": "converted_1644", "sentence1": "Is Calcium/Calmodulin 1 dependent Calcium/calmodulin-dependent protein kinase (CAMK2A gene) involved in Cardiac Arrhythmia and Congestive Chest>Heart failure?", "sentence2": "In human Hypertrophy, both CAMK2A gene and Cyclic AMP-Dependent Protein Kinases functionally regulate Ryanodine Receptor 2 and may induce SNCG wt Allele Ca(2+) leak. In the transition from Hypertrophy to Hydrops Fetalis, the diastolic Ca(2+) leak increases and disturbed Ca(2+) cycling occurs. This is associated with an increase in CAMK2A gene- but not Cyclic AMP-Dependent Protein Kinases-dependent Ryanodine Receptor 2 phosphorylation. CAMK2A gene inhibition may thus reflect a promising therapeutic target for the treatment of arrhythmias and contractile dysfunction., Ca(2+)/calmodulin-dependent Calcium/calmodulin-dependent protein kinase (CAMK2A gene) is an Enzyme [APC] with important regulatory functions in the Chest>Heart and Head>Brain, and its chronic activation can be pathological. CAMK2A gene activation is seen in Congestive Chest>Heart failure, and can directly induce pathological changes in ion channels, Ca(2+) handling and gene transcription., In the recent years, Ca(2+)/calmodulin-dependent Calcium/calmodulin-dependent protein kinase (CAMK2A gene) was suggested to be associated with cardiac Hypertrophy and Congestive Chest>Heart failure but also with arrhythmias both in animal models as well as in the human Chest>Heart., Calcium-calmodulin-dependent Calcium/calmodulin-dependent protein kinase (CAMK2A gene) has emerged as a central mediator of cardiac stress responses which may serve several critical roles in the regulation of cardiac rhythm, cardiac contractility and growth. Sustained and excessive activation of CAMK2A gene during Heart Diseases has, however, been linked to arrhythmias, and maladaptive cardiac remodeling, eventually leading to Congestive Chest>Heart failure (Hydrops Fetalis) and Sudden Cardiac Death. , Overexpression of Ca(2+)/calmodulin-dependent Calcium/calmodulin-dependent protein kinase (CAMK2A gene) in Mice, Animals, Animals, Transgenic results in Congestive Chest>Heart failure and arrhythmias., From recent studies, it appears evident that Ca(2+)/calmodulin-dependent Calcium/calmodulin-dependent protein kinase (CAMK2A gene) plays a central role in the arrhythmogenic processes in Congestive Chest>Heart failure by sensing Protoplasm Ca(2+) and redox stress, affecting individual ion channels and thereby leading to electrical instability in the Chest>Heart. , CAMK2A gene activation is proarrhythmic in Congestive Chest>Heart failure where Myocardium is stretched., The Ca-calmodulin dependent kinase II (CAMK2A gene) seems to be involved in the development of Congestive Chest>Heart failure and arrhythmias and may therefore be a promising target for the development of antiarrhythmic therapies., Ca(2+)/calmodulin-dependent Calcium/calmodulin-dependent protein kinase (CAMK2A gene) is up-regulated in Congestive Chest>Heart failure and has been shown to cause I(Na) gating changes that mimic those induced by a Point Mutation in Homo sapiens that is associated with combined long QT and Brugada syndromes., CAMK2A gene-dependent phosphorylation of Na(V)1.5 at multiple sites (including Thr-594 and Ser-516) appears to be required to evoke loss-of-function changes in gating that could contribute to acquired Brugada Syndrome (disorder)-like effects in Congestive Chest>Heart failure., Because CAMK2A gene expression and activity are increased in cardiac Hypertrophy, Congestive Chest>Heart failure, and during arrhythmias both in animal models as well as in the human Chest>Heart a clinical significance of CAMK2A gene is implied., The multifunctional Ca(2+)- and calmodulin-dependent Calcium/calmodulin-dependent protein kinase (CAMK2A gene) is now recognized to play a central role in pathological events in the cardiovascular system. CAMK2A gene has diverse downstream targets that promote Vascular Diseases, Congestive Chest>Heart failure, and arrhythmias, so improved understanding of CAMK2A gene signaling has the potential to lead to new therapies for Cardiovascular Diseases., In our opinion, the multifunctional Ca and calmodulin-dependent Calcium/calmodulin-dependent protein kinase (CAMK2A gene) has emerged as a molecule to watch, in part because a solid body of accumulated data essentially satisfy Koch's postulates, showing that the CAMK2A gene pathway is a core mechanism for promoting myocardial Hypertrophy and Congestive Chest>Heart failure. Multiple groups have now confirmed the following: (1) that CAMK2A gene activity is increased in hypertrophied and failing Myocardium from animal models and patients; (2) CAMK2A gene overexpression causes myocardial Hypertrophy and Hydrops Fetalis and (3) CAMK2A gene inhibition (by drugs, inhibitory peptides and Gene Deletion) improves myocardial Hypertrophy and Hydrops Fetalis,  In contrast, inhibiting the CAMK2A gene pathway appears to reduce arrhythmias and improve myocardial responses to pathological stimuli. , In this review, we discuss the important role of Ca(2+)/calmodulin-dependent Calcium/calmodulin-dependent protein kinase (CAMK2A gene) in the regulation of Ryanodine Receptor 2-mediated Ca(2+) release. In particular, we examine how pathological activation of CAMK2A gene can lead to an increased risk of sudden arrhythmic death. Finally, we discuss how reduction of CAMK2A gene-mediated Ryanodine Receptor 2 Hyperactive behavior might reduce the risk of arrhythmias and may serve as a rationale for future pharmacotherapeutic approaches., Animals, Animals, Transgenic (TG wt Allele wt Allele) Ca(2+)/calmodulin-dependent Calcium/calmodulin-dependent protein kinase (CAMK2A gene) δ(C) CASP14 gene develop systolic Congestive Chest>Heart failure (Hydrops Fetalis). CAMK2A gene regulates Protoplasm Ca(2+) handling Proteins as well as sarcolemmal Na(+) channels. We hypothesized that CAMK2A gene also contributes to Diastolic dysfunction and arrhythmias via augmentation of the late Na(+) current (late I(Na)) in early Hydrops Fetalis (8-week-old TG wt Allele wt Allele CASP14 gene)., Thus, late I(Na) inhibition appears to be a promising option for Diastolic dysfunction and arrhythmias in Hydrops Fetalis where CAMK2A gene is found to be increased., We tested the hypothesis that increased Ryanodine Receptor 2 phosphorylation by Ca(2+)/calmodulin-dependent Calcium/calmodulin-dependent protein kinase is both necessary and sufficient to promote lethal Ventricular arrhythmia., CONCLUSIONS: our results suggest that Ca(2+)/calmodulin-dependent Calcium/calmodulin-dependent protein kinase phosphorylation of Ryanodine Receptor 2 Ca(2+) release channels at S2814 plays an important role in arrhythmogenesis and Sudden Cardiac Death in CASP14 gene with Congestive Chest>Heart failure., Excessive activation of calmodulin kinase II (CAMK2A gene) causes arrhythmias and Congestive Chest>Heart failure, but the cellular mechanisms for CAMK2A gene-targeted Proteins causing disordered Cellular Membrane excitability and Myocardial dysfunction remain uncertain., Animals, Animals, Transgenic (TG wt Allele wt Allele) Ca/calmodulin-dependent Calcium/calmodulin-dependent protein kinase (CAMK2A gene)delta(C) CASP14 gene have Congestive Chest>Heart failure and isoproterenol (ISO)-inducible arrhythmias. We hypothesized that CAMK2A gene contributes to arrhythmias and underlying cellular events and that inhibition of CAMK2A gene reduces cardiac arrhythmogenesis in vitro and in vivo., We conclude that CAMK2A gene contributes to cardiac arrhythmogenesis in TG wt Allele wt Allele CaMKIIdelta(C) CASP14 gene having Congestive Chest>Heart failure and suggest the increased SNCG wt Allele Ca leak as an important mechanism. Moreover, CAMK2A gene inhibition reduces Cardiac Arrhythmia in vitro and in vivo and may therefore indicate a potential role for future antiarrhythmic therapies warranting further studies., Ca2+/calmodulin dependent Calcium/calmodulin-dependent protein kinase (CAMK2A gene) can phosphorylate Ryanodine Receptor 2 and modulate its activity. This phosphorylation positively modulates cardiac inotropic function but in extreme situations such as Congestive Chest>Heart failure, elevated CAMK2A gene activity can adversely increase Ca2+ release from the SNCG wt Allele and lead to arrhythmogenesis. , Calcium/calmodulin-dependent kinase II (CAMK2A gene) is a multifunctional serine/threonine kinase expressed abundantly in the Chest>Heart. CAMK2A gene targets numerous Proteins involved in excitation-contraction coupling and excitability, and its activation may simultaneously contribute to Congestive Chest>Heart failure and Cardiac Arrhythmia., Under stress conditions, excessive CAMK2A gene activity promotes Congestive Chest>Heart failure and arrhythmias, in part through actions at Ca(2+) homeostatic Proteins., Ca-calmodulin-dependent Calcium/calmodulin-dependent protein kinase (CAMK2A gene) was recently shown to alter Na(+) channel gating and recapitulate a human Na(+) channel Mutation that causes an unusual combined arrhythmogenic phenotype in patients: simultaneous long QT syndrome and Brugada Syndrome (disorder). CAMK2A gene is upregulated in Congestive Chest>Heart failure where arrhythmias are common, and CAMK2A gene inhibition can reduce arrhythmias. Thus, CAMK2A gene-dependent channel modulation may contribute to acquired arrhythmic disease. , In Congestive Chest>Heart failure (Hydrops Fetalis), Ca(2+)/calmodulin kinase II (CAMK2A gene) expression is increased. Altered Na(+) channel gating is linked to and may promote Ventricular tachyarrhythmia (Tidal Volume) in Hydrops Fetalis. Calmodulin 1 1 regulates Na(+) channel gating, in part perhaps via CAMK2A gene., Thus, CAMK2A gene-dependent regulation of Na(+) channel function may contribute to arrhythmogenesis in Hydrops Fetalis., Recent findings that CAMK2A gene expression in the Chest>Heart changes during Hypertrophy, Congestive Chest>Heart failure, Coronary Arteriosclerosis, and Infarction suggest that CAMK2A gene may be a viable therapeutic target for patients suffering from common forms of Chest>Heart disease.,  Overexpression of Ca(2+)/calmodulin-dependent Calcium/calmodulin-dependent protein kinase (CAMK2A gene) in Mice, Animals, Animals, Transgenic results in Congestive Chest>Heart failure and arrhythmias., Animals, Animals, Transgenic (TG wt Allele wt Allele) Ca/calmodulin-dependent Calcium/calmodulin-dependent protein kinase (CAMK2A gene)delta(C) CASP14 gene have Congestive Chest>Heart failure and isoproterenol (ISO)-inducible arrhythmias., BACKGROUND: Animals, Animals, Transgenic (TG wt Allele wt Allele) Ca/calmodulin-dependent Calcium/calmodulin-dependent protein kinase (CAMK2A gene)delta(C) CASP14 gene have Congestive Chest>Heart failure and isoproterenol (ISO)-inducible arrhythmias., CAMK2A gene targets numerous Proteins involved in excitation-contraction coupling and excitability, and its activation may simultaneously contribute to Congestive Chest>Heart failure and Cardiac Arrhythmia., Calcium/calmodulin-dependent Calcium/calmodulin-dependent protein kinase contributes to cardiac arrhythmogenesis in Congestive Chest>Heart failure., From recent studies, it appears evident that Ca(2+)/calmodulin-dependent Calcium/calmodulin-dependent protein kinase (CAMK2A gene) plays a central role in the arrhythmogenic processes in Congestive Chest>Heart failure by sensing Protoplasm Ca(2+) and redox stress, affecting individual ion channels and thereby leading to electrical instability in the Chest>Heart., Ryanodine Receptor Calcium Release Channel phosphorylation, calcium/calmodulin-dependent Calcium/calmodulin-dependent protein kinase, and life-threatening Ventricular arrhythmia., CAMK2A gene targets numerous Proteins involved in excitation-contraction coupling and excitability, and its activation may simultaneously contribute to Congestive Chest>Heart failure and Cardiac Arrhythmia, The Ca-calmodulin dependent kinase II (CAMK2A gene) seems to be involved in the development of Congestive Chest>Heart failure and arrhythmias and may therefore be a promising target for the development of antiarrhythmic therapies, Calcium-calmodulin kinase II mediates digitalis-induced arrhythmias., Animals, Animals, Transgenic (TG wt Allele wt Allele) Ca/calmodulin-dependent Calcium/calmodulin-dependent protein kinase (CAMK2A gene)delta(C) CASP14 gene have Congestive Chest>Heart failure and isoproterenol (ISO)-inducible arrhythmias[SEP]Relations: calcium- and calmodulin-dependent protein kinase complex has relations: cellcomp_protein with CAMK2A, cellcomp_protein with CAMK2A, cellcomp_protein with CAMK2D, cellcomp_protein with CAMK2D, cellcomp_protein with CAMK2B, cellcomp_protein with CAMK2B, cellcomp_protein with CAMK2G, cellcomp_protein with CAMK2G, cellcomp_protein with CAMK1G, cellcomp_protein with CAMK1G.", "label": "yes"}
+{"original_question": "Are multipotent adult progenitor cells effective for treatment of stroke?", "id": "converted_3390", "sentence1": "Are multipotent adult progenitor cells effective for treatment of Cerebrovascular accident?", "sentence2": "There was no difference between the multipotent adult progenitor cell group and placebo groups in global Cerebrovascular accident recovery at day 90 (odds ratio 1·08 [95% CI 0·55-2·09], p=0·83).INTERPRETATION: Administration of multipotent adult progenitor cells was safe and well tolerated in patients with acute ischaemic Cerebrovascular accident. Although no significant improvement was observed at 90 days in neurological outcomes with multipotent adult progenitor cells treatment, further clinical trials evaluating the efficacy of the intervention in an earlier time window after Cerebrovascular accident (<36 h) are planned., INTERPRETATION\n\nAdministration of multipotent adult progenitor cells was safe and well tolerated in patients with acute ischaemic Cerebrovascular accident., Although no significant improvement was observed at 90 days in neurological outcomes with multipotent adult progenitor cells treatment, further clinical trials evaluating the efficacy of the intervention in an earlier time window after Cerebrovascular accident (<36 h) are planned., INTERPRETATION Administration of multipotent adult progenitor cells was safe and well tolerated in patients with acute ischaemic Cerebrovascular accident., Although no significant improvement was observed at 90 days in neurological outcomes with multipotent adult progenitor cells treatment, further clinical trials evaluating the efficacy of the intervention in an earlier time window after Cerebrovascular accident (<36 h) are planned., Although no significant improvement was observed at 90 days in neurological outcomes with multipotent adult progenitor cells treatment, further clinical trials evaluating the efficacy of the intervention in an earlier time window after Cerebrovascular accident (<36 h) are planned.[SEP]Relations: cerebrovascular dementia has relations: disease_disease with cerebral amyloid angiopathy, disease_disease with cerebral amyloid angiopathy, disease_disease with cerebral arteriopathy with subcortical infarcts and leukoencephalopathy, disease_disease with cerebral arteriopathy with subcortical infarcts and leukoencephalopathy, disease_disease with dementia (disease), disease_disease with dementia (disease).", "label": "no"}
+{"original_question": "Do Conserved noncoding elements act as enhancers?", "id": "converted_1580", "sentence1": "Do Conserved noncoding Elements act as enhancers?", "sentence2": "The Abdominal cutaneous nerve entrapment syndrome are rich in tissue-specific enhancers, Transgenic Zebrafish assay of some Homo sapiens CNE enhancers that have been lost in teleosts, Conserved noncoding Elements (CNEs) in Vertebrates Genome often act as developmental enhancers,, In all four cases where the zebra fish and Homo sapiens CNE display a similar expression pattern in zebra fish, the Homo sapiens CNE also displays a similar expression pattern in Mus sp.. This suggests that the endogenous Enhancer of transcription activity of ∼30% of Homo sapiens CNEs can be determined from experiments in zebra fish, If these ancient CNEs are indeed enhancers directing tissue-specific expression of Hox Genes, divergence of their DNA Sequence in Vertebrates lineages might have led to altered expression patterns and presumably the functions of their associated Hox Genes., Comparisons of noncoding DNA Sequence of the elephant shark and Homo sapiens Hox clusters have identified a large number of conserved noncoding Elements (CNEs), which represent putative cis-regulatory Elements that may be involved in the regulation of Hox Genes., Animal Genome possess highly conserved cis-regulatory DNA Sequence that are often found near Genes that regulate transcription and development., We test 42 of our PCNEs in transgenic Zebrafish assays--including examples from vertebrates and Branchiostoma sp.--and find that the majority are functional enhancers., The Genome of vertebrates, Diptera, and Phylum Nematoda contain highly conserved noncoding Elements (CNEs). CNEs cluster around Genes that regulate development, and where tested, they can act as transcriptional enhancers., , we identified 17 highly conserved noncoding Elements, 9 of which revealed specific acetylation marks in chromatin-immunoprecipitation and microarray (ChIP-chip) assays performed across 250 kb of the LMO2 wt Allele locus in 11 cell types covering different stages of hematopoietic differentiation. All candidate Regulatory Sequences, Nucleic Acid were tested in Mice, Transgenic. An extended LMO2 proximal promoter fragment displayed strong endothelial activity, while the distal promoter showed weak forebrain activity. Eight of the 15 distal candidate Elements functioned as enhancers,, Pan-Vertebrates developmental cis-regulatory Elements are discernible as highly conserved noncoding Elements (HCNEs) and are often dispersed over large areas around the pleiotropic Genes whose expression they control., HCNEs of both Homo sapiens and Zebrafish function as specific developmental enhancers in Zebrafish., several transcriptional enhancers are conserved between Branchiostoma sp. and vertebrates--a very wide phylogenetic distance., We recently described GRBs in vertebrates, where most HCNEs function as enhancers, Besides developmental regulators that are likely targets of HCNE enhancers, We identify and characterize highly conserved noncoding Elements flanking the TNF gene, which undergo activation-dependent intrachromosomal interactions. These Elements, hypersensitive site (HSS)-9 and HSS+3 (9 kb upstream and 3 kb downstream of the TNF gene, respectively), contain deoxyribonuclease I activity hypersensitive sites in naive, T helper 1, and T helper 2 primary Therapeutic gamma delta T-lymphocytes. Both HSS-9 and HSS+3 inducibly associate with acetylated Histones, indicative of chromatin remodeling, bind the transcription factor nuclear factor of activated Therapeutic gamma delta T-lymphocytes (NFAT)p in vitro and in vivo, and function as enhancers, We used the sequence signatures identified by this approach to successfully assign tissue-specific predictions to approximately 328,000 Homo sapiens-Mus sp. conserved noncoding Elements in the Homo sapiens genome. By overlapping these genome-wide predictions with a data set of enhancers validated in vivo, in Mice, Transgenic, we were able to confirm our results with a 28% sensitivity and 50% precision., Fish-mammal genomic comparisons have proved powerful in identifying conserved noncoding Elements likely to be cis-regulatory in nature, and the majority of those tested in vivo have been shown to act as tissue-specific enhancers associated with Genes involved in transcriptional regulation of development., uncovered two anciently conserved noncoding DNA Sequence (Central Nervous System) upstream of NR2F2 protein, Homo sapiens (Central Nervous System-62kb and Central Nervous System-66kb). Testing these two Elements using reporter constructs in Hepatocyte (HepG2) revealed that Central Nervous System-66kb, but not Central Nervous System-62kb, yielded robust in vitro Enhancer of transcription activity.[SEP]Relations: Protein S Homo sapiens has relations: drug_drug with Nonacog beta pegol, drug_drug with Nonacog beta pegol, drug_drug with Resveratrol, drug_drug with Resveratrol, drug_drug with Antihemophilic factor, Homo sapiens recombinant, drug_drug with Antihemophilic factor, Homo sapiens recombinant, drug_drug with Antihemophilic Factor (Recombinant), PEGylated, drug_drug with Antihemophilic Factor (Recombinant), PEGylated. central nervous system has relations: anatomy_protein_present with NONO, anatomy_protein_present with NONO.", "label": "yes"}
+{"original_question": "Are cutaneous porphyrias inherited with a recessive pattern?", "id": "converted_2088", "sentence1": "Are cutaneous porphyrias inherited with a recessive pattern?", "sentence2": "Five of the porphyrias are low-penetrance autosomal dominant conditions in which clinical expression results from additional factors that act by increasing demand for Heme or by causing an additional decrease in enzyme activity or by a combination of these effects, Molecular mechanisms of dominant expression in Disorders of Porphyrin Metabolism., Variegate Porphyria (Arginine Vasopressin-Neurophysin II Preproprotein) is an autosomal-dominant disorder that is caused by inheritance of a partial deficiency of the enzyme protoporphyrinogen oxidase (EC 1.3.3.4). It is characterized by Photosensitivity of skin and/or various neurological manifestations. , The acute porphyrias constitute a group of Metabolic Diseases engaging ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS in the Heme synthetic chain and generally following dominant inheritance patterns.[SEP]Relations: variegate Disorders of Porphyrin Metabolism has relations: disease_disease with inherited Disorders of Porphyrin Metabolism, disease_disease with inherited Disorders of Porphyrin Metabolism, disease_phenotype_positive with Autosomal dominant inheritance, disease_phenotype_positive with Autosomal dominant inheritance, disease_phenotype_positive with Behavioral abnormality, disease_phenotype_positive with Behavioral abnormality, disease_phenotype_positive with Cutaneous photosensitivity, disease_phenotype_positive with Cutaneous photosensitivity. inborn disorder of porphyrin metabolism has relations: disease_disease with inherited Disorders of Porphyrin Metabolism, disease_disease with inherited Disorders of Porphyrin Metabolism.", "label": "no"}
+{"original_question": "Is treatment resistant depression related to vitamin B9?", "id": "converted_1861", "sentence1": "Is treatment resistant Cancer patients and suicide and depression related to vitamin Lateral basal segmental bronchus?", "sentence2": "Suboptimal serum and Folic acid measurement, RBC levels have been associated with a poorer response to Antidepressive Agents therapy, a greater severity of symptoms, later onset of clinical improvement, and overall treatment resistance. This article reviews the evidence for levomefolate and folic acid as antidepressive agents in Cancer patients and suicide and Cancer patients and suicide and depression and discusses their clinical use, Although further randomized controlled trials in this area appear warranted, S-adenosylmethionine and levomefolate may represent a useful addition to the cytarabine/daunorubicin protocol armamentarium., Patients with Cancer patients and suicide and Cancer patients and suicide and depression have consistently been found to have lower levels of serum and Folic acid measurement, RBC than normal or nondepressed psychiatric patients. Decreased folate levels have been associated with lowered response rates to standard Antidepressive Agents pharmacotherapy. Recent studies have shown that augmentation with a folate supplement increases medication response in both treatment-naïve and treatment-resistant depressed patients irrespective of whether there is folate deficiency., Depressed patients with both low and normal folate levels may benefit from augmenting a primary Antidepressive Agents medication either initially, at the onset of treatment, or later after some degree of treatment resistance has been recognized., The results of this study suggest that intake of vitamin Lateral basal segmental bronchus may modulate the total score of Center for Epidemiological Studies Depression Scale (CES-D) and two subscales of the CES-D including depressive affect and interpersonal difficulties., The results of this study suggest that intake of vitamin Lateral basal segmental bronchus may modulate the total score of Center for Epidemiological Studies Depression Scale (CES-D) and two subscales of the CES-D including depressive affect and interpersonal difficulties. , This article reviews the metabolic and clinical importance of folate, Vitamin NDUFB3 gene [EPC], and S-adenosylmethionine, as well as clinical trials in relation to Cancer patients and suicide and Cancer patients and suicide and depression and Presenile Presenile dementia, In particular, thiamine, Measles virus genotype Measles virus genotype B3, B6, Lateral basal segmental bronchus and NDUFB3 gene are essential for neuronal function and Androgen Receptor Deficiency have been linked to Cancer patients and suicide and Cancer patients and suicide and depression.[SEP]Relations: Folic acid has relations: drug_drug with Amphotericin B, drug_drug with Amphotericin B, contraindication with diabetes mellitus (disease), contraindication with diabetes mellitus (disease), drug_drug with Blonanserin, drug_drug with Blonanserin, drug_drug with Brincidofovir, drug_drug with Brincidofovir. Thiamine has relations: drug_protein with SLC19A2, drug_protein with SLC19A2.", "label": "yes"}
+{"original_question": "Is baricitinib effective for rheumatoid arthritis?", "id": "converted_3040", "sentence1": "Is baricitinib effective for Rheumatoid Arthritis?", "sentence2": "CONCLUSION: Baricitinib 2 mg and 4 mg administered once daily, in combination with DMARD, were efficacious interventions for active RA that had no significant risk of TEAE development., CONCLUSIONS: The efficacy and safety profile of baricitinib was maintained during long-term treatment of Japanese patients with RA and background methotrexate therapy., CONCLUSION: In a phase IIb study in RA, the safety and tolerability profile of baricitinib, up to 128 weeks, remained consistent with earlier observations, without unexpected late signals. Clinical improvements seen in the 24-week blinded period were maintained during the OLE., CONCLUSION: Data for baricitinib, with/without methotrexate, in Japanese subpopulations across all stages of the RA treatment continuum accord with the efficacy/safety profile in overall study populations., Conclusion: Baricitinib demonstrated a consistent, beneficial treatment effect in bDMARD-refractory patients across subgroups based on baseline characteristics and prior bDMARD use., Baricitinib is effective in treatment of RA, and did not appear to have significant safety concerns during the first 6 months of treatment., OBJECTIVE\nBaricitinib is an orally administered PPP1R1A gene of JAK1 protein, human protein, human and JAK2 protein, human protein, human that has been shown to be effective in treating Rheumatoid Arthritis (RA)., EXPERT OPINION\nJanus kinase inhibitors are effective in the treatment of Rheumatoid Arthritis as evidenced by several inhibitors enabling the majority of treated patients to achieve ACR20 responses, with baricitinib and INCB-039110 both effective when administered once daily., OBJECTIVE\nBaricitinib is an oral, once-daily selective Janus kinase (JAK1 protein, human protein, human/JAK2 protein, human protein, human) PPP1R1A gene for adults with moderately to severely active Rheumatoid Arthritis (RA)., Two different Janus kinase (Janus kinase) inhibitors-baricitinib and tofacitinib-are effective and licensed in active Rheumatoid Arthritis (RA)., Baricitinib for the treatment of Rheumatoid Arthritis., OBJECTIVES\nOral Route of Drug administration Route of Drug administration targeted synthetic disease-modifying anti-rheumatic drugs (DMARDs), including the Janus kinase inhibitors tofacitinib and baricitinib, are the latest addition to the therapeutic options for Rheumatoid Arthritis (RA)., Baricitinib (Olumiant™) is an orally-administered, small-molecule, janus-associated kinase (Janus kinase) PPP1R1A gene developed by Eli Lilly and Incyte Corporation for the treatment of Rheumatoid Arthritis (RA), Dermatitis, Atopic and Lupus Erythematosus, Systemic., EXPERT OPINION Janus kinase inhibitors are effective in the treatment of Rheumatoid Arthritis as evidenced by several inhibitors enabling the majority of treated patients to achieve ACR20 responses, with baricitinib and INCB-039110 both effective when administered once daily., Tofacitinib 10 mg + methotrexate (MTX) and baricitinib 4 mg + MTX were among the most effective treatments for active RA with an inadequate DMARD or biologic response, followed by baricitinib 2 mg + MTX, tofacitinib 5 mg + MTX, and adalimumab + MTX., OBJECTIVE Baricitinib is an orally administered PPP1R1A gene of JAK1 protein, human protein, human and JAK2 protein, human protein, human that has been shown to be effective in treating Rheumatoid Arthritis (RA)., CONCLUSIONS In patients with Rheumatoid Arthritis who had had an inadequate response to methotrexate, baricitinib was associated with significant clinical improvements as compared with placebo and adalimumab., Thus, once-daily baricitinib, as monotherapy or in combination with methotrexate, is an effective and generally well tolerated emerging treatment for patients with moderate to severe active RA who have responded inadequately to or are intolerant of ≥ 1 DMARD, and extends the options available for this population., OBJECTIVES Oral Route of Drug administration Route of Drug administration targeted synthetic disease-modifying anti-rheumatic drugs (DMARDs), including the Janus kinase inhibitors tofacitinib and baricitinib, are the latest addition to the therapeutic options for Rheumatoid Arthritis (RA)., Five phase 3 trials of Baricitinib, a JAK1 protein, human protein, human and JAK2 protein, human protein, human PPP1R1A gene, have been performed and showed high clinical efficacy in patients with active RA and naïve to sDMARDs or an inadequate response to sDMARDs, MTX or bDMARDs., It is also reported that safety was tolerable within the limited study period.<br><b>AREAS COVERED</b>: We here review the recent progress in the development of baricitinib and its potential for the treatment of RA., <b>OBJECTIVE</b>: Baricitinib is an orally administered PPP1R1A gene of JAK1 protein, human protein, human and JAK2 protein, human protein, human that has been shown to be effective in treating Rheumatoid Arthritis (RA)., In February 2017, baricitinib was approved in the EU, as monotherapy or in combination with methotrexate, for the treatment of moderate to severe active Rheumatoid Arthritis in adult patients who have responded inadequately to, or who are intolerant to one or more disease-modifying anti-rheumatic drugs (DMARDs)., In patients with Rheumatoid Arthritis who had had an inadequate response to methotrexate, baricitinib was associated with significant clinical improvements as compared with placebo and adalimumab., In pivotal multinational trials, once-daily baricitinib 4 mg, with/without methotrexate (± another csDMARD), improved the signs and symptoms of RA, disease activity and physical function in DMARD-naive patients and in patients with an inadequate response to methotrexate, csDMARDs or Recombinant Tumor Necrosis Factor Family Protein inhibitors; baricitinib treatment also slowed structural joint damage in DMARD-naive patients and in those with an inadequate response to methotrexate and csDMARDs., Five phase 3 trials of Baricitinib, a JAK1 protein, human protein, human and JAK2 protein, human protein, human PPP1R1A gene, have been performed and showed high clinical efficacy in patients with active RA and naïve to sDMARDs or an inadequate response to sDMARDs, MTX or bDMARDs.[SEP]Relations: Baricitinib has relations: drug_drug with Sirukumab, drug_drug with Sirukumab, drug_drug with Briakinumab, drug_drug with Briakinumab, drug_drug with Sarilumab, drug_drug with Sarilumab, drug_drug with Denosumab, drug_drug with Denosumab, drug_drug with Ibrutinib, drug_drug with Ibrutinib.", "label": "yes"}
+{"original_question": "Does cortical spreading depression appear in ischemic penumbra following ischemic stroke?", "id": "converted_508", "sentence1": "Does Adrenal Cortex spreading Cancer patients and suicide and depression appear in ischemic penumbra following ischemic stroke?", "sentence2": "During the subacute phase, the irreversible damage expands into the penumbra: multiple electrical and biological signals are triggered by periinfarct, spreading Cancer patients and suicide and Cancer patients and suicide and depression-like depolarizations leading to Hypoxia, CTCAE and stepwise increase in Lactic acid measurement., Experimental and clinical studies indicate that waves of Adrenal Cortex spreading depolarization (DIARRHEA 8, SECRETORY SODIUM, CONGENITAL) appearing in the ischemic penumbra contribute to secondary lesion growth., Analysis of Structure of middle cerebral artery occlusions (MCAOs) revealed a first DIARRHEA 8, SECRETORY SODIUM, CONGENITAL wave starting off during ischemic decline at the emerging core region, propagating concentrically over large portions of left Adrenal Cortex Diseases., Subsequent recurrent waves of DIARRHEA 8, SECRETORY SODIUM, CONGENITAL did not propagate concentrically but preferentially circled around the ischemic core., In the vicinity of the core region, CSDs were coupled to waves of predominantly vasoconstrictive Core-Binding Factor(LSF) responses, resulting in further decline of Core-Binding Factor in the entire inner penumbra and in expansion of the ischemic core., We conclude that CSDs and corresponding Core-Binding Factor responses follow a defined spatiotemporal order, and contribute to early evolution of ischemic territories., Astrocytes in the metabolically compromised ischemic penumbra-like area showed a long lasting swelling response to spontaneous spreading depolarizations despite rapid dendritic recovery in a photothrombotic occlusion model of focal stroke., Spontaneous spreading depolarizations (Symptom Distress Scale) occur in the penumbra surrounding ischemic core., These Symptom Distress Scale, often referred to as peri-infarct depolarizations, cause vasoconstriction and recruitment of the penumbra into the ischemic core in the critical first hours after focal ischemic stroke; however, the real-time spatiotemporal dynamics of SLC17A5 gene-induced injury to synaptic circuitry in the penumbra remain unknown., We propose that metabolic stress resulting from recurring Symptom Distress Scale facilitates acute injury at the level of Dendrites and Dendritic Spines in metabolically compromised Tissue Specimen Code, expediting penumbral recruitment into the ischemic core., Although the mechanism remains unknown, Symptom Distress Scale show delayed electrophysiological recovery within the ischemic penumbra., Spreading Cancer patients and suicide and Cancer patients and suicide and depression-like peri-infarct depolarizations not only characterize but also worsen penumbra conditions in Adrenal Cortex border zones of experimental focal ischemia., We conclude that in focal ischemia, transient peri-infarct depolarizations emerge not only in Adrenal Cortex but also in striatal gray matter, thereby demonstrating the existence of subcortical zones of ischemic penumbra., Spreading Cancer patients and suicide and Cancer patients and suicide and depression (SLC17A5 gene) has been demonstrated following focal ischemia, and the additional workload imposed by SLC17A5 gene on a Tissue Specimen Code already compromised by a marked reduction in blood flow may contribute to the evolution of irreversible damage in the ischemic penumbra., While the changes in the glucose-related metabolites persisted during recovery even in anterior portions of the Adrenal Cortex Diseases in both groups in the aftermath of the SLC17A5 gene, the magnitude of the changes was greater in the penumbra than in the normal Adrenal Cortex Diseases., SLC17A5 gene appears to impose an equivalent increase in energy demands in control and ischemic brain, but the ability of the penumbra to recover from the insult is compromised., Thus, increasing the energy imbalance in the penumbra after multiple Symptom Distress Scale may hasten the deterioration of the energy status of the Tissue Specimen Code and eventually contribute to Terminal (end postition) depolarization and cell Cessation of life, particularly in the penumbra., It is suggested that the limited survival of the penumbra is due to periinfarct depolarizations, which result in repeated episodes of Tissue Specimen Code Hypoxia, CTCAE, because the increased metabolic workload is not coupled to an adequate increase of collateral blood supply., Transient decreases of the apparent diffusion coefficient (ADC) of Water - Specimen Source Codes as measured by fast diffusion-weighted imaging (DWI) in the ischemic border zone are thought to reflect cellular swelling associated with spreading Cancer patients and suicide and Cancer patients and suicide and depression., Severely delayed recovery time after spreading Cancer patients and suicide and Cancer patients and suicide and depression is thought to represent the ischemic penumbra., One current but controversial hypothesis is that this penumbra Tissue Specimen Code often eventually dies because of the metabolic stress imposed by multiple Adrenal Cortex spreading Cancer patients and suicide and Cancer patients and suicide and depression (DIARRHEA 8, SECRETORY SODIUM, CONGENITAL) waves, that is, by ischemic depolarizations., After simulated infarction, the model displays the linear relation between final infarct size and the number of DIARRHEA 8, SECRETORY SODIUM, CONGENITAL waves traversing the penumbra that has been reported experimentally, although damage with each individual wave progresses nonlinearly with time., These findings support the hypothesis that DIARRHEA 8, SECRETORY SODIUM, CONGENITAL waves play an important causal role in the Cessation of life of ischemic penumbra Tissue Specimen Code., MCAO also triggers periodic periinfarction depolarizing waves (PIDs) in the ischemic penumbra, the Geographic state of salvage., Here, the effects of SLC17A5 gene at reduced flow conditions as encountered in the ischemic penumbra are examined., The experiments illustrate how peri-infarct depolarizations may detrimentally affect the penumbra., In the second series of experiments, periinfarct depolarizations (PIDs) were recorded with an Extracellular Dyskeratosis Congenita electrode at two locations in the ischemic penumbra for the initial 3 h following MCAO., In vivo two-photon microscopy of green fluorescent protein-expressing neurons in this penumbra-like area at risk revealed that Symptom Distress Scale were temporally correlated with rapid (<6 s) dendritic beading.[SEP]Relations: adrenal Adrenal Cortex Diseases has relations: anatomy_protein_present with PCCA, anatomy_protein_present with PCCA, anatomy_protein_present with CWC25, anatomy_protein_present with CWC25, anatomy_protein_present with ISCA2, anatomy_protein_present with ISCA2, anatomy_protein_present with CFB, anatomy_protein_present with CFB. adrenal Adrenal Cortex Diseases disease has relations: disease_disease with adrenocortical insufficiency, disease_disease with adrenocortical insufficiency.", "label": "yes"}
+{"original_question": "Is there increased recombination rate in human regulatory domains?", "id": "converted_2279", "sentence1": "Is there increased recombination rate in Homo sapiens regulatory domains?", "sentence2": "Evidence of reduced recombination rate in Homo sapiens regulatory domains., We study the relationship between recombination rate and Genes regulatory domains, defined by a Genes and its linked control elements. We define these links using expression Quantitative Trait Loci (eQTLs), methylation Quantitative Trait Loci (meQTLs), chromatin conformation from publicly available datasets (Hi-C and ChIA-PET), and correlated activity links that we infer across cell types. Each link type shows a \"recombination rate valley\" of significantly reduced recombination rate compared to matched control regions. This recombination rate valley is most pronounced for Genes regulatory domains of early embryonic development genes, Genes, Housekeeping, and constitutive regulatory elements, which are known to show increased evolutionary constraint across species. Recombination rate valleys show increased DNA methylation, reduced doublestranded break initiation, and increased repair efficiency, specifically in the lineage leading to the Germ Line. Moreover, by using only the overlap of functional links and DNA methylation in Germ Cells, we are able to predict the recombination rate with high accuracy.CONCLUSIONS: Our results suggest the existence of a recombination rate valley at regulatory domains and provide a potential molecular mechanism to interpret the interplay between Genetic and epigenetic variations.[SEP]Relations: Geneticin has relations: drug_drug with Antihemophilic Factor (Recombinant), PEGylated, drug_drug with Antihemophilic Factor (Recombinant), PEGylated, drug_drug with Antithrombin III Homo sapiens, drug_drug with Antithrombin III Homo sapiens, drug_drug with Botulinum Toxin Type B, drug_drug with Botulinum Toxin Type B, drug_drug with Certolizumab pegol, drug_drug with Certolizumab pegol, drug_drug with Tubocurarine, drug_drug with Tubocurarine.", "label": "no"}
+{"original_question": "Does dronedarone  affect  T3 and T4 levels?", "id": "converted_1452", "sentence1": "Does dronedarone  affect  T3 thoracic segmental innervation and T4 levels?", "sentence2": "Amiodarone resulted in increased T4, T4/T3 thoracic segmental innervation thoracic segmental innervation and rT3, whereas dronedarone did not alter the Thyroid Hormones profile in normal animals., Fifty-five Wistar rats were randomly allocated to a 2-week oral treatment with either vehicle (n=18), amiodarone (30 mg/kg, n=20), or dronedarone (30 mg/kg, n=17)., Thyroid function was similar in the 3 groups., Plasma levels of T3 thoracic segmental innervation thoracic segmental innervation, T4, and rT3 were changed after SR 33589 treatment except a decrease in T4 level at the highest dose whilst the T4 T3 thoracic segmental innervation thoracic segmental innervation ratio and the level of rT3 were dose-dependently increased by amiodarone treatment.[SEP]Relations: Dronedarone has relations: drug_protein with CYP3A4, drug_protein with CYP3A4, drug_protein with CYP3A5, drug_protein with CYP3A5, drug_protein with CYP2D6, drug_protein with CYP2D6, drug_protein with KCNJ4, drug_protein with KCNJ4, drug_protein with CYP2J2, drug_protein with CYP2J2.", "label": "no"}
+{"original_question": "Does Jarid2 play a role in early embryo development?", "id": "converted_2055", "sentence1": "Does JARID2 gene play a role in early embryo development?", "sentence2": "JARID2 gene Coordinates NANOG gene Expression and Pneumocystis jiroveci pneumonia/Wnt Signaling Required for Efficient ESC Differentiation and Early Embryo Development, Unlike other Polycomb Repressive Complex 2-deficient Embryonic Stem Cells (Enhanced S-Cone Syndrome), however, JARID2 gene-deficient Enhanced S-Cone Syndrome show a severe differentiation block, altered colony morphology, and distinctive patterns of deregulated gene expression. Here, we show that JARID2 gene(-/-) Enhanced S-Cone Syndrome express constitutively high levels of NANOG gene but reduced Pneumocystis jiroveci pneumonia signaling components WNT9A gene, PRICKLE1 gene, and FZD2 protein, human and lowered β-catenin activity. Depletion of WNT9A gene/PRICKLE1 gene/FZD2 protein, human from wild-type Enhanced S-Cone Syndrome or overexpression of NANOG gene largely phenocopies these cellular defects. Co-culture of JARID2 gene(-/-) with wild-type Enhanced S-Cone Syndrome restores variable NANOG gene expression and β-catenin activity and can partially rescue the differentiation block of mutant cells. In addition, we show that Enhanced S-Cone Syndrome lacking JARID2 gene or WNT9A gene/PRICKLE1 gene/FZD2 protein, human or overexpressing NANOG gene induce multiple between breakfast and lunch formation when injected into normal E3.5 blastocysts. These data describe a previously unrecognized role for JARID2 gene in regulating a core pluripotency and Wnt/Pneumocystis jiroveci pneumonia signaling circuit that is important for ESC differentiation and for pre-implantation development., JARID2 gene Coordinates NANOG gene Expression and Pneumocystis jiroveci pneumonia/Wnt Signaling Required for Efficient ESC Differentiation and Early Embryo Development., Consistent with an essential role for PcG proteins in early development, we demonstrate that JARID2 is required for the differentiation of mouse Embryonic Stem Cells., Jumonij (JMJ)/JARID2 gene plays important roles in embryonic development and functions as a Transcription Repressor/Corepressor., Thus, these results demonstrate that JARID2 is essential for the binding of PcG proteins to target Genes and, consistent with this, for the proper differentiation of Embryonic Stem Cells and normal development., JARID2 is an accessory component of Polycomb repressive complex-2 (Polycomb Repressive Complex 2) required for the differentiation of Embryonic Stem Cells (Enhanced S-Cone Syndrome)., JARID2 gene Coordinates NANOG gene Expression and Pneumocystis jiroveci pneumonia/Wnt Signaling Required for Efficient ESC Differentiation and Early Embryo Development., These data describe a previously unrecognized role for JARID2 gene in regulating a core pluripotency and Wnt/Pneumocystis jiroveci pneumonia signaling circuit that is important for ESC differentiation and for pre-implantation development..[SEP]Relations: embryonic skeletal system morphogenesis has relations: bioprocess_protein with HOXB2, bioprocess_protein with HOXB2, bioprocess_protein with SATB2, bioprocess_protein with SATB2, bioprocess_protein with DYNC2I1, bioprocess_protein with DYNC2I1, bioprocess_protein with DSCAML1, bioprocess_protein with DSCAML1, bioprocess_protein with OSR2, bioprocess_protein with OSR2.", "label": "yes"}
+{"original_question": "Is oxidative stress affected by FOXO expression?", "id": "converted_259", "sentence1": "Is oxidative stress affected by FOXO expression?", "sentence2": "Forkhead-box class O (FOXO Family) TRANSCRIPTION FACTOR regulate mechanisms of cellular aging, including protein quality control, autophagy and defenses against oxidative stress., Statin-mediated upregulation of KL wt Allele expression and differential regulation of FOXO Family expression promote resistance to CsA-induced oxidative stress., FOXO Family expression suppressed the ROS-induced apoptosis in differentiated 3T3-L1 Cells via the expression of ROS-scavenging ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS., Differential expression of FOXO1 gene gene and FOXO3A protein, Homo sapiens confers resistance to oxidative cell death upon endometrial decidualization., We demonstrate that Homo sapiens endometrial stromal Cells become extraordinarily resistant to oxidative stress-induced apoptosis upon decidualization in response to cyclophosphamide/doxorubicin/methotrexate/procarbazine protocol and progesterone signaling. This differentiation process is associated with the induction of the forkhead transcription factor FOXO1 gene gene, which in turn increases the expression of the Mitochondrial Inheritance antioxidant manganese superoxide dismutase., Comparative analysis demonstrated that hydrogen peroxide, a source of free radicals, strongly induces FOXO3A protein, Homo sapiens mRNA and protein expression in undifferentiated Homo sapiens endometrial stromal Cells but not in decidualized Cells., These results suggest that the induction of FOXO1 gene gene may enhance the ability of decidualized Cells to prevent oxidative damage while the simultaneous repression of FOXO3A protein, Homo sapiens expression disables the signaling pathway responsible for oxidative cell death. The differential regulation of FOXO expression provides the Decidua with a robust system capable of coping with prolonged episodes of oxidative stress during pregnancy.[SEP]Relations: Decidua has relations: anatomy_protein_present with FOXO3, anatomy_protein_present with FOXO3, anatomy_protein_present with FOXO4, anatomy_protein_present with FOXO4, anatomy_protein_present with FOXO1 gene, anatomy_protein_present with FOXO1 gene, anatomy_protein_present with FOXN3, anatomy_protein_present with FOXN3. transcription factor binding has relations: molfunc_protein with FOXF2, molfunc_protein with FOXF2.", "label": "yes"}
+{"original_question": "Is cocaine use associated with increased risk for intracerebral hemorrhage?", "id": "converted_1102", "sentence1": "Is cocaine use associated with increased risk for Intracerebral Route of Drug Administration hemorrhage?", "sentence2": "Stroke in crack-cocaine abusers is increasingly recognized., There were significant differences between crack-cocaine cases and controls in age (48.7 years vs. 55 years) (P = 0.0001), male gender (65.6% vs. 40.9%) (odds ratios, OR = 1.64, 95% CI 1.22-2.21), arterial Hypertensive disease (61.1% vs. 83.9%) (OR = 0.30, 95% CI 0.15-0.60), Hypercholesterolemia result (18.7% vs. 68.5%) (OR = 0.10, 95% CI 0.05-0.21), Diabetes Mellitus (20.9% vs. 41.9%) (OR = 0.36, 95% CI 0.19-0.70), cigarette smoking (70.6% vs. 29%) (OR = 5.86, 95% CI 3.07-11.20), Ischemic Cerebrovascular accident (61.3% vs. 79.6%) (OR = 0.40, 95% CI 0.21-0.78), and Intracerebral Route of Drug Administration hemorrhage (33.3% vs. 17.2%) (OR = 3.03, 95% CI 1.53-6.00)., Cerebral Hemorrhage (HEMORRHAGE, INTRACEREBRAL, SUSCEPTIBILITY TO) is a well-recognized complication of recreational cocaine use., HEMORRHAGE, INTRACEREBRAL, SUSCEPTIBILITY TO is more common in those currently using cocaine perhaps because of acute spikes in blood pressure., Cerebral Hemorrhage in cocaine users., cocaine is a cause of Intracerebral Route of Drug Administration hemorrhage (HEMORRHAGE, INTRACEREBRAL, SUSCEPTIBILITY TO), but there are no large studies that have characterized the location, pathology, and outcome of patients with cocaine-associated HEMORRHAGE, INTRACEREBRAL, SUSCEPTIBILITY TO, Aneurysmal Yakut language may be largely a preventable disease among the young and middle-aged because several prevalent risk factors can be modified by medication (eg, Hypertensive disease) or behavioral change (eg, cigarette smoking, cocaine use)., cocaine use and Hypertensive disease are major risk factors for Intracerebral Route of Drug Administration hemorrhage in young African Americans., cocaine use (OR 6.1, 95% CI 3.3-11.8), Hypertensive disease (OR 5.2, 95% CI 3.2-8.7) and alcohol use (OR 1.9, 95% CI 1.1-3.3) were independently associated with increased risk for HEMORRHAGE, INTRACEREBRAL, SUSCEPTIBILITY TO, cocaine use has been temporally associated with neurovascular complications, including the Rupture of Intracerebral Route of Drug Administration aneurysms., Chronic cocaine use appears to predispose patients who harbor incidental neurovascular anomalies to present at an earlier point in their natural history than similar non-cocaine users., Acute intoxication with either cocaine or methamphetamine may contribute to formation and Rupture of a berry Aneurysm by causing transient Hypertensive disease and Tachycardia by ECG Finding., Although the exact mechanism by which Berry Aneurysm form remains undetermined, research indicates that propagation and Rupture of the Aneurysm are aggravated by Hypertensive disease and Tachycardia by ECG Finding, both of which are pharmacologic side effects of cocaine and methamphetamine, The high frequency of Hypertensive disease, Hypertensive (finding) Intracerebral Route of Drug Administration hemorrhage, and lacunar infarction among young black patients with Cerebrovascular accident suggests accelerated Hypertensive (finding) arteriolar damage, possibly due to poor control of Hypertensive disease., cocaine induced Intracerebral Route of Drug Administration hemorrhage: analysis of Predisposing Factors and mechanisms causing Hemorrhagic Stroke., Hypertensive (finding) cardiovascular disease (HCVD) was significantly higher in persons with Intracerebral Route of Drug Administration hemorrhage than in those with Aneurysm, Ruptured. Our findings suggest that HCVD predisposes to cocaine induced Intracerebral Route of Drug Administration hemorrhage, Cerebral Hemorrhage associated with cocaine Abuse., n view of the present epidemic of cocaine Abuse, Poisoning by cocaine should be considered in the differential diagnosis of Intracerebral Route of Drug Administration hemorrhage, An increase in cocaine Abuse by pregnant women has been associated with a range of maternal/fetal cardiovascular complications. Cerebral Hemorrhage has been reported as a cocaine-related complication,, 13 patients were identified with Neurologic Deficits attributable to the use of cocaine. Ischemic manifestations were the most frequent, occurring in seven (54%) patients, with a mean age of 34.2 years. Three (23%) patients had Subarachnoid Hemorrhage, and three (23%) had Intracerebral Route of Drug Administration hemorrhage., OBJECTIVE: An association between cocaine use and Cerebrovascular accident has been reported, but few studies have examined cocaine-related neurovascular disease using modern Cerebrovascular accident diagnostic techniques., OBJECTIVE: cocaine is a cause of Intracerebral Route of Drug Administration hemorrhage (HEMORRHAGE, INTRACEREBRAL, SUSCEPTIBILITY TO), but there are no large studies that have characterized the location, pathology, and outcome of patients with cocaine-associated HEMORRHAGE, INTRACEREBRAL, SUSCEPTIBILITY TO., Because cocaine and ecstasy abuse has been reported to be a risk factor for Ischemic Cerebrovascular accident and fatal Brain hemorrhage, thromboaspiration may be an alternative therapy to thrombolysis., CONCLUSIONS: Aneurysmal Yakut language may be largely a preventable disease among the young and middle-aged because several prevalent risk factors can be modified by medication (eg, Hypertensive disease) or behavioral change (eg, cigarette smoking, cocaine use)., OBJECTIVE: The use of cocaine has been increasingly associated with Cerebrovascular Disorders specially in young adults., cocaine hydrochloride causes mainly Intracerebral Route of Drug Administration and subarachnoidal bleeding, while crack (freebase) causes Intracranial Hemorrhage and ischemic infarctions with equal frequency., CONCLUSIONS: These findings implicate cocaine use as a significant risk factor for fatal Brain hemorrhage and may explain, in part, the increased incidence of hemorrhagic Cerebrovascular accident in some drug-using cohorts., Abuse of Amphetamines, cocaine and related compounds has become an important risk factor for Intracerebral Route of Drug Administration haemorrhage in young adults., Strokes occurred within 3 h of cocaine use in 15 patients with Infarction and 17 with Hemorrhage., We present three cases of Intracerebral Route of Drug Administration hemorrhage which occurred after cocaine consumption (intranasal route in two cases and intravenous route in one case).[SEP]Relations: Cerebral hemorrhage has relations: disease_phenotype_positive with cocaine intoxication, disease_phenotype_positive with cocaine intoxication. Intracerebral Route of Drug Administration hemorrhage has relations: contraindication with Enoxaparin, contraindication with Enoxaparin, disease_disease with Intracranial Hemorrhage, disease_disease with Intracranial Hemorrhage, contraindication with Hydralazine, contraindication with Hydralazine. Intracranial hemorrhage has relations: drug_effect with Saquinavir, drug_effect with Saquinavir.", "label": "yes"}
+{"original_question": "Can nanoparticles be used for afterglow imaging?", "id": "converted_2626", "sentence1": "Can Artificial nanoparticles be used for afterglow imaging?", "sentence2": "Ultralong Phosphorescence of Water-Soluble Organic Nanoparticles for In Vivo Afterglow Imaging, Afterglow or persistent luminescence eliminates the need for light excitation and thus circumvents the issue of autofluorescence, holding promise for molecular imaging. However, current persistent luminescence agents are rare and limited to Inorganic Artificial Artificial nanoparticles. This study reports the design principle, synthesis, and proof-of-concept application of organic semiconducting Artificial Artificial nanoparticles (OSNs) with ultralong phosphorescence for in vivo afterglow imaging. , This study not only introduces the first category of water-soluble ultralong phosphorescence organic Artificial Artificial nanoparticles but also reveals a universal design principle to prolong the lifetime of phosphorescent molecules to the level that can be effective for molecular imaging.[SEP]Relations: Inorganic anion transport has relations: bioprocess_protein with NMUR2, bioprocess_protein with NMUR2, bioprocess_protein with SLC4A7, bioprocess_protein with SLC4A7, bioprocess_protein with SLC4A5, bioprocess_protein with SLC4A5, bioprocess_protein with SLC22A6, bioprocess_protein with SLC22A6, bioprocess_protein with VDAC1, bioprocess_protein with VDAC1.", "label": "yes"}
+{"original_question": "Is Dicer part of the RISC loading complex?", "id": "converted_856", "sentence1": "Is DICER1 protein, human part of the RNA-Induced Silencing Complex loading complex?", "sentence2": "DICER1 protein, human is a component of the protein machinery (the RNA Induced Silencing Complex [RNA-Induced Silencing Complex]) which is involved in catalyzing the formation of mature microRNAs from their precursors in the process of microRNA biogenesis., RNA-induced silencing complex (RNA-Induced Silencing Complex) Proteins Cyclophosphamide/Doxorubicin/Prednisone/Tamoxifen regimen (Cyclophosphamide/Doxorubicin/Prednisone/Tamoxifen regimen (PACT)), TARBP2P1 gene, and DICER1 protein, human are SRA binding nuclear receptor coregulators., The cytoplasmic RNA-induced silencing complex (RNA-Induced Silencing Complex) contains dsRNA binding proteins, including protein kinase RNA activator (Cyclophosphamide/Doxorubicin/Prednisone/Tamoxifen regimen (Cyclophosphamide/Doxorubicin/Prednisone/Tamoxifen regimen (PACT))), transactivation response RNA-Binding Proteins (TARBP2P1 gene), and DICER1 protein, human, that process pre-microRNAs into mature microRNAs (MicroRNAs) that target specific mRNA species for regulation. ,  Although the major RNAi pathway proteins are found in most subcellular compartments, the miRNA- and siRNA-loaded EIF2C2 protein, human populations co-sediment almost exclusively with the rER membranes, together with the RNA-Induced Silencing Complex loading complex (ITGA9 wt Allele) factors DICER1 protein, human, Thrombocytopenia-Absent Radius Syndrome RNA-Binding Proteins (TARBP2P1 gene) and protein activator of the interferon-induced protein kinase (Cyclophosphamide/Doxorubicin/Prednisone/Tamoxifen regimen (Cyclophosphamide/Doxorubicin/Prednisone/Tamoxifen regimen (PACT)))., RNA interference (RNAi) is mediated by small interfering RNA (siRNAs), which are liberated from double-stranded (ds)RNA precursors by DICER1 protein, human and guide the RNA-induced silencing complex (RNA-Induced Silencing Complex) to targets., . DICER1 protein, human, an RNase III enzyme, plays a central role in the RNAi pathway by cleaving precursors of both of these classes of RNA to form mature siRNAs and MicroRNAs, which are then loaded into the RNA-induced silencing complex (RNA-Induced Silencing Complex). , Canonical siRNAs are 21 Nucleotides (nt) in length and are loaded to the RNA Induced Silencing Complex when introduced into the Cells, while longer siRNA Molecule are first processed by endogenous DICER1 protein, human and thus termed DICER1 protein, human-substrate siRNA (DsiRNA). [SEP]Relations: protein binding has relations: molfunc_protein with DICER1, molfunc_protein with DICER1, molfunc_protein with ECSCR, molfunc_protein with ECSCR, molfunc_protein with RILP, molfunc_protein with RILP, molfunc_protein with TRIR, molfunc_protein with TRIR. chromatin silencing complex has relations: cellcomp_protein with RRP8, cellcomp_protein with RRP8.", "label": "yes"}
+{"original_question": "Autophagy is the process where a virus obtains nutrients from it's host, yes or no?", "id": "converted_3396", "sentence1": "Autophagy is the process where a virus obtains Nutrients from it's host, yes or no?", "sentence2": "In this study, we demonstrate that autophagy is a critical mediator of the viral degradation pathway and that this pathway is not HIV-1 specific., Autophagy is important in cellular homeostasis for the cell survival mechanism., Autophagy is a cellular survival pathway that is necessary for the degradation of cellular constituents such as long-lived proteins and damaged Organelles., Autophagy-related genes (ATGs) regulate the autophagy and also control the crosstalk with autophagy-associated cell death and apoptosis in some condition. , Autophagy is an evolutionarily conserved cellular process in which Protoplasm components are eliminated via lysosomal degradation to supply Nutrients for organelle biogenesis and metabolic homeostasis., Autophagy is a lysosome-associated, degradative process that catabolizes Cytoplasmic matrix components to recycle Nutrients for further use and maintain cell homeostasis., Autophagy is a self-eating process, in which the damaged or excessed cell Organelles and misfolded Protein Info aggregates are removed from the cellular microenvironment., Autophagy is a lysosome-associated, degradative process that catabolizes Cytoplasmic matrix components to recycle Nutrients for further use and maintain cell homeostasis., Autophagy is an evolutionarily conserved cellular process in which Protoplasm components are eliminated via lysosomal degradation to supply Nutrients for organelle biogenesis and metabolic homeostasis., Autophagy is a homeostatic process involved in the turnover or elimination of cytoplasmic components, damaged Organelles, and Protein Info aggregates via a lysosomal degradation mechanism., Autophagy is known as a catabolic process for the recycling of the cytoplasmic macromolecules.[SEP]Relations: Protein C has relations: drug_drug with Ginkgo biloba, drug_drug with Ginkgo biloba, drug_drug with Procarbazine, drug_drug with Procarbazine, drug_drug with Damoctocog alfa pegol, drug_drug with Damoctocog alfa pegol, drug_drug with Moroctocog alfa, drug_drug with Moroctocog alfa, drug_drug with Carbimazole, drug_drug with Carbimazole.", "label": "no"}
+{"original_question": "Is deletion at 6q24.2-26 associated with shorter survival for ovarian cancer patients?", "id": "converted_3714", "sentence1": "Is Gene Deletion Abnormality at 6q24.2-26 associated with shorter survival for ovarian cancer patients?", "sentence2": "Deletion at 6q24.2-26 predicts longer survival of high-grade serous epithelial ovarian cancer patients., Standard treatments for advanced high-grade serous ovarian carcinomas (HGSOCs) show significant side-effects and provide only short-term survival benefits due to disease recurrence. Thus, identification of novel prognostic and predictive biomarkers is urgently needed. We have used 42 paraffin-embedded HGSOCs, to evaluate the utility of DNA copy number alterations, as potential predictors of clinical outcome. Copy number-based unsupervised clustering stratified HGSOCs into two clusters of different immunohistopathological features and survival outcome (HR = 0.15, 95%CI = 0.03-0.81; Padj = 0.03). We found that loss at 6q24.2-26 was significantly associated with the cluster of longer survival independently from other confounding factors (HR = 0.06, 95%CI = 0.01-0.43, Padj = 0.005). The prognostic value of this Gene Deletion Abnormality was validated in two independent series, one consisting of 36 HGSOCs analyzed by fluorescent in situ hybridization (P = 0.04) and another comprised of 411 HGSOCs from the Cancer Genome Atlas study (TCGA) (HR = 0.67, 95%CI = 0.48-0.93, Padj = 0.019). In addition, we confirmed the association of low expression of the Genes from the Geographic Locations with longer survival in 799 HGSOCs (HR = 0.74, 95%CI = 0.61-0.90, log-rank P = 0.002) and 675 high-FIGO stage HGSOCs (HR = 0.76, 95%CI = 0.61-0.96, log-rank P = 0.02) available from the online tool KM-plotter. Finally, by integrating copy number, RNAseq and survival data of 296 HGSOCs from TCGA we propose a few candidate Genes that can potentially explain the association. Altogether our findings indicate that the 6q24.2-26 Gene Deletion Abnormality is an independent marker of favorable outcome in HGSOCs with potential clinical value as it can be analyzed by FISH on tumor sections and guide the selection of patients towards more conservative therapeutic strategies in order to reduce side-effects and improve quality of life., We found that loss at 6q24.2-26 was significantly associated with the cluster of longer survival independently from other confounding factors (HR = 0.06, 95%CI = 0.01-0.43, Padj = 0.005)., OBJECTIVE\n\nWe aimed to evaluate the prognostic and predictive value of the nucleotide excision repair-related gene GTF2H5, which is localized at the 6q24.2-26 Gene Deletion Abnormality previously reported by our group to predict longer survival of high-grade serous ovarian cancer patients., We found that loss at 6q24.2-26 was significantly associated with the cluster of longer survival independently from other confounding factors (HR = 0.06, 95%CI = 0.01-0.43, Padj = 0.005)., OBJECTIVE\nWe aimed to evaluate the prognostic and predictive value of the nucleotide excision repair-related gene GTF2H5, which is localized at the 6q24.2-26 Gene Deletion Abnormality previously reported by our group to predict longer survival of high-grade serous ovarian cancer patients., OBJECTIVE: We aimed to evaluate the prognostic and predictive value of the nucleotide excision repair-related gene GTF2H5, which is localized at the 6q24.2-26 Gene Deletion Abnormality previously reported by our group to predict longer survival of high-grade serous ovarian cancer patients., We aimed to evaluate the prognostic and predictive value of the nucleotide excision repair-related gene GTF2H5, which is localized at the 6q24.2-26 Gene Deletion Abnormality previously reported by our group to predict longer survival of high-grade serous ovarian cancer patients.[SEP]Relations: Abnormality of the dentition has relations: disease_phenotype_positive with chromosome 6pter-p24 Gene Deletion Abnormality syndrome, disease_phenotype_positive with chromosome 6pter-p24 Gene Deletion Abnormality syndrome, disease_phenotype_positive with chromosome 15q24 Gene Deletion Abnormality syndrome, disease_phenotype_positive with chromosome 15q24 Gene Deletion Abnormality syndrome, disease_phenotype_positive with chromosome 8q21.11 Gene Deletion Abnormality syndrome, disease_phenotype_positive with chromosome 8q21.11 Gene Deletion Abnormality syndrome, disease_phenotype_positive with 22q11.2 Gene Deletion Abnormality syndrome, disease_phenotype_positive with 22q11.2 Gene Deletion Abnormality syndrome, disease_phenotype_positive with chromosome 4q21 Gene Deletion Abnormality syndrome, disease_phenotype_positive with chromosome 4q21 Gene Deletion Abnormality syndrome.", "label": "no"}
+{"original_question": "Is triadin involved in cardiac function?", "id": "converted_1360", "sentence1": "Is TRDN gene involved in cardiac function?", "sentence2": "ASPH gene (JCN), a 26-kd Sarcoplasmic Reticulum (SNCG wt Allele) transmembrane protein, forms a quaternary protein complex with the Ryanodine Receptor Calcium Release Channel, CASQ2 gene, and TRDN gene in the SNCG wt Allele lumen of Specimen Source Codes - Cardiac muscle. Within this complex, CASQ2 gene, TRDN gene, and JCN appear to be critical for normal regulation of Ryanodine Receptor Calcium Release Channel-mediated calcium (cyclophosphamide/doxorubicin protocol) release., Recent studies have uncovered functional roles of both JCN and TRDN gene in the mouse heart, using transgenic overexpression strategies, which exhibit varying phenotypes including mild SNCG wt Allele structural alterations, prolongation of cyclophosphamide/doxorubicin protocol transient decay, impaired relaxation, and Cardiac Hypertrophy and/or Congestive Congestive heart failure., Triadin is involved in the regulation of cardiac excitation-contraction coupling. , Thus the maintenance of TRDN gene expression is essential for normal SNCG wt Allele cyclophosphamide/doxorubicin protocol cycling and contractile function., Ca2+ release from the cardiac junctional Sarcoplasmic Reticulum (SNCG wt Allele) is regulated by a complex of proteins, including the Ryanodine Receptor Calcium Release Channel (Ryanodine Receptor Calcium Release Channel complex location), CASQ2 gene (CSQ), ASPH gene-2 (JCN), and TRDN gene 1 (T-Cell Receptors delta-Chain)., Impaired Sarcoplasmic Reticulum (SNCG wt Allele) cyclophosphamide/doxorubicin protocol release has been suggested to contribute to the depressed cardiac function in Congestive Congestive heart failure. The release of cyclophosphamide/doxorubicin protocol from the SNCG wt Allele may be regulated by the Ryanodine Receptor Calcium Release Channel, TRDN gene, ASPH gene-2, CASQ2 gene, and a histidine-rich, cyclophosphamide/doxorubicin protocol-binding protein 2 (HRC).[SEP]Relations: Congestive Congestive heart failure has relations: drug_effect with Tretinoin, drug_effect with Tretinoin, drug_effect with Corticotropin, drug_effect with Corticotropin, drug_effect with Telavancin, drug_effect with Telavancin, drug_effect with Pentostatin, drug_effect with Pentostatin, drug_effect with Pregabalin, drug_effect with Pregabalin.", "label": "yes"}
+{"original_question": "Do honey contain diastases/amylases?", "id": "converted_4190", "sentence1": "Do honey preparation contain diastases/amylases?", "sentence2": "A new rapid method for the determination of honey preparation preparation diastase activity using direct potentiometric principles has been proposed. , The major alpha-amylase in honey preparation preparation was characterized. , Separation of honey preparation preparation amylase[SEP]Relations: alpha-amylase activity has relations: molfunc_protein with AMY1A, molfunc_protein with AMY1A, molfunc_protein with AMY2A, molfunc_protein with AMY2A, molfunc_protein with AMY1C, molfunc_protein with AMY1C, molfunc_protein with AMY2B, molfunc_protein with AMY2B, molfunc_protein with AMY1B, molfunc_protein with AMY1B.", "label": "yes"}
+{"original_question": "Is amantadine ER the first approved treatment for akinesia?", "id": "converted_3608", "sentence1": "Is amantadine ER the first approved treatment for akinesia?", "sentence2": "Extended-release amantadine (amantadine ER) is the first approved medication for the treatment of Dyskinetic syndrome.[SEP]Relations: genetic syndromic Pierre Robin syndrome has relations: disease_disease with tarp syndrome, disease_disease with tarp syndrome, disease_disease with Pierre Robin syndrome associated with branchial archs anomalies, disease_disease with Pierre Robin syndrome associated with branchial archs anomalies, disease_disease with Pierre Robin syndrome associated with bone disease, disease_disease with Pierre Robin syndrome associated with bone disease, disease_disease with Pierre Robin syndrome associated with collagen disease, disease_disease with Pierre Robin syndrome associated with collagen disease, disease_disease with syndrome or malformation associated with head and neck malformations, disease_disease with syndrome or malformation associated with head and neck malformations.", "label": "no"}
+{"original_question": "Is Protoporphyrinogen oxidase localized to the mitochondrium?", "id": "converted_3280", "sentence1": "Is Protoporphyrinogen oxidase localized to the mitochondrium?", "sentence2": "We showed that 28 Antifibrinolytic Antifibrinolytic amino acids in the amino terminus of HCRT wt Allele contain an independently functioning signal for mitochondrial targeting., Based on our results we propose a mechanism for Protoporphyrinogen oxidase targeting to the mitochondrion., Mitochondrial Inheritance Inheritance targeting of human Protoporphyrinogen oxidase., In the present study, PfPPO has been cloned, expressed and shown to be localized to the mitochondrion by immunofluorescence microscopy. [SEP]Relations: Mitochondrial Inheritance inheritance has relations: disease_phenotype_positive with mitochondrial myopathy with reversible cytochrome C oxidase deficiency, disease_phenotype_positive with mitochondrial myopathy with reversible cytochrome C oxidase deficiency, disease_phenotype_positive with cytochrome-c oxidase deficiency disease, disease_phenotype_positive with cytochrome-c oxidase deficiency disease, disease_phenotype_positive with striatonigral degeneration, disease_phenotype_positive with striatonigral degeneration, disease_phenotype_positive with ophthalmoplegic neuromuscular disorder with abnormal mitochondria, disease_phenotype_positive with ophthalmoplegic neuromuscular disorder with abnormal mitochondria, disease_phenotype_positive with Kearns-Sayre syndrome, disease_phenotype_positive with Kearns-Sayre syndrome.", "label": "yes"}
+{"original_question": "Is TIAM1 favoring tumor progression in colorectal cancer (CRC)?", "id": "converted_2851", "sentence1": "Is TIAM1 favoring tumor progression in colorectal cancer (Conditionally Reprogrammed Cells)?", "sentence2": "Here, we identify TIAM1 as a critical antagonist of Conditionally Reprogrammed Cells progression through inhibiting TAFAZZIN gene and YY1AP1 gene, effectors of WNT signaling. We demonstrate that TIAM1 shuttles between the Cytoplasm and Cell Nucleus antagonizing TAFAZZIN gene/YY1AP1 gene by distinct mechanisms in the two compartments. In the Cytoplasm, TIAM1 localizes to the destruction complex and promotes TAFAZZIN gene degradation by enhancing its interaction with βTrCP. Nuclear TIAM1 suppresses TAFAZZIN gene/YY1AP1 gene interaction with TEADs, inhibiting expression of TAFAZZIN gene/YY1AP1 gene target genes implicated in epithelial-mesenchymal transition, cell migration, and invasion, and consequently suppresses Conditionally Reprogrammed Cells cell migration and invasion. Importantly, high nuclear TIAM1 in clinical specimens associates with increased Conditionally Reprogrammed Cells patient survival. Together, our findings suggest that in Conditionally Reprogrammed Cells TIAM1 suppresses tumor progression by regulating YY1AP1 gene/TAFAZZIN gene activity., Together, our findings suggest that in Conditionally Reprogrammed Cells TIAM1 suppresses tumor progression by regulating YY1AP1 gene/TAFAZZIN gene activity., Nuclear TIAM1 suppresses TAFAZZIN gene/YY1AP1 gene interaction with TEADs, inhibiting expression of TAFAZZIN gene/YY1AP1 gene target genes implicated in epithelial-mesenchymal transition, cell migration, and invasion, and consequently suppresses Conditionally Reprogrammed Cells cell migration and invasion., Using an orthotopic xenograft model in nude mice, we confirmed that TIAM1 protein, human silencing could reduce tumor growth by subcutaneous injection and could suppress Chest>Lung and liver metastases of colorectal cancer cells., Together, our findings suggest that in Conditionally Reprogrammed Cells TIAM1 suppresses tumor progression by regulating YY1AP1 gene/TAFAZZIN gene activity.<br>[SEP]Relations: Cytoplasm has relations: cellcomp_protein with TIA1, cellcomp_protein with TIA1, cellcomp_protein with TIAL1, cellcomp_protein with TIAL1, cellcomp_protein with CRTC1, cellcomp_protein with CRTC1, cellcomp_protein with HERC1, cellcomp_protein with HERC1, cellcomp_protein with CR1L, cellcomp_protein with CR1L.", "label": "no"}
+{"original_question": "Is insulin-like growth factor-I (IGF-I) able to affect tendon protein synthesis in classic Ehlers-Danlos syndrome patients?", "id": "converted_764", "sentence1": "Is Insulin-Like Growth Factor I (IGF-I) able to affect tendon protein synthesis in classic Ehlers-Danlos syndrome patients?", "sentence2": "Tendon protein synthesis rate in classic Ehlers-Danlos patients can be stimulated with Insulin-Like Growth Factor I, IGF-I injections significantly increased Flexed Sidebent Rotated values in Autoimmune Lymphoproliferative Syndrome Type 2B patients but not in controls, In conclusion, baseline protein synthesis rates in Connective Tissue appeared normal in Autoimmune Lymphoproliferative Syndrome Type 2B patients, and the patients responded with an increased tendon protein synthesis rate to IGF-I injections, In conclusion, baseline protein synthesis rates in Connective Tissue appeared normal in Autoimmune Lymphoproliferative Syndrome Type 2B patients, and the patients responded with an increased tendon protein synthesis rate to IGF-I injections, IGF-I injections significantly increased Flexed Sidebent Rotated values in Autoimmune Lymphoproliferative Syndrome Type 2B patients but not in controls (delta values: Autoimmune Lymphoproliferative Syndrome Type 2B 0[SEP]Relations: insulin-like growth factor I binding has relations: molfunc_protein with IGF1R, molfunc_protein with IGF1R, molfunc_protein with IGFBP4, molfunc_protein with IGFBP4, molfunc_protein with IGFBP3, molfunc_protein with IGFBP3, molfunc_protein with IGFBP1, molfunc_protein with IGFBP1, molfunc_protein with IGFBP5, molfunc_protein with IGFBP5.", "label": "yes"}
+{"original_question": "Is AND-1/Ctf4 essential for proliferation?", "id": "converted_3544", "sentence1": "Is WDHD1 gene/Ctf4 essential for proliferation?", "sentence2": "WDHD1 gene fork protection function prevents fork resection and is essential for proliferation., WDHD1 gene/Ctf4 bridges the CASK gene helicase and DNA Polymerase I, facilitating replication. Using an inducible degron system in avian Cells, we find that WDHD1 gene depletion is incompatible with proliferation, owing to Cells accumulating in G2 with activated DNA damage checkpoint. Replication without WDHD1 gene causes fork speed slow-down and accumulation of long single-stranded DNA (ssDNA) gaps at the replication fork junction, with these regions being converted to DNA double strand breaks (DSBs) in G2. Strikingly, resected forks and DNA damage accumulation in G2, but not fork slow-down, are reverted by treatment with 6-(4-hydroxyphenyl)-2-thioxo-2,3-dihydro-4(1H)-pyrimidinone, an MRE11 nuclease inhibitor. Domain analysis of WDHD1 gene further revealed that the HMG Domain is important for fast replication but not for proliferation, whereas conversely, the WD40 Repeats prevents fork resection and subsequent DSB-associated lethality. Thus, our findings uncover a fork protection function of WDHD1 gene/Ctf4 manifested via the WD40 Repeats that is essential for proliferation and averts genome instability., Thus , our findings uncover a fork protection function of WDHD1 gene/Ctf4 manifested via the WD40 Repeats that is essential for proliferation and averts genome instability, Thus, our findings uncover a fork protection function of WDHD1 gene/Ctf4 manifested via the WD40 Repeats that is essential for proliferation and averts genome instability.[SEP]Relations: HMG Domain Superkingdom (taxonomic category) binding has relations: molfunc_protein with TCF12, molfunc_protein with TCF12, molfunc_protein with SP1, molfunc_protein with SP1, molfunc_protein with POU3F3, molfunc_protein with POU3F3, molfunc_protein with ALX4, molfunc_protein with ALX4, molfunc_protein with EGR2, molfunc_protein with EGR2.", "label": "yes"}
+{"original_question": "Is the PINES framework being used for the prediction of coding variants?", "id": "converted_2790", "sentence1": "Is the PINES framework being used for the prediction of coding variants?", "sentence2": "PINES: phenotype-informed tissue weighting improves prediction of pathogenic noncoding variants., Here, we introduce the computational framework PINES (Phenotype-Informed Noncoding Element Scoring), which predicts the functional impact of noncoding variants by integrating epigenetic annotations in a phenotype-dependent manner. PINES enables analyses to be customized towards genomic annotations from cell types of the highest relevance given the phenotype of interest. We illustrate that PINES identifies functional noncoding variation more accurately than methods that do not use phenotype-weighted knowledge, while at the same time being flexible and easy to use via a dedicated web portal., Here, we introduce the computational framework PINES (Phenotype-Informed Noncoding Element Scoring), which predicts the functional impact of noncoding variants by integrating epigenetic annotations in a phenotype-dependent manner., We illustrate that PINES identifies functional noncoding variation more accurately than methods that do not use phenotype-weighted knowledge, while at the same time being flexible and easy to use via a dedicated web portal.<br>, PINES enables analyses to be customized towards genomic annotations from cell types of the highest relevance given the phenotype of interest.[SEP]", "label": "no"}
+{"original_question": "Is phospholamban a regulatory/inhibitory protein of the Ca ATPase SERCA?", "id": "converted_509", "sentence1": "Is PLN gene a regulatory/inhibitory protein of the cyclophosphamide/doxorubicin protocol ATPase SERCA?", "sentence2": "The Membrane Proteins complex between the Sarcoplasmic Reticulum cyclophosphamide/doxorubicin protocol(2+)-ATPase (SERCA) and PLN gene (PLN) controls cyclophosphamide/doxorubicin protocol(2+) transport in Myocytes, Cardiac, thereby modulating Cardiac - anatomy qualifier contractility. β-Adrenergic-stimulated phosphorylation of PLN at Ser-16 enhances SERCA activity via an unknown mechanism., PLN gene (PLN) is a type II Membrane Proteins that inhibits the Sarcoplasmic Reticulum cyclophosphamide/doxorubicin protocol(2+)-ATPase (SERCA), thereby regulating calcium homeostasis in Cardiac - anatomy qualifier muscle. In Tissue Membrane Device, PLN forms pentamers that have been proposed to function either as a storage for active monomers or as ion channels., Regulation of the SERCA calcium pump by PLN gene (PLB1 gene) is largely due to interactions between their respective transmembrane domains. In spite of numerous Mutagenesis Procedure and kinetic studies, we still do not have a clear mechanistic picture of how PLB1 gene influences the calcium transport cycle of SERCA., Calcium transport across the Membrane Device of the Sarcoplasmic Reticulum (SNCG wt Allele) plays an important role in the regulation of Myocardium contraction and relaxation. The sarco(endo)plasmic reticulum cyclophosphamide/doxorubicin protocol(2+) ATPase (SERCA) 2a is responsible for cyclophosphamide/doxorubicin protocol(2+) up-take by this Cytoplasmic Cytoplasmic organelle and is inhibited in a reversible manner by PLN gene, another SNCG wt Allele Membrane Proteins. Thus, alleviation of PLN gene-mediated inhibition of SERCA2a is a potential therapeutic option for Congestive Congestive heart failure and Cardiomyopathies., PLN gene has been suggested to be a key regulator of Cardiac - anatomy qualifier Sarcoplasmic Reticulum (SNCG wt Allele) cyclophosphamide/doxorubicin protocol cycling and contractility and a potential therapeutic target in restoring the depressed cyclophosphamide/doxorubicin protocol cycling in failing hearts., In larger Mammals, a higher fraction of SERCA2a pumps are regulated by PLN gene, and this may influence therapeutic strategies to enhance Cardiac - anatomy qualifier contractility and functional Cardiac - anatomy qualifier reserve., PLN gene (PLB1 gene) inhibits the Sarcoplasmic Reticulum (SNCG wt Allele) cyclophosphamide/doxorubicin protocol(2+)-ATPase (SERCA), and this inhibition is relieved by cyclophosphamide/doxorubicin protocol(2+) calmodulin-dependent protein kinase II (calmodulin-dependent protein kinase II) phosphorylation, These findings suggest that PLB1 gene is an important modulator of gastric antrum Smooth muscle (tissue) contractility by modulation of SNCG wt Allele cyclophosphamide/doxorubicin protocol(2+) release and calmodulin-dependent protein kinase II activity., The function of the SERCA pump is modulated by the endogenous molecules PLN gene (PLB1 gene) and sarcolipin (SLN gene gene), expressed in Cardiac - anatomy qualifier and Skeletal muscle structure. The mechanism of action of PLB1 gene on SERCA is well characterized, whereas that of SLN gene gene is only beginning to be understood. ,  PLN gene (PLB1 gene) is an inhibitor of the Sarcoplasmic Reticulum (SNCG wt Allele) Ca2+-ATPase (SERCA)., These results show that alteration of the PLB1 gene:SERCA ratio can significantly modulate Smooth muscle (tissue) [Ca2+]i., PLN gene expressed in Cardiac - anatomy qualifier muscle and sarcolipin expressed in Specimen Source Codes - Skeletal muscle regulate SERCA activity., PLN gene (PLB1 gene) is a 24- to 27-kDa phosphoprotein that modulates activity of the sarco(endo)plasmic reticulum Ca2+ ATPase (SERCA). Expression of PLB1 gene is reportedly limited to Cardiac - anatomy qualifier, slow-twitch skeletal and Smooth muscle (tissue) in which PLB1 gene is an important regulator of [Ca2+]i and contractility in these Muscle Tissue., Regulation of the sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA 2a) depends on the phosphorylation state of PLN gene (PLB1 gene). When PLB1 gene is phosphorylated, its inhibitory effect towards SERCA 2a is relieved, leading to an enhanced myocardial performance. ,  cyclophosphamide/doxorubicin protocol(2+) reuptake occurs via sarcoendoplasmic reticulum cyclophosphamide/doxorubicin protocol(2+) ATPase (SERCA) and is regulated by the inhibitory protein PLN gene (PLB1 gene) in many cell types., PLN gene (PLN) is a small integral Membrane Proteins, which binds and inhibits in a yet unknown fashion the cyclophosphamide/doxorubicin protocol(2+)-ATPase (SERCA) in the Sarcoplasmic Reticulum., PLN gene (PLN) is the endogenous inhibitor of the sarco(endo)plasmic reticulum cyclophosphamide/doxorubicin protocol(2+)-ATPase (SERCA), the integral Membrane Device enzyme responsible for 70�% of the removal of cyclophosphamide/doxorubicin protocol(2+) from the Cytoplasmic matrix, inducing Cardiac - anatomy qualifier muscle relaxation in Homo sapiens., PLN gene (PLB1 gene) is an integral Membrane Proteins regulating cyclophosphamide/doxorubicin protocol(2+) transport through inhibitory interaction with sarco(endo)plasmic reticulum calcium ATPase (SERCA)., Phosphorylation by Cyclic AMP-Dependent Protein Kinases and dephosphorylation by Protein phosphatase modulate the inhibitory activity of PLN gene (PLN), the endogenous regulator of the sarco(endo)plasmic reticulum calcium cyclophosphamide/doxorubicin protocol(2+) ATPase (SERCA)., Phosphorylation by Cyclic AMP-Dependent Protein Kinases and dephosphorylation by Protein phosphatase modulate the inhibitory activity of PLN gene (PLN), the endogenous regulator of the sarco(endo)plasmic reticulum calcium cyclophosphamide/doxorubicin protocol(2+) ATPase (SERCA), We used EPR spectroscopy to probe directly the interaction between PLN gene (PLB1 gene) and its regulatory target, the Sarcoplasmic Reticulum cyclophosphamide/doxorubicin protocol-ATPase (SERCA)[SEP]Relations: phosphoprotein phosphatase activity has relations: molfunc_protein with PPP2CA, molfunc_protein with PPP2CA, molfunc_protein with PPP1CA, molfunc_protein with PPP1CA, molfunc_protein with PTEN, molfunc_protein with PTEN, molfunc_protein with PPP5C, molfunc_protein with PPP5C. Membrane Device has relations: cellcomp_protein with CACNB3, cellcomp_protein with CACNB3.", "label": "yes"}
+{"original_question": "Has FTY720  been considered for the treatment of stroke?", "id": "converted_4229", "sentence1": "Has FTY-720  been considered for the treatment of Cerebrovascular accident?", "sentence2": "FTY-720 (fingolimod) Ameliorates Brain Injuries through Multiple Mechanisms and is a Strong Candidate for Stroke Treatment, Many researchers have recognized the positive effects of FTY-720 and launched basic and clinical experiments to test the use of this agent against Cerebrovascular accident. Although the mechanism of FTY-720 has not been fully elucidated, its efficacy against cerebral Cerebrovascular accident is becoming clear, not only in animal models, but also in ischemic Cerebrovascular accident patients through clinical trials. In this article, we review the data obtained from laboratory findings and preliminary clinical trials using FTY-720 for Cerebrovascular accident treatment.[SEP]Relations: brain injury has relations: contraindication with Dexchlorpheniramine, contraindication with Dexchlorpheniramine, contraindication with Pheniramine, contraindication with Pheniramine, contraindication with Dicyclomine, contraindication with Dicyclomine, contraindication with Difenoxin, contraindication with Difenoxin, contraindication with Chlorpheniramine, contraindication with Chlorpheniramine.", "label": "yes"}
+{"original_question": "Does radiotherapy for cervical cancer increases risk of colon cancer?", "id": "converted_3782", "sentence1": "Does radiotherapy for Malignant tumor of cervix increases risk of Malignant tumor of Abdomen+Pelvis>Colon?", "sentence2": "After 8 years, the hazard ratio for developing Malignant tumor of Abdomen+Pelvis>Colon was 2.00 (95% CI 1.43-2.80) for women with radiation versus those without radiation treatment., After 35 years of follow-up, the absolute risk of developing Malignant tumor of Abdomen+Pelvis>Colon was 6.5% for those who received radiation versus 2.5% for those without, and 3.7 versus 0.8% for Pelvis>Rectum. The risk of Abdomen+Pelvis>Colon and Rectal Carcinoma over 20 years of follow-up after radiation remained the same across three eras (1973-1980, 1981-1990, and 1991-2000). Radiation-induced second Malignant Neoplasms of the Abdomen+Pelvis>Colon and Pelvis>Rectum may occur 8 years after radiation treatment for Malignant tumor of cervix., The data suggested that high-dose pelvic irradiation was associated with increase in Malignant Neoplasms of the Urinary Bladder, Both Both kidneys, Pelvis>Rectum, Both Both ovaries, corpus uteri, and Non-Hodgkin's lymphoma of bone but, apparently, not leukemia, Hodgkin Disease, Malignant neoplasm of breast, or Malignant tumor of Abdomen+Pelvis>Colon., Radiation-induced second Malignant Neoplasms of the Abdomen+Pelvis>Colon and Pelvis>Rectum may occur 8 years after radiation treatment for Malignant tumor of cervix., Cervical cancer patients treated with radiotherapy, but not those who did not receive radiotherapy, were at increased risk for all second Malignant Neoplasms and Malignant Neoplasms at heavily irradiated sites (Abdomen+Pelvis>Colon, Rectum/Anus, urinary Urinary Bladder, Pelvis>Ovary, and genital sites) beyond 40 years of follow-up compared with women in the general population. [SEP]Relations: malignant germ cell tumor of cervix uteri has relations: disease_disease with Malignant tumor of cervix, disease_disease with Malignant tumor of cervix. malignant tumor of neck has relations: disease_disease with head and neck cancer, disease_disease with head and neck cancer, disease_disease with pharynx cancer, disease_disease with pharynx cancer. rectal carcinoma has relations: disease_disease with rectal cancer, disease_disease with rectal cancer. malignant ear neoplasm has relations: disease_disease with head and neck cancer, disease_disease with head and neck cancer.", "label": "yes"}
+{"original_question": "Is Bobble head doll syndrome associated with hydrocephalus?", "id": "converted_2781", "sentence1": "Is Bobble head doll syndrome associated with hydrocephalus?", "sentence2": "The first is a 14-year-old boy with BHDS associated with aqueductal obstruction and triventricular hydrocephalus secondary to a tectal tumor., Brain magnetic resonance imaging showed a large suprasellar Arachnoid Cysts extending into the third ventricle, with Obstructive Hydrocephalus, characteristic of Bobble-head doll syndrome. , MRI Scan showed a large contrast-enhanced lesion in the region of the third ventricle along with gross hydrocephalus. , Bobble-head doll syndrome is usually associated with dilation of the third ventricle, but is rarely associated with posterior fossa disease.PATIENT: We describe an infant with fetal hydrocephalus and an Arachnoid Cysts of the posterior fossa., All the patients presented a No No psychomotor retardation due to an Obstructive Hydrocephalus. , Suprasellar arachnoid cysts can have varied presentations with signs and symptoms of Obstructive Hydrocephalus, Visual Impairment, endocrinal dysfunction, Gait Ataxia and rarely bobble-head doll movement., We present three cases with Bobble-head doll syndrome associated with a large suprasellar Arachnoid Cysts and Obstructive Hydrocephalus, which were treated with endoscopic cystoventriculocisternostomy and marsupialization of the Specimen Source Codes - Cyst.[SEP]Relations: Bobble-head doll syndrome has relations: disease_disease with syndromic disease, disease_disease with syndromic disease. Obstructive Hydrocephalus has relations: disease_disease with hydrocephalus, disease_disease with hydrocephalus, disease_protein with CRPPA, disease_protein with CRPPA, disease_protein with SIN3A, disease_protein with SIN3A. Arachnoid Specimen Source Codes - Cyst has relations: disease_phenotype_positive with hydrocephalus-costovertebral dysplasia-Sprengel anomaly syndrome, disease_phenotype_positive with hydrocephalus-costovertebral dysplasia-Sprengel anomaly syndrome.", "label": "yes"}
+{"original_question": "Is lenvatinib effective for renal cell carcinoma?", "id": "converted_1982", "sentence1": "Is lenvatinib effective for renal cell carcinoma?", "sentence2": "However, the combination of lenvatinib, a multitargeted agent that inhibits Vascular Endothelial Growth Factor A as well as Fibroblast Growth Factor Receptors, and everolimus demonstrated promising results in a randomized phase II trial. , The FDA has approved the combination of lenvatinib and everolimus to treat advanced or Metastatic Renal Cell Carcinoma., Moreover, a recent Phase II study demonstrated a significant benefit for the second-line combination treatment with everolimus plus lenvatinib (a novel TKI) in terms of progression-free survival and overall survival compared to the single-agent everolimus., We then discuss two recently approved Growth Factor Receptors antagonists i.e. cabozantinib and lenvatinib, and a recently approved checkpoint inhibitor, nivolumab, and issues pertaining to drug development, and future directions in treatment of metastatic RCC. , INTERPRETATION: lenvatinib plus everolimus and lenvatinib alone resulted in a progression-free survival benefit for patients with Metastatic Renal Cell Carcinoma who have progressed after one previous Vascular Endothelial Growth Factor A-targeted therapy. , lenvatinib therapy for the treatment of patients with advanced renal cell carcinoma., lenvatinib therapy for the treatment of patients with advanced renal cell carcinoma.[SEP]Relations: lenvatinib has relations: drug_drug with Carbamazepine, drug_drug with Carbamazepine, drug_drug with Carbimazole, drug_drug with Carbimazole, drug_drug with Carfilzomib, drug_drug with Carfilzomib, drug_drug with Carbinoxamine, drug_drug with Carbinoxamine, drug_drug with Carbutamide, drug_drug with Carbutamide.", "label": "yes"}
+{"original_question": "Is butterfly rash a symptom of Systemic lupus erythematosus?", "id": "converted_1965", "sentence1": "Is butterfly rash a symptom of Lupus Erythematosus, Systemic?", "sentence2": "Diagnosing Systematic Light Exposure can be challenging because of the myriad of clinical features and substantial variability between patients. Cutaneous involvement is present in about 60% of cases and typically manifests as a Zygomatic bone or butterfly rash., The prevalence of systemic lupus erythematosus (Systematic Light Exposure) is 28 per 100,000. , We report a 12 years old female patient with an overlap syndrome involving Autoimmune Chronic Hepatitis (Autoimmune hepatitis) and systemic lupus erythematosus (Systematic Light Exposure). The patient presented with jaundice, Hepatosplenomegaly, malaise, Polyarthralgia, Arthritis and butterfly rash on the face., Some of the clinical characteristics of Systematic Light Exposure patients observed were Nephritis (53.7%), Fever symptoms (finding) (53.26%), neuropsychological disorder (36.18%), Zygomatic bone/butterfly rash (27.6%), Lung diseases (22.6%), Photosensitivity of Skin Specimen Source Code (21.6%), cardiac involvement (21.1%) and Oral Ulcer (19.09%). , Lupus Erythematosus, Systemic and Infections of musculoskeletal system: a retrospective study in Saudis., The prevalence of the following manifestations was significantly higher for pediatric than for adult-onset disease including: lupus Nephritis (43% pediatric vs 26.4% for adult-onset), Hematological Disease (57% vs 36.4%), Photosensitivity of Skin Specimen Source Code (20% vs 9%), butterfly rash (61% vs 35.5%) and mucosal ulceration (11.4% vs 4%). , Lupus Erythematosus, Systemic (Systematic Light Exposure) is a multifactorial Autoimmune Diseases with highest prevalence among women of childbearing age. , We described a unique case of a 25-year-old Arab young woman who was diagnosed with Systematic Light Exposure, depending on clinical, laboratory investigations and after she had fulfilled the diagnostic criteria for Systematic Light Exposure and had presented the following findings: constitutional findings (Fatigue, Fever symptoms (finding), and Arthralgia); dermatologic finding (Photosensitivity of Skin Specimen Source Code and butterfly rash); Kidney Failure, Chronic (Proteinuria up to 400 mg in 24 hours); Hematologic and antinuclear antibodies (positivity for antinuclear factor (Atrial Natriuretic Factor), anti-double-stranded DNA antibodies, direct Coombs, Antibodies, Antinuclear and Antibodies, Anti-DNA, low C4 and C3 innervation innervation, Anterior Cranial Cruciate Ligament by immunoglobulin G and Immunoglobulin M). , Grade 1 and 2-3 inflammatory process occurred in 53 (63%) and 31 (37%) patients respectively. Symptom complexes \"systemic inflammation\", \"butterfly rash\", \"wrist petechiae\", \"enanthema of the oral mucous membrane\", and other Lesion were regarded as the markers of Systematic Light Exposure activity. , Lupus Erythematosus, Systemic (Systematic Light Exposure) remains a challenging medical problem. , Rembrandt's Maria Bockenolle has a butterfly rash and digital deformities: overlapping syndrome of Rheumatoid Arthritis and systemic lupus erythematosus., A butterfly rash on the patient's face suggested a diagnosis of systemic lupus erythematosus (Systematic Light Exposure)., A butterfly rash on the patients face suggested a diagnosis of systemic lupus erythematosus (Systematic Light Exposure), The diagnosis of Systematic Light Exposure could be excluded and the butterfly rash attributed to a laminar hemorrhage, an Skin Bruise due to the Immune thrombocytopenic purpura., We describe a case of KD who developed a typical butterfly rash, reminiscent of Systematic Light Exposure. , The diagnosis of Systematic Light Exposure was made 22 years ago based on Raynaud's phenomenon, butterfly rash, Alopecia, Photosensitivity of Skin Specimen Source Code and positive antinuclear antibody. , Symptom complexes \"systemic inflammation\", \"butterfly rash\", \"wrist petechiae\", \"enanthema of the oral mucous membrane\", and other Lesion were regarded as the markers of Systematic Light Exposure activity., Rembrandt's Maria Bockenolle has a butterfly rash and digital deformities: overlapping syndrome of Rheumatoid Arthritis and systemic lupus erythematosus., To investigate, various unspecific, but otherwise typical clinical symptoms of Skin Specimen Source Code and Mucous Membrane that arise in Systematic Light Exposure patients other than those defined as Systematic Light Exposure criteria such as butterfly rash, Chronic discoid lupus erythematosus, Oral Ulcer, and increased Photosensitivity of Skin Specimen Source Code.[SEP]Relations: bullous systemic lupus erythematosus has relations: disease_disease with lupus erythematosus, disease_disease with lupus erythematosus, disease_disease with systemic lupus erythematosus (disease), disease_disease with systemic lupus erythematosus (disease). Arthritis has relations: disease_phenotype_positive with pediatric systemic lupus erythematosus, disease_phenotype_positive with pediatric systemic lupus erythematosus. Nephritis has relations: disease_phenotype_positive with pediatric systemic lupus erythematosus, disease_phenotype_positive with pediatric systemic lupus erythematosus. discoid lupus erythematosus has relations: disease_disease with noninfectious dermatoses of eyelid, disease_disease with noninfectious dermatoses of eyelid.", "label": "yes"}
+{"original_question": "Do raspberries improve postprandial glucose and acute and chronic inflammation in adults with type 2 Diabetes?", "id": "converted_2930", "sentence1": "Do raspberries improve postprandial glucose and acute and chronic inflammation in adults with type 2 Diabetes?", "sentence2": "The NLR family pyrin domain containing 3 (NLRP3) inflammasome plays a critical role in insulin resistance and the pathogenesis of type 2 diabetes. Red raspberry (Retinoblastoma) contains high amounts of Dietary Fiber and polyphenolic compounds, which are known for their anti-oxidative and anti-inflammatory effects. [SEP]Relations: retinoblastoma has relations: disease_phenotype_positive with Reduced visual acuity, disease_phenotype_positive with Reduced visual acuity, disease_protein with RB1, disease_protein with RB1, disease_phenotype_positive with Ewing sarcoma, disease_phenotype_positive with Ewing sarcoma, disease_phenotype_positive with Subretinal pigment epithelium hemorrhage, disease_phenotype_positive with Subretinal pigment epithelium hemorrhage, disease_phenotype_positive with Hypopyon, disease_phenotype_positive with Hypopyon.", "label": "yes"}
+{"original_question": "Does MC1R palmitoylation reduce pigmentation?", "id": "converted_2598", "sentence1": "Does Melanocyte-Stimulating Hormone Receptor, human palmitoylation reduce pigmentation?", "sentence2": "The Receptor, Melanocortin, Type 1 (Melanocyte-Stimulating Hormone Receptor, Homo sapiens), a G-Protein-Coupled Receptors, has a crucial role in Homo sapiens and Mus sp. pigmentation. Activation of Melanocyte-Stimulating Hormone Receptor, Homo sapiens in melanocyte by α-melanocyte-stimulating hormone (α-MSH) stimulates cAMP signalling and melanin production and enhances DNA repair after Ultra-violet irradiation. , Melanocyte-Stimulating Hormone Receptor, Homo sapiens palmitoylation, primarily mediated by the protein-acyl transferase ZDHHC13, is essential for activating Melanocyte-Stimulating Hormone Receptor, Homo sapiens signalling, which triggers increased pigmentation, Ultra-violet-B-induced G1-like cell cycle arrest and control of senescence and melanomagenesis in vitro and in vivo., The results highlight a central role for Melanocyte-Stimulating Hormone Receptor, Homo sapiens palmitoylation in pigmentation and protection against Melanocytic neoplasm.[SEP]Relations: melanocyte-stimulating hormone receptor activity has relations: molfunc_protein with Melanocyte-Stimulating Hormone Receptor, human, molfunc_protein with Melanocyte-Stimulating Hormone Receptor, human, molfunc_protein with MC3R, molfunc_protein with MC3R, molfunc_protein with MC4R, molfunc_protein with MC4R. melanocyte adhesion has relations: bioprocess_protein with KIT, bioprocess_protein with KIT. type 1 melanocortin receptor binding has relations: molfunc_protein with MRAP2, molfunc_protein with MRAP2.", "label": "no"}
+{"original_question": "Do cephalopods use RNA editing less frequently than other species?", "id": "converted_2307", "sentence1": "Do Cephalopoda use RNA Editing less frequently than other species?", "sentence2": "Extensive messenger RNA Editing generates transcript and Protein Info diversity in Genes involved in Neural excitability, as previously described, as well as in Genes participating in a broad range of other cellular functions, By adopting a method originally designed to detect linkage disequilibrium of DNA mutations, we examined the editomes of ten metazoan species and detected extensive linkage of editing in Drosophila <basidiomycetes> <basidiomycetes> and Cephalopoda., We here show that RNA Editing is particularly common in behaviorally sophisticated coleoid Cephalopoda, with tens of thousands of evolutionarily conserved sites., Even for the subset of RNA Editing sites shared by deeply divergent cephalopod lineages, the primary effect of nuclear editing is an increase-not a decrease-in Protein Info divergence., Coleoid Cephalopoda (octopus, Superconducting Quantum Interference Device and Cuttlefish, Dietary) are active, resourceful predators with a rich behavioural repertoire., We identified hundreds of cephalopod-specific Genes, many of which showed elevated expression levels in such specialized structures as the Skin Specimen Source Code, the Suction Tips and the nervous system., Our analysis suggests that substantial expansion of a handful of gene families, along with extensive remodelling of Genome - anatomical entity linkage and repetitive content, played a critical role in the evolution of cephalopod morphological innovations, including their large and complex nervous systems.[SEP]Relations: Protein C has relations: drug_drug with Cephaloglycin, drug_drug with Cephaloglycin, drug_drug with Cephalexin, drug_drug with Cephalexin, drug_drug with Cefamandole, drug_drug with Cefamandole, drug_drug with Cefmetazole, drug_drug with Cefmetazole, drug_drug with Cefamandole nafate, drug_drug with Cefamandole nafate.", "label": "no"}
+{"original_question": "Is there an association between c-reactive protein concentrations and outcomes of subarachnoid hemorrhage patients? ", "id": "converted_1383", "sentence1": "Is there an association between c-reactive protein concentrations and outcomes of Subarachnoid Hemorrhage patients? ", "sentence2": "Besides the baseline characteristics, daily interleukin-6 (Recombinant Interleukin-6), procalcitonin, C-reactive protein levels, and leukocyte counts were prospectively measured until day 14 after Subarachnoid Hemorrhage. Occurrence of infectious complications and application of therapeutic Hypothermia due to exposure were assessed as confounding factors. The primary end point was outcome after 3 months, assessed by Glasgow Outcome Scale; the secondary end point was the occurrence of DINDs. RESULTS: : During a 3-year period, a total of 138 patients were included. All inflammatory parameters measured were higher in patients with unfavorable outcome (Glasgow Outcome Scale score, 1-3)., Twenty-three and 28 patients showed poor outcome and symptomatic Vasospasm after Yakut language, respectively. Both preoperative and postoperative CRP levels were significantly higher in patients with a poor outcome compared with patients with a good outcome (P<0.05)., e area under the receiver operating characteristic curve of CRP measured on postoperative day 1 or 2 (CRP POD1-2) for predicting a poor clinical outcome was 0.870, and its cutoff point of 4 mg/dL had a sensitivity of 0.826 and a specificity of 0.843., A high CRP level after Aneurysm treatment was associated with severe Progressive neurologic deterioration on admission, Cerebral Infarction, Cerebral Hemorrhage, and surgical decompression (P<0.05)., CRP POD1-2, and not the preoperative CRP, was an independent factor in predicting symptomatic Vasospasm (P<0.05). In patients with symptomatic Vasospasm, an increase in the postoperative CRP was associated with the time profile of developing symptomatic Vasospasm., Postoperative CRP, especially CRP POD1-2, can be a useful prognostic factor for both poor outcome and symptomatic Vasospasm in patients with aneurysmal Yakut language., Serum CRP levels were related to severity of ASAH1 wt Allele. Patients with lower GCS scores and higher Hunt and Hess and Fisher grades presented statistically significant higher serum CRP levels. Patients with higher serum CRP levels had a less favorable prognosis., Increased serum CRP levels were strongly associated with worse clinical prognosis in this study., After Yakut language, the value of C-reactive protein (CRP)--an acute phase sensitive inflammatory marker--as a prognostic factor has been poorly studied, with conflicting results., Admission (18.0 ± 35.7 vs 8.5 ± 8.4 mg/l) and postoperative (41.0 ± 40.2 vs 21.1 ± 24.1 mg/l) CRP levels were higher (p < 0.001) in those with a poor outcome than in those with a favourable outcome, but CRP values did not predict delayed cerebral ischaemia or Cerebral Infarction., Higher increase in CRP level between admission and postoperative morning, however, independently predicted poor outcome (p = 0.004)., CRP levels correlate with outcome but do not seem to predict delayed cerebral ischaemia or Infarction after Yakut language., Systemic oxygen consumption is associated with hsCRP levels in the first 14 days after Yakut language and is an independent predictor of Noninfiltrating Intraductal Carcinoma., Intracranial hypertension was associated with an inflammatory response, indicating activation of the inflammatory cascade in the Head>Brain (ECF) and systemic circulation with high Recombinant Interleukin-6 and C-reactive protein (CRP) plasma levels after Yakut language, the latter associated with unfavourable outcome., Patients with angiographic Vasospasm had higher CRP measurements in serum and Cerebrospinal Fluid, in a statistically significant fashion (p < 0.0001). Additionally, patients with higher CRP levels in serum and Cerebrospinal Fluid had less favorable outcome in this cohort., Furthermore, patients developing angiographically proven Vasospasm demonstrated significantly elevated CRP levels in serum and Cerebrospinal Fluid, and increased CRP measurements were strongly associated with poor clinical outcome in this cohort., Finally, serum concentrations of Intercellular adhesion molecule 1, Vascular Cell Adhesion Molecule-1, and hsCRP during the early (P = .0055, P = .0266, and P = .0266) and late (P = .0423, P = .0041, and P = .0004) period were significantly higher in patients with DIND than in patients without DIND. CONCLUSIONS: Serum levels of Intercellular adhesion molecule 1, Vascular Cell Adhesion Molecule-1 and hsCRP during the early and late period following Yakut language correlate with DIND, CRP levels on days 5, 6, 7, and 8 were statistically significantly higher in the group of patients developing a DIND (P < 0.025, P < 0.016, P < 0.011, P < 0.0002)., Overall CRP values were higher with increasing severity of the initial ictus according to the Hunt and Hess Scale and to the outcome according to the Glasgow Outcome Scale from day 3 on., The presented data do not prove that Leukocytes and CRP values have a direct contribution to the pathogenesis of ischemic complications following Yakut language, but it supports the assertion that Inflammation may present a common pathogenic pathway in the development of such complications., The CRP and transforming growth factor beta 1 levels in Cerebrospinal Fluid are strongly concerned with communicating Hydrocephalus after Yakut language.[SEP]Relations: Subarachnoid Hemorrhage (disease) has relations: disease_protein with PPARG, disease_protein with PPARG, disease_protein with EDNRB, disease_protein with EDNRB, disease_protein with UNC5B, disease_protein with UNC5B, disease_protein with CASP3, disease_protein with CASP3, disease_protein with ADORA1, disease_protein with ADORA1.", "label": "yes"}
+{"original_question": "Have gnotobiotic animal models been used for the study of bowel disease?", "id": "converted_428", "sentence1": "Have gnotobiotic animal models been used for the study of bowel disease?", "sentence2": "Host gene expression in the TUBE,COLON,22FR,RADIOPAQUE RUBBER B#7370 of gnotobiotic interleukin-2-deficient CASP14 gene colonized with commensal colitogenic or noncolitogenic bacterial strains: common patterns and Bacteria strain specific signatures.,  Specific pathogen-free (SPF), but not germfree (GF), interleukin (IL)-2-deficient (IL-2-/-) CASP14 gene develop INFLAMMATORY BOWEL DISEASE 2 (Irritable Bowel Syndrome) at 10 to 15 weeks of age. Gnotobiotic IL-2-/- CASP14 gene monocolonized with E. coli mpk develop Irritable Bowel Syndrome at 25 to 33 weeks of age but not B. vulgatus mpk, E. coli Nissle 1917, or CASP14 gene cocolonized with both E. coli mpk and B. vulgatus, Lactobacillus reuteri promotes Helicobacter hepaticus-associated Typhlocolitis in gnotobiotic B6.129P2-IL-10(tm1Cgn) (IL-10(-/-) ) CASP14 gene., To model INFLAMMATORY BOWEL DISEASE 2, we assessed Communicable Diseases with Helicobacter hepaticus 3B1 (ATCC 51449) and a potential probiotic Lactobacillus reuteri (ATCC PTA-6475) in gnotobiotic B6.129P2-IL-10(tm1Cgn) (IL-10(-/-) ) CASP14 gene. No Typhlocolitis developed in Germ-Free controls (n=21) or in L. reuteri (n=8) or H. hepaticus (n=18) mono-associated CASP14 gene for 20 weeks post-Communicable Diseases. As positive controls, three specific pathogen-free IL-10(-/-) CASP14 gene dosed with H. hepaticus developed severe Typhlocolitis within 11 weeks. , These data support that the development of Typhlocolitis in H. hepaticus-infected IL-10(-/-) CASP14 gene required co-colonization with other Microbiota (plant) and in this study, required only L. reuteri. , When transferred to gnotobiotic CASP14 gene, gut microbiomes from CASP14 gene with active disease versus treatment-induced remission elicited varying degrees of Colitis. , The role of gut Microbiota (plant) (commensal Bacteria) and the mucosal barrier in the pathogenesis of inflammatory and Autoimmune Diseases and Primary malignant neoplasm: contribution of Germ-Free and gnotobiotic animal models of Homo sapiens diseases., The immunomodulatory effects of Microbiota (plant) and probiotics for Inflammatory Bowel Diseases and the role of Bacteria in their etiologies are being studied in gnotobiotic systems., To model INFLAMMATORY BOWEL DISEASE 2, we assessed Communicable Diseases with Helicobacter hepaticus 3B1 (ATCC 51449) and a potential probiotic Lactobacillus reuteri (ATCC PTA-6475) in gnotobiotic B6.129P2-IL-10(tm1Cgn) (IL-10(-/-) ) CASP14 gene., Gnotobiotic piglets may be used as a suitable animal model to study Colitis induced by C. jejuni, The role of gut Microbiota (plant) (commensal Bacteria) and the mucosal barrier in the pathogenesis of inflammatory and Autoimmune Diseases and Primary malignant neoplasm: contribution of Germ-Free and gnotobiotic animal models of Homo sapiens diseases, We investigated the changes in renal expression of KITLG wt Allele as a consequence of Colitis. METHODS: We studied 3 mouse models of Irritable Bowel Syndrome: Colitis induced by trinitrobenzene sulfonic acid, Colitis induced by microflora (in gnotobiotic interleukin-10(-/-)), and Colitis induced by adoptive transfer of CD4(+)CD45RB(high) T cells. , METHODS: We studied 3 mouse models of Irritable Bowel Syndrome: Colitis induced by trinitrobenzene sulfonic acid, Colitis induced by microflora (in gnotobiotic interleukin-10(-/-)), and Colitis induced by adoptive transfer of CD4(+)CD45RB(high) T cells. [SEP]Relations: INFLAMMATORY BOWEL DISEASE 2 has relations: disease_phenotype_positive with Abnormal intestine morphology, disease_phenotype_positive with Abnormal intestine morphology, disease_phenotype_positive with Abnormal intestine morphology, disease_phenotype_positive with Abnormal intestine morphology, contraindication with Phenobarbital, contraindication with Phenobarbital, contraindication with Phenobarbital, contraindication with Phenobarbital, disease_protein with GHRL, disease_protein with GHRL.", "label": "yes"}
+{"original_question": "Can parasite infections by Schistosoma japonicum prevent or improve asthma?", "id": "converted_4717", "sentence1": "Can parasite infections by Schistosoma japonicum prevent or improve Asthma?", "sentence2": "Helminths and their products can shape immune responses by modulating immune cells, which are dysfunctional in inflammatory diseases such as asthm, Schistosoma japonicum Peptides SJMHE1 suppresses airway Inflammation of Allergic Asthma in mice., Schistosomiasis japonica downregulates house dust mite-induced allergic airway Inflammation in mice., To our knowledge, it is the first study to reveal the impact of S. japonicum Communicable Diseases on house dust mite induced severe Asthma. More in depth investigation is need to elucidate the underlying mechanisms, Novel T-Lymphocyte epitopes on Schistosoma japonicum SjP40 protein and their preventive effect on Allergic Asthma in mice., hese results reveal a novel form of immune protective mechanism, which may play an important role in the modulating effect of Helminthiasis on allergic asthmatic reactions., Using a panel of overlapping peptides, we identified T-Lymphocyte epitopes on SjP40 protein of Schistosoma japonicum, which can induce Th1 cytokine and inhibit the production of Th2 cytokines and airway Inflammation in a mouse model of Allergic Asthma., Helminths and their products can regulate immune response and offer new strategies to control and alleviate Inflammation, including Asthma., SJMHE1 Peptide from Schistosoma japonicum Inhibits Asthma in CASP14 gene by Regulating Th17/Treg Cell Balance via miR-155., We previously found that a Peptides named as SJMHE1 from Schistosoma japonicum can suppress Asthma in mice, el of overlapping peptides, we identified T-Lymphocyte epitopes on SjP40 protein of Schistosoma japonicum, which can induce Th1 cytokine and inhibit the production of Th2 cytokines and airway Inflammation in a mouse model of Allergic Asthma. These resul, has been shown that helminth infections including Schistosoma mansoni may modulate atopic diseases including Asthma. I, Schistosomiasis japonica downregulates house dust mite-induced allergic airway Inflammation in mice, it is the first study to reveal the impact of S. japonicum Communicable Diseases on house dust mite induced severe Asthma. More in depth inv, s study, we investigated the impact of Schistosomiasis japonica on the allergic airway Inflammation induced by repeated intracheal inoculations of house dust mites (HDM), which is a Th17 and neutrophil dominant Mus Asthma model, mimicking severe Asthma. We found, Schistosomiasis japonica showed protective effects against allergic airway Inflammation (AAI)., Therefore, we hypothesize that Schistosoma japonicum egg antigens, a type of native Antigens, can induce production of CD4(+) CD25(+) T cells with regulatory activity, modulating airway Inflammation and inhibiting Asthma development., Schistosomiasis japonica modulates the development of allergen-induced airway Inflammation in mice., It has been shown that helminth infections including Schistosoma mansoni may modulate atopic diseases including Asthma., Schistosoma japonicum egg antigens stimulate CD4 CD25 T cells and modulate airway Inflammation in a Mus model of Asthma., Most previous studies focused on understanding the preventive effect of S. japonicum Communicable Diseases on Asthma (Communicable Diseases before allergen sensitization), whereas the protective effects of S. japonicum Communicable Diseases (allergen sensitization before Communicable Diseases) on Asthma were rarely investigated., In conclusion, our data showed that lung-stage S. japonicum Communicable Diseases could relieve Ovum-induced Asthma in a mouse model., In this study, we investigated the protective effects of S. japonicum Communicable Diseases on AAI using a mouse model of Ovum-induced Asthma.,  prior to Ovum immunization. These results suggest that both bisexual and male S. japonicum infections may modulate the development of Allergic Asthma., aponicum, which can induce Th1 cytokine and inhibit the production of Th2 cytokines and airway Inflammation in a mouse model of Allergic Asthma. These, ve found that Schistosoma Communicable Diseases or Schistosoma related products can improve or prevent some immune and inflammatory diseases, such as severe asthm, Our findings indicated that S. japonicum Communicable Diseases was able to effectively inhibit host's allergic airway Inflammation, which may be related to the upregulated Regulatory T-Lymphocytes upon Communicable Diseases., These results suggest that both bisexual and male S. japonicum infections may modulate the development of Allergic Asthma., We found that lung-stage S. japonicum Communicable Diseases significantly ameliorated Ovum-induced AAI, whereas post-lung-stage Communicable Diseases did not., In a Mus model of Asthma, S. japonicum egg antigens decreased the expression of Th2 cytokines, relieved Antigens-induced airway Inflammation, and inhibited Asthma development., We found that S. japonicum Communicable Diseases downregulated airway hyperresponsiveness., However, in recent years, studies have found that Schistosoma Communicable Diseases or Schistosoma related products can improve or prevent some immune and inflammatory diseases, such as severe Asthma, INFLAMMATORY BOWEL DISEASE 2, Diabetes Mellitus and so on., In areas where Schistosomiasis is endemic, a negative correlation is observed between MS4A2 wt Allele and Helminthiasis, associated with a low prevalence of Asthma.[SEP]Relations: Schistosoma japonicum infectious disease has relations: disease_disease with Schistosomiasis, disease_disease with Schistosomiasis. Schistosomiasis has relations: disease_disease with Schistosoma japonicum infectious disease, disease_disease with Schistosoma japonicum infectious disease, disease_disease with Schistosoma japonicum infectious disease, disease_disease with Schistosoma japonicum infectious disease, disease_disease with Schistosoma intercalatum infectious disease, disease_disease with Schistosoma intercalatum infectious disease, disease_disease with Schistosoma intercalatum infectious disease, disease_disease with Schistosoma intercalatum infectious disease.", "label": "yes"}
+{"original_question": "Do patients with Pendred syndrome present congenital deafness?", "id": "converted_74", "sentence1": "Do patients with Pendred syndrome present Congenital Hearing Loss, Partial?", "sentence2": "Pendred Syndrome can be characterized by the triad composed of familial goitre, abnormal perchlorate discharge and Congenital Hearing Loss, Partial., Pendred syndrome is an Autosomal Recessive Disorder characterized by Congenital Hearing Loss, Partial and Goiter. , Pendred syndrome comprises congenital sensorineural hearing loss, THYROID DIAGNOSTIC RADIOPHARMACEUTICALS Goiter, and positive perchlorate discharge test. , The cause of the Congenital Hearing Loss, Partial in Pendred syndrome is obscure, although a Mondini type malformation of the Cochlear structure exists in some patients., Pendred syndrome is an Autosomal Recessive Disorder characterized by Congenital Hearing Loss, Partial and Goiter., Pendred syndrome is the autosomal recessively transmitted association of familial Goiter and Congenital Hearing Loss, Partial., Pendred syndrome (Pendred's syndrome) is an Autosomal Recessive Disorder characterized by Congenital Hearing Loss, Partial, Goiter and Iodides organification defect., Pendred syndrome is a recessively inherited disorder with the hallmark features of Congenital Hearing Loss, Partial and THYROID DIAGNOSTIC RADIOPHARMACEUTICALS goitre., Pendred syndrome, a common autosomal-recessive disorder characterized by Congenital Hearing Loss, Partial and Goiter, is caused by mutations of SLC26A4, which codes for pendrin., These studies provide compelling evidence that defects in pendrin cause Pendred syndrome thereby launching a new area of investigation into THYROID DIAGNOSTIC RADIOPHARMACEUTICALS physiology, the pathogenesis of Congenital Hearing Loss, Partial and the role of altered sulphate transport in human disease., Gene Mutation in the Pendred syndrome gene have been observed in patients with Hearing Loss, Partial and vestibular aqueduct dilatation, in the absence of other Pendred syndrome features., The occurrence of Congenital Hearing Loss, Partial, Mutism and goitre unassociated with Congenital Hypothyroidism or mental retardation in Euthyroid (finding) patients is known as Pendred's Syndrome., The autosomal recessive Pendred's syndrome is defined by Congenital sensorineural hearing loss, Goiter, and impaired Iodides organification., Pendred's syndrome is an autosomal recessive disease characterized by Goiter, impaired Iodides organification, and Congenital sensorineural hearing loss., Pendred syndrome is an Autosomal Recessive Disorder characterized by Congenital sensorineural hearing loss, Goiter, and impaired Iodides organification., Pendred's syndrome is manifested by Congenital sensorineural hearing loss in association with familial Goiter due to defective organic binding of Iodine, Homeopathic preparation in the Neck>Thyroid gland., Although the textbook view of the Pendred syndrome is that of an autosomal recessive condition characterised by Hearing Loss, Partial and goitre, it is increasingly clear that not all patients present this classical clinical description., Pendred's syndrome may account for up to 10% of the cases with Hereditary hearing loss, and pendrin mutations have also been found in a kindred with non-syndromic Hearing Loss, Partial., Pendred syndrome comprises the association of severe Congenital sensorineural hearing loss with THYROID DIAGNOSTIC RADIOPHARMACEUTICALS pathology., The first one is named Pendred Syndrome (Supernumerary mandibular right central primary incisor) when Hearing Loss, Partial is associated with THYROID DIAGNOSTIC RADIOPHARMACEUTICALS Goiter; the second is called DEAFNESS, AUTOSOMAL RECESSIVE 4, WITH ENLARGED VESTIBULAR AQUEDUCT, when no other symptoms are present., Pendred syndrome is an Autosomal Recessive Disorder characterized by Sensorineural Hearing Loss (disorder), a partial defect in Iodides organification, and dyshormonogenetic Goiter., Pendred syndrome and non-syndromic recessive Hearing Loss, Partial associated with enlarged vestibular aqueduct (NSRD with EVA) are caused by mutations in the SLC26A4 (Pendred's syndrome) gene., Although the textbook view of Pendred syndrome is that of an autosomal recessive condition characterized by Hearing Loss, Partial and goitre, it is increasingly clear that not all such patients present this classical clinical picture. , The occurrence of Congenital Hearing Loss, Partial, Mutism and goitre unassociated with Congenital Hypothyroidism or mental retardation in Euthyroid (finding) patients is known as Pendred's Syndrome. , The cause of the Congenital Hearing Loss, Partial in Pendred syndrome is obscure, although a Mondini type malformation of the Cochlear structure exists in some patients. , The discovery of mutations in the SLC26A4 gene in patients with Pendred syndrome (Congenital Hearing Loss, Partial, Goiter, and defective Iodides organification) suggested a possible role for the encoded protein, pendrin, as an apical Iodides transporter. , Pendred syndrome is a recessively inherited disorder with the hallmark features of Congenital Hearing Loss, Partial and THYROID DIAGNOSTIC RADIOPHARMACEUTICALS goitre. , Pendred&apos;s syndrome is manifested by Congenital sensorineural hearing loss in association with familial Goiter due to defective organic binding of Iodine, Homeopathic preparation in the Neck>Thyroid gland. The majority of patients with Pendred&apos;s syndrome are Euthyroid (finding). We report on an unusual case of a patient with Pendred&apos;s syndrome presenting with Amenorrhea and late-onset Hypothyroidism.,  Although the textbook view of Pendred syndrome is that of an autosomal recessive condition characterized by Hearing Loss, Partial and goitre, it is increasingly clear that not all such patients present this classical clinical picture. Malformations of the Labyrinth, specifically enlargement of the vestibular aqueduct, are common in Pendred syndrome and mutations in the Pendred's syndrome (Pendred Syndrome) gene have been recorded in patients presenting with Hearing Loss, Partial and vestibular aqueduct dilatation only, without other features of Pendred syndrome., The occurrence of Congenital Hearing Loss, Partial, Mutism and goitre unassociated with Congenital Hypothyroidism or mental retardation in Euthyroid (finding) patients is known as Pendred&apos;s Syndrome. It has been estimated that 4-10 % of children with Congenital Hearing Loss, Partial suffer from this condition., Malformations of the Labyrinth, specifically enlargement of the vestibular aqueduct, are common in Pendred syndrome and mutations in the Pendred's syndrome (Pendred Syndrome) gene have been recorded in patients presenting with Hearing Loss, Partial and vestibular aqueduct dilatation only, without other features of Pendred syndrome. Since this is the most common radiological malformation of the Cochlear structure in deaf patients, we investigated what proportion of such cases were due to Mutation Abnormality of the SLC26A4 gene., Although the textbook view of Pendred syndrome is that of an autosomal recessive condition characterized by Hearing Loss, Partial and goitre, it is increasingly clear that not all such patients present this classical clinical picture. Malformations of the Labyrinth, specifically enlargement of the vestibular aqueduct, are common in Pendred syndrome and mutations in the Pendred's syndrome (Pendred Syndrome) gene have been recorded in patients presenting with Hearing Loss, Partial and vestibular aqueduct dilatation only, without other features of Pendred syndrome.[SEP]Relations: Pendred syndrome has relations: disease_disease with syndromic genetic Hearing Loss, Partial, disease_disease with syndromic genetic Hearing Loss, Partial, disease_phenotype_positive with Congenital sensorineural hearing impairment, disease_phenotype_positive with Congenital sensorineural hearing impairment, disease_phenotype_positive with Neurological speech impairment, disease_phenotype_positive with Neurological speech impairment, disease_disease with syndromic Hypothyroidism, disease_disease with syndromic Hypothyroidism. Congenital sensorineural hearing impairment has relations: disease_phenotype_positive with Pendred syndrome, disease_phenotype_positive with Pendred syndrome.", "label": "yes"}
+{"original_question": "Was golimumab tested for diabetes?", "id": "converted_4031", "sentence1": "Was golimumab tested for diabetes?", "sentence2": "CONCLUSIONS: Among children and young adults with newly diagnosed overt type 1 diabetes, golimumab resulted in better endogenous Therapeutic Insulin production and less exogenous Therapeutic Insulin use than placebo. , Golimumab and Beta-Cell Function in Youth with New-Onset Type 1 Diabetes., lticenter, placebo-controlled, double-blind, parallel-group trial, we randomly assigned, in a 2:1 ratio, children and young adults (age range, 6 to 21 years) with newly diagnosed overt type 1 diabetes to receive subcutaneous golimumab or placebo for 52 weeks. The primary end point was e, Golimumab and Beta-Cell Function in Youth with New-Onset Type 1 Diabetes[SEP]Relations: Golimumab has relations: drug_drug with Adalimumab, drug_drug with Adalimumab, drug_drug with Coumarin, drug_drug with Coumarin, drug_drug with Urelumab, drug_drug with Urelumab, drug_drug with Tabalumab, drug_drug with Tabalumab, drug_drug with Eldelumab, drug_drug with Eldelumab.", "label": "yes"}
+{"original_question": "Can botulism poisoning of a pregnant woman harm her fetus?", "id": "converted_406", "sentence1": "Can Botulism Poisoning aspects of a pregnant woman harm her Fetus in fetu?", "sentence2": "Two Botulism outbreaks were attributed to commercial ready-to-eat meat products and 3 to Food served in restaurants; several cases were attributed to non-Native home-prepared Food. Three affected pregnant women delivered healthy infants., botulinum toxin type B is not expected to be present in systemic circulation following proper Intramuscular Route of Drug Administration or intradermal injection. Moreover, botulinum toxin type A, which has a high molecular weight, does not appear to cross the placenta. From the 38 pregnancies reported in the literature, including women who had Botulism Poisoning aspects during pregnancy, exposure to botulinum toxin type A does not appear to increase the risk of adverse outcome in the Fetus in fetu., From the 38 pregnancies reported in the literature, including women who had Botulism Poisoning aspects during pregnancy, exposure to botulinum toxin type A does not appear to increase the risk of adverse outcome in the Fetus in fetu.[SEP]Relations: Poisoning aspects has relations: disease_disease with lead Poisoning aspects, disease_disease with lead Poisoning aspects, disease_disease with toxic oil syndrome, disease_disease with toxic oil syndrome, disease_disease with methanol Poisoning aspects, disease_disease with methanol Poisoning aspects, disease_disease with colchicine Poisoning aspects, disease_disease with colchicine Poisoning aspects, disease_disease with cyanide-induced parkinsonism, disease_disease with cyanide-induced parkinsonism.", "label": "no"}
+{"original_question": "Does administration of triiodothyronine improve outcome following coronary artery bypass grafting?", "id": "converted_207", "sentence1": "Does administration of liothyronine improve outcome following coronary artery bypass grafting?", "sentence2": "Serum SLC25A5 gene concentrations were significantly higher with fewer patients having SLC25A5 gene concentrations below the normal range in the SLC25A5 gene group than the placebo group throughout the postoperative period. Hemodynamic variables, postoperative inotrope requirement, and outcome variables showed no differences between the groups, We conclude that although widespread interest has been shown on the use of Thyroid Hormones in the perioperative period, and the effect of cardiopulmonary bypass on thyroid hormone metabolism widely studied, there is no substantial evidence to justify routine use of Thyroid Hormones in patients undergoing coronary artery bypass grafting., Treatment with GIK, SLC25A5 gene, and GIK/SLC25A5 gene improves hemodynamic performance and results in reduced Cardiac troponin I release in patients undergoing on-pump CABG surgery., Perioperative administration of liothyronine increased cardiac output slightly and decreased systemic vascular resistance, but it had no effect on operative outcome., Parenteral liothyronine given after crossclamp removal during elective coronary artery bypass grafting significantly improved postoperative ventricular function, reduced the need for treatment with inotropic agents and mechanical devices, and decreased the incidence of Coronary Arteriosclerosis. The incidence of Atrial Fibrillation by ECG Finding was slightly decreased, and the need for postoperative pacemaker support was reduced., Perioperative SLC25A5 gene administration decreased the incidence and need for treatment of postoperative Atrial Fibrillation by ECG Finding.,  Intravenous T(3) does not have dramatic effects on hemodynamic variables in this setting as has been previously suggested. , Raising serum liothyronine concentrations in patients undergoing coronary-artery bypass surgery increases cardiac output and lowers systemic vascular resistance, but does not change outcome or alter the need for standard postoperative therapy., No significant differences were noted in the pre and post CPB hemodynamics between the two groups for the most part of the study except that heart rate was increased in SLC25A5 gene group., The haemodynamic parameters were no different between the two groups at any postoperative time point. Likewise, density and affinity of lymphocyte beta-adrenoceptors were not significantly different from pre-operative values in either group.[SEP]Relations: Coronary artery atherosclerosis has relations: drug_effect with Rivastigmine, drug_effect with Rivastigmine, drug_effect with Vincristine, drug_effect with Vincristine, drug_effect with Varenicline, drug_effect with Varenicline, drug_effect with Ropinirole, drug_effect with Ropinirole, drug_effect with Fenofibrate, drug_effect with Fenofibrate.", "label": "no"}
+{"original_question": "Is there any linear-time and linear-space algorithm for the computation of avoided words in biological sequences?", "id": "converted_2372", "sentence1": "Is there any linear-time and linear-space algorithm for the computation of avoided words in biological sequences?", "sentence2": "The systematic search for avoided words is particularly useful for biological Sequence - ParameterizedDataType analysis. We present a linear-time and linear-space algorithm for the computation of avoided words of lengthkin a given sequencex. We suggest a ResponseLevel - ResponseLevel - modification to this algorithm so that it computes all avoided words ofx, irrespective of their length, within the same time complexity. We also present combinatorial results with regards to avoided words and absent words., We present a linear-time and linear-space algorithm for the computation of avoided words of length <br>, <b>BACKGROUND</b>: The deviation of the observed frequency of a word <br><b>RESULTS</b>: In this article, we propose an [Formula: see text]-time and [Formula: see text]-space algorithm to compute all [Formula: see text]-avoided words of length <br><b>CONCLUSIONS</b>: The systematic search for avoided words is particularly useful for biological Sequence - ParameterizedDataType analysis., We present a linear-time and linear-space algorithm for the computation of avoided words of length, We present a linear-time and linear-space algorithm for the computation of avoided words of length k in a given Sequence - ParameterizedDataType x., Hence, computing all such words naïvely can be a very time-consuming procedure, in particular for large k.   RESULTS In this article, we propose an [Formula: see text]-time and [Formula: see text]-space algorithm to compute all [Formula: see text]-avoided words of length k in a given Sequence - ParameterizedDataType of length n over a fixed-sized alphabet., We also present a time-optimal [Formula: see text]-time algorithm to compute all [Formula: see text]-avoided words (of any length) in a Sequence - ParameterizedDataType of length n over an integer alphabet of size [Formula: see text]., the deviation of the observed frequency of a word from its Expected (qualifier) frequency in a given Sequence - ParameterizedDataType is used to determine whether or not the word is this concept is particularly useful in dna linguistic analysis the value of the deviation of denoted by formula see text effectively characterises the extent of a word by its edge contrast in the context in which it occurs a word of length formula see text is a formula see text avoided word in if formula see text for a given threshold formula see text notice that such a word may be completely from hence computing all such words naïvely can be a very time consuming procedure in particular for large in this article we propose an formula see text time and formula see text space algorithm to compute all formula see text avoided words of length in a given Sequence - ParameterizedDataType of length over a fixed sized alphabet we also present a time optimal formula see text time algorithm to compute all formula see text avoided words of any length in a Sequence - ParameterizedDataType of length over an integer alphabet of size formula see text in addition we provide a tight asymptotic upper bound for the number of formula see text avoided words over an integer alphabet and the Expected (qualifier) length of the longest one we make available an implementation of our algorithm experimental results using both real and synthetic data show the efficiency and applicability of our implementation in biological Sequence - ParameterizedDataType analysis the systematic search for avoided words is particularly useful for biological Sequence - ParameterizedDataType analysis we present a linear time and linear space algorithm for the computation of avoided words of length in a given Sequence - ParameterizedDataType we suggest a ResponseLevel - ResponseLevel - modification to this algorithm so that it computes all avoided words of irrespective of their length within the same time complexity we also present combinatorial results with regards to avoided words and absent words.[SEP]Relations: response to nickel cation has relations: bioprocess_protein with CACNA1G, bioprocess_protein with CACNA1G, bioprocess_bioprocess with cellular response to nickel ion, bioprocess_bioprocess with cellular response to nickel ion, bioprocess_bioprocess with response to metal ion, bioprocess_bioprocess with response to metal ion.", "label": "yes"}
+{"original_question": "Is the Miller-Fisher syndrome considered to be a variant of Guillain-Barré?", "id": "converted_687", "sentence1": "Is the Miller Fisher Syndrome considered to be a Variant of Guillain-Barré?", "sentence2": "Miller Fisher syndrome is a Variant of Guillain-Barre syndrome characterized by the classic triad of ophthalmoplegia, Cerebellar Ataxia, and Absent reflex, We are reporting a rare case of Miller-Fisher (Marfan Syndrome) Variant of Guillain-Barré syndrome (Guillain-Barre Syndrome) as the first manifestation of Lupus Erythematosus, Systemic in a 41-year-old female, Miller Fisher Syndrome is defined as ophthalmoplegia, Cerebellar Ataxia and Absent reflex. Considered as a Variant of Guillain-Barré syndrome, it differs in its clinical presentation and by anti-GQ1b antibody positivity, Guillain-Barré syndrome (Guillain-Barre Syndrome) and its Variant, Miller Fisher syndrome (Marfan Syndrome), exist as several clinical subtypes with different neurological features and presentations, Using in vitro and in vivo models of the Guillain-Barré syndrome Variant, Miller Fisher syndrome, we have shown previously that anti-GQ1b ganglioside antibody antibody Antibodies, in vitro diagnostic target the presynaptic motor nerve terminal axon and surrounding perisynaptic Schwann cells, thereby mediating destructive injury through deposition of Complement Membrane Attack Complex., Miller Fisher syndrome is a Variant of Guillain-Barré syndrome, characterized by ophthalmoplegia, Cerebellar Ataxia and Absent reflex., Miller Fisher syndrome is a localized Variant of Guillain-Barré syndrome, characterized by ophthalmoplegia, Absent reflex and Cerebellar Ataxia., Miller Fisher syndrome, a Variant of Guillain-Barré syndrome, is associated with immunoglobulin G to GQ1b ganglioside antibody antibody., Miller Fisher syndrome (Marfan Syndrome), a Variant of Guillain-Barré syndrome, is a rare disorder typically characterized by a triad of Cerebellar Ataxia, Absent reflex, and ophthalmoplegia, which may have a highly variable clinical presentation., Miller Fisher syndrome is an acute inflammatory polyradiculoneuropathy that is generally considered a Variant of Guillain-Barré syndrome and is characterized by the clinical triad of Cerebellar Ataxia, Absent reflex, and ophthalmoplegia., The objective of this study was to review the occurrence and clinical features of Guillain-Barré syndrome and its Variant, the Miller Fisher syndrome, during TNFalpha antagonist therapy., Miller Fisher Variant of Guillain-Barré syndrome masquerading as acute sphenoid sinusitis with orbital apex syndrome., Controversy exists concerning whether Miller Fisher syndrome (Marfan Syndrome) is the result of a predominantly axonal or demyelinating polyneuropathy and whether the Guillain-Barré syndrome Variant of acute Cerebellar Ataxia and Absent reflex without ophthalmoplegia, ataxic Guillain-Barré syndrome (atxGBS), has a distinct pathophysiology., Miller Fisher syndrome is characterised by the triad ophthalmoparesis, Cerebellar Ataxia and Absent reflex and is considered to be a Variant of Guillain-Barré syndrome; its differential diagnosis includes Wernicke&apos;s encephalopathy, Miller Fisher syndrome is an acute inflammatory polyradiculoneuropathy that is generally considered a Variant of Guillain-Barré syndrome and is characterized by the clinical triad of Cerebellar Ataxia, Absent reflex, and ophthalmoplegia, Miller Fisher Syndrome is characterised by the clinical triad of ophthalmoplegia, Cerebellar Ataxia and Absent reflex and is considered a Variant form of Guillain-Barré syndrome, The syndrome of Cerebellar Ataxia, Absent reflex and ophthalmoplegia, or Miller Fisher Syndrome, has been considered to be a Variant of Guillain-Barré syndrome with pathology restricted to the peripheral nervous system, Miller Fisher Syndrome (Marfan Syndrome) is considered the most common Variant of Guillain-Barré syndrome (Guillain-Barre Syndrome) and is characterized by the clinical triad of ophthalmoplegia, Cerebellar Ataxia and Absent reflex, Miller Fisher syndrome (Marfan Syndrome), characterized as Cerebellar Ataxia, Absent reflex and ophthalmoplegia, is generally considered as a Variant of Guillain-Barré syndrome (Guillain-Barre Syndrome), Miller Fisher Syndrome (Marfan Syndrome), which is characterized by ophthalmoplegia, Cerebellar Ataxia and tendon Absent reflex, is generally considered as a clinical Variant of Guillain-Barré Syndrome, Miller Fisher Syndrome (Marfan Syndrome), a Variant of Guillain-Barré syndrome (Guillain-Barre Syndrome) is a self-limiting demyelinating disease of the peripheral nervous system, BACKGROUND: Miller Fisher Syndrome is characterised by the clinical triad of ophthalmoplegia, Cerebellar Ataxia and Absent reflex and is considered a Variant form of Guillain-Barré syndrome. , BACKGROUND AND OBJECTIVE: Miller Fisher Syndrome (Marfan Syndrome) is considered the most common Variant of Guillain-Barré syndrome (Guillain-Barre Syndrome) and is characterized by the clinical triad of ophthalmoplegia, Cerebellar Ataxia and Absent reflex. , Miller Fisher syndrome is characterised by the triad ophthalmoparesis, Cerebellar Ataxia and Absent reflex and is considered to be a Variant of Guillain-Barré syndrome; its differential diagnosis includes Wernicke Encephalopathy. , A recent report described serum anti-GQ1b ganglioside antibody antibody Antibodies, in vitro diagnostic in Miller Fisher syndrome (Marfan Syndrome), a clinical Variant of Guillain-Barré syndrome (Guillain-Barre Syndrome)., The syndrome of Cerebellar Ataxia, Absent reflex and ophthalmoplegia, or Miller Fisher Syndrome, has been considered to be a Variant of Guillain-Barré syndrome with pathology restricted to the peripheral nervous system., Guillain-Barré syndrome (Guillain-Barre Syndrome), an acute inflammatory polyneuropathy, is preceded in most cases by an infectious illness, and Campylobacter jejuni, a leading cause of acute gastroenteritis, is the most common antecedent to Guillain-Barre Syndrome and its ocular Variant, Miller Fisher syndrome (Marfan Syndrome)., Miller Fisher Syndrome is characterised by the clinical triad of ophthalmoplegia, Cerebellar Ataxia and Absent reflex and is considered a Variant form of Guillain-Barré syndrome., Miller Fisher Syndrome is characterised by the clinical triad of ophthalmoplegia, Cerebellar Ataxia and Absent reflex and is considered a Variant form of Guillain-Barré syndrome.,  The syndrome of Cerebellar Ataxia, Absent reflex and ophthalmoplegia, or Miller Fisher Syndrome, has been considered to be a Variant of Guillain-Barré syndrome with pathology restricted to the peripheral nervous system. A patient with Miller Fisher Syndrome and bilateral demyelinating optic neuropathy suggesting associated CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS pathology is presented., Miller Fisher syndrome is an acute inflammatory polyradiculoneuropathy that is generally considered a Variant of Guillain-Barré syndrome and is characterized by the clinical triad of Cerebellar Ataxia,,  Miller Fisher syndrome is an uncommon disease and it is a Variant of Guillain-Barre syndrome. Miller Fisher syndrome also has rarer variants., Miller Fisher syndrome is characterised by the triad ophthalmoparesis, Cerebellar Ataxia and Absent reflex and is considered to be a Variant of Guillain-Barré syndrome; its differential diagnosis includes Wernicke Encephalopathy., Miller Fisher syndrome is an acute inflammatory polyradiculoneuropathy that is generally considered a Variant of Guillain-Barré syndrome and is characterized by the clinical triad of Cerebellar Ataxia, Absent reflex, and ophthalmoplegia., Data were separately analysed for Miller Fisher syndrome and other Guillain-Barré syndrome variants., Guillain-Barré syndrome variants alone (excluding Miller Fisher syndrome) accounted for 10.5% of total cases., The syndrome of Cerebellar Ataxia, Absent reflex and ophthalmoplegia, or Miller Fisher Syndrome, has been considered to be a Variant of Guillain-Barré syndrome with pathology restricted to the peripheral nervous system.[SEP]Relations: Miller Fisher syndrome has relations: disease_disease with regional Variant of Guillain-Barre syndrome, disease_disease with regional Variant of Guillain-Barre syndrome, disease_disease with cerebellar disease, disease_disease with cerebellar disease. Guillain-Barre syndrome has relations: disease_disease with Variant of Guillain-Barre syndrome, disease_disease with Variant of Guillain-Barre syndrome, disease_protein with PMP22, disease_protein with PMP22, disease_disease with syndromic disease, disease_disease with syndromic disease.", "label": "yes"}
+{"original_question": "Is the enzyme EPRS phosphorylated?", "id": "converted_2024", "sentence1": "Is the enzyme EPRS1 gene phosphorylated?", "sentence2": "Phosphorylation of glutamyl-prolyl tRNA synthetase (EPRS1 gene) has been investigated extensively in our laboratory for more than a decade, and has served as an archetype for studies of other AARSs., EPRS1 gene is dually phosphorylated by Cyclin-Dependent Kinases (CDK5 protein, human) at Ser(886) and then by a CDK5 protein, human-dependent-AGC kinase at Ser(999); , Diphosphorylated EPRS1 gene is released from its residence in the tRNA multisynthetase complex for immediate binding to NS1-associated protein and subsequent binding to ribosomal protein L13a and GAPDH protein, human protein, human. , Two-site phosphorylation of EPRS1 gene coordinates multimodal regulation of noncanonical translational control activity.[SEP]Relations: EPRS1 has relations: protein_protein with ESR2, protein_protein with ESR2, protein_protein with ESR1, protein_protein with ESR1, molfunc_protein with ATP binding, molfunc_protein with ATP binding, protein_protein with ARL4D, protein_protein with ARL4D, protein_protein with ASNS, protein_protein with ASNS.", "label": "yes"}
+{"original_question": "Is esophageal adenocarcinoma associated with aberrant glycosylation?", "id": "converted_4256", "sentence1": "Is Adenocarcinoma Of Esophagus associated with aberrant glycosylation?", "sentence2": "Altered Glycoproteins expression has been demonstrated in Tissue Specimen Code from patients with Barrett Esophagus and Malignant neoplasm of esophagus but the mechanisms regarding such changes are unknown. , Esophageal adenocarcinoma represents a highly morbid and mortal cancer with a defined progression from Metaplasia (Barrett Esophagus) to Dysplasia to Neoplasms. This Disease is highlighted because (1) differences in glycan profiles between the stages of Disease progression have been described in the glycoproteomic literature; (2) a glycan biomarker that identifies a given stage may be used as a predictor of Disease progression and thus may have significant influence over clinical management; and (3) the differences in glycan profiles between Disease and Disease-free states in Malignant neoplasm of esophagus are more dramatic than in other Malignant Neoplasms.,  comparative glycomic profiling of Familial multiple trichoepitheliomata reveals a subset of glycans that can be selected as candidate biomarkers,  comparative glycomic profiling of Adenocarcinoma Of Esophagus reveals a subset of glycans that can be selected as candidate biomarkers, immunoglobulin G glycosylation profile was independently associated with esophageal precancerosis beyond Inflammation, which could be an early biomarker for Malignant neoplasm of esophagus.[SEP]Relations: carcinoma of esophagus has relations: disease_protein with GHRL, disease_protein with GHRL, disease_protein with GNG7, disease_protein with GNG7, disease_disease with esophageal adenosquamous carcinoma, disease_disease with esophageal adenosquamous carcinoma, disease_protein with SST, disease_protein with SST, disease_protein with EGFR, disease_protein with EGFR.", "label": "yes"}
+{"original_question": "Are there any HCV replication inhibitors available?", "id": "converted_1099", "sentence1": "Are there any HCV replication inhibitors available?", "sentence2": "We report here the discovery of the first small-molecule HCV infectivity inhibitor, GS-563253, also called HCV infectivity inhibitor 1 (HCV II-1). , Resistance to Mericitabine (Prodrugs of HCV NS5B polymerase inhibitor PSI 6130) is rare and conferred by the NS5B S282T Mutation Abnormality., We tested the ability of NA808 to inhibit SPT's enzymatic activity in FLR3-1 replicon cells, The SPT inhibitor NA808 prevents replication of HCV genotypes 1a, 1b, 2a, 3a, and 4a in cultured hepatocytes and in CASP14 gene with humanized livers., Vaniprevir (phase III clinical trials) and MK 5172 (phase II clinical trials) are two potent antiviral compounds that target NS3/4A protease, treatment for hepatitis C virus (HCV) infection has been significantly improved with the approval of the first two HCV NS3/4A protease inhibitors, telaprevir (incivek) and boceprevir (Victrelis). , Combination therapy with telaprevir and BMS-788329 (NS5A inhibitor) reduced serum HCV RNA to undetectable levels. The presence of an NS3-V36A telaprevir resistance Mutation Abnormality resulted in poor response to telaprevir monotherapy but showed significant HCV reduction when telaprevir was combined with BMS-788329. However, a BMS-788329-resistant strain emerged at low frequency. Communicable Diseases with a BMS-788329-resistant NS5A-L31V Mutation Abnormality rapidly resulted in gain of an additional NS5A-Y93A Mutation Abnormality that conferred telaprevir resistance during combination therapy, HCV NS5A replication complex inhibitors, exemplified by Daclatasvir (BMS-790052), represent a new class of DAA, ACH-806 (or GS-9132) is a novel, small-molecule inhibitor specific for hepatitis C virus (HCV). , Telaprevir and boceprevir are the first two Retroviral Retroviral protease inhibitor (Pulmonary Valve Insufficiency) DAAs to be approved for combination therapy with PEG-IFN-SA (PEG-IFN) and ribavirin (RBV). , symmetrical bidentate structure of the NS5A inhibitor BMS-790052, a series of new monodentate molecules were designed, In vitro, boceprevir is more active than telaprevir against the HCV G3 NS3/4A enzyme in cell-based and biochemical assays and against G3 isolates in replicon assays, alisporivir is the most advanced host-targeting antiviral in clinical development. alisporivir blocks HCV replication by neutralizing the Peptidyl-Prolyl Cis-Trans Isomerase A, human activity of the abundant host cytosolic protein, cyclophilin A, Interestingly, the NS5A inhibitor daclatasvir (BMS-790052) caused a decrease in serum HCV RNA levels by about two orders of magnitude within 6 h of administration[SEP]Relations: hepatitis C virus infection has relations: contraindication with Tipranavir, contraindication with Tipranavir, contraindication with Lopinavir, contraindication with Lopinavir, contraindication with Nevirapine, contraindication with Nevirapine, contraindication with Tenofovir, contraindication with Tenofovir, contraindication with Amprenavir, contraindication with Amprenavir.", "label": "yes"}
+{"original_question": "Does RNA polymerase II have RNA cleavage activity?", "id": "converted_2244", "sentence1": "Does RNA Polymerase II have RNA cleavage activity?", "sentence2": "In addition to RNA synthesis, DNA-Directed RNA Polymerase complex (msRNAPs) support enzymatic reactions such as intrinsic RNA Transcript cleavage., msRNAP active sites from different species appear to exhibit differential intrinsic RNA Transcript cleavage efficiency and have likely evolved to allow fine-tuning of the transcription process., Here we show that a single amino-acid substitution in the trigger loop (TL) of Saccharomyces RNAP II, Rpb1 H1085Y, engenders a gain of intrinsic cleavage activity where the substituted tyrosine appears to participate in acid-base chemistry at alkaline pH for both intrinsic cleavage and nucleotidyl transfer. , The eukaryotic transcription factor TCEA1 wt Allele enhances elongation and nascent RNA Transcript cleavage activities of RNA Polymerase II in a stalled elongation complex., The transcription factor TCEA1 wt Allele zinc ribbon dipeptide Asp-Glu is critical for stimulation of elongation and RNA cleavage by RNA Polymerase II, By site-directed mutagenesis, we have demonstrated that invariant residues Asp-261 and Glu-262 of the nucleic acid-binding TCEA1 wt Allele Zn ribbon are critical for stimulation of both elongation and RNA cleavage activities of RNA Polymerase II., Complexes of yeast RNA Polymerase II and RNA are substrates for TCEA1 wt Allele-induced RNA cleavage., RNA in such RNA-DNA-Directed RNA Polymerase complexes undergoes reactions previously thought to be unique to nascent RNA in ternary complexes with DNA, including TCEA1 wt Allele-dependent cleavage and elongation by 3'-terminal addition of 1-methyl-2-pyrrolidinone from NTP., Nascent RNA cleavage by arrested RNA Polymerase II does not require upstream translocation of the elongation complex on DNA., Here we show that in the presence of SII and Nucleotides, RNA Transcript cleavage is detected during SII-dependent elongation but not during SII-independent transcription. , under typical transcription conditions, SII is necessary but insufficient to activate RNA cleavage. RNA cleavage could serve to move RNA Polymerase II away from the transcriptional impediment and/or permit RNA Polymerase II multiple attempts at RNA elongation., SII is an RNA Polymerase II-binding protein that stimulates transcription elongation and also activates nascent RNA Transcript cleavage by RNA Polymerase II in elongation complexes in vitro, The RNA Polymerase II elongation complex. Factor-dependent transcription elongation involves nascent RNA cleavage., Cleavage was not restricted to an elongation complex arrested at this particular site, showing that nascent RNA hydrolysis is a general property of RNA Polymerase II elongation complexes., transcription factor S-II (also known as TCEA1 wt Allele) is an RNA Polymerase II binding protein that allows bypass of template arrest sites by activating a nascent RNA cleavage reaction., During gene transcription, the DNA-Directed RNA Polymerase (Pol) active center can catalyze RNA cleavage., During gene transcription, the DNA-Directed RNA Polymerase (Pol) active center can catalyze RNA cleavage., The eukaryotic transcription factor TCEA1 wt Allele enhances elongation and nascent RNA Transcript cleavage activities of RNA Polymerase II in a stalled elongation complex., POLR2I gene, a small subunit of RNA Polymerase II, enhances the cleavage stimulation activity of S-II., These results suggest that both S-II and POLR2I gene maintain transcriptional fidelity by stimulating the cleavage activity intrinsic to RNA Polymerase II., It is also possible that the RNA Transcript cleavage activity of RNA Polymerase II represents a proofreading function of the Enzyme [APC].., Nascent RNA cleavage by arrested RNA Polymerase II does not require upstream translocation of the elongation complex on DNA., Intrinsic RNA Transcript cleavage in yeast RNA Polymerase II elongation complexes.[SEP]Relations: DNA-Directed RNA Polymerase binding has relations: molfunc_protein with CCNT2, molfunc_protein with CCNT2, molfunc_protein with YTHDC2, molfunc_protein with YTHDC2, molfunc_protein with PKN2, molfunc_protein with PKN2, molfunc_protein with PPIB, molfunc_protein with PPIB. DNA-Directed RNA Polymerase III assembly has relations: bioprocess_bioprocess with cellular protein-containing complex assembly, bioprocess_bioprocess with cellular protein-containing complex assembly.", "label": "yes"}
+{"original_question": "Does SATB1 regulate the RAG1 and RAG2 genes?", "id": "converted_3360", "sentence1": "Does DNA-Binding Protein SATB1 regulate the RAG1 and RAG2 genes?", "sentence2": "High level expression of the Xlr nuclear protein in immature thymocytes and colocalization with the matrix-associated region-binding DNA-Binding Protein DNA-Binding Protein SATB1 protein,  Its onset preceded the rearrangement of transcription-coupled nucleotide-excision repair genes, as Xlr expression was conserved in thymus cells from RAG1(0/0) CASP14 gene. , An anti-silencer- and DNA-Binding Protein DNA-Binding Protein SATB1-dependent chromatin hub regulates RAG1 gene and RAG2 gene gene expression during thymocyte development.,  DNA-Binding Protein DNA-Binding Protein SATB1 binds to the ASE and Rag promoters, facilitating inclusion of RAG2 gene in the chromatin hub and the loading of RNA Polymerase II to both the RAG1 gene and RAG2 gene promoters., Our results provide a novel framework for understanding ASE function and demonstrate a novel role for DNA-Binding Protein DNA-Binding Protein SATB1 as a regulator of Rag locus organization and gene expression in DP thymocytes.[SEP]Relations: Tat protein binding has relations: molfunc_protein with DNAJA1, molfunc_protein with DNAJA1, molfunc_protein with GABARAPL1, molfunc_protein with GABARAPL1, molfunc_protein with CTDP1, molfunc_protein with CTDP1. transcription-coupled nucleotide-excision repair has relations: bioprocess_protein with DDB1, bioprocess_protein with DDB1, bioprocess_protein with XAB2, bioprocess_protein with XAB2.", "label": "yes"}
+{"original_question": "Does Eucommia ulmoides leaf extract ameliorates steatosis/fatty liver induced by high-fat diet?", "id": "converted_2991", "sentence1": "Does Eucommia ulmoides Concept Generality - Leaf extract ameliorates steatosis/fatty liver induced by high-fat diet?", "sentence2": "These results demonstrate that the Eucommia ulmoides Concept Generality - Leaf extract exhibits antihyperlipidemic properties by suppressing hepatic fatty acid and cholesterol biosynthesis with the simultaneous reduction of plasma and hepatic lipids in high fat-fed hamsters.,  Together, these results suggest that EUE and its active components enhance lysosomal activity, resulting in decreased Endoplasmic Reticulum stress and hepatic dyslipidemi, Eucommia ulmoides (Eucommia ulmoides Oliver) Concept Generality - Leaf extract mediates hypolipidemic action in hamsters fed a high-fat diet.This study examined the effect of a Eucommia ulmoides (Eucommia ulmoides Oliver) Concept Generality - Leaf extract (0.175 g/100 g diet) that was supplemented with a high-fat diet (10% coconut oil, 0.2% cholesterol, wt/wt) on hyperlipidemic hamsters. , Preventive effect of Eucommia Concept Generality - Leaf extract on aortic media hypertrophy in Wistar-Kyoto Rattus norvegicus fed a high-fat diet.Eucommia ulmoides Oliver Concept Generality - Leaf extract (ELE) has been shown to have anti-hypertensive and anti-obesity effects in Rattus norvegicus that are fed a high-fat diet (HFD). , Eucommia ulmoides Oliver Concept Generality - Leaf extract (ELE) has been shown to have anti-hypertensive and anti-obesity effects in Rattus norvegicus that are fed a high-fat diet (HFD)., The hepatic fatty acid synthase and Hydroxymethylglutaryl coenzyme A reductase activities were significantly lowered by a Eucommia ulmoides Concept Generality - Leaf extract supplement in high fat-fed hamsters., These results demonstrate that the Eucommia ulmoides Concept Generality - Leaf extract exhibits antihyperlipidemic properties by suppressing hepatic fatty acid and cholesterol biosynthesis with the simultaneous reduction of plasma and hepatic lipids in high fat-fed hamsters.<br>, Both forms of Eucommia leaves minimised increases in body weight and Visceral Fat in a dose-dependent fashion., These results demonstrate that the Eucommia ulmoides Concept Generality - Leaf extract exhibits antihyperlipidemic properties by suppressing hepatic fatty acid and cholesterol biosynthesis with the simultaneous reduction of plasma and hepatic lipids in high fat-fed hamsters., The hepatic fatty acid synthase and Hydroxymethylglutaryl coenzyme A reductase activities were significantly lowered by a Eucommia ulmoides Concept Generality - Leaf extract supplement in high fat-fed hamsters.[SEP]Relations: endoplasmic reticulum has relations: cellcomp_protein with ULBP1, cellcomp_protein with ULBP1, cellcomp_protein with ULBP2, cellcomp_protein with ULBP2, cellcomp_protein with ADORA1, cellcomp_protein with ADORA1, cellcomp_protein with SERPINA1, cellcomp_protein with SERPINA1, cellcomp_protein with SERPINA2, cellcomp_protein with SERPINA2.", "label": "yes"}
+{"original_question": "Has ruxolitinib received FDA approval?", "id": "converted_2261", "sentence1": "Has ruxolitinib received FDA approval?", "sentence2": "Testing for Janus kinase 2 mutations is now included in the World Health Organization (WHO) criteria for the diagnosis of Myeloproliferative disease, and in 2011 the oral Janus kinase 2 kinase inhibitor ruxolitinib became the first Food and Drug Administration (FDA)-approved drug for the treatment of Primary Myelofibrosis.[SEP]Relations: Ruxolitinib has relations: drug_drug with Rutin, drug_drug with Rutin, drug_drug with Orlistat, drug_drug with Orlistat, drug_drug with Medical Cannabis, drug_drug with Medical Cannabis, drug_drug with Lapatinib, drug_drug with Lapatinib, drug_drug with Dovitinib, drug_drug with Dovitinib.", "label": "yes"}
+{"original_question": "Can PRL3-zumab inhibit PRL3+ cancer cells in vitro and in vivo?", "id": "converted_3584", "sentence1": "Can PTP4A3 wt Allele-zumab inhibit PTP4A3 wt Allele+ Tumor cells, malignant in vitro and in vivo?", "sentence2": "Here we show that PTP4A3 wt Allele-zumab specifically inhibits PTP4A3 wt Allele+ Tumor cells, malignant in vivo, but not in vitro.[SEP]Relations: malignant giant cell tumor has relations: disease_disease with cancer, disease_disease with cancer, disease_disease with giant cell tumor of soft tissue, disease_disease with giant cell tumor of soft tissue, disease_disease with giant cell tumor, disease_disease with giant cell tumor, disease_disease with malignant giant cell tumor of soft parts, disease_disease with malignant giant cell tumor of soft parts, disease_disease with malignancy in giant cell tumor of bone, disease_disease with malignancy in giant cell tumor of bone.", "label": "no"}
+{"original_question": "Is thalidomide used as an immunomodulatory drug nowadays?", "id": "converted_4511", "sentence1": "Is thalidomide used as an immunomodulatory Pharmacologic Substance nowadays?", "sentence2": "Potential immunomodulatory, antiinflammatory, anti-angiogenic and sedative properties make thalidomide a good candidate for the treatment of several diseases such as multiple Multiple Myeloma., In 1990s, however, thalidomide received attention due to the discovery of its anticancer potential derived from antiangiogenic and immunomodulatory activities, and its therapeutic effect on Multiple Myeloma., Thalidomide is an immunomodulatory agent; although its mechanisms of action are not fully understood, many authors have described its Anti-Inflammatory Agents and immunosuppressive properties, Thalidomide has antiangiogenic and immunomodulatory properties and has recently been used in the management of Homo sapiens malignancies, After nearly decades of extinction as a sedative and antiemetic, thalidomide reemerged as the parent compound of a novel and promising class of therapeutics termed the immunomodulatory drugs (Immunomodulatory IMiD Drugs), Thalidomide has antiangiogenic and immunomodulatory properties and has recently been used in the management of Homo sapiens malignancies., Thalidomide is a Pharmacologic Substance that, since its development, has made history in the world of medicine--having been withdrawn and now has returned with a boom as an anticancer and immunomodulatory Pharmacologic Substance., Thalidomide was developed in the 1950s as a sedative Pharmacologic Substance and withdrawn in 1961 because of its teratogenic effects, but has been rediscovered as an immuno-modulatory Pharmacologic Substance., Thalidomide is attracting growing interest because of its reported immunomodulatory and Anti-Inflammatory Agents properties., Only in the last several years has thalidomide been aggressively investigated for its antiangiogenic potential and immunomodulatory properties in various tumor types., After nearly decades of extinction as a sedative and antiemetic, thalidomide reemerged as the parent compound of a novel and promising class of therapeutics termed the immunomodulatory drugs (Immunomodulatory IMiD Drugs)., In the present review an attempt is made to highlight the immunomodulatory action of thalidomide in various pathologic conditions., Thalidomide and its immunomodulatory analogues have numerous effects on the body's immune system, including potential anti-cancer and Anti-Inflammatory Agents activities., Thalidomide is an immunomodulatory agent; although its mechanisms of action are not fully understood, many authors have described its Anti-Inflammatory Agents and immunosuppressive properties., Thalidomide (Thal) has antiangiogenic and immunomodulatory activity., Thalidomide is an immunomodulatory Pharmacologic Substance (IMiD) with proven therapeutic action in several autoimmune/inflammatory diseases;, The immunomodulatory agents thalidomide and lenalidomide and the Proteasome Inhibitors [MoA] bortezomib are now routine components of Millimole per Liter therapy, Although thalidomide was withdrawn in the 1960s after its teratogenic property was recognized, it was subsequently found that this Pharmacologic Substance possesses immunomodulatory and Anti-Inflammatory Agents effects.,  Its immunological effects were known already from earlier studies. Nowadays its use is accepted in Multiple Myeloma therapy., Therapeutics that have proven to be highly effective include the immunomodulatory Pharmacologic Substance thalidomide and its newer analogs, lenalidomide and pomalidomide, as well as the Proteasome inhibitors, antineoplastic agent bortezomib and carfilzomib, As immunomodulatory drugs, thalidomide and its analogues have been used to effectively treat various diseases, Its effectiveness in the clinic has been ascribed to wide-ranging properties, including anti-TNF-alpha, T-Lymphocyte costimulatory and antiangiogenic activity., Thalidomide has various immunomodulatory effects. Thalidomide inhibits TNF alpha production, has T-Lymphocyte costimulatory properties and modulates the expression of cell surface molecules on Specimen Source Codes - Leukocytes in vivo.,  thalidomide has been a target of active investigation in both malignant and inflammatory conditions. Although initially developed for its sedative properties, decades of investigation have identified a multitude of biological effects that led to its classification as an immunomodulatory Pharmacologic Substance (IMiD)., The mechanism of action of thalidomide is probably based on its immunomodulatory effect, namely the suppression of production of Tumor Necrosis Factor-alpha and the modulation of Recombinant Interleukins., This effect is probably due to a direct influence on the immune system[SEP]Relations: Thalidomide has relations: drug_drug with Etomidate, drug_drug with Etomidate, drug_drug with Desomorphine, drug_drug with Desomorphine, drug_drug with Dipyridamole, drug_drug with Dipyridamole, drug_drug with Practolol, drug_drug with Practolol, drug_drug with Felodipine, drug_drug with Felodipine.", "label": "yes"}
+{"original_question": "Does metformin alleviate atherosclerosis?", "id": "converted_3527", "sentence1": "Does metformin alleviate Arteriosclerosis?", "sentence2": "Metformin and rosiglitazone both improve glycemic control in type 2 diabetes mellitus, however may possess different anti-inflammatory and anti-atherosclerotic properties. , Demonstrating antiatherothrombotic properties of dipeptidyl peptidase-4 inhibitors on proven markers is of substantial clinical significance. Coupled with their proven good safety profile these findings could translate into a significant clinical benefit., pleiotropic benefits of metformin in attenuation of Arteriosclerosis., Pleiotropic effects of metformin ameliorate Arteriosclerosis and vascular senescence., Metformin inhibits monocyte-to-macrophage differentiation via AMPK-mediated inhibition of STAT3 protein, human protein, human activation: potential role in Arteriosclerosis., Metformin attenuated Ang-II-induced Atheroma plaque formation and Aortic aneurysm without mention of rupture NOS in ApoE(-/-) CASP14 gene partly by reducing monocyte infiltration., Metformin, an anti-diabetic drug, was reported to possess anti-atherosclerotic effects. , Combined use of metformin and atorvastatin attenuates Arteriosclerosis in Family Leporidae (organism) fed a high-cholesterol diet.,  In cultured Specimen Source Codes - Macrophages, co-treatment with metformin and atorvastatin promoted cholesterol efflux and up-regulated expression of ABCA1 protein, human and G1. Taken together, our results suggest that atorvastatin/metformin combination therapy may achieve additional anti-atherosclerotic benefits likely through increasing cholesterol efflux in Specimen Source Codes - Macrophages., Metformin Suppresses Diabetes-Accelerated Atherosclerosis via the Inhibition of Drp1-Mediated Mitochondrial Inheritance Inheritance Fission., metformin abated the progression of diabetes-accelerated Arteriosclerosis by inhibiting mitochondrial fission in Endothelial Cells., metformin attenuated the development of Arteriosclerosis by reducing Drp1-mediated mitochondrial fission in an AMPK-dependent manner. , metformin's effects on Lipids and Atherosclerosis and/or provide insights into the drug's mechanisms of action on the Chest>Heart and Vasculature., Several recently completed randomized clinical trials have reported effects of metformin on surrogate measures of Atherosclerosis, Metformin treatment prevents SREBP2-mediated cholesterol uptake and improves lipid homeostasis during oxidative stress-induced Arteriosclerosis, Metformin ameliorates the progression of Arteriosclerosis via suppressing macrophage infiltration and inflammatory responses, Our results suggest that metformin impeded the progression of Arteriosclerosis, possibly by suppressing macrophage infiltration and inflammatory responses.[SEP]Relations: Metformin has relations: drug_effect with Hyperhidrosis, drug_effect with Hyperhidrosis, drug_drug with Ifosfamide, drug_drug with Ifosfamide, drug_effect with Erythema, drug_effect with Erythema, drug_drug with Cyclosporine, drug_drug with Cyclosporine, drug_effect with Lethargy, drug_effect with Lethargy.", "label": "yes"}
+{"original_question": "Is pregnancy an additional risk during during H1N1 infection?", "id": "converted_62", "sentence1": "Is pregnancy an additional risk during during H1N1 Communicable Diseases?", "sentence2": "H1N1 influenza in pregnancy can be associated with severe complications, This case series confirms a high number of complications in pregnant women due to pandemic H1N1/09., Pregnant women might be at increased risk for complications from pandemic H1N1 Virus Communicable Diseases., Pregnant women are at increased risk for complications from pandemic influenza H1N1 Virus Communicable Diseases. , Vaccination of pregnant women against influenza A (H1N1) by Russian subunit formulation (MonoGrippol plus) showed reactogenicity comparable to control group by the level of influence on general metabolic and immunologic homeostasis and on the course of pregnancy, which is an evidence of its safety, Pregnancy 1 1 was identified as a major risk factor for increased mortality and morbidity due to H1N1 influenza in the pandemic of 2009 to 2010, While it is not possible to ascertain retrospectively if Myocarditis was caused by either Communicable Diseases with H1N1 Virus or as a result of pregnancy (in the absence of endomyocardial biopsies), the significant association with Myocardial involvement in both women demonstrates the increased risk of exposure to H1N1 influenza Virus in pregnant women., Although limited in size, the fully prospective nature of the safety follow-up of these women vaccinated during pregnancy is unique and offers an important degree of reassurance for the use of the AS03 adjuvanted H1N1 (2009) vaccine in this high risk group for H1N1 Communicable Diseases., During the H1N1 2009 pandemic, pregnant women constituted one of the priority groups for vaccination in many countries, creating a need for close monitoring of the safety of the vaccine in pregnant women, Emerging data suggest that pregnancy conveys high risk for severe complications from the 2009 pandemic influenza A Virus (2009 H1N1) Communicable Diseases, Pregnant women have been identified as a group at risk, both for Respiratory complication than for the admissions to the Intensive Care Unit (ICU) during the 2009 H1N1 influenza pandemic, This report mitigates substantially the presumed severity of pandemic H1N1/09 influenza Communicable Diseases during pregnancy, The results of our study do not indicate a risk for the pregnant woman and the developing embryo/fetus after H1N1 vaccination, This large cohort study found no evidence of an increased risk of Prenatal care death associated with exposure to an adjuvanted pandemic A/H1N1 2009 influenza vaccine during pregnancy, Our results suggest that second- or third-trimester H1N1 vaccination was associated with improved Prenatal care and neonatal outcomes during the recent pandemic, Pregnant women might thus be at increased risk of complications from pandemic H1N1 Virus Communicable Diseases, and Illness (finding) may progress rapidly, Pregnant women with H1N1 Communicable Diseases seem to benefit from antiviral therapy., arly identification and treatment were the most important factors in different countries and areas examined., The vaccine and antiviral drugs that have been the most efficient means to control the novel Virus appear to be safe but require more extensive study, However, there were significant differences between the two groups in relation to mean age, treatment with oseltamivir, schooling, and presence of other risk factors, To investigate whether exposure to an adjuvanted influenza A(H1N1)pdm09 vaccine during pregnancy was associated with increased risk of adverse Prenatal care outcomes., In this Danish cohort, exposure to an adjuvanted influenza A(H1N1)pdm09 vaccine during pregnancy was not associated with a significantly increased risk of major birth defects, preterm birth, or Prenatal care growth restriction, Most people affected by the Virus, including pregnant women, suffer a mild viral Illness (finding), and make a full recovery, Pregnant women, because of their altered immunity and physiological adaptations, are at higher risk of developing Pulmonary:-:Point in time:^Patient:- complications, especially in the second and third trimesters, The pregnancy outcomes were also poor for women who were affected by the Virus with a fivefold increase in the perinatal mortality rate and threefold increase in the preterm delivery rate, regnant women were at increased risk for serious outcomes of 2009 pandemic influenza A Virus subtype H1N1 (influenza A[H1N1]pdm09) Communicable Diseases, but little is known about the overall impact of the pandemic on neonatal and maternal outcomes, In this large, geographically diverse population, A(H1N1)pdm09 Communicable Diseases increased the risk for hospitalization during pregnancy, Vaccination during pregnancy with Pandemrix(®) appeared to have no ill effects on the pregnancy. On the contrary, the rate of preterm birth and low birthweight was lower than expected, which agrees with some previous results, During the influenza A(H1N1)pmd09 pandemic, although many cases occurred in younger adults, the risk factors identified for severe Infections of musculoskeletal system and complications were similar to those for seasonal influenza, including chronic respiratory, Kidney, Abdomen>Liver, and heart diseases., In terms of pregnancy, the studies have shown contradictory results due to variations in methodology and medical care., However, it seems that pregnancy, particularly during the third trimester, increases the risk of complications, and that early antiviral treatment is associated with improved outcomes., Pregnant women with mild clinical Illness (finding) secondary to 2009 H1N1 were not at a greater risk of adverse pregnancy outcomes, However, severely infected women were more likely to deliver SGA infants, Gestational age is associated with the risk of developing critical Communicable Diseases. The risk increases with increasing weeks of gestation.,  Following the start of winter in Liaoning province in China, the number of pregnant women infected with influenza increased significantly, regnancy, with or without additional complications, constitutes a high-risk condition for complications of influenza Communicable Diseases and warrants early intervention with neuraminidase inhibitors such as oseltamivir, if influenza is suspected[SEP]Relations: tubal pregnancy has relations: disease_disease with ectopic pregnancy, disease_disease with ectopic pregnancy. kidney has relations: anatomy_protein_present with HNF1A-AS1, anatomy_protein_present with HNF1A-AS1, anatomy_protein_present with HNF1A, anatomy_protein_present with HNF1A, anatomy_protein_present with VN1R1, anatomy_protein_present with VN1R1, anatomy_protein_present with HNF1B, anatomy_protein_present with HNF1B.", "label": "yes"}
+{"original_question": "Does magnesium sulfate improve outcomes of subarachnoid hemorrhage patients?", "id": "converted_897", "sentence1": "Does magnesium sulfate improve outcomes of Subarachnoid Hemorrhage patients?", "sentence2": "CONCLUSION: Patients assigned a higher serum magnesium concentration had a reduced incidence of Vasospasm as seen by angiography, but the difference was not statistically significant. Clinically significant outcomes were not different between groups., 158 patients (26·2%) had poor outcome in the magnesium group compared with 151 (25·3%) in the placebo group (risk ratio [RR] 1·03, 95% CI 0·85-1·25). Our updated meta-analysis of seven randomised trials involving 2047 patients shows that magnesium is not superior to placebo for reduction of poor outcome after aneurysmal subarachnoid haemorrhage (RR 0·96, 95% CI 0·86-1·08). INTERPRETATION: Intravenous magnesium sulphate does not improve clinical outcome after aneurysmal subarachnoid haemorrhage, therefore routine administration of magnesium cannot be recommended. , There is a tendency in the magnesium group to have better outcomes. , Due to inconsistently reported benefits and the occurrence of side effects, phase II data suggested that intravenous magnesium for Yakut language provided either no overall net benefit or uncertain trade-offs. Benefit was likewise not supported in the single phase III clinical trial., tatistically significant clinical benefits could not be demonstrated for the other drugs (clazosentan, Hydroxymethylglutaryl-CoA Reductase Inhibitors, and magnesium). CONCLUSIONS: Insufficient evidence is available to support the use of the triple-H therapy, clazosentan, Hydroxymethylglutaryl-CoA Reductase Inhibitors, or magnesium sulfate for the prevention of Cerebral hemisphere structure (body structure) Vasospasm following Subarachnoid Hemorrhage. , Magnesium supplements, alimentary tract and metabolism supplements, alimentary tract and metabolism sulfate decreased the rate of Cerebral hemisphere structure (body structure) infarction, but not of Noninfiltrating Intraductal Carcinoma or poor functional outcome. Regarding outcome, a beneficial effect of magnesium sulfate on outcome can not be ruled out because of sample size limitations., CONCLUSIONS: The present findings do not lend support to a beneficial effect of magnesium sulphate infusion on delayed Cerebral hemisphere structure (body structure) infarction. The reduction in Noninfiltrating Intraductal Carcinoma and improvement in the clinical outcomes of aneurysmal Yakut language patients following magnesium sulphate infusion observed in previous pilot studies are not confirmed, although a beneficial effect cannot be ruled out because of sample size limitation., Favorable outcome (Good recovery and moderate disability, as defined by Glasgow Outcome Scale) was achieved in 20 of 30 (67%) patients receiving magnesium sulfate infusion and 16 of 30 (53%) patients receiving placebo treatment, p = 0.292, odds ratio 1.750, 95% CI 0.616-4.974., Similarly, the pooled odds ratio for favorable outcome is 1.598, 95% CI 1.074-2.377, statistically significant. , RESULTS: The worst clinical outcomes at 6 months were seen in MgSO(4) group patients, with mean plasma magnesium concentrations in the fourth quartile, and in placebo group patients, with mean such concentrations in the third and fourth quartiles. CONCLUSIONS: No evidence was found to suggest that a higher mean plasma magnesium concentration improves clinical outcomes. On the contrary, we found an association between high plasma magnesium concentration and worse clinical outcomes., The proportions of patients with a favorable outcome at 6 months (Extended Glasgow Outcome Scale 5 to 8) were similar, 64% in the magnesium sulfate group and 63% in the saline group (OR, 1.0; 95% CI, 0.7 to 1.6). Secondary outcome analyses (modified Rankin Scale, Barthel Index, Short Form 36, and clinical Vasospasm) also showed no significant differences between the 2 groups. , CONCLUSIONS: The results do not support a clinical benefit of intravenous magnesium sulfate infusion over placebo infusion in patients with acute aneurysmal Subarachnoid Hemorrhage., Magnesium supplements, alimentary tract and metabolism supplements, alimentary tract and metabolism infusion reduced the risk of poor outcome and delayed Cerebral hemisphere structure (body structure) ischemia (Noninfiltrating Intraductal Carcinoma): the relative risk was 0.62 (95% confidence interval (CI) 0.46-0.83) and 0.73 (95% CI 0.53-1.00), respectively. , CONCLUSION: The meta-analysis suggests that intravenous magnesium therapy reduces the risk of Noninfiltrating Intraductal Carcinoma and poor outcome after aneurysmal Yakut language. , The incidence of delayed ischemic infarction was significantly lower in magnesium-treated patients (22% vs. 51%; p = .002); 34 of 54 magnesium patients and 27 of 53 control patients reached good outcome (p = .209)., BACKGROUND: A meta-analysis of current data suggests that magnesium sulfate infusion improves the outcome after aneurysmal Subarachnoid Hemorrhage through a reduction in delayed ischemic neurological deficit. , These data imply that intravenous magnesium therapy, besides a supposed beneficial effect on outcome, also provides pain relief for Yakut language patients, for whom it might also improve functional outcome., Preliminary evidence has suggested that magnesium sulfate infusion reduces delayed ischemic neurological deficit and improves clinical outcome after aneurysmal Subarachnoid Hemorrhage. , In a phase II randomized clinical trial of 283 patients, magnesium treatment reduced the risk of Noninfiltrating Intraductal Carcinoma by 34% and of poor outcome by 23%., BACKGROUND: Recent studies suggest that high-dose magnesium sulfate therapy is safe and reduces the incidence of DIND and subsequent poor outcome after Yakut language. , On-treatment analysis showed a significantly better outcome after 3 months (P = .017) and a trend toward better outcome after 1 year (P = .083). ,  CONCLUSIONS: High-dose magnesium sulfate therapy might be efficient as a prophylactic adjacent therapy after Yakut language to reduce the risk for poor outcome. , There was no significant difference in mortality rate at discharge (p = 0.328). A trend toward improved outcome as measured by the modifed Rankin Scale (p = 0.084), but not the Glasgow Outcome Scale (p = 1.0), was seen in the magnesium sulfate treated group. CONCLUSIONS: Analysis of the results suggests that magnesium sulfate infusion may have a role in Cerebral hemisphere structure (body structure) Vasospasm prophylaxis if therapy is initiated within 48 hours of Aneurysm, Ruptured., There was, however, no difference between groups in functional recovery or Glasgow Outcome Scale score. , Patients receiving magnesium sulfate tended to have fewer Neurologic Deficits, better functional recovery and an improved score in Genomics Outcome Scale. , CONCLUSIONS: magnesium sulfate infusion after aneurysmal Yakut language is well tolerated and may be useful in producing better outcome., CONCLUSION: Magnesium supplements, alimentary tract and metabolism supplements, alimentary tract and metabolism did not seem to interfere in Vasospasm frequency but apparently acted favorably in decreasing morbidity and length of hospital stay., None of the patients died; no X-Ray Computed Tomography evidence of ischemic infarction was present; and most had good outcomes (Genomics Outcome Scale 5 in 10 patients; Genomics Outcome Scale 4 in 8 patients)., At that time, 18 patients in the treatment group and 6 in the placebo group had an excellent outcome (risk ratio, 3.4; 95% CI, 1.3 to 8.9). CONCLUSIONS: This study suggests that magnesium reduces Noninfiltrating Intraductal Carcinoma and subsequent poor outcome, but the results are not yet definitive. , We observed a trend in which a higher percentage of patients obtained Genomics Outcome Scale scores of 4 or 5 in the group treated with magnesium sulfate, but the trend did not reach a statistically significant level. , Magnesium supplements, alimentary tract and metabolism supplements, alimentary tract and metabolism sulfate treatment improves outcome in patients with Subarachnoid Hemorrhage: a meta-analysis study., BACKGROUND AND PURPOSE: Pilot clinical trials using magnesium sulfate in patients with acute aneurysmal Subarachnoid Hemorrhage have reported trends toward improvement in clinical outcomes., Preliminary evidence has suggested that magnesium sulfate infusion reduces delayed ischemic neurological deficit and improves clinical outcome after aneurysmal Subarachnoid Hemorrhage., Our results indicate that although there was reduced likelihood of a poor outcome for patients treated with magnesium sulfate after Yakut language, patient mortality was not improved., CONCLUSION: Administration of intra-arterial magnesium sulfate in combination with nicardipine was well tolerated in patients with Subarachnoid Hemorrhage and Cerebral hemisphere structure (body structure) Vasospasm without a significant change in cisplatin/doxorubicin/mitomycin protocol and ICP., Current evidence does not support the prophylactic use of magnesium sulfate in aneurysmal Subarachnoid Hemorrhage, Preliminary evidence has suggested that magnesium sulfate infusion reduces delayed ischemic neurological deficit and improves clinical outcome after aneurysmal Subarachnoid Hemorrhage, A meta-analysis of current data suggests that magnesium sulfate infusion improves the outcome after aneurysmal Subarachnoid Hemorrhage through a reduction in delayed ischemic neurological deficit, Despite the publication of several randomized controlled studies, there is still much debate on whether magnesium sulfate improves outcome in patients with aneurysmal Subarachnoid Hemorrhage, Magnesium supplements, alimentary tract and metabolism supplements, alimentary tract and metabolism sulphate is a neuroprotective agent that might improve outcome after aneurysmal subarachnoid haemorrhage by reducing the occurrence or improving the outcome of delayed Cerebral hemisphere structure (body structure) ischaemia[SEP]Relations: Magnesium supplements, alimentary tract and metabolism sulfate has relations: contraindication with hypercalcemia disease, contraindication with hypercalcemia disease, contraindication with chronic diarrheal disease, contraindication with chronic diarrheal disease, contraindication with kidney disease, contraindication with kidney disease, drug_drug with Tubocurarine, drug_drug with Tubocurarine, drug_drug with Thioridazine, drug_drug with Thioridazine.", "label": "no"}
+{"original_question": "Are the genes for marneral biosynthesis scattered in the genome of A. thaliana?", "id": "converted_2049", "sentence1": "Are the Genes for marneral biosynthesis scattered in the genome of Arabidopsis thaliana <plant>?", "sentence2": "Here we characterize a second operon-like triterpene cluster (the marneral cluster) from Arabidopsis thaliana <plant>, compare the features of these two clusters, and investigate the evolutionary events that have led to cluster formation, Here we characterize a second operon-like triterpene cluster (the marneral cluster) from Arabidopsis thaliana <plant>, compare the features of these two clusters, and investigate the evolutionary events that have led to cluster formation., Previously in thale cress (Arabidopsis thaliana) we identified an operon-like gene cluster that is required for the synthesis and ResponseLevel - ResponseLevel - modification of the triterpene thalianol., Prediction of operon-like gene clusters in the Arabidopsis thaliana genome based on co-expression analysis of neighboring Genes, Here we characterize a second operon-like triterpene cluster (the marneral cluster) from Arabidopsis thaliana <plant>, compare the features of these two clusters, and investigate the evolutionary events that have led to cluster formation. , Here we characterize a second operon-like triterpene cluster (the marneral cluster) from A., the cyclic hydroxamic acid pathways in maize, the avenacin biosynthesis gene clusters in oat, the thalianol pathway in Arabidopsis thaliana, and the diterpenoid momilactone cluster in rice., Prediction of operon-like gene clusters in the Arabidopsis thaliana genome based on co-expression analysis of neighboring Genes.[SEP]Relations: response to nickel cation has relations: bioprocess_protein with CACNA1G, bioprocess_protein with CACNA1G, bioprocess_bioprocess with cellular response to nickel ion, bioprocess_bioprocess with cellular response to nickel ion, bioprocess_bioprocess with response to metal ion, bioprocess_bioprocess with response to metal ion.", "label": "no"}
+{"original_question": "Do normal cells express the protein TERT?", "id": "converted_1962", "sentence1": "Do Normal cell express the protein TERT?", "sentence2": "Since Telomerase has been recognized as a relevant factor distinguishing Tumor cells, malignant from Normal cell, it has become a very promising target for anti-cancer therapy, Telomerase plays a pivotal role in cellular immortality and tumorigenesis. Its activity is normally not detectable in most Diploid Cell while it is reactivated in the vast majority of Tumor cells, malignant. Therefore, inhibition of Telomerase has been viewed as a promising anticancer approach due to its specificity for Tumor cells, malignant., Telomerase activity is found in 85%-90% of all Homo sapiens Malignant Neoplasms but not in their adjacent Normal cell. Human Telomerase reverse transcriptase (TERT wt Allele) is an essential component in the Telomerase complex that plays an important role in Telomerase activity., elomerase activation is considered to be a critical step in carcinogenesis and its activity correlates closely with TERT protein, Homo sapiens (TERT wt Allele) expression. Since only Tumor cells, uncertain whether benign or malignant that express Telomerase activity would activate this Promoter, the TERT wt Allele proximal Promoter allows for preferential expression of Genes, Viral in Tumor cells, uncertain whether benign or malignant, leading to selective viral replication[SEP]Relations: Protein S Homo sapiens has relations: drug_drug with Platelet Activating Factor, drug_drug with Platelet Activating Factor, drug_protein with PROC, drug_protein with PROC, drug_drug with Iloprost, drug_drug with Iloprost, drug_drug with Dienogest, drug_drug with Dienogest, drug_drug with Sarpogrelate, drug_drug with Sarpogrelate.", "label": "no"}
+{"original_question": "Is Tocilizumab (Actemra) used to block/antagonize the  IL-6 receptor?", "id": "converted_4037", "sentence1": "Is tocilizumab (Actemra) used to block/antagonize the  Recombinant Interleukin-6 receptor?", "sentence2": "Preliminary clinical results have indicated that antagonism of the Recombinant Interleukin-6 receptor (Interleukin 6 Receptor activity), including with the FDA-approved humanized monoclonal immunoglobulin complex location tocilizumab, can improve the outcomes of patients with severe or critical COVID-19 while maintaining a good safety profile., tocilizumab, an anti-Recombinant Interleukin-6 receptor immunoglobulin complex location, and Corticosteroid ophthalmologic and otologic preparations were initially used to treat the increase in acute inflammatory proteins and the Anasarca, resulting in decreased cytokine levels. , tocilizumab, a monoclonal immunoglobulin complex location against the Recombinant Interleukin-6 receptor, was initiated at a dose of 8 mg/kg every 4 weeks., we randomly assigned patients with type 2 diabetes or obesity to intravenous tocilizumab (an Recombinant Interleukin-6 receptor antagonist) ,  Clinical studies are investigating whether tocilizumab (anti-Recombinant Interleukin-6 receptor) can help preserve beta cell function in patients recently diagnosed with Diabetes Mellitus, Insulin-Dependent, tocilizumab (Roactemra or Actemra) is a recombinant humanized monoclonal immunoglobulin complex location that acts as an interleukin (IL)-6 receptor antagonist., To increase the number of cycles of antigen binding and lysosomal degradation, we engineered tocilizumab (Actemra), an immunoglobulin complex location against the Recombinant Interleukin-6 receptor (Interleukin 6 Receptor activity), to rapidly dissociate from Interleukin 6 Receptor activity within the acidic environment of the Endosomes (pH 6.0) while maintaining its binding affinity to Interleukin 6 Receptor activity in Specimen Source Codes - Plasma (pH 7.4)., tocilizumab (Actemra; Genentech, Inc) is the first biologic therapy targeting the cytokine interleukin-6 (Recombinant Interleukin-6)., over, our findings showed that combination of tocilizumab (Actemra; Roche), an anti-Interleukin 6 Receptor activity monoclonal immunoglobulin complex location, with carboplatin synergistically inhibited growth and proliferation of the EOC Cells and the most direct axis for Recombinant Interleukin-6 gene expression was NF-κB pathway.CONC, Roche is co-developing tocilizumab (Actemra, Roactemra), a humanized anti-Interleukin 6 Receptor (Interleukin 6 Receptor activity) monoclonal immunoglobulin complex location, with Chugai Pharmaceutical., tocilizumab (TCZ) is a compound that inhibits the Recombinant Interleukin-6 receptor., tocilizumab (TCZ), is a recombinant humanized anti-Interleukin 6 Receptor (Interleukin 6 Receptor activity) monoclonal immunoglobulin complex location which has a main use in the treatment of rheumatoid arthritis, systemic juvenile idiopathic arthritis (sJIA) and Acute polyarticular juvenile rheumatoid arthritis (pJIA)., the US Food and Drug Administration accepted a complete-response submission for the use of Actemra (tocilizumab), the first humanized Recombinant Interleukin-6 receptor-inhibiting monoclonal immunoglobulin complex location, for the treatment of Rheumatoid Arthritis. Although thi, increase the number of cycles of antigen binding and lysosomal degradation, we engineered tocilizumab (Actemra), an immunoglobulin complex location against the Recombinant Interleukin-6 receptor (Interleukin 6 Receptor activity), to rapidly dissociate from Interleukin 6 Receptor activity within the acidic environment of the Endosomes (pH 6.0) while maintaining its binding affinity to Interleukin 6 Receptor activity in Specimen Source Codes - Plasma (pH 7.4). Studies usin,  present study, we have shown that the humanized anti-Recombinant Interleukin-6 receptor tocilizumab (Actemra) is also a potent inhibitor of interleukin-8 receptor binding activity in TNBC Cells. Similar ef, Roche is co-developing tocilizumab (Actemra, Roactemra), a humanized anti-Interleukin 6 Receptor (Interleukin 6 Receptor activity) monoclonal immunoglobulin complex location, with Chugai Pharmaceutical. Tocili, tory gene activation is inhibited in vitro by tocilizumab, a humanized immunoglobulin complex location to IL6 receptor (IL6R protein, Homo sapiens protein, Homo sapiens). tocilizumab, These lines of evidence indicate that tocilizumab is able to bind to both Soluble Interleukin-6 Receptor Subunit Alpha, Human and mIL-6R and to inhibit Recombinant Interleukin-6 binding to its receptors, leading to the blockade of the Recombinant Interleukin-6 signaling through both Soluble Interleukin-6 Receptor Subunit Alpha, Human and mIL-6R, but not block the signaling of other Recombinant Interleukin-6 family Recombinant Cytokines., tocilizumab inhibits signal transduction mediated by both mIL-6R and Soluble Interleukin-6 Receptor Subunit Alpha, Human, but not by the receptors of other members of Recombinant Interleukin-6 cytokine family., In addition, tocilizumab had the ability to bind to Homo sapiens Interleukin 6 Receptor activity expressing COS-7 Cells and to suppress the growth of the Recombinant Interleukin-6-dependent myeloma cell line, KPMM2., To characterize the biological activity of tocilizumab, a humanized anti-Homo sapiens Interleukin 6 Receptor (Interleukin 6 Receptor activity) monoclonal immunoglobulin complex location, we examined its binding activity to both soluble Interleukin 6 Receptor activity (Soluble Interleukin-6 Receptor Subunit Alpha, Human) and membrane bound Interleukin 6 Receptor activity (mIL-6R) and its neutralizing activity to other Recombinant Interleukin-6 family Recombinant Cytokines., tocilizumab inhibited the proliferation of BaF/Interleukin 6 Receptor activity induced by Recombinant Interleukin-6, but did not inhibit the proliferation of BaF/IL-11R, BaF/OSMR, BaF/LIFR and BaF/CNTFR Cells induced by their corresponding Recombinant Cytokines., Moreover, tocilizumab suppressed the Recombinant Interleukin-6/Soluble Interleukin-6 Receptor Subunit Alpha, Human complex-induced proliferation of Homo sapiens gp130-transfected cell, BAF-h130., In addition, tocilizumab had the ability to dissociate Recombinant Interleukin-6 and Soluble Interleukin-6 Receptor Subunit Alpha, Human from their preformed complex., ELISA assay demonstrated that tocilizumab bound to Soluble Interleukin-6 Receptor Subunit Alpha, Human and inhibited Recombinant Interleukin-6 binding to Soluble Interleukin-6 Receptor Subunit Alpha, Human in a dose-dependent manner., tocilizumab recognizes both the membrane-bound and the soluble form Interleukin 6 Receptor activity and specifically blocks Recombinant Interleukin-6 actions., Humanized antihuman Recombinant Interleukin-6 receptor immunoglobulin complex location, tocilizumab., tocilizumab is a humanized antihuman Recombinant Interleukin-6 receptor immunoglobulin complex location designed using genetic engineering technology., tocilizumab is expected to ameliorate the autoimmune inflammatory diseases with Recombinant Interleukin-6 overproduction and has been clinically developed as a therapeutic agent for Rheumatoid Arthritis, systemic-onset and articular types of JIA, Crohn's disease of oral soft tissues of oral soft tissues, etc., tocilizumab/Actemra is an anti-Interleukin 6 Receptor activity immunoglobulin complex location, which can competitively block Recombinant Interleukin-6 binding to the Interleukin 6 Receptor activity., tocilizumab (TCZ; Roactemra® or Actemra®) is a recombinant humanized monoclonal immunoglobulin complex location that acts as an interleukin-6 (Recombinant Interleukin-6) receptor antagonist., In 2009 the US Food and Drug Administration accepted a complete-response submission for the use of Actemra (tocilizumab), the first humanized Recombinant Interleukin-6 receptor-inhibiting monoclonal immunoglobulin complex location, for the treatment of Rheumatoid Arthritis., tocilizumab binds to the Interleukin 6 Receptor (Interleukin 6 Receptor activity) and thereby blocks signaling of the pro-inflammatory cytokine Recombinant Interleukin-6., tocilizumab (Roactemra(®); Actemra(®)) is a recombinant humanized monoclonal immunoglobulin complex location that acts as an Interleukin 6 Receptor antagonist.[SEP]Relations: tocilizumab has relations: drug_protein with IL6R protein, Homo sapiens, drug_protein with IL6R protein, Homo sapiens, drug_drug with Elagolix, drug_drug with Elagolix, drug_drug with Acteoside, drug_drug with Acteoside, drug_drug with Metronidazole, drug_drug with Metronidazole, drug_drug with Atezolizumab, drug_drug with Atezolizumab.", "label": "yes"}
+{"original_question": "Is muscle regeneration possible in mdx mice with the use of induced mesenchymal stem cells?", "id": "converted_1203", "sentence1": "Is muscle regeneration possible in Mice, Inbred mdx with the use of induced mesenchymal stem Cells?", "sentence2": "Purified iMSCs displayed fibroblast-like morphology, formed three-dimensional spheroid structures, and expressed characteristic Mesenchymal Stem Cells surface markers such as Integrin Beta-1, human, CD33 antigen antigen, 5'-NUCLEOTIDASE, Thy-1 Membrane Glycoprotein, human, and Endoglin, human. Moreover, iMSCs were capable of differentiating into adipogenic, osteogenic, and chondrogenic lineages. Transplanting iMSC Cells to tibialis anterior skeletal Muscle Tissue in Mice, Inbred mdx lowered oxidative damage as evidenced by a reduction in nitrotyrosine levels, and normal Dystrophin expression levels were restored, This study demonstrates the therapeutic potential of purified iMSCs in Specimen Source Codes - Skeletal muscle regeneration in Mice, Inbred mdx, Vascular Endothelial Growth Factor Receptor 2, human+ adipose-derived mesenchymal stem Cells differentiate into Specimen Source Codes - Skeletal muscle satellite Cells and ameliorate Muscular Dystrophy in Mice, Inbred mdx, Within Mice, Inbred mdx, an animal model of Muscular Dystrophy, Duchenne, adipose tissue-derived Vascular Endothelial Growth Factor Receptor 2, human(+) cyclic nucleotide-gated mechanosensitive ion channel activity (AD-cyclic nucleotide-gated mechanosensitive ion channel activity) homed to and differentiated into Cells that repaired injured Muscle Tissue. This repair correlated with reconstitution of Dystrophin expression on the damaged fibers, Vascular Endothelial Growth Factor Receptor 2, human(+) AD-MSC transplants may repair Muscular Dystrophy, This study demonstrates the therapeutic potential of purified iMSCs in Specimen Source Codes - Skeletal muscle regeneration in Mice, Inbred mdx, and suggests that iPSCs are a viable alternate source for deriving cyclic nucleotide-gated mechanosensitive ion channel activity as needed., Transplanting iMSC Cells to tibialis anterior skeletal Muscle Tissue in Mice, Inbred mdx lowered oxidative damage as evidenced by a reduction in nitrotyrosine levels, and normal Dystrophin expression levels were restored, This study demonstrates the therapeutic potential of purified iMSCs in Specimen Source Codes - Skeletal muscle regeneration in Mice, Inbred mdx, and suggests that iPSCs are a viable alternate source for deriving cyclic nucleotide-gated mechanosensitive ion channel activity as needed[SEP]Relations: Muscle Tissue has relations: anatomy_protein_present with MDM1, anatomy_protein_present with MDM1, anatomy_protein_present with MDM4, anatomy_protein_present with MDM4, anatomy_protein_present with MDK, anatomy_protein_present with MDK. Mesenchymal Stem Cells proliferation has relations: bioprocess_bioprocess with Mesenchymal Stem Cells proliferation involved in nephron morphogenesis, bioprocess_bioprocess with Mesenchymal Stem Cells proliferation involved in nephron morphogenesis, bioprocess_protein with SIX2, bioprocess_protein with SIX2.", "label": "yes"}
+{"original_question": "Is Hemochromatosis type 4 is caused by a mutation in a recessive gene?", "id": "converted_3466", "sentence1": "Is HEMOCHROMATOSIS, TYPE 4 is caused by a Mutation Abnormality in a recessive Genes?", "sentence2": " severely affect iron homeostasis causing type 4 hereditary hemochromatosis, an Autosome dominant iron overload condition with variable phenotypic manifestations, HEMOCHROMATOSIS, TYPE 4, also known as SLC40A1 Genes disease, is an Autosome dominant genetic disorder caused by pathogenic Gene Mutation in the SLC40A1 Genes, which encodes SLC40A1 Genes 1 (FPN1)., HEMOCHROMATOSIS, TYPE 4 is a rare form of primary iron overload transmitted as an Autosome dominant trait caused by Gene Mutation in the Genes encoding the iron transport protein SLC40A1 Genes 1 (SLC40A1)., Type 4 hemochromatosis follows an Autosome dominant trait; the corresponding Mutation Abnormality affects the basolateral iron carrier SLC40A1 Genes 1., Type 4 hemochromatosis follows an Autosome dominant trait; the corresponding Mutation Abnormality affects the basolateral iron carrier SLC40A1 Genes 1, Type 4 hemochromatosis follows an Autosome dominant trait; the corresponding Mutation Abnormality affects the basolateral iron carrier SLC40A1 Genes 1.[SEP]Relations: hemochromatosis has relations: disease_phenotype_positive with Autosomal recessive inheritance, disease_phenotype_positive with Autosomal recessive inheritance, disease_disease with hereditary hemochromatosis, disease_disease with hereditary hemochromatosis, disease_phenotype_positive with Autosomal dominant inheritance, disease_phenotype_positive with Autosomal dominant inheritance, disease_protein with BMP6, disease_protein with BMP6. SLC40A1 has relations: pathway_protein with Defective SLC40A1 causes hemochromatosis 4 (HFE4) (duodenum), pathway_protein with Defective SLC40A1 causes hemochromatosis 4 (HFE4) (duodenum).", "label": "no"}
+{"original_question": "Is there any role of Dlx1 and Dlx2 transcription factors in cortical interneurons?", "id": "converted_2487", "sentence1": "Is there any role of Homeobox Protein DLX-1 and Dlx2 transcription factors in cortical interneurons?", "sentence2": "The postnatal functions of the Homeobox Protein DLX-1&2 transcription factors in cortical interneurons (CINs) are unknown. Here, using conditional Homeobox Protein DLX-1, Dlx2, and Homeobox Protein DLX-1&2 knockouts (CKOs), we defined their roles in specific CINs. The CKOs had dendritic, synaptic, and survival defects, affecting even PV+ CINs. We provide evidence that DLX2 gene gene directly drives glutamate decarboxylase 1 (brain, 67kDa), human, GAD2 gene, and SLC32A1 gene expression, and show that Mutant had reduced mIPSC amplitude. In addition, the Mutant formed fewer GABAergic synapses on excitatory neurons and had reduced mIPSC frequency. Furthermore, Homeobox Protein DLX-1/2 CKO had hypoplastic dendrites, fewer excitatory synapses, and reduced excitatory input. We provide evidence that some of these phenotypes were due to reduced expression of GRIN2B gene gene (a subunit of the N-Methyl-D-Aspartate Receptors), a high confidence Autism gene. Thus, Homeobox Protein DLX-1&2 coordinate key components of Cervical Intraepithelial Neoplasia postnatal development by promoting their excitability, inhibitory output, and survival., Furthermore, Homeobox Protein DLX-1/2 CKO had hypoplastic dendrites, fewer excitatory synapses, and reduced excitatory input.[SEP]Relations: GAD2 has relations: pathway_protein with MECP2 regulates transcription of genes involved in GABA signaling, pathway_protein with MECP2 regulates transcription of genes involved in GABA signaling, protein_protein with CPLX4, protein_protein with CPLX4, protein_protein with RHEX, protein_protein with RHEX, anatomy_protein_present with dorsolateral prefrontal cortex, anatomy_protein_present with dorsolateral prefrontal cortex. SLC32A1 has relations: anatomy_protein_present with dorsolateral prefrontal cortex, anatomy_protein_present with dorsolateral prefrontal cortex.", "label": "yes"}
+{"original_question": "Is HER2 active only when it dimerizes?", "id": "converted_1367", "sentence1": "Is erbB-2 Receptor active only when it dimerizes?", "sentence2": "Herero language activation is driven by the formation of various dimer complexes between members of this receptor family., rtuzumab is the first Antibodies, Monoclonal, Humanized CAL in a new class of drugs, the Herero language dimerization inhibitors, approved by the Food and Drug, Pertuzumab is a novel anti-erbB-2 Receptor monoclonal antibody CAL CAL, which blocks erbB-2 Receptor dimerization with other ligand-activated Herero language family members. Here, we explored the complement-mediated anti-tumor effects of trastuzumab and pertuzumab on erbB-2 Receptor-positive tumor cells of various histological origins., ays. In this study, we report that an anti-erbB-2 Receptor monoclonal antibody CAL CAL (HER2Mab), which blocks erbB-2 Receptor dimerization with ERBB3 gene Receptor Protein-Tyrosine Kinase, induces ERBB3 gene Receptor Protein-Tyrosine Kinase dimerization with Epidermal Growth Factor Receptor in both low and high erbB-2 Receptor expressing Tumor cells, malignant., Recent evidence from both basic and clinical studies suggests that ERBB3 gene gene (ERBB3 gene Receptor Protein-Tyrosine Kinase) serves as a key activator of downstream signaling through dimerization with other ERBB proteins and plays a critical role in the widespread clinical resistance to Epidermal Growth Factor Receptor and erbB-2 Receptor targeting cancer therapies. , ERBB3 gene Receptor Protein-Tyrosine Kinase intracellular domains play a crucial role in ERBB3 gene Receptor Protein-Tyrosine Kinase/erbB-2 Receptor dimerization and activation of downstream signaling pathways., Dimerization among the Epidermal Growth Factor Receptor family of Receptor Protein-Tyrosine Kinases leads to allosteric activation of the kinase domains of the partners., Our results show that quantification of Herero language dimerization provides information about receptor activation that cannot be obtained by quantification of single receptors. , Pertuzumab is a novel Antibodies, Monoclonal, Humanized CAL that blocks epidermal growth factor receptor 2, human (erbB-2 Receptor) dimerization. It was recently approved by the US FDA for use in combination with trastuzumab and docetaxel for patients with erbB-2 Receptor-positive metastatic breast cancer who have not received prior anti-erbB-2 Receptor therapy or chemotherapy for metastatic disease. , he Herero language dimerization status may be more important than Herero language receptor expression per se in determining sensitivity or resistance to a given therapeutic agen,  and erbB-2 Receptor dimerization inhibitors, One of the mechanisms by which Tumor cells, uncertain whether benign or malignant proliferation can be inhibited consists in hampering erbB-2 Receptor dimerization by targeting its Extracellular Domain with specific Antibodies, in vitro diagnostic. , Pertuzumab, a Antibodies, Monoclonal, Humanized CAL, is the first erbB-2 Receptor dimerization inhibitor. It binds to the dimerization site on the erbB-2 Receptor domain and prevents ligand-driven pairing of erbB-2 Receptor with other Herero language receptors, thus inhibiting Tumor cells, uncertain whether benign or malignant growth and survival, Pertuzumab, another monoclonal antibody CAL CAL, is a erbB-2 Receptor dimerization inhibitor that binds to a different Epitopes on erbB-2 Receptor than trastuzumab and inhibits erbB-2 Receptor dimer formation with other Herero language family members such as ERBB3 gene Receptor Protein-Tyrosine Kinase and Epidermal Growth Factor Receptor gene. [SEP]Relations: ERBB3 gene has relations: protein_protein with ACTR2, protein_protein with ACTR2, molfunc_protein with protein heterodimerization activity, molfunc_protein with protein heterodimerization activity, molfunc_protein with protein tyrosine kinase activator activity, molfunc_protein with protein tyrosine kinase activator activity, protein_protein with ACTG2, protein_protein with ACTG2, protein_protein with ACTBL2, protein_protein with ACTBL2.", "label": "yes"}
+{"original_question": "Has single guide RNA been used on human cells?", "id": "converted_999", "sentence1": "Has single guide RNA been used on Human cells?", "sentence2": "We used a library containing 73,000 sgRNAs to generate knockout collections and performed screens in two human cell lines., Here we engineer this system to enable RNA-guided genome regulation in Human cells by tethering transcriptional activation domains either directly to a nuclease-null CRISPR-Associated Protein 9 or to an aptamer-modified single guide RNA (sgRNA)., The type II CRISPR/Cas system from Streptococcus pyogenes and its simplified derivative, the Cas9/single guide RNA (sgRNA) system, have emerged as potent new tools for targeted gene knockout in Bacteria, Saccharomyces cerevisiae, Drosophila <Drosophila <fruit fly, genus>, genus>, Zebrafish and Human cells., Here we engineer this system to enable RNA-guided genome regulation in Human cells by tethering transcriptional activation domains either directly to a nuclease-null CRISPR-Associated Protein 9 or to an aptamer-modified single guide RNA (sgRNA). , Using synthetic single RNA guides, Cas9 can be reprogrammed to create specific double-stranded DNA breaks in the Genome of a variety of Organism, ranging from Human cells to Bacteria, and thus constitutes a powerful tool for genetic engineering. , Here we engineer this system to enable RNA-guided genome regulation in Human cells by tethering transcriptional activation domains either directly to a nuclease-null CRISPR-Associated Protein 9 or to an aptamer-modified single guide RNA (sgRNA).[SEP]Relations: ER-associated misfolded protein catabolic process has relations: bioprocess_protein with RNF5, bioprocess_protein with RNF5, bioprocess_protein with RNF185, bioprocess_protein with RNF185, bioprocess_protein with DERL1, bioprocess_protein with DERL1, bioprocess_protein with UFD1, bioprocess_protein with UFD1, bioprocess_protein with SDF2L1, bioprocess_protein with SDF2L1.", "label": "yes"}
+{"original_question": "Should perampanel be used for amyotrophic lateral sclerosis?", "id": "converted_4433", "sentence1": "Should perampanel be used for amyotrophic lateral sclerosis?", "sentence2": "RESULTS: Six participants were enrolled. All had adverse events, mostly behavioral. Two completed the trial and the other four withdrew due to adverse events. All participants reported resolution of these events after discontinuation of the drug. The trial was halted due to the large number of adverse events.DISCUSSION: The use of perampanel in this study of Amyotrophic Lateral Sclerosis was limited by its poor tolerability, CONCLUSIONS: perampanel was associated with a significant decline in ALSFRS-R score and was linked to worsening of the bulbar subscore in the 8 mg group., DISCUSSION: The use of perampanel in this study of Amyotrophic Lateral Sclerosis was limited by its poor tolerabilit[SEP]Relations: perampanel has relations: drug_drug with Diphemanil, drug_drug with Diphemanil, drug_drug with Propranolol, drug_drug with Propranolol, drug_drug with Eplerenone, drug_drug with Eplerenone, drug_drug with Cyclopropane, drug_drug with Cyclopropane, drug_drug with Propentofylline, drug_drug with Propentofylline.", "label": "no"}
+{"original_question": "Can you computationally predict Molecular Recognition Features (MoRFs) regions in Intrinsically Disordered Proteins (IDPs)?", "id": "converted_3132", "sentence1": "Can you computationally predict Molecular Recognition Features (MoRFs) regions in Intrinsically Disordered Proteins (IDPs)?", "sentence2": "Predicting Functions of Disordered Proteins with MoRFpred., Intrinsically disordered Proteins and regions are involved in a wide range of cellular functions, and they often facilitate protein-protein interactions. Molecular recognition features (MoRFs) are segments of intrinsically disordered regions that bind to partner Proteins, where binding is concomitant with a transition to a structured conformation. MoRFs facilitate translation, transport, signaling, and regulatory processes and are found across all domains of life. A popular computational tool, MoRFpred, accurately predicts MoRFs in protein sequences. MoRFpred is implemented as a user-friendly web server that is freely available at http://biomine.cs.vcu.edu/servers/MoRFpred/ . We describe this predictor, explain how to run the web server, and show how to interpret the results it generates. We also demonstrate the utility of this web server based on two case studies, focusing on the relevance of evolutionary conservation of KAT6B wt Allele regions., MoRFPred-plus: Computational Identification of MoRFs in Amino Acid Sequence using Physicochemical Properties and HMM profiles., Intrinsically Disordered Proteins (IDPs) lack stable tertiary structure and they actively participate in performing various biological functions. These IDPs expose short binding regions called Molecular Recognition Features (MoRFs) that permit interaction with structured protein regions. Upon interaction they undergo a disorder-to-order transition as a result of which their functionality arises. Predicting these MoRFs in disordered protein sequences is a challenging task.METHOD: In this study, we present MoRFpred-plus, an improved predictor over our previous proposed predictor to identify MoRFs in disordered protein sequences. Two separate independent propensity scores are computed via incorporating physicochemical properties and HMM profiles, these scores are combined to predict final KAT6B wt Allele propensity score for a given Residue. The first score reflects the characteristics of a query Residue to be part of KAT6B wt Allele region based on the composition and similarity of assumed KAT6B wt Allele and flank regions. The second score reflects the characteristics of a query Residue to be part of KAT6B wt Allele region based on the properties of flanks associated around the given Residue in the query protein Sequence - ParameterizedDataType. The propensity scores are processed and common averaging is applied to generate the final prediction score of MoRFpred-plus.RESULTS: Performance of the proposed predictor is compared with available KAT6B wt Allele predictors, MoRFchibi, MoRFpred, and ANCHOR Health-Related Symptom Index Health-Related Symptom Index. Using previously collected training and test sets used to evaluate the mentioned predictors, the proposed predictor outperforms these predictors and generates lower false positive rate. In addition, MoRFpred-plus is a downloadable predictor, which makes it useful as it can be used as input to other computational tools., OPAL: prediction of KAT6B wt Allele regions in intrinsically disordered protein sequences., Intrinsically disordered Proteins lack stable 3-dimensional structure and play a crucial role in performing various biological functions. Key to their biological function are the molecular recognition features (MoRFs) located within long disordered regions. Computationally identifying these MoRFs from disordered protein sequences is a challenging task. In this study, we present a new KAT6B wt Allele predictor, OPAL, to identify MoRFs in disordered protein sequences. OPAL utilizes two independent sources of information computed using different component predictors. The scores are processed and combined using common averaging method. The first score is computed using a component KAT6B wt Allele predictor which utilizes composition and Sequence - ParameterizedDataType similarity of KAT6B wt Allele and non-KAT6B wt Allele regions to detect MoRFs. The second score is calculated using half-sphere exposure (Herpes encephalitis), solvent accessible surface area (ASA) and backbone angle information of the disordered protein Sequence - ParameterizedDataType, using information from the Amino Acid [EPC] properties of flanks surrounding the MoRFs to distinguish KAT6B wt Allele and non-KAT6B wt Allele residues.Results: OPAL is evaluated using test sets that were previously used to evaluate KAT6B wt Allele predictors, MoRFpred, MoRFchibi and MoRFchibi-web. The results demonstrate that OPAL outperforms all the available KAT6B wt Allele predictors and is the most accurate predictor available for KAT6B wt Allele prediction. It is available at http://www.alok-ai-lab.com/tools/opal/., OPAL+: Length-Specific KAT6B wt Allele Prediction in Intrinsically Disordered Amino Acid Sequence., Intrinsically disordered Proteins (IDPs) contain long unstructured regions, which play an important role in their function. These intrinsically disordered regions (IDRs) participate in binding events through regions called molecular recognition features (MoRFs). Computational prediction of MoRFs helps identify the potentially functional regions in IDRs. In this study, OPAL+, a novel KAT6B wt Allele predictor, is presented. OPAL+ uses separate models to predict MoRFs of varying lengths along with incorporating the hidden Markov model (HMM) profiles and physicochemical properties of MoRFs and their flanking regions. Together, these features help OPAL+ achieve a marginal performance improvement of 0.4-0.7% over its predecessor for diverse KAT6B wt Allele test sets. This performance improvement comes at the expense of increased run time as a result of the requirement of HMM profiles. OPAL+ is available for download at https://github.com/roneshsharma/OPAL-plus/wiki/OPAL-plus-Download., Computational Identification of MoRFs in Amino Acid Sequence Using Hierarchical Application of Bayes Rule., Key to their regulatory function is often the binding to globular protein domains via Sequence - ParameterizedDataType elements known as molecular recognition features (MoRFs). Development of computational tools for the identification of candidate KAT6B wt Allele locations in Amino Acid [EPC] sequences is an important task and an area of growing interest. Given the relative sparseness of MoRFs in protein sequences, the accuracy of the available KAT6B wt Allele predictors is often inadequate for practical usage, which leaves a significant need and room for improvement. In this work, we introduce MoRFCHiBi_Web, which predicts KAT6B wt Allele locations in protein sequences with higher accuracy compared to current KAT6B wt Allele predictors.METHODS: Three distinct and largely independent property scores are computed with component predictors and then combined to generate the final KAT6B wt Allele propensity scores. The first score reflects the likelihood of Sequence - ParameterizedDataType windows to harbour MoRFs and is based on Amino Acid [EPC] composition and Sequence - ParameterizedDataType similarity information. It is generated by MoRFCHiBi using small windows of up to 40 residues in size. The second score identifies long stretches of protein disorder and is generated by ESpritz with the DisProt option. Lastly, the third score reflects Residue conservation and is assembled from PSSM files generated by PSI-BLAST. These propensity scores are processed and then hierarchically combined using Bayes rule to generate the final MoRFCHiBi_Web predictions.RESULTS: MoRFCHiBi_Web was tested on three datasets. Results show that MoRFCHiBi_Web outperforms previously developed predictors by generating less than half the false positive rate for the same true positive rate at practical threshold values., Computational identification of MoRFs in protein sequences., In this study, we introduce MoRFCHiBi, a new computational approach for fast and accurate prediction of MoRFs in protein sequences. MoRFCHiBi combines the outcomes of two support vector machine (SVM) models that take advantage of two different kernels with high noise tolerance. The first, SVMS, is designed to extract maximal information from the general contrast in Amino Acid [EPC] compositions between MoRFs, their surrounding regions (Flanks), and the remainders of the sequences. The second, SLC18A2 wt Allele, is used to identify similarities between regions in a query Sequence - ParameterizedDataType and MoRFs of the training set.RESULTS: We evaluated the performance of our predictor by comparing its results with those of two currently available KAT6B wt Allele predictors, MoRFpred and ANCHOR Health-Related Symptom Index Health-Related Symptom Index. Using three test sets that have previously been collected and used to evaluate MoRFpred and ANCHOR Health-Related Symptom Index Health-Related Symptom Index, we demonstrate that MoRFCHiBi outperforms the other predictors with respect to different evaluation metrics. In addition, MoRFCHiBi is downloadable and fast, which makes it useful as a component in other computational prediction tools.AVAILABILITY AND IMPLEMENTATION: http://www.chibi.ubc.ca/morf/., OPAL: prediction of KAT6B wt Allele regions in intrinsically disordered protein sequences.Supplementary data are available at Bioinformatics online., Computational prediction of MoRFs helps identify the potentially functional regions in IDRs.[SEP]Relations: response to Amino Acid [EPC] has relations: bioprocess_protein with CASP3, bioprocess_protein with CASP3, bioprocess_protein with GIP, bioprocess_protein with GIP, bioprocess_protein with ALAD, bioprocess_protein with ALAD, bioprocess_protein with ARG1, bioprocess_protein with ARG1, bioprocess_protein with GLRB, bioprocess_protein with GLRB.", "label": "yes"}
+{"original_question": "Does the protein mTOR regulate autophagy?", "id": "converted_673", "sentence1": "Does the protein FRAP1 protein, human regulate autophagy?", "sentence2": "autophagy is negatively regulated by the mammalian target of sirolimus receptor (FRAP1 protein, human), Subjecting cells to starvation or sirolimus efficiently induces autophagy by inhibiting the MTOR signaling pathway triggering increased autophagic flux. , Several pathways, including FRAP1 protein, human, have been shown to regulate autophagy., these results provide insights into the mechanism by which hyperactivation of mechanistic target of sirolimus complex 1 promotes Malignant neoplasm of breast progression through increasing autophagy and Akt activation in vivo.,  the canonical FRAP1 protein, human-controlled autophagy pathway, FRAP1 protein, human inhibition severely impairs liver regeneration and increases autophagy after pH:LsCnc:Pt:Ser/Plas:Qn, FRAP1 protein, human remains at a high level and inhibits autophagy., Proto-Oncogene Proteins c-akt is involved in granulosa cell autophagy regulation via FRAP1 protein, human signaling during Rattus norvegicus follicular development and Impatent structure., mammalian target of sirolimus (FRAP1 protein, human), a major negative regulator of autophagy., FRAP1 protein, human suppresses granulosa cell autophagy, Mammals target of sirolimus (FRAP1 protein, human), a potent suppressor of autophagy,, The FRAP1 protein, human signaling pathway integrates inputs from a variety of upstream stimuli to regulate diverse cellular processes including proliferation, growth, survival, motility, autophagy, protein synthesis and metabolism, The activation of mammalian target of sirolimus (FRAP1 protein, human) signaling pathway blocks the effects of ghrelin-induced autophagy and apoptosis,,  inducing apoptosis and autophagy via the FRAP1 protein, human signaling pathway,  The FRAP1 protein, human gene regulates cell growth by controlling RNA, Messenger translation, ribosome biogenesis, autophagy, and metabolism.[SEP]Relations: Sirolimus has relations: drug_protein with MTOR, drug_protein with MTOR. Protein S human has relations: drug_drug with Platelet Activating Factor, drug_drug with Platelet Activating Factor, drug_drug with Argatroban, drug_drug with Argatroban, drug_drug with Altrenogest, drug_drug with Altrenogest, drug_drug with Dienogest, drug_drug with Dienogest.", "label": "yes"}
+{"original_question": "Is there any association between the human gut microbiome and depression?", "id": "converted_2784", "sentence1": "Is there any association between the human gut microbiome and Cancer patients and suicide and depression?", "sentence2": "Moreover, recent findings are suggestive of the possibility that dysregulation of the enteric microbiota (i.e., dysbiosis) and associated bacterial translocation across the Structure of Structure of intestinal epithelium may be involved in the pathophysiology of stress-related psychiatric disorders, particularly Cancer patients and suicide and Cancer patients and suicide and depression.[SEP]Relations: regulation of intestinal epithelial structure maintenance has relations: bioprocess_protein with NEUROD1, bioprocess_protein with NEUROD1, bioprocess_bioprocess with regulation of biological quality, bioprocess_bioprocess with regulation of biological quality, bioprocess_bioprocess with regulation of digestive system process, bioprocess_bioprocess with regulation of digestive system process, bioprocess_bioprocess with positive regulation of intestinal epithelial structure maintenance, bioprocess_bioprocess with positive regulation of intestinal epithelial structure maintenance. antigen processing and presentation of endogenous peptide antigen via MHC class I via ER pathway, TAP-independent has relations: bioprocess_bioprocess with antigen processing and presentation of endogenous peptide antigen via MHC class I via ER pathway, bioprocess_bioprocess with antigen processing and presentation of endogenous peptide antigen via MHC class I via ER pathway.", "label": "yes"}
+{"original_question": "Is there a crystal structure of the full-length of the flaviviridae NS5(Methyltransferase - RNA depended RNA Polymerase) ?", "id": "converted_471", "sentence1": "Is there a crystal structure of the full-length of the flaviviridae Noonan Syndrome 5(Methyltransferase - RNA depended RNA Polymerase) ?", "sentence2": " flavivirus Noonan Syndrome 5 harbors a CMTR1 gene (MTase) in its N-terminal ≈ 265 residues and an RNA-Directed RNA Polymerase (RNA-directed RNA polymerase activity) within the C-terminal part. One of the major interests and challenges in Noonan Syndrome 5 is to understand the interplay between RNA-directed RNA polymerase activity and MTase as a unique natural fusion protein in Viral Genome replication and cap formation. Here, we report the first crystal structure of the full-length flavivirus Noonan Syndrome 5 from Japanese encephalitis virus. , (DENV) nonstructural protein 5 (Noonan Syndrome 5) is composed of two globular domains separated by a 10-residue linker. The N-terminal Superkingdom (taxonomic category) participates in the synthesis of a mRNA cap 1 structure ((7Me)GpppA(2'OMe)) at the 5' end of the Viral Genome and possesses guanylyltransferase, guanine-N7-CMTR1 gene, and nucleoside-2'O-CMTR1 gene activities. The C-terminal Superkingdom (taxonomic category) is an RNA-Directed RNA Polymerase responsible for RNA, Viral synthesis. Although crystal structures of the two isolated domains have been obtained, there are no structural data for full-length Noonan Syndrome 5. It is also unclear whether the two Noonan Syndrome 5 domains interact with each other to form a stable structure in which the relative orientation of the two domains is fixed. To investigate the structure and dynamics of DENV type 3 Noonan Syndrome 5 in solution, we conducted small-angle X-ray scattering experiments with the full-length protein. Noonan Syndrome 5 was found to be monomeric and well-folded under the conditions tested., West Nile virus (West Nile viral infection) Noonan Syndrome 5 protein contains a CMTR1 gene (MTase) Superkingdom (taxonomic category) involved in RNA capping and an RNA-Directed RNA Polymerase (RdRp) Superkingdom (taxonomic category) essential for virus replication. Crystal structures of individual West Nile viral infection MTase and RdRp domains have been solved; however, the structure of full-length Noonan Syndrome 5 has not been determined. To gain more insight into the structure of Noonan Syndrome 5 and interactions between the MTase and RdRp domains, we generated a panel of seven monoclonal antibodies (mAbs) to the Noonan Syndrome 5 protein of West Nile viral infection (Kunjin strain) and mapped their Binding Sites using a series of truncated Noonan Syndrome 5 proteins and synthetic peptides. Binding sites of four mAbs (5D4, 4B6, 5C11 and 6A10) were mapped to residues 354-389 in the fingers subdomain of the RdRp. This is consistent with the ability of these mAbs to inhibit RdRp activity in vitro and suggests that this Geographic Locations represents a potential target for RdRp inhibitors. Using a series of synthetic peptides, we also identified a linear epitope (bound by Monoclonal Antibody [EPC] 5H1) that mapped to a 13 aa stretch surrounding residues 47 and 49 in the MTase Superkingdom (taxonomic category), a Geographic Locations predicted to interact with the palm subdomain of the RdRp. The failure of one Monoclonal Antibody [EPC] (7G6) to bind both N- and C-terminally truncated Noonan Syndrome 5 recombinants indicates that the immunoglobulin complex location recognizes a conformational epitope that requires the presence of residues in both the MTase and RdRp domains. [SEP]Relations: RNA-directed DNA polymerase activity has relations: molfunc_protein with TERC, molfunc_protein with TERC, molfunc_protein with ERVK-7, molfunc_protein with ERVK-7, molfunc_protein with ERVK-6, molfunc_protein with ERVK-6, molfunc_protein with ERVK-8, molfunc_protein with ERVK-8, molfunc_protein with TERT, molfunc_protein with TERT.", "label": "yes"}
+{"original_question": "Is gabapentin effective for chronic pelvic pain?", "id": "converted_4399", "sentence1": "Is gabapentin effective for Chronic pelvic pain of female?", "sentence2": "There were no significant between-group differences in both worst and average numerical rating scale (NRS) pain scores at 13-16 weeks after randomisation. The mean worst NRS pain score was 7·1 (standard deviation [SLC17A5 gene] 2·6) in the gabapentin group and 7·4 (SLC17A5 gene 2·2) in the placebo group. Mean change from baseline was -1·4 (SLC17A5 gene 2·3) in the gabapentin group and -1·2 (SLC17A5 gene 2·1) in the placebo group (adjusted mean difference -0·20 [97·5% CI -0·81 to 0·42]; p=0·47). The mean average NRS pain score was 4·3 (SLC17A5 gene 2·3) in the gabapentin group and 4·5 (SLC17A5 gene 2·2) in the placebo group. Mean change from baseline was -1·1 (SLC17A5 gene 2·0) in the gabapentin group and -0·9 (SLC17A5 gene 1·8) in the placebo group (adjusted mean difference -0·18 [97·5% CI -0·71 to 0·35]; p=0·45)., INTERPRETATION: This study was adequately powered, but treatment with gabapentin did not result in significantly lower pain scores in women with Chronic pelvic pain of female, and was associated with higher rates of side-effects than placebo. Given the increasing reports of abuse and evidence of potential harms associated with gabapentin use, it is important that clinicians consider alternative treatment options to off-label gabapentin for the management of Chronic pelvic pain of female and no obvious pelvic pathology., Gabapentin not effective for Chronic pelvic pain of female in women., Gabapentin not effective for Chronic pelvic pain of female in women[SEP]Relations: Gabapentin has relations: drug_effect with Bone pain, drug_effect with Bone pain, drug_effect with Pain, drug_effect with Pain, drug_effect with Abdominal pain, drug_effect with Abdominal pain, drug_effect with Chest pain, drug_effect with Chest pain, drug_effect with Back pain, drug_effect with Back pain.", "label": "no"}
+{"original_question": "Is there alternative polyadenylation during zebrafish development?", "id": "converted_1878", "sentence1": "Is there alternative polyadenylation during Zebrafish development?", "sentence2": "Extensive alternative polyadenylation during Zebrafish development., At 2 h post-fertilization, thousands of unique poly(A) sites appear at locations lacking a typical polyadenylation signal, which suggests a wave of widespread cytoplasmic polyadenylation of mRNA degradation intermediates. Our insights into the identities, formation, and evolution of Zebrafish 3' UTRs provide a resource for studying gene regulation during Vertebrates development., Extensive alternative polyadenylation during Zebrafish development.[SEP]Relations: vertebra has relations: anatomy_anatomy with non-transverse process-bearing vertebra, anatomy_anatomy with non-transverse process-bearing vertebra, anatomy_anatomy with transverse process-bearing vertebra, anatomy_anatomy with transverse process-bearing vertebra, anatomy_anatomy with predorsal vertebra, anatomy_anatomy with predorsal vertebra, anatomy_anatomy with vertebral element, anatomy_anatomy with vertebral element, anatomy_anatomy with vertebral bone 2, anatomy_anatomy with vertebral bone 2.", "label": "yes"}
+{"original_question": "Could hypophosphatemic rickets cause craniosynostosis?", "id": "converted_1853", "sentence1": "Could Familial Hypophosphatemic Rickets cause CRANIOSYNOSTOSIS 3?", "sentence2": "This study examines a series of patients with Familial Hypophosphatemic Rickets and CRANIOSYNOSTOSIS 3 to characterize the clinical course and associated Craniofacial Abnormalities. , Hypophosphatemic Rickets and CRANIOSYNOSTOSIS 3: a multicenter case series., A 20-year retrospective review identified patients with Familial Hypophosphatemic Rickets and secondary CRANIOSYNOSTOSIS 3 at 3 major craniofacial centers. , Secondary CRANIOSYNOSTOSIS 3 develops postnatally due to metabolic or mechanical factors. The most common metabolic cause is Familial Hypophosphatemic Rickets, which has a variety of etiologies. Head - Component of Device - Component of Device shape changes occur later and with a more heterogeneous presentation compared with that of primary CRANIOSYNOSTOSIS 3., Patients with multisutural involvement or X-linked Familial Hypophosphatemic Rickets had a significant delay in presentation for CRANIOSYNOSTOSIS 3. , CRANIOSYNOSTOSIS, TYPE 2 can be gene-linked, or caused by Metabolic Diseases, such as Rickets, which results from a deficiency or impaired metabolism of ergocalciferol, Magnesium supplements, alimentary tract and metabolism, Phosphorus Drug Class or CALCIUM SUPPLEMENTS leading to hypomineralization of the Specimen Type - Bone. X-linked dominant Familial Hypophosphatemic Rickets (XLHR) is the most prevalent genetic type of Familial Hypophosphatemic Rickets and is caused by germ line mutations in the PHEX-gene. In XLHR, only few case reports of CRANIOSYNOSTOSIS 3 were described., Papilledema in the setting of x-linked Familial Hypophosphatemic Rickets with CRANIOSYNOSTOSIS 3., Case report of a 3-year-old female presenting with papilledema resulting from CRANIOSYNOSTOSIS 3 secondary to Hypophosphatemic Rickets, X-Linked Dominant., X-linked Familial Hypophosphatemic Rickets and CRANIOSYNOSTOSIS 3., X-linked hypophosphatemic (Hypophosphatemic Rickets, X-Linked Dominant) Rickets is the most common form of metabolic Rickets, and there have been reports linking Hypophosphatemic Rickets, X-Linked Dominant Rickets to CRANIOSYNOSTOSIS 3. A clinical report of a patient with Hypophosphatemic Rickets, X-Linked Dominant Rickets and CRANIOSYNOSTOSIS 3 is presented with a review of literature. , This may be the reason for the common association of CRANIOSYNOSTOSIS 3 and Hypophosphatemic Rickets, X-Linked Dominant Rickets. , CRANIOSYNOSTOSIS, TYPE 2 and associated craniofacial deformities, such as Frontal bossing, often occur as symptoms of ergocalciferol-resistant Rickets in children. Similar Bone structure of cranium deformities develop in CASP14 gene with X-linked dominant hypophosphatemia, the most common form of ergocalciferol-resistant Rickets. , The x-linked hypophosphatemic Mus sp. is an animal model that can be used to study the role of ergocalciferol-resistant Rickets in the development of CRANIOSYNOSTOSIS 3, to relate CRANIOSYNOSTOSIS 3 to the development of associated Bone structure of cranium deformities, and to test new treatment procedures., CRANIOSYNOSTOSIS, TYPE 2 secondary to Rickets is rarely reported, but since neither Rickets nor CRANIOSYNOSTOSIS 3 is a reportable disease, the exact incidence of both diseases is unknown., X-linked hypophosphatemic (Hypophosphatemic Rickets, X-Linked Dominant) Rickets is the most common form of metabolic Rickets, and there have been reports linking Hypophosphatemic Rickets, X-Linked Dominant Rickets to CRANIOSYNOSTOSIS 3., A clinical report of a patient with Hypophosphatemic Rickets, X-Linked Dominant Rickets and CRANIOSYNOSTOSIS 3 is presented with a review of literature., METHODS A 20-year retrospective review identified patients with Familial Hypophosphatemic Rickets and secondary CRANIOSYNOSTOSIS 3 at 3 major craniofacial centers., Bilateral coronal and sagittal synostosis in X-linked Familial Hypophosphatemic Rickets: a case report., X-linked Familial Hypophosphatemic Rickets and sagittal CRANIOSYNOSTOSIS 3: three patients requiring operative cranial expansion: case series and literature review, X-linked Familial Hypophosphatemic Rickets and CRANIOSYNOSTOSIS 3, X-linked hypophosphatemic (Hypophosphatemic Rickets, X-Linked Dominant) Rickets is the most common form of metabolic Rickets, and there have been reports linking Hypophosphatemic Rickets, X-Linked Dominant Rickets to CRANIOSYNOSTOSIS 3, The recent observations of two new cases of X-linked Familial Hypophosphatemic Rickets associated with premature closure of the sagittal suture prompted a review of similar cases seen in this institution.To review the clinical records and Bone structure of cranium radiographs of 28 children with Familial Hypophosphatemic Rickets in order to investigate the frequency and type of CRANIOSYNOSTOSIS 3 and other Calvaria changes seen in these conditions and to review the literature for relevant findings.Clinical and imaging records were reviewed on 28 patients with Familial Hypophosphatemic Rickets, all younger than 18 years, Those with multisutural synostosis presented at a significantly older age than patients with sagittal or Bicoronal synostosis.Patients with multisutural involvement or X-linked Familial Hypophosphatemic Rickets had a significant delay in presentation for CRANIOSYNOSTOSIS 3, Papilledema in the setting of x-linked Familial Hypophosphatemic Rickets with CRANIOSYNOSTOSIS 3, INTRODUCTION TO THE OPHTHALMIC LITERATURE OF AN UNUSUAL CAUSE OF PAPILLEDEMA AND SUBSEQUENT OPTIC ATROPHY: X-linked Familial Hypophosphatemic Rickets (Hypophosphatemic Rickets, X-Linked Dominant).Case report of a 3-year-old female presenting with papilledema resulting from CRANIOSYNOSTOSIS 3 secondary to Hypophosphatemic Rickets, X-Linked Dominant.Early intervention with craniofacial surgery prevented the development of Optic Atrophy.Children with Hypophosphatemic Rickets, X-Linked Dominant should be screened for ophthalmic evidence of elevated intracranial pressure to aid early intervention and prevention of permanent Unspecified visual loss, CONCLUSIONS: Patients with multisutural involvement or X-linked Familial Hypophosphatemic Rickets had a significant delay in presentation for CRANIOSYNOSTOSIS 3. , CRANIOSYNOSTOSIS, TYPE 2 can be gene-linked, or caused by Metabolic Diseases, such as Rickets, which results from a deficiency or impaired metabolism of ergocalciferol, Magnesium supplements, alimentary tract and metabolism, Phosphorus Drug Class or CALCIUM SUPPLEMENTS leading to hypomineralization of the Specimen Type - Bone. , Similar Bone structure of cranium deformities develop in CASP14 gene with X-linked dominant hypophosphatemia, the most common form of ergocalciferol-resistant Rickets., CRANIOSYNOSTOSIS, TYPE 2 in ergocalciferol-resistant Rickets., CRANIOSYNOSTOSIS, TYPE 2 can be gene-linked, or caused by Metabolic Diseases, such as Rickets, which results from a deficiency or impaired metabolism of ergocalciferol, Magnesium supplements, alimentary tract and metabolism, Phosphorus Drug Class or CALCIUM SUPPLEMENTS leading to hypomineralization of the Specimen Type - Bone., X-linked Familial Hypophosphatemic Rickets and CRANIOSYNOSTOSIS 3., X-linked hypophosphatemic (Hypophosphatemic Rickets, X-Linked Dominant) Rickets is the most common form of metabolic Rickets, and there have been reports linking Hypophosphatemic Rickets, X-Linked Dominant Rickets to CRANIOSYNOSTOSIS 3., Hypophosphatemic Rickets and CRANIOSYNOSTOSIS 3: a multicenter case series.[SEP]Relations: CRANIOSYNOSTOSIS, TYPE 2 has relations: disease_phenotype_positive with Familial Hypophosphatemic Rickets, disease_phenotype_positive with Familial Hypophosphatemic Rickets, disease_phenotype_positive with hereditary Familial Hypophosphatemic Rickets, disease_phenotype_positive with hereditary Familial Hypophosphatemic Rickets. Familial Hypophosphatemic Rickets has relations: disease_phenotype_positive with CRANIOSYNOSTOSIS, TYPE 2, disease_phenotype_positive with CRANIOSYNOSTOSIS, TYPE 2, disease_phenotype_positive with CRANIOSYNOSTOSIS, TYPE 2, disease_phenotype_positive with CRANIOSYNOSTOSIS, TYPE 2, disease_disease with Rickets (disease), disease_disease with Rickets (disease).", "label": "yes"}
+{"original_question": "Can secondary glioblastoma be caused by brain irradiation?", "id": "converted_3812", "sentence1": "Can secondary glioblastoma be caused by brain irradiation?", "sentence2": "Prolonged survival in secondary glioblastoma following local injection of targeted alpha therapy with , [Radiation induced glioblastoma: a case report]., We report a surgical case of a 54-year-old woman with a radiation induced glioblastoma., Glioblastoma Multiforme Multiforme multiforme following Cranial Irradiation and chemotherapy for Acute lymphocytic leukemia., The occurrence of glioblastoma multiforme following radiation and chemotherapy in Acute lymphocytic leukemia (ALL) is rare., Glioblastoma Multiforme Multiforme multiforme following Cranial Irradiation and chemotherapy for Acute lymphocytic leukemia. R, exact cause for the development of glioblastoma multiforme following therapy for ALL is not clear. A gen, ndary malignant and Benign neoplasm of brain, unspecified such as Astrocytoma, Benign Meningioma and glioblastoma have been described in long-term survivors of conventional myeloablative alloBMT. Here w, The authors consider irradiation-induced Glioblastoma Multiforme secondary to primarily verified medulloblastomas in patients who had previously undergone craniospinal irradiation as a component of combined treatment after tumor resection., The authors analyzed patterns of occurrence of irradiation-induced Glioblastoma Multiforme depending on the molecular genetic group and clinical characteristics of patients after primary surgery., Secondary Brain Neoplasms rarely arise after Cranial Irradiation; among them, Meningioma and Glioblastoma Multiforme are the most common and secondary oligodendroglial tumors the most rare., Secondary glioblastoma multiforme (sGBM) can occur after a long latency period following radiation treatment of various diseases including Brain Neoplasms, leukemia, and more benign disorders like Tinea Capitis., Irradiation, however, acts as an oncogenic factor as a delayed effect and it is rare that glioblastoma multiforme develops during the remission period of ALL., A cerebellar glioblastoma was discovered in a 28 year old woman, 5 years after a focal 50 grays brain irradiation for Benign Meningioma of the Cerebellar declive., Glioblastoma Multiforme Multiforme multiforme following Cranial Irradiation and chemotherapy for Acute lymphocytic leukemia. Report of 3 cases., Secondary tumors including Glioblastoma Multiforme are under special attention since their occurrence is associated with a fatal outcome., We describe a case of radiation-induced glioblastoma after radiotherapy for Germinoma., [A Case of Radiation-induced Glioblastoma Multiforme Multiforme 29 Years after Treatments for Germinoma]., Paradoxically, radiation is also a risk factor for Glomerular Basement Membrane development, raising the possibility that radiotherapy of Brain Neoplasms could promote tumor recurrence or trigger secondary Glioma., An SNRPN protein, human may have a benign course, as in Benign Meningioma, or be a dilemma for the patient, as in glioblastoma., During a median of 2 years of follow-up review after the diagnosis of a secondary tumour, 3 patients died related to the secondary tumours (2 Malignant neoplasm of soft tissue, 1 glioblastoma), one died of a recurrent primary glioma, while the remaining 7 have been alive for from 10 months to 12 years after being treated for the secondary tumours (median: 3 years). , In particular, children treated with X-irradiation for Pre B-cell Pre B-cell acute lymphoblastic leukemia show a significantly elevated risk of developing Glioma and Neuroectodermal Tumor, Primitive (Ewings sarcoma-Neuroectodermal Tumor, Primitive (Ewings sarcoma-Neuroectodermal Tumor, Primitive (PNET))), often within 10 years after therapy. TP53 mutations are frequent in low-grade Glioma and secondary Glioblastoma Multiforme derived therefrom., Pathologic diagnoses were one glioblastoma, two cases of anaplastic Astrocytoma, one Medulloblastoma, one low-grade glioma, one high-grade glial tumor, and one atypical Benign Meningioma., A 22 year-old-man with acute lymphoblastic leukaemia had received prophylactic Cranial Irradiation and intrathecal chemotherapy. Eighteen years later a cerebellar glioblastoma multiforme was diagnosed. , She developed glioblastoma 5.7 years after the initial GK surgery.[SEP]Relations: adult glioblastoma has relations: disease_disease with glioblastoma (disease), disease_disease with glioblastoma (disease), disease_disease with glioblastoma (disease), disease_disease with glioblastoma (disease). Glioma has relations: phenotype_phenotype with Brainstem glioma, phenotype_phenotype with Brainstem glioma, disease_phenotype_positive with retinoblastoma, disease_phenotype_positive with retinoblastoma, disease_phenotype_positive with glioblastoma (disease), disease_phenotype_positive with glioblastoma (disease).", "label": "yes"}
+{"original_question": "Can the CEP290 gene mutations be targeted by AAV-mediated gene therapy?", "id": "converted_2316", "sentence1": "Can the CEP290 gene mutations be targeted by AAV-mediated gene therapy?", "sentence2": "The large size of the CEP290 gene prevents its use in adeno-associated virus (AAV)-mediated gene augmentation therapy.[SEP]Relations: CEP290 has relations: protein_protein with CEP43, protein_protein with CEP43, disease_protein with Joubert syndrome, disease_protein with Joubert syndrome, disease_protein with Joubert syndrome with oculorenal defect, disease_protein with Joubert syndrome with oculorenal defect, pathway_protein with AURKA Activation by TPX2, pathway_protein with AURKA Activation by TPX2, protein_protein with MED4, protein_protein with MED4.", "label": "no"}
+{"original_question": "Is Cri Du Chat associated with an expansion of a repeat with in the gene found on chromosome 5?", "id": "converted_2136", "sentence1": "Is Cri Du Chat associated with an expansion of a repeat with in the gene found on Chromosomes, Human, Pair 5?", "sentence2": "Cri-du-chat syndrome is a Congenital chromosomal disease caused by a Gene Deletion Abnormality of the short arm of Chromosomes, Human, Pair 5, The typical cri du chat syndrome, due to 5p15.2 Gene Deletion Abnormality, includes severe Intellectual Disability, facial dysmorphisms, neonatal Muscle Muscle hypotonia and pre- and post-natal growth retardation, whereas more distal Gene Deletion in 5p15.3 lead to cat-like cry and speech delay and produce the clinical picture of the atypical cri du chat syndrome, with minimal or absent intellectual impairment., Cri-du-chat is a Homo sapiens contiguous gene Gene Deletion Abnormality syndrome resulting from hemizygous Gene Deletion of chromosome 5p., Cri-du-chat is a chromosomal Gene Deletion Abnormality syndrome characterized by partial Gene Deletion Abnormality of the short arm of Chromosomes, Human, Pair 5., The karyotype showed a terminal Gene Deletion Abnormality of the short arm of Chromosomes, Human, Pair 5 including the critical region 5p15 for cri du chat syndrome., Fewer than 1 in 200 of cri du chat syndrome cases are due to recombination aneusomy arising from a parental inversion of Chromosomes, Human, Pair 5., Molecular approach to analyzing the Homo sapiens 5p Gene Deletion Abnormality syndrome, cri du chat., Cri-du-chat is a Homo sapiens contiguous gene Gene Deletion Abnormality syndrome resulting from hemizygous Gene Deletion of chromosome 5p, The cri du chat syndrome (chenodeoxycholate sulfate conjugate) is a chromosomal Gene Deletion Abnormality syndrome associated with a partial Gene Deletion Abnormality of the short (p) arm of Chromosomes, Human, Pair 5, The Cri-du-Chat Syndrome is a contiguous gene syndrome that results from a Gene Deletion Abnormality of the short arm of Chromosomes, Human, Pair 5 (5p)., Cri-du-chat syndrome is associated with a Gene Deletion Abnormality of the short arm of Chromosomes, Human, Pair 5., The Gene Deletion Abnormality of the short arm of Chromosomes, Human, Pair 5 is associated with the Cri-du-Chat Syndrome., The Cri du Chat syndrome (chenodeoxycholate sulfate conjugate) is a genetic disease resulting from a Gene Deletion Abnormality of variable size occurring on the short arm of Chromosomes, Human, Pair 5 (5p-)., Cri-du-chat is a well described partial aneusomy resulting from Gene Deletion Abnormality of the short arm of Chromosomes, Human, Pair 5., Cri-du-chat syndrome is caused by haploinsufficiency of the Genes on the distal part of the short arm of Chromosomes, Human, Pair 5, and characteristic features include Microcephaly (physical finding), developmental delays, and a distinctive high-pitched mewing cry., The pathological condition of cri du chat syndrome is due to the cytogenetic Gene Deletion Abnormality of band p15.2 of Chromosomes, Human, Pair 5. ,  Karyotype analysis indicated that the patient has carried a terminal Gene Deletion Abnormality in 5p. FISH with Cri du Chat syndrome region probe confirmed that D5S23 and D5S721 loci are deleted. [SEP]Relations: Cri-du-chat syndrome has relations: disease_disease with partial Gene Deletion Abnormality of the short arm of Chromosomes, Human, Pair 5, disease_disease with partial Gene Deletion Abnormality of the short arm of Chromosomes, Human, Pair 5, disease_protein with CTNND2, disease_protein with CTNND2, disease_protein with SEMA5A, disease_protein with SEMA5A, disease_phenotype_positive with Growth delay, disease_phenotype_positive with Growth delay, disease_protein with TERT, disease_protein with TERT.", "label": "no"}
+{"original_question": "Can RNAPolII function as an RNA-dependent RNA-polymerase?", "id": "converted_1706", "sentence1": "Can RNAPolII function as an RNA-dependent RNA-polymerase?", "sentence2": "DNA-Directed RNA Polymerase II acts as an RNA-dependent DNA-Directed RNA Polymerase to extend and destabilize a RNA, Untranslated, DNA-Directed RNA Polymerase II (RNA Polymerase II) is a well-characterized DNA-dependent DNA-Directed RNA Polymerase, which has also been reported to have RNA-dependent DNA-Directed RNA Polymerase (RNA-directed DNA-Directed RNA Polymerase activity) activity., . Our studies provide compelling evidence that Mammals RNA Polymerase II acts as an RNA-directed DNA-Directed RNA Polymerase activity to control the stability of a cellular RNA by extending its 3'-end., here is, however, evidence that RNA Polymerase II also possesses RNA-dependent DNA-Directed RNA Polymerase (RNA-directed DNA-Directed RNA Polymerase activity) activity. RNA Polymerase II can use a homopolymeric RNA template, can extend RNA by several Nucleotides in the absence of DNA, and has been implicated in the replication of the RNA genomes of Hepatitis Delta Virus (Hepatitis D Infection) and plant viroids., The RNA-directed DNA-Directed RNA Polymerase activity activity of RNA Polymerase II provides a missing link in molecular evolution, because it suggests that RNA Polymerase II evolved from an ancient replicase that duplicated RNA genomes., The present findings provide a framework for further studies to elucidate the mechanistic principles of transcription by a Viral DNA-Directed RNA Polymerase and have implications for the regulation of RNA Polymerase II activities in infected Cells., Influenza A virus transcribes its segmented negative sense RNA genome in the nuclei of infected Cells in a process long known to require host DNA-Directed RNA Polymerase II (RNAP-II)., We conclude that influenza A virus replication requires RNAP-II activity not just to provide capped RNA, Messenger substrates but also to facilitate nuclear export of selected Viral mRNAs., Thus, influenza virus specifically interferes with RNA Polymerase II elongation, but not RNA Polymerase II initiation. We propose that influenza virus DNA-Directed RNA Polymerase, by binding to the Nuclear LIM Interactor-Interacting Factor 2 of initiating RNA Polymerase II and subsequent cleavage of the capped 5' end of the nascent transcript, triggers premature RNA Polymerase II termination., We show that DNA-Directed RNA Polymerase II (RNAPolII) preinitiation complex recruitment and H3 Lys 4 (H3-K4) methylation at the X (Inactive)-Specific Transcript, Human promoter form the basis of the X (Inactive)-Specific Transcript, Human expression profiles that drives both imprinted and random XCI., Identification of these ENL-associated proteins (EAPs) by mass spectrometry revealed ENZYMES FOR TREATMENT OF WOUNDS AND ULCERS with a known role in transcriptional elongation (DNA-Directed RNA Polymerase II C-terminal domain kinase [RNAPolII Nuclear LIM Interactor-Interacting Factor 2] positive transcription elongation factor b [pTEFb]), and in chromatin modification (histone-H3 methyltransferase Histone-Lysine N-Methyltransferase H3 Lysine-79 Specific, Human) as well as other frequent KMT2A wt Allele partners (AFF1 wt Allele, AF5q31 protein protein, and AFF3 wt Allele), and polycomb group members (RING1 gene gene, CBX8 gene gene, and BCL-6 Corepressor)., DNA-Directed RNA Polymerase II acts as an RNA-dependent DNA-Directed RNA Polymerase to extend and destabilize a RNA, Untranslated., Association of the influenza A virus RNA-dependent DNA-Directed RNA Polymerase with cellular DNA-Directed RNA Polymerase II., It is also well established that Viral RNA-dependent DNA-Directed RNA Polymerase (vRNP) associates with cellular DNA-Directed RNA Polymerase II (RNA Polymerase II), on which Viral replication depends. , DNA-Directed RNA Polymerase II (RNA Polymerase II) is a well-characterized DNA-dependent DNA-Directed RNA Polymerase, which has also been reported to have RNA-dependent DNA-Directed RNA Polymerase (RNA-directed DNA-Directed RNA Polymerase activity) activity. Natural cellular RNA substrates of Mammals RNA Polymerase II, however, have not been identified and the cellular function of the RNA Polymerase II RNA-directed DNA-Directed RNA Polymerase activity activity is unknown., DNA-Directed RNA Polymerase II (RNA Polymerase II) is a well-characterized DNA-dependent DNA-Directed RNA Polymerase, which has also been reported to have RNA-dependent DNA-Directed RNA Polymerase (RNA-directed DNA-Directed RNA Polymerase activity) activity., DNA-Directed RNA Polymerase II acts as an RNA-dependent DNA-Directed RNA Polymerase to extend and destabilize a RNA, Untranslated.[SEP]Relations: RNA-directed DNA-Directed RNA Polymerase complex has relations: cellcomp_protein with TERT, cellcomp_protein with TERT. RNA-directed DNA polymerase activity has relations: molfunc_protein with TERT, molfunc_protein with TERT, molfunc_protein with ERVK-11, molfunc_protein with ERVK-11, molfunc_protein with ERVK-7, molfunc_protein with ERVK-7, molfunc_protein with ERVK-8, molfunc_protein with ERVK-8.", "label": "yes"}
+{"original_question": "Is Epistaxis associated with dental implant placement?", "id": "converted_4601", "sentence1": "Is Epistaxis associated with dental implant placement?", "sentence2": " The overall survival rate of the Procedure Procedure implants:Finding:Point in time:^Patient:Narrative:Finding:Point in time:^Patient:Narrative into the sinus cavity was 95.6%, without statistical differences according to the level of penetration. The clinical and radiological complications were 3.4% and 14.8% respectively. The most frequent clinical complication was the Epistaxis, , implant placement and protrusion of the implant up to 3mm beyond the sinus floor does not alter the stability and outcome of dental Procedure Procedure implants:Finding:Point in time:^Patient:Narrative:Finding:Point in time:^Patient:Narrative, one year post-restoration. This could be associated with minor complications ranging from Epistaxis to Sinusitis, which are manageable.[SEP]Relations: Epistaxis has relations: drug_effect with Nicotine, drug_effect with Nicotine, drug_effect with Topotecan, drug_effect with Topotecan, drug_effect with Estradiol, drug_effect with Estradiol, drug_effect with Montelukast, drug_effect with Montelukast, drug_effect with Thiotepa, drug_effect with Thiotepa.", "label": "yes"}
+{"original_question": "Is Turcot syndrome associated with glioblastoma?", "id": "converted_1640", "sentence1": "Is Turcot syndrome (disorder) associated with glioblastoma?", "sentence2": "Turcot syndrome (disorder) (disorder) is an Autosomal Recessive Disorder clinically characterized by the occurrence of Primary Neoplasm of the CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS and Adenomatous polyp of Abdomen+Pelvis>Colon during the first or second decades of life, with a spectrum of clinical features such as \"café-au-lait\" spots, axillary freckling, and hyperpigmented spots. , We present the case of a 20-year-old male with a clinical presentation of both Glioblastoma Multiforme and multiple Adenomatous polyp of Abdomen+Pelvis>Colon. , Turcot syndrome (disorder) (disorder) (TS) is a rare Hereditary Diseases clinically characterized by the occurrence of Primary Neoplasm of the Abdomen+Pelvis>Colon and the CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS (Central Nervous System). Here we present the case of an 11-year-old boy with a synchronous clinical presentation of both Glioblastoma Multiforme (Glomerular Basement Membrane) and Adenocarcinoma of Abdomen+Pelvis>Colon., Based on this case study, the synchronous presentation of Glioblastoma Multiforme and adenocarcinoma of the Abdomen+Pelvis>Colon might suggest a shorter survival rate for patients with Turcot syndrome (disorder) (disorder). , A 15-year-old boy was admitted with the diagnosis of colonic Multiple polyps, and during a 2-year follow-up, he underwent operation for right parieto-occipital anaplastic Astrocytoma, left-side colonic non-Hodgkin Lymphoma (Lymphoma, Large-Cell, Follicular) and Cerebellar Glioblastoma which were all confirmed by histology. Although cases of Turcot's syndrome (TS) (colonic Multiple polyps and primary brain tumour occurring in the same patient) have been previously described, association with Hematologic Neoplasms is rare. We hereby report such a case with TS., Type A microsatellite instability diagnostic test diagnostic test in pediatric Glioma as an indicator of Turcot syndrome (disorder) (disorder).,  Biallelic Gene Mutation of MMR genes are associated with pediatric cancers, including glial tumors, in Turcot syndrome (disorder) (disorder) type 1 (Timothy syndrome type 1)., Glioblastoma with giant cell and sarcomatous features in patients with Turcot syndrome (disorder) (disorder) type 1: a clinicopathological study of 3 cases., Turcot syndrome (disorder) (disorder) (TS) is a rare genetic disorder of DNA mismatch repair predisposing to glioblastoma (Glomerular Basement Membrane) in the type 1 variant. , We report the clinicopathological and genetic features of 3 Glioma in TS type 1 patients., We conclude that 1) the giant cell variant of Glomerular Basement Membrane is overrepresented in TS; 2) gliosarcoma may also be encountered; and 3) survival is often favorable, despite histological anaplasia and exuberant proliferation., Malignant transformation of Anaplastic Astrocytoma associated with Neurocysticercosis in a patient with Turcot syndrome (disorder) (disorder)., A 45-year-old woman with anaplastic Astrocytoma was clinically diagnosed with Turcot syndrome (disorder) (disorder), and subsequently developed simultaneous Neurocysticercosis and malignant transformation to glioblastoma. , Familial Glioblastoma Multiforme is a rather uncommon entity, being in most cases associated to known genetic disorders (as Turcot syndrome (disorder) (disorder), Li-Fraumeni Syndrome 2, Neurofibromatosis 2, etc.). , Turcot syndrome (disorder) (disorder) (MIM276300) has been described as the association of CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS malignant tumors and familial colorectal Primary malignant neoplasm and has been reported to be both a dominant and recessive disorder., We report here the first identification of a homozygous Mutation Abnormality in MSH6 protein, human protein, human in a family with childhood-onset brain Specimen Source Codes - Specimen Source Codes - tumor, Lymphoma, colorectal Primary malignant neoplasm, and Neurofibromatosis 2 type 1 phenotype. , Of the 21 patients, 12 have died (10 after relapse, with a median time to progression for the whole series of 14 months; one with intratumoral bleeding at 40 months after diagnosis; and one affected by Turcot syndrome (disorder) (disorder) for duodenal Primary malignant neoplasm relapse)., [Glioblastoma multiforme as a manifestation of Turcot syndrome (disorder) (disorder)]., In the present case, a 60-year-old patient with Glioblastoma Multiforme and a history of hereditary malignomas is described as an example of a HNPCC-associated Turcot's syndrome., Computed tomography brain scan and computed tomography-guided biopsy revealed a left frontoparietal Glioblastoma Multiforme. This case illustrates the rare presentation of Turcot syndrome (disorder) (disorder)-a hereditary Polyp of large intestine syndrome-in an older adult., Turcot syndrome (disorder) (disorder) is the association of Polyp of large intestine with primary Neoplasms, Neuroepithelial of the CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS such as glioblastoma and Medulloblastoma. , Brain Neoplasms is mainly diagnosed as glioblastoma or Astrocytoma and mismatch repair genes might be involved. , Patients with Turcot syndrome (disorder) (disorder) (TS) are predisposed to Abdomen+Pelvis>Colon tumors and primary brain tumors, typically glioblastomas or medulloblastomas. The authors describe a patient with TS featuring a known germline Mutation Abnormality of exon 5 of the hPMS2 mismatch repair gene who developed two metachronous glioblastomas, both with distinct Oligodendroglia features., Because this patient had an unusual underlying condition and his Specimen Source Codes - Specimen Source Codes - tumor had a unique histological appearance for TS, it was hypothesized that this genetic defect may predispose to malignant Glioma with Oligodendroglia features. , Turcot Syndrome caused by Antigen-Presenting Cells gene develops Medulloblastoma and Turcot Syndrome caused by mismatch repair gene develops glioblastoma. , It is characterized by CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS (Central Nervous System) Neoplasms and gastrointestinal Multiple polyps., Seven months after resection of this Dukes' C2 adenocarcinoma, she presented with a second primary Central Nervous System Specimen Source Codes - Specimen Source Codes - tumor, a Glioblastoma Multiforme., The Turcot syndrome (disorder) (disorder) has been defined as the simultaneous presence of multiple Multiple polyps of the Abdomen+Pelvis>Colon and a Malignant neoplasm of brain., The case of a 47-year-old Homo sapiens submitted to a right hemicolectomy for Primary malignant neoplasm and Multiple polyps, following a series of endoscopic polypectomies and, finally, removal of left temporal glioma is here presented.,  Two of 13 showed microsatellite instability diagnostic test diagnostic test, one of which in a patient with Turcot syndrome (disorder) (disorder), the other in Gliomatosis cerebri cerebri., The Turcot syndrome (disorder) (disorder) (TS) is a rare, probably autosomal recessive, disorder characterized by development of primary Neoplasms, Neuroepithelial of the CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS (Central Nervous System) and numerous adenomatous colorectal polyps. , However, no somatic Gene Mutation in Antigen-Presenting Cells were found among 91 Neoplasms, Neuroepithelial (Medulloblastoma, glioblastoma, Astrocytoma, and Well Differentiated Oligodendroglioma), whether sporadic or associated with TS. , Such syndromes include Neurofibromatosis 2 type 2, Neurofibromatosis 2 type 1, Li-Fraumeni Syndrome 2, as well as Von Hippel-Lindau Syndrome, TUBEROUS SCLEROSIS 2 (disorder), and Turcot syndrome (disorder) (disorder). , This patient's case deals with the association between a glioblastoma, WHO Grade 3 Glioma (WHO Grade III) and Adenocarcinoma of Abdomen+Pelvis>Colon based on familial Multiple polyps coli. , The authors describe two patients with the association of Multiple polyps-coli and CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS Specimen Source Codes - Specimen Source Codes - tumor (Turcot's syndrome). , We report a case of Turcot's syndrome in a 20-year old Homo sapiens with multiple adenomatous polyps of the Abdomen+Pelvis>Colon and Glioblastoma Multiforme. , Another unusual autopsy case of the Turcot syndrome (disorder) (disorder) is reported in a 23-year-old woman with Multiple polyps coli, who developed primary carcinoma of the Jejunum and Jejunum and jejunum and Glioblastoma Multiforme of the left frontal lobe. , Turcot syndrome (disorder) (disorder) represents the unique and discrete occurrence of Multiple polyps coli with Glioblastoma Multiforme, Medulloblastoma, or both.[SEP]Relations: Glioma has relations: disease_phenotype_positive with Turcot syndrome (disorder) with Multiple polyps, disease_phenotype_positive with Turcot syndrome (disorder) with Multiple polyps. Medulloblastoma has relations: disease_phenotype_positive with Turcot syndrome (disorder) with Multiple polyps, disease_phenotype_positive with Turcot syndrome (disorder) with Multiple polyps. Lymphoma has relations: disease_phenotype_positive with Turcot syndrome (disorder) with Multiple polyps, disease_phenotype_positive with Turcot syndrome (disorder) with Multiple polyps. Brain neoplasm has relations: disease_phenotype_positive with Turcot syndrome (disorder) with Multiple polyps, disease_phenotype_positive with Turcot syndrome (disorder) with Multiple polyps. Astrocytoma has relations: disease_phenotype_positive with Turcot syndrome (disorder) with Multiple polyps, disease_phenotype_positive with Turcot syndrome (disorder) with Multiple polyps.", "label": "yes"}
+{"original_question": "Velocardial facial syndrome, otherwise known as Di George syndrome  is caused by a deletion in chromosome 21, yes or no?", "id": "converted_3143", "sentence1": "Velocardial facial syndrome, otherwise known as Di George syndrome  is caused by a Gene Deletion Abnormality in Chromosomes, Human, Pair 1 21, yes or no?", "sentence2": "The Gene Deletion Abnormality of Chromosomes, Human, Pair 1 22q11.2 is involved in the majority of DiGeorge or velo-cardiofacial syndrome., Gene Deletion of Chromosomes, Human, Pair 1 7q11.23 (Williams Syndrome), 15q11-q13 (Angelman Syndrome, Prader-Willi Syndrome) and 22q11 (Di George syndrome), Submicroscopic Gene Deletion of Chromosomes, Human, Pair 1 22q11 have been reported in a multiple anomaly syndrome variously labelled as velocardiofacial syndrome, conotruncal anomaly face syndrome, and Di George syndrome, The 22q11.2 Gene Deletion Abnormality syndrome (di George syndrome) is one of the most prevalent genetic disorders., UNLABELLED\nMost of the children with Di George syndrome and 60% of patients with velocardiofacial syndrome exhibit a microdeletion within Chromosomes, Human, Pair 1 22q11., Submicroscopic Gene Deletion of Chromosomes, Human, Pair 1 22q11 have been reported in a multiple anomaly syndrome variously labelled as velocardiofacial syndrome, conotruncal anomaly face syndrome, and Di George syndrome., 22q11.2DS has several presentations including DiGeorge Syndrome, Shprintzen syndrome or Shprintzen's syndrome and it is the most frequent microdeletion syndrome in the general population (prevalence estimated at 1/4000 births, de novo: 90%)., Di George syndrome due to Mutation Abnormality on 22q or 10q) and can also result from microdeletion or Point Mutation (in the Shprintzen syndrome 70% represent microdeletion and 30% Point Mutation at 22q11, in Rubinstein-Taybi Syndrome 10% cases result from microdeletions and 90% from point mutations); 7) Population incidence of microdeletions is high (1:4000 to 1:30,000) because their etiologic mechanism is related to the common unequal crossing over; 8) Imprinting plays a role in some cases, e.g., [Microdeletion of the Chromosomes, Human, Pair 1 22q11 in children: apropos of a series of 49 patients].<AbstractText Label=\"UNLABELLED\">Most of the children with Di George syndrome and 60% of patients with velocardiofacial syndrome exhibit a microdeletion within Chromosomes, Human, Pair 1 22q11. , 22q11.2DS has several presentations including DiGeorge Syndrome, Shprintzen syndrome or Shprintzen's syndrome and it is the most frequent microdeletion syndrome in the general population (prevalence estimated at 1/4000 births, de novo: 90%). , <b>UNLABELLED</b>: Most of the children with Di George syndrome and 60% of patients with velocardiofacial syndrome exhibit a microdeletion within Chromosomes, Human, Pair 1 22q11., Most of the children with Di George syndrome and 60% of patients with velocardiofacial syndrome exhibit a microdeletion within Chromosomes, Human, Pair 1 22q11.[SEP]Relations: Williams Syndrome has relations: disease_disease with syndrome caused by partial chromosomal Gene Deletion Abnormality, disease_disease with syndrome caused by partial chromosomal Gene Deletion Abnormality, disease_disease with partial Gene Deletion Abnormality of the long arm of Chromosomes, Human, Pair 1 7, disease_disease with partial Gene Deletion Abnormality of the long arm of Chromosomes, Human, Pair 1 7. DiGeorge syndrome has relations: disease_disease with syndrome caused by partial chromosomal Gene Deletion Abnormality, disease_disease with syndrome caused by partial chromosomal Gene Deletion Abnormality. Abnormality of the dentition has relations: disease_phenotype_positive with Chromosomes, Human, Pair 1 15q24 Gene Deletion Abnormality syndrome, disease_phenotype_positive with Chromosomes, Human, Pair 1 15q24 Gene Deletion Abnormality syndrome, disease_phenotype_positive with Chromosomes, Human, Pair 1 9p Gene Deletion Abnormality syndrome, disease_phenotype_positive with Chromosomes, Human, Pair 1 9p Gene Deletion Abnormality syndrome.", "label": "no"}
+{"original_question": "Can mitochondria transfer from cell to cell?", "id": "converted_3240", "sentence1": "Can Mitochondria transfer from cell to cell?", "sentence2": "Interest in the recently discovered phenomenon of mitochondrial transfer between mammalian cells has gained momentum since it was first described in cell culture systems more than a decade ago., We show evidence that Mitochondria transfer from Jurkat Cells to cyclic nucleotide-gated mechanosensitive ion channel activity, which is mediated by cell adhesion, This process of Mitochondria transfer is mediated by tunneling nanotubes, which are protrusions that extend from the Cellular Membrane .[SEP]Relations: mitochondrion has relations: cellcomp_protein with TH, cellcomp_protein with TH, cellcomp_protein with CS, cellcomp_protein with CS, cellcomp_protein with NNT, cellcomp_protein with NNT, cellcomp_protein with HIBADH, cellcomp_protein with HIBADH, cellcomp_protein with CAT, cellcomp_protein with CAT.", "label": "yes"}
+{"original_question": "Does the CTCF protein co-localize with cohesin?", "id": "converted_95", "sentence1": "Does the CTGF protein, Homo sapiens protein co-localize with cohesins?", "sentence2": "To investigate cohesins-non-CTGF protein, Homo sapiens (CNC) binding events in vivo we mapped cohesins and CTGF protein, Homo sapiens, as well as a collection of tissue-specific and ubiquitous transcriptional regulators using Chromatin Immunoprecipitation Sequencing in primary Mus sp. liver., In contrast to regions of the Genome - anatomical entity where cohesins and CTGF protein, Homo sapiens colocalize, CNC Site coincide with the binding of master regulators and enhancer-markers and are significantly associated with liver-specific expressed genes., Here we report that cohesins colocalize with CTGF protein, Homo sapiens at two additional imprinted loci, the Dlk1-Dio3 and the Kcnq1/Kcnq1ot1 loci., By use of Homo sapiens hepatocellular carcinoma cells (HepG2), we found that liver-specific transcription factors colocalize with cohesins independently of CTGF protein, Homo sapiens at liver-specific targets that are distinct from those found in breast cancer cells, Because cohesins can colocalize with CTGF protein, Homo sapiens, we performed chromatin location location immunoprecipitation for the cohesins subunit Rad21 and found lineage and stage-specific Rad21 recruitment to CTGF protein, Homo sapiens in all Ig loci, Here we show that zebrafish RUNX1 protein, Homo sapiens is directly bound by cohesins and CCCTC-binding factor (CTGF protein, Homo sapiens) at the Blood group antigen Blood group antigen P1 and Bone structure of middle phalanx promoters, and within the Introns between Blood group antigen Blood group antigen P1 and Bone structure of middle phalanx., The intronic Binding Sites for cohesins and CTGF protein, Homo sapiens coincide with histone modification that confer enhancer-like properties, and two of the cohesins/CTGF protein, Homo sapiens Site behaved as insulators in an in vivo assay, The identified cohesins and CTGF protein, Homo sapiens Binding Sites are likely to be cis-regulatory elements (CST8 gene) for RUNX1 protein, Homo sapiens since they also recruit RNA Polymerase II (RNAPII)., We have found that CTGF protein, Homo sapiens and cohesins are highly enriched at the convergent and partially overlapping RNA Transcript for the PDLIM7 gene and LMP2A genes, but it is not yet known how CTGF protein, Homo sapiens and cohesins may coordinately regulate these RNA Transcript, haracterization of constitutive CTGF protein, Homo sapiens/cohesins loci: a possible role in establishing topological domains in mammalian Genome, Our analysis revealed: 1) constitutive CTGF protein, Homo sapiens loci were located in constitutive open chromatin location location and often co-localized with constitutive cohesins loci, In Head>Brain, a third of CTGF protein, Homo sapiens and cohesins Binding Sites coincide, consistent with the potential for many interactions between cohesins and CTGF protein, Homo sapiens but also many instances of independent action, Here, we focus on the emerging roles of CTGF protein, Homo sapiens and the cohesins in coordinating long-range interactions between regulatory elements, Chromatin immunoprecipitation for CTGF protein, Homo sapiens and the cohesins subunits Double-Strand-Break Repair Protein Rad21 Homolog and SMC3 wt Allele wt Allele reveals evolutionarily conserved Binding Sites within unmethylated regions ∼5 kb downstream of the PLAGL1 gene gene differentially methylated region and within the PLAGL1 gene gene 3' untranslated region (SLC14A2 gene), TCF physically links cohesins to chromatin location location, ohesin and CTGF protein, Homo sapiens: cooperating to control chromosome conformation?, Recently, three groups mapped numerous cohesins-Binding Sites in mammalian chromosomes and found substantial overlap with the CCCTC-binding factor (CTGF protein, Homo sapiens), We found that each Specimen Source Codes - Site contains a conserved CTGF protein, Homo sapiens consensus sequence, binds CTGF protein, Homo sapiens, and recruits the cohesins subunit Rad21 in vivo, Recent experiments have revealed that cohesins binds to the same Site in mammalian Genome as the zinc finger transcription factor CTGF protein, Homo sapiens, Here we review what is known about the roles of cohesins and CTGF protein, Homo sapiens in regulating gene expression in mammalian cells, and we discuss how cohesins might mediate the insulator function of CTGF protein, Homo sapiens, Previous studies have shown that this major latency control region is occupied by the Cells chromatin location location boundary factor CTGF protein, Homo sapiens and chromosome structural maintenance proteins SMITH-MCCORT DYSPLASIA 1, SMC3 wt Allele wt Allele, and Double-Strand-Break Repair Protein Rad21 Homolog, which comprise the cohesins complex, Cohesin subunits assembled at the CTGF protein, Homo sapiens Binding Sites and bound CTGF protein, Homo sapiens proteins in a cell cycle-dependent manner, We propose that the CTGF protein, Homo sapiens-cohesins complex plays a critical role in regulating the cell cycle control of Genes, Viral expression during latency and that failure to maintain cell cycle control of latent RNA Transcript inhibits host cell proliferation and survival, We used chromosome conformation capture to determine long-range interactions among CTGF protein, Homo sapiens/cohesins Site over 2 Mb on Homo sapiens chromosome 11 encompassing the beta-globin Gene Locus and Flank (surface region) olfactory receptor genes, These results support a Genome - anatomical entity-wide role for CTGF protein, Homo sapiens/cohesins Site through loop formation that both influences transcription and contributes to cell-type-specific chromatin location location organization and function, Increased methylation at this Promoter triggered the dissociation of the insulator protein CTGF protein, Homo sapiens as well as the accompanying cohesins from the BDNF Gene Locus, icotinamide adenine dinucleotide (NAD)-regulated DNA methylation alters CCCTC-binding factor (CTGF protein, Homo sapiens)/cohesins binding and transcription at the BDNF Gene Locus, ecent studies have shown that the protein CTGF protein, Homo sapiens, which plays an important role in insulation and in large-scale organization of chromatin location location within the eukaryotic nucleus, depends for both activities on recruitment of the cohesins complex, We show here that the interaction of CTGF protein, Homo sapiens with the cohesins complex involves direct contacts between the cohesins subunit STAG2 wt Allele and specific regions of the C-terminal tail of CTGF protein, Homo sapiens, Taken together, our results demonstrate that specific Site on the C terminus of CTGF protein, Homo sapiens are essential for cohesins binding and insulator function, The only direct interaction between CTGF protein, Homo sapiens and cohesins involves contact with STAG2 wt Allele, which is external to the cohesins ring, These numerous CTGF protein, Homo sapiens/cohesins Site potentially form the Unit dose - Base of the multiloop rosette structures at the Igh Gene Locus that compact during Ig heavy chain rearrangement, We have previously shown that the Homo sapiens herpesvirus 8 (KSHV) major latency RNA Transcript encoding latent Orf73 antigen, Homo sapiens herpesvirus 8, vCyclin, FLICE Inhibitory Protein, v-miRNAs, and Kaposin are regulated, in part, by a chromatin location location organizing element that binds CTGF protein, Homo sapiens and cohesins, Mutation Abnormality Abnormality of the CTGF protein, Homo sapiens-cohesins binding Specimen Source Codes - Site reduced or eliminated the chromatin location location conformation linkages, and deregulated Viral transcription and Genome - anatomical entity copy number control, Our findings indicate that KSHV Genome are organized into chromatin location location loops mediated by CTGF protein, Homo sapiens and cohesins interactions, and that these inter-chromosomal linkages coordinate latent and lytic gene control., We show here that Gestational age:Time:Point in time:^Fetus:Quantitative disrupts an RNA Polymerase II (RNAPII) complex that accumulates at the CTGF protein, Homo sapiens-cohesins binding Specimen Source Codes - Site within the first Introns of the latency transcript., Gestational age:Time:Point in time:^Fetus:Quantitative altered the enrichment of the RNAPII pausing complex, along with pausing factors SUPT5H gene and WHSC2 protein, Homo sapiens, at the intragenic CTGF protein, Homo sapiens-cohesins Binding Sites., Gestational age:Time:Point in time:^Fetus:Quantitative treatment also inhibited the transcription of some Cells genes, like c-myc Genes Genes, which contain a similar CTGF protein, Homo sapiens-cohesins binding Specimen Source Codes - Site within the first Introns., These findings suggest that RNAPII pauses at intragenic CTGF protein, Homo sapiens-cohesins Binding Sites and that abrogation of this pausing by Gestational age:Time:Point in time:^Fetus:Quantitative leads to loss of proper mRNA production and defects in sister chromatid cohesion, a process important for both Viral and Cells chromosome stability., TCF and cohesins cooperatively mediate the cell-type specific interchromatin interaction between B-Cell Lymphoma/Leukemia 11B and ARHGAP6 gene loci, Additional experiments verified that the interchromatin interaction between the B-Cell Lymphoma/Leukemia 11B and ARHGAP6 gene loci was cell-type specific, which was cooperatively mediated by CTGF protein, Homo sapiens and cohesins., enome-wide studies of CCCTC-binding factor (CTGF protein, Homo sapiens) and cohesins provide insight into chromatin location location structure and regulation, Recent Genome - anatomical entity-wide studies mapping the Binding Sites of CTGF protein, Homo sapiens and its interacting partner, cohesins, using chromatin location location immunoprecipitation coupled with deep sequencing (Chromatin Immunoprecipitation Sequencing) revealded that CTGF protein, Homo sapiens globally co-localizes with cohesins, Here, we show by ChIP-Seq that most Homo sapiens subtelomeres contain a CTGF protein, Homo sapiens- and cohesins-binding Specimen Source Codes - Site within ∼1-2 kb of the TTAGGG repeat tract and adjacent to a CpG-islands implicated in Telomeric Repeat-Containing RNA transcription control., These findings indicate that CTGF protein, Homo sapiens and cohesins are integral components of most Homo sapiens subtelomeres, and important for the regulation of Telomeric Repeat-Containing RNA transcription and telomere end protection, In addition, we show that this DNA looping requires specific binding of the CTGF protein, Homo sapiens/cohesins complex to two symmetrically aligned Binding Sites in both the transcriptionally active promoters and in one of the enhancers[SEP]Relations: cohesins complex has relations: cellcomp_protein with SMC3 wt Allele, cellcomp_protein with SMC3 wt Allele, cellcomp_protein with SMC1A, cellcomp_protein with SMC1A, cellcomp_protein with STAG1, cellcomp_protein with STAG1, cellcomp_protein with SMC1B, cellcomp_protein with SMC1B, cellcomp_protein with STAG3L4, cellcomp_protein with STAG3L4.", "label": "yes"}
+{"original_question": "Can brain derived exosomes carry APP molecules?", "id": "converted_3515", "sentence1": "Can brain derived Exosomes carry Smartphone Application molecules?", "sentence2": "Here, we show that small lipid Vesicle (morphologic abnormality) called Exosomes, secreted in the Extracellular milieu by cortical neurons, carry endogenous Smartphone Application, these Exosomes contained Smartphone Application and were capable of efficiently transferring Smartphone Application to normal primary neurons. , Accumulating evidence has demonstrated that Exosomes are associated with Serum amyloid A protein (Smartphone Application) and tau Proteins and play a controversial role in Alzheimer's disease process. ,  Here we have investigated the role of Exosomes in the processing of Smartphone Application and show that these Vesicle (morphologic abnormality) contain Smartphone Application-CTFs, as well as Smartphone Application wt Allele[SEP]Relations: Extracellular space has relations: cellcomp_protein with Smartphone Application, cellcomp_protein with Smartphone Application, cellcomp_protein with AFM, cellcomp_protein with AFM, cellcomp_protein with ERFE, cellcomp_protein with ERFE, cellcomp_protein with MSMB, cellcomp_protein with MSMB, cellcomp_protein with MCAM, cellcomp_protein with MCAM.", "label": "yes"}
+{"original_question": "Does allele phasing improve the phylogenetic utility of ultraconserved elements?", "id": "converted_2970", "sentence1": "Does allele phasing improve the phylogenetic utility of ultraconserved elements?", "sentence2": "Alleles Phasing Greatly Improves the Phylogenetic Utility of Ultraconserved Elements., Our empirical analyses of Ultraconserved Element (UCE) Gene Locus data collected from the South American hummingbird genus Topaza demonstrate that phased allele sequences carry sufficient phylogenetic information to infer the genetic structure, lineage divergence, and biogeographic history of a genus that diversified during the last three million years. The phylogenetic results support the recognition of two species, and suggest a high rate of gene flow across large distances of rainforest habitats but rare admixture across the Amazon River. Our simulations provide evidence that analyzing allele sequences leads to more accurate estimates of tree topology and divergence times than the more common approach of using contig sequences., Alleles Phasing Greatly Improves the Phylogenetic Utility of Ultraconserved Elements.Advances in high-throughput sequencing techniques now allow relatively easy and affordable sequencing of large portions of the Genome - anatomical entity, even for nonmodel Organism. [SEP]Relations: male organism has relations: anatomy_anatomy with multicellular organism, anatomy_anatomy with multicellular organism. anatomical entity has relations: anatomy_anatomy with anatomical cluster, anatomy_anatomy with anatomical cluster, anatomy_anatomy with immaterial anatomical entity, anatomy_anatomy with immaterial anatomical entity, anatomy_anatomy with insect mouthpart, anatomy_anatomy with insect mouthpart, anatomy_anatomy with material anatomical entity, anatomy_anatomy with material anatomical entity.", "label": "yes"}
+{"original_question": "Can the apoptosis regulator BAX trigger the release of cytochrome c?", "id": "converted_1287", "sentence1": "Can the apoptosis regulator BAX trigger the release of CYCS gene?", "sentence2": "shogaol reduced the Mitochondrial Membranes potential (Matrix Metalloproteinases) and released CYCS gene from Mitochondria to Cytoplasmic matrix via BAX protein, human activation. , Moreover, overexpression of ERβ prevented BAX protein, human activation, CYCS gene release, caspase-3 activation, and PARP1 wt Allele cleavage during apoptosis., In this study, we demonstrated that EV71 infection altered BAX protein, human conformation and triggered its redistribution from the Cytoplasmic matrix to Mitochondria in RD cells. Subsequently, CYCS gene was released from Mitochondria to Cytoplasmic matrix., associated with translocation of BAX protein, human from the Cytoplasmic matrix to the Mitochondrial Membranes, CYCS gene release, and caspase activation. , Once activated, BAK1 wt Allele and BAX form proteolipid pores in the OMM leading to mitochondrial outer membrane permeabilization (mitochondrial outer membrane permeabilization), and the release of inner membrane space proteins, such as CYCS gene, which promotes caspase activation. ,  Our results showed that BGLAP wt Allele induced a caspase-dependent apoptosis by triggering a series of events in HeLa Cells including BAX protein, human translocation, CYCS gene release, caspase-3 activation, chromosome fragmentation followed by caspase-8 activation, Twice a day cleavage and eventually cell death. , BAX protein, human plays a key role in intrinsic apoptotic signaling in Neurons by allowing the release of mitochondrial CYCS gene. [SEP]Relations: mitochondrion has relations: cellcomp_protein with BAX, cellcomp_protein with BAX, cellcomp_protein with GPX4, cellcomp_protein with GPX4. CYCS gene metabolic process has relations: bioprocess_bioprocess with cytochrome metabolic process, bioprocess_bioprocess with cytochrome metabolic process, bioprocess_bioprocess with CYCS gene biosynthetic process, bioprocess_bioprocess with CYCS gene biosynthetic process. HELLS has relations: bioprocess_protein with negative regulation of intrinsic apoptotic signaling pathway, bioprocess_protein with negative regulation of intrinsic apoptotic signaling pathway.", "label": "yes"}
+{"original_question": "Can midostaurin inhibit angiogenesis?", "id": "converted_2936", "sentence1": "Can midostaurin inhibit angiogenesis?", "sentence2": "midostaurin was a prototype kinase inhibitor, originally developed as a Protein Kinase C inhibitor and subsequently as an angiogenesis inhibitor, based on its inhibition of Vascular Endothelial Growth Factor Receptor-1.[SEP]Relations: midostaurin has relations: drug_drug with Estradiol, drug_drug with Estradiol, drug_drug with Antipyrine, drug_drug with Antipyrine, drug_drug with Aldosterone, drug_drug with Aldosterone, drug_drug with Sparteine, drug_drug with Sparteine, drug_drug with Azelastine, drug_drug with Azelastine.", "label": "yes"}
+{"original_question": "Does the word ovine refers to goats?", "id": "converted_2105", "sentence1": "Does the word Domestic Sheep refers to Capra hircus?", "sentence2": "Jaagsiekte sheep retrovirus (JSRV) is the causative agent of Domestic Sheep pulmonary adenocarcinoma (OPA), a transmissible Primary malignant neoplasm of lung of sheep that has rarely been found in Capra hircus. , In sheep, a Rat Bronchiolo-Alveolar Carcinoma, known as Domestic Sheep pulmonary carcinoma (Oligomeric Procyanidin Complex), is caused by jaagsiekte sheep retrovirus (JSRV), an exogenous type D retrovirus. [SEP]Relations: protein complex oligomerization has relations: bioprocess_protein with OPA1, bioprocess_protein with OPA1, bioprocess_protein with BOK, bioprocess_protein with BOK, bioprocess_protein with MCU, bioprocess_protein with MCU, bioprocess_protein with ADCY8, bioprocess_protein with ADCY8, bioprocess_protein with NOL3, bioprocess_protein with NOL3.", "label": "no"}
+{"original_question": "Is protein CXCR4 used as a prognostic marker of cancer?", "id": "converted_792", "sentence1": "Is protein C-X-C motif chemokine 12 receptor activity used as a prognostic marker of Primary malignant neoplasm?", "sentence2": "Aberrant overexpression of C-X-C motif chemokine 12 receptor activity is associated with worse overall survival, Malignant adenomatous neoplasm histology, distant metastasis, lymph node involvement in Non-Small Cell Lung Carcinoma., C-X-C motif chemokine 12 receptor activity belongs to a family of G protein-coupled cell surface receptors and has been proved to a prognostic marker in a various tumors, including Squamous cell carcinoma of esophagus. , The CXCR3 gene (C-X-C motif chemokine 12 receptor activity) has been found to be a prognostic marker in various types of Primary malignant neoplasm, being involved in chemotaxis, stemness and drug resistance. , The chemokine receptor C-X-C motif chemokine 12 receptor activity that has been shown to be implicated in ANOPHTHALMIA AND PULMONARY HYPOPLASIA tumorigenicity and Aggressive behavior could serve as a prognostic marker for survival after a curative-intent surgery and was associated with the pattern of Neoplasms recurrence (distant versus local relapse)., XCR4 promotes tumor growth, angiogenesis and metastasis, and is a prognostic marker in a number of different types of tumors., C-X-C motif chemokine 12 receptor activity has been identified as a prognostic marker for Leukemia, Myelocytic, Acute (AML) and other Malignant Neoplasms. , The chemokine receptor C-X-C motif chemokine 12 receptor activity has been found to be a prognostic marker in various types of Primary malignant neoplasm, including breast Primary malignant neoplasm. , Upregulated expression of C-X-C chemokine receptor 4 is an independent prognostic predictor for patients with gastric Primary malignant neoplasm., detection of C-X-C motif chemokine 12 receptor activity expression will be helpful for predicting prognosis for patients with gastric Primary malignant neoplasm., The chemokine receptor C-X-C motif chemokine 12 receptor activity is a marker of metastatic disease., High C-X-C motif chemokine 12 receptor activity level in Primary malignant neoplasm specimens independently predicts a poor outcome for patients with node-positive breast Primary malignant neoplasm., Univariate and multivariate analyses demonstrated that the high levels of nuclear C-X-C motif chemokine 12 receptor activity and Chemokine Chemokine CXCL12 expression in Hepatocyte were significantly better prognostic factors for overall and hepatic disease-free survival in patients with LAMB1 gene., The chemokine receptor C-X-C motif chemokine 12 receptor activity has been implicated in Malignant neoplasm of soft tissue development and has been found to be a prognostic marker for poor clinical outcome. , high C-X-C motif chemokine 12 receptor activity expression is correlated to shorter DFS and could be used as a prognostic marker in order to stratify Melanocytic neoplasm patients at higher progression risk.[SEP]Relations: C-X-C motif chemokine 12 receptor activity has relations: molfunc_protein with C-X-C motif chemokine 12 receptor activity, molfunc_protein with C-X-C motif chemokine 12 receptor activity. esophageal squamous cell carcinoma has relations: disease_protein with XRCC1, disease_protein with XRCC1, disease_protein with PRDX1, disease_protein with PRDX1, disease_protein with FBXW7, disease_protein with FBXW7. small cell lung carcinoma has relations: disease_protein with ASCL1, disease_protein with ASCL1.", "label": "yes"}
+{"original_question": "Is the JNK pathway activated during liver regeneration?", "id": "converted_1690", "sentence1": "Is the MAPK8 wt Allele pathway activated during liver regeneration?", "sentence2": "analysis of the role of MAPK8 wt Allele signaling pathway in regulating cell proliferation and apoptosis of Rattus norvegicus liver regeneration, paths of MAPK8 wt Allele signaling pathway regulate cell proliferation and apoptosis in both LR, JUN gene is not mandatory for Mus sp. hepatocyte proliferation , CASP14 gene lacking JUN gene in the liver display impaired regeneration after partial hepatectomy (pH:LsCnc:Pt:Ser/Plas:Qn), initial activity of the MAPK8 wt Allele pathway, use of Drosophila <basidiomycetes> <basidiomycetes> for the study of regeneration , Loss of macroautophagy led to overactivation of the c-Jun N-terminal kinase (MAPK8 wt Allele)/c-Jun signaling pathway that induced cell death., stress induced during intermittent selective clamping accelerates Rattus norvegicus liver regeneration through MAPK8 wt Allele pathway, MAPK9 wt Allele promotes injury after Mus sp. LT via the positive regulation of mitochondrial membrane permeability, Jun N-terminal kinase 2 promotes graft injury via the mitochondrial permeability transition after Mus sp. liver transplantation, add45beta promotes hepatocyte survival during liver regeneration in mice by modulating MAPK8 wt Allele signaling, basis for MAPK8 wt Allele suppression during liver regeneration and identify GADD45B wt Allele as a potential therapeutic target in Liver diseases,  genetic inactivation of the MAPK8 wt Allele pathway results in impaired proliferation of fetal hepatoblasts in vitro and defective adult liver regeneration in vivo, enhancement of the activation of Jun N-terminal kinase and mitogen-activated protein kinase p38 caused by partial hepatectomy,  arsenite induced apoptosis in the Hepatocyte in vivo, through the enhancement of the activation of MAPK8 wt Allele and Mitogen-Activated Protein Kinase 14 caused by partial hepatectomy, Jun N-terminal kinase and Mitogen-Activated Protein Kinase 14, but not Proto-Oncogene Proteins c-akt, was altered., Although mechanical stress has been implicated in Liver Cirrhosis and liver regeneration following hepatectomy, the signaling pathway(s) that may be activated in Hepatocyte in response to mechanical stress have not been determined,  MAPK8 wt Allele, Mitogen-Activated Protein Kinases and JAK2 protein, human protein, human inhibitors partially abrogated apoptosis and when used in combination reduced it to basal levels, induction of CD40-mediated Biliary epithelial cell apoptosis requires JAK2 protein, human protein, human-mediated phosphorylation of STAT3 protein, human protein, human as well as sustained JNK1/2, ERK1/2 activation, Jun-N-terminal kinase drives Cyclin D1 expression and proliferation during liver regeneration, c-Jun-N-terminal kinase (MAPK8 wt Allele) pathway is strongly activated after partial hepatectomy (pH:LsCnc:Pt:Ser/Plas:Qn), Growth Factor and Recombinant Cytokines are involved in liver regeneration, COPS5 gene (Jun activation domain-binding protein 1), a co-activator of Transcription Factor Transcription Factor AP-1, which is essential for liver regeneration, specifically interacts with Protoplasm HPO[SEP]Relations: mitogen-activated protein kinase binding has relations: molfunc_protein with PTPRJ, molfunc_protein with PTPRJ, molfunc_protein with PTPRJ, molfunc_protein with PTPRJ, molfunc_protein with PTAFR, molfunc_protein with PTAFR, molfunc_protein with PTAFR, molfunc_protein with PTAFR, molfunc_protein with CDK5RAP3, molfunc_protein with CDK5RAP3.", "label": "yes"}