{"original_question": "Is Baloxavir effective for influenza?", "id": "converted_0", "sentence1": "Is Baloxavir effective for influenza?", "sentence2": "Baloxavir marboxil (Xofluza\u2122; baloxavir) is an oral cap-dependent endonuclease inhibitor that has been developed by Roche and Shionogi. The drug blocks influenza virus proliferation by inhibiting the initiation of mRNA synthesis. In February 2018, baloxavir received its first global approval in Japan for the treatment of Influenza virus vaccine or Herpesvirus 1, Cercopithecine infections.  This article summarized the milestones in the development of baloxavir leading to this first global approval for Influenza virus vaccine or Herpesvirus 1, Cercopithecine infections. Baloxavir acid (BXA), derived from the prodrug baloxavir marboxil (BXM), potently and selectively inhibits the cap-dependent endonuclease within the polymerase PA subunit of Influenza virus vaccine and B viruses. Characterization of influenza virus variants induced by treatment with the endonuclease inhibitor baloxavir marboxil. Baloxavir Marboxil for Uncomplicated Influenza in Adults and Adolescents. BACKGROUND: Baloxavir marboxil is a selective inhibitor of influenza cap-dependent endonuclease. It has shown therapeutic activity in preclinical models of Influenza virus vaccine and Herpesvirus 1, Cercopithecine infections, including strains resistant to current antiviral agents. CONCLUSIONS: Single-dose baloxavir was without evident safety concerns, was superior to placebo in alleviating influenza symptoms, and was superior to both oseltamivir and placebo in reducing the viral load 1 day after initiation of the trial regimen in patients with uncomplicated influenza. A single oral dose of baloxavir is usually well tolerated; it hastens alleviation of influenza symptoms and shortens the duration of viral shedding. Japan was the first country to approve baloxavir marboxil as a treatment for influenza. This article summarized the milestones in the development of baloxavir leading to this first global approval for Influenza virus vaccine or Herpesvirus 1, Cercopithecine infections.<br> In February 2018, baloxavir received its first global approval in Japan for the treatment of Influenza virus vaccine or Herpesvirus 1, Cercopithecine infections.[SEP]", "label": "yes"}
{"original_question": "Are there microbes in human breast milk?", "id": "converted_1", "sentence1": "Are there microbes in human Breast Milk Specimen?", "sentence2": "Contrary to long-held dogma, human Milk Specimen is not sterile. Instead, it provides infants a rich source of diverse Bacteria, particularly microbes belonging to the Staphylococcus, Streptococcus species species, and Pseudomonas genera. The origins of the Bacteria in Milk Specimen are thought to include the maternal gastrointestinal tract (via an entero-mammary pathway) and through bacterial exposure of the Breast during nursing.[SEP]", "label": "yes"}
{"original_question": "Is cariprazine effective for treatment of bipolar disorder?", "id": "converted_2", "sentence1": "Is cariprazine effective for treatment of Bipolar Disorder Type 2?", "sentence2": "BACKGROUND: We evaluated the safety/tolerability of longer-term open-label treatment with cariprazine in patients who had responded to cariprazine for acute bipolar mania. Clinically relevant response and remission outcomes in cariprazine-treated patients with Bipolar I disorder. Cariprazine is FDA approved for the acute treatment of SCHIZOPHRENIA 2 (disorder) and Manic mood or mixed episodes associated with Bipolar I disorder in adults. DISCUSSION: Cariprazine-treated patients with Bipolar I disorder attained clinically significant improvement in Manic mood symptoms as shown by significantly greater rates of response and remission versus placebo; improvement in Manic mood symptoms did not induce depressive symptoms. OBJECTIVE: Cariprazine, a dopamine D3/D2 partial agonist atypical antipsychotic with preferential binding to D3 receptors, is approved for the treatment of SCHIZOPHRENIA 2 (disorder) and Manic mood or mixed episodes associated with Bipolar I disorder. <b>BACKGROUND</b>: Cariprazine was approved for treating SCHIZOPHRENIA 2 (disorder) and Bipolar Disorder Type 2, and currently is being evaluated for treating Cancer patients and suicide and Cancer patients and suicide and depression in clinical trials in the United States.[SEP]", "label": "yes"}
{"original_question": "Is Bobble head doll syndrome associated with hydrocephalus?", "id": "converted_3", "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]", "label": "yes"}
{"original_question": "Can breastfeeding confer protection from type I diabetes?", "id": "converted_4", "sentence1": "Can breastfeeding confer protection from type I diabetes?", "sentence2": "In the neonate and infant, among other benefits, lactation confers protection from future both type 1 and type 2 diabetes.[SEP]", "label": "yes"}
{"original_question": "Can pets affect infant microbiomed?", "id": "converted_5", "sentence1": "Can pets affect infant microbiomed?", "sentence2": "Since there is some evidence that pets also alter the gut microbial composition of infants, changes to the gut microbiome are putative pathways by which Positron-Emission Tomography exposure can reduce these risks to health. The impact of Positron-Emission Tomography ownership varies under different birth scenarios; however, in common, exposure to pets increased the abundance of two Bacteria, Ruminococcus species species and Oscillospira, which have been negatively associated with childhood MS4A2 wt Allele and BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20. As a common effect in all birth scenarios, pre- and postnatal Positron-Emission Tomography exposure enriched the abundance of Oscillospira and/or Ruminococcus species species (P\u2009<\u20090.05) with more than a twofold greater likelihood of high abundance. Among vaginally born infants with maternal intrapartum antibiotic prophylaxis exposure, Streptococcaceae were substantially and significantly reduced by Positron-Emission Tomography exposure (P\u2009<\u20090.001, FDRp\u2009=\u20090.03), reflecting an 80% decreased likelihood of high abundance (OR 0.20, 95%CI, 0.06-0.70) for Positron-Emission Tomography exposure during pregnancy alone and a 69% reduced likelihood (OR 0.31, 95%CI, 0.16-0.58) for exposure in the pre- and postnatal time periods. Exposure to household furry pets influences the gut microbiota of infant at 3-4\u00a0months following various birth scenarios.[SEP]", "label": "yes"}
{"original_question": "Is there any association between the human gut microbiome and depression?", "id": "converted_6", "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]", "label": "yes"}
{"original_question": "Are whole-genome duplications more divergent than small-scale duplications in yeast?", "id": "converted_7", "sentence1": "Are whole-genome duplications more divergent than small-scale duplications in Saccharomyces cerevisiae?", "sentence2": "Also, we observe that Membrane Transport Proteins and glycolytic Genes have a higher probability to be retained in duplicate after WGD and subsequent gene loss, both in the model as in S. cerevisiae, which leads to an increase in glycolytic flux after WGD We show that the retention of Genes in duplicate in the model, corresponds nicely with those retained in duplicate after the ancestral WGD in S. cerevisiae Thus, our model confirms the hypothesis that WGD has been important in the adaptation of Saccharomyces cerevisiae to the new, glucose-rich environment that arose after the appearance of Angiosperm. Whole-genome duplicates tend to exhibit less profound phenotypic effects when Delete - Document Availability Status, are functionally less divergent, and are associated with a different set of functions than their small-scale duplicate counterparts. The results uncover the WGD as a major source for the evolution of a complex interconnected block of transcriptional pathways. These selected pairs, both WGD and Speech Sound Disorders, tend to have decelerated functional evolution, have higher propensities of co-clustering into the same protein complexes, and share common interacting partners. Moreover, we find additional transcriptional profiles that are suggestive of neo- and subfunctionalization of duplicate gene copies. These patterns are strongly correlated with the functional dependencies and Sequence - ParameterizedDataType divergence profiles of gene copies. Functional and transcriptional divergence between the copies after gene duplication has been considered the main driver of innovations . Whole-genome duplicates tend to exhibit less profound phenotypic effects when Delete - Document Availability Status, are functionally less divergent, and are associated with a different set of functions than their small-scale duplicate counterparts. Empirical data shows that whole-genome duplications (WGDs) are more likely to be retained than small-scale duplications (SSDs), though their relative contribution to the functional fate of duplicates remains unexplored.[SEP]", "label": "yes"}
{"original_question": "Do yeast LTR give rise to circular DNA?", "id": "converted_8", "sentence1": "Do Saccharomyces cerevisiae LTR give rise to DNA, Circular?", "sentence2": "Circular retrotransposition products generated by a LINE retrotransposon Formation of Extrachromosomal Circular DNA from Long Terminal Repeats of Retrotransposons in Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae Ty eccDNA can arise from the circularization of extrachromosomal linear DNA during the transpositional life cycle of retrotransposons, or from circularization of genomic Ty DNA Circularization may happen through nonhomologous end-joining (Non-Homologous DNA End-Joining) of Long Terminal Repeat (LTRs) flanking Ty elements, by Ty autointegration, or by LTR-LTR recombination We have recently shown that Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae LTR elements generate circular DNAs through recombination events between their flanking Long Terminal Repeat (LTRs). Similarly, circular DNAs can be generated by recombination between LTRs residing at different genomic loci, in which case the DNA, Circular will contain the Introns. A recent study on circular DNAs in Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae found that transposable element sequence residing in circular structures mostly corresponded to full-length transposable elements.[SEP]", "label": "yes"}
{"original_question": "Is cohesin linked to myeloid differentiation?", "id": "converted_9", "sentence1": "Is cohesins linked to myeloid differentiation?", "sentence2": "Consistent with a role for inflammatory signals in promoting myeloid differentiation of hematopoietic stem and Stem cells (HPSCs), cohesins mutations in HSPCs led to reduced inflammatory gene expression and increased resistance to differentiation-inducing inflammatory stimuli. These findings uncover an unexpected dependence of inducible gene expression on cohesins, link cohesins with myeloid differentiation, and may help explain the prevalence of cohesins mutations in Homo sapiens Leukemia, Myelocytic, Acute. Consistent with a role for inflammatory signals in promoting myeloid differentiation of hematopoietic stem and Stem cells (HPSCs), cohesins mutations in HSPCs led to reduced inflammatory gene expression and increased resistance to differentiation-inducing inflammatory stimuli. These findings uncover an unexpected dependence of inducible gene expression on cohesins, link cohesins with myeloid differentiation, and may help explain the prevalence of cohesins mutations in Homo sapiens Leukemia, Myelocytic, Acute.<br>[SEP]", "label": "yes"}
{"original_question": "Is pembrolizumab effective against Ewing's sarcoma?", "id": "converted_10", "sentence1": "Is pembrolizumab effective against Ewing's sarcoma of bone?", "sentence2": "None of the 13 patients with Ewing's sarcoma of bone of bone had an objective response.  Between March 13, 2015, and Feb 18, 2016, we enrolled 86 patients, 84 of whom received pembrolizumab (42 in each disease cohort) and 80 of whom were evaluable for response (40 in each disease cohort).[SEP]", "label": "no"}
{"original_question": "Can gene therapy restore auditory function?", "id": "converted_11", "sentence1": "Can Genes therapy restore auditory function?", "sentence2": "Gene therapy restores auditory and vestibular function in a mouse model of Usher syndrome type 1c. We demonstrate recovery of Genes and protein expression, restoration of sensory cell function, rescue of complex auditory function and recovery of hearing and balance behavior to near wild-type levels. The data represent unprecedented recovery of inner ear function and suggest that biological therapies to treat Hearing Loss, Partial may be suitable for translation to Homo sapiens with genetic inner ear disorders.[SEP]", "label": "yes"}
{"original_question": "Is the PINES framework being used for the prediction of coding variants?", "id": "converted_12", "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 erythropoietin effective for treatment of amyotrophic lateral sclerosis?", "id": "converted_13", "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\u2005Intrauterine fortnightly did not change the course of Amyotrophic Lateral Sclerosis. At 12\u2005months, 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\u2005h 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]", "label": "no"}
{"original_question": "Is celecoxib effective for treatment of amyotrophic lateral sclerosis?", "id": "converted_14", "sentence1": "Is celecoxib effective for treatment of amyotrophic lateral sclerosis?", "sentence2": "NTERPRETATION: At the dosage studied, celecoxib did not have a beneficial effect on research subjects with Amyotrophic Lateral Sclerosis, and it was safe. A biological effect of celecoxib was not demonstrated in the Cerebrospinal Fluid. Further studies of celecoxib at a dosage of 800 mg/day in Amyotrophic Lateral Sclerosis are not warranted. Prostaglandin E(2) levels in Cerebrospinal Fluid were not elevated at baseline and did not decline with treatment.<br><b>INTERPRETATION</b>: At the dosage studied, celecoxib did not have a beneficial effect on research subjects with Amyotrophic Lateral Sclerosis, and it was safe.[SEP]", "label": "no"}
{"original_question": "Are ultraconserved enhancers important for normal development?", "id": "converted_15", "sentence1": "Are ultraconserved enhancers important for normal development?", "sentence2": "Ultraconserved Enhancers Are Required for Normal Development. However, initial deletion studies in CASP14 gene revealed that loss of such extraordinarily constrained sequences had no immediate impact on viability. Here, we show that ultraconserved enhancers are required for normal development.  Here, we show that ultraconserved enhancers are required for normal development.[SEP]", "label": "yes"}
{"original_question": "Is chlorotoxin a peptide?", "id": "converted_16", "sentence1": "Is chlorotoxin a peptide?", "sentence2": "chlorotoxin peptide  Chlorotoxin (cyclophosphamide) is a 36-amino-acid disulfide-containing peptide derived from the Venom (disposition) of the scorpion Leiurus quinquestriatus. The mature Odontobuthus doriae chlorotoxin peptide has a 35-amino-acid residue and four disulfide bounds.  Chlorotoxin (cyclophosphamide), a disulfide-rich peptide from the scorpion Leiurus quinquestriatus,[SEP]", "label": "yes"}
{"original_question": "Does vesatolimod inhibit TLR7?", "id": "converted_17", "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]", "label": "no"}
{"original_question": "Is selenocysteine an aminoacid?", "id": "converted_18", "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]", "label": "yes"}
{"original_question": "Is Tecovirimat effective for smallpox?", "id": "converted_19", "sentence1": "Is tecovirimat effective for smallpox?", "sentence2": "Oral tecovirimat for the Treatment of Smallpox. CONCLUSIONS: On the basis of its efficacy in two animal models and pharmacokinetic and safety data in Homo sapiens, tecovirimat is being advanced as a therapy for smallpox in accordance with the FDA Animal Rule. Background: tecovirimat (ST-246) is being developed as an antiviral therapeutic for smallpox for use in the event of an accidental or intentional release.  Conclusions: tecovirimat treatment initiated up to 8 days following a lethal aerosol MPXV challenge improves survival and, when initiated earlier than 5 days after challenge, provides protection from clinical effects of disease, supporting the conclusion that it is a promising smallpox antiviral therapeutic candidate. tecovirimat: First Global Approval. In July 2018, oral tecovirimat was approved in the USA for the treatment of human smallpox disease caused by Smallpox Viruses in adults and paediatric patients weighing \u2265\u00a013\u00a0kg. An intravenous formulation of tecovirimat is undergoing phase I development for the treatment of smallpox infection.  Brincidofovir, an oral antiviral in late stage development, has proven effective against Orthopoxvirus in vitro and in vivo, has a different mechanism of action from tecovirimat (the only oral smallpox antiviral currently in the US Strategic National Stockpile), and has a resistance profile that reduces concerns in the scenario of a bioterror attack using genetically engineered smallpox. Treatment with the smallpox antiviral tecovirimat (ST-246) alone or in combination with ACAM2000 vaccination is effective as a postsymptomatic therapy for monkeypox virus infection. tecovirimat appears to be an effective smallpox therapeutic in nonhuman primates, suggesting that it is reasonably likely to provide therapeutic benefit in smallpox-infected Homo sapiens.[SEP]", "label": "yes"}
{"original_question": "Can simvastatin alleviate depressive symptoms?", "id": "converted_20", "sentence1": "Can simvastatin alleviate depressive symptoms?", "sentence2": "Simvastatin-treated patients experienced significantly more reductions in HDRS scores compared to the placebo group by the end of the trial (p=0.02). Early improvement and response rates were significantly greater in the simvastatin group than the placebo group (p=0.02 and p=0.01, respectively) but remission rate was not significantly different between the two groups (p=0.36). In conclusion, simvastatin seems to be a safe and effective adjuvant therapy for patients suffering from major depressive disorder.[SEP]", "label": "yes"}
{"original_question": "Is P. gingivalis bacteria found in brain?", "id": "converted_21", "sentence1": "Is P. gingivalis bacteria found in Head>Brain?", "sentence2": "studies using animal model of Periodontitis and Homo sapiens post-mortem Head>Brain tissues from subjects with cytarabine/daunorubicin protocol strongly suggest that a gram-negative periodontal pathogen, Porphyromonas gingivalis (Pg) and/or its product gingipain is/are translocated to the Head>Brain. The polymicrobial dysbiotic subgingival biofilm microbes associated with Periodontal Diseases appear to contribute to developing pathologies in distal body sites, including the Head>Brain.[SEP]", "label": "yes"}
{"original_question": "Is ibudilast effective for multiple sclerosis?", "id": "converted_22", "sentence1": "Is ibudilast effective for Multiple Sclerosis?", "sentence2": "Ibudilast slowed brain atrophy in Parts per million (qualifier value) and SPMS patients in a multicenter phase 2b study.  Ibudilast inhibits several CNP gene, macrophage migration inhibitory factor, and toll-like receptor 4 and can cross the blood-brain barrier, with potential salutary effects in progressive Multiple Sclerosis. CONCLUSIONS: In a phase 2 trial involving patients with progressive Multiple Sclerosis, ibudilast was associated with slower progression of brain atrophy than placebo but was associated with higher rates of gastrointestinal side effects, Headache, and Cancer patients and suicide and Cancer patients and suicide and depression. Specifically, the current evidence regarding treatment of progressive MS with ocrelizumab, simvastatin, ibudilast, thioctic acid, high-dose biotin, siponimod, and cell-based therapies are discussed. Based on our knowledge of pathophysiology, three therapeutic strategies are proposed: anti-inflammatory (ocrelizumab, siponimod\u2026); remyelinating (opicinumab); and neuroprotective (high-dose biotin, ibudilast, simvastatin\u2026).  Current article provides an overview of the pharmacology of Irritable Bowel Syndrome with a focus on preclinical and clinical data supporting its potential neuroprotective benefits for neurological conditions, including Multiple Sclerosis, Neuropathic pain, medication overuse Headache, Cerebrovascular accident, Opioids, Alcohol - Recreational Drug Use Code and methamphetamine abuse. Design, rationale, and baseline characteristics of the randomized double-blind phase II clinical trial of ibudilast in progressive Multiple Sclerosis. METHODS: SPRINT-MS is a randomized, placebo-controlled, phase II trial of ibudilast in patients with POLYDACTYLY, POSTAXIAL, WITH PROGRESSIVE MYOPIA. CONCLUSION: SPRINT-MS is designed to evaluate the safety and efficacy of ibudilast as a treatment for POLYDACTYLY, POSTAXIAL, WITH PROGRESSIVE MYOPIA while simultaneously validating five different imaging biomarkers as outcome metrics for use in future phase II proof-of-concept POLYDACTYLY, POSTAXIAL, WITH PROGRESSIVE MYOPIA trials. Ibudilast for the treatment of Multiple Sclerosis. AREAS COVERED: This article reviews various studies looking at ibudilast as a potential therapy for MS. It summarizes prior and current clinical trials of ibudilast in MS as well as its pharmacology.EXPERT OPINION: Although ibudilast has not been found to decrease the focal inflammatory activity in relapsing MS, it was shown to have an effect on preserving brain volume and disability progression. Ibudilast may have a role in the treatment of progressive MS phenotypes. Adverse events with ibudilast included No gastrointestinal symptom, Headache, and Cancer patients and suicide and Cancer patients and suicide and depression.<br><b>CONCLUSIONS</b>: In a phase 2 trial involving patients with progressive Multiple Sclerosis, ibudilast was associated with slower progression of brain atrophy than placebo but was associated with higher rates of gastrointestinal side effects, Headache, and Cancer patients and suicide and Cancer patients and suicide and depression. It summarizes prior and current clinical trials of ibudilast in MS as well as its pharmacology.<br><b>EXPERT OPINION</b>: Although ibudilast has not been found to decrease the focal inflammatory activity in relapsing MS, it was shown to have an effect on preserving brain volume and disability progression.[SEP]", "label": "yes"}
{"original_question": "Does gepotidacin activate bacterial topoisomerase?", "id": "converted_23", "sentence1": "Does gepotidacin activate bacterial topoisomerase?", "sentence2": "GSK2140944 is a novel bacterial topoisomerase inhibitor in development for the treatment of Bacterial Infections.[SEP]", "label": "no"}
{"original_question": "Is durvalumab used for lung cancer treatment?", "id": "converted_24", "sentence1": "Is durvalumab used for Primary malignant neoplasm of lung treatment?", "sentence2": "In the phase III PACIFIC trial consolidation with durvalumab, an anti-PDL-1 immunoglobulin complex location, was associated with survival benefit in patients diagnosed with LA-Non-Small Cell Lung Carcinoma who responded to concurrent chemoradiotherapy. METHODS: An electronic literature search was performed of public databases (MEDLINE, Excerpta Medica dataBASE [EMBASE], and Cochrane) and conference proceedings for trials using Substance with programmed cell death protein 1 inhibitor mechanism of action (substance) (nivolumab and pembrolizumab) and CD274 wt Allele inhibitors (atezolizumab, durvalumab, and avelumab) in patients with Non-Small Cell Lung Carcinoma. Durvalumab in non-small-cell Primary malignant neoplasm of lung patients: current developments. Single-agent durvalumab showed clinical efficacy and a manageable safety profile in advanced non-small-cell Primary malignant neoplasm of lung, particularly the \u226525% CD274 wt Allele+ population. Six drugs including one CTLA-4 blocker (ipilimumab), two PD-1 blockers (nivolumab and pembrolizumab) and three CD274 wt Allele blockers (atezolizumab, avelumab and durvalumab) are approved for the treatment of different types of Malignant Neoplasms including both Solid Neoplasm such as Melanocytic neoplasm, Primary malignant neoplasm of lung, Malignant Head and Neck Neoplasm, Malignant neoplasm of urinary bladder and Merkel cell carcinoma as well as Hematologic Neoplasms such as classic Hodgkin's lymphoma.  PURPOSE OF REVIEW: The therapeutic armamentarium for advanced non-small-cell Primary malignant neoplasm of lung has evolved considerably over the past years. Immune Checkpoint Inhibitors targeting programmed cell death-1 such as pembrolizumab and nivolumab or programmed cell death ligand 1 such as atezolizumab, durvalumab and avelumab have shown favorable efficacy results in this patient population in the first-line and second-line setting. In addition, preclinical and early clinical evidence suggests that chemotherapy and radiation may work synergistically with anti-PD-1/CD274 wt Allele therapy to promote Antitumor immunity, which has led to the initiation of clinical trials testing these drugs in patients with stage III Non-Small Cell Lung Carcinoma. A preliminary report of a randomized phase III trial, the PACIFIC trial, demonstrated an impressive increase in median progression-free survival with consolidative durvalumab, a CD274 wt Allele inhibitor, compared with observation after cCRT.  ICI, such as the Substance with programmed cell death protein 1 inhibitor mechanism of action (substance) nivolumab and pembrolizumab and the CD274 wt Allele inhibitor atezolizumab, have already been marketed for the treatment of pretreated patients with advanced Non-Small Cell Lung Carcinoma. The PACIFIC trial assessing durvalumab after standard chemoradiotherapy for locally advanced Non-Small Cell Lung Carcinoma has already met its primary endpoint and the potential of durvalumab will be reinforced if phase III randomized studies of first-line (MYSTIC trial) and second or subsequent (ARCTIC trial) lines of therapy demonstrate superiority over the current standard of care.<br>[SEP]", "label": "yes"}
{"original_question": "Is  LRP1 interacting with Urokinase receptor?", "id": "converted_25", "sentence1": "Is  LRP1 interacting with Urokinase receptor?", "sentence2": "Interaction with a complex formed by urokinase and its inhibitor SERPINE1 wt Allele induces Cell surface down regulation and recycling of the receptor via the clathrin-coated pathway, a process dependent on the association to RPSA wt Allele-1. Here we investigated whether direct interaction between Urokinase Plasminogen Activator Receptor, a glycosyl-phosphatidylinositol-anchored protein, and RPSA wt Allele, a transmembrane receptor, Direct binding of domain 3 (D3) of Urokinase Plasminogen Activator Receptor to RPSA wt Allele is required for clearance of urokinase-SERPINE1 wt Allele-occupied Urokinase Plasminogen Activator Receptor[SEP]", "label": "yes"}
{"original_question": "Is obesity related to cognitive decline?", "id": "converted_26", "sentence1": "Is obesity related to Mental deterioration?", "sentence2": "The initial results suggests that obese children have higher cognitive scores and that this result is driven by those who are female, non-indigenous and live in an urban region. On the other end of the weight distribution, indigenous children who are severely Thin (qualifier value) or Thin (qualifier value) have significantly lower cognitive scores, a relationship that holds after correcting for possible bias and appears to strengthen between ages of five and eight. BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20 is associated with decreased cognitive function, reduced gray matter volume, and impaired white matter integrity in cognition-related brain areas in patients with Major Depressive Disorder. The data suggest that being overweight or obese in midlife may be more detrimental to subsequent age-related Mental deterioration than being overweight or obese at later stages of the life span Poor cognitive performance was present in 37% of the sample. General obesity (BMI>or = 25) and poor cognition were strongly associated in the presence of BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20, Abdominal. Poor cognition was negatively associated with overweight (BMI 23-25) with normal waist circumference. BMI could be used as a candidate risk marker to identify people at higher risk of Cognition Disorders, and as an intervention target for modifications of cognitive outcomes. BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20 is a common medical illness that is increasingly recognised as conferring risk of decline in cognitive performance, independent of other comorbid medical conditions. Overweight and obesity are associated with an increased risk of subnormal intellectual performance in young adult males. Subjects with low birth weight and adolescent overweight/obesity are at particular risk of subnormal performance. Impairments in cognitive function have been associated with obesity in both people and Rodent. BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20 in the pre-school years was associated with poorer outcomes for some cognitive measures in this study. Stronger relationships between obesity and cognition or educational attainment may emerge later in childhood. There is parallel evidence that people who are overweight or obese tend to perform worse on a variety of cognitive tasks While research in this area is growing, our knowledge of obesity-related cognitive dysfunction and brain alterations has not yet been synthesized. The present review integrates the recent literature regarding patterns of obesity-related cognitive dysfunction and brain alterations and also indicates potential mechanisms for these neuropathological changes. The review culminates in a preliminary model of obesity-related cognitive dysfunction and suggestions for future research, including the potential reversibility of these changes with weight-loss.<br> Evidence for the increased prevalence of Diabetes Mellitus and obesity is reviewed as it relates to Mental deterioration. These articles indicate that the age of onset of Type 1 Diabetes Mellitus may be relevant to future cognitive function and that disease duration of Type 2 Diabetes Mellitus and sociocultural factors are related to Mental deterioration during the aging process. This special issue concludes with a conceptual framework for linking obesity and Diabetes Mellitus with accelerated Mental deterioration as related to the aging process. The adverse effects of Diabetes Mellitus and obesity on cognitive functioning are increasingly well recognized. Moreover, these studies show that distressing environmental circumstances can adversely influence Impaired cognition associated with obesity and Diabetes Mellitus.[SEP]", "label": "yes"}
{"original_question": "Is cabozantinib effective for hepatocellular carcinoma?", "id": "converted_27", "sentence1": "Is cabozantinib effective for hepatocellular carcinoma?", "sentence2": "However, clinical trials of nonselective kinase inhibitors with c-Met activity (Tivantinib, cabozantinib, Foretinib, and golvatinib) in patients with altretamine/cisplatin/cyclophosphamide protocol have failed so far to demonstrate significant efficacy.  More recently, promising outcomes have also been reported with new agents, such as nivolumab and cabozantinib.  Positive results in recent phase III clinical trials have confirmed the high value of anti-angiogenic therapies for altretamine/cisplatin/cyclophosphamide protocol in both first (sorafenib and lenvatinib) and second line (regorafenib and cabozantinib) treatment modalities.  Expert opinion: Based on favorable phase III clinical trial data, sorafenib and lenvatinib are considered promising agents for altretamine/cisplatin/cyclophosphamide protocol as first-line systemic chemotherapy. Moreover, regorafenib and cabozantinib are useful second-line therapies after the failure of sorafenib. cabozantinib in Patients with Advanced and Progressing Liver carcinoma. BACKGROUND: cabozantinib inhibits Protein Tyrosine Kinase, including vascular endothelial growth factor receptors 1, 2, and 3, MET wt Allele wt Allele, and AXL protein, human protein, human, which are implicated in the progression of hepatocellular carcinoma and the development of resistance to sorafenib, the standard initial treatment for advanced disease.  Median overall survival was 10.2 months with cabozantinib and 8.0 months with placebo (hazard ratio for Cessation of life, 0.76; 95% confidence interval [CI], 0.63 to 0.92; P=0.005). Median progression-free survival was 5.2 months with cabozantinib and 1.9 months with placebo (hazard ratio for disease progression or Cessation of life, 0.44; 95% CI, 0.36 to 0.52; P<0.001), and the objective response rates were 4% and less than 1%, respectively (P=0.009). CONCLUSIONS: Among patients with previously treated Advanced Liver carcinoma, treatment with cabozantinib resulted in longer overall survival and progression-free survival than placebo.  Positive phase III-study data have been published for lenvatinib as first-line and cabozantinib as second-line therapy.  More recently, regorafenib and nivolumab have received approval in the second-line setting after sorafenib, with further positive phase 3 studies emerging in the first line (lenvatinib non-inferior to sorafenib) and second line versus placebo (cabozantinib and ramucirumab).  The rapidly changing treatment landscape due to the emergence of new treatment options (sorafenib and lenvatinib equally effective in first line; regorafenib, cabozantinib, and ramucirumab showing OS benefit in second line with nivolumab approved by the FDA based on response rate) underscores the importance of re-assessing the role of the first approved systemic agent in altretamine/cisplatin/cyclophosphamide protocol, sorafenib. Rationale for use, clinical trial data, and current recommendations for cabozantinib in Malignant neoplasm of kidney, Malignant neoplasm of thyroid, Malignant neoplasm of prostate, Malignant neoplasm of liver, and Primary malignant neoplasm of lung are detailed in this article. CONCLUSIONS: Among patients with previously treated Advanced Liver carcinoma, treatment with cabozantinib resulted in longer overall survival and progression-free survival than placebo. The most common high-grade events were Palmar-plantar erythrodysesthesia syndrome (17% with cabozantinib vs. 0% with placebo), Hypertensive disease (16% vs. 2%), increased aspartate aminotransferase level (12% vs. 7%), Fatigue (10% vs. 4%), and Diarrhea (10% vs. 2%).<br><b>CONCLUSIONS</b>: Among patients with previously treated Advanced Liver carcinoma, treatment with cabozantinib resulted in longer overall survival and progression-free survival than placebo. cabozantinib in Patients with Advanced and Progressing Liver carcinoma.Among patients with previously treated Advanced Liver carcinoma, treatment with cabozantinib resulted in longer overall survival and progression-free survival than placebo.  CONCLUSIONS Among patients with previously treated Advanced Liver carcinoma, treatment with cabozantinib resulted in longer overall survival and progression-free survival than placebo. CONCLUSIONS Among patients with previously treated Advanced Liver carcinoma, treatment with cabozantinib resulted in longer overall survival and progression-free survival than placebo. CONCLUSIONS The tyrosine kinase inhibitors sorafenib (first line) and regorafenib (second line) have been approved for hepatocellular carcinoma, and the immune checkpoint inhibitor nivolumab obtained conditional approval for sorafenib-experienced patients in the United States. The principal advancements in the treatment of hepatocellular carcinoma (altretamine/cisplatin/cyclophosphamide protocol) are the use of new systemic treatments such as lenvatinib in first-line treatment and regorafenib, cabozantinib and ramucirumab in second-line treatment due to their benefits in terms of overall survival. Recently, a few systemic chemotherapies proved to be effective for advanced stage altretamine/cisplatin/cyclophosphamide protocol in phase III studies: lenvatinib as the first line of therapy, and regorafenib, cabozantinib, and ramucirumab as second-line therapy. <b>BACKGROUND</b>: The approval of the tyrosine kinase inhibitor sorafenib in 2007 marked a milestone in the treatment of hepatocellular carcinoma, as sorafenib was the first systemic therapy to show a survival benefit in patients with Advanced Liver carcinoma. We also elaborate the unmet need of biomarkers to guide treatment decisions and discuss the emerging field of immunotherapy in hepatocellular carcinoma.<br><b>CONCLUSIONS</b>: The tyrosine kinase inhibitors sorafenib (first line) and regorafenib (second line) have been approved for hepatocellular carcinoma, and the immune checkpoint inhibitor nivolumab obtained conditional approval for sorafenib-experienced patients in the United States. cabozantinib in the treatment of hepatocellular carcinoma. The approval of the tyrosine kinase inhibitor sorafenib in 2007 marked a milestone in the treatment of hepatocellular carcinoma, as sorafenib was the first systemic therapy to show a survival benefit in patients with Advanced Liver carcinoma. Among patients with previously treated Advanced Liver carcinoma, treatment with cabozantinib resulted in longer overall survival and progression-free survival than placebo. More recently, promising outcomes have also been reported with new agents, such as nivolumab and cabozantinib.  Positive phase III-study data have been published for lenvatinib as first-line and cabozantinib as second-line therapy.[SEP]", "label": "yes"}
{"original_question": "Is Tisagenlecleucel effective for B-Cell Lymphoma?", "id": "converted_28", "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 B-cell precursor 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]", "label": "yes"}
{"original_question": "Is ADP-ribosylation a PTM?", "id": "converted_29", "sentence1": "Is ADP-ribosylation a PTM?", "sentence2": "ADP-ribosylation is a PTM, in which PARP1 gene use nicotinamide adenine dinucleotide (NAD) (NAD) (NAD+) to modify target proteins with ADP-ribose Poly-ADP-ribosylation (Poly ADP Ribosylation) is a Post-Translational Protein Processing (PTM) that is critically involved in many biological processes that are linked to cell stress responses. ADP-ribosylation is a post-translational modification (PTM) implicated in several crucial cellular processes, ranging from regulation of DNA repair and chromatin structure to cell metabolism and stress responses.[SEP]", "label": "yes"}
{"original_question": "Does epidural anesthesia for pain management during labor affect the Apgar score of the the infant?", "id": "converted_30", "sentence1": "Does epidural anesthesia for pain management during labor affect the Apgar score of the the infant?", "sentence2": "We retrospectively analyzed 93 consecutive single-pregnancy patients who underwent cesarean section with combined spinal-epidural anesthesia. The patients were divided into two groups, depending on the use of 6% Idiopathic Hypereosinophilic Syndrome 130/0.4: group A (461\u00a0\u00b1\u00a0167\u00a0ml of saline-based Idiopathic Hypereosinophilic Syndrome was administered; 43 patients) and group B (Idiopathic Hypereosinophilic Syndrome not administered; 50 patients). The major outcome was umbilical cord chloride level at delivery. The volume infused from operating room admission until delivery was not significantly different between groups. The umbilical cord chloride level at delivery was statistically significantly higher in group A than in group B, but clinically similar (108\u00a0\u00b1\u00a02 vs. 107\u00a0\u00b1\u00a02\u00a0mmol/l, P\u00a0=\u00a00.02). No differences were observed in the Apgar score or other umbilical cord laboratory data at delivery (Na+, K+, pH, base excess) CONCLUSION Subarachnoid or epidural sufentanil, in the doses used in this study, associated with local anesthetics, had the same effect on the duration of labor after analgesia and in the Apgar score of newborns. CONCLUSION Subarachnoid or epidural sufentanil, in the doses used in this study, associated with local anesthetics, had the same effect on the duration of labor after analgesia and in the Apgar score of newborns.[SEP]", "label": "no"}
{"original_question": "Is phospholipid hydroperoxide glutathione peroxidase a selenoprotein?", "id": "converted_31", "sentence1": "Is phospholipids hydroperoxide glutathione peroxidase a Selenoproteins?", "sentence2": "GLUTATHIONE PEROXIDASE (GPX1 gene) is the major Selenoproteins in most Body tissue in animal allergen extracts. The selenoenzyme GPX4 gene is essential for early embryogenesis and cell viability for its unique function to prevent phospholipids oxidation. the major Selenoproteins expressed by Germ Cells in the Testis, the phospholipids hydroperoxide glutathione peroxidase (PHGPx/GPx4)[SEP]", "label": "yes"}
{"original_question": "Is inositol effective for trichotillomania?", "id": "converted_32", "sentence1": "Is inositol effective for Trichotillomania?", "sentence2": "Patients assigned to inositol failed to show significantly greater reductions on primary or secondary outcomes measures compared with placebo (all P>0.05). This is the first study assessing the efficacy of inositol in the treatment of Trichotillomania, but found no differences in symptom reductions between inositol and placebo. At study endpoint, 42.1% of patients were 'much or very much improved' on inositol compared with 35.3% on placebo. Conclusions \u2022 The review indicates that yoga, aerobic exercise, acupuncture, biofeedback, hypnosis, and inositol and acetylcysteine all show promise in the treatment of excoriation disorder and other body-focused repetitive behaviors, such as Trichotillomania. Future studies should examine whether inositol may be beneficial in controlling pulling behavior in a subgroup of individuals with Trichotillomania.[SEP]", "label": "no"}
{"original_question": "Is TIAM1 favoring tumor progression in colorectal cancer (CRC)?", "id": "converted_33", "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 \u03b2TrCP. 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]", "label": "no"}
{"original_question": "Is pacritinib effective for treatment of myelofibrosis?", "id": "converted_34", "sentence1": "Is pacritinib effective for treatment of Primary Myelofibrosis?", "sentence2": "Pacritinib and its use in the treatment of patients with Primary Myelofibrosis who have THROMBOCYTOPENIA 2 (disorder). Pacritinib, a dual JAK2 protein, human protein, human and FLT3 gene gene PPP1R1A gene which also inhibits IRAK1 protein, human protein, human, has demonstrated the ability to favorably impact fluorouracil/methotrexate protocol-associated Splenomegaly and symptom burden, while having limited Bone Marrow Suppression with manageable Gastrointestinal:-:Point in time:^Patient:- toxicity. Other JAKis, such as fedratinib and pacritinib, proved to be useful in fluorouracil/methotrexate protocol.  Conclusions and Relevance: In patients with Primary Myelofibrosis and THROMBOCYTOPENIA 2 (disorder), including those with prior anti-Janus kinase therapy, pacritinib twice daily was more effective than Behavioral activation therapy, including ruxolitinib, for reducing Splenomegaly and symptoms. Developments of Janus kinase inhibitors, such as ruxolitinib, pacritinib, momelotinib, and febratinib enabled the effective management in fluorouracil/methotrexate protocol patients.   Pacritinib (cisplatin/cyclophosphamide/doxorubicin protocol), a multi-kinase PPP1R1A gene with specificity for JAK2 protein, human protein, human, FLT3 gene gene, and IRAK1 protein, human protein, human but sparing JAK1 protein, human protein, human, has demonstrated clinical activity in fluorouracil/methotrexate protocol with minimal Bone Marrow Suppression.  Pacritinib could be a treatment option for patients with Primary Myelofibrosis, including those with baseline cytopenias for whom options are particularly limited. Conclusions and Relevance In patients with Primary Myelofibrosis and THROMBOCYTOPENIA 2 (disorder), including those with prior anti-Janus kinase therapy, pacritinib twice daily was more effective than Behavioral activation therapy, including ruxolitinib, for reducing Splenomegaly and symptoms. Expert commentary: Pacritinib has demonstrated promising results in patients with Primary Myelofibrosis and THROMBOCYTOPENIA 2 (disorder). Pacritinib, a dual JAK2 protein, human protein, human and FLT3 gene gene PPP1R1A gene, improves disease-related symptoms and signs with manageable Gastrointestinal:-:Point in time:^Patient:- toxicity in patients with Primary Myelofibrosis with Splenomegaly and high-risk features, without causing overt Bone Marrow Suppression, and therefore may provide an important treatment option for a range of patients with Primary Myelofibrosis. Pacritinib is an active agent in patients with fluorouracil/methotrexate protocol, offering a potential treatment option for patients with preexisting Genus Anemia and THROMBOCYTOPENIA 2 (disorder). Pacritinib (cisplatin/cyclophosphamide/doxorubicin protocol), a multi-kinase PPP1R1A gene with specificity for JAK2 protein, human protein, human, FLT3 gene gene, and IRAK1 protein, human protein, human but sparing JAK1 protein, human protein, human, has demonstrated clinical activity in fluorouracil/methotrexate protocol with minimal Bone Marrow Suppression. This article examines the role of JAK2 protein, human protein, human and FLT3 gene gene signaling in Primary Myelofibrosis and provides an overview of the clinical development of pacritinib as a new therapy for Primary Myelofibrosis. Pacritinib appears to be an effective agent for the control of fluorouracil/methotrexate protocol-related symptoms and Splenomegaly with potentially fewer haematological side-effects when compared with ruxolitinib and seems a particularly promising agent for anaemic and thrombocytopenic patients.  Expert commentary: Pacritinib has demonstrated promising results in patients with Primary Myelofibrosis and THROMBOCYTOPENIA 2 (disorder).[SEP]", "label": "yes"}
{"original_question": "Can exposure to heavy metals like lead(Pb) or cadmium(Cd) cause changes in DNA methylation patterns in Isoetes sinensis?", "id": "converted_35", "sentence1": "Can exposure to heavy metals like lead(HTN3 gene) or cadmium(pyrimethamine) cause changes in DNA methylation patterns in Isoetes sinensis?", "sentence2": "DNA methylation in endangered plants after exposure to heavy metals, the Isoetes sinensis, an endangered plant, was stressed with three different concentrations of two heavy metals lead (HTN3 gene) and cadmium (pyrimethamine) The results showed that the DNA methylated profile of I. sinensis was affected by HTN3 gene and pyrimethamine stress. The proportion of DNA methylation (including hypermethylation) by both HTN3 gene and pyrimethamine stresses is nearly equal (39.04% and 39.71%), but the proportion of DNA demethylation by pyrimethamine is higher than that by HTN3 gene (46.86% than 33.92%). There was no significant difference in the amount of DNA methylation among control check (Creatine Kinase), HTN3 gene stress group, and pyrimethamine stress group (Creatine Kinase 46.96%, HTN3 gene 48.23%, and pyrimethamine 48.1%). However, full-methylation level of HTN3 gene stress group (28.34%) and pyrimethamine stress group (20.25%) was lower than control (33.91%), in contrast, hemi-methylation level HTN3 gene stress group (19.89%) and pyrimethamine stress group (27.85%) were higher than control (13.04%). Consistently, a dramatic change in DNA methylation patterns was detected in excess Cu-exposed H. verticillata. Hydrilla verticillata employs two different ways to affect DNA methylation under excess copper stress.Because of the accumulation of heavy metals, Hydrilla verticillata (L.f.) Royle, a rooted submerged perennial aquatic herb, is being developed as a potential tool to clean the aquatic ecosystem polluted by heavy metals.  The proportion of DNA methylation (including hypermethylation) by both HTN3 gene and pyrimethamine stresses is nearly equal (39.04% and 39.71%), but the proportion of DNA demethylation by pyrimethamine is higher than that by HTN3 gene (46.86% than 33.92%).<br>[SEP]", "label": "yes"}
{"original_question": "Has Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) been reported to be a plasminogen receptor in pathogenic bacteria?", "id": "converted_36", "sentence1": "Has Glyceraldehyde 3-phosphate dehydrogenase (GAPDH protein, human) been reported to be a PLG gene receptor in pathogenic bacteria?", "sentence2": "binding of PLG gene (angiostatin, human) to bacterial surfaces, as it has been shown that this interaction contributes to bacterial adhesion to host cells, invasion of host tissues, and evasion of the immune system. Several Bacterial Proteins are known to serve as receptors for angiostatin, human including glyceraldehyde-3-phosphate dehydrogenase (GAPDH protein, human protein, human), Moreover, several Protein Isoforms of the glyceraldehyde 3-phosphate dehydrogenase (GAPDH protein, human protein, human) and galectin (Galanin, human (30 aa, ~3 kDa)) were identified in both antigenic extracts as PLG gene-binding proteins. Purified GAPDH protein, human protein, human was found to bind human PLG gene and Fibrinogen containing hemostatics in Far-Western blot and ELISA-based assays. GAPDH protein, human protein, human exhibits a high affinity for plasmin and a significantly lower affinity for PLG gene. Moreover, several Protein Isoforms of the glyceraldehyde 3-phosphate dehydrogenase (GAPDH protein, human protein, human) and galectin (Galanin, human (30 aa, ~3 kDa)) were identified in both antigenic extracts as PLG gene-binding proteins.[SEP]", "label": "yes"}
{"original_question": "Can CPX-351 be used for the treatment of tuberculosis?", "id": "converted_37", "sentence1": "Can CPX-351 be used for the treatment of tuberculosis?", "sentence2": "CPX-351 is a novel liposomal formulation of cytarabine and daunorubicin which has recently been FDA approved for treatment of RUNX1 gene (Leukemia, Myelocytic, Acute).[SEP]", "label": "no"}
{"original_question": "Does lucatumumab bind to CD140?", "id": "converted_38", "sentence1": "Does lucatumumab bind to CD140?", "sentence2": "Lucatumumab is a fully humanized anti-CD40 Antigens Antigens antibody that blocks interaction of CD40 Antigens Antigens Ligand with CD40 Antigens Antigens and also mediates antibody-dependent cell-mediated cytotoxicity (ADCC).  Phase I study of the anti-CD40 Antigens Antigens humanized monoclonal antibody lucatumumab (CHIR-12.12) in relapsed Chronic Lymphocytic Leukemia. Saturation of CD40 Antigens Antigens receptor on CLL cells was uniform at all doses post-treatment but also persisted at trough time points in the 3.0 mg/kg or greater cohorts.[SEP]", "label": "no"}
{"original_question": "Does simvastatin improve outcomes of aneurysmal subarachnoid hemorrhage?", "id": "converted_39", "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\u22642, 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 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. 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 Compared to control intervention, simvastatin intervention was found to have no influence on delayed ischaemic deficit, delayed cerebral infarction, mRS\u22642, 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\u22642, 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]", "label": "no"}
{"original_question": "Is pazopanib an effective treatment of glioblastoma?", "id": "converted_40", "sentence1": "Is pazopanib an effective treatment of glioblastoma?", "sentence2": "RESULTS: The six-month progression-free survival (PFS) rates in phase II (n = 41) were 0% and 15% in the PTEN/EGFRvIII-positive and PTEN/EGFRvIII-negative cohorts, respectively, leading to early termination.  Single-agent pazopanib did not prolong PFS in this patient population but showed in situ biological activity as demonstrated by radiographic responses.[SEP]", "label": "no"}
{"original_question": "Are de novo mutations in regulatory elements responsible for neurodevelopmental disorders?", "id": "converted_41", "sentence1": "Are de novo Gene Mutation in regulatory elements responsible for Neurodevelopmental Disorders?", "sentence2": "The role of de novo Gene Mutation in regulatory elements affecting Genes associated with Developmental Disabilities, or other Genes, has been essentially unexplored. We identified de novo Gene Mutation in three classes of putative regulatory elements in almost 8,000 patients with Developmental Disabilities. Here we show that de novo Gene Mutation in highly evolutionarily conserved Prenatal care brain-active elements are significantly and specifically enriched in Neurodevelopmental Disorders. We identified a significant twofold enrichment of recurrently mutated elements. We estimate that, genome-wide, 1-3% of patients without a diagnostic coding variant carry Pathogenic Variant de novo Gene Mutation in Prenatal care brain-active regulatory elements and that only 0.15% of all possible Gene Mutation within highly conserved Prenatal care brain-active elements cause Neurodevelopmental Disorders with a dominant mechanism. We estimate that, genome-wide, 1-3% of patients without a diagnostic coding variant carry Pathogenic Variant de novo Gene Mutation in Prenatal care brain-active regulatory elements and that only 0.15% of all possible Gene Mutation within highly conserved Prenatal care brain-active elements cause Neurodevelopmental Disorders with a dominant mechanism. Here we show that de novo Gene Mutation in highly evolutionarily conserved Prenatal care brain-active elements are significantly and specifically enriched in Neurodevelopmental Disorders. We estimate that, genome-wide, 1-3% of patients without a diagnostic coding variant carry Pathogenic Variant de novo Gene Mutation in Prenatal care brain-active regulatory elements and that only 0.15% of all possible Gene Mutation within highly conserved Prenatal care brain-active elements cause Neurodevelopmental Disorders with a dominant mechanism.  Here we show that de novo Gene Mutation in highly evolutionarily conserved Prenatal care brain-active elements are significantly and specifically enriched in Neurodevelopmental Disorders.  De novo Gene Mutation in regulatory elements in Neurodevelopmental Disorders.We previously estimated that 42% of patients with severe Developmental Disabilities carry Pathogenic Variant de novo Gene Mutation in coding sequences.[SEP]", "label": "yes"}
{"original_question": "Are phagosomal proteins ubiquitinated?", "id": "converted_42", "sentence1": "Are phagosomal proteins ubiquitinated?", "sentence2": "Phagosomal proteins are ubiquitylated, and ubiquitylation was found to be required for formation of acidic multivesicular structures. membranes of the bacterial phagosome are enriched with Ubiquitinated Proteins in a way that requires its Dot/Icm type IV secretion system, suggesting the involvement of effectors in the manipulation of the host ubiquitination machinery.[SEP]", "label": "yes"}
{"original_question": "Does tremelimumab improve survival of mesothelioma patients?", "id": "converted_43", "sentence1": "Does tremelimumab improve survival of Malignant mesothelioma patients?", "sentence2": "BACKGROUND: Tremelimumab, an anti-CTLA4 monoclonal antibody, initially showed good activity when used alone in patients with Malignant Malignant 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 Malignant Malignant 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\u00b77 months (95% CI 6\u00b78-8\u00b79) in the tremelimumab group and 7\u00b73 months (5\u00b79-8\u00b77) in the placebo group (hazard ratio 0\u00b792 [95% CI 0\u00b776-1\u00b712], p=0\u00b741).  INTERPRETATION: Tremelimumab did not significantly prolong overall survival compared with placebo in patients with previously treated malignant Malignant Malignant mesothelioma. BACKGROUND Tremelimumab, an anti-CTLA4 monoclonal antibody, initially showed good activity when used alone in patients with Malignant Malignant 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 Malignant Malignant mesothelioma. Median overall survival in the intention-to-treat population did not differ between the treatment groups: 7\u00b77 months (95% CI 6\u00b78-8\u00b79) in the tremelimumab group and 7\u00b73 months (5\u00b79-8\u00b77) in the placebo group (hazard ratio 0\u00b792 [95% CI 0\u00b776-1\u00b712], p=0\u00b741). BACKGROUND Tremelimumab, an anti-CTLA4 monoclonal antibody, initially showed good activity when used alone in patients with Malignant Malignant 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 Malignant Malignant mesothelioma. Median overall survival in the intention-to-treat population did not differ between the treatment groups: 7\u00b77 months (95% CI 6\u00b78-8\u00b79) in the tremelimumab group and 7\u00b73 months (5\u00b79-8\u00b77) in the placebo group (hazard ratio 0\u00b792 [95% CI 0\u00b776-1\u00b712], p=0\u00b741).  <b>BACKGROUND</b>: Tremelimumab, an anti-CTLA4 monoclonal antibody, initially showed good activity when used alone in patients with Malignant Malignant 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]", "label": "no"}
{"original_question": "Can enasidenib be used for the treatment of acute myeloid leukemia?", "id": "converted_44", "sentence1": "Can enasidenib be used for the treatment of acute myeloid leukemia?", "sentence2": "In August 2017, the United States Federal Drug Administration (FDA) approved enasidenib (Idhifa, Celgene/Agios) for adults with relapsed and refractory acute myelogenous leukemia (Leukemia, Myelocytic, Acute) with an IDH2 gene gene mutation.[SEP]", "label": "yes"}
{"original_question": "Is collagen the most abundant human protein?", "id": "converted_45", "sentence1": "Is collagen the most abundant human Protein Info?", "sentence2": "As the most abundant Protein Info in the body, collagen is essential to maintain the normal structure and strength of Connective Tissue, such as XXX bone, Skin Specimen Source Code, Cartilage, and blood vessels. Collagen is the most abundant Protein Info family in Mammals. Collagen is a fibrillar Protein Info that conforms the conjunctive and connective tissues in the Human body structure, essentially Skin Specimen Source Code, joints, and XXX bone. This Molecule is one of the most abundant in many of the living organisms due to its connective role in biological structures.[SEP]", "label": "yes"}
{"original_question": "Is the enzyme ERAP2 associated with the disease birdshot chorioretinopathy?", "id": "converted_46", "sentence1": "Is the Enzyme [APC] ERAP2 gene associated with the Disease birdshot chorioretinopathy?", "sentence2": "Allele-specific Alterations in the Peptidome Underlie the Joint Association of HLA-A*29:02 and Endoplasmic Reticulum Aminopeptidase 2 (ERAP2 gene gene) with Birdshot Chorioretinopathy. Birdshot Chorioretinopathy is also associated with ERAP1 gene (ERAP2 gene gene), an Enzyme [APC] involved in processing HLA class I ligands, thus implicating the A*29:02 peptidome in this Disease.  A genome-wide association study identifies a functional ERAP2 gene gene haplotype associated with birdshot chorioretinopathy.[SEP]", "label": "yes"}
{"original_question": "Does Panitumumab prolong survival of biliary tract cancer patients?", "id": "converted_47", "sentence1": "Does panitumumab prolong survival of biliary tract cancer patients?", "sentence2": "panitumumab in combination with gemcitabine and oxaliplatin does not prolong survival in wild-type Human Oncogene K-Ras advanced biliary tract cancer: A randomized phase 2 trial (Vecti-BIL study). CONCLUSIONS: panitumumab in combination with chemotherapy does not improve ORR, PFS and OS in patients with Human Oncogene K-Ras wild-type, advanced Biliary Tract Cancer.  No survival differences were observed: the median overall survival was 9.9 months in arm A and 10.2 months in arm B (P\u2009=\u2009.42). In a subgroup analysis, no differences in PFS according to the site of the primary tumor were observed; patients with Primary cholangiocarcinoma of intrahepatic biliary tract treated with panitumumab may have had a survival benefit in comparison with the control group (15.1 vs 11.8 months, P\u2009=\u2009.13).  CONCLUSIONS panitumumab in combination with chemotherapy does not improve ORR, PFS and OS in patients with Human Oncogene K-Ras wild-type, advanced Biliary Tract Cancer. CONCLUSIONS panitumumab in combination with chemotherapy does not improve ORR, PFS and OS in patients with Human Oncogene K-Ras wild-type, advanced Biliary Tract Cancer. Despite many clinical trials being conducted with molecular targeted agents including erlotinib, cetuximab, panitumumab, bevacizumab, sorafenib, cediranib, trametinib and vandetanib, no agent has shown to be effective for advanced biliary tract cancer. Adding panitumumab to standard protocols does not prolong survival but provokes additional adverse effects.[SEP]", "label": "no"}
{"original_question": "Is lucatumumab a polyclonal antibody?", "id": "converted_48", "sentence1": "Is lucatumumab a polyclonal antibody?", "sentence2": "A phase 1 study of lucatumumab, a fully Homo sapiens anti-CD40 antagonist monoclonal antibody administered intravenously to patients with relapsed or refractory multiple myeloma. In this open-label, multicentre, phase 1 study a fully Homo sapiens anti-CD40 antagonist monoclonal antibody, lucatumumab, was evaluated in patients with relapsed/refractory multiple myeloma (Millimole per Liter).[SEP]", "label": "no"}
{"original_question": "Is lithium effective for treatment of amyotrophic lateral sclerosis?", "id": "converted_49", "sentence1": "Is lithium effective for treatment of amyotrophic lateral sclerosis?", "sentence2": "In terms of Disease-modifying treatment options, several drugs such as Dexpramipexole, pioglitazone, lithium, and many others have been tested in large multicenter trials, albeit with disappointing results. Despite several positive case reports and short studies, further controlled researches have failed to substantiate any positive effects of lithium exposure in amyotrophic lateral sclerosis.  The effect of lithium was different for UNC13A carriers (p = 0.027), but not for C9orf72 carriers (p = 0.22). The 12-month survival probability for UNC13A carriers treated with Lithium antipsychotics Carbonate - Consent Type improved from 40.1% (95% CI 23.2-69.1) to 69.7% (95% CI 50.4-96.3). Studies in Amyotrophic Lateral Sclerosis showed consistently negative results and presented evidence against the use of lithium for the treatment of this Disease. BACKGROUND Lithium antipsychotics antipsychotics has neuroprotective effects in \"U\" lymphocyte and animal models of amyotrophic lateral sclerosis (Amyotrophic Lateral Sclerosis), and a small pilot study in patients with Amyotrophic Lateral Sclerosis showed a significant effect of lithium on survival. In a pilot clinical study that we recently published we found that lithium administration slows the progression of Amyotrophic Lateral Sclerosis (Amyotrophic Lateral Sclerosis) in Homo sapiens patients. BACKGROUND Lithium antipsychotics antipsychotics has neuroprotective effects in \"U\" lymphocyte and animal models of amyotrophic lateral sclerosis (Amyotrophic Lateral Sclerosis), and a small pilot study in patients with Amyotrophic Lateral Sclerosis showed a significant effect of lithium on survival. BACKGROUND A neuroprotective effect of lithium in amyotrophic lateral sclerosis (Amyotrophic Lateral Sclerosis) has been recently reported. Lithium antipsychotics antipsychotics delays progression of amyotrophic lateral sclerosis.Amyotrophic Lateral Sclerosis is a devastating Neurodegenerative Disorders with no effective treatment.  Lithium antipsychotics antipsychotics in patients with amyotrophic lateral sclerosis (LiCALS): a phase 3 multicentre, randomised, double-blind, placebo-controlled trial.<AbstractText Label=\"BACKGROUND\" NlmCategory=\"BACKGROUND\">Lithium antipsychotics antipsychotics has neuroprotective effects in \"U\" lymphocyte and animal models of amyotrophic lateral sclerosis (Amyotrophic Lateral Sclerosis), and a small pilot study in patients with Amyotrophic Lateral Sclerosis showed a significant effect of lithium on survival.  <b>INTRODUCTION</b>: Lithium antipsychotics antipsychotics was proposed in 2008 as an effective candidate in the treatment of Amyotrophic Lateral Sclerosis after a report claimed that it was able to delay functional deterioration by 40% and that none of the 16 patients treated with a combination of lithium plus riluzole had died during a 15-month follow-up period. A recently published study also ruled out any possible modest effect.<br><b>CONCLUSIONS</b>: There is evidence to suggest that lithium has no short-term benefits in Amyotrophic Lateral Sclerosis. A comparison of the group of patients treated with lithium+riluzole and the control group treated with riluzole alone showed no statistically significant differences in rates of functional decline, deterioration of respiratory function, or survival time. None of the patients treated with lithium died during the 15 months of the follow-up, and Disease progression was markedly attenuated when compared with age-, Disease duration-, and sex-matched control patients treated with riluzole for the same amount of time.[SEP]", "label": "no"}
{"original_question": "Should dacomitinib be used for treatment of glioblastoma patients?", "id": "converted_50", "sentence1": "Should dacomitinib be used for treatment of glioblastoma patients?", "sentence2": "Expert opinion: Despite the poor global results of dacomitinib in recurrent GB shown in a phase II trial, some patients had a significant benefit.  Conclusions: dacomitinib has a limited single-agent activity in recurrent GB with EGFR amplification. Expert opinion: Despite the poor global results of dacomitinib in recurrent GB shown in a phase II trial, some patients had a significant benefit. Expert opinion: Despite the poor global results of dacomitinib in recurrent GB shown in a phase II trial, some patients had a significant benefit.[SEP]", "label": "no"}
{"original_question": "Are there ultraconserved regions in the budding yeast (Saccharomyces cerevisiae)?", "id": "converted_51", "sentence1": "Are there ultraconserved regions in the Cell budding yeast (Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae)?", "sentence2": "The systematic analysis of ultraconserved genomic regions in the Cell Cell budding yeast. In the evolution of species, a kind of special DNA Sequence, termed ultraconserved DNA Sequence (UCSs), have been inherited without any change, which strongly suggests those DNA Sequence should be crucial for the species to survive or adapt to the environment. However, the UCSs are still regarded as mysterious genetic DNA Sequence so far. Here, we present a systematic study of ultraconserved genomic regions in the Cell Cell budding yeast based on the publicly available genome DNA Sequence, in order to reveal their relationship with the adaptability or fitness advantages of the Cell Cell budding yeast.Results: Our results indicate that, in addition to some fundamental biological functions, the UCSs play an important role in the adaptation of Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae to the acidic environment, which is backed up by the previous observation. Besides that, we also find the highly unchanged genes are enriched in some other pathways, such as the nutrient-sensitive signaling pathway. To facilitate the investigation of unique UCSs, the UCSC Genome - anatomical entity - anatomical entity Browser was utilized to visualize the chromosomal position and related annotations of UCSs in S.cerevisiae genome. Here, we present a systematic study of ultraconserved genomic regions in the Cell Cell budding yeast based on the publicly available genome DNA Sequence, in order to reveal their relationship with the adaptability or fitness advantages of the Cell Cell budding yeast. Motivation In the evolution of species, a kind of special DNA Sequence, termed ultraconserved DNA Sequence (UCSs), have been inherited without any change, which strongly suggests those DNA Sequence should be crucial for the species to survive or adapt to the environment. The systematic analysis of ultraconserved genomic regions in the Cell Cell budding yeast.<AbstractText Label=\"Motivation\">In the evolution of species, a kind of special DNA Sequence, termed ultraconserved DNA Sequence (UCSs), have been inherited without any change, which strongly suggests those DNA Sequence should be crucial for the species to survive or adapt to the environment.  Here, we present a systematic study of ultraconserved genomic regions in the Cell Cell budding yeast based on the publicly available genome DNA Sequence, in order to reveal their relationship with the adaptability or fitness advantages of the Cell Cell budding yeast.  Here, we present a systematic study of ultraconserved genomic regions in the Cell Cell budding yeast based on the publicly available genome DNA Sequence, in order to reveal their relationship with the adaptability or fitness advantages of the Cell Cell budding yeast.<br><b>Results</b>: Our results indicate that, in addition to some fundamental biological functions, the UCSs play an important role in the adaptation of Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae to the acidic environment, which is backed up by the previous observation.[SEP]", "label": "yes"}
{"original_question": "Is there any role for HUWE1 in MYC signalling?", "id": "converted_52", "sentence1": "Is there any role for HUWE1 in MYC protein, human signalling?", "sentence2": "HUWE1 is a critical colonic Tumor Suppressor Genes that prevents MYC protein, human protein, human signalling, DNA damage accumulation and tumour initiation. To determine the importance of HUWE1, we chose to examine its function in Malignant neoplasm of colon and/or rectum, where it is Mutation Abnormality in up to 15 per cent of Neoplasms. Modelling of identified Gene Mutation showed that they inactivate the E3 ubiquitin ligase activity of HUWE1. Genetic Gene Deletion Abnormality of HUWE1 protein, human rapidly accelerated tumourigenic in CASP14 gene carrying loss of the intestinal Tumor Suppressor Genes Apc, with a dramatic increase in tumour initiation. Mechanistically, this phenotype was driven by increased MYC protein, human protein, human and rapid DNA damage accumulation leading to loss of the second copy of Apc The increased levels of DNA damage sensitised HUWE1 protein, human-deficient Neoplasms to DNA-damaging agents and to Gene Deletion Abnormality of the anti-apoptotic protein MCL1. Taken together, these data identify HUWE1 as a bona fide Tumor Suppressor Genes in the Structure of Structure of intestinal epithelium and suggest a potential vulnerability of HUWE1-Mutation Abnormality Neoplasms to DNA-damaging agents and inhibitors of Apoptosis Inhibiting Proteins.[SEP]", "label": "yes"}
{"original_question": "Do raspberries improve postprandial glucose and acute and chronic inflammation in adults with type 2 Diabetes?", "id": "converted_53", "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]", "label": "yes"}
{"original_question": "Are Mesenchymal stem cells (MSC) multipotent cells?", "id": "converted_54", "sentence1": "Are Mesenchymal stem cells (MSC) multipotent cells?", "sentence2": "multipotent mesenchymal bone marrow-derived stem cells multipotent hESC-derived mesenchymal cells (MILES-CARPENTER X-LINKED INTELLECTUAL DEVELOPMENTAL DISORDER)[SEP]", "label": "yes"}
{"original_question": "Is there a deep-learning algorithm for protein solubility prediction?", "id": "converted_55", "sentence1": "Is there a deep-learning algorithm for Protein Info solubility prediction?", "sentence2": "DeepSol: a deep learning framework for Sequence - ParameterizedDataType-based Protein Info solubility prediction. Protein solubility plays a vital role in pharmaceutical research and production yield. For a given Protein Info, the extent of its solubility can represent the quality of its function, and is ultimately defined by its Sequence - ParameterizedDataType. Thus, it is imperative to develop novel, highly accurate in silico Sequence - ParameterizedDataType-based Protein Info solubility predictors. In this work we propose, DeepSol, a novel Deep Learning-based Protein Info solubility predictor. The backbone of our framework is a convolutional neural network that exploits k-mer structure and additional Sequence - ParameterizedDataType and structural features extracted from the Protein Info Sequence - ParameterizedDataType. DeepSol: a deep learning framework for Sequence - ParameterizedDataType-based Protein Info solubility prediction.<AbstractText Label=\"Motivation\" NlmCategory=\"UNASSIGNED\">Protein solubility plays a vital role in pharmaceutical research and production yield.[SEP]", "label": "yes"}
{"original_question": "Have machine learning methods been used to predict the severity of major depressive disorder(MDD)?", "id": "converted_56", "sentence1": "Have machine learning methods been used to predict the severity of major depressive disorder(Major Depressive Disorder)?", "sentence2": "Here, we conduct a meta-review to identify predictors of response to Antidepressive Agents therapy in order to select robust input features for machine learning models of treatment response.  machine learning framework involving EEG-based functional connectivity to diagnose major depressive disorder (Major Depressive Disorder). Identification of risk factors of treatment resistance may be useful to guide treatment selection, avoid inefficient trial-and-error, and improve major depressive disorder (Major Depressive Disorder) care. We extended the work in predictive modeling of treatment resistant depression (T-Cell Receptors delta-Chain) via partition of the data from the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) cohort into a training and a testing dataset. persistence and severity of major depressive disorder from baseline self-reports  These results confirm that clinically useful Major Depressive Disorder risk-stratification models can be generated from baseline patient self-reports and that ML methods improve on conventional methods in developing such models Furthermore, machine learning weighting factors may reflect an objective biomarker of major depressive disorder illness severity, based on abnormalities of Head>Brain structure. Notably, while the only information provided for training the classifiers was T(1)-weighted scans plus a categorical label (major depressive disorder versus controls), both relevance vector machine and support vector machine 'weighting factors' (used for making predictions) correlated strongly with subjective ratings of illness severity. BACKGROUND Although variation in the long-term course of major depressive disorder (Major Depressive Disorder) is not strongly predicted by existing symptom subtype distinctions, recent research suggests that prediction can be improved by using machine learning methods. BACKGROUND Although variation in the long-term course of major depressive disorder (Major Depressive Disorder) is not strongly predicted by existing symptom subtype distinctions, recent research suggests that prediction can be improved by using machine learning methods. BACKGROUND Growing evidence documents the potential of machine learning for developing Head>Brain based diagnostic methods for major depressive disorder (Major Depressive Disorder). OBJECTIVE We aimed to integrate neural data and an advanced machine learning technique to predict individual major depressive disorder (Major Depressive Disorder) patient severity. Furthermore, machine learning weighting factors may reflect an objective biomarker of major depressive disorder illness severity, based on abnormalities of Head>Brain structure. <b>BACKGROUND</b>: Although variation in the long-term course of major depressive disorder (Major Depressive Disorder) is not strongly predicted by existing symptom subtype distinctions, recent research suggests that prediction can be improved by using machine learning methods.[SEP]", "label": "yes"}
{"original_question": "Can midostaurin inhibit angiogenesis?", "id": "converted_57", "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]", "label": "yes"}
{"original_question": "Does Groucho related gene 5 (GRG5) have a role only in late development?", "id": "converted_58", "sentence1": "Does Groucho related gene 5 (TLE5 gene) have a role only in late development?", "sentence2": "Groucho related gene 5 (TLE5 gene) is a HSD17B4 gene that has been implicated in late Embryo and postnatal Mus sp. development. Here, we describe a previously unknown role of TLE5 gene in early developmental stages by analyzing its function in stem cell fate decisions. By both loss and gain of function approaches we demonstrate that ablation of TLE5 gene deregulates the Embryonic Stem Cells (ESTERASE C) pluripotent state whereas its overexpression leads to enhanced self-renewal and acquisition of Primary malignant neoplasm cell-like properties. The malignant characteristics of Teratoma generated by Enhanced S-Cone Syndrome that overexpress TLE5 gene reveal its pro-oncogenic potential. Here, we describe a previously unknown role of TLE5 gene in early developmental stages by analyzing its function in stem cell fate decisions. Groucho related gene 5 (TLE5 gene) is involved in Embryo and neural stem cell state decisions.Groucho related gene 5 (TLE5 gene) is a HSD17B4 gene that has been implicated in late Embryo and postnatal Mus sp. development.[SEP]", "label": "no"}
{"original_question": "Are there tools for reviewing variant calls?", "id": "converted_59", "sentence1": "Are there tools for reviewing variant calls?", "sentence2": "VIPER: a web application for rapid expert review of variant calls. With the rapid development in next-generation sequencing, cost and time requirements for genomic sequencing are decreasing, enabling applications in many areas such as cancer research. Many tools have been developed to analyze genomic variation ranging from single nucleotide Variant to whole chromosomal aberrations. As sequencing throughput increases, the number of Variant called by such tools also grows. Often employed manual inspection of such calls is thus becoming a time-consuming procedure. We developed the Variant InsPector and Expert Rating tool (VIPER) to speed up this process by integrating the Integrative Genomics Viewer into a web application. analysts can then quickly iterate through Variant, apply filters and make decisions based on the generated images and variant metadata. VIPER was successfully employed in analyses with manual inspection of more than 10 000 calls.Availability and implementation: VIPER is implemented in Java and Javascript and is freely available at https://github.com/MarWoes/viper. Variant Review with the Integrative Genomics Viewer. VIPER: a web application for rapid expert review of variant calls.Supplementary data are available at Bioinformatics online. We developed the Variant InsPector and Expert Rating tool (VIPER) to speed up this process by integrating the Integrative Genomics Viewer into a web application.[SEP]", "label": "yes"}
{"original_question": "Has ivosidenib been FDA approved for use against acute myeloid leukemia?", "id": "converted_60", "sentence1": "Has ivosidenib been FDA approved for use against acute myeloid leukemia?", "sentence2": "The FDA approved ivosidenib for patients with IDH1-mutant relapsed/refractory acute myeloid leukemia.[SEP]", "label": "yes"}
{"original_question": "Are Copy Number Variants (CNVs) depleted in regions of low mappability?", "id": "converted_61", "sentence1": "Are Copy Number Variants (CNVs) depleted in regions of low mappability?", "sentence2": "Homo sapiens copy number Variant are enriched in regions of low mappability. Applying PopSV to 640 human genomes, we find that low-mappability regions are approximately 5\u00a0times more likely to harbor germline CNVs, in stark contrast to the nearly uniform distribution observed for somatic CNVs in 95 cancer genomes. In addition to known enrichments in segmental duplication and near centromeres and telomere, we also report that CNVs are enriched in specific types of satellite and in some of the most recent families of DNA Transposable Elements. Finally, using this comprehensive approach, we identify 3455 regions with recurrent CNVs that were missing from existing catalogs. In particular, we identify 347 Genes with a novel exonic CNV in low-mappability regions, including 29 Genes previously associated with Disease. Homo sapiens copy number Variant are enriched in regions of low mappability.Copy number Variant (CNVs) are known to affect a large portion of the human genome and have been implicated in many diseases.[SEP]", "label": "no"}
{"original_question": "Is Adar3 involved in learning and memory?", "id": "converted_62", "sentence1": "Is Adar3 involved in learning and memory?", "sentence2": "Adar3 Is Involved in Learning and Memory in CASP14 gene.  The newest member of the A-I editing family of ADAR proteins, the vertebrate-specific ADARB2 gene, is highly expressed in the Head>Brain, but its functional significance is unknown. In vitro studies have suggested that ADARB2 gene acts as a negative regulator of A-I RNA editing but the scope and underlying mechanisms are also unknown. Meta-analysis of published data indicates that mouse Adar3 expression is highest in the hippocampus, thalamus, Amygdaloid structure, and olfactory region. Consistent with this, we show that mice lacking exon 3 of Adar3 (which encodes two Double-Stranded RNA Binding Motif) have increased levels of Anxiety Disorders and deficits in hippocampus-dependent short- and long-term memory formation. RNA sequencing revealed a dysregulation of genes involved in synaptic function in the hippocampi of Adar3-deficient mice. We also show that ADARB2 gene transiently translocates from the Cytoplasm to the Cell Nucleus upon KCl-mediated activation in SH-SY5Y cells. These results indicate that ADARB2 gene contributes to cognitive processes in Mammals. Adar3 Is Involved in Learning and Memory in CASP14 gene.-deficient mice.[SEP]", "label": "yes"}
{"original_question": "There is no drug available to prevent HIV infection, Pre-exposure prophylaxis (PrEP), yes or no?", "id": "converted_63", "sentence1": "There is no drug available to prevent Human immunodeficiency virus II infection, Pre-exposure prophylaxis (HIV: PrEP and PEP), yes or no?", "sentence2": "pre-exposure prophylaxis with generic tenofovir disoproxil fumarate/emtrictabine in London - analysis of pharmacokinetics, safety and outcomes. The antiviral agent tenofovir is highly effective for the treatment of HIV and hepatitis B virus infections, and the older prodrug tenofovir disoproxil fumarate (tenofovir disoproxil fumarate) is also a component of daily preexposure prophylaxis (HIV: HIV: PrEP and PEP and PEP) to reduce the risk of Human immunodeficiency virus II infection in high-risk populations.  Following US Food and Drugs Administration approval in July 2012 of daily oral tenofovir and emtricitabine for pre-exposure prophylaxis (HIV: HIV: PrEP and PEP and PEP) to prevent Human immunodeficiency virus II infection in high-risk individuals in the USA, there has been much controversy about the implementation of this HIV: HIV: PrEP and PEP and PEP regimen in other countries throughout the world, and in Europe in particular. Daily oral pre-exposure prophylaxis (HIV: HIV: PrEP and PEP and PEP) is the use of antiretroviral drugs by HIV-negative people to prevent Human immunodeficiency virus II infection. HIV pre-exposure prophylaxis (HIV: HIV: PrEP and PEP and PEP) is a new approach that involves the ongoing use of antiretroviral medications by HIV-negative individuals to reduce the risk of Human immunodeficiency virus II infection. CONCLUSIONS Combined ART + HIV: HIV: PrEP and PEP and PEP is likely to prevent more HIV Infections than either strategy alone, but with higher prevalence of drug resistance. INTRODUCTION Use of pre-exposure prophylaxis (HIV: HIV: PrEP and PEP and PEP) among people who inject drugs (PWID) has been shown to be effective in preventing HIV transmission. Pre-exposure prophylaxis (HIV: HIV: PrEP and PEP and PEP) is an experimental approach to HIV prevention and consists of antiretroviral drugs to be taken before potential HIV exposure in order to reduce the risk of Human immunodeficiency virus II infection and continued during periods of risk. HIV pre-exposure prophylaxis (HIV: HIV: PrEP and PEP and PEP) is the use of one or more antiretroviral medications (in combination) to prevent Human immunodeficiency virus II infection. The most commonly used HIV: HIV: PrEP and PEP and PEP medication (Truvada<br> The use of antiretrovirals as pre-exposure prophylaxis (HIV: HIV: PrEP and PEP and PEP) is highly efficacious in HIV prevention.[SEP]", "label": "no"}
{"original_question": "Does allele phasing improve the phylogenetic utility of ultraconserved elements?", "id": "converted_64", "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 organisms.[SEP]", "label": "yes"}
{"original_question": "Have yeast prions become important models for the study of the basic mechanisms underlying human amyloid diseases?", "id": "converted_65", "sentence1": "Have Saccharomyces cerevisiae Prions become important models for the study of the basic mechanisms underlying human Serum amyloid A protein diseases?", "sentence2": "Endogenous Saccharomyces cerevisiae amyloids that control heritable traits and are frequently used as models for human Serum Serum amyloid A protein A protein diseases are termed Saccharomyces cerevisiae Prions Fibrous cross-\u03b2 aggregates (amyloids) and their transmissible forms (Prions) cause diseases in Mammals (including Homo sapiens) and control heritable traits in Saccharomyces cerevisiae.  These infectious Saccharomyces cerevisiae amyloidoses are outstanding models for the many common human Serum Serum amyloid A protein A protein-based diseases that are increasingly found to have some infectious characteristics. Yeast Prions (infectious proteins) were discovered by their outr\u00e9 genetic properties and have become important models for an array of human prion and Serum Serum amyloid A protein A protein diseases. Yeast Prions are models for both rare mammalian Prion Diseases and for several very common amyloidoses such as ALZHEIMER DISEASE, FAMILIAL, 1, Diabetes Mellitus, Non-Insulin-Dependent, and Parkinson Disease.  Yeast Prions are important models for human Serum Serum amyloid A protein A protein diseases in general, particularly because new evidence is showing infectious aspects of several human amyloidoses not previously classified as Prions.  Mechanism of Serum Serum amyloid A protein A protein formation is critical for a complete understanding of the Saccharomyces cerevisiae prion phenomenon and human Serum Serum amyloid A protein A protein-related diseases.  Yeast Prions are important models for human Serum Serum amyloid A protein A protein diseases in general, particularly because new evidence is showing infectious aspects of several human amyloidoses not previously classified as Prions. Endogenous Saccharomyces cerevisiae amyloids that control heritable traits and are frequently used as models for human Serum Serum amyloid A protein A protein diseases are termed Saccharomyces cerevisiae Prions. Mechanism of Serum Serum amyloid A protein A protein formation is critical for a complete understanding of the Saccharomyces cerevisiae prion phenomenon and human Serum Serum amyloid A protein A protein-related diseases. Here we summarize the results of studies of Prions of the Saccharomyces cerevisiae Saccharomyces cerevisiae and of the use of Saccharomyces cerevisiae model for investigation of some human amyloidoses, such as Prion Diseases, Alzheimer's, Parkinson's, and Huntington Disease. Yeast Prions increasingly are serving as models for the understanding and treatment of many mammalian amyloidoses. Yeast Prions, based on self-seeded highly ordered Fibrous aggregates (amyloids), serve as a model for human Serum Serum amyloid A protein A protein diseases. These infectious Saccharomyces cerevisiae amyloidoses are outstanding models for the many common human Serum Serum amyloid A protein A protein-based diseases that are increasingly found to have some infectious characteristics.<br> The Saccharomyces cerevisiae system has provided considerable insight into the biology of Serum Serum amyloid A protein A protein and Prions. Yeast Prions are important models for human Serum Serum amyloid A protein A protein diseases in general, particularly because new evidence is showing infectious aspects of several human amyloidoses not previously classified as Prions. We also review studies of the roles of chaperones, aggregate-collecting proteins, and other cellular components using Saccharomyces cerevisiae that have led the way in improving the understanding of similar processes that must be operating in many human amyloidoses.[SEP]", "label": "yes"}
{"original_question": "Is dupilumab effective for treatment of asthma?", "id": "converted_66", "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 Recombinant Interleukin-4 receptor \u03b1 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 \u03b22-agonists. CONCLUSIONS: Dupilumab 300\u00a0mg q2w significantly improved AR-associated nasal symptoms in patients with uncontrolled persistent Asthma and comorbid PAR. 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\u00a0III development across the world for the treatment of Asthma and Nasal Polyps as well as for Dermatitis, Atopic in paediatric patients. BACKGROUND Dupilumab (an anti-interleukin-4-receptor-\u03b1 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]", "label": "yes"}
{"original_question": "Does Eucommia ulmoides leaf extract ameliorates steatosis/fatty liver induced by high-fat diet?", "id": "converted_67", "sentence1": "Does Eucommia ulmoides Concept Generality - Leaf extract ameliorates steatosis/fatty liver induced by high-fat diet?", "sentence2": "These results demonstrate that the Du-zhong 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 Du-zhong (Eucommia ulmoides Oliver) Concept Generality - Leaf extract mediates hypolipidemic action in hamsters fed a high-fat diet.This study examined the effect of a Du-zhong (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 Du-zhong Concept Generality - Leaf extract supplement in high fat-fed hamsters. These results demonstrate that the Du-zhong 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 Du-zhong 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 Du-zhong Concept Generality - Leaf extract supplement in high fat-fed hamsters.[SEP]", "label": "yes"}
{"original_question": "Is verubecestat effective for Alzheimer\u2019s Disease?", "id": "converted_68", "sentence1": "Is verubecestat effective for Alzheimer\u2019s Disease?", "sentence2": "The lack of efficacy of verubecestat in mild-to-moderate cytarabine/daunorubicin protocol raises important questions about the timing of intervention with BACE-1 inhibitors, and anti-amyloid therapies in general, in cytarabine/daunorubicin protocol treatment. This reaction was applied to the preparation of verubecestat, which is currently undergoing clinical evaluation for the treatment of ALZHEIMER DISEASE, FAMILIAL, 1. Verubecestat is an PPP1R1A gene of \u03b2-site amyloid precursor protein cleaving enzyme 1 (BACE1 protein, human protein, human) being evaluated in clinical trials for the treatment of ALZHEIMER DISEASE, FAMILIAL, 1.  CONCLUSIONS: Verubecestat did not reduce cognitive or functional decline in patients with mild-to-moderate ALZHEIMER DISEASE, FAMILIAL, 1 and was associated with treatment-related adverse events.  Randomized Trial of Verubecestat for Mild-to-Moderate Alzheimer's Disease.Verubecestat did not reduce cognitive or functional decline in patients with mild-to-moderate ALZHEIMER DISEASE, FAMILIAL, 1 and was associated with treatment-related adverse events.  CONCLUSIONS Verubecestat did not reduce cognitive or functional decline in patients with mild-to-moderate ALZHEIMER DISEASE, FAMILIAL, 1 and was associated with treatment-related adverse events. Verubecestat did not reduce cognitive or functional decline in patients with mild-to-moderate ALZHEIMER DISEASE, FAMILIAL, 1 and was associated with treatment-related adverse events.[SEP]", "label": "no"}
{"original_question": "Is galcanezumab effective for treatment of migraine?", "id": "converted_69", "sentence1": "Is galcanezumab effective for treatment of Migraine Disorders?", "sentence2": "Importance: Galcanezumab (LY2951742), a Monoclonal Antibody [EPC] against CALCA gene (Calcitonin Gene-Related Peptide), is one of a novel class of new medicines for Migraine Disorders prevention. Conclusions and Relevance: Monthly subcutaneous injections of galcanezumab, both 120 mg and 300 mg, demonstrated efficacy (repeated-measures analysis) for the preventive treatment of Migraine Disorders and support further development in larger phase 3 studies.  PURPOSE OF REVIEW: Monoclonal Antibodies (mAbs) targeting the calcitonin-gene-related peptide (Calcitonin Gene-Related Peptide) pathway have been developed for episodic and chronic Migraine Disorders prevention, either through binding the Calcitonin Gene-Related Peptide ligand (eptinezumab, fremanezumab, galcanezumab) or the Calcitonin-Gene Related Peptide Receptor (erenumab). Background Safety findings from a Phase 2b study of galcanezumab, a Antibodies, Monoclonal, Humanized against CALCA gene, for prevention of Migraine Disorders (NCT02163993) are reported here. Safety of galcanezumab in patients with episodic Migraine Disorders: A randomized placebo-controlled dose-ranging Phase 2b study. Currently, there is considerable excitement regarding monoclonal antibodies against CALCA gene (eptinezumab, galcanezumab, fremanezumab) and the CALCA gene receptor (erenumab). To date, these monoclonal antibodies have shown promising efficacy in clinical trials, with no major safety concerns. If ongoing long-term studies show that their efficacy can be maintained, this may herald a new era for effective antimigraine therapies. Calcitonin-Gene Related Peptide Receptor antagonists such as ubrogepant are effective for acute relief of Migraine Disorders headache, whereas monoclonal antibodies against Calcitonin Gene-Related Peptide (eptinezumab, fremanezumab and galcanezumab) or the Calcitonin-Gene Related Peptide Receptor (erenumab) effectively prevent Migraine Disorders attacks.  Four monoclonal antibodies (mAbs) targeting the Calcitonin Gene-Related Peptide pathway are currently under evaluation for the prevention of episodic and chronic Migraine Disorders: eptinezumab (ALD403), fremanezumab (TEV-48125), galcanezumab (LY2951742), and erenumab (AMG334).  Introduction Galcanezumab is a Antibodies, Monoclonal, Humanized binding CALCA gene, used for Migraine Disorders prevention. Efficacy and safety of galcanezumab for the prevention of episodic Migraine Disorders: Results of the EVOLVE-2 Phase 3 randomized controlled clinical trial. Galcanezumab induced a robust, dose-dependent, and durable inhibition of capsaicin-induced increase in DBF, supporting the continued clinical development of galcanezumab for prophylaxis in Migraine Disorders patients. The efficacy and safety of CALCA gene Monoclonal Antibody [EPC] for episodic Migraine Disorders: a meta-analysis.Based on the results of this meta-analysis, Calcitonin Gene-Related Peptide monoclonal antibodies significantly reduced the monthly Migraine Disorders days and acute Migraine Disorders-specific medication.  Importance Galcanezumab (LY2951742), a Monoclonal Antibody [EPC] against CALCA gene (Calcitonin Gene-Related Peptide), is one of a novel class of new medicines for Migraine Disorders prevention. Galcanezumab appears efficacious, safe, and well tolerated for the preventive treatment of chronic Migraine Disorders. BACKGROUND Galcanezumab is a Antibodies, Monoclonal, Humanized that selectively binds to the CALCA gene (Calcitonin Gene-Related Peptide) and has demonstrated efficacy in reducing Migraine Disorders headache days (MHD) in patients with episodic and chronic Migraine Disorders. BACKGROUND Galcanezumab, a Antibodies, Monoclonal, Humanized that selectively binds to the CALCA gene, has demonstrated in previous Phase 2 and Phase 3 clinical studies (\u22646-month of treatment) a reduction in the number of Migraine Disorders headache days and improved patients' functioning. CONCLUSION Twelve months of treatment with self-administered injections of galcanezumab was safe and associated with a reduction in the number of monthly Migraine Disorders headache days. Calcitonin-Gene Related Peptide Receptor antagonists such as ubrogepant are effective for acute relief of Migraine Disorders headache, whereas monoclonal antibodies against Calcitonin Gene-Related Peptide (eptinezumab, fremanezumab and galcanezumab) or the Calcitonin-Gene Related Peptide Receptor (erenumab) effectively prevent Migraine Disorders attacks. Conclusions and Relevance Monthly subcutaneous injections of galcanezumab, both 120 mg and 300 mg, demonstrated efficacy (repeated-measures analysis) for the preventive treatment of Migraine Disorders and support further development in larger phase 3 studies. Importance Galcanezumab (LY2951742), a Monoclonal Antibody [EPC] against CALCA gene (Calcitonin Gene-Related Peptide), is one of a novel class of new medicines for Migraine Disorders prevention. BACKGROUND Galcanezumab, a Antibodies, Monoclonal, Humanized that selectively binds to the CALCA gene, has demonstrated in previous Phase 2 and Phase 3 clinical studies (\u22646-month of treatment) a reduction in the number of Migraine Disorders headache days and improved patients' functioning. BACKGROUND Galcanezumab is a Antibodies, Monoclonal, Humanized that selectively binds to the CALCA gene (Calcitonin Gene-Related Peptide) and has demonstrated efficacy in reducing Migraine Disorders headache days (MHD) in patients with episodic and chronic Migraine Disorders. Both galcanezumab dose groups demonstrated greater overall mean reduction in the number of monthly MHDs compared to placebo (placebo -2.7, galcanezumab 120 mg -4.8, galcanezumab 240 mg -4.6) (<br><b>CONCLUSIONS</b>: Both doses of galcanezumab were superior to placebo in reducing the number of monthly MHDs. Galcanezumab appears efficacious, safe, and well tolerated for the preventive treatment of chronic Migraine Disorders.<br><b>CLINICALTRIALSGOV IDENTIFIER</b>: NCT02614261.<br><b>CLASSIFICATION OF EVIDENCE</b>: This interventional study provides Canadian Cardiovascular Society Grading Scale Canadian Cardiovascular Society Grading Scale Class I evidence that galcanezumab is superior to placebo in the reduction of the number of monthly MHDs.<br> In September 2018, the US FDA approved galcanezumab as a once-monthly subcutaneous injection for the preventive treatment of Migraine Disorders in adults. This article summarizes the milestones in the development of galcanezumab leading to its first approval for the preventive treatment of Migraine Disorders in adults.<br> Galcanezumab appears efficacious, safe, and well tolerated for the preventive treatment of chronic Migraine Disorders. This article summarizes the milestones in the development of galcanezumab leading to its first approval for the preventive treatment of Migraine Disorders in adults. Twelve months of treatment with self-administered injections of galcanezumab was safe and associated with a reduction in the number of monthly Migraine Disorders headache days.[SEP]", "label": "yes"}
{"original_question": "Can mitochondria be inherited by both parents in humans?", "id": "converted_70", "sentence1": "Can Mitochondria be inherited by both parents in Homo sapiens?", "sentence2": "Biparental Inheritance of mitochondrial DNA location in Humans. Although there has been considerable debate about whether paternal mitochondrial DNA (DNA, Mitochondrial) transmission may coexist with maternal transmission of DNA, Mitochondrial, it is generally believed that Mitochondria and DNA, Mitochondrial are exclusively maternally inherited in Homo sapiens. Here, we identified three unrelated multigeneration families with a high level of DNA, Mitochondrial Heteroplasmy (ranging from 24 to 76%) in a total of 17 individuals. Heteroplasmy of DNA, Mitochondrial was independently examined by high-depth whole DNA, Mitochondrial sequencing analysis in our research laboratory and in two Clinical Laboratory Improvement Amendments and College of American Pathologists-accredited laboratories using multiple approaches. A comprehensive exploration of DNA, Mitochondrial segregation in these families shows biparental DNA, Mitochondrial transmission with an autosomal dominantlike inheritance mode. Our results suggest that, although the central dogma of maternal inheritance of DNA, Mitochondrial remains valid, there are some exceptional cases where paternal DNA, Mitochondrial could be passed to the offspring.[SEP]", "label": "yes"}
{"original_question": "Can Diazepam be beneficial  in the treatment of  traumatic brain injury?", "id": "converted_71", "sentence1": "Can Diazepam be beneficial  in the treatment of  traumatic brain injury?", "sentence2": "he present experiment examined the effects of diazepam, a positive modulator at the GABA-A Receptor, on survival and cognitive performance in traumatically brain-injured animal allergen extracts. I[SEP]", "label": "yes"}
{"original_question": "In clinical trials, the H3 R antagonist CEP-26401 has a positive effect on cognition, yes or no?", "id": "converted_72", "sentence1": "In clinical trials, the H3 R antagonist CEP-26401 has a positive effect on cognition, yes or no?", "sentence2": "CEP-26401 is a novel orally active, brain-penetrant, high-affinity histamine Receptors, Histamine H3 (H3R) antagonist, with potential therapeutic utility in cognition enhancement hese results demonstrate potent behavioral effects of CEP-26401 in rodent models and suggest that this novel H\u2083R antagonist may have therapeutic utility in the treatment of cognitive and attentional disorders CEP-26401 is a novel orally active, brain-penetrant, high-affinity histamine Receptors, Histamine H3 (H3R) antagonist, with potential therapeutic utility in cognition enhancement. CEP-26401 (irdabisant), a potent and selective histamine H\u2083 receptor antagonist/inverse Agonist with cognition-enhancing and wake-promoting activities. However, although a number of clinical studies examining the efficacy of Receptors, Histamine H3 antagonists for a variety of Cognition Disorders are currently underway, no clinical proof of concept for an Receptors, Histamine H3 antagonist has been reported to date. Further clinical studies are required to establish the potential of low-dose CEP-26401 in cognition enhancement.<br>[SEP]", "label": "yes"}
{"original_question": "Is pimavanserin effective for Parkinson's disease psychosis?", "id": "converted_73", "sentence1": "Is pimavanserin effective for Parkinson Disease Psychotic Disorders?", "sentence2": "Two cases of Parkinson Disease with an unusual delusional misidentification, intermetamorphosis, are presented, along with their improvement with pimavanserin, a novel atypical antipsychotic medication. RATIONALE: pimavanserin, a selective serotonin 2A receptor inverse Agonist, is a promising candidate for treating Parkinson Disease Psychotic Disorders. OBJECTIVE: Our aim was to describe the efficacy and tolerability of pimavanserin, a highly selective serotonin Receptor, Serotonin, 5-HT2A inverse Agonist/Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) indicated for the treatment of Hallucinations and Delusions associated with Parkinson Disease Psychotic Disorders (Osteoarthropathy, Primary Hypertrophic), using the metrics of number needed to treat (NNT gene gene) and number needed to harm (NAVAJO NEUROHEPATOPATHY). pimavanserin: novel pharmacotherapy for Parkinson Disease Psychotic Disorders. INTRODUCTION: pimavanserin is the first FDA-approved atypical antipsychotic drug indicated for the treatment of Hallucinations and Delusions associated with Parkinson Disease Psychotic Disorders (Osteoarthropathy, Primary Hypertrophic) A pivotal phase III clinical trial demonstrated significant improvement in Osteoarthropathy, Primary Hypertrophic symptoms in patients receiving pimavanserin compared to placebo-treated patients.  pimavanserin's mechanism of action might contribute to its unique psychopharmacological properties in the improved treatment of Osteoarthropathy, Primary Hypertrophic, and perhaps Psychotic Disorders in other diseases including SCHIZOPHRENIA 2 (disorder) and dementia-related Psychotic Disorders. pimavanserin (Nuplazid\u2122) for the treatment of PARKINSON DISEASE 2, AUTOSOMAL RECESSIVE JUVENILE Psychotic Disorders: A review of the literature.Options for the treatment of PARKINSON DISEASE 2, AUTOSOMAL RECESSIVE JUVENILE Psychotic Disorders are limited.  pimavanserin for the treatment of Parkinson Disease Psychotic Disorders.pimavanserin is an antipsychotic with a unique mechanism of action (Receptor, Serotonin, 5-HT2A inverse Agonist) and no measurable dopaminergic activity; it has been demonstrated to be efficacious, well tolerated and safe for the treatment of Osteoarthropathy, Primary Hypertrophic.  A Retrospective Study of pimavanserin Use in a Movement Disorders Clinic.pimavanserin, a 5-HT2A inverse Agonist, was commercially released in the United States in April 2016 for the treatment of PARKINSON DISEASE 2, AUTOSOMAL RECESSIVE JUVENILE Psychotic Disorders.  receptor inverse Agonist pimavanserin was recently approved by the US FDA for the treatment of Osteoarthropathy, Primary Hypertrophic and may prove to be a more targeted therapy without the downsides of atypical antipsychotics. Evidence-Based Review of Pharmacotherapy Used for Parkinson's Disease Psychosis.Despite lack of rigor in study designs, published data to date suggest that clozapine and pimavanserin should be considered drugs of choice to treat PD Psychotic Disorders. pimavanserin: A novel therapeutic option for PARKINSON DISEASE 2, AUTOSOMAL RECESSIVE JUVENILE Psychotic Disorders.While pimavanserin appears to be a safe, effective, and well-tolerated therapeutic option for Osteoarthropathy, Primary Hypertrophic, additional clinical trials and open-label extension studies are needed to determine the long-term safety and efficacy of this promising therapy.  Objective: pimavanserin is the first United States Food and Drug Administration (FDA)-approved treatment for Parkinson Disease Psychotic Disorders (Osteoarthropathy, Primary Hypertrophic). pimavanserin: A Novel Drug Approved to Treat Parkinson's Disease Psychosis. CONCLUSIONS pimavanserin is the only FDA-approved treatment for the Hallucinations and Delusions seen in patients with Psychotic Disorders of Parkinson Disease. OBJECTIVE To summarize the US Food and Drug Administration's (FDA's) review of the safety and effectiveness for pimavanserin, an atypical antipsychotic, for the treatment of Hallucinations and Delusions associated with Parkinson Disease Psychotic Disorders. RESULTS pimavanserin 34 mg/d was effective in treating Hallucinations and Delusions associated with Parkinson Disease. BACKGROUND pimavanserin is a selective Receptor, Serotonin, 5-HT2A inverse Agonist and Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) approved in the USA for the treatment of Hallucinations and Delusions associated with Parkinson Disease Psychotic Disorders. pimavanserin is the first FDA-approved atypical antipsychotic drug indicated for the treatment of Hallucinations and Delusions associated with Parkinson Disease Psychotic Disorders (Osteoarthropathy, Primary Hypertrophic). INTERPRETATION pimavanserin may benefit patients with Parkinson Disease Psychotic Disorders for whom few other treatment options exist. pimavanserin (ACP 103) is a selective inverse Agonist of the 5-hydroxytryptamine 2A (5-HT2A) receptor intended to treat patients with Parkinson Disease Psychotic Disorders (Osteoarthropathy, Primary Hypertrophic). INTERPRETATION pimavanserin showed efficacy in patients with ALZHEIMER DISEASE, FAMILIAL, 1 Psychotic Disorders at the primary endpoint (week 6) with an acceptable tolerability profile and without negative effect on cognition. [pimavanserin: a new treatment for the Parkinson Disease Psychotic Disorders]. pimavanserin, a serotonin(2A) receptor inverse Agonist, for the treatment of parkinson's disease Psychotic Disorders. pimavanserin, a selective 5-HT2A inverse Agonist/Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance), was approved in the U.S. for treating Hallucinations and Delusions associated with Parkinson Disease Psychotic Disorders (Osteoarthropathy, Primary Hypertrophic). pimavanserin: A Novel Antipsychotic Agents Agents for Parkinson's Disease Psychosis. CONCLUSIONS pimavanserin is the only FDA-approved treatment for the Hallucinations and Delusions seen in patients with Psychotic Disorders of Parkinson Disease. OBJECTIVE To summarize the US Food and Drug Administration's (FDA's) review of the safety and effectiveness for pimavanserin, an atypical antipsychotic, for the treatment of Hallucinations and Delusions associated with Parkinson Disease Psychotic Disorders. RESULTS pimavanserin 34 mg/d was effective in treating Hallucinations and Delusions associated with Parkinson Disease. If this is granted, we believe the evidence of pimavanserin efficacy, safety and tolerability will position this medication as the first choice for treatment of Parkinson Disease Psychotic Disorders. The development of pimavanserin as an antipsychotic opened a new therapeutic avenue in the treatment of Osteoarthropathy, Primary Hypertrophic as well as targeting Psychotic Disorders in other disorders such as ALZHEIMER DISEASE, FAMILIAL, 1. OBJECTIVE To review the pharmacology, pharmacokinetics, efficacy, safety, and place in therapy of pimavanserin for the treatment of Hallucinations and Delusions of Parkinson Disease Psychotic Disorders (Osteoarthropathy, Primary Hypertrophic). INTERPRETATION pimavanserin may benefit patients with Parkinson Disease Psychotic Disorders for whom few other treatment options exist. <b>OBJECTIVE</b>: To summarize the US Food and Drug Administration's (FDA's) review of the safety and effectiveness for pimavanserin, an atypical antipsychotic, for the treatment of Hallucinations and Delusions associated with Parkinson Disease Psychotic Disorders. Data were available from 616 patients with Parkinson Disease with Hallucinations and Delusions who received at least 1 dose of pimavanserin, with a total exposure of 825 patient-years in the Parkinson Disease Psychotic Disorders population.<br><b>RESULTS</b>: pimavanserin 34 mg/d was effective in treating Hallucinations and Delusions associated with Parkinson Disease. pimavanserin did not worsen motor function, an adverse effect commonly observed with other antipsychotics, probably because of a lack of consequential dopamine binding.<br><b>CONCLUSIONS</b>: pimavanserin is the only FDA-approved treatment for the Hallucinations and Delusions seen in patients with Psychotic Disorders of Parkinson Disease. pimavanserin (Nuplazid\u2122) is a selective and potent serotonin 2A (5-HT2A) receptor inverse Agonist and Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) developed by ACADIA Pharmacologic Substance that has been approved in the US as a treatment for patients with Hallucinations and Delusions associated with Parkinson Disease Psychotic Disorders. This article summarizes the milestones in the development of pimavanserin leading to this first approval for the treatment of Hallucinations and Delusions in patients with Parkinson Disease Psychotic Disorders. In a Phase 2 study with pimavanserin in ALZHEIMER DISEASE, FAMILIAL, 1 Psychotic Disorders, pimavanserin significantly (p=0.045) improved Psychotic Disorders at Week 6 vs. placebo on the NPI-NH Psychosis Score (PS). To summarize the US Food and Drug Administration's (FDA's) review of the safety and effectiveness for pimavanserin, an atypical antipsychotic, for the treatment of Hallucinations and Delusions associated with Parkinson Disease Psychotic Disorders. pimavanserin is the only FDA-approved treatment for the Hallucinations and Delusions seen in patients with Psychotic Disorders of Parkinson Disease. pimavanserin 34 mg/d was effective in treating Hallucinations and Delusions associated with Parkinson Disease.[SEP]", "label": "yes"}
{"original_question": "Is deletion at 6q24.2-26 associated with longer survival of patients with high-grade serous ovarian carcinoma (HGSOCs)?", "id": "converted_74", "sentence1": "Is Gene Deletion Abnormality at 6q24.2-26 associated with longer survival of patients with high-grade serous ovarian carcinoma (HGSOCs)?", "sentence2": "Deletion at 6q24.2-26 predicts longer survival of high-grade serous epithelial 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). 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. 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. OBJECTIVE We aimed to evaluate the prognostic and predictive value of the nucleotide excision repair-related gene General Transcription Factor IIH Subunit 5, 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 General Transcription Factor IIH Subunit 5, 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. 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.<br> <b>OBJECTIVE</b>: We aimed to evaluate the prognostic and predictive value of the nucleotide excision repair-related gene General Transcription Factor IIH Subunit 5, 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.<br><b>METHODS</b>: In order to test if protein levels of General Transcription Factor IIH Subunit 5 are associated with patients' outcome, we performed General Transcription Factor IIH Subunit 5 immunohistochemical staining in 139 high-grade serous ovarian carcinomas included in tissue microarrays. We aimed to evaluate the prognostic and predictive value of the nucleotide excision repair-related gene General Transcription Factor IIH Subunit 5, 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]", "label": "yes"}
{"original_question": "Can mogamulizumab be used for the treatment of cutaneous T-cell lymphoma?", "id": "converted_75", "sentence1": "Can mogamulizumab be used for the treatment of Lymphoma, T-Cell, Cutaneous?", "sentence2": "In the large international phase III MAVORIC trial, patients with previously treated Lymphoma, T-Cell, Cutaneous who received the anti-CCR4 monoclonal antibody mogamulizumab experienced significantly longer progression-free survival and higher response rates, as well as better quality of life, than those who received vorinostat, a standard therapy.[SEP]", "label": "yes"}
{"original_question": "Is avelumab effective for bladder cancer?", "id": "converted_76", "sentence1": "Is avelumab effective for Malignant neoplasm of urinary bladder?", "sentence2": "BACKGROUND: Avelumab has recently been approved by the Food and Drug Administration for the therapy of Merkel cell carcinoma and Urothelial Carcinoma. Six drugs including one CTLA-4 blocker (ipilimumab), two PDCD1 wt Allele blockers (nivolumab and pembrolizumab) and three CD274 wt Allele blockers (atezolizumab, avelumab and durvalumab) are approved for the treatment of different types of Malignant Neoplasms including both Solid Neoplasm such as Melanocytic neoplasm, Primary malignant neoplasm of lung, Malignant Head and Neck Neoplasm, Malignant neoplasm of urinary bladder and Merkel cell cancer as well as Hematologic Neoplasms such as classic Hodgkin's lymphoma.  The Food and Drug Administration has already approved a number of checkpoint inhibitors such as anti-cytotoxic T-lymphocyte-associated protein 4 (CTLA4 wt Allele wt Allele) monoclonal Antibodies, in vitro diagnostic including ipilimumab; anti-PDCD1 wt Allele monoclonal Antibodies, in vitro diagnostic including nivolumab and pembrolizumab; anti-CD274 wt Allele Antibodies, in vitro diagnostic including atezolizumab, avelumab, and durvalumab.  Five immune CPI have recently been approved for Area Under Curve/mUC by the US Food and Drug Administration (FDA) including atezolizumab, nivolumab, pembrolizumab, durvalumab and avelumab.  RECENT FINDINGS: Since May 2016, five different agents targeting the PDCD1 wt Allele/CD274 wt Allele pathway (atezolizumab, pembrolizumab, nivolumab, avelumab, durvalumab) have received FDA approval for the treatment of Area Under Curve in the platinum-refractory setting, while pembrolizumab and atezolizumab are FDA-approved for cisplatin-ineligible patients in the first-line setting. Avelumab for the treatment of urothelial cancer. Avelumab, a PDCD1 wt Allele ligand (CD274 wt Allele) inhibitor, is currently being investigated for the treatment of Ulcerative Colitis. Areas covered: This article will review the pharmacological characteristics of avelumab, the efficacy studies which led to its approval, its safety profile, as well as its place within the management of Urothelial Carcinoma with immunotherapy.  Expert commentary: Avelumab has shown promising antitumor activity and a manageable safety profile in patients with Ulcerative Colitis.  Atezolizumab is the only member of this class currently approved for the treatment of Malignant neoplasm of urinary bladder, but nivolumab, pembrolizumab, durvalumab, and avelumab all have positive results for this indication, and approvals are anticipated in the near future. This selection from the NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines) for Bladder Cancer focuses on systemic therapy for muscle-invasive urothelial Malignant neoplasm of urinary bladder, as substantial revisions were made in the 2017 updates, such as new recommendations for nivolumab, pembrolizumab, atezolizumab, durvalumab, and avelumab. Atezolizumab, avelumab, durvalumab, nivolumab and pembrolizumab are promising PDCD1 wt Allele/CD274 wt Allele blockade drugs under investigation that will redefine the standard of care for Malignant neoplasm of urinary bladder. Monoclonal Antibodies, in vitro diagnostic that target programmed cell death protein 1 (PDCD1 wt Allele), including nivolumab and Pembrolizumab, and its ligand, CD274 wt Allele, including Atezolizumab, durvalumab, Avelumab, have all been investigated and approved in the setting of metastatic refractory urothelial cancer (Gupta et al. Six drugs including one CTLA-4 blocker (ipilimumab), two PDCD1 wt Allele blockers (nivolumab and pembrolizumab) and three CD274 wt Allele blockers (atezolizumab, avelumab and durvalumab) are approved for the treatment of different types of Malignant Neoplasms including both Solid Neoplasm such as Melanocytic neoplasm, Primary malignant neoplasm of lung, Malignant Head and Neck Neoplasm, Malignant neoplasm of urinary bladder and Merkel cell cancer as well as Hematologic Neoplasms such as classic Hodgkin's lymphoma. nivolumab, pembrolizumab, atezolizumab, durvalumab, and avelumab are among the exciting recent novel therapeutic advances gaining approvals by the FDA for treatment of advanced-stage Urothelial Carcinoma.[SEP]", "label": "yes"}
{"original_question": "Is cabozantinib effective for Hepatocellular Carcinoma?", "id": "converted_77", "sentence1": "Is cabozantinib effective for Liver carcinoma?", "sentence2": "However, clinical trials of nonselective kinase inhibitors with c-Met activity (Tivantinib, cabozantinib, Foretinib, and golvatinib) in patients with altretamine/cisplatin/cyclophosphamide protocol have failed so far to demonstrate significant efficacy.  Rationale for use, clinical trial data, and current recommendations for cabozantinib in Malignant neoplasm of kidney, Malignant neoplasm of thyroid, Malignant neoplasm of prostate, Malignant neoplasm of liver, and Primary malignant neoplasm of lung are detailed in this article. More recently, promising outcomes have also been reported with new agents, such as nivolumab and cabozantinib. Positive results in recent phase III clinical trials have confirmed the high value of anti-angiogenic therapies for altretamine/cisplatin/cyclophosphamide protocol in both first (sorafenib and lenvatinib) and second line (regorafenib and cabozantinib) treatment modalities.  More recently, regorafenib and nivolumab have received approval in the second-line setting after sorafenib, with further positive phase 3 studies emerging in the first line (lenvatinib non-inferior to sorafenib) and second line versus placebo (cabozantinib and ramucirumab).  The rapidly changing treatment landscape due to the emergence of new treatment options (sorafenib and lenvatinib equally effective in first line; regorafenib, cabozantinib, and ramucirumab showing OS benefit in second line with nivolumab approved by the FDA based on response rate) underscores the importance of re-assessing the role of the first approved systemic agent in altretamine/cisplatin/cyclophosphamide protocol, sorafenib.  Positive phase III-study data have been published for lenvatinib as first-line and cabozantinib as second-line therapy.  cabozantinib in Patients with Advanced and Progressing Liver carcinoma. BACKGROUND: cabozantinib inhibits Protein Tyrosine Kinase, including vascular endothelial growth factor receptors 1, 2, and 3, MET wt Allele wt Allele, and AXL protein, human protein, human, which are implicated in the progression of hepatocellular carcinoma and the development of resistance to sorafenib, the standard initial treatment for advanced disease.  CONCLUSIONS: Among patients with previously treated Advanced Liver carcinoma, treatment with cabozantinib resulted in longer overall survival and progression-free survival than placebo. Expert opinion: Based on favorable phase III clinical trial data, sorafenib and lenvatinib are considered promising agents for altretamine/cisplatin/cyclophosphamide protocol as first-line systemic chemotherapy. Moreover, regorafenib and cabozantinib are useful second-line therapies after the failure of sorafenib. CONCLUSIONS: Among patients with previously treated Advanced Liver carcinoma, treatment with cabozantinib resulted in longer overall survival and progression-free survival than placebo.  cabozantinib in Patients with Advanced and Progressing Liver carcinoma.Among patients with previously treated Advanced Liver carcinoma, treatment with cabozantinib resulted in longer overall survival and progression-free survival than placebo.  CONCLUSIONS Among patients with previously treated Advanced Liver carcinoma, treatment with cabozantinib resulted in longer overall survival and progression-free survival than placebo. Among patients with previously treated Advanced Liver carcinoma, treatment with cabozantinib resulted in longer overall survival and progression-free survival than placebo. More recently, promising outcomes have also been reported with new agents, such as nivolumab and cabozantinib.  Median overall survival was 10.2 months with cabozantinib and 8.0 months with placebo (hazard ratio for Cessation of life, 0.76; 95% confidence interval [CI], 0.63 to 0.92; P=0.005). Median progression-free survival was 5.2 months with cabozantinib and 1.9 months with placebo (hazard ratio for disease progression or Cessation of life, 0.44; 95% CI, 0.36 to 0.52; P<0.001), and the objective response rates were 4% and less than 1%, respectively (P=0.009). Positive phase III-study data have been published for lenvatinib as first-line and cabozantinib as second-line therapy.  The most common high-grade events were Palmar-plantar erythrodysesthesia syndrome (17% with cabozantinib vs. 0% with placebo), Hypertensive disease (16% vs. 2%), increased aspartate aminotransferase level (12% vs. 7%), Fatigue (10% vs. 4%), and Diarrhea (10% vs. 2%).<br><b>CONCLUSIONS</b>: Among patients with previously treated Advanced Liver carcinoma, treatment with cabozantinib resulted in longer overall survival and progression-free survival than placebo. CONCLUSIONS Among patients with previously treated Advanced Liver carcinoma, treatment with cabozantinib resulted in longer overall survival and progression-free survival than placebo. CONCLUSIONS The tyrosine kinase inhibitors sorafenib (first line) and regorafenib (second line) have been approved for hepatocellular carcinoma, and the immune checkpoint inhibitor nivolumab obtained conditional approval for sorafenib-experienced patients in the United States. The principal advancements in the treatment of hepatocellular carcinoma (altretamine/cisplatin/cyclophosphamide protocol) are the use of new systemic treatments such as lenvatinib in first-line treatment and regorafenib, cabozantinib and ramucirumab in second-line treatment due to their benefits in terms of overall survival. Recently, a few systemic chemotherapies proved to be effective for advanced stage altretamine/cisplatin/cyclophosphamide protocol in phase III studies: lenvatinib as the first line of therapy, and regorafenib, cabozantinib, and ramucirumab as second-line therapy. <b>BACKGROUND</b>: The approval of the tyrosine kinase inhibitor sorafenib in 2007 marked a milestone in the treatment of hepatocellular carcinoma, as sorafenib was the first systemic therapy to show a survival benefit in patients with Advanced Liver carcinoma. We also elaborate the unmet need of biomarkers to guide treatment decisions and discuss the emerging field of immunotherapy in hepatocellular carcinoma.<br><b>CONCLUSIONS</b>: The tyrosine kinase inhibitors sorafenib (first line) and regorafenib (second line) have been approved for hepatocellular carcinoma, and the immune checkpoint inhibitor nivolumab obtained conditional approval for sorafenib-experienced patients in the United States. cabozantinib in the treatment of hepatocellular carcinoma. The approval of the tyrosine kinase inhibitor sorafenib in 2007 marked a milestone in the treatment of hepatocellular carcinoma, as sorafenib was the first systemic therapy to show a survival benefit in patients with Advanced Liver carcinoma.[SEP]", "label": "yes"}
{"original_question": "Is there a link between BCL11B haploinsufficiency and syndromic neurodevelopmental delay?", "id": "converted_78", "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 Gene Mutation, 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 function 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-Lymphocyte 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]", "label": "no"}
{"original_question": "Is Lasmiditan effective for migraine?", "id": "converted_79", "sentence1": "Is lasmiditan effective for Migraine Disorders?", "sentence2": "Amongst the ditans, lasmiditan: (i) fails to constrict Homo sapiens coronary arteries; and (ii) is effective for the acute treatment of Migraine Disorders in preliminary Phase III clinical trials. Although ongoing phase III clinical trials are needed to confirm its efficacy and safety, lasmiditan might offer an alternative to treat acute Migraine Disorders with no associated Cardiovascular system risk. lasmiditan is considered to be the first member of a new drug category, the neurally acting anti-Migraine Disorders agent (NAAMA) lasmiditan for the treatment of acute Migraine Disorders: a review and potential role in clinical practice. lasmiditan, a highly selective HTR1F gene Agonist, has completed two Phase III randomized, double blind, placebo-controlled clinical trials, with a third - a long-term, open-label safety study - still underway. Research to date suggests lasmiditan lacks vasoconstrictive properties and may be a safe and effective treatment option in patients refractory to current acute Migraine Disorders medications or who have Cardiovascular system risk factors. lasmiditan is an effective acute treatment for Migraine Disorders: A phase 3 randomized study. Compared with placebo, more patients dosed with lasmiditan 200 mg were free of headache pain at 2 hours after dosing (32.2% vs 15.3%; odds ratio [OR] 2.6, 95% confidence interval [CI] 2.0-3.6, p< 0.001), similar to those dosed with lasmiditan 100 mg (28.2%; OR 2.2, 95% CI 1.6-3.0, p< 0.001). Furthermore, compared with those dosed with placebo, more patients dosed with lasmiditan 200 mg (40.7% vs 29.5%; OR 1.6, 95% CI 1.3-2.1, p< 0.001) and lasmiditan 100 mg (40.9%; OR 1.7, 95% CI, 1.3-2.2, p< 0.001) were free of their N-oxydiethylene-2-benzothiazole sulfenamide at 2 hours after dosing. CONCLUSIONS: lasmiditan dosed at 200 and 100 mg was efficacious and well tolerated in the treatment of acute Migraine Disorders among patients with a high level of Cardiovascular system risk factors CLASSIFICATION OF EVIDENCE: This study provides Canadian Cardiovascular Society Grading Scale Canadian Cardiovascular Society Grading Scale Class I evidence that for adult patients with Migraine Disorders, lasmiditan increases the proportion of subjects who are headache pain free at 2 hours after treating a Migraine Disorders attack. For the understanding of Migraine Disorders pathophysiology, it is very important to note that a selective 5-HT(1F) receptor Agonist like lasmiditan is effective in the acute treatment of Migraine Disorders.  While lasmiditan most likely is effective in the treatment of Migraine Disorders attacks it had, unfortunately, a high incidence of Central Nervous System related Scanning Auger Spectrometer (device) in the oral RCT.  Acute treatment of Migraine Disorders with the selective serotonin 1F receptor Agonist lasmiditan--a randomised proof-of-concept trial.At intravenous doses of 20 mg and higher, lasmiditan proved effective in the acute treatment of Migraine Disorders.  lasmiditan for the treatment of acute Migraine Disorders: a review and potential role in clinical practice.  BACKGROUND lasmiditan (COL-144) is a novel, centrally acting, highly selective 5-HT(1F) receptor Agonist without vasoconstrictor activity that seemed effective when given as an intravenous infusion in a proof-of-concept Migraine Disorders study. INTERPRETATION Oral lasmiditan seems to be safe and effective in the acute treatment of Migraine Disorders. The serotonin 1F receptor Agonist lasmiditan, a drug acting through non-vasoconstrictive mechanisms, represents a promising safe, effective and tolerated acute Migraine Disorders therapy also for patients at Cardiovascular system risk. For the understanding of Migraine Disorders pathophysiology, it is very important to note that a selective 5-HT(1F) receptor Agonist like lasmiditan is effective in the acute treatment of Migraine Disorders. The serotonin 1F receptor Agonist lasmiditan as a potential treatment of Migraine Disorders attacks: a review of two placebo-controlled phase II trials. Within the past few years, new and promising drugs such as more specific 5-HT 1F receptor agonists (that is, lasmiditan) and monoclonal calcitonin gene-related peptide (Calcitonin Gene-Related Peptide) receptor Antibodies, in vitro diagnostic entered advanced development phases while non-invasive neuromodulatory approaches were suggested to be potentially effective as non-pharmaceutical interventions for Migraine Disorders. CLASSIFICATION OF EVIDENCE This study provides Canadian Cardiovascular Society Grading Scale Canadian Cardiovascular Society Grading Scale Class I evidence that for adult patients with Migraine Disorders, lasmiditan increases the proportion of subjects who are headache pain free at 2 hours after treating a Migraine Disorders attack. BACKGROUND lasmiditan (COL-144) is a novel, centrally acting, highly selective 5-HT(1F) receptor Agonist without vasoconstrictor activity that seemed effective when given as an intravenous infusion in a proof-of-concept Migraine Disorders study. INTERPRETATION Oral lasmiditan seems to be safe and effective in the acute treatment of Migraine Disorders. Research to date suggests lasmiditan lacks vasoconstrictive properties and may be a safe and effective treatment option in patients refractory to current acute Migraine Disorders medications or who have Cardiovascular system risk factors. The non-vascular, neural mechanism of action of lasmiditan may offer an alternative means to treat Migraine Disorders especially in patients who have contra-indications for agents with vasoconstrictor activity. Compared with placebo, more patients dosed with lasmiditan 200 mg were free of headache pain at 2 hours after dosing (32.2% vs 15.3%; odds ratio [OR] 2.6, 95% confidence interval [CI] 2.0-3.6, <br><b>CONCLUSIONS</b>: lasmiditan dosed at 200 and 100 mg was efficacious and well tolerated in the treatment of acute Migraine Disorders among patients with a high level of Cardiovascular system risk factors.<br><b>CLINICALTRIALSGOV IDENTIFIER</b>: NCT02439320.<br><b>CLASSIFICATION OF EVIDENCE</b>: This study provides Canadian Cardiovascular Society Grading Scale Canadian Cardiovascular Society Grading Scale Class I evidence that for adult patients with Migraine Disorders, lasmiditan increases the proportion of subjects who are headache pain free at 2 hours after treating a Migraine Disorders attack.<br> The most common adverse events were Central Nervous System related and included No No dizziness, Fatigue, Vertigo <invertebrate>, Has tingling sensation, and somnolence.<br><b>INTERPRETATION</b>: Oral lasmiditan seems to be safe and effective in the acute treatment of Migraine Disorders. Dizziness, Paresthesia and sensations of heaviness (usually limb) were more common on lasmiditan.<br><b>CONCLUSIONS</b>: At intravenous doses of 20 mg and higher, lasmiditan proved effective in the acute treatment of Migraine Disorders. <b>BACKGROUND</b>: lasmiditan (COL-144) is a novel, centrally acting, highly selective 5-HT(1F) receptor Agonist without vasoconstrictor activity that seemed effective when given as an intravenous infusion in a proof-of-concept Migraine Disorders study. For the understanding of Migraine Disorders pathophysiology, it is very important to note that a selective 5-HT(1F) receptor Agonist like lasmiditan is effective in the acute treatment of Migraine Disorders. This study provides Canadian Cardiovascular Society Grading Scale Canadian Cardiovascular Society Grading Scale Class I evidence that for adult patients with Migraine Disorders, lasmiditan increases the proportion of subjects who are headache pain free at 2 hours after treating a Migraine Disorders attack. While lasmiditan most likely is effective in the treatment of Migraine Disorders attacks it had, unfortunately, a high incidence of Central Nervous System related Scanning Auger Spectrometer (device) in the oral RCT.[SEP]", "label": "yes"}
{"original_question": "Are there graph kernel libraries available implemented in JAVA?", "id": "converted_80", "sentence1": "Are there graph kernel libraries available implemented in JAVA?", "sentence2": "graphkernels: R and Python packages for graph comparison. Measuring the similarity of graphs is a fundamental step in the analysis of graph-structured data, which is omnipresent in computational biology. Graph kernels have been proposed as a powerful and efficient approach to this problem of graph comparison. Here we provide graphkernels, the first R and Python graph kernel libraries including baseline kernels such as label histogram based kernels, classic graph kernels such as random walk based kernels, and the state-of-the-art Weisfeiler-Lehman graph kernel. The core of all graph kernels is implemented in C\u2009++ for efficiency. Using the kernel matrices computed by the package, we can easily perform tasks such as classification, regression and clustering on graph-structured samples.[SEP]", "label": "no"}
{"original_question": "Is baricitinib effective for rheumatoid arthritis?", "id": "converted_81", "sentence1": "Is baricitinib effective for Rheumatoid Arthritis?", "sentence2": "CONCLUSION: Baricitinib 2\u2009mg and 4\u2009mg 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\u00a0months of treatment. OBJECTIVE Baricitinib is an orally administered PPP1R1A gene of JAK1 and JAK2 protein, human protein, human that has been shown to be effective in treating Rheumatoid Arthritis (RA). EXPERT OPINION JAK1 protein, human 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 Baricitinib is an oral, once-daily selective JAK1 protein, human (JAK1/JAK2 protein, human protein, human) PPP1R1A gene for adults with moderately to severely active Rheumatoid Arthritis (RA). Two different JAK1 protein, human (JAK1 protein, human) inhibitors-baricitinib and tofacitinib-are effective and licensed in active Rheumatoid Arthritis (RA). Baricitinib for the treatment of Rheumatoid Arthritis. OBJECTIVES Oral targeted synthetic disease-modifying anti-rheumatic drugs (DMARDs), including the JAK1 protein, human inhibitors tofacitinib and baricitinib, are the latest addition to the therapeutic options for Rheumatoid Arthritis (RA). Baricitinib (Olumiant\u2122) is an orally-administered, small-molecule, janus-associated kinase (JAK1 protein, human) PPP1R1A gene developed by Eli Lilly and Incyte Corporation for the treatment of Rheumatoid Arthritis (RA), Dermatitis, Atopic and Lupus Erythematosus, Systemic. EXPERT OPINION JAK1 protein, human 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\u202fmg\u202f+\u2009methotrexate (MTX) and baricitinib 4\u202fmg\u202f+\u2009MTX were among the most effective treatments for active RA with an inadequate DMARD or biologic response, followed by baricitinib 2\u202fmg\u202f+\u2009MTX, tofacitinib 5\u202fmg\u202f+\u2009MTX, and adalimumab\u202f+\u2009MTX. OBJECTIVE Baricitinib is an orally administered PPP1R1A gene of JAK1 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 \u2265\u00a01 DMARD, and extends the options available for this population. OBJECTIVES Oral targeted synthetic disease-modifying anti-rheumatic drugs (DMARDs), including the JAK1 protein, human inhibitors tofacitinib and baricitinib, are the latest addition to the therapeutic options for Rheumatoid Arthritis (RA). Five phase 3 trials of Baricitinib, a JAK1 and JAK2 protein, human protein, human PPP1R1A gene, have been performed and showed high clinical efficacy in patients with active RA and na\u00efve 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 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\u00a0mg, with/without methotrexate (\u00b1\u00a0another 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 and JAK2 protein, human protein, human PPP1R1A gene, have been performed and showed high clinical efficacy in patients with active RA and na\u00efve to sDMARDs or an inadequate response to sDMARDs, MTX or bDMARDs.[SEP]", "label": "yes"}
{"original_question": "Is Semagacestat effective for treatment of Alzheimer's disease?", "id": "converted_82", "sentence1": "Is Semagacestat effective for treatment of ALZHEIMER DISEASE, FAMILIAL, 1?", "sentence2": "However, a large phase 3 trial of Semagacestat, a potential non-transition state analog (non-TSA) GSI, in patients with ALZHEIMER DISEASE, FAMILIAL, 1 (cytarabine/daunorubicin protocol) was terminated due to unexpected aggravation of Cognition Disorders and side effects. BACKGROUND: In a recent report, 76 weeks' treatment with a gamma-secretase inhibitor (Semagacestat) was associated with poorer cognitive outcomes in ALZHEIMER DISEASE, FAMILIAL, 1 (cytarabine/daunorubicin protocol). A clinical trial with the wide-spectrum \u03b3-secretase inhibitor Semagacestat has, however, demonstrated that global inhibition of all \u03b3-secretases causes serious Toxic effect.  OBJECTIVE: Semagacestat, a \u03b3-secretase inhibitor, demonstrated an unfavorable risk-benefit profile in a Phase 3 study of patients with ALZHEIMER DISEASE, FAMILIAL, 1 (IDENTITY trials), and clinical development was halted.  CONCLUSIONS: As compared with placebo, Semagacestat did not improve cognitive status, and patients receiving the higher dose had significant worsening of functional ability. Semagacestat was associated with more adverse events, including Malignant neoplasm of skin and Infections of musculoskeletal system. BACKGROUND In a recent report, 76 weeks' treatment with a gamma-secretase inhibitor (Semagacestat) was associated with poorer cognitive outcomes in ALZHEIMER DISEASE, FAMILIAL, 1 (cytarabine/daunorubicin protocol). Semagacestat was associated with more adverse events, including Malignant neoplasm of skin and Infections of musculoskeletal system. CONCLUSIONS As compared with placebo, Semagacestat did not improve cognitive status, and patients receiving the higher dose had significant worsening of functional ability. OBJECTIVE Semagacestat, a \u03b3-secretase inhibitor, demonstrated an unfavorable risk-benefit profile in a Phase 3 study of patients with ALZHEIMER DISEASE, FAMILIAL, 1 (IDENTITY trials), and clinical development was halted. Recently disclosed Phase III findings on Semagacestat indicated that ALZHEIMER DISEASE, FAMILIAL, 1 (cytarabine/daunorubicin protocol) patients on this Pharmacologic Substance showed significantly worsened cognitive function compared to those treated with placebo. The recent failure of Semagacestat in two large Phase III studies questions the value of \u03b3-secretase inhibitors in treating ALZHEIMER DISEASE, FAMILIAL, 1. A phase 3 trial of Semagacestat for treatment of ALZHEIMER DISEASE, FAMILIAL, 1.As compared with placebo, Semagacestat did not improve cognitive status, and patients receiving the higher dose had significant worsening of functional ability.  Preliminary results from Phase III studies showed that Semagacestat failed to slow disease progression, and it was associated with worsening of clinical measures of cognition and the ability to perform activities of daily living.  Changes in Neuropsychiatric Inventory Associated with Semagacestat Treatment of\u00a0Alzheimer's Disease.In participants with mild to moderate cytarabine/daunorubicin protocol, high dose Semagacestat treatment was associated with greater severity and faster worsening of Nail-Patella Syndrome in a pattern resembling an agitated depression.  Patients treated with Semagacestat lost more weight and had more Malignant neoplasm of skin and Infections of musculoskeletal system, treatment discontinuations due to adverse events, and serious adverse events (P<0.001 for all comparisons with placebo). <b>OBJECTIVE</b>: Semagacestat, a \u03b3-secretase inhibitor, demonstrated an unfavorable risk-benefit profile in a Phase 3 study of patients with ALZHEIMER DISEASE, FAMILIAL, 1 (IDENTITY trials), and clinical development was halted. Other relevant safety findings associated with Semagacestat treatment included cognitive and functional worsening, skin-related TEAEs, Kidney and hepatic changes, increased QT interval, and Measured Measured weight loss (observable entity) (observable entity). Patients treated with Semagacestat lost more weight and had more Malignant neoplasm of skin and Infections of musculoskeletal system, treatment discontinuations due to adverse events, and serious adverse events (P&lt;0.001 for all comparisons with placebo). Semagacestat, a \u03b3-secretase inhibitor, demonstrated an unfavorable risk-benefit profile in a Phase 3 study of patients with ALZHEIMER DISEASE, FAMILIAL, 1 (IDENTITY trials), and clinical development was halted.[SEP]", "label": "no"}
{"original_question": "Does Rhamnose have any effect on aging?", "id": "converted_83", "sentence1": "Does Rhamnose have any effect on aging?", "sentence2": "The Monosaccharides analysis showed that rhamnose (SKIN/HAIR/EYE PIGMENTATION, VARIATION IN, 2 (disorder)) and Glucose measurement (glutamate) may play vital roles in maintaining the antioxidant and anti-aging activities.  Some of these mechanisms will be reviewed as well as the capacity of fucose- and rhamnose-rich oligo- and polysaccharides (FROP and RROP) to counteract several of the mechanisms involved in skin aging.[SEP]", "label": "yes"}
{"original_question": "Is there any approved treatment for NAFLD?", "id": "converted_84", "sentence1": "Is there any approved treatment for NAFLD?", "sentence2": "Non-alcoholic fatty Hepatobiliary Disorder (NAFLD) is the leading chronic hepatic condition worldwide and new approaches to management and treatment are limited. Non-alcoholic fatty Hepatobiliary Disorder (NAFLD) has become one of the most prominent forms of chronic Hepatobiliary Disorder worldwide, reflecting the epidemic of global obesity. Those with the progressive Variant of NAFLD, Nonalcoholic Steatohepatitis (NASH), are at significantly increased risk of multisystem morbidity and mortality. However, there are currently no approved pharmacologic therapies for NASH. Although much progress has been made in enhancing our understanding of NAFLD pathogenesis, development of pharmacologic treatments has been hindered by challenges in clinical trial enrollment and complexities in clinical trial design.  Nonalcoholic fatty Hepatobiliary Disorder (NAFLD) is the most prevalent Hepatobiliary Disorder worldwide, and there is no approved pharmacotherapy. Nonalcoholic fatty Hepatobiliary Disorder (NAFLD) has an increasing prevalence worldwide. At present, no specific pharmacotherapy is approved for NAFLD.[SEP]", "label": "no"}
{"original_question": "Can pazopanib be used for treatment von Hippel-Lindau disease?", "id": "converted_85", "sentence1": "Can pazopanib be used for treatment Von Hippel-Lindau Syndrome?", "sentence2": "Variable response of Clinical Nurse Specialists hemangioblastomas to pazopanib in a single patient with Von Hippel-Lindau Syndrome: Case report. Treatment of Renal Cell Carcinoma with Protein-tyrosine kinase inhibitor (disposition) (TKIs) such as pazopanib is now first line therapy, but their effect on VHL-associated Clinical Nurse Specialists Hemoglobin, Sickle remains unknown. We report the use of pazopanib in a patient with VHL disease for treatment of Conventional (Clear Cell) Renal Cell Carcinoma who also harbored multiple Clinical Nurse Specialists Hemoglobin, Sickle.  pazopanib in patients with Von Hippel-Lindau Syndrome: a single-arm, single-centre, phase 2 trial. INTERPRETATION: pazopanib was associated with encouraging preliminary activity in Von Hippel-Lindau Syndrome, with a side-effect profile consistent with that seen in previous trials. pazopanib could be considered as a treatment choice for patients with Von Hippel-Lindau Syndrome and growing Lesion, or to reduce the size of unresectable Lesion in these patients.  Recurrent multiple Clinical Nurse Specialists hemangioblastomas with VHL disease treated with pazopanib: a case report and literature review.  Here, we report a 37-year-old woman's case with recurrent and rapidly progressive VHL-associated hemangioblastomas, causing severe Disability:Type:Pt:^Patient:Nom. She was treated 24 months with pazopanib, a multityrosine kinase inhibitor (TKI) targeting Vascular Endothelial Growth Factor A and PDGF-\u03b2 pathways.  pazopanib therapy for Cerebellar Hemangioblastoma in Von Hippel-Lindau Syndrome: case report. Here we provide the first report demonstrating clinical and radiological anti-tumor response using pazopanib, a small molecule multi-receptor tyrosine kinase inhibitor, in a patient with treatment-refractory VHL-associated Clinical Nurse Specialists Hemangioblastoma.  pazopanib could be considered as a treatment choice for patients with Von Hippel-Lindau Syndrome and growing Lesion, or to reduce the size of unresectable Lesion in these patients. METHODS In this non-randomised, single-centre, open-label, phase 2 trial, adult patients with clinical manifestations of Von Hippel-Lindau Syndrome were recruited from the University of Texas MD Anderson Cancer Center (Houston, TX, USA) and were treated with pazopanib (800 mg orally daily) for 24 weeks, with an option to continue treatment if desired by the patient and treating physician. We aimed to assess the activity and safety of pazopanib in patients with Von Hippel-Lindau Syndrome. INTERPRETATION pazopanib was associated with encouraging preliminary activity in Von Hippel-Lindau Syndrome, with a side-effect profile consistent with that seen in previous trials. FINDINGS Between Jan 18, 2012, and Aug 10, 2016, we screened 37 patients with genetically confirmed or clinical features consistent with Von Hippel-Lindau Syndrome, of whom 31 eligible patients were treated with pazopanib. pazopanib therapy for Cerebellar Hemangioblastoma in Von Hippel-Lindau Syndrome: case report.von Hippel-Lindau (VHL) disease is a genetically acquired multisystem tumor syndrome of the Viscera and CENTRAL NERVOUS SYSTEM DIAGNOSTIC RADIOPHARMACEUTICALS (Clinical Nurse Specialists).  Recurrent multiple Clinical Nurse Specialists hemangioblastomas with VHL disease treated with pazopanib: a case report and literature review.Hemangioblastoma is a rare benign neoplasm, accounting for less than 2% of all primitive Brain Neoplasms.  We aimed to assess the activity and safety of pazopanib in patients with Von Hippel-Lindau Syndrome.<br><b>METHODS</b>: In this non-randomised, single-centre, open-label, phase 2 trial, adult patients with clinical manifestations of Von Hippel-Lindau Syndrome were recruited from the University of Texas MD Anderson Cancer Center (Houston, TX, USA) and were treated with pazopanib (800 mg orally daily) for 24 weeks, with an option to continue treatment if desired by the patient and treating physician. This study is registered with ClinicalTrials.gov, number NCT01436227, and is closed to accrual.<br><b>FINDINGS</b>: Between Jan 18, 2012, and Aug 10, 2016, we screened 37 patients with genetically confirmed or clinical features consistent with Von Hippel-Lindau Syndrome, of whom 31 eligible patients were treated with pazopanib. Treatment-related serious adverse events included one case each of Appendicitis and Gastritis and one patient had a fatal Clinical Nurse Specialists bleed.<br><b>INTERPRETATION</b>: pazopanib was associated with encouraging preliminary activity in Von Hippel-Lindau Syndrome, with a side-effect profile consistent with that seen in previous trials. pazopanib could be considered as a treatment choice for patients with Von Hippel-Lindau Syndrome and growing Lesion, or to reduce the size of unresectable Lesion in these patients. We aimed to assess the activity and safety of pazopanib in patients with Von Hippel-Lindau Syndrome. In this non-randomised, single-centre, open-label, phase 2 trial, adult patients with clinical manifestations of Von Hippel-Lindau Syndrome were recruited from the University of Texas MD Anderson Cancer Center (Houston, TX, USA) and were treated with pazopanib (800 mg orally daily) for 24 weeks, with an option to continue treatment if desired by the patient and treating physician. pazopanib was associated with encouraging preliminary activity in Von Hippel-Lindau Syndrome, with a side-effect profile consistent with that seen in previous trials. pazopanib could be considered as a treatment choice for patients with Von Hippel-Lindau Syndrome and growing Lesion, or to reduce the size of unresectable Lesion in these patients. Between Jan 18, 2012, and Aug 10, 2016, we screened 37 patients with genetically confirmed or clinical features consistent with Von Hippel-Lindau Syndrome, of whom 31 eligible patients were treated with pazopanib.[SEP]", "label": "yes"}
{"original_question": "Is Netrin-1 a secreted protein?", "id": "converted_86", "sentence1": "Is NTN1 gene a secreted Protein Info?", "sentence2": "The axon guidance cues netrin-1 is a secreted Protein Info overexpressed in many different Primary malignant neoplasm tissues NTN1 gene is a secreted Protein Info that directs long-range axon guidance during early stages of neural circuit formation and continues to be expressed in the mammalian forebrain during the postnatal period of peak synapse formation.   NTN1 gene, a Laminin-related secreted Protein Info, displays proto-oncogenic activity in Malignant Neoplasms. NTN1 gene, a multifunctional secreted Protein Info, is up-regulated in Primary malignant neoplasm and Inflammation. etrin-1 is a Laminin-related secreted Protein Info, is highly induced after Tissue injury, and may serve as a marker of injury. Netrins are a family of secreted Protein Info related to Laminin and act as tropic cues directing axon growth and cell migration during neural development.[SEP]", "label": "yes"}
{"original_question": "Is the yeast (Saccharomyces cerevisiae) genome organized into topologically associated domains (TADs)?", "id": "converted_87", "sentence1": "Is the yeast (Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae) Genome - anatomical entity organized into topologically associated domains (Tietz syndrome)?", "sentence2": "Recent advances in our understanding of the three-dimensional organization of the eukaryotic nucleus have rendered the spatial distribution of Genes increasingly relevant. In a recent work (Tsochatzidou et al., Nucleic Acids Res 45:5818-5828, 2017), we proposed the existence of a functional compartmentalization of the yeast Genome - anatomical entity according to which, Genes occupying the chromosomal regions at the nuclear periphery have distinct structural, functional and evolutionary characteristics compared to their centromeric-proximal counterparts. Around the same time, it was also shown that the Genome - anatomical entity of Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae is organized in topologically associated domains (Tietz syndrome), which are largely associated with the replication timing. Form and function of topologically associating genomic domains in budding yeast. Although similar structures appear to be conserved in fission yeast, computational modeling and analysis of high-throughput chromosome conformation capture (Hi-C) data have been used to argue that the small, highly constrained budding yeast chromosomes could not have these structures. In contrast, herein we analyze Hi-C data for budding yeast and identify 200-kb scale Tietz syndrome, whose boundaries are enriched for transcriptional activity. Furthermore, these boundaries separate regions of similarly timed replication origins connecting the long-known effect of genomic context on replication timing to Genome - anatomical entity architecture. To investigate the molecular basis of aminoglutethimide/danazol/hydrocortisone/tamoxifen formation, we performed Hi-C experiments on Cells depleted for the Forkhead Transcription Factors, FOXO1 wt Allele and FOXG1 wt Allele, previously associated with replication timing. Forkhead factors do not regulate aminoglutethimide/danazol/hydrocortisone/tamoxifen formation, but do promote longer-range genomic interactions and control interactions between origins near the centromere. Thus, our work defines spatial organization within the budding yeast nucleus, demonstrates the conserved role of Genome - anatomical entity architecture in regulating DNA replication, and identifies a molecular mechanism specifically regulating interactions between pericentric origins. Around the same time, it was also shown that the Genome - anatomical entity of Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae is organized in topologically associated domains (Tietz syndrome), which are largely associated with the replication timing. Around the same time, it was also shown that the Genome - anatomical entity of Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae or Saccharomyces cerevisiae or Saccharomyces cerevisiae cerevisiae cerevisiae is organized in topologically associated domains (Tietz syndrome), which are largely associated with the replication timing.  In contrast, herein we analyze Hi-C data for budding yeast and identify 200-kb scale Tietz syndrome, whose boundaries are enriched for transcriptional activity.[SEP]", "label": "yes"}
{"original_question": "As of Feb 2019, are major brain gangliosides a target for the treatment of Alzheimer's disease?", "id": "converted_88", "sentence1": "As of Feb 2019, are major brain gangliosides a target for the treatment of ALZHEIMER DISEASE, FAMILIAL, 1?", "sentence2": "An understanding of the mechanism on the interaction of Ganglioside Ganglioside GM1 and A\u03b2s in cytarabine/daunorubicin protocol may contribute to the development of new neuroregenerative therapies for this disorder. Abnormal ganglioside metabolism also may occur in cytarabine/daunorubicin protocol brains Continuous intraventricular infusion of Ganglioside Ganglioside GM1 has recently been shown to have a significant beneficial effect in ALZHEIMER DISEASE 2 of early onset (cytarabine/daunorubicin protocol Type I). Gangliosides--a new therapeutic agent against Cerebrovascular accident and ALZHEIMER DISEASE, FAMILIAL, 1. Gangliosides--a new therapeutic agent against Cerebrovascular accident and ALZHEIMER DISEASE, FAMILIAL, 1.Gangliosides are glycosphingolipids localized to the outer leaflet of the Plasma membrane of vertebrate cells.  Continuous intraventricular infusion of Ganglioside Ganglioside GM1 has recently been shown to have a significant beneficial effect in ALZHEIMER DISEASE 2 of early onset (cytarabine/daunorubicin protocol Type I).<br>[SEP]", "label": "yes"}
{"original_question": "Is Miller-Dieker syndrome associated with abnormalities of chromosome 1?", "id": "converted_89", "sentence1": "Is Miller-Dieker syndrome associated with abnormalities of chromosome 1?", "sentence2": "A complete ophthalmic examination is not routinely performed on infants with Miller-Dieker syndrome (Miller Dieker syndrome, chromosome 17p13.3 microdeletion).  Chromosomes, Human, Pair 1 microdeletions within 17p13.3 can result in either isolated LISSENCEPHALY SYNDROME, NORMAN-ROBERTS TYPE sequence (Classical Lissencephaly) or Miller-Dieker syndrome (Miller Dieker syndrome).  We report a Fetus in fetu with LISSENCEPHALY SYNDROME, NORMAN-ROBERTS TYPE diagnosed as Miller-Dieker Syndrome postnatally. G banded chromosome analysis revealed 45,X,psu dic(17;Y)(p13;p11.32).ish dic (17;Y)(LIS1-,RARA+, SRY+, DYZ3+) by G-banding analysis using high resolution banding technique. Fetal delayed cortical development will be the findings to perform further investigations including fluorescence in situ hybridization analysis for Miller Dieker syndrome, a 17p13.3 microdeletion syndrome, pre/postnatally. This will be the first case of Miller Dieker syndrome with unbalanced translocation between deleted short arm of Chromosomes, Human, Pair 17 and Y chromosome.  We report the finding of a 2.5-Mb Genes region quadruplication of Chromosomes, Human, Pair 1 17p13.3. This region is well characterized for the Gene Deletion Abnormality leading to Miller-Dieker syndrome but has an unclear replication phenotype.  Both Gene Deletion have overlapped with the critical region of Miller-Dieker syndrome (Miller Dieker syndrome) and involved candidate genes such as PAFAH1B1 Genes Genes, YWHAE protein, Homo sapiens protein, Homo sapiens and CRK protein, Homo sapiens protein, Homo sapiens. In addition, SNP array and FISH analyses on the parental peripheral blood samples demonstrated that both 17p13.3 and 17p13.3p13.2 Gene Deletion were of de novo origin. Miller-Dieker syndrome (Miller Dieker syndrome) is caused by a heterozygous Gene Deletion Abnormality of chromosome 17p13.3 involving the genes LIS1 and YWHAE protein, Homo sapiens protein, Homo sapiens (coding for 14.3.3\u03b5) and leads to Aspects of congenital Aspects of congenital malformations during cortical development. We studied after Cessation of life a 3-month-old girl whose karyotype was 45,XX,-15,-17,+der(17),t(15;17)(q13;p13.3) and thus combines abnormalities of chromosome 15 associated with the Prader-Willi Syndrome and of Chromosomes, Human, Pair 17 associated with the Miller-Dieker syndrome. The Miller-Dieker syndrome (Miller Dieker syndrome), a syndrome with LISSENCEPHALY SYNDROME, NORMAN-ROBERTS TYPE, distinctive craniofacial features, growth impairment, and profound developmental failure, has been associated with a Gene Deletion Abnormality of the distal part of chromosome band 17p13. The Miller-Dieker syndrome (type I LISSENCEPHALY SYNDROME, NORMAN-ROBERTS TYPE) is a Malformations of Cortical Development, Group II which is associated with microdeletions in the short arm of Chromosomes, Human, Pair 17. Detection of submicroscopic Gene Deletion in band 17p13 in patients with the Miller-Dieker syndrome. A 15-month-old girl with Miller-Dieker syndrome, a contiguous Genes Gene Deletion Abnormality syndrome involving chromosome 17p13.3 and resulting in LISSENCEPHALY SYNDROME, NORMAN-ROBERTS TYPE, was diagnosed with Pre B-cell acute lymphoblastic leukemia. A computed tomography scan revealed evidence of LISSENCEPHALY SYNDROME, NORMAN-ROBERTS TYPE, and chromosomal analysis showed a microdeletion on the short arm of Chromosomes, Human, Pair 17 (17p13.3), confirming the diagnosis as Miller-Dieker syndrome. Familial Miller-Dieker syndrome associated with pericentric inversion of Chromosomes, Human, Pair 17. The Miller-Dieker syndrome (Miller Dieker syndrome), a rare Congenital Disorders manifested by characteristic facial abnormalities and LISSENCEPHALY SYNDROME, NORMAN-ROBERTS TYPE (smooth Head>Brain), is associated with microdeletions of the distal Mandibular left third molar prosthesis region. Miller-Dieker syndrome (Miller Dieker syndrome), a disorder manifesting the severe Head>Brain malformation LISSENCEPHALY SYNDROME, NORMAN-ROBERTS TYPE (\"smooth Head>Brain\"), is caused, in the majority of cases, by a chromosomal microdeletion of the distal short arm of Chromosomes, Human, Pair 17. The Miller-Dieker syndrome (Miller Dieker syndrome), composed of characteristic facial abnormalities and a severe Malformations of Cortical Development, Group II affecting the Cerebral cortex, is caused by visible or submicroscopic Gene Deletion of chromosome band 17p13. Microdeletions including YWHAE protein, Homo sapiens protein, Homo sapiens in the Miller-Dieker syndrome region on chromosome 17p13.3 result in facial dysmorphisms, growth restriction, and No No cognitive impairment. Identification of the functional PFN1 Genes, its localization to chromosome subband 17p13.3, and demonstration of its Gene Deletion Abnormality in some patients with Miller-Dieker syndrome. HIC1 gene Genes is a candidate tumor suppressor Genes which is frequently hypermethylated in Homo sapiens Neoplasms, and its location within the Miller-Dieker syndrome's critical Gene Deletion Abnormality region at chromosome 17p13.3 makes it a candidate Genes for involvement in this Genes Gene Deletion Abnormality syndrome. A complete ophthalmic examination is not routinely performed on infants with Miller-Dieker syndrome (Miller Dieker syndrome, chromosome 17p13.3 microdeletion). About 15% of patients with isolated LISSENCEPHALY SYNDROME, NORMAN-ROBERTS TYPE and more than 90% of patients with Miller-Dieker syndrome have microdeletions in a critical 350-kilobase region in chromosome 17p13.3 (ref. Chromosomes, Human, Pair 1 aberrations in which Epilepsy is a major and consistent finding include Angelman Syndrome due to loss of the maternal 15q11.2-q12 Anatomical segmentation, Tetrasomy of the maternal Anatomical segmentation 15pter-q13 due to an additional inv dup chromosome, Miller-Dieker syndrome due to Gene Deletion Abnormality of the 17p13.3 Anatomical segmentation including the lissencephaly1 Genes, Ring Chromosomes, Human, Pair 1 20 Syndrome, and Wolf-Hirschhorn Syndrome due to Gene Deletion Abnormality of at least the 4p16.3 Anatomical segmentation. Miller-Dieker syndrome and 5p partial trisomy in a child carrying a derivative chromosome with a microdeletion in 17p13.3 telomeric to the LIS1 and the D17S379 loci. The Miller-Dieker syndrome, a disorder of neuronal migration, is caused by Gene Deletion of chromosome 17p13.3. The girl was diagnosed by subtelomeric FISH and array-CGH, showing a 4.43-Mb heterozygous Gene Deletion Abnormality on chromosome 10p that involved 14 genes and a 3.22-Mb single-copy gain on chromosome Mandibular left third molar prosthesis, which includes the critical region of the Miller-Dieker syndrome and 61 genes. Detection of submicroscopic Gene Deletion in band 17p13 in patients with the Miller-Dieker syndrome.The Miller-Dieker syndrome (Miller Dieker syndrome), a syndrome with LISSENCEPHALY SYNDROME, NORMAN-ROBERTS TYPE, distinctive craniofacial features, growth impairment, and profound developmental failure, has been associated with a Gene Deletion Abnormality of the distal part of chromosome band 17p13.  Microdeletions including YWHAE protein, Homo sapiens protein, Homo sapiens in the Miller-Dieker syndrome region on chromosome 17p13.3 result in facial dysmorphisms, growth restriction, and No No cognitive impairment.Microdeletions of chromosome 17p13.3 involving YWHAE protein, Homo sapiens protein, Homo sapiens present with growth restriction, craniofacial dysmorphisms, structural abnormalities of Head>Brain and No No cognitive impairment.  Unbalanced translocation (15;17)(q13;13.3) with apparent Prader-Willi Syndrome but without Miller-Dieker syndrome.We studied after Cessation of life a 3-month-old girl whose karyotype was 45,XX,-15,-17,+der(17),t(15;17)(q13;p13.3) and thus combines abnormalities of chromosome 15 associated with the Prader-Willi Syndrome and of Chromosomes, Human, Pair 17 associated with the Miller-Dieker syndrome.  The Miller-Dieker syndrome (Miller Dieker syndrome), a rare Congenital Disorders manifested by characteristic facial abnormalities and LISSENCEPHALY SYNDROME, NORMAN-ROBERTS TYPE (smooth Head>Brain), is associated with microdeletions of the distal Mandibular left third molar prosthesis region.  A revision of the LISSENCEPHALY SYNDROME, NORMAN-ROBERTS TYPE and Miller-Dieker syndrome critical regions in chromosome 17p13.3.Miller-Dieker syndrome (Miller Dieker syndrome) is a multiple malformation syndrome characterized by classical LISSENCEPHALY SYNDROME, NORMAN-ROBERTS TYPE and a characteristic facies.  Case Report of Proliferative Peripheral retinopathy in Two Familial Lissencephaly Infants with Miller-Dieker Syndrome.A complete ophthalmic examination is not routinely performed on infants with Miller-Dieker syndrome (Miller Dieker syndrome, chromosome 17p13.3 microdeletion).  Identification of the functional PFN1 Genes, its localization to chromosome subband 17p13.3, and demonstration of its Gene Deletion Abnormality in some patients with Miller-Dieker syndrome.Profilin is a conserved actin-monomer-binding protein which is found in all Eukaryota, including Saccharomyces cerevisiae.  We propose that essentially no loss of Mandibular left third molar prosthesis material has occurred and confirm previous reports that the critical region for the production of the Miller-Dieker phenotype is located subterminally in the 17p13.3 region.<br> A review of the literature revealed five additional patients in three families, who had Miller-Dieker syndrome and an abnormality of Mandibular left third molar prosthesis. We propose that essentially no loss of Mandibular left third molar prosthesis material has occurred and confirm previous reports that the critical region for the production of the Miller-Dieker phenotype is located subterminally in the 17p13.3 region. Miller-Dieker syndrome: LISSENCEPHALY SYNDROME, NORMAN-ROBERTS TYPE and monosomy Mandibular left third molar prosthesis. Thus, we propose that monosomy of distal Mandibular left third molar prosthesis may be the cause of Miller-Dieker syndrome in some patients. Miller-Dieker syndrome with der(17)t(12;17)(q24.33;p13.3)pat presenting with a potential risk of mis-identification as a de novo submicroscopic Gene Deletion Abnormality of 17p13.3. Most cases of Miller-Dieker syndrome have a de novo Gene Deletion Abnormality involving 17p13.3.[SEP]", "label": "no"}
{"original_question": "Does the interaction of MOV10 and RNASEH2 promote L1 retrotransposition?", "id": "converted_90", "sentence1": "Does the interaction of MOV10 gene and RNASEH2 promote L1 retrotransposition?", "sentence2": "Interplay between RNASEH2 and MOV10 gene gene controls Long Interspersed Nucleotide Element-1 retrotransposition. We show that MOV10 gene gene interacts with RNASEH2, and their interplay is crucial for restricting L1 retrotransposition.  Furthermore, we show that RNASEH2-MOV10 gene gene-mediated L1 restriction downregulates expression of the rheumatoid arthritis-associated inflammatory cytokines and matrix-degrading proteinases in Synoviocytes, implicating a potential causal relationship between them and disease development in terms of disease predisposition.[SEP]", "label": "no"}
{"original_question": "Has the protein SIRT2 been associated to cervical cancer?", "id": "converted_91", "sentence1": "Has the protein Sirtuin 2 been associated to cervical cancer?", "sentence2": "A progressive increase in the expression of both Sirtuin 2 and NAD-Dependent Protein Deacetylase Sirtuin-7 was noted during cancer progression in the following order: normal\u2009<\u2009preneoplasia\u2009<\u2009cancer.  We demonstrate that treatment of cervical cancer cells with a RhoGDI\u03b1-derived K52-trifluoroacetylated, substrate-derived peptidic sirtuin PPP1R1A gene severely impairs cell proliferation.[SEP]", "label": "yes"}
{"original_question": "Are recessive coding variants responsible for the majority of undiagnosed nonconsanguineous individuals?", "id": "converted_92", "sentence1": "Are recessive coding variants responsible for the majority of undiagnosed nonconsanguineous individuals?", "sentence2": "Our results suggest that recessive coding variants account for a small fraction of currently undiagnosed nonconsanguineous individuals, and that the role of noncoding variants, incomplete penetrance, and polygenic mechanisms need further exploration.[SEP]", "label": "no"}
{"original_question": "Is the NLM medical text indexer (MTI) still useful and relevant?", "id": "converted_93", "sentence1": "Is the NLM medical text indexer (MTI) still useful and relevant?", "sentence2": "12 years on - Is the NLM medical text indexer still useful and relevant? Facing a growing workload and dwindling resources, the US National Library of Medicine (NLM) created the Indexing Initiative project in 1996. This cross-library team's mission is to explore indexing methodologies for ensuring quality and currency of NLM document collections. The NLM Medical Text Indexer (MTI) is the main product of this project and has been providing automated indexing recommendations since 2002. After all of this time, the questions arise whether MTI is still useful and relevant.METHODS: To answer the question about MTI usefulness, we track a wide variety of statistics related to how frequently MEDLINE indexers refer to MTI recommendations, how well MTI performs against Homo sapiens indexing, and how often MTI is used. To answer the question of MTI relevancy compared to other available tools, we have participated in the 2013 and 2014 BioASQ Challenges. The BioASQ Challenges have provided us with an unbiased comparison between the MTI system and other systems performing the same task.RESULTS: Indexers have continually increased their use of MTI recommendations over the years from 15.75% of the articles they index in 2002 to 62.44% in 2014 showing that the indexers find MTI to be increasingly useful. The MTI performance statistics show significant improvement in Precision (+0.2992) and F1 (+0.1997) with modest gains in Recall (+0.0454) over the years. MTI consistency is comparable to the available indexer consistency studies. MTI performed well in both of the BioASQ Challenges ranking within the top tier teams.CONCLUSIONS: Based on our findings, yes, MTI is still relevant and useful, and needs to be improved and expanded. The BioASQ Challenge results have shown that we need to incorporate more machine learning into MTI while still retaining the indexing rules that have earned MTI the indexers' trust over the years. We also need to expand MTI through the use of full text, when and where it is available, to provide coverage of indexing terms that are typically only found in the full text. The role of MTI at NLM is also expanding into new areas, further reinforcing the idea that MTI is increasingly useful and relevant. The role of MTI at NLM is also expanding into new areas, further reinforcing the idea that MTI is increasingly useful and relevant. CONCLUSIONS Based on our findings, yes, MTI is still relevant and useful, and needs to be improved and expanded. 12 years on - Is the NLM medical text indexer still useful and relevant?Based on our findings, yes, MTI is still relevant and useful, and needs to be improved and expanded.  The role of MTI at NLM is also expanding into new areas, further reinforcing the idea that MTI is increasingly useful and relevant. After all of this time, the questions arise whether MTI is still useful and relevant.<br><b>METHODS</b>: To answer the question about MTI usefulness, we track a wide variety of statistics related to how frequently MEDLINE indexers refer to MTI recommendations, how well MTI performs against Homo sapiens indexing, and how often MTI is used. The MTI performance statistics show significant improvement in Precision (+0.2992) and F<br><b>CONCLUSIONS</b>: Based on our findings, yes, MTI is still relevant and useful, and needs to be improved and expanded. The role of MTI at NLM is also expanding into new areas, further reinforcing the idea that MTI is increasingly useful and relevant.<br> After all of this time, the questions arise whether MTI is still useful and relevant. The role of MTI at NLM is also expanding into new areas, further reinforcing the idea that MTI is increasingly useful and relevant. Based on our findings, yes, MTI is still relevant and useful, and needs to be improved and expanded.[SEP]", "label": "yes"}
{"original_question": "Has strimvelis been approved by the European Medicines Agency?", "id": "converted_94", "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 (acetaldehyde dehydrogenase (acetylating) activity-SCID) who lack a suitable matched related bone marrow donor.[SEP]", "label": "yes"}
{"original_question": "Is treatment with Bacillus Calmette Guerin used for bladder cancer?", "id": "converted_95", "sentence1": "Is treatment with Bacillus Calmette Guerin used for Urinary Bladder cancer?", "sentence2": "Intravesical Bacillus Calmette-Guerin (BCG) is the best treatment modality for progression of non-muscle invasive Urinary Bladder cancer.  this result indicates that they may be used as putative biomarkers for monitoring changes in Urinary Bladder carcinogenesis in response to BCG immunotherapy. response of urothelial precancerous lesions to intravesical BCG treatment Urinary Bladder cancer (BC Original Formula Original Formula) is a major clinical issue.METHODS: We performed immunohistochemistry to assess the role of Homo sapiens epidermal growth factor receptor-2 (HER-2-neu peptide vaccine-neu peptide vaccine) and microsatellite instability (Microsatellite Instability) factors MutL homologue 1 (MLH1 gene gene) and MutS homologue 2 (DNA Mismatch Repair Protein DNA Mismatch Repair Protein MSH2, human, Homo sapiens) in predicting recurrence and progression of SLC25A4 gene high-grade BCs having undergone transurethral resection of Urinary Bladder tumor (Transurethral resection of neoplasm of Urinary Bladder) alone or Transurethral resection of neoplasm of Urinary Bladder\u2009+\u2009intravesical instillations of bacillus Calmette-Guerin (BCG). To evaluate the efficacy and safety of a tailored endovesical immunotherapy protocol with biweekly BCG for elderly Patients with high risk non muscle invasive Urinary Bladder cancer  Bacillus of Calmette-Guerin (BCG) therapy for high risk non muscle invasive Urinary Bladder cancer treatment in older patients. BCG (Bacillus of Calmette Guerin) has been used for more than 20 years and is currently the most active agent for superficial Urinary Bladder cancer therapy. BCG (Bacillus of Calmette Guerin) therapy of high-risk superficial Urinary Bladder cancer. Production of interleukin-5 binding activity, a classical T(H)2 cytokine, following bacillus Calmette guerin immunotherapy of Urinary Bladder cancer. Intravesical Bacillus Calmette-Guerin is used to treat patients with superficial Urinary Bladder cancer. There is some evidence that BCG therapy improves survival and progression rates of patients with high-risk superficial Urinary Bladder cancer decreasing the proportion who require radical cystectomy. Local immunotherapy with bacillus Calmette-Guerin (BCG) is an effective and frequently used treatment for superficial Urinary Bladder cancer. CONCLUSIONS Intravesical bacillus Calmette-Guerin is a viable therapeutic option in patients with high risk superficial Urinary Bladder cancer and concomitant Lymphoma or Chronic Lymphocytic Leukemia, treatment with low dose oral steroids or treatment with inhaled steroids. PURPOSE Bacillus Calmette-Guerin is the most effective therapy for nonmuscle invasive Urinary Bladder cancer. INTRODUCTION Bacillus Calmette-Guerin (BCG) is a live attenuated strain of Mycobacterium bovis that has been used to treat Urothelial Carcinoma since 1976, and has been reported to eradicate disease in more than 70% of patients with in situ and stage I disease. Intravesical administration of bacillus Calmette-Guerin has been shown to be highly effective treatment of superficial Urinary Bladder cancer. Intravesical bacillus Calmette-Guerin therapy for superficial Urinary Bladder cancer: effect of bacillus Calmette-Guerin viability on treatment results. We describe a 53 year- old man with a disseminated bacillus Calmette-Guerin (BCG) infection after intravescical instillation for Urinary Bladder carcinoma. We tested the hypothesis that tumor expression of natural cytotoxicity receptor ligands can serve as a Disease Predictive Factor for the response to intravesical bacillus Calmette-Guerin in patients with nonmuscle invasive, high grade Urinary Bladder cancer. Bacillus Calmette-Guerin immunotherapy has been found by a number of investigators to be effective in the treatment and prevention of superficial Urinary Bladder cancer. Pancreatic Hormones Hormones and Psoas Abscess as a late complication of intravesical administration of bacillus Calmette-Guerin for Urinary Bladder cancer: a case report and review of the literature.This case illustrates the fact that although intravesical administration of bacillus Calmette-Guerin is generally considered to be safe, it is not exempt from complications and these could appear immediately after treatment or as a delayed complication many years later. Effects of local bacillus Calmette-Guerin therapy in patients with Urinary Bladder carcinoma on immunocompetent Cells of the Urinary Bladder wall.The antitumoral effects of intravesical bacillus Calmette-Guerin against recurrent superficial urothelial Urinary Bladder cancer seem to be linked to immunological effector mechanisms.  Fatal Sepsis (Invertebrate) following intravesical bacillus Calmette-Guerin administration for Urinary Bladder cancer.Intravesical administration of bacillus Calmette-Guerin has been shown to be highly effective treatment of superficial Urinary Bladder cancer.  Intravesical bacillus Calmette-Guerin therapy for superficial Urinary Bladder cancer: effect of bacillus Calmette-Guerin viability on treatment results.We treated 40 patients with superficial Urinary Bladder cancer via intravesical bacillus Calmette-Guerin for 1) prophylaxis against tumor recurrence, 2) residual carcinoma or 3) flat carcinoma in situ.  Bacillus Calmette-Guerin immunotherapy for Urinary Bladder cancer.Bacillus Calmette-Guerin immunotherapy has been found by a number of investigators to be effective in the treatment and prevention of superficial Urinary Bladder cancer.  Safety and efficacy of intravesical bacillus Calmette-Guerin instillations in Steroids treated and immunocompromised patients.Intravesical bacillus Calmette-Guerin is a viable therapeutic option in patients with high risk superficial Urinary Bladder cancer and concomitant Lymphoma or Chronic Lymphocytic Leukemia, treatment with low dose oral steroids or treatment with inhaled steroids.  Our results suggest that intralesional bacillus Calmette-Guerin immunotherapy can afford long term protection from transplanted Urinary Bladder cancer, and that live bacillus Calmette-Guerin is superior to levamisole and P3 + Re-glycolipid + bacillus Calmette-Guerin cell walls in the treatment of Urinary Bladder cancer. A randomized controlled prospective evaluation of intravesical and percutaneous bacillus Calmette-Guerin immunotherapy was done in 57 patients with Carcinoma, Transitional Cell of the Urinary Bladder. Up to 90% of patients with high grade superficial Urinary Bladder tumors experience tumor recurrence and up to 50% have progression despite bacillus Calmette-Guerin treatment. We review how the bacillus Calmette-Guerin vaccine evolved to become standard therapy for superficial Urinary Bladder cancer. We reviewed the historical literature describing the origin of the bacillus Calmette-Guerin vaccine as an anticancer agent and its singular success as the most effective immunotherapy used against a Homo sapiens neoplasm.[SEP]", "label": "yes"}
{"original_question": "Is eculizumab used for treatment of myasthenia gravis?", "id": "converted_96", "sentence1": "Is eculizumab used for treatment of Myasthenia Gravis?", "sentence2": "Eculizumab treatment improved symptoms compared with placebo in a phase II study in patients with refractory gMG. D Eculizumab (Soliris) has been approved in several countries for refractory forms of generalized seropositive severe Myasthenia Gravis.  The humanized monoclonal antibody eculizumab (Soliris\u00ae) is a complement inhibitor indicated for use in anti-acetylcholine receptor (AChR) antibody-positive adults with generalized Myasthenia Gravis (gMG) in the USA, refractory gMG in the EU, or gMG with symptoms that are difficult to control with high-dose IVIg therapy or PLEX in Japan.  Although several questions remain, such as duration of treatment, cost effectiveness and long-term efficacy and tolerability, current evidence indicates that eculizumab is a valuable emerging therapy for patients with refractory gMG. The 2 exceptions are Acetylcholinesterase Inhibitors and complement inhibition with eculizumab, which was recently approved by the US Food and Drug Administration for Myasthenia Gravis. INTRODUCTION A phase 2 study of eculizumab for treating Myasthenia Gravis (MG) used the quantitative Myasthenia Gravis score (QMG) and Myasthenia Gravis activities of daily living profile (MG-ADL) to evaluate baseline disease severity and treatment response. QMG and MG-ADL correlations: Study of eculizumab treatment of Myasthenia Gravis. rituximab seems to be particularly effective in MuSK Myasthenia Gravis, and eculizumab arises as an option in refractory AChR Myasthenia Gravis. Results from a phase 2 study suggested that eculizumab, a terminal complement inhibitor, produced clinically meaningful improvements in patients with anti-acetylcholine receptor antibody-positive refractory generalised Myasthenia Gravis. Safety and efficacy of eculizumab in anti-acetylcholine receptor antibody-positive refractory generalised Myasthenia Gravis (REGAIN): a phase 3, randomised, double-blind, placebo-controlled, multicentre study. The humanized monoclonal antibody eculizumab (Soliris\u00ae) is a complement inhibitor indicated for use in anti-acetylcholine receptor (AChR) antibody-positive adults with generalized Myasthenia Gravis (gMG) in the USA, refractory gMG in the EU, or gMG with symptoms that are difficult to control with high-dose IVIg therapy or PLEX in Japan. Eculizumab (Soliris) has been approved in several countries for refractory forms of generalized seropositive severe Myasthenia Gravis. Eculizumab: A Review in Generalized Myasthenia Gravis. A randomized, double-blind, placebo-controlled phase II study of eculizumab in patients with refractory generalized Myasthenia Gravis. Eculizumab: A Review in Generalized Myasthenia Gravis.)  <b>INTRODUCTION</b>: A phase 2 study of eculizumab for treating Myasthenia Gravis (MG) used the quantitative Myasthenia Gravis score (QMG) and Myasthenia Gravis activities of daily living profile (MG-ADL) to evaluate baseline disease severity and treatment response. Correlations were then analyzed between these assessments.<br><b>METHODS</b>: Patients were given eculizumab or placebo during the first 16-week treatment period of the crossover study, with treatment assignments reversed for the second treatment period following a 5-week washout. A phase 2 study of eculizumab for treating Myasthenia Gravis (MG) used the quantitative Myasthenia Gravis score (QMG) and Myasthenia Gravis activities of daily living profile (MG-ADL) to evaluate baseline disease severity and treatment response. The 2 exceptions are Acetylcholinesterase Inhibitors and complement inhibition with eculizumab, which was recently approved by the US Food and Drug Administration for Myasthenia Gravis.[SEP]", "label": "yes"}
{"original_question": "Can cardiospheres be produced from skin fibroblasts?", "id": "converted_97", "sentence1": "Can cardiospheres be produced from skin fibroblasts?", "sentence2": "Therefore, there is an emerging interest in generating cardiosphere-like stem cells from Diploid Cell via somatic reprogramming.  Here we provide the detailed protocol for generating induced cardiospheres (iCS) for cardiac regeneration by somatic reprogramming of mouse fibroblasts using a panel of pluripotent transcription factors and cardiotrophic growth factors.[SEP]", "label": "yes"}
{"original_question": "Does Axitinib prolong survival of Pancreatic Cancer patients?", "id": "converted_98", "sentence1": "Does Axitinib prolong survival of Pancreatic Cancer patients?", "sentence2": "CONCLUSIONS: Axitinib/gemcitabine, while tolerated, did not provide survival benefit over gemcitabine alone in patients with advanced Malignant neoplasm of pancreas from Japan or other regions. RESULTS: Among Japanese patients, median overall survival was not estimable (95% confidence interval, 7.4 months-not estimable) with axitinib/gemcitabine (n = 58) and 9.9 months (95% confidence interval, 7.4-10.5) with placebo/gemcitabine (n = 56) (hazard ratio 1.093 [95% confidence interval, 0.525-2.274]). Median survival follow-up (range) was 5.1 months (0.02-12.3) with axitinib/gemcitabine vs. 5.4 months (1.8-10.5) with placebo/gemcitabine. Similarly, no difference was detected in overall survival between axitinib/gemcitabine and placebo/gemcitabine in patients from North America or the European Union.  At an interim analysis in January, 2009, the independent data monitoring committee concluded that the futility boundary had been crossed. Median overall survival was 8\u00b75 months (95% CI 6\u00b79-9\u00b75) for gemcitabine plus axitinib (n=314, data missing for two patients) and 8\u00b73 months (6\u00b79-10\u00b73) for gemcitabine plus placebo (n=316; hazard ratio 1\u00b7014, 95% CI 0\u00b7786-1\u00b7309; one-sided p=0\u00b75436).  INTERPRETATION: The addition of axitinib to gemcitabine does not improve overall survival in advanced Malignant neoplasm of pancreas.  INTERPRETATION The addition of axitinib to gemcitabine does not improve overall survival in advanced Malignant neoplasm of pancreas. However, as with other Protein Tyrosine Kinase inhibitors of the same class, axitinib does not prolong overall survival; therefore, selection of second-line Protein Tyrosine Kinase inhibitor therapy, including axitinib, must be carefully considered to maximize outcomes for each patient. CONCLUSIONS Axitinib/gemcitabine, while tolerated, did not provide survival benefit over gemcitabine alone in patients with advanced Malignant neoplasm of pancreas from Japan or other regions. Similarly, no difference was detected in overall survival between axitinib/gemcitabine and placebo/gemcitabine in patients from North America or the European Union. Axitinib/gemcitabine, while tolerated, did not provide survival benefit over gemcitabine alone in patients with advanced Malignant neoplasm of pancreas from Japan or other regions. The addition of axitinib to gemcitabine does not improve overall survival in advanced Malignant neoplasm of pancreas.[SEP]", "label": "no"}
{"original_question": "Is there any association between suicide and autism in adolescents, yes or no?", "id": "converted_99", "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 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. 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]", "label": "yes"}
{"original_question": "Is lactotransferrin a tumour suppressor?", "id": "converted_100", "sentence1": "Is lactotransferrin a tumour suppressor?", "sentence2": "LTF protein, human protein, human (lactotransferrin, or LTF protein, human gene) plays important role in innate immunity, and its anti-tumor function has also been reported in multiple cancers. We previously reported that LTF protein, human protein, human is significantly down-regulated in nasopharyngeal carcinoma (Nasopharyngeal carcinoma) and acts as a tumor suppressor by suppressing Proto-Oncogene Proteins c-akt signaling. The tumor suppressor function of lactotransferrin (LTF protein, human protein, human) has been reported in a variety of Neoplasms, including GC, nasopharyngeal carcinoma (Nasopharyngeal carcinoma) and Malignant neoplasm of prostate. LTF protein, human gene (LTF protein, human protein, human) has been confirmed to act as a tumor suppressor in multiple cancers LTF protein, human gene acts as a tumor suppressor in nasopharyngeal carcinoma by repressing Proto-Oncogene Proteins c-akt through multiple mechanisms. LTF protein, human protein, human is likely to be a candidate tumor suppressor and downregulates the development of Nasopharyngeal carcinoma by inhibiting Nasopharyngeal carcinoma proliferation through induction of cell cycle arrest and modulation of the MAPK signaling pathway.[SEP]", "label": "yes"}
{"original_question": "Are there tools for visualizing and processing long-read sequencing data?", "id": "converted_101", "sentence1": "Are there tools for visualizing and processing long-read sequencing data?", "sentence2": "NanoPack: visualizing and processing long-read sequencing data. Here we describe NanoPack, a set of tools developed for visualization and processing of long-read sequencing data from Oxford Nanopore Technologies and Pacific Biosciences.Availability and implementation: The NanoPack tools are written in Python3 and released under the GNU GPL3.0 License. The source code can be found at https://github.com/wdecoster/nanopack, together with links to separate scripts and their documentation. The scripts are compatible with Linux, Mac OS and the MS Windows 10 subsystem for Linux and are available as a graphical user interface, a web service at http://nanoplot.bioinf.be and command line tools. Summary Here we describe NanoPack, a set of tools developed for visualization and processing of long-read sequencing data from Oxford Nanopore Technologies and Pacific Biosciences. NanoPack: visualizing and processing long-read sequencing data.Supplementary data are available at Bioinformatics online. <b>Summary</b>: Here we describe NanoPack, a set of tools developed for visualization and processing of long-read sequencing data from Oxford Nanopore Technologies and Pacific Biosciences.<br><b>Availability and implementation</b>: The NanoPack tools are written in Python3 and released under the GNU GPL3.0 License. Here we describe NanoPack, a set of tools developed for visualization and processing of long-read sequencing data from Oxford Nanopore Technologies and Pacific Biosciences.[SEP]", "label": "yes"}
{"original_question": "Has Hesperidin any role as a Neuroprotective Agent?", "id": "converted_102", "sentence1": "Has hesperidin any role as a Neuroprotective Agent?", "sentence2": "Neuroprotective effect of hesperetin and nano-hesperetin on recognition memory impairment and the elevated oxygen stress in rat model of Alzheimer's disease hesperidin attenuates depression-related symptoms in CASP14 gene with mild Traumatic Brain Injury Neuroprotective Effects of hesperidin on Cerebral Vasospasm The neuroprotective effect of hesperidin in NMDA-induced retinal injury acts by suppressing oxidative stress and excessive calpain activation. This study suggests a potential neuroprotective role of hesperidin against 3-NP-induced Huntington's disease-like manifestations. hesperidin potentiates the neuroprotective effects of diazepam and gabapentin against pentylenetetrazole-induced convulsions in CASP14 gene: Possible behavioral, biochemical and mitochondrial alterations. hesperidin, a flavanoglycone abundantly present in Fruit, Citrus, is reported to have antioxidant, anti-inflammatory, and neuroprotective properties. PURPOSE hesperidin, a Cardiac Glycosides Flavonoids, is thought to act as an anti-Primary malignant neoplasm agent, since it has been found to exhibit both pro-apoptotic and anti-proliferative effects in several Primary malignant neoplasm cell types. hesperidin is a flavonone Cardiac Glycosides, belonging to the Flavonoids family, which is widely found in Citrus species and acts as a potent antioxidant and anticancer agent. BACKGROUND hesperidin, a flavanone present in Fruit, Citrus, has been identified as a potent anticancer agent because of its proapoptotic and antiproliferative characteristics in some Tumor cells, uncertain whether benign or malignant. Oxidative stress and Primary malignant neoplasm; the role of hesperidin, a citrus natural bioflavonoid, as a Primary malignant neoplasm chemoprotective agent. Our data suggests that hesperidin exerts its neuroprotective effect against rotenone due to its antioxidant, maintenance of mitochondrial function, and antiapoptotic properties in a Neuroblastoma cell line. Taken together, these results demonstrate potent antioxidant and neuroprotective effects of hesperetin, implying its potential role in protecting Neurons against various types of insults associated with many neurodegenerative diseases. The neuroprotective effect of hesperidin in NMDA-induced retinal injury acts by suppressing oxidative stress and excessive calpain activation.We found that hesperidin, a plant-derived bioflavonoid, may be a candidate agent for neuroprotective treatment in the retina, after screening 41 materials for anti-oxidative properties in a primary retinal cell culture under oxidative stress.  Neuroprotective effects of hesperidin, a plant flavanone, on rotenone-induced oxidative stress and apoptosis in a cellular model for Parkinson Disease.Rotenone a widely used Pesticides that inhibits NADH dehydrogenase (ubiquinone) has been used to investigate the pathobiology of Lugano Lymphoma Response Classification Progressive Disease by PET both in vitro and in vivo.  Cytoprotective effects of hesperetin and hesperidin against amyloid \u03b2-induced impairment of glucose transport through downregulation of neuronal autophagy. hesperidin potentiates the neuroprotective effects of diazepam and gabapentin against pentylenetetrazole-induced convulsions in CASP14 gene: Possible behavioral, biochemical and mitochondrial alterations.TMPRSS11A gene possesses potent anticonvulsant activity which might be mediated through modulation of gamma-amino butyric acid/benzodiazepine receptor action. Antioxidant and neuroprotective effects of hesperidin and its aglycone hesperetin.The present study evaluated antioxidant and neuroprotective activities of hesperidin, a flavanone mainly isolated from Fruit, Citrus, and its aglycone hesperetin using cell-free bioassay system and primary cultured rat cortical cells.  Potential neuroprotective effects of hesperidin on 3-nitropropionic acid-induced Neurotoxicity Syndromes in Rattus norvegicus. hesperidin inhibits glutamate release and exerts neuroprotection against excitotoxicity induced by Kainic Acid in the Hippocampus Hippocampus hippocampus of Rattus norvegicus. Emerging evidences indicate hesperidin, a citrus flavanone, attenuates neurodegenerative processes and related complications. Potential anti-inflammatory effects of hesperidin from the genus Citrus. Antioxidant and neuroprotective effects of hesperidin and its aglycone hesperetin. hesperidin is a Flavonoids present in high concentration in citrus species and has numerous biological properties, principally antioxidant and anti-inflammatory.[SEP]", "label": "yes"}
{"original_question": "Are apoE mimetics being considered as a treatment against Alzheimer's disease?", "id": "converted_103", "sentence1": "Are Apolipoprotein E mimetics being considered as a treatment against Alzheimer's disease?", "sentence2": "The apolipoprotein-E-mimetic COG112 protects Amyloid beta-Protein Precursor intracellular domain-overexpressing animals from Alzheimer's disease-like pathological features. Studies show that administration of apolipoprotein E (Apolipoprotein E) and Apolipoprotein E-derived small Peptides mimetics protect AD mouse models against these AD-like features.[SEP]", "label": "yes"}
{"original_question": "Can you computationally predict Molecular Recognition Features (MoRFs) regions in Intrinsically Disordered Proteins (IDPs)?", "id": "converted_104", "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 Protein Sequences 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 Protein Sequences. 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 Protein Sequences 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 Sequence 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]", "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_105", "sentence1": "Velocardial facial syndrome, otherwise known as DiGeorge 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 (DiGeorge 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 DiGeorge Syndrome The 22q11.2 Gene Deletion Abnormality syndrome (di George syndrome) is one of the most prevalent genetic disorders. UNLABELLED Most of the children with DiGeorge 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 DiGeorge Syndrome. 22q11.2DS has several presentations including Di George's 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%). DiGeorge 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 DiGeorge Syndrome and 60% of patients with velocardiofacial syndrome exhibit a microdeletion within Chromosomes, Human, Pair 1 22q11.  22q11.2DS has several presentations including Di George's 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 DiGeorge Syndrome and 60% of patients with velocardiofacial syndrome exhibit a microdeletion within Chromosomes, Human, Pair 1 22q11. Most of the children with DiGeorge Syndrome and 60% of patients with velocardiofacial syndrome exhibit a microdeletion within Chromosomes, Human, Pair 1 22q11.[SEP]", "label": "no"}
{"original_question": "Is the protein Asporin related to disease?", "id": "converted_106", "sentence1": "Is the protein Asporin related to disease?", "sentence2": "Accumulating evidence demonstrates the involvement of ASPN gene in OSTEOARTHRITIS SUSCEPTIBILITY 1 pathogenesis. Asporin has been reported as a tumor suppressor in Malignant neoplasm of breast, while ASPN gene-activated invasion has been described in Malignant neoplasm of stomach. Asporin has been implicated as an Oncogenes in various types of Homo sapiens Malignant Neoplasms;   These results suggested that ASPN gene promoted the tumor growth and metastasis of Cytogenetic Complete Response, and it could be a potential therapeutic target for Cytogenetic Complete Response patients in future. Our results suggest that ASPN is a stromally expressed biomarker that correlates with disease progression, and is observed in reactive stroma.[SEP]", "label": "yes"}
{"original_question": "Can TAD disruption lead to disease?", "id": "converted_107", "sentence1": "Can aminoglutethimide/danazol/hydrocortisone/tamoxifen disruption lead to Disease?", "sentence2": "its perturbation will lead to Homo sapiens Disease, highlighting the accumulating evidence that links the diverse 3 Days Genome - anatomical entity architecture components to a multitude of Homo sapiens diseases and the emerging mechanisms by which 3 Days Genome - anatomical entity derangement causes Disease phenotypes. aminoglutethimide/danazol/hydrocortisone/tamoxifen boundaries are insulators of genomic neighborhoods. In this issue, Sun et\u00a0al. show that Disease-associated tandem repeats are located to aminoglutethimide/danazol/hydrocortisone/tamoxifen boundaries and affect their insulation.  Recent studies of aminoglutethimide/danazol/hydrocortisone/tamoxifen boundaries disrupted in engineered mouse models show that boundary mutations can recapitulate Homo sapiens developmental disorders as a result of aberrant promoter-enhancer interactions in the affected Tietz syndrome Similar boundary disruptions in certain Malignant Neoplasms can result in Oncogenes overexpression, and CTCF binding sites at boundaries appear to be hyper-mutated across Malignant Neoplasms. the disruption of these structures by genomic rearrangements can result in gene misexpression and Disease. aminoglutethimide/danazol/hydrocortisone/tamoxifen disruption as oncogenic driver. Recent studies have shown that aminoglutethimide/danazol/hydrocortisone/tamoxifen disruption is often found in Tumor cells, malignant and contributes to oncogenesis through two mechanisms. Disruption of aminoglutethimide/danazol/hydrocortisone/tamoxifen boundaries results in aberrant gene expression by exposing Genes to inappropriate regulatory elements. However, it is not clear to which extent aminoglutethimide/danazol/hydrocortisone/tamoxifen regions are conserved in evolution and whether disruption of Tietz syndrome by evolutionary rearrangements can alter gene expression. Disruption of this organization by structural variations can lead to ectopic interactions between enhancers and Promoter, and to alteration of Genes expression patterns. Disruption of Tietz syndrome can result in altered gene expression and is associated to genetic diseases and Malignant Neoplasms. Gene Gene Deletion Abnormality Abnormality in 2q35 excluding the IHH gene leads to fetal severe limb anomalies and suggests a disruption of chromatin architecture. We demonstrate that disruption of Tietz syndrome can rewire long-range regulatory architecture and result in Pathogenic Variant phenotypes.  Disruption of aminoglutethimide/danazol/hydrocortisone/tamoxifen boundaries results in aberrant gene expression by exposing Genes to inappropriate regulatory elements.  Disruption of Tietz syndrome can result in altered gene expression and is associated to genetic diseases and Malignant Neoplasms.  Disruption of a aminoglutethimide/danazol/hydrocortisone/tamoxifen boundary causes ectopic chromosomal contacts and long-range transcriptional misregulation.  Recent studies of aminoglutethimide/danazol/hydrocortisone/tamoxifen boundaries disrupted in engineered mouse models show that boundary mutations can recapitulate Homo sapiens developmental disorders as a result of aberrant promoter-enhancer interactions in the affected Tietz syndrome.  Recent studies have shown that aminoglutethimide/danazol/hydrocortisone/tamoxifen disruption is often found in Tumor cells, malignant and contributes to oncogenesis through two mechanisms.  Disruption of this organization by structural variations can lead to ectopic interactions between enhancers and Promoter, and to alteration of Genes expression patterns.  Similar boundary disruptions in certain Malignant Neoplasms can result in Oncogenes overexpression, and CTCF binding sites at boundaries appear to be hyper-mutated across Malignant Neoplasms.  However, it is not clear to which extent aminoglutethimide/danazol/hydrocortisone/tamoxifen regions are conserved in evolution and whether disruption of Tietz syndrome by evolutionary rearrangements can alter gene expression.[SEP]", "label": "yes"}
{"original_question": "Is L-4F an apoE mimetic peptide?", "id": "converted_108", "sentence1": "Is L-4F an apoE mimetic peptide?", "sentence2": "APOA1 gene mimetic peptide 4F suppresses Tumor-Associated Macrophage and Malignant neoplasm of pancreas progression. L-4F, an APOA1 gene (APOA1 gene) mimetic peptide, is engineered to mimic the anti-inflammatory and anti-oxidative functionalities of APOA1 gene.[SEP]", "label": "no"}
{"original_question": "Can oleuropein aglycone interfere with amyloid aggregation?", "id": "converted_109", "sentence1": "Can oleuropein Aglycone interfere with Serum amyloid A protein aggregation?", "sentence2": "oleuropein, a Substance with phenol structure secoiroid glycoside, is the main polyphenols in the olive oil. It has been reported that the Aglycone form of oleuropein (Olea (plant)) interferes in vitro and in vivo with Serum Serum amyloid A protein A protein aggregation of a number of proteins/peptides involved in Serum Serum amyloid A protein A protein, particularly neurodegenerative, diseases avoiding the growth of toxic oligomers and displaying protection against Cognitive deterioration.[SEP]", "label": "yes"}
{"original_question": "Is Apelin usually decreased in diabetes?", "id": "converted_110", "sentence1": "Is APLN gene usually decreased in Diabetes Mellitus?", "sentence2": "APLN gene has been shown to act on Glucose measurement and lipid metabolism but also to modulate insulin secretion. Moreover, different studies in both animal allergen extracts and Homo sapiens have shown that plasma APLN protein, human concentrations are usually increased during BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20 and type 2 Diabetes Mellitus. Upregulated expression of RETN protein, human, SERPINA12 gene, APLN protein, human and TNF-\u03b1 plays a significant role in induction of insulin resistance linked with BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20 and type 2 Diabetes Mellitus. Moreover, different studies in both animal allergen extracts and Homo sapiens have shown that plasma APLN protein, human concentrations are usually increased during BODY MASS INDEX QUANTITATIVE TRAIT LOCUS 20 and type 2 Diabetes Mellitus. APLN gene levels are increased in morbidly obese subjects with Diabetes Mellitus, Noninsulin-Dependent, 3. In men at risk for Diabetes Mellitus (HbA1c 5.7-6.4%, FPG 100-125mg/dl, or OGTT-2h-PG 140-199mg/dl), the risk for developing Diabetes Mellitus was higher in those with higher plasma APLN protein, human concentration than in those with lower plasma APLN protein, human concentrations (10.6%/year vs. 5.1%/year, p<0.001).<br><b>CONCLUSIONS</b>: Plasma APLN protein, human is a novel biomarker for predicting type 2 Diabetes Mellitus in men.<br>[SEP]", "label": "no"}
{"original_question": "Is actin present in the nucleus?", "id": "converted_111", "sentence1": "Is Actins present in the nucleus?", "sentence2": "Moreover, inhibition of ATM kinase or deficiency in Nuclear (incident type) Actins polymerization causes carcinogenic RET/PTC chromosome rearrangements after DSBs induction in Human cells.  Our findings establish that Nuclear (incident type) Actins-based mobility shapes chromatin organization by generating repair domains that are essential for homology-directed repair in Eukaryotic Cells. The discovery of Nuclear (incident type) Actins opened new perspective on the field, suggesting that the Nuclear (incident type) activities of Actins reflect the functions of primordial Actins-like proteins.  The revitalization of research into Nuclear (incident type) Actins occurred after it was found that cellular stresses induce the Nuclear (incident type) localization and alter the structure of Actins.  While it is long known that Actins is part of the Nuclear (incident type) proteome, its properties and functions as regulated, functional and dynamically assembled Microfilaments are only recently emerging.[SEP]", "label": "yes"}
{"original_question": "Can miR-122 target RUNX2?", "id": "converted_112", "sentence1": "Can miR-122 target RUNX2 gene?", "sentence2": "MIR122 gene functions as a tumor suppressor by inhibiting proliferation and inducing apoptosis, which is achieved by directly targeting RUNX2 gene gene.[SEP]", "label": "yes"}
{"original_question": "Tocilizumab is an anti-TNF antibody, yes or no?", "id": "converted_113", "sentence1": "Tocilizumab is an anti-Recombinant Tumor Necrosis Factor Family Protein antibody, yes or no?", "sentence2": "was treated with tocilizumab, an anti-interleukin-6 receptor monoclonal antibody CAL CAL  Tocilizumab (TCZ) is a humanized monoclonal antibody CAL CAL against Recombinant Interleukin-6\u00a0receptor licensed in 2009 that has demonstrated clinical efficacy in various adult Rheumatoid Arthritis populations. Rheumatoid Arthritis management guidelines and recommendations consider TCZ as one of the bDMARDS indicated after methotrexate or other conventional synthetic DMARDs and/or Recombinant Tumor Necrosis Factor Family Protein inhibitors failure in adult Rheumatoid Arthritis Tocilizumab (Roactemra or Actemra) is a recombinant humanized monoclonal antibody CAL CAL that acts as an interleukin (IL)-6 receptor antagonist. METHODS Patients (n = 93) were treated with an anti-Recombinant Interleukin-6 receptor antibody (tocilizumab) or Recombinant Tumor Necrosis Factor Family Protein-\u03b1 inhibitors for 16 weeks. The recent development of biological agents, namely, anti-tumour necrosis factor alpha (Recombinant Tumor Necrosis Factor Family Protein-\u03b1) agents (infliximab, adalimumab and etanercept), anti- ocaratuzumab CAL (rituximab) and anti-interleukin 6 receptor (interleukin-6 receptor activity) monoclonal antibody CAL CAL (tocilizumab), represents a major breakthrough for the treatment of immune-mediated disorders. Recently, an anti-Recombinant Interleukin-6 receptor monoclonal antibody CAL CAL, tocilizumab, has been licensed for the treatment as monotherapy or in combination with methotrexate of moderate to severe Rheumatoid Arthritis, when disease modifying anti-rheumatic drugs or anti-tumour necrosis factors (Recombinant Tumor Necrosis Factor Family Protein) have failed. Tocilizumab is a monoclonal humanized anti-Recombinant Interleukin-6-receptor antibody used for the treatment of rheumatoid arthritis. Indeed, worldwide clinical trials of Recombinant Tumor Necrosis Factor Family Protein inhibiting biologic disease modifying antirheumatic drugs (bDMARDs) including infliximab, adalimumab, golimumab, certolizumab pegol, and etanercept as well as the humanized anti-human Recombinant Interleukin-6 receptor antibody, tocilizumab, have demonstrated outstanding clinical efficacy and tolerable safety profiles, resulting in worldwide approval for using these bDMARDs to treat moderate to severe active Rheumatoid Arthritis in patients with an inadequate response to synthetic disease modifying antirheumatic drugs (sDMARDs). Tocilizumab is a humanized anti-Recombinant Interleukin-6 receptor monoclonal antibody CAL CAL, which binds to circulating soluble Recombinant Interleukin-6 receptor and membrane-expressed Recombinant Interleukin-6 receptor, inhibiting Recombinant Interleukin-6 binding to both forms of Recombinant Interleukin-6 receptor. Subsequent options include a Recombinant Tumor Necrosis Factor Family Protein-alpha antagonist, followed by rituximab or possibly abatacept; (2) Tocilizumab, a monoclonal antibody CAL CAL, inhibits interleukin-6 receptors. Tocilizumab (TCZ) is a monoclonal antibody CAL CAL which inhibits the interleukin-6 receptor.[SEP]", "label": "no"}
{"original_question": "Is it possible to analyze exosomes with FACS?", "id": "converted_114", "sentence1": "Is it possible to analyze Exosomes with Fluorescence-Activated Cell Sorting?", "sentence2": "whose presence was validated by a bead-exosome Fluorescence-Activated Cell Sorting assay. We analyzed Exosomes from Mouse antigen (C57Bl/6) and Breast, Chest>Lung, and Malignant neoplasm of ovary patient samples and cultured cancer cells with different approaches, including nanoparticle tracking analysis, biolayer interferometry, Fluorescence-Activated Cell Sorting, and electron microscopy. we applied a technique to generate native fluorescent Exosomes characterized by Vesicle (morphologic abnormality) integrity, size, density, markers expression, and quantifiable by direct Fluorescence-Activated Cell Sorting analysis we used a novel strategy for generating metabolically-labeled fluorescent Exosomes that can be counted by flow cytometry assay (Fluorescence-Activated Cell Sorting) and characterized.[SEP]", "label": "yes"}
{"original_question": "Can prevnar 13 be used in children?", "id": "converted_115", "sentence1": "Can prevnar 13 be used in children?", "sentence2": "PCV13 is approved for routine vaccination of all infants as a 4-dose series at age 2, 4, 6, and 12-15 months for children who previously received 1 or more doses of the 7-valent pneumococcal conjugate vaccine (PCV7), and for children with underlying medical conditions that increase their risk for pneumococcal disease or its complications.  Based on published immunogenicity and safety data, as well as the recent recommendations by the ACIP for routine use in infants and indications for high-risk pediatric patients, PCV13 is a revised formulation of pneumococcal vaccine that should be included on pharmacy formularies. To review the immunogenicity, efficacy, and safety of the 13-valent pneumococcal conjugate vaccine (PCV13) for use in pediatric patients.[SEP]", "label": "yes"}
{"original_question": "Was stelara developed by Amgen?", "id": "converted_116", "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\u00ae, Janssen, Inc., Horsham, newton per square metre, USA) is recommended after anti-tumour necrosis factor failure.[SEP]", "label": "no"}
{"original_question": "Can mitochondria pass through membrane nanotubes?", "id": "converted_117", "sentence1": "Can Mitochondria pass through membrane nanotubes?", "sentence2": "Membrane nanotubes (MNTs) act as \"highways\" between Cells to facilitate the transfer of multiple signals and play an important role in many diseases. Our previous work reported on the transfer of Mitochondria via MNTs between Myocytes, Cardiac (Myasthenic Syndromes, Congenital) and cardiac myofibroblasts (MFs) Membrane nanotubes play important functional roles in numerous cell activities such as cellular transport and communication.[SEP]", "label": "yes"}
{"original_question": "Are protamines ubiquitously expressed?", "id": "converted_118", "sentence1": "Are protamines ubiquitously expressed?", "sentence2": "protamines are Nuclear Proteins which are specifically expressed in haploid male Germ Cells.[SEP]", "label": "no"}
{"original_question": "Are Crocus sativus compounds being considered against Alzheimer's disease?", "id": "converted_119", "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 A\u03b2 pathological manifestations.[SEP]", "label": "yes"}
{"original_question": "Are there any anti-amyloid antibody approved as drug for Alzheimer's disease treatment?", "id": "converted_120", "sentence1": "Are there any anti-amyloid antibody approved as Pharmacologic Substance for ALZHEIMER DISEASE, FAMILIAL, 1 treatment?", "sentence2": "Treatment with memantine, a noncompetitive NMDA receptor Substance with receptor Substance with receptor antagonist mechanism of action (substance) mechanism of action (substance) which is an approved Pharmacologic Substance for treatment of ALZHEIMER DISEASE, FAMILIAL, 1, rescued protein phosphatase-2A activity by decreasing its demethylation at Leu309 selectively and attenuated ALZHEIMER DISEASE, FAMILIAL, 1-like pathology and cognitive impairment in adeno-associated virus vector-1-I1PP2A Rattus norvegicus.  anti-Amyloid agents (13.30%) no new drugs have been approved during the past 15\u00a0years; and the available medications are not cost-effective.[SEP]", "label": "no"}
{"original_question": "Do Crocus sativus extracts loosen the blood-brain barrier?", "id": "converted_121", "sentence1": "Do Crocus sativus antigen extracts loosen the Blood - brain barrier function?", "sentence2": "Crocus sativus antigen antigen Extract Tightens the Blood-Brain Barrier, Reduces Amyloid \u03b2 Load and Related Toxic effect in 5XFAD Mice. In vitro results showed that Crocus sativus antigen antigen extract increases the Tightness sensation quality of a cell-based Blood - brain barrier function (Blood - brain barrier anatomy) model and enhances transport of A\u03b2. Further in vivo studies confirmed the effect of Crocus sativus antigen antigen extract (50 mg/kg/day, added to mice diet) on the Blood - brain barrier anatomy Tightness sensation quality and function that was associated with reduced A\u03b2 load and related pathological changes in 5XFAD mice used as an cytarabine/daunorubicin protocol model. Reduced A\u03b2 load could be explained, at least in part, by Crocus sativus antigen antigen extract effect to enhance A\u03b2 clearance pathways including Blood - brain barrier anatomy clearance, enzymatic degradation and ApoE clearance pathway.[SEP]", "label": "no"}
{"original_question": "Are artificial blood cells available?", "id": "converted_122", "sentence1": "Are artificial blood cells available?", "sentence2": "The critical point for the break through for artificial blood products did not come yet but could be ahead- We suggest a novel method that uses artificial blood cells (hemoglobin vesicles, Hb-Vs) as photosensitizers in dye laser treatment (at 595-nm wavelength) for Port-Wine Stain (i.e., Capillary malformation (disorder) presenting as red birthmarks) based on the results of Animal allergens experiments.[SEP]", "label": "no"}
{"original_question": "Have apolipoprotein mimetics been used in clinical trials?", "id": "converted_123", "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": "Is the Philadelphia chromosome a fusion between parts of chromosomes 1 and 9?", "id": "converted_124", "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]", "label": "no"}
{"original_question": "Can therapeutic levels of  Vedolizumab be found in the breast milk of nursing mothers following treatment for Inflammatory bowel disease?", "id": "converted_125", "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 vedolizumab 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]", "label": "no"}
{"original_question": "Does RUNX2 inhibit astrocyte differentiation?", "id": "converted_126", "sentence1": "Does RUNX2 gene inhibit astrocyte differentiation?", "sentence2": "The method was able to recapitulate experimentally validated cell-fate determinants, and validation of two predicted cell-fate determinants confirmed that overexpression of estrogen receptor alpha, human and RUNX2 gene gene in mouse neural stem cells induces neuronal and astrocyte differentiation, respectively.[SEP]", "label": "no"}
{"original_question": "Are cardenolides inhibitors of Na+/K+ ATPase?", "id": "converted_127", "sentence1": "Are cardenolides inhibitors of Na+/K+ ATPase?", "sentence2": ". Previously, we reported that a variety of cardenolides impart anti-transmissible gastroenteritis Genus: Coronavirus (TGEV) activity in Sus scrofa testicular (ST) cells, through targeting of the Cellular Membrane sodium/potassium pump, Na+/K+-ATPase.  : We found evidence for low cardenolides by HPLC, but substantial Toxic effect when extracts were assayed on Na+ /K+ -ATPases. Cardenolides have shown significant antitumor activity due to their ability to inhibit the Na+K+ATPase Enzyme [APC], and the expression of this Enzyme [APC] is increased in Tumor cells, uncertain whether benign or malignant.[SEP]", "label": "yes"}
{"original_question": "Can antisense threapy be used for Huntington's disease?", "id": "converted_128", "sentence1": "Can antisense threapy be used for Huntington Disease?", "sentence2": "In this issue of Neurons, Kordasiewicz et\u00a0al. (2012) show the benefit of transient antisense oligonucleotide (ASO) therapy to degrade Hodgkin Disease protein, human mRNA and elicit sustained therapeutic benefit in Hodgkin Disease CASP14 gene. \"Hodgkin Disease protein, human holiday\": progress toward an antisense therapy for Huntington Disease.[SEP]", "label": "yes"}
{"original_question": "Is collagen matrix of human articular cartilage changing with disease?", "id": "converted_129", "sentence1": "Is collagen Matrix Pharmaceutical Inc. of human Structure of articular cartilage changing with Disease?", "sentence2": "The collagen Matrix Pharmaceutical Inc. 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 Pharmaceutical Inc.. 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]", "label": "no"}
{"original_question": "Is ustekinumab a polyclonal antibody?", "id": "converted_130", "sentence1": "Is ustekinumab a polyclonal antibody?", "sentence2": "Ustekinumab Ab Ab, a Homo sapiens monoclonal IgG1 antibody targeting the p40-subunit shared by interleukin (IL)12 and interleukin-23 binding activity, represents a potential treatment for Dermatitis, Atopic (cytarabine/daunorubicin protocol).[SEP]", "label": "no"}
{"original_question": "Is Pim-1 a protein phosphatase?", "id": "converted_131", "sentence1": "Is Pim-1 a protein phosphatase?", "sentence2": "Pim-1 proto-oncogene, AURKA gene (PIM-1) phosphorylates a series of substrates to exert its oncogenic function in numerous Malignant Neoplasms. The PIM1 gene is associated with multiple cellular functions including proliferation, survival, differentiation, apoptosis, tumorigenesis, immune regulation and Inflammation in Vertebrates.[SEP]", "label": "no"}
{"original_question": "Is myc a tumour suppressor gene?", "id": "converted_132", "sentence1": "Is myc a tumour suppressor gene?", "sentence2": "oncogenic MYC protein, human, a master transcription factor that turns on anabolic metabolism to promote cell growth in many Malignant Neoplasms.  he MYC gene  the proto-oncogene protein c-MYC however, other Genes such as the c-myc Proto-Oncogenes are promising targets for anticancer therapy[SEP]", "label": "no"}
{"original_question": "Is CD63 an exosomal marker?", "id": "converted_133", "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]", "label": "yes"}
{"original_question": "Is subdural empyema a complication of sinusitis?", "id": "converted_134", "sentence1": "Is Subdural space Empyema a complication of sinusitis?", "sentence2": "Acute and chronic sinusitis can give rise to a wide array of Intracranial Route of Drug Administration and orbital complications. These complications include Cerebral abscess, Subdural space Empyema,  A computed tomography scan showed bilateral Nasal sinus disease, and magnetic resonance imaging showed a right frontal abscess and Subdural space Empyema. Frontal Sinusitis complicated by a Cerebral abscess and Subdural space Empyema. In older children, sinusitis and Ear Inflammation media are usually the source for Subdural space empyem Empyema, Subdural as a complication of sinusitis in the pediatric population. Second, Subdural space Empyema appears to arise in the setting of subacute rather than acute frontal sinusitis. Empyema, Subdural is a rare but potentially life-threatening complication following paranasal sinusitis and should be considered as a neurological emergency. [Empyema, Subdural as a complication of sinusitis. INTRODUCTION Empyema, Subdural is an uncommon but serious complication of sinusitis. Intracranial Subdural space Empyema is most frequently a complication of sinusitis or, less frequently, Ear Inflammation or neurosurgical procedures. Empyema, Subdural is a rare complication of sinusitis although very severe. Empyema, Subdural is a rare complication of sinusitis in children. Empyema, Subdural is a rare but serious complication of paranasal sinusitis which may result in Cessation of life or permanent disability in a significant proportion of cases. We report a case of Subdural space Empyema secondary to frontal sinusitis in an otherwise healthy immunocompetent adolescent boy. Empyema, Subdural is a rare but life-threatening complication of paranasal sinusitis, Ear Inflammation media, or mastoid disease. Wolf in Sheep's Clothing Subdural Empyema: A Rare Complication of Acute Sinusitis. Interhemispheric and Infratentorial Subdural Empyema with Preseptal cellulitis as Complications of Sinusitis: A Case Report. Empyema, Subdural as a complication of sinusitis in the pediatric population.<AbstractText Label=\"OBJECTIVE\" NlmCategory=\"OBJECTIVE\">Sinusitis is a rare cause of Intracranial Route of Drug Administration Communicable Diseases in children.  [Empyema, Subdural as a complication of sinusitis.  Intracranial Subdural space Empyema is most frequently a complication of sinusitis or, less frequently, Ear Inflammation or neurosurgical procedures.  Streptococcus pluranimalium: A novel Homo sapiens pathogen?<AbstractText Label=\"INTRODUCTION\" NlmCategory=\"BACKGROUND\">We present the first case of a Subdural space Empyema caused by Streptococcus pluranimalium, in a healthy adolescent male as a possible complication of subclinical frontal sinusitis.  <AbstractText Label=\"DISCUSSION\" NlmCategory=\"CONCLUSIONS\">The diagnosis of Subdural space Empyema as a complication of asymptomatic sinusitis in an immunocompetent patient with no history of Fever symptoms (finding) or upper respiratory symptoms was unanticipated.  Second, Subdural space Empyema appears to arise in the setting of subacute rather than acute frontal sinusitis.  Bifrontal decompressive craniectomy for acute Subdural space Empyema.<AbstractText Label=\"INTRODUCTION\" NlmCategory=\"BACKGROUND\">Empyema, Subdural is an uncommon but serious complication of sinusitis.  Empyema, Subdural is a rare but potentially life-threatening complication following paranasal sinusitis and should be considered as a neurological emergency.  We present a patient with Subdural space Empyema in whom the diagnosis was delayed, followed by a discussion of Infection - Infection - suppurative complications of sinusitis.  <AbstractText Label=\"CASE REPORT\" NlmCategory=\"METHODS\">We report an unusual case of sinusitis-associated acute Subdural space Empyema in a 13-year-old patient, presenting in a catastrophic manner with acutely raised Intracranial Route of Drug Administration pressure.  The symptoms of Subdural space Empyema may be mild and may be the same as those associated with sinusitis, or the Communicable Diseases may result in alteration of the level of consciousness and Focal Neurologic Deficits. We report the clinical and radiological course of an adolescent with a Subdural space Empyema secondary to sinusitis. We report two cases of Subdural space Empyema secondary to sinusitis in persons without impaired immunity. Empyema, Subdural as a complication of sinusitis. Furthermore, Subdural space Empyema usually is related to sinus infections, particularly those caused by Streptococcus milleri, an anaerobic Organism. Empyema, Subdural is an uncommon but serious complication of sinusitis.[SEP]", "label": "yes"}
{"original_question": "Anaplasma phagocytophilum is an obligate gram-negative, intracellular bacterium, yes  or no", "id": "converted_135", "sentence1": "Anaplasma phagocytophilum is an obligate gram-negative, Intracellular bacterium, yes  or no", "sentence2": "The genus Anaplasma belonging to the Anaplasmataceae family (order Rickettsiales) comprises obligate Intracellular Gram-negative bacteria of veterinary and public health importance. Six species and five types of strains genetically related are currently assigned to the genus Anaplasma including Anaplasma marginale, A. centrale, A. bovis, A. phagocytophilum, A. ovis and A. platys as classified species, and \"A. capra\", A. odocolei sp. nov. Human granulocytic anaplasmosis (HGA), an increasingly recognized febrile tick-borne illness, is caused by a gram-negative obligate Intracellular bacterium Anaplasma phagocytophilum[SEP]", "label": "yes"}
{"original_question": "Is the crystal structure of Pim-1 available?", "id": "converted_136", "sentence1": "Is the crystal structure of Pim-1 available?", "sentence2": "Recent crystallographic studies of Pim-1 have identified unique structural features but have not provided insight into how the MAP Kinase Kinase Kinase recognizes its target substrates.  a co-crystal structure of lead molecule (HS38) in complex with DAPK3 gene gene, a dual Pim/DAPK3 gene gene inhibitor (HS56) The crystal structure of this fluoromethyl 2,2-difluoro-1-(trifluoromethyl)vinyl ether with PIM1 confirmed the predicted binding mode and Protein Info-ligand interactions except those in the acidic ribose pocket.  Using the determined X-ray crystal structure of PIM1 complexed to the fluoromethyl 2,2-difluoro-1-(trifluoromethyl)vinyl ether 1-R as a control, we discuss the importance of including the Protein Info flexibility inherent in the ensemble docking protocol, for the accuracy of the structure prediction of the bound state.  Here, we describe the crystal structure of LONP1 gene in complex with a newly developed pyrido[4,3-d]pyrimidine-derivative inhibitor (SKI-O-068). Crystallographic and docking data analyses have been undertaken using inhibitor complexes  The crystal structures of LONP1 gene in apo form and bound with Adenylyl Imidodiphosphate have been solved[SEP]", "label": "yes"}
{"original_question": "Do tumour-associated macrophages have a prognostic role in gliomas?", "id": "converted_137", "sentence1": "Do tumour-associated macrophages have a prognostic role in Glioma?", "sentence2": "Increasing evidence suggests that tumour-associated macrophages/microglia (TAMs) facilitate tumour progression by acquiring a M2-like phenotype. Our objective was to investigate the prognostic value of TAMs in Glioma using automated quantitative double immunofluorescence. This is the first study to use automated quantitative immunofluorescence to determine the prognostic impact of TAMs. Our results suggest that M2-like TAMs hold an unfavourable prognostic value in high-grade Glioma and may contribute to a pro-tumourigenic microenvironment. Our data revealed that the amount of especially MSR1 wt Allele+ TAMs increases with malignancy grade. In grade III-IV, high MSR1 wt Allele expression was associated with shorter survival, while high IBA-1 intensity correlated with a longer survival. In grade IV, MSR1 wt Allele showed independent prognostic value when adjusting for clinical data and the methylation status of O6-methylguanine-DNA methyltransferase.[SEP]", "label": "yes"}
{"original_question": "Is TNF-\u03b1 an activator of pancreatic stellate cells?", "id": "converted_138", "sentence1": "Is TNF-\u03b1 an activator of Pancreatic Stellate Cells?", "sentence2": "TNF-\u03b1 is the prime factor responsible for the activation of Pancreatic Stellate Cells Activated PSCs expressed interleukin-33 receptor binding in the Cell Nucleus, and the expression was increased by IL-1\u03b2, TNF-\u03b1, becaplermin, and IFN-\u03b3, but not TGF-\u03b21.[SEP]", "label": "yes"}
{"original_question": "Can mitochondria transfer from cell to cell?", "id": "converted_139", "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]", "label": "yes"}