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2,329,400
The Course and Neonatal Outcome of Choroid Plexus Extension to the Anterior Horn at the Routine Anatomy Scan.
Our objective was to examine the pregnancy course and immediate neonatal outcome of fetuses with an isolated extension of choroid plexus (CP) to the anterior horn during the second trimester.</AbstractText>We prospectively collected the cases referred to us between July 2012 and January 2021 with isolated finding of CP extension to the anterior horn. Relevant clinical and demographic information was recorded, and a full anatomy scan including a comprehensive neurosonogram was performed. In cases of confirmed isolated extension of CP to the anterior horns, women were offered further investigation including fetal MRI, and ultrasound follow up.</AbstractText>We collected 29 eligible cases for analysis. The mean gestational age (GA&#x2009;&#xb1;&#x2009;SD) for diagnosis and referral was 19.24&#x2009;&#xb1;&#x2009;2.3&#x2009;weeks. No other intracranial anomalies were detected in any of the cases, and the finding resolved at 25&#x2009;&#xb1;&#x2009;2.6&#x2009;weeks. The average extension length and width to the anterior horn were 0.7&#x2009;&#xb1;&#x2009;0.3&#xa0;cm, and 0.5&#x2009;&#xb1;&#x2009;0.1&#xa0;cm, respectively. Eleven fetuses (38%) had choroid plexus cyst (CPC) in addition to the extension. Ten patients (35%) completed a fetal brain MRI, with no identified abnormalities. Gross neurological exam and Apgar score at birth were normal.</AbstractText>Extension of CP to anterior horn with or without CPC at mid-trimester seems to have spontaneous resolution with likely a good prognosis and no further implications.</AbstractText>&#xa9; 2022 American Institute of Ultrasound in Medicine.</CopyrightInformation>
2,329,401
Hypothalamic insulin expression remains unaltered after short-term fasting in female rats.
Our previous study showed that 6-h fasting increased insulin expression in the hypothalamus of male rats. We, therefore, wanted to examine if this phenomenon occurs in female rats and whether it depended on the estrus cycle phase.</AbstractText>Female rats in proestrus or diestrus were either exposed to 6-h fasting or had ad libitum access to food. The serum, cerebrospinal fluid, and hypothalamic insulin levels were determined using radioimmunoassay. The hypothalamic insulin mRNA expression was measured by RT-qPCR, while the hypothalamic insulin distribution was assessed immunohistochemically.</AbstractText>Albeit the short-term fasting lowered circulating insulin, both hypothalamic insulin mRNA expression and hypothalamic insulin content remained unaltered. As for the hypothalamic insulin distribution, strong insulin immunopositivity was noted primarily in ependymal cells lining the upper part of the third ventricle and some neurons mainly located within the periventricular nucleus. The pattern of insulin distribution was similar between the controls and the females exposed to fasting regardless of the estrous cycle phase.</AbstractText>The findings of this study indicate that the control of insulin expression in the hypothalamus differs from that in the pancreatic beta cells during short-term fasting. Furthermore, they also imply that the regulation of insulin expression in the female hypothalamus is different from males but independent of the estrus cycle phase.</AbstractText>&#xa9; 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</CopyrightInformation>
2,329,402
Nicotinamide Mononucleotide Adenylyl Transferase 2 Inhibition Aggravates Neurological Damage after Traumatic Brain Injury in a Rat Model.
Nicotinamide mononucleotide adenylyl transferase 2 (NMNAT2) is a crucial factor for the survival of neuron. The role of NMNAT2 in damage following traumatic brain injury (TBI) remains unknown. This study was designed to investigate the role of NMNAT2 in TBI-induced neuronal degeneration and neurological deficits in rats.</AbstractText>The TBI model was established in Sprague-Dawley rats by a weight-dropping method. Real-time polymerase chain reaction, western blot, immunofluorescence, Fluoro-Jade C staining, and neurological score analyses were carried out.</AbstractText>NMNAT2 mRNA and protein levels were increased in the injured-side cortex at 6 hours and peaked 12 hours after TBI. Knocking down NMNAT2 with an injection of small interfering RNA in lateral ventricle significantly exacerbated neuronal degeneration and neurological deficits after TBI, which were accompanied by increased expression of BCL-2-associated X protein (Bax).</AbstractText>NMNAT2 expression is increased and NMNAT2 exhibits neuroprotective activity in the early stages after TBI, and Bax signaling pathway may be involved in the process. Thus, NMNAT2 is likely to be an important target to prevent secondary damage following TBI.</AbstractText>
2,329,403
An Unusual Case of Malignant Melanoma with Metastasis to the Placenta During Pregnancy.
We describe an unusual case of metastatic melanoma of the brain with an unknown primary site during pregnancy.</AbstractText>A 35-year-old woman in the third trimester of pregnancy presented with ataxia, nausea, vomiting, headaches and diplopia. CT of the brain revealed a hyper-attenuating 2.1 cm mass in the fourth ventricle with mild obstructive hydrocephalus. A healthy newborn was delivered by urgent caesarean section. Craniotomy and resection of the brain lesion confirmed melanoma. Pathology of the placenta reported a 'focal nest of melanocytes identified in intervillous space'.</AbstractText>Brain and maternal placenta pathology findings were consistent with melanoma, making this case relevant because of the possibility of metastatic melanoma in a fetus.</AbstractText>Epidemiological data on congenital and infantile melanoma are scarce. Also, there is no database for long-term follow-up of children born to pregnant mothers with metastatic melanoma. Delayed presentation of melanoma in the child cannot be ruled out.</AbstractText>Melanoma brain metastasis is an uncommon initial presentation during pregnancy.During pregnancy, vague symptoms such as headaches and nausea can easily be attributed to the pregnancy itself rather than more serious conditions like cancer.Metastatic melanoma diagnosed during pregnancy with disease in the placenta is a rare occurrence and should trigger close follow-up of the neonate secondary to concerns of transplacental metastasis.</AbstractText>&#xa9; EFIM 2022.</CopyrightInformation>
2,329,404
Partial Obstruction of Ventricular Catheters Affects Performance in a New Catheter Obstruction Model of Hydrocephalus.
One of the major causes of cerebral ventricular shunt failure is proximal catheter occlusion. We describe a novel ventricular cerebrospinal fluid (CSF) flow replicating system that assesses pressure and flow responses to varying degrees of catheter occlusion.</AbstractText>Ventricular catheter performance was assessed during conditions of partial and complete occlusion. The catheters were placed into a three-dimensionally-printed phantom ventricular replicating system. Artificial CSF was pumped through the ventricular system at a constant rate of 1 mL/min to mimic CSF flow, with the proximal end of the catheter in the phantom ventricle. Pressure transducer and flow rate sensors were used to measure intra-phantom pressure, outflow pressure, and CSF flow rates. The catheters were also inserted into silicone tubing and pressure was measured in the same manner for comparison with the phantom.</AbstractText>Pressure measured in the ventricle phantom did not change when the outflow of the ventricular catheter was partially occluded. However, the intraventricular phantom pressure significantly increased when the outflow catheter was 100% occluded. The flow through the catheter showed no significant difference in rate with any degree of partial occlusion of the catheter. At the distal end of the partially occluded catheters, there was less pressure compared with the nonoccluded catheters. This difference in pressure in partially occluded catheters correlated with the percentage of catheter hole occlusion.</AbstractText>Our model mimics the physiological dynamics of the CSF flow in partially and completely obstructed ventricular catheters. We found that partial occlusion of the catheter had no effect on the CSF flow rate, but did reduce outflow pressure from the catheter.</AbstractText>
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Vitamin C Deficiency Reduces Neurogenesis and Proliferation in the SVZ and Lateral Ventricle Extensions of the Young Guinea Pig Brain.
Although scurvy, the severe form of vitamin C deficiency, has been almost eradicated, the prevalence of subclinical vitamin C deficiency is much higher than previously estimated and its impact on human health might not be fully understood. Vitamin C is an essential molecule, especially in the central nervous system where it performs numerous, varied and critical functions, including modulation of neurogenesis and neuronal differentiation. Although it was originally considered to occur only in the embryonic brain, it is now widely accepted that neurogenesis also takes place in the adult brain. The subventricular zone (SVZ) is the neurogenic niche where the largest number of new neurons are born; however, the effect of vitamin C deficiency on neurogenesis in this key region of the adult brain is unknown. Therefore, through BrdU labeling, immunohistochemistry, confocal microscopy and transmission electron microscopy, we analyzed the proliferation and cellular composition of the SVZ and the lateral ventricle (LVE) of adult guinea pigs exposed to a vitamin-C-deficient diet for 14 and 21 days. We found that neuroblasts in the SVZ and LVE were progressively and significantly decreased as the days under vitamin C deficiency elapsed. The neuroblasts in the SVZ and LVE decreased by about 50% in animals with 21 days of deficiency; this was correlated with a reduction in BrdU positive cells in the SVZ and LVE. In addition, the reduction in neuroblasts was not restricted to a particular rostro-caudal area, but was observed throughout the LVE. We also found that vitamin C deficiency altered cellular morphology at the ultrastructural level, especially the cellular and nuclear morphology of ependymal cells of the LVE. Therefore, vitamin C is essential for the maintenance of the SVZ cell populations required for normal activity of the SVZ neurogenic niche in the adult guinea pig brain. Based on our results from the guinea pig brain, we postulate that vitamin C deficiency could also affect neurogenesis in the human brain.
2,329,406
Meridianins Inhibit GSK3&#x3b2; In Vivo and Improve Behavioral Alterations Induced by Chronic Stress.
Major depression disorder (MDD) is a severe mental alteration with a multifactorial origin, and chronic stress is one of the most relevant environmental risk factors associated with MDD. Although there exist some therapeutical options, 30% of patients are still resistant to any type of treatment. GSK3&#x3b2; inhibitors are considered very promising therapeutic tools to counteract stress-related affectations. However, they are often associated with excessive off-target effects and undesired secondary alterations. Meridianins are alkaloids with an indole framework linked to an aminopyrimidine ring from Antarctic marine ascidians. Meridianins could overcome several of the aforementioned limitations since we previously demonstrated that they can inhibit GSK3&#x3b2; activity without the associated neurotoxic or off-target effects in rodents. Here, we show that meridianins delivered into the lateral ventricle inhibited GSK3&#x3b2; in several brain regions involved with stress-related symptoms. We also observed changes in major signaling pathways in the prefrontal cortex (Akt and PKA) and hippocampus (PKC and GluR1). Moreover, meridianins increased synaptic activity, specifically in the CA1 but not in the CA3 or other hippocampal subfields. Finally, we chronically treated the mice subjected to an unpredictable mild chronic stress (CUMS) paradigm with meridianins. Our results showed improvements produced by meridianins in behavioral alterations provoked by CUMS. In conclusion, meridianins could be of therapeutic interest to patients with stress-related disorders such as MDD.
2,329,407
Extraventricular site indicates higher grade but better prognosis in adult supratentorial ependymomas: a 14-year single-center retrospective cohort.
Supratentorial extraventricular ependymoma (STEE) and supratentorial intraventricular ependymoma (STIE) are two subsets of supratentorial ependymoma (SE). These two subsets have similar gene features and only differ in original sites: STEE occurs in the brain parenchyma, and STIE is located in ventricles and surrounded by cerebral spinal fluid. The present study aims to depict the diversities of these two subsets and elucidate the potential effects of the anatomic site on the tumor with the same type, grade, and molecular features. Sixty-six consecutive adult SE patients from 2008 to 2021 were enrolled in our study. Clinical data, pathological features, and long-term outcomes were analyzed retrospectively. Results demonstrated that adult STEE presented with a higher proportion of WHO grade 3 (P = .028) and higher Ki-67 index (&#x2265;10%) (P = .019) compared to adult STIE. Survival analysis demonstrated that patients of grade 3 STEE exhibited a significantly longer overall survival (OS) than patients of grade 3 STIE (median OS, 24.4 months vs. 13.0 months; P = .004). Grade 2 (hazard ratio (HR) = 0.217; P &lt; .001) and gross total resection (GTR) (HR = 0.156; P &lt; .001) were identified as favorable prognostic factors for all adult SE. The STEE was also associated with a lesser hazard of death for patients of grade 3 on multivariate analysis (HR = 0.263; P = .047). These findings suggested that the extraventricular site was an indicator for higher grade and better prognosis in adult supratentorial ependymoma.
2,329,408
Longitudinal in Utero Analysis of Engrailed-1 Knockout Mouse Embryonic Phenotypes Using High-Frequency Ultrasound.
Large-scale international efforts to generate and analyze loss-of-function mutations in each of the approximately 20,000 protein-encoding gene mutations are ongoing using the "knockout" mouse as a model organism. Because one-third of gene knockouts are expected to result in embryonic lethality, it is important to develop non-invasive in utero imaging methods to detect and monitor mutant phenotypes in mouse embryos. We describe the utility of 3-D high-frequency (40-MHz) ultrasound (HFU) for longitudinal in utero imaging of mouse embryos between embryonic days (E) 11.5 and E14.5, which represent critical stages of brain and organ development. Engrailed-1 knockout (En1-ko) mouse embryos and their normal control littermates were imaged with HFU in 3-D, enabling visualization of morphological phenotypes in the developing brains, limbs and heads of the En1-ko embryos. Recently developed deep learning approaches were used to automatically segment the embryonic brain ventricles and bodies from the 3-D HFU images, allowing quantitative volumetric analyses of the En1-ko brain phenotypes. Taken together, these results show great promise for the application of longitudinal 3-D HFU to analyze knockout mouse embryos in utero.
2,329,409
Mortality and complications 1&#xa0;year after treatment of hydrocephalus with endoscopic third ventriculostomy and ventriculoperitoneal shunt in children at Queen Elizabeth Central Hospital, Malawi.
Over the past two decades, the management of hydrocephalus has witnessed the addition of endoscopic third ventriculostomy with or without choroid plexus cauterization (ETV&#x2009;&#xb1;&#x2009;CPC) to the traditional methods including ventriculoperitoneal shunt insertion (VPSI). We conducted this study to assess mortality and complications with surgical implications associated with the two procedures in children with hydrocephalus.</AbstractText>We reviewed our operating theater registry to identify children below 17&#xa0;years old who underwent hydrocephalus surgery for the first time in 2016. The patients were followed for up to 1&#xa0;year from the date of the initial operation. Their vital status was confirmed by follow-up visits by a community nurse. Descriptive analyses were used to describe the characteristics of the patients and evaluate the study outcomes (i.e., mortality and complications).</AbstractText>One hundred fifty-three patients were eligible for the study; 56% were males and 73.2% had primary ETV&#x2009;&#xb1;&#x2009;CPC. Complete 1-year follow-up data was available for 79 patients, and 73.4% of these had ETV&#x2009;&#xb1;&#x2009;CPC. One-year success (event-free) rates for ETV and VPSI were similar at 67.4% and 66.7%, respectively. ETVs in infants under 6&#xa0;months performed poorly; failing in half the infants, who were subsequently converted to VPS. Shunt sepsis was very high, 21.4% (95% CI 10.3-36.8). The majority of surgical complications (81.8%) occurred within 3&#xa0;months of surgery.</AbstractText>ETV&#x2009;&#xb1;&#x2009;CPC and VPSI carry a similar frequency of mortality and complications in our setting, and therefore, both should be considered as a treatment option for patients with hydrocephalus. As VP shunt is still used for managing most of the patients, there is still a need to prioritize measures to reduce shunt infections.</AbstractText>&#xa9; 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Austria, part of Springer Nature.</CopyrightInformation>
2,329,410
Favine/CCDC3 deficiency accelerated atherosclerosis and thrombus formation is associated with decreased MEF2C-KLF2 pathway.
Currently, no mouse models manifest calcification and thrombus formation, which is frequently associated with human atherosclerosis. We demonstrated that lack of Favine/CCDC3 in apoE knockout mice accelerated atherosclerosis accompanied by large cholesterol crystals and calcification, and also promoted thrombus formation in the left ventricle and arteries. Circulating Favine was detectable in WT mouse plasma. RNA-sequencing analysis of aortae in DKO mice showed similar gene expression patterns of human atherosclerosis with unstable and vulnerable plaques. Importantly, human <i>FAVINE</i> mRNA expressions were lower in atheroma plaque than in adjacent intact aortic tissue and decreased with the progression of atherosclerosis. Pathway analysis of aortae in DKO mice suggested the decrease of the MEF2C-KLF2-mediated transcriptional pathway. Favine insufficiency and its attenuated downstream pathways may increase atherosclerosis progression with calcification and thrombus, which have not previously been fully modeled in experimental animals. Favine and its downstream pathways may have therapeutic potential for atherosclerosis.
2,329,411
Amylin regulates testosterone levels via steroidogenesis-related enzymes in the central nervous system of male mice.
Amylin is a peripheral satiation signal polypeptide co-secreted with insulin by pancreatic &#x3b2;-cells in response to nutrient ingestion. Amylin participates in the eating-inhibitory effect and regulates energy metabolism by acting on the central nervous system (CNS). However, the role of amylin in regulating the biosynthesis of steroid hormones, such as testosterone, through the hypothalamic-pituitary-gonadal axis (HPG) remains unexplored. However, only limited evidence is available on the involvement of amylin in steroid synthesis, we hypothesize that amylin regulates testosterone levels via steroidogenesis-related enzymes in the CNS. In this study, we elucidated the effect of intraperitoneal injection of amylin on the protein expression of steroidogenesis-related enzymes, including 3&#x3b2;-hydroxysteroid dehydrogenase (3&#x3b2;-HSD), cytochrome P450 17A1 (CYP17A1), and steroidogenic acute regulatory protein (StAR), and phospho-extracellular signal-regulated kinase (pERK). Additionally, the effect of amylin on testosterone levels in male mice was examined. Our results suggested that 3&#x3b2;-HSD and CYP17A1 neurons were widely expressed in the CNS of male mice, whereas StAR neurons were mainly expressed in the zona incerta (ZI) and locus coeruleus (LC) regions. Intraperitoneal injection of amylin significantly reduced (p&#xa0;&lt;&#xa0;0.01) the expression of 3&#x3b2;-HSD, CYP17A1, and StAR in ZI and other areas near the third ventricle (3&#xa0;V) but increased (p&#xa0;&lt;&#xa0;0.01) pERK expression, brain testosterone levels, serum FSH, serum LH, and decreased (p&#xa0;&lt;&#xa0;0.01) serum testosterone levels in mice. In conclusion, amylin regulates testosterone levels via steroidogenesis-related enzymes in the central nervous system of male mice.
2,329,412
Glial functions in the blood-brain communication at the circumventricular organs.
The circumventricular organs (CVOs) are located around the brain ventricles, lack a blood-brain barrier (BBB) and sense blood-derived molecules. This review discusses recent advances in the importance of CVO functions, especially glial cells transferring periphery inflammation signals to the brain. The CVOs show size-limited vascular permeability, allowing the passage of molecules with molecular weight &lt;10,000. This indicates that the lack of an endothelial cell barrier does not mean the free movement of blood-derived molecules into the CVO parenchyma. Astrocytes and tanycytes constitute a dense barrier at the distal CVO subdivision, preventing the free diffusion of blood-derived molecules into neighboring brain regions. Tanycytes in the CVOs mediate communication between cerebrospinal fluid and brain parenchyma <i>via</i> transcytosis. Microglia and macrophages of the CVOs are essential for transmitting peripheral information to other brain regions <i>via</i> toll-like receptor 2 (TLR2). Inhibition of TLR2 signaling or depletion of microglia and macrophages in the brain eliminates TLR2-dependent inflammatory responses. In contrast to TLR2, astrocytes and tanycytes in the CVOs of the brain are crucial for initiating lipopolysaccharide (LPS)-induced inflammatory responses <i>via</i> TLR4. Depletion of microglia and macrophages augments LPS-induced fever and chronic sickness responses. Microglia and macrophages in the CVOs are continuously activated, even under normal physiological conditions, as they exhibit activated morphology and express the M1/M2 marker proteins. Moreover, the microglial proliferation occurs in various regions, such as the hypothalamus, medulla oblongata, and telencephalon, with a marked increase in the CVOs, due to low-dose LPS administration, and after high-dose LPS administration, proliferation is seen in most brain regions, except for the cerebral cortex and hippocampus. A transient increase in the microglial population is beneficial during LPS-induced inflammation for attenuating sickness response. Transient receptor potential receptor vanilloid 1 expressed in astrocytes and tanycytes of the CVOs is responsible for thermoregulation upon exposure to a warm environment less than 37&#xb0;C. Alternatively, Na <sub><i>x</i></sub> expressed in astrocytes and tanycytes of the CVOs is crucial for maintaining body fluid homeostasis. Thus, recent findings indicate that glial cells in the brain CVOs are essential for initiating neuroinflammatory responses and maintaining body fluid and thermal homeostasis.
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Case report: Atypical teratoid/rhabdoid tumor of the lateral ventricle in a male adolescent (case-based review and diagnostic challenges in developing countries).
Atypical teratoid/rhabdoid tumor (AT/RT) is a rare and highly malignant central nervous system (CNS) embryonal neoplasm: it accounts for &lt;2% of all pediatric CNS tumors and occurs mainly in infants and young children. The primary site of this tumor is usually the posterior cranial fossa. Supratentorial and, in detail, latero-ventricular location is extremely uncommon, especially in adolescents. This tumor is characterized by rapid growth and spread in cerebrospinal fluid and, therefore, it is characterized by a poor prognosis. Neurological signs and symptoms are related the location of the tumor. The radiological features of AT/RT are nonspecific. Immunohistochemical staining for loss of nuclear integrase interactor 1 (INI1) expression is considered a reliable criterion for the diagnosis of this type of tumor. AT/RT has been linked to mutations of&#xa0;SMARCB1 or, rarely, SMARCA4 genes, which function as tumor suppressor genes. Currently, there is no validated protocol of treatment for children with AT/RT, and multimodality treatment (consisting of surgery, chemotherapy, and radiation therapy) is considered. In this case report, we describe a 15-year-old adolescent with an AT/RT of the left lateral ventricle. Despite the late diagnosis, the multimodal therapeutic approach provided a good outcome for our patient at 21 months' follow-up. Based on our case-based review, early diagnosis and a multimodal approach to treatment play a key role in improving the survival of patients with this diagnosis. Implementing a system supporting pathological and molecular analyses for developing countries and, in general, for non-academic centers is of primary importance to timely diagnose and treat rare tumors, such as AT/RT.
2,329,414
How much can AI see in early pregnancy: A multi-center study of fetus head characterization in week 10-14 in ultrasound using deep learning.<Pagination><StartPage>107170</StartPage><MedlinePgn>107170</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.cmpb.2022.107170</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0169-2607(22)00551-X</ELocationID><Abstract><AbstractText Label="PURPOSE" NlmCategory="OBJECTIVE">To investigate if artificial intelligence can identify fetus intracranial structures in pregnancy week 11-14; to provide an automated method of standard and non-standard sagittal view classification in obstetric ultrasound examination METHOD AND MATERIALS: We proposed a newly designed scheme based on deep learning (DL) - Fetus Framework to identify nine fetus intracranial structures: thalami, midbrain, palate, 4th ventricle, cisterna magna, nuchal translucency (NT), nasal tip, nasal skin, and nasal bone. Fetus Framework was trained and tested on a dataset of 1528 2D sagittal-view ultrasound images from 1519 females collected from Shenzhen People's Hospital. Results from Fetus Framework were further used for standard/non-standard (S-NS) plane classification, a key step for NT measurement and Down Syndrome assessment. S-NS classification was also tested with 156 images from the Longhua branch of Shenzhen People's Hospital. Sensitivity, specificity, and area under the curve (AUC) were evaluated for comparison among Fetus Framework, three classic DL models, and human experts with 1-, 3- and 5-year ultrasound training. Furthermore, 4 physicians with more than 5 years of experience conducted a reader study of diagnosing fetal malformation on a dataset of 316 standard images confirmed by the Fetus framework and another dataset of 316 standard images selected by physicians. Accuracy, sensitivity, specificity, precision, and F1-Score of physicians' diagnosis on both sets are compared.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Nine intracranial structures identified by Fetus Framework in validation are all consistent with that of senior radiologists. For S-NS sagittal view identification, Fetus Framework achieved an AUC of 0.996 (95%CI: 0.987, 1.000) in internal test, at par with classic DL models. In external test, FF reaches an AUC of 0.974 (95%CI: 0.952, 0.995), while ResNet-50 arrives at AUC&#x223c;0.883, 95% CI 0.828-0.939, Xception AUC&#x223c;0.890, 95% CI 0.834-0.946, and DenseNet-121 AUC&#x223c;0.894, 95% CI 0.839-0.949. For the internal test set, the sensitivity and specificity of the proposed framework are (0.905, 1), while the first-, third-, and fifth-year clinicians are (0.619, 0.986), (0.690, 0.958), and (0.798, 0.986), respectively. For the external test set, the sensitivity and specificity of FF is (0.989, 0.797), and first-, third-, and fifth-year clinicians are (0.533, 0.875), (0.609, 0.844), and (0.663, 0.781), respectively.On the fetal malformation classification task, all physicians achieved higher accuracy and F1-Score on Fetus selected standard images with statistical significance (p&#xa0;&lt;&#xa0;0.01).</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">We proposed a new deep learning-based Fetus Framework for identifying key fetus intracranial structures. The framework was tested on data from two different medical centers. The results show consistency and improvement from classic models and human experts in standard and non-standard sagittal view classification during pregnancy week 11-13+6.</AbstractText><AbstractText Label="CLINICAL RELEVANCE/APPLICATION" NlmCategory="CONCLUSIONS">With further refinement in larger population, the proposed model can improve the efficiency and accuracy of early pregnancy test using ultrasound examination.</AbstractText><CopyrightInformation>Copyright &#xa9; 2022 Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lin</LastName><ForeName>Qi</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>Department of Ultrasound, Shenzhen People's Hospital, The Second Clinical Medical College, Jinan University, The First Affiliated Hospital, Southern University of Science and Technology, Shenzhen, Guangdong, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhou</LastName><ForeName>Yuli</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Ultrasound, Shenzhen People's Hospital, The Second Clinical Medical College, Jinan University, The First Affiliated Hospital, Southern University of Science and Technology, Shenzhen, Guangdong, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shi</LastName><ForeName>Siyuan</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Illuminate, LLC, Shenzhen, Guangdong, China; Microport Prophecy, Shanghai, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Yujuan</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Ultrasound, Shenzhen People's Hospital, The Second Clinical Medical College, Jinan University, The First Affiliated Hospital, Southern University of Science and Technology, Shenzhen, Guangdong, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yin</LastName><ForeName>Shaoli</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Ultrasound, Shenzhen People's Hospital, The Second Clinical Medical College, Jinan University, The First Affiliated Hospital, Southern University of Science and Technology, Shenzhen, Guangdong, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Xuye</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Ultrasound, Shenzhen People's Hospital, The Second Clinical Medical College, Jinan University, The First Affiliated Hospital, Southern University of Science and Technology, Shenzhen, Guangdong, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Peng</LastName><ForeName>Qihui</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>Department of Ultrasound, Shenzhen People's Hospital, The Second Clinical Medical College, Jinan University, The First Affiliated Hospital, Southern University of Science and Technology, Shenzhen, Guangdong, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Huang</LastName><ForeName>Shaoting</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Ultrasound, Shenzhen People's Hospital, The Second Clinical Medical College, Jinan University, The First Affiliated Hospital, Southern University of Science and Technology, Shenzhen, Guangdong, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jiang</LastName><ForeName>Yitao</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Illuminate, LLC, Shenzhen, Guangdong, China; Microport Prophecy, Shanghai, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cui</LastName><ForeName>Chen</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Illuminate, LLC, Shenzhen, Guangdong, China; Microport Prophecy, Shanghai, China. Electronic address: cuichen@microport.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>She</LastName><ForeName>Ruilian</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Obstetric, Shenzhen People's Hospital, The Second Clinical Medical College, Jinan University, The First Affiliated Hospital, Southern University of Science and Technology), Shenzhen, Guangdong, China. Electronic address: zhe.ruilian@szhospital.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xu</LastName><ForeName>Jinfeng</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Ultrasound, Shenzhen People's Hospital, The Second Clinical Medical College, Jinan University, The First Affiliated Hospital, Southern University of Science and Technology, Shenzhen, Guangdong, China. Electronic address: xujinfeng@szhospital.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dong</LastName><ForeName>Fajin</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Department of Ultrasound, Shenzhen People's Hospital, The Second Clinical Medical College, Jinan University, The First Affiliated Hospital, Southern University of Science and Technology, Shenzhen, Guangdong, China. Electronic address: dongfajin@szhospital.com.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016448">Multicenter Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>10</Month><Day>02</Day></ArticleDate></Article><MedlineJournalInfo><Country>Ireland</Country><MedlineTA>Comput Methods Programs Biomed</MedlineTA><NlmUniqueID>8506513</NlmUniqueID><ISSNLinking>0169-2607</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D011247" MajorTopicYN="N">Pregnancy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000077321" MajorTopicYN="Y">Deep Learning</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001185" MajorTopicYN="N">Artificial Intelligence</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012680" MajorTopicYN="N">Sensitivity and Specificity</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014463" MajorTopicYN="N">Ultrasonography</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005333" MajorTopicYN="N">Fetus</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Artificial intelligence</Keyword><Keyword MajorTopicYN="N">Obstetrics and gynecology</Keyword><Keyword MajorTopicYN="N">Ultrasound</Keyword></KeywordList><CoiStatement>Declaration of Competing of Interest We declare that we have no financial and personal relationships with other people or organizations that can inappropriately influence our work, there is no professional or other personal interest of any nature or kind in any product, service and/or company that could be construed as influencing the position presented in, or the review of, the manuscript entitled.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>3</Month><Day>29</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>9</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>9</Month><Day>30</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>10</Month><Day>23</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>11</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>10</Month><Day>22</Day><Hour>18</Hour><Minute>27</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36272307</ArticleId><ArticleId IdType="doi">10.1016/j.cmpb.2022.107170</ArticleId><ArticleId IdType="pii">S0169-2607(22)00551-X</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36272057</PMID><DateRevised><Year>2022</Year><Month>10</Month><Day>22</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1522-1709</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Oct</Month><Day>22</Day></PubDate></JournalIssue><Title>Sleep &amp; breathing = Schlaf &amp; Atmung</Title><ISOAbbreviation>Sleep Breath</ISOAbbreviation></Journal>Clinical study of transcranial sonography image characteristics in patients with obstructive sleep apnea.
To investigate if artificial intelligence can identify fetus intracranial structures in pregnancy week 11-14; to provide an automated method of standard and non-standard sagittal view classification in obstetric ultrasound examination METHOD AND MATERIALS: We proposed a newly designed scheme based on deep learning (DL) - Fetus Framework to identify nine fetus intracranial structures: thalami, midbrain, palate, 4th ventricle, cisterna magna, nuchal translucency (NT), nasal tip, nasal skin, and nasal bone. Fetus Framework was trained and tested on a dataset of 1528 2D sagittal-view ultrasound images from 1519 females collected from Shenzhen People's Hospital. Results from Fetus Framework were further used for standard/non-standard (S-NS) plane classification, a key step for NT measurement and Down Syndrome assessment. S-NS classification was also tested with 156 images from the Longhua branch of Shenzhen People's Hospital. Sensitivity, specificity, and area under the curve (AUC) were evaluated for comparison among Fetus Framework, three classic DL models, and human experts with 1-, 3- and 5-year ultrasound training. Furthermore, 4 physicians with more than 5 years of experience conducted a reader study of diagnosing fetal malformation on a dataset of 316 standard images confirmed by the Fetus framework and another dataset of 316 standard images selected by physicians. Accuracy, sensitivity, specificity, precision, and F1-Score of physicians' diagnosis on both sets are compared.</AbstractText>Nine intracranial structures identified by Fetus Framework in validation are all consistent with that of senior radiologists. For S-NS sagittal view identification, Fetus Framework achieved an AUC of 0.996 (95%CI: 0.987, 1.000) in internal test, at par with classic DL models. In external test, FF reaches an AUC of 0.974 (95%CI: 0.952, 0.995), while ResNet-50 arrives at AUC&#x223c;0.883, 95% CI 0.828-0.939, Xception AUC&#x223c;0.890, 95% CI 0.834-0.946, and DenseNet-121 AUC&#x223c;0.894, 95% CI 0.839-0.949. For the internal test set, the sensitivity and specificity of the proposed framework are (0.905, 1), while the first-, third-, and fifth-year clinicians are (0.619, 0.986), (0.690, 0.958), and (0.798, 0.986), respectively. For the external test set, the sensitivity and specificity of FF is (0.989, 0.797), and first-, third-, and fifth-year clinicians are (0.533, 0.875), (0.609, 0.844), and (0.663, 0.781), respectively.On the fetal malformation classification task, all physicians achieved higher accuracy and F1-Score on Fetus selected standard images with statistical significance (p&#xa0;&lt;&#xa0;0.01).</AbstractText>We proposed a new deep learning-based Fetus Framework for identifying key fetus intracranial structures. The framework was tested on data from two different medical centers. The results show consistency and improvement from classic models and human experts in standard and non-standard sagittal view classification during pregnancy week 11-13+6.</AbstractText><AbstractText Label="CLINICAL RELEVANCE/APPLICATION" NlmCategory="CONCLUSIONS">With further refinement in larger population, the proposed model can improve the efficiency and accuracy of early pregnancy test using ultrasound examination.</AbstractText>Copyright &#xa9; 2022 Elsevier B.V. All rights reserved.</CopyrightInformation>
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Protective effect of N-acetyl cysteine on the mitochondrial dynamic imbalance in temporal lobe epilepsy: Possible role of mTOR.
Understanding the underlying molecular mechanisms involved in epilepsy is critical for the development of more effective therapies. It is believed that mTOR (Mechanistic Target of Rapamycin kinases) activity and the mitochondrial dynamic balance change during epilepsy. mTOR affects mitochondrial fission by stimulating the translation of mitochondrial fission process 1 (MTFP1). In This study, the protective role of N-acetylcysteine was studied in temporal lobe epilepsy (TLE) through the regulation of mTOR and mitochondrial dynamic proteins. Rats received N-acetylcysteine (oral administration) seven days before induction of epilepsy, followed by one day after epilepsy. TLE was induced by microinjection of kainite into the left lateral ventricle. The total mTOR and Drp1 levels in the hippocampus were evaluated by western blotting. MFN1 was assessed using immunohistochemistry, and the expression of Fis.1 and MTFP1 (fission-related proteins) and OPA (fusion-related protein) were detected by real-time PCR. The mitochondrial membrane potential was measured by Rhodamin 123. The results showed that 72&#xa0;h after induction of epilepsy, the mTOR protein level increased, and the balance of the mitochondrial dynamic was disturbed; however, oral administration of NAC decreased the mTOR protein level and improved the mitochondrial dynamic. These findings indicate that NAC plays a neuroprotective role in temporal lobe epilepsy, probably through decreasing the mTOR protein level, which can improve the imbalance in the mitochondrial dynamic.
2,329,416
Treatment with 1,25-Dihydroxyvitamin D3 Delays Choroid Plexus Infiltration and BCSFB Injury in MRL/lpr Mice Coinciding with Activation of the PPAR&#x3b3;/NF-&#x3ba;B/TNF-&#x3b1; Pathway and Suppression of TGF-&#x3b2;/Smad Signaling.
Neuropsychiatric systemic lupus erythematosus (NPSLE) is a serious complication of systemic lupus erythematosus (SLE) involving the nervous system with high morbidity and mortality. A key hypothesis in NPSLE is that a disrupted barrier allows autoantibodies and immune components of peripheral blood to penetrate into the central nervous system (CNS), resulting in inflammation and damage. The blood cerebrospinal fluid barrier (BCSFB), which consists of the choroid plexus and the hypothalamic tanycytes, has long been regarded as an immunological sanctuary site. 1,25-Dihydroxyvitamin D3 [1,25-(OH)<sub>2</sub>D<sub>3</sub>] is the active form of vitamin D, which plays multiple roles in inflammation and immunoregulation. In this study, we investigated the possible protective effects of 1,25-dihydroxyvitamin D3 against BCSFB dysfunction in NPSLE in MRL/lpr mice and explored the mechanism by which 1,25-dihydroxyvitamin D3 inhibits the progression of NPSLE. In this study, we found that supplementation with 1,25-dihydroxyvitamin D3 markedly improved serological and immunological indices, delayed inflammatory infiltration, delayed neuronal deformation, and upregulated the expression of brain-derived neurotrophic factor (BDNF) proteins in the brain. Furthermore, 1,25-dihydroxyvitamin D3 downregulated proinflammatory cytokines such as nuclear factor kappa-B (NF-&#x3ba;B) and tumor necrosis factor-&#x3b1; (TNF-&#x3b1;) by activating peroxisome proliferator-activated receptor &#x3b3; (PPAR&#x3b3;), and it reduced the expression of the TGF-&#x3b2;/Smad signaling pathway. Our findings demonstrate that 1,25-dihydroxyvitamin D3 delayed cell infiltration into the choroid plexus and decreased markers suggestive of cognitive decline in MRL/lpr mice, and the mechanism may be related to protection against BCSFB disruption through activation of the anti-inflammatory PPAR&#x3b3;/NF-&#x3ba;B/TNF-&#x3b1; pathway as well as upregulation of BDNF and inhibition of the TGF-&#x3b2;/Smad signaling pathway. These findings provide a novel direction for the study of NPSLE.
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The assessment of fetal cardiac output in maternal hypothyroidism under levothyroxine treatment.<Pagination><StartPage>1434</StartPage><EndPage>1438</EndPage><MedlinePgn>1434-1438</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1111/echo.15474</ELocationID><Abstract><AbstractText Label="OBJECTIVE">In this study, we investigated whether maternal hypothyroidism has a role in the cardiac output (CO) of the fetus or not.</AbstractText><AbstractText Label="METHODS">Pregnant women between 33 and 37 gestational weeks known to have hypothyroidism and using levothyroxine were accepted as the case group. Gestational age-matched healthy euthyroid pregnant women constituted the control group. Fetal echocardiography was performed. Diameters and the velocity waveform of the pulmonary artery (PA) and aortic valves were measured. Velocity time integral (VTI) was also measured from the ventricular outflow tract. CO was calculated using VTI &#xd7; &#x3c0; (Aortic Valve or Pulmonary Valve diameter/2) 2 &#xd7; heart rate formula.</AbstractText><AbstractText Label="RESULTS">The aortic and PA annulus were measured larger in the control group. (p&#xa0;=&#xa0;.003, p&#xa0;=&#xa0;.005, respectively). Furthermore, the right and left CO of the case group were lower than the control group. Whereas the mean combined CO (ml/min) of the case group was 674.8&#xa0;&#xb1;&#xa0;146.2, it was 827.8&#xa0;&#xb1;&#xa0;167.9 in the control group (p&#xa0;&amp;lt;&#xa0;.001). Additionally, a negative correlation was observed between thyroid-stimulating hormone and aortic VTI (r:-.480; p:.006).</AbstractText><AbstractText Label="CONCLUSION">The findings of our study suggest that the CO of the fetus may be affected by maternal hypothyroidism.</AbstractText><CopyrightInformation>&#xa9; 2022 Wiley Periodicals LLC.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Tugrul Ersak</LastName><ForeName>Duygu</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Obstetrics and Gynecology, University of Health Sciences, Ankara City Hospital, Ankara, Turkey.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Oluklu</LastName><ForeName>Deniz</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Obstetrics and Gynecology, University of Health Sciences, Ankara City Hospital, Ankara, Turkey.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Uyan Hendem</LastName><ForeName>Derya</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Obstetrics and Gynecology, University of Health Sciences, Ankara City Hospital, Ankara, Turkey.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Turgut</LastName><ForeName>Ezgi</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Department of Obstetrics and Gynecology, University of Health Sciences, Ankara City Hospital, Ankara, Turkey.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>G&#xf6;nc&#xfc; Ayhan</LastName><ForeName>&#x15e;ule</ForeName><Initials>&#x15e;</Initials><AffiliationInfo><Affiliation>Department of Obstetrics and Gynecology, University of Health Sciences, Ankara City Hospital, Ankara, Turkey.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kara</LastName><ForeName>&#xd6;zg&#xfc;r</ForeName><Initials>&#xd6;</Initials><AffiliationInfo><Affiliation>Department of Obstetrics and Gynecology, University of Health Sciences, Ankara City Hospital, Ankara, Turkey.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>&#x15e;ahin</LastName><ForeName>Dilek</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Obstetrics and Gynecology, University of Health Sciences, Ankara City Hospital, Ankara, Turkey.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>10</Month><Day>20</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Echocardiography</MedlineTA><NlmUniqueID>8511187</NlmUniqueID><ISSNLinking>0742-2822</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>Q51BO43MG4</RegistryNumber><NameOfSubstance UI="D013974">Thyroxine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011247" MajorTopicYN="N">Pregnancy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013974" MajorTopicYN="Y">Thyroxine</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002302" MajorTopicYN="N">Cardiac Output</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005333" MajorTopicYN="N">Fetus</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007037" MajorTopicYN="Y">Hypothyroidism</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">cardiac output</Keyword><Keyword MajorTopicYN="N">fetal echocardiography</Keyword><Keyword MajorTopicYN="N">levothyroxine</Keyword><Keyword MajorTopicYN="N">maternal hypothyroidism</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>9</Month><Day>13</Day></PubMedPubDate><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>7</Month><Day>20</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>10</Month><Day>2</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>10</Month><Day>22</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>11</Month><Day>16</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>10</Month><Day>21</Day><Hour>0</Hour><Minute>9</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36266738</ArticleId><ArticleId IdType="doi">10.1111/echo.15474</ArticleId></ArticleIdList><ReferenceList><Title>REFERENCES</Title><Reference><Citation>Delitala AP, Capobianco G, Cherchi PL, Dessole S, Delitala G. Thyroid function and thyroid disorders during pregnancy: a review and care pathway. Arch Ggynecol Obstet. 2019;299(2):327-338.</Citation></Reference><Reference><Citation>Kotani T, Imai K, Ushida T, et&#xa0;al. Pregnancy outcomes in women with thyroid diseases. JMA. 2022;5(2):216-223.</Citation></Reference><Reference><Citation>Casey BM, Dashe JS, Wells CE, et&#xa0;al. Subclinical hypothyroidism and pregnancy outcomes. Obstet Gynecol. 2005;105(2):239-245.</Citation></Reference><Reference><Citation>Burrow GN, Fisher DA, Larsen PR. Maternal and fetal thyroid function. N Engl J Med. 1994;331(16):1072-1078.</Citation></Reference><Reference><Citation>Klein I, Ojamaa K. Thyroid hormone and the cardiovascular system. N Engl J Med. 2001;344(7):501-509.</Citation></Reference><Reference><Citation>Grattan MJ, Thomas DS, Hornberger LK, Hamilton RM, Midodzi WK, Vohra S. Maternal hypothyroidism may be associated with CHD in offspring. Cardiol Young. 2015;25(7):1247-1253.</Citation></Reference><Reference><Citation>Mark PD, Andreassen M, Petersen CL, Kjaer A, Faber J. Treatment of subclinical hyperthyroidism: effect on left ventricular mass and function of the heart using magnetic resonance imaging technique. Endocr Connect. 2015;4(1):37-42.</Citation></Reference><Reference><Citation>Balducci G, Acquafredda A, Amendola F, Natuzzi M, Laforgia N, Cavallo L. Cardiac function in congenital hypothyroidism: impairment and response to L-T4 therapy. Pediatr Cardiol. 1991;12(1):28-32.</Citation></Reference><Reference><Citation>Winter J, Kulkarni A, Craft M, et&#xa0;al. Depressed left and right ventricular cardiac output in fetuses of diabetic mothers. Echo Res Pract. 2018;5(1):19-26.</Citation></Reference><Reference><Citation>Turgut E, Sakcak B, Uyan Hendem D, Oluklu D, Goncu Ayhan S, Sahin D. Decreased fetal cardiac output in pregnant women with severe SARS-Cov-2 infection. Echocardiography. 2022;39(6):803-10.</Citation></Reference><Reference><Citation>Tay J, Foo L, Masini G, et&#xa0;al. Early and late preeclampsia are characterized by high cardiac output, but in the presence of fetal growth restriction, cardiac output is low: insights from a prospective study. Am J Obstet Gynecol. 2018;218(5):517. e1-e12.</Citation></Reference><Reference><Citation>Liu M, Yu J, Fu X, Wan W. Quantitative assessment of cardiac function in fetuses of women with maternal gestational thyroid dysfunction using VVI echocardiography. Med Sci Monit. 2015;21:2956.</Citation></Reference><Reference><Citation>Ghanbari M, Jeddi S, Bagheripuor F, Ghasemi A. The effect of maternal hypothyroidism on cardiac function and tolerance to ischemia-reperfusion injury in offspring male and female rats. J Endocrinol Invest. 2015;38(8):915-922.</Citation></Reference><Reference><Citation>Stagnaro-Green A. Thyroid disease in pregnancy: a touch of clarity. Thyroid. 2022;32(4):347-348.</Citation></Reference><Reference><Citation>Obstetrics ISoUi, Cardiac screening examination of the fetus: guidelines for performing the'basic'and'extended basic'cardiac scan. Ultrasound Obstet Gynecol 2006;27(1):107-113.</Citation></Reference><Reference><Citation>Mao S, Wang Y, Jiang G, Zhao Z. Effects of levothyroxine therapy on left and right ventricular function in neonates with congenital hypothyroidism: a tissue Doppler echocardiography study. Eur J Pediatr. 2007;166(12):1261-1265.</Citation></Reference><Reference><Citation>Goldenthal MJ, Weiss HR, Mar&#xed;n-Garc&#xed;a J, Bioenergetic remodeling of heart mitochondria by thyroid hormone. Mol Cell Biochem. 2004;265(1):97-106.</Citation></Reference><Reference><Citation>Klemperer JD, Klein I, Gomez M, et&#xa0;al. Thyroid hormone treatment after coronary-artery bypass surgery. N Eng J Med. 1995;333(23):1522-1527.&lt;/bib</Citation></Reference><Reference><Citation>Gittenberger-de Groot AC, Bartelings MM, Poelmann RE, Haak MC, Jongbloed MR. Embryology of the heart and its impact on understanding fetal and neonatal heart disease. Sem Fetal and Neonatal Med. 2013;18(5):237-44.</Citation></Reference><Reference><Citation>Stevens RJ, Nishio ML, Hood DA. Effect of hypothyroidism on the expression of cytochrome c and cytochrome c oxidase in heart and muscle during development. Mol Cell Biochem. 1995;143(2):119-127.</Citation></Reference><Reference><Citation>Reed TD, Babu GJ, Ji Y, Zilberman A, Ver Heyen M, Wuytack F, et&#xa0;al. The expression of SR calcium transport ATPase and the Na+/Ca2+ exchanger are antithetically regulated during mouse cardiac development and in hypo/hyperthyroidism. J Mol Cell Cardiol. 2000;32(3):453-464.</Citation></Reference><Reference><Citation>Van Deventer HE, Mendu DR, Remaley AT, Soldin SJ. Inverse log-linear relationship between thyroid-stimulating hormone and free thyroxine measured by direct analog immunoassay and tandem mass spectrometry. Clin Chem. 2011;57(1):122-127.</Citation></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36266256</PMID><DateRevised><Year>2022</Year><Month>11</Month><Day>07</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1601-0825</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Oct</Month><Day>20</Day></PubDate></JournalIssue><Title>Oral diseases</Title><ISOAbbreviation>Oral Dis</ISOAbbreviation></Journal>Porphyromonas gingivalis outer membrane vesicles in cerebral ventricles activate microglia in mice.
In this study, we investigated whether maternal hypothyroidism has a role in the cardiac output (CO) of the fetus or not.</AbstractText>Pregnant women between 33 and 37 gestational weeks known to have hypothyroidism and using levothyroxine were accepted as the case group. Gestational age-matched healthy euthyroid pregnant women constituted the control group. Fetal echocardiography was performed. Diameters and the velocity waveform of the pulmonary artery (PA) and aortic valves were measured. Velocity time integral (VTI) was also measured from the ventricular outflow tract. CO was calculated using VTI &#xd7; &#x3c0; (Aortic Valve or Pulmonary Valve diameter/2) 2 &#xd7; heart rate formula.</AbstractText>The aortic and PA annulus were measured larger in the control group. (p&#xa0;=&#xa0;.003, p&#xa0;=&#xa0;.005, respectively). Furthermore, the right and left CO of the case group were lower than the control group. Whereas the mean combined CO (ml/min) of the case group was 674.8&#xa0;&#xb1;&#xa0;146.2, it was 827.8&#xa0;&#xb1;&#xa0;167.9 in the control group (p&#xa0;&amp;lt;&#xa0;.001). Additionally, a negative correlation was observed between thyroid-stimulating hormone and aortic VTI (r:-.480; p:.006).</AbstractText>The findings of our study suggest that the CO of the fetus may be affected by maternal hypothyroidism.</AbstractText>&#xa9; 2022 Wiley Periodicals LLC.</CopyrightInformation>
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Update Reference Charts: Fetal Biometry between the 15th and 42nd Week of Gestation.
This study was designed to establish new reference charts for BPD (biparietal diameter), OFD (occipitofrontal diameter), HC (head circumference), CM (cisterna magna), TCD (transverse cerebellar diameter), PCV (posterior cerebral ventricle), AC (abdominal circumference), FL (femur length), and HL (humerus length) and extend known charts to 42 weeks of gestation. These new charts were compared to studies carried out by Snijders and Nicolaides, the INTERGROWTH 21st Project, and the WHO Fetal Growth Charts.</AbstractText>In this retrospective cross-sectional single-center study of 12,972 low-risk pregnancies, biometric data between the 15th and 42nd weeks of gestation were evaluated. Only one examination per pregnancy was selected for statistical analysis. Descriptive analysis for the 5th, 50th, and 95th quantile was performed for each parameter as listed above. Regression models were used to fit the mean and the SD at each gestational age.</AbstractText>Initially the reference curves for BPD, OFD, HC, AC, FL, and HL show a linear increase, which changes into a cubic increase towards the end of pregnancy. The results of this study show statistically noticeable differences from the percentile curves of the studies listed above.</AbstractText>The percentile curves in this study differ from the commonly used ones. The presented standard curves can be used as a reference in prenatal diagnostics.</AbstractText>Thieme. All rights reserved.</CopyrightInformation>
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Disease characteristics and patterns of familial colloid cyst of the third ventricle: An international survey of the Colloid Cyst Survivors Group.
Colloid cysts of the third ventricle are rare benign tumors, accounting for approximately 1% of all intracranial tumors. Familial colloid cysts are less common, only 25 cases have been previously reported in the literature. We aim to describe demographic and disease-specific characteristics to reduce the knowledge gap with this potentially life-threatening tumor.</AbstractText>We conducted a retrospective cohort study of 211 colloid cyst patients from the Colloid Cyst Survivors Group who completed a survey that included demographicandclinical data andinquired aboutfamily members diagnosed with a colloid cyst. Datawascollected from October 14th, 2021 to October 27th, 2021. We compared our data with previously published cases from the literature.</AbstractText>A total of 211 responses from patients with a previous diagnosis of a colloid cyst completed our survey. 11.8&#xa0;% were familial colloid cysts, of this group 60.8&#xa0;% were symptomatic and 39.2&#xa0;% incidental. We observed significant difference between symptom incidence between reports from the literature and our cohort: headache 75.5&#xa0;% versus 49&#xa0;% (p&#xa0;=&#xa0;0.005); imbalance 13.2&#xa0;% versus 31.4&#xa0;% (p&#xa0;=&#xa0;0.03); nausea 11.3&#xa0;% versus 29.4&#xa0;% (p&#xa0;=&#xa0;0.02), and difficulty walking 1.9&#xa0;% versus 19.6&#xa0;% (p&#xa0;=&#xa0;0.003). Additionally, we found first degree family member as the most frequent relative diagnosed with this disease.</AbstractText>Our study involved the largestcohortof patients with familial colloid cysts. According to previous literature, siblings are the most prevalent family member affected by this disease, specifically among monozygotic twins. This suggests strong inheritance patterns and even genetic mechanism underlying the development of this disease.</AbstractText>Copyright &#xa9; 2022 Elsevier Ltd. All rights reserved.</CopyrightInformation>
2,329,420
Ventriculorenal shunts in the treatment of pediatric and adult hydrocephalus-historical perspective and analysis of current practice.
Hydrocephalus is a complex pathology that can have a significant impact on the quality of life in all age groups. Cerebrospinal fluid (CSF) diversions from the lateral ventricle to the peritoneal cavity are regarded as the treatment of first intent, but they have a high revision rate, and there are multiple factors which can impair their proper insertion and function. One of the many alternatives to peritoneal shunting is redirecting the CSF towards the renal system. A literature search was conducted to identify the particularities of these types of shunts and what clinical context rendered them&#xa0;feasible in pediatric and adult patient populations. Twenty-eight studies were found to meet the selection criteria. The shunts were classified into ventriculopyeloureteral, ventriculoureteral, and ventriculovesical. Their main advantage was that they did not depend on absorption&#xa0;properties of the tissues, like in the case of the peritoneum. However, several issues with ascending infections, bladder pressure imbalance, distal shunt migration, and calculus formation were noted. Literature suggests that the urinary tract can have the potential of diverting CSF when the peritoneum or atrium is not available, but further research is required to establish their proper role in current practice.
2,329,421
Cardiac-derived extracellular matrix: A decellularization protocol for heart regeneration.<Pagination><StartPage>e0276224</StartPage><MedlinePgn>e0276224</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">e0276224</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0276224</ELocationID><Abstract><AbstractText>Extracellular matrix (ECM) is a fundamental component of the heart, guiding vital cellular processes during organ homeostasis. Most cardiovascular diseases lead to a remarkable remodeling of the ECM, accompanied by the formation of a fibrotic tissue that heavily compromises the heart function. Effective therapies for managing fibrosis and promoting physiological ECM repair are not yet available. The production of a decellularized extracellular matrix (d-ECM) serving as a three-dimensional and bioactive scaffold able to modulate cellular behavior and activities is considered crucial to achieve a successful regeneration. The protocol represents a step-by-step method to obtain a decellularized cardiac matrix through the combination of sodium dodecyl sulphate (SDS) and Triton X-100. Briefly, cardiac samples obtained from left ventricles of explanted, pathological human hearts were dissected and washed to remove residual body fluids. Samples were then snap-frozen and sliced by a cryostat into 350 &#x3bc;m thick sections. The sections obtained were decellularized using a solution containing 1% Triton X-100 and 1% SDS in combination, for 24 hours, until observing the color change from brownish-red to translucent-white. As a result, the protocol shows efficiency in preserving ECM architecture and protein composition during the whole process, suggesting that it is worthwhile, highly reproducible and produces a well- preserved decellularized extracellular matrix from cardiac samples. Notwithstanding, some limitations need to be addressed, such as the risk for microbial contamination and the unpredictable trend of the protocol when applied to decellularize samples other than myocardium, vessels, or skin. These issues require antibiotics mixture supplement during the procedure followed by UV sterilization, and appropriate adjustments for a tissue-specific utilization, respectively. The protocol is intended to produce a cardiac d-ECM for cell settlement, representing the ideal scaffold for tissue engineering purposes.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Belviso</LastName><ForeName>Immacolata</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Department of Public Health, University of Naples Federico II, Naples, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sacco</LastName><ForeName>Anna Maria</ForeName><Initials>AM</Initials><AffiliationInfo><Affiliation>Department of Public Health, University of Naples Federico II, Naples, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cozzolino</LastName><ForeName>Domenico</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Public Health, University of Naples Federico II, Naples, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nurzynska</LastName><ForeName>Daria</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Medicine, Surgery and Dentistry, Scuola Medica Salernitana, University of Salerno, Baronissi, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Di Meglio</LastName><ForeName>Franca</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Department of Public Health, University of Naples Federico II, Naples, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Castaldo</LastName><ForeName>Clotilde</ForeName><Initials>C</Initials><Identifier Source="ORCID">0000-0003-1475-5036</Identifier><AffiliationInfo><Affiliation>Department of Public Health, University of Naples Federico II, Naples, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Romano</LastName><ForeName>Veronica</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>Department of Public Health, University of Naples Federico II, Naples, Italy.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>10</Month><Day>19</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS One</MedlineTA><NlmUniqueID>101285081</NlmUniqueID><ISSNLinking>1932-6203</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>9002-93-1</RegistryNumber><NameOfSubstance UI="D017830">Octoxynol</NameOfSubstance></Chemical><Chemical><RegistryNumber>368GB5141J</RegistryNumber><NameOfSubstance UI="D012967">Sodium Dodecyl Sulfate</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000900">Anti-Bacterial Agents</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017830" MajorTopicYN="N">Octoxynol</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012967" MajorTopicYN="N">Sodium Dodecyl Sulfate</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005109" MajorTopicYN="Y">Extracellular Matrix</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D023822" MajorTopicYN="Y">Tissue Engineering</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012038" MajorTopicYN="N">Regeneration</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000900" MajorTopicYN="N">Anti-Bacterial Agents</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054457" MajorTopicYN="N">Tissue Scaffolds</DescriptorName></MeshHeading></MeshHeadingList><CoiStatement>The authors have declared that no competing interests exist.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>3</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>9</Month><Day>23</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>10</Month><Day>19</Day><Hour>13</Hour><Minute>44</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>10</Month><Day>20</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>10</Month><Day>22</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId 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Extracellular matrix (ECM) is a fundamental component of the heart, guiding vital cellular processes during organ homeostasis. Most cardiovascular diseases lead to a remarkable remodeling of the ECM, accompanied by the formation of a fibrotic tissue that heavily compromises the heart function. Effective therapies for managing fibrosis and promoting physiological ECM repair are not yet available. The production of a decellularized extracellular matrix (d-ECM) serving as a three-dimensional and bioactive scaffold able to modulate cellular behavior and activities is considered crucial to achieve a successful regeneration. The protocol represents a step-by-step method to obtain a decellularized cardiac matrix through the combination of sodium dodecyl sulphate (SDS) and Triton X-100. Briefly, cardiac samples obtained from left ventricles of explanted, pathological human hearts were dissected and washed to remove residual body fluids. Samples were then snap-frozen and sliced by a cryostat into 350 &#x3bc;m thick sections. The sections obtained were decellularized using a solution containing 1% Triton X-100 and 1% SDS in combination, for 24 hours, until observing the color change from brownish-red to translucent-white. As a result, the protocol shows efficiency in preserving ECM architecture and protein composition during the whole process, suggesting that it is worthwhile, highly reproducible and produces a well- preserved decellularized extracellular matrix from cardiac samples. Notwithstanding, some limitations need to be addressed, such as the risk for microbial contamination and the unpredictable trend of the protocol when applied to decellularize samples other than myocardium, vessels, or skin. These issues require antibiotics mixture supplement during the procedure followed by UV sterilization, and appropriate adjustments for a tissue-specific utilization, respectively. The protocol is intended to produce a cardiac d-ECM for cell settlement, representing the ideal scaffold for tissue engineering purposes.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Belviso</LastName><ForeName>Immacolata</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Department of Public Health, University of Naples Federico II, Naples, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sacco</LastName><ForeName>Anna Maria</ForeName><Initials>AM</Initials><AffiliationInfo><Affiliation>Department of Public Health, University of Naples Federico II, Naples, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cozzolino</LastName><ForeName>Domenico</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Public Health, University of Naples Federico II, Naples, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nurzynska</LastName><ForeName>Daria</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Medicine, Surgery and Dentistry, Scuola Medica Salernitana, University of Salerno, Baronissi, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Di Meglio</LastName><ForeName>Franca</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Department of Public Health, University of Naples Federico II, Naples, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Castaldo</LastName><ForeName>Clotilde</ForeName><Initials>C</Initials><Identifier Source="ORCID">0000-0003-1475-5036</Identifier><AffiliationInfo><Affiliation>Department of Public Health, University of Naples Federico II, Naples, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Romano</LastName><ForeName>Veronica</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>Department of Public Health, University of Naples Federico II, Naples, Italy.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>10</Month><Day>19</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS One</MedlineTA><NlmUniqueID>101285081</NlmUniqueID><ISSNLinking>1932-6203</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>9002-93-1</RegistryNumber><NameOfSubstance UI="D017830">Octoxynol</NameOfSubstance></Chemical><Chemical><RegistryNumber>368GB5141J</RegistryNumber><NameOfSubstance UI="D012967">Sodium Dodecyl Sulfate</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000900">Anti-Bacterial Agents</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017830" MajorTopicYN="N">Octoxynol</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012967" MajorTopicYN="N">Sodium Dodecyl Sulfate</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005109" MajorTopicYN="Y">Extracellular Matrix</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D023822" MajorTopicYN="Y">Tissue Engineering</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012038" MajorTopicYN="N">Regeneration</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000900" MajorTopicYN="N">Anti-Bacterial Agents</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054457" MajorTopicYN="N">Tissue Scaffolds</DescriptorName></MeshHeading></MeshHeadingList><CoiStatement>The authors have declared that no competing interests exist.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>3</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>9</Month><Day>23</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>10</Month><Day>19</Day><Hour>13</Hour><Minute>44</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>10</Month><Day>20</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>10</Month><Day>22</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId 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Feb 27;6(9):2927&#x2013;2945. doi: 10.1016/j.bioactmat.2021.02.010 ; PMCID: PMC7930362.</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.bioactmat.2021.02.010</ArticleId><ArticleId IdType="pmc">PMC7930362</ArticleId><ArticleId IdType="pubmed">33732964</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36260426</PMID><DateRevised><Year>2022</Year><Month>10</Month><Day>19</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1930-613X</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Oct</Month><Day>19</Day></PubDate></JournalIssue><Title>Military medicine</Title><ISOAbbreviation>Mil Med</ISOAbbreviation></Journal><ArticleTitle>Standardization of Pulmonary Embolism Evaluation and Management Through Implementation of a Pulmonary Embolism Response Team: A Single-Center Experience at Brooke Army Medical Center.</ArticleTitle><ELocationID EIdType="pii" ValidYN="Y">usac318</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1093/milmed/usac318</ELocationID><Abstract><AbstractText Label="INTRODUCTION" NlmCategory="BACKGROUND">Pulmonary embolism (PE) is associated with significant rates of morbidity and mortality. Management of PE is complex, and adverse patient events are not uncommon. Brooke Army Medical Center (BAMC) is among several select institutions that have implemented multidisciplinary pulmonary embolism response teams (PERTs) to improve PE outcomes. PERT structure varies among institutions and often involves specialty expertise from a variety of departments within the hospital. PE response teams aim to improve the diagnosis and treatment for patients with acute PE. Here, we report our initial experience with this intervention.<AbstractText Label="MATERIALS AND METHODS" NlmCategory="METHODS">We developed a multidisciplinary PERT and implemented a standardized algorithm to guide the evaluation, management, and disposition of patients with acute PE. Patients with PE were identified in the pre-PERT period (2015-2017) and the post-PERT period (2020-2021). A retrospective analysis of clinical characteristics, management strategies, and outcomes was performed for both cohorts.<AbstractText Label="RESULTS" NlmCategory="RESULTS">A total of 68 patients with acute PE were analyzed, 38 patients before PERT adoption, and 30 patients post-PERT. Baseline characteristics between the two cohorts were similar. A statistically significant increase in the evaluation for right ventricle dysfunction was noted in the post-PERT cohort, with 80% of patients having pro-brain natriuretic peptide labs obtained compared to 47% in the pre-PERT cohort (P&#x2009;=&#x2009;.005). Furthermore, 97% of patients in the post-PERT cohort had a transthoracic echocardiogram compared to 55% in the pre-PERT cohort (P&#x2009;=&#x2009;.0001). Six patients in the pre-PERT cohort underwent catheter-directed thrombolysis, compared to zero in the post-PERT cohort (P&#x2009;=&#x2009;.006). There were no differences in other treatment modalities. There was no statistically significant difference in length of stay between the two cohorts.<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">To our knowledge, this is the first report describing the successful implementation of a PERT at a military treatment facility to guide the evaluation, management, and treatment of PE. The implementation of the PERT improved the appropriate diagnostic evaluation for patients with intermediate-risk PE and reduced the use of non-guideline-based catheter-directed thrombolysis. This initiative serves as an example of what could be applied across other military treatment facilities within the Defense Health Agency.
2,329,422
Positive Predictive Value of Endoscopic Findings to Diagnose Vocal Fold Paresis.
Laryngoscopy corresponding with laryngeal electromyography (LEMG) is essential in diagnosing vocal fold paresis. However, baseline asymmetry or other diseases oftentimes confound the exam, making diagnosis difficult. There is currently no agreed upon endoscopic criteria proven to reliably correlate with LEMG findings. We define a set of endoscopic findings termed "paresis triad" that, when present together, reliably correlate with LEMG. The paresis triad consists of (1) hypocontraction of the weak side of the larynx with increased ventricular show, (2) hypercontraction of the intact side with bulging of the false fold covering the ventricle, and (3) tilting of the interarytenoid cleft to the weak side.</AbstractText>We performed a retrospective review of patients with laryngeal asymmetry on laryngoscopy. Patients were divided into two groups: those with consistent paresis triad findings across all pitches and intensities, and those without. All patients underwent LEMG by a neurolaryngologist blinded to the laryngoscopic findings. The endoscopies were then rereviewed in a blinded manner by a second laryngologist to assess inter- and intrarater reliability for identification of the triad.</AbstractText>Twelve patients met inclusion criteria (age 50 +/-15, 7F:5M). Nine had the paresis triad. Three had an inconsistent triad. All patients with the paresis triad had LEMG findings consistent with neurologic injury on the suspected side. All patients with inconsistent triad findings had normal LEMG.</AbstractText>Our findings suggest the proposed laryngoscopic paresis triad may be useful objective criteria to diagnose paresis without the need for LEMG. Further prospective studies should examine a larger series of patients.</AbstractText>4 Laryngoscope, 133:1712-1716, 2023.</AbstractText>&#xa9; 2022 The American Laryngological, Rhinological and Otological Society, Inc.</CopyrightInformation>
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Endoscopic third ventricolustomy as treatment option for normal pressure hydrocephalus.
This descriptive cross-sectional study was performed on 24 patients with normal pressure hydrocephalus who underwent endoscopic third ventriculostomy. The patients were selected by the available sampling method, and the data was collected through a researcher-made checklist. Data were analyzed using SPSS-26 software. Among 24 patients, 62.5% were male and the mean age was 70.85 &#xb1; 9.1 years. The results showed that there was no statistically significant relationship between age (p value = 0.43) and sex (p value = 0.37) with the success and failure rate of the surgical method. There was a significant difference between movement disorders (p value = 0.00) and dementia (p value = 0.00) before and after surgery, while there was no statistically significant difference between urinary disorders before and after surgery. (p value = 0.22). Endoscopic third ventriculostomy is an effective surgical method in the treatment of patients with normal pressure hydrocephalus and it improves the symptoms of movement disorder and dementia.
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Ectopic foci do not co-locate with ventricular epicardial stretch during early acute regional ischemia in isolated pig&#xa0;hearts.<Pagination><StartPage>e15492</StartPage><MedlinePgn>e15492</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">e15492</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.14814/phy2.15492</ELocationID><Abstract><AbstractText>Ectopic activation during early acute regional ischemia may initiate fatal reentrant arrhythmias. However, the origin of this ectopy remains poorly understood. Studies suggest that systolic stretch arising from dyskinesia in ischemic tissue may cause ectopic depolarization due to cardiac mechanosensitivity. The aim of this study was to investigate the link between mechanical stretch and ectopic electrical activation during early acute regional ischemia. We used a recently developed optical mapping technique capable of simultaneous imaging of mechanical deformation and electrical activation in isolated hearts. Eight domestic swine hearts were prepared in left ventricular working mode (LVW), in which the left ventricle was loaded and contracting. In an additional eight non-working (NW) hearts, contraction was pharmacologically suppressed with blebbistatin and the left ventricle was not loaded. In both groups, the left anterior descending coronary artery was tied below the first diagonal branch. Positive mechanical stretch (bulging) during systole was observed in the ischemic zones of LVW, but not NW, hearts. During ischemia phase 1a (0-15&#x2009;min post-occlusion), LVW hearts had more ectopic beats than NW hearts (median: 19, interquartile range: 10-28 vs. median: 2, interquartile range: 1-6; p&#xa0;=&#xa0;0.02); but the difference during phase 1b (15-60&#x2009;min post-occlusion) was not significant (median: 27, interquartile range: 22-42 vs. median: 16, interquartile range: 12-31; p&#xa0;=&#xa0;0.37). Ectopic beats arose preferentially from the ischemic border zone in both groups (p&#x2009;&lt;&#x2009;0.01). In LVW hearts, local mechanical stretch was only occasionally co-located with ectopic foci (9 of 69 ectopic beats). Despite the higher rate of ectopy observed in LVW hearts during ischemia phase 1a, the ectopic beats generally did not arise by the hypothesized mechanism in which ectopic foci are generated by co-local epicardial mechanical stretch.</AbstractText><CopyrightInformation>&#xa9; 2022 The Authors. Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Hanyu</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Biomedical Engineering, University of Alabama at Birmingham, Birmingham, Alabama, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yu</LastName><ForeName>Han</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Biomedical Engineering, University of Alabama at Birmingham, Birmingham, Alabama, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Walcott</LastName><ForeName>Gregory P</ForeName><Initials>GP</Initials><AffiliationInfo><Affiliation>Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rogers</LastName><ForeName>Jack M</ForeName><Initials>JM</Initials><Identifier Source="ORCID">0000-0002-3236-4154</Identifier><AffiliationInfo><Affiliation>Department of Biomedical Engineering, University of Alabama at Birmingham, Birmingham, Alabama, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01-HL115108</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Physiol Rep</MedlineTA><NlmUniqueID>101607800</NlmUniqueID><ISSNLinking>2051-817X</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D013552" MajorTopicYN="N">Swine</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006321" MajorTopicYN="Y">Heart</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001145" MajorTopicYN="Y">Arrhythmias, Cardiac</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016277" MajorTopicYN="N">Ventricular Function, Left</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007511" MajorTopicYN="N">Ischemia</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading></MeshHeadingList><CoiStatement>The authors declares that there is no conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>9</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>6</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>9</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>10</Month><Day>19</Day><Hour>2</Hour><Minute>2</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>10</Month><Day>20</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>10</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36259098</ArticleId><ArticleId IdType="pmc">PMC9579492</ArticleId><ArticleId IdType="doi">10.14814/phy2.15492</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Akaishi, M. , Weintraub, W. 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Ectopic activation during early acute regional ischemia may initiate fatal reentrant arrhythmias. However, the origin of this ectopy remains poorly understood. Studies suggest that systolic stretch arising from dyskinesia in ischemic tissue may cause ectopic depolarization due to cardiac mechanosensitivity. The aim of this study was to investigate the link between mechanical stretch and ectopic electrical activation during early acute regional ischemia. We used a recently developed optical mapping technique capable of simultaneous imaging of mechanical deformation and electrical activation in isolated hearts. Eight domestic swine hearts were prepared in left ventricular working mode (LVW), in which the left ventricle was loaded and contracting. In an additional eight non-working (NW) hearts, contraction was pharmacologically suppressed with blebbistatin and the left ventricle was not loaded. In both groups, the left anterior descending coronary artery was tied below the first diagonal branch. Positive mechanical stretch (bulging) during systole was observed in the ischemic zones of LVW, but not NW, hearts. During ischemia phase 1a (0-15&#x2009;min post-occlusion), LVW hearts had more ectopic beats than NW hearts (median: 19, interquartile range: 10-28 vs. median: 2, interquartile range: 1-6; p&#xa0;=&#xa0;0.02); but the difference during phase 1b (15-60&#x2009;min post-occlusion) was not significant (median: 27, interquartile range: 22-42 vs. median: 16, interquartile range: 12-31; p&#xa0;=&#xa0;0.37). Ectopic beats arose preferentially from the ischemic border zone in both groups (p&#x2009;&lt;&#x2009;0.01). In LVW hearts, local mechanical stretch was only occasionally co-located with ectopic foci (9 of 69 ectopic beats). Despite the higher rate of ectopy observed in LVW hearts during ischemia phase 1a, the ectopic beats generally did not arise by the hypothesized mechanism in which ectopic foci are generated by co-local epicardial mechanical stretch.<CopyrightInformation>&#xa9; 2022 The Authors. Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Hanyu</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Biomedical Engineering, University of Alabama at Birmingham, Birmingham, Alabama, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yu</LastName><ForeName>Han</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Biomedical Engineering, University of Alabama at Birmingham, Birmingham, Alabama, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Walcott</LastName><ForeName>Gregory P</ForeName><Initials>GP</Initials><AffiliationInfo><Affiliation>Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rogers</LastName><ForeName>Jack M</ForeName><Initials>JM</Initials><Identifier Source="ORCID">0000-0002-3236-4154</Identifier><AffiliationInfo><Affiliation>Department of Biomedical Engineering, University of Alabama at Birmingham, Birmingham, Alabama, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01-HL115108</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Physiol Rep</MedlineTA><NlmUniqueID>101607800</NlmUniqueID><ISSNLinking>2051-817X</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D013552" MajorTopicYN="N">Swine</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006321" MajorTopicYN="Y">Heart</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001145" MajorTopicYN="Y">Arrhythmias, Cardiac</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016277" MajorTopicYN="N">Ventricular Function, Left</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007511" MajorTopicYN="N">Ischemia</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading></MeshHeadingList><CoiStatement>The authors declares that there is no conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>9</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>6</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>9</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>10</Month><Day>19</Day><Hour>2</Hour><Minute>2</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>10</Month><Day>20</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>10</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36259098</ArticleId><ArticleId IdType="pmc">PMC9579492</ArticleId><ArticleId IdType="doi">10.14814/phy2.15492</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Akaishi, M. , Weintraub, W. 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Scientific Reports, 8, 10506.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6043572</ArticleId><ArticleId IdType="pubmed">30002391</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36259095</PMID><DateRevised><Year>2022</Year><Month>10</Month><Day>19</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1467-1107</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Oct</Month><Day>19</Day></PubDate></JournalIssue><Title>Cardiology in the young</Title><ISOAbbreviation>Cardiol Young</ISOAbbreviation></Journal><ArticleTitle>Is native aortic valvuloplasty at time of Norwood operation in infants with hypoplastic left heart syndrome and aortic stenosis safe?</ArticleTitle><Pagination><StartPage>1</StartPage><EndPage>2</EndPage><MedlinePgn>1-2</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1017/S1047951122003225</ELocationID><Abstract>In hypoplastic left heart syndrome, the size and function of the left ventricle vary and are dependent on the patency of the aortic valve. A patent native aortic valve, permitting left ventricular ejection, can augment cardiac output. We performed a retrospective chart review of patients with hypoplastic left heart syndrome and a stenotic aortic valve who underwent native aortic valvuloplasty at the time of Norwood and found that none of the eight patients identified had clinically significant aortic insufficiency. This case series suggests that surgical aortic valvuloplasty at Norwood is associated with aortic valve patency/augmented systemic cardiac output without the development of clinically significant aortic regurgitation at intermediate follow-up in a limited cohort.
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Upfront Radiosurgery for Treatment of Symptomatic Obstructive Hydrocephalus due to Brain Tumors.
Introduction Hydrocephalus is a build-up of cerebrospinal fluid (CSF) in the brain and is characterized by abnormal dilatation of the cerebral ventricles. Patients can be either asymptomatic, have symptoms related to primary tumors, or have hydrocephalus-related symptoms. Generally, symptomatic patients are candidates for ventriculoperitoneal (VP) shunt placement to reduce acute symptoms. Little evidence exists regarding the resolution of symptomatic hydrocephalus secondary to brain tumors using stereotactic radiosurgery (SRS) alone as a primary treatment option. Methods The present study is a retrospective series of eight patients (six men and two women) diagnosed with obstructive hydrocephalus due to brain tumors treated with radiosurgery between April 2013 and February 2021. The primary endpoint of the present study is to report our institutional experience regarding the control of symptomatic obstructive hydrocephalus due to brain tumors treated with upfront radiosurgery. Results The mean age was 52 years (range, 5-79). The most common presenting symptoms included headache (100%), vision-related symptoms (75%), and ataxia (37.5%). All patients showed symptom improvement after radiosurgery, five (62.5%) patients showed resolution in less than three days and the rest of the patients resolved hydrocephalus in a longer timeframe (more than three days). All patients lowered their Evans index compared to the index documented before radiosurgery, in a range from 0.02 to 0.17. Conclusion Radiosurgery is a non-invasive alternative treatment for primary and secondary brain tumors that debut with obstructive hydrocephalus, tumors expected to have a high alpha/beta ratio might be suitable to attempt radiosurgery to avoid permanently implanted devices such as VP shunts or other invasive procedures such as a third ventriculostomy. The present study demonstrated that in selected cases SRS can lead to hydrocephalus symptom resolution along with a decrease in ventricular size in a relatively short time frame. Little evidence exists regarding the effect of SRS on symptomatic hydrocephalus resolution and further histology-specific&#xa0;studies are required. We acknowledge that this approach requires immediate access to radiosurgery and close clinical follow-up to ensure success.
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Novelty in Impact of Neurorehabilitation in a Classic Case of Syringomyelia.
A fluid-filled hole inside the parenchyma or central canal of the spinal cord causes syringomyelia, a neurological condition. It is most frequently linked to type 1 Chiari malformations. Syringomyelia can be caused by tumors in the spinal cord, trauma, and post-traumatic or infectious adhesive arachnoiditis. Syringomyelia is shown to have a prevalence of 8.4/100,000 to 0.9/10,000 in certain studies, making it one of the few unusual cases. A large proportion of patients are between 20 and 50 years of age. In our case, the patient is a 17-year-old boy who complained of tingling and weakness in both lower extremities, as well as loss of sensation in both hands. MRI of his spine revealed a Chiari I malformation involving evidence of medulla, fourth ventricle, and cerebellar vermis displacement into the foramen magnum. Arnold Chiari's malformation with cord syringomyelia and tonsillar herniation was diagnosed based on the symptoms and investigation findings. The goal of this case is to highlight the benefits of exercise treatment in improving the patient's quality of life, as physiotherapy protocol instillation is not practiced on a daily basis for such conditions.
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Creation of a novel course for the advanced emergency medicine ultrasound focused practice designation examination.
The American Board of Emergency Medicine recently established a new certification pathway in advanced emergency medicine ultrasound (AEMUS). Eligible applicants come from a wide range of experience but must pass the same examination to become certified. This study sought to evaluate a novel review course targeting a wide range of learners for a new examination.</AbstractText>This was a cross-sectional study evaluating the outcomes of the American College of Emergency Physicians (ACEP) AEMUS review course. The program evaluation survey was designed to collect outcomes across multiple Kirkpatrick levels, including overall satisfaction, topic-specific satisfaction, topic-specific coverage, topic-specific confidence before and after the course, topic-specific perceived knowledge before and after the course, and changes in practice.</AbstractText>Seventy-four of 79 participants (93.7%) completed the survey. Mean course satisfaction was 4.59/5.00 (95% CI 4.47-4.72). Confidence to pass examination components increased for the following topics: administration, advanced left ventricle (LV), education, head and neck, hepatobiliary, male genitourinary, musculoskeletal, nonobstetric gynecology, pediatrics, physics, procedures, research, right ventricle, and venous/arterial. Perceived knowledge increased for the following topics: administration, advanced LV, education, head and neck, male genitourinary, musculoskeletal, pediatrics, physics, procedures, renal/bladder, research, right ventricle, and venous/arterial. Fifty-three of 74 participants (71.6%) stated they would change their practice based on the course. Examples of changes in practice include increased use of ultrasound for advanced abdominal, musculoskeletal, pediatric, and procedural applications. Future work will determine the impact on longer-term outcomes and focused practice designation (FPD) examination pass rates.</AbstractText>The ACEP AEMUS FPD review course demonstrated high levels of satisfaction, increased participant confidence, increased perceived knowledge, and several self-reported changes in participants' ultrasound practice.</AbstractText>&#xa9; 2022 Society for Academic Emergency Medicine.</CopyrightInformation>
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A Case of Non-Germinomatous Germ Cell Tumors of the Frontal Lobe Arising From the Lateral Ventricle With a Synchronous Pineal Lesion.
Non-germinomatous germ cell tumours (NGGCT) are rare intracranial tumours that account for 1% to 3% of cases. They are usually seen in the pineal and suprasellar regions. NGGCT of the frontal lobe arising from the lateral ventricle with a synchronous pineal lesion is uncommon. We present a case of NGGCT with multifocal lesions in the pineal gland, frontal lobe, and pons treated with chemotherapy followed by craniospinal irradiation (CSI).
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Harmonization of Multi-Center Diffusion Tensor Tractography in Neonates with Congenital Heart Disease: Optimizing Post-Processing and Application of ComBat.<ELocationID EIdType="pii" ValidYN="Y">100114</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.ynirp.2022.100114</ELocationID><Abstract><AbstractText>Advanced brain imaging of neonatal macrostructure and microstructure, which has prognosticating importance, is more frequently being incorporated into multi-center trials of neonatal neuroprotection. Multicenter neuroimaging studies, designed to overcome small sample sized clinical cohorts, are essential but lead to increased technical variability. Few harmonization techniques have been developed for neonatal brain microstructural (diffusion tensor) analysis. The work presented here aims to remedy two common problems that exist with the current state of the art approaches: 1) variance in scanner and protocol in data collection can limit the researcher's ability to harmonize data acquired under different conditions or using different clinical populations. 2) The general lack of objective guidelines for dealing with anatomically abnormal anatomy and pathology. Often, subjects are excluded due to subjective criteria, or due to pathology that could be informative to the final analysis, leading to the loss of reproducibility and statistical power. This proves to be a barrier in the analysis of large multi-center studies and is a particularly salient problem given the relative scarcity of neonatal imaging data. We provide an objective, data-driven, and semi-automated neonatal processing pipeline designed to harmonize compartmentalized variant data acquired under different parameters. This is done by first implementing a search space reduction step of extracting the along-tract diffusivity values along each tract of interest, rather than performing whole-brain harmonization. This is followed by a data-driven outlier detection step, with the purpose of removing unwanted noise and outliers from the final harmonization. We then use an empirical Bayes harmonization algorithm performed at the along-tract level, with the output being a lower dimensional space but still spatially informative. After applying our pipeline to this large multi-site dataset of neonates and infants with congenital heart disease (n= 398 subjects recruited across 4 centers, with a total of n=763 MRI pre-operative/post-operative time points), we show that infants with single ventricle cardiac physiology demonstrate greater white matter microstructural alterations compared to infants with bi-ventricular heart disease, supporting what has previously been shown in literature. Our method is an open-source pipeline for delineating white matter tracts in subject space but provides the necessary modular components for performing atlas space analysis. As such, we validate and introduce Diffusion Imaging of Neonates by Group Organization (DINGO), a high-level, semi-automated framework that can facilitate harmonization of subject-space tractography generated from diffusion tensor imaging acquired across varying scanners, institutions, and clinical populations. Datasets acquired using varying protocols or cohorts are compartmentalized into subsets, where a cohort-specific template is generated, allowing for the propagation of the tractography mask set with higher spatial specificity. Taken together, this pipeline can reduce multi-scanner technical variability which can confound important biological variability in relation to neonatal brain microstructure.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Meyers</LastName><ForeName>Benjamin</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Department of Radiology, University of Pittsburgh School of Medicine, Pittsburgh, PA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Vincent K</ForeName><Initials>VK</Initials><AffiliationInfo><Affiliation>Department of Radiology, University of Pittsburgh School of Medicine, Pittsburgh, PA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dennis</LastName><ForeName>Lauren</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Radiology, University of Pittsburgh School of Medicine, Pittsburgh, PA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wallace</LastName><ForeName>Julia</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Radiology, University of Pittsburgh School of Medicine, Pittsburgh, PA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schmithorst</LastName><ForeName>Vanessa</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>Department of Radiology, University of Pittsburgh School of Medicine, Pittsburgh, PA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Votava-Smith</LastName><ForeName>Jodie K</ForeName><Initials>JK</Initials><AffiliationInfo><Affiliation>Division of Cardiology, Department of Pediatrics, Children's Hospital of Los Angeles and Keck School of Medicine University of Southern California, Los Angeles, CA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rajagopalan</LastName><ForeName>Vidya</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>Department of Radiology, Children's Hospital of Los Angeles and Keck School of Medicine University of Southern California Los Angeles, CA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Herrup</LastName><ForeName>Elizabeth</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Department of Critical Care Medicine, University of Pittsburgh, Pittsburgh, PA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Baust</LastName><ForeName>Tracy</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Critical Care Medicine, University of Pittsburgh, Pittsburgh, PA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tran</LastName><ForeName>Nhu N</ForeName><Initials>NN</Initials><AffiliationInfo><Affiliation>Division of Cardiology, Department of Pediatrics, Children's Hospital of Los Angeles and Keck School of Medicine University of Southern California, Los Angeles, CA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hunter</LastName><ForeName>Jill</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Radiology, Texas Children's Hospital, Houston, TX.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Licht</LastName><ForeName>Daniel J</ForeName><Initials>DJ</Initials><AffiliationInfo><Affiliation>Department of Neurology, Children's Hospital of Philadelphia, Philadelphia, PA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gaynor</LastName><ForeName>J William</ForeName><Initials>JW</Initials><AffiliationInfo><Affiliation>Department of Surgery, Children's Hospital of Philadelphia, Philadelphia, PA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Andropoulos</LastName><ForeName>Dean B</ForeName><Initials>DB</Initials><AffiliationInfo><Affiliation>Department of Anesthesiology, Texas Children's Hospital, Houston, TX.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Panigrahy</LastName><ForeName>Ashok</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Radiology, University of Pittsburgh School of Medicine, Pittsburgh, PA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Biomedical Informatics, University of Pittsburgh School of Medicine, Pittsburgh, PA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ceschin</LastName><ForeName>Rafael</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Radiology, University of Pittsburgh School of Medicine, Pittsburgh, PA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Biomedical Informatics, University of Pittsburgh School of Medicine, Pittsburgh, PA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>K01 HL153942</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>K23 NR019121</GrantID><Acronym>NR</Acronym><Agency>NINR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL128818</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL152740</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>06</Month><Day>20</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Neuroimage Rep</MedlineTA><NlmUniqueID>9918227365206676</NlmUniqueID><ISSNLinking>2666-9560</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Congenital Heart Disease</Keyword><Keyword MajorTopicYN="N">Diffusion Tensor Imaging</Keyword><Keyword 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Advanced brain imaging of neonatal macrostructure and microstructure, which has prognosticating importance, is more frequently being incorporated into multi-center trials of neonatal neuroprotection. Multicenter neuroimaging studies, designed to overcome small sample sized clinical cohorts, are essential but lead to increased technical variability. Few harmonization techniques have been developed for neonatal brain microstructural (diffusion tensor) analysis. The work presented here aims to remedy two common problems that exist with the current state of the art approaches: 1) variance in scanner and protocol in data collection can limit the researcher's ability to harmonize data acquired under different conditions or using different clinical populations. 2) The general lack of objective guidelines for dealing with anatomically abnormal anatomy and pathology. Often, subjects are excluded due to subjective criteria, or due to pathology that could be informative to the final analysis, leading to the loss of reproducibility and statistical power. This proves to be a barrier in the analysis of large multi-center studies and is a particularly salient problem given the relative scarcity of neonatal imaging data. We provide an objective, data-driven, and semi-automated neonatal processing pipeline designed to harmonize compartmentalized variant data acquired under different parameters. This is done by first implementing a search space reduction step of extracting the along-tract diffusivity values along each tract of interest, rather than performing whole-brain harmonization. This is followed by a data-driven outlier detection step, with the purpose of removing unwanted noise and outliers from the final harmonization. We then use an empirical Bayes harmonization algorithm performed at the along-tract level, with the output being a lower dimensional space but still spatially informative. After applying our pipeline to this large multi-site dataset of neonates and infants with congenital heart disease (n= 398 subjects recruited across 4 centers, with a total of n=763 MRI pre-operative/post-operative time points), we show that infants with single ventricle cardiac physiology demonstrate greater white matter microstructural alterations compared to infants with bi-ventricular heart disease, supporting what has previously been shown in literature. Our method is an open-source pipeline for delineating white matter tracts in subject space but provides the necessary modular components for performing atlas space analysis. As such, we validate and introduce Diffusion Imaging of Neonates by Group Organization (DINGO), a high-level, semi-automated framework that can facilitate harmonization of subject-space tractography generated from diffusion tensor imaging acquired across varying scanners, institutions, and clinical populations. Datasets acquired using varying protocols or cohorts are compartmentalized into subsets, where a cohort-specific template is generated, allowing for the propagation of the tractography mask set with higher spatial specificity. Taken together, this pipeline can reduce multi-scanner technical variability which can confound important biological variability in relation to neonatal brain microstructure.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Meyers</LastName><ForeName>Benjamin</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Department of Radiology, University of Pittsburgh School of Medicine, Pittsburgh, PA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Vincent K</ForeName><Initials>VK</Initials><AffiliationInfo><Affiliation>Department of Radiology, University of Pittsburgh School of Medicine, Pittsburgh, PA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dennis</LastName><ForeName>Lauren</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Radiology, University of Pittsburgh School of Medicine, Pittsburgh, PA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wallace</LastName><ForeName>Julia</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Radiology, University of Pittsburgh School of Medicine, Pittsburgh, PA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schmithorst</LastName><ForeName>Vanessa</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>Department of Radiology, University of Pittsburgh School of Medicine, Pittsburgh, PA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Votava-Smith</LastName><ForeName>Jodie K</ForeName><Initials>JK</Initials><AffiliationInfo><Affiliation>Division of Cardiology, Department of Pediatrics, Children's Hospital of Los Angeles and Keck School of Medicine University of Southern California, Los Angeles, CA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rajagopalan</LastName><ForeName>Vidya</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>Department of Radiology, Children's Hospital of Los Angeles and Keck School of Medicine University of Southern California Los Angeles, CA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Herrup</LastName><ForeName>Elizabeth</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Department of Critical Care Medicine, University of Pittsburgh, Pittsburgh, PA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Baust</LastName><ForeName>Tracy</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Critical Care Medicine, University of Pittsburgh, Pittsburgh, PA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tran</LastName><ForeName>Nhu N</ForeName><Initials>NN</Initials><AffiliationInfo><Affiliation>Division of Cardiology, Department of Pediatrics, Children's Hospital of Los Angeles and Keck School of Medicine University of Southern California, Los Angeles, CA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hunter</LastName><ForeName>Jill</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Radiology, Texas Children's Hospital, Houston, TX.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Licht</LastName><ForeName>Daniel J</ForeName><Initials>DJ</Initials><AffiliationInfo><Affiliation>Department of Neurology, Children's Hospital of Philadelphia, Philadelphia, PA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gaynor</LastName><ForeName>J William</ForeName><Initials>JW</Initials><AffiliationInfo><Affiliation>Department of Surgery, Children's Hospital of Philadelphia, Philadelphia, PA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Andropoulos</LastName><ForeName>Dean B</ForeName><Initials>DB</Initials><AffiliationInfo><Affiliation>Department of Anesthesiology, Texas Children's Hospital, Houston, TX.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Panigrahy</LastName><ForeName>Ashok</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Radiology, University of Pittsburgh School of Medicine, Pittsburgh, PA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Biomedical Informatics, University of Pittsburgh School of Medicine, Pittsburgh, PA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ceschin</LastName><ForeName>Rafael</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Radiology, University of Pittsburgh School of Medicine, Pittsburgh, PA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Biomedical Informatics, University of Pittsburgh School of Medicine, Pittsburgh, PA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>K01 HL153942</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>K23 NR019121</GrantID><Acronym>NR</Acronym><Agency>NINR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL128818</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL152740</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>06</Month><Day>20</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Neuroimage Rep</MedlineTA><NlmUniqueID>9918227365206676</NlmUniqueID><ISSNLinking>2666-9560</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Congenital Heart Disease</Keyword><Keyword MajorTopicYN="N">Diffusion Tensor Imaging</Keyword><Keyword 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JAMA Pediatrics. 2016;94158(4). doi:10.1001/jamapediatrics.2015.4450</Citation><ArticleIdList><ArticleId IdType="doi">10.1001/jamapediatrics.2015.4450</ArticleId><ArticleId IdType="pmc">PMC5083633</ArticleId><ArticleId IdType="pubmed">26902528</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36258282</PMID><DateRevised><Year>2022</Year><Month>10</Month><Day>18</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1467-1107</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Oct</Month><Day>19</Day></PubDate></JournalIssue><Title>Cardiology in the young</Title><ISOAbbreviation>Cardiol Young</ISOAbbreviation></Journal><ArticleTitle>The prognostic role of liver volumetry in Fontan patients.</ArticleTitle><Pagination><StartPage>1</StartPage><EndPage>6</EndPage><MedlinePgn>1-6</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1017/S1047951122002992</ELocationID><Abstract><AbstractText Label="BACKGROUND AND HYPOTHESES" NlmCategory="UNASSIGNED">High venous pressures and associated hepatic congestion are important drivers for Fontan-associated liver disease. The prognostic significance of hepatomegaly as a marker of congestion however is not well defined and is further explored in this research study.<AbstractText Label="METHODS" NlmCategory="METHODS">Fontan patients who have had liver ultrasound scans were identified from the Prince Sultan Cardiac Centre Fontan Database and had their anatomic, surgical, clinical histories abstracted from the electronic medical records following institutional ethics approval. Liver volumes were determined retrospectively from reviewing individual US images, and these, divided into tertiles, were analysed in the context of the predefined endpoints of (i) Primary - death or heart or liver transplantation, or (ii) Secondary - combined endpoint of death, transplantation, arrhythmia, or protein-losing enteropathy.<AbstractText Label="RESULTS" NlmCategory="RESULTS">Mean indexed liver volumes for the entire cohort (n = 199) were 1065.1 &#xb1; 312.1 ml/m<sup>2</sup>, range 387 to 2071 ml/m<sup>2</sup>. Patients with the largest liver volumes (highest tertile) were less likely to have a functioning fenestration compared to those in the lowest tertile 44% versus 56% p = 0.016 and experienced the highest burden of mortality and heart or heart-liver transplantation, p = 0.016, and were more likely to reach the composite endpoint of death, protein-losing enteropathy, arrhythmia, or transplantation, p = 0.010. Liver volumes had an overall predictive accuracy for the combined outcome of 61% (CI 53%, 67%, p = 0.009).<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Liver volumetry may serve as a potentially important congestion biomarker for adverse outcomes after the Fontan operation.
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Student Team Achievement Division as a tool for peer assisted co-operative learning in neuroanatomy.
Student Team Achievement Division (STAD) is a co-operative learning approach premised on a group learning activity that emphazises learning as a social exchange of knowledge between students, in which each student is accountable for his or her own learning and is also encouraged to assist others in achieving their goals. It promotes the cognitive, psychomotor, and emotional growth of students involved in the team. By random sequencing, 60 participants were allocated to interventional group (n=30) and control group (n=30). The participants of the interventional group were subjected to STAD strategy and participants of the control group were instructed to do a conventional self learning on the ventricles of brain. The outcomes were statistically analysed. It was found that the performance of the students is far better with STAD approach than conventional self learning. Our study has shown that Students team Achievement Division can be used as an effective tool for Peer assisted Co-operative Learning in Anatomy. Further studies can be done to investigate the contribution of STAD to teaching other disciplines of Anatomy and other basic medical sciences.
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Chronic lipopolysaccharide impairs motivation when delivered to the ventricles, but not when delivered peripherally in male rats.
Increased neuroinflammation relative to controls is observed in major depression. Moreover, depressive disorders are significantly elevated in conditions which increase neuroinflammation (e.g., brain injury, Parkinson's disease, Alzheimer's disease). To better understand the relationship between neuroinflammation and depression, additional research is needed. The current set of studies made use of the progressive ratio (PR) task in male rats, a stable measure of motivation which can be evaluated daily and thus is ideally suited for examining a potential role for chronic neuroinflammation in depressive-like behavior. Lipopolysaccharide (LPS) was used to induce an inflammatory response. Experiment 1 confirmed prior acute LPS administration experiments for sensitivity of the PR task, with a large effect at 2&#xa0;mg/kg, a partial effect at 1&#xa0;mg/kg, and no effect at 0.5&#xa0;mg/kg. Experiment 2 evaluated a dose-response of continuous s.c. LPS infusion but found no significant elevation in brain cytokines after 14 days at any doses of 0.1, 0.5, 1, or 2&#xa0;mg/kg/week. Experiment 3 assessed motivation during continuous s.c. infusion of a large 5&#xa0;mg/kg/week LPS dose and found no significant impairments in motivation, but transient decreases in rates of lever pressing (i.e., only motoric deficits). Experiment 4 measured motivation during continuous ICV infusion of 10.5&#xa0;&#x3bc;g/kg/week LPS and found significantly decreased motivation without changes to rates of lever pressing (i.e., only motivational deficits). Together these results suggest that the PR task is efficient for evaluating models of chronic inflammation, and that the adaptive response to chronic LPS exposure, even when delivered centrally, may necessitate alternative strategies for generating long-term neuroinflammation.
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Endoscope-assisted far lateral craniotomy for resection of posterior fossa neurocysticercosis: illustrative case.
Neurocysticercosis is a parasitic infection that commonly affects the ventricles, subarachnoid spaces, and spinal cord of the central nervous system. The authors report an unusual manifestation of purely posterior fossa neurocysticercosis treated with endoscope-assisted open craniotomy for resection.</AbstractText>A 67-year-old male presented with 2 months of progressive dizziness, gait ataxia, headaches, decreased hearing, and memory impairment. Imaging revealed an extra-axial cystic lesion occupying the foramen magnum and left cerebellopontine angle with significant mass effect and evidence of early hydrocephalus. Gross-total resection was accomplished via a left far lateral craniotomy with open endoscopic assistance, and pathological findings were consistent with neurocysticercosis. Postoperatively, he was noted to have a sixth nerve palsy, and adjuvant therapy included albendazole. By 9 months postoperatively, he exhibited complete resolution of an immediate postoperative sixth nerve palsy in addition to all preoperative symptoms. His hydrocephalus resolved and did not require permanent cerebrospinal fluid (CSF) diversion.</AbstractText>When combined with traditional skull base approaches, open endoscopic techniques allow for enhanced visualization and resection of complex lesions otherwise inaccessible under the microscope alone. Recognition and obliteration of central nervous system neurocysticercosis can facilitate excellent neurological recovery without the need for CSF diversion.</AbstractText>
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Primary intracranial extraosseous Ewing's sarcoma of the skull base in an elderly adult: illustrative case.
Primary extraosseous intracranial Ewing's sarcoma, also known as a peripheral primitive neuroectodermal tumor or "small round blue cell tumor," is an extremely rare entity with limited representation in the literature beyond the pediatric population.</AbstractText>A 67-year-old male suffering occipital headache, nausea, and gait disturbance was found to have a large, avidly contrast-enhancing cerebellopontine angle mass extending into the cervical spinal canal with associated mass effect on medulla, cerebellum, fourth ventricle, and cervical spinal cord. This mass was not present on the imaging from 8 years prior. He underwent surgical debulking and pathology results demonstrated a malignant small round cell tumor showing diffuse immunopositivity for cytokeratins, CD99 and NKX2.2 with EWRS1-FLI1 rearrangement in 84% of the nuclei confirmatory of Ewing's sarcoma. After 14 cycles of chemotherapy and 6 weeks of radiotherapy, 22 months after discovery, the patient remains in clinical and radiographic remission with complete return to his baseline functioning.</AbstractText>Primary skull base extraosseous Ewing's sarcoma should be considered in the differential diagnosis even in the elderly population when imaging studies demonstrate aggressive tumor growth patterns. Tumor debulking to establish a diagnosis followed by adjuvant chemoradiation therapy can result in clinical improvement with remission.</AbstractText>
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Multiple drug transporters contribute to the brain transfer of levofloxacin.<Pagination><StartPage>445</StartPage><EndPage>457</EndPage><MedlinePgn>445-457</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1111/cns.13989</ELocationID><Abstract><AbstractText Label="AIMS">The aim of this study was to assess the influence of the major transporters at blood-brain barrier and blood-cerebrospinal fluid barrier on levofloxacin (LVFX) pharmacokinetics in rat. To explore the different effects of transporters on drug concentrations in cerebrospinal fluid (CSF) and brain extracellular fluid (ECF).</AbstractText><AbstractText Label="METHODS">High-performance liquid chromatography coupled with microdialysis was used to continuously and synchronously measure unbound concentrations of LVFX in rat blood, hippocampal ECF, and lateral ventricle CSF for comprehensive characterization of brain pharmacokinetics. The role of transporters in the brain efflux mechanism of LVFX was analyzed in the absence and presence of various transporter inhibitors.</AbstractText><AbstractText Label="RESULTS">Following LVFX (50&#x2009;mg/kg) administration, the unbound partition coefficient of LVFX in brain ECF and CSF (K<sub>p,uu,ECF</sub> and K<sub>p,uu,CSF</sub> ) were 34.0&#x2009;&#xb1;&#x2009;1.7% and 41.2&#x2009;&#xb1;&#x2009;2.4%, respectively. When probenecid was coadministered with LVFX, the AUC and the mean residence time (MRT) in rat blood increased significantly (p&#x2009;&lt;&#x2009;0.05). After MK571 intervention, 1.35-fold and 1.16-fold increases in K<sub>p,uu,ECF</sub> and K<sub>p,uu,CSF</sub> were observed, respectively (p&#x2009;&lt;&#x2009;0.05). Treatment with Ko143 increased the levels of LVFX in brain ECF. The difference in LVFX concentration in brain ECF and CSF was &lt;3-fold with or without treatment with transporter inhibitors.</AbstractText><AbstractText Label="CONCLUSION">Efflux of LVFX from the central nervous system (CNS) involves multidrug resistance-associated proteins (MRPs), breast cancer resistance protein (BCRP), and organic anion transporters (OATs). MRPs play an important role in mediating the brain/CSF-to-blood efflux of LVFX. LVFX concentrations in CSF can be used as a surrogate to predict the concentrations inside brain parenchyma.</AbstractText><CopyrightInformation>&#xa9; 2022 The Authors. CNS Neuroscience &amp; Therapeutics published by John Wiley &amp; Sons Ltd.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Cen</LastName><ForeName>Yuying</ForeName><Initials>Y</Initials><Identifier Source="ORCID">0000-0002-3560-0298</Identifier><AffiliationInfo><Affiliation>Medical School of Chinese PLA, Beijing, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Neurology, The First Medical Centre, Chinese PLA General Hospital, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shan</LastName><ForeName>Yuheng</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Medical School of Chinese PLA, Beijing, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Neurology, The First Medical Centre, Chinese PLA General Hospital, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhao</LastName><ForeName>Jiahua</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Medical School of Chinese PLA, Beijing, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Neurology, The First Medical Centre, Chinese PLA General Hospital, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xu</LastName><ForeName>Xiaojiao</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Medical School of Chinese PLA, Beijing, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Neurology, The First Medical Centre, Chinese PLA General Hospital, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nie</LastName><ForeName>Zhiyong</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>State Key Laboratory of Toxicology and Medical Countermeasures, Institute of Pharmacology and Toxicology, Academy of Military Medical Sciences, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Jiatang</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Neurology, The First Medical Centre, Chinese PLA General Hospital, Beijing, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>10</Month><Day>17</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>CNS Neurosci Ther</MedlineTA><NlmUniqueID>101473265</NlmUniqueID><ISSNLinking>1755-5930</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000070997">ATP Binding Cassette Transporter, Subfamily G, Member 2</NameOfSubstance></Chemical><Chemical><RegistryNumber>6GNT3Y5LMF</RegistryNumber><NameOfSubstance UI="D064704">Levofloxacin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D027425">Multidrug Resistance-Associated Proteins</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000070997" MajorTopicYN="Y">ATP Binding Cassette Transporter, Subfamily G, Member 2</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001812" MajorTopicYN="N">Blood-Brain Barrier</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001921" MajorTopicYN="Y">Brain</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D064704" MajorTopicYN="Y">Levofloxacin</DescriptorName><QualifierName UI="Q000493" MajorTopicYN="N">pharmacokinetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D027425" MajorTopicYN="Y">Multidrug Resistance-Associated Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">blood-brain barrier</Keyword><Keyword MajorTopicYN="N">blood-cerebrospinal fluid barrier</Keyword><Keyword MajorTopicYN="N">drug transporters</Keyword><Keyword MajorTopicYN="N">levofloxacin</Keyword><Keyword MajorTopicYN="N">pharmacokinetics</Keyword></KeywordList><CoiStatement>There are no conflicts of interest to declare.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>9</Month><Day>7</Day></PubMedPubDate><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>6</Month><Day>20</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>9</Month><Day>21</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>10</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2023</Year><Month>1</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>10</Month><Day>18</Day><Hour>0</Hour><Minute>22</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36253925</ArticleId><ArticleId IdType="pmc">PMC9804084</ArticleId><ArticleId IdType="doi">10.1111/cns.13989</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Hayakawa I, Furuhama K, Takayama S, Osada Y. 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Xenobiotica. 2015;45(6):547&#x2010;555.</Citation><ArticleIdList><ArticleId IdType="pubmed">25539457</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedBookArticle><BookDocument><PMID Version="1">29262022</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK470256</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-22652">Anatomy, Thorax, Heart
The heart is a muscular organ situated in the center of the chest behind the sternum. It consists of four chambers: the two upper chambers are called the right and left atria, and the two lower chambers are called the right and left ventricles. The right atrium and ventricle together are often called the right heart, and the left atrium and left ventricle together functionally form the left heart.
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Single-Nucleotide Polymorphisms in Exonic and Promoter Regions of Transcription Factors of Second Heart Field Associated with Sporadic Congenital Cardiac Anomalies.
Multiple second heart field (SHF) transcription factors are involved in cardiac development. In this article we evaluate the relationship between SHF transcription factor polymorphisms and congenital heart disease (CHD). Ten polymorphisms were used for genotyping, and three of these were used for the luciferase assay. The risk of CHD was increased 4.31 times and 1.54 times in the C allele of <i>GATA5</i>: rs6061243 G&gt;C and G allele of <i>TBX20</i>: rs336283 A&gt;G, respectively. The minor alleles of <i>SMYD1</i>: rs1542088 T&gt;G, <i>MEF2C</i>: rs80043958 A&gt;G and <i>GATA5</i>: rs6587239 T&gt;C increased the risk of the simple types of CHD. The minor alleles of <i>GATA5</i>: rs41305803 G&gt;A and <i>MEF2C</i>: rs304154 A&gt;G increased the risk of tetralogy of Fallot (TOF). The minor alleles of <i>TBX20</i>: rs336284 A&gt;G and <i>SMYD1</i>: rs88387557 T&gt;G only increased the risk of a single ventricle (SV). Luciferase assays revealed that the minor alleles of rs304154 and rs336284 decreased the transcriptional levels of <i>MEF2C</i> and <i>TBX20,</i> respectively (p&lt;0.01). When combined with <i>HLTF</i>, the G promoter showed a higher expression level than the A promoter in rs80043958 (p&lt;0.01). Our findings suggest that minor alleles of SNPs in the exonic and promoter regions of transcription factors in the SHF can increase the risks of sporadic CHD.
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Extended endoscopic endonasal approach for resecting anterior intrinsic third ventricular craniopharyngioma.
The surgical treatment of the extended endoscopic endonasal approach (EEEA) is a safe and effective treatment for suprasellar craniopharyngiomas. However, due to damage to the hypothalamus and third ventricle floor (TVF), EEEA is generally regarded as unsuitable in treating intrinsic third ventricle craniopharyngioma (ITVC) that is entirely within the third ventricle. Until now, there have been only a small number of reports using EEEA to treat TVC via</i> a supra-infrachiasmatic approach. Given that the translamina terminalis (TLT) corridor was used in the transcranial subfrontal approach, EEEA via</i> a suprachiasmatic approach may be feasible and practical to treat ITVC. In the current study, we accumulated experience applying the suprachiasmatic translamina terminalis (STLT) corridor for anterior treatment of ITVC.</AbstractText>From March 2016 to December 2020, 14 patients with ITVC in our center were analyzed retrospectively. All patients underwent surgery by EEEA via</i> an STLT corridor. The multilayer reconstruction technique was adopted to achieve skull base reconstruction. Data concerning the patient's tumor resection, vision, hypophyseal hormone, and complications were collected.</AbstractText>Gross-total resection was achieved in 13 (92.8%) of14 patients, with achievement of near-total (90%) resection in the remaining 1 patient. Nine cases (64.3%) were papillary craniopharyngiomas, and the other 5 cases were adamantinomatous subtypes. Postoperatively, 3 patients with pituitary insufficiency received hormone replacement therapy. No permanent diabetes insipidus or hypothalamic obesity was found. All pairs showed significant improvement or stability in vision except 1 patient who encountered visual deterioration. No other neurological deficit occurred postoperatively. Observation results for the exudation of nasal tissue and the length of hospitalization were satisfactory. After a mean follow-up period of 26.2 months, tumor recurrence was not observed.</AbstractText>TLT is a minimally invasive corridor used in EEEA for treating anterior ITVC without increasing risks of visual and hormonal deficits. The multilayered reconstruction technique we used is a safe and effective method for achieving watertight closure and avoiding cerebrospinal fluid leaks and infection. The endonasal approach via</i> STLT provides a new, safe and efficacious operative strategy that should be considered a surgical alternative in treating ITVC.</AbstractText>Copyright &#xa9; 2022 Zhou, Wei, Jin, Hei, Jia, Lin, Yang, Jiang, Liu and Gao.</CopyrightInformation>
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Role of endoscopic endonasal approach for craniopharyngiomas extending into the third ventricle in adults.
&#x2022;EAA is an innovative, promising, safe and effective approach for 3VCPs.&#x2022;Key of success is surgeon learning curve in endoscopy and patients selection.&#x2022;With correct indications, EEA gives GTR and morbidity rate similar to other routes.&#x2022;Clinical, tumoral and anatomical features should be considered for EEA selection.
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Chronic Subdural Hematoma (cSDH): A review of the current state of the art.
Incidence of Chronic Subdural Hematoma (cSDH) is rising worldwide, partly due to an aging population, but also due to increased use of antithrombotic medication. Many recent studies have emerged to address current cSDH management strategies.</AbstractText>What is the state of the art of cSDH management.</AbstractText>Review.</AbstractText>Head trauma, antithrombotic use and craniocerebral disproportion increase the risk of cSDH development. Most patients present with disorientation, GCS 13-15, and symptoms arising from cortical irritation and increased intracranial pressure. cSDH occurs bilaterally in 9-22%. CT allows assessment of cerebral compression (herniation, hematoma thickness, ventricle collapse, midline shift), hematoma age and presence of membranes, factors that ultimately determine treatment urgency and surgical approach. Recurrence remains the principle complication (9-33%), occurring more commonly with older age and bilateral cSDHs.</AbstractText>While incompletely understood, it is generally believed that injury in the dural cell layer results in bleeding from bridging veins, resulting in a hematoma formation, with or without a preceding hygroma, in a potential space approximating the junction between the dura and arachnoid. Neovascularization and leaking from the outer membrane are thought to propagate this process. Evidence that MMA embolization may reduce recurrence rates is a potentially exciting new treatment option, but also supports the theory that the MMA is implicated in the cSDH pathophysiology. The use of steroids remains a controversial topic without clear treatment guidelines. cSDH represents a common neurosurgical problem with burr-hole treatment remaining the gold standard, often in conjunction with subgaleal drains. MMA embolization to stop recurrence may represent an important evolution in understanding the pathophysiology of cSDH and improving treatment.</AbstractText>&#xa9; 2021 The Authors.</CopyrightInformation>
2,329,439
Extracellular signal-regulated kinase-dependent phosphorylation of histone H3 serine 10 is involved in the pathogenesis of traumatic brain injury.<Pagination><StartPage>828567</StartPage><MedlinePgn>828567</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">828567</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.3389/fnmol.2022.828567</ELocationID><Abstract><AbstractText>Traumatic brain injury (TBI) induces a series of epigenetic changes in brain tissue, among which histone modifications are associated with the deterioration of TBI. In this study, we explored the role of histone H3 modifications in a weight-drop model of TBI in rats. Screening for various histone modifications, immunoblot analyses revealed that the phosphorylation of histone H3 serine 10 (p-H3S10) was significantly upregulated after TBI in the brain tissue surrounding the injury site. A similar posttraumatic regulation was observed for phosphorylated extracellular signal-regulated kinase (p-ERK), which is known to phosphorylate H3S10. In support of the hypothesis that ERK-mediated phosphorylation of H3S10 contributes to TBI pathogenesis, double immunofluorescence staining of brain sections showed high levels and colocalization of p-H3S10 and p-ERK predominantly in neurons surrounding the injury site. To test the hypothesis that inhibition of ERK-H3S10 signaling ameliorates TBI pathogenesis, the mitogen-activated protein kinase-extracellular signal-regulated kinase kinase (MEK) 1/2 inhibitor U0126, which inhibits ERK phosphorylation, was administered into the right lateral ventricle of TBI male and female rats via intracerebroventricular cannulation for 7 days post trauma. U0126 administration indeed prevented H3S10 phosphorylation and improved motor function recovery and cognitive function compared to vehicle treatment. In agreement with our findings in the rat model of TBI, immunoblot and double immunofluorescence analyses of brain tissue specimens from patients with TBI demonstrated high levels and colocalization of p-H3S10 and p-ERK as compared to control specimens from non-injured individuals. In conclusion, our findings indicate that phosphorylation-dependent activation of ERK-H3S10 signaling participates in the pathogenesis of TBI and can be targeted by pharmacological approaches.</AbstractText><CopyrightInformation>Copyright &#xa9; 2022 Zhang, Yang, Hou, Zhou, Bi, Yang, Lu, Ding, Ding, Zou, Guo, Sch&#xe4;fer and Huang.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Yu</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Anesthesiology, Xiangya Hospital Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Xin</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Anesthesiology, Xiangya Hospital Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hou</LastName><ForeName>Xinran</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Anesthesiology, Xiangya Hospital Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhou</LastName><ForeName>Wen</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Department of Anesthesiology, Xiangya Hospital Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bi</LastName><ForeName>Changlong</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Xiangya Hospital Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Zhuanyi</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Xiangya Hospital Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lu</LastName><ForeName>Sining</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Medical College of Xiangya, Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ding</LastName><ForeName>Zijin</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Department of Anesthesiology, Xiangya Hospital Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ding</LastName><ForeName>Zhuofeng</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Department of Anesthesiology, Xiangya Hospital Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zou</LastName><ForeName>Yu</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Anesthesiology, Xiangya Hospital Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Guo</LastName><ForeName>Qulian</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>Department of Anesthesiology, Xiangya Hospital Central South University, Changsha, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>National Clinical Research Center for Geriatric Disorders, Xiangya Hospital Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sch&#xe4;fer</LastName><ForeName>Michael K E</ForeName><Initials>MKE</Initials><AffiliationInfo><Affiliation>Department of Anesthesiology, University Medical Center, Johannes Gutenberg University Mainz, Mainz, Germany.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Focus Program Translational Neurosciences and Research Center of Immunotherapy of the Johannes Gutenberg University Mainz, Mainz, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Huang</LastName><ForeName>Changsheng</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Anesthesiology, Xiangya Hospital Central South University, Changsha, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>National Clinical Research Center for Geriatric Disorders, Xiangya Hospital Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>09</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Front Mol Neurosci</MedlineTA><NlmUniqueID>101477914</NlmUniqueID><ISSNLinking>1662-5099</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">ERK</Keyword><Keyword MajorTopicYN="N">H3S10</Keyword><Keyword MajorTopicYN="N">histone modification</Keyword><Keyword MajorTopicYN="N">phosphorylation</Keyword><Keyword MajorTopicYN="N">traumatic brain injury</Keyword></KeywordList><CoiStatement>The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2021</Year><Month>12</Month><Day>30</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>9</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>10</Month><Day>17</Day><Hour>4</Hour><Minute>22</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>10</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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Traumatic brain injury (TBI) induces a series of epigenetic changes in brain tissue, among which histone modifications are associated with the deterioration of TBI. In this study, we explored the role of histone H3 modifications in a weight-drop model of TBI in rats. Screening for various histone modifications, immunoblot analyses revealed that the phosphorylation of histone H3 serine 10 (p-H3S10) was significantly upregulated after TBI in the brain tissue surrounding the injury site. A similar posttraumatic regulation was observed for phosphorylated extracellular signal-regulated kinase (p-ERK), which is known to phosphorylate H3S10. In support of the hypothesis that ERK-mediated phosphorylation of H3S10 contributes to TBI pathogenesis, double immunofluorescence staining of brain sections showed high levels and colocalization of p-H3S10 and p-ERK predominantly in neurons surrounding the injury site. To test the hypothesis that inhibition of ERK-H3S10 signaling ameliorates TBI pathogenesis, the mitogen-activated protein kinase-extracellular signal-regulated kinase kinase (MEK) 1/2 inhibitor U0126, which inhibits ERK phosphorylation, was administered into the right lateral ventricle of TBI male and female rats via intracerebroventricular cannulation for 7 days post trauma. U0126 administration indeed prevented H3S10 phosphorylation and improved motor function recovery and cognitive function compared to vehicle treatment. In agreement with our findings in the rat model of TBI, immunoblot and double immunofluorescence analyses of brain tissue specimens from patients with TBI demonstrated high levels and colocalization of p-H3S10 and p-ERK as compared to control specimens from non-injured individuals. In conclusion, our findings indicate that phosphorylation-dependent activation of ERK-H3S10 signaling participates in the pathogenesis of TBI and can be targeted by pharmacological approaches.<CopyrightInformation>Copyright &#xa9; 2022 Zhang, Yang, Hou, Zhou, Bi, Yang, Lu, Ding, Ding, Zou, Guo, Sch&#xe4;fer and Huang.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Yu</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Anesthesiology, Xiangya Hospital Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Xin</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Anesthesiology, Xiangya Hospital Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hou</LastName><ForeName>Xinran</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Anesthesiology, Xiangya Hospital Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhou</LastName><ForeName>Wen</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Department of Anesthesiology, Xiangya Hospital Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bi</LastName><ForeName>Changlong</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Xiangya Hospital Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Zhuanyi</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Xiangya Hospital Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lu</LastName><ForeName>Sining</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Medical College of Xiangya, Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ding</LastName><ForeName>Zijin</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Department of Anesthesiology, Xiangya Hospital Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ding</LastName><ForeName>Zhuofeng</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Department of Anesthesiology, Xiangya Hospital Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zou</LastName><ForeName>Yu</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Anesthesiology, Xiangya Hospital Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Guo</LastName><ForeName>Qulian</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>Department of Anesthesiology, Xiangya Hospital Central South University, Changsha, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>National Clinical Research Center for Geriatric Disorders, Xiangya Hospital Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sch&#xe4;fer</LastName><ForeName>Michael K E</ForeName><Initials>MKE</Initials><AffiliationInfo><Affiliation>Department of Anesthesiology, University Medical Center, Johannes Gutenberg University Mainz, Mainz, Germany.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Focus Program Translational Neurosciences and Research Center of Immunotherapy of the Johannes Gutenberg University Mainz, Mainz, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Huang</LastName><ForeName>Changsheng</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Anesthesiology, Xiangya Hospital Central South University, Changsha, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>National Clinical Research Center for Geriatric Disorders, Xiangya Hospital Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>09</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Front Mol Neurosci</MedlineTA><NlmUniqueID>101477914</NlmUniqueID><ISSNLinking>1662-5099</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">ERK</Keyword><Keyword MajorTopicYN="N">H3S10</Keyword><Keyword 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Retrospective review of cases with coronary CTA and compare with available catheter angiography, pathology, surgical reports, and outcomes from Mar 2015 to May 2022. In our cohort of 16 patients, 3 were positive for RVDCC, confirmed by pathologic evaluation, and there was concordance for presence or absence of RVDCC with catheter angiography in 5 patients (4 negatives for RVDCC, 1 positive). Clinical follow up for the 8 patients that underwent RV decompression had no clinical evidence of myocardial ischemia. Our findings suggest that coronary CTA is reliable as first-line imaging for determination of RVDCC in neonates with PA IVS. These findings, if supported by further prospective study, may reserve invasive coronary angiography for cases with diagnostic uncertainty or at the time of necessary transcatheter interventions.
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Cardiac function in critically ill patients with severe COVID: A prospective cross-sectional study in mechanically ventilated patients.<Pagination><StartPage>154166</StartPage><MedlinePgn>154166</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.jcrc.2022.154166</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0883-9441(22)00195-2</ELocationID><Abstract><AbstractText Label="PURPOSE">To evaluate cardiac function in mechanically ventilated patients with COVID-19.</AbstractText><AbstractText Label="MATERIALS AND METHODS">Prospective, cross-sectional multicenter study in four university-affiliated hospitals in Chile. All consecutive patients with COVID-19 ARDS requiring mechanical ventilation admitted between April and July 2020 were included. We performed systematic transthoracic echocardiography assessing right and left ventricular function within 24 h of intubation.</AbstractText><AbstractText Label="RESULTS">140 patients aged 57 &#xb1; 11, 29% female were included. Cardiac output was 5.1 L/min [IQR 4.5-6.2] and 86% of the patients required norepinephrine. ICU mortality was 29% (40 patients). Fifty-four patients (39%) exhibited right ventricle dilation out of whom 20 patients (14%) exhibited acute cor pulmonale (ACP). Eight out of the twenty patients with ACP exhibited pulmonary embolism (40%). Thirteen patients (9%) exhibited left ventricular systolic dysfunction (ejection fraction &lt;45%). In the multivariate analysis acute cor pulmonale and PaO<sub>2</sub>/FiO<sub>2</sub> ratio were independent predictors of ICU mortality.</AbstractText><AbstractText Label="CONCLUSIONS">Right ventricular dilation is highly prevalent in mechanically ventilated patients with COVID-19 ARDS. Acute cor pulmonale was associated with reduced pulmonary function and, in only 40% of patients, with co-existing pulmonary embolism. Acute cor pulmonale is an independent risk factor for ICU mortality.</AbstractText><CopyrightInformation>Copyright &#xa9; 2022 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Valenzuela</LastName><ForeName>Emilio Daniel</ForeName><Initials>ED</Initials><AffiliationInfo><Affiliation>Departamento de Medicina Intensiva, Facultad de Medicina, Pontificia Universidad Cat&#xf3;lica de Chile, Santiago, Chile. Electronic address: eevalenzuela@uc.cl.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mercado</LastName><ForeName>Pablo</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Departamento de Paciente Cr&#xed;tico, Cl&#xed;nica Alemana de Santiago, Facultad de Medicina Cl&#xed;nica Alemana - Universidad del Desarrollo, Santiago, Chile.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pairumani</LastName><ForeName>Ronald</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Unidad de Cuidados Intensivos, Hospital Barros Luco Trudeau, Santiago, Chile.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Medel</LastName><ForeName>Juan Nicol&#xe1;s</ForeName><Initials>JN</Initials><AffiliationInfo><Affiliation>Unidad de Pacientes Cr&#xed;ticos, Departamento de Medicina, Hospital Cl&#xed;nico Universidad de Chile, Santiago, Chile.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Petruska</LastName><ForeName>Edward</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Unidad de Cuidados Intensivos, Hospital Barros Luco Trudeau, Santiago, Chile.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ugalde</LastName><ForeName>Diego</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Unidad de Pacientes Cr&#xed;ticos, Departamento de Medicina, Hospital Cl&#xed;nico Universidad de Chile, Santiago, Chile.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Morales</LastName><ForeName>Felipe</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Unidad de Cuidados Intensivos, Hospital Barros Luco Trudeau, Santiago, Chile.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Eisen</LastName><ForeName>Daniela</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Unidad de Pacientes Cr&#xed;ticos, Departamento de Medicina, Hospital Cl&#xed;nico Universidad de Chile, Santiago, Chile.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Araya</LastName><ForeName>Carla</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Unidad de Cuidados Intensivos, Hospital Barros Luco Trudeau, Santiago, Chile.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Montoya</LastName><ForeName>Jorge</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Unidad de Pacientes Cr&#xed;ticos, Departamento de Medicina, Hospital Cl&#xed;nico Universidad de Chile, Santiago, Chile.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gonzalez</LastName><ForeName>Alejandra</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Departamento de Medicina Intensiva, Facultad de Medicina, Pontificia Universidad Cat&#xf3;lica de Chile, Santiago, Chile.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rovegno</LastName><ForeName>Maximiliano</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Departamento de Medicina Intensiva, Facultad de Medicina, Pontificia Universidad Cat&#xf3;lica de Chile, Santiago, Chile.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ramirez</LastName><ForeName>Javier</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Departamento de Medicina Intensiva, Facultad de Medicina, Pontificia Universidad Cat&#xf3;lica de Chile, Santiago, Chile.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Aguilera</LastName><ForeName>Javiera</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Departamento de Paciente Cr&#xed;tico, Cl&#xed;nica Alemana de Santiago, Facultad de Medicina Cl&#xed;nica Alemana - Universidad del Desarrollo, Santiago, Chile.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hern&#xe1;ndez</LastName><ForeName>Glenn</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Departamento de Medicina Intensiva, Facultad de Medicina, Pontificia Universidad Cat&#xf3;lica de Chile, Santiago, Chile.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bruhn</LastName><ForeName>Alejandro</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Departamento de Medicina Intensiva, Facultad de Medicina, Pontificia Universidad Cat&#xf3;lica de Chile, Santiago, Chile.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Slama</LastName><ForeName>Michel</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Medical Intensive Care Unit, CHU Sud Amiens, Amiens, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bakker</LastName><ForeName>Jan</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Departamento de Medicina Intensiva, Facultad de Medicina, Pontificia Universidad Cat&#xf3;lica de Chile, Santiago, Chile; Department of intensive Care Adults, Erasmus MC University Medical Center, Rotterdam, Netherlands; Department of Pulmonary and Critical Care, New York University, NYU Langone Health, New York, USA; Department of Pulmonary and Critical Care, Columbia University Medical Center, New York, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016448">Multicenter Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>10</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Crit Care</MedlineTA><NlmUniqueID>8610642</NlmUniqueID><ISSNLinking>0883-9441</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>J Crit Care. 2023 Feb;73:154217</RefSource><PMID Version="1">36379138</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011660" MajorTopicYN="Y">Pulmonary Heart Disease</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012121" MajorTopicYN="N">Respiration, Artificial</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016638" MajorTopicYN="N">Critical Illness</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003430" MajorTopicYN="N">Cross-Sectional Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011446" MajorTopicYN="N">Prospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000086382" MajorTopicYN="Y">COVID-19</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011655" MajorTopicYN="Y">Pulmonary Embolism</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006333" MajorTopicYN="Y">Heart Failure</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012128" MajorTopicYN="Y">Respiratory Distress Syndrome</DescriptorName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Acute cor pulmonale</Keyword><Keyword MajorTopicYN="N">COVID-19</Keyword><Keyword MajorTopicYN="N">Cardiac function</Keyword><Keyword MajorTopicYN="N">Mechanical ventilation</Keyword><Keyword MajorTopicYN="N">Mortality</Keyword><Keyword MajorTopicYN="N">Right ventricular dilation</Keyword></KeywordList><CoiStatement>Declaration of Competing Interest The authors declare no conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>5</Month><Day>8</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>8</Month><Day>29</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>9</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>10</Month><Day>17</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>11</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>10</Month><Day>16</Day><Hour>18</Hour><Minute>20</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36244256</ArticleId><ArticleId IdType="pmc">PMC9557772</ArticleId><ArticleId IdType="doi">10.1016/j.jcrc.2022.154166</ArticleId><ArticleId IdType="pii">S0883-9441(22)00195-2</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Shi S., Qin M., Shen B., Cai Y., Liu T., Yang F., et al. 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Am J Respir Crit Care Med. 2020;202(5):690&#x2013;699.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC7462405</ArticleId><ArticleId IdType="pubmed">32667207</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedBookArticle><BookDocument><PMID Version="1">33232069</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK564399</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-105879">Upper Airway Obstruction
The upper airway consists of the nasal cavities, oral cavity, pharynx, and larynx. The pharynx is further subdivided into the nasopharynx, oropharynx, and hypopharynx. The larynx is divided into three regions, dependent on their relationship to the vocal cords (glottis). These areas are the supraglottis, glottis, and subglottis. The supraglottis consists of the epiglottis, the arytenoids, the aryepiglottic folds, the false cords, and the ventricles. The subglottis is the subregion just below the free edge of the vocal cords to the inferior margin of the cricoid. The narrowest part of an adult airway is the glottis. The narrowest part of a pediatric airway is the cricoid.&#xa0; Upper airway obstruction varies from narrowing to partial or complete occlusion of any of these anatomic structures, potentially leading to a compromise in ventilation. Given the urgency related to this issue, it is crucial that healthcare professionals fully understand and appreciate the signs and symptoms that indicate upper airway obstruction. When forming a differential diagnosis for upper airway obstruction, it is important to determine the level at which the obstruction is occurring. A vital clinical sign is noisy breathing, which can be described as 'stertor' or 'stridor'. &#x2018;Stertor&#x2019; is noisy breathing which occurs above the larynx. &#x2018;Stridor&#x2019; is noisy breathing that occurs at the level of the larynx or below.&#xa0; Stridor can be further subdivided as inspiratory (level of the supraglottis), expiratory (level of the glottis), and biphasic (level of the subglottis or trachea). Upper airway obstruction can be partial or complete. A partial obstruction can be chronic or acute, therefore it is crucial to take a good history and perform an efficient and comprehensive exam to determine the etiology of the obstruction and therefore the urgency of subsequent management. Left untreated, upper airway obstruction can have significant long-term or fatal effects.&#xa0;
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Peripheral VA-ECMO left ventricular dysfunction: A combined biventricular assistance two case-report.<Pagination><StartPage>583</StartPage><EndPage>586</EndPage><MedlinePgn>583-586</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.redare.2021.04.007</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S2341-1929(22)00177-9</ELocationID><Abstract><AbstractText>We report 2 patients with cardiogenic shock that developed severe left ventricular dysfunction due to a non-opening aortic valve while on peripheral VA-ECMO (Veno-Arterial Extracorporeal Membrane Oxygenator). Patients were managed combining a LV (Left Ventricle) mechanical assist device, and central VA - ECMO to support the right ventricle, thus providing full circulatory and respiratory assistance. Patients were able to bridge to cardiac transplantation. We therefore recommend such combination in patients with severe LV dysfunction while on p-ECMO (peripheral ECMO) support.</AbstractText><CopyrightInformation>Copyright &#xa9; 2021 Sociedad Espa&#xf1;ola de Anestesiolog&#xed;a, Reanimaci&#xf3;n y Terap&#xe9;utica del Dolor. Publicado por Elsevier Espa&#xf1;a, S.L.U. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Gonz&#xe1;lez-Pizarro</LastName><ForeName>P</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Servicio de Anestesiolog&#xed;a, Cuidados Cr&#xed;ticos y Dolor, Hospital Universitario La Paz, Madrid, Spain. Electronic address: pgpizarro@gmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>&#xc1;lvarez Bartolom&#xe9;</LastName><ForeName>A</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Servicio de Anestesiolog&#xed;a, Cuidados Cr&#xed;ticos y Dolor, Hospital Universitario Puerta de Hierro, Majadahonda, Madrid, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Garc&#xed;a Fern&#xe1;ndez</LastName><ForeName>J</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Servicio de Anestesiolog&#xed;a, Cuidados Cr&#xed;ticos y Dolor, Hospital Universitario Puerta de Hierro, Majadahonda, Madrid, Spain; Departamento de Cirug&#xed;a, Facultad de Medicina, Universidad Aut&#xf3;noma, Madrid, Spain.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>10</Month><Day>12</Day></ArticleDate></Article><MedlineJournalInfo><Country>Spain</Country><MedlineTA>Rev Esp Anestesiol Reanim (Engl Ed)</MedlineTA><NlmUniqueID>101778594</NlmUniqueID><ISSNLinking>2341-1929</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015199" MajorTopicYN="Y">Extracorporeal Membrane Oxygenation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012770" MajorTopicYN="N">Shock, Cardiogenic</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018487" MajorTopicYN="Y">Ventricular Dysfunction, Left</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Case report</Keyword><Keyword MajorTopicYN="N">Clinical management</Keyword><Keyword MajorTopicYN="N">Critical care</Keyword><Keyword MajorTopicYN="N">Cuidados cr&#xed;ticos</Keyword><Keyword MajorTopicYN="N">ECMO</Keyword><Keyword MajorTopicYN="N">Gesti&#xf3;n cl&#xed;nica</Keyword><Keyword MajorTopicYN="N">Informe de caso</Keyword><Keyword MajorTopicYN="N">Shock</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2021</Year><Month>3</Month><Day>7</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2021</Year><Month>4</Month><Day>7</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>10</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>11</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>10</Month><Day>14</Day><Hour>22</Hour><Minute>5</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36241508</ArticleId><ArticleId IdType="doi">10.1016/j.redare.2021.04.007</ArticleId><ArticleId IdType="pii">S2341-1929(22)00177-9</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36241450</PMID><DateRevised><Year>2022</Year><Month>10</Month><Day>14</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1097-685X</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Sep</Month><Day>02</Day></PubDate></JournalIssue><Title>The Journal of thoracic and cardiovascular surgery</Title><ISOAbbreviation>J Thorac Cardiovasc Surg</ISOAbbreviation></Journal>Comparison of long-term outcomes of atrial switch with Rastelli and physiological repair using left ventricle-to-pulmonary artery conduit for levo-transposition of the great arteries.
We report 2 patients with cardiogenic shock that developed severe left ventricular dysfunction due to a non-opening aortic valve while on peripheral VA-ECMO (Veno-Arterial Extracorporeal Membrane Oxygenator). Patients were managed combining a LV (Left Ventricle) mechanical assist device, and central VA - ECMO to support the right ventricle, thus providing full circulatory and respiratory assistance. Patients were able to bridge to cardiac transplantation. We therefore recommend such combination in patients with severe LV dysfunction while on p-ECMO (peripheral ECMO) support.<CopyrightInformation>Copyright &#xa9; 2021 Sociedad Espa&#xf1;ola de Anestesiolog&#xed;a, Reanimaci&#xf3;n y Terap&#xe9;utica del Dolor. Publicado por Elsevier Espa&#xf1;a, S.L.U. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Gonz&#xe1;lez-Pizarro</LastName><ForeName>P</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Servicio de Anestesiolog&#xed;a, Cuidados Cr&#xed;ticos y Dolor, Hospital Universitario La Paz, Madrid, Spain. Electronic address: pgpizarro@gmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>&#xc1;lvarez Bartolom&#xe9;</LastName><ForeName>A</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Servicio de Anestesiolog&#xed;a, Cuidados Cr&#xed;ticos y Dolor, Hospital Universitario Puerta de Hierro, Majadahonda, Madrid, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Garc&#xed;a Fern&#xe1;ndez</LastName><ForeName>J</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Servicio de Anestesiolog&#xed;a, Cuidados Cr&#xed;ticos y Dolor, Hospital Universitario Puerta de Hierro, Majadahonda, Madrid, Spain; Departamento de Cirug&#xed;a, Facultad de Medicina, Universidad Aut&#xf3;noma, Madrid, Spain.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>10</Month><Day>12</Day></ArticleDate></Article><MedlineJournalInfo><Country>Spain</Country><MedlineTA>Rev Esp Anestesiol Reanim (Engl Ed)</MedlineTA><NlmUniqueID>101778594</NlmUniqueID><ISSNLinking>2341-1929</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015199" MajorTopicYN="Y">Extracorporeal Membrane Oxygenation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012770" MajorTopicYN="N">Shock, Cardiogenic</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018487" MajorTopicYN="Y">Ventricular Dysfunction, Left</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Case report</Keyword><Keyword MajorTopicYN="N">Clinical management</Keyword><Keyword MajorTopicYN="N">Critical care</Keyword><Keyword MajorTopicYN="N">Cuidados cr&#xed;ticos</Keyword><Keyword MajorTopicYN="N">ECMO</Keyword><Keyword MajorTopicYN="N">Gesti&#xf3;n cl&#xed;nica</Keyword><Keyword MajorTopicYN="N">Informe de caso</Keyword><Keyword MajorTopicYN="N">Shock</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2021</Year><Month>3</Month><Day>7</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2021</Year><Month>4</Month><Day>7</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>10</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>11</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>10</Month><Day>14</Day><Hour>22</Hour><Minute>5</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36241508</ArticleId><ArticleId IdType="doi">10.1016/j.redare.2021.04.007</ArticleId><ArticleId IdType="pii">S2341-1929(22)00177-9</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36241450</PMID><DateRevised><Year>2022</Year><Month>10</Month><Day>14</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1097-685X</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Sep</Month><Day>02</Day></PubDate></JournalIssue><Title>The Journal of thoracic and cardiovascular surgery</Title><ISOAbbreviation>J Thorac Cardiovasc Surg</ISOAbbreviation></Journal><ArticleTitle>Comparison of long-term outcomes of atrial switch with Rastelli and physiological repair using left ventricle-to-pulmonary artery conduit for levo-transposition of the great arteries.</ArticleTitle><ELocationID EIdType="pii" ValidYN="Y">S0022-5223(22)00911-4</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.jtcvs.2022.08.018</ELocationID><Abstract><AbstractText Label="OBJECTIVES" NlmCategory="OBJECTIVE">The objectives of this study was to compare the long-term outcomes of anatomic repair using atrial switch with the Rastelli procedure versus physiological repair with left ventricle-to-pulmonary artery conduit for patients with levo-transposition of the great arteries, ventricular septal defect, and left ventricular outflow tract obstruction.<AbstractText Label="METHODS" NlmCategory="METHODS">Of patients with levo-transposition of the great arteries who underwent biventricular repair between 1978 and 2001, 31 hospital survivors after anatomic repair of atrial switch and the Rastelli (anatomic group) and 14 hospital survivors after physiological repair with left ventricle-to-pulmonary artery conduit (physiological group) were enrolled. Survival rates, reoperation rates, and most recent conditions were compared.<AbstractText Label="RESULTS" NlmCategory="RESULTS">The overall survival rate at 20&#xa0;years was 79.7% (95% CI, 66.4%-95.6%) in the anatomic group and 85.1% (95% CI, 68.0%-100%) in the physiological group (P&#xa0;=&#xa0;.87). The reoperation rate at 10 years was 19.8% (95% CI, 5.6%-34.0%) in the anatomic group and 52.0% (95% CI, 25.0%-79.1%) in the physiological group (P = .067). Only patients in the physiological group underwent systemic tricuspid valve replacement. The anatomic group showed a better cardiac index at catheterization (2.79&#xa0;&#xb1;&#xa0;0.75&#xa0;L/min/m<sup>2</sup> vs 2.30&#xa0;&#xb1;&#xa0;0.54&#xa0;L/min/m<sup>2</sup>; P&#xa0;=&#xa0;.035), lower serum brain natriuretic peptide (73&#xa0;&#xb1;&#xa0;86 pg/mL vs 163&#xa0;&#xb1;&#xa0;171 pg/mL; P&#xa0;=&#xa0;.024), and better maximal oxygen uptake in the treadmill test (64.1&#xa0;&#xb1;&#xa0;16.5% vs 52.7&#xa0;&#xb1;&#xa0;17.8% of predicted normal; P&#xa0;=&#xa0;.036), although the period until most recent catheterization, blood inspection, and treadmill testing were earlier in the anatomic group.<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Preservation of the left ventricle as the systemic ventricle using anatomic repair contributes to better cardiopulmonary condition compared with physiological repair.
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Curative effect of zinc-selenium tea on rat's cardiotoxicity induced by long-term exposure to nonylphenol.
This study aimed to explore whether zinc-selenium tea has an curative effect on the cardiotoxicity induced by nonylphenol (NP), and to compare the effect of zinc-selenium tea and green tea. After drinking of zinc-selenium tea or green tea, compared with the control group, the left ventricular anterior wall became thinner, and the left ventricular end-diastolic diameter increased, the anterior wall of the left ventricle became thin at the end of diastole in the NP group. The serum myocardial enzymes aspartate aminotransferase, creatine kinase, creatine kinase isoenzyme, lactate dehydrogenase, and &#x3b1;-hydroxybutyrate dehydrogenase in the NP group were significantly increased, and the serum myocardial enzymes were significantly decreased after the intervention of zinc-selenium tea. Proteins and mRNA expressions of Collagen I and Collagen III in the tea groups were lower than those in the NP group. In the green tea and zinc-selenium tea intervention groups, the disorder and degree of myocardial fiber were alleviated to varying degrees. The disturbance, breakage, and inflammatory cell infiltration of myocardial fibers in zinc-selenium tea and green tea groups were less than that of NP group. After tea intervention, collagen I and collagen III in the myocardium decreased. The intervention effect of zinc-selenium tea was better than that of green tea. Zinc-selenium tea and green tea could interfere with the cardiotoxicity indued by NP, which would alleviate the myocardial fibrosis by reducing expressions of collagen I and collagen III. Moreover, the curative effect of zinc-selenium tea was better than that of green tea.
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Road to a rare diagnosis: Description of novel unbalanced translocation causing partial trisomy 17p.
Trisomy 17 is a rare chromosomal disorder. Existing literature on the topic is limited and mostly refer to mosaic Trisomy 17 cases. Our report summarizes the 70-day clinical course of a late preterm neonate with partial Trisomy 17p karyotype 46,XY,der(14)t(14;17)(p11.1;p11.2) dpat. Trisomy 17 due to unbalanced translocation is rare, and our case elaborates the clinical presentation with intestinal malfunction without any anatomical pathology and urethral diverticulum and the ethical dilemma in decision-making. The male proband was born at 35&#x2009;weeks with antenatal findings of multiple neurological and other abnormalities such as cystic hygroma, absent corpus collosum, high riding third ventricle, absent cavum septum pellucidum, indented occiput, absent ductus venous, and intrauterine growth restriction. The postnatal findings included significant facial dysmorphisms with short palpebral fissures, hypertelorism, low set ears, micrognathia, hirsutism, and single palmar creases, central hypotonia, and hyperreflexia of upper limbs bilaterally. Genital-urinary assessment revealed a urinary diverticulum and significantly underdeveloped scrotum with undescended testes. Infant had excessive irritability and resistance to sleep despite increasing doses of analgesia and sedation, and persistent respiratory and feeding difficulties. Enteral nutrition could not be established due to profuse and persistent diarrhea, necessitating use of total parenteral nutrition. Microarray assay exhibited a pathogenic copy number gain of approximately 21.4&#xa0;Mb of chromosome region 17p13.3p11.2. Follow-up chromosome analysis and FISH revealed an abnormal male karyotype with a derivative chromosome 14, resulting from an unbalanced translocation between the short arm of one chromosome 14 and the short arm of one chromosome 17, effectively resulting in trisomy 17p11.2. It was derived from a paternal balanced t(14;17)(p11.1;p11.2) as shown by chromosome analysis and FISH studies. The rarity of this chromosomal disorder contributed to difficulty with prognosis and led to bioethical dilemma regarding life-sustaining measures and quality of life. Through shared decision-making processes and in consideration of poor prognosis, parents decided to withdraw life-sustaining care and the proband died at postnatal day of life 70.
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Full cervical cord tractography: A new method for clinical use.
Despite recent improvements in diffusion-weighted imaging, spinal cord tractography is not used in routine clinical practice because of difficulties in reconstructing tractograms, with a pertinent tri-dimensional-rendering, in a long post-processing time. We propose a new full tractography approach to the cervical spinal cord without extensive manual filtering or multiple regions of interest seeding that could help neurosurgeons manage various spinal cord disorders. Four healthy volunteers and two patients with either cervical intramedullary tumors or spinal cord injuries were included. Diffusion-weighted images of the cervical spinal cord were acquired using a Philips 3 Tesla machine, 32 diffusion directions, 1,000 s/mm<sup>2</sup> <i>b</i>-value, 2 &#xd7; 2 &#xd7; 2 mm voxel size, reduced field-of-view (ZOOM), with two opposing phase-encoding directions. Distortion corrections were then achieved using the FSL software package, and tracking of the full cervical spinal cord was performed using the DSI Studio software (quantitative anisotropy-based deterministic algorithm). A unique region of avoidance was used to exclude everything that is not of the nervous system. Fiber tracking parameters used adaptative fractional anisotropy from 0.015 to 0.045, fiber length from 10 to 1,000 mm, and angular threshold of 90&#xb0;. In all participants, a full cervical cord tractography was performed from the medulla to the C7 spine level. On a ventral view, the junction between the medulla and spinal cord was identified with its pyramidal bulging, and by an invagination corresponding to the median ventral sulcus. On a dorsal view, the fourth ventricle-superior, middle, and inferior cerebellar peduncles-was seen, as well as its floor and the obex; and gracile and cuneate tracts were recognized on each side of the dorsal median sulcus. In the case of the intramedullary tumor or spinal cord injury, the spinal tracts were seen to be displaced, and this helped to adjust the neurosurgical strategy. This new full tractography approach simplifies the tractography pipeline and provides a reliable 3D-rendering of the spinal cord that could help to adjust the neurosurgical strategy.
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Striatal Neurons Partially Expressing a Dopaminergic Phenotype: Functional Significance and Regulation.
Since the discovery of striatal neurons expressing dopamine-synthesizing enzymes, researchers have attempted to identify their phenotype and functional significance. In this study, it was shown that in transgenic mice expressing green fluorescent protein (GFP) under the tyrosine hydroxylase (TH) gene promoter, (i) there are striatal neurons expressing only TH, only aromatic L-amino acid decarboxylase (AADC), or both enzymes of dopamine synthesis; (ii) striatal neurons expressing dopamine-synthesizing enzymes are not dopaminergic since they lack a dopamine transporter; (iii) monoenzymatic neurons expressing individual complementary dopamine-synthesizing enzymes produce this neurotransmitter in cooperation; (iv) striatal nerve fibers containing only TH, only AADC, or both enzymes project into the lateral ventricles, providing delivery pathways for L-3,4-dihydroxyphenylalanine and dopamine to the cerebrospinal fluid; and (v) striatal GFP neurons express receptor genes for various signaling molecules, i.e., classical neurotransmitters, neuropeptides, and steroids, indicating fine regulation of these neurons. Based on our data, it is assumed that the synthesis of dopamine by striatal neurons is a compensatory response to the death of nigral dopaminergic neurons in Parkinson's disease, which opens broad prospects for the development of a fundamentally novel antiparkinsonian therapy.
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Novel Insight into the Role of the Kiss1/GPR54 System in Energy Metabolism in Major Metabolic Organs.
The Kiss1/GPR54 system is a multifunctional genetic system with an essential role in regulating energy balance and metabolic homeostasis. In the mammalian hypothalamus, two major populations of neurons, the rostral periventricular region of the third ventricle (RP3V) and the arcuate nucleus (ARC), produced kisspeptin. Kiss1<sup>ARC</sup> neurons input kisspeptin and glutamate to feeding-associated neurons to regulate energy intake and expenditure balance. Kisspeptin in the peripheral circulation is involved in lipid accumulation in adipose tissue. In the hepatic and pancreatic circuits, kisspeptin signaling affects insulin secretion, suggesting the critical role of the Kiss1/GPR54 system in regulating glucose and lipid metabolism. In addition, this review also predicts the role of the Kiss1/GPRS4 system in skeletal muscle in association with exercise performance. Recent studies have focused on the link between kisspeptin signaling and energy homeostasis, further investigation of potential function is warranted. Therefore, this review summarizes the role of the Kiss1/GPRS4 system in the major metabolic organs in relation to energy metabolism homeostasis, aiming to endow the reader with a critical and updated view of the Kiss1/GPR54 system in energy metabolism.
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Current Understanding of the Neural Stem Cell Niches.
Neural stem cells (NSCs) are self-renewing, multipotent cells which give rise to all components of the central nervous system (CNS) during embryogenesis, but also activate in response to injury and disease and maintain a certain level of neurogenic activity throughout adulthood. This activity takes place in specialized regions of the brain, the neurovascular niches, whose main role is to control the behaviour of the CNS. In adult mammals, two main "canonical" niches have been described: The subventricular zone (SVZ) of the lateral ventricles and the subgranular zone (SGZ) of the dentate gyrus. This review discusses our current understanding of the neural stem cells and their canonical niches, as well as their structure, behaviours, and role in neural disease.
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A Predictive Nomogram for Postoperative Hydrocephalus After Intra- and Paraventricular Tumor Resection: A Retrospective Study of 196 Patients.
Hydrocephalus is a common complication of intra- and paraventricular tumors both before and after tumor resection. We investigated the risk factors for postoperative hydrocephalus and established a predictive nomogram to improve surgical planning and adjust the frequency of postoperative clinical and radiographic monitoring.</AbstractText>A retrospective study of 196 intra- and paraventricular tumor patients with follow-up data was conducted to investigate the risk factors for postoperative hydrocephalus via univariate and multivariate Cox regression analyses. We developed a nomogram incorporating these factors based on multivariate analysis and according to scores calculated by the predictive model; a hazard function curve was used to compared risk of hydrocephalus.</AbstractText>Among the 196 patients, 33 had postoperative hydrocephalus. Intraventricular tumor (P&#xa0;= 0.005), glioblastoma (P&#xa0;= 0.010), preoperative hydrocephalus (P&#xa0;= 0.007), and radiotherapy (P&#xa0;= 0.033) were independent risk factors for postoperative hydrocephalus. The nomogram including these independent risk factors had moderate predictive accuracy, with a concordance index of 0.716 (95% confidence interval [CI]: 0.605-0.828), while the area under the curve values at 6, 12, and 24&#xa0;months were 0.708 (95% CI: 0.563-0.853), 0.763 (95% CI: 0.656-0.870) and 0.861 (95% CI: 0.779-0.943), respectively. The hazard function showed differences between the lower and higher nomogram score groups. The higher the nomogram score, the higher the risk of postoperative hydrocephalus (P&#xa0;&lt;&#xa0;0.001).</AbstractText>The established nomogram performs well for predicting postoperative hydrocephalus. Clinicians can use this nomogram to review their practice regarding hydrocephalus associated with intra- and paraventricular tumors, plan surgical treatment and adjust the frequency of postoperative clinical and radiographic monitoring.</AbstractText>Copyright &#xa9; 2022 Elsevier Inc. All rights reserved.</CopyrightInformation>
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Treatment of arrhythmia disorders in the adult with congenital heart disease: A lesion-specific review.<Pagination><StartPage>1072</StartPage><EndPage>1083</EndPage><MedlinePgn>1072-1083</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.33963/KP.a2022.0235</ELocationID><Abstract><AbstractText>There are now more adults living with a history of congenital heart disease than there are children. Modern electrophysiologists must familiarize themselves with the most common congenital lesions requiring electrophysiologic care as adults. Advancements in this field have been made most notably with high-resolution 3D imaging and electroanatomic mapping, left ventricular cannulation techniques, alternative pacing strategies, intracardiac echo, and transeptal access tools.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Knijnik</LastName><ForeName>Leonardo</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Emory University Adult Congenital Heart Center, Atlanta, GA, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lloyd</LastName><ForeName>Michael S</ForeName><Initials>MS</Initials><AffiliationInfo><Affiliation>Emory University Adult Congenital Heart Center, Atlanta, GA, United States. Mlloyd2@emory.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016421">Editorial</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>10</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>Poland</Country><MedlineTA>Kardiol Pol</MedlineTA><NlmUniqueID>0376352</NlmUniqueID><ISSNLinking>0022-9032</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002648" MajorTopicYN="N">Child</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017115" MajorTopicYN="Y">Catheter Ablation</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006330" MajorTopicYN="Y">Heart Defects, Congenital</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001145" MajorTopicYN="N">Arrhythmias, Cardiac</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D021621" MajorTopicYN="N">Imaging, Three-Dimensional</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">ICD</Keyword><Keyword MajorTopicYN="N">ablation</Keyword><Keyword MajorTopicYN="N">arrhythmia</Keyword><Keyword MajorTopicYN="N">congenital heart disease</Keyword><Keyword MajorTopicYN="N">pacemaker</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>10</Month><Day>13</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>10</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>12</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>10</Month><Day>13</Day><Hour>7</Hour><Minute>13</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36226762</ArticleId><ArticleId IdType="doi">10.33963/KP.a2022.0235</ArticleId><ArticleId IdType="pii">VM/OJS/J/92280</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36226672</PMID><DateRevised><Year>2022</Year><Month>10</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1467-1107</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Oct</Month><Day>13</Day></PubDate></JournalIssue><Title>Cardiology in the young</Title><ISOAbbreviation>Cardiol Young</ISOAbbreviation></Journal>MRI evaluation of right heart functions in children with mild cystic fibrosis.
There are now more adults living with a history of congenital heart disease than there are children. Modern electrophysiologists must familiarize themselves with the most common congenital lesions requiring electrophysiologic care as adults. Advancements in this field have been made most notably with high-resolution 3D imaging and electroanatomic mapping, left ventricular cannulation techniques, alternative pacing strategies, intracardiac echo, and transeptal access tools.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Knijnik</LastName><ForeName>Leonardo</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Emory University Adult Congenital Heart Center, Atlanta, GA, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lloyd</LastName><ForeName>Michael S</ForeName><Initials>MS</Initials><AffiliationInfo><Affiliation>Emory University Adult Congenital Heart Center, Atlanta, GA, United States. Mlloyd2@emory.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016421">Editorial</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>10</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>Poland</Country><MedlineTA>Kardiol Pol</MedlineTA><NlmUniqueID>0376352</NlmUniqueID><ISSNLinking>0022-9032</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002648" MajorTopicYN="N">Child</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017115" MajorTopicYN="Y">Catheter Ablation</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006330" MajorTopicYN="Y">Heart Defects, Congenital</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001145" MajorTopicYN="N">Arrhythmias, Cardiac</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D021621" MajorTopicYN="N">Imaging, Three-Dimensional</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">ICD</Keyword><Keyword MajorTopicYN="N">ablation</Keyword><Keyword MajorTopicYN="N">arrhythmia</Keyword><Keyword MajorTopicYN="N">congenital heart disease</Keyword><Keyword MajorTopicYN="N">pacemaker</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>10</Month><Day>13</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>10</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>12</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>10</Month><Day>13</Day><Hour>7</Hour><Minute>13</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36226762</ArticleId><ArticleId IdType="doi">10.33963/KP.a2022.0235</ArticleId><ArticleId IdType="pii">VM/OJS/J/92280</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36226672</PMID><DateRevised><Year>2022</Year><Month>10</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1467-1107</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Oct</Month><Day>13</Day></PubDate></JournalIssue><Title>Cardiology in the young</Title><ISOAbbreviation>Cardiol Young</ISOAbbreviation></Journal><ArticleTitle>MRI evaluation of right heart functions in children with mild cystic fibrosis.</ArticleTitle><Pagination><StartPage>1</StartPage><EndPage>6</EndPage><MedlinePgn>1-6</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1017/S1047951122003249</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">This study aimed to assess the ventricular anatomy, function of the right ventricle, and the haemodynamic findings of pulmonary artery in children with cystic fibrosis using cardiac MRI.<AbstractText Label="PATIENTS" NlmCategory="METHODS">This prospective study consisted of 32 children with mild cystic fibrosis and 30 age-matched healthy control participants.<AbstractText Label="METHODS" NlmCategory="METHODS">Cardiac MRI was used to assess right ventricular volumes, anatomy, and function and to assessment of haemodynamic findings of pulmonary artery in the control and study groups. Haemodynamic findings of pulmonary arteries were determined using pulmonary arteries peak velocity (cm/s), and pulmonary arteries time-to-peak velocity (ms) and pulmonary artery systolic pressure. All data of children with mild cystic fibrosis were compared with those of 30 age-matched healthy control group participants.<AbstractText Label="RESULTS" NlmCategory="RESULTS">Our patients and their age-matched controls were aged from 6 to 17 years and from 7 to 15 years, respectively. We found that ejection fraction (%), cardiac output (L/ml), cardiac output (L/ml/m<sup>2</sup>), and systolic volume (ml/m<sup>2</sup>) were significantly lower in children with cystic fibrosis (p &lt; 0.01). Right ventricular anterior wall thickness (mm) was significantly higher in children with cystic fibrosis (p = 0.01). No significant difference was observed between the haemodynamic parameters of pulmonary artery in the patient group.<AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">In our study, cardiac MRI was used to investigate whether the right ventricle was affected functionally and anatomically in children with mild cystic fibrosis. We detected a significant decrease in right ventricular systolic functions and notable alterations in the right ventricular geometry of children with mild cystic fibrosis. These alterations usually manifest themselves as hypertrophy of the right ventricle. Our study's results demonstrate no relationship between the development of pulmonary hypertension in mild cystic fibrosis children.
2,329,450
Chronic high-fat diet induces overeating and impairs synaptic transmission in feeding-related brain regions.
Obesity is linked to overeating, which can exacerbate unhealthy weight gain. However, the mechanisms for mediating such linkages are elusive. In the current study, we hypothesized that synaptic remodeling occurs in feeding-related brain regions of obese mice. To investigate this, we established a high-fat diet (HFD)-induced obese mouse model and observed that these mice consumed excessive calories. The effect of chronic HFD feeding on lipid droplet accumulation in different brain structures was also investigated. We found that lipid droplets accumulated on the ependyma of the third ventricle (3V), which is surrounded by key areas of the hypothalamus that are involved in feeding. Then, the spontaneous synaptic activity of miniature excitatory postsynaptic current (mEPSC) and miniature inhibitory postsynaptic current (mIPSC) was recorded in these hypothalamic areas. HFD induced a decreased amplitude of mEPSC in the arcuate nucleus (ARC) and the ventromedial hypothalamus (VMH), meanwhile, increased the frequency in the VMH. In addition, HFD reduced the frequency of mIPSC in the lateral hypothalamus (LH) and increased the amplitude of mIPSC in the paraventricular nucleus of the hypothalamus (PVH). Subsequently, we also measured the synaptic activity of nucleus accumbens (NAc) neurons, which play a vital role in the hedonic aspect of eating, and discovered that HFD diminished the frequency of both mEPSC and mIPSC in the NAc. These findings suggest that chronic HFD feeding leads to lipid accumulation and synaptic dysfunction in specific brain regions, which are associated with energy homeostasis and reward regulation, and these impairments may lead to the overeating of obesity.
2,329,451
Anesthetic management of a patient with trisomy 18 undergoing esophageal banding and preceding gastrostomy-A case report.
A patient diagnosed with trisomy 18 is at great risk of perioperative morbidity and mortality, especially with complex congenital cardiac anomalies. Here, we report successful anesthetic management of palliative esophageal-banding and gastrostomy for trachea-esophageal fistula in a patient who had a complex congenital heart disease with trisomy 18.
2,329,452
An International Aircraft Transport of a Neonate From Georgia to Japan.
International air transport over long distances necessitates considerable effort. It is even more challenging when the patient is a neonate and has a congenital disease. We hereby report a case of an international aircraft transport of a neonate from Tbilisi, Georgia to Osaka, Japan. The patient was transported to Osaka University Hospital after being diagnosed with a double outlet right ventricle (DORV), requiring surgical intervention. This unique experience has raised four issues: 1) language issues for referral and consultation; 2) medical equipment and healthcare professionals required to accompany the transport for adequate care; 3) scheduling of the international flight; and 4) the administrative procedures such as&#xa0;birth certificate, passport, and healthcare insurance. In this report, we describe how the patient was successfully transported, received treatment, and discharged home.
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Unusual presentation of a common neurosurgical shunt procedure in an adult patient.<Pagination><StartPage>2050313X221129770</StartPage><MedlinePgn>2050313X221129770</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">2050313X221129770</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1177/2050313X221129770</ELocationID><Abstract><AbstractText>Ventriculoperitoneal shunt surgery is one of the treatments of hydrocephalus. It involves placing a shunt from the cerebral ventricles to the peritoneum serving as a drainage point. Infection and catheter blockage are some of the possible complications resulting from this procedure. In some cases, other incidents such as peritoneal shunt migration have also been described. Here, we present the case of a 73-year-old male patient treated with ventriculoperitoneal shunt for a normal pressure hydrocephalus. After an initial blockage of the ventricular catheter, a revision surgery was performed with only mild improvement of his neurological symptoms. A repeat shunt series X-ray showed a migration of the distal catheter into the scrotum through an inguinal hernia. He was successfully treated with a laparoscopic repair of the inguinal hernia and repositioning of the distal catheter into the peritoneal cavity. Scrotal migration and hydrocele are unusual presentations and complications of ventriculoperitoneal shunts. Close follow-up of patients with a ventriculoperitoneal shunt should be performed if they experience worsening of their neurological symptoms. Shunt integrity should be assessed and any complications should be managed.</AbstractText><CopyrightInformation>&#xa9; The Author(s) 2022.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ndongo Sonfack</LastName><ForeName>Davaine Joel</ForeName><Initials>DJ</Initials><Identifier Source="ORCID">0000-0001-5638-1285</Identifier><AffiliationInfo><Affiliation>Faculty of Medicine, Laval University, Qu&#xe9;bec, QC, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tarabay</LastName><ForeName>Bilal</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Division of Neurosurgery, University of Montreal, Centre Hospitalier de l'Universit&#xe9; de Montr&#xe9;al, Montr&#xe9;al, QC, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shedid</LastName><ForeName>Daniel</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Division of Neurosurgery, University of Montreal, Centre Hospitalier de l'Universit&#xe9; de Montr&#xe9;al, Montr&#xe9;al, QC, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yuh</LastName><ForeName>Sung-Joo</ForeName><Initials>SJ</Initials><AffiliationInfo><Affiliation>Division of Neurosurgery, University of Montreal, Centre Hospitalier de l'Universit&#xe9; de Montr&#xe9;al, Montr&#xe9;al, QC, Canada.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>10</Month><Day>08</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>SAGE Open Med Case Rep</MedlineTA><NlmUniqueID>101638686</NlmUniqueID><ISSNLinking>2050-313X</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Ventriculoperitoneal shunt complications</Keyword><Keyword MajorTopicYN="N">hydrocephalus</Keyword><Keyword MajorTopicYN="N">peritoneal shunt migration</Keyword></KeywordList><CoiStatement>The author(s) declared no potential conflicts of interest with respect to the research, authorship and/or publication of this article.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>8</Month><Day>2</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>9</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>10</Month><Day>13</Day><Hour>2</Hour><Minute>25</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>10</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>10</Month><Day>14</Day><Hour>6</Hour><Minute>1</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36225226</ArticleId><ArticleId IdType="pmc">PMC9549185</ArticleId><ArticleId IdType="doi">10.1177/2050313X221129770</ArticleId><ArticleId IdType="pii">10.1177_2050313X221129770</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Paff M, Alexandru -Abrams D, Muhonen M, et al. 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Spontaneous knot formation in the peritoneal catheter: a rare cause of ventriculoperitoneal shunt malfunction. Pediatr Neurosurg 2012; 48(5): 310&#x2013;312.</Citation><ArticleIdList><ArticleId IdType="pubmed">23816925</ArticleId></ArticleIdList></Reference><Reference><Citation>Thaker NG, Mammis A, Yanni DS, et al. Distal subgaleal-peritoneal shunt migration into the abdominal wall with subsequent formation of a pre-peritoneal pseudocyst: a rare complication. J Surg Case Rep 2010; 2010(7): 9.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC3649147</ArticleId><ArticleId IdType="pubmed">24946343</ArticleId></ArticleIdList></Reference><Reference><Citation>Hauser T, Auer C, Ludwiczek J, et al. Treatment options for scrotal migration of ventriculoperitoneal shunts: case illustration and systematic review of 48 cases. 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Med Ultrason 2012; 14(2): 158&#x2013;160.</Citation><ArticleIdList><ArticleId IdType="pubmed">22675718</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle> <PubmedBookArticle><BookDocument><PMID Version="1">32809748</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK560913</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-28757">Schizencephaly
Ventriculoperitoneal shunt surgery is one of the treatments of hydrocephalus. It involves placing a shunt from the cerebral ventricles to the peritoneum serving as a drainage point. Infection and catheter blockage are some of the possible complications resulting from this procedure. In some cases, other incidents such as peritoneal shunt migration have also been described. Here, we present the case of a 73-year-old male patient treated with ventriculoperitoneal shunt for a normal pressure hydrocephalus. After an initial blockage of the ventricular catheter, a revision surgery was performed with only mild improvement of his neurological symptoms. A repeat shunt series X-ray showed a migration of the distal catheter into the scrotum through an inguinal hernia. He was successfully treated with a laparoscopic repair of the inguinal hernia and repositioning of the distal catheter into the peritoneal cavity. Scrotal migration and hydrocele are unusual presentations and complications of ventriculoperitoneal shunts. Close follow-up of patients with a ventriculoperitoneal shunt should be performed if they experience worsening of their neurological symptoms. Shunt integrity should be assessed and any complications should be managed.<CopyrightInformation>&#xa9; The Author(s) 2022.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ndongo Sonfack</LastName><ForeName>Davaine Joel</ForeName><Initials>DJ</Initials><Identifier Source="ORCID">0000-0001-5638-1285</Identifier><AffiliationInfo><Affiliation>Faculty of Medicine, Laval University, Qu&#xe9;bec, QC, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tarabay</LastName><ForeName>Bilal</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Division of Neurosurgery, University of Montreal, Centre Hospitalier de l'Universit&#xe9; de Montr&#xe9;al, Montr&#xe9;al, QC, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shedid</LastName><ForeName>Daniel</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Division of Neurosurgery, University of Montreal, Centre Hospitalier de l'Universit&#xe9; de Montr&#xe9;al, Montr&#xe9;al, QC, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yuh</LastName><ForeName>Sung-Joo</ForeName><Initials>SJ</Initials><AffiliationInfo><Affiliation>Division of Neurosurgery, University of Montreal, Centre Hospitalier de l'Universit&#xe9; de Montr&#xe9;al, Montr&#xe9;al, QC, Canada.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>10</Month><Day>08</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>SAGE Open Med Case Rep</MedlineTA><NlmUniqueID>101638686</NlmUniqueID><ISSNLinking>2050-313X</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Ventriculoperitoneal shunt complications</Keyword><Keyword MajorTopicYN="N">hydrocephalus</Keyword><Keyword MajorTopicYN="N">peritoneal shunt migration</Keyword></KeywordList><CoiStatement>The author(s) declared no potential conflicts of interest with respect to the research, authorship and/or publication of this article.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>8</Month><Day>2</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>9</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>10</Month><Day>13</Day><Hour>2</Hour><Minute>25</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>10</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>10</Month><Day>14</Day><Hour>6</Hour><Minute>1</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36225226</ArticleId><ArticleId IdType="pmc">PMC9549185</ArticleId><ArticleId IdType="doi">10.1177/2050313X221129770</ArticleId><ArticleId IdType="pii">10.1177_2050313X221129770</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Paff M, Alexandru -Abrams D, Muhonen M, et al. 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Med Ultrason 2012; 14(2): 158&#x2013;160.</Citation><ArticleIdList><ArticleId IdType="pubmed">22675718</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle> <PubmedBookArticle><BookDocument><PMID Version="1">32809748</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK560913</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-28757">Schizencephaly</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Veerapaneni</LastName><ForeName>Poornachand</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>University of Arkansas Medical Sciences</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Veerapaneni</LastName><ForeName>Karthika Durga</ForeName><Initials>KD</Initials><AffiliationInfo><Affiliation>University of Arkansas Medical Sciences</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yadala</LastName><ForeName>Sisira</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>University of Arkansas for Medical Sciences</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>Schizencephaly&#xa0;is a rare congenital neuronal migration disorder characterized by the presence of a full-thickness cleft, lined with heterotopic gray matter and filled with&#xa0;cerebrospinal fluid (CSF), which connects the pial surface of the cerebral hemisphere with the ependymal surface of the lateral ventricle. Schizencephaly was first described by Wilmarth in 1887.&#xa0;The term was coined from the Greek word "schizen" 'to divide' and introduced by Yakovlev and Wadsworth in 1946, based on their work on cadavers,&#xa0;that classified schizencephaly into two types. These are: Type I (closed-lip): Cleft is fused, preventing CSF passage. Type II (open-lip): A cleft is present, which permits CSF to pass between the ventricular cavity and subarachnoid space. Schizencephaly can be either unilateral or bilateral&#xa0;and has a prevalence of 1.48 per 100,000 live births. Recent literature classifies schizencephaly into three types, as the full-thickness cleft containing CSF is not mandatory for the definition. Type 1 (trans-mantle): No CSF-containing cleft on magnetic resonance imaging (MRI), but contains a trans-mantle column of abnormal gray matter. Type 2 (closed-lip): Presence of cleft containing CSF, but the lining lips of abnormal gray matter are abutting and opposed to each other. Type 3 (open-lip): Presence of cleft containing CSF. The lining lips of abnormal gray matter are not abutting each other.
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[Pulmonary Vascular Remodeling Characteristics of Pulmonary Arterial Hypertension Mouse Model Induced by Left Pneumonectomy and Jugular Vein Injection of Monocrotaline Pyrrole].<Pagination><StartPage>821</StartPage><EndPage>827</EndPage><MedlinePgn>821-827</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.12182/20220960508</ELocationID><Abstract><AbstractText Label="OBJECTIVE" NlmCategory="UNASSIGNED">To compare and investigate the differences and characteristics of pulmonary vascular remodeling in three mouse models of pulmonary arterial hypertension (PAH) constructed by left pneumonectomy, jugular vein injection of monocrotaline pyrrole, and left pneumonectomy combined with jugular vein injection of monocrotaline pyrrole, to explore for a PAH animal model that approximates the clinical pathogenesis of PAH, and to create a model that will provide sound basis for thorough investigation into the pathogenesis of severe PAH.</AbstractText><AbstractText Label="METHODS" NlmCategory="UNASSIGNED">59 male C57/BL mice (10-12 weeks, 24-30 g) were randomized into four groups, a control group ( <i>n</i>=9), a group that had left pneumonectomy (PE, <i>n</i>=15), a group that had jugular vein injection of monocrotaline pyrrole (MCTP, <i>n</i>=15), and the last group that had left pneumonectomy combined with jugular injection of monocrotaline pyrrole (P+M, <i>n</i>=20). To evaluate the effect of modeling and the characteristics of pulmonary vascular remodeling, hemodynamic and morphological parameters, including right ventricular systolic pressure (RVSP), right ventricle/(left ventricle plus septum) (RV/LV+S), percent of wall thickness in the pulmonary artery (WT%), muscularization of non-muscular arteries, neointima formation, and vascular obstruction score (VOS), were measured in each group.</AbstractText><AbstractText Label="RESULTS" NlmCategory="UNASSIGNED">1) Compared with those of the control group, the RVSP, RV/LV+S, WT%, and the degree of small pulmonary arteries muscularization in the P+M group were significantly increased ( <i>P</i>&lt;0.01). The MCTP group had just slightly higher findings for these indicators ( <i>P</i>&lt;0.05), while no significant change in these indicators was observed in the PE group ( <i>P</i>&gt;0.05). 2) Neointima formation in the acinus pulmonary arteries, which caused obvious stenosis of the lumen, was observed in the P+M group, the VOS being 1.25&#xb1;0.80 points ( <i>P</i>&lt;0.001). In contrast, neointima formation was not observed in the MCTP group or the PE groups, the VOS being 0 point ( <i>P</i>&gt;0.05).</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="UNASSIGNED">Left pneumonectomy combined with jugular intravenous injection of MCTP could induce severe PAH formation in mouse. The model provides a good simulation of neointima formation, the characteristic pathological change of clinical severe PAH.</AbstractText><CopyrightInformation>Copyright&#xa9; by Editorial Board of Journal of Sichuan University (Medical Sciences).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Gu</LastName><ForeName>Li</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Key Laboratory of Birth Defects and Related Diseases of Women and Children of the Ministry of Education, Sichuan University, Chengdu 610041, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Pediatrics, the First People's Hospital of Yibin, Yibin 644000, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Cai-Jun</ForeName><Initials>CJ</Initials><AffiliationInfo><Affiliation>Key Laboratory of Birth Defects and Related Diseases of Women and Children of the Ministry of Education, Sichuan University, Chengdu 610041, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Pediatric Pulmonology and Immunology, West China Second University Hospital, Sichuan University, Chengdu 610041, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xie</LastName><ForeName>Liang</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Key Laboratory of Birth Defects and Related Diseases of Women and Children of the Ministry of Education, Sichuan University, Chengdu 610041, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Pediatric Pulmonology and Immunology, West China Second University Hospital, Sichuan University, Chengdu 610041, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gu</LastName><ForeName>Ling</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Key Laboratory of Birth Defects and Related Diseases of Women and Children of the Ministry of Education, Sichuan University, Chengdu 610041, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Pediatric Pulmonology and Immunology, West China Second University Hospital, Sichuan University, Chengdu 610041, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yu</LastName><ForeName>Li</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Key Laboratory of Birth Defects and Related Diseases of Women and Children of the Ministry of Education, Sichuan University, Chengdu 610041, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Pediatric Pulmonology and Immunology, West China Second University Hospital, Sichuan University, Chengdu 610041, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Han-Min</ForeName><Initials>HM</Initials><AffiliationInfo><Affiliation>Key Laboratory of Birth Defects and Related Diseases of Women and Children of the Ministry of Education, Sichuan University, Chengdu 610041, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Pediatric Pulmonology and Immunology, West China Second University Hospital, Sichuan University, Chengdu 610041, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>NHC Key Laboratory of Chronobiology (Sichuan University), Chengdu 610041, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>chi</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D000081262">Randomized Controlled Trial, Veterinary</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>China</Country><MedlineTA>Sichuan Da Xue Xue Bao Yi Xue Ban</MedlineTA><NlmUniqueID>101162609</NlmUniqueID><ISSNLinking>1672-173X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>23291-96-5</RegistryNumber><NameOfSubstance UI="C014114">monocrotaline pyrrole</NameOfSubstance></Chemical><Chemical><RegistryNumber>73077K8HYV</RegistryNumber><NameOfSubstance UI="D016686">Monocrotaline</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006976" MajorTopicYN="Y">Hypertension, Pulmonary</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007601" MajorTopicYN="N">Jugular Veins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016686" MajorTopicYN="N">Monocrotaline</DescriptorName><QualifierName UI="Q000031" MajorTopicYN="N">analogs &amp; derivatives</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D058426" MajorTopicYN="N">Neointima</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011013" MajorTopicYN="N">Pneumonectomy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000081029" MajorTopicYN="Y">Pulmonary Arterial Hypertension</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011651" MajorTopicYN="N">Pulmonary Artery</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D066253" MajorTopicYN="N">Vascular Remodeling</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Animal model</Keyword><Keyword MajorTopicYN="N">Mouse</Keyword><Keyword MajorTopicYN="N">Pulmonary arterial hypertension</Keyword><Keyword MajorTopicYN="N">Pulmonary vascular remodeling</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>10</Month><Day>12</Day><Hour>23</Hour><Minute>50</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>10</Month><Day>13</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>10</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36224684</ArticleId><ArticleId IdType="doi">10.12182/20220960508</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36224293</PMID><DateRevised><Year>2022</Year><Month>10</Month><Day>12</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1619-0904</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Oct</Month><Day>12</Day></PubDate></JournalIssue><Title>Journal of artificial organs : the official journal of the Japanese Society for Artificial Organs</Title><ISOAbbreviation>J Artif Organs</ISOAbbreviation></Journal>Trans-subclavian approach for Impella CP implantation using the chimney graft in a pediatric patient with fulminant myocarditis during extracorporeal support.
Impella is a device effective for the treatment of cardiogenic shock. However, among small children, its application has limitations due to left ventricle size and vasculature and the turning diameter of the aortic arch. Herein, we report an 11-year-old girl with fulminant myocarditis who was successfully managed with Impella CP implantation via the right subclavian artery using a polyethylene terephthalate chimney graft. Compared with insertion via the femoral artery, this method has several advantages. That is, it can address limitations in aortic arch diameter and facilitate equable fixation of the Impella device in small pediatric patients.
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Vox2Surf: Implicit Surface Reconstruction from Volumetric Data.
Surface reconstruction from volumetric T1-weighted and T2-weighted images is a time-consuming multi-step process that often involves careful parameter fine-tuning, hindering a more wide-spread utilization of surface-based analysis particularly in large-scale studies. In this work, we propose a fast surface reconstruction method that is based on directly learning a continuous-valued signed distance function (SDF) as implicit surface representation. This continuous representation implicitly encodes the boundary of the surface as the zero isosurface. Given the predicted SDF, the target 3D surface is reconstructed by applying the marching cubes algorithm. Our implicit reconstruction method concurrently predicts the surfaces of the brain parenchyma, the white matter and pial surfaces, the subcortical structures, and the ventricles. Evaluation based on data from the Human Connectome Project indicates that surface reconstruction of a total of 22 cortical and subcortical structures can be completed in less than 20 min.
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A fetus with Bosch-Boonstra-Schaaf optic atrophy syndrome characterized by bilateral ventricle widening: A case report and related literature review.<Pagination><StartPage>e30558</StartPage><MedlinePgn>e30558</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">e30558</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1097/MD.0000000000030558</ELocationID><Abstract><AbstractText Label="RATIONALE" NlmCategory="BACKGROUND">Bosch-Boonstra-Schaaf optic atrophy syndrome (BBSOAS) is a rare neurodevelopmental disorder caused by loss-of-function variants in the Nuclear Receptor Subfamily 2 Group F Member 1 (NR2F1). Here, we report a case of fetal BBSOAS. The fetus is typically featured by bilateral ventricle widening in the late second trimester, meanwhile, a 7.94-Mb deletion fragment on 5q14.3q15 involving the whole NR2F1 gene was confirmed by copy number variation sequencing (CNV-Seq) combined with karyotyping analysis. Our aim is to provide comprehensive prenatal clinical management strategy for fetal BBSOAS.</AbstractText><AbstractText Label="PATIENT CONCERNS" NlmCategory="METHODS">A 29-year-old primipara and her husband were referred to our prenatal diagnosis center due to the widening of bilateral ventricles at 29 + 1 weeks of gestation age.</AbstractText><AbstractText Label="DIAGNOSES" NlmCategory="METHODS">Ultrasound revealed the fetal widening posterior horns of bilateral ventricles at the GA of 27 + 3 weeks, 11 mm on the left and 10 mm on the right. At the following 29 + 1 weeks, ultrasound showed the posterior horn of the left lateral ventricle: 12 mm while the width of the right decreased to 9 mm, and intracranial arachnoid cyst. Furthermore, MRI confirmed that intracranial cyst might originate from an enlarged cisterna venae magnae cerebri, with mild dilation of 13.5 mm on the left ventricle. The fetal karyotyping analysis and CNV-Seq detection confirmed a 7.94-Mb deleted fragment on 5q14.3q15 (89340000_97280000) through the amniocentesis at 29 + 4 weeks of GA.</AbstractText><AbstractText Label="INTERVENTIONS" NlmCategory="METHODS">The fetus was closely monitored and underwent the following assessment by the multidisciplinary team.</AbstractText><AbstractText Label="OUTCOMES" NlmCategory="RESULTS">The pregnancy was terminated in the end.</AbstractText><AbstractText Label="LESSONS" NlmCategory="CONCLUSIONS">It is vital to use molecular and cytogenetical detections combined with a dynamic development history to make a definite diagnosis and evaluate the genetic status for the fetuses with BBSOAS.</AbstractText><CopyrightInformation>Copyright &#xa9; 2022 the Author(s). Published by Wolters Kluwer Health, Inc.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Sun</LastName><ForeName>Yu</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Graduate School of Xuzhou Medical University, Jiangsu Xuzhou, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Prenatal Diagnosis Medical Center, Xuzhou Central Hospital, Xuzhou Clinical School of Xuzhou Medical University, Xuzhou, Jiangsu, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of obstetrics, Fengxian People's Hospital, Xuzhou, Jiangsu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Guo</LastName><ForeName>Lili</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Prenatal Diagnosis Medical Center, Xuzhou Central Hospital, Xuzhou Clinical School of Xuzhou Medical University, Xuzhou, Jiangsu, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Graduate School of Bengbu Medical College, Bengbu, Anhui, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sha</LastName><ForeName>Jing</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Prenatal Diagnosis Medical Center, Xuzhou Central Hospital, Xuzhou Clinical School of Xuzhou Medical University, Xuzhou, Jiangsu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tao</LastName><ForeName>Huimin</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Graduate School of Xuzhou Medical University, Jiangsu Xuzhou, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Prenatal Diagnosis Medical Center, Xuzhou Central Hospital, Xuzhou Clinical School of Xuzhou Medical University, Xuzhou, Jiangsu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Xuezhen</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Prenatal Diagnosis Medical Center, Xuzhou Central Hospital, Xuzhou Clinical School of Xuzhou Medical University, Xuzhou, Jiangsu, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Graduate School of Bengbu Medical College, Bengbu, Anhui, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Ying</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Prenatal Diagnosis Medical Center, Xuzhou Central Hospital, Xuzhou Clinical School of Xuzhou Medical University, Xuzhou, Jiangsu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhai</LastName><ForeName>Jingfang</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Graduate School of Xuzhou Medical University, Jiangsu Xuzhou, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Prenatal Diagnosis Medical Center, Xuzhou Central Hospital, Xuzhou Clinical School of Xuzhou Medical University, Xuzhou, Jiangsu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wu</LastName><ForeName>Jiebin</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Graduate School of Xuzhou Medical University, Jiangsu Xuzhou, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Prenatal Diagnosis Medical Center, Xuzhou Central Hospital, Xuzhou Clinical School of Xuzhou Medical University, Xuzhou, Jiangsu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhao</LastName><ForeName>Yongxiu</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of laboratory, Taixing Maternity and Child Health Care Hospital, Taixing, Jiangsu, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Medicine (Baltimore)</MedlineTA><NlmUniqueID>2985248R</NlmUniqueID><ISSNLinking>0025-7974</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051838">COUP Transcription Factor I</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051838" MajorTopicYN="N">COUP Transcription Factor I</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D056915" MajorTopicYN="N">DNA Copy Number Variations</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005333" MajorTopicYN="N">Fetus</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008607" MajorTopicYN="Y">Intellectual Disability</DescriptorName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015418" MajorTopicYN="Y">Optic Atrophies, Hereditary</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009896" MajorTopicYN="Y">Optic Atrophy</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011247" MajorTopicYN="N">Pregnancy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016216" MajorTopicYN="N">Ultrasonography, Prenatal</DescriptorName></MeshHeading></MeshHeadingList><CoiStatement>The authors have no conflicts of interest to disclose.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>10</Month><Day>12</Day><Hour>1</Hour><Minute>52</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>10</Month><Day>13</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>10</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36221391</ArticleId><ArticleId IdType="pmc">PMC9543064</ArticleId><ArticleId IdType="doi">10.1097/MD.0000000000030558</ArticleId><ArticleId IdType="pii">00005792-202210070-00068</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Rech ME, McCarthy JM, Chen CA, et al. . 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Bosch-Boonstra-Schaaf optic atrophy syndrome presenting as new-onset psychosis in a 32-year-old man: a case report and literature review. J Psychiatr Pract. 2020;26:58&#x2013;62.</Citation><ArticleIdList><ArticleId IdType="pubmed">31913971</ArticleId></ArticleIdList></Reference><Reference><Citation>Armentano M, Filosa A, Andolfi G, Studer M. COUP-TFI is required for the formation of commissural projections in the forebrain by regulating axonal growth. Development. 2006;133:4151&#x2013;62.</Citation><ArticleIdList><ArticleId IdType="pubmed">17021036</ArticleId></ArticleIdList></Reference><Reference><Citation>Huang RN, Chen JY, Pan H, Liu QQ. Correlation between mild fetal ventriculomegaly, chromosomal abnormalities, and copy number variations. J Matern Fetal Neonatal Med. 2020; 28:1&#x2013;9.</Citation><ArticleIdList><ArticleId IdType="pubmed">33371747</ArticleId></ArticleIdList></Reference><Reference><Citation>Chen X, Jiang Y, Chen R, et al. . Clinical efficiency of simultaneous CNV-seq and whole-exome sequencing for testing fetal structural anomalies. J Transl Med. 2022;20:10.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC8722033</ArticleId><ArticleId IdType="pubmed">34980134</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedBookArticle><BookDocument><PMID Version="1">32119505</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK554618</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-86596">Coronary Arteriovenous Fistula
Coronary arteriovenous fistula (CAVF) is a rare form of congenital heart disease. However, it is the most common type of congenital coronary artery anomalies..An arteriovenous fistula is&#xa0;an abnormal conduit between the artery and vein, typically bypassing the capillaries in between.&#xa0;When present between the coronary artery and cardiac chambers, it is called a coronary cameral fistula.&#xa0; The fistula can also be present between a coronary artery and another adjacent vessel&#xa0;from pulmonary or systemic circulation. A patent fistula provides a low resistance flow, shunting the blood directly from an artery into a vein, cardiac chamber, or another low-pressure vessel like the pulmonary artery. Patients with CAVF can develop symptoms at birth or a later age, depending on the type of fistula and the presence of collateral circulation. Studies have reported an association between ventricular arrhythmias and sudden cardiac death syndromes in young adults and athletes in certain types of coronary anomalies like the anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA). Exertional dyspnea and angina pectoris from&#xa0;myocardial ischemia&#xa0;or endocardial fibrosis are the predominant symptoms in adults. Typically, these patients have extensive collateral formation. Human coronary circulation comprises of two main epicardial coronary arteries. They arise from the coronary ostia located in the coronary sinus of Valsalva situated just above the aortic valve cusps. The aortic valve is tricuspid and consists of the right coronary cusp, left coronary cusp, and noncoronary cusp. The left coronary artery (LCA) originates from the left coronary sinus and branches into the left circumflex and the left anterior descending artery (LAD). The left circumflex artery supplies the anterolateral and posterolateral left ventricular walls. The left anterior descending artery supplies the anterior septum, the anterior free wall at the base and mid cavity level, apical septum, anterior wall, and apical cap. The right coronary artery (RCA)&#xa0; arises from the anterior aortic sinus or the right coronary sinus. It supplies the right atrium, right ventricle, sinoatrial (SA) node, and atrioventricular (AV) node. The posterior descending artery, a branch of RCA, provides blood supply to the inferior septum, the inferior free wall, and posterior left ventricular segments. The right coronary artery dominant variant is 80%. The right coronary artery is the most common site of origin for CAVFs, found in approximately 50% of patients. Other sites include the left anterior descending artery in 35% to 40%, the left circumflex artery in 5% to 20%, and both coronary arteries in 5%. Approximately 90% of the fistulas drain into the low-pressure venous circulation. The most common drainage sites are the right ventricle 41%, right atrium 26%, pulmonary artery 17%, coronary sinus 7%, left atrium 26%, left ventricle 3%, and superior vena cava 1%. A coronary arteriovenous fistula may lead to coronary artery dilatation due to increased flow, hyperkinetic pulmonary artery hypertension due to the large left to right shunt, congestive heart failure, myocardial ischemia from coronary steal phenomenon and thrombosis or aneurysm of fistula.
2,329,457
Expanded endoscopic endonasal approach for the resection of midline craniopharyngiomas with hypothalamic involvement.
With relevant surrounding neurological structures and potential involvement of the hypothalamus, the surgical management of craniopharyngiomas is complex. Compared to the transcranial approach, the expanded endoscopic endonasal approach provides direct access to the supradiaphragmatic and retrochiasmatic areas without crossing nerves and arteries.</AbstractText>Based on our substantial experience of 68 patients operated on between 2008 and 2022 by endoscopic surgery, our strategy has evolved such that all of our midline infundibular craniopharyngiomas with hypothalamic involvement are currently treated with an expanded endonasal route, except for tumours isolated to the third ventricle. Vascularized mucosal nasoseptal flaps are required for closure. Fine details of the related anatomy and surgical technique are described.</AbstractText>Expanded endoscopic endonasal approach is a safe and effective route for resection of midline suprasellar craniopharyngiomas with hypothalamic involvement in centres of expertise.</AbstractText>&#xa9; 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Austria, part of Springer Nature.</CopyrightInformation>
2,329,458
Morphometric evaluation of great vein of Galen and its clinical implications.
The Galenic venous system plays a vital role in the drainage of blood from deeper parts of the brain. This venous system is contributed by many major veins. These veins are located closer to the pineal gland making the surgical approach in this region difficult. Any accidental injury or occlusion of the vein of Galen could lead to devasting results. Thus, studying the dimensions of the vein of Galen is more important. Hence, we aimed to evaluate the morphometry and trajectory to the vein of Galen. About 100 computed tomographic venography records were evaluated and the length, diameter of vein of Galen, angle between straight sinus and vein of Galen and distance from internal occipital protuberance and roof of fourth ventricle to vein of Galen were studied. The mean length and diameter of vein of Galen were 9.8&#xb1;2.7 and 4.08&#xb1;1.04 respectively. The mean angle between straight sinus and vein of Galen was 64.2&#xb0;. The mean distance between external occipital protuberance and roof of fourth ventricle to vein of Galen were 52&#xb1;6.9 and 33.3&#xb1;4.5 respectively. No significant morphometric differences were observed between the age groups as well as between the sexs. The results obtained from this study may be helpful for the neurosurgeons in better understanding of the anatomy of the Galenic venous system and to adopt a safe surgical approach to improve the efficacy of the surgeries of the pineal gland and also in the region of vein of Galen.
2,329,459
Single Versus Double Hadad-Bassagasteguy Flap in Expanded Endoscopic Skull-Base Surgery.
The reconstruction of dural defects, after endoscopic removal of skull-base lesions, remains challenging when a large defect or a high flow intraoperative cerebrospinal fluid (CSF) leak is observed. The aim of this study is to describe our preliminary experience with a double Hadad-Bassagasteguy (H-B) flap technique for skull-base repair, comparing its efficacy with the use of a single H-B flap in our series. A retrospective chart review was conducted on patients who underwent exclusive endoscopic endonasal skull-base surgery at our Referral Skull Base Center from December 2014 to January 2018. Data on patient demographics, pathology, preoperative and postoperative imaging, intraoperative findings, surgical route, defect size, reconstruction techniques and repair materials, were analyzed. Patients were divided into double and single H-B flap groups. In the single and double H-B groups, the postoperative CSF leak rates were 37.5% (6 of 16 patients) and 4.5% (1 of 22 patients), respectively. The difference between the two groups was statistically significant (<i>p</i>&#x2009;=&#x2009;0.0470). In patients with defects&#x2009;&gt;&#x2009;4&#xa0;cm or high-flow intraoperative CSF leakage related to the opening of the third ventricle, the double H-B flap was successfully placed with no occurrence of postoperative CSF leakage. The double H-B flap significantly reduced the postoperative CSF leakage rate after expanded transnasal skull-base surgery. Particularly in challenging cases, where a large skull-base defect or a high-flow intraoperative CSF leak was observed, this reconstructive method proved to be very effective, with no evidence of postoperative CSF fistulas.
2,329,460
Intracranial tumors mimicking benign paroxysmal positional vertigo: A case series.
A few intracranial lesions may present only with positional vertigo which are very easy to misdiagnose as benign paroxysmal positional vertigo (BPPV); the clinicians should pay more attention to this disease.</AbstractText>To analyze the clinical characteristics of 6 patients with intracranial tumors who only presented with positional vertigo to avoid misdiagnosing the disease.</AbstractText>Six patients with intracranial tumors who only presented with positional vertigo treated in our clinic between May 2015 to May 2019 were reviewed, and the clinical symptoms, features of nystagmus, imaging presentation, and final diagnosis of the patients were evaluated.</AbstractText>All patients presented with positional vertigo and positional nystagmus induced by the changes in head position or posture, including one case with downbeating nystagmus in a positional test, two cases with left-beating nystagmus, one case with apogeotropic nystagmus in a roll test, one case with right-beating nystagmus, and one case with left-beating and upbeating nystagmus. Brain MRI showed the regions of the tumors were in the vermis of the cerebellum, the fourth ventricle, the lateral ventricle, and the cerebellar hemisphere.</AbstractText>Copyright &#xa9; 2022 Chen, Sun, Mu, Jiang, Wang, Zhang, Qu, Li, Zhou, Zhao, Yu and Sun.</CopyrightInformation>
2,329,461
Case Report: A novel desmoplakin mutation in a taiwanese woman with familial dilated cardiomyopathy that necessitated heart transplantation.
Around one-third of patients diagnosed with idiopathic dilated cardiomyopathy (DCM) turn out to be familial cases, in only a few of which the identification of a pathogenic/likely pathogenic variant could be achieved. Cardiomyopathy caused by desmoplakin gene mutations represents a distinct form with a high prevalence of left ventricle involvement. We report a novel desmoplakin mutation carried by two individuals in a Taiwanese family, in which the proband recovered well after heart transplantation and under medical control, while her son had received an implantable cardioverter defibrillator and has been under guideline-directed medical therapy. The present study broadens the genetic spectrum of this disease entity and strengthens the notion that a detailed family history with genetic study contributes to the early detection and treatment of inherited diseases.
2,329,462
PPMS: A framework to Profile Primary MicroRNAs from Single-cell RNA-sequencing datasets.<ELocationID EIdType="pii" ValidYN="Y">bbac419</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1093/bib/bbac419</ELocationID><Abstract><AbstractText Label="MOTIVATION">Single-cell/nuclei RNA-sequencing (scRNA-seq) technologies can simultaneously quantify gene expression in thousands of cells across the genome. However, the majority of the noncoding RNAs, such as microRNAs (miRNAs), cannot currently be profiled at the same scale. MiRNAs are a class of small noncoding RNAs and play an important role in gene regulation. MiRNAs originate from the processing of primary transcripts, known as primary-microRNAs (pri-miRNAs). The pri-miRNA transcripts, independent of their cognate miRNAs, can also function as long noncoding RNAs, code for micropeptides or even interact with DNA, acting like enhancers. Therefore, it is apparent that the significance of scRNA-seq pri-miRNA profiling expands beyond using pri-miRNA as proxies of mature miRNAs. However, there are no computational methods that allow profiling and quantification of pri-miRNAs at the single-cell-type resolution.</AbstractText><AbstractText Label="RESULTS">We have developed a simple yet effective computational framework to profile pri-MiRNAs from single-cell RNA-sequencing datasets (PPMS). Based on user input, PPMS can profile pri-miRNAs at cell-type resolution. PPMS can be applied to both newly produced and publicly available datasets obtained via single cell or single-nuclei RNA-seq. It allows users to (i) investigate the distribution of pri-miRNAs across cell types and cell states and (ii) establish a relationship between the number of cells/reads sequenced and the detection of pri-miRNAs. Here, to demonstrate its efficacy, we have applied PPMS to publicly available scRNA-seq data generated from (i) individual chambers (ventricles and atria) of the human heart, (ii) human pluripotent stem cells during their differentiation into cardiomyocytes (the heart beating cells) and (iii) hiPSCs-derived cardiomyocytes infected with severe acute respiratory syndrome&#xa0;coronavirus 2.</AbstractText><CopyrightInformation>&#xa9; The Author(s) 2022. Published by Oxford University Press.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ji</LastName><ForeName>Jiahui</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>National Heart and Lung Institute, Imperial College London, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Anwar</LastName><ForeName>Maryam</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>National Heart and Lung Institute, Imperial College London, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Petretto</LastName><ForeName>Enrico</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>London Institute of Medical Sciences, MRC, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Duke-NUS Medical School, Singapore.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institute of Big Data and Artificial Intelligence, China Pharmaceutical University (CPU), 211198 Nanjing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Emanueli</LastName><ForeName>Costanza</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>National Heart and Lung Institute, Imperial College London, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Srivastava</LastName><ForeName>Prashant Kumar</ForeName><Initials>PK</Initials><Identifier Source="ORCID">0000-0003-1454-5493</Identifier><AffiliationInfo><Affiliation>National Heart and Lung Institute, Imperial College London, UK.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>RG/20/9/35101</GrantID><Acronym>BHF_</Acronym><Agency>British Heart Foundation</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>20/0006187</GrantID><Agency>Diabetes UK early-career grants</Agency><Country/></Grant><Grant><GrantID>RG/15/5/31446</GrantID><Agency>British Heart Foundation Programme Grant</Agency><Country/></Grant><Grant><GrantID>101016072</GrantID><Agency>European Union's Horizon 2020</Agency><Country/></Grant><Grant><GrantID>RGS\R2\202413</GrantID><Agency>The Royal Society</Agency><Country/></Grant><Grant><GrantID>CH/15/1/31199</GrantID><Agency>Personal Chair Awards</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Brief Bioinform</MedlineTA><NlmUniqueID>100912837</NlmUniqueID><ISSNLinking>1467-5463</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D035683">MicroRNAs</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D058727">RNA, Small Untranslated</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012323" MajorTopicYN="N">RNA Processing, Post-Transcriptional</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000086382" MajorTopicYN="Y">COVID-19</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005786" MajorTopicYN="N">Gene Expression Regulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D035683" MajorTopicYN="Y">MicroRNAs</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D058727" MajorTopicYN="Y">RNA, Small Untranslated</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>6</Month><Day>2</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>7</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>8</Month><Day>30</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>10</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>11</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>10</Month><Day>9</Day><Hour>14</Hour><Minute>2</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36209413</ArticleId><ArticleId IdType="pmc">PMC9677482</ArticleId><ArticleId IdType="doi">10.1093/bib/bbac419</ArticleId><ArticleId IdType="pii">6754044</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Gomes CPDC, Schroen B, Kuster GM, et al. . 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Nucleic Acids Res 2005;33(Web Server issue):W741&#x2013;8.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC1160236</ArticleId><ArticleId IdType="pubmed">15980575</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedBookArticle><BookDocument><PMID Version="1">30252249</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK525993</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-901">Neuroanatomy, Hypothalamus
Landmarks defining the regions of the hypothalamus include the lamina terminalis, pituitary gland, mammillary bodies, and superior hypothalamic sulcus. The hypothalamus is a bilateral collection of nuclei divided into three zones surrounding the third ventricle and the mammillary bodies. Generally, the periventricular zone nuclei regulate the endocrine system, and the medial and lateral nuclei regulate autonomic&#xa0;and somatic behavior. The hypothalamus is centrally located in the brain, and it connects to the brainstem via the dorsal longitudinal fasciculus, cerebral cortex via the medial forebrain bundle, hippocampus via the fornix, amygdala via the stria terminalis, thalamus via the mammillothalamic tract, pituitary via median eminence, and retina via the retinohypothalamic tract.
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Pineal Gland Tumour With Drop Metastases: A Case Report.
Pineal gland tumours are reported rarely in Malayasia and early diagnosis and intervention promise a better prognosis for patients. We report a rare case of pineal gland tumour with drop metastases in the fourth ventricle in a 20-year-old young male with Parinaud syndrome. The patient, who had no&#xa0;underlying medical illnesses, presented with neurological symptoms and limb weakness associated with tremors and blurring of vision which worsened over a span of four months. The patient was having difficulty in ambulating with reduced power over the lower limbs with tremors as well as Parinaud syndrome indicated through the limitation of upward gaze, light-near dissociation of the pupils and convergence nystagmus. An MRI&#xa0;showed the presence of a pineal gland tumour with drop metastases in the fourth ventricle with calcification. The patient underwent an endoscopic third ventriculostomy and tumour biopsy. The biopsy indicated a pineal gland tumour with a germinoma subset and the patient was subjected to radiotherapy. Latency of diagnosis is an important prognostic factor as it reduces the survival rate for these patients hence the following discussion on the pineal gland tumour and its diagnostic dilemma.
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Multi-task longitudinal forecasting with missing values on Alzheimer's disease.<Pagination><StartPage>107056</StartPage><MedlinePgn>107056</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.cmpb.2022.107056</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0169-2607(22)00438-2</ELocationID><Abstract><AbstractText Label="BACKGROUND AND OBJECTIVE" NlmCategory="OBJECTIVE">Machine learning techniques typically used in dementia assessment are not able to learn multiple tasks jointly and deal with time-dependent heterogeneous data containing missing values. In this paper, we reformulate SSHIBA, a recently introduced Bayesian multi-view latent variable model, for jointly learning diagnosis, ventricle volume, and ADAS score in dementia on longitudinal data with missing values.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">We propose a novel Bayesian Variational inference framework capable of simultaneously imputing missing values and combining information from several views. This way, we can combine different data views from different time-points in a common latent space and learn the relationships between each time-point, using the semi-supervised formulation to fully exploit the temporal structure of the data and handle missing values. In turn, the model can combine all the available information to simultaneously model and predict multiple output variables.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">We applied the proposed model to jointly predict diagnosis, ventricle volume, and ADAS score in dementia. The comparison of imputation strategies demonstrated the superior performance of the semi-supervised formulation of the model, improving the best baseline methods. Moreover, the performance in simultaneous prediction of diagnosis, ventricle volume, and ADAS score led to an improved prediction performance over the best baseline method.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">The results demonstrate that the proposed SSHIBA framework can learn an excellent imputation of the missing values and outperforming the baselines while simultaneously predicting three different tasks.</AbstractText><CopyrightInformation>Copyright &#xa9; 2022. Published by Elsevier B.V.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Sevilla-Salcedo</LastName><ForeName>Carlos</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Signal Theory and Communications Department, University Carlos III of Madrid, Legan&#xe9;s 28911 Spain. Electronic address: sevisal@tsc.uc3m.es.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Imani</LastName><ForeName>Vandad</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>A.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>M Olmos</LastName><ForeName>Pablo</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Signal Theory and Communications Department, University Carlos III of Madrid, Legan&#xe9;s 28911 Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>G&#xf3;mez-Verdejo</LastName><ForeName>Vanessa</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>Signal Theory and Communications Department, University Carlos III of Madrid, Legan&#xe9;s 28911 Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tohka</LastName><ForeName>Jussi</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>A.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><CollectiveName>Alzheimer&#x2019;s Disease Neuroimaging Initiative</CollectiveName><AffiliationInfo><Affiliation>Data used in preparation of this article were obtained from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database (adni.loni.usc.edu). As such, the investigators within the ADNI contributed to the design and implementation of ADNI and/or provided data but did not participate in analysis or writing of this report. This work involved human subjects or animals in its research. Approval of all ethical and experimental procedures and protocols was granted by the Institutional Data Access/Ethics Committee of the ADNI. A complete listing of ADNI investigators can be found at: http://adni.loni.usc.edu/wpcontent/uploads/how_to_apply/ADNI_Acknowledgement_List.pdf. This work involved human subjects or animals in its research. Approval of all ethical and experimental procedures and protocols was granted by the Institutional Data Access/Ethics Committee of the Alzheimer's Disease Neuroimaging Initiative (ADNI).</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>08</Month><Day>02</Day></ArticleDate></Article><MedlineJournalInfo><Country>Ireland</Country><MedlineTA>Comput Methods Programs Biomed</MedlineTA><NlmUniqueID>8506513</NlmUniqueID><ISSNLinking>0169-2607</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000544" MajorTopicYN="Y">Alzheimer Disease</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001499" MajorTopicYN="N">Bayes Theorem</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000069550" MajorTopicYN="N">Machine Learning</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012107" MajorTopicYN="N">Research Design</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Alzheimer&#x2019;s disease</Keyword><Keyword MajorTopicYN="N">Longitudinal data</Keyword><Keyword MajorTopicYN="N">Missing values</Keyword><Keyword MajorTopicYN="N">Multi-task</Keyword></KeywordList><CoiStatement>Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>2</Month><Day>4</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>6</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>8</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>10</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>11</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>10</Month><Day>3</Day><Hour>18</Hour><Minute>12</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36191353</ArticleId><ArticleId IdType="doi">10.1016/j.cmpb.2022.107056</ArticleId><ArticleId IdType="pii">S0169-2607(22)00438-2</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36191246</PMID><DateRevised><Year>2022</Year><Month>10</Month><Day>03</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">2066-8643</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Oct</Month><Day>03</Day></PubDate></JournalIssue><Title>Medical ultrasonography</Title><ISOAbbreviation>Med Ultrason</ISOAbbreviation></Journal>Unusual echocardiographic finding as cause of acute coronary syndrome with ST- segment elevation.
Biventricular metastatic heart tumors from gynecological malignancies presented as an acute coronary syndrome with ST segment elevation are an unusual finding. We present a case of stage-4 vulvar carcinoma that metastasized in both the left and right ventricle. The particularity of the case is the echocardiographic aspect in the emergency room: multiple, large, hyperechogenic masses disseminated in the myocardium, with pericardial extension, in context of acute coronary syndrome with ST segment elevation.
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Analysis of the risk factors of post-operative seizure in pediatric patients with hydrocephalus undergoing endoscopic third ventriculostomy.
The cause and mechanism of epilepsy after endoscopic third ventriculostomy (ETV) have still remained elusive. This single-center study aimed to explore and analyze the risk factors of post-operative seizure in pediatric patients with hydrocephalus undergoing ETV.</AbstractText>Data of pediatric patients with hydrocephalus who were treated with ETV from October 1, 2015, to November 31, 2021, were retrospectively analyzed. Basic demographic characteristics, etiology of hydrocephalus, surgical details, and laboratory measurements were collected. An early postoperative seizure was defined as the occurrence of at least one clinical seizure within 24 h of ETV.</AbstractText>A total of 50 participants were included in the study, of whom 5 (10.00%) cases were in postoperative epilepsy group and 45 (90.00%) cases were in non-epilepsy group. Epilepsy patients were younger than those without epilepsy, while no statistically significant difference was found (P = 0.0836). In the age subgroup, children with epilepsy were younger than 2 years old. All patients with epilepsy received Ringer's solution intraoperatively. The mean postoperative serum calcium and potassium concentrations were significantly lower in patients with epilepsy than in those without epilepsy (Pcalcium</sub> = 0.0429; Ppotassium</sub> = 0.0250). Moreover, a faster decrease of serum potassium and calcium levels was found in children with epilepsy compared with those without epilepsy after ETV.</AbstractText>The decrease of serum calcium and potassium levels, younger age, and using Ringer's solution as irrigation fluid were risk factors for epilepsy after ETV.</AbstractText>&#xa9; 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.</CopyrightInformation>
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A medical image segmentation method based on multi-dimensional statistical features.
Medical image segmentation has important auxiliary significance for clinical diagnosis and treatment. Most of existing medical image segmentation solutions adopt convolutional neural networks (CNNs). Althought these existing solutions can achieve good image segmentation performance, CNNs focus on local information and ignore global image information. Since Transformer can encode the whole image, it has good global modeling ability and is effective for the extraction of global information. Therefore, this paper proposes a hybrid feature extraction network, into which CNNs and Transformer are integrated to utilize their advantages in feature extraction. To enhance low-dimensional texture features, this paper also proposes a multi-dimensional statistical feature extraction module to fully fuse the features extracted by CNNs and Transformer and enhance the segmentation performance of medical images. The experimental results confirm that the proposed method achieves better results in brain tumor segmentation and ventricle segmentation than state-of-the-art solutions.
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Diffusion-weighted imaging hyperintensities during the chronic stage of intracerebral hemorrhage with surgery: A new clinical situation or post-surgery artifact?
Diffusion-weighted imaging (DWI) hyperintensities were occasionally seen at previous hematoma in patients several months after intracerebral hemorrhage with surgery. Whether they are newly occurred clinical situations or post-surgery changes is unknown. This study aims to investigate the prevalence and possible mechanisms for this phenomenon.</AbstractText>We retrospectively reviewed the MRI database for intracerebral hemorrhage with surgery after 3 months of disease onset in our hospital. We also prospectively performed repeated multimodal MRI scans for two patients at the chronic stage after surgery for intracerebral hemorrhage.</AbstractText>We found that 14 out of 23 patients (60.9%) had DWI hyperintensities at the site of previous hematoma 3 months after intracerebral hemorrhage with surgery. All the DWI lesions were hyperintense on T1- and T2-weighted imaging, most of which appeared long and narrow in shape. The DWI lesions were usually located adjacent to the thin wall of the previous hematoma cavity close to the lateral ventricle. They were more associated with the basal ganglia hemorrhage than with the lobar hemorrhage (P</i> = 0.02) and were more frequently seen for those with intraventricular hemorrhage than without (P</i> = 0.02). Prospectively repeated MRI exams of two patients revealed unchanged DWI hyperintensity during the 18- and 2-month follow-up, respectively.</AbstractText>The DWI lesions at previous hematoma were commonly seen in patients after surgery for intracerebral hemorrhage at the chronic stage which would persist for years. We hypothesized a possible mechanism by which extracellular methemoglobin "islands" are formed with delayed or no absorption by macrophages from adjacent thin residual brain tissue. Unnecessary further examinations and treatment would be avoided by realizing this imaging phenomenon.</AbstractText>Copyright &#xa9; 2022 Chen, Li, Guo, Han, Liu, Tian, Cui, Dong and Yu.</CopyrightInformation>
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Relationship between adult subventricular neurogenesis and Alzheimer's disease: Pathologic roles and therapeutic implications.
Alzheimer's disease (AD) is a neurodegenerative disease that is characterized by irreversible cognitive declines. Senile plaques formed by amyloid-&#x3b2; (A&#x3b2;) peptides and neurofibrillary tangles, consisting of hyperphosphorylated tau protein accumulation, are prominent neuropathological features of AD. Impairment of adult neurogenesis is also a well-known pathology in AD. Adult neurogenesis is the process by which neurons are generated from adult neural stem cells. It is closely related to various functions, including cognition, as it occurs throughout life for continuous repair and development of specific neural pathways. Notably, subventricular zone (SVZ) neurogenesis, which occurs in the lateral ventricles, transports neurons to several brain regions such as the olfactory bulb, cerebral cortex, striatum, and hippocampus. These migrating neurons can affect cognitive function and behavior in different neurodegenerative diseases. Despite several studies indicating the importance of adult SVZ neurogenesis in neurodegenerative disorders, the pathological alterations and therapeutic implications of impaired adult neurogenesis in the SVZ in AD have not yet been fully explained. In this review, we summarize recent progress in understanding the alterations in adult SVZ neurogenesis in AD animal models and patients. Moreover, we discuss the potential therapeutic approaches for restoring impaired adult SVZ neurogenesis. Our goal is to impart to readers the importance of adult SVZ neurogenesis in AD and to provide new insights through the discussion of possible therapeutic approaches.
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A large left ventricle and extremely low ejection fraction in a 5-month-old girl with ALCAPA.<Pagination><StartPage>71</StartPage><EndPage>72</EndPage><MedlinePgn>71-72</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.hjc.2022.09.007</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S1109-9666(22)00140-3</ELocationID><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Yu</LastName><ForeName>Juemin</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Cardiac Surgery, Guangdong Cardiovascular Institute, Guangdong Provincial Key Laboratory of South China Structural Heart Disease, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong Province, 510000, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Xiaobing</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Cardiac Surgery, Guangdong Cardiovascular Institute, Guangdong Provincial Key Laboratory of South China Structural Heart Disease, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong Province, 510000, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhuang</LastName><ForeName>Jian</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Cardiac Surgery, Guangdong Cardiovascular Institute, Guangdong Provincial Key Laboratory of South China Structural Heart Disease, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong Province, 510000, China. Electronic address: zhuangjian5413@163.com.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>09</Month><Day>28</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Hellenic J Cardiol</MedlineTA><NlmUniqueID>101257381</NlmUniqueID><ISSNLinking>1109-9666</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007223" MajorTopicYN="N">Infant</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D063748" MajorTopicYN="Y">Bland White Garland Syndrome</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013318" MajorTopicYN="N">Stroke Volume</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003330" MajorTopicYN="Y">Coronary Vessel Anomalies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011651" MajorTopicYN="N">Pulmonary Artery</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Anomalous left coronary artery from the pulmonary artery</Keyword><Keyword MajorTopicYN="N">Cardiac function</Keyword><Keyword MajorTopicYN="N">Congenital heart disease</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>8</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>9</Month><Day>23</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>9</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>10</Month><Day>2</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2023</Year><Month>2</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>10</Month><Day>1</Day><Hour>19</Hour><Minute>36</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36181998</ArticleId><ArticleId IdType="doi">10.1016/j.hjc.2022.09.007</ArticleId><ArticleId IdType="pii">S1109-9666(22)00140-3</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36181389</PMID><DateRevised><Year>2022</Year><Month>10</Month><Day>01</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1932-8494</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Oct</Month><Day>01</Day></PubDate></JournalIssue><Title>Anatomical record (Hoboken, N.J. : 2007)</Title><ISOAbbreviation>Anat Rec (Hoboken)</ISOAbbreviation></Journal>Comparative gross anatomy of epicardiac ganglionated nerve plexi on the human and sheep cardiac ventricles.
This study aimed to examine the distribution and quantitative parameters of the epicardiac ventricular neural ganglionated plexus in the hearts of humans and sheep, highlighting the differences of this plexus in humans and large models. Five non-sectioned pressure distended whole hearts of the human newborns and 10 hearts of newborn German black-faced lambs were investigated applying a histochemical method for acetylcholinesterase to stain epicardiac neural structures with their subsequent stereomicroscopic examination. In humans, the ventricular nerves are spread by four epicardiac nerve subplexuses, that is, the left and right coronary as well as the left and middle dorsal. In sheep, the ventricular nerves are spread by five epicardiac nerve subplexuses, that is, the left and right coronary, the left and middle dorsal and the right ventral ones. The ventricular epicardium involved up to 129 ganglia in humans and up to 198-in sheep. The largest number of the ventricular ganglionic cells in humans were located on the ventral side, in front of the conus arteriosus, while on sheep ventricles, the most numerous neurons distributed on the dorsal wall of the left ventricle. This comparative study of the morphological patterns of the human and sheep ventricles demonstrates that the sheep heart is neuroanatomically distinct from the human one and this must be taking into consideration using the sheep model for the heart physiology experiments.
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Predictors of survival for pediatric extracorporeal cardiopulmonary resuscitation: A systematic review and meta-analysis.<Pagination><StartPage>e30860</StartPage><MedlinePgn>e30860</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">e30860</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1097/MD.0000000000030860</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">The use of extracorporeal cardiopulmonary resuscitation (ECPR) has improved survival in patients with cardiac arrest; however, factors predicting survival remain poorly characterized. A systematic review and meta-analysis was conducted to examine the predictors of survival of ECPR in pediatric patients.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">We searched EMBASE, PubMed, SCOPUS, and the Cochrane Library from 2010 to 2021 for pediatric ECPR studies comparing survivors and non-survivors. Thirty outcomes were analyzed and classified into 5 categories: demographics, pre-ECPR laboratory measurements, pre-ECPR co-morbidities, intra-ECPR characteristics, and post-ECPR complications.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Thirty studies (n&#x2005;=&#x2005;3794) were included. Pooled survival to hospital discharge (SHD) was 44% (95% CI: 40%-47%, I2&#x2005;=&#x2005;67%). Significant predictors of survival for pediatric ECPR include the pre-ECPR lab measurements of PaO2, pH, lactate, PaCO2, and creatinine, pre-ECPR comorbidities of single ventricle (SV) physiology, renal failure, sepsis, ECPR characteristics of extracorporeal membrane oxygenation (ECMO) duration, ECMO flow rate at 24 hours, cardiopulmonary resuscitation (CPR) duration, shockable rhythm, intra-ECPR neurological complications, and post-ECPR complications of pulmonary hemorrhage, renal failure, and sepsis.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">Prior to ECPR initiation, increased CPR duration and lactate levels had among the highest associations with mortality, followed by pH. After ECPR initiation, pulmonary hemorrhage and neurological complications were most predictive for survival. Clinicians should focus on these factors to better inform potential prognosis of patients, advise appropriate patient selection, and improve ECPR program effectiveness.</AbstractText><CopyrightInformation>Copyright &#xa9; 2022 the Author(s). Published by Wolters Kluwer Health, Inc.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Sood</LastName><ForeName>Nitish</ForeName><Initials>N</Initials><Identifier Source="ORCID">0000-0003-1516-0691</Identifier><AffiliationInfo><Affiliation>Medical College of Georgia at Augusta University, Augusta, GA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sangari</LastName><ForeName>Anish</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Medical College of Georgia at Augusta University, Augusta, GA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Goyal</LastName><ForeName>Arnav</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Medical College of Georgia at Augusta University, Augusta, GA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Conway</LastName><ForeName>J Arden S</ForeName><Initials>JAS</Initials><AffiliationInfo><Affiliation>Department of Pediatrics, Division of Critical Care Medicine, Medical College of GA at Augusta University, Augusta, GA, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D017418">Meta-Analysis</PublicationType><PublicationType UI="D000078182">Systematic Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Medicine (Baltimore)</MedlineTA><NlmUniqueID>2985248R</NlmUniqueID><ISSNLinking>0025-7974</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>33X04XA5AT</RegistryNumber><NameOfSubstance UI="D019344">Lactic Acid</NameOfSubstance></Chemical><Chemical><RegistryNumber>AYI8EX34EU</RegistryNumber><NameOfSubstance UI="D003404">Creatinine</NameOfSubstance></Chemical><Chemical><RegistryNumber>S88TT14065</RegistryNumber><NameOfSubstance UI="D010100">Oxygen</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D016887" MajorTopicYN="Y">Cardiopulmonary Resuscitation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002648" MajorTopicYN="N">Child</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003404" MajorTopicYN="N">Creatinine</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019344" MajorTopicYN="N">Lactic Acid</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009422" MajorTopicYN="Y">Nervous System Diseases</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010100" MajorTopicYN="N">Oxygen</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051437" MajorTopicYN="Y">Renal Insufficiency</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018805" MajorTopicYN="Y">Sepsis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015996" MajorTopicYN="N">Survival Rate</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading></MeshHeadingList><CoiStatement>The authors have no funding and conflicts of interest to disclose.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>10</Month><Day>1</Day><Hour>1</Hour><Minute>2</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>10</Month><Day>2</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>10</Month><Day>5</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36181012</ArticleId><ArticleId IdType="pmc">PMC9524896</ArticleId><ArticleId IdType="doi">10.1097/MD.0000000000030860</ArticleId><ArticleId IdType="pii">00005792-202209300-00010</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Matos RI, Watson RS, Nadkarni VM, et al. . 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Pre-excitation is a term that refers to the premature activation of the ventricles. Previously used when referring to Wolff-Parkinson-White (WPW), pre-excitation has been expanded to include any rhythm with antegrade ventricular or retrograde atrial activation via an accessory pathway. These pathways may be partially or completely separate from the normal conduction system. The Lown-Ganong-Levine (LGL) pattern was described in 1952 by Bernard Lown, William Francis Ganong, and Samual Levine and is theorized to involve an accessory pathway that partially or completely bypasses the atrioventricular (AV) node resulting in the direct activation of the bundle of His by the sinoatrial (SA) node.&#xa0;Lown-Ganong-Levine (LGL) syndrome is an outdated clinical diagnosis with no known unique underlying anatomic correlate.&#xa0;
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Single cell and spatial transcriptomic analyses reveal microglia-plasma cell crosstalk in the brain during Trypanosoma brucei infection.<Pagination><StartPage>5752</StartPage><MedlinePgn>5752</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">5752</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1038/s41467-022-33542-z</ELocationID><Abstract><AbstractText>Human African trypanosomiasis, or sleeping sickness, is caused by the protozoan parasite Trypanosoma brucei and induces profound reactivity of glial cells and neuroinflammation when the parasites colonise the central nervous system. However, the transcriptional and functional responses of the brain to chronic T. brucei infection remain poorly understood. By integrating single cell and spatial transcriptomics of the mouse brain, we identify that glial responses triggered by infection are readily detected in the proximity to the circumventricular organs, including the lateral and 3<sup>rd</sup> ventricle. This coincides with the spatial localisation of both slender and stumpy forms of T. brucei. Furthermore, in silico predictions and functional validations led us to identify a previously unknown crosstalk between homeostatic microglia and Cd138<sup>+</sup> plasma cells mediated by IL-10 and B cell activating factor (BAFF) signalling. This study provides important insights and resources to improve understanding of the molecular and cellular responses in the brain during infection with African trypanosomes.</AbstractText><CopyrightInformation>&#xa9; 2022. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Quintana</LastName><ForeName>Juan F</ForeName><Initials>JF</Initials><Identifier Source="ORCID">0000-0002-5092-5576</Identifier><AffiliationInfo><Affiliation>Wellcome Centre for Integrative Parasitology (WCIP), University of Glasgow, Glasgow, UK. juan.quintana@glasgow.ac.uk.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>School of Biodiversity, One Health, and Veterinary Medicine (SBOHVM), MVLS, University of Glasgow, Glasgow, UK. juan.quintana@glasgow.ac.uk.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chandrasegaran</LastName><ForeName>Praveena</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Wellcome Centre for Integrative Parasitology (WCIP), University of Glasgow, Glasgow, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>School of Biodiversity, One Health, and Veterinary Medicine (SBOHVM), MVLS, University of Glasgow, Glasgow, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sinton</LastName><ForeName>Matthew C</ForeName><Initials>MC</Initials><Identifier Source="ORCID">0000-0003-1292-799X</Identifier><AffiliationInfo><Affiliation>Wellcome Centre for Integrative Parasitology (WCIP), University of Glasgow, Glasgow, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>School of Biodiversity, One Health, and Veterinary Medicine (SBOHVM), MVLS, University of Glasgow, Glasgow, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Briggs</LastName><ForeName>Emma M</ForeName><Initials>EM</Initials><Identifier Source="ORCID">0000-0002-6740-8882</Identifier><AffiliationInfo><Affiliation>Wellcome Centre for Integrative Parasitology (WCIP), University of Glasgow, Glasgow, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institute for Immunology and Infection Research, School of Biological Sciences, University of Edinburgh, Edinburgh, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Otto</LastName><ForeName>Thomas D</ForeName><Initials>TD</Initials><Identifier Source="ORCID">0000-0002-1246-7404</Identifier><AffiliationInfo><Affiliation>Wellcome Centre for Integrative Parasitology (WCIP), University of Glasgow, Glasgow, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>School of Infection and Immunity, MVLS, University of Glasgow, Glasgow, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Heslop</LastName><ForeName>Rhiannon</ForeName><Initials>R</Initials><Identifier Source="ORCID">0000-0002-4332-4393</Identifier><AffiliationInfo><Affiliation>Wellcome Centre for Integrative Parasitology (WCIP), University of Glasgow, Glasgow, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>School of Biodiversity, One Health, and Veterinary Medicine (SBOHVM), MVLS, University of Glasgow, Glasgow, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bentley-Abbot</LastName><ForeName>Calum</ForeName><Initials>C</Initials><Identifier Source="ORCID">0000-0002-0087-0028</Identifier><AffiliationInfo><Affiliation>Wellcome Centre for Integrative Parasitology (WCIP), University of Glasgow, Glasgow, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>School of Biodiversity, One Health, and Veterinary Medicine (SBOHVM), MVLS, University of Glasgow, Glasgow, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Loney</LastName><ForeName>Colin</ForeName><Initials>C</Initials><Identifier Source="ORCID">0000-0002-0508-1781</Identifier><AffiliationInfo><Affiliation>School of Infection and Immunity, MVLS, University of Glasgow, Glasgow, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>MRC Centre for Virus Research, University of Glasgow, Glasgow, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>de Lecea</LastName><ForeName>Luis</ForeName><Initials>L</Initials><Identifier Source="ORCID">0000-0002-8921-5942</Identifier><AffiliationInfo><Affiliation>Stanford University School of Medicine, Stanford, CA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mabbott</LastName><ForeName>Neil A</ForeName><Initials>NA</Initials><Identifier Source="ORCID">0000-0001-7395-1796</Identifier><AffiliationInfo><Affiliation>The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Edinburgh, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>MacLeod</LastName><ForeName>Annette</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Wellcome Centre for Integrative Parasitology (WCIP), University of Glasgow, Glasgow, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>School of Biodiversity, One Health, and Veterinary Medicine (SBOHVM), MVLS, University of Glasgow, Glasgow, UK.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>218648/Z/19/Z</GrantID><Acronym>WT_</Acronym><Agency>Wellcome Trust</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>BBS/E/D/20002174</GrantID><Acronym>BB_</Acronym><Agency>Biotechnology and Biological Sciences Research Council</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>221640/Z/20/Z</GrantID><Acronym>WT_</Acronym><Agency>Wellcome Trust</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>204820/Z/16/Z</GrantID><Acronym>WT_</Acronym><Agency>Wellcome Trust</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>104111/Z/14/ZR</GrantID><Acronym>WT_</Acronym><Agency>Wellcome Trust</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>BBS/E/D/20231762</GrantID><Acronym>BB_</Acronym><Agency>Biotechnology and Biological Sciences Research Council</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>209511/Z/17/Z</GrantID><Acronym>WT_</Acronym><Agency>Wellcome Trust</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>MC_UU_12014/7</GrantID><Acronym>MRC_</Acronym><Agency>Medical Research Council</Agency><Country>United Kingdom</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>09</Month><Day>30</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Nat Commun</MedlineTA><NlmUniqueID>101528555</NlmUniqueID><ISSNLinking>2041-1723</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D053264">B-Cell Activating Factor</NameOfSubstance></Chemical><Chemical><RegistryNumber>130068-27-8</RegistryNumber><NameOfSubstance UI="D016753">Interleukin-10</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D053264" MajorTopicYN="N">B-Cell Activating Factor</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001921" MajorTopicYN="N">Brain</DescriptorName><QualifierName UI="Q000469" MajorTopicYN="N">parasitology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016753" MajorTopicYN="N">Interleukin-10</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017628" MajorTopicYN="N">Microglia</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010271" MajorTopicYN="Y">Parasites</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010950" MajorTopicYN="N">Plasma Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D059467" MajorTopicYN="N">Transcriptome</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014346" MajorTopicYN="Y">Trypanosoma brucei brucei</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014353" MajorTopicYN="Y">Trypanosomiasis, African</DescriptorName><QualifierName UI="Q000469" MajorTopicYN="N">parasitology</QualifierName></MeshHeading></MeshHeadingList><CoiStatement>The authors declare no competing interests.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>4</Month><Day>5</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>9</Month><Day>21</Day></PubMedPubDate><PubMedPubDate 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Human African trypanosomiasis, or sleeping sickness, is caused by the protozoan parasite Trypanosoma brucei and induces profound reactivity of glial cells and neuroinflammation when the parasites colonise the central nervous system. However, the transcriptional and functional responses of the brain to chronic T. brucei infection remain poorly understood. By integrating single cell and spatial transcriptomics of the mouse brain, we identify that glial responses triggered by infection are readily detected in the proximity to the circumventricular organs, including the lateral and 3<sup>rd</sup> ventricle. This coincides with the spatial localisation of both slender and stumpy forms of T. brucei. Furthermore, in silico predictions and functional validations led us to identify a previously unknown crosstalk between homeostatic microglia and Cd138<sup>+</sup> plasma cells mediated by IL-10 and B cell activating factor (BAFF) signalling. This study provides important insights and resources to improve understanding of the molecular and cellular responses in the brain during infection with African trypanosomes.<CopyrightInformation>&#xa9; 2022. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Quintana</LastName><ForeName>Juan F</ForeName><Initials>JF</Initials><Identifier Source="ORCID">0000-0002-5092-5576</Identifier><AffiliationInfo><Affiliation>Wellcome Centre for Integrative Parasitology (WCIP), University of Glasgow, Glasgow, UK. juan.quintana@glasgow.ac.uk.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>School of Biodiversity, One Health, and Veterinary Medicine (SBOHVM), MVLS, University of Glasgow, Glasgow, UK. juan.quintana@glasgow.ac.uk.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chandrasegaran</LastName><ForeName>Praveena</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Wellcome Centre for Integrative Parasitology (WCIP), University of Glasgow, Glasgow, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>School of Biodiversity, One Health, and Veterinary Medicine (SBOHVM), MVLS, University of Glasgow, Glasgow, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sinton</LastName><ForeName>Matthew C</ForeName><Initials>MC</Initials><Identifier Source="ORCID">0000-0003-1292-799X</Identifier><AffiliationInfo><Affiliation>Wellcome Centre for Integrative Parasitology (WCIP), University of Glasgow, Glasgow, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>School of Biodiversity, One Health, and Veterinary Medicine (SBOHVM), MVLS, University of Glasgow, Glasgow, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Briggs</LastName><ForeName>Emma M</ForeName><Initials>EM</Initials><Identifier Source="ORCID">0000-0002-6740-8882</Identifier><AffiliationInfo><Affiliation>Wellcome Centre for Integrative Parasitology (WCIP), University of Glasgow, Glasgow, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institute for Immunology and Infection Research, School of Biological Sciences, University of Edinburgh, Edinburgh, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Otto</LastName><ForeName>Thomas D</ForeName><Initials>TD</Initials><Identifier Source="ORCID">0000-0002-1246-7404</Identifier><AffiliationInfo><Affiliation>Wellcome Centre for Integrative Parasitology (WCIP), University of Glasgow, Glasgow, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>School of Infection and Immunity, MVLS, University of Glasgow, Glasgow, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Heslop</LastName><ForeName>Rhiannon</ForeName><Initials>R</Initials><Identifier Source="ORCID">0000-0002-4332-4393</Identifier><AffiliationInfo><Affiliation>Wellcome Centre for Integrative Parasitology (WCIP), University of Glasgow, Glasgow, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>School of Biodiversity, One Health, and Veterinary Medicine (SBOHVM), MVLS, University of Glasgow, Glasgow, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bentley-Abbot</LastName><ForeName>Calum</ForeName><Initials>C</Initials><Identifier Source="ORCID">0000-0002-0087-0028</Identifier><AffiliationInfo><Affiliation>Wellcome Centre for Integrative Parasitology (WCIP), University of Glasgow, Glasgow, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>School of Biodiversity, One Health, and Veterinary Medicine (SBOHVM), MVLS, University of Glasgow, Glasgow, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Loney</LastName><ForeName>Colin</ForeName><Initials>C</Initials><Identifier Source="ORCID">0000-0002-0508-1781</Identifier><AffiliationInfo><Affiliation>School of Infection and Immunity, MVLS, University of Glasgow, Glasgow, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>MRC Centre for Virus Research, University of Glasgow, Glasgow, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>de Lecea</LastName><ForeName>Luis</ForeName><Initials>L</Initials><Identifier Source="ORCID">0000-0002-8921-5942</Identifier><AffiliationInfo><Affiliation>Stanford University School of Medicine, Stanford, CA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mabbott</LastName><ForeName>Neil A</ForeName><Initials>NA</Initials><Identifier Source="ORCID">0000-0001-7395-1796</Identifier><AffiliationInfo><Affiliation>The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Edinburgh, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>MacLeod</LastName><ForeName>Annette</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Wellcome Centre for Integrative Parasitology (WCIP), University of Glasgow, Glasgow, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>School of Biodiversity, One Health, and Veterinary Medicine (SBOHVM), MVLS, University of Glasgow, Glasgow, UK.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>218648/Z/19/Z</GrantID><Acronym>WT_</Acronym><Agency>Wellcome Trust</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>BBS/E/D/20002174</GrantID><Acronym>BB_</Acronym><Agency>Biotechnology and Biological Sciences Research Council</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>221640/Z/20/Z</GrantID><Acronym>WT_</Acronym><Agency>Wellcome Trust</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>204820/Z/16/Z</GrantID><Acronym>WT_</Acronym><Agency>Wellcome Trust</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>104111/Z/14/ZR</GrantID><Acronym>WT_</Acronym><Agency>Wellcome Trust</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>BBS/E/D/20231762</GrantID><Acronym>BB_</Acronym><Agency>Biotechnology and Biological Sciences Research Council</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>209511/Z/17/Z</GrantID><Acronym>WT_</Acronym><Agency>Wellcome Trust</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>MC_UU_12014/7</GrantID><Acronym>MRC_</Acronym><Agency>Medical Research Council</Agency><Country>United Kingdom</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>09</Month><Day>30</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Nat Commun</MedlineTA><NlmUniqueID>101528555</NlmUniqueID><ISSNLinking>2041-1723</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D053264">B-Cell Activating Factor</NameOfSubstance></Chemical><Chemical><RegistryNumber>130068-27-8</RegistryNumber><NameOfSubstance UI="D016753">Interleukin-10</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D053264" MajorTopicYN="N">B-Cell Activating Factor</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001921" MajorTopicYN="N">Brain</DescriptorName><QualifierName UI="Q000469" MajorTopicYN="N">parasitology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016753" MajorTopicYN="N">Interleukin-10</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017628" MajorTopicYN="N">Microglia</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010271" MajorTopicYN="Y">Parasites</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010950" MajorTopicYN="N">Plasma Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D059467" MajorTopicYN="N">Transcriptome</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014346" MajorTopicYN="Y">Trypanosoma brucei brucei</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014353" MajorTopicYN="Y">Trypanosomiasis, African</DescriptorName><QualifierName UI="Q000469" MajorTopicYN="N">parasitology</QualifierName></MeshHeading></MeshHeadingList><CoiStatement>The authors declare no competing interests.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>4</Month><Day>5</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>9</Month><Day>21</Day></PubMedPubDate><PubMedPubDate 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Zenodo10.1101/2022.03.25.485502 (2022).</Citation><ArticleIdList><ArticleId IdType="pmc">PMC9525673</ArticleId><ArticleId IdType="pubmed">36180478</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36180012</PMID><DateRevised><Year>2022</Year><Month>11</Month><Day>05</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1532-9488</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Sep</Month><Day>28</Day></PubDate></JournalIssue><Title>Seminars in thoracic and cardiovascular surgery</Title><ISOAbbreviation>Semin Thorac Cardiovasc Surg</ISOAbbreviation></Journal><ArticleTitle>Early Experience With Reverse Double Switch Operation for the Borderline Left Heart.</ArticleTitle><ELocationID EIdType="pii" ValidYN="Y">S1043-0679(22)00226-X</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1053/j.semtcvs.2022.09.009</ELocationID><Abstract>This study reviews our early experience with the "reverse" double switch operation (R-DSO) for borderline left hearts. A retrospective review of children with borderline left hearts who underwent R-DSO between 2017 and 2021 was conducted. Patient characteristics and early hemodynamic and clinical outcomes were collected. R-DSO was performed in 8 patients with no operative or postoperative deaths; 5 underwent decompressing bidirectional Glenn. Left ventricular (LV) poor-compliance was the dominant pathophysiology. Four patients had undergone staged LV recruitment but were not candidates for anatomical biventricular circulation due to LV hypoplasia and/or diastolic dysfunction. 7/8 patients had risk factors for Fontan circulation including pulmonary vein stenosis, pulmonary hypertension, and pulmonary artery stenosis. Median age at R-DSO was 3.7 years (19 months-12 years). All patients were in sinus rhythm at discharge. At median follow-up of 15 months (57 days-4.1 years) no mortalities, reoperations or heart transplants had occurred. All patients had normal morphologic LV systolic function. In one patient, pre-existing pulmonary hypertension (HTN) resolved after R-DSO. Reinterventions included transcatheter mitral valve replacement for residual mitral stenosis and neo-pulmonary balloon valvuloplasty. In 4 patients follow-up catheterization done at a median of 519 days (320 days-4 years) demonstrated median cardiac index of 3.2 L/min/m<sup>2</sup> (2.2-4); median sub-pulmonary left ventricular end diastolic pressure was 9 mm Hg (7-15); median inferior vena cava/baffle pressure was 8 mm Hg (7-13). R-DSO is an alternative to anatomical biventricular repair or single ventricle palliation in patients with borderline left hearts and can result in low inferior vena cava pressures and favorable early results. This approach can also relieve pulmonary HTN and allow future transplant candidacy.
2,329,472
Increment of CSF fractalkine-positive microvesicles preceded the spatial memory impairment in amyloid beta neurotoxicity.
Fractalkine (CX3</sub>CL1</sub>) is a key chemokine, affects neuronal cell communication and involves in Alzheimer's disease pathogenesis. Microvesicles (MVs) participate in neuronal cells' cross-talk in physiological and pathological states. Microvesicles released in cerebrospinal fluid (CSF) may provide a valuable footprint of brain changes. Little information is available regarding the release of fractalkine-positive MVs (CX3</sub>CL1</sub>+</sup> -MVs) in the nervous system.</AbstractText>We induced cognitive impairment by bilateral injection of amyloid-beta (A&#x3b2;) into the cerebral ventricles. We analyzed the CSF by flow cytometry in two experiments (trained and untrained) to elucidate the presence of CX3</sub>CL1</sub>+</sup> -MVs. The hippocampal TNF-&#x3b1; as an inflammatory factor was assessed by immunohistochemistry.</AbstractText>The A&#x3b2; induced spatial memory impairment after two weeks, verified by a decrease in the escape latency in Morris water maze test. It caused an increase in the anxiety-like behaviors demonstrated by a decrease in entries into the open arms of elevated plus maze test. The A&#x3b2; increased the percent of the positive area for TNF-&#x3b1; staining. Histological evaluation of the hippocampus confirmed the tissue injuries. The CSF levels of CX3</sub>CL1</sub>+</sup> -MVs, increased 2 and 7&#xa0;days after A&#x3b2; injection. The A&#x3b2; increased the TNF-&#x3b1; staining and provided an inflammatory context to facilitate the MVs release. The rise of CX3</sub>CL1</sub>+</sup> -MVs was transient and subsided after two weeks. Both trained and untrained experiments showed a similar rise pattern of CX3</sub>CL1</sub>+</sup> -MVs.</AbstractText>Increase of fractalkine-positive microvesicles preceded the cognitive impairment, more studies are required to approve the CX3</sub>CL1</sub>+</sup> -MVs as a potential biomarker in the early diagnosis of Alzheimer's disease.</AbstractText>Copyright &#xa9; 2022 Elsevier Ltd. All rights reserved.</CopyrightInformation>
2,329,473
A novel modular modeling approach for understanding different electromechanics between left and right heart in rat.
While ion channels and transporters involved in excitation-contraction coupling have been linked and constructed as comprehensive computational models, validation of whether each individual component of a model can be reused has not been previously attempted. Here we address this issue while using a novel modular modeling approach to investigate the underlying mechanism for the differences between left ventricle (LV) and right ventricle (RV). Our model was developed from modules constructed using the module assembly principles of the CellML model markup language. The components of three existing separate models of cardiac function were disassembled as to create smaller modules, validated individually, and then the component parts were combined into a new integrative model of a rat ventricular myocyte. The model was implemented in OpenCOR using the CellML standard in order to ensure reproducibility. Simulated action potential (AP), Ca<sup>2+</sup> transient, and tension were in close agreement with our experimental measurements: LV AP showed a prolonged duration and a more prominent plateau compared with RV AP; Ca<sup>2+</sup> transient showed prolonged duration and slow decay in LV compared to RV; the peak value and relaxation of tension were larger and slower, respectively, in LV compared to RV. Our novel approach of module-based mathematical modeling has established that the ionic mechanisms underlying the APs and Ca<sup>2+</sup> handling play a role in the variation in force production between ventricles. This simulation process also provides a useful way to reuse and elaborate upon existing models in order to develop a new model.
2,329,474
TCB-2, a 5-hydroxytryptamine 2A receptor agonist, disrupts prepulse inhibition in the ventral pallidum and nucleus accumbens.
The 5-hydroxytryptamine 2A (5-HT<sub>2A</sub>) receptor plays an important role in schizophrenia. The 5-HT<sub>2A</sub> receptor is also involved in the regulation of prepulse inhibition (PPI) in rodents. The aim of this study was to determine whether selective 5-HT<sub>2A</sub> receptor agonizts or antagonists may alter PPI in rats and to identify the critical brain regions in which the activity of 5-HT<sub>2A</sub> receptors regulates PPI. The results showed that infusion of the 5-HT<sub>2A</sub> receptor agonist TCB-2 into the lateral ventricle disrupted PPI, but the 5-HT<sub>2A</sub> receptor antagonist M100907 had no such effect. In addition, local infusion of TCB-2 into the nucleus accumbens and ventral pallidum disrupted PPI, whereas the same manipulation in the medial prefrontal cortex, ventral hippocampus, and ventral tegmental area did not disrupt PPI. In conclusion, agonism of 5-HT<sub>2A</sub> receptors in the ventral pallidum and nucleus accumbens can disrupt PPI. The ventral pallidum and nucleus accumbens are critical brain regions responsible for the regulation of PPI by serotonin. These findings contribute to the extensive exploration of the molecular and neural mechanisms underlying the regulatory effect of 5-HT<sub>2A</sub> receptor activity on PPI, especially the neural circuits modulated by 5-HT<sub>2A</sub> receptor activity.
2,329,475
The choroid plexus: a missing link in our understanding of brain development and function.<Pagination><StartPage>919</StartPage><EndPage>956</EndPage><MedlinePgn>919-956</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1152/physrev.00060.2021</ELocationID><Abstract><AbstractText>Studies of the choroid plexus lag behind those of the more widely known blood-brain barrier, despite a much longer history. This review has two overall aims. The first is to outline long-standing areas of research where there are unanswered questions, such as control of cerebrospinal fluid (CSF) secretion and blood flow. The second aim is to review research over the past 10 years where the focus has shifted to the idea that there are choroid plexuses located in each of the brain's ventricles that make specific contributions to brain development and function through molecules they generate for delivery via the CSF. These factors appear to be particularly important for aspects of normal brain growth. Most research carried out during the twentieth century dealt with the choroid plexus, a brain barrier interface making critical contributions to the composition and stability of the brain's internal environment throughout life. More recent research in the twenty-first century has shown the importance of choroid plexus-generated CSF in neurogenesis, influence of sex and other hormones on choroid plexus function, and choroid plexus involvement in circadian rhythms and sleep. The advancement of technologies to facilitate delivery of brain-specific therapies via the CSF to treat neurological disorders is a rapidly growing area of research. Conversely, understanding the basic mechanisms and implications of how maternal drug exposure during pregnancy impacts the developing brain represents another key area of research.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Saunders</LastName><ForeName>Norman R</ForeName><Initials>NR</Initials><Identifier Source="ORCID">0000-0001-6660-7639</Identifier><AffiliationInfo><Affiliation>Department of Neuroscience, The Alfred Centre, Monash University, Melbourne, Victoria, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dziegielewska</LastName><ForeName>Katarzyna M</ForeName><Initials>KM</Initials><Identifier Source="ORCID">0000-0002-0070-904X</Identifier><AffiliationInfo><Affiliation>Department of Neuroscience, The Alfred Centre, Monash University, Melbourne, Victoria, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fame</LastName><ForeName>Ryann M</ForeName><Initials>RM</Initials><Identifier Source="ORCID">0000-0002-8244-2624</Identifier><AffiliationInfo><Affiliation>Department of Pathology, Boston Children's Hospital, Boston, Massachusetts.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lehtinen</LastName><ForeName>Maria K</ForeName><Initials>MK</Initials><AffiliationInfo><Affiliation>Department of Pathology, Boston Children's Hospital, Boston, Massachusetts.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liddelow</LastName><ForeName>Shane A</ForeName><Initials>SA</Initials><Identifier Source="ORCID">0000-0002-0840-1437</Identifier><AffiliationInfo><Affiliation>Neuroscience Institute, NYU Grossman School of Medicine, New York, New York.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Neuroscience and Physiology, NYU Grossman School of Medicine, New York, New York.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Ophthalmology, NYU Grossman School of Medicine, New York, New York.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Parekh Center for Interdisciplinary Neurology, NYU Grossman School of Medicine, New York, New York.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>P50 HD105351</GrantID><Acronym>HD</Acronym><Agency>NICHD NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 NS088566</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>09</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Physiol Rev</MedlineTA><NlmUniqueID>0231714</NlmUniqueID><ISSNLinking>0031-9333</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002831" MajorTopicYN="Y">Choroid Plexus</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001812" MajorTopicYN="Y">Blood-Brain Barrier</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001921" MajorTopicYN="N">Brain</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001692" MajorTopicYN="N">Biological Transport</DescriptorName><QualifierName UI="Q000502" 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Studies of the choroid plexus lag behind those of the more widely known blood-brain barrier, despite a much longer history. This review has two overall aims. The first is to outline long-standing areas of research where there are unanswered questions, such as control of cerebrospinal fluid (CSF) secretion and blood flow. The second aim is to review research over the past 10 years where the focus has shifted to the idea that there are choroid plexuses located in each of the brain's ventricles that make specific contributions to brain development and function through molecules they generate for delivery via the CSF. These factors appear to be particularly important for aspects of normal brain growth. Most research carried out during the twentieth century dealt with the choroid plexus, a brain barrier interface making critical contributions to the composition and stability of the brain's internal environment throughout life. More recent research in the twenty-first century has shown the importance of choroid plexus-generated CSF in neurogenesis, influence of sex and other hormones on choroid plexus function, and choroid plexus involvement in circadian rhythms and sleep. The advancement of technologies to facilitate delivery of brain-specific therapies via the CSF to treat neurological disorders is a rapidly growing area of research. Conversely, understanding the basic mechanisms and implications of how maternal drug exposure during pregnancy impacts the developing brain represents another key area of research.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Saunders</LastName><ForeName>Norman R</ForeName><Initials>NR</Initials><Identifier Source="ORCID">0000-0001-6660-7639</Identifier><AffiliationInfo><Affiliation>Department of Neuroscience, The Alfred Centre, Monash University, Melbourne, Victoria, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dziegielewska</LastName><ForeName>Katarzyna M</ForeName><Initials>KM</Initials><Identifier Source="ORCID">0000-0002-0070-904X</Identifier><AffiliationInfo><Affiliation>Department of Neuroscience, The Alfred Centre, Monash University, Melbourne, Victoria, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fame</LastName><ForeName>Ryann M</ForeName><Initials>RM</Initials><Identifier Source="ORCID">0000-0002-8244-2624</Identifier><AffiliationInfo><Affiliation>Department of Pathology, Boston Children's Hospital, Boston, Massachusetts.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lehtinen</LastName><ForeName>Maria K</ForeName><Initials>MK</Initials><AffiliationInfo><Affiliation>Department of Pathology, Boston Children's Hospital, Boston, Massachusetts.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liddelow</LastName><ForeName>Shane A</ForeName><Initials>SA</Initials><Identifier Source="ORCID">0000-0002-0840-1437</Identifier><AffiliationInfo><Affiliation>Neuroscience Institute, NYU Grossman School of Medicine, New York, New York.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Neuroscience and Physiology, NYU Grossman School of Medicine, New York, New York.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Ophthalmology, NYU Grossman School of Medicine, New York, New York.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Parekh Center for Interdisciplinary Neurology, NYU Grossman School of Medicine, New York, New York.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>P50 HD105351</GrantID><Acronym>HD</Acronym><Agency>NICHD NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 NS088566</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>09</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Physiol Rev</MedlineTA><NlmUniqueID>0231714</NlmUniqueID><ISSNLinking>0031-9333</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002831" MajorTopicYN="Y">Choroid Plexus</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001812" MajorTopicYN="Y">Blood-Brain Barrier</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001921" MajorTopicYN="N">Brain</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001692" MajorTopicYN="N">Biological Transport</DescriptorName><QualifierName UI="Q000502" 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Prevalence trends and individual patterns of antiepileptic drug use in pregnancy 2006-2016: a study in the five Nordic countries, United States, and Australia. Pharmacoepidemiol Drug Saf 29: 913&#x2013;922, 2020. doi:10.1002/pds.5035.</Citation><ArticleIdList><ArticleId IdType="doi">10.1002/pds.5035</ArticleId><ArticleId IdType="pubmed">32492755</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36173474</PMID><DateRevised><Year>2022</Year><Month>09</Month><Day>29</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1573-7241</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Sep</Month><Day>29</Day></PubDate></JournalIssue><Title>Cardiovascular drugs and therapy</Title><ISOAbbreviation>Cardiovasc Drugs Ther</ISOAbbreviation></Journal><ArticleTitle>The SGLT2i Dapagliflozin Reduces RV Mass Independent of Changes in RV Pressure Induced by Pulmonary Artery Banding.</ArticleTitle><ELocationID EIdType="doi" ValidYN="Y">10.1007/s10557-022-07377-1</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Sodium glucose linked transporter 2 (SGLT2) inhibition not only reduces morbidity and mortality in patients with diagnosed heart failure but also prevents the development of heart failure hospitalization in those at risk. While studies to date have focused on the role of SGLT2 inhibition in left ventricular failure, whether this drug class is efficacious in the treatment and prevention of right heart failure has not been explored.<AbstractText Label="HYPOTHESIS" NlmCategory="OBJECTIVE">We hypothesized that SGLT2 inhibition would reduce the structural, functional, and molecular responses to pressure overload of the right ventricle.<AbstractText Label="METHODS" NlmCategory="METHODS">Thirteen-week-old Fischer F344 rats underwent pulmonary artery banding (PAB) or sham surgery prior to being randomized to receive either the SGLT2 inhibitor: dapagliflozin (0.5&#xa0;mg/kg/day) or vehicle by oral gavage. After 6&#xa0;weeks of treatment, animals underwent transthoracic echocardiography and invasive hemodynamic studies. Animals were then terminated, and their hearts harvested for structural and molecular analyses.<AbstractText Label="RESULTS" NlmCategory="RESULTS">PAB induced features consistent with a compensatory response to increased right ventricular (RV) afterload with elevated mass, end systolic pressure, collagen content, and alteration in calcium handling protein expression (all p&#x2009;&lt;&#x2009;0.05 when compared to sham&#x2009;+&#x2009;vehicle). Dapagliflozin reduced RV mass, including both wet and dry weight as well as normalizing the protein expression of SERCA 2A, phospho-AMPK and LC3I/II ratio expression (all p&#x2009;&lt;&#x2009;0.05).<AbstractText Label="SIGNIFICANCE" NlmCategory="CONCLUSIONS">Dapagliflozin reduces the structural, functional, and molecular manifestations of right ventricular pressure overload. Whether amelioration of these early changes in the RV may ultimately lead to a reduction in RV failure remains to be determined.
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CSF circulation and dispersion yield rapid clearance from intracranial compartments.
In this paper, we used a computational model to estimate the clearance of a tracer driven by the circulation of cerebrospinal fluid (CSF) produced in the choroid plexus (CP) located within the lateral ventricles. CSF was assumed to exit the subarachnoid space (SAS) via different outflow routes such as the parasagittal dura, cribriform plate, and/or meningeal lymphatics. We also modelled a reverse case where fluid was produced within the spinal canal and absorbed in the choroid plexus in line with observations on certain iNPH patients. No directional interstitial fluid flow was assumed within the brain parenchyma. Tracers were injected into the foramen magnum. The models demonstrate that convection in the subarachnoid space yields rapid clearance from both the SAS and the brain interstitial fluid and can speed up intracranial clearance from years, as would be the case for purely diffusive transport, to days.
2,329,477
Plastic bronchitis: A rare complication following a motor vehicle collision.
Plastic bronchitis, more appropriately termed chyloptysis, is a rare and potentially fatal condition caused by chylous coating of the airways. These cast coating can dislodge and become an obstructive mass in the patient's airway, necessitating rapid intervention. PB is well described to occur following single ventricle physiology heart disease corrective procedures, particularly following Fontan procedures. It is less commonly seen in traumatic settings. We present the youngest known case of a traumatic injury induced plastic bronchitis. A 19-year-old man was involved in a motor vehicle accident with airbag deployment. The airbags struck him in the chest; however, the patient felt well at the time and did not seek medical attention. Several months later the patient began coughing up milky white masses identified as casts. He was initially diagnosed with asthma but did not respond to therapy. He ultimately was found to have evidence of thoracic duct injury. Options for therapy were discussed, including possible thoracic duct ligation. The patient opted to continue a lowfat diet and has remained cast free. This case highlights the importance of considering plastic bronchitis in patients with cast production and a history of trauma to the chest.
2,329,478
Proximal ventricular shunt catheter occlusion model.
Proximal ventricular shunt catheter occlusion remains a problematic cause of shunt malfunction, and there is no consistent in vivo or in vitro model to help clinicians and researchers study this phenomenon.</AbstractText>An in vitro model utilizing standard proximal ventricular catheter and biological occluding agents mimicking choroid plexus was designed, constructed, and calibrated to occlude consistently within a specified timeframe. Hydrostatic pressure differential of 100 cmH2</sub>O was used as a driving force to generate flow through the catheter. Chalaza and vitelline membranes were harvested from avian eggs and used as occluding agents. Successful occlusion was defined as a greater than 90% reduction in volumetric flow rate through distal outlet. Histological sections of occluded catheters were performed and interpreted by a neuropathologist.</AbstractText>Initial trials demonstrated successful standard catheter occlusion within 24&#xa0;h using chalaza, vitelline membrane, and combination treatments. Repeat trials demonstrated consistency in successful occlusion within 5&#xa0;min utilizing only vitelline membrane treatment. Histopathology demonstrated the vitelline membrane to consist of a thin, superficial layer of extraembryonic ectoderm; the chalaza was observed to consist of strands of mucin protein.</AbstractText>An in vitro model of proximal ventricular shunt catheter occlusion was developed and calibrated for successful occlusion within 5&#xa0;min. Future studies may utilize this model to rapidly test occlusion-resistant shunt designs and de-obstruction techniques.</AbstractText>&#xa9; 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.</CopyrightInformation>
2,329,479
Multi-disciplinary collaborative consensus guidance statement on the assessment and treatment of postacute sequelae of SARS-CoV-2 infection (PASC) in children and adolescents.<Pagination><StartPage>1241</StartPage><EndPage>1269</EndPage><MedlinePgn>1241-1269</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/pmrj.12890</ELocationID><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Malone</LastName><ForeName>Laura A</ForeName><Initials>LA</Initials><Identifier Source="ORCID">0000-0002-9836-822X</Identifier><AffiliationInfo><Affiliation>Kennedy Krieger Institute, Department of Neurology, Johns Hopkins Medicine, Baltimore, Maryland, United States.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Physical Medicine and Rehabilitation, Johns Hopkins Medicine, Baltimore, Maryland, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Morrow</LastName><ForeName>Amanda</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Kennedy Krieger Institute, Department of Physical Medicine and Rehabilitation, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Yuxi</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Rehabilitation Medicine, Montefiore Medical Center, Bronx, New York, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Curtis</LastName><ForeName>Donna</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Pediatric Infectious Diseases Children's Hospital Colorado and University of Colorado School of Medicine Aurora, Aurora, Colorado, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>de Ferranti</LastName><ForeName>Sarah D</ForeName><Initials>SD</Initials><AffiliationInfo><Affiliation>Department of Pediatrics, Harvard Medical School, Department of Cardiology, Boston Children's Hospital, Boston, Massachusetts, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Desai</LastName><ForeName>Monika</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Rehabilitation Medicine, Montefiore Medical Center/Albert Einstein School of Medicine, Bronx, New York, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fleming</LastName><ForeName>Talya K</ForeName><Initials>TK</Initials><Identifier Source="ORCID">0000-0002-2034-8253</Identifier><AffiliationInfo><Affiliation>Department of Physical Medicine and Rehabilitation, JFK Johnson Rehabilitation Institute at Hackensack Meridian Health, Edison, New Jersey, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Giglia</LastName><ForeName>Therese M</ForeName><Initials>TM</Initials><AffiliationInfo><Affiliation>Director of the Center on Cardiac Anticoagulation and Thrombosis and Director of the Infant Single Ventricle Monitoring Program, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hall</LastName><ForeName>Trevor A</ForeName><Initials>TA</Initials><AffiliationInfo><Affiliation>Department of Pediatrics, Oregon Health &amp; Science University, Portland, Oregon.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Henning</LastName><ForeName>Ellen</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Department of Behavioral Psychology, Kennedy Krieger Institute, Baltimore, Maryland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jadhav</LastName><ForeName>Sneha</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Psychiatric Mental Health Program, Kennedy Krieger Institute, Baltimore, Maryland, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Johnston</LastName><ForeName>Alicia M</ForeName><Initials>AM</Initials><AffiliationInfo><Affiliation>Division of Infectious Diseases, Department of Pediatrics, Boston Children's Hospital, Boston, Massachusetts, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kathirithamby</LastName><ForeName>Dona Rani C</ForeName><Initials>DRC</Initials><AffiliationInfo><Affiliation>Department of Rehabilitation Medicine and Department of Pediatrics, Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kokorelis</LastName><ForeName>Christina</ForeName><Initials>C</Initials><Identifier Source="ORCID">0000-0001-6486-4391</Identifier><AffiliationInfo><Affiliation>Department of Physical Medicine and Rehabilitation, Johns Hopkins University and Kennedy Krieger Institute, Baltimore, Maryland, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lachenauer</LastName><ForeName>Catherine</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Division of Infectious Diseases, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Lilun</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Otolaryngology, Head and Neck Surgery, Robert Wood Johnson Medical School, New Brunswick, New Jersey, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lin</LastName><ForeName>Henry C</ForeName><Initials>HC</Initials><AffiliationInfo><Affiliation>Department of Pediatrics, Oregon Health &amp; Science University, Portland, Oregon, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Locke</LastName><ForeName>Tran</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Otolaryngology-Head and Neck Surgery Baylor College of Medicine Houston, Houston, Texas, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>MacArthur</LastName><ForeName>Carol</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Otolaryngology, Head &amp; Neck Surgery, Oregon Health &amp; Science University, Oregon, Portland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mann</LastName><ForeName>Michelle</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Pediatric Pulmonology, Baylor College of Medicine, Texas Children's Hospital, Houston, Texas, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>McGrath-Morrow</LastName><ForeName>Sharon A</ForeName><Initials>SA</Initials><AffiliationInfo><Affiliation>Department of Pediatrics, Division of Pediatric Pulmonary Children's Hospital of Philadelphia and the University of Pennsylvania.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ng</LastName><ForeName>Rowena</ForeName><Initials>R</Initials><Identifier Source="ORCID">0000-0001-7193-4300</Identifier><AffiliationInfo><Affiliation>Neuropsychology Department, Kennedy Krieger Institute; Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ohlms</LastName><ForeName>Laurie</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Otolaryngology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Risen</LastName><ForeName>Sarah</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Pediatric Neurology and Developmental Neuroscience, Texas Children's Hospital and Baylor College of Medicine, Houston, Texas, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sadreameli</LastName><ForeName>S Christy</ForeName><Initials>SC</Initials><AffiliationInfo><Affiliation>Eudowood Division of Pediatric Respiratory Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sampsel</LastName><ForeName>Sarah</ForeName><Initials>S</Initials><Identifier Source="ORCID">0000-0002-7496-8482</Identifier><AffiliationInfo><Affiliation>SLSampsel Consulting, Albuquerque, New Mexico, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tejtel</LastName><ForeName>S Kristen Sexson</ForeName><Initials>SKS</Initials><AffiliationInfo><Affiliation>Pediatric Cardiology, Texas Children's Hospital/Baylor College of Medicine, Houston, Texas, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Silver</LastName><ForeName>Julie K</ForeName><Initials>JK</Initials><AffiliationInfo><Affiliation>Department of Physical Medicine and Rehabilitation, Harvard Medical School, Spaulding Rehabilitation Hospital, Boston, Massachusetts, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Simoneau</LastName><ForeName>Tregony</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Division of Pulmonary Medicine, Department of Pediatrics, Boston Children's Hospital and Harvard Medical School, Boston, Massachusetts, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Srouji</LastName><ForeName>Rasha</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Neurology, Boston Children's Hospital, Boston, Massachusetts, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Swami</LastName><ForeName>Sanjeev</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Pediatrics, Division of Infectious Diseases, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Torbey</LastName><ForeName>Souraya</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Kennedy Krieger Institute, Johns Hopkins School of Medicine, Baltimore, Maryland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gutierrez</LastName><ForeName>Monica Verduzco</ForeName><Initials>MV</Initials><Identifier Source="ORCID">0000-0003-0964-5908</Identifier><AffiliationInfo><Affiliation>Department of Rehabilitation Medicine, Long School of Medicine at UT Health Science Center San Antonio, San Antonio, Texas, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Williams</LastName><ForeName>Cydni Nicole</ForeName><Initials>CN</Initials><AffiliationInfo><Affiliation>Oregon Health &amp; Science University, Department of Pediatrics, Division of Pediatric Critical Care, Pediatric Critical Care and Neurotrauma Recovery Program, Portland, Oregon, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zimmerman</LastName><ForeName>Lori Allison</ForeName><Initials>LA</Initials><AffiliationInfo><Affiliation>Pediatrics, Boston Children's Hospital, Boston, Massachusetts, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Vaz</LastName><ForeName>Louise Elaine</ForeName><Initials>LE</Initials><AffiliationInfo><Affiliation>Division of Pediatric Infectious Diseases, Department of Pediatrics, Oregon Health &amp; Science University, Portland, Oregon, United States.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>K23 HL150229</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>10</Month><Day>08</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PM R</MedlineTA><NlmUniqueID>101491319</NlmUniqueID><ISSNLinking>1934-1482</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D002648" MajorTopicYN="N">Child</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000293" MajorTopicYN="N">Adolescent</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000086382" MajorTopicYN="Y">COVID-19</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D032921" MajorTopicYN="N">Consensus</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000086402" MajorTopicYN="N">SARS-CoV-2</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018450" MajorTopicYN="N">Disease Progression</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>8</Month><Day>11</Day></PubMedPubDate><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>3</Month><Day>29</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>8</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>9</Month><Day>29</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>10</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>9</Month><Day>28</Day><Hour>7</Hour><Minute>12</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36169159</ArticleId><ArticleId IdType="pmc">PMC9538628</ArticleId><ArticleId IdType="doi">10.1002/pmrj.12890</ArticleId></ArticleIdList><ReferenceList><Title>REFERENCES</Title><Reference><Citation>Ludvigsson JF. 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Principles of Inclusion and Engagement; https://www.aapmr.org/about-aapm-r/advancing-diversity-and-inclusion/principles-of-inclusion-and-engagement, Accessed 8/13/2021.</Citation></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36168997</PMID><DateRevised><Year>2022</Year><Month>09</Month><Day>28</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1467-1107</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Sep</Month><Day>28</Day></PubDate></JournalIssue><Title>Cardiology in the young</Title><ISOAbbreviation>Cardiol Young</ISOAbbreviation></Journal>Right ventricle-dependent coronary circulation diagnosed by non-invasive ferumoxytol-enhanced 4D cardiac magnetic resonance angiography in pulmonary atresia with intact ventricular septum.
Pulmonary atresia with intact ventricular septum is a complex cyanotic congenital heart lesion with the potential for myocardial ischaemia due to the presence of coronary artery anomalies. We present a case of a two-day-old baby with postnatal diagnosis of pulmonary atresia with intact ventricular septum in whom non-invasive ferumoxytol-enhanced 4D cardiac magnetic resonance angiography was used for the assessment of coronary artery anatomy.
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Massive cardiopulmonary cement embolism with cardiac perforation after vertebroplasty: a case series.
The prevalence of cement embolism after percutaneous vertebroplasty ranges from 2.1 to 26%, in literature. Even if most cases remain asymptomatic, intracardiac cement embolism becomes symptomatic in up to 8.3% of the cases.</AbstractText>We report a case series of two cases with massive cardiopulmonary cement embolism, which lead to perforation of the right ventricle and needed cardiothoracic surgery.</AbstractText>As this entity affects different fields of medical specialties and may lead to fatal outcome, we believe that the efforts of better understanding its development, avoidance, detection, and treatment need to be intensified. For this purpose, systematic and interdisciplinary studies to follow up patients after vertebroplasty are needed.</AbstractText>&#xa9; The Author(s) 2022. Published by Oxford University Press on behalf of the European Society of Cardiology.</CopyrightInformation>
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Surgical Treatment of Pineal Region Tumors: An 18&#xa0;year-Experience at a Single Institution.
The pineal tumor was once considered as a restricted area for surgery. Such cases are rare, with many different opinions on surgical treatment. This study aimed to review our experience of tumor treatment in the pineal region and explore the optimal treatment strategy.</AbstractText>The clinical data of 72 patients with pineal tumors from January 1997 to May 2015 (18&#xa0;years) were retrospectively analyzed. Preoperative preparation, pathology type, tumor resection rate, surgical approach, and follow-up outcomes were used as the indicators to evaluate the treatment efficacy.</AbstractText>The Krause approach was used in 46 cases, the Poppen approach in 10 cases, and the transcallosal-lateral ventricle-choroid fissure approach in 16 cases. The postoperative pathological results were as follows: 24 cases of germinoma, 11 of teratoma, 15 of glioma, 6 of meningioma, 11 of Pineocytoma, 2 of cholesteatoma, 2 of cavernous hemangioma, and 1 of choriocarcinoma. Further, the study included 64 cases of total surgical resections, 8 of subtotal resections, and 2 deaths. The follow-up period was from 7&#xa0;months to 10&#xa0;years. Further, 51 (70.8%) patients were followed up. The multivariate regression model showed that the surgical method and the pathological type contributed significantly to predicting outcomes.</AbstractText>The type of pathology, extent of excision, and surgical approach had a significant impact on the prognosis of patients. The transcallosal-lateral ventricle-choroid fissure approach for large and medium-sized pineal tumors near the posterior part of the third ventricle had good efficacy.</AbstractText>Copyright &#xa9; 2022. Published by Elsevier Inc.</CopyrightInformation>
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The effects of citalopram, SB-334867 and orexin-1, alone or in various combinations, on the anxiogenic-like effects of REM sleep deprivation in male mice.
Sleep deprivation may induce anxiety. On the other hand, anxiety disorders elicit main changes in the quality of sleep. Moreover, orexin and citalopram play a role in the modulation of insomnia and mood diseases. Thus, we planned preclinical research to evaluate the effect of combinations of orexin agents and citalopram on anxiety behavior in rapid eye movement (REM) sleep-deprived mice. For drug intracerebroventricular (i.c.v.) infusion, the guide cannula was surgically implanted in the left lateral ventricle of mice. REM sleep deprivation was conducted via water tank apparatus for 24&#x2009;h. The anxiety behavior of mice was evaluated using the elevated plus maze (EPM). Our results revealed that REM sleep deprivation reduced the percentage of open arm time (%OAT) and the percentage of the open arm entries (%OAE) but not closed arm entries (locomotor activity) in the EPM test, presenting an anxiogenic response ( P &#x2009;&lt;&#x2009;0.05). We found a sub-threshold dose of SB-334867, orexin-1 receptor antagonist, and orexin-1 which did not alter anxiety reaction in the REM sleep-deprived mice ( P &#x2009;&gt;&#x2009;0.05). Intraperitoneal (i.p.) injections of citalopram (5 and 10 mg/kg) increased both %OAT and %OAE ( P &#x2009;&lt;&#x2009;0.001) representing an anxiolytic effect, but not locomotor activity in the REM sleep-deprived mice. Interestingly, co-treatment of citalopram (1, 5 and 10 mg/kg; i.p.) and SB-334867 (0.1&#x2009;&#xb5;g/mouse; i.c.v.) potentiated the anxiolytic effect in the REM sleep-deprived mice. On the other hand, co-treatment of different dosages of citalopram along with a sub-threshold dose of orexin-1 did not alter %OAT, %OAE, and locomotor activity in the REM sleep-deprived mice. We found a synergistic anxiolytic effect of citalopram and SB-334867 in the REM sleep-deprived mice. These results suggested an interaction between citalopram and SB-334867 to prevent anxiogenic behavior in the REM sleep-deprived mice.
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Incidental accumulation of Technetium-99m pertechnetate in subacute cerebral infarction: A case report.
When interpreting nuclear medicine images, unexpected findings are sometimes encountered. Recognizing these findings and determining the mechanism of their occurrence could have a significant impact on early diagnosis of critical diseases and the appropriate management of patients.</AbstractText>A 59-year-old man was admitted to the emergency room due to left hemiparesis, left hemifacial palsy, and mild dysarthria. After 2 wk of hospitalization, the patient complained of dry eyes and mouth. Thus, salivary scintigraphy was performed to evaluate the functional status of his salivary glands. Incidental accumulation in the right frontoparietal area was found on salivary scintigraphy. Fluid-attenuated inversion recovery phase magnetic resonance (FLAIR phase MR) image showed diffuse high signal intensity in the same area. Anterior and posterior horns of the right lateral ventricle were obliterated and the midline was slightly shifted to the left side due to right frontoparietal swelling. On salivary scintigraphy, Tc-99m pertechnetate was incidentally accumulated in a subacute cerebral infarction lesion. Two years after the diagnosis of acute infarction, the second series of salivary scintigraphy showed no abnormal activity in the brain. FLAIR phase MR image also demonstrated markedly decreased high signal intensity in the previous infarction lesion without evidence of swelling indicating chronic cerebral infarction.</AbstractText>This case highlights that Tc-99m pertechnetate could accumulate in a subacute cerebral infarction lesion. The mechanism of an unexpected uptake of Tc-99m pertechnetate in unusual sites should be evaluated and kept in mind for better interpretation.</AbstractText>&#xa9;The Author(s) 2022. Published by Baishideng Publishing Group Inc. All rights reserved.</CopyrightInformation>
2,329,484
The neural stem cell properties of Pkd2l1<sup>+</sup> cerebrospinal fluid-contacting neurons <i>in vivo</i>.
The neural stem cells (NSCs) in the ventricular-subventricular zone of the adult mammalian spinal cord may be of great benefit for repairing spinal cord injuries. However, the sources of NSCs remain unclear. Previously, we have confirmed that cerebrospinal fluid-contacting neurons (CSF-cNs) have NSC potential <i>in vitro</i>. In this study, we verified the NSC properties of CSF-cNs <i>in vivo</i>. In mouse spinal cords, Pkd2l1<sup>+</sup> CSF-cNs localized around the central canal express NSC markers. <i>In vitro</i>, Pkd2l1<sup>+</sup> CSF-cNs form a neurosphere and express NSC markers. Activation and proliferation of CSF-cNs can be induced by injection of the neurotrophic factors basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) into the lateral ventricle. Spinal cord injury (SCI) also induces NSC activation and proliferation of CSF-cNs. Collectively, our results demonstrate that Pkd2l1<sup>+</sup> CSF-cNs have NSC properties <i>in vivo</i> and may be involved in SCI recovery.
2,329,485
Risk factors for delirium after surgery for craniocerebral injury in the neurosurgical intensive care unit.
Postoperative delirium is common in patients who undergo neurosurgery for craniocerebral injury. However, there is no specific medical test to predict postoperative delirium to date.</AbstractText>To explore risk factors for postoperative delirium in patients with craniocerebral injury in the neurosurgery intensive care unit (ICU).</AbstractText>A retrospective analysis was performed in 120 patients with craniocerebral injury admitted to Hainan People's Hospital/Hainan Hospital Affiliated to Hainan Medical University, The First Affiliated Hospital of Hainan Medical University, and The Second Affiliated Hospital of Hainan Medical University between January 2018 and January 2020. The patients were categorized into groups based on whether delirium occurred. Of them, 25 patients with delirium were included in the delirium group, and 95 patients without delirium were included in the observation group. Logistic regression analysis was used to explore the association between sex, age, educational level, Glasgow coma scale (GCS), complications (with or without concussion, cerebral contusion, hypoxemia and ventricular compression) and site of injury and delirium.</AbstractText>The GCS score above 8 and concomitant disease of cerebral concussion, cerebral contusion, hypoxemia and ventricular compression, and damage to the frontal lobe were associated with delirium in patients admitted to neurosurgical intensive care unit (ICU) (all P</i> &lt; 0.05). However, age, sex, administration more than three medicines, and educational level were not significantly associated with the onset of delirium in patients with craniocerebral injury in the neurosurgical ICU (P</i> &lt; 0.05). Multivariate logistic regression analysis showed that GCS score above 8, cerebral concussion, cerebral contusion, hypoxemia, ventricle compression, and frontal lobe disorders were independent risk factors for delirium in patients with craniocerebral injury in the neurosurgical ICU (P</i> &lt; 0.05).</AbstractText>GCS score, concussive concussion, cerebral contusion, hypoxemia, ventricle compression, and damage to frontal lobe are risk factors of postoperative delirium.</AbstractText>&#xa9;The Author(s) 2022. Published by Baishideng Publishing Group Inc. All rights reserved.</CopyrightInformation>
2,329,486
High-Grade Supratentorial Intraventricular Tumours in Adults.
High-grade Intraventricular tumours are rarely encountered. Many of these tumours will have similar patterns on imaging of signal intensity and contrast enhancement. As IVT are regularly not targetable by radiation or systemic therapy, until now, surgical resection presents the treatment of choice.
2,329,487
An Alzheimer's Disease Mechanism Based on Early Pathology, Anatomy, Vascular-Induced Flow, and Migration of Maximum Flow Stress Energy Location with Increasing Vascular Disease.
This paper suggests a chemical mechanism for the earliest stages of Alzheimer's disease (AD). Cerebrospinal fluid (CSF) flow stresses provide the energy needed to induce molecular conformation changes leading to AD by initiating amyloid-&#x3b2; (A&#x3b2;) and tau aggregation. Shear and extensional flow stresses initiate aggregation in the laboratory and in natural biophysical processes. Energy-rich CSF flow regions are mainly found in lower brain regions. MRI studies reveal flow stress "hot spots" in basal cisterns and brain ventricles that have chaotic flow properties that can distort molecules such as A&#x3b2; and tau trapped in these regions into unusual conformations. Such fluid disturbance is surrounded by tissue deformation. There is strong mapping overlap between the locations of these hot spots and of early-stage AD pathology. Our mechanism creates pure and mixed protein dimers, followed by tissue surface adsorption, and long-term tissue agitation ultimately inducing chemical reactions forming more stable, toxic oligomer seeds that initiate AD. It is proposed that different flow stress energies and flow types in different basal brain regions produce different neurotoxic aggregates. Proliferating artery hardening is responsible for enhanced heart systolic pulses that drive energetic CSF pulses, whose critical maximum systolic pulse energy location migrates further from the heart with increasing vascular disease. Two glymphatic systems, carotid and basilar, are suggested to contain the earliest A&#x3b2; and tau AD disease pathologies. A key to the proposed AD mechanism is a comparison of early chronic traumatic encephalopathy and AD pathologies. Experiments that test the proposed mechanism are needed.
2,329,488
NO<sub>2</sub> exposure contributes to cardiac hypertrophy in male mice through apoptosis signaling pathways.<Pagination><StartPage>136576</StartPage><MedlinePgn>136576</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.chemosphere.2022.136576</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0045-6535(22)03069-7</ELocationID><Abstract><AbstractText>Nitrogen dioxide (NO<sub>2</sub>) is one of the most common indoor and outdoor air pollutants. Inhalation of NO<sub>2</sub> is associated with an increased risk of health problems, especially cardiovascular diseases. However, the underlying pathogenic mechanisms still remain unclear. In this study, we exposed C57BL/6J mice to NO<sub>2</sub> (2.5&#xa0;ppm, 5&#xa0;h/d) for 28 days and found that NO<sub>2</sub> inhalation induced cardiac dysfunction in male mice, but not in female mice, including left ventricular dilation and cardiac systolic dysfunction. Pathological staining showed that NO<sub>2</sub> inhalation induced eccentric hypertrophy with enlarged individual cardiomyocytes, dilated left ventricle, and thinning of the left ventricular wall in male mice. The transcriptional analysis suggested that NO<sub>2</sub> exposure could disrupt Ca<sup>2+</sup> homeostasis, actin cytoskeletal reorganization, myocardial contractility, and vascular dilation in male mice. The Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis indicated that differentially expressed genes (DEGs) were closely associated with the apoptotic signaling pathways. These findings suggested that NO<sub>2</sub> exposure caused cardiac eccentric hypertrophy and cardiac dysfunction through apoptotic signaling pathways, and contributed to cardiotoxicity.</AbstractText><CopyrightInformation>Copyright &#xa9; 2022 Elsevier Ltd. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ji</LastName><ForeName>Shaoyang</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>College of Environment and Resource, Research Center of Environment and Health, Shanxi University, Taiyuan, Shanxi, 030006, PR China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Guo</LastName><ForeName>Yuqiong</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>College of Environment and Resource, Research Center of Environment and Health, Shanxi University, Taiyuan, Shanxi, 030006, PR China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Guangke</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>College of Environment and Resource, Research Center of Environment and Health, Shanxi University, Taiyuan, Shanxi, 030006, PR China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sang</LastName><ForeName>Nan</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>College of Environment and Resource, Research Center of Environment and Health, Shanxi University, Taiyuan, Shanxi, 030006, PR China. Electronic address: sangnan@sxu.edu.cn.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>09</Month><Day>22</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Chemosphere</MedlineTA><NlmUniqueID>0320657</NlmUniqueID><ISSNLinking>0045-6535</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>S7G510RUBH</RegistryNumber><NameOfSubstance UI="D009585">Nitrogen Dioxide</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000199">Actins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000393">Air Pollutants</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009585" MajorTopicYN="N">Nitrogen Dioxide</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000199" MajorTopicYN="N">Actins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006332" MajorTopicYN="N">Cardiomegaly</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000393" MajorTopicYN="Y">Air Pollutants</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006331" MajorTopicYN="Y">Heart Diseases</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Air NO(2) exposure</Keyword><Keyword MajorTopicYN="N">Apoptotic signaling pathways</Keyword><Keyword MajorTopicYN="N">Cardiac hypertrophy</Keyword><Keyword MajorTopicYN="N">Cardiotoxicity</Keyword><Keyword MajorTopicYN="N">Eccentric hypertrophy</Keyword><Keyword MajorTopicYN="N">Structural and functional abnormality</Keyword></KeywordList><CoiStatement>Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>6</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>9</Month><Day>6</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>9</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>9</Month><Day>27</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>10</Month><Day>27</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>9</Month><Day>26</Day><Hour>15</Hour><Minute>14</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36155018</ArticleId><ArticleId IdType="doi">10.1016/j.chemosphere.2022.136576</ArticleId><ArticleId IdType="pii">S0045-6535(22)03069-7</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36154555</PMID><DateRevised><Year>2022</Year><Month>09</Month><Day>26</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1532-2378</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Sep</Month><Day>26</Day></PubDate></JournalIssue><Title>Animal biotechnology</Title><ISOAbbreviation>Anim Biotechnol</ISOAbbreviation></Journal>In ovo feeding of creatine monohydrate increases performances of hatching and development in breeder chicks.
Nitrogen dioxide (NO<sub>2</sub>) is one of the most common indoor and outdoor air pollutants. Inhalation of NO<sub>2</sub> is associated with an increased risk of health problems, especially cardiovascular diseases. However, the underlying pathogenic mechanisms still remain unclear. In this study, we exposed C57BL/6J mice to NO<sub>2</sub> (2.5&#xa0;ppm, 5&#xa0;h/d) for 28 days and found that NO<sub>2</sub> inhalation induced cardiac dysfunction in male mice, but not in female mice, including left ventricular dilation and cardiac systolic dysfunction. Pathological staining showed that NO<sub>2</sub> inhalation induced eccentric hypertrophy with enlarged individual cardiomyocytes, dilated left ventricle, and thinning of the left ventricular wall in male mice. The transcriptional analysis suggested that NO<sub>2</sub> exposure could disrupt Ca<sup>2+</sup> homeostasis, actin cytoskeletal reorganization, myocardial contractility, and vascular dilation in male mice. The Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis indicated that differentially expressed genes (DEGs) were closely associated with the apoptotic signaling pathways. These findings suggested that NO<sub>2</sub> exposure caused cardiac eccentric hypertrophy and cardiac dysfunction through apoptotic signaling pathways, and contributed to cardiotoxicity.<CopyrightInformation>Copyright &#xa9; 2022 Elsevier Ltd. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ji</LastName><ForeName>Shaoyang</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>College of Environment and Resource, Research Center of Environment and Health, Shanxi University, Taiyuan, Shanxi, 030006, PR China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Guo</LastName><ForeName>Yuqiong</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>College of Environment and Resource, Research Center of Environment and Health, Shanxi University, Taiyuan, Shanxi, 030006, PR China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Guangke</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>College of Environment and Resource, Research Center of Environment and Health, Shanxi University, Taiyuan, Shanxi, 030006, PR China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sang</LastName><ForeName>Nan</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>College of Environment and Resource, Research Center of Environment and Health, Shanxi University, Taiyuan, Shanxi, 030006, PR China. Electronic address: sangnan@sxu.edu.cn.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>09</Month><Day>22</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Chemosphere</MedlineTA><NlmUniqueID>0320657</NlmUniqueID><ISSNLinking>0045-6535</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>S7G510RUBH</RegistryNumber><NameOfSubstance UI="D009585">Nitrogen Dioxide</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000199">Actins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000393">Air Pollutants</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009585" MajorTopicYN="N">Nitrogen Dioxide</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000199" MajorTopicYN="N">Actins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006332" MajorTopicYN="N">Cardiomegaly</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000393" MajorTopicYN="Y">Air Pollutants</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006331" MajorTopicYN="Y">Heart Diseases</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Air NO(2) exposure</Keyword><Keyword MajorTopicYN="N">Apoptotic signaling pathways</Keyword><Keyword MajorTopicYN="N">Cardiac hypertrophy</Keyword><Keyword MajorTopicYN="N">Cardiotoxicity</Keyword><Keyword MajorTopicYN="N">Eccentric hypertrophy</Keyword><Keyword MajorTopicYN="N">Structural and functional abnormality</Keyword></KeywordList><CoiStatement>Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>6</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>9</Month><Day>6</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>9</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>9</Month><Day>27</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>10</Month><Day>27</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>9</Month><Day>26</Day><Hour>15</Hour><Minute>14</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36155018</ArticleId><ArticleId IdType="doi">10.1016/j.chemosphere.2022.136576</ArticleId><ArticleId IdType="pii">S0045-6535(22)03069-7</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36154555</PMID><DateRevised><Year>2022</Year><Month>09</Month><Day>26</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1532-2378</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Sep</Month><Day>26</Day></PubDate></JournalIssue><Title>Animal biotechnology</Title><ISOAbbreviation>Anim Biotechnol</ISOAbbreviation></Journal><ArticleTitle>In ovo feeding of creatine monohydrate increases performances of hatching and development in breeder chicks.</ArticleTitle><Pagination><StartPage>1</StartPage><EndPage>11</EndPage><MedlinePgn>1-11</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1080/10495398.2022.2126368</ELocationID><Abstract>The current investigation was conducted to test the potential effects of in ovo feeding of creatine monohydrate (CMH) on hatchability, embryonic mortality, hatching weight, and development of heart and gastrointestinal tract (main organs and regions) of breeder chick embryos. Rhode Island Red fertile eggs were randomly distributed into seven experimental treatments: untreated egg (control), a sterile buffered solution (0.50% NaCl), and five solutions containing increased levels of CMH (0.50, 1.00, 1.50, and 2.00%) + 0.50% NaCl, being separated in four groups/replicates (three with 15 eggs and one with 16 eggs), totaling 61 eggs/treatment and a total of 427 fertile eggs used. All-in ovo injected groups with CMH decreased the hatchability and increased the intermediary embryonic mortality. At hatching, all-in ovo injected groups with CMH also increased the hatching weight and stimulated the development of the heart and the total length of the gastrointestinal tract, especially important organs for digestion of nutrients (yolk sac, pro-ventricle and gizzard) and regions for nutrient absorption (jejunum&#x2009;+&#x2009;ileum and colon&#x2009;+&#x2009;rectum). Conclusively, the in ovo feeding using CMH showed positive impacts on hatching weight and the development of gastrointestinal tract of chicks. However, caused negative impacts on hatchability.
2,329,489
Heterogeneity in the size of the apical surface of cortical progenitors.<Pagination><StartPage>363</StartPage><EndPage>376</EndPage><MedlinePgn>363-376</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/dvdy.539</ELocationID><Abstract><AbstractText Label="BACKGROUND">The apical surface (AS) of epithelial cells is highly specialized; it is important for morphogenetic processes that are essential to shape organs and tissues and it plays a role in morphogen and growth factor signaling. Apical progenitors in the mammalian neocortex are pseudoepithelial cells whose apical surface lines the ventricle. Whether changes in their apical surface sizes are important for cortical morphogenesis and/or other aspects of neocortex development has not been thoroughly addressed.</AbstractText><AbstractText Label="RESULTS">Here we show that apical progenitors are heterogeneous with respect to their apical surface area. In Efnb1 mutants, the size of the apical surface is modified and this correlates with discrete alterations of tissue organization without impacting apical progenitors proliferation.</AbstractText><AbstractText Label="CONCLUSIONS">Altogether, our data reveal heterogeneity in apical progenitors AS area in the developing neocortex and shows a role for Ephrin B1 in controlling AS size. Our study also indicates that changes in AS size do not have strong repercussion on apical progenitor behavior.</AbstractText><CopyrightInformation>&#xa9; 2022 The Authors. Developmental Dynamics published by Wiley Periodicals LLC on behalf of American Association for Anatomy.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Badouel</LastName><ForeName>Caroline</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Molecular, Cellular and Developmental Biology Unit (MCD), Centre de Biologie Int&#xe9;grative (CBI), CNRS, UPS, Universit&#xe9; de Toulouse, Toulouse, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Audouard</LastName><ForeName>Christophe</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Molecular, Cellular and Developmental Biology Unit (MCD), Centre de Biologie Int&#xe9;grative (CBI), CNRS, UPS, Universit&#xe9; de Toulouse, Toulouse, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Davy</LastName><ForeName>Alice</ForeName><Initials>A</Initials><Identifier Source="ORCID">0000-0003-2134-4526</Identifier><AffiliationInfo><Affiliation>Molecular, Cellular and Developmental Biology Unit (MCD), Centre de Biologie Int&#xe9;grative (CBI), CNRS, UPS, Universit&#xe9; de Toulouse, Toulouse, France.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>10</Month><Day>07</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Dev Dyn</MedlineTA><NlmUniqueID>9201927</NlmUniqueID><ISSNLinking>1058-8388</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D036387">Ephrin-B1</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009474" MajorTopicYN="Y">Neurons</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019579" MajorTopicYN="Y">Neocortex</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D036387" MajorTopicYN="N">Ephrin-B1</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008322" MajorTopicYN="N">Mammals</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">ephrin</Keyword><Keyword MajorTopicYN="N">morphogenesis</Keyword><Keyword MajorTopicYN="N">mouse</Keyword><Keyword MajorTopicYN="N">neural progenitors</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>9</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>4</Month><Day>7</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>9</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>9</Month><Day>26</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2023</Year><Month>3</Month><Day>8</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>9</Month><Day>25</Day><Hour>13</Hour><Minute>56</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36153792</ArticleId><ArticleId IdType="doi">10.1002/dvdy.539</ArticleId></ArticleIdList><ReferenceList><Title>REFERENCES</Title><Reference><Citation>Tyler S. 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PLoS Biol. 2020;18(1):e3000581. doi:10.1371/journal.pbio.3000581</Citation></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36153781</PMID><DateRevised><Year>2022</Year><Month>09</Month><Day>25</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1876-7931</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Sep</Month><Day>25</Day></PubDate></JournalIssue><Title>Journal of ultrasound</Title><ISOAbbreviation>J Ultrasound</ISOAbbreviation></Journal>Effect of prone position on right ventricular dysfunction due to pulmonary embolism assessed by speckle tracking echocardiography.
Prone position has shown beneficial hemodynamic effects in patients with right ventricular dysfunction associated with acute respiratory distress syndrome decreasing the right ventricle afterload. We describe the case of a 57-year-old man with right ventricular dysfunction associated with pulmonary thromboembolism with severe hypoxemia that required mechanical ventilation in prone position. With this maneuver, we verified an improvement not only in his oxygenation, but also in his right ventricular function assessed with speckle tracking echocardiography. Our case shows the potential beneficial effect of the prone position maneuver in severely hypoxemic patients with right ventricular dysfunction associated with pulmonary thromboembolism.
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Long-term outcomes of elderly patients receiving continuous flow left ventricular support.<Pagination><StartPage>5685</StartPage><MedlinePgn>5685</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1111/jocs.16973</ELocationID><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Vasavada</LastName><ForeName>Advait</ForeName><Initials>A</Initials><Identifier Source="ORCID">0000-0002-7756-6606</Identifier><AffiliationInfo><Affiliation>M. P. Shah Medical College, Jamnagar, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Llerena-Velastegui</LastName><ForeName>Jordan</ForeName><Initials>J</Initials><Identifier Source="ORCID">0000-0002-3876-1150</Identifier><AffiliationInfo><Affiliation>Pontifical Catholic University of Ecuador, Quito, Ecuador.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Velastegui-Zurita</LastName><ForeName>Sebastian</ForeName><Initials>S</Initials><Identifier Source="ORCID">0000-0002-1310-2802</Identifier><AffiliationInfo><Affiliation>Pontifical Catholic University of Ecuador, Quito, Ecuador.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016422">Letter</PublicationType><PublicationType UI="D016420">Comment</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>09</Month><Day>24</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Card Surg</MedlineTA><NlmUniqueID>8908809</NlmUniqueID><ISSNLinking>0886-0440</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="CommentOn"><RefSource>J Card Surg. 2020 Dec;35(12):3405-3408</RefSource><PMID Version="1">33001467</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006333" MajorTopicYN="Y">Heart Failure</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016027" MajorTopicYN="Y">Heart Transplantation</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>9</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>9</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>9</Month><Day>26</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2023</Year><Month>1</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>9</Month><Day>25</Day><Hour>2</Hour><Minute>22</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36153654</ArticleId><ArticleId IdType="doi">10.1111/jocs.16973</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedBookArticle><BookDocument><PMID Version="1">33085446</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK563299</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-42827">Bidirectional Glenn Procedure or Hemi-Fontan<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Salik</LastName><ForeName>Irim</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Westchester MC/New York Med. College</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mehta</LastName><ForeName>Bhupen</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Westchester Medical Center</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ambati</LastName><ForeName>Shashikanth</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Albany Medical Center</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>The bidirectional Glenn (BDG) and hemi-Fontan are surgical techniques used to create superior cavopulmonary anastomosis, the second stage repair in Fontan completion. They are performed in patients with an anatomic or functional single ventricle. Whether it is right or left, the single ventricle must therefore provide blood supply to the higher resistance systemic circulation and the lower resistance pulmonary circulation until surgical correction is undertaken. The BDG procedure or hemi-Fontan helps to eliminate volume load on the single ventricle and simplify the operative procedure at Fontan. Several centers have reported decreased mortality and morbidity of the Fontan procedure in those who have undergone BDG procedure or hemi-Fontan. All the patients with a single ventricle must eventually undergo a Fontan procedure to achieve separation of their systemic and pulmonary circulations. A patient with a completed Fontan procedure has systemic venous return diverted to the pulmonary circulation, driven by central venous pressure and affected by intrathoracic pressure changes and systemic ventricular relaxation. As of 2018, there are an estimated 50,000 to 70,000 patients with a Fontan circulation, with 40% of these patients older than 18.&#xa0;About 1000 Fontan procedures are performed annually in the United States.</AbstractText><CopyrightInformation>Copyright &#xa9; 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-42827" sec="article-42827.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42827" sec="article-42827.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42827" sec="article-42827.s3">Anatomy and Physiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42827" sec="article-42827.s4">Indications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42827" sec="article-42827.s5">Contraindications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42827" sec="article-42827.s6">Equipment</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42827" sec="article-42827.s7">Personnel</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42827" sec="article-42827.s8">Preparation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42827" sec="article-42827.s9">Technique or Treatment</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42827" sec="article-42827.s10">Complications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42827" sec="article-42827.s11">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42827" sec="article-42827.s12">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42827" sec="article-42827.s13">Nursing, Allied Health, and Interprofessional Team Interventions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42827" sec="article-42827.s14">Nursing, Allied Health, and Interprofessional Team Monitoring</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42827" sec="article-42827.s15">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42827" sec="article-42827.s17">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>9</Month><Day>26</Day></ContributionDate><ReferenceList><Reference><Citation>Rychik J, Atz AM, Celermajer DS, Deal BJ, Gatzoulis MA, Gewillig MH, Hsia TY, Hsu DT, Kovacs AH, McCrindle BW, Newburger JW, Pike NA, Rodefeld M, Rosenthal DN, Schumacher KR, Marino BS, Stout K, Veldtman G, Younoszai AK, d'Udekem Y, American Heart Association Council on Cardiovascular Disease in the Young and Council on Cardiovascular and Stroke Nursing Evaluation and Management of the Child and Adult With Fontan Circulation: A Scientific Statement From the American Heart Association. 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J Thorac Cardiovasc Surg. 2011 Sep;142(3):511-6.</Citation><ArticleIdList><ArticleId IdType="pubmed">21704339</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">33085446</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">32644426</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK559000</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-19038">Cavum Veli Interpositi<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>De Leucio</LastName><ForeName>Alessandro</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Hopital universitaire des enfants Reine Fabiola</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dossani</LastName><ForeName>Rimal H.</ForeName><Initials>RH</Initials><AffiliationInfo><Affiliation>Louisiana State Un Health Sciences Cr</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>The velum interpositum (VI) is a membrane resulting from the superposition of two layers of the tela choroidea of the third ventricle demarcating a potential space containing cerebrospinal fluid (CSF) located in the region between the internal cerebral veins (ICV) and the posterior medial choroidal artery. Kruse, in 1930 defined the dilatation of this space as &#x201c;cavum veli interpositi&#x201d; (CVI). Other names frequently used to describe this structure are &#x201c;ventriculi tertii, &#x201c;cisterna interventricularis,&#x201d; &#x201c;transverse fissure,&#x201d; and &#x201c;sub-trigonal fissure.&#x201d; CVI has a triangular shape with the wide base dorsally and the apex pointing anteriorly, reaching as far forward as the foramen of Monroe. <b>Boundaries: </b> Superiorly: the&#xa0;fornix&#xa0;and&#xa0;the hippocampal commissure, Inferiorly: the tela choroidea of the third ventricle and the&#xa0;internal cerebral veins, Laterally: the thalami, Anteriorly: &#xa0;the roof of the third ventricle and the interventricular foramina; Posteriorly: the splenium of the&#xa0;corpus callosum and the habenular commissure.</AbstractText><CopyrightInformation>Copyright &#xa9; 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-19038" sec="article-19038.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19038" sec="article-19038.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19038" sec="article-19038.s3">Etiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19038" sec="article-19038.s4">Epidemiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19038" sec="article-19038.s5">Pathophysiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19038" sec="article-19038.s6">Histopathology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19038" sec="article-19038.s7">History and Physical</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19038" sec="article-19038.s8">Evaluation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19038" sec="article-19038.s9">Treatment / Management</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19038" sec="article-19038.s10">Differential Diagnosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19038" sec="article-19038.s11">Prognosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19038" sec="article-19038.s12">Complications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19038" sec="article-19038.s13">Deterrence and Patient Education</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19038" sec="article-19038.s14">Pearls and Other Issues</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19038" sec="article-19038.s15">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19038" sec="article-19038.s16">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19038" sec="article-19038.s22">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>9</Month><Day>26</Day></ContributionDate><ReferenceList><Reference><Citation>Macpherson P, Teasdale E. 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Clin Neurol Neurosurg. 2019 Oct;185:105494.</Citation><ArticleIdList><ArticleId IdType="pubmed">31472394</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32644426</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">32644376</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK558950</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-30596">Fontan Completion<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Madonna</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Seattle Children&#x2019;s</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shahjehan</LastName><ForeName>Rai Dilawar</ForeName><Initials>RD</Initials><AffiliationInfo><Affiliation>Conemaugh Memorial Medical Center</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>The Fontan procedure provides a palliative treatment option for pediatric patients with functionally single ventricle congenital heart disease, with an estimated incidence of 0.08 to 0.4 per 1,000 live births. Total right heart bypass was described in 1971&#xa0;for tricuspid atresia with the Fontan procedure, or the total cavopulmonary connection (TCPC) procedure. There is a relatively recent history of staged procedures created to achieve this result established on the premise that systemic venous return can be surgically connected directly to the pulmonary circulation, as long as the pulmonary pressures are low. This will effectively allow the systemic venous circulation to bypass the heart.&#xa0; Patients need to be carefully selected to ensure optimal surgical outcomes. Surgical modifications ushered in different eras, and overall, patients are living longer with better outcomes.&#xa0;Morbidity still remains high with multiple extracardiac manifestations of Fontan circulation after the completion of the procedure.&#xa0;Efforts are ongoing to improve understanding of long-term Fontan patients, functional status, and possible innovations in tackling disparities&#xa0;and improving long-term outcomes.</AbstractText><CopyrightInformation>Copyright &#xa9; 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-30596" sec="article-30596.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30596" sec="article-30596.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30596" sec="article-30596.s3">Anatomy and Physiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30596" sec="article-30596.s4">Indications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30596" sec="article-30596.s5">Contraindications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30596" sec="article-30596.s6">Equipment</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30596" sec="article-30596.s7">Personnel</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30596" sec="article-30596.s8">Preparation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30596" sec="article-30596.s9">Technique or Treatment</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30596" sec="article-30596.s10">Complications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30596" sec="article-30596.s11">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30596" sec="article-30596.s12">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30596" sec="article-30596.s13">Nursing, Allied Health, and Interprofessional Team Interventions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30596" sec="article-30596.s14">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30596" sec="article-30596.s15">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>9</Month><Day>26</Day></ContributionDate><ReferenceList><Reference><Citation>van der Ven JPG, van den Bosch E, Bogers AJCC, Helbing WA. 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J Am Coll Cardiol. 2017 Jun 06;69(22):2745-2747.</Citation><ArticleIdList><ArticleId IdType="pubmed">28571640</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32644376</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">30725892</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK537207</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-18886">Cardiac Dominance
The bidirectional Glenn (BDG) and hemi-Fontan are surgical techniques used to create superior cavopulmonary anastomosis, the second stage repair in Fontan completion. They are performed in patients with an anatomic or functional single ventricle. Whether it is right or left, the single ventricle must therefore provide blood supply to the higher resistance systemic circulation and the lower resistance pulmonary circulation until surgical correction is undertaken. The BDG procedure or hemi-Fontan helps to eliminate volume load on the single ventricle and simplify the operative procedure at Fontan. Several centers have reported decreased mortality and morbidity of the Fontan procedure in those who have undergone BDG procedure or hemi-Fontan. All the patients with a single ventricle must eventually undergo a Fontan procedure to achieve separation of their systemic and pulmonary circulations. A patient with a completed Fontan procedure has systemic venous return diverted to the pulmonary circulation, driven by central venous pressure and affected by intrathoracic pressure changes and systemic ventricular relaxation. As of 2018, there are an estimated 50,000 to 70,000 patients with a Fontan circulation, with 40% of these patients older than 18.&#xa0;About 1000 Fontan procedures are performed annually in the United States.<CopyrightInformation>Copyright &#xa9; 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-42827" sec="article-42827.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42827" sec="article-42827.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42827" sec="article-42827.s3">Anatomy and Physiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42827" sec="article-42827.s4">Indications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42827" sec="article-42827.s5">Contraindications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42827" sec="article-42827.s6">Equipment</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42827" sec="article-42827.s7">Personnel</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42827" sec="article-42827.s8">Preparation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42827" sec="article-42827.s9">Technique or Treatment</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42827" sec="article-42827.s10">Complications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42827" sec="article-42827.s11">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42827" sec="article-42827.s12">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42827" sec="article-42827.s13">Nursing, Allied Health, and Interprofessional Team Interventions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42827" sec="article-42827.s14">Nursing, Allied Health, and Interprofessional Team Monitoring</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42827" sec="article-42827.s15">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42827" sec="article-42827.s17">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>9</Month><Day>26</Day></ContributionDate><ReferenceList><Reference><Citation>Rychik J, Atz AM, Celermajer DS, Deal BJ, Gatzoulis MA, Gewillig MH, Hsia TY, Hsu DT, Kovacs AH, McCrindle BW, Newburger JW, Pike NA, Rodefeld M, Rosenthal DN, Schumacher KR, Marino BS, Stout K, Veldtman G, Younoszai AK, d'Udekem Y, American Heart Association Council on Cardiovascular Disease in the Young and Council on Cardiovascular and Stroke Nursing Evaluation and Management of the Child and Adult With Fontan Circulation: A Scientific Statement From the American Heart Association. 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J Thorac Cardiovasc Surg. 2011 Sep;142(3):511-6.</Citation><ArticleIdList><ArticleId IdType="pubmed">21704339</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">33085446</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">32644426</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK559000</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-19038">Cavum Veli Interpositi</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>De Leucio</LastName><ForeName>Alessandro</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Hopital universitaire des enfants Reine Fabiola</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dossani</LastName><ForeName>Rimal H.</ForeName><Initials>RH</Initials><AffiliationInfo><Affiliation>Louisiana State Un Health Sciences Cr</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>The velum interpositum (VI) is a membrane resulting from the superposition of two layers of the tela choroidea of the third ventricle demarcating a potential space containing cerebrospinal fluid (CSF) located in the region between the internal cerebral veins (ICV) and the posterior medial choroidal artery. Kruse, in 1930 defined the dilatation of this space as &#x201c;cavum veli interpositi&#x201d; (CVI). Other names frequently used to describe this structure are &#x201c;ventriculi tertii, &#x201c;cisterna interventricularis,&#x201d; &#x201c;transverse fissure,&#x201d; and &#x201c;sub-trigonal fissure.&#x201d; CVI has a triangular shape with the wide base dorsally and the apex pointing anteriorly, reaching as far forward as the foramen of Monroe. <b>Boundaries: </b> Superiorly: the&#xa0;fornix&#xa0;and&#xa0;the hippocampal commissure, Inferiorly: the tela choroidea of the third ventricle and the&#xa0;internal cerebral veins, Laterally: the thalami, Anteriorly: &#xa0;the roof of the third ventricle and the interventricular foramina; Posteriorly: the splenium of the&#xa0;corpus callosum and the habenular commissure.<CopyrightInformation>Copyright &#xa9; 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-19038" sec="article-19038.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19038" sec="article-19038.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19038" sec="article-19038.s3">Etiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19038" sec="article-19038.s4">Epidemiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19038" sec="article-19038.s5">Pathophysiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19038" sec="article-19038.s6">Histopathology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19038" sec="article-19038.s7">History and Physical</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19038" sec="article-19038.s8">Evaluation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19038" sec="article-19038.s9">Treatment / Management</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19038" sec="article-19038.s10">Differential Diagnosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19038" sec="article-19038.s11">Prognosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19038" sec="article-19038.s12">Complications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19038" sec="article-19038.s13">Deterrence and Patient Education</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19038" sec="article-19038.s14">Pearls and Other Issues</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19038" sec="article-19038.s15">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19038" sec="article-19038.s16">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19038" sec="article-19038.s22">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>9</Month><Day>26</Day></ContributionDate><ReferenceList><Reference><Citation>Macpherson P, Teasdale E. 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Clin Neurol Neurosurg. 2019 Oct;185:105494.</Citation><ArticleIdList><ArticleId IdType="pubmed">31472394</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32644426</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">32644376</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK558950</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-30596">Fontan Completion</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Madonna</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Seattle Children&#x2019;s</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shahjehan</LastName><ForeName>Rai Dilawar</ForeName><Initials>RD</Initials><AffiliationInfo><Affiliation>Conemaugh Memorial Medical Center</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>The Fontan procedure provides a palliative treatment option for pediatric patients with functionally single ventricle congenital heart disease, with an estimated incidence of 0.08 to 0.4 per 1,000 live births. Total right heart bypass was described in 1971&#xa0;for tricuspid atresia with the Fontan procedure, or the total cavopulmonary connection (TCPC) procedure. There is a relatively recent history of staged procedures created to achieve this result established on the premise that systemic venous return can be surgically connected directly to the pulmonary circulation, as long as the pulmonary pressures are low. This will effectively allow the systemic venous circulation to bypass the heart.&#xa0; Patients need to be carefully selected to ensure optimal surgical outcomes. Surgical modifications ushered in different eras, and overall, patients are living longer with better outcomes.&#xa0;Morbidity still remains high with multiple extracardiac manifestations of Fontan circulation after the completion of the procedure.&#xa0;Efforts are ongoing to improve understanding of long-term Fontan patients, functional status, and possible innovations in tackling disparities&#xa0;and improving long-term outcomes.<CopyrightInformation>Copyright &#xa9; 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-30596" sec="article-30596.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30596" sec="article-30596.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30596" sec="article-30596.s3">Anatomy and Physiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30596" sec="article-30596.s4">Indications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30596" sec="article-30596.s5">Contraindications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30596" sec="article-30596.s6">Equipment</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30596" sec="article-30596.s7">Personnel</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30596" sec="article-30596.s8">Preparation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30596" sec="article-30596.s9">Technique or Treatment</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30596" sec="article-30596.s10">Complications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30596" sec="article-30596.s11">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30596" sec="article-30596.s12">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30596" sec="article-30596.s13">Nursing, Allied Health, and Interprofessional Team Interventions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30596" sec="article-30596.s14">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30596" sec="article-30596.s15">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>9</Month><Day>26</Day></ContributionDate><ReferenceList><Reference><Citation>van der Ven JPG, van den Bosch E, Bogers AJCC, Helbing WA. 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A Pilot Study of Inspiratory Muscle Training to Improve Exercise Capacity in Patients with Fontan Physiology. 2018 WinterSemin Thorac Cardiovasc Surg. 30(4):462-469.</Citation><ArticleIdList><ArticleId IdType="pubmed">30063966</ArticleId></ArticleIdList></Reference><Reference><Citation>Goldberg DJ, Shaddy RE, Ravishankar C, Rychik J. The failing Fontan: etiology, diagnosis and management. Expert Rev Cardiovasc Ther. 2011 Jun;9(6):785-93.</Citation><ArticleIdList><ArticleId IdType="pubmed">21714609</ArticleId></ArticleIdList></Reference><Reference><Citation>Gewillig M, Brown SC. The Fontan circulation after 45&#x2005;years: update in physiology. Heart. 2016 Jul 15;102(14):1081-6.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC4941188</ArticleId><ArticleId IdType="pubmed">27220691</ArticleId></ArticleIdList></Reference><Reference><Citation>Attard C, Huang J, Monagle P, Ignjatovic V. Pathophysiology of thrombosis and anticoagulation post Fontan surgery. 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Extracardiac conduit Fontan procedure without cardiopulmonary bypass. Ann Thorac Surg. 1998 Nov;66(5):1826-8.</Citation><ArticleIdList><ArticleId IdType="pubmed">9875809</ArticleId></ArticleIdList></Reference><Reference><Citation>Petrossian E, Reddy VM, McElhinney DB, Akkersdijk GP, Moore P, Parry AJ, Thompson LD, Hanley FL. Early results of the extracardiac conduit Fontan operation. J Thorac Cardiovasc Surg. 1999 Apr;117(4):688-96.</Citation><ArticleIdList><ArticleId IdType="pubmed">10096963</ArticleId></ArticleIdList></Reference><Reference><Citation>Jacobs JP, Mayer JE, Mavroudis C, O'Brien SM, Austin EH, Pasquali SK, Hill KD, Overman DM, St Louis JD, Karamlou T, Pizarro C, Hirsch-Romano JC, McDonald D, Han JM, Becker S, Tchervenkov CI, Lacour-Gayet F, Backer CL, Fraser CD, Tweddell JS, Elliott MJ, Walters H, Jonas RA, Prager RL, Shahian DM, Jacobs ML. The Society of Thoracic Surgeons Congenital Heart Surgery Database: 2017 Update on Outcomes and Quality. Ann Thorac Surg. 2017 Mar;103(3):699-709.</Citation><ArticleIdList><ArticleId IdType="pubmed">28219544</ArticleId></ArticleIdList></Reference><Reference><Citation>d'Udekem Y, Xu MY, Galati JC, Lu S, Iyengar AJ, Konstantinov IE, Wheaton GR, Ramsay JM, Grigg LE, Millar J, Cheung MM, Brizard CP. Predictors of survival after single-ventricle palliation: the impact of right ventricular dominance. J Am Coll Cardiol. 2012 Mar 27;59(13):1178-85.</Citation><ArticleIdList><ArticleId IdType="pubmed">22440217</ArticleId></ArticleIdList></Reference><Reference><Citation>Kotani Y, Chetan D, Zhu J, Saedi A, Zhao L, Mertens L, Redington AN, Coles J, Caldarone CA, Van Arsdell GS, Honjo O. Fontan Failure and Death in Contemporary Fontan Circulation: Analysis From the Last Two Decades. Ann Thorac Surg. 2018 Apr;105(4):1240-1247.</Citation><ArticleIdList><ArticleId IdType="pubmed">29397930</ArticleId></ArticleIdList></Reference><Reference><Citation>Menon S, Chennapragada M, Ugaki S, Sholler GF, Ayer J, Winlaw DS. The Lymphatic Circulation in Adaptations to the Fontan Circulation. Pediatr Cardiol. 2017 Jun;38(5):886-892.</Citation><ArticleIdList><ArticleId IdType="pubmed">28210768</ArticleId></ArticleIdList></Reference><Reference><Citation>Downing TE, Allen KY, Glatz AC, Rogers LS, Ravishankar C, Rychik J, Faerber JA, Fuller S, Montenegro LM, Steven JM, Spray TL, Nicolson SC, Gaynor JW, Goldberg DJ. Long-term survival after the Fontan operation: Twenty years of experience at a single center. J Thorac Cardiovasc Surg. 2017 Jul;154(1):243-253.e2.</Citation><ArticleIdList><ArticleId IdType="pubmed">28341469</ArticleId></ArticleIdList></Reference><Reference><Citation>Backer CL. The functionally univentricular heart: which is better--right or left ventricle? J Am Coll Cardiol. 2012 Mar 27;59(13):1186-7.</Citation><ArticleIdList><ArticleId IdType="pubmed">22440218</ArticleId></ArticleIdList></Reference><Reference><Citation>Gordon-Walker TT, Bove K, Veldtman G. Fontan-associated liver disease: A review. J Cardiol. 2019 Sep;74(3):223-232.</Citation><ArticleIdList><ArticleId IdType="pubmed">30928109</ArticleId></ArticleIdList></Reference><Reference><Citation>Potter BJ, Leong-Sit P, Fernandes SM, Feifer A, Mayer JE, Triedman JK, Walsh EP, Landzberg MJ, Khairy P. Effect of aspirin and warfarin therapy on thromboembolic events in patients with univentricular hearts and Fontan palliation. Int J Cardiol. 2013 Oct 09;168(4):3940-3.</Citation><ArticleIdList><ArticleId IdType="pubmed">23870650</ArticleId></ArticleIdList></Reference><Reference><Citation>Luo S, Honjo O. Late deaths after Fontan procedure: the next frontier. Curr Opin Cardiol. 2019 Mar;34(2):156-163.</Citation><ArticleIdList><ArticleId IdType="pubmed">30575650</ArticleId></ArticleIdList></Reference><Reference><Citation>Atz AM, Zak V, Mahony L, Uzark K, D'agincourt N, Goldberg DJ, Williams RV, Breitbart RE, Colan SD, Burns KM, Margossian R, Henderson HT, Korsin R, Marino BS, Daniels K, McCrindle BW, Pediatric Heart Network Investigators Longitudinal Outcomes of Patients&#xa0;With&#xa0;Single Ventricle After&#xa0;the&#xa0;Fontan&#xa0;Procedure. J Am Coll Cardiol. 2017 Jun 06;69(22):2735-2744.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC5604334</ArticleId><ArticleId IdType="pubmed">28571639</ArticleId></ArticleIdList></Reference><Reference><Citation>d'Udekem Y. Cardiorespiratory Fitness, Not the Severity&#xa0;of the Condition, Dictates Late Outcomes After Fontan Procedures. J Am Coll Cardiol. 2017 Jun 06;69(22):2745-2747.</Citation><ArticleIdList><ArticleId IdType="pubmed">28571640</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32644376</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">30725892</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK537207</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-18886">Cardiac Dominance</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Shahoud</LastName><ForeName>James S.</ForeName><Initials>JS</Initials><AffiliationInfo><Affiliation>Lake Erie College of Osteopathic Med.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ambalavanan</LastName><ForeName>Manoj</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>University of Illinois at Chicago</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tivakaran</LastName><ForeName>Vijai S.</ForeName><Initials>VS</Initials><AffiliationInfo><Affiliation>Kettering Health Network</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>Heart dominance is described by which coronary artery branch gives off the posterior descending artery and supplies the inferior wall, and is characterized as left, right, or codominant. The posterior descending artery (PDA) is also known as the posterior interventricular artery because it runs along the posterior interventricular sulcus to the apex of the heart. It is at the apex where it meets the left anterior descending artery that is traveling along the anterior surface of the heart. The posterior descending artery is responsible for supplying the posterior third of the interventricular septum, including the posterior and inferior wall of the left ventricle. The vessel most commonly originates from either the right coronary artery (right dominant), left circumflex artery (left dominant), or both (codominant). There have been physiologic variants described in case reports such as an origin from the left anterior descending artery, referred to as &#x201c;superdominant.&#x201d; Estimates are that 70 to 80% of the population is right heart dominant with the posterior descending artery originating from the right coronary artery. Approximately 5 to 10% of the population is left heart dominant with the PDA originating from the left circumflex artery, and about 10 to 20% is codominant with the PDA supplied by both the left circumflex artery and right coronary artery. Small branches from the dominant artery&#xa0;perfuse the atrioventricular node. Theoretically, decreased perfusion to the atrioventricular node may result in dysfunction, adding further significance to the cardiac dominance of the patient.
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Microendoscopic transventricular deep brain stimulation of the anterior nucleus of the thalamus as a safe treatment in intractable epilepsy: A feasibility study.
Deep brain stimulation (DBS) of the anterior nucleus of the thalamus (ANT) is proposed in patients with severe intractable epilepsy. When used, the transventricular approach increases the risk of bleeding due the anatomy around the entry point in the thalamus. To avoid such a complication, we used a transventricular microendoscopic technique.</AbstractText>We performed a retrospective study of nine adult patients who were surgically treated for refractory epilepsy between 2010 and 2019 by DBS of the anterior thalamic nucleus.</AbstractText>Endoscopy provides a direct visual control of the entry point of the lead in the thalamus through the ventricle by avoiding ependymal vessels. No hemorrhage was recorded and accuracy was systematically checked by intraoperative stereotactic MRI. We reported a responder rate improvement in 88.9% of patients at 1 year and in 87.5% at 2 years. We showed a significant decrease in global seizure count per month one year after DBS (68.1%; P=0.013) leading to an overall improvement in quality of life. No major adverse effect was recorded during the follow-up. ANT DBS showed a prominent significant effect with a decrease of the number of generalized seizures.</AbstractText>We aimed at a better ANT/lead collimation using a vertical transventricular approach under microendoscopic monitoring. This technique permitted to demonstrate the safety and the accuracy of the procedure.</AbstractText>Copyright &#xa9; 2022 Elsevier Masson SAS. All rights reserved.</CopyrightInformation>
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Assessment of foetal ventriculomegaly from prenatal to early postnatal period: a single-centre retrospective cohort study.
The aim of this study was to evaluate the early neonatal outcomes of cases with foetal ventriculomegaly (VM) and to investigate the aetiological and prognostic factors according to the degree of VM in a single tertiary referring centre. The medical records of 87 foetuses diagnosed with VM (&#x2265;10&#x2009;mm) within 6&#x2009;years were evaluated. Postnatal evaluation and early neonatal prognosis were determined in 39 cases divided into two groups as mild (10-15&#x2009;mm, 30 cases) and severe (&gt;15&#x2009;mm, 9 cases) according to the ventricular size. The mean gestational age at which foetal VM was detected was 22&#x2009;+&#x2009;3&#x2009;weeks. In terms of severity, severe cases of VM were more frequent in terminated pregnancies. There was no difference in gestational age, birth weight, fifth minute Apgar scores, or cord blood gases between mild and severe cases at delivery. Isolated VM was detected in 63% of mild and 22% of severe cases. In severe cases, the need for intensive care and surgery was higher than in mild cases. Antenatal VM regressed in 50% of mild cases and 22% of severe cases. Increasing knowledge about neonatal prognosis, the factors involved in aetiology, and the degree of VM will guide the management of foetal VM.IMPACT STATEMENT<b>What is already known in this subject?</b> Some cases of foetal VM resolve spontaneously, and postnatal ultrasonography can detect normal ventricle sizes. While 74.6% of isolated VM cases show spontaneous regression, this rate is 52.1% in nonisolated cases. The gestational week at the time of diagnosis, the degree and cause of VM, intrauterine progression and the presence of any genetic, infectious, cerebral, or extracerebral disorders all influence the prognosis.<b>What do the results of this study add?</b> Antenatal VM regressed in 50% of mild cases and 22% of severe cases. In severe cases, the need for intensive care and surgery was higher than in mild cases. The higher frequency of accompanying cerebral findings in severe cases was striking.<b>What are the implications of these findings for clinical practice and/or further research?</b> The current study revealed that isolated VM with ventricular diameter less than 15&#x2009;mm, after excluding out chromosomal abnormalities and prenatal infections, and no prior history of VM, has a favourable neonatal prognosis in terms of mortality and morbidity. In cases of foetal VM, increased knowledge of neonatal prognosis will guide pregnancy care and postnatal follow-up planning. Prospective multicentre studies on the neonatal period are required to bridge the gap between foetal VM and long-term consequences.
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Impaired Neurovascular Function Underlies Poor Neurocognitive Outcomes and Is Associated with Nitric Oxide Bioavailability in Congenital Heart Disease.
We use a non-invasive MRI proxy of neurovascular function (pnvf) to assess the ability of the vasculature to supply baseline metabolic demand, to compare pediatric and young adult congenital heart disease (CHD) patients to normal referents and relate the proxy to neurocognitive outcomes and nitric oxide bioavailability. In a prospective single-center study, resting-state blood-oxygen-level-dependent (BOLD) and arterial spin labeling (ASL) MRI scans were successfully obtained from 24 CHD patients (age = 15.4 &#xb1; 4.06 years) and 63 normal referents (age = 14.1 &#xb1; 3.49) years. Pnvf was computed on a voxelwise basis as the negative of the ratio of functional connectivity strength (FCS) estimated from the resting-state BOLD acquisition to regional cerebral blood flow (rCBF) as estimated from the ASL acquisition. Pnvf was used to predict end-tidal CO2 (P<sub>ET</sub>CO2) levels and compared to those estimated from the BOLD data. Nitric oxide availability was obtained via nasal measurements (nNO). Pnvf was compared on a voxelwise basis between CHD patients and normal referents and correlated with nitric oxide availability and neurocognitive outcomes as assessed via the NIH Toolbox. Pnvf was shown as highly predictive of P<sub>ET</sub>CO2 using theoretical modeling. Pnvf was found to be significantly reduced in CHD patients in default mode network (DMN, comprising the ventromedial prefrontal cortex and posterior cingulate/precuneus), salience network (SN, comprising the insula and dorsal anterior cingulate), and central executive network (CEN, comprising posterior parietal and dorsolateral prefrontal cortex) regions with similar findings noted in single cardiac ventricle patients. Positive correlations of Pnvf in these brain regions, as well as the hippocampus, were found with neurocognitive outcomes. Similarly, positive correlations between Pnvf and nitric oxide availability were found in frontal DMN and CEN regions, with particularly strong correlations in subcortical regions (putamen). Reduced Pnvf in CHD patients was found to be mediated by nNO. Mediation analyses further supported that reduced Pnvf in these regions underlies worse neurocognitive outcome in CHD patients and is associated with nitric oxide bioavailability. Impaired neuro-vascular function, which may be non-invasively estimated via combined arterial-spin label and BOLD MR imaging, is a nitric oxide bioavailability dependent factor implicated in adverse neurocognitive outcomes in pediatric and young adult CHD.
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Bridging with Veno-Arterial Extracorporeal Membrane Oxygenation in Children: A 10-Year Single-Center Experience.
Veno-arterial extracorporeal membrane oxygenation (V-A ECMO) is frequently used in children with and without congenital heart disease (CHD). This study, of a single-center and retrospective design, evaluated the use and timing of V-A ECMO in a pediatric cohort who underwent V-A ECMO implantation between January 2009 and December 2019. The patients were divided into a pre-/non-surgical group and a post-surgical group. Among the investigated variables were age, gender, weight, duration of ECMO, ECMO indication, and ventricular physiology, with only the latter being statistically relevant between the two groups. A total of 111 children (58 male/53 female), with a median age of 87 days (IQR: 7-623) were supported using V-A ECMO. The pre-/non-surgical group consisted of 59 patients and the post-surgical group of 52 patients. Survival at discharge was 49% for the pre-/non-surgical group and 21% for the surgical group (<i>p</i> = 0.04). Single-ventricle physiology was significant for a worse outcome (<i>p</i> = 0.0193). Heart anatomy still has the biggest role in the outcomes of children on ECMO. Nevertheless, children with CHD can be successfully bridged with ECMO to cardiac operation.
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Liver X Receptor Regulation of Glial Cell Functions in the CNS.
In this review, we discuss the role of liver X receptors (LXRs) in glial cells (microglia, oligodendrocytes and astrocytes) in the central nervous system (CNS). LXRs are oxysterol-activated nuclear receptors that, in adults, regulate genes involved in cholesterol homeostasis, the modulation of inflammatory responses and glutamate homeostasis. The study of LXR knockout mice has revealed that LXR&#x3b2; plays a key role in maintaining the health of dopaminergic neurons in the substantia nigra, large motor neurons in the spinal cord and retinal ganglion cells in the eye. In the peripheral nervous system (PNS), LXR&#x3b2; is responsible for the health of the spiral ganglion neurons (SGNs) in the cochlea. In addition, LXRs are essential for the homeostasis of the cerebrospinal fluid (CSF), and in LXR&#x3b1;&#x3b2;<sup>-/-</sup> mice, the lateral ventricles are empty and lined with lipid-laden cells. As LXR&#x3b1;&#x3b2;<sup>-/-</sup> mice age, lipid vacuoles accumulate in astrocytes surrounding blood vessels. By seven months of age, motor coordination becomes impaired, and there is a loss of motor neurons in the spinal cord of LXR&#x3b2;<sup>-/-</sup> mice. During development, migration of neurons in the cortex and cerebellum is retarded in LXR&#x3b2;<sup>-/-</sup> mice. Since LXRs are not expressed in dopaminergic or motor neurons in adult mice, the neuroprotective effects of LXRs appear to come from LXRs in glial cells where they are expressed. However, despite the numerous neurological deficits in LXR<sup>-</sup><sup>/</sup><sup>-</sup> rodents, multiple sclerosis has the clear distinction of being the only human neurodegenerative disease in which defective LXR signaling has been identified. In this review, we summarize the regulation and functions of LXRs in glial cells and analyze how targeting LXRs in glial cells might, in the future, be used to treat neurodegenerative diseases and, perhaps, disorders caused by aberrant neuronal migration during development.
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Beneficial Effects of Empagliflozin Are Mediated by Reduced Renal Inflammation and Oxidative Stress in Spontaneously Hypertensive Rats Expressing Human C-Reactive Protein.
Gliflozins (inhibitors of sodium-glucose cotransporter 2) show many beneficial actions beyond their antidiabetic effects. The underlying mechanisms of these additional protective effects are still not well understood, especially under non-diabetic conditions. Therefore, we analyzed the effects of empagliflozin in young (3-month-old) and adult (12-month-old) male spontaneously hypertensive rats (SHR) expressing human C-reactive protein (CRP) in the liver. SHR-CRP rats are a non-diabetic model of metabolic syndrome, inflammation, and organ damage. Empagliflozin was given in a daily dose of 10 mg/kg body weight for 8 weeks. Both age groups of SHR-CRP rats treated with empagliflozin had lower body weight, decreased weight of fat depots, reduced ectopic fat accumulation in the liver and kidneys, and decreased levels of plasma insulin and &#x3b2;-hydroxybutyrate. Empagliflozin effectively reduced ectopic renal fat accumulation, and was associated with decreased inflammation. Exclusively in young rats, decreased microalbuminuria after empagliflozin treatment was accompanied by attenuated oxidative stress. In adult animals, empagliflozin also improved left ventricle function. In conclusion, in young animals, the beneficial renoprotective effects of empagliflozin could be ascribed to reduced lipid deposition in the kidney and the attenuation of oxidative stress and inflammation. In contrast, hepatic lipid metabolism was ameliorated in adult rats.
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Primary Cilia Influence Progenitor Function during Cortical Development.
Corticogenesis is an intricate process controlled temporally and spatially by many intrinsic and extrinsic factors. Alterations during this important process can lead to severe cortical malformations. Apical neuronal progenitors are essential cells able to self-amplify and also generate basal progenitors and/or neurons. Apical radial glia (aRG) are neuronal progenitors with a unique morphology. They have a long basal process acting as a support for neuronal migration to the cortical plate and a short apical process directed towards the ventricle from which protrudes a primary cilium. This antenna-like structure allows aRG to sense cues from the embryonic cerebrospinal fluid (eCSF) helping to maintain cell shape and to influence several key functions of aRG such as proliferation and differentiation. Centrosomes, major microtubule organising centres, are crucial for cilia formation. In this review, we focus on how primary cilia influence aRG function during cortical development and pathologies which may arise due to defects in this structure. Reporting and cataloguing a number of ciliary mutant models, we discuss the importance of primary cilia for aRG function and cortical development.
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Human antimicrobial peptide LL-37 contributes to Alzheimer's disease progression.
As a prime mover in Alzheimer's disease (AD), microglial activation requires membrane translocation, integration, and activation of the metamorphic protein chloride intracellular channel 1 (CLIC1), which is primarily cytoplasmic under physiological conditions. However, the formation and activation mechanisms of functional CLIC1 are unknown. Here, we found that the human antimicrobial peptide (AMP) LL-37 promoted CLIC1 membrane translocation and integration. It also activates CLIC1 to cause microglial hyperactivation, neuroinflammation, and excitotoxicity. In mouse and monkey models, LL-37 caused significant pathological phenotypes linked to AD, including elevated amyloid-&#x3b2;, increased neurofibrillary tangles, enhanced neuronal death and brain atrophy, enlargement of lateral ventricles, and impairment of synaptic plasticity and cognition, while Clic1 knockout and blockade of LL-37-CLIC1 interactions inhibited these phenotypes. Given AD's association with infection and that overloading AMP may exacerbate AD, this study suggests that LL-37, which is up-regulated upon infection, may be a driving force behind AD by acting as an endogenous agonist of CLIC1.
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Racemose neurocysticercosis simulating tuberculous meningitis.
We report a patient with racemose neurocysticercosis, highlighting the diagnostic and management issues. A 37-year-old male had headaches, fever, and seizures for 8&#xa0;months. He had a positive tuberculin test, cerebrospinal fluid pleocytosis, and hydrocephalus and exudates on MRI. His symptoms rapidly resolved following antitubercular and prednisolone treatment. After 2&#xa0;months, he was readmitted with headache and vomiting, and his brain MRI revealed communicating hydrocephalus with a cyst in the lateral ventricle and subarachnoid space, which was confirmed as neurocysticercosis on the third ventriculostomy. The patient was managed with dexamethasone and a ventriculoperitoneal shunt. This case highlights that meningitis symptoms, CSF pleocytosis, and positive tuberculin tests may not always suggest tubercular etiology.