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Standard values for MRI brain biometry throughout the first year of life.
Brain structures in the infant brain are investigated reliably using cranial magnetic resonance imaging. However, the lack of quantitative standard values for various brain regions results in data interpretation that is often subjective or based on small patient cohorts. The aim of this study was to create simple linear measurements to assess brain structures in infancy.</AbstractText>We assessed cranial magnetic resonance imaging sessions of 131 children without intracerebral pathology retrospectively for size of various brain structures throughout the first year of life.</AbstractText>Standard values for the size and the growth rate of 14 brain structures including lateral ventricles, frontal subarachnoid space, pons, medulla oblongata, cerebellar vermis, pituitary gland, optical nerve, corpus callosum and the tegmentovermian angle were defined.</AbstractText>Our study offers reference values for the biometric assessment of the infant brain. Especially in children with multiple brain malformations, it is essential to know the normal absolute and relative size of brain structures.</AbstractText>Copyright &#xa9; 2022 Taiwan Pediatric Association. Published by Elsevier B.V. All rights reserved.</CopyrightInformation>
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Deformation-based morphometry identifies deep brain structures protected by ocrelizumab.
Despite advancements in treatments for multiple sclerosis, insidious disease progression remains an area of unmet medical need, for which atrophy-based biomarkers may help better characterize the progressive biology.</AbstractText>We developed and applied a method of longitudinal deformation-based morphometry to provide voxel-level assessments of brain volume changes and identified brain regions that were significantly impacted by disease-modifying therapy.</AbstractText>Using brain MRI data from two identically designed pivotal trials of relapsing multiple sclerosis (total N&#xa0;=&#xa0;1483), we identified multiple deep brain regions, including the thalamus and brainstem, where volume loss over time was reduced by ocrelizumab (p&#xa0;&lt;&#xa0;0.05), a humanized anti-CD20&#xa0;+&#xa0;monoclonal antibody approved for the treatment of multiple sclerosis. Additionally, identified brainstem shrinkage, as well as brain ventricle expansion, was associated with a greater risk for confirmed disability progression (p&#xa0;&lt;&#xa0;0.05).</AbstractText>The identification of deep brain structures has a strong implication for developing new biomarkers of brain atrophy reduction to advance drug development for multiple sclerosis, which has an increasing focus on targeting the progressive biology.</AbstractText>Copyright &#xa9; 2022 The Author(s). Published by Elsevier Inc. All rights reserved.</CopyrightInformation>
2,330,302
A Mechanical Bridge to Recovery as a Bridge to Discovery: Learning From Few and Applying to Many.<Pagination><StartPage>562</StartPage><EndPage>564</EndPage><MedlinePgn>562-564</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1161/CIRCULATIONAHA.120.052141</ELocationID><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Taleb</LastName><ForeName>Iosif</ForeName><Initials>I</Initials><Identifier Source="ORCID">0000-0002-0029-5019</Identifier><AffiliationInfo><Affiliation>Division of Cardiovascular Medicine (I.T., E.T., J.C.F., S.G.D.), University of Utah Health, Salt Lake City.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Nora Eccles Harrison Cardiovascular Research and Training Institute (I.T., E.T., S.G.D.), University of Utah Health, Salt Lake City.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tseliou</LastName><ForeName>Eleni</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Division of Cardiovascular Medicine (I.T., E.T., J.C.F., S.G.D.), University of Utah Health, Salt Lake City.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Nora Eccles Harrison Cardiovascular Research and Training Institute (I.T., E.T., S.G.D.), University of Utah Health, Salt Lake City.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fang</LastName><ForeName>James C</ForeName><Initials>JC</Initials><Identifier Source="ORCID">0000-0003-2427-9504</Identifier><AffiliationInfo><Affiliation>Division of Cardiovascular Medicine (I.T., E.T., J.C.F., S.G.D.), University of Utah Health, Salt Lake City.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Drakos</LastName><ForeName>Stavros G</ForeName><Initials>SG</Initials><Identifier Source="ORCID">0000-0002-1223-327X</Identifier><AffiliationInfo><Affiliation>Division of Cardiovascular Medicine (I.T., E.T., J.C.F., S.G.D.), University of Utah Health, Salt Lake City.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Nora Eccles Harrison Cardiovascular Research and Training Institute (I.T., E.T., S.G.D.), University of Utah Health, Salt Lake City.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 HL132067</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL135121</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32 HL007576</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>02</Month><Day>21</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Circulation</MedlineTA><NlmUniqueID>0147763</NlmUniqueID><ISSNLinking>0009-7322</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006333" MajorTopicYN="N">Heart Failure</DescriptorName><QualifierName UI="Q000628" MajorTopicYN="Y">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016027" MajorTopicYN="Y">Heart Transplantation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006353" MajorTopicYN="Y">Heart-Assist Devices</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">heart failure</Keyword><Keyword MajorTopicYN="N">heart ventricles</Keyword><Keyword MajorTopicYN="N">heart-assist devices</Keyword></KeywordList><CoiStatement>Conflict of Interest Disclosures: All other authors have nothing to disclose.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>2</Month><Day>21</Day><Hour>17</Hour><Minute>9</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>2</Month><Day>22</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>3</Month><Day>11</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35188797</ArticleId><ArticleId IdType="mid">NIHMS1772572</ArticleId><ArticleId IdType="pmc">PMC8900596</ArticleId><ArticleId IdType="doi">10.1161/CIRCULATIONAHA.120.052141</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Birks EJ, Drakos SG, Patel SR, Lowes BD, Selzman CH, Starling RC, Trivedi J, Slaughter MS, Alturi P, Goldstein D, Maybaum S, Um JY, Margulies KB, Stehlik J, Cunningham C, Farrar DJ and Rame JE. Prospective Multicenter Study of Myocardial Recovery Using Left Ventricular Assist Devices (RESTAGE-HF [Remission from Stage D Heart Failure]): Medium-Term and Primary End Point Results. Circulation. 2020;142:2016&#x2013;2028.</Citation><ArticleIdList><ArticleId IdType="pubmed">33100036</ArticleId></ArticleIdList></Reference><Reference><Citation>Burkhoff D, Topkara VK, Sayer G and Uriel N. Reverse Remodeling With Left Ventricular Assist Devices. Circ Res. 2021;128:1594&#x2013;1612.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC9132540</ArticleId><ArticleId IdType="pubmed">33983828</ArticleId></ArticleIdList></Reference><Reference><Citation>Drakos SG, Pagani FD, Lundberg MS and Baldwin JT. Advancing the Science of Myocardial Recovery With Mechanical Circulatory Support: A Working Group of the National, Heart, Lung, and Blood Institute. JACC Basic Transl Sci. 2017;2:335&#x2013;340.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC5516933</ArticleId><ArticleId IdType="pubmed">28736756</ArticleId></ArticleIdList></Reference><Reference><Citation>Cluntun AA, Badolia R, Lettlova S, Parnell KM, Shankar TS, Diakos NA, Olson KA, Taleb I, Tatum SM, Berg JA, Cunningham CN, Van Ry T, Bott AJ, Krokidi AT, Fogarty S, Skedros S, Swiatek WI, Yu X, Luo B, Merx S, Navankasattusas S, Cox JE, Ducker GS, Holland WL, McKellar SH, Rutter J and Drakos SG. The pyruvate-lactate axis modulates cardiac hypertrophy and heart failure. Cell Metab. 2020.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC7933116</ArticleId><ArticleId IdType="pubmed">33333007</ArticleId></ArticleIdList></Reference><Reference><Citation>Shankar TS, Ramadurai DKA, Steinhorst K, Sommakia S, Badolia R, Thodou Krokidi A, Calder D, Navankasattusas S, Sander P, Kwon OS, Aravamudhan A, Ling J, Dendorfer A, Xie C, Kwon O, Cheng EHY, Whitehead KJ, Gudermann T, Richardson RS, Sachse FB, Schredelseker J, Spitzer KW, Chaudhuri D and Drakos SG. Cardiac-specific deletion of voltage dependent anion channel 2 leads to dilated cardiomyopathy by altering calcium homeostasis. Nat Commun. 2021;12:4583.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC8319341</ArticleId><ArticleId IdType="pubmed">34321484</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">35188133</PMID><DateCompleted><Year>2022</Year><Month>04</Month><Day>07</Day></DateCompleted><DateRevised><Year>2022</Year><Month>04</Month><Day>07</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1940-087X</ISSN><JournalIssue CitedMedium="Internet"><Issue>180</Issue><PubDate><Year>2022</Year><Month>Feb</Month><Day>03</Day></PubDate></JournalIssue><Title>Journal of visualized experiments : JoVE</Title><ISOAbbreviation>J Vis Exp</ISOAbbreviation></Journal>Isolation and Characterization of the Immune Cells from Micro-dissected Mouse Choroid Plexuses.<ELocationID EIdType="doi" ValidYN="Y">10.3791/63487</ELocationID><Abstract><AbstractText>The brain is no longer considered as an organ functioning in isolation; accumulating evidence suggests that changes in the peripheral immune system can indirectly shape brain function. At the interface between the brain and the systemic circulation, the choroid plexuses (CP), which constitute the blood-cerebrospinal fluid barrier, have been highlighted as a key site of periphery-to-brain communication. CP produce the cerebrospinal fluid, neurotrophic factors, and signaling molecules that can shape brain homeostasis. CP are also an active immunological niche. In contrast to the brain parenchyma, which is populated mainly by microglia under physiological conditions, the heterogeneity of CP immune cells recapitulates the diversity found in other peripheral organs. The CP immune cell diversity and activity change with aging, stress, and disease and modulate the activity of the CP epithelium, thereby indirectly shaping brain function. The goal of this protocol is to isolate murine CP and identify about 90% of the main immune subsets that populate them. This method is a tool to characterize CP immune cells and understand their function in orchestrating periphery-to-brain communication. The proposed protocol may help decipher how CP immune cells indirectly modulate brain function in health and across various disease conditions.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Dominguez-Belloso</LastName><ForeName>Amaia</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Brain-Immune Communication Lab, Institut Pasteur.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schmutz</LastName><ForeName>Sandrine</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Cytometry platform, CB UTechS, Institut Pasteur.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Novault</LastName><ForeName>Sophie</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Cytometry platform, CB UTechS, Institut Pasteur.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Travier</LastName><ForeName>Laetitia</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Brain-Immune Communication Lab, Institut Pasteur; laetitia.travier@pasteur.fr.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Deczkowska</LastName><ForeName>Aleksandra</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Brain-Immune Communication Lab, Institut Pasteur; aleksandra.deczkowska@pasteur.fr.</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><PublicationType UI="D059040">Video-Audio Media</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>02</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Vis Exp</MedlineTA><NlmUniqueID>101313252</NlmUniqueID><ISSNLinking>1940-087X</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000375" MajorTopicYN="N">Aging</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</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><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002829" MajorTopicYN="N">Choroid</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002831" MajorTopicYN="Y">Choroid Plexus</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>2</Month><Day>21</Day><Hour>8</Hour><Minute>44</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>2</Month><Day>22</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>4</Month><Day>8</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35188133</ArticleId><ArticleId IdType="doi">10.3791/63487</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">35188128</PMID><DateCompleted><Year>2022</Year><Month>04</Month><Day>07</Day></DateCompleted><DateRevised><Year>2022</Year><Month>08</Month><Day>05</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1940-087X</ISSN><JournalIssue CitedMedium="Internet"><Issue>180</Issue><PubDate><Year>2022</Year><Month>Feb</Month><Day>01</Day></PubDate></JournalIssue><Title>Journal of visualized experiments : JoVE</Title><ISOAbbreviation>J Vis Exp</ISOAbbreviation></Journal>Generation and Characterization of Right Ventricular Myocardial Infarction Induced by Permanent Ligation of the Right Coronary Artery in Mice.
The brain is no longer considered as an organ functioning in isolation; accumulating evidence suggests that changes in the peripheral immune system can indirectly shape brain function. At the interface between the brain and the systemic circulation, the choroid plexuses (CP), which constitute the blood-cerebrospinal fluid barrier, have been highlighted as a key site of periphery-to-brain communication. CP produce the cerebrospinal fluid, neurotrophic factors, and signaling molecules that can shape brain homeostasis. CP are also an active immunological niche. In contrast to the brain parenchyma, which is populated mainly by microglia under physiological conditions, the heterogeneity of CP immune cells recapitulates the diversity found in other peripheral organs. The CP immune cell diversity and activity change with aging, stress, and disease and modulate the activity of the CP epithelium, thereby indirectly shaping brain function. The goal of this protocol is to isolate murine CP and identify about 90% of the main immune subsets that populate them. This method is a tool to characterize CP immune cells and understand their function in orchestrating periphery-to-brain communication. The proposed protocol may help decipher how CP immune cells indirectly modulate brain function in health and across various disease conditions.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Dominguez-Belloso</LastName><ForeName>Amaia</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Brain-Immune Communication Lab, Institut Pasteur.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schmutz</LastName><ForeName>Sandrine</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Cytometry platform, CB UTechS, Institut Pasteur.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Novault</LastName><ForeName>Sophie</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Cytometry platform, CB UTechS, Institut Pasteur.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Travier</LastName><ForeName>Laetitia</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Brain-Immune Communication Lab, Institut Pasteur; laetitia.travier@pasteur.fr.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Deczkowska</LastName><ForeName>Aleksandra</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Brain-Immune Communication Lab, Institut Pasteur; aleksandra.deczkowska@pasteur.fr.</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><PublicationType UI="D059040">Video-Audio Media</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>02</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Vis Exp</MedlineTA><NlmUniqueID>101313252</NlmUniqueID><ISSNLinking>1940-087X</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000375" MajorTopicYN="N">Aging</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</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><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002829" MajorTopicYN="N">Choroid</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002831" MajorTopicYN="Y">Choroid Plexus</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>2</Month><Day>21</Day><Hour>8</Hour><Minute>44</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>2</Month><Day>22</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>4</Month><Day>8</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35188133</ArticleId><ArticleId IdType="doi">10.3791/63487</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">35188128</PMID><DateCompleted><Year>2022</Year><Month>04</Month><Day>07</Day></DateCompleted><DateRevised><Year>2022</Year><Month>08</Month><Day>05</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1940-087X</ISSN><JournalIssue CitedMedium="Internet"><Issue>180</Issue><PubDate><Year>2022</Year><Month>Feb</Month><Day>01</Day></PubDate></JournalIssue><Title>Journal of visualized experiments : JoVE</Title><ISOAbbreviation>J Vis Exp</ISOAbbreviation></Journal><ArticleTitle>Generation and Characterization of Right Ventricular Myocardial Infarction Induced by Permanent Ligation of the Right Coronary Artery in Mice.</ArticleTitle><ELocationID EIdType="doi" ValidYN="Y">10.3791/63508</ELocationID><Abstract>Right ventricular infarction (RVI) is a common presentation in clinical practice. Severe RVI can lead to fatal hemodynamic dysfunction and arrhythmia. In contrast to the extensively used mouse myocardial infarction (MI) model generated by left coronary artery ligation, the RVI mouse model is rarely employed due to the difficulty associated with model generation. Research on the mechanisms and treatment of RVI-induced RV remodeling and dysfunction requires animal models to mimic the pathophysiology of RVI in patients. This study introduces a feasible procedure for RVI model generation in C57BL/6J mice. Further, this model was characterized based on the following: infarct size evaluation at 24 h after MI, assessment of cardiac remodeling and function with echocardiography, RV hemodynamics assessment, and histology of the infarct zone at 4 weeks after RVI. In addition, a coronary vasculature cast was performed to observe the coronary arterial arrangement in RV. This mouse model of RVI would facilitate the research on mechanisms of right heart failure and seek new therapeutic targets of RV remodeling.
2,330,303
Hypertensive primary intraventricular hemorrhage: a systematic review.
Primary intraventricular hemorrhage (PIVH) is a special subtype of intraventricular hemorrhage (IVH) without a hemorrhagic parenchymal component. Different conditions may cause this uncommon hemorrhage including trauma, vascular anomalies, coagulation disorders, and others. Frequently, PIVH is associated with structural vascular anomalies such as aneurysms, arteriovenous malformations, and dural fistulas. Traditionally, hypertension has been considered a predisposing factor for PIVH. A wide variety of studies have been published describing patients with PIVH; however, studies describing exclusively patients with hypertensive PIVH are lacking in the literature. For this reason, the features of PIVH secondary to hypertension are not well described. The purpose of this study is to analyze and describe the characteristics of hypertensive PIVH. A PubMed and Scopus search adhering to Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines was performed to include studies reporting patients with hypertensive PIVH. The search yielded 19 articles reporting retrospective case series. The diagnosis of hypertensive PIVH should be established in patients meeting the following criteria: (a) elevation of blood pressure is observed at admission, (b) a cerebral angiography is negative for vascular anomalies, and (c) other causes of intracranial hemorrhage are ruled out. The prognosis is poorer in patients who present with low Glasgow Coma Score (GCS), old age, hydrocephalus, or more extensive intraventricular bleeding. The results of this study show that hypertension is the most common cause of PIVH, followed by hemorrhage caused by vascular anomalies. Hypertension may be a direct cause of PIVH, but also it may be a predisposing factor for bleeding in cases of an associated vascular anomaly.
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Ventriculomegaly thresholds for prediction of symptomatic post-hemorrhagic ventricular dilatation in preterm infants.
Benefits from early surgical intervention in preterm infants with intraventricular hemorrhage (IVH) prior to symptomatic ventriculomegaly must be weighed against risks of surgery. We calculated thresholds of common ventriculomegaly indices at a late-intervention institution to predict subsequent symptomatic ventriculomegaly requiring neurosurgery.</AbstractText>We retrospectively reviewed neuroimaging and neurosurgical outcomes in preterm infants with grade III/IV IVH between 2007 and 2020. Frontal-occipital horn ratio (FOHR), frontal-temporal horn ratio (FTHR), anterior horn width (AHW), and ventricular index (VI) were measured. Area under the receiver operating curve (AUC) for predicting intervention (initiated after progressive symptomatic ventriculomegaly) was calculated for diagnostic scan, scans during weeks 1-4, and maximum measurement prior to intervention. Threshold values that optimized sensitivity and specificity were derived.</AbstractText>A total of 1254 scans in 132 patients were measured. In all, 37 patients had a neurosurgical intervention. All indices differed between those with and without intervention from the first diagnostic scan (p&#x2009;&lt;&#x2009;0.001). AUC of maximum measurement was 97.1% (95% CI 94.6-99.7) for FOHR, 97.7% (95% CI 95.6-99.8) for FTHR, 96.6% (95% CI 93.9-99.4) for AHW, and 96.8% (95% CI 94.0-99.5) for VI. Calculated thresholds were FOHR 0.66, FTHR 0.62, AHW 15.5&#x2009;mm, and VI 8.4&#x2009;mm&#x2009;&gt;&#x2009;p97 (sensitivities &gt;86.8%, specificities &gt;90.1%).</AbstractText>Ventriculomegaly indices were greater for patients who developed progressive persistent ventriculomegaly from the first diagnostic scan and predicted neurosurgical intervention.</AbstractText>We derived thresholds of common ventriculomegaly indices (ventricular index, anterior frontal horn width, fronto-occipital horn and fronto-temporal horn index) to best predict the development of progressive symptomatic post-hemorrhage hydrocephalus in preterm infants with intraventricular hemorrhage. While current thresholds were established by a priori expert consensus, we report the first data-driven derivation of ventriculomegaly thresholds across all indices for the prediction of symptomatic hydrocephalus. Data-derived thresholds will more precisely weigh the risks and benefits of early intervention.</AbstractText>&#xa9; 2022. The Author(s), under exclusive licence to the International Pediatric Research Foundation, Inc.</CopyrightInformation>
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Gene expression of hypoxia-inducible factor (HIF), HIF regulators, and putative HIF targets in ventricle and telencephalon of Trachemys scripta acclimated to 21&#xa0;&#xb0;C or 5&#xa0;&#xb0;C and exposed to normoxia, anoxia or reoxygenation.
In anoxia-sensitive mammals, hypoxia inducible factor (HIF) promotes cellular survival in hypoxia, but also tumorigenesis. By comparison, anoxia-tolerant vertebrates likely need to circumvent a prolonged upregulation of HIF to survive long-term anoxia, making them attractive biomedical models for investigating HIF regulation. To lend insight into the role of HIF in anoxic Trachemys scripta ventricle and telencephalon, 21&#xa0;&#xb0;C- and 5&#xa0;&#xb0;C-acclimated turtles were exposed to normoxia, anoxia (24&#xa0;h at 21&#xa0;&#xb0;C; 24&#xa0;h or 14 d at 5&#xa0;&#xb0;C) or anoxia + reoxygenation and the gene expression of HIF-1&#x3b1; (hif1a) and HIF-2&#x3b1; (hif2a), two regulators of HIF, and eleven putative downstream targets of HIF quantified by qPCR. Changes in gene expression with anoxia at 21&#xa0;&#xb0;C differentially aligned with a circumvention of HIF activity. Whereas hif1a and hif2a expression was unaffected in ventricle and telencephalon, and BCL2 interacting protein 3 gene expression reduced by 30% in telencephalon, gene expression of vascular endothelial growth factor-A increased in ventricle (4.5-fold) and telencephalon (1.5-fold), and hexokinase 1 (2-fold) and hexokinase 2 (3-fold) gene expression increased in ventricle. At 5&#xa0;&#xb0;C, the pattern of gene expression in ventricle or telencephalon was unaltered with oxygenation state. However, cold acclimation in normoxia induced downregulation of HIF-1&#x3b1;, HIF-2&#x3b1;, and HIF target gene expression in telencephalon. Overall, the findings lend support to the postulation that prolonged activation of HIF is counterproductive for long-term anoxia survival. Nevertheless, quantification of the effect of anoxia and acclimation temperature on HIF binding activity and regulation at the protein level are needed to provide a strong scientific framework whereby new strategies for oxygen related pathologies can be developed.
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Pharmacological neuroprotection and clinical trials of novel therapies for neonatal peri-intraventricular hemorrhage: a comprehensive review.
Peri-intraventricular hemorrhage (PIVH) is a serious condition for preterm infants, caused by traumatic or spontaneous rupture of the germinal matrix (GM) capillary network in the cerebral ventricles. It is a common source of morbidity and mortality in neonates, and risk correlates with earlier delivery, low birth weight, maternal-fetal infection, and vital sign derangements, among others. PIVH typically occurs in the first 72&#xa0;h of life, and symptoms, when present, manifest most commonly within the first week of life. Prevention remains the primary goal in management, predominantly via prolonging of gestation. Current therapy protocols are center-dependent without consistent consensus guidelines, but infant positioning, homeostatic stabilization, and neuroprotection offer potential options. In this update of pharmacologic neuroprotective therapies for PIVH, we highlight commonly utilized therapies and review the investigative literature. Further multi-institutional clinical trials and basic research studies are required.
2,330,307
Prognostic Implication of DNA Methylation Signature in Atypical Choroid Plexus Papilloma With Intracranial Dissemination.
An underestimation of pathologic diagnosis could be expected if disseminated choroid plexus tumors (CPTs) are diagnosed as lower grade tumors. Thus, molecular diagnosis using genome-wide DNA methylation profiling may be useful for clarifying the malignant potential of the tumor entity. Herein, we report a 2.7-year-old girl of pathologically atypical choroid plexus papilloma with intracranial dissemination. She was treated without radiotherapy and has been well, without recurrence for 32 months following the diagnosis. Subsequently, after a year from the diagnosis, T-stochastic neighbor embedding analysis was performed on methylation data of the case and compared with those of reference data of CPTs, revealing that the case was separated from the cluster of "Plexus tumor subclass pediatric B," which includes a majority of choroid plexus carcinomas with the worst prognosis of these entities, and was categorized into the cluster of "Plexus tumor subclass pediatric A" consisting of choroid plexus papilloma and atypical choroid plexus papillomas diagnosed pathologically. Our case indicates the clinical significance of molecular confirmation for diagnosis among CPTs, particularly lower grade tumors with dissemination.
2,330,308
Engineering in-plane mechanics of electrospun polyurethane scaffolds for cardiovascular tissue applications.
Effective cardiovascular tissue surrogates require high control of scaffold structural and mechanical features to match native tissue properties, which are dependent on tissue-specific mechanics, function heterogenicity, and morphology. Bridging scaffold processing variables with native tissue properties is recognized as a priority for advancing biomechanical performance of biomedical materials and, when translated to the clinical practice, their efficacy. Accordingly, this study selected electrospinning on a rotating cylindrical target as an apparatus of broad application and mapped the relationship between key processing variables and scaffold mechanics and structure. This information was combined with mechanical anisotropy ranges of interest for the three main categories of tissue surrogated in cardiovascular tissue engineering: heart valve leaflets, ventricle wall, and large diameter blood vessels. Specifically, three processing variables have been considered: the rotational velocity and the rastering velocity of the mandrel and the dry (single nozzle - polymer only) vs wet (double nozzle - polymer plus phosphate buffer saline solution) fabrication configuration. While the dry configuration is generally utilized to obtain micro-fiber based polymeric mats, the wet fabrication is representative of processing conditions utilized to incorporate cells, growth factors, or micro-particles within the fibrous scaffold matrix. Dry and wet processed electrospun mats were fabricated with tangential and rastering velocities within the 0.3-9.0&#xa0;m/s and 0.16-8&#xa0;cm/s range respectively. Biaxial mechanics, fiber network, and pore micro-architectures were measured for each combination of velocities and for each fabrication modality (dry and wet). Results allowed identification of the precise combination of rotational and rastering velocities, for both dry and wet conditions, that is able to recapitulate the native cardiovascular tissue anisotropy ratio. By adopting a simple and broadly utilized electrospinning layout, this study is meant to provide a repeatable and easy to access methodology to improve biomimicry of the in plane-mechanics of heart valve leaflets, ventricular wall, and large diameter blood vessels.
2,330,309
Analysis of complications in intraventricular neuroendoscopy in children: proposal for a standardization system.
Although intraventricular neuroendoscopy is considered a minimally invasive technique with good results, there is nevertheless a risk of developing certain complications. As no agreement apparently exists concerning the classification of these complications, we aim to propose a form of classification based on the results of our series, comparing them with recent publications. We undertook a retrospective study of 170 children who underwent intraventricular neuroendoscopy between 2003 and September 2020 at our center. Data were recorded on demographic and clinical variables: age, gender, presenting symptoms, etiology, number of procedures, type of procedure, and complications. Complications were divided into two main groups, intraoperative and postoperative, and in subgroups. The intraoperative complications included one group of systemic alterations and another group of surgical problems. The postoperative complications were divided into six groups: systemic, neurologic, hormone, fluid, hemorrhagic and death. A total of 202 neuroendoscopic procedures were performed in 170 children. The mean age at first surgery was 71&#xa0;months (22-122). The most common etiology of the hydrocephalus was intraventricular tumors (32.9%), followed by aqueductal stenosis (13.5%). The most usual presenting sign was intracranial hypertension. The procedure most used was third ventriculostomy (62.9%). During the procedures, we experienced 5 surgical intraoperative complications (2.47% per procedure). In the postoperative period, there were 23.7% systemic complications per procedure, 12.87% neurologic, 8.41% hormone, 10.9% fluid, 0.5% hemorrhagic, and 0.99% for postoperative death. The rate of complications associated with intraventricular neuroendoscopy was similar in our series to those already published. Comparative studies require standardization for the analysis of neuroendoscopic complications.
2,330,310
Predictors of Left Main Coronary Artery Disease in the ISCHEMIA Trial.<Pagination><StartPage>651</StartPage><EndPage>661</EndPage><MedlinePgn>651-661</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.jacc.2021.11.052</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0735-1097(21)08389-3</ELocationID><Abstract><AbstractText Label="BACKGROUND">Detection of&#xa0;&#x2265;50% diameter stenosis left main coronary artery disease (LMD) has prognostic and therapeutic implications. Noninvasive stress imaging or an exercise tolerance test (ETT) are the most common methods to detect obstructive coronary artery disease, though stress test markers of LMD remain ill-defined.</AbstractText><AbstractText Label="OBJECTIVES">The authors sought to identify markers of LMD as detected on coronary computed tomography angiography (CTA), using clinical and stress testing parameters.</AbstractText><AbstractText Label="METHODS">This was a post hoc analysis of ISCHEMIA (International Study of Comparative Health Effectiveness With Medical and Invasive Approaches), including randomized and nonrandomized participants who had locally determined moderate or severe ischemia on nonimaging ETT, stress nuclear myocardial perfusion imaging, or stress echocardiography followed by CTA to exclude LMD. Stress tests were read by core laboratories. Prior coronary artery bypass grafting was an exclusion. In a stepped multivariate model, the authors identified predictors of LMD, first without and then with stress testing parameters.</AbstractText><AbstractText Label="RESULTS">Among 5,146 participants (mean age 63 years, 74% male), 414 (8%) had LMD. Predictors of LMD were older age (P&#xa0;&lt; 0.001), male sex (P&#xa0;&lt; 0.01), absence of prior myocardial infarction (P&#xa0;&lt; 0.009), transient ischemic dilation of the left ventricle on stress echocardiography (P&#xa0;=&#xa0;0.05), magnitude of ST-segment depression on ETT (P&#xa0;=&#xa0;0.004), and peak metabolic equivalents achieved on ETT (P&#xa0;=&#xa0;0.001). The models were weakly predictive of LMD (C-index 0.643 and 0.684).</AbstractText><AbstractText Label="CONCLUSIONS">In patients with moderate or severe ischemia, clinical and stress testing parameters were weakly predictive of LMD on CTA. For most patients with moderate or severe ischemia, anatomical imaging is needed to rule out LMD. (International Study of Comparative Health Effectiveness With Medical and Invasive Approaches [ISCHEMIA]; NCT01471522).</AbstractText><CopyrightInformation>Copyright &#xa9; 2022 American College of Cardiology Foundation. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Senior</LastName><ForeName>Roxy</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Northwick Park Hospital-Royal Brompton Hospital, London, United Kingdom. Electronic address: roxysenior@cardiac-research.org.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Reynolds</LastName><ForeName>Harmony R</ForeName><Initials>HR</Initials><AffiliationInfo><Affiliation>New York University Grossman School of Medicine, New York, New York, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Min</LastName><ForeName>James K</ForeName><Initials>JK</Initials><AffiliationInfo><Affiliation>Cleerly, Inc, New York, New York, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Berman</LastName><ForeName>Daniel S</ForeName><Initials>DS</Initials><AffiliationInfo><Affiliation>Cedars-Sinai Medical Center, Los Angeles, California, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Picard</LastName><ForeName>Michael H</ForeName><Initials>MH</Initials><AffiliationInfo><Affiliation>Massachusetts General Hospital, Boston, Massachusetts, USA; Harvard Medical School, Boston, Massachusetts, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chaitman</LastName><ForeName>Bernard R</ForeName><Initials>BR</Initials><AffiliationInfo><Affiliation>St Louis University School of Medicine Center for Comprehensive Cardiovascular Care, St Louis, Missouri, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shaw</LastName><ForeName>Leslee J</ForeName><Initials>LJ</Initials><AffiliationInfo><Affiliation>Cleerly, Inc, New York, New York, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Page</LastName><ForeName>Courtney B</ForeName><Initials>CB</Initials><AffiliationInfo><Affiliation>Duke Clinical Research Institute, Durham, North Carolina, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Govindan</LastName><ForeName>Sajeev C</ForeName><Initials>SC</Initials><AffiliationInfo><Affiliation>Government Medical College, Calicut, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lopez-Sendon</LastName><ForeName>Jose</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Hospital Universitario La Paz, Idipaz, UAM, CIBER-CV, Madrid, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Peteiro</LastName><ForeName>Jesus</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>CHUAC, Universidad de A Coru&#xf1;a, CIBER-CV, A Coruna, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wander</LastName><ForeName>Gurpreet S</ForeName><Initials>GS</Initials><AffiliationInfo><Affiliation>Dayanand Medical College &amp; Hospital, Punjab, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Drozdz</LastName><ForeName>Jaroslaw</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department Cardiology Medical University, Lodz, Poland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Marin-Neto</LastName><ForeName>Jose</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Hospital das Clinicas da Faculdade de Medicina de Ribeirao Preto da Universidade de Sao Paulo, Sao Paulo, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Selvanayagam</LastName><ForeName>Joseph B</ForeName><Initials>JB</Initials><AffiliationInfo><Affiliation>Flinders Medical Centre, Adelaide, South Australia, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Newman</LastName><ForeName>Jonathan D</ForeName><Initials>JD</Initials><AffiliationInfo><Affiliation>New York University Grossman School of Medicine, New York, New York, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Thuaire</LastName><ForeName>Christophe</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>C.H. Louis Pasteur, Le Coudray, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Christopher</LastName><ForeName>Johann</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>CARE Hospital, Hyderabad, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jang</LastName><ForeName>James J</ForeName><Initials>JJ</Initials><AffiliationInfo><Affiliation>Kaiser Permanente/San Jose Medical Center, San Jose, California, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kwong</LastName><ForeName>Raymond Y</ForeName><Initials>RY</Initials><AffiliationInfo><Affiliation>Brigham and Women's Hospital, Boston, Massachusetts, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bangalore</LastName><ForeName>Sripal</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>New York University Grossman School of Medicine, New York, New York, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Stone</LastName><ForeName>Gregg W</ForeName><Initials>GW</Initials><AffiliationInfo><Affiliation>Icahn School of Medicine at Mount Sinai, Cardiovascular Research Foundation, New York, New York, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>O'Brien</LastName><ForeName>Sean M</ForeName><Initials>SM</Initials><AffiliationInfo><Affiliation>Duke Clinical Research Institute, Durham, North Carolina, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Boden</LastName><ForeName>William E</ForeName><Initials>WE</Initials><AffiliationInfo><Affiliation>VA New England Healthcare System, Boston University School of Medicine, Boston, Massachusetts, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Maron</LastName><ForeName>David J</ForeName><Initials>DJ</Initials><AffiliationInfo><Affiliation>Department of Medicine, Stanford University School of Medicine, Stanford, California, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hochman</LastName><ForeName>Judith S</ForeName><Initials>JS</Initials><AffiliationInfo><Affiliation>New York University Grossman School of Medicine, New York, New York, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><CollectiveName>ISCHEMIA Research Group</CollectiveName></Author></AuthorList><Language>eng</Language><DataBankList CompleteYN="Y"><DataBank><DataBankName>ClinicalTrials.gov</DataBankName><AccessionNumberList><AccessionNumber>NCT01471522</AccessionNumber></AccessionNumberList></DataBank></DataBankList><GrantList CompleteYN="Y"><Grant><GrantID>UL1 TR001445</GrantID><Acronym>TR</Acronym><Agency>NCATS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>U01 HL105462</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>U01 HL105561</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>U01 HL105907</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>U01 HL105565</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>UL1 TR002243</GrantID><Acronym>TR</Acronym><Agency>NCATS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016448">Multicenter Study</PublicationType><PublicationType UI="D016449">Randomized Controlled Trial</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Am Coll Cardiol</MedlineTA><NlmUniqueID>8301365</NlmUniqueID><ISSNLinking>0735-1097</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>J Am Coll Cardiol. 2022 Feb 22;79(7):662-664</RefSource><PMID Version="1">35177195</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015331" MajorTopicYN="N">Cohort Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000072226" MajorTopicYN="N">Computed Tomography Angiography</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="Y">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003324" MajorTopicYN="N">Coronary Artery Disease</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="Y">diagnostic imaging</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003331" MajorTopicYN="N">Coronary Vessels</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D038622" MajorTopicYN="Y">Internationality</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D055414" MajorTopicYN="N">Myocardial Perfusion Imaging</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D049268" MajorTopicYN="N">Positron-Emission Tomography</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011237" MajorTopicYN="N">Predictive Value of Tests</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000072098" MajorTopicYN="N">Single Photon Emission Computed Tomography Computed Tomography</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="Y">methods</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">coronary CT angiography</Keyword><Keyword MajorTopicYN="N">coronary artery disease</Keyword><Keyword MajorTopicYN="N">stable ischemic heart disease</Keyword><Keyword MajorTopicYN="N">stress testing</Keyword></KeywordList><CoiStatement>Funding Support and Author Disclosures This project was supported in part by Clinical Translational Science Award Nos. 11UL1 TR001445 and UL1 TR002243 from the National Center for Advancing Translational Sciences, and National Heart, Lung, and Blood Institute grants U01HL105907, U01HL105462, and U01HL105561, and U01HL105565. Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the National Center for Advancing Translational Sciences, the National Heart, Lung, and Blood Institute, the National Institutes of Health, or the Department of Health and Human Services. Medications and/or devices were provided by Abbott Vascular, Medtronic, Abbott Laboratories (formerly St. Jude Medical), Royal Philips NV (formerly Volcano Corporation), Omron Healthcare, Amgen, Arbor Pharmaceuticals, AstraZeneca Pharmaceuticals, Merck Sharp &amp; Dohme Corp, Sunovion Pharmaceuticals, and Espero BioPharma. Arbor Pharmaceuticals and AstraZeneca Pharmaceuticals made financial donations. Drs Senior, Reynolds, Min, Berman, Picard, Chaitman, Shaw, Page, Govindan, Sendon, Peteiro, Wander. Drozdz, Marin-Neto, Selvanayagam, Newman, Thuaire, Christopher, Jang, Kwong, Bangalore, Stone, O&#x2019;Brien, Boden, Maron, and Hochman have received grants from the National Heart, Lung, and Blood Institute during the conduct of the study. Dr Hochman is principal investigator for the ISCHEMIA trial. Dr Reynolds has received nonfinancial support from Abbott Vascular; has received nonfinancial support from Siemens; and has received nonfinancial support from BioTelemetry, outside the submitted work. Dr Min has received grants from Cleerly Inc, GE Healthcare, and Arineta, outside the submitted work. Dr Berman has received grants from GE, CSMC Heartflow, and Bayer; and receives software royalties from Cedars-Sinai Medical Center outside the submitted work. Dr Chaitman has received personal fees from Merck, NovoNordisk, Lilly, Johnson and Johnson, Daiichi-Sankyo, Imbria, Xylocor, Sanofi, Tricida, and Xylocor outside the submitted work. Dr Sendon has received grants from Bayer, Merck, Pfizer, Menarini, Sanofi, Boehringer Ingelheim, and Amgen; and has received personal fees from Pfizer, Menarini, Sanofi, and Boehringer Ingelheim outside the submitted work. Dr Bangalore has received grants from Abbott Vascular; and has received personal fees from Abbott Vascular, Biotronik, Pfizer, Amgen, and Reata outside the submitted work. Dr Stone has received personal fees from Terumo, Amaranth, Shockwave, Valfix, TherOx, Reva, Vascular Dynamics, Robocath, HeartFlow, Gore, Ablative Solutions, Matrizyme, Miracor, Neovasc, V-wave, Abiomed, Claret, Sirtex, Ancora, Qool Therapeutics, SpectraWave, MAIA Pharmaceuticals, Orchestra Biomed, and Vectorious; and has received fees from Valfix, Ancora, Qool Therapeutics, Cagent, Applied Therapeutics, Biostar family of funds, MedFocus family of funds, SpectraWave, Orchestra Biomed, Aria, and Cardiac Success, outside the submitted work. Dr Boden has received grants from Abbvie, Amarin, and Amgen; and has received personal fees from Amgen, Cleveland Clinic Clinical Coordinating Center, and Janssen, outside the submitted work.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2021</Year><Month>7</Month><Day>20</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2021</Year><Month>11</Month><Day>3</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2021</Year><Month>11</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>2</Month><Day>18</Day><Hour>5</Hour><Minute>33</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>2</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>3</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35177194</ArticleId><ArticleId IdType="mid">NIHMS1767313</ArticleId><ArticleId IdType="pmc">PMC8875308</ArticleId><ArticleId IdType="doi">10.1016/j.jacc.2021.11.052</ArticleId><ArticleId IdType="pii">S0735-1097(21)08389-3</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Task Force M, Montalescot G, Sechtem U et al. 2013 ESC guidelines on the management of stable coronary artery disease: the Task Force on the management of stable coronary artery disease of the European Society of Cardiology. 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Journal of the American College of Cardiology 1996;27:1171&#x2013;7.</Citation><ArticleIdList><ArticleId IdType="pubmed">8609338</ArticleId></ArticleIdList></Reference><Reference><Citation>Hochman JS Reynolds HR,Bangalore S et al. Baseline Characteristics and Risk Profiles of Participants in the ISCHEMIA Randomized Clinical Trial. JAMA Cardiol 2019;4(3):273&#x2013;86.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6439551</ArticleId><ArticleId IdType="pubmed">30810700</ArticleId></ArticleIdList></Reference><Reference><Citation>Rink LD, Feigenbaum H, Godley RW et al. Echocardiographic detection of left main coronary artery obstruction. Circulation 1982;65:719&#x2013;24.</Citation><ArticleIdList><ArticleId IdType="pubmed">7060251</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35177162</PMID><DateRevised><Year>2022</Year><Month>02</Month><Day>18</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1467-1107</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Feb</Month><Day>18</Day></PubDate></JournalIssue><Title>Cardiology in the young</Title><ISOAbbreviation>Cardiol Young</ISOAbbreviation></Journal>Mini right axillary thoracotomy for congenital heart defect repair can become a safe surgical routine.
Detection of&#xa0;&#x2265;50% diameter stenosis left main coronary artery disease (LMD) has prognostic and therapeutic implications. Noninvasive stress imaging or an exercise tolerance test (ETT) are the most common methods to detect obstructive coronary artery disease, though stress test markers of LMD remain ill-defined.</AbstractText>The authors sought to identify markers of LMD as detected on coronary computed tomography angiography (CTA), using clinical and stress testing parameters.</AbstractText>This was a post hoc analysis of ISCHEMIA (International Study of Comparative Health Effectiveness With Medical and Invasive Approaches), including randomized and nonrandomized participants who had locally determined moderate or severe ischemia on nonimaging ETT, stress nuclear myocardial perfusion imaging, or stress echocardiography followed by CTA to exclude LMD. Stress tests were read by core laboratories. Prior coronary artery bypass grafting was an exclusion. In a stepped multivariate model, the authors identified predictors of LMD, first without and then with stress testing parameters.</AbstractText>Among 5,146 participants (mean age 63 years, 74% male), 414 (8%) had LMD. Predictors of LMD were older age (P&#xa0;&lt; 0.001), male sex (P&#xa0;&lt; 0.01), absence of prior myocardial infarction (P&#xa0;&lt; 0.009), transient ischemic dilation of the left ventricle on stress echocardiography (P&#xa0;=&#xa0;0.05), magnitude of ST-segment depression on ETT (P&#xa0;=&#xa0;0.004), and peak metabolic equivalents achieved on ETT (P&#xa0;=&#xa0;0.001). The models were weakly predictive of LMD (C-index 0.643 and 0.684).</AbstractText>In patients with moderate or severe ischemia, clinical and stress testing parameters were weakly predictive of LMD on CTA. For most patients with moderate or severe ischemia, anatomical imaging is needed to rule out LMD. (International Study of Comparative Health Effectiveness With Medical and Invasive Approaches [ISCHEMIA]; NCT01471522).</AbstractText>Copyright &#xa9; 2022 American College of Cardiology Foundation. All rights reserved.</CopyrightInformation>
2,330,311
[Endoscopic biopsy of a frontal lobe tumor infiltrating the lateral ventricle using intraoperative navigation].
The authors describe the clinical observation of a patient with a paraventricular tumor of the left frontal lobe and demonstrate the effectiveness of endoscopic biopsy of a volumetric mass of such localization through the lateral ventricle using intraoperative navigation. The disease manifested with convulsive seizures two years before the patient was admitted to the hospital. During this period of time, he was repeatedly examined. The dimensions of the volumetric formation remained unchanged. Based on the data obtained, it was not possible to accurately verify the type of tumor. Anticonvulsant therapy was ineffective. The patient underwent surgery - endoscopic partial removal of the tumor (biopsy) and opening of the tumor cyst through the left lateral ventricle using intraoperative navigation. Clinical improvement in the patient's condition was achieved. After the operation, the headaches and the seizures stopped.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Dudanov</LastName><ForeName>I P</ForeName><Initials>IP</Initials><Identifier Source="ORCID">0000-0003-1317-8580</Identifier><AffiliationInfo><Affiliation>Petrozavodsk State University, Petrozavodsk, Russia.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>City Mariinsky Hospital&#xbb;, St. Petersburg, Russia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Podgornyak</LastName><ForeName>M Yu</ForeName><Initials>MY</Initials><Identifier Source="ORCID">0000-0001-8973-5318</Identifier><AffiliationInfo><Affiliation>City Mariinsky Hospital&#xbb;, St. Petersburg, Russia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Legzdain</LastName><ForeName>M A</ForeName><Initials>MA</Initials><Identifier Source="ORCID">0000-0002-6682-3320</Identifier><AffiliationInfo><Affiliation>City Mariinsky Hospital&#xbb;, St. Petersburg, Russia.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Kirov Military Medical Academy, St. Petersburg, Russia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pavlov</LastName><ForeName>O A</ForeName><Initials>OA</Initials><Identifier Source="ORCID">0000-0001-8230-8006</Identifier><AffiliationInfo><Affiliation>City Mariinsky Hospital&#xbb;, St. Petersburg, Russia.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Kirov Military Medical Academy, St. Petersburg, Russia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Simeshchenko</LastName><ForeName>P I</ForeName><Initials>PI</Initials><Identifier Source="ORCID">0000-0002-2684-2156</Identifier><AffiliationInfo><Affiliation>City Mariinsky Hospital&#xbb;, St. Petersburg, Russia.</Affiliation></AffiliationInfo></Author></AuthorList><Language>rus</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><VernacularTitle>Endoskopicheskaya biopsiya opukholi lobnoi doli golovnogo mozga, prorastayushchei v bokovoi zheludochek, s ispol'zovaniem intraoperatsionnoi navigatsii.</VernacularTitle></Article><MedlineJournalInfo><Country>Russia (Federation)</Country><MedlineTA>Zh Nevrol Psikhiatr Im S S Korsakova</MedlineTA><NlmUniqueID>9712194</NlmUniqueID><ISSNLinking>1997-7298</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D001706" MajorTopicYN="N">Biopsy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004724" MajorTopicYN="Y">Endoscopy</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005625" MajorTopicYN="N">Frontal Lobe</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020547" MajorTopicYN="Y">Lateral Ventricles</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012640" MajorTopicYN="N">Seizures</DescriptorName></MeshHeading></MeshHeadingList><OtherAbstract Type="Publisher" Language="rus">&#x41e;&#x43f;&#x438;&#x441;&#x430;&#x43d;&#x43e; &#x43a;&#x43b;&#x438;&#x43d;&#x438;&#x447;&#x435;&#x441;&#x43a;&#x43e;&#x435; &#x43d;&#x430;&#x431;&#x43b;&#x44e;&#x434;&#x435;&#x43d;&#x438;&#x435; &#x43f;&#x430;&#x446;&#x438;&#x435;&#x43d;&#x442;&#x430; &#x441; &#x43f;&#x430;&#x440;&#x430;&#x432;&#x435;&#x43d;&#x442;&#x440;&#x438;&#x43a;&#x443;&#x43b;&#x44f;&#x440;&#x43d;&#x43e;&#x439; &#x43e;&#x43f;&#x443;&#x445;&#x43e;&#x43b;&#x44c;&#x44e; &#x43b;&#x435;&#x432;&#x43e;&#x439; &#x43b;&#x43e;&#x431;&#x43d;&#x43e;&#x439; &#x434;&#x43e;&#x43b;&#x438; &#x438; &#x43f;&#x440;&#x43e;&#x434;&#x435;&#x43c;&#x43e;&#x43d;&#x441;&#x442;&#x440;&#x438;&#x440;&#x43e;&#x432;&#x430;&#x43d;&#x430; &#x44d;&#x444;&#x444;&#x435;&#x43a;&#x442;&#x438;&#x432;&#x43d;&#x43e;&#x441;&#x442;&#x44c; &#x44d;&#x43d;&#x434;&#x43e;&#x441;&#x43a;&#x43e;&#x43f;&#x438;&#x447;&#x435;&#x441;&#x43a;&#x43e;&#x439; &#x431;&#x438;&#x43e;&#x43f;&#x441;&#x438;&#x438; &#x43e;&#x431;&#x44a;&#x435;&#x43c;&#x43d;&#x43e;&#x433;&#x43e; &#x43e;&#x431;&#x440;&#x430;&#x437;&#x43e;&#x432;&#x430;&#x43d;&#x438;&#x44f; 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&#x43f;&#x430;&#x446;&#x438;&#x435;&#x43d;&#x442;&#x430; &#x432; &#x441;&#x442;&#x430;&#x446;&#x438;&#x43e;&#x43d;&#x430;&#x440;. &#x412; &#x442;&#x435;&#x447;&#x435;&#x43d;&#x438;&#x435; &#x44d;&#x442;&#x43e;&#x433;&#x43e; &#x43f;&#x435;&#x440;&#x438;&#x43e;&#x434;&#x430; &#x432;&#x440;&#x435;&#x43c;&#x435;&#x43d;&#x438; &#x43d;&#x435;&#x43e;&#x434;&#x43d;&#x43e;&#x43a;&#x440;&#x430;&#x442;&#x43d;&#x43e; &#x43e;&#x431;&#x441;&#x43b;&#x435;&#x434;&#x43e;&#x432;&#x430;&#x43b;&#x441;&#x44f;, &#x440;&#x430;&#x437;&#x43c;&#x435;&#x440;&#x44b; &#x43e;&#x431;&#x44a;&#x435;&#x43c;&#x43d;&#x43e;&#x433;&#x43e; &#x43e;&#x431;&#x440;&#x430;&#x437;&#x43e;&#x432;&#x430;&#x43d;&#x438;&#x44f; &#x43e;&#x441;&#x442;&#x430;&#x432;&#x430;&#x43b;&#x438;&#x441;&#x44c; &#x431;&#x435;&#x437; &#x438;&#x437;&#x43c;&#x435;&#x43d;&#x435;&#x43d;&#x438;&#x439;. &#x41d;&#x430; &#x43e;&#x441;&#x43d;&#x43e;&#x432;&#x430;&#x43d;&#x438;&#x438; &#x43f;&#x43e;&#x43b;&#x443;&#x447;&#x435;&#x43d;&#x43d;&#x44b;&#x445; &#x434;&#x430;&#x43d;&#x43d;&#x44b;&#x445; &#x442;&#x43e;&#x447;&#x43d;&#x43e; &#x432;&#x435;&#x440;&#x438;&#x444;&#x438;&#x446;&#x438;&#x440;&#x43e;&#x432;&#x430;&#x442;&#x44c; &#x442;&#x438;&#x43f; &#x43e;&#x43f;&#x443;&#x445;&#x43e;&#x43b;&#x438; &#x43d;&#x435; &#x43f;&#x440;&#x435;&#x434;&#x441;&#x442;&#x430;&#x432;&#x43b;&#x44f;&#x43b;&#x43e;&#x441;&#x44c; &#x432;&#x43e;&#x437;&#x43c;&#x43e;&#x436;&#x43d;&#x44b;&#x43c;. &#x41f;&#x440;&#x43e;&#x442;&#x438;&#x432;&#x43e;&#x44d;&#x43f;&#x438;&#x43b;&#x435;&#x43f;&#x442;&#x438;&#x447;&#x435;&#x441;&#x43a;&#x430;&#x44f; &#x442;&#x435;&#x440;&#x430;&#x43f;&#x438;&#x44f; &#x431;&#x44b;&#x43b;&#x430; &#x43d;&#x435;&#x44d;&#x444;&#x444;&#x435;&#x43a;&#x442;&#x438;&#x432;&#x43d;&#x43e;&#x439;. &#x411;&#x43e;&#x43b;&#x44c;&#x43d;&#x43e;&#x43c;&#x443; &#x43f;&#x440;&#x43e;&#x432;&#x435;&#x434;&#x435;&#x43d;&#x43e; &#x44d;&#x43d;&#x434;&#x43e;&#x441;&#x43a;&#x43e;&#x43f;&#x438;&#x447;&#x435;&#x441;&#x43a;&#x43e;&#x435; &#x447;&#x430;&#x441;&#x442;&#x438;&#x447;&#x43d;&#x43e;&#x435; &#x443;&#x434;&#x430;&#x43b;&#x435;&#x43d;&#x438;&#x435; &#x43e;&#x43f;&#x443;&#x445;&#x43e;&#x43b;&#x438; (&#x431;&#x438;&#x43e;&#x43f;&#x441;&#x438;&#x44f;) &#x438; &#x432;&#x441;&#x43a;&#x440;&#x44b;&#x442;&#x438;&#x435; &#x43a;&#x438;&#x441;&#x442;&#x44b; &#x43e;&#x43f;&#x443;&#x445;&#x43e;&#x43b;&#x438; &#x447;&#x435;&#x440;&#x435;&#x437; &#x43b;&#x435;&#x432;&#x44b;&#x439; &#x431;&#x43e;&#x43a;&#x43e;&#x432;&#x43e;&#x439; &#x436;&#x435;&#x43b;&#x443;&#x434;&#x43e;&#x447;&#x435;&#x43a; &#x441; &#x43f;&#x440;&#x438;&#x43c;&#x435;&#x43d;&#x435;&#x43d;&#x438;&#x435;&#x43c; &#x438;&#x43d;&#x442;&#x440;&#x430;&#x43e;&#x43f;&#x435;&#x440;&#x430;&#x446;&#x438;&#x43e;&#x43d;&#x43d;&#x43e;&#x439; &#x43d;&#x430;&#x432;&#x438;&#x433;&#x430;&#x446;&#x438;&#x438;. &#x414;&#x43e;&#x441;&#x442;&#x438;&#x433;&#x43d;&#x443;&#x442;&#x43e; &#x43a;&#x43b;&#x438;&#x43d;&#x438;&#x447;&#x435;&#x441;&#x43a;&#x43e;&#x435; &#x443;&#x43b;&#x443;&#x447;&#x448;&#x435;&#x43d;&#x438;&#x435; &#x432; &#x441;&#x43e;&#x441;&#x442;&#x43e;&#x44f;&#x43d;&#x438;&#x438; &#x43f;&#x430;&#x446;&#x438;&#x435;&#x43d;&#x442;&#x430;. &#x41f;&#x43e;&#x441;&#x43b;&#x435; &#x43e;&#x43f;&#x435;&#x440;&#x430;&#x446;&#x438;&#x438; &#x43f;&#x435;&#x440;&#x435;&#x441;&#x442;&#x430;&#x43b;&#x438; &#x431;&#x435;&#x441;&#x43f;&#x43e;&#x43a;&#x43e;&#x438;&#x442;&#x44c; &#x433;&#x43e;&#x43b;&#x43e;&#x432;&#x43d;&#x44b;&#x435; &#x431;&#x43e;&#x43b;&#x438;, &#x43f;&#x440;&#x435;&#x43a;&#x440;&#x430;&#x442;&#x438;&#x43b;&#x438;&#x441;&#x44c; &#x441;&#x443;&#x434;&#x43e;&#x440;&#x43e;&#x436;&#x43d;&#x44b;&#x435; &#x43f;&#x440;&#x438;&#x441;&#x442;&#x443;&#x43f;&#x44b;.
2,330,312
Fully automated intracardiac 4D flow MRI post-processing using deep learning for biventricular segmentation.
4D flow MRI allows for a comprehensive assessment of intracardiac blood flow, useful for assessing cardiovascular diseases, but post-processing requires time-consuming ventricular segmentation throughout the cardiac cycle and is prone to subjective errors. Here, we evaluate the use of automatic left and right ventricular (LV and RV) segmentation based on deep learning (DL) network that operates on short-axis cine bSSFP images.</AbstractText>A previously published DL network was fine-tuned via retraining on a local database of 106 subjects scanned at our institution. In 26 test subjects, the ventricles were segmented automatically by the network and manually by 3 human observers on bSSFP MRI. The bSSFP images were then registered to the corresponding 4D flow images to apply the segmentation to 4D flow velocity data. Dice coefficients and the relative deviation between measurements (automatic vs. manual and interobserver manual) of various hemodynamic parameters were assessed.</AbstractText>The automated segmentation resulted in similar Dice scores (LV: 0.92, RV: 0.86) and lower relative deviations from manual segmentation in left ventricular (LV) average kinetic energy (KE) (8%) and RV KE (15%) than the Dice scores (LV: 0.91, RV: 0.87) and relative deviations between manual segmentation observers (LV KE: 11%, p = 0.01; RV KE: 19%, p = 0.03).</AbstractText>The automated post-processing method using deep learning resulted in hemodynamic measurements that differ from a manual observer's measurements equally or less than the variation between manual observers. This approach can be used to decrease post-processing time on intraventricular 4D flow data and mitigate interobserver variability.</AbstractText>&#x2022; Our proposed method allows for fully automated post-processing of intraventricular 4D flow MRI data. &#x2022; Our method resulted in hemodynamic measurements that matched those derived from manual segmentation equally as well as interobserver variability. &#x2022; Our method can be used to greatly accelerate intraventricular 4D flow post-processing and improve interobserver repeatability.</AbstractText>&#xa9; 2022. The Author(s), under exclusive licence to European Society of Radiology.</CopyrightInformation>
2,330,313
Transcriptional heterogeneity of ventricular zone cells in the ganglionic eminences of the mouse forebrain.
The ventricular zone (VZ) of the nervous system contains radial glia cells that were originally considered relatively homogenous in their gene expression, but a detailed characterization of transcriptional diversity in these VZ cells has not been reported. Here, we performed single-cell RNA sequencing to characterize transcriptional heterogeneity of neural progenitors within the VZ and subventricular zone (SVZ) of the ganglionic eminences (GEs), the source of all forebrain GABAergic neurons. By using a transgenic mouse line to enrich for VZ cells, we characterize significant transcriptional heterogeneity, both between GEs and within spatial subdomains of specific GEs. Additionally, we observe differential gene expression between E12.5 and E14.5 VZ cells, which could provide insights into temporal changes in cell fate. Together, our results reveal a previously unknown spatial and temporal genetic diversity of VZ cells in the ventral forebrain that will aid our understanding of initial fate decisions in the forebrain.
2,330,314
A robotic magnetic resonance-guided high-intensity focused ultrasound platform for neonatal neurosurgery: Assessment of targeting accuracy and precision in a brain phantom.
Intraventricular hemorrhage (IVH) is one of the most serious neurovascular complications resulting from premature birth. It can result in clotting of blood within the ventricles, which causes a buildup of cerebrospinal fluid that can lead to posthemorrhagic ventricular dilation and posthemorrhagic hydrocephalus. Currently, there are no direct treatments for these blood clots as the standard of care is invasive surgery to insert a shunt. Magnetic resonance-guided high-intensity focused ultrasound (MRgHIFU) has been investigated as a noninvasive treatment to lyse blood clots. However, current MRgHIFU systems are not suitable in the context of treating IVH in neonates.</AbstractText>We have developed a robotic MRgHIFU neurosurgical platform designed to treat the neonatal brain. This platform facilitates ergonomic patient positioning and directs treatment through their open anterior fontanelle while providing a larger treatment volume. The platform is based on an MR-compatible robot developed by our group. Further development of the platform has warranted investigation of its targeting ability to assess its feasibility in the neonatal brain. This study aimed to quantify the platform's targeting accuracy, precision, and repeatability using a brain phantom and clinical MRI system.</AbstractText>A thermosensitive brain-mimicking phantom was developed to test the platform's targeting accuracy. Rectangular grid patterns were created with HIFU thermal energy "lesions" in the phantoms by targeting specific coordinate points. The intended target locations were demarcated by inserting carbon fiber rods through a targeting assessment template. Coordinates for the intended and actual targets were derived from T2-weighted MRI scans, and the centroid distance between them was measured. Subsequently, the platform's targeting accuracy was quantified according to equations derived from ISO Standard 9283:1998.</AbstractText>HIFU ablation resulted in distinct thermal lesions within the thermosensitive phantoms, which appeared as discrete hypointense regions in T2-weighted MR scans. A total of 127 target points were included in the data analysis, which yielded a targeting accuracy of 0.6&#xa0;mm and targeting precision of 1.2&#xa0;mm.</AbstractText>The robotic MRgHIFU platform was shown to have a high degree of accuracy, precision, and repeatability. The results demonstrate the platform's functionality when targeting through simulated brain matter. These results serve as an initial verification of the platform targeting ability and showed promise toward the final application in a neonatal brain.</AbstractText>&#xa9; 2022 American Association of Physicists in Medicine.</CopyrightInformation>
2,330,315
Systematic scoping review of papilledema in vestibular schwannoma without hydrocephalus.
Vestibular schwannoma is a common pathology encountered by neurosurgeons worldwide. Often vestibular schwannoma presents with obstructive hydrocephalus. Papilledema is present in 8% of the patients with vestibular schwannoma, primarily due to obstructive hydrocephalus. Hyperproteinorrhachia is believed to be responsible for papilledema in the absence of hydrocephalus in vestibular schwannoma. However, there is a paucity of literature on the mechanism of papilledema in vestibular schwannoma patients with hydrocephalus.</AbstractText>The aim of this study was to conduct a scoping review of scientific literature on papilledema in vestibular schwannoma patients without hydrocephalus.</AbstractText>Design: This was a systematic scoping review and critical appraisal. Literature Search from PubMed was done following PRISMA-ScR (Preferred Reporting Items for Systematic Reviews and Meta-Analyses Extension for Scoping Reviews) and Joanna Briggs Institute guidelines for conducting and reporting scoping reviews.</AbstractText>A total of seven studies, including eight patients, were identified for inclusion in the review. The studies were heterogeneous in terms of reporting for various variables. All the included studies were case reports, with the earliest publication in 1954 and the latest publication in 2020. The mean age of the patients in the included studies was 35 years, with a minimum age of 20 years and maximum age of 64 years. Approximately 62.5% were females, and 37.5% were males in the included study. Only three studies have studied cerebrospinal fluid (CSF) proteins levels in these patients.</AbstractText>There is paucity in literature and a lack of evidence to conclusively state hyperproteinorrhachia as an antecedent to the development of papilledema in vestibular schwannoma patients without hydrocephalus. Younger age and female gender are risk factors for developing papilledema in the absence of hydrocephalus in vestibular schwannoma patients. Brainstem compression due to the large size of vestibular schwannoma can still have a patent aqueduct of Sylvius and no obstruction to CSF flow. The development of papilledema in vestibular schwannoma is a complex interplay of multiple factors that must be studied comprehensively for complete understanding.</AbstractText>
2,330,316
miR-137 and miR-122, two outer subventricular zone non-coding RNAs, regulate basal progenitor expansion and neuronal differentiation.
Cortical expansion in primate brains relies on enlargement of germinal zones during a prolonged developmental period. Although most mammals have two cortical germinal zones, the ventricular zone (VZ) and subventricular zone (SVZ), gyrencephalic species display an additional germinal zone, the outer subventricular zone (oSVZ), which increases the number and diversity of neurons generated during corticogenesis. How the oSVZ emerged during evolution is poorly understood, but recent studies suggest a role for non-coding RNAs, which allow tight genetic program regulation during development. Here, using in&#xa0;vivo functional genetics, single-cell RNA sequencing, live imaging, and electrophysiology to assess progenitor and neuronal properties in mice, we identify two oSVZ-expressed microRNAs (miRNAs), miR-137 and miR-122, which regulate key cellular features of cortical expansion. miR-137 promotes basal progenitor self-replication and superficial layer neuron fate, whereas miR-122 decreases the pace of neuronal differentiation. These findings support a cell-type-specific role of miRNA-mediated gene expression in cortical expansion.
2,330,317
Ellagic acid and allopurinol decrease H<sub>2</sub>O<sub>2</sub> concentrations, epileptiform activity and astrogliosis after status epilepticus in the hippocampus of adult rats.
Status epilepticus (SE) can result in an overproduction of hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>), which contributes to oxidative stress and brain injury during different phases of epileptogenesis and seizures. The purpose of this study was to evaluate the effects of ellagic acid and allopurinol administered after SE on H<sub>2</sub>O<sub>2</sub> concentrations, electrical activity and GFAP immunoreactivity in the hippocampus of rats evaluated on Day 18 after SE. H<sub>2</sub>O<sub>2</sub> levels were measured using an online technique with high temporal resolution and simultaneous electrical activity recording. For this purpose, the lateral ventricles of male Wistar rats (200-250&#xa0;g) were injected with pilocarpine (2.4&#xa0;mg/2&#xa0;&#xb5;l) to induce SE. After SE, rats were injected with ellagic acid (50&#xa0;mg/kg i.p., and two additional doses at 24 and 48&#xa0;h) or allopurinol (50&#xa0;mg/kg i.p., single dose). Administration of ellagic acid or allopurinol after SE significantly reduced the H<sub>2</sub>O<sub>2</sub> concentrations and decreased the presence of epileptiform activity and GFAP immunoreactivity in the hippocampus 18&#xa0;days after SE. In conclusion, the administration of antioxidants potentially reduces oxidative stress, which indicates the possible attenuation of the neurobiological consequences after SE.
2,330,318
Effects of vasopressin administration in the oral cavity on cardiac function and hemodynamics in rats.
The vasoconstrictive effect of epinephrine in local anesthetics affects the heart, which leads to hesitation among dentists in injecting local anesthetics into patients with cardiovascular disease. Due to its vasoconstrictive effects, the present study investigated the effects of vasopressin administration on cardiac function in rats.</AbstractText>Experiment 1 aimed to determine the vasopressin concentration that could affect cardiac function. An arterial catheter was inserted into the male Wistar rats. Next, 0.03, 0.3, and 3.0 U/mL arginine vasopressin (AVP) (0.03V, 0.3V, and 3.0V) was injected into the tongue, and the blood pressure was measured. The control group received normal saline only. In Experiment 2, following anesthesia infiltration, a pressure-volume catheter was placed in the left ventricle. Baseline values of end-systolic elastance, end-diastolic volume, end-systolic pressure, stroke work, stroke volume, and end-systolic elastance were recorded. Next, normal saline and 3.0V AVP were injected into the tongue to measure their effect on hemodynamic and cardiac function.</AbstractText>After 3.0V administration, systolic blood pressures at 10 and 15 min were higher than those of the control group; they increased at 10 min compared with those at baseline. The diastolic blood pressures at 5-15 min were higher than those of the control group; they increased at 5 and 10 min compared with those at baseline. The preload decreased at 5 and 10 min compared to that at baseline. However, the afterload increased from 5 to 15 min compared with that of the control group; it increased at 10 min compared with that at baseline. Stroke volume decreased at 10 and 15 min compared with that of the control group; it decreased from 5 to 15 min compared with that at baseline. Stroke work decreased from 5 to 15 min compared with that of the control group; it decreased from 5 to 15 min compared with that at baseline.</AbstractText>Our results showed that 3.0 U/mL concentration of vasopressin resulted in increased blood pressure, decreased stroke volume and stoke work, decreased preload and increased afterload, without any effect on myocardial contractility.</AbstractText>Copyright &#xa9; 2022 Journal of Dental Anesthesia and Pain Medicine.</CopyrightInformation>
2,330,319
Gamma knife radiosurgery cured hydrocephalus in non-hemorrhagic brain stem arteriovenous malformation.
A 13-year-old boy, with a history of intermittent headache and transient diplopia, was found to have non-hemorrhagic cerebral arteriovenous malformation in the midbrain tegmental region associated with hydrocephalus. Gamma knife radiosurgery was performed at 16 Gy with 75% marginal dose. Posttreatment course was uneventful. Follow-up MR imaging at one year after the treatment revealed complete disappearance of the abnormal vascular flow voids. The size of each ventricle at the treatment and at one year after treatment were as follows; 60.2 cc and 20.9 cc in the lateral ventricles, 3.7 cc and 2.7 cc in the third ventricle. The hydrocephalus might be caused by obstructive mechanism but mostly by high venous pressure due to the shunt blood flow. The goal of treatment for hydrocephalus should be nidus obstruction and normalizing the vascular flow.
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[Evolving Exploration of the Pathogenesis of CNS Germ Cell Tumors with Regard to Precision Medicine].
Genomic and epigenomic analyses have progressed the exploration of the pathogenesis of CNS germ cell tumors(GCTs)in the past decade. GCTs are characterized by mutations in MAPK or PI3K pathways(55%)and unstable chromosomes, especially 12p gain(45%), as well as global hypomethylation in germinoma. Highly specific microRNA, miR-371a-3p, can be a diagnostic marker in serum and cerebrospinal fluid. Tumor cell content examined in H-E specimens has a prognostic value in germinoma: cases with higher tumor cell content show a worse prognosis. 12p gain in non-germinomatous GCTs(NGGCTs)has an unfavorable prognostic significance. PD-L1 and PD-1 are highly expressed in germinomas and the tumor cell microenvironment, respectively, highlighting the potential effectiveness of immune checkpoint inhibitors. Clinical trials from the Children's Oncology Group(COG)in the US and the Society for Paediatric Oncology(SIOP)in Europe and Japan have shown that whole ventricular irradiation is the most appropriate for germinomas, and that radiation fields can be reduced to the whole ventricle or a local area for localized NGGCTs. Toward personalized medicine, investigations into the structural abnormalities and variants in non-coding regions are needed to develop targeted therapy. A stratified treatment regimen is expected by incorporating newly-found biomarkers to reduce the treatment burden for generally young patients and circumvent late toxicity and sequelae. Establishing effective treatments is crucial for relapsed GCT that has a dismal prognosis.
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Stereotactic Ventriculostomy Guide.
Introduction Based on the anatomy of the frontal horn, a stereotactic ventriculostomy guidance system that does not need an elaborate setup and is suitable for ventricles of all sizes was developed.&#xa0;The objective of this paper is to describe this system and present the results of a cadaveric study in which this system was used. Method The system has a midline-based plate that is contoured to snugly fit the top of the head. It has two probe holders, one on each side at pre-set angles in coronal and sagittal planes, which enables the probe holders to point at the foramen of Monro. A cadaver study was done on eight donors.&#xa0;First, using the guidance system a 1.4 mm endoscope was inserted into the right frontal horn through a twist drill hole. Next, the scope was inserted into the right frontal horn on the same donors using the freehand method. Result With the guide, all eight ventricles were entered into on the first trial, and the foramen of Monro was visible end-on. With freehand technique: six ventricles were entered on the first try; however, the foramen of Monro was visible end-on only in one. In the other two, two to three&#xa0;attempts were needed. The guide facilitated 100% visibility for the end-on visibility of the foramen of Monro upon insertion and the results were statistically significant with t=7, df=7, p-value=0.000106. Conclusion This is a simple system, which is easy to use. The cadaveric study showed a high degree of accuracy to access the ventricles. The data shows significant improvement compared to the freehand technique.
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Analysis of a Novel Entry Point for Freehand Ventriculostomy Using Computerized Tomography Scans.
Background External ventricular drain (EVD)&#xa0;placement is one of the most common procedures in neurosurgery. Neurosurgeons generally prefer to access the ventricles via Kocher's point since it is the most common point of entry to this area; however, this point is used to describe different anatomic landmarks and is not well-defined. Objective The present study aims to describe and provide an anatomical assessment of a novel ventriculostomy access point&#xa0;developed by the authors using computerized tomography (CT) scans performed on 100 patients. Materials and methods Data were collected from 100 randomly selected patients with normal ventricular anatomy found on their 1.0 mm-slice CT scans&#xa0;performed at the Burdenko Neurosurgical Center from March 2019 to June 2021. The CT inclusion criteria were: CT slices&#xa0;&lt; or = to 1 mm and absence of&#xa0;brain herniation. Patients with brain mass lesions, severe brain edema, and pneumocephalus were excluded. Age, gender, and ventricular size were not&#xa0;exclusion criteria. Results The mean patient age was 43.58 years (range 4-73),&#xa0;with 50 men and 50 women. The mean Evan's index was 25.7 % (SD=4.38 %, range 10.2-41.0 %). No differences were found between the angles of EVD placement on either side&#xa0;(89.50&#xb1;1.22 degrees on the right and 89.60&#xb1;1.14 degrees on the left). Hence, nearly all EVD cases had been placed perpendicularly to the skull surface at a pinpoint location. Conclusion The proposed point of successful ventriculostomy placement in this study was 3 cm from the bregma along the coronal suture. The angle of EVD placement was approximately 90 degrees in almost all patients and was independent of the patient's age and the side of the head that was entered. Little correlation&#xa0;was found between the value of the entry angle and Evan's index. The point is simply identifiable, and its entry is easily accessible in practice.
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Central Nervous System Stimulants Limit Caffeine Transport at the Blood-Cerebrospinal Fluid Barrier.
Caffeine, a common ingredient in energy drinks, crosses the blood-brain barrier easily, but the kinetics of caffeine across the blood-cerebrospinal fluid barrier (BCSFB) has not been investigated. Therefore, 127 autopsy cases (Group A, 30 patients, stimulant-detected group; and Group B, 97 patients, no stimulant detected group) were examined. In addition, a BCSFB model was constructed using human vascular endothelial cells and human choroid plexus epithelial cells separated by a filter, and the kinetics of caffeine in the BCSFB and the effects of 4-aminopyridine (4-AP), a neuroexcitatory agent, were studied. Caffeine concentrations in right heart blood (Rs) and cerebrospinal fluid (CSF) were compared in the autopsy cases: caffeine concentrations were higher in Rs than CSF in Group A compared to Group B. In the BCSFB model, caffeine and 4-AP were added to the upper layer, and the concentration in the lower layer of choroid plexus epithelial cells was measured. The CSF caffeine concentration was suppressed, depending on the 4-AP concentration. Histomorphological examination suggested that choroid plexus epithelial cells were involved in inhibiting the efflux of caffeine to the CSF. Thus, the simultaneous presence of stimulants and caffeine inhibits caffeine transfer across the BCSFB.
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The Effect of RADA16-I and CDNF on Neurogenesis and Neuroprotection in Brain Ischemia-Reperfusion Injury.
Scaffold materials, neurotrophic factors, and seed cells are three elements of neural tissue engineering. As well-known self-assembling peptide-based hydrogels, RADA16-I and modified peptides are attractive matrices for neural tissue engineering. In addition to its neuroprotective effects, cerebral dopamine neurotrophic factor (CDNF) has been reported to promote the proliferation, migration, and differentiation of neural stem cells (NSCs). However, the role of RADA16-I combined with CDNF on NSCs remains unknown. First, the effect of RADA16-I hydrogel and CDNF on the proliferation and differentiation of cultured NSCs was investigated. Next, RADA16-I hydrogel and CDNF were microinjected into the lateral ventricle (LV) of middle cerebral artery occlusion (MCAO) rats to activate endogenous NSCs. CDNF promoted the proliferation of NSCs, while RADA16-I induced the neural differentiation of NSCs in vitro. Importantly, both RADA16-I and CDNF promoted the proliferation, migration, and differentiation of endogenous NSCs by activating the ERK1/2 and STAT3 pathways, and CDNF exerted an obvious neuroprotective effect on brain ischemia-reperfusion injury. These findings provide new information regarding the application of the scaffold material RADA16-I hydrogel and the neurotrophic factor CDNF in neural tissue engineering and suggest that RADA16-I hydrogel and CDNF microinjection may represent a novel therapeutic strategy for the treatment of stroke.
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Metabolites and Genes behind Cardiac Metabolic Remodeling in Mice with Type 1 Diabetes Mellitus.
Metabolic remodeling is at the heart of diabetic cardiomyopathy. High glycemic fluctuations increase metabolic stress in the type 1 diabetes mellitus (T1DM) heart. There is a lack of understanding on how metabolites and genes affect metabolic remodeling in the T1DM heart. We hypothesize that differential expression of metabolic genes and metabolites synergistically influence metabolic remodeling preceding T1DM cardiomyopathy. To test our hypothesis, we conducted high throughput analysis of hearts from adult male hyperglycemic <i>Ins2</i><sup>+/-</sup> (Akita) and littermate normoglycemic <i>Ins2</i><sup>+/+</sup> (WT) mice. The Akita mouse is a spontaneous, genetic model of T1DM that develops increased levels of consistent glycemic variability without the off-target cardiotoxic effects present in chemically- induced models of T1DM. After validating the presence of a T1DM phenotype, we conducted metabolomics via LC-MS analysis and genomics via next-generation sequencing in left ventricle tissue from the Akita heart. Ingenuity Pathway Analyses revealed that 108 and 30 metabolic pathways were disrupted within the metabolomics and genomics datasets, respectively. Notably, a comparison between the two analyses showed 15 commonly disrupted pathways, including ketogenesis, ketolysis, cholesterol biosynthesis, acetyl CoA hydrolysis, and fatty acid biosynthesis and beta-oxidation. These identified metabolic pathways predicted by the differential expression of metabolites and genes provide the foundation for understanding metabolic remodeling in the T1DM heart. By limited experiment, we revealed a predicted disruption in the metabolites and genes behind T1DM cardiac metabolic derangement. Future studies targeting these genes and metabolites will unravel novel therapies to prevent/improve metabolic remodeling in the T1DM heart.
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Interplay of Ferritin Accumulation and Ferroportin Loss in Ageing Brain: Implication for Protein Aggregation in Down Syndrome Dementia, Alzheimer's, and Parkinson's Diseases.
Iron accumulates in the ageing brain and in brains with neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and Down syndrome (DS) dementia. However, the mechanisms of iron deposition and regional selectivity in the brain are ill-understood. The identification of several proteins that are involved in iron homeostasis, transport, and regulation suggests avenues to explore their function in neurodegenerative diseases. To uncover the molecular mechanisms underlying this association, we investigated the distribution and expression of these key iron proteins in brain tissues of patients with AD, DS, PD, and compared them with age-matched controls. Ferritin is an iron storage protein that is deposited in senile plaques in the AD and DS brain, as well as in neuromelanin-containing neurons in the Lewy bodies in PD brain. The transporter of ferrous iron, Divalent metal protein 1 (DMT1), was observed solely in the capillary endothelium and in astrocytes close to the ventricles with unchanged expression in PD. The principal iron transporter, ferroportin, is strikingly reduced in the AD brain compared to age-matched controls. Extensive blood vessel damage in the basal ganglia and deposition of punctate ferritin heavy chain (FTH) and hepcidin were found in the caudate and putamen within striosomes/matrix in both PD and DS brains. We suggest that downregulation of ferroportin could be a key reason for iron mismanagement through disruption of cellular entry and exit pathways of the endothelium. Membrane damage and subsequent impairment of ferroportin and hepcidin causes oxidative stress that contributes to neurodegeneration seen in DS, AD, and in PD subjects. We further propose that a lack of ferritin contributes to neurodegeneration as a consequence of failure to export toxic metals from the cortex in AD/DS and from the substantia nigra and caudate/putamen in PD brain.
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Aging Activates the Immune System and Alters the Regenerative Capacity in the Zebrafish Heart.
Age-associated organ failure and degenerative diseases have a major impact on human health. Cardiovascular dysfunction has an increasing prevalence with age and is one of the leading causes of death. In contrast to humans, zebrafish have extraordinary regeneration capacities of complex organs including the heart. In addition, zebrafish has recently become a model organism in research on aging. Here, we have compared the ventricular transcriptome as well as the regenerative capacity after cryoinjury of old and young zebrafish hearts. We identified the immune system as activated in old ventricles and found muscle organization to deteriorate upon aging. Our data show an accumulation of immune cells, mostly macrophages, in the old zebrafish ventricle. Those immune cells not only increased in numbers but also showed morphological and behavioral changes with age. Our data further suggest that the regenerative response to cardiac injury is generally impaired and much more variable in old fish. Collagen in the wound area was already significantly enriched in old fish at 7 days post injury. Taken together, these data indicate an 'inflammaging'-like process in the zebrafish heart and suggest a change in regenerative response in the old.
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Essential Roles of Efferent Duct Multicilia in Male Fertility.
Cilia are microtubule-based hair-like organelles on the cell surface. Cilia have been implicated in various biological processes ranging from mechanosensation to fluid movement. Ciliary dysfunction leads to a plethora of human diseases, known as ciliopathies. Although non-motile primary cilia are ubiquitous, motile multicilia are found in restricted locations of the body, such as the respiratory tract, the oviduct, the efferent duct, and the brain ventricles. Multicilia beat in a whip-like motion to generate fluid flow over the apical surface of an epithelium. The concerted ciliary motion provides the driving force critical for clearing airway mucus and debris, transporting ova from the ovary to the uterus, maintaining sperm in suspension, and circulating cerebrospinal fluid in the brain. In the male reproductive tract, multiciliated cells (MCCs) were first described in the mid-1800s, but their importance in male fertility remained elusive until recently. MCCs exist in the efferent ducts, which are small, highly convoluted tubules that connect the testis to the epididymis and play an essential role in male fertility. In this review, we will introduce multiciliogenesis, discuss mouse models of male infertility with defective multicilia, and summarize our current knowledge on the biological function of multicilia in the male reproductive tract.
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Dlx1/2-dependent expression of Meis2 promotes neuronal fate determination in the mammalian striatum.
The striatum is a central regulator of behavior and motor function through the actions of D1 and D2 medium-sized spiny neurons (MSNs), which arise from a common lateral ganglionic eminence (LGE) progenitor. The molecular mechanisms of cell fate specification of these two neuronal subtypes are incompletely understood. Here, we found that deletion of murine Meis2, which is highly expressed in the LGE and derivatives, led to a large reduction in striatal MSNs due to a block in their differentiation. Meis2 directly binds to the Zfp503 and Six3 promoters and is required for their expression and specification of D1 and D2 MSNs, respectively. Finally, Meis2 expression is regulated by Dlx1/2 at least partially through the enhancer hs599 in the LGE subventricular zone. Overall, our findings define a pathway in the LGE whereby Dlx1/2 drives expression of Meis2, which subsequently promotes the fate determination of striatal D1 and D2 MSNs via Zfp503 and Six3.
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Case Report: Need for Caution in the Diagnosis of GFAP Astrocytopathy-A Case of GFAP Astrocytopathy Coexistent With Primary Central Nervous System Lymphoma.
We reported a case of primary central nervous system lymphoma (PCNSL) coexistent with glial fibrillary acidic protein (GFAP) astrocytopathy, and discussed the problems needing attention in the diagnosis and differential diagnosis of GFAP astrocytopathy. Our patient was a 51-year-old female who presented with somnolence for a month, and memory declination for 10 days. Brain magnetic resonance imaging (MRI) demonstrated multiple abnormal enhancement lesions in bilateral basal ganglia and around the third ventricle, as well as transient T2-weighted hyper-intensity lesions at the splenium of the corpus callosum during the course of the disease. The cerebrospinal fluid (CSF) was positive for anti-GFAP antibodies by antigen-transfected HEK293 cell-based assay (indirect immunofluorescence assay). She was initially diagnosed with autoimmune GFAP astrocytopathy. After treatment with corticosteroids for about 2 months, she displayed poor response and even worsened clinical manifestations when the dose of prednisone reduced to 45 mg. Stereotactic brain biopsy was adopted and the diagnosis of large B-cell lymphoma, non-germinal center type was established on pathological examination. The results of brain biopsy also showed perivascular inflammation and CD8+ T cell infiltration, which also accorded with GFAP astrocytopathy. After chemotherapy with rituximab and methotrexate, the patient showed clinical and radiological improvement significantly. Our findings suggest that positivity of GFAP antibody calls for cautious interpretation. Cancer screening appropriate for age, sex, and risk factors is recommended for GFAP antibody-positive patients, especially for patients with atypical clinical and radiologic manifestations.
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Apoptotic changes and aquaporin-1 expression in the choroid plexus of cerebral malaria patients.
Cerebral malaria (CM) is associated with sequestration of parasitized red blood cells (PRBCs) in the capillaries. Often, the association of CM with cerebral oedema is related with high mortality rate. Morphological changes of the choroid plexus (CP) and caspase-3 expression in CM have not been reported. In addition, limited knowledge is known regarding the role of aquaporin (AQP)-1 in CM. The present study evaluated changes in the CP, explored apoptotic changes and AQP-1 expression in CP epithelial cells (CPECs) in fatal CM patients.</AbstractText>CP from fatal Plasmodium falciparum malaria patients (5 non-CM [NCM], 16 CM) were retrieved and prepared for histopathological evaluation. Caspase-3 and AQP-1 expressions in CPECs were investigated by immunohistochemistry.</AbstractText>Histologically, apoptotic changes in CPECs were significantly observed in the CM group compared with the NCM and normal control (NC) groups (p&#x2009;&lt;&#x2009;0.05). These changes included cytoplasmic and nuclear condensation/shrinkage of CPECs and detachment of CPECs from the basement membrane. The apoptotic changes were positively correlated with caspase-3 expression in the nuclei of CPECs. In addition, AQP-1 expression in CPECs was significantly decreased in the CM group compared with the NCM and NC groups (all p&#x2009;&lt;&#x2009;0.001). A negative correlation (rs</sub>&#x2009;=&#x2009;&#x2009;-&#x2009;0.450,&#xa0;p&#x2009;=&#x2009;0.024) was documented between caspase-3 expression in the nuclei of CPECs and AQP-1.</AbstractText>Apoptotic changes and altered AQP-1 expression may contribute to CPEC dysfunction and subsequently reduce cerebrospinal fluid production, affecting the water homeostasis in the brains of patients with CM.</AbstractText>&#xa9; 2022. The Author(s).</CopyrightInformation>
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Genetic and histopathological associations with outcome in pediatric pilocytic astrocytoma.<Pagination><StartPage>504</StartPage><EndPage>512</EndPage><MedlinePgn>504-512</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.3171/2021.9.PEDS21405</ELocationID><Abstract><AbstractText Label="OBJECTIVE">Pilocytic astrocytomas (PAs) have a generally favorable prognosis; however, progression or recurrence after resection is possible. The prognostic value of histopathological qualifiers (defined below) or BRAF alterations is not well understood. The aim of this study was to identify the prognostic value of genetic and histopathological features of pediatric PAs.</AbstractText><AbstractText Label="METHODS">Patients treated for a WHO grade I PA at a single institution were analyzed for histopathological and genetic features and outcomes. "Histopathological qualifier" refers to designations such as "WHO grade I PA with increased proliferative index." BRAF alterations include gene fusions and point mutations. Patients with neurofibromatosis type 1 were excluded.</AbstractText><AbstractText Label="RESULTS">A total of 222 patients were analyzed (51% female, mean age 9.6 years). Tumors were located in the cerebellum/fourth ventricle (51%), optic pathway/hypothalamus (15%), brainstem (12%), and cerebral cortex (11%). BRAF alterations were screened for in 77 patients and identified in 56 (73%). Histopathological qualifiers were present in 27 patients (14%). Resection was performed in 197 patients (89%), 41 (21%) of whom displayed tumor progression or recurrence after resection. Tumor progression or recurrence was not associated with histopathologic qualifiers (p = 0.36) or BRAF alterations (p = 0.77). Ki-67 proliferative indices were not predictive of progression or recurrence (p = 0.94). BRAF alterations, specifically KIAA1549 fusions, were associated with cerebellar/fourth ventricular tumor location (p &lt; 0.0001) and younger patient age (p = 0.03). Patients in whom gross-total resection was achieved had lower rates of progression and recurrence (p &lt; 0.0001).</AbstractText><AbstractText Label="CONCLUSIONS">Histopathological features/qualifiers and BRAF alterations were not associated with tumor recurrence/progression in pediatric PAs. The extent of resection was the only factor analyzed that predicted outcome.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Cler</LastName><ForeName>Samuel J</ForeName><Initials>SJ</Initials><AffiliationInfo><Affiliation>1Department of Neurosurgery, Washington University School of Medicine, St. Louis, Missouri.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Skidmore</LastName><ForeName>Alexander</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>1Department of Neurosurgery, Washington University School of Medicine, St. Louis, Missouri.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yahanda</LastName><ForeName>Alexander T</ForeName><Initials>AT</Initials><AffiliationInfo><Affiliation>1Department of Neurosurgery, Washington University School of Medicine, St. Louis, Missouri.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mackey</LastName><ForeName>Kimberly</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>2South Georgia Medical Center, Valdosta, Georgia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rubin</LastName><ForeName>Joshua B</ForeName><Initials>JB</Initials><AffiliationInfo><Affiliation>3Department of Neuroscience, Washington University School of Medicine, St. Louis.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>4Department of Pediatrics, Washington University School of Medicine, Division of Hematology and Oncology, St. Louis.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cluster</LastName><ForeName>Andrew</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>4Department of Pediatrics, Washington University School of Medicine, Division of Hematology and Oncology, St. Louis.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Perkins</LastName><ForeName>Stephanie</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>4Department of Pediatrics, Washington University School of Medicine, Division of Hematology and Oncology, St. Louis.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>5Department of Radiation Oncology, Washington University School of Medicine, St. Louis.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gauvain</LastName><ForeName>Karen</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>4Department of Pediatrics, Washington University School of Medicine, Division of Hematology and Oncology, St. Louis.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>King</LastName><ForeName>Allison A</ForeName><Initials>AA</Initials><AffiliationInfo><Affiliation>4Department of Pediatrics, Washington University School of Medicine, Division of Hematology and Oncology, St. Louis.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Limbrick</LastName><ForeName>David D</ForeName><Initials>DD</Initials><AffiliationInfo><Affiliation>1Department of Neurosurgery, Washington University School of Medicine, St. Louis, Missouri.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>McEvoy</LastName><ForeName>Sean</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>1Department of Neurosurgery, Washington University School of Medicine, St. Louis, Missouri.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Park</LastName><ForeName>Tae Sung</ForeName><Initials>TS</Initials><AffiliationInfo><Affiliation>1Department of Neurosurgery, Washington University School of Medicine, St. Louis, Missouri.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Smyth</LastName><ForeName>Matthew D</ForeName><Initials>MD</Initials><AffiliationInfo><Affiliation>1Department of Neurosurgery, Washington University School of Medicine, St. Louis, Missouri.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mian</LastName><ForeName>Ali Y</ForeName><Initials>AY</Initials><AffiliationInfo><Affiliation>6Department of Radiology, Washington University School of Medicine, St. Louis; and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chicoine</LastName><ForeName>Michael R</ForeName><Initials>MR</Initials><AffiliationInfo><Affiliation>1Department of Neurosurgery, Washington University School of Medicine, St. Louis, Missouri.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dahiya</LastName><ForeName>Sonika</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>7Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Strahle</LastName><ForeName>Jennifer M</ForeName><Initials>JM</Initials><AffiliationInfo><Affiliation>1Department of Neurosurgery, Washington University School of Medicine, St. Louis, Missouri.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 CA251112</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL129241</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>K24 HL148305</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>K12 HL137942</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>UH3 HL143192</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>U01 HL143477</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>U01 HL133994</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>UL1 TR000448</GrantID><Acronym>TR</Acronym><Agency>NCATS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P30 CA091842</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>02</Month><Day>11</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Neurosurg Pediatr</MedlineTA><NlmUniqueID>101463759</NlmUniqueID><ISSNLinking>1933-0707</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="D048493">Proto-Oncogene Proteins B-raf</NameOfSubstance></Chemical></ChemicalList><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="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001932" MajorTopicYN="Y">Brain Neoplasms</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D048493" MajorTopicYN="N">Proto-Oncogene Proteins B-raf</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009364" MajorTopicYN="N">Neoplasm Recurrence, Local</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001254" MajorTopicYN="Y">Astrocytoma</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002528" MajorTopicYN="Y">Cerebellar Neoplasms</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">BRAF</Keyword><Keyword MajorTopicYN="N">glioma</Keyword><Keyword MajorTopicYN="N">oncology</Keyword><Keyword MajorTopicYN="N">pediatrics</Keyword><Keyword MajorTopicYN="N">pilocytic astrocytoma</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2021</Year><Month>8</Month><Day>9</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2021</Year><Month>9</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2023</Year><Month>5</Month><Day>29</Day><Hour>6</Hour><Minute>41</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>2</Month><Day>12</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>2</Month><Day>11</Day><Hour>20</Hour><Minute>3</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35148515</ArticleId><ArticleId IdType="doi">10.3171/2021.9.PEDS21405</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35148513</PMID><DateRevised><Year>2022</Year><Month>04</Month><Day>29</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1933-0693</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Feb</Month><Day>11</Day></PubDate></JournalIssue><Title>Journal of neurosurgery</Title><ISOAbbreviation>J Neurosurg</ISOAbbreviation></Journal>Clinical features and surgical outcomes of intracranial and spinal cord subependymomas.<Pagination><StartPage>1</StartPage><EndPage>12</EndPage><MedlinePgn>1-12</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.3171/2021.12.JNS211643</ELocationID><ELocationID EIdType="pii" ValidYN="Y">2021.12.JNS211643</ELocationID><Abstract><AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">Subependymomas are low-grade ependymal tumors whose clinical characteristics, radiographic features, and postsurgical outcomes are incompletely characterized due to their rarity. The authors present an institutional case series and a systematic literature review to achieve a better understanding of subependymomas.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">Adult patients with histologically confirmed subependymoma or mixed subependymoma-ependymoma surgically treated at a tertiary hospital between 1992 and 2020 were identified. A systematic literature review of the PubMed, Embase, Web of Science, and Google Scholar databases from inception until December 4, 2020, was conducted according to PRISMA guidelines. Data extracted from both groups included demographics, radiographic features, tumor characteristics, management, and follow-up variables.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Forty-eight unique patients with subependymoma were identified by chart review; of these patients, 8 (16.7%) had mixed subependymoma-ependymoma tumors. The median age at diagnosis was 49 years (IQR 19.8 years), and 26 patients (54.2%) were male. Forty-two patients (87.5%) had intracranial subependymomas, and 6 (12.5%) had spinal tumors. The most common presentation was headache (n = 20, 41.7%), although a significant number of tumors were diagnosed incidentally (n = 16, 33.3%). Among the 42 patients with intracranial tumors, 15 (35.7%) had hydrocephalus, and the most common surgical strategy was a suboccipital approach with or without C1 laminectomy (n = 26, 61.9%). Gross-total resection (GTR) was achieved in 33 cases (68.7%), and 2 patients underwent adjuvant radiotherapy. Most patients had no major postsurgical complications (n = 34, 70.8%), and only 1 (2.1%) had recurrence after GTR. Of 2036 reports initially identified in the systematic review, 39 were eligible for inclusion, comprising 477 patients. Of 462 patients for whom tumor location was reported, 406 (87.9%) were intracranial, with the lateral ventricle as the most common location (n = 214, 46.3%). Spinal subependymomas occurred in 53 patients (11.5%), with 3 cases (0.6%) in multiple locations. Similar to the case series at the authors' institution, headache was the most common presenting symptom (n = 231, 54.0%) among the 428 patients whose presentation was reported. Twenty-seven patients (6.3%) were diagnosed incidentally, and 36 cases (8.4%) were found at autopsy. Extent of resection was reported for 350 patients, and GTR was achieved in 250 (71.4%). Fifteen of 337 patients (4.5%) had recurrence or progression.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">The authors' case series and literature review demonstrate that patients with subependymoma are well managed with resection and generally have a favorable prognosis.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Rincon-Torroella</LastName><ForeName>Jordina</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>1Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, Maryland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rakovec</LastName><ForeName>Maureen</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>1Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, Maryland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Khalafallah</LastName><ForeName>Adham M</ForeName><Initials>AM</Initials><AffiliationInfo><Affiliation>1Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, Maryland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Ann</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>1Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, Maryland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bettegowda</LastName><ForeName>Anya</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>1Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, Maryland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kut</LastName><ForeName>Carmen</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>2Department of Radiation Oncology and Molecular Radiation Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rodriguez</LastName><ForeName>Fausto J</ForeName><Initials>FJ</Initials><AffiliationInfo><Affiliation>3Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Weingart</LastName><ForeName>Jon</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>1Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, Maryland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Luciano</LastName><ForeName>Mark</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>1Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, Maryland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Olivi</LastName><ForeName>Alessandro</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>1Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, Maryland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jallo</LastName><ForeName>George I</ForeName><Initials>GI</Initials><AffiliationInfo><Affiliation>4Department of Neurosurgery, Johns Hopkins Medicine, Institute for Brain Protection Sciences, Johns Hopkins All Children's Hospital, St. Petersburg, Florida; and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Brem</LastName><ForeName>Henry</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>1Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, Maryland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mukherjee</LastName><ForeName>Debraj</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>1Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, Maryland.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>5Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lim</LastName><ForeName>Michael</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>1Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, Maryland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bettegowda</LastName><ForeName>Chetan</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>1Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, Maryland.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R25 NS065729</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>02</Month><Day>11</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Neurosurg</MedlineTA><NlmUniqueID>0253357</NlmUniqueID><ISSNLinking>0022-3085</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">PRISMA guidelines</Keyword><Keyword MajorTopicYN="N">ependymoma</Keyword><Keyword MajorTopicYN="N">oncology</Keyword><Keyword MajorTopicYN="N">spinal tumor</Keyword><Keyword MajorTopicYN="N">subependymoma</Keyword><Keyword MajorTopicYN="N">systematic review</Keyword><Keyword MajorTopicYN="N">ventricular tumor</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2021</Year><Month>7</Month><Day>2</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2021</Year><Month>12</Month><Day>2</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>2</Month><Day>11</Day><Hour>20</Hour><Minute>3</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>2</Month><Day>12</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>2</Month><Day>12</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>aheadofprint</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35148513</ArticleId><ArticleId IdType="doi">10.3171/2021.12.JNS211643</ArticleId><ArticleId IdType="pii">2021.12.JNS211643</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35148502</PMID><DateRevised><Year>2022</Year><Month>02</Month><Day>11</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1933-0693</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Feb</Month><Day>11</Day></PubDate></JournalIssue><Title>Journal of neurosurgery</Title><ISOAbbreviation>J Neurosurg</ISOAbbreviation></Journal>Surgical management of colloid cysts of the third ventricle: a single-institution comparison of endoscopic and microsurgical resection.
Pilocytic astrocytomas (PAs) have a generally favorable prognosis; however, progression or recurrence after resection is possible. The prognostic value of histopathological qualifiers (defined below) or BRAF alterations is not well understood. The aim of this study was to identify the prognostic value of genetic and histopathological features of pediatric PAs.</AbstractText>Patients treated for a WHO grade I PA at a single institution were analyzed for histopathological and genetic features and outcomes. "Histopathological qualifier" refers to designations such as "WHO grade I PA with increased proliferative index." BRAF alterations include gene fusions and point mutations. Patients with neurofibromatosis type 1 were excluded.</AbstractText>A total of 222 patients were analyzed (51% female, mean age 9.6 years). Tumors were located in the cerebellum/fourth ventricle (51%), optic pathway/hypothalamus (15%), brainstem (12%), and cerebral cortex (11%). BRAF alterations were screened for in 77 patients and identified in 56 (73%). Histopathological qualifiers were present in 27 patients (14%). Resection was performed in 197 patients (89%), 41 (21%) of whom displayed tumor progression or recurrence after resection. Tumor progression or recurrence was not associated with histopathologic qualifiers (p = 0.36) or BRAF alterations (p = 0.77). Ki-67 proliferative indices were not predictive of progression or recurrence (p = 0.94). BRAF alterations, specifically KIAA1549 fusions, were associated with cerebellar/fourth ventricular tumor location (p &lt; 0.0001) and younger patient age (p = 0.03). Patients in whom gross-total resection was achieved had lower rates of progression and recurrence (p &lt; 0.0001).</AbstractText>Histopathological features/qualifiers and BRAF alterations were not associated with tumor recurrence/progression in pediatric PAs. The extent of resection was the only factor analyzed that predicted outcome.</AbstractText>
2,330,333
Endoscopic Transcortical-Transventricular Approach in Treating Third Ventricular Craniopharyngiomas-Case Series With Technical Note and Literature Review.
A paradigm shift toward less radicality in the treatment of craniopharyngioma (CP) has increasingly gained recognition. In selected patients, a less invasive approach aiming at cyst decompression may be suitable.</AbstractText>To present our experience with the endoscopic transcortical-transventricular approach (ETTA) for the treatment of CP located in the third ventricle, describe our surgical technique, and explore the results reported in the literature.</AbstractText>Data for third ventricular CPs treated using ETTA in 2 tertiary medical centers between 2006 and 2020 were retrospectively reviewed. Cystic, mixed lesion, new, and recurrent cases were included. ETTA aimed at cyst fenestration, subtotal or partial tumor resection, managing the hydrocephalus, or a combination of these modalities. Fractionated radiotherapy (RT) was performed (54 Gy in 30 fractions).</AbstractText>The described approach was performed in 13 patients with a mean age of 30.2 years. Tumor excision was attempted in 10 patients. Cystic fenestration alone was conducted in 3 patients, followed by intracystic catheter implantation in 2 patients. Permanent diabetes insipidus developed in 3 patients, and 1 patient experienced a surgical site infection. The recurrence rate for ETTA + RT (pre-ETTA in 33.3%) was 2/9 (22.2%) after a mean follow-up of 21.3 months. Four patients did not undergo RT after ETTA, and all these patients experienced recurrences after a mean follow-up of 15.5 months. Hydrocephalus resolved in all 6 patients who presented with accompanying hydrocephalus.</AbstractText>ETTA combined with adjuvant RT is a safe and effective option in the management of cystic or predominantly cystic CP extending into the third ventricle. This procedure also effectively treats the accompanying hydrocephalus.</AbstractText>Copyright &#xa9; Congress of Neurological Surgeons 2022. All rights reserved.</CopyrightInformation>
2,330,334
Typical linear radial periventricular enhancement in a patient with glial fibrillary acidic protein (GFAP) astrocytopathy.
We describe an unusual case of corticosteroid-responsive autoimmune meningoencephalomyelitis with linear perivascular gadolinium enhancement but in the absence of anti- glial fibrillary acidic protein (GFAP) antibodies (ABs) in the cerebral spinal fluid (CSF).</AbstractText>The patient's clinical symptoms, brain magnetic resonance imaging (MRI) features, serum and CSF analysis and treatment were reviewed.</AbstractText>A 47-year-old female experienced a subacute course with bilateral lower limbs weakness, unsteady walking, and dysuria. Brain MRI revealed typical radial perivascular gadolinium enhancement extending from the lateral ventricles to the white matter; MRI spine revealed lesions distributed in the entire spinal cord. Immunohistochemical staining of a brain biopsy revealed CD3+ T cells and CD20+ B cells cuffing around brain vessels, accompanied by CD68+ macrophages. CSF was negative for anti-GFAP ABs while serum was positive for anti-GFAP ABs (1:100). The patient responded well to corticosteroid.</AbstractText>There are no uniform diagnostic criteria for autoimmune GFAP astrocytopathy. Our case suggested the importance of typical MRI findings in the diagnosis of this rare disease. Early treatments are very important to alleviate symptoms.</AbstractText>&#xa9; 2022. Fondazione Societ&#xe0; Italiana di Neurologia.</CopyrightInformation>
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Isolation and culture of neural stem cells from adult mouse subventricular zone for genetic and pharmacological treatments with proliferation analysis.
Neural stem cells (NSCs) from the subventricular zone (SVZ) of the mouse brain can be expanded <i>in vitro</i> and grown as neurospheres, which can be stored long-term in liquid nitrogen. Here, we present a protocol for isolation and culture of NSCs from the adult mouse SVZ. We describe how to grow and expand primary NSCs to neurospheres, followed by differentiation and nucleofection/pharmacological treatments. Finally, we describe RNA extraction, EdU labeling of the cells, and immunofluorescent analysis to examine their proliferation. For complete details on the use and execution of this protocol, please refer to Radecki et&#xa0;al. (2020).
2,330,336
Predictors of Late Mortality in Patients With Surgically Resected Cardiac Myxomas: A Single-Center Experience.
Background and objective Myxomas are the most common cardiac tumors. This study aimed to analyze the possible risk factors associated with late mortality in this group of patients and assess long-term survival. Methods A retrospective study was conducted among patients who underwent myxomas resection between January 2008 and July 2019 in our service. The patients' preoperative, intraoperative, and postoperative data were analyzed. Multivariate logistic regression was performed to identify predictors of mortality at five years. The Kaplan-Meier curve and Cox proportion-adjusted survival curves were used to assess mortality at five and 10 years. Results A total of 108 patients with cardiac myxomas were identified. All cardiac tumors resected were confirmed as myxomas on histopathological examination. Ninety-six patients&#xa0;presented with left-side myxomas (94 left-atria and two left-ventricle) and 12 with right-side myxomas (11 right-atria, one right-ventricle); 78 of the tumors were capsulated, and 30 were sessile-papillary. The mean dimensions were 37 &#xb1;6.1 mm on the left side and 41 &#xb1;6.7 mm on the right side. Surgical excision was successful in all cases, with 25% requiring interatrial septum patch repair. Recurrence occurred in 2.77% of the patients. Multivariate logistic regression showed chronic kidney disease (CKD) (OR: 7.96, 95% CI: 1.469-43.125, p=0,016) to be an independent predictor for five-year mortality. The mean follow-up period was 7.13 &#xb1;2.965 years, and the Kaplan-Meier curve&#xa0;cumulative proportion survival of patients at five years and 10 years were 100% and 88.8%, respectively. There was no statistically significant difference in late-term survival between patients with and without CKD in the Cox proportion-adjusted survival curve (p=0.275). Conclusions Patients with myxomas have a good long-term prognosis following surgical resection. The multivariate logistic regression showed CKD to be an independent predictor of five-year mortality.
2,330,337
Subcortical Brain Volumes Relate to Neurocognition in First-Episode Schizophrenia, Bipolar Disorder, Major Depression Disorder, and Healthy Controls.
To explore differences and similarities in relationships between subcortical structure volumes and neurocognition among the four subject groups, including first-episode schizophrenia (FES), bipolar disorder (BD), major depression disorder (MDD), and healthy controls (HCs).</AbstractText>We presented findings from subcortical volumes and neurocognitive analyses of 244 subjects (109 patients with FES; 63 patients with BD, 30 patients with MDD, and 42 HCs). Using the FreeSurfer software, volumes of 16 selected subcortical structures were automatically segmented and analyzed for relationships with results from seven neurocognitive tests from the MATRICS (Measurement and Treatment Research to Improve Cognition in Schizophrenia) Cognitive Consensus Battery (MCCB).</AbstractText>Larger left lateral ventricle volumes in FES and BD, reduced bilateral hippocampus and amygdala volumes in FES, and lower bilateral amygdala volumes in BD and MDD were presented compared with HCs, and both FES and BD had a lower bilateral amygdala volume than MDD; there were seven cognitive dimension, five cognitive dimension, and two cognitive dimension impairments in FES, BD, and MDD, respectively; significant relationships were found between subcortical volumes and neurocognition in FES and BD but not in MDD and HCs; besides age and years of education, some subcortical volumes can predict neurocognitive performances variance.</AbstractText>The different degrees of subcortical volume lessening may contribute to the differences in cognitive impairment among the three psychiatric disorders.</AbstractText>Copyright &#xa9; 2022 Shi, Guo, Liu, Xue, Fan, Li, Fan, An, Wang, Tan, Yang and Tan.</CopyrightInformation>
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Kidins220/ARMS modulates brain morphology and anxiety-like traits in adult mice.
Kinase D interacting substrate of 220&#x2009;kDa (Kidins220), also known as ankyrin repeat-rich membrane spanning (ARMS), is a transmembrane scaffold protein that participates in fundamental aspects of neuronal physiology including cell survival, differentiation, and synaptic plasticity. The Kidins220 constitutive knockout line displays developmental defects in the nervous and cardiovascular systems that lead to embryonic lethality, which has so far precluded the study of this protein in the adult. Moreover, Kidins220 mRNA is tightly regulated by alternative splicing, whose impact on nervous system physiology has not yet been addressed in vivo. Here, we have asked to what extent the absence of Kidins220 splicing and the selective knockout of Kidins220 impact on adult brain homeostasis. To answer this question, we used a floxed line that expresses only the full-length, non-spliced Kidins220 mRNA, and a forebrain-specific, CaMKII-Cre driven Kidins220 conditional knockout (cKO) line. Kidins220 cKO brains are characterized by enlarged ventricles in the absence of cell death, and by deficient dendritic arborization in several cortical regions. The deletion of Kidins220 leads to behavioral changes, such as reduced anxiety-like traits linked to alterations in TrkB-BDNF signaling and sex-dependent alterations of hippocampal-dependent spatial memory. Kidins220 floxed mice present similarly enlarged brain ventricles and increased associative memory. Thus, both the absolute levels of Kidins220 expression and its splicing pattern are required for the correct brain development and related expression of behavioral phenotypes. These findings are relevant in light of the increasing evidence linking mutations in the human KIDINS220 gene to the onset of severe neurodevelopmental disorders.
2,330,339
Biventricular mechanical pattern of the athlete's heart: comprehensive characterization using three-dimensional echocardiography.<Pagination><StartPage>1594</StartPage><EndPage>1604</EndPage><MedlinePgn>1594-1604</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1093/eurjpc/zwac026</ELocationID><Abstract><AbstractText Label="AIMS">While left ventricular (LV) adaptation to regular, intense exercise has been thoroughly studied, data concerning the right ventricular (RV) mechanical changes and their continuum with athletic performance are scarce. The aim of this study was to characterize biventricular morphology and function and their relation to sex, age, and sports classes in a large cohort of elite athletes using three-dimensional (3D) echocardiography.</AbstractText><AbstractText Label="METHODS AND RESULTS">Elite, competitive athletes (n = 422) and healthy, sedentary volunteers (n = 55) were enrolled. Left ventricular and RV end-diastolic volumes (EDVi) and ejection fractions (EFs) were measured. To characterize biventricular mechanics, LV and RV global longitudinal (GLS) and circumferential strains (GCS) were quantified. All subjects underwent cardiopulmonary exercise testing to determine peak oxygen uptake (VO2/kg). Athletes had significantly higher LV and RV EDVi compared with controls (athletes vs. controls; LV EDVi: 81 &#xb1; 13 vs. 62 &#xb1; 11 mL/m2, RV EDVi: 82 &#xb1; 14 vs. 63 &#xb1; 11 mL/m2; P &amp;lt; 0.001). Concerning biventricular systolic function, athletes had significantly lower resting LV and RV EF (LV EF: 57 &#xb1; 4 vs. 61 &#xb1; 5%; RV EF: 55 &#xb1; 5 vs. 59 &#xb1; 5%; P &amp;lt; 0.001). The exercise-induced relative decrease in LV GLS (9.5 &#xb1; 10.7%) and LV GCS (10.7 &#xb1; 9.8%) was similar; however, the decrement in RV GCS (14.8 &#xb1; 17.8%) was disproportionately larger compared with RV GLS (1.7 &#xb1; 15.4%, P &amp;lt; 0.01). Right ventricular EDVi was found to be the strongest independent predictor of VO2/kg by multivariable linear regression.</AbstractText><AbstractText Label="CONCLUSION">Resting LV mechanics of the athlete's heart is characterized by a balanced decrement in GLS and GCS; however, RV GCS decreases disproportionately compared with RV GLS. Moreover, this mechanical pattern is associated with better exercise capacity.</AbstractText><CopyrightInformation>&#xa9; The Author(s) 2022. Published by Oxford University Press on behalf of the European Society of Cardiology.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>F&#xe1;bi&#xe1;n</LastName><ForeName>Alexandra</ForeName><Initials>A</Initials><Identifier Source="ORCID">0000-0002-8449-0638</Identifier><AffiliationInfo><Affiliation>Heart and Vascular Center, Semmelweis University, V&#xe1;rosmajor str. 68, Budapest H-1122, Hungary.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ujv&#xe1;ri</LastName><ForeName>Adrienn</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Heart and Vascular Center, Semmelweis University, V&#xe1;rosmajor str. 68, Budapest H-1122, Hungary.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tokodi</LastName><ForeName>M&#xe1;rton</ForeName><Initials>M</Initials><Identifier Source="ORCID">0000-0003-3036-4131</Identifier><AffiliationInfo><Affiliation>Heart and Vascular Center, Semmelweis University, V&#xe1;rosmajor str. 68, Budapest H-1122, Hungary.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lakatos</LastName><ForeName>B&#xe1;lint K&#xe1;roly</ForeName><Initials>BK</Initials><Identifier Source="ORCID">0000-0002-7627-5620</Identifier><AffiliationInfo><Affiliation>Heart and Vascular Center, Semmelweis University, V&#xe1;rosmajor str. 68, Budapest H-1122, Hungary.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kiss</LastName><ForeName>Orsolya</ForeName><Initials>O</Initials><AffiliationInfo><Affiliation>Heart and Vascular Center, Semmelweis University, V&#xe1;rosmajor str. 68, Budapest H-1122, Hungary.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Sports Medicine, Semmelweis University, Budapest, Hungary.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Babity</LastName><ForeName>M&#xe1;t&#xe9;</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Heart and Vascular Center, Semmelweis University, V&#xe1;rosmajor str. 68, Budapest H-1122, Hungary.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Z&#xe1;modics</LastName><ForeName>M&#xe1;rk</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Heart and Vascular Center, Semmelweis University, V&#xe1;rosmajor str. 68, Budapest H-1122, Hungary.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Syd&#xf3;</LastName><ForeName>N&#xf3;ra</ForeName><Initials>N</Initials><Identifier Source="ORCID">0000-0001-9999-4321</Identifier><AffiliationInfo><Affiliation>Heart and Vascular Center, Semmelweis University, V&#xe1;rosmajor str. 68, Budapest H-1122, Hungary.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Sports Medicine, Semmelweis University, Budapest, Hungary.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Csulak</LastName><ForeName>Emese</ForeName><Initials>E</Initials><Identifier Source="ORCID">0000-0001-7683-8000</Identifier><AffiliationInfo><Affiliation>Heart and Vascular Center, Semmelweis University, V&#xe1;rosmajor str. 68, Budapest H-1122, Hungary.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>V&#xe1;g&#xf3;</LastName><ForeName>Hajnalka</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Heart and Vascular Center, Semmelweis University, V&#xe1;rosmajor str. 68, Budapest H-1122, Hungary.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Sports Medicine, Semmelweis University, Budapest, Hungary.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Szab&#xf3;</LastName><ForeName>Lili&#xe1;na</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Heart and Vascular Center, Semmelweis University, V&#xe1;rosmajor str. 68, Budapest H-1122, Hungary.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kiss</LastName><ForeName>Anna R&#xe9;ka</ForeName><Initials>AR</Initials><AffiliationInfo><Affiliation>Heart and Vascular Center, Semmelweis University, V&#xe1;rosmajor str. 68, Budapest H-1122, Hungary.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sz&#x171;cs</LastName><ForeName>Andrea</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Heart and Vascular Center, Semmelweis University, V&#xe1;rosmajor str. 68, Budapest H-1122, Hungary.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hizoh</LastName><ForeName>Istvan</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Heart and Vascular Center, Semmelweis University, V&#xe1;rosmajor str. 68, Budapest H-1122, Hungary.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Merkely</LastName><ForeName>B&#xe9;la</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Heart and Vascular Center, Semmelweis University, V&#xe1;rosmajor str. 68, Budapest H-1122, Hungary.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Sports Medicine, Semmelweis University, Budapest, Hungary.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kov&#xe1;cs</LastName><ForeName>Attila</ForeName><Initials>A</Initials><Identifier Source="ORCID">0000-0003-2320-6434</Identifier><AffiliationInfo><Affiliation>Heart and Vascular Center, Semmelweis University, V&#xe1;rosmajor str. 68, Budapest H-1122, Hungary.</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></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Eur J Prev Cardiol</MedlineTA><NlmUniqueID>101564430</NlmUniqueID><ISSNLinking>2047-4873</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>Eur J Prev Cardiol. 2022 Jun 07;:</RefSource><PMID Version="1">35671162</PMID></CommentsCorrections><CommentsCorrections RefType="ErratumIn"><RefSource>Eur J Prev Cardiol. 2022 Aug 10;:</RefSource><PMID Version="1">35947476</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D056352" MajorTopicYN="N">Athletes</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D059267" MajorTopicYN="Y">Cardiomegaly, Exercise-Induced</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019560" MajorTopicYN="Y">Echocardiography, Three-Dimensional</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013318" MajorTopicYN="N">Stroke Volume</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016277" MajorTopicYN="N">Ventricular Function, Left</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016278" MajorTopicYN="N">Ventricular Function, Right</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Athlete&#x2019;s heart</Keyword><Keyword MajorTopicYN="N">Echocardiography</Keyword><Keyword MajorTopicYN="N">Right ventricle</Keyword><Keyword MajorTopicYN="N">Three-dimensional</Keyword></KeywordList><CoiStatement>Conflict of interest: none declared.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2021</Year><Month>11</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>1</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>2</Month><Day>3</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>2</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>9</Month><Day>11</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>2</Month><Day>9</Day><Hour>17</Hour><Minute>13</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35139228</ArticleId><ArticleId IdType="doi">10.1093/eurjpc/zwac026</ArticleId><ArticleId IdType="pii">6525230</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35138473</PMID><DateRevised><Year>2022</Year><Month>02</Month><Day>09</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1875-8312</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Feb</Month><Day>09</Day></PubDate></JournalIssue><Title>The international journal of cardiovascular imaging</Title><ISOAbbreviation>Int J Cardiovasc Imaging</ISOAbbreviation></Journal>The additional use of strain measurements for timing of treatment in severe aortic regurgitation.
Assessment of severity and need for intervention in clinical practice often is in need for a thorough echocardiography regarding function of the ventricles and additional valvular dysfunction. Despite the indications recommended in the current guidelines, there is still need for further research to identify patients with a severe valvular dysfunction but a potential reversible status regarding the function of the ventricles. Strain imaging is suggested in the current literature to be an additional tool to identify ventricular dysfunction in the setting of preserved left ventricular ejection fraction.
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Multimodal biological brain age prediction using magnetic resonance imaging and angiography with the identification of predictive regions.
Biological brain age predicted using machine learning models based on high-resolution imaging data has been suggested as a potential biomarker for neurological and cerebrovascular diseases. In this work, we aimed to develop deep learning models to predict the biological brain age using structural magnetic resonance imaging and angiography datasets from a large database of 2074 adults (21-81&#x2009;years). Since different imaging modalities can provide complementary information, combining them might allow to identify more complex aging patterns, with angiography data, for instance, showing vascular aging effects complementary to the atrophic brain tissue changes seen in T1-weighted MRI sequences. We used saliency maps to investigate the contribution of cortical, subcortical, and arterial structures to the prediction. Our results show that combining T1-weighted and angiography MR data led to a significantly improved brain age prediction accuracy, with a mean absolute error of 3.85&#x2009;years comparing the predicted and chronological age. The most predictive brain regions included the lateral sulcus, the fourth ventricle, and the amygdala, while the brain arteries contributing the most to the prediction included the basilar artery, the middle cerebral artery M2 segments, and the left posterior cerebral artery. Our study proposes a framework for brain age prediction using multimodal imaging, which gives accurate predictions and allows identifying the most predictive regions for this task, which can serve as a surrogate for the brain regions that are most affected by aging.
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GABA-ergic agents modulated the effects of histamine on the behaviour of male mice in the elevated plus maze test.
What is the central question of this study? Is there an interaction between histamine and the GABAergic system in modulation of anxiety in mice? What is the main finding and its importance? There is a synergistic anxiogenic effect between histamine and bicuculline in mice. This effect may be due to a direct or an indirect effect of the histaminergic system on the GABAergic system.</AbstractText>It has been documented that both histaminergic and GABAergic systems participate in the neurobiology of anxiety behaviour. In the current research, we investigated the effects of the histaminergic system and GABAA</sub> receptor agents on anxiety-related behaviours and their interaction using the elevated plus maze test in mice. Intraperitoneal (i.p.) administration of muscimol (0.12 and 0.25&#xa0;mg/kg) increased the open arm time (OAT) (P&#xa0;&lt;&#xa0;0.001) without affecting the open arm entries (OAE) and locomotor activity, showing an anxiolytic effect. i.p. injection of bicuculline (0.5 and 1&#xa0;mg/kg) decreased OAT (P&#xa0;&lt;&#xa0;0.001) but not OAE and locomotor activity, suggesting an anxiogenic behaviour. Intracerebroventricular (i.c.v.) microinjection of histamine (2.5 and 5&#xa0;&#x3bc;g/mouse) resulted in a decline in OAT (P&#xa0;&lt;&#xa0;0.001) but not OAE and locomotor activity, indicating an anxiogenic response. Co-administration of histamine with GABAergic agents, muscimol (0.06&#xa0;mg/kg; i.p.) and bicuculline (0.25&#xa0;mg/kg; i.p.), decreased (P&#xa0;&lt;&#xa0;0.001) and increased (P&#xa0;&lt;&#xa0;0.05), respectively, the anxiogenic-like response to the effective dose (5&#xa0;&#x3bc;g/mouse; i.c.v.) of histamine. In addition, co-treatment of effective doses of histamine (2.5 and 5&#xa0;&#x3bc;g/mouse;i.c.v.) with an effective dose of muscimol (0.12&#xa0;mg/kg; i.p.) and a non-effective dose of bicuculline (0.25&#xa0;mg/kg; i.p.) significantly decreased OAT (P&#xa0;&lt;&#xa0;0.001), suggesting a likely interaction between the histaminergic and GABAergic systems in the regulation of anxiety. The results demonstrated a synergistic anxiogenic-like effect between histamine and bicuculline in mice. In conclusion, our results present an interaction between the histaminergic and GABAergic systems in anxiolytic/anxiogenic-like behaviours in the elevated plus maze test.</AbstractText>&#xa9; 2022 The Authors. Experimental Physiology &#xa9; 2022 The Physiological Society.</CopyrightInformation>
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Hydatid cyst in the third ventricle of the brain: case report of an exceptionally rare condition.
Hydatid disease is an endemic zoonotic disease caused by the cestode Echinococcus multilocularis and Echinococcus granulosus. Intra-ventricular hydatid cysts are extremely rare. Even more rarely, and to the best of our knowledge, only three cases of third ventricle involvement have been reported. Herein, we present the fourth case of an intraventricular hydatid cyst in a pediatric patient located in the third ventricle. It is about a 7-year-old girl, of a rural origin, admitted for intracranial hypertension, deterioration of the general status, and weakness on the right side of her body. A cerebral magnetic resonance imaging (MRI) showed the presence of a rounded cystic formation in the third ventricle. The patient was operated through a transfrontal transventricular approach, and the cyst was removed. Postoperative course was uneventful. Hydatid disease should be considered part of the differential diagnosis for cystic lesions of the central nervous system, especially in endemic regions. Total removal of the cysts without rupture is a challenge, but best treatment remains an active nationwide prevention.
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Rosette-forming glioneuronal tumours: two case reports and a review of the literature.
Rosette-forming glioneuronal tumour (RGNT) is a rare central nervous system (CNS) neoplasm that typically arises in the fourth ventricle. It is even more uncommon to arise outside the midline. In this paper, we report two cases of RGNT: one located in the fourth ventricle (a typical site), and the other in the right cerebellar hemisphere (a rare site). Both cases were misdiagnosed on imaging, and the results were inconsistent with the pathological diagnosis. The aim of the article is to deepen medical practitioners' understanding of RGNT by learning from these two cases, summarising cases located in the cerebellar hemispheres and systematically reviewing RGNT.
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Acute Exercise Regulates hTERT Gene Expression and Alternative Splicing in the hTERT-BAC Transgenic Mouse Model.
Aerobic exercise maintains telomere length through increased human telomerase reverse transcriptase (hTERT) expression and telomerase enzyme activity. The impact of acute exercise on hTERT alternative splicing (AS) is unknown.</AbstractText>This study aimed to examine hTERT AS in response to acute treadmill running.</AbstractText>A bacterial artificial chromosome mouse model containing the 54-kilobase hTERT gene locus inserted into its genome (hTERT-BAC) was utilized. The gastrocnemius, left ventricle, and brain were excised before (Pre), upon cessation (Post), and during recovery (1, 24, 48, and 72 h; n = 5/time point) from treadmill running (30 min at 60% maximum speed). Full-length (FL) hTERT and the "minus beta" (-&#x3b2;) AS variant (skips exons 7 and 8 and does not code for active telomerase) were measured by gel-based and droplet digital reverse transcription-polymerase chain reaction methods. SF3B4 and SRSF2 protein expression were measured by Western blotting.</AbstractText>Compared with Pre, FL hTERT increased at Post before decreasing during recovery in the gastrocnemius (48 and 72 h; P &#x2264; 0.001) and left ventricle (24 h; P = 0.004). The percentage of FL hTERT in the gastrocnemius also increased during recovery (1 and 72 h; P &#x2264; 0.017), whereas a decrease was observed in the left ventricle (1, 24, and 48 h; P &#x2264; 0.041). hTERT decreased in the brain (48 h), whereas FL hTERT percentage remained unaltered. SF3B4 protein expression decreased throughout recovery in the gastrocnemius and tended to be associated with FL hTERT (r = -0.348, P = 0.075) and -&#x3b2; in opposite directions (r = 0.345, P = 0.067).</AbstractText>Endurance exercise increased hTERT gene expression, and altered FL hTERT splicing in contractile tissues and may maintain telomere length necessary to improve the function and health of the organism.</AbstractText>Copyright &#xa9; 2022 by the American College of Sports Medicine.</CopyrightInformation>
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Ventricular features as reliable differentiators between bvFTD and other dementias.
Lateral ventricles are reliable and sensitive indicators of brain atrophy and disease progression in behavioral variant frontotemporal dementia (bvFTD). We aimed to investigate whether an automated tool using ventricular features could improve diagnostic accuracy in bvFTD across neurodegenerative diseases.</AbstractText>Using 678 subjects -69 bvFTD, 38 semantic variant, 37 primary non-fluent aphasia, 218 amyloid&#xa0;+&#xa0;mild cognitive impairment, 74 amyloid&#xa0;+&#xa0;Alzheimer's Dementia and 242 normal controls- with a total of 2750 timepoints, lateral ventricles were segmented and differences in ventricular features were assessed between bvFTD, normal controls and other dementia cohorts.</AbstractText>Ventricular antero-posterior ratio (APR) was the only feature that was significantly different and increased faster in bvFTD compared to all other cohorts. We achieved a 10-fold cross-validation accuracy of 80% (77% sensitivity, 82% specificity) in differentiating bvFTD from all other cohorts with other ventricular features (i.e., total ventricular volume and left-right lateral ventricle ratios), and 76% accuracy using only the single APR feature.</AbstractText>Ventricular features, particularly the APR, might be reliable and easy-to-implement markers for bvFTD diagnosis. We have made our ventricle feature estimation and bvFTD diagnostic tool publicly available, allowing application of our model in other studies.</AbstractText>Copyright &#xa9; 2022 The Authors. Published by Elsevier Inc. All rights reserved.</CopyrightInformation>
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Olig2 defines a subset of neural stem cells that produce specific olfactory bulb interneuron subtypes in the subventricular zone of adult mice.
Distinct neural stem cells (NSCs) reside in different regions of the subventricular zone (SVZ) and generate multiple olfactory bulb (OB) interneuron subtypes in the adult brain. However, the molecular mechanisms underlying such NSC heterogeneity remain largely unknown. Here, we show that the basic helix-loop-helix transcription factor Olig2 defines a subset of NSCs in the early postnatal and adult SVZ. Olig2-expressing NSCs exist broadly but are most enriched in the ventral SVZ along the dorsoventral axis complementary to dorsally enriched Gsx2-expressing NSCs. Comparisons of Olig2-expressing NSCs from early embryonic to adult stages using single cell transcriptomics reveal stepwise developmental changes in their cell cycle and metabolic properties. Genetic studies further show that cross-repression contributes to the mutually exclusive expression of Olig2 and Gsx2 in NSCs/progenitors during embryogenesis, but that their expression is regulated independently from each other in adult NSCs. Finally, lineage-tracing and conditional inactivation studies demonstrate that Olig2 plays an important role in the specification of OB interneuron subtypes. Altogether, our study demonstrates that Olig2 defines a unique subset of adult NSCs enriched in the ventral aspect of the adult SVZ.
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Extended Ischemic Recovery After Implantation of Human Mesenchymal Stem Cell Aggregates Indicated by Sodium MRI at 21.1&#xa0;T.
Extended therapeutic application remains a significant issue in the use of stem cell therapies to treat ischemic stroke. Along these lines, neurological recovery in a rodent model of ischemic stroke was evaluated following implantation of human mesenchymal stem cell aggregates (hMSC-agg), labeled with micron-sized particles of iron oxide, directly into the lateral ventricle contralateral to the ischemic lesion hemisphere. Longitudinally, disease progression and response to hMSC-agg therapy were assessed by <sup>1</sup>H and <sup>23</sup>Na magnetic resonance imaging (MRI) at 21.1&#xa0;T to investigate cellular localization, migration, and recovery over an extended timeframe. MRI provides quantifiable metrics of tissue status through sodium distributions in addition to traditional proton imaging. Quantitative <sup>23</sup>Na MRI revealed a significant decrease of sodium concentrations following hMSC aggregate implantation, indicating recovery of homeostasis. This result correlates positively with extended neurological recovery assessed by behavioral analysis and immunohistochemistry. These findings demonstrate the potential of implanted hMSC aggregate therapy to provide extended treatment for ischemic stroke, as well as the robustness of MRI for monitoring such approaches. This method potentially can be translated to a clinical setting for the assessment of extended cell therapy efficacy.
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Laryngeal tuberculosis: a neglected diagnosis.
A 24-year-old woman visited the Ear Nose Throat (ENT) outpatient department with complaints of hoarseness for 2&#x2009;months not responding to conservative management. Laryngoscopic examination revealed a whitish ulceroproliferative lesion in the anterior commissure and anterior two-thirds of bilateral true vocal cords with surrounding necrosis. In view of the above findings, the patient was planned for biopsy under general anaesthesia. Intraoperative findings showed multiple whitish necrotic friable tissue involving anterior two-thirds of bilateral false vocal cords, ventricle, bilateral true vocal cords, both aryepiglottic folds and laryngeal surface of epiglottis. Postoperative histopathology was consistent with tuberculosis. A pulmonology consultation was taken, and the patient was started on anti-tuberculosis chemotherapy. One month post therapy, the voice was symptomatically better. A flexible fibreoptic laryngoscopic examination was done, which revealed almost complete resolution of the lesion with minimal ulceration at the anterior one-third of right true vocal cord.
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Impact of physiological factors on longitudinal structural MRI measures of the brain.
Longitudinal MRI is used in clinical research studies to examine illness progression, neurodevelopment, and the effect of medical interventions. Such studies typically report changes in brain volume of less than 5%.&#xa0;However, there is a concern that these findings could be obscured or confounded by small changes in brain volume estimates caused by physiological factors such as, dehydration, blood pressure, caffeine levels, and circadian rhythm. In this study, MRI scans using the ADNI-III protocol were acquired from 20 participants&#xa0;(11 female)&#xa0;at two time points (mean interval&#xa0;=&#xa0;20.3 days). Hydration, systolic and diastolic blood pressure, caffeine intake, and time of day were recorded at both visits. Images were processed using FreeSurfer. Three&#xa0;a priori hypothesised brain regions (hippocampus, lateral ventricles, and total brain) were selected, and an exploratory analysis was conducted on FreeSurfer's auto-segmented brain regions. There was no significant effect of the physiological factors on changes in the hypothesised brain regions.&#xa0;We provide estimates for the maximum percentage change in regional brain volumes that could be expected to occur from normal variation in each of the physiological measures.&#xa0;In this study, normal variations in physiological parameters did not have a detectable effect on longitudinal changes in brain volume.
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Exosomes derived from bone-marrow mesenchymal stem cells alleviate cognitive decline in AD-like mice by improving BDNF-related neuropathology.
Alzheimer's disease (AD) is a neurodegenerative disease characterized by a progressive decline in cognitive ability. Exosomes derived from bone-marrow mesenchymal stem cells (BMSC-exos) are extracellular vesicles that can execute the function of bone-marrow mesenchymal stem cells (BMSCs). Given the versatile therapeutic potential of BMSC and BMSC-exos, especially their neuroprotective effect, the aim of this study was to investigate the potential effect of BMSC-exos on AD-like behavioral dysfunction in mice and explore the possible molecular mechanism.</AbstractText>BMSC-exos were extracted from the supernatant of cultured mouse BMSCs, which were isolated from the femur and tibia of adult C57BL/6 mice, purified and sorted via flow cytometry, and cultured in vitro. BMSC-exos were identified via transmission electron microscopy, and typical marker proteins of exosomes were also detected via Western blot. A sporadic AD mouse model was established by intracerebroventricular injection of streptozotocin (STZ). Six weeks later, BMSC-exos were administered via lateral ventricle injection or caudal vein injection lasting five consecutive days, and the control mice were&#xa0;intracerebroventricularly administered an equal volume of solvent. Behavioral performance was observed via the open field test (OFT), elevated plus maze test (EPM), novel object recognition test (NOR), Y maze test (Y-maze), and tail suspension test (TST). The mRNA and protein expression levels of IL-1&#x3b2;, IL-6, and TNF-&#x3b1; in the hippocampus were measured via quantitative polymerase chain reaction (qPCR) and Western blot, respectively. Moreover, the protein expression of A&#x3b2;1-42</sub>, BACE, IL-1&#x3b2;, IL-6, TNF-&#x3b1;, GFAP, p-Tau (Ser396), Tau5, synaptotagmin-1 (Syt-1), synapsin-1, and brain-derived neurotrophic factor (BDNF) in the hippocampus was detected using Western blot, and the expression of GFAP, IBA1, A&#x3b2;1-42</sub> and DCX in the hippocampus was measured via immunofluorescence staining.</AbstractText>Lateral ventricle administration, but not caudal vein injection of BMSC-exos improved AD-like behaviors in the STZ-injected mouse model, as indicated by the increased number of rearing, increased frequency to the central area, and increased duration and distance traveled in the central area in the OFT, and improved preference index of the novel object in the NOR. Moreover, the hyperactivation of microglia and astrocytes in the hippocampus of the model mice was inhibited after treatment with BMSC-exos via lateral ventricle administration, accompanied by the reduced expression of IL-1&#x3b2;, IL-6, TNF-&#x3b1;, A&#x3b2;1-42,</sub> and p-Tau and upregulated protein expression of synapse-related proteins and BDNF. Furthermore, the results of the Pearson test showed that the preference index of the novel object in the NOR was positively correlated with the hippocampal expression of BDNF, but negatively correlated with the expression of GFAP, IBA1, and IL-1&#x3b2;. Apart from a positive correlation between the hippocampal expression of BDNF and Syt-1, BDNF abundance was found to be negatively correlated with markers of glial activation and the expression of the inflammatory cytokines, A&#x3b2;1-42</sub>, and p-Tau, which are characteristic neuropathological features of AD.</AbstractText>Lateral ventricle administration, but not caudal vein injection of BMSC-exos, can improve AD-like behavioral performance in STZ-injected mice, the mechanism of which might be involved in the regulation of glial activation and its associated neuroinflammation and BDNF-related neuropathological changes in the hippocampus.</AbstractText>&#xa9; 2022. The Author(s).</CopyrightInformation>
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Cross-Modality Multi-Atlas Segmentation via Deep Registration and Label Fusion.
Multi-atlas segmentation (MAS) is a promising framework for medical image segmentation. Generally, MAS methods register multiple atlases, i.e., medical images with corresponding labels, to a target image; and the transformed atlas labels can be combined to generate target segmentation via label fusion schemes. Many conventional MAS methods employed the atlases from the same modality as the target image. However, the number of atlases with the same modality may be limited or even missing in many clinical applications. Besides, conventional MAS methods suffer from the computational burden of registration or label fusion procedures. In this work, we design a novel cross-modality MAS framework, which uses available atlases from a certain modality to segment a target image from another modality. To boost the computational efficiency of the framework, both the image registration and label fusion are achieved by well-designed deep neural networks. For the atlas-to-target image registration, we propose a bi-directional registration network (BiRegNet), which can efficiently align images from different modalities. For the label fusion, we design a similarity estimation network (SimNet), which estimates the fusion weight of each atlas by measuring its similarity to the target image. SimNet can learn multi-scale information for similarity estimation to improve the performance of label fusion. The proposed framework was evaluated by the left ventricle and liver segmentation tasks on the MM-WHS and CHAOS datasets, respectively. Results have shown that the framework is effective for cross-modality MAS in both registration and label fusion https://github.com/NanYoMy/cmmas.
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The right ventricle after cardiac surgery, hypotheses and evidences, and the role of advanced echocardiography modalities.<Pagination><StartPage>126</StartPage><EndPage>127</EndPage><MedlinePgn>126-127</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.33963/KP.a2022.0037</ELocationID><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kossaify</LastName><ForeName>Antoine</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Cardiology, University Hospital Notre Dame des Secours, University Saint Esprit Kaslik, USEK, School of Medicine, Kaslik, Lebanon. antoinekossaify@yahoo.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kossaify</LastName><ForeName>Mikhael</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Cardiology, University Hospital Notre Dame des Secours, University Saint Esprit Kaslik, USEK, School of Medicine, Kaslik, Lebanon.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Massetti</LastName><ForeName>Massimo</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular and Thoracic sciences, Catholic University of the Sacred Heart, Cardiovascular surgery division, Gemelli University Hospital, Rome, Italy.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>02</Month><Day>07</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="D006348" MajorTopicYN="Y">Cardiac Surgical Procedures</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004452" MajorTopicYN="N">Echocardiography</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="Y">Heart Ventricles</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>2</Month><Day>7</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>2</Month><Day>7</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>2</Month><Day>8</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>3</Month><Day>8</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>2</Month><Day>7</Day><Hour>12</Hour><Minute>16</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35129833</ArticleId><ArticleId IdType="doi">10.33963/KP.a2022.0037</ArticleId><ArticleId IdType="pii">VM/OJS/J/88376</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">35129181</PMID><DateCompleted><Year>2022</Year><Month>04</Month><Day>05</Day></DateCompleted><DateRevised><Year>2022</Year><Month>04</Month><Day>05</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1940-087X</ISSN><JournalIssue CitedMedium="Internet"><Issue>179</Issue><PubDate><Year>2022</Year><Month>Jan</Month><Day>20</Day></PubDate></JournalIssue><Title>Journal of visualized experiments : JoVE</Title><ISOAbbreviation>J Vis Exp</ISOAbbreviation></Journal>Four-Dimensional Computed Tomography-Guided Valve Sizing for Transcatheter Pulmonary Valve Replacement.
The measurements of the right ventricle (RV) and pulmonary artery (PA), for selecting the optimal prosthesis size for transcatheter pulmonary valve replacement (TPVR), vary considerably. Three-dimensional (3D) computed tomography (CT) imaging for device size prediction is insufficient to assess the displacement of the right ventricular outflow tract (RVOT) and PA, which could increase the risk of stent misplacement and paravalvular leak. The aim of this study is to provide a dynamic model to visualize and quantify the anatomy of the RVOT to PA over the entire cardiac cycle by four-dimensional (4D) cardiac CT reconstruction to obtain an accurate quantitative evaluation of the required valve size. In this pilot study, cardiac CT from sheep J was chosen to illustrate the procedures. 3D cardiac CT was imported into 3D reconstruction software to build a 4D sequence which was divided into eleven frames over the cardiac cycle to visualize the deformation of the heart. Diameter, cross-sectional area, and circumference of five imaging planes at the main PA, sinotubular junction, sinus, basal plane of the pulmonary valve (BPV), and RVOT were measured at each frame in 4D straightened models prior to valve implantation to predict the valve size. Meanwhile, dynamic changes in the RV volume were also measured to evaluate right ventricular ejection fraction (RVEF). 3D measurements at the end of the diastole were obtained for comparison with the 4D measurements. In sheep J, 4D CT measurements from the straightened model resulted in the same choice of valve size for TPVR (30 mm) as 3D measurements. The RVEF of sheep J from pre-CT was 62.1 %. In contrast with 3D CT, the straightened 4D reconstruction model not only enabled accurate prediction for valve size selection for TPVR but also provided an ideal virtual reality, thus presenting a promising method for TPVR and the innovation of TPVR devices.
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Spontaneous intracerebral pseudoaneurysm rupture and meningiomatosis: A case report and review of the literature.
We report the first case of a spontaneous ruptured anterior cerebral artery pseudoaneurysm in a patient affected by meningiomatosis.</AbstractText>A 71-year-old female patient was admitted to our emergency department after acute loss of consciousness. An urgent head CT scan showed third ventricle hemorrhage and a giant extra-axial tumor with associated peritumoral bleeding. A second, smaller, and right-sided tumor was detected at the posterior third of the superior sagittal sinus, indicative of meningiomatosis diagnosis. A following CT angiogram showed an hypervascularized lesion at the right frontal convexity and a ruptured A2 pseudoaneurysm. Tumor removal was performed through right frontal craniotomy. After the initial debulking and removal of the peritumoral hemorrhage, the A2 segment associated with the bleeding pseudoaneurysm was surgically coagulated.</AbstractText>We report the unique occurrence of two relatively rare neurological entities: meningiomatosis and intracranial pseudoaneurysm. In our experience, their simultaneous and acute presentation is associated to poor prognosis.</AbstractText>Copyright: &#xa9; 2022 Surgical Neurology International.</CopyrightInformation>
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Adult gangliocytoma arising within the lateral ventricle: A case report and review of the literature.
Gangliocytomas are rare neuronal tumors with an incidence of &lt;1% of all central nervous system (CNS) neoplasms. They occur mostly in the pediatric age group, localizing within the cerebral cortex, most often the temporal lobe.</AbstractText>We report a case of an intracranial gangliocytoma arising within the lateral ventricle in a 66-year-old female. Magnetic resonance imaging of the brain showed a diffusely enhancing lobulated mass situated within the frontal horn of the right lateral ventricle with extension into the foramen of Monro and obstructive hydrocephalus. The patient underwent an interhemispheric transcallosal approach with gross total resection and relief of her hydrocephalus. Pathological examination showed clusters of highly pleomorphic neuron-like cells without evidence of neoplastic glial cells. Histopathological and immunohistochemistry findings were consistent with the diagnosis of gangliocytoma (World Health Organization Grade 1).</AbstractText>Gangliocytomas are rare low-grade CNS neoplasms that can present in an older population within unusual locations and should be included within the differential whenever a suspicious lesion is encountered.</AbstractText>Copyright: &#xa9; 2022 Surgical Neurology International.</CopyrightInformation>
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A Comparative Analysis of CSF and the Blood Levels of Monoamines As Neurohormones in Rats during Ontogenesis.
According to the literature, the cerebrospinal fluid (CSF) in the cerebral ventricles contains numerous neuron-derived physiologically active substances that can function as neurohormones and contribute to volume neurotransmission in the periventricular region of the brain. This study was aimed at carrying out a comparative analysis of CSF and the blood levels of monoamines in rats during ontogenesis as an indicator of age-related characteristics of monoamine transport to body fluids and their function as neurohormones in volume neurotransmission in the periventricular region of the brain. We have shown that CSF in the perinatal period and adulthood contains the most functionally significant monoamines: dopamine, noradrenaline, and serotonin. A comparison of the monoamine levels in the CSF and blood of animals of different age groups revealed that CSF contains monoamines of predominantly neuronal (cerebral) origin and almost no monoamines derived from the general circulation. We also established that monoamines are found in the CSF at physiologically active levels that allow them to act as neurohormones in both reversible volume neurotransmission in the adult brain and irreversible regulation of brain development in the perinatal period.
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Emergency department point-of-care biomarkers and day 90 functional outcome in spontaneous intracerebral hemorrhage: A single-center pilot study.
Spontaneous intracerebral hemorrhage (sICH) results in high morbidity and mortality rates, thus identifying strategies for timely prognosis and treatment is important. The present study aimed to analyze the relationship between emergency department point-of-care (POC) blood biomarkers and day 90 functional outcome (FO) in patients with acute (&lt;8 h) sICH. On-site POC determinations, including complete blood count, glucose, cardiac troponin I, D-dimer and C-reactive protein, and derived inflammatory indexes were performed for a cohort of 35 patients. The primary endpoint was a favorable day 90 FO (modified Rankin Score &#x2264;3). Secondary endpoints included early neurological worsening (ENW), day 7/discharge neurological impairment, day 90 independence assessment (Barthel Index &lt;60), hematoma enlargement and perihematomal edema (PHE) growth. A favorable three-month FO was reported in 16 (46%) participants. Older age, previous history of ischemic stroke and initial imagistic parameters, including intraventricular hemorrhage, enlarged contralateral ventricle and cerebral atrophy, significantly predicted an unfavorable FO. The admission D-dimer similarly predicted day 90 FO and the independence status, along with ENW and a more severe day 7/discharge neurological status. The D-dimer also correlated with the initial neurological status and PHE. PHE growth correlated with granulocytes, systemic immune-inflammation index and glycemia. The results suggested that a lower admission D-dimer could indicate an improved day 90 FO of patients with sICH, while also anticipating the development of PHE growth and ENW.
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Influence of the microenvironment dynamics on extracellular matrix evolution under hypoxic ischemic conditions in the myocardium.
The extracellular matrix (ECM) consists of &#xfb01;brillary and non-&#xfb01;brillary components in the extracellular zone, and fulfills structural and signaling roles. Cardiac insult can lead to cardiomyocyte death, which subsequently determines dynamic changes of ECM composition and regulates cellular responses, ultimately contributing to cardiac repair. The present retrospective study on a small batch selected from the database of the Pathology Department of 'Sf. Pantelimon' Hospital aimed to determine which molecules may have a role in the dynamics of ECM using histopathology and immunohistochemistry methods. The study batch was composed of cases with cardiac ischemic conditions who died at various ages of myocardial infarcts. Tissue samples were taken from the myocardium of the left ventricle (anterior and lateral walls), and multiple series of histological sections were produced and analyzed using immunohistochemistry for collagen type I (Col-1), tenascin C (Tn-C), matrix metalloproteinase 9, CD34, and CD68. Col-1 and Tn-C showed variable patterns of fibrillar plexiform network, associated with a high micro-vascular density of newly formed capillaries revealed by CD34, and an interstitial infiltrate with histiocytes demonstrated by CD68 presence. The ECM represents therefore a polymorphic microenvironment with its own dynamics that is in continuous change, involving a large spectrum of heterogenous molecules, which play different roles in myocardium remodeling under hypoxic ischemic conditions.
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Associations of maternal angiogenic factors during pregnancy with alterations in cardiac development in childhood at 10 years of age.<Pagination><StartPage>100</StartPage><EndPage>111</EndPage><MedlinePgn>100-111</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.ahj.2022.01.016</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0002-8703(22)00025-4</ELocationID><Abstract><AbstractText Label="AIM">To examine whether maternal angiogenic factors in the first half of pregnancy are associated with offspring left and right cardiac development.</AbstractText><AbstractText Label="METHODS">In a population-based prospective cohort among 2,415 women and their offspring, maternal first and second trimester plasma PlGF and sFlt-1 concentrations were measured. Cardiac MRI was performed in their offspring at 10 years.</AbstractText><AbstractText Label="RESULTS">Maternal angiogenic factors were not associated with childhood cardiac outcomes in the total population. In children born small-for-their-gestational-age, higher maternal first trimester PlGF concentrations were associated with a lower childhood left ventricular mass&#xa0; (-0.24 SDS&#xa0; [95%CI -0.42, -0.05 per SDS increase in maternal PlGF]), whereas higher sFlt-1 concentrations were associated with higher childhood left ventricular mass&#xa0; (0.22 SDS&#xa0; [95%CI 0.09, 0.34 per SDS increase in maternal sFlt-1]). Higher second trimester maternal sFlt-1 concentrations were also associated with higher childhood left ventricular mass&#xa0; (P-value &lt;.05). In preterm born children, higher maternal first and second trimester sFlt-1/PlGF ratio were associated with higher childhood left ventricular mass&#xa0; (0.30 SDS&#xa0; [95%CI 0.01, 0.60], 0.22 SDS&#xa0; [95%CI -0.03, 0.40]) per SDS increase in maternal sFlt-1/PlGF ratio in first and second trimester respectively). No effects on other childhood cardiac outcomes were present within these higher-risk children.</AbstractText><AbstractText Label="CONCLUSIONS">In a low-risk population, maternal angiogenic factors are not associated with childhood cardiac ventricular structure, and function within the normal range. In children born small for their gestational age or preterm, an imbalance in maternal angiogenic factors in the first half of pregnancy was associated with higher childhood left ventricular mass only.</AbstractText><CopyrightInformation>Copyright &#xa9; 2022 The Authors. Published by Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Bongers-Karmaoui</LastName><ForeName>Meddy N</ForeName><Initials>MN</Initials><AffiliationInfo><Affiliation>The Generation R Study Group, Erasmus University Medical Center, Rotterdam, The Netherlands; Department of Pediatrics, Sophia Children's Hospital, Erasmus University Medical Center, Rotterdam, The Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jaddoe</LastName><ForeName>Vincent W V</ForeName><Initials>VWV</Initials><AffiliationInfo><Affiliation>The Generation R Study Group, Erasmus University Medical Center, Rotterdam, The Netherlands; Department of Pediatrics, Sophia Children's Hospital, Erasmus University Medical Center, Rotterdam, The Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Roest</LastName><ForeName>Arno A W</ForeName><Initials>AAW</Initials><AffiliationInfo><Affiliation>Department of Pediatrics, Leiden University Medical Center, Leiden, The Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Helbing</LastName><ForeName>Willem A</ForeName><Initials>WA</Initials><AffiliationInfo><Affiliation>Department of Pediatrics, Sophia Children's Hospital, Erasmus University Medical Center, Rotterdam, The Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Steegers</LastName><ForeName>Eric A P</ForeName><Initials>EAP</Initials><AffiliationInfo><Affiliation>Department of Obstetrics &amp; Gynecology, Erasmus University Medical Center, Rotterdam, The Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gaillard</LastName><ForeName>Romy</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>The Generation R Study Group, Erasmus University Medical Center, Rotterdam, The Netherlands; Department of Pediatrics, Sophia Children's Hospital, Erasmus University Medical Center, Rotterdam, The Netherlands. Electronic address: r.gaillard@erasmusmc.nl.</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>02</Month><Day>04</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Am Heart J</MedlineTA><NlmUniqueID>0370465</NlmUniqueID><ISSNLinking>0002-8703</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D043925">Angiogenesis Inducing Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015415">Biomarkers</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011257">Pregnancy Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.10.1</RegistryNumber><NameOfSubstance UI="D040281">Vascular Endothelial Growth Factor Receptor-1</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D043925" MajorTopicYN="N">Angiogenesis Inducing Agents</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015415" MajorTopicYN="N">Biomarkers</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002648" MajorTopicYN="N">Child</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007231" MajorTopicYN="N">Infant, Newborn</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011225" MajorTopicYN="Y">Pre-Eclampsia</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011247" MajorTopicYN="N">Pregnancy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011257" MajorTopicYN="Y">Pregnancy Proteins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011446" MajorTopicYN="N">Prospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D040281" MajorTopicYN="N">Vascular Endothelial Growth Factor Receptor-1</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Childhood cardiac development</Keyword><Keyword MajorTopicYN="N">Maternal PlGF</Keyword><Keyword MajorTopicYN="N">Maternal sFlt-1</Keyword><Keyword MajorTopicYN="N">Pregnancy</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2021</Year><Month>8</Month><Day>26</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2021</Year><Month>12</Month><Day>23</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>1</Month><Day>29</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>2</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>4</Month><Day>12</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>2</Month><Day>6</Day><Hour>20</Hour><Minute>30</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35123935</ArticleId><ArticleId IdType="doi">10.1016/j.ahj.2022.01.016</ArticleId><ArticleId IdType="pii">S0002-8703(22)00025-4</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35123790</PMID><DateRevised><Year>2022</Year><Month>02</Month><Day>06</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1097-685X</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2021</Year><Month>Nov</Month><Day>25</Day></PubDate></JournalIssue><Title>The Journal of thoracic and cardiovascular surgery</Title><ISOAbbreviation>J Thorac Cardiovasc Surg</ISOAbbreviation></Journal>Right heart failure and patient selection for isolated tricuspid valve surgery.
To examine whether maternal angiogenic factors in the first half of pregnancy are associated with offspring left and right cardiac development.</AbstractText>In a population-based prospective cohort among 2,415 women and their offspring, maternal first and second trimester plasma PlGF and sFlt-1 concentrations were measured. Cardiac MRI was performed in their offspring at 10 years.</AbstractText>Maternal angiogenic factors were not associated with childhood cardiac outcomes in the total population. In children born small-for-their-gestational-age, higher maternal first trimester PlGF concentrations were associated with a lower childhood left ventricular mass&#xa0; (-0.24 SDS&#xa0; [95%CI -0.42, -0.05 per SDS increase in maternal PlGF]), whereas higher sFlt-1 concentrations were associated with higher childhood left ventricular mass&#xa0; (0.22 SDS&#xa0; [95%CI 0.09, 0.34 per SDS increase in maternal sFlt-1]). Higher second trimester maternal sFlt-1 concentrations were also associated with higher childhood left ventricular mass&#xa0; (P-value &lt;.05). In preterm born children, higher maternal first and second trimester sFlt-1/PlGF ratio were associated with higher childhood left ventricular mass&#xa0; (0.30 SDS&#xa0; [95%CI 0.01, 0.60], 0.22 SDS&#xa0; [95%CI -0.03, 0.40]) per SDS increase in maternal sFlt-1/PlGF ratio in first and second trimester respectively). No effects on other childhood cardiac outcomes were present within these higher-risk children.</AbstractText>In a low-risk population, maternal angiogenic factors are not associated with childhood cardiac ventricular structure, and function within the normal range. In children born small for their gestational age or preterm, an imbalance in maternal angiogenic factors in the first half of pregnancy was associated with higher childhood left ventricular mass only.</AbstractText>Copyright &#xa9; 2022 The Authors. Published by Elsevier Inc. All rights reserved.</CopyrightInformation>
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CRMP4 is required for the positioning and maturation of newly generated neurons in adult mouse hippocampus.
Adult neurogenesis is a phenomenon in which neural stem cells differentiate and mature to generate new neurons in the adult brain. In mammals, the sites where adult neurogenesis occurs are limited to the subgranular zone (SGZ) of the hippocampal dentate gyrus and the subventricular zone. In the hippocampus, newly generated neurons migrate into the granule cell layer (GCL) and are integrated into neural circuits. Previous studies have revealed that CRMP4, a member of the CRMP family, is expressed in immature neurons in the hippocampal SGZ of the adult brain. However, the role of CRMP4 in adult neurogenesis is unknown. To study the role of CRMP4 in hippocampal adult neurogenesis, we compared adult neurogenesis between wild type and CRMP4-/- mice. In CRMP4-/- mice, the number of doublecortin (DCX)-positive cells was comparable to that in wild-type mice, and some DCX-positive cells were ectopically located in the granule cell layer, suggesting that CRMP4 is involved in the migration of adult neurogenesis. In addition, the number of calretinin-positive new neurons in the SGZ was significantly increased, whereas the number of EdU/NeuN-double positive neurons was decreased in CRMP4-/- mice, suggesting that CRMP4 plays an important role in neuronal maturation. Because CRMP4 is expressed in immature neurons, its expression may regulate the migration from the SGZ to the GCL during neuronal maturation in hippocampal adult neurogenesis.
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Effects of white matter hyperintensities distribution and clustering on late-life cognitive impairment.
White matter hyperintensities (WMH) are a key hallmark of subclinical cerebrovascular disease and are known to impair cognition. Here, we parcellated WMH using a novel system that segments WMH based on both lobar regions and distance from the ventricles, dividing the brain into a coordinate system composed of 36 distinct parcels ('bullseye' parcellation), and then investigated the effect of distribution on cognition using two different analytic approaches. Data from a well characterized sample of healthy older adults (58 to 84&#xa0;years) who were free of dementia were included. Cognition was evaluated using 12 computerized tasks, factored onto 4 indices representing episodic memory, speed of processing, fluid reasoning and vocabulary. We first assessed the distribution of WMH according to the bullseye parcellation and tested the relationship between WMH parcellations and performance across the four cognitive domains. Then, we used a data-driven approach to derive latent variables within the WMH distribution, and tested the relation between these latent components and cognitive function. We observed that different, well-defined cognitive constructs mapped to specific WMH distributions. Speed of processing was correlated with WMH in the frontal lobe, while in the case of episodic memory, the relationship was more ubiquitous, involving most of the parcellations. A principal components analysis revealed that the 36 bullseye regions factored onto 3 latent components representing the natural aggrupation of WMH: fronto-parietal periventricular (WMH principally in the frontal and parietal lobes and basal ganglia, especially in the periventricular region); occipital; and temporal and juxtacortical WMH (involving WMH in the temporal lobe, and at the juxtacortical region from frontal and parietal lobes). We found that fronto-parietal periventricular and temporal &amp; juxtacortical WMH were independently associated with speed of processing and episodic memory, respectively. These results indicate that different cognitive impairment phenotypes might present with specific WMH distributions. Additionally, our study encourages future research to consider WMH classifications using parcellations systems other than periventricular and deep localizations.
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Morphine promotes migration and lung metastasis of mouse melanoma cells.
Morphine is an analgesic agent used for cancer pain management. There have been recent concerns that the immunosuppressant properties of morphine can also promote cancer metastasis. Morphine is an agonist for toll like receptor 4 (TLR4) that has a dual role in cancer development. The promotor or inhibitor role of morphine in cancer progression remains controversial. We investigated the effects of morphine on migration and metastasis of melanoma cells through TLR4 activation.</AbstractText>Mouse melanoma cells (B16F10) were treated with only morphine (0, 0.1, 1, and 10 &#x3bc;M) or in combination with a TLR4 inhibitor (morphine10 &#x3bc;M +CLI-095 1&#x3bc;M) for either 12 or 24 hours. Migration of cells was analyzed by transwell migration assays. Twenty C57BL/6 male mice were inoculated with B16F10 cells via the left ventricle of the heart and then randomly divided into two groups (n&#xa0;=&#xa0;10 each) that received either morphine (10 mg.kg-1</sup>, sub-q) or PBS injection for 21 days (control group). Animals were euthanized and their lungs removed for evaluation of metastatic nodules.</AbstractText>Morphine (0.1, 1, and 10 &#x3bc;M) increased cell migration after 12 hours (p &lt; 0.001) and after 24 hours of treatment with morphine (10 &#x3bc;M) (p &lt; 0.001). Treatment with CLI-095 suppressed migration compared to cells treated with morphine alone (p &lt; 0.001). Metastatic nodules&#xa0;in the&#xa0;morphine-treated group (64 nodules) were significantly higher than in the control group (40 nodules) (p &lt; 0.05).</AbstractText>Morphine increases the migration and metastasis of mouse melanoma cells by activating TLR4.</AbstractText>Copyright &#xa9; 2022 Sociedade Brasileira de Anestesiologia. Published by Elsevier Espa&#xf1;a, S.L.U. All rights reserved.</CopyrightInformation>
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Developmental thyroid disruption permanently affects the neuroglial output in the murine subventricular zone.
Neural stem cells (NSCs) in the adult brain are a source of neural cells for brain injury repair. We investigated whether their capacity to generate new neurons and glia is determined by thyroid hormone (TH) during development because serum levels peak during postnatal reorganization of the main NSC niche, the subventricular zone (SVZ). Re-analysis of mouse transcriptome data revealed increased expression of TH transporters and deiodinases in postnatal SVZ NSCs, promoting local TH action, concomitant with a burst in neurogenesis. Inducing developmental hypothyroidism reduced NSC proliferation, disrupted expression of genes implicated in NSC determination and TH signaling, and altered the neuron/glia output in newborns. Three-month-old adult mice recovering from developmental hypothyroidism had fewer olfactory interneurons and underperformed on short-memory odor tests, dependent on SVZ neurogenesis. Our data provide readouts permitting comparison with adverse long-term events following thyroid disruptor exposure and ideas regarding the etiology of prevalent neurodegenerative diseases in industrialized countries.
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Sex-specific effects of prenatal hypoxia on the cardiac endothelin system in adult offspring.
Fetal hypoxia, a major consequence of complicated pregnancies, impairs offspring cardiac tolerance to ischemia-reperfusion (I/R) insult; however, the mechanisms remain unknown. Endothelin-1 (ET-1) signaling through the endothelin A receptors (ET<sub>A</sub>) is associated with cardiac dysfunction. We hypothesized that prenatal hypoxia exacerbates cardiac susceptibility to I/R via increased ET-1 and ET<sub>A</sub> levels, whereas ET<sub>A</sub> inhibition ameliorates this. Pregnant Sprague-Dawley rats were exposed to normoxia (21% O<sub>2</sub>) or hypoxia (11% O<sub>2</sub>) on <i>gestational days 15-21</i>. Offspring were aged to 4 mo, and hearts were aerobically perfused or subjected to ex vivo I/R, with or without preinfusion with an ET<sub>A</sub> antagonist (ABT-627). ET-1 levels were assessed with ELISA in aerobically perfused and post-I/R left ventricles (LV). ET<sub>A</sub> and ET<sub>B</sub> levels were assessed by Western blotting in nonperfused LV. As hypothesized, ABT-627 infusion tended to improve post-I/R recovery in hypoxic females (<i>P</i> = 0.0528); however, surprisingly, ABT-627 prevented post-I/R recovery only in the hypoxic males (<i>P</i> &lt; 0.001). ET-1 levels were increased in post-I/R LV in both sexes regardless of the prenatal exposure (<i>P</i> &lt; 0.01). ET<sub>A</sub> expression was similar among all groups, whereas ET<sub>B</sub> (isoform C) levels were decreased in prenatally hypoxic females (<i>P</i> &lt; 0.05). In prenatally hypoxic males, ET<sub>A</sub> signaling may be essential for tolerance to I/R, whereas in prenatally hypoxic females, ET<sub>A</sub> may contribute to cardiac dysfunction. Our data illustrate that understanding the prenatal history has critical implications for treatment strategies in adult chronic diseases.<b>NEW &amp; NOTEWORTHY</b> We demonstrated that prenatal hypoxia (a common condition of pregnancy) can have profound differential effects on treatment strategies in adult cardiovascular disease. Our data using a rat model of prenatal hypoxia demonstrated that, as adults, although inhibition of endothelin (ET<sub>A</sub>) receptors before an ex vivo cardiac ischemic insult improved recovery in females, it strikingly prevented recovery in males. Our data indicate a sex-specific effect of prenatal hypoxia on the cardiac ET-1 system in adult offspring.
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Reverse Trans-Sellar Neuroendoscopic Management of a Large Rathke's Cleft Cyst Causing Obstructive Hydrocephalus: A Case Report.
Symptomatic Rathke's cleft cysts (RCCs) can be treated by surgical procedures, usually through an endonasal transsphenoidal corridor using either a microscope or an endoscope. We report a large suprasellar extended RCC causing obstructive hydrocephalus, which was efficiently managed by a novel surgical route named "reverse" trans-sellar approach using transventricular neuroendoscopy. A 48-year-old woman complained of persistent headache and a tendency to fall that had begun 6 months previously. The images obtained from MRI scan showed intra- and supra-sellar cystic masses occupying the third ventricle with obstruction of the foramina of Monro and the aqueduct of Sylvius. The cystic wall showed a slight enhancement, and the cystic contents showed iso-signal intensity on T1-and T2-weighted images. Instead of trans-nasal trans-sellar surgery, we decided to operate using a conventional transventricular endoscope. A thin cystic capsule, which blocked the foramina of Monro and the aqueduct of Sylvius, was fenestrated and removed and a third ventriculostomy was performed. The defect in the infundibulum between sellar and suprasellar cysts was widened and used as a corridor to drain cystic contents (reverse trans-sellar route). The final pathological finding revealed an RCC with focal metaplasia. We efficiently managed a large RCC by transventricular neuroendoscopic surgery with cyst fenestration and third ventriculostomy and simultaneously drained the sellar contents using a novel surgical route. Reverse trans-sellar neuroendoscopic surgery is a relevant treatment option for selective patients with large suprasellar extensions of RCCs.
2,330,365
Extraventricular Neurocytoma: Clinical Investigation of Heterogenous Prognosis.
Extraventricular neurocytoma (EVN) is an extremely rare neuronal neoplasm that arises outside the ventricle. The clinical implication of the heterogenous prognosis of this rare tumor has not yet been clarified. Herein, we analyzed our institutional series of EVN.</AbstractText>A total of eight consecutive cases were enrolled and investigated. The prognosis of EVN was analyzed and compared to that of central neurocytoma (CN).</AbstractText>There were two male and six female patients, and the median age was 36.5 years. The median tumor size was 38 mm, and the most common location of the tumor was the frontal lobe (3, 37.5%), followed by the parietal and temporal lobes. In brain imaging, four (50%) tumors showed peritumoral edema and three (37.5%) tumors showed calcification. All patients underwent gross total resection, and two (25%) underwent adjuvant radiotherapy. The 5-year overall survival (OS) was 55.6%, and the 2-year progression-free survival (PFS) was 42.9%. The OS and PFS of EVN were poor compared to those of CN. Although EVN is a single disease entity, individual patients showed varying prognosis. One patient showed no recurrence during the 7-year follow-up period; however, another patient had a recurrence 4 months after surgery and died 2 years later.</AbstractText>EVN may be a heterogenous disease entity. Additional cases with long-term followup are needed to develop optimal management protocols.</AbstractText>Copyright &#xa9; 2022 The Korean Brain Tumor Society, The Korean Society for Neuro-Oncology, and The Korean Society for Pediatric Neuro-Oncology.</CopyrightInformation>
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Abnormal corneal nerve morphology and brain volume in patients with schizophrenia.
Neurodevelopmental and neurodegenerative pathology occur in Schizophrenia. This study compared the utility of corneal confocal microscopy (CCM), an ophthalmic imaging technique with MRI brain volumetry in quantifying neuronal pathology and its relationship to cognitive dysfunction and symptom severity in schizophrenia. Thirty-six subjects with schizophrenia and 26 controls underwent assessment of cognitive function, symptom severity, CCM and MRI brain volumetry. Subjects with schizophrenia had lower cognitive function (P&#x2009;&#x2264;&#x2009;0.01), corneal nerve fiber density (CNFD), length (CNFL), branch density (CNBD), CNBD:CNFD ratio (P&#x2009;&lt;&#x2009;0.0001) and cingulate gyrus volume (P&#x2009;&lt;&#x2009;0.05) but comparable volume of whole brain (P&#x2009;=&#x2009;0.61), cortical gray matter (P&#x2009;=&#x2009;0.99), ventricle (P&#x2009;=&#x2009;0.47), hippocampus (P&#x2009;=&#x2009;0.10) and amygdala (P&#x2009;=&#x2009;0.68). Corneal nerve measures and cingulate gyrus volume showed no association with symptom severity (P&#x2009;=&#x2009;0.35-0.86 and P&#x2009;=&#x2009;0.50) or cognitive function (P&#x2009;=&#x2009;0.35-0.86 and P&#x2009;=&#x2009;0.49). Corneal nerve measures were not associated with metabolic syndrome (P&#x2009;=&#x2009;0.61-0.64) or diabetes (P&#x2009;=&#x2009;0.057-0.54). The area under the ROC curve distinguishing subjects with schizophrenia from controls was 88% for CNFL, 84% for CNBD and CNBD:CNFD ratio, 79% for CNFD and 73% for the cingulate gyrus volume. This study has identified a reduction in corneal nerve fibers and cingulate gyrus volume in schizophrenia, but no association with symptom severity or cognitive dysfunction. Corneal nerve loss identified using CCM may act as a rapid non-invasive surrogate marker of neurodegeneration in patients with schizophrenia.
2,330,367
Paraneoplastic Neuromyelitis Optica Spectrum Disorder Associated With Lung Adenocarcinoma: A Case Report.
Neuromyelitis Optica spectrum disorder is an inflammatory demyelinating disease affecting the central nervous system (CNS), characterized by triad optic neuritis, transverse myelitis, and area postrema syndrome. Antibodies directed against aquaporin-4 (AQP-4), a water channel expressed on the astrocytic membrane, are supposed to play a pathogenic role and are detected in ~80% of cases. Clinical signs of Neuromyelitis Optica spectrum disorder (NMOSD) in elderly patients should arouse the suspicion of paraneoplastic etiology. In this article, we discussed a case of a 76-year-old woman with a 2-month history of confusion, dysarthria, and progressive bilateral leg weakness. A whole-body CT scan showed a neoformation of 5 cm in diameter in the median lobe infiltrating the mediastinal pleura. The tumor had already spread to both the upper and lower right lobes, parietal pleura, and multiple lymph nodes. Pleural cytology revealed adenocarcinoma cells. The brain MRI documented hyperintense alteration in fluid-attenuated inversion recovery (FLAIR) images, involving the anterior portion of the corpus callosum and the periependymal white matter surrounding the lateral ventricles, with mild contrast enhancement on the same areas and meningeal tissue. T2-weighted spinal cord MRI sequences showed extended signal hyperintensity from bulbo-cervical junction to D7 metamer, mainly interesting the central component and the gray matter. Cerebrospinal fluid analysis revealed no neoplastic cells. Serum AQP-4 immunoglobulin (IgG) antibodies were found. Meanwhile, the patient rapidly developed progressive paraparesis and decreased level of consciousness. High-dose intravenous methylprednisolone therapy was started but her conditions rapidly deteriorated. No other treatment was possible.
2,330,368
Perivascular space is associated with brain atrophy in patients with multiple sclerosis.
Perivascular space (PVS) is associated with neurodegenerative and neuroimmune diseases. Multiple sclerosis (MS) is traditionally a neuroimmune disease. However, studies show neurodegeneration also plays a vital role in MS. At present, most studies conclude severer PVS in MS is an imaging marker of neuroinflammation, while a 7T MRI study suggests that PVS in MS is associated with neurodegeneration.</AbstractText>In this study, 82 MS patients (n=82) and 32 healthy controls (n=32) were enrolled. The following indexes were measured: the number, size and distribution of PVS, the PVS score, corpus callosum index (CCI), corpus callosum area (CCA), the ratio of the corpus callosum to the cranium (CCR), aligned third ventricle width (a3VW), and unaligned third ventricle width (u3VW).</AbstractText>The PVS score (4 vs.</i> 3, P=0.041), PVSs number (103.280&#xb1;45.107 vs.</i> 87.625&#xb1;30.139, P=0.035), and enlarged perivascular spaces (EPVSs) number (9 vs.</i> 1, P&lt;0.001) of MS patients were significantly higher than in the healthy controls. PVSs number (23.5 vs.</i> 13) and EPVSs number (1 vs.</i> 0) in the basal ganglia (BG), and EPVSs number (3 vs.</i> 0) in centrum semiovale (CSO) of MS patients were significantly higher than in the healthy controls, P&lt;0.001. In MS patients, PVS was correlated with age and hypertension but not to the extended disability status scale (EDSS) score and other clinical data. In MS patients, PVS score was correlated with CCA (rs=0.272; P=0.013) and the CCR (rs=0.219; P=0.048), and PVSs number was correlated with CCA (rs=0.255; P=0.021), the correlation disappeared after adjusting hypertension and age. In MS patients in remission, PVSs number was correlated with CCA (rs=0.487; P=0.019), CCR (rs=0.479; P=0.021), and PVS score was correlated with CCA (rs=0.453; P=0.03). After adjustment of hypertension and age, the total number of PVSs was correlated with CCA (rs=0.419; P=0.049).</AbstractText>The PVS load in MS patients was heavier than healthy people, especially in BG and CSO. PVS was not correlated with EDSS in MS patients. The PVS of MS patients was associated with CCA and CCR, and PVSs number was independently related with CCA in MS patients in remission.</AbstractText>2022 Quantitative Imaging in Medicine and Surgery. All rights reserved.</CopyrightInformation>
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Natriuresis During an Acute Intravenous Sodium Chloride Infusion in Conscious Sprague Dawley Rats Is Mediated by a Blood Pressure-Independent &#x3b1;<sub>1</sub>-Adrenoceptor-Mediated Mechanism.
The mechanisms that sense alterations in total body sodium content to facilitate sodium homeostasis in response to an acute sodium challenge that does not increase blood pressure have not been fully elucidated. We hypothesized that the renal sympathetic nerves are critical to mediate natriuresis via &#x3b1;<sub>1</sub>- or &#x3b2;-adrenoceptors signal transduction pathways to maintain sodium balance in the face of acute increases in total body sodium content that do not activate the pressure-natriuresis mechanism. To address this hypothesis, we used acute bilateral renal denervation (RDNX), an anteroventral third ventricle (AV3V) lesion and &#x3b1;<sub>1</sub>- or &#x3b2;-antagonism during an acute 1M NaCl sodium challenge in conscious male Sprague Dawley rats. An acute 1M NaCl infusion did not alter blood pressure and evoked profound natriuresis and sympathoinhibition. Acute bilateral RDNX attenuated the natriuretic and sympathoinhibitory responses evoked by a 1M NaCl infusion [peak natriuresis (&#x3bc;eq/min) sham 14.5 &#xb1; 1.3 vs. acute RDNX: 9.2 &#xb1; 1.4, <i>p</i> &lt; 0.05; plasma NE (nmol/L) sham control: 44 &#xb1; 4 vs. sham 1M NaCl infusion 11 &#xb1; 2, <i>p</i> &lt; 0.05; acute RDNX control: 42 &#xb1; 6 vs. acute RDNX 1M NaCl infusion 25 &#xb1; 3, <i>p</i> &lt; 0.05]. In contrast, an AV3V lesion did not impact the cardiovascular, renal excretory or sympathoinhibitory responses to an acute 1M NaCl infusion. Acute i.v. &#x3b1;<sub>1</sub>-adrenoceptor antagonism with terazosin evoked a significant drop in baseline blood pressure and significantly attenuated the natriuretic response to a 1M NaCl load [peak natriuresis (&#x3bc;eq/min) saline 17.2 &#xb1; 1.4 vs. i.v. terazosin 7.8 &#xb1; 2.5, <i>p</i> &lt; 0.05]. In contrast, acute &#x3b2;-adrenoceptor antagonism with i.v. propranolol infusion did not impact the cardiovascular or renal excretory responses to an acute 1M NaCl infusion. Critically, the natriuretic response to an acute 1M NaCl infusion was significantly blunted in rats receiving a s.c. infusion of the &#x3b1;<sub>1</sub>-adrenoceptor antagonist terazosin at a dose that did not lower baseline blood pressure [peak natriuresis (&#x3bc;eq/min) sc saline: 18 &#xb1; 1 vs. sc terazosin 7 &#xb1; 2, <i>p</i> &lt; 0.05]. Additionally, a s.c. infusion of the &#x3b1;<sub>1</sub>-adrenoceptor antagonist terazosin further attenuated the natriuretic response to a 1M NaCl infusion in acutely RDNX animals. Collectively these data indicate a specific role of a blood pressure-independent renal sympathetic nerve-dependent &#x3b1;<sub>1</sub>-adrenoceptor-mediated pathway in the natriuretic and sympathoinhibitory responses evoked by acute increases in total body sodium.
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Imaging of Dentate Nucleus Pathologies: A Case Series.
The dentate nucleus is the largest cerebellar nucleus, and it controls cognition and voluntary movement. It is found in each cerebellar hemisphere medially and posterolateral to the lateral ventricle. Pathologies of the dentate nucleus can be detected using computed tomography and magnetic resonance imaging of the brain. Here, we present a case series of seven different dentate nucleus diseases and their neuroimaging findings recovered from archives of our institution.
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Constitutive activation of canonical Wnt signaling disrupts choroid plexus epithelial fate.
The choroid plexus secretes cerebrospinal fluid and is critical for the development and function of the brain. In the telencephalon, the choroid plexus epithelium arises from the Wnt- expressing cortical hem. Canonical Wnt signaling pathway molecules such as nuclear &#x3b2;-CATENIN are expressed in the mouse and human embryonic choroid plexus epithelium indicating that this pathway is active. Point mutations in human &#x3b2;-CATENIN are known to result in the constitutive activation of canonical Wnt signaling. In a mouse model that recapitulates this perturbation, we report a loss of choroid plexus epithelial identity and an apparent transformation of this tissue to a neuronal identity. Aspects of this phenomenon are recapitulated in human embryonic stem cell derived organoids. The choroid plexus is also disrupted when &#x3b2;-Catenin is conditionally inactivated. Together, our results indicate that canonical Wnt signaling is required in a precise and regulated manner for normal choroid plexus development in the mammalian brain.
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Papillary Craniopharyngioma: A Type of Tumor Primarily Impairing the Hypothalamus - A Comprehensive Anatomo-Clinical Characterization of 350 Well-Described Cases.
Papillary craniopharyngiomas (PCPs) represent a rare histological type of craniopharyngiomas (CPs) usually involving the hypothalamus. This study systematically analyzes the clinical-anatomical correlation between tumor topography and symptoms related to hypothalamic dysfunction in the largest series of PCPs ever gathered.</AbstractText>From 5,346 CP reports published from 1856 to 2021, we selected 350 well-described cases of the squamous-papillary type. Clinical presentation, tumor topography, severity of hypothalamic adhesion, patient outcome, and tumor recurrence were thoroughly analyzed.</AbstractText>PCPs predominantly occur in adult (96.3%), male (61.7%) patients presenting with headache (63.4%), visual alterations (56.2%), and psychiatric disturbances (50.4%). Most PCPs are solid (50%), round (72%) lesions that occupy the third ventricle (3V, 94.8%) and show low-risk severity adhesions to the hypothalamus (66.8%). Two major topographical categories can be found: strictly 3V (57.5%), growing above an intact 3V floor, and not-strictly or infundibulo-tuberal (32.9%), expanding at the infundibulum and/or tuber cinereum. The hypothalamic syndrome predominated among strictly 3V PCPs (p &lt; 0.001). Psychiatric symptoms (p &lt; 0.001) and high-risk hypothalamic attachments (p = 0.031) related to unfavorable postoperative outcomes among patients treated from 2006 onwards. The not-strictly 3V topography was identified as the major predictor of high-risk hypothalamic attachments (71.2% correctly predicted), which, along with incomplete tumor removal (p = 0.018), underlies the higher tumor recurrence of this topography (p = 0.001).</AbstractText>This systematic review evidences that PCP topography is a major determinant of hypothalamic-related symptoms, type of hypothalamic attachments, and tumor recurrence rate. Accurate preoperative definition of PCP-hypothalamus relationships is essential for the judicious, safe management of these complex lesions.</AbstractText>&#xa9; 2021 S. Karger AG, Basel.</CopyrightInformation>
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[Craniopharyngioma Mimicking Chordoid Glioma].
Entirely intrinsic third ventricular craniopharyngiomas showed characteristics of a round/oval shaped tumor, with rare calcification and cyst formation, and pathologically squamous-papillary type with a positive BRAF<sup>V600E</sup> mutation. We report an extremely rare case of entirely intrinsic third ventricular craniopharyngioma, pathologically adamantiomatous but with BRAF<sup>V600E</sup> mutation genetically, developed in a 35-year-old female. It was oval-shaped, with no calcification or cyst, and showed homogeneous enhancement. As shown in this case, it was difficult to differentiate this pathology from chordoid glioma of third ventricle, and the difficulty of this differential diagnosis has not been well documented in previous studies. Our case further implied the importance of molecular diagnosis for subclassification of craniopharyngioma. The BRAF<sup>V600E</sup>-mutated craniopharyngioma could be the target for the development of treatment with preoperative BRAF-inhibitors. Therefore, differentiation between entirely intrinsic third ventricular craniopharyngiomas and chordoid glioma could be new issue. In this report, we discuss about the preoperative differential diagnosis from chordoid glioma and the literature review. (Received 12 August, 2021; Accepted 21 September, 2021; Published 1 February, 2022).
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Hemorrhagic Stroke: Endoscopic Aspiration.
Intracerebral hemorrhage (ICH) and intraventricular hemorrhage (IVH) carry a very dismal prognosis. Several medical and surgical attempts have been made to reduce mortality and to improve neurological outcomes in survivors. Aggressive surgical treatment of ICH through craniotomy and microsurgical evacuation did not prove to be beneficial to these patients, compared to the best medical treatment. Similarly, the conventional treatment of IVH using an EVD is often effective in controlling ICP only initially, as it is very likely for the EVD to become obstructed by blood clots, requiring frequent replacements with a consequent increase of infection rates.Minimally invasive techniques have been proposed to manage these cases. Some are based on fibrinolytic agents that are infused in the hemorrhagic site through catheters with a single burr hole. Others are possible thanks to the development of neuroendoscopy. Endoscopic removal of ICH through a mini-craniotomy or a single burr hole, and via a parafascicular white matter trajectory, proved to reduce mortality in this population, and further randomized trials are expected to show whether also a better neurological outcome can be obtained in survivors. Moreover, endoscopy offers the opportunity to access the ventricular system to aspirate blood clots in patients with IVH. In such cases, the restoration of patency of the entire CSF pathway has the potential to improve outcome and reduce complications and now it is believed to decrease shunt-dependency.
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Electro-energetics of Biventricular, Septal and Conduction System Pacing.
Abnormal electrical activation of the ventricles creates abnormalities in cardiac mechanics. Local contraction patterns, as reflected by strain, are not only out of phase, but also show opposing length changes in early and late activated regions. Consequently, the efficiency of cardiac pump function (the amount of stroke work generated by a unit of oxygen consumed), is approximately 30% lower in dyssynchronous than in synchronous hearts. Maintaining good cardiac efficiency appears important for long-term outcomes. Biventricular, left ventricular septal, His bundle and left bundle branch pacing may minimise the amount of pacing-induced dyssynchrony and efficiency loss when compared to conventional right ventricular pacing. An extensive animal study indicates maintenance of mechanical synchrony and efficiency during left ventricular septal pacing and data from a few clinical studies support the idea that this is also the case for left bundle branch pacing and His bundle pacing. This review discusses electro-mechanics and mechano-energetics under the various paced conditions and provides suggestions for future research.
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Endoscopic third ventriculostomy for adults with hydrocephalus: creating a prognostic model for success: protocol for a retrospective multicentre study (Nordic ETV).<Pagination><StartPage>e055570</StartPage><MedlinePgn>e055570</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">e055570</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1136/bmjopen-2021-055570</ELocationID><Abstract><AbstractText Label="INTRODUCTION" NlmCategory="BACKGROUND">Endoscopic third ventriculostomy (ETV) is becoming an increasingly widespread treatment for hydrocephalus, but research is primarily based on paediatric populations. In 2009, Kulkarni <i>et al</i> created the ETV Success score to predict the outcome of ETV in children. The purpose of this study is to create a prognostic model to predict the success of ETV for adult patients with hydrocephalus. The ability to predict who will benefit from an ETV will allow better primary patient selection both for ETV and shunting. This would reduce additional second procedures due to primary treatment failure. A success score specific for adults could also be used as a communication tool to provide better information and guidance to patients.</AbstractText><AbstractText Label="METHODS AND ANALYSIS" NlmCategory="METHODS">The study will adhere to the Transparent Reporting of a multivariable prediction model for Individual Prognosis Or Diagnosis reporting guidelines and conducted as a retrospective chart review of all patients&#x2265;18 years of age treated with ETV at the participating centres between 1 January 2010 and 31 December 2018. Data collection is conducted locally in a standardised database. Univariate analysis will be used to identify several strong predictors to be included in a multivariate logistic regression model. The model will be validated using K-fold cross validation. Discrimination will be assessed using area under the receiver operating characteristic curve (AUROC) and calibration with calibration belt plots.</AbstractText><AbstractText Label="ETHICS AND DISSEMINATION" NlmCategory="BACKGROUND">The study is approved by appropriate ethics or patient safety boards in all participating countries.</AbstractText><AbstractText Label="TRIAL REGISTRATION NUMBER" NlmCategory="BACKGROUND">NCT04773938; Pre-results.</AbstractText><CopyrightInformation>&#xa9; Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Tefre</LastName><ForeName>Sondre</ForeName><Initials>S</Initials><Identifier Source="ORCID">0000-0002-9516-4440</Identifier><AffiliationInfo><Affiliation>Department of Neurosurgery, Rigshospitalet, Copenhagen, Denmark sondre.tefre@regionh.dk.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lilja-Cyron</LastName><ForeName>Alexander</ForeName><Initials>A</Initials><Identifier Source="ORCID">0000-0003-2915-249X</Identifier><AffiliationInfo><Affiliation>Department of Neurosurgery, Rigshospitalet, Copenhagen, Denmark.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Arvidsson</LastName><ForeName>Lisa</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Karolinska University Hospital, Stockholm, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bartek</LastName><ForeName>Jiri</ForeName><Initials>J</Initials><Identifier Source="ORCID">0000-0002-2911-1914</Identifier><AffiliationInfo><Affiliation>Department of Neurosurgery, Karolinska University Hospital, Stockholm, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Corell</LastName><ForeName>Alba</ForeName><Initials>A</Initials><Identifier Source="ORCID">0000-0002-6329-2392</Identifier><AffiliationInfo><Affiliation>Department of Neurosurgery, Sahlgrenska University Hospital, Goteborg, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Forsse</LastName><ForeName>Axel</ForeName><Initials>A</Initials><Identifier Source="ORCID">0000-0002-0325-0262</Identifier><AffiliationInfo><Affiliation>Department of Neurosurgery, Odense University Hospital, Odense, Denmark.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Glud</LastName><ForeName>Andreas N&#xf8;rgaard</ForeName><Initials>AN</Initials><Identifier Source="ORCID">0000-0003-3339-6120</Identifier><AffiliationInfo><Affiliation>Department of Neurosurgery, Aarhus University Hospital, Aarhus, Denmark.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hamdeh</LastName><ForeName>Sami Abu</ForeName><Initials>SA</Initials><Identifier Source="ORCID">0000-0001-6173-8357</Identifier><AffiliationInfo><Affiliation>Department of Neurosurgery, Uppsala University Hospital, Uppsala, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hansen</LastName><ForeName>Frederik Lundgaard</ForeName><Initials>FL</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Aarhus University Hospital, Aarhus, Denmark.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Huotarinen</LastName><ForeName>Antti</ForeName><Initials>A</Initials><Identifier Source="ORCID">0000-0002-7212-5780</Identifier><AffiliationInfo><Affiliation>Department of Neurosurgery NeuroCenter, Kuopio University Hospital, Kuopio, Pohjois-Savo, Finland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Johansson</LastName><ForeName>Conny</ForeName><Initials>C</Initials><Identifier Source="ORCID">0000-0001-8612-7173</Identifier><AffiliationInfo><Affiliation>Department of Neurosurgery, University Hospital of Ume&#xe5;, Ume&#xe5;, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>K&#xe4;m&#xe4;r&#xe4;inen</LastName><ForeName>Olli-Pekka</ForeName><Initials>OP</Initials><Identifier Source="ORCID">0000-0002-6111-3725</Identifier><AffiliationInfo><Affiliation>Department of Neurosurgery NeuroCenter, Kuopio University Hospital, Kuopio, Pohjois-Savo, Finland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Korhonen</LastName><ForeName>Tommi</ForeName><Initials>T</Initials><Identifier Source="ORCID">0000-0002-5500-9200</Identifier><AffiliationInfo><Affiliation>Department of Neurosurgery, Oulu University Hospital, Oulu, Finland.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Research Unit of Clinical Neuroscience, University of Oulu, Oulu, Finland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kotkansalo</LastName><ForeName>Anna</ForeName><Initials>A</Initials><Identifier Source="ORCID">0000-0002-3182-7786</Identifier><AffiliationInfo><Affiliation>Department of Neurosurgery and Brain Injury Centre, Turku University Hospital, Turku, Finland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mansoor</LastName><ForeName>Nadia Mauland</ForeName><Initials>NM</Initials><Identifier Source="ORCID">0000-0001-5668-3275</Identifier><AffiliationInfo><Affiliation>Department of Neurosurgery, St Olavs Hospital Universitetssykehuset i Trondheim, Trondheim, Tr&#xf8;ndelag, Norway.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mendoza Mireles</LastName><ForeName>Eduardo Erasmo</ForeName><Initials>EE</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Oslo University Hospital Ullevaal, Oslo, Norway.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Neurosurgery, Rikshospitalet University Hospital, Oslo, Norway.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Miscov</LastName><ForeName>Rares</ForeName><Initials>R</Initials><Identifier Source="ORCID">0000-0003-0302-3497</Identifier><AffiliationInfo><Affiliation>Department of Neurosurgery, Aalborg University Hospital, Aalborg, North Denmark Region, Denmark.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Munthe</LastName><ForeName>Sune</ForeName><Initials>S</Initials><Identifier Source="ORCID">0000-0002-4793-9803</Identifier><AffiliationInfo><Affiliation>Department of Neurosurgery, Odense University Hospital, Odense, Denmark.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nittby-Redebrandt</LastName><ForeName>Henrietta</ForeName><Initials>H</Initials><Identifier Source="ORCID">0000-0003-0140-8107</Identifier><AffiliationInfo><Affiliation>Department of Neurosurgery, Lund University Hospital, Lund, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Obad</LastName><ForeName>Nina</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Haukeland University Hospital, Bergen, Norway.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pedersen</LastName><ForeName>Lars Kjelsberg</ForeName><Initials>LK</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, University Hospital of North Norway, Tromso, Norway.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Posti</LastName><ForeName>Jussi</ForeName><Initials>J</Initials><Identifier Source="ORCID">0000-0002-5925-5193</Identifier><AffiliationInfo><Affiliation>Department of Neurosurgery and Brain Injury Centre, Turku University Hospital, Turku, Finland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Raj</LastName><ForeName>Rahul</ForeName><Initials>R</Initials><Identifier Source="ORCID">0000-0003-4243-9591</Identifier><AffiliationInfo><Affiliation>Department of Neurosurgery, Helsinki University Hospital and University of Helsinki, Helsinki, Finland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Satop&#xe4;&#xe4;</LastName><ForeName>Jarno</ForeName><Initials>J</Initials><Identifier Source="ORCID">0000-0002-2674-0301</Identifier><AffiliationInfo><Affiliation>Department of Neurosurgery, Helsinki University Hospital and University of Helsinki, Helsinki, Finland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>St&#xe5;hl</LastName><ForeName>Nils</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Lund University Hospital, Lund, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tetri</LastName><ForeName>Sami</ForeName><Initials>S</Initials><Identifier Source="ORCID">0000-0002-1387-9136</Identifier><AffiliationInfo><Affiliation>Department of Neurosurgery, Oulu University Hospital, Oulu, Finland.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Research Unit of Clinical Neuroscience, University of Oulu, Oulu, Finland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tobieson</LastName><ForeName>Lovisa</ForeName><Initials>L</Initials><Identifier Source="ORCID">0000-0003-2284-846X</Identifier><AffiliationInfo><Affiliation>Department of Neurosurgery in Link&#xf6;ping, and Department of Biomedical and Clinical Sciences, Link&#xf6;ping University, Linkoping, &#xd6;sterg&#xf6;tland, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Juhler</LastName><ForeName>Marianne</ForeName><Initials>M</Initials><Identifier Source="ORCID">0000-0003-2652-7495</Identifier><AffiliationInfo><Affiliation>Department of Neurosurgery, Rigshospitalet, Copenhagen, Denmark.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><DataBankList CompleteYN="Y"><DataBank><DataBankName>ClinicalTrials.gov</DataBankName><AccessionNumberList><AccessionNumber>NCT04773938</AccessionNumber></AccessionNumberList></DataBank></DataBankList><PublicationTypeList><PublicationType UI="D000078325">Clinical Trial Protocol</PublicationType><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>01</Month><Day>31</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>BMJ Open</MedlineTA><NlmUniqueID>101552874</NlmUniqueID><ISSNLinking>2044-6055</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="D006849" MajorTopicYN="Y">Hydrocephalus</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007223" MajorTopicYN="N">Infant</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015337" MajorTopicYN="N">Multicenter Studies as Topic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011379" MajorTopicYN="N">Prognosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020542" MajorTopicYN="Y">Third Ventricle</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014696" MajorTopicYN="N">Ventriculostomy</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">epidemiology</Keyword><Keyword MajorTopicYN="Y">neuropathology</Keyword><Keyword MajorTopicYN="Y">neuroradiology</Keyword><Keyword MajorTopicYN="Y">neurosurgery</Keyword></KeywordList><CoiStatement>Competing interests: None declared.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>2</Month><Day>2</Day><Hour>5</Hour><Minute>32</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>2</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>3</Month><Day>22</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35105647</ArticleId><ArticleId IdType="pmc">PMC8808390</ArticleId><ArticleId IdType="doi">10.1136/bmjopen-2021-055570</ArticleId><ArticleId IdType="pii">bmjopen-2021-055570</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Reddy GK, Bollam P, Caldito G, et al. . 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Missing data and multiple imputation in clinical epidemiological research. Clin Epidemiol 2017;9:157&#x2013;66. 10.2147/CLEP.S129785</Citation><ArticleIdList><ArticleId IdType="doi">10.2147/CLEP.S129785</ArticleId><ArticleId IdType="pmc">PMC5358992</ArticleId><ArticleId IdType="pubmed">28352203</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35105393</PMID><DateRevised><Year>2022</Year><Month>02</Month><Day>02</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1467-1107</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Feb</Month><Day>02</Day></PubDate></JournalIssue><Title>Cardiology in the young</Title><ISOAbbreviation>Cardiol Young</ISOAbbreviation></Journal>Very preterm and very low birthweight infant with pulmonary atresia intact ventricular septum, right ventricle-dependent coronary circulation, and discontinuous pulmonary arteries.
Prematurity and low birthweight are associated with increased mortality in infants undergoing cardiac surgery. Pulmonary atresia with intact ventricular septum and right ventricle-dependent coronary circulation carries one of the highest risks of mortality. We present a patient who was born at 28 weeks of gestation at 1.2 kg, with pulmonary atresia intact ventricular septum, right ventricle-dependent coronary circulation, coronary artery atresia, and discontinuous pulmonary arteries, who successfully underwent palliation with a modified Blalock-Taussig shunt, pulmonary arterioplasty, and subsequently a bidirectional Glenn.
2,330,377
Primary Progressive Multiple Sclerosis in a Portuguese Patient With Neurofibromatosis Type 1.
Neurofibromatosis type 1 (NF1) is a frequent genetic neurocutaneous syndrome and multiple sclerosis (MS) is an acquired demyelinating disease of the central nervous system. The association of both these diseases is rare. In this case report, we describe a 25-year-old man with gait impairment, upper limbs tremor, slurred speech, and urinary symptoms in the form of urinary urgency and incontinence. These symptoms started a year earlier and had a progressive course. Examination revealed scattered caf&#xe9;-au-lait spots, right ptosis, bilateral horizontal and vertical nystagmus, mild dysarthria, quadriparesis with generalized hyperreflexia and bilateral Babinski signs, upper limb tremor, bilateral proprioceptive errors, bilateral appendicular dysmetria, and severe gait ataxia. Brain MRI showed lesions involving the deep and subcortical white matter, as well as thalami, with no enhancement after administration of gadolinium, suggestive of focal areas of signal intensity (FASI) in the setting of NF1. There were also oval lesions in the periventricular white matter, perpendicular to the ventricles and involving the corpus callosum, which were atypical for FASI. Spinal MRI also demonstrated several lesions, which mildly enhance after administration of gadolinium. Cerebrospinal fluid (CSF) examination revealed mild lymphocytic pleocytosis (18/&#x3bc;L), mildly elevated protein (0.53 g/L), normal glucose, and positive oligoclonal IgG bands. Extensive laboratory workup, including microbiological CSF studies, aquaporin-4-IgG, myelin-oligodendrocyte glycoprotein-IgG, autoimmune screening, and viral serology, was negative. The genetic study revealed a new mutation in the NF1 gene that was not previously reported. We intend to discuss the genetic and autoimmune mechanisms by which MS and NF1 appear to be related and draw attention to this association because a timely diagnosis of MS is important to prevent further disability in NF1 patients.
2,330,378
The Intraventricular Pseudocyst as a Complication of Ventriculoperitoneal Shunt: A Rare Case Report and Review of Literature.
Ventriculoperitoneal shunting is the most common treatment for hydrocephalus. Various complications can occur, including the formation of a pseudocyst. Reviewing the literature, we report a rare case of intraventricular pseudocyst as a complication of ventriculoperitoneal shunt in a child. A seven-month-old child with a ventriculoperitoneal shunt presented with a large intraventricular cyst on computed tomography of the skull. It was decided to remove the ventriculoperitoneal shunt, perform an endoscopic fenestration of the pseudocyst, and place an external ventricular shunt. After 14 days of antibiotic treatment, a new ventriculoperitoneal shunt was placed. The child grew up with delayed milestones and epilepsy. Pseudocysts may be a possible complication of ventriculoperitoneal shunting. It is rare for pseudocysts to be located inside the ventricle, as in the present case; the pathophysiology is unclear, and the child can have sequelae after treatment.
2,330,379
Clinical Outcome, Cognitive Function, and Quality of Life after Endoscopic Third Ventriculostomy versus Ventriculo-Peritoneal Shunt in Non-Tumor Hydrocephalus.
Endoscopic Third Ventriculostomy (ETV) is increasingly being accepted as the treatment of choice in place of Ventriculo-Peritoneal (VP) Shunt for hydrocephalus. However, their differences in cognitive and Quality of Life (QOL) scores have not been studied much in children.</AbstractText>To compare the outcome, cognitive function, and QOL between ETV and VP shunt.</AbstractText>Patients of non-tumor hydrocephalus treated with ETV or/and VP shunt underwent cognitive assessment (using modified child MMSE standardized as per the age group) and QOL (using PedsQL as per the age group in Physical, Emotional, Social, and School Functioning domains) in addition to the outcome of not requiring additional intervention.</AbstractText>Out of 139 patients, there were 29 infants and 40 children upto 14 years. Among these children, ETV was the primary intervention in 45, VP shunt in 24, and could be studied for a mean follow-up of 1.7 years. Though ETV required lesser additional intervention than VP shunt (19.2% vs. 28.6%) in toddlers and older children, there was no overall significant difference. Subnormal cognitive scores were noted in 25%, 40%, and 50% after ETV, single shunt procedure, and multiple shunt procedures, respectively, with no statistically significant difference. Among the different domains of QOL, the child reported scores in the social domain were significantly better after ETV than VP shunt (475[+13] vs. 387[+43], P value 0.03), whereas most other scores were non-significantly better following ETV.</AbstractText>Patients who underwent ETV show a trend for better clinical outcome, cognitive function, and QOL with significantly better child-reported QOL scores in the social domain.</AbstractText>
2,330,380
Complications Encountered with ETV in Infants with Congenital Hydrocephalus.
Hydrocephalus is an abnormal excessive accumulation of cerebrospinal fluid (CSF) in the cavity and spaces of the brain. Endoscopic third ventriculostomy (ETV) has been an established treatment modality for congenital hydrocephalus. However, in very young infants, the results are challenging. In our study, we have evaluated whether ETV really offers an acceptable complication-free postoperative course.</AbstractText>To study the complication and mortality rate in infants having congenital hydrocephalus treated with ETV.</AbstractText>This is a single-center prospective study conducted at the Department of Neurosurgery, K. G. M. U, Lucknow, from January 2019 to February 2020. We studied 40 infants presenting with clinical and radiological features suggestive of congenital hydrocephalus. Follow-up was done at the first, third, and sixth months after discharge.</AbstractText>Nineteen infants (47.5%) required a second CSF diversion procedure at 6 months of follow-up. The failure rate was significantly higher in infants less than 3 months of age (P value of 0.04). The ETV site bulge was the most frequent complication encountered in the postoperative period, occurring in 20% of the cases. Eventually, all these infants required a ventriculoperitoneal shunt; 15% developed clinical features consistent with the diagnosis of post-ETV meningitis. The ETV site CSF leak occurred in 10% of the patients. Subdural hygroma developed in 7.5% of the patients; 17.5% of the patients contributed to mortality with a mean time of expiry of 22 days post-procedure. All these deaths had multifactorial causes and could not be said as a complication or failure of ETV.</AbstractText>We do not recommend ETV for infants less than 3 months because of a high failure rate. The ETV site bulge was the most reliable and earliest marker of failure and a second CSF diversion surgery should be immediately considered.</AbstractText>
2,330,381
Endoscopic Third Ventriculostomy And Choroid Plexus Coagulation in Infants: Current Concepts and Illustrative Cases.
The global burden of pediatric hydrocephalus is high, causing significant morbidity and mortality among children especially in low- and middle-income countries. It is commonly treated with ventriculoperitoneal shunting, but in recent years, the combined use of endoscopic third ventriculostomy (ETV) and choroid plexus coagulation (CPC) has enabled patients to live without a shunt.</AbstractText>We aim to give an overview of ETV+CPC for the treatment of hydrocephalus in infants, focusing on patient selection, perioperative care, and long-term follow-up.</AbstractText>We summarize observational studies and randomized trials on the efficacy and safety ETV+CPC, mainly from Uganda and North America. The equipment needs and operative steps of ETV+CPC are enumerated. At the end of the article, three illustrative cases of infants who underwent ETV+CPC with differing outcomes are presented.</AbstractText>The likelihood of success following ETV+CPC is the highest among infants older than 1 month, those with noninfectious hydrocephalus (e.g., aqueductal stenosis and myelomeningocele), and those previously without a shunt. Poor outcomes are seen in patients with posthemorrhagic hydrocephalus or evidence of cisternal scarring. Failure of ETV+CPC most commonly occurs within 3-6 months of surgery.</AbstractText>ETV+CPC is an effective and safe alternative to ventriculoperitoneal shunting in appropriately selected infants with hydrocephalus. Long-term studies on functional and neurocognitive outcomes following ETV+CPC will help guide clinicians in decision making, allowing as many children as possible to attain shunt freedom.</AbstractText>
2,330,382
Endoscopic Third Ventriculostomy - A Review.
Endoscopic third ventriculostomy (ETV) has become a proven modality for treating obstructive and selected cases of communicating hydrocephalus.</AbstractText>This review aims to summarize the indications, preoperative workup, surgical technique, results, postoperative care, complications, advantages, and limitations of an ETV.</AbstractText>A thorough review of PubMed and Google Scholar was performed. This review is based on the relevant articles and authors' experience.</AbstractText>ETV is indicated in obstructive hydrocephalus and selected cases of communicating hydrocephalus. Studying preoperative imaging is critical, and a detailed assessment of interthalamic adhesions, the thickness of floor, arteries or membranes below the third ventricle floor, and prepontine cistern width is essential. Blunt perforation in a thin floor, while bipolar cautery at low settings and water jet dissection are preferred in a thick floor. The appearance of stoma pulsations and intraoperative ventriculostomography reassure stoma and basal cistern patency. The intraoperative decision for shunt, external ventricular drainage, or Ommaya reservoir can be taken. Magnetic resonance ventriculography and cine phase-contrast magnetic resonance imaging can determine stoma patency. Good postoperative care with repeated cerebrospinal fluid drainage enhances outcomes in selected cases. Though the complications mostly occur in an early postoperative phase, delayed lethal ones may happen. Watching live surgeries, assisting expert surgeons, and practicing on cadavers and models can shorten the learning curve.</AbstractText>ETV is an excellent technique for managing obstructive and selected cases of communicating hydrocephalus. Good case selection, methodical technique, and proper training under experts are vital.</AbstractText>
2,330,383
Lumboperitoneal Shunts - Patient Selection, Technique, and Complication Avoidance: An Experience of 426 Cases.
Lumboperitoneal shunt is a known procedure for communicating hydrocephalus. Being an extracranial procedure, it can also be utilized in normal-sized ventricles.</AbstractText>To report our experience of lumboperitoneal shunt done with a minimal follow-up of 12 months with an emphasis on patient selection, technique, and complication avoidance.</AbstractText>This was a retrospective analysis of patients who underwent LP shunt during October 2014-October 2019 at the authors' institute. Inclusion criteria were patients with communicating hydrocephalus due to tubercular meningitis, normal pressure hydrocephalus, idiopathic intracranial hypertension, and postoperative refractory cerebrospinal fluid leaks. Data were collected for demographics, Glasgow coma scale and Glasgow outcome scale, vision, gait, memory, urinary incontinence, failed attempts, and complications.</AbstractText>A total of 426 patients underwent the LP shunt procedure. The commonest indication was tubercular meningitis followed by idiopathic intracranial hypertension and normal pressure hydrocephalus. Age ranged from 16 to 72 years. There were 255 male and 171 female patients. The mean follow-up was 41 &#xb1; 8 months. Overall, 301 patients (70.6%) had neurological improvement. Shunt-related complications occurred in 112 (26.29%) patients, of which shunt block was the commonest. Other complications were infection in 17 (3.9%) patients and extrusion in four (0.9%) patients. Transient postural headache was seen in 46 (10.7%) patients, which gradually improved.</AbstractText>Lumboperitoneal shunt was found to be a safe and effective treatment in appropriately selected communicating hydrocephalus patients. A meticulous technique reduces the complication rate.</AbstractText>
2,330,384
Neurofibromatosis Type 1 Related Hydrocephalus.
The prevalence of hydrocephalus among patients with neurofibromatosis type I (NF1) is estimated to be between 1 and 13%. Aqueductal webs, chiasmatic-hypothalamic tumors, and thalamic mass effect related to NF changes are the common causes of NF1-related hydrocephalus. Brain tumors and moyamoya syndrome may mimic the clinical presentation of hydrocephalus in children with NF1, and should be ruled out while evaluating children with headaches. Treatment of NF1-related hydrocephalus should be personally tailored, including shunts, endoscopic procedures such as septostomy and third ventriculostomy, and tumor resection or debulking. Despite these personalized treatments, many of the primary treatments (including shunts and endoscopic procedures) fail, and patients should be screened and followed accordingly. In the current manuscript, we review the causes of NF1-related hydrocephalus, as well as treatment options.
2,330,385
Diagnostic Nuances and Surgical Management of Arrested Hydrocephalus.
Hydrocephalus is characterized by the increased volume of cerebrospinal fluid (CSF) with enlarged cerebral ventricles. In nearly 50% of the patients, if left untreated, the balance between CSF production and absorption is achieved, resulting in arrested hydrocephalus (AH). However, 15% of them who are diagnosed as arrested can progress over a period of time. Importantly, a large fraction of patients with hydrocephalus in India, may not have access to tertiary level care. Therefore, both progressive hydrocephalus and insidious progression of AH with related mortality and morbidity could be higher in India. The pathophysiology behind AH and insidious progression of AH are poorly established. Unfortunately, there are no established clinical or radiological parameters identifying or predicting AH from progressive hydrocephalous. Diagnosis is often based on a combination of neurological, psychometric, and magnetic resonance imaging (MRI) findings. Invasive monitoring of intracranial pressure (ICP) and telemetric ICP measurement is increasingly helping surgeons to detect insidious progressive AH in the early stages. In patients with AH, surgery may not be always necessary and a conservative approach is often adopted. On the contrary, AH that becomes progressive may require intervention. Surgical intervention should not be delayed and endoscopic third ventriculostomy (ETV) is preferable over shunt placement. Importantly, comprehensive counseling and the appropriate selection of patients are pivotal in improving outcomes and reducing complications.
2,330,386
Prenatal Ventriculomegaly - Diagnosis, Prognostication and Management.
Fetal ventriculomegaly (VM) refers to the abnormal enlargement of one or more ventricles of the brain in-utero. The enlargement may or may not be related to ventricular obstruction and increased intracranial pressure; therefore, the term "hydrocephalus" is not used. VM is diagnosed usually in the mid-trimester when the atrial diameter (AD) of the lateral ventricle is more than 10 mm on one or both sides. A thorough workup is then required to identify the cause as the etiology is diverse. Fetal magnetic resonance imaging (MRI) may yield additional information. Serial ultrasound follow-up would be required to assess its progression with advancing gestation. The prognosis and long-term outcomes greatly depend upon the etiology, the severity at diagnosis, progression, and associations. This article reviews the definitions, diagnosis, and workup of fetal VM, discusses follow-up protocols and prognosis, and examines the role of fetal therapy, including fetoscopic surgery in its prenatal management.
2,330,387
Genetics and Molecular Pathogenesis of Human Hydrocephalus.
Hydrocephalus is a neurological disorder with an incidence of 80-125 per 100,000 live births in the United States. The molecular pathogenesis of this multidimensional disorder is complex and has both genetic and environmental influences. This review aims to discuss the genetic and molecular alterations described in human hydrocephalus, from well-characterized, heritable forms of hydrocephalus (e.g., X-linked hydrocephalus from L1CAM variants) to those affecting cilia motility and other complex pathologies such as neural tube defects and Dandy-Walker syndrome. Ventricular zone disruption is one key pattern among congenital and acquired forms of hydrocephalus, with abnormalities in cadherins, which mediate neuroepithelium/ependymal cell junctions and contribute to the pathogenesis and severity of the disease. Given the relationship between hydrocephalus pathogenesis and neurodevelopment, future research should elucidate the genetic and molecular mechanisms that regulate ventricular zone integrity and stem cell biology.
2,330,388
Exogenous polyserine and polyleucine are toxic to recipient cells.
Repeat-associated non-AUG (RAN) translation of mRNAs/transcripts responsible for polyglutamine (polyQ) diseases may generate peptides containing different mono amino acid tracts such as polyserine (polyS) and polyleucine (polyL). The propagation of aggregated polyQ from one cell to another is also an intriguing feature of polyQ proteins. However, whether the RAN translation-related polyS and polyL have the ability to propagate remains unclear, and if they do, whether the exogenous polyS and polyL exert toxicity on the recipient cells is also not known yet. In the present study, we found that aggregated polyS and polyL peptides spontaneously enter neuron-like cells and astrocytes in vitro. Aggregated polyS led to the degeneration of the differentiated neuron-like cultured cells. Likewise, the two types of aggregates taken up by astrocytes induced aberrant differentiation and cell death in vitro. Furthermore, injection of each of the two types of aggregates into the ventricles of adult mice resulted in their behavioral changes. The polyS-injected mice showed extensive vacuolar degeneration in the brain. Thus, the RAN translation-related proteins containing polyS and polyL have the potential to propagate and the proteins generated by all polyQ diseases might exert universal toxicity in the recipient cells.
2,330,389
Learning Pediatric Point-of-Care Ultrasound: How Many Cases Does Mastery of Image Interpretation Take?
Using an education and assessment tool, we examined the number of cases necessary to achieve a performance benchmark in image interpretation of pediatric soft tissue, cardiac, lung, and focused assessment with sonography for trauma (FAST) point-of-care ultrasound (POCUS) applications. We also determined interpretation difficulty scores to derive which cases provided the greatest diagnostic challenges.</AbstractText>Pediatric emergency physicians participated in web-based pediatric POCUS courses sponsored by their institution as a credentialing priority. Participants deliberately practiced cases until they achieved diagnostic interpretation scores of combined 90% accuracy, sensitivity, and specificity.</AbstractText>Of the 463 who enrolled, 379 (81.9%) completed cases. The median (interquartile range) number of cases required to achieve the performance benchmark for soft tissue was 94 (68-128); cardiac, 128 (86-201); lung, 87 (25-118); and FAST, 93 (68-133) (P &lt; 0001). Specifically, cases completed to achieve benchmark were higher for cardiac relative to other applications (P &lt; 0.0001 for all comparisons). In soft tissue cases, a foreign body was more difficult to diagnose than cobblestoning and hypoechoic collections (P = 0.036). Poor cardiac function and abnormal ventricles were more difficult to interpret with accuracy than normal (P &lt; 0.0001) or pericardial effusion cases (P = 0.01). The absence of lung sliding was significantly more difficult to interpret than normal lung cases (P = 0.028). The interpretation difficulty of various FAST imaging findings was not significantly different.</AbstractText>There was a significant variation in number of cases required to reach a performance benchmark. We also identified the specific applications and imaging findings that demonstrated the greatest diagnostic challenges. These data may inform future credentialing guidelines and POCUS learning interventions.</AbstractText>Copyright &#xa9; 2021 Wolters Kluwer Health, Inc. All rights reserved.</CopyrightInformation>
2,330,390
Aptamer-Based Screen of Neuropsychiatric Lupus Cerebrospinal Fluid Reveals Potential Biomarkers That Overlap With the Choroid Plexus Transcriptome.
As no gold-standard diagnostic test exists for neuropsychiatric systemic lupus erythematosus (NPSLE), we undertook this study to execute a broad screen of NPSLE cerebrospinal fluid (CSF) using an aptamer-based platform.</AbstractText>CSF was obtained from NPSLE patients and subjected to proteomic assay using the aptamer-based screen. Potential biomarkers were identified and validated in independent NPSLE cohorts in comparison to other neurologic diseases.</AbstractText>Forty proteins out of the 1,129 screened were found to be elevated in NPSLE CSF. Based on enzyme-linked immunosorbent assay validation, CSF levels of angiostatin, &#x3b1;2-macroglobulin, DAN, fibronectin, hepatocellular carcinoma clone 1, IgM, lipocalin 2, macrophage colony-stimulating factor (M-CSF), and serine protease inhibitor G1 were significantly elevated in a predominantly White NPSLE cohort (n = 24), compared to patients with other neurologic diseases (n = 54), with CSF IgM (area under the curve [AUC] 0.95) and M-CSF (AUC 0.91) being the most discriminatory proteins. In a second Hong Kong-based NPSLE cohort, CSF IgM (AUC 0.78) and lipocalin 2 (AUC 0.85) were the most discriminatory proteins. Several CSF proteins exhibited high diagnostic specificity for NPSLE in both cohorts. Elevated CSF complement C3 was associated with an acute confusional state. Eleven molecules elevated in NPSLE CSF exhibited concordant elevation in the choroid plexus, suggesting shared origins.</AbstractText>Lipocalin 2, M-CSF, IgM, and complement C3 emerge as promising CSF biomarkers of NPSLE with diagnostic potential.</AbstractText>&#xa9; 2022 American College of Rheumatology.</CopyrightInformation>
2,330,391
Recovery of right ventricular function after bilateral lung transplantation for pediatric pulmonary hypertension.
Lung transplantation is a therapeutic option for end-stage pediatric pulmonary hypertension (PH). Right ventricular (RV) recovery post-lung transplant in children with PH has not been well-described, and questions persist about the peri-operative course and post-transplant cardiac function after lung transplantation in medically refractory PH patients with baseline RV dysfunction.</AbstractText>A single-center chart review identified patients with childhood PH who subsequently underwent bilateral orthotopic lung transplantation between 2000 and 2020. Twenty-six patients met criteria; three were excluded due to echocardiograms not available for digital review. RV fractional area change (FAC) and left ventricular eccentricity index (LVEI) were determined prior to transplantation, and at 1, 3, 6, and 12-month post-transplantation.</AbstractText>Fourteen of 23 patients had baseline RV dysfunction. The median age at transplantation was 16.5&#xa0;years and 13.9&#xa0;years for those with and without baseline RV dysfunction, respectively. Of the 14 with baseline RV dysfunction, 12 (86%) were alive 1-year post-transplantation. All patients with baseline RV dysfunction had increased RV-FAC post-transplantation with normalization of RV-FAC in 70% at 3&#xa0;months and 100% of patients by 12-month post-transplantation. Duration of ventilation (p&#xa0;=&#xa0;.4), intensive care unit (p&#xa0;=&#xa0;.5), or hospital stay (p&#xa0;=&#xa0;.9) was not associated with pre-transplant RV function.</AbstractText>Among pediatric patients with PH and RV dysfunction, pre-transplantation RV function was not associated with short-term outcomes. All patients with baseline RV dysfunction had improvement in RV function, justifying consideration of lung transplantation among pediatric patients with end-stage PH and RV dysfunction.</AbstractText>&#xa9; 2022 Wiley Periodicals LLC.</CopyrightInformation>
2,330,392
An atypical case of hemodialysis access stent migration.
Endovascular stent fractures are commonly seen in arteries but are rare events in the venous system. Stents deployed in hemodialysis vascular accesses can fracture and migrate to proximal locations. Complications associated with stent fracture include in-stent stenosis and central vein stenosis. In this report, we present a unique case of a hemodialysis access stent fracture that migrated to the left ventricle and manifested with chest pain.
2,330,393
Coblation debulking of a paediatric laryngeal plexiform neurofibroma: a pragmatic response to a rare tumour.
Laryngeal neurofibroma is a rare but important differential diagnosis in a patient presenting with stridor. In paediatric patients, these lesions present a management conundrum: complete surgical resection is the established treatment of choice, but an aggressive approach can be detrimental to developing anatomy. We report the case of a plexiform neurofibroma affecting the right hemilarynx of a 3-year-old boy. Endoscopy revealed a large tumour, involving the right aryepiglottic fold and extending into the piriform sinus, ventricle and the false cord. Given the patient's young age and the challenging tumour location, the lesion was debulked, rather than resected, using coblation (low-temperature plasma radiofrequency ablation). At 30&#xa0;months follow-up, the neurofibroma has mildly increased in size-in line with expectations that these lesions exhibit slow growth throughout childhood-but there are no significant respiratory symptoms and there is no functional impairment.
2,330,394
Computational Modeling and Simulation to Quantify the Effects of Obstructions on the Performance of Ventricular Catheters Used in Hydrocephalus Treatment.
Pediatric hydrocephalus is a debilitating condition that affects an estimated 1-2 in 1000 newborns, and there is no cure. A traditional treatment is surgical insertion of a shunt system which was designed 50&#xa0;years ago, and minimal ensuing progress has been made in improving the failure rate of these devices resulting in the need for multiple brain surgeries during an affected child's lifetime for shunt replacement. A first step toward decreasing the failure rate is to optimize the ventricular catheter component of the shunt to minimize its propensity for obstruction. Given the many geometric properties and patient specific in vivo conditions needed to characterize the fluid dynamics affecting ventricular catheter performance, validated computational simulation is an efficient method to rapidly explore and evaluate the effects of this large parameter space to inform improved design and to investigate patient specific shunt performance. This chapter provides the details on how to build a computational model of a ventricle and implanted catheter, analyze the fluid dynamics through an obstructed catheter, and postprocess the results to predict catheter performance for varying geometry and in vivo conditions.
2,330,395
Toxicity of high-molecular-weight polyethylene glycols in Sprague Dawley rats.
Polyethylene glycol (PEG) is present in a variety of products. Little is known regarding the accumulation of high-molecular-weight PEGs or the long-term effects resulting from PEG accumulation in certain tissues, especially the choroid plexus. We evaluated the toxicity of high-molecular-weight PEGs administered to Sprague Dawley rats. Groups of 12 rats per sex were administered subcutaneous injections of 20, 40, or 60 kDa PEG or intravenous injections of 60 kDa PEG at 100 mg PEG/kg body weight/injection once a week for 24 weeks. A significant decrease in triglycerides occurred in the 60 kDa PEG groups. PEG treatment led to a molecular-weight-related increase in PEG in plasma and a low level of PEG in cerebrospinal fluid. PEG was excreted in urine and feces, with a molecular-weight-related decrease in the urinary excretion. A higher prevalence of anti-PEG IgM was observed in PEG groups; anti-PEG IgG was not detected. PEG treatment produced a molecular-weight-related increase in vacuolation in the spleen, lymph nodes, lungs, and ovaries/testes, without an inflammatory response. Mast cell infiltration at the application site was noted in all PEG-treated groups. These data indicate that subcutaneous and intravenous exposure to high-molecular-weight PEGs produces anti-PEG IgM antibody responses and tissue vacuolation without inflammation.
2,330,396
Mouse models characterize GNAO1 encephalopathy as a neurodevelopmental disorder leading to motor anomalies: from a severe G203R to a milder C215Y mutation.
GNAO1 encephalopathy characterized by a wide spectrum of neurological deficiencies in pediatric patients originates from de novo heterozygous mutations in the gene encoding G&#x3b1;o, the major neuronal G protein. Efficient treatments and even the proper understanding of the underlying etiology are currently lacking for this dominant disease. Adequate animal models of GNAO1 encephalopathy are urgently needed. Here we describe establishment and characterization of mouse models of the disease based on two point mutations in GNAO1 with different clinical manifestations. One of them is G203R leading to the early-onset epileptic seizures, motor dysfunction, developmental delay and intellectual disability. The other is C215Y producing much milder clinical outcomes, mostly-late-onset hyperkinetic movement disorder. The resultant mouse models show distinct phenotypes: severe neonatal lethality in GNAO1[G203R]/&#x2009;+&#x2009;mice vs. normal vitality in GNAO1[C215Y]/&#x2009;+&#x2009;. The latter model further revealed strong hyperactivity and hyperlocomotion in a panel of behavioral assays, without signs of epilepsy, recapitulating the patients' manifestations. Importantly, despite these differences the two models similarly revealed prenatal brain developmental anomalies, such as enlarged lateral ventricles and decreased numbers of neuronal precursor cells in the cortex. Thus, our work unveils GNAO1 encephalopathy as to a large extent neurodevelopmental malady. We expect that this understanding and the tools we established will be instrumental for future therapeutic developments.
2,330,397
The Wilms Tumor Gene <i>wt1a</i> Contributes to Blood-Cerebrospinal Fluid Barrier Function in Zebrafish.
The Wilms tumor suppressor gene <i>Wt1</i> encodes a zinc finger transcription factor, which is highly conserved among vertebrates. It is a key regulator of urogenital development and homeostasis but also plays a role in other organs including the spleen and the heart. More recently additional functions for Wt1 in the mammalian central nervous system have been described. In contrast to mammals, bony fish possess two paralogous <i>Wt1</i> genes, namely <i>wt1a</i> and <i>wt1b.</i> By performing detailed <i>in situ</i> hybridization analyses during zebrafish development, we discovered new expression domains for <i>wt1a</i> in the dorsal hindbrain, the caudal medulla and the spinal cord. Marker analysis identified <i>wt1a</i> expressing cells of the dorsal hindbrain as ependymal cells of the choroid plexus in the myelencephalic ventricle. The choroid plexus acts as a blood-cerebrospinal fluid barrier and thus is crucial for brain homeostasis. By employing <i>wt1a</i> mutant larvae and a dye accumulation assay with fluorescent tracers we demonstrate that Wt1a is required for proper choroid plexus formation and function. Thus, Wt1a contributes to the barrier properties of the choroid plexus in zebrafish, revealing an unexpected role for Wt1 in the zebrafish brain.
2,330,398
LncRNA GAS5/miR-137 Is a Hypoxia-Responsive Axis Involved in Cardiac Arrest and Cardiopulmonary Cerebral Resuscitation.
Cardiac arrest/cardiopulmonary resuscitation (CA/CPR) represents one of the devastating medical emergencies and is associated with high mortality and neuro-disability. Post-cardiac arrest syndrome (PCAS) is mechanistically ascribed to acute systemic ischemia/reperfusion(I/R) injury. The lncRNA/microRNA/mRNA networks have been found to play crucial roles in the pathogenesis of the hypoxia-responsive diseases. Nonetheless, the precise molecular mechanisms by which lncRNA/miRNA/mRNA axes are involved in the astrocyte-microglia crosstalk in CA/CPR have not been fully elucidated.</AbstractText>We collected and purified the exosomes from the blood of CA/CPR patients and supernatant of OGD/R-stimulated astrocytes. On the basis of microarray analysis, bioinformatic study, and luciferase activity determination, we speculated that lncRNA GAS5/miR-137 is implicated in the astrocyte-microglia crosstalk under the insult of systemic I/R injury. The regulation of lncRNA GAS5/miR-137 on INPP4B was examined by cellular transfection in OGD/R cell culture and by lateral ventricle injection with miR-137 agomir in CA/CPR mice model. Flow cytometry and immunofluorescence staining were performed to detect the microglial apoptosis, M1/M2 phenotype transformation, and neuroinflammation. Neurological scoring and behavior tests were conducted in CA/CPR group, with miR-137 agomir lateral-ventricle infusion and in their controls.</AbstractText>In all the micRNAs, miR-137 was among the top 10 micRNAs that experienced greatest changes, in both the blood of CA/CPR patients and supernatant of OGD/R-stimulated astrocytes. Bioinformatic analysis revealed that miR-137 was sponged by lncRNA GAS5, targeting INPP4B, and the result was confirmed by Luciferase activity assay. qRT-PCR and Western blotting showed that lncRNA GAS5 and INPP4B were over-expressed whereas miR-137 was downregulated in the blood of CA/CPR patients, OGD/R-stimulated astrocytes, and brain tissue of CA/CPR mice. Silencing lncRNA GAS5 suppressed INPP4B expression, but over-expression of miR-137 negatively modulated its expression. Western blotting exhibited that PI3K and Akt phosphorylation was increased when lncRNA GAS5 was silenced or miR-137 was over-expressed. However, PI3K and Akt phosphorylation was notably suppressed in the absence of miR-137, almost reversing their phosphorylation in the silencing lncRNA GAS5 group. Then we found that GAS5 siRNA or miR-137 mimic significantly increased cell viability and alleviated apoptosis after OGD/R injury. Furthermore, over-expression of miR-137 attenuated microglial apoptosis and neuroinflammation in CA/CPR mice model, exhibiting significantly better behavioral tests after CA/CPR.</AbstractText>LncRNA GAS5/miR-137 may be involved in the astrocyte-microglia communication that inhibits PI3K/Akt signaling activation via</i> regulation of INPP4B during CA/CPR.</AbstractText>Copyright &#xa9; 2022 Jing, Tuxiu, Xiaobing, Guijun, Lulu, Jie, Lu, Liying, Xiaoxing and Jingjun.</CopyrightInformation>
2,330,399
Application of Evans Index in Normal Pressure Hydrocephalus Patients: A Mini Review.
With an ever-growing aging population, the prevalence of normal pressure hydrocephalus (NPH) is increasing. Clinical symptoms of NPH include cognitive impairment, gait disturbance, and urinary incontinence. Surgery can improve symptoms, which leads to the disease's alternative name: treatable dementia. The Evans index (EI), defined as the ratio of the maximal width of the frontal horns to the maximum inner skull diameter, is the most commonly used index to indirectly assess the condition of the ventricles in NPH patients. EI measurement is simple, fast, and does not require any special software; in clinical practice, an EI &gt;0.3 is the criterion for ventricular enlargement. However, EI's measurement methods, threshold setting, correlation with ventricle volume, and even its clinical value has been questioned. Based on the EI, the z-EI and anteroposterior diameter of the lateral ventricle index were derived and are discussed in this review.