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2,329,600 | Factors Associated With Gastrostomy Tube Complications in Infants With Congenital Heart Disease.<Pagination><StartPage>273</StartPage><EndPage>279</EndPage><MedlinePgn>273-279</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.jss.2022.07.022</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0022-4804(22)00472-3</ELocationID><Abstract><AbstractText Label="INTRODUCTION">Children with congenital heart disease (CHD) often experience feeding intolerance due to aspiration, inability to tolerate feed volume, or reflux within the first few months of life, requiring a surgically placed gastrostomy tube (GT) for durable enteral access. However, complications such as GT dislodgement, cellulitis, and leakage related to GT use are common. GT-related complications can lead to unscheduled pediatric surgery clinic or emergency room (ER) visits, which can be time consuming for the family and increase overall healthcare costs. We sought to identify factors associated with GT complications within 2 wk after GT surgery and 1-y after discharge home following GT placement in infants with CHD.</AbstractText><AbstractText Label="METHODS">We performed a retrospective cohort study using the Society of Thoracic Surgeons database and electronic medical records from a tertiary children's hospital. We identified infants <1 y old underwent CHD surgery followed by GT surgery between September 2013-August 2018. Demographics, pre-operative feeding regimen, comorbidities, and GT-related utilization were measured. Postoperative GT complications (e.g., GT cellulitis, leakage, dislodgement, obstruction, and granulation tissue) within 2 wk after the GT surgery and an unplanned pediatric surgery clinic or ER visit within 1-y after discharge home were captured. Bivariate comparisons and multivariable logistic regression evaluated factors associated with GT complications and unplanned clinic or ER visits. A Kaplan-Meier failure curve examined the timing of ER/clinic visits.</AbstractText><AbstractText Label="RESULTS">Of 152 infants who underwent CHD then GT surgeries, 66% (N = 101) had postoperative GT complications. Overall, 83 unscheduled clinic visits were identified after discharge, with 37% (N = 31) due to concerns about granulation tissue. Of 137 ER visits, 48% (N = 66) were due to accidental GT dislodgement. Infants who were hospitalized for ≥2 wk after GT surgery had more complications than those discharged home within 2 wk of the GT surgery (40.6% versus 15.7%, P = 0.002). Infants receiving oral nutrition before CHD surgery (38.6% versus 60%, P=<0.001) or with single ventricle defects (19.8% versus 37.3%, P = 0.02) had fewer GT complications. After adjusting for type of cardiac anomaly, infants receiving oral nutrition prior to CHD surgery had a decreased likelihood of GT complications (odds ratio OR 0.46; 95% confidence intervals CI:0.23-0.93). A Kaplan-Meier failure curve demonstrated that 50% of the cohort experienced a complication leading to an unscheduled ER/clinic visit within 6 mo after discharge.</AbstractText><AbstractText Label="CONCLUSIONS">Unplanned visits to the ER or pediatric surgery clinic occur frequently for infants with CHD requiring a surgically placed GT. Oral feedings before cardiac surgery associated with fewer GT complications. Prolonged hospitalization associated with more GT complications. Optimizing outpatient care and family education regarding GT maintenance may reduce unscheduled visits for this high-risk, device-dependent infant population.</AbstractText><CopyrightInformation>Copyright © 2022 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Tran</LastName><ForeName>Nhu N</ForeName><Initials>NN</Initials><AffiliationInfo><Affiliation>Fetal and Neonatal Institute, Division of Neonatology, Children's Hospital Los Angeles, Department of Pediatrics, Keck School of Medicine of the University of Southern California, Los Angeles, California. Electronic address: ntran@chla.usc.edu.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mahdi</LastName><ForeName>Elaa M</ForeName><Initials>EM</Initials><AffiliationInfo><Affiliation>Division of Pediatric Surgery, Children's Hospital Los Angeles, Los Angeles, CA Department of Surgery, Keck School of Medicine of the University of Southern California, Los Angeles, California.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ourshalimian</LastName><ForeName>Shadassa</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Division of Pediatric Surgery, Children's Hospital Los Angeles, Los Angeles, CA Department of Surgery, Keck School of Medicine of the University of Southern California, Los Angeles, California.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sanborn</LastName><ForeName>Stephanie</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Clinical Nutrition and Lactation Services, Children's Hospital Los Angeles, Los Angeles, California.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Alquiros</LastName><ForeName>Maria Theresa</ForeName><Initials>MT</Initials><AffiliationInfo><Affiliation>Division of Cardiothoracic Surgery, Children's Hospital Los Angeles, Los Angeles, CA Department of Surgery, Keck School of Medicine of the University of Southern California, Los Angeles, California.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kingston</LastName><ForeName>Paige</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Division of Pediatric Surgery, Children's Hospital Los Angeles, Los Angeles, CA Department of Surgery, Keck School of Medicine of the University of Southern California, Los Angeles, California.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lascano</LastName><ForeName>Danny</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Division of Pediatric Surgery, Children's Hospital Los Angeles, Los Angeles, CA Department of Surgery, Keck School of Medicine of the University of Southern California, Los Angeles, California.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Herrington</LastName><ForeName>Cynthia</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Division of Cardiothoracic Surgery, Children's Hospital Los Angeles, Los Angeles, CA Department of Surgery, Keck School of Medicine of the University of Southern California, Los Angeles, California.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Votava-Smith</LastName><ForeName>Jodie K</ForeName><Initials>JK</Initials><AffiliationInfo><Affiliation>Division of Cardiology, Children's Hospital Los Angeles and Keck School of Medicine, University of Southern California, Los Angeles, California.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kelley-Quon</LastName><ForeName>Lorraine I</ForeName><Initials>LI</Initials><AffiliationInfo><Affiliation>Division of Pediatric Surgery, Children's Hospital Los Angeles, Los Angeles, CA Department of Surgery, Keck School of Medicine of the University of Southern California, Los Angeles, California; Department of Population and Public Health Sciences, University of Southern California, Los Angeles, California.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>UL1 TR001855</GrantID><Acronym>TR</Acronym><Agency>NCATS 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>08</Month><Day>26</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Surg Res</MedlineTA><NlmUniqueID>0376340</NlmUniqueID><ISSNLinking>0022-4804</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007223" MajorTopicYN="N">Infant</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007231" MajorTopicYN="N">Infant, Newborn</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002648" MajorTopicYN="N">Child</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005774" MajorTopicYN="Y">Gastrostomy</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002481" MajorTopicYN="N">Cellulitis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007441" MajorTopicYN="N">Intubation, Gastrointestinal</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006330" MajorTopicYN="Y">Heart Defects, Congenital</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011183" MajorTopicYN="N">Postoperative Complications</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Complications</Keyword><Keyword MajorTopicYN="N">Congenital heart disease</Keyword><Keyword MajorTopicYN="N">Gastrostomy tube</Keyword><Keyword MajorTopicYN="N">Infants</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>2</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>7</Month><Day>8</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>7</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="pmc-release"><Year>2023</Year><Month>12</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>8</Month><Day>29</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>10</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>8</Month><Day>28</Day><Hour>18</Hour><Minute>9</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36030602</ArticleId><ArticleId IdType="mid">NIHMS1898583</ArticleId><ArticleId IdType="pmc">PMC10231870</ArticleId><ArticleId IdType="doi">10.1016/j.jss.2022.07.022</ArticleId><ArticleId IdType="pii">S0022-4804(22)00472-3</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Virani SS, Alonso A, Benjamin EJ, et al. 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Pediatr Qual Saf. 2017;2:e016.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6132912</ArticleId><ArticleId IdType="pubmed">30229155</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedBookArticle><BookDocument><PMID Version="1">31536269</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK546663</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-32811">Physiology, AV Junction<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Tandon</LastName><ForeName>Shan</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Medical University of the Americas</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Alzahrani</LastName><ForeName>Talal</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Taibah University</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>Atrioventricular (AV) junction is the area separating atria and the ventricles of the heart. Specifically, when talking about the AV junction, the focus is put more on its contents, the AV node and the nonbranching bundle of His. The AV junction plays a role in the pathology including atrioventricular nodal re-entrant tachycardia (AVNRT) and junctional rhythms which are rhythms that originate at the AV junction due to disruption in communication from the SA node.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-32811" sec="article-32811.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32811" sec="article-32811.s2">Issues of Concern</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32811" sec="article-32811.s3">Cellular Level</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32811" sec="article-32811.s4">Development</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32811" sec="article-32811.s5">Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32811" sec="article-32811.s6">Mechanism</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32811" sec="article-32811.s7">Pathophysiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32811" sec="article-32811.s8">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32811" sec="article-32811.s9">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32811" sec="article-32811.s10">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>8</Month><Day>29</Day></ContributionDate><ReferenceList><Reference><Citation>George SA, Faye NR, Murillo-Berlioz A, Lee KB, Trachiotis GD, Efimov IR. At the Atrioventricular Crossroads: Dual Pathway Electrophysiology in the Atrioventricular Node and its Underlying Heterogeneities. Arrhythm Electrophysiol Rev. 2017 Dec;6(4):179-185.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC5739891</ArticleId><ArticleId IdType="pubmed">29326832</ArticleId></ArticleIdList></Reference><Reference><Citation>Wessels A, Markman MW, Vermeulen JL, Anderson RH, Moorman AF, Lamers WH. The development of the atrioventricular junction in the human heart. Circ Res. 1996 Jan;78(1):110-7.</Citation><ArticleIdList><ArticleId IdType="pubmed">8603493</ArticleId></ArticleIdList></Reference><Reference><Citation>van Weerd JH, Christoffels VM. The formation and function of the cardiac conduction system. Development. 2016 Jan 15;143(2):197-210.</Citation><ArticleIdList><ArticleId IdType="pubmed">26786210</ArticleId></ArticleIdList></Reference><Reference><Citation>Voss F, Eckardt L, Busch S, Estner HL, Steven D, Sommer P, von Bary C, Neuberger HR. [AV-reentrant tachycardia and Wolff-Parkinson-White syndrome : Diagnosis and treatment]. Herzschrittmacherther Elektrophysiol. 2016 Dec;27(4):381-389.</Citation><ArticleIdList><ArticleId IdType="pubmed">27878364</ArticleId></ArticleIdList></Reference><Reference><Citation>Mangi MA, Jones WM, Mansour MK, Napier L. StatPearls [Internet] StatPearls Publishing; Treasure Island (FL): 2022. Aug 22, Atrioventricular Block Second-Degree.</Citation><ArticleIdList><ArticleId IdType="pubmed">0</ArticleId></ArticleIdList></Reference><Reference><Citation>Kesler K, Lahham S. Tachyarrhythmia in Wolff-Parkinson-White Syndrome. West J Emerg Med. 2016 Jul;17(4):469-70.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC4944806</ArticleId><ArticleId IdType="pubmed">27429700</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31536269</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">30725661</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK536976</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-26507">Pacemaker Syndrome | Atrioventricular (AV) junction is the area separating atria and the ventricles of the heart. Specifically, when talking about the AV junction, the focus is put more on its contents, the AV node and the nonbranching bundle of His. The AV junction plays a role in the pathology including atrioventricular nodal re-entrant tachycardia (AVNRT) and junctional rhythms which are rhythms that originate at the AV junction due to disruption in communication from the SA node.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-32811" sec="article-32811.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32811" sec="article-32811.s2">Issues of Concern</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32811" sec="article-32811.s3">Cellular Level</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32811" sec="article-32811.s4">Development</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32811" sec="article-32811.s5">Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32811" sec="article-32811.s6">Mechanism</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32811" sec="article-32811.s7">Pathophysiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32811" sec="article-32811.s8">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32811" sec="article-32811.s9">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32811" sec="article-32811.s10">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>8</Month><Day>29</Day></ContributionDate><ReferenceList><Reference><Citation>George SA, Faye NR, Murillo-Berlioz A, Lee KB, Trachiotis GD, Efimov IR. At the Atrioventricular Crossroads: Dual Pathway Electrophysiology in the Atrioventricular Node and its Underlying Heterogeneities. Arrhythm Electrophysiol Rev. 2017 Dec;6(4):179-185.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC5739891</ArticleId><ArticleId IdType="pubmed">29326832</ArticleId></ArticleIdList></Reference><Reference><Citation>Wessels A, Markman MW, Vermeulen JL, Anderson RH, Moorman AF, Lamers WH. The development of the atrioventricular junction in the human heart. Circ Res. 1996 Jan;78(1):110-7.</Citation><ArticleIdList><ArticleId IdType="pubmed">8603493</ArticleId></ArticleIdList></Reference><Reference><Citation>van Weerd JH, Christoffels VM. The formation and function of the cardiac conduction system. Development. 2016 Jan 15;143(2):197-210.</Citation><ArticleIdList><ArticleId IdType="pubmed">26786210</ArticleId></ArticleIdList></Reference><Reference><Citation>Voss F, Eckardt L, Busch S, Estner HL, Steven D, Sommer P, von Bary C, Neuberger HR. [AV-reentrant tachycardia and Wolff-Parkinson-White syndrome : Diagnosis and treatment]. Herzschrittmacherther Elektrophysiol. 2016 Dec;27(4):381-389.</Citation><ArticleIdList><ArticleId IdType="pubmed">27878364</ArticleId></ArticleIdList></Reference><Reference><Citation>Mangi MA, Jones WM, Mansour MK, Napier L. StatPearls [Internet] StatPearls Publishing; Treasure Island (FL): 2022. Aug 22, Atrioventricular Block Second-Degree.</Citation><ArticleIdList><ArticleId IdType="pubmed">0</ArticleId></ArticleIdList></Reference><Reference><Citation>Kesler K, Lahham S. Tachyarrhythmia in Wolff-Parkinson-White Syndrome. West J Emerg Med. 2016 Jul;17(4):469-70.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC4944806</ArticleId><ArticleId IdType="pubmed">27429700</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31536269</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">30725661</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK536976</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-26507">Pacemaker Syndrome</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Iqbal</LastName><ForeName>Arshad Muhammad</ForeName><Initials>AM</Initials><AffiliationInfo><Affiliation>Oak Hill Hospital, Brooksville, FL</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jamal</LastName><ForeName>Syed F.</ForeName><Initials>SF</Initials><AffiliationInfo><Affiliation>National institute of Cardiovascular Diseases, Karachi, Pakistan.</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>Pacemakers have become an established modality for long-term management of life-threatening arrhythmias and improve the quality of life of affected patients significantly. Pacemakers have also become a cornerstone in the management of cardiomyopathies. Conventionally, these devices pace the ventricle in isolation, often leading to improper or mistimed atrial and ventricular contraction causing a reduction in cardiac output. This may be due to mistimed atrial contraction occurring against closed atrioventricular (AV) valve or atrial contraction occurring too close to ventricular contraction, producing back pressure in venous circulation systems and loss of atrial contribution to the ventricular output. Since the invention of this therapy in 1958, physicians have reported reductions in cardiac output as a response to ventricular pacing. Although baroreceptor reflexes do compensate for this by increasing peripheral vascular resistance, this is not always the case. In patients who fail to compensate for the loss of cardiac output with these mechanisms, a wide variety of symptoms are noted and mostly attributable to a loss in cardiac output and decreased peripheral resistance. This phenomenon and the resulting constellation of signs and symptoms is referred to as pacemaker syndrome. |
2,329,601 | Transtemporal brain contrast-enhanced ultrasound in children: preliminary experience in patients without neurological disorders. | To evaluate the use of transtemporal brain contrast-enhanced ultrasound (CEUS) to assess cerebral blood perfusion in a cohort of children without neurological disorders.</AbstractText>We included pediatric patients who were undergoing a clinically-indicated CEUS study. Brain scans were performed with a Siemens Sequoia scanner and a 4V1 transducer, that was placed on the left transtemporal bone. Brain scans were performed simultaneously with the images of the clinically-indicated organ of interest. Qualitative and quantitative analysis was performed to evaluate the hemispherical blood flow at the level of the midbrain during the wash-in and wash-out phases of the time-intensity curve. Clinical charts were reviewed to evaluate post-CEUS adverse events.</AbstractText>Five patients were evaluated (mean age 5.8 ± 5.1 years). Qualitatively, more avid enhancement in the midbrain than the cortex was observed. Structures depicted ranged between the centrum semiovale at the level of the lateral ventricles and the midbrain. A quantitative analysis conducted on four patients demonstrated less avid perfusion on the contralateral (i.e. right) side, with a mean left/right ratio ranging between 1.51 and 4.07. In general, there was a steep positive wash-in slope starting at approximately 10 s after contrast injection, reaching a peak intensity around 15-26 s on the left side, and 17-29 s on the right side. No adverse events were reported.</AbstractText>Transtemporal brain CEUS is feasible and safe in the pediatric population and allows qualitative and quantitative assessment of cerebral perfusion.</AbstractText>© 2022. Società Italiana di Ultrasonologia in Medicina e Biologia (SIUMB).</CopyrightInformation> |
2,329,602 | Strain-dependent stress relaxation behavior of healthy right ventricular free wall. | The increasing evidence of stress-strain hysteresis in large animal or human myocardium calls for extensive characterizations of the passive viscoelastic behavior of the myocardium. Several recent studies have investigated and modeled the viscoelasticity of the left ventricle while the right ventricle (RV) viscoelasticity remains poorly understood. Our goal was to characterize the biaxial viscoelastic behavior of RV free wall (RVFW) using two modeling approaches. We applied both quasi-linear viscoelastic (QLV) and nonlinear viscoelastic (NLV) theories to experimental stress relaxation data from healthy adult ovine. A three-term Prony series relaxation function combined with an Ogden strain energy density function was used in the QLV modeling, while a power-law formulation was adopted in the NLV approach. The ovine RVFW exhibited an anisotropic and strain-dependent viscoelastic behavior relative to anatomical coordinates, and the NLV model showed a higher capacity in predicting strain-dependent stress relaxation than the QLV model. From the QLV fitting, the relaxation term associated with the largest time constant played the dominant role in the overall relaxation behavior at most strains from early to late diastole, whereas the term associated with the smallest time constant was pronounced only at low strains at early diastole. From the NLV fitting, the parameters showed a nonlinear dependence on the strain. Overall, our study characterized the anisotropic, nonlinear viscoelasticity to capture the elastic and viscous resistances of the RVFW during diastole. These findings deepen our understanding of RV myocardium dynamic mechanical properties. STATEMENT OF SIGNIFICANCE: Although significant progress has been made to understand the passive elastic behavior of the right ventricle free wall (RVFW), its viscoelastic behavior remains poorly understood. In this study, we originally applied both quasi-linear viscoelastic (QLV) and nonlinear viscoelastic (NLV) models to published experimental data from healthy ovine RVFW. Our results revealed an anisotropic and strain-dependent viscoelastic behavior of the RVFW. The parameters from the NLV fitting showed nonlinear relationships with the strain, and the NLV model showed a higher capacity in predicting strain-dependent stress relaxation than the QLV model. These findings characterize the anisotropic, nonlinear viscoelasticity of RVFW to fully capture the total (elastic and viscous) resistance that is critical to diastolic function. |
2,329,603 | Topoisomerase IIA in adult NSCs regulates SVZ neurogenesis by transcriptional activation of Usp37. | Topoisomerase IIA (TOP2a) has traditionally been known as an important nuclear enzyme that resolves entanglements and relieves torsional stress of DNA double strands. However, its function in genomic transcriptional regulation remains largely unknown, especially during adult neurogenesis. Here, we show that TOP2a is preferentially expressed in neurogenic niches in the brain of adult mice, such as the subventricular zone (SVZ). Conditional knockout of Top2a in adult neural stem cells (NSCs) of the SVZ significantly inhibits their self-renewal and proliferation, and ultimately reduces neurogenesis. To gain insight into the molecular mechanisms by which TOP2a regulates adult NSCs, we perform RNA-sequencing (RNA-Seq) plus chromatin immunoprecipitation sequencing (ChIP-Seq) and identify ubiquitin-specific protease 37 (Usp37) as a direct TOP2a target gene. Importantly, overexpression of Usp37 is sufficient to rescue the impaired self-renewal ability of adult NSCs caused by Top2a knockdown. Taken together, this proof-of-principle study illustrates a TOP2a/Usp37-mediated novel molecular mechanism in adult neurogenesis, which will significantly expand our understanding of the function of topoisomerase in the adult brain. |
2,329,604 | Minimally Invasive Resection of Intraventricular Pilocytic Astrocytoma Using the Aurora Surgiscope in an Adult Patient: Technical Note. | Pilocytic astrocytomas account for approximately 5%-6% of all gliomas and are most commonly diagnosed between the ages of 8 and 13 years. Although they may occur throughout the neuraxis, approximately two thirds arise from the cerebellum and optic pathway. Other locations of origin include midline structures such as thalamus, hypothalamus, and periventricular regions. Surgical approaches to lateral or third ventricular tumors include anterior transcallosal, subfrontal translamina terminalis, and anterior transcortical approaches. The Aurora Surgiscope is a single-use, disposable minimally invasive neurological endoscope designed for intraparenchymal hemorrhage evacuation. We present the successful use of this system to aid resection of a large intraventricular pilocytic astrocytoma.</AbstractText>A 29-year-old man presented with signs of developing hydrocephalus and was found to have a large intraventricular tumor, which was later identified to be a rare intraventricular pilocytic astrocytoma. A ventriculostomy was performed as a temporizing measure, and he was transferred to our tertiary care facility for surgical management. Sulcal dissection was performed, and the endoscope was inserted to create a minimally invasive corridor to the lateral ventricle. Using the endoscope, bimanual surgery using multiple instruments simultaneously was possible and enabled gross total resection of the tumor.</AbstractText>The patient tolerated the procedure well and was discharged at his neurological baseline level.</AbstractText>Extensive sulcal dissection preceding placement of the endoscope allowed access to the intraventricular space with minimal passage of parenchymal tissue. High-definition visualization was provided and allowed the operating surgeon to freely use both hands during surgery.</AbstractText>Copyright © 2022 Elsevier Inc. All rights reserved.</CopyrightInformation> |
2,329,605 | SETD4 cells contribute to brain development and maintain adult stem cell reservoir for neurogenesis. | Cellular quiescence facilitates maintenance of neural stem cells (NSCs) and their subsequent regenerative functions in response to brain injury and aging. However, the specification and maintenance of NSCs in quiescence from embryo to adulthood remain largely unclear. Here, using Set domain-containing protein 4 (SETD4), an epigenetic determinant of cellular quiescence, we mark a small but long-lived NSC population in deep quiescence in the subventricular zone of adult murine brain. Genetic lineage tracing shows that SETD4<sup>+</sup> cells appear before neuroectoderm formation and contribute to brain development. In the adult, conditional knockout of Setd4 resulted in quiescence exit of NSCs, generating newborn neurons in the olfactory bulb and contributing to damage repair. However, long period deletion of SETD4 lead to exhaustion of NSC reservoir or SETD4 overexpression caused quiescence entry of NSCs, leading to suppressed neurogenesis. This study reveals the existence of long-lived deep quiescent NSCs and their neurogenetic capacities beyond activation. |
2,329,606 | Brain morphological alterations and their correlation to tumor differentiation and duration in patients with lung cancer after platinum chemotherapy. | Chemotherapy-related brain impairments and changes can occur in patients with lung cancer after platinum chemotherapy and have a substantial impact on survivors' quality of life. Therefore, it is necessary to understand the brain neuropathological alterations and response mechanisms to provide a theoretical basis for rehabilitation strategies. This study aimed to investigate the related brain morphological changes and clarified their correlation with clinical and pathological indicators in patients with lung cancer after platinum chemotherapy.</AbstractText>Overall, 28 patients with chemotherapy, 56 patients without chemotherapy, and 41 healthy controls were categorized in three groups, matched for age, sex, and years of education, and included in the cross-sectional comparison of brain volume and cortical thickness. 14 matched patients before and after chemotherapy were subjected to paired comparison for longitudinal observation of brain morphological changes. Three-dimensional T1</sub>-weighted images were acquired from all participants, and quantitative parameters were calculated using the formula of the change from baseline. Correlation analysis was performed to evaluate the relationship between abnormal morphological indices and clinical information of patients.</AbstractText>Brain regions with volume differences among the three groups were mainly distributed in frontal lobe and limbic cortex. Additionally, significant differences in cerebrospinal fluid were observed in most ventricles, and the main brain regions with cortical thickness differences were the gyrus rectus and medial frontal cortex of the frontal lobe, transverse temporal gyrus of the temporal lobe, insular cortex, anterior insula, and posterior insula of the insular cortex. According to the paired comparison, decreased brain volumes in the patients after chemotherapy appeared in some regions of the frontal, parietal, temporal, and occipital lobes; limbic cortex; insular cortex; and lobules VI-X and decreased cortical thickness in the patients after chemotherapy was found in the frontal, temporal, limbic, and insular cortexes. In the correlation analysis, only the differentiation degree of the tumor and duration after chemotherapy were significantly correlated with imaging indices in the abnormal brain regions.</AbstractText>Our findings illustrate the platinum-related brain reactivity morphological alterations which provide more insights into the neuropathological mechanisms of patients with lung cancer after platinum chemotherapy and empirical support for the details of brain injury related to cancer and chemotherapy.</AbstractText>Copyright © 2022 Lv, Ma, Chen, Liu, Xin, Lu, Su, Li, Yang, Ma, Rong, Dong, Chen, Zhang, Han and Zhang.</CopyrightInformation> |
2,329,607 | Epidermal Growth Factor Receptor Kinase Inhibitor Ameliorates β-Amyloid Oligomer-Induced Alzheimer Disease in Swiss Albino Mice. | Alzheimer's disease (AD) is one of the major neurodegenerative disorders, and its incidence increases globally every year. Currently, available AD drugs symptomatically treat AD with multiple adverse effects. Gefitinib (GE) is an epidermal growth factor receptor (EGFR) kinase inhibitor. EGFR is the preferred target for the treatment of AD, whereas the effect of GE in AD conditions is limited. The present study was designed to explore the ameliorative potential of GE in Aβ<sub>1-42</sub> oligomer-induced neurotoxicity in AD mice. AD was induced by intracerebroventricular (i.c.v.) injection of Aβ<sub>1-42</sub> oligomer (4 μg/4 μL) into the lateral ventricles of the mouse brain. The test compound, i.e., GE (2 and 4 mg/kg of body weight), was administered orally on days 10, 13, 16, 19, 22, 25, and 28, and the reference drug, i.e., donepezil (DP, 2 mg/kg), was administered orally from the 10th to 28th days. The behavioral changes were screened by the Morris water maze (MWM) test. Furthermore, biomarkers i.e., brain acetylcholinesterase (AChE), thiobarbituric acid reactive substances (TBARS), and reduced glutathione (GSH) levels were estimated from brain samples. The AD-associated histopathological changes were analyzed by hematoxylin and eosin staining. The administration of GE significantly ameliorated the AD-associated behavioral, biochemical, and histopathological changes. The ameliorative effect of GE against the Aβ<sub>1-42</sub> oligomer-associated neurotoxicity was due to its potent inhibition of EGFR kinase activation, as well as its antioxidant and antilipid peroxidative effect. |
2,329,608 | Epilepsy in Pediatric Patients-Evaluation of Brain Structures' Volume Using VolBrain Software. | Epilepsy is one of the most frequent serious brain disorders. Approximately 30,000 of the 150,000 children and adolescents who experience unprovoked seizures are diagnosed with epilepsy each year. Magnetic resonance imaging is the method of choice in diagnosing and monitoring patients with this condition. However, one very effective tool using MR images is volBrain software, which automatically generates information about the volume of brain structures. A total of 57 consecutive patients (study group) suffering from epilepsy and 34 healthy patients (control group) who underwent MR examination qualified for the study. Images were then evaluated by volBrain. Results showed atrophy of the brain and particular structures-GM, cerebrum, cerebellum, brainstem, putamen, thalamus, hippocampus and nucleus accumbens volume. Moreover, the statistically significant difference in the volume between the study and the control group was found for brain, lateral ventricle and putamen. A volumetric analysis of the CNS in children with epilepsy confirms a decrease in the volume of brain tissue. A volumetric assessment of brain structures based on MR data has the potential to be a useful diagnostic tool in children with epilepsy and can be implemented in clinical work; however, further studies are necessary to enhance the effectiveness of this software. |
2,329,609 | Using DeepLabCut as a Real-Time and Markerless Tool for Cardiac Physiology Assessment in Zebrafish. | DeepLabCut (DLC) is a deep learning-based tool initially invented for markerless pose estimation in mammals. In this study, we explored the possibility of adopting this tool for conducting markerless cardiac physiology assessment in an important aquatic toxicology model of zebrafish (<i>Danio rerio</i>). Initially, high-definition videography was applied to capture heartbeat information at a frame rate of 30 frames per second (fps). Next, 20 videos from different individuals were used to perform convolutional neural network training by labeling the heart chamber (ventricle) with eight landmarks. Using Residual Network (ResNet) 152, a neural network with 152 convolutional neural network layers with 500,000 iterations, we successfully obtained a trained model that can track the heart chamber in a real-time manner. Later, we validated DLC performance with the previously published ImageJ Time Series Analysis (TSA) and Kymograph (KYM) methods. We also evaluated DLC performance by challenging experimental animals with ethanol and ponatinib to induce cardiac abnormality and heartbeat irregularity. The results showed that DLC is more accurate than the TSA method in several parameters tested. The DLC-trained model also detected the ventricle of zebrafish embryos even in the occurrence of heart abnormalities, such as pericardial edema. We believe that this tool is beneficial for research studies, especially for cardiac physiology assessment in zebrafish embryos. |
2,329,610 | Impact and Modifiers of Ventricular Pacing in Patients With Single Ventricle Circulation.<Pagination><StartPage>902</StartPage><EndPage>914</EndPage><MedlinePgn>902-914</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.jacc.2022.05.053</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0735-1097(22)05425-0</ELocationID><Abstract><AbstractText Label="BACKGROUND">Palliation of the single ventricle (SV) circulation is associated with a burden of lifelong complications. Previous studies have identified that the need for a permanent ventricular pacing system (PPM<sub>v</sub>) may be associated with additional adverse long-term outcomes.</AbstractText><AbstractText Label="OBJECTIVES">The goal of this study was to quantify the attributable risk of PPM<sub>v</sub> in patients with SV, and to identify modifiable risk factors.</AbstractText><AbstractText Label="METHODS">This international study was sponsored by the Pediatric and Congenital Electrophysiology Society. Centers contributed baseline and longitudinal data for functionally SV patients with PPM<sub>v</sub>. Enrollment was at implantation. Controls were matched 1:1 to PPM<sub>v</sub> subjects by ventricular morphology and sex, identified within center, and enrolled at matched age. Primary outcome was transplantation or death.</AbstractText><AbstractText Label="RESULTS">In total, 236 PPM<sub>v</sub> subjects and 213 matched controls were identified (22 centers, 9 countries). Median age at enrollment was 5.3 years (quartiles: 1.5-13.2 years), follow-up 6.9 years (3.4-11.6 years). Median percent ventricular pacing (Vp) was 90.8% (25th-75th percentile: 4.3%-100%) in the PPM<sub>v</sub> cohort. Across 213 matched pairs, multivariable HR for death/transplant associated with PPM<sub>v</sub> was 3.8 (95% CI 1.9-7.6; P < 0.001). Within the PPM<sub>v</sub> population, higher Vp (HR: 1.009 per %; P = 0.009), higher QRS z-score (HR: 1.19; P = 0.009) and nonapical lead position (HR: 2.17; P = 0.042) were all associated with death/transplantation.</AbstractText><AbstractText Label="CONCLUSIONS">PPM<sub>v</sub> in patients with SV is associated with increased risk of heart transplantation and death, despite controlling for increased associated morbidity of the PPM<sub>v</sub> cohort. Increased Vp, higher QRS z-score, and nonapical ventricular lead position are all associated with higher risk of adverse outcome and may be modifiable risk factors.</AbstractText><CopyrightInformation>Copyright © 2022 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Chubb</LastName><ForeName>Henry</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Division of Pediatric Cardiology, Department of Pediatrics, Stanford University, Stanford, California, USA; Division of Pediatric Cardiothoracic Surgery, Department of Cardiothoracic Surgery, Stanford University, Stanford, California, USA. Electronic address: mhchubb@stanford.edu.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bulic</LastName><ForeName>Anica</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Labatt Family Heart Centre, The Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mah</LastName><ForeName>Douglas</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Boston Children's Hospital, Boston, Massachusetts, USA; Department of Pediatrics, Harvard Medical School, Boston, Massachusetts, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Moore</LastName><ForeName>Jeremy P</ForeName><Initials>JP</Initials><AffiliationInfo><Affiliation>Division of Cardiology, Department of Pediatrics, UCLA Health System, Los Angeles, California, USA; Division of Cardiology, Department of Medicine, Ahmanson/UCLA Adult Congenital Heart Disease Center, Los Angeles, California, USA; UCLA Cardiac Arrhythmia Center, UCLA Health System, Los Angeles, California, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Janousek</LastName><ForeName>Jan</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Children's Heart Centre, Second Faculty of Medicine, Charles University in Prague and Motol University Hospital, Prague, Czech Republic.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fumanelli</LastName><ForeName>Jennifer</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Children's Heart Centre, Second Faculty of Medicine, Charles University in Prague and Motol University Hospital, Prague, Czech Republic; Pediatric Cardiology Unit, Department of Women's and Child's Health, University of Padova, Padova, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Asaki</LastName><ForeName>S Yukiko</ForeName><Initials>SY</Initials><AffiliationInfo><Affiliation>Primary Children's Hospital, University of Utah, Salt Lake City, Utah, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pflaumer</LastName><ForeName>Andreas</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>The Royal Children's Hospital, MCRI and University of Melbourne, Melbourne, Victoria, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hill</LastName><ForeName>Allison C</ForeName><Initials>AC</Initials><AffiliationInfo><Affiliation>Division of Cardiology, Children's Hospital Los Angeles, Los Angeles, California, USA; Keck School of Medicine, University of Southern California, Los Angeles, California, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Escudero</LastName><ForeName>Carolina</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Pediatrics, Division of Pediatric Cardiology, University of Alberta, Stollery Children's Hospital, Edmonton, Alberta, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kwok</LastName><ForeName>Sit Yee</ForeName><Initials>SY</Initials><AffiliationInfo><Affiliation>Cardiology Centre, Department of Paediatrics and Adolescent Medicine, Hong Kong Children's Hospital, Hong Kong SAR, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mangat</LastName><ForeName>Jasveer</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Paediatric Cardiology, Great Ormond Street, London, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ochoa Nunez</LastName><ForeName>Luis A</ForeName><Initials>LA</Initials><AffiliationInfo><Affiliation>University of Iowa Healthcare, Iowa City, Iowa, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Balaji</LastName><ForeName>Seshadri</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Pediatrics, Division of Cardiology, Oregon Health & Science University, Portland, Oregon, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rosenthal</LastName><ForeName>Eric</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Paediatric Cardiology, Evelina London Children's Hospital, London, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Regan</LastName><ForeName>William</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Paediatric Cardiology, Evelina London Children's Hospital, London, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Horndasch</LastName><ForeName>Michaela</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Congenital Heart Diseases and Pediatric Cardiology, German Heart Center Munich, Munich, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Asakai</LastName><ForeName>Hiroko</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Paediatrics, University of Tokyo Hospital, Tokyo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tanel</LastName><ForeName>Ronn</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Division of Pediatric Cardiology, Department of Pediatrics, UCSF School of Medicine, San Francisco, California, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Czosek</LastName><ForeName>Richard J</ForeName><Initials>RJ</Initials><AffiliationInfo><Affiliation>The Heart Institute, Cincinnati Children's Hospital Medical Center, Ohio, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Young</LastName><ForeName>Ming-Lon</ForeName><Initials>ML</Initials><AffiliationInfo><Affiliation>Joe DiMaggio Children's Hospital, Hollywood, Florida, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bradley</LastName><ForeName>David J</ForeName><Initials>DJ</Initials><AffiliationInfo><Affiliation>University of Michigan, CS Mott Children's Hospital, Ann Arbor, Michigan, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Paul</LastName><ForeName>Thomas</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Pediatric Cardiology, Georg-August-University Medical Center, Göttingen, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fischbach</LastName><ForeName>Peter</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Sibley Heart Center, Atlanta, Georgia, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Malloy-Walton</LastName><ForeName>Lindsey</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Children's Mercy Hospital, University of Missouri, Kansas City, Missouri, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>McElhinney</LastName><ForeName>Doff B</ForeName><Initials>DB</Initials><AffiliationInfo><Affiliation>Division of Pediatric Cardiology, Department of Pediatrics, Stanford University, Stanford, California, USA; Division of Pediatric Cardiothoracic Surgery, Department of Cardiothoracic Surgery, Stanford University, Stanford, California, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dubin</LastName><ForeName>Anne M</ForeName><Initials>AM</Initials><AffiliationInfo><Affiliation>Division of Pediatric Cardiology, Department of Pediatrics, Stanford University, Stanford, California, USA.</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>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 Aug 30;80(9):915-917</RefSource><PMID Version="1">36007990</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D002648" MajorTopicYN="N">Child</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015331" MajorTopicYN="N">Cohort Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006330" MajorTopicYN="Y">Heart Defects, Congenital</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016027" MajorTopicYN="Y">Heart Transplantation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000080039" MajorTopicYN="Y">Univentricular Heart</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Fontan</Keyword><Keyword MajorTopicYN="N">Glenn</Keyword><Keyword MajorTopicYN="N">cardiac resynchronization therapy</Keyword><Keyword MajorTopicYN="N">cardiac transplant</Keyword><Keyword MajorTopicYN="N">congenital heart disease</Keyword><Keyword MajorTopicYN="N">electrical dyssynchrony</Keyword><Keyword MajorTopicYN="N">heart failure</Keyword><Keyword MajorTopicYN="N">pediatric</Keyword><Keyword MajorTopicYN="N">single ventricle</Keyword></KeywordList><CoiStatement>Funding Support and Author Disclosures Drs Janousek and Fumanelli were supported by the Ministry of Health, Czech Republic: conceptual development of research organization, Motol University Hospital, Prague, Czech Republic. Dr Balaji has been a medical advisor/consultant to “yoR labs” (stock options). All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>2</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>5</Month><Day>4</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>5</Month><Day>23</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>8</Month><Day>25</Day><Hour>21</Hour><Minute>3</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>8</Month><Day>26</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>8</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36007989</ArticleId><ArticleId IdType="doi">10.1016/j.jacc.2022.05.053</ArticleId><ArticleId IdType="pii">S0735-1097(22)05425-0</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36007868</PMID><DateRevised><Year>2022</Year><Month>09</Month><Day>18</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1532-9488</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Aug</Month><Day>23</Day></PubDate></JournalIssue><Title>Seminars in thoracic and cardiovascular surgery</Title><ISOAbbreviation>Semin Thorac Cardiovasc Surg</ISOAbbreviation></Journal>Impact of Anatomical Sub-types and Shunt Types on Aortopulmonary Collaterals in Hypoplastic Left Heart Syndrome. | This study aims to clarify the relation of development of aortopulmonary collateral arteries (APCs) with anatomical sub-types and the shunt types at Norwood procedure in patients with hypoplastic left heart syndrome (HLHS). A total of 140 patients with HLHS who completed 3 staged palliation between 2003 and 2019 were included. Incidence of APCs and corresponding interventions were examined using angiogram by cardiac catheterization, with respect to the anatomical sub-types and shunt types. Totally, APCs were observed in 87 (62%) of the patients; pre-stage II in 32 (23%), pre-stage III in 64 (46%), and after stage III in 40 (29%). The incidence of APCs before stage II was significantly higher in patients with aortic atresia/mitral atresia (AA/MA) compared with other sub-types (P = 0.022). Patients with right ventricle to pulmonary artery conduit (RVPAC) had a higher incidence of APCs originating from the descending aorta, compared with those with modified Blalock-Taussig shunt (20% vs 2%, P= 0.002). Interventions for APCs were performed in 58 (41%) patients; before stage II in 10 (7%), after stage II in 7 (5%), before stage III in 22 (16%), and after stage III in 32 (23%). Patients with AA/MA had more interventions before stage II (P= 0.019), and patients with aortic stenosis/mitral stenosis (AS/MS) had a lower incidence of interventions after stage III (P= 0.047). More than half of the patients with HLHS developed APCs. Before stage II, patients with AA/MA sub-type had a higher incidence of APCs, and those with RVPAC had significantly more APCs from the descending aorta. |
2,329,611 | Thalamic nuclei atrophy at high and heterogenous rates during cognitively unimpaired human aging. | The thalamus is a central integration structure in the brain, receiving and distributing information among the cerebral cortex, subcortical structures, and the peripheral nervous system. Prior studies clearly show that the thalamus atrophies in cognitively unimpaired aging. However, the thalamus is comprised of multiple nuclei involved in a wide range of functions, and the age-related atrophy of individual thalamic nuclei remains unknown. Using a recently developed automated method of identifying thalamic nuclei (3T or 7T MRI with white-matter-nulled MPRAGE contrast and THOMAS segmentation) and a cross-sectional design, we evaluated the age-related atrophy rate for 10 thalamic nuclei (AV, CM, VA, VLA, VLP, VPL, pulvinar, LGN, MGN, MD) and an epithalamic nucleus (habenula). We also used T1-weighted images with the FreeSurfer SAMSEG segmentation method to identify and measure age-related atrophy for 11 extra-thalamic structures (cerebral cortex, cerebral white matter, cerebellar cortex, cerebellar white matter, amygdala, hippocampus, caudate, putamen, nucleus accumbens, pallidum, and lateral ventricle). In 198 cognitively unimpaired participants with ages spanning 20-88 years, we found that the whole thalamus atrophied at a rate of 0.45% per year, and that thalamic nuclei had widely varying age-related atrophy rates, ranging from 0.06% to 1.18% per year. A functional grouping analysis revealed that the thalamic nuclei involved in cognitive (AV, MD; 0.53% atrophy per year), visual (LGN, pulvinar; 0.62% atrophy per year), and auditory/vestibular (MGN; 0.64% atrophy per year) functions atrophied at significantly higher rates than those involved in motor (VA, VLA, VLP, and CM; 0.37% atrophy per year) and somatosensory (VPL; 0.32% atrophy per year) functions. A proximity-to-CSF analysis showed that the group of thalamic nuclei situated immediately adjacent to CSF atrophied at a significantly greater atrophy rate (0.59% atrophy per year) than that of the group of nuclei located farther from CSF (0.36% atrophy per year), supporting a growing hypothesis that CSF-mediated factors contribute to neurodegeneration. We did not find any significant hemispheric differences in these rates of change for thalamic nuclei. Only the CM thalamic nucleus showed a sex-specific difference in atrophy rates, atrophying at a greater rate in male versus female participants. Roughly half of the thalamic nuclei showed greater atrophy than all extra-thalamic structures examined (0% to 0.54% per year). These results show the value of white-matter-nulled MPRAGE imaging and THOMAS segmentation for measuring distinct thalamic nuclei and for characterizing the high and heterogeneous atrophy rates of the thalamus and its nuclei across the adult lifespan. Collectively, these methods and results advance our understanding of the role of thalamic substructures in neurocognitive and disease-related changes that occur with aging. |
2,329,612 | Accuracy and reliability of magnetic resonance imaging in the diagnosis of idiopathic intracranial hypertension. | To determine the diagnostic utility of brain magnetic resonance imaging (MRI) findings in patients with idiopathic intracranial hypertension (IIH) and to investigate the significance of evaluating radiological findings together with neurological and ophthalmological data in the diagnosis of IIH.</AbstractText>All consecutive patients diagnosed with IIH in our tertiary neuro-ophthalmology center between January 1, 2018 and March 15, 2020, were included in the study. The clinical, radiological, and ophthalmological findings of IIH patients were compared with the control group with similar demographic characteristics.</AbstractText>A total of 98 patients, 49 cases and 49 controls, were included in the study. Lateral ventricular index had the highest area under the curve (AUC) value (0.945) for prediction of disease group followed by sella height category (AUC = 0.915) and optic nerve tortuosity (AUC = 0.855) According to the multivariate model we developed, caudate index (OR = 0.572, 95% CI 0.329-0.996), lateral ventricle index (OR = 3.969, 95% CI 1.851-8.509) and bilateral optic nerve tortuosity (OR = 22,784, 95% CI 2.432-213.450) were significant predictors for disease group.</AbstractText>Tortuosity in the optic nerve, lateral ventricular index and caudate index can be used as MRI parameters supporting the diagnosis of IIH in clinically suspicious cases. A holistic approach to the clinical and radiological findings of the cases in the diagnosis of IIH can prevent overdiagnosis and enable early correct diagnosis.</AbstractText>Copyright © 2022 Elsevier B.V. All rights reserved.</CopyrightInformation> |
2,329,613 | Diagnostic approach to fetal ventriculomegaly. | Ventriculomegaly (VM) is defined as an enlargement of the lateral ventricles of the developing fetal brain. The diagnosis is easily made by measuring the lateral ventricle width at the level of the atrium, which is normally <10 mm. VM is defined as mild when the atrial width is 10-12 mm, moderate 12-15 mm, severe >15 mm. VM is a non-specific sonographic sign which is common to different pathological entities and genetic conditions. When no associated anomaly can be found VM is defined as isolated. Since the prognosis of fetal VM mainly depends on the presence of associated anomalies, a careful diagnostic approach is necessary to rule out CNS and extra- CNS fetal anomalies. Magnetic Resonance Imaging can be a useful diagnostic tool complementary to ultrasound in order to recognize subtle brain anomalies, particularly cortical disorders. In this review the diagnostic approach to fetal VM will be discussed starting from ultrasound screening, moving to neurosonographic and MRI examination and genetic evaluation, in order to recognize the cause of VM and offer the appropriate counselling to the parents. |
2,329,614 | Aortic Arch Phenotypes in Double Outlet Right Ventricle (DORV)-Implications for Surgery and Multi-Modal Imaging. | Abnormal aortic arches (AAAs) cover a spectrum of malformations, including abnormal laterality, branching patterns, and flow-limiting narrowing, which themselves vary from tubular hypoplasia, through discrete coarctation, to complete interruption of the arch. Neonatal surgery within the first days of life is necessary for most of these morphologies. Patch aortoplasty is widely used as it can offer a good haemodynamic result, being tailored to each combination of presenting pathologies. Our study hypothesis was that arch malformations are frequent in DORV and exhibit a plethora of phenotypes. We reviewed 54 post-mortem heart specimens from the UCL Cardiac Archive, analysing morphological features that would potentially influence the surgical repair, and taking relevant measurements of surgical importance. AAAs were found in half of the specimens, including 22.2% with aortic arch narrowing. In total, 70% and 30% of narrow arches had a subpulmonary and subaortic interventricular defect, respectively. Z-scores were significantly negative for all cases with tubular hypoplasia. We concluded that arch malformations are a common finding among hearts with DORV. Surgery on the neonatal aortic arch in DORV, performed in conjunction with other interventions that aim to balance pulmonary to systemic flow (Qp/Qs), should be anticipated and form an important part of multi-modal imaging. |
2,329,615 | Valve Endothelial Cell Exposure to High Levels of Flow Oscillations Exacerbates Valve Interstitial Cell Calcification.<ELocationID EIdType="pii" ValidYN="Y">393</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.3390/bioengineering9080393</ELocationID><Abstract><AbstractText>The aortic valve facilitates unidirectional blood flow to the systemic circulation between the left cardiac ventricle and the aorta. The valve's biomechanical function relies on thin leaflets to adequately open and close over the cardiac cycle. A monolayer of valve endothelial cells (VECs) resides on the outer surface of the aortic valve leaflet. Deeper within the leaflet are sublayers of valve interstitial cells (VICs). Valve tissue remodeling involves paracrine signaling between VECs and VICs. Aortic valve calcification can result from abnormal paracrine communication between these two cell types. VECs are known to respond to hemodynamic stimuli, and, specifically, flow abnormalities can induce VEC dysfunction. This dysfunction can subsequently change the phenotype of VICs, leading to aortic valve calcification. However, the relation between VEC-exposed flow oscillations under pulsatile flow to the progression of aortic valve calcification by VICs remains unknown. In this study, we quantified the level of flow oscillations that VECs were exposed to under dynamic culture and then immersed VICs in VEC-conditioned media. We found that VIC-induced calcification was augmented under maximum flow oscillations, wherein the flow was fully forward for half the cardiac cycle period and fully reversed for the other half. We were able to computationally correlate this finding to specific regions of the aortic valve that experience relatively high flow oscillations and that have been shown to be associated with severe calcified deposits. These findings establish a basis for future investigations on engineering calcified human valve tissues and its potential for therapeutic discovery of aortic valve calcification.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hsu</LastName><ForeName>Chia-Pei Denise</ForeName><Initials>CD</Initials><AffiliationInfo><Affiliation>Department of Biomedical Engineering, Florida International University, Miami, FL 33199, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tchir</LastName><ForeName>Alexandra</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Biomedical Engineering, Florida International University, Miami, FL 33199, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mirza</LastName><ForeName>Asad</ForeName><Initials>A</Initials><Identifier Source="ORCID">0000-0003-4515-2203</Identifier><AffiliationInfo><Affiliation>Department of Biomedical Engineering, Florida International University, Miami, FL 33199, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chaparro</LastName><ForeName>Daniel</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Biomedical Engineering, Florida International University, Miami, FL 33199, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Herrera</LastName><ForeName>Raul E</ForeName><Initials>RE</Initials><AffiliationInfo><Affiliation>Miami Cardiac & Vascular Institute, Baptist Health South Florida, Miami, FL 33199, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hutcheson</LastName><ForeName>Joshua D</ForeName><Initials>JD</Initials><AffiliationInfo><Affiliation>Department of Biomedical Engineering, Florida International University, Miami, FL 33199, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ramaswamy</LastName><ForeName>Sharan</ForeName><Initials>S</Initials><Identifier Source="ORCID">0000-0003-4108-7141</Identifier><AffiliationInfo><Affiliation>Department of Biomedical Engineering, Florida International University, Miami, FL 33199, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>08</Month><Day>16</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Bioengineering (Basel)</MedlineTA><NlmUniqueID>101676056</NlmUniqueID><ISSNLinking>2306-5354</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">oscillatory flow</Keyword><Keyword MajorTopicYN="N">paracrine signaling</Keyword><Keyword MajorTopicYN="N">shear stress</Keyword><Keyword MajorTopicYN="N">valve calcification</Keyword></KeywordList><CoiStatement>The authors declare no conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>7</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>8</Month><Day>3</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>8</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>8</Month><Day>25</Day><Hour>7</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>8</Month><Day>26</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>8</Month><Day>26</Day><Hour>6</Hour><Minute>1</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36004918</ArticleId><ArticleId IdType="pmc">PMC9405348</ArticleId><ArticleId IdType="doi">10.3390/bioengineering9080393</ArticleId><ArticleId IdType="pii">bioengineering9080393</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Yadgir S., Johnson C.O., Aboyans V., Adebayo O.M., Adedoyin R.A., Afarideh M., Alahdab F., Alashi A., Alipour V., Arabloo J., et al. 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The valve's biomechanical function relies on thin leaflets to adequately open and close over the cardiac cycle. A monolayer of valve endothelial cells (VECs) resides on the outer surface of the aortic valve leaflet. Deeper within the leaflet are sublayers of valve interstitial cells (VICs). Valve tissue remodeling involves paracrine signaling between VECs and VICs. Aortic valve calcification can result from abnormal paracrine communication between these two cell types. VECs are known to respond to hemodynamic stimuli, and, specifically, flow abnormalities can induce VEC dysfunction. This dysfunction can subsequently change the phenotype of VICs, leading to aortic valve calcification. However, the relation between VEC-exposed flow oscillations under pulsatile flow to the progression of aortic valve calcification by VICs remains unknown. In this study, we quantified the level of flow oscillations that VECs were exposed to under dynamic culture and then immersed VICs in VEC-conditioned media. We found that VIC-induced calcification was augmented under maximum flow oscillations, wherein the flow was fully forward for half the cardiac cycle period and fully reversed for the other half. We were able to computationally correlate this finding to specific regions of the aortic valve that experience relatively high flow oscillations and that have been shown to be associated with severe calcified deposits. These findings establish a basis for future investigations on engineering calcified human valve tissues and its potential for therapeutic discovery of aortic valve calcification.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hsu</LastName><ForeName>Chia-Pei Denise</ForeName><Initials>CD</Initials><AffiliationInfo><Affiliation>Department of Biomedical Engineering, Florida International University, Miami, FL 33199, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tchir</LastName><ForeName>Alexandra</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Biomedical Engineering, Florida International University, Miami, FL 33199, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mirza</LastName><ForeName>Asad</ForeName><Initials>A</Initials><Identifier Source="ORCID">0000-0003-4515-2203</Identifier><AffiliationInfo><Affiliation>Department of Biomedical Engineering, Florida International University, Miami, FL 33199, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chaparro</LastName><ForeName>Daniel</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Biomedical Engineering, Florida International University, Miami, FL 33199, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Herrera</LastName><ForeName>Raul E</ForeName><Initials>RE</Initials><AffiliationInfo><Affiliation>Miami Cardiac & Vascular Institute, Baptist Health South Florida, Miami, FL 33199, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hutcheson</LastName><ForeName>Joshua D</ForeName><Initials>JD</Initials><AffiliationInfo><Affiliation>Department of Biomedical Engineering, Florida International University, Miami, FL 33199, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ramaswamy</LastName><ForeName>Sharan</ForeName><Initials>S</Initials><Identifier Source="ORCID">0000-0003-4108-7141</Identifier><AffiliationInfo><Affiliation>Department of Biomedical Engineering, Florida International University, Miami, FL 33199, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>08</Month><Day>16</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Bioengineering (Basel)</MedlineTA><NlmUniqueID>101676056</NlmUniqueID><ISSNLinking>2306-5354</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">oscillatory flow</Keyword><Keyword MajorTopicYN="N">paracrine signaling</Keyword><Keyword MajorTopicYN="N">shear stress</Keyword><Keyword MajorTopicYN="N">valve calcification</Keyword></KeywordList><CoiStatement>The authors declare no conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>7</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>8</Month><Day>3</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>8</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>8</Month><Day>25</Day><Hour>7</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>8</Month><Day>26</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>8</Month><Day>26</Day><Hour>6</Hour><Minute>1</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36004918</ArticleId><ArticleId IdType="pmc">PMC9405348</ArticleId><ArticleId IdType="doi">10.3390/bioengineering9080393</ArticleId><ArticleId IdType="pii">bioengineering9080393</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Yadgir S., Johnson C.O., Aboyans V., Adebayo O.M., Adedoyin R.A., Afarideh M., Alahdab F., Alashi A., Alipour V., Arabloo J., et al. 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Biomech. 2017;65:40–48. doi: 10.1016/j.jbiomech.2017.09.035.</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.jbiomech.2017.09.035</ArticleId><ArticleId IdType="pubmed">29054608</ArticleId></ArticleIdList></Reference><Reference><Citation>Otto C.M., Prendergast B. Aortic-Valve Stenosis—From Patients at Risk to Severe Valve Obstruction. N. Engl. J. Med. 2014;371:744–756. doi: 10.1056/NEJMra1313875.</Citation><ArticleIdList><ArticleId IdType="doi">10.1056/NEJMra1313875</ArticleId><ArticleId IdType="pubmed">25140960</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36004502</PMID><DateRevised><Year>2022</Year><Month>09</Month><Day>10</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1097-0177</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Aug</Month><Day>25</Day></PubDate></JournalIssue><Title>Developmental dynamics : an official publication of the American Association of Anatomists</Title><ISOAbbreviation>Dev Dyn</ISOAbbreviation></Journal><ArticleTitle>Maternal and zygotic ZFP57 regulate coronary vascular formation and myocardium maturation in mouse embryo.</ArticleTitle><ELocationID EIdType="doi" ValidYN="Y">10.1002/dvdy.530</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Genomic and epigenomic dynamics both play critical roles during embryogenesis. Zfp57 maintains genomic imprinting with both maternal and zygotic functions. In our previous study, we found that maternal and zygotic Zfp57 modulate NOTCH signaling during cardiac development. In this study, we investigated Zfp57 mutants from E11.5 to E13.5 to delineate its function during cardiac development.<AbstractText Label="RESULTS" NlmCategory="RESULTS">Here, we describe novel roles of maternal and zygotic Zfp57 during cardiovascular system development. We found that maternal and zygotic Zfp57 was required for coronary vascular development. Maternal and zygotic loss of Zfp57 perturbed the sprouting of the sinus venosus-derived endothelial cells and led to underdeveloped coronary vasculature, meanwhile, there was an ectopic overproduction of blood islands over the ventricles. Furthermore, loss of Zfp57 and failed vasculature disturbed myocardium maturation. Loss of maternal and zygotic Zfp57 resulted in hyper trabeculation and failed myocardium compaction. Zfp57 zygotic mutant (M<sup>+</sup> Z<sup>-</sup> ) hearts displayed noncompaction cardiomyopathy at E18.5.<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Our results suggest that maternal and zygotic ZFP57 are essential for coronary vascular formation and myocardium maturation in mice. Our research provides evidence for the role of genomic imprinting during embryogenesis. |
2,329,616 | Evaluation of biventricular longitudinal myocardial function in normal fetuses at different gestational ages using ultrasonic velocity vector imaging. | This study aimed to evaluate biventricular myocardial function and biventricular longitudinal global myocardial function of fetuses at different gestational weeks using ultrasonic velocity vector imaging.</AbstractText>A total of 127 pregnant women were enrolled and divided into five groups according to the gestational age of their fetuses. The velocity, strain, and strain rate of the left and right ventricles were measured, and these biventricular parameters were compared between the groups. The global parameters of the biventricular myocardium were also compared.</AbstractText>A pairwise comparison revealed that the differences in biventricular velocity and strain rate between groups in adjacent gestational weeks were not statistically significant (P</i> > 0.05), but velocity increased with gestational age. A comparison of fetal longitudinal global myocardial parameters revealed that the global velocity, strain, and strain rate of the right ventricle were higher than those of the left ventricle, and the differences were statistically significant (P</i> < 0.05) in all groups.</AbstractText>The peak velocities of the fetal left and right ventricles increased with gestational age, but the global strain and strain rate did not, suggesting that fetal myocardial function is mature and constant in the middle and late stages of pregnancy and can more reliably reflect myocardial deformation. The peak systolic velocity, global strain, and peak strain rate of the right ventricle were higher than those of the left ventricle, suggesting that the right ventricle dominates longitudinal systolic movement from the second trimester of pregnancy.</AbstractText>Copyright © 2022 Hou, Liu, Xie, Duan, Lv, Li and Zhang.</CopyrightInformation> |
2,329,617 | Cardiovocal Syndrome Associated With Idiopathic Pulmonary Arterial Hypertension: A Case Report and Literature Review. | Cardiovocal syndrome is left recurrent laryngeal nerve palsy associated with cardiovascular disease. Herein, we report a rare case of left recurrent laryngeal nerve palsy caused by idiopathic pulmonary arterial hypertension. A 40-year-old woman diagnosed with idiopathic pulmonary arterial hypertension was referred to our department for occult infection foci in the ear, nose, and throat (ENT). She had no apparent subjective symptoms in the ENT area, including hoarseness. Flexible laryngoscopy revealed left vocal cord paralysis, and contrast-enhanced computed tomography revealed dilatation of the pulmonary trunk, bilateral pulmonary arteries, and right ventricle, suggesting compression of the left recurrent laryngeal nerve. In our daily practice, when we encounter a left recurrent laryngeal nerve palsy that seems to be endogenous, cardiovascular lesions should be ruled out. |
2,329,618 | Automation of ischemic myocardial scar detection in cardiac magnetic resonance imaging of the left ventricle using machine learning. | Machine learning techniques can be applied to cardiac magnetic resonance imaging (CMR) scans in order to differentiate patients with and without ischemic myocardial scarring (IMS). However, processing the image data in the CMR scans requires manual work that takes a significant amount of time and expertise. We propose to develop and test an AI method to automatically identify IMS in CMR scans to streamline processing and reduce time costs.</AbstractText>CMR scans from 170 patients (138 IMS & 32 without IMS as identified by a clinical expert) were processed using a multistep automatic image data selection algorithm. This algorithm consisted of cropping, circle detection, and supervised machine learning to isolate focused left ventricle image data. We used a ResNet-50 convolutional neural network to evaluate manual vs. automatic selection of left ventricle image data through calculating accuracy, sensitivity, specificity, F1 score, and area under the receiver operating characteristic curve (AUROC).</AbstractText>The algorithm accuracy, sensitivity, specificity, F1 score, and AUROC were 80.6%, 85.6%, 73.7%, 83.0%, and 0.837, respectively, when identifying IMS using manually selected left ventricle image data. With automatic selection of left ventricle image data, the same parameters were 78.5%, 86.0%, 70.7%, 79.7%, and 0.848, respectively.</AbstractText>Our proposed automatic image data selection algorithm provides a promising alternative to manual selection when there are time and expertise limitations. Automatic image data selection may also prove to be an important and necessary step toward integration of machine learning diagnosis and prognosis in clinical workflows.</AbstractText> |
2,329,619 | DNGR-1-tracing marks an ependymal cell subset with damage-responsive neural stem cell potential. | Cells with latent stem ability can contribute to mammalian tissue regeneration after damage. Whether the central nervous system (CNS) harbors such cells remains controversial. Here, we report that DNGR-1 lineage tracing in mice identifies an ependymal cell subset, wherein resides latent regenerative potential. We demonstrate that DNGR-1-lineage-traced ependymal cells arise early in embryogenesis (E11.5) and subsequently spread across the lining of cerebrospinal fluid (CSF)-filled compartments to form a contiguous sheet from the brain to the end of the spinal cord. In the steady state, these DNGR-1-traced cells are quiescent, committed to their ependymal cell fate, and do not contribute to neuronal or glial lineages. However, trans-differentiation can be induced in adult mice by CNS injury or in vitro by culture with suitable factors. Our findings highlight previously unappreciated ependymal cell heterogeneity and identify across the entire CNS an ependymal cell subset wherein resides damage-responsive neural stem cell potential. |
2,329,620 | Cavum septum pellucidum nomogram during the second trimester of pregnancy. | This study aimed to determine cavum septum pellucidum (CSP) nomogram values between 15-28 weeks of gestation. Routine biometric measurements and CSP width were measured by transabdominal ultrasonography in 6042 structurally normal foetuses between 15-28 weeks of gestation. Distribution of CSP width by the week of pregnancy and percentile values were calculated. The mean week of gestation (GW) was 21 ± 1.7, and the mean biparietal diameter (BPD) was 50.2 ± 5.8 mm. The CSP width range was 1.6-7.7 mm at 15-28 weeks, and the mean CSP width was 4.1 ± 0.8 mm. CSP width was found to have a significant correlation between a gestational week (CSP = GW X 0.2705-1.6121; R = 0.62; <i>p</i> < .01) and BPD (CSP = BPD X 0.0859-0.273; R = 0.651; p 0.01). CSP width was found to differ significantly according to gestational weeks, and percentile distributions were calculated. Between 15 and 28 weeks of gestation, the 95th percentile values of CSP width were found to be 3.7-7 mm. Our study was determined that CSP width increased linearly between 15-28 weeks of gestation. For this reason, we think that it would be more appropriate to use CSP width percentile values in the examination of the foetus. Impact statement<b>What is already known on this subject?</b> The cavum septum pellucidum can be easily identified and evaluated by ultrasonography after 18 weeks of pregnancy. CSP can be associated with severe brain anomalies if it is not visualised or deformed. Moreover; large CSP may be associated with chromosomal abnormalities.<b>What do the results of this study add?</b> Our study showed that CSP width increased linearly between 15-28 weeks of gestation. CSP width was found to differ significantly according to gestational weeks, and between 15 and 28 weeks of gestation, the 95th percentile values of CSP width were found to be 3.7-7 mm.<b>What are the implications of these findings for clinical practice and/or further research?</b> We reported that it would be more appropriate to use CSP percentile values according to the gestational week in the definition of abnormal CSP. |
2,329,621 | Cardiac efficiency and Starling's Law of the Heart.<Pagination><StartPage>4265</StartPage><EndPage>4285</EndPage><MedlinePgn>4265-4285</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1113/JP283632</ELocationID><Abstract><AbstractText>The formulation by Starling of The Law of the Heart states that 'the [mechanical] energy of contraction, however measured, is a function of the length of the muscle fibre'. Starling later also stated that 'the oxygen consumption of the isolated heart … is determined by its diastolic volume, and therefore by the initial length of its muscular fibres'. This phrasing has motivated us to extend Starling's Law of the Heart to include consideration of the efficiency of contraction. In this study, we assessed both mechanical efficiency and crossbridge efficiency by studying the heat output of isolated rat ventricular trabeculae performing force-length work-loops over ranges of preload and afterload. The combination of preload and afterload allowed us, using our modelling frameworks for the end-systolic zone and the heat-force zone, to simulate cases by recreating physiologically feasible loading conditions. We found that across all cases examined, both work output and change of enthalpy increased with initial muscle length; hence it can only be that the former increases more than the latter to yield increased mechanical efficiency. In contrast, crossbridge efficiency increased with initial muscle length in cases where the extent of muscle shortening varied greatly with preload. We conclude that the efficiency of cardiac contraction increases with increasing initial muscle length and preload. An implication of our conclusion is that the length-dependent activation mechanism underlying the cellular basis of Starling's Law of the Heart is an energetically favourable process that increases the efficiency of cardiac contraction. KEY POINTS: Ernest Starling in 1914 formulated the Law of the Heart to describe the mechanical property of cardiac muscle whereby force of contraction increases with muscle length. He subsequently, in 1927, showed that the oxygen consumption of the heart is also a function of the length of the muscle fibre, but left the field unclear as to whether cardiac efficiency follows the same dependence. A century later, the field has gained an improved understanding of the factors, including the distinct effects of preload and afterload, that affect cardiac efficiency. This understanding presents an opportunity for us to investigate the elusive length-dependence of cardiac efficiency. We found that, by simulating physiologically feasible loading conditions using a mechano-energetics framework, cardiac efficiency increased with initial muscle length. A broader physiological importance of our findings is that the underlying cellular basis of Starling's Law of the Heart is an energetically favourable process that yields increased efficiency.</AbstractText><CopyrightInformation>© 2022 The Authors. The Journal of Physiology published by John Wiley & Sons Ltd on behalf of The Physiological Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Han</LastName><ForeName>June-Chiew</ForeName><Initials>JC</Initials><Identifier Source="ORCID">0000-0002-6396-7628</Identifier><AffiliationInfo><Affiliation>Auckland Bioengineering Institute, University of Auckland, Auckland, New Zealand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Taberner</LastName><ForeName>Andrew J</ForeName><Initials>AJ</Initials><Identifier Source="ORCID">0000-0002-0452-0308</Identifier><AffiliationInfo><Affiliation>Auckland Bioengineering Institute, University of Auckland, Auckland, New Zealand.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Engineering Science, University of Auckland, Auckland, New Zealand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Loiselle</LastName><ForeName>Denis S</ForeName><Initials>DS</Initials><Identifier Source="ORCID">0000-0002-6928-4019</Identifier><AffiliationInfo><Affiliation>Auckland Bioengineering Institute, University of Auckland, Auckland, New Zealand.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Physiology, University of Auckland, Auckland, New Zealand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tran</LastName><ForeName>Kenneth</ForeName><Initials>K</Initials><Identifier Source="ORCID">0000-0002-8651-3557</Identifier><AffiliationInfo><Affiliation>Auckland Bioengineering Institute, University of Auckland, Auckland, New Zealand.</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>09</Month><Day>10</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Physiol</MedlineTA><NlmUniqueID>0266262</NlmUniqueID><ISSNLinking>0022-3751</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006321" MajorTopicYN="N">Heart</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009200" MajorTopicYN="N">Myocardial Contraction</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009206" MajorTopicYN="N">Myocardium</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D046749" MajorTopicYN="Y">Starlings</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Frank-Starling mechanism</Keyword><Keyword MajorTopicYN="N">cardiac energetics</Keyword><Keyword MajorTopicYN="N">force-length relation</Keyword><Keyword MajorTopicYN="N">mechanical efficiency</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>7</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>8</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>8</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>10</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>8</Month><Day>23</Day><Hour>12</Hour><Minute>23</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35998082</ArticleId><ArticleId IdType="pmc">PMC9826111</ArticleId><ArticleId IdType="doi">10.1113/JP283632</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Abraham, D. , & Mao, L. 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The patients had left ventricular ejection fraction (LVEF) < 50% and were implanted between November 2015 and April 2019. The HBP indications were as follows: 1) bradycardia and atrioventricular conduction disturbances with expected high pacing burden, 2) IVCD, LVEF ≤ 35%, with an indication for resynchronization therapy, 3) the need to upgrade to resynchronization therapy due to pacing-induced cardiomyopathy. Pacing parameters and echocardiographic and clinical data were assessed for up to 2 years of follow-up (FU).</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">His bundle pacing was successful in 154 (85.1%) patients. Eighty-two patients completed a 6-month FU. The mean age was 70.6 ± 9.23 years, and 79% were males. At 6 months FU LVEF improved from 35.3 ± 8.22% to 43.1 ± 10.14% (p < 0.0001), and indexed left ventricular end-systolic volume (LVESVi) decreased from 63.1 ± 25.21 mL/m² to 51.9 ± 22.79 mL/m² (p < 0.0001). In 53.1%, the LVESVi reduction was greater than 15%. The improvement in LVEF and LVESVi was also observed after 24 months of FU.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">His bundle pacing in permanently paced patients when LVEF is reduced below 50% is associated with improvement in LVEF and reverse left ventricle remodeling.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Gardas</LastName><ForeName>Rafal</ForeName><Initials>R</Initials><Identifier Source="ORCID">0000-0003-0002-1955</Identifier><AffiliationInfo><Affiliation>Department of Electrocardiology and Heart Failure, Medical University of Silesia, Katowice, Poland. rafal.gardas@gmail.com.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Electrocardiology, Leszek Giec Upper-Silesian Medical Center of the Silesian Medical University, Katowice, Poland. rafal.gardas@gmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Golba</LastName><ForeName>Krzysztof S</ForeName><Initials>KS</Initials><AffiliationInfo><Affiliation>Department of Electrocardiology and Heart Failure, Medical University of Silesia, Katowice, Poland.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Electrocardiology, Leszek Giec Upper-Silesian Medical Center of the Silesian Medical University, Katowice, Poland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Loboda</LastName><ForeName>Danuta</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Electrocardiology and Heart Failure, Medical University of Silesia, Katowice, Poland.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Electrocardiology, Leszek Giec Upper-Silesian Medical Center of the Silesian Medical University, Katowice, Poland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Biernat</LastName><ForeName>Jolanta</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Electrocardiology and Heart Failure, Medical University of Silesia, Katowice, Poland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Soral</LastName><ForeName>Tomasz</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Electrocardiology and Heart Failure, Medical University of Silesia, Katowice, Poland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kulesza</LastName><ForeName>Piotr</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department of Electrocardiology and Heart Failure, Medical University of Silesia, Katowice, Poland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sajdok</LastName><ForeName>Mateusz</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Electrocardiology and Heart Failure, Medical University of Silesia, Katowice, Poland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zub</LastName><ForeName>Kamil</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Electrocardiology and Heart Failure, Medical University of Silesia, Katowice, Poland.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>08</Month><Day>23</Day></ArticleDate></Article><MedlineJournalInfo><Country>Poland</Country><MedlineTA>Cardiol J</MedlineTA><NlmUniqueID>101392712</NlmUniqueID><ISSNLinking>1898-018X</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">His bundle pacing</Keyword><Keyword MajorTopicYN="N">heart failure</Keyword><Keyword MajorTopicYN="N">permanent pacing</Keyword><Keyword MajorTopicYN="N">resynchronization therapy</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>6</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>8</Month><Day>7</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>8</Month><Day>6</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>8</Month><Day>23</Day><Hour>5</Hour><Minute>33</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>8</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>8</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>aheadofprint</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35997047</ArticleId><ArticleId IdType="doi">10.5603/CJ.a2022.0079</ArticleId><ArticleId IdType="pii">VM/OJS/J/90497</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35997027</PMID><DateRevised><Year>2022</Year><Month>08</Month><Day>23</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1467-1107</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Aug</Month><Day>23</Day></PubDate></JournalIssue><Title>Cardiology in the young</Title><ISOAbbreviation>Cardiol Young</ISOAbbreviation></Journal>Contemporary risk factors for a longer hospital stay following bidirectional cavopulmonary anastomosis. | The formulation by Starling of The Law of the Heart states that 'the [mechanical] energy of contraction, however measured, is a function of the length of the muscle fibre'. Starling later also stated that 'the oxygen consumption of the isolated heart … is determined by its diastolic volume, and therefore by the initial length of its muscular fibres'. This phrasing has motivated us to extend Starling's Law of the Heart to include consideration of the efficiency of contraction. In this study, we assessed both mechanical efficiency and crossbridge efficiency by studying the heat output of isolated rat ventricular trabeculae performing force-length work-loops over ranges of preload and afterload. The combination of preload and afterload allowed us, using our modelling frameworks for the end-systolic zone and the heat-force zone, to simulate cases by recreating physiologically feasible loading conditions. We found that across all cases examined, both work output and change of enthalpy increased with initial muscle length; hence it can only be that the former increases more than the latter to yield increased mechanical efficiency. In contrast, crossbridge efficiency increased with initial muscle length in cases where the extent of muscle shortening varied greatly with preload. We conclude that the efficiency of cardiac contraction increases with increasing initial muscle length and preload. An implication of our conclusion is that the length-dependent activation mechanism underlying the cellular basis of Starling's Law of the Heart is an energetically favourable process that increases the efficiency of cardiac contraction. KEY POINTS: Ernest Starling in 1914 formulated the Law of the Heart to describe the mechanical property of cardiac muscle whereby force of contraction increases with muscle length. He subsequently, in 1927, showed that the oxygen consumption of the heart is also a function of the length of the muscle fibre, but left the field unclear as to whether cardiac efficiency follows the same dependence. A century later, the field has gained an improved understanding of the factors, including the distinct effects of preload and afterload, that affect cardiac efficiency. This understanding presents an opportunity for us to investigate the elusive length-dependence of cardiac efficiency. We found that, by simulating physiologically feasible loading conditions using a mechano-energetics framework, cardiac efficiency increased with initial muscle length. A broader physiological importance of our findings is that the underlying cellular basis of Starling's Law of the Heart is an energetically favourable process that yields increased efficiency.<CopyrightInformation>© 2022 The Authors. The Journal of Physiology published by John Wiley & Sons Ltd on behalf of The Physiological Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Han</LastName><ForeName>June-Chiew</ForeName><Initials>JC</Initials><Identifier Source="ORCID">0000-0002-6396-7628</Identifier><AffiliationInfo><Affiliation>Auckland Bioengineering Institute, University of Auckland, Auckland, New Zealand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Taberner</LastName><ForeName>Andrew J</ForeName><Initials>AJ</Initials><Identifier Source="ORCID">0000-0002-0452-0308</Identifier><AffiliationInfo><Affiliation>Auckland Bioengineering Institute, University of Auckland, Auckland, New Zealand.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Engineering Science, University of Auckland, Auckland, New Zealand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Loiselle</LastName><ForeName>Denis S</ForeName><Initials>DS</Initials><Identifier Source="ORCID">0000-0002-6928-4019</Identifier><AffiliationInfo><Affiliation>Auckland Bioengineering Institute, University of Auckland, Auckland, New Zealand.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Physiology, University of Auckland, Auckland, New Zealand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tran</LastName><ForeName>Kenneth</ForeName><Initials>K</Initials><Identifier Source="ORCID">0000-0002-8651-3557</Identifier><AffiliationInfo><Affiliation>Auckland Bioengineering Institute, University of Auckland, Auckland, New Zealand.</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>09</Month><Day>10</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Physiol</MedlineTA><NlmUniqueID>0266262</NlmUniqueID><ISSNLinking>0022-3751</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006321" MajorTopicYN="N">Heart</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009200" MajorTopicYN="N">Myocardial Contraction</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009206" MajorTopicYN="N">Myocardium</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D046749" MajorTopicYN="Y">Starlings</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Frank-Starling mechanism</Keyword><Keyword MajorTopicYN="N">cardiac energetics</Keyword><Keyword MajorTopicYN="N">force-length relation</Keyword><Keyword MajorTopicYN="N">mechanical efficiency</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>7</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>8</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>8</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>10</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>8</Month><Day>23</Day><Hour>12</Hour><Minute>23</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35998082</ArticleId><ArticleId IdType="pmc">PMC9826111</ArticleId><ArticleId IdType="doi">10.1113/JP283632</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Abraham, D. , & Mao, L. 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Distinct contributions of the thin and thick filaments to length‐dependent activation in heart muscle. eLife, 6, e24081.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC5365314</ArticleId><ArticleId IdType="pubmed">28229860</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35997047</PMID><DateRevised><Year>2022</Year><Month>08</Month><Day>23</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1898-018X</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Aug</Month><Day>23</Day></PubDate></JournalIssue><Title>Cardiology journal</Title><ISOAbbreviation>Cardiol J</ISOAbbreviation></Journal><ArticleTitle>The usefulness of His bundle pacing in a heterogeneous population of patients with impaired left ventricular systolic function.</ArticleTitle><ELocationID EIdType="doi" ValidYN="Y">10.5603/CJ.a2022.0079</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">His bundle pacing (HBP) maintains a physiological activation pattern of ventricular activation, and in patients with intraventricular conduction delay (IVCD) it can normalize wide QRS duration.<AbstractText Label="METHODS" NlmCategory="METHODS">A total of 181 patients from the HBP registry were enrolled into a the study, which was conducted at the Department of Electrocardiology in Katowice, Poland. The patients had left ventricular ejection fraction (LVEF) < 50% and were implanted between November 2015 and April 2019. The HBP indications were as follows: 1) bradycardia and atrioventricular conduction disturbances with expected high pacing burden, 2) IVCD, LVEF ≤ 35%, with an indication for resynchronization therapy, 3) the need to upgrade to resynchronization therapy due to pacing-induced cardiomyopathy. Pacing parameters and echocardiographic and clinical data were assessed for up to 2 years of follow-up (FU).<AbstractText Label="RESULTS" NlmCategory="RESULTS">His bundle pacing was successful in 154 (85.1%) patients. Eighty-two patients completed a 6-month FU. The mean age was 70.6 ± 9.23 years, and 79% were males. At 6 months FU LVEF improved from 35.3 ± 8.22% to 43.1 ± 10.14% (p < 0.0001), and indexed left ventricular end-systolic volume (LVESVi) decreased from 63.1 ± 25.21 mL/m² to 51.9 ± 22.79 mL/m² (p < 0.0001). In 53.1%, the LVESVi reduction was greater than 15%. The improvement in LVEF and LVESVi was also observed after 24 months of FU.<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">His bundle pacing in permanently paced patients when LVEF is reduced below 50% is associated with improvement in LVEF and reverse left ventricle remodeling.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Gardas</LastName><ForeName>Rafal</ForeName><Initials>R</Initials><Identifier Source="ORCID">0000-0003-0002-1955</Identifier><AffiliationInfo><Affiliation>Department of Electrocardiology and Heart Failure, Medical University of Silesia, Katowice, Poland. rafal.gardas@gmail.com.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Electrocardiology, Leszek Giec Upper-Silesian Medical Center of the Silesian Medical University, Katowice, Poland. rafal.gardas@gmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Golba</LastName><ForeName>Krzysztof S</ForeName><Initials>KS</Initials><AffiliationInfo><Affiliation>Department of Electrocardiology and Heart Failure, Medical University of Silesia, Katowice, Poland.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Electrocardiology, Leszek Giec Upper-Silesian Medical Center of the Silesian Medical University, Katowice, Poland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Loboda</LastName><ForeName>Danuta</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Electrocardiology and Heart Failure, Medical University of Silesia, Katowice, Poland.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Electrocardiology, Leszek Giec Upper-Silesian Medical Center of the Silesian Medical University, Katowice, Poland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Biernat</LastName><ForeName>Jolanta</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Electrocardiology and Heart Failure, Medical University of Silesia, Katowice, Poland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Soral</LastName><ForeName>Tomasz</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Electrocardiology and Heart Failure, Medical University of Silesia, Katowice, Poland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kulesza</LastName><ForeName>Piotr</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department of Electrocardiology and Heart Failure, Medical University of Silesia, Katowice, Poland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sajdok</LastName><ForeName>Mateusz</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Electrocardiology and Heart Failure, Medical University of Silesia, Katowice, Poland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zub</LastName><ForeName>Kamil</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Electrocardiology and Heart Failure, Medical University of Silesia, Katowice, Poland.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>08</Month><Day>23</Day></ArticleDate></Article><MedlineJournalInfo><Country>Poland</Country><MedlineTA>Cardiol J</MedlineTA><NlmUniqueID>101392712</NlmUniqueID><ISSNLinking>1898-018X</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">His bundle pacing</Keyword><Keyword MajorTopicYN="N">heart failure</Keyword><Keyword MajorTopicYN="N">permanent pacing</Keyword><Keyword MajorTopicYN="N">resynchronization therapy</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>6</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>8</Month><Day>7</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>8</Month><Day>6</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>8</Month><Day>23</Day><Hour>5</Hour><Minute>33</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>8</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>8</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>aheadofprint</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35997047</ArticleId><ArticleId IdType="doi">10.5603/CJ.a2022.0079</ArticleId><ArticleId IdType="pii">VM/OJS/J/90497</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35997027</PMID><DateRevised><Year>2022</Year><Month>08</Month><Day>23</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1467-1107</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Aug</Month><Day>23</Day></PubDate></JournalIssue><Title>Cardiology in the young</Title><ISOAbbreviation>Cardiol Young</ISOAbbreviation></Journal><ArticleTitle>Contemporary risk factors for a longer hospital stay following bidirectional cavopulmonary anastomosis.</ArticleTitle><Pagination><StartPage>1</StartPage><EndPage>7</EndPage><MedlinePgn>1-7</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1017/S1047951122002694</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Despite high survival after bidirectional cavopulmonary anastomosis, a considerable number of patients suffer significant post-operative morbidities related to prolonged length of stay.<AbstractText Label="METHODS" NlmCategory="METHODS">A single-center retrospective cohort study of all consecutive patients undergoing a first-time bidirectional cavopulmonary anastomosis from 2006 to 2019.<AbstractText Label="RESULTS" NlmCategory="RESULTS">Prolonged length of stay was defined as hospital stay greater than the 75th percentile for our cohort. Of 195 patients who met inclusion criteria, the median post-operative length of stay was 8 days (interquartile range, 4-15 days). Prolonged length of stay was defined as greater than 15 days. In multivariate analysis, greater than mild systemic atrioventricular valve regurgitation (odds ratio 3.7, 95% CI 1.05-13.068, p = 0.04), longer length of stay after the initial palliative procedure (odds ratio 1.028, 95% CI 1.004-1.05, p = 0.02), and pre-operative higher superior vena cava oxygen saturation (odds ratio 0.922, 95% CI 0.85-0.99, p = 0.04) maintained statistical significance as independent risk and protective factors for prolonged length of stay. A one-level increase in the severity of pre-operative systemic atrioventricular valve regurgitation was associated with a multiplicative change in the odds ratio of prolonged length of stay of 5.45 (p = 0.005) independent of the severity of systemic ventricular dysfunction.<AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">Pre-operative characteristics with greater than mild systemic atrioventricular valve regurgitation, longer length of stay after the initial palliative procedure, and lower superior vena cava oxygen saturation were associated with prolonged length of stay after a first-time bidirectional cavopulmonary anastomosis. |
2,329,622 | Ocular Manifestations Leading to a Diagnosis of Joubert Syndrome Related Disorder. | Joubert syndrome is an inherited disorder of rare occurrence usually presenting as developmental delay, hypotonia, hyperpnea and ataxia. The diagnosis is confirmed by characteristic findings in neuroimaging. Involvement of ocular, renal and hepatic systems can be present. Joubert syndrome presenting first to an ophthalmologist is very uncommon.</AbstractText>A twenty-one-year female, with history of delayed milestones, infantile hemiplegia with hearing and visual impairment was referred for visual assessment. On systemic examination, ataxic gait was present. CT head showed hypoplasia of postero-inferior portion of vermis with communication between 4th ventricle and cisterna magna with variable degree of cerebellar dysgenesis. The neurological, ophthalmological and radiological findings of this patient were consistent with Joubert syndrome related disorder.</AbstractText>We hereby report a case of Joubert syndrome related disorder with ocular involvement which after correlation with neurological findings and neuroimaging led us to the diagnosis of this rare disorder. The renal and hepatic functions in these patients need to be monitored.</AbstractText>© NEPjOPH.</CopyrightInformation> |
2,329,623 | Association of complement component 4 with neuroimmune abnormalities in the subventricular zone in schizophrenia and autism spectrum disorders. | An early inflammatory insult is the most recognized risk factor associated with neurodevelopmental psychiatric disorders, even more so than genetic variants. Notably, complement component 4 (C4), a molecule involved in inflammatory responses, has been strongly associated with schizophrenia (SZ) and its role in other neurodevelopmental disorders, such as autism (ASD), is an area of active investigation. However, while C4 in SZ has been implicated in the context of synaptic pruning, little is known about its neuroinflammatory role. The subventricular zone (SVZ) is a region heavily involved in neurodevelopment and neuroimmune interactions through the lifespan; thus, it is a region wherein C4 may play a vital role in disease pathology. Using in situ hybridization with radioactive riboprobes and RNAscope, we identified robust astrocytic expression of C4 in the SVZ and in the septum pellucidum. C4 was also expressed in ependyma, neurons, and Ki67<sup>+</sup> progenitor cells. Examination of mRNA levels showed elevated C4 in both ASD and SZ, with higher expression in SZ compared to controls. Targeted transcriptomic analysis of inflammatory pathways revealed a strong association of complement system genes with SZ, and to a lesser extent, ASD, as well as generalized immune dysregulation without a strong association with known infectious pathways. Analysis of differentially expressed genes (DEGs) showed that ASD DEGs were enriched in adaptive immune system functions such as Th cell differentiation, while SZ DEGs were enriched in innate immune system functions, including NF-κB and toll like receptor signaling. Moreover, the number of Ki67<sup>+</sup> cells was significantly higher in ASD compared to SZ and controls. Taken together, these results support a role for C4 into inflammatory-neuroimmune dysregulation observed in SZ and ASD pathology. |
2,329,624 | Morphological evaluation of the normal and hydrocephalic third ventricle on cranial magnetic resonance imaging in children: a retrospective study. | Third ventricle morphological changes reflect changes in the ventricular system in pediatric hydrocephalus, so visual inspection of the third ventricle shape is standard practice. However, normal pediatric reference data are not available.</AbstractText>To investigate both the normal development of the third ventricle in the 0-18-year age group and changes in its biometry due to hydrocephalus.</AbstractText>For this retrospective study, we selected individuals ages 0-18 years who had magnetic resonance imaging (MRI) from 2012 to 2020. We included 700 children (331 girls) who had three-dimensional (3-D) T1-weighted sequences without and 25 with hydrocephalus (11 girls). We measured the distances between the anatomical structures limiting the third ventricle by dividing the third ventricle into anterior and posterior regions. We made seven linear measurements and three index calculations using 3DSlicer and MRICloud pipeline, and we analyzed the results of 23 age groups in normal and hydrocephalic patients using SPSS (v. 23).</AbstractText>Salient findings are: (1) The posterior part of the third ventricle is more affected by both developmental and hydrocephalus-related changes. (2) For third ventricle measurements, gender was insignificant while age was significant. (3) Normal third ventricular volumetric development showed a segmental increase in the 0-18 age range. The hydrocephalic third ventricle volume cut-off value in this age group was 3 cm3</sup>.</AbstractText>This study describes third ventricle morphometry using a linear measurement method. The ratios defined in the midsagittal plane were clinically useful for diagnosing the hydrocephalic third ventricle. The linear and volumetric reference data and ratios are expected to help increase diagnostic accuracy in distinguishing normal and hydrocephalic third ventricles.</AbstractText>© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.</CopyrightInformation> |
2,329,625 | Prenatal androgen treatment impairs the suprachiasmatic nucleus arginine-vasopressin to kisspeptin neuron circuit in female mice. | Polycystic ovary syndrome (PCOS) is associated with elevated androgen and luteinizing hormone (LH) secretion and with oligo/anovulation. Evidence indicates that elevated androgens impair sex steroid hormone feedback regulation of pulsatile LH secretion. Hyperandrogenemia in PCOS may also disrupt the preovulatory LH surge. The mechanisms through which this might occur, however, are not fully understood. Kisspeptin (KISS1) neurons of the rostral periventricular area of the third ventricle (RP3V) convey hormonal cues to gonadotropin-releasing hormone (GnRH) neurons. In rodents, the preovulatory surge is triggered by these hormonal cues and coincident timing signals from the central circadian clock in the suprachiasmatic nucleus (SCN). Timing signals are relayed to GnRH neurons, in part, <i>via</i> projections from SCN arginine-vasopressin (AVP) neurons to RP3V<sup>KISS1</sup> neurons. Because rodent SCN cells express androgen receptors (AR), we hypothesized that these circuits are impaired by elevated androgens in a mouse model of PCOS. In prenatally androgen-treated (PNA) female mice, SCN <i>Ar</i> expression was significantly increased compared to that found in prenatally vehicle-treated mice. A similar trend was seen in the number of <i>Avp</i>-positive SCN cells expressing <i>Ar</i>. In the RP3V, the number of kisspeptin neurons was preserved. Anterograde tract-tracing, however, revealed reduced SCN<sup>AVP</sup> neuron projections to the RP3V and a significantly lower proportion of RP3V<sup>KISS1</sup> neurons with close appositions from SCN<sup>AVP</sup> fibers. Functional assessments showed, on the other hand, that RP3V<sup>KISS1</sup> neuron responses to AVP were maintained in PNA mice. These findings indicate that PNA changes some of the neural circuits that regulate the preovulatory surge. These impairments might contribute to ovulatory dysfunction in PNA mice modeling PCOS. |
2,329,626 | Dyke-Davidoff-Masson syndrome: A rare case of hemiatrophy of brain-Case report from Nepal. | Dyke-Davidoff-Masson syndrome (DDMS) is a rare neurological disorder that results from brain injury during intrauterine or early years of life. Prominent cortical sulci, dilated lateral ventricles, cerebral hemiatrophy, hyperpneumatization of the sinus, and compensatory hypertrophy of the skull are the characteristic findings. We describe a female patient who presented with a history of seizure, right-sided body weakness, and neuroimaging features of left cerebral hemiatrophy, dilatation of left lateral ventricle, left frontal sinus hyperpneumatization, asymmetric calvarial thickening, and elevation of the petrous ridge. |
2,329,627 | Association of fetal hydrocephalus with other embryological anomalies: A prenatal ultrasound-based study. | To determine the incidence of fetal hydrocephalus in pregnant women and to identify the association of fetal hydrocephalus with other embryological anomalies.</AbstractText>This comparative cross-sectional study was conducted on 36 pregnant women at a private ultrasound clinic in Karachi over a period of eight months. The participants were divided into age groups, 21-30 years and 31-40 years. Toshiba APLIO 300 ultrasound machine was used to assess fetal age by measuring biparietal diameter (BPD) and femur length, whereas atrium of lateral ventricle was measured to diagnose fetal hydrocephalus.</AbstractText>Twenty-two cases of fetal hydrocephalus were observed in maternal age of 21-30 years with a p-value of 0.011. Severe dilatation of ≥15mm was observed in 85.7% cases in age group of 31-40 years. Cranial anomalies were found in 20 cases with significant results while extracranial anomalies were observed in cases of severe dilatation only. Hydrocephalus was prevalent in male fetuses and was observed in 30 (83.33%) fetuses.</AbstractText>Most cases of fetal hydrocephalus were observed in women of younger age (p=0.011). Fetal hydrocephalus of severe type exhibiting ventricular dilatation >15mm was observed in fetuses of male gender.</AbstractText>Copyright: © Pakistan Journal of Medical Sciences.</CopyrightInformation> |
2,329,628 | Predicting Hematoma Expansion after Spontaneous Intracranial Hemorrhage Through a Radiomics Based Model. | Intracranial hemorrhage (ICH) is characterized as bleeding into the brain tissue, intracranial space, and ventricles and is the second most disabling form of stroke. Hematoma expansion (HE) following ICH has been correlated with significant neurological decline and death. For early detection of patients at risk, deep learning prediction models were developed to predict whether hematoma due to ICH will expand. This study aimed to explore the feasibility of HE prediction using a radiomic approach to help clinicians better stratify HE patients and tailor intensive therapies timely and effectively.</AbstractText>Two hundred ICH patients with known hematoma evolution, were enrolled in this study. An open-source python package was utilized for the extraction of radiomic features from both non-contrast computed tomography (NCCT) and magnetic resonance imaging (MRI) scans through characterization algorithms. A total of 99 radiomic features were extracted and different features were selected for network inputs for the NCCT and MR models. Seven supervised classifiers: Support Vector Machine, Naïve Bayes, Decision Tree, Random Forest, Logistic Regression, K-Nearest Neighbor and Multilayer Perceptron were used to build the models. A training:testing split of 80:20 and 20 iterations of Monte Carlo cross validation were performed to prevent overfitting and assess the variability of the networks, respectively. The models were fed training datasets from which they learned to classify the data based on pre-determined radiomic categories.</AbstractText>The highest sensitivity among the NCCT classifier models was seen with the support vector machine (SVM) and logistic regression (LR) of 72 ± 0.3% and 73 ± 0.5%, respectively. The MRI classifier models had the highest sensitivity of 68 ± 0.5% and 72 ± 0.5% for the SVM and LR models, respectively.</AbstractText>This study indicates that the NCCT radiomics model is a better predictor of HE and that SVM and LR classifiers are better predictors of HE due to their more cautious approach indicated by a higher sensitivity metric.</AbstractText> |
2,329,629 | Living on a Thread: A Case of Critical Left Main Coronary Artery Disease With an Unusual Presentation.<Pagination><StartPage>e26942</StartPage><MedlinePgn>e26942</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">e26942</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.7759/cureus.26942</ELocationID><Abstract><AbstractText>The left main disease is significant stenosis of the left coronary artery, which is responsible of supplying blood to a major portion of the left ventricle. In this report, we describe a unique case of critical left main disease with a special clinical presentation. A 66-year-old male with insignificant past medical history presented with dyspepsia. Patient presented twice to the emergency department seeking for help for his persistent complaint. During his second visit, patient was diagnosed with type one myocardial infarction and underwent coronary angiography which showed 90% stenosis in the left main coronary artery. Patient underwent successful coronary artery bypass grafting and was sent home. This case is a unique representation of type 1 myocardial infarction as the peak troponin I level does not correlate with the extent of the myocardium being jeopardized. A big portion of the heart is at risk of injury with the 90% stenosis found in this patient's left main coronary artery, yet the peak troponin I level is minimum. This report provides a possible explanation of the discrepancy between the peak troponin I level and the extent of the myocardium being jeopardized and describes a common yet easily missed clinical presentation of acute coronary syndrome. Left main disease is a relatively uncommon presentation of acute coronary syndrome, with potentially serious detrimental consequences. Discrepancies do occur among patients of critical left main disease, and promptly diagnosing and managing is of great importance.</AbstractText><CopyrightInformation>Copyright © 2022, Asfour et al.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Asfour</LastName><ForeName>Issa</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Internal Medicine, East Tennessee State University, Johnson City, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jbara</LastName><ForeName>Manar</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Cardiology, East Tennessee State University, Johnson City, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>07</Month><Day>17</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Cureus</MedlineTA><NlmUniqueID>101596737</NlmUniqueID><ISSNLinking>2168-8184</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">atypical symptoms</Keyword><Keyword MajorTopicYN="N">cardiac troponin</Keyword><Keyword MajorTopicYN="N">cardio vascular disease</Keyword><Keyword MajorTopicYN="N">coronary artery bypass grafting(cabg)</Keyword><Keyword MajorTopicYN="N">left main coronary artery disease</Keyword><Keyword MajorTopicYN="N">significant coronary artery disease</Keyword></KeywordList><CoiStatement>The authors have declared that no competing interests exist.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>7</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>8</Month><Day>22</Day><Hour>3</Hour><Minute>45</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>8</Month><Day>23</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>8</Month><Day>23</Day><Hour>6</Hour><Minute>1</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35989810</ArticleId><ArticleId IdType="pmc">PMC9380753</ArticleId><ArticleId IdType="doi">10.7759/cureus.26942</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Singh A, Museedi AS, Grossman SA. StatPearls [Internet] Treasure Island (FL): StatPearls Publishing; 2022. Acute coronary syndrome.</Citation><ArticleIdList><ArticleId IdType="pubmed">29083796</ArticleId></ArticleIdList></Reference><Reference><Citation>State-of-the-art diagnosis of myocardial infarction. Vafaie M. Diagnosis (Berl) 2016;3:137–142.</Citation><ArticleIdList><ArticleId IdType="pubmed">29536900</ArticleId></ArticleIdList></Reference><Reference><Citation>Main left coronary artery disease. Clinical experience from 1964-1974. Cohen MV, Gorlin R. Circulation. 1975;52:275–285.</Citation><ArticleIdList><ArticleId IdType="pubmed">1080085</ArticleId></ArticleIdList></Reference><Reference><Citation>Management of left main disease: an update. Fajadet J, Capodanno D, Stone GW. Eur Heart J. 2019;40:1454–1466.</Citation><ArticleIdList><ArticleId IdType="pubmed">29718158</ArticleId></ArticleIdList></Reference><Reference><Citation>Troponin elevation in coronary vs. non-coronary disease. Agewall S, Giannitsis E, Jernberg T, Katus H. Eur Heart J. 2011;32:404–411.</Citation><ArticleIdList><ArticleId IdType="pubmed">21169615</ArticleId></ArticleIdList></Reference><Reference><Citation>Left main coronary artery disease: a review of the spectrum of noninvasive diagnostic modalities. Sareen N, Ananthasubramaniam K. J Nucl Cardiol. 2016;23:1411–1429.</Citation><ArticleIdList><ArticleId IdType="pubmed">26487011</ArticleId></ArticleIdList></Reference><Reference><Citation>Fourth Universal Definition of Myocardial Infarction (2018) Thygesen K, Alpert JS, Jaffe AS, Chaitman BR, Bax JJ, Morrow DA, White HD. J Am Coll Cardiol. 2018;72:2231–2264.</Citation><ArticleIdList><ArticleId IdType="pubmed">30153967</ArticleId></ArticleIdList></Reference><Reference><Citation>Troponin T levels and infarct size by SPECT myocardial perfusion imaging. Arruda-Olson AM, Roger VL, Jaffe AS, Hodge DO, Gibbons RJ, Miller TD. http://linkinghub.elsevier.com/retrieve/pii/S1936878X11001963. JACC Cardiovasc Imaging. 2011;4:523–533.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC3239221</ArticleId><ArticleId IdType="pubmed">21565741</ArticleId></ArticleIdList></Reference><Reference><Citation>Estimation of infarct size using serum troponin T concentration in patients with acute myocardial infarction. Omura T, Teragaki M, Tani T, et al. http://jstage.jst.go.jp/article/circj1960/57/11/57_11_1062/_article. Jpn Circ J. 1993;57:1062–1070.</Citation><ArticleIdList><ArticleId IdType="pubmed">8230683</ArticleId></ArticleIdList></Reference><Reference><Citation>The content and distribution of troponin I, troponin T, myoglobin, and alpha-hydroxybutyric acid dehydrogenase in the human heart. Swaanenburg JC, Visser-VanBrummen PJ, DeJongste MJ, Tiebosch AT. http://academic.oup.com/ajcp/article-lookup/doi/10.1309/054C-QV78-MTVF-YACW. Am J Clin Pathol. 2001;115:770–777.</Citation><ArticleIdList><ArticleId IdType="pubmed">11345843</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35989537</PMID><DateRevised><Year>2023</Year><Month>03</Month><Day>09</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1467-1107</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Aug</Month><Day>22</Day></PubDate></JournalIssue><Title>Cardiology in the young</Title><ISOAbbreviation>Cardiol Young</ISOAbbreviation></Journal>Defining the optimal historical control group for a phase 1 trial of mesenchymal stromal cell delivery through cardiopulmonary bypass in neonates and infants. | The left main disease is significant stenosis of the left coronary artery, which is responsible of supplying blood to a major portion of the left ventricle. In this report, we describe a unique case of critical left main disease with a special clinical presentation. A 66-year-old male with insignificant past medical history presented with dyspepsia. Patient presented twice to the emergency department seeking for help for his persistent complaint. During his second visit, patient was diagnosed with type one myocardial infarction and underwent coronary angiography which showed 90% stenosis in the left main coronary artery. Patient underwent successful coronary artery bypass grafting and was sent home. This case is a unique representation of type 1 myocardial infarction as the peak troponin I level does not correlate with the extent of the myocardium being jeopardized. A big portion of the heart is at risk of injury with the 90% stenosis found in this patient's left main coronary artery, yet the peak troponin I level is minimum. This report provides a possible explanation of the discrepancy between the peak troponin I level and the extent of the myocardium being jeopardized and describes a common yet easily missed clinical presentation of acute coronary syndrome. Left main disease is a relatively uncommon presentation of acute coronary syndrome, with potentially serious detrimental consequences. Discrepancies do occur among patients of critical left main disease, and promptly diagnosing and managing is of great importance.<CopyrightInformation>Copyright © 2022, Asfour et al.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Asfour</LastName><ForeName>Issa</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Internal Medicine, East Tennessee State University, Johnson City, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jbara</LastName><ForeName>Manar</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Cardiology, East Tennessee State University, Johnson City, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>07</Month><Day>17</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Cureus</MedlineTA><NlmUniqueID>101596737</NlmUniqueID><ISSNLinking>2168-8184</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">atypical symptoms</Keyword><Keyword MajorTopicYN="N">cardiac troponin</Keyword><Keyword MajorTopicYN="N">cardio vascular disease</Keyword><Keyword MajorTopicYN="N">coronary artery bypass grafting(cabg)</Keyword><Keyword MajorTopicYN="N">left main coronary artery disease</Keyword><Keyword MajorTopicYN="N">significant coronary artery disease</Keyword></KeywordList><CoiStatement>The authors have declared that no competing interests exist.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>7</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>8</Month><Day>22</Day><Hour>3</Hour><Minute>45</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>8</Month><Day>23</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>8</Month><Day>23</Day><Hour>6</Hour><Minute>1</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35989810</ArticleId><ArticleId IdType="pmc">PMC9380753</ArticleId><ArticleId IdType="doi">10.7759/cureus.26942</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Singh A, Museedi AS, Grossman SA. StatPearls [Internet] Treasure Island (FL): StatPearls Publishing; 2022. Acute coronary syndrome.</Citation><ArticleIdList><ArticleId IdType="pubmed">29083796</ArticleId></ArticleIdList></Reference><Reference><Citation>State-of-the-art diagnosis of myocardial infarction. Vafaie M. Diagnosis (Berl) 2016;3:137–142.</Citation><ArticleIdList><ArticleId IdType="pubmed">29536900</ArticleId></ArticleIdList></Reference><Reference><Citation>Main left coronary artery disease. Clinical experience from 1964-1974. Cohen MV, Gorlin R. Circulation. 1975;52:275–285.</Citation><ArticleIdList><ArticleId IdType="pubmed">1080085</ArticleId></ArticleIdList></Reference><Reference><Citation>Management of left main disease: an update. Fajadet J, Capodanno D, Stone GW. Eur Heart J. 2019;40:1454–1466.</Citation><ArticleIdList><ArticleId IdType="pubmed">29718158</ArticleId></ArticleIdList></Reference><Reference><Citation>Troponin elevation in coronary vs. non-coronary disease. Agewall S, Giannitsis E, Jernberg T, Katus H. Eur Heart J. 2011;32:404–411.</Citation><ArticleIdList><ArticleId IdType="pubmed">21169615</ArticleId></ArticleIdList></Reference><Reference><Citation>Left main coronary artery disease: a review of the spectrum of noninvasive diagnostic modalities. Sareen N, Ananthasubramaniam K. J Nucl Cardiol. 2016;23:1411–1429.</Citation><ArticleIdList><ArticleId IdType="pubmed">26487011</ArticleId></ArticleIdList></Reference><Reference><Citation>Fourth Universal Definition of Myocardial Infarction (2018) Thygesen K, Alpert JS, Jaffe AS, Chaitman BR, Bax JJ, Morrow DA, White HD. J Am Coll Cardiol. 2018;72:2231–2264.</Citation><ArticleIdList><ArticleId IdType="pubmed">30153967</ArticleId></ArticleIdList></Reference><Reference><Citation>Troponin T levels and infarct size by SPECT myocardial perfusion imaging. Arruda-Olson AM, Roger VL, Jaffe AS, Hodge DO, Gibbons RJ, Miller TD. http://linkinghub.elsevier.com/retrieve/pii/S1936878X11001963. JACC Cardiovasc Imaging. 2011;4:523–533.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC3239221</ArticleId><ArticleId IdType="pubmed">21565741</ArticleId></ArticleIdList></Reference><Reference><Citation>Estimation of infarct size using serum troponin T concentration in patients with acute myocardial infarction. Omura T, Teragaki M, Tani T, et al. http://jstage.jst.go.jp/article/circj1960/57/11/57_11_1062/_article. Jpn Circ J. 1993;57:1062–1070.</Citation><ArticleIdList><ArticleId IdType="pubmed">8230683</ArticleId></ArticleIdList></Reference><Reference><Citation>The content and distribution of troponin I, troponin T, myoglobin, and alpha-hydroxybutyric acid dehydrogenase in the human heart. Swaanenburg JC, Visser-VanBrummen PJ, DeJongste MJ, Tiebosch AT. http://academic.oup.com/ajcp/article-lookup/doi/10.1309/054C-QV78-MTVF-YACW. Am J Clin Pathol. 2001;115:770–777.</Citation><ArticleIdList><ArticleId IdType="pubmed">11345843</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35989537</PMID><DateRevised><Year>2023</Year><Month>03</Month><Day>09</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1467-1107</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Aug</Month><Day>22</Day></PubDate></JournalIssue><Title>Cardiology in the young</Title><ISOAbbreviation>Cardiol Young</ISOAbbreviation></Journal><ArticleTitle>Defining the optimal historical control group for a phase 1 trial of mesenchymal stromal cell delivery through cardiopulmonary bypass in neonates and infants.</ArticleTitle><Pagination><StartPage>1</StartPage><EndPage>6</EndPage><MedlinePgn>1-6</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1017/S1047951122002633</ELocationID><Abstract><AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">The Mesenchymal Stromal Cell Delivery through Cardiopulmonary Bypass in Pediatric Cardiac Surgery study is a prospective, open-label, single-centre, dose-escalation phase 1 trial assessing the safety/feasibility of delivering mesenchymal stromal cells to neonates/infants during cardiac surgery. Outcomes will be compared with historical data from a similar population. We aim to define an optimal control group for use in the Mesenchymal Stromal Cell Delivery through Cardiopulmonary Bypass in Pediatric Cardiac Surgery trial.<AbstractText Label="METHODS" NlmCategory="METHODS">Consecutive patients who underwent a two-ventricle repair without aortic arch reconstruction within the first 6 months of life between 2015 and 2020 were studied using the same inclusion/exclusion criteria as the Phase 1 Mesenchymal Stromal Cell Delivery through Cardiopulmonary Bypass in Pediatric Cardiac Surgery trial (n = 169). Patients were allocated into one of three diagnostic groups: ventricular septal defect type, Tetralogy of Fallot type, and transposition of the great arteries type. To determine era effect, patients were analysed in two groups: Group A (2015-2017) and B (2018-2020). In addition to biological markers, three post-operative scoring methods (inotropic and vasoactive-inotropic scores and the Pediatric Risk of Mortality-III) were assessed.<AbstractText Label="RESULTS" NlmCategory="RESULTS">All values for three scoring systems were consistent with complexity of cardiac anomalies. Max inotropic and vasoactive-inotropic scores demonstrated significant differences between all diagnosis groups, confirming high sensitivity. Despite no differences in surgical factors between era groups, we observed lower inotropic and vasoactive-inotropic scores in group B, consistent with improved post-operative course in recent years at our centre.<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Our studies confirm max inotropic and vasoactive-inotropic scores as important quantitative measures after neonatal/infant cardiac surgery. Clinical outcomes should be compared within diagnostic groupings. The optimal control group should include only patients from a recent era. This initial study will help to determine the sample size of future efficacy/effectiveness studies. |
2,329,630 | Detection of Cardiac Functions of Fetus with Diabetic Metabolic Disease through PEG-PCLNano Micelle and Ultrasound Technique.<Pagination><StartPage>24</StartPage><EndPage>33</EndPage><MedlinePgn>24-33</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.14715/cmb/2022.68.3.4</ELocationID><Abstract><AbstractText Label="UNLABELLED">The study was to probe into the application of ultrasound technique in gestational diabetes mellitus (GDM) and research the progress of PEG-PCL nano micelle and ultrasound technique.</AbstractText><AbstractText Label="METHOD" NlmCategory="METHODS">210 patients with a singleton pregnancy fetus, who received the fetal echocardiography in Yuhang District First People's Hospital from March 2019 to March 2020, were selected as the subjects, including 101 fetuses who were confirmed as gestational diabetes mellitus(GDM), and 109 normal fetuses (control group). The ultrasound cardiogram technique was employed to detect the thickness of the fetus ventricle septum, mitral/tricuspid annular displacement, left/right TEI indexes, and so on. The mean value of three cardiac cycles was taken as the test results. Finally, SPSS17.0 software was applied to the analysis of data. The nano micelle was made from the amphiphilic block copolymers (PEG-PCL) using the dialysis method/solvent evaporation method. The nanoscale ultrasound contrast agent was prepared from Decafluoropentane which was imaging gas. The characterizations were studied using the optical microscope, and transmission electron microscopy (TEM). The temperature sensitivity and ultrasound sensitivity of the nano-ultrasound contrast agent were analyzed with the particle size as the evaluation index. The in-vitro ultrasound contrast experiment was conducted to study the contrast-enhanced effect.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">The fetal Tei index of the case group was higher than that of the control group, of which P<0.05 had statistical significance. However, the thickness of the fetus ventricle septum, Em, Am, and Em/Am of mitral/tricuspid annular were not significantly different from those of the control group (P>0.05). The nano ultrasonic contrast agent prepared through the ultrasonic injection method had a uniform particle size and a hollow shell-core structure under an electron projection microscope. The particle size of the nano-ultrasound contrast agent varied with temperature, and its microbubbles were generated under ultrasonic conditions. As compared with the blank degassed water group, a real linear echo appeared inside the contrast agent group, with small and even echo spots. The back echo remained with no obvious attenuation and lasted for a longer period. However, the blank degassed group had no distinct echo intensity and spot.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">PEG-PCL nano-ultrasound contrast agent achieved an excellent imaging effect; there was no obvious change to heart function and structure of the fetus, when gestational diabetes pregnant had blood sugar perfectly controlled, however, the fetus's heart function may change in the last trimester.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ran</LastName><ForeName>Hongmei</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Ultrasound, Linping District First People's Hospital, Hangzhou, 311100, China. ncdx1209@163.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Yunlong</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Ultrasound, Linping District First People's Hospital, Hangzhou, 311100, China. ncdx1209@163.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yu</LastName><ForeName>Dingding</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Obstetrics, Linping District First People's Hospital, Hangzhou, 311100, China. ncdx1209@163.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhou</LastName><ForeName>Guoli</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Department of Laboratory, Linping District First People's Hospital, Hangzhou, 311100, China. ncdx1209@163.com.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>03</Month><Day>31</Day></ArticleDate></Article><MedlineJournalInfo><Country>France</Country><MedlineTA>Cell Mol Biol (Noisy-le-grand)</MedlineTA><NlmUniqueID>9216789</NlmUniqueID><ISSNLinking>0145-5680</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D003287">Contrast Media</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008823">Micelles</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D003287" MajorTopicYN="N">Contrast Media</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016640" MajorTopicYN="Y">Diabetes, Gestational</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005333" MajorTopicYN="N">Fetus</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008823" MajorTopicYN="N">Micelles</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011247" MajorTopicYN="N">Pregnancy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016216" MajorTopicYN="N">Ultrasonography, Prenatal</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>4</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>8</Month><Day>21</Day><Hour>14</Hour><Minute>36</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>8</Month><Day>22</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>8</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35988192</ArticleId><ArticleId IdType="doi">10.14715/cmb/2022.68.3.4</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedBookArticle><BookDocument><PMID Version="1">30969587</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK539765</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-41528">Atrioventricular Reciprocating Tachycardia<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Jabbour</LastName><ForeName>Fouad</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>SUNY Upstate University Hospital</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Grossman</LastName><ForeName>Shamai A.</ForeName><Initials>SA</Initials><AffiliationInfo><Affiliation>HVD Med Sch</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>Atrioventricular reciprocating tachycardia (AVRT) is a macroreentrant tachycardia that needs an accessory pathway to bypass the regular conduction system. Atrioventricular reentry tachycardia has a circuit that consists of two different pathways consisted of the regular conduction system through the AV node and an accessory pathway that enables communication between the atrium with the ventricle. After an extra beat of ectopic atrial or ventricular origin, these two pathways enable a difference between the refractory period and conduction time to allow tachycardia to persist  Atrioventricular reentry tachycardia and Wolf-Parkinson-White syndrome are often used interchangeably. However, to be specific, AVRT is the most common type of arrhythmia associated with the Wolf Parkinson White syndrome. Other examples of arrhythmia include AVNRT, atrial fibrillation with preexcitation, and atrial flutter.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-41528" sec="article-41528.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-41528" sec="article-41528.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-41528" sec="article-41528.s3">Etiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-41528" sec="article-41528.s4">Epidemiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-41528" sec="article-41528.s5">History and Physical</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-41528" sec="article-41528.s6">Evaluation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-41528" sec="article-41528.s7">Treatment / Management</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-41528" sec="article-41528.s8">Differential Diagnosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-41528" sec="article-41528.s9">Prognosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-41528" sec="article-41528.s10">Complications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-41528" sec="article-41528.s11">Deterrence and Patient Education</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-41528" sec="article-41528.s12">Pearls and Other Issues</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-41528" sec="article-41528.s13">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-41528" sec="article-41528.s14">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-41528" sec="article-41528.s16">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>8</Month><Day>22</Day></ContributionDate><ReferenceList><Reference><Citation>Bardy GH, Packer DL, German LD, Gallagher JJ. Preexcited reciprocating tachycardia in patients with Wolff-Parkinson-White syndrome: incidence and mechanisms. Circulation. 1984 Sep;70(3):377-91.</Citation><ArticleIdList><ArticleId IdType="pubmed">6744541</ArticleId></ArticleIdList></Reference><Reference><Citation>Akhtar M, Lehmann MH, Denker ST, Mahmud R, Tchou P, Jazayeri M. Electrophysiologic mechanisms of orthodromic tachycardia initiation during ventricular pacing in the Wolff-Parkinson-White syndrome. 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Part 8: adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010 Nov 02;122(18 Suppl 3):S729-67.</Citation><ArticleIdList><ArticleId IdType="pubmed">20956224</ArticleId></ArticleIdList></Reference><Reference><Citation>Lim SH, Anantharaman V, Teo WS, Goh PP, Tan AT. Comparison of treatment of supraventricular tachycardia by Valsalva maneuver and carotid sinus massage. Ann Emerg Med. 1998 Jan;31(1):30-5.</Citation><ArticleIdList><ArticleId IdType="pubmed">28140013</ArticleId></ArticleIdList></Reference><Reference><Citation>DiMarco JP, Miles W, Akhtar M, Milstein S, Sharma AD, Platia E, McGovern B, Scheinman MM, Govier WC. Adenosine for paroxysmal supraventricular tachycardia: dose ranging and comparison with verapamil. Assessment in placebo-controlled, multicenter trials. The Adenosine for PSVT Study Group. 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Circulation. 1999 Jan 19;99(2):262-70.</Citation><ArticleIdList><ArticleId IdType="pubmed">9892593</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">30969587</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">29493981</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK482359</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-17970">Second-Degree Atrioventricular Block | Atrioventricular reciprocating tachycardia (AVRT) is a macroreentrant tachycardia that needs an accessory pathway to bypass the regular conduction system. Atrioventricular reentry tachycardia has a circuit that consists of two different pathways consisted of the regular conduction system through the AV node and an accessory pathway that enables communication between the atrium with the ventricle. After an extra beat of ectopic atrial or ventricular origin, these two pathways enable a difference between the refractory period and conduction time to allow tachycardia to persist  Atrioventricular reentry tachycardia and Wolf-Parkinson-White syndrome are often used interchangeably. However, to be specific, AVRT is the most common type of arrhythmia associated with the Wolf Parkinson White syndrome. Other examples of arrhythmia include AVNRT, atrial fibrillation with preexcitation, and atrial flutter.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-41528" sec="article-41528.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-41528" sec="article-41528.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-41528" sec="article-41528.s3">Etiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-41528" sec="article-41528.s4">Epidemiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-41528" sec="article-41528.s5">History and Physical</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-41528" sec="article-41528.s6">Evaluation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-41528" sec="article-41528.s7">Treatment / Management</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-41528" sec="article-41528.s8">Differential Diagnosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-41528" sec="article-41528.s9">Prognosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-41528" sec="article-41528.s10">Complications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-41528" sec="article-41528.s11">Deterrence and Patient Education</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-41528" sec="article-41528.s12">Pearls and Other Issues</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-41528" sec="article-41528.s13">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-41528" sec="article-41528.s14">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-41528" sec="article-41528.s16">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>8</Month><Day>22</Day></ContributionDate><ReferenceList><Reference><Citation>Bardy GH, Packer DL, German LD, Gallagher JJ. Preexcited reciprocating tachycardia in patients with Wolff-Parkinson-White syndrome: incidence and mechanisms. Circulation. 1984 Sep;70(3):377-91.</Citation><ArticleIdList><ArticleId IdType="pubmed">6744541</ArticleId></ArticleIdList></Reference><Reference><Citation>Akhtar M, Lehmann MH, Denker ST, Mahmud R, Tchou P, Jazayeri M. Electrophysiologic mechanisms of orthodromic tachycardia initiation during ventricular pacing in the Wolff-Parkinson-White syndrome. J Am Coll Cardiol. 1987 Jan;9(1):89-100.</Citation><ArticleIdList><ArticleId IdType="pubmed">3794115</ArticleId></ArticleIdList></Reference><Reference><Citation>Page RL, Joglar JA, Caldwell MA, Calkins H, Conti JB, Deal BJ, Estes NA, Field ME, Goldberger ZD, Hammill SC, Indik JH, Lindsay BD, Olshansky B, Russo AM, Shen WK, Tracy CM, Al-Khatib SM, Evidence Review Committee Chair‡ 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Circulation. 2016 Apr 05;133(14):e471-505.</Citation><ArticleIdList><ArticleId IdType="pubmed">26399662</ArticleId></ArticleIdList></Reference><Reference><Citation>Chiu SN, Wang JK, Wu MH, Chang CW, Chen CA, Lin MT, Wu ET, Hua YC, Lue HC, Taipei Pediatric Cardiology Working Group Cardiac conduction disturbance detected in a pediatric population. J Pediatr. 2008 Jan;152(1):85-9.</Citation><ArticleIdList><ArticleId IdType="pubmed">18154906</ArticleId></ArticleIdList></Reference><Reference><Citation>Fitzsimmons PJ, McWhirter PD, Peterson DW, Kruyer WB. The natural history of Wolff-Parkinson-White syndrome in 228 military aviators: a long-term follow-up of 22 years. Am Heart J. 2001 Sep;142(3):530-6.</Citation><ArticleIdList><ArticleId IdType="pubmed">11526369</ArticleId></ArticleIdList></Reference><Reference><Citation>Kalbfleisch SJ, el-Atassi R, Calkins H, Langberg JJ, Morady F. Differentiation of paroxysmal narrow QRS complex tachycardias using the 12-lead electrocardiogram. J Am Coll Cardiol. 1993 Jan;21(1):85-9.</Citation><ArticleIdList><ArticleId IdType="pubmed">8417081</ArticleId></ArticleIdList></Reference><Reference><Citation>Neumar RW, Otto CW, Link MS, Kronick SL, Shuster M, Callaway CW, Kudenchuk PJ, Ornato JP, McNally B, Silvers SM, Passman RS, White RD, Hess EP, Tang W, Davis D, Sinz E, Morrison LJ. Part 8: adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010 Nov 02;122(18 Suppl 3):S729-67.</Citation><ArticleIdList><ArticleId IdType="pubmed">20956224</ArticleId></ArticleIdList></Reference><Reference><Citation>Lim SH, Anantharaman V, Teo WS, Goh PP, Tan AT. Comparison of treatment of supraventricular tachycardia by Valsalva maneuver and carotid sinus massage. Ann Emerg Med. 1998 Jan;31(1):30-5.</Citation><ArticleIdList><ArticleId IdType="pubmed">28140013</ArticleId></ArticleIdList></Reference><Reference><Citation>DiMarco JP, Miles W, Akhtar M, Milstein S, Sharma AD, Platia E, McGovern B, Scheinman MM, Govier WC. Adenosine for paroxysmal supraventricular tachycardia: dose ranging and comparison with verapamil. Assessment in placebo-controlled, multicenter trials. The Adenosine for PSVT Study Group. 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Circulation. 1999 Jan 19;99(2):262-70.</Citation><ArticleIdList><ArticleId IdType="pubmed">9892593</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">30969587</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">29493981</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK482359</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-17970">Second-Degree Atrioventricular Block</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Mangi</LastName><ForeName>Muhammad Asif</ForeName><Initials>MA</Initials><AffiliationInfo><Affiliation>University of Toledo</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jones</LastName><ForeName>Wesley M.</ForeName><Initials>WM</Initials><AffiliationInfo><Affiliation>Advocate Christ Medical Center</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mansour</LastName><ForeName>Mohamed K.</ForeName><Initials>MK</Initials><AffiliationInfo><Affiliation>Sheikh Shakhbout Medical City (in partnership with Mayoclinic), Abu-Dhabi, United Arab Emirates</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Napier</LastName><ForeName>Laura</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Advocate Christ Medical Center</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>An electrical impulse from the sinoatrial node has to travel through the atria, to the atrioventricular node, and down the His-Purkinje system to reach the ventricles and create a ventricular contraction. This process is reflected on ECG as the PR interval which leads to a QRS complex. A delay in conduction in this system results in an atrioventricular conduction block or a prolongation of the PR interval on ECG. Conduction blocks are classified as either first-degree block, second-degree block, or third-degree block. The second-degree atrioventricular block is the focus of this activity. There are two types of second-degree atrioventricular blocks: Mobitz type I, also known as, Wenckebach and Mobitz type II. In general, patients with second degree AV block may have no symptoms or may experience symptoms like syncope and lightheadedness.The second degree heart block may be temporary or permanent, depending on the impairment of the conduction system. The mobitz type ll block does have the potential to progress to a complete heart block and if unrecognized, can lead to death. |
2,329,631 | Molecular neurobiological markers in the onset of sodium appetite. | Sodium appetite is a motivational state involving homeostatic behavior, seeking the ingest of salty substances after sodium loss. There is a temporal dissociation between sodium depletion (SD) and the appearance of sodium appetite. However, the responsible mechanisms for this delay remain poorly elucidated. In the present study, we measured the temporal changes at two and 24 h after SD in the gene expression of key elements within excitatory, inhibitory, and sensory areas implicated in the signaling pathways involved in the onset of sodium appetite. In SD rats, we observed that the expression of critical components within the brain control circuit of sodium appetite, including Angiotensin-type-1 receptor (Agtr1a), Oxytocin-(OXT-NP)-neurophysin-I, and serotonergic-(5HT)-type-2c receptor (Htr2c) were modulated by SD, regardless of time. However, we observed reduced phosphorylation of mitogen-activated protein kinases (MAPK) at the paraventricular nucleus (PVN) and increased oxytocin receptor (Oxtr) mRNA expression at the anteroventral of the third ventricle area (AV3V), at two hours after SD, when sodium appetite is inapparent. At twenty-four hours after SD, when sodium appetite is released, we observed a reduction in the mRNA expression of the transient receptor potential channel 1gene (Trpv1) and Oxtr in the AV3V and the dorsal raphe nucleus, respectively. The results indicate that SD exerts a coordinated timing effect, promoting the appearance of sodium appetite through changes in MAPK activity and lower Trpv1 channel and Oxtr expression that trigger sodium consumption to reestablish the hydroelectrolytic homeostasis. |
2,329,632 | A hidden infection: Racemose neurocysticercosis causing hydrocephalus; a case report. | Neurocysticercosis (NCC) is the most common helminthic central nervous system infection (CNS) in the Western hemisphere and the most common cause of acquired epilepsy worldwide. Due to its relatively prolonged latent period and clinical similarity to other infectious diseases - including bacterial or viral meningitis and other helminthic infections - NCC may be difficult to diagnose, especially for clinicians who rarely encounter it.</AbstractText>This case report discusses a patient with obstructive hydrocephalus and eosinophilic meningitis secondary to racemose NCC. The diagnosis process was initially complicated by the patient's history of pork allergy and absence of radiographic evidence of helminthic CNS infection. Further investigation showed a 4th ventricle multi-cystic lesion causing hydrocephalus which prompted a surgical intervention with a ventriculoperitoneal shunt (VPS) in conjunction with anti-helminthic medical treatment. At 1-year follow-up, the patient has reported recurrence of VPS related complications.</AbstractText>Larval cysts typically deposit within the brain parenchyma, making them easily detected on head computed tomography (CT) scans and leading to neurologic sequelae such as epilepsy. In this case, the absence of CT evidence of NCC and the patient's lifelong history of pork allergy slowed the diagnosis process.</AbstractText>Racemose NCC is a rare subset of the disease in which cyst clusters occupy the extra parenchymal space, thereby changing the symptomatic profile and making the cysts more difficult to visualize in imaging studies. In this case, magnetic resonance imaging (MRI) was the best imaging modality to diagnosis extra parenchymal NCC and guide its surgical management.</AbstractText>Copyright © 2022 The Authors. Published by Elsevier Ltd.. All rights reserved.</CopyrightInformation> |
2,329,633 | Supratentorial extra-axial RELA fusion-positive ependymoma misdiagnosed as meningioma by intraoperative histological and cytological examinations: a case report. | Dura-attached supratentorial extra-axial ependymoma is a very rare type of tumor, with only nine reported cases. Preoperative diagnosis of dura-attached supratentorial extra-axial ependymoma is difficult and often radiologically misdiagnosed as a meningioma. We report a case of dura-attached supratentorial extra-axial ependymoma that was misdiagnosed using intraoperative histological and cytological examinations.</AbstractText>A 26-year-old Japanese man with headache and nausea was referred to our medical facility. Magnetic resonance imaging revealed a cystic mass of 70 × 53 × 57 mm in the left temporoparietal lobe. A peritumoral band with hyperintensity on T2-weighted imaging was observed at the periphery of the lesion, suggesting an extra-axial lesion with no apparent connection to the ventricle. A dural tail sign was also noted on the gadolinium-enhanced T1-weighted image. Preoperative clinical diagnosis was meningioma. Proliferated tumor cells in sheets with intermingled branching vessels were observed in the frozen tissue. Perivascular rosettes were inconspicuous, and the tumor cells had rhabdoid cytoplasm. The tumor was intraoperatively diagnosed as a meningioma, suspected to be a rhabdoid meningioma. Perivascular rosettes were evident in the formalin-fixed paraffin-embedded tissues, suggesting ependymoma. The tumor cells had eosinophilic cytoplasm without a rhabdoid appearance. Anaplastic features, such as high tumor cellularity, increased mitotic activity, microvascular proliferation, and necrosis, were observed. Ependymal differentiation was confirmed on the basis of ultrastructural analysis. Molecular analysis detected C11orf95-RELA fusion gene. The final diagnosis was RELA fusion-positive ependymoma, World Health Organization grade III.</AbstractText>Owing to its unusual location, dura-attached supratentorial extra-axial ependymomas are frequently misdiagnosed as meningiomas. Neuropathologists should take great precaution in intraoperatively diagnosing this rare subtype of ependymoma to avoid misdiagnosis of the lesion as other common dura-attached tumors.</AbstractText>© 2022. The Author(s).</CopyrightInformation> |
2,329,634 | Neuroblast migration along cellular substrates in the developing porcine brain. | In the past decade it has become evident that neuroblasts continue to supply the human cortex with interneurons via unique migratory streams shortly following birth. Owing to the size of the human brain, these newborn neurons must migrate long distances through complex cellular landscapes to reach their final locations. This process is poorly understood, largely because of technical difficulties in acquiring and studying neurotypical postmortem human samples along with diverging developmental features of well-studied mouse models. We reasoned that migratory streams of neuroblasts utilize cellular substrates, such as blood vessels, to guide their trek from the subventricular zone to distant cortical targets. Here, we evaluate the association between young interneuronal migratory streams and their preferred cellular substrates in gyrencephalic piglets during the developmental equivalent of human birth, infancy, and toddlerhood. |
2,329,635 | Spectrum of qualitative and quantitative imaging of pilomyxoid, intermediate pilomyxoid and pilocytic astrocytomas in relation to their genetic alterations. | Pilomyxoid astrocytomas (PMA) are pediatric brain tumors predominantly located in the suprasellar region, third ventricle and posterior fossa, which are considered to be more clinically aggressive than pilocytic astrocytomas (PA). Another entity, intermediate pilomyxoid tumors (IPT), exists within the spectrum of pilocytic/pilomyxoid astrocytomas. The 2021 WHO CNS classification refrained from assigning grade 1 or 2 status to PMA, thereby reflecting the need to further elucidate their clinical and imaging characteristics.</AbstractText>We included a total of 15 patients with PMA, IPT and suprasellar PA. We retrospectively evaluated immunohistochemistry, imaging findings and diffusion characteristics within these tumors as well as whole exome sequencing for three of the cases.</AbstractText>87% of the tumors were supratentorial with 11 cases suprasellar in location, 1 case located in the frontal white matter and 1 in the hippocampus. 6 cases demonstrated intraventricular extension. ADC values were higher in PMA and IPT than PA. 3 cases demonstrated KIAA1549-BRAF-fusion, 2 had BRAF[Formula: see text]-mutation and 6 were BRAF-wildtype. All cases had recurrence/progression on follow-up.</AbstractText>PMA and IPT do not demonstrate aggressive imaging characteristics in respect to their diffusion imaging with ADC values being higher than PA. Lack of BRAF-alteration in PMA corresponded to atypical location of tumors with atypical driver mutations and mechanisms.</AbstractText>© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.</CopyrightInformation> |
2,329,636 | Immune Microenvironment and Lineage Tracing Help to Decipher Rosette-Forming Glioneuronal Tumors: A Multi-Omics Analysis. | Rosette-forming glioneuronal tumors (RGNT) are rare low-grade primary central nervous system (CNS) tumors. The methylation class (MC) RGNT (MC-RGNT) delineates RGNT from other neurocytic CNS tumors with similar histological features. We performed a comprehensive molecular analysis including whole-exome sequencing, RNAseq, and methylome on 9 tumors with similar histology, focusing on the immune microenvironment and cell of origin of RGNT. Three RGNT in this cohort were plotted within the MC-RGNT and characterized by FGFR1 mutation plus PIK3CA or NF1 mutations. RNAseq analysis, validated by immunohistochemistry, identified 2 transcriptomic groups with distinct immune microenvironments. The "cold" group was distinguishable by a low immune infiltration and included the 3 MC-RGNT and 1 MC-pilocytic astrocytoma; the "hot" group included other tumors with a rich immune infiltration. Gene set enrichment analysis showed that the "cold" group had upregulated NOTCH pathway and mainly oligodendrocyte precursor cell and neuronal phenotypes, while the "hot" group exhibited predominantly astrocytic and neural stem cell phenotypes. In silico deconvolution identified the cerebellar granule cell lineage as a putative cell of origin of RGNT. Our study identified distinct tumor biology and immune microenvironments as key features relevant to the pathogenesis and management of RGNT. |
2,329,637 | A Case Report of Severe Posterior Reversible Encephalopathy Syndrome Due to Accelerated Hypertension in a Young Patient. | Posterior reversible encephalopathy syndrome (PRES) refers to white matter vasogenic edema primarily affecting the brain's posterior occipital and parietal lobes, causing acute neurological symptoms like headaches, visual symptoms, seizures, and altered mental status. We present the case of a 32-year-old male with uncontrolled hypertension, altered mental status, and left-sided weakness. He had a rapid neurological decline, and a computed tomography (CT) head showed blurring of gray-white matter interfaces in the right posterior parietal lobe, suggesting infarction or PRES. Magnetic resonance imaging (MRI) of the brain suggested worsening with acute-early subacute infarction involving the right temporal, parietal, and occipital lobes and diffuse cerebral edema causing compression of the right ventricle with diffuse sulcal effacement and central downward herniation. There were flair hyperintensities in the bifrontal, pons, and cerebellum. Given the history of uncontrolled hypertension, the right hemispheric infarction and edema were thought to be due to secondary complications of severe PRES. He underwent urgent bilateral craniectomies with dural augmentation and external ventricular drain placement to control the intracranial pressure the next day. His mental status, as well as neurologic function, showed gradual improvement in the next few months. A high index of suspicion and rapid treatment can pave the way for a quick recovery and help reduce morbidity and death. |
2,329,638 | Duct-like diverticulum at the base of third ventricle tumors: a morphological signature diagnostic of papillary craniopharyngioma. | This study describes and characterizes a narrow, hollow tubular structure, termed as duct-like diverticulum (DV), found specifically at the basal midline of papillary craniopharyngiomas (PCPs) located within the third ventricle (3V). The presence of this structure was systematically investigated on autopsy studies and magnetic resonance imaging (MRI) scans of 3536 craniopharyngioma (CP) cases published in the medical literature from 1911 to 2021, as well as in other twelve 3V tumor categories (n = 1470 cases). A basal DV was observed in a total of 50 PCPs, including two of our own cases. This DV corresponds to a tubular-shaped recess invaginated at the midline bottom of the tumor, following the same angled trajectory as the pituitary stalk. It can be easily seen as a hypointense linear structure on T1- and T2-weighted MRI scans, with two main length types: long DVs (74%), which reach the tumor center, and short DVs (26%), which penetrate the tumor only a few millimeters. The DV sign identifies the papillary CP type with a specificity of 100% and a sensitivity of 33% in the overall CP population. This finding also serves to establish the strictly intra-3V location of the lesion with a 95% specificity and 42% sensitivity among papillary CPs. No similar basal DV was found in adamantinomatous CPs nor among other categories of strictly 3V tumors. Consequently, the presence of a diverticulum in a 3V tumor represents a morphological signature pathognomonic of the papillary type and a valuable sign to reliably define the strictly 3V topography. |
2,329,639 | The neurodevelopmental gene MSANTD2 belongs to a gene family formed by recurrent molecular domestication of Harbinger transposons at the base of vertebrates. | The formation of new genes is a major source of organism evolutionary innovation. Beyond their mutational effects, transposable elements can be co-opted by host genomes to form different types of sequences including novel genes, through a mechanism named molecular domestication.We report the formation of four genes through molecular domestication of Harbinger transposons, three in a common ancestor of jawed vertebrates about 500 million years ago and one in sarcopterygians approx. 430 million years ago. Additionally, one processed pseudogene arose approx. 60 million years ago in simians. In zebrafish, Harbinger-derived genes are expressed during early development but also in adult tissues, and predominantly co-expressed in male brain. In human, expression was detected in multiple organs, with major expression in the brain particularly during fetal development. We used CRISPR/Cas9 with direct gene knock-out in the F0 generation and the morpholino antisense oligonucleotide knock-down technique to study in zebrafish the function of one of these genes called MSANTD2, which has been suggested to be associated to neuro-developmental diseases such as autism spectrum disorders and schizophrenia in human. MSANTD2 inactivation led to developmental delays including tail and nervous system malformation at one day post fertilization. Affected embryos showed dead cell accumulation, major anatomical defects characterized by impaired brain ventricle formation and alterations in expression of some characteristic genes involved in vertebrate nervous system development. Hence, the characterization of MSANTD2 and other Harbinger-derived genes might contribute to a better understanding of the genetic innovations having driven the early evolution of the vertebrate nervous system. |
2,329,640 | Cross-sectional reference values of cerebral ventricle for Chinese neonates born at 25-41 weeks of gestation. | To establish the cross-sectional reference values of cerebral ventricular size for the Chinese newborns by the most correlated explanatory variables. The anterior horn width (AHW), thalamo-occipital distance (TOD), and ventricular index (VI) were collected prospectively from 1- to 7-day neonates without potential neurological problems. All neonates were delivered or treated at the Hunan Provincial Maternal and Child Health Care Hospital or Second Xiangya Hospital of Central South University between February and August 2021. The most correlated explanatory variables were identified with the max-min normalization and multiple regression. The reference values were then established based on the above variables. Additionally, intraclass correlation coefficients (ICC) were applied to evaluate the reliability of the overall data collection process. This prospective study consisted of 1848 neonates. The AHW was most highly correlated with GA; the TOD and VI were most strongly correlated with birth weight. All the foregoing correlations were positive ones. Heteroscedasticity and influential points existed in both TOD and VI. The ICCAHW</sub> was the largest to a specific rater or between raters, the ICCTOD</sub> the second largest, and the ICCVI</sub> the smallest.</AbstractText>We recommend using the GA-based AHW reference values and birth weight-based TOD and VI ones. We also present a comparison of GA-based upper limits from all available reference intervals. Moreover, we determine that measurement errors are the primary cause of influential points and heteroscedasticity in TOD and VI studies and infer that the studies of TOD and VI are vulnerable to them.</AbstractText>• Reference values of infantile cerebral ventricles are vital in diagnosing and treating cerebral ventricular dilatation. • Precursors established gestational age-based reference values subjectively.</AbstractText>• We set cross-sectional reference values based on the most correlated variables for Chinese neonates and compared all available gestational age-based upper limits. • Influential points and heteroscedasticity mainly caused by measurement errors are common in TOD and VI studies.</AbstractText>© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.</CopyrightInformation> |
2,329,641 | Craniopharyngiomas: Surgery and Radiotherapy. | Taking into account the benign nature of craniopharyngiomas, the main method of treatment is the resection of the tumor. However, the tendency of these tumors to invade critical structures (such as optic pathways, the hypothalamic-pituitary system, the Willis circle vessels) often limits the possibility of a radical surgery.Craniopharyngiomas of the third ventricle represent the greatest challenge for surgery. After radical surgery, hypothalamic disorders often occur, including not only obesity but also cognitive, emotional, mental, and metabolic disturbances. Metabolic disorders associated with damage to the hypothalamus progress after surgery and lead to impaired functions of the internal organs. This process is irreversible and, in many cases, becomes the direct cause of mortality. The life expectancy of patients with the surgically affected hypothalamus is significantly shorter than in patients with preserved diencephalic function. The incidence of hypothalamic disorders after surgery can reach 40%.Even with macroscopically total resection, craniopharyngiomas can recur in 10-30% of cases, and in the presence of tumor remnants and with no further radiation treatment, the risk of recurrence significantly increases to up to 50-85% according to various studies. For this reason, the observation of patients with residual tumors after surgery is an incorrect strategy.Radiation therapy significantly improves progression-free survival (PFS), and the use of stereotactic irradiation techniques ensures conformity of irradiation of tumor remnants with a complicated shape and location (Iwata H et al., J Neurooncol 106(3):571-577, 2012; Aggarwal et al., Pituitary 16(1):26-33, 2013; Savateev et al., Zh Vopr Neirokhir Im N N Burdenko 81(3):94-106; 2017), which potentially reduces the risk of undesirable postradiation effects. Therefore, the quality of life in patients with craniopharyngiomas infiltrating the hypothalamus is significantly higher after non-radical operations with subsequent stereotactic radiation than after a total or subtotal removal. |
2,329,642 | Hydrocephalus associated to posterior fossa tumor-like sarcoidosis: A case report and literature review. | Intracranial inflammatory pseudotumors (IIPT) are one of the differential diagnosis for the central nervous system (CNS) tumors. They represent a rare condition that may mimic clinically and radiologically intracranial tumors and induce their complications. Among their etiologies, neurosarcoidosis is one of the less known and less frequent. To the best of our knowledge, only two cases of posterior fossa IIPT have been reported in the literature. We present here the 3rd case related to a neurosarcoidosis.</AbstractText>We report the case of a 55-year-old female patient who presented with an altered state of consciousness associated to severe intracranial hypertension syndrome for four months. Glasgow coma scale on admission was 14/15. Brain imaging revealed bilateral cerebellar micronodular meningeal enhancement regarding the mesencephalon and the pons, as well as a nodular lesion of the 4th ventricle causing a triventricular acute hydrocephalus. The patient had a ventriculo-peritoneal shunt with a favorable outcome. Afterwards, she underwent a salivary gland biopsy which confirmed the diagnosis of neurosarcoidosis.</AbstractText>Posterior fossa IIPT are very rare, mainly when located in the posterior fossa, leading to confusion with other pathologies. MRI has an important role in the diagnosis of these lesions, and the determination of their etiology. It shows other than the IIPT itself, many other signs such as leptomeningeal enhancement, nodular lesions or pituitary stalk thickening. These signs can orientate towards the diagnosis. Treatment may associate to symptomatic approach, corticosteroids. Surgical resection may be proposed when the diagnosis remains doubtful.</AbstractText> |
2,329,643 | Synergistic antidepressant effects of citalopram and SB-334867 in the REM sleep-deprived mice: Possible role of BDNF. | This study was done to evaluate the effect of co-treatment of orexin agents along with citalopram on the modulation of depression-like behavior and the expression of BDNF in the prefrontal cortex (PFC) of sleep-deprived male mice. A sleep deprivation model was performed in which rapid eye movement (REM) sleep was completely prohibited, and non-REM sleep was intensely reduced for 24 h. For drug microinjection, the guide cannula was surgically fixed in the left lateral ventricle of mice. Furthermore, we used the open-field test (OFT), forced swim test (FST), tail suspension test (TST), and splash test for recording depression-like behavior as well as Real-Time PCR amplification for assessing the expression of BDNF in the PFC of REM sleep-deprived mice. Our results revealed that REM sleep deprivation did not change locomotor activity while increased depressive-like behavior in FST, TST, and splash tests. However, the expression of BDNF was decreased in the PFC. Intraperitoneally (i.p.) administration of citalopram induced antidepressant effect in the normal and REM sleep-deprived mice. Moreover, intracerebroventricular (i.c.v.) microinjection of a non-effective dose of SB-334867, an orexin antagonist, potentiated the antidepressant-like effect of citalopram. On the other hand, a non-significant dosage of orexin-1 reversed the antidepressant effect of citalopram in the normal and REM sleep-deprived animals. Furthermore, our results showed that injection of citalopram alone or with SB-334867 increased the mRNA expression level of BDNF in the PFC of REM sleep-deprived mice. These data suggest that REM sleep deprivation interferes with the neural systems underlying the depression-like process and supports a likely interaction of the orexin system with citalopram on the modulation of depression-like behavior in REM sleep-deprived mice. |
2,329,644 | Correlations between sleep disturbance and brain structures associated with neurodegeneration in the National Alzheimer's Coordinating Center Uniform Data Set. | This study aimed to 1) determine the association between sleep disturbance and brain structure volumes, 2) the moderation effect of apolipoprotein ε4 genotype on sleep disturbance and brain structures, and 3) the moderation effect of sleep disturbance on cognitive status and regional brain volumes. Using the National Alzheimer's Coordinating Center Uniform Data Set (n = 1,533), multiple linear regressions were used to evaluate the association between sleep disturbance and brain volumes. Sleep disturbance was measured using one question from the NPI-Q. After controlling for intracranial volume, age, sex, years of education, race, ethnicity, and applying the FDR correction, total cerebrospinal fluid volume, left lateral ventricle volume, total lateral ventricle volume, and total third ventricle volume demonstrated significantly higher means for those with sleep disturbance. Total brain volume, total white and gray matter volume, total cerebrum brain volume (including gray but not white matter), left hippocampus volume, total hippocampal volume, the left, right, and total frontal lobe cortical gray matter volume, and the left, right, and total temporal lobe cortical gray matter volume demonstrated significantly lower mean volumes for those with sleep disturbance. Sleep disturbance moderated the association between cognitive status and lateral ventricular volumes. These findings suggest that disrupted sleep is associated with atrophy across multiple brain regions and ventricular hydrocephalus ex vacuo. |
2,329,645 | Involvement of the ERK signaling pathways in the NAc in propofol-seeking behavior induced by cues in rats. | Propofol, an intravenous short-acting anesthetic, has the potential to induce craving and relapse. Accumulated evidence demonstrates that extracellular signal-regulated kinase (ERK) plays an essential role in drug reward and relapse. In the previous study, we demonstrated that the ERK signaling pathways in the Nucleus accumbens (NAc) were involved in propofol reward. However, the role of the ERK signaling pathways in propofol relapse is still unknown. We first trained rats to self-administer propofol for 14 days, then evaluated propofol-seeking behavior of relapse induced by a contextual cues and conditioned cues after 14-day withdrawal. Meanwhile, MEK inhibitor U0126 was used to investigate the role of the ERK signal pathways in propofol-seeking behavior induced by contextual cues and conditioned cues. Results showed that the number of active nose-poke responses in propofol-seeking behavior induced by conditioned cues was much higher compared to contextual cues. U0126 (5.0 μg/side, Lateral Ventricle (LV)) pretreatment significantly decreased the active responses induced by conditioned cues, which was associated with a large decline in the expression of p-ERK in the NAc. Moreover, microinjectionofU0126 (2.0 μg/side) in the NAc also attenuated the active responses of propofol-seeking behavior. Additionally, microinjections with U0126 in the LV (5.0 μg/side) or NAc (2.0 μg/side) both failed to alter sucrose self-administration or locomotor activity of rats. Therefore, we conclude that ERK phosphorylation in the NAc maybe involved in propofol relapse. |
2,329,646 | Endoscopic Endonasal Eustachian Tube Obliteration as a Treatment for Tension Pneumocephalus After Translabyrinthine Resection of Vestibular Schwannoma. | Cerebrospinal fluid leak and pneumocephalus are rare but potentially devastating complications associated with translabyrinthine resection of cerebellopontine angle masses. Persistent pneumocephalus despite proximal eustachian tube (ET) obliteration is rare. We describe, to our knowledge, the first report of successful management of tension pneumocephalus by endoscopic endonasal ET obliteration using a novel V-loc (Covidien; Medtronic, Minneapolis, MN) suture technique.</AbstractText>A 63-year-old man presented with altered mental status 10 months after translabyrinthine excision of a left cerebellopontine angle vestibular schwannoma measuring 2.8 × 2.9 × 3.3 cm. Computed tomography demonstrated diffuse ventriculomegaly and new pneumocephalus along the right frontal lobe, lateral ventricles, and third ventricle, and air within the left translabyrinthine resection cavity.</AbstractText>The patient underwent left-sided endoscopic endonasal ET obliteration using 2-0, 9-inch V-loc suture.</AbstractText>Postoperatively, the patient's mental status improved with a decrease in size of the lateral and third ventricles on computed tomography.</AbstractText>Endoscopic endonasal ET obliteration, a technique previously applied to recalcitrant cerebrospinal fluid leaks, is a safe and reasonable alternative to reentering the original surgical site for patients with pneumocephalus after lateral skull base surgery. Utilizing a V-loc suture for this technique instead of a traditional suture may improve procedural ease and speed.</AbstractText>Copyright © 2022, Otology & Neurotology, Inc.</CopyrightInformation> |
2,329,647 | Probing Caffeine Administration as a Medical Management for Hydrocephalus: An Experimental Study. | Hydrocephalus is currently managed by cerebrospinal fluid diversion from the cerebral ventricles to other body sites, but this is complicated by obstruction and infection in young infants, thus adding to morbidity and mortality. Studies have reported caffeine to be a pleiotropic neuroprotective drug in the developing brain due to its antioxidant, anti-inflammatory, and antiapoptotic properties, with improved white matter microstructural development. In this study, we investigate the use of caffeine administration as a possible means of pharmacological management for hydrocephalus.</AbstractText>A total of 76 three-day-old mice pups from 10 dams were divided into four groups: hydrocephalus was induced in the pups in two groups by intracisternal injection of kaolin suspension, and their dams were given either caffeine (50 mg/kg by gavage) or water daily for 21 days; the dams in the other 2 (non-hydrocephalic) groups similarly had either caffeine or water; the pups received caffeine administered via lactation. Developmental neurobehavioral tests were performed until day 21, when the pups were sacrificed. Their brains were removed and processed for Cresyl and Golgi staining; both quantitative and qualitative analyses were then carried out.</AbstractText>Improved developmental motor activities and reflexes were observed in the hydrocephalus + caffeine-treated pups. Caffeine administration was associated with reduced cell death and increased dendritic arborization of the neurons in the sensorimotor cortex and striatum of hydrocephalic mice pups.</AbstractText>Caffeine administration appears to have promise as an adjunct in hydrocephalus management, and its use needs to be further explored.</AbstractText>Copyright © 2022 Elsevier Inc. All rights reserved.</CopyrightInformation> |
2,329,648 | Microsurgical Management of Fourth Ventricle Lesions Via the Median Suboccipital Keyhole Telovelar Approach. | In this 2-year retrospective analysis, 13 patients with fourth ventricle lesions who underwent microsurgical resection via the midline suboccipital keyhole telovelar approach were analyzed. This is the first study to investigate the surgical outcome and complications of using this approach to resect various types of lesions in the fourth ventricle. We aimed to clarify whether this approach has met its promise of lesion dissection. Three patients (23.1%) had intraoperative extraventricular drains. There were no immediate postoperative deaths. Gross total resection was achieved in 84.6% of the cases. The Fisher exact test showed there was no statistically significant correlation between lesion location, lesion size, brainstem invasion, and extent of resection. About two third (69.2%) of the cases were free of complications. New or worsening gait/focal motor disturbance (15.4%) was the most common neurological deficit in the immediate postoperative period. One patient (7.7%) had worse gait disturbance/motor deficit following surgical intervention. Two patients (15.4%) developed meningitis. Two patients (15.4%) required postoperative cerebrospinal fluid diversion after tumor resection, of these 2 patients, 1 (7.7%) eventually needed a permanent shunt. There were no cases of cerebellar mutism and bulbar paralysis. The median suboccipital keyhole telovelar approach provides relative wide access to resect most fourth ventricle tumors completely and with satisfactory results. In contrast, this requires the appropriate patient selection and skilled surgeons. |
2,329,649 | Detection of left ventricular wall motion abnormalities from volume rendering of 4DCT cardiac angiograms using deep learning. | The presence of left ventricular (LV) wall motion abnormalities (WMA) is an independent indicator of adverse cardiovascular events in patients with cardiovascular diseases. We develop and evaluate the ability to detect cardiac wall motion abnormalities (WMA) from dynamic volume renderings (VR) of clinical 4D computed tomography (CT) angiograms using a deep learning (DL) framework.</AbstractText>Three hundred forty-three ECG-gated cardiac 4DCT studies (age: 61 ± 15, 60.1% male) were retrospectively evaluated. Volume-rendering videos of the LV blood pool were generated from 6 different perspectives (i.e., six views corresponding to every 60-degree rotation around the LV long axis); resulting in 2058 unique videos. Ground-truth WMA classification for each video was performed by evaluating the extent of impaired regional shortening visible (measured in the original 4DCT data). DL classification of each video for the presence of WMA was performed by first extracting image features frame-by-frame using a pre-trained Inception network and then evaluating the set of features using a long short-term memory network. Data were split into 60% for 5-fold cross-validation and 40% for testing.</AbstractText>Volume rendering videos represent ~800-fold data compression of the 4DCT volumes. Per-video DL classification performance was high for both cross-validation (accuracy = 93.1%, sensitivity = 90.0% and specificity = 95.1%, κ: 0.86) and testing (90.9, 90.2, and 91.4% respectively, κ: 0.81). Per-study performance was also high (cross-validation: 93.7, 93.5, 93.8%, κ: 0.87; testing: 93.5, 91.9, 94.7%, κ: 0.87). By re-binning per-video results into the 6 regional views of the LV we showed DL was accurate (mean accuracy = 93.1 and 90.9% for cross-validation and testing cohort, respectively) for every region. DL classification strongly agreed (accuracy = 91.0%, κ: 0.81) with expert visual assessment.</AbstractText>Dynamic volume rendering of the LV blood pool combined with DL classification can accurately detect regional WMA from cardiac CT.</AbstractText>Copyright © 2022 Chen, Contijoch, Colvert, Manohar, Kahn, Narayan and McVeigh.</CopyrightInformation> |
2,329,650 | Grade III solitary fibrous tumor/hemangiopericytoma: An enthralling intracranial tumor-A case report and literature review. | Hemangiopericytomas account for less than 1% of all intracranial tumors. In 2016, World Health Organization (WHO) unified the two terms into a single medical condition known as solitary fibrous tumor/hemangiopericytoma (SFT/HPC). Our patient is an 80-year-old woman with a past medical history of sick sinus syndrome status post pacemaker placement. She presented to the emergency department with progressive headaches for one month duration. Her headaches worsened at night, waking her up from sleep. They also increased in intensity by bending forward. Review of systems was significant for bilateral lower extremity weakness accompanied by difficulty walking. The motor exam was remarkable for right upper and right lower extremity 3/5 weakness. The gait was ataxic. A Computed tomography scan of the head without contrast revealed a large dural-based right parietal hyperdense mass with surrounding edema, mass effect, and compression of the right lateral ventricle atrium. A right-to-left midline shift was also noted. Given the fact that our patient had a pacemaker, she was not a candidate for a brain MRI. Neurosurgery successfully resected the mass. Histopathological studies confirmed WHO grade III anaplastic solitary fibrous tumor/hemangiopericytoma. The patient was discharged on adjuvant radiation with imaging surveillance given the grade and the extent of resection. This case highlights a rare type of intracranial mass that resembles meningioma on imaging studies. It also illustrates that solitary fibrous tumor/hemangiopericytoma should be kept as a differential diagnosis for brain masses, given its aggressive nature, and its potential of metastasis and recurrence. |
2,329,651 | Posterior Fossa Calcifying Pseudoneoplasm of the Neuraxis (CAPNON): Presentation of Three Surgical Cases. | Calcifying pseudoneoplasm of the neuraxis (CAPNON) is an extremely rare entity with fewer than 150 cases reported in the literature and mostly with a supratentorial or spinal location. Posterior fossa CAPNON has been reported scarcely, and association with perilesional edema is a topic not yet approached which might play a significant role in treatment decision and clinical progression. Our objective is to report, to our knowledge, the first series of 3 posterior fossa CAPNON surgically treated in a single institution and assess features that help provide a systematic approach to diagnosis and timely treatment.</AbstractText>This was a monocentric, retrospective study of surgical patients diagnosed with a posterior fossa CAPNON in the last 5 years. A thorough bibliographic research was conducted.</AbstractText>Three patients were included. Locations involved IV ventricle, right cerebellopontine angle with extension to foramen magnum, and cerebellar vermis. Two of them presented with symptoms linked to acute hydrocephalus, and the other one presented with progressive cranial nerve palsy and brainstem compression signs. The 3 of them showed radiological signs of perilesional edema on their preoperative magnetic resonance imaging. Gross total resection was accomplished in one case, with near and subtotal resections in the others. There were no complications. The outcome was favorable in all cases.</AbstractText>It is essential to contemplate this infrequent diagnosis in cases of calcified lesions involving the posterior fossa. When symptoms manifest, surgery should be considered. Perilesional edema could be associated with symptomatic progression and hence a sign suggesting the need for surgical treatment.</AbstractText>Copyright © 2022 Elsevier Inc. All rights reserved.</CopyrightInformation> |
2,329,652 | Implications of Transfusion in Adults with Congenital Heart Disease Undergoing Cardiac Surgery.<Pagination><StartPage>218</StartPage><EndPage>227</EndPage><MedlinePgn>218-227</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s00246-022-02981-2</ELocationID><Abstract><AbstractText>The number of adults with congenital heart disease (CHD) requiring cardiovascular (CV) surgery is increasing rapidly in today's era. We hypothesized that exposure to perioperative blood products is associated with worse outcomes in adults. All adults (≥ 18 years old) undergoing CV surgery with Cardio-Pulmonary Bypass (CPB) between 2015 and 2020 were reviewed retrospectively. Associations between transfusion and outcomes were studied by univariable logistic regression and Wilcoxon rank sum tests. Cox/ logistic regression was used to assess (a) postoperative ventilation time and length of stay, and (b) major complications, respectively. Of 323 patients, 170 (53%) received blood products perioperatively. The median age was 27 (interquartile range [IQR]: 22-36) years, there were 181 (46%) males, and 16 (5%) patients had single ventricle anatomy. Patients receiving products experienced more complications (OR: 6.6, 95% CI: [2.9, 14.7], p < 0.001) specifically, cardiac arrest (OR: 8.8, 95% CI: [1.1, 71.9], p = 0.04). Transfusion was associated with greater frequency of thrombosis ((OR: 7.8, 95% CI: [1.8, 34.7], p = 0.01)), longer ventilation time (HR: 3.0, 95% CI: [2.4, 3.9], p < 0.001), and longer hospital length of stay (HR: 2.7, 95% CI: [2.1, 3.4], p < 0.001). Longer CPB time (OR: 1.0, 95% CI: [1.0, 1.1], p < 0.001) and prior cardiac surgery (OR: 1.6, 95% CI: [1.3, 2.1], p < 0.001) were independent predictors of perioperative blood product transfusion. Adults who received perioperative blood products experienced more complications and worse in-hospital outcomes. Future research on optimizing blood product transfusion based on risk prediction is needed to optimize outcomes in adults with CHD.</AbstractText><CopyrightInformation>© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Dutta</LastName><ForeName>Puja</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department of Cardiac Surgery, Boston Children's Hospital, Boston, MA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Emani</LastName><ForeName>Sirisha</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Cardiac Surgery, Boston Children's Hospital, Boston, MA, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Surgery, Harvard Medical School, Boston, MA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nathan</LastName><ForeName>Meena</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Cardiac Surgery, Boston Children's Hospital, Boston, MA, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Surgery, Harvard Medical School, Boston, MA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Emani</LastName><ForeName>Sitaram</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Cardiac Surgery, Boston Children's Hospital, Boston, MA, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Surgery, Harvard Medical School, Boston, MA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ibla</LastName><ForeName>Juan C</ForeName><Initials>JC</Initials><AffiliationInfo><Affiliation>Division of Cardiac Anesthesia, Department of Anesthesiology, Critical Care, and Pain Medicine, Boston Children's Hospital, 300 Longwood Ave, Boston, MA, 02215, USA. juan.ibla@childrens.harvard.edu.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Anesthesia, Harvard Medical School, Boston, MA, USA. juan.ibla@childrens.harvard.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>08</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Pediatr Cardiol</MedlineTA><NlmUniqueID>8003849</NlmUniqueID><ISSNLinking>0172-0643</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D055815" MajorTopicYN="N">Young Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000293" MajorTopicYN="N">Adolescent</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006348" MajorTopicYN="Y">Cardiac Surgical Procedures</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006330" MajorTopicYN="Y">Heart Defects, Congenital</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001803" MajorTopicYN="N">Blood Transfusion</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002315" MajorTopicYN="N">Cardiopulmonary Bypass</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011183" MajorTopicYN="N">Postoperative Complications</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Adult congenital heart disease (ACHD)</Keyword><Keyword MajorTopicYN="N">Blood product conservation</Keyword><Keyword MajorTopicYN="N">Outcomes</Keyword><Keyword MajorTopicYN="N">Perioperative care</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>4</Month><Day>5</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>7</Month><Day>21</Day></PubMedPubDate><PubMedPubDate 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Semin thorac cardiovasc surg pediatr card surg annu 17(1):9–21. https://doi.org/10.1053/j.pcsu.2014.01.004</Citation><ArticleIdList><ArticleId IdType="doi">10.1053/j.pcsu.2014.01.004</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35963835</PMID><DateRevised><Year>2022</Year><Month>08</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1878-0938</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Aug</Month><Day>08</Day></PubDate></JournalIssue><Title>Cardiovascular revascularization medicine : including molecular interventions</Title><ISOAbbreviation>Cardiovasc Revasc Med</ISOAbbreviation></Journal>Conservative treatment for cavity spilling coronary perforations. | The number of adults with congenital heart disease (CHD) requiring cardiovascular (CV) surgery is increasing rapidly in today's era. We hypothesized that exposure to perioperative blood products is associated with worse outcomes in adults. All adults (≥ 18 years old) undergoing CV surgery with Cardio-Pulmonary Bypass (CPB) between 2015 and 2020 were reviewed retrospectively. Associations between transfusion and outcomes were studied by univariable logistic regression and Wilcoxon rank sum tests. Cox/ logistic regression was used to assess (a) postoperative ventilation time and length of stay, and (b) major complications, respectively. Of 323 patients, 170 (53%) received blood products perioperatively. The median age was 27 (interquartile range [IQR]: 22-36) years, there were 181 (46%) males, and 16 (5%) patients had single ventricle anatomy. Patients receiving products experienced more complications (OR: 6.6, 95% CI: [2.9, 14.7], p < 0.001) specifically, cardiac arrest (OR: 8.8, 95% CI: [1.1, 71.9], p = 0.04). Transfusion was associated with greater frequency of thrombosis ((OR: 7.8, 95% CI: [1.8, 34.7], p = 0.01)), longer ventilation time (HR: 3.0, 95% CI: [2.4, 3.9], p < 0.001), and longer hospital length of stay (HR: 2.7, 95% CI: [2.1, 3.4], p < 0.001). Longer CPB time (OR: 1.0, 95% CI: [1.0, 1.1], p < 0.001) and prior cardiac surgery (OR: 1.6, 95% CI: [1.3, 2.1], p < 0.001) were independent predictors of perioperative blood product transfusion. Adults who received perioperative blood products experienced more complications and worse in-hospital outcomes. Future research on optimizing blood product transfusion based on risk prediction is needed to optimize outcomes in adults with CHD.<CopyrightInformation>© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Dutta</LastName><ForeName>Puja</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department of Cardiac Surgery, Boston Children's Hospital, Boston, MA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Emani</LastName><ForeName>Sirisha</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Cardiac Surgery, Boston Children's Hospital, Boston, MA, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Surgery, Harvard Medical School, Boston, MA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nathan</LastName><ForeName>Meena</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Cardiac Surgery, Boston Children's Hospital, Boston, MA, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Surgery, Harvard Medical School, Boston, MA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Emani</LastName><ForeName>Sitaram</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Cardiac Surgery, Boston Children's Hospital, Boston, MA, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Surgery, Harvard Medical School, Boston, MA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ibla</LastName><ForeName>Juan C</ForeName><Initials>JC</Initials><AffiliationInfo><Affiliation>Division of Cardiac Anesthesia, Department of Anesthesiology, Critical Care, and Pain Medicine, Boston Children's Hospital, 300 Longwood Ave, Boston, MA, 02215, USA. juan.ibla@childrens.harvard.edu.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Anesthesia, Harvard Medical School, Boston, MA, USA. juan.ibla@childrens.harvard.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>08</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Pediatr Cardiol</MedlineTA><NlmUniqueID>8003849</NlmUniqueID><ISSNLinking>0172-0643</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D055815" MajorTopicYN="N">Young Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000293" MajorTopicYN="N">Adolescent</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006348" MajorTopicYN="Y">Cardiac Surgical Procedures</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006330" MajorTopicYN="Y">Heart Defects, Congenital</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001803" MajorTopicYN="N">Blood Transfusion</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002315" MajorTopicYN="N">Cardiopulmonary Bypass</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011183" MajorTopicYN="N">Postoperative Complications</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Adult congenital heart disease (ACHD)</Keyword><Keyword MajorTopicYN="N">Blood product conservation</Keyword><Keyword MajorTopicYN="N">Outcomes</Keyword><Keyword MajorTopicYN="N">Perioperative care</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>4</Month><Day>5</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>7</Month><Day>21</Day></PubMedPubDate><PubMedPubDate 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Semin thorac cardiovasc surg pediatr card surg annu 17(1):9–21. https://doi.org/10.1053/j.pcsu.2014.01.004</Citation><ArticleIdList><ArticleId IdType="doi">10.1053/j.pcsu.2014.01.004</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35963835</PMID><DateRevised><Year>2022</Year><Month>08</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1878-0938</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Aug</Month><Day>08</Day></PubDate></JournalIssue><Title>Cardiovascular revascularization medicine : including molecular interventions</Title><ISOAbbreviation>Cardiovasc Revasc Med</ISOAbbreviation></Journal><ArticleTitle>Conservative treatment for cavity spilling coronary perforations.</ArticleTitle><ELocationID EIdType="pii" ValidYN="Y">S1553-8389(22)00703-5</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.carrev.2022.08.007</ELocationID><Abstract>Coronary perforation leading to shunting to other cardiac chambers is a rare complication of percutaneous coronary intervention (PCI), and most cases reported aggressive treatment with either a covered stent, coiling, or protamine injection. We report herein two cases, one of a fairly large cavity-spilling perforation of the left anterior descending coronary artery into the right ventricle and one spilling in the coronary vein. Both iatrogenic shunts were treated conservatively, and angiographic follow-up showed spontaneous resolution, suggesting that the outcome in this type of perforation may be favorable with conservative therapy. We also propose a management strategy on how to differentiate such contrast extravasations, find which cavity is communicating with the vessel and when to intervene more decisively. SOCIAL MEDIA ABSTRACT: We report herein two "fortunate" perforations, one of a fairly large cavity-spilling perforation from the left anterior descending coronary artery into the right ventricle and one spilling in the coronary vein. The angiographic follow-up showed spontaneous healing due to spilling in low-pressure cavities. A "no-touch" strategy is preferred if the patient remains asymptomatic and the pericardium free of fluid. |
2,329,653 | Correction to: Basal Recess in Third Ventricle Tumors: A Pathological Feature Defining a Clinical-Topographical Subpopulation of Papillary Craniopharyngiomas.<Pagination><StartPage>1042</StartPage><MedlinePgn>1042</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1093/jnen/nlac072</ELocationID><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Pascual</LastName><ForeName>José María</ForeName><Initials>JM</Initials></Author><Author ValidYN="Y"><LastName>Prieto</LastName><ForeName>Ruth</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Carrasco</LastName><ForeName>Rodrigo</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Barrios</LastName><ForeName>Laura</ForeName><Initials>L</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016425">Published Erratum</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Neuropathol Exp Neurol</MedlineTA><NlmUniqueID>2985192R</NlmUniqueID><ISSNLinking>0022-3069</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="ErratumFor"><RefSource>J Neuropathol Exp Neurol. 2022 Apr 27;81(5):330-343</RefSource><PMID Version="1">35472085</PMID></CommentsCorrections></CommentsCorrectionsList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>8</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>8</Month><Day>14</Day><Hour>6</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>8</Month><Day>13</Day><Hour>15</Hour><Minute>12</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35962995</ArticleId><ArticleId IdType="doi">10.1093/jnen/nlac072</ArticleId><ArticleId IdType="pii">6665892</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35962970</PMID><DateRevised><Year>2023</Year><Month>03</Month><Day>08</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1933-0715</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Aug</Month><Day>12</Day></PubDate></JournalIssue><Title>Journal of neurosurgery. Pediatrics</Title><ISOAbbreviation>J Neurosurg Pediatr</ISOAbbreviation></Journal>Etiology- and region-specific characteristics of transependymal cerebrospinal fluid flow. | Transependymal flow (TEF) of CSF, often delineated as T2-weighted hyperintensity adjacent to the lateral ventricles on MRI, is a known imaging finding, usually in the setting of CSF flow disturbances. Specific radiological features of TEF and their relationships with clinical markers of hydrocephalus and underlying disease pathology are not known. Here, the authors describe the radiological features and clinical associations of TEF with implications for CSF circulation in the setting of intracranial pathology.</AbstractText>After obtaining IRB review and approval, the authors reviewed the radiological records of all patients who underwent intracranial imaging with CT or MRI at St. Louis Children's Hospital, St. Louis, Missouri, between 2008 and 2019 to identify individuals with TEF. Then, under direct review of imaging, TEF pattern, degree, and location and underlying pathology and other radiological and clinical features pertaining to CSF circulation and CSF disturbances were noted.</AbstractText>TEF of CSF was identified in 219 patients and was most prevalent in the setting of neoplasms (72%). In 69% of the overall cohort, TEF was seen adjacent to the anterior aspect of the frontal horns and the posterior aspect of the occipital horns of the lateral ventricles, and nearly half of these patients also had TEF dorsal to the third ventricle near the splenium of the corpus callosum. This pattern was independently associated with posterior fossa medulloblastoma when compared with pilocytic astrocytoma (OR 4.75, 95% CI 1.43-18.53, p = 0.0157). Patients with congenital or neonatal-onset hydrocephalus accounted for 13% of patients and were more likely to have TEF circumferentially around the ventricles without the fronto-occipital distribution. Patients who ultimately required permanent CSF diversion surgery were more likely to have the circumferential TEF pattern, a smaller degree of TEF, and a lack of papilledema at the time of CSF diversion surgery.</AbstractText>CSF transmigration across the ependyma is usually restricted to specific periventricular regions and is etiology specific. Certain radiological TEF characteristics are associated with tumor pathology and may reflect impaired or preserved ependymal fluid handling and global CSF circulation. These findings have implications for TEF as a disease-specific marker and in understanding CSF handling within the brain.</AbstractText> |
2,329,654 | Drugs and Endogenous Factors as Protagonists in Neurogenic Stimulation. | Neurogenesis is a biological process characterized by new neurons formation from stem cells. For decades, it was believed that neurons only multiplied during development and in the postnatal period but the discovery of neural stem cells (NSCs) in mature brain promoted a revolution in neuroscience field. In mammals, neurogenesis consists of migration, differentiation, maturation, as well as functional integration of newborn cells into the pre-existing neuronal circuit. Actually, NSC density drops significantly after the first stages of development, however in specific places in the brain, called neurogenic niches, some of these cells retain their ability to generate new neurons and glial cells in adulthood. The subgranular (SGZ), and the subventricular zones (SVZ) are examples of regions where the neurogenesis process occurs in the mature brain. There, the potential of NSCs to produce new neurons has been explored by new advanced methodologies and in neuroscience for the treatment of brain damage and/or degeneration. Based on that, this review highlights endogenous factors and drugs capable of stimulating neurogenesis, as well as the perspectives for the use of NSCs for neurological and neurodegenerative diseases. |
2,329,655 | Is the Choroid Plexus Needed? | Choroid plexectomy was first performed around 1910. Later, the technique evolved into subtotal choroid plexus cauterization (CPC) but was largely abandoned following the invention of the ventriculoperitoneal shunt. Over time, with improved understanding of the pathophysiology of hydrocephalus and improvement in endoscopic techniques and equipment, the procedure of CPC was reintroduced. However, little is known about the biomolecular consequences of ablation of a significant portion of the choroid plexus on metabolic brain homeostasis, neurogenesis, and neuroimmunology.</AbstractText>The physiological functions of choroid plexus in neurogenesis and neuroimmunology and its role in diseases, such as AD and MS, should alert to possible as yet to be determined consequences. Studies, both in children and in adults, are needed not only on the success in hydrodynamic stabilization of hydrocephalus but also on the long-term outcome, especially premature neurodegeneration and inflammatory changes and on compensatory metabolic mechanisms.</AbstractText>The value of CPC for treatment of hydrocephalus in medically underserved areas should be remembered, yet when alternative treatment options are available, we cannot responsibly advocate against or for the use of CPC. Therefore, perhaps a more detailed discussion of risks and benefits of a CPC with parents would be best to include the possible implications in brain development and function.</AbstractText>© 2022 S. Karger AG, Basel.</CopyrightInformation> |
2,329,656 | Differential vulnerability of thalamic nuclei in multiple sclerosis. | Investigating differential vulnerability of thalamic nuclei in multiple sclerosis (MS).</AbstractText>In a secondary analysis of prospectively collected datasets, we pooled 136 patients with MS or clinically isolated syndrome and 71 healthy controls all scanned with conventional 3D-T1 and white-matter-nulled magnetization-prepared rapid gradient echo (WMn-MPRAGE) and tested for cognitive performance. T1-based thalamic segmentation was compared with the reference WMn-MPRAGE method. Volumes of thalamic nuclei were compared according to clinical phenotypes and cognitive profile.</AbstractText>T1- and WMn-MPRAGE provided comparable segmentations (0.84 ± 0.13 < volume-similarity-index < 0.95 ± 0.03). Medial and posterior thalamic groups were significantly more affected than anterior and lateral groups. Cognitive impairment related to volume loss of the anterior group.</AbstractText>Thalamic nuclei closest to the third ventricle are more affected, with cognitive consequences.</AbstractText> |
2,329,657 | [Clinical characteristics and literature review of 12 cases of granulosa cell tumor of head and neck]. | <b>Objective:</b>To investigate the clinical and pathological features, treatment, prognostic and its influence factors of granulosa cell tumor of head and neck. <b>Methods:</b>The clinical medical records of 12 patients with head and neck granulosa cell tumor confirmed by pathology for diagnosis and treatment in Beijing Tongren Hospital affiliated to Capital Medical University were reviewed and collected. <b>Results:</b>The follow-up durations were 4-57 months, with a median of 23 months. The origination of twelve cases were reviewed: 3 cases of the vocal cords, 2 cases of the retroannular region, 1 cases of the ventricular bands, 1 cases of the interarytenoid region, 1 cases of the paraglottic space, 1 cases of the epiglottis, 1 cases of the soft palate, 1 cases of the ventricle of larynx, 1 cases of the trapezius muscle. All 12 patients were undergoing surgical treatment in our hospital, including one who had postoperative adjuvant radiotherapy after second operation. <b>Conclusion:</b>Granulosa cell tumor occurs in the head and neck, usually a benign tumor with diverse morphology, and its diagnosis is mainly based on tumor histopathological examination. Surgical local excision is used in most cases, especially minimally invasive surgery is recommended, with lower postoperative recurrence rate and better prognosis.<CopyrightInformation>Copyright© by the Editorial Department of Journal of Clinical Otorhinolaryngology Head and Neck Surgery.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Xuejun</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Otorhinolaryngology Head and Neck Surgery，Beijing Tongren Hospital，Capital Medical University，Key Laboratory of Otolaryngology Head and Neck Surgery，Ministry of Education，Beijing，100730，China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Feng</LastName><ForeName>Lifei</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Otorhinolaryngology Head and Neck Surgery，Beijing Tongren Hospital，Capital Medical University，Key Laboratory of Otolaryngology Head and Neck Surgery，Ministry of Education，Beijing，100730，China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yin</LastName><ForeName>Gaofei</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Department of Otorhinolaryngology Head and Neck Surgery，Beijing Tongren Hospital，Capital Medical University，Key Laboratory of Otolaryngology Head and Neck Surgery，Ministry of Education，Beijing，100730，China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Pingdong</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department of Otorhinolaryngology Head and Neck Surgery，Beijing Tongren Hospital，Capital Medical University，Key Laboratory of Otolaryngology Head and Neck Surgery，Ministry of Education，Beijing，100730，China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhong</LastName><ForeName>Qi</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>Department of Otorhinolaryngology Head and Neck Surgery，Beijing Tongren Hospital，Capital Medical University，Key Laboratory of Otolaryngology Head and Neck Surgery，Ministry of Education，Beijing，100730，China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fang</LastName><ForeName>Jugao</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Otorhinolaryngology Head and Neck Surgery，Beijing Tongren Hospital，Capital Medical University，Key Laboratory of Otolaryngology Head and Neck Surgery，Ministry of Education，Beijing，100730，China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Yang</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Otorhinolaryngology Head and Neck Surgery，Beijing Tongren Hospital，Capital Medical University，Key Laboratory of Otolaryngology Head and Neck Surgery，Ministry of Education，Beijing，100730，China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>chi</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>China</Country><MedlineTA>Lin Chuang Er Bi Yan Hou Tou Jing Wai Ke Za Zhi</MedlineTA><NlmUniqueID>101303164</NlmUniqueID><ISSNLinking>2096-7993</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006106" MajorTopicYN="Y">Granulosa Cell Tumor</DescriptorName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006258" MajorTopicYN="Y">Head and Neck Neoplasms</DescriptorName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009333" MajorTopicYN="N">Neck</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009364" MajorTopicYN="N">Neoplasm Recurrence, Local</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010051" MajorTopicYN="Y">Ovarian Neoplasms</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011379" MajorTopicYN="N">Prognosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading></MeshHeadingList><OtherAbstract Type="Publisher" Language="chi"><b>目的：</b>探讨头颈部颗粒细胞瘤（GCT）的临床特征、病理表现、治疗手段、预后及其影响因素。 <b>方法：</b>回顾并收集在首都医科大学附属北京同仁医院诊治，经病理证实的12例头颈部GCT患者的临床病历资料。 <b>结果：</b>随访4～57个月，中位随访23个月。12例患者中，肿瘤原发于声带3例、环后区2例、室带1例、杓间区1例、声门旁间隙1例、会厌1例、软腭1例、喉室1例、斜方肌内1例。12例患者均接受手术治疗，其中1例二次手术并在术后辅助放射治疗。 <b>结论：</b>GCT好发于头颈部，通常为良性肿瘤，形态多样，其确诊主要依据肿瘤组织病理学检查。大多采用手术局部切除，尤其推荐微创手术，术后复发率较低，预后较好。. |
2,329,658 | Organization of the ventricular zone of the cerebellum. | The roof of the fourth ventricle (4V) is located on the ventral part of the cerebellum, a region with abundant vascularization and cell heterogeneity that includes tanycyte-like cells that define a peculiar glial niche known as ventromedial cord. This cord is composed of a group of biciliated cells that run along the midline, contacting the ventricular lumen and the subventricular zone. Although the complex morphology of the glial cells composing the cord resembles to tanycytes, cells which are known for its proliferative capacity, scarce or non-proliferative activity has been evidenced in this area. The subventricular zone of the cerebellum includes astrocytes, oligodendrocytes, and neurons whose function has not been extensively studied. This review describes to some extent the phenotypic, morphological, and functional characteristics of the cells that integrate the roof of the 4V, primarily from rodent brains. |
2,329,659 | The effects of mango leaf extract during adolescence and adulthood in a rat model of schizophrenia. | There is evidence that in schizophrenia, imbalances in inflammatory and oxidative processes occur during pregnancy and in the early postnatal period, generating interest in the potential therapeutic efficacy of anti-inflammatory and antioxidant compounds. Mangiferin is a polyphenolic compound abundant in the leaves of <i>Mangifera indica L.</i> that has robust antioxidant and anti-inflammatory properties, making it a potential candidate for preventive or co-adjuvant therapy in schizophrenia. Hence, this study set-out to evaluate the effect of mango leaf extract (MLE) in a model of schizophrenia based on maternal immune activation, in which Poly I:C (4 mg/kg) is administered intravenously to pregnant rats. Young adult (postnatal day 60-70) or adolescent (postnatal day 35-49) male offspring received MLE (50 mg/kg of mangiferin) daily, and the effects of MLE in adolescence were compared to those of risperidone, assessing behavior, brain magnetic resonance imaging (MRI), and oxidative/inflammatory and antioxidant mediators in the adult offspring. MLE treatment in adulthood reversed the deficit in prepulse inhibition (PPI) but it failed to attenuate the sensitivity to amphetamine and the deficit in novel object recognition (NOR) induced. By contrast, adolescent MLE treatment prevented the sensorimotor gating deficit in the PPI test, producing an effect similar to that of risperidone. This MLE treatment also produced a reduction in grooming behavior, but it had no effect on anxiety or novel object recognition memory. MRI studies revealed that adolescent MLE administration partially counteracted the cortical shrinkage, and cerebellum and ventricle enlargement. In addition, MLE administration in adolescence reduced iNOS mediated inflammatory activation and it promoted the expression of biomarkers of compensatory antioxidant activity in the prefrontal cortex and hippocampus, as witnessed through the reduction of Keap1 and the accumulation of NRF2 and HO1. Together, these findings suggest that MLE might be an alternative therapeutic or preventive add-on strategy to improve the clinical expression of schizophrenia in adulthood, while also modifying the time course of this disease at earlier stages in populations at high-risk. |
2,329,660 | How to Optimize ECLS Results beyond Ventricular Unloading: From ECMO to CentriMag<sup>®</sup> eVAD. | CentriMag<sup>®</sup> extracorporeal VAD support could represent a more physiological choice than conventional ECMO in primary cardiogenic shock. We therefore evaluated the outcome of patients with primary cardiogenic shock who were supported with CentriMag<sup>®</sup> extracorporeal VAD implantation versus conventional ECMO. We retrospectively reviewed all extracorporeal life supports implanted for primary cardiogenic shock between January 2009 and December 2018 at our institution. Among 212 patients, 143 cases (67%) were treated exclusively with ECMO (Group 1) and 69 cases (33%) with extracorporeal VAD implantation (Group 2, 48 of whom as conversion of ECMO). ECLS mean duration was 8.37 ± 8.43 days in Group 1 and 14.25 ± 10.84 days in Group 2 (<i>p</i> = 0.001), while the mean rates of the highest predicted flow were 61.21 ± 16.01% and 79.49 ± 18.42% (<i>p</i> = 0.001), respectively. Increasing mechanical support flow was related to in-hospital mortality and overall mortality in Group 1 (HR 11.36, CI 95%: 2.19-44.20), but not in Group 2 (HR 1.48, CI 95%: 0.32-6.80). High-flow ECMO patients had lower survival with respect to high-flow extracorporeal VAD patients (<i>p</i> = 0.027). In the setting of high-flow mechanical circulatory support, CentriMag<sup>®</sup> extracorporeal VAD optimized patient survival, granting long-term assistance and physiological circulation patterns. |
2,329,661 | Right Cortical Infarction and a Reduction in Putamen Volume May Be Correlated with Empathy in Patients after Subacute Ischemic Stroke-A Multimodal Magnetic Resonance Imaging Study. | Empathy has not been well studied in patients following ischemic stroke. We aimed to evaluate the relationships of multimodal neuroimaging parameters with the impairment of empathy in patients who had experienced subacute ischemic stroke. Patients who had experienced a first-event acute ischemic stroke were recruited, and we assessed their empathy using the Chinese version of the Empathy Quotient (EQ) 3 months after the index stroke. Multimodal magnetic resonance imaging (MRI) was conducted in all the participants to identify acute infarction and assess brain volumes, white matter integrity, and other preexisting abnormalities. We quantified the brain volumes of various subcortical structures, the ventricles, and cortical lobar atrophy. The microstructural integrity of the white matter was reflected in the mean fractional anisotropy (FA) and mean diffusivity (MD), and the regional mean values of FA and MD were quantified after mapping using the ICBM_DTI_81 Atlas. Twenty-three (56.1%) men and 18 (43.9%) women (mean age: 61.73 years, range: 41-77 years) were included. The median National Institutes of Health Stroke Scale (NIHSS) score at discharge was 1 (range: 0-4). On univariate analysis, the EQ was correlated with right cortical infarction (r = -0.39, <i>p</i> = 0.012), putamen volume (r = 0.382, <i>p</i> = 0.014), right putamen volume (r = 0.338, <i>p</i> = 0.031), and the FA value of the right sagittal stratum. EQ did not correlated with the MD value in any region of interest or pre-existing brain abnormalities. Multiple stepwise linear regression models were used to identify factors associated with EQ. After adjusting for age and the NIHSS score on admission, the frequency of right cortical infarcts negatively correlated with EQ (standardized β = -0.358, 95% confidence interval =-0.708 to -0.076, <i>p</i> = 0.016), and the putamen volume positively correlated with EQ (standardized β = 0.328, 95% confidence interval =0.044 to 0.676, <i>p</i> = 0.027). In conclusion, in patients who have experienced subacute ischemic stroke, right cortical infarction and a smaller putamen volume are associated with the impairment of empathy. |
2,329,662 | Regulation of APD and Force by the Na<sup>+</sup>/Ca<sup>2+</sup> Exchanger in Human-Induced Pluripotent Stem Cell-Derived Engineered Heart Tissue. | The physiological importance of NCX in human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) is not well characterized but may depend on the relative strength of the current, compared to adult cardiomyocytes, and on the exact spatial arrangement of proteins involved in Ca2+ extrusion. Here, we determined NCX currents and its contribution to action potential and force in hiPSC-CMs cultured in engineered heart tissue (EHT). The results were compared with data from rat and human left ventricular tissue. The NCX currents in hiPSC-CMs were larger than in ventricular cardiomyocytes isolated from human left ventricles (1.3 ± 0.2 pA/pF and 3.2 ± 0.2 pA/pF for human ventricle and EHT, respectively, p < 0.05). SEA0400 (10 µM) markedly shortened the APD90 in EHT (by 26.6 ± 5%, p < 0.05) and, to a lesser extent, in rat ventricular tissue (by 10.7 ± 1.6%, p < 0.05). Shortening in human left ventricular preparations was small and not different from time-matched controls (TMCs; p > 0.05). Force was increased by the NCX block in rat ventricle (by 31 ± 5.4%, p < 0.05) and EHT (by 20.8 ± 3.9%, p < 0.05), but not in human left ventricular preparations. In conclusion, hiPSC-CMs possess NCX currents not smaller than human left ventricular tissue. Robust NCX block-induced APD shortening and inotropy makes EHT an attractive pharmacological model. |
2,329,663 | Hydrocephalus in <i>Nfix<sup>-/-</sup></i> Mice Is Underpinned by Changes in Ependymal Cell Physiology. | Nuclear factor one X (NFIX) is a transcription factor required for normal ependymal development. Constitutive loss of <i>Nfix</i> in mice (<i>Nfix<sup>-/-</sup></i>) is associated with hydrocephalus and sloughing of the dorsal ependyma within the lateral ventricles. Previous studies have implicated NFIX in the transcriptional regulation of genes encoding for factors essential to ependymal development. However, the cellular and molecular mechanisms underpinning hydrocephalus in <i>Nfix<sup>-/-</sup></i> mice are unknown. To investigate the role of NFIX in hydrocephalus, we examined ependymal cells in brains from postnatal <i>Nfix<sup>-/-</sup></i> and control (<i>Nfix<sup>+/+</sup></i>) mice using a combination of confocal and electron microscopy. This revealed that the ependymal cells in <i>Nfix<sup>-/-</sup></i> mice exhibited abnormal cilia structure and disrupted localisation of adhesion proteins. Furthermore, we modelled ependymal cell adhesion using epithelial cell culture and revealed changes in extracellular matrix and adherens junction gene expression following knockdown of <i>NFIX</i>. Finally, the ablation of <i>Nfix</i> from ependymal cells in the adult brain using a conditional approach culminated in enlarged ventricles, sloughing of ependymal cells from the lateral ventricles and abnormal localisation of adhesion proteins, which are phenotypes observed during development. Collectively, these data demonstrate a pivotal role for NFIX in the regulation of cell adhesion within ependymal cells of the lateral ventricles. |
2,329,664 | Duct-like Recess in the Infundibular Portion of Third Ventricle Craniopharyngiomas: An MRI Sign Identifying the Papillary Type. | Papillary craniopharyngiomas (PCPs) are particularly challenging lesions requiring accurate diagnosis to plan the best therapy. Our aim was to define a narrow duct-like recess identified on MR imaging at the base of papillary craniopharyngiomas with a strict third ventricle location.</AbstractText>A duct-like recess at the infundibular portion of craniopharyngiomas was observed on conventional T1WI and T2WI in 3 strict third ventricle papillary craniopharyngiomas in our craniopharyngioma series (n</i> = 125). We systematically investigated this finding on the MR imaging of 2582 craniopharyngiomas and 10 other categories of third ventricle tumors (n</i> = 690) published in the modern era (1986-2020). The diagnostic value and significance of this finding are addressed.</AbstractText>The duct-like recess was recognized in 52 papillary craniopharyngiomas, including 3 of our own cases, as a narrow canal-shaped cavity invaginated at the tumor undersurface, just behind the optic chiasm. This structure largely involves papillary craniopharyngiomas with a strict third ventricle topography (96%), follows the same diagonal trajectory as the pituitary stalk, and finishes at a closed end. The duct-like recess sign identifies the papillary craniopharyngioma type with a specificity of 100% and a sensitivity of 38% in the overall craniopharyngioma population. This finding can also establish the strictly intra-third ventricle location of the lesion with a 90% specificity and 33% sensitivity. These recesses appear as hypointense circular spots on axial/coronal T1WI and T2WI. Their content apparently corresponds to CSF freely flowing within the suprasellar cistern.</AbstractText>The presence of a duct-like recess at the infundibular portion of a third ventricle tumor represents a distinctive hallmark of papillary craniopharyngiomas that can be used as a simple MR imaging sign to reliably diagnose these lesions.</AbstractText>© 2022 by American Journal of Neuroradiology.</CopyrightInformation> |
2,329,665 | Atypical clinical presentation of glioblastoma mimicking autoimmune meningitis in an adult. | Glioblastoma (GBM) is the most malignant type of glial tumor associated with a very unfavorable prognosis. Typical radiological features of GBM include the presence of a tumor with irregular contrast-enhancing margins and central necrosis surrounded by a wide area of vasogenic edema. Here, we presented an atypical clinical presentation of GBM mimicking autoimmune meningitis. A 69-years-old previously healthy male was admitted to the emergency room due to signs of increasing cognitive impairment, weight loss, changes in behavior, difficulty in walking, and prolonged episodes of nausea over the past month. An magnetic resonance imaging (MRI) brain scan revealed hyperintense changes of the periventricular area surrounding brain ventricles in T2 and FLAIR, and post-contrast leptomeningeal enhancement and thickening of meninges involving cerebellar sulci. An additional MRI scan of the cervical spine showed an in-core contrastenhancing lesion on the C7-Th1 level as well as leptomeningeal thickening and post-contrast-enhancement around the spinal cord. Various laboratory tests and two stereotactic biopsies were performed with no essential to diagnosis clinical findings. A couple of months after first hospital admission, the patient died. Post-mortem examination of the brain revealed numerous foci of abnormal tissue inside the subarachnoid space, lateral ventricles, and cerebral aqueduct. Histological examination showed diffuse malignant astroglial neoplasm, and diagnosis of glioblastoma NOS WHO G IV was established. Even though the appearance of usual GBM is widely recognizable, one must bear in mind the possibility of unusual presentation. The presented case highlights the diagnostic difficulties of diffuse glioblastoma with atypical clinical presentation. |
2,329,666 | Costs of pediatric hydrocephalus treatment for the Brazilian public health system in the Northeast of Brazil. | To estimate the costs of the surgical treatment of pediatric hydrocephalus, specifically ventriculoperitoneal shunt (VPS) and endoscopic third ventriculostomy (ETV), for the Brazilian public health system (SUS).</AbstractText>Retrospective cohort study of health records of patients < 14 years of age with a diagnosis of hydrocephalus who underwent VPS or ETV between September 2009 and June 2016, regularly followed up for 24 months.</AbstractText>Seventy-six medical records were included. The groups of children who underwent VPS and ETV consisted of 60 and 16 patients, respectively. Complications during 2 years of follow-up were identified in 56% of the children undergoing VPS and in 18% of those undergoing ETV (p = 0.0103). The initial cost of VPS was lower than that of ETV up to approximately 1 year of post-surgical follow-up. After that, VPS generated higher expenses for the SUS due to higher rates of late post-surgical complications and repeated readmissions.</AbstractText>Higher public expenditures were observed in the group of children undergoing VPS due to higher rates of infectious and mechanical complications requiring repeated hospitalizations and prosthesis replacements. Public policies must be tailored to offer the best treatment to children with hydrocephalus and to make judicious use of public resources without compromising the quality of treatment.</AbstractText>© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.</CopyrightInformation> |
2,329,667 | Tax1 banding protein 1 exacerbates heart failure in mice by activating ITCH-P73-BNIP3-mediated cardiomyocyte apoptosis.<Pagination><StartPage>2562</StartPage><EndPage>2572</EndPage><MedlinePgn>2562-2572</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/s41401-022-00950-2</ELocationID><Abstract><AbstractText>Tax1 banding protein 1 (Tax1bp1) was originally identified as an NF-κB regulatory protein that participated in inflammatory, antiviral and innate immune processes. Tax1bp1 also functions as an autophagy receptor that plays a role in autophagy. Our previous study shows that Tax1bp1 protects against cardiomyopathy in STZ-induced diabetic mice. In this study we investigated the role of Tax1bp1 in heart failure. Pressure overload-induced heart failure model was established in mice by aortic banding (AB) surgery, and angiotensin II (Ang II)-induced heart failure model was established by infusion of Ang II through osmotic minipump for 4 weeks. We showed that the expression levels of Tax1bp1 in the heart were markedly increased 2 and 4 weeks after AB surgery. Knockdown of Tax1bp1 in mouse hearts significantly ameliorated both AB- and Ang II infusion-induced heart failure parameters. On the contrary, AB-induced heart failure was aggravated in cardiac-specific Tax1bp1 transgenic mice. Similar results were observed in neonatal rat cardiomyocytes (NRCMs) under Ang II insult. We demonstrated that the pro-heart failure effect of Tax1bp1 resulted from its interaction with the E3 ligase ITCH to promote the transcription factor P73 ubiquitination and degradation, causing enhanced BCL2 interacting protein 3 (BNIP3)-mediated cardiomyocyte apoptosis. Knockdown ITCH or BNIP3 in NRCMs significantly reduced Ang II-induced apoptosis in vitro. Similarly, BNIP3 knockdown attenuated heart failure in cardiac-specific Tax1bp1 transgenic mice. In the left ventricles of heart failure patients, Tax1bp1 expression level was significantly increased; Tax1bp1 gene expression was negatively correlated with left ventricular ejection fraction in heart failure patients. Collectively, the Tax1bp1 increase in heart failure enhances ITCH-P73-BNIP3-mediated cardiomyocyte apoptosis and induced cardiac injury. Tax1bp1 may serve as a potent therapeutic target for the treatment of heart failure.• Cardiac Tax1bp1 transgene mice were more vulnerable to cardiac dysfunction under stress.• Cardiac Tax1bp1 transgene mice were more vulnerable to cardiac dysfunction under stress.• Knockout of Tax1bp1 in mouse hearts ameliorated heart failure induced by pressure overload.• Tax1bp1 interacts with the E3 ligase Itch to promote P73 ubiquitination and degradation, causing enhanced BNIP3-mediated apoptosis.• Tax1bp1 may become a target of new therapeutic methods for treating heart failure.</AbstractText><CopyrightInformation>© 2022. The Author(s), under exclusive licence to Shanghai Institute of Materia Medica, Chinese Academy of Sciences and Chinese Pharmacological Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y" EqualContrib="Y"><LastName>Wu</LastName><ForeName>Qing-Qing</ForeName><Initials>QQ</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cardiovascular Research Institute, Wuhan University, Wuhan, 430060, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Hubei Key Laboratory of Metabolic and Chronic Diseases, Wuhan, 430060, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Yao</LastName><ForeName>Qi</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cardiovascular Research Institute, Wuhan University, Wuhan, 430060, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Hubei Key Laboratory of Metabolic and Chronic Diseases, Wuhan, 430060, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hu</LastName><ForeName>Tong-Tong</ForeName><Initials>TT</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cardiovascular Research Institute, Wuhan University, Wuhan, 430060, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Hubei Key Laboratory of Metabolic and Chronic Diseases, Wuhan, 430060, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wan</LastName><ForeName>Ying</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cardiovascular Research Institute, Wuhan University, Wuhan, 430060, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Hubei Key Laboratory of Metabolic and Chronic Diseases, Wuhan, 430060, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xie</LastName><ForeName>Qing-Wen</ForeName><Initials>QW</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cardiovascular Research Institute, Wuhan University, Wuhan, 430060, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Hubei Key Laboratory of Metabolic and Chronic Diseases, Wuhan, 430060, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhao</LastName><ForeName>Jin-Hua</ForeName><Initials>JH</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cardiovascular Research Institute, Wuhan University, Wuhan, 430060, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Hubei Key Laboratory of Metabolic and Chronic Diseases, Wuhan, 430060, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yuan</LastName><ForeName>Yuan</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cardiovascular Research Institute, Wuhan University, Wuhan, 430060, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Hubei Key Laboratory of Metabolic and Chronic Diseases, Wuhan, 430060, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tang</LastName><ForeName>Qi-Zhu</ForeName><Initials>QZ</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China. qztang@whu.edu.cn.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cardiovascular Research Institute, Wuhan University, Wuhan, 430060, China. qztang@whu.edu.cn.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Hubei Key Laboratory of Metabolic and Chronic Diseases, Wuhan, 430060, China. qztang@whu.edu.cn.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>08</Month><Day>10</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Acta Pharmacol Sin</MedlineTA><NlmUniqueID>100956087</NlmUniqueID><ISSNLinking>1671-4083</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000998">Antiviral Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C505650">BNIP3 protein, rat</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C508686">BNip3 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008565">Membrane Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D024101">Mitochondrial Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016328">NF-kappa B</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019253">Proto-Oncogene Proteins c-bcl-2</NameOfSubstance></Chemical><Chemical><RegistryNumber>11128-99-7</RegistryNumber><NameOfSubstance UI="D000804">Angiotensin II</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.3.2.27</RegistryNumber><NameOfSubstance UI="D044767">Ubiquitin-Protein Ligases</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000804" MajorTopicYN="N">Angiotensin II</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000998" MajorTopicYN="N">Antiviral Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003921" MajorTopicYN="Y">Diabetes Mellitus, Experimental</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006333" MajorTopicYN="Y">Heart Failure</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008565" MajorTopicYN="N">Membrane Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008822" MajorTopicYN="N">Mice, Transgenic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D024101" MajorTopicYN="N">Mitochondrial Proteins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D032383" MajorTopicYN="N">Myocytes, Cardiac</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016328" MajorTopicYN="N">NF-kappa B</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019253" MajorTopicYN="N">Proto-Oncogene Proteins c-bcl-2</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013318" MajorTopicYN="N">Stroke Volume</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D044767" MajorTopicYN="N">Ubiquitin-Protein Ligases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016277" MajorTopicYN="N">Ventricular Function, Left</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">BCL2 interacting protein 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Clin Chim Acta. 2020;506:72–83. doi: 10.1016/j.cca.2020.02.024.</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.cca.2020.02.024</ArticleId><ArticleId IdType="pubmed">32092316</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35948726</PMID><DateRevised><Year>2022</Year><Month>08</Month><Day>10</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1572-8595</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Aug</Month><Day>10</Day></PubDate></JournalIssue><Title>Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing</Title><ISOAbbreviation>J Interv Card Electrophysiol</ISOAbbreviation></Journal>Novel insights into the substrate involved in maintenance of ventricular fibrillation: results from continuous multipolar mapping in a canine model. | Tax1 banding protein 1 (Tax1bp1) was originally identified as an NF-κB regulatory protein that participated in inflammatory, antiviral and innate immune processes. Tax1bp1 also functions as an autophagy receptor that plays a role in autophagy. Our previous study shows that Tax1bp1 protects against cardiomyopathy in STZ-induced diabetic mice. In this study we investigated the role of Tax1bp1 in heart failure. Pressure overload-induced heart failure model was established in mice by aortic banding (AB) surgery, and angiotensin II (Ang II)-induced heart failure model was established by infusion of Ang II through osmotic minipump for 4 weeks. We showed that the expression levels of Tax1bp1 in the heart were markedly increased 2 and 4 weeks after AB surgery. Knockdown of Tax1bp1 in mouse hearts significantly ameliorated both AB- and Ang II infusion-induced heart failure parameters. On the contrary, AB-induced heart failure was aggravated in cardiac-specific Tax1bp1 transgenic mice. Similar results were observed in neonatal rat cardiomyocytes (NRCMs) under Ang II insult. We demonstrated that the pro-heart failure effect of Tax1bp1 resulted from its interaction with the E3 ligase ITCH to promote the transcription factor P73 ubiquitination and degradation, causing enhanced BCL2 interacting protein 3 (BNIP3)-mediated cardiomyocyte apoptosis. Knockdown ITCH or BNIP3 in NRCMs significantly reduced Ang II-induced apoptosis in vitro. Similarly, BNIP3 knockdown attenuated heart failure in cardiac-specific Tax1bp1 transgenic mice. In the left ventricles of heart failure patients, Tax1bp1 expression level was significantly increased; Tax1bp1 gene expression was negatively correlated with left ventricular ejection fraction in heart failure patients. Collectively, the Tax1bp1 increase in heart failure enhances ITCH-P73-BNIP3-mediated cardiomyocyte apoptosis and induced cardiac injury. Tax1bp1 may serve as a potent therapeutic target for the treatment of heart failure.• Cardiac Tax1bp1 transgene mice were more vulnerable to cardiac dysfunction under stress.• Cardiac Tax1bp1 transgene mice were more vulnerable to cardiac dysfunction under stress.• Knockout of Tax1bp1 in mouse hearts ameliorated heart failure induced by pressure overload.• Tax1bp1 interacts with the E3 ligase Itch to promote P73 ubiquitination and degradation, causing enhanced BNIP3-mediated apoptosis.• Tax1bp1 may become a target of new therapeutic methods for treating heart failure.<CopyrightInformation>© 2022. The Author(s), under exclusive licence to Shanghai Institute of Materia Medica, Chinese Academy of Sciences and Chinese Pharmacological Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y" EqualContrib="Y"><LastName>Wu</LastName><ForeName>Qing-Qing</ForeName><Initials>QQ</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cardiovascular Research Institute, Wuhan University, Wuhan, 430060, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Hubei Key Laboratory of Metabolic and Chronic Diseases, Wuhan, 430060, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Yao</LastName><ForeName>Qi</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cardiovascular Research Institute, Wuhan University, Wuhan, 430060, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Hubei Key Laboratory of Metabolic and Chronic Diseases, Wuhan, 430060, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hu</LastName><ForeName>Tong-Tong</ForeName><Initials>TT</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cardiovascular Research Institute, Wuhan University, Wuhan, 430060, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Hubei Key Laboratory of Metabolic and Chronic Diseases, Wuhan, 430060, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wan</LastName><ForeName>Ying</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cardiovascular Research Institute, Wuhan University, Wuhan, 430060, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Hubei Key Laboratory of Metabolic and Chronic Diseases, Wuhan, 430060, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xie</LastName><ForeName>Qing-Wen</ForeName><Initials>QW</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cardiovascular Research Institute, Wuhan University, Wuhan, 430060, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Hubei Key Laboratory of Metabolic and Chronic Diseases, Wuhan, 430060, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhao</LastName><ForeName>Jin-Hua</ForeName><Initials>JH</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cardiovascular Research Institute, Wuhan University, Wuhan, 430060, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Hubei Key Laboratory of Metabolic and Chronic Diseases, Wuhan, 430060, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yuan</LastName><ForeName>Yuan</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cardiovascular Research Institute, Wuhan University, Wuhan, 430060, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Hubei Key Laboratory of Metabolic and Chronic Diseases, Wuhan, 430060, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tang</LastName><ForeName>Qi-Zhu</ForeName><Initials>QZ</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China. qztang@whu.edu.cn.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cardiovascular Research Institute, Wuhan University, Wuhan, 430060, China. qztang@whu.edu.cn.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Hubei Key Laboratory of Metabolic and Chronic Diseases, Wuhan, 430060, China. qztang@whu.edu.cn.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>08</Month><Day>10</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Acta Pharmacol Sin</MedlineTA><NlmUniqueID>100956087</NlmUniqueID><ISSNLinking>1671-4083</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000998">Antiviral Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C505650">BNIP3 protein, rat</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C508686">BNip3 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008565">Membrane Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D024101">Mitochondrial Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016328">NF-kappa B</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019253">Proto-Oncogene Proteins c-bcl-2</NameOfSubstance></Chemical><Chemical><RegistryNumber>11128-99-7</RegistryNumber><NameOfSubstance UI="D000804">Angiotensin II</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.3.2.27</RegistryNumber><NameOfSubstance UI="D044767">Ubiquitin-Protein Ligases</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000804" MajorTopicYN="N">Angiotensin II</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000998" MajorTopicYN="N">Antiviral Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003921" MajorTopicYN="Y">Diabetes Mellitus, Experimental</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006333" MajorTopicYN="Y">Heart Failure</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008565" MajorTopicYN="N">Membrane Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008822" MajorTopicYN="N">Mice, Transgenic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D024101" MajorTopicYN="N">Mitochondrial Proteins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D032383" MajorTopicYN="N">Myocytes, Cardiac</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016328" MajorTopicYN="N">NF-kappa B</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019253" MajorTopicYN="N">Proto-Oncogene Proteins c-bcl-2</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013318" MajorTopicYN="N">Stroke Volume</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D044767" MajorTopicYN="N">Ubiquitin-Protein Ligases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016277" MajorTopicYN="N">Ventricular Function, Left</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">BCL2 interacting protein 3</Keyword><Keyword MajorTopicYN="N">ITCH</Keyword><Keyword MajorTopicYN="N">P73</Keyword><Keyword MajorTopicYN="N">Tax1 banding protein 1</Keyword><Keyword MajorTopicYN="N">apoptosis</Keyword><Keyword MajorTopicYN="N">heart failure</Keyword></KeywordList><CoiStatement>The authors declare no competing interests.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>3</Month><Day>4</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>6</Month><Day>26</Day></PubMedPubDate><PubMedPubDate PubStatus="pmc-release"><Year>2023</Year><Month>10</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>8</Month><Day>11</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>10</Month><Day>5</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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Clin Chim Acta. 2020;506:72–83. doi: 10.1016/j.cca.2020.02.024.</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.cca.2020.02.024</ArticleId><ArticleId IdType="pubmed">32092316</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35948726</PMID><DateRevised><Year>2022</Year><Month>08</Month><Day>10</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1572-8595</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Aug</Month><Day>10</Day></PubDate></JournalIssue><Title>Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing</Title><ISOAbbreviation>J Interv Card Electrophysiol</ISOAbbreviation></Journal><ArticleTitle>Novel insights into the substrate involved in maintenance of ventricular fibrillation: results from continuous multipolar mapping in a canine model.</ArticleTitle><ELocationID EIdType="doi" ValidYN="Y">10.1007/s10840-022-01333-7</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">While the triggers for ventricular fibrillation (VF) are well-known, the substrate required for its maintenance remains elusive. We have previously demonstrated dynamic spatiotemporal changes across VF from electrical induction of VF to asystole. Those data suggested that VF drivers seemed to reside in the distal RV and LV. However, signals from these areas were not recorded continuously. The aim of this study was to map these regions of significance with stationary basket electrodes from induction to asystole to provide further insights into the critical substrate for VF rhythm sustenance in canines.<AbstractText Label="METHODS" NlmCategory="METHODS">In six healthy canines, three multipolar basket catheters were positioned in the distal right ventricle (RV), RV outflow tract, and distal left ventricle (LV), and remained in place throughout the study. VF was induced via direct current application from an electrophysiologic catheter. Surface and intracardiac electrograms were recorded simultaneously and continuously from baseline, throughout VF, and until asystole, in order to get a complete electrophysiologic analysis of VF. Focused data analysis was also performed via two defined stages of VF: early VF (immediately after induction of VF to 10 min) and late VF (after 10 min up to VF termination and asystole).<AbstractText Label="RESULTS" NlmCategory="RESULTS">VF was continuously mapped for a mean duration of 54 ± 9 min (range 42-70 min). Immediately after initiation of VF in the early phase, the distal LV region appeared to drive the maintenance of VF. Towards the terminal stage of VF, the distal RV region appeared to be responsible for VF persistence. In all canines, we noted local termination of VF in the LV, while VF on surface ECG continued; conversely, subsequent spontaneous termination of VF in the RV was associated with termination of VF on surface ECG into a ventricular escape rhythm. Continuous mapping of VF showed trends towards an increase in peak-to-peak ventricular electrogram cycle length (p = 0.06) and a decrease in the ventricular electrogram amplitude (p = 0.06) after 40 min. Once we could no longer discern surface QRS activity, we demonstrated local ventricular myocardial capture in both the RV and LV but could not reinitiate sustained VF despite aggressive ventricular burst pacing.<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">This study describes the evolution of VF from electrical initiation to spontaneous VF termination without hemodynamic support in healthy canines. These data are hypothesis-generating and suggest that critical substrate for VF maintenance may reside in both the distal RV and LV depending on stage of VF. Further studies are needed to replicate these findings with hemodynamic support and to translate such findings into clinical practice. Ventricular fibrillation maintenance may be dependent on critical structures in the distal RV. ECG: electrocardiogram; LV: left ventricle; RV: right ventricle; RVOT: right ventricular outflow tract; VF: ventricular fibrillation. |
2,329,668 | Senility and COVID-19 as two possible risk factors for loss of consciousness: A rare case report. | and Importance: More than two years after the start of the COVID-19 pandemic, the world is still grappling with this dilemma. COVID-19 covers a wide range of symptoms. Loss of consciousness (LOC) is a very rare symptom that can threaten a patient's life and blur the prognosis of recovery.</AbstractText>An 89-year-old woman was presented to the emergency department with LOC (Glasgow Coma Scale (GCS) score = 3) without any history of the underlying disease and was immediately admitted to the intensive care unit. In brain imaging, severe small vessel disease was diagnosed by observing partial dilatation of the ventricles, sulcus, and hypodense areas in the periventricular area. Lung imaging propounded COVID-19 by detecting the ground glass pattern with 50%-75% involvement. After detecting severe acute respiratory syndrome coronavirus 2 nucleic acid by reverse transcription-polymerase chain reaction, COVID-19 treatment was performed according to the national protocol. Finally, she was discharged after 26 days of hospitalization with partial recovery.</AbstractText>COVID-19-induced cytokine storm along with old age appears to increase LOC risk. It can be claimed that COVID-19-induced LOC can be considered as one of the symptoms of COVID-19 in the elderly population. Therefore, more attention should be paid to this population, which is more at risk.</AbstractText>Few reports illustrate the LOC as a COVID-19 presentation. This report highlights the fact that older people are more at risk for COVID-19-induced LOC than other age groups and should be given more care.</AbstractText>© 2022 The Authors.</CopyrightInformation> |
2,329,669 | Intra-Parenchymal Cerebellar Metastasis-A Rare Presentation of Castration-Resistant Prostate Cancer. | Intracranial metastases from prostate carcinoma are uncommon and usually manifest as dural secondaries in the supratentorial compartment. We present an unusual case of intra-parenchymal posterior fossa prostatic metastasis in a 61-year-old gentleman and discuss the diagnostic and management challenges involved. A 61-year-old hypertensive, diabetic man presented with gait unsteadiness for 1-month duration and no other neurological deficits. He had previously undergone bilateral orchiectomy for prostate carcinoma with multiple osseous metastases. Magnetic resonance imaging showed a well-defined lobulated, intraventricular, peripherally enhancing lesion in the fourth ventricle with obstructive hydrocephalus. He underwent sub-occipital craniectomy and decompression, and histological examination was consistent with metastatic prostate adenocarcinoma. Although cerebellar secondaries are atypical, a suspicion of metastasis should be upheld in all patients with the history of prostate carcinoma, regardless of their location and radiological characteristics of the intracranial lesion. |
2,329,670 | Inducible motor neuron differentiation of human induced pluripotent stem cells in vivo. | Transplantation of neural progenitor cells (NPCs) derived from human-induced pluripotent stem cells (hiPSCs) is one of the promising treatment strategies for motor neuron diseases (MNDs). However, the inefficiency in committed differentiation of NPCs in vivo limits its application. Here, we tried to establish a potential therapeutic strategy for MNDs by in vivo directional differentiation of hiPSCs engineered with motor neuron (MN) specific transcription factors and Tet-On system.</AbstractText>We engineered hiPSCs with three MN-specific transcription factors and Tet-On system. The engineered cells were directly transplanted into immunodeficient mice through subcutaneous, intra-spinal cord and intracerebroventricular injections. Following doxycycline (Dox) induction, teratoma formation, and motor MN differentiation were evaluated.</AbstractText>We generated genetically engineered hiPSCs, in which the expression of Ngn2, Isl1, and Lhx3 was controlled by a drug-inducible transgenic system. These cells showed normal pluripotency and proliferative capacity, and were able to directionally differentiate into mature motor neurons (MNs) and NPCs with high efficiency in spinal cords and cerebral lateral ventricles under the induction of Dox. The grafts showed long-term survival in the recipient mice without formation of teratoma.</AbstractText>The induced mature MNs and NPCs were expected to replace the damaged endogenous MNs directly, and play a role of de novo stem cell stock for long-term neuron damage repair, respectively. Therefore, in vivo directional differentiation of the hiPSCs engineered with MN-specific transcription factors and Tet-On system via Dox induction could be a potential therapeutic strategy for MNDs with high efficacy and safety.</AbstractText>© 2022 The Authors. Cell Proliferation published by Beijing Institute for Stem Cell and Regenerative Medicine and John Wiley & Sons Ltd.</CopyrightInformation> |
2,329,671 | Anaesthesia for elite athletes.<Pagination><StartPage>825</StartPage><EndPage>834</EndPage><MedlinePgn>825-834</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1097/EJA.0000000000001719</ELocationID><Abstract><AbstractText Label="BACKGROUND">Sports participation has been growing rapidly since the 1960s. Anaesthesiologists are increasingly confronted with athletes in a peri-operative setting. The right choice of type of anaesthesia technique, pain management of injuries, specific physiologic adaptations of the athlete and knowledge of prohibited substances are eminent for a correct approach of this subpopulation.</AbstractText><AbstractText Label="PURPOSE">This review aims to give an overview of athletes' specific anaesthetic management in peri-operative and postoperative settings and to guide the nonspecialised anaesthetist.</AbstractText><AbstractText Label="METHODS">We comprehensively reviewed the literature, gathered all the information available on, and synthesised it in a narrative way, regarding preoperative evaluation, intraoperative implications and postoperative pain management of the elite athlete undergoing a surgical procedure.</AbstractText><AbstractText Label="RESULTS">An anaesthesiologist should recognise the most common benign ECG findings in athletes like bradycardia, isolated left ventricle hypertrophy on voltage criteria and early repolarisation as normal features in the athlete's heart. Isotonic physiology typically produces four-chamber dilation. In contrast, isometric stress creates high intravascular pressure leading to left ventricular hypertrophy. Pre-operative evaluation should also identify possible consumers of performance-enhancing drugs. Intraoperative points of interest for the anaesthesiologist is mainly avoiding drugs on the prohibited list of the World Anti-Doping Agency (WADA). Postoperative and chronic pain management are still developing fields in this population. The International Olympic Committee (IOC) proposed treating acute pain with a combination of paracetamol, non-steroidal anti-inflammatory drugs (NSAIDs), topical analgesics, injectable NSAIDs and local anaesthetics. It may be suggested that chronic pain management in elite athletes could benefit from treatment in specialised multidisciplinary pain clinics.</AbstractText><AbstractText Label="CONCLUSION">This literature review aims to serve as a guide for the anaesthesiologist taking care of the elite athlete.</AbstractText><CopyrightInformation>Copyright © 2022 European Society of Anaesthesiology and Intensive Care. Unauthorized reproduction of this article is prohibited.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Bourgonjon</LastName><ForeName>Bram</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>From the Department of Anaesthesiology, GZA Antwerpen (BB), Department of Anaesthesiology, AZ Turnhout, Turnhout (KV), Department of Anaesthesiology, ASZ Aalst, Aalst, Belgium (NT) and Institute of Applied Health Sciences, Epidemiology Group, School of Medicine, Medical Sciences and Nutrition, University of Aberdeen; Department of Anaesthesia, NHS Grampian, Aberdeen, UK (PF).</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Vermeylen</LastName><ForeName>Kris</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Tytgat</LastName><ForeName>Niek</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Forget</LastName><ForeName>Patrice</ForeName><Initials>P</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>08</Month><Day>09</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Eur J Anaesthesiol</MedlineTA><NlmUniqueID>8411711</NlmUniqueID><ISSNLinking>0265-0215</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000700">Analgesics</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000894">Anti-Inflammatory Agents, Non-Steroidal</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000700" MajorTopicYN="N">Analgesics</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000758" MajorTopicYN="Y">Anesthesia</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000894" MajorTopicYN="N">Anti-Inflammatory Agents, Non-Steroidal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D056352" MajorTopicYN="N">Athletes</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004300" MajorTopicYN="Y">Doping in Sports</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013177" MajorTopicYN="Y">Sports</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>8</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>9</Month><Day>16</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>8</Month><Day>9</Day><Hour>8</Hour><Minute>22</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35943185</ArticleId><ArticleId IdType="doi">10.1097/EJA.0000000000001719</ArticleId><ArticleId IdType="pii">00003643-990000000-00023</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Statistical Office of the European Communities. 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Scand J Med Sci Sports 2016; 26:4–7.</Citation></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35942899</PMID><DateRevised><Year>2022</Year><Month>08</Month><Day>09</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1467-1107</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Aug</Month><Day>09</Day></PubDate></JournalIssue><Title>Cardiology in the young</Title><ISOAbbreviation>Cardiol Young</ISOAbbreviation></Journal>Acute vasodilator response testing in the adult Fontan circulation using non-invasive 4D Flow MRI: a proof-of-principle study. | Sports participation has been growing rapidly since the 1960s. Anaesthesiologists are increasingly confronted with athletes in a peri-operative setting. The right choice of type of anaesthesia technique, pain management of injuries, specific physiologic adaptations of the athlete and knowledge of prohibited substances are eminent for a correct approach of this subpopulation.</AbstractText>This review aims to give an overview of athletes' specific anaesthetic management in peri-operative and postoperative settings and to guide the nonspecialised anaesthetist.</AbstractText>We comprehensively reviewed the literature, gathered all the information available on, and synthesised it in a narrative way, regarding preoperative evaluation, intraoperative implications and postoperative pain management of the elite athlete undergoing a surgical procedure.</AbstractText>An anaesthesiologist should recognise the most common benign ECG findings in athletes like bradycardia, isolated left ventricle hypertrophy on voltage criteria and early repolarisation as normal features in the athlete's heart. Isotonic physiology typically produces four-chamber dilation. In contrast, isometric stress creates high intravascular pressure leading to left ventricular hypertrophy. Pre-operative evaluation should also identify possible consumers of performance-enhancing drugs. Intraoperative points of interest for the anaesthesiologist is mainly avoiding drugs on the prohibited list of the World Anti-Doping Agency (WADA). Postoperative and chronic pain management are still developing fields in this population. The International Olympic Committee (IOC) proposed treating acute pain with a combination of paracetamol, non-steroidal anti-inflammatory drugs (NSAIDs), topical analgesics, injectable NSAIDs and local anaesthetics. It may be suggested that chronic pain management in elite athletes could benefit from treatment in specialised multidisciplinary pain clinics.</AbstractText>This literature review aims to serve as a guide for the anaesthesiologist taking care of the elite athlete.</AbstractText>Copyright © 2022 European Society of Anaesthesiology and Intensive Care. Unauthorized reproduction of this article is prohibited.</CopyrightInformation> |
2,329,672 | [Periventricular changes following hydrocephalus: quantitative MR-based assessment of tissue characteristics]. | To study tissue characteristics of periventricular white matter in patients with open hydrocephalus using DWI MRI and their correlations with CSF flow parameters.</AbstractText>MRI was performed in 55 patients (35 women and 20 men) with open normal pressure hydrocephalus, as well as 16 patients with malignant occlusive hydrocephalus and interstitial edema (control group). We determined the correlations between severity of hydrocephalus, periventricular lesions and CSF flow parameters considering MR data. Dimensions of ventricular system were assessed using the Evans' index, periventricular changes - using visual four-level scale with calculation of apparent diffusion coefficient (ADC) and fractional anisotropy coefficient (FA).</AbstractText>Among patients with open hydrocephalus, ACD range for periventricular white matter was 1.57±0.15·10-</sup>3</sup> mm2</sup>/s in subgroup of patients without periventricular changes (n</i>=29) and 1.62±0.11×10-</sup>3</sup> mm2</sup>/s in patients with periventricular changes (n</i>=26). In the control group, mean ADC was 1.76±0.18·10-</sup>3</sup> mm2</sup>/s (p</i><0.05). In patients with open hydrocephalus, FA coefficient in the areas of periventricular changes was 0.70-0.80, in case of occlusive hydrocephalus - 0.68-0.82. There was a significant relationship between the Evans' index and CSF pulsation velocity amplitude, Evans' index and stroke volume, Evans' index and cerebral aqueduct cross-sectional area in patients with open hydrocephalus. Periventricular changes were pronounced in patients with open hydrocephalus and Evans' index > 0.4 (p</i><0.05).</AbstractText>According to MR data, periventricular changes in patients with open hydrocephalus differ from true periventricular interstitial edema following occlusive hydrocephalus. Severity of periventricular changes in patients with open hydrocephalus depends on patient age and width of the ventricles, but does not correlate with CSF flow parameters. In our opinion, periventricular changes are associated with dysfunction of glymphatic system. Further research is required to study the functioning of glymphatic system and related processes.</AbstractText> |
2,329,673 | Elevated salivary kynurenic acid levels related to enlarged choroid plexus and severity of clinical phenotypes in treatment-resistant schizophrenia. | Patients with treatment-resistant schizophrenia (TRS) suffer severe, long-term psychotic symptoms and chronic stress. Salivary kynurenic acid (KYNA) and choroid plexus were evidenced to relate to psychological stress. We hypothesized that TRS patients would have higher salivary KYNA levels than patients who respond to antipsychotics (NTRS) and healthy controls (HC), and increased salivary KYNA levels are associated with clinical phenotypes and choroid plexus volume. A total of 66 HC participants, 53 patients with TRS and 46 with NTRS were enrolled. Salivary KYNA levels were measured by liquid chromatography-tandem mass spectrometry, choroid plexus volume by magnetic resonance imaging, and cognitive functions with the MATRICS Consensus Cognitive Battery. The TRS group had significantly higher salivary KYNA levels than the NTRS group (p = 0.003), who in turn had higher salivary KYNA than HC (p = 0.02). Higher salivary KYNA levels were associated with larger choroid plexus volume (r = 0.48, p = 0.004); lower attention/vigilance (r = -0.44, p = 0.004), verbal learning (r = -0.44, p = 0.004), total MCCB score (r = -0.42, p = 0.005); and a higher total PANSS score (r = 0.48, p = 0.004) in TRS patients. An enlarged choroid plexus also related to worse attention/vigilance (r = -0.39, p = 0.03), verbal learning (r = -0.55, p = 0.001), total MCCB score (r = -0.41, p = 0.02) and clinical symptoms (r = 0.48, p = 0.004) in TRS patients only. We conclude that elevated salivary KYNA levels and associated choroid plexus enlargement are clinically relevant indicators of TRS, with salivary KYNA being particularly valuable as a peripheral marker. Our findings should benefit TRS research and benefit the improvement of personalized treatment. |
2,329,674 | Investigation of serum adropin levels and its relationship with hypothalamic atrophy in patients with multiple sclerosis. | Adropin is expressed in vascular endothelial cells and regulates nitric oxide (NO) bioavailability by upregulating nitric oxide. In recent years, some studies have revealed its relationship with the pathogenesis of multiple sclerosis (MS). Our aim in this study is to determine serum adropin levels in MS patients and to investigate adropin levels's relationship with hypothalamic atrophy.</AbstractText>A total of 80 people, 40 of whom had MS and 40 of whom were healthy volunteers, were included in the study. Serum samples were taken from all participants. Hypothalamus and pituitary diameters were calculated from magnetic resonance imaging of MS patients. The relationship between serum adropin levels and demographic characteristics, Expanded Disability Status Scale (EDSS), and hypothalamic atrophy were evaluated.</AbstractText>The levels of adropin were 848,282±139,229 ng/L in patients with MS and 2957,108±284,034 ng/L in the healthy controls. MS patients had significantly lower levels of adropin than the healthy controls (p = 0.003). Adropin has the highest diagnostic value (AUC=0.874, (95% CI, 0,800-0,947) as cut-off value (838.00), sensitivity (80.43%) and specificity (70.64%) in the MS group. In the study, serum adropin levels were not significantly correlated with 3 ventricle diameter (3VD) and pituitary diameter (PD) size (p = 0,968) and no significant relationships were determined between adropin and other clinical parameters.</AbstractText>As a potential diagnostic marker, adropin levels were significantly lower in MS patients than in those without. Comprehensive studies are needed to verify this entity.</AbstractText>Copyright © 2022. Published by Elsevier B.V.</CopyrightInformation> |
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A unique MCS device, a percutaneous right ventricular assist device (pRVAD), approved for use by the Food and Drug Administration (FDA) in 2014, works by temporarily off-loading the RV through a single, dual lumen catheter with extracorporeal mechanical support and is capable of shunting blood from the right atrium (RA) to the main PA. Although initially approved as venous-venous extracorporeal membrane oxygenation (VV-ECMO) device, this work will focus on the use of RV support, as ambulatory VV-ECMO strategies have been described previously. The catheter is most commonly inserted through the right internal jugular (IJ) vein into the PA and connected to an external pump, allowing flow up to 5 L/min. This device may be an attractive choice for the treatment of RV shock due to its percutaneous, minimally invasive insertion and removal and its ability to allow patient ambulation while the device is in place. This protocol discusses in detail the equipment, hemodynamic effects, indications, contraindications, complications, currently available research in the literature, and step-by-step instructions on how to implant, manage, and extract the device, along with the guidance on use and troubleshooting complications from one of the largest, single-center experiences with the device. |
2,329,676 | Characterization of TRPV4-mediated signaling pathways in an optimized human choroid plexus epithelial cell line.<Pagination><StartPage>C1823</StartPage><EndPage>C1842</EndPage><MedlinePgn>C1823-C1842</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1152/ajpcell.00193.2022</ELocationID><Abstract><AbstractText>The objectives of these studies were twofold: <i>1</i>) to characterize the human choroid plexus papilloma (HIBCPP) cell line as a model of the blood-cerebrospinal fluid barrier (BCSFB) via morphology, tightness, and polarization of transporters in choroid plexus epithelia (CPe), and <i>2</i>) to utilize Ussing-style electrophysiology to elucidate signaling pathways associated with the activation of the transient receptor potential vanilloid 4 (TRPV4) channel involved in cerebrospinal fluid (CSF) secretion. RT-PCR was implemented to determine gene expression of cell fate markers, junctional complex proteins, and transporters of interest. Scanning electron microscopy and confocal three-dimensional renderings of cultures grown on permeable supports were utilized to delineate the morphology of the brush border, junctional complexes, and polarization of key transporters. Electrophysiology was used to understand and explore TRPV4-mediated signaling in the HIBCPP cell line, considering both short-circuit current (<i>I</i><sub>sc</sub>) and conductance responses. HIBCPP cells grown under optimized culture conditions exhibited minimal multilayering, developed an intermediate resistance monolayer, retained differentiation properties, and expressed, and correctly localized, junctional proteins and native transporters. We found that activation of TRPV4 resulted in a robust, multiphasic change in electrogenic ion flux and increase in conductance accompanied by substantial fluid secretion. This response appears to be modulated by a number of different effectors, implicating phospholipase C (PLC), protein kinase C (PKC), and phosphoinositide 3-kinase (PI3K) in TRPV4-mediated ion flux. The HIBCPP cell line is a representative model of the human BCSFB, which can be utilized for studies of transporter function, intracellular signaling, and regulation of CSF production.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hulme</LastName><ForeName>Louise</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Biology, Indiana University Purdue University Indianapolis, Indianapolis, Indiana.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hochstetler</LastName><ForeName>Alexandra</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Biology, Indiana University Purdue University Indianapolis, Indianapolis, Indiana.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schwerk</LastName><ForeName>Christian</ForeName><Initials>C</Initials><Identifier Source="ORCID">0000-0002-1706-0259</Identifier><AffiliationInfo><Affiliation>Department of Pediatrics, Pediatric Infectious Diseases, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schroten</LastName><ForeName>Horst</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Pediatrics, Pediatric Infectious Diseases, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ishikawa</LastName><ForeName>Hiroshi</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Laboratory of Clinical Regenerative Medicine, University of Tsukuba, Ibaraki, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tung</LastName><ForeName>Chun-Yu</ForeName><Initials>CY</Initials><AffiliationInfo><Affiliation>Department of Biology, Indiana University Purdue University Indianapolis, Indianapolis, Indiana.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Perrin</LastName><ForeName>Benjamin</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Department of Biology, Indiana University Purdue University Indianapolis, Indianapolis, Indiana.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Blazer-Yost</LastName><ForeName>Bonnie</ForeName><Initials>B</Initials><Identifier Source="ORCID">0000-0002-1899-4555</Identifier><AffiliationInfo><Affiliation>Department of Biology, Indiana University Purdue University Indianapolis, Indianapolis, Indiana.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>X81XWH-16-PRMRP-IIRA</GrantID><Agency>Department of Defense Investigator Initiated Research Award</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>08</Month><Day>08</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Am J Physiol Cell Physiol</MedlineTA><NlmUniqueID>100901225</NlmUniqueID><ISSNLinking>0363-6143</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>EC 2.7.1.-</RegistryNumber><NameOfSubstance UI="D019869">Phosphatidylinositol 3-Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D026901">Membrane Transport Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C416986">TRPV4 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D050916">TRPV Cation Channels</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002831" MajorTopicYN="Y">Choroid Plexus</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019869" MajorTopicYN="Y">Phosphatidylinositol 3-Kinases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001812" MajorTopicYN="N">Blood-Brain Barrier</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D026901" MajorTopicYN="N">Membrane Transport Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004847" MajorTopicYN="N">Epithelial Cells</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050916" MajorTopicYN="N">TRPV Cation Channels</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">blood-cerebrospinal fluid barrier</Keyword><Keyword MajorTopicYN="N">choroid plexus</Keyword><Keyword MajorTopicYN="N">human choroid plexus cell line</Keyword><Keyword MajorTopicYN="N">transepithelial transport</Keyword><Keyword MajorTopicYN="N">transient potential vanilloid receptor 4</Keyword></KeywordList><CoiStatement>No conflicts of interest, financial or otherwise, are declared by the 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RT-PCR was implemented to determine gene expression of cell fate markers, junctional complex proteins, and transporters of interest. Scanning electron microscopy and confocal three-dimensional renderings of cultures grown on permeable supports were utilized to delineate the morphology of the brush border, junctional complexes, and polarization of key transporters. Electrophysiology was used to understand and explore TRPV4-mediated signaling in the HIBCPP cell line, considering both short-circuit current (<i>I</i><sub>sc</sub>) and conductance responses. HIBCPP cells grown under optimized culture conditions exhibited minimal multilayering, developed an intermediate resistance monolayer, retained differentiation properties, and expressed, and correctly localized, junctional proteins and native transporters. We found that activation of TRPV4 resulted in a robust, multiphasic change in electrogenic ion flux and increase in conductance accompanied by substantial fluid secretion. This response appears to be modulated by a number of different effectors, implicating phospholipase C (PLC), protein kinase C (PKC), and phosphoinositide 3-kinase (PI3K) in TRPV4-mediated ion flux. The HIBCPP cell line is a representative model of the human BCSFB, which can be utilized for studies of transporter function, intracellular signaling, and regulation of CSF production.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hulme</LastName><ForeName>Louise</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Biology, Indiana University Purdue University Indianapolis, Indianapolis, Indiana.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hochstetler</LastName><ForeName>Alexandra</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Biology, Indiana University Purdue University Indianapolis, Indianapolis, Indiana.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schwerk</LastName><ForeName>Christian</ForeName><Initials>C</Initials><Identifier Source="ORCID">0000-0002-1706-0259</Identifier><AffiliationInfo><Affiliation>Department of Pediatrics, Pediatric Infectious Diseases, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schroten</LastName><ForeName>Horst</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Pediatrics, Pediatric Infectious Diseases, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ishikawa</LastName><ForeName>Hiroshi</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Laboratory of Clinical Regenerative Medicine, University of Tsukuba, Ibaraki, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tung</LastName><ForeName>Chun-Yu</ForeName><Initials>CY</Initials><AffiliationInfo><Affiliation>Department of Biology, Indiana University Purdue University Indianapolis, Indianapolis, Indiana.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Perrin</LastName><ForeName>Benjamin</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Department of Biology, Indiana University Purdue University Indianapolis, Indianapolis, Indiana.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Blazer-Yost</LastName><ForeName>Bonnie</ForeName><Initials>B</Initials><Identifier Source="ORCID">0000-0002-1899-4555</Identifier><AffiliationInfo><Affiliation>Department of Biology, Indiana University Purdue University Indianapolis, Indianapolis, Indiana.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>X81XWH-16-PRMRP-IIRA</GrantID><Agency>Department of Defense Investigator Initiated Research Award</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>08</Month><Day>08</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Am J Physiol Cell Physiol</MedlineTA><NlmUniqueID>100901225</NlmUniqueID><ISSNLinking>0363-6143</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>EC 2.7.1.-</RegistryNumber><NameOfSubstance UI="D019869">Phosphatidylinositol 3-Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D026901">Membrane Transport Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C416986">TRPV4 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D050916">TRPV Cation Channels</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002831" MajorTopicYN="Y">Choroid Plexus</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019869" MajorTopicYN="Y">Phosphatidylinositol 3-Kinases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001812" MajorTopicYN="N">Blood-Brain Barrier</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D026901" MajorTopicYN="N">Membrane Transport Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004847" MajorTopicYN="N">Epithelial Cells</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050916" MajorTopicYN="N">TRPV Cation Channels</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">blood-cerebrospinal fluid barrier</Keyword><Keyword MajorTopicYN="N">choroid plexus</Keyword><Keyword MajorTopicYN="N">human choroid plexus cell line</Keyword><Keyword MajorTopicYN="N">transepithelial transport</Keyword><Keyword MajorTopicYN="N">transient potential vanilloid receptor 4</Keyword></KeywordList><CoiStatement>No conflicts of interest, financial or otherwise, are declared by the 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Baseline and procedural vitals were reported. Significant adverse events related to sedation were defined as an escalation in care or need for any additional/increased inotropic support to maintain pre-procedural haemodynamics. Minor adverse events were defined as changes from baseline haemodynamics that resolved without intervention. To assess whether sedation was adequate, echocardiogram reports were reviewed for completeness.<AbstractText Label="RESULTS" NlmCategory="RESULTS">From September to December 2020, five interstage patients (age 29-69 days) were sedated with 3 mcg/kg intranasal dexmedetomidine. The median sedation onset time and duration time was 24 minutes (range 12-43 minutes) and 60 minutes (range 33-60 minutes), respectively. Sedation was deemed adequate in all patients as complete echocardiograms were accomplished without a rescue dose. When compared to baseline, three (60%) patients had a >10% reduction in heart rate, one (20%) patient had a >10% reduction in oxygen saturations, and one (20%) patient had a >30% decrease in blood pressure. Amongst all patients, no significant complications occurred and haemodynamic changes from baseline did not result in need for intervention or interruption of study.<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Intranasal dexmedetomidine may be a reasonable option for echocardiography sedation in infants with shunt-dependent single ventricle heart disease, and further investigation is warranted to ensure efficacy and safety in an outpatient setting. |
2,329,677 | Determinants and Prognostic Implications of Hepatorenal Dysfunction in Adults With Congenital Heart Disease.<Pagination><StartPage>1742</StartPage><EndPage>1750</EndPage><MedlinePgn>1742-1750</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.cjca.2022.07.018</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0828-282X(22)00501-3</ELocationID><Abstract><AbstractText Label="BACKGROUND">There are limited data on the prognostic role of hepatorenal function indices in ambulatory patients with congenital heart disease (CHD). The purpose of this study was to determine the prevalence, risk factors, and prognostic implications of hepatorenal dysfunction, as measured by Model for End-Stage Liver Disease Excluding International Normalised Ratio (MELD-XI) score, in adults with CHD.</AbstractText><AbstractText Label="METHODS">In this retrospective study of CHD patients with comprehensive metabolic panels (2003-2019), mild/moderate and severe hepatorenal dysfunction was defined as MELD-XI 11-15 and > 15, respectively.</AbstractText><AbstractText Label="RESULTS">Of 4977 patients, 1376 (28%) had hepatorenal dysfunction (mild/moderate: n = 935 [19%]; severe: n = 441 [9%]). Hepatorenal dysfunction was most common in Fontan/unrepaired single ventricle (46%) and right heart disease (31%). Baseline MELD-XI was associated with all-cause mortality (HR 1.27, CI 1.21-1.33; P < 0.001) after adjustment for age, sex, and congenital heart lesion. In 3864 patients with serial MELD-XI data, there was a temporal increase in MELD-XI, and this was associated with an increased risk of mortality (HR 1.24, CI 1.15-1.36, per unit increase in MELD-XI; P = 0.004), independently from the baseline MELD-XI score. In the subset of 1856 patients that underwent surgical/transcatheter interventions, there was a postoperative reduction in MELD-XI, and this was associated with a lower risk of mortality (HR 0.94, CI 0.90-0.98, per unit decrease in MELD-XI; P = 0.008), independently from the baseline MELD-XI score.</AbstractText><AbstractText Label="CONCLUSIONS">Hepatorenal dysfunction was common in adults with CHD. Both baseline MELD-XI score and temporal changes in MELD-XI were associated with clinical outcomes, and therefore could be used to monitor therapeutic response to interventions and for deterioration in clinical status.</AbstractText><CopyrightInformation>Copyright © 2022 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Egbe</LastName><ForeName>Alexander C</ForeName><Initials>AC</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota, USA. Electronic address: egbe.alexander@mayo.edu.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Miranda</LastName><ForeName>William R</ForeName><Initials>WR</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Anderson</LastName><ForeName>Jason H</ForeName><Initials>JH</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Katta</LastName><ForeName>Renuka R</ForeName><Initials>RR</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Goda</LastName><ForeName>Ahmed Y</ForeName><Initials>AY</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Andi</LastName><ForeName>Kartik</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kamath</LastName><ForeName>Patrick S</ForeName><Initials>PS</Initials><AffiliationInfo><Affiliation>Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Connolly</LastName><ForeName>Heidi M</ForeName><Initials>HM</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>K23 HL141448</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL158517</GrantID><Acronym>HL</Acronym><Agency>NHLBI 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><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>08</Month><Day>04</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Can J Cardiol</MedlineTA><NlmUniqueID>8510280</NlmUniqueID><ISSNLinking>0828-282X</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011379" MajorTopicYN="N">Prognosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D058625" MajorTopicYN="Y">End Stage Liver Disease</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012720" MajorTopicYN="N">Severity of Illness Index</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006330" MajorTopicYN="Y">Heart Defects, Congenital</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading></MeshHeadingList><CoiStatement><b>Conflict of Interest:</b> none</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate 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The American journal of cardiology. 2020;130:137–142.</Citation><ArticleIdList><ArticleId IdType="pubmed">32703525</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedBookArticle><BookDocument><PMID Version="1">32310404</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK555944</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-17742">Aortic Regurgitation<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Dewaswala</LastName><ForeName>Nakeya</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>University of Miami / JFK Medical Center</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chait</LastName><ForeName>Robert</ForeName><Initials>R</Initials></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>Aortic regurgitation (AR), also known as aortic insufficiency, is the reverse blood flow from the aorta into the left ventricle (LV) during diastole. AR can result from either valve leaflets or primary aortic root disease.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-17742" sec="article-17742.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17742" sec="article-17742.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17742" sec="article-17742.s3">Etiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17742" sec="article-17742.s4">Epidemiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17742" sec="article-17742.s5">Pathophysiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17742" sec="article-17742.s6">History and Physical</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17742" sec="article-17742.s7">Evaluation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17742" sec="article-17742.s8">Treatment / Management</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17742" sec="article-17742.s9">Differential Diagnosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17742" sec="article-17742.s10">Prognosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17742" sec="article-17742.s11">Complications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17742" sec="article-17742.s12">Deterrence and Patient Education</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17742" sec="article-17742.s13">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17742" sec="article-17742.s14">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17742" sec="article-17742.s17">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>8</Month><Day>8</Day></ContributionDate><ReferenceList><Reference><Citation>Bekeredjian R, Grayburn PA. 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Circulation. 2003 Nov 18;108(20):2432-8.</Citation><ArticleIdList><ArticleId IdType="pubmed">14623790</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32310404</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">31536186</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK546577</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-21940">Neuroanatomy, Fourth Ventricle<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Roesch</LastName><ForeName>Zachary K.</ForeName><Initials>ZK</Initials><AffiliationInfo><Affiliation>Creighton University School of Medicine</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tadi</LastName><ForeName>Prasanna</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Asram Medical College, Eluru, India</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>The ventricles of the brain are the sites of cerebrospinal fluid (CSF) production. The lateral ventricles are the largest, and most proximal, ventricles in the central nervous system (CNS). CSF produced in the lateral ventricles goes into the interventricular foramen of Monro. The interventricular foramen of Monro connects the lateral ventricles to the third ventricle. The third ventricle connects to the fourth ventricle through the cerebral aqueduct of Sylvius. CSF flows through this entire pathway and then exits the fourth ventricle into the surrounding CNS tissue or the central spinal canal. This article will focus on the anatomy, function, and clinical relevance of the fourth ventricle.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-21940" sec="article-21940.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-21940" sec="article-21940.s2">Structure and Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-21940" sec="article-21940.s3">Embryology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-21940" sec="article-21940.s4">Blood Supply and Lymphatics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-21940" sec="article-21940.s5">Surgical Considerations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-21940" sec="article-21940.s6">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-21940" sec="article-21940.s7">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-21940" sec="article-21940.s9">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>8</Month><Day>8</Day></ContributionDate><ReferenceList><Reference><Citation>Adigun OO, Al-Dhahir MA. 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Sep 12, Dandy Walker Malformation.</Citation><ArticleIdList><ArticleId IdType="pubmed">0</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31536186</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">31334969</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK544249</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-17808">Neuroanatomy, Area Postrema<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Mirza</LastName><ForeName>Mariam</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>University of Illinois</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>M Das</LastName><ForeName>Joe</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Bahrain Specialist Hospital, Juffair, Bahrain</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>The area postrema is a highly vascular paired structure in the medulla oblongata in the brainstem. It lies in the caudal fourth ventricular floor, overlying the inferior portion of vagal trigone while facing the foramen of Magendie and rostral to the obex, the inferior point of the floor of the fourth ventricle. It is between the funiculus separans and the gracilis tubercle, lying adjacent to the nucleus of tractus solitarius. The description of the structure has been as ‘arched wings’ that are open on the sides of the fourth ventricle, as they separate upward from the central canal.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-17808" sec="article-17808.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17808" sec="article-17808.s2">Structure and Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17808" sec="article-17808.s3">Embryology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17808" sec="article-17808.s4">Blood Supply and Lymphatics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17808" sec="article-17808.s5">Nerves</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17808" sec="article-17808.s6">Muscles</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17808" sec="article-17808.s7">Physiologic Variants</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17808" sec="article-17808.s8">Surgical Considerations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17808" sec="article-17808.s9">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17808" sec="article-17808.s10">Other Issues</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17808" sec="article-17808.s11">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17808" sec="article-17808.s14">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>8</Month><Day>8</Day></ContributionDate><ReferenceList><Reference><Citation>Sarnat HB, Flores-Sarnat L, Boltshauser E. 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Mult Scler. 2019 Mar;25(3):325-329.</Citation><ArticleIdList><ArticleId IdType="pubmed">30463481</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31334969</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">30725818</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK537133</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-19371">Physiology, Chemoreceptor Trigger Zone<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>MacDougall</LastName><ForeName>Megan R.</ForeName><Initials>MR</Initials><AffiliationInfo><Affiliation>Western University of the Health Sci.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sharma</LastName><ForeName>Sandeep</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Mery Fitzgerald Hospital</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>The chemoreceptor trigger zone (CTZ) for emesis, also commonly known as the area postrema (AP), is located within the dorsal surface of the medulla oblongata, on the floor of the fourth ventricle of the brain. The CTZ contains receptors that detect emetic agents in the blood and relays that information to the vomiting center, which is responsible for inducing the vomiting reflex.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-19371" sec="article-19371.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19371" sec="article-19371.s2">Cellular Level</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19371" sec="article-19371.s3">Development</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19371" sec="article-19371.s4">Mechanism</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19371" sec="article-19371.s5">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19371" sec="article-19371.s6">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19371" sec="article-19371.s7">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>8</Month><Day>8</Day></ContributionDate><ReferenceList><Reference><Citation>Miller AD, Leslie RA. The area postrema and vomiting. Front Neuroendocrinol. 1994 Dec;15(4):301-20.</Citation><ArticleIdList><ArticleId IdType="pubmed">7895890</ArticleId></ArticleIdList></Reference><Reference><Citation>Popescu BF, Lennon VA, Parisi JE, Howe CL, Weigand SD, Cabrera-Gómez JA, Newell K, Mandler RN, Pittock SJ, Weinshenker BG, Lucchinetti CF. Neuromyelitis optica unique area postrema lesions: nausea, vomiting, and pathogenic implications. Neurology. 2011 Apr 05;76(14):1229-37.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC3068006</ArticleId><ArticleId IdType="pubmed">21368286</ArticleId></ArticleIdList></Reference><Reference><Citation>Becker DE. Nausea, vomiting, and hiccups: a review of mechanisms and treatment. Anesth Prog. 2010 Winter;57(4):150-6; quiz 157.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC3006663</ArticleId><ArticleId IdType="pubmed">21174569</ArticleId></ArticleIdList></Reference><Reference><Citation>Bhargava KP, Dixit KS. Role of the chemoreceptor trigger zone in histamine-induced emesis. Br J Pharmacol. 1968 Nov;34(3):508-13.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC1703476</ArticleId><ArticleId IdType="pubmed">4387255</ArticleId></ArticleIdList></Reference><Reference><Citation>Bhargava KP, Dixit KS, Gupta YK. Enkephalin receptors in the emetic chemoreceptor trigger zone of the dog. Br J Pharmacol. 1981 Mar;72(3):471-5.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC2071585</ArticleId><ArticleId IdType="pubmed">6266566</ArticleId></ArticleIdList></Reference><Reference><Citation>Gokozan HN, Baig F, Corcoran S, Catacutan FP, Gygli PE, Takakura AC, Moreira TS, Czeisler C, Otero JJ. Area postrema undergoes dynamic postnatal changes in mice and humans. J Comp Neurol. 2016 Apr 15;524(6):1259-69.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC4747799</ArticleId><ArticleId IdType="pubmed">26400711</ArticleId></ArticleIdList></Reference><Reference><Citation>Hornby PJ. Central neurocircuitry associated with emesis. Am J Med. 2001 Dec 03;111 Suppl 8A:106S-112S.</Citation><ArticleIdList><ArticleId IdType="pubmed">11749934</ArticleId></ArticleIdList></Reference><Reference><Citation>Horn CC. Why is the neurobiology of nausea and vomiting so important? Appetite. 2008 Mar-May;50(2-3):430-4.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC2274963</ArticleId><ArticleId IdType="pubmed">17996982</ArticleId></ArticleIdList></Reference><Reference><Citation>O'Brien C. Nausea and vomiting. Can Fam Physician. 2008 Jun;54(6):861-3.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC2426995</ArticleId><ArticleId IdType="pubmed">18556493</ArticleId></ArticleIdList></Reference><Reference><Citation>Griddine A, Bush JS. StatPearls [Internet] StatPearls Publishing; Treasure Island (FL): 2023. Feb 15, Ondansetron.</Citation><ArticleIdList><ArticleId IdType="pubmed">0</ArticleId></ArticleIdList></Reference><Reference><Citation>Chatterjee S, Rudra A, Sengupta S. Current concepts in the management of postoperative nausea and vomiting. Anesthesiol Res Pract. 2011;2011:748031.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC3216269</ArticleId><ArticleId IdType="pubmed">22110499</ArticleId></ArticleIdList></Reference><Reference><Citation>Horn CC, Wallisch WJ, Homanics GE, Williams JP. Pathophysiological and neurochemical mechanisms of postoperative nausea and vomiting. Eur J Pharmacol. 2014 Jan 05;722:55-66.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC3915298</ArticleId><ArticleId IdType="pubmed">24495419</ArticleId></ArticleIdList></Reference><Reference><Citation>Shosha E, Dubey D, Palace J, Nakashima I, Jacob A, Fujihara K, Takahashi T, Whittam D, Leite MI, Misu T, Yoshiki T, Messina S, Elsone L, Majed M, Flanagan E, Gadoth A, Huebert C, Sagen J, Greenberg BM, Levy M, Banerjee A, Weinshenker B, Pittock SJ. Area postrema syndrome: Frequency, criteria, and severity in AQP4-IgG-positive NMOSD. Neurology. 2018 Oct 23;91(17):e1642-e1651.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6205685</ArticleId><ArticleId IdType="pubmed">30258024</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">30725818</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">30020694</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK513322</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-18916">Alcoholic Cardiomyopathy<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Shaaban</LastName><ForeName>Adnan</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Lebanese University</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gangwani</LastName><ForeName>Manesh Kumar</ForeName><Initials>MK</Initials><AffiliationInfo><Affiliation>Mercy Hospital St. Louis</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pendela</LastName><ForeName>Venkata Satish</ForeName><Initials>VS</Initials><AffiliationInfo><Affiliation>Rochester General Hospital</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Vindhyal</LastName><ForeName>Mohinder R.</ForeName><Initials>MR</Initials></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>Alcohol-induced toxicity leads to non-ischemic dilated cardiomyopathy characterized by loss of contractile function and dilatation of myocardial ventricles. These findings are coupled with a clinical history of heavy alcohol use in the absence of coronary artery disease as a supportive etiology. Alcohol use is an important cause for non-ischemic cardiomyopathy and accounts for 10% of all cases of dilated cardiomyopathies. The major risk factor for developing ACM is chronic alcohol abuse; however, there is no specific cutoff value for the amount of alcohol consumption that would lead to the development of ACM.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-18916" sec="article-18916.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18916" sec="article-18916.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18916" sec="article-18916.s3">Etiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18916" sec="article-18916.s4">Epidemiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18916" sec="article-18916.s5">Pathophysiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18916" sec="article-18916.s6">Histopathology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18916" sec="article-18916.s7">History and Physical</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18916" sec="article-18916.s8">Evaluation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18916" sec="article-18916.s9">Treatment / Management</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18916" sec="article-18916.s10">Differential Diagnosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18916" sec="article-18916.s11">Prognosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18916" sec="article-18916.s12">Complications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18916" sec="article-18916.s13">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18916" sec="article-18916.s14">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18916" sec="article-18916.s16">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>8</Month><Day>8</Day></ContributionDate><ReferenceList><Reference><Citation>Mirijello A, Tarli C, Vassallo GA, Sestito L, Antonelli M, d'Angelo C, Ferrulli A, De Cosmo S, Gasbarrini A, Addolorato G. 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Mayo Clin Proc. 2014 Mar;89(3):382-93.</Citation><ArticleIdList><ArticleId IdType="pubmed">24582196</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">30020694</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">28613509</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK430758</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-26735">Patent Ductus Arteriosus<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Gillam-Krakauer</LastName><ForeName>Maria</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Vanderbilt University Medical Center</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mahajan</LastName><ForeName>Kunal</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Holy Heart Advanced Cardiac Care Centre</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>The ductus arteriosus is a fetal vessel that allows the oxygenated blood from the placenta to bypass the lungs in utero. At birth, the lungs fill with air with the first breaths, pulmonary vascular resistance drops, and blood flows from the right ventricle to the lungs for oxygenation. The increased arterial oxygen tension and the decreased flow through the ductus arteriosus allow the ductus to constrict. The ductus arteriosus is functionally closed by 12 to 24 hours of age in healthy, full-term newborns. Permanent (anatomic) closure is complete within 2 to 3 weeks.  In the premature infant, the ductus arteriosus does not close rapidly and may require pharmacologic or surgical closure to treat side effects. Anatomy During fetal life, the ductus is a normal structure that permits blood leaving the right ventricle to bypass the pulmonary circulation and enter the descending aorta. Less than 10% of this blood enters the pulmonary circulation. After birth, the ductus closes within 24-48 hours. The ductus is a remnant of the distal sixth aortic arch and connects the proximal descending aorta to the main pulmonary artery. The ductus can be found just posterior to the arch of the aorta where it enters the anterior pulmonary artery. The ductus has a conical shape which is large at the aortic end and narrow at the pulmonary end. However, the shape, size, and length of the ductus are very variable. For surgeons, an anatomical marker of the patent ductus is the recurrent laryngeal nerve which loops posteriorly around the ductus and ascends behind the aorta en route to the larynx. The recurrent laryngeal nerve is often injured during surgical ligature of the ductus. The Patent ductus is classified based on its angiographic features and includes the following: Type A: Conical. Type B: Window. Type C: Tubular. Type D: Complex. Type E: Elongated.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-26735" sec="article-26735.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26735" sec="article-26735.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26735" sec="article-26735.s3">Etiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26735" sec="article-26735.s4">Epidemiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26735" sec="article-26735.s5">Pathophysiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26735" sec="article-26735.s6">History and Physical</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26735" sec="article-26735.s7">Evaluation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26735" sec="article-26735.s8">Treatment / Management</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26735" sec="article-26735.s9">Differential Diagnosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26735" sec="article-26735.s10">Prognosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26735" sec="article-26735.s11">Complications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26735" sec="article-26735.s12">Postoperative and Rehabilitation Care</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26735" sec="article-26735.s13">Consultations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26735" sec="article-26735.s14">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26735" sec="article-26735.s15">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26735" sec="article-26735.s19">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>8</Month><Day>8</Day></ContributionDate><ReferenceList><Reference><Citation>Fink D, Nitzan I, Bin-Nun A, Mimouni F, Hammerman C. 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AR can result from either valve leaflets or primary aortic root disease.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-17742" sec="article-17742.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17742" sec="article-17742.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17742" sec="article-17742.s3">Etiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17742" sec="article-17742.s4">Epidemiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17742" sec="article-17742.s5">Pathophysiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17742" sec="article-17742.s6">History and Physical</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17742" sec="article-17742.s7">Evaluation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17742" sec="article-17742.s8">Treatment / Management</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17742" sec="article-17742.s9">Differential Diagnosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17742" sec="article-17742.s10">Prognosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17742" sec="article-17742.s11">Complications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17742" sec="article-17742.s12">Deterrence and Patient Education</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17742" sec="article-17742.s13">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17742" sec="article-17742.s14">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17742" sec="article-17742.s17">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>8</Month><Day>8</Day></ContributionDate><ReferenceList><Reference><Citation>Bekeredjian R, Grayburn PA. 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The lateral ventricles are the largest, and most proximal, ventricles in the central nervous system (CNS). CSF produced in the lateral ventricles goes into the interventricular foramen of Monro. The interventricular foramen of Monro connects the lateral ventricles to the third ventricle. The third ventricle connects to the fourth ventricle through the cerebral aqueduct of Sylvius. CSF flows through this entire pathway and then exits the fourth ventricle into the surrounding CNS tissue or the central spinal canal. This article will focus on the anatomy, function, and clinical relevance of the fourth ventricle.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-21940" sec="article-21940.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-21940" sec="article-21940.s2">Structure and Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-21940" sec="article-21940.s3">Embryology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-21940" sec="article-21940.s4">Blood Supply and Lymphatics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-21940" sec="article-21940.s5">Surgical Considerations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-21940" sec="article-21940.s6">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-21940" sec="article-21940.s7">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-21940" sec="article-21940.s9">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>8</Month><Day>8</Day></ContributionDate><ReferenceList><Reference><Citation>Adigun OO, Al-Dhahir MA. 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Sep 12, Dandy Walker Malformation.</Citation><ArticleIdList><ArticleId IdType="pubmed">0</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31536186</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">31334969</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK544249</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-17808">Neuroanatomy, Area Postrema</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Mirza</LastName><ForeName>Mariam</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>University of Illinois</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>M Das</LastName><ForeName>Joe</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Bahrain Specialist Hospital, Juffair, Bahrain</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>The area postrema is a highly vascular paired structure in the medulla oblongata in the brainstem. It lies in the caudal fourth ventricular floor, overlying the inferior portion of vagal trigone while facing the foramen of Magendie and rostral to the obex, the inferior point of the floor of the fourth ventricle. It is between the funiculus separans and the gracilis tubercle, lying adjacent to the nucleus of tractus solitarius. The description of the structure has been as ‘arched wings’ that are open on the sides of the fourth ventricle, as they separate upward from the central canal.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-17808" sec="article-17808.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17808" sec="article-17808.s2">Structure and Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17808" sec="article-17808.s3">Embryology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17808" sec="article-17808.s4">Blood Supply and Lymphatics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17808" sec="article-17808.s5">Nerves</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17808" sec="article-17808.s6">Muscles</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17808" sec="article-17808.s7">Physiologic Variants</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17808" sec="article-17808.s8">Surgical Considerations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17808" sec="article-17808.s9">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17808" sec="article-17808.s10">Other Issues</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17808" sec="article-17808.s11">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17808" sec="article-17808.s14">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>8</Month><Day>8</Day></ContributionDate><ReferenceList><Reference><Citation>Sarnat HB, Flores-Sarnat L, Boltshauser E. 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Mult Scler. 2019 Mar;25(3):325-329.</Citation><ArticleIdList><ArticleId IdType="pubmed">30463481</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31334969</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">30725818</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK537133</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-19371">Physiology, Chemoreceptor Trigger Zone</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>MacDougall</LastName><ForeName>Megan R.</ForeName><Initials>MR</Initials><AffiliationInfo><Affiliation>Western University of the Health Sci.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sharma</LastName><ForeName>Sandeep</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Mery Fitzgerald Hospital</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>The chemoreceptor trigger zone (CTZ) for emesis, also commonly known as the area postrema (AP), is located within the dorsal surface of the medulla oblongata, on the floor of the fourth ventricle of the brain. The CTZ contains receptors that detect emetic agents in the blood and relays that information to the vomiting center, which is responsible for inducing the vomiting reflex.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-19371" sec="article-19371.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19371" sec="article-19371.s2">Cellular Level</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19371" sec="article-19371.s3">Development</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19371" sec="article-19371.s4">Mechanism</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19371" sec="article-19371.s5">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19371" sec="article-19371.s6">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19371" sec="article-19371.s7">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>8</Month><Day>8</Day></ContributionDate><ReferenceList><Reference><Citation>Miller AD, Leslie RA. The area postrema and vomiting. Front Neuroendocrinol. 1994 Dec;15(4):301-20.</Citation><ArticleIdList><ArticleId IdType="pubmed">7895890</ArticleId></ArticleIdList></Reference><Reference><Citation>Popescu BF, Lennon VA, Parisi JE, Howe CL, Weigand SD, Cabrera-Gómez JA, Newell K, Mandler RN, Pittock SJ, Weinshenker BG, Lucchinetti CF. Neuromyelitis optica unique area postrema lesions: nausea, vomiting, and pathogenic implications. Neurology. 2011 Apr 05;76(14):1229-37.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC3068006</ArticleId><ArticleId IdType="pubmed">21368286</ArticleId></ArticleIdList></Reference><Reference><Citation>Becker DE. Nausea, vomiting, and hiccups: a review of mechanisms and treatment. Anesth Prog. 2010 Winter;57(4):150-6; quiz 157.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC3006663</ArticleId><ArticleId IdType="pubmed">21174569</ArticleId></ArticleIdList></Reference><Reference><Citation>Bhargava KP, Dixit KS. 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Neurology. 2018 Oct 23;91(17):e1642-e1651.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6205685</ArticleId><ArticleId IdType="pubmed">30258024</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">30725818</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">30020694</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK513322</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-18916">Alcoholic Cardiomyopathy</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Shaaban</LastName><ForeName>Adnan</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Lebanese University</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gangwani</LastName><ForeName>Manesh Kumar</ForeName><Initials>MK</Initials><AffiliationInfo><Affiliation>Mercy Hospital St. Louis</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pendela</LastName><ForeName>Venkata Satish</ForeName><Initials>VS</Initials><AffiliationInfo><Affiliation>Rochester General Hospital</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Vindhyal</LastName><ForeName>Mohinder R.</ForeName><Initials>MR</Initials></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>Alcohol-induced toxicity leads to non-ischemic dilated cardiomyopathy characterized by loss of contractile function and dilatation of myocardial ventricles. These findings are coupled with a clinical history of heavy alcohol use in the absence of coronary artery disease as a supportive etiology. Alcohol use is an important cause for non-ischemic cardiomyopathy and accounts for 10% of all cases of dilated cardiomyopathies. The major risk factor for developing ACM is chronic alcohol abuse; however, there is no specific cutoff value for the amount of alcohol consumption that would lead to the development of ACM.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-18916" sec="article-18916.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18916" sec="article-18916.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18916" sec="article-18916.s3">Etiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18916" sec="article-18916.s4">Epidemiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18916" sec="article-18916.s5">Pathophysiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18916" sec="article-18916.s6">Histopathology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18916" sec="article-18916.s7">History and Physical</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18916" sec="article-18916.s8">Evaluation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18916" sec="article-18916.s9">Treatment / Management</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18916" sec="article-18916.s10">Differential Diagnosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18916" sec="article-18916.s11">Prognosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18916" sec="article-18916.s12">Complications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18916" sec="article-18916.s13">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18916" sec="article-18916.s14">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18916" sec="article-18916.s16">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>8</Month><Day>8</Day></ContributionDate><ReferenceList><Reference><Citation>Mirijello A, Tarli C, Vassallo GA, Sestito L, Antonelli M, d'Angelo C, Ferrulli A, De Cosmo S, Gasbarrini A, Addolorato G. 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Genetic Etiology for Alcohol-Induced Cardiac Toxicity. J Am Coll Cardiol. 2018 May 22;71(20):2293-2302.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC5957753</ArticleId><ArticleId IdType="pubmed">29773157</ArticleId></ArticleIdList></Reference><Reference><Citation>Kycina P, Murin J. Alcoholic cardiomyopathy and cardiovascular events - an insight from the Liptov region. Bratisl Lek Listy. 2013;114(6):337-41.</Citation><ArticleIdList><ArticleId IdType="pubmed">23731046</ArticleId></ArticleIdList></Reference><Reference><Citation>Hassan AKM, Fouad DA, Refaiy A. Demographic features and prevalence of myocarditis in patients undergoing transarterial endomyocardial biopsy for unexplained cardiomyopathy. Egypt Heart J. 2017 Mar;69(1):29-35.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC5839358</ArticleId><ArticleId IdType="pubmed">29622952</ArticleId></ArticleIdList></Reference><Reference><Citation>Tønnesen H. Alcohol abuse and postoperative morbidity. 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Mayo Clin Proc. 2014 Mar;89(3):382-93.</Citation><ArticleIdList><ArticleId IdType="pubmed">24582196</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">30020694</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">28613509</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK430758</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-26735">Patent Ductus Arteriosus</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Gillam-Krakauer</LastName><ForeName>Maria</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Vanderbilt University Medical Center</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mahajan</LastName><ForeName>Kunal</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Holy Heart Advanced Cardiac Care Centre</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>The ductus arteriosus is a fetal vessel that allows the oxygenated blood from the placenta to bypass the lungs in utero. At birth, the lungs fill with air with the first breaths, pulmonary vascular resistance drops, and blood flows from the right ventricle to the lungs for oxygenation. The increased arterial oxygen tension and the decreased flow through the ductus arteriosus allow the ductus to constrict. The ductus arteriosus is functionally closed by 12 to 24 hours of age in healthy, full-term newborns. Permanent (anatomic) closure is complete within 2 to 3 weeks.  In the premature infant, the ductus arteriosus does not close rapidly and may require pharmacologic or surgical closure to treat side effects. Anatomy During fetal life, the ductus is a normal structure that permits blood leaving the right ventricle to bypass the pulmonary circulation and enter the descending aorta. Less than 10% of this blood enters the pulmonary circulation. After birth, the ductus closes within 24-48 hours. The ductus is a remnant of the distal sixth aortic arch and connects the proximal descending aorta to the main pulmonary artery. The ductus can be found just posterior to the arch of the aorta where it enters the anterior pulmonary artery. The ductus has a conical shape which is large at the aortic end and narrow at the pulmonary end. However, the shape, size, and length of the ductus are very variable. For surgeons, an anatomical marker of the patent ductus is the recurrent laryngeal nerve which loops posteriorly around the ductus and ascends behind the aorta en route to the larynx. The recurrent laryngeal nerve is often injured during surgical ligature of the ductus. The Patent ductus is classified based on its angiographic features and includes the following: Type A: Conical. Type B: Window. Type C: Tubular. Type D: Complex. Type E: Elongated.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-26735" sec="article-26735.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26735" sec="article-26735.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26735" sec="article-26735.s3">Etiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26735" sec="article-26735.s4">Epidemiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26735" sec="article-26735.s5">Pathophysiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26735" sec="article-26735.s6">History and Physical</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26735" sec="article-26735.s7">Evaluation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26735" sec="article-26735.s8">Treatment / Management</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26735" sec="article-26735.s9">Differential Diagnosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26735" sec="article-26735.s10">Prognosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26735" sec="article-26735.s11">Complications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26735" sec="article-26735.s12">Postoperative and Rehabilitation Care</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26735" sec="article-26735.s13">Consultations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26735" sec="article-26735.s14">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26735" sec="article-26735.s15">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26735" sec="article-26735.s19">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>8</Month><Day>8</Day></ContributionDate><ReferenceList><Reference><Citation>Fink D, Nitzan I, Bin-Nun A, Mimouni F, Hammerman C. 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J Thorac Cardiovasc Surg. 2018 Nov;156(5):1937-1944.</Citation><ArticleIdList><ArticleId IdType="pubmed">30007780</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">28613509</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">28613490</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK430739</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-19975">Cor Pulmonale</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Garrison</LastName><ForeName>Daniel M.</ForeName><Initials>DM</Initials></Author><Author ValidYN="Y"><LastName>Pendela</LastName><ForeName>Venkata Satish</ForeName><Initials>VS</Initials><AffiliationInfo><Affiliation>Rochester General Hospital</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Memon</LastName><ForeName>Jawedulhadi</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>King Fahad Hospital</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>Cor pulmonale is a Latin word that means "pulmonary heart," its definition varies, and presently, there is no consensual definition. Cor pulmonale can be defined as an alteration in the structure (e.g., hypertrophy or dilatation) and function of the right ventricle (RV) of the heart caused by a primary disorder of the respiratory system resulting in pulmonary hypertension. Right-sided heart failure secondary to left-sided heart failure, or congenital heart disease is not considered cor pulmonale. |
2,329,678 | Preservation of frontal white matter tracts in ventricular surgery: favoring an anterior interhemispheric transcallosal approach vs a transcortical transfrontal transventricular approach. | Secondary to the creation of a surgical corridor and retraction, white matter tracts degenerate, causing long-term scarring with potential neurological consequences. Third and lateral ventricle tumors require surgery that may lead to cognitive impairment. Our objective is to compare the long-term consequences of a transcortical transfrontal approach and an interhemispheric transcallosal approach on corpus callosum and frontal white matter tracts degeneration. Surgical patients with ventricular tumor accessible through both approaches were included and clinico-radiological data were retrospectively analyzed. The primary endpoint was the callosotomy length at 3-month post-operative T1 MRI, corrected by the extension of the tumor and the use of neuronavigation. Secondary outcomes included perioperative criteria such as bleeding, use of retractors and duration, FLAIR hypersignal on 3-month MRI, and re-do surgeries. To assess white matter tract interruption, 3-month FLAIR hypersignal was superposed to a tractography atlas. Seventy patients were included, 57 (81%) in the transfrontal group and 13 (19%) in the interhemispheric group. There was no difference in the mean callosotomy length on 3-month MRI (12.3 mm ± 5.60 transfrontal vs 11.7 mm ± 3.92 interhemispheric, p = 0.79) on univariate and multivariate analyses. The callosotomy length was inferior by - 3.13 mm for tumors located exclusively in the third ventricle (p = 0.016), independent of the approach. Retractors were used more often in transfrontal approaches (60% vs 33%, p < 0.001). The extent of frontal FLAIR hypersignal was higher after transfrontal approach (14.1 mm vs 0.525 mm, p < 0.001), correlated to the use of retractors (p < 0.05). After the interhemispheric approach, no tract other than corpus callosum was interrupted, whereas, after the transfrontal approach, frontal arcuate fibers and projections from the thalamus were interrupted in all patients, the cingulum in 19 (33%), the superior fronto-occipital fasciculus in 15 (26%), and the superior longitudinal fasciculus in 2 (3%). Transfrontal and interhemispheric approaches to the third and lateral ventricles both lead to the same long-term damage to the corpus callosum, but the transfrontal approach interrupts several white matter tracts essential to cognitive tasks such as attention and planning, even in the non-dominant hemisphere. These results encourage all neurosurgeons to be familiar with both approaches and favor the interhemispheric approach when both can give access to the tumor with a comparable risk. Neuropsychological studies are necessary to correlate these anatomical findings to cognitive outcomes. |
2,329,679 | Left Ventricular Segmental Strain Identifies Unique Myocardial Deformation Patterns After Intrinsic and Extrinsic Stressors in Mice. | We used segmental strain analysis to evaluate whether intrinsic (diet-induced obesity [DIO]) and extrinsic (unpredictable chronic mild stress [UCMS]) stressors can alter deformational patterns of the left ventricle. Six-week-old male C57BL/6J mice were randomized into the lean or obese group (n = 24/group). Mice underwent 12 wk of DIO with a high-fat diet (HFD). At 18 wk, lean and obese mice were further randomized into UCMS and non-UCMS groups (UCMS, 7 h/d, 5 d/wk, for 8 wk). Echocardiography was performed at baseline (6 wk), post-HFD (18 wk) and post-UCMS (26 wk). Machine learning was applied to the DIO and UCMS groups. There was robust predictive accuracy (area under the receiver operating characteristic curve [AUC] = 0.921) when comparing obese with lean mice, with radial strain changes in the lateral (-64%, p ≤ 0.001) and anterior free (-53%, p &lt; 0.001) walls being most informative. The ability to predict mice that underwent UCMS, irrespective of diet, was assessed (AUC = 0.886), revealing longitudinal strain rate of the anterior midwall and radial strain of the posterior septal wall as the top features. The wall segments indicate a predilection for changes in deformation patterns to the free wall (DIO) and septal wall (UCMS), indicating disease-specific alterations to the myocardium. |
2,329,680 | Biventricular biaxial mechanical testing and constitutive modelling of fetal porcine myocardium passive stiffness. | The evaluation of fetal heart mechanical function is becoming increasingly important for determining the prognosis and making subsequent decisions on the treatment and management of congenital heart diseases. Finite Element (FE) modelling can potentially provide detailed information on fetal hearts, and help perform virtual interventions to assist in predicting outcomes and supporting clinical decisions. Previous FE studies have enabled an improved understanding of healthy and diseased fetal heart biomechanics. However, to date, the mechanical properties of the fetal myocardium have not been well characterized which limits the reliability of such modelling. Here, we characterize the passive mechanical properties of late fetal and neonatal porcine hearts via biaxial mechanical testing as a surrogate for human fetal heart mechanical properties. We used samples from both the right and left ventricles over the late gestational period from 85 days of gestation to birth. Constitutive modelling was subsequently performed with a transversely isotropic Fung-type model and a Humphrey-type model, using fiber orientations identified with histology. We found no significant difference in mechanical stiffness across all age groups and between the right and left ventricular samples. This was likely due to the similarity in LV and RV pressures in the fetal heart, and similar gestational maturity across these late gestational ages. We thus recommend using the constitutive model for the average stress-stress behaviour of the tissues in future modelling work. Furthermore, we characterized the variability of the stiffness to inform such work. |
2,329,681 | A recurrent homozygous missense DPM3 variant leads to muscle and brain disease. | Biallelic pathogenic variants in the genes encoding the dolichol-phosphate mannose synthase subunits (DPM) which produce mannosyl donors for glycosylphosphatidylinositols, N-glycan and protein O- and C-mannosylation, are rare causes of congenital disorders of glycosylation. Pathogenic variants in DPM1 and DPM2 are associated with muscle-eye-brain (MEB) disease, whereas DPM3 variants have mostly been reported in patients with isolated muscle disease-dystroglycanopathy. Thus far, only one affected individual with compound heterozygous DPM3 variants presenting with myopathy, mild intellectual disability, seizures, and nonspecific white matter abnormalities (WMA) around the lateral ventricles has been described. Here we present five affected individuals from four unrelated families with global developmental delay/intellectual disability ranging from mild to severe, microcephaly, seizures, WMA, muscle weakness and variable cardiomyopathy. Exome sequencing of the probands revealed an ultra-rare homozygous pathogenic missense DPM3 variant NM_018973.4:c.221A&gt;G, p.(Tyr74Cys) which segregated with the phenotype in all families. Haplotype analysis indicated that the variant arose independently in three families. Functional analysis did not reveal any alteration in the N-glycosylation pathway caused by the variant; however, this does not exclude its pathogenicity in the function of the DPM complex and related cellular pathways. This report provides supporting evidence that, besides DPM1 and DPM2, defects in DPM3 can also lead to a muscle and brain phenotype. |
2,329,682 | Myocardial work: The analytical methodology and clinical utilities.<Pagination><StartPage>46</StartPage><EndPage>59</EndPage><MedlinePgn>46-59</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.hjc.2022.07.007</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S1109-9666(22)00114-2</ELocationID><Abstract><AbstractText>The evaluation of left ventricular (LV) systolic function is an essential part of the clinical practice of cardiology. Although left ventricular ejection fraction (LVEF) is the most validated and widely used parameter, it has fundamental limitations. LV strain is more sensitive to detect subtle myocardial dysfunction when LVEF was preserved, but it is load-dependent. Invasive left ventricular pressure-volume loop (LV-PVL) is the reliable standard to evaluate cardiac function, but its wide clinical application is limited by the risk of invasive LV pressure detection. Until the advent of non-invasive LV pressure-strain loop (LV-PSL), things have changed. LV-PSL is in good agreement with regional myocardial oxygen consumption and metabolism. Compared with traditional echocardiographic parameters or LV strain, myocardial work (MW) derived from LV-PSL is a more advanced tool that combines deformation as well as hemodynamics through integration of global longitudinal strain and non-invasive LV systolic pressure. In recent years, researches on MW are going on in full swing and show many advantages of MW. This review described the method and discussed the applications, advantages, limitations, and prospects of MW in multiple cardiovascular diseases. The goal is to provide the readers new insights for evaluating LV systolic function and promote the incorporation of MW into daily practice.</AbstractText><CopyrightInformation>Copyright © 2022 Hellenic Society of Cardiology. Published by Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Xinhao</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Shandong, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Pengfei</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Shandong, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Mengmeng</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Shandong, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Mei</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Shandong, China. Electronic address: zhangmei@email.sdu.edu.cn.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>08</Month><Day>02</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Hellenic J Cardiol</MedlineTA><NlmUniqueID>101257381</NlmUniqueID><ISSNLinking>1109-9666</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013318" MajorTopicYN="N">Stroke Volume</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016277" MajorTopicYN="Y">Ventricular Function, Left</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018487" MajorTopicYN="Y">Ventricular Dysfunction, Left</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004452" MajorTopicYN="N">Echocardiography</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">echocardiography</Keyword><Keyword MajorTopicYN="N">global longitudinal strain</Keyword><Keyword MajorTopicYN="N">myocardial work</Keyword><Keyword MajorTopicYN="N">pressure-strain loop</Keyword><Keyword MajorTopicYN="N">systolic function</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>2</Month><Day>11</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>7</Month><Day>3</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>7</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>8</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2023</Year><Month>2</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>8</Month><Day>5</Day><Hour>19</Hour><Minute>28</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35931412</ArticleId><ArticleId IdType="doi">10.1016/j.hjc.2022.07.007</ArticleId><ArticleId IdType="pii">S1109-9666(22)00114-2</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35931345</PMID><DateRevised><Year>2022</Year><Month>09</Month><Day>05</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1532-9488</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Aug</Month><Day>02</Day></PubDate></JournalIssue><Title>Seminars in thoracic and cardiovascular surgery</Title><ISOAbbreviation>Semin Thorac Cardiovasc Surg</ISOAbbreviation></Journal>Subcutaneous Treprostinil Improves Surgical Candidacy for Next Stage Palliation in Single Ventricle Patients With High-Risk Hemodynamics. | The evaluation of left ventricular (LV) systolic function is an essential part of the clinical practice of cardiology. Although left ventricular ejection fraction (LVEF) is the most validated and widely used parameter, it has fundamental limitations. LV strain is more sensitive to detect subtle myocardial dysfunction when LVEF was preserved, but it is load-dependent. Invasive left ventricular pressure-volume loop (LV-PVL) is the reliable standard to evaluate cardiac function, but its wide clinical application is limited by the risk of invasive LV pressure detection. Until the advent of non-invasive LV pressure-strain loop (LV-PSL), things have changed. LV-PSL is in good agreement with regional myocardial oxygen consumption and metabolism. Compared with traditional echocardiographic parameters or LV strain, myocardial work (MW) derived from LV-PSL is a more advanced tool that combines deformation as well as hemodynamics through integration of global longitudinal strain and non-invasive LV systolic pressure. In recent years, researches on MW are going on in full swing and show many advantages of MW. This review described the method and discussed the applications, advantages, limitations, and prospects of MW in multiple cardiovascular diseases. The goal is to provide the readers new insights for evaluating LV systolic function and promote the incorporation of MW into daily practice.<CopyrightInformation>Copyright © 2022 Hellenic Society of Cardiology. Published by Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Xinhao</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Shandong, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Pengfei</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Shandong, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Mengmeng</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Shandong, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Mei</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Shandong, China. Electronic address: zhangmei@email.sdu.edu.cn.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>08</Month><Day>02</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Hellenic J Cardiol</MedlineTA><NlmUniqueID>101257381</NlmUniqueID><ISSNLinking>1109-9666</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013318" MajorTopicYN="N">Stroke Volume</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016277" MajorTopicYN="Y">Ventricular Function, Left</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018487" MajorTopicYN="Y">Ventricular Dysfunction, Left</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004452" MajorTopicYN="N">Echocardiography</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">echocardiography</Keyword><Keyword MajorTopicYN="N">global longitudinal strain</Keyword><Keyword MajorTopicYN="N">myocardial work</Keyword><Keyword MajorTopicYN="N">pressure-strain loop</Keyword><Keyword MajorTopicYN="N">systolic function</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>2</Month><Day>11</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>7</Month><Day>3</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>7</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>8</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2023</Year><Month>2</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>8</Month><Day>5</Day><Hour>19</Hour><Minute>28</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35931412</ArticleId><ArticleId IdType="doi">10.1016/j.hjc.2022.07.007</ArticleId><ArticleId IdType="pii">S1109-9666(22)00114-2</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35931345</PMID><DateRevised><Year>2022</Year><Month>09</Month><Day>05</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1532-9488</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Aug</Month><Day>02</Day></PubDate></JournalIssue><Title>Seminars in thoracic and cardiovascular surgery</Title><ISOAbbreviation>Semin Thorac Cardiovasc Surg</ISOAbbreviation></Journal><ArticleTitle>Subcutaneous Treprostinil Improves Surgical Candidacy for Next Stage Palliation in Single Ventricle Patients With High-Risk Hemodynamics.</ArticleTitle><ELocationID EIdType="pii" ValidYN="Y">S1043-0679(22)00191-5</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1053/j.semtcvs.2022.07.011</ELocationID><Abstract>Single ventricle (SV) patients with pulmonary vascular disease (SV-PVD) are considered poor surgical candidates for Glenn or Fontan palliation. Given limited options for Stage 1 (S1) and Stage 2 (S2) SV patients with SV-PVD, we report on the use of subcutaneous treprostinil (TRE) to treat SV-PVD in this population. This single-center, retrospective cohort study examined SV patients who were not candidates for subsequent surgical palliation due to SV-PVD and were treated with TRE. The primary outcome was ability to progress to the next surgical stage; secondary outcomes included changes in hemodynamics after TRE initiation. Between 3/2014 and 8/2021, 17 SV patients received TRE for SV-PVD: 11 after S1 and 6 after S2 (median PVR 4.1 [IQR 3.2-4.8] WU*m<sup>2</sup> and 5.0 [IQR 1.5-6.1] WU*m<sup>2</sup>, respectively). Nine of 11 (82%) S1 progressed to S2, and 2 (18%) underwent heart transplant (HTx). Three of 6 (50%) S2 progressed to Fontan, 1 underwent HTx and 2 are awaiting Fontan on TRE. TRE significantly decreased PVR in S1 patients with median post-treatment PVR of 2.0 (IQR 1.5-2.6) WU*m<sup>2</sup>. TRE can allow for further surgical palliation in select pre-Fontan patients with SV-PVD, obviating the need for HTx. Improvement in PVR was significant in S1 patients and persisted beyond discontinuation of therapy for most patients. |
2,329,683 | Pulmonary valve involvement and left ventricular thrombosis in Behçet's disease: a case report and literature review.<Pagination><StartPage>1607</StartPage><MedlinePgn>1607</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.55563/clinexprheumatol/nocnjd</ELocationID><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Wu</LastName><ForeName>Tingting</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Xiangya Hospital, Central South University, Changsha, Hunan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lulu</LastName><ForeName>Zheng</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Xiangya Hospital, Central South University, Changsha, Hunan, China. zhenglulu_csu@126.com.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType><PublicationType UI="D016422">Letter</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>08</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>Italy</Country><MedlineTA>Clin Exp Rheumatol</MedlineTA><NlmUniqueID>8308521</NlmUniqueID><ISSNLinking>0392-856X</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D001528" MajorTopicYN="Y">Behcet Syndrome</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006331" MajorTopicYN="Y">Heart Diseases</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="D011664" MajorTopicYN="Y">Pulmonary Valve</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013927" MajorTopicYN="Y">Thrombosis</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>2</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>6</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>8</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>9</Month><Day>17</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>8</Month><Day>5</Day><Hour>13</Hour><Minute>3</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35930481</ArticleId><ArticleId IdType="doi">10.55563/clinexprheumatol/nocnjd</ArticleId><ArticleId IdType="pii">18450</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35930273</PMID><DateRevised><Year>2022</Year><Month>08</Month><Day>05</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1557-8518</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Aug</Month><Day>05</Day></PubDate></JournalIssue><Title>Metabolic syndrome and related disorders</Title><ISOAbbreviation>Metab Syndr Relat Disord</ISOAbbreviation></Journal>Impact of Prediabetes on Cardiac Function Among Primary Care Patients. | <b><i>Background:</i></b> Prediabetes is a novel risk factor recently associated with changes in the left ventricle. Our aim is to determine if prediabetes is associated with heart failure (HF) and structural heart disease. <b><i>Methods:</i></b> We conducted a cross-sectional study and performed screening echocardiograms to consecutive primary care patients. We calculated the hemoglobin A1c (HbA1c) within 3 months of the echocardiogram and classified patients as having normal glucose, low-risk or high-risk prediabetes or diabetes. Our primary outcome was HF defined as an ejection fraction (EF) <50% and HF with preserved EF. Our secondary outcome was structural heart disease defined as having either a large atrium, left ventricular hypertrophy, or low EF. <b><i>Results:</i></b> We included 15,056 patients who underwent a screening echocardiogram and had a recorded HbA1c. Only 2794 patients had a normal blood glucose, 4201 had low-risk prediabetes, 2499 had high-risk prediabetes, and the remainder had diabetes. The adjusted odds ratio (ORs) of HF for low-risk prediabetes, high-risk prediabetes and diabetes were 1.38 [confidence interval (95% CI) 1.07-1.78] (<i>P</i> = 0.01), 1.47 (95% CI 1.05-2.01) (<i>P</i> = 0.01), and 1.60 (95% CI 1.16-2.01) (<i>P</i> < 0.01), respectively, when compared with normoglycemic patients. The adjusted OR of HF with preserved EF for low- and high-risk prediabetes and diabetes were 1.17 (95% CI 0.86-1.60) (<i>P</i> = 0.30), 1.60 (95% CI 1.15-2.21) (<i>P</i> < 0.01), and 1.63 (95% CI 1.24-2.13) (<i>P</i> < 0.01), respectively, when compared with normoglycemic patients. <b><i>Conclusions:</i></b> Prediabetes is a prevalent condition associated with structural heart disease and HF. |
2,329,684 | Left ventricular assist devices: A historical perspective at the intersection of medicine and engineering.<Pagination><StartPage>2343</StartPage><EndPage>2360</EndPage><MedlinePgn>2343-2360</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1111/aor.14371</ELocationID><Abstract><AbstractText>Over the last half-century, left ventricular assist device (LVAD) technology has progressed from conceptual therapy for failed cardiopulmonary bypass weaning to an accepted destination therapy for advanced heart failure. The history of LVAD engineering is defined by an initial development phase, which demonstrated the feasibility of such an approach, to the more recent three major generations of commercial devices. In this review, we explore the engineering challenges of LVADs, how they were addressed over time, and the clinical outcomes that resulted from each major technological development. The first generation of commercial LVADs were pulsatile devices, which lacked the appropriate durability due to their number of moving components and hemocompatibility. The second generation of LVADs was defined by replacement of complex, pulsatile pumps with primarily axial, continuous-flow systems with an impeller in the blood passageway. These devices experienced significant commercial success, but the presence of excessive trauma to the blood and in-situ bearing resulted in an unacceptable burden of adverse events. Third generation centrifugal-flow pumps use magnetically suspended rotors within the pump chamber. Superior outcomes with this newest generation of devices have been observed, particularly with respect to hemocompatibility-related adverse events including pump thrombosis, with fully magnetically levitated devices. The future of LVAD engineering includes wireless charging foregoing percutaneous drivelines and more advanced pump control mechanisms, including synchronization of the pump flow with the native cardiac cycle, and varying pump output based on degree of physical exertion using sensor or advanced device-level data triggers.</AbstractText><CopyrightInformation>© 2022 International Center for Artificial Organ and Transplantation (ICAOT) and Wiley Periodicals LLC.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Goodman</LastName><ForeName>Daniel</ForeName><Initials>D</Initials><Identifier Source="ORCID">0000-0003-0250-0271</Identifier><AffiliationInfo><Affiliation>College of Osteopathic Medicine, Des Moines University, Des Moines, Iowa, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Stulak</LastName><ForeName>John</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Division of Cardiovascular Surgery, Mayo Clinic, Rochester, Minnesota, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rosenbaum</LastName><ForeName>Andrew N</ForeName><Initials>AN</Initials><Identifier Source="ORCID">0000-0001-9202-0233</Identifier><AffiliationInfo><Affiliation>Department of Cardiovascular Diseases, Mayo Clinic Minnesota, Rochester, Minnesota, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>08</Month><Day>05</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Artif Organs</MedlineTA><NlmUniqueID>7802778</NlmUniqueID><ISSNLinking>0160-564X</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006353" MajorTopicYN="Y">Heart-Assist Devices</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006333" MajorTopicYN="Y">Heart Failure</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013927" MajorTopicYN="Y">Thrombosis</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">LVAD</Keyword><Keyword MajorTopicYN="N">engineering</Keyword><Keyword MajorTopicYN="N">heart failure</Keyword><Keyword MajorTopicYN="N">history</Keyword><Keyword MajorTopicYN="N">technology</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>7</Month><Day>6</Day></PubMedPubDate><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>5</Month><Day>6</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>7</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>8</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>11</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>8</Month><Day>5</Day><Hour>4</Hour><Minute>13</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35929377</ArticleId><ArticleId IdType="doi">10.1111/aor.14371</ArticleId></ArticleIdList><ReferenceList><Title>REFERENCES</Title><Reference><Citation>Stewart GC, Mehra MR. 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Artif Organs. 2019;43(3):222-8.</Citation></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35929033</PMID><DateRevised><Year>2022</Year><Month>08</Month><Day>05</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">1019-5149</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Jan</Month><Day>25</Day></PubDate></JournalIssue><Title>Turkish neurosurgery</Title><ISOAbbreviation>Turk Neurosurg</ISOAbbreviation></Journal>The Morphology and Morphometry of the Human Interthalamic Adhesion Using Cadaveric Brains and Magnetic Resonance Images and Their Clinical Significance. | Over the last half-century, left ventricular assist device (LVAD) technology has progressed from conceptual therapy for failed cardiopulmonary bypass weaning to an accepted destination therapy for advanced heart failure. The history of LVAD engineering is defined by an initial development phase, which demonstrated the feasibility of such an approach, to the more recent three major generations of commercial devices. In this review, we explore the engineering challenges of LVADs, how they were addressed over time, and the clinical outcomes that resulted from each major technological development. The first generation of commercial LVADs were pulsatile devices, which lacked the appropriate durability due to their number of moving components and hemocompatibility. The second generation of LVADs was defined by replacement of complex, pulsatile pumps with primarily axial, continuous-flow systems with an impeller in the blood passageway. These devices experienced significant commercial success, but the presence of excessive trauma to the blood and in-situ bearing resulted in an unacceptable burden of adverse events. Third generation centrifugal-flow pumps use magnetically suspended rotors within the pump chamber. Superior outcomes with this newest generation of devices have been observed, particularly with respect to hemocompatibility-related adverse events including pump thrombosis, with fully magnetically levitated devices. The future of LVAD engineering includes wireless charging foregoing percutaneous drivelines and more advanced pump control mechanisms, including synchronization of the pump flow with the native cardiac cycle, and varying pump output based on degree of physical exertion using sensor or advanced device-level data triggers.<CopyrightInformation>© 2022 International Center for Artificial Organ and Transplantation (ICAOT) and Wiley Periodicals LLC.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Goodman</LastName><ForeName>Daniel</ForeName><Initials>D</Initials><Identifier Source="ORCID">0000-0003-0250-0271</Identifier><AffiliationInfo><Affiliation>College of Osteopathic Medicine, Des Moines University, Des Moines, Iowa, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Stulak</LastName><ForeName>John</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Division of Cardiovascular Surgery, Mayo Clinic, Rochester, Minnesota, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rosenbaum</LastName><ForeName>Andrew N</ForeName><Initials>AN</Initials><Identifier Source="ORCID">0000-0001-9202-0233</Identifier><AffiliationInfo><Affiliation>Department of Cardiovascular Diseases, Mayo Clinic Minnesota, Rochester, Minnesota, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>08</Month><Day>05</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Artif Organs</MedlineTA><NlmUniqueID>7802778</NlmUniqueID><ISSNLinking>0160-564X</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006353" MajorTopicYN="Y">Heart-Assist Devices</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006333" MajorTopicYN="Y">Heart Failure</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013927" MajorTopicYN="Y">Thrombosis</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">LVAD</Keyword><Keyword MajorTopicYN="N">engineering</Keyword><Keyword MajorTopicYN="N">heart failure</Keyword><Keyword MajorTopicYN="N">history</Keyword><Keyword MajorTopicYN="N">technology</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>7</Month><Day>6</Day></PubMedPubDate><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>5</Month><Day>6</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>7</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>8</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>11</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>8</Month><Day>5</Day><Hour>4</Hour><Minute>13</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35929377</ArticleId><ArticleId IdType="doi">10.1111/aor.14371</ArticleId></ArticleIdList><ReferenceList><Title>REFERENCES</Title><Reference><Citation>Stewart GC, Mehra MR. 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Artif Organs. 2019;43(3):222-8.</Citation></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35929033</PMID><DateRevised><Year>2022</Year><Month>08</Month><Day>05</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">1019-5149</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Jan</Month><Day>25</Day></PubDate></JournalIssue><Title>Turkish neurosurgery</Title><ISOAbbreviation>Turk Neurosurg</ISOAbbreviation></Journal><ArticleTitle>The Morphology and Morphometry of the Human Interthalamic Adhesion Using Cadaveric Brains and Magnetic Resonance Images and Their Clinical Significance.</ArticleTitle><ELocationID EIdType="doi" ValidYN="Y">10.5137/1019-5149.JTN.36551-21.2</ELocationID><Abstract><AbstractText Label="AIM" NlmCategory="OBJECTIVE">An interthalamic adhesion (ITA) is a midplane rod-like neuroanatomical mass connecting two thalami over the cavity of the third ventricle. It is present in approximately 70-80% of healthy humans. The absence of an ITA has been considered as a midline defect of the brain associated with schizophrenia. The aim of the present study was to determine the prevalence, location, and dimensions of ITAs in Indian brains.<AbstractText Label="MATERIAL AND METHODS" NlmCategory="METHODS">We examined 100 brains (50 cadaveric and 50 MR images) in the midsagittal plane for the presence or absence of ITAs, their location in the lateral wall of the third ventricle, and dimensions.<AbstractText Label="RESULTS" NlmCategory="RESULTS">ITA found in 87 brains (87%), four showed duplication (4%). Both its duplication and absence were more frequent among male. It was most commonly located in the anterosuperior quadrant with posterosuperior extension. The mean of horizontal diameter (7.13±4.31 mm) was longer than the vertical (5.13 ±3.17) in all the brains. Its average area (37.98±41.47 mm2) showed huge variation (ranges between 4.40 mm2 to 203 mm2) and was significantly higher in females (61.23±56.22 mm2) than males (36.44±43.21 mm2) (p = 0.026). No correlation was found between the surface area of the ITA and the length of the third ventricle.<AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">Absence and duplication of ITA are fairly common in Indian brains with significant male predominance. Morphometric data are robust to advocate for the presence of sex differences in the ITA size, although not associated with surrounding thalamic or third ventricle anatomy. |
2,329,685 | Joubert-Plus syndrome with an atretic cephalocele: a case report. | Joubert syndrome is a rare heterogeneous disease affecting the cerebellum. It usually presents with hypotonia, abnormal breathing pattern, with distinctive cerebellar and brain stem malformation called the molar tooth sign. It may present with different organ involvement or with other neurological alterations such as Dandy-Walker syndrome. Joubert syndrome with dandy walker syndrome is called Joubert-Plus syndrome, an exceedingly rare entity. Dandy-Walker syndrome is defined by hypoplasia and upward rotation of the cerebellar vermis and cystic dilation of the fourth ventricle. Atretic cephalocele is another rare diagnosis which is characterized by a herniation of intracranial contents through a skull defect. Herein, we present a case of a 6-month-old patient who presented with floppiness and a scalp nodule. After further evaluation, he was diagnosed with Joubert-Plus syndrome with an atretic cephalocele. |
2,329,686 | Paternal De Novo Variant of <i>TAOK1</i> in a Fetus With Structural Brain Abnormalities. | A dilated lateral ventricle is a relatively common finding on prenatal ultrasound, and the causes are complex. We aimed to explore the etiology of a fetus with a dilated lateral ventricle. Trio whole-exome sequencing was performed to detect causative variants. A <i>de novo</i> variant of <i>TAOK1</i> (NM_020791.2: c.227A>G) was detected in the proband and evaluated for potential functional impacts using a variety of prediction tools. Droplet digital polymerase chain reaction was used to exclude the parental mosaicism and to verify the phasing of the <i>de novo</i> variant. Based on peripheral blood analysis, the parents did not exhibit mosaicism at this site, and the <i>de novo</i> variant was paternally derived. Here, we describe a fetus with a <i>de novo</i> likely pathogenic variant of <i>TAOK1</i> who had a dilated lateral ventricle and a series of particular phenotypes. This case expands the clinical spectrum of <i>TAOK1</i>-associated disorders. We propose a method for solving genetic disorders in which the responsible genes have not yet gone through ClinGen curation, particularly for prenatal cases. |
2,329,687 | Beasts and Gods: Hippocampal quarrels before memory. | The first description and naming of the hippocampus is usually credited to Arantius (c. 1530 - 1589), whose comparison of the swelling inside the temporal horn of the lateral ventricle to a seahorse (hippocampus) or silkworm (bombyx) was published in the 1587 edition of the Anatomicarum Observationum Liber. However, in the 17<sup>th</sup> century, the term hippocampus was rarely used and its precise anatomy remained a mystery. The 18<sup>th</sup> century saw the hippocampus referred to as a wide range of animals and divinities. These terminological issues provoked heated discussions in the French Académie Royale des Sciences, culminating in the seminal description of the hippocampus in the 1780s by Félix Vicq d'Azyr (1748-1794). However, it is striking that no hypothesis concerning the function of the hippocampus was proposed, and its link with memory was not established until the mid-20<sup>th</sup> century. |
2,329,688 | Amitriptyline improves cognitive and neuronal function in a rat model that mimics dementia with lewy bodies. | Dementia with Lewy bodies (DLB), a highly prevalent neurodegenerative disorder, causes motor and cognitive deficits. The main pathophysiologies of DLB are glutamate excitotoxicity and accumulation of Lewy bodies comprising α-synuclein (α-syn) and β-amyloid (Aβ). Amitriptyline (AMI) promotes expression of glutamate transporter-1 and glutamate reuptake. In this study, we measured the effects of AMI on behavioral and neuronal function in a DLB rat model. We used rivastigmine (RIVA) as a positive control. To establish the DLB rat model, male Wistar rats were stereotaxically injected with recombinant adenoassociated viral vector with the SNCA gene (10 μg/10 μL) and Aβ (5 μg/2.5 μL) into the left ventricle and prefrontal cortex, respectively. AMI (10 mg/kg/day, i.p.), RIVA (2 mg/kg/day, i.p.), or saline was injected intraperitoneally after surgery. From the 29th day, behavioral tests were performed to evaluate the motor and cognitive functions of the rats. Immunohistochemical staining was used to assess neuronal changes. We measured the α-syn level, number of newborn cells, and neuronal density in the hippocampus and in the nigrostriatal dopaminergic system. The DLB group exhibited deficit in object recognition. Both the AMI and RIVA treatments reversed these deficits. Histologically, the DLB rats exhibited cell loss in the substantia nigra pars compacta and in the hippocampal CA1 area. AMI reduced this cell loss, but RIVA did not. In addition, the DLB rats exhibited a lower number of newborn cells and higher α-syn levels in the dentate gyrus (DG). AMI did not affect α-syn accumulation but recovered neurogenesis in the DG of the rats, whereas RIVA reversed the α-syn accumulation but did not affect neurogenesis in the rats. We suggest that AMI may have potential for use in the treatment of DLB. |
2,329,689 | Structural Brain Network Reorganization Following Anterior Callosotomy for Colloid Cysts: Connectometry and Graph Analysis Results. | The plasticity of the neural circuits after injuries has been extensively investigated over the last decades. Transcallosal microsurgery for lesions affecting the third ventricle offers an interesting opportunity to investigate the whole-brain white matter reorganization occurring after a selective resection of the genu of the corpus callosum (CC).</AbstractText>Diffusion MRI (dMRI) data and neuropsychological testing were collected pre- and postoperatively in six patients with colloid cysts, surgically treated with a transcallosal-transgenual approach. Longitudinal connectometry analysis on dMRI data and graph analysis on structural connectivity matrix were implemented to analyze how white matter pathways and structural network topology reorganize after surgery.</AbstractText>Although a significant worsening in cognitive functions (e.g., executive and memory functioning) at early postoperative, a recovery to the preoperative status was observed at 6 months. Connectometry analysis, beyond the decrease of quantitative anisotropy (QA) near the resection cavity, showed an increase of QA in the body and forceps major CC subregions, as well as in the left intra-hemispheric corticocortical associative fibers. Accordingly, a reorganization of structural network topology was observed between centrality increasing in the left hemisphere nodes together with a rise in connectivity strength among mid and posterior CC subregions and cortical nodes.</AbstractText>A structural reorganization of intra- and inter-hemispheric connective fibers and structural network topology were observed following the resection of the genu of the CC. Beyond the postoperative transient cognitive impairment, it could be argued anterior CC resection does not preclude neural plasticity and may subserve the long-term postoperative cognitive recovery.</AbstractText>Copyright © 2022 Ciavarro, Grande, Bevacqua, Morace, Ambrosini, Pavone, Grillea, Vangelista and Esposito.</CopyrightInformation> |
2,329,690 | Prenatal Diagnosis of Otocephaly: A Rare Facial Anomaly. | Otocephaly is a rare malformation characterized by agnathia (absence of the mandible), melotia (medially displaced ear pinna), aglossia (absence of the tongue) and microstomia (small oral aperture). This results due to failure of migration of the neural crest cells and is a defect of the first branchial arch. It is incompatible with life and early prenatal diagnosis is useful.</AbstractText>Our patient a primigravida with 19 weeks 6 days gestation was referred for micrognathia and polyhydramnios. On ultrasound examination, she had unilateral mild ventriculomegaly and posterior fossa cyst in the fetal brain. The fetus had agnathia and anophthalmia. There was an echogenic intracardiac focus and echogenic bowel. The stomach was not seen clearly. This could be due to agnathia and microstomia leading to swallowing difficulties. The patient was explained about the guarded prognosis. The pregnancy was terminated. A diagnosis of otocephaly was made.</AbstractText>Otocephaly is a rare disorder of development of the first branchial arch. The reported incidence is 1 in 70,000. It is mostly lethal due to respiratory difficulties and may be associated with cranial and extracranial malformations. Most case reports have found that it is sporadic and could be due to mutations in the PRRX1 gene. Other anomalies that may be associated with otocephaly are neural tube defects, cephalocele, dysgenesis of corpus callosum, atresia of the third ventricle, midline probocis, hypotelorism, renal ectopia, cyclopia, vertebral and rib abnormalities, tracheo esophageal fistula, cardiac anomalies and adrenal hypoplasia. Most of the cases reported so far were diagnosed in the second or the third trimester. Facial anomaly screening has undergone a huge evolution in the recent years. In addition to the usual facial screening, we recommend mandibular arch screening in the first and early second trimester. If there is a doubt the patient may be called back at 15 to 16 weeks of gestation considering the fact that these anomalies are usually lethal and medical termination is safer earlier in pregnancy than later. MRI may be a handy tool to confirm antenatal diagnosis as it can detect the abnormal ears. Agnathia and polyhydramnios occur together in the third trimester but in the first or second trimester polyhydramnios may not be observed.</AbstractText>Otocephaly, though rare, poses a clinical challenge for both patient and the reporting doctor. Considering the time limitation for termination of pregnancy in our country, early prenatal diagnosis is important. A detailed face evaluation in the first trimester can help detect this defect as early as 11-14 weeks. Early diagnosis of lethal anomalies helps in completing the fetal work up and offering a safer termination. Correct diagnosis and work up of fetal anomalies allows for documentation and awareness of the presence of these conditions in our population.</AbstractText>© Federation of Obstetric & Gynecological Societies of India 2021.</CopyrightInformation> |
2,329,691 | Injuries in Underbody Blast Fatalities: Identification of Five Distinct Mechanisms of Head Injury. | Previous research has shown that injuries to the head and neck were prevalent in 73% of all mounted fatalities of underbody blast. The mechanisms that cause such injuries to the central nervous system (CNS) are not yet known. The aim of this study was to identify the head and spinal injuries in fatalities due to underbody blast (UBB) and then develop hypotheses on the causative mechanisms. All U.K. military fatalities from UBB with an associated head injury that occurred during 2007-2013 in the Iraq and Afghanistan conflicts were identified retrospectively. Computed tomography post-mortems (CTPMs) were interrogated for injuries to the head, neck, and spine. All injuries were documented and classified using a radiology classification. Pearson's chi-square and Fisher's exact tests were used to show a relationship between variables and form a hypothesis for injury mechanisms. There were 50 fatalities from UBB with an associated head injury. Of these, 46 had complete CTPMs available for analysis. Chi-square and Fisher's exact tests showed a relationship between lateral ventricle blood and injuries to the abdomen and thorax. Five partially overlapping injury constellations were identified: 1.multiple-level spinal injury with skull fracture and brainstem injury, 2.peri-mesencephalic hemorrhage, 3.spinal and brainstem injury, 4.parenchymal contusions with injury to C0-C1, and 5.an "eggshell" pattern of fractures from direct impact. These injury constellations can now be used to propose injury mechanisms to develop mitigation strategies or clinical treatments. |
2,329,692 | Effect of cilia-induced surface velocity on cerebrospinal fluid exchange in the lateral ventricles. | Ciliary motility disorders are known to cause hydrocephalus. The instantaneous velocity of cerebrospinal fluid (CSF) flow is dominated by artery pulsation, and it remains unclear why ciliary dysfunction results in hydrocephalus. In this study, we investigated the effects of cilia-induced surface velocity on CSF flow using computational fluid dynamics. A geometric model of the human ventricles was constructed using medical imaging data. The CSF produced by the choroid plexus and cilia-induced surface velocity were given as the velocity boundary conditions at the ventricular walls. We developed healthy and reduced cilia motility models based on experimental data of cilia-induced velocity in healthy wild-type and Dpcd-knockout mice. The results indicate that there is almost no difference in intraventricular pressure between healthy and reduced cilia motility models. Additionally, it was found that newly produced CSF from the choroid plexus did not spread to the anterior and inferior horns of the lateral ventricles in the reduced cilia motility model. These findings suggest that a ciliary motility disorder could delay CSF exchange in the anterior and inferior horns of the lateral ventricles. |
2,329,693 | An induced pluripotent stem cell line (YCMi006-A) generated from a patient with hypertrophic cardiomyopathy who carries the ACTA1 mutation p.Ile343Met.<Pagination><StartPage>102874</StartPage><MedlinePgn>102874</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.scr.2022.102874</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S1873-5061(22)00223-9</ELocationID><Abstract><AbstractText>Hypertrophic cardiomyopathy (HCM) is a common inherited cardiovascular disease and is characterized by hypertrophy of the left ventricle. We reprogrammed peripheral blood mononuclear cells (PBMCs) from a HCM patient into pluripotent stem cells (iPSC) (YCMi006-A) carrying a heterozygous c.1029C > G mutation in ACTA1. The YCMi006-A cells expressed high levels of pluripotent markers, had a normal 46XX karyotype and demonstrated the capacity to differentiate into derivatives of all three germ layers. This cell line can be a valuable tool for investigating the pathogenesis of HCM.</AbstractText><CopyrightInformation>Copyright © 2022 The Author(s). Published by Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Hyoeun</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Biochemistry and Molecular Biology, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul 03722, South Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Hyeong-Jin</ForeName><Initials>HJ</Initials><AffiliationInfo><Affiliation>Department of Biochemistry and Molecular Biology, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul 03722, South Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Oh</LastName><ForeName>Jaewon</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Division of Cardiology, Severance Cardiovascular Hospital, Cardiovascular Research Institute, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul 03722, South Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Seung-Tae</ForeName><Initials>ST</Initials><AffiliationInfo><Affiliation>Department of Laboratory Medicine, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul 03722, South Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Won</LastName><ForeName>Dongju</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Laboratory Medicine, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul 03722, South Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Choi</LastName><ForeName>Hyo-Kyoung</ForeName><Initials>HK</Initials><AffiliationInfo><Affiliation>Research Group of Healthcare, Korea Food Research Institute, Wanju-gun, Jeollabuk-do, 55365, South Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Choi</LastName><ForeName>Jong Rak</ForeName><Initials>JR</Initials><AffiliationInfo><Affiliation>Department of Laboratory Medicine, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul 03722, South Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Sangwoo</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Biomedical Systems Informatics and Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul 03722, South Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Hyoung-Pyo</ForeName><Initials>HP</Initials><AffiliationInfo><Affiliation>Department of Environmental Medical Biology, Institute of Tropical Medicine, Brain Korea 21 PLUS Project for Medical Science, Yonsei Genome Center, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul 03722, South Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Seok-Jun</ForeName><Initials>SJ</Initials><AffiliationInfo><Affiliation>Department of Biomedical Science, Department of Integrative Biological Sciences & BK21 FOUR Educational Research Group for Age-associated Disorder Control Technology, Chosun University, Gwangju 61452, South Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Park</LastName><ForeName>Sahng Wook</ForeName><Initials>SW</Initials><AffiliationInfo><Affiliation>Department of Biochemistry and Molecular Biology, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul 03722, South Korea; Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Brain Korea 21 Project, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul 03722, South Korea. Electronic address: SWPARK64@yuhs.ac.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kang</LastName><ForeName>Seok-Min</ForeName><Initials>SM</Initials><AffiliationInfo><Affiliation>Division of Cardiology, Severance Cardiovascular Hospital, Cardiovascular Research Institute, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul 03722, South Korea. Electronic address: smkang@yuhs.ac.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Seung-Hyun</ForeName><Initials>SH</Initials><AffiliationInfo><Affiliation>Department of Biochemistry and Molecular Biology, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul 03722, South Korea; Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Brain Korea 21 Project, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul 03722, South Korea. Electronic address: tiger815@yuhs.ac.</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>07</Month><Day>28</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Stem Cell Res</MedlineTA><NlmUniqueID>101316957</NlmUniqueID><ISSNLinking>1873-5061</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D002312" MajorTopicYN="Y">Cardiomyopathy, Hypertrophic</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="Y">Cell Line</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D057026" MajorTopicYN="Y">Induced Pluripotent Stem Cells</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007963" MajorTopicYN="N">Leukocytes, Mononuclear</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009154" MajorTopicYN="N">Mutation</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>6</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>7</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>7</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>8</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>8</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>8</Month><Day>2</Day><Hour>18</Hour><Minute>14</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35917599</ArticleId><ArticleId IdType="doi">10.1016/j.scr.2022.102874</ArticleId><ArticleId IdType="pii">S1873-5061(22)00223-9</ArticleId></ArticleIdList></PubmedData></PubmedArticle>
<PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35917584</PMID><DateRevised><Year>2022</Year><Month>08</Month><Day>02</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">2327-9109</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Aug</Month><Day>02</Day></PubDate></JournalIssue><Title>Applied neuropsychology. Adult</Title><ISOAbbreviation>Appl Neuropsychol Adult</ISOAbbreviation></Journal>Impaired recollection and initially preserved familiarity in a patient with bilateral fornix transection following third ventricle colloid cyst removal: A two-year follow-up study. | Hypertrophic cardiomyopathy (HCM) is a common inherited cardiovascular disease and is characterized by hypertrophy of the left ventricle. We reprogrammed peripheral blood mononuclear cells (PBMCs) from a HCM patient into pluripotent stem cells (iPSC) (YCMi006-A) carrying a heterozygous c.1029C > G mutation in ACTA1. The YCMi006-A cells expressed high levels of pluripotent markers, had a normal 46XX karyotype and demonstrated the capacity to differentiate into derivatives of all three germ layers. This cell line can be a valuable tool for investigating the pathogenesis of HCM.<CopyrightInformation>Copyright © 2022 The Author(s). Published by Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Hyoeun</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Biochemistry and Molecular Biology, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul 03722, South Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Hyeong-Jin</ForeName><Initials>HJ</Initials><AffiliationInfo><Affiliation>Department of Biochemistry and Molecular Biology, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul 03722, South Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Oh</LastName><ForeName>Jaewon</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Division of Cardiology, Severance Cardiovascular Hospital, Cardiovascular Research Institute, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul 03722, South Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Seung-Tae</ForeName><Initials>ST</Initials><AffiliationInfo><Affiliation>Department of Laboratory Medicine, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul 03722, South Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Won</LastName><ForeName>Dongju</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Laboratory Medicine, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul 03722, South Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Choi</LastName><ForeName>Hyo-Kyoung</ForeName><Initials>HK</Initials><AffiliationInfo><Affiliation>Research Group of Healthcare, Korea Food Research Institute, Wanju-gun, Jeollabuk-do, 55365, South Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Choi</LastName><ForeName>Jong Rak</ForeName><Initials>JR</Initials><AffiliationInfo><Affiliation>Department of Laboratory Medicine, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul 03722, South Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Sangwoo</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Biomedical Systems Informatics and Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul 03722, South Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Hyoung-Pyo</ForeName><Initials>HP</Initials><AffiliationInfo><Affiliation>Department of Environmental Medical Biology, Institute of Tropical Medicine, Brain Korea 21 PLUS Project for Medical Science, Yonsei Genome Center, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul 03722, South Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Seok-Jun</ForeName><Initials>SJ</Initials><AffiliationInfo><Affiliation>Department of Biomedical Science, Department of Integrative Biological Sciences & BK21 FOUR Educational Research Group for Age-associated Disorder Control Technology, Chosun University, Gwangju 61452, South Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Park</LastName><ForeName>Sahng Wook</ForeName><Initials>SW</Initials><AffiliationInfo><Affiliation>Department of Biochemistry and Molecular Biology, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul 03722, South Korea; Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Brain Korea 21 Project, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul 03722, South Korea. Electronic address: SWPARK64@yuhs.ac.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kang</LastName><ForeName>Seok-Min</ForeName><Initials>SM</Initials><AffiliationInfo><Affiliation>Division of Cardiology, Severance Cardiovascular Hospital, Cardiovascular Research Institute, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul 03722, South Korea. Electronic address: smkang@yuhs.ac.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Seung-Hyun</ForeName><Initials>SH</Initials><AffiliationInfo><Affiliation>Department of Biochemistry and Molecular Biology, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul 03722, South Korea; Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Brain Korea 21 Project, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul 03722, South Korea. Electronic address: tiger815@yuhs.ac.</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>07</Month><Day>28</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Stem Cell Res</MedlineTA><NlmUniqueID>101316957</NlmUniqueID><ISSNLinking>1873-5061</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D002312" MajorTopicYN="Y">Cardiomyopathy, Hypertrophic</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="Y">Cell Line</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D057026" MajorTopicYN="Y">Induced Pluripotent Stem Cells</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007963" MajorTopicYN="N">Leukocytes, Mononuclear</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009154" MajorTopicYN="N">Mutation</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>6</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>7</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>7</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>8</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>8</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>8</Month><Day>2</Day><Hour>18</Hour><Minute>14</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35917599</ArticleId><ArticleId IdType="doi">10.1016/j.scr.2022.102874</ArticleId><ArticleId IdType="pii">S1873-5061(22)00223-9</ArticleId></ArticleIdList></PubmedData></PubmedArticle>
<PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35917584</PMID><DateRevised><Year>2022</Year><Month>08</Month><Day>02</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">2327-9109</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Aug</Month><Day>02</Day></PubDate></JournalIssue><Title>Applied neuropsychology. Adult</Title><ISOAbbreviation>Appl Neuropsychol Adult</ISOAbbreviation></Journal><ArticleTitle>Impaired recollection and initially preserved familiarity in a patient with bilateral fornix transection following third ventricle colloid cyst removal: A two-year follow-up study.</ArticleTitle><Pagination><StartPage>1</StartPage><EndPage>13</EndPage><MedlinePgn>1-13</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1080/23279095.2022.2104162</ELocationID><Abstract><AbstractText Label="OBJECTIVE" NlmCategory="UNASSIGNED">Recognition memory is widely accepted as a dual process-based model, namely familiarity and recollection. However, the location of their specific neurobiological substrates remains unclear. Similar to hippocampal damage, fornix damage has been associated with recollection memory but not familiarity memory deficits. To understand the neural basis of recognition memory, determining the importance of the fornix and its hippocampal connections is essential.<AbstractText Label="METHODS" NlmCategory="UNASSIGNED">Recognition memory was examined in a 45-year-old male who underwent a complete bilateral fornix section following the removal of a third ventricle colloid cyst. The application of familiarity and recollection for recognition memory decisions was investigated <i>via</i> an immediate and delayed associative recognition test and an immediate and delayed forced-choice task in the patient and a control group (<i>N</i> = 15) over a two-year follow-up period. Complete demographic, neuropsychological, neuropsychiatric, and neuroradiological characterizations of this patient were performed.<AbstractText Label="RESULTS" NlmCategory="UNASSIGNED">Persistent immediate and delayed verbal recollection memory deficits were observed in the patient. Moreover, delayed familiarity-based recognition memory declined gradually over the follow-up period, immediate familiarity-based recognition memory was unaffected, and reduced non-verbal memory improved.<AbstractText Label="CONCLUSION" NlmCategory="UNASSIGNED">The present findings support models that the extended hippocampal system, including the fornices, does not appear to play a role in familiarity memory but is particularly important for recollection memory. Moreover, our study suggests that bilateral fornix transection may be associated with relatively functional recovery of non-verbal memory. |
2,329,694 | Inhibition of Dyrk1A Attenuates LPS-Induced Neuroinflammation via the TLR4/NF-κB P65 Signaling Pathway. | Dual-specificity tyrosine phosphorylation-regulated kinase 1A (Dyrk1A) is a highly conserved protein kinase, playing a key role in the regulation of physiological brain functions and pathological processes. In Alzheimer's disease (AD), Dyrk1A promotes hyperphosphorylation of tau protein and abnormal aggregation of amyloid-β protein (Aβ). This study investigated the role of Dyrk1A in regulating neuroinflammation, another critical factor that contributes to AD. In the present study, we used an immortalized murine BV2 microglia cell line induced by lipopolysaccharide (LPS) to study neuroinflammation. The expression and activity of Dyrk1A kinase were both increased by inflammation. Dyrk1A inhibition using harmine or siRNA silencing significantly reduced the production of proinflammatory factors in LPS-stimulated BV2 cells. Reactive oxygen species (ROS), tumor necrosis factor-α (TNF-α), and nitric oxide (NO), as well as the expression of the inflammatory proteins, cyclooxygenase 2 (COX2), and inducible nitric synthase (iNOS), were attenuated. In vivo, in ICR mice injected with LPS into the left lateral cerebral ventricle, harmine (20 mg/kg) administration decreased the expression of inflammatory proteins in the cortex and hippocampus of mice brain. In addition, immunohistochemical detection of ionized calcium-binding adapter molecule 1 (Iba1) and Nissl staining showed that harmine significantly attenuated microglia activation and neuronal damage in the CA1 region of hippocampus. Further mechanistic studies indicated that Dyrk1A suppression may be related to inhibition of the TLR4/NF-κB signaling pathway in LPS-induced neuroinflammation. Taken together, our studies suggest that Dyrk1A may be a novel target for the treatment of neurodegenerative diseases with an inflammatory component. |
2,329,695 | Lumbar-peritoneal shunt for idiopathic normal pressure hydrocephalus and secondary normal pressure hydrocephalus. | Normal-pressure hydrocephalus is a clinical syndrome consisting of dilated cerebral ventricles with the clinical triad of gait disturbance, cognitive impairment and/or urinary dysfunction. Lumbar-peritoneal (LP) shunt could improve idiopathic normal pressure hydrocephalus (iNPH) while its effectiveness on secondary NPH (sNPH) is elusive. We compared the clinical results of the patients who received LP shunt surgery between iNPH and sNPH.</AbstractText>We retrospectively analyzed the patients who received LP shunt surgery in a single center from January 1, 2017, to June 30, 2017. Patients selected for LP shunt placement had at least two of three cardinal symptoms of iNPH. The symptoms should persist for more than 3 months with compatible brain magnetic resonance imaging findings. All patients were followed up with iNPH grading scale (iNPHGS) and Modified Rankin Scale (MRS) for evaluation.</AbstractText>Thirty-three patients (23 male and 10 female patients) with mean age 76-year-old completed follow-up in this study, and 17 patients received lumbar drainage tests and intracranial pressure measurements. Both iNPH (n</i> = 22) and sNPH (n</i> = 11) groups did not have major complications such as infection, nerve root injury, or shunt failure. Both groups have significant improvement in iNPHGS and MRS. Interestingly, we found the correlation between both opening intracranial pressure and pressure gradient difference to the improvement percentage from LP shunt.</AbstractText>The safety and effectiveness for sNPH patients who received LP shunt placement are equivalent to the iNPH patients. Lumbar drainage test provides prerequisite outcome prediction and should be considered to identify NPH patients planned to receive LP shunt.</AbstractText>Copyright: © 2021 Tzu Chi Medical Journal.</CopyrightInformation> |
2,329,696 | Normal Echocardiographic Reference Values of the Right Ventricular to Left Ventricular Endsystolic Diameter Ratio and the Left Ventricular Endsystolic Eccentricity Index in Healthy Children and in Children With Pulmonary Hypertension. | An accurate assessment of the right and left ventricle and their interaction is important in pediatric pulmonary hypertension (PH). Our objective was to provide normal reference values for the right ventricular to left ventricular endsystolic (RV/LVes) ratio and the LV endsystolic eccentricity index (LVes EI) in healthy children and in children with PH.</AbstractText>We conducted an echocardiographic study in 769 healthy children (median age: 3.36 years; range: 1 day-18 years) and validated abnormal values in 44 children with PH (median age: 2.1 years; range: 0.1 months-17.7 years). We determined the effects of gender, age, body length, body weight, and body surface area (BSA) on RV/LVes ratio and LVes EI values. The RV/LVes ratio and LVes EI were measured from the parasternal short axis view between papillary muscle from the endocardial to endocardial surfaces.</AbstractText>Both, the RV/LVes ratio and the LVes EI were highly age-dependent: (i) neonates RV/LVes ratio [median 0.83 (range 0.53-1.37)], LVes EI [1.21 (0.92-1.45)]; (ii) 12-24 months old: RV/LVes ratio: [0.55 (0.35-0.80)], LVes EI: [1.0 (0.88-1.13)]; iii) 18th year of life RV/LVes ratio: [0.53 (0.32-0.74)], LVes EI: [1.0 (0.97-1.07)]. Healthy neonates had high LVes EI and RV/LVes ratios, both gradually decreased within the first year of life and until BSA values of about 0.5 m2</sup>, body weight to about 15 kg and body length to about 75 cm, but were almost constant thereafter. Children (>1 year) and adolescents with PH had significantly higher RV/LVes ratio (no PH: median 0.55, IQR 0.49-0.60; PH: 1.02, 0.87-1.26; p</i> < 0.001) and higher LVes EI values (no PH: 1.00, 0.98-1.00; PH: 1.53, 1.26-1.71; p</i> < 0.001) compared to those without PH. To predict the presence of PH in children > 1 year, we found the following best cutoff values: RV/LVes ratio ≥ 0.67 (sensitivity: 1.00, specificity: 0.95) and LVes EI ≥ 1.06 (sensitivity: 1.00, specificity: 0.97).</AbstractText>We provide normal echocardiographic reference values of the RV/LVes ratio and LVes EI in healthy children, as well as statistically determined cutoffs for the increased values in children with PH.</AbstractText>Copyright © 2022 Schweintzger, Kurath-Koller, Burmas, Grangl, Fandl, Noessler, Avian, Gamillscheg, Chouvarine, Hansmann and Koestenberger.</CopyrightInformation> |
2,329,697 | Improved Ca<sup>2+</sup> release synchrony following selective modification of I<sub>tof</sub> and phase 1 repolarization in normal and failing ventricular myocytes.<Pagination><StartPage>52</StartPage><EndPage>62</EndPage><MedlinePgn>52-62</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.yjmcc.2022.07.009</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0022-2828(22)00146-8</ELocationID><Abstract><AbstractText>Loss of ventricular action potential (AP) early phase 1 repolarization may contribute to the impaired Ca<sup>2+</sup> release and increased risk of sudden cardiac death in heart failure. Therefore, restoring AP phase 1 by augmenting the fast transient outward K<sup>+</sup> current (I<sub>tof</sub>) might be beneficial, but direct experimental evidence to support this proposition in failing cardiomyocytes is limited. Dynamic clamp was used to selectively modulate the contribution of I<sub>tof</sub> to the AP and Ca<sup>2+</sup> transient in both normal (guinea pig and rabbit) and in failing rabbit cardiac myocytes. Opposing native I<sub>tof</sub> in non-failing rabbit myocytes increased Ca<sup>2+</sup> release heterogeneity, late Ca<sup>2+</sup> sparks (LCS) frequency and AP duration. (APD). In contrast, increasing I<sub>tof</sub> in failing myocytes and guinea pig myocytes (the latter normally lacking I<sub>tof</sub>) increased Ca<sup>2+</sup> transient amplitude, Ca<sup>2+</sup> release synchrony, and shortened APD. Computer simulations also showed faster Ca<sup>2+</sup> transient decay (mainly due to fewer LCS), decreased inward Na<sup>+</sup>/Ca<sup>2+</sup> exchange current and APD. When the I<sub>tof</sub> conductance was increased to ~0.2 nS/pF in failing cells (a value slightly greater than seen in typical human epicardial myocytes), Ca<sup>2+</sup> release synchrony improved and AP duration decreased slightly. Further increases in I<sub>tof</sub> can cause Ca<sup>2+</sup> release to decrease as the peak of the bell-shaped I<sub>Ca</sub>-voltage relationship is passed and premature AP repolarization develops. These results suggest that there is an optimal range for I<sub>tof</sub> enhancement that may support Ca<sup>2+</sup> release synchrony and improve electrical stability in heart failure with the caveat that uncontrolled I<sub>tof</sub> enhancement should be avoided.</AbstractText><CopyrightInformation>Copyright © 2022 The Authors. Published by Elsevier Ltd.. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Fowler</LastName><ForeName>Ewan D</ForeName><Initials>ED</Initials><AffiliationInfo><Affiliation>School of Physiology, Pharmacology & Neuroscience, Faculty of Biomedical Sciences, University of Bristol, University Walk, Bristol BS8 1TD, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Nan</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>School of Physiology, Pharmacology & Neuroscience, Faculty of Biomedical Sciences, University of Bristol, University Walk, Bristol BS8 1TD, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hezzell</LastName><ForeName>Melanie J</ForeName><Initials>MJ</Initials><AffiliationInfo><Affiliation>University of Bristol Veterinary School, Langford, Bristol BS40 5DU, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chanoit</LastName><ForeName>Guillaume</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>University of Bristol Veterinary School, Langford, Bristol BS40 5DU, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hancox</LastName><ForeName>Jules C</ForeName><Initials>JC</Initials><AffiliationInfo><Affiliation>School of Physiology, Pharmacology & Neuroscience, Faculty of Biomedical Sciences, University of Bristol, University Walk, Bristol BS8 1TD, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cannell</LastName><ForeName>Mark B</ForeName><Initials>MB</Initials><AffiliationInfo><Affiliation>School of Physiology, Pharmacology & Neuroscience, Faculty of Biomedical Sciences, University of Bristol, University Walk, Bristol BS8 1TD, UK. Electronic address: mark.cannell@bristol.ac.uk.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>MR/N002903/1</GrantID><Acronym>MRC_</Acronym><Agency>Medical Research Council</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>PG/15/106/31915</GrantID><Acronym>BHF_</Acronym><Agency>British Heart Foundation</Agency><Country>United Kingdom</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D017426">Clinical Trial, Phase I</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>07</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Mol Cell Cardiol</MedlineTA><NlmUniqueID>0262322</NlmUniqueID><ISSNLinking>0022-2828</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>9NEZ333N27</RegistryNumber><NameOfSubstance UI="D012964">Sodium</NameOfSubstance></Chemical><Chemical><RegistryNumber>SY7Q814VUP</RegistryNumber><NameOfSubstance UI="D002118">Calcium</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011817" MajorTopicYN="N">Rabbits</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006168" MajorTopicYN="N">Guinea Pigs</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D032383" MajorTopicYN="Y">Myocytes, Cardiac</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000200" MajorTopicYN="N">Action Potentials</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006333" MajorTopicYN="Y">Heart Failure</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012964" MajorTopicYN="N">Sodium</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002118" MajorTopicYN="N">Calcium</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Arrhythmias</Keyword><Keyword MajorTopicYN="N">Calcium cycling/excitation-contraction coupling</Keyword><Keyword MajorTopicYN="N">Electrophysiology</Keyword><Keyword MajorTopicYN="N">Heart failure</Keyword><Keyword MajorTopicYN="N">Sudden cardiac death</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>3</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>7</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>7</Month><Day>20</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>8</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>11</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>7</Month><Day>31</Day><Hour>19</Hour><Minute>23</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35908686</ArticleId><ArticleId IdType="doi">10.1016/j.yjmcc.2022.07.009</ArticleId><ArticleId IdType="pii">S0022-2828(22)00146-8</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedBookArticle><BookDocument><PMID Version="1">32644681</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK559255</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-20993">Elevated Hemidiaphragm<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Patel</LastName><ForeName>Paula R.</ForeName><Initials>PR</Initials><AffiliationInfo><Affiliation>Wyckoff Heights Medical Center</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bechmann</LastName><ForeName>Samuel</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>New Jersey Medical School</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>The diaphragm is a thin, dome-shaped muscular structure that functions as a respiratory pump and is the primary muscle for inspiration. Elevated hemidiaphragm occurs when one side of the diaphragm becomes weak from muscular disease or loss of innervation due to phrenic nerve injury. Patients may present with difficulty breathing, but more commonly elevated hemidiaphragm is found on imaging as an incidental finding, and patients are asymptomatic. The phrenic nerve runs in the fascia over the anterior scalene muscle. An anesthesiologist commonly performs interscalene blocks for shoulder surgery, such as a rotator cuff repair, humeral fracture, total shoulder replacement, and other arm surgery. phrenic nerve paralysis is a known complication from the interscalene block. It has been observed in many case reports and series in both anesthesia and neurosurgical literature, but only a single case report in the emergency medicine literature. The diaphragm is the primary muscle for inspiration along with secondary muscles such as the sternocleidomastoid, external intercostals, and scalene muscles. During inspiration, the diaphragm flattens pulling air into the lungs, whereas during expiration, the diaphragm relaxes, allowing air to flow out of the lungs passively. As the diaphragm flattens during inspiration subatmospheric, negative pressure is created within the thoracic cavity that overcomes atmospheric pressure.  This forms a vacuum that facilitates the movement of air into the lungs. Also, as the diaphragm contracts, the floor of the thoracic cavity moves downward, and the walls move outward. This causes inflation of the lungs and allows for gas exchange to occur. As the diaphragm relaxes, the tension on the chest wall muscles decreases, causing the muscles to recoil and passively push the air out during expiration. The diaphragm has three points of origin, creating a C shape that culminates in a stable, dense fibrous center tendon. The sternal group of muscle fibers is attached to the posterior aspect of the xiphoid process. The costal group of muscle fibers originates from the inner surface of seven to twelfth ribs. The lumbar group of muscular fibers arises from the medial and lateral arcuate ligaments and anterior longitudinal ligament, and lumbar vertebral bodies of L2-L3. There are three openings in the diaphragm, allowing structures to pass between the thoracic and abdominal cavity. The esophageal hiatus through which the esophagus and vagus nerve pass, the aortic hiatus through which the aorta, azygos vein and thoracic duct pass, and the caval hiatus through which the inferior vena cava passes. The diaphragm anatomically separates the thoracic cavity from the abdominal cavity, making the diaphragm the base of the thoracic cavity and the apex of the abdominal cavity. The diaphragm is separated into the right and left half. Each side has it's own blood supply from the inferior and superior phrenic arteries arising directly from the aorta, subcostal and intercostal arteries. Phrenic veins drain blood from the diaphragm directly into the inferior vena cava. The diaphragm is innervated by the ipsilateral phrenic nerve that arises from the cervical nerve roots of C3-C5. The phrenic nerve emerges through the anterior scalene muscle on either side of the neck and courses posteriorly to the subclavian vein. Both phrenic nerves enter into the thoracic cavity through the thoracic aperture. In the thoracic cavity, the right and left phrenic nerves follow different paths. The right phrenic nerve descends anteriorly over the right atrium of the heart and exits through the inferior vena cava opening to innervate the inferior surface of the hemidiaphragm. The left phrenic nerve crosses the aortic arch and pericardium overlying the left ventricle until it pierces through the diaphragm to innervate the inferior surface of the left hemidiaphragm. Sensory innervation of the diaphragm is from the intercostal nerves 6-11. Elevated Hemidiaphragm is a condition where one portion of the diaphragm is higher than the other. Often elevated hemidiaphragm is asymptomatic and visualized as an incidental finding on radiologic studies like chest X-ray or chest CT (computed tomography). Patients are typically asymptomatic due to the compensation and recruitment of other inspiratory muscles, and often the healthy hemidiaphragm compensates to maintain the pressure gradient required for adequate gas exchange. However, evidence suggests that the function of the contralateral, healthy hemidiaphragm may be impacted by lower abdominal pressure. In severe cases of unilateral hemidiaphragm paralysis, patients may lose their inspiratory capacity, which can impair the ability of the heart to pump efficiently. Under normal circumstances, the intrathoracic pressure and contraction of the diaphragm overcome the force of gravity and propel blood into the right atrium from the inferior vena cava (IVC). When the pressure gradient cannot be maintained, the right atrium will collapse, and the patient may present as though they have cardiac tamponade. Accurate diagnosis, treatment, and management of elevated hemidiaphragm are essential in patients presenting with dyspnea and multi-organ involvement.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-20993" sec="article-20993.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-20993" sec="article-20993.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-20993" sec="article-20993.s3">Etiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-20993" sec="article-20993.s4">Epidemiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-20993" sec="article-20993.s5">Pathophysiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-20993" sec="article-20993.s6">History and Physical</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-20993" sec="article-20993.s7">Evaluation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-20993" sec="article-20993.s8">Treatment / Management</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-20993" sec="article-20993.s9">Differential Diagnosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-20993" sec="article-20993.s10">Prognosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-20993" sec="article-20993.s11">Complications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-20993" sec="article-20993.s12">Consultations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-20993" sec="article-20993.s13">Deterrence and Patient Education</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-20993" sec="article-20993.s14">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-20993" sec="article-20993.s15">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-20993" sec="article-20993.s17">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>8</Month><Day>1</Day></ContributionDate><ReferenceList><Reference><Citation>Roussos C, Macklem PT. 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J Trauma Acute Care Surg. 2014 Feb;76(2):303-9; discussion 309-10.</Citation><ArticleIdList><ArticleId IdType="pubmed">24458038</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32644681</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">29763051</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK499876</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-28599">Right Ventricular Hypertrophy<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Bhattacharya</LastName><ForeName>Priyanka T.</ForeName><Initials>PT</Initials><AffiliationInfo><Affiliation>University of Pennsylvania</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ellison</LastName><ForeName>Matthew B.</ForeName><Initials>MB</Initials><AffiliationInfo><Affiliation>WVU Medicine</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>Right ventricular hypertrophy (RVH) is an abnormal enlargement or pathologic increase in muscle mass of the right ventricle in response to pressure overload, most commonly due to severe lung disease. The right ventricle is considerably smaller than the left ventricle and produces electrical forces that are largely obscured by those generated by the larger left ventricle. Size and function of the right ventricle are adversely affected by the following: Pulmonary hypertension with or without left ventricular dysfunction. Conditions that affect the tricuspid valve leading to significant tricuspid regurgitation (TR). <b>Anatomy and Physiology</b> The right ventricle is composed of inflow (sinus) and outflow (conus) regions, separated by a muscular ridge, the crista supraventricularis. The inflow region includes the tricuspid valve (TV), the chordae/papillary muscles as well as the body of the RV. The RV body boundaries are formed by the RV free wall, extending from the interventricular septum's anterior and posterior aspects. The standard septal curvature convexes toward the RV cavity and imparts a crescent shape to the right ventricle when cross-sectioned. The RV's interior surface is heavily trabeculated; this feature along with the moderator band and more apical insertion of the TV-annulus impart key morphologic differences that distinguish the RV from the LV by echocardiography. In contrast, the infundibulum is a smooth, funnel-shaped outflow portion of the RV that ends at the pulmonic valve. Thus, the RV has a complex geometry, with traditional RV free-wall thickness of 0.3-0.5 cm, imparting greater distensibility and larger cavity volumes in the RV versus the LV, despite lower end-diastolic filling pressures. This translates to an RVEF that is typically 35% to 45% (versus 55% to 65% in the LV) yet generates the identical SV as the LV. Changes in preload, afterload, and intrinsic contractility of the ventricle influence the systolic function of the RV, like the LV. Differences in RV muscle fiber orientation dictate that the body of the RV shortens symmetrically in the longitudinal and radial planes; thus, longitudinal shortening accounts for a much larger proportion of RV ejection than in the LV. The relatively conspicuous RV shortening along the longitudinal axis can measure RV systolic function using uncomplicated techniques that do not require geometric assumptions or meticulous endocardial definition, both being known limitations to the noninvasive assessment of RV systolic function.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-28599" sec="article-28599.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28599" sec="article-28599.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28599" sec="article-28599.s3">Etiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28599" sec="article-28599.s4">Epidemiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28599" sec="article-28599.s5">Pathophysiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28599" sec="article-28599.s6">History and Physical</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28599" sec="article-28599.s7">Evaluation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28599" sec="article-28599.s8">Treatment / Management</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28599" sec="article-28599.s9">Differential Diagnosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28599" sec="article-28599.s10">Staging</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28599" sec="article-28599.s11">Prognosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28599" sec="article-28599.s12">Pearls and Other Issues</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28599" sec="article-28599.s13">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28599" sec="article-28599.s14">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28599" sec="article-28599.s19">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>8</Month><Day>1</Day></ContributionDate><ReferenceList><Reference><Citation>Keramida K, Lazaros G, Nihoyannopoulos P. 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PLoS One. 2017;12(3):e0174118.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC5360271</ArticleId><ArticleId IdType="pubmed">28323875</ArticleId></ArticleIdList></Reference><Reference><Citation>Anand V, Garg S, Duval S, Thenappan T. A systematic review and meta-analysis of trials using statins in pulmonary arterial hypertension. Pulm Circ. 2016 Sep;6(3):295-301.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC5019082</ArticleId><ArticleId IdType="pubmed">27683606</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">29763051</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">29489250</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK482119</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-23440">Increased Intracranial Pressure<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Pinto</LastName><ForeName>Venessa L.</ForeName><Initials>VL</Initials><AffiliationInfo><Affiliation>Baylor College of Medicine</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tadi</LastName><ForeName>Prasanna</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Asram Medical College, Eluru, India</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Adeyinka</LastName><ForeName>Adebayo</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>The Brooklyn Hospital Center</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>Intracranial hypertension (IH) is a clinical condition that is associated with an elevation of the pressures within the cranium. The pressure in the cranial vault is measured in millimeters of mercury (mm Hg) and is normally less than 20 mm Hg. The cranium is a rigid structure that contains three main components: brain, cerebrospinal fluid, and blood. Any increase in the volume of its contents will increase the pressure within the cranial vault. The Monroe-Kellie Doctrine states that the contents of the cranium are in a state of constant volume. That is, the total volumes of the brain tissues, cerebrospinal fluid (CSF), and intracranial blood are fixed. An increase in the volume of one component will result in a decrease in volume in one or two of the other components. The clinical implication of the change in volume of the component is a decrease in cerebral blood flow or herniation of the brain. CSF is a clear fluid found in the subarachnoid spaces and ventricles that cushions the brain and spinal cord. It is secreted by the choroid plexus in the lateral ventricles, travels to the third ventricle via the foramen of Monroe. From the third ventricle, CSF reaches the fourth ventricle through the aqueduct of Sylvius. From here, it flows into the subarachnoid space via the foramina of Magendie and Luschka and is eventually reabsorbed into the dural venous sinuses by arachnoid granulation.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-23440" sec="article-23440.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23440" sec="article-23440.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23440" sec="article-23440.s3">Etiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23440" sec="article-23440.s4">Epidemiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23440" sec="article-23440.s5">Pathophysiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23440" sec="article-23440.s6">History and Physical</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23440" sec="article-23440.s7">Evaluation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23440" sec="article-23440.s8">Treatment / Management</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23440" sec="article-23440.s9">Differential Diagnosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23440" sec="article-23440.s10">Prognosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23440" sec="article-23440.s11">Deterrence and Patient Education</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23440" sec="article-23440.s12">Pearls and Other Issues</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23440" sec="article-23440.s13">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23440" sec="article-23440.s14">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23440" sec="article-23440.s15">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>8</Month><Day>1</Day></ContributionDate><ReferenceList><Reference><Citation>Mokri B. 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Anesth Analg. 2017 Dec;125(6):1999-2008.</Citation><ArticleIdList><ArticleId IdType="pubmed">28806209</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">29489250</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">28613702</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK431048</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-28600">Right Ventricular Myocardial Infarction<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Jeffers</LastName><ForeName>Jeremiah L.</ForeName><Initials>JL</Initials><AffiliationInfo><Affiliation>WVU Medicine</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Boyd</LastName><ForeName>Katharine L.</ForeName><Initials>KL</Initials><AffiliationInfo><Affiliation>Wyckoff Heights Medical Center</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Parks</LastName><ForeName>Lance J.</ForeName><Initials>LJ</Initials><AffiliationInfo><Affiliation>West Virginia University</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>Infarction of the right ventricle with or without left ventricular involvement is becoming a more commonly diagnosed entity as the tools for diagnosis and options for treatment evolves. This activity will discuss the pertinent topics related to the pathophysiology, diagnosis, and treatment of right ventricular myocardial infarction (RVMI). RVMI was first identified in patients with inferior wall MI who had elevated right ventricular (RV) filling pressures and RV failure, with normal values for the left ventricle (LV). RVMI can occur with or without LV involvement. When inferior MI is associated with RVMI, patients show more bradycardia, need for pacing, hypotension, and mortality.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-28600" sec="article-28600.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28600" sec="article-28600.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28600" sec="article-28600.s3">Etiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28600" sec="article-28600.s4">Epidemiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28600" sec="article-28600.s5">Pathophysiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28600" sec="article-28600.s6">History and Physical</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28600" sec="article-28600.s7">Evaluation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28600" sec="article-28600.s8">Treatment / Management</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28600" sec="article-28600.s9">Differential Diagnosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28600" sec="article-28600.s10">Prognosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28600" sec="article-28600.s11">Pearls and Other Issues</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28600" sec="article-28600.s12">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28600" sec="article-28600.s13">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28600" sec="article-28600.s15">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>8</Month><Day>1</Day></ContributionDate><ReferenceList><Reference><Citation>Mactier I, Dalzell JR, Carrick D. 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Int J Cardiovasc Imaging. 2019 Jan;35(1):77-85.</Citation><ArticleIdList><ArticleId IdType="pubmed">30109454</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">28613702</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35907200</PMID><DateRevised><Year>2023</Year><Month>05</Month><Day>10</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1933-0715</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Jul</Month><Day>29</Day></PubDate></JournalIssue><Title>Journal of neurosurgery. Pediatrics</Title><ISOAbbreviation>J Neurosurg Pediatr</ISOAbbreviation></Journal>Endoscopic third ventriculostomy in previously shunt-treated patients. | Loss of ventricular action potential (AP) early phase 1 repolarization may contribute to the impaired Ca<sup>2+</sup> release and increased risk of sudden cardiac death in heart failure. Therefore, restoring AP phase 1 by augmenting the fast transient outward K<sup>+</sup> current (I<sub>tof</sub>) might be beneficial, but direct experimental evidence to support this proposition in failing cardiomyocytes is limited. Dynamic clamp was used to selectively modulate the contribution of I<sub>tof</sub> to the AP and Ca<sup>2+</sup> transient in both normal (guinea pig and rabbit) and in failing rabbit cardiac myocytes. Opposing native I<sub>tof</sub> in non-failing rabbit myocytes increased Ca<sup>2+</sup> release heterogeneity, late Ca<sup>2+</sup> sparks (LCS) frequency and AP duration. (APD). In contrast, increasing I<sub>tof</sub> in failing myocytes and guinea pig myocytes (the latter normally lacking I<sub>tof</sub>) increased Ca<sup>2+</sup> transient amplitude, Ca<sup>2+</sup> release synchrony, and shortened APD. Computer simulations also showed faster Ca<sup>2+</sup> transient decay (mainly due to fewer LCS), decreased inward Na<sup>+</sup>/Ca<sup>2+</sup> exchange current and APD. When the I<sub>tof</sub> conductance was increased to ~0.2 nS/pF in failing cells (a value slightly greater than seen in typical human epicardial myocytes), Ca<sup>2+</sup> release synchrony improved and AP duration decreased slightly. Further increases in I<sub>tof</sub> can cause Ca<sup>2+</sup> release to decrease as the peak of the bell-shaped I<sub>Ca</sub>-voltage relationship is passed and premature AP repolarization develops. These results suggest that there is an optimal range for I<sub>tof</sub> enhancement that may support Ca<sup>2+</sup> release synchrony and improve electrical stability in heart failure with the caveat that uncontrolled I<sub>tof</sub> enhancement should be avoided.<CopyrightInformation>Copyright © 2022 The Authors. Published by Elsevier Ltd.. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Fowler</LastName><ForeName>Ewan D</ForeName><Initials>ED</Initials><AffiliationInfo><Affiliation>School of Physiology, Pharmacology & Neuroscience, Faculty of Biomedical Sciences, University of Bristol, University Walk, Bristol BS8 1TD, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Nan</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>School of Physiology, Pharmacology & Neuroscience, Faculty of Biomedical Sciences, University of Bristol, University Walk, Bristol BS8 1TD, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hezzell</LastName><ForeName>Melanie J</ForeName><Initials>MJ</Initials><AffiliationInfo><Affiliation>University of Bristol Veterinary School, Langford, Bristol BS40 5DU, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chanoit</LastName><ForeName>Guillaume</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>University of Bristol Veterinary School, Langford, Bristol BS40 5DU, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hancox</LastName><ForeName>Jules C</ForeName><Initials>JC</Initials><AffiliationInfo><Affiliation>School of Physiology, Pharmacology & Neuroscience, Faculty of Biomedical Sciences, University of Bristol, University Walk, Bristol BS8 1TD, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cannell</LastName><ForeName>Mark B</ForeName><Initials>MB</Initials><AffiliationInfo><Affiliation>School of Physiology, Pharmacology & Neuroscience, Faculty of Biomedical Sciences, University of Bristol, University Walk, Bristol BS8 1TD, UK. Electronic address: mark.cannell@bristol.ac.uk.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>MR/N002903/1</GrantID><Acronym>MRC_</Acronym><Agency>Medical Research Council</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>PG/15/106/31915</GrantID><Acronym>BHF_</Acronym><Agency>British Heart Foundation</Agency><Country>United Kingdom</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D017426">Clinical Trial, Phase I</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>07</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Mol Cell Cardiol</MedlineTA><NlmUniqueID>0262322</NlmUniqueID><ISSNLinking>0022-2828</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>9NEZ333N27</RegistryNumber><NameOfSubstance UI="D012964">Sodium</NameOfSubstance></Chemical><Chemical><RegistryNumber>SY7Q814VUP</RegistryNumber><NameOfSubstance UI="D002118">Calcium</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011817" MajorTopicYN="N">Rabbits</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006168" MajorTopicYN="N">Guinea Pigs</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D032383" MajorTopicYN="Y">Myocytes, Cardiac</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000200" MajorTopicYN="N">Action Potentials</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006333" MajorTopicYN="Y">Heart Failure</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012964" MajorTopicYN="N">Sodium</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002118" MajorTopicYN="N">Calcium</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Arrhythmias</Keyword><Keyword MajorTopicYN="N">Calcium cycling/excitation-contraction coupling</Keyword><Keyword MajorTopicYN="N">Electrophysiology</Keyword><Keyword MajorTopicYN="N">Heart failure</Keyword><Keyword MajorTopicYN="N">Sudden cardiac death</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>3</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>7</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>7</Month><Day>20</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>8</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>11</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>7</Month><Day>31</Day><Hour>19</Hour><Minute>23</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35908686</ArticleId><ArticleId IdType="doi">10.1016/j.yjmcc.2022.07.009</ArticleId><ArticleId IdType="pii">S0022-2828(22)00146-8</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedBookArticle><BookDocument><PMID Version="1">32644681</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK559255</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-20993">Elevated Hemidiaphragm</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Patel</LastName><ForeName>Paula R.</ForeName><Initials>PR</Initials><AffiliationInfo><Affiliation>Wyckoff Heights Medical Center</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bechmann</LastName><ForeName>Samuel</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>New Jersey Medical School</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>The diaphragm is a thin, dome-shaped muscular structure that functions as a respiratory pump and is the primary muscle for inspiration. Elevated hemidiaphragm occurs when one side of the diaphragm becomes weak from muscular disease or loss of innervation due to phrenic nerve injury. Patients may present with difficulty breathing, but more commonly elevated hemidiaphragm is found on imaging as an incidental finding, and patients are asymptomatic. The phrenic nerve runs in the fascia over the anterior scalene muscle. An anesthesiologist commonly performs interscalene blocks for shoulder surgery, such as a rotator cuff repair, humeral fracture, total shoulder replacement, and other arm surgery. phrenic nerve paralysis is a known complication from the interscalene block. It has been observed in many case reports and series in both anesthesia and neurosurgical literature, but only a single case report in the emergency medicine literature. The diaphragm is the primary muscle for inspiration along with secondary muscles such as the sternocleidomastoid, external intercostals, and scalene muscles. During inspiration, the diaphragm flattens pulling air into the lungs, whereas during expiration, the diaphragm relaxes, allowing air to flow out of the lungs passively. As the diaphragm flattens during inspiration subatmospheric, negative pressure is created within the thoracic cavity that overcomes atmospheric pressure.  This forms a vacuum that facilitates the movement of air into the lungs. Also, as the diaphragm contracts, the floor of the thoracic cavity moves downward, and the walls move outward. This causes inflation of the lungs and allows for gas exchange to occur. As the diaphragm relaxes, the tension on the chest wall muscles decreases, causing the muscles to recoil and passively push the air out during expiration. The diaphragm has three points of origin, creating a C shape that culminates in a stable, dense fibrous center tendon. The sternal group of muscle fibers is attached to the posterior aspect of the xiphoid process. The costal group of muscle fibers originates from the inner surface of seven to twelfth ribs. The lumbar group of muscular fibers arises from the medial and lateral arcuate ligaments and anterior longitudinal ligament, and lumbar vertebral bodies of L2-L3. There are three openings in the diaphragm, allowing structures to pass between the thoracic and abdominal cavity. The esophageal hiatus through which the esophagus and vagus nerve pass, the aortic hiatus through which the aorta, azygos vein and thoracic duct pass, and the caval hiatus through which the inferior vena cava passes. The diaphragm anatomically separates the thoracic cavity from the abdominal cavity, making the diaphragm the base of the thoracic cavity and the apex of the abdominal cavity. The diaphragm is separated into the right and left half. Each side has it's own blood supply from the inferior and superior phrenic arteries arising directly from the aorta, subcostal and intercostal arteries. Phrenic veins drain blood from the diaphragm directly into the inferior vena cava. The diaphragm is innervated by the ipsilateral phrenic nerve that arises from the cervical nerve roots of C3-C5. The phrenic nerve emerges through the anterior scalene muscle on either side of the neck and courses posteriorly to the subclavian vein. Both phrenic nerves enter into the thoracic cavity through the thoracic aperture. In the thoracic cavity, the right and left phrenic nerves follow different paths. The right phrenic nerve descends anteriorly over the right atrium of the heart and exits through the inferior vena cava opening to innervate the inferior surface of the hemidiaphragm. The left phrenic nerve crosses the aortic arch and pericardium overlying the left ventricle until it pierces through the diaphragm to innervate the inferior surface of the left hemidiaphragm. Sensory innervation of the diaphragm is from the intercostal nerves 6-11. Elevated Hemidiaphragm is a condition where one portion of the diaphragm is higher than the other. Often elevated hemidiaphragm is asymptomatic and visualized as an incidental finding on radiologic studies like chest X-ray or chest CT (computed tomography). Patients are typically asymptomatic due to the compensation and recruitment of other inspiratory muscles, and often the healthy hemidiaphragm compensates to maintain the pressure gradient required for adequate gas exchange. However, evidence suggests that the function of the contralateral, healthy hemidiaphragm may be impacted by lower abdominal pressure. In severe cases of unilateral hemidiaphragm paralysis, patients may lose their inspiratory capacity, which can impair the ability of the heart to pump efficiently. Under normal circumstances, the intrathoracic pressure and contraction of the diaphragm overcome the force of gravity and propel blood into the right atrium from the inferior vena cava (IVC). When the pressure gradient cannot be maintained, the right atrium will collapse, and the patient may present as though they have cardiac tamponade. Accurate diagnosis, treatment, and management of elevated hemidiaphragm are essential in patients presenting with dyspnea and multi-organ involvement.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-20993" sec="article-20993.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-20993" sec="article-20993.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-20993" sec="article-20993.s3">Etiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-20993" sec="article-20993.s4">Epidemiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-20993" sec="article-20993.s5">Pathophysiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-20993" sec="article-20993.s6">History and Physical</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-20993" sec="article-20993.s7">Evaluation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-20993" sec="article-20993.s8">Treatment / Management</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-20993" sec="article-20993.s9">Differential Diagnosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-20993" sec="article-20993.s10">Prognosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-20993" sec="article-20993.s11">Complications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-20993" sec="article-20993.s12">Consultations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-20993" sec="article-20993.s13">Deterrence and Patient Education</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-20993" sec="article-20993.s14">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-20993" sec="article-20993.s15">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-20993" sec="article-20993.s17">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>8</Month><Day>1</Day></ContributionDate><ReferenceList><Reference><Citation>Roussos C, Macklem PT. 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Multicenter review of diaphragm pacing in spinal cord injury: successful not only in weaning from ventilators but also in bridging to independent respiration. J Trauma Acute Care Surg. 2014 Feb;76(2):303-9; discussion 309-10.</Citation><ArticleIdList><ArticleId IdType="pubmed">24458038</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32644681</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">29763051</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK499876</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-28599">Right Ventricular Hypertrophy</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Bhattacharya</LastName><ForeName>Priyanka T.</ForeName><Initials>PT</Initials><AffiliationInfo><Affiliation>University of Pennsylvania</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ellison</LastName><ForeName>Matthew B.</ForeName><Initials>MB</Initials><AffiliationInfo><Affiliation>WVU Medicine</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>Right ventricular hypertrophy (RVH) is an abnormal enlargement or pathologic increase in muscle mass of the right ventricle in response to pressure overload, most commonly due to severe lung disease. The right ventricle is considerably smaller than the left ventricle and produces electrical forces that are largely obscured by those generated by the larger left ventricle. Size and function of the right ventricle are adversely affected by the following: Pulmonary hypertension with or without left ventricular dysfunction. Conditions that affect the tricuspid valve leading to significant tricuspid regurgitation (TR). <b>Anatomy and Physiology</b> The right ventricle is composed of inflow (sinus) and outflow (conus) regions, separated by a muscular ridge, the crista supraventricularis. The inflow region includes the tricuspid valve (TV), the chordae/papillary muscles as well as the body of the RV. The RV body boundaries are formed by the RV free wall, extending from the interventricular septum's anterior and posterior aspects. The standard septal curvature convexes toward the RV cavity and imparts a crescent shape to the right ventricle when cross-sectioned. The RV's interior surface is heavily trabeculated; this feature along with the moderator band and more apical insertion of the TV-annulus impart key morphologic differences that distinguish the RV from the LV by echocardiography. In contrast, the infundibulum is a smooth, funnel-shaped outflow portion of the RV that ends at the pulmonic valve. Thus, the RV has a complex geometry, with traditional RV free-wall thickness of 0.3-0.5 cm, imparting greater distensibility and larger cavity volumes in the RV versus the LV, despite lower end-diastolic filling pressures. This translates to an RVEF that is typically 35% to 45% (versus 55% to 65% in the LV) yet generates the identical SV as the LV. Changes in preload, afterload, and intrinsic contractility of the ventricle influence the systolic function of the RV, like the LV. Differences in RV muscle fiber orientation dictate that the body of the RV shortens symmetrically in the longitudinal and radial planes; thus, longitudinal shortening accounts for a much larger proportion of RV ejection than in the LV. The relatively conspicuous RV shortening along the longitudinal axis can measure RV systolic function using uncomplicated techniques that do not require geometric assumptions or meticulous endocardial definition, both being known limitations to the noninvasive assessment of RV systolic function.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-28599" sec="article-28599.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28599" sec="article-28599.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28599" sec="article-28599.s3">Etiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28599" sec="article-28599.s4">Epidemiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28599" sec="article-28599.s5">Pathophysiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28599" sec="article-28599.s6">History and Physical</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28599" sec="article-28599.s7">Evaluation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28599" sec="article-28599.s8">Treatment / Management</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28599" sec="article-28599.s9">Differential Diagnosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28599" sec="article-28599.s10">Staging</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28599" sec="article-28599.s11">Prognosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28599" sec="article-28599.s12">Pearls and Other Issues</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28599" sec="article-28599.s13">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28599" sec="article-28599.s14">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28599" sec="article-28599.s19">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>8</Month><Day>1</Day></ContributionDate><ReferenceList><Reference><Citation>Keramida K, Lazaros G, Nihoyannopoulos P. 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PLoS One. 2017;12(3):e0174118.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC5360271</ArticleId><ArticleId IdType="pubmed">28323875</ArticleId></ArticleIdList></Reference><Reference><Citation>Anand V, Garg S, Duval S, Thenappan T. A systematic review and meta-analysis of trials using statins in pulmonary arterial hypertension. Pulm Circ. 2016 Sep;6(3):295-301.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC5019082</ArticleId><ArticleId IdType="pubmed">27683606</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">29763051</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">29489250</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK482119</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-23440">Increased Intracranial Pressure</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Pinto</LastName><ForeName>Venessa L.</ForeName><Initials>VL</Initials><AffiliationInfo><Affiliation>Baylor College of Medicine</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tadi</LastName><ForeName>Prasanna</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Asram Medical College, Eluru, India</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Adeyinka</LastName><ForeName>Adebayo</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>The Brooklyn Hospital Center</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>Intracranial hypertension (IH) is a clinical condition that is associated with an elevation of the pressures within the cranium. The pressure in the cranial vault is measured in millimeters of mercury (mm Hg) and is normally less than 20 mm Hg. The cranium is a rigid structure that contains three main components: brain, cerebrospinal fluid, and blood. Any increase in the volume of its contents will increase the pressure within the cranial vault. The Monroe-Kellie Doctrine states that the contents of the cranium are in a state of constant volume. That is, the total volumes of the brain tissues, cerebrospinal fluid (CSF), and intracranial blood are fixed. An increase in the volume of one component will result in a decrease in volume in one or two of the other components. The clinical implication of the change in volume of the component is a decrease in cerebral blood flow or herniation of the brain. CSF is a clear fluid found in the subarachnoid spaces and ventricles that cushions the brain and spinal cord. It is secreted by the choroid plexus in the lateral ventricles, travels to the third ventricle via the foramen of Monroe. From the third ventricle, CSF reaches the fourth ventricle through the aqueduct of Sylvius. From here, it flows into the subarachnoid space via the foramina of Magendie and Luschka and is eventually reabsorbed into the dural venous sinuses by arachnoid granulation.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-23440" sec="article-23440.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23440" sec="article-23440.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23440" sec="article-23440.s3">Etiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23440" sec="article-23440.s4">Epidemiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23440" sec="article-23440.s5">Pathophysiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23440" sec="article-23440.s6">History and Physical</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23440" sec="article-23440.s7">Evaluation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23440" sec="article-23440.s8">Treatment / Management</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23440" sec="article-23440.s9">Differential Diagnosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23440" sec="article-23440.s10">Prognosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23440" sec="article-23440.s11">Deterrence and Patient Education</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23440" sec="article-23440.s12">Pearls and Other Issues</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23440" sec="article-23440.s13">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23440" sec="article-23440.s14">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23440" sec="article-23440.s15">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>8</Month><Day>1</Day></ContributionDate><ReferenceList><Reference><Citation>Mokri B. 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This activity will discuss the pertinent topics related to the pathophysiology, diagnosis, and treatment of right ventricular myocardial infarction (RVMI). RVMI was first identified in patients with inferior wall MI who had elevated right ventricular (RV) filling pressures and RV failure, with normal values for the left ventricle (LV). RVMI can occur with or without LV involvement. When inferior MI is associated with RVMI, patients show more bradycardia, need for pacing, hypotension, and mortality.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-28600" sec="article-28600.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28600" sec="article-28600.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28600" sec="article-28600.s3">Etiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28600" sec="article-28600.s4">Epidemiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28600" sec="article-28600.s5">Pathophysiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28600" sec="article-28600.s6">History and Physical</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28600" sec="article-28600.s7">Evaluation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28600" sec="article-28600.s8">Treatment / Management</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28600" sec="article-28600.s9">Differential Diagnosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28600" sec="article-28600.s10">Prognosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28600" sec="article-28600.s11">Pearls and Other Issues</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28600" sec="article-28600.s12">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28600" sec="article-28600.s13">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28600" sec="article-28600.s15">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>8</Month><Day>1</Day></ContributionDate><ReferenceList><Reference><Citation>Mactier I, Dalzell JR, Carrick D. 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Int J Cardiovasc Imaging. 2019 Jan;35(1):77-85.</Citation><ArticleIdList><ArticleId IdType="pubmed">30109454</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">28613702</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35907200</PMID><DateRevised><Year>2023</Year><Month>05</Month><Day>10</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1933-0715</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Jul</Month><Day>29</Day></PubDate></JournalIssue><Title>Journal of neurosurgery. Pediatrics</Title><ISOAbbreviation>J Neurosurg Pediatr</ISOAbbreviation></Journal><ArticleTitle>Endoscopic third ventriculostomy in previously shunt-treated patients.</ArticleTitle><Pagination><StartPage>1</StartPage><EndPage>9</EndPage><MedlinePgn>1-9</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.3171/2022.6.PEDS22177</ELocationID><Abstract><AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">Endoscopic third ventriculostomy (ETV) is an option for treatment of hydrocephalus, including for patients who have a history of previous treatment with CSF shunt insertion. The purpose of this study was to report the success of postshunt ETV by using data from a multicenter prospective registry.<AbstractText Label="METHODS" NlmCategory="METHODS">Prospectively collected data in the Hydrocephalus Clinical Research Network (HCRN) Core Data Project (i.e., HCRN Registry) were reviewed. Children who underwent ETV between 2008 and 2019 and had a history of previous treatment with a CSF shunt were included. A Kaplan-Meier survival curve was created for the primary outcome: time from postshunt ETV to subsequent CSF shunt placement or revision. Univariable Cox proportional hazards models were created to evaluate for an association between clinical and demographic variables and subsequent shunt surgery. Postshunt ETV complications were also identified and categorized.<AbstractText Label="RESULTS" NlmCategory="RESULTS">A total of 203 children were included: 57% male and 43% female; 74% White, 23% Black, and 4% other race. The most common hydrocephalus etiologies were postintraventricular hemorrhage secondary to prematurity (56, 28%) and aqueductal stenosis (42, 21%). The ETV Success Score ranged from 10 to 80. The median patient age was 4.1 years. The overall success of postshunt ETV at 6 months was 41%. Only the surgeon's report of a clear view of the basilar artery was associated with a lower likelihood of postshunt ETV failure (HR 0.43, 95% CI 0.23-0.82, p = 0.009). None of the following variables were associated with postshunt ETV success: age at the time of postshunt ETV, etiology of hydrocephalus, sex, race, ventricle size, number of previous shunt operations, ETV performed at time of shunt infection, and use of external ventricular drainage. Overall, complications were reported in 22% of patients, with CSF leak (8.6%) being the most common complication.<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Postshunt ETV was successful in treating hydrocephalus, without subsequent need for a CSF shunt, in 41% of patients, with a clear view of the basilar artery being the only variable significantly associated with success. Complications occurred in 22% of patients. ETV is an option for treatment of hydrocephalus in children who have previously undergone shunt placement, but with a lower than expected likelihood of success. |
2,329,698 | Late-onset obstructive hydrocephalus associated with occipital encephalocele with large skull defect successfully treated by endoscopic third ventriculostomy. | Hydrocephalus is one of the most common presentations of occipital encephaloceles and usually develops within the first year of life. This case report presents a rare case of late-onset obstructive hydrocephalus associated with occipital encephalocele with an extraordinarily large occipital skull defect.</AbstractText>At birth, a newborn girl presented with an absence of a vast amount of occipital cranium and skin and was diagnosed with occipital hydroencephalomeningocele. Under meticulous sterile management, the affected area was successfully epithelialized, and the patient was discharged without infectious complication. Despite an obstructed cerebral aqueduct, she grew without any signs of hydrocephalus until the age of 7 years. Her gait gradually worsened, and imaging tests at the age of 8 years revealed markedly enlarged lateral and third ventricles but not the fourth ventricle. Endoscopic third ventriculostomy successfully relieved her symptoms with improvement of hydrocephalus.</AbstractText>This is the first case of late-onset obstructive hydrocephalus associated with an occipital encephalocele characterized by large-scale cranial bony defects. Although further investigation is required to elucidate the mechanism of hydrocephalus, this rare phenomenon should be noted during neurological and radiological follow-up.</AbstractText>© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.</CopyrightInformation> |
2,329,699 | Ependymal Cilia: Physiology and Role in Hydrocephalus.<Pagination><StartPage>927479</StartPage><MedlinePgn>927479</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">927479</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.3389/fnmol.2022.927479</ELocationID><Abstract><AbstractText>Cerebrospinal fluid (CSF), a colorless liquid that generally circulates from the lateral ventricles to the third and fourth ventricles, provides essential nutrients for brain homeostasis and growth factors during development. As evidenced by an increasing corpus of research, CSF serves a range of important functions. While it is considered that decreased CSF flow is associated to the development of hydrocephalus, it has recently been postulated that motile cilia, which line the apical surfaces of ependymal cells (ECs), play a role in stimulating CSF circulation by cilia beating. Ependymal cilia protrude from ECs, and their synchronous pulsing transports CSF from the lateral ventricle to the third and fourth ventricles, and then to the subarachnoid cavity for absorption. As a result, we postulated that malfunctioning ependymal cilia could disrupt normal CSF flow, raising the risk of hydrocephalus. This review aims to demonstrate the physiological functions of ependymal cilia, as well as how cilia immobility or disorientation causes problems. We also conclude conceivable ways of treatment of hydrocephalus currently for clinical application and provide theoretical support for regimen improvements by investigating the relationship between ependymal cilia and hydrocephalus development.</AbstractText><CopyrightInformation>Copyright © 2022 Ji, Tang, Chen, Wang, Tan, Liao, Tong and Xiao.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ji</LastName><ForeName>Weiye</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Diagnosis and Treatment Center for Hydrocephalus, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tang</LastName><ForeName>Zhi</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Yibing</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Diagnosis and Treatment Center for Hydrocephalus, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Chuansen</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Diagnosis and Treatment Center for Hydrocephalus, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tan</LastName><ForeName>Changwu</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Diagnosis and Treatment Center for Hydrocephalus, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liao</LastName><ForeName>Junbo</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Diagnosis and Treatment Center for Hydrocephalus, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tong</LastName><ForeName>Lei</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Diagnosis and Treatment Center for Hydrocephalus, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xiao</LastName><ForeName>Gelei</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Diagnosis and Treatment Center for Hydrocephalus, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>07</Month><Day>12</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Front Mol Neurosci</MedlineTA><NlmUniqueID>101477914</NlmUniqueID><ISSNLinking>1662-5099</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">cerebrospinal fluid</Keyword><Keyword MajorTopicYN="N">ependymal cilia</Keyword><Keyword MajorTopicYN="N">hydrocephalus</Keyword><Keyword MajorTopicYN="N">pathogenesis</Keyword><Keyword 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As evidenced by an increasing corpus of research, CSF serves a range of important functions. While it is considered that decreased CSF flow is associated to the development of hydrocephalus, it has recently been postulated that motile cilia, which line the apical surfaces of ependymal cells (ECs), play a role in stimulating CSF circulation by cilia beating. Ependymal cilia protrude from ECs, and their synchronous pulsing transports CSF from the lateral ventricle to the third and fourth ventricles, and then to the subarachnoid cavity for absorption. As a result, we postulated that malfunctioning ependymal cilia could disrupt normal CSF flow, raising the risk of hydrocephalus. This review aims to demonstrate the physiological functions of ependymal cilia, as well as how cilia immobility or disorientation causes problems. We also conclude conceivable ways of treatment of hydrocephalus currently for clinical application and provide theoretical support for regimen improvements by investigating the relationship between ependymal cilia and hydrocephalus development.<CopyrightInformation>Copyright © 2022 Ji, Tang, Chen, Wang, Tan, Liao, Tong and Xiao.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ji</LastName><ForeName>Weiye</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Diagnosis and Treatment Center for Hydrocephalus, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tang</LastName><ForeName>Zhi</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Yibing</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Diagnosis and Treatment Center for Hydrocephalus, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Chuansen</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Diagnosis and Treatment Center for Hydrocephalus, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tan</LastName><ForeName>Changwu</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Diagnosis and Treatment Center for Hydrocephalus, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liao</LastName><ForeName>Junbo</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Diagnosis and Treatment Center for Hydrocephalus, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tong</LastName><ForeName>Lei</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Diagnosis and Treatment Center for Hydrocephalus, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xiao</LastName><ForeName>Gelei</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Diagnosis and Treatment Center for Hydrocephalus, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>07</Month><Day>12</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Front Mol Neurosci</MedlineTA><NlmUniqueID>101477914</NlmUniqueID><ISSNLinking>1662-5099</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">cerebrospinal fluid</Keyword><Keyword MajorTopicYN="N">ependymal cilia</Keyword><Keyword MajorTopicYN="N">hydrocephalus</Keyword><Keyword MajorTopicYN="N">pathogenesis</Keyword><Keyword 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Loss of Rsph9 causes neonatal hydrocephalus with abnormal development of motile cilia in mice. Sci. Rep. 10:12435. 10.1038/s41598-020-69447-4</Citation><ArticleIdList><ArticleId IdType="doi">10.1038/s41598-020-69447-4</ArticleId><ArticleId IdType="pmc">PMC7382491</ArticleId><ArticleId IdType="pubmed">32709945</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35903026</PMID><DateRevised><Year>2022</Year><Month>07</Month><Day>29</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1467-1107</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Jul</Month><Day>29</Day></PubDate></JournalIssue><Title>Cardiology in the young</Title><ISOAbbreviation>Cardiol Young</ISOAbbreviation></Journal><ArticleTitle>Incidence and recovery of post-surgical heart block in children following cardiac surgery.</ArticleTitle><Pagination><StartPage>1</StartPage><EndPage>7</EndPage><MedlinePgn>1-7</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1017/S1047951122002025</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">A subset of patients who develop post-surgical heart block have recovery of atrioventricular node function. Factors predicting recovery are not understood. We investigated our centre's incidence of post-surgical heart block and examine factors associated with recovery of atrioventricular node function.<AbstractText Label="METHODS" NlmCategory="METHODS">We conducted a single-centre retrospective study of patients 0 - 21 years who underwent cardiac surgery between January 2010 and December 2019 and experienced post-operative heart block. Data including patient and clinical characteristics and operative variables were collected and analysed.<AbstractText Label="RESULTS" NlmCategory="RESULTS">Of 6333 surgical hospitalisations, 128 (2%) patients developed post-operative heart block. Of the 128 patients, 90 (70%) had return of atrioventricular node function, and 38 (30%) had pacemaker placement. Of the 38 patients who underwent pacemaker placement, 6 (15.8%) had recovery of atrioventricular node function noted on long-term follow-up. Median time from onset of heart block to late atrioventricular node recovery was 13 days (Interquartile range: 5 - 117). Patients with single-ventricle physiology (p = 0.04), greater weight (p = 0.03), and shorter cardiopulmonary bypass time (p = 0.015) were more likely to have recovery. The use of post-operative steroids was similar between all groups (p = 0.445). Infectious or wound complications were similar between pacemaker groups (p = 1).<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Two per cent of patients who underwent congenital cardiac surgery developed post-operative heart block, and 0.6% underwent pacemaker placement. Early recovery of atrioventricular node was associated with greater weight at the time of surgery, single-ventricle physiology, and shorter cardiopulmonary bypass time. Late recovery of atrioventricular node conduction following pacemaker placement occurred in 15.8% of patients. |
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