Unnamed: 0 int64 0 2.34M | titles stringlengths 5 21.5M | abst stringlengths 1 21.5M |
|---|---|---|
2,329,900 | MRI-Based Risk Assessment for Incomplete Resection of Brain Metastases. | Recent studies demonstrated that gross total resection of brain metastases cannot always be achieved. Subtotal resection (STR) can result in an early recurrence and might affect patient survival. We initiated a prospective observational study to establish a MRI-based risk assessment for incomplete resection of brain metastases.</AbstractText>All patients in whom ≥1 brain metastasis was resected were prospectively included in this study (DRKS ID: DRKS00021224; Nov 2020 - Nov 2021). An interdisciplinary board of neurosurgeons and neuroradiologists evaluated the pre- and postoperative MRI (≤48h after surgery) for residual tumor. Extensive neuroradiological analyses were performed to identify risk factors for an unintended STR which were integrated into a regression tree analysis to determine the patients' individual risk for a STR.</AbstractText>We included 150 patients (74 female; mean age: 61 years), in whom 165 brain metastases were resected. A STR was detected in 32 cases (19.4%) (median residual tumor volume: 1.36ml, median EORrel</sub>: 93.6%), of which 6 (3.6%) were intended STR (median residual tumor volume: 3.27ml, median EORrel</sub>: 67.3%) - mainly due to motor-eloquent location - and 26 (15.8%) were unintended STR (uSTR) (median residual tumor volume: 0.64ml, median EORrel</sub>: 94.7%). The following risk factors for an uSTR could be identified: subcortical metastasis ≥5mm distant from cortex, diffuse contrast agent enhancement, proximity to the ventricles, contact to falx/tentorium and non-transcortical approaches. Regression tree analysis revealed that the individual risk for an uSTR was mainly associated to the distance from the cortex (distance ≥5mm vs. <5mm: OR 8.0; 95%CI: 2.7 - 24.4) and the contrast agent patterns (diffuse vs. non-diffuse in those with distance ≥5mm: OR: 4.2; 95%CI: 1.3 - 13.7). The preoperative tumor volume was not substantially associated with the extent of resection.</AbstractText>Subcortical metastases ≥5mm distant from cortex with diffuse contrast agent enhancement showed the highest incidence of uSTR. The proposed MRI-based assessment allows estimation of the individual risk for uSTR and can help indicating intraoperative imaging.</AbstractText>Copyright © 2022 Rosenstock, Pöser, Wasilewski, Bauknecht, Grittner, Picht, Misch, Onken and Vajkoczy.</CopyrightInformation> |
2,329,901 | Radiomics and Machine Learning for Detecting Scar Tissue on CT Delayed Enhancement Imaging. | Delayed enhancement CT (CT-DE) has been evaluated as a tool for the detection of myocardial scar and compares well to the gold standard of MRI with late gadolinium enhancement (MRI-LGE). Prior work has established that high performance can be achieved with manual reading; however, few studies have looked at quantitative measures to differentiate scar and healthy myocardium on CT-DE or automated analysis.</AbstractText>Eighteen patients with clinically indicated MRI-LGE were recruited for CT-DE at multiple 80 and 100 kV post contrast imaging. Left ventricle segmentation was performed on both imaging modalities, along with scar segmentation on MRI-LGE. Segmentations were registered together and scar regions were estimated on CT-DE. 93 radiomic features were calculated and analysed for their ability to differentiate between scarred and non-scarred myocardium regions. Machine learning (ML) classifiers were trained using the strongest set of radiomic features to classify segments containing scar on CT-DE. Features and classifiers were compared across both tube voltages and combined-energy images.</AbstractText>There were 59 and 51 statistically significant features in the 80 and 100 kV images respectively. Combined-energy imaging increased this to 63 with more features having area under the curve (AUC) above 0.9. The 10 highest AUC features for each image were used in the ML classifiers. The 100 kV images produced the best ML classifier, a support vector machine with an AUC of 0.88 (95% CI 0.87-0.90). Comparable performance was achieved with both the 80 kV and combined-energy images.</AbstractText>CT-DE can be quantitatively analyzed using radiomic feature calculations. These features may be suitable for ML classification techniques to prospectively identify AHA segments with performance comparable to previously reported manual reading. Future work on larger CT-DE datasets is warranted to establish optimum imaging parameters and features.</AbstractText>Copyright © 2022 O'Brien, Williams, Rajani and Niederer.</CopyrightInformation> |
2,329,902 | Reexpansion Pulmonary Edema following Tube Thoracostomy in a Pediatric Patient with Anterior Mediastinal Mass. | Reexpansion pulmonary edema (RPE) is an exceedingly rare and potentially fatal complication of a rapidly reexpanded lung following evacuation of air or fluid from the pleural space secondary to conditions such as a mediastinal mass, pleural effusion, or pneumothorax. Clinical presentations can range from mild radiographic changes to acute respiratory failure and hemodynamic instability. The rapidly progressive nature of the disease makes it important for clinicians to appropriately diagnose and manage patients who develop RPE. We present a case of a child with a large malignant pleural effusion who developed severe RPE after tube thoracostomy and ultimately required venoarterial extracorporeal membrane oxygenation (VA-ECMO). The patient was 7-year-old Caucasian male with newly diagnosed ambiguous T cell myeloid leukemia. A chest computerized tomography (CT) demonstrated a large pleural effusion causing tracheal shift and left bronchus compression as well as an anterior mediastinal mass causing compression of the right atria and right ventricle. Tube thoracostomy was performed in the operating room (OR) with deep sedation. The procedure was complicated with hypoxemia, bradycardia, and pulseless cardiac arrest. After return of spontaneous circulation, the child continued to have refractory hypoxemia, profound hypotension, and frothy secretions. Endotracheal intubation was performed with a size 5.0 cuffed endotracheal tube. Chest radiograph demonstrated opacification of the left hemithorax with chest infiltrates. Patient required VA-ECMO for circulatory support. Supportive therapy of RPE was continued and decannulation was done on day three. Tracheal extubation was performed on day five. |
2,329,903 | Quantification of Intracranial Structures Volume in Fetuses Using 3-D Volumetric MRI: Normal Values at 19 to 37 Weeks' Gestation. | The purpose of this study is to establish a reference of intracranial structure volumes in normal fetuses ranging from 19 to 37 weeks' gestation (mean 27 weeks).</AbstractText>A retrospective analysis of 188 MRI examinations (1.5 T) of fetuses with a normal brain appearance (19-37 gestational weeks) from January 2018 to December 2021 was included in this study. Three dimensional (3-D) volumetric parameters from slice-to-volume reconstructed (SVR) images, such as total brain volume (TBV), cortical gray matter volume (GMV), subcortical brain tissue volume (SBV), intracranial cavity volume (ICV), lateral ventricles volume (VV), cerebellum volume (CBV), brainstem volume (BM), and extra-cerebrospinal fluid volume (e-CSFV), were quantified by manual segmentation from two experts. The mean, SD, minimum, maximum, median, and 25th and 75th quartiles for intracranial structures volume were calculated per gestational week. A linear regression analysis was used to determine the gestational weekly age-related change adjusted for sex. A t</i>-test was used to compare the mean TBV and ICV values to previously reported values at each gestational week. The formulas to calculate intracranial structures volume derived from our data were created using a regression model. In addition, we compared the predicted mean TBV values derived by our formula with the expected mean TBV predicted by the previously reported Jarvis' formula at each time point. For intracranial volumes, the intraclass correlation coefficient (ICC) was calculated to convey association within and between observers.</AbstractText>The intracranial volume data are shown in graphs and tabular summaries. The male fetuses had significantly larger VV compared with female fetuses (p</i> = 0.01). Measured mean ICV values at 19 weeks are significantly different from those published in the literature (p</i> < 0.05). Means were compared with the expected TBV generated by the previously reported formula, showing statistically differences at 22, 26, 29, and 30 weeks' gestational age (GA) (all p</i> < 0.05). A comparison between our data-derived formula and the previously reported formula for TBV showed very similar values at every GA. The predicted TBV means derived from the previously reported formula were all within the 95% confidence interval (CI</i>) of the predicted means of this study. Intra- and inter-observer agreement was high, with an intraclass correlation coefficient larger than 0.98.</AbstractText>We have shown that the intracranial structural volume of the fetal brain can be reliably quantified using 3-D volumetric MRI with a high degree of reproducibility and reinforces the existing data with more robust data in the earlier second and third stages of pregnancy.</AbstractText>Copyright © 2022 Ren, Zhu, Wang, Gui, Jiang and Dong.</CopyrightInformation> |
2,329,904 | [Value of three-dimensional speckle-tracking imaging in evaluating left ventricular systolic function and its correlation with peripheral arterial elasticity in children with simple obesity: a prospective study].<Pagination><StartPage>566</StartPage><EndPage>571</EndPage><MedlinePgn>566-571</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.7499/j.issn.1008-8830.2111122</ELocationID><ELocationID EIdType="pii" ValidYN="Y">1008-8830(2022)05-0566-06</ELocationID><Abstract><AbstractText Label="OBJECTIVES" NlmCategory="OBJECTIVE">To study the application of three-dimensional speckle-tracking imaging in evaluating left ventricular systolic function and its correlation with peripheral arterial elasticity in children with simple obesity.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">Random sampling combined with convenience sampling was used to obtain research samples, and then the samples were divided into an obesity group (23 cases), an overweight group (21 cases), and a normal group (24 cases). Three-dimensional speckle-tracking imaging was used to measure the global longitudinal strain (GLS), global radial strain (GRS), and global circumferential strain (GCS) of the left ventricle. An automatic arteriosclerosis tester was used to measure ankle-brachial index (ABI) and brachial-ankle pulse wave velocity (baPWV). These parameters were compared among the three groups. The correlation of three-dimensional speckle-tracking parameters with ABI and baPWV was evaluated.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">There were no significant differences in GLS, GRS, and GCS between the obesity and normal groups (<i>P</i>>0.05). The overweight group had a significantly higher GLS than the normal group [(-24±7) vs (-19±12), <i>P</i><0.05]. The obesity and overweight groups had a significantly lower ABI than the normal group [(1.00±0.09)/(1.09±0.13) vs (2.25±0.13), <i>P</i><0.05). The obesity group had a significantly higher baPWV than the normal group [(978±109) vs (905±22), <i>P</i><0.05]. In the children with obesity, GLS was positively correlated with baPWV (<i>r</i>=0.516, <i>P</i><0.05) , but not correlated with ABI (<i>P</i>>0.05), and GCS and GRS had no significant correlation with ABI or baPWV (<i>P</i>>0.05).</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">There are varying degrees of changes in left ventricular systolic function and peripheral arterial elasticity in children with simple obesity, and there is a certain correlation between them.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhou</LastName><ForeName>Li</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Cardiac Functions Examination, General Hospital of Ningxia Medical University, Yinchuan 750004, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Shu-Xia</ForeName><Initials>SX</Initials><AffiliationInfo><Affiliation>Department of Cardiac Functions Examination, General Hospital of Ningxia Medical University, Yinchuan 750004, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Fang</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Department of Cardiac Functions Examination, General Hospital of Ningxia Medical University, Yinchuan 750004, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cao</LastName><ForeName>Wei</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Department of Cardiac Functions Examination, General Hospital of Ningxia Medical University, Yinchuan 750004, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Ting-Ting</ForeName><Initials>TT</Initials><AffiliationInfo><Affiliation>Department of Cardiac Functions Examination, General Hospital of Ningxia Medical University, Yinchuan 750004, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ye</LastName><ForeName>Jing-Jing</ForeName><Initials>JJ</Initials><AffiliationInfo><Affiliation>Department of Cardiac Functions Examination, General Hospital of Ningxia Medical University, Yinchuan 750004, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Na</LastName><ForeName>Li-Sha</ForeName><Initials>LS</Initials><AffiliationInfo><Affiliation>Department of Cardiac Functions Examination, General Hospital of Ningxia Medical University, Yinchuan 750004, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhao</LastName><ForeName>Hai-Ping</ForeName><Initials>HP</Initials></Author></AuthorList><Language>chi</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><VernacularTitle>三维斑点追踪成像技术对单纯性肥胖儿童左心室收缩功能的评价及其与外周动脉弹性相关性的前瞻性研究.</VernacularTitle></Article><MedlineJournalInfo><Country>China</Country><MedlineTA>Zhongguo Dang Dai Er Ke Za Zhi</MedlineTA><NlmUniqueID>100909956</NlmUniqueID><ISSNLinking>1008-8830</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D055109" MajorTopicYN="N">Ankle Brachial Index</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002648" MajorTopicYN="N">Child</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019560" MajorTopicYN="Y">Echocardiography, Three-Dimensional</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004548" MajorTopicYN="N">Elasticity</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009765" MajorTopicYN="N">Obesity</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D050177" MajorTopicYN="Y">Overweight</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011446" MajorTopicYN="N">Prospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D063177" MajorTopicYN="N">Pulse Wave Analysis</DescriptorName></MeshHeading></MeshHeadingList><OtherAbstract Type="Publisher" Language="chi"><AbstractText><b>目的</b>: 应用三维斑点追踪成像技术评价单纯性肥胖儿童左心室收缩功能，并探讨其与外周动脉弹性的相关性。<b>方法</b>: 采用随机结合方便抽样的方法，获取研究样本。将样本分为3组：肥胖组（23例）、超重组（21例）和正常组（24例）。采用三维斑点追踪成像技术测量左心室整体长轴应变（global longitudinal strain，GLS）、整体径向应变（global radial strain，GRS）及整体环向应变（global circumferential strain，GCS），全自动动脉硬化测试仪测量踝臂指数（ankle brachial index，ABI）、脉搏波传导速度（brachial ankle pulse wave velocity，baPWV）。比较3组各参数的差异性并探讨三维斑点追踪各参数与ABI、baPWV的相关性。<b>结果</b>: 肥胖组与正常组左心室GLS、GRS、GCS差异无统计学意义（<i>P</i>>0.05）。超重组左心室GLS高于正常组［（-24±7）vs（-19±12），<i>P</i><0.05］。肥胖组ABI（1.00±0.09）、超重组ABI（1.09±0.13）均低于正常组（2.25±0.13）（<i>P</i><0.05）；肥胖组baPWV高于正常组［（978±109）vs（905±22），<i>P</i><0.05］。肥胖儿童左心室GLS与baPWV呈正相关（<i>r</i>=0.516，<i>P</i><0.05），与ABI无相关性（<i>P</i>>0.05）；左心室GCS、GRS与ABI、baPWV无相关性（<i>P</i>>0.05）。<b>结论</b>: 单纯性肥胖儿童左心室收缩功能和外周动脉弹性发生不同程度的改变且二者有一定的相关性。.</AbstractText></OtherAbstract><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Child</Keyword><Keyword MajorTopicYN="N">Correlation</Keyword><Keyword MajorTopicYN="N">Elasticity</Keyword><Keyword MajorTopicYN="N">Obesity</Keyword><Keyword MajorTopicYN="N">Three-dimensional speckle-tracking imaging</Keyword></KeywordList><CoiStatement>所有作者均声明不存在利益冲突。</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>6</Month><Day>1</Day><Hour>10</Hour><Minute>25</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>6</Month><Day>2</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>6</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35644198</ArticleId><ArticleId IdType="pmc">PMC9154371</ArticleId><ArticleId IdType="doi">10.7499/j.issn.1008-8830.2111122</ArticleId><ArticleId IdType="pii">1008-8830(2022)05-0566-06</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Qin W, Liu F, Wan C. A U-shaped association of body mass index and all-cause mortality in heart failure patients: a dose-response meta-analysis of prospective cohort studies[J]. Cardiovasc Ther, 2017, 35(2): 12232. DOI: 10.1111/1755-5922.12232.</Citation><ArticleIdList><ArticleId IdType="doi">10.1111/1755-5922.12232</ArticleId><ArticleId IdType="pubmed">27783461</ArticleId></ArticleIdList></Reference><Reference><Citation>Mukherjee D, Ojha C. Obesity paradox in contemporary cardiology practice[J]. JACC Cardiovasc Interv, 2017, 10(13): 1293-1294. DOI: 10.1016/j.jcin.2017.03.048.</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.jcin.2017.03.048</ArticleId><ArticleId IdType="pubmed">28683934</ArticleId></ArticleIdList></Reference><Reference><Citation>Biasucci LM, Graziani F, Rizzello V, et al. . Paradoxical preservation of vascular function in severe obesity[J]. Am J Med, 2010, 123(8): 727-734. DOI: 10.1016/j.amjmed.2010.02.016.</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.amjmed.2010.02.016</ArticleId><ArticleId IdType="pubmed">20670727</ArticleId></ArticleIdList></Reference><Reference><Citation>李秀娟, 陆永萍. 三维斑点追踪技术的临床应用及研究进展[J]. 中国心血管杂志, 2017, 22(1): 65-68. DOI: 10.3969/j.issn.1007-5410.2017.01.014.</Citation><ArticleIdList><ArticleId IdType="doi">10.3969/j.issn.1007-5410.2017.01.014</ArticleId></ArticleIdList></Reference><Reference><Citation>中国肥胖问题工作组 . 中国学龄儿童青少年超重、肥胖筛查体重指数值分类标准[J]. 中华流行病学杂志, 2004, 25(2): 97-102. DOI: 10.3760/j.issn:0254-6450.2004.02.003.</Citation><ArticleIdList><ArticleId IdType="doi">10.3760/j.issn:0254-6450.2004.02.003</ArticleId><ArticleId IdType="pubmed">15132858</ArticleId></ArticleIdList></Reference><Reference><Citation>邓艺雯, 章春泉, 许燕, 等. 三维斑点追踪技术评估单纯性肥胖儿童左室心肌应变早期变化[J]. 中国超声医学杂志, 2018, 34(3): 217-220. DOI: 10.3969/j.issn.1002-0101.2018.03.009.</Citation><ArticleIdList><ArticleId IdType="doi">10.3969/j.issn.1002-0101.2018.03.009</ArticleId><ArticleId IdType="pubmed">29929803</ArticleId></ArticleIdList></Reference><Reference><Citation>康楠, 王静, 刘丽文, 等. 运动负荷超声心动图评估肥厚型心肌病患者心肌收缩力和心脏-血管耦联的研究[J]. 中国超声医学杂志, 2020, 36(11): 998-1002. DOI: 10.3969/j.issn.1002-0101.2020.11.010.</Citation><ArticleIdList><ArticleId IdType="doi">10.3969/j.issn.1002-0101.2020.11.010</ArticleId><ArticleId IdType="pubmed">32558388</ArticleId></ArticleIdList></Reference><Reference><Citation>罗向红, 杨娅, 李治安. 应用超声初步探讨高血压患者心-血管耦联[J]. 中华超声影像学杂志, 2011, 20(11): 921-924. DOI: 10.3760/cma.j.issn.1004-4477.2011.11.001.</Citation><ArticleIdList><ArticleId IdType="doi">10.3760/cma.j.issn.1004-4477.2011.11.001</ArticleId><ArticleId IdType="pubmed">22078957</ArticleId></ArticleIdList></Reference><Reference><Citation>王庆庆, 高云华, 夏红梅, 等. 超声三维斑点追踪技术对肥胖和非肥胖2型糖尿病患者心脏功能的评价[J]. 中国超声医学杂志, 2015, 31(5): 413-415.</Citation><ArticleIdList><ArticleId IdType="pubmed">25273104</ArticleId></ArticleIdList></Reference><Reference><Citation>曾丽琴, 张军, 拓胜军, 等. 二维斑点追踪成像技术评价早期单纯性肥胖大鼠左心室收缩功能[J]. 中国医学影像技术, 2018, 34(4): 481-485. DOI: 10.13929/j.1003-3289.201709107.</Citation><ArticleIdList><ArticleId IdType="doi">10.13929/j.1003-3289.201709107</ArticleId><ArticleId IdType="pmc">PMC5994664</ArticleId><ArticleId IdType="pubmed">29607652</ArticleId></ArticleIdList></Reference><Reference><Citation>许燕, 章春泉, 邓艺雯, 等. 三维斑点追踪技术评价肥胖儿童左室心肌应变及其与C反应蛋白相关性研究[J]. 中国超声医学杂志, 2018, 34(10): 888-891. DOI: 10.3969/j.issn.1002-0101.2018.10.007.</Citation><ArticleIdList><ArticleId IdType="doi">10.3969/j.issn.1002-0101.2018.10.007</ArticleId></ArticleIdList></Reference><Reference><Citation>晁慧娟, 马瑾, 唐碧雯, 等. 体质量指数与中心动脉血流动力学指标的关系研究[J]. 上海交通大学学报(医学版), 2019, 39(12): 1422-1426. DOI: 10.3969/j.issn.1674-8115.2019.12.013.</Citation><ArticleIdList><ArticleId IdType="doi">10.3969/j.issn.1674-8115.2019.12.013</ArticleId><ArticleId IdType="pubmed">31690975</ArticleId></ArticleIdList></Reference><Reference><Citation>Dangardt F, Charakida M, Georgiopoulos G, et al. . Association between fat mass through adolescence and arterial stiffness: a population-based study from the Avon Longitudinal Study of Parents and Children[J]. Lancet Child Adolesc Health, 2019, 3(7): 474-481. DOI: 10.1016/S2352-4642(19)30105-1.</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/S2352-4642(19)30105-1</ArticleId><ArticleId IdType="pmc">PMC6558973</ArticleId><ArticleId IdType="pubmed">31126896</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35644135</PMID><DateRevised><Year>2022</Year><Month>06</Month><Day>01</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">2193-6323</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>May</Month><Day>29</Day></PubDate></JournalIssue><Title>Journal of neurological surgery. Part A, Central European neurosurgery</Title><ISOAbbreviation>J Neurol Surg A Cent Eur Neurosurg</ISOAbbreviation></Journal>Endoscopic Endonasal Resection of a Cavernous Malformation of the Third Ventricle: Case Report and Literature Review. | <b>目的</b>: 应用三维斑点追踪成像技术评价单纯性肥胖儿童左心室收缩功能，并探讨其与外周动脉弹性的相关性。<b>方法</b>: 采用随机结合方便抽样的方法，获取研究样本。将样本分为3组：肥胖组（23例）、超重组（21例）和正常组（24例）。采用三维斑点追踪成像技术测量左心室整体长轴应变（global longitudinal strain，GLS）、整体径向应变（global radial strain，GRS）及整体环向应变（global circumferential strain，GCS），全自动动脉硬化测试仪测量踝臂指数（ankle brachial index，ABI）、脉搏波传导速度（brachial ankle pulse wave velocity，baPWV）。比较3组各参数的差异性并探讨三维斑点追踪各参数与ABI、baPWV的相关性。<b>结果</b>: 肥胖组与正常组左心室GLS、GRS、GCS差异无统计学意义（<i>P</i>>0.05）。超重组左心室GLS高于正常组［（-24±7）vs（-19±12），<i>P</i><0.05］。肥胖组ABI（1.00±0.09）、超重组ABI（1.09±0.13）均低于正常组（2.25±0.13）（<i>P</i><0.05）；肥胖组baPWV高于正常组［（978±109）vs（905±22），<i>P</i><0.05］。肥胖儿童左心室GLS与baPWV呈正相关（<i>r</i>=0.516，<i>P</i><0.05），与ABI无相关性（<i>P</i>>0.05）；左心室GCS、GRS与ABI、baPWV无相关性（<i>P</i>>0.05）。<b>结论</b>: 单纯性肥胖儿童左心室收缩功能和外周动脉弹性发生不同程度的改变且二者有一定的相关性。.</OtherAbstract><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Child</Keyword><Keyword MajorTopicYN="N">Correlation</Keyword><Keyword MajorTopicYN="N">Elasticity</Keyword><Keyword MajorTopicYN="N">Obesity</Keyword><Keyword MajorTopicYN="N">Three-dimensional speckle-tracking imaging</Keyword></KeywordList><CoiStatement>所有作者均声明不存在利益冲突。</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>6</Month><Day>1</Day><Hour>10</Hour><Minute>25</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>6</Month><Day>2</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>6</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35644198</ArticleId><ArticleId IdType="pmc">PMC9154371</ArticleId><ArticleId IdType="doi">10.7499/j.issn.1008-8830.2111122</ArticleId><ArticleId IdType="pii">1008-8830(2022)05-0566-06</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Qin W, Liu F, Wan C. A U-shaped association of body mass index and all-cause mortality in heart failure patients: a dose-response meta-analysis of prospective cohort studies[J]. Cardiovasc Ther, 2017, 35(2): 12232. DOI: 10.1111/1755-5922.12232.</Citation><ArticleIdList><ArticleId IdType="doi">10.1111/1755-5922.12232</ArticleId><ArticleId IdType="pubmed">27783461</ArticleId></ArticleIdList></Reference><Reference><Citation>Mukherjee D, Ojha C. Obesity paradox in contemporary cardiology practice[J]. JACC Cardiovasc Interv, 2017, 10(13): 1293-1294. DOI: 10.1016/j.jcin.2017.03.048.</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.jcin.2017.03.048</ArticleId><ArticleId IdType="pubmed">28683934</ArticleId></ArticleIdList></Reference><Reference><Citation>Biasucci LM, Graziani F, Rizzello V, et al. . Paradoxical preservation of vascular function in severe obesity[J]. Am J Med, 2010, 123(8): 727-734. DOI: 10.1016/j.amjmed.2010.02.016.</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.amjmed.2010.02.016</ArticleId><ArticleId IdType="pubmed">20670727</ArticleId></ArticleIdList></Reference><Reference><Citation>李秀娟, 陆永萍. 三维斑点追踪技术的临床应用及研究进展[J]. 中国心血管杂志, 2017, 22(1): 65-68. DOI: 10.3969/j.issn.1007-5410.2017.01.014.</Citation><ArticleIdList><ArticleId IdType="doi">10.3969/j.issn.1007-5410.2017.01.014</ArticleId></ArticleIdList></Reference><Reference><Citation>中国肥胖问题工作组 . 中国学龄儿童青少年超重、肥胖筛查体重指数值分类标准[J]. 中华流行病学杂志, 2004, 25(2): 97-102. DOI: 10.3760/j.issn:0254-6450.2004.02.003.</Citation><ArticleIdList><ArticleId IdType="doi">10.3760/j.issn:0254-6450.2004.02.003</ArticleId><ArticleId IdType="pubmed">15132858</ArticleId></ArticleIdList></Reference><Reference><Citation>邓艺雯, 章春泉, 许燕, 等. 三维斑点追踪技术评估单纯性肥胖儿童左室心肌应变早期变化[J]. 中国超声医学杂志, 2018, 34(3): 217-220. DOI: 10.3969/j.issn.1002-0101.2018.03.009.</Citation><ArticleIdList><ArticleId IdType="doi">10.3969/j.issn.1002-0101.2018.03.009</ArticleId><ArticleId IdType="pubmed">29929803</ArticleId></ArticleIdList></Reference><Reference><Citation>康楠, 王静, 刘丽文, 等. 运动负荷超声心动图评估肥厚型心肌病患者心肌收缩力和心脏-血管耦联的研究[J]. 中国超声医学杂志, 2020, 36(11): 998-1002. DOI: 10.3969/j.issn.1002-0101.2020.11.010.</Citation><ArticleIdList><ArticleId IdType="doi">10.3969/j.issn.1002-0101.2020.11.010</ArticleId><ArticleId IdType="pubmed">32558388</ArticleId></ArticleIdList></Reference><Reference><Citation>罗向红, 杨娅, 李治安. 应用超声初步探讨高血压患者心-血管耦联[J]. 中华超声影像学杂志, 2011, 20(11): 921-924. DOI: 10.3760/cma.j.issn.1004-4477.2011.11.001.</Citation><ArticleIdList><ArticleId IdType="doi">10.3760/cma.j.issn.1004-4477.2011.11.001</ArticleId><ArticleId IdType="pubmed">22078957</ArticleId></ArticleIdList></Reference><Reference><Citation>王庆庆, 高云华, 夏红梅, 等. 超声三维斑点追踪技术对肥胖和非肥胖2型糖尿病患者心脏功能的评价[J]. 中国超声医学杂志, 2015, 31(5): 413-415.</Citation><ArticleIdList><ArticleId IdType="pubmed">25273104</ArticleId></ArticleIdList></Reference><Reference><Citation>曾丽琴, 张军, 拓胜军, 等. 二维斑点追踪成像技术评价早期单纯性肥胖大鼠左心室收缩功能[J]. 中国医学影像技术, 2018, 34(4): 481-485. DOI: 10.13929/j.1003-3289.201709107.</Citation><ArticleIdList><ArticleId IdType="doi">10.13929/j.1003-3289.201709107</ArticleId><ArticleId IdType="pmc">PMC5994664</ArticleId><ArticleId IdType="pubmed">29607652</ArticleId></ArticleIdList></Reference><Reference><Citation>许燕, 章春泉, 邓艺雯, 等. 三维斑点追踪技术评价肥胖儿童左室心肌应变及其与C反应蛋白相关性研究[J]. 中国超声医学杂志, 2018, 34(10): 888-891. DOI: 10.3969/j.issn.1002-0101.2018.10.007.</Citation><ArticleIdList><ArticleId IdType="doi">10.3969/j.issn.1002-0101.2018.10.007</ArticleId></ArticleIdList></Reference><Reference><Citation>晁慧娟, 马瑾, 唐碧雯, 等. 体质量指数与中心动脉血流动力学指标的关系研究[J]. 上海交通大学学报(医学版), 2019, 39(12): 1422-1426. DOI: 10.3969/j.issn.1674-8115.2019.12.013.</Citation><ArticleIdList><ArticleId IdType="doi">10.3969/j.issn.1674-8115.2019.12.013</ArticleId><ArticleId IdType="pubmed">31690975</ArticleId></ArticleIdList></Reference><Reference><Citation>Dangardt F, Charakida M, Georgiopoulos G, et al. . Association between fat mass through adolescence and arterial stiffness: a population-based study from the Avon Longitudinal Study of Parents and Children[J]. Lancet Child Adolesc Health, 2019, 3(7): 474-481. DOI: 10.1016/S2352-4642(19)30105-1.</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/S2352-4642(19)30105-1</ArticleId><ArticleId IdType="pmc">PMC6558973</ArticleId><ArticleId IdType="pubmed">31126896</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35644135</PMID><DateRevised><Year>2022</Year><Month>06</Month><Day>01</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">2193-6323</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>May</Month><Day>29</Day></PubDate></JournalIssue><Title>Journal of neurological surgery. Part A, Central European neurosurgery</Title><ISOAbbreviation>J Neurol Surg A Cent Eur Neurosurg</ISOAbbreviation></Journal><ArticleTitle>Endoscopic Endonasal Resection of a Cavernous Malformation of the Third Ventricle: Case Report and Literature Review.</ArticleTitle><ELocationID EIdType="doi" ValidYN="Y">10.1055/s-0041-1741070</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND"> Suprasellar and third ventricle cavernous malformations (CMs) are uncommon. Conventional approaches such as interhemispheric and translamina terminalis approaches are often used to resect these lesions. Here we demonstrate the use of the endoscopic endonasal approach for a third ventricle CM.<AbstractText Label="CASE DESCRIPTION" NlmCategory="METHODS"> A 31-year-old man presented with progressive symptoms of headache and visual disturbance as well as short-term memory deficit over a 6-month period. Neurologic examination revealed bitemporal hemianopsia. Radiologic images showed a suprasellar lesion extending into the third ventricle as well as obstructive hydrocephalus. The patient was operated on using an endoscopic endonasal approach and histopathology revealed a diagnosis of CM. Transient diabetes insipidus and adrenal insufficiency were reported postoperatively.<AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS"> This report demonstrates safe resection of a third ventricle CM via the endonasal route. |
2,329,905 | Pre-treatment with morphine prevents lipopolysaccharide-induced acute respiratory distress syndrome in rats via activation of opioid receptors. | Acute respiratory distress syndrome (ARDS), a severe medical condition, is among the major causes of death in critically ill patients. Morphine is used as a therapeutic agent against severe pain. The mechanisms of its reactions over ARDS are not fully understood. The aim of this study was to assess the mechanism of morphine in rats with ARDS.</AbstractText>Rats were injected with lipopolysaccharide to induce ARDS, and some rats were pre-treated with graded doses of morphine in the lateral ventricles to assess survival and non-infected mortality. Immunohistochemical and HE staining were performed to measure MPO and CD68 activity in the lungs and lung injury. ELISA was conducted to detect the inflammatory factor levels in the plasma and BALF. Co-labeling of μ-opioid receptor (MOR) and c-Fos was observed in the brain tissues. MOR-positive cells in brain tissues were evaluated using immunohistochemistry. The effect of MOR antagonists on ARDS was examined in rats by pre-injection of naloxone or methylnaltrexone. The expression of MyD88, TLR4, and NF-κB was lastly assessed.</AbstractText>Dose-independent improvement was observed in respiratory capacity and lung injury in ARDS rats after morphine pre-injection, along with reduced inflammatory factors in the plasma and BALF. MOR-positive cells were elevated after morphine, which occurred within the ventral part of the gigantocellular reticular nucleus (GiV). Naloxone and methylnaltrexone blocked the effects of morphine via central and peripheral MOR. Morphine activated TLR pathway in a MyD88-dependent manner.</AbstractText>Morphine activates MOR within the GiV and the TLR pathway to attenuate ARDS in rats.</AbstractText>Copyright © 2022 Elsevier Inc. All rights reserved.</CopyrightInformation> |
2,329,906 | Dosimetric advantages of volumetric modulated arc therapy (VMAT) with deep inspiration breath hold (DIBH) technique in Halcyon Linac for left breast cancer treatment. | To evaluate the dosimetric advantages of incorporating the deep inspiration breath hold (DIBH) technique into left breast cancer volumetric modulated arc therapy (VMAT) treatment under Halcyon Linac and to investigate the correlation between mean heart dose (MHD) and distance from the heart to target volumes in left breast cancer VMAT treatment. Fifteen Post-lumpectomy, left-sided breast patients treated between January 2017 and October 2020 were selected. Two plans were generated for each patient using Eclipse treatment planning system (TPS) with the prescription of 50.4 Gy to planning target volume (PTV) breast and 58.8 Gy to PTV boost in 28 fractions. For each patient, DIBH and free breathing (FB) VMAT treatment plans under Halcyon Linac were generated. Dosimetric parameters, monitor unit and beam-on time of both DIBH and FB groups were compared. Three-dimensional distances from heart surface to each target volume were measured on computed tomography images using the TPS contouring tool and their correlation with MHD was evaluated by Pearson's correlation coefficient (r). Comparable target coverage was shown in both groups. Mean dose to heart, left anterior descending artery, and left ventricle in Halcyon-DIBH-VMAT group were significantly reduced by 0.49 Gy, 1.19 Gy, and 0.57 Gy, respectively, compared to Halcyon-FB-VMAT (p < 0.001). A significant lung dose reduction was also achieved in Halcyon-DIBH-VMAT group. There was also a strong negative correlation between MHD and distance from heart surface to PTV boost in both FB and DIBH group (r = -0.741, p < 0.001), but not observed for distance from heart surface to PTV breast. Incorporating DIBH into left breast cancer VMAT treatment under Halcyon Linac demonstrated significant cardiac and lung dose reduction. It was also demonstrated that MHD had a strong negative correlation with distance from heart surface to PTV boost but relatively independent of distance from heart surface to PTV breast. Recognizing the distance from the heart surface to PTV boost as the main factor in affecting MHD could potentially facilitate clinical treatment planning workflow and decision. |
2,329,907 | Pericardial adiposity is independently linked to adverse cardiovascular phenotypes: a CMR study of 42 598 UK Biobank participants.<Pagination><StartPage>1471</StartPage><EndPage>1481</EndPage><MedlinePgn>1471-1481</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1093/ehjci/jeac101</ELocationID><Abstract><AbstractText Label="AIMS">We evaluated independent associations of cardiovascular magnetic resonance (CMR)-measured pericardial adipose tissue (PAT) with cardiovascular structure and function and considered underlying mechanism in 42 598 UK Biobank participants.</AbstractText><AbstractText Label="METHODS AND RESULTS">We extracted PAT and selected CMR metrics using automated pipelines. We estimated associations of PAT with each CMR metric using linear regression adjusting for age, sex, ethnicity, deprivation, smoking, exercise, processed food intake, body mass index, diabetes, hypertension, height cholesterol, waist-to-hip ratio, impedance fat measures, and magnetic resonance imaging abdominal visceral adiposity measures. Higher PAT was independently associated with unhealthy left ventricular (LV) structure (greater wall thickness, higher LV mass, more concentric pattern of LV hypertrophy), poorer LV function (lower LV global function index, lower LV stroke volume), lower left atrial ejection fraction, and lower aortic distensibility. We used multiple mediation analysis to examine the potential mediating effect of cardiometabolic diseases and blood biomarkers (lipid profile, glycaemic control, inflammation) in the PAT-CMR relationships. Higher PAT was associated with cardiometabolic disease (hypertension, diabetes, high cholesterol), adverse serum lipids, poorer glycaemic control, and greater systemic inflammation. We identified potential mediation pathways via hypertension, adverse lipids, and inflammation markers, which overall only partially explained the PAT-CMR relationships.</AbstractText><AbstractText Label="CONCLUSION">We demonstrate association of PAT with unhealthy cardiovascular structure and function, independent of baseline comorbidities, vascular risk factors, inflammatory markers, and multiple non-invasive and imaging measures of obesity. Our findings support an independent role of PAT in adversely impacting cardiovascular health and highlight CMR-measured PAT as a potential novel imaging biomarker of cardiovascular risk.</AbstractText><CopyrightInformation>© The Author(s) 2022. Published by Oxford University Press on behalf of the European Society of Cardiology.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ardissino</LastName><ForeName>Maddalena</ForeName><Initials>M</Initials><Identifier Source="ORCID">0000-0002-2654-8117</Identifier><AffiliationInfo><Affiliation>National Heart and Lung Institute, Imperial College London, Hammersmith Hospital, London W12 0NN, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>McCracken</LastName><ForeName>Celeste</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>William Harvey Research Institute, NIHR Barts Biomedical Research Centre, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Division of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, National Institute for Health Research Oxford Biomedical Research Centre, Oxford University Hospitals NHS Foundation Trust, Oxford OX3 9DUUK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bard</LastName><ForeName>Andrew</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>William Harvey Research Institute, NIHR Barts Biomedical Research Centre, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Antoniades</LastName><ForeName>Charalambos</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Division of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, National Institute for Health Research Oxford Biomedical Research Centre, Oxford University Hospitals NHS Foundation Trust, Oxford OX3 9DUUK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Acute Vascular Imaging Centre, Radcliffe Department of Medicine, University of Oxford, Oxford OX1 2JD, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Neubauer</LastName><ForeName>Stefan</ForeName><Initials>S</Initials><Identifier Source="ORCID">0000-0001-9017-5645</Identifier><AffiliationInfo><Affiliation>Division of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, National Institute for Health Research Oxford Biomedical Research Centre, Oxford University Hospitals NHS Foundation Trust, Oxford OX3 9DUUK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Harvey</LastName><ForeName>Nicholas C</ForeName><Initials>NC</Initials><AffiliationInfo><Affiliation>MRC Lifecourse Epidemiology Centre, University of Southampton, Southampton SO16 6YD, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>NIHR Southampton Biomedical Research Centre, University of Southampton and University Hospital Southampton NHS Foundation Trust, Southampton SO16 6YDUK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Petersen</LastName><ForeName>Steffen E</ForeName><Initials>SE</Initials><AffiliationInfo><Affiliation>William Harvey Research Institute, NIHR Barts Biomedical Research Centre, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Barts Heart Centre, St Bartholomew's Hospital, Barts Health NHS Trust, West Smithfield EC1A 7BE, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Health Data Research UK, London, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Alan Turing Institute, London, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Raisi-Estabragh</LastName><ForeName>Zahra</ForeName><Initials>Z</Initials><Identifier Source="ORCID">0000-0002-7757-5465</Identifier><AffiliationInfo><Affiliation>William Harvey Research Institute, NIHR Barts Biomedical Research Centre, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Barts Heart Centre, St Bartholomew's Hospital, Barts Health NHS Trust, West Smithfield EC1A 7BE, UK.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>MC_PC_17228</GrantID><Acronym>MRC_</Acronym><Agency>Medical Research Council</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>MC_QA137853</GrantID><Acronym>MRC_</Acronym><Agency>Medical Research Council</Agency><Country>United Kingdom</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Eur Heart J Cardiovasc Imaging</MedlineTA><NlmUniqueID>101573788</NlmUniqueID><ISSNLinking>2047-2404</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015415">Biomarkers</NameOfSubstance></Chemical><Chemical><RegistryNumber>97C5T2UQ7J</RegistryNumber><NameOfSubstance UI="D002784">Cholesterol</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008055">Lipids</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D050154" MajorTopicYN="Y">Adiposity</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018070" MajorTopicYN="N">Biological Specimen Banks</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010496" MajorTopicYN="N">Pericardium</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009765" MajorTopicYN="N">Obesity</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008279" MajorTopicYN="N">Magnetic Resonance Imaging</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015415" MajorTopicYN="N">Biomarkers</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010641" MajorTopicYN="N">Phenotype</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006973" MajorTopicYN="Y">Hypertension</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007249" MajorTopicYN="N">Inflammation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006113" MajorTopicYN="N" Type="Geographic">United Kingdom</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002784" MajorTopicYN="N">Cholesterol</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008055" MajorTopicYN="N">Lipids</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">arterial stiffness</Keyword><Keyword MajorTopicYN="N">cardiometabolic disease</Keyword><Keyword MajorTopicYN="N">cardiovascular magnetic resonance</Keyword><Keyword MajorTopicYN="N">left atrium</Keyword><Keyword MajorTopicYN="N">left ventricle</Keyword><Keyword MajorTopicYN="N">pericardial fat</Keyword></KeywordList><CoiStatement>Conflict of interest: S.E.P. provides consultancy to and owns stock of Circle Cardiovascular Imaging Inc, Calgary, Alberta, Canada. CA and SN are Founders, Share holders and Directors of Caristo Diagnostics, a CT Image analysis spinout company from the University of Oxford. C.A. is also inventor of relevant patents US10,695,023B2, PCT/GB2017/053262, GB2018/1818049.7, GR20180100490, and GR20180100510, licensed through exclusive license to Caristo Diagnostics. The remaining authors have no disclosures.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>1</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>4</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>5</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>6</Month><Day>1</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>5</Month><Day>31</Day><Hour>20</Hour><Minute>12</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35640889</ArticleId><ArticleId IdType="pmc">PMC9584621</ArticleId><ArticleId IdType="doi">10.1093/ehjci/jeac101</ArticleId><ArticleId IdType="pii">6595873</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Wong CX, Ganesan AN, Selvanayagam JB. Epicardial fat and atrial fibrillation: current evidence, potential mechanisms, clinical implications, and future directions. Eur Heart J 2017;38:1294–302.</Citation><ArticleIdList><ArticleId IdType="pubmed">26935271</ArticleId></ArticleIdList></Reference><Reference><Citation>Batal O, Schoenhagen P, Shao M, Ayyad AE, Van Wagoner DR, Halliburton SS, et al. . Left atrial epicardial adiposity and atrial fibrillation. Circ Arrhythmia Electrophysiol 2010;3:230–6.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC2974566</ArticleId><ArticleId IdType="pubmed">20504944</ArticleId></ArticleIdList></Reference><Reference><Citation>Kenchaiah S, Ding J, Carr JJ, Allison MA, Budoff MJ, Tracy RP, et al. . Pericardial fat and the risk of heart failure. J Am Coll Cardiol 2021;77:2638–52.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC8218602</ArticleId><ArticleId IdType="pubmed">34045020</ArticleId></ArticleIdList></Reference><Reference><Citation>Greif M, Becker A, Von Ziegler F, Lebherz C, Lehrke M, Broedl UC, et al. . Pericardial adipose tissue determined by dual source CT is a risk factor for coronary atherosclerosis. Arterioscler Thromb Vasc Biol 2009;29:781–6.</Citation><ArticleIdList><ArticleId IdType="pubmed">19229071</ArticleId></ArticleIdList></Reference><Reference><Citation>Shah R V, Anderson A, Ding J, Budoff M, Rider O, Petersen SE, et al. . Pericardial, but not hepatic, fat by CT is associated with CV outcomes and structure. JACC Cardiovasc Imaging 2017; 10:1016–27.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC5591038</ArticleId><ArticleId IdType="pubmed">28330662</ArticleId></ArticleIdList></Reference><Reference><Citation>Zimmermann GS, Ruether T, Von Ziegler F, Greif M, Tittus J, Schenzle J, et al. . Increased pericardial adipose tissue in smokers. J Clin Med 2021;10:3382.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC8348719</ArticleId><ArticleId IdType="pubmed">34362164</ArticleId></ArticleIdList></Reference><Reference><Citation>Ruparelia N, Chai JT, Fisher EA, Choudhury RP. Inflammatory processes in cardiovascular disease: a route to targeted therapies. Nat Rev Cardiol 2017;14:133–44.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC5525550</ArticleId><ArticleId IdType="pubmed">27905474</ArticleId></ArticleIdList></Reference><Reference><Citation>Bard A, Raisi-Estabragh Z, Ardissino M, Lee AM, Pugliese F, Dey D, et al. . Automated quality-controlled cardiovascular magnetic resonance pericardial fat quantification using a convolutional neural network in the UK biobank. Front Cardiovasc Med 2021;8:1–11.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC8294033</ArticleId><ArticleId IdType="pubmed">34307493</ArticleId></ArticleIdList></Reference><Reference><Citation>
UK Biobank Coordinating Centre . UK Biobank: Protocol for a large-scale prospective epidemiological resource. 2007. p. 1–112. https://www.ukbiobank.ac.uk/media/gnkeyh2q/study-rationale.pdf (13 December 2021, date last accessed)</Citation></Reference><Reference><Citation>Petersen SE, Matthews PM, Francis JM, Robson MD, Zemrak F, Boubertakh R, et al. . UK Biobank’s cardiovascular magnetic resonance protocol. J Cardiovasc Magn Reson 2015;18:8.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC4736703</ArticleId><ArticleId IdType="pubmed">26830817</ArticleId></ArticleIdList></Reference><Reference><Citation>Bai W, Suzuki H, Huang J, Francis C, Wang S, Tarroni G, et al. . A population-based phenome-wide association study of cardiac and aortic structure and function. Nat Med 2020;26:1654–62.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC7613250</ArticleId><ArticleId IdType="pubmed">32839619</ArticleId></ArticleIdList></Reference><Reference><Citation>
UK Biobank . Body Composition Measurement. https://biobank.ndph.ox.ac.uk/showcase/ukb/docs/body_composition.pdf (13 December 2021, date last accessed)</Citation></Reference><Reference><Citation>West J, Dahlqvist Leinhard O, Romu T, Collins R, Garratt S, Bell JD, et al. . Feasibility of MR-based body composition analysis in large scale population studies. PLoS One 2016;11:e0163332.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC5035023</ArticleId><ArticleId IdType="pubmed">27662190</ArticleId></ArticleIdList></Reference><Reference><Citation>Townsend P, Phillimore P, Beattie A. Health and deprivation: inequality and the North. Nurs Stand 1988;2:34–4.</Citation></Reference><Reference><Citation>Craig CL, Marshall AL, Sjöström M, Bauman AE, Booth ML, Ainsworth BE, et al. . International physical activity questionnaire: 12-country reliability and validity. Med Sci Sports Exerc 2003;35:1381–95.</Citation><ArticleIdList><ArticleId IdType="pubmed">12900694</ArticleId></ArticleIdList></Reference><Reference><Citation>Ong KL, Ding J, McClelland RL, Cheung BMY, Criqui MH, Barter PJ, et al. . Relationship of pericardial fat with biomarkers of inflammation and hemostasis, and cardiovascular disease: the Multi-Ethnic Study of Atherosclerosis. Atherosclerosis 2015;239:386–92.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC4361311</ArticleId><ArticleId IdType="pubmed">25682037</ArticleId></ArticleIdList></Reference><Reference><Citation>Ong K-L, Ding J, McClelland RL, Cheung BMY, Criqui MH, Barter PJ, et al. . Relationship of pericardial fat with lipoprotein distribution: the Multi-Ethnic study of atherosclerosis. Atherosclerosis 2015;241:664–70.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC4510019</ArticleId><ArticleId IdType="pubmed">26117404</ArticleId></ArticleIdList></Reference><Reference><Citation>Aung N, Sanghvi MM, Piechnik SK, Neubauer S, Munroe PB, Petersen SE. The effect of blood lipids on the left ventricle. J Am Coll Cardiol 2020;76:2477–88.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC7613249</ArticleId><ArticleId IdType="pubmed">33213727</ArticleId></ArticleIdList></Reference><Reference><Citation>Yu Q. Li B. mma: an R package for mediation analysis with multiple mediators. J Open Res Softw 2017;5:11.</Citation></Reference><Reference><Citation>Van Hout MJP, Dekkers IA, Westenberg JJM, Schalij MJ, Scholte AJHA, Lamb HJ. The impact of visceral and general obesity on vascular and left ventricular function and geometry: a cross-sectional magnetic resonance imaging study of the UK Biobank. Eur Heart J Cardiovasc Imaging 2020;21:273–81.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC7031704</ArticleId><ArticleId IdType="pubmed">31722392</ArticleId></ArticleIdList></Reference><Reference><Citation>Mahmoud I, Dykun I, Kärner L, Hendricks S, Totzeck M, Al-Rashid F, et al. . Epicardial adipose tissue differentiates in patients with and without coronary microvascular dysfunction. Int J Obes 2021;45:2058–63.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC8380538</ArticleId><ArticleId IdType="pubmed">34172829</ArticleId></ArticleIdList></Reference><Reference><Citation>Nelson AJ, Worthley MI, Psaltis PJ, Carbone A, Dundon BK, Dundon RF, et al. . Validation of cardiovascular magnetic resonance assessment of pericardial adipose tissue volume. J Cardiovasc Magn Reson 2009;11:1–8.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC2684106</ArticleId><ArticleId IdType="pubmed">19416534</ArticleId></ArticleIdList></Reference><Reference><Citation>Mahajan R, Kuklik P, Grover S, Brooks AG, Wong CX, Sanders P, et al. . Cardiovascular magnetic resonance of total and atrial pericardial adipose tissue: a validation study and development of a 3 dimensional pericardial adipose tissue model. J Cardiovasc Magn Reson 2013;15:73.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC3765997</ArticleId><ArticleId IdType="pubmed">24498950</ArticleId></ArticleIdList></Reference><Reference><Citation>Rosito GA, Massaro JM, Hoffmann U, Ruberg FL, Mahabadi AA, Vasan RS, et al. . Pericardial fat, visceral abdominal fat, cardiovascular disease risk factors, and vascular calcification in a community-based sample the framingham heart study. Circulation 2008;117:605–13.</Citation><ArticleIdList><ArticleId IdType="pubmed">18212276</ArticleId></ArticleIdList></Reference><Reference><Citation>Al-Talabany S, Mordi I, Graeme Houston J, Colhoun HM, Weir-McCall JR, Matthew SZ, et al. . Epicardial adipose tissue is related to arterial stiffness and inflammation in patients with cardiovascular disease and type 2 diabetes. BMC Cardiovasc Disord 2018;18:1–8.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC5809843</ArticleId><ArticleId IdType="pubmed">29433433</ArticleId></ArticleIdList></Reference><Reference><Citation>Kim JS, Kim SW, Lee JS, Lee SK, Abbott R, Lee KY, et al. . Association of pericardial adipose tissue with left ventricular structure and function: a region-specific effect? Cardiovasc Diabetol 2021;20:26.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC7836147</ArticleId><ArticleId IdType="pubmed">33494780</ArticleId></ArticleIdList></Reference><Reference><Citation>Mahabadi AA, Lehmann N, Möhlenkamp S, Pundt N, Dykun I, Roggenbuck U, et al. . Noncoronary measures enhance the predictive value of cardiac CT above traditional risk factors and CAC score in the general population. JACC Cardiovasc Imaging 2016;9:1177–85.</Citation><ArticleIdList><ArticleId IdType="pubmed">27450878</ArticleId></ArticleIdList></Reference><Reference><Citation>Mahabadi AA, Anapliotis V, Dykun I, Hendricks S, Al-Rashid F, Lüdike P, et al. . Epicardial fat and incident heart failure with preserved ejection fraction in patients with coronary artery disease. Int J Cardiol 2022;357:140–5.</Citation><ArticleIdList><ArticleId IdType="pubmed">35395282</ArticleId></ArticleIdList></Reference><Reference><Citation>Mazurek T, Zhang LF, Zalewski A, Mannion JD, Diehl JT, Arafat H, et al. . Human epicardial adipose tissue is a source of inflammatory mediators. Circulation 2003;108:2460–66.</Citation><ArticleIdList><ArticleId IdType="pubmed">14581396</ArticleId></ArticleIdList></Reference><Reference><Citation>Iacobellis G, Bianco AC. Epicardial adipose tissue: emerging physiological, pathophysiological and clinical features. Trends Endocrinol Metab 2011;22:450–7.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC4978122</ArticleId><ArticleId IdType="pubmed">21852149</ArticleId></ArticleIdList></Reference><Reference><Citation>Xie Z, Zhu J, Li W, Liu L, Zhuo K, Yang R, et al. . Relationship of epicardial fat volume with coronary plaque characteristics, coronary artery calcification score, coronary stenosis, and CT-FFR for lesion-specific ischemia in patients with known or suspected coronary artery disease. Int J Cardiol 2021;332:8–14.</Citation><ArticleIdList><ArticleId IdType="pubmed">33775790</ArticleId></ArticleIdList></Reference><Reference><Citation>Chang KF, Lin G, Huang PC, Juan YH, Wang CH, Tsai SY, et al. . Left ventricular function and myocardial triglyceride content on 3T cardiac MR predict major cardiovascular adverse events and readmission in patients hospitalized with acute heart failure. J Clin Med 2020;9:1–15.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC7019990</ArticleId><ArticleId IdType="pubmed">31936313</ArticleId></ArticleIdList></Reference><Reference><Citation>Raisi-Estabragh Z, McCracken C, Condurache D, Aung N, Vargas JD, Naderi H, et al. . Left atrial structure and function are associated with cardiovascular outcomes independent of left ventricular measures: a UK Biobank CMR study. Eur Hear J - Cardiovasc Imaging 2021:jeab266.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC9365306</ArticleId><ArticleId IdType="pubmed">34907415</ArticleId></ArticleIdList></Reference><Reference><Citation>Raisi-Estabragh Z, McCracken C, Gkontra P, Jaggi A, Ardissino M, Cooper J, et al. . Associations of meat and fish consumption with conventional and radiomics cardiovascular magnetic resonance phenotypes in the UK biobank. Front Cardiovasc Med 2021;8:667849.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC8133433</ArticleId><ArticleId IdType="pubmed">34026874</ArticleId></ArticleIdList></Reference><Reference><Citation>Teijeira-Fernandez E, Eiras S, Grigorian-Shamagian L, Fernandez A, Adrio B, Gonzalez-Juanatey JR. Epicardial adipose tissue expression of adiponectin is lower in patients with hypertension. J Hum Hypertens 2008;22:856–63.</Citation><ArticleIdList><ArticleId IdType="pubmed">18650840</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35640546</PMID><DateRevised><Year>2022</Year><Month>12</Month><Day>02</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1422-6421</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>May</Month><Day>31</Day></PubDate></JournalIssue><Title>Cells, tissues, organs</Title><ISOAbbreviation>Cells Tissues Organs</ISOAbbreviation></Journal>Acute Response of Engineered Cardiac Tissue to Pressure and Stretch. | The heart is a dynamic organ, and the cardiac tissue experiences changes in pressure and stretch during the cardiac cycle. Existing cell culture and animal models are limited in their capacity to decouple and tune specific hemodynamic stresses implicated in the development of physiological and pathophysiological cardiac tissue remodeling. This study focused on creating a system to subject engineered cardiac tissue to either pressure or stretch stimuli in isolation and the subsequent evaluation of acute tissue remodeling. We developed a cardiac tissue chip containing three-dimensional (3-D) cell-laden hydrogel constructs and cultured them within systems where we could expose them to either pressure changes or volume changes as seen in the left ventricle. Acute cellular remodeling with each condition was qualitatively and quantitatively assessed using histology, immunohistochemistry, gene expression studies, and soluble factor analysis. Using our unique model systems, we isolated the effects of pressure and stretch on engineered cardiac tissue. Our results confirm that both pressure and stretch mediate acute stress responses in the engineered cardiac tissue. However, both experimental conditions elicited a similar acute phase injury response within this timeframe. This study demonstrates our ability to subject engineered cardiac tissue to either pressure or stretch stimuli in isolation, both of which elicited acute tissue remodeling responses. |
2,329,908 | Bovine intracranial neoplasia: A retrospective case series. | This case series describes the clinical and pathological findings of intracranial neoplasms in cattle, a rare entity. Data and archived tissues from 24 intracranial tumors were reviewed and investigated by immunohistochemistry for S100, glial fibrillary acidic protein, synaptophysin, pancytokeratin, vimentin, neuron-specific enolase, oligodendrocyte transcription factor 2, and isocitrate dehydrogenase 1. Ages of affected cattle ranged from 6 months to 14 years (5.7 ± 3.6 years; mean ± SD). Predominant clinical signs were altered mental state, central vestibular dysfunction, and cerebellar incoordination. Twelve gliomas, all high grade, were the most common tumors observed: oligodendrogliomas (n = 6), astrocytomas (n = 4), and undefined gliomas (n = 2). The oligodendrogliomas were located in the brainstem and extended into the ventricles, whereas all astrocytomas were located in the forebrain. Isocitrate dehydrogenase 1 gene mutation as described in humans was not detected. The 5 meningiomas exhibited microcystic, chordoid, atypical, papillary, and anaplastic subtypes. Metastatic carcinomas (n = 4) were the only secondary tumor type present, and these were located at the level of the medulla with infiltration of cranial nerves and in one case leptomeningeal carcinomatosis. In addition, 2 medulloblastomas and 1 choroid plexus carcinoma were diagnosed. Immunohistochemistry for vimentin and pancytokeratin was particularly useful to distinguish meningiomas and choroid plexus carcinoma (positive for vimentin only) from mestastatic carcinomas (positive for cytokeratin only) as all showed a papillary growth pattern. Overall, the morphological features were comparable with other species and the human and canine classifications could be applied. |
2,329,909 | The subcommissural organ maintains features of neuroepithelial cells in the adult mouse. | The subcommissural organ (SCO) is a part of the circumventricular organs located in the dorsocaudal region of the third ventricle at the entrance of the aqueduct of Sylvius. The SCO comprises epithelial cells and produces high molecular weight glycoproteins, which are secreted into the third ventricle and become part of Reissner's fibre in the cerebrospinal fluid. Abnormal development of the SCO has been linked with congenital hydrocephalus, a condition characterized by excessive accumulation of cerebrospinal fluid in the brain. In the present study, we characterized the SCO cells in the adult mouse brain to gain insights into the possible role of this brain region. Immunohistochemical analyses revealed that expression of Pax6, a transcription factor essential for SCO differentiation during embryogenesis, is maintained in the SCO at postnatal stages from P0 to P84. SCO cells in the adult brain expressed known neural stem/progenitor cell (NSPC) markers, Sox2 and vimentin. The adult SCO cells also expressed proliferating marker PCNA, although expression of another proliferation marker Ki67, indicating a G<sub>2</sub> /M phase, was not detected. The SCO cells did not incorporate BrdU, a marker for DNA synthesis in the S phase. Therefore, the SCO cells have a potential for proliferation but are quiescent for cell division in the adult. The SCO cells also expressed GFAP, a marker for astrocytes or NSPCs, but not NeuN (for neurons). A few cells positive for Iba1 (microglia), Olig2 (for oligodendrocytes) and PDGFRα (oligodendrocyte progenitors) existed within or on the periphery of the SCO. These findings revealed that the SCO cells have a unique feature as secretory yet immature neuroepithelial cells in the adult mouse brain. |
2,329,910 | The shadow in the darkness: Case report on adhesive intestinal obstruction secondary to ventriculoperitoneal shunt catheter in an elderly patient. | Shunt placement is an effective therapy for hydrocephalus. Ventriculoperitoneal shunt draining excess cerebrospinal fluid connects the cerebral ventricles to the abdominal cavity. However, intestinal obstruction may ensue as an infrequent complication of the shunt.</AbstractText>A 65 years old female patient presented with abdominal pain, abdominal bloating, and ceased passage of flatus and stool for six days. She had a history of undergoing a VP shunt procedure due to midbrain obstruction and supratentorial hydrocephalus. Conservative treatment at another local hospital couldn't relieve her symptoms. Laboratory investigations revealed elevated CRP and neutrophils. CT scan showed distended small bowel loops with aerated effusion. Thus, she was admitted to our hospital and underwent an emergent laparotomy following diagnostic modalities completion.</AbstractText>Adhesive intestinal obstruction secondary to ventriculoperitoneal shunt is a rare but fatal shunt complication. The possible mechanisms involved include rubbing movements between the greater omentum and the catheter, cerebrospinal fluid reaction with abdominal organs, immunological rejection of the catheter, and deposition of brain tumor cells with the resultant abdominal metastatic lesions. Laparoscopic and laparotomy are warranted in the surgical management of the disease.</AbstractText>A high index of suspicion for adhesive intestinal obstruction is key to timely diagnosis and treatment.</AbstractText>© 2022 The Authors.</CopyrightInformation> |
2,329,911 | Resection of Pontine Cavernoma with Hemorrhage via Unilateral Uvulotonsillar Keyhole Approach. | The telovelar approach and its modifications are widely used to remove lesions of the fourth ventricle and brainstem. We offer a variant of a unilateral uvulotonsillar approach, which is performed using an open-door keyhole suboccipital craniotomy (Video 1). A 56-year-old woman presented with symptoms of 2 months' duration. Preoperative examination revealed paresis of the left sixth cranial nerve, left seventh nerve paralysis, right-sided hemihypoesthesia, right-sided severe hemiparesis owing to which the patient could not move independently, and dynamic ataxia in the left limbs. Magnetic resonance imaging showed a cavernoma with hemorrhage in the left side of the pons. The surgery was performed in the prone position. After a median skin and soft tissue incision about 6-7 cm long, an open-door keyhole craniotomy was performed. Dura over the left cerebellar hemisphere was opened in a semilunar fashion. The dissection of the uvulotonsillar fissure was performed from its cranial part, where the medial trunk of the cortical segment of the posterior inferior cerebellar artery was the reference point. Following the dissection, the tela choroidea was incised, and the left half of the rhomboid fossa was exposed. After the mapping, the floor of the fourth ventricle was incised in the suprafacial triangle. Cavernoma and hematoma were removed. Hemostasis was achieved. Dura was closed. The attached bone flap was then turned upward and reattached using nonresorbable sutures. Postoperatively, the patient had resolution of sensory and motor disturbances on the right half of the body, and coordination was improved in the left limbs. Postoperative imaging confirmed complete removal of the lesion. |
2,329,912 | Calibration of cine MRI segmentation probability for uncertainty estimation using a multi-task cross-task learning architecture. | While deep learning has shown potential in solving a variety of medical image analysis problems including segmentation, registration, motion estimation, etc., their applications in the real-world clinical setting are still not affluent due to the lack of reliability caused by the failures of deep learning models in prediction. Furthermore, deep learning models need a large number of labeled datasets. In this work, we propose a novel method that incorporates uncertainty estimation to detect failures in the segmentation masks generated by CNNs. Our study further showcases the potential of our model to evaluate the correlation between the uncertainty and the segmentation errors for a given model. Furthermore, we introduce a multi-task cross-task learning consistency approach to enforce the correlation between the pixel-level (segmentation) and the geometric-level (distance map) tasks. Our extensive experimentation with varied quantities of labeled data in the training sets justifies the effectiveness of our model for the segmentation and uncertainty estimation of the left ventricle (LV), right ventricle (RV), and myocardium (Myo) at end-diastole (ED) and end-systole (ES) phases from cine MRI images available through the MICCAI 2017 ACDC Challenge Dataset. Our study serves as a proof-of-concept of how uncertainty measure correlates with the erroneous segmentation generated by different deep learning models, further showcasing the potential of our model to flag low-quality segmentation from a given model in our future study. |
2,329,913 | Bullseye EVD: preclinical evaluation of an intra-procedural system to confirm external ventricular drainage catheter positioning. | External ventricular drainage (EVD) is a life-saving procedure indicated for elevated intracranial pressure. A catheter is inserted into the ventricles to drain cerebrospinal fluid and release the pressure on the brain. However, the standard freehand EVD technique results in catheter malpositioning in up to 60.1% of procedures. This proof-of-concept study aimed to evaluate the registration accuracy of a novel image-based verification system "Bullseye EVD" in a preclinical cadaveric model of catheter placement.</AbstractText>Experimentation was performed on both sides of 3 cadaveric heads (n = 6). After a pre-interventional CT scan, a guidewire simulating the EVD catheter was inserted as in a clinical EVD procedure. 3D structured light images (Einscan, Shining 3D, China) were acquired of an optical tracker placed over the guidewire on the surface of the scalp, along with three distinct cranial regions (scalp, face, and ear). A computer vision algorithm was employed to determine the guidewire position based on the pre-interventional CT scan and the intra-procedural optical imaging. A post-interventional CT scan was used to validate the performance of the Bullseye optical imaging system in terms of trajectory and offset errors.</AbstractText>Optical images which combined facial features and exposed scalp within the surgical field resulted in the lowest trajectory and offset errors of 1.28° ± 0.38° and 0.33 ± 0.19 mm, respectively. Mean duration of the optical imaging procedure was 128 ± 35 s.</AbstractText>The Bullseye EVD system presents an accurate patient-specific method to verify freehand EVD positioning. Use of facial features was critical to registration accuracy. Workflow automation and development of a user interface must be considered for future clinical evaluation.</AbstractText>© 2022. CARS.</CopyrightInformation> |
2,329,914 | Shunt Over-drainage, Slit Ventricle Syndrome, Programmable Valves and Anti-Siphon Devices. A Narrative Review of a Multifactorial and Intractable Problem. | The current management strategy of hydrocephalus mainly involves the insertion of a ventriculoperitoneal shunt and is inherently related with a complication widely known as shunt over-drainage. Albeit this is a well-recognized complication, the true incidence and severity of this phenomenon remains undefined and most probably underdiagnosed, necessitating a more comprehensive pathophysiologic and therapeutic consideration. The slit ventricle syndrome is intimately related with the entity of shunt over-drainage, although who's the definition of the former is implicated by a lack of universally accepted inclusion criteria. Another point of controversy is related with the absence of widely accepted criteria that would be able to discriminate the existing differentiations between these two entities. This is reflected in the fact that there are many proposed, relevant, treatment protocols. The background for all this data is based on the uncertainty and ambiguity regarding the pathophysiological mechanisms that are implicated. Current efforts are centered on the implementation of precautionary measures, as well as on treatment of both of these entities. Currently, there are enough evidence that support the concept that prevention of siphoning via the use of gravitational valves or antisiphon devices is the most efficacious means contained in our current therapeutic armamentarium. We attempt to present an overview of this complex entity, emphasizing on the hydrodynamics of the cerebrospinal fluid circulation in conditions harboring a ventriculoperitoneal shunt, the effect of the siphoning effect and the role of programmable valves and anti-siphon devices in our effort to eliminate this phenomenon. Based on an extensive literature review and on expert opinion, we concluded that the insertion of an anti-siphon device (gravitational shunt valves) could reliably address the issue of over-drainage, when a patient assumes a vertical position. Besides that, there are ongoing prospective studies centered on the safety and efficacy of adjustable gravitational valves, whose results are of ultimate importance. It is of paramount importance to be recognized that, due to the complexity of the pathophysiology of shunted hydrocephalus, lifelong follow-up of patients with ventriculoperitoneal shunts is necessary. |
2,329,915 | Simple Predictors for Cardiac Fibrosis in Patients with Type 2 Diabetes Mellitus: The Role of Circulating Biomarkers and Pulse Wave Velocity. | Cardiac fibrosis is the basis of structural and functional disorders in patients with diabetes mellitus (T2DM). A wide range of laboratory and instrumental methods is used for its prediction. The study aimed to identify simple predictors of cardiac fibrosis in patients with T2DM based on the analysis of circulating fibrosis biomarkers and arterial stiffness. The study included patients with T2DM (n = 37) and cardiovascular risk factors (RF, n = 27) who underwent ECHO, cardiac magnetic resonance imaging (MRI), pulse wave analysis (PWV), reactive hyperemia (RH), peripheral arterial tonometry, carotid ultrasonography, and assessment of serum fibrosis biomarkers. As a control group, 15 healthy subjects were examined. Left ventricular concentric hypertrophy was accompanied by an increased serum galectin-3 level in T2DM patients. There was a relationship between the PICP and HbA1c levels in both main groups (R2 = 0.309; p = 0.014). A negative correlation between PICP level and the global longitudinal strain (GLS) was found (r = −0.467; p = 0.004). The RH index had a negative correlation with the duration of diabetes (r = −0.356; p = 0.03), the carotid-femoral PWV (r = −0.371; p = 0.024), and the carotid intima-media thickness (r = −0.622; p < 0.001). The late gadolinium-enhanced (LGE) cardiac MRI was detected in 22 (59.5%) T2DM and in 4 (14.85%) RF patients. Diabetes, its baseline treatment with metformin, HbA1c and serum TIMP-1 levels, and left ventricle hypertrophy had moderate positive correlations with LGE findings (p < 0.05). Using the multivariate regression analysis, increased TIMP-1 level was identified as an independent factor associated with cardiac fibrosis. |
2,329,916 | Predictive Value of the Third Ventricle Width for Neurological Status in Multiple Sclerosis. | The third ventricle width (3VW) is an easily calculated measure of brain atrophy. The aim of this study was to evaluate the relation of 3VW to cognitive impairment with adjustment for demographic and clinical confounders, including depression, anxiety, and fatigue, as well as to disability in patients with multiple sclerosis (MS). Symbol Digit Modalities Test, California Verbal Learning Test, Brief Visuospatial Memory Test-Revised, Expanded Disability Status Scale (EDSS), Hospital Anxiety and Depression Scale, and Modified Fatigue Impact Scale (MFIS) were analysed in 93 patients with MS. Neuropsychological performance was compared to that of 150 healthy controls. Axial images from 3D FLAIR were used to measure 3VW. In total, 25% of MS patients were impaired in at least two neuropsychological tests. Cognitive impairment and EDSS were associated with 3VW. Age and 3VW were the strongest predictors of cognitive impairment. The multiple regression model including age, 3VW, education, EDSS, and MFIS explained 63% of the variance of neuropsychological tests results, whereas 3VW, age and duration of the disease were significant predictors of EDSS. This study confirms the predictive value of 3VW for neurological status of patients with MS, especially for cognitive impairment after adjustment for demographic and clinical confounders. |
2,329,917 | Biventricular Conversion for Hypoplastic Left Heart Variants: An Update. | Ongoing concerns with single-ventricle palliation morbidity and poor outcomes from primary biventricular strategies for neonates with borderline left heart structures have led some centers to attempt alternative strategies to obviate the need for ultimate Fontan palliation and limit the risk to the child during the vulnerable neonatal period. In certain patients who are traditionally palliated toward single-ventricle circulation, biventricular circulation is possible. This review aims to delineate the current knowledge regarding converting certain patients with borderline left heart structures from single-ventricle palliation toward biventricular circulation. |
2,329,918 | Single-Cell and Single-Nucleus RNAseq Analysis of Adult Neurogenesis. | The complexity of adult neurogenesis is becoming increasingly apparent as we learn more about cellular heterogeneity and diversity of the neurogenic lineages and stem cell niches within the adult brain. This complexity has been unraveled in part due to single-cell and single-nucleus RNA sequencing (sc-RNAseq and sn-RNAseq) studies that have focused on adult neurogenesis. This review summarizes 33 published studies in the field of adult neurogenesis that have used sc- or sn-RNAseq methods to answer questions about the three main regions that host adult neural stem cells (NSCs): the subventricular zone (SVZ), the dentate gyrus (DG) of the hippocampus, and the hypothalamus. The review explores the similarities and differences in methodology between these studies and provides an overview of how these studies have advanced the field and expanded possibilities for the future. |
2,329,919 | Activation of Nkx2.5 transcriptional program is required for adult myocardial repair. | The cardiac developmental network has been associated with myocardial regenerative potential. However, the embryonic signals triggered following injury have yet to be fully elucidated. Nkx2.5 is a key causative transcription factor associated with human congenital heart disease and one of the earliest markers of cardiac progenitors, thus it serves as a promising candidate. Here, we show that cardiac-specific RNA-sequencing studies reveal a disrupted embryonic transcriptional profile in the adult Nkx2.5 loss-of-function myocardium. nkx2.5<sup>-/-</sup> fish exhibit an impaired ability to recover following ventricular apex amputation with diminished dedifferentiation and proliferation. Complex network analyses illuminate that Nkx2.5 is required to provoke proteolytic pathways necessary for sarcomere disassembly and to mount a proliferative response for cardiomyocyte renewal. Moreover, Nkx2.5 targets embedded in these distinct gene regulatory modules coordinate appropriate, multi-faceted injury responses. Altogether, our findings support a previously unrecognized, Nkx2.5-dependent regenerative circuit that invokes myocardial cell cycle re-entry, proteolysis, and mitochondrial metabolism to ensure effective regeneration in the teleost heart. |
2,329,920 | Serial T2-Weighted Thoracic and Abdominal Lymphatic Imaging in Fontan Patients-New Insights into Dynamics of Lymphatic Abnormalities after Total Cavopulmonary Connection. | Lymphatic congestion in single-ventricle patients has been associated with increased morbidity and poor outcomes. Little is known about the dynamics of lymphatic abnormalities over time, on their association with clinical presentation or response to catheter interventions. This retrospective, single-center study describes Fontan patients who underwent at least two magnetic resonance imaging (MRI) studies. T2-weighted lymphatic imaging was used to classify thoracic and abdominal (para-aortic and portal-venous) lymphatic abnormalities. The relationship between lymphatic congestion and hemodynamic changes after cardiac catheter interventions, clinical presentation and MRI data was analyzed. A total of 33 Fontan patients underwent at least two cardiac MRI studies. Twenty-two patients had two, eight had three and three had four lymphatic imaging studies (total of 80 MRIs studies). No significant changes in lymphatic classification between MRI 1 and 2 were observed for thoracic (<i>p</i> = 0.400), para-aortic (0.670) and portal-venous (<i>p</i> = 0.822) abnormalities. No significant correlation between lymphatic classification and hemodynamic changes after intervention or MRI parameters was found. This study illustrates thoracic and abdominal lymphatic abnormalities in serial T2-weighted imaging after Fontan. Fontan patients did not demonstrate significant changes in their lymphatic perfusion, despite clinical or hemodynamic changes. We assume that lymphatic congestion might develop after total cavopulmonary connection (TCPC) and remain relatively stable, despite further intervention targeting hemodynamic parameters. |
2,329,921 | A method for intracerebroventricular cannulation of young broiler chicks. | The site-specific administration of neuroactive substances or pharmacological agents is a routine practice in neurological studies. To facilitate chronic treatments intercranial cannulae are often implanted in the skull. These surgical procedures are widely described and well-documented for rodents, as the most common animal model, and even refined over the years. However, precise descriptions of proper procedure for third ventricle cannulation in young broiler chicks is not readily available. This absence is surprising, as chicken models are often used in the investigation of physiological control of the metabolism and ingestion. Furthermore, as a commercial animal, there is also a particular interest in elucidating the central regulation of feed intake and metabolism to optimize feeding and living conditions for broilers. The brain nuclei that serve as the regulatory centers of feeding and metabolism are the arcuate nucleus, the ventromedial hypothalamic nucleus, and the lateral hypothalamus, which are all located near the third ventricle. Here, we provide a full protocol for intracerebroventricular (i.c.v.) cannulation of 7-day old broiler chicks, as well as a review of some of the advances made in rodent i.c.v. cannulations and whether these advances are applicable to cannulations in chickens. Using the surgical procedure described here, we were able to achieve a success rate of proper implantation of 88%, with a mortality rate of less than 1% (<i>n</i> = 224).•Detailed procedure for i.c.v. canula implantation in the third ventricle of 7d-old broiler chicks.•Cement cap with anchoring screws is necessary in broilers, glue does not provide sufficient stability.•Carboxylate cement and self-adhesive resin cement were tested as an alternative for methyl methacrylate cement. |
2,329,922 | Nonalcoholic fatty liver disease and health outcomes: An umbrella review of systematic reviews and meta-analyses. | A large number of systemic reviews and meta-analyses have explored the relationship between nonalcoholic fatty liver disease (NAFLD) and multiple health outcomes. The aim of this study is to conduct an umbrella review to assess the strength and evidence for the association between NAFLD and health outcomes.</AbstractText>We systematically identified the present meta-analyses of observational studies reporting an association between NAFLD and health outcomes. For each meta-analysis, we assessed the quality with AMSTAR2 and graded the epidemiologic evidence.</AbstractText>Fifty-four articles comprising 111 unique meta-analyses were included in this study. Eighty-five unique outcomes showed significant associations (P</i> ← 0.05), whereas 26 unique outcomes showed insignificant associations, and we cannot assess the epidemiologic evidence. For 85 significant health outcomes, four outcomes (carotid intima-media thickness (C-IMT), peak A velocity, left ventricle end-diastolic diameter, incident chronic kidney disease (CKD) in adult patients) was graded as high quality of evidence, 23 outcomes were graded as the moderate quality of evidence, and the remaining 58 outcomes were graded as weak quality of evidence. Fourty-seven (87.03%) studies showed critically low methodological quality.</AbstractText>In this umbrella review, only four statistically significant health outcomes showed high epidemiologic evidence. NAFLD seems to relate to an increased risk of C-IMT, peak A velocity, left ventricle end-diastolic diameter, and incident CKD in adult patients.</AbstractText>© The Author(s), 2022.</CopyrightInformation> |
2,329,923 | Experimental approaches for manipulating choroid plexus epithelial cells. | Choroid plexus (ChP) epithelial cells are crucial for the function of the blood-cerebrospinal fluid barrier (BCSFB) in the developing and mature brain. The ChP is considered the primary source and regulator of CSF, secreting many important factors that nourish the brain. It also performs CSF clearance functions including removing Amyloid beta and potassium. As such, the ChP is a promising target for gene and drug therapy for neurodevelopmental and neurological disorders in the central nervous system (CNS). This review describes the current successful and emerging experimental approaches for targeting ChP epithelial cells. We highlight methodological strategies to specifically target these cells for gain or loss of function in vivo. We cover both genetic models and viral gene delivery systems. Additionally, several lines of reporters to access the ChP epithelia are reviewed. Finally, we discuss exciting new approaches, such as chemical activation and transplantation of engineered ChP epithelial cells. We elaborate on fundamental functions of the ChP in secretion and clearance and outline experimental approaches paving the way to clinical applications. |
2,329,924 | FRESH 3D Bioprinting a Ventricle-like Cardiac Construct Using Human Stem Cell-Derived Cardiomyocytes. | Here we describe a method to engineer a contractile ventricle-like chamber composed of human stem cell-derived cardiomyocytes using freeform reversible embedding of suspended hydrogels (FRESH) 3D bioprinting. To do this, we print a support structure using a collagen type I ink and a cellular component using a high-density cell ink supplemented with fibrinogen. The gelation of the collagen and the fibrinogen into fibrin is initiated by pH change and enzymatic crosslinking, respectively. Fabrication of the ventricle-like chamber is completed in three distinct phases: (i) materials preparation, (ii) bioprinting, and (iii) tissue maturation. In this protocol, we describe the method to print the construct from a high-density cell ink composed of human stem cell-derived cardiomyocytes and primary fibroblasts (~300 × 10<sup>6</sup> cells/mL) using our open-source dual-extruder bioprinter. Additional details are provided on FRESH support preparation, bioink preparation, dual-extruder needle alignment, print parameter selection, and post-processing. This protocol can also be adapted by altering the 3D model design, cell concentration, or cell type to FRESH 3D bioprint other cardiac tissue constructs. |
2,329,925 | Deconstructing the functional neuroanatomy of the choroid plexus: an ontogenetic perspective for studying neurodevelopmental and neuropsychiatric disorders. | The choroid plexus (CP) is a delicate and highly vascularized structure in the brain comprised of a dense network of fenestrated capillary loops that help in the synthesis, secretion and circulation of cerebrospinal fluid (CSF). This unique neuroanatomical structure is comprised of arachnoid villi stemming from frond-like surface projections-that protrude into the lumen of the four cerebral ventricles-providing a key source of nutrients to the brain parenchyma in addition to serving as a 'sink' for central nervous system metabolic waste. In fact, the functions of the CP are often described as being analogous to those of the liver and kidney. Beyond forming a barrier/interface between the blood and CSF compartments, the CP has been identified as a modulator of leukocyte trafficking, inflammation, cognition, circadian rhythm and the gut brain-axis. In recent years, advances in molecular biology techniques and neuroimaging along with the use of sophisticated animal models have played an integral role in shaping our understanding of how the CP-CSF system changes in relation to the maturation of neural circuits during critical periods of brain development. In this article we provide an ontogenetic perspective of the CP and review the experimental evidence implicating this structure in the pathophysiology of neurodevelopmental and neuropsychiatric disorders. |
2,329,926 | Dyssynchronous Left Ventricular Activation is Insufficient for the Breakdown of Wringing Rotation. | Cardiac resynchronization therapy is a valuable tool to restore left ventricular function in patients experiencing dyssynchronous ventricular activation. However, the non-responder rate is still as high as 40%. Recent studies suggest that left ventricular torsion or specifically the lack thereof might be a good predictor for the response of cardiac resynchronization therapy. Since left ventricular torsion is governed by the muscle fiber orientation and the heterogeneous electromechanical activation of the myocardium, understanding the relation between these components and the ability to measure them is vital. To analyze if locally altered electromechanical activation in heart failure patients affects left ventricular torsion, we conducted a simulation study on 27 personalized left ventricular models. Electroanatomical maps and late gadolinium enhanced magnetic resonance imaging data informed our in-silico model cohort. The angle of rotation was evaluated in every material point of the model and averaged values were used to classify the rotation as clockwise or counterclockwise in each segment and sector of the left ventricle. 88% of the patient models (<i>n</i> = 24) were classified as a wringing rotation and 12% (<i>n</i> = 3) as a rigid-body-type rotation. Comparison to classification based on <i>in vivo</i> rotational NOGA XP maps showed no correlation. Thus, isolated changes of the electromechanical activation sequence in the left ventricle are not sufficient to reproduce the rotation pattern changes observed <i>in vivo</i> and suggest that further patho-mechanisms are involved. |
2,329,927 | Case Report: A Very Low Birth Weight Female Infant With Congenital Bilateral Periventricular Leukomalacia, Born to a Mother With Coronavirus Disease 2019. | A 26-year-old primipara woman with COVID-19 performed an emergency Cesarean section due to further hypoxemia at 28 weeks 5/7 days gestation. The female neonate was born weighing 1,347 gram with an Apgar score of four at 1 min, three at 5 min, and eight at 10 min. RT-PCR from nasopharyngeal swabs for COVID-19 were performed at birth, 24 h, and 48 h after birth, all of which were negative. On head ultrasound bilateral cystic lesions were found in the anterior horn of the lateral ventricles at birth. A brain magnetic resonance imaging (MRI) test at 56 days of life (corrected 36 weeks and 6/7 days) revealed cystic lesions with T1 low signal, T2 high signal, and T2 Flair high signal around the anterior horn of the lateral ventricle and We diagnose it as Grade 2 periventricular leukomalacia (PVL). She was discharged on day 64 of life, with no abnormality on exam. While the majority of neonates born to women with COVID-19 during pregnancy have favorable outcome, we report a case of a neonate with Grade 2 periventricular leukomalacia and this should prompt clinicians to monitor fetal cerebral function and structure shortly after birth. |
2,329,928 | Lifespan Volume Trajectories From Non-harmonized T1-Weighted MRI Do Not Differ After Site Correction Based on Traveling Human Phantoms. | Multi-site imaging consortiums strive to increase participant numbers by pooling data across sites, but scanner related differences can bias results. This study combines data from three research MRI centers, including three different scanner models from two vendors, to examine non-harmonized T1-weighted brain imaging protocols in two cohorts. First, 23 human traveling phantoms were scanned twice each at all three sites (six scans per person; 138 scans total) to quantify within-participant variability of brain volumes (total brain, white matter, gray matter, lateral ventricles, thalamus, caudate, putamen and globus pallidus), and to calculate site-specific correction factors for each structure. Sample size calculations were used to determine the number of traveling phantoms needed to achieve effect sizes for observed differences to help guide future studies. Next, cross-sectional lifespan volume trajectories were examined in 856 healthy participants (5-91 years of age) scanned at these sites. Cross-sectional trajectories of volume versus age for each structure were then compared before and after application of traveling phantom based site-specific correction factors, as well as correction using the open-source method ComBat. Although small systematic differences between sites were observed in the traveling phantom analysis, correction for site using either method had little impact on the lifespan trajectories. Only white matter had small but significant differences in the intercept parameter after ComBat correction (but not traveling phantom based correction), while no other fits differed. This suggests that age-related changes over the lifespan outweigh systematic differences between scanners for volumetric analysis. This work will help guide pooling of multisite datasets as well as meta-analyses of data from non-harmonized protocols. |
2,329,929 | A Slice-Low-Rank Plus Sparse (slice-L + S) Reconstruction Method for k-t Undersampled Multiband First-Pass Myocardial Perfusion MRI. | The synergistic use of k-t undersampling and multiband (MB) imaging has the potential to provide extended slice coverage and high spatial resolution for first-pass perfusion MRI. The low-rank plus sparse (L + S) model has shown excellent performance for accelerating single-band (SB) perfusion MRI.</AbstractText>A MB data consistency method employing ESPIRiT maps and through-plane coil information was developed. This data consistency method was combined with the temporal L + S constraint to form the slice-L + S method. Slice-L + S was compared to SB L + S and the sequential operations of split slice-GRAPPA and SB L + S (seq-SG-L + S) using synthetic data formed from multislice SB images. Prospectively k-t undersampled MB data were also acquired and reconstructed using seq-SG-L + S and slice-L + S.</AbstractText>Using synthetic data with total acceleration rates of 6-12, slice-L + S outperformed SB L + S and seq-SG-L + S (N = 7 subjects) with respect to normalized RMSE and the structural similarity index (P < 0.05 for both). For the specific case with MB factor = 3 and rate 3 undersampling, or for SB imaging with rate 9 undersampling (N = 7 subjects), the normalized RMSE values were 0.037 ± 0.007, 0.042 ± 0.005, and 0.031 ± 0.004; and the structural similarity index values were 0.88 ± 0.03, 0.85 ± 0.03, and 0.89 ± 0.02 for SB L + S, seq-SG-L + S, and slice-L + S, respectively (P < 0.05 for both). For prospectively undersampled MB data, slice-L + S provided better image quality than seq-SG-L + S for rate 6 (N = 7) and rate 9 acceleration (N = 7) as scored by blinded experts.</AbstractText>Slice-L + S outperformed SB-L + S and seq-SG-L + S and provides 9 slice coverage of the left ventricle with a spatial resolution of 1.5 mm × 1.5 mm with good image quality.</AbstractText>© 2022 The Authors. Magnetic Resonance in Medicine published by Wiley Periodicals LLC on behalf of International Society for Magnetic Resonance in Medicine.</CopyrightInformation> |
2,329,930 | Metabolic characterization of amniotic fluid of fetuses with isolated choroid plexus cyst. | To investigate the amino acid (AA)-related metabolic characteristics of amniotic fluid (AF) obtained by ultrasound-guided amniocentesis from fetuses with isolated choroid plexus cysts of the central nervous system.</AbstractText>Ultrasound-guided amniocentesis was performed on 17 fetuses with isolated choroid plexus cysts (ICPCs) and 17 normal fetuses. The AF samples from normal pregnancies were matched with the case samples in a 1:1 ratio based upon gestational age. The AF samples from the 34 fetuses were analyzed by liquid chromatography-mass spectrometry (LC-MS). Then, the peak areas of the metabolites were analyzed by principal component analysis (PCA), partial least squares discriminant analysis (PLS-DA) and univariate statistical analysis.</AbstractText>This study ultimately identified 31 AAs. Seven differentially abundant AAs were screened out, including citrulline, ethanolamine, aspartic acid, valine, 5-hydroxylysine, proline, and isoleucine (p-value<0.05). A total of 4 metabolic pathways were significantly altered in the ICPC group: valine, leucine and isoleucine biosynthesis; valine, leucine and isoleucine degradation; pantothenate and coenzyme A (CoA) biosynthesis; and arginine biosynthesis.</AbstractText>The results of this study indicate that fetuses with ICPC have disrupted levels of citrulline, ethanolamine, aspartic acid, valine, 5-hydroxylysine, proline, and isoleucine, which may ultimately affect fetal glucose and lipid metabolism.</AbstractText>© 2022 Walter de Gruyter GmbH, Berlin/Boston.</CopyrightInformation> |
2,329,931 | Intracranial pressure and optic disc changes in a rat model of obstructive hydrocephalus. | The kaolin induced obstructive hydrocephalus (OHC) model is well known for its ability to increase intracranial pressure (ICP) in experimental animals. Papilledema (PE) which is a predominant hallmark of elevated ICP in the clinic has not yet been studied in this model using high-resolution digital fundus microscopy. Further, the long-term effect on ICP and optic nerve head changes have not been fully demonstrated. In this study we aimed to monitor epidural ICP after induction of OHC and to examine changes in the optic disc. In addition, we validated epidural ICP to intraventricular ICP in this disease model.</AbstractText>Thirteen male Sprague-Dawley rats received an injection into the cisterna magna containing either kaolin-Ringer's lactate suspension (n = 8) or an equal amount of Ringer's lactate solution (n = 5). Epidural ICP was recorded post-operatively, and then continuously overnight and followed up after 1 week. The final epidural ICP value after 1 week was confirmed with simultaneous ventricular ICP measurement. Optic disc photos (ODP) were obtained preoperatively at baseline and after one week and were assessed for papilledema.</AbstractText>All animals injected with kaolin developed OHC and had significant higher epidural ICP (15.49 ± 2.47 mmHg) compared to control animals (5.81 ± 1.33 mmHg) on day 1 (p < 0.0001). After 1 week, the epidural ICP values were subsided to normal range in hydrocephalus animals and there was no significant difference in epidural ICP between the groups. Epidural ICP after 1 week correlated with the ventricular ICP with a Pearson's r = 0.89 (p < 0.0001). ODPs from both groups showed no signs of acute papilledema, but 5 out of 8 (62.5%) of the hydrocephalus animals were identified with peripapillary changes.</AbstractText>We demonstrated that the raised ICP at day 1 in the hydrocephalus animals was completely normalized within 1 week and that epidural ICP measurements are valid method in this model. No acute papilledema was identified in the hydrocephalus animals, but the peripapillary changes indicate a potential gliosis formation or an early state of a growing papilledema in the context of lateral ventricle dilation and increased ICP.</AbstractText>© 2022. The Author(s).</CopyrightInformation> |
2,329,932 | Two cases of spinal tanycytic ependymomas occurring in brothers with a neurofibromatosis type 2 gene mutation. | Tanycytic ependymomas are a rare spinal cord tumour arising from tanycyte cells lining the ventricle or spinal central canal. This is the first report of familial spinal tanycytic ependymoma occurring in two first degree relatives. Both patients underwent surgical resection of the intra-medullary tumours with good overall recovery. Genetic analysis identified that the brothers shared a previously unreported mutation in the NF-2 gene. NF-2 mutations in spinal tanycytic ependymomas may be more common than initially thought and consideration should be given to screening the neural axis for other tumours and genetic counselling. |
2,329,933 | Microstructural Deformations Within the Depth of the Lamina Cribrosa in Response to Acute In Vivo Intraocular Pressure Modulation. | The lamina cribrosa (LC) is a leading target for initial glaucomatous damage. We investigated the in vivo microstructural deformation within the LC volume in response to acute IOP modulation while maintaining fixed intracranial pressure (ICP).</AbstractText>In vivo optic nerve head (ONH) spectral-domain optical coherence tomography (OCT) scans (Leica, Chicago, IL, USA) were obtained from eight eyes of healthy adult rhesus macaques (7 animals; ages = 7.9-14.4 years) in different IOP settings and fixed ICP (8-12 mm Hg). IOP and ICP were controlled by cannulation of the anterior chamber and the lateral ventricle of the brain, respectively, connected to a gravity-controlled reservoir. ONH images were acquired at baseline IOP, 30 mm Hg (H1-IOP), and 40 to 50 mm Hg (H2-IOP). Scans were registered in 3D, and LC microstructure measurements were obtained from shared regions and depths.</AbstractText>Only half of the eyes exhibited LC beam-to-pore ratio (BPR) and microstructure deformations. The maximal BPR change location within the LC volume varied between eyes. BPR deformer eyes had a significantly higher baseline connective tissue volume fraction (CTVF) and lower pore aspect ratio (P = 0.03 and P = 0.04, respectively) compared to BPR non-deformer. In all eyes, the magnitude of BPR changes in the anterior surface was significantly different (either larger or smaller) from the maximal change within the LC (H1-IOP: P = 0.02 and H2-IOP: P = 0.004).</AbstractText>The LC deforms unevenly throughout its depth in response to IOP modulation at fixed ICP. Therefore, analysis of merely the anterior LC surface microstructure will not fully capture the microstructure deformations within the LC. BPR deformer eyes have higher CTVF than BPR non-deformer eyes.</AbstractText> |
2,329,934 | Exercise intervention prevents early aged hypertension-caused cardiac dysfunction through inhibition of cardiac fibrosis.<Pagination><StartPage>4390</StartPage><EndPage>4401</EndPage><MedlinePgn>4390-4401</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.18632/aging.204077</ELocationID><Abstract><AbstractText Label="BACKGROUND">An inappropriate accumulation of fibrillar collagen is a common pathologic feature of early aged hypertensive heart disease, but little information regarding the effects of exercise training on cardiac fibrosis in hypertension is available. The purpose of this study was to evaluate the effects of exercise training on cardiac fibrotic pathways in early aged hypertensive rats.</AbstractText><AbstractText Label="METHODS">Masson's trichrome staining and Western blotting were performed on the excised left ventricle from twenty male spontaneously hypertensive rats at age of 48 weeks, which were randomly divided into either a sedentary hypertensive group (SHR) or exercise hypertensive group (SHR-EX, running on a treadmill running occurred 5 days/week for 60 min/day, for 12 weeks), and from age-matched male Wistar-Kyoto normotensive controls (WKY).</AbstractText><AbstractText Label="RESULTS">Interstitial fibrosis was reduced in the SHR-Ex group when compared with the SHR group. The fibrotic-related protein levels of AT<sub>1</sub>R, FGF23, LOX-2, TGF-β, CTGF, p-Smad 2/3, MMP-2/TIMP-2, MMP-9/TIMP-1, uPA and collagen I were decreased in the SHR-EX group, when compared with the SHR group.</AbstractText><AbstractText Label="CONCLUSIONS">Exercise training suppresses early aged hypertensive heart-induced LOX-2/TGF-β-mediated fibrotic pathways associated with decreasing AT<sub>1</sub>R and FGF23, which might provide a new therapeutic effect for exercise training to prevent adverse cardiac fibrosis and myocardial abnormalities in early aged hypertension.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hong</LastName><ForeName>Yi</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>The First Rehabilitation Hospital of Shanghai, Shanghai, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Ai-Lun</ForeName><Initials>AL</Initials><AffiliationInfo><Affiliation>Department of Sports Sciences, University of Taipei, Taipei, Taiwan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wong</LastName><ForeName>James K S</ForeName><Initials>JKS</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Asia University Hospital, Taichung, Taiwan.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Bioinformatics and Medical Engineering, Asia University, Taichung, Taiwan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Masodsai</LastName><ForeName>Kunanya</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Faculty of Sports Science, Chulalongkorn University, Bangkok, Thailand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Shin-Da</ForeName><Initials>SD</Initials><AffiliationInfo><Affiliation>Department of Physical Therapy, Graduate Institute of Rehabilitation Science, China Medical University, Taichung, Taiwan.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Physical Therapy, Asia University, Taichung, Taiwan.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>School of Rehabilitation Medicine, Weifang Medical University, Shandong, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lin</LastName><ForeName>Yi-Yuan</ForeName><Initials>YY</Initials><AffiliationInfo><Affiliation>Department of Exercise and Health Science, National Taipei University of Nursing and Health Sciences, Taipei, Taiwan.</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>05</Month><Day>23</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Aging (Albany NY)</MedlineTA><NlmUniqueID>101508617</NlmUniqueID><ISSNLinking>1945-4589</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016212">Transforming Growth Factor beta</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005081" MajorTopicYN="N">Exercise Therapy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005355" MajorTopicYN="N">Fibrosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006331" MajorTopicYN="Y">Heart Diseases</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006973" MajorTopicYN="Y">Hypertension</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009206" MajorTopicYN="N">Myocardium</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011918" MajorTopicYN="N">Rats, Inbred SHR</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011921" MajorTopicYN="N">Rats, Inbred WKY</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016212" MajorTopicYN="N">Transforming Growth Factor beta</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">aging</Keyword><Keyword MajorTopicYN="N">hypertension</Keyword><Keyword MajorTopicYN="N">myocardial fibrosis</Keyword><Keyword MajorTopicYN="N">treadmill training</Keyword></KeywordList><CoiStatement><b>CONFLICTS OF INTEREST:</b> The authors declare no conflicts of interest related to this study.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2021</Year><Month>12</Month><Day>2</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>5</Month><Day>2</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>5</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>6</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>5</Month><Day>23</Day><Hour>11</Hour><Minute>3</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35604403</ArticleId><ArticleId IdType="pmc">PMC9186761</ArticleId><ArticleId IdType="doi">10.18632/aging.204077</ArticleId><ArticleId IdType="pii">204077</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Whelton PK, Carey RM, Aronow WS, Casey DE Jr, Collins KJ, Dennison Himmelfarb C, DePalma SM, Gidding S, Jamerson KA, Jones DW, MacLaughlin EJ, Muntner P, Ovbiagele B, et al.. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Hypertension. 2018; 71:1269–324. 10.1161/HYP.0000000000000066</Citation><ArticleIdList><ArticleId IdType="doi">10.1161/HYP.0000000000000066</ArticleId><ArticleId IdType="pubmed">29133354</ArticleId></ArticleIdList></Reference><Reference><Citation>Kearney PM, Whelton M, Reynolds K, Muntner P, Whelton PK, He J. Global burden of hypertension: analysis of worldwide data. Lancet. 2005; 365:217–23. 10.1016/S0140-6736(05)17741-1</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/S0140-6736(05)17741-1</ArticleId><ArticleId IdType="pubmed">15652604</ArticleId></ArticleIdList></Reference><Reference><Citation>Yip GW, Fung JW, Tan YT, Sanderson JE. Hypertension and heart failure: a dysfunction of systole, diastole or both? J Hum Hypertens. 2009; 23:295–306. 10.1038/jhh.2008.141</Citation><ArticleIdList><ArticleId IdType="doi">10.1038/jhh.2008.141</ArticleId><ArticleId IdType="pubmed">19037230</ArticleId></ArticleIdList></Reference><Reference><Citation>Díez J, Querejeta R, López B, González A, Larman M, Martínez Ubago JL. Losartan-dependent regression of myocardial fibrosis is associated with reduction of left ventricular chamber stiffness in hypertensive patients. Circulation. 2002; 105:2512–7. 10.1161/01.cir.0000017264.66561.3d</Citation><ArticleIdList><ArticleId IdType="doi">10.1161/01.cir.0000017264.66561.3d</ArticleId><ArticleId IdType="pubmed">12034658</ArticleId></ArticleIdList></Reference><Reference><Citation>Weber KT, Janicki JS, Pick R, Capasso J, Anversa P. Myocardial fibrosis and pathologic hypertrophy in the rat with renovascular hypertension. Am J Cardiol. 1990; 65:1G–7G. 10.1016/0002-9149(90)90952-w</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/0002-9149(90)90952-w</ArticleId><ArticleId IdType="pubmed">2138851</ArticleId></ArticleIdList></Reference><Reference><Citation>Müller-Brunotte R, Kahan T, López B, Edner M, González A, Díez J, Malmqvist K. Myocardial fibrosis and diastolic dysfunction in patients with hypertension: results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA). J Hypertens. 2007; 25:1958–66. 10.1097/HJH.0b013e3282170ada</Citation><ArticleIdList><ArticleId IdType="doi">10.1097/HJH.0b013e3282170ada</ArticleId><ArticleId IdType="pubmed">17762662</ArticleId></ArticleIdList></Reference><Reference><Citation>Pi M, Ye R, Han X, Armstrong B, Liu X, Chen Y, Sun Y, Quarles LD. Cardiovascular Interactions between Fibroblast Growth Factor-23 and Angiotensin II. Sci Rep. 2018; 8:12398. 10.1038/s41598-018-30098-1</Citation><ArticleIdList><ArticleId IdType="doi">10.1038/s41598-018-30098-1</ArticleId><ArticleId IdType="pmc">PMC6098163</ArticleId><ArticleId IdType="pubmed">30120363</ArticleId></ArticleIdList></Reference><Reference><Citation>Rodríguez C, Martínez-González J. The Role of Lysyl Oxidase Enzymes in Cardiac Function and Remodeling. Cells. 2019; 8:1483. 10.3390/cells8121483</Citation><ArticleIdList><ArticleId IdType="doi">10.3390/cells8121483</ArticleId><ArticleId IdType="pmc">PMC6953057</ArticleId><ArticleId IdType="pubmed">31766500</ArticleId></ArticleIdList></Reference><Reference><Citation>Yang J, Savvatis K, Kang JS, Fan P, Zhong H, Schwartz K, Barry V, Mikels-Vigdal A, Karpinski S, Kornyeyev D, Adamkewicz J, Feng X, Zhou Q, et al.. Targeting LOXL2 for cardiac interstitial fibrosis and heart failure treatment. Nat Commun. 2016; 7:13710. 10.1038/ncomms13710</Citation><ArticleIdList><ArticleId IdType="doi">10.1038/ncomms13710</ArticleId><ArticleId IdType="pmc">PMC5171850</ArticleId><ArticleId IdType="pubmed">27966531</ArticleId></ArticleIdList></Reference><Reference><Citation>Lu M, Qin Q, Yao J, Sun L, Qin X. Induction of LOX by TGF-β1/Smad/AP-1 signaling aggravates rat myocardial fibrosis and heart failure. IUBMB Life. 2019; 71:1729–39. 10.1002/iub.2112</Citation><ArticleIdList><ArticleId IdType="doi">10.1002/iub.2112</ArticleId><ArticleId IdType="pubmed">31317653</ArticleId></ArticleIdList></Reference><Reference><Citation>Dobaczewski M, Chen W, Frangogiannis NG. Transforming growth factor (TGF)-β signaling in cardiac remodeling. J Mol Cell Cardiol. 2011; 51:600–6. 10.1016/j.yjmcc.2010.10.033</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.yjmcc.2010.10.033</ArticleId><ArticleId IdType="pmc">PMC3072437</ArticleId><ArticleId IdType="pubmed">21059352</ArticleId></ArticleIdList></Reference><Reference><Citation>Chen MM, Lam A, Abraham JA, Schreiner GF, Joly AH. CTGF expression is induced by TGF- beta in cardiac fibroblasts and cardiac myocytes: a potential role in heart fibrosis. J Mol Cell Cardiol. 2000; 32:1805–19. 10.1006/jmcc.2000.1215</Citation><ArticleIdList><ArticleId IdType="doi">10.1006/jmcc.2000.1215</ArticleId><ArticleId IdType="pubmed">11013125</ArticleId></ArticleIdList></Reference><Reference><Citation>Grotendorst GR, Okochi H, Hayashi N. A novel transforming growth factor beta response element controls the expression of the connective tissue growth factor gene. Cell Growth Differ. 1996; 7:469–80.</Citation><ArticleIdList><ArticleId IdType="pubmed">9052988</ArticleId></ArticleIdList></Reference><Reference><Citation>Ducharme A, Frantz S, Aikawa M, Rabkin E, Lindsey M, Rohde LE, Schoen FJ, Kelly RA, Werb Z, Libby P, Lee RT. Targeted deletion of matrix metalloproteinase-9 attenuates left ventricular enlargement and collagen accumulation after experimental myocardial infarction. J Clin Invest. 2000; 106:55–62. 10.1172/JCI8768</Citation><ArticleIdList><ArticleId IdType="doi">10.1172/JCI8768</ArticleId><ArticleId IdType="pmc">PMC517910</ArticleId><ArticleId IdType="pubmed">10880048</ArticleId></ArticleIdList></Reference><Reference><Citation>Hayashidani S, Tsutsui H, Ikeuchi M, Shiomi T, Matsusaka H, Kubota T, Imanaka-Yoshida K, Itoh T, Takeshita A. Targeted deletion of MMP-2 attenuates early LV rupture and late remodeling after experimental myocardial infarction. Am J Physiol Heart Circ Physiol. 2003; 285:H1229–35. 10.1152/ajpheart.00207.2003</Citation><ArticleIdList><ArticleId IdType="doi">10.1152/ajpheart.00207.2003</ArticleId><ArticleId IdType="pubmed">12775562</ArticleId></ArticleIdList></Reference><Reference><Citation>Heymans S, Luttun A, Nuyens D, Theilmeier G, Creemers E, Moons L, Dyspersin GD, Cleutjens JP, Shipley M, Angellilo A, Levi M, Nübe O, Baker A, et al.. Inhibition of plasminogen activators or matrix metalloproteinases prevents cardiac rupture but impairs therapeutic angiogenesis and causes cardiac failure. Nat Med. 1999; 5:1135–42. 10.1038/13459</Citation><ArticleIdList><ArticleId IdType="doi">10.1038/13459</ArticleId><ArticleId IdType="pubmed">10502816</ArticleId></ArticleIdList></Reference><Reference><Citation>Tayebjee MH, Lip GY, Blann AD, Macfadyen RJ. Effects of age, gender, ethnicity, diurnal variation and exercise on circulating levels of matrix metalloproteinases (MMP)-2 and -9, and their inhibitors, tissue inhibitors of matrix metalloproteinases (TIMP)-1 and -2. Thromb Res. 2005; 115:205–10. 10.1016/j.thromres.2004.08.023</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.thromres.2004.08.023</ArticleId><ArticleId IdType="pubmed">15617743</ArticleId></ArticleIdList></Reference><Reference><Citation>Heymans S, Lupu F, Terclavers S, Vanwetswinkel B, Herbert JM, Baker A, Collen D, Carmeliet P, Moons L. Loss or inhibition of uPA or MMP-9 attenuates LV remodeling and dysfunction after acute pressure overload in mice. Am J Pathol. 2005; 166:15–25. 10.1016/S0002-9440(10)62228-6</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/S0002-9440(10)62228-6</ArticleId><ArticleId IdType="pmc">PMC1602291</ArticleId><ArticleId IdType="pubmed">15631996</ArticleId></ArticleIdList></Reference><Reference><Citation>Yang HL, Hsieh PL, Hung CH, Cheng HC, Chou WC, Chu PM, Chang YC, Tsai KL. Early Moderate Intensity Aerobic Exercise Intervention Prevents Doxorubicin-Caused Cardiac Dysfunction Through Inhibition of Cardiac Fibrosis and Inflammation. Cancers (Basel). 2020; 12:1102. 10.3390/cancers12051102</Citation><ArticleIdList><ArticleId IdType="doi">10.3390/cancers12051102</ArticleId><ArticleId IdType="pmc">PMC7281105</ArticleId><ArticleId IdType="pubmed">32354131</ArticleId></ArticleIdList></Reference><Reference><Citation>Ma Y, Kuang Y, Bo W, Liang Q, Zhu W, Cai M, Tian Z. Exercise Training Alleviates Cardiac Fibrosis through Increasing Fibroblast Growth Factor 21 and Regulating TGF-β1-Smad2/3-MMP2/9 Signaling in Mice with Myocardial Infarction. Int J Mol Sci. 2021; 22:12341. 10.3390/ijms222212341</Citation><ArticleIdList><ArticleId IdType="doi">10.3390/ijms222212341</ArticleId><ArticleId IdType="pmc">PMC8623999</ArticleId><ArticleId IdType="pubmed">34830222</ArticleId></ArticleIdList></Reference><Reference><Citation>Mayumi E, Nishitani A, Yuki Y, Nakatsu T, Toyonaga S, Mashima K, Ogawa H, Hirohata S, Usui S, Shinohata R, Sakaguchi K, Kusachi S. Increased blood pressure levels relative to subjective feelings of intensity of exercise determined with the Borg scale in male patients with hypertension. Clin Exp Hypertens. 2008; 30:191–201. 10.1080/10641960802068436</Citation><ArticleIdList><ArticleId IdType="doi">10.1080/10641960802068436</ArticleId><ArticleId IdType="pubmed">18425699</ArticleId></ArticleIdList></Reference><Reference><Citation>Brock CM, King DS, Wofford MR, Harrell TK. Exercise, insulin resistance, and hypertension: a complex relationship. Metab Syndr Relat Disord. 2005; 3:60–5. 10.1089/met.2005.3.60</Citation><ArticleIdList><ArticleId IdType="doi">10.1089/met.2005.3.60</ArticleId><ArticleId IdType="pubmed">18370711</ArticleId></ArticleIdList></Reference><Reference><Citation>Spina RJ, Turner MJ, Ehsani AA. Exercise training enhances cardiac function in response to an afterload stress in older men. Am J Physiol. 1997; 272:H995–1000. 10.1152/ajpheart.1997.272.2.H995</Citation><ArticleIdList><ArticleId IdType="doi">10.1152/ajpheart.1997.272.2.H995</ArticleId><ArticleId IdType="pubmed">9124464</ArticleId></ArticleIdList></Reference><Reference><Citation>Smart N, Haluska B, Jeffriess L, Marwick TH. Exercise training in systolic and diastolic dysfunction: effects on cardiac function, functional capacity, and quality of life. Am Heart J. 2007; 153:530–6. 10.1016/j.ahj.2007.01.004</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.ahj.2007.01.004</ArticleId><ArticleId IdType="pubmed">17383289</ArticleId></ArticleIdList></Reference><Reference><Citation>Chen Hi HI, Chiang IP, Jen CJ. Exercise Training Increases Acetylcholine-Stimulated Endothelium-Derived Nitric Oxide Release in Spontaneously Hypertensive Rats. J Biomed Sci. 1996; 3:454–60. 10.1007/BF02258049</Citation><ArticleIdList><ArticleId IdType="doi">10.1007/BF02258049</ArticleId><ArticleId IdType="pubmed">11725126</ArticleId></ArticleIdList></Reference><Reference><Citation>Doggrell SA, Brown L. Rat models of hypertension, cardiac hypertrophy and failure. Cardiovasc Res. 1998; 39:89–105. 10.1016/s0008-6363(98)00076-5</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/s0008-6363(98)00076-5</ArticleId><ArticleId IdType="pubmed">9764192</ArticleId></ArticleIdList></Reference><Reference><Citation>Weber KT. Fibrosis and hypertensive heart disease. Curr Opin Cardiol. 2000; 15:264–72. 10.1097/00001573-200007000-00010</Citation><ArticleIdList><ArticleId IdType="doi">10.1097/00001573-200007000-00010</ArticleId><ArticleId IdType="pubmed">11139090</ArticleId></ArticleIdList></Reference><Reference><Citation>Schelbert EB, Fonarow GC, Bonow RO, Butler J, Gheorghiade M. Therapeutic targets in heart failure: refocusing on the myocardial interstitium. J Am Coll Cardiol. 2014; 63:2188–98. 10.1016/j.jacc.2014.01.068</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.jacc.2014.01.068</ArticleId><ArticleId IdType="pubmed">24657693</ArticleId></ArticleIdList></Reference><Reference><Citation>Li X, Wang K. Effects of moderate-intensity endurance exercise on angiotensin II and angiotensin II type I receptors in the rat heart. Mol Med Rep. 2017; 16:2439–44. 10.3892/mmr.2017.6864</Citation><ArticleIdList><ArticleId IdType="doi">10.3892/mmr.2017.6864</ArticleId><ArticleId IdType="pmc">PMC5548009</ArticleId><ArticleId IdType="pubmed">28656283</ArticleId></ArticleIdList></Reference><Reference><Citation>Fatini C, Guazzelli R, Manetti P, Battaglini B, Gensini F, Vono R, Toncelli L, Zilli P, Capalbo A, Abbate R, Gensini GF, Galanti G. RAS genes influence exercise-induced left ventricular hypertrophy: an elite athletes study. Med Sci Sports Exerc. 2000; 32:1868–72. 10.1097/00005768-200011000-00008</Citation><ArticleIdList><ArticleId IdType="doi">10.1097/00005768-200011000-00008</ArticleId><ArticleId IdType="pubmed">11079515</ArticleId></ArticleIdList></Reference><Reference><Citation>Chiao YA, Ramirez TA, Zamilpa R, Okoronkwo SM, Dai Q, Zhang J, Jin YF, Lindsey ML. Matrix metalloproteinase-9 deletion attenuates myocardial fibrosis and diastolic dysfunction in ageing mice. Cardiovasc Res. 2012; 96:444–55. 10.1093/cvr/cvs275</Citation><ArticleIdList><ArticleId IdType="doi">10.1093/cvr/cvs275</ArticleId><ArticleId IdType="pmc">PMC3500048</ArticleId><ArticleId IdType="pubmed">22918978</ArticleId></ArticleIdList></Reference><Reference><Citation>Ichihara S, Senbonmatsu T, Price E Jr, Ichiki T, Gaffney FA, Inagami T. Angiotensin II type 2 receptor is essential for left ventricular hypertrophy and cardiac fibrosis in chronic angiotensin II-induced hypertension. Circulation. 2001; 104:346–51. 10.1161/01.cir.104.3.346</Citation><ArticleIdList><ArticleId IdType="doi">10.1161/01.cir.104.3.346</ArticleId><ArticleId IdType="pubmed">11457756</ArticleId></ArticleIdList></Reference><Reference><Citation>Agarwal D, Haque M, Sriramula S, Mariappan N, Pariaut R, Francis J. Role of proinflammatory cytokines and redox homeostasis in exercise-induced delayed progression of hypertension in spontaneously hypertensive rats. Hypertension. 2009; 54:1393–400. 10.1161/HYPERTENSIONAHA.109.135459</Citation><ArticleIdList><ArticleId IdType="doi">10.1161/HYPERTENSIONAHA.109.135459</ArticleId><ArticleId IdType="pmc">PMC2780026</ArticleId><ArticleId IdType="pubmed">19841289</ArticleId></ArticleIdList></Reference><Reference><Citation>Leosco D, Parisi V, Femminella GD, Formisano R, Petraglia L, Allocca E, Bonaduce D. Effects of exercise training on cardiovascular adrenergic system. Front Physiol. 2013; 4:348. 10.3389/fphys.2013.00348</Citation><ArticleIdList><ArticleId IdType="doi">10.3389/fphys.2013.00348</ArticleId><ArticleId IdType="pmc">PMC3842896</ArticleId><ArticleId IdType="pubmed">24348425</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">35604150</PMID><DateCompleted><Year>2022</Year><Month>05</Month><Day>25</Day></DateCompleted><DateRevised><Year>2023</Year><Month>07</Month><Day>01</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1940-087X</ISSN><JournalIssue CitedMedium="Internet"><Issue>183</Issue><PubDate><Year>2022</Year><Month>May</Month><Day>05</Day></PubDate></JournalIssue><Title>Journal of visualized experiments : JoVE</Title><ISOAbbreviation>J Vis Exp</ISOAbbreviation></Journal>Utilizing the Precision-Cut Lung Slice to Study the Contractile Regulation of Airway and Intrapulmonary Arterial Smooth Muscle. | Smooth muscle cells (SMC) mediate the contraction of the airway and the intrapulmonary artery to modify airflow resistance and pulmonary circulation, respectively, hence playing a critical role in the homeostasis of the pulmonary system. Deregulation of SMC contractility contributes to several pulmonary diseases, including asthma and pulmonary hypertension. However, due to limited tissue access and a lack of culture systems to maintain in vivo SMC phenotypes, molecular mechanisms underlying the deregulated SMC contractility in these diseases remain fully identified. The precision-cut lung slice (PCLS) offers an ex vivo model that circumvents these technical difficulties. As a live, thin lung tissue section, the PCLS retains SMC in natural surroundings and allows in situ tracking of SMC contraction and intracellular Ca<sup>2+</sup> signaling that regulates SMC contractility. Here, a detailed mouse PCLS preparation protocol is provided, which preserves intact airways and intrapulmonary arteries. This protocol involves two essential steps before subjecting the lung lobe to slicing: inflating the airway with low-melting-point agarose through the trachea and infilling pulmonary vessels with gelatin through the right ventricle. The PCLS prepared using this protocol can be used for bioassays to evaluate Ca<sup>2+</sup>-mediated contractile regulation of SMC in both the airway and the intrapulmonary arterial compartments. When applied to mouse models of respiratory diseases, this protocol enables the functional investigation of SMC, thereby providing insight into the underlying mechanism of SMC contractility deregulation in diseases. |
2,329,935 | Lateral Ventricular Volume Asymmetry and Optic Nerve Sheath Diameter Predict Intracranial Pressure in Traumatic Brain Injury Patients. | Various noninvasive methods of intracranial pressure (ICP) measurement have been proposed. Each has unique advantages and limitations. This study was aimed at investigating the relationships between lateral ventricular asymmetry on admission computed tomography, optic nerve sheath diameter (ONSD), and ICP in traumatic brain injury (TBI) patients.</AbstractText>A prospective observational study was conducted in the patients admitted to our department between October 2018 and October 2020. 20 patients with moderate-severe TBI with a Glasgow Coma Scale of 3-12 were enrolled. Lateral ventricle volume (LVV) value measurements were conducted using ITK-SNAP software. The lateral ventricular volume ratio (LVR) was quantified by dividing the larger LVV by the smaller.</AbstractText>ONSD and LVR had a good correlation with ICP. Admission LVR of >1.735 was shown to have a sensitivity of 90.9% and a specificity of 88.9% for prediction of ICP increase (AUC = 0.879; standard error = 0.091; 95% CI = 0.701 to 1.0; significance level p</i> < 0.004). Admission ONSD of >5.55 mm was shown to have a sensitivity of 81.8% and a specificity of 88.9% for prediction of ICP increase (AUC = 0.919; standard error = 0.062; 95% CI = 0.798 to 1.0; significance level p</i> < 0.002). Combining the ONSD and LVR, the sensitivity could be improved to 90.9% in parallel test, and the specificity could be improved to 100% in serial test.</AbstractText>ONSD and LVR measurements can diagnose elevated ICP in traumatic brain injury patients. ONSD combining with LVR may further improve the diagnostic evaluation.</AbstractText>Copyright © 2022 Yang Wang et al.</CopyrightInformation> |
2,329,936 | Feasibility of endoscopic endonasal resection of intrinsic third ventricular craniopharyngioma in adults. | Intrinsic third ventricular craniopharyngiomas (IVCs) are usually considered as a contraindication of endoscopic endonasal approach (EEA). The aim of this study is to evaluate the safety and feasibility of EEA for the resection of IVCs based on MRI topographical diagnosis and surgical findings. We reviewed the data of 22 patients who were diagnosed to be IVCs according to five MRI criteria and underwent surgery through EEA. Sixteen IVCs were resected using endoscopic endonasal infrachiasmatic corridor, five IVCs by using endoscopic endonasal suprachiasmatic trans-lamina terminalis corridor, and one IVC by using both the infrachiasmatic and suprachiasmatic corridors. During the operation, all the 22 cases were verified to be IVCs. Gross total resection was achieved in 21 (95.5%) patients. After surgery, visual improvement was observed in 14 (63.6%) patients, no change in 6 (27.3%) patients, and some deterioration in 2 (9.1%) patients. An improvement in intellectual ability was observed in nine (40.9%) patients, no change in twelve (54.5%) patients, and some deterioration in one (4.5%) patient. Fifteen of the 22 patients (68.2%) developed new endocrinological deficit. One postoperative cerebral spinal fluid leakage occurred. EEA can be used as a safe and efficacious approach for the radical resection of IVCs. The combination of the five MRI criteria may serve as an accurate preoperative diagnostic tool to define the topographical relationships between craniopharyngiomas and the third ventricle. The endoscopic transnasal view from below has the advantage of clarifying the relationship between tumors and the third ventricle floor. |
2,329,937 | Magnetic Resonance Imaging Evaluation of Perivascular Space Abnormalities in Neuromyelitis Optica.<Pagination><StartPage>173</StartPage><EndPage>183</EndPage><MedlinePgn>173-183</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/ana.26419</ELocationID><Abstract><AbstractText Label="OBJECTIVE">Astrocytes outline the perivascular space (PVS) and regulate fluid exchange through the aquaporin-4 water channel. As neuromyelitis optica is an autoimmune astrocytopathy targeting aquaporin-4, we hypothesized that it could be associatied with PVS abnormalities.</AbstractText><AbstractText Label="METHODS">A total of 34 patients, and 46 age- and sex-matched healthy controls from two independent cohorts (exploratory and validation dataset) underwent a standardized 3.0-T magnetic resonance imaging protocol including conventional and diffusion tensor imaging. Susceptibility-weighted imaging was also acquired in the exploratory dataset. We evaluated macroscopic and microstructural abnormalities of PVS in terms of enlargement and water diffusivity (DTI-ALPS index). In the exploration dataset, a susceptibility-weighted sequence was used to draw the regions of interest for the DTI-ALPS index calculation in areas having veins perpendicular to lateral ventricles. Between-group comparisons, correlations, and regression models were run to assess associations between PVS abnormalities, and clinical and magnetic resonance imaging variables.</AbstractText><AbstractText Label="RESULTS">Patients had a higher frequency of severe PVS enlargement in the centrum semiovale (29.4% vs 8.7%), which correlated with brain atrophy, deep grey matter atrophy, and poorer cognitive performance (r-values range: -0.44, -0.36; p values: 0.01-0.046). In both datasets, patients had reduced DTI-ALPS index compared with controls (p values 0.004-0.038). Lower DTI-ALPS index, deep gray matter volume, and cortical volume could discriminate between patients and controls (R<sup>2</sup>  = 0.62), whereas lower DTI-ALPS index, higher number of myelitis, and higher T2-lesion volume were associated with worse disability (R<sup>2</sup>  = 0.55).</AbstractText><AbstractText Label="INTERPRETATION">Patients with neuromyelitis optica spectrum disorder are characterized by abnormal enlargement and impaired water diffusion along the PVS, whose clinical implications suggest a direct correlation with disease pathogenesis and severity. ANN NEUROL 2022;92:173-183.</AbstractText><CopyrightInformation>© 2022 The Authors. Annals of Neurology published by Wiley Periodicals LLC on behalf of American Neurological Association.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Cacciaguerra</LastName><ForeName>Laura</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Vita-Salute San Raffaele University, Milan, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Carotenuto</LastName><ForeName>Antonio</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pagani</LastName><ForeName>Elisabetta</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mistri</LastName><ForeName>Damiano</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Radaelli</LastName><ForeName>Marta</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Martinelli</LastName><ForeName>Vittorio</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Filippi</LastName><ForeName>Massimo</ForeName><Initials>M</Initials><Identifier Source="ORCID">0000-0002-5485-0479</Identifier><AffiliationInfo><Affiliation>Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Vita-Salute San Raffaele University, Milan, Italy.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Neurorehabilitation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Neurophysiology Service, IRCCS San Raffaele Scientific Institute, Milan, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rocca</LastName><ForeName>Maria A</ForeName><Initials>MA</Initials><Identifier Source="ORCID">0000-0003-2358-4320</Identifier><AffiliationInfo><Affiliation>Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Vita-Salute San Raffaele University, Milan, Italy.</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>06</Month><Day>11</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Ann Neurol</MedlineTA><NlmUniqueID>7707449</NlmUniqueID><ISSNLinking>0364-5134</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051401">Aquaporin 4</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D051401" MajorTopicYN="N">Aquaporin 4</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001284" MajorTopicYN="N">Atrophy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D056324" MajorTopicYN="N">Diffusion Tensor Imaging</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008279" MajorTopicYN="N">Magnetic Resonance Imaging</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009471" MajorTopicYN="Y">Neuromyelitis Optica</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading></MeshHeadingList><CoiStatement>Nothing to report.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>5</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="received"><Year>2021</Year><Month>12</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>5</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>5</Month><Day>22</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>7</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>5</Month><Day>21</Day><Hour>3</Hour><Minute>2</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35596582</ArticleId><ArticleId IdType="pmc">PMC9544484</ArticleId><ArticleId IdType="doi">10.1002/ana.26419</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Wuerfel J, Haertle M, Waiczies H, et al. Perivascular spaces‐‐MRI marker of inflammatory activity in the brain. Brain 2008;131:2332–2340.</Citation><ArticleIdList><ArticleId IdType="pubmed">18676439</ArticleId></ArticleIdList></Reference><Reference><Citation>Wingerchuk DM, Banwell B, Bennett JL, et al. International consensus diagnostic criteria for neuromyelitis optica spectrum disorders. Neurology 2015;85:177–189.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC4515040</ArticleId><ArticleId IdType="pubmed">26092914</ArticleId></ArticleIdList></Reference><Reference><Citation>Lucchinetti CF, Guo Y, Popescu BF, et al. The pathology of an autoimmune astrocytopathy: lessons learned from neuromyelitis optica. Brain Pathol 2014;24:83–97.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC3905574</ArticleId><ArticleId IdType="pubmed">24345222</ArticleId></ArticleIdList></Reference><Reference><Citation>Saadoun S, Papadopoulos MC. Aquaporin‐4 in brain and spinal cord oedema. Neuroscience 2010;168:1036–1046.</Citation><ArticleIdList><ArticleId IdType="pubmed">19682555</ArticleId></ArticleIdList></Reference><Reference><Citation>Roemer SF, Parisi JE, Lennon VA, et al. Pattern‐specific loss of aquaporin‐4 immunoreactivity distinguishes neuromyelitis optica from multiple sclerosis. Brain 2007;130:1194–1205.</Citation><ArticleIdList><ArticleId IdType="pubmed">17282996</ArticleId></ArticleIdList></Reference><Reference><Citation>Wardlaw JM, Benveniste H, Nedergaard M, et al. Perivascular spaces in the brain: anatomy, physiology and pathology. Nat Rev Neurol 2020;16:137–153.</Citation><ArticleIdList><ArticleId IdType="pubmed">32094487</ArticleId></ArticleIdList></Reference><Reference><Citation>Sepehrband F, Cabeen RP, Choupan J, et al. Perivascular space fluid contributes to diffusion tensor imaging changes in white matter. Neuroimage 2019;197:243–254.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6591070</ArticleId><ArticleId IdType="pubmed">31051291</ArticleId></ArticleIdList></Reference><Reference><Citation>Taoka T, Masutani Y, Kawai H, et al. Evaluation of glymphatic system activity with the diffusion MR technique: diffusion tensor image analysis along the perivascular space (DTI‐ALPS) in Alzheimer's disease cases. Jpn J Radiol 2017;35:172–178.</Citation><ArticleIdList><ArticleId IdType="pubmed">28197821</ArticleId></ArticleIdList></Reference><Reference><Citation>Gouveia‐Freitas K, Bastos‐Leite AJ. Perivascular spaces and brain waste clearance systems: relevance for neurodegenerative and cerebrovascular pathology. Neuroradiology 2021;63:1581–1597.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC8460534</ArticleId><ArticleId IdType="pubmed">34019111</ArticleId></ArticleIdList></Reference><Reference><Citation>Chen HL, Chen PC, Lu CH, et al. Associations among cognitive functions, plasma DNA, and diffusion tensor image along the perivascular space (DTI‐ALPS) in patients with Parkinson's disease. Oxid Med Cell Longev 2021;2021:4034509.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC7904342</ArticleId><ArticleId IdType="pubmed">33680283</ArticleId></ArticleIdList></Reference><Reference><Citation>Carotenuto A, Cacciaguerra L, Pagani E, et al. Glymphatic system impairment in multiple sclerosis: relation with brain damage and disability. Brain 2021. doi:10.1093/brain/awab454</Citation><ArticleIdList><ArticleId IdType="doi">10.1093/brain/awab454</ArticleId><ArticleId IdType="pubmed">34919648</ArticleId></ArticleIdList></Reference><Reference><Citation>Kurtzke JF. Rating neurologic impairment in multiple sclerosis: an expanded disability status scale (EDSS). Neurology 1983;33:1444–1452.</Citation><ArticleIdList><ArticleId IdType="pubmed">6685237</ArticleId></ArticleIdList></Reference><Reference><Citation>Cacciaguerra L, Valsasina P, Meani A, et al. Volume of hippocampal subfields and cognitive deficits in neuromyelitis optica spectrum disorders. Eur J Neurol 2021;28:4167–4177.</Citation><ArticleIdList><ArticleId IdType="pubmed">34415660</ArticleId></ArticleIdList></Reference><Reference><Citation>Meng H, Xu J, Pan C, et al. Cognitive dysfunction in adult patients with neuromyelitis optica: a systematic review and meta‐analysis. J Neurol 2017;264:1549–1558.</Citation><ArticleIdList><ArticleId IdType="pubmed">27909800</ArticleId></ArticleIdList></Reference><Reference><Citation>Amato MP, Portaccio E, Goretti B, et al. The Rao's brief repeatable battery and Stroop test: normative values with age, education and gender corrections in an Italian population. Mult Scler 2006;12:787–793.</Citation><ArticleIdList><ArticleId IdType="pubmed">17263008</ArticleId></ArticleIdList></Reference><Reference><Citation>Sumowski JF, Benedict R, Enzinger C, et al. Cognition in multiple sclerosis: state of the field and priorities for the future. Neurology 2018;90:278–288.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC5818015</ArticleId><ArticleId IdType="pubmed">29343470</ArticleId></ArticleIdList></Reference><Reference><Citation>Valverde S, Cabezas M, Roura E, et al. Improving automated multiple sclerosis lesion segmentation with a cascaded 3D convolutional neural network approach. Neuroimage 2017;155:159–168.</Citation><ArticleIdList><ArticleId IdType="pubmed">28435096</ArticleId></ArticleIdList></Reference><Reference><Citation>Battaglini M, Jenkinson M, De Stefano N. Evaluating and reducing the impact of white matter lesions on brain volume measurements. Hum Brain Mapp 2012;33:2062–2071.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6870255</ArticleId><ArticleId IdType="pubmed">21882300</ArticleId></ArticleIdList></Reference><Reference><Citation>Smith SM, Zhang Y, Jenkinson M, et al. Accurate, robust, and automated longitudinal and cross‐sectional brain change analysis. Neuroimage 2002;17:479–489.</Citation><ArticleIdList><ArticleId IdType="pubmed">12482100</ArticleId></ArticleIdList></Reference><Reference><Citation>Patenaude B, Smith SM, Kennedy DN, Jenkinson M. A Bayesian model of shape and appearance for subcortical brain segmentation. Neuroimage 2011;56:907–922.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC3417233</ArticleId><ArticleId IdType="pubmed">21352927</ArticleId></ArticleIdList></Reference><Reference><Citation>Potter GM, Chappell FM, Morris Z, Wardlaw JM. Cerebral perivascular spaces visible on magnetic resonance imaging: development of a qualitative rating scale and its observer reliability. Cerebrovasc Dis 2015;39:224–231.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC4386144</ArticleId><ArticleId IdType="pubmed">25823458</ArticleId></ArticleIdList></Reference><Reference><Citation>Andersson JLR, Graham MS, Drobnjak I, et al. Towards a comprehensive framework for movement and distortion correction of diffusion MR images: within volume movement. Neuroimage 2017;152:450–466.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC5445723</ArticleId><ArticleId IdType="pubmed">28284799</ArticleId></ArticleIdList></Reference><Reference><Citation>Basser PJ, Mattiello J, LeBihan D. MR diffusion tensor spectroscopy and imaging. Biophys J 1994;66:259–267.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC1275686</ArticleId><ArticleId IdType="pubmed">8130344</ArticleId></ArticleIdList></Reference><Reference><Citation>Abdul‐Rahman HS, Gdeisat MA, Burton DR, et al. Fast and robust three‐dimensional best path phase unwrapping algorithm. Appl Optics 2007;46:6623–6635.</Citation><ArticleIdList><ArticleId IdType="pubmed">17846656</ArticleId></ArticleIdList></Reference><Reference><Citation>Sun H, Wilman AH. Background field removal using spherical mean value filtering and Tikhonov regularization. Magn Reson Med 2014;71:1151–1157.</Citation><ArticleIdList><ArticleId IdType="pubmed">23666788</ArticleId></ArticleIdList></Reference><Reference><Citation>Alexander DC, Pierpaoli C, Basser PJ, Gee JC. Spatial transformations of diffusion tensor magnetic resonance images. IEEE Trans Med Imaging 2001;20:1131–1139.</Citation><ArticleIdList><ArticleId IdType="pubmed">11700739</ArticleId></ArticleIdList></Reference><Reference><Citation>Taoka T, Ito R, Nakamichi R, et al. Reproducibility of diffusion tensor image analysis along the perivascular space (DTI‐ALPS) for evaluating interstitial fluid diffusivity and glymphatic function: CHanges in Alps index on multiple conditiON acquIsition eXperiment (CHAMONIX) study. Jpn J Radiol 2022;40:147–158.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC8803717</ArticleId><ArticleId IdType="pubmed">34390452</ArticleId></ArticleIdList></Reference><Reference><Citation>Ringstad G, Vatnehol SAS, Eide PK. Glymphatic MRI in idiopathic normal pressure hydrocephalus. Brain 2017;140:2691–2705.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC5841149</ArticleId><ArticleId IdType="pubmed">28969373</ArticleId></ArticleIdList></Reference><Reference><Citation>Smith SM, Jenkinson M, Johansen‐Berg H, et al. Tract‐based spatial statistics: voxelwise analysis of multi‐subject diffusion data. Neuroimage 2006;31:1487–1505.</Citation><ArticleIdList><ArticleId IdType="pubmed">16624579</ArticleId></ArticleIdList></Reference><Reference><Citation>Jessen NA, Munk AS, Lundgaard I, Nedergaard M. The Glymphatic system: a Beginner's guide. Neurochem Res 2015;40:2583–2599.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC4636982</ArticleId><ArticleId IdType="pubmed">25947369</ArticleId></ArticleIdList></Reference><Reference><Citation>Wiseman SJ, Bastin ME, Jardine CL, et al. Cerebral small vessel disease burden is increased in systemic lupus erythematosus. Stroke 2016;47:2722–2728.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC5079231</ArticleId><ArticleId IdType="pubmed">27703087</ArticleId></ArticleIdList></Reference><Reference><Citation>Troili F, Cipollini V, Moci M, et al. Perivascular unit: this must be the place. The anatomical crossroad between the immune, vascular and nervous system. Front Neuroanat 2020;14:17.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC7177187</ArticleId><ArticleId IdType="pubmed">32372921</ArticleId></ArticleIdList></Reference><Reference><Citation>Zhang Z, Zhou H, Liu X, et al. Identification of the clinical and neuroimaging characteristics in children with neuromyelitis optica spectrum disorders: a case series. Transl Pediatr 2021;10:2459–2466.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC8578765</ArticleId><ArticleId IdType="pubmed">34765469</ArticleId></ArticleIdList></Reference><Reference><Citation>Hyun JW, Park G, Kwak K, et al. Deep gray matter atrophy in neuromyelitis optica spectrum disorder and multiple sclerosis. Eur J Neurol 2017;24:437–445.</Citation><ArticleIdList><ArticleId IdType="pubmed">28009104</ArticleId></ArticleIdList></Reference><Reference><Citation>Tian DC, Xiu Y, Wang X, et al. Cortical thinning and ventricle enlargement in Neuromyelitis Optica Spectrum disorders. Front Neurol 2020;11:872.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC7481470</ArticleId><ArticleId IdType="pubmed">32973658</ArticleId></ArticleIdList></Reference><Reference><Citation>Saji E, Arakawa M, Yanagawa K, et al. Cognitive impairment and cortical degeneration in neuromyelitis optica. Ann Neurol 2013;73:65–76.</Citation><ArticleIdList><ArticleId IdType="pubmed">23378324</ArticleId></ArticleIdList></Reference><Reference><Citation>Iliff JJ, Wang M, Liao Y, et al. A paravascular pathway facilitates CSF flow through the brain parenchyma and the clearance of interstitial solutes, including amyloid beta. Sci Transl Med 2012;4:147ra111.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC3551275</ArticleId><ArticleId IdType="pubmed">22896675</ArticleId></ArticleIdList></Reference><Reference><Citation>Iliff JJ, Nedergaard M. Is there a cerebral lymphatic system? Stroke 2013;44:S93–S95.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC3699410</ArticleId><ArticleId IdType="pubmed">23709744</ArticleId></ArticleIdList></Reference><Reference><Citation>Yokota H, Vijayasarathi A, Cekic M, et al. Diagnostic performance of Glymphatic system evaluation using diffusion tensor imaging in idiopathic Normal pressure hydrocephalus and mimickers. Curr Gerontol Geriatr Res 2019;2019:5675014.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6609364</ArticleId><ArticleId IdType="pubmed">31320896</ArticleId></ArticleIdList></Reference><Reference><Citation>Hasan‐Olive MM, Enger R, Hansson HA, et al. Loss of perivascular aquaporin‐4 in idiopathic normal pressure hydrocephalus. Glia 2019;67:91–100.</Citation><ArticleIdList><ArticleId IdType="pubmed">30306658</ArticleId></ArticleIdList></Reference><Reference><Citation>Schubert JJ, Veronese M, Marchitelli L, et al. Dynamic (11)C‐PiB PET shows cerebrospinal fluid flow alterations in Alzheimer disease and multiple sclerosis. J Nucl Med 2019;60:1452–1460.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6785797</ArticleId><ArticleId IdType="pubmed">30850505</ArticleId></ArticleIdList></Reference><Reference><Citation>Prineas JW, Lee S. Multiple sclerosis: destruction and regeneration of astrocytes in acute lesions. J Neuropathol Exp Neurol 2019;78:140–156.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6330170</ArticleId><ArticleId IdType="pubmed">30605525</ArticleId></ArticleIdList></Reference><Reference><Citation>Masaki K, Suzuki SO, Matsushita T, et al. Connexin 43 astrocytopathy linked to rapidly progressive multiple sclerosis and neuromyelitis optica. PLoS One 2013;8:e72919.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC3749992</ArticleId><ArticleId IdType="pubmed">23991165</ArticleId></ArticleIdList></Reference><Reference><Citation>Richard C, Ruiz A, Cavagna S, et al. Connexins in neuromyelitis optica: a link between astrocytopathy and demyelination. Brain 2020;143:2721–2732.</Citation><ArticleIdList><ArticleId IdType="pubmed">32889550</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedBookArticle><BookDocument><PMID Version="1">29939609</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK507832</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-22431">Grief Reaction<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Mughal</LastName><ForeName>Saba</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Azhar</LastName><ForeName>Yusra</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Dow University of Health Sciences</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mahon</LastName><ForeName>Margaret M.</ForeName><Initials>MM</Initials><AffiliationInfo><Affiliation>National Institutes of Health Clinical Center</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Siddiqui</LastName><ForeName>Waqas J.</ForeName><Initials>WJ</Initials><AffiliationInfo><Affiliation>Drexel University</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>Grief is a natural and universal response to the loss of a loved one. The grief experience is not a state but a process. Most individuals recover adequately within a year after the loss; however, some individuals experience an extension of the standard grieving process. This condition has been identified as complicated grief or prolonged grief disorder, and it results from failure to transition from acute to integrated grief. Symptoms of acute grief include tearfulness, sadness, and insomnia and typically require no treatment. Intense grief over the loss of a significant person may trigger the acute onset of myocardial infarction (MI). The impact may be higher with cardiovascular risk. Complicated grief has prolonged symptoms of painful emotions and sorrow for more than one year. Complicated grief has also been termed as, 'prolonged grief disorder, 'persistent complex bereavement disorder, 'pathological grief' and 'traumatic grief'. Both the ICD-11 and DSM-5 have approved diagnoses of 'prolonged grief disorder.' All of these conditions depict intense, impaired, and prolonged grief. Patients show a preoccupation with the deceased and feel inner emptiness, no interest in life, and sleep poorly. There is a correlation between complicated grief and acute coronary syndrome (ACS). It has been estimated that 7-10% of those bereaved do not adapt to the loss and, in turn, develop complicated grief. The terms grief, mourning, and bereavement have slightly different meanings: <b>Grief</b> is a person's emotional response to loss. <b>Mourning</b> is an outward expression of that grief, including cultural and religious customs surrounding the death. It is also the process of adapting to life after loss. <b>Bereavement</b> is a period of grief and mourning after a loss. <b>Anticipatory Grief</b> is a response to an expected loss. It affects both the person diagnosed with a terminal illness as well as their families. . <b>Disenfranchised grief </b>as defined by Kenneth Doka (1989) is a "grief that persons experience when they incur a loss that is not or cannot be openly acknowledged, publicly mourned, or socially supported." Physicians regularly encounter losses in the form of patient deaths. Grief in healthcare providers is unsanctioned and may play a role in physician burnout. To adequately address the crisis of physician burnout, we need to address the under-recognized role of grief in the physician's clinical experience.  . <b>Takosubo Cardiomyopathy (Broken Heart Syndrome)</b>: is a weakening of the left ventricle caused by severe emotional or physical stress such as loss of a loved one, sudden illness, a serious accident, or a natural disaster (e.g., earthquake). It almost exclusively occurs in women and resolves within a month.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-22431" sec="article-22431.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22431" sec="article-22431.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22431" sec="article-22431.s3">Etiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22431" sec="article-22431.s4">Epidemiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22431" sec="article-22431.s5">Pathophysiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22431" sec="article-22431.s6">History and Physical</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22431" sec="article-22431.s7">Evaluation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22431" sec="article-22431.s8">Treatment / Management</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22431" sec="article-22431.s9">Differential Diagnosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22431" sec="article-22431.s10">Prognosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22431" sec="article-22431.s11">Complications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22431" sec="article-22431.s12">Deterrence and Patient Education</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22431" sec="article-22431.s13">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22431" sec="article-22431.s14">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22431" sec="article-22431.s15">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>5</Month><Day>22</Day></ContributionDate><ReferenceList><Reference><Citation>Kim SM, Kown SH. [Influential Factors of Complicated Grief of Bereaved Spouses from Cancer Patient]. J Korean Acad Nurs. 2018 Feb;48(1):59-69.</Citation><ArticleIdList><ArticleId IdType="pubmed">29535285</ArticleId></ArticleIdList></Reference><Reference><Citation>Edmondson D, Newman JD, Whang W, Davidson KW. Emotional triggers in myocardial infarction: do they matter? Eur Heart J. 2013 Jan;34(4):300-6.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC3549526</ArticleId><ArticleId IdType="pubmed">23178642</ArticleId></ArticleIdList></Reference><Reference><Citation>Iglewicz A, Shear MK, Reynolds CF, Simon N, Lebowitz B, Zisook S. Complicated grief therapy for clinicians: An evidence-based protocol for mental health practice. Depress Anxiety. 2020 Jan;37(1):90-98.</Citation><ArticleIdList><ArticleId IdType="pubmed">31622522</ArticleId></ArticleIdList></Reference><Reference><Citation>Mauro C, Reynolds CF, Maercker A, Skritskaya N, Simon N, Zisook S, Lebowitz B, Cozza SJ, Shear MK. Prolonged grief disorder: clinical utility of ICD-11 diagnostic guidelines. Psychol Med. 2019 Apr;49(5):861-867.</Citation><ArticleIdList><ArticleId IdType="pubmed">29909789</ArticleId></ArticleIdList></Reference><Reference><Citation>Zisook S, Iglewicz A, Avanzino J, Maglione J, Glorioso D, Zetumer S, Seay K, Vahia I, Young I, Lebowitz B, Pies R, Reynolds C, Simon N, Shear MK. Bereavement: course, consequences, and care. Curr Psychiatry Rep. 2014 Oct;16(10):482.</Citation><ArticleIdList><ArticleId IdType="pubmed">25135781</ArticleId></ArticleIdList></Reference><Reference><Citation>Li J, Tendeiro JN, Stroebe M. Guilt in bereavement: Its relationship with complicated grief and depression. Int J Psychol. 2019 Aug;54(4):454-461.</Citation><ArticleIdList><ArticleId IdType="pubmed">29508381</ArticleId></ArticleIdList></Reference><Reference><Citation>Lathrop D. Disenfranchised Grief and Physician Burnout. Ann Fam Med. 2017 Jul;15(4):375-378.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC5505460</ArticleId><ArticleId IdType="pubmed">28694277</ArticleId></ArticleIdList></Reference><Reference><Citation>Pore N, Burley M. When a broken heart is real: Takotsubo cardiomyopathy. Nurse Pract. 2012 Oct 10;37(10):48-52.</Citation><ArticleIdList><ArticleId IdType="pubmed">23014180</ArticleId></ArticleIdList></Reference><Reference><Citation>Bellini S, Erbuto D, Andriessen K, Milelli M, Innamorati M, Lester D, Sampogna G, Fiorillo A, Pompili M. Depression, Hopelessness, and Complicated Grief in Survivors of Suicide. Front Psychol. 2018;9:198.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC5852099</ArticleId><ArticleId IdType="pubmed">29568278</ArticleId></ArticleIdList></Reference><Reference><Citation>Ito M, Nakajima S, Fujisawa D, Miyashita M, Kim Y, Shear MK, Ghesquiere A, Wall MM. Brief measure for screening complicated grief: reliability and discriminant validity. PLoS One. 2012;7(2):e31209.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC3279351</ArticleId><ArticleId IdType="pubmed">22348057</ArticleId></ArticleIdList></Reference><Reference><Citation>Prigerson HG, Maciejewski PK, Reynolds CF, Bierhals AJ, Newsom JT, Fasiczka A, Frank E, Doman J, Miller M. Inventory of Complicated Grief: a scale to measure maladaptive symptoms of loss. Psychiatry Res. 1995 Nov 29;59(1-2):65-79.</Citation><ArticleIdList><ArticleId IdType="pubmed">8771222</ArticleId></ArticleIdList></Reference><Reference><Citation>Jordan JR, Baker J, Matteis M, Rosenthal S, Ware ES, Family Loss Project The grief evaluation measure (GEM): an initial validation study. Death Stud. 2005 May;29(4):301-32.</Citation><ArticleIdList><ArticleId IdType="pubmed">15849881</ArticleId></ArticleIdList></Reference><Reference><Citation>Shear MK, Wang Y, Skritskaya N, Duan N, Mauro C, Ghesquiere A. Treatment of complicated grief in elderly persons: a randomized clinical trial. JAMA Psychiatry. 2014 Nov;71(11):1287-95.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC5705174</ArticleId><ArticleId IdType="pubmed">25250737</ArticleId></ArticleIdList></Reference><Reference><Citation>Shear MK, Reynolds CF, Simon NM, Zisook S, Wang Y, Mauro C, Duan N, Lebowitz B, Skritskaya N. Optimizing Treatment of Complicated Grief: A Randomized Clinical Trial. JAMA Psychiatry. 2016 Jul 01;73(7):685-94.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC5735848</ArticleId><ArticleId IdType="pubmed">27276373</ArticleId></ArticleIdList></Reference><Reference><Citation>Morris S, Schaefer K, Rosowsky E. Primary Care for the Elderly Bereaved: Recommendations for Medical Education. J Clin Psychol Med Settings. 2018 Dec;25(4):463-470.</Citation><ArticleIdList><ArticleId IdType="pubmed">29500657</ArticleId></ArticleIdList></Reference><Reference><Citation>Rogalla KB. Anticipatory Grief, Proactive Coping, Social Support, and Growth: Exploring Positive Experiences of Preparing for Loss. Omega (Westport) 2020 May;81(1):107-129.</Citation><ArticleIdList><ArticleId IdType="pubmed">29516784</ArticleId></ArticleIdList></Reference><Reference><Citation>Hardy B. Meeting the needs of carers of people at the end of life. Nurs Stand. 2018 Apr 28;33(1):59-65.</Citation><ArticleIdList><ArticleId IdType="pubmed">29583171</ArticleId></ArticleIdList></Reference><Reference><Citation>BrintzenhofeSzoc KM, Smith ED, Zabora JR. Screening to predict complicated grief in spouses of cancer patients. Cancer Pract. 1999 Sep-Oct;7(5):233-9.</Citation><ArticleIdList><ArticleId IdType="pubmed">10687592</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">29939609</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35595088</PMID><DateRevised><Year>2022</Year><Month>06</Month><Day>24</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1552-6259</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>May</Month><Day>17</Day></PubDate></JournalIssue><Title>The Annals of thoracic surgery</Title><ISOAbbreviation>Ann Thorac Surg</ISOAbbreviation></Journal>Midterm Follow-up of the Transatrial-to-Left Ventricle Cannulation for Acute Type A Dissection. | Grief is a natural and universal response to the loss of a loved one. The grief experience is not a state but a process. Most individuals recover adequately within a year after the loss; however, some individuals experience an extension of the standard grieving process. This condition has been identified as complicated grief or prolonged grief disorder, and it results from failure to transition from acute to integrated grief. Symptoms of acute grief include tearfulness, sadness, and insomnia and typically require no treatment. Intense grief over the loss of a significant person may trigger the acute onset of myocardial infarction (MI). The impact may be higher with cardiovascular risk. Complicated grief has prolonged symptoms of painful emotions and sorrow for more than one year. Complicated grief has also been termed as, 'prolonged grief disorder, 'persistent complex bereavement disorder, 'pathological grief' and 'traumatic grief'. Both the ICD-11 and DSM-5 have approved diagnoses of 'prolonged grief disorder.' All of these conditions depict intense, impaired, and prolonged grief. Patients show a preoccupation with the deceased and feel inner emptiness, no interest in life, and sleep poorly. There is a correlation between complicated grief and acute coronary syndrome (ACS). It has been estimated that 7-10% of those bereaved do not adapt to the loss and, in turn, develop complicated grief. The terms grief, mourning, and bereavement have slightly different meanings: <b>Grief</b> is a person's emotional response to loss. <b>Mourning</b> is an outward expression of that grief, including cultural and religious customs surrounding the death. It is also the process of adapting to life after loss. <b>Bereavement</b> is a period of grief and mourning after a loss. <b>Anticipatory Grief</b> is a response to an expected loss. It affects both the person diagnosed with a terminal illness as well as their families. . <b>Disenfranchised grief </b>as defined by Kenneth Doka (1989) is a "grief that persons experience when they incur a loss that is not or cannot be openly acknowledged, publicly mourned, or socially supported." Physicians regularly encounter losses in the form of patient deaths. Grief in healthcare providers is unsanctioned and may play a role in physician burnout. To adequately address the crisis of physician burnout, we need to address the under-recognized role of grief in the physician's clinical experience.  . <b>Takosubo Cardiomyopathy (Broken Heart Syndrome)</b>: is a weakening of the left ventricle caused by severe emotional or physical stress such as loss of a loved one, sudden illness, a serious accident, or a natural disaster (e.g., earthquake). It almost exclusively occurs in women and resolves within a month.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-22431" sec="article-22431.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22431" sec="article-22431.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22431" sec="article-22431.s3">Etiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22431" sec="article-22431.s4">Epidemiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22431" sec="article-22431.s5">Pathophysiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22431" sec="article-22431.s6">History and Physical</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22431" sec="article-22431.s7">Evaluation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22431" sec="article-22431.s8">Treatment / Management</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22431" sec="article-22431.s9">Differential Diagnosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22431" sec="article-22431.s10">Prognosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22431" sec="article-22431.s11">Complications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22431" sec="article-22431.s12">Deterrence and Patient Education</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22431" sec="article-22431.s13">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22431" sec="article-22431.s14">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22431" sec="article-22431.s15">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>5</Month><Day>22</Day></ContributionDate><ReferenceList><Reference><Citation>Kim SM, Kown SH. [Influential Factors of Complicated Grief of Bereaved Spouses from Cancer Patient]. J Korean Acad Nurs. 2018 Feb;48(1):59-69.</Citation><ArticleIdList><ArticleId IdType="pubmed">29535285</ArticleId></ArticleIdList></Reference><Reference><Citation>Edmondson D, Newman JD, Whang W, Davidson KW. Emotional triggers in myocardial infarction: do they matter? Eur Heart J. 2013 Jan;34(4):300-6.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC3549526</ArticleId><ArticleId IdType="pubmed">23178642</ArticleId></ArticleIdList></Reference><Reference><Citation>Iglewicz A, Shear MK, Reynolds CF, Simon N, Lebowitz B, Zisook S. Complicated grief therapy for clinicians: An evidence-based protocol for mental health practice. Depress Anxiety. 2020 Jan;37(1):90-98.</Citation><ArticleIdList><ArticleId IdType="pubmed">31622522</ArticleId></ArticleIdList></Reference><Reference><Citation>Mauro C, Reynolds CF, Maercker A, Skritskaya N, Simon N, Zisook S, Lebowitz B, Cozza SJ, Shear MK. Prolonged grief disorder: clinical utility of ICD-11 diagnostic guidelines. Psychol Med. 2019 Apr;49(5):861-867.</Citation><ArticleIdList><ArticleId IdType="pubmed">29909789</ArticleId></ArticleIdList></Reference><Reference><Citation>Zisook S, Iglewicz A, Avanzino J, Maglione J, Glorioso D, Zetumer S, Seay K, Vahia I, Young I, Lebowitz B, Pies R, Reynolds C, Simon N, Shear MK. Bereavement: course, consequences, and care. Curr Psychiatry Rep. 2014 Oct;16(10):482.</Citation><ArticleIdList><ArticleId IdType="pubmed">25135781</ArticleId></ArticleIdList></Reference><Reference><Citation>Li J, Tendeiro JN, Stroebe M. Guilt in bereavement: Its relationship with complicated grief and depression. Int J Psychol. 2019 Aug;54(4):454-461.</Citation><ArticleIdList><ArticleId IdType="pubmed">29508381</ArticleId></ArticleIdList></Reference><Reference><Citation>Lathrop D. Disenfranchised Grief and Physician Burnout. Ann Fam Med. 2017 Jul;15(4):375-378.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC5505460</ArticleId><ArticleId IdType="pubmed">28694277</ArticleId></ArticleIdList></Reference><Reference><Citation>Pore N, Burley M. When a broken heart is real: Takotsubo cardiomyopathy. Nurse Pract. 2012 Oct 10;37(10):48-52.</Citation><ArticleIdList><ArticleId IdType="pubmed">23014180</ArticleId></ArticleIdList></Reference><Reference><Citation>Bellini S, Erbuto D, Andriessen K, Milelli M, Innamorati M, Lester D, Sampogna G, Fiorillo A, Pompili M. Depression, Hopelessness, and Complicated Grief in Survivors of Suicide. Front Psychol. 2018;9:198.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC5852099</ArticleId><ArticleId IdType="pubmed">29568278</ArticleId></ArticleIdList></Reference><Reference><Citation>Ito M, Nakajima S, Fujisawa D, Miyashita M, Kim Y, Shear MK, Ghesquiere A, Wall MM. Brief measure for screening complicated grief: reliability and discriminant validity. PLoS One. 2012;7(2):e31209.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC3279351</ArticleId><ArticleId IdType="pubmed">22348057</ArticleId></ArticleIdList></Reference><Reference><Citation>Prigerson HG, Maciejewski PK, Reynolds CF, Bierhals AJ, Newsom JT, Fasiczka A, Frank E, Doman J, Miller M. Inventory of Complicated Grief: a scale to measure maladaptive symptoms of loss. Psychiatry Res. 1995 Nov 29;59(1-2):65-79.</Citation><ArticleIdList><ArticleId IdType="pubmed">8771222</ArticleId></ArticleIdList></Reference><Reference><Citation>Jordan JR, Baker J, Matteis M, Rosenthal S, Ware ES, Family Loss Project The grief evaluation measure (GEM): an initial validation study. Death Stud. 2005 May;29(4):301-32.</Citation><ArticleIdList><ArticleId IdType="pubmed">15849881</ArticleId></ArticleIdList></Reference><Reference><Citation>Shear MK, Wang Y, Skritskaya N, Duan N, Mauro C, Ghesquiere A. Treatment of complicated grief in elderly persons: a randomized clinical trial. JAMA Psychiatry. 2014 Nov;71(11):1287-95.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC5705174</ArticleId><ArticleId IdType="pubmed">25250737</ArticleId></ArticleIdList></Reference><Reference><Citation>Shear MK, Reynolds CF, Simon NM, Zisook S, Wang Y, Mauro C, Duan N, Lebowitz B, Skritskaya N. Optimizing Treatment of Complicated Grief: A Randomized Clinical Trial. JAMA Psychiatry. 2016 Jul 01;73(7):685-94.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC5735848</ArticleId><ArticleId IdType="pubmed">27276373</ArticleId></ArticleIdList></Reference><Reference><Citation>Morris S, Schaefer K, Rosowsky E. Primary Care for the Elderly Bereaved: Recommendations for Medical Education. J Clin Psychol Med Settings. 2018 Dec;25(4):463-470.</Citation><ArticleIdList><ArticleId IdType="pubmed">29500657</ArticleId></ArticleIdList></Reference><Reference><Citation>Rogalla KB. Anticipatory Grief, Proactive Coping, Social Support, and Growth: Exploring Positive Experiences of Preparing for Loss. Omega (Westport) 2020 May;81(1):107-129.</Citation><ArticleIdList><ArticleId IdType="pubmed">29516784</ArticleId></ArticleIdList></Reference><Reference><Citation>Hardy B. Meeting the needs of carers of people at the end of life. Nurs Stand. 2018 Apr 28;33(1):59-65.</Citation><ArticleIdList><ArticleId IdType="pubmed">29583171</ArticleId></ArticleIdList></Reference><Reference><Citation>BrintzenhofeSzoc KM, Smith ED, Zabora JR. Screening to predict complicated grief in spouses of cancer patients. Cancer Pract. 1999 Sep-Oct;7(5):233-9.</Citation><ArticleIdList><ArticleId IdType="pubmed">10687592</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">29939609</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35595088</PMID><DateRevised><Year>2022</Year><Month>06</Month><Day>24</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1552-6259</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>May</Month><Day>17</Day></PubDate></JournalIssue><Title>The Annals of thoracic surgery</Title><ISOAbbreviation>Ann Thorac Surg</ISOAbbreviation></Journal><ArticleTitle>Midterm Follow-up of the Transatrial-to-Left Ventricle Cannulation for Acute Type A Dissection.</ArticleTitle><ELocationID EIdType="pii" ValidYN="Y">S0003-4975(22)00703-2</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.athoracsur.2022.04.050</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">It is still controversial as to which cannulation strategy for acute type A aortic dissection (AAD) is optimal. Antegrade perfusion to diminish further organ malperfusion and ischemia is preferable.<AbstractText Label="METHODS" NlmCategory="METHODS">We retrospectively analyzed a total of 420 patients who underwent AAD surgery from January 2001 to December 2020. Group A included 229 patients with a transatrial cannulation; group B included 191 patients with all other additionally used cannulation sites. A retrospective analysis was conducted at 30 days and according to clinical outcome and midterm mortality. Risk factors for probability of death were analyzed by multifactorial logistic regression.<AbstractText Label="RESULTS" NlmCategory="RESULTS">The calculated risk scores and demographic preoperative variables were comparable except for hyperlipoproteinemia (P = .011) and redo operation in group B (P < .001) and more pericardial tamponade in group A (P = .006). In addition, fewer patients with postoperative new onset of renal failure were observed in group A (P = .039), although new onset of dialysis was not different between the groups (P = .878). Patients in group A were discharged from the hospital significantly earlier (P = .004). Nevertheless, although significantly more total arch surgery was performed in group A, shorter operation times (P < .001) and lower transfusion rates were observed in group A. Patients' follow-up after a median time of 3.6 (0.6-7.6) years showed no difference in 30-day, 1-year, and long-term mortality. Multivariate logistic regression revealed aortic valve stenosis (P = .041), coronary artery bypass graft surgical procedures (P = .014), preoperative cardiopulmonary resuscitation (P < .001), and length of surgery (P = .032) as the strongest risk factors for mortality.<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Transatrial cannulation for AAD operation was safe and successfully performed under emergent conditions. Although no benefit in mortality was achieved, clinical benefits of shorter operation times, less transfusion, better kidney preservation, and earlier discharge of the patient were observed. |
2,329,938 | A taxonomy for brainstem cavernous malformations: subtypes of medullary lesions. | Medullary cavernous malformations are the least common of the brainstem cavernous malformations (BSCMs), accounting for only 14% of lesions in the authors' surgical experience. In this article, a novel taxonomy for these lesions is proposed based on clinical presentation and anatomical location.</AbstractText>The taxonomy system was applied to a large 2-surgeon experience over a 30-year period (1990-2019). Of 601 patients who underwent microsurgical resection of BSCMs, 551 were identified who had the clinical and radiological information needed for inclusion. These 551 patients were classified by lesion location: midbrain (151 [27%]), pons (323 [59%]), and medulla (77 [14%]). Medullary lesions were subtyped on the basis of their predominant surface presentation. Neurological outcomes were assessed according to the modified Rankin Scale (mRS), with an mRS score ≤ 2 defined as favorable.</AbstractText>Five distinct subtypes were defined for the 77 medullary BSCMs: pyramidal (3 [3.9%]), olivary (35 [46%]), cuneate (24 [31%]), gracile (5 [6.5%]), and trigonal (10 [13%]). Pyramidal lesions are located in the anterior medulla and were associated with hemiparesis and hypoglossal nerve palsy. Olivary lesions are found in the anterolateral medulla and were associated with ataxia. Cuneate lesions are located in the posterolateral medulla and were associated with ipsilateral upper-extremity sensory deficits. Gracile lesions are located outside the fourth ventricle in the posteroinferior medulla and were associated with ipsilateral lower-extremity sensory deficits. Trigonal lesions in the ventricular floor were associated with nausea, vomiting, and diplopia. A single surgical approach was preferred (> 90% of cases) for each medullary subtype: the far lateral approach for pyramidal and olivary lesions, the suboccipital-telovelar approach for cuneate lesions, the suboccipital-transcisterna magna approach for gracile lesions, and the suboccipital-transventricular approach for trigonal lesions. Of these 77 patients for whom follow-up data were available (n = 73), 63 (86%) had favorable outcomes and 67 (92%) had unchanged or improved functional status.</AbstractText>This study confirms that the constellation of neurological signs and symptoms associated with a hemorrhagic medullary BSCM subtype is useful for defining the BSCM clinically according to a neurologically recognizable syndrome at the bedside. The proposed taxonomical classifications may be used to guide the selection of surgical approaches, which may enhance the consistency of clinical communications and help improve patient outcomes.</AbstractText> |
2,329,939 | Cytokine receptor gp130 promotes postnatal proliferation of cardiomyocytes required for the normal functional development of the heart.<Pagination><StartPage>H103</StartPage><EndPage>H120</EndPage><MedlinePgn>H103-H120</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1152/ajpheart.00698.2021</ELocationID><Abstract><AbstractText>Mammalian ventricular cardiomyocytes are premature at birth and exhibit substantial phenotypic changes before weaning. Mouse ventricular myocytes undergo cell division several times after birth; however, the regulatory mechanisms and roles of cardiomyocyte division in postnatal heart development remain unclear. Here, we investigated the physiological role of glycoprotein 130 (gp130), the main subunit of multifunctional receptors for the IL-6 family of cytokines, in postnatal cardiomyocyte proliferation. Pharmacological inhibition of gp130 within the first month after birth induced significant systolic dysfunction of the left ventricle in mice. Consistently, mice with postnatal cardiomyocyte-specific gp130 depletion exhibited impaired left ventricular contractility compared with control mice. In these mice, cardiomyocytes exhibited a moderately decreased size and dramatically inhibited proliferation in the left ventricle but not in the right ventricle. Stereological analysis revealed that this change significantly decreased the number of cardiomyocytes in the left ventricle. Furthermore, IL-6 was mainly responsible for promoting ventricular cardiomyocyte proliferation by activating the JAK/STAT3 pathway. Taken together, the IL-6/gp130/JAK/STAT3 axis plays a crucial role in the physiological postnatal proliferation and hypertrophy of left ventricular cardiomyocytes to ensure normal cardiac functional development.<b>NEW & NOTEWORTHY</b> Although cardiomyocytes undergo proliferation in the early postnatal period, the regulatory mechanisms and physiological importance of this process have not been clarified. We found that the pharmacological and genetic depletion of gp130 in preweaning mice resulted in significant impairment of cardiomyocyte proliferation, thinning of the myocardium, and systolic dysfunction of the left but not right ventricle by perturbing JAK/STAT3 signaling. Thus, the IL-6/gp130/JAK/STAT3 axis is crucial for the postnatal functional development of the left ventricle.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kawagishi</LastName><ForeName>Hiroyuki</ForeName><Initials>H</Initials><Identifier Source="ORCID">0000-0001-7622-341X</Identifier><AffiliationInfo><Affiliation>Department of Biotechnology, Institute for Biomedical Sciences, Shinshu University, Matsumoto, Japan.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Molecular Pharmacology, Shinshu University School of Medicine, Matsumoto, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nakada</LastName><ForeName>Tsutomu</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Instrumental Analysis, Research Center for Supports to Advanced Science, Shinshu University, Matsumoto, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Numaga-Tomita</LastName><ForeName>Takuro</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Molecular Pharmacology, Shinshu University School of Medicine, Matsumoto, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Larrañaga</LastName><ForeName>Maite</ForeName><Initials>M</Initials><Identifier Source="ORCID">0000-0002-4390-8372</Identifier><AffiliationInfo><Affiliation>Basic Sciences Department, Faculty of Medicine and Health Sciences, Universitat Internacional de Catalunya, Barcelona, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Guo</LastName><ForeName>Ang</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Pharmaceutical Sciences, North Dakota State University, Fargo, North Dakota.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Song</LastName><ForeName>Long-Sheng</ForeName><Initials>LS</Initials><AffiliationInfo><Affiliation>Division of Cardiovascular Medicine, Department of Internal Medicine and François M. Abboud Cardiovascular Research Center, University of Iowa Carver College of Medicine, Iowa City, Iowa.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yamada</LastName><ForeName>Mitsuhiko</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Molecular Pharmacology, Shinshu University School of Medicine, Matsumoto, Japan.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><DataBankList CompleteYN="Y"><DataBank><DataBankName>figshare</DataBankName><AccessionNumberList><AccessionNumber>10.6084/m9.figshare.17476613</AccessionNumber><AccessionNumber>10.6084/m9.figshare.17477048</AccessionNumber><AccessionNumber>10.6084/m9.figshare.17477399</AccessionNumber><AccessionNumber>10.6084/m9.figshare.19761844</AccessionNumber><AccessionNumber>10.6084/m9.figshare.17477597</AccessionNumber></AccessionNumberList></DataBank></DataBankList><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>05</Month><Day>20</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Am J Physiol Heart Circ Physiol</MedlineTA><NlmUniqueID>100901228</NlmUniqueID><ISSNLinking>0363-6135</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006023">Glycoproteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015850">Interleukin-6</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018121">Receptors, Cytokine</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D050796">STAT3 Transcription Factor</NameOfSubstance></Chemical><Chemical><RegistryNumber>133483-10-0</RegistryNumber><NameOfSubstance UI="D050822">Cytokine Receptor gp130</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>Am J Physiol Heart Circ Physiol. 2022 Jul 1;323(1):H125-H127</RefSource><PMID Version="1">35657617</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D050822" MajorTopicYN="N">Cytokine Receptor gp130</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006023" MajorTopicYN="N">Glycoproteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015850" MajorTopicYN="Y">Interleukin-6</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008322" MajorTopicYN="N">Mammals</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D032383" MajorTopicYN="Y">Myocytes, Cardiac</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018121" MajorTopicYN="N">Receptors, Cytokine</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050796" MajorTopicYN="N">STAT3 Transcription Factor</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">cardiomyocyte</Keyword><Keyword MajorTopicYN="N">gp130</Keyword><Keyword MajorTopicYN="N">interleukin-6</Keyword><Keyword MajorTopicYN="N">neonate</Keyword><Keyword MajorTopicYN="N">proliferation</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>5</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>6</Month><Day>16</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>5</Month><Day>20</Day><Hour>11</Hour><Minute>53</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35594067</ArticleId><ArticleId IdType="doi">10.1152/ajpheart.00698.2021</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">35593629</PMID><DateCompleted><Year>2022</Year><Month>05</Month><Day>24</Day></DateCompleted><DateRevised><Year>2022</Year><Month>05</Month><Day>24</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0023-1207</ISSN><JournalIssue CitedMedium="Print"><Issue>5</Issue><PubDate><Year>2022</Year></PubDate></JournalIssue><Title>Khirurgiia</Title><ISOAbbreviation>Khirurgiia (Mosk)</ISOAbbreviation></Journal>[Early and long-term results after the Norwood procedure]. | Mammalian ventricular cardiomyocytes are premature at birth and exhibit substantial phenotypic changes before weaning. Mouse ventricular myocytes undergo cell division several times after birth; however, the regulatory mechanisms and roles of cardiomyocyte division in postnatal heart development remain unclear. Here, we investigated the physiological role of glycoprotein 130 (gp130), the main subunit of multifunctional receptors for the IL-6 family of cytokines, in postnatal cardiomyocyte proliferation. Pharmacological inhibition of gp130 within the first month after birth induced significant systolic dysfunction of the left ventricle in mice. Consistently, mice with postnatal cardiomyocyte-specific gp130 depletion exhibited impaired left ventricular contractility compared with control mice. In these mice, cardiomyocytes exhibited a moderately decreased size and dramatically inhibited proliferation in the left ventricle but not in the right ventricle. Stereological analysis revealed that this change significantly decreased the number of cardiomyocytes in the left ventricle. Furthermore, IL-6 was mainly responsible for promoting ventricular cardiomyocyte proliferation by activating the JAK/STAT3 pathway. Taken together, the IL-6/gp130/JAK/STAT3 axis plays a crucial role in the physiological postnatal proliferation and hypertrophy of left ventricular cardiomyocytes to ensure normal cardiac functional development.<b>NEW & NOTEWORTHY</b> Although cardiomyocytes undergo proliferation in the early postnatal period, the regulatory mechanisms and physiological importance of this process have not been clarified. We found that the pharmacological and genetic depletion of gp130 in preweaning mice resulted in significant impairment of cardiomyocyte proliferation, thinning of the myocardium, and systolic dysfunction of the left but not right ventricle by perturbing JAK/STAT3 signaling. Thus, the IL-6/gp130/JAK/STAT3 axis is crucial for the postnatal functional development of the left ventricle.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kawagishi</LastName><ForeName>Hiroyuki</ForeName><Initials>H</Initials><Identifier Source="ORCID">0000-0001-7622-341X</Identifier><AffiliationInfo><Affiliation>Department of Biotechnology, Institute for Biomedical Sciences, Shinshu University, Matsumoto, Japan.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Molecular Pharmacology, Shinshu University School of Medicine, Matsumoto, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nakada</LastName><ForeName>Tsutomu</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Instrumental Analysis, Research Center for Supports to Advanced Science, Shinshu University, Matsumoto, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Numaga-Tomita</LastName><ForeName>Takuro</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Molecular Pharmacology, Shinshu University School of Medicine, Matsumoto, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Larrañaga</LastName><ForeName>Maite</ForeName><Initials>M</Initials><Identifier Source="ORCID">0000-0002-4390-8372</Identifier><AffiliationInfo><Affiliation>Basic Sciences Department, Faculty of Medicine and Health Sciences, Universitat Internacional de Catalunya, Barcelona, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Guo</LastName><ForeName>Ang</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Pharmaceutical Sciences, North Dakota State University, Fargo, North Dakota.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Song</LastName><ForeName>Long-Sheng</ForeName><Initials>LS</Initials><AffiliationInfo><Affiliation>Division of Cardiovascular Medicine, Department of Internal Medicine and François M. Abboud Cardiovascular Research Center, University of Iowa Carver College of Medicine, Iowa City, Iowa.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yamada</LastName><ForeName>Mitsuhiko</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Molecular Pharmacology, Shinshu University School of Medicine, Matsumoto, Japan.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><DataBankList CompleteYN="Y"><DataBank><DataBankName>figshare</DataBankName><AccessionNumberList><AccessionNumber>10.6084/m9.figshare.17476613</AccessionNumber><AccessionNumber>10.6084/m9.figshare.17477048</AccessionNumber><AccessionNumber>10.6084/m9.figshare.17477399</AccessionNumber><AccessionNumber>10.6084/m9.figshare.19761844</AccessionNumber><AccessionNumber>10.6084/m9.figshare.17477597</AccessionNumber></AccessionNumberList></DataBank></DataBankList><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>05</Month><Day>20</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Am J Physiol Heart Circ Physiol</MedlineTA><NlmUniqueID>100901228</NlmUniqueID><ISSNLinking>0363-6135</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006023">Glycoproteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015850">Interleukin-6</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018121">Receptors, Cytokine</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D050796">STAT3 Transcription Factor</NameOfSubstance></Chemical><Chemical><RegistryNumber>133483-10-0</RegistryNumber><NameOfSubstance UI="D050822">Cytokine Receptor gp130</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>Am J Physiol Heart Circ Physiol. 2022 Jul 1;323(1):H125-H127</RefSource><PMID Version="1">35657617</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D050822" MajorTopicYN="N">Cytokine Receptor gp130</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006023" MajorTopicYN="N">Glycoproteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015850" MajorTopicYN="Y">Interleukin-6</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008322" MajorTopicYN="N">Mammals</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D032383" MajorTopicYN="Y">Myocytes, Cardiac</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018121" MajorTopicYN="N">Receptors, Cytokine</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050796" MajorTopicYN="N">STAT3 Transcription Factor</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">cardiomyocyte</Keyword><Keyword MajorTopicYN="N">gp130</Keyword><Keyword MajorTopicYN="N">interleukin-6</Keyword><Keyword MajorTopicYN="N">neonate</Keyword><Keyword MajorTopicYN="N">proliferation</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>5</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>6</Month><Day>16</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>5</Month><Day>20</Day><Hour>11</Hour><Minute>53</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35594067</ArticleId><ArticleId IdType="doi">10.1152/ajpheart.00698.2021</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">35593629</PMID><DateCompleted><Year>2022</Year><Month>05</Month><Day>24</Day></DateCompleted><DateRevised><Year>2022</Year><Month>05</Month><Day>24</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0023-1207</ISSN><JournalIssue CitedMedium="Print"><Issue>5</Issue><PubDate><Year>2022</Year></PubDate></JournalIssue><Title>Khirurgiia</Title><ISOAbbreviation>Khirurgiia (Mosk)</ISOAbbreviation></Journal><ArticleTitle>[Early and long-term results after the Norwood procedure].</ArticleTitle><Pagination><StartPage>59</StartPage><EndPage>67</EndPage><MedlinePgn>59-67</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.17116/hirurgia202205159</ELocationID><Abstract><AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">To assess the early and long-term results after the Norwood procedure and to identify predictors of aortic recoarctation and arterial hypertension.<AbstractText Label="MATERIAL AND METHODS" NlmCategory="METHODS">We have operated on 2789 infants in the department of congenital heart diseases of the Meshalkin National Medical Research Center between January 2015 and December 2018. The current single-center prospective cohort study included 39 (1.4%) patients with hypoplastic left heart syndrome who underwent the Norwood procedure.<AbstractText Label="RESULTS" NlmCategory="RESULTS">In-hospital mortality was 15.3% (<i>n</i>=6). An inter-stage mortality was 10.2% (<i>n</i>=4). Recoarctation of the aorta and Sano shunt stenosis in inter-stage period occurred in 8 (24.2%) and 4 patients (12.1%), respectively. Body mass <3 kg was the only risk factor of recoarctation (OR 7.08, 95% CI 1.17; 42.79, <i>p</i>=0.033). We found no risk factors of Sano shunt stenosis. There were no signs of recoarctation and Sano shunt dysfunction in the early postoperative period. Arterial hypertension developed in 14 (48.3%) patients. We found the correlation between systolic blood pressure and ventricular ejection fraction (β coefficient -0.88, 95% CI -1.33; -0.44, <i>p</i>=0.001). The only risk factor of arterial hypertension was increased stiffness of the aorta.<AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">The early and inter-stage mortality are still the issues after the Norwood procedure. Postoperative reduced ejection fraction of single ventricle is one of the most common complications that could be related with residual arterial hypertension.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Soynov</LastName><ForeName>I A</ForeName><Initials>IA</Initials><Identifier Source="ORCID">0000-0003-3691-2848</Identifier><AffiliationInfo><Affiliation>Meshalkin National Medical Research Center, Novosibirsk, Russia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gorbatykh</LastName><ForeName>A V</ForeName><Initials>AV</Initials><Identifier Source="ORCID">0000-0003-4017-4198</Identifier><AffiliationInfo><Affiliation>Almazov National Medical Research Center, St. Petersburg, Russia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kulyabin</LastName><ForeName>Yu Yu</ForeName><Initials>YY</Initials><Identifier Source="ORCID">0000-0002-2361-5847</Identifier><AffiliationInfo><Affiliation>Meshalkin National Medical Research Center, Novosibirsk, Russia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Arkhipov</LastName><ForeName>A N</ForeName><Initials>AN</Initials><Identifier Source="ORCID">0000-0003-3234-5436</Identifier><AffiliationInfo><Affiliation>Meshalkin National Medical Research Center, Novosibirsk, Russia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nichay</LastName><ForeName>N R</ForeName><Initials>NR</Initials><Identifier Source="ORCID">0000-0002-1763-9535</Identifier><AffiliationInfo><Affiliation>Meshalkin National Medical Research Center, Novosibirsk, Russia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zubritskiy</LastName><ForeName>A V</ForeName><Initials>AV</Initials><Identifier Source="ORCID">0000-0003-4666-2571</Identifier><AffiliationInfo><Affiliation>Meshalkin National Medical Research Center, Novosibirsk, Russia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Voitov</LastName><ForeName>A V</ForeName><Initials>AV</Initials><Identifier Source="ORCID">0000-0003-3797-4899</Identifier><AffiliationInfo><Affiliation>Meshalkin National Medical Research Center, Novosibirsk, Russia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gorbatykh</LastName><ForeName>Yu N</ForeName><Initials>YN</Initials><Identifier Source="ORCID">0000-0002-6204-5381</Identifier><AffiliationInfo><Affiliation>Meshalkin National Medical Research Center, Novosibirsk, Russia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Galstyan</LastName><ForeName>M G</ForeName><Initials>MG</Initials><Identifier Source="ORCID">0000-0003-3870-169X</Identifier><AffiliationInfo><Affiliation>Meshalkin National Medical Research Center, Novosibirsk, Russia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bogachev-Prokophiev</LastName><ForeName>A V</ForeName><Initials>AV</Initials><Identifier Source="ORCID">0000-0003-4625-4631</Identifier><AffiliationInfo><Affiliation>Meshalkin National Medical Research Center, Novosibirsk, Russia.</Affiliation></AffiliationInfo></Author></AuthorList><Language>rus</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><VernacularTitle>Rannie i otdalennye rezul'taty posle protsedury Norvud.</VernacularTitle></Article><MedlineJournalInfo><Country>Russia (Federation)</Country><MedlineTA>Khirurgiia (Mosk)</MedlineTA><NlmUniqueID>0412765</NlmUniqueID><ISSNLinking>0023-1207</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D003251" MajorTopicYN="N">Constriction, Pathologic</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006973" MajorTopicYN="Y">Hypertension</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007223" MajorTopicYN="N">Infant</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D058327" MajorTopicYN="Y">Norwood Procedures</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011446" MajorTopicYN="N">Prospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading></MeshHeadingList><OtherAbstract Type="Publisher" Language="rus"><AbstractText Label="ЦЕЛЬ ИССЛЕДОВАНИЯ" NlmCategory="UNASSIGNED">Оценить ранние и отдаленные результаты хирургической коррекции синдрома гипоплазии левых отделов сердца, а также выявить предикторы рекоарктации аорты и артерильной гипертензии.<AbstractText Label="МАТЕРИАЛ И МЕТОДЫ" NlmCategory="UNASSIGNED">С января 2015 г. по декабрь 2018 г. на базе НМИЦ им. Е.Н. Мешалкина в отделении врожденных пороков сердца прооперированы 2789 пациентов в возрасте до 1 года. В настоящее одноцентровое проспективное, когортное исследование включены 39 (1,4%) пациентов с синдромом гипоплазии левых отделов, которым выполнили процедуру Norwood.<AbstractText Label="РЕЗУЛЬТАТЫ" NlmCategory="UNASSIGNED">Госпитальная летальность составила 15,3% (<i>n</i>=6), отдаленная летальность в межэтапном периоде — 10,2% (<i>n</i>=4). Рекоарктация аорты и дисфункция шунта Sano в межэтапном периоде развились в 8 (24,2%) и 4 (12,1%) случаях соответственно. Единственным фактором риска развития рекоарктации была масса тела пациента <3 кг, OR 7,08 (95% ДИ 1,17; 42,79); <i>p</i>=0,033. Факторов риска дисфункции шунта Sano не выявлено. В раннем послеоперационном периоде признаков рекоарктации и дисфункции шунта не диагностировано. Артериальная гипертензия отмечена у 14 (48,3%) пациентов. При проведении линейного регрессионного анализа установлено влияние систолического артериального давления на сократительную способность желудочка β coef. (95% ДИ –0,88 (–1,33; –0,44); <i>p</i>=0,001. Единственным фактором риска развития артериальной гипертензии была повышенная жесткость восходящей аорты, OR 27,5 (95% ДИ 3,8; 198); <i>p</i>=0,018.<AbstractText Label="ЗАКЛЮЧЕНИЕ" NlmCategory="UNASSIGNED">Ранняя послеоперационная и межэтапная летальность представляет проблему после процедуры Норвуда у детей с синдромом гипоплазии левых отделов сердца. В отдаленном периоде наиболее частым осложнением является снижение сократительной способности единственного желудочка, что может быть связано с артериальной гипертензией. |
2,329,940 | Asymptomatic choroid plexus carcinoma in an infant: Report of one case. | Choroid Plexus Carcinomas (CPC) are rare malignant brain neoplasms of choroid plexus epithelium, with a tendency to occur in infants and children, especially those who are under two years of age. The Main symptoms of CPC include nausea, vomiting, headache, irritability, blurred vision, and seizures. Few studies discuss the therapeutic methods to treat this tumor. However, most of these studies confirmed the poor prognosis of it.</AbstractText>A two-year-old girl presented with a headache due to head trauma, normal consciousness, GCS 15/15, and without intracranial hypertension symptoms. Computed Tomography (CT) has shown a large heterogeneous lesion in the region of the right lateral ventricle. Magnetic resonance imaging (MRI) showed a large poorly-defined mass in the right lateral ventricle with mild dilatation of the ipsilateral lateral ventricle, and midline shift and marked edema surrounding it. In this case, the mass has been discovered by accident. The histological diagnosis was choroid plexus carcinoma (WHO grade 3), curettage of the right lateral ventricle was performed.</AbstractText>CPC is a serious condition with a poor prognosis. Early diagnosis and appropriate approaches are required in order to reduce mortality and morbidity rates.</AbstractText>© 2022 The Authors.</CopyrightInformation> |
2,329,941 | Congenital Hydrocephalus and Associated Risk Factors: An Institution-Based Case-Control Study, Dessie Town, North East Ethiopia. | Congenital hydrocephalus is one of the commonest congenital anomalies of the central nervous system. It is characterized by extensive accumulation of cerebrospinal fluid within the ventricles of the brain due to an imbalance between synthesis and absorption of cerebrospinal fluid. This study was planned to investigate the incidence and associated risk factors of congenital hydrocephalus.</AbstractText>Unmatched case-control study was conducted in 34 (cases) and 104 (controls) pregnant women. Maternal data were collected from a structured questionnaire, and fetal-related data were recorded from obstetric ultrasound. Epi-info 7 and SPSS version 24 were used for data entry and analysis, respectively. The association between congenital hydrocephalus and risk factors was evaluated using binary logistic regression.</AbstractText>The incidence of congenital hydrocephalus was 2.67 per 1000 pregnancies. The result of multivariate logistic regression indicated that alcohol use and iron with folic acid supplementation during pregnancy were significantly associated with the development of congenital hydrocephalus (OR: 7.64, 95% CI: 1.97-29.66 and p-value: 0.003 and OR: 0.186, 95% CI: 0.07-0.49 and p-value: 0.001, respectively). Maternal exposure to typhus and typhoid and use of antibiotics during early pregnancy were also significantly associated with congenital hydrocephalus. Moreover, significant association was also observed between the simultaneous development of spina bifida and congenital hydrocephalus (p-value 0.03).</AbstractText>In conclusion, alcohol consumption, unprescribed use of antibiotics and infection during pregnancy as well as absence of folic acid supplementation may predispose to congenital hydrocephalus.</AbstractText>© 2022 Abebe et al.</CopyrightInformation> |
2,329,942 | Pediatric synchronous multifocal and disseminated cerebrospinal classic medulloblastoma revealed by bilateral decreased visual acuity: a case report. | Medulloblastoma (MB) is a rapidly growing malignant solid tumor that arises from stem cells located in the subependymal germinal matrix or outer granular layer of the cerebellum. It represents 15 to 30% of pediatric brain tumors and less than 1% of primary brain tumors. The reason for the high incidence of MB in children compared to adults is the embryonic origin of the tumor. In typical cases, MB manifests as a solitary lesion in the fourth ventricle or in the cerebellar parenchyma; cases of synchronous multifocal and disseminated MB are quite rare in patients without familial tumor syndromes. To date, only 7 cases in adults and a single pediatric case with Gorlin syndrome have been described previously. Here, the authors report a new case of synchronous multifocal classic cerebrospinal histologically confirmed MB in a 10-year-old male patient revealed by bilateral decreased visual acuity without any other localizing neurological signs. The authors will proceed with a review of the current literature regarding this rare entity. |
2,329,943 | Regulation of choroid plexus development and its functions. | The choroid plexus (ChP) is an extensively vascularized tissue that protrudes into the brain ventricular system of all vertebrates. This highly specialized structure, consisting of the polarized epithelial sheet and underlying stroma, serves a spectrum of functions within the central nervous system (CNS), most notably the production of cerebrospinal fluid (CSF). The epithelial cells of the ChP have the competence to tightly modulate the biomolecule composition of CSF, which acts as a milieu functionally connecting ChP with other brain structures. This review aims to eloquently summarize the current knowledge about the development of ChP. We describe the mechanisms that control its early specification from roof plate followed by the formation of proliferative regions-cortical hem and rhombic lips-feeding later development of ChP. Next, we summarized the current knowledge on the maturation of ChP and mechanisms that control its morphological and cellular diversity. Furthermore, we attempted to review the currently available battery of molecular markers and mouse strains available for the research of ChP, and identified some technological shortcomings that must be overcome to accelerate the ChP research field. Overall, the central principle of this review is to highlight ChP as an intriguing and surprisingly poorly known structure that is vital for the development and function of the whole CNS. We believe that our summary will increase the interest in further studies of ChP that aim to describe the molecular and cellular principles guiding the development and function of this tissue. |
2,329,944 | Four-dimensional computed tomography of the left ventricle, Part I: Motion artifact reduction. | Standard four-dimensional computed tomography (4DCT) cardiac reconstructions typically include spiraling artifacts that depend not only on the motion of the heart but also on the gantry angle range over which the data was acquired. We seek to reduce these motion artifacts and, thereby, improve the accuracy of left ventricular wall positions in 4DCT image series.</AbstractText>We use a motion artifact reduction approach (ResyncCT) that is based largely on conjugate pairs of partial angle reconstruction (PAR) images. After identifying the key locations where motion artifacts exist in the uncorrected images, paired subvolumes within the PAR images are analyzed with a modified cross-correlation function in order to estimate 3D velocity and acceleration vectors at these locations. A subsequent motion compensation process (also based on PAR images) includes the creation of a dense motion field, followed by a backproject-and-warp style compensation. The algorithm was tested on a 3D printed phantom, which represents the left ventricle (LV) and on challenging clinical cases corrupted by severe artifacts.</AbstractText>The results from our preliminary phantom test as well as from clinical cardiac scans show crisp endocardial edges and resolved double-wall artifacts. When viewed as a temporal series, the corrected images exhibit a much smoother motion of the LV endocardial boundary as compared to the uncorrected images. In addition, quantitative results from our phantom studies show that ResyncCT processing reduces endocardial surface distance errors from 0.9 ± 0.8 to 0.2 ± 0.1 mm.</AbstractText>The ResyncCT algorithm was shown to be effective in reducing motion artifacts and restoring accurate wall positions. Some perspectives on the use of conjugate-PAR images and on techniques for CT motion artifact reduction more generally are also given.</AbstractText>© 2022 American Association of Physicists in Medicine.</CopyrightInformation> |
2,329,945 | Pathologically Verified Corticobasal Degeneration Mimicking Richardson's Syndrome Coexisting with Clinically and Radiologically Shunt-Responsive Normal Pressure Hydrocephalus. | Normal pressure hydrocephalus (NPH) manifests as gait instability, cognitive impairment, and urinary incontinence. This clinical triad of NPH sometimes occurs with ventriculomegaly in patients with neurodegenerative disease. Patients with pathologically verified neurodegenerative diseases, such as progressive supranuclear palsy (PSP), have received antemortem diagnoses of NPH.</AbstractText>This study presents clinical and pathological features of a patient with pathologically verified corticobasal degeneration (CBD) coexisting with clinically shunt-responsive NPH.</AbstractText>We performed clinical, radiological, and pathological evaluations in a patient with CBD whose antemortem diagnosis was PSP Richardson's syndrome (PSP-RS) coexisting with shunt-responsive NPH.</AbstractText>A 59-year-old woman developed bradykinesia and gait instability and then frequent falls, urinary incontinence, and supranuclear vertical gaze palsy followed. At 63 years of age, her gait disturbance and urinary incontinence had deteriorated rapidly, and cognitive impairment was disclosed. There were typical findings of NPH with ventriculomegaly and disproportionately enlarged subarachnoid space hydrocephalus as well as a 2-layer appearance with decreased and increased cerebral blood perfusion. Shunt placement ameliorated gait instability for more than 1 year and improved radiological indicators of NPH. However, atrophy of the midbrain progressed with time after transient increases in size. Although the antemortem diagnosis was probable PSP-RS, pathological evaluation verified CBD. There were severe discontinuities of the ependymal lining of the lateral ventricles and subependymal rarefaction and gliosis with tau-positive deposition.</AbstractText>Shunt surgery could ameliorate NPH symptoms in patients with 4-repeat tauopathies. Careful assessments of clinical findings are necessary to predict the benefits of shunts as a therapeutic option for patients with neurodegenerative diseases coexisting with NPH.</AbstractText>© 2022 The Authors. Movement Disorders Clinical Practice published by Wiley Periodicals LLC. on behalf of International Parkinson and Movement Disorder Society.</CopyrightInformation> |
2,329,946 | Increasing miR-126 Can Prevent Brain Injury after Intracerebral Hemorrhage in Rats by Regulating ZEB1. | Studies have found that microRNA (miR) is abnormally expressed in intracerebral hemorrhage (ICH) and is considered a therapeutic target for ICH.</AbstractText>To investigate the expression and role of miR-126 in the ICH rat model.</AbstractText>The ICH rat model was established, and miR-126 agomir and ZEB1 antagomir were injected into the lateral ventricle of ICH rats. The neurological function and water content of brain tissue were evaluated 48 hours later. Brain tissue around the hematoma of rats was taken to detect the expression of miR-126, ZEB1, glial fibrillary acidic protein (GFAP), and inflammatory cytokines (TNF-α</i>, IL-1β</i>, and IL-6). The luciferase reporter gene was applied to analyze the relationship between miR-126 and ZEB1.</AbstractText>miR-126 was downregulated in the ICH rat model, while ZEB1 was upregulated. miR-126 agomir or ZEB1 antagomir injection could improve neurological function and cerebral edema in ICH rats. In addition, it could also reduce the expression of TNF-α</i>, IL-1β</i>, IL-6, and GFAP in the brain tissue of ICH rats. Luciferase reporter gene showed that ZEB1 could be targeted and regulated by miR-126.</AbstractText>miR-126 is downregulated in ICH rats, and miR-126 can reduce brain injury in ICH rats by inhibiting ZEB1 expression.</AbstractText>Copyright © 2022 Yue Liu et al.</CopyrightInformation> |
2,329,947 | Deep Learning Achieves Neuroradiologist-Level Performance in Detecting Hydrocephalus Requiring Treatment. | In large clinical centers a small subset of patients present with hydrocephalus that requires surgical treatment. We aimed to develop a screening tool to detect such cases from the head MRI with performance comparable to neuroradiologists. We leveraged 496 clinical MRI exams collected retrospectively at a single clinical site from patients referred for any reason. This diagnostic dataset was enriched to have 259 hydrocephalus cases. A 3D convolutional neural network was trained on 16 manually segmented exams (ten hydrocephalus) and subsequently used to automatically segment the remaining 480 exams and extract volumetric anatomical features. A linear classifier of these features was trained on 240 exams to detect cases of hydrocephalus that required treatment with surgical intervention. Performance was compared to four neuroradiologists on the remaining 240 exams. Performance was also evaluated on a separate screening dataset of 451 exams collected from a routine clinical population to predict the consensus reading from four neuroradiologists using images alone. The pipeline was also tested on an external dataset of 31 exams from a 2nd clinical site. The most discriminant features were the Magnetic Resonance Hydrocephalic Index (MRHI), ventricle volume, and the ratio between ventricle and brain volume. At matching sensitivity, the specificity of the machine and the neuroradiologists did not show significant differences for detection of hydrocephalus on either dataset (proportions test, p > 0.05). ROC performance compared favorably with the state-of-the-art (AUC 0.90-0.96), and replicated in the external validation. Hydrocephalus cases requiring treatment can be detected automatically from MRI in a heterogeneous patient population based on quantitative characterization of brain anatomy with performance comparable to that of neuroradiologists. |
2,329,948 | Apolipoprotein C1 promotes glioblastoma tumorigenesis by reducing KEAP1/NRF2 and CBS-regulated ferroptosis. | Glioblastoma (GBM), a malignant brain tumor, is a world-wide health problem because of its poor prognosis and high rates of recurrence and mortality. Apolipoprotein C1 (APOC1) is the smallest of apolipoproteins, implicated in many diseases. Recent studies have shown that APOC1 promotes tumorigenesis and development of several types of cancer. In this study we investigated the role of APOC1 in GBM tumorigenesis. Using in silico assays we showed that APOC1 was highly expressed in GBM tissues and its expression was closely related to GBM progression. We showed that APOC1 protein expression was markedly increased in four GBM cell lines (U251, U138, A172 and U87) compared to the normal brain glia cell lines (HEB, HA1800). In U251 cells, overexpression of APOC1 promoted cell proliferation, migration, invasion and colony information, which was reversed by APOC1 knockdown. APOC1 knockdown also markedly inhibited the growth of GBM xenografts in the ventricle of nude mice. We further demonstrated that APOC1 reduced ferroptosis by inhibiting KEAP1, promoting nuclear translocation of NRF2 and increasing expression of HO-1 and NQO1 in GBM cells. APOC1 also induced ferroptosis resistance by increasing cystathionine beta-synthase (CBS) expression, which promoted trans-sulfuration and increased GSH synthesis, ultimately leading to an increase in glutathione peroxidase-4 (GPX4). Thus, APOC1 plays a key role in GBM tumorigenesis, conferring resistance to ferroptosis, and may be a promising therapeutic target for GBM. |
2,329,949 | Choroid Plexus Volume and Permeability at Brain MRI within the Alzheimer Disease Clinical Spectrum. | Background Mounting evidence suggests that the choroid plexus (CP) plays an important role in the pathophysiology of Alzheimer disease (AD), but its imaging profile in cognitive impairment remains unclear. Purpose To evaluate CP volume, permeability, and susceptibility by using MRI in patients at various stages of cognitive impairment. Materials and Methods This retrospective study evaluated patients with cognitive symptoms who underwent 3.0-T MRI of the brain, including dynamic contrast-enhanced (DCE) imaging and quantitative susceptibility mapping (QSM), between January 2013 and May 2020. CP volume was automatically segmented using three-dimensional T1-weighted sequences; the volume transfer constant (ie, <i>K</i><sup>trans</sup>) and fractional plasma volume (ie, <i>V</i><sub>p</sub>) were determined using DCE MRI, and susceptibility was assessed using QSM. The effects of CP volume, expressed as the ratio to intracranial volume, on cognition were evaluated using multivariable linear regression adjusted for age, sex, education, apolipoprotein E ε4 allele status, and volumetric measures. Results A total of 532 patients with cognitive symptoms (mean age, 72 years ± 9 [SD]; 388 women) were included: 78 with subjective cognitive impairment (SCI), 158 with early mild cognitive impairment (MCI), 149 with late MCI, and 147 with AD. Among these, 132 patients underwent DCE MRI and QSM. CP volume was greater in patients at more severe stages (ratio of intracranial volume × 10<sup>3</sup>: 0.9 ± 0.3 for SCI, 1.0 ± 0.3 for early MCI, 1.1 ± 0.3 for late MCI, and 1.3 ± 0.4 for AD; <i>P</i> < .001). Lower <i>K</i><sup>trans</sup> (<i>r</i> = -0.19; <i>P</i> = .03) and <i>V</i><sub>p</sub> (<i>r</i> = -0.20; <i>P</i> = .02) were negatively associated with CP volume; susceptibility was not (<i>r</i> = 0.15; <i>P</i> = .10). CP volume was negatively associated with memory (<i>B</i> = -0.67; standard error of the mean [SEM], 0.21; <i>P</i> = .01), executive function (<i>B</i> = -0.90; SEM, 0.31; <i>P</i> = .01), and global cognition (<i>B</i> = -0.82; SEM, 0.32; <i>P</i> = .01). Conclusion Among patients with cognitive symptoms, larger choroid plexus volume was associated with severity of cognitive impairment in the Alzheimer disease spectrum. Published under a CC BY 4.0 license. <i>Online supplemental material is available for this article</i>. See also the editorial by Chiang in this issue. |
2,329,950 | Analysis of the Therapeutic Effect and Prognostic Factors of 126 Patients With Hypertensive Cerebral Hemorrhage Treated by Soft-Channel Minimally Invasive Puncture and Drainage. | Surgery is the main method for the clinical treatment of hypertensive cerebral hemorrhage. Traditional craniotomy faces the disadvantages of the long operation time, easy to cause secondary injury to patients during the operation, and prone to infection after the operation, which is not conducive to the rehabilitation of patients. At present, it is urgent to find a surgical scheme, which can clear hematoma in time, protect brain tissue, and effectively reduce surgical trauma in the clinic.</AbstractText>The case database of our hospital was consulted, and the clinical data of patients with hypertensive intracerebral hemorrhage (HICH) treated with soft channel minimally invasive puncture and drainage from February 2018 to October 2021 were retrospectively analyzed. Patients were evaluated for efficacy, and the changes in serum C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), homocysteine (Hcy), endothelin (ET), and vasopressin (AVP) levels before surgery, 3 days after surgery, and 7 days after surgery were analyzed. Clinical data were collected and Logistic regression was used to analyze the prognostic factors.</AbstractText>Finally, according to the inclusion and exclusion criteria, 126 patients were selected as the research object. Among them, there were 24 cases (19.05%) of recovery, 47 cases (37.30%) of markedly effective, 34 cases (26.98%) of effective, 11 cases (8.73%) of ineffective, and 10 cases (7.94%) of death. The total effective rate was 83.33%. The hematoma was basically removed in 116 cases (92.06%). The average evacuation time of hematoma was (7.82 ± 1.63) days. Post-operative intracranial infection occurred in 2 cases (1.59%) and post-operative rebleeding occurred in 5 cases (3.97%). The average hospital stay was (34.16 ± 16.59) days. Serum CRP, TNF-α, IL-6, Hcy, ET, and AVP levels of all patients on the third and seventh days after surgery were lower than those before surgery, and those on the seventh day after surgery were lower than those on the third day after surgery (p</i> < 0.05). The differences in pre-operative Glasgow Coma Scale (GCS) score, bleeding volume, ventricular rupture, complicated cerebral hernia, and attack time to surgery between the good prognosis group and the bad prognosis group were statistically significant (p</i> < 0.05). Pre-operative GCS score, bleeding volume, ventricular rupture, complicated cerebral hernia, and onset time to surgery were all independent factors that affect the prognosis of patients (p</i> < 0.05).</AbstractText>Soft-channel minimally invasive puncture and drainage treatment of HICH has a significant effect, which is conducive to the complete removal of hematoma, reducing hospitalization time, while adjusting the balance and stability of various cytokines, and improving patient prognosis. Pre-operative GCS score, bleeding volume, rupture into the ventricle, complicated cerebral hernia, and time from onset to operation are all independent factors that affect the prognosis of patients.</AbstractText>Copyright © 2022 Wu and Zhang.</CopyrightInformation> |
2,329,951 | Modeling the Properties of White Matter Tracts Using Diffusion Tensor Imaging to Characterize Patterns of Injury in Aging and Neurodegenerative Disease. | Diffusion tensor imaging (DTI) is a relatively novel magnetic resonance-based imaging methodology that can provide valuable insight into the microstructure of white matter tracts of the brain. In this paper, we evaluated the reliability and reproducibility of deriving a semi-automated pseudo-atlas DTI tractography method vs. standard atlas-based analysis alternatives, for use in clinical cohorts with neurodegeneration and ventriculomegaly. We showed that the semi-automated pseudo-atlas DTI tractography method was reliable and reproducible across different cohorts, generating 97.7% of all tracts. However, DTI metrics obtained from both methods were significantly different across the majority of cohorts and white matter tracts (<i>p</i> < 0.001). Despite this, we showed that both methods produced patterns of white matter injury that are consistent with findings reported in the literature and with DTI profiles generated from these methodologies. Scatter plots comparing DTI metrics obtained from each methodology showed that the pseudo-atlas method produced metrics that implied a more preserved neural structure compared to its counterpart. When comparing DTI metrics against a measure of ventriculomegaly (i.e., Evans' Index), we showed that the standard atlas-based method was able to detect decreasing white matter integrity with increasing ventriculomegaly, while in contrast, metrics obtained using the pseudo-atlas method were sensitive for stretch or compression in the posterior limb of the internal capsule. Additionally, both methods were able to show an increase in white matter disruption with increasing ventriculomegaly, with the pseudo-atlas method showing less variability and more specificity to changes in white matter tracts near to the ventricles. In this study, we found that there was no true gold-standard for DTI methodologies or atlases. Whilst there was no congruence between absolute values from DTI metrics, differing DTI methodologies were still valid but must be appreciated to be variably sensitive to different changes within white matter injury occurring concurrently. By combining both atlas and pseudo-atlas based methodologies with DTI profiles, it was possible to navigate past such challenges to describe white matter injury changes in the context of confounders, such as neurodegenerative disease and ventricular enlargement, with transparency and consistency. |
2,329,952 | Thioredoxin-Interacting Protein (TXNIP) Knockdown Protects against Sepsis-Induced Brain Injury and Cognitive Decline in Mice by Suppressing Oxidative Stress and Neuroinflammation. | Sepsis-associated encephalopathy (SAE) is linked to increased morbidity and mortality rates in patients with sepsis. Increased cytokine production and neuronal apoptosis are implicated in the pathogenesis of the SAE. Neuroinflammation plays a major role in sepsis-induced brain injury. Thioredoxin-interacting protein (TXNIP), an inhibitor of thioredoxin, is associated with oxidative stress and inflammation. However, whether the TXNIP is involved in the sepsis-induced brain injury and the underlying mechanism is yet to be elucidated. Therefore, the present study was aimed at elucidating the effects of TXNIP knockdown on sepsis-induced brain injury and cognitive decline in mice. Lipopolysaccharide (LPS) was injected intraperitoneally to induce sepsis brain injury in mice. The virus-carrying control or TXNIP shRNA was injected into the lateral ventricle of the brain 4 weeks before the LPS treatment. The histological changes in the hippocampal tissues, encephaledema, and cognitive function were detected, respectively. Also, the 7-day survival rate was recorded. Furthermore, the alterations in microglial activity, oxidative response, proinflammatory factors, apoptosis, protein levels (TXNIP and NLRP3 inflammasome), and apoptosis were examined in the hippocampal tissues. The results demonstrated that the TXNIP and NLRP3 inflammasome expression levels were increased at 6, 12, and 24 h post-LPS injection. TXNIP knockdown dramatically ameliorated the 7-day survival rate, cognitive decline, brain damage, neuronal apoptosis, and the brain water content, inhibited the activation of microglia, downregulated the NLRP3/caspase-1 signaling pathway, and reduced the oxidative stress and the neuroinflammatory cytokine levels at 24 h post-LPS injection. These results suggested a crucial effect of TXNIP knockdown on the mechanism of brain injury and cognitive decline in sepsis mice via suppressing oxidative stress and neuroinflammation. Thus, TXNIP might be a potential therapeutic target for SAE patients. |
2,329,953 | Effect of Baseline Impedance in Radiofrequency Delivery on Lesion Characteristics and the Relationship Between Impedance and Steam Pops. | To explore the effects of baseline impedance (R) and power (P) on radiofrequency ablation (RFA) lesion characteristics and their correlation with steam pops using ThermoCool SmartTouch-SF (STSF) catheters in the porcine heart.</AbstractText>A porcine left ventricle was submerged in 37°C saline ex vivo</i>, and the experiment was performed with various P</i> (P</i> = 30, 40, 50, and 60 W) and multiple R</i> loads (R</i> = 80-100, 100-140, 140-180, and 180-220 Ω) to reach the target ablation index (AI; AI = 350, 450, and 500) or reach the target ablation time using a fixed contact force (CF; CF = 10-15 g) and the same saline irrigation (30 W/8 ml/min or 40-60 W/15 ml/min), repeated five times under each condition.</AbstractText>The surface diameter, maximum diameter, depth, and volume of the lesions were strongly correlated with the AI (P</i> = 40 W, R</i> = 100-140 Ω, CF = 10-15 g) (r</i> = 0.5412; r</i> = 0.7889; r</i> = 0.9366; and r</i> = 0.913, respectively; all p</i> < 0.05). As the value of R</i> increased, the maximum diameter, depth, and volume of the lesions significantly increased (AI = 350, P</i> = 30 W). Moreover, the higher the baseline value of R</i>, the greater the absolute value of the R</i> decrease (r</i> = 0.9035, p</i> < 0.05, Y</i> = 0.2759 × X</i> - 18.33). Under high power and high impedance, the occurrence rate of steam pops was high (P</i> = 60 W, R</i> = 180-220 Ω, AI when a steam pop occurred: 480 ± 26.5, ablation time: 11.29 ± 1.04 s).</AbstractText>Radiofrequency catheter ablation (RFCA) in power-controlled mode resulted in various lesion characteristics that were related to diverse baseline Rs. In addition, the incidence of steam pops was strongly correlated with high baseline R</i> and high P</i>.</AbstractText>Copyright © 2022 Qu, Guo, Sun, Wang, Zhang and Li.</CopyrightInformation> |
2,329,954 | Reduced melatonin levels may facilitate glioblastoma initiation in the subventricular zone. | There is increasing evidence that glioblastoma, a highly aggressive brain tumour, originates from a neural stem cell (NSC) located in the subventricular zone (SVZ) of the lateral cerebral ventricle. Using the most advanced <i>in vivo</i> imaging techniques, Gengatharan and colleagues recently identified a day/night difference in the adult SVZ-NSC division. They reported that the circadian melatonin rhythm and its receptor control the day/night difference in NSC division with high mitotic activity during the day and low activity at night. Expression of melatonin and its receptor diminishes during ageing, which eliminates the regulatory effect of melatonin on NSC mitosis. Moreover, the circadian melatonin rhythm is dampened by light-at-night with the potential of altering the circadian mitotic cycle of NSC in the SVZ. Also, men with a lower melatonin amplitude than women exhibit a 60% higher rate of glioblastoma incidence. Given that ageing contributes significantly to glioblastoma initiation and progression, we suggest that the decline in circadian melatonin synthesis and release as well as its receptors in the SVZ, which also diminish with an ageing act in concert with other factors to facilitate glioblastoma initiation and growth. |
2,329,955 | α-lipoic acid ameliorates inflammation state and oxidative stress by reducing the content of bioactive lipid derivatives in the left ventricle of rats fed a high-fat diet. | Lipid mediators derived from arachidonic acid (AA) are implicated with the occurrence of inflammation and oxidative stress. The current knowledge of AA metabolism focuses on searching for the therapeutic strategy to subvert affected AA metabolism. The aim of our study was to evaluate the potential protective effect of chronic α-lipoic acid (α-LA) supplementation on myocardial inflammation state and oxidative stress in obesity-related cardiovascular dysfunction. The experiment was carried out on male Wistar rats receiving a standard or a high-fat diets with intragastric α-LA administration for 8 weeks. Plasma and myocardial AA concentrations were determined using the gas-liquid chromatography (GLC). The Western blot technique was used to examine the expression of proteins from the inflammatory pathway. The content of selected cytokines, inflammatory mediators, and oxidative stress indicators was detected by the ELISA, colorimetric, and multiplex assay kits. Our results revealed that α-LA caused a notable reduction in AA content, mainly in the phospholipid fraction with a simultaneous diminishment in the synthesis of pro-inflammatory mediators, i.e., prostaglandin E2, leukotrienes B4 and C4 by decreasing the expression of COX-2 and 5-LOX. α-LA also augmented the level of antioxidative SOD2 and GSH and decreased the level of lipid peroxidation products, which improved oxidative system impairment in the left ventricle tissue. The data clearly showed that α-lipoic acid has a significant role in inflammation and oxidative stress development ameliorating the risk of cardiac obesity induced by high-fat feeding. |
2,329,956 | Transcortical Endoscopic Removal of Residual Craniopharyngioma in the Third Ventricle: Surgical Video. | Excision through craniotomy is used for pediatric craniopharyngioma removal. However, residual tumors can sometimes be found in the blind spot of the microscopic field, such as the third ventricle wall, back of the optic chiasm, and brainstem surface, during surgery. Video 1 demonstrates the surgery using a flexible endoscope for the removal of residual tumor located within the blind spot of the first resection. The written consent was obtained from the patient's family. A 4-year-old child complained of vomiting, and the radiologic findings showed obstructive hydrocephalus and a calcified suprasellar mass lesion that extended to the third ventricle. The tumor was treated with a right frontotemporal craniotomy. The pathologic diagnosis was craniopharyngioma. Postoperative magnetic resonance imaging showed residual tumor detected at the roof of the third ventricle, back of the optic chiasm, and interpeduncular fossa. The residual tumors were removed using a flexible endoscope via a transcortical, transventricular approach. Postoperative magnetic resonance imaging showed no residual tumors. Although histologically benign, craniopharyngiomas may be locally aggressive and their close proximity to vital structures makes them one of our controversial management dilemmas. Recurrence may occur following even a presumed total excision and radiation therapy. Residual tumors located in the third ventricle are resected through various approaches, such as the transsphenoidal or transcallosal approach. Our approach using a flexible endoscope was minimally invasive and useful for the removal of residual tumor of the third ventricle in craniopharyngioma surgery because the approach offered a wide field of view and visual angle and forceps could be applied according to the view. |
2,329,957 | Tany-Seq: Integrated Analysis of the Mouse Tanycyte Transcriptome. | The ability to maintain energy homeostasis is necessary for survival. Recently, an emerging role for ependymogial cells, which line the third ventricle in the hypothalamus in the regulation of energy homeostasis, has been appreciated. These cells are called tanycytes and are physically at the interface of brain communication with peripheral organs and have been proposed to mediate the transport of circulating hormones from the third ventricle into the parenchyma of the hypothalamus. Despite the important role tanycytes have been proposed to play in mediating communication from the periphery to the brain, we understand very little about the ontology and function of these cells due to their limited abundance and lack of ability to genetically target this cell population reliably. To overcome these hurdles, we integrated existing hypothalamic single cell RNA sequencing data, focusing on tanycytes, to allow for more in-depth characterization of tanycytic cell types and their putative functions. Overall, we expect this dataset to serve as a resource for the research community. |
2,329,958 | Transduction of Brain Neurons in Juvenile Chum Salmon (<i>Oncorhynchus keta</i>) with Recombinant Adeno-Associated Hippocampal Virus Injected into the Cerebellum during Long-Term Monitoring. | <i>Corpus cerebelli</i> in juvenile chum salmon is a multiprojective region of the brain connected via afferent and efferent projections with the higher regions of the brainstem and synencephalon, as well as with multiprojection regions of the <i>medulla oblongata</i> and spinal cord. During the postembryonic development of the cerebellum in chum salmon, <i>Oncorhynchus keta</i>, the lateral part of the juvenile cerebellum gives rise to the caudomedial part of the definitive cerebellum, which is consistent with the data reported for zebrafish and mouse cerebellum. Thus, the topographic organization of the cerebellum and its efferents are similar between fish (chum salmon and zebrafish) and mammals, including mice and humans. The distributions of recombinant adeno-associated viral vectors (rAAVs) after an injection of the base vector into the cerebellum have shown highly specific patterns of transgene expression in bipolar neurons in the latero-caudal lobe of the juvenile chum <i>tectum opticum</i>. The distribution of rAAVs in the dorsal thalamus, epithalamus, <i>nucleus rotundus</i>, and pretectal complex indicates the targeted distribution of the transgene via the thalamo-cerebellar projections. The detection of GFP expression in the cells of the epiphysis and posterior tubercle of juvenile chum salmon is associated with the transgene's distribution and with the cerebrospinal fluid flow, the brain ventricles and its outer surface. The direct delivery of the rAAV into the central nervous system by intracerebroventricular administration allows it to spread widely in the brain. Thus, the presence of special projection areas in the juvenile chum salmon cerebellum, as well as outside it, and the identification of the transgene's expression in them confirm the potential ability of rAAVs to distribute in both intracerebellar and afferent and efferent extracerebellar projections of the cerebellum. |
2,329,959 | Trappc9 Deficiency Impairs the Plasticity of Stem Cells. | Genetic mutations of <i>trappc9</i> cause intellectual disability with the atrophy of brain structures and variable obesity by poorly understood mechanisms. Trappc9-deficient mice develop phenotypes resembling pathological changes in humans and appear overweight shortly after weaning, and thus are useful for studying the pathogenesis of obesity. Here, we investigated the effects of trappc9 deficiency on the proliferation and differentiation capacity of adipose-derived stem cells (ASCs). We isolated ASCs from mice before overweight was developed and found that trappc9-null ASCs exhibited signs of premature senescence and cell death. While the lineage commitment was retained, trappc9-null ASCs preferred adipogenic differentiation. We observed a profound accumulation of lipid droplets in adipogenic cells derived from trappc9-deficient ASCs and marked differences in the distribution patterns and levels of calcium deposited in osteoblasts obtained from trappc9-null ASCs. Biochemical studies revealed that trappc9 deficiency resulted in an upregulated expression of rab1, rab11, and rab18, and agitated autophagy in ASCs. Moreover, we found that the content of neural stem cells in both the subventricular zone of the lateral ventricle and the subgranular zone of the dentate gyrus vastly declined in trappc9-null mice. Collectively, our results suggest that obesity, as well as brain structure hypoplasia induced by the deficiency of trappc9, involves an impairment in the plasticity of stem cells. |
2,329,960 | Neurogenesis of Subventricular Zone Progenitors in the Premature Cortex of Ferrets Facilitated by Neonatal Valproic Acid Exposure. | The present study evaluated the neurogenesis of neonatal valproic acid (VPA) exposure on subventricular zone progenitors of the developing cerebral cortex in ferrets. VPA was injected at a dose of 200 µg/g of body weight into ferret infants on postnatal days 6 and 7. Two different thymidine analogues, 5-ethynyl-2'-deoxyuridine (EdU) and 5-bromo-2'-deoxyuridine (BrdU), were injected with a 48 h interval to label proliferating cells before and after VPA exposure. Two hours after BrdU injection, BrdU single- and EdU/BrdU double-labeled cells, but not EdU single-labeled cells, were significantly denser in both the inner and outer subventricular zones of VPA-exposed infants than in control infants. Notably, more than 97% of BrdU single- and EdU/BrdU double-labeled cells were immunopositive for Pax6, a stable marker for basal radial glia (bRG), in both groups. In contrast, the percentage of cells positively immunostained for Cux1, a postmitotic marker for upper-layer cortical neurons, in both EdU single- and BrdU single-labeled cells, was significantly higher in VPA-exposed infants than in control infants. These findings suggest that neonatal VPA exposure facilitates bRG proliferation, including self-renewal, followed by their differentiation into upper layer cortical neurons in the premature cortex of ferrets. |
2,329,961 | Medulla oblongata volume as a promising predictor of survival in amyotrophic lateral sclerosis. | Unconventional magnetic resonance imaging studies of the brainstem have recently acquired a growing interest in amyotrophic lateral sclerosis (ALS) pathology since they provide a unique opportunity to evaluate motor tract degeneration and bulbar lower motor neuron involvement. The aim of this study was to investigate the role of brainstem structures as accurate biomarkers of disease severity and predictors of survival.</AbstractText>A total of 60 ALS patients and 30 healthy controls subjects (CS) were recruited in this study. Patients were divided in two subgroups according to the onset of the disease: 42 spinal (S-ALS) and 18 bulbar (B-ALS). All subjects underwent 3D-structural MRI. Brainstem volume both of the entire cohort of ALS patients and S-ALS and B-ALS onset were compared with those of CS. In addition the two ALS subgroups were tested for differences in brainstem volumes. Volumetric, vertex-wise, and voxel-based approaches were implemented to assess correlations between MR structural features and clinical characteristics expressed as ALSFRS-r and its bulbar (ALSFSR-r-B) and spinal subscores (ALSFSR-r-S). ROC curves were performed to test the accuracy of midbrain, pons, and medulla oblongata volumes able to discriminate patients dichotomized into long and short survivors by using Two-Steps cluster analysis. Univariate and multivariate survival analyses were carried out to test the prognostic role of brainstem structures' volume, trichotomized by applying a k-means clustering algorithm.</AbstractText>Both the entire cohort of ALS patients and B-ALS and S-ALS showed significant lower volumes of both medulla oblongata and pons compared to CS. Furthermore, B-ALS showed a significant lower volume of medulla oblongata, compared to S-ALS. Lower score of ALSFRS-r correlated to atrophy in the anterior compartment of midbrain, pons, and medulla oblongata, as well as in the posterior portion of only this latter region. ALSFSR-r-S positively correlated with shape deformation and density reduction of the anterior portion of the entire brainstem, along the corticospinal tracts. ALSFSR-r-B instead showed a positive correlation with shape deformation of the floor of the fourth ventricle in the medulla oblongata and the crus cerebri in the midbrain. Only medulla oblongata volume demonstrated a significant accuracy to discriminate long and short survivors ALS patients (ROC AUC 0.76, p < 0.001). Univariate and multivariate analysis confirmed the survival predictive role of the medulla oblongata (log rank test p: 0.003).</AbstractText>Our findings suggest that brainstem volume may reflect the impairment of corticospinal and corticobulbar tracts as well as lower bulbar motor neurons. Furthermore, medulla oblongata could be used as an early predictor of survival in ALS patients.</AbstractText>Copyright © 2022 The Author(s). Published by Elsevier Inc. All rights reserved.</CopyrightInformation> |
2,329,962 | Periventricular gradient of T<sub>1</sub> tissue alterations in multiple sclerosis. | Pathology in multiple sclerosis is not homogenously distributed. Recently, it has been shown that structures adjacent to CSF are more severely affected. A gradient of brain tissue involvement was shown with more severe pathology in periventricular areas and in proximity to brain surfaces such as the subarachnoid spaces and ependyma, and hence termed the "surface-in" gradient. Here, we study whether (i) the surface-in gradient of periventricular tissue alteration measured by T1</sub> relaxometry is already present in early multiple sclerosis patients, (ii) how it differs between early and progressive multiple sclerosis patients, and (iii) whether the gradient-derived metrics in normal-appearing white matter and lesions correlate better with physical disability than conventional MRI-based metrics.</AbstractText>Forty-seven patients with early multiple sclerosis, 52 with progressive multiple sclerosis, and 92 healthy controls were included in the study. Isotropic 3D T1</sub> relaxometry maps were obtained using the Magnetization-Prepared 2 Rapid Acquisition Gradient Echoes sequence at 3 T. After spatially normalizing the T1</sub> maps into a study-specific common space, T1</sub> inter-subject variability within the healthy cohort was modelled voxel-wise, yielding a normative T1</sub> atlas. Individual comparisons of each multiple sclerosis patient against the atlas were performed by computing z-scores. Equidistant bands of voxels were defined around the ventricles in the supratentorial white matter; the z-scores in these bands were analysed and compared between the early and progressive multiple sclerosis cohorts. Correlations between both conventional and z-score-gradient-derived MRI metrics and the Expanded Disability Status Scale were assessed.</AbstractText>Patients with early and progressive multiple sclerosis demonstrated a periventricular gradient of T1</sub> relaxation time z-scores. In progressive multiple sclerosis, z-score-derived metrics reflecting the gradient of tissue abnormality in normal-appearing white matter were more strongly correlated with disability (maximal rho = 0.374) than the conventional lesion volume and count (maximal rho = 0.189 and 0.21 respectively). In early multiple sclerosis, the gradient of normal-appearing white matter volume with z-scores > 2 at baseline correlated with clinical disability assessed at two years follow-up.</AbstractText>Our results suggest that the surface-in white matter gradient of tissue alteration is detectable with T1 relaxometry and is already present at clinical disease onset. The periventricular gradients correlate with clinical disability. The periventricular gradient in normal-appearing white matter may thus qualify as a promising biomarker for monitoring of disease activity from an early stage in all phenotypes of multiple sclerosis.</AbstractText>Copyright © 2022 The Author(s). Published by Elsevier Inc. All rights reserved.</CopyrightInformation> |
2,329,963 | [Anatomy of the left ventricle for endocardial ablation].<Pagination><StartPage>161</StartPage><EndPage>174</EndPage><MedlinePgn>161-174</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s00399-022-00859-7</ELocationID><Abstract><AbstractText>As with all cardiac interventions, performing left ventricular ablation requires profound knowledge of cardiac anatomy. The aim of this article is to provide an overview of left ventricular anatomy and to characterize complex and clinically relevant structures from an electrophysiologist-centered perspective. In addition to the different access routes, the trabecular network, the left ventricular outflow tract, and the left ventricular conduction system, complex anatomical structures such as the aortomitral continuity and the left ventricular summit are also explained. In addition, this article offers multiple clinical examples that combine ECG, anatomy, and electrophysiologic study.</AbstractText><CopyrightInformation>© 2022. The Author(s), under exclusive licence to Springer Medizin Verlag GmbH, ein Teil von Springer Nature.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Wolfes</LastName><ForeName>Julian</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Klinik für Kardiologie II-Rhythmologie, Universitätsklinikum Münster, Albert-Schweitzer-Campus 1, 48149, Münster, Deutschland. julian.wolfes@ukmuenster.de.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ellermann</LastName><ForeName>Christian</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Klinik für Kardiologie II-Rhythmologie, Universitätsklinikum Münster, Albert-Schweitzer-Campus 1, 48149, Münster, Deutschland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Köbe</LastName><ForeName>Julia</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Klinik für Kardiologie II-Rhythmologie, Universitätsklinikum Münster, Albert-Schweitzer-Campus 1, 48149, Münster, Deutschland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lange</LastName><ForeName>Philipp S</ForeName><Initials>PS</Initials><AffiliationInfo><Affiliation>Klinik für Kardiologie II-Rhythmologie, Universitätsklinikum Münster, Albert-Schweitzer-Campus 1, 48149, Münster, Deutschland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Leitz</LastName><ForeName>Patrick</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Klinik für Kardiologie II-Rhythmologie, Universitätsklinikum Münster, Albert-Schweitzer-Campus 1, 48149, Münster, Deutschland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rath</LastName><ForeName>Benjamin</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Klinik für Kardiologie II-Rhythmologie, Universitätsklinikum Münster, Albert-Schweitzer-Campus 1, 48149, Münster, Deutschland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Willy</LastName><ForeName>Kevin</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Klinik für Kardiologie II-Rhythmologie, Universitätsklinikum Münster, Albert-Schweitzer-Campus 1, 48149, Münster, Deutschland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Güner</LastName><ForeName>Fatih</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Klinik für Kardiologie II-Rhythmologie, Universitätsklinikum Münster, Albert-Schweitzer-Campus 1, 48149, Münster, Deutschland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Frommeyer</LastName><ForeName>Gerrit</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Klinik für Kardiologie II-Rhythmologie, Universitätsklinikum Münster, Albert-Schweitzer-Campus 1, 48149, Münster, Deutschland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Eckardt</LastName><ForeName>Lars</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Klinik für Kardiologie II-Rhythmologie, Universitätsklinikum Münster, Albert-Schweitzer-Campus 1, 48149, Münster, Deutschland.</Affiliation></AffiliationInfo></Author></AuthorList><Language>ger</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><VernacularTitle>Anatomie des linken Ventrikels als Grundlage für endokardiale Ablationen.</VernacularTitle><ArticleDate DateType="Electronic"><Year>2022</Year><Month>05</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>Germany</Country><MedlineTA>Herzschrittmacherther Elektrophysiol</MedlineTA><NlmUniqueID>9425873</NlmUniqueID><ISSNLinking>0938-7412</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D017115" MajorTopicYN="Y">Catheter Ablation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004562" MajorTopicYN="N">Electrocardiography</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D022062" MajorTopicYN="N">Electrophysiologic Techniques, Cardiac</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004699" MajorTopicYN="N">Endocardium</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017180" MajorTopicYN="Y">Tachycardia, Ventricular</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading></MeshHeadingList><OtherAbstract Type="Publisher" Language="ger"><AbstractText>Die Durchführung einer linksventrikulären Ablation setzt, wie bei grundsätzlich allen kardialen Interventionen, eine gute Kenntnis der kardialen Anatomie voraus. Ziel dieses Artikels ist es, eine Übersicht über die Anatomie des linken Ventrikels zu geben und komplexe klinisch relevante Strukturen aus einer untersucherzentrierten Perspektive zu charakterisieren. Neben den unterschiedlichen Zugangswegen, dem Trabekelwerk, dem linksventrikulären Ausflusstrakt und dem spezifischen Reizleitungssystem, sollen im Folgenden auch komplexe anatomische Strukturen wie die aortomitrale Kontinuität und der linksventrikuläre Summit erläutert und kartiert werden. Darüber hinaus bietet dieser Artikel mehrere klinische Fälle, die eine Verbindung zwischen EKG, Anatomie und Ablation ermöglichen sollen.</AbstractText><CopyrightInformation>© 2022. The Author(s), under exclusive licence to Springer Medizin Verlag GmbH, ein Teil von Springer Nature.</CopyrightInformation></OtherAbstract><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Aortomitral continuity</Keyword><Keyword MajorTopicYN="N">Conduction system</Keyword><Keyword MajorTopicYN="N">Landmarks</Keyword><Keyword MajorTopicYN="N">Left ventricular summit</Keyword><Keyword MajorTopicYN="N">Ventricular tachycardia</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>2</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>4</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>5</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>6</Month><Day>11</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>5</Month><Day>13</Day><Hour>17</Hour><Minute>2</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35556156</ArticleId><ArticleId IdType="doi">10.1007/s00399-022-00859-7</ArticleId><ArticleId IdType="pii">10.1007/s00399-022-00859-7</ArticleId></ArticleIdList><ReferenceList><Title>Literatur</Title><Reference><Citation>Hartzler GO (1983) Electrode catheter ablation of refractory focal ventricular tachycardia. J Am Coll Cardiol 2(6):1107–1113. https://doi.org/10.1016/s0735-1097(83)80337-4</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/s0735-1097(83)80337-4</ArticleId><ArticleId IdType="pubmed">6630783</ArticleId></ArticleIdList></Reference><Reference><Citation>Morady F (1999) Radio-frequency ablation as treatment for cardiac arrhythmias. N Engl J Med 340(7):534–544. https://doi.org/10.1056/NEJM199902183400707</Citation><ArticleIdList><ArticleId IdType="doi">10.1056/NEJM199902183400707</ArticleId><ArticleId IdType="pubmed">10021475</ArticleId></ArticleIdList></Reference><Reference><Citation>Sapp JL, Wells GA, Parkash R, Stevenson WG, Blier L, Sarrazin JF et al (2016) Ventricular Tachycardia Ablation versus Escalation of Antiarrhythmic Drugs. N Engl J Med 375(2):111–121. https://doi.org/10.1056/NEJMoa1513614</Citation><ArticleIdList><ArticleId IdType="doi">10.1056/NEJMoa1513614</ArticleId><ArticleId IdType="pubmed">27149033</ArticleId></ArticleIdList></Reference><Reference><Citation>Kuck KH, Schaumann A, Eckardt L, Willems S, Ventura R, Delacretaz E et al (2010) Catheter ablation of stable ventricular tachycardia before defibrillator implantation in patients with coronary heart disease (VTACH): a multicentre randomised controlled trial. Lancet 375(9708):31–40. https://doi.org/10.1016/S0140-6736(09)61755-4</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/S0140-6736(09)61755-4</ArticleId><ArticleId IdType="pubmed">20109864</ArticleId></ArticleIdList></Reference><Reference><Citation>Wasmer K, Reinecke H, Heitmann M, Dechering DG, Reinke F, Lange PS et al (2020) Clinical, procedural and long-term outcome of ischemic VT ablation in patients with previous anterior versus inferior myocardial infarction. Clin Res Cardiol 109(10):1282–1291. https://doi.org/10.1007/s00392-020-01622-z</Citation><ArticleIdList><ArticleId IdType="doi">10.1007/s00392-020-01622-z</ArticleId><ArticleId IdType="pubmed">32157380</ArticleId><ArticleId IdType="pmc">7515937</ArticleId></ArticleIdList></Reference><Reference><Citation>Ho SY (2009) Anatomy and myoarchitecture of the left ventricular wall in normal and in disease. Eur J Echocardiogr 10(8):iii3–7. https://doi.org/10.1093/ejechocard/jep159</Citation><ArticleIdList><ArticleId IdType="doi">10.1093/ejechocard/jep159</ArticleId><ArticleId IdType="pubmed">19889656</ArticleId></ArticleIdList></Reference><Reference><Citation>Ho SY (2009) Anatomic insights for catheter ablation of ventricular tachycardia. Heart Rhythm 6(8 Suppl):77–80. https://doi.org/10.1016/j.hrthm.2009.02.008</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.hrthm.2009.02.008</ArticleId></ArticleIdList></Reference><Reference><Citation>Santangeli P, Di Biase L, Lakkireddy D, Burkhardt JD, Pillarisetti J, Michowitz Y et al (2010) Radiofrequency catheter ablation of ventricular arrhythmias in patients with hypertrophic cardiomyopathy: safety and feasibility. Heart Rhythm 7(8):1036–1042. https://doi.org/10.1016/j.hrthm.2010.05.022</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.hrthm.2010.05.022</ArticleId><ArticleId IdType="pubmed">20493276</ArticleId></ArticleIdList></Reference><Reference><Citation>Eckardt L, Doldi F, Busch S, Duncker D, Estner H, Kuniss M et al (2022) 10-year Follow-up of Interventional Electrophysiology—Updated German survey during the COVID-19 pandemic</Citation></Reference><Reference><Citation>O’Connor M, Robson R, Kirby A, Wignall T, Hooks DA (2019) Anatomically guided ventricular transseptal access to the left ventricle for catheter ablation of ventricular tachycardia in the presence of mechanical aortic and mitral valves. JACC Clin Electrophysiol 5(1):138–139. https://doi.org/10.1016/j.jacep.2018.10.001</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.jacep.2018.10.001</ArticleId><ArticleId IdType="pubmed">30678782</ArticleId></ArticleIdList></Reference><Reference><Citation>Santangeli P, Hyman MC, Muser D, Callans DJ, Shivkumar K, Marchlinski FE (2020) Outcomes of Percutaneous trans-right atrial access to the left ventricle for catheter ablation of ventricular tachycardia in patients with mechanical aortic and mitral valves. JAMA Cardiol. https://doi.org/10.1001/jamacardio.2020.4414</Citation><ArticleIdList><ArticleId IdType="doi">10.1001/jamacardio.2020.4414</ArticleId><ArticleId IdType="pubmed">32997112</ArticleId><ArticleId IdType="pmc">7941197</ArticleId></ArticleIdList></Reference><Reference><Citation>Yorgun H, Canpolat U, Nof E, Beinart R, Aydin A, Sabuncu T et al (2020) Transapical left ventricular access for ventricular tachycardia ablation in patients with mechanical aortic and mitral valve prosthesis. Circ Arrhythm Electrophysiol 13(10):e8893. https://doi.org/10.1161/CIRCEP.120.008893</Citation><ArticleIdList><ArticleId IdType="doi">10.1161/CIRCEP.120.008893</ArticleId><ArticleId IdType="pubmed">32921133</ArticleId></ArticleIdList></Reference><Reference><Citation>Ho SY, Ernst S (2012) Anatomy for cardiac electrophysiologists: a practical handbook. Cardiotext Publishing. Hopkins, Minnesota</Citation></Reference><Reference><Citation>Sanchez-Quintana D, Doblado-Calatrava M, Cabrera JA, Macias Y, Saremi F (2015) Anatomical basis for the cardiac interventional electrophysiologist. Biomed Res Int 2015:547364. https://doi.org/10.1155/2015/547364</Citation><ArticleIdList><ArticleId IdType="doi">10.1155/2015/547364</ArticleId><ArticleId IdType="pubmed">26665006</ArticleId><ArticleId IdType="pmc">4668306</ArticleId></ArticleIdList></Reference><Reference><Citation>Lam JH, Ranganathan N, Wigle ED, Silver MD (1970) Morphology of the human mitral valve. I. Chordae tendineae: a new classification. Circulation 41(3):449–458. https://doi.org/10.1161/01.cir.41.3.449</Citation><ArticleIdList><ArticleId IdType="doi">10.1161/01.cir.41.3.449</ArticleId><ArticleId IdType="pubmed">5415982</ArticleId></ArticleIdList></Reference><Reference><Citation>Desimone CV, Hu T, Ebrille E, Syed FF, Vaidya VR, Cha YM et al (2014) Catheter ablation related mitral valve injury: the importance of early recognition and rescue mitral valve repair. J Cardiovasc Electrophysiol 25(9):971–975. https://doi.org/10.1111/jce.12439</Citation><ArticleIdList><ArticleId IdType="doi">10.1111/jce.12439</ArticleId><ArticleId IdType="pubmed">24758402</ArticleId><ArticleId IdType="pmc">4459508</ArticleId></ArticleIdList></Reference><Reference><Citation>Kitzman DW, Scholz DG, Hagen PT, Ilstrup DM, Edwards WD (1988) Age-related changes in normal human hearts during the first 10 decades of life. Part II (maturity): a quantitative anatomic study of 765 specimens from subjects 20 to 99 years old. Mayo Clin Proc 63(2):137–146. https://doi.org/10.1016/s0025-6196(12)64946-5</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/s0025-6196(12)64946-5</ArticleId><ArticleId IdType="pubmed">3276974</ArticleId></ArticleIdList></Reference><Reference><Citation>Iwai S, Cantillon DJ, Kim RJ, Markowitz SM, Mittal S, Stein KM et al (2006) Right and left ventricular outflow tract tachycardias: evidence for a common electrophysiologic mechanism. J Cardiovasc Electrophysiol 17(10):1052–1058. https://doi.org/10.1111/j.1540-8167.2006.00539.x</Citation><ArticleIdList><ArticleId IdType="doi">10.1111/j.1540-8167.2006.00539.x</ArticleId><ArticleId IdType="pubmed">16800855</ArticleId></ArticleIdList></Reference><Reference><Citation>Haqqani HM, Tschabrunn CM, Tzou WS, Dixit S, Cooper JM, Riley MP et al (2011) Isolated septal substrate for ventricular tachycardia in nonischemic dilated cardiomyopathy: incidence, characterization, and implications. Heart Rhythm 8(8):1169–1176. https://doi.org/10.1016/j.hrthm.2011.03.008</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.hrthm.2011.03.008</ArticleId><ArticleId IdType="pubmed">21392586</ArticleId></ArticleIdList></Reference><Reference><Citation>Cheung JW, Anderson RH, Markowitz SM, Lerman BB (2019) Catheter ablation of arrhythmias originating from the left ventricular outflow tract. JACC Clin Electrophysiol 5(1):1–12. https://doi.org/10.1016/j.jacep.2018.11.012</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.jacep.2018.11.012</ArticleId><ArticleId IdType="pubmed">30678772</ArticleId></ArticleIdList></Reference><Reference><Citation>Anderson RH (2000) Clinical anatomy of the aortic root. Heart 84(6):670–673. https://doi.org/10.1136/heart.84.6.670</Citation><ArticleIdList><ArticleId IdType="doi">10.1136/heart.84.6.670</ArticleId><ArticleId IdType="pubmed">11083753</ArticleId><ArticleId IdType="pmc">1729505</ArticleId></ArticleIdList></Reference><Reference><Citation>Kuroki K, Sato A, Yamagami F, Nogami A, Aonuma K (2017) Life-threatening aortic dissection with cardiac tamponade during catheter ablation for ventricular tachycardia originating from left coronary cusp. J Cardiovasc Electrophysiol 28(10):1224–1225. https://doi.org/10.1111/jce.13277</Citation><ArticleIdList><ArticleId IdType="doi">10.1111/jce.13277</ArticleId><ArticleId IdType="pubmed">28635147</ArticleId></ArticleIdList></Reference><Reference><Citation>Whitman IR, Gladstone RA, Badhwar N, Hsia HH, Lee BK, Josephson SA et al (2017) Brain emboli after left ventricular Endocardial ablation. Circulation 135(9):867–877. https://doi.org/10.1161/CIRCULATIONAHA.116.025546</Citation><ArticleIdList><ArticleId IdType="doi">10.1161/CIRCULATIONAHA.116.025546</ArticleId><ArticleId IdType="pubmed">28119381</ArticleId></ArticleIdList></Reference><Reference><Citation>Anderson RH, Spicer DE, Hlavacek AM, Cook AC, Backer CL (2013) Wilcox’s surgical anatomy of the heart. Cambridge University Press</Citation><ArticleIdList><ArticleId IdType="doi">10.1017/CBO9781139028561</ArticleId></ArticleIdList></Reference><Reference><Citation>Elizari MV (2017) The normal variants in the left bundle branch system. J Electrocardiol 50(4):389–399. https://doi.org/10.1016/j.jelectrocard.2017.03.004</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.jelectrocard.2017.03.004</ArticleId><ArticleId IdType="pubmed">28341304</ArticleId></ArticleIdList></Reference><Reference><Citation>Kapa S, Gaba P, DeSimone CV, Asirvatham SJ (2017) Fascicular ventricular arrhythmias: Pathophysiologic mechanisms, anatomical constructs, and advances in approaches to management. Circ Arrhythm Electrophysiol. https://doi.org/10.1161/CIRCEP.116.002476</Citation><ArticleIdList><ArticleId IdType="doi">10.1161/CIRCEP.116.002476</ArticleId><ArticleId IdType="pubmed">28183845</ArticleId><ArticleId IdType="pmc">5319731</ArticleId></ArticleIdList></Reference><Reference><Citation>Demoulin JC, Kulbertus HE (1973) Left hemiblocks revisited from the histopathological viewpoint. Am Heart J 86(5):712–713. https://doi.org/10.1016/0002-8703(73)90354-2</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/0002-8703(73)90354-2</ArticleId><ArticleId IdType="pubmed">4743340</ArticleId></ArticleIdList></Reference><Reference><Citation>Kulbertus HE (1975) Concept of left hemiblocks revisited. A histopathological and experimental study. Adv Cardiol 14:126–135. https://doi.org/10.1159/000397645</Citation><ArticleIdList><ArticleId IdType="doi">10.1159/000397645</ArticleId><ArticleId IdType="pubmed">1136876</ArticleId></ArticleIdList></Reference><Reference><Citation>De Almeida MC, Lopes F, Fontes P, Barra F, Guimaraes R, Vilhena V (2015) Ungulates heart model: a study of the Purkinje network using India ink injection, transparent specimens and computer tomography. Anat Sci Int 90(4):240–250. https://doi.org/10.1007/s12565-014-0255-9</Citation><ArticleIdList><ArticleId IdType="doi">10.1007/s12565-014-0255-9</ArticleId><ArticleId IdType="pubmed">25316088</ArticleId></ArticleIdList></Reference><Reference><Citation>McAlpine WA (1975) Heart and Coronary Arteries: An Anatomical Atlas for Clinical Diagnosis, Radiological Investigation, and Surgical Treatment Bd. 0, Berlin, Heidelberg</Citation><ArticleIdList><ArticleId IdType="doi">10.1007/978-3-642-65983-6</ArticleId></ArticleIdList></Reference><Reference><Citation>El-Maasarany S, Ferrett CG, Firth A, Sheppard M, Henein MY (2005) The coronary sinus conduit function: anatomical study (relationship to adjacent structures). Europace 7(5):475–481. https://doi.org/10.1016/j.eupc.2005.05.013</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.eupc.2005.05.013</ArticleId><ArticleId IdType="pubmed">16087113</ArticleId></ArticleIdList></Reference><Reference><Citation>Hori Y, Nakahara S, Mine S, Anjo N, Fujii A, Ueda Y et al (2016) Pathological autopsy of a patient that underwent a successful ablation of an electrical storm from the left ventricular summit. Heart Vessels 31(12):2068–2073. https://doi.org/10.1007/s00380-016-0847-5</Citation><ArticleIdList><ArticleId IdType="doi">10.1007/s00380-016-0847-5</ArticleId><ArticleId IdType="pubmed">27178756</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35554772</PMID><DateRevised><Year>2022</Year><Month>05</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1573-7241</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>May</Month><Day>13</Day></PubDate></JournalIssue><Title>Cardiovascular drugs and therapy</Title><ISOAbbreviation>Cardiovasc Drugs Ther</ISOAbbreviation></Journal>Long-term Dexamethasone Treatment Increases Cardiac Galectin-3 Levels. | As with all cardiac interventions, performing left ventricular ablation requires profound knowledge of cardiac anatomy. The aim of this article is to provide an overview of left ventricular anatomy and to characterize complex and clinically relevant structures from an electrophysiologist-centered perspective. In addition to the different access routes, the trabecular network, the left ventricular outflow tract, and the left ventricular conduction system, complex anatomical structures such as the aortomitral continuity and the left ventricular summit are also explained. In addition, this article offers multiple clinical examples that combine ECG, anatomy, and electrophysiologic study.<CopyrightInformation>© 2022. The Author(s), under exclusive licence to Springer Medizin Verlag GmbH, ein Teil von Springer Nature.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Wolfes</LastName><ForeName>Julian</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Klinik für Kardiologie II-Rhythmologie, Universitätsklinikum Münster, Albert-Schweitzer-Campus 1, 48149, Münster, Deutschland. julian.wolfes@ukmuenster.de.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ellermann</LastName><ForeName>Christian</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Klinik für Kardiologie II-Rhythmologie, Universitätsklinikum Münster, Albert-Schweitzer-Campus 1, 48149, Münster, Deutschland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Köbe</LastName><ForeName>Julia</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Klinik für Kardiologie II-Rhythmologie, Universitätsklinikum Münster, Albert-Schweitzer-Campus 1, 48149, Münster, Deutschland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lange</LastName><ForeName>Philipp S</ForeName><Initials>PS</Initials><AffiliationInfo><Affiliation>Klinik für Kardiologie II-Rhythmologie, Universitätsklinikum Münster, Albert-Schweitzer-Campus 1, 48149, Münster, Deutschland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Leitz</LastName><ForeName>Patrick</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Klinik für Kardiologie II-Rhythmologie, Universitätsklinikum Münster, Albert-Schweitzer-Campus 1, 48149, Münster, Deutschland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rath</LastName><ForeName>Benjamin</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Klinik für Kardiologie II-Rhythmologie, Universitätsklinikum Münster, Albert-Schweitzer-Campus 1, 48149, Münster, Deutschland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Willy</LastName><ForeName>Kevin</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Klinik für Kardiologie II-Rhythmologie, Universitätsklinikum Münster, Albert-Schweitzer-Campus 1, 48149, Münster, Deutschland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Güner</LastName><ForeName>Fatih</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Klinik für Kardiologie II-Rhythmologie, Universitätsklinikum Münster, Albert-Schweitzer-Campus 1, 48149, Münster, Deutschland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Frommeyer</LastName><ForeName>Gerrit</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Klinik für Kardiologie II-Rhythmologie, Universitätsklinikum Münster, Albert-Schweitzer-Campus 1, 48149, Münster, Deutschland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Eckardt</LastName><ForeName>Lars</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Klinik für Kardiologie II-Rhythmologie, Universitätsklinikum Münster, Albert-Schweitzer-Campus 1, 48149, Münster, Deutschland.</Affiliation></AffiliationInfo></Author></AuthorList><Language>ger</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><VernacularTitle>Anatomie des linken Ventrikels als Grundlage für endokardiale Ablationen.</VernacularTitle><ArticleDate DateType="Electronic"><Year>2022</Year><Month>05</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>Germany</Country><MedlineTA>Herzschrittmacherther Elektrophysiol</MedlineTA><NlmUniqueID>9425873</NlmUniqueID><ISSNLinking>0938-7412</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D017115" MajorTopicYN="Y">Catheter Ablation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004562" MajorTopicYN="N">Electrocardiography</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D022062" MajorTopicYN="N">Electrophysiologic Techniques, Cardiac</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004699" MajorTopicYN="N">Endocardium</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017180" MajorTopicYN="Y">Tachycardia, Ventricular</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading></MeshHeadingList><OtherAbstract Type="Publisher" Language="ger">Die Durchführung einer linksventrikulären Ablation setzt, wie bei grundsätzlich allen kardialen Interventionen, eine gute Kenntnis der kardialen Anatomie voraus. Ziel dieses Artikels ist es, eine Übersicht über die Anatomie des linken Ventrikels zu geben und komplexe klinisch relevante Strukturen aus einer untersucherzentrierten Perspektive zu charakterisieren. Neben den unterschiedlichen Zugangswegen, dem Trabekelwerk, dem linksventrikulären Ausflusstrakt und dem spezifischen Reizleitungssystem, sollen im Folgenden auch komplexe anatomische Strukturen wie die aortomitrale Kontinuität und der linksventrikuläre Summit erläutert und kartiert werden. Darüber hinaus bietet dieser Artikel mehrere klinische Fälle, die eine Verbindung zwischen EKG, Anatomie und Ablation ermöglichen sollen.<CopyrightInformation>© 2022. The Author(s), under exclusive licence to Springer Medizin Verlag GmbH, ein Teil von Springer Nature.</CopyrightInformation></OtherAbstract><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Aortomitral continuity</Keyword><Keyword MajorTopicYN="N">Conduction system</Keyword><Keyword MajorTopicYN="N">Landmarks</Keyword><Keyword MajorTopicYN="N">Left ventricular summit</Keyword><Keyword MajorTopicYN="N">Ventricular tachycardia</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>2</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>4</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>5</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>6</Month><Day>11</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>5</Month><Day>13</Day><Hour>17</Hour><Minute>2</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35556156</ArticleId><ArticleId IdType="doi">10.1007/s00399-022-00859-7</ArticleId><ArticleId IdType="pii">10.1007/s00399-022-00859-7</ArticleId></ArticleIdList><ReferenceList><Title>Literatur</Title><Reference><Citation>Hartzler GO (1983) Electrode catheter ablation of refractory focal ventricular tachycardia. J Am Coll Cardiol 2(6):1107–1113. https://doi.org/10.1016/s0735-1097(83)80337-4</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/s0735-1097(83)80337-4</ArticleId><ArticleId IdType="pubmed">6630783</ArticleId></ArticleIdList></Reference><Reference><Citation>Morady F (1999) Radio-frequency ablation as treatment for cardiac arrhythmias. N Engl J Med 340(7):534–544. https://doi.org/10.1056/NEJM199902183400707</Citation><ArticleIdList><ArticleId IdType="doi">10.1056/NEJM199902183400707</ArticleId><ArticleId IdType="pubmed">10021475</ArticleId></ArticleIdList></Reference><Reference><Citation>Sapp JL, Wells GA, Parkash R, Stevenson WG, Blier L, Sarrazin JF et al (2016) Ventricular Tachycardia Ablation versus Escalation of Antiarrhythmic Drugs. N Engl J Med 375(2):111–121. https://doi.org/10.1056/NEJMoa1513614</Citation><ArticleIdList><ArticleId IdType="doi">10.1056/NEJMoa1513614</ArticleId><ArticleId IdType="pubmed">27149033</ArticleId></ArticleIdList></Reference><Reference><Citation>Kuck KH, Schaumann A, Eckardt L, Willems S, Ventura R, Delacretaz E et al (2010) Catheter ablation of stable ventricular tachycardia before defibrillator implantation in patients with coronary heart disease (VTACH): a multicentre randomised controlled trial. Lancet 375(9708):31–40. https://doi.org/10.1016/S0140-6736(09)61755-4</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/S0140-6736(09)61755-4</ArticleId><ArticleId IdType="pubmed">20109864</ArticleId></ArticleIdList></Reference><Reference><Citation>Wasmer K, Reinecke H, Heitmann M, Dechering DG, Reinke F, Lange PS et al (2020) Clinical, procedural and long-term outcome of ischemic VT ablation in patients with previous anterior versus inferior myocardial infarction. Clin Res Cardiol 109(10):1282–1291. https://doi.org/10.1007/s00392-020-01622-z</Citation><ArticleIdList><ArticleId IdType="doi">10.1007/s00392-020-01622-z</ArticleId><ArticleId IdType="pubmed">32157380</ArticleId><ArticleId IdType="pmc">7515937</ArticleId></ArticleIdList></Reference><Reference><Citation>Ho SY (2009) Anatomy and myoarchitecture of the left ventricular wall in normal and in disease. Eur J Echocardiogr 10(8):iii3–7. https://doi.org/10.1093/ejechocard/jep159</Citation><ArticleIdList><ArticleId IdType="doi">10.1093/ejechocard/jep159</ArticleId><ArticleId IdType="pubmed">19889656</ArticleId></ArticleIdList></Reference><Reference><Citation>Ho SY (2009) Anatomic insights for catheter ablation of ventricular tachycardia. Heart Rhythm 6(8 Suppl):77–80. https://doi.org/10.1016/j.hrthm.2009.02.008</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.hrthm.2009.02.008</ArticleId></ArticleIdList></Reference><Reference><Citation>Santangeli P, Di Biase L, Lakkireddy D, Burkhardt JD, Pillarisetti J, Michowitz Y et al (2010) Radiofrequency catheter ablation of ventricular arrhythmias in patients with hypertrophic cardiomyopathy: safety and feasibility. Heart Rhythm 7(8):1036–1042. https://doi.org/10.1016/j.hrthm.2010.05.022</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.hrthm.2010.05.022</ArticleId><ArticleId IdType="pubmed">20493276</ArticleId></ArticleIdList></Reference><Reference><Citation>Eckardt L, Doldi F, Busch S, Duncker D, Estner H, Kuniss M et al (2022) 10-year Follow-up of Interventional Electrophysiology—Updated German survey during the COVID-19 pandemic</Citation></Reference><Reference><Citation>O’Connor M, Robson R, Kirby A, Wignall T, Hooks DA (2019) Anatomically guided ventricular transseptal access to the left ventricle for catheter ablation of ventricular tachycardia in the presence of mechanical aortic and mitral valves. JACC Clin Electrophysiol 5(1):138–139. https://doi.org/10.1016/j.jacep.2018.10.001</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.jacep.2018.10.001</ArticleId><ArticleId IdType="pubmed">30678782</ArticleId></ArticleIdList></Reference><Reference><Citation>Santangeli P, Hyman MC, Muser D, Callans DJ, Shivkumar K, Marchlinski FE (2020) Outcomes of Percutaneous trans-right atrial access to the left ventricle for catheter ablation of ventricular tachycardia in patients with mechanical aortic and mitral valves. JAMA Cardiol. https://doi.org/10.1001/jamacardio.2020.4414</Citation><ArticleIdList><ArticleId IdType="doi">10.1001/jamacardio.2020.4414</ArticleId><ArticleId IdType="pubmed">32997112</ArticleId><ArticleId IdType="pmc">7941197</ArticleId></ArticleIdList></Reference><Reference><Citation>Yorgun H, Canpolat U, Nof E, Beinart R, Aydin A, Sabuncu T et al (2020) Transapical left ventricular access for ventricular tachycardia ablation in patients with mechanical aortic and mitral valve prosthesis. Circ Arrhythm Electrophysiol 13(10):e8893. https://doi.org/10.1161/CIRCEP.120.008893</Citation><ArticleIdList><ArticleId IdType="doi">10.1161/CIRCEP.120.008893</ArticleId><ArticleId IdType="pubmed">32921133</ArticleId></ArticleIdList></Reference><Reference><Citation>Ho SY, Ernst S (2012) Anatomy for cardiac electrophysiologists: a practical handbook. Cardiotext Publishing. Hopkins, Minnesota</Citation></Reference><Reference><Citation>Sanchez-Quintana D, Doblado-Calatrava M, Cabrera JA, Macias Y, Saremi F (2015) Anatomical basis for the cardiac interventional electrophysiologist. Biomed Res Int 2015:547364. https://doi.org/10.1155/2015/547364</Citation><ArticleIdList><ArticleId IdType="doi">10.1155/2015/547364</ArticleId><ArticleId IdType="pubmed">26665006</ArticleId><ArticleId IdType="pmc">4668306</ArticleId></ArticleIdList></Reference><Reference><Citation>Lam JH, Ranganathan N, Wigle ED, Silver MD (1970) Morphology of the human mitral valve. I. Chordae tendineae: a new classification. Circulation 41(3):449–458. https://doi.org/10.1161/01.cir.41.3.449</Citation><ArticleIdList><ArticleId IdType="doi">10.1161/01.cir.41.3.449</ArticleId><ArticleId IdType="pubmed">5415982</ArticleId></ArticleIdList></Reference><Reference><Citation>Desimone CV, Hu T, Ebrille E, Syed FF, Vaidya VR, Cha YM et al (2014) Catheter ablation related mitral valve injury: the importance of early recognition and rescue mitral valve repair. J Cardiovasc Electrophysiol 25(9):971–975. https://doi.org/10.1111/jce.12439</Citation><ArticleIdList><ArticleId IdType="doi">10.1111/jce.12439</ArticleId><ArticleId IdType="pubmed">24758402</ArticleId><ArticleId IdType="pmc">4459508</ArticleId></ArticleIdList></Reference><Reference><Citation>Kitzman DW, Scholz DG, Hagen PT, Ilstrup DM, Edwards WD (1988) Age-related changes in normal human hearts during the first 10 decades of life. Part II (maturity): a quantitative anatomic study of 765 specimens from subjects 20 to 99 years old. Mayo Clin Proc 63(2):137–146. https://doi.org/10.1016/s0025-6196(12)64946-5</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/s0025-6196(12)64946-5</ArticleId><ArticleId IdType="pubmed">3276974</ArticleId></ArticleIdList></Reference><Reference><Citation>Iwai S, Cantillon DJ, Kim RJ, Markowitz SM, Mittal S, Stein KM et al (2006) Right and left ventricular outflow tract tachycardias: evidence for a common electrophysiologic mechanism. J Cardiovasc Electrophysiol 17(10):1052–1058. https://doi.org/10.1111/j.1540-8167.2006.00539.x</Citation><ArticleIdList><ArticleId IdType="doi">10.1111/j.1540-8167.2006.00539.x</ArticleId><ArticleId IdType="pubmed">16800855</ArticleId></ArticleIdList></Reference><Reference><Citation>Haqqani HM, Tschabrunn CM, Tzou WS, Dixit S, Cooper JM, Riley MP et al (2011) Isolated septal substrate for ventricular tachycardia in nonischemic dilated cardiomyopathy: incidence, characterization, and implications. Heart Rhythm 8(8):1169–1176. https://doi.org/10.1016/j.hrthm.2011.03.008</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.hrthm.2011.03.008</ArticleId><ArticleId IdType="pubmed">21392586</ArticleId></ArticleIdList></Reference><Reference><Citation>Cheung JW, Anderson RH, Markowitz SM, Lerman BB (2019) Catheter ablation of arrhythmias originating from the left ventricular outflow tract. JACC Clin Electrophysiol 5(1):1–12. https://doi.org/10.1016/j.jacep.2018.11.012</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.jacep.2018.11.012</ArticleId><ArticleId IdType="pubmed">30678772</ArticleId></ArticleIdList></Reference><Reference><Citation>Anderson RH (2000) Clinical anatomy of the aortic root. Heart 84(6):670–673. https://doi.org/10.1136/heart.84.6.670</Citation><ArticleIdList><ArticleId IdType="doi">10.1136/heart.84.6.670</ArticleId><ArticleId IdType="pubmed">11083753</ArticleId><ArticleId IdType="pmc">1729505</ArticleId></ArticleIdList></Reference><Reference><Citation>Kuroki K, Sato A, Yamagami F, Nogami A, Aonuma K (2017) Life-threatening aortic dissection with cardiac tamponade during catheter ablation for ventricular tachycardia originating from left coronary cusp. J Cardiovasc Electrophysiol 28(10):1224–1225. https://doi.org/10.1111/jce.13277</Citation><ArticleIdList><ArticleId IdType="doi">10.1111/jce.13277</ArticleId><ArticleId IdType="pubmed">28635147</ArticleId></ArticleIdList></Reference><Reference><Citation>Whitman IR, Gladstone RA, Badhwar N, Hsia HH, Lee BK, Josephson SA et al (2017) Brain emboli after left ventricular Endocardial ablation. Circulation 135(9):867–877. https://doi.org/10.1161/CIRCULATIONAHA.116.025546</Citation><ArticleIdList><ArticleId IdType="doi">10.1161/CIRCULATIONAHA.116.025546</ArticleId><ArticleId IdType="pubmed">28119381</ArticleId></ArticleIdList></Reference><Reference><Citation>Anderson RH, Spicer DE, Hlavacek AM, Cook AC, Backer CL (2013) Wilcox’s surgical anatomy of the heart. Cambridge University Press</Citation><ArticleIdList><ArticleId IdType="doi">10.1017/CBO9781139028561</ArticleId></ArticleIdList></Reference><Reference><Citation>Elizari MV (2017) The normal variants in the left bundle branch system. J Electrocardiol 50(4):389–399. https://doi.org/10.1016/j.jelectrocard.2017.03.004</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.jelectrocard.2017.03.004</ArticleId><ArticleId IdType="pubmed">28341304</ArticleId></ArticleIdList></Reference><Reference><Citation>Kapa S, Gaba P, DeSimone CV, Asirvatham SJ (2017) Fascicular ventricular arrhythmias: Pathophysiologic mechanisms, anatomical constructs, and advances in approaches to management. Circ Arrhythm Electrophysiol. https://doi.org/10.1161/CIRCEP.116.002476</Citation><ArticleIdList><ArticleId IdType="doi">10.1161/CIRCEP.116.002476</ArticleId><ArticleId IdType="pubmed">28183845</ArticleId><ArticleId IdType="pmc">5319731</ArticleId></ArticleIdList></Reference><Reference><Citation>Demoulin JC, Kulbertus HE (1973) Left hemiblocks revisited from the histopathological viewpoint. Am Heart J 86(5):712–713. https://doi.org/10.1016/0002-8703(73)90354-2</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/0002-8703(73)90354-2</ArticleId><ArticleId IdType="pubmed">4743340</ArticleId></ArticleIdList></Reference><Reference><Citation>Kulbertus HE (1975) Concept of left hemiblocks revisited. A histopathological and experimental study. Adv Cardiol 14:126–135. https://doi.org/10.1159/000397645</Citation><ArticleIdList><ArticleId IdType="doi">10.1159/000397645</ArticleId><ArticleId IdType="pubmed">1136876</ArticleId></ArticleIdList></Reference><Reference><Citation>De Almeida MC, Lopes F, Fontes P, Barra F, Guimaraes R, Vilhena V (2015) Ungulates heart model: a study of the Purkinje network using India ink injection, transparent specimens and computer tomography. Anat Sci Int 90(4):240–250. https://doi.org/10.1007/s12565-014-0255-9</Citation><ArticleIdList><ArticleId IdType="doi">10.1007/s12565-014-0255-9</ArticleId><ArticleId IdType="pubmed">25316088</ArticleId></ArticleIdList></Reference><Reference><Citation>McAlpine WA (1975) Heart and Coronary Arteries: An Anatomical Atlas for Clinical Diagnosis, Radiological Investigation, and Surgical Treatment Bd. 0, Berlin, Heidelberg</Citation><ArticleIdList><ArticleId IdType="doi">10.1007/978-3-642-65983-6</ArticleId></ArticleIdList></Reference><Reference><Citation>El-Maasarany S, Ferrett CG, Firth A, Sheppard M, Henein MY (2005) The coronary sinus conduit function: anatomical study (relationship to adjacent structures). Europace 7(5):475–481. https://doi.org/10.1016/j.eupc.2005.05.013</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.eupc.2005.05.013</ArticleId><ArticleId IdType="pubmed">16087113</ArticleId></ArticleIdList></Reference><Reference><Citation>Hori Y, Nakahara S, Mine S, Anjo N, Fujii A, Ueda Y et al (2016) Pathological autopsy of a patient that underwent a successful ablation of an electrical storm from the left ventricular summit. Heart Vessels 31(12):2068–2073. https://doi.org/10.1007/s00380-016-0847-5</Citation><ArticleIdList><ArticleId IdType="doi">10.1007/s00380-016-0847-5</ArticleId><ArticleId IdType="pubmed">27178756</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35554772</PMID><DateRevised><Year>2022</Year><Month>05</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1573-7241</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>May</Month><Day>13</Day></PubDate></JournalIssue><Title>Cardiovascular drugs and therapy</Title><ISOAbbreviation>Cardiovasc Drugs Ther</ISOAbbreviation></Journal><ArticleTitle>Long-term Dexamethasone Treatment Increases Cardiac Galectin-3 Levels.</ArticleTitle><ELocationID EIdType="doi" ValidYN="Y">10.1007/s10557-022-07344-w</ELocationID><Abstract><AbstractText Label="PURPOSE" NlmCategory="OBJECTIVE">Glucocorticoids, which are widely prescribed around the world, cause cardiac remodeling in long-term treatment by triggering insulin resistance and increasing blood pressure. However, its role in cardiac remodeling remains unclear. Galectin-3 (gal-3) is a member of a beta-galactoside-binding animal lectins, upregulated as a result of insulin resistance and in the pressure-overloaded myocardium and regulate cardiac remodeling. We hypothesized that gal-3 may be upregulated in the myocardium with prolonged use of glucocorticoids and associated with cardiac hypertrophy.<AbstractText Label="METHODS" NlmCategory="METHODS">To examine the involvement of glucocorticoids in gal-3 levels in rat myocardium, sixteen female Wistar Albino rats were assigned to control (C; n = 8) and dexamethasone (Dex; n = 8) groups. Daily dexamethasone was injected subcutaneously for 28 days at a dose of 1 mg.kg<sup>-1</sup>. Control animals were injected with the same volume of saline. The body weight and heart weights were determined. Gal-3 levels in myocardium were determined by Western blot.<AbstractText Label="RESULTS" NlmCategory="RESULTS">Our data shows that dexamethasone administration resulted in significant increase in heart weight (p < 0.05) and HW/BW ratios (p < 0.001) and 28 days of dexamethasone administration with the dose of 1 mg.kg<sup>-1</sup> caused a twofold increase in the gal-3 expression in the left ventricle (p < 0.001).<AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">The finding of the current study is the first to show that dexamethasone causes an increase in gal-3 levels in myocardium. Our study provides an important step in the development of possible therapeutics by determining that dexamethasone causes an increase in gal-3 levels in the myocardium and raises awareness about the follow-up of patients receiving long-term glucocorticoid therapy. |
2,329,964 | Measurement of CSF pulsation from EPI-based human fMRI. | It is recently discovered that the glymphatic system and meningeal lymphatic system are the primary routes for the clearance of brain waste products. The CSF flow is part of these systems, facilitating the clearance procedure. Nonetheless, the relationship between CSF flow and brain functional activity has been underexplored. To investigate CSF dynamics and functional brain activity simultaneously, recent studies have proposed a CSF inflow index measured on edge slices (CSFedge) of echo-planar imaging (EPI) based functional magnetic resonance imaging (fMRI), however, it lacks the quantitative aspect of the CSF pulsation. We proposed a new method for quantifying CSF pulsation (CSFpulse) based on an interslice CSF pulsation model in the 4<sup>th</sup> ventricle of EPI-based fMRI. The proposed CSFpulse successfully detected the higher CSF flow during the resting state than the typical task states (visual and motor) (p<.05), which is consistent with previous studies based on phase contrast (PC) MRI and CSF volume MRI, while it was not detected in CSFedge based indices or baseline CSF signals in various regions of interest (ROIs). Moreover, CSFpulse demonstrated dynamic functional changes in CSF pulsation: it decreased during the activation-on blocks while it increased during the activation-off blocks. CSFpulse significantly correlated with stroke volume measured using PC MRI, a standard method for CSF pulsation quantification, under the same functional state, while CSFedge based indices or CSF ROIs showed no correlation with the PC MRI stroke volume. Lastly, the correlation of CSFpulse with global BOLD was weaker than that of CSFedge, suggesting that CSFpulse may reflect distinct CSF physiological information that is less affected by global BOLD effects. Based on these results, the proposed CSFpulse provides CSF pulsatility information more accurately in a quantitative manner than CSFedge based indices from the recent CSF studies or the conventional ROI-based analysis. In addition to the high correlation with PC MRI, CSFpulse is much faster than PC MRI and provides information of functional brain activations simultaneously, advantageous over PC MRI or CSF volume MRI. Accordingly, the suggested CSFpulse can be used for investigating intra-subject functional changes in BOLD and CSF pulsation simultaneously and inter-subject CSF pulsation variations based on conventional EPI-based fMRI, which warrants further investigation. |
2,329,965 | A Combined Human <i>in Silico</i> and CRISPR/Cas9-Mediated <i>in Vivo</i> Zebrafish Based Approach to Provide Phenotypic Data for Supporting Early Target Validation. | The clinical heterogeneity of heart failure has challenged our understanding of the underlying genetic mechanisms of this disease. In this respect, large-scale patient DNA sequencing studies have become an invaluable strategy for identifying potential genetic contributing factors. The complex aetiology of heart failure, however, also means that <i>in vivo</i> models are vital to understand the links between genetic perturbations and functional impacts as part of the process for validating potential new drug targets. Traditional approaches (e.g., genetically-modified mice) are optimal for assessing small numbers of genes, but less practical when multiple genes are identified. The zebrafish, in contrast, offers great potential for higher throughput <i>in vivo</i> gene functional assessment to aid target prioritisation, by providing more confidence in target relevance and facilitating gene selection for definitive loss of function studies undertaken in mice. Here we used whole-exome sequencing and bioinformatics on human patient data to identify 3 genes (<i>API5</i>, <i>HSPB7</i>, and <i>LMO2</i>) suggestively associated with heart failure that were also predicted to play a broader role in disease aetiology. The role of these genes in cardiovascular system development and function was then further investigated using <i>in vivo</i> CRISPR/Cas9-mediated gene mutation analysis in zebrafish. We observed multiple impacts in F0 knockout zebrafish embryos (crispants) following effective somatic mutation, including changes in ventricle size, pericardial oedema, and chamber malformation. In the case of <i>lmo2</i>, there was also a significant impact on cardiovascular function as well as an expected reduction in erythropoiesis. The data generated from both the human <i>in silico</i> and zebrafish <i>in vivo</i> assessments undertaken supports further investigation of the potential roles of <i>API5</i>, <i>HSPB7</i>, and <i>LMO2</i> in human cardiovascular disease. The data presented also supports the use of human <i>in silico</i> genetic variant analysis, in combination with zebrafish crispant phenotyping, as a powerful approach for assessing gene function as part of an integrated multi-level drug target validation strategy. |
2,329,966 | Pro-Arrhythmic Effects of Discontinuous Conduction at the Purkinje Fiber-Ventricle Junction Arising From Heart Failure-Induced Ionic Remodeling - Insights From Computational Modelling. | Heart failure is associated with electrical remodeling of the electrical properties and kinetics of the ion channels and transporters that are responsible for cardiac action potentials. However, it is still unclear whether heart failure-induced ionic remodeling can affect the conduction of excitation waves at the Purkinje fiber-ventricle junction contributing to pro-arrhythmic effects of heart failure, as the complexity of the heart impedes a detailed experimental analysis. The aim of this study was to employ computational models to investigate the pro-arrhythmic effects of heart failure-induced ionic remodeling on the cardiac action potentials and excitation wave conduction at the Purkinje fiber-ventricle junction. Single cell models of canine Purkinje fiber and ventricular myocytes were developed for control and heart failure. These single cell models were then incorporated into one-dimensional strand and three-dimensional wedge models to investigate the effects of heart failure-induced remodeling on propagation of action potentials in Purkinje fiber and ventricular tissue and at the Purkinje fiber-ventricle junction. This revealed that heart failure-induced ionic remodeling of Purkinje fiber and ventricular tissue reduced conduction safety and increased tissue vulnerability to the genesis of the unidirectional conduction block. This was marked at the Purkinje fiber-ventricle junction, forming a potential substrate for the genesis of conduction failure that led to re-entry. This study provides new insights into proarrhythmic consequences of heart failure-induced ionic remodeling. |
2,329,967 | The endogenous progenitor response following traumatic brain injury: a target for cell therapy paradigms. | Although there is ample evidence that central nervous system progenitor pools respond to traumatic brain injury, the reported effects are variable and likely contribute to both recovery as well as pathophysiology. Through a better understanding of the diverse progenitor populations in the adult brain and their niche-specific reactions to traumatic insult, treatments can be tailored to enhance the benefits and dampen the deleterious effects of this response. This review provides an overview of endogenous precursors, the associated effects on cognitive recovery, and the potential of exogenous cell therapeutics to modulate these endogenous repair mechanisms. Beyond the hippocampal dentate gyrus and subventricular zone of the lateral ventricles, more recently identified sites of adult neurogenesis, the meninges, as well as circumventricular organs, are also discussed as targets for endogenous repair. Importantly, this review highlights that progenitor proliferation alone is no longer a meaningful outcome and studies must strive to better characterize precursor spatial localization, transcriptional profile, morphology, and functional synaptic integration. With improved insight and a more targeted approach, the stimulation of endogenous neurogenesis remains a promising strategy for recovery following traumatic brain injury. |
2,329,968 | Multidrug-Resistant <i>Corynebacterium striatum</i> Developed During Treatment of Ommaya Reservoir Infection. | <i>Corynebacterium striatum</i>, a common component of the skin and mucosal microbiota of both immunocompetent and immunocompromised individuals, has become an emerging pathogen, colonizing indwelling medical devices and causing infections at multiple sites. A 3-year-old boy with an Ommaya reservoir in the right ventricle and a medical history of grade 3 intraventricular hemorrhage, Hirschsprung disease, catheter-related methicillin-resistant <i>Staphylococcus aureus</i> bacteremia, and congenital central hypoventilation syndrome was hospitalized for Ommaya reservoir infection with <i>C. striatum</i>. He was treated with ampicillin, to which the initial isolate was susceptible. <i>C. striatum</i> may have acquired multiple-drug resistance during the antibiotic treatment due to biofilm production. The Ommaya reservoir was replaced by external ventricular drainage. Cultures of the removed Ommaya reservoir, and cerebrospinal fluid samples grew <i>C. striatum</i>, which was susceptible to meropenem and vancomycin and resistant to other antibiotics. The antibiotic was switched to vancomycin to treat this new multidrug-resistant strain. After 8 days of vancomycin treatment, the cerebrospinal fluid culture obtained by a lumbar puncture was negative for <i>C. striatum</i>. In cases of device-associated infections caused by biofilm-producing bacteria, it is desirable to remove the device as soon as possible. |
2,329,969 | Ginsenoside Rh2 mitigates doxorubicin-induced cardiotoxicity by inhibiting apoptotic and inflammatory damage and weakening pathological remodelling in breast cancer-bearing mice.<Pagination><StartPage>e13246</StartPage><MedlinePgn>e13246</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">e13246</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1111/cpr.13246</ELocationID><Abstract><AbstractText Label="OBJECTIVES" NlmCategory="OBJECTIVE">There are presently a few viable ways to reduce cardiotoxicity of doxorubicin (Dox). The combination of chemotherapy agents with natural compounds delivers greater efficacy and reduces adverse effects in recent researches for cancer treatment. Here, we examined the potential effect of ginsenoside Rh2 on a Dox-based regimen in chemotherapy treatment.</AbstractText><AbstractText Label="MATERIALS AND METHODS" NlmCategory="METHODS">Human breast tumour (MDA-MB-231) xenograft nude mice, human cardiac ventricle fibroblasts, and human umbilical vein endothelial cells (HUVEC) were employed in the present study. Histology, immunohistochemistry, immunofluorescence, western blot, antibody array, and RNA-sequencing analyses were utilized to assess the protective effect of Rh2 on cardiotoxicity induced by Dox and the underlying mechanisms.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Rh2-reduced cardiotoxicity by inhibiting the cardiac histopathological changes, apoptosis and necrosis, and consequent inflammation. Pathological remodelling was attenuated by reducing fibroblast to myofibroblast transition (FMT) and endothelial-mesenchymal transition (EndMT) in hearts. RNA-sequencing analysis showed that Dox treatment predominantly targets cell cycle and attachment of microtubules and boosted tumour necrosis, chemokine and interferon-gamma production, response to cytokine and chemokine, and T cell activation, whereas Rh2 regulated these effects. Intriguingly, Rh2 also attenuated fibrosis via promoting senescence in myofibroblasts and reversing established myofibroblast differentiation in EndMT.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Rh2 regulates multiple pathways in the Dox-provoked heart, proposing a potential candidate for cancer supplement and therapy-associated cardiotoxicity.</AbstractText><CopyrightInformation>© 2022 The Authors. Cell Proliferation published by John Wiley & Sons Ltd.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hou</LastName><ForeName>Jingang</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Intelligent Synthetic Biology Center, Daejeon, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yun</LastName><ForeName>Yeejin</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon, South Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cui</LastName><ForeName>Changhao</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Research and Development Team 4, Sempio Foods Company, Cheongju, South Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Sunchang</ForeName><Initials>S</Initials><Identifier Source="ORCID">0000-0003-0238-7205</Identifier><AffiliationInfo><Affiliation>Intelligent Synthetic Biology Center, Daejeon, Republic of Korea.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon, South Korea.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>P0014633</GrantID><Agency>Advancement of Active Biomedical material Project, funded by the Ministry of Trade</Agency><Country/></Grant><Grant><GrantID>321109041SB010</GrantID><Agency>Development of industrialization technology for crop virus and pest Project, funded by the Ministry of Agriculture, Food and Rural Affairs</Agency><Country/></Grant><Grant><GrantID>2011-0031955</GrantID><Agency>Intelligent Synthetic Biology Center of the Global Frontier Project, funded by the Ministry of Education, Science and Technology</Agency><Country/></Grant><Grant><Agency>KAIST Cross-Generation Collaborative Lab project</Agency><Country/></Grant><Grant><GrantID>2021-153-0028-0019-002B</GrantID><Agency>Multi-Department Research and Business Development Program, funded by Sejong city</Agency><Country/></Grant><Grant><GrantID>NRF-2021M3A9C4001028</GrantID><Agency>The Bio-Synergy Research Project of the Ministry of Science, ICT and Future Planning through the National Research Foundation</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>05</Month><Day>09</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Cell Prolif</MedlineTA><NlmUniqueID>9105195</NlmUniqueID><ISSNLinking>0960-7722</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D036145">Ginsenosides</NameOfSubstance></Chemical><Chemical><RegistryNumber>63231-63-0</RegistryNumber><NameOfSubstance UI="D012313">RNA</NameOfSubstance></Chemical><Chemical><RegistryNumber>78214-33-2</RegistryNumber><NameOfSubstance UI="C055305">ginsenoside Rh2</NameOfSubstance></Chemical><Chemical><RegistryNumber>80168379AG</RegistryNumber><NameOfSubstance UI="D004317">Doxorubicin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001943" MajorTopicYN="Y">Breast Neoplasms</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D066126" MajorTopicYN="Y">Cardiotoxicity</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004317" MajorTopicYN="N">Doxorubicin</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D042783" MajorTopicYN="N">Endothelial Cells</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D036145" MajorTopicYN="N">Ginsenosides</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008819" MajorTopicYN="N">Mice, Nude</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D032383" MajorTopicYN="N">Myocytes, Cardiac</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009336" MajorTopicYN="N">Necrosis</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018384" MajorTopicYN="N">Oxidative Stress</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012313" MajorTopicYN="N">RNA</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><CoiStatement>We declare no conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>4</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>1</Month><Day>20</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>4</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>5</Month><Day>11</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>6</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>5</Month><Day>10</Day><Hour>0</Hour><Minute>43</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35534947</ArticleId><ArticleId IdType="pmc">PMC9201376</ArticleId><ArticleId IdType="doi">10.1111/cpr.13246</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Siegel RL, Miller KD, Fuchs HE, Jemal A. Cancer statistics, 2021. CA Cancer J Clin. 2021;71(1):7‐33.</Citation><ArticleIdList><ArticleId IdType="pubmed">33433946</ArticleId></ArticleIdList></Reference><Reference><Citation>Wang D, Fulthorpe R, Liss SN, Edwards EA. Identification of estrogen‐responsive genes by complementary deoxyribonucleic acid microarray and characterization of a novel early estrogen‐induced gene: EEIG1. Mol Endocrinol. 2004;18(2):402‐411.</Citation><ArticleIdList><ArticleId IdType="pubmed">14605097</ArticleId></ArticleIdList></Reference><Reference><Citation>Khongorzul P, Ling CJ, Khan FU, Ihsan AU, Zhang J. Antibody–drug conjugates: a comprehensive review. Mol Cancer Res. 2020;18(1):3‐19.</Citation><ArticleIdList><ArticleId IdType="pubmed">31659006</ArticleId></ArticleIdList></Reference><Reference><Citation>Blagosklonny MV. Analysis of FDA approved anticancer drugs reveals the future of cancer therapy. Cell Cycle. 2004;3(8):1033‐1040.</Citation><ArticleIdList><ArticleId IdType="pubmed">15254418</ArticleId></ArticleIdList></Reference><Reference><Citation>Bisogno G, Jenney M, Bergeron C, et al. Addition of dose‐intensified doxorubicin to standard chemotherapy for rhabdomyosarcoma (EpSSG RMS 2005): a multicentre, open‐label, randomised controlled, phase 3 trial. Lancet Oncol. 2018;19(8):1061‐1071.</Citation><ArticleIdList><ArticleId IdType="pubmed">29941280</ArticleId></ArticleIdList></Reference><Reference><Citation>Cardinale D, Colombo A, Lamantia G, et al. Anthracycline‐induced cardiomyopathy: clinical relevance and response to pharmacologic therapy. J Am Coll Cardiol. 2010;55(3):213‐220.</Citation><ArticleIdList><ArticleId IdType="pubmed">20117401</ArticleId></ArticleIdList></Reference><Reference><Citation>Levitt G, Anazodo A, Burch M, Bunch K. Cardiac or cardiopulmonary transplantation in childhood cancer survivors: an increasing need? Eur J Cancer. 2009;45(17):3027‐3034.</Citation><ArticleIdList><ArticleId IdType="pubmed">19744853</ArticleId></ArticleIdList></Reference><Reference><Citation>Ichikawa Y, Ghanefar M, Bayeva M, et al. Cardiotoxicity of doxorubicin is mediated through mitochondrial iron accumulation. J Clin Invest. 2014;124(2):617‐630.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC3904631</ArticleId><ArticleId IdType="pubmed">24382354</ArticleId></ArticleIdList></Reference><Reference><Citation>Hu C, Zhang X, Wei W, et al. Matrine attenuates oxidative stress and cardiomyocyte apoptosis in doxorubicin‐induced cardiotoxicity via maintaining AMPKα/UCP2 pathway. Acta Pharmaceutica Sinica B. 2019;9(4):690‐701.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6664099</ArticleId><ArticleId IdType="pubmed">31384530</ArticleId></ArticleIdList></Reference><Reference><Citation>Sachinidis A. Cardiotoxicity and heart failure: lessons from human‐induced pluripotent stem cell‐derived cardiomyocytes and anticancer drugs. Cell. 2020;9(4):1001.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC7226145</ArticleId><ArticleId IdType="pubmed">32316481</ArticleId></ArticleIdList></Reference><Reference><Citation>Gyöngyösi M, Lukovic D, Zlabinger K, et al. Liposomal doxorubicin attenuates cardiotoxicity via induction of interferon‐related DNA damage resistance. Cardiovasc Res. 2020;116(5):970‐982.</Citation><ArticleIdList><ArticleId IdType="pubmed">31346605</ArticleId></ArticleIdList></Reference><Reference><Citation>Foucquier J, Guedj M. Analysis of drug combinations: current methodological landscape. Pharmacol Res Perspe. 2015;3(3):e00149.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC4492765</ArticleId><ArticleId IdType="pubmed">26171228</ArticleId></ArticleIdList></Reference><Reference><Citation>Mamounas EP, Bryant J, Lembersky B, et al. Paclitaxel after doxorubicin plus cyclophosphamide as adjuvant chemotherapy for node‐positive breast cancer: results from NSABP B‐28. J Clin Oncol. 2005;23(16):3686‐3696.</Citation><ArticleIdList><ArticleId IdType="pubmed">15897552</ArticleId></ArticleIdList></Reference><Reference><Citation>Sonowal H, Pal PB, Wen J‐J, Awasthi S, Ramana KV, Srivastava SK. Aldose reductase inhibitor increases doxorubicin‐sensitivity of colon cancer cells and decreases cardiotoxicity. Sci Rep. 2017;7(1):3182.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC5466629</ArticleId><ArticleId IdType="pubmed">28600556</ArticleId></ArticleIdList></Reference><Reference><Citation>Wang Y, Ma Q, Zhang S, et al. Digoxin enhances the anticancer effect on non‐small cell lung cancer while reducing the cardiotoxicity of Adriamycin. Front Pharmacol. 2020;11:186.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC7059749</ArticleId><ArticleId IdType="pubmed">32180730</ArticleId></ArticleIdList></Reference><Reference><Citation>Rocca A, Cortesi P, Cortesi L, et al. Phase II study of liposomal doxorubicin, docetaxel and trastuzumab in combination with metformin as neoadjuvant therapy for HER2‐positive breast cancer. Ther Adv Med Oncol. 2021;13: 1758835920985632.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC7876584</ArticleId><ArticleId IdType="pubmed">33613693</ArticleId></ArticleIdList></Reference><Reference><Citation>Lin S, Chang C, Hsu C, et al. Natural compounds as potential adjuvants to cancer therapy: preclinical evidence. Br J Pharmacol. 2020;177(6):1409‐1423.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC7056458</ArticleId><ArticleId IdType="pubmed">31368509</ArticleId></ArticleIdList></Reference><Reference><Citation>Sritharan S, Sivalingam N. A comprehensive review on time‐tested anticancer drug doxorubicin. Life Sci. 2021;278:119527.</Citation><ArticleIdList><ArticleId IdType="pubmed">33887349</ArticleId></ArticleIdList></Reference><Reference><Citation>Mohajeri M, Sahebkar A. Protective effects of curcumin against doxorubicin‐induced toxicity and resistance: a review. Crit Rev Oncol/Hematol. 2018;122:30‐51.</Citation><ArticleIdList><ArticleId IdType="pubmed">29458788</ArticleId></ArticleIdList></Reference><Reference><Citation>Christidi E, Brunham LR. Regulated cell death pathways in doxorubicin‐induced cardiotoxicity. Cell Death Dis. 2021;12(4):339.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC8017015</ArticleId><ArticleId IdType="pubmed">33795647</ArticleId></ArticleIdList></Reference><Reference><Citation>Shin H, Kwon H, Lee J, et al. Doxorubicin‐induced necrosis is mediated by poly‐(ADP‐ribose) polymerase 1 (PARP1) but is independent of p53. Sci Rep. 2015;5(1):15798.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC4629133</ArticleId><ArticleId IdType="pubmed">26522181</ArticleId></ArticleIdList></Reference><Reference><Citation>Zhang W, Lavine KJ, Epelman S, et al. Necrotic myocardial cells release damage‐associated molecular patterns that provoke fibroblast activation in vitro and trigger myocardial inflammation and fibrosis in vivo. J Am Heart Assoc. 2015;4(6):e001993.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC4599537</ArticleId><ArticleId IdType="pubmed">26037082</ArticleId></ArticleIdList></Reference><Reference><Citation>Gong T, Liu L, Jiang W, Zhou R. DAMP‐sensing receptors in sterile inflammation and inflammatory diseases. Nat Rev Immunol. 2020;20(2):95‐112.</Citation><ArticleIdList><ArticleId IdType="pubmed">31558839</ArticleId></ArticleIdList></Reference><Reference><Citation>Gulati A, Jabbour A, Ismail TF, et al. Association of fibrosis with mortality and sudden cardiac death in patients with nonischemic dilated cardiomyopathy. JAMA. 2013;309(9):896‐908.</Citation><ArticleIdList><ArticleId IdType="pubmed">23462786</ArticleId></ArticleIdList></Reference><Reference><Citation>Sweeney M, Corden B, Cook SA. Targeting cardiac fibrosis in heart failure with preserved ejection fraction: mirage or miracle? EMBO Mol Med. 2020;12(10):e10865.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC7539225</ArticleId><ArticleId IdType="pubmed">32955172</ArticleId></ArticleIdList></Reference><Reference><Citation>Baci D, Bosi A, Parisi L, et al. Innate immunity effector cells as inflammatory drivers of cardiac fibrosis. Int J Mol Sci. 2020;21(19):7165.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC7583949</ArticleId><ArticleId IdType="pubmed">32998408</ArticleId></ArticleIdList></Reference><Reference><Citation>Münch J, Avanesov M, Bannas P, et al. Serum matrix metalloproteinases as quantitative biomarkers for myocardial fibrosis and sudden cardiac death risk stratification in patients with hypertrophic cardiomyopathy. J Card Fail. 2016;22(10):845‐850.</Citation><ArticleIdList><ArticleId IdType="pubmed">27018569</ArticleId></ArticleIdList></Reference><Reference><Citation>Spinale FG, Janicki JS, Zile MR. Membrane‐associated matrix proteolysis and heart failure. Circul Res. 2013;112(1):195‐208.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC4026203</ArticleId><ArticleId IdType="pubmed">23287455</ArticleId></ArticleIdList></Reference><Reference><Citation>Meyer K, Hodwin B, Ramanujam D, Engelhardt S, Sarikas A. Essential role for premature senescence of Myofibroblasts in myocardial fibrosis. J Am Coll Cardiol. 2016;67(17):2018‐2028.</Citation><ArticleIdList><ArticleId IdType="pubmed">27126529</ArticleId></ArticleIdList></Reference><Reference><Citation>Garrison G, Huang SK, Okunishi K, et al. Reversal of myofibroblast differentiation by prostaglandin E(2). Am J Respir Cell Mol Biol. 2013;48(5):550‐558.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC3707380</ArticleId><ArticleId IdType="pubmed">23470625</ArticleId></ArticleIdList></Reference><Reference><Citation>Desai VD, Hsia HC, Schwarzbauer JE. Reversible modulation of Myofibroblast differentiation in adipose‐derived mesenchymal stem cells. PLoS One. 2014;9(1):e86865.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC3900664</ArticleId><ArticleId IdType="pubmed">24466271</ArticleId></ArticleIdList></Reference><Reference><Citation>Yan C, Xu Z, Huang W. Cellular senescence affects cardiac regeneration and repair in ischemic heart disease. Aging Dis. 2021;12(2):552‐569.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC7990367</ArticleId><ArticleId IdType="pubmed">33815882</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedBookArticle><BookDocument><PMID Version="22">26389391</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK65954</ArticleId></ArticleIdList><Book><Publisher><PublisherName>National Cancer Institute (US)</PublisherName><PublisherLocation>Bethesda (MD)</PublisherLocation></Publisher><BookTitle book="pdqcis">PDQ Cancer Information Summaries</BookTitle><PubDate><Year>2002</Year></PubDate><BeginningDate><Year>2002</Year></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="pdqcis" part="CDR0000574295">Childhood Astrocytomas Treatment (PDQ®): Patient Version | This PDQ cancer information summary has current information about the treatment of childhood astrocytomas. It is meant to inform and help patients, families, and caregivers. It does not give formal guidelines or recommendations for making decisions about health care. Editorial Boards write the PDQ cancer information summaries and keep them up to date. These Boards are made up of experts in cancer treatment and other specialties related to cancer. The summaries are reviewed regularly and changes are made when there is new information. The date on each summary ("Date Last Modified") is the date of the most recent change. The information in this patient summary was taken from the health professional version, which is reviewed regularly and updated as needed, by the PDQ Pediatric Treatment Editorial Board. |
2,329,970 | [Algorithm for the management of laryngeal obstruction in pediatrics]. | The larynx is at the aerodigestive crossroads; any pathology that involves it will have an impact on breathing, swallowing and/or the voice. It`s divided into three regions: supraglottis (includes epiglottis, ventricular bands and laryngeal ventricles), glottis (space limited by the vocal cords) and subglottis (narrowest area of pediatric airway and the only point of larynx completely surrounded by cartilage: the cricoid ring). Laryngeal obstruction can present as a potentially fatal acute condition or as a chronic process. The main symptom is inspiratory or biphasic stridor. The etiology varies widely according to age and it may be of congenital, inflammatory, infectious, traumatic, neoplastic or iatrogenic origin. We describe the pathologies that cause laryngeal obstruction, either those that occur very often or those which are important for their severity, their guiding symptoms to the presumptive diagnosis, additional studies and treatment.<CopyrightInformation>Sociedad Argentina de Pediatría.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Cuestas</LastName><ForeName>Giselle</ForeName><Initials>G</Initials><Identifier Source="ORCID">0000-0001-8514-713X</Identifier><AffiliationInfo><Affiliation>Sección de Endoscopia Respiratoria, División de Otorrinolaringología, Hospital General de Niños Dr. Pedro de Elizalde, Ciudad Autónoma de Buenos Aires, Argentina. giselle_cuestas@yahoo.com.ar.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rodríguez</LastName><ForeName>Hugo</ForeName><Initials>H</Initials><Identifier Source="ORCID">0000-0001-5785-681Xr</Identifier><AffiliationInfo><Affiliation>Servicio de Endoscopia Respiratoria, Hospital de Pediatría S.A.M.I.C. "Prof. Dr. Juan P. Garrahan", Ciudad Autónoma de Buenos Aires, Argentina.</Affiliation></AffiliationInfo></Author></AuthorList><Language>spa</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><VernacularTitle>Algoritmo para el manejo de la obstrucción laríngea en pediatría.</VernacularTitle></Article><MedlineJournalInfo><Country>Argentina</Country><MedlineTA>Arch Argent Pediatr</MedlineTA><NlmUniqueID>0372460</NlmUniqueID><ISSNLinking>0325-0075</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000402" MajorTopicYN="Y">Airway Obstruction</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000465" MajorTopicYN="N">Algorithms</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002648" MajorTopicYN="N">Child</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007818" MajorTopicYN="Y">Laryngeal Diseases</DescriptorName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007830" MajorTopicYN="Y">Larynx</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010372" MajorTopicYN="Y">Pediatrics</DescriptorName></MeshHeading></MeshHeadingList><OtherAbstract Type="Publisher" Language="spa">La laringe se localiza en la encrucijada aerodigestiva; cualquier patología que la comprometa tendrá repercusión en la respiración, la deglución y/o la voz. Se divide en tres regiones: la supraglotis (comprende la epiglotis, las bandas ventriculares y los ventrículos laríngeos), la glotis (espacio limitado por las cuerdas vocales) y la subglotis (zona más estrecha de la vía aérea pediátrica y único punto rodeado en su totalidad por cartílago: el anillo cricoides). La obstrucción laríngea se puede presentar como una condición aguda potencialmente fatal o como un proceso crónico. El síntoma principal es el estridor inspiratorio o bifásico. La etiología varía mucho según la edad y puede ser de origen congénito, inflamatorio, infeccioso, traumático, neoplásico o iatrogénico. Se describen las patologías que ocasionan obstrucción laríngea con más frecuencia o que revisten importancia por su gravedad, sus síntomas orientadores para el diagnóstico presuntivo, los estudios complementarios y el tratamiento. |
2,329,971 | Preoperative Third Ventricle Floor Bowing is Associated with Increased Surgical Success Rate in Patients Undergoing Endoscopic Third Ventriculostomy - A Systematic Review and Meta-analysis. | Endoscopic third ventriculostomy (ETV) is a procedure that involves devising an opening in the third ventricle floor, allowing cerebrospinal fluid to flow into the prepontine cistern and the subarachnoid space. Third ventricular floor bowing (TVFB) serves as an indicator of intraventricular obstruction in hydrocephalus and existence of pressure gradient across third ventricular floor, which is the prerequisite of a successful ETV.</AbstractText>In this systematic review and meta-analysis, we aimed to synthesize the latest evidence on the TVFB as a marker for surgical success in patients undergoing ETV.</AbstractText>We performed a comprehensive search on topics that assesses the association of TVFB with the surgical success in patients undergoing ETV from several electronic databases.</AbstractText>There was a total of 568 subjects from six studies. TVFB was associated with 85% (81-88%) ETV success. TVFB was associated with OR 4.13 [2.59, 6.60], P < 0.001; I2</sup>: 6% for ETV success. Subgroup analysis on pediatric patients showed 86% (82-91%) success rate. In terms of value for ETV success compared to ETV Success Score (ETVSS), a high ETVSS does not significantly differ (P = 0.31) from TVFB and TVFB was associated with OR 3.14 [1.72, 5.73], P < 0.001; I2</sup>: 69% compared to intermediate/moderate ETVSS. Funnel plot analysis showed an asymmetrical funnel plot due to the presence of an outlier. Upon sensitivity analysis by removing the outlier, the OR was 3.62 [2.22, 5.89], P < 0.001; I2</sup>: 0% for successful surgery in TVFB.</AbstractText>TVFB was associated with an increased rate of successful surgery in adults and children undergoing ETV.</AbstractText> |
2,329,972 | Transcallosal Suprachoroidal Approach for a Small Third Ventricular Colloid Cyst. | The interhemispheric transcallosal approach provides an elegant pathway to access the lesions of the third ventricle. However, every step of this approach is fraught with hazards which must be negotiated delicately. A comprehensive knowledge of surgical anatomy coupled with technical skill is necessary for optimum surgical results.</AbstractText>This video aims to address the surgical nuances of the suprachoroidal transcallosal approach while accessing the lesions around the foramen of Monro in the anterior and middle part of the third ventricle.</AbstractText>A 16-year-old boy presented with worsening headaches with episodes of speech arrest and blank stare for 6 years, which had become more frequent over the past 4-5 months. Radiology showed a subcentimeteric colloid cyst at the foramen of monro. A transcallosal corridor was used to reach the foramen of monro, and the suprachoroidal access was adopted to uncover the colloid cyst and excise it completely preserving the deep veins.</AbstractText>The patient had uneventful recovery and radiology showed complete excision of the cyst.</AbstractText>Transcallosal approach, being minimally invasive, exploits the natural extra-axial corridor (interhemispheric) obviating the need for a cortical incision. The suprachoroidal approach mitigates the risks of thalamostriate vein injury, basal ganglia stroke, and hemiparesis.</AbstractText> |
2,329,973 | Community-Acquired Meningitis Complicated by Pyogenic Ventriculitis: A Case Report. | Ventriculitis is the inflammation of the ependymal lining of the ventricles in the brain which usually occurs as a complication of meningitis, intraventricular devices, intracranial surgery, or brain abscess. Common clinical features include fever, altered mental status, headache, and neck rigidity. Some commonly associated organisms are <i>Streptococcus,</i> gram-negative <i>Bacillus</i>, <i>Staphylococcus</i>, and <i>Meningococcus.</i> Here, we report the case of a 57-year-old female presenting with fever, headache, and altered mental status, along with positive physical examination findings of Kernig's and Brudzinski's signs without any focal neurological deficits. Cerebrospinal fluid analysis findings were consistent with bacterial infection with neutrophilic leukocytosis, high protein, and low glucose. The blood culture was positive for <i>Streptococcus pneumoniae</i>. Magnetic resonance imaging was negative for enhancement of the meninges but showed fluid-filled layering in the ventricles consistent with pyogenic ventriculitis. The patient improved clinically within three days of initiation of empiric antibiotics. |
2,329,974 | The hidden continuum of HIV-associated cardiomyopathy: A focussed review with case reports. | HIV-associated cardiomyopathy (HIVAC) is a poorly understood group of diseases with a poor prognosis once ventricular dysfunction is present. Cardiovascular magnetic resonance has revealed a previously unappreciated burden of asymptomatic myocardial abnormalities in people living with HIV, including abnormalities already present at the time of HIV diagnosis. These abnormalities include thickened, inflamed ventricles that bear resemblance to cases of symptomatic HIVAC that are reported on in this article. Our understanding and the significance of asymptomatic HIV-associated myocardial pathology will be explored as early disease on a continuum towards more advanced cardiomyopathy. The need for prospective research in persons naïve to anti-retroviral therapy is emphasised as it may provide key findings to better understand this elusive disease process. |
2,329,975 | Multiscale Contrasts Between the Right and Left Ventricle Biomechanics in Healthy Adult Sheep and Translational Implications. | Cardiac biomechanics play a significant role in the progression of structural heart diseases (SHDs). SHDs alter baseline myocardial biomechanics leading to single or bi-ventricular dysfunction. But therapies for left ventricle (LV) failure patients do not always work well for right ventricle (RV) failure patients. This is partly because the basic knowledge of baseline contrasts between the RV and LV biomechanics remains elusive with limited discrepant findings. The aim of the study was to investigate the multiscale contrasts between LV and RV biomechanics in large animal species. We hypothesize that the adult healthy LV and RV have distinct passive anisotropic biomechanical properties. <i>Ex vivo</i> biaxial tests were performed in fresh sheep hearts. Histology and immunohistochemistry were performed to measure tissue collagen. The experimental data were then fitted to a Fung type model and a structurally informed model, separately. We found that the LV was stiffer in the longitudinal (outflow tract) than circumferential direction, whereas the RV showed the opposite anisotropic behavior. The anisotropic parameter <i>K</i> from the Fung type model accurately captured contrasting anisotropic behaviors in the LV and RV. When comparing the elasticity in the same direction, the LV was stiffer than the RV longitudinally and the RV was stiffer than the LV circumferentially, suggesting different filling patterns of these ventricles during diastole. Results from the structurally informed model suggest potentially stiffer collagen fibers in the LV than RV, demanding further investigation. Finally, type III collagen content was correlated with the low-strain elastic moduli in both ventricles. In summary, our findings provide fundamental biomechanical differences between the chambers. These results provide valuable insights for guiding cardiac tissue engineering and regenerative studies to implement chamber-specific matrix mechanics, which is particularly critical for identifying biomechanical mechanisms of diseases or mechanical regulation of therapeutic responses. In addition, our results serve as a benchmark for image-based inverse modeling technologies to non-invasively estimate myocardial properties in the RV and LV. |
2,329,976 | Hemodynamic alterations following a cerebellar arteriovenous malformation resection: Case report and densitometric quantitative analysis from CT imaging. | Cerebellar arteriovenous malformations (cAVMs) are rare and challenging lesions with an aggressive natural history. The mechanisms whereby a patient can worsen clinically after a supratentorial AVM resection include an acute alteration in cerebral hemodynamics, which is a known cause of postoperative hyperemia, edema and/or hemorrhage. These phenomena has not been described for cAVMS. Moreover, the underlying pathophysiology of edema and hemorrhage after AVM resection still remains controversial.</AbstractText>We report a patient that presented an abrupt neurological deterioration after cAVM surgical resection. Emergent external ventricular drainage to treat incipient hydrocephalus only partially reverted the patient's deterioration. Consecutive post-surgery CT images revealed fourth ventricle compression secondary to cerebellar swelling that concurred with a new neurological deterioration. Densitometric analysis was performed in these CT images to reveal the nature of these changes as well as their evolution over time.</AbstractText>Importantly, we demonstrated a dynamic increase in the cerebellum mean density at the interval of Hounsfield values which correspond to hyperemia values. These changes were dynamic, and when hyperemia resolved and cerebellar density returned to basal levels, the fourth ventricle re-expanded and the patient neurologically recovered.</AbstractText>This study demonstrated the utility of quantitative CT image analysis in the context of hemodynamic alterations following cAVM resection. Densitometric CT analysis demonstrated that hyperemic changes, but not ischemic ones, were time-dependent and were responsible for swelling and hemorrhage that conditioned neurological status and patient's evolution.</AbstractText>Copyright © 2021 Sociedad Española de Neurocirugía. Published by Elsevier España, S.L.U. All rights reserved.</CopyrightInformation> |
2,329,977 | Re-Do endoscopic third ventriculostomy. Retrospective analysis of 13 patients. | Indication for endoscopic third ventriculostomy (ETV) in the treatment for noncommunicating hydrocephalus is widely accepted. There is controversy regarding the indication of a second procedure (re-ETV) when the first has failed. The objective of this work is to revise ETV failures in a series in which re-ETV was performed and to describe the factors related to its prognosis.</AbstractText>Retrospective study of pediatric patients with ETV failure treated by re-ETV between 2003 and 2018. Gender, age in first and second ETV, time to failure of first ETV, etiology of hydrocephalus, previous presence of shunt, ETV-SS in the first and second ETV, intraoperative findings, success of the second procedure and follow-up were collected. The ETV-SS result was grouped into high (≥ 80), moderate (50-70) or low (≤ 40) scores. Endoscopic procedure failure was considered clinical worsening or the absence of radiological criteria for improvement (reduction in ventricular size or presence of ETV flow artifact in the floor of third ventricle).</AbstractText>Of 97 ETV carried out in this period, 47 failures were registered, with 13 re-ETV performed. Of these, 8 were classified as successful (61.53%). Re-ETV was successful in 4/4 cases in which etiology was tectal tumor or aqueduct stenosis. In the group with a high ETV-SS score there was a higher rate of success (75%) than in the group with a moderate score (40%). 9 patients presented shunt prior to first ETV and in them, success was 66.6% compared to 50% in the group without prior shunt. All re-ETV were performed without complications. In 11 of the 13 procedures a closed stoma was found and the remaining 2 cases, we found a punctate opening. The mean follow-up after re-ETV was 61.23 months.</AbstractText>The selection of patients for re-VET should be cautious. Factors such as age, etiology, and previous shunt (ETV-SS factors) have prognostic influence. However, there are specific factors which indicate favorable prognostic for re-VET such as a longer time to failure of the first procedure, the finding of a closed/punctate stoma or the loss of flow artifact in the follow-up MRI.</AbstractText>Copyright © 2021 Sociedad Española de Neurocirugía. Published by Elsevier España, S.L.U. All rights reserved.</CopyrightInformation> |
2,329,978 | Ideal trajectory for frontal ventriculostomy: Radiological study and anatomical study. | Several techniques have been described to improve the accuracy of the freehand procedure for frontal ventriculostomy and reduce complications due to suboptimal placement or misplacement of the catheter tip. To date, none of the available studies have found a reliable, low cost and consistent technique. We aimed to provide a standardized protocol for freehand frontal ventriculostomy.</AbstractText>In the first part of the radiological study, 125 CT scans were used to measure the length of the catheter using 2 right-sided entry points. In the second part, a grid of 24 entry points on the frontal bone was used in 50 CT scans to record the distance from the cranial surface to the Foramen of Monro (FM). Ventriculostomy was performed on six cadaveric heads using a grid of 9 entry points, comparing a 5 ml syringe with the freehand technique to reach the target.</AbstractText>The first part of the radiological study showed a length from the cranial surface to the FM was overall 67,38 ± 1,03 mm. For the second part, the mean length of the 24 selected points was 68,54 ± 2,73 mm without statistical difference. In the anatomical study, the FM was reached 8 times (14.8%) with the syringe vs 31 times (57.4%) with the freehand technique, and the ventricles 43 (79.6%) vs 37 (68.5%). The mean lengths from the skull to the FM were 71.33 ± 4.21 mm.</AbstractText>In this study, we showed the optimal length of a frontal ventricular catheter. We have also demonstrated that the portion of the frontal bone above the superior temporal lines matches a sphere in which the center is the FM.</AbstractText>Copyright © 2022 Elsevier B.V. All rights reserved.</CopyrightInformation> |
2,329,979 | Endoscopic Management of Lateral Ventricle Arachnoid Cysts-Case Series with Proposed Classification. | We present a case series of 7 patients with intraventricular arachnoid cysts of lateral ventricle managed with endoscopic treatment with proposed classification of the cyst based on anatomic extent.</AbstractText>In all patients, the lateral ventricle arachnoid cyst was primarily located in the trigone and body of the lateral ventricle. Proposed classification is based on extension of the arachnoid cyst. Type 1 is an arachnoid cyst located in the lateral ventricle only, type 2 is a lateral ventricle arachnoid cyst extending to the quadrigeminal cistern, and type 3 is the lateral ventricle arachnoid cyst extending to the velum interpositum cistern.</AbstractText>Two patients were managed with multiple fenestration and septostomy, and in 1 patient where the cyst was not adherent to the ventricular wall it was excised completely. Two patients who had a lateral ventricle cyst located in the atrium but extending to quadrigeminal cyst were managed with 3 fenestrations. Two patients with a lateral ventricle arachnoid cyst located into the atrium of lateral ventricle and extending to the velum interpositum cistern through the choroid fissure were managed with 3 endoscopic fenestrations. Postoperatively, patients were followed clinically and by radiologic imaging. None of the patients reported recurrence until the latest follow-up.</AbstractText>Multiple endoscopic fenestrations for lateral ventricle arachnoid cyst according to its location and anatomic extension help to reduce recurrence and good outcome. Cyst excision is recommended only when the cyst wall is easily separable from the lateral ventricle wall. Intraoperative use of thulium light amplification by stimulated emission of radiation helps in achieving early hemostasis and easy perforation of the thick cyst wall.</AbstractText>Copyright © 2022 Elsevier Inc. All rights reserved.</CopyrightInformation> |
2,329,980 | Influence of heart rate on right ventricular function assessed by right heart catheterization and echocardiography in healthy anesthetized dogs.<Pagination><StartPage>166</StartPage><MedlinePgn>166</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">166</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1186/s12917-022-03271-y</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Right ventricular (RV) functional assessment has received considerable attention in veterinary medicine since various diseases, such as cardiovascular, respiratory, endocrine, and neoplastic disease, may affect RV function. Heart rate (HR) is an important factor that can influence RV function through changes in loading condition and contractility. However, no study has yet evaluated the association between HR and RV function in the same individuals. This study aimed to evaluate the influence of elevated HR on RV function using right heart catheterization and echocardiography, and investigate the association between right heart catheterization and echocardiographic indices.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Right atrial pacing was performed in eight dogs at 120, 140, 160, and 180 bpm. With an increase in HR, the RV systolic volume, RV diastolic volume, and stroke volume significantly decreased; however, the cardiac output, end-systolic elastance (Ees), and effective arterial elastance (Ea) significantly increased. Significant changes were not observed in RV pressure and Ees/Ea. The RV area normalized by body weight, RV fractional area change normalized by body weight (RV FACn), and tricuspid annular plane systolic excursion normalized by body weight (TAPSEn) significantly decreased with increased HR. Peak systolic myocardial velocity of the lateral tricuspid annulus (RV s'), RV strain, and RV strain rate of only the RV free wall analysis (RV-SrL<sub>3seg</sub>) showed no significant changes with the increase in HR; however, there was an increase in the RV strain rate of the RV global analysis (RV-SrL<sub>6seg</sub>). Multiple regression analysis revealed that HR, RV FACn, and RV- SrL<sub>6seg</sub> had significant associations with the Ees, and the TAPSEn and RV-SrL<sub>3seg</sub> with Ees/Ea.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Decreased venous return and shortened relaxation time decreased the RV FAC, TAPSE, RV s', and RV strain, and might underestimate the RV function. Ees increased with the increase in HR, reflecting the myocardial force-frequency relation; as a result, RV-SrL<sub>6seg</sub> could be a useful tool for Ees estimation. Additionally, the RV-SrL<sub>3seg</sub> could detect RV performance, reflecting the balance between RV contractility and RV afterload.</AbstractText><CopyrightInformation>© 2022. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Yuchi</LastName><ForeName>Yunosuke</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Laboratory of Veterinary Internal Medicine, School of Veterinary Medicine, Faculty of Veterinary Science, Nippon Veterinary and Life Science University, 1-7-1 Kyonan-cho, Musashino-shi, Tokyo, 180-8602, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Suzuki</LastName><ForeName>Ryohei</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Laboratory of Veterinary Internal Medicine, School of Veterinary Medicine, Faculty of Veterinary Science, Nippon Veterinary and Life Science University, 1-7-1 Kyonan-cho, Musashino-shi, Tokyo, 180-8602, Japan. ryoheisuzuki0130@gmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kanno</LastName><ForeName>Haruka</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Laboratory of Veterinary Internal Medicine, School of Veterinary Medicine, Faculty of Veterinary Science, Nippon Veterinary and Life Science University, 1-7-1 Kyonan-cho, Musashino-shi, Tokyo, 180-8602, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Saito</LastName><ForeName>Takahiro</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Laboratory of Veterinary Internal Medicine, School of Veterinary Medicine, Faculty of Veterinary Science, Nippon Veterinary and Life Science University, 1-7-1 Kyonan-cho, Musashino-shi, Tokyo, 180-8602, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Teshima</LastName><ForeName>Takahiro</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Laboratory of Veterinary Internal Medicine, School of Veterinary Medicine, Faculty of Veterinary Science, Nippon Veterinary and Life Science University, 1-7-1 Kyonan-cho, Musashino-shi, Tokyo, 180-8602, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Matsumoto</LastName><ForeName>Hirotaka</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Laboratory of Veterinary Internal Medicine, School of Veterinary Medicine, Faculty of Veterinary Science, Nippon Veterinary and Life Science University, 1-7-1 Kyonan-cho, Musashino-shi, Tokyo, 180-8602, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Koyama</LastName><ForeName>Hidekazu</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Laboratory of Veterinary Internal Medicine, School of Veterinary Medicine, Faculty of Veterinary Science, Nippon Veterinary and Life Science University, 1-7-1 Kyonan-cho, Musashino-shi, Tokyo, 180-8602, Japan.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>05</Month><Day>06</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>BMC Vet Res</MedlineTA><NlmUniqueID>101249759</NlmUniqueID><ISSNLinking>1746-6148</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001835" MajorTopicYN="N">Body Weight</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006328" MajorTopicYN="N">Cardiac Catheterization</DescriptorName><QualifierName UI="Q000662" MajorTopicYN="N">veterinary</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004283" MajorTopicYN="Y">Dog Diseases</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004285" MajorTopicYN="N">Dogs</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004452" MajorTopicYN="N">Echocardiography</DescriptorName><QualifierName UI="Q000662" MajorTopicYN="N">veterinary</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006339" MajorTopicYN="N">Heart Rate</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013318" MajorTopicYN="N">Stroke Volume</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018497" MajorTopicYN="Y">Ventricular Dysfunction, Right</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000662" MajorTopicYN="N">veterinary</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016278" MajorTopicYN="N">Ventricular Function, Right</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Bowditch effect</Keyword><Keyword MajorTopicYN="N">Elastance</Keyword><Keyword MajorTopicYN="N">Force-frequency relation</Keyword><Keyword MajorTopicYN="N">Pressure–volume loop</Keyword><Keyword MajorTopicYN="N">Right ventricular contractility</Keyword><Keyword MajorTopicYN="N">Right ventricular performance</Keyword><Keyword MajorTopicYN="N">Strain</Keyword><Keyword MajorTopicYN="N">Strain rate</Keyword><Keyword MajorTopicYN="N">Two-dimensional speckle tracking echocardiography</Keyword></KeywordList><CoiStatement>The authors declare that they have no competing interests.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2021</Year><Month>7</Month><Day>23</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>4</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>5</Month><Day>7</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>5</Month><Day>8</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>5</Month><Day>11</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35524303</ArticleId><ArticleId IdType="pmc">PMC9074250</ArticleId><ArticleId IdType="doi">10.1186/s12917-022-03271-y</ArticleId><ArticleId IdType="pii">10.1186/s12917-022-03271-y</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Reinero C, Visser LC, Kellihan HB, Masseau I, Rozanski E, Clercx C, et al. ACVIM consensus statement guidelines for the diagnosis, classification, treatment, and monitoring of pulmonary hypertension in dogs. J Vet Intern Med. 2020;34:549–573. doi: 10.1111/jvim.15725.</Citation><ArticleIdList><ArticleId IdType="doi">10.1111/jvim.15725</ArticleId><ArticleId IdType="pmc">PMC7097566</ArticleId><ArticleId IdType="pubmed">32065428</ArticleId></ArticleIdList></Reference><Reference><Citation>Borgarelli M, Abbott J, Braz-Ruivo L, Chiavegato D, Crosara S, Lamb K, et al. Prevalence and Prognostic Importance of Pulmonary Hypertension in Dogs with Myxomatous Mitral Valve Disease. J Vet Intern Med. 2015;29:569–574. doi: 10.1111/jvim.12564.</Citation><ArticleIdList><ArticleId IdType="doi">10.1111/jvim.12564</ArticleId><ArticleId IdType="pmc">PMC4895522</ArticleId><ArticleId IdType="pubmed">25818210</ArticleId></ArticleIdList></Reference><Reference><Citation>Jaffey JA, Wiggen K, Leach SB, Masseau I, Girens RE, Reinero CR. Pulmonary hypertension secondary to respiratory disease and/or hypoxia in dogs: Clinical features, diagnostic testing and survival. Vet J. 2019;251:105347. doi: 10.1016/j.tvjl.2019.105347.</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.tvjl.2019.105347</ArticleId><ArticleId IdType="pubmed">31492386</ArticleId></ArticleIdList></Reference><Reference><Citation>Visser LC, Wood JE, Johnson LR. Survival characteristics and prognostic importance of echocardiographic measurements of right heart size and function in dogs with pulmonary hypertension. J Vet Intern Med. 2020;34:1379–1388. doi: 10.1111/jvim.15826.</Citation><ArticleIdList><ArticleId IdType="doi">10.1111/jvim.15826</ArticleId><ArticleId IdType="pmc">PMC7379050</ArticleId><ArticleId IdType="pubmed">32501601</ArticleId></ArticleIdList></Reference><Reference><Citation>Maughan WL, Shoukas AA, Sagawa K, Weisfeldt ML. Instantaneous pressure-volume relationship of the canine right ventricle. Circ Res. 1979;44:309–315. doi: 10.1161/01.RES.44.3.309.</Citation><ArticleIdList><ArticleId IdType="doi">10.1161/01.RES.44.3.309</ArticleId><ArticleId IdType="pubmed">761311</ArticleId></ArticleIdList></Reference><Reference><Citation>Vonk Noordegraaf A, Westerhof BE, Westerhof N. The Relationship Between the Right Ventricle and its Load in Pulmonary Hypertension. J Am Coll Cardiol. 2017;69:236–243. doi: 10.1016/j.jacc.2016.10.047.</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.jacc.2016.10.047</ArticleId><ArticleId IdType="pubmed">28081831</ArticleId></ArticleIdList></Reference><Reference><Citation>Vonk-Noordegraaf A, Haddad F, Chin KM, Forfia PR, Kawut SM, Lumens J, et al. Right heart adaptation to pulmonary arterial hypertension: Physiology and pathobiology. J Am Coll Cardiol. 2013;62(25 SUPPL.):22–33. doi: 10.1016/j.jacc.2013.10.027.</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.jacc.2013.10.027</ArticleId><ArticleId IdType="pubmed">24355638</ArticleId></ArticleIdList></Reference><Reference><Citation>Lahm T, Douglas IS, Archer SL, Bogaard HJ, Chesler NC, Haddad F, et al. Assessment of right ventricular function in the research setting: Knowledge gaps and pathways forward an official American thoracic society research statement. Am J Respir Crit Care Med. 2018;198:e15–43. doi: 10.1164/rccm.201806-1160ST.</Citation><ArticleIdList><ArticleId IdType="doi">10.1164/rccm.201806-1160ST</ArticleId><ArticleId IdType="pmc">PMC6835085</ArticleId><ArticleId IdType="pubmed">30109950</ArticleId></ArticleIdList></Reference><Reference><Citation>Visser LC, Scansen BA, Brown NV, Schober KE, Bonagura JD. Echocardiographic assessment of right ventricular systolic function in conscious healthy dogs following a single dose of pimobendan versus atenolol. J Vet Cardiol. 2015;17:161–172. doi: 10.1016/j.jvc.2015.04.001.</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.jvc.2015.04.001</ArticleId><ArticleId IdType="pubmed">26213150</ArticleId></ArticleIdList></Reference><Reference><Citation>Rudski LG, Lai WW, Afilalo J, Hua L, Handschumacher MD, Chandrasekaran K, et al. Guidelines for the Echocardiographic Assessment of the Right Heart in Adults: A Report from the American Society of Echocardiography. Endorsed by the European Association of Echocardiography, a registered branch of the European Society of Cardiology. J Am Soc Echocardiogr. 2010;23:685–713. doi: 10.1016/j.echo.2010.05.010.</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.echo.2010.05.010</ArticleId><ArticleId IdType="pubmed">20620859</ArticleId></ArticleIdList></Reference><Reference><Citation>Vezzosi T, Domenech O, Costa G, Marchesotti F, Venco L, Zini E, et al. Echocardiographic evaluation of the right ventricular dimension and systolic function in dogs with pulmonary hypertension. J Vet Intern Med. 2018;32:1541–1548. doi: 10.1111/jvim.15253.</Citation><ArticleIdList><ArticleId IdType="doi">10.1111/jvim.15253</ArticleId><ArticleId IdType="pmc">PMC6189358</ArticleId><ArticleId IdType="pubmed">30216561</ArticleId></ArticleIdList></Reference><Reference><Citation>Amundsen BH, Helle-Valle T, Edvardsen T, Torp H, Crosby J, Lyseggen E, et al. Noninvasive myocardial strain measurement by speckle tracking echocardiography: Validation against sonomicrometry and tagged magnetic resonance imaging. J Am Coll Cardiol. 2006;47:789–793. doi: 10.1016/j.jacc.2005.10.040.</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.jacc.2005.10.040</ArticleId><ArticleId IdType="pubmed">16487846</ArticleId></ArticleIdList></Reference><Reference><Citation>Johnson LR, Boon J, Orton EC. Clinical characteristics of 53 dogs with Doppler-derived evidence of pulmonary hypertension: 1992–1996. J Vet Intern Med. 1999;13:440–447.</Citation><ArticleIdList><ArticleId IdType="pubmed">10499728</ArticleId></ArticleIdList></Reference><Reference><Citation>Hsiao S-H, Lin S-K, Wang W-C, Yang S-H, Gin P-L, Liu C-P. Severe tricuspid regurgitation shows significant impact in the relationship among peak systolic tricuspid annular velocity, tricuspid annular plane systolic excursion, and right ventricular ejection fraction. J Am Soc Echocardiogr. 2006;19:902–910. doi: 10.1016/j.echo.2006.01.014.</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.echo.2006.01.014</ArticleId><ArticleId IdType="pubmed">16825000</ArticleId></ArticleIdList></Reference><Reference><Citation>Morita T, Nakamura K, Osuga T, Yokoyama N, Morishita K, Sasaki N, et al. Changes in right ventricular function assessed by echocardiography in dog models of mild RV pressure overload. Echocardiography. 2017;34:1040–1049. doi: 10.1111/echo.13560.</Citation><ArticleIdList><ArticleId IdType="doi">10.1111/echo.13560</ArticleId><ArticleId IdType="pubmed">28493465</ArticleId></ArticleIdList></Reference><Reference><Citation>Morita T, Nakamura K, Osuga T, Yokoyama N, Morishita K, Sasaki N, et al. Effect of acute volume overload on echocardiographic indices of right ventricular function and dyssynchrony assessed by use of speckle tracking echocardiography in healthy dogs. Am J Vet Res. 2019;80:51–60. doi: 10.2460/ajvr.80.1.51.</Citation><ArticleIdList><ArticleId IdType="doi">10.2460/ajvr.80.1.51</ArticleId><ArticleId IdType="pubmed">30605034</ArticleId></ArticleIdList></Reference><Reference><Citation>Chetboul V, Damoiseaux C, Lefebvre HP, Concordet D, Desquilbet L, Gouni V, et al. Quantitative assessment of systolic and diastolic right ventricular function by echocardiography and speckle-tracking imaging: A prospective study in 104 dogs. J Vet Sci. 2018;19:683–692. doi: 10.4142/jvs.2018.19.5.683.</Citation><ArticleIdList><ArticleId IdType="doi">10.4142/jvs.2018.19.5.683</ArticleId><ArticleId IdType="pmc">PMC6167344</ArticleId><ArticleId IdType="pubmed">30041288</ArticleId></ArticleIdList></Reference><Reference><Citation>Wu CC, Takeuchi M. Echocardiographic assessment of right ventricular systolic function. Cardiovascular Diagnosis and Therapy. 2018;8:70–79. doi: 10.21037/cdt.2017.06.05.</Citation><ArticleIdList><ArticleId IdType="doi">10.21037/cdt.2017.06.05</ArticleId><ArticleId IdType="pmc">PMC5835653</ArticleId><ArticleId IdType="pubmed">29541612</ArticleId></ArticleIdList></Reference><Reference><Citation>Janssen PML, Periasamy M. Determinants of frequency-dependent contraction and relaxation of mammalian myocardium. J Mol Cell Cardiol. 2007;43:523–531. doi: 10.1016/j.yjmcc.2007.08.012.</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.yjmcc.2007.08.012</ArticleId><ArticleId IdType="pmc">PMC2093987</ArticleId><ArticleId IdType="pubmed">17919652</ArticleId></ArticleIdList></Reference><Reference><Citation>Landis JR, Koch GG. The Measurement of Observer Agreement for Categorical Data. Biometrics. 1977;33:159. doi: 10.2307/2529310.</Citation><ArticleIdList><ArticleId IdType="doi">10.2307/2529310</ArticleId><ArticleId IdType="pubmed">843571</ArticleId></ArticleIdList></Reference><Reference><Citation>Chetboul V, Serres F, Gouni V, Tissier R, Pouchelon J. Noninvasive assessment of systolic left ventricular torsion by 2-dimensional speckle tracking imaging in the awake dog: repeatability, reproducibility, and comparison with tissue Doppler imaging variables. J Vet Intern Med. 2008;22:342–350. doi: 10.1111/j.1939-1676.2007.0037.x.</Citation><ArticleIdList><ArticleId IdType="doi">10.1111/j.1939-1676.2007.0037.x</ArticleId><ArticleId IdType="pubmed">18312281</ArticleId></ArticleIdList></Reference><Reference><Citation>Weidemann F, Jamal F, Sutherland GR, Claus P, Kowalski M, Hatle L, et al. Myocardial function defined by strain rate and strain during alterations in inotropic states and heart rate. Am J Physiol Circ Physiol. 2002;283:H792–H799. doi: 10.1152/ajpheart.00025.2002.</Citation><ArticleIdList><ArticleId IdType="doi">10.1152/ajpheart.00025.2002</ArticleId><ArticleId IdType="pubmed">12124229</ArticleId></ArticleIdList></Reference><Reference><Citation>Donald DE, Essex HE. Pressure Studies After Inactivation of the Major Portion of the Canine Right Ventricle. Am J Physiol. 1954;176:155–161. doi: 10.1152/ajplegacy.1953.176.1.155.</Citation><ArticleIdList><ArticleId IdType="doi">10.1152/ajplegacy.1953.176.1.155</ArticleId><ArticleId IdType="pubmed">13124512</ArticleId></ArticleIdList></Reference><Reference><Citation>Starr I, Jeffers WA, Meade RH. The absence of conspicuous increments of venous pressure after severe damage to the right ventricle of the dog, with a discussion of the relation between clinical congestive failure and heart disease. Am Heart J. 1943;26:291–301. doi: 10.1016/S0002-8703(43)90325-4.</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/S0002-8703(43)90325-4</ArticleId></ArticleIdList></Reference><Reference><Citation>Sunagawa K, Maughan WL, Sagawa K. Optimal arterial resistance for the maximal stroke work studied in isolated canine left ventricle. Circ Res. 1985;56:586–595. doi: 10.1161/01.RES.56.4.586.</Citation><ArticleIdList><ArticleId IdType="doi">10.1161/01.RES.56.4.586</ArticleId><ArticleId IdType="pubmed">3978773</ArticleId></ArticleIdList></Reference><Reference><Citation>Ohte N, Cheng CP, Little WC. Tachycardia exacerbates abnormal left ventricular-arterial coupling in heart failure. Heart Vessels. 2003;18:136–141. doi: 10.1007/s00380-003-0697-9.</Citation><ArticleIdList><ArticleId IdType="doi">10.1007/s00380-003-0697-9</ArticleId><ArticleId IdType="pubmed">12955429</ArticleId></ArticleIdList></Reference><Reference><Citation>McConnell MV, Solomon SD, Rayan ME, Come PC, Goldhaber SZ, Lee RT. Regional Right Ventricular Dysfunction Detected by Echocardiography in Acute Pulmonary Embolism. Am J Cardiol. 1996;78:469–473. doi: 10.1016/S0002-9149(96)00339-6.</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/S0002-9149(96)00339-6</ArticleId><ArticleId IdType="pubmed">8752195</ArticleId></ArticleIdList></Reference><Reference><Citation>Wright L, Dwyer N, Power J, Kritharides L, Celermajer D, Marwick TH. Right Ventricular Systolic Function Responses to Acute and Chronic Pulmonary Hypertension: Assessment with Myocardial Deformation. J Am Soc Echocardiogr. 2016;29:259–266. doi: 10.1016/j.echo.2015.11.010.</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.echo.2015.11.010</ArticleId><ArticleId IdType="pubmed">26944627</ArticleId></ArticleIdList></Reference><Reference><Citation>Priebe HJ. Differential effects of isoflurane on regional right and left ventricular performances, and on coronary, systemic, and pulmonary hemodynamics in the dog. Anesthesiology. 1987;66:262–272. doi: 10.1097/00000542-198703000-00002.</Citation><ArticleIdList><ArticleId IdType="doi">10.1097/00000542-198703000-00002</ArticleId><ArticleId IdType="pubmed">3826683</ArticleId></ArticleIdList></Reference><Reference><Citation>Kerbaul F, Rondelet B, Motte S, Fesler P, Hubloue I, Ewalenko P, et al. Isoflurane and desflurane impair right ventricular-pulmonary arterial coupling in dogs. Anesthesiol. 2004;101:1357–1362. doi: 10.1097/00000542-200412000-00016.</Citation><ArticleIdList><ArticleId IdType="doi">10.1097/00000542-200412000-00016</ArticleId><ArticleId IdType="pubmed">15564943</ArticleId></ArticleIdList></Reference><Reference><Citation>Sanchez AA, Levy PT, Sekarski TJ, Hamvas A, Holland MR, Singh GK. Effects of Frame Rate on Two-Dimensional Speckle Tracking-Derived Measurements of Myocardial Deformation in Premature Infants. Echocardiography. 2015;32:839–847. doi: 10.1111/echo.12716.</Citation><ArticleIdList><ArticleId IdType="doi">10.1111/echo.12716</ArticleId><ArticleId IdType="pmc">PMC4324397</ArticleId><ArticleId IdType="pubmed">25109389</ArticleId></ArticleIdList></Reference><Reference><Citation>Suzuki R, Matsumoto H, Teshima T, Koyama H. Influence of heart rate on myocardial function using two-dimensional speckle-tracking echocardiography in healthy dogs. J Vet Cardiol. 2013;15:139–146. doi: 10.1016/j.jvc.2012.12.004.</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.jvc.2012.12.004</ArticleId><ArticleId IdType="pubmed">23643819</ArticleId></ArticleIdList></Reference><Reference><Citation>Vitarelli A, Terzano C. Do we have two hearts? New insights in right ventricular function supported by myocardial imaging echocardiography. Hear Fail Rev. 2010;15:39–61. doi: 10.1007/s10741-009-9154-x.</Citation><ArticleIdList><ArticleId IdType="doi">10.1007/s10741-009-9154-x</ArticleId><ArticleId IdType="pubmed">19866357</ArticleId></ArticleIdList></Reference><Reference><Citation>Caivano D, Rishniw M, Birettoni F, Petrescu VF, Porciello F. Transverse right ventricle strain and strain rate assessed by 2-dimensional speckle tracking echocardiography in dogs with pulmonary hypertension. Vet Sci. 2020;7:1–10.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC7157588</ArticleId><ArticleId IdType="pubmed">32046130</ArticleId></ArticleIdList></Reference><Reference><Citation>Yuchi Y, Suzuki R, Teshima T, Matsumoto H, Koyama H. Investigation of the influence of manual ventilation-controlled respiration on right ventricular pressure-volume loops and echocardiographic variables in healthy anesthetized dogs. Am J Vet Res. 2021;82:865–871. doi: 10.2460/ajvr.82.11.865.</Citation><ArticleIdList><ArticleId IdType="doi">10.2460/ajvr.82.11.865</ArticleId><ArticleId IdType="pubmed">34669489</ArticleId></ArticleIdList></Reference><Reference><Citation>Brimioulle S, Wauthy P, Ewalenko P, Rondelet B, Vermeulen F, Kerbaul F, et al. Single-beat estimation of right ventricular end-systolic pressure-volume relationship. Am J Physiol Circ Physiol. 2003;284:H1625–H1630. doi: 10.1152/ajpheart.01023.2002.</Citation><ArticleIdList><ArticleId IdType="doi">10.1152/ajpheart.01023.2002</ArticleId><ArticleId IdType="pubmed">12531727</ArticleId></ArticleIdList></Reference><Reference><Citation>Visser LC, Scansen BA, Schober KE, Bonagura JD. Echocardiographic assessment of right ventricular systolic function in conscious healthy dogs: Repeatability and reference intervals. J Vet Cardiol. 2015;17:83–96. doi: 10.1016/j.jvc.2014.10.003.</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.jvc.2014.10.003</ArticleId><ArticleId IdType="pubmed">25547662</ArticleId></ArticleIdList></Reference><Reference><Citation>Gentile-Solomon JM, Abbott JA. Conventional echocardiographic assessment of the canine right heart: reference intervals and repeatability. J Vet Cardiol. 2016;18:234–247. doi: 10.1016/j.jvc.2016.05.002.</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.jvc.2016.05.002</ArticleId><ArticleId IdType="pubmed">27453517</ArticleId></ArticleIdList></Reference><Reference><Citation>Yuchi Y, Suzuki R, Teshima T, Matsumoto H, Koyama H. Utility of tricuspid annular plane systolic excursion normalized by right ventricular size indices in dogs with postcapillary pulmonary hypertension. J Vet Intern Med. 2021;35:107–119. doi: 10.1111/jvim.15984.</Citation><ArticleIdList><ArticleId IdType="doi">10.1111/jvim.15984</ArticleId><ArticleId IdType="pmc">PMC7848373</ArticleId><ArticleId IdType="pubmed">33277735</ArticleId></ArticleIdList></Reference><Reference><Citation>Visser LC, Sintov DJ, Oldach MS. Evaluation of tricuspid annular plane systolic excursion measured by two-dimensional echocardiography in healthy dogs: repeatability, reference intervals, and comparison with M-mode assessment. J Vet Cardiol. 2018;20:165–174. doi: 10.1016/j.jvc.2018.04.002.</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.jvc.2018.04.002</ArticleId><ArticleId IdType="pubmed">29724583</ArticleId></ArticleIdList></Reference><Reference><Citation>Cornell CC, Kittleson MD, Della Torre P, Häggström J, Lombard CW, Pedersen HD, et al. Allometric scaling of M-mode cardiac measurements in normal adult dogs. J Vet Intern Med. 2004;18:311–321. doi: 10.1111/j.1939-1676.2004.tb02551.x.</Citation><ArticleIdList><ArticleId IdType="doi">10.1111/j.1939-1676.2004.tb02551.x</ArticleId><ArticleId IdType="pubmed">15188817</ArticleId></ArticleIdList></Reference><Reference><Citation>Suzuki R, Matsumoto H, Teshima T, Koyama H. Effect of age on myocardial function assessed by two-dimensional speckle-tracking echocardiography in healthy beagle dogs. J Vet Cardiol. 2013;15:243–252. doi: 10.1016/j.jvc.2013.07.001.</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.jvc.2013.07.001</ArticleId><ArticleId IdType="pubmed">24054982</ArticleId></ArticleIdList></Reference><Reference><Citation>Bland JM, Altman DG. Statistics Notes: Measurement error proportional to the mean. BMJ. 1996;313:106–106. doi: 10.1136/bmj.313.7049.106.</Citation><ArticleIdList><ArticleId IdType="doi">10.1136/bmj.313.7049.106</ArticleId><ArticleId IdType="pmc">PMC2351517</ArticleId><ArticleId IdType="pubmed">8688716</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedBookArticle><BookDocument><PMID Version="1">32491430</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK557498</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-19397">Chiari II Malformation | Chiari II malformation (CM-II), commonly known as Arnold-Chiari malformation, is a relatively common congenital malformation characterized by beaked midbrain, downward displacement of the tonsils, and cerebellar vermis, and spinal myelomeningocele. This malformation is frequently misunderstood as a more severe version of Chiari I malformation (CM-I). However, these are two distinct diseases with overlapping imaging findings. Interestingly, most patients who have myelomeningocele also have CM-II and are typically associated with hydrocephalus. There are many additional findings associated with CM-II, including cerebellar dysplasia, elongation of the lower pons and the medulla, and the fourth ventricle displacing into the cervical canal. The diagnosis is primarily based on the patient’s neuroanatomy on MRI. The treatment is typically centered upon surgical interventions. Prognosis is dependent on the extent of the malformations and the symptoms of the patient. |
2,329,981 | Subventricular zone adult mouse neural stem cells require insulin receptor for self-renewal. | The insulin receptor (INSR) is an evolutionarily conserved signaling protein that regulates development and cellular metabolism. INSR signaling promotes neurogenesis in Drosophila; however, a specific role for the INSR in maintaining adult neural stem cells (NSCs) in mammals has not been investigated. We show that conditionally deleting the Insr gene in adult mouse NSCs reduces subventricular zone NSCs by ∼70% accompanied by a corresponding increase in progenitors. Insr deletion also produced hyposmia caused by aberrant olfactory bulb neurogenesis. Interestingly, hippocampal neurogenesis and hippocampal-dependent behaviors were unperturbed. Highly aggressive proneural and mesenchymal glioblastomas had high INSR/insulin-like growth factor (IGF) pathway gene expression, and isolated glioma stem cells had an aberrantly high ratio of INSR:IGF type 1 receptor. Moreover, INSR knockdown inhibited GBM tumorsphere growth. Altogether, these data demonstrate that the INSR is essential for a subset of normal NSCs, as well as for brain tumor stem cell self-renewal. |
2,329,982 | Cerebrospinal fluid-based boron delivery system may help increase the uptake boron for boron neutron capture therapy in veterinary medicine: A preliminary study with normal rat brain cells. | Boron neutron capture therapy (BNCT) is a non-invasive type of radiation therapy developed for humans and translated to veterinary medicine. However, clinical trials on BNCT for patients with brain tumors are on-going. To improve the therapeutic efficacy of BNCT for brain tumors, we developed a boron delivery system that involves the cerebrospinal fluid (CSF), in contrast to the conventional method that involves intravenous (IV) administration. This study aimed to investigate the time-concentration profile of boron in the CSF as well as the uptake rate of boron by the brain cells after administering L-p‑boronophenylalanine (BPA) into the lateral ventricle of normal rats. Brain cell uptake rates were compared between the CSF-based and IV administration methods. The CSF-based and IV administration methods achieved comparable brain cell uptake levels; however, the former method involved lower BPA doses than the latter method. These findings suggest that the CSF method may reduce the economic and physical burdens associated with this treatment in brain tumor patients. Future studies should validate these findings in rat models of brain tumors. |
2,329,983 | Review of Cerebrospinal Fluid Physiology and Dynamics: A Call for Medical Education Reform. | The flow of cerebrospinal fluid (CSF) has been described as a unidirectional system with the choroid plexus serving as the primary secretor of CSF and the arachnoid granulations as primary reabsorption site. This theory of neurosurgical forefathers has been universally adopted and taught as dogma. Many neuroscientists have found difficulty reconciling this theory with common pathologies, and recent studies have found that this "classic" hypothesis may not represent the full picture.</AbstractText>To review modern CSF dynamic theories and to call for medical education reform.</AbstractText>We reviewed the literature from January 1990 to December 2020. We searched the PubMed database using key terms "cerebrospinal fluid circulation," "cerebrospinal fluid dynamics," "cerebrospinal fluid physiology," "glymphatic system," and "glymphatic pathway." We selected articles with a primary aim to discuss either CSF dynamics and/or the glymphatic system.</AbstractText>The Bulat-Klarica-Orešković hypothesis purports that CSF is secreted and reabsorbed throughout the craniospinal axis. CSF demonstrates similar physiology to that of water elsewhere in the body. CSF "circulates" throughout the subarachnoid space in a pulsatile to-and-fro fashion. Osmolarity plays a critical role in CSF dynamics. Aquaporin-4 and the glymphatic system contribute to CSF volume and flow by establishing osmolarity gradients and facilitating CSF movement. Multiple studies demonstrate that the choroid plexus does not play any significant role in CSF circulation.</AbstractText>We have highlighted major studies to illustrate modern principles of CSF dynamics. Despite these, the medical education system has been slow to reform curricula and update learning resources.</AbstractText>Copyright © Congress of Neurological Surgeons 2022. All rights reserved.</CopyrightInformation> |
2,329,984 | False-positive results in transcranial motor evoked potentials for outcome prognostication during surgery for supratentorial lesions. | During monitoring of motor evoked potentials (MEP) elicited by transcranial electrical stimulation (TES) for prognostication of postoperative motor deficit, significant MEP changes without postoperative deterioration of motor function represent false-positive results. We aimed to investigate this phenomenon in a large series of patients who underwent resection of supratentorial lesions. TES was applied in 264 patients during resection of motor-eloquent supratentorial lesions. MEP were recorded bilaterally from arm, leg, and/ or facial muscles. The threshold criterion was applied assessing percentage increase in threshold level, which was considered significant if being > 20% higher on affected side than on the unaffected side. Subcortical stimulation was additionally applied to estimate the distance to corticospinal tract. Motor function was evaluated at 24 h after surgery and at 3-month follow-up. Patients with false-positive results were analyzed regarding tumor location, tumor volume, and characteristics of the monitoring. MEP were recorded from 399 muscles (264 arm muscles, 75 leg muscles, and 60 facial muscles). Motor function was unchanged postoperatively in 359 muscles in 228 patients. Among these cases, the threshold level did not change significantly in 354 muscles in 224 patients, while it increased significantly in the remaining 5 muscles in 4 patients (abductor pollicis brevis in all four patients and orbicularis oris in one patient), leading to a false-positive rate of 1.1%. Tumor volume, opening the ventricle, and negative subcortical stimulation did not significantly correlate with false-positive results, while the tumor location in the parietal lobe dorsal to the postcentral gyrus correlated significantly (p = 0.012, odds ratio 11.2, 95% CI 1.8 to 69.8). False-negative results took place in 1.1% of cases in a large series of TES-MEP monitoring using the threshold criterion. Tumor location in the parietal lobe dorsal to the postcentral gyrus was the only predictor of false-positive results. |
2,329,985 | Cardiac Magnetic Resonance to Predict Coronary Artery Compression in Transcatheter Pulmonary Valve Implantation Into Conduits.<Pagination><StartPage>979</StartPage><EndPage>988</EndPage><MedlinePgn>979-988</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.jcin.2022.02.047</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S1936-8798(22)00544-1</ELocationID><Abstract><AbstractText Label="OBJECTIVES">The aim of this study was to evaluate the accuracy of cardiac magnetic resonance (CMR) in predicting coronary artery (CA) compression during transcatheter pulmonary valve implantation (TPVi).</AbstractText><AbstractText Label="BACKGROUND">TPVi is a widely available option to treat dysfunctional right ventricle (RV)-to-pulmonary artery (PA) conduits, but CA compression is an absolute contraindication. CMR can evaluate coronary anatomy, but its utility in predicting CA compression is not well established.</AbstractText><AbstractText Label="METHODS">After Institutional Review Board approval was obtained, all patients at 9 centers with attempted TPVi in RV-PA conduits and recent CMR (≤12 months) were analyzed. A core laboratory reviewed all CMR studies for the shortest orthogonal distance from a CA to the conduit, the shortest distance from a CA to the most stenotic area of the conduit, and subjective assessment of CA compression risk.</AbstractText><AbstractText Label="RESULTS">Among 231 patients, TPVi was successful in 198 (86%); in 24 (10%), balloon testing precluded implantation (documented CA compression or high risk). Distance to the RV-PA conduit ≤2.1 mm (area under the curve [AUC]: 0.70) and distance to most stenotic area ≤13.1 mm (AUC: 0.69) predicted CA compression. Subjective assessment had the highest AUC (0.78), with 96% negative predictive value. Both distances and qualitative assessment remained independently associated with CA compression when controlling for abnormal coronary anatomy or degree of conduit calcification.</AbstractText><AbstractText Label="CONCLUSIONS">CMR can help predict the risk for CA compression during TPVi in RV-PA conduits but cannot completely exclude CA compression. CMR may assist in patient selection and counseling families prior to TPVi, although balloon testing remains essential.</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>Romans</LastName><ForeName>Ryan A</ForeName><Initials>RA</Initials><AffiliationInfo><Affiliation>Ward Family Heart Center, Children's Mercy Kansas City, Kansas City, Missouri, USA. Electronic address: raromans@cmh.edu.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lu</LastName><ForeName>Jimmy C</ForeName><Initials>JC</Initials><AffiliationInfo><Affiliation>Division of Cardiology, Department of Pediatrics, C.S. Mott Children's Hospital and University of Michigan Congenital Heart Center, Ann Arbor, Michigan, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Balasubramanian</LastName><ForeName>Sowmya</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Division of Cardiology, Department of Pediatrics, C.S. Mott Children's Hospital and University of Michigan Congenital Heart Center, Ann Arbor, Michigan, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Whiteside</LastName><ForeName>Wendy</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Division of Cardiology, Department of Pediatrics, C.S. Mott Children's Hospital and University of Michigan Congenital Heart Center, Ann Arbor, Michigan, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yu</LastName><ForeName>Sunkyung</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Division of Cardiology, Department of Pediatrics, C.S. Mott Children's Hospital and University of Michigan Congenital Heart Center, Ann Arbor, Michigan, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Aldoss</LastName><ForeName>Osamah T</ForeName><Initials>OT</Initials><AffiliationInfo><Affiliation>Division of Pediatric Cardiology, University of Iowa Hospitals and Clinics, Iowa City, Iowa, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Armstrong</LastName><ForeName>Aimee K</ForeName><Initials>AK</Initials><AffiliationInfo><Affiliation>The Heart Center, Nationwide Children's Hospital, Columbus, Ohio, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Boe</LastName><ForeName>Brian A</ForeName><Initials>BA</Initials><AffiliationInfo><Affiliation>The Heart Center, Nationwide Children's Hospital, Columbus, Ohio, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Balzer</LastName><ForeName>David T</ForeName><Initials>DT</Initials><AffiliationInfo><Affiliation>Division of Cardiology, Department of Pediatrics, St. Louis Children's Hospital, St. Louis, Missouri, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Christensen</LastName><ForeName>Jason T</ForeName><Initials>JT</Initials><AffiliationInfo><Affiliation>Division of Cardiology, Department of Pediatrics, Children's Hospital and Medical Center, Omaha, Nebraska, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jones</LastName><ForeName>Thomas K</ForeName><Initials>TK</Initials><AffiliationInfo><Affiliation>Division of Cardiology, Department of Pediatrics, Seattle Children's Hospital, Seattle, Washington, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Keeshan</LastName><ForeName>Britton</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Division of Cardiology, Department of Pediatrics, Yale School of Medicine, New Haven, Connecticut, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>McLennan</LastName><ForeName>Daniel</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Division of Cardiology, Herma Heart Institute at Children's Wisconsin, Milwaukee, Wisconsin, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nicholson</LastName><ForeName>George T</ForeName><Initials>GT</Initials><AffiliationInfo><Affiliation>Division of Cardiology, Department of Pediatrics, Monroe Carrell Jr. Children's Hospital at Vanderbilt, Nashville, Tennessee, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Patel</LastName><ForeName>Neil</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Children's Hospital Los Angeles and The Heart Institute, Los Angeles, California, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Salavitabar</LastName><ForeName>Arash</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>The Heart Center, Nationwide Children's Hospital, Columbus, Ohio, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shahanavaz</LastName><ForeName>Shabana</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Division of Cardiology, Department of Pediatrics, Cincinnati Children's Hospital, Cincinnati, Ohio, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sullivan</LastName><ForeName>Patrick M</ForeName><Initials>PM</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Children's Hospital Los Angeles and The Heart Institute, Los Angeles, California, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Turner</LastName><ForeName>Mariel E</ForeName><Initials>ME</Initials><AffiliationInfo><Affiliation>Department of Pediatrics, Division of Cardiology, Columbia University Irving Medical Center, New York, New York, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zampi</LastName><ForeName>Jeffrey D</ForeName><Initials>JD</Initials><AffiliationInfo><Affiliation>Division of Cardiology, Department of Pediatrics, C.S. Mott Children's Hospital and University of Michigan Congenital Heart Center, Ann Arbor, Michigan, 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>JACC Cardiovasc Interv</MedlineTA><NlmUniqueID>101467004</NlmUniqueID><ISSNLinking>1936-8798</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>JACC Cardiovasc Interv. 2022 May 9;15(9):989-991</RefSource><PMID Version="1">35512923</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D006328" MajorTopicYN="N">Cardiac Catheterization</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003331" MajorTopicYN="N">Coronary Vessels</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019918" MajorTopicYN="Y">Heart Valve Prosthesis Implantation</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009682" MajorTopicYN="N">Magnetic Resonance Spectroscopy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011651" MajorTopicYN="N">Pulmonary Artery</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011664" MajorTopicYN="Y">Pulmonary Valve</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">cardiac magnetic resonance</Keyword><Keyword MajorTopicYN="N">congenital heart disease</Keyword><Keyword MajorTopicYN="N">transcatheter pulmonary valve implantation</Keyword></KeywordList><CoiStatement>Funding Support and Author Disclosures This research was supported by funding from the Percy J. Murphy and Mary C. Murphy Endowed Children’s Research Fund. This grant does not have any relationship with industry. The 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>2021</Year><Month>6</Month><Day>21</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>2</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>2</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>5</Month><Day>5</Day><Hour>21</Hour><Minute>4</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>5</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>5</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35512922</ArticleId><ArticleId IdType="doi">10.1016/j.jcin.2022.02.047</ArticleId><ArticleId IdType="pii">S1936-8798(22)00544-1</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35512837</PMID><DateRevised><Year>2022</Year><Month>05</Month><Day>05</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1438-8782</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>May</Month><Day>05</Day></PubDate></JournalIssue><Title>Ultraschall in der Medizin (Stuttgart, Germany : 1980)</Title><ISOAbbreviation>Ultraschall Med</ISOAbbreviation></Journal>Aorto-Left Ventricular Tunnel - Prenatal Diagnosis and Outcome. | The aim of this study was to evaluate the accuracy of cardiac magnetic resonance (CMR) in predicting coronary artery (CA) compression during transcatheter pulmonary valve implantation (TPVi).</AbstractText>TPVi is a widely available option to treat dysfunctional right ventricle (RV)-to-pulmonary artery (PA) conduits, but CA compression is an absolute contraindication. CMR can evaluate coronary anatomy, but its utility in predicting CA compression is not well established.</AbstractText>After Institutional Review Board approval was obtained, all patients at 9 centers with attempted TPVi in RV-PA conduits and recent CMR (≤12 months) were analyzed. A core laboratory reviewed all CMR studies for the shortest orthogonal distance from a CA to the conduit, the shortest distance from a CA to the most stenotic area of the conduit, and subjective assessment of CA compression risk.</AbstractText>Among 231 patients, TPVi was successful in 198 (86%); in 24 (10%), balloon testing precluded implantation (documented CA compression or high risk). Distance to the RV-PA conduit ≤2.1 mm (area under the curve [AUC]: 0.70) and distance to most stenotic area ≤13.1 mm (AUC: 0.69) predicted CA compression. Subjective assessment had the highest AUC (0.78), with 96% negative predictive value. Both distances and qualitative assessment remained independently associated with CA compression when controlling for abnormal coronary anatomy or degree of conduit calcification.</AbstractText>CMR can help predict the risk for CA compression during TPVi in RV-PA conduits but cannot completely exclude CA compression. CMR may assist in patient selection and counseling families prior to TPVi, although balloon testing remains essential.</AbstractText>Copyright © 2022 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.</CopyrightInformation> |
2,329,986 | [Gastrointestinal stromal tumor with right ventricle metastases: report of a case]. | 胃肠道间质瘤（gastrointestinal stromal tumors）最常发生部位为胃、小肠、结直肠及食管，其转移瘤多见于肝脏、腹膜。检索到国内外报道胃肠道间质瘤转移至心脏的临床案例仅有4例，临床极为罕见。本文报道1例胃肠道间质瘤心脏转移病例。. |
2,329,987 | Hemodynamic Response to Fluid Boluses in Patients with Single-Ventricle Parallel Circulation. | The purpose of this study is to assess the effect of fluid bolus in response to a hypotensive episode by evaluating high-fidelity hemodynamic data obtained from children with single-ventricle anatomy and parallel circulation. Single center, retrospective analysis of hemodynamic and oximetric data after fluid bolus administrations within the first 2 weeks post-surgery. A baseline (- 60 to - 10 min), hypotensive episode (- 10 to 0 min), and response interval (0 to 60 min) were defined to quantify the dynamics of vital signs. The responses assessed include heart rate, blood pressure, oxygen saturation, oxygen extraction ratios, and pulmonary-to-systemic flow ratios. Mixed effects models were used to account for the repeated measures over the response interval. The analysis included 67 fluid boluses. There is a decrease in heart rate and an increase in blood pressure during the response in comparison to the hypotensive time. These vitals rapidly return to the baseline values. The boluses induced a significant decrease in renal and cerebral oxygen extraction ratios, with no significant change in arterial oxygen saturation or pulmonary-to-systemic flow ratio. The type of bolus (normal saline versus albumin) did not affect the response in blood pressure. However, in comparison with albumin, normal saline had a more favorable effect on the renal and cerebral oxygen extraction ratios. This study demonstrates that fluid boluses are an effective rescue medication for hypotensive episodes in children with parallel circulation by improving hemodynamics, as well as markers of oxygen delivery. The type of bolus (normal saline versus albumin) did not affect the blood pressure response. However, normal saline had a more pronounced effect on the renal and cerebral oxygen extraction ratios than albumin. |
2,329,988 | Surgical resection of giant extrasellar thyrotropinoma: Use of orbitozygomatic and endoscopic endonasal approach. | Thyrotropinomas (TSHoma) are rare pituitary adenomas.</AbstractText>A 34-year-old female presented with mild bitemporal field defect in third trimester with intact pituitary function. MRI demonstrated an enhancing lesion from the posterior planum to suprasellar, interpeduncular and prepontine cisterns with chiasmal compression and right fetal posterior communicating artery encasement. With no sellar expansion, the differentials included meningioma or craniopharyngioma. She underwent a postpartum expanded endoscopic endonasal transtuberculum transchiasmatic sulcus approach [Video 1]. The lesion was debulked in the chiasmatic cistern to decompress the chiasm with preservation of superior hypophyseal perforators. Pituitary transposition and midclival approach to access the retrosellar component was not undertaken pending formal histology as the lesion encased the perforators and was atypical for the outlined differentials. In addition, the diaphragm was intact. Postoperatively, visual field normalized and the patient developed mild diabetes insipidus. Following the diagnosis of TSHoma (with an abnormal thyroid function test [TFT]) and due to patient preference and slightly increased risk of CSF leak with revisional endoscopic procedure, she underwent an orbitozygomatic craniotomy (pretemporal and transsylvian approach) without tentorial division to resect the disease in the interpeduncular and prepontine cisterns [Video 1]. The anatomical triangles and tumor characteristics facilitated this. A residual cuff was left along the base of the stalk and the floor of the third ventricle to preserve the superior hypophyseal and thalamoperforators. Postoperatively, the patient had normal TFT without any neurological deficit.</AbstractText>Operative treatment strategy is presented for a rare large challenging multicompartmental extrasellar TSHoma using endoscopic endonasal and open skull base approaches.</AbstractText>Copyright: © 2022 Surgical Neurology International.</CopyrightInformation> |
2,329,989 | Favorable management of symptomatic cerebellar hemangioblastoma presenting with obstructive hydrocephalus during pregnancy: A case report and literature review. | Cerebellar hemangioblastoma is a highly vascular benign tumor and the growth rate of hemangioblastomas is believed to often accelerate during pregnancy; however, the reason for this rapid increase in size remains poorly understood. There are several case reports of symptomatic hemangioblastoma during pregnancy; however, the favorable management strategy has not been well established.</AbstractText>A 35-year-old woman, gravida 2 para 1, with no significant medical history presented with vertigo and difficulty walking at around 11 weeks of pregnancy and was referred to our institute at 30 weeks of gestation because of worsening symptoms. Brain magnetic resonance imaging revealed a 5.6 cm cystic lesion with a mural nodule in the right cerebellar hemisphere and the lesion blocked cerebrospinal fluid drainage from the fourth ventricle and brainstem, resulting in obstructive hydrocephalus. After obtaining the patient's consent, a multidisciplinary team consisting of obstetricians and neurosurgeons decided to perform resection of the intracranial lesion following delivery of the fetus by emergency cesarean section in view of the symptoms of increased intracranial pressure. The patient's general condition was confirmed to be stable postoperatively and she was discharged on the 16th</sup> day of her hospitalization without any neurological deficits or fetal complications.</AbstractText>Urgent tumor resection combined with cesarean section can be planned once fetal lung maturity is confirmed. Most cases of symptomatic hemangioblastoma during pregnancy have an uneventful gestational course and a favorable outcome for both mother and child.</AbstractText>Copyright: © 2022 Surgical Neurology International.</CopyrightInformation> |
2,329,990 | Endoscopic third ventriculostomy for noncommunicating hydrocephalus by vertebrobasilar dolichoectasia: A case report. | Vertebrobasilar dolichoectasia (VBD) is a vasculopathy characterized by the elongation, widening, and tortuosity of a cerebral artery. Rarely, hydrocephalus results when the extended basilar artery impairs communication of the cerebral ventricle and cerebrospinal fluid dynamics. We experienced such a case when a patient underwent endoscopic third ventriculostomy (ETV) for noncommunicating hydrocephalus with VBD.</AbstractText>A 54-year-old man presented with cognitive dysfunction and was diagnosed with VBD by magnetic resonance imaging (MRI). Seven years later, he exhibited subacute impaired consciousness due to acute noncommunicating hydrocephalus, undergoing external ventricular drainage (EVD) that improved consciousness. After EVD removal, the noncommunicating hydrocephalus did not recur; however, 7 months later, subacute consciousness impairment due to noncommunicating hydrocephalus was again observed. MRI showed a significant dilation of both lateral ventricles and ballooning of the third ventricle while the right posterior cerebral artery shifted slightly posteriorly. The patient underwent ETV and clinical symptoms improved. One year after the treatment, MRI observed a patent ETV fenestration and no deleterious changes in clinical symptoms were observed.</AbstractText>ETV can be an effective treatment for the noncommunicating hydrocephalus with VBD when performed with preoperative assessment of vascular anatomy and attention to vascular injury.</AbstractText>Copyright: © 2022 Surgical Neurology International.</CopyrightInformation> |
2,329,991 | Primary intracranial marginal zone B-cell lymphoma of mucosa-associated lymphoid tissue arising in the lateral ventricle: Case report and review of pathogenesis. | Primary central nervous system lymphoma (PCNSL) is an aggressive extranodal subtype of nonHodgkin's lymphoma. Ventricle-predominant PCNSL, arising in the CNS ventricular system, is a rare entity. In over 90% of cases, PCNSL is classified as diffuse large B-cell lymphoma. Rarely, PCNSL may be classified as marginal zone B-cell lymphoma (MZBCL) of mucosa-associated lymphoid tissue (MALT). Taken together, a primary MALT-type MZBCL arising in a cerebral ventricle is an extremely rare presentation.</AbstractText>A 69-year-old female presented with a persistent left frontal headache for 1 year. Magnetic resonance imaging revealed an enhancing soft-tissue lesion within the left lateral ventricle, with associated periventricular edema. We performed an excisional biopsy of the tumor, which grossly had the appearance of a meningioma. Histopathology of the tumor was consistent with MZBCL of the MALT type. The patient was treated with Rituximab and Ibrutinib. Six months after surgery, she remained neurologically intact and free of disease.</AbstractText>We report the case of a primary MALT-type MZBCL arising in the CNS ventricular system, with characteristics mimicking meningioma. This lymphoma involved the lateral ventricle and likely originated from the choroid plexus. Meningothelial cells and epithelial cells in the choroid plexus may acquire MALT in response to chronic inflammatory stimuli, such as infection or autoimmune disease. In rare cases, MALT lymphoma may develop as part of this pathogenesis.</AbstractText>Copyright: © 2022 Surgical Neurology International.</CopyrightInformation> |
2,329,992 | Treatment of refractory giant suprasellar arachnoid cyst by endoscopic expansion of a fenestrated stoma. | Although endoscopic ventriculo-cysto-cisternostomy is considered to be effective for suprasellar arachnoid cysts, we encountered a giant suprasellar arachnoid cyst that recurred despite surgery using this technique.</AbstractText>The patient was a 9-month-old boy. Magnetic resonance imaging revealed a huge suprasellar arachnoid cyst extending from the suprasellar region to the anterior skull base and both middle cranial fossa. First, an endoscopic procedure was performed to open the cyst wall between the right ventricle and the cyst and between the cyst and the prepontine cistern. Although the cyst initially shrank, it recurred over the next 2 months, and hence, we performed another endoscopic surgery. At the second surgery, both the previously opened stomas were found to be occluded. To reopen the cyst wall between the ventricle and the cyst, multiple holes were made with monopolar electrodes, and forceps were used to connect the holes by grasping and twisting the cyst wall so that the stoma was much larger than at the previous surgery. Postoperatively, the cyst shrank and the patient's head circumference stopped expanding.</AbstractText>Following the treatment of large cysts, the stoma might become narrower as the cyst shrinks, resulting in obstruction. Using the technique reported here might prevent occlusion of large arachnoid cysts.</AbstractText>Copyright: © 2022 Surgical Neurology International.</CopyrightInformation> |
2,329,993 | Hydrocephalus owing to ventriculoperitoneal shunt dysfunction. | A 43-year-old woman presented to our hospital with headache accompanied with nausea and intermittent vomiting without abdominal pain. The patient had undergone ventriculoperitoneal shunt placement for hydrocephalus owing to quadrigeminal cistern arachnoid cyst. Cranial computed tomography demonstrated enlarged bilateral ventricles, and the abdominal radiograph demonstrated a reverse U-shaped catheter that seemed to have been fractured in the left peritoneal cavity. |
2,329,994 | Porcine choroid plexus-Riems cell line demonstrates altered polarization of transport proteins compared with the native epithelium. | The choroid plexus epithelium (CPe) forms a barrier between the cerebral blood supply and the cerebrospinal fluid (CSF), establishing the blood-CSF barrier (BCSFB). CSF is actively secreted by the CPe via tightly controlled processes involving multiple channels, transporters, and pumps. The importance of controlling CSF production and composition has been accentuated recently with an appreciation of CSF dysfunction in many pathologies. For mechanistic studies of CSF production, isolated CPe cell lines are valuable for the testing of hypotheses and potential drug targets. Although several continuous CPe cell lines have been described, none appear to have all the characteristics of the native epithelium and each must be used judiciously. The porcine choroid plexus-Riems (PCP-R) cell line forms a high-resistance monolayer characteristic of a barrier epithelium. Conservation of this phenotype is unusual among CPe cell lines, making this model useful for studies of the effects of infection, injury, and drugs on permeability. We have recently discovered that, although this line expresses many of the transporters expressed in the native tissue, some are mispolarized. As a result, inferences regarding fluid/electrolyte flux and the resultant CSF production should be pursued with caution. Furthermore, extended culture periods and changes in media composition result in significant morphological and functional variability. These studies provide a more detailed characterization of the PCP-R cell line concerning transporter expression, polarization, and functionality, as well as plasticity in culture, with the goal to provide the scientific community with information necessary to optimize future experiments with this model. |
2,329,995 | A case of acquired von Willebrand disease in severe pediatric pulmonary hypertension contributing to bleeding following reverse Potts shunt. | The reverse Potts shunt is increasingly used as a palliative measure for end-stage pulmonary arterial hypertension (PAH) as a means to offload the right ventricle and improve functional status. This case report describes a child who developed significant hemothorax after reverse Potts shunt that required surgical exploration, blood product administration, and prolonged intensive care hospitalization. Despite lack of preoperative bleeding symptoms, testing revealed acquired von Willebrand disease (aVWD), with subsequent resolution of bleeding. Alterations in von Willebrand factor, including aVWD, have been reported in children with severe PAH but have not previously been associated with bleeding after reverse Potts shunt procedure. As bleeding is a recognized postoperative morbidity in PAH patients undergoing reverse Potts shunt, we highlight a potential role for preoperative testing for aVWD as perioperative factor replacement therapy may improve postoperative outcomes. |
2,329,996 | Ingenuity pathway analysis of the human cardiac cell Atlas identifies differences between right and left ventricular cardiomyocytes. | Pharmaceuticals for left ventricular (LV) dysfunction do not have similar success in right ventricular (RV) failure, which may reflect biological differences between the ventricles. In this study, we performed Ingenuity Pathway Analysis of the Human Cell Atlas to understand how the transcriptomic signatures of the RV and LV differ. |
2,329,997 | Emerging therapies: The potential roles SGLT2 inhibitors, GLP1 agonists, and ARNI therapy for ARNI pulmonary hypertension. | Pulmonary hypertension (PH) is a highly morbid condition. PH due to left heart disease (PH-LHD) has no specific therapies and pulmonary arterial hypertension (PAH) has substantial residual risk despite several approved therapies. Multiple lines of experimental evidence link metabolic dysfunction to the pathogenesis and outcomes in PH-LHD and PAH, and novel metabolic agents hold promise to improve outcomes in these populations. The antidiabetic sodium-glucose cotransporter 2 (SGLT2) inhibitors and glucagon-like peptide-1 (GLP1) agonists targeting metabolic dysfunction and improve outcomes in patients with LHD but have not been tested specifically in patients with PH. The angiotensin receptor/neprilysin inhibitors (ARNIs) produce significant improvements in cardiac hemodynamics and may improve metabolic dysfunction that could benefit the pulmonary circulation and right ventricle function. On the basis of promising preclinical work with these medications and clinical rationale, we explore the potential of SGLT2 inhibitors, GLP1 agonists, and ARNIs as therapies for both PH-LHD and PAH. |
2,329,998 | Strong ACE-2 expression in the choroidal vessels: do high choroid plexuses serve as a gateway for SARS-CoV-2 infection on the human brain?<Pagination><StartPage>3025</StartPage><EndPage>3029</EndPage><MedlinePgn>3025-3029</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.26355/eurrev_202204_28633</ELocationID><ELocationID EIdType="pii" ValidYN="Y">28633</ELocationID><Abstract><AbstractText Label="OBJECTIVE">Previous studies have confirmed the key mechanism by which SARS-CoV-2 enters human cells. It is well established that ACE2 is the receptor that can mark the beginning of the infection. In light of this, the organs that express higher levels of ACE2 are generally considered at higher risk, while those with lower levels should be somehow more protected. This - if related to the scarcity of ace2-expressing cells in the brain - seems to contrast with the presence of a variety of neurological symptoms that follow infection with ace2.  The aim of this work was to analyze ACE2 expression in the human brain, focusing on the choroid plexuses.</AbstractText><AbstractText Label="PATIENTS AND METHODS">Twenty brain samples were obtained at autopsy from ten human fetuses and from ten adult subjects. All samples were selected to contain the choroid plexus. Specimens were fixed in 10% formalin, routinely processed and paraffin embedded. 5-micron sections were stained with Hematoxylin and Eosin (H&E) and immunostained with a commercial anti-human ACE2 rabbit monoclonal antibody at 1:100 dilution.</AbstractText><AbstractText Label="RESULTS">We analyzed 20 samples by immunohistochemistry, and we noted that, as far as fetal samples are concerned, a strong reactivity for ACE2 was detected in the myxoid stroma of the choroid plexuses and in the endothelial cells in fetuses. The complete absence of the ACE2 marker was detected in epithelial cells, neurons and glial cells of the cerebral cortex, both in fetuses and in adults. Whereas a  strong but selective reactivity for ACE2 was also detected in adult choroid plexuses, mainly localized in the endothelial cells of the choroid capillaries.</AbstractText><AbstractText Label="CONCLUSIONS">Our study shows a strong expression of ACE in the fetal and adult brain choroid plexuses. This new histopathological finding may clarify the susceptibility of the human brain to SARS-COV-2 infection. Our data indicate the choroid plexus as the entry gate of virus for in the human brain; therefore, the entrance of SARS-CoV-2 into the cerebrospinal fluid through the choroid plexuses might represent the mechanism utilized by this coronavirus to cause direct injury to brain cells.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Piras</LastName><ForeName>M</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Medical Sciences and Public Health, University of Cagliari, Electron Microscopy Laboratory, Division Pathological Anatomy, Cagliari, Italy. monica.piras@unica.it.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cau</LastName><ForeName>F</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Manchia</LastName><ForeName>M</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Paribello</LastName><ForeName>P</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Saba</LastName><ForeName>L</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Suri</LastName><ForeName>J S</ForeName><Initials>JS</Initials></Author><Author ValidYN="Y"><LastName>Faa</LastName><ForeName>G</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Pichiri</LastName><ForeName>G</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Cerrone</LastName><ForeName>G</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Scano</LastName><ForeName>A</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Orrù</LastName><ForeName>G</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>La Nasa</LastName><ForeName>G</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Coghe</LastName><ForeName>F</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Castagnola</LastName><ForeName>M</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Fanni</LastName><ForeName>D</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Gerosa</LastName><ForeName>C</ForeName><Initials>C</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Italy</Country><MedlineTA>Eur Rev Med Pharmacol Sci</MedlineTA><NlmUniqueID>9717360</NlmUniqueID><ISSNLinking>1128-3602</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>EC 3.4.17.23</RegistryNumber><NameOfSubstance UI="D000085962">Angiotensin-Converting Enzyme 2</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000085962" MajorTopicYN="Y">Angiotensin-Converting Enzyme 2</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000086382" MajorTopicYN="Y">COVID-19</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002829" MajorTopicYN="N">Choroid</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002831" MajorTopicYN="N">Choroid Plexus</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D042783" MajorTopicYN="N">Endothelial Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000086402" MajorTopicYN="N">SARS-CoV-2</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>5</Month><Day>3</Day><Hour>12</Hour><Minute>55</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>5</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>5</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35503602</ArticleId><ArticleId IdType="doi">10.26355/eurrev_202204_28633</ArticleId><ArticleId IdType="pii">28633</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35503304</PMID><DateRevised><Year>2022</Year><Month>06</Month><Day>09</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1477-111X</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>May</Month><Day>03</Day></PubDate></JournalIssue><Title>Perfusion</Title><ISOAbbreviation>Perfusion</ISOAbbreviation></Journal>The incremental value of myocardial viability, evaluated by 18F-fluorodeoxyglucose positron emission tomography, and cardiovascular magnetic resonance for mortality prediction in patients with previous myocardial infarction and symptomatic heart failure. | Previous studies have confirmed the key mechanism by which SARS-CoV-2 enters human cells. It is well established that ACE2 is the receptor that can mark the beginning of the infection. In light of this, the organs that express higher levels of ACE2 are generally considered at higher risk, while those with lower levels should be somehow more protected. This - if related to the scarcity of ace2-expressing cells in the brain - seems to contrast with the presence of a variety of neurological symptoms that follow infection with ace2.  The aim of this work was to analyze ACE2 expression in the human brain, focusing on the choroid plexuses.</AbstractText>Twenty brain samples were obtained at autopsy from ten human fetuses and from ten adult subjects. All samples were selected to contain the choroid plexus. Specimens were fixed in 10% formalin, routinely processed and paraffin embedded. 5-micron sections were stained with Hematoxylin and Eosin (H&E) and immunostained with a commercial anti-human ACE2 rabbit monoclonal antibody at 1:100 dilution.</AbstractText>We analyzed 20 samples by immunohistochemistry, and we noted that, as far as fetal samples are concerned, a strong reactivity for ACE2 was detected in the myxoid stroma of the choroid plexuses and in the endothelial cells in fetuses. The complete absence of the ACE2 marker was detected in epithelial cells, neurons and glial cells of the cerebral cortex, both in fetuses and in adults. Whereas a  strong but selective reactivity for ACE2 was also detected in adult choroid plexuses, mainly localized in the endothelial cells of the choroid capillaries.</AbstractText>Our study shows a strong expression of ACE in the fetal and adult brain choroid plexuses. This new histopathological finding may clarify the susceptibility of the human brain to SARS-COV-2 infection. Our data indicate the choroid plexus as the entry gate of virus for in the human brain; therefore, the entrance of SARS-CoV-2 into the cerebrospinal fluid through the choroid plexuses might represent the mechanism utilized by this coronavirus to cause direct injury to brain cells.</AbstractText> |
2,329,999 | The Surprise Question as a Trigger for Primary Palliative Care Interventions for Children with Advanced Heart Disease. | There is significant uncertainty in describing prognosis and a lack of reliable entry criteria for palliative care studies in children with advanced heart disease (AHD). This study evaluates the utility of the surprise question-"Would you be surprised if this child died within the next year?"-to predict one-year mortality in children with AHD and assess its utility as entry criteria for future trials. This is a prospective cohort study of physicians and nurses caring for children (1 month-19 years) with AHD hospitalized ≥ 7 days. AHD was defined as single ventricle physiology, pulmonary vein stenosis or pulmonary hypertension, or any cardiac diagnosis with signs of advanced disease. Primary physicians were asked the surprise question and medical record review was performed. Forty-nine physicians responded to the surprise question for 152 patients. Physicians responded "No, I would not be surprised if this patient died" for 54 (36%) patients, 20 (37%) of whom died within 1 year, predicting one-year mortality with 77% sensitivity, 73% specificity, 37% positive predictive value, and 94% negative predictive value. Patients who received a "No" response had an increased 1-year risk of death (hazard ratio 7.25, p < 0.001). Physician years of experience, subspecialty, and self-rated competency were not associated with the accuracy of the surprise question. The surprise question offers promise as a bedside screening tool to identify children with AHD at high risk for mortality and help physicians identify patients who may benefit from palliative care and advance care planning discussions. |
Subsets and Splits
No community queries yet
The top public SQL queries from the community will appear here once available.