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2,329,300 | Impact of severe valvular heart disease in adult congenital heart disease patients.<Pagination><StartPage>983308</StartPage><MedlinePgn>983308</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">983308</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.3389/fcvm.2022.983308</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="UNASSIGNED">The clinical impact of valvular heart disease (VHD) in adult congenital heart disease (ACHD) patients is unascertained. Aim of our study was to assess the prevalence and clinical impact of severe VHD (S-VHD) in a real-world contemporary cohort of ACHD patients.</AbstractText><AbstractText Label="MATERIALS AND METHODS" NlmCategory="UNASSIGNED">Consecutive patients followed-up at our ACHD Outpatient Clinic from September 2014 to February 2021 were enrolled. Clinical characteristics and echocardiographic data were prospectively entered into a digitalized medical records database. VHD at the first evaluation was assessed and graded according to VHD guidelines. Clinical data at follow-up were collected. The study endpoint was the occurrence of cardiac mortality and/or unplanned cardiac hospitalization during follow-up.</AbstractText><AbstractText Label="RESULTS" NlmCategory="UNASSIGNED">A total of 390 patients (median age 34 years, 49% males) were included and S-VHD was present in 101 (25.9%) patients. Over a median follow-up time of 26 months (IQR: 12-48), the study composite endpoint occurred in 76 patients (19.5%). The cumulative endpoint-free survival was significantly lower in patients with S-VHD <i>vs.</i> patients with non-severe VHD (Log rank <i>p</i> < 0.001). At multivariable analysis, age and atrial fibrillation at first visit (<i>p</i> = 0.029 and <i>p</i> = 0.006 respectively), lower %Sat O<sub>2</sub>, higher NYHA class (<i>p</i> = 0.005 for both), lower LVEF (<i>p</i> = 0.008), and S-VHD (<i>p</i> = 0.015) were independently associated to the study endpoint. The likelihood ratio test demonstrated that S-VHD added significant prognostic value (<i>p</i> = 0.017) to a multivariate model including age, severe CHD, atrial fibrillation, %Sat O2, NYHA, LVEF, and right ventricle systolic pressure > 45 mmHg.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="UNASSIGNED">In ACHD patients, the presence of S-VHD is independently associated with the occurrence of cardiovascular mortality and hospitalization. The prognostic value of S-VHD is incremental above other established prognostic markers.</AbstractText><CopyrightInformation>Copyright © 2022 Graziani, Iannaccone, Meucci, Lillo, Delogu, Grandinetti, Perri, Galletti, Amodeo, Butera, Secinaro, Lombardo, Lanza, Burzotta, Crea and Massetti.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Graziani</LastName><ForeName>Francesca</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Medicine, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Iannaccone</LastName><ForeName>Giulia</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular and Pulmonary Sciences, Università Cattolica del Sacro Cuore, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Meucci</LastName><ForeName>Maria Chiara</ForeName><Initials>MC</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Medicine, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lillo</LastName><ForeName>Rosa</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Medicine, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome, Italy.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Cardiovascular and Pulmonary Sciences, Università Cattolica del Sacro Cuore, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Delogu</LastName><ForeName>Angelica Bibiana</ForeName><Initials>AB</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular and Pulmonary Sciences, Università Cattolica del Sacro Cuore, Rome, Italy.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Unit of Pediatrics, Pediatric Cardiology, Department of Women and Child Health and Public Health, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Grandinetti</LastName><ForeName>Maria</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Medicine, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Perri</LastName><ForeName>Gianluigi</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Pediatric Cardiac Surgery Unit, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Galletti</LastName><ForeName>Lorenzo</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Pediatric Cardiac Surgery Unit, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Amodeo</LastName><ForeName>Antonio</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Pediatric Cardiac Surgery Unit, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Butera</LastName><ForeName>Gianfranco</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Pediatric Cardiology Unit, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Secinaro</LastName><ForeName>Aurelio</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Advanced Cardiovascular Imaging Unit, Department of Imaging, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lombardo</LastName><ForeName>Antonella</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Medicine, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome, Italy.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Cardiovascular and Pulmonary Sciences, Università Cattolica del Sacro Cuore, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lanza</LastName><ForeName>Gaetano Antonio</ForeName><Initials>GA</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Medicine, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome, Italy.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Cardiovascular and Pulmonary Sciences, Università Cattolica del Sacro Cuore, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Burzotta</LastName><ForeName>Francesco</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Medicine, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome, Italy.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Cardiovascular and Pulmonary Sciences, Università Cattolica del Sacro Cuore, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Crea</LastName><ForeName>Filippo</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Medicine, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome, Italy.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Cardiovascular and Pulmonary Sciences, Università Cattolica del Sacro Cuore, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Massetti</LastName><ForeName>Massimo</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Medicine, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome, Italy.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Cardiovascular and Pulmonary Sciences, Università Cattolica del Sacro Cuore, Rome, Italy.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>11</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Front Cardiovasc Med</MedlineTA><NlmUniqueID>101653388</NlmUniqueID><ISSNLinking>2297-055X</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">adult congenital heart disease (ACHD)</Keyword><Keyword MajorTopicYN="N">hospitalization</Keyword><Keyword MajorTopicYN="N">mortality</Keyword><Keyword MajorTopicYN="N">prognosis</Keyword><Keyword MajorTopicYN="N">valvular heart disease</Keyword></KeywordList><CoiStatement>The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed 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(2022) 43:561–632. 10.1093/eurheartj/ehab395</Citation><ArticleIdList><ArticleId IdType="doi">10.1093/eurheartj/ehab395</ArticleId><ArticleId IdType="pubmed">34453165</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36523262</PMID><DateRevised><Year>2022</Year><Month>12</Month><Day>16</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1467-1107</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Dec</Month><Day>16</Day></PubDate></JournalIssue><Title>Cardiology in the young</Title><ISOAbbreviation>Cardiol Young</ISOAbbreviation></Journal>Mid-cavitary hypertrophy after myocarditis in a patient with operated medulloblastoma. | A 16-month-old girl was referred for tachycardia and upper respiratory tract infection. Echocardiographic examination revealed pericardial effusion, mild mitral regurgitation, and left ventricle systolic dysfunction. Patient was positive for Parainfluenza type 4 virus. Her laboratory tests revealed increased troponin I level. The patient was treated with intravenous immunoglobulin considering acute viral myopericarditis. Two weeks after treatment, midventricular hypertrophy was detected. |
2,329,301 | Rare adult pilocytic astrocytoma of the septum pellucidum with novel RIN2::BRAF fusion. | Pilocytic astrocytoma is mostly a pediatric tumor with the majority of patients under age 20. Although tumors can occur throughout neuraxis, most tumors are in the cerebellum and optic chiasm. Pilocytic astrocytoma in unusual locations is often associated with different genetic alterations than the classic KIAA1549::BRAF fusion. We report a rare adult pilocytic astrocytoma of the septum pellucidum that presented with progressive headache. A detailed genomic evaluation found a fusion between BRAF and a novel partner RIN2, a gene overexpressed in both low-grade glioma and glioblastoma. The RIN2::BRAF transcript encodes a chimeric protein containing a dimerization domain SH2 and an intact kinase domain, consistent with a prototypic oncogenic kinase rearrangement. In addition, we discuss the potential oncogenic mechanisms of BRAF signaling and its implication in targeted therapy with kinase inhibitors. |
2,329,302 | Personalization of biomechanical simulations of the left ventricle by in-vivo cardiac DTI data: Impact of fiber interpolation methods. | Simulations of cardiac electrophysiology and mechanics have been reported to be sensitive to the microstructural anisotropy of the myocardium. Consequently, a personalized representation of cardiac microstructure is a crucial component of accurate, personalized cardiac biomechanical models. <i>In-vivo</i> cardiac Diffusion Tensor Imaging (cDTI) is a non-invasive magnetic resonance imaging technique capable of probing the heart's microstructure. Being a rather novel technique, issues such as low resolution, signal-to noise ratio, and spatial coverage are currently limiting factors. We outline four interpolation techniques with varying degrees of data fidelity, different amounts of smoothing strength, and varying representation error to bridge the gap between the sparse <i>in-vivo</i> data and the model, requiring a 3D representation of microstructure across the myocardium. We provide a workflow to incorporate <i>in-vivo</i> myofiber orientation into a left ventricular model and demonstrate that personalized modelling based on fiber orientations from <i>in-vivo</i> cDTI data is feasible. The interpolation error is correlated with a trend in personalized parameters and simulated physiological parameters, strains, and ventricular twist. This trend in simulation results is consistent across material parameter settings and therefore corresponds to a bias introduced by the interpolation method. This study suggests that using a tensor interpolation approach to personalize microstructure with <i>in-vivo</i> cDTI data, reduces the fiber uncertainty and thereby the bias in the simulation results. |
2,329,303 | [The relationship between left ventricular artery coupling and left ventricular work and their predictive value on prognosis in septic shock].<Pagination><StartPage>3749</StartPage><EndPage>3755</EndPage><MedlinePgn>3749-3755</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.3760/cma.j.cn112137-20220620-01351</ELocationID><Abstract><AbstractText><b>Objective:</b> To explore the relationship between left ventricular artery coupling and left ventricular work in patients with septic shock, and further clarified their predictive value for the prognosis of septic shock. <b>Methods:</b> In total, 56 patients with septic shock admitted in the Department of Critical Care Medicine of Peking Union Medical College Hospital were retrospectively enrolled between January 2016 and July 2021. The hemodynamic indexes and clinical data monitored by pulse indicator continuous cardiac output (PICCO) at different time points were collected. To reveal alterations of arterial elastance index (EaI), end-systolic elastance index (EesI), EaI/EesI, stroke work (SW), total cardiac function (PVA), and left ventricular ejection efficiency (LVEf) in patients with septic shock at different time points. The patients were divided into the death group (<i>n</i>=20) and survival group (<i>n</i>=36) according to the outcome of the ICU. The relationship between left ventricular work and left ventricular arterial coupling and its prognostic value were statistically analyzed. <b>Results:</b> A total of 56 patients were enrolled, 32 males and 24 females, aged (61±15) years. There was a significantly difference in EaI/EesI and LVEf between survivors and non-survivors with septic shock at 6 h (<i>P</i><0.05). Further analysis showed that the correlation between EaI/EesI and LVEf was most evident at 6 h after intervention. EaI/EesI was negatively correlated with SW (<i>r</i><sub>s</sub>=-0.500, <i>P</i><0.001), and highly negative with LVEf (<i>r</i><sub>s</sub>=-0.959, <i>P</i><0.001). Both univariate logistic regression and multivariate regression analysis showed that EaI/EesI (adjusted <i>OR</i>=42.783, 95%<i>CI</i>: 2.725-671.819, <i>P</i>=0.008) and LVEf (adjusted <i>OR</i>=2.293, 95%<i>CI</i>:1.222-4.301, <i>P</i>=0.010) were risk factors for ICU prognosis of patients with septic shock. The receiver operating characteristic (ROC) curve analysis showed that EaI/EesI [area under the curve (AUC)=0.742±0.083, <i>P</i>=0.004; cut-off value 6.10, sensitivity 88.9%, specificity 65.0%] and LVEf (AUC=0.733±0.084, <i>P</i>=0.006; cut-off value 0.24, sensitivity 88.8%, specificity 60.0%) were both effective indicators for predicting the prognosis of patients with septic shock in the ICU. Moreover, EaI/EesI had a better prognosis value than LVEf (ΔAUC=0.120, <i>Z</i>=6.528, <i>P</i>=0.036). <b>Conclusion:</b> It's indicated that EaI/EesI was significantly correlated with SW and LVEf after 6 h of septic shock intervention; EaI/EesI and LVEf are risk factors and effective predictors of ICU prognosis in patients with septic shock. The predictive efficacy of EaI/EesI is greater than LVEF.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhou</LastName><ForeName>G S</ForeName><Initials>GS</Initials><AffiliationInfo><Affiliation>Department of Critical Care Medicine, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100710, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>J J</ForeName><Initials>JJ</Initials><AffiliationInfo><Affiliation>Department of Critical Care Medicine, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100710, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>H M</ForeName><Initials>HM</Initials><AffiliationInfo><Affiliation>Department of Critical Care Medicine, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100710, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Q</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>Department of Critical Care Medicine, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100710, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>X T</ForeName><Initials>XT</Initials><AffiliationInfo><Affiliation>Department of Critical Care Medicine, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100710, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>D W</ForeName><Initials>DW</Initials><AffiliationInfo><Affiliation>Department of Critical Care Medicine, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100710, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>chi</Language><GrantList CompleteYN="Y"><Grant><GrantID>Z201100005520038</GrantID><Agency>Capital Clinic Research and Demonstration Application of Diagnosis and Treatment Project</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D004740">English Abstract</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>China</Country><MedlineTA>Zhonghua Yi Xue Za Zhi</MedlineTA><NlmUniqueID>7511141</NlmUniqueID><ISSNLinking>0376-2491</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012772" MajorTopicYN="Y">Shock, Septic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011379" MajorTopicYN="N">Prognosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001158" MajorTopicYN="N">Arteries</DescriptorName></MeshHeading></MeshHeadingList><OtherAbstract Type="Publisher" Language="chi"><AbstractText><b>目的：</b> 探寻左心室动脉偶联与左心做功在感染性休克患者中的关系，明确二者对感染性休克预后的预测价值。 <b>方法：</b> 回顾性分析2016年1月1日至2021年7月31日北京协和医院重症医学科56例感染性休克患者的临床资料。收集不同时间点脉搏指示连续心排血量技术（PICCO）监测血流动力学指标及临床资料，揭示在不同时间点感染性休克患者动脉弹性指数（EaI）、左心室收缩末弹性指数（EesI）、EaI/EesI、心脏每搏功（SW）、心脏总功（PVA）、左心室射血效率（LVEf）的变化规律。根据重症监护病房（ICU）结局将患者分为死亡组（<i>n</i>=20）和存活组（<i>n</i>=36），分析两组患者在不同时间点左心室做功及左心室-动脉偶联的关系及其预后价值。 <b>结果：</b> 共纳入56例感染性休克患者，男32例，女24例，年龄（61±15）岁。死亡组及生存组EaI/EesI、LVEf在入ICU 6 h差异均有统计学意义（均<i>P</i><0.05）。进一步分析发现干预6 h后左心室动脉偶联与左心做功的相关性最明显，EaI/EesI与SW呈中度负相关（<i>r</i><sub>s</sub>=-0.500，<i>P</i><0.001），与LVEf呈高度负相关（<i>r</i><sub>s</sub>=-0.959，<i>P</i><0.001）。单因素logistic回归及多因素回归分析均显示EaI/EesI（校正<i>OR</i>=42.783，95%<i>CI</i>：2.725~671.819，<i>P</i>=0.008）、LVEf（校正<i>OR</i>=2.293，95%<i>CI</i>：1.222~4.301，<i>P</i>=0.010）是感染性休克患者住院预后的危险因素。受试者工作特征（ROC）曲线分析提示EaI/EesI［曲线下面积（AUC）=0.742±0.083，<i>P</i>=0.004］、LVEf（AUC=0.733±0.084，<i>P</i>=0.006）均是预测感染性休克患者ICU预后的有效指标，其中EaI/EesI预测感染性休克患者预后的最佳cut-off值为6.10，灵敏度为88.9%，特异度为65.0%；LVEf预测感染性休克患者预后的最佳cut-off值为0.24，灵敏度为88.8%，特异度为60.0%；EaI/EesI预测效能大于LVEf（ΔAUC=0.120，<i>Z</i>=6.528，<i>P</i>=0.036）。 <b>结论：</b> 感染性休克干预6 h后，EaI/EesI与SW、LVEf明显相关；EaI/EesI、LVEf是感染性休克患者ICU预后的危险因素及有效预测指标，EaI/EesI预测效能大于LVEf。.</AbstractText></OtherAbstract></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>12</Month><Day>14</Day><Hour>22</Hour><Minute>16</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>12</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>12</Month><Day>17</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36517424</ArticleId><ArticleId IdType="doi">10.3760/cma.j.cn112137-20220620-01351</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36517010</PMID><DateRevised><Year>2022</Year><Month>12</Month><Day>14</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1880-2206</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Dec</Month><Day>13</Day></PubDate></JournalIssue><Title>Magnetic resonance in medical sciences : MRMS : an official journal of Japan Society of Magnetic Resonance in Medicine</Title><ISOAbbreviation>Magn Reson Med Sci</ISOAbbreviation></Journal>Measurement of Turbulent Kinetic Energy in Hypertrophic Cardiomyopathy Using Triple-velocity Encoding 4D Flow MR Imaging.<ELocationID EIdType="doi" ValidYN="Y">10.2463/mrms.mp.2022-0051</ELocationID><Abstract><AbstractText Label="PURPOSE" NlmCategory="OBJECTIVE">The turbulent kinetic energy (TKE) estimation based on 4D flow MRI has been currently developed and can be used to estimate the pressure gradient. The objective of this study was to validate the clinical value of 4D flow-based TKE measurement in patients with hypertrophic cardiomyopathy (HCM).</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">From April 2018 to March 2019, we recruited 28 patients with HCM. Based on echocardiography, they were divided into obstructed HCM (HOCM) and non-obstructed HCM (HNCM). Triple-velocity encoding 4D flow MRI was performed. The volume-of-interest from the left ventricle to the aortic arch was drawn semi-automatically. We defined peak turbulent kinetic energy (TKE<sub>peak</sub>) as the highest TKE phase in all cardiac phases.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">TKE<sub>peak</sub> was significantly higher in HOCM than in HNCM (14.83 ± 3.91 vs. 7.11 ± 3.60 mJ, P < 0.001). TKE<sub>peak</sub> was significantly higher in patients with systolic anterior movement (SAM) than in those without SAM (15.60 ± 3.96 vs. 7.44 ± 3.29 mJ, P < 0.001). Left ventricular (LV) mass increased proportionally with TKE<sub>peak</sub> (P = 0.012, r = 0.466). When only the asymptomatic patients were extracted, a stronger correlation was observed (P = 0.001, r = 0.842).</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">TKE measurement based on 4D flow MRI can detect the flow alteration induced by systolic flow jet and LV outflow tract geometry, such as SAM in patients with HOCM. The elevated TKE is correlated with increasing LV mass. This indicates that increasing cardiac load, by pressure loss due to turbulence, induces progression of LV hypertrophy, which leads to a worse prognosis.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Iwata</LastName><ForeName>Kotomi</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Radiology, Nippon Medical School.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sekine</LastName><ForeName>Tetsuro</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Radiology, Nippon Medical School Musashi Kosugi Hospital.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Matsuda</LastName><ForeName>Junya</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Medicine, Nippon Medical School.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tachi</LastName><ForeName>Masaki</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Radiology, Nippon Medical School.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Imori</LastName><ForeName>Yoichi</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Medicine, Nippon Medical School.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Amano</LastName><ForeName>Yasuo</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Radiology, Nihon University School of Medicine.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ando</LastName><ForeName>Takahiro</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Radiology, Nippon Medical School.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Obara</LastName><ForeName>Makoto</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Philips Electronics Japan Ltd.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Crelier</LastName><ForeName>Gerard</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>GyroTools LLC.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ogawa</LastName><ForeName>Masashi</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Radiology, Nippon Medical School.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Takano</LastName><ForeName>Hitoshi</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Medicine, Nippon Medical School.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kumita</LastName><ForeName>Shinichiro</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Radiology, Nippon Medical School.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>12</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>Japan</Country><MedlineTA>Magn Reson Med Sci</MedlineTA><NlmUniqueID>101153368</NlmUniqueID><ISSNLinking>1347-3182</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">4D flow magnetic resonance imaging</Keyword><Keyword MajorTopicYN="N">energy loss</Keyword><Keyword MajorTopicYN="N">hypertrophic cardiomyopathy</Keyword><Keyword MajorTopicYN="N">left ventricular mass</Keyword><Keyword MajorTopicYN="N">turbulent kinetic energy</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>12</Month><Day>14</Day><Hour>20</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>12</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>12</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>aheadofprint</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36517010</ArticleId><ArticleId IdType="doi">10.2463/mrms.mp.2022-0051</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36517009</PMID><DateRevised><Year>2022</Year><Month>12</Month><Day>14</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1880-2206</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Dec</Month><Day>13</Day></PubDate></JournalIssue><Title>Magnetic resonance in medical sciences : MRMS : an official journal of Japan Society of Magnetic Resonance in Medicine</Title><ISOAbbreviation>Magn Reson Med Sci</ISOAbbreviation></Journal>Associating the Severity of Emphysema with Coronary Flow Reserve and Left Atrial Conduit Function for the Emphysema Patients with Known or Suspected Coronary Artery Disease. | <b>Objective:</b> To explore the relationship between left ventricular artery coupling and left ventricular work in patients with septic shock, and further clarified their predictive value for the prognosis of septic shock. <b>Methods:</b> In total, 56 patients with septic shock admitted in the Department of Critical Care Medicine of Peking Union Medical College Hospital were retrospectively enrolled between January 2016 and July 2021. The hemodynamic indexes and clinical data monitored by pulse indicator continuous cardiac output (PICCO) at different time points were collected. To reveal alterations of arterial elastance index (EaI), end-systolic elastance index (EesI), EaI/EesI, stroke work (SW), total cardiac function (PVA), and left ventricular ejection efficiency (LVEf) in patients with septic shock at different time points. The patients were divided into the death group (<i>n</i>=20) and survival group (<i>n</i>=36) according to the outcome of the ICU. The relationship between left ventricular work and left ventricular arterial coupling and its prognostic value were statistically analyzed. <b>Results:</b> A total of 56 patients were enrolled, 32 males and 24 females, aged (61±15) years. There was a significantly difference in EaI/EesI and LVEf between survivors and non-survivors with septic shock at 6 h (<i>P</i><0.05). Further analysis showed that the correlation between EaI/EesI and LVEf was most evident at 6 h after intervention. EaI/EesI was negatively correlated with SW (<i>r</i><sub>s</sub>=-0.500, <i>P</i><0.001), and highly negative with LVEf (<i>r</i><sub>s</sub>=-0.959, <i>P</i><0.001). Both univariate logistic regression and multivariate regression analysis showed that EaI/EesI (adjusted <i>OR</i>=42.783, 95%<i>CI</i>: 2.725-671.819, <i>P</i>=0.008) and LVEf (adjusted <i>OR</i>=2.293, 95%<i>CI</i>:1.222-4.301, <i>P</i>=0.010) were risk factors for ICU prognosis of patients with septic shock. The receiver operating characteristic (ROC) curve analysis showed that EaI/EesI [area under the curve (AUC)=0.742±0.083, <i>P</i>=0.004; cut-off value 6.10, sensitivity 88.9%, specificity 65.0%] and LVEf (AUC=0.733±0.084, <i>P</i>=0.006; cut-off value 0.24, sensitivity 88.8%, specificity 60.0%) were both effective indicators for predicting the prognosis of patients with septic shock in the ICU. Moreover, EaI/EesI had a better prognosis value than LVEf (ΔAUC=0.120, <i>Z</i>=6.528, <i>P</i>=0.036). <b>Conclusion:</b> It's indicated that EaI/EesI was significantly correlated with SW and LVEf after 6 h of septic shock intervention; EaI/EesI and LVEf are risk factors and effective predictors of ICU prognosis in patients with septic shock. The predictive efficacy of EaI/EesI is greater than LVEF.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhou</LastName><ForeName>G S</ForeName><Initials>GS</Initials><AffiliationInfo><Affiliation>Department of Critical Care Medicine, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100710, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>J J</ForeName><Initials>JJ</Initials><AffiliationInfo><Affiliation>Department of Critical Care Medicine, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100710, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>H M</ForeName><Initials>HM</Initials><AffiliationInfo><Affiliation>Department of Critical Care Medicine, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100710, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Q</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>Department of Critical Care Medicine, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100710, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>X T</ForeName><Initials>XT</Initials><AffiliationInfo><Affiliation>Department of Critical Care Medicine, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100710, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>D W</ForeName><Initials>DW</Initials><AffiliationInfo><Affiliation>Department of Critical Care Medicine, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100710, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>chi</Language><GrantList CompleteYN="Y"><Grant><GrantID>Z201100005520038</GrantID><Agency>Capital Clinic Research and Demonstration Application of Diagnosis and Treatment Project</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D004740">English Abstract</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>China</Country><MedlineTA>Zhonghua Yi Xue Za Zhi</MedlineTA><NlmUniqueID>7511141</NlmUniqueID><ISSNLinking>0376-2491</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012772" MajorTopicYN="Y">Shock, Septic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011379" MajorTopicYN="N">Prognosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001158" MajorTopicYN="N">Arteries</DescriptorName></MeshHeading></MeshHeadingList><OtherAbstract Type="Publisher" Language="chi"><b>目的：</b> 探寻左心室动脉偶联与左心做功在感染性休克患者中的关系，明确二者对感染性休克预后的预测价值。 <b>方法：</b> 回顾性分析2016年1月1日至2021年7月31日北京协和医院重症医学科56例感染性休克患者的临床资料。收集不同时间点脉搏指示连续心排血量技术（PICCO）监测血流动力学指标及临床资料，揭示在不同时间点感染性休克患者动脉弹性指数（EaI）、左心室收缩末弹性指数（EesI）、EaI/EesI、心脏每搏功（SW）、心脏总功（PVA）、左心室射血效率（LVEf）的变化规律。根据重症监护病房（ICU）结局将患者分为死亡组（<i>n</i>=20）和存活组（<i>n</i>=36），分析两组患者在不同时间点左心室做功及左心室-动脉偶联的关系及其预后价值。 <b>结果：</b> 共纳入56例感染性休克患者，男32例，女24例，年龄（61±15）岁。死亡组及生存组EaI/EesI、LVEf在入ICU 6 h差异均有统计学意义（均<i>P</i><0.05）。进一步分析发现干预6 h后左心室动脉偶联与左心做功的相关性最明显，EaI/EesI与SW呈中度负相关（<i>r</i><sub>s</sub>=-0.500，<i>P</i><0.001），与LVEf呈高度负相关（<i>r</i><sub>s</sub>=-0.959，<i>P</i><0.001）。单因素logistic回归及多因素回归分析均显示EaI/EesI（校正<i>OR</i>=42.783，95%<i>CI</i>：2.725~671.819，<i>P</i>=0.008）、LVEf（校正<i>OR</i>=2.293，95%<i>CI</i>：1.222~4.301，<i>P</i>=0.010）是感染性休克患者住院预后的危险因素。受试者工作特征（ROC）曲线分析提示EaI/EesI［曲线下面积（AUC）=0.742±0.083，<i>P</i>=0.004］、LVEf（AUC=0.733±0.084，<i>P</i>=0.006）均是预测感染性休克患者ICU预后的有效指标，其中EaI/EesI预测感染性休克患者预后的最佳cut-off值为6.10，灵敏度为88.9%，特异度为65.0%；LVEf预测感染性休克患者预后的最佳cut-off值为0.24，灵敏度为88.8%，特异度为60.0%；EaI/EesI预测效能大于LVEf（ΔAUC=0.120，<i>Z</i>=6.528，<i>P</i>=0.036）。 <b>结论：</b> 感染性休克干预6 h后，EaI/EesI与SW、LVEf明显相关；EaI/EesI、LVEf是感染性休克患者ICU预后的危险因素及有效预测指标，EaI/EesI预测效能大于LVEf。.</OtherAbstract></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>12</Month><Day>14</Day><Hour>22</Hour><Minute>16</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>12</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>12</Month><Day>17</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36517424</ArticleId><ArticleId IdType="doi">10.3760/cma.j.cn112137-20220620-01351</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36517010</PMID><DateRevised><Year>2022</Year><Month>12</Month><Day>14</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1880-2206</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Dec</Month><Day>13</Day></PubDate></JournalIssue><Title>Magnetic resonance in medical sciences : MRMS : an official journal of Japan Society of Magnetic Resonance in Medicine</Title><ISOAbbreviation>Magn Reson Med Sci</ISOAbbreviation></Journal><ArticleTitle>Measurement of Turbulent Kinetic Energy in Hypertrophic Cardiomyopathy Using Triple-velocity Encoding 4D Flow MR Imaging.</ArticleTitle><ELocationID EIdType="doi" ValidYN="Y">10.2463/mrms.mp.2022-0051</ELocationID><Abstract><AbstractText Label="PURPOSE" NlmCategory="OBJECTIVE">The turbulent kinetic energy (TKE) estimation based on 4D flow MRI has been currently developed and can be used to estimate the pressure gradient. The objective of this study was to validate the clinical value of 4D flow-based TKE measurement in patients with hypertrophic cardiomyopathy (HCM).<AbstractText Label="METHODS" NlmCategory="METHODS">From April 2018 to March 2019, we recruited 28 patients with HCM. Based on echocardiography, they were divided into obstructed HCM (HOCM) and non-obstructed HCM (HNCM). Triple-velocity encoding 4D flow MRI was performed. The volume-of-interest from the left ventricle to the aortic arch was drawn semi-automatically. We defined peak turbulent kinetic energy (TKE<sub>peak</sub>) as the highest TKE phase in all cardiac phases.<AbstractText Label="RESULTS" NlmCategory="RESULTS">TKE<sub>peak</sub> was significantly higher in HOCM than in HNCM (14.83 ± 3.91 vs. 7.11 ± 3.60 mJ, P < 0.001). TKE<sub>peak</sub> was significantly higher in patients with systolic anterior movement (SAM) than in those without SAM (15.60 ± 3.96 vs. 7.44 ± 3.29 mJ, P < 0.001). Left ventricular (LV) mass increased proportionally with TKE<sub>peak</sub> (P = 0.012, r = 0.466). When only the asymptomatic patients were extracted, a stronger correlation was observed (P = 0.001, r = 0.842).<AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">TKE measurement based on 4D flow MRI can detect the flow alteration induced by systolic flow jet and LV outflow tract geometry, such as SAM in patients with HOCM. The elevated TKE is correlated with increasing LV mass. This indicates that increasing cardiac load, by pressure loss due to turbulence, induces progression of LV hypertrophy, which leads to a worse prognosis.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Iwata</LastName><ForeName>Kotomi</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Radiology, Nippon Medical School.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sekine</LastName><ForeName>Tetsuro</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Radiology, Nippon Medical School Musashi Kosugi Hospital.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Matsuda</LastName><ForeName>Junya</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Medicine, Nippon Medical School.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tachi</LastName><ForeName>Masaki</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Radiology, Nippon Medical School.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Imori</LastName><ForeName>Yoichi</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Medicine, Nippon Medical School.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Amano</LastName><ForeName>Yasuo</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Radiology, Nihon University School of Medicine.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ando</LastName><ForeName>Takahiro</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Radiology, Nippon Medical School.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Obara</LastName><ForeName>Makoto</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Philips Electronics Japan Ltd.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Crelier</LastName><ForeName>Gerard</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>GyroTools LLC.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ogawa</LastName><ForeName>Masashi</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Radiology, Nippon Medical School.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Takano</LastName><ForeName>Hitoshi</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Medicine, Nippon Medical School.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kumita</LastName><ForeName>Shinichiro</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Radiology, Nippon Medical School.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>12</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>Japan</Country><MedlineTA>Magn Reson Med Sci</MedlineTA><NlmUniqueID>101153368</NlmUniqueID><ISSNLinking>1347-3182</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">4D flow magnetic resonance imaging</Keyword><Keyword MajorTopicYN="N">energy loss</Keyword><Keyword MajorTopicYN="N">hypertrophic cardiomyopathy</Keyword><Keyword MajorTopicYN="N">left ventricular mass</Keyword><Keyword MajorTopicYN="N">turbulent kinetic energy</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>12</Month><Day>14</Day><Hour>20</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>12</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>12</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>aheadofprint</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36517010</ArticleId><ArticleId IdType="doi">10.2463/mrms.mp.2022-0051</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36517009</PMID><DateRevised><Year>2022</Year><Month>12</Month><Day>14</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1880-2206</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Dec</Month><Day>13</Day></PubDate></JournalIssue><Title>Magnetic resonance in medical sciences : MRMS : an official journal of Japan Society of Magnetic Resonance in Medicine</Title><ISOAbbreviation>Magn Reson Med Sci</ISOAbbreviation></Journal><ArticleTitle>Associating the Severity of Emphysema with Coronary Flow Reserve and Left Atrial Conduit Function for the Emphysema Patients with Known or Suspected Coronary Artery Disease.</ArticleTitle><ELocationID EIdType="doi" ValidYN="Y">10.2463/mrms.mp.2022-0025</ELocationID><Abstract><AbstractText Label="PURPOSE" NlmCategory="OBJECTIVE">Pulmonary emphysema may associate with ischemic heart disease through systemic microvascular abnormality as a common pathway. Stress cardiovascular MR (CMR) allows for the assessment of global coronary flow reserve (CFR). The purpose of this study was to evaluate the association between the emphysema severity and the multiple MRI parameters in the emphysema patients with known or suspected coronary artery disease (CAD).<AbstractText Label="METHODS" NlmCategory="METHODS">A total of 210 patients with known or suspected CAD who underwent both 3.0T CMR including cine CMR, stress and rest perfusion CMR, stress and rest phase-contrast (PC) cine CMR of coronary sinus, and late gadolinium enhancement (LGE) CMR, and lung CT within 6 months were studied. Global CFR, volumes and functions of both ventricles and atria, and presence or absence of myocardial ischemia and infarction were evaluated. Emphysema severity was visually determined on lung CT by Goddard method.<AbstractText Label="RESULT" NlmCategory="RESULTS">Seventy nine (71.0 ± 7.9 years, 75 male) of 210 patients with known or suspected CAD had emphysema on lung CT. Goddard score was significantly correlated with CFR (r = -0.246, P = 0.029), left ventricular end-diastolic volume index (LV EDVI) (r = -0.230, P = 0.041), right ventricular systolic volume index (RV SVI) (r = -0.280, P = 0.012), left atrial (LA) total emptying volume index (r = -0.269, P = 0.017), LA passive emptying volume index (r = -0.309, P = 0.006), LA systolic strain (Es) (r = -0.244, P = 0.030), and LA conduit strain (Ee) (r = -0.285, P = 0.011) in the patients with emphysema. Multiple linear regression analysis revealed LA conduit function was independently associated with emphysema severity as determined by Goddard method (beta = -0.361, P = 0.006).<AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">LA conduit function independently associates with emphysema severity in the emphysema patients with known or suspected CAD after adjusting age, sex, smoking, and the CMR indexes including CFR. These findings suggest that impairment of LA function predominantly occurs prior to the reduction of the CFR in the emphysema patients with known or suspected CAD. |
2,329,304 | p53/p21 pathway activation contributes to the ependymal fate decision downstream of GemC1. | Multiciliated ependymal cells and adult neural stem cells are components of the adult neurogenic niche, essential for brain homeostasis. These cells share a common glial cell lineage regulated by the Geminin family members Geminin and GemC1/Mcidas. Ependymal precursors require GemC1/Mcidas expression to massively amplify centrioles and become multiciliated cells. Here, we show that GemC1-dependent differentiation is initiated in actively cycling radial glial cells, in which a DNA damage response, including DNA replication-associated damage and dysfunctional telomeres, is induced, without affecting cell survival. Genotoxic stress is not sufficient by itself to induce ependymal cell differentiation, although the absence of p53 or p21 in progenitors hinders differentiation by maintaining cell division. Activation of the p53-p21 pathway downstream of GemC1 leads to cell-cycle slowdown/arrest, which permits timely onset of ependymal cell differentiation in progenitor cells. |
2,329,305 | Endurance exercise under short-duration intermittent hypoxia promotes endurance performance via improving muscle metabolic properties in mice. | This study was designed to (1) investigate the effects of acute exercise under intermittent hypoxia on muscle mRNA and protein levels, and (2) clarify the mechanisms by which exercise under intermittent hypoxia improves endurance capacity. Experiment-1: Male mice were subjected to either acute endurance exercise, exercise under hypoxia (14% O<sub>2</sub> ), exercise under intermittent hypoxia (Int, three cycles of room air [10 min] and 14% O<sub>2</sub> [15 min]). At 3 h after exercise under intermittent hypoxia, sirtuin-6 mRNA levels and nuclear prolyl hydroxylases-2 protein levels were significantly upregulated in white gastrocnemius muscle in the Int group. Experiment-2: Mice were assigned to sedentary control (Sed), normoxic exercise-trained (ET), hypoxic exercise-trained (HYP) or exercise-trained under intermittent hypoxia (INT) groups. Exercise capacity was significantly greater in the INT group than in the ET and HYP group. Activity levels of citrate synthase were significantly greater in the INT group than in the HYP group in soleus (SOL) and red gastrocnemius muscles. In SOL, nuclear N-terminal PGC1α levels were considerably increased by the INT training (95% confidence interval [CI]: 1.09-1.79). The INT significantly increased pyruvate dehydrogenase complex activity levels in left ventricle (LV). Monocarboxylate transporter-4 protein levels were significantly increased after the INT training in LV. Capillary-to-fiber ratio values were significantly increased in SOL and were substantially increased in LV (CI: 1.10-1.22) after the INT training. These results suggest that exercise training under intermittent hypoxia represents a beneficial strategy for increasing endurance performance via improving metabolic properties and capillary profiles in several hind-leg muscles and the heart. |
2,329,306 | A rare coronary anomaly: The single left coronary artery with coronary artery fistula draining into the right ventricular outflow tract.<Pagination><StartPage>65</StartPage><EndPage>66</EndPage><MedlinePgn>65-66</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1111/echo.15508</ELocationID><Abstract><AbstractText>A previously healthy 9-year-old girl was referred to us for the evaluation of a murmur on a routine clinical examination. Routine electrocardiogram and chest x-ray were normal. The cardiac enzymes were normal. Combining ultrasound and CCTA, it was confirmed that the hemodynamics of the heart was a left-to-right shunt and that RVOT stole blood from the left ventricle through the single coronary artery (SCA).</AbstractText><CopyrightInformation>© 2022 Wiley Periodicals LLC.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Jie</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Radiology, Wuhan Asia Heart Hospital, Wuhan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hu</LastName><ForeName>Ping</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department of Radiology, Wuhan Asia Heart Hospital, Wuhan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ku</LastName><ForeName>Lei-Zhi</ForeName><Initials>LZ</Initials><AffiliationInfo><Affiliation>Department of Radiology, Wuhan Asia Heart Hospital, Wuhan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xia</LastName><ForeName>Juan</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Radiology, Wuhan Asia Heart Hospital, Wuhan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ma</LastName><ForeName>Xiao-Jing</ForeName><Initials>XJ</Initials><AffiliationInfo><Affiliation>Department of Radiology, Wuhan Asia Heart Hospital, Wuhan, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>12</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Echocardiography</MedlineTA><NlmUniqueID>8511187</NlmUniqueID><ISSNLinking>0742-2822</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002648" MajorTopicYN="N">Child</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017023" MajorTopicYN="N">Coronary Angiography</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006330" MajorTopicYN="Y">Heart Defects, Congenital</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005402" MajorTopicYN="Y">Fistula</DescriptorName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003324" MajorTopicYN="Y">Coronary Artery Disease</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003330" MajorTopicYN="Y">Coronary Vessel Anomalies</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">congenital heart disease</Keyword><Keyword MajorTopicYN="N">coronary artery fistula</Keyword><Keyword MajorTopicYN="N">single coronary artery</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>11</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>9</Month><Day>7</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>11</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>12</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2023</Year><Month>1</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>12</Month><Day>13</Day><Hour>5</Hour><Minute>13</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36511159</ArticleId><ArticleId IdType="doi">10.1111/echo.15508</ArticleId></ArticleIdList><ReferenceList><Title>REFERENCES</Title><Reference><Citation>Ishii Y, Suzuki T, Kobayashi T, et al. Single coronary artery with right ventricular fistula: case report and literature review. Congenit Heart Dis. 2010;1:56-59.</Citation></Reference><Reference><Citation>Carretero JM, Palacios JR, Prada FH. Single coronary artery-right ventricular fistula. Cardiol Young. 2012,2:209-212.</Citation></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36510796</PMID><DateRevised><Year>2022</Year><Month>12</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1467-1107</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Dec</Month><Day>13</Day></PubDate></JournalIssue><Title>Cardiology in the young</Title><ISOAbbreviation>Cardiol Young</ISOAbbreviation></Journal>Experiences and insights from partners of individuals with single-ventricle CHD: a pilot qualitative research study. | A previously healthy 9-year-old girl was referred to us for the evaluation of a murmur on a routine clinical examination. Routine electrocardiogram and chest x-ray were normal. The cardiac enzymes were normal. Combining ultrasound and CCTA, it was confirmed that the hemodynamics of the heart was a left-to-right shunt and that RVOT stole blood from the left ventricle through the single coronary artery (SCA).<CopyrightInformation>© 2022 Wiley Periodicals LLC.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Jie</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Radiology, Wuhan Asia Heart Hospital, Wuhan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hu</LastName><ForeName>Ping</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department of Radiology, Wuhan Asia Heart Hospital, Wuhan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ku</LastName><ForeName>Lei-Zhi</ForeName><Initials>LZ</Initials><AffiliationInfo><Affiliation>Department of Radiology, Wuhan Asia Heart Hospital, Wuhan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xia</LastName><ForeName>Juan</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Radiology, Wuhan Asia Heart Hospital, Wuhan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ma</LastName><ForeName>Xiao-Jing</ForeName><Initials>XJ</Initials><AffiliationInfo><Affiliation>Department of Radiology, Wuhan Asia Heart Hospital, Wuhan, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>12</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Echocardiography</MedlineTA><NlmUniqueID>8511187</NlmUniqueID><ISSNLinking>0742-2822</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002648" MajorTopicYN="N">Child</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017023" MajorTopicYN="N">Coronary Angiography</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006330" MajorTopicYN="Y">Heart Defects, Congenital</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005402" MajorTopicYN="Y">Fistula</DescriptorName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003324" MajorTopicYN="Y">Coronary Artery Disease</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003330" MajorTopicYN="Y">Coronary Vessel Anomalies</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">congenital heart disease</Keyword><Keyword MajorTopicYN="N">coronary artery fistula</Keyword><Keyword MajorTopicYN="N">single coronary artery</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>11</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>9</Month><Day>7</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>11</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>12</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2023</Year><Month>1</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>12</Month><Day>13</Day><Hour>5</Hour><Minute>13</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36511159</ArticleId><ArticleId IdType="doi">10.1111/echo.15508</ArticleId></ArticleIdList><ReferenceList><Title>REFERENCES</Title><Reference><Citation>Ishii Y, Suzuki T, Kobayashi T, et al. Single coronary artery with right ventricular fistula: case report and literature review. Congenit Heart Dis. 2010;1:56-59.</Citation></Reference><Reference><Citation>Carretero JM, Palacios JR, Prada FH. Single coronary artery-right ventricular fistula. Cardiol Young. 2012,2:209-212.</Citation></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36510796</PMID><DateRevised><Year>2022</Year><Month>12</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1467-1107</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Dec</Month><Day>13</Day></PubDate></JournalIssue><Title>Cardiology in the young</Title><ISOAbbreviation>Cardiol Young</ISOAbbreviation></Journal><ArticleTitle>Experiences and insights from partners of individuals with single-ventricle CHD: a pilot qualitative research study.</ArticleTitle><Pagination><StartPage>1</StartPage><EndPage>5</EndPage><MedlinePgn>1-5</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1017/S1047951122003882</ELocationID><Abstract><AbstractText Label="INTRODUCTION" NlmCategory="BACKGROUND">With advances in care, an increasing number of individuals with single-ventricle CHD are surviving into adulthood. Partners of individuals with chronic illness have unique experiences and challenges. The goal of this pilot qualitative research study was to explore the lived experiences of partners of individuals with single-ventricle CHD.<AbstractText Label="METHODS" NlmCategory="METHODS">Partners of patients ≥18 years with single-ventricle CHD were recruited and participated in Experience Group sessions and 1:1 interviews. Experience Group sessions are lightly moderated groups that bring together individuals with similar circumstances to discuss their lived experiences, centreing them as the experts. Formal inductive qualitative coding was performed to identify salient themes.<AbstractText Label="RESULTS" NlmCategory="RESULTS">Six partners of patients participated. Of these, four were males and four were married; all were partners of someone of the opposite sex. Themes identified included uncertainty about their partners' future health and mortality, becoming a lay CHD specialist, balancing multiple roles, and providing positivity and optimism. Over time, they took on a role as advocates for their partners and as repositories of medical history to help navigate the health system. Despite the uncertainties, participants described championing positivity and optimism for the future.<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">In this first-of-its-kind pilot study, partners of individuals with single-ventricle CHD expressed unique challenges and experiences in their lives. There is a tacit need to design strategies to help partners cope with those challenges. Further larger-scale research is required to better understand the experiences of this unique population. |
2,329,307 | Development of the Periventricular Nucleus as a Brain Center, Containing Dopaminergic Neurons and Neurons Expressing Individual Enzymes of Dopamine Synthesis. | We have recently shown that the periventricular nucleus (PeVN) of adult rats is a "mixed dopaminergic (DAergic) center" containing three thousand neurons: DAergic neurons and those expressing one of the dopamine (DA)-synthesizing enzymes. This study aims to evaluate the development of the PeVN as a mixed DAergic center in rats in the perinatal period, critical for brain morphogenesis. During this period, the PeVN contains DAergic neurons and monoenzymatic neurons expressing individual enzymes of DA synthesis: tyrosine hydroxylase (TH) or aromatic L-amino acid decarboxylase (AADC). In the perinatal period, the total number of such neurons triples, mainly due to monoenzymatic neurons; the content of L-DOPA, the end product of monoenzymatic TH neurons, doubles; and the content of DA, the end product of monoenzymatic AADC neurons and DAergic neurons, increases sixfold. Confocal microscopy has shown that, in the PeVN, all types of neurons and their processes are in close relationships, which suggests their mutual regulation by L-DOPA and DA. In addition, monoenzymatic and DAergic fibers are close to the third cerebral ventricle, located in the subependymal zone, between ependymal cells and in the supraependymal zone. These observations suggest that these fibers deliver L-DOPA and DA to the cerebrospinal fluid, participating in the neuroendocrine regulation of the brain. |
2,329,308 | Zebrafish as an Orthotopic Tumor Model for Retinoblastoma Mimicking Routes of Human Metastasis. | Retinoblastoma (RB) is the most common eye cancer in children that has a high mortality rate when left untreated. Mouse models for retinoblastoma have been established but are time- and cost-intensive. The aim of this work was to evaluate an orthotopic transplantation model of retinoblastoma in zebrafish that also allows for tracking migratory routes and to explore advantages and disadvantages with respect to drug testing.</AbstractText>Three fluorescence-labeled retinoblastoma cell lines (RB355, WERI-RB-1, Y79) were injected into the left eye of two-day-old zebrafish, while the un-injected right eye served as control. The migratory trajectories of injected retinoblastoma cells were observed until 8 days post injection (dpi), both in lateral and dorsal view, and measuring fluorescence intensity of injected cells was done for RB355 cells.</AbstractText>Time until the onset of migration and routes for all three retinoblastoma cell lines were comparable and resulted in migration into the brain and ventricles of the forebrain, midbrain and hindbrain. Involvement of the optic nerve was observed in 10% of injections with the RB355 cell line, 15% with Y79 cells and 5% with WERI-RB-1 cells. Fluorescence intensity of injected RB355 cells showed an initial increase until five dpi, but then decreased with high variability until the end of observation.</AbstractText>The zebrafish eye is well suited for the analysis of migratory routes in retinoblastoma and closely mirrors patterns of retinoblastoma metastases in humans.</AbstractText> |
2,329,309 | Early Coronary Artery Calcification Progression over Two Years in Breast Cancer Patients Treated with Radiation Therapy: Association with Cardiac Exposure (BACCARAT Study).<ELocationID EIdType="pii" ValidYN="Y">5724</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.3390/cancers14235724</ELocationID><Abstract><AbstractText>Background: Radiotherapy (RT) for breast cancer (BC) can induce coronary artery disease many years after RT. At an earlier stage, during the first two years after RT, we aimed to evaluate the occurrence of increased coronary artery calcium (CAC) and its association with cardiac exposure. Methods: This prospective study included 101 BC patients treated with RT without chemotherapy. Based on CAC CT scans performed before and two years after RT, the event ‘CAC progression’ was defined by an increase in overall CAC score (CAC RT+ two years—CAC before RT > 0). Dosimetry was evaluated for whole heart, left ventricle (LV), and coronary arteries. Multivariable logistic regression models were used to assess association with doses. Results: Two years after RT, 28 patients presented the event ‘CAC progression’, explained in 93% of cases by a higher CAC score in the left anterior descending coronary (LAD). A dose−response relationship was observed with LV exposure (for Dmean LV: OR = 1.15, p = 0.04). LAD exposure marginally explained increased CAC in the LAD (for D2 LV: OR =1.03, p = 0.07). Conclusion: The risk of early CAC progression may be associated with LV exposure. This progression might primarily be a consequence of CAC increase in the LAD and its exposure.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Honaryar</LastName><ForeName>Manoj Kumar</ForeName><Initials>MK</Initials><Identifier Source="ORCID">0000-0002-6784-0309</Identifier><AffiliationInfo><Affiliation>INSERM U 1018, CESP, Radiation Epidemiology Team, 94800 Villejuif, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Allodji</LastName><ForeName>Rodrigue</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>INSERM U 1018, CESP, Radiation Epidemiology Team, 94800 Villejuif, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institute Gustave Roussy, 94800 Villejuif, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>University Paris-Saclay, 94800 Villejuif, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ferrières</LastName><ForeName>Jean</ForeName><Initials>J</Initials><Identifier Source="ORCID">0000-0001-6144-1297</Identifier><AffiliationInfo><Affiliation>Department of Cardiology and INSERM UMR 1295, Rangueil University Hospital, 31400 Toulouse, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Panh</LastName><ForeName>Loïc</ForeName><Initials>L</Initials><Identifier Source="ORCID">0000-0002-2775-8546</Identifier><AffiliationInfo><Affiliation>Department of Cardiology, Clinique Pasteur, 31076 Toulouse, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Locquet</LastName><ForeName>Médéa</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Laboratory of Epidemiology, Institute for Radiation Protection and Nuclear Safety (IRSN), 92260 Fontenay-Aux-Roses, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jimenez</LastName><ForeName>Gaelle</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Department of Radiation Oncology (Oncorad), Clinique Pasteur, 31076 Toulouse, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lapeyre</LastName><ForeName>Matthieu</ForeName><Initials>M</Initials><Identifier Source="ORCID">0000-0002-2517-2111</Identifier><AffiliationInfo><Affiliation>Department of Radiology (GRX), Clinique Pasteur, 31076 Toulouse, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Camilleri</LastName><ForeName>Jérémy</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Radiation Oncology (Oncorad), Clinique Pasteur, 31076 Toulouse, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Broggio</LastName><ForeName>David</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Dosimetry, Institute for Radiation Protection and Nuclear Safety (IRSN), 92260 Fontenay-Aux-Roses, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>de Vathaire</LastName><ForeName>Florent</ForeName><Initials>F</Initials><Identifier Source="ORCID">0000-0002-8374-9281</Identifier><AffiliationInfo><Affiliation>INSERM U 1018, CESP, Radiation Epidemiology Team, 94800 Villejuif, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institute Gustave Roussy, 94800 Villejuif, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>University Paris-Saclay, 94800 Villejuif, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jacob</LastName><ForeName>Sophie</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Laboratory of Epidemiology, Institute for Radiation Protection and Nuclear Safety (IRSN), 92260 Fontenay-Aux-Roses, France.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList 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Protoc. 2018;7:e178. doi: 10.2196/resprot.9906.</Citation><ArticleIdList><ArticleId IdType="doi">10.2196/resprot.9906</ArticleId><ArticleId IdType="pmc">PMC6242210</ArticleId><ArticleId IdType="pubmed">30274965</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedBookArticle><BookDocument><PMID Version="1">36508532</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK587358</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-146287">Pulmonary Hypertension Due to Lung Disease or Hypoxia | Background: Radiotherapy (RT) for breast cancer (BC) can induce coronary artery disease many years after RT. At an earlier stage, during the first two years after RT, we aimed to evaluate the occurrence of increased coronary artery calcium (CAC) and its association with cardiac exposure. Methods: This prospective study included 101 BC patients treated with RT without chemotherapy. Based on CAC CT scans performed before and two years after RT, the event ‘CAC progression’ was defined by an increase in overall CAC score (CAC RT+ two years—CAC before RT > 0). Dosimetry was evaluated for whole heart, left ventricle (LV), and coronary arteries. Multivariable logistic regression models were used to assess association with doses. Results: Two years after RT, 28 patients presented the event ‘CAC progression’, explained in 93% of cases by a higher CAC score in the left anterior descending coronary (LAD). A dose−response relationship was observed with LV exposure (for Dmean LV: OR = 1.15, p = 0.04). LAD exposure marginally explained increased CAC in the LAD (for D2 LV: OR =1.03, p = 0.07). Conclusion: The risk of early CAC progression may be associated with LV exposure. This progression might primarily be a consequence of CAC increase in the LAD and its exposure.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Honaryar</LastName><ForeName>Manoj Kumar</ForeName><Initials>MK</Initials><Identifier Source="ORCID">0000-0002-6784-0309</Identifier><AffiliationInfo><Affiliation>INSERM U 1018, CESP, Radiation Epidemiology Team, 94800 Villejuif, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Allodji</LastName><ForeName>Rodrigue</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>INSERM U 1018, CESP, Radiation Epidemiology Team, 94800 Villejuif, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institute Gustave Roussy, 94800 Villejuif, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>University Paris-Saclay, 94800 Villejuif, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ferrières</LastName><ForeName>Jean</ForeName><Initials>J</Initials><Identifier Source="ORCID">0000-0001-6144-1297</Identifier><AffiliationInfo><Affiliation>Department of Cardiology and INSERM UMR 1295, Rangueil University Hospital, 31400 Toulouse, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Panh</LastName><ForeName>Loïc</ForeName><Initials>L</Initials><Identifier Source="ORCID">0000-0002-2775-8546</Identifier><AffiliationInfo><Affiliation>Department of Cardiology, Clinique Pasteur, 31076 Toulouse, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Locquet</LastName><ForeName>Médéa</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Laboratory of Epidemiology, Institute for Radiation Protection and Nuclear Safety (IRSN), 92260 Fontenay-Aux-Roses, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jimenez</LastName><ForeName>Gaelle</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Department of Radiation Oncology (Oncorad), Clinique Pasteur, 31076 Toulouse, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lapeyre</LastName><ForeName>Matthieu</ForeName><Initials>M</Initials><Identifier Source="ORCID">0000-0002-2517-2111</Identifier><AffiliationInfo><Affiliation>Department of Radiology (GRX), Clinique Pasteur, 31076 Toulouse, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Camilleri</LastName><ForeName>Jérémy</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Radiation Oncology (Oncorad), Clinique Pasteur, 31076 Toulouse, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Broggio</LastName><ForeName>David</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Dosimetry, Institute for Radiation Protection and Nuclear Safety (IRSN), 92260 Fontenay-Aux-Roses, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>de Vathaire</LastName><ForeName>Florent</ForeName><Initials>F</Initials><Identifier Source="ORCID">0000-0002-8374-9281</Identifier><AffiliationInfo><Affiliation>INSERM U 1018, CESP, Radiation Epidemiology Team, 94800 Villejuif, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institute Gustave Roussy, 94800 Villejuif, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>University Paris-Saclay, 94800 Villejuif, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jacob</LastName><ForeName>Sophie</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Laboratory of Epidemiology, Institute for Radiation Protection and Nuclear Safety (IRSN), 92260 Fontenay-Aux-Roses, France.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>AEPET2016-JF</GrantID><Agency>Fédération française de cardiologie</Agency><Country/></Grant><Grant><GrantID>CE2016-SJ</GrantID><Agency>Électricité de France (France)</Agency><Country/></Grant><Grant><GrantID>755523</GrantID><Agency>H2020 Euratom research and training program 2014-2018</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>11</Month><Day>22</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Cancers (Basel)</MedlineTA><NlmUniqueID>101526829</NlmUniqueID><ISSNLinking>2072-6694</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">breast cancer</Keyword><Keyword MajorTopicYN="N">cardiotoxicity</Keyword><Keyword MajorTopicYN="N">coronary artery calcification</Keyword><Keyword MajorTopicYN="N">dosimetry</Keyword><Keyword 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2,329,310 | Systemic arterial pulsatility (SAPi) in advanced heart failure: a novel hemodynamic risk stratification tool.<Pagination><StartPage>1093</StartPage><EndPage>1094</EndPage><MedlinePgn>1093-1094</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s00380-022-02217-6</ELocationID><Abstract><AbstractText>Systemic arterial pulsatility index (SAPi) is a novel hemodynamic marker for ventriculo-arterial coupling (VAC), as it integrates the contractile properties of the left ventricle with the aortic impendence. SAPi can identify heart failure patients at increased risk for adverse events. Systemic pulsatility decreases as heart failure progresses, and there is a decrease in pulse pressure accompanied by an increase in left ventricular filling pressure. Decreasing SAPi is associated with worse prognosis in advanced heart failure patients.</AbstractText><CopyrightInformation>© 2022. Springer Japan KK, part of Springer Nature.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Mazimba</LastName><ForeName>Sula</ForeName><Initials>S</Initials><Identifier Source="ORCID">0000-0001-6451-2118</Identifier><AffiliationInfo><Affiliation>UVA Division of Cardiovascular Medicine, University of Virginia Health System, 1215 Lee St, PO Box 800158, Charlottesville, Virginia, United States. SM8SD@hscmail.mcc.virginia.edu.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bilchick</LastName><ForeName>Kenneth C</ForeName><Initials>KC</Initials><AffiliationInfo><Affiliation>UVA Division of Cardiovascular Medicine, University of Virginia Health System, 1215 Lee St, PO Box 800158, Charlottesville, Virginia, United States.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016422">Letter</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>12</Month><Day>09</Day></ArticleDate></Article><MedlineJournalInfo><Country>Japan</Country><MedlineTA>Heart Vessels</MedlineTA><NlmUniqueID>8511258</NlmUniqueID><ISSNLinking>0910-8327</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006333" MajorTopicYN="Y">Heart Failure</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006439" MajorTopicYN="N">Hemodynamics</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001158" MajorTopicYN="N">Arteries</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001794" MajorTopicYN="N">Blood Pressure</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018570" MajorTopicYN="N">Risk Assessment</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016277" MajorTopicYN="N">Ventricular Function, Left</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>11</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>12</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2023</Year><Month>6</Month><Day>26</Day><Hour>6</Hour><Minute>42</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>12</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>12</Month><Day>9</Day><Hour>11</Hour><Minute>14</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36484814</ArticleId><ArticleId IdType="doi">10.1007/s00380-022-02217-6</ArticleId><ArticleId IdType="pii">10.1007/s00380-022-02217-6</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Mazimba S, Mwansa H, Breathett K, Strickling JE, Shah K, McNamara C, Mehta N, Kwon Y, Lamp J, Feng L, Tallaj J, Pamboukian S, Mubanga M, Matharoo J, Lim S, Salerno M, Mwansa V, Bilchick KC (2022) Systemic arterial pulsatility index (SAPi) predicts adverse outcomes in advanced heart failure patients. 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Circulation 102(15):1788–1794</Citation><ArticleIdList><ArticleId IdType="doi">10.1161/01.CIR.102.15.1788</ArticleId><ArticleId IdType="pubmed">11023933</ArticleId></ArticleIdList></Reference><Reference><Citation>Kane CJ, Salama AA, Pislaru C, Kane GC, Pislaru SV, Lin G (2022) Low pulmonary artery pulsatility index by echocardiography is associated with increased mortality in pulmonary hypertension. J Am Soc Echocardiogr. https://doi.org/10.1016/j.echo.2022.09.003</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.echo.2022.09.003</ArticleId><ArticleId IdType="pubmed">36368437</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36484131</PMID><DateRevised><Year>2022</Year><Month>12</Month><Day>09</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1467-1107</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Dec</Month><Day>09</Day></PubDate></JournalIssue><Title>Cardiology in the young</Title><ISOAbbreviation>Cardiol Young</ISOAbbreviation></Journal>Facilitators and barriers of physical activity participation in children with a single ventricle physiology: a mixed-methods study.<Pagination><StartPage>1</StartPage><EndPage>8</EndPage><MedlinePgn>1-8</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1017/S1047951122003754</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">The present study focuses on assessing the physical activity level of children with Fontan circulation for Hypoplastic Left Heart Syndrome and identifying potential barriers and facilitators toward their participation in physical activity.</AbstractText><AbstractText Label="PATIENTS AND METHODS" NlmCategory="METHODS">Seven children aged 5-16 years (mean (SD) 8.8 (3.7) years) with a Fontan procedure for hypoplastic left heart syndrome, their parents (n = 7), and siblings (n = 1) were recruited. Data were collected using a mixed-methods approach: (i) children wore an activity monitor for 7 days to record physical activity, with sedentary time and level of activity calculated from accelerometer data; (ii) children completed a bespoke questionnaire recording limitations in physical activity; (iii) parents completed a semi-structured interview discussing perceptions about their child's physical activity participation. Qualitative data were analysed using thematic analysis.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Activity monitors data recorded highly active children with a mean (SD) of 153(36) minutes/day spent in moderate-to-vigorous physical activity. Time spent in sedentary behaviour was also high (57.5% of total accelerometer wearing-time). Four key themes relating to parental perceptions of physical activity were identified: (i) A new lease of life -post-Fontan; (ii) Setting limits - managing limitations; (iii) The wider world - how others set limits; and (iv) "I fear the future" - parental concerns.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">Following completion of the Fontan circulation, children engaged in higher levels of physical activity in comparison to the national average. However, more than half their time was spent in sedentary behaviour. Fears and anxiety from parents and teachers may act as a barrier toward physical activity participation.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Leo</LastName><ForeName>Donato Giuseppe</ForeName><Initials>DG</Initials><Identifier Source="ORCID">0000-0002-0709-3073</Identifier><AffiliationInfo><Affiliation>Department of Cardiovascular and Metabolic Medicine, Institute of Life Course and Medical Sciences, Faculty of Health and Life Sciences, University of Liverpool, Liverpool, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Liverpool Centre for Cardiovascular Science, University of Liverpool and Liverpool Heart and Chest, Liverpool, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lane</LastName><ForeName>Deirdre A</ForeName><Initials>DA</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular and Metabolic Medicine, Institute of Life Course and Medical Sciences, Faculty of Health and Life Sciences, University of Liverpool, Liverpool, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Liverpool Centre for Cardiovascular Science, University of Liverpool and Liverpool Heart and Chest, Liverpool, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Riley</LastName><ForeName>Marlene</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Paediatric Cardiac Surgery, Alder Hey Children's Hospital, Liverpool, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lotto</LastName><ForeName>Attilio A</ForeName><Initials>AA</Initials><AffiliationInfo><Affiliation>Liverpool Centre for Cardiovascular Science, University of Liverpool and Liverpool Heart and Chest, Liverpool, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Paediatric Cardiac Surgery, Alder Hey Children's Hospital, Liverpool, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>School of Nursing and Allied Health, Faculty of Health, Liverpool John Moores University, Liverpool, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lotto</LastName><ForeName>Robyn R</ForeName><Initials>RR</Initials><Identifier Source="ORCID">0000-0002-4305-0513</Identifier><AffiliationInfo><Affiliation>Liverpool Centre for Cardiovascular Science, University of Liverpool and Liverpool Heart and Chest, Liverpool, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>School of Nursing and Allied Health, Faculty of Health, Liverpool John Moores University, Liverpool, UK.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>12</Month><Day>09</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Cardiol Young</MedlineTA><NlmUniqueID>9200019</NlmUniqueID><ISSNLinking>1047-9511</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Congenital heart disease</Keyword><Keyword MajorTopicYN="N">hypoplastic left heart syndrome</Keyword><Keyword MajorTopicYN="N">mixed-methods</Keyword><Keyword MajorTopicYN="N">physical activity</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>12</Month><Day>9</Day><Hour>4</Hour><Minute>21</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>12</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>12</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>aheadofprint</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36484131</ArticleId><ArticleId IdType="doi">10.1017/S1047951122003754</ArticleId><ArticleId IdType="pii">S1047951122003754</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36484129</PMID><DateRevised><Year>2022</Year><Month>12</Month><Day>09</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1467-1107</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Dec</Month><Day>09</Day></PubDate></JournalIssue><Title>Cardiology in the young</Title><ISOAbbreviation>Cardiol Young</ISOAbbreviation></Journal>Wayfinding through the "ocean of the great unknown": how lactating parents establish a direct breastfeeding relationship with an infant with critical CHD. | Systemic arterial pulsatility index (SAPi) is a novel hemodynamic marker for ventriculo-arterial coupling (VAC), as it integrates the contractile properties of the left ventricle with the aortic impendence. SAPi can identify heart failure patients at increased risk for adverse events. Systemic pulsatility decreases as heart failure progresses, and there is a decrease in pulse pressure accompanied by an increase in left ventricular filling pressure. Decreasing SAPi is associated with worse prognosis in advanced heart failure patients.<CopyrightInformation>© 2022. Springer Japan KK, part of Springer Nature.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Mazimba</LastName><ForeName>Sula</ForeName><Initials>S</Initials><Identifier Source="ORCID">0000-0001-6451-2118</Identifier><AffiliationInfo><Affiliation>UVA Division of Cardiovascular Medicine, University of Virginia Health System, 1215 Lee St, PO Box 800158, Charlottesville, Virginia, United States. SM8SD@hscmail.mcc.virginia.edu.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bilchick</LastName><ForeName>Kenneth C</ForeName><Initials>KC</Initials><AffiliationInfo><Affiliation>UVA Division of Cardiovascular Medicine, University of Virginia Health System, 1215 Lee St, PO Box 800158, Charlottesville, Virginia, United States.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016422">Letter</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>12</Month><Day>09</Day></ArticleDate></Article><MedlineJournalInfo><Country>Japan</Country><MedlineTA>Heart Vessels</MedlineTA><NlmUniqueID>8511258</NlmUniqueID><ISSNLinking>0910-8327</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006333" MajorTopicYN="Y">Heart Failure</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006439" MajorTopicYN="N">Hemodynamics</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001158" MajorTopicYN="N">Arteries</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001794" MajorTopicYN="N">Blood Pressure</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018570" MajorTopicYN="N">Risk Assessment</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016277" MajorTopicYN="N">Ventricular Function, Left</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>11</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>12</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2023</Year><Month>6</Month><Day>26</Day><Hour>6</Hour><Minute>42</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>12</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>12</Month><Day>9</Day><Hour>11</Hour><Minute>14</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36484814</ArticleId><ArticleId IdType="doi">10.1007/s00380-022-02217-6</ArticleId><ArticleId IdType="pii">10.1007/s00380-022-02217-6</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Mazimba S, Mwansa H, Breathett K, Strickling JE, Shah K, McNamara C, Mehta N, Kwon Y, Lamp J, Feng L, Tallaj J, Pamboukian S, Mubanga M, Matharoo J, Lim S, Salerno M, Mwansa V, Bilchick KC (2022) Systemic arterial pulsatility index (SAPi) predicts adverse outcomes in advanced heart failure patients. 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Circulation 102(15):1788–1794</Citation><ArticleIdList><ArticleId IdType="doi">10.1161/01.CIR.102.15.1788</ArticleId><ArticleId IdType="pubmed">11023933</ArticleId></ArticleIdList></Reference><Reference><Citation>Kane CJ, Salama AA, Pislaru C, Kane GC, Pislaru SV, Lin G (2022) Low pulmonary artery pulsatility index by echocardiography is associated with increased mortality in pulmonary hypertension. J Am Soc Echocardiogr. https://doi.org/10.1016/j.echo.2022.09.003</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.echo.2022.09.003</ArticleId><ArticleId IdType="pubmed">36368437</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36484131</PMID><DateRevised><Year>2022</Year><Month>12</Month><Day>09</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1467-1107</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Dec</Month><Day>09</Day></PubDate></JournalIssue><Title>Cardiology in the young</Title><ISOAbbreviation>Cardiol Young</ISOAbbreviation></Journal><ArticleTitle>Facilitators and barriers of physical activity participation in children with a single ventricle physiology: a mixed-methods study.</ArticleTitle><Pagination><StartPage>1</StartPage><EndPage>8</EndPage><MedlinePgn>1-8</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1017/S1047951122003754</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">The present study focuses on assessing the physical activity level of children with Fontan circulation for Hypoplastic Left Heart Syndrome and identifying potential barriers and facilitators toward their participation in physical activity.<AbstractText Label="PATIENTS AND METHODS" NlmCategory="METHODS">Seven children aged 5-16 years (mean (SD) 8.8 (3.7) years) with a Fontan procedure for hypoplastic left heart syndrome, their parents (n = 7), and siblings (n = 1) were recruited. Data were collected using a mixed-methods approach: (i) children wore an activity monitor for 7 days to record physical activity, with sedentary time and level of activity calculated from accelerometer data; (ii) children completed a bespoke questionnaire recording limitations in physical activity; (iii) parents completed a semi-structured interview discussing perceptions about their child's physical activity participation. Qualitative data were analysed using thematic analysis.<AbstractText Label="RESULTS" NlmCategory="RESULTS">Activity monitors data recorded highly active children with a mean (SD) of 153(36) minutes/day spent in moderate-to-vigorous physical activity. Time spent in sedentary behaviour was also high (57.5% of total accelerometer wearing-time). Four key themes relating to parental perceptions of physical activity were identified: (i) A new lease of life -post-Fontan; (ii) Setting limits - managing limitations; (iii) The wider world - how others set limits; and (iv) "I fear the future" - parental concerns.<AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">Following completion of the Fontan circulation, children engaged in higher levels of physical activity in comparison to the national average. However, more than half their time was spent in sedentary behaviour. Fears and anxiety from parents and teachers may act as a barrier toward physical activity participation.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Leo</LastName><ForeName>Donato Giuseppe</ForeName><Initials>DG</Initials><Identifier Source="ORCID">0000-0002-0709-3073</Identifier><AffiliationInfo><Affiliation>Department of Cardiovascular and Metabolic Medicine, Institute of Life Course and Medical Sciences, Faculty of Health and Life Sciences, University of Liverpool, Liverpool, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Liverpool Centre for Cardiovascular Science, University of Liverpool and Liverpool Heart and Chest, Liverpool, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lane</LastName><ForeName>Deirdre A</ForeName><Initials>DA</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular and Metabolic Medicine, Institute of Life Course and Medical Sciences, Faculty of Health and Life Sciences, University of Liverpool, Liverpool, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Liverpool Centre for Cardiovascular Science, University of Liverpool and Liverpool Heart and Chest, Liverpool, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Riley</LastName><ForeName>Marlene</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Paediatric Cardiac Surgery, Alder Hey Children's Hospital, Liverpool, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lotto</LastName><ForeName>Attilio A</ForeName><Initials>AA</Initials><AffiliationInfo><Affiliation>Liverpool Centre for Cardiovascular Science, University of Liverpool and Liverpool Heart and Chest, Liverpool, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Paediatric Cardiac Surgery, Alder Hey Children's Hospital, Liverpool, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>School of Nursing and Allied Health, Faculty of Health, Liverpool John Moores University, Liverpool, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lotto</LastName><ForeName>Robyn R</ForeName><Initials>RR</Initials><Identifier Source="ORCID">0000-0002-4305-0513</Identifier><AffiliationInfo><Affiliation>Liverpool Centre for Cardiovascular Science, University of Liverpool and Liverpool Heart and Chest, Liverpool, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>School of Nursing and Allied Health, Faculty of Health, Liverpool John Moores University, Liverpool, UK.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>12</Month><Day>09</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Cardiol Young</MedlineTA><NlmUniqueID>9200019</NlmUniqueID><ISSNLinking>1047-9511</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Congenital heart disease</Keyword><Keyword MajorTopicYN="N">hypoplastic left heart syndrome</Keyword><Keyword MajorTopicYN="N">mixed-methods</Keyword><Keyword MajorTopicYN="N">physical activity</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>12</Month><Day>9</Day><Hour>4</Hour><Minute>21</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>12</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>12</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>aheadofprint</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36484131</ArticleId><ArticleId IdType="doi">10.1017/S1047951122003754</ArticleId><ArticleId IdType="pii">S1047951122003754</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36484129</PMID><DateRevised><Year>2022</Year><Month>12</Month><Day>09</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1467-1107</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Dec</Month><Day>09</Day></PubDate></JournalIssue><Title>Cardiology in the young</Title><ISOAbbreviation>Cardiol Young</ISOAbbreviation></Journal><ArticleTitle>Wayfinding through the "ocean of the great unknown": how lactating parents establish a direct breastfeeding relationship with an infant with critical CHD.</ArticleTitle><Pagination><StartPage>1</StartPage><EndPage>12</EndPage><MedlinePgn>1-12</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1017/S1047951122003808</ELocationID><Abstract><AbstractText Label="INTRODUCTION" NlmCategory="BACKGROUND">Lactating parents of infants hospitalised for critical congenital heart disease (CHD) face significant barriers to direct breastfeeding. While experiences of directly breastfeeding other hospitalised neonates have been described, studies including infants with critical CHD are scarce. There is no evidence-based standard of direct breastfeeding care for these infants, and substantial practice variation exists.<AbstractText Label="AIM" NlmCategory="OBJECTIVE">To explain how direct breastfeeding is established with an infant hospitalised for critical CHD, from lactating parents' perspectives.<AbstractText Label="MATERIALS & METHODS" NlmCategory="METHODS">This study is a qualitative grounded dimensional analysis of interviews with 30 lactating parents of infants with critical CHD who directly breastfed within 3 years. Infants received care from 26 United States cardiac centres; 57% had single ventricle physiology. Analysis included open, axial, and selective coding; memoing; member checking; and explanatory matrices.<AbstractText Label="RESULTS" NlmCategory="RESULTS">Findings were represented by a conceptual model, "Wayfinding through the 'ocean of the great unknown'." The core process of Wayfinding involved a nonlinear trajectory requiring immense persistence in navigating obstacles, occurring in a context of life-and-death consequences for the infant. Wayfinding was characterised by three subprocesses: navigating the relationship with the healthcare team; protecting the direct breastfeeding relationship; and doing the long, hard work. Primary influencing conditions included relentless concern about weight gain, the infant's clinical course, and the parent's previous direct breastfeeding experience.<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">For parents, engaging in the Wayfinding process to establish direct breastfeeding was feasible and meaningful - though challenging. The conceptual model of Wayfinding explains how direct breastfeeding can be established and provides a framework for research and practice. |
2,329,311 | Different profiles of lipoprotein particles associate various degrees of cardiac involvement in adolescents with morbid obesity.<Pagination><StartPage>887771</StartPage><MedlinePgn>887771</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">887771</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.3389/fped.2022.887771</ELocationID><Abstract><AbstractText Label="INTRODUCTION" NlmCategory="UNASSIGNED">Dyslipidemia secondary to obesity is a risk factor related to cardiovascular disease events, however a pathological conventional lipid profile (CLP) is infrequently found in obese children. The objective is to evaluate the advanced lipoprotein testing (ALT) and its relationship with cardiac changes, metabolic syndrome (MS) and inflammatory markers in a population of morbidly obese adolescents with normal CLP and without type 2 diabetes mellitus, the most common scenario in obese adolescents.</AbstractText><AbstractText Label="METHODS" NlmCategory="UNASSIGNED">Prospective case-control research of 42 morbidly obese adolescents and 25 normal-weight adolescents, whose left ventricle (LV) morphology and function had been assessed. The ALT was obtained by proton nuclear magnetic resonance spectroscopy, and the results were compared according to the degree of cardiac involvement - normal heart, mild LV changes, and severe LV changes (specifically LV remodeling and systolic dysfunction) - and related to inflammation markers [highly-sensitive C-reactive protein and glycoprotein A (GlycA)] and insulin-resistance [homeostatic model assessment for insulin-resistance (HOMA-IR)]. A second analysis was performed to compare our results with the predominant ALT when only body mass index and metabolic syndrome criteria were considered.</AbstractText><AbstractText Label="RESULTS" NlmCategory="UNASSIGNED">The three cardiac involvement groups showed significant increases in HOMA-IR, inflammatory markers and ALT ratio LDL-P/HDL-P (40.0 vs. 43.9 vs. 47.1, <i>p</i> 0.012). When only cardiac change groups were considered, differences in small LDL-P (565.0 vs. 625.1 nmol/L, <i>p</i> 0.070), VLDL size and GlycA demonstrated better utility than just traditional risk factors to predict which subjects could present severe LV changes [AUC: 0.79 (95% CI: 0.54-1)]. In the second analysis, an atherosclerotic ALT was detected in morbidly obese subjects, characterized by a significant increase in large VLDL-P, small LDL-P, ratio LDL-P/HDL-P and ratio HDL-TG/HDL-C. Subjects with criteria for MS presented overall worse ALT (specially in triglyceride-enriched particles) and remnant cholesterol values.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="UNASSIGNED">ALT parameters and GlycA appear to be more reliable indicators of cardiac change severity than traditional CV risk factors. Particularly, the overage of LDL-P compared to HDL-P and the increase in small LDL-P with cholesterol-depleted LDL particles appear to be the key ALT's parameters involved in LV changes. Morbidly obese adolescents show an atherosclerotic ALT and those with MS present worse ALT values.</AbstractText><CopyrightInformation>© 2022 Siurana, Sabaté-Rotés, Amigó, Martínez-Micaelo, Arciniegas, Riaza, Mogas, Rosés-Noguer, Ventura and Yeste.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Siurana</LastName><ForeName>José M</ForeName><Initials>JM</Initials><AffiliationInfo><Affiliation>Department of Pediatric Cardiology, Hospital HM Nens, HM Hospitales, Barcelona, Spain.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Autonomous University of Barcelona, Barcelona, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sabaté-Rotés</LastName><ForeName>Anna</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Autonomous University of Barcelona, Barcelona, Spain.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Pediatric Cardiology, Vall d'Hebron University Hospital, Barcelona, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Amigó</LastName><ForeName>Núria</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Biosfer Teslab, Reus, Spain.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Basic Medical Sciences, Universitat Rovira I Virgili, Institut D'Investigació Sanitària Pere Virgili (IISPV), Tarragona, Spain.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Instituto de Salud Carlos III (ISCIII), Madrid, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Martínez-Micaelo</LastName><ForeName>Neus</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Biosfer Teslab, Reus, Spain.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Basic Medical Sciences, Universitat Rovira I Virgili, Institut D'Investigació Sanitària Pere Virgili (IISPV), Tarragona, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Arciniegas</LastName><ForeName>Larry</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Pediatric Endocrinology, Vall d'Hebron University Hospital, Barcelona, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Riaza</LastName><ForeName>Lucia</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Pediatric Radiology, Vall d'Hebron University Hospital, Barcelona, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mogas</LastName><ForeName>Eduard</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Department of Pediatric Endocrinology, Vall d'Hebron University Hospital, Barcelona, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rosés-Noguer</LastName><ForeName>Ferran</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Autonomous University of Barcelona, Barcelona, Spain.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Pediatric Cardiology, Vall d'Hebron University Hospital, Barcelona, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ventura</LastName><ForeName>Paula S</ForeName><Initials>PS</Initials><AffiliationInfo><Affiliation>Department of Pediatric Endocrinology, Hospital HM Nens, HM Hospitales, Barcelona, Spain.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Fundació Institut d'Investigació en Ciències de la Salut Germans Trias i Pujol (IGTP), Badalona, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yeste</LastName><ForeName>Diego</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Autonomous University of Barcelona, Barcelona, Spain.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Pediatric Endocrinology, Vall d'Hebron University Hospital, Barcelona, Spain.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Instituto de Salud Carlos III (ISCIII), Madrid, Spain.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>11</Month><Day>22</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Front Pediatr</MedlineTA><NlmUniqueID>101615492</NlmUniqueID><ISSNLinking>2296-2360</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">adolescents</Keyword><Keyword MajorTopicYN="N">atherosclerotic phenotype</Keyword><Keyword MajorTopicYN="N">cardiac changes</Keyword><Keyword MajorTopicYN="N">lipoprotein subclasses</Keyword><Keyword MajorTopicYN="N">metabolic syndrome</Keyword><Keyword MajorTopicYN="N">morbid obesity</Keyword><Keyword MajorTopicYN="N">small LDL particles</Keyword><Keyword MajorTopicYN="N">systolic dysfunction</Keyword></KeywordList><CoiStatement>NA has a patent and is stock owner of Biosfer Teslab, the company that commercializes the lipoprotein profiling described in the present manuscript. This study received funding from Novo Nordisk Pharma S.A. through “The Growth and Development Group” of the Vall d’Hebron Research Institute. The funder was not involved in the study design, collection, analysis, interpretation of data, the writing of this article or the decision to submit it for publication. All authors declare no other competing interests.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>3</Month><Day>2</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>11</Month><Day>2</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>12</Month><Day>9</Day><Hour>4</Hour><Minute>2</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>12</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>12</Month><Day>10</Day><Hour>6</Hour><Minute>1</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36483472</ArticleId><ArticleId IdType="pmc">PMC9723388</ArticleId><ArticleId IdType="doi">10.3389/fped.2022.887771</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>World Health Organization. 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The objective is to evaluate the advanced lipoprotein testing (ALT) and its relationship with cardiac changes, metabolic syndrome (MS) and inflammatory markers in a population of morbidly obese adolescents with normal CLP and without type 2 diabetes mellitus, the most common scenario in obese adolescents.</AbstractText>Prospective case-control research of 42 morbidly obese adolescents and 25 normal-weight adolescents, whose left ventricle (LV) morphology and function had been assessed. The ALT was obtained by proton nuclear magnetic resonance spectroscopy, and the results were compared according to the degree of cardiac involvement - normal heart, mild LV changes, and severe LV changes (specifically LV remodeling and systolic dysfunction) - and related to inflammation markers [highly-sensitive C-reactive protein and glycoprotein A (GlycA)] and insulin-resistance [homeostatic model assessment for insulin-resistance (HOMA-IR)]. A second analysis was performed to compare our results with the predominant ALT when only body mass index and metabolic syndrome criteria were considered.</AbstractText>The three cardiac involvement groups showed significant increases in HOMA-IR, inflammatory markers and ALT ratio LDL-P/HDL-P (40.0 vs. 43.9 vs. 47.1, p</i> 0.012). When only cardiac change groups were considered, differences in small LDL-P (565.0 vs. 625.1 nmol/L, p</i> 0.070), VLDL size and GlycA demonstrated better utility than just traditional risk factors to predict which subjects could present severe LV changes [AUC: 0.79 (95% CI: 0.54-1)]. In the second analysis, an atherosclerotic ALT was detected in morbidly obese subjects, characterized by a significant increase in large VLDL-P, small LDL-P, ratio LDL-P/HDL-P and ratio HDL-TG/HDL-C. Subjects with criteria for MS presented overall worse ALT (specially in triglyceride-enriched particles) and remnant cholesterol values.</AbstractText>ALT parameters and GlycA appear to be more reliable indicators of cardiac change severity than traditional CV risk factors. Particularly, the overage of LDL-P compared to HDL-P and the increase in small LDL-P with cholesterol-depleted LDL particles appear to be the key ALT's parameters involved in LV changes. Morbidly obese adolescents show an atherosclerotic ALT and those with MS present worse ALT values.</AbstractText>© 2022 Siurana, Sabaté-Rotés, Amigó, Martínez-Micaelo, Arciniegas, Riaza, Mogas, Rosés-Noguer, Ventura and Yeste.</CopyrightInformation> |
2,329,312 | Neural precursor cells tune striatal connectivity through the release of IGFBPL1. | The adult brain retains over life endogenous neural stem/precursor cells (eNPCs) within the subventricular zone (SVZ). Whether or not these cells exert physiological functions is still unclear. In the present work, we provide evidence that SVZ-eNPCs tune structural, electrophysiological, and behavioural aspects of striatal function via secretion of insulin-like growth factor binding protein-like 1 (IGFBPL1). In mice, selective ablation of SVZ-eNPCs or selective abrogation of IGFBPL1 determined an impairment of striatal medium spiny neuron morphology, a higher failure rate in GABAergic transmission mediated by fast-spiking interneurons, and striatum-related behavioural dysfunctions. We also found IGFBPL1 expression in the human SVZ, foetal and induced-pluripotent stem cell-derived NPCs. Finally, we found a significant correlation between SVZ damage, reduction of striatum volume, and impairment of information processing speed in neurological patients. Our results highlight the physiological role of adult SVZ-eNPCs in supporting cognitive functions by regulating striatal neuronal activity. |
2,329,313 | Kisspeptin-neuron control of LH pulsatility and ovulation. | Feedback from oestradiol (E2) plays a critical role in the regulation of major events in the physiological menstrual cycle including the release of gonadotrophins to stimulate follicular growth, and the mid-cycle luteinising hormone (LH) surge that leads to ovulation. E2 predominantly exerts its action <i>via</i> oestrogen receptor-alpha (ERα), however, as gonadotrophin releasing hormone (GnRH) neurons lack ERα, E2-feedback is posited to be indirectly mediated <i>via</i> upstream neurons. Kisspeptin (KP) is a neuropeptide expressed in hypothalamic KP-neurons that control GnRH secretion and plays a key role in the central mechanism regulating the hypothalamic-pituitary-gonadal (HPG) axis. In the rodent arcuate (ARC) nucleus, KP is co-expressed with Neurokinin B and Dynorphin; and thus, these neurons are termed 'Kisspeptin-Neurokinin B-Dynorphin' (KNDy) neurons. ARC KP-neurons function as the 'GnRH pulse generator' to regulate GnRH pulsatility, as well as mediating negative feedback from E2. A second KP neuronal population is present in the rostral periventricular area of the third ventricle (RP3V), which includes anteroventral periventricular (AVPV) nucleus and preoptic area neurons. These RP3V KP-neurons mediate positive feedback to induce the mid-cycle luteinising hormone (LH) surge and subsequent ovulation. Here, we describe the role of KP-neurons in these two regions in mediating this differential feedback from oestrogens. We conclude by considering reproductive diseases for which exploitation of these mechanisms could yield future therapies. |
2,329,314 | Experimental brain infection with cysticercosis in sheep. | <AbstractText Label="OBJECTIVE." NlmCategory="UNASSIGNED">To explore the feasibility of developing a sheep model of neurocysticercosis (NCC) by intracranial infection with T. solium oncospheres.</AbstractText><AbstractText Label="MATERIALS AND METHODS." NlmCategory="UNASSIGNED">We carried out an experimental infection model of NCC in sheep. Approximately 10 T. solium oncospheres previously cultured for 30 days were inoculated intracranially into ten sheep. The oncospheres, in 0.1 mL of physiological saline, were injected into the parietal lobe through an 18-gauge needle.</AbstractText><AbstractText Label="RESULTS." NlmCategory="UNASSIGNED">After three months, granulomas were found in two sheep. In a third sheep we identified a 5 mm diameter cyst in the right lateral ventricle and histological evaluation confirmed that the cyst corresponded to a T. solium larva. Immunohistochemistry with monoclonal antibodies directed against membrane components and excretory/secretory antigens of the T. solium cyst was also used to confirm the etiology of the found granulomas. One of them showed reactivity to the monoclonal antibodies used, thus confirming that it was a cysticercus.</AbstractText><AbstractText Label="CONCLUSION." NlmCategory="UNASSIGNED">This experiment is the proof of concept that it is possible to infect sheep with cysticercosis by intracranial inoculation.</AbstractText> |
2,329,315 | Superior cardiometabolic and cellular adaptive responses to multiple versus single daily sessions of high-intensity interval training in Wistar rats. | This study aimed to compare in rats the cardiometabolic and cellular adaptative responses to 8 weeks of high-intensity interval training (HIIT) performed in a single (1xHIIT) or three shorter daily sessions (3xHIIT). Male Wistar rats were assigned to untrained (n = 10), 1xHIIT (n = 10), and 3xHIIT (n = 10) groups. Both HIIT groups performed 15 min of a treadmill run five times per week for 8 weeks. The 1xHIIT performed single daily sessions of 15 min, and the 3xHIIT performed three daily sessions of 5 min with an interval of 4 h between sessions. Resting VO<sub>2</sub> and VO<sub>2</sub>max were measured using a metabolic chamber; blood pressure and heart rate were measured by plethysmography; body composition was estimated by DEXA; Glucose and insulin tolerance tests were performed; after euthanasia, hearts, gastrocnemius, and visceral fat were harvested for analysis of cardiac function, histology, and morphology. Mitochondrial densities of the gastrocnemius and left ventricle muscles were determined by electron microscopy. 3xHIIT induced similar positive adaptative responses to 1xHIIT on resting VO<sub>2</sub> and VO<sub>2</sub>max, cardiac function, and mitochondria density. 3xHIIT was superior to 1xHIIT in reducing visceral fat weight and adipocyte size and improving insulin tolerance. Multiple short daily bouts of HIIT may be superior to single HIIT daily sessions in improving cardiometabolic and cellular adaptations in rats. |
2,329,316 | Comparing the findings and diagnostic sensitivity of cardiovascular magnetic resonance in biopsy confirmed acute myocarditis with infarct-like vs. heart failure presentation.<Pagination><StartPage>69</StartPage><MedlinePgn>69</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">69</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1186/s12968-022-00903-y</ELocationID><Abstract><AbstractText Label="BACKGROUND">Cardiovascular magnetic resonance (CMR) is considered the reference imaging modality in providing a non-invasive diagnosis of acute myocarditis (AM), as it allows for the detection of myocardial injury associated with AM. However, the diagnostic sensitivity and pattern of CMR findings appear to differ according to clinical presentation.</AbstractText><AbstractText Label="METHODS">This is a retrospective cross-sectional study. Consecutive adult patients presenting to a single tertiary centre in South Africa between August 2017 and January 2022 with AM confirmed on endomyocardial biopsy (EMB) were enrolled. Patients with infarct-like symptoms, defined as those presenting primarily with chest pain syndrome with associated ST-T wave changes on electrocardiogram, or heart failure (HF) symptoms, defined as clinical signs and symptoms of HF without significant chest discomfort, were compared using contrasted CMR and parametric techniques with EMB confirmation of AM as diagnostic gold standard.</AbstractText><AbstractText Label="RESULTS">Forty-one patients were identified including 23 (56%) with infarct-like symptoms and 18 (44%) with HF symptoms. On CMR, the infarct-like group had significantly higher ejection fractions of both ventricles (LVEF 55.3 ± 15.3% vs. 34.4 ± 13.5%, p < 0.001; RVEF 57.3 ± 10.9% vs. 42.9 ± 18.2%, p = 0.008), without significant differences in end diastolic volumes (LVEDVI 82.7 ± 30.3 ml/m<sup>2</sup> vs. 103.4 ± 35.9 ml/m<sup>2</sup>, p = 0.06; RVEDVI 73.7 ± 22.1 ml/m<sup>2</sup> vs. 83.9 ± 29.9 ml/m<sup>2</sup>, p = 0.25). Myocardial oedema was detected more frequently on T2-weighted imaging (91.3% vs. 61.1%, p = 0.03) and in more myocardial segments [3.0 (IQR 2.0-4.0) vs. 1.0 (IQR 0-1.0), p = 0.003] in the infarct-like group. Despite the absence of a significant statistical difference in the prevalence of late gadolinium enhancement (LGE) between the two groups (95.7% vs. 72.2%, p = 0.07), the infarct-like group had LGE detectable in significantly more ventricular segments [4.5 (IQR 2.3-6.0) vs. 2.0 (IQR 0-3.3), p = 0.02] and in a different distribution. The sensitivity of the original Lake Louise Criteria (LLC) was 91.3% in infarct-like patients and 55.6% in HF patients. When the updated LLC, which included the use of parametric myocardial mapping techniques, were applied, the sensitivity improved to 95.7% and 72.2% respectively.</AbstractText><AbstractText Label="CONCLUSION">The pattern of CMR findings and its diagnostic sensitivity appears to differ in AM patients presenting with infarct-like and HF symptoms. Although the sensitivity of the LLC improved with the addition of parametric mapping in the HF group, it remained lower than that of the infarct-like group, and suggests that EMB should be considered earlier in the course of patients with clinically suspected AM presenting with HF.</AbstractText><CopyrightInformation>© 2022. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hassan</LastName><ForeName>Karim</ForeName><Initials>K</Initials><Identifier Source="ORCID">0000-0002-1141-9486</Identifier><AffiliationInfo><Affiliation>Division of Cardiology, Department of Medicine, Stellenbosch University, Tygerberg Hospital, E8, 8/F Tygerberg Hospital, Francie Van Zijl Drive, Parow, Cape Town, 7505, South Africa. hsskar@gmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Doubell</LastName><ForeName>Anton</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Division of Cardiology, Department of Medicine, Stellenbosch University, Tygerberg Hospital, E8, 8/F Tygerberg Hospital, Francie Van Zijl Drive, Parow, Cape Town, 7505, South Africa.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kyriakakis</LastName><ForeName>Charles</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Division of Cardiology, Department of Medicine, Stellenbosch University, Tygerberg Hospital, E8, 8/F Tygerberg Hospital, Francie Van Zijl Drive, Parow, Cape Town, 7505, South Africa.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Joubert</LastName><ForeName>Lloyd</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Division of Cardiology, Department of Medicine, Stellenbosch University, Tygerberg Hospital, E8, 8/F Tygerberg Hospital, Francie Van Zijl Drive, Parow, Cape Town, 7505, South Africa.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Robbertse</LastName><ForeName>Pieter-Paul</ForeName><Initials>PP</Initials><AffiliationInfo><Affiliation>Division of Cardiology, Department of Medicine, Stellenbosch University, Tygerberg Hospital, E8, 8/F Tygerberg Hospital, Francie Van Zijl Drive, Parow, Cape Town, 7505, South Africa.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Van Zyl</LastName><ForeName>Gert</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Division of Medical Virology, National Health Laboratory Services, Tygerberg Hospital, Cape Town, South Africa.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zaharie</LastName><ForeName>Dan</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Division of Anatomical Pathology, National Health Laboratory Services, Tygerberg Hospital, Cape Town, South Africa.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Herbst</LastName><ForeName>Philip</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Division of Cardiology, Department of Medicine, Stellenbosch University, Tygerberg Hospital, E8, 8/F Tygerberg Hospital, Francie Van Zijl Drive, Parow, Cape Town, 7505, South Africa.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>12</Month><Day>07</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Cardiovasc Magn Reson</MedlineTA><NlmUniqueID>9815616</NlmUniqueID><ISSNLinking>1097-6647</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D003287">Contrast Media</NameOfSubstance></Chemical><Chemical><RegistryNumber>AU0V1LM3JT</RegistryNumber><NameOfSubstance UI="D005682">Gadolinium</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003430" MajorTopicYN="N">Cross-Sectional Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003287" MajorTopicYN="Y">Contrast Media</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005682" MajorTopicYN="N">Gadolinium</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011237" MajorTopicYN="N">Predictive Value of Tests</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009682" MajorTopicYN="N">Magnetic Resonance Spectroscopy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006333" MajorTopicYN="Y">Heart Failure</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Cardiac magnetic resonance imaging</Keyword><Keyword MajorTopicYN="N">Lake Louise criteria</Keyword><Keyword MajorTopicYN="N">Myocarditis</Keyword><Keyword MajorTopicYN="N">Parametric mapping</Keyword><Keyword MajorTopicYN="N">Viral myocarditis</Keyword></KeywordList><CoiStatement>The authors declare that they have no competing interests.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>5</Month><Day>13</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>11</Month><Day>21</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>12</Month><Day>8</Day><Hour>10</Hour><Minute>28</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>12</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>12</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36476480</ArticleId><ArticleId IdType="pmc">PMC9730564</ArticleId><ArticleId IdType="doi">10.1186/s12968-022-00903-y</ArticleId><ArticleId 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Radiology. 2014;273(2):383–392. doi: 10.1148/radiol.14132540.</Citation><ArticleIdList><ArticleId IdType="doi">10.1148/radiol.14132540</ArticleId><ArticleId IdType="pubmed">24910904</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36475546</PMID><DateRevised><Year>2022</Year><Month>12</Month><Day>07</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">2724-5772</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Dec</Month><Day>07</Day></PubDate></JournalIssue><Title>Minerva cardiology and angiology</Title><ISOAbbreviation>Minerva Cardiol Angiol</ISOAbbreviation></Journal>In-hospital outcomes in nonagenarian patients undergoing primary percutaneous coronary intervention. | Cardiovascular magnetic resonance (CMR) is considered the reference imaging modality in providing a non-invasive diagnosis of acute myocarditis (AM), as it allows for the detection of myocardial injury associated with AM. However, the diagnostic sensitivity and pattern of CMR findings appear to differ according to clinical presentation.</AbstractText>This is a retrospective cross-sectional study. Consecutive adult patients presenting to a single tertiary centre in South Africa between August 2017 and January 2022 with AM confirmed on endomyocardial biopsy (EMB) were enrolled. Patients with infarct-like symptoms, defined as those presenting primarily with chest pain syndrome with associated ST-T wave changes on electrocardiogram, or heart failure (HF) symptoms, defined as clinical signs and symptoms of HF without significant chest discomfort, were compared using contrasted CMR and parametric techniques with EMB confirmation of AM as diagnostic gold standard.</AbstractText>Forty-one patients were identified including 23 (56%) with infarct-like symptoms and 18 (44%) with HF symptoms. On CMR, the infarct-like group had significantly higher ejection fractions of both ventricles (LVEF 55.3 ± 15.3% vs. 34.4 ± 13.5%, p < 0.001; RVEF 57.3 ± 10.9% vs. 42.9 ± 18.2%, p = 0.008), without significant differences in end diastolic volumes (LVEDVI 82.7 ± 30.3 ml/m2</sup> vs. 103.4 ± 35.9 ml/m2</sup>, p = 0.06; RVEDVI 73.7 ± 22.1 ml/m2</sup> vs. 83.9 ± 29.9 ml/m2</sup>, p = 0.25). Myocardial oedema was detected more frequently on T2-weighted imaging (91.3% vs. 61.1%, p = 0.03) and in more myocardial segments [3.0 (IQR 2.0-4.0) vs. 1.0 (IQR 0-1.0), p = 0.003] in the infarct-like group. Despite the absence of a significant statistical difference in the prevalence of late gadolinium enhancement (LGE) between the two groups (95.7% vs. 72.2%, p = 0.07), the infarct-like group had LGE detectable in significantly more ventricular segments [4.5 (IQR 2.3-6.0) vs. 2.0 (IQR 0-3.3), p = 0.02] and in a different distribution. The sensitivity of the original Lake Louise Criteria (LLC) was 91.3% in infarct-like patients and 55.6% in HF patients. When the updated LLC, which included the use of parametric myocardial mapping techniques, were applied, the sensitivity improved to 95.7% and 72.2% respectively.</AbstractText>The pattern of CMR findings and its diagnostic sensitivity appears to differ in AM patients presenting with infarct-like and HF symptoms. Although the sensitivity of the LLC improved with the addition of parametric mapping in the HF group, it remained lower than that of the infarct-like group, and suggests that EMB should be considered earlier in the course of patients with clinically suspected AM presenting with HF.</AbstractText>© 2022. The Author(s).</CopyrightInformation> |
2,329,317 | Connecting the dots: alterations in bioelectric activity at acupuncture Ting (Jing-Well) points following CV4 cranial manipulation. | The mechanisms by which osteopathic cranial manipulative medicine (OCMM) promotes health and healing have yet to be fully elucidated. One commonly utilized OCMM technique, compression of the fourth ventricle (CV4), has been theorized to balance autonomic nervous system (ANS) activity. There is growing evidence that the ANS also plays a significant mechanistic role in acupuncture. Potential connections between OCMM and acupuncture meridian theory largely remain unknown.</AbstractText>By measuring specific electrical parameters at acupuncture points that have been shown to correlate with ANS activity, the objectives of this study were to: 1) determine if CV4 has any influence on the bioelectric properties of the acupuncture meridian system; and 2) determine if CV4 affects the ANS.</AbstractText>A total of 77 males and females ages 18-78 years, all volunteers recruited by local flyers and personal or phone contact, were randomized into CV4 (n=40) and Sham (n=37) groups. All CV4 participants were treated by the same physician utilizing standard CV4 protocol. The Sham treatment, performed by a different physician, consisted of the supine participant's occiput resting passively on the physician's finger pads for a similar duration as those in the CV4 group. Among several devices developed to assess ANS activity at acupuncture points, evidence suggests that the Apparatus for Meridian Identification (AMI) is the most accurate and valid. Utilizing the AMI, bioelectric skin parameters were measured immediately before and after CV4 or Sham treatments. Student's or Welch's t tests and Wilcoxon tests were utilized for analysis of normally and non-normally distributed data, respectively.</AbstractText>Statistical significance was determined with a p value less than 0.05. Sham treatments showed insignificant (p=0.754) before vs. after differences in ANS activity measured at acupuncture points, whereas CV4 treatment significantly (p=0.00015) affected ANS activity.</AbstractText>This research suggests that CV4 has demonstrable biophysical effects on the acupuncture meridian system occurring via the ANS, and that the underlying mechanisms of OCMM and acupuncture may be related. Further studies are needed to clarify this.</AbstractText>© 2022 the author(s), published by De Gruyter, Berlin/Boston.</CopyrightInformation> |
2,329,318 | Role of cardiac mitofusins in cardiac conduction following simulated ischemia-reperfusion.<Pagination><StartPage>21049</StartPage><MedlinePgn>21049</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">21049</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1038/s41598-022-25625-0</ELocationID><Abstract><AbstractText>Mitochondrial dysfunction induced by acute cardiac ischemia-reperfusion (IR), may increase susceptibility to arrhythmias by perturbing energetics, oxidative stress production and calcium homeostasis. Although changes in mitochondrial morphology are known to impact on mitochondrial function, their role in cardiac arrhythmogenesis is not known. To assess action potential duration (APD) in cardiomyocytes from the Mitofusins-1/2 (Mfn1/Mfn2)-double-knockout (Mfn-DKO) compared to wild-type (WT) mice, optical-electrophysiology was conducted. To measure conduction velocity (CV) in atrial and ventricular tissue from the Mfn-DKO and WT mice, at both baseline and following simulated acute IR, multi-electrode array (MEA) was employed. Intracellular localization of connexin-43 (Cx43) at baseline was evaluated by immunohistochemistry, while Cx-43 phosphorylation was assessed by Western-blotting. Mfn-DKO cardiomyocytes demonstrated an increased APD. At baseline, CV was significantly lower in the left ventricle of the Mfn-DKO mice. CV decreased with simulated-ischemia and returned to baseline levels during simulated-reperfusion in WT but not in atria of Mfn-DKO mice. Mfn-DKO hearts displayed increased Cx43 lateralization, although phosphorylation of Cx43 at Ser-368 did not differ. In summary, Mfn-DKO mice have increased APD and reduced CV at baseline and impaired alterations in CV following cardiac IR. These findings were associated with increased Cx43 lateralization, suggesting that the mitofusins may impact on post-MI cardiac-arrhythmogenesis.</AbstractText><CopyrightInformation>© 2022. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y" EqualContrib="Y"><LastName>Kwek</LastName><ForeName>Xiu-Yi</ForeName><Initials>XY</Initials><AffiliationInfo><Affiliation>National Heart Research Institute Singapore, National Heart Centre, Singapore, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Hall</LastName><ForeName>Andrew R</ForeName><Initials>AR</Initials><AffiliationInfo><Affiliation>The Hatter Cardiovascular Institute, Institute of Cardiovascular Science, University College London, London, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Lim</LastName><ForeName>Wei-Wen</ForeName><Initials>WW</Initials><AffiliationInfo><Affiliation>National Heart Research Institute Singapore, National Heart Centre, Singapore, Singapore.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cardiovascular and Metabolic Disorders Program, Duke-National University of Singapore Medical School, Singapore, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Katwadi</LastName><ForeName>Khairunnisa</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Cardiovascular and Metabolic Disorders Program, Duke-National University of Singapore Medical School, Singapore, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Soong</LastName><ForeName>Poh Loong</ForeName><Initials>PL</Initials><AffiliationInfo><Affiliation>Yong Loo Lin School of Medicine, National University Singapore, Singapore, Singapore.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cardiovascular Translational Program, Cardiovascular Research Institute (CVRI), National University of Singapore, Singapore, Singapore.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Medicine, National University Hospital of Singapore (NUHS), Singapore, Singapore.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Ternion Biosciences, Singapore, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Grishina</LastName><ForeName>Elina</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Ternion Biosciences, Singapore, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lin</LastName><ForeName>Kun-Han</ForeName><Initials>KH</Initials><AffiliationInfo><Affiliation>Ternion Biosciences, Singapore, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Crespo-Avilan</LastName><ForeName>Gustavo</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>National Heart Research Institute Singapore, National Heart Centre, Singapore, Singapore.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cardiovascular and Metabolic Disorders Program, Duke-National University of Singapore Medical School, Singapore, Singapore.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Biochemistry, Medical Faculty, Justus Liebig-University, Giessen, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yap</LastName><ForeName>En Ping</ForeName><Initials>EP</Initials><AffiliationInfo><Affiliation>National Heart Research Institute Singapore, National Heart Centre, Singapore, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ismail</LastName><ForeName>Nur Izzah</ForeName><Initials>NI</Initials><AffiliationInfo><Affiliation>Centre for Cardiovascular Genomics and Medicine (CCGM), Lui Che Woo Institute of Innovative Medicine, Chinese University of Hong Kong (CUHK), Hong Kong, SAR, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Medicine and Therapeutics, Faculty of Medicine, Chinese University of Hong Kong (CUHK), Hong Kong, SAR, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Hong Kong Hub of Paediatric Excellence (HK HOPE), Hong Kong Children's Hospital (HKCH), Kowloon Bay, Hong Kong, SAR, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chinda</LastName><ForeName>Kroekkiat</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Physiology, Faculty of Medical Science, Naresuan University, Phitsanulok, Thailand.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Integrative Cardiovascular Research Unit, Faculty of Medical Science, Naresuan University, Phitsanulok, Thailand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chung</LastName><ForeName>Ying Ying</ForeName><Initials>YY</Initials><AffiliationInfo><Affiliation>Centre for Vision Research, Duke-National University of Singapore Medical School, Singapore, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wei</LastName><ForeName>Heming</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Research Laboratory, KK Women's & Children's Hospital, Singapore, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shim</LastName><ForeName>Winston</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Health and Social Sciences Cluster, Singapore Institute of Technology, Singapore, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Montaigne</LastName><ForeName>David</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Inserm, CHU Lille, Institut Pasteur Lille, U1011-European Genomic Institute for Diabetes (EGID), University of Lille, 59000, Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tinker</LastName><ForeName>Andrew</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Centre for Clinical Pharmacology, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ong</LastName><ForeName>Sang-Bing</ForeName><Initials>SB</Initials><AffiliationInfo><Affiliation>Centre for Cardiovascular Genomics and Medicine (CCGM), Lui Che Woo Institute of Innovative Medicine, Chinese University of Hong Kong (CUHK), Hong Kong, SAR, China. sangbingong@cuhk.edu.hk.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Medicine and Therapeutics, Faculty of Medicine, Chinese University of Hong Kong (CUHK), Hong Kong, SAR, China. sangbingong@cuhk.edu.hk.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Hong Kong Hub of Paediatric Excellence (HK HOPE), Hong Kong Children's Hospital (HKCH), Kowloon Bay, Hong Kong, SAR, China. sangbingong@cuhk.edu.hk.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Joint Laboratory of Bioresources and Molecular Research of Common Diseases, Kunming Institute of Zoology-The Chinese University of Hong Kong (KIZ-CUHK), Chinese Academy of Sciences, Kunming, Yunnan, China. sangbingong@cuhk.edu.hk.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Shenzhen Research Institute (SZRI), Chinese University of Hong Kong (CUHK), Shenzhen, China. sangbingong@cuhk.edu.hk.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hausenloy</LastName><ForeName>Derek J</ForeName><Initials>DJ</Initials><AffiliationInfo><Affiliation>National Heart Research Institute Singapore, National Heart Centre, Singapore, Singapore. derek.hausenloy@duke-nus.edu.sg.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>The Hatter Cardiovascular Institute, Institute of Cardiovascular Science, University College London, London, UK. derek.hausenloy@duke-nus.edu.sg.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cardiovascular and Metabolic Disorders Program, Duke-National University of Singapore Medical School, Singapore, Singapore. derek.hausenloy@duke-nus.edu.sg.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Yong Loo Lin School of Medicine, National University Singapore, Singapore, Singapore. derek.hausenloy@duke-nus.edu.sg.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>FS/10/039/28270</GrantID><Acronym>BHF_</Acronym><Agency>British Heart Foundation</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>RG/15/15/31742</GrantID><Acronym>BHF_</Acronym><Agency>British Heart Foundation</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>MR/J003530/1</GrantID><Acronym>MRC_</Acronym><Agency>Medical Research Council</Agency><Country>United Kingdom</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>12</Month><Day>06</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Sci Rep</MedlineTA><NlmUniqueID>101563288</NlmUniqueID><ISSNLinking>2045-2322</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D050071">Bone Density Conservation Agents</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D054849" MajorTopicYN="N">Cardiac Electrophysiology</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D050071" MajorTopicYN="Y">Bone Density Conservation Agents</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006259" MajorTopicYN="Y">Craniocerebral Trauma</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007511" MajorTopicYN="N">Ischemia</DescriptorName></MeshHeading></MeshHeadingList><CoiStatement>E.G. is employed by Ternion Biosciences. K.H.L. and P.L.S. are founders and scientific advisors of Ternion Biosciences, Singapore. 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Although changes in mitochondrial morphology are known to impact on mitochondrial function, their role in cardiac arrhythmogenesis is not known. To assess action potential duration (APD) in cardiomyocytes from the Mitofusins-1/2 (Mfn1/Mfn2)-double-knockout (Mfn-DKO) compared to wild-type (WT) mice, optical-electrophysiology was conducted. To measure conduction velocity (CV) in atrial and ventricular tissue from the Mfn-DKO and WT mice, at both baseline and following simulated acute IR, multi-electrode array (MEA) was employed. Intracellular localization of connexin-43 (Cx43) at baseline was evaluated by immunohistochemistry, while Cx-43 phosphorylation was assessed by Western-blotting. Mfn-DKO cardiomyocytes demonstrated an increased APD. At baseline, CV was significantly lower in the left ventricle of the Mfn-DKO mice. CV decreased with simulated-ischemia and returned to baseline levels during simulated-reperfusion in WT but not in atria of Mfn-DKO mice. Mfn-DKO hearts displayed increased Cx43 lateralization, although phosphorylation of Cx43 at Ser-368 did not differ. In summary, Mfn-DKO mice have increased APD and reduced CV at baseline and impaired alterations in CV following cardiac IR. These findings were associated with increased Cx43 lateralization, suggesting that the mitofusins may impact on post-MI cardiac-arrhythmogenesis.<CopyrightInformation>© 2022. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y" EqualContrib="Y"><LastName>Kwek</LastName><ForeName>Xiu-Yi</ForeName><Initials>XY</Initials><AffiliationInfo><Affiliation>National Heart Research Institute Singapore, National Heart Centre, Singapore, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Hall</LastName><ForeName>Andrew R</ForeName><Initials>AR</Initials><AffiliationInfo><Affiliation>The Hatter Cardiovascular Institute, Institute of Cardiovascular Science, University College London, London, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Lim</LastName><ForeName>Wei-Wen</ForeName><Initials>WW</Initials><AffiliationInfo><Affiliation>National Heart Research Institute Singapore, National Heart Centre, Singapore, Singapore.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cardiovascular and Metabolic Disorders Program, Duke-National University of Singapore Medical School, Singapore, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Katwadi</LastName><ForeName>Khairunnisa</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Cardiovascular and Metabolic Disorders Program, Duke-National University of Singapore Medical School, Singapore, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Soong</LastName><ForeName>Poh Loong</ForeName><Initials>PL</Initials><AffiliationInfo><Affiliation>Yong Loo Lin School of Medicine, National University Singapore, Singapore, Singapore.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cardiovascular Translational Program, Cardiovascular Research Institute (CVRI), National University of Singapore, Singapore, Singapore.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Medicine, National University Hospital of Singapore (NUHS), Singapore, Singapore.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Ternion Biosciences, Singapore, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Grishina</LastName><ForeName>Elina</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Ternion Biosciences, Singapore, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lin</LastName><ForeName>Kun-Han</ForeName><Initials>KH</Initials><AffiliationInfo><Affiliation>Ternion Biosciences, Singapore, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Crespo-Avilan</LastName><ForeName>Gustavo</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>National Heart Research Institute Singapore, National Heart Centre, Singapore, Singapore.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cardiovascular and Metabolic Disorders Program, Duke-National University of Singapore Medical School, Singapore, Singapore.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Biochemistry, Medical Faculty, Justus Liebig-University, Giessen, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yap</LastName><ForeName>En Ping</ForeName><Initials>EP</Initials><AffiliationInfo><Affiliation>National Heart Research Institute Singapore, National Heart Centre, Singapore, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ismail</LastName><ForeName>Nur Izzah</ForeName><Initials>NI</Initials><AffiliationInfo><Affiliation>Centre for Cardiovascular Genomics and Medicine (CCGM), Lui Che Woo Institute of Innovative Medicine, Chinese University of Hong Kong (CUHK), Hong Kong, SAR, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Medicine and Therapeutics, Faculty of Medicine, Chinese University of Hong Kong (CUHK), Hong Kong, SAR, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Hong Kong Hub of Paediatric Excellence (HK HOPE), Hong Kong Children's Hospital (HKCH), Kowloon Bay, Hong Kong, SAR, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chinda</LastName><ForeName>Kroekkiat</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Physiology, Faculty of Medical Science, Naresuan University, Phitsanulok, Thailand.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Integrative Cardiovascular Research Unit, Faculty of Medical Science, Naresuan University, Phitsanulok, Thailand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chung</LastName><ForeName>Ying Ying</ForeName><Initials>YY</Initials><AffiliationInfo><Affiliation>Centre for Vision Research, Duke-National University of Singapore Medical School, Singapore, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wei</LastName><ForeName>Heming</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Research Laboratory, KK Women's & Children's Hospital, Singapore, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shim</LastName><ForeName>Winston</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Health and Social Sciences Cluster, Singapore Institute of Technology, Singapore, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Montaigne</LastName><ForeName>David</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Inserm, CHU Lille, Institut Pasteur Lille, U1011-European Genomic Institute for Diabetes (EGID), University of Lille, 59000, Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tinker</LastName><ForeName>Andrew</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Centre for Clinical Pharmacology, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ong</LastName><ForeName>Sang-Bing</ForeName><Initials>SB</Initials><AffiliationInfo><Affiliation>Centre for Cardiovascular Genomics and Medicine (CCGM), Lui Che Woo Institute of Innovative Medicine, Chinese University of Hong Kong (CUHK), Hong Kong, SAR, China. sangbingong@cuhk.edu.hk.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Medicine and Therapeutics, Faculty of Medicine, Chinese University of Hong Kong (CUHK), Hong Kong, SAR, China. sangbingong@cuhk.edu.hk.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Hong Kong Hub of Paediatric Excellence (HK HOPE), Hong Kong Children's Hospital (HKCH), Kowloon Bay, Hong Kong, SAR, China. sangbingong@cuhk.edu.hk.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Joint Laboratory of Bioresources and Molecular Research of Common Diseases, Kunming Institute of Zoology-The Chinese University of Hong Kong (KIZ-CUHK), Chinese Academy of Sciences, Kunming, Yunnan, China. sangbingong@cuhk.edu.hk.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Shenzhen Research Institute (SZRI), Chinese University of Hong Kong (CUHK), Shenzhen, China. sangbingong@cuhk.edu.hk.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hausenloy</LastName><ForeName>Derek J</ForeName><Initials>DJ</Initials><AffiliationInfo><Affiliation>National Heart Research Institute Singapore, National Heart Centre, Singapore, Singapore. derek.hausenloy@duke-nus.edu.sg.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>The Hatter Cardiovascular Institute, Institute of Cardiovascular Science, University College London, London, UK. derek.hausenloy@duke-nus.edu.sg.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cardiovascular and Metabolic Disorders Program, Duke-National University of Singapore Medical School, Singapore, Singapore. derek.hausenloy@duke-nus.edu.sg.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Yong Loo Lin School of Medicine, National University Singapore, Singapore, Singapore. derek.hausenloy@duke-nus.edu.sg.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>FS/10/039/28270</GrantID><Acronym>BHF_</Acronym><Agency>British Heart Foundation</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>RG/15/15/31742</GrantID><Acronym>BHF_</Acronym><Agency>British Heart Foundation</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>MR/J003530/1</GrantID><Acronym>MRC_</Acronym><Agency>Medical Research Council</Agency><Country>United Kingdom</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>12</Month><Day>06</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Sci Rep</MedlineTA><NlmUniqueID>101563288</NlmUniqueID><ISSNLinking>2045-2322</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D050071">Bone Density Conservation Agents</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D054849" MajorTopicYN="N">Cardiac Electrophysiology</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D050071" MajorTopicYN="Y">Bone Density Conservation Agents</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006259" MajorTopicYN="Y">Craniocerebral Trauma</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007511" MajorTopicYN="N">Ischemia</DescriptorName></MeshHeading></MeshHeadingList><CoiStatement>E.G. is employed by Ternion Biosciences. K.H.L. and P.L.S. are founders and scientific advisors of Ternion Biosciences, Singapore. 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JCI Insight. 2019;4:125908. doi: 10.1172/jci.insight.125908.</Citation><ArticleIdList><ArticleId IdType="doi">10.1172/jci.insight.125908</ArticleId><ArticleId IdType="pmc">PMC6777811</ArticleId><ArticleId IdType="pubmed">31434798</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36473799</PMID><DateRevised><Year>2023</Year><Month>05</Month><Day>19</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1535-6302</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Nov</Month><Day>17</Day></PubDate></JournalIssue><Title>Current problems in diagnostic radiology</Title><ISOAbbreviation>Curr Probl Diagn Radiol</ISOAbbreviation></Journal><ArticleTitle>Gastroenteropancreatic Neuroendocrine Tumor Metastasis to the Heart: Evaluation of Imaging Manifestations.</ArticleTitle><ELocationID EIdType="pii" ValidYN="Y">S0363-0188(22)00154-2</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1067/j.cpradiol.2022.11.011</ELocationID><Abstract>Neuroendocrine tumors (NET) may affect the heart by cardiac metastasis or carcinoid heart disease. NET metastasis to the heart is rare, with limited data characterizing it. We sought to evaluate <sup>68</sup>Ga-DOTATATE PET scan imaging features and associated cardiac imaging characteristics where available in those with NET cardiac metastases. <sup>68</sup>Ga-DOTATATE positron emission tomography (PET)/CT scans performed on patients with gastroenteropancreatic (GEP) NET at our institution were reviewed for cardiac involvement. Those identified with cardiac metastases had their electronic medical record, transthoracic echocardiogram (TTE) and cardiac magnetic resonance imaging (MRI) reviewed for characterization. From a total of 1426 <sup>68</sup>Ga-DOTATATE PET/CT scans performed on patients with GEP-NET, 25 (1.75%) had cardiac uptake consistent with metastasis. Of these, 22 had myocardial metastases (29 distinct myocardial lesions: left ventricle - 16, right ventricle - 6, and ventricular septum -7) and 3 had periradial lymph node involvement only. NET patients with cardiac metastases as identified by DOTATATE scan did not appear to have any hemodynamically significant TTE features, aside from those (2/25) who had concomitant carcinoid heart disease. Of the 14 patients who had available TTE for review, only one with high metastatic cardiac tumor burden had detectable cardiac mass. Of the 6 cases who had available MRI, all had metastatic cardiac lesions seen with excellent correlation with tumor localization on <sup>68</sup>Ga-DOTATATE PET scan. <sup>68</sup>Ga-DOTATATE PET has excellent capability for the diagnosis of cardiac NET metastasis. Cardiac MRI may provide further anatomic and tissue characterization evaluation. Those with myocardial NET metastases without carcinoid heart disease did not have significant hemodynamic effect based on echocardiographic criteria. |
2,329,319 | A finite element model of the embryonic zebrafish heart electrophysiology.<Pagination><StartPage>107281</StartPage><MedlinePgn>107281</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.cmpb.2022.107281</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0169-2607(22)00662-9</ELocationID><Abstract><AbstractText Label="BACKGROUND AND OBJECTIVE" NlmCategory="OBJECTIVE">In the last 30 years, a growing interest has involved the study of zebrafish thanks to its physiological characteristics similar to those of humans. The aim of the following work is to create an electrophysiological computational model of the zebrafish heart and lay the foundation for the development of an in-silico model of the zebrafish heart that will allow to study the correlation between pathologies and drug administration with the main electrophysiological parameters as the ECG signal.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">The model considers a whole body and the two chambers of three days post fertilization (3 dpf) zebrafish. A four-variable phenomenological action potential model describes the action potential of different heart regions. Tissue conductivity was calibrated to reproduce the experimentally described activation sequence.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">The model is able to correctly reproduce the activation sequence and times found in literature, with activation of the atrium and ventricle that correspond to 36 and 59 ms, respectively, and a delay of 14 ms caused by the presence of the atrioventricular band (AV band). Moreover, the obtained in-silico ECG reflects the main characteristics of the zebrafish ECG in good agreement with experimental records, a P-wave with a duration of approximately the total atrial activation, followed by a QRS complex of approximately 109 ms corresponding to ventricle activation.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">The model allows the assessment of the main electrophysiological parameters in terms of activation sequence and timing, reproducing monopolar and bipolar ECG signals in line with experimental data. Coupling the proposed model with an electrophysiological detailed action potential model of zebrafish will represent a significant breakthrough toward the development of an in-silico zebrafish heart.</AbstractText><CopyrightInformation>Copyright © 2022. Published by Elsevier B.V.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Cestariolo</LastName><ForeName>Ludovica</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Laboratory of Biological Structure Mechanics (LaBS), Department of Chemistry, Materials and Chemical Engineering "Giulio Natta", Politecnico di Milano, Milan, Italy. Electronic address: ludovica.cestariolo@polimi.it.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Luraghi</LastName><ForeName>Giulia</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Laboratory of Biological Structure Mechanics (LaBS), Department of Chemistry, Materials and Chemical Engineering "Giulio Natta", Politecnico di Milano, Milan, Italy. Electronic address: giulia.luraghi@polimi.it.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>L'Eplattenier</LastName><ForeName>Pierre</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Livermore Software Technology Corporation, CA, US. Electronic address: pierre.leplattenier@ansys.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rodriguez Matas</LastName><ForeName>Jose Felix</ForeName><Initials>JF</Initials><AffiliationInfo><Affiliation>Laboratory of Biological Structure Mechanics (LaBS), Department of Chemistry, Materials and Chemical Engineering "Giulio Natta", Politecnico di Milano, Milan, Italy. Electronic address: josefelix.rodriguezmatas@polimi.it.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>11</Month><Day>28</Day></ArticleDate></Article><MedlineJournalInfo><Country>Ireland</Country><MedlineTA>Comput Methods Programs Biomed</MedlineTA><NlmUniqueID>8506513</NlmUniqueID><ISSNLinking>0169-2607</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015027" MajorTopicYN="Y">Zebrafish</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020342" MajorTopicYN="N">Finite Element Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006325" MajorTopicYN="Y">Heart Atria</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004594" MajorTopicYN="N">Electrophysiology</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004562" MajorTopicYN="N">Electrocardiography</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Action potential</Keyword><Keyword MajorTopicYN="N">Computational model</Keyword><Keyword MajorTopicYN="N">ECG</Keyword><Keyword MajorTopicYN="N">Electrophysiology</Keyword><Keyword MajorTopicYN="N">Zebrafish</Keyword></KeywordList><CoiStatement>Conflict of interest statement Pierre L'Eplattenier reports a financial relationship with Livermore Software Technology Corporation outside the submitted work.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>8</Month><Day>8</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>11</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>11</Month><Day>26</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>12</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2023</Year><Month>2</Month><Day>8</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>12</Month><Day>5</Day><Hour>18</Hour><Minute>17</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36470034</ArticleId><ArticleId IdType="doi">10.1016/j.cmpb.2022.107281</ArticleId><ArticleId IdType="pii">S0169-2607(22)00662-9</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36469699</PMID><DateRevised><Year>2022</Year><Month>12</Month><Day>05</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1536-0237</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Dec</Month><Day>06</Day></PubDate></JournalIssue><Title>Journal of thoracic imaging</Title><ISOAbbreviation>J Thorac Imaging</ISOAbbreviation></Journal>Myocardial Work Measurement With Functional Capacity Evaluation in Primary Systemic Hypertension Patients: Comparison Between Left Ventricle With and Without Hypertrophy. | In the last 30 years, a growing interest has involved the study of zebrafish thanks to its physiological characteristics similar to those of humans. The aim of the following work is to create an electrophysiological computational model of the zebrafish heart and lay the foundation for the development of an in-silico model of the zebrafish heart that will allow to study the correlation between pathologies and drug administration with the main electrophysiological parameters as the ECG signal.</AbstractText>The model considers a whole body and the two chambers of three days post fertilization (3 dpf) zebrafish. A four-variable phenomenological action potential model describes the action potential of different heart regions. Tissue conductivity was calibrated to reproduce the experimentally described activation sequence.</AbstractText>The model is able to correctly reproduce the activation sequence and times found in literature, with activation of the atrium and ventricle that correspond to 36 and 59 ms, respectively, and a delay of 14 ms caused by the presence of the atrioventricular band (AV band). Moreover, the obtained in-silico ECG reflects the main characteristics of the zebrafish ECG in good agreement with experimental records, a P-wave with a duration of approximately the total atrial activation, followed by a QRS complex of approximately 109 ms corresponding to ventricle activation.</AbstractText>The model allows the assessment of the main electrophysiological parameters in terms of activation sequence and timing, reproducing monopolar and bipolar ECG signals in line with experimental data. Coupling the proposed model with an electrophysiological detailed action potential model of zebrafish will represent a significant breakthrough toward the development of an in-silico zebrafish heart.</AbstractText>Copyright © 2022. Published by Elsevier B.V.</CopyrightInformation> |
2,329,320 | A compartmentalized mathematical model of the β<sub>1</sub>- and β<sub>2</sub>-adrenergic signaling systems in ventricular myocytes from mouse in heart failure.<Pagination><StartPage>C263</StartPage><EndPage>C291</EndPage><MedlinePgn>C263-C291</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1152/ajpcell.00366.2022</ELocationID><Abstract><AbstractText>Mouse models of heart failure are extensively used to research human cardiovascular diseases. In particular, one of the most common is the mouse model of heart failure resulting from transverse aortic constriction (TAC). Despite this, there are no comprehensive compartmentalized mathematical models that describe the complex behavior of the action potential, [Ca<sup>2+</sup>]<sub>i</sub> transients, and their regulation by β<sub>1</sub>- and β<sub>2</sub>-adrenergic signaling systems in failing mouse myocytes. In this paper, we develop a novel compartmentalized mathematical model of failing mouse ventricular myocytes after TAC procedure. The model describes well the cell geometry, action potentials, [Ca<sup>2+</sup>]<sub>i</sub> transients, and β<sub>1</sub>- and β<sub>2</sub>-adrenergic signaling in the failing cells. Simulation results obtained with the failing cell model are compared with those from the normal ventricular myocytes. Exploration of the model reveals the sarcoplasmic reticulum Ca<sup>2+</sup> load mechanisms in failing ventricular myocytes. We also show a larger susceptibility of the failing myocytes to early and delayed afterdepolarizations and to a proarrhythmic behavior of Ca<sup>2+</sup> dynamics upon stimulation with isoproterenol. The mechanisms of the proarrhythmic behavior suppression are investigated and sensitivity analysis is performed. The developed model can explain the existing experimental data on failing mouse ventricular myocytes and make experimentally testable predictions of a failing myocyte's behavior.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Asfaw</LastName><ForeName>Tesfaye Negash</ForeName><Initials>TN</Initials><AffiliationInfo><Affiliation>Department of Mathematics and Statistics, Georgia State University, Atlanta, Georgia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bondarenko</LastName><ForeName>Vladimir E</ForeName><Initials>VE</Initials><Identifier Source="ORCID">0000-0003-4356-4669</Identifier><AffiliationInfo><Affiliation>Department of Mathematics and Statistics, Georgia State University, Atlanta, Georgia.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Neuroscience Institute, Georgia State University, Atlanta, Georgia.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>12</Month><Day>05</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Am J Physiol Cell Physiol</MedlineTA><NlmUniqueID>100901225</NlmUniqueID><ISSNLinking>0363-6143</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018663">Adrenergic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>SY7Q814VUP</RegistryNumber><NameOfSubstance UI="D002118">Calcium</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="Y">Heart Ventricles</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D032383" MajorTopicYN="N">Myocytes, Cardiac</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008962" MajorTopicYN="N">Models, Theoretical</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006333" MajorTopicYN="Y">Heart Failure</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012519" MajorTopicYN="N">Sarcoplasmic Reticulum</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018663" MajorTopicYN="N">Adrenergic Agents</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000200" MajorTopicYN="N">Action Potentials</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002118" MajorTopicYN="N">Calcium</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Ca2+ dynamics</Keyword><Keyword MajorTopicYN="N">action potential</Keyword><Keyword MajorTopicYN="N">delayed afterdepolarization</Keyword><Keyword MajorTopicYN="N">late Na+ current</Keyword><Keyword MajorTopicYN="N">β1- and β2-adrenergic receptors</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>12</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2023</Year><Month>2</Month><Day>2</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>12</Month><Day>5</Day><Hour>8</Hour><Minute>53</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36468844</ArticleId><ArticleId IdType="doi">10.1152/ajpcell.00366.2022</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">36468701</PMID><DateCompleted><Year>2022</Year><Month>12</Month><Day>06</Day></DateCompleted><DateRevised><Year>2022</Year><Month>12</Month><Day>09</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1940-087X</ISSN><JournalIssue CitedMedium="Internet"><Issue>189</Issue><PubDate><Year>2022</Year><Month>Nov</Month><Day>18</Day></PubDate></JournalIssue><Title>Journal of visualized experiments : JoVE</Title><ISOAbbreviation>J Vis Exp</ISOAbbreviation></Journal>An Apical Resection Model in the Adult Xenopus tropicalis Heart. | Mouse models of heart failure are extensively used to research human cardiovascular diseases. In particular, one of the most common is the mouse model of heart failure resulting from transverse aortic constriction (TAC). Despite this, there are no comprehensive compartmentalized mathematical models that describe the complex behavior of the action potential, [Ca<sup>2+</sup>]<sub>i</sub> transients, and their regulation by β<sub>1</sub>- and β<sub>2</sub>-adrenergic signaling systems in failing mouse myocytes. In this paper, we develop a novel compartmentalized mathematical model of failing mouse ventricular myocytes after TAC procedure. The model describes well the cell geometry, action potentials, [Ca<sup>2+</sup>]<sub>i</sub> transients, and β<sub>1</sub>- and β<sub>2</sub>-adrenergic signaling in the failing cells. Simulation results obtained with the failing cell model are compared with those from the normal ventricular myocytes. Exploration of the model reveals the sarcoplasmic reticulum Ca<sup>2+</sup> load mechanisms in failing ventricular myocytes. We also show a larger susceptibility of the failing myocytes to early and delayed afterdepolarizations and to a proarrhythmic behavior of Ca<sup>2+</sup> dynamics upon stimulation with isoproterenol. The mechanisms of the proarrhythmic behavior suppression are investigated and sensitivity analysis is performed. The developed model can explain the existing experimental data on failing mouse ventricular myocytes and make experimentally testable predictions of a failing myocyte's behavior.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Asfaw</LastName><ForeName>Tesfaye Negash</ForeName><Initials>TN</Initials><AffiliationInfo><Affiliation>Department of Mathematics and Statistics, Georgia State University, Atlanta, Georgia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bondarenko</LastName><ForeName>Vladimir E</ForeName><Initials>VE</Initials><Identifier Source="ORCID">0000-0003-4356-4669</Identifier><AffiliationInfo><Affiliation>Department of Mathematics and Statistics, Georgia State University, Atlanta, Georgia.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Neuroscience Institute, Georgia State University, Atlanta, Georgia.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>12</Month><Day>05</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Am J Physiol Cell Physiol</MedlineTA><NlmUniqueID>100901225</NlmUniqueID><ISSNLinking>0363-6143</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018663">Adrenergic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>SY7Q814VUP</RegistryNumber><NameOfSubstance UI="D002118">Calcium</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="Y">Heart Ventricles</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D032383" MajorTopicYN="N">Myocytes, Cardiac</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008962" MajorTopicYN="N">Models, Theoretical</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006333" MajorTopicYN="Y">Heart Failure</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012519" MajorTopicYN="N">Sarcoplasmic Reticulum</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018663" MajorTopicYN="N">Adrenergic Agents</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000200" MajorTopicYN="N">Action Potentials</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002118" MajorTopicYN="N">Calcium</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Ca2+ dynamics</Keyword><Keyword MajorTopicYN="N">action potential</Keyword><Keyword MajorTopicYN="N">delayed afterdepolarization</Keyword><Keyword MajorTopicYN="N">late Na+ current</Keyword><Keyword MajorTopicYN="N">β1- and β2-adrenergic receptors</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>12</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2023</Year><Month>2</Month><Day>2</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>12</Month><Day>5</Day><Hour>8</Hour><Minute>53</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36468844</ArticleId><ArticleId IdType="doi">10.1152/ajpcell.00366.2022</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">36468701</PMID><DateCompleted><Year>2022</Year><Month>12</Month><Day>06</Day></DateCompleted><DateRevised><Year>2022</Year><Month>12</Month><Day>09</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1940-087X</ISSN><JournalIssue CitedMedium="Internet"><Issue>189</Issue><PubDate><Year>2022</Year><Month>Nov</Month><Day>18</Day></PubDate></JournalIssue><Title>Journal of visualized experiments : JoVE</Title><ISOAbbreviation>J Vis Exp</ISOAbbreviation></Journal><ArticleTitle>An Apical Resection Model in the Adult Xenopus tropicalis Heart.</ArticleTitle><ELocationID EIdType="doi" ValidYN="Y">10.3791/64719</ELocationID><Abstract>It is known that in adult mammals, the heart has lost its regenerative capacity, making heart failure one of the leading causes of death worldwide. Previous research has demonstrated the regenerative ability of the heart of the adult Xenopus tropicalis, an anuran amphibian with a diploid genome and a close evolutionary relationship with mammals. Additionally, studies have shown that following ventricular apex resection, the heart can regenerate without scarring in X. tropicalis. Consequently, these previous results suggest that X. tropicalis is an appropriate alternative vertebrate model for the study of adult heart regeneration. A surgical model of cardiac regeneration in the adult X. tropicalis is presented herein. Briefly, the frogs were anesthetized and fixed; then, a small incision was made with iridectomy scissors, penetrating the skin and pericardium. Gentle pressure was applied to the ventricle, and the apex of the ventricle was then cut out with scissors. Cardiac injury and regeneration were confirmed by histology at 7-30 days post resection (dpr). This protocol established an apical resection model in adult X. tropicalis, which can be employed to elucidate the mechanisms of adult heart regeneration. |
2,329,321 | Expansion of the mutation spectrum and phenotype of <i>USP7</i>-related neurodevelopmental disorder. | Hao-fountain syndrome (HAFOUS) is a neurodevelopmental syndrome characterized by global developmental and severe language delays, behavioral abnormalities (including autism), and mild dysmorphic impairment of intellectual development. It is a dominant genetic disease caused by USP7</i> gene (*602519) mutations on chromosome 16p13.2. So far, only 15 cases with 14 deleterious variants in the USP7</i> gene have been reported.</AbstractText>This study describes three unrelated patients with USP7</i> variants. Besides, we identified novel de novo</i> heterozygous USP7</i> variants using trio-whole exome sequencing and verified by Sanger sequencing. Furthermore, clinical characteristics were evaluated by reviewing the medical records.</AbstractText>The three identified variants, i.e., one frameshift variant (c.247_250del, p.Glu83Argfs × 18) and two missense variants (c.992A > G, p.Tyr331Cys; c.835T > G, p.Leu279Val) are unreported. The predominant clinical manifestations of the three patients included: DD/ID; language impairment; abnormal behavior; abnormal brain magnetic resonance (dilation of lateral ventricles, dilation of Virchow-Robin spaces, dilated the third ventricle, abnormal cerebral white matter morphology in bilateral occipital lobes, hypodysplasia of the corpus callosum, arachnoid cyst, delayed myelination, and widened subarachnoid space); some also had facial abnormalities.</AbstractText>In summary, DD/ID is the most prevalent clinical phenotype of HAFOUS, although some patients also exhibit language and behavioral abnormalities. For the first time in China, we identified three variants of the USP7</i> gene using whole-genome sequence data. This work expands the USP7</i> gene mutation spectrum and provides additional clinical data on the clinical phenotype of HAFOUS.</AbstractText>Copyright © 2022 Zheng, Mei, Li, Wei, Wang, Huang, Zhang, Huang, Liu, Gu and Liu.</CopyrightInformation> |
2,329,322 | Incidental and Clinical Significance of Slit Ventricles in Fixed Pressure Valves. | Slit ventricle syndrome (SVS) is a recognized delayed complication of cerebrospinal fluid (CSF) shunting in children. It had been linked to the use of low-pressure shunts and considered an argument for the use of programmable valves. In this study, we aim to assess the rate of SVS in children that were shunted using fixed-pressure valves.</AbstractText>This study is a retrospective cohort study that occurred in King Abdulaziz Medical City, Jeddah, which reviews 100 patients with a median age of 15.5 months that were shunted by using fixed pressure valves during the period from 2010 to 2018. Fixed low-pressure valves were used in 69% of patients, while fixed medium-pressure valves were used in 31% of patients. SVS was defined by the presence of slit-like ventricles (fronto-occipital [F-O] horns ratio was ≤ 0.2 on any post-shunt CT scan) and the occurrence of slit-like ventricle-related symptoms (chronic headache, nausea, vomiting, and altered conscious level_ in the absence of other causes of shunt malfunction.</AbstractText>The overall SVS rate in the cohort was 6%. Nine children had slit-like ventricles, but only six of them were symptomatic. Relatively higher SVS rates were observed in younger male children, obstructive hydrocephalus, and medium-pressure valves. Slit-like ventricle-related symptoms in the absence of a slit-like ventricle were reported in 24 out of 91 (26%) patients. A total of 42 patients underwent shunt revisions for other complications. All SVS patients were treated conservatively. There was a temporal fluctuation in the F-O horns ratio and in some patients with SVS their F-O horns ratio returned to normal at further follow-up without intervention.</AbstractText>The overall SVS rate following the use of fixed-pressure CSF valves in children is low and managed conservatively. Not all patients with slit-like ventricles are symptomatic and the radiological appearance of SVS may improve on further follow-up without intervention. Fixed pressure valves remain an acceptable device in the treatment of hydrocephalus in children.</AbstractText>Copyright © 2022, Alghamdi et al.</CopyrightInformation> |
2,329,323 | Sublethal exposure to Microcystis aeruginosa extracts during the yolk-sac larval stage reduces aerobic swimming speed in juvenile zebrafish.<Pagination><StartPage>1443</StartPage><EndPage>1447</EndPage><MedlinePgn>1443-1447</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s10695-022-01151-8</ELocationID><Abstract><AbstractText>This study examined whether the aerobic swimming capacity of zebrafish juveniles is affected by the exposure of the yolk-sac larvae to sublethal concentration of Microcystis aeruginosa extract (200 mg dw L<sup>-1</sup>). Critical swimming speed significantly decreased in the pre-exposed fish (9.2 ± 1.0 vs 11.3 ± 1.4 TL s<sup>-1</sup> in the control group). Exposure did not have any significant effects on the shape of the heart ventricle, rate of skeletal abnormalities, and growth or survival rates. Decreased swimming performance due to the early and short exposure to M. aeruginosa could have negative impacts on fish in the wild.</AbstractText><CopyrightInformation>© 2022. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kekelou</LastName><ForeName>Athina</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Biology Department, University of Crete, Heraklion, Greece.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dimitriadi</LastName><ForeName>Anastasia</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Biology Department, University of Crete, Heraklion, Greece.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Koumoundouros</LastName><ForeName>George</ForeName><Initials>G</Initials><Identifier Source="ORCID">0000-0002-9738-0403</Identifier><AffiliationInfo><Affiliation>Biology Department, University of Crete, Heraklion, Greece. gkoumound@uoc.gr.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>MIS-5033021</GrantID><Agency>European Social Fund-ESF, State Scholarships Foundation, ІKΥ (Greece & EU)</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>12</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Fish Physiol Biochem</MedlineTA><NlmUniqueID>100955049</NlmUniqueID><ISSNLinking>0920-1742</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015027" MajorTopicYN="Y">Zebrafish</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007814" MajorTopicYN="N">Larva</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013550" MajorTopicYN="N">Swimming</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D046931" MajorTopicYN="Y">Microcystis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015017" MajorTopicYN="N">Yolk Sac</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Critical swimming speed</Keyword><Keyword MajorTopicYN="N">CyanoHABs</Keyword><Keyword MajorTopicYN="N">Fish</Keyword><Keyword MajorTopicYN="N">Yolk-sac larvae</Keyword></KeywordList><CoiStatement>The authors declare no competing interests.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>8</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>11</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>12</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>12</Month><Day>22</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>12</Month><Day>3</Day><Hour>11</Hour><Minute>15</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36462100</ArticleId><ArticleId IdType="pmc">PMC9763139</ArticleId><ArticleId IdType="doi">10.1007/s10695-022-01151-8</ArticleId><ArticleId IdType="pii">10.1007/s10695-022-01151-8</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Fleming A, Keynes R, Tannahill D. 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Biotech Histochem. 2007;82:23–28. doi: 10.1080/10520290701333558.</Citation><ArticleIdList><ArticleId IdType="doi">10.1080/10520290701333558</ArticleId><ArticleId IdType="pubmed">17510811</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36462099</PMID><DateRevised><Year>2023</Year><Month>05</Month><Day>11</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1868-601X</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Dec</Month><Day>03</Day></PubDate></JournalIssue><Title>Translational stroke research</Title><ISOAbbreviation>Transl Stroke Res</ISOAbbreviation></Journal>Stroke and Neurogenesis: Bridging Clinical Observations to New Mechanistic Insights from Animal Models.<ELocationID EIdType="doi" ValidYN="Y">10.1007/s12975-022-01109-1</ELocationID><Abstract><AbstractText>Stroke was the 2nd leading cause of death and a major cause of morbidity. Unfortunately, there are limited means to promote neurological recovery post-stroke, but research has unearthed potential targets for therapies to encourage post-stroke neurogenesis and neuroplasticity. The occurrence of neurogenesis in adult mammalian brains, including humans, was not widely accepted until the 1990s. Now, adult neurogenesis has been extensively studied in human and mouse neurogenic brain niches, of which the subventricular zone of the lateral ventricles and subgranular zone of the dentate gyrus are best studied. Numerous other niches are under investigation for neurogenic potential. This review offers a basic overview to stroke in the clinical setting, a focused summary of recent and foundational research literature on cortical neurogenesis and post-stroke brain plasticity, and insights regarding how the meninges and choroid plexus have emerged as key players in neurogenesis and neuroplasticity in the context of focal cerebral ischemia disrupting the anterior circulation. The choroid plexus and meninges are vital as they are integral sites for neuroimmune interactions, glymphatic perfusion, and niche signaling pertinent to neural stem cells and neurogenesis. Modulating neuroimmune interactions with a focus on astrocyte activity, potentially through manipulation of the choroid plexus and meningeal niches, may reduce the exacerbation of stroke by inflammatory mediators and create an environment conducive to neurorecovery. Furthermore, addressing impaired glymphatic perfusion after ischemic stroke likely supports a neurogenic environment by clearing out inflammatory mediators, neurotoxic metabolites, and other accumulated waste. The meninges and choroid plexus also contribute more directly to promoting neurogenesis: the meninges are thought to harbor neural stem cells and are a niche amenable to neural stem/progenitor cell migration. Additionally, the choroid plexus has secretory functions that directly influences stem cells through signaling mechanisms and growth factor actions. More research to better understand the functions of the meninges and choroid plexus may lead to novel approaches for stimulating neuronal recovery after ischemic stroke.</AbstractText><CopyrightInformation>© 2022. This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Passarelli</LastName><ForeName>Joshua P</ForeName><Initials>JP</Initials><AffiliationInfo><Affiliation>Tufts University School of Medicine, Boston, MA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nimjee</LastName><ForeName>Shahid M</ForeName><Initials>SM</Initials><AffiliationInfo><Affiliation>Department of Neurological Surgery, The Ohio State University Wexner Medical Center, Biomedical Research Tower, 460 W 12th Avenue, Columbus, OH, 43210, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Townsend</LastName><ForeName>Kristy L</ForeName><Initials>KL</Initials><AffiliationInfo><Affiliation>Department of Neurological Surgery, The Ohio State University Wexner Medical Center, Biomedical Research Tower, 460 W 12th Avenue, Columbus, OH, 43210, USA. kristy.townsend@osumc.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>12</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Transl Stroke Res</MedlineTA><NlmUniqueID>101517297</NlmUniqueID><ISSNLinking>1868-4483</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Adult stem cell</Keyword><Keyword MajorTopicYN="N">Brain</Keyword><Keyword MajorTopicYN="N">Central nervous system (CNS)</Keyword><Keyword MajorTopicYN="N">Choroid plexus</Keyword><Keyword MajorTopicYN="N">Inflammation</Keyword><Keyword MajorTopicYN="N">Ischemia</Keyword><Keyword MajorTopicYN="N">Meninges</Keyword><Keyword MajorTopicYN="N">Neural stem cell</Keyword><Keyword MajorTopicYN="N">Neurogenesis</Keyword><Keyword MajorTopicYN="N">Plasticity</Keyword><Keyword MajorTopicYN="N">Regeneration</Keyword><Keyword MajorTopicYN="N">Remodeling</Keyword><Keyword MajorTopicYN="N">Stroke</Keyword><Keyword MajorTopicYN="N">Tissue stem cell</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>10</Month><Day>13</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>11</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>11</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>12</Month><Day>3</Day><Hour>11</Hour><Minute>15</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>12</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>12</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>aheadofprint</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36462099</ArticleId><ArticleId IdType="doi">10.1007/s12975-022-01109-1</ArticleId><ArticleId IdType="pii">10.1007/s12975-022-01109-1</ArticleId></ArticleIdList><ReferenceList><Title>References</Title><Reference><Citation>Collaborators GBDCoD. 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Critical swimming speed significantly decreased in the pre-exposed fish (9.2 ± 1.0 vs 11.3 ± 1.4 TL s<sup>-1</sup> in the control group). Exposure did not have any significant effects on the shape of the heart ventricle, rate of skeletal abnormalities, and growth or survival rates. Decreased swimming performance due to the early and short exposure to M. aeruginosa could have negative impacts on fish in the wild.<CopyrightInformation>© 2022. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kekelou</LastName><ForeName>Athina</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Biology Department, University of Crete, Heraklion, Greece.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dimitriadi</LastName><ForeName>Anastasia</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Biology Department, University of Crete, Heraklion, Greece.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Koumoundouros</LastName><ForeName>George</ForeName><Initials>G</Initials><Identifier Source="ORCID">0000-0002-9738-0403</Identifier><AffiliationInfo><Affiliation>Biology Department, University of Crete, Heraklion, Greece. gkoumound@uoc.gr.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>MIS-5033021</GrantID><Agency>European Social Fund-ESF, State Scholarships Foundation, ІKΥ (Greece & EU)</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>12</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Fish Physiol Biochem</MedlineTA><NlmUniqueID>100955049</NlmUniqueID><ISSNLinking>0920-1742</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015027" MajorTopicYN="Y">Zebrafish</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007814" MajorTopicYN="N">Larva</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013550" MajorTopicYN="N">Swimming</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D046931" MajorTopicYN="Y">Microcystis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015017" MajorTopicYN="N">Yolk Sac</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Critical swimming speed</Keyword><Keyword MajorTopicYN="N">CyanoHABs</Keyword><Keyword MajorTopicYN="N">Fish</Keyword><Keyword MajorTopicYN="N">Yolk-sac larvae</Keyword></KeywordList><CoiStatement>The authors declare no competing interests.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>8</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>11</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>12</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>12</Month><Day>22</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>12</Month><Day>3</Day><Hour>11</Hour><Minute>15</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36462100</ArticleId><ArticleId IdType="pmc">PMC9763139</ArticleId><ArticleId IdType="doi">10.1007/s10695-022-01151-8</ArticleId><ArticleId IdType="pii">10.1007/s10695-022-01151-8</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Fleming A, Keynes R, Tannahill D. 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Biotech Histochem. 2007;82:23–28. doi: 10.1080/10520290701333558.</Citation><ArticleIdList><ArticleId IdType="doi">10.1080/10520290701333558</ArticleId><ArticleId IdType="pubmed">17510811</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36462099</PMID><DateRevised><Year>2023</Year><Month>05</Month><Day>11</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1868-601X</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Dec</Month><Day>03</Day></PubDate></JournalIssue><Title>Translational stroke research</Title><ISOAbbreviation>Transl Stroke Res</ISOAbbreviation></Journal><ArticleTitle>Stroke and Neurogenesis: Bridging Clinical Observations to New Mechanistic Insights from Animal Models.</ArticleTitle><ELocationID EIdType="doi" ValidYN="Y">10.1007/s12975-022-01109-1</ELocationID><Abstract>Stroke was the 2nd leading cause of death and a major cause of morbidity. Unfortunately, there are limited means to promote neurological recovery post-stroke, but research has unearthed potential targets for therapies to encourage post-stroke neurogenesis and neuroplasticity. The occurrence of neurogenesis in adult mammalian brains, including humans, was not widely accepted until the 1990s. Now, adult neurogenesis has been extensively studied in human and mouse neurogenic brain niches, of which the subventricular zone of the lateral ventricles and subgranular zone of the dentate gyrus are best studied. Numerous other niches are under investigation for neurogenic potential. This review offers a basic overview to stroke in the clinical setting, a focused summary of recent and foundational research literature on cortical neurogenesis and post-stroke brain plasticity, and insights regarding how the meninges and choroid plexus have emerged as key players in neurogenesis and neuroplasticity in the context of focal cerebral ischemia disrupting the anterior circulation. The choroid plexus and meninges are vital as they are integral sites for neuroimmune interactions, glymphatic perfusion, and niche signaling pertinent to neural stem cells and neurogenesis. Modulating neuroimmune interactions with a focus on astrocyte activity, potentially through manipulation of the choroid plexus and meningeal niches, may reduce the exacerbation of stroke by inflammatory mediators and create an environment conducive to neurorecovery. Furthermore, addressing impaired glymphatic perfusion after ischemic stroke likely supports a neurogenic environment by clearing out inflammatory mediators, neurotoxic metabolites, and other accumulated waste. The meninges and choroid plexus also contribute more directly to promoting neurogenesis: the meninges are thought to harbor neural stem cells and are a niche amenable to neural stem/progenitor cell migration. Additionally, the choroid plexus has secretory functions that directly influences stem cells through signaling mechanisms and growth factor actions. More research to better understand the functions of the meninges and choroid plexus may lead to novel approaches for stimulating neuronal recovery after ischemic stroke.<CopyrightInformation>© 2022. This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Passarelli</LastName><ForeName>Joshua P</ForeName><Initials>JP</Initials><AffiliationInfo><Affiliation>Tufts University School of Medicine, Boston, MA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nimjee</LastName><ForeName>Shahid M</ForeName><Initials>SM</Initials><AffiliationInfo><Affiliation>Department of Neurological Surgery, The Ohio State University Wexner Medical Center, Biomedical Research Tower, 460 W 12th Avenue, Columbus, OH, 43210, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Townsend</LastName><ForeName>Kristy L</ForeName><Initials>KL</Initials><AffiliationInfo><Affiliation>Department of Neurological Surgery, The Ohio State University Wexner Medical Center, Biomedical Research Tower, 460 W 12th Avenue, Columbus, OH, 43210, USA. kristy.townsend@osumc.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>12</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Transl Stroke Res</MedlineTA><NlmUniqueID>101517297</NlmUniqueID><ISSNLinking>1868-4483</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Adult stem cell</Keyword><Keyword MajorTopicYN="N">Brain</Keyword><Keyword MajorTopicYN="N">Central nervous system (CNS)</Keyword><Keyword MajorTopicYN="N">Choroid plexus</Keyword><Keyword MajorTopicYN="N">Inflammation</Keyword><Keyword MajorTopicYN="N">Ischemia</Keyword><Keyword MajorTopicYN="N">Meninges</Keyword><Keyword MajorTopicYN="N">Neural stem cell</Keyword><Keyword MajorTopicYN="N">Neurogenesis</Keyword><Keyword MajorTopicYN="N">Plasticity</Keyword><Keyword MajorTopicYN="N">Regeneration</Keyword><Keyword MajorTopicYN="N">Remodeling</Keyword><Keyword MajorTopicYN="N">Stroke</Keyword><Keyword MajorTopicYN="N">Tissue stem cell</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>10</Month><Day>13</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>11</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>11</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>12</Month><Day>3</Day><Hour>11</Hour><Minute>15</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>12</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>12</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>aheadofprint</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36462099</ArticleId><ArticleId IdType="doi">10.1007/s12975-022-01109-1</ArticleId><ArticleId IdType="pii">10.1007/s12975-022-01109-1</ArticleId></ArticleIdList><ReferenceList><Title>References</Title><Reference><Citation>Collaborators GBDCoD. 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Overexpression of slit2 decreases neuronal excitotoxicity, accelerates glymphatic clearance, and improves cognition in a multiple microinfarcts model. Mol Brain. 2020;13:135.</Citation><ArticleIdList><ArticleId IdType="pubmed">33028376</ArticleId><ArticleId IdType="pmc">7542754</ArticleId><ArticleId IdType="doi">10.1186/s13041-020-00659-5</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36462027</PMID><DateRevised><Year>2022</Year><Month>12</Month><Day>03</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1432-1971</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Dec</Month><Day>03</Day></PubDate></JournalIssue><Title>Pediatric cardiology</Title><ISOAbbreviation>Pediatr Cardiol</ISOAbbreviation></Journal><ArticleTitle>Impact of Maternal-Fetal Environment on Outcomes Following the Hybrid Procedure in the Single Ventricle Population.</ArticleTitle><ELocationID EIdType="doi" ValidYN="Y">10.1007/s00246-022-03063-z</ELocationID><Abstract>Treatment of infants with hypoplastic left heart syndrome (HLHS) remains challenging, and those affected remain with significant risks for mortality and morbidity throughout their lifetimes. The maternal-fetal environment (MFE) has been shown to affect outcomes for infants with HLHS after the Norwood procedure. The hybrid procedure, comprised of both catheterization and surgical components, is a less invasive option for initial intervention compared to the Norwood procedure. It is unknown how the MFE impacts outcomes following the hybrid procedure. This is a single-center, retrospective study of infants born with HLHS who underwent hybrid palliation from January 2009 to August 2021. Predictor variables analyzed included fetal, maternal, and postnatal factors. The primary outcome was mortality prior to Stage II palliation. We studied a 144-subject cohort. There was a statistically significant difference in mortality prior to stage II palliation in infants with prematurity, small for gestational age, and aortic atresia subtype (p < 0.001, p = 0.009, and p = 0.008, respectively). There was no difference in mortality associated with maternal diabetes, hypertension, obesity, smoking or illicit drug use, or advanced maternal age. State and national area deprivation index scores were associated with increased risk of mortality in the entire cohort, such that infants born in areas with higher deprivation had a higher incidence of mortality. Several markers of an impaired MFE, including prematurity, small for gestational age, and higher deprivation index scores, are associated with mortality following hybrid palliation. Individual maternal comorbidities were not associated with higher mortality. The MFE may be a target for prenatal counseling and future interventions to improve pregnancy and neonatal outcomes in this population. |
2,329,324 | External-internal cranial expansion to treat patients with craniocerebral disproportion due to post-shunt craniosynostosis: a case series. | Secondary craniosynostosis subsequent to shunting is one of the late complications of ventricular shunt placement in the early childhood. Several interventions have been used to treat high intracranial pressure associated with this condition. This study aimed to evaluate the patients' clinical symptoms and head circumference before and after a method of decompressive craniotomy, coined as external-internal cranial expansion (EICE).</AbstractText>A retrospective study was conducted, and the patients who had undergone EICE for the treatment of post-shunt craniosynostosis between 2010 and 2020 were enrolled. This approach was a combination of a hinge multiple-strut decompressive craniectomy and internal cranial flap thinning by drill. Data, extracted from medical records, were used to evaluate the patients' symptoms and head circumferences before and 12 months after surgery.</AbstractText>A total of 16 patients were enrolled in the study, of which eight were females. Before the surgery, 9 patients (56.2%) suffered from visual impairment, and all had intractable headache. Papilledema was recorded in all, with 3 cases having optic disc paleness. After cranial expansion, only two patients had headaches, diagnosed as migraine-type and psychosomatic headaches, respectively. In two patients, progressive visual impairments got worsening after surgery, which would be due to severe preoperative optic nerve atrophy. Patients' head circumferences significantly increased after the surgery (mean of 48.97 ± 4.28 cm vs. 45.78 ± 4.31 cm; P value < 0.0001).</AbstractText>In lower resource countries, where newer technologies like distraction osteogenesis is not easily available, external-internal cranial expansion can be considered an effective alternative for patients with post-shunt craniosynostosis.</AbstractText>© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.</CopyrightInformation> |
2,329,325 | [Immediate, medium- and long-term outcomes of percutaneous coronary intervention with very long drug eluting stent : An observational multicentric study].<Pagination><StartPage>8</StartPage><EndPage>15</EndPage><MedlinePgn>8-15</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.ancard.2022.11.006</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0003-3928(22)00209-8</ELocationID><Abstract><AbstractText Label="INTRODUCTION" NlmCategory="BACKGROUND">Very long coronary lesions account for 20% of coronary stenoses in the real world. There are few data on the effectiveness of angioplasty of these lesions with very long active stents (DES) in the literature. We conducted this study to assess the long-term outcomes of angioplasty with DES length ≥ 40 mm in a population with multiple cardiovascular risk factors.</AbstractText><AbstractText Label="PATIENTS AND METHODS" NlmCategory="METHODS">This is a retrospective, multicenter, descriptive, and prognostic study, conducted between January 2015 and January 2020, in four Tunisian centers, including all patients who underwent angioplasty with a DES of length ≥ 40 mm with a follow-up of at least one year. The primary outcome was a combined criteria (major cardiovascular and Cerebral events: MACCE) (stroke, acute coronary syndrome, revascularization of the target lesion: TLR, cardiovascular death: CVD).</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">We included 480 procedures. More than half of the patients had at least three risk factors. The prevalence of high blood pressure, diabetes and smoking were 61.1%, 56.6% and 60.4%, respectively. The treated lesions were complex: 23.54% calcified lesions, 8.75% chronic occlusions, 25% bifurcation lesions and 12.08% ostial lesions. The average length of the stents was 47.72 mm. We noted 17 cases of per-procedural complications (3.55%). The median follow-up was 35 months (extremes 1-60 months). The rate of stent thrombosis was 0.83%. The incidence of MACCE, TLR and CVD were respectively 16.25%, 8.12% and 5.2%. In multivariate analysis, diabetes (HR = 1.7, 95% CI [1.01-2.9]), dyslipidemia (HR = 2.08, 95% CI [1.3-3.3]), familial coronary artery disease (HR = 1.9, 95% CI [1.01-3.6]), left ventricle dysfunction (HR = 2.07, 95% CI [1.1-3.6]) and bifurcation lesions (HR = 1.9, 95% CI [1.2-3.14]) were the independent predictors of MACCE, while statin intake (HR = 0.38, 95% CI [0.19-0.78]) was a protective factor.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">Angioplasty with very long DES is associated with low levels of MACCE, TLR, stent thrombosis and CVD in our population. Therefore, it could be an interesting alternative to cardiac surgery. Randomized comparative studies of the two treatment options are needed.</AbstractText><CopyrightInformation>Copyright © 2022. Published by Elsevier Masson SAS.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hammami</LastName><ForeName>Rania</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Service de Cardiologie de Sfax, Hôpital Hedi Chaker Sfax, Faculté de médecine de Sfax, Université de Sfax, 3029, Tunisie. Electronic address: raniahammami@yahoo.fr.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Boughariou</LastName><ForeName>Aimen</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Service de Cardiologie de Sfax, Hôpital Hedi Chaker Sfax, Faculté de médecine de Sfax, Université de Sfax, 3029, Tunisie.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jdidi</LastName><ForeName>Jihen</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Service de Médecine préventive, Faculté de médecine de Sfax, Université de Sfax, Tunisie.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cheikhrouhou</LastName><ForeName>Anis</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Service de Cardiologie de Sfax, Hôpital Hedi Chaker Sfax, Faculté de médecine de Sfax, Université de Sfax, 3029, Tunisie.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Abdelmoula</LastName><ForeName>Yacine</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Service de Cardiologie de Sfax, Hôpital Hedi Chaker Sfax, Faculté de médecine de Sfax, Université de Sfax, 3029, Tunisie.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Thabet</LastName><ForeName>Houssem</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Service de Cardiologie, Hôpital Sahloul, Sousse, Tunisie.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gribaa</LastName><ForeName>Rim</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Service de Cardiologie, Hôpital Sahloul, Sousse, Tunisie.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kacem</LastName><ForeName>Marwen</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Service de Cardiologie, Hôpital Sahloul, Sousse, Tunisie.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mrad</LastName><ForeName>Imtinene Ben</ForeName><Initials>IB</Initials><AffiliationInfo><Affiliation>Service de Cardiologie, Hôpital Habib Thameur, Tunis, Tunisie.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Belkahla</LastName><ForeName>Noufeil</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Service de Cardiologie, Hôpital Habib Thameur, Tunis, Tunisie.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Abdessalem</LastName><ForeName>Aymen Ben</ForeName><Initials>AB</Initials><AffiliationInfo><Affiliation>Service de Cardiologie, Hôpital Farhat Hached, Sousse, Tunisie.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ameur</LastName><ForeName>Zied Ben</ForeName><Initials>ZB</Initials><AffiliationInfo><Affiliation>Service de Cardiologie, Hôpital Farhat Hached, Sousse, Tunisie.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hejri</LastName><ForeName>Ernez</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Service de Cardiologie, Hôpital Farhat Hached, Sousse, Tunisie.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kraiem</LastName><ForeName>Sondos</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Service de Cardiologie, Hôpital Habib Thameur, Tunis, Tunisie.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Naffeti</LastName><ForeName>Ilyes</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Service de Cardiologie, Hôpital Sahloul, Sousse, Tunisie.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Abid</LastName><ForeName>Leila</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Service de Cardiologie de Sfax, Hôpital Hedi Chaker Sfax, Faculté de médecine de Sfax, Université de Sfax, 3029, Tunisie.</Affiliation></AffiliationInfo></Author></AuthorList><Language>fre</Language><PublicationTypeList><PublicationType UI="D064888">Observational Study</PublicationType><PublicationType UI="D016448">Multicenter Study</PublicationType><PublicationType UI="D004740">English Abstract</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><VernacularTitle>Les résultats immédiats, à moyen et à long terme de l'angioplastie coronaire par stent actif très long : à propos d'une étude multicentrique observationnelle.</VernacularTitle><ArticleDate DateType="Electronic"><Year>2022</Year><Month>11</Month><Day>28</Day></ArticleDate></Article><MedlineJournalInfo><Country>France</Country><MedlineTA>Ann Cardiol Angeiol (Paris)</MedlineTA><NlmUniqueID>0142167</NlmUniqueID><ISSNLinking>0003-3928</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D054855" MajorTopicYN="Y">Drug-Eluting Stents</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009203" MajorTopicYN="Y">Myocardial Infarction</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003324" MajorTopicYN="Y">Coronary Artery Disease</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D062645" MajorTopicYN="Y">Percutaneous Coronary Intervention</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013927" MajorTopicYN="Y">Thrombosis</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003920" MajorTopicYN="Y">Diabetes Mellitus</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Angioplastie</Keyword><Keyword MajorTopicYN="N">décès cardiovasculaire</Keyword><Keyword MajorTopicYN="N">stent actif</Keyword><Keyword MajorTopicYN="N">thrombose</Keyword></KeywordList><CoiStatement>Déclaration de liens d'intérêts Les auteurs déclarent ne pas avoir de liens d'intérêts.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>7</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>11</Month><Day>5</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>11</Month><Day>7</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>12</Month><Day>2</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2023</Year><Month>2</Month><Day>8</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>12</Month><Day>1</Day><Hour>22</Hour><Minute>3</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36456251</ArticleId><ArticleId IdType="doi">10.1016/j.ancard.2022.11.006</ArticleId><ArticleId IdType="pii">S0003-3928(22)00209-8</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36455711</PMID><DateRevised><Year>2023</Year><Month>05</Month><Day>30</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1532-9488</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Nov</Month><Day>29</Day></PubDate></JournalIssue><Title>Seminars in thoracic and cardiovascular surgery</Title><ISOAbbreviation>Semin Thorac Cardiovasc Surg</ISOAbbreviation></Journal>Palliated Hypoplastic Left Heart Syndrome Patients Experience Superior Waitlist and Comparable Post-Heart Transplant Survival to Non-Single Ventricle Congenital Heart Disease Patients.<ELocationID EIdType="pii" ValidYN="Y">S1043-0679(22)00271-4</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1053/j.semtcvs.2022.08.019</ELocationID><Abstract><AbstractText>Congenital heart disease (CHD) is a well-established risk factor for inferior waitlist and post-heart transplant survival in children. Differences in outcomes between CHD subgroups are understudied. The present study compared outcomes for palliated hypoplastic left heart syndrome (HLHS) patients to other non-single ventricle CHD (non-SVCHD) and non-CHD patients. United Network for Organ Sharing was used to identify children (age < 18) listed for heart transplant in the United States between 2016 and 2021. CHD sub-diagnoses were only available for United Network for Organ Sharing status 1a after 2015, thereby defining the cohort. Waitlist outcomes were studied using competing-risk time-to-event analysis for transplantation, mortality/decompensation, and alive-on-waitlist. Multivariable Cox proportional hazards regression analyses were used to identify factors associated with inferior post-transplant survival. Patients included: palliated-HLHS (n = 477), non-SVCHD (n = 686), and non-CHD (n = 1261). At listing, Palliated-HLHS patients were older than non-SVCHD (median 2-year [IQR 0-8] vs median 0-year [0-3], respectively) and younger than non-CHD (median 7-year [0-14]) (P < 0.001 vs both), and were more likely to be white (P < 0.01 vs both). Upon time-to-event analysis, rates of waitlist mortality/decompensation rates were greater among non-SVCHD than palliated-HLHS. Post-transplant survival was comparable between palliated-HLHS and non-SVCHD (P = 0.920) but worse compared to non-CHD (P < 0.001). Both palliated-HLHS (HR 2.40 [95% CI 1.68-3.42]) and non-SVSCHD (2.04 [1.39-2.99]) were independently associated with post-transplant mortality. Palliated-HLHS patients with heart failure experience significantly worse post-transplant outcomes than non-CHD but, compared to other CHD patients, experience superior waitlist and comparable post-transplant survival. While a high-risk cohort, HLHS patients can achieve gratifying waitlist and post-transplant survival.</AbstractText><CopyrightInformation>Copyright © 2022 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Greenberg</LastName><ForeName>Jason W</ForeName><Initials>JW</Initials><AffiliationInfo><Affiliation>The Heart Institute, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio. Electronic address: jasongreenbergmd@gmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Raees</LastName><ForeName>Muhammad Aanish</ForeName><Initials>MA</Initials><AffiliationInfo><Affiliation>The Heart Institute, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dani</LastName><ForeName>Alia</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>The Heart Institute, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Heydarian</LastName><ForeName>Haleh C</ForeName><Initials>HC</Initials><AffiliationInfo><Affiliation>The Heart Institute, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chin</LastName><ForeName>Clifford</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>The Heart Institute, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zafar</LastName><ForeName>Farhan</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>The Heart Institute, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lehenbauer</LastName><ForeName>David G</ForeName><Initials>DG</Initials><AffiliationInfo><Affiliation>The Heart Institute, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Morales</LastName><ForeName>David L S</ForeName><Initials>DLS</Initials><AffiliationInfo><Affiliation>The Heart Institute, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 HL147957</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>11</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Semin Thorac Cardiovasc Surg</MedlineTA><NlmUniqueID>8917640</NlmUniqueID><ISSNLinking>1043-0679</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Clinical outcomes</Keyword><Keyword MajorTopicYN="N">Congenital cardiac surgery</Keyword><Keyword MajorTopicYN="N">Congenital heart disease</Keyword><Keyword MajorTopicYN="N">Heart transplantation</Keyword><Keyword MajorTopicYN="N">Hypoplastic left heart syndrome</Keyword><Keyword MajorTopicYN="N">Norwood procedure</Keyword><Keyword MajorTopicYN="N">Quality improvement</Keyword></KeywordList><CoiStatement><b>Disclosures:</b> The authors declare no conflicts of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>8</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>8</Month><Day>31</Day></PubMedPubDate><PubMedPubDate PubStatus="pmc-release"><Year>2024</Year><Month>5</Month><Day>29</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>12</Month><Day>2</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>12</Month><Day>2</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>12</Month><Day>1</Day><Hour>19</Hour><Minute>25</Minute></PubMedPubDate></History><PublicationStatus>aheadofprint</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36455711</ArticleId><ArticleId IdType="mid">NIHMS1853639</ArticleId><ArticleId IdType="pmc">PMC10225473</ArticleId><ArticleId IdType="doi">10.1053/j.semtcvs.2022.08.019</ArticleId><ArticleId IdType="pii">S1043-0679(22)00271-4</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Krasuski RA, Bashore TM. 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J Hear Lung Transplant. 2009;28(12):1292–1298. doi:10.1016/j.healun.2009.06.013</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.healun.2009.06.013</ArticleId><ArticleId IdType="pmc">PMC4269350</ArticleId><ArticleId IdType="pubmed">19782580</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36455710</PMID><DateRevised><Year>2023</Year><Month>05</Month><Day>30</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1532-9488</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Nov</Month><Day>29</Day></PubDate></JournalIssue><Title>Seminars in thoracic and cardiovascular surgery</Title><ISOAbbreviation>Semin Thorac Cardiovasc Surg</ISOAbbreviation></Journal>Force Profiles of Single Ventricle Atrioventricular Leaflets in Response to Annular Dilation and Leaflet Tethering. | Congenital heart disease (CHD) is a well-established risk factor for inferior waitlist and post-heart transplant survival in children. Differences in outcomes between CHD subgroups are understudied. The present study compared outcomes for palliated hypoplastic left heart syndrome (HLHS) patients to other non-single ventricle CHD (non-SVCHD) and non-CHD patients. United Network for Organ Sharing was used to identify children (age < 18) listed for heart transplant in the United States between 2016 and 2021. CHD sub-diagnoses were only available for United Network for Organ Sharing status 1a after 2015, thereby defining the cohort. Waitlist outcomes were studied using competing-risk time-to-event analysis for transplantation, mortality/decompensation, and alive-on-waitlist. Multivariable Cox proportional hazards regression analyses were used to identify factors associated with inferior post-transplant survival. Patients included: palliated-HLHS (n = 477), non-SVCHD (n = 686), and non-CHD (n = 1261). At listing, Palliated-HLHS patients were older than non-SVCHD (median 2-year [IQR 0-8] vs median 0-year [0-3], respectively) and younger than non-CHD (median 7-year [0-14]) (P < 0.001 vs both), and were more likely to be white (P < 0.01 vs both). Upon time-to-event analysis, rates of waitlist mortality/decompensation rates were greater among non-SVCHD than palliated-HLHS. Post-transplant survival was comparable between palliated-HLHS and non-SVCHD (P = 0.920) but worse compared to non-CHD (P < 0.001). Both palliated-HLHS (HR 2.40 [95% CI 1.68-3.42]) and non-SVSCHD (2.04 [1.39-2.99]) were independently associated with post-transplant mortality. Palliated-HLHS patients with heart failure experience significantly worse post-transplant outcomes than non-CHD but, compared to other CHD patients, experience superior waitlist and comparable post-transplant survival. While a high-risk cohort, HLHS patients can achieve gratifying waitlist and post-transplant survival.<CopyrightInformation>Copyright © 2022 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Greenberg</LastName><ForeName>Jason W</ForeName><Initials>JW</Initials><AffiliationInfo><Affiliation>The Heart Institute, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio. Electronic address: jasongreenbergmd@gmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Raees</LastName><ForeName>Muhammad Aanish</ForeName><Initials>MA</Initials><AffiliationInfo><Affiliation>The Heart Institute, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dani</LastName><ForeName>Alia</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>The Heart Institute, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Heydarian</LastName><ForeName>Haleh C</ForeName><Initials>HC</Initials><AffiliationInfo><Affiliation>The Heart Institute, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chin</LastName><ForeName>Clifford</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>The Heart Institute, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zafar</LastName><ForeName>Farhan</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>The Heart Institute, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lehenbauer</LastName><ForeName>David G</ForeName><Initials>DG</Initials><AffiliationInfo><Affiliation>The Heart Institute, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Morales</LastName><ForeName>David L S</ForeName><Initials>DLS</Initials><AffiliationInfo><Affiliation>The Heart Institute, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 HL147957</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>11</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Semin Thorac Cardiovasc Surg</MedlineTA><NlmUniqueID>8917640</NlmUniqueID><ISSNLinking>1043-0679</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Clinical outcomes</Keyword><Keyword MajorTopicYN="N">Congenital cardiac surgery</Keyword><Keyword MajorTopicYN="N">Congenital heart disease</Keyword><Keyword MajorTopicYN="N">Heart transplantation</Keyword><Keyword MajorTopicYN="N">Hypoplastic left heart syndrome</Keyword><Keyword MajorTopicYN="N">Norwood procedure</Keyword><Keyword MajorTopicYN="N">Quality improvement</Keyword></KeywordList><CoiStatement><b>Disclosures:</b> The authors declare no conflicts of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>8</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>8</Month><Day>31</Day></PubMedPubDate><PubMedPubDate PubStatus="pmc-release"><Year>2024</Year><Month>5</Month><Day>29</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>12</Month><Day>2</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>12</Month><Day>2</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>12</Month><Day>1</Day><Hour>19</Hour><Minute>25</Minute></PubMedPubDate></History><PublicationStatus>aheadofprint</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36455711</ArticleId><ArticleId IdType="mid">NIHMS1853639</ArticleId><ArticleId IdType="pmc">PMC10225473</ArticleId><ArticleId IdType="doi">10.1053/j.semtcvs.2022.08.019</ArticleId><ArticleId IdType="pii">S1043-0679(22)00271-4</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Krasuski RA, Bashore TM. 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Explanted fetal bovine tricuspid valves were sutured onto image-derived annuli and ventricular mounts. Control valves (CON) were secured to a size-matched hypoplastic left heart syndrome (HLHS)-type annulus and compared to: (1) normal tricuspid valves secured to a size-matched saddle-shaped annulus, (2) HLHS-type annulus with LT, (3) HLHS-type annulus with annular dilation (dilation valves), or (4) a combined disease model with both dilation and tethering (disease valves). The specimens were tested in a systemic heart simulator at various single ventricle physiologies. Leaflet forces were measured using optical strain sensors sutured to each leaflet edge. Average force in the anterior leaflet was 43.2% lower in CON compared to normal tricuspid valves (P < 0.001). LT resulted in a 6.6% increase in average forces on the anterior leaflet (P = 0.04), 10.7% increase on the posterior leaflet (P = 0.03), and 14.1% increase on the septal leaflet (P < 0.001). In dilation valves, average septal leaflet forces increased relative to the CON by 42.2% (P = 0.01). In disease valves, average leaflet forces increased by 54.8% in the anterior leaflet (P < 0.001), 37.6% in the posterior leaflet (P = 0.03), and 79.9% in the septal leaflet (P < 0.001). The anterior leaflet experiences the highest forces in the normal tricuspid annulus under single ventricle physiology conditions. Annular dilation resulted in an increase in forces on the septal leaflet and LT resulted in an increase in forces across all 3 leaflets. Annular dilation and LT combined resulted in the largest increase in leaflet forces across all 3 leaflets. |
2,329,326 | Difficulties interpreting concentrations in fatal cases: example of 2,5-dimethoxy-4-chloroamphetamine.<Pagination><StartPage>383</StartPage><EndPage>392</EndPage><MedlinePgn>383-392</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s11419-022-00628-8</ELocationID><Abstract><AbstractText Label="PURPOSE">Death related to the use of drugs is evident when drugs are detected in biological matrices within toxic levels, but sometimes it can be less obvious. Intoxications after 2,5-dimethoxy-4-chloroamphetamine (DOC) use are occurring but up to date, only one fatality has been reported. Here we present the case of a young woman admitted to hospital as she presented vomiting, convulsions and cardiorespiratory arrest.</AbstractText><AbstractText Label="METHODS">Blood ethanol concentration was determined using gas chromatography with flame ionization detection and toxicological screenings (blood, gastric content and hair samples) were performed using liquid chromatography with diode array detection, gas chromatography or liquid chromatography with mass spectrometry detection.</AbstractText><AbstractText Label="RESULTS">Her health state declined with cardiac troubles, organs failure and cerebral edema till death occurring 4 days later. The autopsy revealed the presence of hemorrhagic infiltration inside the left ventricle, pulmonary edema and hemorrhagic infiltration of the terminal ileum. The analysis of biological fluids confirmed the presence of DOC (< 10 ng/mL in cardiac blood sample), buprenorphine, cocaine and cannabis metabolites. The analysis of hair highlighted a history of drugs abuse.</AbstractText><AbstractText Label="CONCLUSION">In the absence of evident identified cause, the hypothesis of a death due to acute drugs use within a history of chronic consumption of drugs has been put forward. The concentration of some substances such as new psychoactive substances can be low in biological matrices but the toxic effects can be additive and lead to death even within young people, hence the importance of the knowledge of consumption history.</AbstractText><CopyrightInformation>© 2022. The Author(s), under exclusive licence to Japanese Association of Forensic Toxicology.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lelievre</LastName><ForeName>Benedicte</ForeName><Initials>B</Initials><Identifier Source="ORCID">0000-0003-4014-4028</Identifier><AffiliationInfo><Affiliation>Laboratoire de Pharmacologie-Toxicologie, CHU Angers, 4 rue Larrey, Angers, France. belelievre@chu-angers.fr.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dupont</LastName><ForeName>Vincent</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>Service de Médecine Légale et Pénitentiaire, CHU Angers, Angers, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Service de Médecine Légale, CHU Rennes, Rennes, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Buchaillet</LastName><ForeName>Celine</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Service de Médecine Légale et Pénitentiaire, CHU Angers, Angers, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Unité Médico Judiciaire, CHI Créteil, Créteil, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jousset</LastName><ForeName>Nathalie</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Service de Médecine Légale et Pénitentiaire, CHU Angers, Angers, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Deguigne</LastName><ForeName>Marie</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Centre Anti Poison, CHU Angers, Angers, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cirimele</LastName><ForeName>Vincent</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>Laboratoire ChemTox, Illkirch, France.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>05</Month><Day>17</Day></ArticleDate></Article><MedlineJournalInfo><Country>Japan</Country><MedlineTA>Forensic Toxicol</MedlineTA><NlmUniqueID>101315563</NlmUniqueID><ISSNLinking>1860-8965</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>8Y1C6K0PCA</RegistryNumber><NameOfSubstance UI="C529482">4-chloro-2,5-dimethoxyamphetamine</NameOfSubstance></Chemical><Chemical><RegistryNumber>CK833KGX7E</RegistryNumber><NameOfSubstance UI="D000661">Amphetamine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="ErratumIn"><RefSource>Forensic Toxicol. 2023 Jan;41(1):185</RefSource><PMID Version="1">36652072</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000293" MajorTopicYN="N">Adolescent</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008401" MajorTopicYN="N">Gas Chromatography-Mass Spectrometry</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000661" MajorTopicYN="Y">Amphetamine</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005410" MajorTopicYN="N">Flame Ionization</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002853" MajorTopicYN="N">Chromatography, Liquid</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001926" MajorTopicYN="Y">Brain Death</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">2,5-dimethoxy-4-chloroamphetamine</Keyword><Keyword MajorTopicYN="N">Fatal</Keyword><Keyword MajorTopicYN="N">New psychoactive 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Behav Brain Res 277:146–192. https://doi.org/10.1016/j.bbr.2014.04.007</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.bbr.2014.04.007</ArticleId><ArticleId IdType="pubmed">24769172</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36454265</PMID><DateRevised><Year>2022</Year><Month>12</Month><Day>01</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1432-1971</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Dec</Month><Day>01</Day></PubDate></JournalIssue><Title>Pediatric cardiology</Title><ISOAbbreviation>Pediatr Cardiol</ISOAbbreviation></Journal>Cardiac MRI-Derived Inferior Vena Cava Cross-Sectional Area Correlates with Measures of Fontan-Associated Liver Disease. | There is currently no clear consensus on screening techniques to evaluate the presence or severity of Fontan-associated liver disease (FALD). Cardiac MRI (CMR) is used routinely for post-Fontan surveillance, but CMR-derived measures that relate to the severity of FALD are not yet defined. This was a cross-sectional single-center study of post-Fontan patients who underwent a CMR. CMR exams were re-analyzed by a single pediatric cardiologist. Surrogates of FALD included Gamma-Glutamyl Transferase (GGT), Fibrosis-4 laboratory score (FIB-4), and imaging findings. Findings consistent with cirrhosis on liver ultrasound included increased liver echogenicity and/or nodularity. Statistical analyses were performed to investigate potential relationships between CMR parameters and markers of FALD. Sixty-one patients were included. A larger inferior vena cava cross-sectional area (IVC-CSA) indexed to height was significantly associated with a higher FIB-4 score (Spearman's ρ = 0.28, p = 0.04), a higher GGT level (Spearman's ρ = 0.40, p = 0.02), and findings consistent with cirrhosis on liver ultrasound (OR 1.17, 95% CI: (1.01, 1.35), p = 0.04). None of the other CMR parameters were associated with markers of FALD. A larger indexed IVC-CSA was associated with higher systemic ventricle end-diastolic pressure (EDP) on cardiac catheterization (Spearman's ρ = 0.39, p = 0.018) as well as older age (Spearman's ρ = 0.46, p =  < 0.001). Indexed IVC-CSA was the only CMR parameter that was associated with markers of FALD. This measure has the potential to serve as an additional non-invasive tool to improve screening strategies for FALD. Visual abstract summarizing the primary findings of this paper. |
2,329,327 | [Diagnosis a fetus with Coffin-Siris syndrome due to variant of SMARCA4 gene by whole exome sequencing]. | To explore the clinical phenotype and genetic basis for a fetus suspected for Coffin-Siris syndrome.</AbstractText>Chromosomal microarray analysis (CMA) and whole exome sequencing (WES) were carried out for the fetus. Candidate variant was verified by Sanger sequencing.</AbstractText>Prenatal ultrasound at 23rd gestational week has revealed fetal ventriculomegaly. No abnormality was found by CMA, while WES revealed that the fetus has harbored a de novo heterozygous c.2851G>A (p.G951R) variant of the SMARCA4 gene, which was predicted to be pathogenic.</AbstractText>Genetic testing should be considered for fetuses featuring progressive widening of lateral cerebral ventricles.</AbstractText> |
2,329,328 | Novel de novo ZNF148 truncating variant causing autism spectrum disorder, attention deficit hyperactivity disorder, and intellectual disability. | ZNF148 gene is a Krüppel-type transcription factor that has transcriptional regulatory function. Heterozygous variant in ZNF148 gene causes an intellectual disability syndrome characterized by global developmental delay, absence, or hypoplasia of corpus callosum, wide intracerebral ventricles, and dysmorphic facial features, while its associations with ASD and ADHD have not been reported. We report a new patient with intellectual disability, autism spectrum disorder (ASD) and attention-deficit hyperactivity disorder (ADHD). The patient had a novel heterozygous truncating variant c.1818dupC (p.Lys607Glnfs*11) in the ZNF148 gene. This variation produces a ZNF148 truncated protein with a deletion of the C-terminal activation domain and may destabilize the protein by affecting the transcriptional activation function. Brain MRI shows normal brain development. Here, we identify a novel ZNF148 heterozygous truncating variant in a patient with distinct phenotypes of ASD and ADHD, which expands the genotype-phenotype spectrum of ZNF148, and indicates ZNF148 is also a potential target gene for ASD. |
2,329,329 | Loculated hydrocephalus: is neuroendoscopy effective and safe? A 90 patients' case series and literature review. | Loculated hydrocephalus is a complex condition in which different non-communicating compartments form within the ventricular system due to different etiology, mainly intraventricular hemorrhage and infection. Since the end of the twentieth century, neuroendoscopy has been explored as a therapeutic option for loculated hydrocephalus with non-univocal results.</AbstractText>We performed a retrospective analysis of 90 patients who underwent endoscopic treatment for loculated hydrocephalus from January 1997 to January 2021 (mean age: 2 years, range 7-21). We included 37 (41.1%) children with multiloculated hydrocephalus, 37 (41.1%) with isolated lateral ventricle, 13 (14.4%) with excluded temporal horn, and 3 (3.3%) with isolated fourth ventricle. We compared our results with those available in literature.</AbstractText>A mean of 1.91 endoscopic procedure/patient were performed (only one endoscopy in 42.2% of cases). Complications of neuroendoscopy and of shunt surgeries were recorded in 17 (18.9%) and 52 (57.8%) children, respectively. Twenty-six (28.9%) children were shunt-free at the last follow-up, 47.8% have only one shunt.</AbstractText>The first goal of neuroendoscopy is to increase the rate of shunt-free patients but, when it is not possible, it aims at simplifying shunt system and reducing the number of surgical procedures. In our series, neuroendoscopy was able to achieve both these goals with an acceptable complication rate. Thus, our results confirmed neuroendoscopy as a valid tool in the long-term management of loculated hydrocephalus. Neuronavigation and intraoperative ultrasound could increase the success rate in cases with distorted anatomy.</AbstractText>© 2022. The Author(s).</CopyrightInformation> |
2,329,330 | Endothelial cell-specific mineralocorticoid receptor activation promotes diastolic dysfunction in diet-induced obese male mice.<Pagination><StartPage>R90</StartPage><EndPage>R101</EndPage><MedlinePgn>R90-R101</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1152/ajpregu.00274.2021</ELocationID><Abstract><AbstractText>Widespread consumption of diets high in fat and fructose (Western diet, WD) has led to increased prevalence of obesity and diastolic dysfunction (DD). DD is a prominent feature of heart failure with preserved ejection fraction (HFpEF). However, the underlying mechanisms of DD are poorly understood, and treatment options are still limited. We have previously shown that deletion of the cell-specific mineralocorticoid receptor in endothelial cells (ECMR) abrogates DD induced by WD feeding in female mice. However, the specific role of ECMR activation in the pathogenesis of DD in male mice has not been clarified. Therefore, we fed 4-wk-old ECMR knockout (ECMRKO) male mice and littermates (LM) with either a WD or chow diet (CD) for 16 wk. WD feeding resulted in DD characterized by increased left ventricle (LV) filling pressure (<i>E</i>/<i>e</i>') and diastolic stiffness [<i>E</i>/<i>e</i>'/LV inner diameter at end diastole (LVIDd)]. Compared with CD, WD in LM resulted in increased myocardial macrophage infiltration, oxidative stress, and increased myocardial phosphorylation of Akt, in concert with decreased phospholamban phosphorylation. WD also resulted in focal cardiomyocyte remodeling, characterized by areas of sarcomeric disorganization, loss of mitochondrial electron density, and mitochondrial fragmentation. Conversely, WD-induced DD and associated biochemical and structural abnormalities were prevented by ECMR deletion. In contrast with our previously reported observations in females, WD-fed male mice exhibited enhanced Akt signaling and a lower magnitude of cardiac injury. 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Truman Memorial Veterans Affairs Hospital, Columbia, Missouri.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Whaley-Connell</LastName><ForeName>Adam T</ForeName><Initials>AT</Initials><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Medicine, University of Missouri, Columbia, Missouri.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Research Service, Harry S. Truman Memorial Veterans Affairs Hospital, Columbia, Missouri.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Division of Nephrology, Department of Medicine, University of Missouri, Columbia, Missouri.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jia</LastName><ForeName>Guanghong</ForeName><Initials>G</Initials><Identifier Source="ORCID">0000-0003-0018-5925</Identifier><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Medicine, University of Missouri, Columbia, Missouri.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Yan</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sharma</LastName><ForeName>Neekun</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Medicine, University of Missouri, Columbia, Missouri.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Naz</LastName><ForeName>Huma</ForeName><Initials>H</Initials><Identifier Source="ORCID">0000-0002-1989-7466</Identifier><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Medicine, University of Missouri, Columbia, Missouri.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Research Service, Harry S. Truman Memorial Veterans Affairs Hospital, Columbia, Missouri.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hans</LastName><ForeName>Chetan</ForeName><Initials>C</Initials><Identifier Source="ORCID">0000-0003-1830-9084</Identifier><AffiliationInfo><Affiliation>Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Division of Cardiovascular Medicine, Department of Medicine, University of Missouri, Columbia, Missouri.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hayden</LastName><ForeName>Melvin R</ForeName><Initials>MR</Initials><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Medicine, University of Missouri, Columbia, Missouri.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hill</LastName><ForeName>Michael A</ForeName><Initials>MA</Initials><AffiliationInfo><Affiliation>Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Medical Pharmacology and Physiology, University of Missouri, Columbia, Missouri.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sowers</LastName><ForeName>James R</ForeName><Initials>JR</Initials><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Medicine, University of Missouri, Columbia, Missouri.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Medical Pharmacology and Physiology, University of Missouri, Columbia, Missouri.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Manrique-Acevedo</LastName><ForeName>Camila</ForeName><Initials>C</Initials><Identifier Source="ORCID">0000-0001-9341-404X</Identifier><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Medicine, University of Missouri, Columbia, Missouri.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Research Service, Harry S. Truman Memorial Veterans Affairs Hospital, Columbia, Missouri.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lastra</LastName><ForeName>Guido</ForeName><Initials>G</Initials><Identifier Source="ORCID">0000-0001-9205-1021</Identifier><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Medicine, University of Missouri, Columbia, Missouri.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Research Service, Harry S. 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Diabetes 64: 1988–2001, 2015. doi:10.2337/db14-0804.</Citation><ArticleIdList><ArticleId IdType="doi">10.2337/db14-0804</ArticleId><ArticleId IdType="pmc">PMC4439570</ArticleId><ArticleId IdType="pubmed">25605806</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">36440832</PMID><DateCompleted><Year>2022</Year><Month>11</Month><Day>29</Day></DateCompleted><DateRevised><Year>2022</Year><Month>12</Month><Day>09</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1940-087X</ISSN><JournalIssue CitedMedium="Internet"><Issue>189</Issue><PubDate><Year>2022</Year><Month>Nov</Month><Day>11</Day></PubDate></JournalIssue><Title>Journal of visualized experiments : JoVE</Title><ISOAbbreviation>J Vis Exp</ISOAbbreviation></Journal>Multiple Intravenous Bolus Dosing and Invasive Hemodynamic Assessment in a Hypoxia-Induced Mouse Pulmonary Artery Hypertension Model. | Widespread consumption of diets high in fat and fructose (Western diet, WD) has led to increased prevalence of obesity and diastolic dysfunction (DD). DD is a prominent feature of heart failure with preserved ejection fraction (HFpEF). However, the underlying mechanisms of DD are poorly understood, and treatment options are still limited. We have previously shown that deletion of the cell-specific mineralocorticoid receptor in endothelial cells (ECMR) abrogates DD induced by WD feeding in female mice. However, the specific role of ECMR activation in the pathogenesis of DD in male mice has not been clarified. Therefore, we fed 4-wk-old ECMR knockout (ECMRKO) male mice and littermates (LM) with either a WD or chow diet (CD) for 16 wk. WD feeding resulted in DD characterized by increased left ventricle (LV) filling pressure (<i>E</i>/<i>e</i>') and diastolic stiffness [<i>E</i>/<i>e</i>'/LV inner diameter at end diastole (LVIDd)]. Compared with CD, WD in LM resulted in increased myocardial macrophage infiltration, oxidative stress, and increased myocardial phosphorylation of Akt, in concert with decreased phospholamban phosphorylation. WD also resulted in focal cardiomyocyte remodeling, characterized by areas of sarcomeric disorganization, loss of mitochondrial electron density, and mitochondrial fragmentation. Conversely, WD-induced DD and associated biochemical and structural abnormalities were prevented by ECMR deletion. In contrast with our previously reported observations in females, WD-fed male mice exhibited enhanced Akt signaling and a lower magnitude of cardiac injury. Collectively, our data support a critical role for ECMR in obesity-induced DD and suggest critical mechanistic differences in the genesis of DD between males and females.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Aroor</LastName><ForeName>Annayya</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Medicine, University of Missouri, Columbia, Missouri.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Research Service, Harry S. Truman Memorial Veterans Affairs Hospital, Columbia, Missouri.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>DeMarco</LastName><ForeName>Vincent G</ForeName><Initials>VG</Initials><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Medicine, University of Missouri, Columbia, Missouri.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Research Service, Harry S. Truman Memorial Veterans Affairs Hospital, Columbia, Missouri.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Whaley-Connell</LastName><ForeName>Adam T</ForeName><Initials>AT</Initials><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Medicine, University of Missouri, Columbia, Missouri.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Research Service, Harry S. Truman Memorial Veterans Affairs Hospital, Columbia, Missouri.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Division of Nephrology, Department of Medicine, University of Missouri, Columbia, Missouri.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jia</LastName><ForeName>Guanghong</ForeName><Initials>G</Initials><Identifier Source="ORCID">0000-0003-0018-5925</Identifier><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Medicine, University of Missouri, Columbia, Missouri.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Yan</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sharma</LastName><ForeName>Neekun</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Medicine, University of Missouri, Columbia, Missouri.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Naz</LastName><ForeName>Huma</ForeName><Initials>H</Initials><Identifier Source="ORCID">0000-0002-1989-7466</Identifier><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Medicine, University of Missouri, Columbia, Missouri.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Research Service, Harry S. Truman Memorial Veterans Affairs Hospital, Columbia, Missouri.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hans</LastName><ForeName>Chetan</ForeName><Initials>C</Initials><Identifier Source="ORCID">0000-0003-1830-9084</Identifier><AffiliationInfo><Affiliation>Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Division of Cardiovascular Medicine, Department of Medicine, University of Missouri, Columbia, Missouri.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hayden</LastName><ForeName>Melvin R</ForeName><Initials>MR</Initials><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Medicine, University of Missouri, Columbia, Missouri.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hill</LastName><ForeName>Michael A</ForeName><Initials>MA</Initials><AffiliationInfo><Affiliation>Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Medical Pharmacology and Physiology, University of Missouri, Columbia, Missouri.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sowers</LastName><ForeName>James R</ForeName><Initials>JR</Initials><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Medicine, University of Missouri, Columbia, Missouri.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Medical Pharmacology and Physiology, University of Missouri, Columbia, Missouri.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Manrique-Acevedo</LastName><ForeName>Camila</ForeName><Initials>C</Initials><Identifier Source="ORCID">0000-0001-9341-404X</Identifier><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Medicine, University of Missouri, Columbia, Missouri.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Research Service, Harry S. Truman Memorial Veterans Affairs Hospital, Columbia, Missouri.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lastra</LastName><ForeName>Guido</ForeName><Initials>G</Initials><Identifier Source="ORCID">0000-0001-9205-1021</Identifier><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Medicine, University of Missouri, Columbia, Missouri.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Research Service, Harry S. Truman Memorial Veterans Affairs Hospital, Columbia, Missouri.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><DataBankList CompleteYN="Y"><DataBank><DataBankName>figshare</DataBankName><AccessionNumberList><AccessionNumber>10.6084/m9.figshare.21561684</AccessionNumber></AccessionNumberList></DataBank></DataBankList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013486">Research Support, U.S. Gov't, Non-P.H.S.</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>11</Month><Day>28</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Am J Physiol Regul Integr Comp Physiol</MedlineTA><NlmUniqueID>100901230</NlmUniqueID><ISSNLinking>0363-6119</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018161">Receptors, Mineralocorticoid</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="D051057">Proto-Oncogene Proteins c-akt</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D042783" MajorTopicYN="N">Endothelial Cells</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006333" MajorTopicYN="Y">Heart Failure</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018161" MajorTopicYN="N">Receptors, Mineralocorticoid</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008820" MajorTopicYN="N">Mice, Obese</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051057" MajorTopicYN="N">Proto-Oncogene Proteins c-akt</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013318" MajorTopicYN="N">Stroke Volume</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009202" MajorTopicYN="Y">Cardiomyopathies</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D066273" MajorTopicYN="N">Diet, Western</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009765" MajorTopicYN="N">Obesity</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">diastolic dysfunction</Keyword><Keyword MajorTopicYN="N">endothelium</Keyword><Keyword MajorTopicYN="N">mineralocorticoid receptor</Keyword><Keyword MajorTopicYN="N">mitochondria</Keyword><Keyword MajorTopicYN="N">oxidative stress</Keyword></KeywordList><CoiStatement>No conflicts of interest, financial or otherwise, are declared by the authors.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pmc-release"><Year>2024</Year><Month>1</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>11</Month><Day>29</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>12</Month><Day>31</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>11</Month><Day>28</Day><Hour>8</Hour><Minute>32</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36440901</ArticleId><ArticleId IdType="pmc">PMC9799154</ArticleId><ArticleId IdType="doi">10.1152/ajpregu.00274.2021</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Gerber Y, Weston SA, Redfield MM, Chamberlain AM, Manemann SM, Jiang R, Killian JM, Roger VL. 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Currently, there is no cure for PAH. It is important to discover new compounds that can be used to treat PAH. The mouse hypoxia-induced PAH model is a widely used model for PAH research. This model recapitulates human clinical manifestations of PAH Group 3 disease and is an important research tool to evaluate the effectiveness of new experimental therapies for PAH. Research using this model often requires the administration of compounds in mice. For a compound that needs to be given directly into the bloodstream, optimizing intravenous (IV) administration is a key part of the experimental procedures. Ideally, the IV injection system should permit multiple injections over a set time course. Although the mouse hypoxia-induced PAH model is very popular in many laboratories, it is technically challenging to perform multiple IV bolus dosing and invasive hemodynamic assessment in this model. 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We have identified 18,420 genes from the GWAS summary data, and of those 1010 non-overlapping genes expression were significantly associated with hypertension after FDR correction (PFDR <0.05) in four tissues (left heart ventricle, aorta, whole blood, and peripheral blood). The KEGG and GO terms were mostly related to autoimmune mechanisms, and the autoimmune-related pathways have also been enriched using GO analysis for PPI genes. We further performed Mendelian randomization analysis, and the results supported a significant association between autoimmunity and hypertension. Moreover, 15 novel hypertension-susceptible genes were identified in all tissues, and five of the genes (<i>RBM6, HLA-DRB5, UHRF1BP1, LYZ,</i> and <i>TMEM116</i>) were associated with autoimmune system, which provide further evidence supporting an autoimmune mechanism in hypertension. In summary, our study supports that an autoimmune mechanism plays an important role in the development of hypertension, and these findings will provide new biological insights that will assist in deciphering the molecular etiology of hypertension.</AbstractText><CopyrightInformation>© 2022 The Authors.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Huang</LastName><ForeName>Lu-Jie</ForeName><Initials>LJ</Initials><AffiliationInfo><Affiliation>Medical Research Center, Xi'an Key Laboratory of Cardiovascular and Cerebrovascular Diseases, Xi'an No.3 Hospital, Xi'an, Shaanxi, 710018, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Qiao-Xia</ForeName><Initials>QX</Initials><AffiliationInfo><Affiliation>Department of Electron Microscope, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, 710061, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Valenzuela</LastName><ForeName>Robert K</ForeName><Initials>RK</Initials><AffiliationInfo><Affiliation>The Jackson Laboratory, Bar Harbor, ME, 04609, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xu</LastName><ForeName>Jia-Chen</ForeName><Initials>JC</Initials><AffiliationInfo><Affiliation>Department of Electron Microscope, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, 710061, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yan</LastName><ForeName>Fang</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Medical Research Center, Xi'an Key Laboratory of Cardiovascular and Cerebrovascular Diseases, Xi'an No.3 Hospital, Xi'an, Shaanxi, 710018, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ma</LastName><ForeName>Jie</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Medical Research Center, Xi'an Key Laboratory of Cardiovascular and Cerebrovascular Diseases, Xi'an No.3 Hospital, Xi'an, Shaanxi, 710018, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>11</Month><Day>21</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Biochem Biophys Rep</MedlineTA><NlmUniqueID>101660999</NlmUniqueID><ISSNLinking>2405-5808</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Autoimmunity</Keyword><Keyword MajorTopicYN="N">BP</Keyword><Keyword MajorTopicYN="N">GWAS</Keyword><Keyword MajorTopicYN="N">Hypertension</Keyword><Keyword MajorTopicYN="N">TWAS</Keyword></KeywordList><CoiStatement>The authors declare no conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>8</Month><Day>31</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>10</Month><Day>29</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>11</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>11</Month><Day>28</Day><Hour>4</Hour><Minute>19</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>11</Month><Day>29</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>11</Month><Day>29</Day><Hour>6</Hour><Minute>1</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36438602</ArticleId><ArticleId IdType="pmc">PMC9682336</ArticleId><ArticleId IdType="doi">10.1016/j.bbrep.2022.101387</ArticleId><ArticleId IdType="pii">S2405-5808(22)00187-X</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Kearney P.M., Whelton M., Reynolds K., Muntner P., Whelton P.K., He J. 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PLoS One. 2017;12</Citation><ArticleIdList><ArticleId IdType="pmc">PMC5395154</ArticleId><ArticleId IdType="pubmed">28419103</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36437722</PMID><DateRevised><Year>2022</Year><Month>11</Month><Day>28</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1875-5739</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Nov</Month><Day>25</Day></PubDate></JournalIssue><Title>Current neurovascular research</Title><ISOAbbreviation>Curr Neurovasc Res</ISOAbbreviation></Journal>Lesion Location Predicts Early Neurological Deterioration in Single Subcortical Infarction. | Hypertension is a leading risk factor of cardiovascular disease and mortality in the population worldwide. Recently, hundreds of genomic loci were reported for hypertension by GWAS, however, the most SNPs are located in intergenic regions of genome, where a functional cause is difficult to determine. In the current study, a TWAS of hypertension was conducted using 452,264 individuals including 84,640 patients. KEGG and GO enrichment analyses were performed for the hypertension-related genes identified via TWAS. PPI network analysis based on the STRING database was also performed to detect TWAS-identified genes in hypertension. We have identified 18,420 genes from the GWAS summary data, and of those 1010 non-overlapping genes expression were significantly associated with hypertension after FDR correction (PFDR <0.05) in four tissues (left heart ventricle, aorta, whole blood, and peripheral blood). The KEGG and GO terms were mostly related to autoimmune mechanisms, and the autoimmune-related pathways have also been enriched using GO analysis for PPI genes. We further performed Mendelian randomization analysis, and the results supported a significant association between autoimmunity and hypertension. Moreover, 15 novel hypertension-susceptible genes were identified in all tissues, and five of the genes (<i>RBM6, HLA-DRB5, UHRF1BP1, LYZ,</i> and <i>TMEM116</i>) were associated with autoimmune system, which provide further evidence supporting an autoimmune mechanism in hypertension. In summary, our study supports that an autoimmune mechanism plays an important role in the development of hypertension, and these findings will provide new biological insights that will assist in deciphering the molecular etiology of hypertension.<CopyrightInformation>© 2022 The Authors.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Huang</LastName><ForeName>Lu-Jie</ForeName><Initials>LJ</Initials><AffiliationInfo><Affiliation>Medical Research Center, Xi'an Key Laboratory of Cardiovascular and Cerebrovascular Diseases, Xi'an No.3 Hospital, Xi'an, Shaanxi, 710018, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Qiao-Xia</ForeName><Initials>QX</Initials><AffiliationInfo><Affiliation>Department of Electron Microscope, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, 710061, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Valenzuela</LastName><ForeName>Robert K</ForeName><Initials>RK</Initials><AffiliationInfo><Affiliation>The Jackson Laboratory, Bar Harbor, ME, 04609, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xu</LastName><ForeName>Jia-Chen</ForeName><Initials>JC</Initials><AffiliationInfo><Affiliation>Department of Electron Microscope, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, 710061, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yan</LastName><ForeName>Fang</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Medical Research Center, Xi'an Key Laboratory of Cardiovascular and Cerebrovascular Diseases, Xi'an No.3 Hospital, Xi'an, Shaanxi, 710018, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ma</LastName><ForeName>Jie</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Medical Research Center, Xi'an Key Laboratory of Cardiovascular and Cerebrovascular Diseases, Xi'an No.3 Hospital, Xi'an, Shaanxi, 710018, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>11</Month><Day>21</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Biochem Biophys Rep</MedlineTA><NlmUniqueID>101660999</NlmUniqueID><ISSNLinking>2405-5808</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Autoimmunity</Keyword><Keyword MajorTopicYN="N">BP</Keyword><Keyword MajorTopicYN="N">GWAS</Keyword><Keyword MajorTopicYN="N">Hypertension</Keyword><Keyword MajorTopicYN="N">TWAS</Keyword></KeywordList><CoiStatement>The authors declare no conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>8</Month><Day>31</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>10</Month><Day>29</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>11</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>11</Month><Day>28</Day><Hour>4</Hour><Minute>19</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>11</Month><Day>29</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>11</Month><Day>29</Day><Hour>6</Hour><Minute>1</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36438602</ArticleId><ArticleId IdType="pmc">PMC9682336</ArticleId><ArticleId IdType="doi">10.1016/j.bbrep.2022.101387</ArticleId><ArticleId IdType="pii">S2405-5808(22)00187-X</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Kearney P.M., Whelton M., Reynolds K., Muntner P., Whelton P.K., He J. 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PLoS One. 2017;12</Citation><ArticleIdList><ArticleId IdType="pmc">PMC5395154</ArticleId><ArticleId IdType="pubmed">28419103</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36437722</PMID><DateRevised><Year>2022</Year><Month>11</Month><Day>28</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1875-5739</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Nov</Month><Day>25</Day></PubDate></JournalIssue><Title>Current neurovascular research</Title><ISOAbbreviation>Curr Neurovasc Res</ISOAbbreviation></Journal><ArticleTitle>Lesion Location Predicts Early Neurological Deterioration in Single Subcortical Infarction.</ArticleTitle><ELocationID EIdType="doi" ValidYN="Y">10.2174/1567202620666221125123008</ELocationID><Abstract>Background- A certain number of patients with single subcortical small infarction (SSSI) in the lenticulostriate artery (LSA) territory present with early neurological deterioration (END). Objective-We sought to identify more specific predicting imaging marker for END in lenticulostriate SSSI patients. Methods-We screened patients in a prospective hospital-based registry of stroke in the first Affiliated Hospital of Zhengzhou University from January 2015 to December 2020. Lesion locations were defined as posterior type when more than half of the lesion was located in the posterior part of the corona radiata divided by the midline, which was drawn between the tangents of the anterior and posterior horns of the lateral ventricle and was adjacent to the lateral ventricle at the same time. END was defined as an increase of ≥2 points in total National Institutes of Health Stroke Scale score or ≥1 point. A multivariate logistic analysis was used to assess the imaging predictors for END. Results-418 patients were enrolled in the final data analysis. Among them, 206 (49. 3％) cases were rated as the posterior type and71（17. 0％）cases had END. A multivariate logistic analysis showed that only posterior type (adjusted odds ratio, 2. 126; 95% confidence interval, 1. 250-3. 614; P = 0. 005) was independently associated with the risk of END. Conclusions-The posterior type of lesion location represented an imaging marker predicting END in the lenticulostriate SSSI patients. |
2,329,332 | Modulation of striatal glutamatergic, dopaminergic and cholinergic neurotransmission pathways concomitant with motor disturbance in rats with kaolin-induced hydrocephalus. | Hydrocephalus is characterized by abnormal accumulation of cerebrospinal fluid in the cerebral ventricles and causes motor impairments. The mechanisms underlying the motor changes remain elusive. Enlargement of ventricles compresses the striatum of the basal ganglia, a group of nuclei involved in the subcortical motor circuit. Here, we used a kaolin-injection juvenile rat model to explore the effects of acute and chronic hydrocephalus, 1 and 5 weeks post-treatment, respectively on the three major neurotransmission pathways (glutamatergic, dopaminergic and cholinergic) in the striatum.</AbstractText>Rats were evaluated for motor impairments. Expressions of presynaptic and postsynaptic protein markers related to the glutamatergic, dopaminergic, and cholinergic connections in the striatum were evaluated. Combined intracellular dye injection and substance P immunohistochemistry were used to distinguish between direct and indirect pathway striatal medium spiny neurons (d and i-MSNs) for the analysis of their dendritic spine density changes.</AbstractText>Hydrocephalic rats showed compromised open-field gait behavior. However, male but not female rats displayed stereotypic movements and compromised rotarod performance. Morphologically, the increase in lateral ventricle sizes was greater in the chronic than acute hydrocephalus conditions. Biochemically, hydrocephalic rats had significantly decreased striatal levels of synaptophysin, vesicular glutamate transporter 1, and glutamatergic postsynaptic density protein 95, suggesting a reduction of corticostriatal excitation. The expression of GluR2/3 was also reduced suggesting glutamate receptor compositional changes. The densities of dendritic spines, morphological correlates of excitatory synaptic foci, on both d and i-MSNs were also reduced. Hydrocephalus altered type 1 (DR1) and 2 (DR2) dopamine receptor expressions without affecting tyrosine hydroxylase level. DR1 was decreased in acute and chronic hydrocephalus, while DR2 only started to decrease later during chronic hydrocephalus. Since dopamine excites d-MSNs through DR1 and inhibits i-MSNs via DR2, our findings suggest that hydrocephalus downregulated the direct basal ganglia neural pathway persistently and disinhibited the indirect pathway late during chronic hydrocephalus. Hydrocephalus also persistently reduced the striatal choline acetyltransferase level, suggesting a reduction of cholinergic modulation.</AbstractText>Hydrocephalus altered striatal glutamatergic, dopaminergic, and cholinergic neurotransmission pathways and tipped the balance between the direct and indirect basal ganglia circuits, which could have contributed to the motor impairments in hydrocephalus.</AbstractText>© 2022. The Author(s).</CopyrightInformation> |
2,329,333 | [Endoscopic Endonasal Surgery for Pediatric Suprasellar Tumors]. | Pediatric suprasellar tumors are difficult to treat. Their sellar-suprasellar location frequently results in compression of the adjacent critical neurovascular structures, making them a challenging surgical entity. Our surgical strategy emphasizes on radical resection of the tumor without compromising visual or cognitive functions. In recent years, the endoscopic endonasal approach has been increasingly used for pediatric suprasellar tumors. We have adopted a "4-hand technique by two neurosurgeons" during endoscopic endonasal surgery to resect aggressive tumors safely. Posterior clinoidectomy and upper clivectomy are useful additional procedures to resect intra-3<sup>rd</sup>-ventricle and retrochiasmatic suprasellar tumors. Here, we present our surgical management strategy and tips for endonasal resection of pediatric suprasellar tumors. |
2,329,334 | [Original Ventriculoperitoneal Shunt for Pediatric Hydrocephalus]. | Although the use of newly developed procedures such as endoscopic third ventriculostomy or coagulation of the choroid plexus has gradually expanded, ventriculoperitoneal(VP)shunts are still not obsolete. They are the most commonly performed surgery for treating pediatric hydrocephalus. Young neurosurgeons may frequently encounter this CSF diversion procedure in clinical practice. However, the VP shunt remains a failure-prone procedure, as exemplified by obstruction, infection, mechanical shunt failure, over drainage, and distal catheter site-specific failures. Therefore, surgery requires exquisite techniques, especially in the pediatric population, to meet the needs of the child's growth. This article sheds light on the refined methodology for pediatric VP shunting with meticulous details of the surgical technique. Neurosurgeons must always remember that appropriate ICP control has a major impact on patient development and that a stably functioning VP shunt can deliver the full potential of children with hydrocephalus. |
2,329,335 | The Effects of Cuprizone on Murine Subventricular Zone-Derived Neural Stem Cells and Progenitor Cells Grown as Neurospheres. | Despite the extensive use of the cuprizone (CPZ) demyelination animal model, there is little evidence regarding the effects of CPZ on a cellular level. Initial studies have suggested that oligodendrocytes (OL) are the main cell targets for CPZ toxicity. However, recent data have revealed additional effects on neural stem cells and progenitor cells (NSC/NPC), which constitute a reservoir for OL regeneration during brain remyelination. We cultured NSC/NPC as neurospheres to investigate CPZ effects on cell mechanisms which are thought to be involved in demyelination and remyelination processes in vivo. Proliferating NSC/NPC cultures exposed to CPZ showed overproduction of intracellular reactive oxygen species and increased progenitor migration at the expense of a significant inhibition of cell proliferation. Although NSC/NPC survival was not affected by CPZ in proliferative conditions, we found that CPZ-treated cultures undergoing cell differentiation were more prone to cell death than controls. The commitment and cell differentiation towards neural lineages did not seem to be affected by CPZ, as shown by the conserved proportions of OL, astrocytes, and neurons. Nevertheless, when CPZ treatment was performed after cell differentiation, we detected a significant reduction in the number and the morphological complexity of OL, astrogliosis, and neuronal damage. We conclude that, in addition to damaging mature OL, CPZ also reduces NSC/NPC proliferation and activates progenitor migration. These results shed light on CPZ direct effects on NSC proliferation and the progression of in vitro differentiation. |
2,329,336 | Giant intracardiac medullary thyroid cancer metastasis.<Pagination><StartPage>5455</StartPage><EndPage>5456</EndPage><MedlinePgn>5455-5456</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1111/jocs.17162</ELocationID><Abstract><AbstractText>We report an unusual case of giant intracardiac medullary thyroid cancer metastasis. A 76-year-old woman with a 9-year history of medullary thyroid cancer presented an unexpected 7.5 cm mass in the right ventricle. Complete resection and tricuspid valve replacement led to 40 months survival.</AbstractText><CopyrightInformation>© 2022 The Authors. Journal of Cardiac Surgery published by Wiley Periodicals LLC.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Tricard</LastName><ForeName>Jérémy</ForeName><Initials>J</Initials><Identifier Source="ORCID">0000-0001-6211-1097</Identifier><AffiliationInfo><Affiliation>Department of Cardiac and Thoracic Surgery, University Hospital of Limoges, Limoges, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chermat</LastName><ForeName>Anaëlle</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Cardiac and Thoracic Surgery, University Hospital of Limoges, Limoges, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Abdelkafi</LastName><ForeName>Ezedin</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Department of Cardiac and Thoracic Surgery, University Hospital of Limoges, Limoges, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Piccardo</LastName><ForeName>Alessandro</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Cardiac and Thoracic Surgery, University Hospital of Limoges, Limoges, France.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>11</Month><Day>24</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Card Surg</MedlineTA><NlmUniqueID>8908809</NlmUniqueID><ISSNLinking>0886-0440</ISSNLinking></MedlineJournalInfo><SupplMeshList><SupplMeshName Type="Disease" UI="C536914">Thyroid cancer, medullary</SupplMeshName></SupplMeshList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006321" MajorTopicYN="N">Heart</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018278" MajorTopicYN="Y">Carcinoma, Neuroendocrine</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013964" MajorTopicYN="Y">Thyroid Neoplasms</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">intracardiac metastasis</Keyword><Keyword MajorTopicYN="N">surgical resection</Keyword><Keyword MajorTopicYN="N">thyroid cancer</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>9</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>10</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>11</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2023</Year><Month>1</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>11</Month><Day>24</Day><Hour>13</Hour><Minute>52</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36423260</ArticleId><ArticleId IdType="doi">10.1111/jocs.17162</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36422991</PMID><DateRevised><Year>2022</Year><Month>11</Month><Day>24</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1477-111X</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Nov</Month><Day>24</Day></PubDate></JournalIssue><Title>Perfusion</Title><ISOAbbreviation>Perfusion</ISOAbbreviation></Journal>Proportional pulmonary pulse pressure: A new index to assess response to veno-arterial extracorporeal membrane oxygenation. | We report an unusual case of giant intracardiac medullary thyroid cancer metastasis. A 76-year-old woman with a 9-year history of medullary thyroid cancer presented an unexpected 7.5 cm mass in the right ventricle. Complete resection and tricuspid valve replacement led to 40 months survival.<CopyrightInformation>© 2022 The Authors. Journal of Cardiac Surgery published by Wiley Periodicals LLC.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Tricard</LastName><ForeName>Jérémy</ForeName><Initials>J</Initials><Identifier Source="ORCID">0000-0001-6211-1097</Identifier><AffiliationInfo><Affiliation>Department of Cardiac and Thoracic Surgery, University Hospital of Limoges, Limoges, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chermat</LastName><ForeName>Anaëlle</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Cardiac and Thoracic Surgery, University Hospital of Limoges, Limoges, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Abdelkafi</LastName><ForeName>Ezedin</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Department of Cardiac and Thoracic Surgery, University Hospital of Limoges, Limoges, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Piccardo</LastName><ForeName>Alessandro</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Cardiac and Thoracic Surgery, University Hospital of Limoges, Limoges, France.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>11</Month><Day>24</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Card Surg</MedlineTA><NlmUniqueID>8908809</NlmUniqueID><ISSNLinking>0886-0440</ISSNLinking></MedlineJournalInfo><SupplMeshList><SupplMeshName Type="Disease" UI="C536914">Thyroid cancer, medullary</SupplMeshName></SupplMeshList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006321" MajorTopicYN="N">Heart</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018278" MajorTopicYN="Y">Carcinoma, Neuroendocrine</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013964" MajorTopicYN="Y">Thyroid Neoplasms</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">intracardiac metastasis</Keyword><Keyword MajorTopicYN="N">surgical resection</Keyword><Keyword MajorTopicYN="N">thyroid cancer</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>9</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>10</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>11</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2023</Year><Month>1</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>11</Month><Day>24</Day><Hour>13</Hour><Minute>52</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36423260</ArticleId><ArticleId IdType="doi">10.1111/jocs.17162</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36422991</PMID><DateRevised><Year>2022</Year><Month>11</Month><Day>24</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1477-111X</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Nov</Month><Day>24</Day></PubDate></JournalIssue><Title>Perfusion</Title><ISOAbbreviation>Perfusion</ISOAbbreviation></Journal><ArticleTitle>Proportional pulmonary pulse pressure: A new index to assess response to veno-arterial extracorporeal membrane oxygenation.</ArticleTitle><Pagination><StartPage>2676591221140744</StartPage><MedlinePgn>2676591221140744</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1177/02676591221140744</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Based on theoretical physiology, the ratio of pulmonary artery pulse pressure to mean pulmonary pressure (PP-MPAP), termed proportional pulmonary pulse pressure, provides a measure of coupling between the right ventricle and the pulmonary circulation. This study tested the hypothesis that lower PP-MPAP ratio was associated with left ventricular (LV) distension in patients with cardiogenic shock who underwent extracorporeal life support (ECLS).<AbstractText Label="METHODS" NlmCategory="METHODS">This is a retrospective observational single-centre study of 22 patients with cardiogenic shock who underwent ECLS as the primary support modality without and with LV distension and Impella unloading. The relationship between post-support PP-MPAP and 12-hour lactate clearance was also assessed.<AbstractText Label="RESULTS" NlmCategory="RESULTS">Of the 22 patients: 10 patients underwent additional Impella unloading due to LV distension (Group 1) and 12 patients on ECLS only without LV distension (Group 2). As predicted by the theoretical model, PP-MPAP on ECLS dropped in Group 1 (pre-Impella) from 0.473 ± 0.067 to 0.372 ± 0.087, <i>p</i> < 0.001; but increased in Group 2 patients without LV distension (0.518 ± 0.070 to 0.549 ± 0.072, <i>p</i> = 0.002). Impella support in Group 1 increased PP-MPAP (0.372 ± 0.087 to 0.615 ± 0.094, <i>p</i> < 0.001). On multiple regression analysis, post-support PP-MPAP was significantly associated with 12-hour lactate clearance.<AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">Changes in PP-MPAP is associated hemodynamic response to ECLS and 12-hour lactate clearance. This simple parameter may guide therapeutic optimization in cardiogenic shock and ECLS. |
2,329,337 | Untargeted metabolomics to evaluate polymyxin B toxicodynamics following direct intracerebroventricular administration into the rat brain. | There is a dearth of studies focused on understanding pharmacokinetics, pharmacodynamics and toxicodynamics of polymyxins following direct administration to the central nervous system (CNS). In this study, for the first time, untargeted metabolomics were employed to ascertain the perturbations of brain metabolism in the rat cerebral cortex following direct brain injection of 0.75 mg/kg polymyxin B (1 and 4 h) through the right lateral ventricle. In the right cortex metabolome, ICV polymyxin B induced a greater perturbation at 1 h compared to negligible effect at 4 h. Pathway enrichment analysis showed that sphingolipid, arginine, and histidine metabolism, together with aminoacyl-tRNA biosynthesis were significantly affected in the right cortex metabolome. Furthermore, intracerebroventricular (ICV) polymyxin B dysregulated the two arms (CDP-choline and CDP-ethanolamine) of the Kennedy pathway that governs the <i>de novo</i> biosynthesis of neuronal phospholipids. Importantly, the key intermediates of metabolic pathways that maintain cellular redox balance (e.g., glutathione metabolism) and mitochondrial function (e.g., electron transport chain) were markedly depleted. The abundance of key metabolites (e.g., <i>N</i>-acetyl-l-glutamate) associated with diverse CNS disorders (e.g., neurodegenerative disease) were also significantly perturbed. The biological significance of these metabolic perturbations on the CNS includes impaired oxidant-antioxidant balance, impaired neuronal lipid homeostasis and mitochondrial dysfunction. Furthermore, ICV polymyxin B caused a significant alteration in the abundance of several metabolic biomarkers associated with cerebral ischemia, oxidative stress as well as certain neurological disorders. These findings may facilitate the development of new pharmacokinetic/pharmacodynamic strategies to attenuate polymyxins ICV related CNS toxicities and stimulate the discovery of safer next-generation polymyxin-like lipopeptide antibiotics. |
2,329,338 | Differential compartmentalization of myeloid cell phenotypes and responses towards the CNS in Alzheimer's disease. | Myeloid cells are suggested as an important player in Alzheimer´s disease (AD). However, its continuum of phenotypic and functional changes across different body compartments and their use as a biomarker in AD remains elusive. Here, we perform multiple state-of-the-art analyses to phenotypically and metabolically characterize immune cells between peripheral blood (n = 117), cerebrospinal fluid (CSF, n = 117), choroid plexus (CP, n = 13) and brain parenchyma (n = 13). We find that CSF cells increase expression of markers involved in inflammation, phagocytosis, and metabolism. Changes in phenotype of myeloid cells from AD patients are more pronounced in CP and brain parenchyma and upon in vitro stimulation, suggesting that AD-myeloid cells are more vulnerable to environmental changes. Our findings underscore the importance of myeloid cells in AD and the detailed characterization across body compartments may serve as a resource for future studies focusing on the assessment of these cells as biomarkers in AD. |
2,329,339 | [Evaluation of left ventricular function with left atrio-ventricular longitudinal strain in patients with lymphoma underwent anthracycline therapy].<Pagination><StartPage>1064</StartPage><EndPage>1068</EndPage><MedlinePgn>1064-1068</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.3760/cma.j.cn112148-20220727-00583</ELocationID><Abstract><AbstractText><b>Objective:</b> To analyze the value of 3-dimensional speckle tracking echocardiograghy (3D-STE) derived strain parameters on the detection of subclinical myocardial deformation alterations in patients with lymphoma treated with anthracycline agents. <b>Methods:</b> This study was a retrospective study. A total of 37 patients with newly diagnosed diffuse large B cell non-Hodgkin lymphoma between December 2012 and December 2014 in Cancer Center, Fudan university were included. 3D-STE strain measurements were performed at baseline (T0),after the completion of two therapy circles (T1) and at the end of anthracycline regimen chemotherapy (Te). Echocardiography images were analyzed on the TTA workstation, and the indexes included left atrial minimum volume (LAVmin), left atrial emptying index (LAEF), left atrial active emptying index (LAAEF), as well as the left ventricular global longitudinal strain (LVGLS), left ventricular global circumferential strain (LVGCS), left atrial global longitudinal strain (LAGLS). The overall left atrioventricular longitudinal strain (LAVGLS) was calculated, which was the sum of the absolute values of LVGLS and LAGLS. The changes of left ventricular strain indexes measured by 3D-STE at different time points of patients were evaluated. <b>Results:</b> Thirty-seven patients with DLBCL, aged (48.3±12.1)years, including 23 males (63.9%), were enrolled. Compared with baseline, LVGLS (T1: (-18.63±4.73)% vs. (-22.13±4.40)%, <i>P</i>=0.001; Te:(-18.26±4.64)% vs. (-22.13±4.40)%, <i>P</i><0.001), LAGLS (T1: (20.41±5.56)% vs. (23.98±5.59)%, <i>P</i>=0.003; Te: (17.60±3.96)% vs. (23.98±5.59)%, <i>P</i><0.001) and LAVGLS (T1: (39.05±7.60)% vs. (46.11±7.77)%, <i>P</i><0.001; Te: (40.34±8.55)% vs. (46.11±7.77)%, <i>P</i><0.001) were all deteriorated at the T1 and Te. While LVGCS ((-21.98±5.82)% vs. (-26.15±7.51)%, <i>P</i>=0.010), LAVmin ((23.93±7.29)ml vs. (20.33±7.03)ml, <i>P</i>=0.029), LAEF ((28.94±11.16)% vs. (35.79±11.12)%, <i>P</i>=0.002) and LAAEF ((11.93±10.00)% vs. (18.10±9.96)%, <i>P</i>=0.013) were decreased only until Te. <b>Conclusions:</b> 3D-STE strain measurements could detect early myocaridial function alteration in patients receiving anthracycline regimen chemotherapy, thus may provide a novel approach to monitor anthracycline caused myocardial toxicity.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Z</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Department of Echocardiography, Zhongshan Hospital, Fudan University, Shanghai 200032, China Shanghai Institute of Cardiovascular disease, Shanghai 200032, China Shanghai Institute of Medical Imaging, Shanghai 200032, China National Clinical Research Center for Interventional Medicine, Shanghai 200032, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Q L</ForeName><Initials>QL</Initials><AffiliationInfo><Affiliation>Department of Medical Oncology, Fudan University Shanghai Cancer Center, Shanghai, 200032 China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shen</LastName><ForeName>Y H</ForeName><Initials>YH</Initials><AffiliationInfo><Affiliation>Department of Echocardiography, Zhongshan Hospital, Fudan University, Shanghai 200032, China Shanghai Institute of Cardiovascular disease, Shanghai 200032, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shu</LastName><ForeName>X H</ForeName><Initials>XH</Initials><AffiliationInfo><Affiliation>Department of Echocardiography, Zhongshan Hospital, Fudan University, Shanghai 200032, China Shanghai Institute of Cardiovascular disease, Shanghai 200032, China Shanghai Institute of Medical Imaging, Shanghai 200032, China Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai 200032, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cheng</LastName><ForeName>L L</ForeName><Initials>LL</Initials><AffiliationInfo><Affiliation>Department of Echocardiography, Zhongshan Hospital, Fudan University, Shanghai 200032, China Shanghai Institute of Cardiovascular disease, Shanghai 200032, China Shanghai Institute of Medical Imaging, Shanghai 200032, China National Clinical Research Center for Interventional Medicine, Shanghai 200032, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>chi</Language><GrantList CompleteYN="Y"><Grant><GrantID>82170359</GrantID><Agency>National Natural Science Foundation of China</Agency><Country/></Grant><Grant><GrantID>2020ZSLC21</GrantID><Agency>Clinical Research Fund of Zhongshan Hospital</Agency><Country/></Grant><Grant><GrantID>2020ZSQN74</GrantID><Agency>Youth Fund of Zhongshan Hospital, Fudan University</Agency><Country/></Grant><Grant><GrantID>19MC1910300</GrantID><Agency>Shanghai Clinical Research Center for Interventional Medicine</Agency><Country/></Grant><Grant><GrantID>202040344</GrantID><Agency>Shanghai Municipal Health Commission Fund</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D004740">English Abstract</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>China</Country><MedlineTA>Zhonghua Xin Xue Guan Bing Za Zhi</MedlineTA><NlmUniqueID>7910682</NlmUniqueID><ISSNLinking>0253-3758</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018943">Anthracyclines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000903">Antibiotics, Antineoplastic</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D061065">Polyketides</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018943" MajorTopicYN="N">Anthracyclines</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016277" MajorTopicYN="N">Ventricular Function, Left</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000903" MajorTopicYN="N">Antibiotics, Antineoplastic</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D061065" MajorTopicYN="Y">Polyketides</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008223" MajorTopicYN="Y">Lymphoma</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading></MeshHeadingList><OtherAbstract Type="Publisher" Language="chi"><AbstractText><b>目的：</b> 评价三维斑点追踪超声心动图（3D-STE）应变指标评估蒽环类药物化疗早期左心功能改变的价值。 <b>方法：</b> 本研究为回顾性研究。选取2012年12月至2014年12月于复旦大学附属肿瘤医院接受以蒽环类药物为基础的化疗方案治疗的弥漫大B淋巴瘤（DLBCL）患者37例。分别于化疗前、化疗2周期后及化疗结束后行3D-STE检查。应用TTA工作站分析患者的超声心动图图像，测量指标包括左心房最小容积（LAVmin）、左心房排空指数（LAEF）、左心房主动排空指数（LAAEF）等左心容积指标，及左心室整体纵向应变（LVGLS）、左心室整体环向应变（LVGCS）、左心房整体纵向应变（LAGLS）等左心应变指标。计算LVGLS与LAGLS的绝对值之和得出左房室整体纵向应变（LAVGLS）。观察纳入患者不同时间点3D-STE测量的左心应变指标变化情况。 <b>结果：</b> 本研究共纳入37例DLBCL患者，年龄（48.3±12.1）岁，其中男性23例（63.9%）。与基线测量值相比，患者化疗2周期后及化疗结束时LVGLS［化疗2周期后：（-18.63±4.73）%比（-22.13±4.40）%，<i>P</i>=0.001；化疗结束：（-18.26±4.64）%比（-22.13±4.40）%，<i>P</i><0.001］、LAGLS［化疗2周期后：（20.41±5.56）%比（23.98±5.59）%，<i>P</i>=0.003；化疗结束：（17.60±3.96）%比（23.98±5.59）%，<i>P</i><0.001］和LAVGLS［化疗2周期后：（39.05±7.60）%比（46.11±7.77）%，<i>P</i><0.001；化疗结束：（40.34±8.55）%比（46.11±7.77）%，<i>P</i><0.001］均降低；LVGCS［（-21.98±5.82）%比（-26.15±7.51）%，<i>P</i>=0.010］、LAVmin［（23.93±7.29）ml比（20.33±7.03）ml，<i>P</i>=0.029］、LAEF［（28.94±11.16）%比（35.79±11.12）%，<i>P</i>=0.002］、LAAEF［（11.93±10.00）%比（18.10±9.96）%，<i>P</i>=0.013］仅在化疗结束后改变，而在化疗2周期后无明显变化（<i>P</i>均>0.05）。 <b>结论：</b> 3D-STE左心应变指标能发现蒽环类药物化疗早期心肌功能改变，可为化疗过程中的心肌毒性监测提供更加敏感的指标。.</AbstractText></OtherAbstract></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>11</Month><Day>23</Day><Hour>23</Hour><Minute>12</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>11</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>11</Month><Day>26</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36418273</ArticleId><ArticleId IdType="doi">10.3760/cma.j.cn112148-20220727-00583</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36418164</PMID><DateRevised><Year>2022</Year><Month>11</Month><Day>23</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1478-5153</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Nov</Month><Day>23</Day></PubDate></JournalIssue><Title>Nursing in critical care</Title><ISOAbbreviation>Nurs Crit Care</ISOAbbreviation></Journal>Nurses' perceptions and use of near infrared spectroscopy in paediatric cardiac intensive care. | <b>Objective:</b> To analyze the value of 3-dimensional speckle tracking echocardiograghy (3D-STE) derived strain parameters on the detection of subclinical myocardial deformation alterations in patients with lymphoma treated with anthracycline agents. <b>Methods:</b> This study was a retrospective study. A total of 37 patients with newly diagnosed diffuse large B cell non-Hodgkin lymphoma between December 2012 and December 2014 in Cancer Center, Fudan university were included. 3D-STE strain measurements were performed at baseline (T0),after the completion of two therapy circles (T1) and at the end of anthracycline regimen chemotherapy (Te). Echocardiography images were analyzed on the TTA workstation, and the indexes included left atrial minimum volume (LAVmin), left atrial emptying index (LAEF), left atrial active emptying index (LAAEF), as well as the left ventricular global longitudinal strain (LVGLS), left ventricular global circumferential strain (LVGCS), left atrial global longitudinal strain (LAGLS). The overall left atrioventricular longitudinal strain (LAVGLS) was calculated, which was the sum of the absolute values of LVGLS and LAGLS. The changes of left ventricular strain indexes measured by 3D-STE at different time points of patients were evaluated. <b>Results:</b> Thirty-seven patients with DLBCL, aged (48.3±12.1)years, including 23 males (63.9%), were enrolled. Compared with baseline, LVGLS (T1: (-18.63±4.73)% vs. (-22.13±4.40)%, <i>P</i>=0.001; Te:(-18.26±4.64)% vs. (-22.13±4.40)%, <i>P</i><0.001), LAGLS (T1: (20.41±5.56)% vs. (23.98±5.59)%, <i>P</i>=0.003; Te: (17.60±3.96)% vs. (23.98±5.59)%, <i>P</i><0.001) and LAVGLS (T1: (39.05±7.60)% vs. (46.11±7.77)%, <i>P</i><0.001; Te: (40.34±8.55)% vs. (46.11±7.77)%, <i>P</i><0.001) were all deteriorated at the T1 and Te. While LVGCS ((-21.98±5.82)% vs. (-26.15±7.51)%, <i>P</i>=0.010), LAVmin ((23.93±7.29)ml vs. (20.33±7.03)ml, <i>P</i>=0.029), LAEF ((28.94±11.16)% vs. (35.79±11.12)%, <i>P</i>=0.002) and LAAEF ((11.93±10.00)% vs. (18.10±9.96)%, <i>P</i>=0.013) were decreased only until Te. <b>Conclusions:</b> 3D-STE strain measurements could detect early myocaridial function alteration in patients receiving anthracycline regimen chemotherapy, thus may provide a novel approach to monitor anthracycline caused myocardial toxicity.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Z</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Department of Echocardiography, Zhongshan Hospital, Fudan University, Shanghai 200032, China Shanghai Institute of Cardiovascular disease, Shanghai 200032, China Shanghai Institute of Medical Imaging, Shanghai 200032, China National Clinical Research Center for Interventional Medicine, Shanghai 200032, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Q L</ForeName><Initials>QL</Initials><AffiliationInfo><Affiliation>Department of Medical Oncology, Fudan University Shanghai Cancer Center, Shanghai, 200032 China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shen</LastName><ForeName>Y H</ForeName><Initials>YH</Initials><AffiliationInfo><Affiliation>Department of Echocardiography, Zhongshan Hospital, Fudan University, Shanghai 200032, China Shanghai Institute of Cardiovascular disease, Shanghai 200032, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shu</LastName><ForeName>X H</ForeName><Initials>XH</Initials><AffiliationInfo><Affiliation>Department of Echocardiography, Zhongshan Hospital, Fudan University, Shanghai 200032, China Shanghai Institute of Cardiovascular disease, Shanghai 200032, China Shanghai Institute of Medical Imaging, Shanghai 200032, China Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai 200032, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cheng</LastName><ForeName>L L</ForeName><Initials>LL</Initials><AffiliationInfo><Affiliation>Department of Echocardiography, Zhongshan Hospital, Fudan University, Shanghai 200032, China Shanghai Institute of Cardiovascular disease, Shanghai 200032, China Shanghai Institute of Medical Imaging, Shanghai 200032, China National Clinical Research Center for Interventional Medicine, Shanghai 200032, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>chi</Language><GrantList CompleteYN="Y"><Grant><GrantID>82170359</GrantID><Agency>National Natural Science Foundation of China</Agency><Country/></Grant><Grant><GrantID>2020ZSLC21</GrantID><Agency>Clinical Research Fund of Zhongshan Hospital</Agency><Country/></Grant><Grant><GrantID>2020ZSQN74</GrantID><Agency>Youth Fund of Zhongshan Hospital, Fudan University</Agency><Country/></Grant><Grant><GrantID>19MC1910300</GrantID><Agency>Shanghai Clinical Research Center for Interventional Medicine</Agency><Country/></Grant><Grant><GrantID>202040344</GrantID><Agency>Shanghai Municipal Health Commission Fund</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D004740">English Abstract</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>China</Country><MedlineTA>Zhonghua Xin Xue Guan Bing Za Zhi</MedlineTA><NlmUniqueID>7910682</NlmUniqueID><ISSNLinking>0253-3758</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018943">Anthracyclines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000903">Antibiotics, Antineoplastic</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D061065">Polyketides</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018943" MajorTopicYN="N">Anthracyclines</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016277" MajorTopicYN="N">Ventricular Function, Left</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000903" MajorTopicYN="N">Antibiotics, Antineoplastic</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D061065" MajorTopicYN="Y">Polyketides</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008223" MajorTopicYN="Y">Lymphoma</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading></MeshHeadingList><OtherAbstract Type="Publisher" Language="chi"><b>目的：</b> 评价三维斑点追踪超声心动图（3D-STE）应变指标评估蒽环类药物化疗早期左心功能改变的价值。 <b>方法：</b> 本研究为回顾性研究。选取2012年12月至2014年12月于复旦大学附属肿瘤医院接受以蒽环类药物为基础的化疗方案治疗的弥漫大B淋巴瘤（DLBCL）患者37例。分别于化疗前、化疗2周期后及化疗结束后行3D-STE检查。应用TTA工作站分析患者的超声心动图图像，测量指标包括左心房最小容积（LAVmin）、左心房排空指数（LAEF）、左心房主动排空指数（LAAEF）等左心容积指标，及左心室整体纵向应变（LVGLS）、左心室整体环向应变（LVGCS）、左心房整体纵向应变（LAGLS）等左心应变指标。计算LVGLS与LAGLS的绝对值之和得出左房室整体纵向应变（LAVGLS）。观察纳入患者不同时间点3D-STE测量的左心应变指标变化情况。 <b>结果：</b> 本研究共纳入37例DLBCL患者，年龄（48.3±12.1）岁，其中男性23例（63.9%）。与基线测量值相比，患者化疗2周期后及化疗结束时LVGLS［化疗2周期后：（-18.63±4.73）%比（-22.13±4.40）%，<i>P</i>=0.001；化疗结束：（-18.26±4.64）%比（-22.13±4.40）%，<i>P</i><0.001］、LAGLS［化疗2周期后：（20.41±5.56）%比（23.98±5.59）%，<i>P</i>=0.003；化疗结束：（17.60±3.96）%比（23.98±5.59）%，<i>P</i><0.001］和LAVGLS［化疗2周期后：（39.05±7.60）%比（46.11±7.77）%，<i>P</i><0.001；化疗结束：（40.34±8.55）%比（46.11±7.77）%，<i>P</i><0.001］均降低；LVGCS［（-21.98±5.82）%比（-26.15±7.51）%，<i>P</i>=0.010］、LAVmin［（23.93±7.29）ml比（20.33±7.03）ml，<i>P</i>=0.029］、LAEF［（28.94±11.16）%比（35.79±11.12）%，<i>P</i>=0.002］、LAAEF［（11.93±10.00）%比（18.10±9.96）%，<i>P</i>=0.013］仅在化疗结束后改变，而在化疗2周期后无明显变化（<i>P</i>均>0.05）。 <b>结论：</b> 3D-STE左心应变指标能发现蒽环类药物化疗早期心肌功能改变，可为化疗过程中的心肌毒性监测提供更加敏感的指标。.</OtherAbstract></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>11</Month><Day>23</Day><Hour>23</Hour><Minute>12</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>11</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>11</Month><Day>26</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36418273</ArticleId><ArticleId IdType="doi">10.3760/cma.j.cn112148-20220727-00583</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36418164</PMID><DateRevised><Year>2022</Year><Month>11</Month><Day>23</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1478-5153</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Nov</Month><Day>23</Day></PubDate></JournalIssue><Title>Nursing in critical care</Title><ISOAbbreviation>Nurs Crit Care</ISOAbbreviation></Journal><ArticleTitle>Nurses' perceptions and use of near infrared spectroscopy in paediatric cardiac intensive care.</ArticleTitle><ELocationID EIdType="doi" ValidYN="Y">10.1111/nicc.12861</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Near-infrared spectroscopy (NIRS) is a non-invasive technology that estimates regional oxygen saturation. Literature demonstrates that NIRS can provide valuable data for clinical staff. However, little research has addressed the nursing care and management of NIRS in the critical care environment.<AbstractText Label="AIMS" NlmCategory="OBJECTIVE">To assess nurses' perception around the use of NIRS and current NIRS practice within PCICUs.<AbstractText Label="STUDY DESIGN" NlmCategory="METHODS">A 53-item cross-sectional electronic survey was developed to assess indications for NIRS, critical value thresholds and interventions, barriers to use, policies and procedures, and nursing perceptions. Descriptive statistics were used to summarize and aggregate data.<AbstractText Label="RESULTS" NlmCategory="RESULTS">Among the 28 responding sites (63.6% response rate), usage of NIRS was variable and patient-dependent. Most nurses reported using NIRS in patients with unstable physiology such as post-operative single ventricle (n = 25, 89.3%) and concern for shock (n = 21, 75.0%). Critically low cerebral values varied among respondents from less than 40 (n = 3, 10.7%) to less than 60 (n = 4, 14.3%), with lower critical values permitted for single ventricle physiology: less than 40 (n = 8, 28.6%) to less than 50 (n = 6, 21.4%). Reported barriers to using NIRS included skin breakdown (n = 9, 32.1%), lack of consistency in decision-making among physicians (n = 13, 46.4%), and not using NIRS data when developing a plan of care (n = 11, 39.3%). Most (n = 24, 85.7%) nurses reported that NIRS provided valuable information and was perceived to be beneficial for patients.<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">NIRS monitoring is a common technology in the care of complex congenital heart disease patients. Most nurses valued this technology, but inconsistencies and practicalities around its use in guiding patient management were found to be problematic.<AbstractText Label="RELEVANCE TO CLINICAL PRACTICE" NlmCategory="CONCLUSIONS">NIRS is commonly used in the PCICU and although nurses perceived NIRS to be useful for their practice, the variability in the interpretation of values and inconsistent protocols and decision-making by physicians was challenging. |
2,329,340 | Decline of stress resilience in aging rats: Focus on choroid plexus-cerebrospinal fluid-hippocampus. | This study was designed to examine the mechanisms underlying decline of stress resilience in aged rats from the perspective of CP-CSF-hippocampus.</AbstractText>Male Wistar rats (7-8 weeks old or 20 months old) were subjected to chronic unpredictable mild stress (CUMS) for 6 weeks. The behavioral tests were conducted to assess anxiety, depression and cognitive function. Hippocampal neurogenesis, apoptosis and synaptic plasticity were detected by western blot (WB) and/or immunofluorescence (IF) assay. Differential expression of growth factors (GFs) and axon guidance proteins (AGPs) in CSF was analyzed using the quantitative proteomics approach. IF and WB were performed to detect expression of occludin-1, Ki-67/Transthyretin, and folate transporters in choroid plexus (CP).</AbstractText>Decreased proliferation, impaired structure and transport function of CP were correlated with CSF composition alterations in stressed aging rats, including reduced 5-Methyltetrahydrofolate, growth factors and axon growth factors. Nutritional support of CSF upon hippocampus was attenuated, therefore affecting hippocampal plasticity. It has led to depression-like behaviors and cognitive deficits in stressful aged rats.</AbstractText>Keeping normal structure and function of CP-CSF system may be a practical strategy for neuropsychological disorders in the elderly. This work provides evidential basis for CP transplant and CSF replacement therapy in future studies.</AbstractText> |
2,329,341 | [The effects of vagus nerve stimulation on hippocampal neuro-inflammatory and α7nAChR expression in rats with intractable epilepsy]. | <b>Objective:</b> To investigate the effects of vagus nerve stimulation(VNS) on hippocampal neuro-inflammatory and α7 nicotinic acetylcholine receptor (α7nAChR) expression in rats with intractable epilepsy (IE). <b>Methods:</b> Eighty adult male SD rats (SPF) were randomly divided into control group, model group, VNS group and MLA+VNS group. There were respectively 20 rats in the control group and MLA+VNS group, and because of model failure and animal death, 15 rats and 14 rats in the model group and VNS group were left respectively . Except the control group, the IE model was established in other groups. Only the vagus nerve was isolated in the control group without electrical stimulation; the model group did not take any intervention measures; the VNS group was treated for 4 weeks with VNS after the model was successful; the MLA(3.4 μg/μl, 5 μl) was given to the lateral ventricle in the MLA+VNS group, and then VNS for 4 weeks. Seizure frequency and duration in each group were observed and recorded. And then the rats were decapitated, the hippocampus were quickly separated and 10% tissue homogenate was prepared. The homogenate was centrifuged and the supernatant was extracted. The activities of AChE and ChAT in the supernatant were measured by spectrophotometry, and the levels of TNF-ɑ, IL-6 and IL-1β were detected by ELISA. The expression of α7nAChR in rat hippocampals was detected by Western blot. The expression of α7nAChR on microglias in rat hippocampals was assesed by double-labeled immunofluorescence. <b>Results:</b> ①After VNS for 4 weeks, the frequency and duration of seizures in rats were decreased significantly, which were lower than those of the model group (P<0.01); After treated with MLA +VNS, the frequency and duration of seizures in rats were also reduced significantly, which were lower than those of the model group, but higher than those of the VNS group (P<0.01).②Compared with the control group, the expression of ChAT in the hippocampus of rats in the model group was decreased significantly and the expression of AChE was increased significantly (P<0.01); Compared with the model group, the expressions of ChAT in the hippocampus of rats in the VNS group and MLA+VNS group were increased significantly and the expressions of AChE were decreased significantly (P<0.01); Compared with the VNS group, in the hippocampus of rats in the MLA+VNS group, the expressions of ChAT and AChE had no significant changes (P>0.05). ③Compared with the control group, the expressions of TNF-ɑ, IL-6 and IL-1β in the hippocampus of rats in the model group were increased significantly (P<0.01). Compared with the model group, the expressions of TNF-ɑ, IL-6 and IL-1β in the hippocampus of rats in the VNS group were decreased significantly (P<0.01). Compared with the VNS group, the expressions of TNF-ɑ, IL-6 and IL-1β in the hippocampus of rats in the MLA+VNS group were increased significantly(P<0.01). ④Compared with the control group, the expression of α7nAChR in hippocampus and microglia of rats in the model group was decreased significantly(P<0.01); Compared with the model group, the expression of α7nAChR in hippocampus and microglia of rats in the VNS group was up-regulated significantly (P<0.01); Compared with the VNS group, coexpression of α7nAChR on microglia wasreduced significantly in the MLA+VNS group (P<0.01). <b>Conclusion:</b> VNS has obvious therapeutic effect on IE rats, and its mechanism may be related to activating hippocampal microglia cholinergic anti-inflammatory pathway directly and inhibiting hippocampal neuro-inflammatory response.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Yong-Ge</ForeName><Initials>YG</Initials><AffiliationInfo><Affiliation>Department of Basic Medicine, Nanyang Medical College, Nanyang 473000.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhou</LastName><ForeName>Shu</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Basic Medicine, Nanyang Medical College, Nanyang 473000.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Biomedical Engineering Research Center, Kunming Medical University, Kunming 650000, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yao</LastName><ForeName>Yin-le</ForeName><Initials>YL</Initials><AffiliationInfo><Affiliation>Department of Basic Medicine, Nanyang Medical College, Nanyang 473000.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wei</LastName><ForeName>Xiao-Ming</ForeName><Initials>XM</Initials><AffiliationInfo><Affiliation>Department of Basic Medicine, Nanyang Medical College, Nanyang 473000.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Shi-Feng</ForeName><Initials>SF</Initials><AffiliationInfo><Affiliation>Department of Basic Medicine, Nanyang Medical College, Nanyang 473000.</Affiliation></AffiliationInfo></Author></AuthorList><Language>chi</Language><PublicationTypeList><PublicationType UI="D004740">English Abstract</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>China</Country><MedlineTA>Zhongguo Ying Yong Sheng Li Xue Za Zhi</MedlineTA><NlmUniqueID>9426407</NlmUniqueID><ISSNLinking>1000-6834</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D064569">alpha7 Nicotinic Acetylcholine Receptor</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014409">Tumor Necrosis Factor-alpha</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015850">Interleukin-6</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D055536" MajorTopicYN="Y">Vagus Nerve Stimulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D064569" MajorTopicYN="N">alpha7 Nicotinic Acetylcholine Receptor</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000069279" MajorTopicYN="Y">Drug Resistant Epilepsy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014409" MajorTopicYN="N">Tumor Necrosis Factor-alpha</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015850" MajorTopicYN="N">Interleukin-6</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017207" MajorTopicYN="N">Rats, Sprague-Dawley</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006624" MajorTopicYN="N">Hippocampus</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012640" MajorTopicYN="N">Seizures</DescriptorName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading></MeshHeadingList><OtherAbstract Type="Publisher" Language="chi"><b>目的:</b> 探讨迷走神经刺激(VNS)对难治性癫痫(IE)模型大鼠海马神经炎性反应及α7nAChR表达的影响。<b>方法:</b> 80只成年雄性SD大鼠,SPF级,随机分为对照组、模型组、VNS组、甲基牛扁亭(MLA)+VNS组,其中对照组与MLA+VNS组分别20只,模型组与VNS组因模型制作失败与动物死亡,分别剩下15只和14只。除对照组之外,其余各组皆通过腹腔注射皮罗卡品建立氯化锂-皮罗卡品IE大鼠模型。对照组仅分离迷走神经,不采取电刺激;模型组不采取任何干预措施;VNS组在模型制作成功后7 d采取VNS,连续4周;MLA+VNS组先侧脑室给药MLA(3.4 μg/μl,5 μl),然后给予VNS,连续4周。观察并记录各组大鼠癫痫发作的次数与持续时间的变化;然后断头处死大鼠,快速分离海马并制备10%组织匀浆,离心并提取上清液,通过分光光度法测定上清液中AChE、ChAT活性;ELISA法检测TNF-ɑ、IL-6和IL-1β表达;Western blot检测海马组织α7nAChR蛋白表达;免疫荧光染色法检测海马组织α7nAChR与小胶质细胞共表达。<b>结果:</b> ①通过VNS治疗4周后,大鼠癫痫发作的频率以及持续的时间都明显低于模型组(P<0.01);MLA阻断后在给予VNS,大鼠癫痫发作的频率以及持续的时间也明显低于模型组,但高于VNS组(P<0.01)。②与对照组比较,模型组大鼠海马组织ChAT表达明显下降,AChE表达明显升高(P<0.01);与模型组比较,VNS组与MLA+VNS组大鼠海马组织ChAT表达明显升高,AChE表达明显降低(P< 0.01);与VNS组比较,MLA+VNS组大鼠海马组织ChAT、AChE表达无明显变化(P>0.05)。③与对照组比较,模型组大鼠海马组织TNF-ɑ、IL-6和IL-1β表达明显升高(P<0.01);与模型组比较,VNS组大鼠海马组织TNF-ɑ、IL-6和IL-1β表达明显降低(P<0.01);与VNS组比较,MLA+VNS组大鼠海马组织TNF-ɑ、IL-6和IL-1β表达明显升高(P<0.01)。④与对照组比较,模型组大鼠海马组织以及小胶质细胞上α7nAChR表达明显降低(P<0.01);与模型组比较,VNS组大鼠海马组织以及小胶质细胞上α7nAChR表达明显上调(P<0.01);与VNS组比较,MLA+VNS组海马小胶质细胞上共表达α7nAChR数量明显减少(P<0.01)。<b>结论:</b> VNS对IE大鼠有明显的治疗作用,其机制可能是通过直接激活海马小胶质细胞CAP,抑制海马神经炎性反应来实现的。. |
2,329,342 | Coordination of Cilia Movements in Multi-Ciliated Cells. | Multiple motile cilia are formed at the apical surface of multi-ciliated cells in the epithelium of the oviduct or the fallopian tube, the trachea, and the ventricle of the brain. Those cilia beat unidirectionally along the tissue axis, and this provides a driving force for directed movements of ovulated oocytes, mucus, and cerebrospinal fluid in each of these organs. Furthermore, cilia movements show temporal coordination between neighboring cilia. To establish such coordination of cilia movements, cilia need to sense and respond to various cues, including the organ's orientation and movements of neighboring cilia. In this review, we discuss the mechanisms by which cilia movements of multi-ciliated cells are coordinated, focusing on planar cell polarity and the cytoskeleton, and highlight open questions for future research. |
2,329,343 | Inflammation of the cardiac coronary artery in ICR mice. | Inflammation of the cardiac coronary artery in ICR mice is occasionally observed in toxicity studies; however, this has not been well explored histologically. Herein, we investigated the detailed histology of the associated lesions in 6-8-week-old ICR mice. Coronary artery inflammation in the right ventricular wall was observed in 10 of 142 mice (7.0%). Histopathological examination revealed hypertrophy of the vascular smooth muscle cells and perivascular infiltration of macrophages in mild cases. In moderate to marked cases, single-cell necrosis of vascular smooth muscle cells, hemorrhage of the tunica media, and fibrinoid necrosis of the vessel wall were observed, in addition to the changes seen in mild cases. Electron microscopic examination of moderate cases revealed a discontinuous internal elastic lamina suggestive of rupture, and vascular smooth muscle cells beneath the elastic lamina showed degeneration and necrosis. These findings suggest that the lesions developed as a rupture of the internal elastic lamina and necrosis of vascular smooth muscle cells, while leaked plasma components caused vascular and perivascular inflammation. In ICR mice, dystrophic calcinosis (DCC) is known to occur rarely in the right ventricle. DCC is defined as focal calcification in necrotic myocardial fibers, the pathogenesis of which is considered to involve ectopic calcification. Since calcification was not observed in any part of the heart, including the inflammation region, the pathophysiology of cardiac arterial inflammation seen in our ICR mice was considered to differ from that of DCC. |
2,329,344 | The predictive value of changes in left atrial volume index for rehospitalization in heart failure with preserved ejection fraction.<Pagination><StartPage>151</StartPage><EndPage>158</EndPage><MedlinePgn>151-158</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/clc.23952</ELocationID><Abstract><AbstractText Label="AIMS" NlmCategory="OBJECTIVE">Left atrial volume index (LAVI) is an adequate analysis to predicate the left ventricle (LV) filling pressures, providing a powerful predictive marker of LV diastolic dysfunction. LAVI is a dynamic morphophysiological marker, and whether LAVI changes can predicate clinical outcomes in HF with preserved ejection fraction (HFpEF) is unknown.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">HFpEF patients were retrospectively studied from the First Affiliated Hospital of Dalian Medical University. Patients were classified into deteriorated, stable and improved groups according to the change in LAVI. Rehospitalization was defined as the main endpoint, the composite outcome of rehospitalization or all-cause death was defined as the secondary endpoint.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">A total of 409 patients were included. In this cohort, the percentage of deteriorated, stable, and improved LAVI were 99 (24.2%), 235 (57.4%), and 75 (18.4%), respectively. During the 22 months follow-up period, 168 patients (41.1%) were rehospitalized, 31 patients (7.5%) died and 182 patients (44.5%) experienced a composite outcome. Multivariate Cox regression showed that compared to improved LAVI, those with deteriorated and stable LAVI experienced higher risk of rehospitalization. Logistic regression showed atrial fibrillation (AF) and higher creatinine were independent predictors of deteriorated LAVI, whereas the use of loop diuretics, calcium channel blockers (CCB), and high level of high-density lipoprotein cholesterol (HDL-C) were significantly associated with improved LAVI.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Change in LAVI provides a powerful and dynamic morphophysiological marker of LV filling status and can be used to evaluate the rehospitalization in HFpEF patients.</AbstractText><CopyrightInformation>© 2022 The Authors. Clinical Cardiology published by Wiley Periodicals, LLC.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hao</LastName><ForeName>Zhujing</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Institute of Cardiovascular Diseases, The First Affiliated Hospital of Dalian Medical University, Dalian, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xu</LastName><ForeName>Guiwen</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Institute of Cardiovascular Diseases, The First Affiliated Hospital of Dalian Medical University, Dalian, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yuan</LastName><ForeName>Mengyang</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Institute of Cardiovascular Diseases, The First Affiliated Hospital of Dalian Medical University, Dalian, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sun</LastName><ForeName>Yuxi</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Institute of Cardiovascular Diseases, The First Affiliated Hospital of Dalian Medical University, Dalian, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tan</LastName><ForeName>Ruopeng</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Institute of Cardiovascular Diseases, The First Affiliated Hospital of Dalian Medical University, Dalian, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Yang</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Institute of Cardiovascular Diseases, The First Affiliated Hospital of Dalian Medical University, Dalian, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xia</LastName><ForeName>Yun-Long</ForeName><Initials>YL</Initials><Identifier Source="ORCID">0000-0001-7985-3273</Identifier><AffiliationInfo><Affiliation>Institute of Cardiovascular Diseases, The First Affiliated Hospital of Dalian Medical University, Dalian, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Cardiology, Institute of Heart and Vascular Diseases, The First Affiliated Hospital of Dalian Medical University, Dalian, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>11</Month><Day>20</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Clin Cardiol</MedlineTA><NlmUniqueID>7903272</NlmUniqueID><ISSNLinking>0160-9289</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006333" MajorTopicYN="Y">Heart Failure</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013318" MajorTopicYN="N">Stroke Volume</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010359" MajorTopicYN="N">Patient Readmission</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006325" MajorTopicYN="N">Heart Atria</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016277" MajorTopicYN="N">Ventricular Function, Left</DescriptorName><QualifierName 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Heart failure with preserved, borderline, and reduced ejection fraction. J Am Coll Cardiol. 2017;70:2476‐2486.</Citation><ArticleIdList><ArticleId IdType="pubmed">29141781</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36403164</PMID><DateRevised><Year>2022</Year><Month>11</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1432-1971</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Nov</Month><Day>20</Day></PubDate></JournalIssue><Title>Pediatric cardiology</Title><ISOAbbreviation>Pediatr Cardiol</ISOAbbreviation></Journal>Impact of Abnormal Potassium on Arrhythmia Risk During Pediatric Digoxin Therapy. | Digoxin is used in children with heart failure and tachyarrhythmia. Its use in patients with single ventricle anatomy has increased following evidence of improved interstage survival after the Norwood procedure. Digoxin has a narrow therapeutic window and may alter serum potassium balance, inducing arrhythmias. We hypothesized digoxin use in the setting of abnormal serum potassium levels is associated with arrhythmias. We reviewed all patients ≤ 18 years who received digoxin while admitted at our institution from 2014 to 2021. Admissions < 2 nights were excluded. We compared patients with a hemodynamically significant arrhythmia to those without. We performed adjusted mixed-effects logistic regression with arrhythmia as the outcome variable and potassium status as the predictor variable; adjusting for weight, route of digoxin administration, digoxin indication, serum creatinine, and number of interacting drugs prescribed. Abnormal potassium was defined as serum levels < 3.5 mmol/L or > 6.0 mmol/L. There were 268 encounters in 171 patients. Potassium levels were abnormal in 75.5% of patients who experienced an arrhythmia during digoxin administration, compared to 42.6% who did not (p < 0.001). Odds of arrhythmia was 138% higher in patients with abnormal potassium receiving digoxin (AOR = 2.38, 95% CI 1.07-5.29, p = 0.03). Receiving intravenous digoxin was also associated with a 7.35 odds of cardiac arrhythmia (AOR 7.35, p = 0.006, 95% CI 1.79-30.26). Odds of arrhythmia is increased during digoxin administration when pediatric patients have abnormal potassium levels. Vigilant attention to potassium levels is essential to prevent adverse outcomes during digoxin therapy. |
2,329,345 | Refractory psychiatric symptoms and seizure associated with Dandy-Walker syndrome: A case report and literature review. | Dandy-Walker syndrome (DWS) is a group of brain malformations which occasionally accompanied by psychotic symptoms. The co-occurrence of DWS and epilepsy in children is quite rare.</AbstractText>We reported a 14-year-old male who presented with a 8-month history of inconsistent upper limb tremor and accidental seizure. The MRI showed the typical alterations of DWS: cystic dilatation of the fourth ventricle, vermian hypoplasia, enlarged posterior fossa. He received the ventriculoperitoneal shunting (VPS) placement for hydrocephalus and had a symptom-free period for 8 days. Then he experienced a recurrence of involuntary upper limb tremor and behavior disturbance after decreasing the pressure of cerebrospinal fluid (CSF) from 150 to 130 mm Hg. After being treated with Olanzapine 10 mg/d, Clonazepam 3 mg/qn and Valproate acid (VPA) 500 mg/bid for nearly a month, his mental status and psychotic symptoms fluctuated. A search of Pub Med showed little report of hydrocephalus and DWS comorbidity with seizure and psychosis. Here we presented the whole process of a rare disease from the very beginning with all his symptoms, examinations and treatments.</AbstractText>VPS placement surgery at an earlier stage may be an effective way to avoid inevitable brain damage so as to improve the clinical outcomes for patients with DWS. Continued treatment with regard to DWS condition may include shunt placement, but it mainly focus on developmental concerns, with occupational and physical therapy along with ongoing supportive psychotherapy to improve the coping skills and quality of life.</AbstractText>Copyright © 2022 the Author(s). Published by Wolters Kluwer Health, Inc.</CopyrightInformation> |
2,329,346 | Von Hippel-Lindau syndrome with a rare complication of dilated cardiomyopathy: a case report.<Pagination><StartPage>489</StartPage><MedlinePgn>489</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">489</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1186/s12872-022-02913-1</ELocationID><Abstract><AbstractText Label="BACKGROUND">Von Hippel-Lindau (VHL) syndrome is an autosomal dominant hereditary disease affecting multiple organs, with pheochromocytoma in 26% of cases. However, VHL syndrome with congestive heart failure and dilated cardiomyopathy as the primary clinical manifestations has been rarely reported.</AbstractText><AbstractText Label="CASE PRESENTATION">A 35-year-old male patient was admitted to the hospital with dyspnea. The patient had a history of cerebellar hemangioblastoma that had been resected, and a one-year history of hypertension. Echocardiography and cardiac magnetic resonance imaging demonstrated a dilated left ventricle, decreased systolic function, and nonischemic myocardial changes. Contrast-enhanced abdominal computed tomography showed pheochromocytoma, neoplastic lesions, and multiple cysts in the kidneys and pancreas. Genetic analysis revealed a missense mutation of the VHL gene, c.269 A > T (p.Asn90Ile), which was identified as the cause of the disease. Dilated cardiomyopathy and VHL syndrome type 2 were diagnosed. The patient was administered a diuretic, α-blocker, β-blocker, and an angiotensin receptor neprilysin inhibitor (ARNI), but refused pheochromocytoma resection. At the six-month follow-up, the patient was asymptomatic with improved cardiac function.</AbstractText><AbstractText Label="CONCLUSION">Cardiac involvement is an atypical manifestation in VHL syndrome. Early diagnosis with genetic screening is essential for avoiding life-threatening complications associated with VHL. The management of this rare manifestation of VHL syndrome requires further investigation.</AbstractText><CopyrightInformation>© 2022. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Yu</LastName><ForeName>Ming</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Cardiology, China-Japan Union Hospital of Jilin University, Xiantai, Street NO.126, Jilin, 130033, Changchun, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Jilin Provincial Engineering Laboratory for Endothelial Function and Genetic Diagnosis of Cardiovascular Disease, Jilin Provincial Cardiovascular Research Institute, 130031, Changchun, Jilin Province, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Du</LastName><ForeName>Beibei</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Department of Cardiology, China-Japan Union Hospital of Jilin University, Xiantai, Street NO.126, Jilin, 130033, Changchun, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Jilin Provincial Engineering Laboratory for Endothelial Function and Genetic Diagnosis of Cardiovascular Disease, Jilin Provincial Cardiovascular Research Institute, 130031, Changchun, Jilin Province, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yao</LastName><ForeName>Shuai</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Neurology, China-Japan Union Hospital of Jilin University, Jilin Province, 130031, Changchun, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ma</LastName><ForeName>Jianghong</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Cardiology, China-Japan Union Hospital of Jilin University, Xiantai, Street NO.126, Jilin, 130033, Changchun, China. 790989241@qq.com.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Jilin Provincial Engineering Laboratory for Endothelial Function and Genetic Diagnosis of Cardiovascular Disease, Jilin Provincial Cardiovascular Research Institute, 130031, Changchun, Jilin Province, China. 790989241@qq.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Ping</ForeName><Initials>P</Initials><Identifier Source="ORCID">0000-0001-7960-6248</Identifier><AffiliationInfo><Affiliation>Department of Cardiology, China-Japan Union Hospital of Jilin University, Xiantai, Street NO.126, Jilin, 130033, Changchun, China. pyang@jlu.edu.cn.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Jilin Provincial Engineering Laboratory for Endothelial Function and Genetic Diagnosis of Cardiovascular Disease, Jilin Provincial Cardiovascular Research Institute, 130031, Changchun, Jilin Province, China. pyang@jlu.edu.cn.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>11</Month><Day>18</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>BMC Cardiovasc Disord</MedlineTA><NlmUniqueID>100968539</NlmUniqueID><ISSNLinking>1471-2261</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006623" MajorTopicYN="Y">von Hippel-Lindau Disease</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010673" MajorTopicYN="Y">Pheochromocytoma</DescriptorName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002311" MajorTopicYN="Y">Cardiomyopathy, Dilated</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000310" MajorTopicYN="Y">Adrenal Gland Neoplasms</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005820" MajorTopicYN="N">Genetic Testing</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Case report</Keyword><Keyword MajorTopicYN="N">Congestive heart failure</Keyword><Keyword MajorTopicYN="N">Dilated cardiomyopathy</Keyword><Keyword MajorTopicYN="N">Pheochromocytoma</Keyword><Keyword MajorTopicYN="N">Von Hippel–Lindau syndrome</Keyword></KeywordList><CoiStatement>The authors declare
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Med Princ Pract. 2016;25(2):196–8. doi: 10.1159/000442525.</Citation><ArticleIdList><ArticleId IdType="doi">10.1159/000442525</ArticleId><ArticleId IdType="pmc">PMC5588357</ArticleId><ArticleId IdType="pubmed">26584481</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedBookArticle><BookDocument><PMID Version="1">31194436</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK542296</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-18915">Cardiomegaly<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Amin</LastName><ForeName>Hina</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>SUNY Upstate Medical University</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>Cardiomegaly means enlargement of the heart. The definition is when the transverse diameter of the cardiac silhouette is greater than or equal to 50% of the transverse diameter of the chest (increased cardiothoracic ratio) on a posterior-anterior projection of a chest radiograph or a computed tomography. It should not be confused with an enlargement of the cardiomediastinal outline. Cardiomegaly is usually a manifestation of another pathologic process and presents with several forms of primary or acquired cardiomyopathies. It may involve enlargement of the right, left, or both ventricles or the atria. Many types of cardiomyopathy, such as dilated cardiomyopathy, are characterized by left ventricular dilation and systolic dysfunction, although right ventricular impairment and diastolic dysfunction can also develop.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-18915" sec="article-18915.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18915" sec="article-18915.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18915" sec="article-18915.s3">Etiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18915" sec="article-18915.s4">Epidemiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18915" sec="article-18915.s5">Pathophysiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18915" sec="article-18915.s6">History and Physical</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18915" sec="article-18915.s7">Evaluation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18915" sec="article-18915.s8">Treatment / Management</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18915" sec="article-18915.s9">Differential Diagnosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18915" sec="article-18915.s10">Prognosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18915" sec="article-18915.s11">Complications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18915" sec="article-18915.s12">Deterrence and Patient Education</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18915" sec="article-18915.s13">Pearls and Other Issues</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18915" sec="article-18915.s14">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18915" sec="article-18915.s15">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18915" sec="article-18915.s16">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>11</Month><Day>20</Day></ContributionDate><ReferenceList><Reference><Citation>Jefferies JL, Towbin JA. 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<PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36400745</PMID><DateRevised><Year>2022</Year><Month>11</Month><Day>29</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1097-0177</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Nov</Month><Day>18</Day></PubDate></JournalIssue><Title>Developmental dynamics : an official publication of the American Association of Anatomists</Title><ISOAbbreviation>Dev Dyn</ISOAbbreviation></Journal>Development of ventricular trabeculae affects electrical conduction in the early endothermic heart. | Cardiomegaly means enlargement of the heart. The definition is when the transverse diameter of the cardiac silhouette is greater than or equal to 50% of the transverse diameter of the chest (increased cardiothoracic ratio) on a posterior-anterior projection of a chest radiograph or a computed tomography. It should not be confused with an enlargement of the cardiomediastinal outline. Cardiomegaly is usually a manifestation of another pathologic process and presents with several forms of primary or acquired cardiomyopathies. It may involve enlargement of the right, left, or both ventricles or the atria. Many types of cardiomyopathy, such as dilated cardiomyopathy, are characterized by left ventricular dilation and systolic dysfunction, although right ventricular impairment and diastolic dysfunction can also develop.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-18915" sec="article-18915.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18915" sec="article-18915.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18915" sec="article-18915.s3">Etiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18915" sec="article-18915.s4">Epidemiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18915" sec="article-18915.s5">Pathophysiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18915" sec="article-18915.s6">History and Physical</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18915" sec="article-18915.s7">Evaluation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18915" sec="article-18915.s8">Treatment / Management</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18915" sec="article-18915.s9">Differential Diagnosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18915" sec="article-18915.s10">Prognosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18915" sec="article-18915.s11">Complications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18915" sec="article-18915.s12">Deterrence and Patient Education</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18915" sec="article-18915.s13">Pearls and Other Issues</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18915" sec="article-18915.s14">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18915" sec="article-18915.s15">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18915" sec="article-18915.s16">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>11</Month><Day>20</Day></ContributionDate><ReferenceList><Reference><Citation>Jefferies JL, Towbin JA. 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<PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36400745</PMID><DateRevised><Year>2022</Year><Month>11</Month><Day>29</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1097-0177</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Nov</Month><Day>18</Day></PubDate></JournalIssue><Title>Developmental dynamics : an official publication of the American Association of Anatomists</Title><ISOAbbreviation>Dev Dyn</ISOAbbreviation></Journal><ArticleTitle>Development of ventricular trabeculae affects electrical conduction in the early endothermic heart.</ArticleTitle><ELocationID EIdType="doi" ValidYN="Y">10.1002/dvdy.552</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">The ventricular trabeculae play a role, among others, in the impulse spreading in ectothermic hearts. Despite the morphological similarity with the early developing hearts of endotherms, this trabecular function in mammalian and avian embryos was poorly addressed.<AbstractText Label="RESULTS" NlmCategory="RESULTS">We simulated impulse propagation inside the looping ventricle and revealed delayed apical activation in the heart with inhibited trabecular growth. This finding was corroborated by direct imaging of the endocardial surface showing early activation within the trabeculae implying preferential spreading of depolarization along with them. Targeting two crucial pathways of trabecular formation (Neuregulin/ErbB and Nkx2.5), we showed that trabecular development is also essential for proper conduction patterning. Persistence of the slow isotropic conduction likely contributed to the pumping failure in the trabeculae-deficient hearts.<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Our results showed the essential role of trabeculae in intraventricular impulse spreading and conduction patterning in the early endothermic heart. Lack of trabeculae leads to the failure of conduction parameters differentiation resulting in primitive ventricular activation with consequent impact on the cardiac pumping function. |
2,329,347 | Complete intraventricular migration of ventriculo-peritoneal shunt: A rare case report. | A ventriculoperitoneal (VP) shunt is a cerebral shunt used to treat hydrocephalus. This is used to remove the excessive accumulation of cerebrospinal fluid inside the ventricles.</AbstractText>We are reporting a rare case of complete intracranial migration of a ventriculoperitoneal shunt, a potentially fatal complication, presenting to us with hydrocephalous. The baby was taken up for surgery with endoscopic assisted shunt removal and shunt revision.</AbstractText>Ventriculoperitoneal shunt is one of the common procedures used in infants and children, however, it is used in all age groups for hydrocephalous. The shunt is associated with multiple large number of complications like obstruction, infection, migration, and separation from the connected site. Etc. Shunt migration is a less common complication of which cranial migration is still less common.</AbstractText>Optimum creation of the sub-galeal space for the shunt chamber, a smaller burr hole, a smaller dural opening, and proper anchorage of the chamber to the pericranium, are some of the measures that may be useful in obviating this complication.</AbstractText>Copyright © 2022. Published by Elsevier Ltd.</CopyrightInformation> |
2,329,348 | Cell proliferation and neurogenesis in the adult telencephalon of the newt Cynops pyrrhogaster. | Urodele amphibians have the ability to regenerate several organs, including the brain. For this reason, the research on neurogenesis in these species after ablation of some parts of the brain has markedly progressed. However, detailed information on the characteristics and fate of proliferated cells as well as the function of newly generated neurons under normal conditions is still limited. In this study, we focused on investigating the proliferative and neurogenic zones as well as the fate of proliferated cells in the adult brain of the Japanese red-bellied newt to clarify the significance of neurogenesis in adulthood. We found that the proximal region of the lateral ventricles in the telencephalon and the preoptic area in the diencephalon were the main sites for continuous cell proliferation in the adult brain. Furthermore, we characterized proliferative cells and analyzed neurogenesis through a combination of 5-ethynyl-2'-deoxyuridine (EdU) labeling and immunohistochemistry using antibodies against the stem cell marker Sox2 and neuronal marker NeuN. Twenty-four hours after EdU injection, most of the EdU-positive cells were Sox2-immunopositive, whereas, EdU-positive signals and NeuN-immunoreactivities were not colocalized. Two months after EdU injection, the colocalization ratio of EdU-positive signals with Sox2-immunoreactivities decreased to approximately 10%, whereas the ratio of colocalization of EdU-positive signals with NeuN-immunoreactivities increased to approximately 60%. Furthermore, a portion of the EdU-incorporated cells developed into γ-aminobutyric acid-producing cells, which are assumed to function as interneurons. On the basis of these results, the significance of newly generated neurons was discussed with special reference to their reproductive behavior. |
2,329,349 | Interleukin-17 Promotes the Infiltration of CD8+ T Cells into the Brain in a Mouse Model for Alzheimer's Disease. | Interleukin-17 (IL-17) family cytokines play critical roles in inflammation and pathogen resistance. Inflammation in the central nervous system, denoted as neuroinflammation, promotes the onset and progression of Alzheimer's disease (AD). Previous studies showed that IL-17A neutralizing antibody treatment alleviated Amyloid β (Aβ) burden in rodent models of AD, while overexpression of IL-17A in mouse lateral ventricles rescued part of the AD pathology. However, the involvement of IL-17 in AD and its mechanism of action remain largely unknown.</AbstractText>To investigate the role of IL-17 in AD, we crossed mice lacking the common receptor of IL-17 signaling (IL-17RA knockout mice) to the APP/PS1 mouse model of AD. We then analyzed the composition of immune cells and cytokines/chemokines during different phases of AD pathology, and interrogated the underlying mechanism by which IL-17 may regulate immune cell infiltration into AD brains.</AbstractText>Ablation of IL-17RA in APP/PS1 mice decreased infiltration of CD8+ T cells and myeloid cells to mouse brain. IL-17 was able to promote the production of myeloid- and T cell-attracting chemokines CXCL1 and CXCL9/10 in primary glial cells. We also observed that IL-17 is upregulated in the late stage of AD development, and ectopic expression of IL-17 via adenoviral infection to the cortex trended towards worsened cognition in APP/PS1 mice, suggesting a pathogenic role of excessive IL-17 in AD.</AbstractText>Our data show that IL-17 signaling promotes neuroinflammation in AD by accelerating the infiltration of CD8+ T lymphocytes and Gr1+ CD11b+ myeloid cells.</AbstractText> |
2,329,350 | Cardio-sarcopenia: A syndrome of concern in aging. | Cardiac alterations in structure and function, namely, the left ventricle, have been intensely studied for decades, in association with aging. In recent times, there has been keen interest in describing myocardial changes that accompany skeletal muscle changes in older adults. Initially described as a cardio-sarcopenia syndrome where alterations in myocardial structure were observed particularly among older adults with skeletal muscle sarcopenia, investigations into this syndrome have spurred a fresh level of interest in the cardiac-skeletal muscle axis. The purpose of this perspective is to summarize the background for this "syndrome of concern," review the body of work generated by various human aging cohorts, and to explore future directions and opportunities for understanding this syndrome. |
2,329,351 | Stereology of gonadotropin-releasing hormone and kisspeptin neurons in PACAP gene-deficient female mice. | The hypothalamic gonadotropin-releasing hormone (GnRH)-kisspeptin neuronal network regulates fertility in all mammals. Pituitary adenylate cyclase-activating polypeptide (PACAP) is a neuropeptide isolated from the hypothalamus that is involved in the regulation of several releasing hormones and trop hormones. It is well-known that PACAP influences fertility at central and peripheral levels. However, the effects of PACAP on GnRH and kisspeptin neurons are not well understood. The present study investigated the integrity of the estrous cycle in PACAP-knockout (KO) mice. The number and immunoreactivity of GnRH (GnRH-ir) neurons in wild-type (WT) and PACAP KO female mice were determined using immunohistochemistry. In addition, the number of kisspeptin neurons was measured by counting kisspeptin mRNA-positive cells in the rostral periventricular region of the third ventricle (RP3V) and arcuate nucleus (ARC) using the RNAscope technique. Finally, the mRNA and protein expression of estrogen receptor alpha (ERα) was also examined. Our data showed that the number of complete cycles decreased, and the length of each cycle was longer in PACAP KO mice. Furthermore, the PACAP KO mice experienced longer periods of diestrus and spent significantly less time in estrus. There was no difference in GnRH-ir or number of GnRH neurons. In contrast, the number of kisspeptin neurons was decreased in the ARC, but not in the R3PV, in PACAP KO mice compared to WT littermates. Furthermore, ERα mRNA and protein expression was decreased in the ARC, whereas in the R3PV region, ERα mRNA levels were elevated. Our results demonstrate that embryonic deletion of PACAP significantly changes the structure and presumably the function of the GnRH-kisspeptin neuronal network, influencing fertility. |
2,329,352 | Case report and literature review: Resection of retroinfundibular craniopharyngioma via endoscopic far-lateral supracerebellar infratentorial approach. | The management of retroinfundibular craniopharyngioma (CP) remains the ultimate challenge for both transsphenoidal and open transcranial surgery because of their anatomical location and proximity to vital neurovascular structures. In this report, we aim to describe the technique and feasibility of a novel approach, the purely endoscopic far-lateral supracerebellar infratentorial approach (EF-SCITA), for resection of retroinfundibular CP.</AbstractText>A 63-year-old women presented with progressive visual disturbance, polyuria, and spiritlessness of a 3-month duration. Imaging studies revealed a typical retroinfundibular CP containing solid and cystic components with calcification, which extended inferiorly in front of the brainstem and upward into the third ventricle. The EF-SCITA approach was attempted for resection of the tumor. During surgery, lateral prone positioning with upper flexion of the head and early CSF release allowed for download retraction of the cerebellum. This, in combination with tentorium incision, created a working corridor toward retrosellar and suprasellar spaces. This approach required working between neurovascular structures in the crural cistern, with tumor removal permitted in supra-oculomotor and infra-oculomotor spaces. After aspiration of the fluid contents through the supra-oculomotor triangle, the solid lesion was found tightly adhering to the distal part of the pituitary stalk, and subtotal resection was achieved for maintaining the integrity of pituitary function. In the immediate postoperative period, the patients exhibited oculomotor paralysis and was discharged with hormonal replacement therapy three weeks after operation. At her three-month follow-up appointment, she reported obvious vision improvement. Physical examinations showed partial alleviation of oculomotor paralysis. Pathological analyses confirmed the diagnosis of papillary CP.</AbstractText>The purely EF-SCITA approach combines the advantages of both the posterolateral approach and endoscopic technique, which offers access to retrosellar and suprasellar spaces with seemingly low risks of postoperative morbidity. It would be a safe and effective alternative for the treatment of retroinfundibular CP, especially those with lateral extension to the temporal lobe or posterolateral extension to the petroclival region. Further observational studies in a larger cohort are urgently needed to assess the long-term efficacy of this minimal access approach.</AbstractText>Copyright © 2022 Bai, Sun, Li, Han, Liang, Feng and Yu.</CopyrightInformation> |
2,329,353 | Right heart failure in left heart disease: imaging, functional, and biochemical aspects of right ventricular dysfunction.<Pagination><StartPage>1009</StartPage><EndPage>1022</EndPage><MedlinePgn>1009-1022</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s10741-022-10276-0</ELocationID><Abstract><AbstractText>For decades, cardiologists have largely underestimated the role of the right heart in heart failure due to left heart disease. Nowadays, the importance of evaluating right ventricular (RV) structure and function in left heart failure is well documented and this concept has been emphasized in the most recent heart failure guidelines. However, several relevant questions remain unanswered such as the following: (a) which imaging technique (standard or 3D echocardiography or strain imaging or cardiac magnetic resonance) and, more, which parameters should be used to grade the severity of RV dysfunction? (b) do less widespread and less applied diagnostic tools such as cardiopulmonary stress testing and bioelectrical impedance analysis play a role in this field? (c) are there specific biochemical aspects of RV failure? (d) why notion of pathophysiology of heart and lung interaction are so well appreciated at an academic level but are not applied in the clinical setting? The present review has been prepared by the Heart Failure (HF) working group of the Italian Society of Cardiology and its main objective is to improve our understanding on RV dysfunction in heart failure.</AbstractText><CopyrightInformation>© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ghio</LastName><ForeName>Stefano</ForeName><Initials>S</Initials><Identifier Source="ORCID">0000-0002-1858-1152</Identifier><AffiliationInfo><Affiliation>Divisione Di Cardiologia, IRCCS Fondazione Policlinico San Matteo, Viale Golgi 19, 27100, Pavia, Italy. s.ghio@smatteo.pv.it.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Acquaro</LastName><ForeName>Mauro</ForeName><Initials>M</Initials><Identifier Source="ORCID">0000-0002-5042-7999</Identifier><AffiliationInfo><Affiliation>Divisione Di Cardiologia, IRCCS Fondazione Policlinico San Matteo, Viale Golgi 19, 27100, Pavia, Italy.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cardiology, Department of Molecular Medicine, University of Pavia, Pavia, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Agostoni</LastName><ForeName>Piergiuseppe</ForeName><Initials>P</Initials><Identifier Source="ORCID">0000-0002-8345-6382</Identifier><AffiliationInfo><Affiliation>Centro Cardiologico Monzino, IRCCS, Milan, Italy.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Clinical Science and Community Health, University of Milan, Milan, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ambrosio</LastName><ForeName>Giuseppe</ForeName><Initials>G</Initials><Identifier Source="ORCID">0000-0002-9677-980X</Identifier><AffiliationInfo><Affiliation>Cardiology and Cardiovascular Pathophysiology, S.Maria Della Misericordia Hospital, University of Perugia, Perugia, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Carluccio</LastName><ForeName>Erberto</ForeName><Initials>E</Initials><Identifier Source="ORCID">0000-0002-9296-4397</Identifier><AffiliationInfo><Affiliation>Cardiology and Cardiovascular Pathophysiology, S.Maria Della Misericordia Hospital, University of Perugia, Perugia, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Castiglione</LastName><ForeName>Vincenzo</ForeName><Initials>V</Initials><Identifier Source="ORCID">0000-0002-9285-2328</Identifier><AffiliationInfo><Affiliation>Interdisciplinary Center for Health Sciences, Scuola Superiore Sant'Anna, Pisa, Italy.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Fondazione Toscana G. Monasterio, Pisa, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Colombo</LastName><ForeName>Davide</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Divisione Di Cardiologia, IRCCS Fondazione Policlinico San Matteo, Viale Golgi 19, 27100, Pavia, Italy.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cardiology, Department of Molecular Medicine, University of Pavia, Pavia, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>D'Alto</LastName><ForeName>Michele</ForeName><Initials>M</Initials><Identifier Source="ORCID">0000-0001-5729-1038</Identifier><AffiliationInfo><Affiliation>Department of Cardiology, University L. Vanvitelli - Monaldi Hospital, Naples, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Delle Grottaglie</LastName><ForeName>Santo</ForeName><Initials>S</Initials><Identifier Source="ORCID">0000-0001-7153-4040</Identifier><AffiliationInfo><Affiliation>Division of Cardiology, Ospedale Medico-Chirurgico Accreditato Villa dei Fiori, Acerra (Naples), Italy.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Zena and Michael A. Wiener Cardiovascular Institute/Marie-Josee and Henry R. Kravis Center for Cardiovascular Health, Mount Sinai School of Medicine, New York, NY, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dini</LastName><ForeName>Frank Lloyd</ForeName><Initials>FL</Initials><AffiliationInfo><Affiliation>Sant'Agostino Medical Center, Milan, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Emdin</LastName><ForeName>Michele</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Interdisciplinary Center for Health Sciences, Scuola Superiore Sant'Anna, Pisa, Italy.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Fondazione Toscana G. Monasterio, Pisa, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fortunato</LastName><ForeName>Martino</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Medical and Surgical Sciences, University of Foggia, Foggia, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Guaricci</LastName><ForeName>Andrea Igoren</ForeName><Initials>AI</Initials><Identifier Source="ORCID">0000-0001-7133-4401</Identifier><AffiliationInfo><Affiliation>Department of Emergency and Organ Transplantation, Institute of Cardiovascular Disease, University Hospital Policlinico of Bari, 70124, Bari, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jacoangeli</LastName><ForeName>Francesca</ForeName><Initials>F</Initials><Identifier Source="ORCID">0000-0003-3244-2164</Identifier><AffiliationInfo><Affiliation>Cardiology and Cardiovascular Pathophysiology, S.Maria Della Misericordia Hospital, University of Perugia, Perugia, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Marra</LastName><ForeName>Alberto M</ForeName><Initials>AM</Initials><AffiliationInfo><Affiliation>Department of Translational Medical Sciences, "Federico II" University Hospital and School of Medicine, Naples, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Paolillo</LastName><ForeName>Stefania</ForeName><Initials>S</Initials><Identifier Source="ORCID">0000-0003-4683-0993</Identifier><AffiliationInfo><Affiliation>Department of Advanced Biomedical Sciences, Federico II University of Naples, Naples, Italy.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Mediterranea Cardiocentro, Naples, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Papa</LastName><ForeName>Sivia</ForeName><Initials>S</Initials><Identifier Source="ORCID">0000-0001-8653-4035</Identifier><AffiliationInfo><Affiliation>Department of Clinical, Anesthesiological and Cardiovascular Sciences, I School of Medicine, Sapienza University of Rome, Policlinico Umberto I, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Scajola</LastName><ForeName>Luca Vicini</ForeName><Initials>LV</Initials><AffiliationInfo><Affiliation>Divisione Di Cardiologia, IRCCS Fondazione Policlinico San Matteo, Viale Golgi 19, 27100, Pavia, Italy.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cardiology, Department of Molecular Medicine, University of Pavia, Pavia, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Correale</LastName><ForeName>Michele</ForeName><Initials>M</Initials><Identifier Source="ORCID">0000-0002-7863-253X</Identifier><AffiliationInfo><Affiliation>Cardiology Unit, University Hospital Policlinico Riuniti, Foggia, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Palazzuoli</LastName><ForeName>Alberto</ForeName><Initials>A</Initials><Identifier Source="ORCID">0000-0002-6235-984X</Identifier><AffiliationInfo><Affiliation>Cardiovascular Diseases Unit, Cardio-Thoracic and Vascular Department, Le Scotte Hospital University of Siena, Siena, Italy.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>11</Month><Day>16</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Heart Fail Rev</MedlineTA><NlmUniqueID>9612481</NlmUniqueID><ISSNLinking>1382-4147</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004452" MajorTopicYN="N">Echocardiography</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018497" MajorTopicYN="Y">Ventricular Dysfunction, Right</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006333" MajorTopicYN="Y">Heart Failure</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019560" MajorTopicYN="Y">Echocardiography, Three-Dimensional</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016278" MajorTopicYN="N">Ventricular Function, Right</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013318" MajorTopicYN="N">Stroke Volume</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Bioelectrical impedance analysis</Keyword><Keyword MajorTopicYN="N">Cardiac magnetic resonance</Keyword><Keyword MajorTopicYN="N">Echocardiography</Keyword><Keyword MajorTopicYN="N">Right heart catheterization</Keyword><Keyword MajorTopicYN="N">Right heart function</Keyword><Keyword MajorTopicYN="N">Strain</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>9</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2023</Year><Month>6</Month><Day>26</Day><Hour>6</Hour><Minute>41</Minute></PubMedPubDate><PubMedPubDate 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Nowadays, the importance of evaluating right ventricular (RV) structure and function in left heart failure is well documented and this concept has been emphasized in the most recent heart failure guidelines. However, several relevant questions remain unanswered such as the following: (a) which imaging technique (standard or 3D echocardiography or strain imaging or cardiac magnetic resonance) and, more, which parameters should be used to grade the severity of RV dysfunction? (b) do less widespread and less applied diagnostic tools such as cardiopulmonary stress testing and bioelectrical impedance analysis play a role in this field? (c) are there specific biochemical aspects of RV failure? (d) why notion of pathophysiology of heart and lung interaction are so well appreciated at an academic level but are not applied in the clinical setting? The present review has been prepared by the Heart Failure (HF) working group of the Italian Society of Cardiology and its main objective is to improve our understanding on RV dysfunction in heart failure.<CopyrightInformation>© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ghio</LastName><ForeName>Stefano</ForeName><Initials>S</Initials><Identifier Source="ORCID">0000-0002-1858-1152</Identifier><AffiliationInfo><Affiliation>Divisione Di Cardiologia, IRCCS Fondazione Policlinico San Matteo, Viale Golgi 19, 27100, Pavia, Italy. s.ghio@smatteo.pv.it.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Acquaro</LastName><ForeName>Mauro</ForeName><Initials>M</Initials><Identifier Source="ORCID">0000-0002-5042-7999</Identifier><AffiliationInfo><Affiliation>Divisione Di Cardiologia, IRCCS Fondazione Policlinico San Matteo, Viale Golgi 19, 27100, Pavia, Italy.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cardiology, Department of Molecular Medicine, University of Pavia, Pavia, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Agostoni</LastName><ForeName>Piergiuseppe</ForeName><Initials>P</Initials><Identifier Source="ORCID">0000-0002-8345-6382</Identifier><AffiliationInfo><Affiliation>Centro Cardiologico Monzino, IRCCS, Milan, Italy.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Clinical Science and Community Health, University of Milan, Milan, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ambrosio</LastName><ForeName>Giuseppe</ForeName><Initials>G</Initials><Identifier Source="ORCID">0000-0002-9677-980X</Identifier><AffiliationInfo><Affiliation>Cardiology and Cardiovascular Pathophysiology, S.Maria Della Misericordia Hospital, University of Perugia, Perugia, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Carluccio</LastName><ForeName>Erberto</ForeName><Initials>E</Initials><Identifier Source="ORCID">0000-0002-9296-4397</Identifier><AffiliationInfo><Affiliation>Cardiology and Cardiovascular Pathophysiology, S.Maria Della Misericordia Hospital, University of Perugia, Perugia, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Castiglione</LastName><ForeName>Vincenzo</ForeName><Initials>V</Initials><Identifier Source="ORCID">0000-0002-9285-2328</Identifier><AffiliationInfo><Affiliation>Interdisciplinary Center for Health Sciences, Scuola Superiore Sant'Anna, Pisa, Italy.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Fondazione Toscana G. Monasterio, Pisa, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Colombo</LastName><ForeName>Davide</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Divisione Di Cardiologia, IRCCS Fondazione Policlinico San Matteo, Viale Golgi 19, 27100, Pavia, Italy.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cardiology, Department of Molecular Medicine, University of Pavia, Pavia, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>D'Alto</LastName><ForeName>Michele</ForeName><Initials>M</Initials><Identifier Source="ORCID">0000-0001-5729-1038</Identifier><AffiliationInfo><Affiliation>Department of Cardiology, University L. Vanvitelli - Monaldi Hospital, Naples, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Delle Grottaglie</LastName><ForeName>Santo</ForeName><Initials>S</Initials><Identifier Source="ORCID">0000-0001-7153-4040</Identifier><AffiliationInfo><Affiliation>Division of Cardiology, Ospedale Medico-Chirurgico Accreditato Villa dei Fiori, Acerra (Naples), Italy.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Zena and Michael A. Wiener Cardiovascular Institute/Marie-Josee and Henry R. Kravis Center for Cardiovascular Health, Mount Sinai School of Medicine, New York, NY, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dini</LastName><ForeName>Frank Lloyd</ForeName><Initials>FL</Initials><AffiliationInfo><Affiliation>Sant'Agostino Medical Center, Milan, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Emdin</LastName><ForeName>Michele</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Interdisciplinary Center for Health Sciences, Scuola Superiore Sant'Anna, Pisa, Italy.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Fondazione Toscana G. Monasterio, Pisa, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fortunato</LastName><ForeName>Martino</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Medical and Surgical Sciences, University of Foggia, Foggia, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Guaricci</LastName><ForeName>Andrea Igoren</ForeName><Initials>AI</Initials><Identifier Source="ORCID">0000-0001-7133-4401</Identifier><AffiliationInfo><Affiliation>Department of Emergency and Organ Transplantation, Institute of Cardiovascular Disease, University Hospital Policlinico of Bari, 70124, Bari, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jacoangeli</LastName><ForeName>Francesca</ForeName><Initials>F</Initials><Identifier Source="ORCID">0000-0003-3244-2164</Identifier><AffiliationInfo><Affiliation>Cardiology and Cardiovascular Pathophysiology, S.Maria Della Misericordia Hospital, University of Perugia, Perugia, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Marra</LastName><ForeName>Alberto M</ForeName><Initials>AM</Initials><AffiliationInfo><Affiliation>Department of Translational Medical Sciences, "Federico II" University Hospital and School of Medicine, Naples, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Paolillo</LastName><ForeName>Stefania</ForeName><Initials>S</Initials><Identifier Source="ORCID">0000-0003-4683-0993</Identifier><AffiliationInfo><Affiliation>Department of Advanced Biomedical Sciences, Federico II University of Naples, Naples, Italy.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Mediterranea Cardiocentro, Naples, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Papa</LastName><ForeName>Sivia</ForeName><Initials>S</Initials><Identifier Source="ORCID">0000-0001-8653-4035</Identifier><AffiliationInfo><Affiliation>Department of Clinical, Anesthesiological and Cardiovascular Sciences, I School of Medicine, Sapienza University of Rome, Policlinico Umberto I, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Scajola</LastName><ForeName>Luca Vicini</ForeName><Initials>LV</Initials><AffiliationInfo><Affiliation>Divisione Di Cardiologia, IRCCS Fondazione Policlinico San Matteo, Viale Golgi 19, 27100, Pavia, Italy.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cardiology, Department of Molecular Medicine, University of Pavia, Pavia, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Correale</LastName><ForeName>Michele</ForeName><Initials>M</Initials><Identifier Source="ORCID">0000-0002-7863-253X</Identifier><AffiliationInfo><Affiliation>Cardiology Unit, University Hospital Policlinico Riuniti, Foggia, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" 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It is important to differentiate from acquired diseases such as post-infarct pseudoaneurysm that need surgical treatment, and cardiac MRI offers an excellent diagnostic tool. |
2,329,354 | Solitary intraventricular tumors in dogs and cats treated with radiotherapy alone or combined with ventriculoperitoneal shunts: A retrospective descriptive case series. | Intraventricular tumors are rare, optimal treatment is not defined. Symptomatic patients often exhibit life-threatening hydrocephalus. With several months time-to-effect after radiotherapy (RT), increased intracranial pressure is concerning. This increase in pressure can be overcome by ventriculoperitoneal shunting (VPS).</AbstractText>Retrospective evaluation of outcome and complications in dogs and cats with intracranial tumors treated with either RT or VPS/RT.</AbstractText>Twelve client-owned cats and dogs.</AbstractText>Dogs and cats with symptomatic intraventricular tumors treated with definitive-intent RT or VPS/RT were included in a retrospective, descriptive case series. Complications, tumor volume evolution, time-to-progression, and survival time were determined.</AbstractText>Twelve animals were included: 1 cat and 5 dogs treated with single-modality RT and 4 cats and 2 dogs treated with VPS/RT. Neurological worsening seen in 4/6 animals during single-modality RT and 2/6 died during RT (suspected brain herniation). All dogs with VPS normalized clinically by the end of RT or earlier. Complications occurred in 4/6 animals, all but 1 were successfully managed surgically. Imaging follow-up in 8 animals surviving RT showed a marked decrease in tumor volume. Median survival time was 162 days (95% confidence interval [CI]: 16; infinity) for animals treated with RT and 1103 days (95%CI: 752; infinity) for animals treated with VPS/RT. Median time-to-progression was 71 days (95%CI: 7; infinity) and 895 days (95%CI: 704; infinity) for each group, respectively. Two dogs died because of intraventricular metastasis 427 and 461 days after single-modality RT.</AbstractText>Ventriculoperitoneal shunting led to rapid normalization of neurological signs and RT had a measurable effect on tumor volume. Combination of VPS/RT seems to be beneficial.</AbstractText>© 2022 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals LLC on behalf of American College of Veterinary Internal Medicine.</CopyrightInformation> |
2,329,355 | Management of pseudomeningocele following posterior fossa tumor surgery with absence of hydrocephalus: A case report.<Pagination><StartPage>107552</StartPage><MedlinePgn>107552</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">107552</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.ijscr.2022.107552</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S2210-2612(22)00798-2</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">The management of pseudomeningocele can be challenging and treatment options vary in the literature. There is currently no algorithm or standard protocol regarding the type and timing of treatment. Until now, there has been a little literature and no case report that used puncture techniques as a conservative treatment. We reported the effectiveness of fluid puncture and pressure dressing as an aggressive nonsurgical management of pseudomeningocele.</AbstractText><AbstractText Label="CASE PRESENTATION" NlmCategory="METHODS">A 5-year-old boy with posterior fossa tumor underwent midline suboccipital craniotomy tumor removal and decompression. A week after the surgery, the patient developed buldging in the operation region. Head CT scan showed pseudomeningocele in suboccipital region, a residual calcified tumor was seen, and no enlargement of ventricle. Conservative management was taken and the patient was managed with fluid puncture and pressure dressing. The reduction in size of the pseudomeningocele appeared within 14 days.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">Pseudomeningocele is a common complication of posterior fossa surgery. Nonsurgical treatment is the management of choice to reduce the symptoms. Fluid puncture and pressure dressing are effective in reducing symptoms. Surgical intervention is recommended when conservative treatment fails.</AbstractText><CopyrightInformation>Copyright © 2022 The Authors. Published by Elsevier Ltd.. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Dustur</LastName><ForeName>Shafhan</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Universitas Airlangga - Dr. Soetomo General Academic Hospital, Surabaya, East Java, Indonesia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Parenrengi</LastName><ForeName>M Arifin</ForeName><Initials>MA</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Universitas Airlangga - Dr. Soetomo General Academic Hospital, Surabaya, East Java, Indonesia. Electronic address: muhammad.arifin@fk.unair.ac.id.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Suryaningtyas</LastName><ForeName>Wihasto</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Universitas Airlangga - Dr. Soetomo General Academic Hospital, Surabaya, East Java, Indonesia.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>08</Month><Day>27</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Int J Surg Case Rep</MedlineTA><NlmUniqueID>101529872</NlmUniqueID><ISSNLinking>2210-2612</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Case report</Keyword><Keyword MajorTopicYN="N">Neoplasm</Keyword><Keyword MajorTopicYN="N">Posterior fossa tumor</Keyword><Keyword MajorTopicYN="N">Pressure dressing</Keyword><Keyword MajorTopicYN="N">Pseudomeningocele</Keyword><Keyword MajorTopicYN="N">Puncture</Keyword></KeywordList><CoiStatement>Declaration of competing interest No conflict of interest in this study.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>7</Month><Day>13</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>8</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>8</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>11</Month><Day>16</Day><Hour>1</Hour><Minute>9</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>11</Month><Day>17</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>11</Month><Day>17</Day><Hour>6</Hour><Minute>1</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36380537</ArticleId><ArticleId IdType="pmc">PMC9468414</ArticleId><ArticleId IdType="doi">10.1016/j.ijscr.2022.107552</ArticleId><ArticleId IdType="pii">S2210-2612(22)00798-2</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Norrdahl S.P., Jones T.L., Dave P., Hersh D.S., Vaughn B., Klimo P. 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Acta Neurochir. 2013;155:2281–2286. doi: 10.1007/s00701-013-1882-y.</Citation><ArticleIdList><ArticleId IdType="doi">10.1007/s00701-013-1882-y</ArticleId><ArticleId IdType="pubmed">24078114</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedBookArticle><BookDocument><PMID Version="1">30252377</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK526121</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-30597">Tricuspid Regurgitation<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Mulla</LastName><ForeName>Sana</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Asuka</LastName><ForeName>Edinen</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>All Saints University School of Medicine, Dominica.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bora</LastName><ForeName>Vaibhav</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>Augusta University</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>Tricuspid regurgitation is comparatively a common anomaly. Structural modifications of any or all of the tricuspid valve apparatus may cause the development of tricuspid regurgitation. <b>Anatomy</b> The right atrioventricular valve apparatus, or tricuspid valve, consists of the following components: 1. Three valve leaflets: It may have as few as two and as many as six leaflets. 2. Annulus. 3. Supporting chordae tendineae. 4. Papillary muscles: From 2 to 9. Just before the onset of the right ventricular systole, the papillary muscle contracts to increase tension in the chordae tendineae so that the 3 valve cusps coapt and thereby prevent regurgitation across the tricuspid valve. The conduction system and the supporting structure of the fibroelastic cardiac skeleton coordinate the actions of the tricuspid valve. The tricuspid valve is located between the right atrium and the right ventricle. It has a valve area of 4 to 6 cm2. The pathophysiological variants of the tricuspid valve include: 1. Ebstein anomaly. 2. Tricuspid atresia. 3. Congenital tricuspid stenosis. 4. Congenital cleft of the anterior leaflet.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-30597" sec="article-30597.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30597" sec="article-30597.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30597" sec="article-30597.s3">Etiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30597" sec="article-30597.s4">Epidemiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30597" sec="article-30597.s5">Pathophysiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30597" sec="article-30597.s6">History and Physical</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30597" sec="article-30597.s7">Evaluation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30597" sec="article-30597.s8">Treatment / Management</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30597" sec="article-30597.s9">Differential Diagnosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30597" sec="article-30597.s10">Prognosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30597" sec="article-30597.s11">Complications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30597" sec="article-30597.s12">Postoperative and Rehabilitation Care</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30597" sec="article-30597.s13">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30597" sec="article-30597.s14">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30597" sec="article-30597.s15">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>11</Month><Day>17</Day></ContributionDate><ReferenceList><Reference><Citation>Wafae N, Hayashi H, Gerola LR, Vieira MC. 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Structural modifications of any or all of the tricuspid valve apparatus may cause the development of tricuspid regurgitation. <b>Anatomy</b> The right atrioventricular valve apparatus, or tricuspid valve, consists of the following components: 1. Three valve leaflets: It may have as few as two and as many as six leaflets. 2. Annulus. 3. Supporting chordae tendineae. 4. Papillary muscles: From 2 to 9. Just before the onset of the right ventricular systole, the papillary muscle contracts to increase tension in the chordae tendineae so that the 3 valve cusps coapt and thereby prevent regurgitation across the tricuspid valve. The conduction system and the supporting structure of the fibroelastic cardiac skeleton coordinate the actions of the tricuspid valve. The tricuspid valve is located between the right atrium and the right ventricle. It has a valve area of 4 to 6 cm2. The pathophysiological variants of the tricuspid valve include: 1. Ebstein anomaly. 2. Tricuspid atresia. 3. Congenital tricuspid stenosis. 4. Congenital cleft of the anterior leaflet.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-30597" sec="article-30597.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30597" sec="article-30597.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30597" sec="article-30597.s3">Etiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30597" sec="article-30597.s4">Epidemiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30597" sec="article-30597.s5">Pathophysiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30597" sec="article-30597.s6">History and Physical</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30597" sec="article-30597.s7">Evaluation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30597" sec="article-30597.s8">Treatment / Management</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30597" sec="article-30597.s9">Differential Diagnosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30597" sec="article-30597.s10">Prognosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30597" sec="article-30597.s11">Complications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30597" sec="article-30597.s12">Postoperative and Rehabilitation Care</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30597" sec="article-30597.s13">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30597" sec="article-30597.s14">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-30597" sec="article-30597.s15">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>11</Month><Day>17</Day></ContributionDate><ReferenceList><Reference><Citation>Wafae N, Hayashi H, Gerola LR, Vieira MC. Anatomical study of the human tricuspid valve. Surg Radiol Anat. 1990;12(1):37-41.</Citation><ArticleIdList><ArticleId IdType="pubmed">2345895</ArticleId></ArticleIdList></Reference><Reference><Citation>Aktas EO, Govsa F, Kocak A, Boydak B, Yavuz IC. Variations in the papillary muscles of normal tricuspid valve and their clinical relevance in medicolegal autopsies. Saudi Med J. 2004 Sep;25(9):1176-85.</Citation><ArticleIdList><ArticleId IdType="pubmed">15448762</ArticleId></ArticleIdList></Reference><Reference><Citation>Xanthos T, Dalivigkas I, Ekmektzoglou KA. Anatomic variations of the cardiac valves and papillary muscles of the right heart. Ital J Anat Embryol. 2011;116(2):111-26.</Citation><ArticleIdList><ArticleId IdType="pubmed">22303639</ArticleId></ArticleIdList></Reference><Reference><Citation>Rogers JH, Bolling SF. The tricuspid valve: current perspective and evolving management of tricuspid regurgitation. Circulation. 2009 May 26;119(20):2718-25.</Citation><ArticleIdList><ArticleId IdType="pubmed">19470900</ArticleId></ArticleIdList></Reference><Reference><Citation>Nath J, Foster E, Heidenreich PA. Impact of tricuspid regurgitation on long-term survival. J Am Coll Cardiol. 2004 Feb 04;43(3):405-9.</Citation><ArticleIdList><ArticleId IdType="pubmed">15013122</ArticleId></ArticleIdList></Reference><Reference><Citation>Mutlak D, Lessick J, Reisner SA, Aronson D, Dabbah S, Agmon Y. Echocardiography-based spectrum of severe tricuspid regurgitation: the frequency of apparently idiopathic tricuspid regurgitation. J Am Soc Echocardiogr. 2007 Apr;20(4):405-8.</Citation><ArticleIdList><ArticleId IdType="pubmed">17400120</ArticleId></ArticleIdList></Reference><Reference><Citation>Tornos Mas P, Rodríguez-Palomares JF, Antunes MJ. Secondary tricuspid valve regurgitation: a forgotten entity. Heart. 2015 Nov;101(22):1840-8.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC4680164</ArticleId><ArticleId IdType="pubmed">26503944</ArticleId></ArticleIdList></Reference><Reference><Citation>Sagie A, Schwammenthal E, Padial LR, Vazquez de Prada JA, Weyman AE, Levine RA. Determinants of functional tricuspid regurgitation in incomplete tricuspid valve closure: Doppler color flow study of 109 patients. J Am Coll Cardiol. 1994 Aug;24(2):446-53.</Citation><ArticleIdList><ArticleId IdType="pubmed">8034882</ArticleId></ArticleIdList></Reference><Reference><Citation>Navia JL, Elgharably H, Javadikasgari H, Ibrahim A, Koprivanac M, Lowry AM, Blackstone EH, Klein AL, Gillinov AM, Roselli EE, Svensson LG. Tricuspid Regurgitation Associated With Ischemic Mitral Regurgitation: Characterization, Evolution After Mitral Surgery, and Value of Tricuspid Repair. Ann Thorac Surg. 2017 Aug;104(2):501-509.</Citation><ArticleIdList><ArticleId IdType="pubmed">28223050</ArticleId></ArticleIdList></Reference><Reference><Citation>Simula DV, Edwards WD, Tazelaar HD, Connolly HM, Schaff HV. Surgical pathology of carcinoid heart disease: a study of 139 valves from 75 patients spanning 20 years. Mayo Clin Proc. 2002 Feb;77(2):139-47.</Citation><ArticleIdList><ArticleId IdType="pubmed">11838647</ArticleId></ArticleIdList></Reference><Reference><Citation>Waller BF, Howard J, Fess S. Pathology of tricuspid valve stenosis and pure tricuspid regurgitation--Part III. Clin Cardiol. 1995 Apr;18(4):225-30.</Citation><ArticleIdList><ArticleId IdType="pubmed">7788951</ArticleId></ArticleIdList></Reference><Reference><Citation>Pritchett AM, Morrison JF, Edwards WD, Schaff HV, Connolly HM, Espinosa RE. Valvular heart disease in patients taking pergolide. Mayo Clin Proc. 2002 Dec;77(12):1280-6.</Citation><ArticleIdList><ArticleId IdType="pubmed">12479512</ArticleId></ArticleIdList></Reference><Reference><Citation>Baseman DG, O'Suilleabhain PE, Reimold SC, Laskar SR, Baseman JG, Dewey RB. Pergolide use in Parkinson disease is associated with cardiac valve regurgitation. Neurology. 2004 Jul 27;63(2):301-4.</Citation><ArticleIdList><ArticleId IdType="pubmed">15277624</ArticleId></ArticleIdList></Reference><Reference><Citation>Frater R. Tricuspid insufficiency. J Thorac Cardiovasc Surg. 2001 Sep;122(3):427-9.</Citation><ArticleIdList><ArticleId IdType="pubmed">11547290</ArticleId></ArticleIdList></Reference><Reference><Citation>Topilsky Y, Tribouilloy C, Michelena HI, Pislaru S, Mahoney DW, Enriquez-Sarano M. Pathophysiology of tricuspid regurgitation: quantitative Doppler echocardiographic assessment of respiratory dependence. Circulation. 2010 Oct 12;122(15):1505-13.</Citation><ArticleIdList><ArticleId IdType="pubmed">20876436</ArticleId></ArticleIdList></Reference><Reference><Citation>Ha JW, Chung N, Jang Y, Rim SJ. Tricuspid stenosis and regurgitation: Doppler and color flow echocardiography and cardiac catheterization findings. Clin Cardiol. 2000 Jan;23(1):51-2.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6655003</ArticleId><ArticleId IdType="pubmed">10680030</ArticleId></ArticleIdList></Reference><Reference><Citation>Shah PM, Raney AA. Tricuspid valve disease. 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The objective of the study was to evaluate targeted neonatal echocardiography (TnECHO) characteristics and the clinical course of preterm infants ≤2 kg undergoing percutaneous PDA closure.<AbstractText Label="METHODS" NlmCategory="METHODS">Retrospective cohort study of prospectively acquired pre- and post-closure TnECHOs to assess hemodynamic changes. Cardiorespiratory parameters in the first 24 h following PDA closure were also evaluated.<AbstractText Label="RESULTS" NlmCategory="RESULTS">Fifty patients were included with a mean age of 30.6 ± 9.6 days and weight of 1188 ± 280 g. LV global longitudinal strain decreased from -20.6 ± 2.6 to -14.9 ± 2.9% (p < 0.001) after 1 h. There was a decrease in LV volume loading, left ventricular output, LV systolic and diastolic parameters. Cardiorespiratory instability occurred in 24 (48%) [oxygenation failure in 44%] but systolic hypotension and/or need for cardiovascular medications was only seen in 6 (12%). Patients with instability had worse baseline respiratory severity score and lower post-closure early diastolic strain rates.<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Percutaneous PDA closure leads to a reduction in echocardiography markers of LV systolic/diastolic function. Post-closure cardiorespiratory instability is characterized primarily by oxygenation failure and may relate to impaired diastolic performance.<AbstractText Label="IMPACT" NlmCategory="CONCLUSIONS">Percutaneous patent ductus arteriosus closure leads to a reduction in echocardiography markers of left ventricular volume loading, cardiac output, and left ventricular systolic/diastolic function. Post-procedural cardiorespiratory instability is characterized primarily by oxygenation failure. Post-procedural cardiorespiratory instability may relate to impaired diastolic performance. |
2,329,356 | InsP<sub>3</sub>R-RyR Ca<sup>2+</sup> channel crosstalk facilitates arrhythmias in the failing human ventricle.<Pagination><StartPage>60</StartPage><MedlinePgn>60</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s00395-022-00967-y</ELocationID><Abstract><AbstractText>Dysregulated intracellular Ca<sup>2+</sup> handling involving altered Ca<sup>2+</sup> release from intracellular stores via RyR channels underlies both arrhythmias and reduced function in heart failure (HF). Mechanisms linking RyR dysregulation and disease are not fully established. Studies in animals support a role for InsP<sub>3</sub> receptor Ca<sup>2+</sup> channels (InsP<sub>3</sub>R) in pathological alterations in cardiomyocyte Ca<sup>2+</sup> handling but whether these findings translate to the divergent physiology of human cardiomyocytes during heart failure is not determined. Using electrophysiological and Ca<sup>2+</sup> recordings in human ventricular cardiomyocytes, we uncovered that Ca<sup>2+</sup> release via InsP<sub>3</sub>Rs facilitated Ca<sup>2+</sup> release from RyR and induced arrhythmogenic delayed after depolarisations and action potentials. InsP<sub>3</sub>R-RyR crosstalk was particularly increased in HF at RyR clusters isolated from the T-tubular network. Reduced SERCA activity in HF further facilitated the action of InsP<sub>3</sub>. Nanoscale imaging revealed co-localisation of InsP<sub>3</sub>Rs with RyRs in the dyad, which was increased in HF, providing a mechanism for augmented Ca<sup>2+</sup> channel crosstalk. Notably, arrhythmogenic activity dependent on InsP<sub>3</sub>Rs was increased in tissue wedges from failing hearts perfused with AngII to promote InsP<sub>3</sub> generation. These data indicate a central role for InsP<sub>3</sub>R-RyR Ca<sup>2+</sup> signalling crosstalk in the pro-arrhythmic action of GPCR agonists elevated in HF and the potential for their therapeutic targeting.</AbstractText><CopyrightInformation>© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Jin</LastName><ForeName>Xin</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Sciences, Laboratory of Experimental Cardiology, KU Leuven, 3000, Leuven, Belgium.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Internal Medicine, Carver College of Medicine, University of Iowa, Iowa City, IA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Amoni</LastName><ForeName>Matthew</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Sciences, Laboratory of Experimental Cardiology, KU Leuven, 3000, Leuven, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Gilbert</LastName><ForeName>Guillaume</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Sciences, Laboratory of Experimental Cardiology, KU Leuven, 3000, Leuven, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dries</LastName><ForeName>Eef</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Sciences, Laboratory of Experimental Cardiology, KU Leuven, 3000, Leuven, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Doñate Puertas</LastName><ForeName>Rosa</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Sciences, Laboratory of Experimental Cardiology, KU Leuven, 3000, Leuven, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tomar</LastName><ForeName>Ashutosh</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Sciences, Laboratory of Experimental Cardiology, KU Leuven, 3000, Leuven, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nagaraju</LastName><ForeName>Chandan K</ForeName><Initials>CK</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Sciences, Laboratory of Experimental Cardiology, KU Leuven, 3000, Leuven, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pradhan</LastName><ForeName>Ankit</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Sciences, Laboratory of Experimental Cardiology, KU Leuven, 3000, Leuven, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yule</LastName><ForeName>David I</ForeName><Initials>DI</Initials><AffiliationInfo><Affiliation>Department of Pharmacology and Physiology, Medical Center School of Medicine and Dentistry, University of Rochester, 601 Elmwood Avenue, Box 711, Rochester, NY, 14642, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Martens</LastName><ForeName>Tobie</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Laboratory for Enteric NeuroScience (LENS), Translational Research Center for Gastrointestinal Disorders (TARGID), KU Leuven, 3000, Leuven, Belgium.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cell and Tissue Imaging Cluster (CIC), KU Leuven, 3000, Leuven, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Menten</LastName><ForeName>Roxane</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Sciences, Laboratory of Experimental Cardiology, KU Leuven, 3000, Leuven, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Vanden Berghe</LastName><ForeName>Pieter</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Laboratory for Enteric NeuroScience (LENS), Translational Research Center for Gastrointestinal Disorders (TARGID), KU Leuven, 3000, Leuven, Belgium.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cell and Tissue Imaging Cluster (CIC), KU Leuven, 3000, Leuven, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rega</LastName><ForeName>Filip</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Sciences, Laboratory of Experimental Cardiology, KU Leuven, 3000, Leuven, Belgium.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Cardiology and Department of Cardiac Surgery, University Hospitals Leuven, Leuven, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sipido</LastName><ForeName>Karin</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Sciences, Laboratory of Experimental Cardiology, KU Leuven, 3000, Leuven, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Roderick</LastName><ForeName>H Llewelyn</ForeName><Initials>HL</Initials><Identifier Source="ORCID">0000-0001-7065-3523</Identifier><AffiliationInfo><Affiliation>Department of Cardiovascular Sciences, Laboratory of Experimental Cardiology, KU Leuven, 3000, Leuven, Belgium. Llewelyn.roderick@kuleuven.be.</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>11</Month><Day>15</Day></ArticleDate></Article><MedlineJournalInfo><Country>Germany</Country><MedlineTA>Basic Res Cardiol</MedlineTA><NlmUniqueID>0360342</NlmUniqueID><ISSNLinking>0300-8428</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019837">Ryanodine Receptor Calcium Release Channel</NameOfSubstance></Chemical><Chemical><RegistryNumber>SY7Q814VUP</RegistryNumber><NameOfSubstance UI="D002118">Calcium</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019837" MajorTopicYN="Y">Ryanodine Receptor Calcium Release Channel</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002118" MajorTopicYN="N">Calcium</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D032383" MajorTopicYN="N">Myocytes, Cardiac</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001145" MajorTopicYN="N">Arrhythmias, Cardiac</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006333" MajorTopicYN="Y">Heart Failure</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020013" MajorTopicYN="N">Calcium Signaling</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Arrhythmia</Keyword><Keyword MajorTopicYN="N">Cardiomyocyte</Keyword><Keyword MajorTopicYN="N">Excitation contraction coupling</Keyword><Keyword MajorTopicYN="N">Heart failure</Keyword><Keyword MajorTopicYN="N">InsP3 signalling</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>6</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>10</Month><Day>31</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>10</Month><Day>13</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>11</Month><Day>15</Day><Hour>11</Hour><Minute>36</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>11</Month><Day>16</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>11</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36378362</ArticleId><ArticleId IdType="doi">10.1007/s00395-022-00967-y</ArticleId><ArticleId IdType="pii">10.1007/s00395-022-00967-y</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Amoni M, Dries E, Ingelaere S, Vermoortele D, Roderick HL, Claus P, Willems R, Sipido KR (2021) Ventricular arrhythmias in ischemic cardiomyopathy-new avenues for mechanism-guided treatment. 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J Physiol 588:4743–4757. https://doi.org/10.1113/jphysiol.2010.197913</Citation><ArticleIdList><ArticleId IdType="doi">10.1113/jphysiol.2010.197913</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36378279</PMID><DateRevised><Year>2023</Year><Month>05</Month><Day>04</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1432-1971</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Nov</Month><Day>15</Day></PubDate></JournalIssue><Title>Pediatric cardiology</Title><ISOAbbreviation>Pediatr Cardiol</ISOAbbreviation></Journal>Development and Initial Validation of a Frailty Score for Pediatric Patients with Congenital and Acquired Heart Disease. | Dysregulated intracellular Ca<sup>2+</sup> handling involving altered Ca<sup>2+</sup> release from intracellular stores via RyR channels underlies both arrhythmias and reduced function in heart failure (HF). Mechanisms linking RyR dysregulation and disease are not fully established. Studies in animals support a role for InsP<sub>3</sub> receptor Ca<sup>2+</sup> channels (InsP<sub>3</sub>R) in pathological alterations in cardiomyocyte Ca<sup>2+</sup> handling but whether these findings translate to the divergent physiology of human cardiomyocytes during heart failure is not determined. Using electrophysiological and Ca<sup>2+</sup> recordings in human ventricular cardiomyocytes, we uncovered that Ca<sup>2+</sup> release via InsP<sub>3</sub>Rs facilitated Ca<sup>2+</sup> release from RyR and induced arrhythmogenic delayed after depolarisations and action potentials. InsP<sub>3</sub>R-RyR crosstalk was particularly increased in HF at RyR clusters isolated from the T-tubular network. Reduced SERCA activity in HF further facilitated the action of InsP<sub>3</sub>. Nanoscale imaging revealed co-localisation of InsP<sub>3</sub>Rs with RyRs in the dyad, which was increased in HF, providing a mechanism for augmented Ca<sup>2+</sup> channel crosstalk. Notably, arrhythmogenic activity dependent on InsP<sub>3</sub>Rs was increased in tissue wedges from failing hearts perfused with AngII to promote InsP<sub>3</sub> generation. These data indicate a central role for InsP<sub>3</sub>R-RyR Ca<sup>2+</sup> signalling crosstalk in the pro-arrhythmic action of GPCR agonists elevated in HF and the potential for their therapeutic targeting.<CopyrightInformation>© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Jin</LastName><ForeName>Xin</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Sciences, Laboratory of Experimental Cardiology, KU Leuven, 3000, Leuven, Belgium.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Internal Medicine, Carver College of Medicine, University of Iowa, Iowa City, IA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Amoni</LastName><ForeName>Matthew</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Sciences, Laboratory of Experimental Cardiology, KU Leuven, 3000, Leuven, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Gilbert</LastName><ForeName>Guillaume</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Sciences, Laboratory of Experimental Cardiology, KU Leuven, 3000, Leuven, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dries</LastName><ForeName>Eef</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Sciences, Laboratory of Experimental Cardiology, KU Leuven, 3000, Leuven, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Doñate Puertas</LastName><ForeName>Rosa</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Sciences, Laboratory of Experimental Cardiology, KU Leuven, 3000, Leuven, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tomar</LastName><ForeName>Ashutosh</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Sciences, Laboratory of Experimental Cardiology, KU Leuven, 3000, Leuven, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nagaraju</LastName><ForeName>Chandan K</ForeName><Initials>CK</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Sciences, Laboratory of Experimental Cardiology, KU Leuven, 3000, Leuven, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pradhan</LastName><ForeName>Ankit</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Sciences, Laboratory of Experimental Cardiology, KU Leuven, 3000, Leuven, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yule</LastName><ForeName>David I</ForeName><Initials>DI</Initials><AffiliationInfo><Affiliation>Department of Pharmacology and Physiology, Medical Center School of Medicine and Dentistry, University of Rochester, 601 Elmwood Avenue, Box 711, Rochester, NY, 14642, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Martens</LastName><ForeName>Tobie</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Laboratory for Enteric NeuroScience (LENS), Translational Research Center for Gastrointestinal Disorders (TARGID), KU Leuven, 3000, Leuven, Belgium.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cell and Tissue Imaging Cluster (CIC), KU Leuven, 3000, Leuven, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Menten</LastName><ForeName>Roxane</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Sciences, Laboratory of Experimental Cardiology, KU Leuven, 3000, Leuven, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Vanden Berghe</LastName><ForeName>Pieter</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Laboratory for Enteric NeuroScience (LENS), Translational Research Center for Gastrointestinal Disorders (TARGID), KU Leuven, 3000, Leuven, Belgium.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cell and Tissue Imaging Cluster (CIC), KU Leuven, 3000, Leuven, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rega</LastName><ForeName>Filip</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Sciences, Laboratory of Experimental Cardiology, KU Leuven, 3000, Leuven, Belgium.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Cardiology and Department of Cardiac Surgery, University Hospitals Leuven, Leuven, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sipido</LastName><ForeName>Karin</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Sciences, Laboratory of Experimental Cardiology, KU Leuven, 3000, Leuven, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Roderick</LastName><ForeName>H Llewelyn</ForeName><Initials>HL</Initials><Identifier Source="ORCID">0000-0001-7065-3523</Identifier><AffiliationInfo><Affiliation>Department of Cardiovascular Sciences, Laboratory of Experimental Cardiology, KU Leuven, 3000, Leuven, Belgium. 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J Physiol 588:4743–4757. https://doi.org/10.1113/jphysiol.2010.197913</Citation><ArticleIdList><ArticleId IdType="doi">10.1113/jphysiol.2010.197913</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36378279</PMID><DateRevised><Year>2023</Year><Month>05</Month><Day>04</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1432-1971</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Nov</Month><Day>15</Day></PubDate></JournalIssue><Title>Pediatric cardiology</Title><ISOAbbreviation>Pediatr Cardiol</ISOAbbreviation></Journal><ArticleTitle>Development and Initial Validation of a Frailty Score for Pediatric Patients with Congenital and Acquired Heart Disease.</ArticleTitle><ELocationID EIdType="doi" ValidYN="Y">10.1007/s00246-022-03045-1</ELocationID><Abstract>Frailty is a multi-dimensional clinical syndrome that is associated with increased morbidity and mortality and decreased quality of life. Children/adolescents with heart disease (HD) perform significantly worse for each frailty domain compared to non-HD peers. Our study aimed to create a composite frailty score (CFS) that can be applied to children/adolescents with HD and evaluate associations between the CFS and outcomes. Children and adolescents (n = 30) with HD (73% single ventricle, 20% heart failure, 7% pulmonary hypertension) were recruited from 2016 to 2017 (baseline). Five frailty domains were assessed at baseline using measures validated for pediatrics: (1) Slowness: 6-min walk test; (2) Weakness: handgrip strength; (3) Fatigue: PedsQL Multi-dimensional Fatigue Scale; (4) Body composition: triceps skinfold thickness; and (5) Physical activity questionnaire. Frailty points per domain (range = 0-5) were assigned based on z-scores or raw questionnaire scores and summed to produce a CFS (0 = least frail; 25 = most frail). Nonparametric bootstrapping was used to identify correlations between CFS and cross-sectional change in outcomes over 2.2 ± 0.2 years. The mean CFS was 12.5 ± 3.5. In cross-sectional analyses of baseline data, correlations (|r|≥ 0.30) were observed between CFS and NYHA class, the number of ancillary specialists, total prescribed medications, heart failure medications/day, exercise test derived chronotropic index and percent predicted VO<sub>2peak</sub>, and between child and parent proxy PEDsQL. At follow-up, CFS was correlated with an increase in the number of heart failure medications (r = 0.31). CFS was associated with cross-sectional outcomes in youth with heart disease. Longitudinal analyses were limited by small sample sizes due to loss to follow-up. |
2,329,357 | Analysis of a cell niche with proliferative potential at the roof of the aqueduct of Sylvius. | The aqueduct of Sylvius connects the third with the fourth ventricle and is surrounded by the Periaqueductal Grey. Here, we report a novel niche of cells in the dorsal section of the aqueduct, hereby named dorsal aqueduct niche or DAN, by applying a battery of selective markers and transgenic mouse lines. The somata of DAN cells are located toward the lumen of the ventricle forming multiple layers in close association with the cerebrospinal fluid (CSF). A single process emerges from the soma and run with the blood vessels. Cells of the DAN express radial glia/stem cell markers such as GFAP, vimentin and nestin, and the glutamate transporter GLAST or the oligodendrocyte precursor/pericyte marker NG2, thereby suggesting their potential for the generation of new cells. Morphologically, DAN cells resemble tanycytes of the third ventricle, which transfer biochemical signals from the CSF to the central nervous system and display proliferative capacity. The aqueduct ependymal lining can proliferate as observed by the integration of BrdU and expression of Ki67. Thus, the dorsal section of the aqueduct of Sylvius possesses cells that may act a niche of new glial cells in the adult mouse brain. |
2,329,358 | Mitral Valve Re-Repair Due to Chordal Pseudo-Elongation Through Repeated Right Anterior Minithoracotomy.<Pagination><StartPage>548</StartPage><EndPage>552</EndPage><MedlinePgn>548-552</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1177/15569845221130038</ELocationID><Abstract><AbstractText Label="OBJECTIVE" NlmCategory="UNASSIGNED">We aim to show the step-by-step surgical technique of mitral valve re-repair by means of a repeated right anterior minithoracotomy in a case of a procedure-related early mitral valve repair failure due to left ventricular positive remodeling and chordal pseudo-elongation.</AbstractText><AbstractText Label="METHODS" NlmCategory="UNASSIGNED">The patient was readdressed to our institution for an early severe mitral valve regurgitation, less than a year after performing a right minithoracotomy mitral valve repair (42-mm annular ring implantation, P2 triangular resection, and P2 neochord positioning). The mechanism was attributed to a positive left ventricle remodeling and neochordal pseudo-elongation. Therefore, we decided to perform a mitral valve re-repair in a redo minimally invasive cardiac surgery. We describe in a video-guided step-by-step fashion the surgical procedure, from the reopening of the right anterior minithoracotomy to the surgical strategy chosen to address the re-repair, guided by the mechanism of the previous repair failure.</AbstractText><AbstractText Label="RESULTS" NlmCategory="UNASSIGNED">We replaced the previously implanted ring with a smaller one and positioned a new polytetrafluoroethylene 4-0 neochord at the P2 level. The patient was discharged home on the fifth postoperative day after an uneventful hospital stay. Predischarge echocardiogram demonstrated undetectable residual mitral valve regurgitation. At 3-month follow-up, echocardiographic and clinical data were encouraging. At 9-month follow-up, the patient endorsed no recurrence of cardiologic symptoms.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="UNASSIGNED">Redo minimally invasive cardiac surgery is a viable option even in case of a mitral valve re-repair due to previous repair failure, especially when procedure related in degenerative mitral disease. Combining the benefits of mitral valve re-repair with those of a minimally invasive surgery may optimize short-term and long-term outcomes.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Celmeta</LastName><ForeName>Bleri</ForeName><Initials>B</Initials><Identifier Source="ORCID">0000-0002-5586-619X</Identifier><AffiliationInfo><Affiliation>Minimally Invasive Cardiac Surgery Department, Galeazzi - Sant'Ambrogio Hospital, Gruppo Ospedaliero San Donato, Milan, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Miceli</LastName><ForeName>Antonio</ForeName><Initials>A</Initials><Identifier Source="ORCID">0000-0002-5666-5402</Identifier><AffiliationInfo><Affiliation>Minimally Invasive Cardiac Surgery Department, Galeazzi - Sant'Ambrogio Hospital, Gruppo Ospedaliero San Donato, Milan, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ferrarini</LastName><ForeName>Matteo</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Minimally Invasive Cardiac Surgery Department, Galeazzi - Sant'Ambrogio Hospital, Gruppo Ospedaliero San Donato, Milan, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Glauber</LastName><ForeName>Mattia</ForeName><Initials>M</Initials><Identifier Source="ORCID">0000-0002-0443-8179</Identifier><AffiliationInfo><Affiliation>Minimally Invasive Cardiac Surgery Department, Galeazzi - Sant'Ambrogio Hospital, Gruppo Ospedaliero San Donato, Milan, Italy.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>11</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Innovations (Phila)</MedlineTA><NlmUniqueID>101257528</NlmUniqueID><ISSNLinking>1556-9845</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008944" MajorTopicYN="Y">Mitral Valve Insufficiency</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008943" MajorTopicYN="N">Mitral Valve</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006349" MajorTopicYN="Y">Heart Valve Diseases</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006348" MajorTopicYN="Y">Cardiac Surgical Procedures</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019060" MajorTopicYN="N">Minimally Invasive Surgical Procedures</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">minimally invasive</Keyword><Keyword MajorTopicYN="N">mitral valve repair</Keyword><Keyword MajorTopicYN="N">mitral valve repair failure</Keyword><Keyword MajorTopicYN="N">repeated mitral valve repair</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>11</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2023</Year><Month>1</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>11</Month><Day>14</Day><Hour>5</Hour><Minute>52</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36373647</ArticleId><ArticleId IdType="doi">10.1177/15569845221130038</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36373478</PMID><DateRevised><Year>2022</Year><Month>11</Month><Day>14</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1525-6006</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Nov</Month><Day>14</Day></PubDate></JournalIssue><Title>Clinical and experimental hypertension (New York, N.Y. : 1993)</Title><ISOAbbreviation>Clin Exp Hypertens</ISOAbbreviation></Journal>MicroRNA153 induces apoptosis by targeting NFATc3 to improve vascular remodeling in pulmonary hypertension. | We aim to show the step-by-step surgical technique of mitral valve re-repair by means of a repeated right anterior minithoracotomy in a case of a procedure-related early mitral valve repair failure due to left ventricular positive remodeling and chordal pseudo-elongation.</AbstractText>The patient was readdressed to our institution for an early severe mitral valve regurgitation, less than a year after performing a right minithoracotomy mitral valve repair (42-mm annular ring implantation, P2 triangular resection, and P2 neochord positioning). The mechanism was attributed to a positive left ventricle remodeling and neochordal pseudo-elongation. Therefore, we decided to perform a mitral valve re-repair in a redo minimally invasive cardiac surgery. We describe in a video-guided step-by-step fashion the surgical procedure, from the reopening of the right anterior minithoracotomy to the surgical strategy chosen to address the re-repair, guided by the mechanism of the previous repair failure.</AbstractText>We replaced the previously implanted ring with a smaller one and positioned a new polytetrafluoroethylene 4-0 neochord at the P2 level. The patient was discharged home on the fifth postoperative day after an uneventful hospital stay. Predischarge echocardiogram demonstrated undetectable residual mitral valve regurgitation. At 3-month follow-up, echocardiographic and clinical data were encouraging. At 9-month follow-up, the patient endorsed no recurrence of cardiologic symptoms.</AbstractText>Redo minimally invasive cardiac surgery is a viable option even in case of a mitral valve re-repair due to previous repair failure, especially when procedure related in degenerative mitral disease. Combining the benefits of mitral valve re-repair with those of a minimally invasive surgery may optimize short-term and long-term outcomes.</AbstractText> |
2,329,359 | Fetal cerebral ventriculomegaly: What do we tell the prospective parents? | Fetal cerebral ventriculomegaly is a relatively common finding, observed during approximately 1% of obstetric ultrasounds. In the second and third trimester, mild (≥10 mm) and severe ventriculomegaly (≥15 mm) are defined according to the measurement of distal lateral ventricles that is included in the routine sonographic examination of central nervous system. A detailed neurosonography and anatomy ultrasound should be performed to detect other associated anomalies in the central nervous system and in other systems, respectively. Fetal MRI might be useful when neurosonography is unavailable or suboptimal. The risk of chromosomal and non-chromosomal genetic disorders associated with ventriculomegaly is high, therefore invasive genetic testing, including microarray, is recommended. Screening for prenatal infections, in particular cytomegalovirus and toxoplasmosis, should also be carried out at diagnosis. The prognosis is determined by the severity of ventriculomegaly and/or by the presence of co-existing abnormalities. Fetal ventriculoamniotic shunting in progressive isolated severe ventriculomegaly is an experimental procedure. After delivery, ventricular-peritoneal shunting or ventriculostomy are the two available options to treat hydrocephalus in specific conditions with similar long-term outcomes. A multidisciplinary fetal neurology team, including perinatologists, geneticists, pediatric neurologists, neuroradiologists and neurosurgeons, can provide parents with the most thorough prenatal counseling. This review outlines the latest evidence on diagnosis and management of pregnancies complicated by fetal cerebral ventriculomegaly. |
2,329,360 | Disruption of the anterior commissure in Olig2 deficient mice. | In the present study, we examined neural circuit formation in the forebrain of the Olig2 knockout (Olig2-KO) mouse model and found disruption of the anterior commissure at the late foetal stage. Axon bundles of the anterior commissure encountered the wall of the third ventricle and ceased axonal extension. L1-CAM immunohistochemistry showed that Olig2-KO mice lose decussation formation in the basal forebrain. DiI tracing revealed that the thin bundles of the anterior commissure axons crossed the midline but ceased further extension into the deep part of the contralateral side. Furthermore, some fractions of DiI-labelled axons were oriented dorsolaterally, which was not observed in the control mouse forebrain. The rostral part of the third ventricle was much wider in the Olig2-KO mice than in wild-type mice, which likely resulted in the delay of midline fusion and subsequent delay and malformation of the anterior commissure. We analysed gene expression alterations in the Olig2-KO mice using a public database and found multiple genes, which are related to axon guidance and epithelial-mesenchymal transition, showing subtle expression changes. These results suggest that Olig2 is essential for anterior commissure formation, likely by regulating multiple biological processes. |
2,329,361 | Unusual Localization of <i>Hysterothylacium incurvum</i> in <i>Xiphias gladius</i> (Linnaeus 1758) Caught in the Atlantic Ocean. | This study represents the first report of <i>Hysterothylacium incurvum</i> within swordfish (<i>Xiphias gladius</i>) heart chambers. Swordfish is a large pelagic teleost, considered one of the most appreciated fish worldwide. Among swordfish parasites, <i>Anisakis</i> sp. and <i>Hysterothylacium</i> sp. have been used to evaluate biological and ecological aspects of this teleost. Between 2021 and 2022, 364 <i>X. gladius</i> hearts, caught from the Atlantic Ocean (FAO 27.IXa and FAO 34 areas), were collected at the Milan fish market (Lombardy, Italy). Three specimens from FAO 27.IXa was positive for seven adult nematodes (<i>p</i> = 1.55%) within the heart chambers. Of these, three specimens were found within the bulbus arteriosus and 4 in the ventricle. All parasites were stored in 70% ethanol and processed for parasitological and molecular analysis using <i>Cox2</i>, <i>ITS regions/ITS-I-5.8S-ITS-II,</i> and rrnS genes. The analysis allowed us to identify the retrieved parasite as <i>H. incurvum</i>. According to our evaluation, the final localization is due to the movement of L3 larvae from the coelomic cavity to the bloodstream, with consequent development to the adult stage within the heart. Finally, the parasite localization, considered non-marketable fish parts, does not pose a significant risk to consumers, also considering the low zoonotic potential of <i>H. incurvum</i>. |
2,329,362 | Improved Locomotor Recovery in a Rat Model of Spinal Cord Injury by BioLuminescent-OptoGenetic (BL-OG) Stimulation with an Enhanced Luminopsin. | Irrespective of the many strategies focused on dealing with spinal cord injury (SCI), there is still no way to restore motor function efficiently or an adequate regenerative therapy. One promising method that could potentially prove highly beneficial for rehabilitation in patients is to re-engage specific neuronal populations of the spinal cord following SCI. Targeted activation may maintain and strengthen existing neuronal connections and/or facilitate the reorganization and development of new connections. BioLuminescent-OptoGenetics (BL-OG) presents an avenue to non-invasively and specifically stimulate neurons; genetically targeted neurons express luminopsins (LMOs), light-emitting luciferases tethered to light-sensitive channelrhodopsins that are activated by adding the luciferase substrate coelenterazine (CTZ). This approach employs ion channels for current conduction while activating the channels through treatment with the small molecule CTZ, thus allowing non-invasive stimulation of all targeted neurons. We previously showed the efficacy of this approach for improving locomotor recovery following severe spinal cord contusion injury in rats expressing the excitatory luminopsin 3 (LMO3) under control of a pan-neuronal and motor-neuron-specific promoter with CTZ applied through a lateral ventricle cannula. The goal of the present study was to test a new generation of LMOs based on opsins with higher light sensitivity which will allow for peripheral delivery of the CTZ. In this construct, the slow-burn <i>Gaussia</i> luciferase variant (sbGLuc) is fused to the opsin CheRiff, creating LMO3.2. Taking advantage of the high light sensitivity of this opsin, we stimulated transduced lumbar neurons after thoracic SCI by intraperitoneal application of CTZ, allowing for a less invasive treatment. The efficacy of this non-invasive BioLuminescent-OptoGenetic approach was confirmed by improved locomotor function. This study demonstrates that peripheral delivery of the luciferin CTZ can be used to activate LMOs expressed in spinal cord neurons that employ an opsin with increased light sensitivity. |
2,329,363 | Multiple Machine Learning Approaches for Morphometric Parameters in Prediction of Hydrocephalus. | The diagnosis of hydrocephalus is mainly based on imaging findings. However, the significance of many imaging indicators may change, especially in some degenerative diseases, and even lead to misdiagnosis.</AbstractText>This study explored the effectiveness of commonly used morphological parameters and typical radiographic findings in hydrocephalus diagnosis. The patients' imaging data were divided into three groups, including the hydrocephalus group, the symptomatic group, and the normal control group. The diagnostic validity and weight of various parameters were compared between groups by multiple machine learning methods.</AbstractText>Our results demonstrated that Evans' ratio is the most valuable diagnostic indicator compared to the hydrocephalus group and the normal control group. But frontal horns' ratio is more useful in diagnosing patients with symptoms. Meanwhile, the sign of disproportionately enlarged subarachnoid space and third ventricle enlargement could be effective diagnostic indicators in all situations.</AbstractText>Both morphometric parameters and radiological features were essential in diagnosing hydrocephalus, but the weights are different in different situations. The machine learning approaches can be applied to optimize the diagnosis of other diseases and consistently update the clinical diagnostic criteria.</AbstractText> |
2,329,364 | The Ipsilateral Interhemispheric Transprecuneal Approach to the Atrium: Technical Considerations and Clinical Outcome on a Series of 7 Patients. | Surgical removal of tumors of the atrium is challenging due to their deep location, vascularization, and to their complex three-dimensional relationships with the highly functional white matter fibers of the region. To assess the feasibility and the effectiveness of the ipsilateral interhemispheric transprecuneus approach (IITA) for tumors involving the atrium and the posterior third of the temporal horn, a retrospective chart review of all patients who had undergone a surgical treatment for intraventricular tumors between January 2008 and January 2017 was performed, and the step-by-step approach is described. Ten patients affected by lesions of the atrium of the lateral ventricle underwent surgical treatment, seven of which were approached through the IITA. The mean age was 42.8 years (range 6-63 years). The symptoms presented included severe, drug-resistant headache (90%), lateral homonymous hemianopsia (50%), seizures (30%), and speech disturbances (30%). Histological examinations revealed seven patients with meningioma (70%), one with a metastasis (10%), one with a choroid plexus papilloma (10%) and one with a cavernoma (10%). In all cases, a gross total removal was obtained. All patients had a significant improvement in their headache. Two patients experienced a worsening of the pre-operative visual disturbances, while two patients had a significant improvement. No patients without pre-operative visual disturbances described a post-operative worsening of visual symptoms. The IITA represents a feasible approach for tumors of the atrium. The three-quarter prone position facilitates the enlargement of the interhemispheric fissure by increasing the working angle and facilitating the exposure of the lateral wall of the atrium. |
2,329,365 | Inhibiting von Hippel‒Lindau protein-mediated Dishevelled ubiquitination protects against experimental parkinsonism. | Dopaminergic neuron degeneration is a hallmark of Parkinson's disease (PD). We previously reported that the inactivation of von Hippel‒Lindau (VHL) alleviated dopaminergic neuron degeneration in a C. elegans model. In this study, we investigated the specific effects of VHL loss and the underlying mechanisms in mammalian PD models. For in vivo genetic inhibition of VHL, AAV-Vhl-shRNA was injected into mouse lateral ventricles. Thirty days later, the mice received MPTP for 5 days to induce PD. Behavioral experiments were conducted on D1, D3, D7, D14 and D21 after the last injection, and the mice were sacrificed on D22. We showed that knockdown of VHL in mice significantly alleviated PD-like syndromes detected in behavioral and biochemical assays. Inhibiting VHL exerted similar protective effects in MPP<sup>+</sup>-treated differentiated SH-SY5Y cells and the MPP<sup>+</sup>-induced C. elegans PD model. We further demonstrated that VHL loss-induced protection against experimental parkinsonism was independent of hypoxia-inducible factor and identified the Dishevelled-2 (DVL-2)/β-catenin axis as the target of VHL, which was evolutionarily conserved in both C. elegans and mammals. Inhibiting the function of VHL promoted the stability of β-catenin by reducing the ubiquitination and degradation of DVL-2. Thus, in vivo overexpression of DVL-2, mimicking VHL inactivation, protected against PD. We designed a competing peptide, Tat-DDF-2, to inhibit the interaction between VHL and DVL-2, which exhibited pharmacological potential for protection against PD in vitro and in vivo. We propose the therapeutic potential of targeting the interaction between VHL and DVL-2, which may represent a strategy to alleviate neurodegeneration associated with PD. |
2,329,366 | Application of AP-MALDI Imaging Mass Microscope for the Rapid Mapping of Imipramine, Chloroquine, and Their Metabolites in the Kidney and Brain of Wild-Type Mice. | Mass spectrometry imaging (MSI) is well-known for the non-labeling visualization of analytes, including drugs and their metabolites in biological samples. In this study, we applied three different tools of MSI, desorption electrospray ionization (DESI)-MSI, matrix-assisted laser desorption ionization (MALDI)-MSI, and a newly developed atmospheric pressure (AP)-MALDI-MSI known as iMScope<sup>TM</sup> QT for rapid mapping of imipramine, chloroquine, and their metabolites in C57BL/6 male wild-type mice. Among three MSI tools, better detection capability for targeted drugs at higher speed (up to 32 pixels/s) was observed in iMScope QT. It revealed that imipramine and its metabolites were significantly accumulated in the renal cortex of mice, but chloroquine and its metabolites were highly accumulated in the renal pelvis and renal medulla of mice. Additionally, a higher accumulation of imipramine was noted in the thalamus, hypothalamus, septum, and hindbrain of mice brains. However, chloroquine and its metabolites showed notable accumulation in the lateral ventricle, fourth ventricle, and fornix of the mice brains. These findings of our study can be helpful in understanding clinically relevant properties, efficacy, and potential side effects of these drugs. Our study also showed the potentiality of iMScope QT for rapid mapping of small drugs and their metabolites in biological samples. |
2,329,367 | Molecular and Functional Characterization of a Novel Kunitz-Type Toxin-like Peptide in the Giant Triton Snail <i>Charonia tritonis</i>. | It has been reported that the giant triton snail (<i>Charonia tritonis</i>) inserts its large proboscis and then injects venom or acid saliva from its salivary gland into its prey, the crown-of-thorns starfish <i>Acanthaster planci</i> (COTS), paralyzing it. A full-length cDNA sequence of the <i>C. tritonis</i> Ct-kunitzin gene was obtained by RACE PCR based on a transcriptomic database constructed by our laboratory (data not published), which contains an open reading frame (ORF) sequence with a length of 384 bp including a 1-32aa Kunitz domain. The Ct-kunitzin peptide was synthesized by solid-phase polypeptide methods according to its conserved amino acid sequence, with a molecular weight of 3746.0 as well as two disulfide bonds. Renatured Ct-kunitzin was injected into mice ventricles to evaluate its potential function. Compared with the normal control group (physiological saline), the spontaneous locomotor activity of the Ct-kunitzin group decreased significantly. There was a significant effect on Ct-kunitzin on mice grip strength in the grip strength test. In addition, Ct-kunitzin exhibited remarkable biological activity in suppressing pain in the pain thresholds test. There were no significant differences between the Ct-kunitzin group and the normal control group in terms of various hematological indexes and histopathological observations. When tested in COTS, the most significant histological change was the destruction, disorganization, and significant reduction in the amount of COTS tube feet tissues. Altogether, the potential paralyzing effect on mice suggests that Ct-kunitzin is a possible agent for novel drug development. |
2,329,368 | The Nematic Chiral Liquid Crystal Structure of the Cardiac Myoarchitecture: Disclinations and Topological Singularities. | This is our second article devoted to the cardiac myoarchitecture considered as a nematic chiral liquid crystal (NCLC). While the first article focused on the myoarchitecture of the left ventricle (LV), this new article extends to the whole ventricular mass and introduces the concept of disclinations and topological singularities, which characterize the differences and relationships between the left and right ventricles (RV). At the level of the ventricular apices, we constantly observed a vortex shape at the LV apex, corresponding, in the terminology of liquid crystals, to a "+1 disclination"; we never observed this at the RV apex. At the level of the interventricular septum (IVS), we identified "-1/2 disclinations" at the anterior and posterior parts. During the perinatal period, there was a significant difference in their distribution, with more "-1/2 disclinations" in the posterior part of the IVS. After birth, concomitant to major physiological changes, the number of "-1/2 disclinations" significantly decreased, both in the anterior and posterior parts of the IVS. Finally, the description of the disclinations must be considered in any attempt to segment the whole ventricular mass, in biomechanical studies, and, more generally, for the characterization of myocardial remodeling. |
2,329,369 | From Macro to Micro: Comparison of Imaging Techniques to Detect Vascular Network Formation in Left Ventricle Decellularized Extracellular Matrix Hydrogels. | <b>Background:</b> Angiogenesis is a crucial process in physiological maintenance and tissue regeneration. To understand the contribution of angiogenesis, it is essential to replicate this process in an environment that reproduces the biochemical and physical properties which are largely governed by the extracellular matrix (ECM). We investigated vascularization in cardiac left ventricular ECM hydrogels to mimic post-myocardial repair. We set out to assess and compare different destructive and non-destructive methods, optical as well as non-optical, to visualize angiogenesis and associated matrix remodeling in myocardial ECM hydrogels. <b>Methods:</b> A total of 100,000, 300,000, and 600,000 Human Pulmonary Microvascular Endothelial Cells (HPMEC) were seeded in left ventricular cardiac ECM hydrogel in 48-well plates. After 1, 7, and 14 days of culture, the HPMEC were imaged by inverted fluorescence microscopy and 3D confocal laser scanning microscopy (Zeiss Cell Discoverer 7). In addition, cell-seeded ECM hydrogels were scanned by optical coherence tomography (OCT). Fixed and paraffin-embedded gels were thin-sectioned and assessed for ECM components via H&E, picrosirius red histochemical staining, and immunostaining for collagen type I. ImageJ-based densitometry was used to quantify vascular-like networks and GraphPad was used for statistical analyses. <b>Results:</b> Qualitative analyses were realized through fluoromicrographs obtained by the confocal laser scanning microscope which allowed us to visualize the extensive vascular-like networks that readily appeared at all seeding densities. Quantification of networks was only possible using fluoromicrographs from inverted microscopy. These showed that, after three days, the number of master junctions was seeding density-dependent. The resolution of optical coherence tomography was too low to distinguish between signals caused by the ECM and cells or networks, yet it did show that gels, irrespective of cells, were heterogeneous. Interestingly, (immuno)histochemistry could clearly distinguish between the cast cardiac-derived matrix and newly deposited ECM in the hydrogels. The H&E staining corroborated the presence of vascular-like network structures, albeit that sectioning inevitably led to the loss of 3D structure. <b>Conclusions:</b> Except for OCT, all methods had complementary merit and generated qualitative and quantitative data that allowed us to understand vascular network formation in organ-derived ECM hydrogels. |
2,329,370 | Isolated Fetal Ventriculomegaly- Postnatal Outcomes and Proposed New Prognostication Classification. | Outcome of Isolated ventriculomegaly diagnosed antenatally depends on size of ventricles and associated malformations. There is scarcity of literature on the guidelines for prognostication based on outcomes as per the ventricle size.</AbstractText>The aim of this work was to study outcome of antenatally detected isolated ventriculomegaly in terms of medical termination, postnatal neuro-developmental milestones, and mortality; and also to propose a new prognostication classification.</AbstractText>Prospective and retrospective observational study on antenatal mothers with isolated ventriculomegaly diagnosed in fetus. Outcomes in terms of termination of pregnancy, postnatal mortality, need of surgery, and morbidity were recorded. Patients were categorized into four groups: Group 1--ventricle size <10 mm, II--11-15 mm, III--16-20 mm, and IV > 20 mm and neuro-developmental milestones were co-related. Association with chromosomal anomalies, congenital heart disease, and maternal infection were also analyzed.</AbstractText>521 antenatal females were referred with fetal anomalies with 163 having CNS malformations. Isolated ventriculomegaly was seen in only 44. Patients of groups 1 and 2 had 100% normal neuro-developmental milestones without any intervention. Group 3 patients had normal neurodevelopmental milestones in 60% only while shunt surgery was required in 40% of patients. All patients of group 4 had poor outcome with only 50% survival. No association with chromosomal anomalies and heart disease was found.</AbstractText>Prognosis of isolated ventriculomegaly depends upon size of ventricles and its progressive increase on serial ultrasounds. New proposed classification is simple and would be useful for the treating surgeons to explain the prognosis to parents so as to relieve them of anxiety.</AbstractText> |
2,329,371 | BAM! Pathogen control at the brain border. | Border-associated macrophages (BAMs) reside at the interface between the brain and the periphery, including the meninges and choroid plexus. In this issue of Immunity, two studies report the dynamics, diversity, and fate of murine BAMs during infection, assigning these cells a neuroprotective role. |
2,329,372 | Echoencephalography of Möbius sequence: A congenital cranial dysinnervation disorder with brainstem calcifications. | Möbius sequence (MBS) previously known as Möbius syndrome is a rare nonprogressive developmental defect of the rhombencephalon leading to congenital abducens (VIth) and facial (VIIth) nerve palsy. Echoencephalography is the first, safe, noninvasive, and cost-effective imaging modality available at bedside. No study on the use of echoencephalography in neonates for the diagnosis of MBS has been previously reported.</AbstractText>In this single tertiary center study, more than 18,000 neonates underwent echoencephalographic imaging over the span of two decades. Imaging was performed through the anterior, posterior, and lambdoid fontanelles. All neonates found to have calcifications of brainstem tegmental nuclei underwent additional imaging studies. Each neonate with MBS was carefully examined by the same investigator.</AbstractText>Five neonates were shown to have punctate, bilateral, symmetrical tegmental pontine calcifications through all three acoustic windows. These calcifications extended caudally in most patients, and rostrally in 2 patients. Brainstem hypoplasia was best seen through the posterior fontanelle. Three out of five infants were noted to have brainstem hypoplasia with straightening of the floor of the fourth ventricle. In two children, facial collicular bulges and hypoglossal eminences were present. All five infants fulfilled clinical diagnostic criteria of MBS. In addition, a wide array of cerebral defects is identified. Echoencephalographic findings were confirmed by other imaging modalities.</AbstractText>Knowledge of echoencephalographic features of MBS should improve its early recognition. A detailed description of the various imaging phenotypes of MBS is necessary to characterize the etiology of this heterogeneous congenital cranial dysinnervation disorder.</AbstractText>© 2022 American Society of Neuroimaging.</CopyrightInformation> |
2,329,373 | Lumboperitoneal Shunt Combined With Ommaya Reservoir Enables Continued Intraventricular Chemotherapy for Leptomeningeal Metastasis With Increased Intracranial Pressure. | Intra-cerebrospinal fluid (CSF) chemotherapy for leptomeningeal metastasis (LM) can be delivered intraventricularly via an Ommaya reservoir. However, hydrocephalus associated with LM can interfere with chemotherapeutic drug distribution, and ventriculoperitoneal shunts can prevent drug distribution to the extra-ventricular CSF space. This study examined the feasibility of combining a lumboperitoneal (LP) shunt with an Ommaya reservoir to both control intracranial pressure and allow for intraventricular chemotherapy.</AbstractText>We identified 16 patients with LM who received both an Ommaya reservoir and an LP shunt, either concurrently or sequentially, and subsequently received intraventricular chemotherapy. The feasibility of this combination for intraventricular chemotherapy was evaluated by assessing 1) the distribution of intraventricularly injected drugs in CSF samples collected 0, 6, and 12 h post-injection and 2) adverse events associated with the procedure and drug administration.</AbstractText>Patients received a median of seven rounds (range 1-37) of intraventricular chemotherapy during a median follow-up period of 5.2 months after LP shunt insertion. Pharmacokinetic data were obtained from six patients. Baseline methotrexate (MTX) levels from Ommaya reservoirs varied from 339.9 µM to 1,523.5 µM. CSF sampled from LP shunt reservoirs revealed an elimination half-life (t1/2</sub>) of 2.63 h, and the mean ratio of MTX concentration at 12 h to that at baseline was 0.05±0.05, ensuring drug distribution from the ventricle to the spinal canal. Nine patients (56%) underwent revision surgery due to catheter migration, malfunction, or infection. Among these patients, CSF infections attributable to intraventricular chemotherapy (n=3) occurred, but no infections occurred in later cases after we began to employ a complete aseptic technique.</AbstractText>LP shunt combined with Ommaya reservoir insertion is a feasible option for achieving both intracranial pressure control and the continuation of intraventricular chemotherapy in patients with LM.</AbstractText>Copyright © 2022 The Korean Brain Tumor Society, The Korean Society for Neuro-Oncology, and The Korean Society for Pediatric Neuro-Oncology.</CopyrightInformation> |
2,329,374 | Endoscopic transcortical expanded transforaminal transvenous transchoroidal approach to third ventricle lesion resection using an endoport. | To investigate the clinical experience and application value of endoscopic resection of lesions in and around the third ventricle using a transcortical expanded transforaminal transvenous transchoroidal approach with an endoport.</AbstractText>Clinical data and follow-up results of seven patients who underwent the removal of lesions in the third ventricle and its adjacent area with an endoport-guided endoscopic system from January 2018 to December 2020 in the Department of Neurosurgery, Zhongshan Hospital Affiliated to Fudan University, were analyzed retrospectively. Two other patients from the Affiliated Pediatric Hospital of Fudan University and the Affiliated Hospital of Guizhou Medical University, respectively, were included in the analysis.</AbstractText>A total of nine cases of third ventricle tumors were included in the study, including six women and three men, with an average age of 37.8 years (4-84 years old) and a follow-up time of 6-44 months. These nine tumor cases included two pilocytic astrocytomas, one diffuse midline glioma (H3 K27-altered), two craniopharyngiomas, two choroid plexus (CP) papillomas, one germinoma, and one pineal parenchymal tumor of intermediate differentiation. Total resection was completed in eight cases, with one near-total resection. There were no complications related to the surgical approach, such as epilepsy, aphasia, or hemiplegia.</AbstractText>The endoscope transcortical expanded transforaminal transvenous transchoroidal approach using an endoport can safely and effectively remove third ventricle lesions. This approach can reach a wide area, from the anterior to the posterior third ventricle.</AbstractText>Copyright © 2022. Published by Elsevier Ltd.</CopyrightInformation> |
2,329,375 | Foxl2a and Foxl2b are involved in midbrain-hindbrain boundary development in zebrafish. | Foxl2 plays conserved central function in ovarian differentiation and maintenance in several fish species. However, its expression pattern and function in fish embryogenesis are still largely unknown. In this study, we first presented a sequential expression pattern of zebrafish foxl2a and foxl2b during embryo development. They were predominantly expressed in the cranial paraxial mesoderm (CPM) and cranial venous vasculature (CVV) during somitogenesis and subsequently expressed in the pharyngeal arches after 48 h post-fertilization (hpf). Then, we compared the brain structures among zebrafish wildtype (WT) and three homozygous foxl2 mutants (foxl2a<sup>-/-</sup>, foxl2b<sup>-/-</sup> and foxl2a<sup>-/-</sup>;foxl2b<sup>-/-</sup>) and found the reduction of the fourth ventricle in the three foxl2 mutants, especially in foxl2a<sup>-/-</sup>;foxl2b<sup>-/-</sup> mutant. Finally, we detected several key transcription factors involved in the gene regulatory network of midbrain-hindbrain boundary (MHB) patterning, such as wnt1, en1b and pax2a. Their expression levels were obviously downregulated in MHB of foxl2a<sup>-/-</sup> and foxl2a<sup>-/-</sup>;foxl2b<sup>-/-</sup> mutants. Thus, we suggest that Foxl2a and Foxl2b are involved in MHB and the fourth ventricle development in zebrafish. The current study provides insights into the molecular mechanism underlying development of brain ventricular system. |
2,329,376 | Rethinking the cilia hypothesis of hydrocephalus. | Dysfunction of motile cilia in ependymal cells has been proposed to be a pathogenic cause of cerebrospinal fluid (CSF) overaccumulation leading to ventricular expansion in hydrocephalus, primarily based on observations of enlarged ventricles in mouse models of primary ciliary dyskinesia. Here, we review human and animal evidence that warrants a rethinking of the cilia hypothesis in hydrocephalus. First, we discuss neuroembryology and physiology data that do not support a role for ependymal cilia as the primary propeller of CSF movement across the ventricles in the human brain, particularly during in utero development prior to the functional maturation of ependymal cilia. Second, we highlight that in contrast to mouse models, motile ciliopathies infrequently cause hydrocephalus in humans. Instead, gene mutations affecting motile cilia function impact not only ependymal cilia but also motile cilia found in other organ systems outside of the brain, causing a clinical syndrome of recurrent respiratory infections and situs inversus, symptoms that do not typically accompany most cases of human hydrocephalus. Finally, we postulate that certain cases of hydrocephalus associated with ciliary gene mutations may arise not necessarily just from loss of cilia-generated CSF flow but also from altered neurodevelopment, given the potential functions of ciliary genes in signaling and neural stem cell fate beyond generating fluid flow. Further investigations are needed to clarify the link between motile cilia, CSF physiology, and brain development, the understanding of which has implications for the care of patients with hydrocephalus and other related neurodevelopmental disorders. |
2,329,377 | Detection of multidrug-resistant <i>Acinetobacter baumannii</i> by metagenomic next-generation sequencing in central nervous system infection after neurosurgery: A case report. | Central nervous system (CNS) infection is one of the most serious complications after neurosurgery. Traditional clinical methods are difficult to diagnose the pathogen of intracranial infection. Due to recent advances in genomic approaches, especially sequencing technologies, metagenomic next-generation sequencing (mNGS) has been applied in many research and clinical settings.</AbstractText>Here, we report a case of CNS infection with Acinetobacter baumannii</i> in a 15-year-old woman, who previously underwent surgery for recurrence of ependymoma in the fourth ventricle. On the eleventh postoperative day, the patient had a high fever and leukocytosis in the cerebrospinal fluid (CSF). mNGS using CSF rapidly and accurately identified the causative pathogen as A. baumannii</i> with carbapenem resistance genes blaOXA-23</i> and blaOXA-51</i>, which were confirmed by subsequent culture and susceptibility tests within 5 days. During the disease, mNGS, culture, and drug susceptibility testing were continued to monitor changes in pathogenic bacteria and adjust medication. At present, there are no case reports on to the use of mNGS for detecting pathogens in postoperative infection with ependymoma and guide medication.</AbstractText>mNGS has great advantages in pathogen identification and even pathogen resistance prediction. Multiple mNGS examinations during the course of the disease play an important role in the dynamic monitoring of pathogens.</AbstractText>Copyright © 2022 Tian, Xia, Zhang and Zhou.</CopyrightInformation> |
2,329,378 | Case report: Prenatal diagnosis of fetal intracranial hemorrhage due to compound mutations in the <i>JAM3</i> gene. | Intracranial hemorrhage is a common complication in preterm infants but occasionally occurs in fetuses. Disruptions of the genes, such as the <i>COL4A1</i> and <i>COL4A2</i> genes<i>,</i> are common genetic causes identified in fetal intracranial hemorrhage; however, the disruptions of the <i>JAM3</i> gene are rarely reported. In the current investigation, fetal intracranial hemorrhage and dilated lateral ventricles were observed in three consecutive siblings in a pedigree. The pregnancies were terminated, and whole-exome sequencing, followed by Sanger sequencing, was performed on the affected fetuses. Pre-implantation genetic testing for monogenic diseases was performed to avoid the recurrence. The compound heterozygous variants of c.712 + 2T > A and c.813C > G p.Tyr271* in the <i>JAM3</i> gene (NM_032801.4) were identified in the proband and its affected brother, which were predicted to be pathogenic. The variant of c.813C > G p.Tyr271* but not c.712 + 2T > A was identified in the fourth fetus, implying a good prognosis. Our findings expanded the spectrum of the pathogenic mutations in the <i>JAM3</i> gene and revealed an important application of fetal whole-exome sequencing in idiopathic fetal intracranial hemorrhage. |
2,329,379 | Acute Glycogen Synthase Kinase-3 Inhibition Modulates Human Cardiac Conduction. | Glycogen synthase kinase 3 (GSK-3) inhibition has emerged as a potential therapeutic target for several diseases, including cancer. However, the role for GSK-3 regulation of human cardiac electrophysiology remains ill-defined. We demonstrate that SB216763, a GSK-3 inhibitor, can acutely reduce conduction velocity in human cardiac slices. Combined computational modeling and experimental approaches provided mechanistic insight into GSK-3 inhibition-mediated changes, revealing that decreased sodium-channel conductance and tissue conductivity may underlie the observed phenotypes. Our study demonstrates that GSK-3 inhibition in human myocardium alters electrophysiology and may predispose to an arrhythmogenic substrate; therefore, monitoring for adverse arrhythmogenic events could be considered. |
2,329,380 | Novel insights into the origin and development of CNS macrophage subsets. | The central nervous system (CNS) hosts a variety of immune cells, including two distinct macrophage populations: microglia are found in the parenchyma, whereas CNS-associated macrophages (CAMs) cover the CNS interfaces, such as the perivascular spaces, the meninges and the choroid plexus. Recent studies have given novel insights into the nature of CAMs as compared to microglia. In this mini-review, we summarise the current knowledge about the ontogenetic relationship and the underlying mechanism for the establishment of CNS macrophages during development. |
2,329,381 | Conditioned medium from BV2 microglial cells having polyleucine specifically alters startle response in mice. | Repeat-associated non-AUG translation (RAN translation) is observed in transcripts that are causative for polyglutamine (polyQ) diseases and generates proteins with mono amino acid tracts such as polyalanine (polyA), polyleucine (polyL) and polyserine (polyS) in neurons, astrocytes and microglia. We have previously shown that microglia with aggregated polyQ led to defective differentiation and degeneration of neuron-like cells. However, it has not been determined whether only microglia containing a specific RAN product, but not other RAN products, is harmful in vitro and in vivo. Here we show that polyL-incorporating microglia specifically led to altered startle response in mice. Aggregated polyA, polyS and polyL induced aberrant differentiation of microglia-like BV2 cells. Differentiated PC12 cells treated with conditioned medium (CM) of polyS- and polyL- but not polyA-incorporating microglia-like BV2 cells showed retraction of neurites and loss of branch of neurites. Injection of the polyL-CM, but not polyA-CM and polyS-CM, into the lateral ventricle lowered startle response in mice. Consistently, polyL induced the highest expression of CD68 in BV2 cells. The lowered startle response was replicated in mice given the polyL-CM in the caudal pontine reticular nucleus (PnC), the key region of startle response. Thus, endogenous RAN proteins having polyL derived from polyQ diseases-causative genes in microglia might specifically impair startle response. |
2,329,382 | Postoperative opioid administration and post-traumatic stress symptoms in preschool children after cardiac surgery. | The purpose of this study was to explore relationships between postoperative opioid administration and posttraumatic stress symptoms (PTSS) in preschool-aged children surviving cardiac surgery.</AbstractText>This was a cross-sectional, descriptive study using survey administration and medical chart review. Primary caregivers of children aged three to six years who underwent cardiac surgery at our institution between 2018 and 2020 were invited to participate. Opioid administration was calculated according to morphine milligram equivalents and indexed to the child's body weight. Caregivers completed the Young Child Posttraumatic Stress Disorder Checklist to explore child PTSS. We used correlational methods to assess the strength and direction of relationships between postoperative opioid administration and child PTSS.</AbstractText>We did not find a statistically significant relationship between total postoperative opioid administration and child PTSS. When analyzing individual opioid agents, morphine did show a significant inverse relationship to YCPC scores (rs</sub> = -.57, p = .017) in children with single ventricle physiology.</AbstractText>Total postoperative opioid administration was not statistically significantly related to child PTSS in our sample. Differing patterns of association were noted among children with single- versus bi-ventricular physiology. Postoperative morphine administration was favorably associated with PTSS in children with single-ventricle physiology.</AbstractText>Nurses caring for preschool children who undergo cardiac surgery should anticipate the potential development of PTSS in their patients. Studies using larger sample sizes and longitudinal design are needed to replicate the significant relationship between morphine administration and PTSS in preschoolers with single-ventricle physiology.</AbstractText>Copyright © 2022. Published by Elsevier Inc.</CopyrightInformation> |
2,329,383 | Pre-operative external ventricle drainage improves neurological outcomes for patients with traumatic intracerebellar hematomas. | Traumatic intracerebellar hematoma (TICH) is a very rare entity with a high morbidity and mortality rate, and there is no consensus on its optimal surgical management. In particular, whether and when to place external ventricle drainage in TICH patients without acute hydrocephalus pre-operation is still controversial.</AbstractText>A single-institutional, retrospective analysis of total of 47 TICH patients with craniectomy hematoma evacuation in a tertiary medical center from January 2009 to October 2020 was performed. Primary outcomes were mortality in hospital and neurological function evaluated by GOS at discharge and 6 months after the ictus. Special attention was paid to the significance of external ventricular drainage (EVD) in TICH patients without acute hydrocephalus on admission.</AbstractText>Analysis of the clinical characteristics of the TICH patients revealed that the odds of use of EVD were seen in patients with IVH, fourth ventricle compression, and acute hydrocephalus. Placement of EVD at the bedside can significantly improve the GCS score before craniotomy, as well as the neurological score at discharge and 6 months. Compared with the only hematoma evacuation (HE) group, there is a trend that EVD can reduce hospital mortality and decrease the occurrence of delayed hydrocephalus, although the difference is not statistically significant. In addition, EVD can reduce the average NICU stay time, but has no effect on the total length of stay. Moreover, our data showed that EVD did not increase the risk of associated bleeding and intracranial infection. Interestingly, in terms of neurological function at discharge and 6 month after the ictus, even though without acute hydrocephalus on admission, the TICH patients can still benefit from EVD insertion.</AbstractText>For TICH patients, perioperative EVD is safe and can significantly improve neurological prognosis. Especially for patients whose GCS dropped by more than 2 points before the operation, EVD can significantly improve the patient's GCS score, reduce the risk of herniation, and gain more time for surgical preparation. Even for TICH patients without acute hydrocephalus on admission CT scan, EVD placement still has positive clinical significance.</AbstractText>Copyright © 2022 Wang, Gao, Zhang, Su, Shi, Wang, Ge, Zhu, Guo, Gao, Shi, Cui, Li, Qu and Wang.</CopyrightInformation> |
2,329,384 | Extracellular vesicles derived from the choroid plexus trigger the differentiation of neural stem cells. | The choroid plexus secrets cerebrospinal fluid (CSF) composed of electrolytes, cytokines, growth factors, metabolites and extracellular vesicles (EVs) that flow through the interconnected brain ventricles. On their course, CSF components can act as signals that affect, for example, neural stem cells (NSCs) residing in niches of the ventricular wall. We studied EV-born CSF signals in an in vitro culture system. We purified EVs from the secretome of a choroid plexus cell line (Z310 cells), and from primary choroid plexus cultures and co-cultured those EVs with NSCs isolated from the niche of the lateral and the third ventricle. EVs<sup>Z310</sup> and EVs<sup>CHP</sup> were purified by differential centrifugation. This yielded fractions of EVs of 50-150-nm diameter that induced a complex multicellular network formation and NSC differentiation. Both types of EV converted the round NSCs to cells that extended long processes that contacted nearby, alike-shaped cells. Mass spectrometry showed that the differentiation-inducing EV<sup>Z310</sup> were enriched for membrane and membrane-associated proteins involved in cell differentiation, membrane trafficking, and membrane organization. We hypothesize that this type of EV <sup>Z310</sup> cargo causes changes of stem cell morphology that leads to multicellular networks in the niches. This cell-shape transition may represent an initial step in NSC differentiation. |
2,329,385 | Sinking skin syndrome in a decompressive craniectomy series: Clinical and radiological features. | The sinking skin syndrome (SSS) is a particular complication after a decompressive craniectomy (DC). It still remains a poorly understood and underestimated entity.</AbstractText>Retrospective case series of craniectomized patients with and without SSS. Clinical and radiological features (DC diameter, shape of craniectomy flap, and midline deviation) were described and relative volumes of intracranial loss were quantified.</AbstractText>Twenty-seven patients (63% with SSS). The most common indication for DC was traumatic brain injury: 48.15%. The p50 diameter of DC was 12.8 cm for patients with SSS and 11.1 cm for patients without (Z score = 0.32). DC area was 81.5 cm2</sup> for patients with SSS and 71.43 cm2</sup> for patients without the syndrome (Z score = 0.61). According to the shape of the craniectomy flap, we classified our patients as: «same level» (51.8%), «sunken» (25.9%), and «extracranial herniation» (14.8%). Two patients (7.4%) had paradoxical herniation. Midline deviation was present in 12 (70.6%) patients with SSS. The 3rd</sup> ventricle volume average was 1.2 cc for patients with SSS versus 2.35 cc for patients without (Z score = 0.04). About 94.11% of patients (16 out of 17) clearly improved after replacement of the cranial defect.</AbstractText>In our series, low 3rd</sup> ventricle volumes had a good relation with SSS. The presence of a sunken flap does not guarantee SSS per se</i> and we propose the following radiologic description: A = sunken, B = same level, C = extracranial herniation, and D = paradoxical. Replacement of the skull defect is the main treatment.</AbstractText>Copyright: © 2022 Surgical Neurology International.</CopyrightInformation> |
2,329,386 | The development of a new, ultra-fine, and flexible neuroendoscope for intracranial observation. | A neuroendoscope is a technical advance that allows surgeons to visualize certain regions of the brain that was previously inaccessible through the use of a surgical microscope. Several neuroendoscope designs have been implemented by other neurosurgeons over the past 5 years. The advantage of a neuroendoscope is the addition of a flexible and narrow tip that allows for safe entry into intracranial structures for clinical observation. However, there are some limitations to this approach. Here, we report the use of a modified angioscope as a newly developed neuroendoscope to be employed in observing intracranial structures.</AbstractText>We report the use of an angioscope that is 1.8 mm in diameter and has both a thin and flexible tip. In this study, the angioscope was inserted into the lumen of an aspirator tube, and the tip of the device was placed at the intracranial area of intended observation area. Image findings were evaluated using an established in vivo</i> goat brain model.</AbstractText>The angioscope was light in weight and maneuverable and could be reached and observed in the blind spot using a surgical microscope. From the cerebellopontine angle, the lower cranial nerves and trigeminal nerve could be observed, and from the cisterna magna, the floor of the fourth ventricle and the aqueduct could be seen.</AbstractText>The angioscope is a useful instrument to observe intracranial locations safely and effectively even within a limited surgical field. Further modifications will be required to use the angioscope in various craniotomy procedures.</AbstractText>Copyright: © 2022 Surgical Neurology International.</CopyrightInformation> |
2,329,387 | HSPB1 overexpression improves hypoxic-ischemic brain damage by attenuating ferroptosis in rats through promoting G6PD expression. | Heat-shock protein B (HSPB1) has a neuroprotective effect on brain injury and is a negative regulator of ferroptosis. Therefore, we infer that HSPB1 plays a protective role in hypoxic-ischemic (HI) brain damage by inhibiting ferroptosis. A neonatal rat model of hypoxic-ischemic (HI) brain damage was established. HSPB1 overexpression plasmid and the negative control were injected into the lateral ventricle of rats 48 h before HI brain damage surgery. HSPB1 and glucose-6-phosphate dehydrogenase (G6PD) levels, infarction rate, iron accumulation, apoptosis, and ferroptosis-related markers were estimated with the assistance of qRT-PCR, 2,3,5-triphenyl tetrazolium chloride (TTC) staining, Prussian blue staining, iron assay kit, TUNEL staining, and Western blot. In vitro, after transfection, HSPB1 and G6PD levels, oxygen-glucose deprivation (OGD)-mediated hippocampal neuron cell viability, apoptosis, iron content, and ferroptosis-related markers were assessed using qRT-PCR, MTT, flow cytometry, iron assay kit, and Western blot. HSPB1 and G6PD were overexpressed in the hippocampus tissues of HI rats. High expression of HSPB1 in HI rats lessened infarction rate and ferritin level, hindered iron accumulation and apoptosis, and promoted GPX4, SLC7A11, and TFR1 levels. In OGD-mediated hippocampal neuron cells, HSPB1 upregulation intensified the viability and repressed apoptosis and ferroptosis, whereas G6PD silencing reversed the effects of HSPB1 upregulation. We documented that HSPB1 overexpression unleashes neuroprotective effects via modulating G6PD expression, which offers a novel target for the prevention and treatment of HI brain damage.<b>NEW & NOTEWORTHY</b> HSPB1 and G6PD were overexpressed in the hippocampus tissues of HI rats. High expression of HSPB1 in HI rats mitigated infarction rate and iron accumulation. HSPB1 overexpression reduced ferritin level, attenuated apoptosis, yet augmented GPX4, SLC7A11, and TFR1 levels in the hippocampus tissues of HI rats. G6PD deletion impaired the protective role of HSPB1 overexpression against HI brain damage-induced ferroptosis. |
2,329,388 | Gene therapy using human FMRP isoforms driven by the human <i>FMR1</i> promoter rescues fragile X syndrome mouse deficits. | Fragile X syndrome (FXS) is caused by the loss of the fragile X messenger ribonucleoprotein 1 (FMRP) encoded by the <i>FMR1</i> gene. Gene therapy using adeno-associated virus (AAV) to restore FMRP expression is a promising therapeutic strategy. However, so far AAV gene therapy tests for FXS only utilized rodent FMRPs driven by promoters other than the human <i>FMR1</i> promoter. Restoration of human FMRP in appropriate cell types and at physiological levels, preferably driven by the human <i>FMR1</i> promoter, would be more suitable for its clinical use. Herein, we generated two human <i>FMR1</i> promoter subdomains that effectively drive gene expression. When AAVs expressing two different human FMRP isoforms under the control of a human <i>FMR1</i> promoter subdomain were administered into bilateral ventricles of neonatal <i>Fmr1</i> <sup>-/y</sup> and wild-type (WT) mice, both human FMRP isoforms were expressed throughout the brain in a pattern reminiscent to that of mouse FMRP. Importantly, human FMRP expression attenuated social behavior deficits and stereotyped and repetitive behavior, and reversed dysmorphological dendritic spines in <i>Fmr1</i> <sup>-/y</sup> mice, without affecting WT mouse behaviors. Our results demonstrate that human <i>FMR1</i> promoter can effectively drive human FMRP expression in the brain to attenuate <i>Fmr1</i> <sup>-/y</sup> mouse deficits, strengthening the notion of using AAV gene therapy for FXS treatment. |
2,329,389 | Frontotemporal-Orbitozygomatic Approach and Its Variants: Technical Nuances and Video Illustration. | The frontotemporal-orbitozygomatic (FTOz) approach is an extension of the traditional pterional approach. It provides the neurosurgeon with a wide access to the skull base with minimal or no brain retraction needed; it also offers a panoramic view that enables various trajectories toward the anterior, middle, and central cranial fossae as well as the upper segment of the posterior cranial fossa. Intracranial lesions that can be addressed using the FTOz approach include large medial sphenoid wing and spheno-orbital meningiomas; suprasellar and parasellar tumors; lesions of the orbital apex, interpeduncular cistern, third ventricle, and upper paraclival regions; and anterior communicating artery and basilar-tip aneurysms. In this article, we discuss the advantages and disadvantages of the FTOz approach and describe related technical nuances and common pitfalls. Our goal was to provide an up-to-date report of this time-tested surgical approach using original high-quality dissections, 3-dimensional models, and 2-dimensional 4K videos to serve as a reliable and practical educational resource for neurosurgery trainees and junior neurosurgeons. A case example is also provided to show the 1-piece orbitozygomatic approach. |
2,329,390 | Preoperative Management of Neonates With Congenital Heart Disease.<ELocationID EIdType="pii" ValidYN="Y">e2022056415F</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1542/peds.2022-056415F</ELocationID><Abstract><AbstractText>Clinicians caring for neonates with congenital heart disease encounter challenges in clinical care as these infants await surgery or are evaluated for further potential interventions. The newborn with heart disease can present with significant pathophysiologic heterogeneity and therefore requires a personalized therapeutic management plan. However, this complex field of neonatal-cardiac hemodynamics can be simplified. We explore some of these clinical quandaries and include specific sections reviewing the anatomic challenges in these patients. We propose this to serve as a primer focusing on the hemodynamics and therapeutic strategies for the preoperative neonate with systolic dysfunction, diastolic dysfunction, excessive pulmonary blood flow, obstructed pulmonary blood flow, obstructed systemic blood flow, transposition physiology, and single ventricle physiology.</AbstractText><CopyrightInformation>Copyright © 2022 by the American Academy of Pediatrics.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ashrafi</LastName><ForeName>Amir H</ForeName><Initials>AH</Initials><AffiliationInfo><Affiliation>CHOC Children's Hospital, Orange, California.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mazwi</LastName><ForeName>Mjaye</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Hospital for Sick Children, Toronto, Ontario.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sweeney</LastName><ForeName>Nathaly</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Rady Children's Hospital, San Diego, California.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>van Dorn</LastName><ForeName>Charlotte S</ForeName><Initials>CS</Initials><AffiliationInfo><Affiliation>Mayo Clinic, Rochester, Minnesota.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Armsby</LastName><ForeName>Laurie B</ForeName><Initials>LB</Initials><AffiliationInfo><Affiliation>Doernbecher Children's Hospital, Portland, Oregon.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Eghtesady</LastName><ForeName>Pirooz</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Washington University School of Medicine, St Louis, Missouri.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ringle</LastName><ForeName>Megan</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Lucile Packard Children's Hospital, Palo Alto, California.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Justice</LastName><ForeName>Lindsey B</ForeName><Initials>LB</Initials><AffiliationInfo><Affiliation>Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gray</LastName><ForeName>Seth B</ForeName><Initials>SB</Initials><AffiliationInfo><Affiliation>Hospital for Sick Children, Toronto, Ontario.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Levy</LastName><ForeName>Victor</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>Lucile Packard Children's Hospital, Palo Alto, California.</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>Pediatrics</MedlineTA><NlmUniqueID>0376422</NlmUniqueID><ISSNLinking>0031-4005</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D007223" MajorTopicYN="N">Infant</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007231" MajorTopicYN="N">Infant, Newborn</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006330" MajorTopicYN="Y">Heart Defects, Congenital</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006439" MajorTopicYN="N">Hemodynamics</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011652" MajorTopicYN="N">Pulmonary Circulation</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006321" MajorTopicYN="N">Heart</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>8</Month><Day>29</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>11</Month><Day>1</Day><Hour>9</Hour><Minute>53</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>11</Month><Day>2</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>11</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36317975</ArticleId><ArticleId IdType="doi">10.1542/peds.2022-056415F</ArticleId><ArticleId IdType="pii">189886</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36317937</PMID><DateRevised><Year>2022</Year><Month>11</Month><Day>01</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1536-0237</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Oct</Month><Day>18</Day></PubDate></JournalIssue><Title>Journal of thoracic imaging</Title><ISOAbbreviation>J Thorac Imaging</ISOAbbreviation></Journal>Influence of Respiration on Collateral Flow in the Fontan Population Using Real-time Phase-contrast Cardiovascular Magnetic Resonance: Collateral Flow Does Not Protect the Ventricle From Volume Deficiency and Diastolic Dysfunction. | Clinicians caring for neonates with congenital heart disease encounter challenges in clinical care as these infants await surgery or are evaluated for further potential interventions. The newborn with heart disease can present with significant pathophysiologic heterogeneity and therefore requires a personalized therapeutic management plan. However, this complex field of neonatal-cardiac hemodynamics can be simplified. We explore some of these clinical quandaries and include specific sections reviewing the anatomic challenges in these patients. We propose this to serve as a primer focusing on the hemodynamics and therapeutic strategies for the preoperative neonate with systolic dysfunction, diastolic dysfunction, excessive pulmonary blood flow, obstructed pulmonary blood flow, obstructed systemic blood flow, transposition physiology, and single ventricle physiology.<CopyrightInformation>Copyright © 2022 by the American Academy of Pediatrics.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ashrafi</LastName><ForeName>Amir H</ForeName><Initials>AH</Initials><AffiliationInfo><Affiliation>CHOC Children's Hospital, Orange, California.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mazwi</LastName><ForeName>Mjaye</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Hospital for Sick Children, Toronto, Ontario.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sweeney</LastName><ForeName>Nathaly</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Rady Children's Hospital, San Diego, California.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>van Dorn</LastName><ForeName>Charlotte S</ForeName><Initials>CS</Initials><AffiliationInfo><Affiliation>Mayo Clinic, Rochester, Minnesota.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Armsby</LastName><ForeName>Laurie B</ForeName><Initials>LB</Initials><AffiliationInfo><Affiliation>Doernbecher Children's Hospital, Portland, Oregon.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Eghtesady</LastName><ForeName>Pirooz</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Washington University School of Medicine, St Louis, Missouri.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ringle</LastName><ForeName>Megan</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Lucile Packard Children's Hospital, Palo Alto, California.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Justice</LastName><ForeName>Lindsey B</ForeName><Initials>LB</Initials><AffiliationInfo><Affiliation>Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gray</LastName><ForeName>Seth B</ForeName><Initials>SB</Initials><AffiliationInfo><Affiliation>Hospital for Sick Children, Toronto, Ontario.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Levy</LastName><ForeName>Victor</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>Lucile Packard Children's Hospital, Palo Alto, California.</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>Pediatrics</MedlineTA><NlmUniqueID>0376422</NlmUniqueID><ISSNLinking>0031-4005</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D007223" MajorTopicYN="N">Infant</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007231" MajorTopicYN="N">Infant, Newborn</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006330" MajorTopicYN="Y">Heart Defects, Congenital</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006439" MajorTopicYN="N">Hemodynamics</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011652" MajorTopicYN="N">Pulmonary Circulation</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006321" MajorTopicYN="N">Heart</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>8</Month><Day>29</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>11</Month><Day>1</Day><Hour>9</Hour><Minute>53</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>11</Month><Day>2</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>11</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36317975</ArticleId><ArticleId IdType="doi">10.1542/peds.2022-056415F</ArticleId><ArticleId IdType="pii">189886</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">36317937</PMID><DateRevised><Year>2022</Year><Month>11</Month><Day>01</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1536-0237</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Oct</Month><Day>18</Day></PubDate></JournalIssue><Title>Journal of thoracic imaging</Title><ISOAbbreviation>J Thorac Imaging</ISOAbbreviation></Journal><ArticleTitle>Influence of Respiration on Collateral Flow in the Fontan Population Using Real-time Phase-contrast Cardiovascular Magnetic Resonance: Collateral Flow Does Not Protect the Ventricle From Volume Deficiency and Diastolic Dysfunction.</ArticleTitle><ELocationID EIdType="doi" ValidYN="Y">10.1097/RTI.0000000000000684</ELocationID><Abstract><AbstractText Label="PURPOSE" NlmCategory="OBJECTIVE">The clinical significance of collateral flow for the ventricular function of patients with univentricular hearts is often debated. This study evaluates the impact of collateral flow on respiration-dependent preload modification and diastolic function in Fontan patients assessed by systemic and pulmonary vein (PV) flow patterns.<AbstractText Label="MATERIALS AND METHODS" NlmCategory="METHODS">Real-time phase-contrast cardiovascular magnetic resonance was performed in the right upper PV, ascending aorta, superior, and inferior vena cava (IVC) in 21 Fontan patients and 11 healthy individuals. The patients' respiratory cycle was divided into 4 periods to generate respiratory-dependent stroke volumes (SVi). Conventional quantitative blood flow measurements were used to quantify and differentiate between low (group A) and high (group B) collateral flow.<AbstractText Label="RESULTS" NlmCategory="RESULTS">Group B showed significantly lower SVi IVC in inspiration, end-inspiration, expiration, and SVi ΔIVC compared with group A (23.6±4.8 mL/m2 to 33.4±8.0; P=0.005). PV flow resulted in a lower mean SVi PV (11.6±7.6 mL/m2, vs. 14.0±11.4 mL/m2) as well as a significantly lower peak systolic S-wave velocity (Smax) (P=0.005), S/D-ratio (Smax/peak diastolic wave velocity) (P=0.015), and shorter diastolic deceleration time (DTD; P=0.030; median DTD=134 ms) compared with group A (DTD=202 ms).<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">This study demonstrates the incapability of Fontan patients to properly increase preload by inspiration in the presence of significant collateral flow. The results further show that collateral flow is associated with a volume-deprived ventricle and impaired diastolic function. |
2,329,391 | Metallothionein synthesis increased by Ninjin-yoei-to, a Kampo medicine protects neuronal death and memory loss after exposure to amyloid β<sub>1-42</sub>. | It is possible that increased synthesis of metallothioneins (MTs), Zn2+</sup>-binding proteins is linked with the protective effect of Ninjin-yoei-to (NYT) on Zn2+</sup> toxicity ferried by amyloid β1-42</sub> (Aβ1-42</sub>).</AbstractText>Judging from the biological half-life (18-20 h) of MTs, the effective period of newly synthesized MT on capturing Zn2+</sup> is estimated to be approximately 2 days. In the present paper, a diet containing 3% NYT was administered to mice for 2 days and then Aβ1-42</sub> was injected into the lateral ventricle of mice.</AbstractText>MT level in the dentate granule cell layer was elevated 2 days after administration of NYT diet, while the administration reduced intracellular Zn2+</sup> level increased 1 h after Aβ1-42</sub> injection, resulting in rescuing neuronal death in the dentate granule cell layer, which was observed 14 days after Aβ1-42</sub> injection. Furthermore, Pre-administration of NYT diet rescued object recognition memory loss via affected perforant pathway long-term potentiation after local injection of Aβ1-42</sub> into the dentate granule cell layer of rats.</AbstractText>The present study indicates that pre-administration of NYT diet for 2 days increases synthesis of MTs, which reduces intracellular Zn2+</sup> toxicity ferried by extracellular Aβ1-42</sub>, resulting in protecting neuronal death in the dentate gyrus and memory loss after exposure to Aβ1-42</sub>.</AbstractText>© 2022. The Author(s).</CopyrightInformation> |
2,329,392 | Novel <i>TPR::ROS1</i> Fusion Gene Activates MAPK, PI3K and JAK/STAT Signaling in an Infant-type Pediatric Glioma. | <AbstractText Label="BACKGROUND/AIM" NlmCategory="OBJECTIVE">Although fusion genes involving the proto-oncogene receptor tyrosine kinase ROS1 are rare in pediatric glioma, targeted therapies with small inhibitors are increasingly being approved for histology-agnostic fusion-positive solid tumors.</AbstractText>Here, we present a 16-month-old boy, with a brain tumor in the third ventricle. The patient underwent complete resection but relapsed two years after diagnosis and underwent a second operation. The tumor was initially classified as a low-grade glioma (WHO grade 2); however, methylation profiling suggested the newly WHO-recognized type: infant-type hemispheric glioma. To further refine the molecular background, and search for druggable targets, whole genome (WGS) and whole transcriptome (RNA-Seq) sequencing was performed.</AbstractText>Concomitant WGS and RNA-Seq analysis revealed several segmental gains and losses resulting in complex structural rearrangements and fusion genes. Among the top-candidates was a novel TPR::ROS1 fusion, for which only the 3' end of ROS1 was expressed in tumor tissue, indicating that wild type ROS1 is not normally expressed in the tissue of origin. Functional analysis by Western blot on protein lysates from transiently transfected HEK293 cells showed the TPR::ROS1 fusion gene to activate the MAPK-, PI3K- and JAK/STAT- pathways through increased phosphorylation of ERK, AKT, STAT and S6. The downstream pathway activation was also confirmed by immunohistochemistry on tumor tissue slides from the patient.</AbstractText>We have mapped the activated oncogenic pathways of a novel ROS1-fusion gene and broadened the knowledge of the newly recognized infant-type glioma subtype. The finding facilitates suitable targeted therapies for the patient in case of relapse.</AbstractText>Copyright © 2022, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.</CopyrightInformation> |
2,329,393 | <i>Npas3</i> regulates stemness maintenance of radial glial cells and neuronal migration in the developing mouse cerebral cortex. | The neuronal PAS domain 3 (NPAS3) is a member of the basic helix-loop-helix (bHLH) PAS family of transcription factors and is implicated in psychiatric and neurodevelopmental disorders. <i>NPAS3</i> is robustly expressed in the cortical ventricle zone (VZ), a transient proliferative zone containing progenitor cells, mainly radial glial cells, destined to give rise to cortical excitatory neurons. However, the role of <i>NPAS3</i> in corticogenesis remains largely unknown. In this study, we knocked down <i>Npas3</i> expression in the neural progenitor cells residing in the cortical VZ to investigate the role of <i>Npas3</i> in cerebral cortical development in mice. We demonstrated that <i>Npas3</i> knockdown profoundly impaired neuronal radial migration and changed the laminar cell fate of the cells detained in the deep cortical layers. Furthermore, the downregulation of <i>Npas3</i> led to the stemness maintenance of radial glial cells and increased the proliferation rate of neural progenitor cells residing in the VZ/subventricular zone (SVZ). These findings underline the function of <i>Npas3</i> in the development of the cerebral cortex and may shed light on the etiology of <i>NPAS3</i>-related disorders. |
2,329,394 | Noninvasive Respiratory Support Does Not Prevent Extubation Failure in High-Risk Norwood Patients. | This study aims to determine whether bilevel positive airway pressure (BiPAP) and continuous positive airway pressure (CPAP) effectively mitigate the risk of extubation failure in children status post-Norwood procedure.</AbstractText>Single-center, retrospective analysis. Extubation events were collected from January 2015 to July 2021. Extubation failure was defined as the need for reintubation within 48 hours of extubation. Demographics, clinical characteristics, and ventilatory settings were compared between successful and failed extubations.</AbstractText>Pediatric cardiovascular ICU.</AbstractText>Neonates following Norwood procedure.</AbstractText>Extubation following the Norwood procedure.</AbstractText>The analysis included 311 extubations. Extubation failure occurred in 31 (10%) extubation attempts within the first 48 hours. On univariate analysis, higher rate of extubation failure was observed when patients were extubated to CPAP/BiPAP relative to patients who were extubated to either high-flow nasal cannula (HFNC) or nasal cannula (NC) (16% vs 7.8%; p</i> = 0.027). On multivariable analysis, the presence of vocal cord anomaly (odds ratio, 3.08; p</i> = 0.005) and lower pre-extubation end-tidal co2</sub> (odds ratio, 0.91; p</i> = 0.006) were simultaneously associated with extubation failure while also controlling for the post-extubation respiratory support (CPAP/BiPAP/HFNC vs NC).</AbstractText>Clinicians should not rely on CPAP or BiPAP as the only supportive measure for a patient at increased risk of extubation failure. CPAP or BiPAP do not mitigate the risk of extubation failure in the Norwood patients. A multisite study is needed to generalize these conclusions.</AbstractText>Copyright © 2022 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of the Society of Critical Care Medicine.</CopyrightInformation> |
2,329,395 | Spontaneous regression of colloid cyst on the third ventricle: a case report with the review of the literature.<Pagination><StartPage>397</StartPage><MedlinePgn>397</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">397</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1186/s12883-022-02933-6</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Colloid cyst (CC) is a rare and benign cyst found in the third ventricle near the foramen of Monro. Although the role of surgical resection is well established in symptomatic large-sized CC, it remains debatable whether surgical removal of CC with no symptoms or minimal symptoms is necessary.</AbstractText><AbstractText Label="CASE PRESENTATION" NlmCategory="METHODS">A 49-year-old male patient visited our institute for incidentally detected intracranial mass. MRI demonstrated typical, 12 mm-sized CC located in the third ventricle. It was noticed that the cyst spontaneously decreased in size from 12 mm to 4 mm on MRI at 18 months after the first visit.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">Although spontaneous regression is a very rare phenomenon in CC, regular imaging study and frequent neurologic examination can be an alternative option for well-selected, asymptomatic cases.</AbstractText><CopyrightInformation>© 2022. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Joo-Hwan</ForeName><Initials>JH</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Chonnam National University Hwasun Hospital and Medical School, 322 Seoyang-ro, Hwasun-eup, Jeollanam-do, 58128, Hwasun-gun, South Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hong</LastName><ForeName>Jong-Hwan</ForeName><Initials>JH</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Chonnam National University Hwasun Hospital and Medical School, 322 Seoyang-ro, Hwasun-eup, Jeollanam-do, 58128, Hwasun-gun, South Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Yeong Jin</ForeName><Initials>YJ</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Chonnam National University Hwasun Hospital and Medical School, 322 Seoyang-ro, Hwasun-eup, Jeollanam-do, 58128, Hwasun-gun, South Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Moon</LastName><ForeName>Kyung-Sub</ForeName><Initials>KS</Initials><Identifier Source="ORCID">0000-0002-1129-1064</Identifier><AffiliationInfo><Affiliation>Department of Neurosurgery, Chonnam National University Hwasun Hospital and Medical School, 322 Seoyang-ro, Hwasun-eup, Jeollanam-do, 58128, Hwasun-gun, South Korea. moonks@chonnam.ac.kr.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>2020R1C1C1007832</GrantID><Agency>Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Minist</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D016454">Review</PublicationType><PublicationType UI="D002363">Case Reports</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>10</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>BMC Neurol</MedlineTA><NlmUniqueID>100968555</NlmUniqueID><ISSNLinking>1471-2377</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D056364" MajorTopicYN="Y">Colloid Cysts</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020542" MajorTopicYN="Y">Third Ventricle</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008279" MajorTopicYN="N">Magnetic Resonance Imaging</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009460" MajorTopicYN="N">Neurologic Examination</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Colloid cyst</Keyword><Keyword MajorTopicYN="N">Natural history</Keyword><Keyword MajorTopicYN="N">Spontaneous regression</Keyword><Keyword MajorTopicYN="N">Third ventricle</Keyword></KeywordList><CoiStatement>The authors declare that we have no conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>5</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>10</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>10</Month><Day>30</Day><Hour>1</Hour><Minute>4</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>10</Month><Day>31</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>11</Month><Day>2</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">36309649</ArticleId><ArticleId IdType="pmc">PMC9617380</ArticleId><ArticleId IdType="doi">10.1186/s12883-022-02933-6</ArticleId><ArticleId IdType="pii">10.1186/s12883-022-02933-6</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Annamalai G, Lindsay KW, Bhattacharya JJ. 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Historically, it has been referred to as idiopathic hypertrophic subaortic stenosis.  HOCM is a significant cause of sudden cardiac death in young people, including well-trained athletes, affecting men and women equally across all races.  In most patients, it results from asymmetric septal hypertrophy causing outflow obstruction of the left ventricle.  It is difficult to diagnose and presents a challenge to medical health professionals in evaluating at-risk athletes.  Unfortunately, hypertrophic obstructive cardiomyopathy is often not diagnosed until a significant cardiac event has occurred. The hypertrophy can occur in any segment of the left ventricle but is most common in the interventricular septum. This often results in obstruction of blood flow through the left ventricular outflow tract. HOCM is a genetic disorder. Defects in several genes have been identified that result in septal hypertrophy. The condition is usually asymptomatic in children but may first present with sudden death in teenagers and adolescents. |
2,329,396 | Comparison of surgery with or without adjuvant radiotherapy in treating central neurocytoma: a single-center retrospective real-world study. | To investigate the efficacy and safety of adjuvant radiotherapy (RT) in patients with central neurocytoma (CN).</AbstractText>The study included 68 patients with CN retrospectively, was further divided into surgery + RT group (31 patients) and surgery alone group (37 patients). Progression-free survival (PFS), overall survival (OS), and adverse reactions (AEs) were compared between the two groups.</AbstractText>The median follow-up duration was 82.2 (interquartile range, 64.7-104.5) months. Patients in the surgery + RT group tended to have longer PFS than those in the surgery alone group (5-year PFS rate: 92.7% vs. 86.3%; P = 0.074). There was no significant difference in OS between the two groups (5-year OS rate: 96.8% vs. 94.3%; P = 0.639). Subgroup analysis revealed a significant improvement in PFS in patients receiving RT after surgery in patients who underwent subtotal resection (STR) (P = 0.045). In the overall population, univariate multivariate analysis revealed that gross total resection (GTR) (P = 0.002), tumor location in the unilateral ventricle (P = 0.008), and MIB-1 (Ki-67) labeling index (LI) < 5% (P = 0.009) were favorable independent prognostic factors for PFS. Whereas tumor location in the unilateral ventricle (P = 0.043) was a favorable independent prognostic factor for OS. Moreover, RT patients experienced AEs (Grade 1-2, well-tolerated).</AbstractText>Adjuvant RT in the treatment of CNs showed satisfactory safety, and postoperative RT could improve PFS in STR patients. Furthermore, GTR, tumor development in the unilateral ventricle, and MIB-1 LI < 5% were found to be favorable factors affecting the prognosis of CNs.</AbstractText>© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</CopyrightInformation> |
2,329,397 | Shunt freedom in slit ventricle syndrome: using paradoxical ventriculomegaly following lumbar shunting to our advantage. Illustrative cases. | The authors present two cases of paradoxical ventriculomegaly after lumboperitoneal (LP) shunting in patients with slit ventricle syndrome (SVS).</AbstractText>After placement of an LP shunt, both patients rapidly developed radiographic and clinically symptomatic ventricular enlargement. The then generous ventricular corridors allowed both patients to be treated by endoscopic third ventriculostomy (ETV) with concurrent removal of their LP shunt. The patients then underwent staged increases in their shunt resistance to the maximum setting and remain asymptomatic.</AbstractText>The authors suggest that this paradoxical ventriculomegaly may have resulted from a pressure gradient between the shunt systems in the intra- and extraventricular spaces due to a noncommunicating etiology of their hydrocephalus. ETV may successfully exploit this newfound obstructive hydrocephalus and provide resolution of the radiographic and clinical hydrocephalus through allowing for improved communication between the cranial and lumbar cerebrospinal fluid spaces in SVS.</AbstractText> |
2,329,398 | Conservative management of intraventricular migration of a gelatin sponge: illustrative case. | Gelatin sponges, such as Gelfoam, are used as hemostatic agents during surgery and are generally absorbed over the course of 4-6 weeks in most body cavities. The time course of the dissolution of Gelfoam sponges within the cerebral ventricles has not been described.</AbstractText>The authors present a case of intraventricular migration of Gelfoam after ventriculoperitoneal shunt placement in a 6-week-old infant. The infant was imaged regularly after ventriculoperitoneal shunt placement, and the Gelfoam sponge persisted within the ventricles on all images until 11 months after surgery. At no time during follow-up did the patient have any symptoms of hydrocephalus requiring retrieval of the sponge or shunt revision.</AbstractText>This is the first case describing time until absorption of a gelatin sponge within the ventricle and successful conservative management.</AbstractText> |
2,329,399 | Neuromedin U-deficient rats do not lose body weight or food intake. | Studies in genetically modified mice establish that essential roles of endogenous neuromedin U (NMU) are anorexigenic function and metabolic regulation, indicating that NMU is expected to be a potential target for anti-obesity agents. However, in central administration experiments in rats, inconsistent results have been obtained, and the essential role of NMU energy metabolism in rats remain unclear. This study aims to elucidate the role of endogenous NMU in rats. We generated NMU knockout (KO) rats that unexpectedly showed no difference in body weight, adiposity, circulating metabolic markers, body temperature, locomotor activity, and food consumption in both normal and high fat chow feeding. Furthermore, unlike reported in mice, expressions of Nmu and NMU receptor type 2 (Nmur2) mRNA were hardly detectable in the rat hypothalamic nuclei regulating feeding and energy metabolism, including the arcuate nucleus and paraventricular nucleus, while Nmu was expressed in pars tuberalis and Nmur2 was expressed in the ependymal cell layer of the third ventricle. These results indicate that the species-specific expression pattern of Nmu and Nmur2 may allow NMU to have distinct functions across species, and that endogenous NMU does not function as an anorexigenic hormone in rats. |
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