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2,328,900 | Salient Central Lesion Volume: A Standardized Novel Fully Automated Proxy for Brain FLAIR Lesion Volume in Multiple Sclerosis. | Quantitative neuroimaging is an important part of multiple sclerosis research and clinical trials, and measures of lesion volume (LV) and brain atrophy are key clinical trial endpoints. However, translation of these endpoints to heterogeneous historical datasets and nonstandardized clinical routine imaging has been difficult. The NeuroSTREAM technique was recently introduced as a robust and broadly applicable surrogate for brain atrophy measurement, but no such surrogate currently exists for conventional T2-LV. Therefore, we sought to develop a fully automated proxy for T2-LV with similar analytic value but increased robustness to common issues arising in clinical routine imaging.</AbstractText>We created an algorithm to identify salient central lesion volume (SCLV), comprised of the subset of lesion voxels within a specific distance to the lateral ventricles (centrality) and with intensity at least a quantitatively-derived amount brighter than normal appearing tissue (salience). We evaluated this method on four datasets (clinical, inter-scanner, scan-rescan, and real-world multi-center), including 1.5T, 3T, Philips, Siemens, and GE scanners with heterogeneous protocols, to assess agreement with conventional T2-LV, comparative relationship with disability, reliability across scanners and between scans, and applicability to real-world scans.</AbstractText>SCLV correlated strongly with conventional T2-LV in both research-quality (r = .90, P < .001) and real-world (r = 0.87, P < 0.001) datasets. It also showed similar correlations with Expanded Disability Status Scale, as conventional T2-LV (r = 0.48 for T2-LV vs. r = 0.45 for SCLV). Inter-scanner reproducibility (ICC) was 0.86, p < 0.001 for SCLV compared to 0.84, p < 0.001 for conventional T2-LV, whereas scan-rescan ICC was 0.999 for SCLV versus 0.997 for T2-LV.</AbstractText>SCLV is a robust, fully-automated proxy for T2-LV in situations where conventional T2-LV is not easily or reliably calculated.</AbstractText>© 2019 by the American Society of Neuroimaging.</CopyrightInformation> |
2,328,901 | Clinical efficacy of gangliosides on premature infants suffering from white matter damage and its effect on the levels of IL-6, NSE and S100β. | This study investigated the clinical efficacy of gangliosides on premature infants suffering from white matter damage and its effect on the levels of IL-6, neuron-specific enolase (NSE) and S100β. Seventy-six cases of premature infants suffering from white matter damage admitted to the Tianjin Central Hospital of Obstetrics and Gynecology from February 2016 to March 2017 were enrolled in this study. They were randomly divided into the control group and the observation group with 38 cases in each group. Control group was given conventional treatment, while the observation group was given ganglioside treatment on the basis of the treatment given to the control group. Craniocerebrum ultrasonic detection was used to observe the condition of white matter around the ventricle of child patients in the two groups, before and after treatment. ELISA was used to detect the levels of IL-6, NSE and S100β. Gesell developmental scale was used to compare the developmental quotient (DQ) of various function regions of the children. The total effective rate of the observation group was higher than that of the control group (P<0.05). The gray value of craniocerebrum ultrasonic detection in the observation group was significantly lower than that in the control group (P<0.05). IL-6, S100β and NSE levels of the child patients in the two groups were significantly declined at 7 and 14 days after birth (P<0.05). After 1 year, the observation group scored significantly higher DQ than the control group in the aspects of social adaptation, gross motor, fine motor, language and personal social contact. The sequel incidence of patients in the observation group was significantly lower than that of the control group (P<0.05). In conclusion, the intervention treatment with ganglioside for premature infants suffering from white matter damage was beneficial and provided a protective effect. It also reduced sequel and produced some promising results. |
2,328,902 | [Effects of Exendin-4 on the differentiation of neural stem cells from subventricular zone of adult mice in vitro]. | To study the effect of exendin-4(Ex-4) on the differentiation of neural stem cells(NSCs) in adult mouse subventricular zone(SVZ)and its mechanism .</AbstractText>NSCs in the SVZ were derived from 5-week C57BL/6J mice and the expression of nestin was detected by immunofluorescence. The cell morphology was observed after the cells treatmed with 100 nmol/L Ex-4 for 14 days.The expressions of nestin and glucagon-like peptide-1 receptor (GLP-1R) were detected by immunofluorescence. GLP-1R was knocked down by using shRNA and the study was divided into four groups: control group, Ex-4 group, GLP-1R knockdown group, GLP-1R knockdown + Ex-4 group. After treatment with 100 nmol/L Ex-4 for 14 d, β-tublin III and glial fibrillary acidic protein (GFAP) were labeled by immunofluorescence and then the proportion of β-tublin III positive cells were counted. Western blot was used to detect the activation of cAMP-response element binding protein (CREB) in NSCs. In order to further study the effects of Ex-4 on mitogen-activated protein kinase(MAPK) and phosphatidylinositol 3-hydroxy kinase (PI3K) pathways, the cells were pretreated with MAPK inhibitor U0126 at a concentration of 0.07 μmol/L for 30 min or PI3K inhibitor LY294002 at 50 μmol for 2 h, respectively. The study was divided into six groups: control group, Ex-4 group, U0126 group, U0126 + Ex-4 group, LY294002 group, LY294002 + Ex-4 group. The activation of CREB in each group was detected by Western blot. The experiment was repeated three times independently.</AbstractText>NSCs were successfully extracted from SVZ of C57BL/6J mice. Immunofluorescence showed that nestin and GLP-1R were positive in NSCs. Compared with the control group, the proportion of neurons differentiated from Ex-4 group was higher. The percentage of neurons in GLP-1R knockdown + Ex-4 group was basically the same as that in control group (P＜0.01). The positive cells of beta-tublin III showed positive activation of GLP-1R and CREB. Western blot showed that CREB was significantly activated in the Ex-4 group, and knockdown of GLP-1R abolished its activation (P＜0.01). U0126 did not affect Ex-4-mediated CERB activation, and LY294002 significantly reduced Ex-4-mediated CREB activation (P＜0.01).</AbstractText>Ex-4 promotes the differentiation of NSCs into neurons in SVZ of adult mice through GLP-1R receptor, which may be achieved through PI3K/CREB pathway.</AbstractText> |
2,328,903 | Resolving the natural myocardial remodelling brought upon by cardiac contraction; a porcine ex-vivo cardiovascular magnetic resonance study of the left and right ventricle.<Pagination><StartPage>35</StartPage><MedlinePgn>35</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">35</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1186/s12968-019-0547-2</ELocationID><Abstract><AbstractText Label="BACKGROUND">The three-dimensional rearrangement of the right ventricular (RV) myocardium during cardiac deformation is unknown. Previous in-vivo studies have shown that myocardial left ventricular (LV) deformation is driven by rearrangement of aggregations of cardiomyocytes that can be characterised by changes in the so-called E3-angle. Ex-vivo imaging offers superior spatial resolution compared with in-vivo measurements, and can thus provide novel insight into the deformation of the myocardial microstructure in both ventricles. This study sought to describe the dynamic changes of the orientations of the cardiomyocytes in both ventricles brought upon by cardiac contraction, with particular interest in the thin-walled RV, which has not previously been described in terms of its micro-architecture.</AbstractText><AbstractText Label="METHODS">The hearts of 14 healthy 20 kg swine were excised and preserved in either a relaxed state or a contracted state. Myocardial architecture was assessed and compared between the two contractional states by quantification of the helical, transmural and E3-angles of the cardiomyocytes using high-resolution diffusion tensor imaging.</AbstractText><AbstractText Label="RESULTS">The differences between the two states of contraction were most pronounced in the endocardium where the E3-angle decreased from 78.6° to 24.8° in the LV and from 82.6° to 68.6° in the RV. No significant change in neither the helical nor the transmural angle was found in the cardiomyocytes of the RV. In the endocardium of the LV, however, the helical angle increased from 35.4° to 47.8° and the transmural angle increased from 3.1° to 10.4°.</AbstractText><AbstractText Label="CONCLUSION">The entire myocardium rearranges through the cardiac cycle with the change in the orientation of the aggregations of cardiomyocytes being the predominant mediator of myocardial wall thickening. Interestingly, differences also exist between the RV and LV, which helps in the explanation of the different physiological capabilities of the ventricles.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Omann</LastName><ForeName>Camilla</ForeName><Initials>C</Initials><Identifier Source="ORCID">0000-0002-9718-201X</Identifier><AffiliationInfo><Affiliation>Department of Cardiothoracic & Vascular Surgery, Aarhus University Hospital, Skejby, Denmark. camillaomann@clin.au.dk.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Clinical Medicine, Aarhus University, Palle Juul-Jensens Boulevard 99, 8200, Aarhus N, Denmark. camillaomann@clin.au.dk.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Agger</LastName><ForeName>Peter</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department of Cardiothoracic & Vascular Surgery, Aarhus University Hospital, Skejby, Denmark.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Clinical Medicine, Aarhus University, Palle Juul-Jensens Boulevard 99, 8200, Aarhus N, Denmark.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Comparative Medicine Lab, Aarhus University Hospital, Skejby, Denmark.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bøgh</LastName><ForeName>Nikolaj</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Department of Cardiothoracic & Vascular Surgery, Aarhus University Hospital, Skejby, Denmark.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Clinical Medicine, Aarhus University, Palle Juul-Jensens Boulevard 99, 8200, Aarhus N, Denmark.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Laustsen</LastName><ForeName>Christoffer</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Clinical Medicine, Aarhus University, Palle Juul-Jensens Boulevard 99, 8200, Aarhus N, Denmark.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>MR Research Centre, Aarhus University, Aarhus, Denmark.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ringgaard</LastName><ForeName>Steffen</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>MR Research Centre, Aarhus University, Aarhus, Denmark.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Stephenson</LastName><ForeName>Robert S</ForeName><Initials>RS</Initials><AffiliationInfo><Affiliation>Department of Clinical Medicine, Aarhus University, Palle Juul-Jensens Boulevard 99, 8200, Aarhus N, Denmark.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Comparative Medicine Lab, Aarhus University Hospital, Skejby, Denmark.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institute of Clinical Sciences, College of Medical and Dental Sciences, The University of Birmingham, Birmingham, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Anderson</LastName><ForeName>Robert H</ForeName><Initials>RH</Initials><AffiliationInfo><Affiliation>Institute of Genetic Medicine, Newcastle University, Newcastle-upon-Tyne, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hjortdal</LastName><ForeName>Vibeke E</ForeName><Initials>VE</Initials><AffiliationInfo><Affiliation>Department of Cardiothoracic & Vascular Surgery, Aarhus University Hospital, Skejby, Denmark.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Clinical Medicine, Aarhus University, Palle Juul-Jensens Boulevard 99, 8200, Aarhus N, Denmark.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Smerup</LastName><ForeName>Morten</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Cardiothoracic & Vascular Surgery, Aarhus University Hospital, Skejby, Denmark.</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>2019</Year><Month>07</Month><Day>01</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Cardiovasc Magn Reson</MedlineTA><NlmUniqueID>9815616</NlmUniqueID><ISSNLinking>1097-6647</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D056324" MajorTopicYN="Y">Diffusion Tensor Imaging</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000000981" MajorTopicYN="Y">diagnostic imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009200" MajorTopicYN="Y">Myocardial Contraction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D032383" MajorTopicYN="N">Myocytes, Cardiac</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011237" MajorTopicYN="N">Predictive Value of Tests</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D034421" MajorTopicYN="N">Sus scrofa</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013997" MajorTopicYN="N">Time Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016277" MajorTopicYN="Y">Ventricular Function, Left</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016278" MajorTopicYN="Y">Ventricular Function, Right</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020257" MajorTopicYN="Y">Ventricular Remodeling</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Diffusion tensor imaging</Keyword><Keyword MajorTopicYN="N">Dynamic rearrangement</Keyword><Keyword MajorTopicYN="N">Micro-structure</Keyword><Keyword MajorTopicYN="N">Myocardial architecture</Keyword><Keyword MajorTopicYN="N">Myocardium</Keyword><Keyword MajorTopicYN="N">Myocyte orientation</Keyword></KeywordList><CoiStatement>The authors declare that they have no competing interests.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year><Month>1</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2019</Year><Month>5</Month><Day>29</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2019</Year><Month>7</Month><Day>2</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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J Cardiovasc Magn Reson. 2017;19:31. doi: 10.1186/s12968-017-0342-x.</Citation><ArticleIdList><ArticleId IdType="doi">10.1186/s12968-017-0342-x</ArticleId><ArticleId IdType="pmc">PMC5345150</ArticleId><ArticleId IdType="pubmed">28279178</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">31256636</PMID><DateRevised><Year>2019</Year><Month>07</Month><Day>01</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1524-4539</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2019</Year><Month>Jul</Month><Day>01</Day></PubDate></JournalIssue><Title>Circulation</Title><ISOAbbreviation>Circulation</ISOAbbreviation></Journal>Evaluation and Management of the Child and Adult With Fontan Circulation: A Scientific Statement From the American Heart Association. | It has been 50 years since Francis Fontan pioneered the operation that today bears his name. Initially designed for patients with tricuspid atresia, this procedure is now offered for a vast array of congenital cardiac lesions when a circulation with 2 ventricles cannot be achieved. As a result of technical advances and improvements in patient selection and perioperative management, survival has steadily increased, and it is estimated that patients operated on today may hope for a 30-year survival of >80%. Up to 70 000 patients may be alive worldwide today with Fontan circulation, and this population is expected to double in the next 20 years. In the absence of a subpulmonary ventricle, Fontan circulation is characterized by chronically elevated systemic venous pressures and decreased cardiac output. The addition of this acquired abnormal circulation to innate abnormalities associated with single-ventricle congenital heart disease exposes these patients to a variety of complications. Circulatory failure, ventricular dysfunction, atrioventricular valve regurgitation, arrhythmia, protein-losing enteropathy, and plastic bronchitis are potential complications of the Fontan circulation. Abnormalities in body composition, bone structure, and growth have been detected. Liver fibrosis and renal dysfunction are common and may progress over time. Cognitive, neuropsychological, and behavioral deficits are highly prevalent. As a testimony to the success of the current strategy of care, the proportion of adults with Fontan circulation is increasing. Healthcare providers are ill-prepared to tackle these challenges, as well as specific needs such as contraception and pregnancy in female patients. The role of therapies such as cardiovascular drugs to prevent and treat complications, heart transplantation, and mechanical circulatory support remains undetermined. There is a clear need for consensus on how best to follow up patients with Fontan circulation and to treat their complications. This American Heart Association statement summarizes the current state of knowledge on the Fontan circulation and its consequences. A proposed surveillance testing toolkit provides recommendations for a range of acceptable approaches to follow-up care for the patient with Fontan circulation. Gaps in knowledge and areas for future focus of investigation are highlighted, with the objective of laying the groundwork for creating a normal quality and duration of life for these unique individuals. |
2,328,904 | Pontine cavernous malformation: microsurgery evading the floor of the fourth ventricle. | This video demonstrates resection of a left pontine cavernous malformation that is abutting the floor of the fourth ventricle (f4V). Even though accessing the lesion through the f4V seems to be reasonable, we used a lateral supracerebellar approach through the middle cerebellar peduncle to preserve especially the abducens and facial nuclei. After total resection the patient was neurologically intact at the 3-month follow-up. Postoperative MRI revealed 3.5-mm pontine tissue between the cavity and f4V that appeared to be absent in preoperative MRI. Approaching pontine lesions through the f4V is not the first choice. In our opinion, the philosophy of safe entry zones is a concept to be reassessed. The video can be found here: https://youtu.be/1Jh6giZc-48. |
2,328,905 | The suboccipital, telovelar, transsuperior fovea approach to dorsal pontine lesions. | Dorsal pons lesions at the facial colliculus level can be accessed with a suboccipital telovelar (SOTV) approach using the superior fovea safe entry zone. Opening the telovelar junction allows visualization of the dorsal pons and lateral entry at the level of the fourth ventricle floor. Typically, a lateral entry into the floor of the fourth ventricle is better tolerated than a midline opening. This video demonstrates the use of the SOTV approach to remove a cavernous malformation at the level of the facial colliculus. This case is particularly interesting because of a large venous anomaly and several telangiectasias in the pons. Dissections in the video are reproduced with permission from the Rhoton Collection (http://rhoton.ineurodb.org). The video can be found here: https://youtu.be/LqzCfN2J3lY. |
2,328,906 | Thalamomesencephalic cavernoma: anterior transcallosal transchoroidal approach. | We present a case of a 62-year-old man with acute onset of diplopia, headache, and vomiting for a bleeding thalamomesencephalic cavernoma. The lesion was removed via the anterior transcallosal transchoroidal approach. His head was slightly flexed and a right paramedian craniotomy for an interhemispheric approach was performed. The interhemispheric fissure was split and, after callosotomy, the choroidal fissure was opened along the tenia fornicis to enter the velum interpositum and enlarge the foramen of Monro. The cavernoma was then identified and resected. There were no long-term postoperative neurological deficits. This approach is a valid alternative for thalamomesencephalic lesions. The video can be found here: https://youtu.be/DJdorbzDnH0. |
2,328,907 | Drug potency on inhibiting late Na<sup>+</sup> current is sensitive to gating modifier and current region where drug effects were measured. | Cardiac late Na+</sup> current (INaL</sub>) contributes to ventricular action potential duration. Pathological increase in INaL</sub> is arrhythmogenic, and inhibition of INaL</sub> offers protection against ventricular repolarization disturbance. Recently, two INaL</sub> datasets generated by different laboratories that assessed current inhibition by a panel of clinical drugs as a part of the Comprehensive in vitro Proarrhythmia Assay (CiPA) initiative were published. The results revealed a surprising degree of data variability despite of the use of a standardized voltage protocol. This study investigated whether remaining procedural differences related to experimental methods and data analysis associated with these datasets can produce differences in INaL</sub> pharmacology.</AbstractText>Whole cell voltage clamp recordings were performed on cells expressing NaV</sub>1.5 α- and β1-subunits to study: 1) the impact of gating modifiers used to augment INaL</sub> (ATX-II vs. veratridine), internal solution composition (with vs. without ATP and GTP), and recording temperature (23 °C vs 37 °C) on stability of INaL</sub> measured across the duration of a patch clamp experiment; 2) mechanisms of each gating modifier on Na+</sup> channels; and 3) effects of six drugs (lidocaine, mexiletine, chloroquine, ranolazine, ritonavir, and verapamil) on INaL</sub> induced by either gating modifier.</AbstractText>Stability of INaL</sub> is affected by the choice of gating modifier, presence of nucleotides in the internal solution, and recording temperature. ATX-II and veratridine produced different changes in Na+</sup> channel gating, inducing mechanistically distinct INaL</sub>. Drug potencies on inhibiting INaL</sub> were dependent on the choice of gating modifier and current region where drug effects were measured.</AbstractText>INaL</sub> pharmacology can be impacted by all experimental factors examined in this study. The effect of gating modifier and current region used to quantify drug inhibition alone led to 30× difference in half inhibitory concentration (IC50</sub>) for ritonavir, demonstrating that substantial difference in drug inhibition can be produced. Drug potencies on inhibiting INaL</sub> derived from different patch clamp studies may thus not be generalizable. For INaL</sub> pharmacology to be useful for in silico modeling or interpreting drug-induced changes in cardiac action potentials or ECG, standardizing INaL</sub> experimental procedures including data analysis methods is necessary to minimize data variability.</AbstractText>Published by Elsevier Inc.</CopyrightInformation> |
2,328,908 | Benznidazole, itraconazole and their combination in the treatment of acute experimental chagas disease in dogs. | Chagas disease (CD) is a serious public health problem in Latin America and its treatment remains neglected. Benznidazole (BZ), the only drug available in Brazil, presents serious side effects and low therapeutic efficacy, especially at the chronic phase. The last clinical trials demonstrated that the first generation of azole compounds were less successful than BZ in CD chemotherapy, which stimulated studies of these compounds associated to BZ and nifurtimox (NF). This study evaluated the therapeutic efficacy of BZ, itraconazole (ITZ) and their combination (BZ + ITZ) in dogs infected with the VL-10 T. cruzi strain in the acute phase of the disease. Twenty young mongrel dogs were inoculated with 2.0 × 10<sup>3</sup> blood trypomastigotes/kg and divided into four groups: treated with BZ, ITZ and BZ + ITZ for 60 days, and control group (INT). The parasitemia of the BZ + ITZ and BZ groups were similar and showed significant reduction compared to the INT group. The group treated with ITZ also showed significant parasitemia reduction compared to the INT group. The global analysis of hemoculture (HC), blood PCR, conventional serology (CS-ELISA), heart qPCR and histopathology techniques, used in the post-treatment evaluation, revealed that BZ + ITZ combination lead to a more reduction of parasitemia during the acute phase and heart qPCR positivity, less cardiac damage (inflammation and fibrosis in the left ventricle) and total survival. According to the classical cure criteria one animal treated with BZ + ITZ can be considered cured in its final evaluation and two other dogs, one of this group and one treated with ITZ were in process of cure. At least for BZ-resistant T. cruzi strains such as VL-10, BZ + ITZ was not effective to induce parasitological cure or a profound and sustained reduction of the parasite burden in blood and infected organs. |
2,328,909 | Thoracoscopic epicardial left ventricular bipolar lead implantation with the use of automated titanium fasteners (Cor-Knot®).<Pagination><StartPage>121</StartPage><MedlinePgn>121</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">121</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1186/s13019-019-0945-4</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Pacemaker implantation techniques using thoracoscopy have been described since about 25 years. However, the published reports concerning types of electrodes refer mostly to monopolar screw-in leads. We report our experience of thoracoscopic implantation of a bipolar suture-on epicardial electrode with monofilamentous sutures tightened by automated fasteners to avoid hand-tied knots.</AbstractText><AbstractText Label="CASE PRESENTATION" NlmCategory="METHODS">A 69-year-old Caucasian female patient with a cardiac resynchronization therapy - defibrillator (CRT-D) due to dilated cardiomyopathy required the implantation of a supplementary left ventricluar resynchronization electrode. Because of unfavorable venous access, we chose a thoracoscopic approach. A bipolar suture-on epicardial electrode, was implanted by means of polypropylene monofilament 2-0 threads and automated titanium fasteners (Cor-Knot®). The intervention was uneventful. The correct function of the device was confirmed postoperatively and the patient was dismissed within 3 days from hospital. Six months after implantation the cardiologic control asserted regular device function and restitution of normal ejection fraction (EF 60%).</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">This case demonstrates the feasibility, safety and effectiveness of automated fasteners in the setting of thoracoscopic implantation of epicardial bipolar suture-on leads.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Schaeffer</LastName><ForeName>Thibault</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of cardiac surgery, University Hospital of Basel, Spitalstrasse 31, CH 4031, Basel, Switzerland. thibaultsch@hotmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mork</LastName><ForeName>Constantin</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of cardiac surgery, University Hospital of Basel, Spitalstrasse 31, CH 4031, Basel, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Erb</LastName><ForeName>Joachim</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of anesthesiology, University Hospital of Basel, Basel, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Reuthebuch</LastName><ForeName>Oliver</ForeName><Initials>O</Initials><AffiliationInfo><Affiliation>Department of cardiac surgery, University Hospital of Basel, Spitalstrasse 31, CH 4031, Basel, Switzerland.</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>2019</Year><Month>06</Month><Day>28</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Cardiothorac Surg</MedlineTA><NlmUniqueID>101265113</NlmUniqueID><ISSNLinking>1749-8090</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>D1JT611TNE</RegistryNumber><NameOfSubstance UI="D014025">Titanium</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D058406" MajorTopicYN="N">Cardiac Resynchronization Therapy</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="Y">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002311" MajorTopicYN="N">Cardiomyopathy, Dilated</DescriptorName><QualifierName UI="Q000628" MajorTopicYN="Y">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010138" MajorTopicYN="Y">Pacemaker, Artificial</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013536" MajorTopicYN="N">Suture Techniques</DescriptorName><QualifierName UI="Q000295" MajorTopicYN="Y">instrumentation</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013537" MajorTopicYN="N">Sutures</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013906" MajorTopicYN="N">Thoracoscopy</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="Y">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014025" MajorTopicYN="Y">Titanium</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Cor-knot</Keyword><Keyword MajorTopicYN="N">Epicardial pacemaker electrode</Keyword><Keyword MajorTopicYN="N">Thoracoscopy</Keyword></KeywordList><CoiStatement>The authors declare that they have no competing interests.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year><Month>4</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2019</Year><Month>6</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2019</Year><Month>6</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>6</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2019</Year><Month>11</Month><Day>12</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31253165</ArticleId><ArticleId IdType="pmc">PMC6599233</ArticleId><ArticleId IdType="doi">10.1186/s13019-019-0945-4</ArticleId><ArticleId IdType="pii">10.1186/s13019-019-0945-4</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Ely SW, Kron IL. 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Pacing Clin Electrophysiol. 2016;39(5):471–477. doi: 10.1111/pace.12836.</Citation><ArticleIdList><ArticleId IdType="doi">10.1111/pace.12836</ArticleId><ArticleId IdType="pubmed">26920816</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">31252392</PMID><DateRevised><Year>2019</Year><Month>06</Month><Day>28</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1933-0693</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2019</Year><Month>Jun</Month><Day>28</Day></PubDate></JournalIssue><Title>Journal of neurosurgery</Title><ISOAbbreviation>J Neurosurg</ISOAbbreviation></Journal>Development and evaluation of a patient-specific surgical simulator for endoscopic colloid cyst resection.<Pagination><StartPage>1</StartPage><EndPage>9</EndPage><MedlinePgn>1-9</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.3171/2019.4.JNS183184</ELocationID><ELocationID EIdType="pii" ValidYN="Y">2019.4.JNS183184</ELocationID><Abstract><AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">Endoscopic resection of third-ventricle colloid cysts is technically challenging due to the limited dexterity and visualization provided by neuroendoscopic instruments. Extensive training and experience are required to master the learning curve. To improve the education of neurosurgical trainees in this procedure, a synthetic surgical simulator was developed and its realism, procedural content, and utility as a training instrument were evaluated.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">The simulator was developed based on the neuroimaging (axial noncontrast CT and T1-weighted gadolinium-enhanced MRI) of an 8-year-old patient with a colloid cyst and hydrocephalus. Image segmentation, computer-aided design, rapid prototyping (3D printing), and silicone molding techniques were used to produce models of the skull, brain, ventricles, and colloid cyst. The cyst was filled with a viscous fluid and secured to the roof of the third ventricle. The choroid plexus and intraventricular veins were also included. Twenty-four neurosurgical trainees performed a simulated colloid cyst resection using a 30° angled endoscope, neuroendoscopic instruments, and image guidance. Using a 19-item feedback survey (5-point Likert scales), participants evaluated the simulator across 5 domains: anatomy, instrument handling, procedural content, perceived realism, and confidence and comfort level.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Participants found the simulator's anatomy to be highly realistic (mean 4.34 ± 0.63 [SD]) and appreciated the use of actual instruments (mean 4.38 ± 0.58). The procedural content was also rated highly (mean 4.28 ± 0.77); however, the perceived realism was rated slightly lower (mean 4.08 ± 0.63). Participants reported greater confidence in their ability to perform an endoscopic colloid cyst resection after using the simulator (mean 4.45 ± 0.68). Twenty-three participants (95.8%) indicated that they would use the simulator for additional training. Recommendations were made to develop complex case scenarios for experienced trainees (normal-sized ventricles, choroid plexus adherent to cyst wall, bleeding scenarios) and incorporate advanced instrumentation such as side-cutting aspiration devices.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">A patient-specific synthetic surgical simulator for training residents and fellows in endoscopic colloid cyst resection was successfully developed. The simulator's anatomy, instrument handling, and procedural content were found to be realistic. The simulator may serve as a valuable educational tool to learn the critical steps of endoscopic colloid cyst resection, develop a detailed understanding of intraventricular anatomy, and gain proficiency with bimanual neuroendoscopic techniques.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Bodani</LastName><ForeName>Vivek P</ForeName><Initials>VP</Initials><AffiliationInfo><Affiliation>1Center for Image Guided Innovation and Therapeutic Intervention, The Hospital for Sick Children, Toronto.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>2Division of Neurosurgery, Department of Surgery, and.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>3Institute of Biomaterials and Biomedical Engineering, University of Toronto; and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Breimer</LastName><ForeName>Gerben E</ForeName><Initials>GE</Initials><AffiliationInfo><Affiliation>1Center for Image Guided Innovation and Therapeutic Intervention, The Hospital for Sick Children, Toronto.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Haji</LastName><ForeName>Faizal A</ForeName><Initials>FA</Initials><AffiliationInfo><Affiliation>4Division of Clinical Neurological Sciences, Western University, London, Ontario, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Looi</LastName><ForeName>Thomas</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>1Center for Image Guided Innovation and Therapeutic Intervention, The Hospital for Sick Children, Toronto.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>3Institute of Biomaterials and Biomedical Engineering, University of Toronto; and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Drake</LastName><ForeName>James M</ForeName><Initials>JM</Initials><AffiliationInfo><Affiliation>1Center for Image Guided Innovation and Therapeutic Intervention, The Hospital for Sick Children, Toronto.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>2Division of Neurosurgery, Department of Surgery, and.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>3Institute of Biomaterials and Biomedical Engineering, University of Toronto; and.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2019</Year><Month>06</Month><Day>28</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Neurosurg</MedlineTA><NlmUniqueID>0253357</NlmUniqueID><ISSNLinking>0022-3085</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">CAD = Canadian dollars</Keyword><Keyword MajorTopicYN="N">EM = electromagnetic</Keyword><Keyword MajorTopicYN="N">IQR = interquartile range</Keyword><Keyword MajorTopicYN="N">PGY = postgraduate year</Keyword><Keyword MajorTopicYN="N">VR = virtual reality</Keyword><Keyword MajorTopicYN="N">colloid cysts</Keyword><Keyword MajorTopicYN="N">hydrocephalus</Keyword><Keyword MajorTopicYN="N">medical education</Keyword><Keyword MajorTopicYN="N">neuroendoscopy</Keyword><Keyword MajorTopicYN="N">simulation training</Keyword><Keyword MajorTopicYN="N">surgical technique</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2018</Year><Month>11</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2019</Year><Month>4</Month><Day>11</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2019</Year><Month>6</Month><Day>29</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>6</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2019</Year><Month>6</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>aheadofprint</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31252392</ArticleId><ArticleId IdType="doi">10.3171/2019.4.JNS183184</ArticleId><ArticleId IdType="pii">2019.4.JNS183184</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">31252383</PMID><DateRevised><Year>2019</Year><Month>06</Month><Day>28</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1933-0715</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2019</Year><Month>Jun</Month><Day>28</Day></PubDate></JournalIssue><Title>Journal of neurosurgery. Pediatrics</Title><ISOAbbreviation>J Neurosurg Pediatr</ISOAbbreviation></Journal>Using a burr hole valve prevents proximal shunt failure in infants and toddlers. | Pacemaker implantation techniques using thoracoscopy have been described since about 25 years. However, the published reports concerning types of electrodes refer mostly to monopolar screw-in leads. We report our experience of thoracoscopic implantation of a bipolar suture-on epicardial electrode with monofilamentous sutures tightened by automated fasteners to avoid hand-tied knots.</AbstractText>A 69-year-old Caucasian female patient with a cardiac resynchronization therapy - defibrillator (CRT-D) due to dilated cardiomyopathy required the implantation of a supplementary left ventricluar resynchronization electrode. Because of unfavorable venous access, we chose a thoracoscopic approach. A bipolar suture-on epicardial electrode, was implanted by means of polypropylene monofilament 2-0 threads and automated titanium fasteners (Cor-Knot®). The intervention was uneventful. The correct function of the device was confirmed postoperatively and the patient was dismissed within 3 days from hospital. Six months after implantation the cardiologic control asserted regular device function and restitution of normal ejection fraction (EF 60%).</AbstractText>This case demonstrates the feasibility, safety and effectiveness of automated fasteners in the setting of thoracoscopic implantation of epicardial bipolar suture-on leads.</AbstractText> |
2,328,910 | Shunt independence in paediatric hydrocephalus: our 16-year experience and review. | Shunt independence remains a matter of debate for neurosurgeons, and little information on this subject is available in the literature. The aims of the study were to analyse the incidence of shunt removal in a series of paediatric patients and to describe our experience with attempts at shunt removal.</AbstractText>Thirty of 212 paediatric patients shunted between 2000 and 2016 at our institution were studied for shunt independence. Variables related to hydrocephalus aetiology, shunt complications, independence trial peculiarities and follow-up were recorded and a descriptive analysis of the data was performed.</AbstractText>Two patients (0.94%) refused to be included in a shunt independence trial and were analysed separately. In the other 28 patients, 29 shunt independence trials were performed, of which 19 (65.52%) were successful, giving a global rate of shunt independence of 8.96% (19/212) in our population. Secondary endoscopic third ventriculostomy was the most frequent type of independence trial and achieved the highest success rate (75%). Spontaneous independence was achieved in just 4/7 cases (57.14%). Planned removal of the shunt in overdrainage cases had a 50% success rate, with transient measures to control intracranial pressure frequently required.</AbstractText>Shunt independence trials should be considered for selected patients in a closely monitored setting. Secondary endoscopic third ventriculostomy at the time of shunt malfunction has the highest success rate whereas planned removal of the shunt in overdrainage is an invasive procedure with more likelihood of failure. Shunt independence should not be presumed.</AbstractText> |
2,328,911 | A simulation study of left ventricular decompression using a double lumen arterial cannula prototype during a veno-arterial extracorporeal membrane oxygenation. | Veno-arterial extracorporeal membrane oxygenation can be vital to support patients in severe or rapidly progressing cardiogenic shock. In cases of left ventricular distension, left ventricular decompression during veno-arterial extracorporeal membrane oxygenation may be a crucial factor influencing the patient outcome. Application of a double lumen arterial cannula for a left ventricular unloading is an alternative, straightforward method for left ventricular decompression during extracorporeal membrane oxygenation in a veno-arterial configuration.</AbstractText>The purpose of this article is to use a mathematical model of the human adult cardiovascular system to analyze the left ventricular function of a patient in cardiogenic shock supported by veno-arterial extracorporeal membrane oxygenation with and without the application of left ventricular unloading using a novel double lumen arterial cannula.</AbstractText>A lumped model of cardiovascular system hydraulics has been coupled with models of non-pulsatile veno-arterial extracorporeal membrane oxygenation, a standard venous cannula, and a drainage lumen of a double lumen arterial cannula. Cardiogenic shock has been induced by decreasing left ventricular contractility to 10% of baseline normal value.</AbstractText>The simulation results indicate that applying double lumen arterial cannula during veno-arterial extracorporeal membrane oxygenation is associated with reduction of left ventricular end-systolic volume, end-diastolic volume, end-systolic pressure, and end-diastolic pressure.</AbstractText>A double lumen arterial cannula is a viable alternative less invasive method for left ventricular decompression during veno-arterial extracorporeal membrane oxygenation. However, to allow for satisfactory extracorporeal membrane oxygenation flow, the cannula design has to be revisited.</AbstractText> |
2,328,912 | Cardiac disease is linked to adiposity in male gorillas (Gorilla gorilla gorilla). | Cardiac disease is a major cause of morbidity and mortality for adult gorillas. Previous research indicates a sex-based difference with predominantly males demonstrating evidence of left ventricular hypertrophy. To evaluate these findings, we analyzed serum markers with cardiac measures in a large sample of gorillas. The study sample included 44 male and 25 female gorillas housed at American Association of Zoo and Aquariums (AZA)-accredited zoos. Serum samples were collected from fasted gorillas during routine veterinary health exams and analyzed to measure leptin, adiponectin, IGF-1, insulin, ferritin, glucose, triglycerides, and cholesterol. Cardiac ultrasonography via transthoracic echocardiogram was performed simultaneously. Three echocardiographic parameters were chosen to assess cardiac disease according to parameters established for captive lowland gorillas: left ventricular internal diameter, inter-ventricular septum thickness, and left ventricular posterior wall thickness. Our data revealed that high leptin, low adiponectin, and lowered cholesterol were significantly and positively correlated with measures of heart thickness and age in males but not in females. Lowered cholesterol in this population would be categorized as elevated in humans. High leptin and low adiponectin are indicative of increased adiposity and suggests a potential parallel with human obesity and cardiovascular disease in males. Interestingly, while females exhibited increased adiposity with age, they did not progress to cardiac disease. |
2,328,913 | The impact of nine weeks swimming exercise on heart function in hypertensive and normotensive rats: role of cardiac oxidative stress. | The purpose of this study was to estimate the effects of 9-week swimming training on cardiodynamic parameters and coronary flow in a rat model of high salt-induced hypertension with a special focus on the role of oxidative stress.</AbstractText>Rats involved in the research were divided randomly into four groups: healthy sedentary (SA), healthy trained (TA), sedentary hypertensive (SHA) and trained hypertensive animals (THA). Trained rats were exposed to 9-week swimming training (5 days/week, 60 min/day). Additionally, in order to induce hypertension animals from SHA and THA groups were on high sodium (8% NaCl solution) diet during 4 weeks. Afterwards all rats were sacrificed and hearts were isolated and retrogradely perfused according to Langendorff technique. The following parameters of cardiac function were continuously recorded: maximum and minimum rate of pressure development in left ventricle, systolic and diastolic left ventricular pressure and heart rate. Coronary flow was measured flowmetrically. Oxidative stress markers were determined in coronary venous effluent.</AbstractText>Our findings demonstrated that 9 weeks of swimming training led to improvement of cardiac contractility, relaxation and systolic capacity of normotensive rats, while this training protocol induced enhanced diastolic function in hypertensive conditions. More pronounced effects of exercise in alleviating oxidative stress were observed in hypertensive rats.</AbstractText>Obvious beneficial exercise-induced cardiac adaptations provide scientific basis for further researches which would thoroughly clarify the mechanisms through which swimming training alters myocardial function both in healthy conditions and in the presence of chronic diseases.</AbstractText> |
2,328,914 | Calaxin is required for cilia-driven determination of vertebrate laterality. | Calaxin is a Ca<sup>2+</sup>-binding dynein-associated protein that regulates flagellar and ciliary movement. In ascidians, calaxin plays essential roles in chemotaxis of sperm. However, nothing has been known for the function of calaxin in vertebrates. Here we show that the mice with a null mutation in <i>Efcab1</i>, which encodes calaxin, display typical phenotypes of primary ciliary dyskinesia, including hydrocephalus, <i>situs inversus</i>, and abnormal motility of trachea cilia and sperm flagella. Strikingly, both males and females are viable and fertile, indicating that calaxin is not essential for fertilization in mice. The 9 + 2 axonemal structures of epithelial multicilia and sperm flagella are normal, but the formation of 9 + 0 nodal cilia is significantly disrupted. Knockout of calaxin in zebrafish also causes <i>situs inversus</i> due to the irregular ciliary beating of Kupffer's vesicle cilia, although the 9 + 2 axonemal structure appears to remain normal. |
2,328,915 | Splenic Blood Flow Increases after Hypothermic Stimulus (Cold Pressor Test): A Perfusion Magnetic Resonance Study. | The Cold Pressor Test (CPT) is a novel diagnostic strategy to noninvasively assess the myocardial microvascular endothelial-dependent function using perfusion magnetic resonance imaging (MRI). Spleen perfusion is modulated by a complex combination of several mechanisms involving the autonomic nervous system and vasoactive mediators release. In this context, the effects of cold temperature on splenic blood flow (SBF) still need to be clarified. Ten healthy subjects were studied by MRI. MRI protocol included the acquisition of GRE T1-weighted sequence ("first pass perfusion") during gadolinium administration (0.1mmol/kg of Gd-DOTA at flow of 3.0 ml/s), at rest and after CPT. Myocardial blood flow (MBF) and SBF were measured by applying Fermi function deconvolution, using the blood pool input function sampled from the left ventricle cavity. MBF and SBF values after performing CPT were significantly higher than rest values (SBF at rest: 0.65 ± 0.15 ml/min/g Vs. SBF after CPT: 0.90 ± 0.14 ml/min/g, p: <0.001; MBF at rest: 0.90 ± 0.068 ml/min/g Vs. MBF after CPT: 1.22 ± 0.098 ml/min/g, p<0.005). Both SBF and MBF increased in all patients during the CPT. In particular, the CPT-induced increase was 43% ± 29% for SBF and 36.5% ± 17% for MBF. CPT increases SBF in normal subjects. The characterization of a standard perfusion response to cold might allow the use of the spleen as reference marker for the adequacy of cold stimulation during myocardial perfusion MRI. |
2,328,916 | Proteolytic Rafts for Improving Intraparenchymal Migration of Minimally Invasively Administered Hydrogel-Embedded Stem Cells. | The physiological spaces (lateral ventricles, intrathecal space) or pathological cavities (stroke lesion, syringomyelia) may serve as an attractive gateway for minimally invasive deployment of stem cells. Embedding stem cells in injectable scaffolds is essential when transplanting into the body cavities as they secure favorable microenvironment and keep cells localized, thereby preventing sedimentation. However, the limited migration of transplanted cells from scaffold to the host tissue is still a major obstacle, which prevents this approach from wider implementation for the rapidly growing field of regenerative medicine. Hyaluronan, a naturally occurring polymer, is frequently used as a basis of injectable scaffolds. We hypothesized that supplementation of hyaluronan with activated proteolytic enzymes could be a viable approach for dissolving the connective tissue barrier on the interface between the scaffold and the host, such as pia mater or scar tissue, thus demarcating lesion cavity. In a proof-of-concept study, we have found that collagenase and trypsin immobilized in hyaluronan-based hydrogel retain 60% and 28% of their proteolytic activity compared to their non-immobilized forms, respectively. We have also shown that immobilized enzymes do not have a negative effect on the viability of stem cells (glial progenitors and mesenchymal stem cells) in vitro. In conclusion, proteolytic rafts composed of hyaluronan-based hydrogels and immobilized enzymes may be an attractive strategy to facilitate migration of stem cells from injectable scaffolds into the parenchyma of surrounding tissue. |
2,328,917 | Interhemispheric Transcallosal Transforaminal Approach and Microscopic Third Ventriculostomy for Intraventricular Craniopharyngioma Associated with Asymmetric Hydrocephalus: Case Report and Literature Review. | We report on a case of a solid adamantinomatous variant of craniopharyngioma located entirely within the third ventricle causing asymmetric obstructive hydrocephalus in a 43-year-old male patient. The patient complaints included intermittent severe headache and progressive bilateral visual field loss. Initially, the lesion was accessed via the bifrontal interhemispheric translamina terminalis approach but total removal was not possible due to short anterior communicating artery which limited the exposure. In the second stage, we used the right interhemispheric transcallosal transforaminal approach and achieved total tumor removal followed by microscopic third ventriculostomy. The present article discusses the selection of appropriate surgical approach based on concise literature review that provides favorable surgical management of these rare lesions. |
2,328,918 | Pathological and molecular studies on Coxsackie virus A-16 isolated from hand, foot, and mouth disease cases in India: Approach using neonatal mouse model. | The present study highlights pathogenesis and molecular aspects of Coxsackie virus A-16 (CVA-16) strains isolated from hand, foot, and mouth disease (HFMD) cases from India using a neonatal mice model. ICR mice were intraperitoneally inoculated with CVA-16/311 strain isolated from HFMD cases. Mice developed hind and forelimb paralysis on day 3 of post infection. Histopathological observations of hind limb muscles showed necrosis, dissolution of muscle fiber cells, infiltration of inflammatory cells, marked dilated ventricle, hemorrhages, and neuronal degeneration in the brain. Immunohistochemical studies revealed high expression of CVA-16/311-specific viral antigen in limb muscles, brain, heart from day 3 till day 7 of post-infection. VP1 gene-based reverse transcription polymerase chain reaction conducted in RNA samples of different tissue organs of infected mice followed by sequencing of the positive amplimers revealed presence of CVA-16/311-specific viral sequences. Phylogenetic analysis based on the VP1 gene showed the presence of B1c sub genotype of CVA-16/311 strain in targeted tissue organs. Sequence analysis revealed major genetic changes in heart, skeletal muscle tissues at the nucleotide and amino acid levels. Genetic changes occurred in organs of mice might predict some potential targets and might act as markers of virulence for neuronal tropism. Pathogenesis and molecular studies of CVA-16 strains isolated from HFMD cases using neonatal mice model was conducted for the first time from India. |
2,328,919 | Multiple ventricular bands and the associated trabecula septomarginalis dextra in the right ventricle of the domestic dog (Canis familiaris). | Ventricular bands are strand-like intraventricular structures extending between adjacent papillary muscles; a papillary muscle and the ventricular wall or the interventricular septum and ventricular wall. Examination of the domestic dog right ventricle documented six ventricular band types. Eighty-five of the 89 examined hearts had at least one right ventricular band. In the current study, the right ventricle of the 85 dog hearts was re-examined for more than one ventricular band type. Seven patterns of multiple different bands were identified in the 24 dog hearts. The patterns (i.e., combinations) of different ventricular bands were grouped into three categories. Category 1 had five different patterns of bands. Each pattern had two different band types. Category 2 had one combination of three different bands. Category 3 had one combination of four different bands. The presence of right ventricular bands around the trabecula septomarginalis dextra was also documented. All 24 dog hearts with multiple ventricular bands had a trabecula septomarginalis dextra. The main goal of this study was documentation of multiple right ventricular band patterns. A secondary goal was documentation of the combined presence of these bands and a trabecula septomarginalis dextra. In the dog, the ventricular bands and trabecula are both thin, strand-like intraventricular structures with variable branching patterns before blending into the ventricular wall. The gross similarity of these structures and lack of information on their combined presence could precipitate their misidentification. |
2,328,920 | Septo-optic dysplasia caused by a novel FLNA splice site mutation: a case report. | Septo-optic dysplasia (SOD), also known as de-Morsier syndrome, is a rare disorder characterized by any combination of optic nerve hypoplasia, pituitary gland hypoplasia, and midline abnormalities of the brain including absence of the septum pellucidum and corpus callosum dysgenesis. The variable presentation of SOD includes visual, neurologic, and/or hypothalamic-pituitary endocrine defects. The unclear aetiology of a large proportion of SOD cases underscores the importance of identifying novel SOD-associated genes.</AbstractText>To identify the disease-causing gene in a male infant with neonatal hypoglycaemia, dysmorphic features, and hypoplasia of the optic nerve and corpus callosum, we designed a targeted next-generation sequencing panel for brain morphogenesis defects. We identified a novel hemizygous deletion, c.6355 + 4_6355 + 5delAG, in intron 38 of the FLNA gene that the patient had inherited from his mother. cDNA studies showed that this variant results in the production of 3 aberrant FLNA transcripts, the most abundant of which results in retention of intron 38 of FLNA.</AbstractText>We report for the first time a case of early-onset SOD associated with a mutation in the FLNA gene. This finding broadens the spectrum of genetic causes of this rare disorder and expands the phenotypic spectrum of the FLNA gene.</AbstractText> |
2,328,921 | Characterizing a perfusion-based periventricular small vessel region of interest. | The periventricular white matter (PVWM) is supplied by terminal distributions of small vessels and is particularly susceptible to developing white matter lesions (WML) associated with cerebral small vessel disease (CSVD). We obtained group-averaged cerebral blood flow (CBF) maps from Arterial Spin Labeled (ASL) perfusion MRI data obtained in 436 middle-aged (50.4 ± 3.5 years) subjects in the NHLBI CARDIA study and in 61 elderly (73.3 ± 6.9 years) cognitively normal subjects recruited from the Penn Alzheimer's Disease Center (ADC) and found that the lowest perfused brain voxels are located within the PVWM. We constructed a white matter periventricular small vessel (PSV) region of interest (ROI) by empirically thresholding the group averaged CARDIA CBF map at CBF < 15 ml/100 g/min. Thereafter we compared CBF in the PSV ROI and in the remaining white matter (RWM) with the location and volume of WML measured with Fluid Attenuated Inversion Recovery (FLAIR) MRI. WM CBF was lower within WML than outside WML voxels (p < <0.0001) in both the PSV and RWM ROIs, however this difference was much smaller (p < <0.0001) in the PSV ROI than in the RWM suggesting a more homogenous reduction of CBF in the PSV region. Normalized WML volumes were significantly higher in the PSV ROI than in the RWM and in the elderly cohort as compared to the middle-aged cohort (p < <0.0001). Additionally, the PSV ROI showed a significantly (p = .001) greater increase in lesion volume than the RWM in the elderly ADC cohort than the younger CARDIA cohort. Considerable intersubject variability in PSV CBF observed in both study cohorts likely represents biological variability that may be predictive of future WML and/or cognitive decline. In conclusion, a data-driven PSV ROI defined by voxels with low perfusion in middle age defines a region with homogeneously reduced CBF that is particularly susceptible to progressive ischemic injury in elderly controls. PSV CBF may provide a mechanistically specific biomarker of CSVD. |
2,328,922 | Thrombus straddling a patent foramen ovale and massive pulmonary embolism: Venous arterial extracorporeal membrane oxygenation as a valuable support tool.<Pagination><StartPage>867</StartPage><EndPage>870</EndPage><MedlinePgn>867-870</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1111/jocs.14123</ELocationID><Abstract><AbstractText>Thrombus straddling a patent foramen ovale and massive pulmonary embolism is a very rare and life-threatening condition. Optimal management can be controversial because different therapeutic options are available and individual approach based in individual risk is needed. We present a case of a thrombus straddling the patent foramen ovale with massive pulmonary embolism, hemodynamic instability, and upper extremity embolism. We performed surgical pulmonary embolectomy, and venous arterial extracorporeal membrane oxygenation was needed to successfully overcome severe right ventricular impairment and pulmonary injury.</AbstractText><CopyrightInformation>© 2019 Wiley Periodicals, Inc.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ayaon Albarrán</LastName><ForeName>Ali</ForeName><Initials>A</Initials><Identifier Source="ORCID">0000-0003-4879-077X</Identifier><AffiliationInfo><Affiliation>Adult Cardiac Surgery Department, La Paz University Hospital, Madrid, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pérez Chulia</LastName><ForeName>Nuria</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Anesthesiology Department, Division of Cardiothoracic Anesthesia, La Paz University Hospital, Madrid, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Meca Aguirrezabalaga</LastName><ForeName>Juan</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Adult Cardiac Surgery Department, La Paz University Hospital, Madrid, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Blázquez González</LastName><ForeName>José Antonio</ForeName><Initials>JA</Initials><AffiliationInfo><Affiliation>Adult Cardiac Surgery Department, La Paz University Hospital, Madrid, Spain.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2019</Year><Month>06</Month><Day>24</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Card Surg</MedlineTA><NlmUniqueID>8908809</NlmUniqueID><ISSNLinking>0886-0440</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006348" MajorTopicYN="N">Cardiac Surgical Procedures</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="Y">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004452" MajorTopicYN="N">Echocardiography</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017548" MajorTopicYN="N">Echocardiography, Transesophageal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017128" MajorTopicYN="N">Embolectomy</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="Y">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015199" MajorTopicYN="N">Extracorporeal Membrane Oxygenation</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="Y">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D054092" MajorTopicYN="N">Foramen Ovale, Patent</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="Y">complications</QualifierName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006331" MajorTopicYN="N">Heart Diseases</DescriptorName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="Y">Heart Ventricles</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011655" MajorTopicYN="N">Pulmonary Embolism</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="Y">complications</QualifierName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013927" MajorTopicYN="N">Thrombosis</DescriptorName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014057" MajorTopicYN="N">Tomography, X-Ray Computed</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">massive pulmonary embolism</Keyword><Keyword MajorTopicYN="N">patent foramen ovale</Keyword><Keyword MajorTopicYN="N">thrombus</Keyword><Keyword MajorTopicYN="N">venous arterial extracorporeal membrane oxygenation</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year><Month>4</Month><Day>21</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2019</Year><Month>5</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2019</Year><Month>5</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>6</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>2</Month><Day>11</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2019</Year><Month>6</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31233236</ArticleId><ArticleId IdType="doi">10.1111/jocs.14123</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">31233017</PMID><DateCompleted><Year>2020</Year><Month>06</Month><Day>10</Day></DateCompleted><DateRevised><Year>2022</Year><Month>05</Month><Day>18</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1940-087X</ISSN><JournalIssue CitedMedium="Internet"><Issue>148</Issue><PubDate><Year>2019</Year><Month>Jun</Month><Day>04</Day></PubDate></JournalIssue><Title>Journal of visualized experiments : JoVE</Title><ISOAbbreviation>J Vis Exp</ISOAbbreviation></Journal>High-Throughput Analysis of Optical Mapping Data Using ElectroMap. | Thrombus straddling a patent foramen ovale and massive pulmonary embolism is a very rare and life-threatening condition. Optimal management can be controversial because different therapeutic options are available and individual approach based in individual risk is needed. We present a case of a thrombus straddling the patent foramen ovale with massive pulmonary embolism, hemodynamic instability, and upper extremity embolism. We performed surgical pulmonary embolectomy, and venous arterial extracorporeal membrane oxygenation was needed to successfully overcome severe right ventricular impairment and pulmonary injury.<CopyrightInformation>© 2019 Wiley Periodicals, Inc.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ayaon Albarrán</LastName><ForeName>Ali</ForeName><Initials>A</Initials><Identifier Source="ORCID">0000-0003-4879-077X</Identifier><AffiliationInfo><Affiliation>Adult Cardiac Surgery Department, La Paz University Hospital, Madrid, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pérez Chulia</LastName><ForeName>Nuria</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Anesthesiology Department, Division of Cardiothoracic Anesthesia, La Paz University Hospital, Madrid, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Meca Aguirrezabalaga</LastName><ForeName>Juan</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Adult Cardiac Surgery Department, La Paz University Hospital, Madrid, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Blázquez González</LastName><ForeName>José Antonio</ForeName><Initials>JA</Initials><AffiliationInfo><Affiliation>Adult Cardiac Surgery Department, La Paz University Hospital, Madrid, Spain.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2019</Year><Month>06</Month><Day>24</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Card Surg</MedlineTA><NlmUniqueID>8908809</NlmUniqueID><ISSNLinking>0886-0440</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006348" MajorTopicYN="N">Cardiac Surgical Procedures</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="Y">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004452" MajorTopicYN="N">Echocardiography</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017548" MajorTopicYN="N">Echocardiography, Transesophageal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017128" MajorTopicYN="N">Embolectomy</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="Y">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015199" MajorTopicYN="N">Extracorporeal Membrane Oxygenation</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="Y">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D054092" MajorTopicYN="N">Foramen Ovale, Patent</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="Y">complications</QualifierName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006331" MajorTopicYN="N">Heart Diseases</DescriptorName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="Y">Heart Ventricles</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011655" MajorTopicYN="N">Pulmonary Embolism</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="Y">complications</QualifierName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013927" MajorTopicYN="N">Thrombosis</DescriptorName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014057" MajorTopicYN="N">Tomography, X-Ray Computed</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">massive pulmonary embolism</Keyword><Keyword MajorTopicYN="N">patent foramen ovale</Keyword><Keyword MajorTopicYN="N">thrombus</Keyword><Keyword MajorTopicYN="N">venous arterial extracorporeal membrane oxygenation</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year><Month>4</Month><Day>21</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2019</Year><Month>5</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2019</Year><Month>5</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>6</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>2</Month><Day>11</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2019</Year><Month>6</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31233236</ArticleId><ArticleId IdType="doi">10.1111/jocs.14123</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">31233017</PMID><DateCompleted><Year>2020</Year><Month>06</Month><Day>10</Day></DateCompleted><DateRevised><Year>2022</Year><Month>05</Month><Day>18</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1940-087X</ISSN><JournalIssue CitedMedium="Internet"><Issue>148</Issue><PubDate><Year>2019</Year><Month>Jun</Month><Day>04</Day></PubDate></JournalIssue><Title>Journal of visualized experiments : JoVE</Title><ISOAbbreviation>J Vis Exp</ISOAbbreviation></Journal><ArticleTitle>High-Throughput Analysis of Optical Mapping Data Using ElectroMap.</ArticleTitle><ELocationID EIdType="doi" ValidYN="Y">10.3791/59663</ELocationID><Abstract>Optical mapping is an established technique for high spatio-temporal resolution study of cardiac electrophysiology in multi-cellular preparations. Here we present, in a step-by-step guide, the use of ElectroMap for analysis, quantification, and mapping of high-resolution voltage and calcium datasets acquired by optical mapping. ElectroMap analysis options cover a wide variety of key electrophysiological parameters, and the graphical user interface allows straightforward modification of pre-processing and parameter definitions, making ElectroMap applicable to a wide range of experimental models. We show how built-in pacing frequency detection and signal segmentation allows high-throughput analysis of entire experimental recordings, acute responses, and single beat-to-beat variability. Additionally, ElectroMap incorporates automated multi-beat averaging to improve signal quality of noisy datasets, and here we demonstrate how this feature can help elucidate electrophysiological changes that might otherwise go undetected when using single beat analysis. Custom modules are included within the software for detailed investigation of conduction, single file analysis, and alternans, as demonstrated here. This software platform can be used to enable and accelerate the processing, analysis, and mapping of complex cardiac electrophysiology. |
2,328,923 | Pretreatment with vildagliptin boosts ischemic-postconditioning effects on cardioprotection and expression profile of genes regulating autophagy and mitochondrial fission/fusion in diabetic heart with reperfusion injury. | The burden of myocardial ischemia/reperfusion (IR) injury is 2-3-folds higher in diabetic patients, so protecting diabetic hearts is clinically important. Here, we investigated the effect of combinational therapy with vildagliptin and ischemic postconditioning (IPostC) on cardioprotection and the expression of genes regulating autophagy and mitochondrial function in diabetic hearts with IR injury. Type 2 diabetes was induced through high-fat diet and streptozotocin protocol in Wistar rats. Vildagliptin was orally administered to diabetic rats 5 weeks before IR injury. Myocardial-IR injury was modeled by ligation of left the coronary artery for 30 min followed by 60-min reperfusion, on a Langendorff-perfusion system. IPostC was applied at early reperfusion as 6 alternative cycles of 10-s reperfusion/ischemia. Creatine-kinase levels were measured spectrometrically, and infarct size was evaluated by TTC staining method. Left ventricles were harvested for assessing the expression levels of autophagy and mitochondrial-related genes using real-time PCR. Induction of diabetes significantly increased creatine-kinase release in comparison to healthy rats, and all treatments significantly reduced the release of enzyme toward control levels (P < 0.05). Only the combination therapy (IPostC + vildagliptin) could significantly reduce the infarct size of diabetic hearts as compared to untreated diabetic-IR group (P < 0.01). The levels of autophagy genes LC3 and p62 were significantly higher in diabetic groups than healthy ones. Induction of IR injury in diabetic hearts enhanced mitochondrial fission (drp-1) and reduced mitochondrial fusion (mfn1 and mfn2) genes. IPostC alone had no significant effect on the gene expression and vildagliptin alone could only affect LC3-II and mfn2 expressions. Nevertheless, administration of combination therapy significantly reduced the expression of both autophagy genes and increased both LC3-II/I and mfn2/1 ratios as compared with diabetic-IR hearts (P < 0.01-0.05). Application of this combination therapy could overcome the diabetes-induced failure of cardioprotection by individual treatments and improve mitochondrial dynamic and autophagy flux. |
2,328,924 | Prostaglandin E<sub>2</sub> and an EP4 receptor agonist inhibit LPS-Induced monocyte chemotactic protein 5 production and secretion in mouse cardiac fibroblasts via Akt and NF-κB signaling. | Prostaglandin E2 (PGE2</sub>) signals through 4 separate G-protein coupled receptor sub-types to elicit a variety of physiologic and pathophysiological effects. We have previously reported that mice lacking the EP4 receptor in the cardiomyocytes develop heart failure with a phenotype of dilated cardiomyopathy. Also, these mice have increased levels of chemokines, like MCP-5, in their left ventricles. We have recently reported that overexpression of the EP4 receptor could improve cardiac function in the myocardial infarction model. Furthermore, we showed that overexpression of EP4 had an anti-inflammatory effect in the whole left ventricle. It has also been shown that PGE2</sub> can antagonize lipopolysaccharide-induced secretion of chemokines/cytokines in various cell types. We therefore hypothesized that PGE2</sub> inhibits lipopolysaccharide (LPS)-induced MCP-5 secretion in adult mouse cardiac fibroblasts via its EP4 receptor.</AbstractText>Our hypothesis was tested using isolated mouse adult ventricular fibroblasts (AVF) treated with LPS. Pre-treatment of the cells with PGE2</sub> and the EP4 agonist CAY10598 resulted in reductions of the pro-inflammatory response induced by LPS. Specifically, we observed reductions in MCP-5 secretion. Western blot analysis showed reductions in phosphorylated Akt and IκBα indicating reduced NF-κB activation. The anti-inflammatory effects of PGE2</sub> and EP4 agonist signaling appeared to be independent of cAMP, p-44/42, or p38 pathways.</AbstractText>Exogenous treatment of PGE2</sub> and the EP4 receptor agonist blocked the pro-inflammatory actions of LPS. Mechanistically, this was mediated via reduced Akt phosphorylation and inhibition of NF-κB.</AbstractText>Copyright © 2019 Elsevier Inc. All rights reserved.</CopyrightInformation> |
2,328,925 | Risperidone administered during adolescence induced metabolic, anatomical and inflammatory/oxidative changes in adult brain: A PET and MRI study in the maternal immune stimulation animal model. | Inflammation and oxidative stress (IOS) are considered key pathophysiological elements in the development of mental disorders. Recent studies demonstrated that the antipsychotic risperidone elicits an antiinflammatory effect in the brain. We administered risperidone for 2-weeks at adolescence to assess its role in preventing brain-related IOS changes in the maternal immune stimulation (MIS) model at adulthood. We also investigated the development of volumetric and neurotrophic abnormalities in areas related to the HPA-axis. Poly I:C (MIS) or saline (Sal) were injected into pregnant Wistar rats on GD15. Male offspring received risperidone or vehicle daily from PND35-PND49. We studied 4 groups (8-15 animals/group): Sal-vehicle, MIS-vehicle, Sal-risperidone and MIS-risperidone. [<sup>18</sup>F]FDG-PET and MRI studies were performed at adulthood and analyzed using SPM12 software. IOS and neurotrophic markers were measured using WB and ELISA assays in brain tissue. Risperidone elicited a protective function of schizophrenia-related IOS deficits. In particular, risperidone elicited the following effects: reduced volume in the ventricles and the pituitary gland; reduced glucose metabolism in the cerebellum, periaqueductal gray matter, and parietal cortex; higher FDG uptake in the cingulate cortex, hippocampus, thalamus, and brainstem; reduced NFκB activity and iNOS expression; and increased enzymatic activity of CAT and SOD in some brain areas. Our study suggests that some schizophrenia-related IOS changes can be prevented in the MIS model. It also stresses the need to search for novel strategies based on anti-inflammatory compounds in risk populations at early stages in order to alter the course of the disease. |
2,328,926 | Dickkopf-1 blocks 17β-estradiol-enhanced object memory consolidation in ovariectomized female mice. | The memory-enhancing effects of 17β-estradiol (E<sub>2</sub>) depend upon rapid activation of several cell-signaling cascades within the dorsal hippocampus (DH). Among the many cell-signaling pathways that mediate memory processes, Wnt/β-catenin signaling has emerged as a potential key player because of its importance to hippocampal development and synaptic plasticity. However, whether E<sub>2</sub> interacts with Wnt/β-catenin signaling to promote memory consolidation is unknown. Therefore, the present study examined whether Wnt/β-catenin signaling within the DH is necessary for E<sub>2</sub>-induced memory consolidation in ovariectomized mice tested in the object recognition and object placement tasks. Ovariectomized C57BL/6 mice received immediate post-training infusions of E<sub>2</sub> or vehicle into the dorsal third ventricle plus the endogenous Wnt/β-catenin antagonist Dickkopf-1 (Dkk-1) or vehicle into the DH to assess whether the memory-enhancing effects of E<sub>2</sub> depend on activation of Wnt/β-catenin signaling. Our results suggest that Dkk-1 blocks E<sub>2</sub>-induced memory enhancement as hypothesized, but may do so by only moderately blunting Wnt/β-catenin signaling while concurrently activating Wnt/JNK signaling. The current study provides novel insights into the mechanisms through which E<sub>2</sub> enhances memory consolidation in the DH, as well as critical information about the mechanistic actions of Dkk-1. |
2,328,927 | Chiari type I and hydrocephalus. | The association between Chiari type I malformation (CIM) and hydrocephalus raises a great interest because of the still unclear pathogenesis and the management implications. The goal of this paper is to review the theories on the cause-effect mechanisms of such a relationship and to analyze the results of the management of this condition.</AbstractText>A review of the literature has been performed, focusing on the articles specifically addressing the problem of CIM and hydrocephalus and on the series reporting about its treatment. Also, the personal authors' experience is briefly discussed.</AbstractText>As far as the pathogenesis is concerned, it seems clear that raised intracranial pressure due to hydrocephalus can cause a transient and reversible tonsillar caudal ectopia ("pressure from above" hypothesis), which is something different from CIM. A "complex" hypothesis, on the other hand, can explain the occurrence of hydrocephalus and CIM because of the venous engorgement resulting from the hypoplasia of the posterior cranial fossa (PCF) and the occlusion of the jugular foramina, leading to cerebellar edema (CIM) and CSF hypo-resorption (hydrocephalus). Nevertheless, such a mechanism can be advocated only in a minority of cases (syndromic craniosynostosis). In non-syndromic CIM subjects, the presence of hydrocephalus could be explained by an occlusion of the basal CSF pathways, which would occur completely in a minority of cases (only 7-10% of CIM patients show hydrocephalus) while it would be partial in the remaining cases (no hydrocephalus). This hypothesis still needs to be demonstrated. As far as the management is concerned, the strategy to treat the hydrocephalus first is commonly accepted. Because of the "obstructive" origin of CIM-related hydrocephalus, the use of endoscopic third ventriculostomy (ETV) is straightforward. Actually, the analysis of the literature, concerning 63 cases reported so far, reveals very high success rates of ETV in treating hydrocephalus (90.5%), CIM (78.5%), and syringomyelia symptoms (76%) as well as in giving a radiological improvement of both CIM (74%) and syringomyelia (89%). The failures of ETV were not attributable to CIM or syringomyelia. Only 11% of cases required PCF decompression after ETV.</AbstractText>The association between CIM and hydrocephalus probably results from different, multifactorial, and not yet completely understood mechanisms, which place the affected patients in a peculiar subgroup among those constituting the heterogeneous CIM population. ETV is confirmed as the best first approach for this subset of patients.</AbstractText> |
2,328,928 | Pathogenesis of hydrocephalus in achondroplastic dwarfs: a review and presentation of a case followed for 22 years. | The purpose of this work is to review the pathogenesis and pathophysiology of hydrocephalus in patients with achondroplasia as a guide to its management throughout life.</AbstractText>A review of the literature related to neurosurgical issues in achondroplasia with specific focus on cerebrospinal fluid physics, clinical management, and outcome of affected individuals. Issues involved in this review are highlighted by a case report of a patient shunted for achondroplasia first shunted in infancy and followed for 22 years. Each of the management issues is explored with respect to this patient.</AbstractText>Head circumferences in achondroplasia are abnormally large in this condition usually caused by excess cerebrospinal fluid in the cortical subarachnoid space. Increase in ventricular size (hydrocephalus) is not rare but should not be treated unless rapidly progressive or symptomatic. The underlying cause of the abnormalities of cerebrospinal fluid dynamics relates to abnormal venous drainage at the skull base. Patients shunted in infancy for hydrocephalus usually remain dependent on the shunt for life, and crises of high intracranial pressure may occur with no distention of the ventricles.</AbstractText>In infants with achondroplasia, large heads and enlarged ventricles without symptoms should be watched initially for progression. If hydrocephalus progresses or if symptoms of intracranial hypertension occur, endoscopic third ventriculostomy can be tried. If shunt is necessary, it should have a high opening pressure and a device to retard siphoning. In the case of recurrent ventricular catheter blockage, it may be necessary to create a communication between the ventricles and the cortical subarachnoid space.</AbstractText> |
2,328,929 | Increased NADPH-diaphorase reactivity in the hypothalamic paraventricular nucleus and tanycytes following systemic administration of leptin in rats. | Leptin, a hormone mainly produced by adipocytes in proportion to fat mass, is a key component in the regulation of energy homeostasis and reproductive, neuroendocrine, immune, and metabolic functions. Leptin binds to the leptin receptor, which is expressed throughout the central nervous system but particularly in neurons of several nuclei of the hypothalamus, such as the arcuate nucleus (ARC) and paraventricular nucleus (PVN). It has been found that nitric oxide (NO) plays an important role in mediating effects of leptin. Since PVN and ARC neurons are known to express leptin receptors, we investigated the effects of leptin on nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) reactivity in the PVN and ARC of male Wistar rats. Our results have shown that systemic administration of leptin resulted in increased NADPH-d positive cell number in the PVN and ARC, suggesting that both the PVN and ARC may be important centers in the hypothalamus for the leptin action, mediated by increased NO production. In addition, we have also observed that hypothalamic tanycytes in the ventral portion of the third ventricle were NADPH-d positive. We speculate that leptin may affect the release of neurohormones and hypothalamic neurogenesis by activating nitric oxide synthase in hypothalamic tanycytes. |
2,328,930 | Surgical Techniques and Long-Term Outcomes of Flexible Neuroendoscopic Aqueductoplasty and Stenting in Infants with Obstructive Hydrocephalus: A Single-Center Study. | To technically review and explore long-term follow-up results of aqueductoplasty and stenting under flexible neuroendoscopy in infantile obstructive hydrocephalus.</AbstractText>The clinical data, surgical techniques, and long-term effects in 14 infants with obstructive hydrocephalus treated by flexible neuroendoscopic aqueductoplasty and stenting between 2008 and 2010 were analyzed retrospectively.</AbstractText>The 14 infants had a mean age of 5.71 ± 3.10 months (range, 2-11 months) and a mean duration of follow-up of 62.64 ± 34.52 months (range, 9-121 months). Subdural effusion was observed in 4 infants (28.6%) after surgery. There were no deaths or serious complications related to intracranial stent placement. Three infants (21.4%) failed, 2 due to proximal aqueduct occlusion from a short stent length and 1 due to intraluminal ependymal adhesion obstruction. One case was abandoned when a second surgical adjustment stent was unsuccessful, and the other 2 cases went to shunt surgery.</AbstractText>Aqueductoplasty with stenting is a feasible and safe surgical procedure for treating infants with midbrain aqueduct stenosis or occlusion. However, the optimal stent material and definitive outcomes after this procedure require additional long-term follow-up studies in large numbers of infants.</AbstractText>Copyright © 2019 Elsevier Inc. All rights reserved.</CopyrightInformation> |
2,328,931 | Myofibroblast modulation of cardiac myocyte structure and function. | After myocardial infarction, resident fibroblasts (Fb) differentiate towards myofibroblasts (MyoFb), generating the scar tissue and the interstitial fibrosis seen in the adjacent myocardium. Fb and MyoFb have the potential to interact with cardiac myocytes (CMs) but insight into the phenotype-specific role and mode of interaction is still incomplete. Our objectives are to further define the modulation of CMs by MyoFbs compared to Fbs, as well as the role of direct contact through gap junctions vs. soluble mediators, using Fbs and CMs from pig left ventricle. Fbs were treated to maintain an undifferentiated state (SD-208) or to attain full differentiation to MyoFb (TGF-β1). Fbs and MyoFbs were co-cultured with CMs, with the possibility of direct contact or separated by a Thincert membrane. Only in direct co-culture, both Fbs and MyoFbs were able to decrease CM viability after 2 days. Only MyoFbs induced significant distal spreading of CMs in both direct and indirect co-culture. MyoFbs, but not Fbs, readily made connections with CMs in direct co-culture and connexin 43 expression in MyoFb was higher than in Fb. When coupled to CMs, MyoFbs reduced the CM action potential duration and hyperpolarized the CM resting membrane potential. Uncoupling reversed these effects. In conclusion, MyoFbs, but not Fbs, alter the CM structural phenotype. MyoFbs, but not Fbs, are likely to electrically connect to CMs and thereby modulate the CM membrane potential. These data provide further support for an active role of MyoFbs in the arrhythmogenic substrate after cardiac remodelling. |
2,328,932 | Proteomics Analysis of Extracellular Matrix Remodeling During Zebrafish Heart Regeneration. | Adult zebrafish, in contrast to mammals, are able to regenerate their hearts in response to injury or experimental amputation. Our understanding of the cellular and molecular bases that underlie this process, although fragmentary, has increased significantly over the last years. However, the role of the extracellular matrix (ECM) during zebrafish heart regeneration has been comparatively rarely explored. Here, we set out to characterize the ECM protein composition in adult zebrafish hearts, and whether it changed during the regenerative response. For this purpose, we first established a decellularization protocol of adult zebrafish ventricles that significantly enriched the yield of ECM proteins. We then performed proteomic analyses of decellularized control hearts and at different times of regeneration. Our results show a dynamic change in ECM protein composition, most evident at the earliest (7 days postamputation) time point analyzed. Regeneration associated with sharp increases in specific ECM proteins, and with an overall decrease in collagens and cytoskeletal proteins. We finally tested by atomic force microscopy that the changes in ECM composition translated to decreased ECM stiffness. Our cumulative results identify changes in the protein composition and mechanical properties of the zebrafish heart ECM during regeneration. |
2,328,933 | Single-Cell Transcriptomics Reveals Chemotaxis-Mediated Intraorgan Crosstalk During Cardiogenesis. | We hypothesized that the differentiation processes of cardiac progenitor cell (CP) from first and second heart fields (FHF and SHF) may undergo the unique instructive gene regulatory networks or signaling pathways, and the precise SHF progression is contingent on the FHF signaling developmental cues.</AbstractText>We investigated how the intraorgan communications control sequential building of discrete anatomic regions of the heart at single-cell resolution.</AbstractText>By single-cell transcriptomic analysis of Nkx2-5 (NK2 homeobox 5) and Isl1 (ISL LIM homeobox 1) lineages at embryonic day 7.75, embryonic day 8.25, embryonic day 8.75, and embryonic day 9.25, we present a panoramic view of distinct CP differentiation hierarchies. Computational identifications of FHF- and SHF-CP descendants revealed that SHF differentiation toward cardiomyocytes underwent numerous step-like transitions, whereas earlier FHF progressed toward cardiomyocytes in a wave-like manner. Importantly, single-cell pairing analysis demonstrated that SHF-CPs were attracted to and expanded FHF-populated heart tube region through interlineage communications mediated by the chemotactic guidance (MIF [macrophage migration inhibitory factor]-CXCR2 [C-X-C motif chemokine receptor 2]). This finding was verified by pharmacological blockade of this chemotaxis in embryos manifesting limited SHF cell migration and contribution to the growth of the outflow tract and right ventricle but undetectable effects on the left ventricle or heart tube initiation. Genetic loss-of-function assay of Cxcr2 showed that the expression domain of CXCR4 was expanded predominantly at SHF. Furthermore, double knockout of Cxcr2/Cxcr4 exhibited defective SHF development, corroborating the redundant function. Mechanistically, NKX2-5 directly bound the Cxcr2 and Cxcr4 genomic loci and activated their transcription in SHF.</AbstractText>Collectively, we propose a model in which the chemotaxis-mediated intraorgan crosstalk spatiotemporally guides the successive process of positioning SHF-CP and promoting primary heart expansion and patterning upon FHF-derived heart tube initiation.</AbstractText> |
2,328,934 | Analysis of FAM19A2/TAFA-2 function. | FAM19A2/TAFA-2, a member of the chemokine CC family, shares 31% sequence identity with MIP-1α, which is known to elevate body temperature and reduce food intake. A single administration of 250 pM of FAM19A2/TAFA-2 to the third ventricle of mice just before the initiation of dark period increased food intake and meal number significantly, but reduced meal size during the dark period. The respiratory exchange rate and energy expenditure were increased significantly during the dark period, while the ambulatory count and vertical activity were not affected. These data suggest that FAM19A2/TAFA-2 participates in the regulation of food intake and metabolic activities. |
2,328,935 | Colloid Cysts: Evolution of Surgical Approach Preference and Management of Recurrent Cysts. | Optimal management of third ventricular colloid cysts remains debated. While microsurgery offers greater resection rates and lower recurrences, endoscopy offers a perceived less invasive option.</AbstractText>To describe the evolution of our practice to favor microsurgery and determine the optimal management of recurrent colloid cysts.</AbstractText>Any patient having undergone surgery for a colloid cyst by the senior author was identified and included in the study cohort. Clinical, radiographic, and operative records were reviewed, with attention paid to those patients requiring recurrent surgery.</AbstractText>Thirty-three patients were treated for intracranial colloid cysts between 1995 and 2017. Two patients had initial surgical treatment at an outside institution prior to presentation at our institution. Microsurgery was used in 15/31 initial cases, endoscopy in 13 cases, and ventriculoperitoneal shunting in 3 cases. Between 1995 and 2005, 89% of colloid cysts (8/9 cases) were resected endoscopically, whereas 74% of colloid cysts (14/19 cases) were resected by microsurgery after 2005. Of the 13 patients treated endoscopically, 6 (46%) required surgery for recurrent cysts. Incomplete cyst wall resection at the initial operation increased the recurrence rate to 55%. There were no recurrences in the microsurgery cohort.</AbstractText>Surgical resection of recurrent colloid cysts should focus on complete removal of the cyst wall to minimize the chance of recurrence. Microsurgery has been shown to provide the highest success rates for cyst wall resection and lowest rates of recurrence and is therefore recommended for patients undergoing surgery for primary and recurrent colloid cysts.</AbstractText>Copyright © 2019 by the Congress of Neurological Surgeons.</CopyrightInformation> |
2,328,936 | In utero Exposure to Anesthetics Alters Neuronal Migration Pattern in Developing Cerebral Cortex and Causes Postnatal Behavioral Deficits in Rats. | During fetal development, cerebral cortical neurons are generated in the proliferative zone along the ventricles and then migrate to their final positions. To examine the impact of in utero exposure to anesthetics on neuronal migration, we injected pregnant rats with bromodeoxyuridine to label fetal neurons generated at embryonic Day (E) 17 and then randomized these rats to 9 different groups receiving 3 different means of anesthesia (oxygen/control, propofol, isoflurane) for 3 exposure durations (20, 50, 120 min). Histological analysis of brains from 54 pups revealed that significant number of neurons in anesthetized animals failed to acquire their correct cortical position and remained dispersed within inappropriate cortical layers and/or adjacent white matter. Behavioral testing of 86 littermates pointed to abnormalities that correspond to the aberrations in the brain areas that are specifically developing during the E17. In the second set of experiments, fetal brains exposed to isoflurane at E16 had diminished expression of the reelin and glutamic acid decarboxylase 67, proteins critical for neuronal migration. Together, these results call for cautious use of anesthetics during the neuronal migration period in pregnancy and more comprehensive investigation of neurodevelopmental consequences for the fetus and possible consequences later in life. |
2,328,937 | Trait Conscientiousness predicts rate of brain atrophy in multiple sclerosis. | Conscientiousness is a core personality trait with favorable prognosis in neuropsychiatric disease.</AbstractText>We aimed to determine whether baseline Conscientiousness predicts future brain atrophy in multiple sclerosis (MS) after accounting for demographic and basic clinical characteristics.</AbstractText>Trait Conscientiousness, clinical features, and Expanded Disability Status Scale (EDSS) were obtained at baseline. Lateral ventricle volume (LVV) was measured longitudinally. In a retrospective general linear mixed effects model, data from 424 patients were analyzed (mean 6 time-points, up to 15 years).</AbstractText><AbstractText Label="RESULTS/CONCLUSION">We observed significant age and Conscientiousness by time-from-baseline interactions indicating that younger age and higher Conscientiousness are associated with reduced progression of brain atrophy.</AbstractText> |
2,328,938 | Effects of Salmon Calcitonin on the Concentrations of Monoamines in Periaqueductal Gray in Formalin Test. | The receptors of salmon calcitonin, located on certain areas of the brain such as the periaqueductal gray matter, are responsible for pain modulation.</AbstractText>The effects of intracerebroventricular injection of salmon calcitonin on the behavioral response to pain and on the levels of monoamines in the periaqueductal gray were explored using a biphasic animal model of pain.</AbstractText>Animal experiment.</AbstractText>A total of 45 male rats were divided into four groups (n=6). Salmon calcitonin was injected into the lateral ventricle of the brain (1.5 nmol, with a volume of 5 μL). After 20 min, 2.5% formalin was subcutaneously injected into the right leg claw, and pain behavior was recorded on a numerical basis. At the time of the formalin test, the periaqueductal gray area was microdialized. High-performance liquid chromatography method was used to gauge the levels of monoamines and their metabolites.</AbstractText>Intracerebroventricular injections of salmon calcitonin resulted in pain reduction in the formalin test (p<0.05). The dialysate concentrations of serotonin, dopamine, norepinephrine, 5-hydroxyindoleacetic acid, 3,4-dihydroxyphenylacetic, and 4-hydroxy-3-methoxyphenylglycol increased in the periaqueductal gray area in different phases of the formalin pain test (p<0.05).</AbstractText>Salmon calcitonin reduced pain by increasing the concentrations of monoamines and the metabolites derived from them in the periaqueductal gray area.</AbstractText> |
2,328,939 | Prognosis of fetuses with ventriculomegaly: An observational retrospective study. | To investigate the prognosis of fetuses with ventriculomegaly (VM).</AbstractText>Clinical data were collected from 234 cases of fetal VM diagnosed by ultrasound between March 2010 and July 2016. VM progression was monitored, and karyotyping and infection screening performed. Magnetic resonance imaging (MRI) was performed where increasing ventricular diameter was noted. Neonatal behavioral neurological assessment (NBNA) was carried out after birth, and Bayley Scales of Infant Development assessment at 6 months.</AbstractText>The in utero outcomes of Group A were better than Group B in 173 pregnancies. Isolated VM (IVM) was associated with better prognosis than nonisolated VM (NIVM); the regression rates were 74.6% (59/79) and 52.1% (49/94), respectively (χ2</sup> = 10.222, .006). The NBNA scores were significantly higher in Group A than Group B (χ2</sup> = 4.231, .004), but not significantly different between IVM and NIVM. The composition ratios of both the psychomotor and mental developmental index (PDI and MDI) scores were not significantly different between Groups A and B (Z = 1.869, .062 and Z = 0.826, .409, respectively). Significant differences in in utero outcomes were observed between IVM and NIVM cases in Groups A and B.</AbstractText>Fetal VM prognosis is affected by the width of ventricle, chromosome abnormalities, coexisted abnormalities, and in utero progression.</AbstractText>© 2019 John Wiley & Sons, Ltd.</CopyrightInformation> |
2,328,940 | Delayed Cerebrospinal Fluid Cleft Formation Through the Midbrain and Thalamus Following Hemicraniectomy and Cranioplasty for Acute Subdural Hematoma. | Cerebrospinal fluid (CSF) cleft formation through brain parenchyma following nonpenetrating traumatic brain injury (TBI) is a rare phenomenon. Here we present a unique case of delayed CSF cleft formation months after initial injury.</AbstractText>A 41-yr-old male presented after a fall with a right convexity acute subdural hematoma and ipsilateral frontal contusion. He underwent emergent hemicraniectomy with subsequent autologous cranioplasty 2 mo later. At 10-mo follow-up his neurological status had improved. His magnetic resonance imaging (MRI) at that time demonstrated encephalomalacia at the site of his prior contusion and punctate right pontine traumatic shearing injury. The patient re-presented to clinic 13 mo after initial injury with 2 mo of progressively worsening dysarthria, left hand numbness, diplopia, and dysphagia. MRI revealed a new tubular-shaped CSF cleft extending from the fourth ventricle, through the right midbrain and thalamus that was not present on prior MRI. Computed tomography cisternogram confirmed communication with the ventricular system, and there was no clinical evidence for elevated CSF pressure. One month later, the patient's symptoms had not improved, and imaging revealed progression of the CSF cleft. Following placement of a ventriculoperitoneal shunt, progression of the cleft ceased. We postulate that this cleft was a late sequela of traumatic shearing injury. We discuss our efforts to diagnose the etiology of the cleft and the rationale for our management strategy.</AbstractText>To our knowledge, this represents the first reported delayed-onset CSF cleft through the midbrain and thalamus after closed TBI.</AbstractText>Copyright © 2019 by the Congress of Neurological Surgeons.</CopyrightInformation> |
2,328,941 | Malignant Transformation of a Rosette-Forming Glioneuronal Tumor with IDH1 Mutation: A Case Report and Literature Review. | Rosette-forming glioneuronal tumor (World Health Organization grade I) is considered as a benign tumor with very low potential for progression. The potential for malignant transformation of this tumor is not known and has never been reported before in literature.</AbstractText>We report a 42-year-old man, diagnosed with rosette-forming glioneuronal tumor of the fourth ventricle with a positive isocitrate dehydrogenase 1 mutation, progressed to glioblastoma after 6 years from diagnosis. We discuss the clinical history, radiological findings, and histopathological characteristic with immunohistochemistry findings observed in this unique case.</AbstractText>Despite being acceptable as benign, based on our observations in this case, there is a potential for malignant transformation of rosette-forming glioneuronal tumor. The role of isocitrate dehydrogenase 1 mutation leading to malignant transformation could not be established as our finding is novel and further prospective studies are required to prove this association.</AbstractText> |
2,328,942 | One Shot Segmentation: Unifying Rigid Detection and Non-Rigid Segmentation Using Elastic Regularization. | This paper proposes a novel approach for the non-rigid segmentation of deformable objects in image sequences, which is based on one-shot segmentation that unifies rigid detection and non-rigid segmentation using elastic regularization. The domain of application is the segmentation of a visual object that temporally undergoes a rigid transformation (e.g., affine transformation) and a non-rigid transformation (i.e., contour deformation). The majority of segmentation approaches to solve this problem are generally based on two steps that run in sequence: a rigid detection, followed by a non-rigid segmentation. In this paper, we propose a new approach, where both the rigid and non-rigid segmentation are performed in a single shot using a sparse low-dimensional manifold that represents the visual object deformations. Given the multi-modality of these deformations, the manifold partitions the training data into several patches, where each patch provides a segmentation proposal during the inference process. These multiple segmentation proposals are merged using the classification results produced by deep belief networks (DBN) that compute the confidence on each segmentation proposal. Thus, an ensemble of DBN classifiers is used for estimating the final segmentation. Compared to current methods proposed in the field, our proposed approach is advantageous in four aspects: (i) it is a unified framework to produce rigid and non-rigid segmentations; (ii) it uses an ensemble classification process, which can help the segmentation robustness; (iii) it provides a significant reduction in terms of the number of dimensions of the rigid and non-rigid segmentations search spaces, compared to current approaches that divide these two problems; and (iv) this lower dimensionality of the search space can also reduce the need for large annotated training sets to be used for estimating the DBN models. Experiments on the problem of left ventricle endocardial segmentation from ultrasound images, and lip segmentation from frontal facial images using the extended Cohn-Kanade (CK+) database, demonstrate the potential of the methodology through qualitative and quantitative evaluations, and the ability to reduce the search and training complexities without a significant impact on the segmentation accuracy. |
2,328,943 | Predictors of early cardiac changes in patients with type 1 diabetes mellitus: An echocardiography-based study. | In patients with type 1 diabetes mellitus (T1DM) imaging studies have demonstrated an increased prevalence of left ventricular diastolic dysfunction and increased left ventricular mass (LVM) unrelated to arterial hypertension and ischemic heart disease. The aim of our study was to identify potential predictors of early subclinical changes in cardiac chamber size and function in such patients. Sixty-one middle-aged asymptomatic normotensive patients with T1DM were included in the study. Conventional and tissue Doppler echocardiography was performed and fasting serum levels of glucose, glycated hemoglobin (HbA1c), lipids, and creatinine were measured. We found moderate bivariate correlations of body mass index (BMI) with left atrial volume (r = 0.47, p < 0.01), LVM (r = 0.42, p < 0.01), left ventricular relative wall thickness (r = 0.32, p = 0.01), and all observed parameters of diastolic function of both ventricles. The five-year average value of HbA1c weakly correlated with the Doppler index of left ventricular filling pressure E/e´sept (r = 0.27, p = 0.04). We found no significant association of diabetes duration, five-year trend of HbA1c, serum lipids, and glomerular filtration rate with cardiac structure and function. After adjusting for other parameters, BMI remained significantly associated with left atrial volume, LVM as well as with the transmitral Doppler ratio E/A. In our study, BMI was the only observed parameter significantly associated with subclinical structural and functional cardiac changes in the asymptomatic middle-aged patients with T1DM. |
2,328,944 | Oligodendroglial tumours: subventricular zone involvement and seizure history are associated with CIC mutation status. | CIC-mutant oligodendroglial tumours linked to better prognosis. We aim to investigate associations between CIC gene mutation status, MR characteristics and clinical features.</AbstractText>Imaging and genomic data from the Cancer Genome Atlas and the Cancer Imaging Archive (TCGA/TCIA) for 59 patients with oligodendroglial tumours were used. Differences between CIC mutation and CIC wild-type were tested using Chi-square test and binary logistic regression analysis.</AbstractText>In univariate analysis, the clinical variables and MR features, which consisted 3 selected features (subventricular zone[SVZ] involvement, volume and seizure history) were associated with CIC mutation status (all p < 0.05). A multivariate logistic regression analysis identified that seizure history (no vs. yes odd ratio [OR]: 28.960, 95 confidence interval [CI]:2.625-319.49, p = 0.006) and SVZ involvement (SVZ- vs. SVZ+ OR: 77.092, p = 0.003; 95% CI: 4.578-1298.334) were associated with a higher incidence of CIC mutation status. The nomogram showed good discrimination, with a C-index of 0.906 (95% CI: 0.812-1.000) and was well calibrated. SVZ- group has increased (SVZ- vs. SVZ+, hazard ratio [HR]: 4.500, p = 0.04; 95% CI: 1.069-18.945) overall survival.</AbstractText>Absence of seizure history and SVZ involvement (-) was associated with a higher incidence of CIC mutation.</AbstractText> |
2,328,945 | Purely Endoscopic Resection of Cavernoma of the Septum Pellucidum. | The intraventricular location of a cavernoma is a rare entity and accounts for approximately 2.5% of all cavernomas of the central nervous system. They are commonly found in the lateral ventricle followed by the third and fourth ventricles. The location in the septum pellucidum is rare, and only four cases have been reported in the international literature. An open craniotomy was performed in all these cases. To the best of our knowledge, this is the first case of a cavernoma of the septum pellucidum successfully resected using a purely endoscopic transventricular approach. |
2,328,946 | Age-Related Hearing Loss Associations With Changes in Brain Morphology. | Age-related hearing loss has been associated with varied auditory cortex morphology in human neuroimaging studies. These findings have suggested that peripheral auditory system declines cause changes in brain morphology but could also be due to latent variables that affect the auditory periphery and brain. The current longitudinal study was designed to evaluate these explanations for pure-tone threshold and brain morphology associations. Thirty adults (mean age at Time 1 = 64.12 ± 10.32 years) were studied at two time points (average duration between visits = 2.62 ± 0.81 years). Small- to medium-effect size associations were observed between high-frequency pure-tone thresholds and auditory cortex gray matter volume at each time point. Although there were significant longitudinal changes in low- and high-frequency hearing measures and brain morphology, those longitudinal changes were not significantly correlated across participants. High-frequency hearing measures at Time 1 were significantly related to more lateral ventricle expansion, such that participants with higher measures exhibited larger increases in ventricle size. This ventricle effect was statistically independent of high-frequency hearing associations with auditory cortex morphology. Together, these results indicate that there are at least two mechanisms for associations between age-related hearing loss and brain morphology. Potential explanations for a direct hearing loss effect on brain morphology, as well as latent variables that likely affect both the inner ear and brain, are discussed. |
2,328,947 | Giant intradural extramedullary spinal ependymoma, a rare arachnoiditis-mimicking condition: case report and literature review. | Ependymomas are tumours arising from the ependymal cells lining the ventricles and the central canal of the spinal cord. They represent the most common intramedullary spinal cord tumour in adults and are very rarely encountered in an extramedullary location. Only 40 cases of intradural extramedullary (IDEM) ependymomas have been reported, all of which were diagnosed pre-operatively as IDEM ependymomas on contrast-enhanced MRI.</AbstractText>We report a 23-year old male presenting with rapidly worsening signs and symptoms of spinal cord disease. A spinal MRI demonstrated a posterior multi-cystic dilatation extended between T1 and T12. Post-contrast sequences showed peri-medullar leptomeningeal enhancement and the diagnosis of spinal arachnoiditis was made. The patient underwent surgery and the spinal cord appeared circumferentially wrapped by an irregular soft tissue. The tissue was sub-totally removed and the pathological diagnosis was ependymoma WHO grade II. The patient experienced an excellent neurological recovery and no further treatments were administered. A small residue is now stable at 2.5 years follow-up.</AbstractText>Giant IDEM ependymomas are rare entities and pre-operative diagnosis can be challenging in some cases. Surgery represents the main treatment option being resolutive in most cases.</AbstractText> |
2,328,948 | Brain renin-angiotensin system in broiler chickens with cold-induced pulmonary hypertension. | 1. The relative expression of angiotensinogen (AGT), renin, angiotensin-converting enzyme (ACE) and angiotensin II type 1 receptor (AT<sub>1</sub>R) was determined using quantitative real-time PCR on tissue from the brain (forebrain, midbrain and hindbrain) to investigate the effect of cold-induced pulmonary hypertension syndrome (PHS) in broilers aged 42 days. Brain angiotensin II (Ang II) and AT<sub>1</sub>R levels were measured using enzyme immunoassay. 2. The right ventricle/total ventricles (RV/TV) ratio of the heart was increased in broilers exposed to cold stress (PHS group) at the end of the experiment. 3. ACE and renin transcripts in three parts of the brain were significantly increased in the PHS group at 42 d of age compared to controls while AGT transcript was significantly increased only in the hindbrain of PHS birds. The amount of AT1R transcript did not differ between control and PHS groups. 4. The amount of Ang II significantly decreased only in the midbrain of PHS birds compared with controls while the amounts of AT<sub>1</sub>R were not different between treatments in the three segments of the brain. 5. It was concluded that brain gene expression of AGT (in the hindbrain), renin, and ACE was upregulated in broilers with PHS whereas Ang II and AT1R levels were not changed. These results provided evidence of diminished involvement of the renin-angiotensin system in the pathogenesis of chicken pulmonary hypertension. |
2,328,949 | Mechanistic investigation of Ca2+ alternans in human heart failure and its modulation by fibroblasts. | Heart failure (HF) is characterized, among other factors, by a progressive loss of contractile function and by the formation of an arrhythmogenic substrate, both aspects partially related to intracellular Ca2+ cycling disorders. In failing hearts both electrophysiological and structural remodeling, including fibroblast proliferation, contribute to changes in Ca2+ handling which promote the appearance of Ca2+ alternans (Ca-alt). Ca-alt in turn give rise to repolarization alternans, which promote dispersion of repolarization and contribute to reentrant activity. The computational analysis of the incidence of Ca2+ and/or repolarization alternans under HF conditions in the presence of fibroblasts could provide a better understanding of the mechanisms leading to HF arrhythmias and contractile function disorders.</AbstractText>The goal of the present study was to investigate in silico the mechanisms leading to the formation of Ca-alt in failing human ventricular myocytes and tissues with disperse fibroblast distributions. The contribution of ionic currents variability to alternans formation at the cellular level was analyzed and the results show that in normal ventricular tissue, altered Ca2+ dynamics lead to Ca-alt, which precede APD alternans and can be aggravated by the presence of fibroblasts. Electrophysiological remodeling of failing tissue alone is sufficient to develop alternans. The incidence of alternans is reduced when fibroblasts are present in failing tissue due to significantly depressed Ca2+ transients. The analysis of the underlying ionic mechanisms suggests that Ca-alt are driven by Ca2+-handling protein and Ca2+ cycling dysfunctions in the junctional sarcoplasmic reticulum and that their contribution to alternans occurrence depends on the cardiac remodeling conditions and on myocyte-fibroblast interactions.</AbstractText>It can thus be concluded that fibroblasts modulate the formation of Ca-alt in human ventricular tissue subjected to heart failure-related electrophysiological remodeling. Pharmacological therapies should thus consider the extent of both the electrophysiological and structural remodeling present in the failing heart.</AbstractText> |
2,328,950 | Transcranial brain sonography for Parkinsonian syndromes. | Substantia nigra (SN) hyperechogenicity has been proved to be a characteristic finding for idiopathic Parkinson's disease (PD), occurring in more than 90% of the patients. This echofeature is owed to increased amounts of iron in the SN region and reflects a functional impairment of the nigrostriatal dopaminergic system. In a prospective blinded study in which a group of patients with early mild signs and symptoms of unclear Parkinsonism were followed until a definite clinical diagnosis of PD, the hyperechogenicity of the SN was demonstrated to be highly predictive of a final diagnosis of PD. For the diagnosis of PD in individuals with early motor symptoms, both the sensitivity and positive predictive value of SN hyperechogenicity were higher than 90% and both the specificity and negative predictive value were higher than 80%. For early differential diagnosis between PD and atypical Parkinsonian syndromes, the sensitivity and positive predictive value of SN hyperechogenicity were higher than 90%, and both the specificity and negative predictive value were higher than 80%. The diagnostic specificity is increased if combining the TCS findings of SN, lenticular nucleus and third ventricle. In asymptomatic adult subjects, SN hyperechogenicity, at least unilaterally, indicates a subclinical functional insufficiency of the nigrostriatal dopaminergic system. Recent papers revealed that SN hyperechogenicity might suggest preclinical PD. Reduced echogenicity of midbrain raphe indicates increased risk of depression in PD patients. Caudate nucleus hyperechogenicity has been associated with drug-induced psychosis, and frontal horn dilatation >20 mm with dementia. Transcranial brain sonography can be a valuable tool for managing patients with Parkinsonian signs and symptoms. |
2,328,951 | Impaired Glymphatic Transport in Spontaneously Hypertensive Rats. | The glymphatic system is a brainwide CSF transport system that uses the perivascular space for fast inflow of CSF. Arterial pulsations are a major driver of glymphatic CSF inflow, and hypertension that causes vascular pathologies, such as arterial stiffening and perivascular alterations, may impede the inflow. We used dynamic contrast-enhanced MRI to assess the effect of hypertension on glymphatic transport kinetics in male young and adult spontaneously hypertensive (SHR) rats compared with age-matched normotensive Wistar-Kyoto rats (WKY). We anesthetized the rats with dexmedetomidine/isoflurane and infused paramagnetic contrast (Gd-DOTA) into the cisterna magna during dynamic contrast-enhanced MRI to quantify glymphatic transport kinetics. Structural MRI analysis showed that cerebroventricular volumes are larger and brain volumes significantly smaller in SHR compared with WKY rats, regardless of age. We observed ventricular reflux of Gd-DOTA in SHR rats only, indicating abnormal CSF flow dynamics secondary to innate hydrocephalus. One-tissue compartment analysis revealed impeded glymphatic transport of Gd-DOTA in SHR compared with WKY rats in both age groups, implying that glymphatic transport, including solute clearance from brain parenchyma, is impaired during evolving hypertension in young SHR, an effect that worsens in states of chronic hypertension. The study demonstrates the suppression of glymphatic clearance in SHR rats and thus offers new insight into the coexistence of hypertension and concomitant vascular pathologies in Alzheimer's disease. The study further highlights the importance of considering the distribution of tracers in the CSF compartment in the analysis of the glymphatic system.<b>SIGNIFICANCE STATEMENT</b> The glymphatic system contributes to the removal of amyloid β from the brain and is disrupted in Alzheimer's disease and aging. Using a rat model of hypertension, we measured gross CSF flow and tracked glymphatic influx and efflux rates with dynamic contrast-enhanced MRI, showing that glymphatic transport is compromised in both early and advanced stages of hypertension. The study provides a new perspective on the importance for brain metabolite and fluid homeostasis of maintaining healthy blood vessels, an increasingly pertinent issue in an aging population that in part may explain the link between vascular pathology and Alzheimer's disease. |
2,328,952 | SU5416 does not attenuate early RV angiogenesis in the murine chronic hypoxia PH model. | Right ventricular (RV) angiogenesis has been associated with adaptive myocardial remodeling in pulmonary hypertension (PH), though molecular regulators are poorly defined. Endothelial cell VEGFR-2 is considered a "master regulator" of angiogenesis in other models, and the small molecule VEGF receptor tyrosine kinase inhibitor SU5416 is commonly used to generate PH in rodents. We hypothesized that SU5416, through direct effects on cardiac endothelial cell VEGFR-2, would attenuate RV angiogenesis in a murine model of PH.</AbstractText>C57 BL/6 mice were exposed to chronic hypoxia (CH-PH) to generate PH and stimulate RV angiogenesis. SU5416 (20 mg/kg) or vehicle were administered at the start of the CH exposure, and weekly thereafter. Angiogenesis was measured after one week of CH-PH using a combination of unbiased stereological measurements and flow cytometry-based quantification of myocardial endothelial cell proliferation. In complementary experiments, primary cardiac endothelial cells from C57 BL/6 mice were exposed to recombinant VEGF (50 ng/mL) or grown on Matrigel in the presence of SU5416 (5 μM) or vehicle.</AbstractText>SU5416 directly inhibited VEGF-mediated ERK phosphorylation, cell proliferation, and Kdr transcription, but not Matrigel tube formation in primary murine cardiac endothelial cells in vitro. SU5416 did not inhibit CH-PH induced RV angiogenesis, endothelial cell proliferation, or RV hypertrophy in vivo, despite significantly altering the expression profile of genes involved in angiogenesis.</AbstractText>These findings demonstrate that SU5416 directly inhibited VEGF-induced proliferation of murine cardiac endothelial cells but does not attenuate CH-PH induced RV angiogenesis or myocardial remodeling in vivo.</AbstractText> |
2,328,953 | Malignant epidermoid arising from the third ventricle: A case report. | Third epidermoid tumors are a rare finding. The appearance of these tumors often makes them difficult to diagnose, and thus they require multimodality imaging.</AbstractText>A 48-year-old male patient reported to our hospital with complaints of vomiting and severe headache. The patient also complained of involuntary micturition for the past five days. We used a combination of computed tomography (CT) and magnetic resonance imaging (MRI) imaging modalities to confirm the presence of a malignant epidermoid cyst arising from the third ventricle. A contrast-enhanced CT of the head demonstrated minimal perilesional enhancement while an MRI revealed a large, lobulated and septated T2 hyperintense mass arising from the third ventricle. The maximum size of the lesion measured 73 mm × 65 mm × 64 mm in size.</AbstractText>Malignant epidermoid arising from the third ventricle in an adult male was reported using a combination of CT, MRI, and MR spectroscopy.</AbstractText> |
2,328,954 | A Fluttering Heart: A Storm is Brewing.<Pagination><StartPage>e3</StartPage><MedlinePgn>e3</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">e3</ELocationID><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Rothstein</LastName><ForeName>Peter</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Houston Methodist DeBakey Heart & Vascular Center, Houston Methodist Hospital, Houston, Texas.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Valderrábano</LastName><ForeName>Miguel</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Houston Methodist DeBakey Heart & Vascular Center, Houston Methodist Hospital, Houston, Texas.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType><PublicationType UI="D059040">Video-Audio Media</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Methodist Debakey Cardiovasc J</MedlineTA><NlmUniqueID>101508600</NlmUniqueID><ISSNLinking>1947-6108</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000889">Anti-Arrhythmia Agents</NameOfSubstance></Chemical></ChemicalList><MeshHeadingList><MeshHeading><DescriptorName UI="D000200" MajorTopicYN="N">Action Potentials</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D056988" MajorTopicYN="N">Anterior Wall Myocardial Infarction</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000889" MajorTopicYN="N">Anti-Arrhythmia Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017115" MajorTopicYN="N">Catheter Ablation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017023" MajorTopicYN="N">Coronary Angiography</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004562" MajorTopicYN="Y">Electrocardiography</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D022062" MajorTopicYN="N">Electrophysiologic Techniques, Cardiac</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006322" MajorTopicYN="N">Heart Aneurysm</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006339" MajorTopicYN="Y">Heart Rate</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D062645" MajorTopicYN="N">Percutaneous Coronary Intervention</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011237" MajorTopicYN="N">Predictive Value of Tests</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017180" MajorTopicYN="N">Tachycardia, Ventricular</DescriptorName><QualifierName UI="Q000175" MajorTopicYN="Y">diagnosis</QualifierName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2019</Year><Month>6</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>6</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2019</Year><Month>8</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31205592</ArticleId><ArticleId IdType="pmc">PMC6557143</ArticleId><ArticleId IdType="sici">i1947-6094-15-1-e3</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Tikiz H, Balbay Y, Atak R, Terzi T, Genç Y, Kütük E. The effect of thrombolytic therapy on left ventricular aneurysm formation in acute myocardial infarction: relationship to successful reperfusion and vessel patency. Clin Cardiol. 2001;24(10):656.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6654946</ArticleId><ArticleId IdType="pubmed">11594411</ArticleId></ArticleIdList></Reference><Reference><Citation>Sapp JL, Wells GA, Parkash R et al. Ventricular tachycardia ablation versus escalation of antiarrhythmic drugs. N Engl J Med. 2016;375:111–21.</Citation><ArticleIdList><ArticleId IdType="pubmed">27149033</ArticleId></ArticleIdList></Reference><Reference><Citation>Al-Khatib SM, Stevenson WG, Ackerman MJ et al. 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. 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Heart Rhythm. 2014 Apr;11(4):533–40.</Citation><ArticleIdList><ArticleId IdType="pubmed">24333283</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">31205307</PMID><DateCompleted><Year>2020</Year><Month>05</Month><Day>27</Day></DateCompleted><DateRevised><Year>2020</Year><Month>05</Month><Day>27</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1940-087X</ISSN><JournalIssue CitedMedium="Internet"><Issue>148</Issue><PubDate><Year>2019</Year><Month>Jun</Month><Day>01</Day></PubDate></JournalIssue><Title>Journal of visualized experiments : JoVE</Title><ISOAbbreviation>J Vis Exp</ISOAbbreviation></Journal>Transthoracic Echocardiographic Examination in the Rabbit Model. | Large animal models such as the rabbit are valuable for translational preclinical research. Rabbits have a similar cardiac electrophysiology compared to that of humans and that of other large animal models such as dogs and pigs. However, the rabbit model has the additional advantage of lower maintenance costs compared to other large animal models. The longitudinal evaluation of cardiac function using echocardiography, when appropriately implemented, is a useful methodology for preclinical assessment of novel therapies for heart failure with reduced ejection fraction (e.g. cardiac regeneration). The correct use of this non-invasive tool requires the implementation of a standardized examination protocol following international guidelines. Here we describe, step by step, a detailed protocol supervised by veterinary cardiologists for performing echocardiography in the rabbit model, and demonstrate how to correctly obtain the different echocardiographic views and imaging planes, as well as the different imaging modes available in a clinical echocardiography system routinely used in human and veterinary patients. |
2,328,955 | 18F-FDG Whole-body PET/MRI of a 30-Week Pregnant Woman With Breast Cancer Revealed Interesting Fetal Findings. | A 35-year-old 30-week pregnant woman was referred to our institution for initial staging of a triple negative invasive ductal carcinoma of the left breast. To avoid fetal radiation exposure from CT, a whole-body F-FDG PET/MRI was performed. Simultaneous acquisition of PET, T1-, T2-, and diffusion-weighted sequences revealed left axillary node extension and no distant metastases. Fetal radiation dose was estimated at 1.9 mGy. Interestingly, low fetal brain uptake and high symmetrical myocardial metabolism in both ventricles were found. Delivery was induced at 37 weeks of amenorrhea, and the patient underwent 4 cycles of neoadjuvant chemotherapy. |
2,328,956 | Malignant Transformation of a Rosette-Forming Glioneuronal Tumor to Glioblastoma. | A rosette-forming glioneuronal tumor (RGNT), a rare brain tumor, presents as a benign feature with a favorable outcome. To date, a few cases with aggressive behaviors, such as recurrence or dissemination, but none with malignant transformation, have been reported. We describe 1 case that recurred as glioblastoma after complete resection of the benign RGNT.</AbstractText>A man aged 58 years presented with headache and dizziness without neurologic symptoms. Magnetic resonance imaging showed a 4 × 2.5 cm, well-demarcated mass in the left cerebellar hemisphere. The patient underwent gross total resection of the tumor and a diagnosis of RGNT was made. There was no evidence of recurrence on serial follow-up. However, a recurrent heterogeneous enhancing mass in the previous surgical cavity was observed on a 7-year postoperative magnetic resonance imaging scan. Reoperation was performed and a histopathological study revealed a glioblastoma.</AbstractText>To the best of our knowledge, this is the first case of spontaneous malignant transformation of an RGNT. Our case may be helpful in better understanding the biological behavior and clinical outcome of RGNT. We emphasize the malignant potential of this rare tumor and the necessity of future large-scaled research for most appropriate therapeutic strategies.</AbstractText>Copyright © 2019. Published by Elsevier Inc.</CopyrightInformation> |
2,328,957 | Endoscopic Fourth Ventriculostomy: Suboccipital Transaqueductal Approach for Fenestration of Isolated Fourth Ventricle: Case Report and Technical Note. | Trapped or isolated fourth ventricle is a known, late sequela after lateral ventricular shunt placement for hydrocephalus, particularly after infection or hemorrhage. It may cause brainstem compression and insidiously present with ataxia, dysarthria, and intracranial hypertension, further delaying diagnosis. There is no universally agreed on treatment algorithm, and options include open fenestration through a suboccipital craniotomy, fourth ventricle shunting, and minimally invasive options including endoscopic stenting and fenestration through a precoronal approach.</AbstractText>We describe a young child with epilepsy and symptomatic brainstem compression from a dilated fourth ventricle, with a history of streptococcal parietal abscess and posthemorrhagic hydrocephalus requiring shunt placement. Given his history of infection and nearly neurologically intact examination, we pursued minimally invasive endoscopy through a suboccipital, transaqueductal approach to fenestrate his fourth ventricle.</AbstractText>Magnetic resonance imaging (MRI) demonstrated complex, loculated hydrocephalus and a dilated fourth ventricle. Under electromagnetic navigation, we endoscopically fenestrated his fourth ventricle using a rarely described suboccipital, transaqueductal approach. He tolerated the procedure without complication and improved neurologically, although his follow-up MRI demonstrated no change in fourth ventricular dilation at 1 year. Although there was no decrease in size of the fourth ventricle on follow-up MRI, we describe an alternative, well-tolerated, suboccipital approach for the management of a trapped fourth ventricle. Fenestration of a web of tissue in the aqueduct of Sylvius provided long-term clinical improvement and may provide a rescue approach for patients who are not candidates for standard approaches.</AbstractText>Copyright © 2019 Elsevier Inc. All rights reserved.</CopyrightInformation> |
2,328,958 | Collection of cerebrospinal fluid from murine lateral ventricles for biomarker determination in mucopolysaccharidosis type IIIA. | Cerebrospinal fluid (CSF) collection is currently the only feasible means to obtain biological fluid for the quantitative determination of biomarkers that may reflect disease activity within the brain. Studies in mouse models of human neurological disease benefit from ascertainment and subsequent analysis of brain tissue that is not afforded in human patients. The CSF provides a translational forum, however, due to the practical constraints presented by the mouse's small size, CSF is often ignored in experimental mouse models.</AbstractText>Here we report a method for the controlled, precise and predictable collection of 10 μL of CSF from the lateral ventricles of adult mice using stereotaxic equipment and a micro-syringe pump.</AbstractText>Collected CSF was clear and manifested the consistency of water and moreover, quantification of a disease-specific biomarker for the neurodegenerative disorder, mucopolysaccharidosis type IIIA (MPS IIIA) was possible in this small volume of CSF. In the naturally occurring mouse model of MPS IIIA, that faithfully recapitulates the human form of the disease, this biomarker was present at concentrations of >100 pmol/mL and undetectable in wild-type mice.</AbstractText>Advantages of this method over the most commonly used cisterna magna collection technique include increased CSF sample volume (10 μL) and reduced blood contamination.</AbstractText>The ability to collect CSF from mouse models of neurological disease enables a forum for translating research outcomes in experimental models to the human equivalent in which CSF collection is also possible.</AbstractText>Copyright © 2019 Elsevier B.V. All rights reserved.</CopyrightInformation> |
2,328,959 | Mapping glutathione utilization in the developing zebrafish (Danio rerio) embryo. | Glutathione (GSH), the most abundant vertebrate endogenous redox buffer, plays key roles in organogenesis and embryonic development, however, organ-specific GSH utilization during development remains understudied. Monochlorobimane (MCB), a dye conjugated with GSH by glutathione-s-transferase (GST) to form a fluorescent adduct, was used to visualize organ-specific GSH utilization in live developing zebrafish (Danio rerio) embryos. Embryos were incubated in 20 μM MCB for 1 h and imaged on an epifluorescence microscope. GSH conjugation with MCB was high during early organogenesis, decreasing as embryos aged. The heart had fluorescence 21-fold above autofluorescence at 24 hpf, dropping to 8.5-fold by 48 hpf; this increased again by 72 hpf to 23.5-fold, and stayed high till 96 hpf (18-fold). The brain had lower fluorescence (10-fold) at 24 and 48 hpf, steadily increasing to 30-fold by 96 hpf. The sensitivity and specificity of MCB staining was then tested with known GSH modulators. A 10-min treatment at 48 hpf with 750 μM tert-butylhydroperoxide, caused organ-specific reductions in staining, with the heart losing 30% fluorescence, and, the brain ventricle losing 47% fluorescence. A 24 h treatment from 24-48 hpf with 100 μM of N-Acetylcysteine (NAC) resulted in significantly increased fluorescence, with the brain ventricle and heart showing 312% and 240% increases respectively, these were abolished upon co-treatment with 5 μM BSO, an inhibitor of the enzyme that utilizes NAC to synthesize GSH. A 60 min 100 μM treatment with ethacrynic acid, a specific GST inhibitor, caused 30% reduction in fluorescence across all measured structures. MCB staining was then applied to test for GSH disruptions caused by the toxicants perfluorooctanesulfonic acid and mono-(2-ethyl-hexyl)phthalate; MCB fluorescence responded in a dose, structure and age-dependent manner. MCB staining is a robust, sensitive method to detect spatiotemporal changes in GSH utilization, and, can be applied to identify sensitive target tissues of toxicants. |
2,328,960 | ERK1/2 communicates GPCR and EGFR signaling pathways to promote CTGF-mediated hypertrophic cardiomyopathy upon Ang-II stimulation.<Pagination><StartPage>14</StartPage><MedlinePgn>14</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">14</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1186/s12860-019-0202-7</ELocationID><Abstract><AbstractText Label="BACKGROUND">Hypertrophic cardiomyopathy occurs along with pathological phenomena such as cardiac hypertrophy, myocardial fibrosis and cardiomyocyte activity. However, few of the specific molecular mechanisms underlying this pathological condition have been mentioned.</AbstractText><AbstractText Label="METHODS">All target proteins and markers expression in the study was verified by PCR and western bloting. H9c2 cell morphology and behavior were analyzed using immunofluorescent and proliferation assays, respectively. And, the CTGF protein secreted in cell culture medium was detected by ELISA.</AbstractText><AbstractText Label="RESULTS">We found that high expression of CTGF and low expression of EGFR were regulated by ERK1/2 signaling pathway during the cardiac hypertrophy induced by Ang-II stimulation. CTGF interacted with EGFR, and the interaction is reduced with the stimulation of Ang-II. ERK1/2 serves as the center of signal control during the cardiac hypertrophy.</AbstractText><AbstractText Label="CONCLUSION">The ERK1/2 cooperates with GPCR and EGFR signaling, and promotes the occurrence and development of cardiac hypertrophy by regulating the expression and binding states of CTGF and EGFR. The study revealed a regulation model based on ERK1/2, suggesting that ERK1/2 signaling pathway may be an important control link for mitigation of hypertrophic cardiomyopathy treatment.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Xin</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Cardiology, The Second Affiliated Hospital of Xi'an Jiaotong University, 157, Fifth West Road, Xi'an, 710004, Shaanxi, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lin</LastName><ForeName>Lin</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Cardiology, The Second Affiliated Hospital of Xi'an Jiaotong University, 157, Fifth West Road, Xi'an, 710004, Shaanxi, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Qing</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>Department of Cardiology, The Second Affiliated Hospital of Xi'an Jiaotong University, 157, Fifth West Road, Xi'an, 710004, Shaanxi, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ni</LastName><ForeName>Yajuan</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Cardiology, The Second Affiliated Hospital of Xi'an Jiaotong University, 157, Fifth West Road, Xi'an, 710004, Shaanxi, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Chaoying</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Cardiology, The Second Affiliated Hospital of Xi'an Jiaotong University, 157, Fifth West Road, Xi'an, 710004, Shaanxi, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Qin</LastName><ForeName>Shuguang</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Cardiology, The Second Affiliated Hospital of Xi'an Jiaotong University, 157, Fifth West Road, Xi'an, 710004, Shaanxi, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wei</LastName><ForeName>Jin</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Cardiology, The Second Affiliated Hospital of Xi'an Jiaotong University, 157, Fifth West Road, Xi'an, 710004, Shaanxi, China. xiweijin88@163.com.</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>2019</Year><Month>06</Month><Day>14</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>BMC Mol Cell Biol</MedlineTA><NlmUniqueID>101741148</NlmUniqueID><ISSNLinking>2661-8850</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D002070">Butadienes</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C526316">CCN2 protein, rat</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009570">Nitriles</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D043562">Receptors, G-Protein-Coupled</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C113580">U 0126</NameOfSubstance></Chemical><Chemical><RegistryNumber>11128-99-7</RegistryNumber><NameOfSubstance UI="D000804">Angiotensin II</NameOfSubstance></Chemical><Chemical><RegistryNumber>139568-91-5</RegistryNumber><NameOfSubstance UI="D055513">Connective Tissue Growth Factor</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.10.1</RegistryNumber><NameOfSubstance UI="C483803">Egfr protein, rat</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.10.1</RegistryNumber><NameOfSubstance UI="D066246">ErbB Receptors</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000804" MajorTopicYN="N">Angiotensin II</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002070" MajorTopicYN="N">Butadienes</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006332" MajorTopicYN="N">Cardiomegaly</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002312" MajorTopicYN="N">Cardiomyopathy, Hypertrophic</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D049108" MajorTopicYN="N">Cell Enlargement</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D055513" MajorTopicYN="N">Connective Tissue Growth Factor</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D066246" MajorTopicYN="N">ErbB Receptors</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020935" MajorTopicYN="Y">MAP Kinase Signaling System</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D032383" MajorTopicYN="N">Myocytes, Cardiac</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009570" MajorTopicYN="N">Nitriles</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010766" MajorTopicYN="N">Phosphorylation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D043562" MajorTopicYN="N">Receptors, G-Protein-Coupled</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">CTGF</Keyword><Keyword MajorTopicYN="N">EGFR</Keyword><Keyword MajorTopicYN="N">ERK1/2</Keyword><Keyword MajorTopicYN="N">Hypertrophic cardiomyopathy</Keyword></KeywordList><CoiStatement>The authors declare that they have no competing interests.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2018</Year><Month>9</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2019</Year><Month>6</Month><Day>2</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2019</Year><Month>6</Month><Day>16</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>6</Month><Day>16</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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Proc Natl Acad Sci U S A. 2015;112(29):E3855–E3863. doi: 10.1073/pnas.1510733112.</Citation><ArticleIdList><ArticleId IdType="doi">10.1073/pnas.1510733112</ArticleId><ArticleId IdType="pmc">PMC4517222</ArticleId><ArticleId IdType="pubmed">26150526</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">31200375</PMID><DateRevised><Year>2019</Year><Month>10</Month><Day>19</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1933-0693</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2019</Year><Month>Jun</Month><Day>14</Day></PubDate></JournalIssue><Title>Journal of neurosurgery</Title><ISOAbbreviation>J Neurosurg</ISOAbbreviation></Journal>Percival S. Bailey: eminent scholar of neurosciences who revealed the workings of the hypothalamus through clinicopathological research on craniopharyngiomas.<Pagination><StartPage>1</StartPage><EndPage>13</EndPage><MedlinePgn>1-13</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.3171/2019.3.JNS183145</ELocationID><ELocationID EIdType="pii" ValidYN="Y">2019.3.JNS183145</ELocationID><Abstract><AbstractText>Percival S. Bailey (1892-1973) was a scholar, neuroscientist, neuropathologist, and neurosurgeon who made decisive contributions in the field of neuro-oncology. Far less known are his groundbreaking insights into understanding hypothalamic physiology through the study of craniopharyngiomas. As one of Harvey W. Cushing's most talented trainees, Bailey was instrumental in developing Cushing's project of a histologically based prognostic classification of brain tumors. He worked at Peter Bent Brigham Hospital on and off between 1919 and 1928, owing to frequent clashes with his mentor. A major cause of this long-term conflict was Bailey's 1921 experimental demonstration of the hypothalamic origin of diabetes insipidus and Fröhlich's syndrome. This finding challenged Cushing's view that both alterations were due to pituitary gland insufficiency. In a seminal monograph written with John F. Fulton in 1929, both authors provided the first comprehensive account of the specific hypothalamic disturbances caused by tumors that originated within the infundibulum and third ventricle. The methodical study of Cushing's craniopharyngioma specimens allowed Bailey to recognize the close contact between these lesions and hypothalamic nuclei, a key concept that Bailey originally advanced for proper surgical planning. This article aims to credit Bailey for his pioneering definition of craniopharyngiomas as tumors with a true intrahypothalamic position.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Prieto</LastName><ForeName>Ruth</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>1Department of Neurosurgery, Puerta de Hierro University Hospital; and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pascual</LastName><ForeName>José M</ForeName><Initials>JM</Initials><AffiliationInfo><Affiliation>2Department of Neurosurgery, La Princesa University Hospital, Madrid, Spain.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2019</Year><Month>06</Month><Day>14</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Neurosurg</MedlineTA><NlmUniqueID>0253357</NlmUniqueID><ISSNLinking>0022-3085</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">3V = third ventricle</Keyword><Keyword MajorTopicYN="N">3VF = third ventricle floor</Keyword><Keyword MajorTopicYN="N">BTR = Brain Tumor Registry</Keyword><Keyword MajorTopicYN="N">CP = craniopharyngioma</Keyword><Keyword MajorTopicYN="N">DI = diabetes insipidus</Keyword><Keyword MajorTopicYN="N">Fröhlich’s syndrome</Keyword><Keyword MajorTopicYN="N">Harvey W. Cushing</Keyword><Keyword MajorTopicYN="N">PBBH = Peter Bent Brigham Hospital</Keyword><Keyword MajorTopicYN="N">Percival S. Bailey</Keyword><Keyword MajorTopicYN="N">craniopharyngioma</Keyword><Keyword MajorTopicYN="N">diabetes insipidus</Keyword><Keyword MajorTopicYN="N">history</Keyword><Keyword MajorTopicYN="N">hypothalamus</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2018</Year><Month>11</Month><Day>6</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2019</Year><Month>3</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>6</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2019</Year><Month>6</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2019</Year><Month>6</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>aheadofprint</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31200375</ArticleId><ArticleId IdType="doi">10.3171/2019.3.JNS183145</ArticleId><ArticleId IdType="pii">2019.3.JNS183145</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">31200374</PMID><DateRevised><Year>2019</Year><Month>06</Month><Day>14</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1933-0693</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2019</Year><Month>Jun</Month><Day>14</Day></PubDate></JournalIssue><Title>Journal of neurosurgery</Title><ISOAbbreviation>J Neurosurg</ISOAbbreviation></Journal>Clinical features and operative technique of transinfundibular craniopharyngioma. | Percival S. Bailey (1892-1973) was a scholar, neuroscientist, neuropathologist, and neurosurgeon who made decisive contributions in the field of neuro-oncology. Far less known are his groundbreaking insights into understanding hypothalamic physiology through the study of craniopharyngiomas. As one of Harvey W. Cushing's most talented trainees, Bailey was instrumental in developing Cushing's project of a histologically based prognostic classification of brain tumors. He worked at Peter Bent Brigham Hospital on and off between 1919 and 1928, owing to frequent clashes with his mentor. A major cause of this long-term conflict was Bailey's 1921 experimental demonstration of the hypothalamic origin of diabetes insipidus and Fröhlich's syndrome. This finding challenged Cushing's view that both alterations were due to pituitary gland insufficiency. In a seminal monograph written with John F. Fulton in 1929, both authors provided the first comprehensive account of the specific hypothalamic disturbances caused by tumors that originated within the infundibulum and third ventricle. The methodical study of Cushing's craniopharyngioma specimens allowed Bailey to recognize the close contact between these lesions and hypothalamic nuclei, a key concept that Bailey originally advanced for proper surgical planning. This article aims to credit Bailey for his pioneering definition of craniopharyngiomas as tumors with a true intrahypothalamic position.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Prieto</LastName><ForeName>Ruth</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>1Department of Neurosurgery, Puerta de Hierro University Hospital; and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pascual</LastName><ForeName>José M</ForeName><Initials>JM</Initials><AffiliationInfo><Affiliation>2Department of Neurosurgery, La Princesa University Hospital, Madrid, Spain.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2019</Year><Month>06</Month><Day>14</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Neurosurg</MedlineTA><NlmUniqueID>0253357</NlmUniqueID><ISSNLinking>0022-3085</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">3V = third ventricle</Keyword><Keyword MajorTopicYN="N">3VF = third ventricle floor</Keyword><Keyword MajorTopicYN="N">BTR = Brain Tumor Registry</Keyword><Keyword MajorTopicYN="N">CP = craniopharyngioma</Keyword><Keyword MajorTopicYN="N">DI = diabetes insipidus</Keyword><Keyword MajorTopicYN="N">Fröhlich’s syndrome</Keyword><Keyword MajorTopicYN="N">Harvey W. Cushing</Keyword><Keyword MajorTopicYN="N">PBBH = Peter Bent Brigham Hospital</Keyword><Keyword MajorTopicYN="N">Percival S. Bailey</Keyword><Keyword MajorTopicYN="N">craniopharyngioma</Keyword><Keyword MajorTopicYN="N">diabetes insipidus</Keyword><Keyword MajorTopicYN="N">history</Keyword><Keyword MajorTopicYN="N">hypothalamus</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2018</Year><Month>11</Month><Day>6</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2019</Year><Month>3</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>6</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2019</Year><Month>6</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2019</Year><Month>6</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>aheadofprint</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31200375</ArticleId><ArticleId IdType="doi">10.3171/2019.3.JNS183145</ArticleId><ArticleId IdType="pii">2019.3.JNS183145</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">31200374</PMID><DateRevised><Year>2019</Year><Month>06</Month><Day>14</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1933-0693</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2019</Year><Month>Jun</Month><Day>14</Day></PubDate></JournalIssue><Title>Journal of neurosurgery</Title><ISOAbbreviation>J Neurosurg</ISOAbbreviation></Journal><ArticleTitle>Clinical features and operative technique of transinfundibular craniopharyngioma.</ArticleTitle><Pagination><StartPage>1</StartPage><EndPage>10</EndPage><MedlinePgn>1-10</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.3171/2019.3.JNS181953</ELocationID><ELocationID EIdType="pii" ValidYN="Y">2019.3.JNS181953</ELocationID><Abstract><AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">Transinfundibular craniopharyngioma (TC) is one of the 4 subtypes of suprasellar craniopharyngioma. In this study, the authors analyzed the clinical features of and operative technique for TC.<AbstractText Label="METHODS" NlmCategory="METHODS">A total of 95 consecutive cases of suprasellar craniopharyngioma that had been resected via the endoscopic expanded endonasal approach were retrospectively reviewed. Patients were divided into 2 groups: 34 in the TC group and 61 in the nontransinfundibular craniopharyngioma (NC) group. Clinical and radiographic features, intraoperative findings, histopathological and genetic findings, and surgical outcomes were analyzed and compared between groups.<AbstractText Label="RESULTS" NlmCategory="RESULTS">Compared with NC, TC was mostly seen in adult patients (97.1%); it was rare in children (2.9%). Clinical presentations tended toward headache, hydrocephalus, and diabetes insipidus. The relatively smaller volume, midline location (consistent with the stalk position), unidentifiable stalk, no shift of the third ventricle, and greater likelihood to involve the third ventricle and cause hydrocephalus were the characteristic features of TC in the preoperative MRI study. According to the degree of vertical extension of the tumor, the 34 TCs could be classified into 3 subtypes: type 1, entity was limited to stalk (n = 2, 5.9%); type 2, tumor extended up to the third ventricle (type 2a) or down to the subdiaphragmatic cavity (type 2b) (n = 23, 67.6%); and type 3, tumor extended in both directions (n = 9, 26.5%). For TC resection, the chiasm-pituitary corridor, lamina terminalis corridor, and pituitary corridor could be used separately or jointly. Most of the TCs originated from the infundibulum-tuber cinereum, grew within and along the long axis of the infundibulum, and the pituitary stalk was not usually preserved in TCs (20.6%), whereas the rate of preservation was higher (80.3%) in NCs. Bilateral hypothalamic injury was found in nearly all TCs if radical resection was performed, whereas the relationship between NCs and hypothalamus was either compression (32.8%) or unilateral invasion (67.2%). Meanwhile, the postoperative endocrine and neuropsychological function outcomes in patients with TC were worse than in patients with NC. The genetic analysis with whole-exome sequencing studies showed no differential mutations of CTNNB1 (β-catenin) and BRAF (V600E) between TC and NC subtypes, but there was a difference between adamantinomatous craniopharyngioma and papillary craniopharyngioma.<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">TC is a special subtype of suprasellar craniopharyngioma, which is remarkably different from NC. Identification of this type of tumor preoperatively is essential for the planning of appropriate surgical approach and degree of excision. |
2,328,961 | Detailed structural assessment of healthy interventricular septum in the presence of remodeling infarct in the free wall - A finite element model. | Computational modelling may improve the fundamental understanding of various mechanisms of diseases more particularly related to clinical challenges. In this study the effect of remodeling infarct presence in the left ventricle on the interventricular septal wall is studied using the finite element methods.</AbstractText>In this study, two rat heart (one model with healthy myocardium and one model with remodeling free wall and healthy septal wall) with magnetic resonance imaging data was gathered to reconstruct three-dimensional (3D) rat heart models. 3D data points from Segment® were imported into SolidEdge® for creation of 3D rat heart models. Abaqus® was used for finite element modeling.</AbstractText>The strain in the healthy interventricular septum of the infarcted left ventricle wall increased when compared to the healthy interventricular septum in the healthy left ventricle. Similarly, the average stress in the healthy left ventricle was observed to have increased on the healthy the interventricular septum where the free wall is subjected to remodeling infarct. When comparing the infarcted models to the healthy model, it was found that the average strain had greatly increased by up to 50.0 %.</AbstractText>The remodeling infarct in the left ventricle has an impact on the healthy interventricular septal wall. Even though the interventricular septal wall was modelled as healthy, it was observed that it has undergone considerable changes in stresses and strains in circumferential and longitudinal direction. The observed changes in myocardial stresses and strains may result in poor global functioning of the heart.</AbstractText> |
2,328,962 | Cardiac hypertrophy is stimulated by altered training intensity and correlates with autophagy modulation in male Wistar rats. | The mechanism for cardiac hypertrophy process that would be a benefit for improvement of cardiovascular endurance needed to be investigated throughly. Specific intensity of training may play a role for homeostasis process in cardiac during training. In the present study, we examine the effect of different intensity of treadmill training on cardiac hypertrophy process and autophagy related gene expression in male wistar rats.</AbstractText>Three different intensities of treadmill training were conducted on 15 male wistar rats (Low Intensity: 10 m/minute, Moderate Intensity: 20 m/minute, and High Intensity: 30 m/minute) compared to 5 sedentary rats as control. Training duration was 30 min per day, frequency was 5 days per week, during 8 weeks period. Heart weight and heart weight/body weight ratio were measured after the experiments. Left ventricle myocardium was taken for microscopic analysis with HE staining. mRNA was extracted from left ventricle myocardium for examining αMHC and autophagy related gene expression (PIK3CA, mTOR, LC3, p62) using semi quantitative PCR.</AbstractText>We observed that altered training intensity might stimulate cardiac hypertrophy process. MI and HI training increased heart weight and heart weight/body weight ratio. This finding is supported by microscopic result in which cardiac hypertrophy was found in MI and HI, with focal fibrosis in HI, and increased αMHC gene expression in MI (p</i> < 0.05) and HI (p</i> = 0.076). We also observed decreased PIK3CA (LI 0.8 fold, MI 0.9 fold), mTOR (LI 0.9 fold, MI 0.9 fold), LC3 (LI 0.9 fold, MI 0.8 fold, HI 0.8 fold), and p62 (LI 0.8 fold, MI 0.9 fold) compared to control. Interestingly, we found increased mTOR (HI 1.1 fold) and p62 (HI 1.1 fold) compared to control.</AbstractText>Training with different intensity creates different cardiac hypertrophy process based on heart weight and heart weight/body weight ratio, microscopic examination and autophagy related gene expression.</AbstractText> |
2,328,963 | Differential expression of myosin heavy chain isoforms in cardiac segments of gnathostome vertebrates and its evolutionary implications. | Immunohistochemical studies of hearts from the lesser spotted dogfish, Scyliorhinus canicula</i> (Chondrichthyes) revealed that the pan-myosin heavy chain (pan-MyHC) antibody MF20 homogeneously labels all the myocardium, while the pan-MyHC antibody A4.1025 labels the myocardium of the inflow (sinus venosus and atrium) but not the outflow (ventricle and conus arteriosus) cardiac segments, as opposed to other vertebrates. We hypothesized that the conventional pattern of cardiac MyHC isoform distribution present in most vertebrates, i.e. MYH6 in the inflow and MYH7 in the outflow segments, has evolved from a primitive pattern that persists in Chondrichthyes. In order to test this hypothesis, we conducted protein detection techniques to identify the MyHC isoforms expressed in adult dogfish cardiac segments and to assess the pan-MyHC antibodies reactivity against the cardiac segments of representative species from different vertebrate groups.</AbstractText>Western and slot blot results confirmed the specificity of MF20 and A4.1025 for MyHC in dogfish and their differential reactivity against distinct myocardial segments. HPLC-ESI-MS/MS and ESI-Quadrupole-Orbitrap revealed abundance of MYH6 and MYH2 in the inflow and of MYH7 and MYH7B in the outflow segments. Immunoprecipitation showed higher affinity of A4.1025 for MYH2 and MYH6 than for MYH7 and almost no affinity for MYH7B. Immunohistochemistry showed that A4.1025 signals are restricted to the inflow myocardial segments of elasmobranchs, homogeneous in all myocardial segments of teleosts and acipenseriforms, and low in the ventricle of polypteriforms.</AbstractText>The cardiac inflow and outflow segments of the dogfish show predominance of fast- and slow-twitch MyHC isoforms respectively, what can be considered a synapomorphy of gnathostomes. The myocardium of the dogfish contains two isomyosins (MYH2 and MYH7B) not expressed in the adult heart of other vertebrates. We propose that these isomyosins lost their function in cardiac contraction during the evolution of gnathostomes, the later acquiring a regulatory role in myogenesis through its intronic miRNA. Loss of MYH2 and MYH7B expression in the heart possibly occurred before the origin of Osteichthyes, being the latter reacquired in polypteriforms. We raise the hypothesis that the slow tonic MYH7B facilitates the peristaltic contraction of the conus arteriosus of fish with a primitive cardiac anatomical design and of the vertebrate embryo.</AbstractText> |
2,328,964 | Region-specific and activity-dependent regulation of SVZ neurogenesis and recovery after stroke. | Stroke is the leading cause of adult disability. Neurogenesis after stroke is associated with repair; however, the mechanisms regulating poststroke neurogenesis and its functional effect remain unclear. Here, we investigate multiple mechanistic routes of induced neurogenesis in the poststroke brain, using both a forelimb overuse manipulation that models a clinical neurorehabilitation paradigm, as well as local manipulation of cellular activity in the peri-infarct cortex. Increased activity in the forelimb peri-infarct cortex via either modulation drives increased subventricular zone (SVZ) progenitor proliferation, migration, and neuronal maturation in peri-infarct cortex. This effect is sensitive to competition from neighboring brain regions. By using orthogonal tract tracing and rabies virus approaches in transgenic SVZ-lineage-tracing mice, SVZ-derived neurons synaptically integrate into the peri-infarct cortex; these effects are enhanced with forelimb overuse. Synaptic transmission from these newborn SVZ-derived neurons is critical for spontaneous recovery after stroke, as tetanus neurotoxin silencing specifically of the SVZ-derived neurons disrupts the formation of these synaptic connections and hinders functional recovery after stroke. SVZ-derived neurogenesis after stroke is activity-dependent, region-specific, and sensitive to modulation, and the synaptic connections formed by these newborn cells are functionally critical for poststroke recovery. |
2,328,965 | Outcomes of Pregnancy in Patients With Prior Right Ventricular Outflow Interventions. | Background The purpose of this study was to compare the incidence of pregnancy-related adverse outcomes ( PRAO ) between patients with versus without hemodynamically significant right ventricle outflow tract ( RVOT) . Methods and Results This was a retrospective cohort study of all pregnant patients with isolated RVOT lesions undergoing evaluation at the Mayo Clinic, 1990 to 2017. Hemodynamic significance was defined as ≥moderate pulmonary/conduit stenosis (≥3 m/s) and/or ≥moderate regurgitation. Patients with concomitant significant left heart disease were excluded. PRAO was defined as cardiovascular, obstetric, and/or neonatal complications occurring during the pregnancy through 6 weeks postpartum. A total of 224 pregnancies in 114 patients with RVOT lesions were identified; 38 pregnancies occurred in 24 patients with hemodynamically significant RVOT . Forty-eight (21%) pregnancies ended in spontaneous abortion. Of the 173 completed pregnancies, median gestational age at delivery was 38 (35-40) weeks and median birth weight 2965 (2065-4122) g. Seven pregnancies (4%) were complicated by cardiovascular events, 14 (8%) by obstetric complications, with adverse neonatal outcomes occurring in 38 (22%). There were no maternal deaths. The incidence of spontaneous abortion and PRAO were similar in both the RVOT and hemodynamically significant RVOT groups. As an isolated condition, Tetralogy of Fallot-pulmonary atresia was associated with spontaneous abortion and neonatal complications. Conclusions The risk of cardiovascular complications was low in patients with isolated RVOT lesions, and hemodynamically significant RVOT lesions were not associated with either cardiovascular complications or PRAO . Further studies are required to explore the factors responsible for PRAO in patients with Tetralogy of Fallot-pulmonary atresia. |
2,328,966 | Prone CT for diagnosis of silicone oil intraventricular migration after intraocular tamponade. | Silicone oil tamponade is a frequent treatment for retinal detachment. Intraventricular migration of this agent is rare, but was described previously in patients with chronic glaucoma and atrophy of the optic disc. We describe a patient with prior silicone oil tamponade in the left eye with a noncontrast computed tomography demonstrating hyperattenuating material along the course of the left optic nerve and in the frontal horns of the lateral ventricles, and emphasize the use of prone noncontrast computed tomography as an important diagnostic tool in order to confirm the low specific gravity of the oil agent. |
2,328,967 | Corrigendum: ECG Imaging to Detect the Site of Ventricular Ischemia Using Torso Electrodes: A Computational Study. | [This corrects the article DOI: 10.3389/fphys.2019.00050.]. |
2,328,968 | Asymmetric Dimethylarginine at Sea Level Is a Predictive Marker of Hypoxic Pulmonary Arterial Hypertension at High Altitude. | <b>Background:</b> Prolonged exposure to altitude-associated chronic hypoxia (CH) may cause high-altitude pulmonary hypertension (HAPH). Chronic intermittent hypobaric hypoxia (CIH) occurs in individuals who commute between sea level and high altitude. CIH is associated with repetitive acute hypoxic acclimatization and conveys the long-term risk of HAPH. As nitric oxide (NO) regulates pulmonary vascular tone and asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of NO synthesis, we investigated whether ADMA concentration at sea level predicts HAPH among Chilean frontiers personnel exposed to 6 months of CIH. <b>Methods:</b> In this prospective study, 123 healthy army draftees were subjected to CIH (5 days at 3,550 m, 2 days at sea level) for 6 months. In 100 study participants with complete data, ADMA, symmetric dimethylarginine (SDMA), L-arginine, arterial oxygen saturation (SaO<sub>2</sub>), systemic blood pressure, and hematocrit were assessed at months 0 (sea level), 1, 4, and 6. Acclimatization to altitude was determined using the Lake Louise Score (LLS) and the presence of acute mountain sickness (AMS). Echocardiography was performed after 6 months of CIH in 43 individuals with either good (<i>n</i> = 23) or poor (<i>n</i> = 20) acclimatization. <b>Results:</b> SaO<sub>2</sub> acutely decreased at altitude and plateaued at 90% thereafter. ADMA increased and SDMA decreased during the study course. The incidence of AMS and the LLS was high after the first ascent (53 and 3.1 ± 2.4) and at 1 month of CIH (47 and 3.0 ± 2.6), but decreased to 20 and 1.4 ± 2.0 at month 6 (both <i>p</i> < 0.001). Eighteen participants (42%) showed a mean pulmonary arterial pressure (mPAP) >25 mm Hg, out of which 9 (21%) were classified as HAPH (mPAP ≥ 30 mm Hg). ADMA at sea level was significantly associated with mPAP at high altitude in month 6 (<i>R</i> = 0.413; <i>p</i> = 0.007). In ROC analysis, a cutoff for baseline ADMA of 0.665 μmol/L was determined to predict HAPH (mPAP > 30 mm Hg) with a sensitivity of 100% and a specificity of 63.6%. <b>Conclusions:</b> ADMA concentration increases during CIH. ADMA at sea level is an independent predictive biomarker of HAPH. SDMA concentration decreases during CIH and shows no association with HAPH. Our data support a role of impaired NO-mediated pulmonary vasodilation in the pathogenesis of HAPH. |
2,328,969 | The Configuration of the Perivascular System Transporting Macromolecules in the CNS. | Large blood vessels entering the CNS are surrounded by perivascular spaces that communicate with the cerebrospinal fluid and, at their termini, with the interstitial space. Solutes and particles can translocate along these perivascular conduits, reportedly in both directions. Recently, this prompted a renewed interest in the intrathecal therapy delivery route for CNS-targeted therapeutics. However, the extent of the CNS coverage by the perivascular system is unknown, making the outcome of drug administration to the CSF uncertain. We traced the translocation of model macromolecules from the CSF into the CNS of rats and non-human primates. Conduits transporting macromolecules were found to extend throughout the parenchyma from both external and internal (fissures) CNS boundaries, excluding ventricles, in large numbers, on average ca. 40 channels per mm<sup>2</sup> in rats and non-human primates. The high density and depth of extension of the perivascular channels suggest that the perivascular route can be suitable for delivery of therapeutics to parenchymal targets throughout the CNS. |
2,328,970 | Upregulation of the lncRNA MEG3 improves cognitive impairment, alleviates neuronal damage, and inhibits activation of astrocytes in hippocampus tissues in Alzheimer's disease through inactivating the PI3K/Akt signaling pathway. | The purpose of this study was to elucidate the expression of the long noncoding RNA (lncRNA) maternally expressed gene 3 (MEG3) in rats with Alzheimer's disease (AD) and to explore its potential mechanisms.</AbstractText>An AD rat model was induced by microinjection of Aβ25-35</sub> . On the first day after successful modeling, pcDNA3.1 plasmid and pcDNA3.1-MEG3 plasmid were continuously infused into the third ventricle through a micro-osmotic pump to interfere with the expression level of MEG3. The spatial learning ability and memory ability, the histopathological changes of hippocampus tissues, the ultrastructure of hippocampal neurons, astrocyte activation as well as the survival and apoptosis of hippocampal neurons in each group was observed. The expression of apoptosis, PI3/Akt signaling pathway-related proteins, glial fibrillary acidic protein, inflammatory factors, malondialdehyde, glutathione-peroxidase, and superoxide dismutase levels were determined. The deposition of amyloid beta (Aβ) in the hippocampus of rats by was observed by Aβ immunohistochemical staining.</AbstractText>Downregulated MEG3 was detected in the tissues of AD rats. In addition, upregulation of MEG3 contributed to an improvement of spatial learning ability and memory ability, inhibited the pathological injury and its apoptosis of hippocampal neurons, decreased Aβ positive expression, inhibited oxidative stress injury and inflammatory injury as well as the activated astrocytes in AD rats via inactivation of the PI3/Akt pathway.</AbstractText>Our study highlights that upregulation of the lncRNA MEG3 improves cognitive impairment, alleviates neuronal damage, and inhibits activation of astrocytes in hippocampus tissues in AD through inhibiting the PI3K/Akt signaling pathway.</AbstractText>© 2019 Wiley Periodicals, Inc.</CopyrightInformation> |
2,328,971 | Cornel iridoid glycoside induces autophagy to protect against tau oligomer neurotoxicity induced by the activation of glycogen synthase kinase-3β. | Tau oligomers are the etiologic molecules of Alzheimer's disease, and correlate strongly with neuronal loss and exhibit neurotoxicity. Recent evidence indicates that small tau oligomers are the most relevant toxic aggregate species. The aim of the present study was to investigate the mechanisms of cornel iridoid glycoside (CIG) on tau oligomers and cognitive functions. We injected wortmannin and GF-109203X (WM/GFX, 200 μM each) into the lateral ventricles to induce tau oligomer and memory impairment in rats. When orally administered with CIG at 60 and 120 mg/kg/day for 14 days, CIG decreased the escape latency in the Morris water maze test. We also found that CIG restored the expression of presynaptic p-synapsin, synaptophysin, and postsynaptic density-95 (PSD-95) decreased by WM/GFX in rat cortex. CIG reduced the accumulation of tau oligomers in the brain of WM/GFX rats and in cells transfected with wild type glycogen synthase kinase-3β (wtGSK-3β). In addition, CIG up-regulated the levels of ATG7, ATG12, Beclin-1, and LC3II in vivo and in vitro, suggesting the restoration of autophagy function. These results suggest that CIG could ameliorate memory deficits and regulate memory-associated synaptic proteins through the clearance of tau oligomers accumulation. Moreover, CIG clears tau oligomers by restoring autophagy function. |
2,328,972 | Adrenalectomy impairs insulin-induced hypophagia and related hypothalamic changes. | Adrenalectomy (ADX) induces hypophagia and glucocorticoids counter-regulate the peripheral metabolic effects of insulin. This study evaluated the effects of ADX on ICV (lateral ventricle) injection of insulin-induced changes on food intake, mRNA expression of hypothalamic neuropeptides (insulin receptor (InsR), proopiomelanocortin, cocaine and amphetamine-regulated transcript (Cart), agouti-related protein, neuropeptide Y (Npy) in the arcuate nucleus of the hypothalamus (ARC), corticotrophin-releasing factor in the paraventricular nucleus of the hypothalamus) and hypothalamic protein content of insulin signaling-related molecules (insulin receptor substrate (IRS) 1, protein kinase B (AKT), extracellular-signal-regulated kinase (ERK1/2), c-Jun N-terminal kinase (JNK), protein tyrosine phosphatase-1B (PTP1B) and T cell protein tyrosine phosphatase (TCPTP)) Compared with sham animals, ADX increased the hypothalamic content of pJNK/JNK, PTP1B and TCPTP, as well as decreased mRNA expression of InsR, and corticosterone (B) treatment reversed these effects. Insulin central injection enhanced hypothalamic content of pAKT/AKT and Cart mRNA expression, decreased Npy mRNA expression and food intake only in sham rats, without effects in ADX and ADX + B rats. Insulin did not alter the hypothalamic phosphorylation of IRS1 and ERK1/2 in the three experimental groups. These data demonstrate that ADX reduces the expression of InsR and increases insulin counter-regulators in the hypothalamus, as well as ADX abolishes hypophagia, activation of hypothalamic AKT pathway and changes in Cart and Npy mRNA expression in the ARC induced by insulin. Thus, the higher levels of insulin counter-regulatory proteins and lower expression of InsR in the hypothalamus are likely to underlie impaired insulin-induced hypophagia and responses in the hypothalamus after ADX. |
2,328,973 | Transient Redirection of SVZ Stem Cells to Oligodendrogenesis by FGFR3 Activation Promotes Remyelination. | Stimulating oligodendrocyte (OL) production from endogenous progenitor cells is an important strategy for myelin repair and functional restoration after disease or injury-induced demyelination. Subventricular zone (SVZ) stem cells are multipotential, generating neurons and oligodendroglia. The factors that regulate the fate of these stem cells are poorly defined. In this study, we show that genetically increasing fibroblast growth factor receptor-3 (FGFR3) activity in adult SVZ stem cells transiently and dramatically redirects their differentiation from the neuronal to the oligodendroglial lineage after pathological demyelination. The increased SVZ-derived oligodendrogenesis leads to improved OL regeneration and myelin repair, not only in the corpus callosum (a normal destination for SVZ-derived oligodendroglial cells), but also in the lower cortical layers. This study identifies FGF signaling as a potent target for improving endogenous SVZ-derived OL regeneration and remyelination. |
2,328,974 | Amitriptyline accumulation in tissues after coated activated charcoal hemoperfusion-a randomized controlled animal poisoning model. | Amitriptyline poisoning (AT) is a common poisoning, and AT possess the ability to promote life-threatening complications by its main action on the central nervous and cardiovascular systems. The pharmacokinetic properties might be altered at toxic levels compared to therapeutic levels. The effect of coated activated charcoal hemoperfusion (CAC-HP) on the accumulation of AT and its active metabolite nortriptyline (NT) in various tissues was studied in a non-blinded randomized controlled animal trial including 14 female Danish Land Race piglets. All piglets were poisoned with amitriptyline 7.5 mg/kg infused in 20 min, followed by orally instilled activated charcoal at 30 min after infusion cessation. The intervention group received 4 h of CAC-HP followed by a 1-h redistribution phase. At study cessation, the piglets were euthanized, and within 20 min, vitreous fluid, liver tissue, ventricle and septum of the heart, diaphragm and lipoic and brain tissues were collected. AT and NT tissue concentrations were quantified by UHPLC-MS/MS. A 4-h treatment with CAC-HP did not affect the tissue accumulation of AT in the selected organs when tested by Mann-Whitney U test (p values between 0.44 and 0.73). For NT concentrations, p values were between 0.13 and 1.00. Although not significant, an interesting finding was that data showed a tendency of increased tissue accumulation of AT and NT in the CAC-HP group compared with the control group. Coated activated charcoal hemoperfusion does not significantly alter the tissue concentration of AT and NT in the AT-poisoned piglet. |
2,328,975 | Insulin Suppresses Type 1 Diabetes Mellitus-Induced Ventricular Cardiomyocyte Damage Associated with the Inhibition of Biomarkers of Inflammation and Oxidative Stress in Rats. | We sought to determine whether insulin can protect against type 1 diabetes mellitus (T1DM)-induced cardiac ultrastructural alterations in an animal model of the disease. This has not been investigated before.</AbstractText>Rats were either injected once with 65 mg/kg streptozotocin (STZ) before being sacrificed after 8 weeks or were treated with a daily injection of insulin 2 days by STZ and continued until being sacrificed.</AbstractText>Harvested tissues obtained from left ventricles in the untreated T1DM rats showed substantial damage to the cardiomyocyte ultrastructure as demonstrated by disintegrated myofibrils and their sarcomeres, damaged mitochondria and lipid droplets, which was substantially protected by insulin. Insulin also significantly inhibited T1DM-induced hyperglycemia (p < 0.001), dyslipidemia (p < 0.0001), malondialdehyde (MDA; p < 0.0001), tumor necrosis factor-alpha (TNF-α; p < 0.001) and interleukin-6 (p < 0.001). We further demonstrated a significant (p ≤ 0.001) correlation between either sarcomere or mitochondrial injury scoring and the serum levels of glucose, dyslipidemia, and biomarkers of oxidative stress (OxS) and inflammation.</AbstractText>These results indicate that insulin effectively suppresses left ventricular cardiomyocyte ultrastructural damage, which substantially slows down the progression of diabetic cardiomyopathy for 8 weeks in a rat model of T1DM, possibly due to the glycemic control and inhibition of dyslipidemia, OxS and inflammation.</AbstractText>© 2019 S. Karger AG, Basel.</CopyrightInformation> |
2,328,976 | RASA1-dependent cellular export of collagen IV controls blood and lymphatic vascular development. | Combined germline and somatic second hit inactivating mutations of the RASA1 gene, which encodes a negative regulator of the Ras signaling pathway, cause blood and lymphatic vascular lesions in the human autosomal dominant vascular disorder capillary malformation-arteriovenous malformation (CM-AVM). How RASA1 mutations in endothelial cells (EC) result in vascular lesions in CM-AVM is unknown. Here, using different murine models of RASA1-deficiency, we found that RASA1 was essential for the survival of EC during developmental angiogenesis in which primitive vascular plexuses are remodeled into hierarchical vascular networks. RASA1 was required for EC survival during developmental angiogenesis because it was necessary for export of collagen IV from EC and deposition in vascular basement membranes. In the absence of RASA1, dysregulated Ras mitogen-activated protein kinase (MAPK) signal transduction in EC resulted in impaired folding of collagen IV and its retention in the endoplasmic reticulum (ER) leading to EC death. Remarkably, the chemical chaperone, 4-phenylbutyric acid, and small molecule inhibitors of MAPK and 2-oxoglutarate dependent collagen IV modifying enzymes rescued ER retention of collagen IV and EC apoptosis and resulted in normal developmental angiogenesis. These findings have important implications with regards an understanding of the molecular pathogenesis of CM-AVM and possible means of treatment. |
2,328,977 | Levo-transposition of the Great Arteries in an Adult Patient: Management Considerations and Treatment Strategy. | Levo-transposition of the great arteries (L-TGA) is a rare congenital heart anomaly associated with the increased risk of developing heart failure (HF) as well as complete heart block at a young age. Due to limited data regarding the treatment strategy in the adult L-TGA sub-population, shared medical decision-making should occur between the patient and a team of physicians. Clinical status, age, and associated cardiac lesions or rhythm disturbances can affect patient outcomes. These factors should be considered prior to pursuing a surgical versus a medicinal approach. |
2,328,978 | Cardiac Magnetic Resonance Imaging and Transthoracic Echocardiography: Investigation of Concordance between the Two Methods for Measurement of the Cardiac Chamber. | <i>Background and objectives:</i> Cardiac magnetic resonance (CMR) imaging is the gold standard method for the detection of ventricular volumes and myocardial edema/scar. Transthoracic echocardiography (TTE) imaging is primarily used in the evaluation of cardiac functions and chamber dimensions. This study aims to investigate whether the chamber diameter measurements are concordant with each other in the same patient group who underwent TTE and CMR. <i>Materials and Methods:</i> The study included 41 patients who underwent TTE and CMR imaging. Ventricular and atrial diameter measurements from TTE-derived standard parasternal long axis and apical four-chamber views and CMR-derived three- and four-chamber views were recorded. The concordance between the two methods was compared using intra-class correlation coefficients (ICC) and Bland-Altman plots. <i>Results:</i> Of the patients, 25 (61%) were male and the mean age was 48.12 ± 16.79. The mean ICC for LVDD between CMR observers was 0.957 (95% CI: 0.918-0.978), while the mean ICC between CMR and TTE measurements were 0.849 (95% CI: 0.709-0.922) and 0.836 (95% CI: 0.684-0.915), respectively. The mean ICC for the right ventricle between CMR observers was 0.985 (95% CI: 0.971-0.992), while the mean ICC between CMR and TTE measurements were 0.869 (95% CI: 0.755-0.930) and 0.892 (95% CI: 0.799-0.942), respectively. Passing-Bablok Regression and Bland-Altman plots indicated high concordance between the two methods. <i>Conclusions:</i> TTE and CMR indicated high concordance in chamber diameter measurements for which the CMR should be considered in patients for whom optimal evaluation with TTE could not be performed due to their limitations. |
2,328,979 | Midbrain area for differentiating Parkinson's disease from progressive supranuclear palsy. | We aimed to investigate the values of midbrain area in diagnosing Parkinson's Disease (PD) and progressive supranuclear palsy (PSP) by using transcranial sonography (TCS). Disease duration effect on brain sonographic findings could decrease the accuracy of TCS in PD and PSP patients. We reduced the disease duration effect on sonographic differences found between PD and PSP patients by using multivariate analysis.</AbstractText>Patients with clinical diagnosis of PSP and PD were recruited. We used SonoSite Edge II Ultrasound system to measure midbrain area, diameter of third ventricle and substantia nigra echogenicity. Diagnostic value of each measured area in sonography was estimated regarding its power for diagnosing PD or PSP. Independent sample t-test, Regression analysis and receiver operating characteristic (ROC) curve were performed using SPSS software.</AbstractText>Of 35 patients, 18 were PD and 17 PSP cases. The mean midbrain area was 4.86 ± 0.71cm2</sup> in PD patients and 3.61 ± 0.85cm2</sup> in those with PSP (P < 0.005). Regression for reducing the effect of disease duration on midbrain area variances between patients with PD and PSP revealed a significant P value (P < 0.005, Adjusted R2</sup> = 0.36). The sensitivity and specificity of midbrain area in diagnosing PD were 83.3% and 70.6% respectively. The sensitivity of the third ventricle size in diagnosing PSP was 82% although its specificity was 62%.</AbstractText>Midbrain area in patients with PD was wider than those with PSP that was not affected by disease duration. Midbrain area was the most accurate index for diagnosing PD by TCS although third ventricle size was the most sensitive one for diagnosing PSP.</AbstractText>Copyright © 2019 Elsevier B.V. All rights reserved.</CopyrightInformation> |
2,328,980 | Calorie restriction activates new adult born olfactory-bulb neurones in a ghrelin-dependent manner but acyl-ghrelin does not enhance subventricular zone neurogenesis. | The ageing and degenerating brain show deficits in neural stem/progenitor cell (NSPC) plasticity that are accompanied by impairments in olfactory discrimination. Emerging evidence suggests that the gut hormone ghrelin plays an important role in protecting neurones, promoting synaptic plasticity and increasing hippocampal neurogenesis in the adult brain. In the present study, we investigated the role of ghrelin with respect to modulating adult subventricular zone (SVZ) NSPCs that give rise to new olfactory bulb (OB) neurones. We characterised the expression of the ghrelin receptor, growth hormone secretagogue receptor (GHSR), using an immunohistochemical approach in GHSR-eGFP reporter mice to show that GHSR is expressed in several regions, including the OB but not in the SVZ of the lateral ventricle. These data suggest that acyl-ghrelin does not mediate a direct effect on NSPC in the SVZ. Consistent with these findings, treatment with acyl-ghrelin or genetic silencing of GHSR did not alter NSPC proliferation within the SVZ. Similarly, using a bromodeoxyuridine pulse-chase approach, we show that peripheral treatment of adult rats with acyl-ghrelin did not increase the number of new adult-born neurones in the granule cell layer of the OB. These data demonstrate that acyl-ghrelin does not increase adult OB neurogenesis. Finally, we investigated whether elevating ghrelin indirectly, via calorie restriction (CR), regulated the activity of new adult-born cells in the OB. Overnight CR induced c-Fos expression in new adult-born OB cells but not in developmentally born cells, whereas neuronal activity was absent following re-feeding. These effects were not present in ghrelin<sup>-/-</sup> mice, suggesting that adult-born cells are uniquely sensitive to changes in ghrelin mediated by fasting and re-feeding. In summary, ghrelin does not promote neurogenesis in the SVZ and OB; however, new adult-born OB cells are activated by CR in a ghrelin-dependent manner. |
2,328,981 | Left Ventricle Segmentation and Quantification from Cardiac Cine MR Images via Multi-task Learning. | Segmentation of the left ventricle and quantification of various cardiac contractile functions is crucial for the timely diagnosis and treatment of cardiovascular diseases. Traditionally, the two tasks have been tackled independently. Here we propose a convolutional neural network based multi-task learning approach to perform both tasks simultaneously, such that, the network learns better representation of the data with improved generalization performance. Probabilistic formulation of the problem enables learning the task uncertainties during the training, which are used to automatically compute the weights for the tasks. We performed a five fold cross-validation of the myocardium segmentation obtained from the proposed multi-task network on 97 patient 4-dimensional cardiac cine-MRI datasets available through the STA-COM LV segmentation challenge against the provided gold-standard myocardium segmentation, obtaining a Dice overlap of 0.849 ± 0.036 and mean surface distance of 0.274 ± 0.083 mm, while simultaneously estimating the myocardial area with mean absolute difference error of 205 ± 198 mm<sup>2</sup>. |
2,328,982 | Hydrogen Sulfide Ameliorates Homocysteine-Induced Cardiac Remodeling and Dysfunction. | Patients with diabetes, a methionine-rich meat diet, or certain genetic polymorphisms show elevated levels of homocysteine (Hcy), which is strongly associated with the development of cardiovascular disease including diabetic cardiomyopathy. However, reducing Hcy levels with folate shows no beneficial cardiac effects. We have previously shown that a hydrogen sulfide (H<sub>2</sub>S), a by-product of Hcy through transsulfuration by cystathionine beta synthase (CBS), donor mitigates Hcy-induced hypertrophy in cardiomyocytes. However, the <i>in vivo</i> cardiac effects of H<sub>2</sub>S in the context of hyperhomocysteinemia (HHcy) have not been studied. We tested the hypothesis that HHcy causes cardiac remodeling and dysfunction <i>in vivo</i>, which is ameliorated by H<sub>2</sub>S. Twelve-week-old male CBS<sup>+/-</sup> (a model of HHcy) and sibling CBS<sup>+/+</sup> (WT) mice were treated with SG1002 (a slow release H<sub>2</sub>S donor) diet for 4 months. The left ventricle of CBS<sup>+/-</sup> mice showed increased expression of early remodeling signals c-Jun and c-Fos, increased interstitial collagen deposition, and increased cellular hypertrophy. Notably, SG1002 treatment slightly reduced c-Jun and c-Fos expression, decreased interstitial fibrosis, and reduced cellular hypertrophy. Pressure volume loop analyses in CBS<sup>+/-</sup> mice revealed increased end systolic pressure with no change in stroke volume (SV) suggesting increased afterload, which was abolished by SG1002 treatment. Additionally, SG1002 treatment increased end-diastolic volume and SV in CBS<sup>+/-</sup> mice, suggesting increased ventricular filling. These results demonstrate SG1002 treatment alleviates cardiac remodeling and afterload in HHcy mice. H<sub>2</sub>S may be cardioprotective in conditions where H<sub>2</sub>S is reduced and Hcy is elevated. |
2,328,983 | Use of Ceftriaxone in Treating Cognitive and Neuronal Deficits Associated With Dementia With Lewy Bodies. | Dementia with Lewy bodies (DLB) is caused by accumulation of Lewy bodies, destruction of mitochondria, and excess of glutamate in synapses, which eventually leads to excitotoxicity, neurodegeneration, and cognitive impairments. Ceftriaxone (CEF) reduces excitotoxicity by increasing glutamate transporter 1 expression and glutamate reuptake. We investigated whether CEF can prevent cognitive decline and neurological deficits and increase neurogenesis in DLB rats. Male Wistar rats infused with viral vector containing human alpha-synuclein (α-syn) gene, <i>SNCA</i>, in the lateral ventricle were used as a rat model of DLB. CEF (100 mg/kg/day, i.p.) was injected in these rats for 27 days. The active avoidance test and object recognition test was performed. Finally, the brains of all the rats were immunohistochemically stained to measure α-syn, neuronal density, and newborn cells in the hippocampus and substantia nigra. The results revealed that DLB rats had learning and object recognition impairments and exhibited cell loss in the nigrostriatal dopaminergic system, and hippocampal CA1, and dentate gyrus (DG). Additionally, DLB rats had fewer newborn cells in the DG and substantia nigra pars reticulata and more α-syn immune-positive cells in the DG. Treatment with CEF improved cognitive function, reduced cell loss, and increased the number of newborn cells in the brain. To our knowledge, this is the first study showing that CEF prevents loss of neurogenesis in the brain of DLB rats. CEF may therefore has clinical potential for treating DLB. |
2,328,984 | The Orphan Nuclear Receptor TLX Represses Hes1 Expression, Thereby Affecting NOTCH Signaling and Lineage Progression in the Adult SEZ. | In the adult subependymal zone (SEZ), neural stem cells (NSCs) apically contacting the lateral ventricle on activation generate progenitors proliferating at the niche basal side. We here show that Tailless (TLX) coordinates NSC activation and basal progenitor proliferation by repressing the NOTCH effector Hes1. Consistent with this, besides quiescence Hes1 expression also increases on Tlx mutation. Since HES1 levels are higher at the apical SEZ, NOTCH activation is increased in Tlx<sup>-/-</sup> NSCs, but not in surrounding basal progenitors. Underscoring the causative relationship between higher HES1/NOTCH and increased quiescence, downregulation of Hes1 only in mutant NSCs normalizes NOTCH activation and resumes proliferation and neurogenesis not only in NSCs, but especially in basal progenitors. Since pharmacological blockade of NOTCH signaling also promotes proliferation of basal progenitors, we conclude that TLX, by repressing Hes1 expression, counteracts quiescence and NOTCH activation in NSCs, thereby relieving NOTCH-mediated lateral inhibition of proliferation in basal progenitors. |
2,328,985 | Bilateral oculomotor nerve palsy in a case of anti-aquaporin-4 antibody-positive neuromyelitis optica spectrum disorder. | Neuromyelitis optica spectrum disorder (NMOSD) has a wide disease spectrum and sometimes shows abnormal eye movement with brainstem manifestations. However, bilateral oculomotor nerve palsy with a midbrain lesion has never been reported in a patient with NMOSD. We describe a 61-year-old woman with progressive ptosis and diplopia. She displayed bilateral oculomotor nerve palsy and hypersomnia. Brain MRI demonstrated abnormal signal intensities in the midbrain and around the third ventricle and hypothalamus with a mild contrast enhancement. A cerebrospinal fluid study indicated elevated protein and pleocytosis. Because serum anti-aquaporin-4 IgG antibody was positive, the patient was diagnosed with neuromyelitis optica spectrum disorder with aquaporin-4 IgG. We report for the first time bilateral oculomotor nerve palsy as an initial manifestation in a patient with aquaporin-4 positive NMOSD. |
2,328,986 | Influence of Intracerebral Hemorrhage Location on Outcomes in Patients With Severe Intraventricular Hemorrhage. | Background and Purpose- We investigated the prognostic significance of spontaneous intracerebral hemorrhage location in presence of severe intraventricular hemorrhage. Methods- We analyzed diagnostic computed tomography scans from 467/500 (excluding primary intraventricular hemorrhage) subjects from the CLEAR (Clot Lysis: Evaluating Accelerated Resolution of Intraventricular Hemorrhage) III trial. We measured intracerebral hemorrhage engagement with specific anatomic regions, and estimated association of each region with blinded assessment of dichotomized poor stroke outcomes: mortality, modified Rankin Scale score of 4 to 6, National Institutes of Health Stroke Scale score of >4, stroke impact scale score of <60, Barthel Index <86, and EuroQol visual analogue scale score of <50 and <70 at days 30 and 180, respectively, using logistic regression models. Results- Frequency of anatomic region involvement consisted of thalamus (332 lesions, 71.1% of subjects), caudate (219, 46.9%), posterior limb internal capsule (188, 40.3%), globus pallidus/putamen (127, 27.2%), anterior limb internal capsule (108, 23.1%), and lobar (29, 6.2%). Thalamic location was independently associated with mortality (days 30 and 180) and with poor outcomes on most stroke scales at day 180 on adjusted analysis. Posterior limb internal capsule and globus pallidus/putamen involvement was associated with increased odds of worse disability at days 30 and 180. Anterior limb internal capsule and caudate locations were associated with decreased mortality on days 30 and 180. Anterior limb internal capsule lesions were associated with decreased long-term morbidity. Conclusions- Acute intracerebral hemorrhage lesion topography provides important insights into anatomic correlates of mortality and functional outcomes even in severe intraventricular hemorrhage causing obstructive hydrocephalus. Models accounting for intracerebral hemorrhage location in addition to volumes may improve outcome prediction and permit stratification of benefit from aggressive acute interventions. Clinical Trial Registration- URL: https://www.clinicaltrials.gov . Unique identifier: NCT00784134. |
2,328,987 | (-)-Phenserine Ameliorates Contusion Volume, Neuroinflammation, and Behavioral Impairments Induced by Traumatic Brain Injury in Mice. | Traumatic brain injury (TBI), a major cause of mortality and morbidity, affects 10 million people worldwide, with limited treatment options. We have previously shown that (-)-phenserine (Phen), an acetylcholinesterase inhibitor originally designed and tested in clinical phase III trials for Alzheimer's disease, can reduce neurodegeneration after TBI and reduce cognitive impairments induced by mild TBI. In this study, we used a mouse model of moderate to severe TBI by controlled cortical impact to assess the effects of Phen on post-trauma histochemical and behavioral changes. Animals were treated with Phen (2.5 mg/kg, IP, BID) for 5 days started on the day of injury and the effects were evaluated by behavioral and histological examinations at 1 and 2 weeks after injury. Phen significantly attenuated TBI-induced contusion volume, enlargement of the lateral ventricle, and behavioral impairments in motor asymmetry, sensorimotor functions, motor coordination, and balance functions. The morphology of microglia was shifted to an active from a resting form after TBI, and Phen dramatically reduced the ratio of activated to resting microglia, suggesting that Phen also mitigates neuroinflammation after TBI. While Phen has potent anti-acetylcholinesterase activity, its (+) isomer Posiphen shares many neuroprotective properties but is almost completely devoid of anti-acetylcholinesterase activity. We evaluated Posiphen at a similar dose to Phen and found similar mitigation in lateral ventricular size increase, motor asymmetry, motor coordination, and balance function, suggesting the improvement of these histological and behavioral tests by Phen treatment occur via pathways other than anti-acetylcholinesterase inhibition. However, the reduction of lesion size and improvement of sensorimotor function by Posiphen were much smaller than with equivalent doses of Phen. Taken together, these results show that post-injury treatment with Phen over 5 days significantly ameliorates severity of TBI. These data suggest a potential development of this compound for clinical use in TBI therapy. |
2,328,988 | [Clinical analysis of sequelae of acute trimethyltin oxide poisoning]. | <b>Objective:</b> Clinical analysis of sequelae of 16 patients with trimethyltin chloride (TMT) poisoning after 2 years. <b>Methods:</b> Sixteen patients with TMT poisoning from a waste recycling company in Ganzhou City in August 2016 were enrolled. They were investigated by questionnaires and assessed by various scales after two years. 6 cases of severe poisoning were examined by head MRI. The scale includes Hamilton Anxiety Scale (HAMA) , Depression Scale (HAMD) , Simple Mental State Examination Scale (MMSE) , Activity of Daily Living (ADL) , International Cooperative Ataxia Rating Scale (ICARS) . <b>Results:</b> 16 cases of TMT poisoning still have headache, dizziness and other symptoms. Instability of walking in 4 patients with severe poisoning, and the brain MRI manifestations included obvious atrophy of temporal lobe, hippocampus, insula lobe, cerebellum and ventricle enlargement. Two patients were rated as severe mixed anxiety and depression, one as moderate mixed anxiety and depression, and one as mild anxiety. 3 cases were diagnosed as dementia and 1 case as mild cognitive impairment. Two cases were totally dependent on living ability. ICARS scores were 66 points and 63 points respectively. Two cases were mildly dependent on living ability. ICARS scores were 28 points and 6 points respectively. There were 2 cases of mild mixed anxiety and depression in mild and moderate poisoning patients, and 1 case of mild cognitive impairment in each patient. They could live independently. ICARS scores were 0. <b>Conclusion:</b> After 2 years of TMT poisoning, some patients still have general clinical symptoms such as dizziness, headache and so on. There are also mental and intellectual symptoms such as anxiety, depression and cognitive impairment. Some of patients with severe poisoning presented with dementia and cerebellar ataxia, and even lost independent living ability.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhu</LastName><ForeName>H B</ForeName><Initials>HB</Initials><AffiliationInfo><Affiliation>Department of Neurology, the First Affiliated Hospital of Gannan Medical University, Ganzhou 341000, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ouyang</LastName><ForeName>G L</ForeName><Initials>GL</Initials></Author><Author ValidYN="Y"><LastName>Lai</LastName><ForeName>Y Y</ForeName><Initials>YY</Initials></Author><Author ValidYN="Y"><LastName>Zhong</LastName><ForeName>S Q</ForeName><Initials>SQ</Initials></Author></AuthorList><Language>chi</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>China</Country><MedlineTA>Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi</MedlineTA><NlmUniqueID>8410840</NlmUniqueID><ISSNLinking>1001-9391</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010087">Oxides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014298">Trimethyltin Compounds</NameOfSubstance></Chemical><Chemical><RegistryNumber>1631-73-8</RegistryNumber><NameOfSubstance UI="C046488">trimethyltin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000203" MajorTopicYN="Y">Activities of Daily Living</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003072" MajorTopicYN="Y">Cognition Disorders</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003704" MajorTopicYN="N">Dementia</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003863" MajorTopicYN="Y">Depression</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018450" MajorTopicYN="N">Disease Progression</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005500" MajorTopicYN="N">Follow-Up Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016273" MajorTopicYN="N">Occupational Exposure</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010087" MajorTopicYN="N">Oxides</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D059027" MajorTopicYN="N">Recycling</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014298" MajorTopicYN="Y">Trimethyltin Compounds</DescriptorName><QualifierName UI="Q000506" MajorTopicYN="N">poisoning</QualifierName></MeshHeading></MeshHeadingList><OtherAbstract Type="Publisher" Language="chi"><b>目的：</b> 分析三甲基氯化锡（TMT）中毒患者2年后所留后遗症的临床表现。 <b>方法：</b> 于2018年9月，对2016年8月赣州市某废料再生产公司的16例TMT中毒患者进行2年后的问卷调查及量表评定，包括汉密尔顿焦虑量表（HAMA）、汉密尔顿抑郁量表（HAMD）、简易智能精神状态检查量表（MMSE）、日常生活能力（ADL）、国际协作共济失调量表（ICARS）；对6例重度中毒患者进行头颅MRI检查。 <b>结果：</b> 16例TMT中毒患者中部分患者仍有头痛、头晕等症状。重度中毒患者：4例行走不稳，并且头颅MRI表现为颞叶、海马、岛叶、小脑萎缩明显及脑室扩大；2例患者评定为重度混合性焦虑和抑郁状态，1例中度混合性焦虑和抑郁状态，1例轻度焦虑状态；3例患者诊断为痴呆，1例为轻度认知功能障碍；2例患者ICARS评分分别为66、63分（完全依赖生活能力），2例ICARS评分分别为28、6分（轻度依赖生活能力），2例ICARS评分均为0分（可独立生活能力）。轻、中度中毒患者：各有2例轻度混合性焦虑和抑郁状态，各有1例为轻度认知功能障碍，所有患者轻、中度ICARS评分均为0分（可独立生活能力）。 <b>结论：</b> 部分患者TMT中毒2年后仍残留头晕、头痛等一般临床症状，也有焦虑、抑郁及认知功能减退等精神智能症状；重度中毒者部分出现痴呆、小脑性共济失调，甚至丧失独立生活能力。. |
2,328,989 | Mitochondrial membranes in cardiac muscle from Antarctic notothenioid fishes vary in phospholipid composition and membrane fluidity. | Antarctic notothenioid fishes are highly stenothermal, yet their tolerance for warming is species-dependent. Because a body of literature points to the loss of cardiac function as underlying thermal limits in ectothermic animals, we investigated potential relationships among properties of ventricular mitochondrial membranes in notothenioids with known differences in both cardiac mitochondrial metabolism and organismal thermal tolerance. Fluidity of mitochondrial membranes was quantified by fluorescence depolarization for the white-blooded Chaenocephalus aceratus and the red-blooded Notothenia coriiceps. In these same membranes, lipid compositions and products of lipid peroxidation, the latter of which can disrupt membrane order, were analyzed in both species and in a second icefish, Pseudochaenichthys georgianus. Mitochondrial membranes from C. aceratus were significantly more fluid than those of the more thermotolerant species N. coriiceps (P < .0001). Consistent with this, ratios of total phosphatidylethanolamine (PE) to total phosphatidylcholine (PC) were lower in membranes from both species of icefishes, compared to those of N. coriiceps (P < .05). However, membranes of N. coriiceps displayed a greater unsaturation index (P < .0001). No differences among species were found in membrane products of lipid peroxidation. With rising temperatures, greater contents of PC in mitochondrial membranes from ventricles of icefishes are likely to promote membrane hyperfluidization at a lower temperature than for cardiac mitochondrial membranes from the red-blooded notothenioid. We propose that physical and chemical properties of the mitochondrial membranes may contribute to some of the observed differences in thermal sensitivity of physiological function among these species. |
2,328,990 | Dopamine-mediated immunomodulation affects choroid plexus function. | Immune system alterations have been implicated in various dopamine-related disorders, such as schizophrenia, bipolar disorder, and attention-deficit/hyperactivity disorder (ADHD). How immunity might be influenced by dopaminergic dysfunction and impact on clinically-relevant behaviors is still uncertain. We performed a peripheral and cerebral immunophenotyping in mice bearing dopaminergic alteration produced by genetic liability (hypofunction of the dopamine transporter DAT) and psychostimulant (amphetamine) administration. We found that DAT hypofunction influences immune tolerance by increasing functional Tregs and adrenomedullin levels in the thymus and spleen, while reducing microglia activation and infiltration of brain monocyte-derived macrophages (mo-MΦ). Remarkably, both DAT hypofunction and amphetamine treatment are associated with a weaker activation of the choroid plexus (CP) gateway. Conversely, amphetamine reactivated the CP in the setting of DAT hypofunction, paralleling its paradoxical ADHD-relevant behavioral effects. These findings add new knowledge on dopaminergic immunopharmacology and support the immunomodulation of CP functionality as a promising therapeutic strategy for neurodevelopmental and psychiatric disorders. |
2,328,991 | Development of arterial hypotension in premature infants with early onset bacterial infections: tools of clinical predication. | Introduction: The safe thresholds of blood pressure in preterm neonates are still unclear. The aim of our study was to substantiate the diagnostic criteria for the syndrome of arterial hypotension (AH) and indications for the appointment of hemodynamic support in premature infants with early onset bacterial infections.</AbstractText>Materials and methods: A prospective cohort study was conducted. 2 experimental groups were formed -premature babies with early onset bacterial infections and AH (n = 58), and control group (n = 62), premature babies without AH. The subjects of the study were a number of risk factors. Simple and multiple logistic regression analyses were used.</AbstractText>Results: In premature infants with AH, compared with those without AH, there are significantly lower values of stroke index of left ventricle (SILV), index of resistance (IR) of the middle cerebral artery, pH, significantly higher level of urea in serum and a higher proportion of children with hypoglycemia. Multiple logistic regression analysis was used to develop a clinical prognostic model for the AH-syndrome. Only prognostic model, which included SILV, blood pH and blood glucose, had high prognostic characteristics and the largest area under the ROC curve.</AbstractText>Conclusions: The following diagnostic criteria can be used for the appointment of medical support for hemodynamics: the digital value of the level of mean blood pressure, expressed in mmHg, is less than the gestational age in weeks, and at least one of the following indicators -pH is less than 7.2, blood glucose level is less than 2.8 mmol/l, SILV is less than the normal ranges.</AbstractText> |
2,328,992 | Echocardiographic Assessment of the Right Ventricle-State of the Art. | Assessment of right ventricular (RV) structure and function by echocardiography has largely been qualitative in the past. More recent approaches emphasise the quantification of RV structure from multiple echocardiographic views and quantification of multiple parameters of RV function. Current echocardiographic examinations should include at least two quantitative measures of RV function. This paper will highlight commonly used measures along with their strengths and weaknesses. With further technical developments in three-dimensional and myocardial deformation imaging and as more outcome data become available it is likely that further quantitative assessment will become routine and be used to guide diagnosis and treatment choices. |
2,328,993 | The surgical results of endoscopic third ventriculostomy in long-standing overt ventriculomegaly in adults with papilledema. | Longstanding overt vetriculomegaly in adults (LOVA) is a type of chronic hydrocephalus presumed to begin during infancy, which manifests in adults after a long and slow clinical course. Only a quite small number of LOVA case series have been published, controversies regarding optimal management still exist. The authors describe a series of symptomatic LOVA patients with papilledema treated successfully using endoscopic third ventriculostomy (ETV) at a single institution.</AbstractText>In the past 7 years, 4 LOVA patients with papilledema were surgically treated using ETV. Clinical features and neuroimaging of all patients were carefully reviewed retrospectively. Changes of the third ventricle transverse diameter, Evan's ratio, frontal occipital horn ratio after operation were measured.</AbstractText>There were two males and two females, with a mean age of 24 (21-29) on first presentation. Presentation symptoms were visual problems (4 cases), headaches (3 cases), hemidysesthesia(1 case), and poor mobility(1 cases). Papilledema and increased intracranial pressure were identified in all 4 cases. The mean follow-up period of this series was 5 years (range 4-6 years). All patients reported improved vision function 3 months and experienced other symptom relief accompanying with normalized intracranial pressure after ETV and did not require any further surgical intervention.</AbstractText>Endoscopic third ventriculostomy provides an effective treatment for LOVA patients with papilledema, which can improve the symptoms of LOVA and relive papilledema. The fundoscopy is of great value in making decisions related to surgical intervention for LOVA patients.</AbstractText>Copyright © 2019 Elsevier B.V. All rights reserved.</CopyrightInformation> |
2,328,994 | Brain ventricle parcellation using a deep neural network: Application to patients with ventriculomegaly. | Numerous brain disorders are associated with ventriculomegaly, including both neuro-degenerative diseases and cerebrospinal fluid disorders. Detailed evaluation of the ventricular system is important for these conditions to help understand the pathogenesis of ventricular enlargement and elucidate novel patterns of ventriculomegaly that can be associated with different diseases. One such disease is normal pressure hydrocephalus (NPH), a chronic form of hydrocephalus in older adults that causes dementia. Automatic parcellation of the ventricular system into its sub-compartments in patients with ventriculomegaly is quite challenging due to the large variation of the ventricle shape and size. Conventional brain labeling methods are time-consuming and often fail to identify the boundaries of the enlarged ventricles. We propose a modified 3D U-Net method to perform accurate ventricular parcellation, even with grossly enlarged ventricles, from magnetic resonance images (MRIs). We validated our method on a data set of healthy controls as well as a cohort of 95 patients with NPH with mild to severe ventriculomegaly and compared with several state-of-the-art segmentation methods. On the healthy data set, the proposed network achieved mean Dice similarity coefficient (DSC) of 0.895 ± 0.03 for the ventricular system. On the NPH data set, we achieved mean DSC of 0.973 ± 0.02, which is significantly (p < 0.005) higher than four state-of-the-art segmentation methods we compared with. Furthermore, the typical processing time on CPU-base implementation of the proposed method is 2 min, which is much lower than the several hours required by the other methods. Results indicate that our method provides: 1) highly robust parcellation of the ventricular system that is comparable in accuracy to state-of-the-art methods on healthy controls; 2) greater robustness and significantly more accurate results on cases of ventricular enlargement; and 3) a tool that enables computation of novel imaging biomarkers for dilated ventricular spaces that characterize the ventricular system. |
2,328,995 | Time course of cardiomyopathy induced by doxorubicin in rats. | Doxorubicin (DOX)-related cardiotoxicity may expose cancer survivors to increased risk of cardiovascular morbidity and mortality. Here, we characterized the time course of DOX-induced cardiomyopathy in rats.</AbstractText>Sprague-Dawley male rats (12 wk old) received doxorubicin hydrochloride (1 mg/kg/d, ip) during 10 consecutive days and they were euthanized one (DOX1), two (DOX2) or four (DOX4) weeks after the last drug injection. Control group received NaCl 0.9% (ip). Hearts were mounted on a Langendorff perfusion system, left ventricle fragments were processed for microscopy and oxidative stress-related assays, and blood was collected for cardiac troponin I assay.</AbstractText>All DOX-treated groups showed swollen and vacuolated cardiomyocytes with myofilaments disarray and mitochondrial damage. These changes were already evident after one week and became more pronounced after four weeks. Cardiac troponin I plasma levels were significantly increased in DOX1 and further increased in DOX4 compared to control group. Increased oxidative damage to lipids was observed in DOX1, and to proteins in DOX4. Glutathione peroxidase activity increased in DOX4. The morphological changes resulted in cardiac remodeling, including interstitial fibrosis, apoptosis and significant impairment of both contractile and relaxation function in DOX 4 compared to control group. Hearts from all animals displayed an early reduction in the responsiveness to norepinephrine.</AbstractText>These findings support the view that DOX cardiotoxicity occurs in a "continuum", and as the hypothesis of an irreversible cardiac injury is being challenged, understanding the progression of morphological and functional changes caused by DOX may allow proper timing of initiation of prophylactic treatment.</AbstractText>Copyright © 2019 Institute of Pharmacology, Polish Academy of Sciences. Published by Elsevier B.V. All rights reserved.</CopyrightInformation> |
2,328,996 | The left lateral occipital cortex exhibits decreased thickness in children with sensorineural hearing loss. | Patients with sensorineural hearing loss (SNHL) tend to show language delay, executive functioning deficits, and visual cognitive impairment, even after intervention with hearing amplification and cochlear implants, which suggest altered brain structures and functions in SNHL patients. In this study, we investigated structural brain MRI in 30 children with SNHL (18 mild to moderate [M-M] SNHL and 12 moderately severe to profound [M-P] SNHL) by comparing gender- and age-matched normal controls (NC). Region-based analyses did not show statistically significant differences in volumes of the cerebrum, basal ganglia, cerebellum, and the ventricles between SNHL and NC. On surface-based analyses, the global and lobar cortical surface area, thickness, and volumes were not statistically significantly different between SNHL and NC participants. Regional surface areas, cortical thicknesses, and cortical volumes were statistically significantly smaller in M-P SNHL compared to NC in the left middle occipital cortex, and left inferior occipital cortex after a correction for multiple comparisons using random field theory (p < 0.02). These regions were identified as areas known to be related to high level visual cognition including the human middle temporal area, lateral occipital area, occipital face area, and V8. The observed regional decreased thickness in M-P SNHL may be associated with dysfunctions of visual cognition in SNHL detectable in a clinical setting. |
2,328,997 | Interhypothalamic adhesions in endoscopic third ventriculostomy. | An interhypothalamic adhesion (IHA) is a gray mater-like band of tissue traversing across the third ventricle anterior to the mammillary bodies and is similar but distinct from an interthalamic adhesion. These rare anatomic anomalies can be detected with magnetic resonance imaging or, incidentally, during endoscopic ventricular surgery.</AbstractText>All cases of interhypothalamic adhesions visualized during endoscopic third ventriculotomy (ETV), outside of the myelomeningocele setting, were identified from two institutions. Retrospective chart and imaging reviews were conducted and compared to intraoperative videos and photos for all cases. IHA variables collected included the following size, location, multiplicity, and associated anatomic anomalies.</AbstractText>Four cases of interhypothalamic adhesions were identified during ETV-all of which, either partially or completely, obscured access to the third ventricular floor. The IHAs in our cohort were duplicated in two patients, large (> 3 mm and severely obstructing access to the third ventricular floor) in three patients, and adherent to the floor of the third ventricle in three patients. All four patients had primary absence of the septum pellucidum. Previous reports found associations of IHAs with other congenital, particularly midline, abnormalities. The IHAs in our cohort affected the surgery in three of four cases including misdirecting the ventriculostomy and requiring retraction or division of the IHA. In no case was postoperative pituitary or hypothalamic dysfunction observed.</AbstractText>Although interhypothalamic adhesions are rare, these anomalies must be recognized as they may hinder access to the third ventricular floor. IHAs may be large, multiple, or adherent to adjacent ventricular structures, they can misdirect or occlude the ventriculostomy or impart risk of bleeding and hypothalamic injury. Techniques for management of IHA include aborting the attempt, re-siting the ventriculostomy, or retracting or dividing the IHA, which enabled technically successful ETV in three of four patients in this series.</AbstractText> |
2,328,998 | Soluble Nogo receptor 1 fusion protein protects neural progenitor cells in rats with ischemic stroke. | Soluble Nogo66 receptor-Fc protein (sNgR-Fc) enhances axonal regeneration following central nervous system injury. However, the underlying mechanisms remain unclear. In this study, we investigated the effects of sNgR-Fc on the proliferation and differentiation of neural progenitor cells. The photothrombotic cortical injury model of ischemic stroke was produced in the parietal cortex of Sprague-Dawley rats. The rats with photothrombotic cortical injury were randomized to receive infusion of 400 μg/kg sNgR-Fc (sNgR-Fc group) or an equal volume of phosphate-buffered saline (photothrombotic cortical injury group) into the lateral ventricle for 3 days. The effects of sNgR-Fc on the proliferation and differentiation of endogenous neural progenitor cells were examined using BrdU staining. Neurological function was evaluated with the Morris water maze test. To further examine the effects of sNgR-Fc treatment on neural progenitor cells, photothrombotic cortical injury was produced in another group of rats that received transplantation of neural progenitor cells from the hippocampus of embryonic Sprague-Dawley rats. The animals were then given an infusion of phosphate-buffered saline (neural progenitor cells group) or sNgR-Fc (sNgR-Fc + neural progenitor cells group) into the lateral ventricle for 3 days. sNgR-Fc enhanced the proliferation of cultured neural progenitor cells in vitro as well as that of endogenous neural progenitor cells in vivo, compared with phosphate-buffered saline, and it also induced the differentiation of neural progenitor cells into neurons. Compared with the photothrombotic cortical injury group, escape latency in the Morris water maze and neurological severity score were greatly reduced, and distance traveled in the target quadrant was considerably increased in the sNgR-Fc group, indicating a substantial improvement in neurological function. Furthermore, compared with phosphate-buffered saline infusion, sNgR-Fc infusion strikingly improved the survival and differentiation of grafted neural progenitor cells. Our findings show that sNgR-Fc regulates neural progenitor cell proliferation, migration and differentiation. Therefore, sNgR-Fc is a potential novel therapy for stroke and neurodegenerative diseases, The protocols were approved by the Committee on the Use of Live Animals in Teaching and Research of the University of Hong Kong (approval No. 4560-17) in November, 2015. |
2,328,999 | Periventricular magnetisation transfer ratio abnormalities in multiple sclerosis improve after alemtuzumab. | In multiple sclerosis (MS), disease effects on magnetisation transfer ratio (MTR) increase towards the ventricles. This periventricular gradient is evident shortly after first symptoms and is independent of white matter lesions.</AbstractText>To explore if alemtuzumab, a peripherally acting disease-modifying treatment, modifies the gradient's evolution, and whether baseline gradients predict on-treatment relapses.</AbstractText>Thirty-four people with relapsing-remitting MS underwent annual magnetic resonance imaging (MRI) scanning (19 receiving alemtuzumab (four scans each), 15 untreated (three scans each)). The normal-appearing white matter was segmented into concentric bands. Gradients were measured over the three bands nearest the ventricles. Mixed-effects models adjusted for age, gender, relapse rate, lesion number and brain parenchymal fraction compared the groups' baseline gradients and evolution.</AbstractText>Untreated, the mean MTR gradient increased (+0.030 pu/band/year) but decreased following alemtuzumab (-0.045 pu/band/year, p</i> = 0.037). Within the alemtuzumab group, there were no significant differences in baseline lesion number (p</i> = 0.568) nor brain parenchymal fraction (p</i> = 0.187) between those who relapsed within 4 years (n</i> = 4) and those who did not (n</i> = 15). However, the baseline gradient was significantly different (p</i> = 0.020).</AbstractText>Untreated, abnormal periventricular gradients worsen with time, but appear reversible with peripheral immunotherapy. Baseline gradients - but not lesion loads or brain volumes - may predict on-treatment relapses. Larger confirmatory studies are required.</AbstractText> |
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