Database : MEDLINE
Search on : Myocarditis [Words]
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[PMID]: 29524647
[Au] Autor:Zhao M; Wu J; Li X; Gao Y
[Ad] Address:Department of Laboratory Medicine, Beijing Hospital, National Center of Gerontology, Beijing, China; Department of Pathophysiology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, China.
[Ti] Title:Urinary candidate biomarkers in an experimental autoimmune myocarditis rat model.
[So] Source:J Proteomics;, 2018 Mar 07.
[Is] ISSN:1876-7737
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Urine is a better source than plasma for biomarker studies, as it can accumulate all changes in the body. Various candidate urinary biomarkers of physiological condition, kidney disease and even brain dysfunction, have been detected in urine; however, urine has rarely been used to reflect cardiac diseases. In this study, urine at day 0, 14, 21 and 28 were collected from the myosin-induced autoimmune myocarditis rat models. The candidate urinary biomarkers were then characterized using the isobaric tandem mass tag labeling approach coupled with offline two-dimensional reverse-phase liquid chromatography and high-resolution mass spectrometry. Compared with controls, forty-six urinary proteins were significantly changed in the myocarditis rats; among them, ten had previously been associated with myocarditis, twelve corresponding gene products had annotated as mainly cardiovascular network genes by the Ingenuity Pathway Analysis, four urinary proteins were validated by western blot, thirteen were reported in previous urine proteome studies of other diseases and twenty-six were reported the first time to be related to myocarditis. SIGNIFICANCE: This is the first study to use isobaric tandem mass tag labeling approach in the urine proteome analysis of experimental autoimmune myocarditis. These findings may provide clues for the pathogenesis of myocarditis. And the study showed that urine can be a good source of myocarditis biomarkers.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 18152 MEDLINE  
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[PMID]: 29524390
[Au] Autor:Gou W; Zhang Z; Yang C; Li Y
[Ad] Address:PICU, First Hospital of Jilin University, Changchun, Jilin, 130021, China.
[Ti] Title:MiR-223/Pknox1 axis protects mice from CVB3-induced viral myocarditis by modulating macrophage polarization.
[So] Source:Exp Cell Res;, 2018 Mar 07.
[Is] ISSN:1090-2422
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Macrophage polarization plays a crucial role in regulating myocardial inflammation and injuries of coxsackievirus B3 (CVB3)-induced viral myocarditis (VM). It has been reported that miR-223 is a potent regulator of inflammatory responses that involved in macrophage polarization. However, the functional roles of miR-223 in CVB3-induced VM still remain unknown. Here, we found that miR-223 expression was significantly down-regulated in heart tissues and heart-infiltrating macrophages of CVB3-infected mice. Up-regulation of miR-223 in vivo protected the mice against CVB3-induced myocardial injuries characterized by the increased body weight and survival, enhanced left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS), relieved inflammation, depressed creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH) and aspartate transaminase (AST) levels, reduced production of interferon (IFN)-γ, interleukin (IL)-6 as well as increased IL-10. We subsequently found that miR-233 up-regulation significantly suppressed the expression of M1 markers (iNOS, TNF-α and CD 86), and promoted the expression of M2 markers (Arginase-1, Fizz-1 and CD 206) in vivo and in vitro. Furthermore, we confirmed that miR-223 directly targeted Pknox1 to inhibit its expression, and the expression of Pknox1 was inversely correlated with miR-223 expression in heart tissues and heart-infiltrating macrophages of CVB3-infected mice. Gain-of-function analyses indicated that Pknox1 overexpression partially reversed the polarization phenotypes regulated by miR-223 overexpression. Taken together, the data suggest that miR-223 protects against CVB3-induced inflammation and myocardial damage, which may partly attribute to the regulation of macrophage polarization via targeting Pknox1.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 18152 MEDLINE  
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[PMID]: 29520196
[Au] Autor:Pizzino F; Recupero A; Pugliatti P; Maffei S; Di Bella G
[Ad] Address:Fondazione Toscana Gabriele Monasterio, UO Patologie Mediche e Chirurgiche del Cuore, Massa, CAP 54100, Italy.
[Ti] Title:RE: Multi-Parameter CMR Approach in Acute Myocarditis to Improve Diagnosis and Prognostic Stratification.
[So] Source:Korean J Radiol;19(2):366-367, 2018 Mar-Apr.
[Is] ISSN:2005-8330
[Cp] Country of publication:Korea (South)
[La] Language:eng
[Pt] Publication type:JOURNAL ARTICLE; COMMENT
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.3348/kjr.2018.19.2.366

  4 / 18152 MEDLINE  
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[PMID]: 29524349
[Au] Autor:Beijerink NJ; Bergmann W; Szatmári V
[Ad] Address:Department of Clinical Sciences of Companion Animals, Utrecht University, Utrecht, The Netherlands.
[Ti] Title:Incomplete endothelialization of an intravascular implant and fatal late-onset bacterial ductal arteritis in a dog with occluded patent ductus arteriosus.
[So] Source:J Vet Intern Med;, 2018 Mar 10.
[Is] ISSN:1939-1676
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:An 18-month-old male Akita Inu dog developed fever and lameness 8 months after successful transcatheter closure of a patent ductus arteriosus with an Amplatz Canine Duct Occluder (ACDO). Corynebacterium species were cultured from 3 blood samples. Echocardiography showed a vegetative process on the aortic valves. The dog died spontaneously 3 days after development of the initial signs. Necropsy confirmed the presence of bacterial ductal arteritis and myocarditis, and revealed an incomplete endothelialization of the intraductal metal implant. The reason for the lack of (neo)endothelialization of the ACDO remains unknown. We conclude that late-onset bacterial device-related ductal arteritis can develop in dogs where the implant is incompletely covered by a protective endothelial layer.
[Pt] Publication type:CASE REPORTS
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1111/jvim.15074

  5 / 18152 MEDLINE  
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[PMID]: 29523179
[Au] Autor:Ralapanawa DMPUK; Kumarihamy KWMPP; Sundararajah M; Jayalath WATA
[Ad] Address:Department of Medicine, University of Peradeniiya, Peradeniya, Sri Lanka. udayapralapanawa@yahoo.com.
[Ti] Title:A young female presenting with heart failure secondary to eosinophilic myocarditis: a case report and review of the literature.
[So] Source:BMC Res Notes;11(1):168, 2018 Mar 09.
[Is] ISSN:1756-0500
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Eosinophilic myocarditis is one of the fatal complications of idiopathic hypereosinophilic syndromes. Given the rarity of this form of myocarditis, it is often under-recognized. We describe a young girl who presented with features of heart failure. To our knowledge, this is the first reported case of eosinophilic myocarditis in a young Sri Lankan female. CASE PRESENTATION: A previously healthy 21 year old Sri Lankan female admitted with shortness of breath for 1 week duration with associated low grade fever and profuse sweating. She was mildly febrile and dyspnoeic with absent ankle oedema. She was tachycardic and had elevated Jugular venous pressure with negative Kussmaul sign. Blood pressure was 100/70 mmHg. Clinically there was no cardiomegaly and heart sounds were slightly muffled with gallop rhythm. Bilateral basal fine end inspiratory crackles and mild hepatosplenomegaly were noted. The laboratory examinations showed leucocytosis with severe eosinophilia with no abnormal cells. Her ESR, Troponin I and Brain natriuretic peptide were elevated with normal CRP and electrocardiogram showed sinus tachycardia with wide spread ST depression. Heart failure was evident on chest X-ray and 2D-echocardiogram showed global left ventricular hypokinesia with 40% ejection fraction and a thin layer of pericardial effusion. Mild hepatosplenomegaly without lymphadenopathy was detected in the ultrasound scan. Bone marrow biopsy showed hypereosinophilia with no evidence of bone marrow infiltration. FIP1L1-PDGFRA fusion transcript and BCR-ABL transcript were not detected. Secondary causes for hypereosinophilia were excluded and the diagnosis of idiopathic hypereosinophilic syndrome and eosinophilic myocarditis was made. She had good response to steroids clinically and biochemically with complete recovery of left ventricular function. She is now on steroid to be continued at least 6 months to 1 year. CONCLUSION: Eosinophilic myocarditis is a rare but fatal disease if left untreated. Hence clinicians should have high index of suspicion to diagnose eosinophilic myocarditis in clinical context of heart failure due to myocarditis. The diagnoses of eosinophilic myocarditis may often be challenged especially in a poor recourse setting. However available investigation should be used to diagnose this condition without delay. Early treatment with systemic steroids may prevent fatal outcome and therapies for this disease have yet to be validated in large prospective studies.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Process
[do] DOI:10.1186/s13104-018-3273-1

  6 / 18152 MEDLINE  
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[PMID]: 29287886
[Au] Autor:Samdani S; Jain A; Meena V; Meena CB
[Ad] Address:Department of Otorhinolaryngology (ENT), Sawai Man Singh Medical College and Attached Group of Hospitals, Jaipur, Rajasthan, India.
[Ti] Title:Cardiac complications in diphtheria and predictors of outcomes.
[So] Source:Int J Pediatr Otorhinolaryngol;104:76-78, 2018 Jan.
[Is] ISSN:1872-8464
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:OBJECTIVE: To study the cardiac complications in diphtheria patients and to study the predictors of outcomes. STUDY DESIGN: Single centre prospective analysis of cardiac complications in diphtheria patients. RESULTS: In this study, there were 60 patients diagnosed with diphtheria with ECG changes. The ECG changes seen were sinus tachycardia (68.3%), T wave inversion (20%), ST segment depression (13.3%), right bundle branch block (5%), multiple atrial ectopics (3.3%). The case fatality rate in our study was 25% (15 patients). High CPK-MB, myoglobulin and cardiac troponin levels were associated with cardiac mortality. In our study, cardiac troponin T had the highest sensitivity (80%) and CK-MB had the highest specificity (95.56%). CONCLUSION: Cardiac involvement is a common complication of infection with C. diphtheria and is associated with high mortality. As diphtheria can be prevented by adequate vaccination, efforts should be maximized for high vaccine coverage with booster doses.
[Mh] MeSH terms primary: Diphtheria/complications
Heart Diseases/etiology
[Mh] MeSH terms secundary: Adolescent
Biomarkers
Child
Child, Preschool
Creatine Kinase
Electrocardiography
Female
Heart Diseases/epidemiology
Humans
Infant
Male
Prospective Studies
Sensitivity and Specificity
Troponin T
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Biomarkers); 0 (Troponin T); EC 2.7.3.2 (Creatine Kinase)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:171231
[St] Status:MEDLINE

  7 / 18152 MEDLINE  
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[PMID]: 29522219
[Au] Autor:Lüscher TF
[Ad] Address:Editorial Office, Zurich Heart House, 8032 Zurich, Center for Molecular Cardiology, Schlieren Campus, University of Zurich, Switzerland and Royal Brompton and Harefield Hospital Trust and Imperial College, London, SW3 6NP, UK.
[Ti] Title:Novel insights in HFpEF, cardiomyopathies, and myocarditis.
[So] Source:Eur Heart J;39(10):819-822, 2018 Mar 07.
[Is] ISSN:1522-9645
[Cp] Country of publication:England
[La] Language:eng
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review
[do] DOI:10.1093/eurheartj/ehy105

  8 / 18152 MEDLINE  
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[PMID]: 29518613
[Au] Autor:Zhang H; Li H; Ge A; Guo E; Liu S; Zhang L
[Ad] Address:Department of Pediatrics, Jining No. 1 People's Hospital, Jining, 272011, China.
[Ti] Title:Long non-coding RNA TUG1 inhibits apoptosis and inflammatory response in LPS-treated H9c2 cells by down-regulation of miR-29b.
[So] Source:Biomed Pharmacother;101:663-669, 2018 Mar 05.
[Is] ISSN:1950-6007
[Cp] Country of publication:France
[La] Language:eng
[Ab] Abstract:OBJECTIVE: Myocarditis is an important cause for cardiovascular morbidity and mortality in children and adults. The lncRNA taurine up-regulated gene 1 (TUG1) plays important roles in cell apoptosis and inflammation in tumor and liver injury. The present study aimed to investigate the role of TUG1 in LPS-injured H9c2 cells and explore the underlying molecular mechanism. METHODS: H9c2 cells were stimulated with LPS to induce inflammatory injury. The expression of TUG1 was altered by transient transfections. Cell viability and apoptotic cell rates were detected by CCK-8 assay and flow cytometry assay, respectively. Inflammatory response was determined by detecting levels of inflammatory cytokines using qRT-PCR and ELISA. Furthermore, western blot analysis was conducted to assess the expression levels of core factors related with apoptosis and activations of NF-κB and JAK/STAT signaling pathways. RESULTS: LPS exposure reduced cell viability but enhanced cell apoptosis and inflammation in H9c2 cells. Moreover, TUG1 expression was down-regulated in LPS-injured H9c2 cells. TUG1 overexpression attenuated LPS-induced injuries in H9c2 cells, evidenced by augmented cell viability, declined apoptotic cell rates and decreased levels of pro-apoptotic factors and inflammatory cytokines. Inversely, TUG1 inhibition exerted the opposite effects. More importantly, TUG1 negatively modulated the expression of miR-29b and miR-29b mimic blocked the effect of TUG1 overexpression on cell viability, apoptosis, inflammation and inactivation of NF-κB and JAK/STAT signaling pathways in LPS-stimulated H9c2 cells. CONCLUSION: This study demonstrated that TUG1 played the anti-apoptotic and anti-inflammatory roles in LPS-injured H9c2 cells via down-regulating miR-29b and inhibiting NF-κB and JAK/STAT pathways.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher

  9 / 18152 MEDLINE  
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[PMID]: 29499204
[Au] Autor:Li H; Xie Y; Liu Y; Qi Y; Tang C; Li X; Zuo K; Sun D; Shen Y; Pang D; Chu Y; Zhao B
[Ad] Address:Jilin Provincial Key Laboratory of Animal Embryo Engineering, Department of Animal Biotechnology, College of Animal Science, Jilin University, Changchun 130062, China; Department of Toxicology, School of Public Health, Beihua University, Jilin 132011, Jilin, China; Heilongjiang Key Laboratory of Ant
[Ti] Title:Alteration in microRNA-25 expression regulate cardiac function via renin secretion.
[So] Source:Exp Cell Res;, 2018 Feb 28.
[Is] ISSN:1090-2422
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Heart failure arises from diverse cardiovascular diseases, including hypertension, ischemic disease and atherosclerosis, valvular insufficiency, myocarditis, and contractile protein mutations. MicroRNAs are dysregulated in heart failure, but identification of the specific microRNAs involved remains incomplete. Here, we evaluate miR-25 expression in the peripheral blood from healthy, dilated cardiomyopathy (DCM), remote infarct (OMI), hypertensive heart disease (HHD), and HHD resulting in heart failure (HHDF) using q-PCR. Interestingly, we discovered miR-25 expression in humans is initially decreased at the onset of heart failure but is later increased in end-stage heart failure. We also show that overexpression of miR-25 in normal mice causes cardiomyocyte fibrosis and apoptosis. However, inhibition of miR-25 in normal mice led to activate renin-angiotensin system (RAS) and high blood pressure, mild heart dilation. Notably, the miR-25 cluster knock-out mice was also characterized high blood pressure and no obvious cardiac function alteration. RNA sequencing showed the alteration of miR-25 target genes in angomir-treated mice, including the renin secretion signal related gene. In vitro, cotransfection with the miR-25 antagomir repressed luciferase activity from a reporter construct containing the Pde3a and Cacnalc untranslated region. In summary, miR-25 expression during different stages of heart disease, offers a new perspective for the role of miR-25 function in heart failure.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  10 / 18152 MEDLINE  
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[PMID]: 29425680
[Au] Autor:Laitinen OH; Svedin E; Kapell S; Hankaniemi MM; Larsson PG; Domsgen E; Stone VM; Määttä JAE; Hyöty H; Hytönen VP; Flodström-Tullberg M
[Ad] Address:The Center for Infectious Medicine, Department of Medicine HS, Karolinska Institutet, Karolinska University Hospital, Stockholm, 141 86, Sweden.
[Ti] Title:New Coxsackievirus 2A and 3C protease antibodies for virus detection and discovery of pathogenic mechanisms.
[So] Source:J Virol Methods;255:29-37, 2018 Feb 06.
[Is] ISSN:1879-0984
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Enteroviruses (EVs), such as the Coxsackie B-viruses (CVBs), are common human pathogens, which can cause severe diseases including meningitis, myocarditis and neonatal sepsis. EVs encode two proteases (2A and 3C ), which perform the proteolytic cleavage of the CVB polyprotein and also cleave host cell proteins to facilitate viral replication. The 2A cause direct damage to the infected heart and tools to investigate 2A and 3C expression may contribute new knowledge on virus-induced pathologies. Here, we developed new antibodies to CVB-encoded 2A and 3C ; Two monoclonal 2A antibodies and one 3C antibody were produced. Using cells infected with selected viruses belonging to the EV A, B and C species and immunocytochemistry, we demonstrate that the 3C antibody detects all of the EV species B (EV-B) viruses tested and that the 2A antibody detects all EV-B viruses apart from Echovirus 9. We furthermore show that the new antibodies work in Western blotting, immunocyto- and immunohistochemistry, and flow cytometry to detect CVBs. Confocal microscopy demonstrated the expression kinetics of 2A and 3C , and revealed a preferential cytosolic localization of the proteases in CVB3 infected cells. In summary, the new antibodies detect proteases that belong to EV species B in cells and tissue using multiple applications.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher


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