WordNet
- inflammation of the myocardium (the muscular tissue of the heart) (同)myocarditis
- a response of body tissues to injury or irritation; characterized by pain and swelling and redness and heat (同)redness, rubor
- arousal to violent emotion (同)inflaming
- of or relating to the myocardium
PrepTutorEJDIC
- 〈U〉〈C〉炎症 / 〈U〉点火,燃焼 / 〈U〉興奮すること,激怒すること
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- 1. 関節リウマチの全身および非関節症状の概要overview of the systemic and nonarticular manifestations of rheumatoid arthritis [show details]
- 2. 関節リウマチにおける冠動脈疾患：病因、危険因子、臨床症状、および診断上の注意点coronary artery disease in rheumatoid arthritis pathogenesis risk factors clinical manifestations and diagnostic implications [show details]
- 3. 心サルコイドーシスのマネージメントと予後management and prognosis of cardiac sarcoidosis [show details]
- 4. 腎不全における炎症inflammation in renal insufficiency [show details]
- 5. 急性心膜炎：臨床症状および診断的評価acute pericarditis clinical presentation and diagnostic evaluation [show details]
English Journal
- Highly sensitive and quantitative human thrombospondin-1 detection by an M55 aptasensor and clinical validation in patients with atherosclerotic disease.
- Ji K1, de Carvalho LP2, Bi X3, Seneviratnankn A2, Bhakoo K4, Chan M5, Yau Li SF6.Author information 1NUS Graduate School for Integrative Sciences and Engineering, National University of Singapore, Singapore 119077, Singapore.2Yong Loo Lin School of Medicine, National University of Singapore, Singapore 119228, Singapore.3Bioprocessing Technology Institute, Agency for Science, Technology and Research, 20 Biopolis Way, #06-01, Singapore 138668, Singapore.4Translational Molecular Imaging Group, Singapore Bioimaging Consortium, Agency for Science, Technology and Research, Singapore 138667, Singapore.5National University Heart Centre, Singapore 119074, Singapore.6Department of Chemistry and NUS Environmental Research Institute, National University of Singapore, Singapore 117543, Singapore; Shenzhen Engineering Laboratory for Eco-efficient Polysilicate Materials, Peking University Shenzhen Graduate School, Shenzhen, P.R.C. 518055. Electronic address: chmlifys@nus.edu.sg.AbstractAptamer-based biosensors (aptasensor) are powerful tools for rapid and sensitive biomarker detection. In this study, we report a DNA aptamer probe evolved from cell-SELEX that can recognize thrombospondin-1 protein in human plasma samples. The KD value of the aptamer M55 binding to thrombospondin-1 was determined as 0.5±0.2μM with an R(2) of 0.9144. A horseradish peroxidase-linked short oligo was complementarily bound onto the 3' end of the aptamer sequence to facilitate the 'smart' design of an M55-aptasensor for quantifying thrombospondin-1 protein in plasma samples. The limit of detection was 6.96fM. Thrombospondin-1 is a glycoprotein with multiple biological functions, including inflammation, platelet aggregation and endothelial cell apoptosis, and is involved in the pathology of atherosclerosis. In total, 118 plasma subjects were analyzed by using the aptasensor measurement with 1μL sample volume and 5min incubation time. The thrombospondin-1 concentrations in ST-Elevation Myocardial Infarction patients with severe atherosclerotic plaque burden were statistically significantly higher than in the healthy volunteers without atherosclerosis conditions, suggesting that thromboposnidn-1 is a potential plasma biomarker for atherosclerosis progression.
- Biosensors & bioelectronics.Biosens Bioelectron.2014 May 15;55:405-11. doi: 10.1016/j.bios.2013.12.012. Epub 2013 Dec 27.
- Aptamer-based biosensors (aptasensor) are powerful tools for rapid and sensitive biomarker detection. In this study, we report a DNA aptamer probe evolved from cell-SELEX that can recognize thrombospondin-1 protein in human plasma samples. The KD value of the aptamer M55 binding to thrombospondin-1
- PMID 24434496
- Loss of duplexmiR-223 (5p and 3p) aggravates myocardial depression and mortality in polymicrobial sepsis.
- Wang X1, Huang W2, Yang Y1, Wang Y2, Peng T3, Chang J4, Caldwell CC5, Zingarelli B6, Fan GC7.Author information 1Department of Pharmacology and Cell Biophysics.2Department of Pathology and Laboratory Medicine.3Critical Illness Research, Lawson Health Research Institute, Ontario N6A 4G5, Canada.4Institute of Biosciences and Technology, Texas A&M Health Science Center, TX, USA.5Department of Surgery, University of Cincinnati College of Medicine, Cincinnati, OH, USA.6Division of Critical Care Medicine, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.7Department of Pharmacology and Cell Biophysics. Electronic address: fangg@ucmail.uc.edu.AbstractSepsis is the leading cause of death in critically ill patients. While myocardial dysfunction has been recognized as a major manifestation in severe sepsis, the underlying molecular mechanisms associated with septic cardiomyopathy remain unclear. In this study, we performed a miRNA array analysis in hearts collected from a severe septic mouse model induced by cecal ligation and puncture (CLP). Among the 19 miRNAs that were dys-regulated in CLP-mouse hearts, miR-223(3p) and miR-223*(5p) were most significantly downregulated, compared with sham-operated mouse hearts. To test whether a drop of miR-223 duplex plays any roles in sepsis-induced cardiac dysfunction and inflammation, a knockout (KO) mouse model with a deletion of the miR-223 gene locus and wild-type (WT) mice were subjected to CLP or sham surgery. We observed that sepsis-induced cardiac dysfunction, inflammatory response and mortality were remarkably aggravated in CLP-treated KO mice, compared with control WTs. Using Western-blotting and luciferase reporter assays, we identified Sema3A, an activator of cytokine storm and a neural chemorepellent for sympathetic axons, as an authentic target of miR-223* in the myocardium. In addition, we validated that miR-223 negatively regulated the expression of STAT-3 and IL-6 in mouse hearts. Furthermore, injection of Sema3A protein into WT mice revealed an exacerbation of sepsis-triggered inflammatory response and myocardial depression, compared with control IgG1 protein-treated WT mice following CLP surgery. Taken together, these data indicate that loss of miR-223/-223* causes an aggravation of sepsis-induced inflammation, myocardial dysfunction and mortality. Our study uncovers a previously unrecognized mechanism underlying septic cardiomyopathy and thereby, may provide a new strategy to treat sepsis.
- Biochimica et biophysica acta.Biochim Biophys Acta.2014 May;1842(5):701-11. doi: 10.1016/j.bbadis.2014.01.012. Epub 2014 Jan 29.
- Sepsis is the leading cause of death in critically ill patients. While myocardial dysfunction has been recognized as a major manifestation in severe sepsis, the underlying molecular mechanisms associated with septic cardiomyopathy remain unclear. In this study, we performed a miRNA array analysis in
- PMID 24486439
- Inhibition of IL-2 inducible T-cell kinase alleviates T-cell activation and murine myocardial inflammation associated with CVB3 infection.
- He F1, Yao H1, Xiao Z1, Han J2, Zou J3, Liu Z4.Author information 1Molecular Immunology Laboratory, Capital Institute of Pediatrics, Beijing 100020, China.2Medical Department, Aerospace 731 Hospital, Beijing 100074, China.3Pathology Laboratory, Capital Institute of Pediatrics, Beijing 100020, China.4Molecular Immunology Laboratory, Capital Institute of Pediatrics, Beijing 100020, China. Electronic address: zheweiliu@163.com.AbstractBACKGROUND: Coxsackievirus B3 (CVB3) infection causes myocarditis, pancreatitis, and aseptic meningitis. Targeting antigen-specific T cell reactions might be a promising way to alleviate the inflammatory response induced by CVB3 infection. IL-2-inducible T-cell kinase (ITK), a member of Tec kinase family expressed mainly in T cells, plays an important role in the activation of T cells. The role of ITK in viral myocarditis induced by CVB3 has not been documented.
- Molecular immunology.Mol Immunol.2014 May;59(1):30-8. doi: 10.1016/j.molimm.2013.12.004. Epub 2014 Jan 22.
- BACKGROUND: Coxsackievirus B3 (CVB3) infection causes myocarditis, pancreatitis, and aseptic meningitis. Targeting antigen-specific T cell reactions might be a promising way to alleviate the inflammatory response induced by CVB3 infection. IL-2-inducible T-cell kinase (ITK), a member of Tec kinase f
- PMID 24462896
Japanese Journal
- The Growth Hormone Secretagogue Hexarelin Protects Rat Cardiomyocytes From <i>in vivo</i> Ischemia/Reperfusion Injury Through Interleukin-1 Signaling Pathway
- International Heart Journal 58(2), 257-263, 2017
- NAID 130005556630
- The Growth Hormone Secretagogue Hexarelin Protects Rat Cardiomyocytes From <i>in vivo</i> Ischemia/Reperfusion Injury Through Interleukin-1 Signaling Pathway
- International Heart Journal, 2017
- NAID 130005450469
- 心血管疾患における無菌性炎症とインフラマソーム
- 岩手医科大学歯学雑誌 41(2.3), 19-28, 2017
- NAID 130005398364
Related Links
- myocardial [mi″o-kahr´de-al] pertaining to the muscular tissue of the heart (the myocardium). myocardial infarction (MI) death of the cells of an area of the heart muscle (myocardium) as a result of oxygen deprivation, which in turn is ...
- Thesaurus Antonyms Related Words Synonyms Legend: Noun 1. myocardial inflammation - inflammation of the myocardium (the muscular tissue of the heart) myocarditis ... In cases where TC is the primary pathology, pericarditis ...
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| 関連記事 | 「myocardial」「inflammation」「myocardia」 |
「myocardial」
- adj.
- 心筋の
「inflammation」
- n.
「myocardia」
- np.