Cardiomyopathy, Dilated/metabolism* ; Humans ; Microfilament Proteins/metabolism* ; Models, Cardiovascular ; Mutation ; Myocytes, Cardiac ; Pluripotent Stem Cells/metabolism* ; Transcription Factors/metabolism* ; Troponin T/metabolism*

OBJECTIVE: To compare the changes in muscle enzyme between children with myocarditis and Duchene/Becker muscular dystrophy (DMD/BMD), and to seek the explanations for variation.
 METHODS: The retrospective analysis for 83 myocarditis children (myocarditis group) and 69 DMD/BMD children (DMD/BMD group), who were collected from Department of Pediatric of Shengjing Hospital affiliated to China Medical University since January 2008 to May 2015, was carried out. At the same time, 24 healthy children from the Department of Pediatric Development served as a control group. The examination indexes included creatine kinase (CK), creatine kinase-isoenzyme MB (CK-MB), creatine kinase isoenzyme MB mass (CK-MB mass), cardiac troponin I (cTnI) and high-sensitive-cTnT (hs-cTnT).
 RESULTS: 1) In the myocarditis group, the CK increased from 100 to 1 000 U/L, reached a peak after 5 days, which lasted for a week and then dropped to the normal; the CK-MB reached a peak after 5 to 7 days and dropped to the normal a month later; the CK-MB mass reached a peak on the first day and dropped to the normal after 3 weeks; the cTn reached to a peak after 5 days and dropped to the normal after about 17 days; hs-cTnT reached to a peak on the first day and dropped to the normal after about 19 days. 2) In the DMD/BMD group, the CK increased significantly and 27 cases had a CK value of more than 10 000 U/L. After the treatment for 1 to 2 weeks, their enzyme rose again after a slight drop. In terms of cTnI, 6 cases showed a moderate increase, 5 of them couldn't drop to the normal level until more than 3 weeks later; the hs-cTnT increased in the 45 cases, which lasted for more than 3 weeks in the 31 cases of them and showed a tendency of persisting increase.
 CONCLUSION The cTnI and hs-cTnT rise significantly and possess wider observation window than CK and CK-MB mass in myocarditis children, with more sensitive and specific changes. The myocardial damage can occur before myasthenia and keep this trend for a long time in the DMD/BMD children. The trend of cTnI change in myocarditis children is similar to hs-cTnT, while hs-cTnT in DMD/BMD children is more sensitive than cTnI.
Biomarkers ; Child ; China ; Creatine Kinase ; blood ; metabolism ; Creatine Kinase, MB Form ; blood ; metabolism ; Female ; Humans ; Male ; Muscle Weakness ; enzymology ; Muscular Dystrophy, Duchenne ; enzymology ; therapy ; Myocarditis ; enzymology ; therapy ; Retrospective Studies ; Time Factors ; Troponin I ; blood ; metabolism ; Troponin T ; blood ; metabolism

PURPOSE: Adipose-derived stem cells (ADSCs) are known to be potentially effective in regeneration of damaged tissue. We aimed to assess the effectiveness of intracoronary administration of ADSCs in reducing the infarction area and improving function after acute transmural myocardial infarction (MI) in a porcine model. MATERIALS AND METHODS: ADSCs were obtained from each pig's abdominal subcutaneous fat tissue by simple liposuction. After 3 passages of 14-days culture, 2 million ADSCs were injected into the coronary artery 30 min after acute transmural MI. At baseline and 4 weeks after the ADSC injection, 99mTc methoxyisobutylisonitrile-single photon emission computed tomography (MIBISPECT) was performed to evaluate the left ventricular volume, left ventricular ejection fraction (LVEF; %), and perfusion defects as well as the myocardial salvage (%) and salvage index. At 4 weeks, each pig was sacrificed, and the heart was extracted and dissected. Gross and microscopic analyses with specific immunohistochemistry staining were then performed. RESULTS: Analysis showed improvement in the perfusion defect, but not in the LVEF in the ADSC group (n=14), compared with the control group (n=14) (perfusion defect, -13.0+/-10.0 vs. -2.6+/-12.0, p=0.019; LVEF, -8.0+/-15.4 vs. -15.9+/-14.8, p=0.181). There was a tendency of reducing left ventricular volume in ADSC group. The ADSCs identified by stromal cell-derived factor-1 (SDF-1) staining were well co-localized by von Willebrand factor and Troponin T staining. CONCLUSION: Intracoronary injection of cultured ADSCs improved myocardial perfusion in this porcine acute transmural MI model.
Adipose Tissue/cytology ; Animals ; Bone Marrow Cells/cytology/*metabolism ; Chemokine CXCL12 ; Coronary Vessels ; Female ; Heart/physiopathology ; Heart Ventricles ; *Mesenchymal Stromal Cells ; Myocardial Infarction/physiopathology/radionuclide imaging/*therapy ; *Stem Cell Transplantation ; Swine ; Technetium Tc 99m Sestamibi/*pharmacology ; Tomography, Emission-Computed, Single-Photon/*methods ; Troponin T ; *Ventricular Function, Left

OBJECTIVETo investigate the expression of Junctophilin 1 (JP1) in cardiogenesis of mammalian.

METHODSCardiac differentiation of embryonic stem cells (ESCs) was generated by hanging drop method. Fetal heart was obtained from the rats aged d 14-20 of gestation. The expression of JP1 and JP2 during cardiogenesis of ESCs and rat embryos was analyzed by RT-PCR or Western blotting. Immunofluorescence staining was employed to reveal the distribution of JP1 and JP2 in embryoid body (EB), probing for merging of JP1 and JP2 and cardiac sarcomeric α-Actinin or Troponin-T. Percentage of JP1 and JP2-positive staining cells was analyzed quantitatively by FCS on d17.

RESULTSJP1 mRNA was up-regulated at the early stage (d 5-11) and then decreased. The expression of JP1 protein was up-regulated at the early stage (d 7-9), then decreased gradually and disappeared after d 15. While JP2 gene and protein expression increased in a time-dependent manner during cardiogenesis of rat embryos. The results of immunofluorescence staining showed that there was a parallel co-localization of JP2 with Troponin-T or α-Actinin on d17, while JP1 failed to express in the sarcomeric positive area at the same time point. Furthermore, FCS analysis showed that about 16.59% of cells were JP2-positive, while no cells were stained positively for JP1 in d17 EBs.

CONCLUSIONJP1 gene is expressed during the whole process of cardiogenesis, while JP1 protein only appears on the early stage. The expression of JP1 in cardiogenesis of ESCs is consistent with that of rat embryos.

Actinin ; genetics ; metabolism ; Animals ; Cell Differentiation ; Cell Line ; Embryonic Stem Cells ; cytology ; metabolism ; Heart ; embryology ; Membrane Proteins ; genetics ; metabolism ; Mice ; Mice, Inbred ICR ; Myocytes, Cardiac ; cytology ; metabolism ; RNA, Messenger ; genetics ; Rats ; Troponin T ; genetics ; metabolism

OBJECTIVETo discuss the diagnostic value of cardiac enzyme and troponin in acute organophosphorus pesticide poisoning (AOPP).

METHODSA retrospective study was performed in the document published in domestic journals and PubMed from 1979 to 2010. The data of the cardiac enzyme and troponin were collected. Statistical analysis was conducted with one-way ANOVA and rank sum test. 2129 cases with AOPP were enrolled.

RESULTSThe levels of creatine kinase (CK), creatine kinase-MB (CK-MB) and cardiac troponin I (cTnI) in milder, moderate and severe poisoning groups were significantly elevated compared by the healthy control group (P < 0.05). The differences were also dramatic among three patients groups (P < 0.05). The ratios of CK-MB to CK in both moderate and severe groups were significantly lower than in healthy controls (P < 0.05). The levels of CK, CK-MB and cTnI were higher especially in patients with intermediate myasthenic syndrome (IMS) than patients without IMS. Meanwhile, the levels of CK and CK-MB were elevated in patients with respiratory failure compared by non-failure ones, but decreased in the ratios of CK-MB to CK (P < 0.05).

CONCLUSIONSThe elevation of CK and CK-MB in serum could not be judged as the criteria of myocardial damage in AOPP, the ratio of CK-MB to CK were more valuable; the value of cTnI in myocardial damage was still in suspect. CK, CK-MB and cTnI could be used as auxiliary criteria of AOPP classification.

Adolescent ; Adult ; Aged ; Aged, 80 and over ; Cardiomyopathies ; diagnosis ; etiology ; Child ; Child, Preschool ; Creatine Kinase ; blood ; Creatine Kinase, MB Form ; blood ; Female ; Humans ; Infant ; Male ; Middle Aged ; Myocardium ; enzymology ; metabolism ; pathology ; Organophosphate Poisoning ; metabolism ; Troponin I ; blood ; Troponin T ; blood ; Young Adult

The purpose of this study was to test whether oxygen carriers could decrease tissue injury in a rat model of acute myocardial infarct. The study included 3 groups: SD rats in group II and group III were subjected to permanent occlusion of their left anterior descending coronary arteries; SD rats in group I were subjected to sham-operation. The success of modeling was assartained by ECG. Then the rats were given drug via caudal veins for 2 days. A quantitative evaluation was made with an automatic device for interpretation of cardiac troponin T (cTnT); heart staining was made for the calculation of myocardial infarction size (MIS); and myocardial tissue was taken and subjected to routine pathological hematoxylin-eosin (HE) staining for showing myocardial cell injury. cTnT in the sham-operation group was significantly lower by comparison with that in the model group (P < 0.01), and it was slightly lower in the oxygen carriers group than that in the model group, but there was no statistically significant difference (P = 0.18); MIS was significantly smaller in the sham-operation group than that in the model group (P < 0.01), and it was greater in the model rats than that in the oxygen carriers rats (P < 0.05). HE staining of myocardicum in the oxygen carriers group was significantly better than that in the model group (P < 0.01). The evidence suggested that oxygen carriers increased oxygen supply to ischemic myocardium, reduced the myocardial injury, and thus might offer a novel treatment of myocardial infarction.
Animals ; Blood Substitutes ; pharmacology ; Hemoglobins ; metabolism ; Male ; Myocardial Infarction ; metabolism ; Oxygen ; metabolism ; Rats ; Rats, Sprague-Dawley ; Troponin T ; metabolism

OBJECTIVETo investigate the role of homeobox gene Nkx2-5 in cardiac myogenesis.

METHODSTwo P19 cell lines, namely cells transfected with exogenous expression of Nkx2-5 gene and non-transfected cells, were cultured in suspension for 4 days to induce cell aggregation, and the cell aggregates were transferred to the Petri dish for further adherent culture. On days 4, 8, 12 and 16 of adherent culture, the expressions of α-sarcomeric actin (α-SA) and cardiac troponin T (cTnT) protein were detected by immunocytochemistry, and the mRNA expressions of GATA-4, α-myosin heavy chain (α-MHC) and atrial natriuretic factor (ANF) genes by RT-PCR.

RESULTSIn the transfected cells, α-SA and cTnT protein expressions were detected on days 8, 12 and 16 of adhere culture, and their expressions increased gradually with time. α-SA and cTnT expression was significantly higher on day 16 than on day 8 of culture (P<0.01). RT-PCR analysis of the transfected cell showed the presence of GATA-4 expression on day 4 of adherent culture, and the expression increased on days 8 and 12 but decreased on day 16. ANF and α-MHC expressions were found on days 8, 12, and 16, increasing gradually over time and showing significant differences from those on day 4 (P<0.05 or P<0.01). The expression of α-MHC was significantly higher on days 12 and 16 than on day 8 (P<0.05 or P<0.01), and ANF expression was significantly higher on day 16 than on days 8 and 12 (P<0.01). The non-transfected cells were negative for the expressions of all these genes.

CONCLUSIONExogenous expression of Nkx2-5 gene can induce P19 cells to express cardiac markers in vitro.

Actins ; metabolism ; Animals ; Atrial Natriuretic Factor ; metabolism ; Cell Culture Techniques ; Cell Differentiation ; Cell Line ; GATA4 Transcription Factor ; metabolism ; Gene Expression ; Homeobox Protein Nkx-2.5 ; Homeodomain Proteins ; genetics ; metabolism ; Mice ; Myocytes, Cardiac ; cytology ; metabolism ; Myosin Heavy Chains ; metabolism ; Transcription Factors ; genetics ; metabolism ; Transfection ; Troponin T ; metabolism

Vitamin D insufficiency may be associated with cardiovascular (CV) mortality in HD patients. To test this hypothesis, we cross-sectionally measured 25-hydroxyvitamin D (25D), 1,25-dihydroxyvitamin D (1,25D), cardiac troponin T (cTnT), and N-terminal pro-B-type natriuretic peptide (NT-pro-BNP) in chronic HD patients. Sixty-five patients (M:F=31:34, age 52.2+/-13.2 yr, DM 41.5%) were selected. Along with the expected low levels of 1,25D, 59 (90.8%) patients had 25D insufficiency (<30 ng/mL) among whom 15 (23.1%) were 25D deficient (<10 ng/mL). The 25D levels showed a negative correlation with cTnT levels (Spearman's rho=-0.44, p<0.01) but not with NT-pro-BNP levels (Spearman's rho=-0.17, p=0.17). The 1,25D levels, however, did not show any relationship with either cTnT or NT-pro-BNP. In multivariate analysis, being male and having low levels of 25D were independent risk factors associated with cTnT elevation (beta=0.44, p<0.01 and beta=-0.48, p<0.01, respectively). In conclusion, not only 1,25D but also 25D are commonly decreased in HD patients. Lower 25D levels appear to be associated with cTnT elevation, predicting worse CV outcome, and are possible to involve cardiac hypertrophy or coronary artery disease.
Biological Markers/*blood ; Coronary Artery Disease/blood/diagnosis ; Electrocardiography/methods ; Female ; Heart Diseases/*blood/diagnosis ; Humans ; Male ; Middle Aged ; Multivariate Analysis ; Nerve Tissue Proteins/blood ; Protein Precursors/blood ; Renal Dialysis/*methods ; Risk Factors ; Troponin T/blood ; Vitamin D/*blood/metabolism

OBJECTIVETo investigate the changes of cardiac T troponin (cTnT) and high-sensitivity C reactive protein (hs-CRP) in children with viral myocarditis (VMC).

METHODSForty children with VMC were examined for cTnT, hs-CRP, and creatine kinase MB (CK-MB) levels.

RESULTSChildren with VMC had significantly higher cTnT, hs-CRP and CK-MB levels than the control group on admission (P<0.01), but obviously decreased after two weeks of treatment. The positivity rate of cTnT and hs-CRP were significantly higher in children with VMC than the control group on admission, and decreased significantly after treatment (P<0.01). The positivity rate of cTnT and hs-CRP were significantly higher than that of CK-MB (P<0.05).

CONCLUSIONSerum cTnT and hs-CRP are sensitive indices for diagnosis of VMC, and their detection have important value in estimation of the patients' condition.

Biomarkers ; blood ; C-Reactive Protein ; metabolism ; Child ; Child, Preschool ; Creatine Kinase, MB Form ; blood ; Female ; Humans ; Male ; Myocarditis ; blood ; virology ; Troponin T ; blood ; Virus Diseases ; blood

OBJECTIVE: To study the postmortem stability of cTnT as well as its expression alteration, and to evaluate it in the diagnosis of early myocardial ischemia in forensic practice. METHODS: Animal model of early myocardial ischemia was established by rabbit coronary artery ligation. The expression of cTnT in myocardium at different postmortem intervals was detected using immunohistochemistry and analyzed using imaging technique and statistics. The results were then compared between the experimental and control groups. RESULTS: In ischemic myocardium, the expression of cTnT showed prominent focal or flaky depletion in myocardial cytoplasm with no expression detected in interstitium. The expression level showed a linear decrease with prolonged postmortem interval, and disappeared completely on day 14 after death while stored at 4 degrees C. However, there were significant differences in the expression levels of cTnT between experimental and control groups from day 1 to day 7 after death. CONCLUSION Immunohistochemical detection of cTnT for diagnosis of early myocardial ischemia in corpses stored at 4 degrees C must be performed within 7 days after death.
Animals ; Female ; Immunohistochemistry ; Male ; Myocardial Ischemia/metabolism* ; Myocardium/metabolism* ; Postmortem Changes ; Rabbits ; Random Allocation ; Time Factors ; Troponin T/metabolism*