• The Korean Journal of Health Service Management
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• v.7 no.3
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• pp.71-82
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• 2013

Arterial stiffness(AS) is an important pathologic state of vascular injury. This study was carried out to elucidate the effect of physiological variables on brachial-ankle pulse wave velocity(BAPWV), index of AS. Four hundred adults(volunteers) participated in this study. Body indices, biochemical, cardiac and inflammatory markers, and right(Rt)- and left(Lt)-BAPWV were measured. Body mass index(BMI), Rt- and Lt-BAPWV, glucose, triglyceride, alkaline phosphatase(ALP), gamma-glutamyl transferase(GGT), creatinine, uric acid, troponin-I(TNI), NT-proBNP and high sensitivity C-reactive protein(hs-CRP) levels were higher than the reference value of each variable. Rt- and Lt-BAPWV were directly correlated with age, body weight, BMI, glucose, ketone, aspartate aminotransferase, alanine aminotransferase, ALP, GGT, total cholesterol, low density lipoprotein, lipoprotein(a), apolipoprotein-B, blood urea nitrogen, heart rate, TNI, creatine kinase, CK-MB, lactic dehydrogenase, myoglobin, hs-CRP, lipase, reumatoid factor, fibrinogen and D-dimer (P<0.05, P<0.01, P<0.001 or P<0.000, respectively), but inversely associated with total bilirubin, uric acid, apolipoprotein-A1 and GFR (P<0.05). These observations suggest that a variety of physiological variables may influence BAPWV, resulting in increased risk or prevention of cardiovascular and/or cerebrovascular attacks. Therefore, physiological variables affecting BAPWV should be regularly controlled.

• The Korean Journal of Physiology and Pharmacology
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• v.12 no.2
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• pp.51-58
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• 2008

Cardiac fibroblasts constitute one of the largest cell populations in the heart, and contribute to structural, biochemical, mechanical and electrical properties of the myocardium. Nonetheless, their cardiac functions, especially electrophysiological properties, have often been disregarded in studies. $Ca^{2+}$-activated $K^+\;(K_{Ca})$ channels can control $Ca^{2+}$ influx as well as a number of $Ca^{2+}$-dependent physiological processes. We, therefore, attempted to identify and characterize $K_{Ca}$ channels in rat Cardiac fibroblasts. First, we showed that the cells cultured from the rat ventricle were cardiac fibroblasts by immunostaining for discoidin domain receptor 2 (DDR-2), a specific fibroblast marker. Secondly, we detected the expression of various $K_{Ca}$ channels by reverse transcription polymerase chain reaction (RT-PCR), and found all three family members of $K_{Ca}$ channels, including large conductance $K_{Ca}$ (BK-${\alpha}1-\;and\;-{\beta}1{\sim}4$subunits), intermediate conductance $K_{Ca}$ (IK), and small conductance $K_{Ca}$ (SK$1{\sim}4$ subunits) channels. Thirdly, we recorded BK, IK, and SK channels by whole cell mode patch clamp technique using their specific blockers. Finally, we performed cell proliferation assay to evaluate the effects of the channels on cell proliferation, and found that the inhibition of IK channel increased the cell proliferation. These results showed the existence of BK, IK, and SK channels in rat ventricular fibroblasts and involvement of IK channel in cell proliferation.

• Biomolecules & Therapeutics
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• v.21 no.3
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• pp.196-203
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• 2013

Recent accumulating studies have reported that hypoxic preconditioning during ex vivo expansion enhanced the self-renewal or differentiation of various stem cells and provide an important strategy for the adequate modulation of oxygen in culture conditions, which might increase the functional bioactivity of these cells for cardiac regeneration. In this study, we proposed a novel priming protocol to increase the functional bioactivity of cardiac progenitor cells (CPCs) for the treatment of cardiac regeneration. Firstly, patient-derived c-$kit^+$ CPCs isolated from the atrium of human hearts by enzymatic digestion and secondly, pivotal target molecules identified their differentiation into specific cell lineages. We observed that hCPCs, in response to hypoxia, strongly activated ERK phosphorylation in ex vivo culture conditioning. Interestingly, pre-treatment with an ERK inhibitor, U0126, significantly enhanced cellular proliferation and tubular formation capacities of CPCs. Furthermore, we observed that hCPCs efficiently maintained the expression of the c-kit, a typical stem cell marker of CPCs, under both hypoxic conditioning and ERK inhibition. We also show that hCPCs, after preconditioning of both hypoxic and ERK inhibition, are capable of differentiating into smooth muscle cells (SMCs) and cardiomyocytes (CMs), but not endothelial cells (ECs), as demonstrated by the strong expression of ${\alpha}$-SMA, Nkx2.5, and cTnT, respectively. From our results, we conclude that the functional bioactivity of patient-derived hCPCs and their ability to differentiate into SMCs and CMs can be efficiently increased under specifically defined culture conditions such as short-term hypoxic preconditioning and ERK inhibition.

• Annals of Laboratory Medicine
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• v.38 no.6
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• pp.538-544
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• 2018

Background: Serum copeptin has been demonstrated to be useful in early risk stratification and prognostication of patients with acute myocardial infarction (AMI). However, the prognostic value of copeptin after percutaneous coronary intervention (PCI) for clinical outcomes remains uncertain. We investigated the prognostic role of serum copeptin levels immediately after successful PCI as a prognostic marker for major adverse cardiac events (MACE; comprising death, repeat PCI, recurrent MI, or coronary artery bypass grafting) in patients with AMI. Methods: A retrospective study was performed in 149 patients with AMI who successfully received PCI. Serum copeptin levels were analyzed in blood samples collected immediately after PCI. The association between copeptin levels and MACE during the follow-up period was evaluated. Results: MACE occurred in 34 (22.8%) patients during a median follow-up of 30.1 months. MACE patients had higher copeptin levels than non-MACE patients did. Multiple logistic regression analysis showed that the increase in serum copeptin levels was associated with increased MACE incidence (odds ratio=1.6, P =0.005). Conclusions: A high level of serum copeptin measured immediately after PCI was associated with MACE in patients with AMI during long-term follow-up. Serum copeptin levels can serve as a prognostic marker in patients with AMI after successful PCI.

• Anatomy and Cell Biology
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• v.51 no.4
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• pp.266-273
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• 2018

The ganglion cardiacum or juxtaductal body is situated along the left recurrent laryngeal nerve in the aortic window and is an extremely large component of the cardiac nerve plexus. This study was performed to describe the morphologies of the ganglion cardiacum or juxtaductal body in human fetuses and to compare characteristics with intracardiac ganglion. Ganglia were immunostained in specimens from five fetuses of gestational age 12-16 weeks and seven fetuses of gestational age 28-34 weeks. Many ganglion cells in the ganglia were positive for tyrosine hydroxylase (TH; sympathetic nerve marker) and chromogranin A, while a few neurons were positive for neuronal nitric oxide synthase (NOS; parasympathetic nerve marker) or calretinin. Another ganglion at the base of the ascending aorta carried almost the same neuronal populations, whereas a ganglion along the left common cardinal vein contained neurons positive for chromogranin A and NOS but no or few TH-positive neurons, suggesting a site-dependent difference in composite neurons. Mixtures of sympathetic and parasympathetic neurons within a single ganglion are consistent with the morphology of the cranial base and pelvic ganglia. Most of the intracardiac neurons are likely to have a non-adrenergic non-cholinergic phenotype, whereas fewer neurons have a dual cholinergic/noradrenergic phenotype. However, there was no evidence showing that chromogranin A- and/or calretinin-positive cardiac neurons corresponded to these specific phenotypes. The present study suggested that the ganglion cardiacum was composed of a mixture of sympathetic and parasympathetic neurons, which were characterized the site-dependent differences in and near the heart.

• Food Science of Animal Resources
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• v.38 no.2
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• pp.259-272
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• 2018

This study aims to investigate the protective effects of kefir against myocardial infarction induced by isoproterenol (ISO). The rats were randomly divided into 4 groups, each group consisting of 8 rats. The control group, the kefir group (5 mL/kg/d kefir administered to rats as intra-gastric gavage for 60 d), the ISO group (100 mg/kg ISO was administered to rats, s.c. on 61. and 62. d), and kefir+ISO group (5 mL/kg/d kefir was administered to rats intra gastric gavage for 60 days prior to ISO, 100 mg/kg in two doses on day 61 and 62). 12 h after the last ISO dose, all rats were decapitated and their blood samples were collected. Cardiac tissue was reserved for histopathological examination. creatine kinase (CK), alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), triglycerides, total cholesterol,very low density lipoprotein (VLDL), low density lipoprotein (LDL), high density lipoprotein (HDL) and glucose were measured by autoanalyzer, whole blood malondialdehyde (MDA), glutathione (GSH) and plasma advanced oxidation protein products (AOPP) levels were measured spectrophotometrically. It was determined that in the group of kefir+ISO, the levels of AST (p<0.001), CK (p<0.001), LDH (p<0.001), MDA (p<0.001) and AOPP (p<0.001) were decreased, while the GSH (p<0.05) increased, compared to ISO group. There were no significant changes in lipid profile and glucose levels between these two groups. In conclusion, by examining cardiac enzymes and histopathological changes in cardiac tissue, it can be concluded that the administration of kefir in myocardial infarction induced by ISO can protect the heart with its antioxidant characteristic and minimize the toxic damage created by ISO.

• Journal of Life Science
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• v.17 no.12
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• pp.1717-1722
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• 2007

In the present study, all of the treadmill exercise-trained SHR expressed clear adaptive changes such as reduced resting heart rate and blood pressures, LPOA, homocysteine Therefore, treadmill exercise was sufficient to induce physiological adaptation in the SHR. Endurance training is known to induce physiological cardiac hypertrophy, while hypertension induces patho logical cardiac hypertrophy that increases cardiomyocyte apoptosis. The pathological adaptation to pressure overload has also been associated with a further increase in the expression of several marker genes including cardiomyocyte ET-1 in the SHR, but not in the exercise-trained SHR. Additionally, there is an increase in the endothelial nitricoxide synthases (eNOS) protein expression of soleus, gastrocnemius, and extensor digitorum longus muscle in the exercise-trained SHR but not in the SHR in the present study. Thus, compared to pathological adaptation to pressure overload, physiological adaptation to exercise training is associated with distinct alterations in cardiac and molecular phenotypes. based on these results, exercise training improves hypertension by cardiovascular regulating genes and hemodynamic parameters.

• Korean Journal of Radiology
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• v.24 no.6
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• pp.512-521
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• 2023

Objective: There is increasing recognition that left atrial (LA) strain can be a prognostic marker of various cardiac diseases. However, its prognostic value in acute myocarditis remains unclear. Therefore, this study aimed to evaluate whether cardiovascular magnetic resonance (CMR)-derived parameters of LA strain can predict outcomes in patients with acute myocarditis. Materials and Methods: We retrospectively analyzed the data of 47 consecutive patients (44.2 ± 18.3 years; 29 males) with acute myocarditis who underwent CMR in 13.5 ± 9.7 days (range, 0-31 days) of symptom onset. Various parameters, including feature-tracked CMR-derived LA strain, were measured using CMR. The composite endpoints included cardiac death, heart transplantation, implantable cardioverter-defibrillator or pacemaker implantation, rehospitalization following a cardiac event, atrial fibrillation, or embolic stroke. The Cox regression analysis was performed to identify associations between the variables derived from CMR and the composite endpoints. Results: After a median follow-up of 37 months, 20 of the 47 (42.6%) patients experienced the composite events. In the multivariable Cox regression analysis, LA reservoir and conduit strains were independent predictors of the composite endpoints, with an adjusted hazard ratio per 1% increase of 0.90 (95% confidence interval [CI], 0.84-0.96; P = 0.002) and 0.91 (95% CI, 0.84-0.98; P = 0.013), respectively. Conclusion: LA reservoir and conduit strains derived from CMR are independent predictors of adverse clinical outcomes in patients with acute myocarditis.

• Tuberculosis and Respiratory Diseases
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• v.59 no.1
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• pp.53-61
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• 2005

Background : Cardiac troponin I (cTnI) is a specific marker of myocardial injury. It is known that a higher level of cTnI is associated with a poor clinical outcome in patients with acute coronary syndrome. An elevation in cTnI is also observed in various noncardiac critical illnesses. This study evaluated whether cTnI is useful for predicting the prognosis in noncardiac critically ill patients. Methods : From June 2003 to July 2004 at Gyeongsang National University Hospital, we enrolled 215 patients (male:142, female:73, mean age:$63{\pm}15$ years ) who were admitted for critical illness other than acute coronary syndrome at the medical intensive care unit(ICU). The severity score of critical illness (SAPS II and SOFA) was determined and serum cTnI level was measured within 24 hours after admission to the ICU. The mortality rate was compared between the cTnI-positive (${\geq}0.1{\mu}g/L$) and cTnI-negative ($cTnI<0.1{\mu}g/L$) patients at the $10^{th}$ and $30^{th}$ day after admission to the ICU. The mean cTnI value was compared between the survivors and non-survivors at the $10^{th}$ and $30^{th}$ day after admission to the ICU in the cTnI-positive patients. The correlation between cTnI and the severity of the critical illness score (SAPS II and SOFA) was also analyzed in cTnI-positive patients. Results : 1) The number of cTnI-negative and positive patients were 95(44%) and 120(56%), respectively. 2) The mortality rate at the $10^{th}$ and $30^{th}$ day after admission to the ICU was significantly higher in the cTnI-positive patients (29%, 41%) than in the cTnI-negative patients (12%, 21%)(p<0.01). 3) In the cTnI-positive patients, the mean value of the cTnI at the $10^{th}$ and $30^{th}$ day after admission to the ICU was significantly higher in the non-survivors ($4.5{\pm}9.2{\mu}g/L$, $3.5{\pm}7.9{\mu}g/L$) than in the survivors($1.8{\pm}3.6{\mu}g/L$, $2.0{\pm}3.9{\mu}g/L$) (p < 0.05). 4) In the cTnI-positive patients, the cTnI level was significantly correlated with the SAPS II score (r=0.24, p<0.001) and SOFA score (r=0.30, p<0.001). Conclusion : The cTnI may be a useful prognostic marker in noncardiac critically ill patients.

• Journal of Veterinary Clinics
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• v.33 no.2
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• pp.81-86
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• 2016

Cystatin C is a low molecular weight 13 kilodalton protein. It is known to be a more sensitive marker of glomerular filtration rate than creatinine in humans. The purpose of the present study was to demonstrate the changes of renal markers including cystatin C according to the severity of chronic mitral valve insufficiency (CMVI) and to investigate the clinical relevance of cystatin C as an early renal marker in dogs with CMVI. A retrospective study was performed to assess renal function according to International Small Animal Cardiac Health Council (ISACHC) system classification of heart failure in dogs with CMVI. Thirty seven dogs were divided into a group 1 (healthy dogs ; n = 10), a group 2 (ISACHC I ; n = 10) and a group 3 (ISACHC II-III ; n = 17). In all dogs, serum concentrations of bun (sUr), creatinine (sCr) and cystatin C (sCys-C) were measured with an automated analyzer. In dogs with CMVI, sCys-C concentrations were significantly correlated with sCr concentrations and were independent of age, BW, SBP, and sex. Renal dysfunction tended to occur more frequently as the severity of CMVI increases. In dogs with mild CMVI, only sCys-C concentrations were statistically higher than in healthy dogs. This study demonstrates the clinical relevance of sCys-C. sCys-C may be a valuable renal marker for early diagnosis of renal dysfunction in dogs with CMVI.