• 대한한의학회지
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• 제32권5호
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• pp.126-133
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• 2011

Objective: We report a case of non-specific Aconiti Tuber poison complaining only of severe peripheral neurotoxicity without cardiac dysfunction. Methods: The authors evaluated the symptom changes of a patient who was hospitalized in an Oriental hospital for fourteen days. The patient received acupuncture, herbal medicine, moxibustion and analgesics. Result: No abnormality in examination for cardiac function or biochemical parameters was present. The severity of pain and dysesthesia in lower extremities gradually receded during the period of treatment with herbal and western medicines. Conclusion: This study provides helpful information for treatment of Aconiti Tuber toxicity.

• 한국생물물리학회:학술대회논문집
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• 한국생물물리학회 1999년도 학술발표회 진행표 및 논문초록
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• pp.29-29
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• 1999

Diabetic cardiomyopathy has been suggested to be caused by the intracellular Ca$\^$2＋/ overload in the myocardium. We have investigated the possible mechanism of the functional defect of cardiac sarcoplasmic reticulum (SR) in diabetic rats with respect to Ca$\^$2＋/-ATPase and phospholamban (PLB) at the transcriptional and translational levels.(omitted)

• The Korean Journal of Physiology and Pharmacology
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• 제3권6호
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• pp.623-630
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• 1999

Decreased cardiac contractility occurs in endotoxicosis, but little is known about the ionic mechanism responsible for myocardial dysfunction. In this study, we examined the changes in $Ca{2+}$ and $K^+$ currents in cardiac myocytes from endotoxin-treated rat. Ventricular myocytes were isolated from normal and endotoxemic rats (ex vivo), that were treated for 10 hours with Salmonella enteritidis lipopolysaccharides (LPS; 1.5 mg/kg) intravenously. Normal cardiac myocytes were also incubated for 6 hours with 200 ng/ml LPS (in vitro). L-type $Ca{2+}$ current $(I_{Ca,L})$ and transient outward $K^+$ current $(I_{to})$ were measured using whole cell patch clamp techniques. Peak $I_{Ca,L}$ was reduced in endotoxemic myocytes (ex vivo; 6.00.4 pA/pF, P＜0.01) compared to normal myocytes (control; 10.90.6 pA/pF). Exposure to endotoxin in vitro also attenuated $I_{Ca,L}$ (8.40.4 pA/pF, P＜0.01). The amplitude of $(I_{to})$ on depolarization to 60 mV was reduced in endotoxin treated myocytes (16.51.5 pA/pF, P＜0.01, ex vivo; 20.00.9 pA/pF, P＜0.01 , in vitro) compared to normal myocytes (control; 24.71.0 pA/pF). There was no voltage shift in steady-state inactivation of $I_{Ca,L}$ and $(I_{to})$ between groups. These results suggest that endotoxin reduces $Ca{2+}$ and $K^+$ currents of rat cardiac myocytes, which may lead to cardiac dysfunction.

• 한국독성학회:학술대회논문집
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• 한국독성학회 2005년도 추계학술대회
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• pp.133-141
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• 2005

• Journal of Chest Surgery
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• 제21권1호
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• pp.164-168
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• 1988

Between November, 1984, and May, 1986, 93 patients underwent combined valvular and coronary artery operation. They were 70 male and 23 female, the age ranging from 29 to 82. From this population 89 patients underwent single valve replacement and 4 patients underwent double valve replacement. Patients with mitral valve disease were in the majority present in the age group between 50 till 70, where as in the group after 60 years, patients with aortic valve disease were dominant. The main indication for aortic valve replacement was aortic stenosis and the indication for mitral valve replacement was equal between mitral stenosis and mitral incompetence, the later was due to papillary dysfunction after myocardial infarction. Dyspnea was a very frequent symptom and it was found in nearly all patients. 28 patients had a previous myocardial infarction and severe left ventricular dysfunction. The grafts were placed prior to valve replacement and periods of myocardial ischemia were kept at a minimum by maintaining coronary perfusion throughout the operation. It is our opinion that simultaneous valve replacement and myocardial revascularization does not increase the risk of cardiac valve replacement substantially.

• The Korean Journal of Physiology and Pharmacology
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• 제25권1호
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• pp.1-14
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• 2021

Cardiovascular disease (CVD) accounts for approximately 30% of all deaths worldwide and its prevalence is constantly increasing despite advancements in medical treatments. Cardiac remodeling and dysfunction are independent risk factors for CVD. Recent studies have demonstrated that cardiac structure and function are genetically influenced, suggesting that understanding the genetic basis for cardiac structure and function could provide new insights into developing novel therapeutic targets for CVD. Regular exercise has long been considered a robust nontherapeutic method of treating or preventing CVD. However, recent studies also indicate that there is inter-individual variation in response to exercise. Nevertheless, the genetic basis for cardiac structure and function as well as their responses to exercise training have yet to be fully elucidated. Therefore, this review summarizes accumulated evidence supporting the genetic contribution to these traits, including findings from population-based studies and unbiased large genomic-scale studies in humans.

• Journal of Ginseng Research
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• 제45권3호
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• pp.450-455
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• 2021

Korean Red Ginseng (KRG) is an herbal oriental medicine known to alleviate cardiovascular dysfunction. To analysis the expression of diabetic cardiac complication-associated genes in db/db mice, we studied the cardiac gene expression following KRG treatment. In result, a total of 585 genes were found to be changed in db/db mice. Among the changed expression, 245 genes were found to 2-fold upregulated, and 340 genes were 2-fold downregulated. In addition, the changed gene expressions were ameliorated by KRG. In conclusion, KRG may be possible to normalize cardiac gene expressions in db/db mice.

• BMB Reports
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• 제49권5호
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• pp.270-275
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• 2016

The Ubiquitin proteasome system (UPS) plays roles in protein degradation, cell cycle control, and growth and inflammatory cell signaling. Dysfunction of UPS in cardiac diseases has been seen in many studies. Cholesterol acts as an inducer of cardiac hypertrophy. In this study, the effect of proteasome inhibitors on the cholesterol-induced hypertrophic growth in H9c2 cells is examined in order to observe whether UPS is involved in cardiac hypertrophy. The treatment of proteasome inhibitors MG132 and Bortezomib markedly reduced cellular surface area and mRNA expression of β-MHC in cholesterol-induced cardiac hypertrophy. In addition, activated AKT and ERK were significantly attenuated by MG132 and Bortezomib in cholesterol-induced cardiac hypertrophy. We demonstrated that cholesterol-induced cardiac hypertrophy was suppressed by proteasome inhibitors. Thus, regulatory mechanism of cholesterol-induced cardiac hypertrophy by proteasome inhibitors may provide a new therapeutic strategy to prevent the progression of heart failure.

• 한국기계가공학회지
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• 제12권4호
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• pp.22-28
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• 2013

It is important to begin left ventricular assist device (LVAD) treatment at appropriate time for heart failure patients who expect cardiac recovery after the therapy. In order to predict the optimal timing of LVAD implantation, we predicted pumping efficacy of LVAD according to the severity of heart failure theoretically. We used LVAD-implanted cardiovascular system model which consist of 8 Windkessel compartments for the simulation study. The time-varying compliance theory was used to simulate ventricular pumping function in the model. The ventricular systolic dysfunction was implemented by increasing the end-systolic ventricular compliance. Using the mathematical model, we predicted cardiac responses such as left ventricular peak pressure, cardiac output, ejection fraction, and stroke work according to the severity of ventricular systolic dysfunction under the treatments of continuous and pulsatile LVAD. Left ventricular peak pressure, which indicates the ventricular loading condition, decreased maximally at the 1st level heart-failure under pulsatile LVAD therapy and 2nd level heart-failure under continuous LVAD therapy. We conclude that optimal timing for pulsatile LVAD treatment is 1st level heart-failure and for continuous LVAD treatment is 2nd level heart-failure when considering LVAD treatment as "bridge to recovery".

• Journal of Chest Surgery
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• 제57권2호
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• pp.225-229
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• 2024

Venovenous (VV) extracorporeal membrane oxygenation (ECMO) is a lifesaving technique for patients experiencing respiratory failure. When VV ECMO fails to provide adequate support despite optimal settings, alternative strategies may be employed. One option is to add another venous cannula to increase venous drainage, while another is to insert an additional arterial return cannula to assist cardiac function. Alternatively, a separate ECMO circuit can be implemented to function in parallel with the existing circuit. We present a case in which the parallel ECMO method was used in a 63-year-old man with respiratory failure due to coronavirus disease 2019, combined with cardiac dysfunction. We installed an additional venoarterial ECMO circuit alongside the existing VV ECMO circuit and successfully weaned the patient from both types of ECMO. In this report, we share our experience and discuss this method.