• Korean Journal of Poultry Science
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• v.29 no.3
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• pp.225-231
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• 2002

Total 240 of ISA Brown layers were employed in this experiment to study the effects of single or mixed feeding of Lactobacillus and yeast on the performance and intestinal microflora of laying hens. They were randomly allocated to six dietary treatments; None(Control), Pichia farinosa(PF), Lactobacillus crispatus avihen1 (LCH), Lactobacillus vaginalis avihen1(LVH), LCH＋PF, and LVH＋PF. Viable microflora were added to meet 3${\times}$10$\^$6/ cfu PF and 10$\^$7/ cfu Lacrobacillus per g of feed. There were four replicates per treatment, and 10 birds per replicates. Laying performance was recorded for 10 weeks, followed by a metabolism trial during which nutrient utilization, pattern of intestinal microflora and fecal NH$\sub$3/ emission were examined. Egg production and daily egg mass of birds fed either single or mixed microorganisms were significantly higher than those of the control(P<0.05). Egg weight and feed intake were not statistically different among all treatments. However, feed conversion ratio tended to improve by the supplementation of microbes. Digestibility of crude protein, ether extract and crude ash tended to improve in Lactobacillus treatments, however, there were not statistically different. With regards to the number of intestinal microbes, number of anaerobes were increased in microbes feeding group. Eggshell quality of PF layers was significantly poorer than those of the other treatments. No consistent trend was found in Haugh Unit among all treatments. Fecal NH$\sub$3/ gas emission was significantly lower in LVH, LVH＋PF and LCH＋PF than the other treatments(P<0.05). From the result of this experiment, it could be concluded that single or mixed feeding of Lactobacillus and yeast improves the laying performance and decreases the fecal ammonia gas emission. No synergic effect was found when both microbes were mixed and fed to the layers.

• The Korean Journal of Physiology and Pharmacology
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• v.5 no.5
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• pp.413-421
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• 2001

An impaired smooth muscle cell (SMC) relaxation of coronary artery by alteration of $K^+$ channels would be the most potential explanation for reduced coronary reserve in left ventricular hypertrophy (LVH), however, this possibility has not been investigated. We performed morphometrical analysis of the coronary artery under electron microscopy and measured $Ca^{2+}-activated\;K\;(K_{Ca})$ currents and delayed rectifier K $(K_{dr})$ currents by whole-cell and inside-out patch-clamp technique in single coronary arterial SMCs from rabbits subjected to isoprenaline-induced cardiac hypertrophy. Coronary arterial SMCs underwent significant changes in ultrastructure. The unitary current amplitude and the open-state probability of $K_{Ca}$ channel were significantly reduced in hypertrophy without open-time and closed-time kinetic. The concentration-response curve of $K_{Ca}$ channel to $Ca^{2+}$ is shifted to the right in hypertrophy. The reduction in the mean single channel current and increase in the open channel noise of $K_{Ca}$ channel by TEA were more sensitive in hypertrophy. $K_{dr}$ current density is significantly reduced in hypertrophy without activation and inactivation kinetics. The sensitivity of $K_{dr}$ current on 4-AP is significantly increased in hypertrophy. This is the first study to report evidence for alterations of $K_{Ca}$ channels and $K_{dr}$ channels in coronary SMCs with LVH. The findings may provide some insight into mechanism of the reduced coronary reserve in LVH.

• Biomedical Science Letters
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• v.25 no.3
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• pp.237-246
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• 2019

Left ventricular hypertrophy (LVH) refers to the expansion and the enlarged myocardium due to the increased resistance to ejection from the left ventricle to the aorta and/or the periphery, or the long-term burden imposed by the blood increase. Hypertension is a major risk factor that accounts for more than 50% of the causes of cardiovascular disease. If hypertension endure in the long term, the myocardium responds to abnormal heartbeat in the heart. Therefore, the prevalence of left ventricular hypertrophy also increases. As a result of genome-wide association study (GWAS) analysis for European people, PDGFC, MARK3, and BCL2 were related to blood pressures. In this study, the genetic polymorphisms of PDGFC, MARK3, and BCL2 were extracted and selected based on Korean genomic and epidemiologic data, and then logistic regression analysis was performed on LVH. As a result, one SNP (rs9307953) in PDGFC gene, four SNPs (rs6575983, rs17679475, rs2273703 and rs10141388) in MARK3 gene and two SNPs (rs17756073 and rs17070739) in BCL2 gene were statistically significant. The rs6575983 of the MARK3 gene showed the highest significance level ($P=7.2{\times}10^{-3}$) among the SNPs and the relative risk of 1.08 (95% confidence interval: 1.06 to 1.45). These results suggest that the polymorphisms of PDGFC, MARK3, and BCL2 not only affect European blood pressures but also correlate with LVH in Korean. These results suggest that increased understanding of the genetic correlations of the pathogenesis of LVH.

• Childhood Kidney Diseases
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• v.15 no.1
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• pp.14-21
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• 2011

Although left Left ventricular hypertrophy (LVH) is not only an adaptive response of the heart to increased cardiac workload in hypertension, it surelybut also is the most potent risk factor of overt cardiovascular complications such as coronary heart disease, heart failure, arrhythmia and stroke in the hypertensive population. Also it has become generally accepted that subclinical cardiovascular disease begins in childhood and LVH is the most readily assessed marker for that. As LVH can be seen in children and adolescents with even mild blood pressure elevation with the reported prevalence of 10 to 47%, aggressive antihypertensive treatment is critical in preventing the development of hypertensive heart disease in that those cases.

• BMB Reports
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• v.37 no.2
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• pp.234-238
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• 2004

This study was designed to investigate, in the Turkish population, the association of methylene tetrahydrofolate reductase (MTHFR) C677T polymorphism and left ventricular hypertrophy (LVH) in patients with type II diabetes mellitus. Our study included 249 patients with type II diabetes mellitus (102 men, 147 women) and 214 healthy volunteers as controls (91 men, 123 women). MTHFR C677T genotypes were determined by polymerase chain reaction, restriction fragment length polymorphism techniques. No differences were observed in the distribution of MTHFR genotypes or allele frequencies in the cases versus the controls. The frequency of the MTHFR-mutated allele (T) was 31.7% in the type II diabetes mellitus versus 31.1% of the controls. The homozygous mutation (T/T) in the MTHFR gene was identified in 12% of the type II diabetes mellitus versus 9.3% of the controls. Patients with the TT genotype showed a higher prevalence of LVH when compared to patients with the CC and CT genotypes (p = 0.01). The MTHFR gene C677T mutation may be a possible risk factor for the development of LVH in the type II diabetic patients.

• The Journal of the Korean life insurance medical association
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• v.19
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• pp.105-107
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• 2000

• Journal of Chest Surgery
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• v.12 no.4
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• pp.350-354
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• 1979

The incidence of congenital aortic valvular stenosis has been known rare, and approximately 3-6% of congenital heart diseases. Recently, we experienced 1 case of congenital aortic valvular stenosis, and which was corrected surgically under extracorporeal circulation successfully. A 11 years old male pt. was admitted to N.M.C. because of dyspnea, dizziness, chest pain and episode of syncope. An auscultation, harsh systolic murmur [Gr. IV/VI] was noted at aortic area and also palpable strong thrill. ECG showed LVH c strain pattern and suspicious LVH finding in simple chest P-A film. In Lt. cardiac catheterization, abrupt pressure change [110mmHg] between LV & Aorta was noted across the aortic valve. And aortic insufficiency was absent, well visualized both coronary arteries and suspicious bicuspid aortic valve in aortography. Valve form was bicuspid, large one was noncoronary cusp and another cusp was Rt. & Lt. coronary cusp which was interpositioned rudimentary commissure. Central aortic orifice was about 5ram in diameter. Valvulotomy was done along the fusioned commissure between noncoronary cusp and Rt. & Lt.coronary cusp, and then short incision was added between Rt. coronary cusp & Lt. coronary cusp. Immediate postoperative course smooth but unknown cardiac arrest was noted in POD second day. Complete recovery was done without sequelae by resuscitation. After operation, clinical symptoms were subsided but systolic murmur [Gr. II/VI] was audible at aortic area, diastolic murmur was absent. ECG showed still remained LVH but much decreased R wave voltage in Lt. precordial leads. Simple chest P-A showed no interval changes compared to preop film. Control Lt. heart catheterization revealed still remained pressure gradient [40ramrig] between LV & Aorta. But much decreased pressure gradient compared to preop pressure gradient [110mmHg].

• Journal of Chest Surgery
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• v.17 no.1
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• pp.32-40
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• 1984

During the past six years from July 1977 to June 1983, fifteen adult patients of patent ductus arteriosus were surgically treated. The results were as follows: 1. Of the 15 patients, their age range was 17 to 34 years with a mean of 24 years, and sexual predominance was women [9. cf. 6 men]. 2. The most common symptom showed exertional dyspnea, and 10 patients were classed in NYHA class II, the rest were all class III. 3. On physical examination, all patients were auscultated continuous murmur, but concomitantly diastolic murmur was noted apical region in 2 patients. 4. On roentgenogram of chest, normal finding was 3 patients, and the other patients were revealed the evidence of pulmonary congestion. 5. The electrocardiogram was normal in 6 patients, but LVH was seen in 5, and 2 patients were LVH+ LAH. 6. Cardiac catheterization was performed in 12, and mean value of SO2[LPA-RV] was 6.3%, Q/Q 2.09, peak systolic pulmonary arterial pressure 45.3 mmHg, and Rp/Rs 0.365. 7. All operations were carried out by posterolateral thoracotomy. In 6 patients, division and suture of ductus were possible, the other patients were treated by division and ligation with heavy silk or Dacron patch. 8. Postoperative complications were hoarseness, persistent murmur, reoperation for bleeding, and atelectasis. Early and late mortality was 20% [3 patients], and cause of death was mainly aneurysmal rupture of previous operative site.

• Korean Journal of Radiology
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• v.23 no.6
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• pp.581-597
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• 2022

Left ventricular (LV) wall thickening, or LV hypertrophy (LVH), is common and occurs in diverse conditions including hypertrophic cardiomyopathy (HCM), hypertensive heart disease, aortic valve stenosis, lysosomal storage disorders, cardiac amyloidosis, mitochondrial cardiomyopathy, sarcoidosis and athlete's heart. Cardiac magnetic resonance (CMR) imaging provides various tissue contrasts and characteristics that reflect histological changes in the myocardium, such as cellular hypertrophy, cardiomyocyte disarray, interstitial fibrosis, extracellular accumulation of insoluble proteins, intracellular accumulation of fat, and intracellular vacuolar changes. Therefore, CMR imaging may be beneficial in establishing a differential diagnosis of LVH. Although various diseases share LV wall thickening as a common feature, the histologic changes that underscore each disease are distinct. This review focuses on CMR multiparametric myocardial analysis, which may provide clues for the differentiation of thickened myocardium based on the histologic features of HCM and its phenocopies.

• Journal of Chest Surgery
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• v.50 no.3
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• pp.144-152
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• 2017

Background: The ubiquitin-proteasome system (UPS) is an important pathway of proteolysis in pathologic hypertrophic cardiomyocytes. We hypothesize that MG132, a proteasome inhibitor, might prevent hypertrophic cardiomyopathy (CMP) by blocking the UPS. Nuclear factor kappa-light-chain-enhancer of activated B cells ($NF-{\kappa}B$) and androgen receptor (AR) have been reported to be mediators of CMP and heart failure. This study drew upon pathophysiologic studies and the analysis of $NF-{\kappa}B$ and AR to assess the cardioprotective effects of MG132 in a left ventricular hypertrophy (LVH) rat model. Methods: We constructed a transverse aortic constriction (TAC)-induced LVH rat model with 3 groups: sham (TAC-sham, n=10), control (TAC-cont, n=10), and MG132 administration (TAC-MG132, n=10). MG-132 (0.1 mg/kg) was injected for 4 weeks in the TAC-MG132 group. Pathophysiologic evaluations were performed and the expression of AR and $NF-{\kappa}B$ was measured in the left ventricle. Results: Fibrosis was prevalent in the pathologic examination of the TAC-cont model, and it was reduced in the TAC-MG132 group, although not significantly. Less expression of AR, but not $NF-{\kappa}B$, was found in the TAC-MG132 group than in the TAC-cont group (p<0.05). Conclusion: MG-132 was found to suppress AR in the TAC-CMP model by blocking the UPS, which reduced fibrosis. However, $NF-{\kappa}B$ expression levels were not related to UPS function.