• Journal of mucopolysaccharidosis and rare diseases
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• v.4 no.1
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• pp.21-25
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• 2018

Fabry disease is a hereditary lysosomal storage disorder caused by the reduction or absence of lysosomal enzyme alpha-galactosidase A and the accumulation of glycosphingolipids, such as globotriaosylceramide (Gb3), in various organs, including the heart. The prevention of cardiac involvement in Fabry disease can only be achieved by enzyme replacement therapy (ERT), and the method of assessing the efficacy of ERT should be confirmed. Changes in the electrocardiogram, such as the shortening of PQ interval, prolongation of QTc and repolarization abnormalities as well as left ventricular hypertrophy in voltage criteria, can be used to identify Fabry disease patients; however, the usefulness of electrocardiograms for evaluating the efficacy of ERT is limited. The assessment of left ventricular hypertrophy using echocardiography has been established to evaluate the efficacy of ERT during long-term period. A new technique involving speckled tracking method might be useful for detecting early cardiac dysfunction and identifying the effect of ERT for a relatively short period. The estimation of left ventricular hypertrophy using cardiac magnetic resonance (CMR) is also useful for assessing the efficacy of ERT. Identifying late gadolinium enhancement in CMR may affect the effectiveness of ERT, and the new technique of T1 mapping might be useful for monitoring the accumulation of Gb3 during ERT. Histopathology in cardiac biopsy specimens is another potentially useful method for identifying the accumulation of GB3; however, the use of histopathology to evaluate of the efficacy of ERT is limited because of the invasive nature of an endomyocardial biopsy.

• Journal of Biomedical Engineering Research
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• v.31 no.4
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• pp.302-309
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• 2010

The present study proposed a method of measuring uroflow and urophonography at the same time for more accurate diagnosis in case uroflow looks normal due to compensatory function hypertrophy in the expression of early obstruction. In case of early obstruction, there happens turbulent uroflow by the obstruction even if the uroflow looks normal and thus obstruction can be detected by measuring and analyzing signal caused by turbulent flow. We implemented a system that can measure both uroflow and urophonography, and evaluated its performance. In the experiment, we observed changes in uroflow and urophonography according to artificial pressure and the degree of obstruction, and confirmed that it is possible to determine the effect of compensatory function hypertrophy by analyzing urophonographyic parameter under the same uroflow. The results of our experiment show that the effect of compensatory function hypertrophy in the early-stage obstruction of lower urinary tract, which is not detectible with uroflowmetry alone, can be assessed through urophonographic analysis.

• Korean Journal of Veterinary Research
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• v.45 no.4
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• pp.537-544
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• 2005

We have examined distribution and expression of caveolin-3 (cav-3), one of three caveolin isoforms from 16-wks-old spontaneously hypertensive rats (SHR) compared with age-matched control wistar-kyoto (WKY) rats. The expression of cav-3 was increased, whereas expression of PKB/Akt and calcineurin (Cn) was not changed in cardiac tissues of SHR compared to WKY rats. Interestingly, expression of cav-3, PKB/Akt and Cn were decreased in plasma membrane fraction in SHR compared to WKY rats. In H9c2 cardiomyoblast cells treated with phenylephrine ($50{\mu}M$, 48hr) or isoproterenol ($10{\mu}M$, 48hr), the expression of cav-3 was markedly enhanced compared to nontreated cells. Upon immunofluorescence analysis, cav-3 was localized in plasma membrane of control H9c2 cells. However phenylephrine or isoproterenol treatment caused translocation of cav-3 to perinuclear region. These results suggest that cav-3 plays as positive regulators in the development of hypertrophy in cardiac tissues of SHR rats.

• The Korean Journal of Physiology and Pharmacology
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• v.19 no.3
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• pp.191-196
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• 2015

Attenuated functional exercise capacity in elderly and diseased populations is a common problem, and stems primarily from physical inactivity. Decreased function and exercise capacity can be restored by maintaining muscular strength and mass, which are key factors in an independent and healthy life. Resistance exercise has been used to prevent muscle loss and improve muscular strength and mass. However, the intensities necessary for traditional resistance training to increase muscular strength and mass may be contraindicated for some at risk populations, such as diseased populations and the elderly. Therefore, an alternative exercise modality is required. Recently, blood flow restriction (BFR) with low intensity resistance exercise (LIRE) has been used for such special populations to improve their function and exercise capacity. Although BFR+LIRE has been intensively studied for a decade, a comprehensive review detailing the effects of BFR+LIRE on both skeletal muscle and vascular function is not available. Therefore, the purpose of this review is to discuss previous studies documenting the effects of BFR+LIRE on hormonal and transcriptional factors in muscle hypertrophy and vascular function, including changes in hemodynamics, and endothelial function.

• Proceedings of the Korean Biophysical Society Conference
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• 2003.06a
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• pp.52-52
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• 2003

Junctate is a newly identified integral ER/SR membrane $Ca^{2+}$ binding protein, which is an alternative splicing form of the same gene generating aspartyl $\square$-hydroxylase and junctin. To elucidate the functional role of junctate in heart, transgenic (TG) mice overexpressing mouse cardiac junctate-1 under the control of mouse $\square$$^{~}$ myosin heavy chain promoter were generated. Overexpression of junctate in mouse heart resulted in cardiac hypertrophy, increased fibrosis, bradycardia, arrhythmias and impaired contractility. Overexpression of junctate also led to down-regulation of SERCA2, calsequestrin, calreticulin and RyR, but to up-regulation of NCX and PMCA. The SR $Ca^{2+}$ content decreased and the L-type $Ca^{2+}$ current density and the action potential durations increased in TG cardiomyocytes, which could be the cause for the bradycardia in TG heart. The present work has provided an important example of pathogenesis leading to cardiac hypertrophy and arrhythmia, which was caused by impaired $Ca^{2+}$ handling by overexpression of junctate in heart.n heart.

• Maxillofacial Plastic and Reconstructive Surgery
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• v.21 no.2
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• pp.215-219
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• 1999

This article discusses the diagnosis, anatomic consideration, and surgical management of masseter muscle hypertrophy. Surgical correction is advised for patients who have esthetic complaints. Esthetic improvement can be achieved by surgery and not by conservative treatment. Recently, the intraoral method, which leaves no scar on the face and minimizes the possibility of injury to the marginal branch of the facial nerve, has been supported by many surgeons. Patients who complained of marked swelling of unilateral or bilateral mandibular angle area and showed abnormal bony growth at the mandibular angle area and enlarged masseter muscle received mandibular angle shaving and excision of the inner layer of masseter muscle with intraoral approach. After operation, physiotherapy was done with EAST(eletrical acupuncture stimulation therapy) for encouraging the mouth opening and reducing the swelling. They showed early maximum mouth opening and reduction of swelling.

• 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.

• Korean Journal of Bronchoesophagology
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• v.6 no.1
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• pp.72-79
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• 2000

Background and Objectives : Adenotonsillar hypertrophy is the most common disorder in pediatric otolaryngology, which should be suspected as a possible cause of obstructive sleep apnea syndrome (OSAS). In the past, most of the adenotonsillectomy were performed because of recurrent infection, but now OSAS is the most common indication in many centers. Materials and Method : A review of 1,945 adenotonsillectomy performed between 1990 and 1998 is presented. We classified into two categories of indication for adenotonsillectomy and analyzed changing trends of indication for adenotonsillectomy. Results : Although recurrent infection remains the predominant indication for surgery, there has been a rise in OSAS as a significant indication from 13.67% in 1990 to 24.26% in 1998. Conclusion : An increase has occurred in the percentage of adenotonsillectomy performed for OSAS due to adenotonsillar hypertrophy. This trend promises to continue as physicians become increasingly aware of the prevalence and seriousness of adenotonsillar hypertrophy as a cause of sleep apnea.

• The Journal of Internal Korean Medicine
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• v.22 no.3
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• pp.463-469
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• 2001

Valvular heart disease is one of the main current of cardiac problems and has many problems must be solved by sequelae and complications, etc. Rheumatic Mitral Stenosis is mainly attacked by rheumatic fever and developed by process of treatment of mitral valve or formation of trace. The purpose of this study is to examine the efficacy of oriental treatment for Cerebral Infarction with Rheumatic Mitral Stenosis. At the time of visiting ER, he was shown the symptoms of dull mentality, Rt. hemiplegia, global aphasia, dysphagia, chest discomfort, insomnia, dyspnea, etc, It showed that Atrial fibrillation in EKG monitoring, Atrial fibrillation, Rheumatic Mitral Stenosis, Ejection-Fraction slope 60% in Cardiac echography, Lt. atrial hypertrophy, Rt. atrial hypertrophy, Rt. ventricular hypertrophy with pulmonary congestion in chest X-ray. From the view of oriental diagnostic criteria. We classified the patient's clinical conditions and treated accordingly. As a result of treatment, symptoms were markedly improved and he was discharged. Further elaboration of oriental diagnostic classification could possibly lead to the fundamental treatment.

• Biomedical Science Letters
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• v.24 no.4
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• pp.311-318
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• 2018

Vitamin C (ascorbic acid) supplementation has been suggested to negatively correlate with obesity in humans and other animals. Previous studies, including ours, have demonstrated that a high-fat diet (HFD) induces obesity and related diseases such as hyperlipidemia, hyperglycemia, insulin resistance, and nonalcoholic fatty liver disease. Here, we investigated the effects of vitamin C on visceral adipocyte hypertrophy and glucose intolerance in C57BL/6J mice. Mice received a low-fat diet (LFD, 10% kcal fat), HFD (45% kcal fat), or the same HFD supplemented with vitamin C (HFD-VC, 1% w/w) for 15 weeks. Visceral adiposity and glucose intolerance were examined using metabolic measurements, histology, and gene expression analyses. Mice in the HFD-VC supplementation group had reduced body weight, mesenteric fat mass, and mesenteric adipocyte size compared with HFD-fed mice. Vitamin C intake in obese mice also decreased the mRNA levels of lipogenesis-related genes (i.e., stearoyl-CoA desaturase 1 and sterol regulatory element-binding protein 1c) in mesenteric adipose tissues, inhibited hyperglycemia, and improved glucose tolerance. In addition, vitamin C attenuated the HFD-induced increase in the size of pancreatic islets. These results suggest that vitamin C suppresses HFD-induced visceral adipocyte hypertrophy and glucose intolerance in part by decreasing the visceral adipose expression of genes involved in lipogenesis.