Sungkyunkwan University

About: Sungkyunkwan University is a education organization based out in Seoul, South Korea. It is known for research contribution in the topics: Graphene & Thin film. The organization has 28229 authors who have published 56428 publications receiving 1352733 citations. The organization is also known as: 성균관대학교.

2014 clinical practice guidelines for overweight and obesity in Korea.

Abstract: The dramatic increase in the prevalence of obesity and its accompanying comorbidities are major health concerns in Korea. Obesity is defined as a body mass index ≥25 kg/m2 in Korea. Current estimates are that 32.8% of adults are obese: 36.1% of men and 29.7% of women. The prevalence of being overweight and obese in national surveys is increasing steadily. Early detection and the proper management of obesity are urgently needed. Weight loss of 5% to 10% is the standard goal. In obese patients, control of cardiovascular risk factors deserves the same emphasis as weight-loss therapy. Since obesity is multifactorial, proper care of obesity requires a coordinated multidisciplinary treatment team, as a single intervention is unlikely to modify the incidence or natural history of obesity.

The mitophagy activator urolithin A is safe and induces a molecular signature of improved mitochondrial and cellular health in humans

Abstract: Urolithin A (UA) is a natural dietary, microflora-derived metabolite shown to stimulate mitophagy and improve muscle health in old animals and in preclinical models of aging1. Here, we report the results of a first-in-human clinical trial in which we administered UA, either as a single dose or as multiple doses over a 4-week period, to healthy, sedentary elderly individuals. We show that UA has a favourable safety profile (primary outcome). UA was bioavailable in plasma at all doses tested, and 4 weeks of treatment with UA at doses of 500 mg and 1,000 mg modulated plasma acylcarnitines and skeletal muscle mitochondrial gene expression in elderly individuals (secondary outcomes). These observed effects on mitochondrial biomarkers show that UA induces a molecular signature of improved mitochondrial and cellular health following regular oral consumption in humans.

Thoracic Sequelae and Complications of Tuberculosis

Abstract: Pulmonary tuberculosis is caused by Mycobacterium tuberculosis when droplet nuclei laden with bacilli are inhaled. In accordance with the virulence of the organism and the defenses of the host, tuberculosis can occur in the lungs and in extrapulmonary organs. A variety of sequelae and complications can occur in the pulmonary and extrapulmonary portions of the thorax in treated or untreated patients. These can be categorized as follows: (a) parenchymal lesions, which include tuberculoma, thin-walled cavity, cicatrization, end-stage lung destruction, aspergilloma, and bronchogenic carcinoma; (b) airway lesions, which include bronchiectasis, tracheobronchial stenosis, and broncholithiasis; (c) vascular lesions, which include pulmonary or bronchial arteritis and thrombosis, bronchial artery dilatation, and Rasmussen aneurysm; (d) mediastinal lesions, which include lymph node calcification and extranodal extension, esophagomediastinal or esophagobronchial fistula, constrictive pericarditis, and fibrosing mediastinitis; (e) pleural lesions, which include chronic empyema, fibrothorax, bronchopleural fistula, and pneumothorax; and (f) chest wall lesions, which include rib tuberculosis, tuberculous spondylitis, and malignancy associated with chronic empyema. These varieties of radiologic manifestations can mimic other disease entities. Therefore, recognition and understanding of the radiologic manifestations of the thoracic sequelae and complications of tuberculosis are important to facilitate diagnosis.

Cisplatin Induces Apoptosis in LLC-PK1 Cells via Activation of Mitochondrial Pathways

Abstract: Cisplatin, a commonly used chemotherapeutic agent, has a major limitation because of its nephrotoxicity. Recent studies have shown that cisplatin causes apoptotic cell death in renal tubule cells, but the underlying molecular mechanisms remain to be elucidated. In this study, cisplatin was found to induce apoptosis in a dose- and duration-dependent manner in cultured proximal tubule (LLC-PK1) cells, as evidenced by DNA laddering and TdT-mediated dUTP nick end-labeling assay. Pretreatment with the specific caspase 9 inhibitor LEHD-CHO completely prevented the apoptosis, whereas the caspase 8 inhibitor IETD-fmk had no effect. Furthermore, the activity of caspase 9 was upregulated about sixfold by cisplatin in a dose-dependent manner. These results implicated the caspase 9-dependent mitochondrial apoptotic pathways. Indeed, cisplatin triggered a duration-dependent translocation of cytochrome c from the mitochondria to the cytosol, by immunofluorescence and Western blots. Cisplatin treatment also resulted in the duration-dependent activation and mitochondrial translocation of the pro-apoptotic molecule Bax, by immunofluorescence. Finally, cisplatin induced a duration-dependent onset of the mitochondrial permeability transition. Our results indicate that cisplatin induces apoptosis in LLC-PK1 cells via activation of mitochondrial signaling pathways. The sequence of events may be summarized as follows: activation of Bax induces mitochondrial permeability transition, leading to release of cytochrome c, activation of caspase 9, and entry into the execution phase of apoptosis. Inhibition of this specific pathway may provide a strategy to minimize cisplatin-induced nephrotoxicity.