Seoul National University Hospital

About: Seoul National University Hospital is a healthcare organization based out in Seoul, South Korea. It is known for research contribution in the topics: Population & Medicine. The organization has 10684 authors who have published 20230 publications receiving 415197 citations. The organization is also known as: Seoul National University Hospital.

Recent progress in genetic and epigenetic research on type 2 diabetes

Abstract: Type 2 diabetes (T2DM) is a common complex metabolic disorder that has a strong genetic predisposition. During the past decade, progress in genetic association studies has enabled the identification of at least 75 independent genetic loci for T2DM, thus allowing a better understanding of the genetic architecture of T2DM. International collaborations and large-scale meta-analyses of genome-wide association studies have made these achievements possible. However, whether the identified common variants are causal is largely unknown. In addition, the detailed mechanism of how these genetic variants exert their effect on the pathogenesis of T2DM requires further investigation. Currently, there are ongoing large-scale sequencing studies to identify rare, functional variants for T2DM. Environmental factors also have a crucial role in the development of T2DM. These could modulate gene expression via epigenetic mechanisms, including DNA methylation, histone modification and microRNA regulation. There is evidence that epigenetic changes are important in the development of T2DM. Recent studies have identified several DNA methylation markers of T2DM from peripheral blood and pancreatic islets. In this review, we will briefly summarize the recent progress in the genetic and epigenetic research on T2DM and discuss how environmental factors, genetics and epigenetics can interact in the pathogenesis of T2DM.

Efficient Induction of Oligodendrocytes from Human Embryonic Stem Cells

Abstract: Oligodendrocytes form myelin sheaths around axons to support rapid nerve conduction in the central nervous system (CNS). Damage to myelin can cause severe CNS disorders. In this study, we attempted to devise a protocol for the induction of oligodendrocytes from human embryonic stem (ES) cells to treat demyelinated axons. Four days after embryoid body formation, human ES cells were differentiated into neural precursors through selection and expansion procedures. Neural precursors were then grown in the presence of epidermal growth factor and then platelet-derived growth factor to generate oligodendrocyte precursor cells. After withdrawal of the growth factors, the cells were treated with thyroid hormone to induce differentiation into oligodendrocytes. This method resulted in approximately 81%-91% oligodendrocyte precursor cells and approximately 81% oligodendrocytes among total cells. The ability of the oligodendrocyte precursors to myelinate axons has been verified by coculturing with rat hippocampal neurons, confirming their biological functionality.

Risk Factors Associated With Sclerotomy Leakage And Postoperative Hypotony After 23-gauge Transconjunctival Sutureless Vitrectomy

Abstract: PURPOSE To investigate the incidence and risk factors of sclertomy leakage and postoperative hypotony after 23-gauge transconjunctival sutureless vitrectomy. METHODS This was a retrospective study including 322 eyes of 292 patients who underwent 23-gauge transconjunctival sutureless vitrectomy by a single surgeon with minimum follow-up period of 1 month. The incidence and risk factors of intraoperative suture placement for leaking sclerotomies and postoperative hypotony (

Diffusion-weighted imaging abnormalities in Wernicke encephalopathy: Reversible cytotoxic edema?

Abstract: Background Wernicke encephalopathy (WE) is a metabolic disorder of the central nervous system resulting from vitamin B 1 deficiency. The exact mechanisms underlying the pathogenesis of the lesions in WE are not completely understood. Vitamin B 1 deficiency is associated with intracellular and extracellular edema by glutamate N-methyl-D-aspartate receptor–mediated excitotoxicity. Conventional magnetic resonance imaging (MRI) cannot differentiate the types of edema. Diffusion-weighted imaging (DWI) has been reported to detect early ischemic damage (cytotoxic edema) as bright areas of high signal intensity (SI) and vasogenic edema as areas of heterogeneous SI. Objectives To describe the DWI findings and to characterize the types of edema in WE using DWI. Setting Tertiary referral center. Design and Methods Two patients with WE underwent DWI and conventional MRI with gadolinium enhancement. Wernicke encephalopathy was diagnosed with salient conventional MRI findings (high SIs in the paramedian thalamus, periaqueductal gray matter, and mamillary bodies) and typical clinical history and symptoms. Apparent diffusion coefficient (ADC) values were measured in abnormal lesions by visual inspection of DWIs and T2-weighted echo planar images. Results T2-weighted and fluid-attenuated inversion recovery MRIs showed high SIs in the bilateral paramedian thalamus, mamillary bodies, and periaqueductal gray matter. The DWIs showed bright high SI in the corresponding lesions, and ADC values were decreased (patient 1: 512-545 × 10 −6 mm 2 /s; patient 2: 576-612 × 10 −6 mm 2 /s). The ADC decrease and the DWI high SI were normalized in 2 weeks with administration of thiamine hydrochloride. Conclusions Abnormalities on DWI and ADC decrease became normalized with adequate therapy. The MRI abnormalities in WE might be owing to the "reversible cytotoxic edema" caused by vitamin B 1 deficiency.