The microRNA miR-34c inhibits vascular smooth muscle cell proliferation and neointimal hyperplasia by targeting stem cell factor.

The fine balance between proliferation and differentiation of vascular smooth muscle cells (VSMCs) is indispensable for the maintenance of healthy blood vessels, whereas an increase in proliferation participates in pathologic cardiovascular events such as atherosclerosis and restenosis. Here we report that microRNA-34c (miR-34c) targets stem cell factor (SCF) to inhibit VSMC proliferation and neointimal hyperplasia. In an animal model, miR-34c was significantly increased in the rat carotid artery after catheter injury.

Ret finger protein mediates Pax7-induced ubiquitination of MyoD in skeletal muscle atrophy.

Skeletal muscle atrophy results from the net loss of muscular proteins and organelles and is caused by pathologic conditions such as nerve injury, immobilization, cancer, and other metabolic diseases. Recently, ubiquitination-mediated degradation of skeletal-muscle-specific transcription factors was shown to be involved in muscle atrophy, although the mechanisms have yet to be defined. Here we report that ret finger protein (RFP), also known as TRIM27, works as an E3 ligase in Pax7-induced degradation of MyoD.

Changes of Epistemological Beliefs and Self-regulated Learning in Problem-based Learning.

Purpose: Epistemological beliefs (EBs) are fundamental assumptions about the nature of knowledge and learning. Self-regulation (SR) is the ability and willingness to effectively use and monitor cognitive strategies. Problem-based learning (PBL) emphasizes meaningful learning through solving ill-structured problems.

Comparison of Learning Styles between Medical College Students and Professional Graduate Medical School Students.

Purpose: The Professional Graduate Medical School (PGMS) was established in 2003 in South Korea to train doctors that had better humanities and various educational backgrounds. By comparing the learning styles between students of the Medical College (MC) and PGMS, we investigated the characteristics of these students.

Methods: The Kolb Learning Style Inventory (LSI) is used to determine learning preferences.

Changes underlying arrhythmia in the transgenic heart overexpressing Refsum disease gene-associated protein.

Previously, we identified a novel neuron-specific protein (PAHX-AP1) that binds to Refsum disease gene product (PAHX), and we developed transgenic (TG) mice that overexpress heart-targeted PAHX-AP1. These mice have atrial tachycardia and increased susceptibility to aconitine-induced arrhythmia. This study was undertaken to elucidate the possible changes in ion channels underlying the susceptibility to arrhythmia in these mice.

A novel murine long-chain acyl-CoA synthetase expressed in brain participates in neuronal cell proliferation.

Refsum disease (RfD) is an autosomal recessive neurologic disorder of the lipid metabolism. We have identified a novel murine long-chain acyl-CoA synthetase (mLACS) associated with the RfD gene using yeast two-hybrid assay. Northern blot analyses revealed that mLACS was expressed mainly in the brain and testis.

Physiological concentration of atrial natriuretic peptide induces endothelial regeneration in vitro.

Both nitric oxide (NO) and natriuretic peptides produce apoptosis of vascular smooth muscle cells. However, there is evidence that NO induces endothelial cell proliferation, which suggests that there is a difference in the response of endothelial cells to natriuretic peptides. The purpose of this study was to investigate the effect of atrial natriuretic peptide (ANP) on human endothelial cell survival.

Augmented natriuretic peptide-induced guanylyl cyclase activity and vasodilation in experimental hyperglycemic rats.

The present study was aimed to investigate whether hyperglycemia may alter the regulation of vascular natriuretic peptide receptors (NPR). The hyperglycemia was induced in rats by the treatment with streptozotocin (50 mg/kg, i.v.