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RISS 인기검색어
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- 발행기관 : Institute of Lifestyle Medicine, Yonsei University (검색결과 5 건)
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New Prophylactic and Therapeutic Strategies for Spinal Cord Injury
Park, Sookyoung,Park, Kanghui,Lee, Youngjeon,Chang, Kyu-Tae,Hong, Yonggeun Institute of Lifestyle Medicine, Yonsei University 2013 Journal of lifestyle medicine Vol.3 No.1
<P>Melatonin production by the pineal gland in the vertebrate brain has attracted much scientific attention. Pineal melatonin is regulated by photoperiodicity, whereas circadian secretion of melatonin produced in the gastrointestinal tract is regulated by food intake. Thus, the circadian rhythm of pineal melatonin depends upon whether a species is diurnal or nocturnal. Spinal cord injury (SCI) involves damage to the spinal cord caused by trauma or disease that results in compromise or loss of body function. Melatonin is the most efficient and commonly used pharmacological antioxidant treatment for SCI. Melatonin is an indolamine secreted by the pineal gland during the dark phase of the circadian cycle. Neurorehabilitation is a complex medical process that focuses on improving function and repairing damaged connections in the brain and nervous system following injury. Physical activity associated with an active lifestyle reduces the risk of obesity, cardiovascular disease, type 2 diabetes, osteoporosis, and depression and protects against neurological conditions, including Parkinson’s disease, Alzheimer’s disease, and ischemic stroke. Physical activity has been shown to increase the gene expression of several brain neurotrophins (brain-derived neurotrophic factor [BDNF], nerve growth factor, and galanin) and the production of mitochondrial uncoupling protein 2, which promotes neuronal survival, differentiation, and growth. In summary, melatonin is a neural protectant, and when combined with therapeutic exercise, the hormone prevents the progression of secondary neuronal degeneration in SCI. The present review briefly describes the pathophysiological mechanisms underlying SCI, focusing on therapeutic targets and combined melatonin and exercise therapy, which can attenuate secondary injury mechanisms with minimal side effects.</P>
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TGFβ Signaling-mediated MicroRNA Regulation in Vascular Smooth Muscle Cells.
Kim, Sunghwan,Kang, Hara Institute of lifestyle medicine 2013 Journal of lifestyle medicine Vol.3 No.2
<P>The discovery of small noncoding microRNAs (miRNAs) increases the complexity of gene expression regulatory mechanisms. The basic mechanism of miRNA biogenesis and regulatory functions of target genes have been widely elucidated. Recently, it has been recognized that regulation of each step of miRNA biogenesis is critical for generating functional miRNAs. Interestingly, cell signaling pathways, including the transforming growth factor β (TGFβ) signaling pathway, have been found to modulate miRNA biosynthesis. TGFβ signaling regulates expression of several miRNAs that are implicated in the development and homeostasis of vascular smooth muscle cells (VSMCs). This review describes recent understanding of the transcriptional and post-transcriptional regulation of miRNA expression by TGF β signaling in VSMCs.</P>
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Regulation of IGFBP-1 in Metabolic Diseases
Bae, Jae-Hoon,Song, Dae-Kyu,Im, Seung-Soon Institute of Lifestyle Medicine, Yonsei University 2013 Journal of lifestyle medicine Vol.3 No.2
<P>Insulin-like growth factor binding proteins (IGFBPs) play a key role in insulin and insulin growth factor signaling and are known to be expressed in several tissues. Studies on the transcriptional regulation of IGFBP genes in various cell types have suggested that IGFBPs control both systemic hormones and regulators. Also, the complex regulatory mechanisms involved in both transcription and translation of IGFBPs provide evidence for molecular mechanisms by which growth factor- and hormone-mediated gene expression are regulated. In particular, IGFBP-1 is known to be an important regulator of IGF activity and mainly regulates metabolism in mammals. In this review, we focus on recent progress in elucidating the transcriptional regulation of IGFBP-1 among IGFBP isoforms.</P>
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Regulation of Cholesterol Metabolism in Liver: Link to NAFLD and Impact of n-3 PUFAs
Bae, Jin-Sik,Oh, Ah-Reum,Cha, Ji-Young Institute of Lifestyle Medicine, Yonsei University 2013 Journal of lifestyle medicine Vol.3 No.1
<P>Non-alcoholic fatty liver disease (NAFLD) is one of the most common causes of chronic liver disease that affects one-third of adults in westernized countries. NAFLD represents a wide spectrum of hepatic alterations, ranging from simple triglyceride accumulation in the liver to steatohepatitis. Several pharmaceutical approaches to NAFLD management have been examined, but no particular treatment has been considered both safe and highly effective. Growing evidence reveal that supplemental fish oil, seal oil and purified n-3 fatty acids can reduce hepatic lipid content in NAFLD through extensive regulation by inhibiting lipogenesis, promoting fatty acid oxidation and suppressing inflammatory responses. Recently, the <I>fat-1</I> transgenic mice capable of converting n-6 to n-3 polyunsaturated fatty acids (PUFAs) have been used to examine the effects of endogenous n-3 PUFAs on NAFLD. The increased n-3 PUFAs in <I>fat-1</I> transgenic mice reduced diet-induced hyperlipidemia and fatty liver through induction of CYP7A1 expression and activation of cholesterol catabolism to bile acid. This article introduces the n-3 PUFAs, and addresses the evidence and mechanisms by which endogenously synthesized n-3 PUFAs or increased dietary n-3 PUFAs may ameliorate NAFLD.</P>
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Statin-induced Myopathy in Skeletal Muscle: the Role of Exercise
Institute of Lifestyle Medicine, Yonsei University 2014 Journal of lifestyle medicine Vol.4 No.2
<P>Statins are widely used drugs to lower cholesterol levels and to reduce the risk of cardiovascular disease. However, it has been reported that statins are associated with adverse side effects of skeletal myopathy. Statin treatment can impair mitochondrial function and induce apoptosis in skeletal muscle in both human and animal models. Ubiquinone plays an essential role in transferring electrons in the mitochondrial electron transfer chain for oxidative phosphorylation. However, statin treatment reduces ubiquinone levels in the cholesterol synthesis pathway, which may be associated with mitochondrial dysfunction. In addition, reactive oxygen species (ROS) production and apoptosis induced by statins may provide cellular and molecular mechanisms in skeletal myopathy. Exercise is the most effective therapy to prevent metabolic and cardiovascular diseases. However, whether exercise provides a benefit to or exacerbation of statin-induced myopathy in skeletal muscle remains poorly investigated. This review will briefly provide a comprehensive summary regarding the effects of statins on skeletal myopathy, and discuss the potential mechanisms of statin-induced myopathy and the role of exercise in statin-induced myopathy in skeletal muscle.</P>
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