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Case Report : Novel LMNA Gene Mutation in a Patient With Atypical Werner`s Syndrome
Yun Jeong Doh,Hee Kyoung Kim,Eui Dal Jung,Seung Hee Choi,Jung Guk Kim,Bo Wan Kim,In Kyu Lee 대한내과학회 2009 The Korean Journal of Internal Medicine Vol.24 No.1
Hutchinson-Gilford progeria syndrome (HGPS) and Werner`s syndrome are representative types of progeroid syndrome. LMNA (Lamin A/C) gene mutation with atypical Werner`s syndrome have recently been reported. Atypical Werner`s syndrome with the severe metabolic complications, the extent of the lipodystrophy is associated with A133L mutation in the LMNA gene and these patients present with phenotypically heterogeneous disorders. We experienced a 15-yr-old Korean female with progeroid features, generalized lipodystrophy, hypertriglyceridemia, fatty liver, steatohepatitis, and type 2 diabetes mellitus. Skin fibroblasts from the patient showed marked abnormal nuclear morphology, compared with that from normal persons. Gene analysis revealed that this patient had T506del of exon 2 in the LMNA gene. We report here the first case of atypical Werner`s syndrome with frameshift mutation that was caused by T506del. (Korean J Intern Med 2009;24:68-72)
The Effect of Metformin on Liver Lipid Accumulation in Mice Fed a High-fat Diet
( Yun Hye Kim ),( Youn Ju Lee ),( Yun Yeong Jeong ),( Yong Woon Kim ),( So Young Park ),( Kyung Oh Doh ),( Jong Yeon Kim ) 한국응용생명화학회 2010 Applied Biological Chemistry (Appl Biol Chem) Vol.53 No.2
Fat accumulation in the liver involves an imbalance in the hepatic uptake of free fatty acids and their metabolism. Fat accumulation in the liver plays a critical role in the initiation of nonalcoholic steatohepatitis, which may progress to liver fibrosis and cirrhosis. The prevention of hepatic fat accumulation, therefore, may be effective therapy for nonalcoholic fatty liver disease. However, the effect of insulin sensitizing drugs on hepatic fat accumulation is still unclear. Here, we show that metformin, the most widely used insulin sensitizer, prevents liver fat accumulation induced by a high-fat diet. Male C57BL/6 mice weighing 18~20 g were grouped as follows for 8 weeks: mice chow diet, high-fat diet pair-fed control, and high-fat diet with metformin. Triglyceride and total cholesterol levels in plasma and liver were measured. AMP-activated protein kinase activity in liver were determined by Western blot. Expressions of SREBP1c and FAS in the liver were measured using RT-PCR. The high-fat diet increased body weight, abdominal fat mass, fat accumulation in the liver, and plasma total cholesterol, as well as liver triglyceride and total cholesterol levels, but plasma triglyceride levels were unchanged. Metformin decreased each of these measures. The high-fat diet decreased liver AMP-activated protein kinase activity as well as SREBP-1c and FAS expressions, and metformin reversed these changes. In conclusion, a high-fat diet induced visceral obesity and hepatic fat accumulation. Metformin prevented visceral obesity, hepatic fat accumulation, and reduced plasma total and LDL-cholesterol concentrations, potentially through modulating AMP-activated protein kinase activity and the expressions of SREBP-1C and FAS.
Doh, Chil-Hoon,Kim, Seong Il,Jeong, Ki-Young,Jin, Bong-Soo,An, Kay Hyeok,Min, Byung Chul,Moon, Seong-In,Yun, Mun-Soo Korean Chemical Society 2006 Bulletin of the Korean Chemical Society Vol.27 No.8
Si-C composites were prepared by the carbonization of polyaniline (PAn) coated on silicone powder. The physical and electrochemical properties of the Si-C composites were characterized by particle-size analysis, X-ray diffraction, scanning electron microscopy, and battery electrochemical tests. The average particle size of Si was increased by the coating of Pan but somewhat reduced by the carbonization to give silicone-carbon composites. The co-existence of crystalline silicone and amorphous-like carbon was confirmed by XRD analyses. SEM photos showed that the silicone particles were well covered with carbonaceous materials, depending on the PAn content. Si-C$\mid$Li cells were fabricated using the Si-C composites and tested using galvanostatic charge-discharge. Si-C$\mid$Li cells gave better electrochemical properties than Si|Li cells. Si-C$\mid$Li cells using Si-C from HCl-undoped precursor PAn showed better electrochemical properties than precursor PAn doped in HCl. The addition of an electrolyte containing 4-fluoroethylene carbonate (FEC) increased the initial discharge capacity. Also, another electrochemical test, the galvanostatic charge-discharge test with GISOC (gradual increasing of the state of charge) was carried out. Si-C(Si:PAn = 50:50 wt. ratio)|Li cell showed 414 mAh/g of reversible specific capacity, 75.7% of IIE (initial intercalation efficiency), 35.4 mAh/g of IICs (surface irreversible specific capacity).
Jeong, Jaewon,Kim, Soojin,Lim, Da-Sol,Kim, Seo-Hea,Doh, Heeju,Kim, So-Dam,Song, Yun Seon The Korean Society for Brain and Neural Science 2017 Experimental Neurobiology Vol.26 No.4
<P>Postconditioning has been shown to protect the mouse brain from ischemic injury. However, the neuroprotective mechanisms of postconditioning remain elusive. We have found that toll-like receptor 5 (TLR5) plays an integral role in postconditioning-induced neuroprotection through Akt/nuclear factor kappa B (NF-κB) activation in cerebral ischemia. Compared to animals that received 30 min of transient middle cerebral artery occlusion (tMCAO) group, animals that also underwent postconditioning showed a significant reduction of up to 60.51% in infarct volume. Postconditioning increased phospho-Akt (p-Akt) levels and NF-κB translocation to the nucleus as early as 1 h after tMCAO and oxygen-glucose deprivation. Furthermore, inhibition of Akt by Akt inhibitor IV decreased NF-κB promoter activity after postconditioning. Immunoprecipitation showed that interactions between TLR5, MyD88, and p-Akt were increased from postconditioning both <I>in vivo</I> and <I>in vitro</I>. Similar to postconditioning, flagellin, an agonist of TLR5, increased NF-κB nuclear translocation and Akt phosphorylation. Our results suggest that postconditioning has neuroprotective effects by activating NF-κB and Akt survival pathways via TLR5 after cerebral ischemia. Additionally, the TLR5 agonist flagellin can simulate the neuroprotective mechanism of postconditioning in cerebral ischemia.</P>
분자표지 활용 무 육종을 위한 High-throughput DNA 추출법 탐색
최정근(Jeong-Keun Choi),박수형(Suhyoung Park),윤도원(Doh-Won Yun),구자환(Ja-Hwan Ku) 한국원예학회 2006 원예과학기술지 Vol.24 No.4
배추과 작물의 자가불화합성은 잡종종자의 생산에 유용하게 이용되어왔다. 자가불화합 특성은 주두측의 S-locus glycoprotein(SLG)와 S-locus receptor kinase(SRK)에 의하여 발현이 조절되는 것으로 보고 되었다. 이에 관련된 연구가 활발하게 진행된 결과 육종 기간과 선발에 소요되는 대면적 재배를 효과적으로 감소시킬 수 있는 다양한 분자표지들이 개발되었다. 본 연구는 유용한 분자 표지를 실질적으로 육종에 활용하고자 할 때 기본적으로 필요한 DNA의 high-throughput 추출법을 밝히고자 수행하였다. 무는 조직내부에 상당량의 polysaccharide가 함유되어 있어 DNA의 추출이 다른 작물에 비하여 까다롭다. 따라서 CTAB법을 변형시킨 다양한 방법이 활용되어 왔으나 다수의 시료에서 단기간에 DNA를 추출하기에는 어려움이 있다. 본 연구에서는 시료 마쇄에 소요되는 노력을 절감하기 위하여 시료의 마쇄 상태가 최종적인 DNA의 수율에 영향을 적게 미치는 것으로 보고된 Xanthogenate 버퍼 이용법과 시중에 판매되고 있는 Dneasy 96-plant kit 및 Wizard Magnetic 96 DNA plant system, 그리고 FB plate와 Xanthogenate 버퍼를 함께 이용하는 방법 중 무의 high-throughput DNA 추출에 효과적인 방법을 찾고자 하였다. 실험 결과 위의 4가지 DNA 추출 방법 모두 목적 DNA를 증폭시킴으로 무의 PCR based selection에는 적합한 것으로 판단되었다. 시약과 팁 등 부대소모품의 가격, 추출에 필요한 노력, DNA의 품질과 PCR 증폭 효율을 비교한 결과 FB plate와 Xanthogenate버퍼를 이용한 방법이 가장 효과적이었음을 밝혔다. The self-incompatibility (SI) has been used for hybrid seed production in Brassica crops. Concerning the SI response, the S-locus glycoprotein (SLG) and the S-locus receptor kinase (SRK) genes were reported to control the SI response in the stigmatic side. Many primers have been developed using sequence of these two specific genes in Brassica crops. The first step of applying these primers into molecular analysis of SI is DNA extraction. In order to analyse thousands of sample in a short time, finding fast and efficient DNA extraction method was required. In this study, four kinds of DNA extraction methods (xanthogenate buffer, FB plate with xanthogenate buffer, Dneasy 96-plant kit, and Wizard Magnetic 96 DNA plant system) were compared for efficiency in radish. All four PCR amplification results show target bands, thus these four methods were considered good for PCR-based selection in radish. Comparing cost, labour, DNA quality and PCR amplification rate, a method using FB plate with xanthogenate buffer was proved efficient for DNA extraction in radish.
The Effect of Metformin on Liver Lipid Accumulation in Mice Fed a High-fat Diet
Kim, Yun-Hye,Lee, Youn-Ju,Jeong, Yun-Yeong,Kim, Yong-Woon,Park, So-Young,Doh, Kyung-Oh,Kim, Jong-Yeon The Korean Society for Applied Biological Chemistr 2010 Applied Biological Chemistry (Appl Biol Chem) Vol.53 No.2
Fat accumulation in the liver involves an imbalance in the hepatic uptake of free fatty acids and their metabolism. Fat accumulation in the liver plays a critical role in the initiation of nonalcoholic steatohepatitis, which may progress to liver fibrosis and cirrhosis. The prevention of hepatic fat accumulation, therefore, may be effective therapy for nonalcoholic fatty liver disease. However, the effect of insulin sensitizing drugs on hepatic fat accumulation is still unclear. Here, we show that metformin, the most widely used insulin sensitizer, prevents liver fat accumulation induced by a high-fat diet. Male C57BL/6 mice weighing 18~20 g were grouped as follows for 8 weeks: mice chow diet, high-fat diet pair-fed control, and high-fat diet with metformin. Triglyceride and total cholesterol levels in plasma and liver were measured. AMP-activated protein kinase activity in liver were determined by Western blot. Expressions of SREBP1c and FAS in the liver were measured using RT-PCR. The high-fat diet increased body weight, abdominal fat mass, fat accumulation in the liver, and plasma total cholesterol, as well as liver triglyceride and total cholesterol levels, but plasma triglyceride levels were unchanged. Metformin decreased each of these measures. The high-fat diet decreased liver AMP-activated protein kinase activity as well as SREBP-1c and FAS expressions, and metformin reversed these changes. In conclusion, a high-fat diet induced visceral obesity and hepatic fat accumulation. Metformin prevented visceral obesity, hepatic fat accumulation, and reduced plasma total and LDL-cholesterol concentrations, potentially through modulating AMP-activated protein kinase activity and the expressions of SREBP-1C and FAS.