http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
한지혜,Joung Kyong Hye,이정국,Kim Ok Soon,정소림,김지민,강예은,Yi Hyon-Seung,이주희,구본정,김현진 대한당뇨병학회 2024 Diabetes and Metabolism Journal Vol.48 No.1
Background: Type 2 diabetes mellitus (T2DM) induces endothelial dysfunction and inflammation, which are the main factors for atherosclerosis and cardiovascular disease. The present study aimed to compare the effects of rosuvastatin monotherapy and rosuvastatin/ezetimibe combination therapy on lipid profile, insulin sensitivity, and vascular inflammatory response in patients with T2DM.Methods: A total of 101 patients with T2DM and dyslipidemia were randomized to either rosuvastatin monotherapy (5 mg/day, <i>n</i>=47) or rosuvastatin/ezetimibe combination therapy (5 mg/10 mg/day, <i>n</i>=45) and treated for 12 weeks. Serum lipids, glucose, insulin, soluble intercellular adhesion molecule-1 (sICAM-1), and peroxiredoxin 4 (PRDX4) levels were determined before and after 12 weeks of treatment.Results: The reduction in low density lipoprotein cholesterol (LDL-C) by more than 50% from baseline after treatment was more in the combination therapy group. The serum sICAM-1 levels increased significantly in both groups, but there was no difference between the two groups. The significant changes in homeostasis model assessment of insulin resistance (HOMA-IR) and PRDX4 were confirmed only in the subgroup in which LDL-C was reduced by 50% or more in the combination therapy group. However, after adjusting for diabetes mellitus duration and hypertension, the changes in HOMA-IR and PRDX4 were not significant between the two groups.Conclusion: Although rosuvastatin/ezetimibe combination therapy had a greater LDL-C reduction effect than rosuvastatin monotherapy, it had no additional effects on insulin sensitivity and vascular inflammatory response. Further studies are needed on the effect of long-term treatment with ezetimibe on insulin sensitivity and vascular inflammatory response.
Treatment with Lobeglitazone Attenuates Hepatic Steatosis in Diet-Induced Obese Mice
Choung, Sorim,Joung, Kyong Hye,You, Bo Ram,Park, Sang Ki,Kim, Hyun Jin,Ku, Bon Jeong Hindawi 2018 PPAR research Vol.2018 No.-
<P>Nonalcoholic fatty liver disease (NAFLD) is strongly associated with insulin resistance. The peroxisome proliferator-activated receptor (PPAR) activators, thiazolidinediones, (TZDs), are insulin sensitizers used as a treatment for NAFLD. However, TZDs are a controversial treatment for NAFLD because of conflicting results regarding hepatic steatosis and fibrosis. To evaluate a possible effective drug for treatment of NAFLD, we investigated the effects of a newly developed TZD, lobeglitazone, with an emphasis on hepatic lipid metabolism. Lobeglitazone treatment for 4 weeks in high fat diet- (HFD-) induced obese mice (HL group) improved insulin resistance and glucose intolerance compared to HFD-induced obese mice (HU group). The gene levels related to hepatic gluconeogenesis also decreased after treatment by lobeglitazone. The livers of mice in the HL group showed histologically reduced lipid accumulation, with lowered total plasma cholesterol and triglyceride levels. In addition, the HL group significantly decreased the hepatic expression of genes associated with lipid synthesis, cholesterol biosynthesis, and lipid droplet development and increased the hepatic expression of genes associated with fatty acid <I>β</I>-oxidation, thus suggesting that lobeglitazone decreased hepatic steatosis and reversed hepatic lipid dysregulation. Livers with steatohepatitis contained increased levels of PPAR<I>γ</I> and phosphorylated PPAR<I>γ</I> at serine 273, leading to downregulation of expression of genes associated with insulin sensitivity. Notably, the treatment of lobeglitazone increased the protein levels of PPAR<I>α</I> and diminished levels of PPAR<I>γ</I> phosphorylated at serine 273, which were increased by a HFD, suggesting that induction of PPAR<I>α</I> and posttranslational modification of PPAR<I>γ</I> in livers by lobeglitazone might be an underlying mechanism of the improvement seen in NAFLD. Taken together, our data showed that lobeglitazone might be an effective treatment for NAFLD.</P>
과학기술분야 학술지 수집전략 개선에 관한 연구 : 1997년/20 02년 원문이용 실적을 중심으로
정현태,황혜경,Joung, Hyun-Tae,Hwang, Hye-Kyong 한국과학기술정보연구원 과학기술정보센터 2003 Journal of Information Science Theory and Practice Vol.34 No.4
본고는 KISTI 학술지 수집전략의 최적화를 위한 방편으로 학술지 원문복사 이용실적을 분석한 것이다. 정보자원개발정책에 부합하는 합리적인 학술지 수집을 목적으로 1997년과 2002년의 원문복사(DDS)실적의 비교분석을 통하여, 주제분야, 언어, 발행국, SCI 자료, 전자자료의 변화 추이가 분석되었다. 이를 통해 이용자 수요에 기초를 둔 학술지 수집정책을 구현하는 업무상의 전략적 가이드라인을 도출하였다. This paper describes the results of a usage analysis on the scientific and technical journals in order to optimize the collection development at KISTI. By comparing usage data for the journals from 1997/2002, this study identifies the short-term changes in journal use, which were shown on the subject field, language, publication country, SCI journal and electronic journal. The changing of journal use has important implications for collection development strategy in sci-tech libraries.
Song, Myoung-Chong,Yang, Hye-Joung,Jeong, Tae-Sook,Kim, Kyong-Tai,Baek, Nam-In 대한약학회 2008 Archives of Pharmacal Research Vol.31 No.5
The aerial parts of Chrysanthemum coronarium L. were extracted with MeOH, and the concentrated extract was partitioned using EtOAc, n-BuOH, and $H_2O$, successively. Repeated column chromatography of the EtOAc and n-BuOH fractions gave a new heterocycle, 5,5'-dibuthoxy-2,2'-bifuran (1) along with five known compounds: methyl trans-ferulate (2), prunasin (3), sambunigrin (4), pterolactam (5), and adenosine (6), which were identified by several spectroscopic methods including NMR and MS. This paper is the first report on the isolation of these compounds from C. coronarium L. The $IC_{50}$ values of compound 1 for human Acyl-CoA:cholesterol acyltransferase (hACAT)-1 and hACAT-2 were 0.16 mM and 0.19 mM, respectively. Compound 2 inhibited low-density lipoprotein (LDL) oxidation with an $IC_{50}$ value of $7.7\;{\mu)M$.
Mitoribosome insufficiency in β cells is associated with type 2 diabetes-like islet failure
Hong Hyun Jung,Joung Kyong Hye,Kim Yong Kyung,Choi Min Jeong,Kang Seul Gi,Kim Jung Tae,Kang Yea Eun,Chang Joon Young,Moon Joon Ho,Jun Sangmi,Ro Hyun-Joo,Lee Yujeong,Kim Hyeongseok,Park Jae-Hyung,Kang 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-
Genetic variations in mitoribosomal subunits and mitochondrial transcription factors are related to type 2 diabetes. However, the role of islet mitoribosomes in the development of type 2 diabetes has not been determined. We investigated the effects of the mitoribosomal gene on β-cell function and glucose homeostasis. Mitoribosomal gene expression was analyzed in datasets from the NCBI GEO website (GSE25724, GSE76894, and GSE76895) and the European Nucleotide Archive (ERP017126), which contain the transcriptomes of type 2 diabetic and nondiabetic organ donors. We found deregulation of most mitoribosomal genes in islets from individuals with type 2 diabetes, including partial downregulation of CRIF1. The phenotypes of haploinsufficiency in a single mitoribosomal gene were examined using β-cell-specific Crif1 (Mrpl59) heterozygous-deficient mice. Crif1beta+/− mice had normal glucose tolerance, but their islets showed a loss of first-phase glucose-stimulated insulin secretion. They also showed increased β-cell mass associated with higher expression of Reg family genes. However, Crif1beta+/− mice showed earlier islet failure in response to high-fat feeding, which was exacerbated by aging. Haploinsufficiency of a single mitoribosomal gene predisposes rodents to glucose intolerance, which resembles the early stages of type 2 diabetes in humans.
Kim, Yong Kyung,Joung, Kyong Hye,Ryu, Min Jeong,Kim, Soung Jung,Kim, Hyeongseok,Chung, Hyo Kyun,Lee, Min Hee,Lee, Seong Eun,Choi, Min Jeong,Chang, Joon Young,Hong, Hyun Jung,Kim, Koon Soon,Lee, Sang-H Springer Verlag 2015 Diabetologia Vol.58 No.4
<P>Although mitochondrial oxidative phosphorylation (OxPhos) dysfunction is believed to be responsible for beta cell dysfunction in insulin resistance and mitochondrial diabetes, the mechanisms underlying progressive beta cell failure caused by defective mitochondrial OxPhos are largely unknown.</P>
Thyroid dysfunction associated with follicular cell steatosis in obese male mice and humans.
Lee, Min Hee,Lee, Jung Uee,Joung, Kyong Hye,Kim, Yong Kyung,Ryu, Min Jeong,Lee, Seong Eun,Kim, Soung Jung,Chung, Hyo Kyun,Choi, Min Jeong,Chang, Joon Young,Lee, Sang-Hee,Kweon, Gi Ryang,Kim, Hyun Jin The Endocrine Society 2015 Endocrinology Vol.156 No.3
<P>Adult thyroid dysfunction is a common endocrine disorder associated with an increased risk of cardiovascular disease and mortality. A recent epidemiologic study revealed a link between obesity and increased prevalence of hypothyroidism. It is conceivable that excessive adiposity in obesity might lead to expansion of the interfollicular adipose (IFA) depot or steatosis in thyroid follicular cells (thyroid steatosis, TS). In this study, we investigated the morphological and functional changes in thyroid glands of obese humans and animal models, diet-induced obese (DIO), ob/ob, and db/db mice. Expanded IFA depot and TS were observed in obese patients. Furthermore, DIO mice showed increased expression of lipogenesis-regulation genes, such as sterol regulatory element binding protein 1 (SREBP-1), peroxisome proliferator-activated receptor γ (PPARγ), acetyl coenzyme A carboxylase (ACC), and fatty acid synthetase (FASN) in the thyroid gland. Steatosis and ultrastructural changes, including distension of the endoplasmic reticulum (ER) and mitochondrial distortion in thyroid follicular cells, were uniformly observed in DIO mice and genetically obese mouse models, ob/ob and db/db mice. Obese mice displayed a variable degree of primary thyroid hypofunction, which was not corrected by PPARγ agonist administration. We propose that systemically increased adiposity is associated with characteristic IFA depots and TS and may cause or influence the development of primary thyroid failure.</P>
강현정 ( Hyeon Jeong Kang ),조혜진 ( Hye Jin Cho ),김경현 ( Kyung Hyun Kim ),정미경 ( Mi Kyong Joung ),신재욱 ( Jae Uk Shin ),진수신 ( Su Sin Jin ) 대한내과학회 2017 대한내과학회지 Vol.92 No.5
위장관기질종양에서 다른 장기로의 전이가 없는 부신 단독으로의 전이는 매우 드물지만 발생이 가능하므로 부신에 종양이 있는 경우에 위장관기질종양 치료 병력이 있다면 반드시 이의 전이 가능성에 대해서 고려하여야 한다. 그리고 고위험 위장관기질종양 환자는 병변에 대한 완전 절제술 후에도 재발이 발생할 가능성이 높아서, 재발률을 낮추고 환자의 예후를 향상시키기 위해서 imatinib 보조 치료를 장기간 시행하는 것이 중요하다. 또한 imatinib 치료를 시작한 이후에 잔존 병소에 대해서는 6-12개월 사이에 수술을 시행하여서 imatinib이차 내성에 의한 병변의 재발을 방지해야 하겠다. 저자들은 위에서 발생한 위장관기질종양을 수술적 절제를 시행하고 imatinib을 이용한 보조화학요법을 유지하였음에도 불구하고, 왼쪽 부신에 원격 재발을 일으킨 사례를 국내에서 처음으로 경험하였기에 문헌고찰과 함께 보고하는 바이다. A 56-year-old male with a gastrointestinal stromal tumor (GIST) underwent surgical resection of the tumor. Nine months after surgery, imatinib therapy was initiated because of the discovery of metastatic tumors in the left adrenal gland and in a lymph node of the peritoneum. Seventeen months later, the patient achieved complete remission (CR) and imatinib therapy was continued. However, 48 months after initiation of imatinib therapy, computed tomography scans revealed a left adrenal gland metastasis and the patient underwent left adrenalectomy. Immunohistochemical staining indicated that the spindle-shaped cells of the resected tumor were positive for C-kit, thus confirming metastasis of the GIST. This is the first report from Korea of an adrenal gland metastasis from a GIST. Worldwide, only two such cases have been reported. Here, we describe the first case of a distant recurrence of a GIST in the left adrenal gland after CR had been achieved with the aid of surgical resection and imatinib therapy. (Korean J Med 2017;92:471-475)