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정현주,김예나,최영식,박요한 고신대학교 의과대학 2009 고신대학교 의과대학 학술지 Vol.24 No.1
Thyroid hemiagenesis is a rare congenital anomaly, in which one thyroid lobe fails to develop. It is reported that thyroid hemiagenesis associated with thyroid diseases such as Graves' disease, Hashimoto's thyroiditis, colloidal goiter and thyroid follicular and papillary cancer. However, Thyroid hemiagenesis associated Hashimoto's thyroiditis haven't reported in Korea. A 31-year-old female patient was clinically hypothyroid with a left-sided goiter. Hemiagenesis of right thyroid lobe indicated on 99mTc pertechnete scan and later confirmed on ultrasonography. The authors report this case with literature review.
란크릭 캅셀(플루옥세틴 20mg)에 대한 프로작 캅셀의 생물학적 동등성 시험
심상범,조요나,오한석,류재환,이경태,김남재,서성훈 경희대학교 동서의학연구소 2001 東西醫學硏究所 論文集 Vol.2000 No.-
Bioequivalence of two flouxetine capsule, ProzacR (Lilly kora Ltd.) and LanclicR (Samsung Pharm. IND. Co.), was evalated according to the guideline of KFDA. Twenty four healthy male volunteers (21-26 years old) were divided into two groups and a randomized 2×2 cross-over study was employed. After 60mg of fluoxetine was orally administered, blood was taken at 1, 2, 3, 4, 5, 6, 7, 8, 10, 12, 24, 32, 48 and 72 hours after administration and just before administration. Plasma was analyzed for fluoxetine and internal standard (clomipramine) by a sensitive and validated HPLC assay. The pharmaco kinetic parameters (AUCt, Cmax and Tmax) wre calculated and ANOVA test was used for the statistical analysis of parameters. Differences in (AUCt, Cmax and Tmax between two capsules were -0.90, 3.46 and -14.08% respectively. All powers (1-β) for AUGt, Cmax and Tmax were more than 0.9. Detectable differences (Δ) and confidence interval were all less than ±20%. All the parameters above met the criteria of KFDA for bioequivalence and indicated that LanclicR capsules are bioequivalent to ProzacR capsules.
Kim, Se-Lim,Kim, Seong Hun,Park, Young Ran,Liu, Yu-Chuan,Kim, Eun-Mi,Jeong, Hwan-Jeong,Kim, Yo Na,Seo, Seung Young,Kim, In Hee,Lee, Seung Ok,Lee, Soo Teik,Kim, Sang-Wook American Association for Cancer Research 2017 Molecular Cancer Research Vol.15 No.2
<P>Balsalazide is a colon-specific prodrug of 5-aminosalicylate that is associated with a reduced risk of colon cancer in patients with ulcerative colitis. Parthenolide, a strong NF-kappa B inhibitor, has recently been demonstrated to be a promising therapeutic agent, promoting apoptosis of cancer cells. In the current study, the antitumor effect of balsalazide combined with parthenolide in human colorectal cancer cells and colitis-associated colon cancers (CAC) was investigated. The results demonstrate that the combination of balsalazide and parthenolide markedly suppress proliferation, nuclear translocation of NF-kappa B, I kappa B-alpha phosphorylation, NF-kappa B DNA binding, and expression of NF-kappa B targets. Apoptosis via NF-kappa B signaling was confirmed by detecting expression of caspases, p53 and PARP. Moreover, treatment of a CAC murine model with parthenolide and balsalazide together resulted in significant recovery of body weight and improvement in histologic severity. Administration of parthenolide and balsalazide to CAC mice also suppressed carcinogenesis as demonstrated by uptake of 18F-fluoro-2-deoxy- D-glucose (FDG) using micro-PET/CT scans. These results demonstrate that parthenolide potentiates the efficacy of balsalazide through synergistic inhibition of NF-kappa B activation and the combination of dual agents prevents colon carcinogenesis from chronic inflammation. (C) 2016 AACR.</P>
Kim, Kook Hwan,Jeong, Yeon Taek,Oh, Hyunhee,Kim, Seong Hun,Cho, Jae Min,Kim, Yo-Na,Kim, Su Sung,Kim, Do Hoon,Hur, Kyu Yeon,Kim, Hyoung Kyu,Ko, TaeHee,Han, Jin,Kim, Hong Lim,Kim, Jin,Back, Sung Hoon,Ko Nature Publishing Group, a division of Macmillan P 2013 Nature medicine Vol.19 No.1
Despite growing interest and a recent surge in papers, the role of autophagy in glucose and lipid metabolism is unclear. We produced mice with skeletal muscle–specific deletion of Atg7 (encoding autophagy-related 7). Unexpectedly, these mice showed decreased fat mass and were protected from diet-induced obesity and insulin resistance; this phenotype was accompanied by increased fatty acid oxidation and browning of white adipose tissue (WAT) owing to induction of fibroblast growth factor 21 (Fgf21). Mitochondrial dysfunction induced by autophagy deficiency increased Fgf21 expression through induction of Atf4, a master regulator of the integrated stress response. Mitochondrial respiratory chain inhibitors also induced Fgf21 in an Atf4-dependent manner. We also observed induction of Fgf21, resistance to diet-induced obesity and amelioration of insulin resistance in mice with autophagy deficiency in the liver, another insulin target tissue. These findings suggest that autophagy deficiency and subsequent mitochondrial dysfunction promote Fgf21 expression, a hormone we consequently term a 'mitokine', and together these processes promote protection from diet-induced obesity and insulin resistance.
Mun, Se Hwan,Kim, Jie Wan,Nah, Seong Su,Ko, Na Young,Lee, Jun Ho,Kim, Ju Dong,Kim, Do Kyun,Kim, Hyuk Soon,Choi, Ji Da,Kim, Soo Hyun,Lee, Chang Keun,Park, Seung Hwa,Kim, Bo Kyung,Kim, Hyung Sik,Kim, Yo Wiley Subscription Services, Inc., A Wiley Company 2009 Vol.60 No.3
<B>Objective</B><P>Interleukin-32 (IL-32) is a recently discovered cytokine that appears to play a critical role in human rheumatoid arthritis (RA). It is highly expressed in synovium and fibroblast-like synoviocytes (FLS) from RA patients, but not in patients with osteoarthritis (OA). This study was undertaken to assess IL-32 levels in RA synovial fluid (SF) and to investigate the secretion and regulation of IL-32 in RA FLS.</P><B>Methods</B><P>FLS and SF were obtained from the joints of RA patients. The secretion and expression of IL-32 and activation of signaling molecules were examined by enzyme-linked immunosorbent assay, immunoblotting, immunoprecipitation, reverse transcriptase–polymerase chain reaction, and small interfering RNA (siRNA) transfection.</P><B>Results</B><P>IL-32 levels were high in RA SF compared with OA SF. Furthermore, RA FLS expressed and secreted IL-32 when stimulated with tumor necrosis factor α (TNFα). TNFα-induced expression of IL-32 was significantly suppressed, in a dose-dependent manner, by inhibitors of Syk, protein kinase Cδ (PKCδ), and JNK and by knockdown of these kinases and c-Jun with siRNA. We also observed that PKCδ mediated the activation of JNK and c-Jun, and experiments using specific inhibitors and siRNA demonstrated that Syk was the upstream kinase for the activation of PKCδ.</P><B>Conclusion</B><P>The present findings suggest that IL-32 may be a newly identified prognostic biomarker in RA, thereby adding valuable knowledge to the understanding of this disease. The results also demonstrate that the production of IL-32 in RA FLS is regulated by Syk/PKCδ-mediated signaling events.</P>
Kim, Don-Kyu,Gang, Gil-Tae,Ryu, Dongryeol,Koh, Minseob,Kim, Yo-Na,Kim, Su Sung,Park, Jinyoung,Kim, Yong-Hoon,Sim, Taebo,Lee, In-Kyu,Choi, Cheol Soo,Park, Seung Bum,Lee, Chul-Ho,Koo, Seung-Hoi,Choi, Hu American Diabetes Association 2013 Diabetes Vol.62 No.9
<P>Type 2 diabetes mellitus (T2DM) is a progressive metabolic disorder with diverse pathological manifestations and is often associated with abnormal regulation of hepatic glucose production. Many nuclear receptors known to control the hepatic gluconeogenic program are potential targets for the treatment of T2DM and its complications. Nevertheless, the therapeutic potential of the estrogen-related receptor γ (ERRγ) in T2DM remains unknown. In this study, we show that the nuclear receptor ERRγ is a major contributor to hyperglycemia under diabetic conditions by controlling hepatic glucose production. Hepatic ERRγ expression induced by fasting and diabetic conditions resulted in elevated levels of gluconeogenic gene expression and blood glucose in wild-type mice. Conversely, ablation of hepatic ERRγ gene expression reduced the expression of gluconeogenic genes and normalized blood glucose levels in mouse models of T2DM: <I>db</I>/<I>db</I> and diet-induced obesity (DIO) mice. In addition, a hyperinsulinemic-euglycemic clamp study and long-term studies of the antidiabetic effects of GSK5182, the ERRγ-specific inverse agonist, in <I>db</I>/<I>db</I> and DIO mice demonstrated that GSK5182 normalizes hyperglycemia mainly through inhibition of hepatic glucose production. Our findings suggest that the ability of GSK5182 to control hepatic glucose production can be used as a novel therapeutic approach for the treatment of T2DM.</P>
Kim, Eunjin,Kang, Jeongwoo,Cho, Minchul,Lee, Sojung,Seo, Eunhee,Choi, Heesook,Kim, Yumi,Kim, Junghee,Kang, Kum Yong,Kim, Kwang Pyo,Han, Jaeyong,Sheen, Yhunyhong,Yum, Young Na,Park, Sue-Nie,Yoon, Do-Yo D. A. Spandidos 2009 MOLECULAR MEDICINE REPORTS Vol.2 No.1
<P>The E6 and E7 oncoproteins of human papilloma virus (HPV) type 16 have been known to cooperatively induce the immortalization and transformation of primary keratinocytes. We established an E7 transgenic mouse model to screen HPV-related biomakers using the omics approach. The methods used to identify HPV-modulated factors were genomics analysis by microarray using the Affymetrix 430 2.0 array to screen E7-modulated genes, and proteomics analysis using nano-LC-ESI-MS/MS to screen E7-modulated proteins with the lung tissue of E7 transgenic mice. According to omics data, cyclin B1, cyclin E2, topoisomerase IIα, calnexin, activated leukocyte cell adhesion molecule CD166, actinin α1, diaphorase 1, gelsolin, platelet glycoprotein, and annexin A2 and A4 were up-regulated in the E7-Tg mice, while proteoglycan 4, sarcolipin, titin, vimentin, drep 1, troponin and cofilin-1 were down-regulated. We further confirmed the significance of differences between the expression levels of the selected factors in E7-Tg and non-Tg mice by real-time PCR. Genes related to cancer cell adhesion, cell cycle and migration, proliferation and apoptosis, as well as to the intermediate filament network and to endoplasmic reticulum proteins, were selected. Taken together, the results suggest that the E7 oncogene modulates the expression levels of cell cycle-related (cyclin B1, cyclin E2) and cell adhesion- and migration-related (actinin α1, CD166) factors, which may play important roles in cellular transformation in cancer. In addition, the solubilization of the rigid intermediate filament network by specific proteolysis mediated via up-regulating gelsolin and down-regulating cofilin-1, as well as increased levels of endoplasmic reticulum protein calnexin with chaperone functions, might also be involved in E7-lung epithelial cells.</P>
( Na Young Kim ),( Dong Ho Lee ),( Joo Sung Kim ),( Hyun Chae Jung ),( In Sung Song ),( Kyung Phil Kang ),( Jung Hoon Lee ),( Jae Il Chung ),( Hyun Cheul Choi ),( Taek Man Nam ),( Sang Hyup Lee ),( Yo 대한소화기학회 2007 SIDDS Vol.9 No.-
Background/Aims: The prevalence of gastric cancer and Helicobacter pylori (Hp) infection is high in Korea. This study was performed to evaluate the prevalence rate of atrophic gastritis (AG) and intestinal metaplasia (IM) and their risk factors in the aspect of Hp virulence factors, environmental and host factors in normal population. Methods: The subjects consisted of 389, 135 H. pylori-negative and 254 H. pylori-positive. AG and IM were scored histologically by the Sydney classification in the antrum and body, respectively. Prevalence rate and bacterial factors such as cagA, vacA m1, m2, and oipA; environmental factors such as smoking, alcohol drinking; host factors such as genetic polymorphisms for IL-IB-511, IL-IRN, TNF-A, IL-10-592, IL-10-819, IL-10-1082, IL-8-251, IL-6-572, GSTP1, and p53 codon 72 were evaluated. Risk factors were calculated by multiple logistic regression analysis. Results: The prevalence rate of AG increased from 25%, 0% in the age of 20s, 45% and 22% in the 40s and 50% and 35% in the over 70s in the antrum and body, respectively (p<0.001). In case of IM it increased from 11.1% and 6.4% in the 30s up to 43% and 43% in over 70s in the antrum and body, respectively, (p<0.001). The positive rates of AG and IM were significantly higher in the Hp-positive than in the Hp-negative subjects. Multivariate analysis showed that the risk factors for AG were Hp infection, age ≥60, cagA and vacA m1 positive. In case of IM the risk factors were Hp infection, age ≥60, smoking, spicy food, occupation (unemployed or non professional vs. professional), IL6-572 G carrier over C/C and IL10-592 C/A vs. A/A. Conclusions: The prevalence rate of AG and IM increased proportional to age. The most risk factor for AG and IM was Hp infection. Bacterial factors were important for AG but environmental and host factors were rather important in case of IM.