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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>
Ahnak deficiency attenuates high-fat diet-induced fatty liver in mice through FGF21 induction
Kim Yo Na,Shin Jae Hoon,Kyeong Dong Soo,Cho Soo Young,김미영,Lim Hee Jung,Jimenez Maria Raquel Rojas,Kim Il Yong,Lee Mi-Ock,Bae Yun Soo,Seong Je Kyung 생화학분자생물학회 2021 Experimental and molecular medicine Vol.53 No.-
The AHNAK nucleoprotein has been determined to exert an anti-obesity effect in adipose tissue and further inhibit adipogenic differentiation. In this study, we examined the role of AHNAK in regulating hepatic lipid metabolism to prevent diet-induced fatty liver. Ahnak KO mice have reportedly exhibited reduced fat accumulation in the liver and decreased serum triglyceride (TG) levels when provided with either a normal chow diet or a high-fat diet (HFD). Gene expression profiling was used to identify novel factors that could be modulated by genetic manipulation of the Ahnak gene. The results revealed that fibroblast growth factor 21 (FGF21) was markedly increased in the livers of Ahnak KO mice compared with WT mice fed a HFD. Ahnak knockdown in hepatocytes reportedly prevented excessive lipid accumulation induced by palmitate treatment and was associated with increased secretion of FGF21 and the expression of genes involved in fatty acid oxidation, which are primarily downstream of PPARα. These results indicate that pronounced obesity and hepatic steatosis are attenuated in HFD-fed Ahnak KO mice. This may be attributed, in part, to the induction of FGF21 and regulation of lipid metabolism, which are considered to be involved in increased fatty acid oxidation and reduced lipogenesis in the liver. These findings suggest that targeting AHNAK may have beneficial implications in preventing or treating hepatic steatosis.
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>