http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Study on Relationship between Tumor Necrosis $Factor-\alpha$ Gene Polymorphism and Obese Patients
Kang Byung-Ku,Lee Si-Hyeong,Shin Jo-Young The Society of Korean Medicine 2005 대한한의학회지 Vol.26 No.1
Objective: A number of candidate genes have been in implicated in the pathogenesis of obesity in humans. Tumor necrosis factor-alpha $(TNF-{\alpha})$ is expressed primarily in adipocytes, and elevated levels of this cytokine have been linked to obesity and insulin resistance. Recently, the A allele of a polymorphism at position 308 in the promoter region of $TNF-{\alpha}$ (G-308A) has been shown to increase transcription of the gene in adipocytes. Therefore, we designed this study to test whether obese and non-obese subjects differ in $TNF-{\alpha}$ genotype distribution, and how the genotypes affect anthropometric parameters, including degrees of body mass index (BMI). Methods : The study included 153 obese but otherwise healthy women ($BMI{\geq}kg/m^2$, range 25-54.7, age range 15-40 years) and 82 non-obese healthy women ($BMI<kg/m^2$, age range 15-40 years). Total fat mass and percent body fat were determined by dual-energy X-ray absorptiometry. Genomic DNA was extracted and used for Ncol restriction fragment length polymorphism (RFLP) based genotyping of $TNF-{\alpha}$. Results: No differences were observed for allelic and genotype frequencies between the obese ($BMI{\geq}25$) and non-obese women. Also, no association of TNF-(l polymorphism was observed with body mass index (BMI) for genotype in obese women. In addition, age, pertent body fat, BMI, and cholesterol levels did not differ by $TNF-{\alpha}$ genotype. However, waist-tohip ratio (WHR) was significantly lower in subjects with $TNF-{\alpha}$ GA or AA genotype (0.94 0.07 vs. 0.920.03, P<0.005). Conclusion: These results suggest that $TNF-{\alpha}$ promoter polymorphism at position-308 is not a significant factor for BMI, but affects the WHR in obese healthy women from Koreans.
Bone Mineral Density in Prediabetic Men
Lee, Ju Hee,Lee, Yun Hyeong,Jung, Kyoung Hye,Kim, Min Kyeong,Jang, Hye Won,Kim, Tae Kyun,Kim, Hyun Jin,Jo, Young Suk,Shong, Minho,Lee, Tae Yong,Ku, Bon Jeong Korean Diabetes Association 2010 Korean diabetes journal Vol.34 No.5
<P><B>Background</B></P><P>There are many studies regarding the effects of insulin on bone metabolism and changes in bone mineral density (BMD) in the setting of diabetes. The effect of prediabetes on BMD is not known.</P><P><B>Methods</B></P><P>A total of 802 men participated in the Korea Rural Genomic Cohort Study (in Geumsan County). According to the results of an oral glucose tolerance test, subjects were classified into normal, prediabetic, and diabetic categories. One hundred twenty-four subjects diagnosed with type 2 diabetes were excluded, leaving 678 subjects for the study inclusion. BMD was estimated with a quantitative ultrasonometer.</P><P><B>Results</B></P><P>The average BMD T scores of normal and prediabetic subjects were -1.34 ± 1.42 and -1.33 ± 1.30, respectively; there was no significant difference in the BMD T scores between these groups. The BMD T score was inversely associated with age and positively correlated with body weight, body mass index, total cholesterol, low density lipoprotein cholesterol, and HbA1c. On multiple linear regression analysis, low density lipoprotein cholesterol was the only statistically significant variable for prediabetes (β = 0.007, <I>P</I> = 0.005). On the stepwise regression analysis, age (β = -0.026, <I>P</I> < 0.001), the body mass index (β = 0.079, <I>P</I> < 0.001), and low density lipoprotein cholesterol (β = 0.004, <I>P</I> = 0.016) were significant variables for prediabetes.</P><P><B>Conclusions</B></P><P>There was no significant difference in the BMD T score between the normal and prediabetic subjects. Further studies are needed regarding the association of fracture risk and changes in BMD with the development of overt diabetes.</P>
KSR1 is coordinately regulated with Notch signaling and oxidative phosphorylation in thyroid cancer
Lee, Jandee,Seol, Mi-Youn,Jeong, Seonhyang,Kwon, Hyeong Ju,Lee, Cho Rok,Ku, Cheol Ryong,Kang, Sang-Wook,Jeong, Jong Ju,Shin, Dong Yeob,Nam, Kee-Hyun,Lee, Eun Jig,Chung, Woong Youn,Jo, Young Suk Journal of Endocrinology (Ltd. by Guarantee) 2015 Journal of molecular endocrinology Vol.54 No.2
<P>Kinase suppressor of RAS1 (KSR1) is a scaffold protein implicated in RAS-mediated RAF activation. However, the molecular function of KSR in papillary thyroid cancer (PTC) is unknown. Thus, this study aimed to characterize the role of KSR1 in patients with PTC. qRT-PCR and immunohistochemistry (IHC) revealed inter-tumor heterogeneities in the expression of KSR1 in PTC tissues. Interestingly, BRAFV600E-positive PTC showed higher <I>KSR1</I> mRNA expression than BRAFV600E-negative PTC (<I>P</I><0.001). Gene Set Enrichment Analysis (GSEA) using public repositories showed that high KSR1 expression coordinately upregulated Notch signaling (nominal <I>P</I>=0.019, false discovery rate (FDR) <I>q</I>-value=0.165); this finding was supported by GeneNetwork analysis, indicating that <I>KSR1</I> expression is positively correlated with <I>NOTCH1</I> expression (<I>ρ</I>=0.677, <I>P</I>=6.15×10<SUP>−9</SUP>). siRNA against KSR1 (siKSR1) significantly decreased ERK phosphorylation induced by BRAFV600E, resulting in reduced expression of <I>NOTCH1</I> and <I>HES1</I>, targets of Notch signaling. GSEA revealed that high KSR1 expression was also associated with downregulation of genes related to oxidative phosphorylation (OxPhos). Consistent with this, electron microscopy showed that PTCs with high KSR1 expression exhibited structural defects of the mitochondrial cristae. Furthermore, siKSR1-transfected BCPAP and 8505C cells generated fewer colonies in colony-forming assays. In addition, GSEA showed that high expression of KSR2 and connector enhancer of KSR1 (CNKSR1) also coordinately upregulated Notch signaling (KSR2: nominal <I>P</I>=0.0097, FDR <I>q</I>-value=0.154 and CNKSR1: nominal <I>P</I><0.0001, FDR <I>q</I>-value=0.00554), and high CNKSR2 was associated with downregulation of the OxPhos gene set (nominal <I>P</I><0.0001, FDR <I>q</I>-value <0.0001). In conclusion, KSR1 is coordinately regulated with Notch signaling and OxPhos in PTC, because its scaffold function might be required to sustain the proliferative signaling and metabolic remodeling associated with this type of cancer.</P>