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Stathmin is a Marker of Progression and Poor Prognosis in Esophageal Carcinoma
Wang, Feng,Xuan, Xiao-Yan,Yang, Xuan,Cao, Lei,Pang, Li-Na,Zhou, Ran,Fan, Qin-Xia,Wang, Liu-Xing Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.8
Stathmin, also called oncoprotein 18, is a founding member of the family of microtubule-destabilizing proteins that play a critical role in the regulation of mitosis. At the same time stathmin has been recognized as one of responsible factors in cancer cells. The aim of this study was to assess stathmin status, its correlations with clinicopathological parameters and its role as a progosnostic marker in EC patients. The protein and mRNA levels of stathmin were examined byimmunohistochemistry (IHC) and in situ hybridization in 100EC tissues and adjacent noncancerous tissues. mRNA and protein expression of stathmin in three EC cell lines(EC9706, ECa109, EC1 commonly used in research) were also analyzed using immunocytochemistry, western blot and in situ hybridization. The prognostic value of Stathmin expression within the tumor tissues were assessed by Cox regression and Kaplan-Meier analysis. We showed that stathmin expression was significantly higher in EC tissues than in adjacent noncancerous tissues. High stathmin immunostaining score in the EC was positively correlated with tumor differentiation, Tumor invasion, Lymph node metastases, and TNM stage. In addition, we demonstrated that three EC cell lines examined, were constitutively expressing a high level of stathmin. Of those, EC-1 showed the strongest mRNA and protein expression for the stathmin analyzed. Kaplan-Meier analysis showed that significantly longer 5-year survival rate was seen in EC patients with high Stathmin expression, compared to those with low expression of Stathmin expression. Furthermore, multivariate Cox proportional hazard analyses revealed that Stathmin was an independent factors affecting the overall survival probability. In conclusion, our data provide a basis for the concept that stathmin might be associated with EC development and progression. High levels of Stathmin expression in the tumor tissues may be a good prognostic marker for patients with EC.
Lei Chi,Dai-Di Fan,Xiao-Xuan Ma,Yan-E Luo,Chen-Hui Zhu 한국생물공학회 2011 Biotechnology and Bioprocess Engineering Vol.16 No.3
To increase the biomass and production of recombinant human-like collagen (RHLC), the effect of controlled fermentor pressure during fed-batch cultivation was investigated using recombinant Escherichia coli producing RHLC. This study focused primarily on the effects of the fermentor pressure on the oxygen transfer capacity. A twostep exponential feeding strategy was used to control the specific growth rate at 0.2 and 0.1/h in the fed-batch and induction phase, respectively. A kinetic model of cell growth was developed, and the specific growth rate, specific glucose uptake rate, concentration of extracellular DNA, and percentage of plasmid loss were calculated and detected. The results demonstrated that increasing the fermentor pressure was an effective way of avoiding the oxygen transfer capacity limitation, and an increase in the dissolved CO2 content did not affect the growth of the recombinant E. coli BL21strain. At the end of the fermentation process, the cell density (represented by the dry cell weight, DCW) reached 77.3 g/L, and the RHLC concentration reached 14.1 g/L. In addition,the oxygen transfer capacity (KLaC^*) decreased drastically at approximately 5 h after induction. This is probably because of the increased concentration of extracellular DNA due to cell lysis, indicating that the cells needed to be harvested.
Wei Ye,Jinhui Sun,Chunchao Li,Xuan-Yan Fan,Fan Gong,Xinqia Huang,Mingzhu Deng,Jia-Qi Chu 대한기생충학ㆍ열대의학회 2020 The Korean Journal of Parasitology Vol.58 No.4
Toxoplasma gondii is an intracellular parasite that causes severe disease when the infection occurs during pregnancy. Adenosine is a purine nucleoside involved in numerous physiological processes; however, the role of adenosine receptors in T. gondii-induced trophoblast cell function has not been investigated until now. The goal of the present study was to evaluate the intracellular signaling pathways regulated by adenosine receptors using a HTR-8/SVneo trophoblast cell model of T. gondii infection. HTR8/SVneo human extravillous trophoblast cells were infected with or without T. gondii and then evaluated for cell morphology, intracellular proliferation of the parasite, adenosine receptor expression, TNF-α production and mitogen-activated protein (MAP) kinase signaling pathways triggered by adenosine A3 receptor (A3AR). HTR8/SVneo cells infected with T. gondii exhibited an altered cytoskeletal changes, an increased infection rate and reduced viability in an infection time-dependent manner. T. gondii significantly promoted increased TNF-α production, A3AR protein levels and p38, ERK1/2 and JNK phosphorylation compared to those observed in uninfected control cells. Moreover, the inhibition of A3AR by A3AR siRNA transfection apparently suppressed the T. gondii infection-mediated upregulation of TNF-α, A3AR production and MAPK activation. In addition, T. gondii-promoted TNF-α secretion was dramatically attenuated by pretreatment with PD098059 or SP600125. These results indicate that A3AR-mediated activation of ERK1/2 and JNK positively regulates TNF-α secretion in T. gondii-infected HTR8/SVneo cells.
( Wen Qian Wei ),( Fang Qi Liu ),( Lei Liu ),( Zuo Feng Li ),( Xiao Yan Zhang ),( Fan Jiang ),( Qu Shi ),( Xiao Yan Zhou ),( Wei Qi Sheng ),( San Jun Cai ),( Xuan Li ),( Ye Xu ),( Peng Nan ) 생화학분자생물학회(구 한국생화학분자생물학회) 2011 BMB Reports Vol.44 No.5
Hereditary non-polyposis Colorectal Cancer (HNPCC) is an autosomal dominant inheritance syndrome. HNPCC is the most common hereditary variant of colorectal cancer (CRC), which accounts for 2-5% CRCs, mainly due to hMLH1 and hMSH2 mutations that impair DNA repair functions. Our study aimed to identify the patterns of hMSH2 and hMLH1 mutations in Chinese HNPCC patients. Ninety-eight unrelated families from China meeting Amsterdam or Bethesda criteria were included in our study. Germline mutations in MLH1 and MSH2 genes, located in the exons and the splice-site junctions, were screened in the 98 probands by direct sequencing. Eleven mutations were found in ten patients (11%), with six in MLH1 (54.5%) and five in MSH2 (45.5%) genes. One patient had mutations in both MLH1 and MSH2 genes. Three novel mutations in MLH1 gene (c.157_160delGAGG, c.2157dupT and c.-64G>T) were found for the first time, and one suspected hotspot in MSH2 (c.1168C>T) was revealed. [BMB reports 2011; 44(5): 317-322]