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- 저자 : ( Wen Wen Tang ) (검색결과 187 건)
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Tang, Yun-Hao,Zhu, Wen-Jiang,Wen, Tian-Fu Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.4
Background: Clinically significant portal hypertension (PHT) is considered as a contraindication for hepatectomy according to the guidelines of the European Association for Study of Liver and the American Association for Study of Liver Diseases. However, this issue remains controversial. Here we performed a metaanalysis to evaluate the impact of PHT on the results of hepatectomy for hepatocellular carcinoma (HCC). Methods: Cohort studies evaluating the impact of clinically significant PHT, defined as oesophageal varices and/or splenomegaly associated with thrombocytopenia, on the results of hepatectomy for HCC were identified using a predefined search strategy. Summary risk ratios (RRs) and 95% confidence intervals (95% CIs) for PHT and outcomes after hepatectomy for HCC were calculated. Results: Seven cohort studies which including 574 cases with PHT and 1,354 cases without PHT were considered eligible for inclusion. The meta-analysis showed that, in all patients, pooled RRs of post-operative liver failure, post-operative ascites, peri-operative blood transfusion, operative mortality, 3- and 5-year overall survival associated with PHT were 2.23 (95% CI: 1.48-3.34, P=0.0001), 1.77 (95% CI: 1.19-2.64, P=0.005), 1.23 (95% CI: 1.03-1.49, P=0.03), 2.58 (95% CI: 1.12-5.96, P=0.03), 0.82 (95% CI: 0.75-0.88, P<0.00001) and 0.76 (95% CI: 0.69-0.85, P<0.00001), respectively. In subgroup analysis, similar results were found in Child-Pugh class A patients. Conclusion: This meta-analysis suggests that presence of oesophageal varices and/or splenomegaly associated with thrombocytopenia is associated with higher rates of post-operative complications and poor long-term survival after hepatectomy for HCC.
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Tang, Chang-Quan,Tang, Rui-Ren,Tang, Chun-Hua,Zeng, Zhi-Wen Korean Chemical Society 2010 Bulletin of the Korean Chemical Society Vol.31 No.5
A novel polyaminopolycarboxylate ligand with many coordination sites, N,N,$N^1,N^1,N^2,N^2$-[( 2,4,6-tri(aminomethyl)-pyridine]hexakis(acetic acid) (TPHA), was designed and synthesized and its lanthanide complexes $Na_6Tb_2$(TPHA)$Cl_6{\cdot}14H_2O$, $Na_6Eu_2$(TPHA)$Cl_6{\cdot}8H_2O$, $Na_6Gd_2$(TPHA)$Cl_6{\cdot}11H_2O$ and $Na_6Sm_2$(TPHA)$Cl_6{\cdot}9H_2O$ were successfully prepared. The ligand and the complexes were characterized by elemental analysis, IR, mass, NMR and TG-DTA. The TG-DTA studies indicated that the complexes had a high thermal stability, whose initial decomposition temperature was over $270^{\circ}C$. The luminescence properties of the complexes in solid state were investigated and the results suggested that $Tb^{3+}$ and $Eu^{3+}$ ions could be sensitized efficiently by the ligand, especially the Tb(III) complex displayed a very strong luminescence intensity (> 10000) and only displayed characteristic metal-centered luminescence. Also, the correlative comparison between the structure of ligand and luminescence properties showed how the number of the coordination atoms of ligand can be a prominent factor in the effectiveness of ligand-to-metal energy transfer.
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CircZNF609 Aggravated Myocardial Ischemia Reperfusion Injury via Mediation of miR-214-3p/PTGS2 Axis
Wen-Qiang Tang,Feng-Rui Yang,Ke-Min Chen,Huan Yang,Yu Liu,Bo Dou 대한심장학회 2022 Korean Circulation Journal Vol.52 No.9
Background and Objectives: Circular RNAs were known to play vital role in myocardial ischemia reperfusion injury (MIRI), while the role of CircZNF609 in MIRI remains unclear. This study was aimed to investigate the function of CircZNF609 in MIRI. Methods: Hypoxia/reoxygenation (H/R) model was established to mimic MIRI in vitro. Quantitative polymerase chain reaction was performed to evaluate gene transcripts. Cellular localization of CircZNF609 and miR-214-3p were visualized by fluorescence in situ hybridization. Cell proliferation was determined by CCK-8. TUNEL assay and flow cytometry were applied to detect apoptosis. Lactate dehydrogenase was determined by commercial kit. ROS was detected by DCFH-DA probe. Direct interaction of indicated molecules was determined by RIP and dual luciferase assays. Western blot was used to quantify protein levels. In vivo model was established to further test the function of CircZNF609 in MIRI. Results: CircZNF609 was upregulated in H/R model. Inhibition of CircZNF609 alleviated H/R induced apoptosis, ROS generation, restored cell proliferation in cardiomyocytes and human umbilical vein endothelial cells. Mechanically, CircZNF609 directly sponged miR-214-3p to release PTGS2 expression. Functional rescue experiments showed that miR-214-3p/PTGS2 axis was involved in the function of circZNG609 in H/R model. Furthermore, data in mouse model revealed that knockdown of CircZNF609 significantly reduced the area of myocardial infarction and decreased myocardial cell apoptosis. Conclusions: CircZNF609 aggravated the progression of MIRI via targeting miR-214-3p/PTGS2 axis, which suggested CircZNF609 might act as a vital modulator in MIRI.
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Tang, Chen-Yi,Man, Xiao-Fei,Guo, Yue,Tang, Hao-Neng,Tang, Jun,Zhou, Ci-La,Tan, Shu-Wen,Wang, Min,Zhou, Hou-De Korean Society for Molecular and Cellular Biology 2017 Molecules and cells Vol.40 No.2
Insulin signaling is coordinated by insulin receptor substrates (IRSs). Many insulin responses, especially for blood glucose metabolism, are mediated primarily through Irs-1 and Irs-2. Irs-1 knockout mice show growth retardation and insulin signaling defects, which can be compensated by other IRSs in vivo; however, the underlying mechanism is not clear. Here, we presented an Irs-1 truncated mutated mouse ($Irs-1^{-/-}$) with growth retardation and subcutaneous adipocyte atrophy. $Irs-1^{-/-}$ mice exhibited mild insulin resistance, as demonstrated by the insulin tolerance test. Phosphatidylinositol 3-kinase (PI3K) activity and phosphorylated Protein Kinase B (PKB/AKT) expression were elevated in liver, skeletal muscle, and subcutaneous adipocytes in Irs-1 deficiency. In addition, the expression of IRS-2 and its phosphorylated version were clearly elevated in liver and skeletal muscle. With miRNA microarray analysis, we found miR-33 was down-regulated in bone marrow stromal cells (BMSCs) of $Irs-1^{-/-}$ mice, while its target gene Irs-2 was up-regulated in vitro studies. In addition, miR-33 was down-regulated in the presence of Irs-1 and which was up-regulated in fasting status. What's more, miR-33 restored its expression in re-feeding status. Meanwhile, miR-33 levels decreased and Irs-2 levels increased in liver, skeletal muscle, and subcutaneous adipocytes of $Irs-1^{-/-}$ mice. In primary cultured liver cells transfected with an miR-33 inhibitor, the expression of IRS-2, PI3K, and phosphorylated-AKT (p-AKT) increased while the opposite results were observed in the presence of an miR-33 mimic. Therefore, decreased miR-33 levels can up-regulate IRS-2 expression, which appears to compensate for the defects of the insulin signaling pathway in Irs-1 deficient mice.
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Tang, Wen-Rui,Fang, Jia-Ying,Wu, Ku-Sheng,Shi, Xiao-Jun,Luo, Jia-Yi,Lin, Kun Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.16
Background: To analyze the mortality distribution of esophageal cancer in China from 1991 to 2012, to forecast the mortality in the future five years, and to provide evidence for prevention and treatment of esophageal cancer. Materials and Methods: Mortality data for esophageal cancer in China from 1991 to 2012 were used to describe its epidemiological characteristics, such as the change of the standardized mortality rate, urban-rural differences, sex and age differences. Trend-surface analysis was used to study the geographical distribution of the mortality. Curve estimation, time series, gray modeling, and joinpoint regression were used to predict the mortality for the next five years in the future. Results: In China, the incidence rate of esophageal cancer from 2007 and the mortality rate of esophageal cancer from 2008 increased yearly, with males at $8.72/10^5$ being higher than females, and the countryside at $15.5/10^5$ being higher than in the city. The mortality rate increased from age 45. Geographical analysis showed the mortality rate increased from southern to eastern China, and from northeast to central China. Conclusions: The incidence rate and the standardized mortality rate of esophageal cancer are rising. The regional disease control for esophageal cancer should be focused on eastern, central and northern regions China, and the key targets for prevention and treatment are rural men more than 45 years old. The mortality of esophageal cancer will rise in the next five years.
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Tang, Qing-Feng,Ji, Qing,Tang, Yu,Hu, Song-Jiao,Bao, Yi-Jie,Peng, Wen,Yin, Pei-Hao Asian Pacific Journal of Cancer Prevention 2013 Asian Pacific journal of cancer prevention Vol.14 No.10
Golgi phosphoprotein 2 (GOLPH2) is a very important biomarker in a variety of diseases. Its biological function is not clear, particularly in gastric cancer. To investigate the role of GOLPH2 in human gastric cancer, and determine its effect on the Th1 lymphocyte response, its expression and that of IL-12A were measured by real-time PCR and immunohistochemistry. The relationship between GOLPH2 and IL-12A was analysed statistically. The effect of GOLPH2 on the Th1 lymphocyte response was investigated with an in vitro co-culture system. The results showed that in human gastric cancer, the expression of GOLPH2 was significantly higher and the expression of IL-12A was lower than in normal gastric mucosal tissues, and the expression levels of GOLPH2 and IL-12A were negatively correlated. In addition, obvious down-regulation of the Th1 response was observed when lymphocytes were co-cultured with gastric cancer SGC7901 cells over-expressing GOLPH2. GOLPH2 down-regulated the expression of IL-12A, and inhibited the expression of TNF-${\alpha}$ and IFN-${\gamma}$. The results indicated that GOLPH2 down-regulates the Th1 response via suppression of IL-12A in human gastric cancer, and this might provide a target for the prevention and treatment.
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LncRNA expression profile analysis of Mg2+-induced osteogenesis by RNA-seq and bioinformatics
Tang Wen,Liu Qing,Tan Wei,Sun Tianshi,Deng Youwen 한국유전학회 2021 Genes & Genomics Vol.43 No.11
Background In recent years, magnesium (Mg) has been extensively studied for manufacturing biodegradable orthopedic devices. Besides other advantages, researches have shown that magnesium-based implants can stimulate osteogenesis thus accelerating orthopedic trauma recovery, but its molecular mechanism is not fully understood. Meanwhile, long non-coding RNA (lncRNA) has been found to play vital role in regulating osteogenic diferentiation. Objective To explore the role of lncRNA in Mg2+ (magnesium ions)-induced osteogenesis. Methods The efect of Mg2+ on mBMSCs proliferation was detected by the CCK-8 assay. The optimum concentration of Mg2+ (7.5 mM) in promoting mBMSCs osteogenesis was determined by ALP staining and Alizarin red staining, western blot and RT-qPCR were performed to detect osteogenic markers expressions. The lncRNAs and mRNAs expression profles of mBMSCs were assessed by RNA-Seq and processed by bioinformatics analysis. The selected lncRNAs expression level was validated by RT-qPCR. Results The efect of Mg2+ in promoting osteogenesis was confrmed and the optimum concentration was determined as 7.5 mM. The lncRNAs and mRNAs diferentially expressed between 7.5 mM Mg2+-treated group and control group was detected and functional analysis revealed that their function were associated with osteogenesis. The ceRNA networks were constructed for H19 and Dubr that aberrantly expressed in two groups. The ceRNA networks of selected lncRNAs (H19 and Dubr) were constructed. Conclusions This study identifed H19 and Dubr as osteogenic associated lncRNAs involved in Mg2+-induced osteogenesis, and they might play their roles through lncRNA-miRNA–mRNA axis.
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