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1. Fetal exposure to angiotensin II type 1 autoantibody induces hepatic insulin resistance in the adolescent offspring of rats | |||
WEI Mingming,ZHANG Suli,YANG Xiaoli,WANG Li,ZHAO Chengrui,LEI Jinghui,WANG Pengli,LIU Huirong | |||
Basic Medicine 09 February 2017 | |||
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Abstract:Fetal origin of adult disease has gained lots of attention in relation to the occurrence of insulin resistance. Studys found offspring of pregnant rats tested positive for angiotensin II type 1 receptor autoantibody (AT1-AA) exhibited both liver damage and systemic insulin resistance during adulthood. But the mechanism and time-course associated with symptom remain unclear. Normal pregnant rats were administered with preeclampsia serum-derived AT1-AA in the second trimester to establish AT1-AA positive pregnant rat models. Compared to saline group, fasting serum glucose and insulin levels, insulin resistance index values were higher, and impaired glucose tolerance, abnormal insulin tolerance, islet compensatory hypertrophy were observed in adolescent and middle-aged offspring of AT1-AA group. Triglyceride and systolic blood pressure levels were elevated in adolescence. Hepatic glycogen synthetase reduced in the third trimester, adolescence and middle age. Expression of insulin receptor subunit, insulin receptor substrate 1/2, and their phosphoprotein decreased in hepatic insulin signaling pathway of adolescent and middle-aged offspring of AT1-AA group. We found the offspring of AT1-AA positive pregnant rats exist insulin resistance in adolescence. Meanwhile, hepatic insulin receptor and downstream receptor pathway disorder may be an important mechanism of insulin resistance in AT1-AA positive pregnant rat offspring. | |||
TO cite this article:WEI Mingming,ZHANG Suli,YANG Xiaoli, et al. Fetal exposure to angiotensin II type 1 autoantibody induces hepatic insulin resistance in the adolescent offspring of rats[OL].[ 9 February 2017] http://en.paper.edu.cn/en_releasepaper/content/4718781 |
2. Angiotensin II type 2 recptor inhibits cell growth and promotes apoptosis in bladder cancer | |||
Pei Nana,Du Hongyan | |||
Basic Medicine 24 November 2016 | |||
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Abstract:Bladder cancer (BCa) is the ninth most common form of cancer in the world. There is a continuing need not only for improving the accuracy of diagnostic markers but also for the development of new treatment strategies. Recent studies have shown that the renin-angiotensin system (RAS), which include the angiotensin II type 1 (AT1R), type 2(AT2R), and Mas receptors, play an important role in tumorigenesis and may guide us in meeting those needs. In this study, we first observed that AT1R and Mas expression levels were significantly upregulated in BCa specimens while AT2R was significantly downregulated. Viral vector mediated overexpression of AT2R induced apoptosis and dramatically suppressed BCa cell proliferation in vitro, suggesting a therapeutic effect. Investigation into the mechanism revealed that the overexpression of AT2R increases the expression levels of caspase-3, caspase-8, and p38 and decreases the expression level of pErk. AT2R overexpression also leads to upregulation of 2 apoptosis-related genes (BCL2A1, TNFSF25) and downregulation of 8 apoptosis-related genes (CASP 6, CASP 9, DFFA, IGF1R, PYCARD, TNF, TNFRSF21, TNFSF10, NAIP) in transduced EJ cells as determined by PCR Array analysis. Taken together, the data suggest that AT1R, AT2R or Mas could be used as a diagnostic marker of BCa and AT2R is a promising novel target gene for BCa gene therapy. | |||
TO cite this article:Pei Nana,Du Hongyan. Angiotensin II type 2 recptor inhibits cell growth and promotes apoptosis in bladder cancer[OL].[24 November 2016] http://en.paper.edu.cn/en_releasepaper/content/4711519 |
3. The involvement of sirtuins during optic nerve injury of rats | |||
MENG Pei,WEI Jiacong,LIANG Jiajian,WANG Jingying,ZHI Ye,CUI Qi,GENG Yiqun | |||
Basic Medicine 04 January 2016 | |||
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Abstract:Sirtuins protects cells from injury while 7 members may have different roles. In this study, we applied young rat optic nerve injury model to analyze the change of Sirt1-7 at different time point to better understand the role of Sirtuins during optic nerve injury. 12 week old adult male F344 rats were used (total n=36). Rats were divided into two groups randomly. One group underwent optic nerve cut and the other group underwent peripheral nerve-optic nerve graft (PN-ON graft) on the left eye. At the time point of 1 day, 3 day, 1 week, 2 week and 4 week, the rats were sacrificed. Retinas of both eyes were removed. Total RNA was extracted and first-strand cDNA was synthesized. Sirt1-7 and housekeeping β-actin quantitative real-time PCR was performed. The quantitative real time PCR profile showed that 7 members of Sirtuins of both groups had time period after surgery. Sirtuin family mRNA transcript levels increased following optic nerve injury with and without peripheral nerve grafting. Sirt1 showed a quite different transcription pattern from the rest of the members. Our data indicated that Sirt1 and Sirts 2-7, or just Sirt2, played opposing roles in optic nerve injury. Sirts 4 and 6 were the only Sirts higher in the PN-graft group, where neuronal survival should be higher, these results suggested that Sirts 4 and 6 played the predominant role for Sirts in neuroprotection or axon regeneration. | |||
TO cite this article:MENG Pei,WEI Jiacong,LIANG Jiajian, et al. The involvement of sirtuins during optic nerve injury of rats[J]. |
4. The Influence of Autophagy in Advanced Atherosclerosis | |||
Zhu Yuning,Fan Wenjing,Zhang Chi,Guo Fang,Li Wei,Wang Yufei,Jiang Zhisheng,Qu Shunlin | |||
Basic Medicine 02 December 2015 | |||
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Abstract:Atherosclerosis (AS) is still the leading cause for cardiovascular disease global morbidity and mortality, such as it is a key cause of cardiopathy, myocardial infarction and peripheral vascular diseases. It does great harm to human health. Macrophages play a crucial role in atherosclerotic plaque stabilization and rupture. In this case, the selectivity of macrophage removal may be beneficial to the stability of the plaques. Autophagy is a catabolic recycling pathway that is triggered by various intracellular or extracellular stimuli and then during autophagy, diverse cytosolic constituents are enveloped by double-membrane vesicles, autophagosomes, which later fuse with lysosomes or the vacuole to degrade their cargo. Because autophagy has the function of maintaining cell homeostasis and promoting cell survival,and therefore imbalance in autophagy is related closely to a diverse range of pathologies including cardiovascular diseases, the leading cause of death in the world. | |||
TO cite this article:Zhu Yuning,Fan Wenjing,Zhang Chi, et al. The Influence of Autophagy in Advanced Atherosclerosis[OL].[ 2 December 2015] http://en.paper.edu.cn/en_releasepaper/content/4665970 |
5. Effect of ADH1B Arg48His polymorphism on DNA damage induced by alcohol in esophageal squamous cell lines | |||
Liang Weijun,Wei Zhang,Tian Dongping,Liu Xi,Xu Zexin,Huang Bo,Su Min | |||
Basic Medicine 16 November 2015 | |||
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Abstract:Previous studies reported that ADH1B Arg48His locus was susceptible to esophageal cancer, especially interacting with alcohol drinking, but the mechanism behind the association is not clear. The current study was to explore the effect of ADH1B Arg48His genotypes on alcohol induced DNA damage in esophageal squamous immortalized cell lines. NE2 and NE3 cell lines were performed sanger sequencing to genotype ADH1B Arg48His locus. After treatment with different concentrations of alcohol, DNA double strand breaks (γ-H2AX immunostaining) were detected by immunocytochemistry. We found that higher concentration of alcohol made more serious of DNA damage. In addition, the degree of DNA double strand breaks of NE3 with homozygote His/His genotype were significant serious than that of NE2 with heterozygote Arg/His genotype. These findings provide an important contribution to understanding the role of ADH1B polymorphisms in esophageal susceptibility and carcinogenesis.????? | |||
TO cite this article:Liang Weijun,Wei Zhang,Tian Dongping, et al. Effect of ADH1B Arg48His polymorphism on DNA damage induced by alcohol in esophageal squamous cell lines[OL].[16 November 2015] http://en.paper.edu.cn/en_releasepaper/content/4661634 |
6. Immunoglobulin A Expression Correlated with Aberrant Proliferation of Esophageal Epithelium | |||
Huang Bo,Wang Jihong,Hu Bin,Wu Xianying,Lin Wenting,Tian Dongping,Su Min,Guo Dan | |||
Basic Medicine 16 November 2015 | |||
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Abstract:Many research groups have recently shown that various cancer types can express immunoglobulin, but investigation of immunoglobulin A, the human most abundant isotype of immunoglobulin and the most prominent antibody at mucosa, expression in esophageal squamous cell carcinoma has been lacking. In this study, IgA protein expression was examined by immunohistochemistry in 197 esophageal tissues including normal, precancerous and squamous cancer, and found that IgA protein expressed in all normal and Esophageal Intraepithelial Neoplasia (EIN) and 96.30% of esophageal cancer (EC) (p > 0.05), but the strong expression (++) rate of IgA in cancer (79.01%) was significantly lower than that of normal (90.12%, p = 0.048) and EIN (95%, p = 0.012). Furthermore, the expression pattern changed from cell membrane in normal to cytoplasm in EIN and cancer. From normal, low EIN to high EIN, with increasing of proliferation, IgA expression had an increasing tendency. In EC, IgA expression positively correlated with Ki-67 immunochemically labeled proliferation (rs = 0.223,p = 0.046) but not other clinicopathological parameters. Ki67 labeling index of IgA strong expression (++) group was significantly higher than that of IgA weak expression (+) group (p = 0.011). To avoid the inference of secretory IgA protein from plasma cell, we validated IgA expression by detecting its protein and messenger RNA meanwhile in EC cell lines (EC109) used immunofluorescence and nested Real-time PCR, respectively. Our results indicated that the capability of EC in producing IgA and IgA expression correlated well with aberrant proliferation of EC.) | |||
TO cite this article:Huang Bo,Wang Jihong,Hu Bin, et al. Immunoglobulin A Expression Correlated with Aberrant Proliferation of Esophageal Epithelium[OL].[16 November 2015] http://en.paper.edu.cn/en_releasepaper/content/4661655 |
7. The effects of collagen genes col-131, col-150, dpy-5 and col-121 on fertility and development of Caenorhabditis elegans | |||
Lu Zhaolian,Fu Ximei,Zhang Yan,Liang Hongmei,Liu Xin,Chen Gen | |||
Basic Medicine 10 October 2015 | |||
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Abstract:5-Fluorouracil (5-FU) treatment in Caenorhabditis elegans(C.elegans) leads to slow developmental rate, reduces brood size, small body size, and truncates lifespan. Using Digital Gene Expression (DGE) profiling analysis, the potential pathways and genes that could be involved in declining the embryos of C. elegans have identified. Here, when C.elegans treated by 5-FU, three down-regulated genes were identified, including col-131, col-150 and dpy-5, which belong to ECM-receptor interaction pathway and Focal adhesion and one up-regulated gene col-121 which acts in Focal adhesion. Furtherly, RNAi-mediated gene knock down method was used to examine their RNAi phenotypes. The result showed that dpy-5(RNAi) worms were short-body, dumpy, and displaying a serious defect in fertility. col-121(RNAi) worms were slender, long, and slightly altered in body development. In addition, col-121(RNAi) worms displayed abnormal body morphology. Furthermore, knocking down of col-131 has subtle side effect in C.elegans fertility; however, col-131 (RNAi) worms could rescue 5-Fu toxic effect on C.elegans on fertility and lifespan defect. Taken together, the results revealed the essential role for col-150, dpy-5 and col-121 in C.elegans fertility decline. Our data also suggested that col-131 may be an essential gene in ECM-receptor interaction pathway and Focal adhesion and regulate other cuticle collagen genes including col-150, dpy-5, and col-121. | |||
TO cite this article:Lu Zhaolian,Fu Ximei,Zhang Yan, et al. The effects of collagen genes col-131, col-150, dpy-5 and col-121 on fertility and development of Caenorhabditis elegans[OL].[10 October 2015] http://en.paper.edu.cn/en_releasepaper/content/4657315 |
8. Heat shock treatment regulates the expression of NFKBIA (IκBα) in a post-transcriptional manner | |||
Mei Zhuzhong,Li Tao,Wang Ni,Chen Xinyu,Ou Xiaoli,Jiang Yong | |||
Basic Medicine 08 January 2014 | |||
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Abstract:IκBα, encoded by NFKBIA, is the prototype inhibitor of transcription factor NF-κB. Notably, the transcription of NFKBIA is directly regulated by NF-κB. In contrast, the contribution of post-transcriptional regulation in the expression of NFKBIA remains obscure. To elucidate the post-transcriptional regulation of NFKBIA, we first aligned the 3?-UTR from several different species (human, mouse, rat, dog and cow). The alignment results revealed that the 3?-UTR sequences were highly conserved among these analyzed species. Dual luciferase assay analysis showed that 3?-UTR of mouse NFKBIA downregulated the expression of associated luciferase gene. Heat shock treatment stabilized NFKBIA mRNA and promote the expression of luciferase gene associated with mouse NFKBIA 3?-UTR. Biotin-labeled RNA pulldown assay followed mass spectrometry analysis identified specific binding proteins to the 3?-UTR of mouse NFKBIA mRNA. Half of them were identified as ribosomal proteins of 40S and 60S ribosome subunits. | |||
TO cite this article:Mei Zhuzhong,Li Tao,Wang Ni, et al. Heat shock treatment regulates the expression of NFKBIA (IκBα) in a post-transcriptional manner[OL].[ 8 January 2014] http://en.paper.edu.cn/en_releasepaper/content/4581250 |
9. Association Between Genetic Variants in pre-miRNA and Colorectal Cancer Risk in a Chinese Population | |||
Lv Meili,Dong Wei,Wei Yonggang,Li Lijuan,Zhang Lushun,Shu Xiaowei,Wang Li,Gao Linbo*,Zhang Lin* | |||
Basic Medicine 28 January 2013 | |||
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Abstract:Background: Single nucleotide polymorphisms (SNPs) in pre-miRNAs may alter microRNA expression levels or processing and then contribute to the susceptibility of cancer development. We hypothesized that SNPs in pre-miRNAs may be association associated with the risk of colorectal cancer (CRC). Methods: We used genotyped four common polymorphisms (i.e., rs11614913, rs3746444, rs2910164, and rs2292832) in pre-miRNAs of 353 CRC patients and 540 healthy controls to investigate the association between the SNPs and the risk of CRC using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) genotyped four common polymorphisms(rs11614913, rs3746444, rs2292832 and rs2910164) in pre-miRNAs of 353 CRC patients and 540 healthy controls to investigate the association between them and the risk of CRC assay..Results: The rs11614913 CT, TT genotypes and T allele were associated with an increased risk of CRC compared with the CC genotype and C allele (CT vs. CC: OR=7.34, 95% CI, 3.76-14.34; TT vs. CC: OR=13.66, 95% CI, 6.76-27.6; T vs. C: OR=1.99, 95% CI, 1.63-2.42, respectively). Interestingly, using the rs2910164 GG genotype as a reference, the rs2910164 GC genotype was associated with an increased risk of CRC (OR=1.49, 95% CI, 1.02-2.18), whereas the rs2910164 CC genotype was associated with a decreased risk of CRC (OR=0.58, 95% CI, 0.37-0.93). When compared with the rs2910164G allele, rs2910164 C allele was associated with a reduced risk of CRC (OR=0.80, 95% CI, 0.66-0.97, P=0.02). significantly increased CRC risk were found to be associated with CT genotype (OR=0.136, 95% CI: 0.070-0.266) and TT genotype (OR=0.073, 95% CI: 0.036-0.148) vs. CC genotype of rs11614913, CT (OR=0.166, 95% CI: 0.037-0.735,) and TT genotype (OR=0.167, 95% CI: 0.038-0.729) vs. CC genotype of rs3746444, and GC genotype (OR=0.670, 95% CI: 0.460-0.977) vs. GG genotype of rs2910164. Unfortunately, there were no statistically significant differences between cases and controls in genotype of rs2292832. When compared with the alleles, significantly increased CRC risk were found to be associated with T allele (OR=0. 530, 95% CI: 0.413-0.613) vs. C allele in rs11614913. There were no statistically significant differences between cases and controls in alleles of rs3746444, rs2292832 and rs2910164.Conculsion: These findings suggest that rs11614913 and rs2910164 polymorphisms may be associated with the etiology of CRC. | |||
TO cite this article:Lv Meili,Dong Wei,Wei Yonggang, et al. Association Between Genetic Variants in pre-miRNA and Colorectal Cancer Risk in a Chinese Population[OL].[28 January 2013] http://en.paper.edu.cn/en_releasepaper/content/4517990 |
10. Influences of Angiotensin I-Converting Enzyme and Endothelial Nitric Oxide Synthase Gene Polymorphisms on Hepatocellular Carcinoma Risks in China | |||
YUAN Fang,ZHANG Lushun,LI Hongyu,LIAO Miao,LV Meili※,ZHANG Chongjie※ | |||
Basic Medicine 11 January 2013 | |||
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Abstract:Aims: Growing evidences suggested that angiotensin-converting enzyme (ACE) gene and endothelial nitric oxide synthase (eNOS) gene have been associated with the risk in a wide range of cancers. The objective of this study was to examine whether two DNA polymorphisms at the ACE insertion/deletion (I/D) and NOS intron 4 variable number of tandem repeats (4a/4b) have been linked with the risk of developing hepatocellular carcinoma (HCC) in a Chinese population. Methods: Polymorphisms of ACE I/D and eNOS 4a/4b were genotyped in 293 HCC patients and 384 healthy control subjects using the polymerase chain reaction (PCR). Results: Frequencies of D allele and DD genotype in ACE gene of HCC patients were significantly different from that in healthy controls. However, no differences were observed in eNOS 4a/4b genotype and allele frequencies between the HCC and controls. Conclusions: These findings indicate that the ACE I/D polymorphism may play a role in HCC progression. | |||
TO cite this article:YUAN Fang,ZHANG Lushun,LI Hongyu, et al. Influences of Angiotensin I-Converting Enzyme and Endothelial Nitric Oxide Synthase Gene Polymorphisms on Hepatocellular Carcinoma Risks in China[OL].[11 January 2013] http://en.paper.edu.cn/en_releasepaper/content/4511647 |
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