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1. Seroprevalence of Hepatitis E among Pregnant Women in Zhenjiang, China | |||
Rui Zhilian,Xiaochun Wang,Yang Yan,Peng Ying,Zhao Xiaoying,Wen Zhang,Fu Xingli,Zhou Chenglin,Yang Shixing,Shen Quan | |||
Basic Medicine 01 April 2017 | |||
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Abstract: Backgroud: HEV is the most common cause of acute viral hepatitis in the worldwide. Most of HEV infections are mild or subclinical, nevertheless, hepatitis E (HE) is characteristically associated with a high occurrence of symptomatic presentations of clinical syndrome in pregnant women. Objectives: So far, only few cases of HE during pregnancy have been reported, and the data of seroprevalence among pregnant women was extremely limited. The aim of this study is to assess the HEV prevalence in the pregnant women in Zhengjiang, China. Materials and Methods: A total of 225 serum samples taken from pregnant women were subjected to detection of anti-HEV. IgM positive samples were tested for HEV RNA by using reverse transcription-nested PCR method. Positive PCR products were sequenced and phylogenetically analyzed. Results: The prevalence of anti-HEV IgG and IgM in pregnant women were 21.8% (49/225) and 3.6% (8/225), respectively. Four of the eight IgM positive samples were positive to HEV RNA. Phylogenetic analyses indicated that the 4 HEV strains had distinct nucleotide sequence and were divided into two different subgenotypes in genotype 4. Conclusions: The prevalences in current study for IgG and IgM were higher than those in the other regions of China. Additional, all of the four strains belonging to genotype 4 suggested that the genotype 4 was the predominant genotype in this area. | |||
TO cite this article:Rui Zhilian,Xiaochun Wang,Yang Yan, et al. Seroprevalence of Hepatitis E among Pregnant Women in Zhenjiang, China[OL].[ 1 April 2017] http://en.paper.edu.cn/en_releasepaper/content/4723385 |
2. 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 |
3. Association Analyses of TBX5 Gene Polymorphisms with Congenital Heart Disease in Tibetan Population of China | |||
Zhaobing Su,Qiuhong Chen,Shinan Wu,Xi Wang,Hong Pan,Jianmin Xiao,Jing Wang | |||
Basic Medicine 19 January 2017 | |||
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Abstract:Objective: TBX5 gene is a member of T-box transcriptional factors that mainly expressed in cardiovascular system and play a significant role in the development of embryonic cardiovascular. The aim of this study is to investigate the association of TBX5 gene polymorphisms with the risk of congenital heart disease (CHD) in the Tibetan population in China. Methods: One hundred and twenty Chinese Tibetan patients with CHD as well as one hundred and twelve matched healthy controls were recruited for this study. And the tagging SNPs were genotyped using Illumina GoldenGate chips. Potential association was evaluated with the chi-square (Χ2) test. Results: The selected tagging SNPs were well genotyped and we found significant differences in allele frequencies and genotype distributions of rs55646156 as well as rs4533090 between CHD patients and controls. The AA genotype of rs55656156 may be am increased risk factor of CHD, while the TT genotype of rs4533090 might be the protective factor against CHD development in Chinese Tibetan population. Conclusions: We have firstly established the association between the tagging SNPs of TBX5 and CHD in the Tibetan population of China in the present study. | |||
TO cite this article:Zhaobing Su,Qiuhong Chen,Shinan Wu, et al. Association Analyses of TBX5 Gene Polymorphisms with Congenital Heart Disease in Tibetan Population of China[OL].[19 January 2017] http://en.paper.edu.cn/en_releasepaper/content/4717734 |
4. Early detection in urinary proteome for the effective early treatment of bleomycin-induced pulmonary fibrosis in a rat model | |||
WU Jianqiang,LI Xundou,GAO Youhe | |||
Basic Medicine 10 January 2017 | |||
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Abstract:Idiopathic pulmonary fibrosis (IPF) is a progressive, fatal fibrotic lung disease. With limited effective treatments available in the late stage, IPF has a very poor prognosis, with an average survival time of under 3 years. Molecular biomarkers are highly desired for IPF, especially for its early phase. Lacking homeostatic control, urine is a better biomarker source than blood for detecting small and early pathological changes.In this study, urine samples were collected from rats with bleomycin-induced pulmonary fibrosis. Samples collected during slight fibrosis were used for early diagnostic biomarker identification; 11 differentially expressed proteins were identified by labeled proteome quantitation, four of which were previously reported to be associated with fibrosis. In samples during fibrosis progression, 30 differentially expressed proteins were identified as biomarkers for disease monitoring, many of which have been reported to be associated with IPF pathogenesis. Then, prednisone treatment was administered at different phases of fibrosis. Early prednisone treatment effectively inhibited pulmonary fibrosis, whereas the same treatment later had very limited effects. Trends in the change of 5 differentially expressed proteins were reversed after prednisone treatment, indicating that these proteins could serve as biomarkers of therapeutic response.Urinary proteomics has been underutilized in respiratory diseases. This is the first application of urinary proteomics to pulmonary fibrosis. Urine proteins could enable early diagnosis and monitoring of both disease progression and treatment efficacy in IPF and probably in other pulmonary diseases. These findings may improve our understanding of the pathogenesis of pulmonary fibrosis. | |||
TO cite this article:WU Jianqiang,LI Xundou,GAO Youhe. Early detection in urinary proteome for the effective early treatment of bleomycin-induced pulmonary fibrosis in a rat model[OL].[10 January 2017] http://en.paper.edu.cn/en_releasepaper/content/4716803 |
5. Shp2 is required in EMT induced by IL-6 in breast cancer cells | |||
Sun Xuan,Zhang Jie,Wang Zhiyong,Ji Wei,Tian Ran,Zhang Fei,Niu Ruifang | |||
Basic Medicine 17 December 2016 | |||
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Abstract:Accumulative evidence demonstrates that protein tyrosine phosphatase Shp2 functions as a powerful tumor promoter in many types of cancers. Abnormal expression of Shp2 has been implicated in many human malignancies. Overexpression of Shp2 in cancer tissues is correlated with cancer metastasis, resistance to targeted therapy, and poor prognosis. The well-known function of Shp2 is its positive role in regulating cellular signaling initiated by growth factors and cytokines, including interleukin-6 (IL-6). Several recent studies have shown that Shp2 is required for epithelial-mesenchymal transition (EMT) triggered by growth factors. However, whether Shp2 is involved in IL-6-signaling-promoted breast cancer EMT and progression remains undefined. In this study, we showed that exogenous and endogenous IL-6 can enhance breast cancer invasion and migration through the promotion of EMT. IL-6 also induces activation of Erk1/2 and phosphorylation of Shp2. Knockdown of Shp2 inhibited IL-6-induced downregulation of E-cadherin, and IL-6 promoted cell migration and invasion. Moreover, by using Shp2 phosphatase mutants, phosphor-tyrosine mimicking, and deficiency mutants, we provided evidence that the phosphatase activity of Shp2 and its tyrosine phosphorylation are necessary for IL-6-induced downregulation of E-cadherin and phosphorylation of Erk1/2. Our findings uncover an important function that links Shp2 to IL-6-promoted breast cancer progression. | |||
TO cite this article:Sun Xuan,Zhang Jie,Wang Zhiyong, et al. Shp2 is required in EMT induced by IL-6 in breast cancer cells[OL].[17 December 2016] http://en.paper.edu.cn/en_releasepaper/content/4714649 |
6. 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 |
7. NMDA receptor blockade suppresses pentylenetetrazole-induced acute seizure and kindling | |||
Yong Qianye,Li Shujun,Wang Huize,Kong Lingwen,Li Siqi,Zhu Xinjian | |||
Basic Medicine 11 October 2016 | |||
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Abstract:N-methyl-D-aspartate (NMDA) receptor plays an important role in the pathophysiology of several neurological diseases, including epilepsy. The present study, therefore, using the non-competitive NMDA receptor antagonist, MK-801 to investigate the role of NMDA receptor in pentylenetetrazole (PTZ)-induced kindling and the possible cellular and molecular mechanisms involved. Our results showed that acute seizure was induced in male C57BL/6 mice with a single dose of PTZ (60mg/kg), while kindling was induced with a subconvulsive dose of PTZ (35mg/kg) for at least 9 injections. Blocking NMDA receptor by non-competitive antagonist MK-801, however, significantly suppressed PTZ-induced acute seizure and the development of kindling. These results indicate that PTZ-induced acute seizure and kindling are dependent on NMDA receptor activation. | |||
TO cite this article:Yong Qianye,Li Shujun,Wang Huize, et al. NMDA receptor blockade suppresses pentylenetetrazole-induced acute seizure and kindling[OL].[11 October 2016] http://en.paper.edu.cn/en_releasepaper/content/4705952 |
8. Mutations in Growth Differentiation Factor 1 (GDF1) are Associated with Ventricular Septal Defect in a Chinese Population | |||
Wang Jing,Bai Tingting,Yan Jinting,Wang Binbin,Liu Shiming,Chen Qiuhong,Xie Xiaodong,Wang Xi,Wu Shinan,Zhang Wei,Pan Hong | |||
Basic Medicine 18 August 2016 | |||
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Abstract:Ventricular septal defect (VSD) is the largest subtype of congenital heart defect (CHD). Previous studies have suggested that mutations of growth/differentiation factor 1 (GDF1) contribute to CHD. This study explored the role of GDF1 in the etiology of VSD. A total of 312 VSD Chinese patients and 250 healthy controls were screened for mutations in the GDF1 gene. Compared with the controls and the public database, one 25-bp deletion (truncation mutation), five point non-synonymous mutations (two located in the protein coding region), and one variant in the 5′-UTR were found in 312 VSD Chinese patients. The dual luciferase assays showed that the c.-47G>C mutation in the 5′-UTR affected the capacity of GDF1 promoter to activate transcription. In the meanwhile, the p.A266T and p.P312T mutations in the mature peptide region repressed the activation of the CAGA-Luc reporter which was the responsive reporter of TGFβ signaling pathway. Our study provides important evidence that GDF1 gene mutations might be associated with VSD. | |||
TO cite this article:Wang Jing,Bai Tingting,Yan Jinting, et al. Mutations in Growth Differentiation Factor 1 (GDF1) are Associated with Ventricular Septal Defect in a Chinese Population[OL].[18 August 2016] http://en.paper.edu.cn/en_releasepaper/content/4701172 |
9. 937nm Laser of Nd:GGG at the Absorption Peak of Vapor | |||
Wang Yufei,Liu Jingyu,Zhang Chunyu | |||
Basic Medicine 14 June 2016 | |||
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Abstract:In this paper we realized an efficient diode-pumped Nd-doped gadolinium gallium garnet (GGG) continuous-wave (CW) quasi-three-level laser operating at 937nm which is at the absorption peak of vapor. Laser actions of 0.5 at.% Nd-doped GGG crystals were also investigated. The maximum output power of 3 W was obtained at the incident pump power of 10.6 W with an optical to optical conversion efficiency of 29%. A maximum output power of 300 mW in the blue spectral range at 468 nm is achieved with 15-mm-long LBO. | |||
TO cite this article:Wang Yufei,Liu Jingyu,Zhang Chunyu. 937nm Laser of Nd:GGG at the Absorption Peak of Vapor[OL].[14 June 2016] http://en.paper.edu.cn/en_releasepaper/content/4696344 |
10. Two novel copy number variations involving the α-globin gene cluster on chromosome 16 cause thalassemia in two Chinese families | |||
HU Lingling,SHANG Xuan,YI Sheng,CAI Ren,LI Zhetao,LIU Cuixian,LIANG Yidan,CAI Decheng,ZHANG Feng,Xu Xiangmin | |||
Basic Medicine 29 May 2016 | |||
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Abstract:The human α-globin gene cluster lies close to the telomere of the short arm on chromosome 16. Copy number variations (CNVs) of this region produce excessive or insufficient α-globin chains which imbalances the β-globin chains, resulting in thalassemia. However, these CNVs usually cannot be precisely defined by traditional methods. Here, we designed a technique strategy and applied it to identify two CNVs involving the α-globin gene cluster causing thalassemia in two Chinese families. A novel 282kb duplication (αααα282) was identified in family A and a novel 235kb deletion (--235) in family B. Proband A is a coinheritance of βCD41-42 and αααα282 and showed severe β-thalassemia intermedia phenotype. Proband B is a compound heterozygote of --235/αCSα genotype and was diagnosed with hemoglobin H disease. The clinical phenotypic features of the CNVs carriers were described, together with a complete picture of molecular structure of these rearrangements. Two CNVs are novel rearrangements in α-globin clusters and the αααα282 is the first to identify the exact insert position of a duplication region from the telomere on chromosome 16. The identification and characterization of these two novel CNVs demonstrates the precision and effectiveness of our strategy in analyzing the structure of unknown CNVs. | |||
TO cite this article:HU Lingling,SHANG Xuan,YI Sheng, et al. Two novel copy number variations involving the α-globin gene cluster on chromosome 16 cause thalassemia in two Chinese families[OL].[29 May 2016] http://en.paper.edu.cn/en_releasepaper/content/4691436 |
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