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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. 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 |
3. 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 |
4. VEGF is involved in the increase of dermal microvessel permeability induced by tryptase | |||
Bai Qianming,Wang Xinhong,Xu Yali,Yin Lianhua,Li Xiaobo | |||
Basic Medicine 31 January 2012 | |||
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Abstract:Mast cells abundantly reside near the dermal vessels and release tryptase in the condition of cutaneous hypersensitivity and allergy, which is meanifested by rapid edema due to increased vascular permeability. However, the mechanism of mast cell tryptase promoting permeability remains to be defined. In this study, we investigated the effect of tryptase/human mast cells (HMC-1) supernatant on the permeability of human dermal microvascular endothelial cells (HDMECs) and studied whether vascular endothelial growth factor (VEGF) is involved in this effect or not. HMC-1 cells released tryptase pro-degranulating agent a23187 dose-dependently and HMC-1 cells density-dependently. Both tryptase and HMC-1 supernatant can promote permeability of HDMECs dramatically dose-dependently, which was resisted by tryptase inhibitor APC366 (a specific tryptase inhibitor) and partially reversed by a VEGF neutralizing antibody. Tryptase added to HDMECs caused a significant increase of mRNA and protein levels of VEGF, VEGF receptors (Flt-1 and Flk-1) by Real-time RT-PCR assay and Western-blot respectively. Our results suggest that mast cells tryptase can up-regulate the expression of VEGF and VEGF receptors. The VEGF neutralizing antibody can block the dermal microvessel hypermeability induced by tryptase. Thus, VEGF is involved in the increase of tryptse-induced dermal microvessel hypermeability and edema. | |||
TO cite this article:Bai Qianming,Wang Xinhong,Xu Yali, et al. VEGF is involved in the increase of dermal microvessel permeability induced by tryptase[OL].[31 January 2012] http://en.paper.edu.cn/en_releasepaper/content/4464501 |
5. A small interfering RNA targeting NF-kappaB p65 alone or combined with 5-FU inhibits the growth of esophageal squmous cell carcinoma in nude mice | |||
TIAN Fang,FAN Tianli,JIANG Yanan,ZHANG Xiaoyan,WANG Xinhua | |||
Basic Medicine 07 November 2011 | |||
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Abstract:NF-κB signaling pathway plays an important role in carcinogenesis. Although constitutive NF-κB activation has been reported in many human tumors, the effect of NF-κB signaling pathway in esophageal squamous cell carcinoma (ESCC) is still poorly understood. To explore the role of NF-κB signaling pathway in ESCC, RNA interference (RNAi) was used to knockdown NF-κB p65 protein level in the ESCC cells and in nude mice. 5-FU was used to investigated whether knockdown NF-κB p65 can potentiate 5-FU's antitumor effect. Animal results indicated that the tumor growth was inhibited in p65 siRNA and p65 siRNA + 5-FU groups compared with control group. Immunohistochemistry, RT-PCR and TUNEL assay showed that p65 siRNA downregulated the expression of p65 and enhanced the sensitivity of EC9706 cells to 5-FU treatment in vivo. Overall, our work indicated that downregulation of p65 can increase the tumor apoptosis and potentiates the effects of 5-FU by suppressing NF-κB signaling pathway. Thus, p65 is an interesting target for ESCC treatment. | |||
TO cite this article:TIAN Fang,FAN Tianli,JIANG Yanan, et al. A small interfering RNA targeting NF-kappaB p65 alone or combined with 5-FU inhibits the growth of esophageal squmous cell carcinoma in nude mice[J]. |
6. More mesenchymal stem cells are recovered from bone marrow aspirates by culturing bone marrow particles and mononuclear cells respectively | |||
Xing Wen,Liu Pengxia,Liu Meng,Yang Shaoguang,Zhao Qinjun,Li Jianping,Lu Shihong,Ren Hongying,Han Zhongchao | |||
Basic Medicine 04 January 2011 | |||
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Abstract:Bone marrow (BM) is the major source of mesenchymal stem cells (MSCs). In most experiments, MSCs were classically cultured from mononuclear cells (MNCs) isolated by density gradient centrifugation method. However, several groups have demonstrated that this method was less efficient for MSCs' recovery. Here, we investigated whether BM particles were the cause and how to isolate them. A total of 20 patients were enrolled. MNCs were cultured by standard adherence and BM particles were cultivated by primary explant culture. For BM from patients 1-10, we first isolated MNCs, then filtered out BM particles. We then compared the morphology and the fibroblastic colony number between cultures of MNCs and BM particles. For BM from patients 11-20, we processed them in opposite order. We then compared the immunophenotype and function between adherent cells expanded from MNCs and BM particles. In addition, for patients 11-20,we cultured the left BM aspirates after BM particles and MNCs were isolated respectively. Adherent cells from BM particles were MSCs. After BM particles were filtered out and cultured separately, MSCs could be recovered completely from MNCs isolated by density gradient centrifugation and no MSCs were left in the residual BM aspirates. BM particles, which have been mostly discarded by the method of density gradient centrifugation, are another important source of MSCs and they can be cultivated reliably by primary explant culture. More MSCs are recovered from a single BM sample by culturing BM particles and MNCs respectively. | |||
TO cite this article:Xing Wen,Liu Pengxia,Liu Meng, et al. More mesenchymal stem cells are recovered from bone marrow aspirates by culturing bone marrow particles and mononuclear cells respectively[J]. |
7. The mechanisms underlying that injury of skin afferents does not produce neuropathic pain: the role of BDNF | |||
Liu Xian-guo,Zhou Li-Jun | |||
Basic Medicine 18 January 2010 | |||
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Abstract:Although a large body of evidence has shown that peripheral nerve injury usually induces neuropathic pain, there are also clinical studies demonstrating that injury of the sural nerve, which almost only innervates skin, fails to do so. The underlying mechanism, however, is largely unknown. In the present work, we found that the transection of either the gastrocnemius-soleus (GS) nerve innervating skeletal muscle or tibial nerve supplying both muscle and skin, but not of the sural nerve produced a lasting mechanical allodynia and thermal hyperalgesia in adult rats. High-frequency stimulation (HFS) or injury of either the tibial nerve or the GS nerve induced late-phase long-term potentiation (L-LTP) of C-fiber-evoked field potentials in spinal dorsal horn, while HFS or injury of the sural nerve only induced early-phase LTP (E-LTP). Furthermore, HFS of the tibial nerve induced L-LTP of C-fiber responses evoked by the stimulation of the sural nerve and the heterotopic L-LTP was completely prevented by spinal application of TrkB-Fc (a BDNF scavenger). Spinal application of low dose BDNF (10pg/ml) enabled HFS of the sural nerve to produce homotopic L-LTP. Finally, we found that injury of the GS nerve but not that of the sural nerve up-regulated BDNF in DRG neurons, and that the up-regulation of BDNF occurred not only in injured neurons but also in many uninjured ones. Therefore, the sural nerve injury failing to produce neuropathic pain may be due to the nerve containing insufficient BDNF under both physiological and pathological conditions. | |||
TO cite this article:Liu Xian-guo,Zhou Li-Jun. The mechanisms underlying that injury of skin afferents does not produce neuropathic pain: the role of BDNF[OL].[18 January 2010] http://en.paper.edu.cn/en_releasepaper/content/39074 |
8. The direction of synaptic plasticity mediated by C-fibers in spinal dorsal horn is decided by Src-family kinases in microglia | |||
Liu Xian-guo,Zhong Yi | |||
Basic Medicine 15 January 2010 | |||
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Abstract:Previous studies have shown that Src-family kinases (SFKs) are selectively activated in spinal microglia following peripheral nerve injury and the activated SFKs play a key role for the development of neuropathic pain. To investigate the underlying mechanism, in the present study the effect of SFKs on long-term potentiation (LTP) at C-fiber synapses in spinal dorsal horn, which is believed as central mechanism of neuropathic pain, was investigated in adult rats. Electrophysiological data revealed that pretreatment with either microglia inhibitor (minocycline, 200 μM) or SFKs inhibitors (PP2, 100 μM and SU6656, 200 μM) reversed the effect of high frequency stimulation (HFS), that is, HFS, which induces long-term potentiation (LTP) normally, induced long-term depression (LTD) after inhibition of either microglia or SFKs. Western blotting analysis showed that the level of phosphorylated SFKs (p-SFKs) in ipsilateral spinal dorsal horn was transiently increased after LTP induced by HFS, starting at 15 min and returning to control level at 60 min after HFS. Double –labeled immunofluorescence staining demonstrated that p-SFKs were highly restricted to microglia. Furthermore, we found that the inhibitory effects of minocycline or SU6656 on spinal LTP were reversed by spinal application of rat recombinant tumor necrosis factor-α (TNF-α 0.5 ng/ml, 200 μl). HFS failed to induce LTP of C-fiber evoked field potentials in tumor necrosis factor-α receptor-1 knock out (TNFR1 -/- ) mice and in rats pretreated with TNF-α neutralization antibody (0.6 μg/ml, 200μl). The results suggested that in spinal dorsal horn activation of SFKs in microglia might control the direction of plastic changes at C-fiber synapses and TNF-α might be involved in the process. | |||
TO cite this article:Liu Xian-guo,Zhong Yi. The direction of synaptic plasticity mediated by C-fibers in spinal dorsal horn is decided by Src-family kinases in microglia[OL].[15 January 2010] http://en.paper.edu.cn/en_releasepaper/content/39023 |
9. Dynamic urinary proteomic analysis | |||
Sun Wei ,Chen Yong ,Gao Youhe | |||
Basic Medicine 24 March 2009 | |||
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Abstract:Human urinary proteome analysis is a convenient and efficient approach for understanding disease processes affecting the kidney and urogenital tract. Many potential biomarkers have been identified in previous differential analyses; however, dynamic variations of the urinary proteome have not been intensively studied, and it is difficult to conclude that potential biomarkers are genuinely associated with disease rather then simply being physiological proteome variations. In this paper, pooled and individual urine samples were used to analyze dynamic variations in the urinary proteome. Five types of pooled samples (first morning void, second morning void, excessive water-drinking void, random void, and 24 h void) collected in 1 day from six volunteers were used to analyze intra-day variations. Six pairs of first morning voids collected a week apart were used to study inter-day, inter-individual, and inter-gender variations. The intra-day, inter-day, inter-individual, and inter-gender variation analyses showed that many proteins were constantly present with relatively stable abundances, and some of these had earlier been reported as potential disease biomarkers. In terms of sensitivity, the main components of the five intra-day urinary proteomes were similar. The advantages and disadvantages of pooling samples are also discussed. | |||
TO cite this article:Sun Wei ,Chen Yong ,Gao Youhe . Dynamic urinary proteomic analysis [OL].[24 March 2009] http://en.paper.edu.cn/en_releasepaper/content/30668 |
10. Comparative Study of Serum Proteins Between Guizhou Miniature Pig And Human | |||
Younan Chen,Shengfang Qin,Jingqiu Cheng | |||
Basic Medicine 15 January 2009 | |||
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Abstract:Porcine liver synthesized proteins performing efficient physiological function in human body is an essential premise for successful liver xenotransplantation. So, we did preliminary study on porcine serum protein and compared with that of human to gain insight into the functional compatibility in xenotransplantation. Venous blood was collected from 30 Guizhou Miniature Pigs (Sus scrofa) and 30 human volunteers. Total Protein (TP) was detected by biuret and Albumin (Alb) was detected by bromocresol green. Serum proteins were electrophoresed in REP electrophoresis system and the percentage of each subtype was calculated. The concentration of porcine Alb was apparently lower than that of human (p<0.05), while the TP level was similar. Consistently, porcine Alb% was lower than that of human while the concentration of porcine Globulin (Glb) and percentage of each subtype (Alpha1, Alpha2, Beta and Gamma Globulin) are higher than that of human (p<0.05). The results suggested that there were definite differences in contents of serum proteins between human and pig, which would lead to potential functional incompatibility after porcine liver was transplanted into human body. | |||
TO cite this article:Younan Chen,Shengfang Qin,Jingqiu Cheng. Comparative Study of Serum Proteins Between Guizhou Miniature Pig And Human[OL].[15 January 2009] http://en.paper.edu.cn/en_releasepaper/content/27906 |
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