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	1. Anti -Munc-18 antibody induced epilepsy by chronic kindling way in rat
	Chen Gong,Xu Ming,Yang Ru,Gao Xiang,Jiang Chengchuan
	Basic Medicine 17 December 2009
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	Abstract:Background Resent investigations implicated that autoantibody underlie some intractable seizure, such an anit-Munc18 (syntaxin-interacting protein) antibody. However, its mechanism is poorly understood. Methods Anit-Munc-18 antibody was microinjected into CA1 area of hippocampus in Sprague-Dawley (SD) rat every other day for five times, followed up that every other week for additional five times. During experimental period, both electroencephalogram（EEG）and epileptiform activity (including spontaneous seizure) were monitored. Results In twelve rats managed with antibody, ten rats （10/12）showed epileptiform EEG and nine rats（9/12）displayed epileptiform activity. Furthermore, 50 %( 5/10) eleptiform EEG and 44% (4/9) eleptiform activity had been retaining until the end of experiment, three rats (33%, 3/9) among displayed spontaneous seizures. These staining sections, from rats managed with antibody, showed abnormal morphology and loss of neuron, increase of apoptosis cell and gliosis. Conclusions Although further study is needed to clarify the role of Munc-18 in epilepsy, our results show that anti-Munc-18 antibody could induce epilepsy by chronic kindling way, which might link to apoptosis and loss of neuron in hippocampal regions.
	TO cite this article:Chen Gong,Xu Ming,Yang Ru, et al. Anti -Munc-18 antibody induced epilepsy by chronic kindling way in rat[OL].[17 December 2009] http://en.paper.edu.cn/en_releasepaper/content/37700


	2. Comparative quantification of microRNA in placenta and circulating nucleic acid isolated from maternal plasma and umbilical cord plasma
	Yang Qi ,Lu Jiafeng ,Ge Qinyu,Lu Zuhong
	Basic Medicine 18 August 2009
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	Abstract:The purpose of this study was to analyze the miRNA expression in placenta, maternal plasma and umbilical cord plasma of patients with mild and severe preeclampsia vs maternal plasma of normal pregnancies. Three families of miRNA was analyzed, which were miR-411, miR-154and miR-18a. The miRNA expression was compared between mPE and sPE in the same kind of sample, and also among the three kinds of sample. The result showed that miR-411 and miR-154 was downexpressed and miR-18a was upexpressed. It also showed that the expression of miRNA in placenta was consistent with maternal plasma, but showed more significant change in maternal plasma of sPE vs mPE. However, the expression of miRNA in umbilical cord plasma showed no markable relationship with placenta and maternal plasma.
	TO cite this article:Yang Qi ,Lu Jiafeng ,Ge Qinyu, et al. Comparative quantification of microRNA in placenta and circulating nucleic acid isolated from maternal plasma and umbilical cord plasma[OL].[18 August 2009] http://en.paper.edu.cn/en_releasepaper/content/34515

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	3. Involvement of STAT5a signaling in morphine-induced up-regulation of the cyclin D1
	Liyuan Guo,Hui Li,Han Liu,Chaoying Li,Mengsen Li,Wei Jiang,Peng He,Shanshan Wang,Michael A McNutt,Gang Li
	Basic Medicine 24 July 2009
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	Abstract:Opioids receptor and cytokine receptor has been verified to have a functional link and interaction. However, if opioid receptor in lymphocytes shares cytokine signal pathway is not well defined. The presented results from confocal microscopy and Western blotting showed that morphine treatment was able to activate cytoplasmic STAT5a in CEM x174 cells, which was then translocated into nuclei and bound to elements of cyclin D1 promoter, and as a consequence the expression of the cyclin D1 was apparently up-regulated. The data from EMSA-superEMSA and ChIP-qPCR further confirmed that morphine was capable of promoting the binding of STAT5a to its elements (proximal and distal), which was abolished by antagonist naloxone. As shown in transient transfection assay, activity of the cyclin D1 promoter was significantly reduced by 82% (distal) and 65% (proximal) in comparison with wild type after two STAT5a elements were mutated. Furthermore, knockdown of the STAT5a was associated with a concurrent silence of morphine-induced expression upregulation？ of the cyclin D1, indicating the involvement of STAT5a in morphine-triggered signaling in regulation of the cyclin D1 expression. The finding provides evidence which demonstrates the cross-talk between mu opioid receptor and cytokine signaling in lymphocytes. Thus, we conclude that morphine may modulate cyclin D1 gene expression via STATs signaling, which will be favorable for further understanding of the pharmacological effect of morphine on immune regulation.
	TO cite this article:Liyuan Guo,Hui Li,Han Liu, et al. Involvement of STAT5a signaling in morphine-induced up-regulation of the cyclin D1[OL].[24 July 2009] http://en.paper.edu.cn/en_releasepaper/content/34079


	4. Effects of uropathogenic Escherichia coli infection on gene expression profiles in human bladder transitional epithelial cells1
	Ge Xin,Dong jie,Chen jinying,Yao ping,Yang dongjing,Zhang yumei
	Basic Medicine 26 May 2009
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	Abstract:Interaction between uropathogenic Escherichia coli (UPEC) and host uroepithelial cells is the key step of the process of urinary tract infection. To further define the role uroepithelial cells play in initiating and modulating the host response to infection with UPEC strains, the human bladder transitional epithelial EJ cells were evaluated for their capacities to allow the adherence and invasion by UPEC132, a clinical strain isolated from China, and a cDNA microarray for 22 000 human genes was used to identify the gene expression differences between EJ cells infected with UPEC132 and uninfected EJ cells. Microscope observation showed that UPEC132 could adhere to EJ cells, and visualization by confocal microscope revealed that this invasive microorganism could be seen within the cells. EJ cells infected with UPEC132 significantly changed mRNA expression of a total of 29 genes, including 28 genes up-regulated and 1 gene down-regulated. Of these, regulators of growth and proliferation (e.g. immediate-early genes), cytokines (e.g. interleukin-6, interleukin-8), and modulators of apoptotic responses were the most prominent. In addition, the deduced signal transduction events based on bioinformatics analysis disclosed the complicated interaction between UPEC and host cells.
	TO cite this article:Ge Xin,Dong jie,Chen jinying, et al. Effects of uropathogenic Escherichia coli infection on gene expression profiles in human bladder transitional epithelial cells1[OL].[26 May 2009] http://en.paper.edu.cn/en_releasepaper/content/32569


	5. The effect of acetylation of FoxO1 on activating Bim expression in response to HDAC inhibitor depsipeptide treatment
	Yang Yang,Zhao Ying,Liao Wenjuan,Yang Jing,Zhu Weiguo
	Basic Medicine 31 March 2009
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	Abstract:Histone deacetylase (HDAC) inhibitors have been shown to induce cell cycle arrest and apoptosis in cancer cells. However, the mechanisms of HDAC inhibitor induced apoptosis are incompletely understood. In previous study, we found that HDAC inhibitor depsipeptide may induce apoptosis of human lung cancer cells through the forkhead box class O1 (FoxO1)-Bim pathway. In this study, we further explore the mechanisms of mediating FoxO1 after depsipeptide treatment in lung cancer cells. We found that depsipeptide-induced expression of Bim was directly dependent on acetylation of FoxO1 that is catalyzed by cAMP-responsive element-binding protein (CREB)-binding protein (CBP). Moreover, our results demonstrated that FoxO1 acetylation is required for the depsipeptide induced activation of Bim and apoptosis, using transfection with a plasmid containing FoxO1 mutated at lysine sites. These data show for the first time that a HDAC inhibitor induces apoptosis through the FoxO1 acetylation-Bim pathway.
	TO cite this article:Yang Yang,Zhao Ying,Liao Wenjuan, et al. The effect of acetylation of FoxO1 on activating Bim expression in response to HDAC inhibitor depsipeptide treatment[OL].[31 March 2009] http://en.paper.edu.cn/en_releasepaper/content/30933


	6. 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


	7. A FoxO1-Bim pathway is involved in HDAC inhibitor depsipeptide induced apoptosis
	Yang Yang,Ying Zhao,Jing Yang,Wei-guo Zhu
	Basic Medicine 17 March 2009
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	Abstract:Histone deacetylase (HDAC) inhibitors have been shown to induce cell cycle arrest and apoptosis in cancer cells. However, the mechanisms of HDAC inhibitor induced apoptosis are not completely understood. In this study, a novel HDAC inhibitor, depsipeptide was found to induce p53-independent apoptosis in human lung cancer cells. Further study showed that Bim, a BH3-only pro-apoptotic protein, was significantly up-regulated by depsipeptide in cancer cells, indicating Bim may play a role in this depsipeptide induced apoptosis. In additional experiments, Bim’s function in depsipeptide-induced apoptosis was confirmed by knock down of Bim with RNAi. Furthermore, depsipeptide-induced expression of Bim was found to be dependent on forkhead transcription factor 1 (FoxO1) by FoxO1 siRNA. These data show for the first time that HDAC inhibitor may induce apoptosis through the FoxO1-Bim pathway.
	TO cite this article:Yang Yang,Ying Zhao,Jing Yang, et al. A FoxO1-Bim pathway is involved in HDAC inhibitor depsipeptide induced apoptosis[OL].[17 March 2009] http://en.paper.edu.cn/en_releasepaper/content/30413


	8. Role of γ-Interferon in Induction of Foxp3 and Conversion of CD4+CD25- T cells to CD4+ Regulatory T Cells
	Wang Zhaojun,Hong Jian,Sun Wei,Xu Guangwu,Li Ningli,Chen Xi,Liu Ailian,Xu Lingyun,Sun Bing,Zang Jingwu
	Basic Medicine 16 January 2009
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	Abstract:γ−Interferon (γ−IFN) is an important Th1 pro-inflammatory cytokine and has a paradoxical effect on experimental autoimmune encephalomyelitis (EAE) in which the disease susceptibility is unexpectedly heightened in γ−IFN deficient mice. In this study, we provided new evidence indicating that γ−IFN was critically required for the conversion of CD4+CD25- T cells to CD4+ regulatory T cells during EAE. The study showed that the added severity of EAE in γ−IFN knockout mice was directly associated with altered encephalitogenic T cell responses, which correlated with reduced frequency and function of CD4+CD25+Foxp3+ regulatory T cells when compared to wild-type mice. It was demonstrated in both human and mouse systems that in vitro γ−IFN treatment of CD4+CD25- T cells converted to CD4+ regulatory T cells characterized by increased expression of Foxp3 and enhanced regulatory function. Mouse CD4+CD25- T cells, when treated in vitro with γ−IFN, acquired marked regulatory properties as evidenced by suppression of EAE by adoptive transfer. The findings have important implications for the understanding of the complex role of γ−IFN in both induction and self regulation of inflammatory processes.
	TO cite this article:Wang Zhaojun,Hong Jian,Sun Wei, et al. Role of γ-Interferon in Induction of Foxp3 and Conversion of CD4+CD25- T cells to CD4+ Regulatory T Cells[OL].[16 January 2009] http://en.paper.edu.cn/en_releasepaper/content/27933


	9. 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


	10. Overexpression of Suppressor of Cytokine Signaling 1 in Islet Graft results in Anti-Apoptosis Effect and Prolonged Survival
	Qin Jie,Jiao Yang ,Chen Xiaobo ,Zhou Shuang ,Liang Chunmin ,Zhong Cuiping
	Basic Medicine 13 January 2009
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	Abstract:A significant portion of islet grafts are destroyed by apoptosis and fail to become functional after transplantation. Strategies which enhance islets’ anti-apoptosis ability may inhibit grafts loss. Aim of this study was to investigate whether overexpression of SOCS1 in islet grafts could achieve anti-apoptosis effect and prolonged grafts survival. We used chimeric adenovirus vector (Ad5F35) to enhance SOCS1 expression in isolated rat islets, and detected its protective action against rTNF-α induced apoptosis. After transplanting SOCS1-overexpressing islets into allogeneic recipients with streptozotocin-induced diabetes, grafts survival and in situ apoptosis were analyzed using immunohistochemistry. The isolated rat islets infected with Ad5F35 containing SOCS1 gene (Ad5F35-SOCS1, MOI=100) showed significantly higher SOCS1 expression than Ad5F35-EGFP and mock infected islets. After treatment with rTNF-α and cycloheximide for 48 hours in vitro, Ad5F35-SOCS1 infected islets exhibited lower apoptotic ratio (8.89±4.03%, P<0.05) than controls (Ad5F35-EGFP: 24.60±6.88%, mock infected: 21.14±5.12%). The diabetic recipients transplanted with Ad5F35-SOCS1 infected islets presented 12.14±2.12 days of normoglycemia, statistically longer than that of recipients transplanted with mock infected islets (6.20±1.48 days, P<0.05). Furthermore, histological analysis indicated that these infected grafts with local overexpression of SOCS1 had preserved islet function and suppressed cell apoptosis in the early posttransplant period. These results demonstrate that overexpression of SOCS1 in islet grafts prior to transplantation can significantly protect them from apoptosis loss and prolong their survival. This approach could be used to improve outcomes of islet transplantation in clinic.
	TO cite this article:Qin Jie,Jiao Yang ,Chen Xiaobo , et al. Overexpression of Suppressor of Cytokine Signaling 1 in Islet Graft results in Anti-Apoptosis Effect and Prolonged Survival[OL].[13 January 2009] http://en.paper.edu.cn/en_releasepaper/content/27693

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