Abstract:In this paper，microRNAs (miRNAs) have recently emerged as a central player of gene regulatory network involved in decision of cell fate. Apoptosis, an active process that leads to cell death, has been shown to be controlled by miRNAs. It has also been implicated in a variety of human disease, such as heart disease, and established as a target process for disease therapy. Tanshinone IIA (TIIA), a monomer of phenanthrenequinones used to treat cardiovascular diseases, is known to insert cardioprotective effects in myocardial infarction by targeting apoptosis through enhancing Bcl-2 expression. To explore the potential link between miRNAs and the anti-apoptotic action of TIIA, we studied the possible involvement of miRNAs. We found that expression of all three members of the miR-34 family, miR-34a, miR-34b and miR-34c that have been known to mediate the apoptotic effect of p53, was robustly upregulated after exposure to either the DNA-damaging agent doxorubicin or pro-oxidant H2O2 for 24 hr. This upregulation caused significant apoptotic cell death, as determined by DNA fragmentation, and the effects were reversed by the antisense to these miRNAs. Pretreatment of cells with TIIA prior to incubation with doxorubicin or H2O2 prevented upregulation of miR-34 and reduced apoptosis. We then established BCL2L2, API5 and TCL1, in addition to BCL2, as the novel target genes for miR-34. We further unraveled that repression of these genes by miR-34 accounts for their proapoptotic effect in cardiomyocytes whereas upregulation of these genes by TIIA through downregulating miR-34 is likely the molecular mechanism for its beneficial effect against ischemic myocardial injuries.

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	1. ELUCIDATION OF ANTI-APOPTOTIC MECHANISMS OF TANSHINONE IIA REVEALS THE ROLE OF MIR-34 IN CARDIOMYOCYTE APOPTOSIS
	CHU Xia,LU Huimin,BAI Yunlong,XIAO Jiening,PAN Zhenwei,LUO Xiaobin,ZHANG Yong,SHAN Hongli,LU Yanjie,YANG Baofeng,WANG Zhiguo
	Basic Medicine 28 December 2010
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	Abstract:In this paper，microRNAs (miRNAs) have recently emerged as a central player of gene regulatory network involved in decision of cell fate. Apoptosis, an active process that leads to cell death, has been shown to be controlled by miRNAs. It has also been implicated in a variety of human disease, such as heart disease, and established as a target process for disease therapy. Tanshinone IIA (TIIA), a monomer of phenanthrenequinones used to treat cardiovascular diseases, is known to insert cardioprotective effects in myocardial infarction by targeting apoptosis through enhancing Bcl-2 expression. To explore the potential link between miRNAs and the anti-apoptotic action of TIIA, we studied the possible involvement of miRNAs. We found that expression of all three members of the miR-34 family, miR-34a, miR-34b and miR-34c that have been known to mediate the apoptotic effect of p53, was robustly upregulated after exposure to either the DNA-damaging agent doxorubicin or pro-oxidant H2O2 for 24 hr. This upregulation caused significant apoptotic cell death, as determined by DNA fragmentation, and the effects were reversed by the antisense to these miRNAs. Pretreatment of cells with TIIA prior to incubation with doxorubicin or H2O2 prevented upregulation of miR-34 and reduced apoptosis. We then established BCL2L2, API5 and TCL1, in addition to BCL2, as the novel target genes for miR-34. We further unraveled that repression of these genes by miR-34 accounts for their proapoptotic effect in cardiomyocytes whereas upregulation of these genes by TIIA through downregulating miR-34 is likely the molecular mechanism for its beneficial effect against ischemic myocardial injuries.
	TO cite this article:CHU Xia,LU Huimin,BAI Yunlong, et al. ELUCIDATION OF ANTI-APOPTOTIC MECHANISMS OF TANSHINONE IIA REVEALS THE ROLE OF MIR-34 IN CARDIOMYOCYTE APOPTOSIS[OL].[28 December 2010] http://en.paper.edu.cn/en_releasepaper/content/4401790


	2. Neural ensemble sparse coding during working memory task in rat prefrontal cortex
	Xu Yunhua,Bai Wenwen,Tian Xin
	Basic Medicine 27 December 2010
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	Abstract:The neural ensemble aims to provide a mechanistic explanation of how groups of neurons acting together during a cognitive processing. It is significant to expressing neural ensemble at a higher precision when neural population activity data are recoded from experiment. In this article, we propose the use of sparse coding as a new methodology to address this issue by recording the activities of neurons in the rat prefrontal cortex during the working memory task in Y-maze. The time information of neural activity is summarized into bin counts using 200 milliseconds windows, and a sparse code for the bin-count matrix is found by means of a linear generative model. The meaningful components are extracted to reconstruct the input by an inverse of the sparsifying transform. None of the feature components are ignored or missed, as the number of the source components is greater than that of neurons. The reconstructed sparse neuronal activities are compared with rate coding. The recording twenty cases dealt show that, using sparse coding, it is possible to identify spatiotemporal patterns of neural activity in the form of reconstructed signal. The results indicate that the spatiotemporal location of neural ensemble could be more precisely detected, using sparse coding.
	TO cite this article:Xu Yunhua,Bai Wenwen,Tian Xin. Neural ensemble sparse coding during working memory task in rat prefrontal cortex[OL].[27 December 2010] http://en.paper.edu.cn/en_releasepaper/content/4401529

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	3. Induced Pluripotent Stem (iPS) Cell：A novel potential resource for Hematopoietic Stem Cell Transplantation (HSCT)
	WANG Jing,CHEN Jing,PAN Xiongfei,BA Kai,GE Yuehua,LIN Yunfeng
	Basic Medicine 23 December 2010
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	Abstract:As a current procedure, hematopoietic stem cell transplantation (HSCT) has been applied for various blood diseases, such as leukemia and lymphoma. However, it sometimes causes significant immunological rejection, which may do harm to the recipients. Several researches have suggested that human iPS cells possess differentiation potentials to hematopoietic progenitor cells and lack of immunologic rejection. The hypothesis may be proposed that human iPS cells could be a novel potential resource for hematopoietic stem cell transplantation (HSCT). It is indicated that iPS cells will be a safer resource for research and clinic applications in future.
	TO cite this article:WANG Jing,CHEN Jing,PAN Xiongfei, et al. Induced Pluripotent Stem (iPS) Cell：A novel potential resource for Hematopoietic Stem Cell Transplantation (HSCT)[OL].[23 December 2010] http://en.paper.edu.cn/en_releasepaper/content/4400271


	4. Inhibitory Activity of Alltride, Sodium Houttuyfonate and Berberine Hydrochloride on Mycobacterium Tuberculosis
	JIANG Xin,LU Chanyi
	Basic Medicine 13 December 2010
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	Abstract:Three Chinese medicine monomers alltride, sodium houttuyfonate and berberine hydrochloride, has been identified some activity against tuberculosis in clinic application in China. To explore the activity and mechanism of them against Mycobacterium tuberculosis and multidrug-resistant Mycobacterium tuberculosis, MICs of them were performed in vitro. Comparison between the proteomes of Mycobacterium tuberculosis H37Rv, treated with and without alltride, differential protein spots were measured by matrix assisted laser desorption ionization time of flight mass spectrometry (MOLDI-TOF-MS). Alltride had the same inhibitory activity on susceptible and multidrug resistant Mycobacterium tuberculosis. Sodium houttuyfonate and berberine hydrochloride were higher inhibitory concentration on multidrug resistant Mycobacterium tuberculosis than susceptible. Four protein spots were downregulated in Mycobacterium tuberculosis H37Rv treated with alltride and identified as Rv2032，Rv0780，Rv1611 and Rv1284 by MOLDI-TOF-MS. The four proteins might be the targets of alltride. These findings suggest the multidrug resistance mechanisms of Mycobacterium tuberculosis are effective to berberine hydrochloride and sodium houttuyfonate. The anti-Mycobacterium tuberculosis mechanisms of these two drugs might be the similar with the one of the existing anti-tuberculosis drugs. Mechanism of alltride was different from them, might be inhibition biosynthesis of some nucleic acid and amino acid.
	TO cite this article:JIANG Xin,LU Chanyi. Inhibitory Activity of Alltride, Sodium Houttuyfonate and Berberine Hydrochloride on Mycobacterium Tuberculosis[OL].[13 December 2010] http://en.paper.edu.cn/en_releasepaper/content/4397485


	5. Suppressor of Cytokine Signaling 1 Inhibits Apoptosis of Islet Grafts Through Caspase 3 and Apoptosis Inducing Factor Pathways
	QIN Jie,SUO Guangjun,ZHONG Cuiping,ZHAO Zhongxin
	Basic Medicine 23 November 2010
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	Abstract:A significant portion of islet grafts can be destroyed by apoptosis and fail to engraft in the early post-transplant period. In order to inhibit graft loss, a number of strategies have been explored to prevent islet cell apoptosis. Recently, we found that overexpression of suppressor of cytokine signaling 1 (SOCS1) in islet grafts could achieve an anti-apoptotic effect and prolong graft survival in rat transplant model. Caspase 3 is the central executioner caspase which can be activated by upstream cascades in caspase-dependent apoptosis pathway. Apoptosis inducing factor (AIF) is the first identified and key protein which can release from mitochondria and translocate to nucleus in caspase-independent apoptosis pathway. In this study, we investigated whether above two pathways were all involved in cytoprotection of SOCS1 in islet grafts. We used a chimeric adenovirus vector (Ad5F35-SOCS1) to enhance SOCS1 expression in isolated rat islets and transplanted them into recipients with streptozotocin-induced diabetes. The expressions of active (cleaved) caspase 3 and AIF on islets were analyzed in vitro and in vivo. The Ad5F35-SOCS1 infected islets with higher SOCS1 expression showed decreased levels of active caspase 3 and intranuclear AIF after treatment with TNF-α and cycloheximide in vitro. The histological analysis also indicated that these infected islets had decreased caspase 3 activation and AIF translocation (to nucleus) in the early post-transplant period. These results demonstrate that the expression of SOCS1 in islet grafts protect them from apoptosis through caspase 3 (caspase-dependent) and AIF (caspase-independent) mediated pathways.
	TO cite this article:QIN Jie,SUO Guangjun,ZHONG Cuiping, et al. Suppressor of Cytokine Signaling 1 Inhibits Apoptosis of Islet Grafts Through Caspase 3 and Apoptosis Inducing Factor Pathways[OL].[23 November 2010] http://en.paper.edu.cn/en_releasepaper/content/4392954


	6. The correlation of fascin over-expression with motility and invasion of tumor cells
	Li Weiping,Ma Gui
	Basic Medicine 12 November 2010
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	Abstract:In the progression of the cancer invasion, carcinoma cells migrate away from primary tumors, traverse to basement membrane and extracellular matrix (ECM), overcome the cell-cell and cell-ECM adhesions, invade surrounding tissue, and come into the metastases through lymphatic and/or blood system .Of all these processes, the acquisition and increase of cell motile and invasive properties play a crucial role in the neoplasm progression. Fascin, an Actin-bundling protein, is considered to induce specific morphological features of membrane protrusion, as well as the changes of cell adhesion and cell interactions, and ultimately enhance the cell motility for subsequent invasion and metastasis, which is significantly negatively correlated with prognosis and survival rate. It is profound to study the involvement of fascin in the mechanism of invasion and metastasis so as to provide effective early diagnosis for potentially aggressive tumors or be used to develop therapeutic strategies that can arrest invasion and even metastases.
	TO cite this article:Li Weiping,Ma Gui. The correlation of fascin over-expression with motility and invasion of tumor cells[OL].[12 November 2010] http://en.paper.edu.cn/en_releasepaper/content/4391408


	7. The motility and invasion of tumor cell and its association with Fascin
	Ma Gui,Li WeiPing
	Basic Medicine 11 June 2010
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	Abstract:In the progression of the cancer, carcinoma cells migrate away from primary tumors, traverse to basement membrane and ECM, overcome the cell-cell and cell-ECM adhesions, invade surrounding tissue, and come into the metastases through lymphatic and/or blood system .Of all these processes, the acquisition and increase of cell motile and invasive properties play a crucial role in the neoplastic progression. Fascin, as an Actin-bundling protein, is prevalently considered to induce specific morphological features of membrane protrusion, as well as the changes of cell adhesion and cell interactions, and ultimately enhance the cell motility for subsequent invasion and metastases, which is significantly associated with bad prognosis. Therefore, fascin over-expression is proposed to be a novel biomarker to provide effective early diagnosis for potentially aggressive tumors or be used to develop therapeutic strategies that can arrest invasion and even metastases.
	TO cite this article:Ma Gui,Li WeiPing. The motility and invasion of tumor cell and its association with Fascin[OL].[11 June 2010] http://en.paper.edu.cn/en_releasepaper/content/4376011


	8. Rapid biomimetic mineralization of chitosan sponges with a facile method in ethanol/water mixed solution
	Li Lihua ,Zhou Changren
	Basic Medicine 18 May 2010
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	Abstract:Mineralization of biopolymers is a hot topic and a promising method for tissue engineering. In this study, biomimetic mineralization of chitosan sponges was performed in a large quantity with a rapid and facile approach. The calcium phosphate apatite was co-precipitated as the precursor for the formation of hydroxyapatite in mixed water-ethanol solution. The component and morphology of the apatite and the nanocomposite hybrid sponges were measured with XRD, TEM, FTIR and ESEM. The mechanism of nucleation and growth of crystals were discussed as well. Results revealed that chitosan matrix improved the crystalline quality of hydroxyapatite (HAP) crystals. With elongation of mineralization time, the mineral layers on the outer surface and inner section of chitosan sponges increased. The chitosan sponge or the microenvironment around it promoted the crystallites quality of HAP phase. Furthermore, the compressive strength and modulus of the HAP-chitosan bio-composites increased to 0.55 MPa and 29.29± 1.25 MPa respectively. Such one-pot approach might be extended to the mineralization of other biopolymers and will have a very broad application in the future.
	TO cite this article:Li Lihua ,Zhou Changren . Rapid biomimetic mineralization of chitosan sponges with a facile method in ethanol/water mixed solution[OL].[18 May 2010] http://en.paper.edu.cn/en_releasepaper/content/4372783


	9. 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


	10. 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

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