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Table of Content

    05 October 2011, Volume 31 Issue 10
    Effects of Fluorosis of Coal Burning on Reproductive and Endocrinology of Male Rats
    2011, 31(10):  1077-1081. 
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    Abstract Objective To study the effects of fluorosis of coal burning on reproductive and endocrinology of male rats. Methods SD rats taken as the experimental objects were randomly assorted into 7 groups: control group,low-dose fluoride group, middle-dose fluoride group, high-dose fluoride group, low-dose fluoride supplemented with nutrition group,middle-dose fluoride supplemented with nutrition group and high-dose fluoride supplemented with nutrition group. The exposed groups were fed with the fodder with different proportions of corn dried by burning coal coming from endemic fluorosis areas, to establish the animal model of coal-burning fluorosis. All rats were killed by femoral arterial exsanguination at three times(90d,120d,180d). Followed by examinations of dental fluorosis,fluorine in urine and the concentrations of intratesticular testosterone and testosterone (T), estradiol (E2),luteinizing hormone (LH), follicle stimulating hormone (FSH), Gonadotropin-Releasing Hormone (GnRH)and Prolactin(PRL) in serum. Results The animal model of fluorosis was successfully established. Compared with the control groups, the level of T, E2 and PRLdeclined more apparently with the increasing fluoride dose and the longer exposure time in exposed groups(p<0.05 or p<0.01),but the level of LH and FSH increased more apparently with the increasing fluoride dose and the longer exposure time in exposed groups(p<0.05 or p<0.01). Compared with the control groups, the level of exposed groups’GnRH declined more apparently with the longer exposure time but increased more apparently with the increasing fluoride dose between exposed groups(p<0.05 or p<0.01). In the same dose of fluoride added nutrition groups sex hormone levels improved (p <0.05 or p <0.01). Conclusions Coal-burning fluorosis had a significant endocrine effect on reproductive and endocrinology of male rats, with the increasing fluoride dose and prolonged exposure, influence increased. Reducing fluoride intake and improving nutritional status can ease the effects of coal-burning fluorosis on reproductive and endocrinology of male rats.
    The inhibitive effects of exogenous S100A8 on Hela cells in vitro
    2011, 31(10):  1082-1087. 
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    Objective To study the effect of exogenous S100A8 on cell proliferation,apoptosis, clone formation, migration and invasion of human cervical cancer cell line Hela. Methods MTT was used to detect the cell proliferation; Hoechst staining was used to detect the cell apoptosis; Flow Cytometry was used to detect the variation of cell cycle; colony-forming assay was used to detect the ability of cell cloning formation; Wound healing assay and Transwell chamber experiment were used to detect the cell migration and invasion ability. Results 1)S100A8 inhibited cell proliferation: MTT indicated that after treatment of GST-hS100A8 for 3d, the OD value of 100 mg/L, 300 mg/L and 1000 mg/L group of GST-hS100A8 decreased by 13.64%, 19.29% and 25.06% compared with GST group, respectively (P<0.05) .In the group of 100 mg/L, the OD value of GST-hS100A8 decreased in a time-dependent manner, especially from 72h(P<0.05). 2)S100A8 promoted cell apoptosis: The result of Hoechst staining showed that cell apoptosis rate in GST-hS100A8 group increased by 5.18 times compared with GST group at 72h(P<0.05). Meanwhile, the result of Flow Cytometry displayed that the peak of apoptosis of GST-hS100A8 was 19.9% at 72h, while the groups of GST and blank were no apoptotic peak. 3) We also found that the effect of GST-hS100A8 on cell cycle was not significant. 4) Colony-forming assay showed that the rate of cloning formation of GST-hS100A8 decreased by 30.2% (P<0.05). 5) The result of wound healing assay indicated that the healing rate of GST-hS100A8 group reduced by 30.1% compared with GST group (P<0.05) at 24h. 6) The result of Transwell indicated that the trans-membrane cell number of GST-hS100A8 group reduced by 48.9%(P<0.05) compared with GST group at 24h. Conclusion Exogenous S100A8 could inhibit cell proliferation, cloning formation, migration, and invasion and induce cell apoptosis on human cervical cancer cell line Hela, which indicated that S100A8 could have the inhibitive effects on cervical cancer.
    Effect of Astragalus injection on the expression of JNK3 after hypoxia /hypoglycemia and reoxygenation in rats hippocampal neurons
    2011, 31(10):  1088-1093. 
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    Objective: Investigate the effect of Astragalus injection on the expression of JNK3(c-jun N terminal kinase) following hypoxia/ hypoglycemia and reoxygenation in rat hippocampal neurons. Methods: 8 days-old hippocampal neurons which had undergone primary cultures were divided randomly into normal control group、hypoxia/ hypoglycemia and reoxygenation group(model group)、Astragalus injection group and vehicle control group. Hippocampal neurons were treated with reoxygenation after deprived of oxygen and glucose for 30 minutes in model group, and expressions of JNK3 were measured by immunohistochemistry and western blotting after reoxygenation 0h、0.5h、2h、6h、24h、72h、120h . Results: Compared with normal control group, the numbers of JNK3-marked neurons and the mean optic density (MOD) of JNK3 protein increased obviously in model group excepted 120h (P<0.05); Compared with model group, the numbers of JNK3–marked neurons and MOD of JNK3 decreased obviously in the Astragalus injection group excepted 120h (P<0.05). Conclusions: Astragalus injection can inhibit the expression of JNK3 protein following hypoxia/ hypoglycemia and reoxygenation, which plays a role in inhibiting hippocampal neuronal apoptosis.
    PPAR-α involves in cardiomyocyte hypertrophy induced by angiotensin Ⅳ
    2011, 31(10):  1094-1098. 
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    Abstract: Objective: To study the role of peroxisome proliferator-activated receptor-α (PPAR-α) signal transduction pathway in cardiomyocyte hypertrophy induced by angiotensin Ⅳ (Ang Ⅳ). Methods: The cardiomyocyte hypertrophic responses were assayed by measuring the cell surface area, protein content, and atrial natriuretic factor (ANF) mRNA expression. In cultured cardiomyocytes, fenofibrate (FF), a selective PPAR-α agonist, and MK886, a selective PPAR-α antagonist, were used to investigate the mechanisms of Ang Ⅳ. The expressions of mRNA and protein were assayed by Real-time PCR and Western blot, respectively. Results: In cultured cardiomyocytes, Ang Ⅳ (0.01, 0.1, 1 nmol/L) can induce cardiomyocyte hypertrophy in a concentration-dependent manner. Meanwhile, the expressions of PPAR-α mRNA and protein decreased significantly. FF at 0.3 μmol/L increased the expressions of PPAR-α both mRNA and protein (P <0.01). All of these effects of FF could be abolished by MK886 at 0.3 μmol/L (P<0.05). Conclusion: PPAR-α signal transduction pathway involves in cardiomyocyte hypertrophy induced by Ang Ⅳ.
    Mechanism of Ginsenosides Regulating Spontaneous Sleep Architecture in Rats
    2011, 31(10):  1104-1109. 
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    Abstract: Objective To study the underling mechanism of the effect of ginsenosides(GS) on spontaneous sleep. Methods Adult SD rats were randomly divided into the control, GS 10 mg/kg (low dose) and 100 mg/kg (high dose) groups. Rats were instrumented with sleep-wake recording electrodes. After recovery from surgical operation, rats were orally administered GS 10 mg/kg and 100 mg/kg or water once per day for 6 days. On GS administration day 1 and day 6, Polygraphic signs of undisturbed sleep-wake activities were recorded for 12h (7:30 ~19:30) after GS administration. Results On GS administration day 1 (acute), 10 mg/kg GS slightly (P?>0.05 but 100mg/kg GS significantly (P?<0.05) increased the non-rapid eye movement (NREM) and total sleep and decreased wakefulness; compared with control, low dose and high dose GS failed to change the level of glutamic acid decarboxylase (GAD) (P?>0.05) but enhanced the expressions of GABAA receptor α,? not ? subunits in rat hypothalamus (P?<0.05). Following 6 days administration (chronic), both 10 and 100mg/kg GS increased markedly NREM and total sleep and decreased wakefulness. Accordingly, low dose GS slightly (P?>0.05) but high dose GS significantly (P? <0.05) increased the level of GAD in rat hypothalamus, whereas the expressions of GABAA receptor α, ? and ? subunits not affected (P?>0.05). Conclusion These results suggest that GS can regulate spontaneous sleep architecture in time and dose-dependent manner in which acute GS treatment is related to its up-regulating GABAA receptor α, ? subtypes whereas chronic GS administration involved in the raised GABA product produced by its over-expressing GAD in rat hypothalamus.
    Inhibitory Effects of Chloroquine on Astrocyte Activation in Vitro
    2011, 31(10):  1110-1114. 
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    Objective To investigate the effects of Chliroquine on Pentylenetetrazole(PTZ)- activitied hippocampal astrocyte of rats. Methods Neonatal rat (24h) hippocampal astrocytes were obtained and divided into contron group, PTZ-activitied group and Chliroquine groups with Chliroquine treatment at 25, 50, 75mg/ L. The cell proliferation, expression of glial fibrillary acidic protein (GFAP) and CyclinD1 after the treatments were detected with MTT assay, immunofluorescence cytochemistry and western bloting respectively. Results In comparison with PTZ-activition group, Chliroquine treatment resulted in significant inhibition of the cell proliferation, GFAP and CyclinD1 in the PTZ-activated astrocytes (P<0.05). Chliroquine at 75mg/L showed the strongest inhibitory effects against astrocyte activation and maintained nearly normol level of astrocyte activation in comparison with the control group. Conclusion Chliroquine could inhibited the activation of astrocytes which activitied by PTZ. So Chliroquine may be used to treat epilepsy.
    Stathmin in non-small cell lung cancer in expression enhanced Stathmin in non-small cell lung cancer in expression enhanced
    2011, 31(10):  1115-1119. 
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    Abstract: Objective Explore Stathmin in non-small cell lung cancer (NSCLC) organization and normal tissue the expression, understand its with NSCLC clinical and pathological features of the relationship between them. Method Using immunohistochemistry and RT - PCR method, detection 43 patients with NSCLC postoperative cancerous tissue and normal tissue samples in Stathmin protein and mRNA expression. Results Stathmin protein and gene in NSCLC positive expression rate respectively 67.44%, 62.79% and significantly higher than normal tissues 16.28% and 20.93% (P < 0.01), its expression and tumor cell differentiation degree and without lymph node metastasis relevant (P < 0.05). Conclusion Stathm in in NSCLC happening development process has played an important role, he may become prediction NSCLC aggressieness of new biology and tailored therapies sensitive indicators.
    TRAIL induced apoptosis in Hela cells by mitochondrial signal pathway
    2011, 31(10):  1120-1123. 
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    Objective To explore the mitochondrial pathway in the apoptosis of Hela cells induced by TRAIL. Methods Apoptotic cells were detected by DNA electrophoresis. The mitochondrial transmembrane potential (∆Ψm), the expressions of Bcl-2, the location of Cyt c and AIF, the caspase-3 activity were tested by confocal laser microscopy, western blot, immunofluorescence and caspase-3 activity assay. Results TRAIL can induce apoptosis in Hela cells. DNA ladders were showed on agarose gel electrophoresis. At the same time, TRAIL induced the decrease of ∆Ψm and Bcl-2, the release of Cyt c, the translocation of mitochondrial AIF to cytoplasm and nuclei, the increase of caspase-3 activity in the time-dependent manner. Conclusion TRAIL induce the apoptosis of Hela cells involves mitochondrial signal pathway.
    Amiloride protects PC12 cells from acid-induced injury via chaperone-mediated autophagic pathway
    Chang-Zhen ZHAO
    2011, 31(10):  1124-1128. 
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    OBJECTIVE: To study the neuroprotective effects of amiloride (Ami), non-selective blocker of acid-sensing ion channels,in the cell death and apoptosis induced by extracellular acid in PC12 cells, and investigate the effects of Ami on chaperone-mediated autophagic pathway. METHODS:The cell viability following acid exposure (pH6.0) was analyzed with 3-(4, 5-dimethylthiazol-2-yl) -2, 5-diphenyltetrazolium bromide (MTT) assay. The degree of cell injury was assessed by a quantitative measurement of lactate dehydrogenase (LDH) released from cytosol to culture medium. Double staining of treated cells with Annexin V and PI was assayed with flow cytometry to determine the apoptotic rate. Western blot was used to examine the expression levels of receptor lysosome-associated membrane protein 2a (Lamp2a). RESULTS: Acid exposure significantly decreased the cell viability, increased the activity of LDH which released to culture medium and raised apoptosis rate. Western bolt analysis shown that acidic exposure led to compensatory induction of Lamp2a protein signaficantly. Co-incubation with Ami (100μM) significantly increased the cell viability, inhibited the release of LDH, reduced the apoptosis rate, and inhibited the overexpression of Lamp2a. CONCLUSION: Ami protects PC12 cells against acid-induced injury via chaperone-mediated autophagic pathway.
    Effect of Culture Supernatant of Toxoplasma gondii on Human acute monocytic leukemia cell line THP-1 and probable mechanisms
    2011, 31(10):  1129-1133. 
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    The study on how to get culture supernatants of Toxoplasma gondii and investigate the inhibitive effects of culture supernatants of Toxoplasma gondii on the proliferation and on the cell cycle of Human acute monocytic leukemia cell line THP-1 in vitro. Methods THP-1 cells (concentration of 5×104mL-1) were harvested in the different cell culture plates. The cells were treated for different hours with different concentrations of Toxoplasma gondii culture supernatant. Growth inhibition rates were tested with the MTT method;Cell cycle were checked by Flow Cytometer. Western blot was used to detect the leves of NF-κB/p65 and cyclin D1 of cells. Results the culture supernatants of Toxoplasma gondii could inhibit the proliferation of THP-1 cells in a time-dose dependent manner. Cell cycle was significantly stopped at G0/G1phase by the culture supernatants with FCM technology. The culture supernatant of Toxoplasma gondii reduced the expressions of gene NF-κB 、cyclin D1 of THP-1 cells. Conclusion The culture supernatant of Toxoplasma gondii may inhibit THP-1 cell and arrest the cell cycle of THP-1 cells at G0/G1phase mainly by regulating the expression of gene NF-κB 、cyclin D1 .
    The inhibitory effects of human umbilical cord blood derived mesenchymal stem cells on allogeneic peripheral blood T lymphocytes
    2011, 31(10):  1134-1138. 
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    Objective To study the influences of human umbilical cord blood derived mesenchymal stem cells (HUCB-MSCs) on allogeneic peripheral blood T lymphocytes. Methods HUCB-MSCs were isolated from normal human umbilical cord blood, isolated and cultured in vitro, and then surface marker were determinate with FCM. After isolating CD3+T cells from normal human peripheral blood, CD3+T cells were mixed with HUCB-MSCs stimulated with PHA or not. Five days later, the effects of HUCB-MSCs on T-cell proliferation was detected by 3H-TdR. Cytokines production of PHA-stimulated T cells in co-culture were investigated with ELISA. T-cell apoptosis affected by HUCB-MSCs were also observed by FCM. Results HUCB-MSCs showed a spindle-shaped fibroblastic morphology in culture. The populations appeared as a homogenous population and were uniformly positive for the expression of CD29, CD44, and HLA-ABC, but negative for the expression of CD14, CD34, CD45, and HLA-DR. In co-culture, MSCs failed to elicit positive responses of T cells (3760 ± 730 counts/min versus 3600 ± 800 counts/min,p=0.85), whereas significantly suppressed PHA-stimulated T-cell proliferation(5230 ± 550 counts/min versus 10500 ± 800 counts/min,p<0.001). Both pro-inflammatory cytokines IFN-γ(510 ± 60 pg/ml versus 1580 ± 100 pg/ml, p<0.001)and TNF-α(590 ± 20 pg/ml versus 1180 ± 30 pg/ml, p<0.001)secreted by T cells were inhibited by HUCB-MSCs while anti-inflammatory cytokines IL-10(105 ± 5 pg/ml versus 17 ± 2 pg/ml, p<0.001)and IL-4 (16.3 ± 8.2 pg/ml versus 4.1 ± 1.8 pg/ml, p<0.001) were up-regulated. In addition, MSCs-inhibited T cells were not apoptotic during 5 days’ culture. Conclusion HUCB-MSCs possessed could inhibit the activity of allogeneic peripheral blood T lymphocytes.
    The effect of PGE-interferon-alpha2a on peripheral T lymphocyte subsets in Patients with chronic hepatitis B
    2011, 31(10):  1139-1143. 
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    【Abstract】 Objective To study the changes of peripheral T lymphocyte subsets and its significance in patients with chronic hepatitis B (CHB) during peginterferon-alph2a treatment. Method Fifty-two patients with chronic hepatitis B were recruited and received peginterferon-alph2a treatment for 48 weeks .Before and during the 12 and 48 weeks of treatment, flow cytometry was used to detect the Peripheral T lymphocyte subsets. Realtime PCR was used to detect the levels of HBV DNA in the serum. Markers of hepatitis B virus infection were detected by ELISA assay and levels of alanine aminotransferase in the serum were also measured by automatic biochemical analyzer. Results The proportion of peripheral blood CD4+、CD4+ / CD8+ in patients with CHB was significantly lower than that in healthy people(P<0.05) and the proportion of peripheral blood CD8+T lymphocytes are increasing(P<0.05). During 12 weeks of INFa treatment the proportion of peripheral blood CD4+T lymphocytes and the ratio of CD4+ / CD8+ increased gradually, the proportion of peripheral blood CD8+T lymphocytes decreased to normal level after 48 weeks’ INFa treatment. At 12 and 48 weeks of INFa treatment resulted in HBeAg negativity in 44.2% patients and 51.9% patients respectively. In 11(21.1%) patients who had seroconvertion from HBeAg to anti-HBeAg, after 12 months of INFa treatment, their proportion of peripheral blood CD4+、CD4+ / CD8+ had increased to level similar to that of the healthy people. Conclusions INFa treatment reduces HBV replication and increases the proportion of peripheral blood CD4+、CD4+ / CD8+ and these patients are prone to have higher sustain virus response and higher biochemical response.
    The usage of three-dimension-image co-registration technique in invasive EEG mornitoring
    2011, 31(10):  1144-1148. 
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    Objective: To confirm the location of the electrode contacts which were implanted into the cranium. Methods: Ten patients who suffering intractable epilepsy underwent intracranial electrodes implantation. Before and after the electrodes implantation head MRI and CT scan were done respectively, then the 3D image data of MRI and CT were co-registered. Results: We got the 3D infused images form which we can easily observe the relationship between cerebrum and the electrode contacts. we can easily see the location of each contact directly and then to conduct the following mapping through the infused images. Conclusion: 3D digital images co-registration technique is useful to confirm the accurate location of the implanted electrode contacts.
    Arrhythmia caused by Sjogren’s syndrome complicated with primary biliary cirrhosis
    2011, 31(10):  1149-1150. 
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    To present a case of multiple arrhythmia caused by Sjogren’s syndrome complicated with primary biliary cirrhosis. To improve the knowledgement of physicians to such kind of patients.
    Protect of Cold Acclimation on Myocardium of Cold Exposure Rat
    2011, 31(10):  1154-1155. 
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    【Absrtact】:Objective:To establish rat model of cold acclimation by different cold exposure,and to form foundation on studying the molecule mechanisms of cold acclimation. Methods:60Sprague-Dawley rats were randomly divided into 3groups with 20 in each, control group ,4℃cold exposure 4h/d group,0℃cold exposure 10h/d group.The plasma levels of monoamine neurotransmitters were analyzed by HPLC-ECD techniques;the content of plasma corticosterone was evaluated by radioactivity immunoassay;myeloperoxidase(MPO) activity of the myocardium were measured by colorimetric method.Results:In different cold stress,plasma levels of monoamine neurotransmitters and corticosterone significantly different(P<0.05).Compared with the cold exposure group,the plasma LDH,CK-MB and myocardium MPO activities in cold acclimation rats after cold exposure were significantly decreased(P<0.05).Conclusion: cold acclimation rat model is established,and cold acclimation can attenuate the myocardial damage caused by cold exposure.
    The role of bone marrow mesenchymal stem cells transp1antation in the treatment of miniature swine acute myocardial infarction model
    2011, 31(10):  1156-1158. 
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    To investigate the treatment role of bone marrow mesenchymal stem cell (MSCs) transp1antation on the model of acute myocardial infarction (AMI) and to observe the survived and transformationed MSCs in the infracted heart after 3 months. Methods: After established models of AMI, 20 miniswines were randomly divided into four groups (n=6), Model group: the animals only established models of AMI; Saline group: AMI immediately followed by saline injection take the place of MSCs implantation; MSCs group: AMI immediately followed by MSCs implantation. Three months after operation, detection the cardiac function in each group and observation the bone marrow-derived mesenchymal stem cell survival and transformation by Immunofluorescence microscopy. Result: Three months later, the ejection fraction (EF%) was significantly improvement in MSCs group [(50.2±5.3)% and (58.9±1.5), P<0.01] compared with saline group and the mass defect percentage(%) was decreased [(1.95±0.22)% and (-1.75±0.19)%, P<0.05] in MSCs group compared with saline group importantly, Immunofluorescence and histochemical results confirm that transplanted MSCs still alive after 3 months, and part of the experiment appears to have differentiated into cardiomyocytes and vascular endothelial cells. Conclusion: MSCs transplantation by directly injection into myocardial infarction can survive 3 months and differentiated into cardiomyocytes and vascular endothelial cells, on the other hand, the same kinds of the opposite sex MSC transplantation can improve cardiac function on the model of acute myocardial infarction .
    The Effect of Smoking On Expressing of Histone Deacetylase 2 in the Lung Tissues of COPD Rats
    2011, 31(10):  1159-1160. 
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    Abstract:Objective To investigate the relationship of histone deacetylase 2 (HDAC2) and the inflammation of chronic obstructive pulmonary disease (COPD) by detecting its expression in lung tissues of COPD rats and normal rats. Methods:We made the COPD rat model by cigarette smoking. According to the time of COPD formation, we divided the rats into four groups, there were 10 rats in every group including the control group. The expression of HDAC2 protein and mRNA were detected by immunohistochemical and in situ hybridization assays. Results:The A values of HDAC2 protein and mRNA in COPD rats lung tissues were lower than that of normal rats (p<0.05). And between the COPD groups the differences were significant (p< 0.05). Conclusion:The expression of HDAC2 in COPD rats was lower than that of normal rats, and depresseded with the progression of COPD.
    Parkinson’s disease and advances in ATP13A2 gene research
    2011, 31(10):  1161-1164. 
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    Parkinson’s disease (PD) is the second most frequent neurodegenerative disease after Alzheimer’s disease, with the cause is the co-activation of environmental and genetic factors. Sixteen gene loci and 11 disease genes have been identified. ATP13A2 gene located on PARK9 implicated in Kufor-Rakeb syndrome (KRS)and early-onset Parkinson’s disease(EOPD). This review will describe the advances concerning the ATP13A2 mutations in PD patients and function of this gene.
    Progress of study on functions of RIP1 in cell signal transduction
    2011, 31(10):  1165-1167. 
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    Since the discovery of the first member ten years ago, the receptor-interacting protein (RIP) family kinases have emerged as essential sensors of cellular stress.The different members integrate both extracellular stress signals transmitted by various cell-surface receptors and signals emanating from intracellular stress. The cascades of events initiated by activated RIPs are complex. Not only are pro-survival, inflammatory and immune responses triggered by RIP kinases via the activation of transcription factors such as NF-κB and AP-1, but opposing, death-inducing programs can also be initiated by the RIP kinases. Hence, RIP kinases are crucial regulators of cell survival and cell death. This article summarizes the recent progress of RIP1 about its expression and function.
    Focusing on the Development and Current Status of International Translational Medicine by Bibliometric Analysis
    WANG Min
    2011, 31(10):  1168-1175. 
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    This study conducts a bibliometric analysis of translational medicine by collecting 5417 papers from Web of Science (WOS) for the period of 1900-2011.Based on bibliometric method, co-occurrence method, citation analysis and some other methods for information visualization, the paper presents a overview of the development process, research model, subject structure and some main contents on translational medicine abroad, which may give a reference to translational medicine research in China.
    Systemic Effects of Chronic Obstructive Pulmonary Disease
    2011, 31(10):  1176-1180. 
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    Chronic Obstructive Pulmonary Disease(COPD)is a common disease, the characteristic of which is airflow limitation and airway remodeling, thus worsening the structure and function of the lung. COPD is not only implicated in the lung, but involve in some other extrapulumonary effects, also called systemic effects, through the systemic inflammation caused by the activation of inflammation mediators. The most frequent systemic effects are: skeletal muscle wasting, cachexia, osteoporosis, etc. And the prevalences of ischemic heart disease, pulmonary hypertension, diabetes mellitus are higher in COPD patients because of the chronic inflammation.
    Recent advances on angiogenesis inhibitor of vasohibin
    2011, 31(10):  1185-1188. 
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    Angiogenic balance in physiological conditions is determined by the levels of angiogenesis activators and inhibitors. Vasohibin is a negative feedback regulator of angiogenesis inhibitor that can be induced by VEGF or bFGF. Vasohibin may play an important role in the regulation of angiogenesis under physiological and pathological conditions. Currently, vasohibin is an important research topic in a relevant field of medicine.