Involvement of endoplasmic reticulum stress in apoptosis of testicular cells induced by low-dose radiation / 华中科技大学学报（医学）（英德文版）

The study examined the role of endoplasmic reticulum stress (ERS) and signaling pathways of inositol-requiring enzyme-1 (IRE1), RNA-activated protein kinase-like ER kinase (PERK) and activating transcription factor-6 (ATF6) in apoptosis of mouse testicular cells treated with low-dose radiation (LDR). In the dose-dependent experiment, the mice were treated with whole-body X-ray irradiation at different doses (25, 50, 75, 100 or 200 mGy) and sacrificed 12 h later. In the time-dependent experiment, the mice were exposed to 75 mGy X-ray irradiation and killed at different time points (3, 6, 12, 18 or 24 h). Testicular cells were harvested for experiments. H(2)O(2) and NO concentrations, and Ca(2+)-ATPase activity were detected by biochemical assays, the calcium ion concentration ([Ca(2+)]i) by flow cytometry using fluo-3 probe, and GRP78 mRNA and protein expressions by quantitative real-time RT-PCR (qRT-PCR) and Western blotting, respectively. The mRNA expressions of S-XBP1, JNK, caspase-12 and CHOP were measured by qRT-PCR, and the protein expressions of IRE1α, S-XBP1, p-PERK, p-eIF2α, ATF6 p50, p-JNK, pro-caspase-12, cleaved caspase-12 and CHOP by Western blotting. The results showed that the concentrations of H2O2 and NO, the mRNA expressions of GRP78, S-XBP1, JNK, caspase-12 and CHOP, and the protein expressions of GRP78, S-XBP1, IRE1α, p-PERK, p-eIF2α, ATF6 p50, p-JNK, pro-caspase-12, cleaved caspase-12 and CHOP were significantly increased in a time- and dose-dependent manner after LDR. But the [Ca(2+)]i and Ca(2+)-ATPase activities were significantly decreased in a time- and dose-dependent manner. It was concluded that the ERS, regulated by IRE1, PERK and ATF6 pathways, is involved in the apoptosis of testicular cells in LDR mice, which is associated with ERS-apoptotic signaling molecules of JNK, caspase-12 and CHOP.

Involvement of endoplasmic reticulum stress in apoptosis of testicular cells induced by low-dose radiation / 华中科技大学学报（医学）（英德文版）

The study examined the role of endoplasmic reticulum stress (ERS) and signaling pathways of inositol-requiring enzyme-1 (IRE1), RNA-activated protein kinase-like ER kinase (PERK) and activating transcription factor-6 (ATF6) in apoptosis of mouse testicular cells treated with low-dose radiation (LDR). In the dose-dependent experiment, the mice were treated with whole-body X-ray irradiation at different doses (25, 50, 75, 100 or 200 mGy) and sacrificed 12 h later. In the time-dependent experiment, the mice were exposed to 75 mGy X-ray irradiation and killed at different time points (3, 6, 12, 18 or 24 h). Testicular cells were harvested for experiments. H2O2 and NO concentrations, and Ca(2+)-ATPase activity were detected by biochemical assays, the calcium ion concentration ([Ca(2+)]i) by flow cytometry using fluo-3 probe, and GRP78 mRNA and protein expressions by quantitative real-time RT-PCR (qRT-PCR) and Western blotting, respectively. The mRNA expressions of S-XBP1, JNK, caspase-12 and CHOP were measured by qRT-PCR, and the protein expressions of IRE1α, S-XBP1, p-PERK, p-eIF2α, ATF6 p50, p-JNK, pro-caspase-12, cleaved caspase-12 and CHOP by Western blotting. The results showed that the concentrations of H2O2 and NO, the mRNA expressions of GRP78, S-XBP1, JNK, caspase-12 and CHOP, and the protein expressions of GRP78, S-XBP1, IRE1α, p-PERK, p-eIF2α, ATF6 p50, p-JNK, pro-caspase-12, cleaved caspase-12 and CHOP were significantly increased in a time- and dose-dependent manner after LDR. But the [Ca(2+)]i and Ca(2+)-ATPase activities were significantly decreased in a time- and dose-dependent manner. It was concluded that the ERS, regulated by IRE1, PERK and ATF6 pathways, is involved in the apoptosis of testicular cells in LDR mice, which is associated with ERS-apoptotic signaling molecules of JNK, caspase-12 and CHOP.

Reliability and validity of Chinese version of the Addiction Severity Index among drug users in the community / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To assess the reliability and validity of a new Chinese version of the Addiction Severity Index (ASI-C) in drug users in the community.</p><p><b>METHODS</b>Three hundred and eighty-one drug users in the community in Chengdu, Sichuan province were recruited. They were interviewed with a questionnaire consisting of the ASI-C revised on the basis of the previous Chinese version and 38 were interviewed for the second time at an interval of 7 days to evaluate test-retest reliability.</p><p><b>RESULTS</b>Cronbach's α coefficients for the internal consistency of the scale varied from 0.49 to 0.86. Test-retest correlation coefficients ranged from 0.50 to 0.93. Criterion validity was found acceptable, as compared with the Symptom Checklist 90 (SCL-90).</p><p><b>CONCLUSION</b>The ASI-C presented acceptable reliability and validity in a sample of drug users in the community.</p>

Application of multi-coeffieient of variation significance test for toxicology study / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To establish the methods of calculating and analyzing the multi-coefficient of variation significance test for the toxicology study.</p><p><b>METHODS</b>The paper aimed to confirm the significance level with the method of Bonferroni and then compared the methods of calculating and analyzing of the experiment groups with the control group respectively.</p><p><b>RESULTS</b>The significance level of multi-coefficient of variation significance test was confirmed as alpha1=0.0167. Compared with the control groups, the activity of ALT in serum both in 30 mg/kg and 60 mg/kg groups did not change in the average significance test, which was not statistically significant (P>0.05), while it changed in the variation significance test, which was of statistical significance (P<0.0167). The activity of AST in serum in 60 mg/kg group did not change in the average significance test (P>0.05), while it changed in the variation significance test (P<0.0167).</p><p><b>CONCLUSION</b>The complete changes of the indexes can only be shown by use of both the average significance test and the variation significance test together.</p>

Effects of over-expressed Smac gene coupling with cisplatin on proliferation and apoptosis of hepatocarcinoma cells / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To investigate the effects of over-expressed Smac gene combined with cisplatin (CDDP) on proliferation and apoptosis of hepatic carcinoma cells.</p><p><b>METHODS</b>The recombinant plasmid pcDNA3.1+-hSmac was introduced into the human hepatic carcinoma SMMC-7721 cells using a liposome-mediated method. The expression of Smac protein was detected by Western blot and flow cytometry. The cells were treated with three different doses of CDDP, 5, 15 and 25microg/ml, for 24 hours after the transfection. MTT colorimetry was used to detect the cellular growth-inhibitory effects; acridine orange-ethidium bromide fluorescent staining (AO/EB) and flow cytometry with annexin V-PI double staining</p><p><b>METHODS</b>were used to detect the changes of cell apoptosis.</p><p><b>RESULTS</b>Western blot and flow cytometry results demonstrated that the Smac protein level in SMMC-7721 cells was significantly increased after the transfection (P less than 0.01). Compared with that of the control group, the over-expressed Smac gene inhibited the cell growth and induced cell apoptosis (P less than 0.01). After being treated with CDDP, the inhibitory rates were increased significantly with increasing concentrations of CDDP compared with that of the control group, and the inhibitory rate of the CDDP-treated plus Smac group was significantly higher than that of the CDDP-treated group (P less than 0.01). The results detected by AO/EB and flow cytometry demonstrated that the apoptotic rates of CDDP-treated plus Smac group were higher than those of the CDDP-treated group (P less than 0.01). The results demonstrated that the Smac over-expression enhanced the effects of cell growth inhibition and apoptotic promotion induced by CDDP.</p><p><b>CONCLUSION</b>The pro-apoptotic Smac gene could be over-expressed in hepatocarcinoma SMMC-7721 cells and inhibit cell growth and induce apoptosis. Moreover the over-expressed Smac could enhance the chemotherapeutic sensitivity of SMMC-7721 to cisplatin. This experimental work may help in further study on the regulatory mechanism of Smac in apoptosis and improve the chemotherapeutic effect on hepatoma.</p>