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1.
Chinese Journal of Industrial Hygiene and Occupational Diseases ; (12): 932-936, 2011.
Article in Chinese | WPRIM | ID: wpr-273571

ABSTRACT

<p><b>OBJECTIVE</b>To explore the effects of workplace violence on sub-health status of nurses and to provide the theoretical basis for preventing the workplace violence in the hospitals and improving the health status of nurses.</p><p><b>METHODS</b>A total of 679 nurses were selected by using stratified cluster sampling method. The Chinese version of workplace violence scale (WVS) and sub-health scale were used to measure workplace violence and sub-health status, respectively.</p><p><b>RESULTS</b>The subjects with middle age (30-45 years) were found to have the highest incidence of physical assault (24.5%) and emotional assault (52.2%) as compared with other subjects (P<0.05). The prevalence (23.6%) of emotional assault of subjects with lowest education levels was significantly lower than that of others (P<0.05). The nurses with work shift were more vulnerable to emotional assault (45.1%) than those without work shift (36.8%)(P<0.05). The prevalence of the workplace violence of nurses in the psychiatric department and emergency department was significantly higher than that of nurses in other departments (P<0.05). The results of multivariate analysis showed that workplace violence was an important risk factor for sub-health status of nurses when other potential confounding factors were taken into account.</p><p><b>CONCLUSION</b>The results of present study showed that workplace violence plays an important role in sub-health status of nurses after adjusting other potential confounding factors. It is important to develop the prevention strategies for reducing the incidence of workplace violence and improving the sub-health status of nurses.</p>


Subject(s)
Adolescent , Adult , Humans , Middle Aged , Young Adult , Health Status , Nursing Staff, Hospital , Psychology , Occupational Health , Surveys and Questionnaires , Violence , Workplace , Psychology
2.
Chinese Journal of Industrial Hygiene and Occupational Diseases ; (12): 270-274, 2011.
Article in Chinese | WPRIM | ID: wpr-272626

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the protective effects of the tert-butylhydroquinone (tBHQ) pretreatment on neurotoxicity and oxidative stress induced by paraquat (PQ) in PC12 cells.</p><p><b>METHODS</b>Cytotoxicity of PC12 cells was measured by MTT assay, following the PC12 cells treatment with different concentrations of 100, 300 micromol/L PQ for 24 h and 48 h. PC12 cells were pretreated with or without 40 micromol/L tBHQ for 4 h, PC12 cells were exposed to PQ at the doses of 0, 100, 300 micromol/L for 24 h and 48 h, respectively. The viability of PC12 cells was measured by MTT assay, the apoptosis rates of PC12 cells were detected by flow cytometry (FCM) and the malondialdehyde (MDA) levels of PC12 cells were examine by thiobarbituric acid (TBA) method.</p><p><b>RESULTS</b>When the exposure doses of PQ were 100 and 300 micromol/L for 24 h, the viability of PC12 cells pretreated with tBHQ was significantly higher than that of PC12 cells only exposed to PQ (P < 0.05 or P < 0.01). When the exposure dose of PQ was 100 micromol/L for 48 h, the viability of PC12 cells pretreated with tBHQ was significantly higher than that of PC12 cells only exposed to PQ (P < 0.01). When the exposure doses of PQ were 100 and 300 micromol/L for 24 h, the apoptosis rates and MDA levels of PC12 cells pretreated with tBHQ were significantly lower than those of PC12 cells only exposed to PQ (P < 0.05 or P < 0.01).</p><p><b>CONCLUSIONS</b>tBHQ pretreatment can reduce the cytotoxicity, apoptosis and oxidative stress induced by PQ in PC12 cells.</p>


Subject(s)
Animals , Rats , Apoptosis , Cell Survival , Hydroquinones , Pharmacology , Oxidative Stress , PC12 Cells , Paraquat , Toxicity , Reactive Oxygen Species
3.
Chinese Journal of Industrial Hygiene and Occupational Diseases ; (12): 2-6, 2011.
Article in Chinese | WPRIM | ID: wpr-293770

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the effect of paraquat on induction of cell damage and miR-133b expression in PC12 cells.</p><p><b>METHODS</b>Cytotoxicity of PC12 cells was measured by MTT assay, following the PC12 cells treatment with 50, 100, or 300 µmol/L paraquat. Cell apoptosis was examined by the method of Annexin V-FITC/PI in flow cytometry (FCM) and the relative level of miR-133b expression was measured by real time RT-PCR, following the PC12 cells treatment with 100 or 300 µmol/L paraquat.</p><p><b>RESULTS</b>Survival rate of PC12 cells treated with 100 or 300 µmol/L paraquat was lower than that of the vehicle control group (P < 0.01, P < 0.05), in the dose dependent pattern. Apoptotic rate of PC12 cells treated with 100, 300 µmol/L paraquat was higher than that of the vehicle control group (P < 0.05). The relative level of miR-133b expression of PC12 cells treated with 300 µmol/L paraquat was higher than that of the vehicle control group (P < 0.05).</p><p><b>CONCLUSIONS</b>Paraquat may cause cell damage and induce apoptosis in PC12 cells, and induce miR-133b expression.</p>


Subject(s)
Animals , Rats , Apoptosis , MicroRNAs , Metabolism , PC12 Cells , Paraquat , Toxicity
4.
Chinese Journal of Industrial Hygiene and Occupational Diseases ; (12): 593-596, 2009.
Article in Chinese | WPRIM | ID: wpr-352826

ABSTRACT

<p><b>OBJECTIVE</b>To explore the effect of deltamethrin (DM) on production of free radical and transcription factor Nrf2 in rats' brain tissue.</p><p><b>METHODS</b>8 male rats were randomly assigned to four groups and administered with 1% W/W tertiary butylhydroquinone (tBHQ) or olive oil for 3 days, prior to exposure to DM and then with 12.50 mg or 0mg DM/Kg BW for 5 days. The level of free radical in rats' hippocampus tissue was detected by electron spin resonance (ESR) spectroscopy. 18 male rats were randomly assigned to three groups and administered with i.p. (daily dose was respectively 0, 3.13, 12.50 mg/kg DM) for five days. After treatment, Nrf2 protein levels in the cytoplasmic and nuclear fractions of both cerebral cortex and hippocampus tissue were measured by western blot.</p><p><b>RESULTS</b>The level of free radical in hippocampus tissue of rats administered by DM and pretreatment with tBHQ prior to DM were increased to a 2.45-fold and 2.97-fold of values of control group, respectively (P < 0.05). Nrf2 protein levels in the cytoplasmic fractions of cerebral cortex of both low and high dose group were significantly increased, 1.68- fold and 1.34- fold of values of control group, respectively. Nrf2 protein levels in the nuclear fractions of cerebral cortex of both low and high dose group were increased in a dose- dependent model, 1.51-fold and 2.29-fold of values of control group, respectively (P < 0.01). Nrf2 protein levels in the cytoplasmic fractions of hippocampus tissue of both low and high dose group were increased in a dose- dependent model, 2.26-fold and 3.58-fold of values of control group, respectively. Nrf2 protein levels in the nuclear fractions of hippocampus tissue of both low and high dose group were increased, 2.42-fold and 2.45-fold of values of control group, respectively (P < 0.01).</p><p><b>CONCLUSION</b>The studies in vivo demonstrate that DM treatment could induce free radical production and expression of Nrf2 protein in both cerebral cortex and hippocampus tissue and activate Nrf2.</p>


Subject(s)
Animals , Male , Rats , Brain , Metabolism , Free Radicals , Metabolism , NF-E2-Related Factor 2 , Metabolism , Nitriles , Toxicity , Pyrethrins , Toxicity , Rats, Sprague-Dawley
5.
Chinese Journal of Industrial Hygiene and Occupational Diseases ; (12): 597-600, 2009.
Article in Chinese | WPRIM | ID: wpr-352825

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the protective effect of the tert-butylhydroquinone (tBHQ) on PC12 cells from neurotoxicity induced by manganese.</p><p><b>METHODS</b>Cytotoxicity of PC12 cells was measured by MTT assay, following the PC12 cells treatment with different concentrations of MnCl₂ (300, 600, 900 μmol/L) for 24, 48 or 72 h. PC12 cells were pretreated with 40 μmol/L tBHQ for 12 h, followed by the treatment of 600 micromol/L or 300 μmol/L MnCl₂ for 72 h. Cytotoxicity of PC12 cells was measured by MTT assay, and cell apoptosis was examined by the method of Annexin V-FITC/PI in flow cytometry (FCM).</p><p><b>RESULTS</b>The proliferation of PC12 cells treated with 300, 600, 900 μmol/L MnCl2 was suppressed in the dose dependent pattern (P < 0.01). Proliferation of PC12 cells treated with 600 μmol/L MnCl₂ was suppressed to 40% of that in control group (P < 0.01), but the proliferation rate of PC12 cell pretreated with 40 μmol/L tBHQ was 180% of that in control group (P < 0.01). Apoptotic rate of PC12 cells treated with 300 micromol/L MnCl₂ was higher than the vehicle control group (P < 0.01). Apoptotic rate of 40 μmol/L tBHQ pretreatment followed by 300 μmol/L MnCl₂ treatment was lower than that of MnCl2 treatment group (P < 0.01). The inhibition rate of apoptosis was 61%.</p><p><b>CONCLUSIONS</b>Manganese may suppress PC12 cells proliferation and induce apoptosis. tBHQ can reduce PC12 cells proliferation suppressed by manganese and attenuate the apoptosis induced by manganese.</p>


Subject(s)
Animals , Rats , Apoptosis , Cell Proliferation , Drug Antagonism , Hydroquinones , Pharmacology , Manganese , Toxicity , PC12 Cells
6.
Chinese Journal of Industrial Hygiene and Occupational Diseases ; (12): 273-277, 2006.
Article in Chinese | WPRIM | ID: wpr-342984

ABSTRACT

<p><b>OBJECTIVE</b>To study the effects of deltamethrin (DM) on the mRNA expression of copper-zinc dependent SOD (CuZn-SOD), glutathione reductase (GR) and gamma glutamylcysteine synthetase (gamma-GCS) light subunit (GCSl), as well as on expression of both mRNA and protein of gamma-GCS heavy subunit (GCSh) and NFE2 related factor 2 (Nrf2) in cerebral cortex and hippocampus of rats.</p><p><b>METHODS</b>Eighteen Wistar male rats were randomizedly divided into three groups, six for each group. The low dosage and high dosage DM treated groups were administrated intraperitoneally with DM (the daily dosage was 3.125, 12.500 mg/kg BWT respectively) for five consecutive days while the control group was administered intraperitoneally with olive oil. The relative amount of mRNA expression of these genes was measured by the method of reverse transcription polymerase chain reaction (RT-PCR) (n = 6). The protein level was detected by the method of immunohistochemistry and image analysis system (n = 4).</p><p><b>RESULTS</b>There was no change in mRNA expression level of CuZn-SOD, GR, GCSh and Nrf2 gene in both cerebral cortex and hippocampus tissue in rats administrated with DM. However, the mRNA level of GCSl gene in cerebral cortex of high dosage group as well as in both cerebral cortex and hippocampus of the low dosage group was significantly lower than that in corresponding tissue in the control group, and was decreased to 71.1%, 63.6% and 75.2% of mRNA level of corresponding tissue in the control group (P < 0.01). There was no obvious effect on protein level of both GCSh and Nrf2 in CA1, CA2, CA3 and dentate gyrus (DG) of hippocampus as well as on that in cerebral cortex in rats treated with DM.</p><p><b>CONCLUSION</b>Under the experimental conditions, there is no obvious effect in the mRNA expression level of CuZn-SOD, GR gene, as well as on expression of both mRNA and protein of Nrf2 gene in both cerebral cortex and hippocampus tissue in rats administered with DM. DM depresses the mRNA expression of GCSl gene, but does not affect the mRNA expression of GCSh gene.</p>


Subject(s)
Animals , Male , Rats , Cerebral Cortex , Metabolism , Dose-Response Relationship, Drug , Gene Expression , Glutamate-Cysteine Ligase , Genetics , Glutathione Reductase , Genetics , Hippocampus , Metabolism , NF-E2-Related Factor 2 , Genetics , Nitriles , Toxicity , Pyrethrins , Toxicity , RNA, Messenger , Genetics , Random Allocation , Rats, Wistar , Reverse Transcriptase Polymerase Chain Reaction , Superoxide Dismutase , Genetics
7.
Chinese Journal of Industrial Hygiene and Occupational Diseases ; (12): 16-19, 2005.
Article in Chinese | WPRIM | ID: wpr-346599

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the effect of cadmium (Cd) on estrogen receptor and to assess its endocrine disrupting action.</p><p><b>METHODS</b>The estrogen receptor rich supernatant was prepared from the ovariectomized Sprague-Dawley rats. The effects of cadmium on estrogen binding were performed using a sing-dose ligand-binding assay. Extract from uterus were treated with various concentrations of cadmium (0, 10(-3), 10(-5) or 10(-7) mol/L) for various pre-incubation time (0, 30, 60, 90 min) by means of orthogonal experimental design with orthogonal layout of L16(4(5)) (the experiment was repeated for 5 times). In addition to the radioinert competitor, each assay included a zero tube and a DES standard curve for quality control purpose. Data for cadmium and the DES standard curve were plotted as percent [3H]-E2 bound versus log (molar concentration), and the IC50 for cadmium was determined. The RBA for cadmium was calculated by dividing the IC50 of DES in terms of the IC50 of cadmium.</p><p><b>RESULTS</b>Cadmium could not block the binding of estradiol to the receptor because hormone binding did not change with increasing cadmium concentration or increasing preincubation time. The results showed that the binding of [3H]-estradiol to uterine cytosols was not significant (P > 0.05). The Bmax (its unit is pmol/mg protein) of various concentrations of cadmium (0, 10(-3), 10(-5) or 10(-7) mol/L) for pre-incubating 0 min is 203.15 +/- 75.16, 203.41 +/- 22.78, 220.82 +/- 45.35, 209.10 +/- 49.66 respectively; The Bmax of them for pre-incubating 30 min is 215.67 +/- 92.97, 139.79 +/- 53.78, 205.27 +/- 23.60, 172.63 +/- 55.09 respectively. The Bmax of them for pre-incubating 60 min is 197.11 +/- 50.68, 203.24 +/- 66.33, 183.92 +/- 31.89, 183.33 +/- 32.70, respectively. The Bmax of them for pre-incubating 90 min is 229.69 +/- 76.88, 175.70 +/- 70.28, 164.26 +/- 24.46, 150.78 +/- 65.97 respectively. Mean IC50 for cadmium is 10(-4) - 10(-3) M. If the affinities of DES binding to estrogen receptors was taken to be 100%, the relative binding affinities of cadmium was 10(-6) - 10(-7). The results indicated that cadmium had only a very poor affinity with estrogen receptor.</p><p><b>CONCLUSION</b>In vitro assay cadmium did not have distinct disrupting effect on binding of estradiol to estrogen receptors from rat uterine.</p>


Subject(s)
Animals , Female , Rats , Cadmium , Toxicity , In Vitro Techniques , Rats, Sprague-Dawley , Receptors, Estrogen , Metabolism , Uterus , Metabolism
8.
Chinese Journal of Experimental and Clinical Virology ; (6): 383-386, 2005.
Article in Chinese | WPRIM | ID: wpr-333000

ABSTRACT

<p><b>BACKGROUND</b>To further probe into the role of CD178 in the pathogenesis of hemorrhagic fever with renal syndrome (HFRS).</p><p><b>METHODS</b>The expression of CD178 and HLA-DR on T cell subsets in peripheral blood of patients with HFRS and their dynamic changes were detected by Flow cytometry.</p><p><b>RESULTS</b>CD4+ CD178+ and CD8+ CD178+ T lymphocytes both in fever and polyuria phases were significantly higher than those in normal controls, while there was no significant difference between the both phases of HFRS (P > 0.05). CD178 expression on CD4+ HLA-DR+ and CD8+ HLA-DR+ T lymphocytes were significantly higher than those in normal controls (P < 0.05, P < 0.01, P < 0.001, P < 0.001), while there was no significant difference between CD4+ HLA-DR+ and CD8+ HLA-DR+ T lymphocytes (P > 0.05).</p><p><b>CONCLUSION</b>CD178 was expressed on both CD4+ and CD8+ T cell subsets, but mainly on CD8+ T cell subsets both in early stage and in later stage in the pathogenesis of HFRS. Cytotoxic T lymphocyte (CTL) might kill target cells infected by hantavirus (HV) and eliminate HV via cell apoptosis mediated by CD178 in early stage of HFRS. In later stage of HFRS, CD178 might reduce antigen-specific T lymphocytes by activation induced cell death (AICD) and help to maintain the homeostasis of immune system.</p>


Subject(s)
Adolescent , Adult , Female , Humans , Male , Middle Aged , Young Adult , CD4-Positive T-Lymphocytes , Cell Biology , Allergy and Immunology , CD8-Positive T-Lymphocytes , Cell Biology , Allergy and Immunology , Fas Ligand Protein , Allergy and Immunology , Flow Cytometry , Hemorrhagic Fever with Renal Syndrome , Blood , Allergy and Immunology , Hemorrhagic Fevers, Viral , Blood , Allergy and Immunology , T-Lymphocyte Subsets , Cell Biology , Allergy and Immunology
9.
Chinese Journal of Epidemiology ; (12): 852-855, 2004.
Article in Chinese | WPRIM | ID: wpr-325019

ABSTRACT

<p><b>OBJECTIVE</b>To study the relationship between cadmium pollution and its adverse effects on female reproductive health status in people living in cadmium polluted area in Zhenghe, Fujian provinces.</p><p><b>METHODS</b>Data through laboratory studies on reproductive health of female residents in Cd-pollution area were studied and compared with those in control areas in Zhenghe.</p><p><b>RESULTS</b>Both prevalence rates of abnormal menstrual cycle and dysmenorrhea in unmarried women in Cd-pollution area (19.1% vs. 42.6%) were significantly higher than those in control area (5.7% vs. 18.9%) and the rates of sterility in married women in Cd-pollution area (6.3%) were significantly higher than those in control area (1.1%). During the first two pregnancies, rates of queasiness, disgorgement, spontaneous abortion and stillbirth in married women in polluted area were 44.7%, 31.7%, 10.27% and 4.23%, significantly higher than those 26.5%, 17.8%, 2.85% and 1.05% in control area, with significant differences (P < 0.05). Results from cumulative odds model analysis showed that: living in Cd-pollution area was a possible risk factor related to female reproductive health (OR = 2.072), after the other risk factors being under control.</p><p><b>CONCLUSION</b>The female reproductive health status of people residing in the cadmium polluted area had already been deteriorated.</p>


Subject(s)
Adult , Female , Humans , Abortion, Spontaneous , Epidemiology , Cadmium , China , Epidemiology , Dysmenorrhea , Epidemiology , Environmental Pollutants , Infertility, Female , Epidemiology , Risk Factors
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