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Background The mining of non-coal underground mines may come into contact with various types of dust, such as lead, zinc, copper, and non-metallic minerals. Dust of various kinds commonly exists in all aspects of mining and selection, and is one of the main occupational hazard groups in non-coal underground mines. Objective To compare the application of two risk assessment methods in the occupational health risk assessment of productive dust in non-coal underground mines, and to provide a reference for the selection of dust hazard health risk assessment methods and the management of dust hazards in non-coal mines. Methods A field investigation of the dust hazards of three typical non-coal underground mining enterprises (lead-zinc mines, copper mines, and fluorite mines) was carried out, and the comprehensive index method and the occupational health risk assessment method from the International Council on Mining and Metals (ICMM) were used to perform risk assessments. The comprehensiveindex method considers the following factors: dust monitoring data, the aerodynamic diameter of dust, hazard control measures, occupational health management, daily usage, and daily exposure time to determine exposure levels. The ICMM method determines the risk level based on the consequences caused by dust, exposure probability, exposure time, and uncertainty coefficient. Kendall consistency test was used to compare agreement between the results generated by the two methods. Results The results generated by the comprehensive index method were as follows: level 3 (medium risk) or level 4 (high risk) for silica dust or lead dust; level 1 (negligible risk) or level 2 (low risk) for other dust (dust with free SiO2 content<10% and containing lead, zinc, and copper, using other dust limit values for comparison), fluorspar mixed dust, fluorine and its compounds, zinc oxide, and copper dust. The risk levels graded by the ICMM method were as follows: level 4 (very high risk) and level 3 (high risk) for exposure to silica dust and lead dust, respectively, and level 1 (tolerable risk) or level 2 (potential risk) for exposure to other dust (dust with free SiO2 content <10% and containing lead, zinc, and copper, using other dust limit values for comparison), fluorspar mixed dust, fluorine and its compounds, zinc oxide, and copper dust. The consistency level between the results graded by the two methods was very high (Kendall W coefficient=0.974, P < 0.05). Conclusion For the occupational health risk assessment of productive dust in non-coal underground mines, the consistency level of risk assessment results between the ICMM method and the comprehensive index method is very high. The ICMM method is more convenient to operate and should be preferred in assessing health risks of dust hazard in non-coal underground mines.
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Background The complex and diverse occupational disease hazards in automobile manufacturing industry pose high occupational health risks to workers. Objective To explore the methods that can accurately reflect the workplace health risk grade of automobile manufacturing enterprises, and to guide enterprises to practice risk classification management. Methods Comprehensive index method, International Commission on Mining and Metals occupational health risk assessment method (ICMM method), and risk index method were used toassess health risks of occupational disease hazards in major workstations such as welding, polishing, and painting in three automobile manufacturing enterprises in Hunan Province. Kappa consistency test was used to test the grading results of the three assessment methods. The re-examine results and detection rate of contraindications of occupational health examinations in the past three years were used to verify the assessment results. Results The results of comprehensive index method showed that the hazards of each selected workstation in enterprises A and B were evaluated as grade 2-3, among which NO2 in enterprise A was grade 3, and welding fume, NO2, and formaldehyde in enterprise B were all grade 3. The hazards of each selected workstation in enterprise C were grade 3-4, among which NO2 and benzene in were grade 4, and welding fume, manganese and its compounds, grinding wheel dust, and xylene were grade 3. The hazards evaluated by ICMM quantitative method were grade 2 and grade 5, among which manganese and its compounds in enterprise A and welding fume, grinding wheel dust, and benzene series in enterprise C were graded as grade 5. The hazards evaluated by risk index method were grade 1-4, among which manganese and its compounds in enterprises A and B were grade 3, and manganese and its compounds and benzene in enterprise C were grade 4. The Kappa value between comprehensive index method and ICMM method was 0.084 (P>0.05), that between comprehensive index method and risk index method was −0.046 (P>0.05), and that between ICMM method and risk index method was 0.014 (P>0.05), indicating poor consistency. By comparing the results of occupational health surveillance with the results of occupational health risk assessment, one worker was found to have occupational contraindication of manganese exposure and 1 worker was found to have excessive manganese in hair in enterprise A. However, the comprehensive index method graded low risk for manganese and its compounds in enterprise A and the result is conservative. The key workstations identified by ICMM method were consistent with the occupational health examination results, but the assessment grades were all extremely high risk, and the results were too strict. One worker was found to be contraindicated to welding fumes, and 2 polishers were found to have severe mixed pulmonary ventilation dysfunction in enterprise C. Mild and moderate pulmonary ventilation dysfunction was found to be common in welding and polishing workstations in each enterprise. The assessment results of welding fumes and grinding wheel dust by the risk index method were negligible risks, which were inconsistent with the occupational health examination results. Conclusion The comprehensive index method, ICMM method, and risk index method can basically identify workstations with serious occupational hazards, but they have certain limitations and applicability. In general, the evaluation results of the comprehensive index method were generates more consistent with the results with occupational health surveillance than the other two methods, is more comprehensive and objective in consideration, and is more suitable for health risk assessment of automobile manufacturing enterprises.
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Obsessive-compulsive disorder (OCD), which has the main clinical features of intrusive obsessions and compulsive behaviors, is listed as one of the top ten disabling diseases by the World Health Organization.Error related negativity(ERN) is a neurocognitive alarm signal in the case of errors.The individual differences in the ERN reflect the variability in reactivity to errors and to an internally generated threat.More and more studies have reported that ERN amplitudes in OCD have significantly increased.As a result, overactive error-monitoring is a core dysfunction disorder in OCD, which is closely related to the key symptoms of OCD including worry, doubt, repeating check behaviors.In addition, the increased ERN amplitudes are expected to serve as a diagnostic or predictive marker of OCD as well as a potential intervention target of this disease.Therefore, further understanding about the relationship between ERN and pathophysiology of OCD plays an important role in the effective diagnosis and treatment of OCD.The current paper aims to review the research results of ERN in patients with OCD and explore the following issues: the common experiment paradigms of ERN in OCD, the brain region sources of ERN in OCD, the characteristic manifestations of ERN in OCD, influencing factors of ERN and clinical value and application of ERN in OCD.In a word, it will provide reference for clinical practice and scientific research in the future.
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Objective To study the relationship between CDC25A (cell division cycle 25A) expression and the development of gastric adenocarcinoma. hTe effect of artesunate (Art) on CDC25A and gastric cancer cells were also investigated.Methods hTe CDC25A protein expression in gastric adenocarcinoma was detected by lfow cytometry assay. SGC-7901 cells were divided into four groups: control group and 30, 60, 120μmol/L Art groups. Cell apoptosis, cell cycle and CDC25A protein expression in SGC-7901 cells were determined by lfow cytometry atfer the treatment of different concentrations of Art (30, 60, 120μmol/L) for 24h, while the same volume of saline was used in the control.Results CDC25A protein expression level in gastric adenocarcinoma (419.69±21.91) was signiifcantly higher than that in normal gastric tissues (316.11±24.23,P<0.01). hTe cell apoptosis rates of 30, 60, 120μmol/L Art groups (5.48%±0.67%, 12.55%±1.17%, 23.43%±2.18%) were significantly higher than that of control group (0.87%±0.14 %,P<0.05), with an Art dose dependent manner. hTe cell proliferation indices of 30, 60, 120μmol/L Art groups (39.18%±0.53%, 35.71%±0.99%, 31.73%±1.02%) were signiifcantly lower than that of control group (44.12%±2.51%,P<0.01). hTe CDC25A protein expression levels of 30, 60, 120μmol/L Art groups (414.80±4.06, 397.86±3.61, 345.68±7.11) were significantly lower than that of control group (433.99±1.56,P<0.01).ConclusionhTe abnormally increased expression level of CDC25A may be involved in the development of gastric adenocarcinoma. Art can inhibit the growth of SGC-7901 cells by down-regulating the expression of CDC25A protein.
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Objective To investigate the effects of periplocin from Cortex Periplocae (CPP) on apoptosis of human lung cancer A549 cells and expression of survivin, and demonstrate its anti-tumor effect and the possible mechanism. Methods Inhibitory effect of CPP at different concentrations (1. 25, 2. 50, 5. 00, 10. 00, 20. 00 ng·mL-1 ) and for different time length (24, 48, 72 h) on A549 cell proliferation was tested by MTT method. Apoptosis rate of A549 cells treated with CPP at different concentrations (2. 50, 5. 00, 10. 00 ng·mL-1 ) were measured using flow cytometry (FCM) for 6, 12, 24, 48, 72 h, respectively. The morphological and ultrastructural changes of the apoptosis cells were observed by acridine orange/ ethidium bromide (AO/ EB) staining and transmission electron microscopy (TEM). The effects of CPP on mRNA and protein expression of apoptosis associated gene survivin were assessed by RT-PCR and Western blotting. Results CPP could significantly inhibit the growth of A549, and the inhibition rate reached (93. 46±2. 35)% . The results of FCM showed that the apoptosis rate of A549 cells treated with CPP was increased significantly as compared to the control group ( P<0. 05). Meanwhile, typical apoptotic peaks were detected. The characteristic morphological changes of apoptosis were observed in A549 exposed to CPP, including cell shrinkage, the nuclei became yellow-red by AO/ EB staining, and typical ultrastructural changes, including nuclear chromatin condensation along the nuclear membrane, vacuolar degeneration of cytoplasm observed by TEM. The result of RT-PCR indicated that survivin mRNA expression decreased obviously in A549 cells exposed to CPP. The protein expression of survivin in A549 cells treated with 10. 0 ng·mL-1 CPP(0. 251±0. 012)was weaker than that in control group(0. 928±0. 016). Conclusion CPP can induce apoptosis in human lung cancer cell lines A549, and the probable mechanism is related to the down-regulation of survivin mRNA and protein.
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Objective To investigate the inhibitory effects of periplocin from cortex periplocae (CPP) on human lung cancer cell line QG56 and to discuss its mechanism. Methods QG56 cells were cultured in vitro. The final concentrations of CPP in control group were 1.25, 2.50, 5.00, 10.00 and 20.00μg/L. QG56 cells were treated with ascending concentration of CPP for 24 h, 48 h and 72 h. The cell proliferation was measured using MTT method. The morphological changes of QG56 cells were observed under inverted microscope. Flow cytometry (FCM) was used to detect the effects of CPP on cell cycle and cell apoptosis. The expression of apoptosis associated gene bax mRNA in QG56 cells was detected by RT-PCR. The expres-sion of bax protein before and after treatment of CPP was examined by SP immunocytochemistry. Results The inhibitory ef-fect of CPP on the proliferation of QG56 cells was increased with the increasing concentrations of CPP and the prolonged du-ration of treatment. The morphological changes were displayed in QG56 exposed to CPP. The results of FCM showed that CPP caused cell cycle arrest at G0/G1 phase. The apoptotic rate of QG56 cells was significantly increased after CPP treatment for 48 h (P<0.05). The expression of bax mRNA was increased in QG56 exposed to CPP. The result of immunocytochemis-try indicated that CPP up-regulated the expression of bax protein. Conclusion CPP showed significant inhibitory effect on human lung cancer cell lines QG56 through inducing cell cycle arrest and apoptosis.
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Objective To observe the effects of drainage with vacuum and closure (VAC) on acute wounds, and explore the mechanism of drainage with VAC in promoting wound healing.Methods Twenty-four acute wounds were inflicted on the backs of 12 New Zealand white rabbits (each rabbit two wounds), and the rabbits were divided into a drainage with VAC group and a control group randomly. The drainage with VAC group was treated with drainage with VAC. The control group was treated with wet saline gauze. The wounds were observed 3 and 7 days after treatment. Patho-morphological changes in tissues from the compressed area were observed by HE staining. The expression level of Cx 43 mRNA was detected using a RT-PCR.Results At the 3rd and 7th day after treatment, the wounds of the drainage with VAC group were clean, fresh and had less edema compared with those of the control group. Pathomorphological tissue changes were more obvious in the drainage with VAC group. The expression of Cx 43 mRNA in the drainage with VAC group had declined significantly compared with the control group.Conclusion Drainage with VAC can promote inflammatory cell infiltration, down-regulate the expression of Cx 43 mRNA, and promote wound healing.
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Objective To investigate the roles of cystatin C (CysC) and serum creatinine (Scr) in acute renal injury of patients with shock. Method A total of 71 patients with shock, 42 male and 29 female, were enrolled from February 2006 to June 2007. Patients with kidney disease or renal insufficiency were excluded. All of patients were assigned to 4 groups as per the duration of shock. The blood samples were taken from patients for measurements of CysC and Scr during the periods of 1 hr,2 hr,and 4 hr of shock and 72 hr and 7 days after correction of shock. The corrected GFR (cGFR) and decreased GFR (dGFR) were calculated. The levels of Scr and dGFR could be used to classify the acute renal injury into stages according to the Acute Kidney Injury Diagnosis Criteria. The positive detection rates of different methods were compared. The levels of CysC, Scr and cGFR were statistically analyzed. Data were studied by using Pearson's correlation analysis, Results The elevation of CysC appeared sooner than that of Scr in all shock patients. Contrarily, the high level of CysC lowered to normal level much slower than that of SCR after correction of shock. The CysC increased 1 hour after shock. The GFR was negatively correlated with CysC and Scr, especially in the early stage of shock. Conclusions The renal dysfunction appears in the early stage of shock. The CysC assayed is more sensitive in the stage 1 of renal injury than Scr.
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Objective To explore the expression of ATP-binding cassette transporter C2(ABCG2) in adriamycin(ADM)-resistant human esophageal cancer cells.Methods The ADM-resistant human esophageal cancer cell(Eca109/ADM) was induced by gradually increasing the ADM concentration in the culture medium of human esophageal cancer cell line(Eca109) and long time screening culture.ABCG2 mRNA and protein of ADM-resistant cells was detected by RT-PCR,flow cytometry(FCM) and Western blot.Drug excretion of Eca109/ADM cells was examined by FCM.The drug resistance index to ADM was detected by MTT.Results The expression of ABCG2 in Eca109/ADM cells was higher than that in Eca109 cells.The drug excretion of Eca109/ADM cells was stronger than Eca109 cells.The Ecal09/ADM cells drug resistance index to ADM was 3.29.Conclusion The ADM-resistant cell line Eca109/ADM was established successfully as an ideal chemoresistant cell model.ABCG2 might be involved in the drug resistance of esophageal cancer cell.
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Objective To investigate the effect and possible mechanism of high mobility group box (HMGB) 1 in the development and progress of rheumatoid arthritis.Methods PBMC and serum samples were obtained from 74 RA patients (38 in active stage and 36 in stable stage) and 26 healthy controls.The expression of HMGB1 mRNA and protein was detected by RT-PCR and ELISA.Flow cytometry analysis ( FCM ) was used to detect the expression of Toll-like receptor 4 on PBMC.Results ①The expression of HMGBI mRNA and protein in active RA patients was significantly higher than that in healthy controls and inactive RA patients [2.63 vs 0.71，0.93 and (10.2±1.2) vs (7.5±1.8)，(8.3±1.8) ng/ml，respectively](P＜0.01 ).② The relative expression of TLR4 protein on CD14+ monocytes and CD3+ lymphocytes in active RA patients was increased than that in inactive RA and healthy controls (P＜0.05 or P＜0.01 ).It was also higher in inactive RA than in healthy controls (P＜0.05 or P＜0.01 ).③ Level of HMGB1 protein in serum of RA patients was positively correlated with ESR，CRP，RF，the numbers of tender joints and swollen joints as well as radiographic changes.Conclusion HMGB1 can be synthesized and released by PBMC of active RA patients，and then bind to TLR4 of PBMC to promote inflammatory responses and bone erosion.
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Objective To study the effects of adenosine triphosphate (ATP) on proliferation of human squamous esophageal carcinoma Eca-109 and hepatoma SMMC-7721 cells in vitro and the underlying mechanism. MethodsMTT assay was used to determine the proliferation of tumor cells. The AO/EB double stained cells were observed under fluorescence microscope. The effects of ATP on the cell cycle, apoptotic rate and apoptosis-related protein were detected by flow cytometry. Results ATP showed inhibitory effects on Eca-109 and SMMC-7721 cells at the concentration of 0.01～0.3 mmol/L. Exposure to 0.3 mmol/L ATP for 72 h, some of SMMC-7721 cells displayed morphological changes of apoptosis, but Eca-109 cells did not show the characteristics of apoptosis markedly. There was no significant change in the apoptotic rate and apoptosis-related protein of the two tumor cell lines treated with ATP 0.03, 0.1 and 0.3 mmol/L for 72 h respectively. The proportion of Eca-109 cells in G0/G1-phase of cellcycle was significantly increased, meanwhile the proportion of Eca-109 cells in S-phase and proliferation index value was significantly decreased by treatment with 0.3 mmol/L ATP. Conclusion ATP inhibited Eca-109 cell proliferation by changing the distribution of cell cycle phase, and its mechanism might not related to apoptosis, but for SMMC-7721 cell, the inhibition of cell proliferation induced by ATP was not related to the change in cell cycle.
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Objective To investigate the effects of selective COX-2 inhibitor nimesulide on growth inhibition,apoptosis and expression of COX-2 of human esophageal carcinoma Eca-109 cell line; and analyzed the correlation with the anti-oncogene,P277~(kip1). Methods MTT assay was used to detect the proliferation of Eca-109 cell. Apoptosis and cell cycle were determined by electronic microscopy and flow cytometry. The expression of COX-2 mRNA was detected by reverse transcription polymerase chain reaction (RT-PCR),the protein expression of COX-2 and P277~(kip1) were examined by Western blot analysis. Results Nimesulide significantly inhibited the proliferation of Eca-109 cell line in a time-and dose-depenent fashion; increased the proportion of cells in the G_0/G_1 phase and induced apoptosis of the cells in a dose-dependent(manner). Meanwhile,nimesulide can down-regulated the expression of COX-2 and up-regulated the expression of P277~(kip1) protein.Conclusion Nimesulide can inhibit the proliferation of Eca-109 cells,cause G_0/G_1 phase cell cycle arrest and induce apoptosis.The mechanism is probably explained with down-regulation of the expression of COX-2 and up-regulation of P277~(kip1) expression.
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Objective To investigate the expressions of EphA2 and its ligand EphrinA1 and their relationship with angiogenesis in gastric carcinoma. Methods Expressions of EphA2,EphrinA1 and CD34-stained microvessel density (MVD) were detected by immunohistochemical assay in gastric carcinoma tissues,adjacent tissues (1.5 to 2 cm from the mass) and normal gastric mucosa (5 to 10 cm from the mass) from 82 cases. The correlations among EphA2 and EphrinA1 expressions,MVD and clinic pathological features were analyzed. Results EphA2,EphrinA1 expressions and MVD in gastric carcinomas tissues were significantly higher than those in adjacent tissues and normal gastric tissues (P
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Aim To study the effects of selective cyclooxygenase-2 (COX-2) inhibitor,nimesulide,on COX-2 expression, cell proliferation and apoptosis of human esophageal carcinoma Eca-109 cell lines. Methods MTT assay was used to observe the proliferative effect;COX-2 mRNA expression was evaluated with RT-PCR; COX-2 protein expression,cell cycle and apoptosis were analyzed with flow cytometry;microscope and agarose gel electrophoresis of DNA were also used to observe the apoptosis. Results Nimesulide significantly inhibited the proliferation of Eca-109 cell lines in a time and dose-depenent fashion, down-regulated the expression of COX-2 mRNA and COX-2 protein in a dose-dependent fashion;nimesulide also decreased the proliferation index and the proportion of cells in S phase, meanwhile increased the proportion of cells in G_0/G_1 phase and induced apoptosis. Conclusion COX-2 selective inhibitor nimesulide inhibits proliferation,induces apoptosis and cell cycle arrest of human esophageal cells via down-regulation of COX-2 expression.
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<p><b>OBJECTIVE</b>To explore the molecular events and mechanism in the carcinogenesis of esophageal epithelium in the high incidence area of esophageal carcinoma.</p><p><b>METHODS</b>Epithelial cells collected from the high incidence area of esophageal carcinoma were used to detect DNA content and ploidy by propidium iodide(PI) stain. The expressions of p53, p16 and cyclin D1 were stained by indirect immunofluorescence of fluorescein isothiocyanate(FTTC), which were detected by flow cytometry (FCM).</p><p><b>RESULTS</b>During the process of carcinogenesis, DNA content increased significantly. The diploid cells decreased while heteroploid cells increased sharply, with a heteroploidy rate of 84.2%. At the same time, the p53 protein accumulated and p16 was deleted. The positive rates of p53 and oncogene cyclin D1 were both 100%(5/5, 6/6) in the cancer group.</p><p><b>CONCLUSION</b>In the early carcinogenesis of esophageal epithelium, DNA content and heteroploidy rates increase with tumor suppressor gene p16 deletion and p53 protein accumulation while oncogene cyclin D1 is overexpressed. Multiple molecular events have already occurred when esophageal carcinoma develops.</p>