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Objective To evaluate the diagnostic value of interferon-γ release assay of blood and pleural effusion for tuberculous pleurisy.Methods Fifty-six adult patients with suspected tuberculous pleurisy were enrolled in our study.The blood and pleural effusion interferon-γ release assay were measured by T-SPOT.TB test in 38 pleural tuberculosis patients and 18 nontuberculous pleurisy controls.The diagnostic sensitivity,specificity,predictive value of T-SPOT.TB in pleural effusion mononuclear cells (PE-MC) and peripheral mononuclear cells (PBMC) were analyzed.Results The sensitivities and specificities,positive predictive values and negative predictive values,respectively,of the PE-MC and PBMC for diagnosing were as follows:86.5％(95％ confidence interval[CI] 71.2％-95.5％) and 100％(95％CI 90.5％-100％);52.9％(95％CI 27.8％-77.0％) and 35.3％(95％CI 14.2％-61.7％);80.0％(95％CI 64.4％-90.9％) and 77.1％(95％CI 62.7％-88.0％);64.3％(95％CI 35.1％-87.2％) and 100％(95％CI 54.1％-100％).By ROC curve analysis,a cut-off value of 47SFC/2.5 × 105 cells in PE-MC showed a sensitivity of 89.2％ and a specificity of 88.2％.Conclusion T-SPOT.TB in PE-MC could be an accurate diagnostic method for tuberculous pleurisy in TB endemic settings.Moreover,47SFC/2.5 × 105 cells might be the optimal cut-off value for diagnosing tuberculous pleurisy.
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Objective To explore the suitable risk assessment model for printing industry, we evaluated the risk of furniture industry using models provided by Singapore Ministry of Manpower (MOM) . Methods According to the occupational-disease-prevention laws and regulations, we improved the MOM and increased the risk assessment of physical agents. Then, we evaluate the risk of furniture industry using the improved MOM. Results The range of wood dust was 1.9-8.9mg/m3, and the percent of pass was 50%. The range of formaldehyde, benzene, methylbenzene and dimethylbenzene was 0.24-0.36 mg/m3, <0.6mg/m3, 3.8-6.7mg/m3 and 6.1-16.1mg/m3 respectively, and their percent of pass was 100%. Furthermore, the noise intensity was 80.8 dB (A), which was under the occupational exposure limit. The risk level of wood dust, formaldehyde, benzene and noise was high, while the risk level of methylbenzene and dimethylbenzene was moderate. Conclusion The improved semi-quantitative risk assessment was appropriate for furniture industry, but its applicability in industrial enterprise needs to be studied further.
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Objective To analyze and evaluate the occupational hazards,engineering protection measures and risk levels in an oil terminal project.Methods Engineering analysis,occupational health survey,inspecting -testing and semi -qualitative semi-quantitative evaluation method (MES method)were used to analyze the production process,the type of occupational hazards,characteristics and concentrated/strong degrees and engineering protection measures of the project. Also,the occupational health risk and the effect of engineering protection were assessed.Results The main occupational hazards of this project were dust,solvent naphtha,benzene,toluene,xylene,hexane,non -methane hydrocarbons, carbon monoxide,carbon dioxide,manganese and its inorganic compounds,hydrochloric acid,hydrogen sulfide,noise, high temperature,power frequency electric field,welding electric arc and so on.Approximately,16.67%of noise samples and 66.67% of high temperature samples exceeded the Chinese National Occupational Health Standards.Except for noise of the fuel pump shed and high temperature of 100000 tons pier and fuel tank,the occupational hazards of other jobs were in line with the national occupational health standards.In normal conditions,the occupational risk levels of all positions were 5 (slightly hazardous),while in special conditions,the occupational risk level of repair welders was 5 (slightly hazardous),of pier operators and tank farm operators were 1 (extremely dangerous),of sewage treatment workers,boiler room operators and electricians were 3 (significant risk ).Conclusion This project can take effective engineering protective measures to control occupational hazards and risk management of special conditions need to be strengthened.
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This study was aimed to investigate the application value of the dual color dual fusion fluorescence in situ hybridization (DCDF-FISH) in BCR/ABL (+) acute lymphoblastic leukemia patients with complex chromosomal translocation. The clinical presentations of a patient with ALL were monitored regularly by bone marrow cell morphology test, chromosome analysis, flow cytometry and DCDF-FISH technique, and the reaction of patients to treatment and disease progression were dynamically observed by DCDF-FISH. The results indicated that the patient showed the typical presentation of B lineage acute lymphoblastic leukemia (B-ALL) with expression of CD10, CD19 and CD34; the chromosome analysis showed 46,XY, i(8), ider(9)t (9; 22) [23]/47, idem, +der(22) t (9;22) [7] karyotype in the bone marrow cells, FISH showed that 83% cells contained BCR/ABL fusion gene in the patient's bone marrow, among which 5% cells showed 1R1G2F signalling model, 14% cells showed 1R1G3F, and 64% cells showed 1R1G4F. The patient got complete remission when the imatinib chemotherapy combined with VTLP was carried out, and the tumor cells decreased to 19%, but the cells with 1R1G2F signal model increased to 18%. The 1R1G2F cell signal model increased up to 38% when patient relapsed. The patient died of the drug-resistance. It is concluded that the BCR/ABL (+) leukemia patient with complex translocation has multiple tumor cell subsets, and the responses of different cell subsets to the treatment are different, therefore the response to therapy and drug resistance of patient can be monitored early by the signal model of DCDF-FISH and the observation of dynamical changes of different cell subset.
Subject(s)
Adult , Humans , Male , Drug Resistance, Neoplasm , Genetics , Fusion Proteins, bcr-abl , Genetics , In Situ Hybridization, Fluorescence , Leukemia, Myelogenous, Chronic, BCR-ABL Positive , Drug Therapy , GeneticsABSTRACT
<p><b>BACKGROUND</b>PDK1 is an essential protein kinase that plays a critical role in mammalian development. Mouse lacking PDK1 leads to multiple abnormalities and embryonic lethality at E9.5. To elucidate the role of PDK1 in the heart, we investigated the cardiac phenotype of mice that lack PDK1 in the heart in different growth periods and the alteration of PDK1 signaling in human failing heart.</p><p><b>METHODS</b>We employed Cre/loxP system to generate PDK1(flox/flox): α-MHC-Cre mice, which specifically deleted PDK1 in cardiac muscle at birth, and tamoxifen-inducible heart-specific PDK1 knockout mice (PDK1(flox/flox):MerCreMer mice), in which PDK1 was deleted in myocardium in response to the treatment with tamoxifen. Transmural myocardial tissues from human failing hearts and normal hearts were sampled from the left ventricular apex to analyze the activity of PDK1/Akt signaling pathways by Western blotting.</p><p><b>RESULTS</b>PDK1(flox/flox): α-MHC-Cre mice died of heart failure at 5 and 10 weeks old. PDK1(flox/flox) -MerCreMer mice died of heart failure from 5 to 21 weeks after the initiation of tamoxifen treatment at 8 weeks old. We found that expression levels of PDK1 in human failing heart tissues were significantly decreased compared with control hearts.</p><p><b>CONCLUSION</b>Our results suggest that PDK1 signaling network takes part in regulating cardiac viability and function in mice, and may be also involved in human heart failure disease.</p>