Carbon monoxide poisoning: a prediction model using meteorological factors and air pollutant.

BACKGROUND: While the influence of meteorology on carbon monoxide (CO) poisoning has been reported, few data are available on the association between air pollutants and the prediction of CO poisoning. Our objective is to explore meteorological and pollutant patterns associated with CO poisoning and to establish a predictive model. RESULTS: CO poisoning was found to be significantly associated with meteorological and pollutant patterns: low temperatures, low wind speeds, low air concentrations of sulfur dioxide (SO2) and ozone (O38h), and high daily temperature changes and ambient CO (r absolute value range: 0.079 to 0.232, all P values < 0.01). Based on the above factors, a predictive model was established: "logitPj = aj - 0.193 * temperature - 0.228 * wind speed + 0.221 * 24 h temperature change + 1.25 * CO - 0.0176 * SO2 + 0.0008 *O38h; j = 1, 2, 3, 4; a1 = -4.12, a2 = -2.93, a3 = -1.98, a4 = -0.92." The proposed prediction model based on combined factors showed better predictive capacity than a model using only meteorological factors as a predictor. CONCLUSION: Low temperatures, wind speed, and SO2 and high daily temperature changes, O38h, and CO are related to CO poisoning. Using both meteorological and pollutant factors as predictors could help facilitate the prevention of CO poisoning.

[Value of detecting p16 gene methylation in the diagnosis of malignant pleural effusion].

OBJECTIVE: To investigate aberrant methylation in the promoter of p16 gene in the sediment cells of pleural effusion and evaluate its clinical significance in the differentiating benign and malignant pleural effusion. METHODS: Using methylation-specific PCR (MSP), aberrant promoter methylation of p16 gene was detected in the sedimental cells of pleural effusion samples from 66 patients with pleural effusion. RESULTS: Of the 66 patients with pleural effusion, 36 had a definite diagnosis of malignant pleural effusion, and the rest were confirmed to have benign pleural effusion. The positivity rate of p16 gene promoter methylation was 69.4% (25/36) in malignant pleural effusion and 13.3% (4/30) in benign pleural effusion specimens, showing a significant difference between them (χ² = 20.915, P < 0.01). The diagnostic sensitivity, specificity and accuracy of aberrant promoter methylation of p16 gene in the 36 malignant cases were 69.4%, 86.7% and 77.3%, respectively. The positive expression of p16 gene promoter methylation in malignant pleural effusion was not correlated to the histological type or the pathological grade of the tumor (P > 0.05). CONCLUSION: Detection of aberrant methylation in p16 gene promoter in the sediment cells of pleural effusion specimens by MSP method allows differentiation between benign and malignant pleural effusion.

[Clinical value of monitoring serum cardiac biomarkers in pulmonary thromboembolism-induced myocardial injury].

OBJECTIVE: To investigate the clinical value of monitoring the serum cardiac biomarkers in patients with pulmonary thromboembolism (PTE) and secondary myocardial injury. METHODS: The serum cardiac biomarkers including aspartate aminotransferase (AST), lactate dehydrogenase (LDH), alpha-hydroxybutyrate dehydrogenase (HBDH), creatine kinase (CK), creatine kinase isoenzyme (CK-MB), cardiac tropnin I (cTnI) and myoglobin (Myo) were measured using immunochemiluminescent assays in 36 patients with PTE, who were diagnosed according to imaging findings in the recent 5 years. The measurements in concomitant non-PTE patients free of heart, liver, or kidney diseases were used as the baseline values of the biomarkers. Correlation analysis of the measurements was conducted in relation to the pulmonary embolism area, pulmonary hypertension and mortality rate. RESULTS: The PTE patients exhibited significantly elevated levels of the serum cardiac biomarkers including AST (56.14-/+15.73 U/L), LDH (303.06-/+94.99 U/L), HBDH (234.67-/+87.86 U/L), CK-MB (26.19-/+12.39 U/L), CK (129.25-/+76.14 U/L), Myo (70.63-/+45.75 ng/ml), and cTnI (0.45-/+0.41 ng/ml) in comparison with the baseline values (P < 0.01). Of these biomarkers, AST and CK-MB showed a significant correlation to the mortality, cTnI was correlated to pulmonary hypertension, and Myo was correlated to pulmonary hypertension and massive pulmonary embolism. CONCLUSION: Measurements of these serum cardiac biomarkers may serve as indicators for diagnosis of myocardial injury secondary to PTE. AST, CK-MB, cTnI, and Myo can help assess the prognosis of the patients.