Separation and determination of triadimefon and its metabolites triadimenol enantiomers in fruit puree by supercritical fluid chromatography.

A method was established for the separation and determination of triadimefon and its metabolite triadimenol enantiomer residues in major complementary fruit puree for infants and young children (banana puree, pineapple puree, and grape puree) by supercritical fluid chromatography. After the samples were extracted with acetonitrile and purified with a solid phase extraction cartridge, Acquity Trefoil CEL2 chiral chromatographic column was adopted for separation, and gradient elution was conducted at the flow rate of 1.0 ml/min under the mobile phase of supercritical carbon dioxide - 0.5% ammonia methanol, the detection wavelength was 220 nm and quantification was conducted with the external standard method. The limits of quantitation of triadimefon and triadimenol enantiomers were both 0.05 mg/kg, the linear ranges were 0.5-50 mg/L, and the linear correlation coefficients were greater than 0.9993. The recoveries in the spiked samples at 0.05, 0.2, and 3.0 mg/kg were from 80.1 to 106%, and the relative standard deviation reached 3.3-7.6%. The method is efficient, rapid, reproducible, and environmentally friendly, enabling accurate analysis of pesticide enantiomers, which can detect the enantiomer residues of triadimefon and its metabolite triadimenol in major complementary fruit puree for infants and young children.

[Comparative study with the effect of stromal cell derived factor-1 on osteogenic differentiation of human healthy and inflammatory periodontal ligament stem cells].

OBJECTIVE: This study aims to compare the osteogenic differentiation capability of stem cells derived from human inflammatory periodontal ligament tissues (iPDLSCs) with those of stem cells derived from healthy periodontal ligament tissues (hPDLSCs). Both types of tissues were induced by stromal cell derived factor (SDF-1) in vitro. METHODS: iPDLSCs and hPDLSCs were primarily cultured by tissue digestion method and purified by limited dilution cloning. The cells were passaged and identified by stem cell surface marker expression through flow cytometry. Then, we used thiazolyl blue tetrazolium bromide to detect and compare the proliferation capabilities of the iPDLSCs and hPDLSCs. Express of bone volumes were detected by alizarin red staining after SDF-1 was added to the cells. Using alkaline phosphatase, we evaluated the osteogenic differentiation capability of the cells induced by SDF-1. The expression levels of the osteogenesis-related genes of the cells induced by SDF-1 were determined by reverse transcription-polymerase chain reaction. RESULTS: After purification, both iPDLSCs and hPDLSCs expressed stem cell markers. hPDLCSs had a higher proliferation capability than iPDLSCs. Osteogenesis-related genes had higher expression levels in the cells induced by SDF-1 than in those without induction (P<0.05). SDF-1 at 50 and 200 ng·mL⁻¹ concentration greatly affected the differen-tiation capabilities of iPDLSCs and hPDLSCs respectively. CONCLUSIONS: iPDLSCs and hPDLSCs had osteogenic differentia-tion capability. The level of osteogenic differentiation in normal and inflamed periodontal ligament stem cells increases after SDF-1 induction.

Three new diterpenoid alkaloids from the roots of Aconitum duclouxii.

Three new C19-diterpenoid alkaloids, ducloudines C (1), D (2), and E (3), were isolated from the roots of Aconitum duclouxii. Their structures were established on the basis of extensive spectroscopic analyses. Ducloudine C (1) is the first aconitine-type C19-diterpenoid alkaloid with a C=O group at C-3 and a C=C bond between C-1 and C-2. All compounds were tested for their biological activities against one pathogenic fungi and two pathogenic bacteria.

[A prospective cohort study on comparison of risk of death of respiratory system diseases between occupational dust exposure and smoking].

OBJECTIVE: To compare the effects of dust exposure and smoking on mortality of respiratory system diseases (RSD). METHODS: Based on the Guangzhou Occupational Health Surveillance Record System established between 1989 and 1992, 80,987 factory workers, aged 30 years old or older, occupationally exposed or not exposed to dusts, were included in a prospective cohort study. RESULTS: (1) The mean age of the cohort was 43.5. Most subjects were workers, had secondary education, and almost all were married. The dust exposure rate was 16.3%, the smoking rate 43.7% and the alcohol-drinking rate 33.5%. (2) The cohort was followed up for 8 years on average, but 35 people (0.04%) were lost for follow up. Among the 1593 deaths, 219 and 90 people died of lung cancer and non-cancer respiratory system diseases (NCRSD) respectively. (3) The adjusted relative risk (RR) of death of lung cancer for smokers, 3.32, was 2.2 times of that for dust exposed workers, 1.53, and the RR of death of NCRSD for dust exposed workers, 2.41, 1.28 times of that for smokers, 1.89, especially for silica dust-exposed workers, 5.72, 3.03 times of that for smokers. Dust exposure combined with smoking caused significantly higher RR of death of RSD. (4) In male, the death risks of RSD were increased with the amount of smoking per day and years of smoking. CONCLUSION: Occupational dust exposure and smoking may cause excessive lung cancer and NCRSD death with synergistic effects. Smoking has higher RR of Lung cancer death than dust exposure. However, the dust exposure contributes to higher RR of NCRSD death. There is a significant dose-effect relationship between smoking and the death risk of RSD.

[A prospective cohort study on the comparison of risk of occupational dust exposure and smoking to death].

OBJECTIVE: To compare the effects of dust exposure and smoking on mortality. METHODS: Based on the Guangzhou Occupational Health Surveillance Record System established in 1989-1992, 80 987 factory workers, aged > or = 30, occupationally exposed to dust and non-exposure to dust, were included in a prospective cohort study. RESULTS: (1) The mean age of the cohort was 43.5. Most subjects were workers, with secondary education, and married. Out of them 16.3% having ever exposed to dust, 43.7% ever smoked and 33.5% drank alcohol. (2) The cohort were traced for 8 years on average, but 35 were lost for follow-up. Malignant neoplasm was most commonly seen among 1539 deaths. (3) The adjusted relative risk (RRs) of death of all causes, malignant neoplasm and cerebro-cardiovascular diseases for dust exposed workers were close to those for smokers. However, the adjusted RRs of death of nasopharynx cancer and respiratory system diseases for dust exposed workers were higher than those for smokers. The adjusted RRs of death of lung cancer and stomach cancer for smokers were 2.2 times and 1.5 times of that for dust exposed workers respectively. Dust exposure combined with smoking caused significantly higher death RR. (4) In males, the adjusted RRs of death of all causes, malignant neoplasm and respiratory system diseases for silica dust exposed workers and the adjusted RR of death of cerebro-cardiovascular diseases for wood dust exposed workers were higher those in smokers. (5) The population attributable risk percentage (PARP) of all causes of death for smokers was 2.5 times of that for dust exposed workers. (6) In males, the risks of death for all causes, malignant neoplasm, lung cancer and stomach cancer increased with the amount of smoking per day and the duration of smoking. The risks of death caused by coronary heart disease and respiratory system diseases were increasing with the amount of smoking per day and the duration of smoking respectively. CONCLUSIONS: The adjusted RRs for dust exposed workers were close to those for smokers with dust exposure and smoking having synergistic effects. Some of the adjusted RRs for smokers were higher than those for dust exposed workers PARP for smokers was higher than that for dust exposed workers. Our findings suggested that there was a significant dose-effect between smoking and risk of deaths.

[A cohort study on the relationship between blood pressure levels and the mortality of cerebro-cardiovascular diseases in Guangzhou workers].

OBJECTIVE: To study the relative risk (RR) of mortalities of cerebro-cardiovascular diseases (CVD) in Guangzhou workers with hypertension. METHOD: Prospective cohort study was conducted in 78,379 workers, aged >or= 35, from 399 factories. Cox regression model were mainly used for data analysis. RESULTS: (1) There were 48,705 male and 29,674 female workers in the cohort. All workers were followed-up for 8 years. 363 CVD deaths (male 305, female 58) mainly died of stroke, coronary heart disease and hypertension. The crude mortalities were 78.58/100,000 person years in male and 24.55/100,000 person years in female. (2) Compared with the optimal or normal blood pressure (ONBP), the RR (95%) of CVD deaths with high blood pressure (HBP) were 6.19 (4.85 - 7.91) in male and 2.78 (1.59 - 4.85) in female. In male, compared with ONBP, the RR of CVD deaths without illness but with 1st-grade HBP at baseline, and of those suffered non-CVD but with 1st-grade HBP at baseline, and of those suffered CVD with 2nd-grade HBP at baseline were 3.98, 3.25 and 3.15 respectively (P < 0.01). (3) After stratifying of age, smoking, drinking, educational levels and occupational exposure, the RR of CVD deaths was higher in those who were younger, or ever-smoking, non-drinking, higher educational level, exposed to occupational hazards and with hypertension. CONCLUSION: There is relationship between BP levels and CVD mortality. High BP may affect CVD deaths at younger age. Comprehensive measures should be used to reduce the risk of CVD deaths.

Smoking, occupational exposure and mortality in workers in Guangzhou, China.

PURPOSE: To compare the mortality risk of smoking and overall occupational exposure in Guangzhou, China. METHODS: Baseline data on smoking and occupational exposure of 82159 workers aged 30+ were retrieved from medical records established in 1988-92. Vital status and causes of death were followed through 1998. RESULTS: During follow-up 1584 workers had died. Adjusted relative risks (RR) with 95% confidence intervals (95%CI) for ever-smoking in men was 1.23 (1.07-1.41) for total deaths, 1.43 (1.17-1.74) for all cancer, 3.77 (2.31-6.14) for lung cancer and 2.54 (1.09-5.92) for stomach cancer (all showing significant linear trends with amount and duration of smoking). The RR in women of 1.10 (0.59-2.06) for total deaths and 1.60 (0.65-3.92) for all cancer were positive but not significant. No significant excess mortality risk was observed for occupational exposure in each gender. In both genders combined, the RR for total deaths was 1.23 (1.08-1.40) for smoking and 1.07 (0.96-1.19) for occupational exposure. If the relationships were causal, 12% of all deaths could be attributed to smoking but only 3% to occupational exposure. CONCLUSION: Smoking was more predictive of premature deaths than overall occupational exposures in middle aged workers. Smoking cessation should be a top priority in occupational health practice.