1.The dose response decrease of lung function associated with the urinary polycyclic aromatic hydrocarbons metabolites in coke oven workers.
Die HU ; Qi-fei DENG ; Su-li HUANG ; Yun-feng HE ; Huan GUO ; Tang-chun WU
Chinese Journal of Industrial Hygiene and Occupational Diseases 2012;30(12):893-897
OBJECTIVETo analyze the relationship between metabolites of polycyclic aromatic hydrocarbons (PAHs) and lung function in coke oven workers, and to provide scientific basis for further exploring the potential mechanism and developing the preventing strategies of the workers' early lung damage.
METHODSWe measured carbon monoxide, sulfur dioxide, benzene soluble matter, particulate matters, and PAHs at different workplaces of a coke oven plant. Detailed information on demography and occupational health condition of 912 workers were collected. We divided these workers into control group and coke oven group according to their workplaces and the different concentrations of COEs in the environment. We detected 10 urinary PAH metabolites and lung function using gas chromatography-mass spectrometry and spirometric tests, respectively.
RESULTSFEV(1.0) (91.12 ± 13.31) and FEV(1.0)/FVC (108.61 ± 20.37) of the coke oven group is significantly lower than the control group (94.16 ± 15.57, 113.45 ± 19.70). In the coke oven group, the hydroxyphenanthrene and 1-hydroxypyrene are negatively correlated with FEV(1.0)/FVC (β = -0.136, β = -0.100), Ptrend < 0.05 for all.
CONCLUSIONThe dose response decrease of lung function is associated with the urinary PAH metabolites in coke oven workers. Indicated that the long exposure to PAHs may cause the early lung damage in coke oven workers, phenanthrene and pyrene may be the main factors.
Adult ; Air Pollutants, Occupational ; urine ; Coke ; Humans ; Lung ; physiopathology ; Male ; Middle Aged ; Occupational Exposure ; analysis ; Phenanthrenes ; urine ; Polycyclic Aromatic Hydrocarbons ; urine ; Pyrenes ; urine ; Respiratory Function Tests
2.Correlation between serum anti-P53 and familial clustering of hepatocellular carcinoma in Guangxi.
Yu PANG ; Guo-jian LI ; Ji-zhou WU ; Jian-lin WU ; Wu-qing CHEN ; Qiu-yue NING ; Ying-hua WEI ; Die-fei HU ; Ling QIN
Chinese Journal of Medical Genetics 2012;29(2):206-209
OBJECTIVETo assess the correlation between familial clustering of hepatocellular carcinoma (HCC) and the level of anti-P53 in human serum in Guangxi.
METHODSEnzyme-linked immunosorbent assay (ELISA) was used to detect anti-P53 in 164 members from 20 HCC families and 164 members from non-cancer control families. Univariate analysis was performed to assess the correlation between seral level of P53 antibody and familial clustering of HCC.
RESULTSThe level of P53 antibody was significantly higher in the members of HCC families than controls (Z=-3.04, P=0.002). After eliminating the interference of hepatitis B virus infection, this tendency still remains (P=0.011). And there was a significant difference between relatives of different degrees from HCC families (chi-square=11.593, P=0.021), with the expression of anti-P53 declining along with decrease in relationship coefficient. Furthermore, the number of individuals with high anti-P53 expression was also significantly greater in HCC families (95/164) than controls (71/164) (P=0.006). And the expression was rising along with the increasing HCC numbers (chi-square=16.068, P=0.000). Anti-P53 level was also greater in HCC families featuring sibling affection than parental affection (chi-square=12.679, P=0.002). Univariate analysis indicated that high expression of anti-P53 is a risk factor for development of HCC (OR=2.087, 95%CI: 1.270-3.431).
CONCLUSIONHigh level of anti-P53 expression may be a factor for the clustering of HCC families in Guangxi, China.
Adolescent ; Adult ; Antibodies, Neoplasm ; blood ; genetics ; Carcinoma, Hepatocellular ; blood ; genetics ; immunology ; Child ; China ; Cluster Analysis ; Family Health ; Female ; Humans ; Liver Neoplasms ; blood ; genetics ; immunology ; Male ; Risk Factors ; Tumor Suppressor Protein p53 ; immunology ; Young Adult
3.Metabolomic changes of neonatal sepsis: an exploratory clinical study.
Ping TONG ; Fu-Rong HUANG ; Jun XU ; Zi-Qi WU ; Xing HU ; Ming LING ; Die WANG ; Bu-Fei WU ; Du-Jiao YANG ; Ai-Min ZHANG
Chinese Journal of Contemporary Pediatrics 2022;24(6):675-680
OBJECTIVES:
To study the metabolic mechanism of neonatal sepsis at different stages by analyzing the metabolic pathways involving the serum metabolites with significant differences in neonates with sepsis at different time points after admission.
METHODS:
A total of 20 neonates with sepsis who were hospitalized in the Department of Neonatology, Hunan Provincial People's Hospital, from January 1, 2019 to January 1, 2020 were enrolled as the sepsis group. Venous blood samples were collected on days 1, 4, and 7 after admission. Ten healthy neonates who underwent physical examination during the same period were enrolled as the control group. Ultra-performance liquid chromatography-quadrupole time-of-flight mass spectrometry was used for the metabonomic analysis of serum samples to investigate the change in metabolomics in neonates with sepsis at different time points.
RESULTS:
On day 1 after admission, the differentially expressed serum metabolites between the sepsis and control groups were mainly involved in the biosynthesis of terpenoid skeleton. For the sepsis group, the differentially expressed serum metabolites between days 1 and 4 after admission were mainly involved in pyruvate metabolism, and those between days 4 and 7 after admission were mainly involved in the metabolism of cysteine and methionine. The differentially expressed serum metabolites between days 1 and 7 after admission were mainly involved in ascorbic acid metabolism.
CONCLUSIONS
The metabolic mechanism of serum metabolites varies at different stages in neonates with sepsis and is mainly associated with terpenoid skeleton biosynthesis, pyruvate metabolism, cysteine/methionine metabolism, and ascorbic acid metabolism.
Ascorbic Acid
;
Cysteine
;
Humans
;
Infant, Newborn
;
Metabolomics
;
Methionine
;
Neonatal Sepsis
;
Pyruvates
;
Sepsis