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排序方式: 共有337条查询结果,搜索用时 15 毫秒
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Jolinda LD Schram Joost Oude Groeniger Merel Schuring Karin I Proper Sandra H van Oostrom Suzan JW Robroek Alex Burdorf 《Scandinavian journal of work, environment & health》2021,47(2):127
Objective:Using a novel mediation method that presents unbiased results even in the presence of exposure–mediator interactions, this study estimated the extent to which working conditions and health behaviors contribute to educational inequalities in self-rated health in the workforce.Methods:Respondents of the longitudinal Survey of Health, Ageing, and Retirement in Europe (SHARE) in 16 countries were selected, aged 50–64 years, in paid employment at baseline and with information on education and self-rated health (N=15 028). Education, health behaviors [including body mass index (BMI)] and working conditions were measured at baseline and self-rated health at baseline and two-year follow-up. Causal mediation analysis with inverse odds weighting was used to estimate the total effect of education on self-rated health, decomposed into a natural direct effect (NDE) and natural indirect effect (NIE).Results:Lower educated workers were more likely to perceive their health as poor than higher educated workers [relative risk (RR) 1.48, 95% confidence interval (CI) 1.37–1.60]. They were also more likely to have unfavorable working conditions and unhealthy behaviors, except for alcohol consumption. When all working conditions were included, the remaining NDE was RR 1.30 (95% CI 1.15–1.44). When BMI and health behaviors were included, the remaining NDE was RR 1.40 (95% CI 1.27–1.54). Working conditions explained 38% and health behaviors and BMI explained 16% of educational inequalities in health. Including all mediators explained 64% of educational inequalities in self-rated health.Conclusions:Working conditions and health behaviors explain over half of the educational inequalities in self-rated health. To reduce health inequalities, improving working conditions seems to be more important than introducing health promotion programs in the workforce. 相似文献
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Characterization of xenobiotic-metabolizing enzymes and nitrosamine metabolism in the human esophagus 总被引:5,自引:2,他引:5
Smith TJ; Liao A; Wang LD; Yang GY; Starcic S; Philbert MA; Yang CS 《Carcinogenesis》1998,19(4):667-672
Esophageal cancer has been associated with tobacco smoking, and
nitrosamines are possible causative agents for this cancer. The present
study investigated the metabolism of the tobacco carcinogens N'-
nitrosonornicotine (NNN), 4-(methylnitrosamino)-1-(3-pyridyl)-1- butanone
(NNK), and N-nitrosodimethylamine (NDMA), as well as the presence of
xenobiotic-metabolizing enzymes in human esophageal tissues from
individuals in the United States and Huixian, Henan Province, China (a
high-risk area for esophageal cancer). All esophageal microsomal samples
activated NNN and the metabolic rate was 2-fold higher in the esophageal
samples from China than the USA. All microsomal samples activated NDMA.
However, most of the microsomal samples did not activate NNK.
Troleandomycin (an inhibitor of cytochrome P450 3A) decreased the formation
of NNN-derived keto acid by 20-26% in the esophageal microsomes. The
activities for NADPH: cytochrome c reductase, ethoxycoumarin O-deethylase,
NAD(P)H: quinone oxidoreductase and glutathione S-transferase were present
in the esophageal samples. Coumarin 7-hydroxylase (a representative
activity for P450 2A6) activity was not detected in the esophageal
microsomal samples. The activities for nitrosamine metabolism and
xenobiotic- metabolizing enzymes were decreased (by 30-50%) in the squamous
cell carcinomas compared with their corresponding non-cancerous mucosa. The
presence of activation and detoxification enzymes in the esophagus may play
an important role in determining the susceptibility of the esophagus to the
carcinogenic effect of nitrosamines. Our results suggest that P450s 3A4 and
2E1 are involved in the activation of NNN and NDMA, respectively, in the
human esophagus.
相似文献
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Immunologic status of hemophilia patients treated with cryoprecipitate or lyophilized concentrate 总被引:1,自引:0,他引:1
We evaluated 37 patients with moderate or severe hemophilia A and six patients with severe factor IX deficiency for clinical or laboratory evidence of immune abnormalities. Patients were assigned to one of four groups according to the type of clotting factor replacement. Twenty patients had received only cryoprecipitate during the two years preceding the evaluation (group I); 11 additional patients were treated predominantly with cryoprecipitate but had also received up to nine bottles of factor VIII concentrate (group II); six patients received factor VIII concentrate (group III); six patients received factor IX concentrate (group IV). There was no clinical or laboratory evidence of immunodeficiency among the 43 patients. The mean absolute number of Th cells was normal in all patient groups, but the mean absolute number of Ts cells was increased compared with controls, both in patients treated with cryoprecipitate and in patients treated with factor VIII or factor IX concentrate. There was no correlation between the Th/Ts ratio and patient age, alanine aminotransferase level, hepatitis serology, in vitro lymphocyte function, or amount of clotting factor administered. Our observations demonstrate that the volunteer or commercial origin of clotting factor replacement cannot fully explain the alterations in lymphocyte subset distribution previously described in patients with hemophilia A. 相似文献
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牛津膝置换是使用最广泛的膝关节单髁置换(UKR)。牛津膝在37年前开始应用,拥有一个全匹配的活动衬垫,因而磨损率非常低。牛津膝最主要的使用指征是膝关节前内侧骨关节炎,这种病人至少占所有需要行膝关节置换术患者的50%。由于这一系统的设计特点,传统UKR的反指征,如年龄、活动量、肥胖、髌股关节损害和软骨钙质沉着症等对于牛津膝均不是反指征。与全膝关节置换(TKR)相比,牛津膝提供更快的康复、更好的功能、更大的活动度和更好的术后满意度,发生并发症更少、程度更轻,病残率和死亡率更低。一个持续超过30年的研究显示在90%的病例中,牛津膝为患者终生提供了优或良的临床结果,且不需要翻修。在最近15年,牛津膝通过微创手术入路植入,涉及6000多例使用该入路牛津膝置换的9个研究报道显示,10年生存率约95%。在许多这样的研究中,医生们在拟行膝关节置换的患者中约50%使用了牛津单髁膝置换。 相似文献
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Graft-versus-host disease (GVHD) is currently encountered after bone marrow transplantation and transfusion. GVHD associated with transfusion (TA-GVHD) in apparently immunocompetent recipients has been recently reported with increasing frequency. A consistent finding in many of these cases is that the recipient received blood from a donor homozygous for one of the recipient's HLA haplotypes. However, the observed frequency of TA-GVHD is much lower than the estimated probability of this donor/recipient combination. The potential role of recipient immune responses in controlling TA-GVHD was investigated using an analogous murine model in which GVHD is induced by the injection of parental lymphoid cells into unirradiated F1 hybrid recipients. The effect of various immune manipulations of the recipient of GVHD induction was assessed by determining the number of donor lymphoid cells required to induce GVHD responses. Whereas depletion of recipient CD4+ cells increased the number of donor cells needed to induce GVHD, depletion of recipient CD8+ and natural killer cells resulted in fewer donor cells being needed to induce a GVHD response. These studies suggest a central role for functioning recipient CD8 and natural killer cells in the down-regulation of TA-GVHD development in recipients. 相似文献