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排序方式: 共有153条查询结果,搜索用时 15 毫秒
1.
扎拥 《解放军保健医学杂志》2009,(3):216-218
目的探讨西藏拉萨地区幽门螺杆菌(Helicobacter pyloric,Hp)感染与冠心病及多种危险因素的关系。为该地区冠心病的防治提供依据。方法分为冠心病组46例和非冠心病组51例,应用检测血抗HpIgG及-C-尿素呼气试验方法检测Hp感染情况,并分别测定各组血脂、血糖、餐后2h血糖、C反应蛋白、纤维蛋白原、白细胞总数。结果冠心病组患者血清抗HpIgG阳性率为50.0%(23/46),明显高于非冠心病组的23.5%(12/51),P〈0.05;冠心病患者Hp现症感染率为54.3%(25/46),明显高于非冠心病组的31.3%(27/51),P〈0.05;冠心病组Hp感染患者血脂、空腹及餐后2h血糖、C反应蛋白、纤维蛋白原较非感染患者明显升高(P〈0.05)。结论Hp感染与冠心病相关,可能是拉萨地区冠心病发病的独立危险因素。 相似文献
2.
We compared the tumor-initiating activities toward mouse skin of two
structurally related polycyclic aromatic hydrocarbon diol epoxides: racemic
anti-1,2,3,4-tetrahydro-5,6-dimethylchrysene-1,2-diol-3,4- epoxide
(5,6-diMeCDE) and racemic anti-1,2,3,4-tetrahydro-5-
methylchrysene-1,2-diol-3,4-epoxide (5-MeCDE). Tumors induced by these diol
epoxides were analysed for mutations in the Ha-ras gene. 5,6- diMeCDE is
derived from the non-planar parent compound 5,6- dimethylchrysene, and
reacts to approximately equal extents with dA and dG in DNA, whereas
5-MeCDE is derived from a nearly planar parent compound, 5-methylchrysene,
and reacts mainly with dG in DNA. 5,6- diMeCDE, at initiating doses of 33,
100 or 400 nmol per mouse, induced 1.2, 2.2 and 6.2 skin tumors per mouse,
respectively. It was significantly less tumorigenic than 5-MeCDE which
induced 3.1, 7.5 and 9.1 skin tumors per mouse at the same doses. Tumors
induced by 5,6- diMeCDE had a large number of CAA-->CTA mutations in
codon 61 of the Ha- ras gene: 50, 55 and 75% of the tumors analysed had
this mutation at the 33, 100 and 400 nmol doses. No mutations were found in
codons 12 and 13 in the tumors induced by 5,6-diMeCDE. In contrast,
CAA-->CTA mutations in codon 61 were rarely seen in tumors induced by
5-MeCDE. At the highest dose of 5-MeCDE, 20% of the tumors analysed had
mutations at G of codons 12 and 13. The results of this comparative study
support the hypothesis that mutations in the Ha-ras gene in mouse skin
tumors induced by PAH diol epoxides occur as a result of their direct
reaction with the gene. However, pathways other than the commonly observed
Ha- ras codon 61 mutations are clearly important in mouse skin
tumorigenesis by these diol epoxides.
相似文献
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In order to study the plasminogen activator inhibitor activity (PAI-1) in subjects at different risk of non-insulin-dependent diabetes and ischaemic heart disease we examined 89 subjects with diet controlled NIDDM (49 Caucasian, 40 Asian), 29 with impaired glucose tolerance (IGT) (13 Caucasian, 16 Asian), and 149 with normal glucose tolerance (67 Caucasian, 82 Asian). Diabetes was diagnosed by WHO criteria and highly specific, monoclonal antibody-based assays were used to measure insulin, intact proinsulin, and des 31,32 proinsulin. Subjects with NIDDM were significantly more obese, had more central distribution of obesity, higher fasting plasma specific insulin concentrations (NIDDM median 74 pmol l−1 vs IGT 41 pmol l−1, p < 0.01 and vs normals 34 pmol l−1, p < 0.001) and higher PAI-1 activity than normals and those with IGT (NIDDM 23.0 ± 6.9 vs IGT 16.8 ± 5.0, p < 0.001 and vs normals 17.1 ± 6.9 AU ml−1, p < 0.001). However, PAI-1 activity was not significantly different between Asian and Caucasian normals (17.5 ± 7.3 vs 16.5 ± 6.4 AU ml−1, p = ns) and diabetic (22.8 ± 7.3 vs 23.1 ± 6.6 AU ml−1, p = ns) subjects. In addition to relationships with obesity and plasma triglyceride, PAI-1 activity, after controlling for age, sex, body mass index, and waist–hip ratio, was related to fasting insulin (partial r = 0.22, p < 0.001), intact proinsulin (partial r = 0.36, p < 0.001), and des 31,32 proinsulin concentrations (partial r = 0.33, p < 0.001) as measured by highly specific assays. The association of PAI-1 with diabetes was weakened but remained statistically significant (p = 0.042) after controlling for age, sex, ethnicity, obesity, plasma triglyceride, and all insulin-like molecules. We conclude that, although PAI-1 activity is raised in subjects with diet-treated NIDDM, it is normal in subjects with IGT and non-diabetic Asians, populations at high risk of NIDDM and ischaemic heart disease. Raised PAI-1 activity may play an important role in the pathogenesis of macrovascular disease in subjects with NIDDM, but is unlikely to explain excess risk of ischaemic heart disease in Asians and those with impaired glucose tolerance. 相似文献
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目的:探讨随访2型糖尿病(T2DM)家系非糖尿病一级亲属5年的胰岛素抵抗和胰岛β细胞功能变化。方法:入选2型糖尿病家系非糖尿病一级亲属组(FDR)32例和正常对照组(NC)18例,基线检测了体质量指数、腰臀比、血压、血脂、血糖和空腹胰岛素(FINS)水平。采用稳态模式(HOMA)评价胰岛素抵抗(HOMA-IR)和胰岛β细胞功能(HOMA-β),5年后进行了相同的随访。结果:5年后FDR组HOMA-IR明显升高(P=0.040),HOMA-β明显降低(P=0.004)。5年后FDR组与NC组HOMA-IR组间无显著差异(P=0.594),HOMA-β明显降低(P=0.000)。多元逐步回归分析显示,FINS、空腹血糖(FBG)、高密度脂蛋白-胆固醇(HDL-C)是影响FDR组胰岛素抵抗的独立危险因素;FBG和FINS是影响FDR组胰岛β细胞功能的独立危险因素。结论:T2DM患者一级亲属非肥胖患者在发生糖尿病之前已经存在胰岛素抵抗和胰岛分泌功能缺陷,且随着病程延长胰岛β细胞功能衰竭可能更明显。 相似文献
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ZA Bhutta 《Archives of disease in childhood》1996,75(3):214-217
The risk factors for mortality were analysed in a consecutive group of 1158 children presenting to the Aga Khan University Medical Center, Karachi, with multidrug resistant typhoid fever that had been proved on culture. There were 19 deaths, representing an overall case fatality rate of 1.6%. Multidrug resistant typhoid was associated with a more severe clinical illness and higher rates of toxicity, hepatomegaly, hypotensive shock, and death. Irrespective of drug resistance status, typhoid fever was found to be a more severe illness in young infants with significantly higher rates of diarrhoea, hypotensive shock, and mortality. Univariate analysis of admission characteristics associated with increased risk for mortality revealed significant association with younger age (p < 0.05), hypotensive shock or hypothermia (p < 0.001), obtundation (p < 0.001), seizures (p < 0.05), anaemia at admission (p < 0.005), and leucocytosis (p < 0.001). Logistic regression analysis of risk factors for mortality showed persistent association of hypothermia, toxicity, and anaemia with mortality. The data provides evidence that multidrug resistant typhoid in childhood is associated with increased risk of mortality, especially in infancy and closer attention to several risk factors for increased morbidity and case fatality rates may lead to improved outcome of treatment. 相似文献