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1.
Chinese Medical Journal ; (24): 1666-1670, 2015.
Article in English | WPRIM | ID: wpr-231717

ABSTRACT

<p><b>BACKGROUND</b>Inflammation plays a pivotal role in the formation and progression of ischemic stroke. Recently, more and more epidemiological studies have focused on the association between C-reactive protein (CRP) -717A > G and -286C > T > A genetic polymorphisms and ischemic stroke. However, the findings of these researches are not conclusive.</p><p><b>METHODS</b>We performed a meta-analysis to determine whether these two polymorphisms are associated with the risk of ischemic stroke. Eligible studies were identified from the database of PubMed, Medline, Embase, Web of Science, CNKI, Weipu, and Wanfang. We calculated odds ratios (ORs) with 95% confidence intervals (CIs) to assess the strength of the association.</p><p><b>RESULTS</b>Four articles were included in our study, including 1926 cases and 2678 controls for -717A > G polymorphism, 652 cases and 1103 controls for -286C > T > A polymorphism. The results of meta-analysis showed that single nucleotide polymorphism (SNP) -717A > G was not significantly associated with the risk of ischemic stroke (GG vs. AA, OR = 1.12, 95% CI = 0.83-1.50, P = 0.207; GG + GA vs. AA, OR = 1.04, 95% CI = 0.93-1.17, P = 0.533; GG vs. GA + AA, OR = 1.10, 95% CI = 0.82-1.47, P = 0.220). Meta-analysis of SNP - 286C > T > A also demonstrated no statistical evidence of a significant association with the risk of ischemic stroke (AA vs. CC, OR = 0.86, 95% CI = 0.59-1.25, P = 0.348; AA vs. CC, OR = 0.92, 95% CI = 0.80-1.06, P = 0.609; AA vs. CC, OR = 0.89, 95% CI = 0.62-1.30, P = 0.374).</p><p><b>CONCLUSIONS</b>This meta-analysis demonstrated little evidence to support a role of CRP gene -717A > G, -286C > T > A polymorphisms in ischemic stroke predisposition. However, to draw comprehensive and more reliable conclusions, further larger studies are needed to validate the association between CRP gene polymorphisms and ischemic stroke in various ethnic groups.</p>


Subject(s)
Humans , Alleles , Brain Ischemia , Genetics , C-Reactive Protein , Genetics , Genetic Predisposition to Disease , Genetics , Genotype , Polymorphism, Single Nucleotide , Genetics , Stroke , Epidemiology , Genetics
2.
Chinese Journal of Endemiology ; (6): 302-305, 2009.
Article in Chinese | WPRIM | ID: wpr-643351

ABSTRACT

Objective To study the effects of different level of iodine nutrition on the thyroid function in women of reproductive age. Methods A total of 100 (50 from each) women of reproductive age but not pregnant were collected from iodine deficient and adequate areas. The questionnaire was obtained individually with items concerning personal history of thyroid diseases, goiters and category of edible salt and drinking water based on the project design. The household salt and drinking water were collected for measuring iodine content, and blood samples were obtained for TSH, FT4 and FT3 testing. Results The coverage of iodized salt and the median level of urinary iodine in iodine deficient women(72.0% and 95.5 μg/L) were obviously lower than that in iodine sufficient women(100.0% and 167.4 μg/L, χ2=16.28, U = 632.00, P < 0.01). Median level of serum TSH in iodine deficient women (2.56 m U/L) appeared in an increasing tendency compared to the iodine sufficient women (1.88 mU/L), but there was no significance (U=990.50, P > 0.05). Serum FT4 mean level in iodine deficient women [(14.7±2.0) pmol/L]was lower than that in iodine sufficient women[(17.0±3.8)pmoI/L, t=3.76, P<0.01]. There was no difference in serum FT3 between two group women[(5.1±1.4), (4.8±0.5)pmoI/L, t = 1.59, P > 0.05]; but FT3/FT4 ratio in iodine deficient women(0.33±0.04) was markedly higher than that in the iodine sufficient women(0.30±0.04, t=3.13, P<0.01). The percentage of thyroid dysfunction in iodine deficient women[20.0% (10/50)]was higher compared with the iodine sufficient women[8.0%(4/50)], but without significance(χ2=2.99, P>0.05). Conclusions Iodine deficiency is a primary cause leading to hypothyroid in women of reproductive age. Long term of iodized salt usage is an efficient way to correct iodine deficiency.

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