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This meta-analysis was undertaken in an attempt to understand the relationships of functional polymorphisms in the SELE and SELP genes to myocardial infarction (MI) risk. The PubMed, CISCOM, CINAHL, Web of Science, Google Scholar, EBSCO, Cochrane Library, and CBM databases were searched for relevant articles published before March 1st, 2013 without any language restrictions. Meta-analysis was conducted using the STATA 12.0 software. Crude odds ratios with 95 % confidence intervals were calculated. The effect of SELE and SELP genetic polymorphisms on the pathogenesis of MI was investigated in this meta-analysis with a total of ten case-control studies, including 2,696 MI patients and 4,724 healthy subjects. Eight single nucleotide polymorphisms were assessed, including polymorphisms 98G/T, 128S/R and 561A/C in the SELE gene, and polymorphisms 715T/P, 599V/L, 290S/N, 562N/D and 2123G/C in the SELP gene. The results of our meta-analysis suggested that SELE genetic polymorphisms might be correlated with an increased risk of MI, especially for 128S/R and 561A/C polymorphisms. A subgroup analysis by ethnicity was conducted to investigate its effects on susceptibility to MI. The results revealed positive significant correlations between SELE genetic polymorphisms and the risk of MI among Asians, but not among Caucasians (all P > 0.05). Nevertheless, no significantly correlations were found between SELP genetic polymorphisms and MI risk (all P > 0.05). In the subgroup analysis by ethnicity, we also did not observe significant associations between SELP genetic polymorphisms and MI risks among both Asians and Caucasians (all P > 0.05). The current meta-analysis suggests that SELE genetic polymorphisms may contribute to the development of MI, especially for the 128S/R and 561A/C polymorphisms among Asians. However, SELP genetic polymorphisms may not be important risk factors in MI.
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http://dx.doi.org/10.1007/s11033-014-3323-2 | DOI Listing |
Cell Mol Biol (Noisy-le-grand)
September 2025
Department of Biology, College of Education for Pure Sciences, University of Kerbala, Kerbala, Iraq.
Gastric cancer is one of the causes of deaths related to cancer across the globe and both genetic and environmental factors are the most prominent. Causes of its pathogenesis. This paper researches the expression of the C-FOS gene.
View Article and Find Full Text PDFPlant Dis
September 2025
South Dakota State University, 2380 Research Parkway, 113B Seed Tech, Brookings, Brookings, South Dakota, United States, 57007;
Bacterial leaf streak (BLS), caused by pv. (), has recently emerged as a significant threat to wheat production in the Northern Great Plains region of the US. Deploying resistant cultivars is an economical and practical method of controlling BLS.
View Article and Find Full Text PDFBrief Funct Genomics
January 2025
School of Mathematics and Statistics, Henan University of Science and Technology, No. 263 Kaiyuan Avenue, Luolong District, Luoyang, Henan 471000, China.
Background: Comorbidities and genetic correlations between gastrointestinal tract diseases and psychiatric disorders have been widely reported, but the underlying intrinsic link between Alzheimer's disease (AD) and inflammatory bowel disease (IBD) is not adequately understood.
Methods: To identify pathogenic cell types of AD and IBD and explore their shared genetic architecture, we developed Pathogenic Cell types and shared Genetic Loci (PCGL) framework, which studied AD and IBD and its two subtypes of ulcerative colitis (UC) and Crohn's disease (CD).
Results: We found that monocytes and CD8 T cells were the enriched pathogenic cell types of AD and IBDs, respectively.
J Integr Neurosci
August 2025
Laboratory of Genomic Research, Research Institute for Genetic and Molecular Epidemiology, Kursk State Medical University, 305041 Kursk, Russia.
G3 (Bethesda)
September 2025
Department of Biology, Stanford University, Stanford, CA 94305, USA.
The ψ directionality index was introduced by Peter & Slatkin (Evolution 67: 3274-3289, 2013) to infer the direction of range expansions from single-nucleotide polymorphism variation. Computed from the joint site frequency spectrum for two populations, ψ uses shared genetic variants to measure the difference in the amount of genetic drift experienced by the populations, associating excess drift with greater distance from the origin of the range expansion. Although ψ has been successfully applied in natural populations, its statistical properties have not been well understood.
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