LDL species heterogeneity in the atherogenic dyslipidemia of polycystic ovary syndrome

One of the important risk factors for coronary heart disease is dyslipidemia. Several lipid abnormalities have been studied in patients with polycystic ovary syndrome (PCOS), but the relationship between PCOS and low-density lipoprotein (LDL) subclass pattern is not clear. A case-control study was designed to look into lipid differences, and LDL size was analyzed by a newly developed polyacrylamide tube gel electrophoresis method. Results indicated that only PCOS status and serum triglyceride levels were independently associated with LDL particle size. The apolipoprotein (Apo)A-I level was higher in PCOS patients with small dense LDL (sdLDL). PCOS seems to result in smaller LDL particle size and higher ApoA-I levels independent of triglyceride levels. After adjusting for triglyceride levels, other traits of insulin resistance syndrome (IRS) were not associated with LDL size phenotype, suggesting that the IRS-related sdLDL is linked most strongly to alterations in triglyceride levels

Association of Hashimoto's thyroiditis with cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) and inducible co-stimulator (ICOS) genes in a Kuwaiti population

Analysing two CTLA-4 markers [exon 1 A49G single nucleotide polymorphism (SNP) and exon 4 3′UTR (AT)n repeat] and the ICOS intron 4 (GT)n marker for their potential association with HT, and exploring the effect of the tested SNPs on the CTLA-4 isoform expression at the mRNA and protein levels. Total of 270 age-gender-ethnically matched subjects were genotyped by fluorescent-labelled restriction fragment length polymorphism, multiplex PCR, and fragment analysis. Sequencing was used to confirm the genotyping results. Expression of the full-length and soluble CTLA-4 mRNAs analysed using real-time PCR. Sera from subjects were screened for sCTLA-4 using ELISA. Tested subjects revealed ten alleles and sixteen genotypes of CTLA-4 3′UTR(AT)n. The 3′UTR(AT)n was significantly associated with HT: allele (AT)15 and genotype 15/15 were found to cause susceptibility to HT (P = 0.004, OR = 2.13, 95 % CI = 1.26-3.58 and P = 0.029, OR = 2.77, 95 % CI = 1.1-6.94, respectively), whereas allele (AT)6 and genotype 6/6 were found to be protective of HT (P = 0.00002, OR = 0.36, 95 % CI = 0.227-0.57 and P = 0.001, OR = 0.357, 95 % CI = 0.1980.64, respectively). SNP A49G and ICOS(GT)n revealed no significant association with HT (P > 0.05). The expression of sCTLA-4 was inversely proportional to the number of 3′UTR(AT)n repeats, with heterozygous and longer (AT)n repeats showing lower levels of sCTLA-4 mRNA than those with shorter alleles in HC and HT (P = 0.001 and P = 0.04, respectively). Significant increase in the serum level of sCTLA-4 was observed in HT patients compared with the HC (P = 0.0007). The novel finding in our study is that the CTLA-4 3′UTR(AT)n proven to be a key player in the pathogenesis of HT