Get help from the best in academic writing.

XRCC1 Polymorphism and Systemic Lupus Erythematosus

XRCC1 Arg399Gln and Arg194Try Gene Polymorphisms and the Risk of Systemic Lupus Erythematosus in Iranian population (a pilot study)
Saeedeh Salimi, Milad Mohammadoo-khorasani, Ehsan Tabatabai, Mahnaz Sandoughi, Zahra Zakeri
Corresponding Author: Milad Mohammadoo-khorasani

Analysis of T-cell Immunoglobulin and Mucin 1 Gene -416G

Association analysis of T-cell immunoglobulin and mucin 1 gene -416G > C polymorphism with asthma in center of Iran.
TIM1, One of the gene family members of T cell immunoglobulin (Ig) domain and mucin domain (TIM) expressing on TH2 cells, promotes producing of Th2 signiture cytokines and increases a series of responses in this cells which could be one of the causes of asthma or asthma-related phenotypes.We are determined to investigate whether a TIM-1 promoter single nucleotide polymorphism (SNP), -416G > C, associated with asthma in Chaharmahal va Bakhtiari and Isfahan, Iran.
In a case-control study existence of the -416G > C polymorphism was examined using polymerase chain reaction (PCR) and restriction fragment length polymorphism in 130 healthy control and 130 asthmatic patient. Additionally, the relationship between this polymorphism genotypes and total serum IgE levels in this iranian population was evaluated.
We discovered no association between the -416G > C polymorphism and asthma susceptibility in this population (p>0.05). But our results showed this significant relation between this polymorphism and serum IgE levels (p<0.05).
These results suggest that -416G > C polymorphism in TIM-1 gene, could not be a predisposing factor for asthma susceptibility in Chaharmahal va Bakhtiari and Isfahan but CC genotype of this SNP can be effective in increasing blood sugar levels in patients with asthma in a subset of Iranian population.
Key words
asthma, T-cell immunoglobulin and mucin domain molecule-1, polymorphism, single nucleotide polymorphism
Asthma is a chronic inflammatory disorder of the airway that result from abnormal (irregular) immune responses and induced by environmental factors in genetically susceptible individuals (p1 Palmer