Stroke has emerged as the second commonest cause of mortality worldwide and is a major public health problem. For the first time, we present here the association of human leucocyte antigen (HLA)-DRB1*/DQB1* alleles and haplotypes with ischaemic stroke in South Indian patients. Ischaemic stroke (IS) cases and controls were genotyped for HLA-DRB1*/DQB1* alleles by polymerase chain reaction sequence-specific primers (PCR-SSP) method. The frequencies of HLA class II alleles such as DRB1*04, DRB1*07, DRB1*11, DRB1*12, DRB1*13, DQB1*02 and DQB1*07 were high in IS patients than in the age- and gender-matched controls, suggesting that the individuals with these alleles are susceptible to ischaemic stroke in South India. The frequencies of alleles such as DRB1*03, DRB1*10, DRB1*14, DQB1*04 and DQB1*05 were less in IS cases than in the controls, suggesting a protective association. Haplotypes DRB1*04-DQB1*0301, DRB1*07-DQB1*02, DRB1*07-DQB1*0301, DRB1*11-DQB1*0301 and DRB1*13-DQB1*06 were found to be high in IS patients conferring susceptibility. The frequency of haplotype DRB1*10-DQB1*05 was high in controls conferring protection. IS-LVD and gender-stratified analysis too confirmed these susceptible and protective associations. Thus, HLA-DRB1*/DQB1* alleles and haplotypes strongly predispose South Indian population to ischaemic stroke. Further studies in different populations with large sample size or the meta-analysis are needed to explain the exact mechanism of associations of HLA gene(s) with IS.

The HLA-DQB1* region exhibits complex associations with autoimmune thyroid disease (AITD). AITD patients (Hashimoto's thyroiditis, HT = 180; Graves' disease, GD = 55) and age/sex matched controls (n = 235) were genotyped for DQB1* alleles by PCR-SSP. Alleles DQB1*02:02, *06:03, *06:09, *03:02, and *03:03 showed an increased risk and *02:01, *05:02, and *06:02 showed a protection toward AITD. Multiple sequence alignment was used to find out the amino acid variations within the peptide-binding pockets of susceptible and/or protective DQB1* alleles. We observed susceptible associations for amino acids 'Glu(P < 0.0007)' and 'Leu(P < 3.8 × 10)' in P1, 'Leu(P < 4.0 × 10)' in P4, 'His(P < 5.0 × 10)' and 'Ala(P < 3.6 × 10)' in P9 toward HT; and 'Gly(P < 0.0004)' in P1 and 'Asp(P < 1.9 × 10)' in P9 towards GD. Protective associations were observed for amino acids 'Ala(P < 8.2 × 10)' and 'Tyr(P < 0.0003)' in P1, 'Gly(P < 4.9 × 10)' and 'Ser(P < 4.9 × 10)' in P4, 'Phe(P < 0.0007)' and 'Ser(P < 0.0016)' in P9 towards HT. Thus, the present study revealed that DQB1* alleles and putative amino acid residues play an important role in susceptibility toward AITD in south India.

The aim of this study was to measure the serum concentrations of heat shock protein (HSP) 70 and C-reactive protein (CRP) and the expression levels of the hsp70 gene among frequent users of mobile phones (FUMPs). We enrolled 120 employees of information technology (IT)/IT enabled service companies (FUMPs; IT professionals) and 102 infrequent users of mobile phones (IFUMPs; people from non-IT professions) as controls. The serum concentrations of HSP70 and CRP were measured by enzyme-linked immunosorbant assay and hsp70 gene expression by reverse transcription polymerase chain reaction. Significantly higher concentrations of serum HSP70 (P < 0.00012) and CRP (P < 0.04) were observed among FUMPs than IFUMPs. A higher level of hsp70 gene expression (fold induction) was observed among FUMPs than IFUMPs (P < 7.06 × 10-13). In contrast to the duration of exposure-dependent increase of serum concentration of CRP, the serum HSP70 concentration was found to be independent of the duration of exposure to mobile phones. Thus, the study convincingly demonstrated the role of serum HSP and CRP as systemic inflammatory biomarkers for mobile phone-induced radiation.