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Articles by S Nair
Total Records ( 4 ) for S Nair
  K. E Holt , Y. Y Teo , H Li , S Nair , G Dougan , J Wain and J. Parkhill

Summary: Here, we present a method for estimating the frequencies of SNP alleles present within pooled samples of DNA using high-throughput short-read sequencing. The method was tested on real data from six strains of the highly monomorphic pathogen Salmonella Paratyphi A, sequenced individually and in a pool. A variety of read mapping and quality-weighting procedures were tested to determine the optimal parameters, which afforded ≥80% sensitivity of SNP detection and strong correlation with true SNP frequency at poolwide read depth of 40x, declining only slightly at read depths 20–40x.

  S Nair , V. D Kekatpure , B. L Judson , A. B Rifkind , R. D Granstein , J. O Boyle , K Subbaramaiah , J. B Guttenplan and A. J. Dannenberg

UV radiation (UVR) and exposure to tobacco smoke, a source of polycyclic aromatic hydrocarbons (PAH), have been linked to skin carcinogenesis. UVR-mediated activation of the aryl hydrocarbon receptor (AhR) stimulates the transcription of CYP1A1 and CYP1B1, which encode proteins that convert PAH to genotoxic metabolites. We determined whether UVR exposure sensitized human keratinocytes to PAH-induced DNA adduct formation. UVR exposure induced CYP1A1 and CYP1B1 in HaCaT cells, an effect that was mimicked by photooxidized tryptophan (aTRP) and FICZ, a component of aTRP. UVR exposure or pretreatment with aTRP or FICZ also sensitized cells to benzo(a)pyrene (B[a]P)-induced DNA adduct formation. NF, an AhR antagonist, suppressed UVR-, aTRP-, and FICZ-mediated induction of CYP1A1 and CYP1B1 and inhibited B[a]P-induced DNA adduct formation. Treatment with 17-AAG, an Hsp90 inhibitor, caused a marked decrease in levels of AhR; inhibited UVR-, aTRP-, and FICZ-mediated induction of CYP1A1 and CYP1B1; and blocked the sensitization of HaCaT cells to B[a]P-induced DNA adduct formation. FICZ has been suggested to be a physiologic ligand of the AhR that may have systemic effects. Hence, studies of FICZ were also carried out in MSK-Leuk1 cells, a model of oral leukoplakia. Pretreatment with -naphthoflavone or 17-AAG blocked FICZ-mediated induction of CYP1A1 and CYP1B1, and suppressed the increased B[a]P-induced DNA adduct formation. Collectively, these results suggest that sunlight may activate AhR signaling and thereby sensitize cells to PAH-mediated DNA adduct formation. Antagonists of AhR signaling may have a role in the chemoprevention of photocarcinogenesis.

  M Luckie , B Irwin , S Nair , J Greenwood and R. Khattar
  No Description
  M Luckie , B Irwin , S Nair , J Greenwood and R. Khattar

Cardiac disease in patients with transfusion-dependent beta-thalassaemia major is well described. Cardiac manifestations may include left ventricular wall thickening and both systolic and diastolic dysfunctions. We describe a group of family members, including a pair of identical twins, each of whom suffered from thalassaemia major requiring multiple transfusions. Cardiac magnetic resonance demonstrated myocardial iron overload, and impairment of systolic function. Echocardiography confirmed both significant left ventricular systolic and diastolic impairment, along with features consistent with left ventricular non-compaction. This finding has not been noted in association with thalassaemia-related cardiac disease before. We then review the cardiac manifestations which occur in association with thalassaemia major.

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