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Articles by G Armstrong
Total Records ( 2 ) for G Armstrong
  Y Liu , S Shete , L. E Wang , R El Zein , C. J Etzel , F. W Liang , G Armstrong , S Tsavachidis , M. R Gilbert , K. D Aldape , J Xing , X Wu , Q Wei and M. L. Bondy

Background: DNA strand breaks pose the greatest threat to genomic stability. Genetically determined mutagen sensitivity predisposes individuals to a variety of cancers, including glioma. However, polymorphisms in DNA strand break repair genes that may determine mutagen sensitivity are not well studied in cancer risk, especially in gliomas.

Methods: We correlated genotype data for tag single-nucleotide polymorphisms (tSNPs) of DNA strand break repair genes with a gamma-radiation-induced mutagen sensitivity phenotype [expressed as mean breaks per cell (B/C)] in samples from 426 glioma patients. We also conducted analysis to assess joint and haplotype effects of single-nucleotide polymorphisms (SNPs) on mutagen sensitivity. We further validate our results in an independent external control group totaling 662 subjects.

Results: Of the 392 tSNPs examined, we found that mutagen sensitivity was modified by one tSNP in the EME2 gene and six tSNPs in the RAD51L1 gene (P < 0.01). Among the six RAD51L1 SNPs tested in the validation set, one (RAD51L1 rs2180611) was significantly associated with mutagen sensitivity (P = 0.025). Moreover, we found a significant dose–response relationship between the mutagen sensitivity and the number of adverse tSNP genotypes. Furthermore, haplotype analysis revealed that RAD51L1 haplotypes F-A (zero adverse allele) and F-E (six adverse alleles) exhibited the lowest (0.42) and highest (0.93) mean B/C values, respectively. A similar dose–response relationship also existed between the mutagen sensitivity and the number of adverse haplotypes.

Conclusion: These results suggest that polymorphisms in and haplotypes of the RAD51L1 gene, which is involved in the double-strand break repair pathway, modulate gamma-radiation-induced mutagen sensitivity.

  A. C.Y To , G Armstrong , I Zeng and M. W.I. Webster

Background— The decision on whether to implant a drug-eluting or bare-metal stent during percutaneous coronary intervention (PCI) depends in part on the perceived likelihood of the patient developing late stent thrombosis. Noncardiac surgery and bleeding are associated with discontinuation of dual antiplatelet therapy and with increased stent thrombosis. We assessed the incidence of and predictors for subsequent noncardiac surgery and bleeding episodes in patients who had undergone PCI.

Methods and Results— Hospital discharge coding data were used to identify all adult patients undergoing public hospital PCI in New Zealand from 1996 to 2001. Hospital admissions during the ensuing 5 years were analyzed for noncardiac surgery and bleeding episodes. Eleven thousand one hundred fifty-one patients (age, 62±11 years; 30% women) underwent PCI, mainly for an acute coronary syndrome (73%). During the 5-year follow-up, 26% of the population underwent at least 1 noncardiac surgical procedure (23% orthopedic, 20% abdominal, 12% urologic, 10% vascular, 35% others) and 8.6% had at least 1 bleeding episode either requiring or occurring during hospitalization. Of those, half were gastrointestinal, and one quarter of bleeding events required blood transfusion. The main clinical predictors of noncardiac surgery were advanced age, previous noncardiac surgery, osteoarthritis, and peripheral vascular disease. A previous bleeding admission and age were the strongest predictors of subsequent bleeding.

Conclusions— Noncardiac surgery is required frequently after PCI, whereas bleeding is less common. Before implanting a drug-eluting or bare-metal stent, individual patient risk stratification by the interventional cardiologist should include assessment of whether there is an increased likelihood of needing noncardiac surgery or developing bleeding.

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