Biomedical subjects

James G Taylor

Publications and source records attributed to James G Taylor.

4 recordsLinked to original sources

PubMed2003

Association between chronic disseminated candidiasis in adult acute leukemia and common IL4 promoter haplotypes.

Chronic disseminated candidiasis (CDC) is a form of Candida species infection observed primarily in patients with acute leukemia. To investigate possible genetic factors associated with CDC, we conducted a pilot study of 40 patients with both leukemia and CDC and 50 control patients with leukemia only. A common haplotype of the IL4 promoter (-1098T/-589C/-33C) was overrepresented in patients with CDC (P= .01; odds ratio [OR], 2.16), whereas another common haplotype (-1098T/-589T/-33T) appeared to be protective against CDC (P= .018; OR, 0.47). Genetic variants of IL4 could contribute to the development of CDC in patients with acute leukemia.

Adolescent↗

PubMed2002

Variants in the VCAM1 gene and risk for symptomatic stroke in sickle cell disease.

Stroke is a major cause of morbidity and mortality in sickle cell (SS) disease. Genetic risk factors have been postulated to contribute to this clinical outcome. The human genome project has substantially increased the catalog of variations in genes, many of which could modify the risk for manifestations of disease outcome in a monogenic disease, namely SS. VCAM1 is a cell adhesion molecule postulated to play a critical role in the pathogenesis of SS disease. We identified a total of 33 single nucleotide polymorphisms (SNPs) by sequencing the entire coding region, 2134 bp upstream of the 5' end of the published cDNA, 217 bp downstream of the 3' end of the cDNA, and selected intronic regions of the VCAM1 locus. Allelic frequencies for selected SNPs were determined in a healthy population. We subsequently analyzed 4 nonsynonymous coding, 2 synonymous coding, and 4 common promoter SNPs in a genetic association study of clinically apparent stroke in SS disease conducted in a cohort derived from a single institution in Jamaica (51 symptomatic cases and 51 matched controls). Of the 10 candidate SNPs analyzed in this pilot study, the variant allele of the nonsynonymous SNP, VCAM1 G1238C, may be associated with protection from stroke (odds ratio [OR] 0.35, 95% confidence interval [CI] 0.15-0.83, P =.04). Further study is required to confirm the importance of this variant in VCAM1 as a clinically useful modifier of outcome in SS disease.

Alleles↗

PubMed2002

Patterns of low-affinity immunoglobulin receptor polymorphisms in stroke and homozygous sickle cell disease.

Symptomatic stroke is a major complication of homozygous sickle cell (SS) disease, with a prevalence of approximately 10%. An elevated peripheral leukocyte count has been identified as a risk factor for hemorrhagic stroke in adults with SS disease. It has been observed that sickle cells coated with immunoglobulin have increased adherence to endothelial cells or phagocytes, possibly via binding to the low-affinity Fcgamma receptors. Common polymorphisms have been described in three low-affinity receptors: FCGR2A, FCGR3A, and FCGR3B; each has been shown to alter biological function, and each has also been associated with disease susceptibility. On the basis of this information, we evaluated common genetic variants of the low-affinity Fcgamma receptors for an association with symptomatic stroke in SS disease in a pilot case-control study of 51 Jamaican adult SS disease stroke cases and 51 SS disease-matched controls. Comparison of allelic distributions between cases and controls at 3 loci, FCGR2A (P = 0.39), FCGR3A (P = 0.67), FCGR3B (P = 0.35), failed to demonstrate a significant association. In a separate analysis, the FCGR2A/FCGR3A two-locus combination does not appear to segregate randomly (P(COR) = 0.0053), suggesting that these two loci could be linked in this population. We conclude that polymorphisms of the low-affinity Fcgamma receptors are not associated with stroke in SS disease.

Adolescent↗

PubMed2002

Using genetic variation to study immunomodulation.

The generation of a draft sequence of a human genome has led to the identification of millions of common variants, known as single nucleotide polymorphisms, which constitute a resource for studying complex diseases. Currently, high-density maps of variants in candidate genes, chromosomal regions or the entire genome should encourage investigation of determinants of human immune response, using quantitative analysis. Ultimately, this approach should identify novel targets for therapeutic intervention.

Adjuvants, Immunologic↗