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Martin J Hessner

Publications and source records attributed to Martin J Hessner.

20 records · Page 2Linked to original sources

The design of a gene chip for functional immunological studies on a high-quality control platform.

We have created an immunology-related microarray chip containing primarily known genes with well-studied functional properties. By looking at known genes rather than expressed sequence tags, we hope to gain a better understanding of immunological pathways and how they work. The immunology gene chip contains genes from the following functional categories: T cell genes; B cell genes; dendritic cell genes; chemokine and cytokine genes; apoptosis genes; cell cycle genes; cell interaction genes; general hematology and immunology genes; and adhesion genes. We have also developed a novel three-color cDNA array platform in which arrays are directly visualized before hybridization, which allows us to select only high-quality chips for our experiments. In an effort to provide quantitative quality control for each array element as well as the entire chip, we have developed Matarray, a software package for image processing and data acquisition. With Matarray, we have built a quantitative data filtering and normalization scheme that has proved to be more efficient than the existing methods. The list of immunology chip genes is available from the authors.

Chemokines↗

Factor V Leiden: a genetic risk factor for thrombotic microangiopathy in patients with normal von Willebrand factor-cleaving protease activity.

Thrombotic microangiopathy (TM) is associated with abnormalities of von Willebrand factor-cleaving protease (VWCP) and other hemostatic factors. This study hypothesized that TM patients might have genetically determined thrombotic risk factors that predispose them to aberrant microvascular thrombosis. DNA samples from 30 white and 12 African American adult TM patients were analyzed for genetic alleles associated with vascular thrombosis, and plasma samples were analyzed for levels of VWCP activity. DNA was analyzed by using allele-specific polymerase chain reaction for factor V 1691A (Leiden), factor II 20 210A, methylenetetrahydrofolate reductase 667T, type 1 plasminogen activator inhibitor 4G/5G, and platelet GPIa 807T. Patients were segregated by race (white or African American) and plasma level of VWCP activity (normal or deficient). The prevalence of factor V Leiden was significantly increased among the white TM patients that had normal VWCP activity: 4 (36%) of 11 patients compared with 6 (3%) of 186 white control subjects possessed the factor V Leiden allele (P <.001; odds ratio, 17.1; 95% confidence interval, 5.4-54.0). No factor V Leiden alleles were detected in 19 white TM patients with intermediate or deficient levels of VWCP activity or in any of 12 African American patients. The prevalence of other thrombosis-associated alleles did not differ between TM patients and control subjects. These findings suggest that factor V Leiden may be a pathogenic risk factor in TM patients that have normal VWCP activity.

3' Untranslated Regions↗