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Biomedical subjects

H Travers

Publications and source records attributed to H Travers.

47 records · Page 3Linked to original sources
PubMed1977

Bowel perforation with candidiasis.

Spontaneous multiple jejunal perforations developed in a relatively normal patient. Candida albicans was cultured from a biopsy specimen of an area of perforation and from peritoneal fluid. Yeasts and pseudohyphae were seen deep within the necrotic mucosa. Serial determinations of precipitating and agglutinating antibodies support the diagnosis of invasive candidiasis causing this unusual presentation.

Adult↗
PubMed1973

Rubella reinfection.

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False Positive Reactions↗
PubMedDate not supplied

Homozygotes for Huntington's disease.

Careful comparison of symptomatic individuals with normal controls has revealed the primary biochemical abnormality in many human genetic diseases, particularly recessive disorders. This strategy has proved less successful for most human disorders which are not recessive, and where a single copy of the aberrant gene has clinically significant effects even though the normal gene product is present. An alternative approach that eliminates the impediment of a normal protein in affected individuals is to study homozygotes for the mutant allele. For virtually all dominant human disorders in which homozygotes have been described, symptoms have been significantly more severe in the homozygote than in the heterozygote. Thus, these disorders do not conform to the classical definition of dominance which states that homozygotes and heterozygotes for a defect are phenotypically indistinguishable. Instead, they display incomplete dominance, indicating that the normal allele may play a role in ameliorating the disease process. The D4S10 locus, defined by the probe G8 and linked to the gene for Huntington's disease (HD), has permitted us to identify individuals with a high probability of being homozygous for this autosomal dominant neurodegenerative disorder. These homozygotes do not differ in clinical expression or course from typical HD heterozygotes. HD appears to be the first human disease of genetically documented homozygosity that displays complete phenotypic dominance.

Genes, Dominant↗
PubMedDate not supplied

The effect of antiplatelet therapy on the incidence of carotid plaque hemorrhage.

Hemorrhage into the carotid atheroma has recently been gaining attention with respect to the pathophysiology of cerebrovascular disease. Many patients are currently receiving platelet agents for various vascular diseases. Some researchers have postulated that antiplatelet therapy may be detrimental by possibly inducing intraplaque hemorrhage or by increasing preexisting hemorrhage. This retrospective study was undertaken to determine if the use of antiplatelet therapy increases the incidence of carotid plaque hemorrhage. Ninety-five consecutive carotid endarterectomies were performed and the atheromas examined microscopically for intraplaque hemorrhage. The atheromas were divided into two groups; those from patients receiving preoperative antiplatelet therapy and those who were not. Forty-five atheromas were removed from patients receiving preoperative antiplatelet therapy; 39 (87%) of these demonstrated intraplaque hemorrhage. Of the 50 atheromas which were removed from patients not receiving preoperative therapy, 45 (90%) showed intraplaque hemorrhage. We conclude that antiplatelet therapy does not increase the incidence of carotid plaque hemorrhage.

Aged↗