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Biomedical subjects

J D Glass

Publications and source records attributed to J D Glass.

180 records · Page 10Linked to original sources

Leucylglycinamide released from oxytocin by human uterine enzyme.

Uteri of pregnant and nonpregnant women contain enzymic activities which inactivate oxytocin. A potent enzyme, which has been partially purified from uterine homogenates, cleaves the prolyl-leucyl peptide bond of oxytocin. This findinig associates for the first time the release of the dipeptide leucylglycinamide with the degradation of neurohypophyseal hormones.

Buffers↗

Enzymatic inactivation of peptide hormones possessing a C-terminal amide group.

A partially purified enzyme extracted from the bladder of the toad, Bufo marinus L., was found to cleave the glycine amide moiety from oxytocin, 8-lysine-vasopressin, 8-arginine-vasopressin, and other hormone analogs terminating in a primary carboxamide group; however, this enzyme does not attack hormone analogs terminating with a methylamide, dimethylamide, or carboxyl group. Preliminary experiments indicate that a functionally similar enzyme is also present in the mammalian kidney, the major target organ of neurohypophyseal antidiuretic hormones. This enzyme, besides inactivating oxytocin and 8-lysine-vasopressin, also cleaves the phenylalanine amide moiety from a tetrapeptide analog of gastrin, another hormone terminating in a primary carboxamide group. Attention is drawn to the possible general significance of "carboxamidopeptidases" for the termination of the action of peptide hormones in which the C-terminal amino acid residue bears a carboxamide group.

Amides↗

AIDS-related CNS cryptococcosis: radiologic-pathologic correlation.

PURPOSE: This study evaluates the effectiveness of cranial CT and MR in detecting autopsy findings of AIDS-related CNS cryptococcosis. METHODS: Final imaging studies compared with pathology were CT in eight patients (five with contrast) and MR in five patients (all with Gd-DTPA). RESULTS: Neither modality effectively identified cryptococcal meningitis. Punctate hyperintensities were seen in all patients with MR and corresponded pathologically to both perivascular spaces dilated by cryptococcal infection and cryptococcomas. Pathologically, cryptococcomas were more common than dilated perivascular spaces. MR detected more cryptococcomas than did CT, but both modalities underestimated the number of lesions seen at autopsy. Contrast enhancement of cryptococcomas and cryptococcal meningitis was uncommon. CONCLUSIONS: CNS cryptococcosis was more effectively demonstrated by MR than by CT, but both modalities underestimated the pathologic extent of the disease. Cryptococcal lesion contrast enhancement was unusual possibly because of the immunocompromised state of our patients and the unique characteristics of the organism itself.

Acquired Immunodeficiency Syndrome↗