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Biomedical subjects

R S Zeiger

Publications and source records attributed to R S Zeiger.

66 records · Page 4Linked to original sources
PubMed1977

Delayed cold-induced urticaria: a dominantly inherited disorder.

A delayed cutaneous response to cold, characterized by areas of erythematous, edematous deep swelling at 9 to 18 hr after experimental ice challenge, was recognized in a 10-yr-old boy and several members of his family. Biopsy of the cold-induced lesion showed edema and an infiltrate of mononuclear cells; mast cells were normal, and immunoglobulins, complement factors, and fibrin were not detected by immunofluorescence techniques. Local cold challenge did not release histamine or induce alterations in the complement system or the enzymes, histaminase, and histamine methyl transferase. The delayed cutaneous response to cold could not be passively transferred with serum or tissue extracts to monkey skin. Family studies suggested an autosomal-dominant mode of inheritance.

Amine Oxidase (Copper-Containing)↗
PubMed1977

Histaminase release from human eosinophils.

Phagocytosis of opsonized zymosan by human eosinophils results in a dose-dependent noncytotoxic release of histaminase as well as arylsulfatase and beta-glucuronidase. The calcium ionophore A23187 also stimulates release of eosinophil histaminase at concentrations of ionophore which barely release arylsulfatase and beta-glucuronidase. Zymosan-induced histaminase release from eosinophils but not from neutrophils was abolished or markedly reduced in the presence of cytochalasin B, suggesting a difference in the mechanisms of histaminase release from the two granulocyte cell types.

Amine Oxidase (Copper-Containing)↗
PubMed1976

Histaminase release from human granulocytes.

Histaminase (EC-1.4.3.6), one of the two catabolic enzymes for histamine, is contained in human granulocytes. Opsonized zymosan or the calcium ionophore A-23187 induce a dose-dependent release of histaminase from human granulocytes in vitro. Release is completed within 30 min, is temperature dependent, and requires divalent cations. Opsonized zymosan-induced histaminase release was maximal in the presence of both calcium and magnesium, whereas ionophore release was magnesium independent. The total cellular content of histaminase could be released by both opsonized zymosan and ionophore. In contrast, only 25% of the cellular beta glucuronidase, a lysosomal enzyme, was released after maximal stimulation with opsonized zymosan; there was minimal release of beta glucuronidase with ionophore. Zymosan- and ionophore-induced histaminase release was inhibited by agents that are presumed to interfere with cell metabolism and disrupt microtubules. Human granulocytes therefore may modulate the effect of histamine by releasing histaminase at a site of inflammation. Studies of granulocyte histaminase release in vitro may also provide a new model to explore granulocyte function and secretion.

Amine Oxidase (Copper-Containing)↗
PubMed1976

Histamine metabolism. II. Cellular and subcellular localization of the catabolic enzymes, histaminase and histamine methyl transferase, in human leukocytes.

Histaminase (EC 1.4.3.6) activity has been demonstrated in human eosinophils and neutrophils, but not in mononuclear cells, with the use of a new and specific thin-layer radiochromatographic enzyme assay. Leukocyte histaminase was physicochemically and functionally similar to histaminase isolated from human placenta and was principally localized to the 27,000-g granule-rich fraction of eosinophil and neutrophil homogenates. Histamine methyl transferase (EC 2.1.1.8), on the other hand, was detected in monocytes but not in granulocytes, eosinophils, lymphocytes, or platelets, and was localized solely to the 100,000-g cell sap supernatant fraction. These data suggest a role of human leukocytes in the catabolism of histamine and therefore in the modulation of histamine-mediated inflammatory reactions.

Amine Oxidase (Copper-Containing)↗
PubMed1976

Histamine metabolism. I. Thin-layer radiochromatographic assays for histaminase and histidine decarboxylase enzyme activities.

Thin-layer radiochromatographic methods for the measurement of histaminase and histidine decarboxylase activities have been developed. The assays are specific for the respective enzymes, are sensitive and reproducible, and can be performed using commercially available substrates. The histaminase assay permits determination of enzyme activity from 2.5 mul of pregnancy sera, 1-2 X 10(6) human granulocytes, and microgram quantities of partially purified human placenta histaminase with an error of less than 5 per cent. The histidine decarboxylase assay permits measurement of nanogram quantities of newly formed histamine from as few as 2 X 10(4) rat peritoneal mast cells or rat basophilic leukemia cells with an error of less than 5 per cent.

Amine Oxidase (Copper-Containing)↗
PubMedDate not supplied

Diagnosis and management of rhinitis during pregnancy.

Chronic nasal symptoms occur commonly in pregnant women. The most frequent causes of rhinitis during pregnancy are allergic rhinitis, bacterial rhinosinusitis and rhinitis medicamentosa. The appropriate diagnosis in the individual pregnant woman can usually be established on the basis of the history, physical examination and nasal cytology. Benefit-risk considerations in the management of gestational rhinitis are discussed in detail.

Diagnosis, Differential↗
PubMedDate not supplied

Osteoporosis in corticosteroid-treated asthmatic patients: clinical correlates.

This study sought to identify clinical and laboratory characteristics associated with the development of osteoporosis in 44 corticosteroid (CS)-treated asthmatic patients. Percentage predicted bone density was inversely correlated with both the duration of CS therapy (r = -.39, p = 0.009) and 24-hour urine calcium excretion (chi 2 = 5.2, p = 0.022). Bone density was not related to prednisone equivalent dose, alternate day versus daily therapy or serum cortisol levels. These data suggest that (1) long duration of CS therapy and increased urine calcium may identify patients at increased risk of developing CS-induced osteoporosis, and (2) urinary loss of calcium may be of particular importance in the pathogenesis of this condition.

Adrenal Cortex Hormones↗