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Biomedical subjects

R B Zurier

Publications and source records attributed to R B Zurier.

At least 91 records · Page 5Linked to original sources
PubMed1980

Suppression by prostaglandin E1 of vascular permeability induced by vasoactive inflammatory mediators.

Systemic treatment of rats with prostaglandin E1 or with its stable derivative, 15-(S)-15-methyl-Prostaglandin E1, markedly reduce the increases in vasopermeability induced by the intradermal injection of histamine, serotonin, bradykinin, C3a, and compound 48/80. This inhibition is dependent on the dose of the vasopermeability factor and the duration of time between injection of the prostaglandin and intradermal injection of vasopermeability factor. The inhibition of associated ultrastructurally with a preservation of tight junctions between endothelial cells. The structure-function specificity of the inhibitory effects of the prostaglandin is shown by the diminished effects of prostaglandin A2, and the lack of inhibition by prostaglandin F2 alpha. These data provide evidence that PGE1 interferes with the local effects of vasopermeability mediators and may explain the earlier observations at PGE1 protects animals from immune complex-induced nephritis.

Animals↗
PubMed1979

Systemic lupus erythematosus.

SLE often presents such a confusing clinical picture that diagnosis is long delayed, and it remains a disease of unknown cause. But early diagnosis and carefully planned therapy can enable many patients to lead nearly normal lives. Recent advances are outlined.

Adrenal Cortex Hormones↗
PubMed1979

Lymphocyte adherence in multiple sclerosis: effect of aspirin.

Peripheral blood lymphocytes from multiple sclerosis (MS) patients form substantially greater numbers of rosettes with measles virus-infected human epithelial cells than do lymphocytes from healthy controls or from patients with other diseases. We have previously shown that prostaglandin E(1)-treated normal lymphocytes exhibit increased lymphocyte adherence, and thus behave like MS lymphocytes in this in vitro system. In this study we describe the effect of prostaglandin synthesis inhibition on lymphocyte adherence in both MS and control patients. Direct addition of aspirin or indomethacin to peripheral blood mononuclear cells from MS patients in vitro reduced lymphocyte adherence to control levels. Ingestion of therapeutic (anti-inflammatory) doses of aspirin (1 g, 4 times daily for 2 d) by MS patients resulted in reduction of lymphocyte adherence to levels seen in healthy controls. A single 325-mg dose of aspirin did not reduce lymphocyte adherence. A dose-dependent reduction in lymphocyte adherence was observed after single doses ranging from 650 mg to 1.3 g; duration of the effect was directly related to the aspirin dose. These observations indicate that treatment of MS patients with aspirin profoundly influences adherence of their lymphocytes to measles virus-infected cells and suggest that the altered cellular response, which results in increased lymphocyte adherence in MS patients, may be mediated by a prostaglandin-sensitive mechanism.

Aspirin↗
PubMed1979

Suppression of immune complex vasculitis in rats by prostaglandin.

Immune complex-induced vascular damage can be markedly suppressed by treatment of rats with either prostaglandin (PG)E1 or its stable derivative, 15-(S)-15-methyl PGE1, but not with PGF2 alpha. In addition, PGD2 and PGE2 also show suppressive effects. The PGE1 derivative is considerably more effective than PGE1 and shows potent anti-inflammatory activity even after oral administration. Suppression of the vasculitis reaction is reflected by a greatly diminished increase in vasopermeability, indicating little or no vascular damage. In suppressed animals, the infiltration of neutrophils is greatly reduced, and those leukocytes that have appeared at tissue sites fail to show phagocytic uptake of immune complexes. In suppressed animals, the skin sites nevertheless show deposits of immune complexes and C3 fixation in vascular walls. Neutrophils harvested from the blood of rats treated with PGE1 show depressed responsiveness in chemotaxis and in enzyme secretion after incubation with chemotactic peptide. These studies indicate that certain PG have potent anti-inflammatory activity, which may be related to their effects on leukocytes.

Administration, Oral↗
PubMed1979

Lymphocyte adherence in multiple sclerosis.

It has been reported that peripheral blood lymphocytes from patients with multiple sclerosis (MS) adhere to measles-infected human epithelial cells in significantly greater numbers than do lymphocytes from healthy volunteers or patients with other neurologic diseases. We have confirmed this observation in three separate studies, and have investigated the relationship of lymphocyte adherence to the clinical state. Lymphocyte adherence determination values correlated with the degree of certainty of the clinical diagnosis of MS, and lymphocyte adherence values in individual patients increased during clinical exacerbations. Judicious use of this test may facilitate the diagnosis of MS.

Epithelium↗
PubMed1979

Eosinophilic fasciitis: a clinicopathologic study.

Eosinophilic fasciitis is a syndrome that is characterized by induration of the skin, peripheral eosinophilia, and a good clinical response to corticosteroid therapy. A skin biopsy specimen from a 69-year-old man who died four months after diagnosis of eosinophilic fasciitis showed that vessel walls in the fascia were invaded by inflammatory cells; endothelial cell proliferation appeared to lead to obliteration of the lumen. No evidence of internal organ involvement was noted at postmortem examination. These findings suggest that, although cutaneous vasculitis may play a role in this disorder, lack of visceral involvement and generally benign course of the disease dictate conservative therapy.

Adrenal Cortex Hormones↗
PubMed1978

Systemic lupus erythematosus. Management during pregnancy.

The course of 27 pregnancies in 13 patients with systemic lupus erythematosus (SLE) is presented. The overall incidence of fetal wastage was 33.3%, a figure significantly higher than that observed in the general population. Although serum C3 complement levels rise during normal pregnancy, mean C3 levels remain within the normal range. Since it is a fall in complement levels in patients with SLE which may herald the onset of symptoms and provide a guide to therapy, assay of serum C3 complement levels remains a valid monitoring device in management of these patients during pregnancy. Flares of SLE during pregnancy generally should be treated vigorously with corticosteroids rather than by therapeutic abortion. Continuation of corticosteroid treatment during the first 2 months postpartum is advised to limit the incidence of exacerbation of SLE activity following delivery.

Antibodies, Antinuclear↗
PubMed1977

Adherence of human peripheral blood lymphocytes to measles-infected cells. Enhancement by prostaglandin E1.

We studied the effect of prostaglandins in vitro on an immune reaction mediated by T cells; adherence of lymphocytes to measles-virus-infected human epithelial cells. Normal human lymphocytes adhered to a mean +/- S.D. 20.1 +/- 5.2 per cent of these HEp-2 cells. The percentage positive cells increased to 50.3 +/- 5.7 when lymphocytes were incubated with 10(-6) M prostaglandin E1 (P less than 0.01 vs. untreated lymphocytes); 10(-8) M and 10(-10) M were as effective. Prostaglandin F2alpha had no effect on lymphocyte adherence. Prostaglandin E1 increased lymphocyte cyclic AMP five to 10 times whereas prostagladin F2alpha did not affect cellular levels of this nucleotide. Dibutyryl cyclic AMP (10(-8) M) increased lymphocyte adherence: positive human epithelial cells increased from 16.0 +/- 2.4 to 38.7 +/- 1.1 per cent (P less than 0.01). Prostagladin E1 also increased adherence of lymphocytes from patients with systemic lupus erythematosus from 21.8 +/- 5.8 to 52.5 +/- 9.2 per cent (P less than 0.01). These results indicate that prostagladin E1 and cyclic AMP may serve to stimulate T-cell function and cell-mediated immunity.

Antigens, Viral↗
PubMed1977

Prostaglandin E treatment of NZB/NZW mice.

NZB/NZW F1 hybrid mice were treated with pharmacologic doses of prostaglandin E1 (PGE1) (200 microng subcutaneously either once or twice daily) from 6 through 52 weeks of age. PGE1-treated mice were protected against development anemia, clinical nephritis, and death. At 52 weeks 18 of 19 treated mice were alive, wherase only 2 of 19 untretreated control mice were alive. None of the 10 mice treated with PGE1 twice daily exhibited significant (greater than 2+) proteinuria at 1 year of age. PGE1 treatment did not prevent development of antibodies to nuclear antigens. The data also suggest that survival of NZB/NZW mice is prolonged when treatment with PGE1 is begun at 24 weeks, an age at which mice already show evidence of nephritis. Thus all 6 mice treated with PGE1 (200 microng sc twice daily) from 24 weeks were alive at 52 weeks, whereas only 2 of 6 untreated control mice were alive. The mechanisms whereby PGE1 treatment influences the course of disease in NZB/NZW mice are not known.

Animals↗
PubMed1977

Cyclic AMP response to prostaglandin E1 in mononuclear cells from peripheral blood and synovial fluid of patients with rheumatoid arthritis.

The cyclic AMP response to prostaglandin E1 (PGE1) was studied in peripheral blood (PB) and synovial fluid (SF) mononuclear cells from patients with rheumatoid arthritis (RA). The PGE1 induced accumulation of cyclic AMP was consistently (7 of 8 patients) less in cell suspensions derived from SF than in suspensions of equivalent numbers of mononuclear cells obtained simultaneously from PB. The high PB/SF cyclic AMP ratio was seen most clearly at the lowest concentration (10(-6)M) of PGE1 tested. There was no correlation between the patients' therapy and cyclic AMP response to PGE1. The high PB/SF cyclic AMP ratio was not accounted for by the presence of platelets in PB cell suspensions.

Arthritis, Rheumatoid↗
PubMed1976

Correction of characteristic abnormalities of microtubule function and granule morphology in Chediak-Higashi syndrome with cholinergic agonists.

Chediak-Higashi (CH) syndrome is a genetic disorder of children and certain animal species including the beige mouse. We have previously described a membrane abnormality in CH mouse polymorphonuclear leukocytes (PMH). Whereas normal mouse PMN do not form surface caps with concanavalin A except after treatment with agents such as colchicine that inhibit microtubule assembly, CH mouse PMN show spontaneous cap formation. This capping is inhibited by 3',5 cyclic guanosine monophosphate and by the cholinergic agonists carbamylcholine and carbamyl beta-methylcholine that increase 3',5' cyclic guanosine monophosphate generation. These data suggested that microtubule function may be impaired in CH syndrome perhaps secondary to an abnormality in 3',5' cyclic guanosine monophosphate generation. The cholinergic agonists were also shown to prevent development of the giant granules that are pathognomonic of CH syndrome in embryonic fibroblasts isolated from CH mice and cultured in vitro. In this report it is shown that an extreme degree of spontaneous concanavalin A cap formation is also characteristic of peripheral blood PMN from two patients with CH syndrome. This indicates an abnormality of microtubule function in CH syndrome in man. 3',5' cyclic guanosine monophasphate, carbamylcholine, and carbamyl beta-methylcholine reduce spontaneous capping in CH cells. In addition, it is shown that monocytes isolated from the patients' blood and incubated in tissue culture generate a large complement of abnormal granules. When the same cells mature in vitro in the presence of carbamylcholine or carbamyl beta-methylcholine, the proportion of cells containing morphologically normal granules is significantly increased. These responses can be reproduced in vivo in the beige (CH) mouse. Animals treated for 3 wk and longer with carbamylcholine or carbamyl beta-methylcholline show normal granule morphology and a normal degree of concanavalin A cap formation in peripheral blood PMN leukocytes.

Adult↗