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Biomedical subjects

S Kenwright

Publications and source records attributed to S Kenwright.

15 recordsLinked to original sources
PubMed1997

Ethics of cloning.

Explore the source record for details and available documents.

Cloning, Molecular↗
PubMed1991

The normocomplementemic urticarial vasculitis syndrome--report of a case and response to colchicine.

A patient with a 15-year history of urticarial vasculitic rashes and chronic vasculitic skin ulceration has been followed at our Connective Tissue Disease Clinic for the past five years. Serum complement levels have been persistently normal. She has been unresponsive to a variety of medications including steroids, dapsone and hydroxychloroquine. She had a dramatic response to colchicine 500 micrograms daily with total clearing of the urticarial vasculitic rash.

Chronic Disease↗
PubMed1977

Nodular lymphoid hyperplasia of the bowel in primary hypogammaglobulinaemia: study of in vivo and in vitro lymphocyte function.

In vitro and in vivo lymphocyte function was studied in six patients with primary hypogammaglobulinaemia and nodular lymphoid hyperplasia (NLH) of the bowel. Lymphocyte transformation, numbers of circulating T and B lymphocytes, and delayed hypersensitivity skin tests did not significantly differ when compared with hypogammaglobulinaemic patients without NLH. However, patients with NLH had higher jejunal juice IgM concentrations and a tendency to higher serum IgM concentrations than those without NLH. The morphological features of NLH are similar to the germinal centres of lymph nodes but more closely resemble the follicle zone of Peyer's patches. These findings suggest that NLH represents a local immune response to antigens originating in the gut lumen.

Adolescent↗
PubMed1974

Sites of competition in the selective hepatic uptake of rifamycin-SV, flavaspidic acid, bilirubin, and bromsulphthalein.

In rats both rifamycin-SV and flavaspidic acid impaired the disappearance of bromsulphthalein (BSP) from plasma. The addition of rifamycin-SV to rat liver supernatant containing BSP did not displace BSP from ligandin or Z protein unless it was added in very high concentration. In similar studies in vitro with flavaspidic acid, BSP was displaced from Z protein even at low concentrations of flavaspidic acid, whereas there was only a minor effect on the binding to ligandin. The intravenous administration of rifamycin to Gunn rats raised the plasma bilirubin concentration slightly after 30 minutes whereas flavaspidic acid was without significant effect. At 30 minutes the amount of bilirubin in the liver was markedly reduced by rifamycin and moderately depressed by flavaspidic acid. Although both the rifamycin and flavaspidic acid lowered the bilirubin in cell sap, the main effect of flavaspidic acid appeared to be on binding to Z protein. Rifamycin reduced the amount bound to both ligandin and Z protein. It is suggested that flavaspidic acid acted on the hepatic uptake of bilirubin and BSP predominantly by competing for binding to Z protein. Rifamycin-SV acted at a different site, probably blocking uptake at the plasma membrane.

Animals↗