Search PubMed⌕ Search

Biomedical subjects

M W Greaves

Publications and source records attributed to M W Greaves.

At least 307 records · Page 17Linked to original sources
PubMed1978

Inflammatory reactions induced by ultraviolet irradiation.

Exposure of human skin to short wavelength ultraviolet (U.V.) leads to increased concentrations of arachidonic acid and prostaglandins E2 and F2, but their role is uncertain. Although the levels of prostaglandins rise as erythema develops the correlation between intensity of erythema and prostaglandin activity is incomplete. There is mounting evidence that prostaglandins may regulate epidermal cell growth and differentiation through a cyclic-AMP dependent mechanism. The possibility therefore arises that prostaglandins, released in response to U. V. exposure, reduce proliferative activity in the exposed epidermis. This can be expected, in turn, to result in protection of skin from the mutagenic action of U. V. irradiation.

Arachidonic Acids↗
PubMed1977

Vascular reactions to histamine and compound 48/80 in human skin: suppression by a histamine H2-receptor blocking agent.

1 The ability of a specific competitive histamine H2-receptor antagonist, cimetidine, to inhibit vascular responses to histamine in human skin provides new evidence that skin blood vessels possess histamine H2 receptors. 2 Simultaneous systemic administration of cimetidine and chlorpheniramine (an H1-receptor antagonist) was more effective than either drug alone in inhibition of the erythematous reaction both to exogenous histamine, and endogenous histamine secreted by skin mast cells in response to compound 48/80. 3 These results suggest that combined therapy of histamine-mediated skin diseases included urticaria and dermatitis using a combination of H1- and H2-histamine receptor antagonists may be more effective than either class of drug alone.

Adult↗
PubMed1977

Failure of prostaglandins, prostaglandin metabolites and arachidonic acid to elicit chemotaxis of human polymorphonuclear leukocytes.

This paper reports chemotactic studies on human polymorphonuclear leukocytes using prostaglandins, prostaglandin precursors and prostaglandin metabolites in vitro. Chemotaxis could not be demonstrated when arachidonic acid, prostaglandins D2, E1, E2, F2alpha, and the prostaglandin metabolites 15 keto E2, 15 keto F2alpha were incubated with polymorphonuclear leukocytes using the Boyden millipore technique.

Arachidonic Acids↗
PubMed1977

Enzymatic histamine degradation by human skin.

1. Degradation of histamine by homogenized human skin in vitro, in the presence of the cofactor S-adenosyl methionine, indicates the presence of the histamine metabolizing enzyme histamine-N-methyl transferase in human skin. Under the experimental conditions described, no significant histamine degradation by diamine oxidase was observed. 2. The enzyme activity is temperature-sensitive with an optimum at 37 degrees C. The enzyme is stable in in intact excised skin at -20 degrees C, but unstable in homogenized skin at this temperature. 3. Little or no enzyme activity is present in mid- or deep dermis, but the distribution of the enzyme between superficial papillary dermis and epidermis is uncertain. 4. The presence of a potent histamine degrading mechanism raises the possibility that histamine-N-methyl transferase activity may be an important modulating factor in histamine-mediated skin disorders.

Chromatography, Thin Layer↗
PubMed1977

Inflammation in human skin induced by ultraviolet irradiation.

Pharmacologically active mediators of inflammation were obtained from suction bullae raised on normal and ultraviolet B (290-320 nm) inflamed human abdominal skin. The exudates obtained from the bullae were examined by superfusion cascade bioassay, by radioimmunoassay for PGF2alpha and by column, thin-layer and gas-liquid chromatography. Ultraviolet B (u.v.-B) irradiation of human skin produced an erythema which appeared after 2 hr, increased in severity up to 24 hr and persisted for more than 48 hr. Bioassayable and radioimmunoassayable prostaglandin activity was elevated at 6 hr, was maximal at 24 hr and had returned to normal 48 hr. Topical application of indomethacin suppressed both the erythema and the increased concentration of PGF2alpha as measured by radioimmunoassay. Chromatographic studies confirmed increased prostaglandin activity at 6 and 24 hr and in addition demonstrated an increase in arachidonic acid-like activity. The results suggest that prostaglandins may play an important role between 6 and 24 hr of u.v.-B-induced erythema. Whether the reduction of erythema by indomethacin can be partially or wholly attributable to inhibition of prostaglandin biosynthesis is uncertain.

Adult↗