Letter: Actinomycetes are bacteria.
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Biomedical subjects
Publications and source records attributed to B Becker.
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The reproducibility of the intraocular pressure response to topical dexamethasone was investigated in 162 persons previously classified as low (NN), intermediate (NG), or high (GG) responders. The concordance of first and second test results was 71% for NN, 74% for NG, and 79% for GG responders, exceeding chance significantly for the NG and GG categories. Quantitative assessment revealed significant correlation of final pressure achieved on first and second tests (r equals .747, P LESS THAN .001). In the course of the study applications of dexamethasone to one eye were noted to have no effect on the intraocular pressure in the contralateral untreated eye, nor did testing of one eye influence the response of the contralateral eye in simultaneous bilateral testing. Using our data to estimate the reproducibility of topical testing in a general population, a value of 73% was obtained. That value was similar to the 65% concordance reported in an identical twin study, suggesting that the limited precision of topical testing accounts for the relatively low concordance found in that study.
We used an in vitro assay utilizing corticosteroids to inhibit transformation of peripheral blood lymphocytes to evaluate a group of 20 patients with pigmentary glaucoma. The pigmentary glaucoma patient group did not manifest the markedly increased cellular sensitivity to corticosteroids associated with primary open-angle glaucoma. If increased sensitivity to corticosteroids plays an essential role in the pathogenesis of primary open-angle glaucoma, then pigmentary glaucoma appears to be etiologically, as well as clinically, a separate entity.
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The corticosteroid concentration required to inhibit phytohemagglutinin stimulated human lymphocyte transformation by 50% was determined for three corticosteroids. The relative potency of hydrocortisone, prednisolone and dexamethasone determined in 16 patients was 1.00, 2.43, and 24.7 respectively. This assay is proposed as an objective tool for comparison of relative corticosteroid potency in man.
Imidazole, given intraperitoneally to rabbits, inhibited the prostaglandin E1-induced (PGE1) elevation of intraocular pressure. The maximum imidaz-le effect occurred at three to six hours after intraperitoneal infection. The prostaglandin E1-induced aqueous humor protein elevation was reduced markedly in the imidazole-pretreated rabbits. Intravenous administration of imidazole also was effective in reducing the intraocular pressure elevation produced by prostaglandin E1. Imidazole pretreatment by subconjunctival, subdermal, or topical routes had no such effect. Imidazole derivatives, 1-methylimidazole and 2-methylimidazole, given intraperitoneally, blocked the effect of PGE1 on intraocular pressure and aqueous humor protein. Imidazole pretreatment also inhibited the elevation of intraocular pressure produced by topical nitrogen mustard, 1 per cent.
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