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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have investigated the effect of ultraviolet-B (UVB) irradiation on the density of epidermal ATPase-positive Langerhans cells, and the modulation of this effect by indomethacin (IND). Depilated backs of albino guinea pigs were exposed to varying doses of UVB (10-550 mJ/cm2). Skin biopsies were taken serially. There was an UVB dose-dependent decrease in the density of dendritic epidermal Langerhans cells, as identified by their membrane ATPase activity. This was accompanied by thinning and shortening, or disappearance of dendritic processes. Such changes were followed by a gradual recovery of the cell density to preirradiation level by day 21. Despite the high doses of UVB given, the maximal decrease in the density of ATPase-positive cells was only 58%. Topical application of IND, a prostaglandin-synthetase inhibitor, after irradiation resulted in a decrease of the erythema; however, the decrease in the density of ATPase-positive cells was still observed. In contrast, guinea pigs that received IND topically prior to irradiation showed a decrease erythemal response, but failed to show any decrease in the density of ATPase-positive cells. Administration of IND orally for 3 days prior to UVB exposure did not prevent the decrease in the cell density. The protective effect of topical IND, applied prior to irradiation, may be explained by its in vitro absorbance at both the UVB and UVA ranges. Topical application of IND 20 min prior to exposure to UVB in 2 human subjects resulted in an increase in the minimal erythema dose, giving a sun protection factor of 1.6, which is comparable to that produced by an equimolar concentration of para-aminobenzoic acid solution. The sun-protective property of IND, together with its activity as a prostaglandin synthetase inhibitor, indicate that it potentially could be a useful sunscreen agent. Its clinical safety and efficacy, however, remain to be determined.
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PMID:Effect of indomethacin on alteration of ATPase-positive Langerhans cell density and cutaneous sunburn reaction induced by ultraviolet-B radiation. 622 48

The canalicular and saccular stages of rat lung development are marked by thinning of mesenchymal tissue. Because cell-cell interactions are important for normal fetal lung development, we investigated whether this regression of mesenchymal tissue is controlled by fibroblast-epithelial cell interactions. Using flow cytometry, thymidine uptake into DNA, and cell doubling time, we observed an increase in the proportion of lung fibroblasts in the G0/G1 phase of the cell cycle with advancing gestation. Conditioned medium of epithelial cells from the canalicular stage of lung development, but not from the pseudoglandular and saccular stages, inhibited fetal lung fibroblast proliferation. Fetal lung epithelial cell growth was not affected by the epithelial cell-conditioned medium. The response of fibroblasts to this epithelial cell-derived growth-inhibitory activity was organ specific but not gestation dependent. The inhibitory effect of epithelial cell-conditioned medium on fibroblast proliferation was overcome by the addition of > 2% fetal bovine serum. The inhibition was not mediated by prostaglandins because 50 microM ibuprofen, a prostaglandin synthase inhibitor, did not block the elaboration of the inhibitory activity by fetal lung epithelial cells. Partial characterization of the fibroblast growth-inhibitory activity in epithelial cell-conditioned medium showed that it was trypsin labile, heat and acid insensitive, and lipid extractable. Its molecular weight appears to be > 3.5 and < 12.5 kD. Transforming growth factor-beta 1 and surfactant proteins B and C did not mimic the inhibitory effect of epithelial cell-conditioned medium. These data suggest that fetal lung epithelial cells elaborate a hydrophobic polypeptide that inhibits fetal lung fibroblast proliferation in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inhibition of fibroblast growth by epithelial cells in fetal rat lung. 759 42

1. The focus of this review is the effects and mechanism of action of p,p'-DDE on eggshell formation in birds. Inhibition of prostaglandin synthesis in the eggshell gland mucosa is a probable mechanism for p,p'-DDE-induced eggshell thinning. 2. The duck is sensitive to p,p'-DDE-induced eggshell thinning but the domestic fowl is not, and studies comparing the two species in regard to the calcium and prostaglandin metabolism of the eggshell gland have shown that eggshell thinning induced by p,p'-DDE in ducks is accompanied by reduced activity of prostaglandin synthetase, reduced levels of prostaglandin E2, and reduced uptake of 45Ca by the eggshell gland mucosa. The content of calcium, bicarbonate, chloride, sodium, and potassium are also reduced in the eggshell gland lumen in ducks exhibiting eggshell thinning. None of these effects are seen in the domestic fowl. 3. Inhibition of prostaglandin synthesis is a specific effect of p,p'-DDE. The detrimental effects of p,p'-DDE on the eggshell gland seem to be unique when comparing the compound with structurally related substances, i.e., similar treatment regimens with o,p'-DDE, p,p'-DDT, o,p'-DDT, and p,p'-DDD do not cause eggshell thinning in ducks. Neither do they inhibit prostaglandin synthesis in the eggshell gland mucosa. 4. Administration of other compounds that do inhibit prostaglandin synthesis, e.g., indomethacin, does cause the same effects as those seen with p,p'-DDE, i.e., eggshell thinning and the described effects on the calcium and prostaglandin metabolism of the eggshell gland.
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PMID:DDE-induced eggshell thinning in birds: effects of p,p'-DDE on the calcium and prostaglandin metabolism of the eggshell gland. 949 Jan 82