Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Epidermal growth factor (EGF) injected into pregnant mice increased the frequency of cleft palate (CP) in cortisone-treated mouse fetuses. EGF alone produced proliferation and thickening of the epithelium of the palatal processes, but CP was not significantly increased over saline injected controls. Cortisone alone produced thinning of the palatal epithelium and caused CP in 61 percent of formed fetuses. The combination of EGF and cortisone treatment induced CP in 100 percent of formed fetuses; epithelial thickening still occurred with the combination treatment. Thus, EGF may be teratogenic under special circumstances. These observations suggest that the relative thickness of the palatal shelf epithelium may not be a critical factor in the fusion of the palatal shelves.
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PMID:Epidermal growth factor potentiates cortisone-induced cleft palate in the mouse. 30 37

Epidermal thinning of mouse tail skin was compared for commercial preparations of clobetasol propionate (Dermovate), clobetasone butyrate (Eumovate), fluocinonide (Metosyn), and hydrocortisone butyrate (Locoid). The thickness measurements were ranked with those for hydrocortisone (1%), betamethasone valerate (Betnovate), triamcinolone acetonide (Ledercort), fluocinolone acetonide (Synlar), and prednisolone stearoylglycolate (Sinistrone) obtained in a previous study (Spearman and Jarrett, 1975). All steroids caused epidermal thinning, except clobetasone butyrate. Some cream and ointment vehicles were also assayed. Epidermal thickening was caused by the cream and ointment vehicles used for Eumovate and also by the cream employed for Locoid formulation.
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PMID:Epidermal thinning: evaluation of commercial corticosteroids. 738 77

Steroid flares are common side effects associated with corticosteroid treatment, and have been recently theorized to be a consequence of drug crystallization. It was previously reported that the lipid bilayer can promote crystallization of cortisone at high local concentrations. Here, we studied the effect of cholesterol on this membrane induced cortisone crystallization. By combining x-ray diffraction and Molecular Dynamics simulations we observe that that the presence of cholesterol suppresses cortisone-induced membrane thinning and cortisone transnucleation. Cortisone located in the head-tail interface of the membranes also in the presence of cholesterol. The cholesterol molecules were found to be tilted and displaced towards the bilayer center as function of cortisone concentration, away from their canonical position. Our results show that membrane cholesterol may play an important role in the ability of lipid bilayers to catalyze the formation of corticosteroid crystallites.
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PMID:Steroid-steroid interactions in biological membranes: Cholesterol and cortisone. 3095 11