PubMed · 10483171
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A R Zlatkina. 1999. [Chronic colitis].. https://pubmed.ncbi.nlm.nih.gov/10483171/
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The effect of pH on the excised skin permeability towards two model lipophilic compounds was studied in the range of pH 1.0-10.0 and 1.0-12.0, for hydrocortisone and testosterone, respectively. Suspensions of the model compounds in appropriate buffers (0.1-0.2 M) were applied to the intact skin, delipidized skin, skin pretreated with Azone or sodium lauryl sulfate solution and the percutaneous penetration was observed for 28 h. Within the studied pH range, up to pH 11.0 no change in the penetration through the skin and skin accumulation was observed for both compounds. Significant, 3-4-fold, increase of penetration of testosterone was noted only at pH 12.0, however the change was neither fast not progressing with time. None of the pretreatment procedure influenced the observed relationship between pH and skin permeability. It is concluded that the lipoidal route of penetration is not affected by solutions at pH within the range 1.0-11.0.
PURPOSE: Cyclophosphamide-induced ovarian failure has been reported to be protective against flares of systemic lupus erythematosus (SLE). We studied whether patients with SLE experience a decrease in disease activity after natural menopause. SUBJECTS AND METHODS: We studied 30 SLE patients with natural menopause who had been observed at least 2 years before and after menopause and who did not receive hormone replacement therapy or danazol. Menopause was defined as the date of the last self-reported menstrual period. Disease activity was assessed retrospectively by medical chart review using standard measures (the SLE disease activity index) during the immediate premenopausal and postmenopausal periods, and 2 (n = 30 patients), 3 (n = 19), and 4 (n = 13) years before and after menopause. We also compared the use of health services and medications. RESULTS: Patients were studied for a mean (+/- SD) of 6.4 +/- 1.7 years (premenopausal, 3.3 +/- 0.9 years; postmenopausal, 3.2 +/- 0.9 years). During the premenopausal periods, the mean disease activity score was 2.3 +/- 2.3 (range, 0 to 9 on a 0 to 105 scale), compared with 2.3 +/- 2.9 (range, 0 to 12; P = 0.37) after menopause. The maximum disease activity score was somewhat greater in the premenopausal period (7.9 +/- 6.0 [range, 0 to 22] vs. 5.8 +/- 5.1 [range, 0 to 22]; P = 0.04). The incidence rates of flares (0.56 per year vs. 0.43 per year, P = 0.20) and severe flares (0.17 per year vs. 0.12 per year, P = 0.33) were similar in the premenopausal and postmenopausal periods. Differences in disease activity scores (mean and maximum) and the number of visits to a rheumatologist's office were only significant when the fourth year before menopause was compared with the fourth year after menopause. CONCLUSIONS: Disease activity is mild during the premenopausal and postmenopausal periods in women with SLE. A modest decrease, especially in the maximum disease activity, is seen after natural menopause.
Nerve growth factor (NGF) has recently been presented as a possible effector of inflammation and bronchial hyperresponsiveness. However, the production of NGF in human airways as well as the regulation of its expression by inflammatory cytokines and glucocorticoids have received little attention. A549 epithelial cells were cultured in Dulbecco's modified Eagle's medium supplemented with 10% foetal bovine serum, and starved for 24 h. The effect of the pro-inflammatory cytokine interleukin-1beta (1-30 U/ml), and of the glucocorticoid dexamethasone (1 microM) on NGF secretion was studied and quantified by enzyme-linked immunosorbent assay (ELISA). In addition, NGF production within the cells was visualized by immunocytochemistry. Under basal conditions, A549 cells produced and secreted NGF (12.6+/-2.0 pg/ml). Stimulation by interleukin-1beta for 24 h induced a dose-dependent increase in NGF production (maximal at 10 U/ml with 59.6+/-3.5% increase, P<0.05). Dexamethasone (1 microM) markedly reduced the constitute NGF secretion by 44.9% (7.0+/-2.1 pg/ml, P<0.001). In addition, the interleukin-1beta-stimulated NGF secretion was inhibited to approximately the same low level (8.5+/-2.5 pg/ml, P<0.001). In conclusion, we here report that human airway A549 epithelial cells are capable of producing NGF. This production is positively regulated by the pro-inflammatory interleukin-1beta, and negatively regulated by dexamethasone.