[My experience in Tanzania].
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Biomedical subjects
Publications and source records attributed to M Gallo.
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Clinical report of a 23-year-old woman with total IgA-deficit, who had suffered for 2 years from a connective tissue disease similar to lupus erythematosus, with severe hemorrhagic retinitis but without any renal involvement.
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Smoking has become a true epidemic that interests a lot of people in the world. The antismoking programmes are at these moments the most important strategy to prevent lung cancer and cardiovascular diseases. This article analyses the compliance and the results of the antismoking campaigns in the world. Data show the long term efficacy of school based smoking prevention programmes and underline their importance even if the methodologies can be different in the various countries. Other data show that the percentage of young smokers is increasing during the last three years; for this reason it is necessary to implement everywhere new programmes against smoking.
The possible mechanisms of the inhibitory effect of Dehydroepiandrosterone (DHEA) on the estrogen-induced growth of MCF-7 human breast cancer cells were explored. The impairment of metabolic pathways, via the inhibition of glucose-6-phosphate dehydrogenase (G6PD) activity, was excluded: G6PD activity in MCF-7 homogenate was reduced by DHEA only at a very high concentration (50 microM), while no inhibitory action on the enzyme activity was detected when DHEA was added at the antimitotic concentrations (0.02-0.5 microM). A steroid receptor mediated effect was explored: DHEA might either activate androgen receptors (AR) or partially displace E2 from estrogen receptor (ER). The pure antiandrogens Flutamide and Hydroxyflutamide reversed the inhibitory effect of DHEA on MCF-7 cell growth, whereas both the nonsteroidal estrogen Diethylstilbestrol and the antiestrogen Tamoxifen were ineffective. Results demonstrate that the AR activation plays a pivotal role in the inhibitory action of DHEA on the E2-induced MCF-7 growth.
Cell to cell interaction, which plays a crucial role in breast cancer growth, may be regulated by steroid hormones. This study examined dihydrotestosterone (DHT) effects on the interaction between the steroid receptor positive MCF-7 and the steroid receptor negative MDA-MB-231 breast cancer cell lines. The growth of MDA-MB-231 cells was inhibited by medium conditioned by MCF-7 cells grown in presence of DHT but not by medium conditioned by MCF-7 cells grown in presence of both DHT and the antiandrogen hydroxyflutamide. Trypsin pretreatment of conditioned medium abolished its growth-inhibitory effect on hormone-unresponsive cells. DHT itself did not affect the growth of MDA-MB-231 cells when directly added to their culture medium. Data suggest that DHT stimulates, via the androgen receptor, the androgen-responsive breast cancer cells to produce a peptide factor(s) capable of inhibiting the growth of hormone-unresponsive cells.