[Identity, culture and psychological discomfort: elements for a metacultural psychotherapy]. / Identità, cultura e disagio psichico: spunti per una psicoterapia metaculturale.

The purpose of this article is to offer observations and insights gained during the implementation of a specific Intervention Project and an experience of clinical work devoted to foreign people, including hot topics in the field of psychology and psychoterapy: the psychic discomfort of migrants. Today multiethnic and multicultural society that are urgently in the modern world is a reality that needs a more consistent focus and a complex response from psychiatry, psychology and science territorial similar. In the therapeutic relationship with an "other culture" the operator will adjust and restructure himself with great flexibility and particular sensitivity. It's always necessary to recognize the sense of cultural diversity for which the bearer is an immigrant. The disorders and mental discomfort can not be nor decontext, nor dehistoric. Metacultural psychotherapy may represent a mode of intervention in the complexity of migration processes that allow reading the psychic discomfort through a review and rethinking of the relationship of care and listening for otherness.

Estrogenic effect of procymidone through activation of MAPK in MCF-7 breast carcinoma cell line.

Procymidone modifies sexual differentiation in vitro and induces estrogenic activity in primary cultured rainbow trout hepatocytes, as shown by an increase in the contents of vitellogenin and heat shock proteins. Since this dicarboximide fungicide is found in human tissues, it was considered of interest to investigate its ability to induce endocrine damage in the MCF-7 human cell line. The mechanism of this estrogenic action was also evaluated. Procymidone 100 microM stimulated cell growth from day 3 up to day 12 and raised the level of pS2 on day 3. Although procymidone does not bind the estrogen receptor (ER), the antiestrogen ICI 182780 inhibited its effect on cell growth and pS2 content, suggesting that the ER is involved indirectly in these effects. In exploring the mechanism of ER indirect activation we found that the antibody against c-Neu receptor (9G6) did not modify procymidone's effects on cell growth and pS2 expression. Thus, procymidone does not bind the c-Neu membrane receptor, excluding this indirect ER activation pathway. We also found that procymidone induced mitogen-activated protein kinase (MAPK) at 15 and 30 min, and that PD 98059, a MAPK (Erk1/2) inhibitor, prevented procymidone's effects on cell growth and pS2, indicating that MAPK activation is responsible for procymidone ER activation. The production of reactive oxygen species (ROS) with these times and elimination of the phenomenon by alpha-tocopherol (alpha-T), a ROS scavenger, is proof that oxygen free-radical production is at the basis of the MAPK activation by procymidone.

Study of potential toxic effects on rainbow trout hepatocytes of surface water treated with chlorine or alternative disinfectants.

This study evaluates the effects of disinfection on the formation of toxic compounds in lake water treated with sodium hypochlorite, chlorine dioxide and peracetic acid (a disinfectant not previously used in drinking water processes). Chlorine reacts with the natural organic matter or contaminants in surface waters and produces a complex mixture of disinfection by-products (DBPs), some of which have been shown to be carcinogenic, mutagenic and/or teratogenic in animal studies. To define the potential toxicity on aquatic animals, disinfected drinking waters obtained from a pilot plant fed with water coming from Lake Trasimeno (Perugia) were collected, adsorbed by using silica C18 cartridges, and then eluted in sequence with ethylacetate, dichloromethane and methanol. The eluates were concentrated under vacuum and resuspended in dimethylsulfoxide (DMSO). Primary cultures of rainbow trout hepatocytes were exposed to three amounts of water concentrate (equivalent to 0.5, 0.25 and 0.125 l of disinfected water per ml of culture medium) for 24 h at 20 degrees C, after which their viability, glutathione content (GSH), free radical production (ROS) and cytochrome P4501A3 expression were determined. The disinfected water samples were collected during different seasons in order to evaluate a possible correlation between seasonal water variations and formation of toxic compounds. None of the water concentrates showed any cytotoxic effect or variations in GSH content, but significant increases in ROS production were detected in the autumn water concentrates from the treatments with sodium hypochlorite and chlorine dioxide. Cytochrome P4501A3 expression was not modified in the hepatocytes exposed to the water concentrates irrespective to the sampling season.

Estrogenic activity of procymidone in rainbow trout (Oncorhynchus mykiss) hepatocytes: a possible mechanism of action.

It is known that procymidone modifies sexual differentiation in vivo and in vitro, and that it induces vitellogenin (Vtg) synthesis in primary cultured rainbow trout hepatocytes. The aim of this study was to evaluate the mechanism underlying this latter in vitro estrogenic action. The cells were treated for 24 h with procymidone 150 microM (with 17beta-estradiol [E2] 20 microM as a positive control) combined with an estrogen receptor (ER) antagonist (tamoxifen 20 microM or ICI 182,780 1 microM) or, given the drug toxic action on the production of reactive oxygen species (ROS), a free radical scavenger (alpha-tocopherol 30 microM). The results from ELISA experiments provided evidence that procymidone Vtg-induction is inhibited by ER antagonists and by alpha-tocopherol suggesting that both ER and ROS are involved in this effect. The ROS detection revealed that the treatment with alpha-tocopherol and tamoxifen completely prevented ROS induction by procymidone, that was not inhibited by ICI 182,780. In exploring the mechanism mediating these events and its timing, we found that procymidone induced mitogen-activated protein kinase (MAPK) at 30 and 60 min, and that this effect was blocked by co-treatment with alpha-tocopherol. In summary, the results of the study clearly support the idea that the estrogenic activity of procymidone in primary cultured trout hepatocytes is mediated by ROS production, and that this activity is similar to that of the ligand-independent ER activation involving MAPK.