ABSTRACT
Objective: Assuming that the difference exist in the manifestation of psychological suffering among genders, the purpose of this review is to summarize the current knowledge on gender differences in vitiligo quality of life and psychological assessment. Methods: We searched in PubMed, Scopus, and Web of Science databases for original articles in English language. Results were screened according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA checklist). Results: The study yielded 107 results; 12 articles have been evaluated as eligible. Each eligible study has been screened and analyzed. The study's qualitative evaluation revealed that 8 papers were classifiable as satisfactory, 4 were classifiable as unsatisfactory. The agreement between the coders was high (% agreement = 84.6%; Cohen's kappa = 0.79). All considered researches (100%) were cross-sectional studies, based on self-report questionnaires. From our analysis, women with vitiligo had a higher risk to experience lower quality of life, and worse mental health in a wide range of psychopathology symptoms than men. A wide heterogeneity of tools is used to investigate the quality of life and psychological symptoms among these patients. Conclusion: Unfortunately, there are few explanatory models proposed in the literature to rationalize these findings. It will be important to investigate in further researches the specific influence of known risk factors for psychopathology in this population to better explore these phenomena.
ABSTRACT
We investigated the role of the A3 adenosine receptor in cells of the astroglial lineage (both rat primary astrocytes and human astrocytoma ADF cells) by means of the selective A3 agonists N6-(3-iodobenzyl)-adenosine-5'-N-methyluronamide (IB-MECA) and CI-IB-MECA, and by utilizing the selective A3 receptor antagonist MRS1191. Exposure of ADF cells to µM concentrations of either agonist resulted in reduction of cell number, likely due to cell death. In both rat astrocytes and human astrocytoma cells, at concentrations 2-3 orders of magnitude lower (which were not associated with cytotoxicity), these same agonists induced a marked reorganization of the cytoskeleton, with appearance of stress fibers and numerous cell protrusions. Functionally, these morphological changes were associated with cell protection, as demonstrated by a significant reduction of spontaneous apoptosis in A3 agonist-treated cells. To confirm a role for the A3 receptor in this effect, MRS1191 completely counteracted CI-IB-MECA-induced reduction of spontaneous apoptosis. In ADF cells, A3 agonists also induced changes in the intracellular distribution of the anti-apoptotic protein Bcl-XL, which became localized in cell protrusions. Also, this effect was specifically antagonized by MRS1191. These dual actions of A3 agonists in vitro may have important in vivo implications. For example, a robust and acute activation of the A3 receptor following massive adenosine release during ischemia may contribute to brain cell death; conversely, a subthreshold activation of this receptor prior to ischemia may trigger protective mechanisms (i.e., induction of stress fibers and of a Bcl-XL-dependent reorganization of cytoskeleton) making the brain more resistant to subsequent insults ("ischemic tolerance").