Comparison between personality profiles of the parents with schizophrenic offspring and normal parents based on MCMI-III

AbstractMCMI-III used to compare the psychiatric profile of the parents with schizophrenic children and parents without schizophrenia in the family. We did not observed any significant differences between fathers in case and control groups in all 27 scales of MCMI-III (p-value>0.10). However the in female subjects the scores of disclosure, debasement, schizoid, avoidant, depressive, dependent, negativistic, masochistic, schizotypal, paranoid and anxiety scales in two groups were significant (P-value<0.05). No significant differences were observed between the scores in desirability, histrionic, narcissistic, antisocial, sadistic, compulsive, borderline, bipolar, alcohol dependence and drug dependence scales in two groups were significant (P-value>0.05)

Level Crossing Analysis of Growing surfaces

We investigate the average frequency of positive slope $\nu_{\alpha}^{+}$, crossing the height $\alpha = h- \bar h$ in the surface growing processes. The exact level crossing analysis of the random deposition model and the Kardar-Parisi-Zhang equation in the strong coupling limit before creation of singularities are given.Comment: 5 pages, two column, latex, three figure

Cortisol regulates the paracrine action of macrophages by inducing vasoactive gene expression in endometrial cells

The human endometrium undergoes inflammation and tissue repair during menstruation. We hypothesized that the local availability of bioactive glucocorticoids plays an important role in immune cell–vascular cell interactions in endometrium during tissue repair at menstruation, acting either directly or indirectly via tissue resident macrophages. We sought to determine whether endometrial macrophages are direct targets for glucocorticoids; whether cortisol-treated macrophages have a paracrine effect on angiogenic gene expression by endometrial endothelial cells; and whether endometrial macrophages express angiogenic factors. Human endometrium (n = 41) was collected with ethical approval and subject consent. Donor peripheral blood monocyte-derived macrophages were treated with estradiol, progesterone, or cortisol. The effect of peripheral blood monocyte-derived macrophage secretory products on the expression of angiogenic RNAs by endothelial cells was examined. Immunofluorescence was used to examine localization in macrophages and other endometrial cell types across the menstrual cycle. Endometrial macrophages express the glucocorticoid receptor. In vitro culture with supernatants from cortisol-treated peripheral blood monocyte-derived macrophages resulted in altered endometrial endothelial cell expression of the angiogenic genes, CXCL2, CXCL8, CTGF, and VEGFC. These data highlight the importance of local cortisol in regulating paracrine actions of macrophages in the endometrium. CXCL2 and CXCL8 were detected in endometrial macrophages in situ. The expression of these factors was highest in the endometrium during the menstrual phase, consistent with these factors having a role in endometrial repair. Our data have indicated that activation of macrophages with glucocorticoids might have paracrine effects by increasing angiogenic factor expression by endometrial endothelial cells. This might reflect possible roles for macrophages in endometrial repair of the vascular bed after menstruation

Neuroendocrine–immune disequilibrium and endometriosis: an interdisciplinary approach

Endometriosis, a chronic disease characterized by endometrial tissue located outside the uterine cavity, affects one fourth of young women and is associated with chronic pelvic pain and infertility. However, an in-depth understanding of the pathophysiology and effective treatment strategies of endometriosis is still largely elusive. Inadequate immune and neuroendocrine responses are significantly involved in the pathophysiology of endometriosis, and key findings are summarized in the present review. We discuss here the role of different immune mechanisms particularly adhesion molecules, protein–glycan interactions, and pro-angiogenic mediators in the development and progression of the disease. Finally, we introduce the concept of endometrial dissemination as result of a neuroendocrine-immune disequilibrium in response to high levels of perceived stress caused by cardinal clinical symptoms of endometriosis