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The primary aim was to evaluate changes in female sexuality across the menopausal period, and the secondary objective was to test the associations of female sexuality domains with vaginal atrophy and its symptoms.A cross-sectional multicenter study was performed involving 518 women, 40 to 55 years of age, consulting outpatient gynecological services at 30 centers across Italy. Vaginal atrophy was identified by the contemporaneous presence of a pH5, subjective vaginal dryness, and an objective sign. The relationships between vaginal atrophy and its main symptoms (vaginal dryness and dyspareunia), and Female Sexual Function Index (FSFI) score and its domains (desire, arousal, orgasm, dyspareunia, lubrication, and sexual satisfaction) were analyzed.The prevalence of sexual dysfunction, as defined by a FSFI score26.55, was 70.6%, increasing from 55% in the years 40 to 45, to 82.8% (P 0.01) in the years 52 to 55 of age. Mean FSFI score decreased from 40 to 45, to 46 to 48 years of age (23.13 ± 9.76 vs 19.49 ± 9.88; P 0.05), and from 48 to 51, to 52 to 55 years of age (21.3 ± 8.06 to 17.59 ± 9.11; P 0.01). Independent determinants of FSFI were age, vaginal atrophy, and the presence of vaginal dryness and dyspareunia (R2 0.208; P = 0.011). FSFI score was independently correlated (R2 0.116) with weight (CR -0.067; 95% confidence interval [CI] -0.126, -0.006; P 0.032), menopausal status (CR -2.406; 95% CI -4.180, -0.63; P 0.008), and vaginal dryness (CR -5.647; 95% CI -7.677, -3.618; P 0.0001). Vaginal dryness was the only variable correlated independently with each FSFI domain, including desire (also correlated with menopausal status), arousal (with age and menopausal status), lubrication (with age), orgasm (with age), satisfaction (with vaginal atrophy and being an ex-smoker), and dyspareunia (with age and spontaneously referred dyspareunia).In the perimenopausal years, FSFI score decreases and sexual dysfunction increases by about 30%. Vaginal dryness is the symptom of vaginal atrophy most closely related to all domains of female sexuality.

To evaluate the association between treatments for vulvovaginal atrophy (VVA) and symptom frequency and severity, quality of life (QoL) and sexual functioning in postmenopausal women.Cross-sectional survey conducted in postmenopausal women aged 45-75 years. Data on demographic and clinical variables, as well as vaginal, vulvar and urinary symptoms were collected. The EuroQoL questionnaire (EQ5D3L), the Day-to-Day Impact of Vaginal Aging (DIVA), the Female Sexual Function Index (FSFI) and the Female Sexual Distress Scale - revised (FSDS-R) were filled out.Association between treatments for VVA and symptom frequency.Women on VVA treatment presented with more severe symptoms. The sexual function score was higher in the treated women (FSFI: 15.6 vs 16.7; p = 0.010), as was the score for sexual distress (FSDS-R: 9.2 vs 12.3, p 0.0005). The systemic hormone group presented with fewer VVA symptoms, lower vaginal impact (DIVA), and better sexual function (FSFI and FSDS-R) and vaginal health. The rates of sexual distress and vulvar atrophy were higher in the non-hormonal treatment group. No significant differences were found according to treatment duration.Postmenopausal women with VVA receiving treatment complained of more severe symptoms than those untreated. Women on systemic treatment had fewer and milder VVA symptoms and presented with better vaginal and vulvar health than women on other treatments. Many women request effective local treatment too late, when VVA symptoms are already severe. Our data suggest that VVA treatments should ideally be initiated when symptoms commence and cause distress, rather than later, when symptoms may have become more severe and even a cause of intolerable distress for the woman.

In addition to its catalytic activities as ecto-NAD+ glycohydrolase (NADase), CD38 displays the ability to transduce signals of biological relevance. Indeed, ligation of CD38 on peripheral blood mononuclear cells (PBMC) by agonistic monoclonal antibodies (mAbs) is followed by the transcription and secretion of a vast array of regulatory cytokines. The present work addresses the issue of whether the signals leading to calcium (Ca2+) mobilization, lymphocyte proliferation and release of cytokines is dependent on the epitopes recognized by the individual mAbs. Competition binding analysis identifies two families of mAbs, namely IB4, IB6 and AT2 on one side and OKT10, SUN-4B7 and AT1 on the other. Each mAb family binds epitopes that are completely or partially common. However, the functional activities of the CD38 molecule can not be simply attributed to the epitopes engaged: for instance, IB4 and OKT10 mAbs, which bind different epitopes, perform as agonistic mAbs in inducing PBMC proliferation and interferon (IFN)-gamma secretion. SUN-4B7 yields intermediate effects, whereas IB6, AT1 and AT2 mAbs are totally ineffective. The effects mediated by IB4 and OKT10 mAbs are apparent in 80% of the healthy individuals studied, whereas the effects of SUN-4B7 mAb operate only in 25% of the donors. Interleukin (IL)-6 secretion was observed in all individuals analyzed, irrespective of the epitopes triggered and of mAbs used to ligate the CD38 molecule. In addition, IB4 is the only mAb able to induce significant intracellular Ca2+ fluxes.

During the last three decades, research focused on cancer treatment has led to the development of many cytotoxic agents. Despite the fact that these efforts have significantly improved the prognosis of certain malignancies such as some lymphomas, leukemias and testicular carcinomas, other tumors such as ovarian, lung and metastatic breast cancer are still associated with a poor prognosis. An innovative approach has recently emerged, thanks to a better understanding of tumor cell biology and many efforts are aimed at finding compounds capable of restoring a more differentiated phenotype to tumor cells, thereby reducing the tumor's aggressiveness and ultimately reverting it to its normal counterpart [1, 2]. Retinoids are the prototype of this new therapeutical approach called "differentiation therapy".

Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a cytokine that stimulates the proliferation and differentiation of bone marrow progenitors. Moreover, the presence and activity of GM-CSF and its receptor (GM-CSF-r) has been documented on tissues and cell lines of a non-hemopoietic origin. In this paper we studied the expression and putative role of GM-CSF and GM-CSF-r in endometrial cancer. The modulation of GM-CSF-r alpha-chain upon progesterone treatment suggests a role for GM-CSF and its receptor in the pathogenesis and development of endometrial cancer.