BackgroundStigma affects all aspects of mental disorders, and is the most important risk factor for promoting mental health. The aim of this study was to explore strategies effective in reducing the stigma toward people with mental disorders in Iran.MethodsThis qualitative study was conducted from 2013 to 2016. All participants were recruited by purposive sampling method. The majority of them were stakeholders of mental health in Iran. Data were collected through eight individual interviews, two focus groups, and six written narratives. The data were collected, coded and analyzed simultaneously. Content analysis was employed to analyze the qualitative interview data.ResultsThe major themes that emerged were: “Emphasis on education and changing attitudes”, “Changing the culture”, “Promoting supportive services”, “Role of various organizations and institutions”, “Integrated reform of structures and policies to improve the performance of custodians”, and “Evidence-based actions”.ConclusionsThis study did not investigate the extent of stigma or its origins, rather it examines strategies appropriate for implementation in Iran. Additional studies are needed to evaluate the effectiveness of strategies for reducing the stigma attached to patients with mental disorders.

No abstract

frequencies of genotypes and alleles of the two T-786C and G894T polymorphisms when patients with ED and normal controls were compared.• In a multiple logistic regression analysis, the odds ratio (OR) of increased ED was strongly associated with the -786C allele [adjusted OR = 3.12, 95% confidence interval (CI) = 2.28-4.25; P = 0.001] and the 894T allele (adjusted OR = 3.87, 95% CI = 2.53-4.87; P = 0.001).• The data showed a higher prevalence of the T-786C CC genotype (adjusted OR = 2.72, 95% CI = 1.88-3.65; P = 0.006), and the G894T GT (adjusted OR = 1.72, 95% CI 1.24-2.83; P = 0.037) and G894T TT genotypes (adjusted OR = 3.42, 95% CI 2.42-4.26; P = 0.001) in patients with ED than in the controls. CONCLUSIONS• The findings of the present study suggest that the eNOS T-786C and G894T polymorphisms are strong predictors of the predisposition to ED in addition to traditional risk factors, signifying a genetic influence for this multifactorial disease.• Further studies in different ethnic populations are needed to better elucidate the role of eNOS gene polymorphism in the pathogenesis of ED.

treatment you received during the 12-week improve meaningful your sexual desire?') and overall patient satisfaction question ('Are you satisfied with the efficacy of your treatment?'). RESULTSThe mean ( SD ) composite score on the BISF-W, increased from 15.8 (2.6) and 15.5 (2.2) at baseline to 33.9 (4.2) and 16.9 (2.6) in the bupropion and placebo groups, respectively ( P = 0.001). The odds ratio (95% confidence interval) for response in the bupropion group relative to placebo was 3.2 (2.1-6.3). The thoughts/desire score more than doubled in patients treated with bupropion ( P = 0.001). At the 12-week evaluation the reduction in the PDS scale was 29.4% in bupropion and 4.7% in the placebo group ( P = 0.01). In response to the GEQ, of patients in the bupropion and placebo groups, 65.3%, and 4.3%, respectively, responded 'Definitely yes' ( P = 0.001). Of patients in the bupropion and placebo groups, 71.8%, and 3.7%, respectively, were definitely satisfied with the efficacy of their treatment, ( P = 0.001). After 12 weeks of treatment, 82 women (78.1%) in the bupropion and five (4.9%) in the placebo group were willing to continue therapy ( P = 0.001). CONCLUSIONSThe results from this study indicate that bupropion SR is an effective and welltolerated treatment for HSDD in ovulating women. Further controlled trials are warranted. KEYWORDShypoactive sexual desire disorder, bupropion, treatment, ovulating women, libido Study Type -Therapy (RCT) Level of Evidence 1b

Educational formats that suit different stages of learning can support primary care doctors to reach higher stages of behavioural change in the topic of depressive disorders. Our findings have practical implications for conducting CME programmes in Iran and are possibly also applicable in other parts of the world.

Parkinson's disease (PD) is one of the most commonly occurring neurodegenerative disorders, with lifetime incidence between 1 and 2% among people older than 65 years. ED is one of the more disabling and poorly addressed aspects of PD. The purpose of this study was to assess the efficacy and safety of sildenafil citrate in Parkinson-emergent ED. Sexual function of participants was assessed using responses to the 15-question International Index of Erectile Function (IIEF), Sexual Encounter Profile (SEP) diary questions 2 and 3, Erectile Dysfunction Inventory of Treatment Satisfaction (EDITS) questionnaire and a Global Efficacy Question 'Has the treatment you have been taking over the study period improved your erections?' This randomized, double-blind, placebocontrolled study, comprised a screening period of at least 1 month, a placebo-lead in period of 1 week and treatment period. Two hundred thirty-six patients entered the trial. These patients had mild-to-moderate PD (stages I-III Hoehn-Yahr) and were experiencing Parkinson-emergent neurogenic ED. They were randomized to receive 100 mg sildenafil on demand 1 h before sexual activity (group 1, n ¼ 118), or similar regimen of placebo (group 2, n ¼ 118). Patients were instructed to use at least 24 doses/attempts at home. At the end of the trial, differences between sildenafil and placebo groups were significant for the IIEF erectile function (EF) score (22.6 ± 4.6 vs 14.8 ± 4.2, P ¼ 0.01), for percent Global Efficacy Question 'Yes' responses (68.1±4.6 vs 12.2±3.2, P ¼ 0.001), for SEP2 'Yes' responses (68.1±4.2 vs 32.5±2.2, P ¼ 0.003), for SEP3 'Yes' responses (75.9±5.4 vs 33.5 ± 4.4, P ¼ 0.004) and for mean EDITS score (69.8 ± 4.2 vs 13.0 ± 2.7, P ¼ 0.004). A normal EF domain score (X26) at end point was achieved by 56.9 and 8.7% of the patients in the sildenafil and placebo groups, respectively (P ¼ 0.001). Sildenafil can be considered as an effective treatment in patients with Parkinson-emergent ED.

In the current study, we tried to evaluate the effect of transcranial direct current stimulation (tDCS) on treatment-resistant major depression. We carried out a double-blind randomized sham-controlled trial was conducted in University Hospitals. Individuals with less than 50% decrease in the intensity of depression after 8 weeks of treatment with selective serotonin reuptake inhibitors were recruited. Thirty patients (16 women) with a mean (SD) age of 47.2 (12.0) years were randomly allocated to 2 groups. For the active group we administered 2-mA stimulation 20 minutes for each session, with 30 seconds ramp-up from 0 and 30 seconds ramp-down. For the sham group we administered 30 seconds ramp-up to 2 mA, 10 seconds stimulation, 30 seconds ramp-down, and 20 minutes no current. The anode was fixed on the center of F3, and the cathode on F4, over the dorsolateral prefrontal cortex. We assessed the Hamilton Depression Rating Scale at the baseline (mean difference = 1.0, P = .630), at the last session of tDCS, and at 1-month postintervention. There were statistically significant differences in the mean Hamilton scores after the intervention, and 1 month later in favor of active group; P < .001, and P = .003, respectively. Mixed analysis of variance showed a significant difference in the mean scores for active group P = .010 and pattern of change during the study P < .001 in favor of active intervention. We concluded that tDCS is an efficient therapy for patients with resistant major depression, and the benefits would remain at least for 1 month.

According to these findings, the authors recommend the use of standardized patients in OSCEs for psychiatric board certification exams.