Previous studies had illustrated the significant neural pathological changes in patients with psychogenic erectile dysfunction (pED), while few works focused on the neural underpinning of the psychosocial status in patients with pED. This study aimed to investigate the associations among the altered cerebral activity patterns, impaired erectile function, and the disrupted psychosocial status in patients with pED. Thirty-two patients with pED and 28 healthy controls (HCs) were included. The amplitude of low-frequency fluctuations (ALFF), region-of-interest-based functional connectivity (FC), as well as Pearson correlation analyses and mediation analyses between neuroimaging outcomes and clinical outcomes were performed. Compared to HCs, patients with pED manifested lower erectile function, disrupted psychosocial status, as well as decreased ALFF in the left dorsolateral prefrontal cortex (dlPFC) and reduced FC between the left dlPFC and left angular gyrus, and left posterior cingulate cortex (PCC) and precuneus, which belonged to the default mode network (DMN). Moreover, both the ALFF of the left dlPFC and FC between the left dlPFC and left PCC and precuneus were significantly correlated with the sexual function and psychosocial status in patients with pED. The disrupted psychosocial status mediated the influence of atypical FC between dlPFC and DMN on decreased erectile function. This study widened our understanding of the important role of psychosocial disorders in pathological neural changes in patients with pED.
IntroductionErectile dysfunction (ED) is the most common male sexual disorder that severely impacts the sexual performance and quality of life of men. As the main subtype of ED, psychogenic ED (pED) has been demonstrated to be a genitourinary disease and also associated with alterations in both brain structure and function. However, the scattered neuroimaging evidence from individual studies has not yet been integrated, and the central pathological alterations associated with pED remain unclear. The objective of this systematic review is to integrate and assess the evidence of the impact of pED on brain structure and function.Methods and analysisFive databases (PubMed, EMBASE, Web of Science, China Biology Medicine Database and China National Knowledge Infrastructure (CNKI)) will be systematically searched from inception to 1 October 2019 (the anticipated completion date of this review), with language restricted to English and Chinese. Studies focusing on the structural or functional alterations in patients with pED will be retrieved. The study selection process will follow the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guideline and quality assessment will be conducted with a customised checklist. After data extraction, a qualitative review will be performed to synthesise the structural and functional brain alterations as well as the correlations between the altered cerebral structures and functions and the clinical characteristics of patients with pED. If the collected data make it feasible, an activation likelihood estimation meta-analysis will also be launched.Ethics and disseminationEthical approval is not required as primary data will not be collected. This review will be published in a peer-reviewed journal and presented at conferences.PROSPERO registration numberCRD42019117206.
Background: Erectile dysfunction (ED) affects many adult men worldwide. Many studies on the brain of psychogenic ED have shown significant cerebral functional changes and reduced volume of gray matter and white matter microstructural alterations in widespread brain regions. Chaihu-Shugan-San (CHSGS) capsule has been used to treat ED from the 20th century in China. However, clinical research of CHSGS capsule in the treatment of ED was lack. We design this study to evaluate the efficacy and safety of CHSGS capsule in the treatment of patients suffering from psychogenic ED. Furthermore, we also aim to provide a new evidence as well as an innovation of the clinical treatment in psychogenic ED. Methods: This study is designed as a multi-center, 3-arms, randomized trial. From the perspective of psychogenic ED, we will divide patients into 3 groups, which are placebo group, tadalafil group and CHSGS group. One hundred thirty-five patients will be randomly allocated to receive placebo, CHSGS capsule or tadalafil oral pharmacotherapy. After the period of 4-week treatment, the outcome of primary assessment changes in the brain MRI, IIEF-5, EHS, and QEQ total scores from baseline. Secondary assessments include the SEAR, HAMA-14, HAMD-17 scores, response rate of the patients and their partners. Discussion: We designed this study based on previous research about psychogenic erectile dysfunction (ED). This study will provide objective evidences to evaluate the effects of CHSGS capsule as an adjuvant treatment for psychogenic ED. Trial registration number: chictr.org.cn, ChiCTR-IOR-1800018301.
Background: Recently, several genome-wide association studies have demonstrated a cumulative association of 17q24 rs1859962 gene variants with prostate cancer (PCa) risk, but conflicting results on this issue have been reported. Hence, we performed a systematic literature review and meta-analysis to assess the association between 17q24 rs1859962 gene and PCa risk. Methods: Systematic literature searches were conducted with PubMed, EMBASE, Science Direct/Elsevier, CNKI, and the Cochrane Library up to January 2019 for studies focusing on the association of 17q24 rs1859962 gene polymorphism with PCa risk. Meta-analysis was performed with Review Manager and stata software. Combined OR were identified with 95% confidence intervals (95% CI) in a random or fixed effects model. Results: Eight studies were identified, including 7863 cases of PCa patients and 17122 normal controls. Our results revealed significant associations between the 17q24 rs1859962 gene polymorphism and PCa in all genetic models (P < 0.05). The combined odds ratios and 95% confidence intervals were as follows: Additive model (odds ratios [ORs] 1.44, 95%, confidence interval [CI] [1.32, 1.57]); Codominant model (ORs 1.22, 95% CI [1.08, 1.39]); Dominant model (ORs 1.25, 95%, CI [1.17, 1.34]); recessive model (ORs 1.27, 95% CI [1.18, 1.36]); allele model (ORs 1.32, 95% CI [1.12, 1.55]). Conclusion: The present study supports the proposed association between the 17q24 gene rs1859962 and PCa progression. Specifically, this polymorphism is suggested to be a risk factor of PCa. However, studies with larger sample sizes are needed to better illuminate the correlation between 17q24 rs1859962 gene polymorphism and PCa.
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