[Research Advances on the Relationship between Overt Hyperthyroidism and Risk of Erectile Dysfunction].

Studies have demonstrated the detrimental effects of overt hyperthyroidism on sexual functioning.Here,we comprehensively reviewed the studies that focused on the association between overt hyperthyroidism and erectile dysfunction (ED).After the systematic searching for relevant studies,we find that overt hyperthyroidism is significantly associated with the high risk of ED.The prevalence of ED in patients with hyperthyroidism ranges from 3.05% to 85%,while that in general population is 2.16% to 33.8%.A study reported that the erectile functioning of the hyperthyroidism patients was improved (International Index of Erectile Function:22.1±6.9 vs. 25.2±5.1) after the achievement of euthyroidism.The underlying mechanism of the increase in the risk of ED by overt hyperthyroidism might be correlated to the dysfunction of hypothalamus-pituitary-thyroid axis,dysregulation of sex hormones,abnormal expression of thyroid hormone receptors,and psychiatric or psychological disturbances (e.g.,depression,anxiety,and irritability).Since limited clinical trials have been conducted,additional well-designed cohorts with sizable samples are warranted to elucidate the evidence and mechanism of hyperthyroidism predisposing to ED.The present review indicates that overt hyperthyroidism and the risk of ED are associated,which reminds the clinicians should assess the thyroid stimulating hormone in hyperthyroidism patients presenting with ED,especially in those without positive conventional laboratory findings for causing ED.

Roles of ARID1A variations in colorectal cancer: a collaborative review.

Colorectal cancer (CRC), a common malignancy, is one of the leading cause of cancer death in adults. AT-rich interaction domain 1A (ARID1A), a critical portion of the SWItch/sucrose non-fermentation (SWI/SNF) chromatin remodeling complexes, shows one of the most frequent mutant genes across different human cancer types. Deleterious variations of ARID1A has been recognized to be correlated the tumorigenesis and the poor prognosis of CRC. Here, we summarize recent advances in the clinical implications and molecular pathogenesis of ARID1A variations in CRC. According to independent data of 23 included studies, ARID1A is mutated in 3.6-66.7%. Consistently, all of the 23 relevant studies report that ARID1A functions as a specific tumor suppressor in CRC. Clinically, ARID1A variation status serves as a biomarker for survival prognosis and various therapies for CRC. Mechanistically, the pathophysiologic impacts of ARID1A variations on CRC may be associated with the co-occurrence variations of other genes (i.e., TP53, KRAS, APC, FBXW7, and PIK3CA) and the regulation of several signaling pathways being affected (i.e., WNT signaling, Akt signaling, and MEK/ERK pathway), leading to cell cycle arrest, chromatin remodeling, chromosome organization, and DNA hypermethylation of the cancer cells. The present review highlights ARID1A serving as a potent tumor suppressor and an important prognostic factor in CRC. ARID1A variations hint towards a promising tool for diagnostic tumor profiling and individualized therapeutic targets for CRC in the future.

Risk of osteoporosis and fracture after hysterectomies without oophorectomies: a systematic review and pooled analysis.

The present study provides evidence that women who underwent hysterectomy without oophorectomies are at a higher risk of osteoporosis and bone fractures than the general population. Early interventions for these susceptible women may help to delay or reduce the risk of osteoporosis and bone fractures. INTRODUCTION: Mounting studies have shown that patients with hysterectomy are at high risk of developing osteoporosis or bone fractures, but the evidence from all the relevant studies has not been previously synthesized. The present study aims to investigate whether women with hysterectomy without oophorectomies have a prominently higher prevalence of osteoporosis or fractures than healthy subjects. METHODS: Four electronic databases were systematically searched to identify the eligible studies. The combined effect was assessed by calculating the relative risk (RR) with a 95% confidence interval (CI). More methodologies for this study were available in the PROSPERO (ID: CRD42021227255). RESULTS: Finally, three observational studies offering osteoporosis cases and two retrospective studies reporting fracture cases were included. One eligible study has provided independent data from three groups of fractures. Synthetic results revealed that hysterectomy without oophorectomies was significantly associated with an increased risk of osteoporosis as compared to the general population (combined RR from three studies = 1.47, 95%CI 1.253 to 1.725, P < 0.001; heterogeneity, I2 = 76.2%, P = 0.015). Consistently, the prevalence of fractures was also significantly higher in patients with hysterectomy without oophorectomies than in healthy controls (pooled RR from four studies = 2.333, 95%CI: 1.314 to 4.144, P = 0.004; heterogeneity, I2 = 92.3%, P < 0.001). CONCLUSIONS: This is the first study to quantify the association between hysterectomy without oophorectomies and osteoporosis/fracture risk through a meta-analysis and has subsequently confirmed its positive relationship. Additional large-sample rigorously prospective cohorts are still warranted to validate the present evidence.

Low prognostic nutritional index is associated with poor outcome in middle-aged and elderly patients with non-metastatic nasopharyngeal carcinoma: a retrospective cohort study.

BACKGROUND: Prognostic nutritional index (PNI) and age are effective prognostic factors for patients with non-metastatic nasopharyngeal carcinoma (NPC), and an interaction between them may exist. However, the age cutoff value is generally set at 45 years in current studies. The clinical implications of PNI in middle-aged and elderly patients are unclear. Therefore, we aimed to uncover this issue. PATIENTS AND METHODS: We retrospectively collected data from 132 middle-aged and elderly (≥ 45 years old) patients with non-metastatic NPC. The association between covariates and the PNI was analyzed using 2 or t-test. The effect of PNI on the prognosis was evaluated using univariate and multivariate Cox regression analyses. Unadjusted and multivariate-adjusted models were applied. Stratified and interactive analyses were performed to investigate the potential source of heterogeneity. RESULTS: Median age (61.0 years versus 59.5 years) and the proportion of patients aged ≥ 60 years (57.6% versus 50.0%) in the low-PNI group were higher than those in the high-PNI group (P > 0.05). The patients with a low PNI had shorter overall survival (OS) (hazard ratio (HR) = 0.86, 95% confidence interval (CI) = 0.80-0.93; P < 0.001) and progression-free survival (PFS) (HR = 0.93, 95% CI = 0.87-0.99; P = 0.034). The results remained stable after three adjusted models of covariates, including age (P < 0.05). No significant interactions were observed in middle-aged (45-59 years) and elderly (≥ 60 years) subgroups for OS and PFS (P for interaction > 0.05). CONCLUSION: Although there is an interaction between PNI and age, PNI is an independent prognostic factor in middle-aged and elderly patients with non-metastatic NPC.

Protective effects of dexmedetomidine in vital organ injury: crucial roles of autophagy.

Vital organ injury is one of the leading causes of global deaths. Accumulating studies have demonstrated that dexmedetomidine (DEX) has an outstanding protective effect on multiple organs for its antiinflammatory and antiapoptotic properties, while the underlying molecular mechanism is not clearly understood. Autophagy, an adaptive catabolic process, has been found to play a crucial role in the organ-protective effects of DEX. Herein, we present a first attempt to summarize all the evidence on the proposed roles of autophagy in the action of DEX protecting against vital organ injuries via a comprehensive review. We found that most of the relevant studies (17/24, 71%) demonstrated that the modulation of autophagy was inhibited under the treatment of DEX on vital organ injuries (e.g. brain, heart, kidney, and lung), but several studies suggested that the level of autophagy was dramatically increased after administration of DEX. Albeit not fully elucidated, the underlying mechanisms governing the roles of autophagy involve the antiapoptotic properties, inhibiting inflammatory response, removing damaged mitochondria, and reducing oxidative stress, which might be facilitated by the interaction with multiple associated genes (i.e., hypoxia inducible factor-1α, p62, caspase-3, heat shock 70 kDa protein, and microRNAs) and signaling cascades (i.e., mammalian target of rapamycin, nuclear factor-kappa B, and c-Jun N-terminal kinases pathway). The authors conclude that DEX hints at a promising strategy in the management of vital organ injuries, while autophagy is crucially involved in the protective effect of DEX.

Molecular mechanisms underlying the renal protective effects of coenzyme Q10 in acute kidney injury.

Coenzyme Q10 (CoQ10), an endogenous antioxidant, has been reported frequently to exert an outstanding protective effect on multiple organ injury, including acute kidney injury (AKI). In this study, we aim to summarize all the current evidence of the protective action of CoQ10 against AKI as there are presently no relevant reviews in the literature. After a systematic search, 20 eligible studies, either clinical trials or experimental studies, were included and further reviewed. CoQ10 treatment exhibited a potent renal protective effect on various types of AKI, such as AKI induced by drugs (e.g., ochratoxin A, cisplatin, gentamicin, L-NAME, and nonsteroidal anti-inflammatory drug), extracorporeal shock wave lithotripsy (ESWL), sepsis, contrast media, and ischemia-reperfusion injury. The renal protective role of CoQ10 against AKI might be mediated by the antiperoxidative, anti-apoptotic, and anti-inflammatory potential of CoQ10. The molecular mechanisms for the protective effects of CoQ10 might be attributed to the regulation of multiple essential genes (e.g., caspase-3, p53, and PON1) and signaling cascades (e.g., Nrf2/HO-1 pathway). This review highlights that CoQ10 may be a potential strategy in the treatment of AKI.

Glycine suppresses kidney calcium oxalate crystal depositions via regulating urinary excretions of oxalate and citrate.

An abnormal urine composition is a key reason for kidney stone formation, but little is known about the roles of small metabolites in the urine during kidney stone formation. Here, we found urine glycine in patients with kidney calcium oxalate (CaOx) stone was significantly lower than that in healthy people via 1 H NMR spectra detection, and investigated the role and underlying mechanism of glycine in the regulation of CaOx stone formation. Our results showed that glycine could significantly attenuate ethylene glycol-induced CaOx crystal depositions in rat kidney via decreasing urine oxalate and increasing urine citrate. Mechanism studies revealed that glycine could decrease urine oxalate through downregulating Slc26a6 expression, whereas increase urine citrate via inhibiting Nadc1 expression. Moreover, glycine decreased the protein expression of both Slc26a6 and Nadc1 via increasing the expression of miRNA-411-3p, which directly bound to the 3'-untranslated regions of Slc26a6 and Nadc1 messenger RNAs, in vitro and in vivo. Together, our results revealed a novel role of glycine in the regulation of kidney CaOx crystal formation and provided a potential target for the treatment of kidney CaOx stone.

miR-199b-5p-DDR1-ERK signalling axis suppresses prostate cancer metastasis via inhibiting epithelial-mesenchymal transition.

BACKGROUND: The investigation of underlying mechanism and the exploitation of novel therapies for metastatic prostate cancer (PCa) are still urgently needed. miR-199b-5p has been suggested to function as tumour suppressor in various human cancers. However, the clinical significance and role of miR-199b-5p in PCa remain unclear. METHODS: The current study sought to investigate the expression status of miR-199b-5p in PCa and the involved molecular mechanisms in PCa metastasis by using bioinformatics analyses, loss-and gain-of-functions and rescue experiments in vitro and in vivo. RESULTS: We demonstrated that miR-199b-5p was significantly downregulated in metastatic PCa tissues and cells when compared with the normal prostate tissue, the localised disease, the weakly metastatic and androgen-dependent PCa cell and the normal prostate epithelial cell. We also found that miR-199b-5p drastically suppressed PCa cell proliferation, migration and invasion in vitro and inhibited xenografts tumour growth and metastasis in vivo. Mechanistically, our results showed that miR-199b-5p could inhibit discoidin domain receptor tyrosine kinase 1 (DDR1) expression by directly targeting its 3'-UTR, thereby hindering epithelial-mesenchymal transition (EMT)-associated traits, which were induced by DDR1 activating ERK signalling pathway. Moreover, PCa patients with low miR-199b-5p expression level had a remarkably shorter overall survival than those with high miR-199b-5p level, indicating an association of miR-199b-5p loss with poor prognosis in patients with PCa. Furthermore, DDR1 was upregulated in PCa, and significantly correlated with high Gleason score, advanced pathological stage, tumour metastasis and shorter overall survival. CONCLUSIONS: Our study, for the first time, provide evidence of a tumour-suppressive function of miR-199b-5p in the invasion and metastasis of PCa, supporting the translational exploitation of miR-199b-5p-based therapeutic approaches for PCa metastases. Also, the miR-199b-5p-DDR1-ERK signalling axis identified in this study represents a novel mechanism of regulating EMT in PCa metastases.

Roles of ferroptosis in urologic malignancies.

Ferroptosis, an iron-dependent form of non-apoptotic cell death, is believed to strongly contribute to the pathogenesis of multiple cancers. Recently, the positive association between ferroptosis and urologic malignancies has drawn considerable attention, while a comprehensive review focused on this issue is absent. Based on this review, ferroptosis has been implicated in the development and therapeutic responses of prostate cancer, kidney cancer, and bladder cancer. Mechanistically, a large number of biomolecules and tumor-associated signaling pathways, including DECR1, PANX2, HSPB1, ACOT8, SUV39H1, NCOA4, PI3K-AKT-mTOR signaling, VHL/HIF-2α pathway, and Hippo/TAZ signaling pathway, have been reported to regulate ferroptosis in urologic cancers. Ferroptosis inducers, such as erastin, ART, CPNPs, and quinazolinyl-arylurea derivatives, exert potential therapeutic effects per se and/or enhance the anticancer response of other anticancer drugs in urologic oncology. A better understanding of ferroptosis may provide a promising way to treat therapy-resistant urologic cancers.

Digoxin reduces the incidence of prostate cancer but increases the cancer-specific mortality: A systematic review and pooled analysis.

Digoxin, a commonly used drug for congestive heart failure and cardiac arrhythmias, has been reported to exert cytotoxic and apoptosis-inducing effects on prostate cancer (PCa) cells. In this study, we aimed to perform a pooled analysis to summarise all the evidence related to the effects of digoxin on PCa development. Four electronic databases were systematically searched to filter the eligible studies. The hazard ratio (HR) with its 95% confidence interval (CI) was calculated. This study was registered on PROSPERO (ID: CRD42021226885). Ten clinical studies with a total of 108,444 participants (15,835 individuals were digoxin users) were included. The pooled result from 6 included studies demonstrated that digoxin usage was correlated with a significant decrease in PCa risk (adjusted RR = 0.892, 95% CI: 0.799-0.997, p = .044) when compared with the nonusers. Synthetic result of 4 eligible studies revealed that digoxin significantly correlated with higher prostate cancer-specific mortality than the controls (adjusted HR = 1.142, 95% CI: 1.005-1.297). No statistical heterogeneity was detected during this analysis (all I2  < 50%, p > .1). Our study confirmed a preventive effect of digoxin usage for the risk of PCa in men. However, digoxin use was associated with a significantly elevated risk of prostate cancer-specific mortality. This finding needs more well-designed studies to better interpret the causality.

Nonalcoholic fatty liver disease and risk of prostatic diseases: Roles of insulin resistance.

Nonalcoholic fatty liver disease (NAFLD), the liver component of metabolic syndrome, is considered to be associated with high risk of prostatic diseases but a systematic review has not been conducted. Under a comprehensive review of the eligible clinical studies, a potential positive association between NAFLD and benign prostatic hyperplasia/prostate cancer (BPH/PCa) has been postulated. Insulin resistance and metabolic aberrations are considered to be the potential mechanism for such association. However, the relationship between NAFLD and other prostatic diseases, that is, prostatic inflammation and lower urinary tract symptoms, seems vague due to limited relevant studies in the literatures. The present review highlights that clinicians should be conscious of the detrimental effect of NAFLD on the development of BPH and PCa.

Is There an Association Between Schizophrenia and Sexual Dysfunction in Both Sexes? A Systematic Review and Meta-Analysis.

BACKGROUND: Mounting clinical studies have reported patients with schizophrenia are at high risk of developing sexual dysfunction (SD), but a directly calculated prevalence of SD is currently lacking. AIM: To further quantify the association between schizophrenia and SD. METHODS: MEDLINE (PubMed), Embase (OVID), the Cochrane Library databases, and the PsycINFO were systematically searched for eligible studies reporting the sexual functioning in patients with schizophrenia. This meta-analysis has been registered on PROSPERO (ID: CRD42019121720, http://www.crd.york.ac.uk/PROSPERO). OUTCOMES: The relationship between schizophrenia and SD was detected by calculating the relative risk (RR) with a 95% confidence interval (CI). The GRADE-profiler was employed to rank the quality of the evidence. RESULTS: 10 observational studies (3 case-control studies and 7 cross-sectional studies) were finally included, enrolling a total of 3,570 participants (mean age 28.6-46.2 years), of whom 1,161 had schizophrenia and the remainders were the healthy control subjects. Synthetic results indicated that schizophrenia was significantly associated with an increased risk of SD regardless of gender (3 studies reporting both sexes: RR = 2.24, 95%CI: 1.66-3.03, P < .001, heterogeneity: I2 = 0.0%, P = .431; 7 studies reporting men: RR = 2.63, 95%CI: 1.68-4.13, P < .001, heterogeneity: I2 = 82.7%, P < .001; 5 studies reporting women: RR = 2.07, 95%CI: 1.46-2.94, P < .001; heterogeneity: I2 = 79.7%, P = .001). In accordance with the GRADE-profiler, the quality of the evidence of primary outcomes was LOW, MODERATE, and LOW in studies including both sexes, men, and women, respectively. CLINICAL IMPLICATIONS: Our findings confirmed the potential link between schizophrenia and SD. Clinicians should routinely assess the sexual functioning for those patients with schizophrenia and further recommend the preferred antipsychotics for them. STRENGTHS & LIMITATIONS: This is the first meta-analysis investigating the association between schizophrenia and the risks of SD in both sexes. Nonetheless, substantial heterogeneities were identified across the selected studies. CONCLUSION: Robust data from this meta-analysis showed increased rates of SD in patients with schizophrenia compared with the general populations. Therefore, more specific psychological and pharmaceutical interventions are needed to help patients with schizophrenia gain a better sexual life. Zhao S, Wang X, Qiang X, et al. Is There an Association Between Schizophrenia and Sexual Dysfunction in Both Sexes? A Systematic Review and Meta-Analysis. J Sex Med 2020;17:1476-1488.

Association Between Overt Hyperthyroidism and Risk of Sexual Dysfunction in Both Sexes: A Systematic Review and Meta-Analysis.

BACKGROUND: Numerous studies have shown the detrimental effects of overt hyperthyroidism on sexual functioning but a quantitative result has not yet been synthesized. AIM: To conduct a systematic review and meta-analysis that quantifies the association between overt hyperthyroidism and the risk of sexual dysfunction (SD). METHODS: A meta-analysis of studies in the literature published prior to February 1, 2020, from 4 electronic databases (MEDLINE, Embase, Cochrane Library databases, and PsychINFO) was conducted. All analyses were performed using the random-effects model comparing individuals with and without overt hyperthyroidism. OUTCOMES: The strength of the association between overt hyperthyroidism and risk of SD was quantified by calculating the relative risk (RR) and the standard mean difierences with 95% CI. The quality of evidence for the reported outcome was based on the Grading of Recommendations Assessment, Development, and Evaluation approach. RESULTS: Of 571 publications, a total of 7 studies involving 323,257 individuals were included. Synthetic results from 7 eligible studies indicated that overt hyperthyroidism led to significant SD in both sexes (pooled RR = 2.59, 95% CI: 1.3-5.17, P = .007; heterogeneity: I2 = 98.8%, P < .001). When we analyzed the data of men and women independently, the pooled results consistently showed that men and women with overt hyperthyroidism were at over 2-fold higher risk of SD than the general populations (RR for males = 2.59, 95% CI: 1.03-6.52, P = .044; RR for females = 2.51, 95% CI: 1.47-4.28, P = .001). Combined standard mean diffierences from those studies providing the Female Sexual Function Index (FSFI) suggested that women with overt hyperthyroidism were associated with a significantly lower FSFI value in FSFI total scores, subscale sexual arousal, lubrication, orgasm, and satisfaction domain (all P < .05). The overall quality of evidence in our study was considered to be moderate. CLINICAL IMPLICATIONS: Clinicians should know the detrimental effects of overt hyperthyroidism on sexual functioning in clinical practice. Measurement of thyroid hormones should be included in the assessment of patients presenting with SD when they show symptoms of clinical hyperthyroidism. STRENGTHS & LIMITATIONS: This is the first meta-analysis quantifying the relationship between overt hyperthyroidism and the risks of SD. However, the combined results were derived from limited retrospective studies along with substantial heterogeneities. CONCLUSION: Our study has confirmed the potentially devastating sexual health consequences caused by overt hyperthyroidism. However, additional rigorous studies with sizable samples are still needed to better elucidate this evidence. Pan Y, Xie Q, Zhang Z, et al. Association Between Overt Hyperthyroidism and Risk of Sexual Dysfunction in Both Sexes: A Systematic Review and Meta-Analysis. J Sex Med 2020;17:2198-2207.

Association between PD-L1 Expression and the Prognosis and Clinicopathologic Features of Renal Cell Carcinoma: A Systematic Review and Meta-Analysis.

The expression of programmed cell death-ligand 1 (PD-L1) and its correlation with the prognosis and clinicopathologic features of renal cell carcinoma (RCC) remain controversial to date. Concerning this issue, we had conducted a meta-analysis of relevant studies searched in the Web of Science, PubMed, EMBASE, and Cochrane Library databases. The Newcastle-Ottawa quality assessment scale was applied to assess the quality of the included studies. The hazard ratio (HR) and its corresponding 95% confidence intervals (CIs) were collected by Stata 12.0 and used for the results of overall survival (OS) and disease-free survival (DFS). A total of 1,644 patients in 8 studies were included in this meta-analysis. Results showed that PD-L1 expression significantly correlated with OS (HR = 1.98, 95% CI: 1.22-3.22, Z = 2.77, p = 0.006) and DFS (HR = 3.70, 95% CI: 2.07-6.62, Z = 4.40, p = 0.0001) in ccRCC. Subgroup analysis indicated that PD-L1 expression significantly correlated with the lymph-gland transfer ratio (HR = 2.45, 95% CI: 1.02-5.92, Z = 1.99, p = 0.05) and tumor necrosis (HR = 6.05, 95% CI: 3.78-9.67, Z = 7.51, p < 0.00001). This meta-analysis suggests that PD-L1 expression is a valuable prognostic tool for patients with ccRCC. Subgroup analyses demonstrated that it was helpful for screening patients with RCC who need anti-PD-1/PD-L1 treatment and support them to benefit from such immune-targeted therapy.

Low intensity extracorporeal shockwave Therapy shifts PDE5i nonresponders to responders.

To evaluate the efficiency of an energy density of 0.05mj/mm2 of low intensity extracorporeal shockwave therapy (Li-ESWT) on erectile dysfunction (ED) patients. A total of 45 ED patients met the inclusion criteria, including 7 PDE5i responders and 38 nonresponders. All the patients have already been delivered 10000 shockwaves of total seven treatment points twice a week for 4 weeks. Simultaneously, questionnaires of International Index of Erectile Function-Erectile Function (IIEF-EF), Erectile Hard Score (EHS) and Minimal Clinical Important Differences (MCID) were evaluated for the efficiency and safety at 8th and 16th weeks. The changes in the IIEF-EF score by MCID suggested that Li-ESWT treatment was effective in 22 PDE5i nonresponders patients (58%) at 8th week. Then at 16th week the number of patients who were effectively treated increased to 27 (71%). Among PDE5i responders, 5 patients (71%) were effective base on MCID at 16th week. Among PDE5i nonresponders 22 patients (58%) achieved erection hard enough for vaginal penetration and increased to 27 (71%) patients at 16th week (EHS ≥3). Moreover, even 3 patients achieved EHS 4 in PDE5i nonresponders at 16th week. Among PDE5i responders, 4 of 7 patients reached EHS of 4 from EHS 3 at 16th week. Apart from this, Li-ESWT treatment was also effective in 9 patients (24%) in PDE5i nonresponders without follow-up PDE5i. Energy flux density (EFD) of 0.05 of Li-ESWT could improve the erectile function of ED patients with PDE5i response. In addition, EFD of 0.05 of Li-ESWT treatment could turn PDE5i nonresponders to responders.

Mesenchymal stem cell-derived exosomes ameliorate erection by reducing oxidative stress damage of corpus cavernosum in a rat model of artery injury.

Erectile dysfunction (ED) is a common ageing male's disease, and vascular ED accounts for the largest proportion of all types of ED. One of the mechanisms of vascular ED in the clinic is arterial insufficiency, which mainly caused by atherosclerosis, trauma and surgical. Moreover, oxidative stress damage after tissue ischemia usually aggravated the progress of ED. As a new way of acellular therapy, mesenchymal stem cell-derived exosomes (MSC-Exos) have great potential in ED treatment. In the current study, we have explored the mechanism of MSC-Exos therapy in a rat model of internal iliac artery injury-induced ED. Compared with intracavernous (IC) injection of phosphate-buffered saline after artery injury, of note, we observed that both mesenchymal stem cells (MSCs) and MSC-Exos through IC injection could improve the erectile function to varying degrees. More specifically, IC injection MSC-Exos could promote cavernous sinus endothelial formation, reduce the organization oxidative stress damage, and improve the nitric oxide synthase and smooth muscle content in the corpus cavernosum. With similar potency compared with the stem cell therapy and other unique advantages, IC injection of MSC- Exos could be an effective treatment to ameliorate erectile function in a rat model of arterial injury.

Is polycystic ovary syndrome associated with risk of female sexual dysfunction? A systematic review and meta-analysis.

The aim of this study was to evaluate whether polycystic ovary syndrome (PCOS) is a risk factor for female sexual dysfunction (FSD) by conducting a systematic review and meta-analysis. The databases PubMed, EMBASE and the Cochrane Library were searched for relevant studies. The association between PCOS and risk of FSD was assessed by relative risk or standard mean differences with 95% confidence interval. The protocol for this meta-analysis is available from PROSPERO (CRD42018102247). Overall, 2626 participants (mean age 25-36 years) were included from 10 studies (five cross-sectional and five case-control studies), 1163 of whom were women with PCOS. The pooled results from eight included studies providing the number of cases revealed no significant association between PCOS and increased risk of FSD (RR = 1.09, 95% CI 0.9 to 1.32; heterogeneity: I2 = 11.0%). The combined overall standard mean difference from five studies reporting Female Sexual Function Index (FSFI) scores showed that patients with PCOS had similar values in total FSFI scores compared with healthy controls (standard mean difference = -0.03, 95% CI -0.12 to 0.05; heterogeneity: I2 = 0.0%). Sensitivity analyses yielded similar results. This meta-analysis suggests no direct association between PCOS and risk of FSD. Well-controlled trials with large sample sizes, however, are needed to validate this evidence.

Parkinson's Disease Is Associated with Risk of Sexual Dysfunction in Men but Not in Women: A Systematic Review and Meta-Analysis.

BACKGROUND: Mounting evidence has emerged suggesting that patients with Parkinson's disease (PD) are susceptible to sexual dysfunction (SD). AIM: To better clarify the relationship between PD and SD. METHODS: PubMed, Embase, Cochrane Library database, and PsychINFO database were systematically searched for pertinent studies evaluating sexual function in the patients with PD. This systematic review and meta-analysis have been registered on PROSPERO (ID: CRD42018108714; http://www.crd.york.ac.uk/PROSPERO). OUTCOMES: The association between PD and SD was assessed using relative risk (RR) with 95% CI. The quality of evidence was ranked by the GRADE profiler. RESULTS: 11 observational studies met the predefined criteria for inclusion, enrolling 30,150 subjects from both the PD group and healthy control group (mean age 54.6-75.1 years). Synthesis results revealed that PD was associated with an elevated risk of SD in males (7 studies; 1.79; 95% CI = 1.26-2.54, P = .001; heterogeneity: I2 = 73.2%, P < .001). However, when restricted to female subjects, the combined RR from 3 eligible studies suggested a lack of significant association between PD and SD (RR = 1.3, 95% CI = 0.64-2.61, P = .469; heterogeneity: I2 = 80.0%, P = .007). The GRADE profiler indicated the overall quality of the evidence was low in studies including males and very low in studies including females. CLINICAL IMPLICATIONS: The current meta-analysis indicated that men with PD were more likely to experience SD than those without PD. In female subjects, however, PD seemed to not be associated with a high prevalence of SD compared with healthy controls. Based on these findings, patients with PD should be routinely assessed for sexual functioning, especially males. STRENGTHS & LIMITATIONS: This is the first systematic review and meta-analysis of the association between PD and the risks of SD in both males and females. However, substantial heterogeneities were detected across the included studies. CONCLUSION: A hazardous effect of PD for developing SD was detected in men but not in women. As a result, sexual function assessment and appropriate therapy are recommended for men with PD in clinical practice. Zhao S, Wang J, Xie Q, et al. Parkinson's Disease Is Associated with Risk of Sexual Dysfunction in Men but Not in Women: A Systematic Review and Meta-Analysis J Sex Med 2019;16:434-446.

Elucidating Mechanisms of Long-Term Gasoline Vehicle Exhaust Exposure-Induced Erectile Dysfunction in a Rat Model.

INTRODUCTION: Exposure to air pollution poses a risk for morbidity in multiple diseases. However, the role of ambient air pollutant emissions in public sexual health is just beginning to be understood and remains controversial. AIM: We have determined to elucidate the specific role of gasoline vehicle exhaust (VE), a crucial source and toxicant of air pollution, in the penile erectile function via a rat model. METHODS: 40 male Sprague Dawley rats, 12 weeks of age, were used in this experiment. Except for the control group (10 rats), rats were equally exposed to VE for total 2 hours, 4 hours, and 6 hours daily for 3 months consecutively. During each VE exposure periods, particulate matter (PM) mass concentrations of PM1, PM2.5, and PM10 were 1.43 ± 0.036, 1.45 ± 0.033, and 1.47 ± 0.037 mg/m3, respectively. MAIN OUTCOME MEASURE: Erectile function, pulmonary function, serum inflammatory factors, and histologic examinations of the lung and penile tissues were evaluated. RESULTS: Our study indicates that in vivo, 4-hour, and 6-hour daily exposure to VE causes significant reduction of erectile function, as judged by intracavernous pressure measurement. Meanwhile, we have observed that the 4-hour and 6-hour VE exposure rats exhibited remarkable increased levels of serum inflammatory factors, decreased total lung capacity and chord compliance, thickened alveoli septum, destroyed alveoli, pulmonary fibrosis, as well as down-regulation of the messenger RNA and protein expression of endothelial and neuronal nitric oxide synthase in the penile tissue when compared with normal control rats. CLINICAL IMPLICATIONS: We speculated that the underlying mechanisms of VE inducing erectile dysfunction could be attributed to systemic inflammation, pulmonary dysfunction, and the reduction of nitric oxide synthase activity in the corpus cavernosum. STRENGTH & LIMITATIONS: For the first time, our study revealed the deleterious effect of VE on penile erection in vivo. However, the VE exposure model might not entirely mimic the natural condition of ambient air pollution. CONCLUSION: Our results raise concerns about the potential role played by long-term exposure to gasoline VE in the development of erectile dysfunction. Zhao S, Wang J, Xie Q, et al. Elucidating Mechanisms of Long-Term Gasoline Vehicle Exhaust Exposure-Induced Erectile Dysfunction in a Rat Model. J Sex Med 2019;16:155-167.

Gout is associated with elevated risk of erectile dysfunction: a systematic review and meta-analysis.

Previous studies investigating the risk of erectile dysfunction (ED) among patients with gout have produced inconsistent evidence. Therefore, the aim of this meta-analysis was to investigate the relationship between gout and the risk of ED. The Embase, Medline, Scopus, Web of Science and Cochrane Library databases were searched for all studies assessing the risk of ED in patients with gout. Relative risks (RR) and corresponding 95% confidence intervals (CI) were adopted to estimate the association between gout and the risk of ED. Sensitivity analyses were applied to evaluate the robustness of results. Overall, 355,761 participants were included from 8 studies (3 cross-sectional and 5 cohort studies). Of these, 85,067 were patients with gout. Synthesis results showed patients with gout had a 1.2-fold higher risk of ED than individual without gout (RR 1.20, 95% CI 1.10-1.31, P < 0.001). The results of sensitivity analysis are consistent with the trend of synthesis results. The present meta-analysis revealed that the risk of ED in patients with gout was dramatically increased when compared with the general population, which suggests that clinicians should assess erectile function when treating an individual who suffers from gout.