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.

The safety and efficacy of esketamine in comparison to dexmedetomidine during drug-induced sleep endoscopy in children with obstructive sleep apnea hypopnea syndrome: A randomized, controlled and prospective clinical trial.

Background and Purpose: Data and high-quality studies of anesthetic methods for children with obstructive sleep apnea hypopnea syndrome (OSAHS) who undergo drug-induced sleep endoscopy (DISE) are limited. Research on pediatric DISE using esketamine has never been reported before. To test the safety and efficacy of esketamine during DISE in children with OSAHS, we compare esketamine (Group K) with dexmedetomidine (Group D) in this study. Methods: 100 children with ASA Ⅰ∼Ⅱ grade, prepared for an elective adenotonsillectomy under general anesthesia, were enrolled in this study and randomized into two groups. Midazolam 0.1 mg/kg was administered intravenously for both groups. In Group D a 1 µg/kg bolus of dexmedetomidine was given over 10 min followed by the infusion rate 1 µg/kg/hr to the end of DISE. Group K received a 1.0 mg/kg IV bolus of esketamine over 10 s followed by the infusion rate 1 mg/kg/hr to the end of DISE. Results: Group K had a higher percentage of success than Group D (p = 0.008). The onset time of Group K was shorter than that of Group D (p = 0.000). The University of Michigan Sedation Scale (UMSS) score of Group K was higher than that of Group D (p = 0.005). The risk of adverse effects (AEs) was lower in Group K (p = 0.000). In Group D, systolic and diastolic blood pressure (SBP and DBP) and heart rate (HR) all decreased, while in Group K, SBP, DBP, and HR hardly changed. Conclusion: Esketamine in comparison to dexmedetomidine provides more effective and safer depth of anesthesia for OSAHS pediatric DISE by ensuring short onset time, deep sedation, and few AEs. Clinical Trial Registration: ClincalTrials.gov, identifier NCT04877639.

Study on the relationship of cPLA2, CK-MB, and membrane phospholipid content in acute myocardial infarction.

Increased plasma creatine kinase-myoglobin (CK-MB) occurs in patients with acute myocardial infarction (AMI), but its underlying relationship with cytosolic phospholipase A2 (cPLA2) is poorly understood. In the present study we sought to determine cPLA2 activation and its relationship with plasma and myocardial CK-MB level and membrane phospholipids (PLs) in an animal model of AMI. AMI was induced in 60 male Sprague-Dawley rats by ligating the left anterior descending of coronary artery. Rats were randomized into six groups at 0 (sham group), 1, 2, 4, 6, and 12 h after AMI onset (ten rats in each group). cPLA2 was detected by reverse transcription polymerase chain reaction and immunohistochemical staining for mRNA and protein expression, respectively. Plasma and myocardial CK-MB activity were measured by inhibition kinetics, and membrane PLs were determined by phosphorus quantitative method. Myocardial cPLA2 expression increased from 1 h and reached a peak at 2 h after AMI onset (p < 0.01) followed by a decrease but still remained high, whereas plasma CK-MB significantly increased in rats from 4 h after the onset of AMI (p < 0.05). During the first 6 h of AMI, a negative correlation existed between myocardial cPLA2 and membrane PLs (r = -0.504, p < 0.01), whereas myocardial cPLA2 levels were positively associated with plasma CK-MB (r = 0.741, p < 0.01) but negatively correlated with myocardial CK-MB in AMI groups (r = -0.785, p < 0.01). Myocardial cPLA2 level increased and is positively correlated with plasma CK-MB activity and negatively correlated with membrane phospholipid content in AMI rats at early stage.

Electrophysiologic characteristics of the Crista terminalis and implications on atrial tachycardia in rabbits.

The objective of this study was to evaluate the electrophysiologic characteristics of Crista terminalis (CT) and their implication in the pathogenesis of atrial tachycardia in rabbits. For this purpose, 27 New Zealand rabbits were used. Using standard glass microelectrode technique, cellular action potentials (APs) of CT and pectinate muscle (PM) were recorded in normal Tyrode's perfusion and Tyrode's perfusion with 4 µM isoproterenol. Longitudinal conduction velocity (V(L)) and transverse conduction velocity (V(T)) of CT were measured. As our data show, CT tissue had a trend of spontaneous phase IV depolarization. Conduction anisotropy (V(L)/V(T)) of CT was 4.53 ± 0.91. The duration of the AP of CT was longer than that of PM cells. APD(20) and APD(90) for CT were 28.1 ± 3.5 and 145.3 ± 7.1 ms; and for PM cells were 21.8 ± 4.1 and 125.3 ± 6.3 ms, respectively (all P values < 0.01). The early and delayed action depolarizations were recorded after isoproterenol perfusion. A fast paroxysmal irregular rhythm was recorded which could be arrested by 0.1 mmol/l Isoptin. It was, therefore, concluded that the latent autorhythmicity, trigger activity, and conduction properties of CT might provide the electrophysiologic basis for the occurrence and sustenance of atrial arrhythmia.

Digitalis does not improve left atrial mechanical dysfunction after successful electrical cardioversion of chronic atrial fibrillation.

This study was designed to investigate whether administration of digitalis could improve mechanical function of left atrial appendage (LAA) and left atrium prospectively in patients with atrial stunning. Fifty-four consecutive patients in whom atrial stunning was observed immediately after cardioversion of chronic atrial fibrillation (AF) were randomized into digitalis or control group for 1 week following cardioversion. Transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE) were performed prior to, immediately following, 1 day after and 1 week after cardioversion to measure transmitral flow velocity and LAA flow velocity. Electrical cardioversion of AF elicited significantly slower left atrial appendage peak emptying velocity (LAA-PEV) and peak filling velocity (LAA-PFV) immediately following cardioversion in both groups. 1 day post cardioversion, there were no significant differences in transmitral E wave, A wave, E/A ratio, LAA-PEV, LAA-PFV or left atrial appendage ejection fraction (LAA-EF) between digitalis and control groups. 1 week post cardioversion, no significant differences were found in transmitral E wave, A wave, E/A ratio, LAA-PEV, LAA-PFV or LAA-EF between the two groups. The occurrence rates of spontaneous echo contrast were not significantly different between digitalis and control groups one day and one week post cardioversion. In conclusion, digitalis did not improve left atrial and appendage mechanical dysfunction following cardioversion of chronic AF. Digitalis did not prevent the development of spontaneous echo contrast in left atrial chamber and appendage. This may be due to the fact that digitalis aggravates intracellular calcium overload induced by chronic AF and has a negative effect on ventricular rate.

Simvastatin inhibits sPLA2 IIa expression in aorta and myocardium.

BACKGROUND AND AIMS: Group IIa secretory phospholipase A2 (sPLA2 IIa) induces atherosclerosis by altering systemic lipoprotein mechanism. The aim of this study was to investigate the expression and localization of sPLA2 IIa in atherosclerosis of rat aorta, myocardium and visceral adipose tissue (VAT) and to explore the effect of simvastatin on sPLA2 IIa expression. METHODS: Thirty male Wistar rats were randomly divided into three groups: control group, test group, and simvastatin group. Control group rats were fed with standard chow, whereas those in the test group were fed with a high cholesterol diet. Simvastatin (5 mg/kg/day per gavage) was given to the rats in simvastatin group in addition to the high cholesterol diet. At the end of 8 weeks, rats were sacrificed and sPLA2 IIa measured by immunocytochemistry. RESULTS: sPLA2 IIa was present in smooth muscle cells, aortic plaques, and also in myocardium and VAT. In addition, sPLA2 IIa expression in myocardium and aorta was much higher in the test group than in control group (p <0.01). However, expression of the enzyme in myocardium and aorta was significantly decreased in the simvastatin group compared to the test group (p <0.05). Immunostaining of sPLA2 IIa was also present in VAT, but no significant changes were found in levels of this enzyme among the three groups (p >0.05). CONCLUSIONS: Myocardium and VAT may be two other important sources of sPLA2 IIa. Our data support the hypothesis that sPLA2 IIa may play a significant role in the pathogenesis of atherosclerosis. Simvastatin may reduce the process of atherosclerosis by decreasing the expression level of sPLA2 IIa in myocardium and aorta.