Sexual Dysfunctions are Predicted by Childhood Sexual Abuse in Women with Opioid Use Disorder

Background: Studies on sexual functioning of populations with substance use disorders (SUDs) are mostly conducted with male substance users. We have very limited information about the sexuality and related factors in women with opioid use disorder (OUD). Objectives: We aimed to evaluate the relationship between childhood traumatic experiences (CTEs) and sexual dysfunctions (SDs) of women with OUD and to compare it with a sample of women who do not have SUD. Methods: Participants included 51 outpatient women with OUD who were on opioid maintenance treatment (OMT) with Buprenorphine/Naloxone and 48 women without SUD. Participants were evaluated by a semi-structured sociodemographic form, the Golombok-Rust Inventory of Sexual Satisfaction (GRISS), the Childhood Trauma Questionnaire (CTQ-28), the Beck Depression Inventory (BDI) and the State-Trait Anxiety Inventory (STAI). Results: In women with OUD; CTQ-28, BDI, STAI, and GRISS scores were significantly higher. In the partial correlation analysis, sexual abuse was found to be significantly correlated with nonsensuality, avoidance and total GRISS score. In stepwise regression model, sexual abuse was found to predict SDs together with depression. Conclusions: CTE, SD, depression, and anxiety rates were higher in the women with OUD. Especially childhood sexual abuse was associated with SDs in this group. Sexual abuse was predicting SDs together with depression. Further investigation of different characteristics of women with SUD may give an opportunity to clinicians to have a better understanding for adaptable treatment strategies.     

NF‐κB/p53‐activated inflammatory response involves in diquat‐induced mitochondrial dysfunction and apoptosis

Inflammation generated by environmental toxicants including pesticides could be one of the factors underlying neuronal cell damage in neurodegenerative diseases. In this study, we investigated the mechanisms by which inflammatory responses contribute to apoptosis in PC12 cells treated with diquat. We found that diquat induced apoptosis, as demonstrated by the activation of caspases and nuclear condensation, inhibition of mitochondrial complex I activity, and decreased ATP level in PC12 cells. Diquat also reduced the dopamine level, indicating that cell death induced by diquat is due to cytotoxicity of dopaminergic neuronal components in these cells. Exposure of PC12 cells to diquat led to the production of reactive oxygen species (ROS), and the antioxidant N‐acetyl‐cystein attenuated the cytotoxicity of caspase‐3 pathways. These results demonstrate that diquat‐induced apoptosis is involved in mitochondrial dysfunction through production of ROS. Furthermore, diquat increased expression of cyclooxygenase‐2 (COX‐2) and tumor necrosis factor‐α (TNF‐α) via inflammatory stimulation. Diquat induced nuclear accumulation of NF‐κB and p53 proteins. Importantly, an inhibitor of NF‐κB nuclear translocation blocked the increase of p53. Both NF‐κB and p53 inhibitors also blocked the diquat‐induced inflammatory response. Pretreatment of cells with meloxicam, a COX‐2 inhibitor, also blocked apoptosis and mitochondrial dysfunction. These results represent a unique molecular characterization of diquat‐induced cytotoxicity in PC12 cells. Our results demonstrate that diquat induces cell damage in part through inflammatory responses via NF‐κB‐mediated p53 signaling. This suggests the potential to generate mitochondrial damage via inflammatory responses and inflammatory stimulation‐related neurodegenerative disease.     

腹腔镜子宫(阴道)骶骨固定术与改良全盆底重建术治疗盆腔脏器脱垂的临床疗效观察

目的探讨经腹腔镜子宫(阴道)骶骨固定术及改良全盆底重建术用于治疗中盆腔缺陷为主的盆腔脏器脱垂(POP)患者的临床疗效。方法纳入2012年3月-2015年3月住院的中盆腔脏器脱垂达到POP-Q分期Ⅱ~Ⅲ期的患者169例,根据手术方式分为改良全盆底重建组81例和腹腔镜下骶骨固定术组88例。按照规范化标准为患者实施手术,手术中对合并盆底功能障碍进行对应处理。围手术期记录患者相应情况,检测手术主客观满意度。所有患者纳入随访,填写盆底功能障碍及性生活质量评估量表。结果骶骨固定术组平均年龄比较[(43.78±7.63)岁vs.(53.01±10.50)岁],两组绝经概率比较(33.0%vs.60.5%),术前压力性尿失禁(SUI)概率比较(46.1%vs.65.4%)显著低于改良全盆底重建组,差异有统计学意义(P<0.05)。与改良全盆底重建组相比,骶骨固定组手术出血量[(60.32±30.27)mlvs.(98.35±40.28)ml]、尿管留置时间[(1.90±0.90)dvs.(2.50±1.10)d]及子宫切除比例(30.7%vs.60.5%)更低,差异有统计学意义(P<0.05)。两组患者手术后12个月时PFIQ-7及PFQI-20评分均较手术前显著下降(P<0.05)。术后12个月时,骶骨固定组的PISQ-12评分显著高于手术前(P<0.05)。结论骶骨固定术及改良全盆底重建术治疗POP患者均具有较好的疗效及安全性,远期预后良好。骶骨固定术改善POP患者性生活质量更为显著。     

Quercetin attenuates domoic acid-induced cognitive deficits in mice

Domoic acid (DA) is one of the best known marine toxins, causative of important neurotoxic alterations. DA effects are documented both in wildlife and experimental assays, showing that this toxin causes severe injuries principally in the hippocampal area. Accumulating evidence indicates that mitochondrial dysfunction and oxidative stress are involved in DA-induced cognitive functional impairment. Therefore, therapeutics targeted to improve mitochondrial function and increase oxidative stress defence could be bene?cial. Quercetin, a bio?avanoid, has been reported to have potent neuroprotective effects and anti-oxidative ability, but its preventive effects on DA-induced mitochondrial dysfunction and cognitive impairment have not been well characterised. In this study, we evaluated the effects of quercetin on DA-induced cognitive deficits in mice and explored its potential mechanism. Our results showed that the oral administration of quercetin to DA-treated mice significantly improved their behavioural performance in a novel objective recognition task and a Morris water maze task. These improvements were mediated, at least in part, by a stimulation of PPARγ coactivator 1α-mediated mitochondrial biogenesis signalling and an amelioration of mitochondrial dysfunction. Moreover, quercetin activated nuclear factorerythroid-2-related factor-2 (Nrf2)-mediated phase II enzymes and decreased reactive oxygen species and protein carbonylation. Furthermore, the AMP-activated protein kinase (AMPK) activity significantly increased in the quercetin-treated group. Taken together, these findings suggest that a reduction in mitochondrial dysfunction through the increase of AMPK activity, coupled with an increase in Nrf2 pathway mediated oxidative defence, may be one of the mechanisms by which quercetin improves cognitive impairment induced by DA in mice.     

Evaluation of a tape removal test to assess neurological deficit after cardiac arrest in rats

BACKGROUND: In animal models of cardiocirculatory arrest (CA) it is of major interest to establish tests that can assess neurological damage after global cerebral ischaemia following CA. We evaluated a tape removal test with regard to detection of sensorimotor deficit, comparing it to the Neurological Deficit Score (NDS) in an established model of global cerebral ischaemia after CA in rats. METHODS: Rats were subjected to either 6 min of CA followed by cardiopulmonary resuscitation (CPR) or a sham operation. At 1, 3 and 7 days from the intervention, two different neurological tests were applied to all animals: in the tape removal test, the time was measured from attachment of adhesive tapes to the front paws until the animals removed them using their teeth and compared to latencies in the sham group. The NDS assessed two parameters ("travel beam" and "stop at the edge of a table"). Receiver operating characteristic (ROC) analysis was used to compare tests. RESULTS: In the tape removal test, all animals of the CPR group showed a clear neurological deficit throughout the observation period with a marked recovery until day 7 (pre-CA: 4s, 1 day: 180 s, 3 days: 165 s, 7 days: 44 s; data are median values). Latencies differed significantly from those of sham-operated animals (1 day: P<0.001, 3 days: P=0.003, 7 days: P=0.006). ROC analysis showed that the tape removal test but not the NDS was appropriate for detecting neurological damage 3 and 7 days after restoration of spontaneous circulation (ROSC). Histological examination confirmed neuronal damage to the hippocampus, cortex, thalamus and striatum. CONCLUSION: In the present study, a clinically relevant sensorimotor deficit after global cerebral ischaemia following cardiac arrest in rats has been quantified for the first time by using a tape removal test. The tape removal test is a sensitive method that can be easily applied to test large numbers of animals in future studies.     

New onset postural tachycardia syndrome following lightning injury

Lightning injuries are one of the top three causes of death from environmental causes. Survivors of lightning injuries may be left with injuries, which may affect either the somatic or autonomic nervous systems. We report on two previously healthy patients who developed severe forms of postural tachycardia syndrome following a lightning injury, and review the literature on the subject.     

自噬在丙泊酚麻醉致老年大鼠术后认知功能障碍中的作用

目的 探讨丙泊酚麻醉对老年大鼠术后认知功能的影响及自噬在其中的作用。方法 将老年大鼠72只,随机分为4组：对照组、丙泊酚组、雷帕霉素组、丙泊酚+雷帕霉素组。雷帕霉素组及丙泊酚+雷帕霉素组于麻醉前5 d ip雷帕霉素10 mg/kg,每天1次,麻醉当日为麻醉前1 h注射,共6 d。丙泊酚组及丙泊酚+雷帕霉素组以20 mg/kg丙泊酚诱导麻醉,并以54 mg/kg/h维持4 h。采用Morris水迷宫评测大鼠学习与记忆功能;Western Blotting技术及免疫荧光观察麻醉后24 h、6 d海马区自噬相关蛋白的表达。结果 与对照组比较,丙泊酚组第1~3天逃避潜伏期显著延长（P<0.05、0.01）,目标象限探索时间明显缩短,穿平台次数明显减少（P<0.05）;麻醉后24 h、6 d海马区自噬相关蛋白LC3B、Beclin-1蛋白表达明显减少,p62蛋白表达明显增多（P<0.05）。与丙泊酚组比较,丙泊酚+雷帕霉素组第1~3天逃避潜伏期缩短,目标象限探索时间显著延长,穿平台次数明显增加（P<0.05）;麻醉后24 h、6 d海马区自噬相关蛋白LC3B、Beclin-1表达明显增多,p62表达明显减少（P<0.05）。结论 丙泊酚连续麻醉4 h可导致老年大鼠空间学习记忆能力损伤,其机制可能与抑制海马区自噬有关。     

艾灸督脉对肾精亏虚型卒中后轻度认知障碍患者认知功能和中医症状的临床疗效研究

背景 卒中后轻度认知障碍（PSMCI）是卒中后患者常见并发症,影响患者全面康复的同时也给其家庭带来了经济和精神方面的压力。 目的 观察艾灸督脉对肾精亏虚型PSMCI患者认知功能及中医症状的临床疗效。 方法 选取2020年7月至2021年7月河南中医药大学第一附属医院康复中心收治的符合纳入标准的PSMCI患者60例为研究对象,采用随机数字表法将其分为艾灸组和对照组,每组30例。对照组患者给予常规基础治疗及常规认知功能康复训练,艾灸组患者在对照组基础上进行艾灸督脉治疗,1次/d,5次/周,持续4周。比较治疗前后两组患者简易智能精神状态量表（MMSE）、蒙特利尔认知评估量表（MoCA）、血管性痴呆中医辨证量表（SDSVD）中肾精亏虚型和脑卒中专用生活质量量表（SS-QOL）评分,并评定两组治疗的临床疗效和安全性。 结果 艾灸组患者治疗前后MMSE、MoCA、SDSVD、SS-QOL评分差值大于对照组（P<0.05）。艾灸组患者治疗后临床疗效优于对照组（P<0.05）。两组患者治疗安全性比较,差异无统计学意义（P>0.05）。 结论 艾灸督脉可以改善PSMCI患者的认知功能和中医症状,临床疗效佳,且安全性较好。     

膈肌保护性通气的概念及进展

急性呼吸窘迫综合征发展至今五十余年,从最初的机械通气治疗到呼吸机相关肺损伤的识别,肺保护通气策略已成临床诊疗共识,但这一策略限制了呼吸机或患者自身呼吸努力对肺部施加的机械压力,脱机困难发生率日趋增加,膈肌功能障碍作用日趋明显,膈肌保护性通气策略应运而出,优化机械通气参数和膈肌负荷,减少人机不同步,可减轻或避免膈肌损伤。但肺保护仍然是机械通气首要考虑的因素,通过最佳方式来降低机械通气的并发症,优化患者呼吸努力,从而达到同时保护肺和膈肌的作用。本文就膈肌保护性通气的概念和进展进行综述。     

非酒精性脂肪性肝病与左心室早期舒张功能不全的相关性研究

背景 非酒精性脂肪性肝病（NAFLD）已成为最常见的慢性肝病,有研究认为NAFLD对心肌结构及功能均有明显影响,但NAFLD是否是心肌结构或功能异常的独立危险因素仍存在争议。 目的 比较NAFLD患者与非NAFLD患者左心室结构及功能指标的异同,初步探究NAFLD与左心室早期舒张功能不全的相关性。 方法 选取2018—2020年北京大学人民医院老年科符合纳入标准的519例住院患者为研究对象,根据腹部超声或CT检查结果分为NAFLD组与非NAFLD组。比较两组患者左心室结构及功能指标差异。以左心室舒张早期左房室瓣血流最大流速与左心房收缩期左房室瓣血流最大流速之比（E/A）<1判定为左心室早期舒张功能不全。采用多因素Logistic回归分析探究NAFLD与左心室早期舒张功能不全的关系。采用FIB-4指数评估NAFLD患者肝纤维化风险,其中FIB-4指数<1.30、1.30~3.25、>3.25分别判定为低风险、中风险、高风险。依据FIB-4指数是否<1.30将NAFLD组患者分为低风险亚组（n=81）和中高风险亚组（n=100）。 结果 519例住院患者中NAFLD患者181例（NAFLD组）、非NAFLD患者338例（非NAFLD组）。与非NAFLD组患者相比,NAFLD组患者E/A较低〔（0.79±0.25）和（0.87±0.34）,t=2.607,P=0.009〕,室间隔舒张末期厚度（IVSd）较厚〔（0.92±0.13）cm和（0.89±0.13）cm,t=-2.525,P=0.012〕。多因素Logistic回归分析结果显示,合并NAFLD是左心室早期舒张功能不全的独立危险因素〔OR=2.941,95%CI（1.736,4.981）,P<0.001〕。中高风险亚组患者E/A低于低风险亚组〔（0.75±0.21）和（0.84±0.28）,t=2.275,P=0.024〕,左心室质量指数（LVMI）高于低风险亚组〔（80.22±14.92）g/m2和（74.72±16.83）g/m2,t=-2.327,P=0.021〕。 结论 合并NAFLD是左心室早期舒张功能不全的独立危险因素,NAFLD患者的肝纤维化风险越高,左心室舒张功能越差。