Autism spectrum disorder (ASD) is a neurodevelopmental condition characterized by impaired social interaction and repetitive behaviors, with increasing evidence implicating immune dysregulation, oxidative stress, and altered transcriptional regulation. This study investigated the pharmacological effects of Rannasangpei (RNSP), a classical Tibetan formulation, and its active constituent crocin-1 in a valproic acid (VPA)-induced mouse model of ASD. Behavioral tests demonstrated that RNSP and crocin-1 markedly reduced VPA-induced repetitive behaviors and improved social interaction. Biochemical analyses revealed that these effects were associated with restoration of redox balance, characterized by increased activities of catalase and superoxide dismutase and decreased levels of malondialdehyde, together with improvement of the GSH/GSSG ratio. Both treatments also attenuated neuroinflammation, as indicated by reduced expression of IL-6, IL-17A, TNF-α, and Lepr, together with recovery of IL-10 in the prefrontal cortex and cerebellum. Transcriptomic profiling further revealed that RNSP and crocin-1 were associated with widespread transcriptional reorganization in the prefrontal cortex (PFC) and cerebellum. In the PFC, these changes involved pathways related to cell-cell adhesion, morphogenesis, and MAPK signaling. In the cerebellum, the dominant enrichment pattern centered on membrane trafficking and cytoskeleton-related processes, with additional enrichment of oxidative stress response pathways. Integration of pathway analysis and representative gene changes indicated region-specific but functionally related alterations in programs linked to intracellular transport, neuronal structure, and synaptic function. Safety evaluation further showed that neither RNSP nor crocin-1 produced obvious systemic toxicity under the present experimental conditions, as indicated by no consistent treatment-related abnormalities in serum biochemical parameters and histological features of major peripheral organs. These findings indicate that RNSP and crocin-1 were associated with changes in oxidative stress, neuroinflammation, and transcriptional regulation across multiple brain regions, supporting their potential therapeutic relevance in ASD.

OBJECTIVE:To delve into the potential association between the dietary sodium-potassium ratio and stroke in the low-sodium diet population. METHODS:Cross-sectional analysis was done utilizing data from the National Health and Nutrition Examination Survey (NHANES) spanning 7 cycles from 2003 to 2016. 7141 samples were selected. Participants were categorized into stroke and non-stroke groups following population characteristics, and the association between dietary sodium-potassium ratio and stroke was analyzed across various categorical variables. Stratification of the dietary sodium-potassium ratio was done using quartiles. Weighted logistic regression models were constructed by adjusting various confounders to examine the sodium-potassium ratio's relationship with stroke. ubgroup analyses stratified by BMI were performed; interaction terms were evaluated with significance threshold p < 0.1. The relation between the sodium-potassium ratio and stroke risk was explored by Restricted Cubic Splines (RCS). RESULTS:Among the 7,141 participants with a dietary sodium intake ≤ 2,300 mg, the dietary sodium-to-potassium ratio was significantly higher in those who had experienced a stroke (ratio = 1.19 (0.51)) compared to those who had not (ratio = 1.11 (0.52)) (p < 0.05). An increased sodium-to-potassium ratio was associated with a higher risk of stroke in the following subgroups: women (Odds Ratio (OR) = 1.31, 95% CI: 1.05-1.62, p = 0.013), individuals with a BMI of 25-30 kg/m² (OR = 2.02, 95% CI: 1.40-2.91, p < 0.001), those with a history of smoking (OR = 1.79, 95% CI: 1.20-2.67, p = 0.004), alcohol consumers (OR = 1.29, 95% CI: 1.00-1.67, p = 0.047), those without coronary heart disease (OR = 1.33, 95% CI: 1.10-1.62, p = 0.003) or diabetes (OR = 1.33, 95% CI: 1.08-1.63, p = 0.006), but with hypertension (OR = 1.28, 95% CI: 1.03-1.59, p = 0.022). Stratified analysis by BMI indicated that the association between the sodium-to-potassium ratio and stroke was strongest and most consistent among overweight individuals (BMI 25-30 kg/m²), with all ORs exceeding 2 and p < 0.001. Additionally, a U-shaped relationship was observed between the dietary sodium-to-potassium ratio and stroke risk. A ratio within the range of 0.46-1.00 was associated with a reduced risk of stroke, with the lowest risk observed at a ratio of 0.76. CONCLUSION:In low-sodium diet population, association between dietary sodium-potassium ratio and stroke risk follows a "U" shaped correlation. However, prospective investigations are warranted to provide additional evidence to support findings.

BackgroundAutism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by impaired social interaction and restricted, repetitive behaviors (RRBs). These symptoms may stem from cognitive flexibility deficits, with dysfunction in the prefrontal cortex (PFC) and related neural circuits proposed as underlying mechanisms.ObjectivesThis study examined whether transcranial direct current stimulation (tDCS) could enhance PFC activity and functional connectivity, thereby improving cognitive flexibility in a valproic acid (VPA)-induced ASD rat model.MethodsPregnant Sprague-Dawley rats were administered VPA (600 mg/kg, E12.5) or saline. VPA-exposed offspring exhibiting curved tails received tDCS and underwent behavioral tests, including the three-chamber social interaction test and cross-maze rule-shifting task, while local field potentials (LFPs) were recorded. Immunohistochemistry was performed to evaluate microglial activation (Iba1 +) and synaptic density (PSD95).ResultsValproic acid -exposed offspring displayed significant social interaction deficits and impaired cognitive flexibility, alongside disrupted functional connectivity in frontal-striato-hippocampal circuits. Neuroinflammatory analysis revealed elevated Iba1+ microglial density (p < 0.05) and increased PSD95 expression (p < 0.05). After tDCS intervention, VPA rats exhibited restored sociability and cognitive performance, normalized functional connectivity, and significantly reduced microglial activation (p < 0.05), though PSD95 levels were unaffected.ConclusionOur results indicate that tDCS ameliorates ASD-like phenotypes in VPA rats, potentially through microglial suppression and PFC network synchronization. These findings support neuromodulation as a promising therapeutic approach for ASD-related cognitive dysfunction.

Objective: To investigate the impact of prenatal and early childhood antimicrobial use on autism spectrum disorders (ASD). Data Sources: We searched PubMed and Embase databases for relevant studies from inception to August 2022. Study Selection and Data Extraction: Peer-reviewed, observational studies were all acceptable. Raw data were extracted into a predefined worksheet and quality analysis was performed using the Newcastle–Ottawa Scale. Data Synthesis: Nineteen studies were identified in the meta-analysis. Prenatal antimicrobial exposure was not associated with ASD ( P = 0.06 > 0.05), whereas early childhood antimicrobial exposure was associated with an increased odds ratio of ASD (OR = 1.17, 95% CI = [1.08-1.27], P value < 0.001). The sibling-matched analysis, with a very limited sample size, suggested that neither prenatal ( P = 0.47 > 0.05) nor early childhood ( P = 0.13 > 0.05) antimicrobial exposure was associated with ASD. Medical professionals may need to take the possible association into consideration when prescribing an antimicrobial in children. Conclusions: Early childhood antimicrobial exposure could increase the incidence of ASD. In future studies, it would be necessary to control for confounding factors, such as genetic factors, parenteral age at birth, or low birthweight, to further validate the association.

脑性瘫痪是由于发育中的胎儿或婴幼儿脑部非进行性损伤所致的一组持续存在的中枢性运动和姿势发育障碍及活动受限症候群,而胆红素脑病是导致脑性瘫痪发生的主要原因之一.本文从脑瘫患儿三级损伤机制的角度出发,对胆红素脑病致脑性瘫痪发病机制各环节及早期诊断等方面进行综述,旨在为胆红素脑病相关性脑性瘫痪的早期防治提供参考.

BACKGROUND:Autism spectrum disorder (ASD) is a group of neurodevelopmental disorders characterized by deficits in social communication and restrictive behaviors. Mouse nerve growth factor (mNGF), a neurotrophic factor, is critical for neuronal growth and survival, and the mNGF treatment is considered a promising therapy for neurodegeneration. In light of this, we aimed to evaluate the effect of mNGF on neurological function in ASD.METHODS:An ASD rat model was established by intraperitoneal injection of valproic acid (VPA). Social behavior, learning, and memory of the rats were measured. TdT-mediated dUTP Nick-end labeling and Nissl assays were performed to detect neuronal apoptosis and survival in the hippocampus and prefrontal cortex. Apoptosis-related proteins and oxidative stress markers were detected.RESULTS:mNGF improved locomotor activity, exploratory behavior, social interaction, and spatial learning and memory in VPA-induced ASD rats. In the hippocampus and prefrontal cortex, mNGF suppressed neuronal apoptosis, increased the number of neurons, superoxide dismutase, and glutathione levels, and decreased reactive oxygen species, nitric oxide, TNF-α, and IL-1β levels compared with the VPA group. In addition, mNGF increased the levels of Bcl-2, p-phosphoinositide-3-kinase (PI3K), and p-serine/threonine kinase (Akt), and decreased the levels of Bax and cleaved caspase-3, while the PI3K inhibitor LY294002 reversed these effects.CONCLUSION:These data suggest that mNGF suppressed neuronal apoptosis and ameliorated the abnormal behaviors in VPA-induced ASD rats, in part, by activating the PI3K/Akt signaling pathway.

Autism spectrum disorder (ASD) is a multifactorial disease, with social difficulties and repetitive behaviors as its core symptoms. With the improvement of diagnostic methods, the detection rate of ASD is increasing year by year.Cognitive flexibility impairment is very obvious in most autistic patients.More and more studies have shown that cognitive flexibility impairment is related to the occurrence and development of core symptoms. However, the mechanism of cognitive flexibility impairment in autism remains unclear. The frontal lobe plays an important role in advanced cognition, and its complete development is related to cognitive function. Recent studies have shown that frontal lobe dysfunction is closely related to cognitive flexibility deficits in autistic patients, and the abnormal changes in the frontal lobe, the associated default mode network dysfunction and frontal striatal circuit defects may be the important mechanisms of cognitive flexibility impairment. Based on the recent clinical and basic studies on cognitive flexibility in autism, this article reviews the mechanisms of frontal lobe and related circuits involved in the impairment of cognitive flexibility in autism.

中医学已经经过了数千年的发展,是我国医疗事业中的瑰宝.随着现代科学技术、互联网大数据以及各种硬件条件的不断突破和发展,中医与各个行业不断交叉融合,中医远程诊疗应运而生.通过文献整理发现,远程诊疗为中医注入了新血液,与中医诊疗技术形成了互补,为中医诊疗技术提供了支持.

Autism spectrum disorder (ASD) is a neurodevelopmental disorder that cannot be cured. The ASD rat model was developed in this study to demonstrate the role and mechanism of ganglioside GM1 (GM1). Rats were given valproic acid (VPA) to create the ASD rat model. The rats’ behaviors were assessed using the Y-maze test, open-field test, three-chamber social interaction test, and Morris water maze test. Relative levels of glutathione (GSH), malondialdehyde (MDA), catalase (CAT), reactive oxygen species (ROS), and superoxide dismutase (SOD) were quantitated using relative kits. Nissl, TUNEL, immunofluorescent, and immunohistochemistry staining techniques were used. GM1 treatment improved the ASD model rats’ behavior disorders, including locomotor activity and exploratory behavior, social interaction, learning and memory capacity, and repetitive behavior. Following GM1 injection, striatal neurons grew and apoptosis decreased. GM1 reduced the excessively elevated α-Syn in ASD by encouraging autophagy. The behavior disorder of ASD model rats was exacerbated by autophagy inhibition, which also increased α-Syn levels. By increasing autophagy, GM1 reduced α-Syn levels and, ultimately, improved behavioral abnormalities in ASD model rats.

Autism is a common neurodevelopmental disorder that severely affects patients' quality of life. We aimed to investigate whether acupuncture at Zusanli (ST36) could alleviate the behavior disorder of autistic rats by inhibiting thioredoxin-interacting protein (TXNIP)-mediated activation of NLRP3. An autism model was induced by intraperitoneal injection of pregnant rats with valproic acid (VPA). The pups' behaviors were analyzed using hot plate, open field, Morris water maze, and 3-chamber social interaction tests. Nissl staining was used to visualize neurons in prefrontal cortex. Levels of TXNIP, NLRP3, interleukin (IL)-1β, and caspase were determined by Western blot or quantitative real-time PCR. After ST36 acupuncture, pain sensitivity, autonomous activity, sociability index, sociability preference index, and learning and memory were improved in the autism model rats. Levels of TXNIP, NLRP3, IL-1β, and caspase 1 were decreased after acupuncture. Interference with TXNIP alleviated the behavior disorders and inhibited NLRP3, caspase 1, and IL-1β levels. In summary, ST36 acupuncture reduced TXNIP expression, inhibited the activation of the NLRP3 inflammasome, and alleviated the behavior disorder related to the prefrontal cortex of the autistic rats. These results point to a potential mechanism for acupuncture-induced improvement of autistic behavioral disorders.

我国面临最重要的社会问题就是人口老龄化,人口老龄化会带来一系列问题,严重限制了我国经济的发展.本文针对我国人口老龄化对经济发展的影响进行深入分析,并提出相应的建议以供参考,以最大程度促进我国经济可持续性稳定发展.

目的:探讨太极拳训练对帕金森病患者运动和平衡功能的影响.方法:对7个中英文数据库进行检索,检索内容包括所有关于探讨太极拳运动对帕金森病患者作用的随机对照试验.检索时间是从建库时间至2022年1月31日.按照Cochrane手册5.1.0标准,由2名研究者独立对每一篇纳入文献进行质量和偏倚风险评估,并提取数据.应用RevMan 5.4.1软件进行Meta分析.结果:共纳入12项随机对照试验,样本量共585例.结果显示,太极拳运动能够降低帕金森病患者的美国帕金森病综合评分量表Ⅲ(The Unified Parkinson's Disease Rating Scale Part Ⅲ,UPDRS Ⅲ)评分[平均差:-3.09(95％置信区间:-4.54～-1.64);P＜0.0001]和计时起立行走测试(Timed Up and Go Test,TUG)评分[平均差:-1.33(95％置信区间:-1.83～-0.84);P＜0.000 01],提高Berg平衡量表评分[平均差:6.73(95％置信区间:6.55～6.90);P＜0.00001],但对6 min步行距离测试(6-minute Walk Test,6-MWT)评分无明显影响[平均差:4.54(95％置信区间:-10.63～19.72),P=0.56].结论:太极拳运动能够提高帕金森病患者的运动和平衡功能,改善生活质量;但是对于步行能力的改善,尚无足够的证据.

Troxerutin is known for its anti-inflammatory and antioxidative effects in nerve impairment. The purpose of this study is to investi-gate the effect of troxerutin and cerebroprotein hydrolysate injections (TCHis) on prenatal valproic acid (VPA)-exposed rats. The VPA was administered to pregnant rats on gestational day 12.5 to induce a model of autism. The offspring were given the treat-ment of TCHis on postnatal day (PND) 21-50. On PND 43-50, the behavioral analysis of offspring was performed after the treat-ment of TCHis for 1 h. On PND 50, the offspring were harvested and the brains were collected. The hippocampus and prefrontal cortex were isolated for relevant biochemical detections. The administration of TCHis increased pain sensitivity and improved abnormal social behaviors in prenatal VPA-exposed rats. Prenatal exposure of VPA induced neuronal loss and apoptosis, enhanced reactive oxygen species (ROS) production, and promoted oxidative stress in hippocampus and prefrontal cortex, whereas these effects were reversed by the postnatal treatment of TCHis. In addition, postnatal administration of TCHis amelio-rated mitochondrial function in hippocampus and prefrontal cortex of prenatal VPA-exposed rats. This study concluded that post-natal treatment of TCHis reduced oxidative stress and ameliorated abnormal behavior in a prenatal VPA-induced rat model of autism.

OBJECTIVE:Emerging evidence suggests that acupuncture plays a neuroprotective role in autism. This study aimed to explore the effect of electroacupuncture at Zusanli (ST36) on autistic-like behaviors and the underlying mechanism. METHOD:Pregnant rats were administered with valproic acid (VPA) on gestational day 12.5 to induce an autism spectrum disorder (ASD) model. The pups were given electroacupuncture at ST36 daily from postnatal day (PND) 28-48. On PND28, the adenoviral vector containing small interfering RNA Nrf2 (Ad-siRNA-Nrf2) was injected into the prefrontal cortex of rats. The behavioral analysis was performed on PND 44-48. On PND48, the animals were euthanized and the brains were collected for further detection. Nissl staining was performed to detect neuronal viability. The biochemical markers of oxidative stress were subsequently measured. RESULT:Electroacupuncture at ST36 ameliorated the locomotor activity, social behavior, spatial learning and memory and repetitive behavior compared with ASD rats. It was notable that the electroacupuncture decreased oxidative stress markers in the tissues of prefrontal cortex, enhanced translocation of nuclear factor erythroid2-related factor2 (Nrf2) from cytoplasm to nucleus, and up-regulated the levels of NADP(H) quinone oxidoreductase (NQO1) and heme oxygenase (HO-1). However, these effects induced by electroacupuncture at ST36 were abolished after injection of Ad-siRNA-Nrf2. CONCLUSION:These data suggested that electroacupuncture at ST36 protected nerve function in ASD rats through Nrf2 activation and the antioxidant response.

经络辨证作为针灸学中最重要的理论基础,但在临床中尚未凸显其重要地位,甚至日益被忽视.通过查阅《素问》《灵枢》等有关篇章,并结合近十年来针灸治疗儿童孤独症的临床观察文献,对比经络辨证与临床应用的选穴发现,经络辨证指导的常用腧穴与临床实际用穴存在较大差异,现代临床应用与经络辨证理论存在脱节的现象.目前,经络辨证并未起到指导现代临床治疗儿童孤独症的作用,古代文献中涉及的诸多腧穴未在儿童孤独症的临床上充分应用.今后,应进一步加强针灸经络辨证治疗儿童孤独症的临床指导作用.

自闭症谱系障碍是一种儿童早期发病的严重神经发育障碍性疾病,临床特征主要表现为社交障碍、刻板行为、兴趣狭窄和感知觉方面的异常.研究发现自闭症儿童会出现技能倒退现象,该文对倒退型自闭症概念、患病率、病因学、临床特点及预后等进行了综述.

目的:研制具有无创、集成、移动便携、可家用特征的孤独症智能治疗头盔.方法:开发了能够集成模拟电针刺激模块、药物离子导入模块、生物反馈模块和网络信息模块功能.结果:头盔安全性高,疗效佳,可实现家庭化、便携化.结论:现代科技与先进通讯技术将传统针刺技术广泛传播,为广大孤独症患儿提供有效、便捷的治疗与帮助,使更多患儿及家庭获益.

目的:分析事件相关电位(ERP)指导下的高频和低频重复经颅磁刺激(rTMS)联合综合康复训练治疗孤独症谱系障碍(ASD)患儿的临床疗效.方法:选取2018年1月至2019年2月在郑州大学第五附属医院住院治疗的ASD儿童60例,随机分为实验组(n=30)和对照组(n=30).两组患儿均接受综合康复治疗,在此基础上,对照组接受常规rTMS治疗,实验组根据ERP指导下的脑功能异常区域进行对应的高频和低频rTMS治疗.采用儿童孤独症评定量表(CARS)、孤独症儿童行为检查量表(ABC)、孤独症治疗评估表(ATEC)比较两组患儿治疗后的疗效.结果:治疗前两组CARS评分、ABC评分及ATEC评分均无显著差异(P>0.05);治疗3个月后,实验组CARS评分(34.63±1.94)显著低于对照组(35.73±1.96,P<0.05),ABC总分(50.10±4.55)显著低于对照组(54.53±5.43,P<0.05),ATEC总分(53.53±4.70)显著低于对照组(59.07±5.95,P<0.05);治疗6个月后,实验组CARS评分(33.87±2.49)显著低于对照组(31.50±2.05,P<0.05),ABC总分(50.00±5.13)显著低于对照组(40.01±4.86,P<0.05),ATEC总分(47.00±5.08)显著低于对照组(54.93±6.70,P<0.05).结论:ERP指导下rTMS治疗方案在ASD治疗上较常规rTMS疗效更显著,可以为ASD患儿的rTMS治疗方案提供一定参考.

目的 实践探索三甲医疗机构在失能失智老人的养老方面的作用与责任.方法 通过社区、养老院、医疗机构及河南相关政策等样本调研法、访谈法、三甲医疗机构医养结合实践、大学教育背景影响,探索失能失智老人解决对策.结果 通过郑大五附院近两年医养结合发展实践,九种方法路径实践医养结合新模式,解决失能失智伴慢性病重症老人系统医康护问题,与养老机构合作推动缓解期的长期照护问题;与社会资本合作补充养老资金短板;开展多层次培训补充人才短板;承担政府项目研究长期保护保险等综合解决方案.结论 失能失智老人健康养老成是重要的民生问题,医康护是刚需,养老机构专业照护人才不足,郑州大学五附院充分利用大学教育背景与9种医康养结合实践经验,拟在解决失能失智老人急性期的救治与康复,也探索通过与养老服务及社会资本密切结合解决稳定期的长期照护与康复问题,是值得借鉴与可复制以及继续发展完善的三甲医疗机构在失能失智老人中发挥引领带动辐射的养老解决模式.