p38MAPK在体外培养星形胶质细胞缺氧/复氧损伤中的表达

目的 建立SD大鼠星形胶质细胞缺氧复氧损伤模型,探讨p38MAPK活性变化与星形胶质细胞损伤的关系.方法 体外培养新生SD大鼠星形胶质细胞,实验设正常对照组（N）、SB203580组（SB组,10 μmol/L）、缺氧/复氧组（H/R组）和缺氧/复氧组＋SB203580阻断p38MAPK组（H/R＋SB组）.应用MTT法、WB法、ELISA法检测缺氧4 h、8 h、复氧6 h、12 h、24 h、48 h时细胞存活率,p38MAPK、p-p38（磷酸化p38MAPK）及TNF-α的变化.结果 培养星形胶质细胞GFAP阳性表达率大于97%.缺氧/复氧使星形胶质细胞活力降低,SB203580阻断p38MAPK细胞活力高于H/R组,各组星形胶质细胞总p38MAPK水平无显著变化,缺氧复氧干预后p-p38表达上调,TNF-α水平显著增高.用SB203580阻断p38MAPK通路后,SB＋H/R组较H/R组p-p38、TNF-α水平降低.SB组总p38MAPK、p-p38、TNF-α水平与N组比较无显著变化.结论 p38MAPK信号通路参与了星形胶质细胞缺氧复氧损伤过程.     

帕金森病伴发认知功能障碍的相关因素分析

目的 探讨认知功能障碍在帕金森病中（Parkinson＇s disease,PD）的发生率及其影响因素.方法 对确诊的PD患者采用蒙特利尔认知评价量表（Montreal Cognitive Assessment MOCA中文版）、汉密尔顿抑郁量表（Hamilt depression scale,HAMD）及Webster功能评分量表进行评定分析PD伴发认知功能障碍的发生情况和相关影响因素.结果 PD伴发认知功能障碍者50例,认知功能障碍的发生率为76.9%,病程、文化程度、Webster评分、HAMD评分与帕金森病伴发认知功能障碍的发生均有统计学意义（P＜0.05）,年龄、性别、婚姻状况、经济情况与帕金森伴发认知功能障碍的发生均无统计学意义（P＞0.05）.回归分析发现病程和PD病情严重程度是PD患者伴发认知功能障碍的危险因素.结论 PD患者有较高认知功能障碍的发生率,PD伴发认知功能障碍的发生可能与PD患者的病程、文化程度、PD患者病情的严重程度及抑郁有关.     

宫颈癌患者心理弹性及家庭关怀度在社会支持与家庭韧性间的中介作用

目的 探讨宫颈癌患者家庭韧性与社会支持、家庭关怀度及心理弹性之间的关系,并分析心理弹性、家庭关怀度在社会支持与家庭韧性之间的中介作用。方法 2022年9月至2023年6月,采用便利抽样法选取江苏省2所三级甲等医院的宫颈癌患者为研究对象,采用一般资料调查表、家庭韧性问卷、心理弹性量表、家庭关怀度量表、社会支持量表对其进行问卷调查,各变量之间进行相关性分析,并通过结构方程模型分析中介效应。结果 Pearson相关性分析显示宫颈癌患者社会支持、家庭关怀度以及心理弹性均与家庭韧性呈显著正相关（P＜0.05）。结构方程模型显示：家庭关怀度对宫颈癌患者家庭韧性的直接效应不显著（P＞0.05）;社会支持对家庭韧性发挥直接效应（效应值为0.370）,并通过家庭关怀、心理弹性发挥间接效应（效应值为0.391）。结论 宫颈癌患者的社会支持越高,家庭韧性水平越高;家庭关怀度和心理弹性在社会支持与家庭韧性之间起链式中介作用。     

Failure to Compensate: Patients With Nerve Injury Use Their Injured Dominant Hand,Even When Their Nondominant Is More Dexterous

ObjectiveTo identify how individuals respond to unilateral upper extremity peripheral nerve injury via compensation (increased use of the nondominant hand). We hypothesized that injury to the dominant hand would have a greater effect on hand use (left vs right choices). We also hypothesized that compensation would not depend on current (postinjury) nondominant hand performance because many patients undergo rehabilitation that is not designed to alter hand use.DesignObservational survey, single-arm.SettingsAcademic research institution and referral center.ParticipantsA total of 48 adults (N=48) with unilateral upper extremity peripheral nerve injury. Another 14 declined participation. Referred sample, including all eligible patients from 16 months at 1 nerve injury clinic and 1 hand therapy clinic.InterventionsNot applicable.Main Outcome MeasuresHand use (% of actions with each hand) via Block Building Task. Dexterity via Jebsen-Taylor Hand Function.ResultsParticipants preferred their dominant hand regardless of whether it was injured: hand usage (dominant/nondominant) did not differ from typical adults, regardless of injured side (P>.07), even though most participants (77%) were more dexterous with their uninjured nondominant hand (mean asymmetry index, ?0.16±0.25). The Block Building Task was sensitive to hand dominance (P=2 × 10^?4) and moderately correlated with Motor Activity Log amount scores (r²=0.33, P<.0001). Compensation was associated only with dominant hand dexterity (P=3.9 × 10^?3), not on nondominant hand dexterity, rehabilitation, or other patient and/or injury factors (P>.1).ConclusionsPatients with peripheral nerve injury with dominant hand injury do not compensate with their unaffected nondominant hand, even if it is more dexterous. For the subset of patients unlikely to recover function with the injured hand, they could benefit from rehabilitation that encourages compensation with the nondominant hand.     

Isoflurane preconditioning ameliorates electromagnetic pulse-induced neural damage by shifting microglia polarization toward anti-inflammatory phenotype via upregulation of SOCS1

With the speedy technological advances during the past few decades, human exposure to the electromagnetic field (EMF) has become increasingly common. Exposure to EMF may induce neural injuries and dysfunction of various organs, likely involving neuroinflammation and activation of microglial cells. Isoflurane preconditioning (IP) is shown to provide neuroprotection in various neurological diseases by inhibiting excessive neuroinflammatory responses. Brain samples harvested from rats exposed to electromagnetic pulse (EMP) with or without IP were subjected to qPCR, Western blot assay, and immunohistochemistry to determine the expression of pro-inflammatory/anti-inflammatory microglia markers and a variety of pro- and anti-inflammatory mediators. Suppressor of cytokine signaling 1 (SOCS1) siRNA was used in cultured N9 microglia cells to examine the roles of SOCS1 in the effect of IP. In both in vivo and in vitro experiments, EMP-exposed microglia were predominantly pro-inflammatory microglia, accompanied by increased expression of pro-inflammatory cytokines and chemokines, and activation of TLR4 pathway, leading to neuronal death. IP reversed the changes induced by EMP and switched the activated microglia to an anti-inflammatory phenotype. SOCS1 siRNA abolished the beneficial effects of IP. IP ameliorates EMP-induced neural injuries by shifting microglia polarization from pro-inflammatory to anti-inflammatory phenotype via upregulation of SOCS1.