目的 探讨 5,10-亚甲基四氢叶酸还原酶(MTHFR)基因rs1801133 位点多态性与脑卒中的相关性.方法共纳入华北理工大学附属医院脑卒中患者 194 例(病例组),再根据脑卒中类型分为缺血性脑卒中(IS)组和出血性脑卒中(ICH)组,无脑卒中相关病史的体检者 221 例为对照组.收集一般资料和多项检验结果,提取空腹外周血中DNA,利用实时荧光 PCR 技术定性定量检测 MTHFR 基因rs1801133 位点多态性.通过χ2 检验评估CC、CT和TT 3 种基因型和C、T等位基因的差异.通过多因素二元Logistic回归分析包括CT、TT两种基因型在内的共 12 种因素与脑卒中的关系.结果 在MTHFR基因rs1801133 位点上相比较:IS组与ICH组基因型和等位基因频数无显著差异(P>0.05);但是病例组及IS、ICH组分别与对照组相比,基因型和等位基因频率差异有统计学意义(P<0.05).在 5 种基因模型(等位基因模型:T vs C;显性模型:CT+ TT vs CC;隐性模型:TT vs CC+CT;共显性杂合子模型:CT vs CC,共显性纯合子模型:TT vs CC)的分析结果中,均提示T等位基因携带者(CT/TT)较CC基因型发生脑卒中的风险增加(OR>1,P<0.05).多因素二元Logistic回归分析表明:TT型、饮酒、高尿酸血症、吸烟、体质量指数、年龄为脑卒中的危险因素(P<0.05).结论 MTHFR基因 rs1801133 位点多态性与脑卒中的发生密切相关,T等位基因携带者发生脑卒中的风险较高,可作为该地区脑卒中发生风险的预测指标.

目的:亚甲基四氢叶酸还原酶基因C677T或A1298C位点多态性是否与出血性脑卒中相关存在争议.文章以此评估亚甲基四氢叶酸还原酶基因C677T或A1298C位点多态性与出血性脑卒中的相关性.方法:检索PubMed、Embase、Web of Science、中国知网、万方数据、维普和中国生物医学服务系统(SinoMed)数据库中的相关文献.由2名人员筛选,提取信息和评价文献质量.建立5种遗传模型:等位基因模型(Tvs.C和Cvs.A)、显性模型[(CT+TT)vs.CC和(AC+CC)vs.AA]、隐性模型[TT vs.(CC+CT)和CC vs.(AA+AC)]、共显性杂合子模型(CT vs.CC和AC vs.AA)及共显性纯合子模型(TT vs.CC和CC vs.AA).利用RevMan 5.4和Stata 14软件,Cochrane'Q检验和I2值评估异质性,合并OR值和95％CI做为效应及指标,亚组分析探索异质性来源,敏感性分析评估结论稳定性,漏斗图、Begg及Egger检验和剪补法评估发表偏倚.结果:纳入24篇高质量观察性研究文献,其中病例对照研究23篇,横断面研究1篇.①亚甲基四氢叶酸还原酶基因C677T位点多态性与出血性脑卒中存在相关性,5 种遗传模型均有显著性意义[Tvs.C:OR=1.39,95％CI:1.18-1.64;(CT+TT)vs.CC:OR=1.46,95％CI:1.18-1.80;TT vs.(CC+CT):OR=1.54,95％CI:1.20-1.96;CT vs.CC:OR=1.31,95％CI:1.08-1.58;TT vs.CC:OR=1.78,95％CI:1.31-2.43].亚组分析提示在亚洲人群中亚甲基四氢叶酸还原酶基因C677T与出血性脑卒中存在相关性,而欧洲和非洲则无,随着年龄的增大,其OR值越大,在控制病例组和对照组混杂因素(年龄和性别)的研究中,合并效应量提示相关性有显著性意义;综合各项假阳性结果报告率,推测假阳性可能性较小.②亚甲基四氢叶酸还原酶基因A1288C位点多态性与出血性脑卒中相关性无显著性意义[Cvs.A:OR=1.16,95％CI:0.98-1.37;(CC+AC)vs.AA:OR=1.19,95％CI:0.96-1.48;CC vs.(AC+AA):OR=1.27,95％CI:0.86-1.88;AC vs.AA:OR=1.04,95％CI:0.71-1.51;CC vs.AA:OR=1.37,95％CI:0.90-2.06];上述位点的亚组分析所得阳性结果,经假阳性结果报告率检验后,结论并不可靠.结论:亚甲基四氢叶酸还原酶基因C677T位点多态性与出血性脑卒中相关,携带突变T等位基因是出血性脑卒中的重要危险因素,尤其是在亚洲人群中,且年龄越大,风险越大.亚甲基四氢叶酸还原酶基因A1298C位点多态性与出血性脑卒中无明显关联.

目的 探讨骨髓间充质干细胞(BMSC)移植对蛛网膜下腔出血(SAH)大鼠早期脑损伤(EBI)的治疗作用及机制.方法 将健康雄性SD大鼠随机分为假手术组、蛛网膜下腔出血(SAH)组、BMSC组、VitE组,每组10只,采用血管内穿刺法构建SAH模型.分离、培养、鉴定BMSC.造模后24 h,将第4代BMSC 3×106个重悬于0.6 mL PBS中,经股静脉注入BMSC组;假手术组、SAH组、VitE组经股静脉注入等量PBS.VitE组给予维生素E(100 mg/kg)灌胃,其他组给予等量橄榄油灌胃.造模后48 h,用改良Garcia评分评估大鼠的神经功能,计算脑组织水含量,用HE染色法观察脑组织病理变化,统计坏死的神经细胞数量,普鲁士蓝染色(铁染色)法检测脑组织铁沉积情况,吸光光度法检测脑组织铁含量、MDA、GSH,Western blotting法检测脑组织NOX2蛋白,ROS探针法检测脑组织ROS.结果 与假手术组比较,SAH组改良Garcia评分低,脑组织含水量高,SAH组神经细胞坏死数量多,脑组织中铁沉积量、铁含量、MDA含量高,GSH含量低,脑组织中NOX2蛋白表达、ROS水平高(P均<0.05);与SAH组比较,BMSC组、VitE组改良Gar-cia评分高,脑组织含水量低,神经细胞坏死数量少,脑组织中铁沉积量、铁含量、MDA含量低,GSH含量高,脑组织中NOX2蛋白表达、ROS水平低(P均<0.05).除改良Garcia评分外,BMSC组、VitE组以上其他指标比较差异有统计学意义(P均<0.05).假手术组神经细胞形态规则,均匀;SAH组神经细胞排列紊乱,细胞核破碎;与SAH组比较,BMSC组神经细胞损伤情况明显改善;VitE组神经细胞损伤修复情况比BMSC组弱.结论 BMSC移植可有效治疗SAH大鼠EBI,其作用机制可能通过NOX2/ROS通路调控铁死亡.

目的 了解临床一线护士心理弹性、心理健康和职业倦怠现状,分析心理弹性在心理健康和职业倦怠间的中介作用.方法 2020年4-7月通过方便抽样法,使用自行设计的问卷、心理弹性问卷、心理健康问卷和职业倦怠量表对华北理工大学附属医院358名临床护士进行问卷调查,并对数据进行分析.结果 护士心理弹性得分为(62.16±15.52)分,心理健康得分为(14.55±3.60)分,职业倦怠总分为(50.32±10.89)分;不同婚育状况、护理执业态度的临床护士职业倦怠得分比较,差异均有统计学意义(均P＜0.05).不同学历、对护理工作的态度、月收入的护士心理健康得分比较,差异均有统计学意义(均P＜0.05).不同性别、工龄、月收入、职称的护士心理弹性得分比较,差异均有统计学意义(均P＜0.05).护士心理健康总分与职业倦怠总分呈负相关(r=-0.530,P＜0.05);心理弹性总分与职业倦怠总分呈负相关(r=-0.556,P＜0.05);心理弹性、心理健康及护士婚姻状况和对护理工作的态度可解释职业倦怠变异的45.3％.结论 华北理工大学附属医院358名临床护士心理弹性水平与一般心理健康是影响职业倦怠状况的重要因子,心理弹性在心理健康与职业倦怠间发挥部分中介作用.

背景:脑老化后神经细胞凋亡增多,其机制不明确.近年研究表明,褪黑素可调节多种凋亡因子的表达,丰富环境作为一种治疗阿尔茨海默病的有效方案已投入临床使用,然而二者合用是否有更好的疗效及其各自的作用机制目前尚不清楚.目的:探讨丰富环境与褪黑素联合干预对SAMP8小鼠学习记忆功能及脑神经细胞凋亡的影响.方法:选用3月龄雄性SAMP8小鼠24只,利用随机数字表法分成4组:对照组、丰富环境组、褪黑素组和联合处理组,每组6只.对照组和褪黑素组小鼠饲养于标准环境,丰富环境组和联合组饲养于丰富环境,直至小鼠满4月龄;满4月龄次日,褪黑素组、联合处理组小鼠开始皮下注射褪黑素8 mg/(kg·d),对照组、丰富环境组皮下注射等量生理盐水,共30 d.给药结束后继续饲养于原环境至11月龄,采用筑巢实验和Morris水迷宫实验评估小鼠学习记忆能力;行为学实验结束后,采用NeuN免疫荧光/TUNEL双标染色及尼氏染色观察海马CA1区细胞凋亡情况,采用Western blot法检测海马中凋亡相关蛋白Caspase-3、Bax、Bcl-2、P53的表达.结果 与结论:①与对照组相比,其他3组小鼠的筑巢实验得分、Morris水迷宫跨平台次数、海马CA1区NeuN免疫反应性、尼氏染色阳性细胞数量、海马中Bcl-2蛋白表达显著增加(P<0.05),联合处理组上述指标值显著多于丰富环境组、褪黑素组(P<0.05);②苏木精-伊红染色显示,与对照组相比,其他3组小鼠海马CA1区神经细胞形态和排列较佳;③与对照组相比,其他3组小鼠的Morris水迷宫逃避潜伏期、海马CA1区免疫荧光/TUNEL双阳性细胞数量及Caspase-3、Bax、P53蛋白表达水平显著降低(P<0.05),联合处理组上述指标值显著低于丰富环境组、褪黑素组(P<0.05);④结果表明,丰富环境和褪黑素对SAMP8小鼠的学习记忆功能、脑神经细胞凋亡具有改善作用,其机制可能与调控小鼠海马神经细胞P53/P21通路来减少细胞凋亡有关;且将丰富环境和褪黑素联合应用的疗效很可能高于单方案治疗.

目的 探讨不同剂量头孢曲松对蛛网膜下腔出血脑水肿及谷氨酸转运蛋白(GLT)-1 蛋白表达的影响和意义.方法 选择 60 只成年雄性SD大鼠建立蛛网下腔出血模型,随机分为假手术(Sham)组、蛛网膜下腔出血(SAH)组、头孢曲松治疗 1(C1)组、头孢曲松治疗 2(C2)组、头孢曲松治疗 3(C3)组.C1、C2、C3 组分别于模型制作后立即按 0.5、1.0、2.0 g/kg于尾静脉注射头孢曲松溶液,均于术后24 h处死各组大鼠,采用干湿重法、免疫组织化学法和 Western印迹分别测定脑含水量及GLT-1蛋白表达量.结果 与Sham 组比较,SAH组脑含水量明显升高,GLT-1 蛋白表达明显降低(P<0.05);与SAH组比较,C1、C2 和C3 组脑含水量明显降低,GLT-1蛋白表达明显升高,且脑组织含水量和GLT-1 蛋白表达呈剂量依赖性(均P<0.05).结论 SAH大鼠脑组织中GLT-1蛋白表达明显降低,不同剂量头孢曲松治疗均可上调 GLT-1蛋白表达水平并减轻脑水肿,呈剂量依赖性,大剂量头孢曲淞治疗SAH效果更佳.

目的 探讨护理专业大学生的灵性健康和学业倦怠水平,分析灵性健康对学业倦怠的影响.方法 采用一般资料调查表、灵性健康问卷和学业倦怠量表于2021年3月对随机整群抽样得到的山西省汾阳市某医学院校护理专业的588名学生进行调查,并对数据进行分析.结果 护理专业大学生学业倦怠检出率为22.62％,学业倦怠总分为(51.42±10.08)分,灵性健康总分为(91.76±12.94)分,灵性健康得分与学业倦怠得分呈负相关(r=-0.320,P＜0.05).分层回归分析显示,灵性健康能独立解释学业倦怠总变异的28％(P＜0.05).结论 护理专业大学生的灵性健康及学业倦怠均有待进一步提高,灵性健康负向预测学业倦怠.护理教育者可以从发展良好的人际关系、明确人生意义、正确认识自我、提高逆商及超越逆境的能力等方面提高学生灵性健康,从而降低学业倦怠.

背景:脑老化可导致学习记忆功能减退,其机制并不明确.近年研究发现,人参皂苷Rg1可提高阿尔茨海默病模型小鼠的学习记忆能力,其机制可能与其改善突触后密度蛋白95的表达相关.目的:探讨人参皂苷Rg1能否通过脑源性神经营养因子/TrkB信号通路改善D-半乳糖诱导衰老小鼠的学习记忆功能与海马区突触后密度蛋白95的表达.方法:取50只雄性昆仑种小鼠,采用随机数字表法分为5组,每组10只:A组不进行任何处理;B组皮下注射D-半乳糖溶液300 mg/(kg·d)建立脑老化模型;C组造模1 h后每天灌胃给予盐酸多奈哌齐;D组造模1 h后每天灌胃给予人参皂苷Rg1;E组造模1 h后每天灌胃给予人参皂苷Rg1,并且腹腔注射选择性TrkB阻断剂ANA-12(每2 d一次).持续给药6周后,进行学习记忆能力(旷场实验、新物体识别实验、Morris水迷宫实验)测试、脑组织形态学观察及小鼠海马区突触后密度蛋白95、脑源性神经营养因子的蛋白表达检测.结果 与结论:①行为学结果显示:B组小鼠学习记忆能力低于A组(P<0.05);C、D组小鼠学习记忆能力高于B组(P<0.05);D组小鼠学习记忆能力低于C组(P<0.05);E组小鼠学习记忆能力低于D组(P<0.05);②苏木精-伊红、Nissl染色显示,与A组相比,B组小鼠海马CA1区正常神经元数量减少,尼氏体表达明显减少;与B组相比,C、D组正常神经元数量增多,尼氏小体颗粒明显增加;与D组相比,E组正常神经元数量减少,尼氏小体颗粒明显减少;③Western blot检测显示,与A组相比,B组脑源性神经营养因子、突触后密度蛋白95的蛋白表达降低(P<0.05);与B组相比,C、D组脑源性神经营养因子、突触后密度蛋白95的蛋白表达升高(P<0.05);D组小鼠海马脑源性神经营养因子、突触后密度蛋白95的蛋白表达低于C组(P<0.05);与D组相比,E组突触后密度蛋白95的蛋白表达降低(P<0.05),脑源性神经营养因子蛋白表达无明显变化(P>0.05);④结果表明,人参皂苷Rg1可改善D-半乳糖诱导的脑老化小鼠神经元损伤与学习记忆能力,并促进海马中突触后密度蛋白95的表达,而脑源性神经营养因/TrkB信号通路可能为其调控机制之一.

MicroRNA (miR)-126 is known to inhibit inflammatory responses in various inflammatory-related diseases, but its role during the cerebral ischemia/reperfusion (I/R) injury remains unknown. The present study aimed to examine the interaction between miR-126 and RAB3A interacting protein (RAB3IP), and explore its potential protective effects during I/R injury. The human neuroblastoma cell line SH-SY5Y was cultured in an oxygen-glucose deprivation/reoxygenation (OGD/R) environment to simulate I/R injury to assess miR-126 expression and cell viability. SH-SY5Y cells cultured in normal conditions were used as a negative control (NC) group. SH-SY5Y cells were transfected with a miR-126 mimic or an NC mimic, then cultured in OGD/R conditions; in rescue experiments, SH-SY5Y cells were co-transfected with RAB3IP overexpression or NC plasmid together with mimic-NC or mimic-miR, and then maintained in an OGD/R environment to evaluate miR-126, RAB3IP expression, cell viability and apoptosis. Cell viability was reduced in the Model group compared with the NC group, suggesting the successful construction of the OGD/R model. miR-126 expression was downregulated in the Model group compared with the NC group. However, following transfection with mimic-miR, cell viability increased compared with the mimic-NC group. Annexin V and PI staining and Hoechst/PI assays also indicated that apoptosis was reduced in the mimic-miR group compared with the mimic-NC group. RAB3IP expression was reduced following mimic-miR transfection. In rescue experiments, miR-126 negatively regulated RAB3IP expression; by contrast, RAB3IP did not affect that of miR-126. In addition, RAB3IP overexpression attenuated the protective effect of miR-126 on OGD/R-induced apoptosis. These findings suggest that miR-126 protects against cerebral I/R injury by targeting RAB3IP.

Objective:To explore the effects and possible mechanisms of melatonin combined with enriched environment on the learning and memory ability of senescence-accelerated mouse prone 8(SAMP8).Methods:Forty-eight SAMP8 male mice aged 4 months were randomly divided into model group, enriched environment group, melatonin group and melatonin combined with enriched environment group (combined intervention group) by random number table method, with 12 mice in each group. Mice in the melatonin group and combined intervention group were subcutaneously injected with melatonin at a dose of 8 mg·kg -1·d -1, and the mice in the model group and the enriched environment group were given the same amount of normal saline instead.The mice in model group and melatonin group were raised in a standard environment, and the mice in enriched environment group and combined intervention group were raised in an enriched environment.The intervention lasted 28 days. The aging degree of mice was scored before and 28 days after the intervention. Morris water maze test was used to detect the learning and memory ability of mice. Nissl staining and TUNEL staining were used to observe the Nissl staining positive cells and apoptotic cells in the CA1 area of hippocampus.ELISA was used to detect the levels of interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in the hippocampus of mice. Western blot was used to detect the levels of amyloid β-protein (Aβ) 1-42, microtubule-associated protein tau (tau) phosphorylated at threonine (Thr) 205 (Tau pT205), Toll-like receptor 4 (TLR4), and nuclear factor-κB (NF-κB) p65 protein in the hippocampus of mice. qRT-PCR was used to detect the levels of TLR4, NF-κB p65 mRNA in the hippocampus of mice. SPSS 22. 0 statistical software was used for repeated measure ANOVA, one-way ANOVA and LSD test. Results:(1) Aging score: after intervention, the aging scores of mice in the four groups were significantly different ( F=120.601, P<0.01). The aging scores of mice in the enriched environment group, melatonin group, and combined intervention group were lower than those in the model group (all P<0.05), while the aging score of mice in the combined intervention group was significantly lower than those in the enriched environment group and melatonin group (both P<0.05). (2) The results of the location navigation experiment showed that the time × group interaction effect of the escape latencies of mice in the four groups were significant ( F=30.524, P<0.001). From the 2nd to 4th day, the escape latencies of mice in the enriched environment group, melatonin group and combined intervention group were all lower than that in the model group (all P<0.05). The results of the space exploration experiment showed that the residence time in the target quadrant and the number of platform crossings of mice in the four groups were significantly different ( F=291.328, 113.482, both P<0.01). The residence time in the target quadrant ((29.45±1.70)s, (32.44±1.55)s, (37.48±0.84) s) and the number of platform crossings ((6.44±0.61) times, (7.16±0.70) times, (12.60±1.23) times) of mice in the enriched environment group, melatonin group and combined intervention group were higher than those in the model group ((15.07±1.28) s, (4.10±0.61) times), while the residence time in the target quadrant and the number of platform crossings of mice in the enriched environment group and the melatonin group were significantly lower than those in the combined intervention group (all P<0.05). (3) Nissl and TUNEL staining showed that the number of Nissl positive neurons in the hippocampal CA1 region of mice in the four groups were significantly different ( F=809.264, P<0.01), and the number of apoptotic cells in the hippocampal CA1 region were also significantly different ( F=1 060.583, P<0.01). The number of Nissl stained positive neurons in the hippocampal CA1 region of mice in the combined intervention group was more than those in the model group, enriched environment group, and melatonin group (all P<0.05), and the number of apoptotic cells were less than those in the model group, enriched environment group, and melatonin group (all P<0.05). (4) The results of ELISA assay showed that there were significantly different in the levels of IL-1β, IL-6 and TNF-α in the hippocampus of mice in the four groups ( F=152.887, 63.506, 432.026, all P<0.01). The contents of IL-1β, IL-6 and TNF-α in the hippocampus of mice in the enriched environment group, melatonin group, and combined intervention group were lower than those in the model group(all P<0.05). Among them, the contents of IL-1β, IL-6 and TNF-α in the hippocampus of mice in the enriched environment group and melatonin group were significantly higher than those in the combined intervention group (all P<0.05). (5) Western blot analysis showed that there were significantly different in the protein expression levels of Aβ1~42, tau pT205, TLR4, NF-κB p65 in the hippocampus of mice in the four groups ( F=122.349, 98.934, 201.635, 116.553, all P<0.01). The protein expression levels of Aβ1-42, tau pT205, TLR4, and NF-κB p65 in the hippocampus of mice in the enriched environment group, melatonin group, and combined intervention group were lower than those in the model group.Among them, the protein expression levels of Aβ1-42, tau pT205, TLR4, NF-κB p65 in the hippocampus of mice in the enriched environment group and melatonin group were significantly higher than those in the combined intervention group (all P<0.05). (6) qRT-PCR showed that the mRNA expression levels of TLR4 and NF-κB p65 in the hippocampus of mice in the four groups were significantly different ( F=42.913, 102.446, both P<0.01). The mRNA expression levels of TLR4 ((0.63±0.05), (0.55±0.04), (0.42±0.03)) and NF-κB p65 ((0.98±0.06), (0.82±0.04), (0.72±0.04)) in the hippocampus of mice in the enriched environment group, melatonin group and combined intervention group were lower than those in the model group ((0.74±0.07), (1.20±0.05)) (all P<0.05). Among them, the mRNA expression levels of TLR4 and NF-κB p65 in the hippocampus of mice in the enriched environment group and melatonin group were significantly higher than those in the combined intervention group (all P<0.05). Conclusion:Melatonin combined with enriched environment can improve the learning and memory ability and neuroinflammatory response of SAMP8 mice, and its mechanism may be related with the down-regulation of TLR4/NF-κB p65 signaling pathway.

临床本科生导师制的构建研究是华北理工大学贯彻国务院办公厅关于加快医学教育创新发展指导意见,全面实施卓越医生教育培养计划2.0的一次有效尝试.本研究是针对目前国内高校本科生导师制存在问题进行分析,通过创新组织形式、优化制度环境、引入专业知识教育与思想政治教育协同育人的理念、重塑师生间的"导学"关系、打造"四有"好导师队伍等方面对临床本科生导师制进行了构建,旨在培养符合新时代要求的卓越医生.

目的 观察盐酸纳美芬联合依达拉奉对原发性脑千损伤患者神经功能重建、氧化应激及炎症因子的影响.方法 回顾性分析2018年2月-2021年1月来华北理工大学附属医院就诊的原发性脑干损伤患者的病例资料,将入选的60例患者按照治疗方法分成二组:对照组(n=30,给予常规综合治疗,包括吸氧、抗休克及抗感染、纠正水及电解质平衡等);观察组(n=30,在对照组的基础上加用盐酸纳美芬联合依达拉奉静脉滴注治疗);二组治疗时间均为两周.分析二组患者人口学特征、神经功能重建相关指标(BDNF、NGF、1GF-1),氧化应激相关指标(SOD、TAOC,MDA),炎症因子(TNF-α、hs-CRP、IL-8)水平.结果 二组患者在性别、年龄、GCS评分及致伤原因等基线资料差异无统计学意义(P＞0.05).治疗后二组血清及观察组脑脊液BDNF、NGF、IGF-1水平均增加且观察组血清BDNF、NGF、IGF-1水平显著高于对照组(P＜0.05);治疗后二组血清及观察组脑脊液TAOC、SOD水平均显著上升,MDA水平均显著下降且观察组血清SOD水平显著高于对照组,而MDA水平显著低于对照组(P＜0.05);治疗后二组血清及观察组脑脊液hs-CRP、TNF-α、IL-8水平与治疗前相比均显著下降,且观察组血清hs-CRP、TNF-α、IL-8水平显著低于对照组(P＜0.05).结论 盐酸纳美芬联合依达拉奉可以抑制原发性脑千损伤患者炎症反应以及调节氧化应激反应,促进患者神经功能重建.

目的 研究新型冠状病毒肺炎(COVID-19)疫情期间临床护士心理弹性状况,分析其影响因素.方法 采用方便抽样的方法,于2020年4月21～27日抽取某三甲医院临床护士358名,使用自行设计的一般情况调查问卷和心理弹性问卷分别调查研究对象的一般资料和心理弹性状况.结果 CO-VID-19疫情期间临床护士心理弹性评分为(62.16±15.517)分.多因素分析显示,家人是否支持参与抗疫一线工作、是否轮转过疫情高风险科室、认为从事护理工作心理压力太大是影响护士心理弹性水平的相关因素(P<0.05).结论 疫情期间护士的心理弹性水平较低,护理管理者应针对相关影响因素采取改进措施,以改善其心理弹性状况.

目的 研究新冠肺炎疫情期护士职业倦怠状况及相关影响因素.方法 于2020年4月,使用自行设计的问卷和职业倦怠量表调查护士的一般资料及职业倦怠状况.结果 护士职业倦怠量表均分为50.32分,有34.92％的护士经历此次疫情后不愿意从事临床护理工作.影响护士职业倦怠的因素包括认为从事护理工作有生命危险、从事护理工作心理压力太大、从事护理工作更受人尊重及从事护理工作能实现自我价值.结论 疫情期护士存有一定的职业倦怠,护理管理者应采取相应措施予以缓解.

目的:探讨头孢曲松(CEF)对蛛网膜下腔出血(SAH)大鼠的神经保护作用,并阐明其可能的作用机制.方法:将48只清洁级雄性SD大鼠随机分为假手术组、SAH组和CEF组,每组16只.采用改良后的血管内穿刺法制备SAH大鼠模型,CEF组大鼠术前5 d开始腹腔注射给药,药物剂量为200 mg·kg-1.模型建立24 h后,对各组大鼠进行神经功能评分,HE染色法观察各组大鼠脑组织神经细胞形态表现并计算其神经细胞坏死数,免疫组织化学染色检测各组大鼠脑组织中星形胶质细胞的活化数,ELISA法检测各组大鼠脑组织中白细胞介素1β(IL-1β)、白细胞介素33(IL-33)、白细胞介素6(IL-6)和肿瘤坏死因子α(TNF-α)水平.结果:与假手术组比较,SAH组大鼠组神经功能评分明显降低(P<0.05);与SAH组比较,CEF组大鼠神经功能评分明显升高(P<0.05).HE染色,假手术组大鼠神经细胞分布排列有序、形态规整,细胞匀称,细胞核居中,染色清楚;SAH组大鼠的神经细胞排列杂乱,形态不规则,呈锥状,胞核收缩、破裂和溶解;CEF组大鼠脑组织神经细胞结构较完整,胞核固缩减轻.与假手术组比较,SAH组大鼠神经细胞坏死数明显增加(P<0.05);与SAH组比较,CEF组大鼠神经细胞坏死数明显减少(P<0.05).免疫组织化学染色,活化的星形胶质细胞形态多呈"分支状",细胞体较小,以细胞质染色为主,突起增粗延长且长短不一.与假手术组比较,SAH组大鼠星形胶质细胞活化数明显增多(P<0.05);与SAH组比较,CEF组大鼠星形胶质细胞活化数明显减少(P<0.05).ELISA法检测,与假手术组比较,SAH组大鼠脑组织中IL-1β、IL-33、IL-6和TNF-α水平明显升高(P<0.05);与SAH组比较,CEF组大鼠脑组织中IL-1β、IL-33、IL-6和TNF-α水平明显降低(P<0.05).结论:CEF能够减轻SAH大鼠脑组织神经细胞的坏死,提高大鼠神经功能评分,具有神经保护作用,其机制可能与抑制星形胶质细胞活化和减轻炎症反应有关.

目的 探讨头孢曲松(CEF)对于大鼠蛛网膜下腔出血后血脑屏障通透性及神经细胞凋亡的影响及其机制.方法 取成年雄性SD大鼠48只,采用血管内动脉穿刺法制作SAH模型,随机分为SAH模型组(SAH组)、头孢曲松低剂量组(50 mg/kg体质量)和头孢曲松高剂量组(200 mg/kg体质量).假手术组(Sham组)只穿刺,不刺破血管.给药72 h后,用Garcia量表对各组大鼠进行神经功能评分;取病灶侧脑组织,用干湿重法测量脑组织水含量;TUNEL荧光染色法观察各组大鼠神经细胞凋亡情况;Western Blot检测MMP-9和Caspase-3蛋白的表达情况.结果 与假手术组比较,SAH模型组Garcia评分降低,凋亡细胞数以及MMP-9和Caspase-3蛋白表达量升高,脑组织含水量升高,差异有统计学意义(P<0.05);与SAH模型组比较,头孢曲松低、高剂量组神经功能评分升高,凋亡细胞数以及MMP-9和Caspase-3蛋白表达量降低,脑组织含水量降低,差异有统计学意义(P<0.05);与头孢曲松低剂量组比较,头孢曲松高剂量组神经功能评分升高,凋亡细胞数以及MMP-9和Caspase-3蛋白表达量降低,脑组织含水量降低,差异有统计学意义(P<0.05).结论 头孢曲松可通过下调SAH后MMP-9的表达,改善血脑屏障的功能,从而起到减轻脑水肿,减少神经细胞凋亡,改善神经功能的作用.

目的 了解供血医院洗涤红细胞产品临床用量及其血型分布特点,为洗涤红细胞产品的合理制备、储存,为更好地做好服务保障提供支持.方法 调查分析2015.8-2017.7间,使用ACP215全自动红细胞处理仪制备洗涤红细胞产品以来的临床供应量,统计分析洗涤红细胞产品临床供血特点.结果 洗涤红细胞产品临床供应量第二阶段较第一阶段有较大增长,增长率为16.22％,两阶段洗涤红细胞产品血型构成比即A∶B∶O∶AB为24∶32∶36∶8.洗涤红细胞产品AB型发放量最少.O型发放量最多,日均发放量O型＞B型＞A型＞AB型呈依次递减态势.结论 洗涤红细胞产品临床应用总体保持增长态势,并与当地供血状况驱于平衡,及时掌握临床用血动态的变化,有助于做好保障工作,确保洗涤红细胞产品的临床最大化综合性效用.

目的 探讨缺血后处理对脑缺血再灌注大鼠海马区神经元自噬表达的影响.方法 采用改良的Pulsinelli四血管闭塞(4-VO)法制作脑缺血再灌注模型,雄性SD大鼠72只随机平均分为3组:假手术组(Sham组)、脑缺血再灌注模型组(CIR组)、脑缺血后处理组(CIP组),每组又分为6 h、24 h、48 h、72 h 4个时间点,通过苏木素-伊红(HE)染色检测海马区各时间点神经元形态及存活数量变化;应用免疫组织化学染色法测定自噬相关基因Beclin-1、LC3-Ⅱ的表达情况;Western印迹检测海马区自噬相关基因Beclin-1、LC3-Ⅱ的蛋白含量.结果 与Sham组比较,其他两组大鼠海马神经元结构破坏,各时间点存活神经元数量显著下降(P<0.05),LC3-Ⅱ、Beclin-1表达显著增加(P<0.05);与CIR组比较,CIP组神经元结构损伤减轻,各时间点存活神经元数量明显增多(P<0.05),LC3-Ⅱ、Beclin-1的表达明显增加,其中24 h表达最高,差异有统计学意义(P<0.05).结论 脑缺血后处理通过促进自噬相关基因表达上升,减轻脑缺血再灌注损伤.

近年来,越来越多的国内医学高校将增强科研和创新思维能力纳入医学本科生的培养过程.与一般的教学方法相比,拔尖创新人才的培养更强调"特殊性",兼具"符合一般"和"针对特殊"两层含义,既符合一般医学人才培养的规律,又适合精英人才的自身特点.根据国家"卓越医生教育培养计划"的建设内容,重点从更新教育理念、创新教育方法、加强人文素质教育、鼓励学生科研创新等方面构建拔尖创新型医学人才培养模式.

Background Acute ischemic stroke causes long-term neurological and neurobehavioral dysfunctions. With the development of clinical medicine, the importance of pre-ischemic exercise intervention has been gradually recognized, but its mechanism remains to be further explored. Objective This study investigates the effects of different exercise intensity preconditioning in changes of hippocampal neurons and the expression of Gadd45β and DNA-PKcs in the hippocampal region after cerebral ischemia-reperfusion in rats. Method 160 SD rats were divided into control group (n=40), cerebral ischemia reperfusion group (I/R group, n=40), middle intensity exercise preconditioning group (EI 1+I/R group, n=40), high intense exercise preconditioning group (EI 2+I/R group, n=40). Stroke was induced by improved Pulsinelli four blood vessel blocking after exercise preconditioning. Morphological changes of neurons in the hippocampal region of rats were observed by HE staining at 6 h, 1d, 3d and 7d after ischemia in each group. Immunohistochemistry method was used to detect the expression of Gadd45β and DNA-PKcs in hippocampus CA1. The mRNA level of Gadd45β and DNA-PKcs in hippocampal CA1 was detected by Real Time PCR. Results Compared with I/R group, the neuronal cell necrosis of was alleviated in EI 1+I/R group, but more serious in EI 2+I/R group; The expression of Gadd45β and DNA-PKcs were significantly higher in the EI 1+ I/R group, but lower in EI 2+I/R group (P<0.01). Conclusion Moderate intensity exercise preconditioning can improve the survival of neurons after cerebral ischemia-reperfusion injury in rats. However, high-intensity motor preconditioning increased the damage and loss of neurons, and its mechanism may be related to the regulation of the expression of Gadd45β and DNA-PKcs in the hippocampus of cerebral ischemia-reperfusion rats, thus protecting and promoting the function of DNA repair system.