高压氧治疗对阿尔茨海默病大鼠海马内神经元凋亡及p38丝裂原蛋白激酶表达的影响

目的 评价高压氧治疗对阿尔茨海默病(alzheimer's disease,AD)大鼠海马内神经元凋亡及p38丝裂原蛋白激酶(p38 mitogenactivated protein kinases,p38MAPK)表达的影响. 方法 18只雄性SD大鼠,体重260 g～290 g,采用随机数字表法分为3组(每组6只):生理盐水组(NS组),海马区注射生理盐水;阿尔茨海默病组(AD组),海马区注射Aβ1-40;高压氧组(HBO组),海马区注射Aβ1-40,并于术后1 d～7d行每天1次的高压氧治疗.应用脑立体定位仪于大鼠海马区注射Aβ1-40制备AD模型.于术前1d和术后1、7、14、21 d行水迷宫行为学测试.于术后21 d水迷宫行为学测试结束后处死大鼠,采用苏木精-伊红染色(hematoxylin-eosin,HE)方法染色海马组织病理结构,TUNEL法标记检测凋亡细胞,免疫印迹法(Western bolt)法测定海马内p38MAPK蛋白磷酸化水平. 结果 术后21 d时,与NS组比较,AD组大鼠上台前路程和逃避潜伏期增加[(379±41)、(1 978±120) cm,(16.0±2.8)、(78.4±10.8)s](P＜0.05);与AD组比较,HBO组大鼠上台前路程和逃避潜伏期减少[(1978±120)、(1 246±96) cm,(78.4±10.8)、(51.7±6.2)s](P＜0.05).与NS组比较,AD组和HBO组大鼠海马组织细胞凋亡率[(6.3±13)％,(45.2±5.1)％]及p38MAPK蛋白磷酸化表达升高(0.16±0.06),(0.54±0.10)(P＜0.05);与AD组比较,HBO组海马组织细胞凋亡率[(45.2±5.1)％,(22.5±3.7)％]及p38 MAPK蛋白磷酸化表达下降[(0.54±0.10),(0.31±0.08)](P＜0.05).结论 高压氧治疗可有效缓解AD大鼠认知功能障碍,且能够抑制海马内神经元凋亡,其机制与降低p38MAPK的磷酸化水平有关.     

基于2-back任务下ERP特征的脑力疲劳客观评价研究

利用事件相关电位(ERP)技术研究2-back任务下长时间的工作记忆所诱发的脑力疲劳的脑电特征变化,从而获取脑力疲劳评价的客观指标。32名健康男性受试者,年龄22～28岁,均分为两组:疲劳组和正常组。疲劳组通过连续执行100 min 2-back任务来诱发脑力疲劳,而正常组在前后分别执行10 min的2-back任务,中间80 min休息。采集实验过程中的主观疲劳评分值、行为绩效及脑电信号并进行分析。任务后疲劳组与正常组相比,思维清晰度和注意力明显减弱,困倦程度增加,综合疲劳感上升,且操作2-back的反应时明显延长,正确率下降,即从主观评价和行为绩效相结合的角度验证了所诱发的脑力疲劳模型的有效性。进一步比较疲劳组与正常组的ERP特征参数的变化情况,结果表明:相比正常组,随着脑力疲劳的加深,疲劳组的P300(F=2.539,P <0.05)和错误相关负波(ERN)(F=10.040,P <0.05)的波幅都明显下降,其他参数则未发生明显变化(均有P> 0.05)。因此,P300和ERN被证实可以作为评价长时间工作记忆任务下脑力疲劳模型的潜在指标,为后期研究脑力疲劳对抗措施提供依据。     

Role of class II P fimbriae and cytokine response in the pathogenesis of Escherichia coli kidney infection in diabetic mice

Background

The role of class II P fimbriae (P fimbriae II) in diabetic kidney infections is uncertain, although some genetic and epidemiological studies suggest a lower prevalence of P fimbriae II genes in Escherichia coli strains isolated from diabetic patients with complicated kidney infections.

A retrospective biochemical,molecular, and neurocognitive review of Saudi patients with argininosuccinic aciduria

A retrospective review was compiled of 54 patients with argininosuccinic aciduria who were either identified through the Saudi National Newborn Screening Program or diagnosed clinically from January 2000 to December 2015. The duration of follow-up is from 2 to 19 years. The majority of patients (65%) originated from the central province of Saudi Arabia. The mean patient age at review was 10 years (2–19 years), 92% received an early diagnosis (<28 days of age) and most were symptomatic at the time of the diagnosis (n?=?34). Normal ammonia at diagnosis was reported in 30% of patients, who were detected under the newborn metabolic screen (n?=?5/16). A very high rate of consanguinity was observed in our cohort (98%). Developmental delay was the most detectable long term neurocognitive consequence followed by seizure disorder; 90.7% (n?=?49) and 62.9% (n = 34) respectively. As expected, the severe neonatal form was the major presentation. The most common variant identified in this cohort was the previously reported founder c.1060C > T; p.(Gln354*) nonsense mutation in the ASL gene. In addition, the frequency of hyperammonemia was higher in patients homozygous for c.1060C > T; p.(Gln354*) compared to the other mutations. Interestingly, frequent thrombocytosis with the mean level of 717 × 10⁹/L (range?=?457–1169?×?10⁹/L) was observed in 96% of the patients with no clear explanation.