Effect of regular swimming exercise to duration-intensity on neurocognitive function in cerebral infarction rat model

Objective: This study investigated the effect of regular swimming exercise according to the duration-intensity on neurocognitive function in a cerebral infarction rat model.

Methods: Forty male Sprague–Dawley 10-week-old rats, weighing 300 ± 50 g, were subjected to photothrombotic cerebral infarction. The remaining 36 rats were randomly divided into four groups (n = 9 per group: non-exercise (group A); swimming exercise of short duration-intensity (5 min/day, group B); swimming exercise of moderate duration-intensity (10 min/day, group C); and swimming exercise of long duration-intensity (20 min/day, group D). Exercise was performed five times a week for 4 weeks, beginning the day after cerebral infarction. Neurocognitive function was evaluated with the Morris water maze test. Immunohistochemistry and western blot analysis examined brain-derived neurotrophic factor (BDNF) and vascular endothelial growth factor (VEGF) at 4 weeks postinfarction.

Results: At 4 weeks postinfarction, escape latency was found to be shorter in group C than in any of groups A, B, or D. Immunohistochemistry revealed the most significant immunoreactivity for BDNF and VEGF in group C. Western blot analysis demonstrated that BDNF and VEGF proteins were markedly expressed in group C.

Conclusions: Regular swimming exercise of moderate duration-intensity may be the most effective exercise protocol for the recovery of neurocognitive function in cerebral infarction rat model.     

乳腺癌21基因检测的研究进展

乳腺癌是一类具有异质性的肿瘤，不同患者的治疗方法和疗效都不相同。尽管目前仍在努力为激素受体（hormone receptor，HR）阳性（+）、人表皮生长因子受体2（human epidermal growth factor receptor 2,HER-2）阴性（-）、淋巴结（axillary lymph node，ALN）阴性（-）的早期乳腺癌患者寻找合适的治疗方法，但其术后是否需要化疗仍然是肿瘤科医生面临的一个难题。以往治疗主要依赖于经典的组织病理学和免疫组织化学技术，随着精准医疗时代的到来，我们需要更定量的诊断方法和合理的个体化治疗。虽然化疗可降低疾病复发风险并提高生存率，但它带来的不良反应事件会降低患者的生活质量，尤其低复发风险（recurrence risk,RS)有可能超过化疗益处。21基因检测不仅可以预测这类早期乳腺癌化疗疗效及评估预后，还可提供精准的个体化治疗方案指导用药，为患者增添信心。本文就乳腺癌21基因检测的研究进展进行综述。     

维生素E有什么希望？

过去15年来，有关动脉粥样硬化的流行病学、基础生物学和实验研究均支持下述假设：抗氧化剂可通过抑制动脉壁低密度脂蛋白的氧化而抑制动脉粥样硬化的发生。这种作用机制可抑制胆固醇酯通过巨噬细胞清除受体在动脉斑块内发生病理性沉积。胆固醇酯病理沉积是一种可引起斑块破裂及心血管事件的过程。同样，生物机制亦已确定，癌基因可被抗氧化剂阻断。     

白细胞介素-8在哺乳动物生殖过程中的作用

白细胞介素-8(IL-8)作为中性粒细胞趋化因子和促血管生成因子,受到人们的重视。研究表明,IL-8促进卵细胞的发育、成熟,诱发排卵;在输卵管和子宫内膜的表达随月经周期而变化;参与胚泡着床和胚胎发育。本文综述IL-8在哺乳动物生殖过程中的重要作用。     

对乙酰氨基酚引起的急性肝衰竭：一项美国多中心前瞻性研究结果

严重的对乙酰氨基酚肝毒性常常会引起急性肝衰竭（ALF），作者在美国的22所三级护理中心调查了由对乙酰氨基酚引起的肝衰竭的发生率、危险因素和预后，用超过6年的时间收集到662例完全符合ALF（包括肝源性凝血症和肝性脑病）标准的患者资料，详细分析后发现：其中有275例（45％）是由对乙酰氨基酚引起的。调查发现，对乙酰氨基酚相关性ALF的年度百分比由1998年的28％上升至2003年的51％。对乙酰氨基酚的中位摄入量为24g（相当于48个高含量的片剂）。在上述275例中，误服过量者有131例（48％），有意服用者（即有自杀倾向者）有122例（44％），还有22例（8％）为不明意图。在误服组中38％同时服用了两种或多种对乙酰氨基酚制剂，63％患者服用了含有镇静剂的复合制剂。据报道，81％患者因为急性或慢性疼痛误服了对乙酰氨基酚和（或）其他镇痛剂。总体上，有178例研究对象（65％）存活，74例（27％）未经肝移植而死亡，23例（8％）进行了肝移植，其中71％的患者仅存活了3周。未接受移植的存活率和肝移植存活率在误服组和有意服用组差别不明显。     

对我院两年护理夜查房情况的分析

为了控制夜间护理质量,了解夜间护理工作存在的主要问题,对我院2年来护理夜查房的资料进行回顾性分析,以利于制定相应的护理管理措施,达到全面提高护理质量的目的。1对象和方法1.1对象2003年9月—2005年9月内科、针推科、外科、骨伤科、急诊科护理夜查房资料530份。1.2方法回顾分析530份夜查房资料中护士仪表、劳动纪律、环境卫生、陪伴管理、重病人护理、医院感染管理6个方面及不同职称护理人员的检查结果。1.3统计学方法采用t检验及χ2检验。2结果2.1夜查房检查结果(见表1)表1530份夜查房分项检查结果项目存在问题例构成比%护士仪表21.05…     

Plasmid DNA encoding transforming growth factor-beta1 suppresses chronic disease in a streptococcal cell wall-induced arthritis model.

Transforming growth factor beta is a potent immunomodulator with both pro- and antiinflammatory activities. Based on its immunosuppressive actions, exogenous TGF-beta has been shown to inhibit autoimmune and chronic inflammatory diseases. To further explore the potential therapeutic role of TGF-beta, we administered a plasmid DNA encoding human TGF-beta1 intramuscularly to rats with streptococcal cell wall-induced arthritis. A single dose of 300 microg plasmid DNA encoding TGF-beta1, but not vector DNA, administered at the peak of the acute phase profoundly suppressed the subsequent evolution of chronic erosive disease typified by disabling joint swelling and deformity (articular index = 8.17+/-0. 17 vs. 1.25+/-0.76, n = 6, day 26, P < 0.01). Moreover, delivery of the TGF-beta1 DNA even as the chronic phase commenced virtually eliminated subsequent inflammation and arthritis. Both radiologic and histopathologic as well as molecular evidence supported the marked inhibitory effect of TGF-beta1 DNA on synovial pathology, with decreases in the inflammatory cell infiltration, pannus formation, cartilage and bone destruction, and the expression of proinflammatory cytokines that characterize this model. Increases in TGF-beta1 protein were detected in the circulation of TGF-beta1 DNA-treated animals, consistent with the observed therapeutic effects being TGF-beta1 dependent. These observations provide the first evidence that gene transfer of plasmid DNA encoding TGF-beta1 provides a mechanism to deliver this potent cytokine that effectively suppresses ongoing inflammatory pathology in arthritis.