临床路径管理对脑出血患者卒中相关性肺炎的干预作用

目的观察临床路径管理对脑出血患者卒中相关性肺炎(SAP)发生与预后的影响。方法根据本院特点制定脑出血临床路径,收集200例发病在3 d内的脑出血患者,最终入组180例,采用非同期队列研究来比较未实施临床路径组70例(对照组)与实施临床路径组110例(路径组)脑出血患者SAP发生率和改良Rankin评分(mRS)。结果 SAP总体发病率为16.11%,对照组发病率为25.71%,路径组SAP发病率为10.00%;实施临床路径后脑出血患者SAP有明显降低(P0.05),但3个月时评分路径组明显降低(P<0.05)。结论脑出血发病后通过实施临床路径...     

早期吞咽功能量化评估在降低卒中相关性肺炎中的效果

目的探讨早期吞咽功能量化评估在降低卒中相关性肺炎中的应用效果。方法选取郑州大学第一附属2017-01-12收治的1320例急性缺血性卒中患者作为对照组,选取同期入住的1440例急性缺血性脑卒中患者为干预组,对照组采用洼田饮水试验进行吞咽功能筛查,干预组在洼田饮水试验的基础上,采用基于增稠剂量化吞咽功能评估方法,并给予个性化饮食指导。结果干预组痊愈率78.16%,对照组为69.68%,2组比较差异有统计学意义(P<0.05);对照组吞咽障碍患者卒中相关性肺炎发生率7.43%(51/686),干预组为2.65%(21/792),组间比较差异有统计学意义(P<0.05)。结论基于增稠剂吞咽功能量化评估使患者的吞咽功能得到明显提高,脑卒中后相关性肺炎的发生率显著降低。     

卒中相关性肺炎血清炎症因子和外周血淋巴细胞亚群的分析

目的 探讨卒中相关性肺炎（SAP）病人血清炎症因子白细胞介素（IL）-1β、IL-6、IL-4、肿瘤坏死因子-α（TNF-α）的水平变化及其临床意义。方法 选取2016年3月至2017年3月收治的48例SAP,根据A2D2S2L评分分为低危（0~2分,14例）、中危（3~9分,15例）、高危（≥10分,19例）三组。入院后次日清晨取空腹静脉血,应用流式细胞仪测定外周血T淋巴细胞亚群（CD3+、CD4+、CD8+）,应用酶联免疫吸附试验法检测血清炎症因子（IL-1β、IL-6、TNF-α、IL-4）。结果 随着危险程度的增高,血清IL-1β、IL-6、IL-4、TNF-α水平均明显增高（P<0.05）,外周血CD3+和CD4+细胞百分比显著增高（P<0.05）。低危组CD4+/CD8+显著高于高危组和中危组（P<0.05）,而后两组无统计学差异（P>0.05）;三组CD3+/CD8+均无显著差异（P>0.05）。结论 血清炎症因子IL-1β、IL-6、TNF-α、IL-4以及T细胞淋巴亚群变化情况反映SAP病人的A2D2S2L评分,血清IL-1β、IL-4、IL-6、TNF-α与A2D2S2L评分呈正相关,T细胞亚群CD3+、CD4+百分比与A2D2S2L评分呈负相关。     

Effect of statin treatment on three-month outcomes in patients with stroke-associated infection: a prospective cohort study

Background and purpose: Infection is a major medical problem in patients with acute stroke. Recent evidences suggest that statins reduce infection‐associated complications. The purpose of this study was to examine the influence of statin treatment on mortality and functional outcomes in patients with stroke‐associated infection. Methods: In this prospective observational cohort study, 514 patients with acute ischaemic stroke or transient ischaemic attack (mean age, 74 ± 11 years; men, 48%) with infection occurring in the first 7 days after admission were included. We examined the effect of in‐hospital statin treatment on mortality and favorable functional outcome (modified Rankin Scale score ≤2) at 3 months follow‐up. Results: Infection occurred at 0.93 ± 1.49 days after admission. All patients had not received statin treatment prior to admission, and 121 patients (24%) received statin at 1.71 ± 1.28 days after admission. Follow‐up at 3 months was completed for 511 patients (99%). National Institutes of Health Stroke Scale score and Charlson index were the most important independent predictors of mortality and functional outcome. Univariate [hazard ratio (HR), 0.82; 95% confidence intervals (CI), 0.47–1.42] and multivariate (HR, 1.68; 95% CI, 0.79–3.56) Cox regression analysis showed that statin did not significantly decrease the morality. In propensity analysis, statin treatment still had no significant association with mortality (HR, 1.54; 95% CI, 0.68–3.47) in the multivariate analyses after adjusting for age, sex, and propensity score. Conclusions: Statin use was not associated with a better functional outcome or survival in patients with stroke‐associated infection.     

法舒地尔对戊四氮点燃大鼠海马丝切蛋白及苔藓纤维出芽的影响

目的 探讨法舒地尔对戊四氮(PTZ)点燃大鼠海马组织中丝切蛋白(cofilin,非磷酸化形式)表达与苔藓纤维出芽程度关系的影响.方法 210只SD雄性大鼠分成戊四氮组、法舒地尔干预组和生理盐水对照组,采用PTZ慢性点燃癫癎模型,应用SABC法检测cofilin表达,用Timm染色检测苔鲜纤维出芽情况.结果 PTZ组大鼠点燃率、病死率与法舒地尔组比较差异无统计学意义.PTZ组和法舒地尔组CA3区苔藓纤维出芽评分差异无统计学意义,与对照组相比差异均有统计学意义(P＜0.05).PTZ组和法舒地尔组海马非磷酸化cofilin表达差异无统计学意义.结论 丝切蛋白可能通过苔藓纤维出芽与癫癎的发生相关.     

TRPC6在匹罗卡品致痫大鼠海马苔藓纤维出芽中的作用

目的 观察传统型瞬时受体电位通道6(TRPC6)蛋白在匹罗卡品致痫大鼠海马中的表达变化,探讨其在海马苔藓纤维出芽中的作用.方法 72只SD大鼠随机分为实验组(n=60)和对照组(n=12).实验组采用氯化锂-匹罗卡品腹腔注射法建立颞叶癫痫模型;对照组腹腔注射等量无菌生理盐水.实验组按癫痫持续状态(SE)后1d、7d、15d、30 d和60 d分为5个亚组,每亚组12只大鼠.以上各亚组及对照组再分为2个小组,分别进行Western blot检测TRPC6及突触重建标志蛋白Synaptophysin在海马中的表达和Timm染色观察海马苔藓纤维出芽并评分.结果 实验组TRPC6蛋白表达量在SE后1d达高峰(P＜0.01),其他时间点均显著高于对照组(P＜0.01).Synaptophysin蛋白表达量在SE后7d、15d、30 d和60 d显著增加(7 d:P＜0.05;15 d、30 d、60 d:P＜0.01),30 d达峰值(P＜0.01).实验组大鼠齿状回内分子层在SE后7d出现Timm颗粒,并呈进行性增加.结论 TRPC6可能参与了苔藓纤维出芽这一过程.     

Effect of growth hormone-releasing peptide on ardiac cholinergic nerve fiber density distribution in a rat model of heart failure

BACKGROUND: Changes in the cardiac autonomic nerve are considered to be important factors in the mechanisms of heart failure. It is possible to reduce or slow down nerve degeneration and necrosis, provided that patients take effective neuroprotectants during the early stages of heart failure. Moreover, it is possible to relieve the pathological process and reduce the risk of death.OBJECTIVE: To study the effect of growth hormone releasing peptide (GHRP) on cardiac cholinergic nerve fiber density distribution in a rat model of heart failure, and verify whether GHRP can ameliorate denervation.DESIGN, TIME AND SETTING: A randomized controlled study was performed at the Key Laboratory of Anatomy, Harbin Medical University, between June and October 2009.MATERIALS: Fifty adult, healthy, female, Wistar rats, weighing (200±20) g, were randomly divided into GHRP (n=30), model (n=10), and sham operation (n=10) groups. GHRP-2 was made in Shanghai, China (batch No. z071212-03).METHODS: Acute myocardial infarction was established by ligating the left anterior descending coronary artery in the GHRP and model groups. Five weeks later, myocardial function was detected using color ultrasound electrocardiograph. Ejection fraction < 60% was considered to be a successful marker of chronic heart failure models. However, the left anterior descending coronary artery was not ligated in the sham operation group. The GHRP group was injected with 100μg/kg GHRP-2, and the other two groups were injected with the same volume of physiological saline, once per day.MAIN OUTCOME MEASURES: After 4 weeks, pathological changes in cardiac cholinergic nerve fibers were detected under optic microscopy following hematoxylin/eosin staining. In addition, density distribution was measured using a multi-function color pathological image system.RESULTS: In the sham operation group, myocardial cells were regular, uniformly stained, and no inflammatory cells were present. In the model group, myocardial cells were unevenly stained, exhibited nuclear atrophy, degeneration, dissolution, or disappearance. In the GHRP group, myocardial damage was less than in the model group; cardiac muscle fibers exhibited slight degeneration. The myocardium in the sham operation group was serried, spreading the cholinergic innervations along the cardiac fiber. In the model group, there was a decreased number of cholinergic nerve fibers decreased, which also became shorter and smaller, compared with the sham operation group (P<0.01). In the GHRP group, cholinergic positive nerve fibers were significantly increased compared with the model group (P<0.01), but still less than the sham surgery group (P<0.05).CONCLUSION: GHRP delayed denervation and reduced nerve reconstitution following heart failure in rats.     

应用生长激素释放肽心力衰竭大鼠心肌胆碱能神经纤维密度分布的变化

BACKGROUND： Changes in the cardiac autonomic nerve are considered to be important factors in the mechanisms of heart failure. It is possible to reduce or slow down nerve degeneration and necrosis, provided that patients take effective neuroprotectants during the early stages of heart failure. Moreover, it is possible to relieve the pathological process and reduce the risk of death. OBJECTIVE： To study the effect of growth hormone releasing peptide （GHRP） on cardiac cholinergic nerve fiber density distribution in a rat model of heart failure, and verify whether GHRP can ameliorate denervation. DESIGN, TIME AND SETTING： A randomized controlled study was performed at the Key Laboratory of Anatomy, Harbin Medical University, between June and October 2009. MATERIALS： Fifty adult, healthy, female, Wistar rats, weighing （200± 20） g, were randomly divided into GHRP （n = 30）, model （n = 10）, and sham operation （n = 10） groups. GHRP-2 was made in Shanghai, China （batch No. z071212-03）. METHODS： Acute myocardial infarction was established by ligating the left anterior descending coronary artery in the GHRP and model groups. Five weeks later, myocardial function was detected using color ultrasound electrocardiograph a successful marker of chronic heart failure models Ejection fraction 〈 60% was considered to be However, the left anterior descending coronary artery was not ligated in the sham operation group. The GHRP group was injected with 100 μ g/kg GHRP-2, and the other two groups were injected with the same volume of physiological saline, once per day. MAIN OUTCOME MEASURES： After 4 weeks, pathological changes in cardiac cholinergic nerve fibers were detected under optic microscopy following hematoxylin/eosin staining. In addition, density distribution was measured using a multi-function color pathological image system. RESULTS： In the sham operation group, myocardial cells were regular, uniformly stained, and no inflammatory cells were present. In the model group, myocardial cells were unevenly stained, exhibited nuclear atrophy, degeneration, dissolution, or disappearance. In the GHRP group, myocardial damage was less than in the model group; cardiac muscle fibers exhibited slight degeneration. The myocardium in the sham operation group was serried, spreading the cholinergic innervations along the cardiac fiber. In the model group, there was a decreased number of cholinergic nerve fibers decreased, which also became shorter and smaller, compared with the sham operation group （P 〈 0.01）. In the GHRP group, cholinergic positive nerve fibers were significantly increased compared with the model group （P 〈 0.01）, but still less than the sham surgery group （P 〈 0.05）. CONCLUSION： GHRP delayed denervation and reduced nerve reconstitution following heart failure in rats.     

Effect of epileptiform abnormality burden on neurologic outcome and antiepileptic drug management after subarachnoid hemorrhage

Objective

To quantify the burden of epileptiform abnormalities (EAs) including seizures, periodic and rhythmic activity, and sporadic discharges in patients with aneurysmal subarachnoid hemorrhage (aSAH), and assess the effect of EA burden and treatment on outcomes.