基于SRK模型的护理人为差错类型分析及管理对策

目的了解护理人为差错的特点及其与不良事件的关系,为减少护理不良事件、保证患者安全提供依据。方法从某三级甲等医院的护士不良事件上报系统收集护理不良事件,根据SRK模型进行人为差错分类。结果共收集护理不良事件806起,其中护理人为差错占74.32%,非人为差错占25.68%;在护理人为差错中,规则型错误所占比例最高(58.43%),其次为技能型疏忽和技能型遗忘(分别为22.37%和11.69%),知识型错误和规则型疏忽占比较少(分别为7.18%和0.33%);不同类型护理人为差错导致的不良事件严重程度比较,差异有统计学意义(P<0.01);知识型错误、规则型错误导致的不良事件严重程度显著高于技能型遗忘和技能型疏忽(均P<0.01)。结论护理人为差错是导致护理不良事件的主要因素,知识型及规则型人为差错引起的护理不良事件后果较严重,需要从组织层面和个人层面防范护理人为差错的发生。     

大鼠脊髓全横断诱导芳香族氨基酸脱酸酶细胞产生5-羟色胺的机制研究

目的:探讨大鼠脊髓损伤(spinal cord injury,SCI)前后芳香族氨基酸脱酸酶(Aromatic L-amino acid decarboxylase,AADC)细胞的分布以及SCI后不同时间段AADC细胞表达5-羟色胺(5-HT)的特点。方法:60只成年雄性Wistar大鼠随机分为正常对照组(12只)、脊髓损伤2d组(24只,其中假手术/Sham组12只)及脊髓损伤60d组(24只,其中假手术/Sham组12只)。使用负压吸引器将大鼠T10-T11脊髓完全离断1~3mm,建立脊髓胸段T10-T11全横断模型。使用BBB评分评价SCI大鼠不同时间点后肢运动功能。各组大鼠在相应时间点灌注取材,并且在灌注前30min腹腔注射外源性5-羟色胺酸(5-HTP)(100mg/kg),免疫荧光法检测脊髓腰段(L段)和骶尾段(S+C段)中AADC和5-HT表达水平。结果:SCI大鼠在术后1~2、3、7、14、28、60d时BBB评分别为0、1.00±0.58、3.30±0.95、6.30±0.10、7.50±0.36、7.87±0.08分。AADC细胞主要在脊髓的背角、中间带、中央管周围等部位表达。正常对照组、脊髓损伤2d组和脊髓损伤60d组AADC表达数量在脊髓L段为:46.75±5.50、49.50±4.87、48.50±6.38个,在脊髓S+C段为1026.50±66.59、1066.75±80.56、1046.25±67.79个,三组结果相比无显著性差异(P0.05)。正常对照组大鼠脊髓L段和S+C段中AADC细胞中未见5-HT的表达,但在SCI2d组和SCI 60d组均观察到AADC细胞表达5-HT,L段两组表达率分别为(44.43±6.03)%和(96.20±1.53)%,S+C段分别为(44.45±5.71)%和(95.14±3.02)%,两组间差异有显著性(P0.05)。结论:AADC细胞在脊髓胸段T10~T11全横断损伤前后脊髓中表达数量和部位相似。SCI后,损伤平面以下脊髓中的AADC细胞功能增加,可利用外源性5-HTP生成5-HT。     

Early and mid-term results of transarticular external fixation in the treatment of supination-external rotation type IV equivalent ankle fractures

Purpose

To investigate the early and mid-term results of open reduction and internal fixation (ORIF) with transarticular external fixation (TEF) but no deltoid ligament repair (DLR) in the treatment of supination-external rotation type IV equivalent (SER IV E) ankle fractures (AO/OTA classification 44-B 3.1) and provide evidence for clinical practice.

A novel heterozygous variant p.(Trp538Arg) of SYNM is identified by whole‐exome sequencing in a Chinese family with dilated cardiomyopathy

Dilated cardiomyopathy (DCM) is a relatively frequent myocardial disease that may lead to heart failure, syncope, and sudden cardiac death. Genetic factors play important roles in the etiology of the disease. To date, at least 50 genes have been identified in patients with DCM, among them, only three mutations have been reported in Synemin (SYNM) gene. In this study, we investigate a Chinese family of three generations with four patients with DCM. Employing whole‐exome sequencing (WES) and bioinformatics strategies, a novel heterozygous missense mutation p.(Trp538Arg) of SYNM was identified and cosegregated with the affected family members. The missense mutation locates in the C‐terminal domain of SYNM and leads to a substitution of tryptophan by arginine and may cause the structure change of synemin protein. In conclusion, we employed WES to detect the mutations of DCM patients and identified a novel likely pathogenic mutation in SYNM gene. Our study not only expands the spectrum of SYNM mutations, it further confirms that mutations in SYMN may underlie nonfamilial DCM, and offers genetic testing information to additional DCM patients.     

Modular-level alterations of single-subject gray matter networks in schizophrenia

Brain Imaging and Behavior - Schizophrenia is often regarded as a psychiatric disorder caused by disrupted connections in the brain. Evidence suggests that the gray matter of schizophrenia patients...     

Impaired white matter microstructure associated with severe depressive symptoms in patients with PD

Brain Imaging and Behavior - Depression is a common occurrence in patients with Parkinson's disease (PD); however, its pathophysiology is still unclear. This study assessed the association...