女性护理专业学生心理健康相关因素分析

目的:分析护理专业学生心理健康的影响因素。方法:于2005-12-01/15按整群抽样法抽取西安市高校在读的护理专业学生515名作为被调查对象。症状自评量表总分≥187为高分组,总分≤116为低分组。高分组与低分组配比的条件是均为女性,年龄相差不超过3岁。采用症状自评量表、简易应对方式问卷、自尊量表、护理专业学生相关状况调查表进行问卷调查。对调查变量进行单因素和多因素Logistic回归分析。结果:共发放问卷515份,其中2名学生生病未填写调查表,应答率为99.6%。调查中有效问卷共507份,有效率为98.8%。症状自评量表总分高分组与低分组学生各100名。①护理专业学生心理健康相关个人因素(计量变量)单因素分析结果:高分组积极应对、自尊水平得分明显低于低分组(20.47±5.02,22.15±6.02;25.91±3.60,30.96±3.25),差异有显著性意义(P<0.05,P<0.01)。高分组消极应对得分明显高于低分组(12.57±4.08,8.00±4.12),差异有显著性意义(P<0.01)。②护理专业学生心理健康相关个人因素(二分类变量)单因素分析结果表明,高分组与低分组比较差异有显著性的因素有独生子女、远离家人、孤独、学习压力大、担心拿不到学位、自我实现需要的满足、经常被人误会、受人歧视、失恋、有知心朋友、无处倾诉苦恼、睡眠型态紊乱、近1年来本人健康改变、适应新环境、经常参加体育活动、担心毕业分配、现有最担心的事情。③多因素分析显示,学习压力大(OR=10.017)、近1年来本人健康改变(OR=4.384)为护理专业学生心理健康状况不良的独立危险因素,而自我实现需要的满足(OR=0.037)、高水平自尊(OR=0.357)是保护因素。结论:护理专业学生心理健康状况与教育、成长、社会环境等多方面因素相关,其心理健康干预需考虑学生的个人因素有针对性地进行。     

股内侧肌和腓肠肌疲劳后反应时的变化及郑氏按摩手法的干预效应

目的:观察股内侧肌和腓肠肌疲劳后反应时的变化及应用郑怀贤教授创立的郑氏按摩手法对这种变化的影响。方法:于2005-05/06选择成都体育学院运动医学系健康男性大学生30人,随机抽签法分为3组:单纯训练组,按摩组,理疗组,每组10人。下肢大强度运动方式:①功率自行车蹬车20min,阻力3档,速度20km/h。②优势腿单脚跳楼梯22级×5组。组间休息1min。③优势腿在CYBEX等动练习器上做膝关节屈伸练习2组,60次/组,角速度为180(°)/s,两组间休息10min。每种运动方式后休息5min。运动结束后,立即进行恢复性治疗。按摩组以郑氏按摩手法重点放松股四头肌、腘绳肌和小腿三头肌15min。理疗组采用自制活血化瘀中药液(红花、川芎、木香、血竭等14种中药组成)和CLJL-3多功能经络治疗仪作中药离子导入,电极安放位置为血海-梁丘,阴-阳陵泉,悬钟-太冲共3对,时间20min。单纯训练组不做特殊处理,自然休息恢复。于运动前、运动后即刻和恢复4h采用肌电图仪分别记录受试者股内侧肌和腓肠肌的肌肉反应时,包括脊髓反射、中间反射和自主肌肉活动肌肉反应时。结果:各组大学生均完成训练和各时段指标测试,全部进入结果分析。①单纯训练组运动后即刻股内侧肌和腓肠肌的脊髓反射时、中间反射时、自主肌肉活动时均比运动前显著延长,差异有显著性意义(P<0.01)Z恢复4h后股内侧肌中间反射时和腓肠肌脊髓反射时仍比运动前显著延长,差异有显著性意义(P<0.01)。②理疗组运动后即刻股内侧肌和腓肠肌的脊髓反射时、中间反射时、自主肌肉活动时均比运动前显著延长,差异有显著性意义(P<0.01)Z恢复4h后股内侧肌脊髓反射时和腓肠肌中间反射时仍比运动前显著延长,差异有显著性意义(P<0.01)。③按摩组运动后即刻股内侧肌和腓肠肌的脊髓反射时、中间反射时、自主肌肉活动时均比运动前显著延长,差异有显著性意义(P<0.01)Z恢复4h后股内侧肌和腓肠肌的脊髓反射时、中间反射时、自主肌肉活动时均与运动前接近,恢复正常,差异无显著性意义(P>0.05)。结论:运动后即刻股内侧肌和腓肠肌的反应时显著性延长,是疲劳后膝关节受伤增加的主要原因之一。郑氏按摩手法可促进股内侧肌和腓肠肌反应时的恢复。     

细胞移植治疗帕金森病诱发运动并发症的研究与进展

细胞移植曾被认为是帕金森病治疗领域最具前途的手段，但是相关并发症的报道却打消了人们最初的热情。移植物导致的并发症是在部分接受细胞移植手术的帕金森病患者中发生的严重而持续的运动障碍，这种运动障碍主要表现为不自主或舞蹈样动作或肌张力的异常。关于移植物诱发异动症的诱因主要有以下几个假说：多巴胺浓度过高、移植物形成的斑片状投射、移植物与宿主的异常投射等。目前，上述假说大部分来源于临床试验，需要控制严格的动物实验进—步验证。由于对帕金森病状态下的运动障碍了解尚不十分透彻，所以还不能确定哪一种假说是诱发移植物诱发的异动症的确切因素。     

127例高龄多病因心力衰竭病人的早期护理

心力衰竭(心衰)是心脏病发展到终末阶段的综合征.随着人口老化进程的加快,心力衰竭患病率正在逐渐增高.据统计,我国≥80岁人群的患病率高达6%～10%,个别地方病死率高达40%[1].临床上高龄心衰病人常是多种病因共存,使病情复杂、预后差、病死率也高.2004年1月-2005年12月,我科共收治病历资料较完整的高龄老年病人127例,早期对其进行护理干预,这对延长病人生命,保证治疗,提供了较好的基础条件.现介绍如下.     

急诊科护士院前急救常见的护理隐患分析

文章编号:1009-6493(2006)3C-0831-02为了探讨院前急救工作的特点及护理隐患,从而采取有效的防范措施,降低院前救护中护理隐患的发生率。通过对2001年1月—2004年12月我院急诊科“120”院前急救病人进行回顾性的总结分析,现报告如下。1资料与方法1.1临床资料选取2001年1月—200     

Protective Effects of Memantine Against Methylmercury-Induced Glutamate Dyshomeostasis and Oxidative Stress in Rat Cerebral Cortex

Methylmercury (MeHg) is one of the ubiquitous environmental toxicant that leads to long-lasting neurological deficits in animals and humans. The identification of the underlying mechanisms has been a main focus of research in the neurotoxicology field. Glutamate (Glu) dyshomeostasis and oxidative stress have been identified as two critical mechanisms mediating MeHg-induced neurotoxicity. However, little has been known of the interaction between these two mechanisms that play in MeHg poisoning in vivo. We, therefore, developed a rat model of MeHg subchronic poisoning to evaluate its neurotoxic effects and investigated the neuroprotective role of memantine, a low-affinity, noncompetitive N-methyl-d-aspartate receptors (NMDARs) antagonist, against MeHg-induced neurotoxicity. Ninety rats were randomly divided into five groups: control, memantine control, MeHg-treated (4 and 12 μmol/kg), and memantine pretreated. Administration of 12 μmol/kg MeHg for 4 weeks significantly elevated total Hg levels, disrupted Glu metabolism, overexcited NMDARs, and led to intracellular calcium overload, which might be critical to excessive reactive oxygen species (ROS) formation in cerebral cortex. Meanwhile, MeHg administration reduced non-enzymatic (non-protein sulfhydryl, NPSH) and enzymatic (superoxide dismutase, SOD and glutathione peroxidase, GSH-Px) antioxidants; caused lipid, protein, and DNA oxidative damage; and enhanced neurocyte apoptosis in cerebral cortex. Moreover, glutamate/aspartate transporter (GLAST) and glutamate transporter-1 (GLT-1) appear to be inhibited by MeHg exposure. Pretreatment with memantine at a dose of 5 μmol/kg significantly prevented MeHg-induced alterations of Glu metabolism and oxidative stress, alleviated neurocyte apoptosis, and pathological injury. In conclusion, the results suggested that Glu dyshomeostasis and oxidative stress resulting from MeHg exposure contributed to neuronal injury. Memantine possesses the ability to attenuate MeHg-induced neurotoxicity through mechanisms involving its NMDARs-binding properties and indirect antioxidation.     

Developing a prediction rule from automated clinical databases to identify high-risk patients in a large population with diabetes

OBJECTIVE: To develop and validate a prediction rule for identifying diabetic patients at high short-term risk of complications using automated data in a large managed care organization. RESEARCH DESIGN AND METHODS: Retrospective cohort analyses were performed in 57,722 diabetic members of Kaiser Permanente, Northern California, aged > or =19 years. Data from 1994 to 1995 were used to model risk for macro- and microvascular complications (n = 3,977), infectious complications (n = 1,580), and metabolic complications (n = 316) during 1996. Candidate predictors (n = 36) included prior inpatient and outpatient diagnoses, laboratory records, pharmacy records, utilization records, and survey data. Using split-sample validation, the risk scores derived from logistic regression models in half of the population were evaluated in the second half. Sensitivity, positive predictive value, and receiver operating characteristics curves were used to compare scores obtained from full models to those derived using simpler approaches. RESULTS: History of prior complications or related outpatient diagnoses were the strongest predictors in each complications set. For patients without previous events, treatment with insulin alone, serum creatinine > or =1.3 mg/dl, use of two or more antihypertensive medications, HbA(1c) >10%, and albuminuria/microalbuminuria were independent predictors of two or all three complications. Several risk scores derived from multivariate models were more efficient than simply targeting patients with elevated HbA(1c) levels for identifying high-risk patients. CONCLUSIONS: Simple prediction rules based on automated clinical data are useful in planning care management for populations with diabetes.     

Cytoskeletal changes during development and aging in the cortex of neurofilament light protein knockout mice

The neurofilament light (NFL) subunit is considered as an obligate subunit polymer for neuronal intermediate filaments comprising the neurofilament (NF) triplet proteins. We examined cytoskeletal protein levels in the cerebral cortex of NFL knockout (KO) mice at postnatal day 4 (P4), 5 months, and 12 months of age compared with age‐matched wild‐type (WT) mice of a similar genetic background (C57BL/6). The absence of NFL protein resulted in a significant reduction of phosphorylated and dephosphorylated NFs (NF‐P, NF‐DP), the medium NF subunit (NFM), and the intermediate filament α‐internexin (INT) at P4. At 5 months, NF‐DP, NFM, and INT remained significantly lower in knockouts. At 12 months, NF‐P was again significantly decreased, and INT significantly increased, in KOs compared with wild type. In addition, protein levels of class III neuron‐specific β‐tubulin and microtubule‐associated protein 2 were significantly increased in NFL KO mice at P4, 5 months, and 12 months, whereas β‐actin levels were significantly decreased at P4. Immunocytochemical studies demonstrated that NF‐DP accumulated abnormally in the perikarya of cortical neurons by 5 months of age in NFL KO mice. Neurons that lacked NF triplet proteins, such as calretinin‐immunolabeled nonpyramidal cells, showed no alterations in density or cytoarchitectural distribution in NFL KO mice at 5 months relative to WT mice, although calretinin protein levels were decreased significantly after 12 months in NFL KO mice. These findings suggest that a lack of NFL protein alters the expression of cytoskeletal proteins and disrupts other NF subunits, causing intracellular aggregation but not gross structural changes in cortical neurons or cytoarchitecture. The data also indicate that changes in expression of other cytoskeletal proteins may compensate for decreased NFs. J. Comp. Neurol. 521:1817–1827, 2013. © 2012 Wiley Periodicals, Inc.     

Influence of gender and age on the Dysphonia Severity Index: A normative study in a Shanghainese population

Dysphonia Severity Index (DSI) is an objective multi-parametric measurement of voice quality, which has been widely used in different countries. Studies indicate that DSI may be influenced by vocal pathology, age and geographical factors, whereas gender does not significantly affect DSI. The purpose of this study was to investigate the effects of gender and age on the DSI and related parameters in a Shanghainese population. The present study measured the DSI and the parameters maximum phonation time (MPT), highest fundamental frequency (HF0), lowest intensity (LI) and Jitter in 187 Shanghainese subjects, including 106 young adults aged 18–23 years (52 males and 54 females) and 81 children aged 7–9 years (44 boys and 37 girls). Two-way analysis of variance indicated that HF0 was significantly higher in female subjects than in male subjects, in both young adults and children. Gender was not significantly associated with MPT, LI, jitter or DSI. With regard to age, MPT and DSI were significantly higher in young adults than in children, and HF0 and LI were significantly lower. No significant associations between age and jitter were detected. In terms of clinic significance, the results of this study may contribute to the establishment of a normal reference range for Shanghainese DSI values, and the influence of gender and age on DSI and its separate components.     

Adenosine A2A receptor deficiency alleviates blast-induced cognitive dysfunction

Traumatic brain injury (TBI), particularly explosive blast-induced TBI (bTBI), has become the most prevalent injury among military personnel. The disruption of cognitive function is one of the most serious consequences of bTBI because its long-lasting effects prevent survivors fulfilling their active duty and resuming normal civilian life. However, the mechanisms are poorly understood and there is no treatment available. This study investigated the effects of adenosine A2A receptor (A2AR) on bTBI-induced cognitive deficit, and explored the underlying mechanisms. After being subjected to moderate whole-body blast injury, mice lacking the A2AR (A2AR knockout (KO)) showed less severity and shorter duration of impaired spatial reference memory and working memory than wild-type mice did. In addition, bTBI-induced cortical and hippocampal lesions, as well as proinflammatory cytokine expression, glutamate release, edema, cell loss, and gliosis in both early and prolonged phases of the injury, were significantly attenuated in A2AR KO mice. The results suggest that early injury and chronic neuropathological damages are important mechanisms of bTBI-induced cognitive impairment, and that the impairment can be attenuated by preventing A2AR activation. These findings suggest that A2AR antagonism is a potential therapeutic strategy for mild-to-moderate bTBI and consequent cognitive impairment.