一种新的对于长期卧床病人的护理模型

长期卧床的病人处置的改善,为减少医院床位的占用和改善病人的生命质量提供了可能。多达60%的英国成年人存在慢性健康问题,而且其中一些人有着多发慢性病导致复杂的健康护理需求。结果是小部分病人需要长期卧床,这就与大量的健康护理以及医院床位需求产生了矛盾。改善对这些疾病处置的策略可潜在减少医院床位的占用以及改善这类病人的生命质量。这个模式以提供人性化、系统化和持续支持的方式对长期卧床病人的健康和生命质量进行改善为目标。构建这个模式的第一步是确认所有长期卧床的病人所需要的护理等级,并标示在模式图上。病案管理是面…     

一种新的稳定多囊卵巢综合征大鼠模型的建立

目的：建立适合运动疗法研究的多囊卵巢综合征（PCOS）大鼠模型．观察模型建立过程中激素水平及卵巢形态的变化规律。方法：实验组（n=25）以丙酸睾酮皮下注射2113龄Wistar雌性大鼠，对照组（n=25）同期皮下注射相同容积茶油，分别在注射第7天、14天、21天、28天观察大鼠肥胖指数、卵巢器官指数、空腹血糖、空腹胰岛素、性激素水平以及卵巢的形态学变化。结果：实验组大鼠在完成28天注射后表现出肥胖、雌激素升高、孕酮下降、空腹胰岛素水平显著升高、空腹血糖，空腹胰岛素显著降低等典型PCOS的激素变化特征。卵巢形态呈现显著的颗粒层细胞减少,膜层增多,窦前卵泡大量聚集．闭锁卵泡增多等多囊卵巢特点。各时间点观察可见雌二醇水平第7天即发生显著改变，血糖水平在各时间点均未有显著改变．而胰岛素水平在各时间点没有显著变化直至第28天实验组显著升高。卵巢形态的变化早期表现膜层增厚和颗粒层减少，第21天闭锁卵泡显著增多，第28天出现窦前卵泡大量聚集。结论：连续28天丙酸睾酮注射诱导的PCOS大鼠模型具有高胰岛素血症、性激素异常的内分泌特征和卵巢多囊改变的形态学特点．并且激素和形态变化符合生理规律具有相当的稳定性，适合运动干预的研究。     

Rate Hysteresis Pacing: How Valuable Is It? A Comparison of the Stimulation Rates of 70 and 50 Beats per Minute and Rate Hysteresis in Patients with Sinus Node Disease

The main disadvantages of VVI pacing are absence of acceleration of the heart rate and loss of atrial synchronization. The alternatives to AAI and DDD pacing are stimulation at a low rate or hysteresis in order to decrease pacing time and thus reduce AV asynchrony. Nine patients who suffered from sinus node disease and who had been given a multiprogrammable pacemaker were monitored at each of three stimulation rates: 70, 50, and 70 bpm with an inhibition rate of 50 bpm (hysteresis).
The total pacing time was shortest (p < 0.05) for the stimulation rate of 50 bpm as compared to 70 bpm and hysteresis. It was also shorter for the hysteresis mode than for the 70 bpm mode (p < 0.05).
Only for hysteresis pacing was there a significant reduction in the number of changes from conducted cardiac rhythm to pacemaker-induced rhythm. Most patients found the 50 bpm mode preferable. None favored the hysteresis mode.
In patients with sinus node disease and intermittent bradycardia being permanently paced, the periods of AV-conducted rhythm may be lengthened by reducing the stimulation rate from 70 bpm, with or without hysteresis pacing, to 50 bpm. In paced patients with sinus node disease and symptoms due to AV asynchrony, it might be worth trying a decrease in the stimulation rate before resorting to other pacemaker systems.     

速度向量成像评价1型糖尿病兔模型心功能演变过程

目的 运用速度向量成像技术(VVI)对糖尿病兔心脏运动功能变化进行监测,并通过不同时期的心肌病理切片对照,探讨糖尿病兔心脏运动功能变化的特点.方法 采用耳缘静脉注射链脲佐菌素(65mg/kg)诱导1型糖尿病兔模型;运用VVI获得糖尿病兔左心室心肌各节段最大收缩期运动速度(Vs)、最大舒张期运动速度(Vd)、最大收缩期应变(Ss)、最大收缩期应变率(SRs)、最大舒张期应变率(SRd)等参数,进行评估其心脏运动功能变化状况;应用10％甲醛固定及石蜡包埋技术制备心肌病理切片.结果 成模2周后即可发现糖尿病兔心脏短轴Ss、SRs、SRd下降,并于成模4～12周后呈逐步减低趋势,与同期心肌病理改变情况一致.结论 VVI可早期发现糖尿病性心肌病心脏运动功能的改变.     

The Role of Rate Hysteresis Pacing in the Hypersensitive Carotid Sinus Syndrome

The ability of rate hysteresis programming with the escape interval longer than the automatic interval lo reduce the hypotensive response to carotid sinus massage at the onset of ventricular pacing was studied in six patients paced for carotid sinus syndrome. Rate hysteresis significantly reduced this hypotensive response and abolished spontaneous symptoms in two patients and symptoms reproduced by carotid sinus massage in four patients.     

The Role of Rate Hysteresis Pacing in the Hypersensitive Carotid Sinus Syndrome

The ability of rate hysteresis programming with the escape interval longer than the automatic interval lo reduce the hypotensive response to carotid sinus massage at the onset of ventricular pacing was studied in six patients paced for carotid sinus syndrome. Rate hysteresis significantly reduced this hypotensive response and abolished spontaneous symptoms in two patients and symptoms reproduced by carotid sinus massage in four patients.     

线栓法制作兔大脑中动脉闭塞脑缺血模型

目的:探讨兔颈内动脉系统的结构和变异及采用线栓法制作兔大脑中动脉闭塞脑缺血模型的可行性。方法:新西兰白兔40只,20只制作脑血管模型,20只制作大脑中动脉闭塞脑缺血模型。0.8号渔线经颈内动脉插至大脑中动脉起始部,观察颅内压、肛温、中心静脉压和股动脉压,48 h后行头颅MRI,过量麻醉处死,取脑进行TTC染色和HE染色。结果:兔颈内动脉起始段与大脑中动脉起始段间距4.2-4.8 cm,多数(85%)无分支,少数(15%)在颈内动脉入颅前向后分出供应耳后部的分支。线栓大脑中动脉后,兔的血压、颅内压逐渐升高,头颅MRI和TTC染色均可见梗死灶,其大小、部位基本一致。结论:线栓法制作兔大脑中动脉闭塞脑缺血模型操作简单,创伤小,制作的模型稳定,成功率高。     

帕金森病基因治疗中病毒载体的研究进展

帕金森病是一种神经节退行性疾病,主要以静止震颤,肌肉僵直和运动减少为临床症状.在其各种治疗方法中基因治疗最有望彻底治愈PD,最有发展前景.但其有效性与安全性与其所选用的载体有很大关系.本文介绍了基因治疗中常用的病毒载体以及它们的特性,并指出PD基因治疗中病毒载体的发展趋势.     

一种新的原位膀胱癌动物模型的建立

目的：建立一种新的,重复性高的裸鼠原位膀胱癌模型。方法：36只裸鼠,分为A、B、C3组,每组12只。A组通过尿道留置24G动脉留置针,将裸鼠膀胱黏膜以针芯划伤,再以多聚赖氨酸预灌注20min,最后注入2×10^6人移性上皮细胞癌细胞株T24,保留灌注1h。B组仅经尿道划伤裸鼠膀胱黏膜后注入2×10^6T24细胞,C组仅经尿道注入多聚赖氨酸后注入2×10^6T24细胞。预设观察期为90d,定期观察裸鼠的健康状况及有无血尿产生,当裸鼠体质量下降〉10%,活动明显减少时认为实验终点达到,处死裸鼠。90d时处死所有动物,行病理学检查。结果：A组所有12只裸鼠均于70d内达到处死标准,动物尸检结合病理切片显示成瘤率为100%,B组9只裸鼠于90d内达到处死标准,另3只存活,动物尸检结合病理切片显示成瘤率为75%,C组动物均正常存活至90d,处死后动物尸检结合病理切片显示成瘤率为0。结论：经尿道机械划伤裸鼠黏膜后注入多聚赖氨酸以建立裸鼠原位膀胱癌模型的方法,是一种稳定、可重复性高的模型。     

速度向量成像技术评价颈总动脉粥样硬化斑块力学状态的研究

目的 应用速度向量成像(VVI) 技术评价颈总动脉壁粥样硬化斑块运动特性及斑块力学的临床价值.方法 对36例动脉粥样硬化斑块患者和对照组30例正常人双侧颈总动脉进行超声检查;并检测出颈总动脉内中膜厚度(IMT),结合同步心电图描记,取颈总动脉长轴、短轴二维图像进行动态存储,运用VVI软件进行脱机分析,计算颈动脉壁粥样斑块部位的运动速度、应变和应变率,并与正常组动脉壁运动参数进行比较.结果颈总动脉粥样斑块处运动速度、应变及应变率低于无斑块处;斑块基底部速度、应变及应变率低于斑块表面;斑块组颈动脉IMT及运动速度均高于正常对照组(P<0.5),软斑块收缩期最大运动速度、最大应变率分别高于硬斑块组,肩部运动速度、应变率高于帽顶部(P<0.5).结论 VVI 技术可用于颈总动脉管壁斑块运动速度、应变及应变率的分析,为研究颈总动脉斑块形成机理和稳定性,提供新的方法.     

Vector mapping in localizing the transverse conduction site of the crista terminalis in patients with typical atrial flutter

BACKGROUND: The difference in the conduction properties of the crista terminalis (CT) along its course, has not been fully clarified. Using the vector mapping method, we localized the transverse conduction (TC) site of the CT and elucidated its conduction capabilities in patients with typical atrial flutter (AF). METHODS: The TC site of the CT was localized by the analysis of the polarity reversal of the double potentials recorded at 10 sites along the CT using a 20-pole deflectable catheter in 17 patients. The conduction capabilities of the TC site were analyzed during incremental pacing delivered from 100 beats/min to 2-to-1 local capture at the low anterior (LARA) and posterior (LPRA) right atrium. RESULTS: At a pacing rate of 100 beats/min, TC at a single site was observed in 15 patients during LARA pacing and 7 patients during LPRA pacing, respectively. TC sites were distributed from superior to middle third of the CT in all patients. TC was bidirectional in 4 sites, but was unidirectional in the remaining 14 sites. Following an increase in the pacing rate, TC was blocked in all 7 sites during LPRA pacing and 11 of 15 sites during LARA pacing. Shift in the location of the TC site was not observed in any of the patients before TC block. The conduction block rate during pacing from LARA was significantly higher than that from LPRA (211 +/- 59 beats/min vs 145 +/- 66 beats/min, P < 0.01). CONCLUSIONS: The superior to middle third of the CT provides TC capabilities. The TC across the CT was caused by a preferential conduction site and most of these TC were unidirectional, and stable in location irrespective of the change in the conduction rate.     

Sustained Human Factor VIII Expression in Hemophilia A Mice Following Systemic Delivery of a Gutless Adenoviral Vector

Gutless adenoviral vectors are devoid of all viral coding regions and display reduced cytotoxicity, diminished immunogenicity, and an increased coding capacity compared with early generation vectors. Using hemophilia A, a deficiency in clotting factor VIII (FVIII), as a model disease, we generated and evaluated a gutless vector encoding human FVIII. The FVIII gutless vector grew to high titer and was reproducibly scaled-up from vector seed lots. Extensive viral DNA analyses revealed no rearrangements of the vector genome. A quantitative PCR assay demonstrated helper virus contamination levels of <2%, with the best preparation containing 0.3% helper virus. We compared the gutless vector with an E1/E2a/E3-deficient (Av3) early generation vector encoding an identical FVIII expression cassette following intravenous administration to hemophilia A mice. Gutless vector-treated mice displayed 10-fold higher FVIII expression levels that were sustained for at least 9 months. In contrast, mice treated with the Av3 vector displayed FVIII levels below the limit of sensitivity of the assay at 3 months. Assessment of hepatotoxicity by measuring the serum levels of liver enzymes demonstrated that the gutless vector was significantly less toxic than the Av3 vector at time points later than 7 days. At the highest dose used, both vectors caused a transient 10-fold increase in liver enzymes 1 day after vector administration, suggesting that this increase was caused by direct toxicity of the input capsid proteins. These data demonstrate that the gutless vector displayed increased duration and levels of FVIII expression, and was significantly less toxic than an analogous early generation vector.