Sandwich Vertebral Fracture in the Study of Adjacent-level Fracture After Vertebral Cement Augmentation

The literature is inconclusive on the development of adjacent-level vertebral fracture after initial cement augmentation. A preliminary hypotheses is that cement injection exaggerates force transmission to the adjacent vertebral bodies, thereby predisposing those levels to future fractures. A sandwich vertebra is an intact vertebral body located between 2 previously cemented vertebrae. The purpose of this study was to determine whether the risk of adjacent-level fracture increased due to load shift after a cement injection procedure. The authors retrospectively investigated the rate of adjacent-level fracture after sandwiching compared with conservative treatment and determined the potential causative factors of sandwich vertebral fracture. Age, sex, weight, height, body mass index, follow-up period, and location of sandwich level (T10-L2 or nonT10-L2 junction) were assessed. Surgical variables, including surgical procedure (vertebroplasty or balloon kyphoplasty), surgical approach (through uni- or bilateral pedicle), volume of cement injected into the painful vertebrae, cement leakage into the intervertebral disk, cumulative number of treated levels, and pre- and postoperative kyphotic angulation of the sandwich region, were also analyzed. Nine of 42 sandwiched levels developed fatigue fractures, whereas 11 of 71 patients treated with conservative therapy sustained new vertebral fractures adjacent to the treated levels. Only preoperative kyphotic angulation was the variable positively associated with sandwich vertebral fracture at follow-up (P=.021). Although subjected to double load shifts, the sandwich vertebra was not prone to structural failure. Thus, cement augmentation protocol does not increase the incidence of adjacent vertebral fracture.     

云南白药外敷治疗静脉穿刺致皮下淤血

目的 探讨云南白药外敷治疗静脉穿刺致皮下淤血的效果.方法 将94例静脉穿刺后引起皮下淤血的患者随机分成观察组(48例)和对照组(46例),观察组采用乙醇调制的云南白药外敷,对照组进行热敷治疗,观察患者淤血消退时间.结果 观察组淤血消退时间显著短于对照组(P＜0.01).结论 云南白药外敷治疗静脉穿刺引起的皮下淤血效果优于传统方法.     

Construction and application of traditional Chinese medicine-oriented care model for stroke

目的 通过理论与临床相结合的研究方式构建中风病辨证施护模式,以提高护理效果和患者满意度.方法 将200例中风病患者按病区分为观察组104例和对照组96例.对照组采用中医常规护理方案;观察组构建中风病辨证施护模式,采用该模式对患者辩证分型施护.连续14d后评价效果.结果 观察组疗效、Barthel指数评价及患者满意度显著高于对照组,并发症发生率显著低于对照组(P<0.05,P<0.01).结论 中风病辩证施护模式应用于临床效果可靠,患者满意,可作为中医临床护理和研究的借鉴.     

新型覆膜支架在腹主动脉瘤腔内修复中的应用

目的 总结腹主动脉瘤腔内修复术使用Endurant支架的经验及体会.方法 回顾分析2010年5月至2011年5月北京协和医院血管外科收治的19例肾下腹主动脉瘤使用Endurant支架行腔内修复术的病例特点、术后并发症和近期随访结果.结果 19例患者均获得手术成功,其中9例为复杂解剖形态的病例.术中同时进行的肾动脉支架、髂内动脉栓塞和髂动脉扩张也均获得成功.术后无Ⅰ、Ⅲ和Ⅳ型内漏发生,4例残余Ⅱ型内漏留待观察.围手术期无死亡病例,30 d并发症主要包括血栓消耗性凝血功能障碍,心肌梗死合并心衰,伤口感染和血肿.全组随访1～12个月,无死亡病例.8例患者完成至少1次CT动脉重建(computer tomography angiography,CTA)检查,5例动脉瘤体直径缩小,3例无改变.1例患者出现单侧髂腿延长支闭塞,行股股动脉转流.1例患者出现继发性ⅠB型内漏,继续观察.结论 腹主动脉瘤腔内修复术使用Endurant支架安全,有效.Endurant支架增加了对于复杂解剖形态的病例的手术成功率,近期疗效满意.     

A CD11d Monoclonal Antibody Treatment Reduces Tissue Injury and Improves Neurological Outcome after Fluid Percussion Brain Injury in Rats

Abstract Traumatic brain injury (TBI) is an international health concern often resulting in chronic neurological abnormalities, including cognitive deficits, emotional disturbances, and motor impairments. An anti-CD11d monoclonal antibody that blocks the CD11d/CD18 integrin and vascular cell adhesion molecule (VCAM)-1 interaction following experimental spinal cord injury improves functional recovery, while reducing the intraspinal number of neutrophils and macrophages, oxidative activity, and tissue damage. Since the mechanisms of secondary injury in the brain and spinal cord are similar, we designed a study to evaluate fully the effects of anti-CD11d treatment after a moderate lateral fluid percussion TBI in the rat. Rats were treated at 2?h after TBI with either the anti-CD11d antibody or an isotype-matched control antibody 1B7, and both short (24- to 72-h) and long (4-week) recovery periods were examined. The anti-CD11d integrin treatment reduced neutrophil and macrophage levels in the injured brain, with concomitant reductions in lipid peroxidation, astrocyte activation, amyloid precursor protein accumulation, and neuronal loss. The reduced neuroinflammation seen in anti-CD11d-treated rats correlated with improved performance on a number of behavioral tests. At 24?h, the anti-CD11d group performed significantly better than the 1B7 controls on several water maze measures of spatial cognition. At 4 weeks post-injury the anti-CD11d-treated rats had better sensorimotor function as assessed by the beam task, and reduced anxiety-like behaviors, as evidenced by elevated-plus maze testing, compared to 1B7 controls. These findings suggest that neuroinflammation is associated with behavioral deficits after TBI, and that anti-CD11d antibody treatment is a viable strategy to improve neurological outcomes after TBI.     

加速康复外科理念指导下围手术期焦虑非药物干预临床应用研究

背景 焦虑是临床常见的围手术期不良反应,可造成不同程度的躯体及心理应激.目前暂无系统、有效的治疗指南可预防或减少围手术期焦虑反应.目的 介绍在加速康复外科理念下非药物干预治疗(non-pharmacologic intervention)在围手术期焦虑的应用进展.内容 阐述围手术期焦虑对机体造成的心理及生理等不良影响,着重从情绪、认知及行为三方面介绍加速康复外科理念指导下围手术期焦虑非药物治疗的临床应用.趋向 围手术期非药物干预与常规药物治疗相比,具有安全、舒适、无药物副作用等优势,治疗效果显著,是抗焦虑治疗措施中不可替代的组成部分.     

护士职业压力与职业倦怠的调查研究

目的1、调查护士在工作中面临的职业压力与工作倦怠程度;2、研究职业压力对工作倦怠的影响。方法采用问卷调查法,对贵州省贵阳市多所医院173名护士的职业压力与工作倦怠状况进行调查分析。结果1、被试的职业压力处于中度水平;2、被试的情感枯竭程度中等,冷漠程度较轻,职业效能感较高。3、被试的职业压力与情感枯竭、冷漠显著正相关。结论职业压力是情感枯竭的一个有效的预测因子,情感枯竭达到一定程度会导致冷漠,冷漠最终将使得职业效能感减退。     

结直肠癌患者运动行为影响因素的研究现状

坚持进行规律的运动可以提高结直肠癌患者的生活质量,降低复发率和病死率,但结直肠癌患者普遍存在运动量不足的现象。多项研究表明,疾病及治疗相关因素均会影响患者的运动水平,导致运动量不足。在分析结直肠癌患者运动行为现状的基础上,从一般人口学资料、社会心理、运动方式及疾病四方面阐述影响结直肠癌患者运动行为的因素,以期为今后开展更有效的运动干预提供参考。     

Reduction of hepatic and adipose tissue glucocorticoid receptor expression with antisense oligonucleotides improves hyperglycemia and hyperlipidemia in diabetic rodents without causing systemic glucocorticoid antagonism

Glucocorticoids (GCs) increase hepatic gluconeogenesis and play an important role in the regulation of hepatic glucose output. Whereas systemic GC inhibition can alleviate hyperglycemia in rodents and humans, it results in adrenal insufficiency and stimulation of the hypothalamic-pituitary-adrenal axis. In the present study, we used optimized antisense oligonucleotides (ASOs) to cause selective reduction of the glucocorticoid receptor (GCCR) in liver and white adipose tissue (WAT) and evaluated the resultant changes in glucose and lipid metabolism in several rodent models of diabetes. Treatment of ob/ob mice with GCCR ASOs for 4 weeks resulted in approximately 75 and approximately 40% reduction in GCCR mRNA expression in liver and WAT, respectively. This was accompanied by approximately 65% decrease in fed and approximately 30% decrease in fasted glucose levels, a 60% decrease in plasma insulin concentration, and approximately 20 and 35% decrease in plasma resistin and tumor necrosis factor-alpha levels, respectively. Furthermore, GCCR ASO reduced hepatic glucose production and inhibited hepatic gluconeogenesis in liver slices from basal and dexamethasone-treated animals. In db/db mice, a similar reduction in GCCR expression caused approximately 40% decrease in fed and fasted glucose levels and approximately 50% reduction in plasma triglycerides. In ZDF and high-fat diet-fed streptozotocin-treated (HFD-STZ) rats, GCCR ASO treatment caused approximately 60% reduction in GCCR expression in the liver and WAT, which was accompanied by a 40-70% decrease in fasted glucose levels and a robust reduction in plasma triglyceride, cholesterol, and free fatty acids. No change in circulating corticosterone levels was seen in any model after GCCR ASO treatment. To further demonstrate that GCCR ASO does not cause systemic GC antagonism, normal Sprague-Dawley rats were challenged with dexamethasone after treating with GCCR ASO. Dexamethasone increased the expression of GC-responsive genes such as PEPCK in the liver and decreased circulating lymphocytes. GCCR ASO treatment completely inhibited the increase in dexamethasone-induced PEPCK expression in the liver without causing any change in the dexamethasone-induced lymphopenia. These studies demonstrate that tissue-selective GCCR antagonism with ASOs may be a viable therapeutic strategy for the treatment of the metabolic syndrome.