A systematic review of the management of hangman’s fractures

During the past 30 years various treatment protocols for hangmans fractures have been attempted. In order to guide the management of hangmans fractures, different classifications have been introduced. However, opinions on operative or nonoperative treatment have not yet been solidified. To evaluate both conservative and operative management of hangmans fractures in the published literature and to provide appropriate guidelines for treatment of hangmans fractures, a systematic review of the literature regarding the management of hangmans fractures was performed. An English literature search from January 1966 to January 2004 was completed with reference to treatment of hangmans fractures. The classification for treatment guidance from the literature was also reviewed. Regarding a primary therapy for hangmans fractures, there were 20 papers (62.5%) that advocated for a conservative treatment and 11 of the remaining 12 papers suggested that conservative treatment was suitable for some stable fractures. The classification of Effendi et al. modified by Levine and Edwards was used widely. Most hangmans fractures could be managed successfully with traction and external immobilization, especially in Effendi Type I, Type II and Levine-Edwards Type II fractures. It is necessary for Levine-Edwards Type IIa and III fractures to be treated with rigid immobilization. Only for some stable Type I and Levine-Edwards Type II injuries, nonrigid external fixation alone was sufficient. Rigid immobilization alone was necessary for most cases. Surgical stabilization is recommended in unstable cases when there is the possibility of later instability, such as Levine-Edwards Type IIa and III fractures with significant dislocation. The classification system proposed by Effendi et al. and modified by Levine and Edwards provided a clinically reasonable guideline for successful management of hangmans fractures.     

单纯内固定与有限内固定结合外固定在治疗高能量闭合性pilon骨折中的比较

【摘要】 目的 比较单纯内固定与有限内固定结合外固定在治疗高能量闭合性pilon骨折中的临床效果,评估两种术式在治疗高能量闭合性Pilon骨折中的优劣。 方法 回顾性分析2001年12月至2010年12月收治的42例高能量闭合性Pilon骨折的临床资料。按手术方式不同分为两组:A组26例,行切开复位单纯内固定手术(ORIF);B组16例,行切开复位有限内固定结合外固定手术(LORIF+ EX)。分析术后两组患者感染、骨延迟愈合或不愈合、创伤性关节炎、关节僵硬等并发症的发生率,测量术后8个月患者关节活动度并根据AOFAS评分标准评价其踝足功能。 结果 术前两组患者在性别、年龄、骨折分型、受伤至手术时间等方面无明显差异(P>0.05),术后随访8~109月个月,平均 37.6个月,两种治疗方法在术后并发症发生率、关节活动度及AOFAS评分并无明显差别(P>0.05)。结论 对于高能量闭合性pilon骨折的治疗,切开复位内固定和切开复位有限内固定结合外固定临床疗效相当,并发症的发生率无明显差别,均可作为其治疗手段。     

腹腔镜辅助中位肛门闭锁成形术11例报告

目的 探讨腹腔镜辅助中位肛门闭锁成形术的可行性。方法 腹腔镜监视下,游离松解直肠;断离修补直肠尿道（阴道）瘘管,其中6例经腹腔镜离断修补,4例经会阴切口离断修补;然后在电刺激仪的引导下经会阴肌肉中心1.0cm左右小切口向盆底肌肉中心分离形成隧道,最后将直肠从隧道中拖出,与会阴皮肤吻合,同时关闭结肠造瘘口。结果 11例患儿均在腹腔镜辅助下完成肛门成形术,腹腔镜手术操作时间平均32.8min（25～78min）,出血量平均5.3ml（2～10ml）,无需要输血者。术后11d去除尿管或膀胱造瘘管,无尿道瘘或憩室出现,无切口感染发生。11例术后随访3～66个月,平均45个月。根据肛门功能临床评分标准评分（6分法）,排便优8例（72.7%）,良3例（27.3%）。结论 腹腔镜辅助中位肛门闭锁成形术处理直肠泌尿系瘘方便,辨认盆底肌中心准确及避免切口污染等优点,是治疗中位肛门闭锁有效方法。     

保护动机理论在糖尿病高危足干预中的应用

目的探讨基于保护动机理论的护理干预在糖尿病高危足患者中的应用效果。方法对40例糖尿病高危足患者进行保护动机理论的综合护理干预,在干预前、后对患者的生存质量、自我效能和糖尿病足相关指标进行测评和调查。结果干预后患者自我效能、生存质量评分及糖尿病足相关指标显著优于干预前(均P<0.01)。结论基于保护动机理论的护理干预对糖尿病高危足患者临床疗效有效,并能改善患者的生存质量。     

交锁髓内钉在治疗肱骨干骨折中对肩关节功能的影响

目的　报告 1996～ 1998年间应用多种型号的交锁髓内钉治疗肱骨干骨折 2 5例的疗效。方法　对肱骨干骨折 2 5例采用交锁髓内针治疗。得到随访 2 1例。随访时间 8～ 32个月 ,平均 17个月。伤者年龄 18～ 70岁 ,平均 39岁。骨折类型 :横断形9例 ,粉碎形 2例 ,斜形 5例 ,螺旋形 5例。肱骨上 1/3骨折 4例 ,中 1/3骨折 16例 ,下 1/3骨折 1例。结果　按Neer评分法测定肩关节功能 ,13例 (6 2 % )合并有不同程度的功能障碍。结论　认为目前的交锁髓内针在治疗肱骨干骨折时会损伤到肩袖 ,因此在选用时应慎重。     

护士心理契约与工作倦怠的相关性分析

目的探讨护士心理契约与工作倦怠的相关性。方法采用整群抽样的方法对衡阳市2所综合性三级甲等医院515名临床护士进行问卷调查,了解护士心理契约和工作倦怠现状,并探讨两者间关系。结果护士心理契约中医院责任得分2.98±0.39,高于护士责任的得分(1.78±0.53),护士工作倦怠总均分为2.80±0.55,护士心理契约与工作倦怠之间呈显著正相关(P0.05,P0.01)。回归分析显示,控制人口学变量后,医院团队责任和护士团队责任可预测情绪衰竭,医院现实责任和医院团队责任可预测玩世不恭,护士团队责任、护士现实责任和护士发展责任可预测成就感低落。结论心理契约是护士工作倦怠的重要影响因素,医院管理者应根据护士心理契约中的不足之处,制订针对性干预措施,以降低护士的工作倦怠。     

人非小细胞肺癌P16基因突变研究

目的探讨ｐ１６基因缺失和突变与人非小细胞肺癌发生、发展的关系。方法应用多重ＰＣＲ、ＳＳＣＰ分析及ＤＮＡ序列分析技术，对４５例人非小细胞肺癌组织中ｐ１６基因外显子１和外显子２进行基因缺失和突变分析。结果４５例肺癌样品中共检出１９例ｐ１６基因缺失，总的缺失率为４２．２％（１９／４５）。其中纯合型缺失８例（１７．８％），半合型缺失１１例（２４．４％）；外显子１缺失７例（１５．６％），外显子２缺失１２例（２６．７％）；ｐ１６基因外显子２的突变检出率为３１．１％（１４／４５）；ＤＮＡ序列分析显示ｐ１６基因７２位密码子无义突变７例，７５位密码子错义突变７例。结论ｐ１６基因的缺失和突变可能与人非小细胞肺癌的发生、发展有关。     

Inhibition of Autophagy by 3-MA Enhances the Effect of 5-FU-Induced Apoptosis in Colon Cancer Cells

Background  5-fluorouracil-(5-FU)-based adjuvant chemotherapy is widely used for the treatment of colorectal cancer. However, 5-FU resistance in the course of treatment has become more common. Therefore, new therapeutic strategies and/or new adjuvant drugs still need to be explored. Methods  Two colon-cancer-derived cell lines, colon26 and HT29, were used to investigate the effect of 5-FU, 3-methyladenine (3-MA, an autophagy inhibitor), or their combination on apoptotic cell death and autophagy. MTT assay, Hochest plus propidium iodide (PI) staining, and DNA fragmentation assay were used to observe apoptosis. Meanwhile, monodansylcadaverine (MDC) was used to detect autophagy. Finally, immunoblotting assay was used to explore the molecular change that occurred. Results  We observed the apoptosis induced by 5-FU in colon cancer cells. Meanwhile, autophagy was also stimulated. The combination treatment of 3-MA and 5-FU significantly increased the apoptotic cell death. By isolating the subcellular fractions of mitochondria and cytosol, we observed that the release of cytochrome c was increased in combination-treated cells. Cytochrome c resulted in the activation of caspase-3, thus activating PARP. Moreover, the anti-apoptotic protein, Bcl-xL, was significantly downregulated by 3-MA. Conclusions  Our results suggest that 5-FU-induced apoptosis in colon cancer cells can be enhanced by the inhibitor of autophagy, 3-MA. Autophagy might play a role as a self-defense mechanism in 5-FU-treated colon cancer cells, and its inhibition could be a promising strategy for the adjuvant chemotherapy of colon cancer.     

IL-1β对ATDC5成软骨分化细胞miR-455-3p的影响

目的：检测IL-1β对ATDC5成软骨分化细胞miR-455-3p表达的影响,探索miR-455-3p在骨关节炎中的作用。方法诱导ATDC5细胞成软骨分化后,予10 ng/ml的IL-1β刺激,在刺激4、12、24、48 h时应用实时荧光定量PCR检测miR-455-3p、C/EBPβ和软骨特征性标记物的表达情况;并利用抑制剂IKK-NBD阻断NF-κB通路后,应用实时荧光定量PCR检测IL-1β作用下miR-455-3p的表达水平。结果在IL-1β作用下的ATDC5成软骨分化细胞中miR-455-3p、C/EBPβ和软骨退变标记物（ MMP13、ADAMTS5）均上调,而软骨基质合成标记物（ ACAN、COL2A1、SOX9）则下调,且后期更为明显;而IKK-NBD可抑制IL-1β诱导的miR-455-3p表达。结论 IL-1β可上调ATDC5成软骨分化细胞miR-455-3p的表达水平,且受NF-κB通路的调节。