锁定肱骨近端接骨板治疗肱骨近端骨折

目的探讨锁定肱骨近端接骨板治疗肱骨近端骨折的临床价值：方法采用切开复位AO锁定肱骨近端接骨板(LPHP)内固定治疗肱骨近端骨折12例。结果所有患随访3～13个月，平均7．5个月。临床疗效评估：优7例，良3例，进步2例，优良率为83．3％。结论LPHP具有固定可靠、减少软组织损伤、保护血运、利于关节囊和肩袖修复、有助于骨折愈合和肩关节功能恢复的特点，值得提倡。     

骨髓间充质干细胞促进骨-肌腱结合部愈合的初步观察

[目的]观察骨髓间充质干细胞对骨-肌腱结合部愈合的影响.[方法]采用骨髓穿刺、全骨髓培养法获取兔骨髓间充质干细胞.36只18周龄新西兰大白兔随机分为2组,实验组将骨髓间充质干细胞与Pluronic F-127载体材料结合后,植入兔髌骨部分切除模型,对照组只进行手术,不植入细胞.在术后6、12、18周进行X线片、大体和组织学观察评估.[结果]X线片显示术后6、12、18周实验组骨-肌腱结合部新生骨面积显著大于对照组（P＜0.01）.大体观察可见实验组骨-腱结合部愈合较早.HE染色显示实验组术后6周有大量的纤维母细胞和类软骨细胞增生,并可见新骨形成;12周,髌腱与松质骨接触面软骨细胞移行带形成;18周,纤维软骨移行带排列更有序.Safranin 0染色显示实验组术后6周,基质染色较深,部分骨-腱结合处可见相对浓染区;12周,基质染色范围明显减少,沿类软骨细胞走行分布;18周,类软骨细胞集中的区域染色较12周有所减退.组织学检查显示实验组术后6、12、18周骨-腱结合部组织愈合明显,较对照组迅速.[结论]骨髓间充质干细胞可以促进骨-肌腱结合部细胞增生,促进其早期愈合.     

纤维组织粘合剂的实验研究

本文应用“冷沉淀”法制备纤维组织粘合剂。对纤维组织粘合剂中主要成份和含量进行了测定,并测定了主要理化性质,建立了动物实验模型,观察了实验兔对纤维粘合剂的反应。     

细胞分化帮助剂提高低浓度As2O3对肝癌细胞凋亡作用的体外实验

目的 研究细胞分化帮助剂（CDA-Ⅱ）促进低浓度三氧化二砷（As2O3）对肝癌细胞株HepG-2，BEL-7402凋亡的协同效应。方法 用四甲基偶氮唑蓝（MTT）法检测单用CDA-Ⅱ或As2O3和联用对肝癌细胞株HepG-2，BEL-7402生长及抑制率的影响；用乳酸脱氢酶（LDH）法检测药物对细胞膜的毒性反应；流式细胞仪（FCM）分析细胞周期和凋亡率变化。结果 单用CDA-Ⅱ和As2O3分别为3．0mg／ml和50μmol／L时，肝癌细胞株BEL-7402，HepG-2发生凋亡达到最大值，而联用5μmol／LAs2O3＋1mg／mlCDA-Ⅱ可达到同样效果；结果显示：该浓度下HepG2的抑制率可达88％；BEL-7402的抑制率在100％；LDH检测表明联用比单用As2O310μmol／L更安全。流式细胞仪结果显示凋亡率联合组为40．2％，明显高于单用组As2O3（11．3％）或CDA-Ⅱ（8．7％）。结论 细胞分化帮助剂1mg／mlCDA-Ⅱ联用5μmol／LAs2O3可促进肝癌细胞株HepG-2，BEL-7402凋亡，可以明显降低As2O3的使用浓度，减少对正常细胞的毒副作用。二者联用具有协同作用。     

踝关节慢性前外侧不稳的手术治疗

目的: 探讨治疗踝关节慢性前外侧不稳定 (踝关节外侧不稳定合并距下关节不稳定) 的合理而有效的手术方式。方法: 自 1999 ~2003年, 应用Chrisman Snook术式, 以腓骨短肌腱前半部分重建距腓前韧带、跟腓韧带和距跟外侧韧带,治疗踝关节慢性前外侧不稳 8例患者,共 13例关节。结果: 术后随诊 6个月~5年, 平均 19个月。术后所有踝关节均达到功能稳定, 关节活动度基本恢复正常, 没有复发性踝关节不稳发生。以Good评级标准作为疗效评价, 10例关节 (77% ) 为优, 2例关节 (15% ) 为良, 1例关节为中 (7% ), 优良率达 92%。结论: Chrisman Snook术式重建了距腓前韧带、跟腓韧带和距跟外侧韧带, 有效地矫正了踝关节外侧不稳定和距下关节不稳定, 是治疗踝关节慢性前外侧严重不稳定的合理而有效的治疗方法。     

原发性胆囊癌CT诊断与鉴别诊断

目的 探讨原发性胆囊癌的CT诊断与鉴别诊断要点。方法 回顾性分析23例原发性胆囊癌CT征象，并与手术和病理对照。结果 本组23例胆囊癌术前CT正确诊断18例，5例误诊，根据CT表现可分为：腔内型8例、厚壁型5例、肿块型10例；其中共8例并肝门和腹膜后淋巴结转移；3例肝内转移；病理结果：腺癌20例，鳞癌3例。结论 原发性胆囊癌CT的诊断价值较高，但仍容易误诊，早期的诊断仍有一定困难，掌握其CT征象，注意鉴别诊断可以提高本病的诊断水平。     

Secondary sulphonylurea failure: what pathogenesis is responsible?

Sulphonylurea (SU) stimulates insulin secretion by pancreatic beta-cells and is generally used as a first-line treatment for type 2 diabetes. However, after long-term SU treatment (six months or over), some patients begin to show an increase in blood glucose once again (secondary SU failure). Two theories have been put forward to explain this failure--dysfunction of the proinsulin conversion machinery or insulin resistance. However, the primary pathogenesis behind secondary SU failure still needs to be investigated. Using a reliable technique that specifically identifies intact proinsulin (IPI), total proinsulin (TPI) and specific insulin (SI), this study aims to discover if a defect in the proinsulin converting mechanism plays a role in SU failure. Three groups were recruited for this study: healthy controls (n=8), SU responders (n=38) and secondary SU failures (n= 46). Serum concentrations of insulin-related molecules released in response to a standard glucose challenge test were compared between the groups. It was found that total SI was lower in the patient groups (P<0.05 compared to the control group), while TPI and IPI showed no distinct difference between the three groups (P>0.05). TPI:SI ratio and IPI:SI ratio showed marked increases in the patient groups (P<0.05 compared to control group), with no obvious quantitative difference between SU responders and secondary SU failures (P>0.05). Similar results for the Homa Insulin Resistant Index were found between the two patient groups. Interestingly, blood glucose at 180 mins after glucose challenge was significantly higher in the secondary SU failure group (P<0.05), with no correlation to SI, while the SU responder group showed good correlation between the parameters (P<0.05). We conclude that type 2 diabetes is associated with obvious dysfunction in the proinsulin-converting process and shows severe SI deficiency in responding to glucose challenge. Dysfunction of the proinsulin conversion mechanism was not an extra cause responsible for SU failure.     

Progressive decrease of proinsulin secretion in sulphonylurea-treated type 2 diabetes

Progressive deterioration of beta-cell function is proposed as a disease-related factor of sulphonylurea (SU) failure in type 2 diabetes. If it gradually worsens over time then disease duration may mirror the progressive beta-cell deterioration. The aim of the present study is to assess whether or not disease duration is influential in remodelling the secretion pattern of insulin-like molecules and in glucose control of SU-treated type 2 diabetes. A research model is used to investigate proinsulin secreting capacity over time, using two groups of patients: i) disease duration <5 years (n=62), comprising SU responders (SUr; n=48) and SU failures (SUf; n=14); and ii) disease duration > or = 5 years (n= 37), comprising an SUr group (n=17) and an SUf group (n=20). Blood samples are taken at 0 h, 0.5 h 1 h, 2 h and 3 h during a standard oral glucose tolerance test and measured for glucose, total proinsulin (TPI), intact proinsulin (IPI) and specific insulin (SI) concentrations. Pairwise comparison of estimated marginal means of blood glucose, SI, IPI and TPI levels at each time point are carried out between groups and subgroups. (SUr vs. SUf). Homa insulin resistance index (IR index) is applied to analyse IR between the groups. It was found that patients with shorter disease duration had higher proinsulin (TPI and IPI) levels at all time points (P<0.05), together with a lower glucose level at 2 h and 3 h (P<0.05). Homa insulin index analysis showed no difference between the two groups (P=0.26). Results also showed that the SUr group had a significantly lower glucose level at Oh and 3h (P<0.05), although no significant difference in insulin and proinsulin levels was found between the SUr and SUf groups. In conclusion, proinsulin may play an important role in glucose control in SU-treated type 2 diabetes, but the effect is reduced in SUf patients.     

小腿内侧逆行筋膜岛状皮瓣修复足部软组织缺损

目的探讨小腿内侧皮瓣在修复足部软组织缺损方面的应用.方法设计应用小腿内侧逆行筋膜岛状皮瓣修复足部软组织缺损15例.其中,男11例,女4例;缺损原因电烧伤3例,皮肤肿瘤2例,慢性溃疡7例,化学烧伤2例,热压伤1例.结果15例病例皮瓣全部成活.足外形、感觉及行走的稳定性均恢复良好.结论小腿内侧逆行岛状皮瓣与足部皮肤组织类似,血运及神经支配有保证,成活率高;蒂部较长,操作简便;特别适用于足跟及底部软组织缺损的修复.     

6岁以下小儿头面部烧伤后体积变化的研究

为探讨小儿头面部烧伤后体积的变化,我们从1991年5月～1997年12月用陈壁教授提出热量计算小儿头面部体积的方法,对30例渡过休克期而生命体征平稳的6岁以下合并头面部重度烧伤的患儿在烧伤后48小时及5天～7天分别出量计算头面部体积,得出每1％头面部烧伤创面每kg体重烧伤后48小时内体积增加6.05±1.08cm3.明显高于目前习用输液公式伤后48小时每kg体重量1％烧伤面积2.7～3ml.为了准确计算此类病人休克期液体丢失量,建议分别计算头面部和其他部位创面伤后丢失量,从而指导临床治疗,提高救治水平.