处女膜修补手术及麻醉方法的改进

目的；增大处女膜粘膜瓣的接触面，减少因麻醉造成的处女膜粘膜水肿，提高修复手术的成功率。方法：手术全部采用1％的卡因行粘膜表面麻醉。53例采用瓦合粘膜瓣法，3例用瓦合粘膜瓣联合阴道粘膜瓣修复法。结果：56例术后一月随访，53例处女膜孔径为一指，成功率94．64％。结论：采用1％的卡因粘膜表面麻醉，瓦合粘膜瓣法及瓦合粘膜联合阴道粘膜瓣修复法对处女膜修复是行之有效的。     

近端/远端复合肌肉动作电位振幅比率在术后面神经功能评估上的价值

目的 探讨近端/远端复合肌肉动作电位振幅比率在术后面神经肿瘤侵犯段功能评估上的价值和对早期面神经修复的指导意义。方法 比较术末面神经近端/远端复合肌肉动作电位振幅比率和术后2周、6个月患侧面神经功能的H-B分级之间的关系。结果 术后6个月面神经H-B分级恢复到Ⅰ-Ⅱ级者,术末近端/远端复合肌肉动作电位振幅比率均>0.3。结论 术末面神经近端/远端复合肌肉动作电位振幅比率是判断术后面神经远期功能,特别是肿瘤侵犯段功能的重要指标,为术中直接修复面神经提供了指导依据。     

颅脑外伤后肢体痉挛状态的显微外科治疗

目的 探讨显微外科治疗颅脑外伤后肢体痉挛状态的疗效.方法 回顾分析2006年7月至2008年7月实施的21例显微外科治疗颅脑外伤后肢体痉挛状态,根据不同病例采用相应的选择性周围神经部分切断术,包括:胫神经、肌皮神经、正中神经、尺神经和腰骶段脊神经后根,共计50个肢体.结果 术后随访2～24个月,全部患者术后立即感相应肢体痉挛状态缓解,随访期间缓解率为98%(49/50).随访期间运动功能改善率为86%(18/21),生活质量提高率为95%(20/21).术后发生肢体麻木、疼痛等感觉异常26个(52%),肌力下降18个(36%),随访期间均见好转.术后痉挛状态复发1个(2%).结论 选择性周围神经部分切断术是治疗颅脑外伤后肢体痉挛状态安全有效的方法.选择适应证及手术时机和术后坚持康复训练是保证疗效的关键.     

原发性眼眶静脉曲张的CT和MRI表现

目的探讨原发性眼眶静脉曲张(POV)的CT及MRI表现。方法临床诊断的30例原发性眼眶静脉曲张患者,9例行CT横断位和冠状位扫描,21例行MR扫描,4例行CT和MR检查。结果30例中30只患眼,左眼18例,右眼12例,均为单侧发病。病变部位眼睑3例,眼眶前部1例,眼眶后部(球后)17例,眼睑和眼眶前部5例,眼睑、眼眶前部和眼眶后部2例,眼眶前部和眼眶后部2例。形态17例为不规则块状,4例为卵圆形,9例为不规则条状。CT冠状位,病变均显示为软组织密度,有明显强化;静脉石2例;眶骨受压变薄、眶腔扩大3例。MR扫描,颈部加压后25例均显示病变,11例呈等T1长T2信号,7例呈长T1长T2信号,1例呈等T1等T2信号,6例呈长T1长T2为主的混杂信号,增强的22例中,14例呈明显均匀强化,8例呈不均匀强化。结论CT横断位和冠状位及颈部加压或俯卧位MRI在原发性眼眶静脉曲张的诊断和鉴别诊断方面有重要价值。     

对数期继代对南方红豆杉细胞培养动力学的影响

目的 解决南方红豆杉细胞生长缓慢及代谢水平低下的问题。方法 对对数期(20d)和静止期(30d)的红豆杉细胞分别进行继代，在整个生长周期中测定了培养基中的碳源、氮源、磷酸盐的变化并分析了红豆杉细胞生长及紫杉醇的合成情况。结果 对数期继代细胞吸收碳源和硝态氮早于静止期继代的细胞，且前者的比生长速度是后者的1．5倍，紫杉醇含量提高了近4倍。结论 对数期继代有利于生物量的积累及紫杉醇的合成。     

CT增强扫描在评价NSCLC血管生成中的临床意义

目的　探讨非小细胞肺癌 (NSCLC)血管内皮生长因子 (VEGF)的表达水平与CT增强程度的关系 ,从影像学角度评价肿瘤血管生成在肺癌诊断、治疗及淋巴结转移中的临床价值。方法　对 30例NSCLC病人进行动态螺旋CT扫描 (SCT) ,测量病灶增强幅度 ,并利用免疫组化技术检测VEGF。对病灶增强值、VEGF阳性表达及淋巴结转移情况进行统计学分析。结果　 30例肺癌病人CT增强值均数为 (36 .2 8± 6 .41 )HU ,VEGF阳性表达 2 1例 ,阴性表达 9例。VEGF在中晚期的阳性表达高于早期病人 (Ρ<0 .0 5) ,淋巴结转移组高于非淋巴结转移组 (Ρ <0 .0 5) ;癌灶增强值与VEGF阳性表达、肿瘤分期及淋巴结转移亦呈正相关。结论　NSCLC的CT增强程度能够反映肿瘤的血管生成 ,并与淋巴结转移密切相关 ,有助于肺癌的诊断、TNM分期 ,而且可以从肿瘤分子生物学行为方面补充目前肺癌分期方法的不足     

嗜铬细胞瘤患者围手术期处理的改进

目的：探讨提高嗜铬细胞瘤患者围手术期安全性的措施。方法：对15例嗜铬细胞瘤患者、术前采用选择性α1受体阻滞剂多沙唑嗪控释片(可多华)控制高血压；11例患者采用3D DCEMRA进行肿瘤定位；术中均采用联合高容量血液稀释(AHH)和术中患者自体血回输纠正血容量。结果：除1例持续性高血压患者需联合钙离子拮抗剂和ACEI药物降压外．其余患者血压控制均为满意；根据3D DCEMRA定位选择手术径路者均顺利完成手术；AHH联合术中自体血回输使14例患者避免了异体输血。结论：本文围手术期处理改进．可多华可明显减少药物的不良反应；采用3D DCEMRA进行肿瘤定位，可增加手术安全性；AHH联合术中自体血回输可减少医疗成本和异体输血，以及由此而引起的并发症。     

角膜损伤后神经再生的实验研究

应用神经组织化学技术观察了兔角膜NA能神经及AchE阳性神经在角膜损伤后的再生,证实术后1月,两种神经均有再生轴突进入植片;术后3月可见交界区和植床内神经密度明显增加;同时,对术后两种神经再生的功能意义进行了讨论。     

Transient Brain Ischaemia Provokes Ca2+, PIP2 and Calpain Responses Prior to Delayed Neuronal Death in Monkeys

To clarify the mechanism of postischaemic delayed cornu Ammonis (CA)-1 neuronal death, we studied correlations among calpain activation and its subcellular localization, the immunoreactivity of phosphatidylinositol 4,5-bisphosphate (PIP₂) and Ca²⁺ mobilization in the monkey hippocampus by two independent experimental approaches: in vivo transient brain ischaemia and in vitro hypoxia-hypoglycaemia of hippocampal acute slices. The CA-1 sector undergoing 20 min of ischaemia in vivo showed microscopically a small number of neuronal deaths on day 1 and almost global neuronal loss on day 5 after ischaemia. Immediately after ischaemia, CA-1 neurons ultrastructurally showed vacuolation and/or disruption of the lysosomes. Western blotting using antibodies against inactivated or activated μ-calpain demonstrated μ-calpain activation specifically in the CA-1 sector immediately after ischaemia. This finding was confirmed in the perikarya of CA-1 neurons by immunohistochemistry. CA-1 neurons on day 1 showed sustained activation of μ-calpain, and increased immunostaining for inactivated and activated forms of μ- and m-calpains and for PIP₂. Activated μ-calpain and PIP₂ were found to be localized at the vacuolated lysosomal membrane or endoplasmic reticulum and mitochondrial membrane respectively, by immunoelectron microscopy. Calcium imaging data using hippocampal acute slices showed that hypoxia-hypoglycaemia in vitro provoked intense Ca²⁺ mobilization with increased PIP₂ immunostaining specifically in CA-1 neurons. These data suggest that transient brain ischaemia increases intracellular Ca²⁺ and PIP₂ breakdown, which will activate calpain proteolytic activity. Therefore, we suggest that activated calpain at the lysosomal membrane, with the possible release of biodegrading enzyme, will cause postischaemic CA-1 neuronal death.     

Influence of Osteoarthritis on Serum Marker Levels of Bone Formation and Resorption in Patients with Benign Prostatic Hypertrophy

Background :
The aim of this study was to investigate the influence of osteoarthritis of lumbar vertebrae on serum bone formation and resorption marker levels of patients with benign prostatic hypertrophy (BPH).
Methods :
Serum levels of carboxyterminal propeptide of type I procollagen (PICP), alkaline phosphatase (ALP), carboxyterminaltelopeptide of type I collagen (ICTP), and prostate-specific antigen (PSA) were examined in 40 patients with BPH, and the presence of osteoarthritis at the lumbar vertebrae of the patients was evaluated by plain x-ray-p.
Results :
Findings of osteoarthritis were observed in 23 of the 40 patients (58%), and 10 of the patients had severe osteoarthritis (involving at least 2 lumbar vertebral bodies). The serum levels of PICP, ALP, ICTP, and PSA of the patients without osteoarthritis findings were not different from those of the patients with osteoarthritis or severe osteoarthritis.
Conclusion :
The influence of osteoarthritis on serum bone formation and resorption marker levels of patients with BPH appears to be rather slight, if there is any influence at all.