低张结肠水灌肠CT检查诊断结肠癌的价值

目的 :探讨低张结肠水灌肠CT检查对结肠癌的CT表现及诊断价值。材料和方法 :肌注 65 4 2 2 0mg后 ,结肠灌注微温生理盐水进行CT扫描。分析经手术病理证实的 3 8例结肠癌资料。结果 :CT显示肿瘤部位准确率为 10 0 % ,CT分期与手术分期符合率为 92 % ,低张结肠水灌肠CT可见病变肠壁增厚、突出腔内的肿块、肠腔狭窄及其浆膜面毛糙 ;可见结肠癌侵犯邻近器官、淋巴结肿大及远处转移。结论 :低张结肠水灌肠CT检查对结肠癌的术前诊断有很大的价值。     

胸腔镜辅助小切口手术诊治肺周围型结节

目的探讨胸腔镜辅助小切口手术在诊断和治疗肺周围型结节病变中的临床应用价值。方法胸腔镜辅助小切口手术诊治肺周围型结节55例，其中单发结节54例，多发结节1例。肺楔形切除术23例；肺叶切除联合淋巴结清扫治疗原发性肺癌32例，采用常规开胸手术器械及胸腔镜用器械切除肺叶，自制淋巴结摘除钳完成淋巴结清扫。结果55例均在胸腔镜下完成手术。手术时间35～180min，平均109min，术中出血量50～400ml，平均122min。均未输血，1例术后漏气术后32d出院，1例切口延迟愈合，术后19d出院，余53例术后住院4～11d，平均8．3d。无严重并发症。术后病理：良性病变15例，原发性肺癌38例，非典型性腺瘤样增生1例，转移性肺癌1例。良性病变行肺楔形切除术，32例原发性肺癌行解剖学肺叶切除联合淋巴结清扫，4例肺癌胸膜广泛播散未手术处理，2例肺癌因肺功能差行姑息性肺楔形切除。结论胸腔镜辅助小切口手术有助于明确诊断肺周围型结节病变，治疗临床早期原发性肺癌的长期疗效有待随访观察。     

霍奇金淋巴瘤组织中H／RS细胞与其背景细胞的微切割及其IgH基因重排检测

目的 从基因水平探讨霍奇金淋巴瘤(HL)组织中H／RS细胞(Hodgkin and Reed-Sternberg cells)是否起源于B细胞、H／RS细胞的克隆性以及与背景淋巴细胞的相互关系。方法 对33例经典霍奇金淋巴瘤(cHL)石蜡刮片组织进行IgH基因重排分析，并对其中6例重排阳性的病例经B细胞特异性激活蛋白(BSAP)免疫标记，将标记阳性的H／RS细胞和背景淋巴细胞进行微切割后进一步行IgH基因重排分析。结果 16例石蜡刮片组织IgH基因重排阳性。对6例经BSAP标记的cHL成功进行了微切割，其中19管H／RS细胞中，有14管出现重排阳性，细胞数目不同的各管阳性率无显著性差异(P=0．290)；12管背景淋巴细胞有2管出现重排阳性，H／RS细胞与背景淋巴细胞的阳性率有显著性差异(P=0．002)。结论 支持H／RS细胞来源于B细胞的理论，认为部分背景淋巴细胞可能具有瘤性增生活性，参与H／RS细胞的前体细胞组成。     

北京自然人群载脂蛋白E基因多态性频率分布研究

应用聚合酶链反应 限制性片段长度多态性技术 (PCR RFLP) ,以北京自然人群为基础 ,采用分层随机抽样的方法进行横断面研究 ,对 1 0 46人进行apoE基因分型 ,并分析不同特点人群apoE基因频率分布特点。结果表明 :1 )本组人群ε2、ε3、ε4基因频率分别为 9.1 %、81 .2 %和 9.7% ,男女和各年龄组间基因频率无显著差异 ;2 )与欧美国家相比 ,本组人群ε2基因频率增高 ,ε4频率减低 ,与日本人群相比也有相同趋势 ;3 )在空腹血糖受损及糖尿病人群中ε2频率明显增高 ;4)在高胆固醇血症人群中ε2频率减低、ε4基因频率增高     

内镜治疗甲状腺功能亢进7例报告

目的总结内镜治疗甲状腺功能亢进（甲亢）的经验。方法7例原发性或继发性甲亢，内镜经胸人路行甲状腺全切或次全切除术。结果7例手术均成功，无中转开放手术。手术时间130～260min，平均168min；术中出血量10～200ml，平均70ml。无喉返、喉上神经损伤，无术后出血等并发症。术后恢复良好，近期随访美容效果满意。随访1～12个月，平均5．1月，无复发，2例出现甲状腺功能低下，1例在术后2个月时恢复。结论内镜治疗甲亢技术安全、可行。除常规手术前甲亢准备外，必须行CT检查确认腺体大小，确定残留腺体的大小和位置。     

微波凝固对变应性鼻炎患者T淋巴细胞亚群的影响及意义

目的　探讨常年性变应性鼻炎 (PAR)患者细胞免疫功能状态及微波凝固治疗的作用机制。方法　观察组 2 5例PAR患者分别于微波治疗前以及治疗 1个月后应用免疫组化法检测鼻粘膜上皮和外周血CD3、CD4、CD8、CD4/CD8水平。健康对照组 1 5例亦作相应检测。结果　PAR患者治疗前鼻粘膜及外周血CD3、CD4明显高于正常人 ,CD8低于正常人 ,CD4/CD8比值升高 ,与正常人比较差异有显著性 (P <0 .0 5)。微波治疗后CD4明显减少 ,CD8升高 ,CD4/CD8接近于健康对照组。结论　PAR患者存在明显的细胞免疫功能障碍 ;微波局部凝固治疗可改善PAR患者的细胞免疫状况。     

Extracellular signal regulated kinases 1/2 signal pathway and responses of astrocytes after diffuse brain injury

BACKGROUND: The treatment of diffuse brain injury during an acute period is focused on relieving degrees of secondary brain injury. Generation and development of pathological changes of secondary brain injury depend on signal conduction, so down-regulating over response of astrocyte through interfering a key link of signal conduction pathway may bring a new thinking for the treatment of diffuse brain injury. OBJECTIVE: To observe the effect of over activity of extracellular signal regulated kinases 1/2 (ERK1/2) signal pathway on the response of astrocyte during an acute period of diffuse brain injury. DESIGN: Completely randomized grouping and controlled animal study. SETTINGS: Department of Neurosurgery, the Third Affiliated Hospital, Nanchang University; Department of Neurosurgery, Union Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology. MATERIALS: A total of 158 healthy male SD rats, of 11 weeks old, weighing 320–370 g, were provided by Experimental Animal Faulty, Tongji Medical College, Huazhong University of Science and Technology. Rabbit-anti-phosphorylated ERK1/2 (pERK1/2) polyclonal antibody was provided by R&D Company; rabbit-anti-glial fibrillary acidic protein (GFAP) polyclonal antibody, SP immunohistochemical kit and horseradish peroxidase (HRP)-labeled goat-anti-rabbit IgG by Santa Cruz Company; specific inhibitor U0126 of ERK1/2 signal pathway by Alexis Company. METHODS: The experiment was carried out in the Laboratory of Neurosurgery, Union Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology from September 2004 to March 2006. ① Detection of pERK1/2 expression: A total of 110 rats were randomly divided into sham operation group (n =5), model group (n =35), high-dosage U0126 group (n =35) and low-dosage U0126 group (n =35). Rats in the sham operation group were only treated with incision of epicranium and fixation of backup plate, but not hit. Rats in the model group were used to establish diffuse brain injury models based on Marmarou free falling body without drug intervention. Rats in the high- and low-dosage U0126 groups were injected into caudal vein with 0.1 and 0.05 mg/kg U0126, respectively, and then, rats were hit to establish injured models. Every 5 rats were collected from model, high- and low-dosage U0126 groups at 5, 30 minutes, 3, 12, 24, 72 hours and 7 days after diffuse brain injury to detect pERK1/2 expression in cortex of parietal lobe based on Western blot technique. ② Distribution of pERK1/2 and positive GFAP cells in brain tissue: Another 48 rats were randomly divided into sham operation group (n =3), model group (n =15), high-dosage U0126 group (n =15) and low-dosage U0126 group (n =15). The intervention and administration were dealt as the same as those mentioned above. Every 3 rats were collected from model, high- and low-dosage U0126 groups at 30 minutes, 3, 12, 24 and 72 hours after model establishment to observe the distribution of pERK1/2 and postive GFAP cells in brain tissue which was cut from coronal section at Bregma –4.8 mm layer with immunohistochemical staining. MAIN OUTCOME MEASURES: pERK1/2 expression in cortex of parietal lobe and distribution of pERK1/2 and positive GFAP cells in brain tissues. RESULTS: ① pERK1/2 expression: After diffuse brain injury, pERK1/2 expression in cortex of parietal lobe was rapidly increased in the model group, reached at peak at 5 minutes and then decreased gradually. But the expression was still in a high level until the 72nd hour and fallen to the basic level on the 7th day. pERK1/2 level was lower in high- and low-dosage U0126 groups than that in model group at various time points (P < 0.01); meanwhile, pERK1/2 level was lower in high-dosage U0126 group than that in low-dosage U0126 group. The results showed that there was a certain dosage dependence on pERK1/2 expression. ② Distribution of pERK1/2 and positive GFAP cells in brain tissue: Positive expression of pERK1/2 lasted in brain tissue from 30 minutes to 72 hours after diffuse brain injury (P < 0.05). In addition, from 30 minutes to 3 hours, brown-yellow stained cells were mainly distributed in plasma, but rarely in nucleus. A lot of positive cells had tree-like apophysis, which was similar to neurons. With the time passing by, more and more nuclei manifested positive stains; moreover, nuclei mainly manifested positive staining until 24 hours after diffuse brain injury. Immune-positive pERK1/2 cells were widely distributed in brain tissue, especially mainly in binding site between deep cortex and cerebral white matter, and then in hippocampus. In addition, ependymal cell and vascular endothelial cells of choroids plexus also manifested strongly positive staining. As compared with model group, positive cells were decreased gradually in high- and low-dosage U0126 groups. However, number of positive cells was less in high-dosage U0126 group than that in low-dosage U0126 group. CONCLUSION: Diffuse brain injury strongly induces the activity of ERK1/2 signal pathway and response of astrocyte; in addition, U0126 can inhibit response of glial cells during an acute period, and the effect manifests dosage dependence.     

原发性前列腺印戒细胞癌(1例报告并文献复习)

目的探讨原发性前列腺印戒细胞癌的临床特征。方法回顾性分析1例原发性前列腺印戒细胞癌患者的临床资料,并结合文献进行复习讨论。结果患者前列腺穿刺活检病理报告为前列腺印戒细胞癌,免疫组织化学检查示PSA( ),PAS、CEA、LCA、CKH(-),行双侧睾丸切除术和氟他胺治疗,术后1月死于肺部转移。结论原发性前列腺印戒细胞癌来自前列腺腺泡上皮,确诊依靠病理组织学和免疫组化检查。临床罕见,恶性程度高,预后较差。     

磁场对荷瘤小鼠TNF及TNFR水平的影响

目的　观察磁场对荷瘤鼠瘤组织内肿瘤坏死因子 (TNF)及肿瘤坏死因子受体 (TNFR)的影响。方法　采用磁场照射荷瘤小鼠瘤区。结果　磁疗组小鼠体内TNF活性明显增强 ,TNFR表达量增多 ,与非磁疗组相比 ,差异有高度显著性 (P <0 .0 1)。结论　磁场具有增强荷瘤小鼠TNF活性并促进TNFR表达的作用。     

脑创伤致迟发性脑梗死临床分析

目的探讨脑创伤后迟发脑梗死的发生机制,临床诊断及救治措施。方法对32例经影像学证实为颅脑创伤后迟发脑梗死患者的临床资料进行回顾分析。结果出院时按GOS标准评价:恢复良好12例、中残5例、重残4例、植物生存3例,死亡8例,其中非手术治疗20例,存活14例,死亡6例,死亡率30%;手术治疗12例,存活10例,死亡2例,死亡率17%。结论及时诊断与合理有效的治疗是提高脑创伤后迟发性脑梗死的治愈率及提高患者生存质量的关键。