Easier node dissection after chemoradiotherapy for lung cancer with collagen insertion at mediastinoscopy

Objective: Induction chemoradiotherapy followed by anatomical resection is a current therapeutic strategy for non-small-cell lung cancer with mediastinal node involvement. Dense peritracheal fibrosis and sclerosis after chemoradiotherapy cause difficult mediastinal node dissection. We evaluated a novel technique to make the mediastinal node dissection easier after induction therapy. Methods: At the end of mediastinoscopic node biopsy for staging of lung cancer, cotton-type collagen was inserted anterior and lateral to the trachea in patients with pathologically confirmed mediastinal node involve-ment (n=45). The induction therapy consisted of concurrent use of platinum-based chemotherapy and hyperfractionated radiotherapy. After the chemoradiotherapy all patients underwent a pulmonary resection with complete mediastinal node dissection 7–12 weeks after the collagen insertion. Surgical findings of the mediastinum and the time for node dissection were compared with those without collagen insertion at mediastinoscopy after chemoradiotherapy (n=5). Results: All five patients without collagen insertion showed sclerotic and fibrotic change of mediastinal nodes with severe adhesion to the trachea. In 42 of 45 patients with collagen insertion (93.3%) the collagen remained unabsorbed and separated the mediastinal nodes from the trachea. Mediastinal node dissection was easily accomplished by removing mediastinal tissues lateral and anterior to the collagen. The rate of mediastinal node separation was significantly higher with collagen insertion than without (p< 0.0001). The times for node dissection in patients with and without collagen insertion showed no significant difference. Conclusion: Cotton-type collagen insertion at staging mediastinoscopy for lung cancer separates the mediastinal nodes from the trachea and makes the node dissection easier after induction chemoradiotherapy.     

自发性气胸的临床特点与治疗对策

目的通过对多种自发性气胸的临床表现采用不同的治疗方法,达到治愈。方法根据不同临床表现及气胸压缩程度采取人工抽气、闭式引流术、胸膜粘连术等检测效果。结论96例病人中治愈90例,说明采用适用的方法可有效地治疗自发性气胸。     

2型糖尿病患者绝经期骨密度与甲状旁腺素、雌激素相关性研究

目的 观察2型糖尿病妇女绝经期骨密度与甲状旁腺素、雌激素相关性研究.方法 测定绝经期2型糖尿病妇女伴骨质疏松（A）组及绝经期2型糖尿病妇女无骨质疏松（B）组的左侧髋部股骨颈、大转子、华氏三角区、及腰椎L2～L4正侧位的骨密度和血清中骨代谢指标,如：骨钙素、碱性磷酸酶、钙、磷、甲状旁腺素、雌二醇、Ⅰ型胶原羧基末端终肽（β-CTx）的浓度,对骨密度与多个变量之间的关系进行相关分析,并对（A）组血清中的甲状旁腺素、雌二醇、骨钙素、β-CTx与不同部位的骨密度之间的关系进行多元逐步回归分析.结果绝经期2型糖尿病妇女（B）组的腰椎、大转子、华氏三角区、股骨颈等骨密度指标明显低于对照组（A）（P＜0.05）;2型糖尿病绝经期妇女血清中雌二醇水平与腰椎L2～L4骨密度呈正相关（P＜0.032）;甲状旁腺素水平与股骨颈骨密度呈负相关（P＜0.034）.结论 绝经期2型糖尿病患者甲状旁腺素和雌激素水平与骨密度密切相关,分别可以用于预测骨质疏松发生的不同部位.     

人冠状动脉的生物力学特性 Ⅱ.二维载荷下的应力-应变关系

本文在生物软组织试验台上,对7例成人的左冠状动脉前室间支、旋支、右冠状动脉、胸廓内动脉以及大隐静脉进行了二维载荷的力学试验。上述血管的二维载荷下的应力-应变关系以指数型应变能函数表达。讨论了血管二维材料常数的意义。     

Active production of anti-human T-lymphotropic virus type I (HTLV-I) IgM antibody in HTLV-I-associated myelopathy

We investigated the presence of anti-human T-lymphotropic virus type I (HTLV-I) IgM in sera and cerebrospinal fluid from patients with HTLV-I-associated myelopathy (HAM) by Western blot analysis. Analyses of 36 serum samples revealed that most patients (31/36; 86.1%) had anti-HTLV-I IgM, whereas only four of 23 (17.4%) HTLV-I carriers had it. In studies of cerebrospinal fluid, anti-HTLV-I IgM was detected in 24 of 36 (66.7%) HAM patients, whereas none was detected in nine HTLV-I carriers. The differences were statistically significant (p less than 0.01). These results suggest that persistent active replication of HTLV-I occurs in the central nervous system as well as in the peripheral blood of HAM patients, and may contribute to the development of HAM.     

Multidrug transport in human glioblastoma cells is inhibited by transforming growth factors type beta 1, beta 2, and beta 1.2

The transforming growth factors type beta 1, beta 2, and beta 1.2 suppress multidrug transport in human pat-1 glioblastoma cells and even in cells that strongly over-express mdr genes and are resistant to inhibition of multidrug transport by chemosensitizers. Thus, inhibition of multidrug transport by cytokines might be a new approach to increase cellular accumulation of chemotherapeutic agents in multidrug resistant glial tumor cells. Interestingly, a member of the more distantly related decapentaplegic subgroup of transforming growth factors, the bone morphogenetic protein BMP 2, did not inhibit multidrug transport.     

ABO血型与肝炎病毒感染关系的探讨

目的：探讨ABO血型与肝炎病毒感染的关系，方法：应用疾病关联分析方法对HBsAg和,抗－HCV阳性献血者与同期健康献血者的ABO血型资料进行比较分析。结果：ABO血型与HBsAg和抗－HCV阳性率之间无显著性相关关系（P＞0．05），结论：乙型肝炎和丙型肝炎病毒感染与ABO血型无显著性相关。     

窒息鼠脑组织型纤溶酶原激活物活性变化与脑水肿的关系

目的：探讨窒息对鼠脑分泌组织型纤溶酶原激活物（TPA）的影响与脑水肿的关系。方法：通过“延迟剖宫产术”致胎鼠宫内窘迫，实验分空白对照组，窒息15min组，窒息30min组，窒息15min复氧30min组，窒息30min复氧30min五个实验组，每组各取8例测试脑组织TAP的活性及含水量，结果：窒息后鼠脑TPA活性与含水量均升高（P＜0．01），结论：窒息可致TAP活性增高，同时发生脑水肿，高活性的TPA可能是脑缺氧缺血致不可逆神经元损伤的一个重要媒介。     

Herpes simplex virus latency in the nervous system – a new model

Permissive herpes simplex virus (HSV) infection in tissue culture results in host cell destruction. Latent HSV infection in vivo occurs in neurons of peripheral sensory ganglia (PSG) and it therefore can not take place in neurons in which the virus has completed a lytic replication cycle similar to that present in vitro. Our hypothesis, based on experimental data and observations in humans, suggests that establishment of latent infection and reactivation of HSV-1 does not involve neuronal cell loss. Latency is established in neurons in which the virus does not replicate and is determined, in part, by the tissue levels of a herpes transactivating protein (Vmw65) that is a component of the viral tegument. We also suggest that reactivation of latent infection does not involve destruction of neurons and is due to replication of virus at the peripheral mucocutaneous tissues to where virus or viral DNA have been transported from the nervous tissue. Alternatively, reactivation is initiated in the PSG using a replication cycle which does not involve irreversible damage to neurons. This model explains the lack of damage to neurons which continue to serve as permanent reservoirs of latent virus for the entire life of the host.     

原发性肝癌患者乙型及丙型肝炎病毒感染的检测

目的　调查原发性肝癌患者乙型及丙型肝炎病毒感染情况。　方法　采用免疫组织化学 SP法检测15 7例原发性肝癌患者乙型肝炎病毒 (HBV)及丙型肝炎病毒 (HCV)感染情况 ,每例患者均有血清学检测资料 ,另取 30例良性肝病组织作对照 ,所有数据用卡方检验。　结果　 15 7例原发性肝癌患者中 HBV感染阳性率为31.8% (5 0 / 15 7) ,HCV感染阳性率为 5 1.0 % (80 / 15 7) ,其中 10 7例原发性肝细胞癌 HBV、HCV感染阳性率分别为39.3% (42 / 10 7) ,4 5 .8% (49/ 10 7) ,5 0例胆管细胞癌 HBV、 HCV感染阳性率分别为 16 .0 % (8/ 5 0 ) ,6 2 .0 %(31/ 5 0 ) ,原发性肝细胞癌、胆管细胞癌 HBV、HCV重叠感染率分别为 2 7.1% (2 9/ 10 7) ,14 .0 % (7/ 5 0 ) ,良性肝病组HBV、HCV感染阳性率分别为 16 .7% (5 / 30 ) ,30 .0 % (9/ 30 )。原发性肝细胞癌 HBV感染、胆管细胞癌 HCV感染率高于良性肝病组 ,差异均有显著性 (P<0 .0 5 )。原发性肝细胞癌 HBV、HCV血清学检测阳性率分别为 87.8%(94 / 10 7) ,13.1% (14 / 10 7) ,胆管细胞癌 HBV、HCV血清学检测阳性率分别为 6 8.0 % (34/ 5 0 ) ,16 .0 % (8/ 5 0 )。　结论　原发性肝癌与 HBV、HCV的感染有密切关系