CD_(44)v_6与肿瘤侵袭和转移研究进展

CD44是由单一基因所编码的具有高度异质性的单链膜表面糖蛋白家族,介导细胞与细胞、细胞与细胞外基质之间的黏附作用,其拼接变异体的不同构成了其基因产物的多样性;尤其拼接变异体V6(CD44v6)被认为具有致瘤性;CD44v6在一定程度上参与了肿瘤的发生发展,是预后因子之一,并且可能作为肿瘤进展的标志物。CD44v6的过表达与肿瘤的侵袭、转移和临床分期有关。对CD44v6的检测不仅能预测患者的预后,而且还可为肿瘤的个体化治疗直接提供信息。     

CD44V6，HIF-1α，VEGF与非小细胞肺癌侵袭和转移的关系

目的 探讨CD44V6、HIF-1α、VEGF在非小细胞肺癌(NSCLC)中的表达与非小细胞肺癌侵袭和转移的关系.方法 通过免疫组化的方法(SP法)测定粘附分子 (CD44V6 )、血管内皮细胞生长因子(VEGF)和缺氧诱导因子(HIF-1α)在非小细胞肺癌组织中的表达情况.结果 CD44V6 、HIF-1α和VEGF在NSCLC组织中阳性表达率分别为85.07%、61.19%和74.63%;CD44V6 、HIF-1α、VEGF蛋白表达与肿块大小、病理类型、组织分程度、淋巴结转移、临床分期密切相关,并且在非小细胞肺癌中的表达相互之间存在相关性;这3种蛋白的共表达与淋巴结转移、临床分期相关.结论 CD44V6 、HIF-1α和VEGF在NSCLC中的阳性表达与NSCLC的侵袭和转移密切相关.     

训练Wistar大鼠急进高原并运动力竭后肾组织病理变化及其防护

目的通过观察训练大鼠急进高原模型肾组织学形态改变和血中肾功能水平以探讨训练对大鼠肾组织的损伤及防护效果。方法于海拔1520m环境设实验组（EG），予中药抗疲Ⅰ号加入常规饲料中喂养，对照组（CG）常规饲料喂养。EG、CG各40只游泳训练4周后，各选35只3h急进海拔3850m环境静息1．5h，从中各选10只作为静息对照采集标本；EG、CG各20只游泳至力竭后，1h、24h采集标本。结果EG与CG相比，血中肾功能水平均有显著性差异；EG肾组织结构正常，结构核清晰、无变性；CG组大鼠运动力竭24h后则出现肾组织损害、肾组织结构紊乱、肾区小管有脱落管型生成等。结论非防护的训练大鼠急进高原后肾功能有损伤，有肾水肿发生，血中肾功变化可以揭示组织损害的程度。提示过度训练、改变运动集训环境或进入高海拔地区作业训练更要特别注重加强劳动和训练防护。     

异常黑胆质性哮喘与ECP、IgE及FEV1的关系研究

目的探讨异常黑胆质性哮喘与嗜酸细胞阳离子蛋白（ECP）、血清总免疫球蛋白E（T-IgE）、血清特异性免疫球蛋白E（S-IgE）、第1秒用力呼气流量（FEV1）之间的关系。方法对76例支气管哮喘患者按维医体液论进行辨证分型，异常黑胆质性哮喘组30例，非异常黑胆质性哮喘组46例，并与正常对照组89例进行对照，分别测定各组血清ECP、T-IgE、S-IgE、FEV1水平。结果血清ECP、T-IgE、S-IgE变化在3组间有显著差异（P〈0．01），异常黑胆质性哮喘组明显高于正常对照组（P〈0．01），异常黑胆质性哮喘组明显高于非异常黑胆质性哮喘组（P〈0．01），非异常黑胆质性哮喘组明显高于正常对照组（P〈0．01），FEV1水平变化在3组间有显著性差异（P〈0.01），异常黑胆质性哮喘组明显低于非异常黑胆质性哮喘组和对照组（P〈0．01），非异常黑胆质性哮喘组也低于正常对照组（P〈0．01）。结论异常黑胆质性哮喘的气道炎症程度更明显，阻塞情况更严重。     

儿童呼吸道感染肺炎衣原体的检测及意义

目的探讨肺炎衣原体(简称CPn)在儿童急性呼吸道感染中的发病情况及临床特征,为临床诊断及治疗提供参考依据。方法急性呼吸道感染患者142例,健康儿童52例,取静脉血,采用酶联免疫吸附试验(ELISA)检测CPn。结果观察组CpnIgG阳性者30例(占21.1%),对照组4例(占7.7%),两组比较差异有统计学意义(P<0.005)。观察组中有CPn急性感染抗体的有22例(占15.5%),对照组中无CPn急性感染,两组比较差异有统计学意义(P<0.005)。下呼吸道感染患者的CPn急性感染率为17.8%,上呼吸道感染患者为4.2%,两组比较P<0.05。CPn急性感染的临床表现无特征性。结论CPn是儿童急性呼吸道感染的重要致病原。     

老年病人压疮危险因素分析及护理对策

目的：探讨老年病人压疮高发危险因素并提出相关护理对策。方法：分析30例老年压疮病人相关资料,使用诺顿评分（NORTON）评估压疮高发因素,分类评价各项相关指标与压疮发病的关系。结果：30例老年压疮病人诺顿评分平均（16.97±3.24）分,其中,3人（10%）≤13分,有很高风险,14人（46.7%）14～18分,有较高风险,5人（16.7%）19～23分,有中等风险;30例老年病人不同程度存在中重度营养不良、低蛋白血症、血清钙降低、肌张力改变、大小便失禁等情况;30例病人均长期卧床,丧失生活自理能力,住院后接受输液治疗,其中10例因躁动需要约束四肢等,这些因素均与压疮的发生相关。结论：应针对老年病人压疮高发因素作好积极的预防和护理措施,提高老年病人生存质量。     

胸腺瘤治疗的现状和进展(附127例临床报告)

目的 总结胸腺瘤的诊断与治疗经验.方法 复习近年文献,结合我科127例胸腺瘤的临床资料,对其手术途径,单纯胸腺瘤和、扩大胸腺瘤切除术=胸腺瘤综合治疗现状和回顾性分析.结果 胸部X线,CT等影像学检查是本病诊断的主要手段.重症肌无力是常见伴随症状,发生率为43.3%(55/127).扩大胸腺瘤切除治疗效果优于单纯胸腺瘤切除.Ⅱ期以上病变进行放疗或化疗及综合治疗可提高疗效.结论 胸腺瘤不宜行单纯切除,无论病理分期如何均应行扩大切除,有利降低复发率.术中发现胸腺肿瘤有明显外侵或累及器官,术后应辅以综合治疗(化疗或放化疗),以提高疗效.     

托吡酯片与丙戊酸钠缓释片治疗儿童癫痫的最小成本分析

目的:探讨2种药物治疗儿童癫痫的成本和效果。方法:72例癫痫患儿分别应用托吡酯片与丙戊酸钠缓释片,观察疗效, 并运用药物经济学原理进行最小成本分析。结果:2种药物有效率分别为76．2％、83．3％(P>0．05);治疗成本分别为1 305．00元、 588．60元。结论:丙戊酸钠缓释片治疗儿童癫痫的经济效果优于托吡酯片。     

Proliferation, development and DNA adduct levels in the mammary gland of rats given 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine and a high fat diet

2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) is a heterocyclic amine derived from cooked meat that is a mammary gland carcinogen in rats. A carcinogenic dose-regimen of PhIP (75 mg/kg, p.o., 10 doses, once per day) was administered to 43-day old female Sprague-Dawley rats, and the rats were then placed on a defined high fat (23.5% corn oil) or low fat (5% corn oil) diet for up to 6 weeks. At various times after carcinogen and diet, and prior to carcinogenesis, we examined the percentage of proliferating cells in terminal end bud (TEB) epithelial structures of the rat mammary gland by proliferating cell nuclear antigen staining, mammary gland architecture by whole mounting, and PhIP-DNA adduct levels in mammary epithelial cells by the 32P-post-labeling assay. Immediately after dosing, the percentage of proliferating epithelial cells in TEBs was significantly higher in PhIP-treated rats than in control rats receiving vehicle only [7.5 +/- 0.9% (n = 99) versus 4.2 +/- 0.6% (n = 127), respectively]. The mammary glands of PhIP-treated rats showed a significantly lower density of alveolar buds (ABs) and a higher density of TEBs than control rats, which suggests that PhIP exposure partially inhibited the normal glandular differentiation of TEBs to ABs. After 6 weeks on the diet, proliferation in TEBs was statistically higher in rats given PhIP plus a high fat diet than in rats given vehicle plus a low fat diet. The mammary glands from rats on a high fat diet also showed a statistically higher density of TEBs when compared with rats on a low fat diet [2.08 +/- 0.34% versus 1.04 +/- 0.20%, respectively (n = 6)]. PhIP-DNA adduct levels were relatively high in mammary epithelial cells of treated rats. At 3 h after the last dose of PhIP, DNA adduct levels [relative adduct labeling (RAL) x 10(7), mean +/- SE] were 10.5 +/- 1.7 (n = 8) and 0.9 +/- 0.2 (n = 7) in epithelial cells isolated from mammary gland and in the liver, respectively. DNA adduct removal rates from the mammary gland were not different between rats on the high fat and low fat diets. Adducts were still detected after 6 weeks on either diet. Thus, events that occurred prior to neoplasia in the mammary glands of PhIP-treated rats include formation of PhIP-DNA adducts at relatively high levels, and enhanced proliferation in TEBs (putative sites of origin of mammary gland carcinomas) and partial inhibition of TEB differentiation. The high fat diet, a promoter of PhIP-induced mammary gland carcinogenesis, appeared to sustain the proliferative effect of PhIP in mammary gland TEBs at a time when PhIP- DNA adducts are still detectable. These early events may contribute to the targeting and carcinogenicity of PhIP to the mammary gland of rats.