胆囊息肉样病变临床病理与癌变关系的探讨

目的　探讨胆囊息肉样病变 (PLG)的临床及病理特征与癌变的关系。方法　回顾性分析经手术切除的15 0例PLG患者临床及病理资料。结果　胆固醇息肉 10 3例 ,占 6 8.7% ;炎性息肉、腺肌瘤及腺瘤样增生 30例 ,占2 0 .0 % ,无恶变 ;腺瘤 17例 ,占 11.3% ,其中癌变 6例 ,恶变率为 35 .0 %。6例癌变者年龄 5 2～ 6 9岁 ,均为广基单发 ,大小为 15mm× 18mm× 2 0mm以上。结论　PLG中年龄 >5 0岁、广基单发、直径 >10mm ,位于颈部的息肉均为癌变的高危因素 ,病理类型以腺瘤最易癌变 ,应早期手术切除。     

妇科肿瘤癌变的基础研究现状

恶性肿瘤是进行性发展的疾病 ,临床发现时多属晚期 ,治疗亦无过多回旋余地 ,病人的生活质量急剧下降 ,故早期诊断、早期治疗极为重要 ,而早期识别癌前病变则是防止肿瘤发生发展并做出早期治疗的重要环节。1　子宫颈癌子宫颈癌是危害妇女健康的主要恶性肿瘤之一 ,近 4 0年来国内外广泛开展了巴氏涂片和宫颈癌普查普治工作 ,使其发病率及病死率都明显下降。但近年来由于人乳头瘤病毒 (HPV)感染增多 ,宫颈癌发病率有明显上升趋势 ,且患者趋于年轻化 ,故针对癌前病变的基础研究引起人们普遍关注。1.1　HPV感染与宫颈癌前病变自 1976年首次从…     

幽门螺杆菌感染与c-myc、p16表达在胃粘膜癌变中的相关性研究

目的 观察胃粘膜癌变过程中幽门螺杆菌(Hp)和c-myc、p16的表达状况，探讨Hp感染与c-myc、p16表达在胃粘膜癌变中的相关性。方法 通过内镜活检和外科手术获取171例胃组织标本，Hp培养确定有无Hp感染；免疫组织化学法检测组织标本中c-myc、p16表达。结果 胃癌(GC)组织中c-myc表达率最高，慢性浅表性胃炎(CSG)和慢性萎缩性胃炎(CAG)伴轻度肠化(IM)组p16表达率显高于其它各组(P＜0．05)。在CAG伴中、重度IM、异型增生(Dys)组中，Hp阳性亚组的c-myc表达率显高于Hp阴性亚组(P＜0．01)，p16阳性表达率显低于Hp阴性亚组(P＜0．01)。结论 Hp感染可能通过激活c-myc、抑制p16，刺激胃粘膜过度增殖，使其具有较高恶变倾向。     

白三烯拮抗剂ONO-1078的一般神经药理特点

目的　观察白三烯拮抗剂ONO-1078对小鼠的一般神经药理作用,评价其对中枢的安全性。方法　测定自发活动、运动及协调能力试验、水迷宫试验、跳台实验以及镇痛试验等,研究ONO-1078(0.2,1.0,5.0mg·kg^-1,ip)对小鼠神经活动的影响。结果　大剂量ONO-1078( 5.0mg·kg^-1)对小鼠自发活动有抑制作用,但是未观察到其它明显的神经作用。结论　ONO-1078对中枢神经系统作用轻微,提示抗脑缺血应用时对中枢神经系统有较好的安全性     

药品上市后的监测(续)

药品不良反应(ADR)的监测,在欧洲国家也习惯称为“上市后药物监测”,以1964年英国黄卡制度(Yellow Card System)的问世而宣告诞生。ADR的监测方法有自发报告系统(Spontaneous reportingsystem,SRS)。集中(或特殊)报告系统(Intensive Re-porting System)、建立数据库和流行病学研究方法等多种方式。由于SRS一直是ADR监测的基本方式,近年来似乎已习惯于把一般的ADR监测看作是SRS。     

Effects of Imbalance of Apoptosis and Proliferation on Large Bowel Carcinogenesis in Mice

OBJECTIVE To observe the pattern of changes in the proliferation and apoptosis at different stages of large bowel carcinoma in mice, and to explore the effects of the imbalance of apoptosis and proliferation at different stages of large-intestine carcinogenesis.METHODS An experimental animal model for large intestine carcinogenesis of KUNMING-strain mice was used. The carcinomas were induced by subcuteneous injection of dimethylhydrazine (DMH) and the distribution and density changes of proliferating and apoptotic cells observed through multistages toward cancer formation. The animals were killed in groups at the 12th, 18th, 24th,and 32nd weeks of carcinoma induction. The apoptotic and proliferating cells were labeled separately using TUNEL and PCNA immunohistochemical staining methodsRF, RESULTS In the normal mouse mucosa, all the apoptotic cells were situated in the superficial layers, however, the proliferating cells were situated in the basement layers, and the amount of both were small. In the early stage of carcinoma induction, the proliferation and the apoptotic cells slightly increased in amount, but there were no obvious changes in their ratio. In the medium stage, the densities of both distinctly increased, but there were no obvious changes in the ratio. In the late stage, the densities of the proliferating and the apoptotic cells in the non-carcinoma mucosa were higher than those at other stages. The proliferating cells in the dysplastic mucosa increased progressively with the increasing degree of the lesions. Although the apoptotic cells increased, their changes did not occur with the degree of the lesions. Their ratio showed a decreasing tendency with the degree of the lesions.CONCLUSIONS (①The presence of an imbalance between cell proliferation and apoptosis was confirmed in the course of large intestine carcinogenesis in a mouse model. ②In the early stage of carcinoma induction both proliferation and apoptosis were at a low level; in the medium stage, they were both at a high level; and in the late stage (that is in carcinoma), proliferation was at a very high level, while apoptosis was at a low level. ③The proliferating cells increased progressively with the degree of dysplasia. There were no obvious changes in the apoptotic cells and their ratio to the proliferating cell sshowed a progressively increasing tendency. ④In the stage of cancer formation, the most essential change was the excessive decrease in the ratio of apoptosis to proliferation. These results support the hypothesis of “Cell Selective Proliferation“, which was raised by authors previously in a study on human large bowel carcinoma.     

大肠腺瘤癌变的处理

报告49例大肠腺瘤与癌变的关系及大肠腺瘤癌变的处理。男性26例，女性23例，平均年龄43．7岁，其中癌变14例，癌变率为28．6％。脉瘤癌变与腺癌的大小、部位、腺癌的数目、组织学类型及病人年龄等因素有关。＜1cm腺癌未发生癌变，≤2cm的癌变率为55％，直肠及乙状结肠的腺癌易恶变。管状腺瘤、绒毛状腺癌、管状绒毛状腺癌的癌变率分别为22．7％、41．2％、20％，绒毛状腺癌最易癌变。癌变腺癌的术式选择应根据癌变浸润深度、病理组织分类、癌细胞分化程度、切缘是否有癌残留以及淋巴管和静脉是否有癌浸润等决定。     

肺间质纤维化合并肺癌四例临床经验总结

特发性肺间质纤维化（idiopathic pulmonary fibrosis，IPF）是弥漫性肺间质性疾病中的一组疾病，其直接致病原因目前仍不清楚。而肺癌则是死亡率极高的恶性肿瘤之一，严重威胁着人类健康。目前认为肺癌的发生是一个多基因参与的、多步骤、多中心、区域性的癌变过程，要经历从癌前病变（包括轻、中、重度不典型增生）、原位癌、癌的浸润和转移等多个步骤。而单个细胞癌变则主要有以下两阶段：①在初次发生致癌物暴露后，细胞内出现基因与分子异常并不断积累；②最终出现细胞的生长增殖失控，发生转移。随着现代影像学技术的不断发展，在临床工作中不时见到肺间质纤维化与肺癌同时或者先后发生在同一患者。     

幽门螺杆菌感染的胃黏膜上皮细皮细胞环氧合酶-2表达及意义

目的探讨幽门螺杆菌(Hp)感染的胃黏膜上皮细胞环氧合酶-2(COX-2)的表达及其在胃黏膜癌变过程中的意义.方法采用快速尿素酶试验和组织学碱性品红染色法检测胃黏膜Hp 感染状况;应用免疫组化法检测胃黏膜上皮细胞COX-2表达状况.结果 32例胃癌中,COX-2表达阳性22例(68.7%).12例Hp阴性的胃黏膜中,有1例(8.3%)COX-2低表达;10例Hp阳性正常胃黏膜中,仅1例(10.0%)COX-2低表达;9例Hp阳性的胃黏膜充血水肿糜烂者中,有5例(55.6%)COX-2表达阳性,与Hp阴性者和Hp阳性正常胃黏膜者比较,差异有统计学意义(P<0.05);10例Hp阳性的轻度萎缩性胃炎伴轻度肠化生者中,COX-2表达阳性5例(50.0%);10例Hp阳性的中重度萎缩性胃炎伴中重度肠化生者中,COX-2表达阳性8例(80.0%);8例Hp阳性的中重度不典型增生者中,COX-2表达阳性6例(75.0%).中重度萎缩性胃炎伴中重度肠化生和不典型增生者的COX-2表达高于轻度萎缩性胃炎伴轻度肠化生者(P<0.05).结论 Hp感染诱导慢性浅表性胃炎黏膜上皮细胞的COX-2表达与黏膜损伤形成有关;根据胃癌发生模式,COX-2表达上调与Hp感染胃黏膜癌变发生相关,且可能在癌前病变形成早期阶段起作用.     

如何治疗癌变的乳腺增生

乳腺增生病分为三型,即乳痛症、乳腺腺病和乳腺囊性增生症.虽然乳痛症和乳腺腺病早期不会发生癌变,乳腺腺病后期和乳腺囊性增生病才可能发生癌变,乳腺囊性增生癌变率也仅在3-8%,但毕竟乳腺增生患者发生乳癌的机率比正常妇女高8-20%,防止乳腺增生癌变固然重要,得了乳癌,更需要科学治疗认真对待.