原发性胆囊癌CD44v6和bcl-2的表达及其与临床病理的关系

目的　探讨CD44v6和bcl 2蛋白在原发性胆囊癌组织中的表达及其与癌组织类型、病理分级和转移状况的关系 ,以及CD44v6表达与bcl 2表达的相关性。方法　应用免疫组织化学方法检测 50例原发性胆囊癌、2 0例胆囊腺瘤和 1 0例慢性胆囊炎组织中CD44v6和bcl 2蛋白的表达。结果　胆囊癌组织中CD44v6和bcl 2表达阳性率分别为82 .0 %和 60 .0 % ,均明显高于胆囊腺瘤 (分别为 45 .0 %和 30 .0 % ,P<0 .0 5) ,并随着胆囊癌细胞分化程度的减低、病理分级的增高和转移而明显增高 (P<0 .0 5)。同时 ,CD44v6的表达与bcl 2表达呈正相关 (r =0 .36 ,P<0 .0 5)。结论　CD44v6和bcl 2均是胆囊癌高度恶性和预后不良的重要指标。胆囊癌CD44v6表达与bcl 2蛋白表达可能具有相互协同作用。     

RP－HPLC法测定复合维生素B片中维生素B_1、B_2、B_6和烟酰胺的含量

用ＲＰ－ＨＰＬＣ法（固定相为μＢｏｎｄｐａｋ Ｃ１８柱，流动相为己烷磺酸钠冰醋酸液，紫外检测波长为２８０ｎｍ）同时测定出复合维生素Ｂ片中四个组分的含量，方法专属性强，省时；维生素Ｂ１、Ｂ２、Ｂ６和烟酰胺的平均回收率和平均相对标准偏差分别为１００．５％，２．０％；９８．０％，１．９％；１０１．８％，１．１％；１００．１％，２．１％（ｎ＝３）。     

同型半胱氨酸对黑质细胞凋亡及NF-κB表达的影响

目的研究同型半胱氨酸(homocysteine,Hcy)对帕金森(parkinson’s disease,PD)大鼠的黑质细胞的细胞凋亡及NF-κB表达的影响作用。方法100只SD鼠随机分为四组,即正常对照组、6-OHDA组、Hcy组、6-OHDA+Hey组,通过脑立体定向注射6-羟多巴胺建立大鼠PD模型,2小时后同侧脑立体定向注射同型半胱氨酸或生理盐水,采用TUNEL法、免疫组化技术,选择实验后后4h、1d、2d、7d及14d为研究时点,观察黑质细胞凋亡的数量;并检测黑质细胞NF-κB p65的表达情况。结果局部注射同型半胱氨酸能明显增加6-羟基多巴胺引起的黑质细胞凋亡,并增加黑质细胞NF-κB p65的表达,与对照组存在显著性差异(P<0.01)。结论Hcy可以促进6-OHDA引起的黑质细胞凋亡,NF-κBp65的激活可能是机制之一。     

恙虫病东方体在无生命培养基内生长的研究

目的　恙虫病东方体 (Orientiatsutsugamushi;Ot)被认为属专性细胞内寄生。特别是制备大量抗原培养难的问题 ,是近一个世纪以来人们渴望解决的难题。为证实是否能在无生命培养基生长。方法　用Vero -E6个单层组织细胞培养OtJL - 90株与标准Gilliam株 ,在合适时取该培养物接种于Ⅲ号无生命固体培养基培养 ,置 36℃ (± 1℃ )培养 18- 2 4h。结果　可见生长一群无色透明或半透明光滑、湿润、圆形或枫叶样小菌落 ,并产生一种难闻的臭味。两种方法培养物分别做了生物学性状鉴定、形态染色、小白鼠致病力、血清学特异性间接免疫荧光检测。各株Ot经两种培养获得培养物特性基本一致。结论　Ot能在细胞内生长也能在无生命培养基内生长 ,解决了Ot大量抗原培养难的困扰。     

原发性胆囊癌CD44v5、CD44v6表达及其临床病理意义的研究

目的 检测胆囊癌组织中CD44v5、CD44v6的表达,并探讨其在胆囊癌发生发展过程中的临床病理意义.方法 采用SP免疫组织化学方法,检测49例胆囊癌、10例胆囊结石伴慢性胆囊炎组织和10例正常胆囊组织中CD44v5、CD44v6蛋白表达情况.结果 CD44v5、CD44v6阳性表达率在胆囊癌组织明显高于良性组织.在胆囊癌中,CD44v5基因表达阳性率与组织学分级无关,CD4 4v6基因表达阳性率与组织学分级有关.有淋巴结转移的胆囊癌组织中,CD44v5、CD44v6阳性表达率明显高于无淋巴结转移者.结论 CD44v5、CD44v6可能在胆囊癌的淋巴结转移中起着重要的作用,CD44v5、CD4 4v6可能是了解胆囊癌病变发生发展生物学行为,淋巴结转移的重要生物学指标.     

Chemokine receptor CCR6 as a prognostic factor after hepatic resection for hepatocellular carcinoma

Background and Aims: Chemokines and their receptors have recently been shown to have major roles in cancer metastasis. The aim of this study was to determine whether the interaction between chemokine receptor 6 (CCR6) and its ligand, macrophage inflammatory protein‐3 alpha (MIP‐3α), correlates with metastasis of hepatocellular carcinoma (HCC). Methods: To observe the reaction of CCR6 expressed cancer cells to MIP‐3α stimulation, chemotactic and actin polymerization assays for both CCR6 high cells (HepG2) and CCR6 low cells (MCF‐7) were performed. CCR6 mRNA levels in tumor specimens from 30 HCC patients were quantified by real‐time polymerase chain reaction. Patients were classified into two groups, high (≥ 20 copies; n = 10) CCR6 and low (<20 copies; n = 20) CCR6 on the basis of CCR6 expression, and the groups were compared with respect to clinicopathological features. Results: When HepG2 cells (CCR6 high) were stimulated with MIP‐3α, they migrated in a dose‐dependent manner, and formation of pseudopodia was observed. These phenomena were not observed in the CCR6 low cells. The incidence of intrahepatic metastasis was higher in the high CCR6 expression group than in the low CCR6 expression group (P < 0.05). Disease‐free survival was significantly poorer in the high CCR6 expression group than in the low CCR6 expression group (P < 0.05). Conclusions: It was indicated that CCR6 might be associated with intrahepatic metastasis of HCC and might be able to become one of the prognostic factor after hepatic resection for HCC.     

白细胞介素6、信号传导和转录活化因子3和血管内皮生长因子在人脑胶质瘤中的表达及相关性研究

目的研究人脑不同级别胶质瘤中白细胞介素（IL）-6，信号传导和转录活化因子3（STAT3）和血管内皮生长因子（VEGF）的表达，探讨IL-6、STAT3和VEGF与肿瘤病理级别和侵袭性的关系。方法采用免疫组织化学法，检测70例人脑胶质瘤，10例脑膜瘤和5例正常脑组织中IL-6、STAT3和VEGF的表达。结果胶质瘤中IL-6、STAT3和VEGF的表达水平在高级别组（Ⅲ、Ⅳ级）明显高于低级别组（Ⅰ、Ⅱ级），两组间差异有统计学意义（P〈0．01），STAT3的表达与IL-6和VEGF的表达均呈正相关（P〈0．01）。结论IL-6、STAT3和VEGF的表达与胶质瘤的恶性程度有密切关系；且三者协同在胶质瘤发生、发展过程中起重要作用。三者的相关性证实VEGF基因由STAT3蛋白调节，而STAT3又由IL-6刺激活化。     

Grave''''s病与血浆白介素-2、6水平变化的相关性研究

目的了解细胞因子在Grave's病的发生、发展过程中的浓度变化及相关关系.方法用放射免疫分析法测定了54例Grave's病无明显眼病组(G1组),25例Grave's病有眼部合并症组(G2组)及31例正常对照组血清中IL-2、IL-6含量.结果 Grave's病患者血浆IL-6浓度水平显著高于正常对照组(P＜0.01);G2组IL-2血浆水平显著高于G1组成和正常对照组(P＜0.02),IL-6水平与IL-2、FT3、FT4、TGA、MCA浓度水平不相关(P＞0.05).结论细胞因子IL-2、IL-6参与了Graves'病的致病过程,观察其浓度变化对探讨Graves'病的发病机理及指导用药均有重要价值.     

Association of donor TNFRSF6 (FAS) gene polymorphism with acute rejection in renal transplant patients: a case-control study.

BACKGROUND: Genetic factors other than HLA have been reported to be associated with the outcome of organ transplantations. Because binding of FasL to its receptor Fas could play an important role in tubulitis and in the death of graft tubular epithelial cells during kidney allograft rejection, a gene polymorphism recently identified in position -671 in the promoter of the TNFRSF6 gene coding for Fas was investigated in donors. METHODS: A case-control study was performed within a cohort of non-hyperimmunized adult patients who had received cadaveric kidney transplants based on the occurrence or absence of acute cellular rejection in the first 6 months after renal transplantation. Each recipient from the acute rejection group (n = 35) was matched for age (+/- 5 years) and number of HLA-DR mismatches with two recipients within the non-acute rejection group (n = 70). RESULTS: The TNFRSF6-GG genotype was more frequent in donors in the group without rejection episodes. In contrast, patients who received a kidney from a TNFRSF6-A carrier were more likely to experience acute rejection episodes (relative risk nearly 2.1). CONCLUSION: This study suggests that donor TNFRSF6 polymorphism directly or indirectly influences acute kidney rejection episodes.