胰腺癌微血管壁通透性的形态学研究

目的 观察胰腺癌微血管壁的通透性相关结构,为胰腺癌药物治疗靶向性的提高提供参考.方法 选取我院切除的中分化胰腺癌10例,对肿瘤中心、边缘、瘤旁、正常/远隔胰腺4个部位进行透射电镜检测.结果 胰腺癌微血管数量和内皮窗孔数量明显少于正常胰腺组织(P<0.05),且内皮间隙和窗孔的内径并不超过正常胰腺组织.胰腺癌微血管内皮间隙内径中位数为12.8～13.2 nm,5～95百分位数为0～24.4 nm,内皮间隙存在局部扩张的现象,最宽处可以达到60.3～76.4 nm.胰腺癌微血管窗孔的内径在40.0nm左右.瘤旁组织破口较多,破口内径平均516.3 mm左右.结论 与正常胰腺组织比较,胰腺癌具有一定的微血管异质性,体现为血供较少和微血管壁通透性较低等特点.     

Cigarette smoke toxicants alter growth and survival of cultured mammalian cells.

Our purpose was to determine the effects of six cigarette toxicants (pyridine, nicotine, 2-ethylpyridine, 3-ethylpyridine, p-cresol, and pyrazine) on three types of cultured mammalian cells (human umbilical vein endothelial cells [HUVECs], human microvascular endothelial cells [HMVECs], and NIH 3T3 cells) using a cell proliferation/survival assay. Synchronized cells were cultured in proliferation or survival medium containing various doses (10(-18)M-10(-2)M) of the tested chemicals. After 48 h, cells were counted using a hemacytometer. The no observable adverse effect level (NOAEL), lowest observable adverse effect level (LOAEL), and the efficacy were determined for each compound in the cell proliferation and survival assays. Pyridine and p-cresol did not show significant effects with any cell types, except at high doses. Derivitization of the pyridine ring altered its potency, especially when an ethyl group or nitrogen was added. In survival medium, nicotine stimulated proliferation of all three cell types at doses found in smoker's serum (10(-8)M-10(-7)M). For HUVEC and HMVEC, 2-ethylpyridine, 3-ethylpyridine, and pyrazine inhibited proliferation in proliferation medium and induced cell death in survival medium at attomolar and femtomolar doses. All chemicals, except pyridine and pyrazine, stimulated NIH 3T3 cell proliferation at low doses and induced cell death at high doses. LOAELs and efficacies revealed that endothelial cells from a developing organ (umbilical cord) were more sensitive to these chemicals than endothelial cells from an adult organ (lung). 3-Ethylpyridine and pyrazine, which induced cell death at low doses, are added to consumer products and should be subjected to further toxicological testing.     

供者表达活化性杀伤细胞免疫球蛋白样受体对造血干细胞移植预后的影响

目的 观察供者表达活化性杀伤细胞免疫球蛋白样受体（aKIR）对受者造血干细胞移植（HSCT）预后的影响。方法 1996年至2001年共行亲缘性人类白细胞抗原（HLA）全相合骨髓移植59例，以序列特异性引物多聚酶链反应法（SSP-PCR）检测供者aKIR的表型。分析供者表达aKIR对受者移植后病毒、细菌和真菌感染及出血、复发、存活情况的影响。结果 供者表达aKIR与受者移植后出血、病毒及细菌感染发生的概率无明显相关性；当供者表达KIR3DS1表型时，发生真菌感染概率增高（X^4．804，P=0．028）。供者表达aKIR对受者HSCT后存活率和白血病复发率均无明显影响。结论 亲缘性HLA全相合HSCT中，供者表达aKIR并不能改善受者的移植效果。     

肝病患者血清诱导间充质干细胞表达肝细胞特异性标志物的实验研究

目的：观察重型肝病患者血清对人骨髓间充质干细胞（MSCs）的诱导分化作用，探讨人MSCs分离培养、体外扩增的条件和方法。方法：从肋骨分离、培养人骨髓MSCs、体外扩增培养、鉴定，并采用重型肝病患者血清诱导培养，分别在诱导培养0、7、14、21、28天时留取细胞，并采用免疫细胞化学方法检测肝特异性标志物（AFP、Alb、CK-18）、用PAS进行糖原染色实验。结果：诱导后5天、MSCs表现为肝细胞样细胞，随着诱导培养时间的延长，肝特异性标志物逐渐出现和成熟。AFP在7天时表达水平最高，培养14、21、28天时表达逐渐减弱；Alb、CK- 18和糖原随着诱导时间的延长，表达逐渐增强。结论：密度梯度离心，贴壁培养和消化时间控制相结合，是一种较为有效的分离纯化方法。重型肝病患者血清能诱导骨髓MSCs表达肝细胞的特异性标志物。     

Effect of naringin on bone cells.

Statin, a HMG-CoA reductase inhibitor, was shown to increase BMP-2 gene expression for bone formation, by blocking the mevalonate pathway in cholesterol production. We investigated the effect of naringin, a flavonoid available commonly in citrus fruits, which was also a HMG-CoA reductase inhibitor, in UMR 106 osteoblastic cell line in vitro. The control group consisted of cells cultured without any intervention for different time intervals (24 h, 48 h, and 72 h), whereas the experimental (naringin) group consisted of cells cultured with naringin of different concentrations (0.001 micromol/L, 0.01 micromol/L, and 0.1 micromol/L) for the same time intervals of the control. Colorimetric Tetrazolium (MTT) assay, total protein content assay, and alkaline phosphatase activity were used to measure the cellular activities. Results for the naringin group showed an increase in MTT assay compared with the control and the effect was dose dependent. At high concentration (0.1 micromol), the increases ranged from 60% to 80%. In the total protein content assay, naringin also showed an increase compared with control and the effect was also dose dependent. At high concentration (0.1 micromol), the increases ranged from 9% to 20%. In the alkaline phosphatase activity assay, naringin at high concentration (0.1 micromol) significantly increased the activity up to 20%. In conclusion, naringin significantly increased bone cell activities in vitro. This is the first study specifically attempted to investigate the effect of naringin on bone cell activities. Besides statin, this provided another example of mevalonate pathway blockage in the cholesterol production pathway by HMG-CoA reductase inhibition will increase the bone cell activities.     

兔关节软骨细胞的分离、培养和形态学特征

[目的]探讨兔关节软骨细胞的分离、培养方法,观察单层高浓度培养时细胞表型表达情况.[方法]无菌条件下,从 2周龄新西兰白兔的颞颌关节及四肢关节髁突面削取软骨片,采用机械-酶消化法分离软骨细胞,经台盼蓝拒染计数,将细胞按 1× 106个 /孔接种于 6孔培养板,传代培养,描绘生长曲线.利用相差显微镜及透射电镜观察细胞形态.应用甲苯胺蓝及Ⅱ型胶原免疫组化对细胞进行鉴定.[结果]每克软骨能获取 1 5× 106个软骨细胞,活性率为 95%.培养 2～ 3 d,细胞贴壁、变形,呈多角形; 8 d左右,细胞融合成层.透射电镜观察显示细胞核圆形,有丰富的粗面内质网、高尔基体及分泌的基质成分.甲苯胺蓝及Ⅱ型胶原染色阳性.细胞传至 5代后,出现"成纤维细胞样".[结论]本研究建立了简单易行的软骨细胞分离、培养方法;初代、第 2代细胞生长良好,适合于实验研究;软骨细胞 5代培养后,细胞表型发生改变.     

Epidemiology of nonmelanoma skin cancer (NMSC) in Europe: accurate and comparable data are needed for effective public health monitoring and interventions

Summary Nonmelanoma skin cancer (NMSC) is the most common malignancy occurring in white populations. It is currently becoming an important challenge in terms of public health management as the increasing incidence rates will probably have a tremendous impact on healthcare costs. Possible factors driving this rise in NMSC numbers are increases in both acute and prolonged UV exposure together with increasing numbers of older people in the population. A better understanding of NMSC epidemiology in Europe is essential if an evidence-based European-wide public health policy is to be developed. It is obvious this can only be achieved by recording and analysing comparative epidemiological data. Finally, by improving the skin examination training for physicians, developing guidelines and exchanging best practices, a high level of healthcare could be provided for NMSC.     

Role of Integrin CD103 in Promoting Destruction of Renal Allografts by CD8+ T Cells

Infiltration of CD8(+)TCRalphabeta(+) T-effector populations (CD8 effectors) into graft epithelial compartments has long been recognized as a key lesion in progression of clinical renal allograft rejection. While the afferent phase of allograft immunity is increasingly well-defined, the efferent pathways by which donor-reactive CD8-effector populations access and ultimately destroy the graft renal tubules (rejection per se) have received remarkably little attention. This is an important gap in our knowledge of transplantation immunology, because epithelial compartments comprise the functional elements of most commonly transplanted organs including not only kidney, but also liver, lung, pancreas, and intestine. Furthermore, there is increasing evidence that attack of graft epithelial elements by CD8-effector populations not only causes short-term graft dysfunction but is also a major contributor to development of chronic allograft nephropathy and late graft loss, which now represent the salient clinical problems. Recent studies of the T-cell integrin, alpha(E)beta(7) (CD103), have provided insight into the mechanisms that promote interaction of CD8 effectors with graft epithelial compartments. The purpose of this communication is to review the known properties of the CD103 molecule and its postulated role in the efferent phase of renal allograft rejection.