细菌脂多糖对NIH3T3细胞增生、胞内游离钙及cAMP浓度的影响

目的 :探讨细菌脂多糖 (lipopolysaccharide,L PS)对 NIH 3T3细胞增生、胞内游离钙及 c AMP浓度的影响。　方法 :以中性红比色法检测细胞生长 ,酚试剂法检测细胞蛋白质合成 ,并动态检测 L PS对胞内游离钙和 c AMP浓度的影响。　结果 :1微量 L PS可促进细胞生长及蛋白质合成 ;2 L PS作用后 3～ 5 min可使胞内游离钙浓度升高 ,作用 1 m in后使 c AMP浓度升高 ,并保持较高水平。　结论 :胞内游离钙 ([Ca2 ]i)及 c AMP是 L PS对 NIH3T3细胞作用过程中重要的信使分子     

Age-related changes in dividing cells of the olfactory epithelium of the maturing guinea pig

Changes in dividing cells of the olfactory epithelium from guinea pigs of different ages were examined by immunohistochemical staining using anti-proliferating cell nuclear antigen antibody. Numerous dividing cells were scattered diffusely in the basal layer of the olfactory epithelium at 1 and 2 months following birth and then gradually decreased with maturation until 4 months. Findings then remained constant between 4 and 24 months. Subsequently, cell numbers were found to decrease as animals became older. The number of olfactory receptor cells did not vary significantly between 1 and 30 months. Although no correlation could be found between the numbers of dividing cells and olfactory receptor cells, it is still possible that the longevity of the olfactory receptor cells changes to maintain the overall size of the neuronal population. Received: 18 February 1998 / Accepted: 9 April 1998     

盆腔静脉瘀血症患者瘀血静脉超微结构观察

为探讨盆腔静脉瘀血症患者瘀血静脉形态学改变,本文对11例瘀血症患者和6例结扎术后无任何症状和体征的妇女盆腔静脉进行了扫描及透射电镜观察.发现瘀血静脉壁间渗出增多;内皮细胞数量增多、体积变小且外形肿胀;细胞表面粗糙,突起增粗,小孔及凹陷增多、变大;细胞质致密并含大量饮液泡,线粒体肿胀而数量增多;染色质呈块状分布于核的周边;内皮细胞间嵌合连接和紧密连接正常存在.这些变化说明缺氧是引起本症盆腔静脉超微结构改变的主要原因,提示本症是一种功能性疾病.     

Immunobiology of T helper cells and antigen-presenting cells in autoimmune thrombocytopenic purpura (ITP)

Autoimmune thrombocytopenic purpura (AITP) is a bleeding disease in which autoantibodies are directed against the individual's own platelets, resulting in enhanced Fc-mediated platelet destruction by macrophages in the reticuloendothelial system. Most research in AITP has focused on characterization of the autoantibodies, while little has been devoted to the cellular immune mechanisms leading to autoantibody production. This report summarizes the current state of the literature and argues that enhanced T helper cell/antigen-presenting cell interactions in patients with AITP are the primary stimulus for the development of antiplatelet autoantibody production. Understanding these events is important for eventually identifying disease-initiating platelet autoantigens and ultimately developing specific immunotherapies for AITP.     

Genotypic analysis of tumor suppressor genes PTEN/MMAC1 and p53 in head and neck squamous cell carcinomas

Objectives: Tumor suppressor gene mutations in both p53 and PTEN/MMAC1 genomic DNA have been detected in many types of cancer. The purpose of this study was to investigate the presence and importance of PTEN/MMAC1 mutations in squamous cell carcinomas. Methods: Exons of each gene were amplified after polymerase chain reaction (PCR) using genomic DNA derived from cell lines of squamous cell carcinoma of the head and neck (SCCHN) and snap-frozen biopsy specimens from primary established head and neck tumors. The amplified and purified DNA was then sequenced directly. Result: As anticipated, point mutations of the p53 gene were found in 80% of cell lines examined. A single base mutation in codon 151 was found in six of 10 cell lines studied. PTEN/MMAC1 gene mutations were found in neither the cell lines tested nor the tumor biopsy samples. Conclusion: This study, as well as a large volume of data, confirms that mutations of the p53 gene are frequent events in head and neck cancer cell lines. Although PTEN/MMAC1 gene mutations have been found in a variety of carcinomas, this gene was not found to be mutated in SCCHN cell lines or in primary squamous cell carcinomas of the head and neck. This information is useful for further studies of mutations in these cell lines. Laryngoscope, 108:1553–1556, 1998     

The role of VCAM-l/VLA-4 in the activation of allogenic T cells by murine macrophages

Vascular cell adhesion molecule 1 (VCAM-1) is a member of immunoglobulin superfamily. The principal ligand for VCAM-1 is integrin α4β/VLA-4 (very late antigen 4). It was reported that VCAM-1 was expressed on macrophages and dendritic cells, but little is known about its function on these professional antigen presenting cells (APC). The present study was performed to investigate the expression of VCAM-1 on macrophages and the role of VCAM-l/VLA-4 in the activation of allogenic T cells by murine macrophages. We analyzed VCAM-1 expression on peritoneal macrophages and macrophage cell line J774A.1 by fluorescence-activated cell sorting (FACS). Using neutralizing antibodies, we further analyzed the role of VCAM-l/VLA-4 interaction in macrophage and allogenic T cell mixed lymphocyte reaction (MLR). We found that VCAM-1 was constitutively expressed on macrophages and its expression level was upregulated by soluble tumor associated antigen (freeze-thaw lysates of FBL-3 leukemia cells) and TNF-a. In MLR assays, we observed that blocking VCAM-l/VLA-4 interaction with anti-VCAM-1 or anti-VLA-4 mAbs caused significant inhibition of the proliferative response and IL-2 production. These results suggest that VCAM-lon macrophages not only facilitates the cell-to-cell contact through adhesive interaction but also plays a role in the costimulation of T cells via its interaction with VLA-4 on the T cells. This work was supported by grants from the National Natural Science Foundation of China.No. (39730420). This is one of papers of the special issue on gene therapy research (Chin J Cancer Res Vol. 9 No. 4 December, 1997).     

Paracrine/autocrine regulation of breast cancer by the insulin-like growth factors

Local environmental signals regulate the growth and development of both normal and malignant breast epithelium. Members of the insulin-like growth factor (IGF) family likely influence both of these processes. The localization of IGF2 to stroma specifically surrounding malignant breast epithelium indicates that this growth factor may play a critical role in the genesis or maintenance of this transformed phenotype. Recent studies have sought to understand the mechanism by which IGF2 expressing fibroblasts are localized to the periphery of malignant breast cancer cells. In addition, the consequences of the expression of IGF-signaling components likely expand beyond their direct effects on mitogenesis. Indirect effects predominantly associated with the IGF2 receptor could also influence the invasive potential of breast tumor cells.     

Antitumor Immunity Induction by Intracellular Hyperthermia Using Magnetite Cationic Liposomes

Induction of antitumor immunity to T-9 rat glioma by intracellular hyperthermia using functional magnetic particles was investigated. Magnetite cationic liposomes (MCLs), which have a positive surface charge, were used as heating mediators for intracellular hyperthermia. Solid T-9 glioma tissues were formed subcutaneously on both femurs of female F344 rats, and MCLs were injected via a needle only into the left solid tumors (treatment side). The rats were then divided into two groups, which received no irradiation, or irradiation for 30 min given three times at 24-h intervals with an alternating magnetic field (118 kHz, 384 Oe). On the treatment side, the tumor tissue disappeared completely in many rats exposed to the magnetic field. The tumor tissue on the opposite side also disappeared completely, even though MCLs were not injected into the right solid tumors. To examine whether a long-lasting and tumor-specific immunity could be generated, the rats that had been cured by the hyperthermia treatment were rechallenged with T-9 cells 3 months later. After a period of transient growth, all tumors disappeared. Furthermore, immuno-cytochemical assay revealed that the immune response induced by the hyperthermia treatment was mediated by both CD8⁺ and CD4⁺ T cells and accompanied by a marked augmentation of tumor-selective cytotoxic T lymphocyte activity. These results suggest that our magnetic particles are potentially effective tools for hyperthermic treatment of solid tumors, because in addition to killing of the tumor cells by heat, a host immune response is induced.     

中华硬蜱叮咬免疫兔后中肠消化细胞形态测量分析

本文采用军事医学科学院生产的多功能系统，对叮咬经不同抗原免疫接种兔后的中华硬蜱中肠消化细胞进行形态学测量分析，以了解蜱中肠受损程度和各种抗原诱导免疫力产生的强弱。结果表明：蜱血餐后其中肠增粗，肠壁增厚：消化细胞数量增加，体积增大；而细胞核相对较小，核体密度、表面积密度变小。中华硬蜱叮咬免疫兔后上述各种吸血后的正常反应不如佐剂对照组，尤以纯化抗原接种组明显，其中肠也增粗，由于大量消化细胞受损伤而脱落，使得消化细胞数减少，由于大量消化细胞受损脱落使消化细胞数减小和消化细胞平均截面面积减小。由于核固缩、核碎裂、核溶解早于细胞碎裂脱落，使细胞核的体密度和表面积密度明显减小。与对照组相比，肠直径、肠壁面积、消化细胞截面数、数面密度、截面面积和消化细胞核的体密度及表面积密度均有显著性或非常显著性差异。受损程度依次为纯化抗原（ＰＡ）组、中肠抗原（ＭＡ）组、唾液腺抗原（ＳＧＡ）组和全虫抗原（ＷＴＡ）组。卵抗原（ＯＡ）组损伤最轻。本实验的五个免疫接种组中有四个组能有效诱导宿主产生免疫力，以１０５ＫＤ纯化抗原接种作用最强，在选择制备抗蜱疫苗时可供参考