促肝细胞生长素诱导人肝癌细胞（BEL－7402）凋亡

本文从细胞学、ＤＮＡ凝胶电泳、流式细胞术三方面研究促肝细胞生长素（ｐＨＧＦ）在体外对肝癌细胞增殖活性的影响。结果表明：ｐＨＧＦ对肝癌ＢＥＬ－７４０２细胞增殖有抑制作用，并存在剂量和时间相关性。其４８ｈ的半数抑制浓度（ＩＤ５０）为０．３７ｍｇ／ｍｌ±０．０４ｍｇ／ｍｌ。而３７℃灭活的ｐＨＧＦ对ＢＥＬ－７４０２细胞增殖在１５ｈ无抑制作用，在２４和４８ｈ抑制作用很弱（ＩＤ５０＞１．５ｍｇ／ｍｌ）。ＤＮＡ凝胶电泳结果表明，ｐＨＧＦ可诱导ＢＥＬ７４０２细胞产生细胞凋亡（Ａｐｏｐｔｏｓｉｓ）。流式细胞术（ＦＣＭ）结果显示：ｐＨＧＦ抑制ＢＥＬ－７４０２细胞增殖过程是先使细胞停留在Ｇ０／Ｇ１期，继而诱导细胞产生凋亡。后两项结果均显示ｐＨＧＦ对人肝癌细胞凋亡的诱导里时间和剂量相关性。     

84例周围血管病的足甲襞微循环观察

对84例周围血管病(脉管炎68例,静脉炎16例)和25例正常健康人进行了足甲襞微循环的对比观察。结果:患病组足甲襞微循环的血管形态、流态、管周状态均较正常健康组有明显差异(P<0.01)。提示:更接近病变部位的局部微循环观察更能代表病变的程度,对临床医生判断病情、选择用药和疗效观察都有很大帮助和参考价值。     

Cytotoxicity of Hemolytic, Cytotoxic Necrotizing Factor 1-Positive and -Negative Escherichia coli to Human T24 Bladder Cells

Approximately one-half of Escherichia coli isolates from patients with cystitis or pyelonephritis produce the pore-forming cytotoxin hemolysin, a molecule with the capacity to lyse erythrocytes and a range of nucleated cell types. A second toxin, cytotoxic necrotizing factor 1 (CNF1), is found in approximately 70% of hemolytic, but rarely in nonhemolytic, isolates. To evaluate the potential interplay of these two toxins, we used epidemiological and molecular biologic techniques to compare the cytotoxicity of hemolytic, CNF1⁺, and CNF1⁻ cystitis strains toward human T24 bladder epithelial cells in vitro. A total of 29 isolates from two collections of cystitis-associated E. coli were evaluated by using methylene blue staining of bladder monolayers at 1-h intervals after inoculation with each strain. Most (20 of 29) isolates damaged or destroyed the T24 monolayer (less than 50% remaining) within 4 h after inoculation. As a group, CNF1⁺ isolates from one collection (11 strains) were less cytotoxic at 4 h than the CNF1⁻ strains in that collection (P = 0.009), but this pattern was not observed among isolates from the second collection (18 strains). To directly evaluate the role of CNF1 in cytotoxicity of hemolytic E. coli without the variables present in multiple clinical isolates, we constructed mutants defective in production of CNF1. Compared to the CNF1⁺ parental isolates, no change in cytotoxicity was detected in these cnf1 mutants. Our results indicate that CNF1 does not have a detectable effect on the ability of hemolytic E. coli to damage human bladder cell monolayers in vitro.     

针刺对实验性脑缺血作用机理的研究进展

缺血性脑血管疾病是一个非常复杂的病理生理过程 ,是多种机制共同作用的结果。本文从针刺对实验性脑缺血在脑组织形态学改变、血液流变学、脑微循环等方面的研究进展作一综述。     

高校学生朋友心理辅导员培训内容与方法研究

目的 学生朋友心理辅导员是高校学生心理健康教育网络系统的重要组成部分。如何在较短的时间里，经过比较系统的培训，让普通的大学生成长为合格的学生朋友心理辅导员并承担起为同学进行心理护理的义务，是构建高校学生心理健康教育网络系统的关健。方法 明确培训目标和担任工作职能，培训内容科学，知识构成合理，培训方法灵活，进行培训前测与后测和培训效果评估，注重实践锻炼和心理督导。结果 培训结业的学员在各方面有比较真显著变化，心态明显改变，知识明显提高、助人技巧明显增强、人际交往明显改善，总体上呈现出积极、友爱、乐观、向上的精神面貌。结论 在高校能够培训出合格的学生朋友心理辅导员，并成为高校学生心理健康教育网络的重要力量。     

中药“神经再生素”促神经生长过程中基因差异性表达的初步研究

为了探索中药“神经再生素”促神经生长过程中基因水平的变化。本实验采用 dd-PCR方法 ,从体外培养背根神经节细胞加药组和不加药组中获得两者的差异表达片段 ,并经反杂交筛选、克隆测序、DNA序列检索分析、Northern验证。结果表明 ,差异显示共获得 8个差异条带 ,一个为下调基因 ,其余为上调基因 ,其中 2个 c DNA序列与 RRAJ5 16 1基因 (增殖相关基因 )、AF196 3 15基因 (锌指样蛋白 DDP2 ) 10 0 %同源 ,2个 c DNA序列与 AK0 0 175 7基因、STA5 SRR基因 (t RNA合成酶 )部分同源。结论是中药“神经再生素”在促神经生长过程中 ,对神经元基因的选择性表达起着重要的调控作用。     

正常人血小板介电谱的实验研究

在100KHz～110MHz范围内,测量人血小板的介电谱,分析了人血小板对交流电场的介电响应的数据特征。利用频域阻抗技术首次测量了正常人血小板交流阻抗,绘制血小板的介电常数和电导率与电场频率的关系曲线。建立了人血小板的介电谱和Cole-Cole图,明确了人血小板的介电频响的数据特征。在射频电场中,人血小板的介电常数和电导率具有频率依赖性,血小板介电谱具有两个特征频率:第一特征频率fC1为6.66MHz,第二特征频率fC2为9.81MHz。     

Neural cell adhesion molecule contributes to hemopoiesis-supporting capacity of stromal cell lines

To clarify mechanisms underlying cell-to-cell interactions between hemopoietic stem cells (HSCs) and stromal cells, we established a stromal cell line (FMS/PA6-P) from day-16 fetal bone marrow (BM) adherent cells using an anti-PA6 monoclonal antibody (mAb) specific for BM stromal cells. Importantly, this FMS/PA6-P cell line, showing homogenous fibroblastic morphology, is absent from hematolymphoid and endothelial lineage markers and maintains a high level of expression of PA6 molecule, recognized by the anti-PA6 mAb, for approximately 20 passages. Further, the cell line expressing a high level of PA6 molecule has a better hemopoiesis-supporting capacity in vitro than other stromal cell lines such as PA6 and MS-5. In fact, the PA6 molecule is closely related to the hemopoiesis-supporting capacity of the stromal cells because the proliferation of HSCs was suppressed to a great extent by the anti-PA6 mAb. Affinity chromatography and mass peptide fingerprinting revealed that the protein reacting with the anti-PA6 mAb is neural cell adhesion molecule (NCAM). The frequencies of long-term cobblestone area-forming cells and long-term culture-initiating cells were significantly suppressed by repression of NCAM in the FMS/PA6-P cells using NCAM small interfering RNA. Our findings clearly indicate that NCAM functions on the maintenance of HSCs.     

血管内皮生长因子反义基因转染对高转移人巨细胞肺癌细胞系生 …

目的 探讨反义血管内皮生长因子（ＶＥＧＦ）基因转染在抑制恶性肿瘤生长和转移的抗肿瘤血管基因治疗中的意义。方法 利用基因重组技术构建正义和反义ＶＥＧＦ１２１ ｃＤＮＡ真核表达载体,用脂质体法转染高转移性人巨细胞肺癌细胞（ＰＧ）,经Ｎｏｒｔｈｅｍ杂交和Ｗｅｓｔｅｒｎ印迹免疫化学检测ＶＥＧＦ ｍＲＮＡ和蛋白质的表达水平,并对转染前后细胞进行体外生长和裸鼠体内生长转移等多项生物学行为实验,结果 转染反义转     

Subchronic exposure to arsenic through drinking water alters expression of cancer-related genes in rat liver

Although arsenic exposure causes liver disease and/or hepatoma, little is known about molecular mechanisms of arsenic-induced liver toxicity or carcinogenesis. We investigated the effects of arsenic on expression of cancer-related genes in a rat liver following subchronic exposure to sodium arsenate (1, 10, 100 ppm in drinking water), by using real-time quantitative RT-PCR and immunohistochemical analyses. Arsenic accumulated in the rat liver dose-dependently and caused hepatic histopathological changes, such as disruption of hepatic cords, sinusoidal dilation, and fatty infiltration. A 1-month exposure to arsenic significantly increased hepatic mRNA levels of cyclin D1 (10 ppm), ILK (1 ppm), and p27(Kip1) (10 ppm), whereas it reduced mRNA levels of PTEN (1 ppm) and beta-catenin (100 ppm). In contrast, a 4-month arsenic exposure showed increased mRNA expression of cyclin D1 (100 ppm), ILK (1 ppm), and p27(Kip1) (1 and 10 ppm), and decreased expression of both PTEN and beta-catenin at all 3 doses. An immunohistochemical study revealed that each protein expression accords closely with each gene expression of mRNA level. In conclusion, subchronic exposure to inorganic arsenate caused pathological changes and altered expression of cyclin D1, p27(Kip1), ILK, PTEN, and beta-catenin in the liver. This implies that arsenic liver toxicity involves disturbances of some cancer-related molecules.