传染性法氏囊病病毒在鸡胚细胞上的优化繁殖

研究了传染性法氏囊病病毒在鸡胚细胞上繁殖上的优化条件，结果表明，鸡胚细胞体外增殖培养后对ＩＢＤＶ的敏感性并不减弱，而且有提高。维持培养基中血清浓度的变化对病毒的繁殖影响不大。     

乳苣水提取物对人肺癌细胞SPCA-1生长的影响

为了探讨乳苣水提取物对体外培养的肺癌细胞SPCA-1的影响,分别用质量浓度为0.5、1、1.25和1.5 g/L(mg/m L)的乳苣水提取物处理SPCA-1细胞,24 h后通过CCK-8法检测发现,与对照组(未处理)相比,处理组细胞增殖活力均显著下降(P0.001).流式细胞仪检测(AnnexinⅤ-FITC/PI染色)发现随着处理浓度的增加,处理组细胞凋亡率都显著提高(P0.05),且呈剂量依赖关系.为了探索乳苣是否对体内肿瘤有抑制作用,构建了SPCA-1细胞的裸鼠皮下瘤模型,通过观察喂食乳苣水提取物后皮下瘤的生长情况发现,与未喂食乳苣水提取物的对照鼠相比,喂食5周后的实验组的瘤体得到明显的抑制.实验结果表明乳苣水提取物能够抑制体外和体内生长的SPCA-1细胞,可以作为一种潜在的预防和治疗肺癌的药物做进一步研究.     

SLE患者外周血淋巴细胞表达BLyS和CD86的变化

采用FACS研究了 2 2例SLE患者外周血淋巴细胞表达BLyS和CD86的变化。结果表明 ,SLE患者外周血BLyS 淋巴细胞和CD19 CD86 淋巴细胞显著增加 ,但二者之间无显著相关。     

污染因子Cu2+对鲫鱼血细胞的影响

在光镜水平上研究了鲫鱼外周血细胞的形态结构。结果发现在鲫鱼外周血中可看到红细胞、淋巴细胞、嗜中性粒细胞、单核细胞和血栓细胞,未发现嗜酸性细胞和嗜碱性粒细胞,描述了上述各种血细胞在光镜下的形态和显微结构。污染后鱼体中淋巴细胞的显著增加,单核细胞增多,伴随着血栓细胞和嗜中性细胞的显著减少是鱼体短期(96h)接触Cu~(2+)后变化的一个指示。这个研究结果同时也被白细胞数量的变化特征所证实,即白细胞在通常的温度污染条件下增多,以抵抗可能由Cu~(2+)所引起的机体感染,从而来保护机体。     

Isolation and purification of BVⅠ-2H from bee venom and analysis of its biological action

The medical use of bee venom for rheumatoid arthritis (RA) has a very long tradition. In this study, isolation and purification of polypeptides from bee venom were carried out on sephadex chromatography, heparin sepharose CL-6B chromatography and HPLC. Several fractions were extracted, and their effects on activation of splenocyte and THP-1 cell were studied. The inhibitory fraction was selected for further studies. Finally, BVⅠ-2H that the HPLC elution profiles was a single peak was isolated by C8 column. ESI- MS detection results showed that BVⅠ-2H was a fraction of bee venom, and the molecular weight of the major component was 644.8. BVⅠ-2H could inhibit ConA-induced splenocyte proliferation, IL-1 production and interfere with splenocyte cycle in mice. Moreover, BVⅠ-2H could inhibit PMA-induced TNFa production in THP-1 cells, which was due to its inhibitory effects on TNFa mRNA expression and protein phosphorylation of IkBa. Our studies indicated that BVⅠ-2H was one of the anti-inflammatory components of bee venom.     

The involvement of the renin-angiotensin system in the regulation of cell proliferation in the rat endometrium

Oestrogens are known to enhance angiotensin biosynthesis by increasing the elaboration of its precursor, angiotensinogen. On the other hand, we found that inhibition of angiotensin-converting enzyme (ACE) suppressed the proliferative response of the rat anterior pituitary gland to oestrogens. To answer the question whether the angiotensin system is involved in the control of the cell proliferation of the uterine epithelium, the effects of an ACE inhibitor, enalapril maleate, and of angiotensins II and IV, alone or together with losartan, an antagonist of angiotensin receptor type 1 (AT1), on endometrial epithelial cell proliferation have been studied. The experiments were performed on ovariectomized female Wistar rats. In the first experiment the animals were injected with a single dose of oestradiol benzoate or received an injection of solvent only. Half of the oestrogen-treated rats were injected additionally with enalapril maleate (EN, twice daily). The incorporation of bromodeoxyuridine (BrDU) into endometrial cell nuclei was used as an index of cell proliferation. It was found that oestradiol alone dramatically increased the BrDU labelling index (LI) of endometrial cell nuclei, and this effect was partially blocked by the simultaneous treatment with EN. In the second experiment, the animals were injected intraperitoneally with angiotensin II (AII), angiotensin IV (AIV) or saline, alone or together with losartan. It was found that AIV induced an increase in the LI in uterine epithelium, and this effect was not blocked by the simultaneous treatment with losartan. The increase in LI in uterine epithelium was also observed in the rats treated with AII and with losartan. These findings suggest an involvement of angiotensin IV in the control of uterine epithelium cell proliferation. Received 12 October 1998; received after revision 6 January 1999; accepted 2 February 1999     

The complexity of parathyroid hormone-related proteinsignalling

Our understanding of the mode of action of parathyroid hormone-related protein (PTHrP) has changed profoundly during the last decade. Most PTHrP activities are mediated by membrane receptors through autocrine/paracrine pathways. However, both endogenous and exogenous PTHrP also appear to have intracrine effects through translocation into the nucleus. The present review proposes unconventional PTHrP signalling, based on novel clues. First, PTHrP binding to its membrane receptor triggers internalization of the whole complex, mediated by beta-arrestin. There is growing evidence that the receptor and arrestin are the effectors of biological responses, rather than the ligand (or in addition to the ligand). Second, the existence of putative PTHrP targets within the cytoplasm is beginning to be supported. Recent findings of interactions between a COOH-terminus of PTHrP and beta-arrestin and between the PTHrP receptor and 14-3-3 proteins represent the starting point for identification of intracellular partners of both the hormone and its receptor.Received 19 June 2003; received after revision 10 July 2003; accepted 21 July 2003     

Angiogenesis and signal transduction in endothelial cells

Endothelial cells receive multiple information from their environment that eventually leads them to progress along all the stages of the process of formation of new vessels. Angiogenic signals promote endothelial cell proliferation, increased resistance to apoptosis, changes in proteolytic balance, cytoskeletal reorganization, migration and, finally, differentiation and formation of a new vascular lumen. We aim to review herein the main signaling cascades that become activated in angiogenic endothelial cells as well as the opportunities of modulating angiogenesis through pharmacological interference with these signaling mechanisms. We will deal mainly with the mitogen-activated protein kinases pathway, which is very important in the transduction of proliferation signals; the phosphatidylinositol-3-kinase/protein kinase B signaling system, particularly essential for the survival of the angiogenic endothelium; the small GTPases involved in cytoskeletal reorganization and migration; and the kinases associated to focal adhesions which contribute to integrate the pathways from the two main sources of angiogenic signals, i.e. growth factors and the extracellular matrix.Received 13 February 2004; received after revision 25 March 2004; accepted 19 April 2004     

The functions of mucosal T cells in containing the indigenous commensal flora of the intestine

There is an immense load of non-pathogenic commensal bacteria in the distal small intestine and the colon of mammals. The physical barrier that prevents penetration (translocation) of these organisms into the body is a simple epithelium comprised of the single enterocyte/colonocyte cell layer with its overlying mucus. In this review, we discuss the roles of intestinal T cells in initiating and regulating innate and adaptive mucosal immune responses of the mucosal immune system that avoid or limit penetration of the commensal intestinal bacteria. Received 9 August 2002; accepted 9 September 2002 RID="*" ID="*"Corresponding author.     

Recombinant expression of perchloric acid-soluble protein reduces cell proliferation

Perchloric acid-soluble protein (PSP) may play an important role in the regulation of cellular physiological functions because it has been highly conserved throughout evolution; however, this role has not been well elucidated. In previous reports, we suggested that PSP regulates cell proliferation. In this study, we examined the effect of PSP expression on proliferation of the normal rat kidney cell line NRK-52E, the rat hepatocyte cell line RLN-10, and the rat hepatoma cell line dRLh-84. Cells transfected with pcDNA-sense-PSP (pcDNA-S-PSP) over-expressed PSP mRNA and protein, and cell proliferation of the transfected cells was suppressed compared with that of cells transfected with pcDNA-empty (pcDNA-E). Cell viability of pcDNA-S-PSP-transfected cells was similar to that of pcDNA-E-transfected cells. Thus, over-expression of PSP suppresses cell proliferation without any influence on cell viability. These findings are the first to report an inhibitory activity of PSP on cell proliferation. Received 27 April 2001; received after revision 8 June 2001; accepted 8 June 2001