Effects of immunosuppressors and cytostatics on the extracellular matrix production in experimental nephropathy

Methylprednisolone increased the content of laminine, cyclosporin increased the content of fibronectin, and cyclophosphamide suppressed the extracellular matrix production in experimental nephrotoxic nephritis and puromycin aminonucleoside nephrosis. Therapy should be chosen with due consideration of the extracellular matrix structure in different morphological variants of chronic glomerulonephritis. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 126, No. 11, pp. 584–587, November, 1998     

糖尿病大鼠肺病理改变及同期肾脏病理变化对比

目的:观察糖尿病(DM)大鼠肺组织改变及与同期肾脏变化的关系.方法:链脲菌素腹腔注射制作糖尿病大鼠模型,4周后胶原、网状纤维染色及透射电镜方法观察糖尿病大鼠肺组织基底膜病理改变,同期观察肾脏改变.结果:DM大鼠4周后肺组织病理改变为毛细血管基底膜及Ⅱ型肺泡上皮细胞基底膜不同程度的增厚及肺间质胶原成分等细胞外基质的增多,与同期糖尿病肾脏病变相平行.结论:DM大鼠4周后肺组织与糖尿病肾病相似,主要表现为微血管病变.     

Cell–matrix adhesion in vascular development

Summary.  Vascular development requires correct interactions among endothelial cells, pericytes and surrounding cells. These interactions involve many cell adhesion interactions, including cell–matrix interactions both with basement membranes and with surrounding extracellular matrices. Investigations of the contributions of these various interactions in vascular development and angiogenesis have been rather uneven and incomplete over the past 10–15 years. There has been considerable concentration on a few receptors, matrix proteins and proteolytic fragments with the goal of finding means to control angiogenesis. Many other potential contributors have received much less attention. Even for those molecules that have been subject to intensive investigation, our knowledge is incomplete. This review will survey the spectrum of extracellular matrix (ECM) proteins and cell–matrix adhesion receptors (particularly integrins) that are likely to contribute to angiogenesis and discuss what is known and not known about the roles of each of them.     

耐药性癫(癎)患者颞叶中细胞周期依赖性蛋白激酶5的表达

目的 研究细胞周期依赖性蛋白激酶5(cyclin dependent kinases 5,CDK5)在耐药性癫(癎)患者颞叶中的表达,探索其在耐药性癫(癎)发病机制中的作用.方法 收集耐药性癫(癎)患者术后脑组织,用荧光定量PCR、免疫组化和Western blot 3种检测方法从基因和蛋白水平分别测定CDK5在耐药性癫(癎)患者颞叶中的表达,并与对照组进行比较.结果 荧光定量PCR发现CDK5 mRAN比对照组明显增加,免疫组化检测显示这种基因的蛋白表达产物主要分布在神经元轴突和胶质细胞中,Western blot检测在相对分子质量35 000处有一蛋白条带,并且可见实验组(颞叶和海马中分别为1.4293±0.1839和2.0733±0.4738)高于对照组(颞叶和海马中分别为0.9680±0.4147和1.403±0.6163,P＜0.05).结论 CDK5在耐药性癫(癎)患者颞叶中表达增强,提示他们可能参与了耐药性癫(癎)的形成.     

酪氨酸激酶抑制剂对气管上皮细胞生长的影响

目的探讨酪氨酸激酶抑制剂(Tyrosine kinase inhibitor,TKI)对培养气管上皮细胞生长的影响.方法通过MMT法、3H-胸腺嘧啶(3H-TdR)掺入法及流式细胞计数,观察3种TKIs:Tyrphostin AG1478、Genistein(Sigma)及金转停对原代培养的大鼠气管上皮细胞增殖、周期及凋亡的影响,以及TKIs对表皮生长因子(EGF)的阻断作用.结果MTT法显示3种TKI均对气管上皮细胞的生长具有时间和剂量依赖性抑制作用,同时,TKI阻断EGF对气管上皮细胞生长的刺激作用,3种TKIs的作用无明显差异;1μmol/L的Tyrphostin AG1478、Genistein及金转停分别使气管上皮细胞的TdR掺入率降低18.3%、20.9%及19.7%,与MTT比色法结果一致.同时,Tyrphostin AG1478不仅加速气管上皮细胞的凋亡而且阻止细胞有丝分裂.TKIs可阻断表皮生长因子(EGF)对气管上皮细胞生长的刺激作用.结论TKIs不仅抑制对原代培养的大鼠气管上皮细胞的生长,加速其凋亡,而且可阻断EGF对气管上皮细胞生长的刺激作用,3种抑制剂的作用无明显差异.     

Distribution of extracellular matrix components and their receptors in human lymphoid tissue and B-cell non-Hodgkin lymphomas

In this study the distribution patterns of various extracellular matrix components and their receptors (i.e. β1 integrins) in B-cell non-Hodgkin lymphomas were examined and compared to those in reactive lymphoid tissue. Neoplastic follicles within follicular lymphomas showed similar patterns to that observed in reactive follicles, which appeared to be strongly associated with the presence of follicular dendritic cells. Diffuse lymphomas of low and intermediate malignancy grade revealed features comparable to those of interfollicular areas of reactive lymphoid tissue, irrespective to which compartment the tumour cells were related. Highly malignant lymphomas, however, displayed unique extracellular matrix configurations, resulting from active matrix degradation by macrophages; this may support rapid tumour growth. Extranodal lymphomas showed virtually the same matrix patterns as their nodal counterparts, suggesting that (malignant) lymphoid cells generate (at least partly) their own specific microenvironment. In reactive lymphoid tissue β1 integrins were mainly found on resident cells and except for α4, α5 (and β1) the lymphoid cells expressed very little, if any, β1 integrins. In comparison, expression of these integrins on lymphoma cells was reduced (follicular lymphomas) or could not be detected at all (diffusely growing lymphomas); this might contribute to the growth pattern and metastatic properties of the tumours.     

ERK信号传导通路调控乙醛刺激的肝星状细胞Na+/Ca2+泵mRNA表达的研究

目的 :探讨Erk信号传导通路调控乙醛刺激的肝星状细胞 (HSC)Na /Ca2 泵mRNA表达的影响。方法 :用链霉蛋白酶和胶原酶原位灌流 ,Metrizamide密度梯度离心分离大鼠肝星状细胞 ,采用RT PCR测定PD980 5 9阻断乙醛激活的肝星状细胞Erk活性后Na /Ca2 泵mRNA表达。结果 :乙醛刺激后 ,HSC后明显促进Na /Ca2 泵mRNA表达 (P<0 0 1) ,不同剂量PD980 5 9对肝星状细胞Na /Ca2 泵mRNA表达的影响无统计学意义。结论 :Erk信号传导通路可能对乙醛刺激的肝星状细胞激活状态的启动无明显影响     

肝纤维化组织中MMP1、TIMP1的表达及其临床意义

目的 :检测肝纤维化组织中基质金属蛋白酶 1 (MMP1 )、基质金属蛋白酶组织抑制因子 1 (TIMP1 )的表达 ,为肝纤维化的诊治提供重要的分子生物学指标。 方法 :采用链霉菌抗生物蛋白 -过氧化酶联接法 (S- P法 )检测70例肝纤维化组织中 MMP1 、TIMP1 的表达。结果:(1) TIMP1 蛋白阳性表达随肝纤维化程度的加重而增强 ,并且呈正相关关系 (r=0 .92 74 ,P <0 .0 1)。 (2 ) MMP1 蛋白阳性表达随肝纤维化程度的加重无明显变化 ,无相关关系(r =0 .2 181,P >0 .0 5 )。 结论:TIMP1 与肝纤维化的发生、发展密切相关 ,随纤维化发生、发展阳性表达增强。从分子水平对肝纤维化、肝硬化病变进行评估 ,为早期诊治肝纤维化和判断预后提供依据。     

IL-2对垂体瘤细胞系RC-4B/C细胞分泌ACTH的影响

目的 :探讨白细胞介素 2 (IL 2 )对垂体瘤细胞系RC 4B/C细胞ACTH分泌的调控作用及其影响因素 .方法 :以放射免疫方法测定培养的垂体瘤细胞系RC 4B/C细胞的培养液中的ACTH浓度 .结果 :IL 2 (1× 10 4～ 5× 10 5U·L-1)促进RC 4B/C细胞分泌ACTH ;蛋白激酶A的抑制剂H 9(1μmol·L-1)和酪氨酸蛋白激酶的抑制剂tyrphostin2 3 (1μmol·L-1)均可显著性抑制IL 2的促ACTH分泌作用 .结论 :IL 2可促进RC 4B/C细胞分泌ACTH ,该作用与蛋白激酶A和酪氨酸蛋白激酶信号转导途径紧密相关     

Acute volaemic changes modify the gastroduodenal resistance to the flow of saline in anaesthetized dogs

The effect of acute and sequential volaemic changes on the gastroduodenal flow of saline was assessed in 23 anaesthetized dogs following two different experimental protocols. Hypervolaemia, by i. v. infusion of saline, induced a gradual decrease on gastroduodenal flow which amounted to 76% below control values (P < 0.001) when volaemic expansion attained 5% of body weight. This effect was volume dependent (17% increase on gastroduodenal flow per volume of infused saline equivalent to 0.5% of body weight, P < 0.001), lasted for at least 90 minutes after infusion was completed and was also obtained by expanding previously bled animals. Hypovolaemia due to bleeding was followed by an increase on gastroduodenal flow of about 88% above control values (P < 0.05) when haemorrhage was equal to 3% of body weight. This effect was also volume dependent (23 % increase on gastroduodenal flow per volume of blood shed equivalent to a 0.5% of body weight, P < 0.01) and was reversed after blood volume was restored. These modifications in the resistance of the gastroduodenal segment to the flow of liquid due to acute volaemic changes suggest that the extracellular fluid volume modulates the contractile activity of the gastroduodenal portion of the gut possibly to set a gastroduodenal handling of liquid adequate to cope with volaemic imbalances.