负压输水光滑管道水力摩擦系数的试验研究

为了研究虹吸进流在某些输水工程改造中取得显著效果的内在机理,通过在实验室内进行复杂起伏管路的局部窝气/没窝气情况下阻力特性试验,并对试验管道(DN50有机玻璃管)的水力摩擦系数进行了试验预估,得到了比基于穆迪图估算更低的数值.为了排除该复杂管路中诸多弯头、球阀等部件对试验结果的干扰,重新搭建了一套前端带有虹吸负压整流装置的简单直管系统,对负压情况下的圆管流动水力摩擦系数进行了试验研究.管道为透明有机玻璃,可视为水力光滑管道.通过测量直管上两相距18.4 m的侧压点,在不同流量下的得到其水力摩擦系数,测试不仅获得比先前学者更低的水力摩擦系数,而且随雷诺数变化表现出一种新的趋势,由此得出负压对管道流动有着重要的影响.     

鸡肺动脉平滑肌细胞培养及免疫组化鉴定

应用组织贴块法、贴块配合差速贴壁法成功培养不同日龄鸡的肺动脉平滑肌细胞。一般需4－7d细胞从组织块边缘长出，再经5－10d长成细胞单层。鸡日龄越小培养的肺动脉平滑肌细胞生长越旺盛。培养的肺动脉平滑肌细胞呈梭形、三角形、圆形核位于中央，胞浆丰富致密。用兔抗鸡α-actin多克隆抗体为一抗做免疫组化染色，平滑肌细胞占95％以上。     

水力光滑圆管临界雷诺数的确定

根据由Prandtle紊流混合长理论推导出的光滑圆管中紊流的速度分布和Nikuratse测得的圆管中紊流的速度剖面图确定的层流边层的区域范围,推导出层流边层厚度的计算公式,提出一个新的水力光滑圆管临界雷诺数计算模型.经试验数据验证,新计算模型确定的临界雷诺数与试验点符合很好.     

Effects of human xeroderma pigmentosum group D gene on proliferation of human vascular smooth muscle cells induced by interleukin-6

AIM: To investigate the effects of human xeroderma pigmentosum group D (XPD) gene on the proliferation of human vascular smooth muscle cells (VSMCs) induced by interleukin-6 (IL-6). METHODS: Recombinant plasmid pEGFP-N2/XPD and vacant plasmid pEGFP-N2 were transfected into VSMCs by liposome, and then these cells were incubated with IL-6 at 1×10⁵ U/L for 48 h. The cells were divided into 6 groups: blank control group; pEGFP-N2 group; pEGFP-N2/XPD group; IL-6 group; IL-6 + pEGFP-N2 group; IL-6 + pEGFP-N2/XPD group. The expression of green fluorescent protein was observed under fluorescence microscope. The cell growth was detected by MTT method. The cell cycle and apoptosis rate were examined by flow cytometre. The expression levels of XPD, Bcl-2, Bax and wild type P53 (wt-P53) were detected by RT-PCR and Western blotting.RESULTS: Green fluorescence was observed in the cells transfected with pEGFP-N2/XPD or pEGFP-N2, indicating successful transfection MTT results showed that the transfection of pEGFP-N2/XPD inhibited the cell growth, and reduced the positive effects of IL-6 on VSMCs growth. Flow cytometry results showed that the transfection of pEGFP-N2/XPD increased the apoptosis rate of VSMCs and the cell numbers in G₀/G₁ phase, decreased the cell numbers in S phase, and reduced the effects that IL-6 decreased the apoptosis rate of VSMCs and the cell numbers in G₀/G₁ phase, and increased the cell numbers in S phase. The results of RT-PCR and Western blotting showed that the transfection of pEGFP-N2/XPD increased the expression of XPD, Bax and wt-P53, decreased the expression of Bcl-2, and reduced the effects that IL-6 decreased the expression of Bax and wt-P53, and increased the expression of Bcl-2. CONCLUSION: XPD gene inhibits VSMCs proliferation, promotes VSMCs apoptosis, and reduces the effects that IL-6 promotes VSMCs proliferation and inhibits VSMCs apoptosis. Therefore, XPD gene is likely to be potential molecular target for treatment of atherosclerosis.     

Role of α1 adrenoceptor in proliferation of hypoxic pulmonary artery smooth muscle cells

AIM: To investigate the role of α₁ and β₂ adrenoceptors(α₁AR and β₂AR) in the proliferation of hypoxic pulmonary artery smooth muscle cells (PASMCs).METHODS: PASMCs were isolated by an explant method from neonatal bovine pulmonary arteries. The cultured PASMCs were exposed to 6.6% O₂ for 6 h, 12 h and 24 h. The method of -TdR incorporation was used to measure the proliferation of PASMCs. _i was assayed with Fura-2/AM. The mRNA expression of α₁AR, β₂AR, c-fos and c-myc was determined by Northern blotting. The effects of activation of α₁AR and β₂AR, and inhibition of α₁AR on the above indexes were observed by treating PASMCs with different AR agonists and antagonists under hypoxic condition.RESULTS: Significant increase in TdR incorporation in hypoxic PASMCs with α₁AR activation was observed, and marked decrease in that was induced by α₁AR inhibition. However, no significant change was found after β₂AR activation. _i , the mRNA expression of c-fos, c-myc, α₁AR and β₂AR in PASMCs were increased after hypoxia.CONCLUSION: Hypoxia induces the increase in _i and mRNA expression of c-fos and c-myc, leading to the proliferation of PASMCs. The hypoxic proliferation of PASMCs is intervened by α₁AR, but not β₂AR. The remodeling of pulmonary arteriole and pulmonary hypertension may be involved in the processes of pulmonary arteriole constriction and proliferation induced by hypoxia through up-regulation of α₁AR.     

CREG inhibits proliferation of VSMCs by modulating internalization of IGF2R/IGFII

AIM: To study the molecular mechanisms of cellular repressor of E1A-stimulated genes (CREG) on the proliferation of human vascular smooth muscle cells (VSMCs) in vitro.METHODS: The pLNCX₂-CREG plasmid and the pSM₂-siCREG plasmid were transfected into VSMCs to produce the cell clones of over-expression and down-expression of CREG, respectively.BrdU assay and FACS cell cycle analysis were performed to detect the proliferation of the cells.The expression and localization of insulin-like growth factor Ⅱ receptor(IGF2R) in the hVSMCs were detected by Western blotting and immunocytochemistry.The expression and secretion of insulin-like growth factor Ⅱ(IGFII) were measured by RT-PCR and ELISA.Alexa 488-labeled rhIGFII was used to investigate the endocysis of the cells.The blockade of IGFII internalization was conducted by treating the cells with both neutralized antibody of IGF2R and recombinant IGF2R peptide to detect the effect of IGFII on HVSMCs growth.Furthermore, Western blotting and signal pathway inhibitor were used to analysis the activation of PI3K/Akt and ERK on VSMCs proliferation.RESULTS: Compared with the control cells, Western blotting identified that the expression of CREG was increased in VSMCs-CREG cells and was decreased in VSMCs-siCREG cells.Meanwhile, the over-expression of CREG in the cells inhibited the proliferation of VSMCs and enhanced the distribution of IGF2R in cellular membrane.Furthermore, over-expression of CREG also accelerated the endocytosis of IGFII in VSMCs-CREG cells, and attenuated the secretion of IGFII into cell medium.Blockade experiments showed that enhancement of IGFII secretion promoted the proliferation of HVSMCs.PI3K/Akt and ERK signal pathways mediated the effect of IGFII on the VSMCs.CONCLUSION: CREG inhibits the proliferation of VSMCs through interfering with the internalization of IGF2R-IGFII.     

球形约束变分不等式的光滑化牛顿方法

研究球形约束变分不等式求解的算法 ,提出一种光滑化牛顿方法 ,证明了该方法具有全局收敛性和超线性收敛     

Effects of probucol on the proliferation of rat vascular smooth muscle cells stimulated by basic fibroblast growth factor and hydrogen peroxide

AIM: To investigate the effect of probucol on proliferation of rat vascular smooth muscle cells(VSMC) stimulated by basic fibroblast growth factor (bFGF) and/or hydrogen peroxide(H₂O₂). METHODS: Effects of probucol on VSMC proliferation and DNA synthesis stimulated by bFGF and/or H₂O₂ were observed by means of MTT test, cell number count and [3H]-TdR incorporation. RESULTS: ①Probucol significantly inhibited proliferation and DNA synthesis in VSMC stimulated by bFGF and/or H₂O₂, with dosage-dependent manner. Cell number, A value and [3H]-TdR incorporation in group probucol+bFGF and group probucol+H₂O₂ were reduced by 40.0%, 39.1%, 45.5% and 46.9%, 45.0%, 39.5%, respectively, compared with group bFGF and group H₂O₂ (P＜0.05, P＜0.01, respectively). ②Pretreatment of VSMC with probucol for 24 h prior to bFGF and/or H₂O₂ stimulation exhibited significant inhibiton of VSMC proliferation and DNA synthesis, but after prestimulation by bFGF and/or H₂O₂ for 24 h, probucol had no influence on VSMC proliferation and DNA synthesis (P＞0.05). CONCLUSION: Probucol dramatically inhibited proliferation and DNA synthesis in VSMC stimulated by bFGF and/or H₂O₂, but had no inhibitory effect on the cell proliferation prestimulated by bFGF and /or H₂O₂.     

Role of NHE-1 in the proliferation and apoptosis of pulmonary artery smooth muscle cell in rats

AIM: To evaluate the role of Na⁺/H⁺ exchanger-1(NHE-1)in the proliferation and apoptosis of pulmonary artery smooth muscle cells in rats. METHODS: Twenty Wistar rats were equally randomized into the control group and 3-week hypoxic group. Intracellular pH (pHi) of the smooth muscle was determined with fluorescence measurement of the pH-sensitive dye BCECF-AM and the expression of NHE-1 mRNA was detected with RT-PCR. The primary culture of pulmonary artery smooth muscle cell in vitro was performed. In situ cell death detection kit (TUNEL) was used to study the effect of specific NHE-1 inhibitor, dimethyl amiloride (DMA), on the apoptosis of muscle cells which had intracellular acidification. RESULTS: pHi value and expression of NHE-1 mRNA of pulmonary artery smooth muscle cell were significantly higher respectively in the hypoxic group than those in the control group (P＜0.01). DMA elevated the apoptotic ratio significantly. The effect was enhanced when DMA concentration was augmented and the time was prolonged. CONCLUSION: With the function of adjusting pHi, NHE-1 may play an important role in the proliferation and apoptosis of pulmonary artery smooth muscle cells.     

浅谈达到桥涵砼施工外观质量的几点看法

为了提高混凝土的外观质量,本文作者详细论述了混凝土施工各工序的施工方法和注意事项。