大黄酸对IL-2诱发T淋巴细胞增殖和细胞[Ca2+]i变化的作用

研究大黄酸对IL-2引起大鼠T淋巴细胞增殖和细胞内[Ca2+]i变化的影响.采用MTT法检测细胞增殖,用单细胞钙成像系统记录胞内游离Ca2+浓度([Ca2+]i).结果表明,大黄酸对IL-2引起的细胞增殖有显著抑制作用,且抑制效果与剂量有关;IL-2引起[Ca2+]i升高,并持续维持高[Ca2+]i水平,[Ca2+]i升高的机制包括胞内Ca2+释放和胞外Ca2+内流;大黄酸显著抑制IL-2引起的[Ca2+]i升高.结果提示大黄酸可抑制T淋巴细胞增殖,作用机制可能与抑制细胞内[Ca2+]i升高相关.     

红树林内源真菌Fusarium sp.#ZZF51吸附Cu2+的研究

采用生物吸附法去除废水中Cu2+,研究了南海红树林内源真菌Fusarium sp.#ZZF51吸附Cu2+的行为特性、吸附模型及吸附机理。结果表明:受试菌吸附Cu2+的吸附平衡时间为90 min,常温常压下吸附最佳pH值为6.5,Cu2+初始浓度50 mg/L,吸附时间90 min,此时受试菌对Cu2+的吸附率和吸附容量分别为82.14%和20.53 mg/g。Langmuir方程比Freundlich方程能更好地描述该受试菌对Cu2+的平衡吸附行为。通过比较受试菌吸附Cu2+前后红外光谱图得知,在吸附过程中,羟基和羰基都起着十分重要的作用。     

啤酒酵母对废水中Cu~(2+)的生物吸附特性

为了用生物吸附法去除废水中铜离子,实验了用工业废弃酿酒酵母吸附Cu2+离子的生物吸附特性。结果表明:酵母吸附Cu2+的吸附平衡时间为3h,最佳条件为初始pH 4~5之间,温度20~30℃。在初始质量浓度为5.0~63.5mg/L,Cu2+去除率达到56%~22%。Langmuir方程比Freundlich方程更好地描述酵母对Cu2+平衡吸附行为。啤酒酵母吸附Cu2+为自发过程。利用废弃啤酒酵母去除废水中Cu2+是可行的。     

纳米羟基磷灰石对Cu2+的吸附

用溶胶-凝胶法制备纳米羟基磷灰石(n-HAP)吸附水溶液中的铜离子(Cu2+),研究反应时间、体系pH值和Cu2+初始浓度等因素对吸附行为的影响,并探讨吸附机理。结果表明:在溶液pH=4.5~7.5,n-HAP对Cu2+的吸附升高趋势近似线性关系;反应60 min时基本达到吸附平衡;pH>7.5时,溶液中Cu2+几乎完全去除,最大吸附量为51.28 mg/g。n-HAP对Cu2+有良好的吸附作用,吸附类型为Langmu ir等温吸附,吸附过程符合拟二级反应动力学方程。     

NH4+-Mg2+-PO43--H+-H2O体系的固液平衡热力学

对NH4+-Mg2+-PO43--H+-H2O体系中固相MgNH4PO4,Mg3(PO4)2,MgHPO4及Mg(OH)2与液相间的热力学平衡关系进行计算,绘制溶液总镁与总磷摩尔比为1-1时该体系的lgcMg-pH图、lgcN-lgcMg图和lgcN-pH图,确定体系中各种固相稳定存在的pH值范围.结果表明,溶液中的氨氮浓度和pH值是影响固相稳定存在的重要因素,MgNH4PO4的稳定区随氨氮浓度的降低而变小并最终消失,当pH=8.5且MgNH4PO4与Mg3(PO4)2共存时,溶液中的氨氮平衡浓度最低.     

甲硫氨酸在Fe3+或In3+掺杂的SnO2:Sb5+电极上的电催化氧化

采用金属离子氯化盐溶胶热分解法制备了Fe3 或In3 掺杂的SnO2:Sb5 电极,并通过线性电位扫描法考察了这种电极材料对甲硫氨酸的电催化氧化性能.根据甲硫氨酸在不同掺杂含量的SnO2:Sb5 (5%)-Fe3 和SnO2:Sb5 (5%)-In3 电极上的电催化氧化情况,确定了Fe3 和In3 离子的最佳掺杂含量分别为0.5%和0.3%.根据扫描速度、甲硫氨酸浓度和转速对甲硫氨酸在Fe3 或In3 掺杂的SnO2:Sb5 电极上的电催化氧化的影响结果可以看出,该电极对甲硫氨酸的电催化氧化性能正比于实验所采用的扫描速度、甲硫氨酸的浓度以及旋转圆盘电极的转速.     

ITO电极上Tris促进[Ru(bpy)3]2+对次黄嘌呤的电催化氧化

研究了在铟锡氧化物（ITO）电极上三羟甲基氨基甲烷（Tris）促进[Ru(bpy)3]2+（bpy = 2,2′-联吡啶）对次黄嘌呤（Hx）的电催化氧化作用. 结果表明，Tris的加入明显地增强了[Ru(bpy)3]2+对Hx的电催化氧化，扫描速度、溶液pH和Hx浓度对Hx电催化氧化均有明显的影响，Hx电催化氧化产物能与Tris发生后续的化学反应，[Ru(bpy)3]2+对Hx的催化氧化是基于后续化学反应增强均相电催化反应（EC′C）的机理. 在10 mmol/L Tris/50 mmol/L NaCl (pH 7.2)缓冲溶液中，Hx的电催化氧化电流在0.10 ~0.15 mmol/L区间随Hx浓度线性地增大，相关系数为0.991，检测限为0.12 μmol/L (S/N = 3).     

污水处理厂污泥对Cu2+、Zn2+吸附性能的研究

以污水处理厂污泥作为吸附剂,研究其对Cu2+、Zn2+吸附性能的差异.结果表明:污泥对Cu2+、Zn2+的吸附量均随着平衡浓度的增大而增大,且均符合Henry型和Freundlich型等温吸附过程,其中污泥对Zn2+的吸附固定能力高于对Cu2+的吸附固定能力;随处理浓度的增大,污泥对Cu2+、Zn2+的解吸率均减小,相...     

壳聚糖对Pb2+吸附性能研究

以壳聚糖为吸附剂,考察溶液pH值、Pb2+初始浓度等条件对壳聚糖吸附性能的影响,研究不同温度下壳聚糖对Pb2+的吸附等温线、热力学和动力学行为,并研究表观活化能.结果表明,当pH为5~6时,壳聚糖对Pb2+的吸附能力达到最大值;随着Pb2+初始浓度增加,平衡吸附量随之增加并达到最大值,此后基本不变;当温度在298~313 K变化时,平衡吸附量随Pb2+平衡浓度增大而增大,达到最大值后基本不变,吸附行为符合Langmuir方程;不同温度下的△G均小于零,且温度越高,△G越小,△H大于零,温度越高越有利于吸附;随着吸附时间延长,初始阶段吸附速率较快,此后逐渐下降,吸附动力学行为符合拟二级速率模型,吸附表观活化能为18.658 kJ/mol.     

UO2+2在人体血浆中形态的计算机模拟研究

引入UO2+2、Ca2+、Fe3+、Zn2+等金属离子和氨基酸、柠檬酸、乳酸等小分子配体建立了UO2+2在人体血浆中的金属离子–小分子配体热力学平衡模型.利用此模型研究了UO2+2在血浆中的形态及加入乙二胺四乙酸(EDTA)和二乙烯三胺五乙酸(DTPA)对血浆中UO2+2形态的影响.研究表明,在正常pH条件下,人体血浆中UO2+2主要以带负电荷的[UO2Ca(CO3)3]2-、电中性的[UO2Ca2(CO3)3](aq)和U(Ⅵ)-氨基酸配位离子的形式存在.当各形态UO2+2的总摩尔浓度[U]=5.0×10-3 mol/L时,血浆中出现固相(UO2)3(PO4)2*4H2O,并随[U]的增加而升高.Ca2+浓度的变化对血浆中UO2+2的形态有较大影响,血浆中Zn2+形态与UO2+2浓度无明显相关.在[U]=1.0×10-3 mol/L,[EDTA]=1.0×10-3 mol/L(或[DTPA]= 2.0×10-3 mol/L)条件下,血浆中UO2+2主要以水溶性小分子[UO2(OH)2EDTA]4-(或[(UO2)2(OH)DTPA]2-)的形态存在,此时固相Ca3(PO4)2溶解.这一结果提示EDTA、DTPA能有效的促排人体内的UO2+2,但同时具有较高的毒副作用.     

Fenton法去除垃圾渗滤液TOC的动力学研究

采用修正后一级反应动力学模型拟合Fenton法处理垃圾渗滤液结果,研究初始pH值、试剂比、H2 O2用量、初始浓度和温度等因素对动力学常数的影响并优化反应参数.结果表明：在考虑运行成本情况下,Fenton法处理渗滤液的最佳去除率为70.3%,此时反应条件初始pH值为3,[H2O2]/[TOC0]为4,[H2O2]/[Fe2+]为5,反应温度为室温.     

氯盐体系中铋湿法冶金的基础研究

根据同时平衡原理，对氯盐体系硫化铋矿浸出过程和三氯化铋水解过程进行了详细的热力学分析，绘制了Ｂｉ２Ｓ３－ＨＣｌ－Ｈ２Ｏ系Ｅ－ｐＨ图，Ｅ－［Ｃｌ－］Ｔ图和Ｅ－［Ｂｉ３＋］Ｔ图以及三氯化铋水解过程ｐＨ－［Ｂｉ３＋］Ｔ和溶解度－ｐＨ图，为铋湿法冶金提供重要的理论依据     

气相中二氧化铬与乙烯反应机理的理论研究

用密度泛函B3LYP/6-311++G(3df,3pd)//6-311G(2d,p)法研究了CrO2(+2A1/4A″)+C2H4生成P1[Cr(OCH2)(+2A"/4A")+CH2O]和P2[CrO(+2Σg/4Σg)+C2H4O]的气相反应,重点对影响反应机理和反应速率的势能面交叉现象进行了讨论,并运用Hammond假设和Yoshizawa等的内禀反应坐标单点垂直激发计算的方法大致确定了势能面交叉点(crossing point(CP))或势能面交叉缝(crossing seam)的位置。研究结果表明,CrO2+活化乙烯C-C键是一个[2+2]类型反应,整个反应经历了重排过程。     

以Cu2+-邻菲啰啉配合物为模板制备铜离子印迹聚合物

采用分子印迹技术,物质的量比为1∶2的Cu2+-邻菲啰啉配合物为模板,4-乙烯基吡啶为功能单体,乙二醇二甲基丙烯酸酯为交联剂,模板、功能单体与交联剂的物质的量比为1∶2∶30,在甲醇中用沉淀聚合法制备了一个铜离子印迹聚合物.该印迹聚合物在室温和pH 5.0的条件下对Cu2+的吸附可以在1h内达到平衡,理论饱和吸附容量(Qmax)为75.01mg/g,印迹因子(IF)为1.77.用该印迹聚合物制备的固相萃取柱对质量浓度为5.0μg/mL的Cu2+的萃取回收率为89.7%,相对标准偏差为4.7%(n=5).表明其有作为分析测定Cu2+时的固相萃取剂的应用前景.     

Cyclic nucleotides control a system which regulates Ca2+ sensitivity of platelet secretion

Cellular responses to extracellular signals are mediated by changes in the intracellular concentrations of one or more second messengers. In platelets, inhibitory agonists increase intracellular cyclic-3',5'-AMP [( cyclic AMP]i (refs 2, 3] whereas excitatory agonists increase [Ca2+]i and/or [1,2-diacylglycerol]i (refs 4-9), and in some cases decrease [cyclic AMP]i (refs 10, 11). Both activation and inhibition of platelet responses have been attributed to an increase in [cyclic-3',5'-GMP]i (refs 8, 12). The activity of protein kinase C, which is associated with the platelet secretory response, is increased by both 1,2-diacylglycerol and Ca2+ (refs 4, 7, 8). The role of cyclic AMP may involve either inhibition of Ca2+ mobilization to the cytosol or stimulation of intracellular Ca2+ uptake, and in addition inhibition of 1,2-diacylglycerol formation. The relationship between cyclic-3',5'-GMP (cyclic GMP) and other second messengers in platelet activation has not been defined. Using platelets made permeable by exposure to an intense electric field, we demonstrate here modulation of the Ca2+ sensitivity of platelet secretion by thrombin, and by 12-O-tetradecanoylphorbol-13-acetate (TPA) and 1-oleyl-2- acetylglycerol ( OAG ), both potent activators of protein kinase C. The effect of thrombin is selectively modified by cyclic GMP and cyclic AMP. The response to OAG and TPA is also modulated by cyclic AMP but to a much lesser extent.     

五元体系Li~+,K~+//Cl~-,B_4O_7~(2-),CO_3~(2-)-H_2O在298K时相平衡的实验研究

采用等温溶解平衡法研究了五元体系 L i+ ,K+ / / Cl- ,B4O2 -7,CO2 -3- H2 O在 2 98K时相关系和平衡液相物化性质。对各组分的溶解度以及密度、折光率、粘度、电导率和 p H值进行了测定 ,并绘制了相关相图 ,得到 5个结晶相区和 3个共饱点。该体系没有固溶体和复盐生成 ,为简单共饱和型体系。     

Quantification of Ca2+-activated K+ channels under hormonal control in pig pancreas acinar cells

Ca2+- and voltage-activated K+ channels are found in many electrically excitable cells and have an important role in regulating electrical activity. Recently, the large K+ channel has been found in the baso-lateral plasma membranes of salivary gland acinar cells, where it may be important in the regulation of salt transport. Using patch-clamp methods to record single-channel currents from excised fragments of baso-lateral acinar cell membranes in combination with current recordings from isolated single acinar cells and two- and three-cell clusters, we have now for the first time characterized the K+ channels quantitatively. In pig pancreatic acini there are 25-60 K+ channels per cell with a maximal single channel conductance of about 200 pS. We have quantified the relationship between internal ionized Ca2+ concentration [( Ca2+]i) membrane potential and open-state probability (p) of the K+ channel. By comparing curves obtained from excised patches relating membrane potential to p, at different levels of [Ca2+]i, with similar curves obtained from intact cells, [Ca2+]i in resting acinar cells was found to be between 10(-8) and 10(-7) M. In microelectrode experiments acetylcholine (ACh), gastrin-cholecystokinin (CCK) as well as bombesin peptides evoked Ca2+-dependent opening of the K+ conductance pathway, resulting in membrane hyperpolarization. The large K+ channel, which is under strict dual control by internal Ca2+ and voltage, may provide a crucial link between hormone-evoked increase in internal Ca2+ concentration and the resulting NaCl-rich fluid secretion.     

Oscillations of intracellular Ca2+ in mammalian cardiac muscle

Contraction of cardiac muscle depends on a transient rise of intracellular calcium concentration ([Ca2+]i) which is initiated by the action potential. It has, however, also been suggested that [Ca2+]i can fluctuate in the absence of changes in membrane potential. The evidence for this is indirect and comes from observations of (1) fluctuations of contractile force in intact cells, (2) spontaneous cellular movements, and (3) spontaneous contractions in cells which have been skinned to remove the surface membrane. The fluctuations in force are particularly prominent when the cell is Ca2+-loaded, and have been attributed to a Ca2+-induced Ca2+ release from the sarcoplasmic reticulum. In these conditions of Ca2+-loading the normal cardiac contraction is followed by an aftercontraction which has been attributed to the synchronization of the fluctuations. The rise of [Ca2+]i which is thought to underlie the aftercontraction also produces a transient inward current. This current, which probably results from a Ca2+-activated nonspecific cation conductance, has been implicated in the genesis of various cardiac arrhythmias. However, despite the potential importance of such fluctuations of [Ca2+]i their existence has, so far, only been inferred from tension measurements. Here we present direct measurements of such oscillations of [Ca2+]i.