二元羧酸对草酸钙结晶的调控作用

采用双扩散法系统研究了凝胶体系中二元羧酸对尿结石主要成分草酸钙结晶的影响,这些羧酸分别为含有0、1、2个羟基的丁二酸、羟基丁二酸、酒石酸,含有1个氨基的L-天冬氨酸,以及含有双键的顺丁烯二酸、反丁烯二酸．对于丁二酸、羟基丁二酸和酒石酸的研究表明,随着羧酸中羟基数目的增加,抑制一水草酸钙(COM)聚集和诱导二水草酸钙(COD)生成的能力逐渐增强;随着羧酸浓度的增大,抑制COM聚集和诱导COD生成的能力也增强;随着结晶时间的增加,COM晶体钝化程度加深．对L-天冬氨酸、顺丁烯二酸和反丁烯二酸的研究表明,三者影响不明显．     

Binding of estradiol to synaptosomal mitochondria: physiological significance

The subsynaptosomal distribution and specific binding of 17beta-estradiol in vitro to mitochondria isolated from presynaptic nerve endings of female rat brain were examined. 17Beta-estradiol is (i) distributed unequally in synaptosomes and mitochondria posses the highest capacity to bind estradiol with respect to the available amount of the hormone. (ii) Estradiol binds specifically to isolated synaptosomal mitochondria. A Michaelis-Menten plot of specific binding was sigmoidal within a concentration range of 0.1-5 nM of added estradiol, with a saturation plateau at 3 nM. Binding of higher estradiol concentrations demonstrated an exponential Michaelis-Menten plot, indicating non-specific binding to mitochondria. Vmax and Km for the sigmoidal-shape range were estimated as 46 +/- 6 fmol of estradiol/mg of mitochondrial proteins and 0.46 +/- 0.07 nM free estradiol respectively. (iii) Estradiol binding is not affected by the removal of ovaries. The results show that inhibition of Na-dependent Ca2+ efflux from mitochondria by estradiol occurs according to an affinity change of the translocator for Na+, at the same estradiol concentrations that show specific binding to mitochondrial membranes. These data imply that physiological concentrations of estradiol, acting on mitochondrial membrane properties, extragenomically modulate the mitochondrial, and consequently the synaptosomal content of Ca2+, and in that way exert a significant change in nerve cell homeostasis.     

Changes in calpastatin localization and expression during calpain activation: a new mechanism for the regulation of intracellular Ca<Superscript>2+</Superscript>-dependent proteolysis

The amount of calpastatin directly available in cytosol is under the control of [Ca²⁺] and [cyclic AMP]. Prolonged calpain activation also promotes degradation of calpastatin. The fluctuation of calpastatin concentration in cell soluble fraction is accompanied by an initial decrease in calpastatin gene expression, followed by a fivefold increase in its expression when the inhibitor protein is degraded. This process can be conceptualized as a mechanism to regulate calpastatin availability in the cell. This conclusion is supported by the fact that calpain, the other component of this proteolytic system, undergoes changes in its levels of expression in a much more limited manner. Furthermore, this process can be observed both in cells exposed to different natural stimuli, or in other cell lines. Modification of calpastatin gene expression might represent a new tool for the in vivo control of the regulatory machinery required for the modulation of Ca²⁺-dependent proteolysis.Received 18 July 2003; received after revision 3 September 2003; accepted 23 September 2003     

Cardiac protective role of a novel erythrocyte-derived depressing factor on rats and its Ca^2＋ mechanism

The cardiac protective role of a novel erythro-cyte-derived depressing factor (EDDF) on spontaneous hy-pertensive rats (SHR), calcium overload (CaO) rats and Wistar rats and its mechanism was evaluated. Mean artery pressure (MAP), heart rate (HR) and LVdp/dtmax were measured by physiological recorder. The effect of EDDF on the Ca2+-ATPase activity in myocardial sarcoplasmic reticu-lum (SR) of CaO rats was determined by inorganic phos-phate assay. Calcium transport in myocytes was measured by 45Ca2+ radioactive isotope measurement. The phosphoryla-tion levels of extracellular signal-regulated protein kinases (ERK1/2) in myocardial tissue of SHR and CaO rats were measured by Western blot method. And the ultrastructures of cardiac muscle cells were observed with the transmission electron microscope. The results indicated that EDDF could significantly decrease MAP, HR and LVdp/dtmax in a dose dependent manner (P < 0.05). It seems that the mechanism might relate with activating the Ca2+-APTase, enhancing the uptake and release of Ca2+ from SR (P < 0.05), decreasing the phosphorylation levels of ERK1/2 of myocytes (P < 0.01) and lightening the ultrastructural lesion of cardiac muscle cells. In CaO rats, the Ca2+-ATPase activity decreased clearly com-pared to control (64.99 7.16 vs 94.48 7.68 nmol·min-1 ·mg-1 protein, P < 0.01), while EDDF (100 mg/mL) could significantly increase the activity (87.93 ?9.54 vs 64.99 ?7.16, P < 0.05, n = 7). Both uptake and release rate of Ca2+ (祄ol 45Ca2+/g protein/min) from myocardial SR of CaO rats re-markably decreased compared to control (32.40 ?2.70 and 15.46 ?1.49 vs 61.09 ?10.89 and 25.47 ?4.29, P < 0.05); EDDF (100 mg/mL) could significantly stimulate their activi-ties (50.48 6.76 and 21.76 2.75 vs 32.40 2.70 and 15.46 1.49, P < 0.05). EDDF could evidently down-regulate the phosphorylation of ERK1/2 in myocardial tissue from SHR and CaO rats (P < 0.01), lighten the ultrastructural lesion of cardiac muscle cells of SHR as well. It is concluded that EDDF seems to play protective roles on both structure and function of heart, which closely related with amelioration of Ca2+ transport and inhibition of Ca2+-MAP kinase pathway.     

氢氧化铝颗粒的附聚动力学研究

以往的氢氧化铝颗粒尺寸对其附聚动力学影响的研究结果不甚相同,本文对此进行了进一步的研究。基于附聚过程的颗粒二元碰撞模型,以粒径ri-1,ri,ri 1的3种颗粒为作用物,按照穷举法,建立了附聚的物理模型。依照附聚模型给出了氢氧化铝颗粒的附聚速率方程,根据差分法求出了附聚的宏观速率,建立了不同粒径颗粒的附聚速率方程组。计算的动力学结果表明:等径颗粒的附聚速率常数要大于不等径颗粒的附聚速率常数;对于等粒径的颗粒,其中粒径最小的颗粒附聚速率常数最大,随着粒径增加,颗粒的附聚速率常数逐渐减少;对于不等径颗粒,其粒径相差越大,附聚的速率常数越小;动力学的计算结果与实验结果能够很好地吻合。     

固定化优势菌降解2，6-二叔丁基酚的研究

用前期研究中获得的2,6-二叔丁基酚(简2,6-DTBP)降解菌(Aeromonas sp.),进行了对2,6-二叔丁基酚的降解性能等研究。结果表明菌株经固定化包埋后,降解底物2,6-DTBP的能力大大提高。在100.0mg/L的初始浓度下其降解率在十二天可达到81%。通过对固定化菌株的降解反应过程的动力学分析,其对底物的降解反应符合一级动力学特征,当2,6-DTBP初始浓度为100mg/L时,固定化菌种其动力学常数为0.1232,半衰期为5.63day。扫描电镜观察到菌种在海藻酸钙包埋载体中能良好地生长和繁殖。     

减水剂对掺电石渣水泥砂浆强度影响的研究及配方确定

采用正交试验法探讨掺入减水剂后各因素对掺电石渣的水泥砂浆强度的影响,确定水泥砂浆强度性能较佳的配方并分析其微观结构.结果表明:掺入减水剂后,对掺电石渣的水泥胶砂试样早期抗压强度的影响从大到小的次序分别为胶砂比、水灰比、电石渣掺量、减水剂掺量、减水剂品种、搅拌时间、减水剂的掺入方式.正交试验法确定的水泥胶砂试样较佳的配方为,电石渣掺量为5%;减水剂为J2,采用后掺方式,其掺量为0.5%;水灰比为0.377;胶砂比为1∶1.5;搅拌时间为9 min.     

钙离子形态对吸附效果的影响研究

通过不同方式配制高钙水,来研究矿物吸附材料对钙离子的吸附规律,同时对吸附过程中的流体力化学效应进行了探讨.实验结果表明,矿物吸附材料对钙的吸附性能与钙在溶液中的存在形态有很大关系:用CaCl2配制的高钙水中,钙主要以离子形态存在,矿物吸附材料对其吸附主要以静电吸附为主,5A沸石对钙离子有筛分效应;用CaO配制的高钙水中,钙主要以Ca(OH)2(2q)、Ca(OH)2(s)沉淀微晶、Ca2 和Ca(OH) 多种形态存在,矿物吸附材料对其吸附有静电吸附、一羟基络合吸附、表面沉淀吸附,同时,矿物吸附材料的加入对氢氧化钙沉淀起晶种作用,可以加速其沉淀;合适的流体剪切力可以提高5A沸石对钙离子的吸附量,此结论证实了吸附过程中流体力化学效应的存在.图4,表2,参7.     

Icariin suppresses bone resorption activity of rabbit osteoclasts in vitro

The effect of icariin on the bone resorption activity of rabbit osteoclasts is assessed in vitro. Osteoclasts were isolated from Japanese white rabbits and cultured on plates with a sterilized bone slice in each well. After treatment with icariin at various concentrations, the bone resorption activity of osteoclasts was evaluated by examining pit areas, superoxide anion (·O2-) generation, size and number of actin rings and intracellular calcium concentration [Ca2 ]i. As revealed by these data, icariin elicited continuous decline of [Ca2 ]i, making actin ring constricted and ·O2- generation decreased. These events resulted in smaller and fewer pits which indicate suppressed bone resorption activity of rabbit osteoclasts by icariin.     

The effects of S4 segments on the voltage-dependence of inactivation for Cav3.1 calcium channels

T-type calcium channels exhibit fast voltage-dependent inactivation, for which the underlying struc- ture-function relationship still remains unclear. To investigate the roles of S4 segments in volt- age-dependent inactivation of T-type calcium channels, we created S4 replacement chimeras between Cav3.1 calcium channels (fast voltage-dependent inactivation) and Cav1.2 calcium channels (little voltage-dependent inactivation) by replacing S4s in Cav3.1 with the corresponding regions in Cav1.2. Wild type and chimeric channels were expressed in Xenopus oocytes and channel currents were re- corded with two-electrode voltage-clamp. We showed that replacing S4 region in domain I shifted voltage-dependence for inactivation of Cav3.1 to the left, and the V0.5 inact and kinact value were signifi- cantly changed. However replacing S4s in domains II―IV had no effects on the voltage-dependent in- activation properties. These results suggest that the roles of S4 segments in domains I―IV are different, and S4 in domain I is likely to be involved in voltage-dependent inactivation process. Its movement during membrane depolarization may trigger a conformational change in the inactivation gate.