富里酸和Ca^(2+)共存对嗜酸性氧化亚铁硫杆菌介导生成次生高铁矿物的影响

为揭示富里酸和Ca^(2+)共存对嗜酸性氧化亚铁硫杆菌(Acidithiobacillus ferrooxidans)氧化酸性矿山废水(AMD)中的Fe^(2+)和形成次生高铁矿物的影响,分析了pH、Fe^(2+)氧化率、铁沉淀率以及次生高铁矿物矿相、基团等相关指标。结果表明,Ca^(2+)确实具有提高嗜酸性氧化亚铁硫杆菌氧化Fe^(2+)的能力。低质量浓度(0.2 g/L)的富里酸对嗜酸性氧化亚铁硫杆菌活性的提高具有促进作用,高质量浓度(0.4 g/L)的富里酸具有抑制作用,而增加Ca^(2+)反过来能够减弱高浓度富里酸对嗜酸性氧化亚铁硫杆菌的抑制作用。对形成的次生高铁矿物进行X射线衍射(XRD)和傅立叶红外光谱(FTIR)分析,结果表明高浓度富里酸促进了另一次生高铁矿物草黄铁矾的生成。

川芎嗪抑制ROCK的表达降低模拟失重大鼠血管Ca^(2+)敏感性

研究失重条件下血管平滑肌收缩性、Ca^(2+)敏感性及其调控通路RhoA-ROCK蛋白表达的变化,以及川芎嗪干预对其的影响。大鼠尾部悬吊模拟失重,在机体前、后部分别选取颈总动脉和肠系膜上动脉。在模拟失重大鼠颈总动脉中,由苯肾上腺素(PHE)或KCl诱发的血管收缩性和Ca^(2+)敏感性增强,RhoA激酶2(ROCK II)的表达、肌球蛋白磷酸酶靶亚基1(MYPT1)和肌球蛋白调节轻链(MLC)的磷酸化水平均上升,血管孵育Y-27632(ROCK特异性抑制剂)后可降低以上变化。模拟失重大鼠灌饲川芎嗪亦可降低以上变化。模拟失重后,大鼠肠系膜上动脉的收缩性和Ca^(2+)敏感性、ROCK II的表达、MYPT1和MLC的磷酸化水平降低,血管孵育Y-27632对以上变化无明显作用。模拟失重大鼠灌饲川芎嗪亦对以上变化无明显作用。结果表明,由RhoA-ROCK调控的血管平滑肌Ca^(2+)敏感性的变化可能是失重条件下机体前后部血管收缩性发生区域性重塑的关键因素。川芎嗪可抑制ROCK蛋白的表达,降低血管平滑肌升高的Ca^(2+)敏感性,从而纠正失重条件下机体前部血管收缩性的增强,但对失重条件下机体后部血管收缩性的减弱无恢复作用。

外源Ca^(2+)对玉米幼苗镉胁迫的缓解效应

本试验以玉米为研究材料,对玉米幼苗进行一定浓度的镉(20mg/L)胁迫,通过对玉米幼苗施加不同浓度的Ca^(2+)(0、2、5、8mmol/L),研究Ca^(2+)对镉胁迫下玉米幼苗的叶绿素、MDA、可溶性糖、可溶性蛋白、游离脯氨酸和POD活性6个生理生化指标的影响。结果表明:施加外源Ca^(2+)显著增加了镉胁迫下南瓜幼苗叶片中叶绿素含量(P<0.05),而MDA含量、可溶性糖含量、游离脯氨酸含量以及POD活性均显著降低(P<0.05),对可溶性蛋白的缓解作用不显著(P>0.05)。其中以5mmol/LCa^(2+)的缓解效果最好。

Ca^(2+) cytochemical changes of hepatotoxicity caused by halothane and sevoflurane in enzyme-induced hypoxic rats

AIM： To investigat the relation between hepatotoxicity of halothane and sevoflurane and altered hepatic calcium homeostasis in enzyme-induced hypoxic rats. METHODS： Forty-eight rats were pretreated with phenobarbital and randomly divided into six groups （eight in each group） and exposed to O2/N2/1.2 MAC anesthetics for 1 h： normal control （NC）, 21% O2/79% N2; hypoxic control （HC）, 14% O2/86% N2; normal sevoflurane （NS）, 21% O2/ N2/1.2MAC sevoflurane; hypoxic sevoflurane （HS）, 14% O2/N2/1.2MAC sevoflurane; normal halothane （NH）21%O2/79%N2/1.2MAC halothane; hypoxic halothane （HH）, 14%O2/N2/1.2MAC halothane. Liver specimens and blood were taken 24 h after exposure to calcium and determined by EDX microanalysis. RESULTS： The liver of all rats given halothane （14% O2） had extensive centrilobular necrosis and denaturation. Morphologic damage was accompanied with an increase in serum glutarnic pyruvic transminase. In groups NH and HH, more calcium was precipitated in cytoplasm and mitochondria. CONCLUSION： These results suggest that halothane increases cytosolic Ca^2＋ concentration in hepatocytes. Elevation in Ca^2＋ concentration is implicated in the mechanism of halothane-induced hepatotoxicity. sevoflurane is less effective in affecting hepatic calcium homeostasis than halothane.

Changes of cytosolic [Ca^(2+)]i in neutrophils in pancreatic microcirculation of rats with caerulein-induced acute pancreatitis under fluid shear stress

AIM: To investigate the fluid shear stress induced changes of [Ca^2+]i in neutrophils in pancreatic microcirculation of experimental acute pancreatitis (AP).METHODS: Wistar rats (n = 36) were randomized into three groups. A model of AP was established by subcutaneous injection of caerulein. Low-shear 30 viscometer was used to provide steady fluid shear stress on separated neutrophils. The mean fluorescent intensity tested by flow cytometry was used as the indication of [Ca2+]i quantity.RESULTS: Under steady shear, cytosolic [Ca^2+]i showed biphasic changes. The shear rate changed from low to high, [Ca^2+]i in different groups decreased slightly and then increased gradually to a high level (P<0.05). A close correlation was observed between the cytosolic [Ca^2+]i level and the alteration of fluid shear stress in regional microcirculation of AP. CONCLUSION: The increase of [Ca^2+]i is highly related to the activation of neutrophils, which contributes to neutrophil adhesion to endothelium in the early phase of AP. The effect of fluid shear stress on [Ca^2+]i may play a crucial role in pancreatic microcirculatory failure of AP.

Ca^(2+) Entry Through TRPC1 Channels Contributes to Intracellular Ca^(2+) Dynamics and Consequent Glutamate Release from Rat Astrocytes

各种不同的刺激作用于星型胶质细胞,可以导致胞浆内Ca2+浓度增加,进而释放更多谷氨酸作用于周边的神经元。大部分Ca2+来源于细胞内,小部分来源于细胞外。Ca2+内流是通过钙池操纵Ca2+通道(SOC)实现的。因此,作者观察在星型胶质细胞内Ca2+激活与谷氨酸释放过程中钙池操纵Ca2+通道(SOC)发挥了什么样的作用。已有研究显示星型胶质细胞所表达的TRPC通道(Ca2+通过瞬时受体电位通道相关蛋白)介导了钙池操纵Ca2+的内流。本文发现培养的星形胶质细胞以及从视皮质中新分离的星形胶质细胞表达TRPC1,TRPC4,和TRPC5。间接免疫组化显示这些蛋白存在于整个细胞中,然而机能检测TRPC1主要表达在质膜上。在新分离的星形胶质细胞中做标记,显示了在细胞发育过程中TRPC表达的改变。应用抗TRPC1的抗体,可以阻断TRPC1通道并且可以测定它们在培养的星形细胞的机械性和激动剂触发的钙离子内流过程中的作用。阻断TRPC1可以减少机械诱导的钙离子依赖性的谷氨酸盐的释放。这些实验数据表明,钙离子通过TRPC1通道的内流有助于钙离子在星形细胞中的信号传导以及由此引起的谷氨酸盐的释放。

Dual mechanisms of Bcl-2 regulation in IP_(3)-receptor-mediated Ca^(2+)release:A computational study

Inositol 1,4,5-trisphosphate receptors(IP_(3)R)-mediated calcium ion(Ca^(2+))release plays a central role in the regulation of cell survival and death.Bcl-2 limits the Ca^(2+)release function of the IP3R through a direct or indirect mechanism.However,the two mechanisms are overwhelmingly complex and not completely understood.Here,we convert the mechanisms into a set of ordinary differential equations.We firstly simulate the time evolution of Ca^(2+)concentration under two different levels of Bcl-2 for the direct and indirect mechanism models and compare them with experimental results available in the literature.Secondly,we employ one-and two-parameter bifurcation analysis to demonstrate that Bcl-2 can suppress Ca^(2+)signal from a global point of view both in the direct and indirect mechanism models.We then use mathematical analysis to clarify that the indirect mechanism is more efficient than the direct mechanism in repressing Ca^(2+)signal.Lastly,we predict that the two mechanisms restrict Ca^(2+)signal synergistically.Together,our study provides theoretical insights into Bcl-2 regulation in IP_(3)R-mediated Ca^(2+)release,which may be instrumental for the successful development of therapies to target Bcl-2 for cancer treatment.

Protective effect of curcumin on tumor necrosis factor-alpha-induced neuronal damage in the rat hippocampus A relationship to the inhibition of neuronal Ca^(2+) influx

BACKGROUND： Previous studies of curcumin have focused mainly on its cytotoxic properties for antitumor therapy. There are few studies addressing the application of curcumin in the prevention and treatment of nervous system diseases. OBJECTIVE： To observe the protective effect of curcumin against tumor necrosis factor-alpha （TNF-α）-induced neuronal damage in the rat hippocampus and to explore the intervention effect of curcumin on Ca^2＋ influx following neuronal damage. DESIGN, TIME AND SETTING： A cell morphological and physiological study was performed at the Institute of Brain Research, Medical College of Jinan University, China, from December 2006 to June 2007. MATERIALS： Curcumin （Sigma, USA） and TNF-α （Sigma, USA） were used in this study. METHODS： Hippocampal neurons were isolated from one-day neonatal rats and primarily cultured for 5 days. Following this they received 1 pmol/L curcumin and 100 ng/mL TNF-a pre-treatment. Dynamic morphological changes were observed for 1 hour by inverted microscopy. At 48 hours post-treatment, static morphological characteristics of the neurons were observed using inverted microscopy. Subsequently, hippocampal neurons were primarily cultured for 7 days, after receiving 1 pmol/L curcumJn and 4.5 ng/mL TNF-a pre-treatment. Intracellular free Ca^2＋ was measured using Fluo 3/acetoxymethyl ester. MAIN OUTCOME MEASURES： Effects of curcumin on TNF-a-induced neuronal damage and Ca^2＋ influx in the rat hippocampus were measured. RESULTS： Following curcumin treatment, TNF-a-induced neurons grew as normal. TNF-a induced a rapid Ca^2＋ influx into the neuronal cytoplasm; however, Ca2＋ fluorescence intensity only slightly increased when neurons were co-perfused with curcumin and TNF-α. CONCLUSION： Curcumin has a protective effect on rat hippocampal neurons possibly by reducing the TNF-α-induced rapid Ca^2＋ influx into neuronal cytoplasm and by maintaining the Ca^2＋ homeostasis.

The fertilization-induced Ca^(2+) oscillation in mouse oocytes is cytoplasmic maturation dependent

Mature eggs (at metaphase Ⅱ stage) produce a series of Ca2+ oscillation at fertilization. To define whether the fertilization-induced Ca2+ oscillation is restrict to the metaphase Ⅱ eggs and cell cycle dependent, mouse oocytes at prophase Ⅰ (arrested at germinal vesicle stage),metaphase Ⅰ, metaphase Ⅱ, as well as the pronuclear embryos at interphase of the first mitotic division derived from fertilization or parthenogenetic activation were inseminated after removal of zona pellucida. The results show that the fertilization-induced Ca2+ oscillation is not specific to metaphase Ⅱ eggs. This is supported by the fact that immature oocytes generated the Ca2+ oscillations at fertilization regardless of their nuclear progression from prophase Ⅰ to metaphase Ⅰ (in vitro matured) stage. More interestingly, it was first found that pronuclear embryos at interphase derived from parthenogenetic activation showed Ca2+ oscillations in response to fertilization while the zygotes at interphase did not after reinsemination or intracytoplasmic injection of sperm extracts which induce Ca2+ oscillations in MII eggs. This suggests that the ability of oocytes to generate Ca2+ oscillation in response to sperm penetration is not regulated in a cell cycle dependent manner but dependent on the cytoplasmic maturation.

复合混凝剂中Ca^(2+)对高溶解态磷坑塘水混凝效果的影响

文章以Ca^(2+)改性后的AlCl_(3)和PACl作为混凝剂进行混凝实验,通过出水浊度、余铝、总磷、絮体粒径及有机物组成等分析改性后混凝剂的作用机理,探讨混凝剂中存在的Ca^(2+)对高磷坑塘水混凝效果的影响机制。浊度去除方面,低投加量下Ca^(2+)可明显降低出水浊度。当投加量为0.10 mmol/L时,PACl出水浊度下降了33.52 NTU,AlCl_(3)出水浊度下降了28.72 NTU。余铝去除方面,当AlCl_(3)作混凝剂时,Ca^(2+)可以通过增加混凝剂的电中和能力来降低出水余铝浓度。溶解态磷去除方面,Ca^(2+)与磷酸根反应或通过压缩双电层和吸附电中和作用来增加溶解态磷的去除率。当投加量为0.20 mmol/L时,Ca^(2+)浓度为0.9 mmol/L,PACl溶解态磷去除率较未改性前提高16.1%。絮体粒径方面,Ca^(2+)可以促进颗粒之间脱稳凝聚,增加絮体粒径和分形维数,AlCl_(3)在0.20 mmol/L投加量下絮体粒径增加79μm。并且Ca^(2+)的加入使AlCl_(3)生成的絮体抗剪切能力更强,但是絮体受到破坏后更不容易恢复,使PACl形成絮体强度因子和恢复因子变大。有机物去除方面,Ca^(2+)可以提高有机物的去除率。对于0.20 mmol/L投加量,Ca^(2+)为0.06 mmol/L投加量条件下AlCl_(3)改性后混凝剂荧光响应值由1100降至800。

The effect of external Ca^(2+) and Ca^(2+)-channel modulators on red-light-induced swelling of protoplasts of Phaseolus radiatus L.

Red-light-induced swelling of the protoplasts isolated from hypocotyl of etiolated mung bean (Phaseolus radiatus L.) was observed only when Ca2+ ions were present in the medium. The optimal CaCl2 concentration was 250 μM. Swelling response declined when Ca2+ was supplied into the medium after red light irradiation. The Ca2+-chelator EGTA eliminated the red-light-induced swelling and 45Ca2+ accumulation in the protoplasts. In contrast, A23187, a Ca2+-ionophore, could mimic the effect of red light in darkness. These results indicate that Ca2+ may play a role in light signal transduction. In addition, swelling response was prevented by TFP and CPZ (both are CaM antagonists), implying the involvement of CaM in red-light-induced and Ca2+ -dependent protoplast swelling.

芪黄健脾滋肾颗粒可改善小鼠系统性红斑狼疮血小板减少:基于Ca^(2+)/CaMKK2/AMPK/mTOR信号通路介导的自噬

目的基于Ca^(2+)/CaMMK2/AMPK/mTOR信号通路介导的自噬探讨芪黄健脾滋肾颗粒(QJZG)对小鼠系统性红斑狼疮血小板减少的影响。方法将24只MRL/lpr狼疮小鼠随机分为模型组、QJZG组、醋酸泼尼松(Pred)组、CaMKK2激活剂组,6只/组;另将6只C57BL/6小鼠设为正常对照(Control)组。Control组、模型组:予10 mL/(kg·d)生理盐水灌胃;QJZG组:芪黄健脾滋肾颗粒+生理盐水配成0.39 g/mL溶液灌胃,剂量3.9 g/(kg·d);Pred组:予小鼠醋酸泼尼松片加生理盐水配成0.273 mg/mL的溶液灌胃,剂量2.73 mg/(kg·d);激活剂组:予10 mL/(kg·d)生理盐水灌胃,另将小鼠腹腔注射CaMKK2激活剂,5 mg/kg,2次/周。检测血小板计数(PLT)、血小板压积(PCT)、血小板分布宽度(PDW)、平均血小板体积(MPV);ELISA法检测血清血小板生成素(TPO)、白介素-6(IL-6)、白介素-10(IL-10)、肿瘤坏死因子-α(TNF-α)、γ干扰素(IFN-γ)水平;流式细胞术检测钙离子荧光强度;Real-time PCR法检测血小板CaMKK2、AMPK2α、mTOR、Beclin1、p62 mRNA表达水平;Western blotting检测血小板CaMKK2、p-CaMKK2、AMPK、p-AMPK、mTOR、p-mTOR、LC3、Beclin1、P62蛋白表达水平。结果与Control组相比,模型组PLT、PCT、IL-10、mTOR、p62 mRNA、p-mTOR、P62水平降低(P<0.01),PDW、MPV、TPO、IL-6、TNF-α、IFN-γ、CaMKK2、AMPK、Bcl-1 mRNA、p-CaMKK2、p-AMPK及血小板自噬蛋白(LC3Ⅱ蛋白、Beclin1蛋白)在血小板内表达量升高(P<0.01)。与模型组比较,QJZG组及Pred组PLT、IL-10、mTOR、p62 mRNA、p-mTOR、P62水平升高(P<0.01),MPV、TPO、IL-6、TNF-α、IFN-γ、CaMKK2、AMPK、Bcl-1 mRNA、p-CaMKK2、p-AMPK及血小板自噬蛋白(LC3Ⅱ蛋白、Beclin1蛋白)在血小板内表达量降低(P<0.05);CaMKK2激活剂组PLT、PCT、IL-10、mTOR、p62 mRNA、p-mTOR、P62水平降低(P<0.01),PDW、MPV、IL-6、TNF-α、IFN-γ、CaMKK2、AMPK、Bcl-1 mRNA、p-CaMKK2、p-AMPK及血小板自噬蛋白(LC3Ⅱ蛋白、Beclin1蛋白)在血小板内表达量升高(P<0.01)。结论QJZG可通过减轻炎症及影响Ca^(2+)/CaMKK2/AMPK/mTOR信号通路抑制血小板自噬改善系统性红斑狼疮血小板减少。

Ca^(2+)/CaN/NFAT信号通路在肿瘤中的研究进展

肿瘤成为危害人类健康的主要原因,其发生发展与免疫炎症密切相关.Ca^(2+)/CaN/NFAT信号通路是目前已知的免疫炎症通路,可促进多种免疫细胞活化,介导免疫炎症因子释放,进而影响机体的免疫功能.目前,Ca^(2+)/CaN/NFAT信号通路在肿瘤中的存在和作用越来越受关注.多项研究表明与该通路与肿瘤发生发展密切相关.故本文从Ca^(2+)/CaN/NFAT信号通路概述、信号通路对肿瘤发生发展的影响、信号通路对肿瘤免疫炎症的作用及与信号通路相关药物在防治肿瘤中的作用四方面进行综述,以期为临床防治肿瘤提供新视角新靶点.

Ca^(2+)-ATPase参与植物耐盐性调控的研究进展

盐胁迫下细胞质Ca^(2+)浓度升高,细胞会激活Ca^(2+)调节的靶酶或者与Ca^(2+)高度亲和的受体蛋白,其中,与Ca^(2+)高度亲和的受体蛋白中,植物钙泵(Ca^(2+)-ATPase)是P型ATP酶,包含内质网Ca^(2+)-ATPases与质膜Ca^(2+)-ATPas‐es,通过主动运输将Ca^(2+)从细胞质转移到质外体或细胞器。大量研究表明,植物的耐盐性在很大程度上与其维持钙泵即Ca^(2+)-ATPase活性的能力有关。多种植物Ca^(2+)-ATPase对盐胁迫表现出敏感性,并受到外源Ca^(2+)的保护,表明外源钙处理与Ca^(2+)-ATPase活性可能在盐胁迫下的细胞内钙稳态和信号转导中起重要作用。该研究概述了植物Ca^(2+)-ATPase类型、结构与性质,亚细胞定位Ca^(2+)-ATPase及外源钙与亚细胞定位Ca^(2+)-ATPase参与植物耐盐调控研究进展,重点对质膜、液泡膜、核膜、内质网及高尔基体Ca^(2+)-ATPases参与植物耐盐调控的研究进展进行了综述,并提出展望。该研究为了解植物耐盐性生理及分子机制提供帮助,同时为作物耐盐栽培提供新思路。

Xiaoyaosan-containing serum inhibits corticosterone-induced apoptosis in PC12 cells by downregulating [Ca^(2+)]_i overload

in hippocampal neurons is an important contributor to depression. [Ca^2＋]i of hippocampal neurons may raise rapidly with increased corticosterone concentrations, leading to apoptosis. The anti-depressant effects of Xiaoyaosan （Free and Easy Wanderer＇s Powder） may inhibit apoptosis by down regulating the [Ca^2＋]i overload. PC12 cells were containing with corticosterone to simulate neuronal injury, dosed with Xiaoyaosan-containing serum, and the following parameters were measured： apoptosis,[Ca^2＋]i overload, and changes in mitochondrial membrane potential （△ψm） and bioenergetics. High-dose Xiaoyaosan-containing serum （the dose of intragastric administration was 2.633 g herb/mL） not only inhibited morphological injury and cell apoptosis, but also suppressed [Ca^2＋]i overload induced by corticosterone. Xiaoyaosan also blocked the decrease in mitochondrial membrane potential and adenosine triphosphate levels induced by corticosterone. Xiaoyaosan dose-dependently suppresses corticosterone-induced apoptosis, potentially via inhibiting [Ca^2＋]ioverload, and prevents impaired mitochondrial bioenergetics by maintaining mitochondrial membrane potential and adenosine triphosphate production, providing a putative mechanism for its antidepressant effects.

Numerical study of IP_3-induced Ca^(2+) spiral pattern evolution

The effect of change in concentration of messenger molecule inositol 1,4,5-trisphosphate （IP3） on intracellular Ca^2＋spiral pattern evolution is studied numerically. The results indicate that when the IP3 concentration decreases from 0.27 μM, a physiologically reasonable value, to different values, the spiral centre drifts to the edge of the medium and disappears for a small enough IP3 concentration. The instability of spiral pattern can be understood in terms of excitability-change controlled by the IP3 concentration. On the other hand, when the IP3 concentration increases from 0.27 μM, a homogeneous area with a high Ca^2＋ concentration emerges and competes with the spiral pattern. A high enough IP3 concentration can lead the homogeneous area to occupy the whole medium. The instability of spiral pattern is ascribed to the change in stability of a stationary state with a high Ca^2＋ concentration.

β-细辛醚通过抑制TRPV4的表达缓解谷氨酸诱导的Ca^(2+)超载

谷氨酸处理会导致Ca^(2+)超载,瞬时受体电位香草素受体4(transient receptor potential vanilloid 4,TRPV4)在其中的作用及可能机制尚不清楚。β-细辛醚能快速透过血脑屏障,对兴奋性毒性具有较强的神经保护作用。文章以高分化的PC12细胞为研究对象,探究β-细辛醚(15、30、60μmol/L)预处理4 h,40 mmol/L谷氨酸处理实时记录对PC12细胞Ca^(2+)浓度的影响,采用钙成像技术检测Ca^(2+)浓度的变化;采用实时荧光定量聚合酶链式反应(polymerase chain reaction,PCR)、Western Blot及免疫荧光技术检测TRPV4的mRNA和蛋白的表达;采用Lipofectiamine 2000脂质体实验转染TRPV4-siRNA和pEX-3-TRPV4,观察沉默和过表达TRPV4对谷氨酸引起Ca^(2+)超载的影响。结果表明:与正常对照组相比,谷氨酸处理5 min可诱导Ca^(2+)超载,显著提高TRPV4的mRNA和蛋白的表达;与模型组相比,β-细辛醚能够剂量依赖性地降低谷氨酸诱导的Ca^(2+)超载和TRPV4的表达;沉默TRPV4抑制细胞Ca^(2+)超载;过表达TRPV4则部分逆转β-细辛醚抑制谷氨酸诱导的Ca^(2+)超载。该研究证明,谷氨酸处理PC12细胞5 min通过上调TRPV4的表达诱导Ca^(2+)超载,β-细辛醚作为TRPV4的拮抗剂,是一种潜在的抑制兴奋性毒性的药物。

活血益肾法联合西药对踝关节骨折术后血清Ca^(2+)、ALP及踝关节功能的影响

目的探讨活血益肾法联合西药对踝关节骨折术后血清Ca^(2+)、碱性磷酸酶(ALP)及踝关节功能的影响。方法选取踝关节骨折术后患者105例,随机分为试验组(n=53)和对照组(n=52)。对照组给予地塞米松治疗,试验组在对照组的基础上加用活血益肾法治疗。比较两组临床疗效、血清Ca^(2+)、ALP、踝关节功能水平变化情况、临床症状改善情况及不良反应发生情况。结果治疗后,试验组踝关节功能恢复优良率显著高于对照组;治疗后,试验组血清Ca^(2+)、ALP水平高于对照组;治疗后,两组肌力背伸、跖屈和背伸关节主动活动度、跖屈关节主动活动度水平均升高,且试验组高于对照组;治疗后,试验组临床各症状改善时间均显著低于对照组;以上组间差异均有统计学意义(P<0.05)。治疗期间,两组不良反应比较差异无统计学意义(P>0.05)。结论踝关节骨折术后应用活血益肾法联合西药效果显著,可有效改善患者血清Ca^(2+)、ALP及踝关节功能水平。

miR-361介导PI3K/Akt/Ca^(2+)通路对大鼠肥大细胞增殖情况及组胺与IL-4表达水平的影响

目的:探讨miR-361介导PI3K/AKt/Ca^(2+)通路对活化大鼠肥大细胞增殖情况及组胺与白细胞介素-4(IL-4)表达水平的影响。方法:将大鼠肥大细胞(RBL-2H3细胞)分为miR-361过表达组、miR-361抑制组、miR-361对照组和正常对照组,miR-361过表达组、miR-361抑制组、miR-361对照组细胞分别转染miR-361过表达、miR-361抑制及miR-361无义序列寡核苷酸片段,测定并比较各组细胞miR-361 mRNA、组胺、IL-4及PI3K/AKt/Ca^(2+)通路相关蛋白水平。结果:miR-361过表达组细胞miR-361 mRNA相对表达水平高于miR-361抑制组、miR-361对照组及正常对照组,差异均有统计学意义(P<0.05)。CCK-8法检测结果显示,miR-361过表达组24、48、72 h细胞增值率均低于miR-361抑制组、miR-361对照组及正常对照组,差异均有统计学意义(P<0.05)。ELISA法检测结果显示,miR-361过表达组细胞组胺和IL-4水平的表达水平低于miR-361抑制组、miR-361对照组及正常对照组,差异均有统计学意义(P<0.05)。Western印迹法检测结果显示,miR-361过表达组细胞p-AKT、AKT、p-PI3K、PI3K蛋白表达水平均高于miR-361抑制组、miR-361对照组及正常对照组,差异均有统计学意义(P<0.05)。结论:miR-361过表达可抑制大鼠肥大细胞的增殖,降低组胺与IL-4的表达水平,其作用机制可能与其能够提高PI3K/AKt/Ca^(2+)通路活性有关。

STIM1和Orai1/TRPCs在右心衰竭Ca^(2+)重塑中的作用

本文总结右心衰竭心肌细胞动作电位变化、心肌细胞内T管和内质网的改变,详细阐述了钙调神经磷酸酶(Calcineurin)-活化细胞活因子(NFAT)通路对心肌收缩力的作用。重点描述基质相互作用因子1(STIM1)和钙释放激活钙通道蛋白1(Orai1)/瞬时受体电位通道(TRPCs)通路在右心室心肌细胞兴奋收缩耦联、肥大及右心室成纤维细胞迁移增强方面的机制。