异丙嗪对下丘脑细胞内游离钙浓度的影响

目的：观察异丙嗪（ｐｒｏｍｅｔｈａｚｉｎｅ,ＰＭＺ）对下丘脑细胞内游离钙浓度（［Ｃａ２＋］ｉ）的影响。方法：以酶法制备家兔下丘脑细胞悬液,运用钙指示剂Ｆｕｒａ－２／ＡＭ作为细胞内游离钙的荧光探针测定下丘脑细胞［Ｃａ２＋］ｉ。结果：１）ＰＭＺ（０４６ｍｍｏｌ／Ｌ）使下丘脑［Ｃａ２＋］ｉ显著升高,且在一定的剂量范围内呈量效关系。２）事先向细胞悬液中加入钙通道阻滞剂维拉帕米可明显抑制ＰＭＺ诱导的［Ｃａ２＋］ｉ升高,但不能完全阻断ＰＭＺ的这种作用。结论：上述结果提示ＰＭＺ可引起下丘脑［Ｃａ２＋］ｉ升高,钙通道开放导致细胞外钙内流是ＰＭＺ引起下丘脑［Ｃａ２＋］ｉ升高的机制之一。     

催化剂种类对间苯二酚甲醛气凝胶结构的影响

首次以Ｋ２ＣＯ３、Ｃａ（ＯＨ）２为催化剂制备ＲＦ炭气凝胶,相同条件下溶胶转变为凝胶的时间（ｔｇ）最低达到４０ｍｉｎ,且密度优于Ｎａ２ＣＯ３催化得到的ＲＦ气交,最低为０．０４７ｇ／ｃｍ＾３。ＴＥＭ表征结果显示：Ｃａ（ＯＨ）２催化得到的气凝胶具有纳米级网络结构,构成网络的球状颗粒均匀,平均直径５～１０ｎｍ,网络结构优于文献报道。     

Ca2+ signals induced from calcium stores in pancreatic islet β cells

In single rat pancreatic β cells, using fura-2 microfluorometry to measure [Ca²⁺]i response upon different stimuli, the ways of calcium regulation have been studied. When the extracellular calcium concentration was 2.5 mmol/L, either 60 mmol/L KCl, 20 mmol/L D-glucose or 0.1 mmol/L tolbutamide induced increase in [Ca²⁺]i. Such increase in [Ca²⁺]i was absent when the same stimuli were applied under zero extracellular calcium. These results indicate that the increase of [Ca²⁺]i is induced by the activation of voltage-dependent calcium channels in β cells. The manifold forms of [Ca²⁺]i change induced by glucose imply that the effects of glucose are complex. 5 mmol/L caffeine or 5 mmol/L MCh increase the [Ca²⁺]i, which is independent of the external calcium, suggesting that [Ca²⁺]i can be regulated by Ca²⁺ release from not only the IP₃-sensitive but also the ryanodine sensitive calcium stores in β cells. The latency of Ca responses for IP₃ pathway (5 s) is faster than that for ryanodine pathway (30 s). It is concluded that there are multiple calcium stores in rat pancreatic β cells.     

过氧化钙的碘量分析法

通过现行的过氧化钙分析法的比较分析,本文推荐用碘量法分析不同工艺生产的过氧化钙．     

Regulation of mitochondrial oxidative phosphorylation by second messenger-mediated signal transduction mechanisms

The mitochondrial oxidative phosphorylation system is responsible for providing the bulk of cellular ATP molecules. There is a growing body of information regarding the regulation of this process by a number of second messenger-mediated signal transduction mechanisms, although direct studies aimed at elucidating this regulation are limited. The main second messengers affecting mitochondrial signal transduction are cAMP and calcium. Other second messengers include ceramide and reactive oxygen species as well as nitric oxide and reactive nitrogen species. This review focuses on available data on the regulation of the mitochondrial oxidative phosphorylation system by signal transduction mechanisms and is organised according to the second messengers involved, because of their pivotal role in mitochondrial function. Future perspectives for further investigations regarding these mechanisms in the regulation of the oxidative phosphorylation system are formulated. Received 11 December 2005; received after revision 14 January 2006; accepted 6 February 2006     

磷酸钙/氧化锆复合陶瓷的微观结构及力学性能

利用冷等静压成形, 经不同的温度烧结制备了不同比例的磷酸钙与钇稳定四方氧化锆系列复合陶瓷, XRD、 SEM及力学性能测试结果表明, 随磷酸钙含量的增加, 陶瓷的相对密度降低, 晶粒尺寸变大, 四方氧化锆(t-ZrO2)减少, 单斜氧化锆(m-ZrO2)增加, 导致力学性能下降; 1 350 ℃烧结含磷酸钙质量分数为12％~15％的样品及1 400 ℃烧结含磷酸钙质量分数为15％的样品以t-ZrO2为主, 并含有少量m-ZrO2和TCP(Ca3(PO4)2), 其相对密度大于95％, 综合力学性能评价分析表明, 它可用于CAD/CAM加工口腔修复材料.      

宣布式可控波形单光子的产生和应用

在时域上操控单光子的波形不但可以应用到基础量子物理研究,也可以应用到量子信息处理.窄线宽纠缠光子对的成功产生让时域上操控单光子的波形成为可能.本文首先介绍了利用四波混频和慢光技术在大光学厚度的冷原子系综中产生窄线宽纠缠光子对,进而获得宣布式可控波形单光子的工作.在此基础上,本文进一步介绍了宣布式可控波形单光子波形的操控.然后介绍宣布式可控波形单光子在基础量子物理和量子通信方面的应用,具体包括:(1)单光子光前驱波;(2)宣布式可控波形单光子与二能级原子相干相互作用;(3)宣布式可控波形单光子差分相位编码量子密钥分发.     

Cadmium-induced autophagy and apoptosis are mediated by a calcium signaling pathway

The cytotoxicity of cadmium (Cd) induced autophagy and apoptosis in MES-13 cells was determined by flow cytometry. Autophagy was also assessed by formation of autophagosomes and processing of LC3. Pharmacological inhibition of autophagy resulted in increased of cell viability, suggesting autophagy plays a role in cell death in Cd-treated mesangial cells. Cd also induced a rapid elevation in cytosolic calcium ([Ca²⁺]_i ), and modulation of [Ca²⁺]_i via treatment with IP ₃R inhibitor or knockdown of calcineurin resulted in a change in the proportion of cell death, suggesting that the release of calcium from the ER plays a crucial role in Cd-induced cell death. Inhibition of Cd-induced ERK activation by PD 98059 suppressed Cd-induced autophagy, and BAPTA-AM eliminated activation of ERK. BAPTA-AM also inhibited Cd-induced mitochondrial depolarization and activation of caspases. These findings demonstrated that Cd induces both autophagy and apoptosis through elevation of [Ca²⁺]_i, followed by Ca²⁺-ERK and Ca²⁺-mitochondria-caspase signaling pathways. Electronic supplementary material  The online version of this article (doi:) contains supplementary material, which is available to authorized users. Received 05 July 2008; received after revision 25 August 2008; accepted 17 September 2008     

关于电子结构的电磁模型

提出了关于电子结构的电磁模型、关于电子能量和质量的新公式,提出电子环形电流假设以取代电子自旋假设等一些新观点,并在下一篇文章中用于解决原子的稳定性等问题.     

过度训练对大鼠心肌线粒体膜和基质游离钙的影响

采用模拟过度训练大鼠模型,观察了大鼠心肌线粒体的MDA、巯基（-SH）、还原型谷胱苷肽（GSH）、磷脂A2（PLA2）、游离钙（Fca2＋）等指标,结果表明：过度训练组大鼠心肌线粒体与对照组相比,-SH含量和GSH含量显著降低（P〈0．01）,PLA2活性显著增加（P〈0．01）;MDA、Fca2＋含量明显升高（P〈0．01）．本文根据以上结果探讨了运动时机体产生的活性氧的氧化过程与过度训练后心肌线粒体膜结构变化以及游离钙之间的关系,提出过度训练后PLA2活性增加可能是其发生机制的关键指标,通过对这一指标的进一步观察能更好地了解过度训练发生的分子机制。