Calcium pyrophosphate dihydrate deposition disease: morphological and microanalytical features

The light microscopic and polarization appearances of calcium pyrophosphate dihydrate crystal deposits in tissues are reviewed. In routine sections haematoxylinophilic crystalline deposits with a feathery or brush-like pattern are typical of calcium pyrophosphate dihydrate. Short rhomboidal crystals showing positive birefringence are seen on polarization; X-ray microanalytical and infrared spectroscopic data support the specificity of these appearances. The appearances of the crystal deposits in decalcified specimens are also described. We include six cases of calcium pyrophosphate dihydrate deposition within periarticular bone; to the best of our knowledge this has not previously been described.     

Expression of the calcium receptor CaR in the parathyroid of secondary hyperparathyroidism patients

The effects of calcium on parathyroid hormone (PTH) has further discovered in recent years. It has been known that calcium ion concentration in the extracellular fluid is a major determinant of PTH secretion. The relationship between serum intact PTH (iPTH) and calcium ion levels is described by a sigmoidal curve. The calcium concentration that produces half-maximal change in PTH release (the midpoint between maximal and minimal     

Autonomic Regulation of Voltage-Gated Cardiac Ion Channels

Altering voltage-gated ion channel currents, by changing channel number or voltage-dependent kinetics, regulates the propagation of action potentials along the plasma membrane of individual cells and from one cell to its neighbors. Functional increases in the number of cardiac sodium channels (Na_V1.5) at the myocardial sarcolemma are accomplished by the regulation of caveolae by β adrenergically stimulated G-proteins. We demonstrate that Na_V1.5, Ca_V1.2a, and K_V1.5 channels specifically localize to isolated caveolar membranes, and to punctate regions of the sarcolemma labeled with caveolin-3. In addition, we show that Na_V1.5, Ca_V1.2a, and K_V1.5 channel antibodies label the same subpopulation of isolated caveolae. Plasma membrane sheet assays demonstrate that Na_V1.5, Ca_V1.2a, and K_V1.5 cluster with caveolin-3. This may have interesting implications for the way in which adrenergic pathways alter the cardiac action potential morphology and the velocity of the excitatory wave.     

粉防己碱舒张离体新西兰白兔阴茎海绵体平滑肌的机制研究

目的观察粉防己碱(tetrandrine,Tet)对阴茎海绵体平滑肌胞内钙释放和胞外钙内流的影响,初步探讨其舒张作用的机制。方法采用离体阴茎海绵体平滑肌肌条张力记录法,观察Tet对去氧肾上腺素(phenylephrine,PE)和氯化钾(KCI)诱导收缩的肌条的影响；采用无Ca~(2 )-复Ca~(2 )实验法,观察Tet对PE诱导的依赖细胞内钙和细胞外钙的肌条收缩反应的影响。结果Tet对PE或kcl诱导的肌条收缩均具有浓度依赖性的抑制作用。100μmol/L Tet可抑制20μmol/L PE引起的依赖细胞内钙和细胞外钙的肌条收缩(P＜0．05)；结论Tet可通过阻滞电压依赖性钙通道、受体依赖性钙通道和抑制细胞内钙库释放,从而介导其对海绵体平滑肌的舒张作用。     

盐酸吗啡普通片及硫酸吗啡控释片在不同溶剂中溶释过程的对照研究

本文采用紫外分光光度法对国产盐酸吗啡普通片及合资厂产硫酸吗啡控释片于蒸馏水、人工胃液、人工肠液中进行体外溶出度和释放度测定。结果表明，两种片剂的溶释均符合中国药典９５版标准，控释片在人工肠液中溶释参数Ｔ５０、Ｔｄ、ｍ与在蒸馏水及人工胃液中的溶释参数差异具显著性（Ｐ＜０．０１），在人工肠液中的释放过程明显缓慢。     

钾通道开放剂降低血管平滑肌细胞内游离钙浓度(英文)

目的:研究PCO—Pin,Nic,Lem及RP对VMSC内[Ca~(2 )]_i的改变及其可能机制。方法:VSMC加入Fura-2 AM 2.5μmol·L~(-1)37℃下孵育50min,[Ca~(2 )]_i用荧光分光光度计检测。结果:4种PCO能较弱地抑制K~ 30 mmol·L~(-1)诱导的[Ca~(2 )]_i增加,但明显抑制ATP 0.1mmol·L~(-1)诱导的[Ca~(2 )]_i峰相及持续相增加,且呈剂量依赖性。格列苯脲完全阻断Pin,Lem及RP的作用,只部分抑制Nic的作用。无钙液中先给4种PCO,能显著抑制ATP诱导的[Ca~(2 )]_i峰相增加。结论:4种PCO均抑制ATP诱导的[Ca~(2 )]_i增加,此作用与减少细胞外钙内流及细胞内钙释放有关。     

Repetitive firing properties in subpopulations of the chick Edinger Westphal nucleus.

The avian Edinger Westphal nucleus, through the ciliary ganglion, controls accommodation, iris constriction, and blood flow through the choroid. In live brainstem slices, the nucleus is easily identifiable as an olive-shaped cluster of neurons dorsal to the oculomotor nerve and nucleus. Intracellular recordings from neurons in the nucleus identified two classes of responses to sustained (300 to 500 ms) injections of depolarizing current. One set of cells fired action potentials for the duration of the pulse while a second set of cells fired action potentials only transiently, during the first 50 to 100 ms, after which they remained silent regardless of the size of the depolarization. Intracellular recordings followed by injections of the fluorescent dye lucifer yellow revealed that repetitively firing cells were located in the lateral half of the nucleus while non-repetitively or transiently firing cells were located in the medial half. These locations correspond to different Edinger Westphal subdivisions which have distinct inputs and target populations. The varying firing patterns are discussed with reference to the known functions of the subdivisions in which they occur. Replacement of calcium by magnesium in the extracellular medium had no effect on the number of action potentials fired by non-repetitively firing cells, suggesting that a calcium-activated potassium current is not responsible for suppressing repetitive firing in these cells. In contrast, in repetitively firing cells removal of extracellular calcium increased the frequency of action potential discharge and decreased the amplitude of afterhyperpolarizations following single action potentials. Addition of cadmium to the bath medium had similar effects.(ABSTRACT TRUNCATED AT 250 WORDS)     

铁骨晶对大鼠钙代谢、骨密度的影响及临床观察

本实验以铁骨晶（多肽钙），进口脱脂奶粉，活性钙冲剂，贝壳钙为钙源添加于大鼠正常饲料中。观察结果表明：上述４组钙的吸收率分别为６４．４％，６９．１％，５９．９％，５１．６％；钙的储留率分别为８９．８％，９３．３％，８５．２％，７９．０％；钙的存留率分别为４３．６％，４９．０％，３２．４％，２６．８％；股骨指数分别为７．０２×１０（－３），６．４３×１０（－３），６．８４×１０（－３）。６．８８×１０（－３）；折断力（牛顿）分别为６０．５４±１２．５５，４６．８１±９．３２，４３．２６±１６．６２，３８．２４±１０．７９。同时以铁骨晶为钙源对７０例（５～６岁）儿童进行了血清Ｃａ，Ｆｅ，Ｚｎ，Ｈｂ及生长发育的检测。铁骨晶组的身高，体重，胸围分别比对照组增加。铁骨晶组血清Ｃａ，Ｆｅ，Ｚｎ，Ｈｂ也均有较好的改善。这表明铁骨晶具有较好的促进钙吸收利用作用，同时能增加骨强度作用。     

Mast cell activation involves plasma membrane potential- and thapsigargin-sensitive intracellular calcium pools

Summary— The regulation and role of the intracellular Ca²⁺ pools were studied in rat peritoneal mast cells. Cytosolic free calcium concentration ([Ca²⁺]i) was monitored in fura-2 loaded mast cells. In the presence of Ca²⁺ and K+, compound 48/80 induced a biphasic increase in [Ca²⁺]i composed of a fast transient phase and an apparent sustained phase. The sustained phase was partially inhibited by the addition of Mn²⁺. DTPA, a cell-impermeant chelator of Mn²⁺, reversed this inhibition, suggesting that a quenching of fura-2 fluorescence occurs in the extracellular medium. In the absence of extracellular Ca²⁺, the transient phase, but not the sustained one, could be preserved, provided that mast cells were depolarized. The transient phase was completely abolished by thapsigargin, a microsomal Ca²⁺-ATPase inhibitor. Maximum histamine release induced by either compound 48/80 or antigen was obtained in the absence of added Ca²⁺ only when mast cells were depolarized. These histamine releases were inhibited by low doses (< 30 nM) of thapsigargin. Thapsigargin at higher doses induced histamine release which was unaffected by changing the plasma membrane potential, but was completely dependent on extracellular Ca²⁺, showing that a Ca²⁺ influx is required for thapsigargin-induced exocytosis. Together, these results suggest that the mobilization of Ca²⁺ from thapsigargin sensitive-intracellular pools induced by compound 48/80 or antigen is sufficient to trigger histamine release. The modulation of these pools by the plasma membrane potential suggest their localization is close to the plasma membrane.