大鼠骨髓间充质干细胞与多孔双相磷酸钙陶瓷支架体外黏附的实验研究

目的研究大鼠骨髓间充质干细胞(marrowmesenchymalstemcells,MSCs)诱导培养后在多孔双相磷酸钙(biphasiccalciumphosphate,BCP)陶瓷支架材料上的黏附和生长。方法SD大鼠MSCs经矿化诱导培养、扩增,具有成骨细胞表型后,与多孔BCP陶瓷支架及普通多孔羟基磷灰石(hydroxyapatite,HA)陶瓷支架体外复合培养,扫描电镜观察比较MSCs在两种材料支架表面的黏附数量和形态;同时以0.5、1.0、2.0、3.0和4.0×106/ml浓度细胞悬液接种于多孔BCP支架材料,检测适宜的接种浓度及单位体积支架材料可黏附MSCs数量。结果大鼠MSCs经诱导培养14d后,行矿化沉积茜素红染色、型胶原免疫细胞化学染色及碱性磷酸酶细胞化学染色,结果均为阳性。大鼠MSCs黏附于多孔BCP陶瓷上的细胞数(88.00±6.58)明显高于HA陶瓷组(39.00±3.65),两组比较差异有统计学意义(P<0.01)。当接种浓度为2.0×106/ml时,单位体积的陶瓷支架材料最多可黏附MSCs数量为1.28×107个/cm3,为细胞适宜接种浓度。结论大鼠MSCs在体外经矿化诱导培养可表达成骨细胞表型,细胞浓度为2.0×106/ml时与多孔BCP陶瓷支架材料具有良好的黏附能力。     

中等强度冲击波负压暴露对豚鼠耳蜗毛细胞游离钙浓度的影响

目的:观察实验性冲击波负压(BUP)暴露对豚鼠耳蜗外毛细胞内游离钙浓度([Ca2 ]i)的影响。方法:在激光共聚焦显微镜下,用钙敏荧光探针Fluo-3作为指示剂,观察豚鼠暴露中等强度实验性BUP后耳蜗外毛细胞[Ca2 ]i的变化。结果:中等强度BUP暴露后8 h,至暴露后24 h和3 d稍有回落,但仍高于正常对照组。上述这些变化与听性脑干反应阈值的升高是一致的。结论:豚鼠暴露中等强度性BUP可引起耳蜗外毛细胞内[Ca2 ]i的明显增高,且可能是听功能损害的主要原因之一。     

福辛普利预处理对缺氧复氧期豚鼠心室肌细胞Na+/Ca2+交换电流的影响

目的:观察福辛普利晚期预处理对缺氧复氧心室肌细胞Na /Ca2 交换电流的影响。方法:应用全细胞膜片钳方法,记录观察酶解的成年豚鼠心室肌细胞Na /Ca2 交换电流在缺氧复氧期的变化。结果:缺氧复氧明显增加心肌Na /Ca2 交换电流,在-100mV和 60mV时较对照组分别增加41.05%及32.75%,福辛普利预处理后可明显抑制缺氧复氧心肌Na /Ca2 交换电流,在-100mV和 60mV时分别减少17.90%及14.20%,有助于减少钙内流,减轻钙超载。结论:福辛普利预处理可抑制缺氧复氧心肌Na /Ca2 交换电流逆向转运。     

快速心房起搏对家兔L-型钙通道和Kv4.3钾通道基因表达的影响

目的观察快速心房起搏对家兔心房L型钙通道亚单位和Kv4.3钾通道基因表达的影响。方法新西兰大耳白家兔36只,随机分成6组,经右颈外静脉穿刺置入电极于右房,分别给予0、3、6、12、24或48h快速心房起搏,停止起搏后取右房组织,应用半定量反转录聚合酶链式反应测定各时相点L型钙通道α1c,β1,α2亚单位,钾通道Kv4.3mRNA的表达水平。结果L型钙通道α1c、β1亚单位在快速起搏6h后表达水平下调,并随着起搏时间的延长进一步下调。α2亚单位的mRNA表达在各时相点无显著差异。Kv4.3的mRNA的表达在快速起搏的24h和48h下降分别达55.50%（P<0.01）和59.12%（P<0.01）。48h后下降达到一个平台期。结论快速心房起搏可导致L型钙通道亚单位和Kv4.3钾通道mRNA表达下调。     

小剂量肝素联用巯甲丙脯酸治疗慢性肺心病急性发作期66例疗效分析

目的探讨综合疗法并用小剂量肝素、巯甲丙脯酸治疗慢性肺心病急性发作期的疗效.方法慢性肺心病急性发作期患者随机分为治疗组(66例)、对照组(62例),两组均进行综合治疗,但治疗组加用了小剂量肝素和巯甲丙脯酸,然后观察并比较其症状、体征、血气指标和血液黏稠度.结果治疗组的血液流变学变化、症状与体征的改善及总好转率明显优于对照组P＜0.01.结论慢性肺心病急性发作期病人在综合治疗的基础上加用小剂量肝素和巯甲丙脯酸可显著提高疗效.     

钙通道阻滞剂在皮肤科的应用

钙通道阻滞剂(CCB)是广泛应用于临床治疗心血管疾病的药物。近年的研究表明，CCB具有稳定肥大细胞膜和阻止脱颗粒，抑制淋巴细胞转化及白介素2产生，降低表皮郎格罕细胞数，扩张血管、抑制血小板聚集、增强红细胞变形能力，抑制细胞的分裂和增殖作用。此外对淋菌的耐药性有逆转作用。用于临床某些过敏性疾病、寒冷性脉管性疾病及银屑病取得了较好的效果，为临床增添了新的治疗手段．给变应性接触性皮炎、耐药性淋病的治疗带来了新的展望。本文对药物的副作用亦有概述。     

次氯酸钠和氢氧化钙对牙本质弹性模量和挠曲强度的影响

目的 :评估 5 %次氯酸钠 (NaOCl)溶液和饱和氢氧化钙 [Ca(OH) 2 ]溶液对牙本质弹性模量和挠曲强度的影响 ,以进一步了解根管治疗过程中药物对牙齿机械性能的影响。方法 :取新鲜拔除的完整前磨牙制成标准规格牙本质条 ,经 5 %NaOCl和饱和Ca(OH) 2 溶液处理 ,三点加荷系统测定其弹性模量和挠曲强度。结果 :5 %NaOCl使牙本质弹性模量和挠曲强度显著降低 ;饱和Ca(OH) 2 溶液使牙本质挠曲强度显著降低 ,对弹性模量无显著影响 ;5 %NaOCl处理后再用饱和Ca(OH) 2 溶液处理对牙本质弹性模量和挠曲强度无进一步影响。结论 :5 %NaOCl和饱和Ca(OH) 2 溶液对牙本质的机械性能有一定影响     

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.