Objective To study the relation between serum calcium level and elevated BaPWV in Chinese subjects.
Methods The relation between serum calcium level and elevated BaPWV was studied in 9 615 subjects. The mean value of left and right BaPWV was analyzed. BaPWV was defined as high when it was31 752.5 cm/s (the upper quartile) either side.
Results The BaPWV and its elevated percentage progressively increased across the quartiles of the serum calcium level (P<0.05). The prevalence of elevated BaPWV was significantly higher in subjects of the second, third and highest quartiles than in those of the lowest quartile (26.9%, 28.4%, and 33.2%vs 23.7%, P=0.0116, P=0.0004, and P<0.0001). Logistic regression analysis revealed that the risk of elevated BaPWV was 1.32- fold higher in subjects of the highest quartile than in those of the lowest quartile (OR=1.32, 95%CI:1.08-1.60).
Conclusion The elevated serum calcium level is related to an elevated BaPWV and a higher risk of arterial stiffness, independent of conventional risk factors, in middle-aged and elderly Chinese subjects.

INTRODUCTIONThe recent studies have shown that rhubarb has not only the effect of removing stasis by purgation, but also intestinal barrier effects[1,2]. In order to further clarify the intestinal barrier mechanism of rhubarb, we studied the effects of rhubarb decoction and the active ingredients of rhubarb on the cytoplasmic free calcium in isolated intestinal mononuclear cells (INT-MNC)

Even though many studies have identified roles of proteasomes in axonal degeneration, the mo-lecular mechanisms by which axonal injury regulates proteasome activity are stil unclear. In the present study, we found evidence indicating that extracellular calcium influx is an upstream regula-tor of proteasome activity during axonal degeneration in injured peripheral nerves. In degenerating axons, the increase in proteasome activity and the degradation of ubiquitinated proteins were sig-nificantly suppressed by extracellular calcium chelation. In addition, electron microscopic findings revealed selective inhibition of neurofilament degradation, but not microtubule depolymerization or mitochondrial swel ing, by the inhibition of calpain and proteasomes. Taken together, our findings suggest that calcium increase and subsequent proteasome activation are an essential initiator of neurofilament degradation in Wal erian degeneration.

Effect of calcium and soy isoflavone supplementation on bone mineral density of women with different menstrual status

平滑肌是胃肠运动的基础,其收缩和舒张涉及电-机械偶联和药物-机械偶联.其中有钙离子和其他信号分子的参与.本文通过电生理特性,钙和钙动员,收缩装置和途径,信号转导途径和交叉对话来总结信号转导在胃肠平滑肌中的作用.

目的:研究ATP对人中性粒细胞内三磷酸肌醇和钙离子的作用.方法:使用结合法测定三磷酸肌醇,根据Fura-2AM荧光变化测定钙离子浓度.结果:ATP刺激细胞三磷酸肌醇的形成和钙离子的释放.结论:ATP促进人中性粒细胞释放elastase酶可能与刺激细胞内三磷酸肌醇的形成和钙离子的释放有关.

肿瘤坏死因子α对大鼠心室肌细胞钙转运的影响

AIM: To study the effects of tumor necrosis factor-alpha (TNF-α) on calcium movement in rat ventricular myocytes. METHODS: Intracellular free Ca2+ concentration was measured with calcium fluorescent probe Fluo-3/AM and laser confocal microscope. L-type calcium current (Ica,L) was recorded with the whole-cell configuration of the patch-clamp techniques. RESULTS: At 2, 20 and 200 μg/L, TNF-α was found to increase intracellular free Ca2+ concentration in a dose-dependent manner illustrated by the increment of calcium fluorescence density with laser confocal microscope. Nicardipine 0.5 μmol/L slightly attenuated TNF-α-induced response. When the cardiac myocytes were exposed to caffeine (100 mmol/L) for 30 min, TNF-α failed to induce any change of intracellular free calcium. However, it was found that TNF-α inhibited Ica,L in whole-cell patch-clamp experiments. At 2, 20, and 200 μg/L, TNF-α decreased peak Ica,L by 3.9 % (-5.1 pA/pF+0.3 pA/pF vs -4.9 pA/pF+0.2 pA/pF, n=9, P＞0.05), 15.7 % (-5.1 pA/pF+0.3 pA/pF vs -4.3 pA/pF+0.3 pA/pF, n=9, P＜0.05) and 19.6 % (-5.1 pA/pF+0.3 pA/ pF vs -4.1 pA/pF+0.4 pA/pF, n=9, P＜0.01), respectively. It shifted the steady-state inactivation curve of Ica,L to the left (V1/2 shifted from -28.7 mV+0.3 mV to -37.8 mV+1.4 mV, n=7, P＜0.05), while it took no effects on steadystate activation and recovery from inactivation. CONCLUSION: TNF-α inhibited Ica,L in rat ventricular myocytes,while increasing the intercellular free Ca2+ level due to the release of Ca2+ from intracellular stores.

Objective:　To observe dynamic changes of intracellular calcium (［Ca2+］i) after spinal cord injury, and to study the relationship between the changes of ［Ca2+］i and the functional damage of the spinal cord.　　Methods:　The rats were subjected to a spinal cord contusion by using a modified Allens method. The ［Ca2+］i in the injured segment of the spinal cord was measured by the technique of La3+ blockage and atomic absorption spectroscopy at 1, 4, 8, 24, 72, and 168 hours after injury. The motor function on the inclined plane was measured at the same time.　　Results:　The spinal cord ［Ca2+］i increased significantly (P<0.05 or P<0.01) after spinal cord injury. There was a significant correlation (P<0.05) between the changes of ［Ca2+］i and the motor function. 　　Conclusions:　［Ca2+］i overload may play an important role in the pathogenesis of spinal cord injury.

Elevated oxidative stress (OS) during aging leads to bone loss. OS increases intracellular Ca2+ ([Ca2+]i), resulting in cellular damage and death. We show earlier that Cx43 hemichannels open in response to OS, which serves as a protective mechanism for osteocytes. However, the underlying mechanism is unknown. Here, we found that treatment with H2O2 increased [Ca2+]i in osteocytes with [Ca2+]i being primarily derived from an extracellular Ca2+source. Hemichannel opening induced by OS was inhibited by the depletion of [Ca2+]i with BAPTA-AM, a Ca2+chelator, suggesting that [Ca2+]i influenced the activity of Cx43 hemichannels. Conversely, blockade of hemichannels had no effect on [Ca2+]i. A biotinylation assay showed that cell surface-expressed Cx43 was increased by OS, which could be inhibited by BAPTA-AM, suggesting that [Ca2+]i is necessary for Cx43 migration to the cell surface in response to OS. Together, these data suggest that increased hemichannel activity induced by OS was likely to be caused by elevated [Ca2+]i through increased Cx43 on the cell surface.

The Ca2+ Over Loading Effect of Oxidized Low Density Lipoprotein on Macrophages

Purpose The Ca2+ over loading effect of oxidized low density lipoprotein (OLDL) on macrophages and its mechanisms were explored in these studies. Methods C57BL/6J mouse peritoneal macrophages were incubated in 10mg/L oxidized low density lipoprotein (OLDL), the intracellular Ca2+ level was determined with the technique of Ca2+ fluorescent indicator, and the membranous Ca2+-ATPase activity was determined with the assay of NADH-oxidizing coupling spectrum-alteration. Results The intracellular Ca2+ level was 2.7 times higher than the control, and the membranous Ca2+-ATPase activity was 24.0% of the control. Conclusion OLDL exerted a Ca2+ over loading effect on macrophages, and this was probably related to the opening of the membranous Ca2+ channels and the inactivating of the membranous Ca2+-ATPase.

The Ca2+ Antagonizing Effect of Chinese Cobra Venom Factor on Formation of Macrophage-derived Foam Cells

Purpose CCVF was isolated from Chinese cobra (Naja naja) venom, its Ca2+ antagonizing effect on formation of macrophage-derived foam cells was explored in these studies. Methods Foam cell models were induced with C57BL/6J mouse peritoneal macrophages incubated in 10mg/L oxidized low density lipoprotein (OLDL), and their intracellular Ca2+ levels influenced both slowly and transiently by CCVF were determined with the technique of Ca2+ fluorescent indicator. Results The intracellular Ca2+ level with the macrophages incubated in 10mg/L OLDL and 10mg/L CCVF was 40.2% of the macrophages incubated in 10mg/L OLDL (P＜0.05); While the transient influence of CCVF on the intracellular Ca2+ levels were not significant. Conclusion CCVF exerted a long-lasting antagonizing role on the enhancement of intracellular Ca2+ levels, thus inhibited the formation of macrophage-derived foam cell.