Objective To summarize the traits of calcium-binding tyrosine phosphorylation regulate gene and the significance in tumor incidence. Methods The domestic and foreign literatures about calcium-binding tyrosine phosphorylation regulate gene involved in the regulation of signaling pathways and research status in a variety of tumors were reviewed. Results Calcium-binding tyrosine phosphorylation regulate gene induced the abnormal proliferation of cells through multiple mechanisms. There was closely relation between the occurrence of many tumors and abnormal expression of calcium-binding tyrosine phosphorylation regulate gene. In the distribution of different epithelial tumors， the pathway of calcium-binding tyrosine phosphorylation regulate gene involved in the regulation was same， and the effect target was similar. Conclusion Further study of the calcium-binding tyrosine phosphorylation regulate gene is expected to provide a new way for clarify the occurrence and development mechanisms of tumors， and can serve as important means of early diagnosis and adjuvant therapy.
Objective To probe the change of the structure and function of the small bowel by injection of different drugs (verapamil, energy compounds or normal saline) via the superior mesenteric artery (SMA) injections.Methods The model of the small intestine ischemia/reperfusion (I/R) injury was made in grey rabbits. Free calcium concentration in mitochondria of the small intestine was determined, and the ultrastructural change was also observed by electron microscopy at the very time of occlusion, 60 minutes after occlusion and 30 minutes after reperfusion. Results The free calcium concentration in mitochondria was more declined in verapamil group (2.976±0.410 nmol/mg.prot) than in N.S. group (4.234±0.542 nmol/mg.prot), Ｐ＜0.01, at 60 minutes after occlusion. At 30 minutes after reperfusion, free calcium concentration in mitochondria was more decreased in energy compunds group (2.401±0.323 nmol/mg.prot) and verapamil group (3.847±0.610 nmol/mg.prot) than in the N.S. group (5.981±1.031 nmol/mg.prot). Conclusion Verapamil and energy compouds have protective effects on the functions and ultrastructures of the I/R of small intestine.
Objective To study the effect of substance P ( SP) on int racellular f ree calcium concent ration in human poorly-differentiated gast ric cancer cell in vitro. Methods Human gast ric cancer cell line MKN45 was cultured in RPMI 1640. Then the cells were loaded with specific calcium fluorescent probe Furu23/ AM. ASN21377642 (NK21 receptor antagonist) , Nicardipine (calcium channel blocker) and different concent rations of SP were used to treat gast ric cancer cells. The concent ration changes of int racellular free calcium were detected by laser scanning confocal microscope. Results It was found that 10 , 50 and 100 nmol/ L SP could significantly increase the int racellular free calcium concent ration of gast ric cancer cells in Hanks solutions , which contain ext racellular calcium ( P lt;0. 05) , and the change was in a dose-dependent manner ( P lt; 0. 05) . When there was ext racellular calcium existed ,the increasing amplitude of intracellular f ree calcium concent ration was significantly higher than that when there was no extracellular calcium ( Plt; 0. 05) . And when Hanks solutions were pretreated with ASN21377642 and Nicardipine , the effects of 100 nmol/ L SP were partly inhibited , and the concent rations of int racellular f ree calcium were significantly lower than those in group s without pret reatment s ( P lt; 0. 05) . Conclusion SP can significantly increase free calcium concent ration in the gastric cancer cells. Releasing of stored calcium in the cells and influx of extracelluar calcium may contribute to the elevation of int racellular free calcium concentration.
Free calcium ions, as a kind of message-transport substance, is important in cellular activity such as cell movement, cell differentiation and cell proliferation. In order to investigate the relationship between free calcium ions and scar contracture, the fibroblasts which originated from hypertrophic scar, keloid and normal skin were used as the experimental target. The fibroblasts from 4th-6th generations of different sources were used; Then the intracellular free calcium ions concentrations were measured respectively by the fluorescent Ca2+ indicator Fura-2/AM and Image analysis system. The results showed that the level of Ca2+ in fibroblasts of hypertrophic scar was higher than that in keloid and normal skin (P lt; 0.01). There was no significant difference between the level of Ca2+ in keloid and in normal skin. The conclusion was that the concentration of intracellular free calcium ions played an important role in the scar contract, but the exact mechanism was still unclear and required further study.
ObjectiveTo summarize the role of ionized free calcium/calmodulin/calmodulin-dependent protein kinase Ⅱ (Ca2+/CaM/CaMKⅡ) signaling pathway in liver fibrosis so as to provide a theoretical basis for the treatment of liver fibrosis. MethodThe recent literature relevant research on the role of Ca2+/CaM/CaMKⅡ signaling pathway in the process of liver fibrosis both domestically and internationally was reviewed. ResultsThe Ca2+/CaM/CaMKⅡ signaling pathway played a bidirectional regulatory role in the process of liver fibrosis, potentially facilitating the activation of hepatic stellate cells and triggering hepatocyte apoptosis through synergistic transforming growth factor-β1 and platelet-derived growth factor pathways. ConclusionsAt present, there is very little research on the role of Ca2+/CaM/CaMKⅡ signaling pathway in the process of liver fibrosis, and there is still insufficient understanding. Future research should focus on the mechanism of this signaling pathway in liver fibrosis, especially its upstream genes or downstream target proteins, which will aid to develop targeted and effective treatment strategies, achieve the reversal of liver fibrosis and even liver cirrhosis, and provide more effective treatment options for patients with liver fibrosis.
Abstract: Objective To observe the combined protective effects of U50 488H and hypothermia preservation on isolated rabbit hearts preconditioned. Methods Forty rabbits were randomly divided into five groups, 8 rabbits in each group. The perfusion model of isolated rabbit hearts was established by the Langendorff device. In the control group: the isolated rabbit hearts were preserved with the University of Wissconsin solution (UW ) for six hours; groupI : the isolated rabbit hearts were preconditioned with St. ThomasII cardioplegic solution containing U50 488H (1. 6mmo l/L ) and then preserved with hypothermic preservation for four hours; groupII ; the precondition was the same as group II , hypothermic preservat ion fo r six hours; group III : the precondit ion was the same as group I , hypothermic preservation for eight hours; group IV : the precondit on was the same as group I , hypothermic preservation for ten hours. The cardiac function, myocardial sarcoplasmic reticulum calcium ion adenosine triphosphatase (SRCa2+ -ATPase) act ivity and calcium ion concentrations in mitochondria were determined at thirty minutes after reperfusion. Results As the hypothermic preservation time increased from four to ten hours, the recovery rate of each index of cardiac function, coronary artery flow (Cf) and SRCa2+ -ATPase activity also decreased, but the calcium ion concentrations in the mitochondria increased. Cardiac function index recovery rates in group I and group II w ere higher than those in group III and groupIV respectively (P lt; 0. 05, 0. 01) ,meanwhile recovery rates of cardiac function index in group III were higher than that in group IV (P lt; 0. 05). Recovery rate of Cf in groupII ( 84. 56%±10. 38%)were higher than those in group III (79. 45%±9. 67% ) and group IV (68. 31%±6. 84% , P lt;0.01) , meanwhile the recovery rate of Cf in group III was higher than that in group IV (P lt; 0. 05). SRCa2+ -A Tpase activity in group II (4. 43±0. 41μmo l/m g?h)were higher than those in control group (3. 04±0. 22Lmo l/mg?h ) , group III (3. 26±0. 29Lmo l/m g?h) and group IV (2. 57±0. 63Lmo l/m g?h, P lt; 0. 05) , SRCa2+ -ATPase activity in group III was higher than that in group IV (P lt; 0. 01). The calcium ion concentrations in mitochondria in group II (38176±4. 30μmo l/g ?dw ) and in the control group (40. 23±3. 75μmol/g ?dw )were less than those in group III (43125±5116μmol/g?dw ) and groupIV (45. 78±3. 26μmol/g?dw , P lt; 0. 05, 0. 01) respect ively. Conclusion The hypothermic preservation time for isolated dono r’s hearts p re-treated with St. Thomas II cardioplegic solution containing U 50 488H should the kep tunder 8h. The myocardial protection effects of both UW solution and U50 488H- containing St. Thomas II cardioplegic solution on isolated dono r’s hearts appear to be the same at 6 hours.
Myocardial stunning is the main pathological basis of heart dysfunction after open heart operation, its exact pathogenesis hasn’t been clarified until today.In recent years,the molecular and cellular studies have revealed possibly crucial pathogenesis of myocardial stunning that delayed recovery of myocardial glucose oxidation causes intracellular H + accumulation which augments H + Na + exchange thus leading to [Na +] i overload.[Na +] i overload increases Na + Ca 2+ exchange resulting in t...
From this experiment we found that acetylcholine (Ach) was the agonist of the colonic smooth muscles, and noradrenaline (NA) the internal anal sphincter(IAS). The contractions of colonic smooth muscles were significantly inhibited under the calcium-free solution (Ｐ＜0.01), but the IAS was not affected. Ryanodine, which can exhaust the intracellular calcium, remarkably depressed the contractions of IAS (Ｐ＜0.01),but had no effect on the colonic smooth muscles. It can be concluded that the contractions of colonic smooth muscles are mainly related to the influx of extracellular calcium; the release of intracellular calcium plays an important role in the contractions of IAS.
目的：探讨雌激素影响人精子顶体反应的可能机制。方法：应用异硫氰酸荧光素标记豌豆凝集素荧光染色法（FITC-PSA）分析精子顶体反应（AR）、以分光光度比色法测定顶体酶（ACE）活性。结果：17β-雌二醇（17β-E2）可促进精子发生AR，并增强精子顶体酶的活性；去除培养液中的Ca2+后，17β-E2不能诱导精子发生AR；PKC抑制剂能明显降低17β-E2所诱导的AR；E2-BSA亦能够促进精子发生AR，其作用与17β-E2无显著差异。结论：雌激素对人精子顶体反应有一定的促进作用，增强精子顶体酶活性可能是其作用途径之一，此过程涉及了胞外Ca2+、PKC及精子膜上的ER或雌激素结合位点的参与。