针对目前用户数据报协议(user datagram protocol,UDP)简单穿越NAT(simple traversal of UDP over NATs,STUN)的过程中,时延较长导致建立peer-to-peer(P2P)连接较慢的问题,提出了一种优化穿越性能的STUN算法。该算法根据客户端向STUN服...针对目前用户数据报协议(user datagram protocol,UDP)简单穿越NAT(simple traversal of UDP over NATs,STUN)的过程中,时延较长导致建立peer-to-peer(P2P)连接较慢的问题,提出了一种优化穿越性能的STUN算法。该算法根据客户端向STUN服务器发送UDP绑定请求的返回信息,计算出端口分配间距,然后利用分配间距提前计算出需要分配的实际传输的端口号,从而实现NAT穿越。搭建系统的服务器和客户端模块,并对算法的NAT穿越进行模拟测试。结果表明,与传统的STUN算法相比,通信双方使用优化的STUN算法建立P2P连接所需的时延较短,数据传输的吞吐量较高。展开更多
A comparative study was performed of the permeability of cell membranous structures in canine stunned myocardium and that of infarct myocardium by using colloidal lanthanum nitrate as an ultrastructure probe. Stunned ...A comparative study was performed of the permeability of cell membranous structures in canine stunned myocardium and that of infarct myocardium by using colloidal lanthanum nitrate as an ultrastructure probe. Stunned myocardium was characterized by mitochondrial swelling, vacuolar formation, a few lanthanum granules deposrting inside cells and intact structure of such membranes as cell membrane, mitochondrial membrane and lysosome membrane.Infarct myocardium was characterized by a large number of lanthanum granules passing through ruptured cell membrane and depositing in the cytoplasm and mitochondria. These results suggest that membranous structure remained intact during the occurrence of stunned myocardium.展开更多
Objective:To observe the effects of inhibition of glycolysis with iodoacetate (IAA) on calcium homeostasis and functional recovery of stunned myocardium in anesthetized dogs. Methods: Atomic absorption spectrophotomet...Objective:To observe the effects of inhibition of glycolysis with iodoacetate (IAA) on calcium homeostasis and functional recovery of stunned myocardium in anesthetized dogs. Methods: Atomic absorption spectrophotometry was employed to measure myocyte calcium and magnesium contents. Hemodynamics were monitored with a multichannel electrophysiologic recorder. Results: In nonischemic canine hearts (control), IAA's inhibition of glycolysis failed to change the [Ca2+] and [Mg2+] levels and cardiac functional conditions, whereas in hearts subjected to 15-minute ischemia , [Ca2+] increased from nonischemic 1.40±0. 20μmol/g to ischemic 1.80±0.17 μmol/g (P<0. 05), while [Mg2+] decreased. After 30 min of reperfusion,[Ca2+] continued to increase from 1.57±0.21 μmol/g (nonischemic area)to 2. 26±0. 09 μmol/g (abnormal area) and 60 min of reperfusion saw a slight restoration (1.54±0. 16 μmol/g in nonischemic area and 2. 21±0.20 μmol/g in abnormal area). In the glycolysis-inhibiting group, the calcium level registered a significant rise after 30 min of reperfusion: 1.57±0.07 μmol/g in nonischemic area and 2. 90? 0.25 μmol/g in abnormal area (P<0. 01).There was a significant difference between the glycolysis-inhibiting group and the group to which IAA was not applied. [Mg2+] maintained at a relatively low level and registered a more remarkable drop during inhibition of glycolysis, P<0.01 in comparison with the non IAA-administered group,suggesting that inhibition of glycolysis could cause severe calcium overload to sustain, in addition to an obvious harm to cardiac function. Left ventricular end-diastolic pressure and diastolic factor T were augmented andp/dt(max)declined. Conclusion: Since in vivo inhibition of glycolysis seemed to lead to severe calcium overload and hemodynamics changes,it might indicate that glycolysis played an importent role in the restoration of calcium homeostasis in postischemic myocardium,and that ATP derived from glycolysis took a significant part in myocardial ion transport both at the stage of ischemia and the early stage of reperfusion and in cardiac functional recovery.展开更多
文摘针对目前用户数据报协议(user datagram protocol,UDP)简单穿越NAT(simple traversal of UDP over NATs,STUN)的过程中,时延较长导致建立peer-to-peer(P2P)连接较慢的问题,提出了一种优化穿越性能的STUN算法。该算法根据客户端向STUN服务器发送UDP绑定请求的返回信息,计算出端口分配间距,然后利用分配间距提前计算出需要分配的实际传输的端口号,从而实现NAT穿越。搭建系统的服务器和客户端模块,并对算法的NAT穿越进行模拟测试。结果表明,与传统的STUN算法相比,通信双方使用优化的STUN算法建立P2P连接所需的时延较短,数据传输的吞吐量较高。
文摘A comparative study was performed of the permeability of cell membranous structures in canine stunned myocardium and that of infarct myocardium by using colloidal lanthanum nitrate as an ultrastructure probe. Stunned myocardium was characterized by mitochondrial swelling, vacuolar formation, a few lanthanum granules deposrting inside cells and intact structure of such membranes as cell membrane, mitochondrial membrane and lysosome membrane.Infarct myocardium was characterized by a large number of lanthanum granules passing through ruptured cell membrane and depositing in the cytoplasm and mitochondria. These results suggest that membranous structure remained intact during the occurrence of stunned myocardium.
文摘Objective:To observe the effects of inhibition of glycolysis with iodoacetate (IAA) on calcium homeostasis and functional recovery of stunned myocardium in anesthetized dogs. Methods: Atomic absorption spectrophotometry was employed to measure myocyte calcium and magnesium contents. Hemodynamics were monitored with a multichannel electrophysiologic recorder. Results: In nonischemic canine hearts (control), IAA's inhibition of glycolysis failed to change the [Ca2+] and [Mg2+] levels and cardiac functional conditions, whereas in hearts subjected to 15-minute ischemia , [Ca2+] increased from nonischemic 1.40±0. 20μmol/g to ischemic 1.80±0.17 μmol/g (P<0. 05), while [Mg2+] decreased. After 30 min of reperfusion,[Ca2+] continued to increase from 1.57±0.21 μmol/g (nonischemic area)to 2. 26±0. 09 μmol/g (abnormal area) and 60 min of reperfusion saw a slight restoration (1.54±0. 16 μmol/g in nonischemic area and 2. 21±0.20 μmol/g in abnormal area). In the glycolysis-inhibiting group, the calcium level registered a significant rise after 30 min of reperfusion: 1.57±0.07 μmol/g in nonischemic area and 2. 90? 0.25 μmol/g in abnormal area (P<0. 01).There was a significant difference between the glycolysis-inhibiting group and the group to which IAA was not applied. [Mg2+] maintained at a relatively low level and registered a more remarkable drop during inhibition of glycolysis, P<0.01 in comparison with the non IAA-administered group,suggesting that inhibition of glycolysis could cause severe calcium overload to sustain, in addition to an obvious harm to cardiac function. Left ventricular end-diastolic pressure and diastolic factor T were augmented andp/dt(max)declined. Conclusion: Since in vivo inhibition of glycolysis seemed to lead to severe calcium overload and hemodynamics changes,it might indicate that glycolysis played an importent role in the restoration of calcium homeostasis in postischemic myocardium,and that ATP derived from glycolysis took a significant part in myocardial ion transport both at the stage of ischemia and the early stage of reperfusion and in cardiac functional recovery.
