随着电网换相型高压直流输电(line commutated converter based high voltage direct current, LCC-HVDC)技术的广泛应用,交直流混联电力系统的交互稳定性问题日益突出。首先基于状态空间平均法建立了考虑非线性换相重叠动态过程的LCC...随着电网换相型高压直流输电(line commutated converter based high voltage direct current, LCC-HVDC)技术的广泛应用,交直流混联电力系统的交互稳定性问题日益突出。首先基于状态空间平均法建立了考虑非线性换相重叠动态过程的LCC换流器传递函数模型。为适应愈加复杂的直流输电系统建模,提出利用模块化思想分别建立LCC-HVDC各子系统小信号模型,并推导了能反映交直流系统和换流器之间电气耦合特性的接口矩阵实现子系统连接,从而模块化建立精确且易于扩展的计及控制链路延时和锁相环输出相位波动的双端LCC-HVDC系统改进小信号模型。最后分析了控制系统参数和控制链路延时对系统小干扰稳定性的影响以及失稳模态的主导因素,揭示了双端LCC-HVDC系统交直流混合谐振机理及送受端交互影响具体过程。研究结果可以为系统参数设计、谐振抑制措施提供理论基础。展开更多
Oxaliplatin, an anticancer drug commonly used to treat colorectal cancer and other tumors, has a number of serious side effects, most notably neuropathy and ototoxicity. To gain insights into its ototoxic profile, oxa...Oxaliplatin, an anticancer drug commonly used to treat colorectal cancer and other tumors, has a number of serious side effects, most notably neuropathy and ototoxicity. To gain insights into its ototoxic profile, oxaliplatin was applied to rat cochlear organ cultures. Consistent with it neurotoxic propensity, oxaliplatin selectively damaged nerve fibers at a very low dose 1 μM. In contrast, the dose required to damage hair cells and spiral ganglion neurons was 50 fold higher (50 μM). Oxailiplatin-induced cochlear lesions initial-ly increased with dose, but unexpectedly decreased at very high doses. This non-linear dose response could be related to depressed oxaliplatin uptake via active transport mechanisms. Previous studies have demon-strated that axonal degeneration involves biologically active processes which can be greatly attenuated by nicotinamide adenine dinucleotide (NAD+). To determine if NAD+would protect spiral ganglion axons and the hair cells from oxaliplatin damage, cochlear cultures were treated with oxaliplatin alone at doses of 10 μM or 50 μM respectively as controls or combined with 20 mM NAD+. Treatment with 10 μM oxaliplatin for 48 hours resulted in minor damage to auditory nerve fibers, but spared cochlear hair cells. However, when cochlear cultures were treated with 10 μM oxaliplatin plus 20 mM NAD+, most auditory nerve fibers were intact. 50 μM oxaliplatin destroyed most of spiral ganglion neurons and cochlear hair cells with apop-totic characteristics of cell fragmentations. However, 50 μM oxaliplatin plus 20 mM NAD+treatment great-ly reduced neuronal degenerations and hair cell missing. The results suggested that NAD+provides signifi-cant protection against oxaliplatin-induced neurotoxicity and ototoxicity, which may be due to its actions of antioxidant, antiapoptosis, and energy supply.展开更多
文摘随着电网换相型高压直流输电(line commutated converter based high voltage direct current, LCC-HVDC)技术的广泛应用,交直流混联电力系统的交互稳定性问题日益突出。首先基于状态空间平均法建立了考虑非线性换相重叠动态过程的LCC换流器传递函数模型。为适应愈加复杂的直流输电系统建模,提出利用模块化思想分别建立LCC-HVDC各子系统小信号模型,并推导了能反映交直流系统和换流器之间电气耦合特性的接口矩阵实现子系统连接,从而模块化建立精确且易于扩展的计及控制链路延时和锁相环输出相位波动的双端LCC-HVDC系统改进小信号模型。最后分析了控制系统参数和控制链路延时对系统小干扰稳定性的影响以及失稳模态的主导因素,揭示了双端LCC-HVDC系统交直流混合谐振机理及送受端交互影响具体过程。研究结果可以为系统参数设计、谐振抑制措施提供理论基础。
文摘Oxaliplatin, an anticancer drug commonly used to treat colorectal cancer and other tumors, has a number of serious side effects, most notably neuropathy and ototoxicity. To gain insights into its ototoxic profile, oxaliplatin was applied to rat cochlear organ cultures. Consistent with it neurotoxic propensity, oxaliplatin selectively damaged nerve fibers at a very low dose 1 μM. In contrast, the dose required to damage hair cells and spiral ganglion neurons was 50 fold higher (50 μM). Oxailiplatin-induced cochlear lesions initial-ly increased with dose, but unexpectedly decreased at very high doses. This non-linear dose response could be related to depressed oxaliplatin uptake via active transport mechanisms. Previous studies have demon-strated that axonal degeneration involves biologically active processes which can be greatly attenuated by nicotinamide adenine dinucleotide (NAD+). To determine if NAD+would protect spiral ganglion axons and the hair cells from oxaliplatin damage, cochlear cultures were treated with oxaliplatin alone at doses of 10 μM or 50 μM respectively as controls or combined with 20 mM NAD+. Treatment with 10 μM oxaliplatin for 48 hours resulted in minor damage to auditory nerve fibers, but spared cochlear hair cells. However, when cochlear cultures were treated with 10 μM oxaliplatin plus 20 mM NAD+, most auditory nerve fibers were intact. 50 μM oxaliplatin destroyed most of spiral ganglion neurons and cochlear hair cells with apop-totic characteristics of cell fragmentations. However, 50 μM oxaliplatin plus 20 mM NAD+treatment great-ly reduced neuronal degenerations and hair cell missing. The results suggested that NAD+provides signifi-cant protection against oxaliplatin-induced neurotoxicity and ototoxicity, which may be due to its actions of antioxidant, antiapoptosis, and energy supply.
