为了研究Ga N开关类功率放大器（PA）的温度特性,通过开展一系列的温度测试来研究温度变化对该Ga N PA各个性能参数的具体影响。测试结果表明：首先,较高的温度（〉80℃）会使Ga N HEMT的电特性发生严重恶化,进而导致器件的性能和可靠...为了研究Ga N开关类功率放大器（PA）的温度特性,通过开展一系列的温度测试来研究温度变化对该Ga N PA各个性能参数的具体影响。测试结果表明：首先,较高的温度（〉80℃）会使Ga N HEMT的电特性发生严重恶化,进而导致器件的性能和可靠性显著下降。其次,对于该开关类Ga N PA来说,随着温度的持续升高,其功率附加效率（PAE）显著降低,不能再保持高效率。而且,随着温度的突变和冲击次数的增加,电路出现显著的退化甚至失效。这些都说明了温度的变化对PA的性能产生了很大的影响,开关类PA对温度的变化非常敏感,而且温度冲击对其性能影响更为显著。这些研究为PA的可靠性设计提供了重要指导。展开更多
Alzheimer＇s disease （AD） is a complex neurological disor- der characterized by a progressive dementia. The amyloid hypothesis states that pathogenesis is driven by the accumu- lation of amyloid β（Aβ） peptides w...Alzheimer＇s disease （AD） is a complex neurological disor- der characterized by a progressive dementia. The amyloid hypothesis states that pathogenesis is driven by the accumu- lation of amyloid β（Aβ） peptides within the brain （Hardy and Higgins, 1992）, which have multiple effects including activation of glial cells and synapse degeneration. For many years therapeutic strategies were based upon the discovery of compounds that reduced the production of Aβ in vitro and in vivo. However, the amyloid hypothesis is not universally accepted; critics pointed out poor correlations between con- centrations of Aβ in the brain and clinical disease and that, although numerous compounds reduced the production of Aβ in animal models, few had any clinical benefit in AD pa- tients. The failure of Aβ-1owering therapies in translational research has resulted in important modifications of the amy- loid hypothesis.展开更多
文摘为了研究Ga N开关类功率放大器（PA）的温度特性,通过开展一系列的温度测试来研究温度变化对该Ga N PA各个性能参数的具体影响。测试结果表明：首先,较高的温度（〉80℃）会使Ga N HEMT的电特性发生严重恶化,进而导致器件的性能和可靠性显著下降。其次,对于该开关类Ga N PA来说,随着温度的持续升高,其功率附加效率（PAE）显著降低,不能再保持高效率。而且,随着温度的突变和冲击次数的增加,电路出现显著的退化甚至失效。这些都说明了温度的变化对PA的性能产生了很大的影响,开关类PA对温度的变化非常敏感,而且温度冲击对其性能影响更为显著。这些研究为PA的可靠性设计提供了重要指导。
文摘Alzheimer＇s disease （AD） is a complex neurological disor- der characterized by a progressive dementia. The amyloid hypothesis states that pathogenesis is driven by the accumu- lation of amyloid β（Aβ） peptides within the brain （Hardy and Higgins, 1992）, which have multiple effects including activation of glial cells and synapse degeneration. For many years therapeutic strategies were based upon the discovery of compounds that reduced the production of Aβ in vitro and in vivo. However, the amyloid hypothesis is not universally accepted; critics pointed out poor correlations between con- centrations of Aβ in the brain and clinical disease and that, although numerous compounds reduced the production of Aβ in animal models, few had any clinical benefit in AD pa- tients. The failure of Aβ-1owering therapies in translational research has resulted in important modifications of the amy- loid hypothesis.
