针对电源噪声影响图像、声音信息的传输质量,系统电源上电时间过长导致延时增大、时序紧张等问题设计了一种可快速启动的高电源抑制比的带隙基准源。通过引入负反馈回路,维持基准电压的稳定,以提升基准源的电源抑制比。设计了快速启动电...针对电源噪声影响图像、声音信息的传输质量,系统电源上电时间过长导致延时增大、时序紧张等问题设计了一种可快速启动的高电源抑制比的带隙基准源。通过引入负反馈回路,维持基准电压的稳定,以提升基准源的电源抑制比。设计了快速启动电路,在电源上电时通过开关管快速导通以拉高基准电压,加速了带隙基准源的启动,在基准建立好之后启动电路停止工作。基于5 V 0.35μm互补金属氧化物半导体(Complementary Metal Oxide Semiconductor,CMOS)工艺设计了基准电压源,仿真结果表明,在-40℃~125℃温度变化范围内,基准源电压变化为5.33 mV,电源抑制比在100 Hz以下达到-90.1 dB,启动时间为9μs。设计的带隙基准电压源启动速度较快,电源抑制比较高。展开更多
apamvcin was first isolated from a strain of Sreptomyces hygroscopicus in the early 1970s froma soil sample taken on Easter Island. Because the antiproliferative effects of rapamycin on yeast cell, as well as B and T ...apamvcin was first isolated from a strain of Sreptomyces hygroscopicus in the early 1970s froma soil sample taken on Easter Island. Because the antiproliferative effects of rapamycin on yeast cell, as well as B and T lymphocytes, it was first identified as an antimicrobial agent with potent immunosuppressive activity and has been used in antirejection therapy.展开更多
文摘针对电源噪声影响图像、声音信息的传输质量,系统电源上电时间过长导致延时增大、时序紧张等问题设计了一种可快速启动的高电源抑制比的带隙基准源。通过引入负反馈回路,维持基准电压的稳定,以提升基准源的电源抑制比。设计了快速启动电路,在电源上电时通过开关管快速导通以拉高基准电压,加速了带隙基准源的启动,在基准建立好之后启动电路停止工作。基于5 V 0.35μm互补金属氧化物半导体(Complementary Metal Oxide Semiconductor,CMOS)工艺设计了基准电压源,仿真结果表明,在-40℃~125℃温度变化范围内,基准源电压变化为5.33 mV,电源抑制比在100 Hz以下达到-90.1 dB,启动时间为9μs。设计的带隙基准电压源启动速度较快,电源抑制比较高。
基金This work was supported by grants from National Natural Science Foundation of China （No. 30971312） and the Key Project of Beijing Municipal Education Commission Sci-Tech Development Program （No. KZ201110025028）.
文摘apamvcin was first isolated from a strain of Sreptomyces hygroscopicus in the early 1970s froma soil sample taken on Easter Island. Because the antiproliferative effects of rapamycin on yeast cell, as well as B and T lymphocytes, it was first identified as an antimicrobial agent with potent immunosuppressive activity and has been used in antirejection therapy.
文摘目的明确癌基因B-RafV600E在Mps1和B-RafWT/MEK/ERK通路之间自动调节的负反馈回路中抵抗作用的具体机制。方法 (1)Sbcl2转染B-RafWT和Mps1-KD,Western blot方法检测p-ERK水平;(2)向B-Raf野生型SK-MEL31、Sbcl2、WM35细胞及V600E突变型SK-MEL28、A375细胞中过表达Mps1,Western blot方法检测p-ERK水平;(3)在SK-MEL31、Sbcl2、WM35细胞中敲低AKT,转染Mps1,Western blot方法检测p-ERK水平;(4)在SK-MEL31、Sbcl2、WM35细胞中敲低内源性B-Raf,过表达外源性RafV600E,Western blot方法检测p-AKT水平;敲低SK-MEL-28、A375细胞中RafV600E,Western blot方法检测p-A K T水平。结果 (1)M p s 1激酶和B-RafWT/MEK/ERK通路之间的自动负反馈通路不依赖Mps1激酶的活性;(2)在野生型SK-MEL31、Sbcl2、WM35细胞中外源性Mps1的表达可诱导AKT磷酸化,抑制ERK活性;V600E突变型SK-MEL28、A375细胞中外源性Mps1的表达不能诱导AKT磷酸化,亦不影响ERK活性。(3)敲低野生型黑色素瘤细胞中的AKT后,Mps1和B-RafWT/MEK/ERK之间的负反馈作用消失。(4)癌基因B-RafV600E通过抑制AKT的磷酸化,进而抵抗Mps1激酶与B-Raf/MEK/ERK通路之间的负反馈调节作用。结论 Mps1和B-RafWT/MEK/ERK通路之间的自动负反馈通路不依赖Mps1激酶的活性,且癌基因B-RafV600E对B-Raf/MEK/ERK/Mps1负反馈通路的抵抗作用是通过抑制AKT的磷酸化实现的。
