We report the radio observations of the eclipsing black widow pulsar J1720-0534, a 3.26 ms pulsar in orbit with a low mass companion of mass 0.029 to 0.034 M⊙. We obtain the phase-connected timing ephemeris and polar...We report the radio observations of the eclipsing black widow pulsar J1720-0534, a 3.26 ms pulsar in orbit with a low mass companion of mass 0.029 to 0.034 M⊙. We obtain the phase-connected timing ephemeris and polarization profile of this millisecond pulsar(MSP) using the Five-hundred-meter Aperture Spherical radio Telescope(FAST), the Green Bank Telescope(GBT), and the Parkes Telescope. For the first time from such a system, an oscillatory polarization angle change was observed from a particular eclipse egress with partial depolarization, indicating 10-milliGauss-level reciprocating magnetic fields oscillating in a length scale of 5 ×10^(3)km(assuming an orbital inclination angle of 90°) outside the companion's magnetosphere. The dispersion measure variation observed during the ingresses and egresses shows the rapid raising of the electron density in the shock boundary between the companion's magnetosphere and the surrounding pulsar wind. We suggest that the observed oscillatory magnetic fields originate from the pulsar wind outside the companion's magnetosphere.展开更多
SRT1720, a new discovered drug, was reported to activate silent information regulator 1（SIRT1） and inhibit the chondrocyte apoptosis. However, the underlying mechanism remains elusive. In the present study, the chon...SRT1720, a new discovered drug, was reported to activate silent information regulator 1（SIRT1） and inhibit the chondrocyte apoptosis. However, the underlying mechanism remains elusive. In the present study, the chondrocytes were extracted from the cartilage tissues of New Zealand white rabbits, cultured in the presence of sodium nitroprusside（SNP）（2.5 mmol/L） and divided into five groups： 1, 5, 10, and 20 μmol/L SRT1720 groups and blank control group（0 μmol/L SRT1720）. MTT assay was used to detect the chondrocyte viability and proliferation, and DAPI staining and flow cytometry to measure the chondrocyte apoptosis. The expression levels of SIRT1, p53, NF-κB/p65, Bax, and peroxisome proliferator-activated receptor gamma coactivator 1-α（PGC-1α） were detected by Western blotting and the expression levels of SIRT1, type Ⅱ collagen, and aggrecan m RNA by RT-PCR. The results showed that in the SRT1720-treated groups, the nuclei of chondrocytes were morphologically intact and had uniform chromatin. In the blank control group, nuclear rupture into debris was observed in chondrocytes. With the SRT1720 concentration increasing, the chondrocyte viability increased, the apoptosis rate decreased, the protein expression levels of SIRT1 and PGC-1α and the m RNA expression levels of type Ⅱ collagen and aggrecan increased（P〈0.05）, and the expression levels of p53, NF-κB and bax decreased（P〈0.05）. It was suggested that SRT1720 inhibits chondrocyte apoptosis by activating the expression of SIRT1 via p53/bax and NF-κB/PGC-1α pathways.展开更多
目的探讨沉默交配型信息调节2同系物-1(silent mating type information regulation2 homolog 1,SIRT1)激活剂SRT1720对重度失血性休克/复苏致大鼠急性肾损伤的治疗作用及机制。方法模型组、SIRT1激活剂SRT1720低、中、高剂量组(20、40...目的探讨沉默交配型信息调节2同系物-1(silent mating type information regulation2 homolog 1,SIRT1)激活剂SRT1720对重度失血性休克/复苏致大鼠急性肾损伤的治疗作用及机制。方法模型组、SIRT1激活剂SRT1720低、中、高剂量组(20、40、80mg/kg)建立重度失血性休克/复苏致大鼠急性肾损伤模型,建模成功后SIRT1激活剂SRT1720各剂量组给予相应药物,对照组、模型组给予等体积生理盐水;随后处死大鼠,测定肾/体比值、肌酐(SCr)、尿素氮(BUN)、肾脏SIRT1、信号转导转录激活剂-3(signal transducers and activators of transcription factor 3,STAT3)mRNA和蛋白水平、白细胞介素-2(IL-2)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)水平。结果与对照组比较,模型组肾/体比值、尿蛋白、SCr、BUN、IL-2、IL-6、TNF-α升高(t值分别为25.632、14.524、18.965、23.654、23.654、18.695、19.547,P均<0.001);与模型组比较,SRT1720各剂量组肾/体比值、尿蛋白、SCr、BUN、IL-2、IL-6、TNF-α降低(t=21.526、19.654、23.654、25.148,32.654、19.654、21.548、25.965、24.967、28.741、30.365、31.654、23.654、18.475、26.548、29.512,30.248、24.659、24.965、22.698、26.985,P均<0.001),且随着SRT1720给药剂量的增加,肾/体比值、尿蛋白、SCr、BUN、IL-2、IL-6、TNF-α逐渐降低,剂量-效应关系明显(t=38.632、19.625、25.847、27.489、26.954、29.547、32.685、34.489、32.362、24.548、29.654、28.415、35.957、32.548,P均<0.001)。与对照组比较,模型组肾SIRT1 mRNA和蛋白水平降低(t=38.635、32.145,P均<0.001),STAT3 m RNA水平升高(t=32.636、30.213,P均<0.001);与模型组比较,SRT1720各剂量组SIRT1 mRNA和蛋白水平升高(t=18.965、23.147、28.476、30.216、23.654、28.471,P均<0.001),STAT3 mRNA和蛋白水平降低(t=22.654、25.489、29.548、33.265、41.326、29.635,P均<0.001),且随着SRT1720给药剂量增加,SIRT1 m RNA和蛋白水平逐渐升高,STAT3 mRNA和蛋白水平逐渐降低,剂量-效应关系明显(t=27.485、28.459、30.215、29.584、29.654、31.145、32.159、30.269,P均<0.001)。结论SIRT1激活剂SRT1720能减轻重度失血性休克/复苏致大鼠急性肾损伤;其机制与SIRT1激活剂SRT1720通过激活大鼠肾脏中SIRT1表达,抑制STAT3表达进而抑制炎性介质表达有关。展开更多
基金The Parkes Radio Telescope (Murriyang) is part of the Australia Telescope National Facility, which is funded by the Australian Government for operation as a National Facility managed by CSIROsupported by the National Natural Science Foundation of China (NSFC) grant Nos. 12041303, 12041304, 11873067, 12133004, 12203045, 12203070, 12203072, 12103013, U2031117 and T2241020+11 种基金the CAS-MPG LEGACY project and the National SKA Program of China No. 2020SKA0120200the Foundation of Science and Technology of Guizhou Province No. ((2021)023)the Foundation of Guizhou Provincial Education Department (No.KY(2021)303)the National Key Research and Development Program of China Nos. 2022YFC2205202 and 2022YFC2205203the Major Science and Technology Program of Xinjiang Uygur Autonomous Region Nos. 2022A03013-1, 2022A03013-3 and 2022A03013-4the National Key Research and Development Program of China No. 2022YFC2205203the 2021 project Xinjiang Uygur autonomous region of China for Tianshan elites and the Youth Innovation Promotion Association of CAS under No. 2023069support from the Youth Innovation Promotion Association CAS (id. 2021055)CAS Project for Young Scientists in Basic Research (grant YSBR-006)the Cultivation Project for FAST Scientific Payoff and Research Achievement of CAMS-CASsupport from Zhejiang Provincial Natural Science Foundation of China under grant No. LY23A030001supported by the NSF Physics Frontiers Center award number 2020265。
文摘We report the radio observations of the eclipsing black widow pulsar J1720-0534, a 3.26 ms pulsar in orbit with a low mass companion of mass 0.029 to 0.034 M⊙. We obtain the phase-connected timing ephemeris and polarization profile of this millisecond pulsar(MSP) using the Five-hundred-meter Aperture Spherical radio Telescope(FAST), the Green Bank Telescope(GBT), and the Parkes Telescope. For the first time from such a system, an oscillatory polarization angle change was observed from a particular eclipse egress with partial depolarization, indicating 10-milliGauss-level reciprocating magnetic fields oscillating in a length scale of 5 ×10^(3)km(assuming an orbital inclination angle of 90°) outside the companion's magnetosphere. The dispersion measure variation observed during the ingresses and egresses shows the rapid raising of the electron density in the shock boundary between the companion's magnetosphere and the surrounding pulsar wind. We suggest that the observed oscillatory magnetic fields originate from the pulsar wind outside the companion's magnetosphere.
基金supported by grants from the National Natural Science Foundation of China(No.81272032)Key Project of Shenzhen Science and Technology Plan(No.201101001)
文摘SRT1720, a new discovered drug, was reported to activate silent information regulator 1（SIRT1） and inhibit the chondrocyte apoptosis. However, the underlying mechanism remains elusive. In the present study, the chondrocytes were extracted from the cartilage tissues of New Zealand white rabbits, cultured in the presence of sodium nitroprusside（SNP）（2.5 mmol/L） and divided into five groups： 1, 5, 10, and 20 μmol/L SRT1720 groups and blank control group（0 μmol/L SRT1720）. MTT assay was used to detect the chondrocyte viability and proliferation, and DAPI staining and flow cytometry to measure the chondrocyte apoptosis. The expression levels of SIRT1, p53, NF-κB/p65, Bax, and peroxisome proliferator-activated receptor gamma coactivator 1-α（PGC-1α） were detected by Western blotting and the expression levels of SIRT1, type Ⅱ collagen, and aggrecan m RNA by RT-PCR. The results showed that in the SRT1720-treated groups, the nuclei of chondrocytes were morphologically intact and had uniform chromatin. In the blank control group, nuclear rupture into debris was observed in chondrocytes. With the SRT1720 concentration increasing, the chondrocyte viability increased, the apoptosis rate decreased, the protein expression levels of SIRT1 and PGC-1α and the m RNA expression levels of type Ⅱ collagen and aggrecan increased（P〈0.05）, and the expression levels of p53, NF-κB and bax decreased（P〈0.05）. It was suggested that SRT1720 inhibits chondrocyte apoptosis by activating the expression of SIRT1 via p53/bax and NF-κB/PGC-1α pathways.
文摘目的探讨沉默交配型信息调节2同系物-1(silent mating type information regulation2 homolog 1,SIRT1)激活剂SRT1720对重度失血性休克/复苏致大鼠急性肾损伤的治疗作用及机制。方法模型组、SIRT1激活剂SRT1720低、中、高剂量组(20、40、80mg/kg)建立重度失血性休克/复苏致大鼠急性肾损伤模型,建模成功后SIRT1激活剂SRT1720各剂量组给予相应药物,对照组、模型组给予等体积生理盐水;随后处死大鼠,测定肾/体比值、肌酐(SCr)、尿素氮(BUN)、肾脏SIRT1、信号转导转录激活剂-3(signal transducers and activators of transcription factor 3,STAT3)mRNA和蛋白水平、白细胞介素-2(IL-2)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)水平。结果与对照组比较,模型组肾/体比值、尿蛋白、SCr、BUN、IL-2、IL-6、TNF-α升高(t值分别为25.632、14.524、18.965、23.654、23.654、18.695、19.547,P均<0.001);与模型组比较,SRT1720各剂量组肾/体比值、尿蛋白、SCr、BUN、IL-2、IL-6、TNF-α降低(t=21.526、19.654、23.654、25.148,32.654、19.654、21.548、25.965、24.967、28.741、30.365、31.654、23.654、18.475、26.548、29.512,30.248、24.659、24.965、22.698、26.985,P均<0.001),且随着SRT1720给药剂量的增加,肾/体比值、尿蛋白、SCr、BUN、IL-2、IL-6、TNF-α逐渐降低,剂量-效应关系明显(t=38.632、19.625、25.847、27.489、26.954、29.547、32.685、34.489、32.362、24.548、29.654、28.415、35.957、32.548,P均<0.001)。与对照组比较,模型组肾SIRT1 mRNA和蛋白水平降低(t=38.635、32.145,P均<0.001),STAT3 m RNA水平升高(t=32.636、30.213,P均<0.001);与模型组比较,SRT1720各剂量组SIRT1 mRNA和蛋白水平升高(t=18.965、23.147、28.476、30.216、23.654、28.471,P均<0.001),STAT3 mRNA和蛋白水平降低(t=22.654、25.489、29.548、33.265、41.326、29.635,P均<0.001),且随着SRT1720给药剂量增加,SIRT1 m RNA和蛋白水平逐渐升高,STAT3 mRNA和蛋白水平逐渐降低,剂量-效应关系明显(t=27.485、28.459、30.215、29.584、29.654、31.145、32.159、30.269,P均<0.001)。结论SIRT1激活剂SRT1720能减轻重度失血性休克/复苏致大鼠急性肾损伤;其机制与SIRT1激活剂SRT1720通过激活大鼠肾脏中SIRT1表达,抑制STAT3表达进而抑制炎性介质表达有关。
