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16篇 您的检索式:作者名="Galileo"
    题名 作者 年代 出处 被引量
1Galileo views of the geology of Callisto显示文摘Greeleya R Klemaszewskia J E Wagnerb R the Galileo Imaging Team 2000Planetary and Space Science2000,48,:1
2锐钛型钛二氧化物纳米颗粒对小鼠的影响:证据表明短时间而不是长时间的暴露会导致小鼠精子结构和功能的异常显示文摘锐钛型钛二氧化物纳米颗粒(TNPs)广泛应用在商业领域,并且存在于不同的产品中。为明确更小剂量的锐钛型钛二氧化物纳米颗粒(ATNPs)间隔一定距离进入体内到达阴囊后是否能诱导精子缺陷的发生,雄性成年小鼠持续3天腹腔内注射100%ATNP(2.5或5mg/kg),然后在注射后1周、2周、3周或5周(长时间暴露)或者是注射后24小时、48小时或120小时(短时间暴露)处死。透射电镜表明在注射后120小时收集到的阴囊脂肪组织中,附睾组织和附睾液均出现炎症反应。在注射后120小时和3周后,睾丸组织间质间隙增大。利用末端脱氧核糖核酸转移酶介导的缺口末端标记技术发现在注射后的雄鼠体内阳性(即凋亡)精子(P=0.002)和间质细胞(P=O.04)数目均显著增加。与对照组相比,短时间暴露而不是长时间暴露的附睾尾部精子鞭毛异常、过量胞浆残余(ERC)的发生率增加,精子无顶体反应的发生率增加(呈剂量依赖性)。ERC与无顶体反应是否存在相关性目前尚不清楚。与对照组相比,暴露120小时组快速运动精子数量和线粒体膜电位均显著下降(P〈0.05),同时,活性氧水平显著增加(P〈0.00001)。这些结果表明在注射后4.8天,ANTP能够引发不育的精子结构和功能的异常,并且通过氧化应激造成DNA的损伤。同时,在暴露后的10天到5周末检测到精子的异常,这表明精子的这种异常是暂时性的。Michelle A Smith Rowan Michael Rolands G Aravindan Soma Dash Syed I Shah Deni S Galileo Patricia A Martin-DeLeon 2015Asian Journal of Andrology2015,17,2:1
3Immunomagnetic separation of neural cell- types 显示文摘Galileo DS Linser PJ 1986Journal of Cell Biology1986,103,5:1
4Triose phosphate export from chloroplasts and cellular sugar content regulate anthocyanin biosynthesis during high light acclimation显示文摘Plants have evolvedmultiple strategies to cope with rapid changes in the environment.During high light(HL)acclimation,the biosynthesis of photoprotective flavonoids,such as anthocyanins,is induced.However,the exact nature of the signal and downstreamfactors forHL induction of flavonoid biosynthesis(FB)is still under debate.Here,we show that carbon fixation in chloroplasts,subsequent export of photosynthates by triose phosphate/phosphate translocator(TPT),and rapid increase in cellular sugar content permit the transcriptional and metabolic activation of anthocyanin biosynthesis during HL acclimation.In combination with genetic and physiological analysis,targeted and whole-transcriptome gene expression studies suggest that reactive oxygen species and phytohormones play only a minor role in rapid HL induction of the anthocyanin branch of FB.In addition to transcripts of FB,sugar-responsive genes showed delayed repression or induction in tpt-2 during HL treatment,and a significant overlapwith transcripts regulated by SNF1-related protein kinase 1(SnRK1)was observed,including a central transcription factor of FB.Analysis of mutants with increased and repressed SnRK1 activity suggests that sugar-induced inactivation of SnRK1 is required for HL-mediated activation of anthocyanin biosynthesis.Our study emphasizes the central role of chloroplasts as sensors for environmental changes as well as the vital function of sugar signaling in plant acclimation.Max-Emanuel Zirngibl Galileo Estopare Araguirang Anastasia Kitashova Kathrin Jahnke Tobias Rolka Christine Kühn Thomas Nägele Andreas S.Richter 2023Plant Communications2023,4,1:1
5Epididymal SPAM1 is a marker for sperm maturation in the mouse显示文摘Chen H Griffiths G Galileo DS 2006Biol Reprod2006,74,5:1
6Risk assessment techniques for civil avia-tion security显示文摘Galileo Tamasi 2011Reliability Engineering & System Safety2011,96,8:1
7Retrovirally introduced antisense integrin RNA inhibits neuroblast migration in vivo显示文摘Galileo D Majors J Horwitz A 1992Neuron1992,9,:1
8Retrovirally introduced antisense integrin RNA inhibits neuroblast migration in vivo显示文摘Galileo DS Majors J Horwitz AF 1992Neuron1992,9,6:1
9Epididymal SPAM1 is a marker for sperm maturation in the mouse显示文摘Chen H Grifliths G Galileo DS Martln- DeLeon PA Biol Re- prod0,74,5:1
10Emigration of neuroepithelial cel s from the hindbrain neural tube in the chick embryo显示文摘Sohal GS Ali MM Galileo DS 0,,06:1
11Retrovirally introduced antisense integrin RNA inhibils neuroblast migration in vivo 显示文摘Galileo D Majors J Horwitz A 1992Neuron1992,9,11:1
12Epididymal SPAM1 is a marker for sperm maturation in the mouse 显示文摘Chen H Griffiths G Galileo DS 2006Biol Reprod2006,74,5:1
13Ground Calibration Targets for MIMR Radiometer System Testing显示文摘Battistelli E Galileo O Bordi R 1998IEEE1998,3498,:1
14Soluble L1 CAM promotes breast cancer cell adhe- sion and migration in vitro, bat not invasion 显示文摘Li Y Galileo DS 2010Cancer Cell Int2010,10,:1
15Leibniz and Newton around the braehistoehrone problem显示文摘HERRERA M D I Galileo Bernoulli 1994Rev Mexieana Fis1994,40,3:1
16Immunometabolic bases of type 2 diabetes in the severity of COVID- 19显示文摘The outbreak of coronavirus disease 2019(COVID-19)is caused by the novel severe acute respiratory syndrome coronavirus-2(SARS-CoV-2).COVID-19 and type 2 diabetes(T2D)have now merged into an ongoing global syndemic that is threatening the lives of millions of people around the globe.For this reason,there is a deep need to understand the immunometabolic bases of the main etiological factors of T2D that affect the severity of COVID-19.Here,we discuss how hyperglycemia contributes to the cytokine storm commonly associated with COVID-19 by stimulating monocytes and macrophages to produce interleukin IL-1β,IL-6,and TNF-αin the airway epithelium.The main mechanisms through which hyperglycemia promotes reactive oxygen species release,inhibition of T cell activation,and neutrophil extracellular traps in the lungs of patients with severe SARS-CoV-2 infection are also studied.We further examine the molecular mechanisms by which proinflammatory cytokines induce insulin resistance,and their deleterious effects on pancreaticβ-cell exhaustion in T2D patients critically ill with COVID-19.We address the effect of excess glucose on advanced glycation end product(AGE)formation and the role of AGEs in perpetuating pneumonia and acute respiratory distress syndrome.Finally,we discuss the contribution of preexisting endothelial dysfunction secondary to diabetes in the development of neutrophil trafficking,vascular leaking,and thrombotic events in patients with severe SARS-CoV-2 infection.As we outline here,T2D acts in synergy with SARSCoV-2 infection to increase the progression,severity,and mortality of COVID-19.We think a better understanding of the T2D-related immunometabolic factors that contribute to exacerbate the severity of COVID-19 will improve our ability to identify patients with high mortality risk and prevent adverse outcomes.Rebeca Viurcos-Sanabria Galileo Escobedo 2021World Journal of Diabetes2021,12,7:0
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