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越崎论坛,如若n维乘性相关向量的坐标是代数数

时间:2019-09-26 15:24来源:信息科学
2018年中国矿业大学海外青年学者“越崎论坛” 广大师生:华南理工大学“海内外优秀青年学者论坛”旨在面向全球邀请拥有不同学术背景的青年才俊,围绕国际科学前沿、热点研究领

2018年中国矿业大学海外青年学者“越崎论坛”

广大师生: 华南理工大学“海内外优秀青年学者论坛”旨在面向全球邀请拥有不同学术背景的青年才俊,围绕国际科学前沿、热点研究领域以及行业产业的技术问题等展开探讨和交流。希望藉此平台,互相启迪、开拓视野,增强国际交流与合作,促进双方共同发展。现将医学院分论坛有关安排通知如下:一、论坛时间2018年10月24日14:00-17:00二、论坛地点华南理工大学大学城校区B2-513会议室 三、论坛议程

广大师生:华南理工大学“海内外优秀青年学者论坛”旨在面向全球邀请青年才俊,围绕国际科学前沿、热点研究领域以及行业产业的技术问题等展开探讨和交流。籍此平台,启迪思维,开拓视野,促进学术交流与合作,本次论坛的具体安排如下:一、论坛时间2018年10月8日下午15:00-16:00二、论坛地点华南理工大学4号楼数学学院4318会议室三、论坛议程1. 15:00-15:05学院领导致欢迎辞;2. 15:05-16:00报告人:沙敏博士,澳大利亚麦考瑞大学,报告题目:代数数的乘性相关性(Multiplicative dependence of algebraic numbers)。欢迎广大师生参加!数学学院2018年9月26日内容摘要:代数数的乘性相关性是数论中的经典课题。我们称n个非零复数a1, ..., an是乘性相关的,如果存在不全为零的整数k1, ..., kn使得乘积a1k1... ankn=1。同理,称一个n维向量是乘性相关的,如果它的n个坐标是乘性相关的。报告将从分析、算术和几何角度开展。从分析角度,考虑到稠密性问题。在实空间或复空间中,虽然乘性相关向量的勒贝格测度为零,但证明它们在空间中是稠密的,并且向量的坐标只需取自某个代数数域。然后通过考虑覆盖半径,这个问题可以被更细致地研究。从算术角度,考虑到n维乘性相关向量的计数问题。比如,如果n维乘性相关向量的坐标是代数数,次数和高度都有上界,那么对于这些向量的个数,给出了关于高度的渐近公式。从几何角度,考虑到代数曲线上的乘性相关点。证明如果曲线定义在一个代数数域K上并且亏格大于零,那么曲线上只有有限个乘性相关点,其坐标来自于K的极大阿贝尓扩张。亏格为零的曲线也有类似结论。报告人简介:沙敏,1983年10月出生,博士。2007年在华南理工大学获得学士学位,2010年在清华大学获得硕士学位,2013年在法国波尔多大学获得博士学位。2013年12月至2016年6月在澳大利亚新南威尔士大学做博士后。2016年6月至今在澳大利亚麦考瑞大学做校级博士后。沙敏博士长期研究数论及其应用。目前主要研究兴趣包括代数数论,椭圆曲线,有限域理论,算术动力系统,线性递归序列,以及数论中的图论问题。在包括Transactions of the American Mathematical Society, International Mathematics Research Notices, Moscow Mathematical Journal, Journal of Combinatorial Theory Series B等国际知名期刊上发表论文多篇。从2012年起担任美国《数学评论》的评论员。于2013年获得欧盟委员会的Alain Bensoussan Fellowship,并于2016年获得麦考瑞大学的Macquarie University Research Fellowship。

资源学院分论坛

日期

附件:

间:2018年6月6日-7日

时间

主办单位:资源与地球科学学院

事项或议程

欢迎全校师生踊跃参加!

地点

第一会场

10月23日

地点:煤层气资源与成藏过程教育部重点实验室319会议室

全天

(文昌校区北门外大学科技园B座)

报到、入住;

时间:2018年6月7日9点

大学城中心酒店

报告一:Particle-based modeling of pull-apart basin development

10月24日

报告人:刘源,博士后, 德国弗莱贝格工业大学

凤凰彩票在线计划,14:00-17:00学术报告主持人:廉哲雄

报告摘要:

报告人:曾筑天(加拿大卡尔加里大学Cumming 医学院博士后)题目:To See the Unseen: Intravital imaging reveals key immune defense mechanisms against bloodstream bacterial infection

1. A scale-independent modeling approach based on the Discrete Element Method has been built to investigate pull-apart basin development.

B2-513会议室

2. The shape of a pull-apart basin is the consequence of both initial strike-slip geometry and its various evolution stages.

报告人:叶浩彬(科罗拉多大学医学院博士后)题目:Management of Leukemia from Metabolic Perspectives

3. Minimum displacements to form pull-apart basins, and minimum ages of initiation for pull-apart basins can be estimated.

欢迎广大师生参加! 医学院2018年10月22日1.报告人:曾筑天(加拿大卡尔加里大学Cumming 医学院博士后)报告题目:To See the Unseen: Intravital imaging reveals key immune defense mechanisms against bloodstream bacterial infection内容摘要:Bloodstream bacterial infection is on the rise due to the wide spread use of indwelling intravenous catheters and immunosuppressive iatrogenic interventions. First-pass clearance of blood-borne bacteria is critical to control bloodstream infections and to prevent systemic dissemination. The liver has been well known as a blood-filtering organ capable of sequestering circulating bacteria via its vast pool of intravascular macrophages-Kupffer cells. However, the molecular mechanism underlying Kupffer cell mediated capture of circulating pathogens under shear conditions remains less understood. Taking advantage of high-speed real time intravital imaging, we visualized the dynamic process of bacterial capture by Kupffer cells, and revealed novel mechanisms utilized by Kupffer cells to catch bacteria. We observed a pattern recognition role for complement receptor-CRIg in the capture of circulating Gram-positive bacteria from the bloodstream by directly binding to the Lipoteichoic Acid of Gram-positive bacteria, such as S. aureus. We also observed a sex-biased difference of Kupffer cells in capture circulating enteropathogenic E. coli . While complement opsonization was indispensable for the capture of EPEC in male mice; however, a faster, complement-independent process involving abundant preexisting antibodies to EPEC was detected in female mice. These antibodies were elicited predominantly in female mice at puberty in response to estrogen regardless of microbiota-colonization conditions. Estrogen-driven antibodies were maternally transferrable to offspring and conferred protection during infancy. Thus, an estrogen-driven, innate antibody-mediated immunological strategy conferred protection to females and their offspring. 报告人简介︰曾筑天博士于2004年至2008年就读于中国科学技术大学生命科学学院,取得学士学位。随后在中国科学技术大学免疫学研究所师从田志刚院士并于2014年7月获得细胞生物学博士学位。2014年8月至今,曾筑天博士在加拿大卡尔加里大学师从国际著名免疫学专家Paul Kubes教授进行博士后研究。在博士及博士后研究期间,曾筑天博士在肝脏天然免疫学及感染应答机制等方向做出一系列具有延续性和创新型的重要研究,主要利用高分辨率活体显微成像技术实现了对肝脏局部免疫细胞和血液中微生物动态相互作用的实时成像观测,揭示了肝脏抗细菌感染免疫的分子细胞机制,发现了全新的由雌激素诱导的天然抗体新群体,并对慢性病毒感染状态下肝脏免疫功能低下致使乙肝病毒不能被有效清除阐明了机制。其研究成果以第一作者身份发表在了Nature Immunology, Cell Host&Microbe, Journal of Experimental Medicine, Journal of Immunology等高水平免疫学期刊上。曾筑天博士是免疫学领域的优秀青年学者,多年来致力于肝脏疾病免疫学基础研究及潜在免疫治疗方法的开发,在肝脏免疫这一重要领域具有坚实的研究基础,具有清晰合理的未来规划以及巨大的发展潜力。曾筑天博士掌握独特的科研技术,能对活体小动物肝脏,肾脏,脾脏等多个脏器免疫细胞进行直接实时动态的显微成像检测及分析,是目前国际上为数不多的能对上述多个脏器进行活体动态成像研究的学者之一。 2.报告人:叶浩彬(科罗拉多大学医学院博士后)报告题目:Management of Leukemia from Metabolic Perspectives内容摘要:Obese leukemia patients have a poorer prognosis compared to normal weight patients, suggesting that obesity-associated conditions protect leukemia cells/leukemia stem cells from chemotherapy. Further, obese population have a higher risk for leukemia, indicating that obesity promotes disease development and progression. However, the biological mechanisms underlying these phenomena remain unknown. In today’s presentation, the author introduces two studies that reveal the mechanisms for the phenomena mentioned above. The first study has demonstrated that adipose tissue functions as a sanctuary for LSCs. Briefly, LSCs are found to be enriched in adipose tissue. Tranome comparisons show that compared to hematopoietic tissue-resident LSCs, adipose-resident LSCs display a pro-inflammatory gene signature, which leads to an inflamed state in adipose tissue, and consequently an increased lipolysis rate as evidenced by elevated serum fatty acids level. Lipolysis-derived fatty acids are utilized by two distinct pathways: 1) fatty acids-induced inflammation pathway and 2) fatty acid oxidation pathway. Interestingly, a LSC subpopulation that has a high-level expression of the fatty acid transporter CD36 (CD36+ LSCs) displays a significantly higher FAO rate compared to CD36- LSCs and is strikingly enriched in adipose tissue. Further, CD36+ LSCs are more chemo-resistant compared to CD36- LSCs partially due to CD36-mediated FAO. More importantly, a CD36+ LSC subpopulation is also observed in primary human leukemia patient samples. Human CD36+ LSCs display a higher FAO rate and are chemo-resistant compared to CD36- LSCs. Collectively, this study shows that the interplay between leukemia cells and adipose tissue creates a unique microenvironment that supports the metabolic demands and survival of a distinct LSC population.The second study demonstrates that leukemic disease causes aberrancies in multiple tissues including adipose tissue, pancreas, gut and gut microbiota to subvert the systemic glucose metabolism to support growth of leukemia cells. Briefly, leukemia mice are found to have characteristics of both type 2 and type 1 diabetes: insulin resistance and insulin defect, conditions that inhibit glucose utilization in normal tissues. Mechanistically, leukemia induces a high-level production of IGFBP1 from adipose tissue, which results in insulin resistance. Further, leukemic disease impairs gut functions causing loss of gut-derived serotonin and dysbiosis. Serotonin loss results in inhibition of insulin secretion and dysbiosis leads to insulin resistance and less production of microbiota-derived short chain fatty acids such as butyrate and propionate. Supplementation of serotonin or SCFAs impedes leukemia progression. Importantly, combination of serotonin and SCFAs supplementations drastically reduce leukemic burden and prolong survival of leukemic mice by directly increasing the uptake and utilization of glucose in normal tissues. Together, these data demonstrate that restoration of normal glucose regulation may be a feasible strategy to suppress systemic growth of malignant cell types. Taking together, these two studies suggest that interventions by targeting either intracellular metabolism of LSCs or systemic metabolism are effective means for disease management.报告人简介︰叶浩彬,博士,男,1986年出生,毕业于罗切斯特大学医学院 (University of Rochester Medical Center),现为科罗拉多大学医学院(University of Colorado Medical Campus)博士后,主要进行白血病病理和白血病干细胞代谢及其微环境研究。已在Cancer Cell、 Cell Stem Cell、blood和Journal of Biological Chemistry等期刊上发表论文及摘要8篇。担任Cancers、International Journal of Molecular Sciences、Molecules和Vaccines等国际学术期刊审稿人。

个人简介:

附件:

刘源,2018年4月博士毕业于德国弗莱贝格工业大学(TU Bergakademie Freiberg),博士论文德国评分获得“magna cum laude”(优秀),现继续博士后研究。专业是构造地质学,研究方向为地质过程的数值模拟,博士阶段师从国际著名岩石力学和数值模拟专家Heinz Konietzky教授,学习用离散元数值模拟方法解决地质构造过程中的断裂扩展问题,属学科交叉研究。首次将离散元(DEM)方法应用到大尺度的地质构造演化模拟中,建立了拉分盆地的断裂和盆地演化过程的数值模型,通过对模型尺度和断裂参数的分析研究,首次基于离散元方法(颗粒流PFC)模拟了拉分盆地形成演化过程中的断裂扩展问题,揭示了菱形拉分盆地的起源问题,给出了计算拉分盆地形成的最小位移和最小时间的方法,为拉分盆地的形成演化过程提供了新的研究思路和方法,相关成果以第一作者兼通讯作者发表于构造地质学界顶级期刊Tectonics(IF:3.784)上。

报告二:Understanding the mechanical properties of shale in nanoscale

报告人:刘扣其博士,美国北达科他大学

报告摘要:Shale, nanoindentation , Modulus, Creep

个人简介:

刘扣其,美国北达科他大学应届博士毕业。主要研究方向为页岩微孔结构分析和微观力学性能表征。博士期间以第一作者发表SCI 论文12 篇(7篇top),参与编著专著一部,参加国际会议10余次。SPE, AAPG, ARMA, SEG, AGU, TSOP 等国际组织会员。Fuel,Energy& Fuel, Marine and petroleum geology, JPSE, JNGSE 等期刊审稿人。

第二会场

地点:大学科技园515会议室(文昌校区北门外大学科技园B座)

编辑:信息科学 本文来源:越崎论坛,如若n维乘性相关向量的坐标是代数数

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