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Search Results: 1 - 10 of 144846 matches for " LI Su-ju "
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Tunable Landau-Zener transitions in a spin-orbit coupled Bose-Einstein condensate
Abraham J. Olson,Su-Ju Wang,Robert J. Niffenegger,Chuan-Hsun Li,Chris H. Greene,Yong P. Chen
Physics , 2013, DOI: 10.1103/PhysRevA.90.013616
Abstract: The Landau-Zener (LZ) transition is one of the most fundamental phenomena in quantum dynamics. It describes nonadiabatic transitions between quantum states near an avoided crossing that can occur in diverse physical systems. Here we report experimental measurements and tuning of LZ transitions between the dressed eigenlevels of a Bose-Einstein condensate (BEC) that is synthetically spin-orbit (SO) coupled. We measure the transition probability as the BEC is accelerated through the SO avoided crossing and study its dependence on the coupling between the diabatic (bare) states, eigenlevel slope, and eigenstate velocity--the three parameters of the LZ model that are independently controlled in our experiments. Furthermore, we performed time-resolved measurements to demonstrate the breaking down of the spin-momentum locking of the spin-orbit-coupled BEC in the nonadiabatic regime, and we determined the diabatic switching time of the LZ transitions. Our observations show quantitative agreement with the LZ model and numerical simulations of the quantum dynamics in the quasimomentum space. The tunable LZ transition may be exploited to enable a spin-dependent atomtronic transistor.
Increased Life Span due to Calorie Restriction in Respiratory-Deficient Yeast
Su-Ju Lin,Leonard Guarente
PLOS Genetics , 2006, DOI: 10.1371/journal.pgen.0020033
Abstract:
Increased life span due to calorie restriction in respiratory-deficient yeast.
Lin Su-Ju,Guarente Leonard
PLOS Genetics , 2006,
Abstract:
General ultracold scattering formalism with isotropic spin orbit coupling
Su-Ju Wang,Chris H. Greene
Physics , 2014,
Abstract: A general treatment of ultracold two-body scattering in the presence of isotropic spin-orbit coupling (SOC) is presented. Owing to the mixing of different partial wave channels, scattering with SOC is in general a coupled multichannel problem. A systematic method is introduced to analytically solve a class of coupled differential equations by recasting the coupled channel problem as a simple eigenvalue problem. The exact Green's matrix in the presence of SOC is found, which readily gives the scattering solutions for any two identical particles in any total angular momentum subspace having negligible center of mass momentum. Application of this formalism to two spin-1 bosons shows the ubiquitous low energy threshold behavior for systems with isotropic SOC. A modified threshold behavior shows up, which does not occur for the spin-orbit coupled spin-1/2 system. We also confirm the parity-breaking mechanism for the spontaneous emergency of handedness, that has been proposed by Duan et. al. [1]. Additionally, a two-body bound state is found for any arbitrarily small and negative scattering length. Our study sheds light on the few-body side of SOC physics and provides one step towards understanding ultracold scattering in a non-Abelian gauge field.
Identification of Potential Calorie Restriction-Mimicking Yeast Mutants with Increased Mitochondrial Respiratory Chain and Nitric Oxide Levels
Bin Li,Craig Skinner,Pablo R. Castello,Michiko Kato,Erin Easlon,Li Xie,Tianlin Li,Shu-Ping Lu,Chen Wang,Felicia Tsang,Robert O. Poyton,Su-Ju Lin
Journal of Aging Research , 2011, DOI: 10.4061/2011/673185
Abstract: Calorie restriction (CR) induces a metabolic shift towards mitochondrial respiration; however, molecular mechanisms underlying CR remain unclear. Recent studies suggest that CR-induced mitochondrial activity is associated with nitric oxide (NO) production. To understand the role of mitochondria in CR, we identify and study Saccharomyces cerevisiae mutants with increased NO levels as potential CR mimics. Analysis of the top 17 mutants demonstrates a correlation between increased NO, mitochondrial respiration, and longevity. Interestingly, treating yeast with NO donors such as GSNO (S-nitrosoglutathione) is sufficient to partially mimic CR to extend lifespan. CR-increased NO is largely dependent on mitochondrial electron transport and cytochrome c oxidase (COX). Although COX normally produces NO under hypoxic conditions, CR-treated yeast cells are able to produce NO under normoxic conditions. Our results suggest that CR may derepress some hypoxic genes for mitochondrial proteins that function to promote the production of NO and the extension of lifespan. 1. Introduction Calorie restriction (CR) extends lifespan in a variety of organisms and has also been shown to ameliorate many age-associated diseases such as diabetes and cancers [1–3]. However, the molecular mechanisms underlying CR-induced beneficial effects are still not fully understood. Owing to a short lifespan and well-established molecular genetic techniques, the budding yeast Saccharomyces cerevisiae represents a powerful system to identify new components in CR signaling pathways and to study these factors at the molecular/genetic level. Yeast lifespan can be studied in two distinct ways: replicative lifespan (RLS) and chronological lifespan (CLS). RLS measures the number of cell divisions an individual yeast cell undergoes before senescence (division potential), whereas CLS measures the length of time cells remain viable at a nondividing state (postmitotic survival). RLS may serve as a model to understand the mechanisms of replicative senescence such as in stem cells, while CLS may be more relevant to postmitotic cell senescence in adult animals [4, 5]. Moderate CR can be imposed in yeast by reducing the glucose concentration from 2% to 0.5% in rich media [6–9], which extends both RLS and CLS. In yeast, CR is suggested to function through reducing the activities of conserved nutrient-sensing pathways. Decreasing the activities of the Ras-cAMP/PKA (cyclic AMP-activated protein kinase A) pathway, Sch9 (homolog of mammalian S6K kinases) and Tor1 kinases have been shown to mimic CR and extend
Temporal variation and regional differences of ecosystem service value of Nanjing City
南京市生态系统服务价值时间变化及区域差异分析

GU Xiang,ZHOU Sheng-lu,ZHANG Hong-fu,LI Su-ju,GENG Zhao,
顾芗
,周生路,张红富,李素菊,耿召

生态学杂志 , 2009,
Abstract: 生态系统服务价值的变化决定着区域的可持续发展,其评估已成为生态学研究的热点之一。本文采用单位面积生态系统服务价值和生态经济协调度(EEH)指数,分析了南京市生态系统服务价值时间变化及区域差异。结果表明:2007年与1997年比较,所处单位面积生态系统服务价值分区不同的区域有建邺区等6个区,2个时段均处于同一单位面积生态系统服务价值分区的区域有高淳县等7个区、县;区域整体单位面积生态系统服务价值大体上呈现郊县>郊区>城区的特点;1997—2007年南京市11区2县属于5种不同类型的生态经济协调度分区,其中建邺区等5个区、县处于生态经济协调区,秦淮区等8个区处于生态经济不协调区。最后,探讨了南京市不同区域生态建设调整措施,为促进生态经济协调发展和实现区域的可持续发展提供决策参考。
ON SHADE TOLERANCE OF 741 POPLAR
“741杨”扦插苗耐阴性的研究

Pei Bac-hua,Guo Jin-qi,Zhang Su-ju,
裴保华
,郭进起

植物生态学报 , 1996,
Abstract: Using black shading net, we set up four light conditions (e. g. 100%, 24. 5%,7. 5% and 2. 5% of full light) under which the cuttings of poplar grown. The effects of light intensity on leaf growth, leaf anatomic structure, chlorophyll content, ligtphotosynthesis curve, growth of newly produced sprouts and biomass were investigated.The results show that 741 poplar is a light tree species. Biomass and other parameters were all higher under 100% light than the other light conditions. The plants had a strong compensation at the level of 24. 5% of full light. The single leaf area, growth rate of newly produced sprouts, chlorophyll content and pettole length were larger, but total biomass was smaller, under full light than 34. 4% of full light conditions. Under 7. 5% of full light, the plants reached their limitation of shade tolerance. The plants were not able to survive for long term under 2. 5% of full light conditions.
Fuzzy Comprehensive Evaluation on the New Cross Combinations of Super-sweet Corn in Guangdong Province
广东省超甜玉米新组合模糊综合评价

WANG Xiao-ming,WANG Zi-ming,LE Su-ju,LIU Guo-guang,
王晓明
,王子明,乐素菊,刘国光

热带亚热带植物学报 , 2004,
Abstract: New cross combinations were subjected to regional test during 2000-2002 in Guangdong Province by using fuzzy comprehensive evaluation method. The evaluation factors included fresh spike yield, plant type traits, growth duration, resistance and quality. The results showed that the fuzzy comprehensive indexes for the combinations could well reflect the practical quality levels of the corn varieties. This method is more accurate in quantifying the factors evaluated in comparison with the weighted aggregative index method. The evaluation values finally obtained could reflect both the relative grades between evaluation factors and the absolute grades directly.
Correction: Sirt1 Regulates Insulin Secretion by Repressing UCP2 in Pancreatic ? Cells
Laura Bordone,Maria Carla Motta,Frederic Picard,Ashley Robinson,Ulupi S. Jhala,Javier Apfeld,Thomas McDonagh,Madeleine Lemieux,Michael McBurney,Akos Szilvasi,Erin J. Easlon,Su-Ju Lin,Leonard Guarente
PLOS Biology , 2012, DOI: 10.1371/journal.pbio.0040295
Abstract:
Sirt1 Regulates Insulin Secretion by Repressing UCP2 in Pancreatic β Cells
Laura Bordone,Maria Carla Motta,Frederic Picard,Ashley Robinson,Ulupi S. Jhala,Javier Apfeld,Thomas McDonagh,Madeleine Lemieux,Michael McBurney,Akos Szilvasi,Erin J. Easlon,Su-Ju Lin,Leonard Guarente
PLOS Biology , 2012, DOI: 10.1371/journal.pbio.0040031
Abstract: Sir2 and insulin/IGF-1 are the major pathways that impinge upon aging in lower organisms. In Caenorhabditis elegans a possible genetic link between Sir2 and the insulin/IGF-1 pathway has been reported. Here we investigate such a link in mammals. We show that Sirt1 positively regulates insulin secretion in pancreatic β cells. Sirt1 represses the uncoupling protein (UCP) gene UCP2 by binding directly to the UCP2 promoter. In β cell lines in which Sirt1 is reduced by SiRNA, UCP2 levels are elevated and insulin secretion is blunted. The up-regulation of UCP2 is associated with a failure of cells to increase ATP levels after glucose stimulation. Knockdown of UCP2 restores the ability to secrete insulin in cells with reduced Sirt1, showing that UCP2 causes the defect in glucose-stimulated insulin secretion. Food deprivation induces UCP2 in mouse pancreas, which may occur via a reduction in NAD (a derivative of niacin) levels in the pancreas and down-regulation of Sirt1. Sirt1 knockout mice display constitutively high UCP2 expression. Our findings show that Sirt1 regulates UCP2 in β cells to affect insulin secretion.
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