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Search Results: 1 - 10 of 97943 matches for " Yu-Tao Lee "
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Roles of liver innate immune cells in nonalcoholic fatty liver disease
Yu-Tao Zhan, Wei An
World Journal of Gastroenterology , 2010,
Abstract: Nonalcoholic fatty liver disease (NAFLD) has become the most common liver disease in the United States and other developed countries and is expected to increase in the next few years. Emerging data suggest that some patients with NAFLD may progress to nonalcoholic steatohepatitis (NASH), cirrhosis and even hepatocellular carcinoma. NAFLD can also promote the development and progression of disease in other organ systems, such as the cardiovascular and endocrine (i.e. diabetes) systems. Thus, understanding the pathogenesis of NAFLD is of great clinical importance and is critical for the prevention and treatment of the disease. Although the “two-hit hypothesis” is generally accepted, the exact pathogenesis of NAFLD has not been clearly established. The liver is an important innate immune organ with large numbers of innate immune cells, including Kupffer cells (KCs), natural killer T (NKT) cells and natural killer (NK) cells. Recent data show that an imbalance in liver cytokines may be implicated in the development of fatty liver disease. For example, Th1 cytokine excess may be a common pathogenic mechanism for hepatic insulin resistance and NASH. Innate immune cells in the liver play important roles in the excessive production of hepatic Th1 cytokines in NAFLD. In addition, liver innate immune cells participate in the pathogenesis of NAFLD in other ways. For example, activated KCs can generate reactive oxygen species, which induce liver injury. This review will focus primarily on the possible effect and mechanism of KCs, NKT cells and NK cells in the development of NAFLD.
2-[2-(Methylamino)benzoyl]-2,3,4,9-tetrahydro-1H-pyrido[3,4-b]indol-1-one
Lin Li,Yu-Tao Zhang
Acta Crystallographica Section E , 2010, DOI: 10.1107/s1600536810019409
Abstract: The title compound, C19H17N3O2, was obtained from fruits of Evodia Rutaecarpa. In the solid state, the dihedral angle between the 2,3,4,9-tetrahydro-1H-pyrido[3,4-b]indol-1-one (tetrahydro-β-carbolinone) unit and the benzoyl ring is 61.46 (3)°. In the crystal, dimers are formed through intermolecular N—H...O hydrogen-bonding interactions. In addition, intramolecular N—H...O hydrogen bonds are also observed. C—H...π contacts connect the dimers, leading to the formation of a three-dimensional supramolecular network.
catena-Poly[[silver(I)-μ-N-(3-pyridylmethyl)pyridine-4-carboxamide] nitrate monohydrate]
Yu-Tao Ma,Qi-Hua Zhao
Acta Crystallographica Section E , 2008, DOI: 10.1107/s1600536807064744
Abstract: In the title compound, {[Ag(C12H11N3O)]NO3·H2O}n, the Ag atom is coordinated by two N atoms from the heterocyclic ligand, giving a linear polycationic chain. Two long Ag...Onitrate interactions [2.667 (3) and 2.840 (3) ] result in a three-dimensional network. The water molecule consolidates the network structure by forming hydrogen bonds, one to the polycationic chain and one to the nitrate anion.
Fak56 functions downstream of integrin alphaPS3betanu and suppresses MAPK activation in neuromuscular junction growth
Pei-I Tsai, Hsiu-Hua Kao, Caroline Grabbe, Yu-Tao Lee, Aurnab Ghose, Tzu-Ting Lai, Kuan-Po Peng, David Van Vactor, Ruth H Palmer, Ruey-Hwa Chen, Shih-Rung Yeh, Cheng-Ting Chien
Neural Development , 2008, DOI: 10.1186/1749-8104-3-26
Abstract: We have generated mutants for the Drosophila FAK gene, Fak56. Null Fak56 mutants display overgrowth of larval neuromuscular junctions (NMJs). Localization of phospho-FAK and rescue experiments suggest that Fak56 is required in presynapses to restrict NMJ growth. Genetic analyses imply that FAK mediates the signaling pathway of the integrin αPS3βν heterodimer and functions redundantly with Src. At NMJs, Fak56 downregulates ERK activity, as shown by diphospho-ERK accumulation in Fak56 mutants, and suppression of Fak56 mutant NMJ phenotypes by reducing ERK activity.We conclude that Fak56 is required to restrict NMJ growth during NMJ development. Fak56 mediates an extracellular signal through the integrin receptor. Unlike its conventional role in activating MAPK/ERK, Fak56 suppresses ERK activation in this process. These results suggest that Fak56 mediates a specific neuronal signaling pathway distinct from that in other cellular processes.Formation and stabilization of neuronal synapses demands communication between pre- and post-synaptic partners, as well as signals from the extracellular matrix (ECM). These signals can reorganize local cytoskeletal structures or be transduced into the nucleus to regulate transcription, thereby modulating neuronal plasticity [1-3]. One major receptor family for ECM signals comprises the transmembrane protein integrins, which have been shown to play critical roles in sequential steps of neuronal wiring, such as in neurite outgrowth, axon guidance, and synaptic formation and maturation [4-7]. In Drosophila, various integrin subunits have been shown to function in motor axon pathfinding and target recognition, and synaptic morphogenesis at neuromuscular junctions (NMJs) [8-10]. Mutant analyses for the integrin subunits αPS3 and βPS indicate that integrin signaling is involved in synaptic growth and arborization of larval NMJs [8-10]. Although specific ECM signals for these integrin receptors are not clear, dynamic NMJ growth is regulated
Effects of intratracheal administration of nuclear factor-kappaB decoy oligodeoxynucleotides on long-term cigarette smoke-induced lung inflammation and pathology in mice
Yu-Tao Li, Bei He, Yu-Zhu Wang, Jing Wang
Respiratory Research , 2009, DOI: 10.1186/1465-9921-10-79
Abstract: Extensive exposure to cigarette smoke is a principal risk factor associated with chronic obstructive pulmonary disease (COPD). COPD is a complex inflammatory disease involving numerous inflammatory cell types, which have the capacity to release multiple inflammatory mediators. An increase in expression of many of these mediators translates to activation of an inflammatory cascade involving cytokines, chemokines, growth factors, enzymes, receptors, and adhesion molecules [1-4]; specific to COPD are increased levels of tumor necrosis factor-α (TNFα), interferon-γ(IFNγ), interleukin-8(IL-8), macrophage inflammatory protein 1α(MIP-1α), monocyte chemoattractant protein 1(MCP-1), GROα, and matrix metalloproteinase(MMP)-9 [1-4].NF-κB is a family of critical transcription factors regulating many cytokines, including IL-8, IL-6, TNF-α, GM-CSF, MIP-1, and MCP-1 [5], as well as MMP-9 expression [6]. In the past few years, five mammalian NF-κB family members have been identified and cloned [7-9]. These include NF-κB1 (p50/p105), NF-κB2 (p52/p100), RelA (p65), RelB, and c-Rel. In resting cells NF-κB is retained in the cytoplasm due to inhibitory protein (I-κB) binding. When the cell is appropriately stimulated, I-κB degradation results in the ability of NF-κB to recognition nuclear localization signals of p65, thus it is rapidly transported into the nucleus where it binds to specific κB recognition elements in the promoters of target genes [10]. Chronic exposure to cigarette smoke causes cellular oxidative stress, a key feature in smoking-induced lung inflammation [11-13], and oxidative stress (particularly hydrogen peroxide) can enhance the DNA binding activity of NF-κB [14].It has been demonstrated in humans and animal models that smoke-induced chronic pulmonary inflammation is associated with increased NF-κB activity in lung cells. Enhanced NF-κB activation has been observed in bronchial biopsies from smokers, macrophages from COPD patients and in guinea pigs exposed to cigar
Discussion About the Climatic Factor of Planation Surface Formation
CHU Yu-chun,XIE Shi-you,XIA Kai-sheng,LIU Yu-tao
Journal of Chongqing Normal University , 2009,
Abstract: Planation surfaces are the final products of geomorphologic evolution after long-term exogenic processes under stable tectonic conditions, and the surface elevations are related to erosion base level. Just because those planation surfaces , formed under stable tectonic conditions and cut cross all strata and tectonic which are older than formation of the surfaces, tectonic processes and lithology have become subsidiary among planation surfaces formation. And the exogenic processes of those planation surfaces development are controlled under the climatic factor, so the climatic factor is the most important ones. In this paper, therefore, the planation surfaces are re-classified by the climatic factor of their Formation. And based on climate geomorphologic principles, their evolvement mechanisms are studied and discussed in detail .they can be classified into four types in this paper,such as warm-wet planation surface,Savanna planation surface,arid planation surface and frigid planation surface.
Serum Autofluorescence, a Potential Serum Marker for the Diagnosis of Liver Fibrosis in Rats
Yu-Tao Zhan,Li Li,Jing Weng,Xin Song,Shao-Qi Yang,Wei An
International Journal of Molecular Sciences , 2012, DOI: 10.3390/ijms130912130
Abstract: Fluctuations in serum autofluorescence (AF) intensity have recently been widely used as markers of certain diseases such as cancer. To determine the diagnostic value of serum AF intensity for liver fibrosis in rats, we induced liver fibrosis by subcutaneous injection of carbon tetrachloride into rats. The rat serum AF intensities were detected at the excitation wavelength of 337 nm and the emission wavelength of 512 nm. The degree of liver fibrosis was evaluated by Van Gieson’s staining. The relationship between serum AF intensity and the degree of liver fibrosis was analyzed by Spearman and Pearson Correlation. The diagnostic sensitivity and specificity of the serum AF was determined by analyzing the receiver operating characteristic (ROC) curves. Our results show that the serum AF intensity in the rat liver fibrosis model increased when compared with control rats eight weeks and twelve weeks post induction of liver fibrosis. However, there was no significant difference in serum AF intensity between fibrotic and control rats at four week post induction. Furthermore, serum AF intensity correlated positively with the severity of the degree of hepatic fibrosis. ROC analysis further suggested that serum AF intensity is a valid marker for staging fibrosis. Therefore, it may potentially be developed as a novel diagnostic tool for hepatic fibrosis.
Impacts of tourist activities on components, properties and heavy metal pollution of soils in the Songshan scenic area
嵩山景区旅游活动对土壤组成性质和重金属污染的影响

MA Jian-Hu,ZHU Yu-Tao,
马建华
,朱玉涛

生态学报 , 2008,
Abstract: 沿嵩山景区登山路线,在嵩阳书院(455m)、老母(715m)、石船(930m)和天爷庙(1490m)采集混合土壤样品,在离景点200 m以外的受旅游活动影响微弱的地方采集对照土壤样品.根据我国土壤常规分析方法或国家标准分析方法开展土壤组成、性质和重金属(Cu、Zn、Pb、Ni、Cd和Cr)含量分析.与对照样相比,景点土壤具有以下特征:①黏粒含量高,质地偏细,相对紧实、干燥,根系分布少,颜色浅.②CEC小,盐基饱和度大,pH高.③有机质含量下降,速效养分减少,肥力衰退.④黏粒部分CaO含量高,SiO2含量相对下降,Saf减小,出现"假淋溶风化现象".⑤土壤重金属含量高于对照样,大部分超过我国棕壤和褐土背景值.土壤Cu和Ni没有发生污染,其它重金属污染程度的次序为:Zn>Pb>Cd>Cr;不同景点重金属污染程度的次序为:嵩阳书院>老母洞>天爷庙>石船.
Plasma Catalytic Synthesis of Silver Nanoparticles

ZHANG Yu-Tao,GUO Ying,MA Teng-Cai,

中国物理快报 , 2011,
Abstract:
The Algorithm for Distributed QoS Multicast Routing with Resource Reservation
结合资源预留的分布式QoS组播路由算法

Du Li,Liu Yu-tao,
杜 荔
,刘玉涛

电子与信息学报 , 2009,
Abstract: To eliminate the affect of the change of resource information on the QoS multicast routing, an algorithm for Distributed QoS Multicast Routing with Resource Reservation(DQMTR) is put forward in this paper. Using resource reservation in the process of path-detecting, DQMTR overcomes the issue. By noting the number of reserved resource, DQMTR resolves the issue of over-reservation. This paper considers the characteristic of differentiated services model to which DQMTR is adapted. The simulation reveals that the algorithm improves the success ratio, and optimizes the average path cost.
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