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Search Results: 1 - 10 of 30282 matches for " Ru-Rong Ji "
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p38 MAPK, microglial signaling, and neuropathic pain
Ru-Rong Ji, Marc R Suter
Molecular Pain , 2007, DOI: 10.1186/1744-8069-3-33
Abstract: Injuries of the nervous system, including peripheral nervous system (PNS, e.g. peripheral nerves, dorsal root ganglia, and dorsal roots) and central nervous system (CNS, e.g. spinal cord and thalamus), often result in neuropathic pain. These injuries may result from diabetic neuropathy, viral infection, major surgeries (e.g. amputation, thoracotomy), spinal cord injury, and stroke [1-3]. Spontaneous pain, described as shooting, lancinating or burning pain, and mechanical allodynia (painful responses to normally innocuous tactile stimuli) are distinct symptoms of neuropathic pain, although neuropathic pain is also characterized by heat hyperalgesia, mechanical hyperalgesia, and cold allodynia. Neuropathic pain is a consequence of neural plasticity, developed both in the PNS (peripheral sensitization) and CNS (central sensitization). After nerve injury, neuropathic pain can arise from injury discharge at the site of axonal injury and ectopic/spontaneous activity in dorsal root ganglion (DRG) neurons [4-6]. Inflammatory mediators (e.g. cytokines) play a critical role in the generation of spontaneous activity and neuropathic pain. Peripheral nerve injury also induces marked phenotypic changes in DRG neurons [1,2]. While spontaneous activity from primary afferents drives central sensitization, central sensitization is responsible for persistent neuropathic pain. Central sensitization may also directly drive neuropathic pain in central neuropathic pain conditions caused by spinal cord injury or stroke. Central sensitization is induced by enhanced synaptic strength in the spinal cord and brain regions, due to an increase in excitatory synaptic transmission (e.g. AMPA and NMDA currents) or/and a reduction in inhibitory synaptic transmission (e.g. GABA currents) [7-9]. In addition to increased primary afferent input, enhanced descending facilitation also contributes to spinal neuron hypersensitivity and neuropathic pain [10,11].Despite our intensive investigation on neuronal
Microglia and Spinal Cord Synaptic Plasticity in Persistent Pain
Sarah Taves,Temugin Berta,Gang Chen,Ru-Rong Ji
Neural Plasticity , 2013, DOI: 10.1155/2013/753656
Abstract: Microglia are regarded as macrophages in the central nervous system (CNS) and play an important role in neuroinflammation in the CNS. Microglial activation has been strongly implicated in neurodegeneration in the brain. Increasing evidence also suggests an important role of spinal cord microglia in the genesis of persistent pain, by releasing the proinflammatory cytokines tumor necrosis factor-alpha (TNFα), Interleukine-1beta (IL-1β), and brain derived neurotrophic factor (BDNF). In this review, we discuss the recent findings illustrating the importance of microglial mediators in regulating synaptic plasticity of the excitatory and inhibitory pain circuits in the spinal cord, leading to enhanced pain states. Insights into microglial-neuronal interactions in the spinal cord dorsal horn will not only further our understanding of neural plasticity but may also lead to novel therapeutics for chronic pain management. 1. Microglia-Synapse Interactions in Healthy CNS Microglia are derived from myeloid precursor cells in the periphery and penetrate the central nervous system (CNS) during embryogenesis [1]. They account for approximately 10–20% of all cells in the CNS, however their distribution varies from one region to another [2, 3]. Microglial density is particularly high in the hippocampus, basal ganglia, substantia nigra, and spinal cord [2, 4]. Microglia are regarded as the resident macrophages in the CNS and, similar to peripheral macrophages, they display different morphology depending upon their physiological states. In the resting physiological state, microglial cells are ramified with slender, radially projecting processes with similar thickness, length, and ramification, whereas in pathological states, microglia can be activated presenting an amoeboid morphology characterized by large soma, short/thick, and radially projecting processes with few ramifications [4–6]. Although most studies have focused on the role of activated microglia and synaptic transmission, both resting and activated microglia dynamically interact with synapses shaping their connectivity and function [7]. Microglial processes constantly and dynamically survey their environment and interact with nearby synapses [8, 9]. In mature CNS, it has been observed that microglial processes interact with axon terminals and dendritic spines in a transient manner, for an average of five minutes and at a rate of approximately one microglial contact per hour [10]. Notably, microglia processes are driven by neuronal activity and can simultaneously interact with both presynaptic and postsynaptic
Acute morphine activates satellite glial cells and up-regulates IL-1β in dorsal root ganglia in mice via matrix metalloprotease-9
Temugin Berta, Tong Liu, Yen-Chin Liu, Zhen-Zhong Xu, Ru-Rong Ji
Molecular Pain , 2012, DOI: 10.1186/1744-8069-8-18
Abstract: Subcutaneous morphine injection (10 mg/kg) induced robust peripheral glial responses, as evidenced by increased GFAP expression in DRGs but not in spinal cords. The acute morphine-induced GFAP expression is transient, peaking at 2 h and declining after 3 h. Acute morphine treatment also increased IL-1β immunoreactivity in SGCs and IL-1β activation in DRGs. MMP-9 and GFAP are expressed in DRG neurons and SGCs, respectively. Confocal analysis revealed a close proximity of MMP-9 and GFAP immunostaining. Importantly, morphine-induced DRG up-regulation of GFAP expression and IL-1β activation was abolished after Mmp9 deletion or naloxone pre-treatment. Finally, intrathecal injections of IL-1β-selective siRNA not only reduced DRG IL-1β expression but also prolonged acute morphine-induced analgesia.Acute morphine induces opioid receptors- and MMP-9-dependent up-regulation of GFAP expression and IL-1β activation in SGCs of DRGs. MMP-9 could mask and shorten morphine analgesia via peripheral neuron-glial interactions. Targeting peripheral glial activation might prolong acute opioid analgesia.Mounting evidence indicates that activation of spinal cord glial cells such as microglia and astrocytes plays a crucial role in the pathogenesis of chronic pain [1-7]. In particular, chronic opioid exposure induces profound changes in spinal cord microglia and astrocytes [8-10]. Upon activation spinal glial cells produce multiple proinflammatory cytokines such as TNF-α, IL-1β, and IL-6 to antagonize morphine analgesia and promote morphine tolerance [11-14], via sensitization of spinal cord dorsal horn neurons [15-17]. For example, IL-1β has been shown to counteract opioid-induced analgesia following both chronic and acute administration of morphine [18]. While intrathecal injection of the inteurleukin-1 receptor (IL-1R) antagonist potentiates acute morphine analgesia [11], intrathecal administration of IL-1β induces heat hyperalgesia [15]. Of interest genetic polymorphism of IL-1R antagon
Acute morphine induces matrix metalloproteinase-9 up-regulation in primary sensory neurons to mask opioid-induced analgesia in mice
Yen-Chin Liu, Temugin Berta, Tong Liu, Ping-Heng Tan, Ru-Rong Ji
Molecular Pain , 2012, DOI: 10.1186/1744-8069-8-19
Abstract: Subcutaneous morphine induced a marked up-regulation of MMP-9 protein in DRGs but not spinal cords. Morphine also increased MMP-9 activity and mRNA expression in DRGs. MMP-9 up-regulation peaked at 2 h but returned to the baseline after 24 h. In DRG tissue sections, MMP-9 is expressed in small and medium-sized neurons that co-express mu opioid receptors (MOR). In DRG cultures, MOR agonists morphine, DAMGO, and remifentanil each increased MMP-9 expression in neurons, whereas the opioid receptor antagonist naloxone and the MOR-selective antagonist D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP) suppressed morphine-induced MMP-9 expression. Notably, subcutaneous morphine-induced analgesia was enhanced and prolonged in Mmp9 knockout mice and also potentiated in wild-type mice receiving intrathecal injection of MMP-9 inhibitors. Consistently, intrathecal injection of specific siRNA targeting MMP-9 reduced MMP-9 expression in DRGs and enhanced and prolonged morphine analgesia. Subcutaneous morphine also produced heat hyperalgesia at 24 h, but this opioid-induced hyperalgesia was not enhanced after MMP-9 deletion or inhibition.Transient MMP-9 up-regulation in DRG neurons can mask opioid analgesia, without modulating opioid-induced hyperalgesia. Distinct molecular mechanisms (MMP-9 dependent and independent) control acute opioid-induced pronociceptive actions (anti-analgesia in the first several hours and hyperalgesia after 24 h). Targeting MMP-9 may improve acute opioid analgesia.Opioids especially mu opioid receptor (MOR) agonists remain to be the most effective treatment for moderate to severe pain. MOR is expressed by primary sensory neurons including small-sized (C-fiber) and medium-sized (Aδ-fiber) neurons in the dorsal root ganglia (DRGs) [1-5]. MOR is also expressed in primary afferent terminals and lamina II interneurons in the spinal cord [1,6-8]. MOR agonist, such as [D-Ala2, N-Me-Phe4, Gly5-ol]-enkephalin (DAMGO) elicits potent presynaptic inhibition via suppress
Large A-fiber activity is required for microglial proliferation and p38 MAPK activation in the spinal cord: different effects of resiniferatoxin and bupivacaine on spinal microglial changes after spared nerve injury
Marc R Suter, Temugin Berta, Yong-Jing Gao, Isabelle Decosterd, Ru-Rong Ji
Molecular Pain , 2009, DOI: 10.1186/1744-8069-5-53
Abstract: SNI induced robust mechanical allodynia and p38 activation in spinal microglia. SNI also induced marked cell proliferation in the spinal cord, and all the proliferating cells (BrdU+) were microglia (Iba1+). Bupivacaine induced a complete sensory and motor blockade and also significantly inhibited p38 activation and microglial proliferation in the spinal cord. In contrast, and although it produced an efficient nociceptive block, RTX failed to inhibit p38 activation and microglial proliferation in the spinal cord.(1) Blocking peripheral input in TRPV1-positive fibers (presumably C-fibers) is not enough to prevent nerve injury-induced spinal microglial activation. (2) Peripheral input from large myelinated fibers is important for microglial activation. (3) Microglial activation is associated with mechanical allodynia.Injuries to peripheral nervous system can result in neuropathic pain and contribute to chronic post-operative pain [1]. Current treatments for persistent post-operative pain are not satisfactory and prevention at early stage might be important for the success [2]. Section of a peripheral nerve induces injury discharges at the time of injury followed by spontaneous activity in the axons and soma of primary sensory neurons. The onset of spontaneous activity is strongly implicated in the generation of neuropathic pain [3-6]. However, the relative contribution of different types of primary afferents to the genesis of spontaneous activity is still under debate. Many studies demonstrated that A-fibers are the principal contributors of ectopic firing from the periphery following nerve injury [7-11]. Some studies also reported spontaneous activity in C-fibers but at different times after nerve injury, either very early during the first 15 minutes [12] or later after a few days [13]. The C-fibers' activity was also found in the neighbouring intact spinal nerve after spinal nerve ligation [5] or after stimulation of a nerve stump with nociceptive mediators [14]. Int
Simplification and Error Analysis Based on Implicit Surface for Measuring Point-sets

WANG Hong-tao,ZHANG Li-yan,DU Ji,LI Zhong-wen,ZHOU Ru-rong,

中国图象图形学报 , 2007,
Abstract: The model reconstruction based on measuring point-sets is a key step in the reverse engineering,it is quite necessary to simplify the measuring point-sets and analyze the reconstruction error in order to improve the reconstruction precision and the reconstruction efficiency and provide essential information for the model reconstruction.In this paper,a new simplification algorithm for measuring point-sets is realized firstly,and then a novel method for reconstruction error analysis where the simplified point-set is fitted by an implicit surface based on compactly supported radial basis function is presented.The experimental results show that the simplification algorithm has higher efficiency and better effect,the error analysis results based on implicit surface can restrict simplification quantity within the limitation of reconstruction precision.
Giant radio galaxies as probes of the ambient WHIM in the era of the SKA
Bo Peng,Ru-Rong Chen,Richard Strom
Physics , 2015,
Abstract: The missing baryons are usually thought to reside in galaxy filaments as warm-hot intergalactic medium (WHIM). From previous studies, giant radio galaxies are usually associated with galaxy groups, which normally trace the WHIM. We propose observations with the powerful SKA1 to make a census of giant radio galaxies in the southern hemisphere, which will probe the ambient WHIM. The radio galaxies discovered will also be investigated to search for dying radio sources. With the highly improved sensitivity and resolution of SKA1, more than 6,000 giant radio sources will be discovered within 250 hours.
Preliminary proteomic difference analysis on the kidney of grass carp, Ctenopharyngodon idellus, in various developmental stages

ZHANG Qiong-Yu,XIE Jin-Yun,ZHAO Ru-Rong,LUO Chen,

水生生物学报 , 2006,
Abstract: 为了研究草鱼在不同发育阶段抗病能力差异的发育遗传学原因,以1龄草鱼和3龄草鱼的免疫器官肾脏为材料研究其在蛋白质组水平的差异。提取1龄草鱼和3龄草鱼肾脏的全蛋白,用二维聚丙烯酰胺凝胶电泳进行蛋白质的分离,染色后,扫描成像,经PDQUST软件分析,分别检测到大约900个蛋白质点。这些蛋白质点主要分布在pH4.5—7之间,其分子量大部分在66.2kDa以下。在3龄草鱼中检测到了3个在1龄草鱼中没有的差异蛋白质点,和20个上调、下调的差异点。经MALDI-TOF质谱分析和数据库搜索,证明在3龄草鱼肾脏中上调的差异点中有4个是与免疫或肾脏发育相关的蛋白质。这些初步的研究结果提示草鱼在不同发育阶段抗病能力的差异可能具有其发育遗传学基础。
Probe into program of eco-environmental construction in Ngari region of Tibet

DENG Kun-mei,YANG Ru-rong,ZHANG Ming-tao,

自然资源学报 , 2003,
Abstract: In this paper,the present situation,course of evolution of eco-environment in Ngari prefecture in Tibet were thoroughly analyzed.And the regional eco-environmental problems such as air temperature rise,precipitation decline,grassland degradation,vegetation vanishing,fre-quent occurrence of natural disasters,malmanagement of eco-environment were also explored.On the basis of the results,the important issues existing in the development were discussed and the following items for sustainable development were projected:1)The sand control engineering pro-ject of Shiquanhe drainage basin and its surrounding region;2)construction of nature protected areas;3)making use of biological engineering measures to scientifically eradicate rats,protect and extend livestock food chain project;4)to set up grassland eco-environmental monitoring and early-warning system;5)to enhance eco-environmental construction of small towns;6)to develop multi-function shelter forest systems dominated by fuel forest and timber forest;7)to carry out farmland ecosystem construction;and8)to build project for controlling contaminations of mining and livestock products processing activities.And the following countermeasures are identified as:(a)Ngari region want to establish and perfect eco-environmental management and supervision or-ganization;(b)to launch investigation of the general situation of nature protected area;(c)to in-tensify law enforcement,and protect and harness the eco-environment according to law;(d)to in-crease scientific and technical input,develop green property and guarantee the environment safe-ty;and(e)to economize fuel forest,and pursue contract system of wood and grass properties,and promote the eco-environment to take the road towards sustainable development.
Interpolation and Blending on Parametric Surfaces

WANG Xiao-Ping,ZHOU Ru-Rong,YU Zhan-Yue,YE Zheng-Lin,

软件学报 , 2004,
Abstract: Representing a curve contained in a surface is very important in dealing with path generation in computer numerical control (CNC) machining and the trimming issues that frequently occur in the field of CAD/CAM. This paper develops methods for tangent direction continuous (G1) and both tangent direction and curvature continuous (G2) interpolation of a range of points on surface with specified tangent and either a curvature vector or a geodesic curvature at every point. As a special case of the interpolation, the blending problems of curves on surface are also discussed. The basic idea is as follows: with the help of the related results of differential geometry, the problem of interpolating curve on a parametric surface is converted to a similar one on its parametric plane. The methods can express the G1 and G2 interpolation curve of an arbitrary sequence of points on a parametric surface in a 2D implicit form, which transforms the geometric problem of surface intersection, usually a troublesome issue, into the algebraic problem of computing an implicit curve in displaying such an interpolation curve. Experimental results show the presented methods are feasible and applicable to CAD/CAM and Computer Graphics.
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