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Search Results: 1 - 10 of 12632 matches for " Shuanglin Hao "
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HSV-mediated expression of interleukin-4 in dorsal root ganglion neurons reduces neuropathic pain
Shuanglin Hao, Marina Mata, Joseph C Glorioso, David J Fink
Molecular Pain , 2006, DOI: 10.1186/1744-8069-2-6
Abstract: Subcutaneous inoculation of S4IL4 in the foot transduced lumbar DRG to produce IL-4. Transgene-mediated expression of IL-4 did not alter thermal latency or tactile threshold in normal animals, but inoculation of S4IL4 1 week after spinal nerve ligation (SNL) reduced mechanical allodynia and reversed thermal hyperalgesia resulting from SNL. Inoculation of S4IL4 1 week before SNL delayed the development of thermal hyperalgesia and tactile allodynia, but did not prevent the ultimate development of these manifestations of neuropathic pain. S4IL4 inoculation suppressed non-noxious-induced expression of c-Fos immunoreactivity in dorsal horn of spinal cord and reversed the upregulation of spinal IL-1β, PGE2, and phosphorylated-p38 MAP kinase, characteristic of neuropathic pain.HSV-mediated expression of IL-4 effectively reduces the behavioral manifestations of neuropathic pain, and reverses some of the biochemical and histologic correlates of neuropathic pain at the spinal level.Neural-immune interactions play a key role in the pathogenesis of neuropathic pain. Partial nerve injury results in the release of proinflammatory cytokines interleukin (IL)-1β, IL-6, and tumor necrosis factor alpha from activated Schwann cells, endothelial cells, and macrophages in nerve [1] to produce direct effects on nociceptive activity [2]. Peripheral nerve damage also activates microglia and astrocytes in spinal cord to release the same proinflammatory cytokines in dorsal horn [3-6], resulting in central sensitization [7,8] and an exaggerated pain response characteristic of neuropathic pain [9-11].IL-4 is a prototypical anti-inflammatory cytokine that modulates macrophage activity through global suppression of proinflammatory cytokines [12-14], in addition to pleiotropic effects on the development of immune cells and the immune response [15]. The broad spectrum of IL-4 action makes it an attractive candidate for suppressing cytokine activation in neuropathic pain, but the short half-life of
Reduction of voltage gated sodium channel protein in DRG by vector mediated miRNA reduces pain in rats with painful diabetic neuropathy
Munmun Chattopadhyay, Zhigang Zhou, Shuanglin Hao, Marina Mata, David J Fink
Molecular Pain , 2012, DOI: 10.1186/1744-8069-8-17
Abstract: Subcutaneous inoculation of the miRNA-expressing HSV vector into the feet of diabetic rats to transduce DRG resulted in a reduction in NaVα subunit levels in DRG neurons, coincident with a reduction in cold allodynia, thermal hyperalgesia and mechanical hyperalgesia.These data support the role of increased NaVα protein in DRG in the pathogenesis of pain in diabetic neuropathy, and provide a proof-of-principle demonstration for the development of a novel therapy that could be used to treat intractable pain in patients with diabetic neuropathy.Pain is a common complication of diabetic neuropathy that, despite substantial advances in understanding of pathophysiology, remains relatively refractory to treatment with available agents [1]. In rats with streptozotocin (STZ) induced diabetes and painful neuropathy, an increase in the alpha (pore-forming) subunit of voltage gated sodium channel isoform 1.7 (NaV1.7) in primary sensory afferent neurons of the dorsal root ganglia (DRG) has been reported [2], a change that correlates with increased amplitude and negative shift of the activation of tetrodotoxin (TTX)-sensitive current in those neurons. A potential pathogenic role for NaV1.7 in the development of pain in this syndrome is supported by the observation that gain of function mutations in NaV1.7 cause inherited spontaneous neuropathic pain syndromes primary erythermalgia [3,4] and paroxysmal extreme pain disorder [5].In previous studies we have constructed a series of herpes simplex virus (HSV)-based gene transfer vectors that effectively transduce DRG in vivo from skin inoculation, and have used these vectors to express inhibitory neurotransmitters [6-8] or neurotrophic factors [9-11]. In order to explicitly test the role of increased levels of NaV in DRG in the pathogenesis of pain in PDN, we constructed a non-replicating herpes simplex virus (HSV)-based vector to reduce NaVα protein in DRG, and compared the effect of NaVα subunit knockdown on pain-related behaviors i
Glial TNFα in the spinal cord regulates neuropathic pain induced by HIV gp120 application in rats
Wenwen Zheng, Handong Ouyang, Xuexing Zheng, Shue Liu, Marina Mata, David J Fink, Shuanglin Hao
Molecular Pain , 2011, DOI: 10.1186/1744-8069-7-40
Abstract: Peripheral gp120 application into the rat sciatic nerve induced mechanical allodynia for more than 7 weeks, and upregulated the expression of spinal TNFα in the mRNA and the protein levels at 2 weeks after gp120 application. Spinal TNFα was colocalized with GFAP (a marker of astrocytes) and Iba1 (a marker of microglia) in immunostaining, suggesting that glia produce TNFα in the spinal cord in this model. Peripheral gp120 application also increased TNFα in the L4/5 DRG. Furthermore, intrathecal administration of TNFα siRNA or soluble TNF receptor reduced gp120 application-induced mechanical allodynia.Our results indicate that TNFα in the spinal cord and the DRG are involved in neuropathic pain, following the peripheral HIV gp120 application, and that blockade of the glial product TNFα reverses neuropathic pain induced by HIV gp120 application.Infection of the central nervous system with the human immunodeficiency virus type 1 (HIV-1) can lead to cognitive, motor and sensory disorders. HIV-associated sensory neuropathy (HIV-SN) is one of the most common forms of peripheral neuropathy, affecting about 30% of people with acquired immune deficiency syndrome (AIDS) [1,2]. The symptoms of HIV-SN are dominated by neuropathic pain [3,4]. The mechanisms underlying HIV-SN remain unclear. Astrocytosis and subsequent neuron death are two hallmarks of HIV infection in the central nervous system[5]. Direct infection of neurons by HIV is thought to be unlikely [6,7]; HIV-1 binds via the external envelope proteins (e.g., gp120) to the chemokine receptors CXCR4 and/or CCR5 (co-receptors of gp120) on the cells. Previous reports have suggested that gp120 application contributes to neurotoxicity in in vitro and nociceptive behaviour in rodents [8-11]. Indeed, it has been demonstrated that gp120 application is capable of producing pain when administered peripherally [12] or centrally [13]. Proposed mechanisms underlying gp120 application induced a chronic nociceptive effect included spin
Maximizers for the Strichartz and the Sobolev-Strichartz inequalities for the Schrodinger equation
Shuanglin Shao
Electronic Journal of Differential Equations , 2009,
Abstract: In this paper, we first show that there exists a maximizer for the non-endpoint Strichartz inequalities for the Schrodinger equation in all dimensions based on the recent linear profile decomposition result. We then present a new proof of the linear profile decomposition for the Schroindger equation with initial data in the homogeneous Sobolev space; as a consequence, there exists a maximizer for the Sobolev-Strichartz inequality.
Sharp linear and bilinear restriction estimates for paraboloids in the cylindrically symmetric case
Shuanglin Shao
Mathematics , 2007,
Abstract: For cylindrically symmetric functions dyadically supported on the paraboloid, we obtain a family of sharp linear and bilinear adjoint restriction estimates. As corollaries, we first extend the ranges of exponents for the classical \textit{linear or bilinear adjoint restriction conjectures} for such functions and verify the \textit{linear adjoint restriction conjecture} for the paraboloid. We also interpret the restriction estimates in terms of solutions to the Schr\"odinger equation and establish the analogous results when the paraboloid is replaced by the lower third of the sphere.
A note on the cone restriction conjecture in the cylindrically symmetric case
Shuanglin Shao
Mathematics , 2007,
Abstract: In this note, we present two arguments showing that the classical \textit{linear adjoint cone restriction conjecture} holds for the class of functions supported on the cone and invariant under the spatial rotation in all dimensions. The first is based on a dyadic restriction estimate, while the second follows from a strengthening version of the Hausdorff-Young inequality and the H\"older inequality in the Lorentz spaces.
On localization of the Schr?dinger maximal operator
Shuanglin Shao
Mathematics , 2010,
Abstract: In \cite{Lee:2006:schrod-converg}, when the spatial variable $x$ is localized, Lee observed that the Schr\"odinger maximal operator $e^{it\Delta}f(x)$ enjoys certain localization property in $t$ for frequency localized functions. In this note, we give an alternative proof of this observation by using the method of stationary phase, and then include two applications: the first is on is on the equivalence of the local and the global Schr\"odinger maximal inequalities; secondly the local Schr\"odinger maximal inequality holds for $f\in H^{3/8+}$, which implies that $e^{it\Delta}f$ converges to $f$ almost everywhere if $f\in H^{3/8+}$. These results are not new. In this note we would like to explore them from a slightly different perspective, where the analysis of the stationary phase plays an important role.
Pointwise convergence of the Schr?dinger maximal operator
Shuanglin Shao
Mathematics , 2012,
Abstract: This paper has been withdrawn by the author due to an error estimate in Lemma 3.1.
On extremisers to a bilinear Strichartz inequality
Shuanglin Shao
Mathematics , 2013,
Abstract: In this note, we show that a pair of Gaussian functions are extremisers to a bilinear Strichartz inequality, and unique up to the symmetry group of the inequality.
Maximizers for the Strichartz inequalities and the Sobolev-Strichartz inequalities for the Schr?dinger equation
Shuanglin Shao
Mathematics , 2008,
Abstract: In this paper, we first show that there exists a maximizer for the non-endpoint Strichartz inequalities for the Schr\"odinger equation in all dimensions based on the recent linear profile decomposition results. We then present a new proof of the linear profile decomposition for the Schr\"oindger equation with initial data in the homogeneous Sobolev space; as a consequence, there exists a maximizer for the Sobolev-Strichartz inequality.
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