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Search Results: 1 - 10 of 357 matches for " Tuo Jingsheng "
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Genetic/Epigenetic Modulation, Ocular Diseases, and Therapeutic Prospective
Jingsheng Tuo,Lai Wei,Nan Hu
Journal of Ophthalmology , 2013, DOI: 10.1155/2013/980608
Peroxisome Proliferator-Activated Receptor and Age-Related Macular Degeneration
Alexandra A. Herzlich,Jingsheng Tuo,Chi-Chao Chan
PPAR Research , 2008, DOI: 10.1155/2008/389507
Abstract: Age-related macular degeneration (AMD) is the leading cause of new blindness in the western world and is becoming more of a socio-medical problem as the proportion of the aged population increases. There are multiple efforts underway to better understand this disease process. AMD involves the abnormal retinal pigment epithelium (RPE), drusen formation, photoreceptor atrophy, and choroidal neovascularization. Peroxisome proliferator-activated receptors (PPARs) play an important role in lipid degeneration, immune regulation, regulation of reactive oxygen species (ROSs), as well as regulation of vascular endothelial growth factor (VEGF), matrix metalloproteinase-9 (MMP-9), and docosahexaenoic acid (DHA). These molecules have all been implicated in the pathogenesis of AMD. In addition, PPAR gamma is expressed in RPE, an essential cell in photoreceptor regeneration and vision maintenance. This review summarizes the interactions between PPAR, AMD-related molecules, and AMD-related disease processes.
Genetic mechanisms and age-related macular degeneration: common variants, rare variants, copy number variations, epigenetics, and mitochondrial genetics
Liu Melissa M,Chan Chi-Chao,Tuo Jingsheng
Human Genomics , 2012, DOI: 10.1186/1479-7364-6-13
Abstract: Age-related macular degeneration (AMD) is a complex and multifaceted disease involving contributions from both genetic and environmental influences. Previous work exploring the genetic contributions of AMD has implicated numerous genomic regions and a variety of candidate genes as modulators of AMD susceptibility. Nevertheless, much of this work has revolved around single-nucleotide polymorphisms (SNPs), and it is apparent that a significant portion of the heritability of AMD cannot be explained through these mechanisms. In this review, we consider the role of common variants, rare variants, copy number variations, epigenetics, microRNAs, and mitochondrial genetics in AMD. Copy number variations in regulators of complement activation genes (CFHR1 and CFHR3) and glutathione S transferase genes (GSTM1 and GSTT1) have been associated with AMD, and several additional loci have been identified as regions of potential interest but require further evaluation. MicroRNA dysregulation has been linked to the retinal pigment epithelium degeneration in geographic atrophy, ocular neovascularization, and oxidative stress, all of which are hallmarks in the pathogenesis of AMD. Certain mitochondrial DNA haplogroups and SNPs in mitochondrially encoded NADH dehydrogenase genes have also been associated with AMD. The role of these additional mechanisms remains only partly understood, but the importance of their further investigation is clear to elucidate more completely the genetic basis of AMD.
Systems Biology Profiling of AMD on the Basis of Gene Expression
Mones S. Abu-Asab,Jose Salazar,Jingsheng Tuo,Chi-Chao Chan
Journal of Ophthalmology , 2013, DOI: 10.1155/2013/453934
Abstract: Genetic pathways underlying the initiation and progression of age-related macular degeneration (AMD) have not been yet sufficiently revealed, and the correlations of AMD’s genotypes, phenotypes, and disease spectrum are still awaiting resolution. We are tackling both problems with systems biology phylogenetic parsimony analysis. Gene expression data (GSE29801: NCBI, Geo) of macular and extramacular specimens of the retinas and retinal pigment epithelium (RPE) choroid complexes representing dry AMD without geographic atrophy (GA), choroidal neovascularization (CNV), GA, as well as pre-AMD and subclinical pre-AMD were polarized against their respective normal specimens and then processed through the parsimony program MIX to produce phylogenetic cladograms. Gene lists from cladograms’ nodes were processed in Genomatix GePS to reveal the affected signaling pathway networks. Cladograms exposed a highly heterogeneous transcriptomic profiles within all the conventional phenotypes. Moreover, clades and nodal synapomorphies did not support the classical AMD phenotypes as valid transcriptomal genotypes. Gene lists defined by cladogram nodes showed that the AMD-related deregulations occurring in the neural retina were different from those in RPE-choroidal tissue. Our analysis suggests a more complex transcriptional profile of the phenotypes than expected. Evaluation of the disease in much earlier stages is needed to elucidate the initial events of AMD. 1. Introduction Age-related macular degeneration (AMD) is the main cause of permanent central blindness in the developed countries [1]. It manifests in drusen formation and degeneration/atrophy of the retinal pigmented epithelium (RPE) and neural retina, as well as the formation of abnormal choroidal capillaries [2, 3]. In addition to aging as the principal risk factor, there are others such as smoking, diet, and genetic predisposition [3, 4]. However, it is not yet sufficiently resolved the exact genetic pathways underlying the initiation and progression of AMD and the relationship between its genotypes and phenotypes [1]. Although a more recent clinical classification of AMD has been published recently [5], we are using that of Newman et al. [1] since the study specimens were categorized in the public data according to their phenotypes (see Table 1 for details), these encompass (1) dry AMD, (2) choroidal neovascularization (CNV) or Wet AMD, (3) geographic atrophy (GA) in macular region of RPE, (4) GA/CNV, (5) pre-AMD, and (6) subclinical pre-AMD. These phenotypes are typically the progressing manifestations of the
Anti-inflammatory recombinant TSG-6 stabilizes the progression of focal retinal degeneration in a murine model
Jingsheng Tuo, Xiaoguang Cao, Defen Shen, Yujuan Wang, Jun Zhang, Joo Oh, Darwin J Prockop, Chi-Chao Chan
Journal of Neuroinflammation , 2012, DOI: 10.1186/1742-2094-9-59
Abstract: Recombinant TSG-6 (400 ng) was administered by intravitreous injection into the right eye of six-week-old Ccl2-/-/Cx3cr1-/- mice. Their left eye was injected with phosphate-buffered saline as a control. Funduscopic pictures were taken before injection and sequentially once a month after injection. The mice were killed two months after injection and the ocular histology examined. Retinal A2E, a major component of lipofuscin, was measured by high performance liquid chromatography. The microarray of ocular mRNA of 92 immunological genes was performed. The genes showing differentiated expression in microarray were further compared between the injected right eye and the contralateral (control) eye by [real-time quantitative reverse transcription polymerase chain reaction] qRT-PCR.The continuous monitoring of the fundus for two months showed a slower progression or alleviation of retinal lesions in the treated right eyes as compared with the untreated left eyes. Among 23 pairs of eyes, the lesion levels improved in 78.3%, stayed the same in 8.7% and progressed in 13.0%. Histology confirmed the clinical observation. Even though there was no difference in the level of A2E between the treated and the untreated eyes, microarray analysis of 92 immune genes showed that IL-17a was substantially decreased after the treatment. Expression of TNF-α showed a similar pattern to IL-17a. The results were consistent in duplicated arrays and confirmed by qRT-PCR.We concluded that intravitreous administration of recombinant TSG-6 might stabilize retinal lesions in Ccl2-/-/Cx3cr1-/- mice on rd8 background. Modulation of ocular immunological gene expressions, especially IL-17a, could be one of the mechanisms.Age-related macular degeneration (AMD) is a common cause of irreversible central blindness in elderly patients worldwide [1]. The pathological features of this neurodegenerative disease include degeneration and atrophy of the photoreceptors and the retinal pigment epithelium (RPE) in the
Design Optimization of TBM Disc Cutters for Different Geological Conditions  [PDF]
Yimin Xia, Kui Zhang, Jingsheng Liu
World Journal of Engineering and Technology (WJET) , 2015, DOI: 10.4236/wjet.2015.34023
Abstract: A novel optimization methodology for the disc cutter designs of tunnel boring machines (TBM) was presented. To fully understand the characteristics and performance of TBM cutters, a comprehensive list of performance parameters were investigated, including maximum equivalent stress and strain, specific energy and wear life which were closely related to the cutting forces and profile geometry of the cutter rings. A systematic method was employed to evaluate an overall performance index by incorporating objectives at all possible geological conditions. The Multi-objective & Multi-geologic Conditions Optimization (MMCO) program was then developed, which combined the updating of finite element model, system evaluation, finite element solving, post-processing and optimization algorithm. Finally, the MMCO was used to optimize the TBM cutters used in a TBM tunnel project in China. The results show that the optimization significantly improves the working performances of the cutters under all geological conditions considered.
Complement component C5a Promotes Expression of IL-22 and IL-17 from Human T cells and its Implication in Age-related Macular Degeneration
Baoying Liu, Lai Wei, Catherine Meyerle, Jingsheng Tuo, H Nida Sen, Zhiyu Li, Sagarika Chakrabarty, Elvira Agron, Chi-Chao Chan, Michael L Klein, Emily Chew, Frederick Ferris, Robert B Nussenblatt
Journal of Translational Medicine , 2011, DOI: 10.1186/1479-5876-9-111
Abstract: Human peripheral blood mononuclear cells (PBMCs) were isolated from the blood of exudative form of AMD patients using a Ficoll gradient centrifugation protocol. Intracellular staining and enzyme-linked immunosorbent assays were used to measure protein expression. Apoptotic cells were detected by staining of cells with the annexin-V and TUNEL technology and analyzed by a FACS Caliber flow cytometer. SNP genotyping was analyzed by TaqMan genotyping assay using the Real-time PCR system 7500.We show that C5a promotes interleukin (IL)-22 and IL-17 expression by human CD4+ T cells. This effect is dependent on B7, IL-1β and IL-6 expression from monocytes. We have also found that C5a could protect human CD4+ cells from undergoing apoptosis. Importantly, consistent with a role of C5a in promoting IL-22 and IL-17 expression, significant elevation in IL-22 and IL-17 levels was found in AMD patients as compared to non-AMD controls.Our results support the notion that C5a may be one of the factors contributing to the elevated serum IL-22 and IL-17 levels in AMD patients. The possible involvement of IL-22 and IL-17 in the inflammation that contributes to AMD may herald a new approach to treat AMD.Age related macular degeneration (AMD) is clinically characterized by degenerative changes in the macula, the region of the retina that permits fine central vision. One of the key pathological features of AMD is the development of large drusen, extracellular deposits located between Bruch's membrane and the retinal pigment epithelium (RPE). These large drusen and the associated RPE changes are the major risk factors for the development of advanced AMD, which can be classified into two subtypes: dry (geographic atrophic) and wet (neovascular) [1]. Inflammation has been suggested to play an important role in AMD pathogenesis [2,3].Genetic studies have demonstrated strong associations between AMD and several gene variants in genes coding for complement proteins, including complement factor H
Interleukin-17 Retinotoxicity Is Prevented by Gene Transfer of a Soluble Interleukin-17 Receptor Acting as a Cytokine Blocker: Implications for Age-Related Macular Degeneration
Daniel Ardeljan, Yujuan Wang, Stanley Park, Defen Shen, Xi Kathy Chu, Cheng-Rong Yu, Mones Abu-Asab, Jingsheng Tuo, Charles G. Eberhart, Timothy W. Olsen, Robert F. Mullins, Gary White, Sam Wadsworth, Abraham Scaria, Chi-Chao Chan
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0095900
Abstract: Age-related macular degeneration (AMD) is a common yet complex retinal degeneration that causes irreversible central blindness in the elderly. Pathology is widely believed to follow loss of retinal pigment epithelium (RPE) and photoreceptor degeneration. Here we report aberrant expression of interleukin-17A (IL17A) and the receptor IL17RC in the macula of AMD patients. In vitro, IL17A induces RPE cell death characterized by the accumulation of cytoplasmic lipids and autophagosomes with subsequent activation of pro-apoptotic Caspase-3 and Caspase-9. This pathology is reduced by siRNA knockdown of IL17RC. IL17-dependent retinal degeneration in a mouse model of focal retinal degeneration can be prevented by gene therapy with adeno-associated virus vector encoding soluble IL17 receptor. This intervention rescues RPE and photoreceptors in a MAPK-dependent process. The IL17 pathway plays a key role in RPE and photoreceptor degeneration and could hold therapeutic potential in AMD.
The BSA-induced Ca(2+) influx during sperm capacitation is CATSPER channel-dependent
Jingsheng Xia, Dejian Ren
Reproductive Biology and Endocrinology , 2009, DOI: 10.1186/1477-7827-7-119
Abstract: BSA-induced changes in intracellular calcium concentration were studied using Fluo-4 and Fura-2 calcium imaging with wild-type and Catsper1 knockout mouse sperm.We found that the fast phase of the BSA-induced rises in intracellular calcium concentration was absent in the Catsper1 knockout sperm and could be restored by an EGFP-CATSPER1 fusion protein. The calcium concentration increases were independent of G-proteins and phospholipase C but could be partially inhibited when intracellular pH was clamped. The changes started in the principal piece and propagated toward the sperm head.We conclude that the initial phase of the increases in intracellular calcium concentration induced by BSA requires the CATSPER channel, but not the voltage-gated calcium channel. Our findings identify the molecular conduit responsible for the calcium entry required for the sperm motility changes that occur during capacitation.During mammalian fertilization, freshly ejaculated sperm do not have the ability to fertilize oocytes until after they undergo capacitation, a functionally defined, but poorly understood maturation process by which sperm become capable of fertilizing eggs [1-3]. Sperm become capacitated in vivo, by interacting with environmental stimuli in the female reproductive tract before encountering eggs. This process can also be mimicked in vitro by incubating sperm in defined capacitation media. Several commonly used components are essential for successful in vitro capacitation in sperm from many mammalian species. Among them are bovine serum albumin (BSA), Ca2+ and bicarbonate (HCO3-) [3]. Capacitation leads to several cellular and behavioral changes, including an increase in tyrosine phosphorylation of sperm proteins, rises in intracellular pH (pHi) and Ca2+ concentration ([Ca2+]i), membrane hyperpolarization, and hyperactivated motility [4-6].Increases in [Ca2+]i and intracellular [pH]i are believed to play central roles in both sperm capacitation and the acrosome reaction
Hedging Against the Interest-rate Risk by Measuring the Yield-curve Movement
Zhongliang Tuo
Quantitative Finance , 2013,
Abstract: By adopting the polynomial interpolation method, we propose an approach to hedge against the interest-rate risk of the default-free bonds by measuring the nonparallel movement of the yield-curve, such as the translation, the rotation and the twist. The empirical analysis shows that our hedging strategies are comparable to traditional duration-convexity strategy, or even better when we have more suitable hedging instruments on hand. The article shows that this strategy is flexible and robust to cope with the interest-rate risk and can help ?fine-tune a position as time changes.
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