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Search Results: 1 - 10 of 23602 matches for " Jialin Zheng "
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Translational Neurodegeneration, a platform to share knowledge and experience in translational study of neurodegenerative diseases
Shengdi Chen, Jialin C Zheng
Translational Neurodegeneration , 2012, DOI: 10.1186/2047-9158-1-1
Abstract: Indeed, the prevalence of neurodegenerative disorders, including Alzheimer's disease (AD) and Parkinson's disease (PD), has increased significantly as global populations age. Specifically, the number of cases of dementia in the developed world is projected to rise from 13.5 million in 2000 to 21.2 million in 2025, and to 36.7 million in 2050[1]. Currently, the number of deaths caused by AD is only next to the number of deaths caused by stroke. As the prevalence of AD grows, so does the cost to a nation. For PD, the second most common neurodegenerative disease after AD, more than 4 million people suffer from this devastating disease worldwide and that will double in the next 25 years [2]. To date, PD is still an incurable progressive neurological disorder that seriously impairs the quality of life.The discovery and application of levodopa (L-dopa) is one of the best examples of translational research for neurodegenerative diseases. In 1910s, L-dopa was first isolated from seedlings of Vicia faba; and in 1938, L-dopa decarboxylase was discovered, which can produce dopamine (DA) from L-dopa. In 1959, DA was found enriched in the basal ganglia; and in 1960, a severe striatal DA deficit was demonstrated in PD patients. These major discoveries and a deepening understanding of the neurochemistry of DA and the neuropathology of PD led to the concept of "DA replacement" with L-dopa. In 1961, L-dopa was tried in PD patients by i.v. treatment. In 1967, oral administration of L-dopa was reported to produce dramatic improvements in PD patients with increasing amounts over long periods [3]. However, the main side effects of increasing L-dopa administration, i.e., dyskinesias and motor fluctuations, became apparent. This clinical finding confused doctors and patients, and a solution was needed. In 1970s, the key cause was found. L-dopa decarboxylase degraded L-dopa to DA in peripheral blood, which can not across the blood-brain barrier. These findings led to the first L-dopa combi
STAT1 Regulates Human Glutaminase 1 Promoter Activity through Multiple Binding Sites in HIV-1 Infected Macrophages
Lixia Zhao, Yunlong Huang, Jialin Zheng
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0076581
Abstract: Mononuclear phagocytes (MP, macrophages and microglia), the main targets of HIV-1 infection in the brain, play a pathogenic role in HIV-associated neurocognitive disorders (HAND) through the production and release of various soluble neurotoxic factors including glutamate. We have previously reported that glutaminase (GLS), the glutamate-generating enzyme, is upregulated in HIV-1 infected MP and in the brain tissues of HIV dementia individuals, and that HIV-1 or interferon-α (IFN-α) regulates human glutaminase 1 (GLS1) promoter through signal transducer and activator of transcription 1 (STAT1) phosphorylation in macrophages. However, there are multiple putative STAT1 binding sites in human GLS1 promoter, the exact molecular mechanism of how HIV-1 or IFN-α regulates human GLS1 promoter remains unclear. To further study the function of the putative STAT1 binding sites, we mutated the sequence of each binding site to ACTAGTCTC and found that six mutants (mut 1,3,4,5,7,8) had significantly higher promoter activity and two mutants (mut 2 and mut 6) completely lost the promoter activity compared with the wild type. To determine whether sites 2 and 6 could interfere with other inhibitory sites, particularly the nearby inhibitory sites 3 and 5, we made double mutants dmut 2/3 and dmut 5/6, and found that both the double mutants had significantly higher activity than the wild type, indicating that sites 3 and 5 are critical inhibitory elements, while sites 2 and 6 are excitatory elements. ChIP assay verified that STAT1 could bind with sites 2/3 and 5/6 within human GLS1 promoter in IFN-α stimulated or HIV-1-infected monocyte-derived macrophages. Interestingly, we found that rat Gls1 promoter was regulated through a similar way as human GLS1 promoter. Together, our data identified critical elements that regulate GLS1 promoter activity.
Mitochondrial Fragmentation Is Involved in Methamphetamine-Induced Cell Death in Rat Hippocampal Neural Progenitor Cells
Changhai Tian, L. Charles Murrin, Jialin C. Zheng
PLOS ONE , 2009, DOI: 10.1371/journal.pone.0005546
Abstract: Methamphetamine (METH) induces neurodegeneration through damage and apoptosis of dopaminergic nerve terminals and striatal cells, presumably via cross-talk between the endoplasmic reticulum and mitochondria-dependent death cascades. However, the effects of METH on neural progenitor cells (NPC), an important reservoir for replacing neurons and glia during development and injury, remain elusive. Using a rat hippocampal NPC (rhNPC) culture, we characterized the METH-induced mitochondrial fragmentation, apoptosis, and its related signaling mechanism through immunocytochemistry, flow cytometry, and Western blotting. We observed that METH induced rhNPC mitochondrial fragmentation, apoptosis, and inhibited cell proliferation. The mitochondrial fission protein dynamin-related protein 1 (Drp1) and reactive oxygen species (ROS), but not calcium (Ca2+) influx, were involved in the regulation of METH-induced mitochondrial fragmentation. Furthermore, our results indicated that dysregulation of ROS contributed to the oligomerization and translocation of Drp1, resulting in mitochondrial fragmentation in rhNPC. Taken together, our data demonstrate that METH-mediated ROS generation results in the dysregulation of Drp1, which leads to mitochondrial fragmentation and subsequent apoptosis in rhNPC. This provides a potential mechanism for METH-related neurodegenerative disorders, and also provides insight into therapeutic strategies for the neurodegenerative effects of METH.
New Insights into Human Resource Management of Large Public Hospitals with Multi Campuses in China  [PDF]
Jialin Yang, Huafeng Cheng
Journal of Human Resource and Sustainability Studies (JHRSS) , 2015, DOI: 10.4236/jhrss.2015.33016
Abstract: Human resource departments of large public hospitals in China deal with new challenges caused by multi-campus structure, such as increased labor demand, difficulty in cost management, lack of professional talents, restriction on employing way and etc. Delphi Method and Focus Group were used as the chief methods to analyze the problems. Countermeasures are researched as staffing optimization, performance management, forming Expert Center, establishing HRM Framework based on the positions among campus and restricting the human resource department. The researches break away from traditional human resource practices, develop new application for future trends, and adapt to the changes of business in the country’s public hospital reform.
Fabrication and Analysis of Vanadium-Based Metal Powders for Selective Laser Melting  [PDF]
Jialin Yang, Jingfeng Li
Journal of Minerals and Materials Characterization and Engineering (JMMCE) , 2018, DOI: 10.4236/jmmce.2018.61005
Abstract: Vanadium Alloy is a type of advanced nuclear material with many ideal properties compared as traditional nuclear materials, which has very wide and important application in first-wall and blanket structural material for fusion power plant applications. So it has attracted increasing attentions, especially on new manufacturing methods, such as selective laser melting and so on. In this paper, the comparative study of the powders obtained by mechanical mixing method, dry grinding method and wet grinding method respectively was performed to evaluate the effect of ball milling process on the microstructure and degree of alloying of the vanadium-based powder mixtures with the nominal composition of V5Cr5Ti vanadium alloy. The powders prepared by dry grinding method exhibits better spherical-like morphology and degree of alloying than those prepared by mechanical mixing method and wet grinding method, which indicates that dry grinding method can be used to prepare the superfine vanadium alloy powders for selective laser melting. This work provides a new method as well as important insights into the preparation of superfine vanadium alloy powders for selective laser melting additive manufacturing technology.
Type I Interferons and Interferon Regulatory Factors Regulate TNF-Related Apoptosis-Inducing Ligand (TRAIL) in HIV-1-Infected Macrophages
Yunlong Huang, Angelique Walstrom, Luwen Zhang, Yong Zhao, Min Cui, Ling Ye, Jialin C. Zheng
PLOS ONE , 2009, DOI: 10.1371/journal.pone.0005397
Abstract: TNF-related apoptosis-inducing ligand (TRAIL) is a member of the TNF family that participates in HIV-1 pathogenesis through the depletion of CD4+ T cells. TRAIL is expressed on the cell membrane of peripheral immune cells and can be cleaved into a soluble, secreted form. The regulation of TRAIL in macrophages during HIV-1 infection is not completely understood. In this study, we investigated the mechanism(s) of TRAIL expression in HIV-1-infected macrophages, an important cell type in HIV-1 pathogenesis. A human monocyte-derived macrophage (MDM) culture system was infected with macrophage-tropic HIV-1ADA, HIV-1JR-FL, or HIV-1BAL strains. TRAIL, predominantly the membrane-bound form, increased following HIV-1 infection. We found that HIV-1 infection also induced interferon regulatory factor (IRF)-1, IRF-7 gene expression and signal transducers and activators of transcription 1 (STAT1) activation. Small interfering RNA knockdown of IRF-1 or IRF-7, but not IRF-3, reduced STAT1 activation and TRAIL expression. Furthermore, the upregulation of IRF-1, IRF-7, TRAIL, and the activation of STAT1 by HIV-1 infection was reduced by the treatment of type I interferon (IFN)-neutralizing antibodies. In addition, inhibition of STAT1 by fludarabine abolished IRF-1, IRF-7, and TRAIL upregulation. We conclude that IRF-1, IRF-7, type I IFNs, and STAT1 form a signaling feedback loop that is critical in regulating TRAIL expression in HIV-1-infected macrophages.
HIV-1-Infected and Immune-Activated Macrophages Induce Astrocytic Differentiation of Human Cortical Neural Progenitor Cells via the STAT3 Pathway
Hui Peng, Lijun Sun, Beibei Jia, Xiqian Lan, Bing Zhu, Yumei Wu, Jialin Zheng
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0019439
Abstract: Diminished adult neurogenesis is considered a potential mechanism in the pathogenesis of HIV-1-associated dementia (HAD). In HAD, HIV-1-infected and immune-activated brain mononuclear phagocytes (MP; perivascular macrophages and microglia) drive central nervous system (CNS) inflammation and may alter normal neurogenesis. We previously demonstrated HIV-1-infected and lipopolysaccharide (LPS) activated monocyte-derived macrophages (MDM) inhibit human neural progenitor cell (NPC) neurogenesis, while enhancing astrogliogenesis through the secretion of the inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α), in vitro and in vivo. Here we further test the hypothesis that HIV-1-infected/activated MDM promote NPC astrogliogenesis via activation of the transcription factor signal transducer and activator of transcription 3 (STAT3), a critical factor for astrogliogenesis. Our results show that LPS-activated MDM-conditioned medium (LPS-MCM) and HIV-infected/LPS-activated MDM-conditioned medium (LPS+HIV-MCM) induced Janus kinase 1 (Jak1) and STAT3 activation. Induction of the Jak-STAT3 activation correlated with increased glia fibrillary acidic protein (GFAP) expression, demonstrating an induction of astrogliogenesis. Moreover, STAT3-targeting siRNA (siSTAT3) decreased MCM-induced STAT3 activation and NPC astrogliogenesis. Furthermore, inflammatory cytokines (including IL-6, IL-1β and TNF-α) produced by LPS-activated and/or HIV-1-infected MDM may contribute to MCM-induced STAT3 activation and astrocytic differentiation. These observations were confirmed in severe combined immunodeficient (SCID) mice with HIV-1 encephalitis (HIVE). In HIVE mice, siRNA control (without target sequence, sicon) pre-transfected NPCs injected with HIV-1-infected MDM showed more astrocytic differentiation and less neuronal differentiation of NPCs as compared to NPC injection alone. siSTAT3 abrogated HIV-1-infected MDM-induced astrogliogenesis of injected NPCs. Collectively, these observations demonstrate that HIV-1-infected/activated MDM induces NPC astrogliogenesis through the STAT3 pathway. This study generates important data elucidating the role of brain inflammation in neurogenesis and may provide insight into new therapeutic strategies for HAD.
Interferon-α Regulates Glutaminase 1 Promoter through STAT1 Phosphorylation: Relevance to HIV-1 Associated Neurocognitive Disorders
Lixia Zhao, Yunlong Huang, Changhai Tian, Lynn Taylor, Norman Curthoys, Yi Wang, Hamilton Vernon, Jialin Zheng
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0032995
Abstract: HIV-1 associated neurocognitive disorders (HAND) develop during progressive HIV-1 infection and affect up to 50% of infected individuals. Activated microglia and macrophages are critical cell populations that are involved in the pathogenesis of HAND, which is specifically related to the production and release of various soluble neurotoxic factors including glutamate. In the central nervous system (CNS), glutamate is typically derived from glutamine by mitochondrial enzyme glutaminase. Our previous study has shown that glutaminase is upregulated in HIV-1 infected monocyte-derived-macrophages (MDM) and microglia. However, how HIV-1 leads to glutaminase upregulation, or how glutaminase expression is regulated in general, remains unclear. In this study, using a dual-luciferase reporter assay system, we demonstrated that interferon (IFN) α specifically activated the glutaminase 1 (GLS1) promoter. Furthermore, IFN-α treatment increased signal transducer and activator of transcription 1 (STAT1) phosphorylation and glutaminase mRNA and protein levels. IFN-α stimulation of GLS1 promoter activity correlated to STAT1 phosphorylation and was reduced by fludarabine, a chemical that inhibits STAT1 phosphorylation. Interestingly, STAT1 was found to directly bind to the GLS1 promoter in MDM, an effect that was dependent on STAT1 phosphorylation and significantly enhanced by IFN-α treatment. More importantly, HIV-1 infection increased STAT1 phosphorylation and STAT1 binding to the GLS1 promoter, which was associated with increased glutamate levels. The clinical relevance of these findings was further corroborated with investigation of post-mortem brain tissues. The glutaminase C (GAC, one isoform of GLS1) mRNA levels in HIV associated-dementia (HAD) individuals correlate with STAT1 (p<0.01), IFN-α (p<0.05) and IFN-β (p<0.01). Together, these data indicate that both HIV-1 infection and IFN-α treatment increase glutaminase expression through STAT1 phosphorylation and by binding to the GLS1 promoter. Since glutaminase is a potential component of elevated glutamate production during the pathogenesis of HAND, our data will help to identify additional therapeutic targets for the treatment of HAND.
Association of genetic polymorphisms in the interleukin-10 promoter with risk of prostate cancer in Chinese
Jie Liu, Bao Song, Xueli Bai, Wenjian Liu, Zengjun Li, Jialin Wang, Yan Zheng, Zhehai Wang
BMC Cancer , 2010, DOI: 10.1186/1471-2407-10-456
Abstract: We genotyped three SNPs of the IL-10 promoter (-1082A/G, -819T/C and -592A/C) using polymerase chain reaction-restriction fragment length polymorphism analysis in 262 subjects with PCa and 270 age-matched healthy controls. Odds ratio and 95% confidence interval were determined by logistic regression for the associations between IL-10 genotypes and haplotypes with the risk of PCa and advanced PCa grade.No significant differences in allele frequency or genotype distribution were observed for any of the IL-10 SNPs between PCa patients and control subjects. Significantly higher frequencies of -1082G, -819C and -592C allele and GCC haplotype were observed, however, in early stage patients in comparison to advanced PCa patients (for -1082 G, 13.9% vs 6.1%, OR = 2.48, P = 0.005; for -819 C 40.3% vs 30.8%, OR = 1.51, P = 0.043; for -512C, 40.3% vs 30.8%, OR = 1.51, P = 0.043; and for haplotype GCC 11.1%vs 5.1%, OR = 2.66, P = 0.008, respectively).Our results identify that IL-10 promoter polymorphisms might not be a risk factor for PCa in Chinese cohorts, but rather incidence of polymorphisms associates with PCa grade, suggesting that IL-10 expression may impact PCa progression.Prostate cancer (PCa) is among the most common malignant tumors in Western males, ranking second only to lung cancer in cancer mortality [1]. PCa incidence in Asian men is significantly lower, however, the incidence of PCa in China has increased significantly in recent years [2]. While age, ethnicity, diet, and geographic factors are believed to contribute to the etiology of this disorder [3-5], genetic variations may play a role in susceptibility to PCa [6]. Recent studies suggest that genetic polymorphisms of genes involved in innate immunity and chronic inflammation, including the anti-inflammatory cytokine Interleukin-10 (IL-10), may impact susceptibility to PCa [6].IL-10 is produced primarily by macrophages and T lymphocytes. It has important anti-inflammatory and immunosuppressive activities, in
TNF-α Affects Human Cortical Neural Progenitor Cell Differentiation through the Autocrine Secretion of Leukemia Inhibitory Factor
Xiqian Lan, Qiang Chen, Yongxiang Wang, Beibei Jia, Lijun Sun, Jialin Zheng, Hui Peng
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0050783
Abstract: Proinflammatory cytokine tumor necrosis factor-alpha (TNF-α) is a crucial effector of immune responses in the brain that participates in the pathogenesis of several acute and chronic neurodegenerative disorders. Accumulating evidence has suggested that TNF-α negatively regulates embryonic and adult neurogenesis. However, the effect of TNF-α on cell fate decision in human neural progenitor cells (NPCs) has rarely been studied. Our previous studies have shown that recombinant TNF-α enhances astrogliogenesis and inhibits neurogenesis of human NPCs through the STAT3 (signal transducer and activator of transcription 3) pathway. In the current study, we further elucidated the specific mechanism involved in TNF-α-induced astrogliogenesis. We found that TNF-α activated STAT3 at delayed time points (6 h and 24 h), whereas conditioned medium collected from TNF-α-treated NPCs induced an immediate STAT3 activation. These data suggest TNF-α plays an indirect role on STAT3 activation and the subsequent NPC differentiation. Further, we showed that TNF-α induced abundant amounts of the IL-6 family cytokines, including Leukemia inhibitory factor (LIF) and Interleukin 6 (IL-6), in human NPCs. TNF-α-induced STAT3 phosphorylation and astrogliogenesis were abrogated by the addition of neutralizing antibody for LIF, but not for IL-6, revealing a critical role of autocrine secretion of LIF in TNF-α-induced STAT3 activation and astrogliogenesis. This study generates important data elucidating the role of TNF-α in neurogenesis and may provide insight into new therapeutic strategies for brain inflammation.
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