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1.
Yu Xiaolin Ji Kunqian Lin Yan Xu Xuebi Wang Wei Li Ying Lu Jian-Qiang Zhao Yuying Yan Chuanzhu 《Neurological sciences》2021,42(12):5123-5130
Neurological Sciences - To report a Chinese family with combined m.14459G>A mutation and m.6064A>T mutation of which the female proband presenting unique Leber hereditary optic... 相似文献
2.
Qingyu Shi Xuebi Tian Yinlin Zhao Huiyu Luo Yuke Tian Ailin Luo 《Rheumatology international》2014,34(1):51-57
The objective of this study is to construct and identify an inducible lentiviral vector containing improved tet-on system and FasL gene and observe its effects on pristane-induced arthritis (PIA). FasL gene was amplified from the spleen of Lewis rats by RT-PCR. The tet-on system was improved with insertion of a chicken chromatin insulator (cHS4) element and an rtTA-dependent, tet-responsive element containing modifications of the tetO sequence (TRE-tight1). Pro-apoptosis effect of the vector pTREFasLcHS4V16 on synovial cells was evaluated by flow cytometer in vitro. Anti-arthritis effects of the vector on PIA after intra-articular injection were observed by clinical evaluation and joint histology. Cytokines in synovial tissue were measured by ELISA. The recombinant inducible lentiviral vector pTREFasLcHS4V16 was successfully constructed. The expression response and the pro-apoptosis effects of the vector were doxycycline dose-dependent. The vector injected intra-articularly attenuated the severity of PIA and decreased the level of cytokines in inflamed joints. pTREFasLcHS4V16 with an improved tet-on system can precisely regulate the expression of FasL gene and apoptosis. Anti-arthritis effects were observed after intra-articular injection of the inducible vector. 相似文献
3.
AN Ke XU Ying TIAN Xuebi GAO Feng TIAN Yuke YANG Hui ZHANG Chuanhan 《Frontiers of medicine.》2008,2(1):63
Neural progenitor cells (NPC) are those that are the source of neural cells for cell transplantation and gene therapy. The shortage in quantity and the limited life spans of primary cultured cells limit its widespread use in basic research. Immortalized NPC, which also possess the capacity of self-renewal and can proliferate infinitely, can produce a large number of NPCs with stable phenotype and genotype. Here we report that an immortalized neural progenitor cell strain, which we named as INPC, was successfully established by gene-transfer of simian virus 40 large T antigen gene mediated by liposomes. The INPC retained the biological characteristics of its original cells and provided a safe and reliable cell platform for the treatment of central nervous system diseases and transgenic cell transplantation. INPC could express low levels of MHC antigens which was down-regulated after differentiation. This indicates that INPC possesses poor immunogenicity. The immortalized cells may show good long-term survival and do not elicit an acute immunological response following transplantation. 相似文献
4.
Patients with chronic pain experience spontaneous or ongoing pain as well as enhanced sensitivity to evoked stimuli. Spontaneous or ongoing pain is rarely evaluated in preclinical studies. In fact, it remains controversial whether ongoing or spontaneous pain even develops in mice after tissue or nerve injury. This study tested a hypothesis that negative reinforcement can be used to unmask the presence of pain in mice with tissue or nerve injury. We found that spinal administration of clonidine or lidocaine did not elicit conditioned place preference (CPP) in uninjured or sham-operated mice. However, these agents produced CPP in mice with chronic inflammation induced by complete Freund's adjuvant (CFA) or following L5/L6 spinal nerve ligation (SNL). These data indicate the presence of non-evoked (ie, stimulus-independent) ongoing pain in mice with chronic inflammation (CFA) or following nerve injury (SNL). In addition, this study validates the use of negative reinforcement to unmask non-evoked ongoing pain in mice. Given the existence of a large collection of transgenic and knockout mice, our data show the application of this approach to elucidate molecular mechanisms underlying non-evoked pain and to contribute to drug discovery for pain. PERSPECTIVE: We demonstrated the presence of non-evoked ongoing pain in mice with chronic inflammation or following nerve injury. The study also validates the use of negative reinforcement to unmask non-evoked pain in mice. We propose to apply this approach to identify molecular mechanisms and effective drugs for chronic pain. 相似文献
5.
Xiao-Gao Jin Song-Qing He Xue-Tao Yan Guangxiong Zhang Li Wan Jintao Wang Yawen Li Xuebi Tian Yuke Tian Ailin Luo 《The journal of pain》2009,10(1):80-89
Neuropathic pain due to nerve injury is associated with overactivity of spinal N-methyl-D-aspartate (NMDA) receptors and nitric oxide synthases (NOS). Spinal NOS and NMDA receptors could act in a concerted manner to excite each other in nociceptive signaling. Among the 3 major NOS isoforms, neuronal NOS (nNOS) has the most functional relationship with NMDA receptors through a PDZ-PDZ (PSD-95, Dlg, ZO-1 homology) postsynapse interaction. However, some nNOS variants lack the PDZ domain, which may result in the changes in the interaction with the NMDA receptor and subsequent localization and enzymatic activity. The aim of this study was to determine which nNOS variants are expressed in the spinal cord in neuropathic rats and deduce their role in neuropathic pain by testing the effects of these kinds of nNOS on nuclear factor-κB (NF-κB) activity in PC12 cells. Western blot analysis revealed that there were at least 3 bands of nNOS (155, 135, and 125 kDa) in the spinal cord and, moreover, that nNOS at 135 kDa decreased significantly after development of neuropathic pain. 5′-RACE-PCR and Southern blots determined that the nNOS at 155 and 135 kDa corresponded to nNOSα and nNOSβ, respectively, which was confirmed by RT-PCR. PC12 cells transfected with the nNOSα gene had no effect on NF-κB activity, but nNOSβ without the PDZ domain significantly decreased that in PC12 cells. Considering the importance of spinal NF-κB signaling in neuropathic rat, it could be concluded that changes in spinal nNOS variants and quantity after peripheral nerve injury implicate nNOS in the generation of neuropathic pain.PerspectiveThis article presents data demonstrating that nNOS variants change in the spinal cord of the rats after neuropathic pain and result in differential effects on NF-κB activity in PC12 cells. These changes in nNOS variants and their different characteristics may account for the spinal NO paradox role in neuropathic pain. Furthermore, these data suggest that nNOSβ? may represent a new therapeutic target for the treatment of chronic neuropathic pain. 相似文献
6.
Feng GAO Yuke TIAN Hui YANG Ke AN Ying XU Xuebi TIAN Chuanhan ZHANG 《Frontiers of Medicine in China》2008,2(1):63-69
Neural progenitor cells (NPC) are those that are the source of neural cells for cell transplantation and gene therapy. The
shortage in quantity and the limited life spans of primary cultured cells limit its widespread use in basic research. Immortalized
NPC, which also possess the capacity of self-renewal and can proliferate infinitely, can produce a large number of NPCs with
stable phenotype and genotype. Here we report that an immortalized neural progenitor cell strain, which we named as INPC,
was successfully established by gene-transfer of simian virus 40 large T antigen gene mediated by liposomes. The INPC retained
the biological characteristics of its original cells and provided a safe and reliable cell platform for the treatment of central
nervous system diseases and transgenic cell transplantation. INPC could express low levels of MHC antigens which was down-regulated
after differentiation. This indicates that INPC possesses poor immunogenicity. The immortalized cells may show good long-term
survival and do not elicit an acute immunological response following transplantation. 相似文献
7.
Ren Hong Lin Yan Li Ying Zhang Xiufang Wang Wei Xu Xuebi Ji Kunqian Zhao Yuying Yan Chuanzhu 《Neurological sciences》2022,43(9):5581-5592
Neurological Sciences - Leber’s hereditary optic neuropathy (LHON) is a common mitochondrial disease. More than 30 variants in the mitochondrial DNA (mtDNA) have been previously described in... 相似文献
8.
Dawei Ye Huilian Bu Genhua Guo Bin Shu Wei Wang Xuehai Guan Hui Yang Xuebi Tian Hongbing Xiang Feng Gao 《Journal of molecular neuroscience : MN》2014,53(4):571-579
Morphine is a potent agonist of μ-opioid receptor and is widely used to relieve severe pain, including cancer pain. Some chemokines, for example, CX3CL1 and CCL2, participate in the regulation of opioid santinociception. In our previous study, we found overexpression of chemokine CXCL10/CXCR3 in spinal cord participated in the development of cancer-induced bone pain, so we supposed that CXCL10 may have influence in morphine analgesia in cancer pain relief. In this study, we found that a single dose of morphine could transiently increase the expression of CXCL10 in spinal cord. Blocking the function of CXCL10 enhanced morphine antinociception in cancer-induced bone pain rats. However, overexpression of CXCL10 induced acute algesia and decreased the analgesic effect of morphine in normal mice. The algesic effect of CXCL10 was blocked by inhibition of CXCR3 and Gi protein. These results suggested that CXCL10 in spinal cord serves as a novel negative regulator of morphine analgesia and provided evidence that activation of CXCL10/CXCR3 in spinal cord may attenuate antinociceptive potency of morphine in cancer pain relief. 相似文献
9.
Ye Tu Ping Yang Yaqun Zhou Xiaoyan Wen Qinqin Li Jing Zhou Jingjing Wang Jinqian Hu Nannan He Kai Wang Chaolong Wang Xuebi Tian Ailin Luo Feng Gao 《International journal of medical sciences》2021,18(5):1198
Rationale: Early invasive ventilation may improve outcomes for critically ill patients with COVID-19. The objective of this study is to explore risk factors for 28-day mortality of COVID-19 patients receiving invasive ventilation.Methods: 74 consecutive adult invasively ventilated COVID-19 patients were included in this retrospective study. The demographic and clinical data were compared between survivors and non-survivors, and Cox regression analysis was used to explore risk factors for 28-day mortality. The primary outcome was 28-day mortality after initiation of invasive ventilation. Secondary outcome was the time from admission to intubation.Results: Of 74 patients with COVID-19, the median age was 68.0 years, 53 (71.6%) were male, 47 (63.5%) had comorbidities with hypertension, and diabetes commonly presented. The most frequent symptoms were fever and dyspnea. The median time from hospital admission to intubation was similar in survivors and non-survivors (6.5 days vs. 5.0 days). The 28-day mortality was 81.1%. High Sequential Organ Failure Assessment (SOFA) score (hazard ratio [HR], 1.54; 95% confidence interval [CI], 1.23-1.92; p < 0.001) and longer time from hospital admission to intubation (HR, 2.41; 95% CI, 1.15-5.07; p = 0.020) were associated with 28-day mortality in invasively ventilated COVID-19 patients.Conclusions: The mortality of invasively ventilated COVID-19 patients was particularly striking. Patients with high SOFA score and receiving delayed invasive ventilation were at high risk of mortality. 相似文献
10.
Wei Wang Yuan Sun Yan Lin Xuebi Xu Dandan Zhao Kunqian Ji Wei Li Yuying Zhao Chuanzhu Yan 《Neuromuscular disorders : NMD》2021,31(6):558-565
Both mitochondrial and nuclear gene mutations can cause cytochrome c oxidase (COX, complex Ⅳ) dysfunction, leading to mitochondrial diseases. Although numerous diseases caused by defects of the COX subunits or COX assembly factors have been documented, clinical cases directly related to mitochondrial cytochrome c oxidase subunit 3 gene (MT-CO3) mutations are relatively rare. Here, we report a 47-year-old female patient presented with mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome. Muscle pathology revealed ragged-red fibres and remarkable COX-deficient muscle fibres. Muscle mitochondrial DNA sequencing analysis identified a novel MT-CO3 variant (m.9553G>A) that changed a highly conserved amino acid to a stop codon (p.Trp116*). This variant was heteroplasmic in multiple tissues, where the mutation load was 13% in oral epithelial cells, 89% in muscle samples, and not detectable in the peripheral blood lymphocytes. Single muscle fiber PCR analysis showed clear segregation of the mutation load with COX deficient fibres. Western blot analysis of the muscle samples revealed a significant decrease in the levels of COX1, COX2, COX3, COX4 and UQCRC2. COX respiration activity was remarkably reduced (58.84%) relative to the controls according to spectrophotometric assays. Taken together, our results indicated that this m.9553G>A variant may be responsible for the MELAS symdrome in the proband by affecting the stability and function of COX. The study expands the clinical and molecular spectrum of COX3-specific mitochondrial diseases. 相似文献