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Background: Cervical spondylosis (CS) is a prevalent disorder that can have a major negative impact on quality of life. Traditional conservative treatment has limited efficacy, and electroacupuncture (EA) is a novel treatment option. We investigated the application and molecular mechanism of EA treatment in a rat model of cervical intervertebral disk degeneration (CIDD). Methods: The CIDD rat model was established, following which rats in the electroacupuncture (EA) group received EA. For overexpression of IL-22 or inhibition of JAK2-STAT3 signaling, the rats were injected intraperitoneally with recombinant IL-22 protein (p-IL-22) or the JAK2-STAT3 (Janus kinase 2—signal transducer and activator of transcription protein 3) inhibitor AG490 after model establishment. Rat nucleus pulposus (NP) cells were isolated and cultured. Cell counting kit-8 and flow cytometry were used to analyze the viability and apoptosis of the NP cells. Expression of IL-22, JAK2 and STAT3 was determined using RT-qPCR. Expression of IL-22/JAK2-STAT3 pathway and apoptosis related proteins was detected by Western blotting (WB). Results: EA protected the NP tissues of CIDD rats by regulating the IL-22/JAK2-STAT3 pathway. Overexpression of IL-22 significantly promoted the expression of tumor necrosis factor (TNF)-α, IL-6, IL-1β, matrix metalloproteinase (MMP)3 and MMP13 compared with the EA group. WB demonstrated that the expression of IL-22, p-JAK2, p-STAT3, caspase-3 and Bax in NP cells of the EA group was significantly reduced and Bcl-2 elevated compared with the model group. EA regulated cytokines and MMP through activation of IL-22/JAK2-STAT3 signaling in CIDD rat NP cells. Conclusion: We demonstrated that EA affected apoptosis by regulating the IL-22/JAK2-STAT3 pathway in NP cells and reducing inflammatory factors in the CIDD rat model. The results extend our knowledge of the mechanisms of action underlying the effects of EA as a potential treatment approach for CS in clinical practice. [ABSTRACT FROM AUTHOR]

Tensile experiments were conducted for Al-7.0Zn-2.5Mg-2.0Cu-0.1Zr-0.2Sc alloy in different aging states (18 h, 24 h, 36 h) with temperature environments including room temperature, −10 °C and −30 °C. Comparative studies were made on the evolution of the precipitate phase in alloys at three kinds of aging times and the evolution of tensile properties in alloys under different ambient temperatures. The findings showed that the precipitates in Al-7.0Zn-2.5Mg-2.0Cu-0.1Zr-0.2Sc alloy were mainly in the GP zone after the solution + aging treatment η' phase, the secondary Al3 (Sc, Zr) phase and the θ' (Al2Cu) phase. As the aging time was prolonged, the η' phase gradually grew and the PFZ gradually widened. At the three test temperatures, the tensile strength (TS) and yield strength (YS) of the alloys both showed a trend of first increasing before decreasing with the extension of aging time, while the elongation (A) and section shrinkage (Z) showed a decreasing trend. As the test temperature decreased, the TS and YS of the alloys increased and the A and Z of the alloys decreased. At room temperature, alloys showed a ductile fracture mode, which changed to mixed ductile and brittle fracture with decreasing test temperature. [ABSTRACT FROM AUTHOR]

Objective: To investigate the potential therapeutic effect in a rheumatoid arthritis model of stable human CD8+ regulatory T cells (hCD8+Tregs) induced by TGF-β1 and rapamycin (RAPA) in vitro.Methods: Human CD8+T cells were isolated from human peripheral blood mononuclear cells and induced/expanded with TGF-β1 and RAPA along with anti-CD3/28 beads and IL-2 in vitro and harvested as hCD8+Tregs. The phenotypes, suppressive characteristics, and stability of the hCD8+Tregs in an inflammatory microenvironment were examined in vitro. Human CD8+Tregs were transfused into an acollagen-induced arthritis (CIA) mouse model, and their therapeutic effects and related mechanisms were investigated.Results: Human CD8+Tregs induced by TGF-β1/RAPA showed high expression of Foxp3 and CD103, exhibited vigorous suppression ability, and were stable in inflammatory microenvironments. In CIA mice, the clinical scores, levels of anti-collagen IgG antibody, and cartilage destruction were significantly reduced after adoptive transfusion with hCD8+Tregs. Moreover, hCD8+Treg treatment significantly reduced the number of Th17 cells, increased the number of CD4+IFN-γ+T cells, and produced self CD4+Foxp3+Tregs in vivo. In an in vitro cell coculture assay, hCD8+Tregs significantly inhibited mouse CD4+ effector T cell proliferation, induced mouse CD4+Foxp3+Treg and CD4+IFN-γ+Th1 cell production, reduced Th17 cell development, and downregulated CD80/86 expression on mature DCs (mDCs).Conclusion: TGF-β1/RAPA can induce hCD8+Tregs with stable suppressive characteristics, which could significantly alleviate the severity of CIA based on their stable suppressive ability in an inflammatory microenvironment and further influence the function of other downstream cell subtypes. Human CD8+Tregs might be a therapeutic strategy for rheumatoid arthritis. [ABSTRACT FROM AUTHOR]

Objective: To investigate the potential therapeutic effect in a rheumatoid arthritis model of stable human CD8 + regulatory T cells (hCD8 + Tregs) induced by TGF- β 1 and rapamycin (RAPA) in vitro ., Methods: Human CD8 + T cells were isolated from human peripheral blood mononuclear cells and induced/expanded with TGF- β 1 and RAPA along with anti-CD3/28 beads and IL-2 in vitro and harvested as hCD8 + Tregs. The phenotypes, suppressive characteristics, and stability of the hCD8 + Tregs in an inflammatory microenvironment were examined in vitro . Human CD8 + Tregs were transfused into an acollagen-induced arthritis (CIA) mouse model, and their therapeutic effects and related mechanisms were investigated., Results: Human CD8 + Tregs induced by TGF- β 1/RAPA showed high expression of Foxp3 and CD103, exhibited vigorous suppression ability, and were stable in inflammatory microenvironments. In CIA mice, the clinical scores, levels of anti-collagen IgG antibody, and cartilage destruction were significantly reduced after adoptive transfusion with hCD8 + Tregs. Moreover, hCD8 + Treg treatment significantly reduced the number of Th17 cells, increased the number of CD4 + IFN- γ + T cells, and produced self CD4 + Foxp3 + Tregs in vivo . In an in vitro cell coculture assay, hCD8 + Tregs significantly inhibited mouse CD4 + effector T cell proliferation, induced mouse CD4 + Foxp3 + Treg and CD4 + IFN- γ + Th1 cell production, reduced Th17 cell development, and downregulated CD80/86 expression on mature DCs (mDCs)., Conclusion: TGF- β 1/RAPA can induce hCD8 + Tregs with stable suppressive characteristics, which could significantly alleviate the severity of CIA based on their stable suppressive ability in an inflammatory microenvironment and further influence the function of other downstream cell subtypes. Human CD8 + Tregs might be a therapeutic strategy for rheumatoid arthritis.