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  1. Article ; Online: Clinical Analysis of Laparoscopic Common Bile Duct Primary Suture and T-Tube Drainage in the Treatment of Common Bile Duct Stones.

    Lu, Jiang / Zhang, Xiao / Zeng, Chao / Gu, Jin-Tao / Cai, Huihua

    Journal of laparoendoscopic & advanced surgical techniques. Part A

    2023  Volume 33, Issue 7, Page(s) 622–625

    Abstract: Background: ...

    Abstract Background:
    MeSH term(s) Humans ; Choledocholithiasis/surgery ; Choledocholithiasis/complications ; Retrospective Studies ; Common Bile Duct/surgery ; Gallstones/surgery ; Gallstones/complications ; Drainage/adverse effects ; Postoperative Complications/etiology ; Length of Stay ; Laparoscopy/adverse effects ; Sutures/adverse effects
    Language English
    Publishing date 2023-05-11
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1381909-4
    ISSN 1557-9034 ; 1092-6429
    ISSN (online) 1557-9034
    ISSN 1092-6429
    DOI 10.1089/lap.2022.0485
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: MicroRNA-98 ameliorates doxorubicin-induced cardiotoxicity via regulating caspase-8 dependent Fas/RIP3 pathway.

    Pan, Yang / Pan, Yu-Miao / Liu, Fang-Tong / Xu, Si-Lun / Gu, Jin-Tao / Hang, Peng-Zhou / Du, Zhi-Min

    Environmental toxicology and pharmacology

    2021  Volume 85, Page(s) 103624

    Abstract: Cardiotoxicity is one of the primary limitations in the clinical use of the anticancer drug doxorubicin (DOX). However, the role of microRNAs (miRNAs) in DOX-induced cardiomyocyte death has not yet been covered. To investigate this, we observed a ... ...

    Abstract Cardiotoxicity is one of the primary limitations in the clinical use of the anticancer drug doxorubicin (DOX). However, the role of microRNAs (miRNAs) in DOX-induced cardiomyocyte death has not yet been covered. To investigate this, we observed a significant increase in miR-98 expression in neonatal rat ventricular myocytes after DOX treatment, and MTT, LIVE/Dead and Viability/Cytotoxicity staining showed that miR-98 mimic inhibited DOX-induced cell death. This was also confirmed by Flow cytometry and Annexin V-FITC/PI staining. Interestingly, the protein expression of caspase-8 was upregulated by miR-98 mimics during this process, whereas Fas and RIP3 were downregulated. In addition, the effect of miR-98 against the expression of Fas and RIP3 were restored by the specific caspase-8 inhibitor Z-IETD-FMK. Thus, we demonstrate that miR-98 protects cardiomyocytes from DOX-induced injury by regulating the caspase-8-dependent Fas/RIP3 pathway. Our findings enhance understanding of the therapeutic role of miRNAs in the treatment of DOX-induced cardiotoxicity.
    MeSH term(s) Animals ; Antibiotics, Antineoplastic ; Cardiotoxicity/genetics ; Cardiotoxicity/metabolism ; Caspase 8/metabolism ; Cell Survival ; Cells, Cultured ; Doxorubicin ; Membrane Potential, Mitochondrial ; MicroRNAs ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/physiology ; Rats, Sprague-Dawley ; Receptor-Interacting Protein Serine-Threonine Kinases/metabolism ; Signal Transduction ; fas Receptor/metabolism ; Rats
    Chemical Substances Antibiotics, Antineoplastic ; Fas protein, rat ; MIRN98 microRNA-98, rat ; MicroRNAs ; fas Receptor ; Doxorubicin (80168379AG) ; Receptor-Interacting Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Ripk3 protein, rat (EC 2.7.11.1) ; Casp8 protein, rat (EC 3.4.22.-) ; Caspase 8 (EC 3.4.22.-)
    Language English
    Publishing date 2021-02-19
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 1318302-3
    ISSN 1872-7077 ; 1382-6689
    ISSN (online) 1872-7077
    ISSN 1382-6689
    DOI 10.1016/j.etap.2021.103624
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Coflex interspinous process dynamic stabilization for lumbar spinal stenosis: Long-term follow-up.

    Du, Ming-Rui / Wei, Fei-Long / Zhu, Kai-Long / Song, Ruo-Min / Huan, Yu / Jia, Bo / Gu, Jin-Tao / Pan, Lu-Xiang / Zhou, Hai-Ying / Qian, Ji-Xian / Zhou, Cheng-Pei

    Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia

    2020  Volume 81, Page(s) 462–468

    Abstract: Objective: To evaluate the long-term efficacy of Coflex dynamic stabilization device in the treatment of lumbar spinal stenosis.: Methods: The clinical and imaging data of 73 patients undergoing Coflex dynamic stabilization surgery from July 2008 to ... ...

    Abstract Objective: To evaluate the long-term efficacy of Coflex dynamic stabilization device in the treatment of lumbar spinal stenosis.
    Methods: The clinical and imaging data of 73 patients undergoing Coflex dynamic stabilization surgery from July 2008 to June 2012 were retrospectively analyzed. All patients had a minimum of 8 years of follow-up. Clinical data were used to assess the clinical efficacy, and radiographic parameters were measured for evaluation of ASD.
    Results: 56 Patients were followed up for 107.6 ± 13.3 months. The visual analogue scale of pain (VAS), Owestry disability index (ODI) and Japanese Orthopedic Association Scores (JOA) improved significantly after surgery. At 6 months after surgery and the last follow-up, lumbar range of motion (ROM) was significantly lower than that before surgery (P < 0.001). ROM was slightly increased at the last follow-up compared with that 6 months after operation (P > 0.05). ROM of adjacent segments increased at 6 months and at the last follow-up compared with that before surgery (P > 0.05). At 6 months after surgery, intervertebral space height (ISH) and intervertebral foramen height (IFH) of implanted segment was significantly higher than that before surgery (P < 0.05). At the last follow-up, there was a decrease in ISH and IFH (P > 0.05). During the follow-up period, a total of 11 patients (19.6%) experienced complications and 6 patients (10.7%) underwent secondary surgery.
    Conclusion: Coflex interspinous process dynamic stabilization is effective in the long-term treatment of lumbar spinal stenosis, the ISH and IFH of implanted segment could be increased in a short period of time.
    MeSH term(s) Adult ; Aged ; Decompression, Surgical/instrumentation ; Female ; Follow-Up Studies ; Humans ; Lumbar Vertebrae/surgery ; Male ; Middle Aged ; Neurosurgical Procedures/instrumentation ; Prostheses and Implants ; Range of Motion, Articular ; Retrospective Studies ; Spinal Stenosis/surgery ; Treatment Outcome
    Language English
    Publishing date 2020-11-01
    Publishing country Scotland
    Document type Journal Article
    ZDB-ID 1193674-5
    ISSN 1532-2653 ; 0967-5868
    ISSN (online) 1532-2653
    ISSN 0967-5868
    DOI 10.1016/j.jocn.2020.09.040
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Blockade of Discoidin Domain Receptor 2 as a Strategy for Reducing Inflammation and Joint Destruction in Rheumatoid Arthritis Via Altered Interleukin-15 and Dkk-1 Signaling in Fibroblast-Like Synoviocytes.

    Mu, Nan / Gu, Jin-Tao / Huang, Tong-Lie / Liu, Nan-Nan / Chen, Hui / Bu, Xin / Zheng, Zhao-Hui / Jia, Bo / Liu, Jun / Wang, Bao-Long / Wang, Ying-Mei / Zhu, Zhen-Feng / Zhang, Yong / Zhang, Ying-Qi / Xue, Xiao-Chang / Li, Meng / Zhang, Wei

    Arthritis & rheumatology (Hoboken, N.J.)

    2020  Volume 72, Issue 6, Page(s) 943–956

    Abstract: Objective: This study was undertaken to uncover the pathophysiologic role of discoidin domain receptor 2 (DDR-2), a putative fibrillar collagen receptor, in inflammation promotion and joint destruction in rheumatoid arthritis (RA).: Methods: In ... ...

    Abstract Objective: This study was undertaken to uncover the pathophysiologic role of discoidin domain receptor 2 (DDR-2), a putative fibrillar collagen receptor, in inflammation promotion and joint destruction in rheumatoid arthritis (RA).
    Methods: In synovial tissue from patients with RA and from mice with collagen antibody-induced arthritis (CAIA) (using Ddr2
    Results: DDR2 messenger RNA (mRNA) expression was significantly associated with the levels of IL-15 and Dkk-1 mRNA in the synovial tissue of RA patients (r
    Conclusion: These results indicate a novel role for activated DDR-2 in RA FLS, showing that DDR-2 is responsible for regulating the expression of IL-15 and Dkk-1 in RA FLS and is involved in the promotion of inflammation and joint destruction during pathophysiologic development of RA. Moreover, DDR-2 inhibition, acting through the H19-miR-103a axis, leads to reductions in the inflammatory reaction and severity of joint destruction in mice with CAIA, suggesting that inhibition of DDR-2 may be a potential therapeutic strategy for RA.
    MeSH term(s) Animals ; Arthritis, Experimental/metabolism ; Arthritis, Rheumatoid/genetics ; Discoidin Domain Receptor 2/metabolism ; Gene Expression Regulation ; Humans ; In Situ Hybridization, Fluorescence ; Inflammation ; Intercellular Signaling Peptides and Proteins/metabolism ; Interleukin-15/metabolism ; Mice ; Mice, Inbred DBA ; MicroRNAs/metabolism ; RNA, Long Noncoding/metabolism ; Signal Transduction/genetics ; Synovial Membrane/metabolism ; Synoviocytes/metabolism
    Chemical Substances Dkk1 protein, mouse ; H19 long non-coding RNA ; Intercellular Signaling Peptides and Proteins ; Interleukin-15 ; MIRN103 microRNA, mouse ; MicroRNAs ; RNA, Long Noncoding ; Discoidin Domain Receptor 2 (EC 2.7.10.1)
    Language English
    Publishing date 2020-05-02
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2756371-6
    ISSN 2326-5205 ; 2326-5191
    ISSN (online) 2326-5205
    ISSN 2326-5191
    DOI 10.1002/art.41205
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: DDR2-CYR61-MMP1 Signaling Pathway Promotes Bone Erosion in Rheumatoid Arthritis Through Regulating Migration and Invasion of Fibroblast-Like Synoviocytes.

    Huang, Tong-Lie / Mu, Nan / Gu, Jin-Tao / Shu, Zhen / Zhang, Kuo / Zhao, Jin-Kang / Zhang, Cun / Hao, Qiang / Li, Wei-Na / Zhang, Wang-Qian / Liu, Nan-Nan / Zhang, Yong / Zhang, Wei / Xue, Xiao-Change / Zhang, Ying-Qi

    Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research

    2019  Volume 34, Issue 4, Page(s) 779–780

    Language English
    Publishing date 2019-03-25
    Publishing country United States
    Document type Published Erratum
    ZDB-ID 632783-7
    ISSN 1523-4681 ; 0884-0431
    ISSN (online) 1523-4681
    ISSN 0884-0431
    DOI 10.1002/jbmr.3688
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: DDR2-CYR61-MMP1 Signaling Pathway Promotes Bone Erosion in Rheumatoid Arthritis Through Regulating Migration and Invasion of Fibroblast-Like Synoviocytes.

    Huang, Tong-Lie / Mu, Nan / Gu, Jin-Tao / Shu, Zhen / Zhang, Kuo / Zhao, Jin-Kang / Zhang, Cun / Hao, Qiang / Li, Wei-Na / Zhang, Wang-Qian / Liu, Nan-Nan / Zhang, Yong / Zhang, Wei / Xue, Xiao-Chang / Zhang, Ying-Qi

    Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research

    2016  Volume 32, Issue 2, Page(s) 407–418

    Abstract: Regulation of matrix metalloproteinases (MMPs) by collagen in the fibroblast-like synoviocytes (FLSs) plays a critical role in joint destruction in rheumatoid arthritis (RA). Our previous study indicated that discoidin receptor 2 (DDR2) mediated collagen ...

    Abstract Regulation of matrix metalloproteinases (MMPs) by collagen in the fibroblast-like synoviocytes (FLSs) plays a critical role in joint destruction in rheumatoid arthritis (RA). Our previous study indicated that discoidin receptor 2 (DDR2) mediated collagen upregulation of MMPs. However, the precise underlying mechanism remains unclear. We report here that CYR61, a secreted, extracellular matrix-associated signaling protein which is capable of regulating a broad range of cellular activities, including cell adhesion, migration, proliferation, and apoptosis, is significantly upregulated in collagen II-stimulated RA FLS. Further studies found that collagen II-activated phosphorylated-DDR2 induces CYR61 through activation of transcription factor activator protein 1 (AP-1). The elevated CYR61, in turn, accelerates MMP1 production via ETS1 (ETS proto-oncogene 1). In addition, CYR61 significantly promotes FLS invasion and migration. Blockade of CYR61 by an adenovirus expressing CYR61 shRNA (Ad-shCYR61) in vivo remarkably ameliorated the severity of arthritis, reduced inflammatory cytokine secretion, and attenuated bone erosion as detected by micro-computed tomography (μCT), in collagen-induced arthritis (CIA) rats. Taken together, we uncovered the Collagen II-DDR2-AP-1-CYR61-ETS1-MMP1 loop in RA FLS. In which, CYR61 acts as a hinge to promote cartilage damage through regulating FLS invasion, migration, and MMP1 production and the inflammatory cascade in RA. Thus, CYR61 may be a promising diagnostic and therapeutic target for RA treatment. © 2016 American Society for Bone and Mineral Research.
    MeSH term(s) Animals ; Arthritis, Experimental/pathology ; Arthritis, Rheumatoid/diagnostic imaging ; Arthritis, Rheumatoid/pathology ; Bone Resorption/pathology ; Cell Movement ; Cysteine-Rich Protein 61/metabolism ; Cytokines/biosynthesis ; Discoidin Domain Receptor 2/metabolism ; Fibroblasts/metabolism ; Fibroblasts/pathology ; Gene Knockdown Techniques ; Humans ; Inflammation/pathology ; Inflammation Mediators/metabolism ; Joints/pathology ; Male ; Matrix Metalloproteinase 1/metabolism ; Phosphorylation ; Rats, Wistar ; Signal Transduction ; Synovial Membrane/pathology ; Synoviocytes/pathology ; Transcription Factor AP-1/metabolism ; Up-Regulation
    Chemical Substances Cysteine-Rich Protein 61 ; Cytokines ; Inflammation Mediators ; Transcription Factor AP-1 ; DDR2 protein, human (EC 2.7.10.1) ; Discoidin Domain Receptor 2 (EC 2.7.10.1) ; Matrix Metalloproteinase 1 (EC 3.4.24.7)
    Language English
    Publishing date 2016-11-03
    Publishing country United States
    Document type Journal Article
    ZDB-ID 632783-7
    ISSN 1523-4681 ; 0884-0431
    ISSN (online) 1523-4681
    ISSN 0884-0431
    DOI 10.1002/jbmr.2993
    Database MEDical Literature Analysis and Retrieval System OnLINE

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