comparing-transperitoneal-retroperitoneal-access-percutaneous

Comparing Transperitoneal Retroperitoneal Access and Percutaneous Puncture for Lumbar Disc Degeneration Modeling in Rabbits

This study compares the efficacy of two methods for inducing intervertebral disc degeneration (IVDD) in rabbits: percutaneous and trans-retroperitoneal ...

Chengdu University of Traditional Chinese Medicine

Most previous studies on acupuncture in the treatment of knee osteoarthritis (KOA) have focused on improving functional efficacy and safety, while related mechanisms have not been systematically reviewed. Acupuncture modulates cytokines to attenuate cartilage extracellular matrix degradation and apoptosis, key to the pathogenesis of KOA, but the mechanisms are complex.

Effects of acupuncture on cartilage p38MAPK and mitochondrial pathways in animal model of knee osteoarthritis: A systematic evaluation and meta-analysis.

The aim of this study was to investigate the protective effects of Tuina (a traditional Chinese massage therapy) on intervertebral disc (IVD) degeneration and the regulatory mechanisms of the transforming growth factor-β1 (TGF-β1)/small mothers against decapentaplegic (Smad) signaling pathway.

Effect of Tuina along "bladder meridian" alleviating intervertebral disc degeneration by regulating the transforming growth factor-β1/Smad signaling pathway in a rabbit model.

To construct a new prediction nomogram to predict the risk of musculoskeletal pain in patients with primary osteoporosis who receive zoledronic acid intravenously for the first time.

Prediction of musculoskeletal pain after the first intravenous zoledronic acid injection in patients with primary osteoporosis: development and evaluation of a new nomogram.

Several previous studies have reported an association between rheumatoid arthritis (RA) and epilepsy, but the causal relationship is unclear. The aim of this study was to assess the connection between RA and epilepsy in a European population using Mendelian randomization (MR).

Causal relationship between rheumatoid arthritis and epilepsy in a European population: a univariate and multivariate Mendelian randomization study.

The homeostasis of gastric mucosa is extremely delicate. Neutrophils, the most abundant immune cells in human circulation, are regarded crutial in the regulation of gastric mucosal immune response. Non-steroidal anti-inflammatory drugs (NSAIDs) induced gastric injury is the second major reason for gastric ulcers. The relations between neutrophils and Indomethacin-induced gastric injury are not fully understood. A mouse model of gastric injury was established using Indomethacin, followed by proteomic analysis (raw data are available via ProteomeXchange with identifier PXD058482). GO functional annotations and KEGG pathway enrichment analysis were conducted on significant differential proteins. The formation of neutrophil extracellular traps (NETs) was observed using ELISA and immunofluorescence. TEM, Western blot and Real-time PCR were applied to observe programmed death of gastric epithelial cells (GECs), and ELISA was conducted to measure levels of TNF-α and IL-1β in the gastric tissue. Deoxyribonuclease 1 (DNase 1), a NETs inhibitor, was administered intraperitoneally to inhibit NETs formation. In vitro, neutrophils were isolated from peripheral blood of mice and co-cultured with mouse GECs cell line, different dosage of Indomethacin were added to the culture dish, the levels of inflammatory factors, formation of NETs and GECs programmed death were assessed in vitro. Poly morphonuclear neutrophils (PMN) were extracted from mouse peripheral blood and single-cell RNA-sequencing (scRNA-seq) was further applied (raw data are available via Genome Sequence Archive with identifier CRA020950) to explore the intracellular mechanism of NETs formation. ELISA and immunofluorescence were performed to validate expression of IL-17 signaling pathway. After Indomethacin gavage, obvious gastric injury was observed. Proteomic analysis indicated that NETs formation played a crucial role in Indomethacin-induced gastric injury. Compared to control group, Indomethacin treatment resulted in NETs formation, elevated levels of TNF-α and IL-1β and GECs programmed death. Inhibition of NETs significantly reduced inflammatory factor levels and mitigated gastric injury caused by indomethacin. In vitro, 200 µL, 400 µL and 600 µL of Indomethacin caused excessive NETs formation in neutrophils. Besides, Indomethacin-induced NETs formation led to GECs programmed death in vitro. scRNA-seq revealed that neutrophils enrichment in the peripheral blood of Indomethacin-induced gastric injury and IL-17 signaling might be the key intracellular of NETs formation. Expressions of neutrophil IL-17R and concentration of IL-17 were significantly higher in model group. NETs formation is pivotal in Indomethacin-induced gastric injury, contributing to programmed cell death of GECs and inflammation; IL-17 signaling might be the key intracellular mechanism of NETs formation.

Article	Year
Effects of acupuncture on cartilage p38MAPK and mitochondrial pathways in animal model of knee osteoarthritis: A systematic evaluation and meta-analysis. Frontiers in neuroscience\| PubMed ID: 36711149	2022
Effect of Tuina along "bladder meridian" alleviating intervertebral disc degeneration by regulating the transforming growth factor-β1/Smad signaling pathway in a rabbit model. Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan\| PubMed ID: 37679987	2023
Prediction of musculoskeletal pain after the first intravenous zoledronic acid injection in patients with primary osteoporosis: development and evaluation of a new nomogram. BMC musculoskeletal disorders\| PubMed ID: 37880626	2023
Causal relationship between rheumatoid arthritis and epilepsy in a European population: a univariate and multivariate Mendelian randomization study. Frontiers in immunology\| PubMed ID: 38817604	2024
The crucial role of neutrophil extracellular traps and IL-17 signaling in indomethacin-induced gastric injury in mice. Scientific reports\| PubMed ID: 40204883	2025

Ye Jiangnan

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