The Sheng Jing (盛京) Hospital was founded by Dugald Christie (missionary) (1855-1936), a Scottish missionary doctor in 1883. It was the base on which the Mukden Medical College was formed, also by Christie, in 1912. In 1949 the Mukden Medical College was absorbed by the China Medical University and the hospital became known as the 2nd Affiliated hospital of the China Medical University. In 1969 it was moved, by Chairman Mao, to Chaoyang but returned to Shenyang in 1983. In 2002 the hospital took over the Third Affiliated Hospital of the China Medical University and set up the Huaxiang Campus. In 2003, on the 120th anniversary of its founding, it restored the name as Shenjing Hospital. It is situated near the famous San Hao Jie (Computer town)三好街. The hospital is one of the largest hospitals in the city of Shenyang, Liaoning Province. Its motto is "United and dedicated; Disciplined and responsible; Caring and trustworthy; Professional and innovative."In 2012 a history of the hospital and Dr Christie was published by Liaoning University Press.The hospital is known for its famous specialists clinic.Address:36 No.
By analyzing the single-cell RNA-Seq libraries we established of OA joints during exercise therapy, we found cartilage intermediate zone might participate in early OA exercise therapy. Early OA rat model was established by 4-week anterior cruciate ligament transection (ACLT). The radiomics was used to evaluate the relative damaged and undamaged area in OA patients’ cartilage. We overexpressed and knocked down CILP in early OA chondrocyte to explore its potential mechanism. The quantitative proteomics was used to examine the protein profiles of the CILP-treated chondorcyte. The Yeast One-Hybrid Assay, Co-Immunoprecipitation (Co-IP), Nrf2 cytosol-nuclei fractionation and ubiquitination assay were used to investigate the potential mechanism in CILP intervention. Western blot, ROS, JC-1, Ferrous ion, MDA and GSH detection, transmission electron microscopy (TEM) were used to explored the therapeutic effect of CILP on OA. Moderate exercise up-regulates CILP in the articular cartilage intermediate zone. CILP recovers the ratio of type II / I collagen, Sox9, α-SMA expression and competitively bind to Keap1 protein and reduce the stability of Keap1-Nrf2 dimer, thereby reducing the degree of Nrf2 ubiquitination and promoting Nrf2 nuclear translocation. Nrf2 nuclear translocation activated SLC7A11, HO-1, GPX4 and SOD-1 expression, then decreased the MDA contents, but increased GSH content, which ultimately inhibited chondrocytes ferroptosis and promoted hyalinization of fibrocartilage. Exercise induced cartilage intermediate zone and CILP-Keap1-Nrf2 axis inhibits hyaline cartilage fibrosis and chondrocyte ferroptosis to alleviate early osteoarthritis.
Objective Axial spondyloarthritis is a chronic inflammatory disease characterized by bone destruction and pathological new bone formation, in which osteoclasts play a key role, and elevated cholesterol levels enhance osteoclast function. This study sought to investigate whether cholesterol metabolic disorder contributes to the severity of spinal inflammation in axial spondyloarthritis. Methods This prospective study enrolled 92 axSpA patients and collected clinical and laboratory data. MRI quantified acute spinal inflammation (SPARCC score), chronic spinal inflammation (vertebral fat fraction, VFF), as well as lipid metabolism-related imaging parameters, including liver fat fraction (LFF) and subcutaneous-to-visceral adipose ratio (SAT/VAT). To identify independent factors associated with imaging spinal inflammation and adjust for potential confounders, univariate linear regression and multivariable linear regression analyses were performed using three incrementally adjusted models: Model 1 adjusted for demographics; Model 2 additionally adjusted for inflammatory markers (CRP, ESR) and disease activity indices (BASDAI, ASDAS-CRP); Model 3 further adjusted for functional/structural impairment scores (BASMI, BASFI, mSASSS). Results In the fully adjusted multivariable regression model (Model 3), current smoking (β = 16.727, P = 0.001), Chol/HDL ratio (β = 4.253, P = 0.021), LDL/HDL ratio (β = 5.114, P = 0.038), and LFF (β = 1.014, P = 0.016) were independently associated with the SPARCC score; while current smoking (β = 3.646, P = 0.040), total cholesterol (β = 1.544, P = 0.050), Chol/HDL ratio (β = 1.399, P = 0.030), and LFF (β = 0.404, P = 0.005) were independently associated with VFF. Conclusion Elevated total Chol, Chol/HDL ratio, and LDL/HDL ratio—collectively reflecting a cholesterol metabolic disorder—were independently and positively associated with the severity of both acute and chronic spinal inflammation. These findings suggest that the cholesterol metabolic status of axSpA patients warrants greater attention in clinical evaluation. Trial Registration: Chinese Clinical Trial Registry, ChiCTR2500113832. Retrospectively registered on 03/12/2025.
Cyclohexane-1,2-dicarboxylic acid diisononyl ester (DINCH), as a "green" alternative to phthalates, has been widely used in consumer products and industrial materials. Consequently, its environmental and human exposure levels continue to rise, necessitating a systematic evaluation of its mechanism of intestinal toxicity. This study developed a strategy integrating "network toxicology-machine learning-molecular simulation-experimental validation": First, multiple databases were combined to identify potential intestinal toxicity targets of DINCH, followed by the construction of a PPI network and the identification of the core pathway "metabolic pathway" through GO/KEGG enrichment. Subsequently, ENO1 was selected by machine learning. Molecular docking and molecular dynamics simulations consistently demonstrate a interaction between DINCH and ENO1. In vitro experiments confirmed that high concentrations of DINCH significantly downregulated ENO1 expression and attenuated the H₂O₂-induced increase in ENO1 levels, leading to ROS accumulation, mitochondrial dysfunction, and lipid peroxidation. Furthermore, experiments with ENO1 gene silencing demonstrated that DINCH-induced lipid peroxidation was dependent on ENO1. Exogenous supplementation of PA significantly reversed DINCH-triggered mitochondrial damage, and lipid peroxidation. NAC and Mito-TEMPO interventions also alleviated the H₂O₂ + DINCH-induced lipid peroxidation. In summary, this study is the first to elucidate the novel molecular mechanism by which DINCH aggravates H2O2-induced ROS-ENO1-dependent oxidative stress, providing critical scientific evidence for revising its safety thresholds, managing exposure risks, and developing next-generation alternative plasticizers.
