Osteoarthritis is a major cause of disability worldwide, and understanding epidemiological trends in osteoarthritis is critical for public health planning and intervention strategies. This study analyzed the global, regional, and national burden on osteoarthritis utilizing the Global Burden of Disease Study 2021. Trends from 1990 to 2021 were primarily assessed, with projections to 2050 based on demographic changes and historical data. In 2021, 607 (95% UI: 538–671) million people worldwide suffered from osteoarthritis, including 46.6 (95% UI: 41.1–51.6) million new cases, and the DALYs was 21.3 (95% UI: 10.2–42.9) million. Age-standardized incidence, prevalence and DALYs rates increased to 535.00/100,000 (95% UI: 472.38–591.97), 6967.29/100,000 (95% UI: 6180.70–7686.06), and 244.50/100,000 (95% UI: 117.06–493.11), with knee osteoarthritis accounting for more than 56%. Age-standardized rates of osteoarthritis were higher in females than in males. East Asia, South Asia, and Western Europe were the regions and China, India, and the United States were the countries with the highest burdens. In addition, high body-mass index led to 4.43 (95% UI: -0.42–12.34) million DALYs, with an increase of 205.10%. Bayesian age-period cohort projections showed that the burden of osteoarthritis would continue to rise from 2021 to 2050. As an ageing population and rising obesity rates, the burden of osteoarthritis will continue to rise, with females and the middle-aged and older age groups being the current populations of concern. Awareness-raising, early detection, and effective management are essential to reduce the burden of osteoarthritis in the coming decades, especially among vulnerable groups.

Background: Macrophage migration inhibitory factor ( MIF ) is a key regulator of inflammatory responses, including in the heart. Plasma MIF is elevated early in the course of acute myocardial infarction. In this study, we hypothesized that plasma MIF may also be increased in acute myocardial ischemia. Methods and Results: Patients undergoing cardiac stress test (stress nuclear myocardial perfusion scan or stress echocardiography) were recruited. Twenty‐two patients had a stress test indicative of myocardial ischemia and were compared with 62 patients who had a negative stress test. Plasma MIF was measured by ELISA before and after the stress test. MIF was also measured in patients with peripheral arterial occlusive disease before and after exercise causing claudication. Gene and protein expression of MIF was measured in mouse cardiac and skeletal muscle tissue by real‐time polymerase chain reaction and western blot, respectively. Plasma MIF was elevated at 5 and 15 minutes after stress (relative to before stress) in patients with a positive test, compared with those with a negative test. In contrast, high‐sensitivity troponin T and C‐reactive protein were not altered after stress in either group. MIF was not altered after exercise in PAOD patients, despite the occurrence of claudication, suggesting that plasma MIF is not a marker for skeletal muscle ischemia. This may be explained by a lower gene and protein expression of MIF in skeletal muscle than the heart. Conclusions: Our results suggest that plasma MIF is an early marker for acute myocardial ischemia.

T-2 toxin is known to cause tissue and cellular damage, with chondrocytes being particularly vulnerable. In contrast, chondroitin sulfate A-selenium nanoparticles (CSA-SeNP) have shown cartilage-protective properties, although the precise molecular mechanism remains incompletely elucidated. This study used T-2 toxin and CSA-SeNP to treat human C28/I2 chondrocytes, and studied their effects on SIRT1-AMPK-FOXO3 pathway and oxidative damage, mitochondrial dysfunction, impaired autophagy, and apoptosis. Autophagy was evaluated by acridine orange (AO) and dansylcadaverine (MDC) staining, transmission electron microscopy observation, and mRFP-GFP-LC3 adenovirus. Oxidative stress (ROS, MDA, SOD, CAT, T-AOC) and mitochondrial function (ATP, SDH, ATPases, membrane potential) were assessed. Western blotting analyzed the expression level of the SIRT1-AMPK-FOXO3 pathway, autophagy markers, and apoptosis. We found that 4-hour exposure to 5 and 20 ng/mL, as well as 12-hour exposure to 5 ng/mL of T-2 toxin, activated the SIRT1-AMPK-FOXO3 pathway compensatively, inducing autophagy but inhibiting degradation of autolysosome, leading to oxidative damage, mitochondrial dysfunction, and increased apoptosis. 12-hour exposure to 20 ng/mL T-2 toxin inhibited this pathway and autophagy, causing serious damage to chondrocytes. CSA-SeNP alleviated the inhibition of the SIRT1-AMPK-FOXO3 pathway induced by T-2 toxin, reducing oxidative damage, mitochondrial dysfunction and apoptosis, thereby restoring autophagy to protect chondrocytes. In summary, T-2 toxin's effects on chondrocyte autophagy were dose- and time-dependent. CSA-SeNP protected against T-2 toxin by activating the SIRT1-AMPK-FOXO3 pathway, suggesting its potential for chondrocyte protection. This study may provide new insights into the development of T-2 toxin detoxification strategies and the method for prevention and treatment of chondrocyte damage.

OBJECTIVE: Identification of interstitial lung disease (ILD) may be difficult in certain cases using pulmonary function tests (PFTs) or subjective radiological analysis. We evaluated the efficacy of quantitative computed tomography (CT) with 3-dimensional (3D) reconstruction for distinguishing ILD patients from healthy controls. MATERIALS AND METHODS: We retrospectively collected chest CT images of 102 ILD patients and 102 healthy matched controls, and measured the following parameters: lung parenchymal volume, emphysema indices low attenuation area LAA910 volume, LAA950 volume, LAA910%, and LAA950%, and mean lung density (MLD) for whole lung, left lung, right lung, and each lobe, respectively. The Mann-Whitney U test was used to compare quantitative CT parameters between groups. Receiver operating characteristic (ROC) curves, Bayesian stepwise discriminant analysis, and deep neural network analysis were used to test the discriminative performance of quantitative CT parameters. Binary logistic regression was performed to identify ILD markers. RESULTS: Total lung volume was lower in ILD patients than controls, while emphysema and MLD values were higher ( P < 0.001) except LAA910 volume in right middle lobe. LAA910 volume, LAA950 volume, LAA910%, LAA950%, and MLD accurately distinguished ILD patients from healthy controls (AUC >0.5, P < 0.05), and high MLD was a significant marker for ILD (OR = 1.047, P < 0.05). CONCLUSIONS: This quantitative CT analysis can effectively identify ILD patients, providing an alternative to subjective image analysis and PFTs.