ObjectiveThe aim of this study was to explore the association between quadriceps strength and synovitis in the knee osteoarthritis (KOA).MethodsThis study was derived from the Osteoarthritis Initiative (OAI) cohort which recruited adults with or at risk of KOA. Knees with complete records of isometric quadriceps strength, effusion-synovitis and Hoffa-synovitis assessments were included. Quadriceps strength was measured isometrically at baseline. Effusion-synovitis and Hoffa-synovitis were measured using Magnetic Resonance Imaging Osteoarthritis Knee Score (MOAKS) at baseline, 1-year and 2-year follow-ups. Generalized estimating equations were used to analyze the associations of baseline quadriceps strength with the effusionsynovitis and Hoffa-synovitis changes in multivariable analyses. Additionally, analyses were stratified on synovitis-driven inflammatory phenotype.Results1513 knees were included in this study. 61.0% of the subjects were female, with an average age of 61.9 years and mean BMI of 29.4 kg/m2. In the whole population, baseline quadriceps strength was negatively associated with the baseline effusion-synovitis and follow-up changes in effusion-synovitis (OR: 0.77-0.86), but no significant association was observed in terms of Hoffa-synovitis. Stratified by synovitis-driven inflammatory phenotypes, baseline quadriceps strength was significantly associated with follow-up changes in effusion-synovitis in the population with existed effusion-synovitis (OR: 0.75-0.79), but not in Hoffa-synovitis.ConclusionHigher baseline quadriceps strength was negatively associated with the changes in effusion-synovitis instead of Hoffa-synovitis, especially in the population with existed effusion-synovitis. Our finding suggested a potential protective role of quadriceps in effusion-synovitis.
Aging is a non-modifiable risk factor for stroke and the global burden of stroke is continuing to increase due to the aging society. Muscle dysfunction, common sequela of stroke, has long been of research interests. Therefore, how to accurately assess muscle function is particularly important. Electrical impedance myography (EIM) has proven to be feasible to assess muscle impairment in patients with stroke in terms of micro structures, such as muscle membrane integrity, extracellular and intracellular fluids. However, EIM alone is not sufficient to assess muscle function comprehensively given the complex contributors to paretic muscle after an insult. This article discusses the potential to combine EIM and other common quantitative methods as ways to improve the assessment of muscle function in stroke survivors. Clinically, these combined assessments provide not only a distinct advantage for greater accuracy of muscle assessment through cross-validation, but also the physiological explanation on muscle dysfunction at the micro level. Different combinations of assessments are discussed with insights for different purposes. The assessments of morphological, mechanical and contractile properties combined with EIM are focused since changes in muscle structures, tone and strength directly reflect the muscle function of stroke survivors. With advances in computational technology, finite element model and machine learning model that incorporate multi-modal evaluation parameters to enable the establishment of predictive or diagnostic model will be the next step forward to assess muscle function for individual with stroke.
A high-methionine (HM) diet leads to hyperhomocysteinemia (HHcy), while gastrointestinal tissue is an important site of net homocysteine (Hcy) production. However, the role of the gut microbiota in host HHcy remains obscure. This study aimed to determine whether gut microbiota ablation could alleviate host HHcy and glucose intolerance and reveal the underlying mechanism. The results showed that the HM diet-induced HHcy and glucose intolerance in mice, while antibiotic administration decreased the plasma level of Hcy and reversed glucose intolerance. HM diet increased intestinal epithelial homocysteine levels, while antibiotic treatment decreased intestinal epithelial homocysteine levels under the HM diet. Gut microbiota depletion had no effect on the gene expression and enzyme activity of CBS and BHMT in the livers of HM diet-fed mice. The HM diet altered the composition of the gut microbiota with marked increases in the abundances of Faecalibaculum and Dubosiella, which were also positively correlated with plasma Hcy concentrations. An in-depth analysis of the bacterial cysteine and methionine metabolism pathways showed that the abundances of two homocysteine biosynthesis-related KEGG orthologies (KOs) were markedly increased in the gut microbiota in HM diet-fed mice. Hcy was detected from Dubosiella newyorkensis-cultured supernatant by liquid chromatography–tandem mass spectrometry (LC‒MS) analysis. In conclusion, these findings suggested that the HM diet-induced HHcy and glucose intolerance in mice, by reshaping the composition of the gut microbiota, which might produce and secrete Hcy.
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