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ObjectiveTo study the association of serum adiponectin and high sensitivity C-reactive protein (hs-CRP) levels to short-term outcome in patients with acute ischemic stroke (AIS). MethodsClinical data of 216 patients with AIS in Beijing Bo'ai Hospital from January, 2019 to September, 2020 were collected. The serum biochemical indicator was measured in all the patients within 24 hours after enrollment, and adiponectin was detected with enzyme-linked immunosorbent assay. Meanwhile, all patients were evaluated with National Institute of Health Stroke Scale (NIHSS). Modified Rankin Scale (mRS) was used to assess the functional outcome 90 days after onset during follow-up. ResultsThe incidence of poor outcome in patients with AIS within 90 days was 48.1%. Compared with the good outcome group, the serum adiponectin was lower (t = 5.861, P < 0.001) and the serum hs-CRP level was higher (Z = 5.525, P < 0.001) poor outcome group. Reduced serum adiponectin (OR = 0.862, 95%CI 0.751 to 0.975, P < 0.001) and increased serum hs-CRP (OR = 1.215, 95%CI 1.015 to 1.455, P < 0.001) were independent risk factors for poor outcome in patients with AIS. The areas under curve (95% CI) of serum adiponectin and hs-CRP for predicting the outcome of patients with AIS were 0.819 (0.761 to 0.877) and 0.722 (0.654 to 0.791), respectively (P < 0.001). The predictive power of serum adiponectin was higher than that of hs-CRP (Z = 2.151, P = 0.032). The optimum cut-off point of adiponectin was < 3.5 mg/L, and the Yoden index was 0.609, yielding a sensitivity of 0.704 and a specificity of 0.905. ConclusionSerum adiponectin and hs-CRP can serve as independent predictors for short functional outcome in patients with AIS.
RESUMO
The interplay between mechanoresponses and a broad range of fundamental biological processes, such as cell cycle progression, growth and differentiation, has been extensively investigated. However, metabolic regulation in mechanobiology remains largely unexplored. Here, we identified glucose transporter 1 (GLUT1)-the primary glucose transporter in various cells-as a novel mechanosensitive gene in orthodontic tooth movement (OTM). Using an in vivo rat OTM model, we demonstrated the specific induction of Glut1 proteins on the compressive side of a physically strained periodontal ligament. This transcriptional activation could be recapitulated in in vitro cultured human periodontal ligament cells (PDLCs), showing a time- and dose-dependent mechanoresponse. Importantly, application of GLUT1 specific inhibitor WZB117 greatly suppressed the efficiency of orthodontic tooth movement in a mouse OTM model, and this reduction was associated with a decline in osteoclastic activities. A mechanistic study suggested that GLUT1 inhibition affected the receptor activator for nuclear factor-κ B Ligand (RANKL)/osteoprotegerin (OPG) system by impairing compressive force-mediated RANKL upregulation. Consistently, pretreatment of PDLCs with WZB117 severely impeded the osteoclastic differentiation of co-cultured RAW264.7 cells. Further biochemical analysis indicated mutual regulation between GLUT1 and the MEK/ERK cascade to relay potential communication between glucose uptake and mechanical stress response. Together, these cross-species experiments revealed the transcriptional activation of GLUT1 as a novel and conserved linkage between metabolism and bone remodelling.