Background The association between nonalcoholic fatty liver disease (NAFLD) and free triiodothyronine (FT3) in euthyroid subjects was in dispute. We aimed to investigate this issue in a population‐based cohort study. Materials and methods A total of 3144 euthyroid subjects at baseline from the Shanghai Nicheng Atherosclerosis Study were selected for the cross‐sectional analysis, and 2089 subjects being followed up after 2.2 years were selected for the longitudinal analysis. NAFLD was diagnosed by ultrasound. The cut‐off point of elevated alanine aminotransferase (ALT) level was 40 U/L. The FIB‐4 index was used to assess the risk of advanced liver fibrosis. Results Age‐adjusted mean levels of FT3 and FT3/free thyroxine (FT4) ratio were higher in subjects with NAFLD than those without NAFLD and linearly increased with a higher risk of NAFLD progression (assessed by levels of ALT and FIB‐4 index) in euthyroid women but not in men. After adjustment for confounding variables, FT3 levels significantly increased with the presence of NAFLD (β = 0.1, P < 0.001) and linearly increased with a higher risk of NAFLD progression in euthyroid women. After a 2.2‐year follow‐up, FT3 levels increased with the occurrence of NAFLD (mean change percentage: 1.4%) and decreased with the remission of NAFLD (mean change percentage: −2.7%) in euthyroid women. Conclusions There are positive associations of FT3 levels with NAFLD and the risk of NAFLD progression in euthyroid women. The changes in FT3 levels with the alteration of NAFLD status may be an adaptive response to maintain energy and metabolic homeostasis.
Hypoxia, a hallmark of cancer, compromises the efficacy of chemotherapy and other oxygen-dependent modalities (e.g., sonodynamic therapy). For monotherapy, this effect becomes more pronounced because of drug resistance and an adaptive tumor microenvironment. To overcome this, here, we reported metal–organic framework (MOF)-based nanotherapeutics (DOX/Ce6@ZIF-8@PDA) to simultaneously deliver Ce6 and doxorubicin for synergistic sonodynamic/chemotherapy. Notably, O2 storage ability of MOFs relieves tumor hypoxia to sensitize the tumor to sonodynamic therapy and chemotherapy. Moreover, polydopamine (PDA) promotes endocytosis and enhances intracellular drug concentration. The pH-responsive property of MOFs enables controlled drug release. The in vitro and in vivo results validate the impressive tumor inhibition, implying the potential of this combination therapy for cancer treatment.
PURPOSE: To evaluate the diagnostic value of shear wave velocity (SWV) ratio for the differential diagnosis of benign and malignant breast lesions. MATERIAL AND METHODS: Our retrospective study included 151 breast lesions that were diagnosed by biopsy and surgical pathology. All of the breast lesions were detected by conventional ultrasound and Virtual Touch tissue quantification (VTQ) and mammography. The sonographic characteristics of the breast lesion, such as the internal echo, shape, margin, color flow, and calcification so on, were also observed. The SWV in lesions and surrounding parenchyma were measured and the SWV ratio between the lesion and surrounding parenchyma was calculated. Pathological results were used as a diagnosis standard to compare the value of SWV ratio, VTQ, and mammography in the diagnosis of benign and malignant breast lesions. RESULTS: The 151 breast lesions included 96 benign lesions and 55 malignant lesions. The cutoff value of VTQ in the diagnosis of benign and malignant breast lesions was 5.01 m/s, of SWV ratio was 2.43, and mammography was BI-RADS 4B. The sensitivity, specificity, accuracy and the area under the ROC curve (AUC) of the SWV ratio were 78.2%, 86.5%, 83.4%, and 0.83 respectively. While of SWV ratio with mammography was 86.4%, 89.4%, 88.3% and 0.87, respectively. The sensitivity, specificity, accuracy, and AUC of SWV ratio and SWV ratio with mammography were statistically higher than those of mammography, no statistically higher than VTQ and VTQ with mammography. CONCLUSION: The SWV ratio can improve the sensitivity without sacrificing diagnostic specificity in the process of breast cancer diagnostic, provide a better diagnostic performance, and avoid unnecessary biopsy or surgery.
Upon recognition of the pathogen components by PRR (pattern recognition receptors), then the cells could be activated to produce inflammatory cytokines and type I interferons. The inflammation is tightly modulated by the host to prevent inappropriate inflammatory responses. MicroRNAs (miRNAs) are non-coding and small RNAs that can inhibit gene expression and participate in various biological functions, including maintaining a balanced immune response in the host. To maintain the balance of the immune response, these pathways are closely regulated by the host to prevent inappropriate reactions of the cells. However, in low vertebrates, the miRNA-mediated inflammatory response regulatory networks remain largely unknown. Here, we report that two miRNAs, miR-20-1 and miR-101a are identified as negative regulators in teleost inflammatory responses. Initially, we find that both miR-20-1 and miR-101a dramatically increased after lipopolysaccharide (LPS) stimulation and Vibrio harveyi infection. Upregulated miR-20-1 and miR-101a inhibit LPS-induced inflammatory cytokines production by targeting TNF receptor-associated factor 6 (TRAF6), thus avoiding excessive inflammation. Moreover, miR-20-1 and miR-101a regulate the inflammatory responses through the TRAF6-mediated nuclear factor kappa (NF-κB) signaling pathways. Collectively, these data indicate that miR-20-1 and miR-101a act as negative regulators through regulating the TRAF6-mediated NF-κB signaling pathway, and participate in the host antibacterial immune responses, which will provide new insight into the intricate networks of the host-pathogen interaction in the lower vertebrates.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.