BackgroundThere is substantial overlap in MRI findings between phyllodes tumors (PTs) and fibroadenomas (FAs). Our study was performed to investigate the value of conventional MRI texture analysis in the differential diagnosis of PTs and FAs.MethodsPreoperative MRI data − including axial T1WI, T2WI<sub>FS</sub> (T2WI with fat suppression), dynamic contrast-enhanced (DCE)-T1WI<sub>2min</sub> and DCE-T1WI<sub>7min</sub> (T1WI post-strengthened for 2 and 7 min, respectively, on DCE-MRI) − of 45 patients with PTs and 67 patients with FAs were retrospectively analyzed. MaZda 4.7 software was used to manually draw the maximum ROIs at the same lesion level of the above MRI images. The optimized feature selection methods included Fisher''s coefficient, probability of classification error and average correction coefficient (POE + ACC), and mutual information (MI) as well as a combination of the above 3 methods (F + POE + ACC + MI [FPM]), respectively. The misclassification rates of PTs and FAs were compared between texture analysis and subjective diagnosis by radiologists.ResultsThe DCE-T1WI<sub>7min</sub> images had the lowest misclassification rate of 10.71% (12/112). The misclassification rate for the radiologists'' analysis (31.25%, 35/112) was higher than that of all the texture analysis, and there was a statistically significant difference between the radiologists'' misclassification rates and those from the FPM method in terms of the T2WI<sub>FS</sub> and DCE-T1WI<sub>2min</sub> images (all p < 0.05), and for the DCE-T1WI<sub>7min</sub> images by using the Fisher and FPM methods (all p < 0.05).ConclusionTexture analysis of conventional MRI can be used as an assistant tool in providing a certain objective basis for differentiating PTs from FAs. 相似文献
microRNAs (miRNAs) play critical roles in embryogenesis, cell differentiation and the pathogenesis of several human diseases, including systemic lupus erythematosus (SLE). Toll-like receptors (TLRs) are also known to exert crucial functions in the immune response activation occurring in the pathogenesis of autoimmune diseases like SLE. Herein, the current study aimed to explore the potential role of miR-152-3p in TLR-mediated inflammatory response in SLE.
Methods
We determined the miR-152-3p expression profiles in CD4+ T cells and peripheral blood mononuclear cells (PBMCs) harvested from patients with SLE and healthy controls, and analyzed the correlation between miR-152-3p expression and clinicopathological parameters. CD70 and CD40L expression patterns in CD4+ T cells were assessed by RT-qPCR and flow cytometry. ChIP was adopted to determine the enrichment of DNA methyltransferase 1 (DNMT1) in the promoter region of myeloid differentiation factor 88 (MyD88).
Results
The obtained findings revealed that miR-152-3p was highly-expressed in CD4+ T cells and PBMCs of patients with SLE, and this high expression was associated with facial erythema, joint pain, double-stranded DNA, and IgG antibody. DNMT1 could be enriched in the MyD88 promoter, and miR-152-3p inhibited the methylation of MyD88 by targeting DNMT1. We also found that silencing miR-152-3p inhibited MyD88 expression not only to repress the autoreactivity of CD4+ T cells and but also to restrain their cellular inflammation, which were also validated in vivo.
Conclusion
Our study suggests that miR-152-3p promotes TLR-mediated inflammatory response in CD4+ T cells by regulating the DNMT1/MyD88 signaling pathway, which highlights novel anti-inflammatory target for SLE treatment.
BACKGROUND. Ebola virus (EBOV) causes periodic outbreaks of life-threatening EBOV disease in Africa. Historically, these outbreaks have been relatively small and geographically contained; however, the magnitude of the EBOV outbreak that began in 2014 in West Africa has been unprecedented. The aim of this study was to describe the viral kinetics of EBOV during this outbreak and identify factors that contribute to outbreak progression.METHODS. From July to December 2014, one laboratory in Sierra Leone processed over 2,700 patient samples for EBOV detection by quantitative PCR (qPCR). Viremia was measured following patient admission. Age, sex, and approximate time of symptom onset were also recorded for each patient. The data was analyzed using various mathematical models to find trends of potential interest.RESULTS. The analysis revealed a significant difference (P = 2.7 × 10–77) between the initial viremia of survivors (4.02 log10 genome equivalents [GEQ]/ml) and nonsurvivors (6.18 log10 GEQ/ml). At the population level, patient viral loads were higher on average in July than in November, even when accounting for outcome and time since onset of symptoms. This decrease in viral loads temporally correlated with an increase in circulating EBOV-specific IgG antibodies among individuals who were suspected of being infected but shown to be negative for the virus by PCR.CONCLUSIONS. Our results indicate that initial viremia is associated with outcome of the individual and outbreak duration; therefore, care must be taken in planning clinical trials and interventions. Additional research in virus adaptation and the impacts of host factors on EBOV transmission and pathogenesis is needed. 相似文献
The human brain can be inherently modeled as a brain network, where nodes denote billions of neurons and edges denote massive connections between neurons. 相似文献