Demographic and clinical characteristics of patients with active TB and controls.

<p>Note: ¹ Erythrocyte sedimentation rate; ²The absolute number of monocytes was determined by white blood cell count; ³% of CD14⁺ Monocytes was determined by flow cytometry.</p

<i>FOXO1</i> is a direct target of miR-582-5p.

<p>(A) Alignment between the predicted miR-582-5p target site of <i>FOXO1</i> 3′UTR region and miR-582-5p. (B) Real time RT-PCR and western blot analysis showing <i>FOXO1</i> mRNA and protein expression levels in THP-1 cells transfected with miR-582-5p mimics or mimics NC, respectively. (C) Co-transfection of miR-582-5p mimics/mimics NC and <i>FOXO1</i> 3′UTR-luciferase reporter vector into HEK-293T cells demonstrated that significant decrease in luciferase activity was only found in reporter vector that contained a wild type sequence (FOXO1-3′UTR-wt), not in vector that contained a mutant sequence (FOXO1-3′UTR-mut) within the miR-582-5p binding site. Values were presented as relative luciferase activity after normalization to Renilla luciferase activity. FOXO1-3′UTR-wt: pMIR-FOXO1-3′UTR-wt vector; FOXO1-3′UTR-mut: pMIR-FOXO1-3′UTR-mut vector. (D) Representative flow cytometric plots showing apoptotic ratio of THP-1 transfected with <i>FOXO1</i> siRNA or negative controls of siRNA (siRNA NC) (left panel). The apoptotic percentage of THP-1 cells transfected with <i>FOXO1</i> siRNA were significantly lower than those transfected with negative control siRNA (siRNA NC) (<i>p</i><0.01).</p

miR-582-5p expression detected by real-time RT-PCR.

<p>(A) Relative expression of miR-582-5p in CD3⁻CD33⁺, CD3⁻CD33⁻, CD3⁺ cell subsets and in PBMCs from patients with active TB (n = 3). miR-582-5p was mainly expressed in CD3⁻CD33⁺ cells. (B) Patients with active TB had significantly higher expression of miR-582-5p as compared with healthy controls. The relative expression of miR-582-5p, as defined by mean -ΔCt, was normalized against U6 snRNA. Two-tailed unpaired t-test was used for statistical analysis between groups.</p

Inhibition of apoptosis in monocytes by miR-582-5p.

<p>(A) Representative flow cytometric plots showing apoptotic percentage of THP-1 cells transfected with miR-582-5p mimics or negative control of mimics (mimics NC). (B) The apoptotic percentage of THP-1 cells transfected with miR-582-5p mimics was significantly lower than those transfected with negative control of microRNA mimics (mimics NC).</p

Frequencies and apoptosis of CD14⁺ peripheral blood monocytes in patients with active TB and healthy controls.

<p>(A) Representative flow cytometric plots showing gating strategy and percentage of monocytes (left panel). Monocytes were defined by high CD14 expression (gate BV). Patients with active TB had significantly elevated frequency of CD14⁺ monocytes compared with healthy controls. Two-tailed unpaired t-test was used for statistical analysis between groups. (B) Representative flow cytometric plots showing apoptosis of monocytes (upper panel). PBMCs from patients with active TB and healthy controls were incubated with RPMI-1640 contained 2% FBS for 24 h at 37°C, and cells were stained with fluorochrome-labeled anti-human CD14, Annexin V and PI. Cells that were positive for Annexin V were defined as apoptosis. Monocytes from patients with active TB had significantly lower percentage of apoptotic cells than that from healthy controls. Mann-Whitney test was used for statistical analysis between groups.</p

List of predicted target genes of miR-582-5p.

<p>List of predicted target genes of miR-582-5p.</p

Micromorphology of Asphalt Modified by Polymer and Carbon Nanotubes through Molecular Dynamics Simulation and Experiments: Role of Strengthened Interfacial Interactions

Polymer modifiers have been used to improve the performances of asphalt binders in pavement engineering. The modifying effect of polymers on asphalt is largely dependent on the morphological characteristics of polymer-modified asphalt. The morphologies of polymer-modified asphalt are composed of a polymer-rich phase, a asphaltene-rich phase, and the interphase between the two phases. Interfacial interactions importantly contribute to the morphology but are commonly overlooked. In this study, carbon nanotubes (CNTs) were selected to improve the interfacial interactions of polymer-modified asphalt. Fluorescence microscopy (FM), scanning electron microscopy (SEM), micro-Raman spectroscopy (MRS), and molecular dynamics (MD) simulation were used to capture the characteristics of the interphase and polymer-rich phase. CNTs-polymer-modified asphalt involves stronger intermolecular forces than those in asphalt-modified by only styrene–butadiene–styrene (SBS) or CNTs. This discrepancy highlights the intensified interfacial interaction in the former material. Raman peak and MD findings reveal that the CC of CNTs interacted with the alkanes and aromatic hydrocarbons of asphalt. SBS were entwined or surrounded with CNTs through the π–π conjugation of the benzene rings of the two components. Consequently, a synergistic effect enhanced the intermolecular force between SBS and CNTs in the interphase. SEM results indicated that CNTs were enriched in the interphase, enhancing mechanical anchorage between the polymer and asphalt. As a result, CNTs increased the roughness of the interphase and produced a prominent cage construction of polymer-rich phase. Moreover, the observed pullout behaviors of CNTs alleviated interfacial failure. FM images displayed that CNTs enhanced the swelling degree of the polymer-rich phase. This effect was realized because CNTs served as a tunnel for transporting saturates, aromatics, and small resin molecules, as shown by molecular dynamics MD analysis. This work revealed the importance of the interfacial interactions on the micromorphologies of polymer-modified asphalt

Evaluating the Significance of Viscoelasticity in Diagnosing Early-Stage Liver Fibrosis with Transient Elastography

<div><p>Transient elastography quantifies the propagation of a mechanically generated shear wave within a soft tissue, which can be used to characterize the elasticity and viscosity parameters of the tissue. The aim of our study was to combine numerical simulation and clinical assessment to define a viscoelastic index of liver tissue to improve the quality of early diagnosis of liver fibrosis. This is clinically relevant, as early fibrosis is reversible. We developed an idealized two-dimensional axisymmetric finite element model of the liver to evaluate the effects of different viscoelastic values on the propagation characteristics of the shear wave. The diagnostic value of the identified viscoelastic index was verified against the clinical data of 99 patients who had undergone biopsy and routine blood tests for staging of liver disease resulting from chronic hepatitis B infection. Liver stiffness measurement (LSM) and the shear wave attenuation fitting coefficient (AFC) were calculated from the ultrasound data obtained by performing transient elastography. Receiver operating curve analysis was used to evaluate the reliability and diagnostic accuracy of LSM and AFC. Compared to LSM, the AFC provided a higher diagnostic accuracy to differentiate early stages of liver fibrosis, namely F1 and F2 stages, with an overall specificity of 81.48%, sensitivity of 83.33% and diagnostic accuracy of 81.82%. AFC was influenced by the level of LSM, ALT. However, there are no correlation between AFC and Age, BMI, TBIL or DBIL. Quantification of the viscoelasticity of liver tissue provides reliable measurement to identify and differentiate early stages of liver fibrosis.</p></div

Finite element model of liver tissue and the mesh generated.

<p>(A) An idealized 3D model. (B) An idealized two-dimensional axisymmetric finite element model of liver tissue adopted in our study. (C) The generated finite element mesh (22,500 finite elements).</p

Peak axial displacements along the depth of propagation for the simulated dataset, viscosity (<i>μ</i>₂) are set as 0/0.5/1/2/4 Pa·s in per subfigure.

<p><b>Young's modulus (E) in each subfigure:</b> (A) E = 4 kPa, (B) E = 6 kPa, (C) E = 8 kPa, and (D) E = 10 kPa.</p