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Additional file 1: Table S1. Baseline tumor markers and inflammation index of patients with colorectal cancer. Fig. S1. Coefficients deviance of the LASSO analysis. Fig. S2. A, B, C X-tile analysis on the optimal cutoff points of NSAP. Fig. S3. A Kaplan-Meier curves for disease-free survival of CRC patients. according to the stage; B according to alpha-fetoprotein (AFP); C according to carcinoembryonic antigen (CEA). Fig. S4. A Calibration curve of nomogram of 1-Year DFS. B Calibration curve of nomogram of 2-Year DFS.

The sample size effect on the deformation behaviors of metallic glasses (MGs) attracts a lot of interest. Here, a series of molecular dynamics simulations have been performed on un-notched and notched MG thin films to fully investigate the influence of sample thickness on their fracture strengths and failure mechanisms. With decreasing sample thickness, the failure strength of un-notched MG thin films decreases slightly and the failure mode changes from shear banding to homogeneous deformation. In contrast to this brittle-to-ductile transition observed in un-notched MG thin films, shear banding prevails for notched MG thin films regardless of sample thickness. Concurrently, a notch strengthening effect is observed in the notched MG thin films when the sample thickness falls close to the shear band (SB) thickness. This significant notch strengthening is due to the failure mode transition from homogeneous deformation in un-notched MGs to shear banding in notched MGs. Based on the energetic model, a theoretical analysis is proposed to rationalize the size effect on failure mechanism transitions of both un-notched and notched MG thin films. The present study offers an understanding of size effect on the un-notched and notched MG thin films, as well as useful guidelines for the design, testing, and engineering of MG for microelectromechanical applications.

The wide existence of saline wastewater has attracted public attention due to its environmental destructiveness. The potential of anammox to treat saline wastewater was systematically evaluated in this study. Three bioreactors with different salinity increasing strategies (R1: inhibition kinetic; R2: gradient increasing; R3: pulsed increasing) were operated to identify the optimal acclimation mode. The results showed that the inhibition of anammox activity by salinity was mainly caused by the loss of enzyme activity. Under the condition of 25.0 g NaCl L−1, the highest nitrogen removal rate of R3 (2.36 ± 0.14 kg N m−3 d−1) indicated that the pulsed strategy might be optimal. Changes in microbial community might be the primary reason lead to different acclimatization results. The relative abundance of anammox bacteria increased by 37.19% in R1 and by 46.81% in R3, but remained stable in R2 with increasing salinity. Dynamic varations in bacterial interactions, proteins, and functional genes revealed the potential resistance mechanisms of bacteria to salinity. The present work provides a novel approach and guidance for the treatment of nitrogen-rich saline wastewater by the anammox process.

Esophageal squamous cell carcinoma (ESCC) is one of the most common and serious malignancies in China. However, the exact mechanisms of tumor formation and progression are unclear. As late diagnosis and poor therapeutic efficacy result in lower survival rates, identifying biomarkers for early detection, prognostic evaluation, and recurrence monitoring of ESCC is necessary. Here we analyzed 10 protein expression profiles of ESCC core tissues and paired normal esophageal epithelial tissues using two-dimensional gel electrophoresis. We excised 29 protein spots with two-fold or greater differential expression between cancer and normal tissues and identified them using matrix-assisted laser desorption/ionization-time-of-flight/time-of-flight mass spectrometry. The role of PA28β in ESCC cell was confirmed using cell growth, colony formation and soft agar in TE-1 cells pre- and post- PA28β transfection. Compared to their expression in the adjacent normal epithelia, 12 proteins, including transgelin (TAGLN), were upregulated in ESCC tissues; 17 proteins, including proteasome activator 28-beta subunit (PA28β), were downregulated (p < 0.05). Western blotting and immunohistochemistry confirmed that PA28β was significantly underexpressed in ESCC tissues. The functional assays demonstrate that PA28β inhibited cell growth, proliferation and malignancy of TE-1 cells. Among the differentially expressed proteins, PA28β is a potential tumor inhibitor.

As previously described, a cell surface-associated adhesive factor (AF) was separated from differentiated rat ascites hepatoma AH136B cells (forming cell islands in vivo) and highly purified by chromatography. AF induces not only aggregation of dissociated AH136B cells or undifferentiated rat ascites hepatoma AH109A cells (present as free cells in vivo), but also adhesiveness characterized by the development of junctional complexes. The localization of AF on the surfaces of AH136B cell islands was investigated using anti-AF IgG (Fab fragment) coupled to peroxidase. AF was detected in the contact region of the lateral surfaces of the AH136B cells and in the intercellular spaces. In contacted free cell surfaces of AH136B cells. Fluorescence studies revealed that biotin-labeled AF did not bind to the apical surface of AH136B cell islands. These results indicate a distinct difference between apical and lateral surfaces of AH136B cells; neither AF nor binding site for AF were localized on the apical surface of AH136B cells, whereas both were localized on the lateral surface. On the other hand, AH136B cells detached from the cell islands, or during the process of partial dissociation from them, showed the loss of the AF localization and binding site of AF on the surfaces. The results suggest that AH136B cell surfaces may be polarized in terms of the AF localization, and this polarization may be lost after cell dissociation.