Jiangbennedsen4691

Poly(2-oxazolines) (POx) are an attractive material of choice for biocompatible and bioactive coatings in medical applications. To prepare POx coatings, the plasma polymerization represents a fast and facile approach that is surface-independent. However, unfavorable factors of this method such as using the low-pressure regimes and noble gases, or poor control over the resulting surface chemistry limit its utilization. Here, we propose to overcome these drawbacks by using well-defined POx-based copolymers prepared by living cationic polymerization as a starting material. Chemically inert polytetrafluoroethylene (PTFE) is selected as a substrate due to its beneficial features for medical applications. The deposited POx layer is additionally post-treated by non-equilibrium plasma generated at atmospheric pressure. For this purpose, diffuse coplanar surface barrier discharge (DCSBD) is used as a source of "cold" homogeneous plasma, as it is operating at atmospheric pressure even in ambient air. Prepared POx coatings possess hydrophilic nature with an achieved water contact angle of 60°, which is noticeably lower in comparison to the initial value of 106° for raw PTFE. Moreover, the increased fibroblasts adhesion in comparison to raw PTFE is achieved, and the physical and biological properties of the POx-modified surfaces remain stable for 30 days.We developed a new nanozyme-based electrochemical immunoassay method for the monitoring of glycated albumin (GA) known to reflect short-term glycaemic levels. For this study, we synthesized urchin-like Pt nanozymes (uPtNZs) and applied them to colorimetric and electrochemical assays for sensitive determination of GA in total human serum albumin (tHSA) using 3,3',5,5'-tetramethylbenzidine (TMB) and thionine as substrates, respectively. The uPtNZs showed peroxidase-mimic activity in the presence of hydrogen peroxide. Boronic acid (BA)-agarose bead was used to capture GA through specific cis-diol interactions. uPtNZs were modified with GA antibody (GA-Ab) to form sandwich complexes with GA/BA-agarose bead. The amount of Ab-uPtNZ/GA/BA-agarose bead complex increased with increasing percentage of GA in 50 mg/mL tHSA. The colorimetric assay exhibited linearity from 0.02 to 10% (10 µg/mL - 5 mg/mL) GA with an LOD of 0.02% (9.2 µg/mL). For electrochemical assay, GA was detected from 0.01 to 20% (5 µg/mL - 10 mg/mL) with an LOD of 0.008% (3.8 µg/mL). The recovery values of measured GA in human plasma samples were from 106 to 107%. These results indicate that electrochemical assay using uPtNZs is a promising method for determining GA.Homologous recombination (HR) mediates the error-free repair of DNA double-strand breaks to maintain genomic stability. Here we characterize C17orf53/MCM8IP, an OB-fold containing protein that binds ssDNA, as a DNA repair factor involved in HR. MCM8IP-deficient cells exhibit HR defects, especially in long-tract gene conversion, occurring downstream of RAD51 loading, consistent with a role for MCM8IP in HR-dependent DNA synthesis. selleck inhibitor Moreover, loss of MCM8IP confers cellular sensitivity to crosslinking agents and PARP inhibition. Importantly, we report that MCM8IP directly associates with MCM8-9, a helicase complex mutated in primary ovarian insufficiency, and RPA1. We additionally show that the interactions of MCM8IP with MCM8-9 and RPA facilitate HR and promote replication fork progression and cellular viability in response to treatment with crosslinking agents. Mechanistically, MCM8IP stimulates the helicase activity of MCM8-9. Collectively, our work identifies MCM8IP as a key regulator of MCM8-9-dependent DNA synthesis during DNA recombination and replication.We explore effects of light dispersion by a wire-grid polarizer (WGP) in imaging polarimetry. The dispersive characteristics of a WGP, combined with off-axis scene incidence, cause significant non-uniformity. The normalized performance measure of contrast due to dispersion of WGP exceeded 0.84 for transmittance and 0.90 for extinction ratio (maximum non-uniformity at 1 and 0 for uniform performance). Dispersion also produces a lateral spread in the imaging plane, which may induce spectral image misregistration. Without higher-order excitation, the misregistration can be at the least a few pixels long in the detector. In the presence of higher-order modes, the dispersive misregistration can be severe and critical for polarized scene extraction. The results emphasize the need for an imaging polarimeter to be designed to manage the dispersive effects.An amendment to this paper has been published and can be accessed via a link at the top of the paper.Apoptosis is fundamental to normal animal development and is the target for many anticancer therapies. Recent studies have explored the consequences of "failed apoptosis" where the apoptotic program is initiated but does not go to completion and does not cause cell death. Nevertheless, this failed apoptosis induces DNA double-strand breaks generating mutations that facilitate tumorigenesis. Whether failed apoptosis is relevant to clinical disease is unknown. BCL-2 interacting killer (BIK) is a stress-induced BH3-only protein that stimulates apoptosis in response to hormone and growth factor deprivation, hypoxia, and genomic stress. It was unclear whether BIK promotes or suppresses tumor survival within the context of breast cancer. We investigated this and show that BIK induces failed apoptosis with limited caspase activation and genomic damage in the absence of extensive cell death. Surviving cells acquire aggressive phenotypes characterized by enrichment of cancer stem-like cells, increased motility and increased clonogenic survival. Furthermore, by examining six independent cohorts of patients (total n = 969), we discovered that high BIK mRNA and protein levels predicted clinical relapse of Estrogen receptor (ER)-positive cancers, which account for almost 70% of all breast cancers diagnosed but had no predictive value for hormone receptor-negative (triple-negative) patients. Thus, this study identifies BIK as a biomarker for tumor recurrence of ER-positive patients and provides a potential mechanism whereby failed apoptosis contributes to cancer aggression.