Herein, we present a novel polymer architecture based on poly(2-oxazoline)s bearing protected thiol functionalities, which can be selectively liberated by irradiation with UV light. Whereas free thiol groups can suffer from oxidation or other spontaneous reactions that degrade polymer performance, this strategy with masked thiol groups offers the possibility of photodeprotection on demand with spatio-temporal control while maintaining polymer integrity. Here, we exploit this potential for a tandem network formation upon irradiation with UV light by thiol deprotection and concurrent crosslinking via thiol-ene coupling. The synthesis of the novel oxazoline monomer 2-2-[(2-nitrobenzyl)thio]ethyl-4,5-dihydrooxazole (NbMEtOxa) carrying 2-nitrobenzyl-shielded thiol groups and its cationic ring-opening copolymerization at varying ratios with 2-ethyl-2-oxazoline (EtOxa) is described. The tandem network formation was exemplarily demonstrated with the photoinitator 2-hydroxy-2-methylpropiophenone (HMPP) and pentaerythritol tetraacrylate (PETA), a commercially available, tetrafunctional vinyl crosslinker. The key findings of the conducted experiments indicate that a ratio of ~10% NbMEtOxa repeat units in the polymer backbone is sufficient for network formation and in-situ gelation in N,N-dimethylformamide.The study of the quality of hospital emergency services is based on analyzing a set of indicators such as the average time of first medical attention, the average time spent in the emergency department, degree of completion of the medical report and others. In this paper, an analysis is presented of one of the quality indicators the rate of return of patients to the emergency service less than 72 h from their discharge. The objective of the analysis was to know the variables that influence the rate of return and which prediction model is the best. In order to do this, the data of the activity of the emergency service of a hospital of a reference population of 290,000 inhabitants were analyzed, and prediction models were created for the binary objective variable (rate of return to emergencies) using the logistic regression techniques, neural networks, random forest, gradient boosting and assembly models. Each of the models was analyzed and the result shows that the best model is achieved through a neural network with activation function tanh, algorithm levmar and three nodes in the hidden layer. This model obtains the lowest mean squared error (MSE) and the best area under the curve (AUC) with respect to the rest of the models used.Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease that affects the lining of the synovial joints leading to stiffness, pain, inflammation, loss of mobility, and erosion of joints. Its pathogenesis is related to aberrant immune responses against the synovium. Dysfunction of innate and adaptive immunity, including dysregulated cytokine networks and immune complex-mediated complement activation, are involved in the progression of RA. At present, drug treatments, including corticosteroids, antirheumatic drugs, and biological agents, are used in order to modulate the altered immune responses. Chronic use of these drugs may cause adverse effects to a significant number of RA patients. Additionally, some RA patients are resistant to these therapies. In recent years, mesenchymal stem/stromal cell (MSCs)-based therapies have been largely proposed as a novel and promising stem cell therapeutic approach in the treatment of RA. MSCs are multipotent progenitor cells that have immunomodulatory properties and can be obtained and expanded easily. Today, nearly one hundred studies in preclinical models of RA have shown promising trends for clinical application. Proof-of-concept clinical studies have demonstrated satisfactory safety profile of MSC therapy in RA patients. The present review discusses MSC-based therapy approaches with a focus on published clinical data, as well as on clinical trials, for treatment of RA that are currently underway.Cellular DNA is constantly being damaged by numerous internal and external mutagenic factors. Probably the most severe type of insults DNA could suffer are the double-strand DNA breaks (DSBs). They sever both DNA strands and compromise genomic stability, causing deleterious chromosomal aberrations that are implicated in numerous maladies, including cancer. Not surprisingly, cells have evolved several DSB repair pathways encompassing hundreds of different DNA repair proteins to cope with this challenge. selleck compound In eukaryotic cells, DSB repair is fulfilled in the immensely complex environment of the chromatin. The chromatin is not just a passive background that accommodates the multitude of DNA repair proteins, but it is a highly dynamic and active participant in the repair process. Chromatin alterations, such as changing patterns of histone modifications shaped by numerous histone-modifying enzymes and chromatin remodeling, are pivotal for proficient DSB repair. Dynamic chromatin changes ensure accessibility to the damaged region, recruit DNA repair proteins, and regulate their association and activity, contributing to DSB repair pathway choice and coordination. Given the paramount importance of DSB repair in tumorigenesis and cancer progression, DSB repair has turned into an attractive target for the development of novel anticancer therapies, some of which have already entered the clinic.Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) has attracted attention as a potential candidate for cancer therapy. However, many primary cancers are resistant to TRAIL, even when combined with standard chemotherapy. The mechanism of TRAIL resistance in cancer cells has not been fully elucidated. The TRAIL death receptor (DR) 3′-untranslated region (3′-UTR) is reported to contain AU-rich elements (AREs) that are important for regulating DR mRNA stability. However, the mechanisms by which DR mRNA stability is determined by its 3′-UTR are unknown. We demonstrate that tristetraprolin (TTP), an ARE-binding protein, has a critical function of regulating DR mRNA stability. DR4 mRNA contains three AREs and DR5 mRNA contains four AREs in 3′-UTR. TTP bound to all three AREs in DR4 and ARE3 in DR5 and enhanced decay of DR4/5 mRNA. TTP overexpression in colon cancer cells changed the TRAIL-sensitive cancer cells to TRAIL-resistant cells, and down-regulation of TTP increased TRAIL sensitivity via DR4/5 expression.