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Nanoencapsulation of living cells within artificial shells is a powerful approach for augmenting the inherent capacity of cells and enabling the acquisition of extrinsic functions. However, the current state of the field requires the development of nanoshells that can dynamically sense and adapt to environmental changes by undergoing transformations in form and composition. This paper reports the compositional transformation of an enzyme‐embedded nanoshell of Fe3+‐trimesic acid complex to an iron phosphate shell in phosphate‐containing media. The cytocompatible transformation allows the nanoshells to release functional molecules without loss of activities and biorecognition, while preserving the initial shell properties, such as cytoprotection. Demonstrations include the lysis and killing of Escherichia coli by lysozyme, and the secretion of interleukin‐2 by Jurkat T cells in response to paracrine stimulation by antibodies. This work on micrometric Transformers will benefit the creation of cell‐in‐shell nanobiohybrids that can interact with their surroundings in active and adaptive ways. [ABSTRACT FROM AUTHOR]

A bi‐directional deformable block‐based motion‐estimation algorithm to improve the accuracy of a motion prediction in a 360‐degree video, used for motion compensated frame‐rate up conversion (MC‐FRUC) is proposed. The block shapes are adaptively deformed to predict a motion based on the coordinate of the current block, considering the geometric property of the equi‐rectangular projection of 360‐degree videos. Experimental results demonstrate that the proposed technique can significantly improve the visual quality of the videos as compared with the conventional MC‐FRUC. [ABSTRACT FROM AUTHOR]

The design and optimization of nanostructures with unique morphologies and properties are at the forefront of biomedical nanotechnology. Cerium oxides are widely used to investigate the effect of morphology on performance. However, elucidating the morphology–activity relationship of cerium oxide nanocrystals in biomedical applications remains challenging. Herein, the therapeutic effects of cerium oxide nanoparticles with different morphologies: cerium oxide nanorods with two different aspect ratios (CeOx NRs_A and CeOx NRs_B), cerium oxide nanopolyhedra (CeOx NPs), and cerium oxide nanocubes (CeOx NCs) are investigated in in vivo and in vitro mild traumatic brain injury (TBI) models. Cerium oxide nanoparticles inhibit oxidative stress and inflammation after mild TBI, alleviating cognitive impairment; furthermore, the therapeutic effect is significantly affected by their morphology. Owing to the higher Ce3+/Ce4+ ratio, exposure of more active crystal surfaces, and greater number of exposed oxygen vacancies, CeOx NRs show better activity than CeOx NPs and CeOx NCs for mild TBI. Among the two investigated types of cerium oxide nanorods, CeOx NRs_A, with a higher Ce3+/Ce4+ ratio on the surface, appear to spread better than CeOx NRs_B in the injured lesions. The factors causing morphology‐controlled biomedical performance, such as Ce3+/Ce4+ molar ratio, surface area, and aspect ratio, are discussed. [ABSTRACT FROM AUTHOR]

Background: B‐ and T‐lymphocyte attenuator (BTLA) and programmed cell death‐1 (PD‐1) inhibit γδ T cell homeostasis and activation. This study aimed to determine whether BTLA and PD‐1 signaling pathways were convergent or independent in human peripheral blood γδ T cells. Herein we demonstrate that the signalings of BTLA and PD‐1 regulated proliferation and cytotoxicity of human γδ T cells, respectively. Methods: Human peripheral blood γδ T cells were cultured with inactivated Jurkat cells in the presence of interleukin‐2 and zoledronate (Zol) for 14 days. Flow cytometry was performed to evaluate the phenotypes and functions of γδ T cells. Results: The proliferation of the γδ T cells was increased when PBMCs were cocultured with inactivated herpes virus entry mediator (HVEM)low Jurkat cells. The cytotoxicity of the expanded γδ T cells was not affected by coculture with inactivated HVEMlow Jurkat cells and was further increased in the presence of anti‐PD‐L1 mAb. These results suggest that the inactivation of the BTLA signaling pathway during expansion could help produce more γδ T cells without compromising γδ T cell function. The inhibition of BTLA or PD‐1 signaling repressed phosphorylation of the src homology region 2‐containing protein tyrosine phosphatase 2 and increased the phosphorylation of protein kinase B in γδ T cells. However, there were no synergistic or additive effects by a combination of BTLA and PD‐1 blockade. Conclusion: These results suggest that BTLA signaling is crucial in regulating γδ T cell proliferation and function and that the BTLA and PD‐1 signaling pathways act independently on the proliferation and cytotoxicity of human peripheral γδ T cells. [ABSTRACT FROM AUTHOR]

Summary: Background: Inflammatory bowel disease (IBD) is accompanied by various extraintestinal manifestations including systemic inflammation and hypercoagulability, which may increase the risk of atherosclerosis and ischaemic heart disease. Aim: To investigate whether IBD is associated with an increased risk of myocardial infarction (MI), stroke or death Methods: The International Classification of Disease, 10th edition codes and the claim codes for rare diseases were used to identify candidates from National Health Insurance Service (NHIS) of South Korea. Patients diagnosed with Crohn's disease (CD) or ulcerative colitis (UC) between 2006 and 2009 were age‐matched 1:3 with NHIS enrolees without IBD. The primary outcomes included newly developed MI, stroke and death. Hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated using Cox regression models. Results: We identified 10 708 patients diagnosed with CD and 26 769 with UC. MI risk was higher in CD patients than in controls (incidence ratio (IR) 1.64 per 1000 person‐years, HR, 1.80; 95% CI, 1.47‐2.21), and this trend was more prominent among patients aged <40 years (IR 0.69 per 1000 person‐years, HR, 2.96; 95% CI, 1.96‐4.47) and among female patients (IR 2.35 per 1000 person‐years, HR, 2.18; 95% CI, 1.61‐2.94). In contrast, only female patients with UC had an increased risk of MI (IR 2.01 per 1000 person‐years, HR, 1.33; 95% CI, 1.13‐1.56). Conclusions: The risk of MI risk is higher in patients with CD than in the general population, and this trend is stronger in female patients and those aged <40 years. [ABSTRACT FROM AUTHOR]

Summary: Background: Tegoprazan is a novel potassium‐competitive acid blocker that has a fast onset of action and can control gastric pH for a prolonged period, which could offer clinical benefit in acid‐related disorders. Aim: To confirm the non‐inferiority of tegoprazan to esomeprazole in patients with erosive oesophagitis (EE). Methods: In this multicentre, randomised, double‐blind, parallel‐group comparison study, 302 Korean patients with endoscopically confirmed EE (Los Angeles Classification Grades A‐D) were randomly allocated to either tegoprazan (50 or 100 mg) or esomeprazole (40 mg) treatment groups for 4 or 8 weeks. The primary endpoint was the cumulative proportion of patients with healed EE confirmed by endoscopy up to 8 weeks from treatment initiation. Symptoms, safety and tolerability were also assessed. Results: The cumulative healing rates at week 8 were 98.9% (91/92), 98.9% (90/91) and 98.9% (87/88) for tegoprazan 50 mg, tegoprazan 100 mg and esomeprazole 40 mg, respectively. Both doses of tegoprazan were non‐inferior to esomeprazole 40 mg. The incidence of adverse events was comparable among the groups, and tegoprazan was well‐tolerated. Conclusion: Once daily administration of tegoprazan 50 or 100 mg showed non‐inferior efficacy in healing EE and tolerability to that of esomeprazole 40 mg. [ABSTRACT FROM AUTHOR]

TopBP1 was initially identified as a topoisomerase II-β-binding protein and it plays roles in DNA replication and repair. We found that TopBP1 is expressed at high levels in lymphoid tissues and is essential for early lymphocyte development. Specific abrogation of TopBP1 expression resulted in transitional blocks during early lymphocyte development. These defects were, in major part, due to aberrant V(D)J rearrangements in pro-B cells, double-negative and double-positive thymocytes. We also show that TopBP1 was located at sites of V(D)J rearrangement. In TopBP1-deficient cells, γ-H2AX foci were found to be increased. In addition, greater amount of γ-H2AX product was precipitated from the regions where TopBP1 was localized than from controls, indicating that TopBP1 deficiency results in inefficient DNA double-strand break repair. The developmental defects were rescued by introducing functional TCR αβ transgenes. Our data demonstrate a novel role for TopBP1 as a crucial factor in V(D)J rearrangement during the development of B, T and iNKT cells. [ABSTRACT FROM AUTHOR]