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In recent years, photothermal therapy (PTT) particularly nanomaterial-based PTT is a promising therapeutic modality and technique for cancer tumor ablation. In addition to killing tumor cells directly through heat, PTT also can induce immunogenic cell death (ICD) to activate the whole-body anti-tumor immune response, including the redistribution and activation of immune effector cells, the expression and secretion of cytokines and the transformation of memory T lymphocytes. When used in combination with immunotherapy, the efficacy of nanomaterial-based PTT can be improved. This article summarized the mechanism of nanomaterial-based PTT against cancer and how nanomaterial-based PTT impacts the tumor microenvironment and induces an immune response. Moreover, we reviewed recent advances of nanomaterial-based photothermal immunotherapy and discussed challenges and future outlook.

Metabolic syndrome (MetS) describes a set of risk factors that can eventually lead to the occurrence of cardiovascular and cerebrovascular disease. A detailed understanding of the MetS mechanism will be helpful in developing effective prevention strategies and appropriate intervention tools. In this article, we discuss the relationship between the clinical symptoms of MetS and differences in the gut microbial community compared with healthy individuals, characterized by the proliferation of potentially harmful bacteria and the inhibition of beneficial ones. Interactions between gut microbiota and host metabolism have been shown to be mediated by a number of factors, including inflammation caused by gut barrier defects, short-chain fatty acids metabolism, and bile acid metabolism. However, although we can clearly establish a causal relationship between gut microbial profiles and MetS in animal experiments, the relationship between them is still controversial in humans. Therefore, we need more clinical studies to augment our understanding of how we can manipulate the gut microbiota and address the role of the gut microbiota in the prevention and treatment of MetS.

Nitrogen is the main limiting nutrient after carbon, hydrogen and oxygen for photosynthetic process, phyto-hormonal, proteomic changes and growth-development of plants to complete its lifecycle. Excessive and inefficient use of N fertilizer results in enhanced crop production costs and atmospheric pollution. Atmospheric nitrogen (71%) in the molecular form is not available for the plants. For world’s sustainable food production and atmospheric benefits, there is an urgent need to up-grade nitrogen use efficiency in agricultural farming system. The nitrogen use efficiency is the product of nitrogen uptake efficiency and nitrogen utilization efficiency, it varies from 30.2 to 53.2%. Nitrogen losses are too high, due to excess amount, low plant population, poor application methods etc., which can go up to 70% of total available nitrogen. These losses can be minimized up to 15–30% by adopting improved agronomic approaches such as optimal dosage of nitrogen, application of N by using canopy sensors, maintaining plant population, drip fertigation and legume based intercropping. A few transgenic studies have shown improvement in nitrogen uptake and even increase in biomass. Nitrate reductase, nitrite reductase, glutamine synthetase, glutamine oxoglutarate aminotransferase and asparagine synthetase enzyme have a great role in nitrogen metabolism. However, further studies on carbon–nitrogen metabolism and molecular changes at omic levels are required by using “whole genome sequencing technology” to improve nitrogen use efficiency. This review focus on nitrogen use efficiency that is the major concern of modern days to save economic resources without sacrificing farm yield as well as safety of global environment, i.e. greenhouse gas emissions, ammonium volatilization and nitrate leaching.

Epigenetic alterations play an important role in tumor progression of diffuse large B-cell lymphoma (DLBCL). However, the biological relevance of epigenetic gene mutations on tumor microenvironment remains to be determined. The core set of genes relating to histone methylation ( KMT2D , KMT2C , EZH2 ), histone acetylation ( CREBBP , EP300 ), DNA methylation ( TET2 ), and chromatin remodeling ( ARID1A ) were detected in the training cohort of 316 patients by whole-genome/exome sequencing (WGS/WES) and in the validation cohort of 303 patients with newly diagnosed DLBCL by targeted sequencing. Their correlation with peripheral blood immune cells and clinical outcomes were assessed. Underlying mechanisms on tumor microenvironment were investigated both in vitro and in vivo. Among all 619 DLBCL patients, somatic mutations in KMT2D (19.5%) were most frequently observed, followed by mutations in ARID1A (8.7%), CREBBP (8.4%), KMT2C (8.2%), TET2 (7.8%), EP300 (6.8%), and EZH2 (2.9%). Among them, CREBBP / EP300 mutations were significantly associated with decreased peripheral blood absolute lymphocyte-to-monocyte ratios, as well as inferior progression-free and overall survival. In B-lymphoma cells, the mutation or knockdown of CREBBP or EP300 inhibited H3K27 acetylation, downregulated FBXW7 expression, activated the NOTCH pathway, and downstream CCL2/CSF1 expression, resulting in tumor-associated macrophage polarization to M2 phenotype and tumor cell proliferation. In B-lymphoma murine models, xenografted tumors bearing CREBBP / EP300 mutation presented lower H3K27 acetylation, higher M2 macrophage recruitment, and more rapid tumor growth than those with CREBBP / EP300 wild-type control via FBXW7-NOTCH-CCL2/CSF1 axis. Our work thus contributed to the understanding of aberrant histone acetylation regulation on tumor microenvironment as an alternative mechanism of tumor progression in DLBCL.

Esophageal cancer is a familiar malignancy with high incidence and mortality, and the overall prognosis is poor. The numbers of cases of and deaths from esophageal cancer have risen rapidly in recent decades. It is one of the most malignant cancers, with more than 0.6 million new cases and 0.54 million deaths worldwide in 2020. Here, we present the global epidemiology of esophageal cancer in 2020 and projections to 2030 and 2040 at different geographical levels of continents, regions and countries, and analyze them by gender, race, geographic region and human development index. We summarize the prospects for the esophageal cancer burden and risk factors in different areas, which will be useful for global esophageal cancer clinical therapy and cancer control planning. Esophageal cancer is one of the most malignant cancers, with more than 0.6 million new cases of esophageal cancer and 0.54 million deaths worldwide in 2020. In current review, we present the global epidemiology of esophageal cancer in 2020 and projections to two decades later at different levels of continents, regions and countries and analyze them in gender, race, geographic region, and human development index. Graph showed global and top 3 countries with the highest incident cases of esophageal cancer in 2020 and projections to 2030 and 2040.

HighlightsrGO/MXene/TiO2/Fe2C heterointerface porous microspheres prepared via scalable method to boost polarization.Customization of hierarchical structure by precisely tuning 2D rGO/MXene intercalation.Optimal reflection loss of -67.4 dB and EAB = 5.47 GHz at low filler loading of 5 wt%. Simulations showed the benefits of 2D nanosheets intercalation on polarization loss.Multi-layer 2D material assemblies provide a great number of interfaces beneficial for electromagnetic wave absorption. However, avoiding agglomeration and achieving layer-by-layer ordered intercalation remain challenging. Here, 3D reduced graphene oxide (rGO)/MXene/TiO2/Fe2C lightweight porous microspheres with periodical intercalated structures and pronounced interfacial effects were constructed by spray-freeze-drying and microwave irradiation based on the Maxwell–Wagner effect. Such approach reinforced interfacial effects via defects introduction, porous skeleton, multi-layer assembly and multi-component system, leading to synergistic loss mechanisms. The abundant 2D/2D/0D/0D intercalated heterojunctions in the microspheres provide a high density of polarization charges while generating abundant polarization sites, resulting in boosted interfacial polarization, which is verified by CST Microwave Studio simulations. By precisely tuning the 2D nanosheets intercalation in the heterostructures, both the polarization loss and impedance matching improve significantly. At a low filler loading of 5 wt%, the polarization loss rate exceeds 70%, and a minimum reflection loss (RLmin) of −67.4 dB can be achieved. Moreover, radar cross-section simulations further confirm the attenuation ability of the optimized porous microspheres. These results not only provide novel insights into understanding and enhancing interfacial effects, but also constitute an attractive platform for implementing heterointerface engineering based on customized 2D hierarchical architectures.

Quantum networks are promising tools for the implementation of long-range quantum communication. The characterization of quantum correlations in networks and their usefulness for information processing is therefore central for the progress of the field, but so far only results for small basic network structures or pure quantum states are known. Here we show that symmetries provide a versatile tool for the analysis of correlations in quantum networks. We provide an analytical approach to characterize correlations in large network structures with arbitrary topologies. As examples, we show that entangled quantum states with a bosonic or fermionic symmetry can not be generated in networks; moreover, cluster and graph states are not accessible. Our methods can be used to design certification methods for the functionality of specific links in a network and have implications for the design of future network structures. The analysis of correlations in quantum networks is a difficult problem in the general case, and have so far been limited to small examples. Here, the authors show how to use symmetries and the inflation technique to derive general network entanglement criteria and certification methods.

Background Epstein-Barr virus (EBV) represents an important pathogenic factor of lymphoma and is significantly associated with poor clinical outcome of diffuse large B-cell lymphoma (DLBCL). Circular RNAs (circRNAs) play an essential role in lymphoma progression. However, the underlying mechanism of circRNA on DLBCL progression related to EBV remains largely unknown. Methods CircRNA was screened by high-throughput sequencing in tumor samples of 12 patients with DLBCL according to EBV infection status. Expression of circEAF2, as well as the relationship with clinical characteristics and prognosis, were further analyzed in tumor samples of 100 DLBCL patients using quantitative real-time PCR. Gain- and loss-of-function experiments were conducted to investigate the biological functions of circEAF2 both in vitro and in vivo. The underlying mechanism of circRNA on DLBCL progression were further determined by RNA sequencing, RNA pull down assay, dual-luciferase reporter assay, rescue experiments and western blotting. Results We identified a novel circRNA circEAF2, which was downregulated in EBV + DLBCL and negatively correlated with EBV infection and DLBCL progression. In EBV-positive B lymphoma cells, circEAF2 overexpression induced lymphoma cell apoptosis and sensitized lymphoma cells to epirubicin. As mechanism of action, circEAF2 specifically targeted EBV-encoded miR-BART19-3p, upregulated APC, and suppressed downstream β-catenin expression, resulting in inactivation of Wnt signaling pathway and inhibition of EBV + DLBCL cell proliferation. In EBV-positive B-lymphoma murine models, xenografted tumors with circEAF2 overexpression presented decreased Ki-67 positivity, increased cell apoptosis and retarded tumor growth. Conclusions CircEAF2 counteracted EBV + DLBCL progression via miR-BART19-3p/APC/β-catenin axis, referring circEAF2 as a potential prognostic biomarker. Therapeutic targeting EBV-encoded miRNA may be a promising strategy in treating EBV-associated lymphoid malignancies.

Assembly of a high-quality genome is important for downstream comparative and functional genomic studies. However, most tools for genome assembly assessment only give qualitative reports, which do not pinpoint assembly errors at specific regions. Here, we develop a new reference-free tool, Clipping information for Revealing Assembly Quality (CRAQ), which maps raw reads back to assembled sequences to identify regional and structural assembly errors based on effective clipped alignment information. Error counts are transformed into corresponding assembly evaluation indexes to reflect the assembly quality at single-nucleotide resolution. Notably, CRAQ distinguishes assembly errors from heterozygous sites or structural differences between haplotypes. This tool can clearly indicate low-quality regions and potential structural error breakpoints; thus, it can identify misjoined regions that should be split for further scaffold building and improvement of the assembly. We have benchmarked CRAQ on multiple genomes assembled using different strategies, and demonstrated the misjoin correction for improving the constructed pseudomolecules. A high-quality genome assembly is essential for various genomic studies in life sciences. Here the authors develop CRAQ, a reference-free method that facilitates the evaluation and improvement of any de novo genome assembly with single nucleotide resolution.

Generating properly differentiated embryonic structures in vitro from pluripotent stem cells remains a challenge. Here we show that instruction of aggregates of mouse embryonic stem cells with an experimentally engineered morphogen signalling centre, that functions as an organizer, results in the development of embryo-like entities (embryoids). In situ hybridization, immunolabelling, cell tracking and transcriptomic analyses show that these embryoids form the three germ layers through a gastrulation process and that they exhibit a wide range of developmental structures, highly similar to neurula-stage mouse embryos. Embryoids are organized around an axial chordamesoderm, with a dorsal neural plate that displays histological properties similar to the murine embryo neuroepithelium and that folds into a neural tube patterned antero-posteriorly from the posterior midbrain to the tip of the tail. Lateral to the chordamesoderm, embryoids display somitic and intermediate mesoderm, with beating cardiac tissue anteriorly and formation of a vasculature network. Ventrally, embryoids differentiate a primitive gut tube, which is patterned both antero-posteriorly and dorso-ventrally. Altogether, embryoids provide an in vitro model of mammalian embryo that displays extensive development of germ layer derivatives and that promises to be a powerful tool for in vitro studies and disease modelling. Following instruction by a morphogen secreting centre, aggregates of mouse embryonic stem cells develop into embryo-like structures organized around an axial mesoderm, which show extensive characteristics of a neurula-stage mouse embryo, with antero-posterior and dorso-ventral patterning of germ layer derivatives.