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BackgroundEsophageal cancer (EC) is the seventh-most prevalent cancer worldwide and is a significant contributor to cancer-related mortality. Metabolic reprogramming in tumors frequently coincides with aberrant immune function alterations, and extensive research has demonstrated that perturbations in energy metabolism within the tumor microenvironment influence the occurrence and progression of esophageal cancer. Current treatment modalities for esophageal cancer primarily include encompass chemotherapy and a limited array of targeted therapies, which are hampered by toxicity and drug resistance issues. Immunotherapy, particularly immune checkpoint inhibitors (ICIs) targeting the PD-1/PD-L1 pathway, has exhibited promising results; however, a substantial proportion of patients remain unresponsive. The optimization of these immunotherapies requires further investigation. Mounting evidence underscores the importance of modulating metabolic traits within the tumor microenvironment (TME) to augment anti-tumor immunotherapy.MethodsWe selected relevant studies on the metabolism of the esophageal cancer tumor microenvironment and immune cells based on our searches of MEDLINE and PubMed, focusing on screening experimental articles and reviews related to glucose metabolism, amino acid metabolism, and lipid metabolism, as well their interactions with tumor cells and immune cells, published within the last five years. We analyzed and discussed these studies, while also expressing our own insights and opinions.ResultsA total of 137 articles were included in the review: 21 articles focused on the tumor microenvironment of esophageal cancer, 33 delved into research related to glucose metabolism and tumor immunology, 30 introduced amino acid metabolism and immune responses, and 17 focused on the relationship between lipid metabolism in the tumor microenvironment and both tumor cells and immune cells.ConclusionThis article delves into metabolic reprogramming and immune alterations within the TME of EC, systematically synthesizes the metabolic characteristics of the TME, dissects the interactions between tumor and immune cells, and consolidates and harnesses pertinent immunotherapy targets, with the goal of enhancing anti-tumor immunotherapy for esophageal cancer and thereby offering insights into the development of novel therapeutic strategies.

The manipulation of micro/nanostructures to customise their inherent material characteristics has garnered considerable attention. In this study, we present the selective activation of gallium arsenide (GaAs) via ultrafast laser-induced decomposition, which correlates with the emergence of ripples on the surface. This instigated a pronounced enrichment in the arsenic (As) concentration around the surface while inducing a depletion of gallium (Ga) at the structural depth. Theoretical simulations based on first principles exhibited a robust inclination towards the phase separation of GaAs, with the gasification of As–As pairs proving more facile than that of Ga–Ga pairs, particularly above the melting point of GaAs. As an illustrative application, a metal-semiconductor hybrid surface was confirmed, showing surface chemical bonding and surface-enhanced Raman scattering (SERS) through the reduction of silver ions on the laser-activated pattern. This laser-induced selective activation holds promise for broader applications, including the controlled growth of Pd and the development of Au/Ag alloy-based platforms, and thereby opens innovative avenues for advancements in semiconductors, solar cell technologies, precision sensing, and detection methodologies.

We illustrated a rare case of malignant solitary fibrous tumor (MSFT) with epithelioid morphology in the occipital region of a 59-year-old female, in which a rare NAB2ex7-STAT6 exon15/16 double fusion subtype was detected by the Next-generation sequencing (NGS) and STAT6 immunohistochemistry (IHC) was diffusely and strongly positively expressed, without recurrence after 20 months of postoperative follow-up. The morphological and molecular genetic aspects and the differential diagnosis are described, and the relevant literature was assessed in order to broaden our understanding and diagnostic capability of this malignancy.

In this paper, the gas-liquid flow pattern and CO2 dissolution transport process of microalgae solution in an air-lift photobioreactor (PBR) are investigated by numerical simulations. In order to promote the gas-liquid mass transfer efficiency to enhance the carbon fixation, we propose different optimization schemes for the structure. Firstly, a two-phase flow model and a mass transfer model are employed to investigate the fluid flow characteristics. The flow state is evaluated by velocity in light direction, turbulent kinetic energy (TKE), gas hold-up and CO2 mass transfer coefficient. The results show that the gas flow rate of 0.2 V/V/min is the optimum value for the inlet. Secondly, CO2 mass transfer and carbon fixation rates are analyzed for different inlet CO2 volume fractions. With the increase of CO2 volume fraction, the carbon fixation rate first increases and then decreases, the highest fixation rate reaching 2.21 × 10−4 mol m−3 s−1 at 6 %. Finally, based on numerical simulations, three optimized structures with different spacing of baffles are proposed and evaluated the performance in comparison with the original. The results show that the gas distribution and CO2 mass transfer are significantly improved, with the one-sided baffle structure is the best. In summary, this study provides a new and useful reference to evaluate the gas-liquid mixing and improve the microalgae carbon fixation rate.

Non-alcoholic fatty liver disease (NAFLD), one of the most common chronic liver diseases with a prevalence of 23%–25% globally, is an independent risk factor for cardiovascular diseases (CVDs). Growing evidence indicates that the development of NAFLD, ranging from non-alcoholic fatty liver (NAFL), non-alcoholic steatohepatitis (NASH), advanced fibrosis to cirrhosis, and even hepatocellular carcinoma, is at substantial risk for CVDs, which clinically contribute to increased cardiovascular morbidity and mortality. Non-invasive serum markers assessing liver fibrosis, such as fibrosis-4 (FIB-4) score, aspartate transaminase-to-platelet ratio index (APRI), and NAFLD fibrosis score (NFS), are expected to be useful tools for clinical management of patients with CVDs. This review aims to provide an overview of the evidence for the relationship between the progression of NAFLD and CVDs and the clinical application of non-invasive markers of liver fibrosis in managing patients with CVDs.

BackgroundPOLE is a critical biomarker for endometrial cancer (ECs) prognosis and therapeutic decision. However, the immune infiltration and immunotherapy-related gene expression in the tumor microenvironment (TME) of POLE-mutated ECs remain unresolved.MethodsThe TCGA database was used to characterize the TME of POLE mutants, which primarily included immune cells and co-expression genes. We used immunohistochemistry (IHC) to determine immune cell abundance and PD-L1 expression in 104 EC tissues, including 11 POLE mutants and 93 wild-type.ResultsThe bioinformatic study found significant differences in gene expression of the chemokine family, immune-cell markers, and lysozyme in POLE mutants, along with immune response activation. In POLE-mutated ECs, the abundance of CD4+T, CD8+T, M1 macrophages, and dendritic cells increased considerably. Furthermore, POLE mutations may enhance immune cell recruitment or activation and lymphocyte homing in ECs. POLE mutants also had increased expression of immune-checkpoint suppressor genes such as PD-L1, CTLA-4, TIM-3, and others. The tumor mutation burden (TMB) was higher in ECs with POLE mutation. In the validation cohort, we discovered that POLE mutations were related to the immune infiltration abundance of CD8+, CD4+, and Foxp3+ cells and PD-L1 expression by IHC. The prognosis of TCGA-ECs showed that the survival time of the CD8, CD4, PD-L1, or Foxp3 over-expression subgroup of the POLE mutants was significantly prolonged compared to the down-regulation subgroup or the POLE wild-type.ConclusionThe infiltration abundance of CD8+ T, CD4+ T, Foxp3+ T cells, and the expression of PD-L1 harbor crucial value for the prognosis or individualized therapy of POLE-mutated ECs.

Abstract Phase‐change random‐access memory (PCRAM) devices suffer from pronounced resistance drift originating from considerable structural relaxation of phase‐change materials (PCMs), which hinders current developments of high‐capacity memory and high‐parallelism computing that both need reliable multibit programming. This work realizes that compositional simplification and geometrical miniaturization of traditional GeSbTe‐like PCMs are feasible routes to suppress relaxation. While to date, the aging mechanisms of the simplest PCM, Sb, at nanoscale, have not yet been unveiled. Here, this work demonstrates that in an optimal thickness of only 4 nm, the thin Sb film can enable a precise multilevel programming with ultralow resistance drift coefficients, in a regime of ≈10−4–10−3. This advancement is mainly owed to the slightly changed Peierls distortion in Sb and the less‐distorted octahedral‐like atomic configurations across the Sb/SiO2 interfaces. This work highlights a new indispensable approach, interfacial regulation of nanoscale PCMs, for pursuing ultimately reliable resistance control in aggressively‐miniaturized PCRAM devices, to boost the storage and computing efficiencies substantially.

Sugar transporters are essential for osmotic process regulation, various signaling pathways and plant growth and development. Currently, few studies are available on the function of sugar transporters in sorghum (Sorghum bicolor L.). In this study, we performed a genome-wide survey of sugar transporters in sorghum. In total, 98 sorghum sugar transporters (SSTs) were identified via BLASTP. These SSTs were classified into three families based on the phylogenetic and conserved domain analysis, including six sucrose transporters (SUTs), 23 sugars will eventually be exported transporters (SWEETs), and 69 monosaccharide transporters (MSTs). The sorghum MSTs were further divided into seven subfamilies, including 24 STPs, 23 PLTs, two VGTs, four INTs, three pGlcT/SBG1s, five TMTs, and eight ERDs. Chromosomal localization of the SST genes showed that they were randomly distributed on 10 chromosomes, and substantial clustering was evident on the specific chromosomes. Twenty-seven SST genes from the families of SWEET, ERD, STP, and PLT were found to cluster in eight tandem repeat event regions. In total, 22 SSTs comprising 11 paralogous pairs and accounting for 22.4% of all the genes were located on the duplicated blocks. The different subfamilies of SST proteins possessed the same conserved domain, but there were some differences in features of the motif and transmembrane helices (TMH). The publicly-accessible RNA-sequencing data and real-time PCR revealed that the SST genes exhibited distinctive tissue specific patterns. Functional studies showed that seven SSTs were mainly located on the cell membrane and membrane organelles, and 14 of the SSTs could transport different types of monosaccharides in yeast. These findings will help us to further elucidate their roles in the sorghum sugar transport and sugar signaling pathways.