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Seasonal influenza results in 3 to 5 million cases of severe disease and 250,000 to 500,000 deaths annually. Macrophages have been implicated in both the resolution and progression of the disease, but the drivers of these outcomes are poorly understood. We probed mouse lung transcriptomic datasets using the Digital Cell Quantifier algorithm to predict immune cell subsets that correlated with mild or severe influenza A virus (IAV) infection outcomes. We identified a unique lung macrophage population that transcriptionally resembled small serosal cavity macrophages and whose presence correlated with mild disease. Until now, the study of serosal macrophage translocation in the context of viral infections has been neglected. Here, we show that pleural macrophages (PMs) migrate from the pleural cavity to the lung after infection with IAV. We found that the depletion of PMs increased morbidity and pulmonary inflammation. There were increased proinflammatory cytokines in the pleural cavity and an influx of neutrophils within the lung. Our results show that PMs are recruited to the lung during IAV infection and contribute to recovery from influenza. This study expands our knowledge of PM plasticity and identifies a source of lung macrophages independent of monocyte recruitment and local proliferation.

Abstract Two-dimensional electrides can acquire topologically non-trivial phases due to intriguing interplay between the cationic atomic layers and anionic electron layers. However, experimental evidence of topological surface states has yet to be verified. Here, via angle-resolved photoemission spectroscopy (ARPES) and scanning tunnelling microscopy (STM), we probe the magnetic Weyl states of the ferromagnetic electride [Gd2C]2+·2e−. In particular, the presence of Weyl cones and Fermi-arc states is demonstrated through photon energy-dependent ARPES measurements, agreeing with theoretical band structure calculations. Notably, the STM measurements reveal that the Fermi-arc states exist underneath a floating quantum electron liquid on the top Gd layer, forming double-stacked surface states in a heterostructure. Our work thus not only unveils the non-trivial topology of the [Gd2C]2+·2e− electride but also realizes a surface heterostructure that can host phenomena distinct from the bulk.

Abstract Background Tumor cells of diffuse-type gastric cancer (DGC) are discohesive and infiltrate into the stroma as single cells or small subgroups, so the stroma significantly impacts DGC progression. Cancer-associated fibroblasts (CAFs) are major components of the tumor stroma. Here, we identified CAF-specific secreted molecules and investigated the mechanism underlying CAF-induced DGC progression. Methods We conducted transcriptome analysis for paired normal fibroblast (NF)-CAF isolated from DGC patient tissues and proteomics for conditioned media (CM) of fibroblasts. The effects of fibroblasts on cancer cells were examined by transwell migration and soft agar assays, western blotting, and in vivo. We confirmed the effect of blocking tubulointerstitial nephritis antigen-like 1 (TINAGL1) in CAFs using siRNA or shRNA. We evaluated the expression of TINAGL1 protein in frozen tissues of DGC and paired normal stomach and mRNA in formalin-fixed, paraffin-embedded (FFPE) tissue using RNA in-situ hybridization (RNA-ISH). Results CAFs more highly expressed TINAGL1 than NFs. The co-culture of CAFs increased migration and tumorigenesis of DGC. Moreover, CAFs enhanced the phosphorylation of focal adhesion kinase (FAK) and mesenchymal marker expression in DGC cells. In an animal study, DGC tumors co-injected with CAFs showed aggressive phenotypes, including lymph node metastasis. However, increased phosphorylation of FAK and migration were reduced by blocking TINAGL1 in CAFs. In the tissues of DGC patients, TINAGL1 was higher in cancer than paired normal tissues and detected with collagen type I alpha 1 chain (COL1A1) in the same spot. Furthermore, high TINAGL1 expression was significantly correlated with poor prognosis in several public databases and our patient cohort diagnosed with DGC. Conclusions These results indicate that TINAGL1 secreted by CAFs induces phosphorylation of FAK in DGC cells and promotes tumor progression. Thus, targeting TINAGL1 in CAFs can be a novel therapeutic strategy for DGC.

AbstractPhilodendron hederaceum (Jacq.) Schott 1829, a species of the Araceae family, is a foliage plant of ornamental value. The complete chloroplast genome sequence of Philodendron hederaceum was obtained by the de novo assembly of NovaSeq 6000 (Illumina Co., San Diego, CA) paired-end short reads and Oxford Nanopore long reads. The complete chloroplast genome of P. hederaceum was 168,609 bp in length, with a large single-copy (LSC) region of 94,393 bp, a small single-copy (SSC) region of 25,774 bp, and a pair of identical inverted repeat regions (IRs) of 24,221 bp. The genome contained a total of 129 genes, including 85 protein-coding genes, 36 transfer RNA (tRNA) genes, and eight ribosomal RNA (rRNA) genes. The phylogenetic analysis of P. hederaceum with 19 related species and two outgroup species revealed the closest taxonomical relationship with Philodendron lanceolatum in the Araceae family.

Sorting single‐walled carbon nanotubes (SWNTs) that are heterogeneous into homogeneous groups based on their electronic type, chirality, and handedness is crucial for optoelectronic and biological applications. To achieve this, researchers have utilized dispersants with different binding affinities to sort SWNTs according to their chiralities. This review article provides an overview of the methods developed for sorting SWNTs using dispersants, with a particular focus on the role played by dispersant binding affinities. The article is organized into six sections, including an introduction, a background on SWNTs and dispersant‐based individualization of SWNTs, information on dispersants and their binding affinities, separation methods for SWNTs based on controlling the dispersant binding affinity, parameters used to control dispersant binding affinity, and a conclusion. It is hoped that this review will enhance understanding of the intricate interactions between dispersants and SWNTs, leading to the development of new SWNT sorting methods for future applications.

Introduction: Magnolia kobus DC has been used as herbal medicine to treat coughs and is known to exert biological effects such as anti-inflammatory, antioxidant, and antibacterial properties. We aimed to define the pharmacological effects of M. kobus leaf ethanol extract (MLEE) on acute lung inflammation and explore the underlying mechanisms of action. Methods: For in vitro investigations, RAW 264.7 cells were pretreated with MLEE (1, 10, and 100 μg/mL) and stimulated with lipopolysaccharide (LPS). For in vivo investigations, BALB/c mice were intratracheally administered with LPS for 24 hours after injection of MLEE (0.3, 3, and 30 mg/kg). Hematoxylin and eosin staining was used for histopathology analysis of lung tissue. The phytochemical constituents of MLEE were analyzed using high-performance liquid chromatography. Results: In RAW 264.7 cells, MLEE reduced the activation of the inflammatory mediators (inducible nitric oxide synthase and cyclooxygenase-2) and the nuclear translocation of nuclear factor (NF)-κB and nuclear factor erythroid-2-related factor 2 (Nrf2). The intraperitoneal injection of MLEE (30 mg/kg) attenuated interstitial edema and immune cell infiltration in LPS-induced acute lung inflammation. MLEE also inhibited the activation of cyclooxygenase-2, NF-κB, and Nrf2 in the lung tissue. Conclusion: Taken together, MLEE exerted an anti-inflammatory effect by inhibiting inflammatory and oxidative mediators on acute lung inflammation suggesting that it might be used as a natural drug for treating acute lung inflammatory diseases.

Abstract Innate immune training involves myelopoiesis, dynamic gene modulation, and functional reprogramming of myeloid cells in response to secondary heterologous challenges. The present study evaluates whether systemic innate immune training can protect tissues from local injury. Systemic pretreatment of mice with β‐glucan, a trained immunity agonist, reduces the mortality rate of mice with bleomycin‐induced lung injury and fibrosis, as well as decreasing collagen deposition in the lungs. β‐Glucan pretreatment induces neutrophil accumulation in the lungs and enhances efferocytosis. Training of mice with β‐glucan results in histone modification in both alveolar macrophages (AMs) and neighboring lung epithelial cells. Training also increases the production of RvD1 and soluble mediators by AMs and efferocytes. Efferocytosis increases trained immunity in AMs by stimulating RvD1 release, thus inducing SIRT1 expression in neighboring lung epithelial cells. Elevated epithelial SIRT1 expression is associated with decreased epithelial cell apoptosis after lung injury, attenuating tissue damage. Further, neutrophil depletion dampens the effects of β‐glucan on macrophage accumulation, epigenetic modification in lung macrophages, epithelial SIRT1 expression, and injury‐mediated fibrosis in the lung. These findings provide mechanistic insights into innate immune training and clues to the potential ability of centrally trained immunity to protect peripheral organs against injury‐mediated disorders.

Background/Aims The Genoss DES™ is a novel, biodegradable, polymer-coated, sirolimus-eluting stent with a cobalt-chromium stent platform and thin strut. Although the safety and effectiveness of this stent have been previously investigated, real-world clinical outcomes data are lacking. Therefore, the aim of this prospective, multicenter trial was to evaluate the clinical safety and effectiveness of the Genoss DES™ in all-comer patients undergoing percutaneous coronary intervention. Methods The Genoss DES registry is a prospective, single-arm, observational trial for evaluation of clinical outcomes after Genoss DES™ implantation in all-comer patients undergoing percutaneous coronary intervention from 17 sites in South Korea. The primary endpoint was a device-oriented composite outcome of cardiac death, target vessel-related myocardial infarction (MI), and clinically driven target lesion revascularization (TLR) at 12 months. Results A total of 1,999 patients (66.4 ± 11.1 years of age; 72.8% male) were analyzed. At baseline, 62.8% and 36.7% of patients had hypertension and diabetes, respectively. The implanted stent number, diameter, and length per patient were 1.5 ± 0.8, 3.1 ± 0.5 mm, and 37.0 ± 25.0 mm, respectively. The primary endpoint occurred in 1.8% patients, with a cardiac death rate of 1.1%, target vessel-related MI rate of 0.2%, and clinically driven TLR rate of 0.8%. Conclusions In this real-world registry, the Genoss DES™ demonstrated excellent safety and effectiveness at 12 months among all-comer patients undergoing percutaneous coronary intervention. These findings suggest that the Genoss DES™ may be a viable treatment option for patients with coronary artery disease.

Abstract Various prospective surgical trials have been conducted on treating patients with gastric cancer. In clinical practice, patients and surgeons may hesitate to participate in prospective surgical trials due to trial-related complications. In this study, we evaluated the effects of participation in prospective surgical trials on surgical outcomes after radical gastrectomy for gastric cancer. This study included 1689 patients who underwent curative gastrectomy for gastric cancer between 2016 and 2020. The propensity score weighting (PSW) method was used to adjust for differences in baseline clinicopathological characteristics between patients who participated and those who did not participate in prospective surgical clinical trials. Perioperative outcomes and overall survival were compared between groups. Of the 1689 patients, 309 (18.3%) participated in surgical clinical trials (SCT group). Before PSW, the SCT group had a similar operation time, intraoperative blood loss, complications, major complications, and hospital stay as the non-SCT group but had superior overall survival. After PSW, overall survival and perioperative outcomes were not significantly different between the groups. The present study suggests that participation in prospective surgical trials was not associated with surgical outcomes. Patients and surgeons may participate in prospective surgical trials without fearing adverse effects on surgical outcomes.

This study focuses on advancing the field of remote sensing image target detection, addressing challenges such as small target detection, complex background handling, and dense target distribution. We propose solutions based on enhancing the YOLOv7 algorithm. Firstly, we improve the multi-scale feature enhancement (MFE) method of YOLOv7, enhancing its adaptability and precision in detecting small targets and complex backgrounds. Secondly, we design a modified YOLOv7 global information DP-MLP module to effectively capture and integrate global information, thereby improving target detection accuracy and robustness, especially in handling large-scale variations and complex scenes. Lastly, we explore a semi-supervised learning model (SSLM) target detection algorithm incorporating unlabeled data, leveraging information from unlabeled data to enhance the model’s generalization ability and performance. Experimental results demonstrate that despite the outstanding performance of YOLOv7, the mean average precision (MAP) can still be improved by 1.9%. Specifically, under testing on the TGRS-HRRSD-Dataset, the MFE and DP-MLP models achieve MAP values of 93.4% and 93.1%, respectively. Across the NWPU VHR-10 dataset, the three models achieve MAP values of 93.1%, 92.1%, and 92.2%, respectively. Significant improvements are observed across various metrics compared to the original model. This study enhances the adaptability, accuracy, and generalization of remote sensing image object detection.

Many helminth life cycles, including hookworm, involve a mandatory lung phase, where myeloid and granulocyte subsets interact with the helminth and respond to infection-induced lung injury. To evaluate these innate subsets in Nippostrongylus brasiliensis infection, reporter mice for myeloid cells (CX3CR1GFP ) and granulocytes (PGRPdsRED ) are employed. Nippostrongylus infection induces lung infiltration of reporter cells, including CX3CR1+ myeloid cells and PGRP+ eosinophils. Strikingly, CX3CR1GFP/GFP mice, which are deficient in CX3CR1, are protected from Nippostrongylus infection with reduced weight loss, lung leukocyte infiltration, and worm burden compared to CX3CR1+/+ mice. This protective effect is specific for CX3CR1 as CCR2-deficient mice do not exhibit reduced worm burdens. Nippostrongylus co-culture with lung Ly6C+ monocytes or CD11c+ cells demonstrates that CX3CR1GFP/GFP monocytes secrete more pro-inflammatory cytokines and actively bind the parasites causing reduced motility. RNA sequencing of Ly6C+ or CD11c+ cells shows Nippostrongylus-induced gene expression changes, particularly in monocytes, associated with inflammation, chemotaxis, and extracellular matrix remodeling pathways. Analysis reveals cytotoxic and adhesion molecules as potential effectors against the parasite, such as Gzma and Gzmb, which are elevated in CX3CR1GFP/GFP monocytes. These studies validate a dual innate cell reporter for lung helminth infection and demonstrate that CX3CR1 impairs monocyte-helminth interaction.