Atomic Bose-Einstein condensate in twisted-bilayer optical lattices.

Observation of strong correlations and superconductivity in twisted-bilayer graphene1-4 has stimulated tremendous interest in fundamental and applied physics5-8. In this system, the superposition of two twisted honeycomb lattices, generating a moiré pattern, is the key to the observed flat electronic bands, slow electron velocity and large density of states9-12. Extension of the twisted-bilayer system to new configurations is highly desired, which can provide exciting prospects to investigate twistronics beyond bilayer graphene. Here we demonstrate a quantum simulation of superfluid to Mott insulator transition in twisted-bilayer square lattices based on atomic Bose-Einstein condensates loaded into spin-dependent optical lattices. The lattices are made of two sets of laser beams that independently address atoms in different spin states, which form the synthetic dimension accommodating the two layers. The interlayer coupling is highly controllable by a microwave field, which enables the occurrence of a lowest flat band and new correlated phases in the strong coupling limit. We directly observe the spatial moiré pattern and the momentum diffraction, which confirm the presence of two forms of superfluid and a modified superfluid to insulator transition in twisted-bilayer lattices. Our scheme is generic and can be applied to different lattice geometries and for both boson and fermion systems. This opens up a new direction for exploring moiré physics in ultracold atoms with highly controllable optical lattices.

Arabidopsis FIN219/JAR1 interacts with phytochrome A under far-red light and jasmonates in regulating hypocotyl elongation via a functional demand manner.

Integration of light and phytohormones is essential for plant growth and development. FAR-RED INSENSITIVE 219 (FIN219)/JASMONATE RESISTANT 1 (JAR1) participates in phytochrome A (phyA)-mediated far-red (FR) light signaling in Arabidopsis and is a jasmonate (JA)-conjugating enzyme for the generation of an active JA-isoleucine. Accumulating evidence indicates that FR and JA signaling integrate with each other. However, the molecular mechanisms underlying their interaction remain largely unknown. Here, the phyA mutant was hypersensitive to JA. The double mutant fin219-2phyA-211 showed a synergistic effect on seedling development under FR light. Further evidence revealed that FIN219 and phyA antagonized with each other in a mutually functional demand to modulate hypocotyl elongation and expression of light- and JA-responsive genes. Moreover, FIN219 interacted with phyA under prolonged FR light, and MeJA could enhance their interaction with CONSTITUTIVE PHOTOMORPHOGENIC 1 (COP1) in the dark and FR light. FIN219 and phyA interaction occurred mainly in the cytoplasm, and they regulated their mutual subcellular localization under FR light. Surprisingly, the fin219-2 mutant abolished the formation of phyA nuclear bodies under FR light. Overall, these data identified a vital mechanism of phyA-FIN219-COP1 association in response to FR light, and MeJA may allow the photoactivated phyA to trigger photomorphogenic responses.

Deciphering the ultra-high plasticity in metal monochalcogenides.

The quest for electronic devices that offer flexibility, wearability, durability and high performance has spotlighted two-dimensional (2D) van der Waals materials as potential next-generation semiconductors. Especially noteworthy is indium selenide, which has demonstrated surprising ultra-high plasticity. To deepen our understanding of this unusual plasticity in 2D van der Waals materials and to explore inorganic plastic semiconductors, we have conducted in-depth experimental and theoretical investigations on metal monochalcogenides (MX) and transition metal dichalcogenides (MX2). We have discovered a general plastic deformation mode in MX, which is facilitated by the synergetic effect of phase transitions, interlayer gliding and micro-cracks. This is in contrast to crystals with strong atomic bonding, such as metals and ceramics, where plasticity is primarily driven by dislocations, twinning or grain boundaries. The enhancement of gliding barriers prevents macroscopic fractures through a pinning effect after changes in stacking order. The discovery of ultra-high plasticity and the phase transition mechanism in 2D MX materials holds significant potential for the design and development of high-performance inorganic plastic semiconductors.

Human Umbilical Cord Mesenchymal Stem Cells Improve Lung Function in Chronic Obstructive Pulmonary Disease Rat Model Through Regulating Lung Microbiota.

BACKGROUND: The use of human umbilical cord mesenchymal stem cells (UC-MSCs) has shown promise in improving the pathophysiological characteristics of rats with chronic obstructive pulmonary disease (COPD). However, more research is needed to understand the exact mechanism behind their therapeutic effects and their impact on lung microbiota. METHODS: To investigate this, rats were randomly assigned to one of 3 groups: Control, COPD + vehicle, and COPD + UC-MSCs group. Lung function changes after UC-MSCs therapy were evaluated weekly for 6 weeks. Additionally, lactate dehydrogenase (LDH), TNF (tumor necrosis factor)-α, IL (interleukin)-6, and IL-1ß level in bronchoalveolar lavage fluid (BALF) were analyzed. Arterial blood gas and weight were recorded. Hematoxylin and eosin (HE) staining was used to examine lung pathology, while changes in the lung microbiota were evaluated through 16S rRNA sequencing. RESULTS: The administration of UC-MSCs in rats led to a progressive amelioration of COPD, as demonstrated by enhanced lung function and reduced inflammatory response. UC-MSCs treatment significantly altered the structure and diversity of the lung microbiota, effectively preventing microbiota dysbiosis. This was achieved by increasing the abundance of Bacteroidetes and reducing the levels of Proteobacteria. Additionally, treatment with UC-MSCs reduced the activation of pathways associated with COPD, including microbial metabolism, ABC transporters, and Quorum sensing. The group of UC-MSCs showed increased metabolic pathways, such as amino acid biosynthesis, purine metabolism, starch and sucrose metabolism, and biosynthesis of secondary metabolites, compared to the COPD group. CONCLUSIONS: The use of UC-MSCs was found to reduce inflammation and improve lung function in rats with COPD. The mechanism may be related to the lung microbiota, as UC-MSCs improved the communities of lung microbiota and regulated dysregulated metabolic pathways.

Identification and Characterization of Alveolar and Recruited Lung Macrophages during Acute Lung Inflammation.

To precisely identify mouse resident alveolar macrophages (AMs) and bone marrow (BM)-derived macrophages, we developed a technique to separately label AMs and BM-derived macrophages with a fluorescent lipophilic dye followed by FACS. We showed that this technique overcomes issues in cell identification related to dynamic shifts in cell surface markers that occurs during lung inflammation. We then used this approach to track macrophage subsets at different time points after intratracheal (i.t.) instillation of Escherichia coli LPS. By isolating BM-derived macrophages and AMs, we demonstrated that BM-derived macrophages were enriched in expression of genes in signal transduction and immune system activation pathways whereas resident AMs were enriched in cellular processes, such as lysosome/phagosome pathways, efferocytosis, and metabolic pathways related to fatty acids and peroxisomes. Taken together, these data indicate that more accurate identification of macrophage origin can result in improved understanding of differential phenotypes and functions between AMs and BM-derived macrophages in the lungs.

Author Correction: Targeting cardiac fibrosis with engineered T cells.

An Amendment to this paper has been published and can be accessed via a link at the top of the paper.

Targeting cardiac fibrosis with engineered T cells.

Fibrosis is observed in nearly every form of myocardial disease1. Upon injury, cardiac fibroblasts in the heart begin to remodel the myocardium by depositing excess extracellular matrix, resulting in increased stiffness and reduced compliance of the tissue. Excessive cardiac fibrosis is an important factor in the progression of various forms of cardiac disease and heart failure2. However, clinical interventions and therapies that target fibrosis remain limited3. Here we demonstrate the efficacy of redirected T cell immunotherapy to specifically target pathological cardiac fibrosis in mice. We find that cardiac fibroblasts that express a xenogeneic antigen can be effectively targeted and ablated by adoptive transfer of antigen-specific CD8+ T cells. Through expression analysis of the gene signatures of cardiac fibroblasts obtained from healthy and diseased human hearts, we identify an endogenous target of cardiac fibroblasts-fibroblast activation protein. Adoptive transfer of T cells that express a chimeric antigen receptor against fibroblast activation protein results in a significant reduction in cardiac fibrosis and restoration of function after injury in mice. These results provide proof-of-principle for the development of immunotherapeutic drugs for the treatment of cardiac disease.

Loss of p73 Expression Contributes to Chronic Obstructive Pulmonary Disease.

Rationale: Multiciliated cell (MCC) loss and/or dysfunction is common in the small airways of patients with chronic obstructive pulmonary disease (COPD), but it is unclear if this contributes to COPD lung pathology. Objectives: To determine if loss of p73 causes a COPD-like phenotype in mice and explore whether smoking or COPD impact p73 expression. Methods: p73floxE7-E9 mice were crossed with Shh-Cre mice to generate mice lacking MCCs in the airway epithelium. The resulting p73Δairway mice were analyzed using electron microscopy, flow cytometry, morphometry, forced oscillation technique, and single-cell RNA sequencing. Furthermore, the effects of cigarette smoke on p73 transcript and protein expression were examined using in vitro and in vivo models and in studies including airway epithelium from smokers and patients with COPD. Measurements and Main Results: Loss of functional p73 in the respiratory epithelium resulted in a near-complete absence of MCCs in p73Δairway mice. In adulthood, these mice spontaneously developed neutrophilic inflammation and emphysema-like lung remodeling and had progressive loss of secretory cells. Exposure of normal airway epithelium cells to cigarette smoke rapidly and durably suppressed p73 expression in vitro and in vivo. Furthermore, tumor protein 73 mRNA expression was reduced in the airways of current smokers (n = 82) compared with former smokers (n = 69), and p73-expressing MCCs were reduced in the small airways of patients with COPD (n = 11) compared with control subjects without COPD (n = 12). Conclusions: Loss of functional p73 in murine airway epithelium results in the absence of MCCs and promotes COPD-like lung pathology. In smokers and patients with COPD, loss of p73 may contribute to MCC loss or dysfunction.

A cell-cycle-dependent GARP-like transcriptional repressor regulates the initiation of differentiation in Giardia lamblia.

Transcriptional regulation of differentiation is critical for parasitic pathogens to adapt to environmental changes and regulate transmission. In response to encystation stimuli, Giardia lamblia shifts the distribution of the cell cycle toward G2 and induces the expression of cyst wall proteins (CWPs) within 2 to 4 h, indicating that key regulatory steps occur within the first 4 h of encystation. However, the role of transcription factors (TFs) in encystation has primarily been investigated at later time points. How TFs initiate encystation and link it to the cell cycle remains enigmatic. Here, we systematically screened six putative early up-regulated TFs for nuclear localization, established their dynamic expression profiles, and determined their functional role in regulating encystation. We found a critical repressor, Golden2, ARR-B, Psr-1­like protein 1 (GARP)­like protein 4 (GLP4), that increases rapidly after 30 min of encystation stimuli and down-regulates encystation-specific markers, including CWPs and enzymes in the cyst N-acetylgalactosamine pathway. Depletion of GLP4 increases cyst production. Importantly, we observe that G2+M cells exhibit higher levels of CWP1, resulting from the activation of myeloblastosis domain protein 2 (MYB2), a TF previously linked to encystation in Giardia. GLP4 up-regulation occurs in G1+S cells, suggesting a role in repressing MYB2 and encystation-specific genes in the G1+S phase of the cell cycle. Furthermore, we demonstrate that depletion of GLP4 up-regulates MYB2 and promotes encystation while overexpression of GLP4 down-regulates MYB2 and represses encystation. Together, these results suggest that Giardia employs a dose-dependent transcriptional response that involves the cell-cycle­regulated repressor GLP4 to orchestrate MYB2 and entry into the encystation pathway.

GABA signaling enforces intestinal germinal center B cell differentiation.

Recent compelling results indicate possible links between neurotransmitters, intestinal mucosal IgA+ B cell responses, and immunoglobulin A nephropathy (IgAN) pathogenesis. Here, we demonstrated that γ-amino butyric acid (GABA) transporter-2 (GAT-2) deficiency induces intestinal germinal center (GC) B cell differentiation and worsens the symptoms of IgAN in a mouse model. Mechanistically, GAT-2 deficiency enhances GC B cell differentiation through activation of GABA-mammalian target of rapamycin complex 1 (mTORC1) signaling. In addition, IgAN patients have lower GAT-2 expression but higher activation of mTORC1 in blood B cells, and both are correlated with kidney function in IgAN patients. Collectively, this study describes GABA signaling-mediated intestinal mucosal immunity as a previously unstudied pathogenesis mechanism of IgAN and challenges the current paradigms of IgAN.

Clustering on hierarchical heterogeneous data with prior pairwise relationships.

BACKGROUND: Clustering is a fundamental problem in statistics and has broad applications in various areas. Traditional clustering methods treat features equally and ignore the potential structure brought by the characteristic difference of features. Especially in cancer diagnosis and treatment, several types of biological features are collected and analyzed together. Treating these features equally fails to identify the heterogeneity of both data structure and cancer itself, which leads to incompleteness and inefficacy of current anti-cancer therapies. OBJECTIVES: In this paper, we propose a clustering framework based on hierarchical heterogeneous data with prior pairwise relationships. The proposed clustering method fully characterizes the difference of features and identifies potential hierarchical structure by rough and refined clusters. RESULTS: The refined clustering further divides the clusters obtained by the rough clustering into different subtypes. Thus it provides a deeper insight of cancer that can not be detected by existing clustering methods. The proposed method is also flexible with prior information, additional pairwise relationships of samples can be incorporated to help to improve clustering performance. Finally, well-grounded statistical consistency properties of our proposed method are rigorously established, including the accurate estimation of parameters and determination of clustering structures. CONCLUSIONS: Our proposed method achieves better clustering performance than other methods in simulation studies, and the clustering accuracy increases with prior information incorporated. Meaningful biological findings are obtained in the analysis of lung adenocarcinoma with clinical imaging data and omics data, showing that hierarchical structure produced by rough and refined clustering is necessary and reasonable.

Transcriptome analysis of long non-coding RNA and mRNA Profiles in VSV-infected BHK-21 Cells.

BACKGROUND: Vesicular stomatitis virus (VSV) is a typical non-segmented negative-sense RNA virus of the genus Vesiculovirus in the family Rhabdoviridae. VSV can infect a wide range of animals, including humans, with oral blister epithelial lesions. VSV is an excellent model virus with a wide range of applications as a molecular tool, a vaccine vector, and an oncolytic vector. To further understand the interaction between VSV and host cells and to provide a theoretical basis for the application prospects of VSV, we analyzed the expression of host differentially expressed genes (DEGs) during VSV infection using RNA-Seq. RESULTS: Our analyses found a total of 1015 differentially expressed mRNAs and 161 differentially expressed LncRNAs in BHK-21 cells infected with VSV for 24 h compared with controls. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment showed that the differentially expressed lncRNAs and their target genes were mainly concentrated in pathways related to apoptosis, cancer, disease, and immune system activation, including the TNF, P53, MAPK, and NF-kappaB signaling pathways. The differentially expressed lncRNA can modulate immune processes by regulating genes involved in these signaling transmissions. Ten randomly selected DEGs, namely, Il12rb2, F2, Masp2, Mcl1, FGF18, Ripk1, Fas, BMF, POLK, and JAG1, were validated using RT-qPCR. As predicted through RNA-Seq analysis, these DEGs underwent either up- or downregulation, suggesting that they may play key regulatory roles in the pathways mentioned previously. CONCLUSIONS: Our study showed that VSV infection alters the host metabolic network and activates immune-related pathways, such as MAPK and TNF. The above findings provide unique insights for further study of the mechanism of VSV-host interactions and, more importantly, provide a theoretical basis for VSV as an excellent vaccine carrier.

Repetitive sulfur dioxide exposure in mice models post-deployment respiratory syndrome.

Soldiers deployed to Iraq and Afghanistan have a higher prevalence of respiratory symptoms than nondeployed military personnel and some have been shown to have a constellation of findings on lung biopsy termed post-deployment respiratory syndrome (PDRS). Since many of the subjects in this cohort reported exposure to sulfur dioxide (SO2), we developed a model of repetitive exposure to SO2 in mice that phenocopies many aspects of PDRS, including adaptive immune activation, airway wall remodeling, and pulmonary vascular (PV) disease. Although abnormalities in small airways were not sufficient to alter lung mechanics, PV remodeling resulted in the development of pulmonary hypertension and reduced exercise tolerance in SO2-exposed mice. SO2 exposure led to increased formation of isolevuglandins (isoLGs) adducts and superoxide dismutase 2 (SOD2) acetylation in endothelial cells, which were attenuated by treatment with the isoLG scavenger 2-hydroxybenzylamine acetate (2-HOBA). In addition, 2-HOBA treatment or Siruin-3 overexpression in a transgenic mouse model prevented vascular remodeling following SO2 exposure. In summary, our results indicate that repetitive SO2 exposure recapitulates many aspects of PDRS and that oxidative stress appears to mediate PV remodeling in this model. Together, these findings provide new insights regarding the critical mechanisms underlying PDRS.NEW & NOTEWORTHY We developed a mice model of "post-deployment respiratory syndrome" (PDRS), a condition in Veterans with unexplained exertional dyspnea. Our model successfully recapitulates many of the pathological and physiological features of the syndrome, revealing involvement of the ROS-isoLGs-Sirt3-SOD2 pathway in pulmonary vasculature pathology. Our study provides additional knowledge about effects and long-term consequences of sulfur dioxide exposure on the respiratory system, serving as a valuable tool for future PDRS research.

Differences in the incidence and mortality of digestive cancer between Global Cancer Observatory 2020 and Global Burden of Disease 2019.

The burden of digestive cancers is increasing worldwide. The Global Cancer Observatory (GLOBOCAN) 2020 and the Global Burden of Disease (GBD) 2019 are two primary cancer databases, which have a significant impact on policy formulation and resource allocation. We aim to compare the incidence and mortality of digestive cancers between them. Digestive cancer (esophageal, stomach, colorectal, liver, gallbladder and pancreatic cancer) incidence was obtained from the Cancer Today and GBD 2019 result tool. The top five countries with the most or minor difference between GLOBOCAN 2020 and GBD 2019 in age-standardized incidence rates (ASIRs) of digestive cancers were identified. A systematic search on the incidence of specific digestive cancer in selected countries from PubMed and Embase was conducted, and 20 of 281 publications were included. The most significant differences in digestive cancers incidence were commonly found in Asian countries (70%), particularly Indonesia, Vietnam and Myanmar, located in Southeast Asia. The ASIRs for most digestive cancers, except liver cancer, in GLOBOCAN 2020 were higher than those in GBD 2019. Gallbladder cancer had the highest average ratio, followed by liver cancer. The most commonly used standard population was Segi's standard population, followed by the World Health Organization standard population. The data sources nor the processing methods of GLOBOCAN 2020 and GBD 2019 were not similar. Low- and middle-income countries without population-based cancer registries were more likely to have selection bias in data collection and amplify regional variations of etiological factors. Better judgments on the quality of cancer data can be made.

Mapping and Functional Dissection of the Rumpless Trait in Piao Chicken Identifies a Causal Loss of Function Mutation in the Novel Gene Rum.

Rumpless chickens exhibit an abnormality in their tail development. The genetics and biology of this trait has been studied for decades to illustrate a broad variation in both the types of inheritance and the severity in the developmental defects of the tail. In this study, we created a backcross pedigree by intercrossing Piao (rumpless) with Xianju (normal) to investigate the genetic mechanisms and molecular basis of the rumpless trait in Piao chicken. Through genome-wide association and linkage analyses, the candidate region was fine-mapped to 798.5 kb (chromosome 2: 86.9 to 87.7 Mb). Whole-genome sequencing analyses identified a single variant, a 4.2 kb deletion, which was completely associated with the rumpless phenotype. Explorations of the expression data identified a novel causative gene, Rum, that produced a long, intronless transcript across the deletion. The expression of Rum is embryo-specific, and it regulates the expression of MSGN1, a key factor in regulating T-box transcription factors required for mesoderm formation and differentiation. These results provide genetic and molecular experimental evidence for a novel mechanism regulating tail development in chicken and report the likely causal mutation for the tail abnormity in the Piao chicken. The novel regulatory gene, Rum, will, due to its role in fundamental embryo development, be of interest for further explorations of a potential role in tail and skeletal development also in other vertebrates.

Recent infection with SARS-CoV-2 in donors was associated with a higher incidence of acute graft-versus-host disease in recipients undergoing allogeneic haematopoietic stem cell transplantation.

The global pandemic has resulted in the common occurrence of SARS-CoV-2 infection in the population. In the post-pandemic era, it is imperative to understand the influence of donor SARS-CoV-2 infection on outcomes after allogeneic haematopoietic stem cell transplantation (allo-HSCT). We retrospectively analysed allo-HSCTs from donors with mild SARS-CoV-2 infection or early recovery stage (ERS) (group 1, n = 65) and late recovery stage (group 2, n = 120). Additionally, we included allo-HSCT from donors without prior SARS-CoV-2 infection as group 0 (n = 194). Transplants from donors with different SARS-CoV-2 infection status had comparable primary engraftment and survival rates. However, group 1 had higher incidences of acute graft-versus-host disease (aGvHD), grade II-IV (41.5% vs. 28.1% in group 0 [p = 0.014] and 30.6% in group 2 [p = 0.067]) and grade III-IV (22.2% vs. 9.6% [p = 0.004] in group 0 and 12.2% in group 2 [p = 0.049]). Conversely, the risk of aGvHD in group 2 was similar to that in group 0 (p > 0.5). Multivariable analysis identified group 1 associated with grade II-IV (hazard ratio [HR] 2.307, p = 0.010) and grade III-IV (HR 2.962, p = 0.001) aGvHD, which yielded no significant risk factors for survival. In conclusion, we preliminarily demonstrated donors in the active infection state or ERS of mild SARS-CoV-2 infection were associated with higher incidences of aGvHD in transplants from related donors.

Glioma induces atypical depression-like behaviors in mice through the 5-HT and glutamatergic synapse pathways.

Glioma patients often undertake psychiatric disorders such as depression and anxiety. There are several clinical epidemiological studies on glioma-associated depression, but basic research and corresponding animal experiments are still lacking. Here, we observed that glioma-bearing mice exhibited atypical depression-like behaviors in orthotopic glioma mouse models. The concentrations of monoamine neurotransmitters were detected by enzyme-linked immunosorbent assay (ELISA), revealing a decrease in 5-hydroxytryptamine (5-HT) levels in para-glioma tissues. The related gene expression levels also altered, detected by quantitative RT-PCR. Then, we developed a glioma-depression comorbidity mouse model. Through sucrose preference test (SPT), forced swimming test (FST), tail suspension test (TST) and other tests, we found that the occurrence of glioma could lead to changes in depression-like behaviors in a chronic unpredictable mild stress (CUMS) mouse model. The results of RNA sequencing (RNA-seq) indicated that the altered expression of glutamatergic synapse related genes in the paratumor tissues might be one of the main molecular features of the comorbidity model. Our findings suggested that the presence of glioma caused and altered depression-like behaviors, which was potentially related to the 5-HT and glutamatergic synapse pathways.

Predicting Invasiveness of Lung Adenocarcinoma at Chest CT with Deep Learning Ternary Classification Models.

Background Preoperative discrimination of preinvasive, minimally invasive, and invasive adenocarcinoma at CT informs clinical management decisions but may be challenging for classifying pure ground-glass nodules (pGGNs). Deep learning (DL) may improve ternary classification. Purpose To determine whether a strategy that includes an adjudication approach can enhance the performance of DL ternary classification models in predicting the invasiveness of adenocarcinoma at chest CT and maintain performance in classifying pGGNs. Materials and Methods In this retrospective study, six ternary models for classifying preinvasive, minimally invasive, and invasive adenocarcinoma were developed using a multicenter data set of lung nodules. The DL-based models were progressively modified through framework optimization, joint learning, and an adjudication strategy (simulating a multireader approach to resolving discordant nodule classifications), integrating two binary classification models with a ternary classification model to resolve discordant classifications sequentially. The six ternary models were then tested on an external data set of pGGNs imaged between December 2019 and January 2021. Diagnostic performance including accuracy, specificity, and sensitivity was assessed. The χ2 test was used to compare model performance in different subgroups stratified by clinical confounders. Results A total of 4929 nodules from 4483 patients (mean age, 50.1 years ± 9.5 [SD]; 2806 female) were divided into training (n = 3384), validation (n = 579), and internal (n = 966) test sets. A total of 361 pGGNs from 281 patients (mean age, 55.2 years ± 11.1 [SD]; 186 female) formed the external test set. The proposed strategy improved DL model performance in external testing (P < .001). For classifying minimally invasive adenocarcinoma, the accuracy was 85% and 79%, sensitivity was 75% and 63%, and specificity was 89% and 85% for the model with adjudication (model 6) and the model without (model 3), respectively. Model 6 showed a relatively narrow range (maximum minus minimum) across diagnostic indexes (accuracy, 1.7%; sensitivity, 7.3%; specificity, 0.9%) compared with the other models (accuracy, 0.6%-10.8%; sensitivity, 14%-39.1%; specificity, 5.5%-17.9%). Conclusion Combining framework optimization, joint learning, and an adjudication approach improved DL classification of adenocarcinoma invasiveness at chest CT. Published under a CC BY 4.0 license. Supplemental material is available for this article. See also the editorial by Sohn and Fields in this issue.

A Non-Flammable and Flexible Aluminum Derived Lithium-Ion Storage Device with a Wide Temperature Range of Operation.

With the rapid development and increasing popularity of electric vehicles and wearables, battery safety has become a leading focus in the field of energy storage research. Specifically, aluminum-ion batteries are gaining increasing attention as low-cost energy-storage systems with high safety levels and theoretical energy density. However, the dense alumina passivation layer on the aluminum anode surface and slow kinetic performance of commonly used ionic liquid electrolytes still render poor performance. This report presents a new type of aluminum-derived lithium-ion battery (ALIB) that maintains a certain discharge performance under damaging conditions, including continuous bending, high- and low-temperature environments, and shearing. This new ALIB effectively meets the current demand for flexible and wearable batteries. The prepared ALIB achieves a stable cycle of 130 mAh g-1 specific capacity and ≈260 Wh kg-1 theoretical energy density at a wide voltage platform of 2 V and a test temperature of 25 °C without undergoing combustion. Additionally, the study analyzes the reaction mechanism of this ALIB based on density functional theory and conducts ex situ XRD and XPS analyses to elucidate the underlying storage mechanism.

Flexible Ti3 C2 Tx MXene Bonded Bio-Derived Carbon Fibers Support Tin Disulfide for Fast and Stable Sodium Storage.

High energy density and flexible electrodes, which have high mechanical properties and electrochemical stability, are critical to the development of wearable electronics. In this work, a free-standing MXene bonded SnS2 composited nitrogen-doped carbon fibers (MXene/SnS2 @NCFs) film is reported as a flexible anode for sodium-ion batteries. SnS2 nanoparticles with high-capacity properties are covalently decorated in bio-derived nitrogen-doped 1D carbon fibers (SnS2 @NCFs) and further assembled with highly conductive MXene sheets. The addition of bacterial cellulose (BC) can further improve the flexibility of the film. The unique 3D structure of points, lines, and planes can not only offset the disadvantage of low conductivity of SnS2 nanoparticles but also expand the distance between MXene sheets, which is conducive to the penetration of electrolytes. More importantly, the MXene sheets and N-doped 1D carbon fibers (NCFs) can accommodate the large volume expansion of SnS2 nanoparticles and trap polysulfide during the cycle. The MXene/SnS2 @NCFs film exhibits better sodium storage and excellent rate performance compared to the SnS2 @NCFs. The in situ XRD and ex situ (XRD, XPS, and HRTEM) techniques are used to analyze the sodiation process and to deeply study the reaction mechanism of the films. Finally, the quasi-solid-state full cells with MXene/SnS2 @NCFs and Na3 V2 (PO4 )3 @carbon cloth (NVP@CC) fully demonstrate the application potential of the flexible electrodes.