Browse Articles

Integratable all-solid-state thin-film microbatteries

Large-scale integration of microbattery systems on chips has long been hindered by the technical barrier between electrochemistry and microelectronics, particularly in terms of the compatibility of microbattery cells and their collective manufacturability. In this work, a silicon-based all-solid-state thin-film microbattery cell is developed at low temperatures for on-chip integration applications. Stress management at the interfaces covering both the resistance to interfacial fracture and the stress dissipation through strain regulation enables microbattery cells to deliver a high-rate performance (34.4 mA cm −2 ), fast charge–discharge properties (1,000,000 cycles at 20 mA cm −2 ), and high-temperature tolerance (150 °C) under zero stack pressure. An intrinsic relationship among lithium utilization ratio, strain, stress, and interface manifestation is uncovered. A collective microfabrication protocol for on-chip microbattery packs is proposed, resulting in a prototype of series-connected microbattery packs. This work focuses on practically addressing the technologies and challenges in engineering on-chip microbattery systems for large-scale integration.

A study focusing on the distinct fine structure of starch in mealy and waxy potatoes

Metaheuristic optimizers integrated with vision transformer model for severity detection and classification via multimodal COVID-19 images

Functional redundancy in the toxic pathway of Bt protein Cry1Ab, but not Cry1Fa, against the Asian corn borer

Crops genetically engineered to produce insecticidal proteins from the bacterium Bacillus thuringiensis (Bt) have been used extensively to control some major crop pests, but their benefits decrease when pests evolve resistance. Better understanding of the genetic basis of resistance is needed to effectively monitor, manage, and counter pest resistance to Bt crops. Resistance to Bt proteins in at least 11 species of Lepidoptera, including many important crop pests, is associated with naturally occurring mutations that disrupt one or more of three larval midgut proteins: cadherin and ATP-binding cassette proteins ABCC2 and ABCC3. Here, we determined how CRISPR/Cas9-mediated mutations disrupting cadherin, ABCC2, and ABCC3 singly and in pairs affect resistance to Bt proteins Cry1Ab and Cry1Fa in the Asian corn borer ( Ostrinia furnacalis ), which is the most damaging pest of corn in Asia and is closely related to the European corn borer ( Ostrinia nubilalis ), a major pest in Europe and North America. The results from bioassays of six knockout strains and their parent susceptible strain support a model in which Cry1Ab can kill larvae via one path requiring ABCC2 or another path requiring cadherin and ABCC3, whereas Cry1Fa uses only the first path. The model’s predictions are generally supported by results from genetic linkage analyses and responses to Cry1Ab and Cry1Fa of Sf9 cells and Xenopus oocytes modified to produce cadherin, ABCC2, and ABCC3 singly or in pairs. The functional redundancy identified here for Cry1Ab could sustain its efficacy against O. furnacalis and may exemplify a widespread natural strategy for delaying resistance.

DSIT UNet a dual stream iterative transformer based UNet architecture for segmenting brain tumors from FLAIR MRI images

Cleavage cascade of the sigma regulator FecR orchestrates TonB-dependent signal transduction

TonB-dependent signal transduction is a versatile mechanism observed in gram-negative bacteria that integrates energy-dependent substrate transport with signal relay. In Escherichia coli , the TonB–ExbBD motor complex energizes the TonB-dependent outer membrane transporter FecA, facilitating ferric citrate import. FecA also acts as a sensor, transmitting signals to the cytoplasmic membrane protein FecR, which eventually activates the cytoplasmic sigma factor FecI, driving transcription of the fec operon. Building on our previous finding that FecR undergoes functional maturation through a three-step cleavage process [T. Yokoyama et al., J. Biol. Chem. 296 , 100673 (2021)], we here describe the complete mechanism of FecR-mediated ferric citrate signaling involving FecA and TonB. The cleavage cascade begins with FecR autoproteolysis prior to membrane integration. The soluble C-terminal domain (CTD) fragment of FecR is cotranslocated with the N-terminal domain (NTD) fragment through a twin-arginine translocation (Tat) system–mediated process. In the periplasm, the interaction between the CTD and NTD fragments prevents further cleavage. Binding of ferric citrate induces a conformational change in FecA, exposing its TonB box to the periplasmic space. This structural alteration is transmitted to the interacting FecR CTD via the motor function of TonB, resulting in the release of the CTD blockage from the NTD. Consequently, the successive cleavage of FecR’s NTD is initiated, culminating in the ferric citrate signal–induced activation of fec gene expression. Our findings reveal that the regulation of FecR cleavage, controlled by the TonB–FecA axis, plays a central role in the bacterial response to ferric citrate signals.

Testing the limits of large language models in debating humans

Abstract Large Language Models (LLMs) have shown remarkable promise in communicating with humans. Their potential use as artificial partners with humans in sociological experiments involving conversation is an exciting prospect. But how viable is it? Here, we rigorously test the limits of agents that debate using LLMs in a preregistered study that runs multiple debate-based opinion consensus games. Each game starts with six humans, six agents, or three humans and three agents. We found that agents can blend in and concentrate on a debate’s topic better than humans, improving the productivity of all players. Yet, humans perceive agents as less convincing and confident than other humans, and several behavioral metrics of humans and agents we collected deviate measurably from each other. We observed that agents are already decent debaters, but their behavior generates a pattern distinctly different from the human-generated data.

Diet-regulated transcriptional plasticity of plant parasites in plant–mutualist environments

Crop pathogens often lack exclusive access to their host and must interact with plants concurrently engaged with numerous other symbionts. Here, we demonstrate that the colonization of hosts by plant–mutualistic mycorrhizal fungi can indirectly induce transcriptional responses of a major plant parasite, the nematode Globodera pallida , via a modified host resource profile. A shift in the resource profile of the root, where the parasite feeds, is perceived and responded to by the parasite through transcriptional changes, potentially to optimize resource intake. Specifically, G. pallida react to reduced host-photosynthate influx due to concurrent mycorrhizal-host symbiosis by upregulating the expression of a sugar transporter ( SWEET3 ) in the nematode intestine. We identify this gene’s role in parasite growth and development, regulated by the putative diet-responsive transcription factor Gp-HBL1. Overall, our data unveil a mechanism by which a parasitic animal responds to fluctuations in host plant quality that is induced by a plant–mutualistic fungus, to enhance parasitism and reproduction.

Predicting relapse after achieving a functional cure for chronic hepatitis B (CHB) using baseline HBsAg and end-of-treatment HBsAb levels

Elevated brain manganese induces motor disease by upregulating the kynurenine pathway of tryptophan metabolism

Elevated brain levels of the essential metals manganese (Mn), copper, or iron induce motor disease. However, mechanisms of metal-induced motor disease are unclear and treatments are lacking. Elucidating the mechanisms of Mn-induced motor disease is particularly important because occupational and environmental Mn overexposure is a global public health problem. To address this, here we combined unbiased transcriptomics and metabolomics with functional studies in a mouse model of human environmental Mn exposure. Transcriptomics unexpectedly revealed that Mn exposure up-regulated expression of metabolic pathways in the brain and liver. Notably, genes in the kynurenine pathway of tryptophan metabolism, which produces neuroactive metabolites that impact neurological function, were up-regulated by Mn. Subsequent unbiased metabolomics revealed that Mn treatment altered kynurenine pathway metabolites in the brain and liver. Functional experiments then demonstrated that pharmacological inhibition of the first and rate-limiting step of the kynurenine pathway fully rescued Mn-induced motor deficits. Finally, elevated Mn directly activates hypoxia-inducible factor (HIF) transcription factors, and additional mechanistic assays identified a role for HIF1, but not HIF2, in regulating expression of hepatic kynurenine pathway genes under physiological or Mn exposure conditions, suggesting that Mn-induced HIF1 activation may contribute to the dysregulation of the kynurenine pathway in Mn toxicity. These findings (1) identify the upregulation of the kynurenine pathway by elevated Mn as a fundamental mechanism of Mn-induced motor deficits; (2) provide a pharmacological approach to treat Mn-induced motor disease; and (3) should broadly advance understanding of the general principles underlying neuromotor deficits caused by metal toxicity.

A method for combing multi-beam bathymetric data to correct the deep sea sub-bottom profile

Virion-associated influenza hemagglutinin clusters upon sialic acid binding visualized by cryoelectron tomography

Influenza viruses are enveloped, negative-sense single-stranded RNA viruses covered in a dense layer of glycoproteins. Hemagglutinin (HA) accounts for 80 to 90% of influenza glycoprotein and plays a role in host cell binding and membrane fusion. While previous studies have characterized structures of purified receptor-free and receptor-bound HA, the effect of receptor binding on HA organization and structure on virions remains unknown. Here, we used cryoelectron tomography to visualize influenza virions bound to a sialic acid receptor mimic. Overall, receptor binding did not result in significant changes in viral morphology; however, we observed rearrangements of HA trimer organization and orientation. Compared to the even interglycoprotein spacing of unliganded HA trimers, receptor binding promotes HA trimer clustering and the formation of a triplet of trimers. Subtomogram averaging and refinement yielded 8 to 10 Å reconstructions that allowed us to visualize specific contacts between HAs from neighboring trimers and identify molecular features that mediate clustering. Taken together, we present structural evidence that receptor binding triggers clustering of HA trimers, revealing an additional layer of HA dynamics and plasticity.

WGCNA analysis reveals hub genes in the Hemarthria compressa roots in response to waterlogging stress

Abstract Hemarthria compressa is a high-quality forage resource in China. In recent years, waterlogging has frequently occurred, adversely affecting the growth and development of H. compressa. In order to investigate the physiological and molecular response mechanisms of H. compressa under waterlogging stress and identify hub genes involved in waterlogging tolerance, H. compressa roots from the GY (waterlogging-tolerant) and N1291 (waterlogging-sensitive) cultivars were selected as experimental materials in this study. The physiological indexes of H. compressa were measured, and transcriptome sequencing was carried out after 8 h and 24 h of waterlogging stress, with 0 h used as the control group. Superoxide dismutase (SOD) and peroxidase (POD) activities were significantly increased in both GY and N1291 under waterlogging stress (P < 0.05). Weighted gene co-expression network analysis (WGCNA) identified a total of four modules significantly associated with waterlogging stress (r>|0.9|, P < 0.05). Gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) enrichment results showed that differentially expressed genes (DEGs) were mainly enriched in the Starch and sucrose metabolism, Plant hormone signal transduction, Ribosome and Glutathione metabolism pathways. Seven hub genes were also retrieved, including Cluster-38255.67514 and Cluster-38255.80127, potentially associated with waterlogging tolerance. It is related to the Ribosome pathway and participates in the process of anti-waterlogging regulation. The results of this experiment provide new insights into the response mechanisms of H. compressa to waterlogging stress and a theoretical framework for the effective selection and breeding of waterlogging-tolerant cultivars.

Sleep homeostasis in lizards and the role of the cortex

Slow-wave sleep (SWS) and rapid eye movement sleep are the two primary components of electrophysiological sleep (e-sleep) in mammals and birds. Slow waves in the cortex not only characterize SWS but are also used as biological markers for sleep homeostasis, given their rebound after sleep deprivation (SD). Recently, it has been reported that the Australian dragon Pogona vitticeps exhibits a two-stage sleep pattern in the dorsal ventricular ridge (DVR), which includes a homologue of the mammalian claustrum (CLA). It remains unclear whether reptilian e-sleep, which has been characterized by activity outside the cortex, compensates for sleep loss, as observed in mammals. We here report a significant rebound in the local field potential (LFP) after 7 h of SD. Meanwhile, the mean bout length of each sleep state remained unaffected. We further investigated a possible role of the cortex in e-sleep regulation and homeostasis in Pogona and found that although a corticotomy had no obvious effect on the LFP features of baseline sleep, it abolished LFP power rebound in the CLA/DVR after SD. These findings suggest that e-sleep homeostasis is a common feature in amniotes and that the cortex is involved in regulating activity rebounds in reptiles and mammals.

Data reconstruction from machine learning models via inverse estimation and Bayesian inference

Focusing a viral risk ranking tool on prediction

Preparing to rapidly respond to emerging infectious diseases is critical. SpillOver: Viral Risk Ranking is an open-source tool developed to assess the risk of novel wildlife-origin viruses spilling over from animals to humans and spreading in human populations. Several risk factors used by the tool depend on evidence of previous zoonotic spillover itself or sustained transmission in humans. Therefore, we reanalyzed the Ranking Comparison after removing eight of the 31 risk factors that require postspillover knowledge and compared the adjusted risk rankings to the originals. The area under the receiver operating characteristic curve deteriorated from 0.94 for the original risk scores to 0.73 for the adjusted ones for predicting the classification as a human virus. We also compared the mean and SD of the risk scores for the human and non-human viruses at the risk factor level. Most excluded spillover-dependent risk factors had dissimilar means between the human and non-human virus classifications, but nonspillover-dependent risk factors frequently showed similar means between the two classifications. The original formulation of the tool depended on the inclusion of spillover-dependent risk factors to quantitatively assess the risk of zoonotic spillover for a novel virus. Future iterations of the tool should omit such risk factors and consider other nonspillover-dependent risk factors to ensure that the tool is fit for risk prediction of novel viruses.

Trunk stability and breathing exercises superior to foam rolling for restoring postural stability after core muscle fatigue in sedentary employees

St3gal5-mediated sialylation of glyco-CD177 on neutrophils restricts neuroinflammation following CNS injury

Neutrophils are the most abundant circulating leukocyte population that play critical roles in neuroinflammation following central nervous system (CNS) injury. CD177, a glycoprotein on neutrophils, is emerging as an important immune regulator which can fundamentally affect multiple human inflammatory diseases. However, the role and regulatory mechanism of CD177 glycobiology of neutrophils in neuroinflammation remain elusive. Here, we show that CD177 + neutrophils expand significantly and infiltrate the injured brain following CNS injury both in the human and mouse. Using single-cell RNA sequencing and genetic approaches, we find CD177 + neutrophils as an anti-inflammatory subset that is critical for modulating neuroinflammation after CNS injury. We further identify St3gal5, a sialyltransferase (ST), that can mediate the sialylation and cell surface presentation of glyco-CD177 on neutrophils. Glycoproteomics reveal downregulated sialylation levels in St3gal5-deficient neutrophils. Neutrophil-specific depletion of St3gal5 prevents the cell surface presentation of CD177 on brain-infiltrated neutrophils and exacerbates neuroinflammation. Administration of the FDA-approved anticonvulsant valproic acid (VPA), an St3gal5 upregulator, promotes the glycosylation of neutrophils and attenuates neuroinflammation following CNS injury. Our study reveals a glycoimmuno-regulatory effect of neutrophils and suggests VPA as a neutrophil glycobiology targeting approach to combat neuroinflammation following CNS injury.

An innovative decision-making approach for unmanned aerial vehicle software selection using bipolar fuzzy aggregation operators

Existential risk narratives about AI do not distract from its immediate harms

There is broad consensus that AI presents risks, but considerable disagreement about the nature of those risks. These differing viewpoints can be understood as distinct narratives, each offering a specific interpretation of AI’s potential dangers. One narrative focuses on doomsday predictions of AI posing long-term existential risks for humanity. Another narrative prioritizes immediate concerns that AI brings to society today, such as the reproduction of biases embedded into AI systems. A significant point of contention is that the “existential risk” narrative, which is largely speculative, may distract from the less dramatic but real and present dangers of AI. We address this “distraction hypothesis” by examining whether a focus on existential threats diverts attention from the immediate risks AI poses today. In three preregistered, online survey experiments (N = 10,800), participants were exposed to news headlines that either depicted AI as a catastrophic risk, highlighted its immediate societal impacts, or emphasized its potential benefits. Results show that i) respondents are much more concerned with the immediate, rather than existential, risks of AI, and ii) existential risk narratives increase concerns for catastrophic risks without diminishing the significant worries respondents express for immediate harms. These findings provide important empirical evidence to inform ongoing scientific and political debates on the societal implications of AI.