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Stretchable energy storage devices, maintaining the capability of steady operation under large mechanical strain, have become increasing more important with the development of stretchable electronic devices. Stretchable supercapacitors (SSCs), with high power density, modest energy density, and superior mechanical properties are regarded as one of the most promising power supplies to stretchable electronic devices. Conductive polymers, such as polyaniline (PANI), polypyrrole (PPy), polythiophene (PTh) and poly(3,4-ehtylenedioxythiophene) (PEDOT), are among the well-studied electroactive materials for the construction of SSCs because of their high specific theoretical capacity, excellent electrochemical activity, light weight, and high flexibility. Much effort has been devoted to developing stretchable, conductive polymer-based SSCs with different device structures, such as sandwich-type and fiber-shaped type SSCs. This review summarizes the material and structural design for conductive polymer-based SSCs and discusses the challenge and important directions in this emerging field.

The two-dimensional topological insulators host a full gap in the bulk band, induced by spin–orbit coupling (SOC) effect, together with the topologically protected gapless edge states. However, it is usually challenging to suppress the bulk conductance and thus to realize the quantum spin Hall (QSH) effect. In this study, we find a mechanism to effectively suppress the bulk conductance. By using the quasiparticle interference technique with scanning tunneling spectroscopy, we demonstrate that the QSH candidate single-layer 1 T ’-WTe 2 has a semimetal bulk band structure with no full SOC-induced gap. Surprisingly, in this two-dimensional system, we find the electron–electron interactions open a Coulomb gap which is always pinned at the Fermi energy ( E F ). The opening of the Coulomb gap can efficiently diminish the bulk state at the E F and supports the observation of the quantized conduction of topological edge states. The conductance from bulk bands in a topological insulator usually blurs effects arising from edge states. Here, Song et al. report a Coulomb gap opened by electron–electron interactions, which effectively suppress the bulk conductance and promote observation of topological edge states in the single-layer 1 T ’-WTe 2 .

Autism spectrum disorder (ASD) is a common neurodevelopmental disorder. The mechanisms underlying ASD are unclear. Astrocyte alterations are noted in ASD patients and animal models. However, whether astrocyte dysfunction is causal or consequential to ASD-like phenotypes in mice is unresolved. Type 2 inositol 1,4,5-trisphosphate 6 receptors (IP3R2)-mediated Ca 2+ release from intracellular Ca 2+ stores results in the activation of astrocytes. Mutations of the IP3R2 gene are associated with ASD. Here, we show that both IP3R2-null mutant mice and astrocyte-specific IP3R2 conditional knockout mice display ASD-like behaviors, such as atypical social interaction and repetitive behavior. Furthermore, we show that astrocyte-derived ATP modulates ASD-like behavior through the P2X2 receptors in the prefrontal cortex and possibly through GABAergic synaptic transmission. These findings identify astrocyte-derived ATP as a potential molecular player in the pathophysiology of ASD. Astrocytes contribute to autism spectrum disorder (ASD) pathophysiology. Here, the authors show that IP3R2 conditional KO mice show ASD-like behaviours and identify astrocyte-derived ATP as a modulator of these behaviours in mice.

Background Endothelial cell (EC) dysfunctions, including turnover enrichment, gap junction disruption, inflammation, and oxidation, play vital roles in the initiation of vascular disorders and atherosclerosis. Hemodynamic forces, i.e., atherprotective pulsatile (PS) and pro-atherogenic oscillatory shear stress (OS), can activate mechanotransduction to modulate EC function and dysfunction. This review summarizes current studies aiming to elucidate the roles of epigenetic factors, i.e., histone deacetylases (HDACs), non-coding RNAs, and DNA methyltransferases (DNMTs), in mechanotransduction to modulate hemodynamics-regulated EC function and dysfunction. Main body of the abstract OS enhances the expression and nuclear accumulation of class I and class II HDACs to induce EC dysfunction, i.e., proliferation, oxidation, and inflammation, whereas PS induces phosphorylation-dependent nuclear export of class II HDACs to inhibit EC dysfunction. PS induces overexpression of the class III HDAC Sirt1 to enhance nitric oxide (NO) production and prevent EC dysfunction. In addition, hemodynamic forces modulate the expression and acetylation of transcription factors, i.e., retinoic acid receptor α and krüppel-like factor-2, to transcriptionally regulate the expression of microRNAs (miRs). OS-modulated miRs, which stimulate proliferative, pro-inflammatory, and oxidative signaling, promote EC dysfunction, whereas PS-regulated miRs, which induce anti-proliferative, anti-inflammatory, and anti-oxidative signaling, inhibit EC dysfunction. PS also modulates the expression of long non-coding RNAs to influence EC function. i.e., turnover, aligmant, and migration. On the other hand, OS enhances the expression of DNMT-1 and -3a to induce EC dysfunction, i.e., proliferation, inflammation, and NO repression. Conclusion Overall, epigenetic factors play vital roles in modulating hemodynamic-directed EC dysfunction and vascular disorders, i.e., atherosclerosis. Understanding the detailed mechanisms through which epigenetic factors regulate hemodynamics-directed EC dysfunction and vascular disorders can help us to elucidate the pathogenic mechanisms of atherosclerosis and develop potential therapeutic strategies for atherosclerosis treatment.

ObjectiveTumour pathology contains rich information, including tissue structure and cell morphology, that reflects disease progression and patient survival. However, phenotypic information is subtle and complex, making the discovery of prognostic indicators from pathological images challenging.DesignAn interpretable, weakly supervised deep learning framework incorporating prior knowledge was proposed to analyse hepatocellular carcinoma (HCC) and explore new prognostic phenotypes on pathological whole-slide images (WSIs) from the Zhongshan cohort of 1125 HCC patients (2451 WSIs) and TCGA cohort of 320 HCC patients (320 WSIs). A ‘tumour risk score (TRS)’ was established to evaluate patient outcomes, and then risk activation mapping (RAM) was applied to visualise the pathological phenotypes of TRS. The multi-omics data of The Cancer Genome Atlas(TCGA) HCC were used to assess the potential pathogenesis underlying TRS.ResultsSurvival analysis revealed that TRS was an independent prognosticator in both the Zhongshan cohort (p<0.0001) and TCGA cohort (p=0.0003). The predictive ability of TRS was superior to and independent of clinical staging systems, and TRS could evenly stratify patients into up to five groups with significantly different prognoses. Notably, sinusoidal capillarisation, prominent nucleoli and karyotheca, the nucleus/cytoplasm ratio and infiltrating inflammatory cells were identified as the main underlying features of TRS. The multi-omics data of TCGA HCC hint at the relevance of TRS to tumour immune infiltration and genetic alterations such as the FAT3 and RYR2 mutations.ConclusionOur deep learning framework is an effective and labour-saving method for decoding pathological images, providing a valuable means for HCC risk stratification and precise patient treatment.

Speeding up the transmission of information carried by waves is of fundamental interest for wave physics, with pivotal significance for underwater communications. To overcome the current limitations in information transfer capacity, here we propose and experimentally validate a mechanism using multipath sound twisting to realize real-time high-capacity communication free of signal-processing or sensor-scanning. The undesired channel crosstalk, conventionally reduced via time-consuming postprocessing, is virtually suppressed by using a metamaterial layer as purely-passive demultiplexer with high spatial selectivity. Furthermore, the compactness of system ensures high information density crucial for acoustics-based applications. A distinct example of complicated image transmission is experimentally demonstrated, showing as many independent channels as the path number multiplied by vortex mode number and an extremely-low bit error rate nearly 1/10 of the forward error correction limit. Our strategy opens an avenue to metamaterial-based high-capacity communication paradigm compatible with the conventional multiplexing mechanisms, with far-reaching impact on acoustics and other domains. Here, the authors demonstrate multipath twisting of acoustic waves with a thin metamaterial layer enabling high-speed transfer of information with no time-consuming post-processing or sensor scanning, showing important application potential in underwater communication.

Hierarchies of Peregrine solution and breather solution are derived in a (2+1)-dimensional variable-coefficient nonlinear Schrödinger equation with partial nonlocality. Based on these solutions, we study the control of the excitation of Peregrine solution and breather solution in different planes. In particular, the localized Peregrine solution and breather solution are firstly reported in two-dimensional space. It is expected that our analysis and results may give new insight into higher-dimensional localized rogue waves in nonlocal media.

Long-term potentiation (LTP) in the hippocampus is the most studied form of synaptic plasticity. Temporal integration of synaptic inputs is essential in synaptic plasticity and is assumed to be achieved through Ca2+ signaling in neurons and astroglia. However, whether these two cell types play different roles in LTP remain unknown. Here, we found that through the integration of synaptic inputs, astrocyte inositol triphosphate (IP3) receptor type 2 (IP3R2)-dependent Ca2+ signaling was critical for late-phase LTP (L-LTP) but not early-phase LTP (E-LTP). Moreover, this process was mediated by astrocyte-derived brain-derived neurotrophic factor (BDNF). In contrast, neuron-derived BDNF was critical for both E-LTP and L-LTP. Importantly, the dynamic differences in BDNF secretion play a role in modulating distinct forms of LTP. Moreover, astrocyte- and neuron-derived BDNF exhibited different roles in memory. These observations enriched our knowledge of LTP and memory at the cellular level and implied distinct roles of astrocytes and neurons in information integration.

Breast cancer, characterized by unique epidemiological patterns and significant heterogeneity, remains one of the leading causes of malignancy-related deaths in women. The increasingly nuanced molecular subtypes of breast cancer have enhanced the comprehension and precision treatment of this disease. The mechanisms of tumorigenesis and progression of breast cancer have been central to scientific research, with investigations spanning various perspectives such as tumor stemness, intra-tumoral microbiota, and circadian rhythms. Technological advancements, particularly those integrated with artificial intelligence, have significantly improved the accuracy of breast cancer detection and diagnosis. The emergence of novel therapeutic concepts and drugs represents a paradigm shift towards personalized medicine. Evidence suggests that optimal diagnosis and treatment models tailored to individual patient risk and expected subtypes are crucial, supporting the era of precision oncology for breast cancer. Despite the rapid advancements in oncology and the increasing emphasis on the clinical precision treatment of breast cancer, a comprehensive update and summary of the panoramic knowledge related to this disease are needed. In this review, we provide a thorough overview of the global status of breast cancer, including its epidemiology, risk factors, pathophysiology, and molecular subtyping. Additionally, we elaborate on the latest research into mechanisms contributing to breast cancer progression, emerging treatment strategies, and long-term patient management. This review offers valuable insights into the latest advancements in Breast Cancer Research, thereby facilitating future progress in both basic research and clinical application.

CRISPR-based assays for the detection of nucleic acids are highly specific, yet they are not fast, sensitive or easy to use. Here we report a one-step fluorescence assay for the detection of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) RNA in nasopharyngeal samples, with a sample-to-answer time of less than 20 minutes and a sensitivity comparable to that of quantitative real-time PCR with reverse transcription (RT–qPCR). The assay uses suboptimal protospacer adjacent motifs, allowing for flexibility in the design of CRISPR RNAs and slowing down the kinetics of Cas12a-mediated collateral cleavage of fluorescent DNA reporters and cis cleavage of substrates, which leads to stronger fluorescence owing to the accumulation of amplicons generated by isothermal recombinase polymerase amplification. In a set of 204 nasopharyngeal samples with RT–qPCR cycle thresholds ranging from 18.1 to 35.8, the assay detected SARS-CoV-2 with a sensitivity of 94.2% and a specificity of 100%, without the need for RNA extraction. Rapid and sensitive assays for nucleic acid testing in one pot that allow for flexibility in assay design may aid the development of reliable point-of-care nucleic acid testing. A one-step fluorescence assay relying on suboptimal protospacer adjacent motifs for Cas12a detects SARS-CoV-2 RNA in nasopharyngeal samples in less than 20 minutes with a sensitivity comparable to that of RT–qPCR.