A noninvasive brain–computer interface is a central task in the comprehensive analysis and understanding of the brain and is an important challenge in international brain-science research. Current implanted brain–computer interfaces are cranial and invasive, which considerably limits their applications. The development of new noninvasive reading and writing technologies will advance substantial innovations and breakthroughs in the field of brain–computer interfaces. Here, we review the theory and development of the ultrasound brain functional imaging and its applications. Furthermore, we introduce latest advancements in ultrasound brain modulation and its applications in rodents, primates, and human; its mechanism and closed-loop ultrasound neuromodulation based on electroencephalograph are also presented. Finally, high-frequency acoustic noninvasive brain–computer interface is prospected based on ultrasound super-resolution imaging and acoustic tweezers.

The cell-specific functions of nitric oxide (NO) in the intestinal microenvironment orchestrate its therapeutic effects in ulcerative colitis. While most biomaterials show promise by eliciting the characteristics of NO, the insufficient storage, burst release, and pro-inflammatory side effects of NO remain as challenges. Herein, we report the development of thiol–disulfide hybrid mesoporous organosilica nanoparticles (MONs) that improve the storage and sustained release of NO, broadening the therapeutic window of NO-based therapy against colitis. The tailored NO-storing nanomaterials coordinated the release of NO and the immunoregulator dexamethasone (Dex) in the intestinal microenvironment, specifically integrating the alleviation of oxidative stress in enterocytes and the reversal of NO-exacerbated macrophage activation. Mechanistically, such a synchronous operation was achieved by a self-motivated process wherein the thiyl radicals produced by NO release cleaved the disulfide bonds to degrade the matrix and release Dex via thiol–disulfide exchange. Specifically, the MON-mediated combination of NO and Dex greatly ameliorated intractable colitis compared with 5-aminosalicylic acid, even after delayed treatment. Together, our results reveal a key contribution of synergistic modulation of the intestinal microenvironment in NO-based colitis therapy and introduce thiol–disulfide hybrid nanotherapeutics for the management of inflammatory diseases and cancer.

Black phosphorus gives several advantages and complementarities over other two-dimensional materials. It has drawn extensive interest owing to its relatively high carrier mobility, wide tunable bandgap, and in-plane anisotropy in recent years. This manuscript briefly reviews the structure and physical properties of black phosphorus and targets on black phosphorus for photonic integrated circuits. Some of the applications are discussed including photodetection, optical modulation, light emission, and polarization conversion. Corresponding recent progresses, associated challenges, and future potentials are covered.

Primary sclerosing cholangitis (PSC) is a biliary disease accompanied by chronic inflammation of the liver and biliary stricture. Mesenchymal stem cells (MSCs) are used to treat liver diseases because of their immune regulation and regeneration-promoting functions. This study was performed to explore the therapeutic potential of human placental MSCs (hP-MSCs) in PSC through the Takeda G protein-coupled receptor 5 (TGR5) receptor pathway. Liver tissues were collected from patients with PSC and healthy donors (n = 4) for RNA sequencing and intrahepatic cholangiocyte organoid construction. hP-MSCs were injected via the tail vein into Mdr2^−/−, bile duct ligation (BDL), and 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) mouse models or co-cultured with organoids to confirm their therapeutic effect on biliary cholangitis. Changes in bile acid metabolic profile were analyzed by liquid chromatography/tandem mass spectrometry (LC-MS/MS). Compared with healthy controls, liver tissues and intrahepatic cholangiocyte organoids from PSC patients were characterized by inflammation and cholestasis, and marked downregulation of bile acid receptor TGR5 expression. hP-MSC treatment apparently reduced the inflammation, cholestasis, and fibrosis in Mdr2^−/−, BDL, and DDC model mice. By activating the phosphatidylinositol 3 kinase/extracellular signal-regulated protein kinase pathway, hP-MSC treatment promoted the proliferation of cholangiocytes, and affected the transcription of downstream nuclear factor κB through regulation of the binding of TGR5 and Pellino3, thereby affecting the cholangiocyte inflammatory phenotype.

Soft carbons have attracted extensive interests as competitive anodes for fast-charging sodium-ion batteries (SIBs); however, the high-rate performance is still restricted by their large ion migration barriers and sluggish reaction kinetics. Herein, we show a molecular design approach toward the fabrication of nitrogen and phosphorus codoped mesoporous soft carbon (NPSC). The key to this strategy lies in the chemical cross-linking reaction between polyphosphoric acid and p-phenylenediamine, associated with pyrolysis induced in-situ self-activation that creates mesoporous structures and rich heteroatoms within the carbon matrix. Thanks to the enlarged interlayer spacing, reduced ion diffusion length, and plentiful active sites, the obtained NPSC delivers a superb rate capacity of 215 mAh g⁻¹ at 10 A g⁻¹ and an ultralong cycle life of 4,700 cycles at 5 A g⁻¹. Remarkably, the full cell shows 99% capacity retention during 100 continuous cycles, and maximum energy and power densities of 191 Wh kg⁻¹ and 9.2 kW kg⁻¹, respectively. We believe that such a synthetic protocol could pave a novel venue to develop soft carbons with unique properties for advanced SIBs.

An optical spectrometer is a basic spectral instrument that probes microscopic physical and chemical properties of macroscopic objects but generally suffers from difficulty in broadband time-resolved measurement. In this work, we report the creation of ultrabroadband white-light laser with a 3-dB bandwidth covering 385 to 1,080 nm, pulse energy of 1.07 mJ, and pulse duration of several hundred femtoseconds by passing 3-mJ pulse energy, 50-fs pulse duration Ti:Sapphire pulse laser through a cascaded fused silica plate and chirped periodically poled lithium niobate crystal. We utilize this unprecedented superflat, ultrabroadband, and intense femtosecond laser light source to build a single-shot (i.e., single-pulse) subpicosecond pulse laser ultraviolet–visible–near-infrared spectrometer and successfully measure various atomic and molecular absorption spectra. The single-shot ultrafast spectrometer may open up a frontier to monitor simultaneously the ultrafast dynamics of multiple physical and chemical processes in various microscopic systems.

Neddylation is necessary for activation of Cullin-RING ligases (CRLs), which degrade various immune regulatory proteins. Our recent study showed that while depletion of neddylation E2–E3 pair Ube2f-Sag in regulatory T (T_reg) cells had no obvious phenotype, the same depletion of either Ube2m or Rbx1 caused inflammation disorders with different severity. Whether these E2s or E3s compensate each other in functional regulations of T_reg cells is, however, previously unknown. In this report, we generated Foxp3^Cre;Ube2m^fl/fl;Ube2f^fl/fl or Foxp3^Cre;Rbx1^fl/fl;Sag^fl/fl double-null mice by simultaneous deletion of both neddylation E2s or E3s in T_reg cells, respectively. Remarkably, Ube2m&Ube2f double-null mice developed much severe autoimmune phenotypes than did Ube2m-null mice, indicating that Ube2m markedly compensates Ube2f in T_reg cells. The minor worsened autoimmune phenotypes seen at the very early stage in Rbx1&Sag double-null than Rbx1-null mice is likely due to already severe phenotypes of the later, indicating a minor compensation of Rbx1 for Sag. The RNA profiling-based analyses revealed that up- and down-regulations of few signaling pathways in T_reg cells are associated with the severity of autoimmune phenotypes. Finally, severer inflammation phenotypes seen in mice with double E3-null than with double E2-null T_reg cells indicate a neddylation-independent mechanism of 2 E3s, also known to serve as the RING component of CRLs in regulation of T_reg cell fitness.

Marine organisms perform a sea of diel rhythmicity. Planktonic diel dynamics have been shown to be driven by light, energy resources, circadian rhythms, and the coordinated coupling of photoautotrophs and heterotrophic bacterioplankton. Here, we explore the diel fluctuation of viral production and decay and their impact on the total and active bacterial community in the coastal and open seawaters of the South China Sea. The results showed that the night-production diel pattern of lytic viral production was concurrent with the lower viral decay at night, contributing to the accumulation of the viral population size during the night for surface waters. The diel variations in bacterial activity, community composition, and diversity were found highly affected by viral dynamics. This was revealed by the finding that bacterial community diversity was positively correlated to lytic viral production in the euphotic zone of the open ocean but was negatively related to lysogenic viral production in the coastal ocean. Such distinct but contrasting correlations suggest that viral life strategies can not only contribute to diversifying bacterial community but also potentially piggyback their host to dominate bacterial community, suggesting the tightly synchronized depth-dependent and habitat-specific diel patterns of virus–host interactions. It further implies that viruses serve as an ecologically important driver of bacterial diel dynamics across the ocean, highlighting the viral roles in bacterial ecological and biogeochemical processes in the ocean.

Comprehensive and quantitative assessment of human physical activity in daily life is valuable for healthcare, especially for those who suffer from obesity and neurological disorders or are at high risk of dementia. Common wearable devices, e.g., smartwatches, are insufficient and inaccurate for monitoring highly dynamic limb movements and assessing human motion. Here, we report a new wearable leg movement monitoring system incorporating a custom-made motion sensor with machine learning algorithm to perceive human motion accurately and comprehensively during diverse walking and running actions. The system enables real-time multimodal perceptions of personal identity, motion state, locomotion speed, and energy expenditure for wearers. A general law of extracting real-time metabolic energy from leg movements is verified although individual gaits show differences. In addition, we propose a novel sensing configuration combining unilateral lower leg movement velocity with its angular rate to achieve high accuracy and good generalizability while simplifying the wearable system. Advanced performances in personal identification (accuracy of 98.7%) and motion-state recognition (accuracy of 93.7%) are demonstrated. The wearable system also exhibites high-precision real-time estimations of locomotion speed (error of 3.04% to 9.68%) and metabolic energy (error of 4.18% to 14.71%) for new subjects across various time-varying conditions. The wearable system allows reliable leg movement monitoring and quantitative assessment of bodily kinematic and kinetic behaviors during daily activities, as well as safe identity authentication by gait parameters, which would greatly facilitate smart life, personal healthcare, and rehabilitation training.

Solid tumor cells live in a highly dynamic mechanical microenvironment. How the extracellular-matrix-generated mechanotransduction regulates tumor cell development and differentiation remains an enigma. Here, we show that a low mechanical force generated from the soft matrix induces dedifferentiation of moderately stiff tumor cells to soft stem-cell-like cells. Mechanistically, integrin β8 was identified to transduce mechano-signaling to trigger tumor cell dedifferentiation by recruiting RhoGDI1 to inactivate RhoA and subsequently Yes-associated protein (YAP). YAP inactivation relieved the inhibition of v-maf avian musculoaponeurotic fibrosarcoma oncogene homolog G (MAFG), allowing MAFG to transactivate the stemness genes NANOG, SOX2, and NESTIN. Inactivation also restored β8 expression, thereby forming a closed mechanical loop. Importantly, MAFG expression is correlated with worse prognosis. Our findings provide mechanical insights into the regulation of tumor cell dedifferentiation, which has therapeutic implications for exploring innovative strategies to attack malignancies.