Explore the vast range of titles available.

Tactile perception is significant for robotic operation in unstructured environments. Whisker-based sensors offer lightweight bio-inspired solutions, yet most rely on single-whisker sensing and are limited by passive interaction and constrained functionality. Here we present a circular array of eight independently actuated whiskers, each driven by a pulse-switchable permanent magnet and tracked by a camera. This design enables simultaneous multi-point sensing and coordinated actuation, supporting diverse functions. Quantitative analyses demonstrate accurate pixel-to-physical mapping, consistent pixel-to-force characterization, and long-term repeatability. In this work, we show that an vibrissae-inspired vision-based magnetic-actuated whisker array integrating distributed perception with active interaction achieves reliable physical mapping, repeatable sensing, and delicate grasping, thereby advancing tactile sensing and laying the foundation for contact-driven exploration, soft manipulation, and adaptive behavior in dynamic environments. Authors present a whisker sensor enabling robots to sense surroundings via vision-tracked, magnetically actuated whiskers. It detects contact and flow, identifies objects and fluids, and gently grasps fragile items.

Autophagy captures intracellular components and delivers them to lysosomes, where they are degraded and recycled to sustain metabolism and to enable survival during starvation 1 – 5 . Acute, whole-body deletion of the essential autophagy gene Atg7 in adult mice causes a systemic metabolic defect that manifests as starvation intolerance and gradual loss of white adipose tissue, liver glycogen and muscle mass 1 . Cancer cells also benefit from autophagy. Deletion of essential autophagy genes impairs the metabolism, proliferation, survival and malignancy of spontaneous tumours in models of autochthonous cancer 6 , 7 . Acute, systemic deletion of Atg7 or acute, systemic expression of a dominant-negative ATG4b in mice induces greater regression of KRAS-driven cancers than does tumour-specific autophagy deletion, which suggests that host autophagy promotes tumour growth 1 , 8 . Here we show that host-specific deletion of Atg7 impairs the growth of multiple allografted tumours, although not all tumour lines were sensitive to host autophagy status. Loss of autophagy in the host was associated with a reduction in circulating arginine, and the sensitive tumour cell lines were arginine auxotrophs owing to the lack of expression of the enzyme argininosuccinate synthase 1. Serum proteomic analysis identified the arginine-degrading enzyme arginase I (ARG1) in the circulation of Atg7 -deficient hosts, and in vivo arginine metabolic tracing demonstrated that serum arginine was degraded to ornithine. ARG1 is predominantly expressed in the liver and can be released from hepatocytes into the circulation. Liver-specific deletion of Atg7 produced circulating ARG1, and reduced both serum arginine and tumour growth. Deletion of Atg5 in the host similarly regulated circulating arginine and suppressed tumorigenesis, which demonstrates that this phenotype is specific to autophagy function rather than to deletion of Atg7 . Dietary supplementation of Atg7 -deficient hosts with arginine partially restored levels of circulating arginine and tumour growth. Thus, defective autophagy in the host leads to the release of ARG1 from the liver and the degradation of circulating arginine, which is essential for tumour growth; this identifies a metabolic vulnerability of cancer. Mice with whole-body or liver-specific deletion of Atg7 release circulating arginase I and have reduced levels of serum arginine, which impairs the growth of allografted arginine-auxotrophic tumours.

Cancer cells depend on nicotinamide adenine dinucleotide phosphate (NADPH) to combat oxidative stress and support reductive biosynthesis. One major NADPH production route is the oxidative pentose phosphate pathway (committed step: glucose-6-phosphate dehydrogenase, G6PD). Alternatives exist and can compensate in some tumors. Here, using genetically-engineered lung cancer mouse models, we show that G6PD ablation significantly suppresses Kras G12D/+ ;Lkb1 -/- (KL) but not Kras G12D/+ ;P53 -/- (KP) lung tumorigenesis. In vivo isotope tracing and metabolomics reveal that G6PD ablation significantly impairs NADPH generation, redox balance, and de novo lipogenesis in KL but not KP lung tumors. Mechanistically, in KL tumors, G6PD ablation activates p53, suppressing tumor growth. As tumors progress, G6PD-deficient KL tumors increase an alternative NADPH source from serine-driven one carbon metabolism, rendering associated tumor-derived cell lines sensitive to serine/glycine depletion. Thus, oncogenic driver mutations determine lung cancer dependence on G6PD, whose targeting is a potential therapeutic strategy for tumors harboring KRAS and LKB1 co-mutations. Cancer cells rely on NADPH to manage oxidative stress and support biosynthesis. Here, the authors show that glucose-6-phosphate dehydrogenase (G6PD) ablation suppresses KRAS -driven lung tumours with LKB1 deficiency, but not with P53 deficiency, by impairing NADPH production, suggesting a potential therapeutic strategy.

The past decades have seen the rapid development of tactile sensors in material, fabrication, and mechanical structure design. The advancement of tactile sensors has heightened the expectation of sensor functions, and thus put forward a higher demand for data processing. However, conventional analysis techniques have not kept pace with the tactile sensor development and still suffer from some severe drawbacks, like cumbersome models, poor efficiency, and expensive costs. Machine learning, with its prominent ability for big data analysis and fast processing speed, can offer many possibilities for tactile data analysis. Herein, the machine learning techniques employed for processing tactile signals are reviewed. Supervised learning and unsupervised learning for analog signals are covered, and processing spike signals with machine learning are summarized. Furthermore, the applications in robotic tactile perception and human activity monitoring are presented. Finally, the current challenges and future prospects in sensors, data, algorithms, and benchmarks are discussed. Tactile sensors have developed rapidly, which increases the need for data processing. While machine learning, rather than conventional approaches, provides new support for tactile data analysis, thanks to its strong capacity for processing massive data quickly, the machine learning methods for tactile data processing and their applications are reviewed. The current issues and future directions are then discussed.

Mitochondrial function supports energy and anabolic metabolism. Pathogenic mitochondrial DNA (mtDNA) mutations impair these processes, causing mitochondrial diseases. Their role in human cancers is less clear; while some cancers harbor high mtDNA mutation burden, others do not. Here we show that a proofreading mutant of DNA polymerase gamma (PolG D256A ) increases the mtDNA mutation burden in non-small-cell lung cancer (NSCLC). This mutation promotes the accumulation of defective mitochondria, reduces tumor cell proliferation and viability, and improves cancer survival. In NSCLC, pathogenic mtDNA mutations enhance glycolysis and create a glucose dependency to support mitochondrial energy, but at the expense of a lower NAD + /NADH ratio that hinders de novo serine synthesis. Thus, mitochondrial function in NSCLC is essential for maintaining adequate serine synthesis, which in turn supports the anabolic metabolism and redox homeostasis required for tumor growth, explaining why these cancers preserve functional mtDNA. The role of pathogenic mitochondrial DNA (mtDNA) mutation in cancer remains to be studied. Here the authors show that high mtDNA mutation burden in lung cancer models leads to increased glycolysis but limited de novo serine synthesis, rendering sensitivity to dietary serine and glycine deprivation.

Macroautophagy (hereafter autophagy) degrades and recycles intracellular components to sustain metabolism and survival during starvation. Host autophagy promotes tumor growth by providing essential tumor nutrients. Autophagy also regulates immune cell homeostasis and function and suppresses inflammation. Although host autophagy does not promote a T-cell anti-tumor immune response in tumors with low tumor mutational burden (TMB), whether this was the case in tumors with high TMB was not known. Here we show that autophagy, especially in the liver, promotes tumor immune tolerance by enabling regulatory T-cell function and limiting stimulator of interferon genes, T-cell response and interferon-γ, which enables growth of high-TMB tumors. We have designated this as hepatic autophagy immune tolerance. Autophagy thereby promotes tumor growth through both metabolic and immune mechanisms depending on mutational load and autophagy inhibition is an effective means to promote an antitumor T-cell response in high-TMB tumors.

TRPM7 is an unusual bi-functional protein containing an ion channel covalently linked to a protein kinase domain. TRPM7 is implicated in regulating cellular and systemic magnesium homeostasis. While the biophysical properties of TRPM7 ion channel and its function are relatively well characterized, the function of the TRPM7 enzymatically active kinase domain is not understood yet. To investigate the physiological role of TRPM7 kinase activity, we constructed mice carrying an inactive TRPM7 kinase. We found that these mice were resistant to dietary magnesium deprivation, surviving three times longer than wild type mice; also they displayed decreased chemically induced allergic reaction. Interestingly, mutant mice have lower magnesium bone content compared to wild type mice when fed regular diet; unlike wild type mice, mutant mice placed on magnesium-depleted diet did not alter their bone magnesium content. Furthermore, mouse embryonic fibroblasts isolated from TRPM7 kinase-dead animals exhibited increased resistance to magnesium deprivation and oxidative stress. Finally, electrophysiological data revealed that the activity of the kinase-dead TRPM7 channel was not significantly altered. Together, our results suggest that TRPM7 kinase is a sensor of magnesium status and provides coordination of cellular and systemic responses to magnesium deprivation.

LKB1 and KRAS are the third most frequent co-mutations detected in non-small cell lung cancer (NSCLC) and cause aggressive tumor growth. Unfortunately, treatment with RAS-RAF-MEK-ERK pathway inhibitors has minimal therapeutic efficacy in LKB1-mutant KRAS-driven NSCLC. Autophagy, an intracellular nutrient scavenging pathway, compensates for Lkb1 loss to support Kras-driven lung tumor growth. Here we preclinically evaluate the possibility of autophagy inhibition together with MEK inhibition as a treatment for Kras-driven lung tumors. We found that the combination of the autophagy inhibitor hydroxychloroquine (HCQ) and the MEK inhibitor Trametinib displays synergistic anti-proliferative activity in Kras G12D/+; Lkb1 -/- (KL) lung cancer cells, but not in Kras G12D/+; p53 -/- (KP) lung cancer cells. In vivo studies using tumor allografts, genetically engineered mouse models (GEMMs) and patient-derived xenografts (PDXs) showed anti-tumor activity of the combination of HCQ and Trametinib on KL but not KP tumors. We further found that the combination treatment significantly reduced mitochondrial membrane potential, basal respiration, and ATP production, while also increasing lipid peroxidation, indicative of ferroptosis, in KL tumor-derived cell lines (TDCLs) and KL tumors compared to treatment with single agents. Moreover, the reduced tumor growth by the combination treatment was rescued by ferroptosis inhibitor. Taken together, we demonstrate that autophagy upregulation in KL tumors causes resistance to Trametinib by inhibiting ferroptosis. Therefore, a combination of autophagy and MEK inhibition could be a novel therapeutic strategy to specifically treat NSCLC bearing co-mutations of LKB1 and KRAS.

Perceiving surface characteristics through tactile interaction typically requires high‐resolution devices or precise spatial scanning to record and analyze a significant amount of information. However, most available tactile sensors require complicated technological processes, redundant layouts, and data acquisition circuits, which limits their ability to provide a real‐time static perception and feedback for potential applications such as robotic manipulation. Drawing inspiration from the sliding tactile (ST) perception mode of the human fingertip, a robust and flexible ST sensor with a low array density of 2.7 cells cm−2 is reported. This innovative sensor has a soft and cambered configuration that allows it to rapidly and accurately recognize the 3D surface features of objects, including grooves as small as 500 μm. Benefiting from the strong correlation between collected electronic responding and local deformation of sensing cell, the ST sensor can adaptively reconstruct surface patterns with the assistance of deep learning, even on unstructured objects. The pattern recognition system based on the robot is demonstrated by accurately classifying a set of mahjong tiles with nearly 100% accuracy, surpassing human tactile perception capabilities in the same task. Herein, a flexible sliding tactile sensor that is inspired by the human fingertip, capable of constructing high‐resolution pattern images using just a few sensor cells, is proposed. Its unique deformation‐induced sensing mechanism provides a strongly correlated static response to unstructured pattern features and applied pressure. When combined with deep learning, this technology enables a robot to automatically classify significant patterns.

Liver kinase B1 (LKB1), also known as serine/threonine kinase 11 (STK11) is the major energy sensor for cells to respond to metabolic stress. Autophagy degrades and recycles proteins, macromolecules, and organelles for cells to survive starvation. To assess the role and cross-talk between autophagy and Lkb1 in normal tissue homeostasis, we generated genetically engineered mouse models where we can conditionally delete Stk11 and autophagy essential gene, Atg7, respectively or simultaneously, throughout the adult mice. We found that Lkb1 was essential for the survival of adult mice, and autophagy activation could temporarily compensate for the acute loss of Lkb1 and extend mouse life span. We further found that acute deletion of Lkb1 in adult mice led to impaired intestinal barrier function, hypoglycemia, and abnormal serum metabolism, which was partly rescued by the Lkb1 loss-induced autophagy upregulation via inhibiting p53 induction. Taken together, we demonstrated that autophagy and Lkb1 work synergistically to maintain adult mouse homeostasis and survival.