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Gut bacteria prime and reinforce mature leaf oviposition preference in beetles via plant mediated feedback
Reply to: “No evidence of neural feature-specific pre-activation during the prediction of an upcoming stimulus”
TAK1 drives inflammatory fibroblast acquisition and shapes myocardial infarction responses in male mice
Gene-in-gene coding generates dual-isoform Fha condensates to control type VI secretion system assembly
qChIP-MS reveals the local chromatin composition by label-free quantitative proteomics
Predictive acoustical processing in human cortical layers
High-impact weather effects on wind and solar power systems under future climate scenarios in China
Targeting arginine metabolism reverses bone immunosuppressive microenvironment and metastasis in ARID1A-deficient triple negative breast cancer
Abstract Bone metastasis is a lethal consequence of breast cancer. AT-rich interaction domain 1 A gene ( ARID1A ), a subunit of the switch/sucrose non-fermentable (SWI/SNF) complex, regulates immunosuppressive tumor microenvironment. However, its specific role in bone metastasis remains unclear. Here, we show that female patients with ARID1A ‑mutated triple negative breast cancer (TNBC) exhibit a higher bone metastasis incidence. Most ARID1A mutations result in loss of protein expression. ARID1A deficiency upregulates the arginine metabolic pathway, increasing ornithine and spermine levels that promote the expansion of polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs) within the bone marrow, thereby facilitating bone metastasis. Targeting key enzymes of arginase 2 (ARG2) and ornithine decarboxylase 1 (ODC1) in arginine metabolic pathway effectively reduces bone metastasis in ARID1A -deficient models. Collectively, these findings reveal that ARID1A deficiency promotes bone metastasis by activating arginine metabolism to expand PMN-MDSCs and potentially offers therapeutic strategies for preventing bone metastasis in female patients with ARID1A -deficient TNBC.
Super-robust and sustainable bamboo structural material enabled by bonding network reconstruction
The widening partisan gap in legislative support for civil rights in the United States
Abstract The history of civil rights legislation offers a window into how American democracy codified social justice over time, and whether this process unfolded gradually or through punctuated shifts. Sixty years after the civil rights movement, we apply natural language processing to legislative archives to track how civil rights has evolved as a policy domain. We show that civil rights legislation has become more common, but also has diverged by party. Divergence accelerated during the early 1990s and mid-2010s—the latter coinciding with the rise of the Black Lives Matter movement and driven by a surge in sponsorship among racial minority Democrats in Congress. Topic modeling reveals that divergence is concentrated in legislation concerning racial minorities, women, and LGBTQ+ populations, while attention to older adults and people with disabilities has declined across both parties. Our findings offer potential insights into party divergence, race and ethnicity politics, and collective action tipping points.
Convergent and divergent brain–cognition development in early adolescence
Abstract How functional brain networks and cognition co-evolve during adolescent development remains poorly understood. Using baseline and Year 2 data from 2949 individuals in the Adolescent Brain Cognitive Development Study, we trained kernel ridge regression models to predict cognitive ability from resting-state functional connectivity. We find that baseline functional connectivity more strongly predicts future cognitive ability than baseline cognitive ability. Models trained on baseline functional connectivity to predict baseline cognition generalize better to Year 2 functional connectivity and cognition, suggesting that brain–cognition relationships strengthen over time. Intriguingly, baseline functional connectivity outperforms longitudinal functional connectivity change in predicting future cognitive ability. While longitudinal functional connectivity change is less reliable than baseline functional connectivity – intraclass correlation coefficient 0.24 vs. 0.56 – shortening scan duration to reduce reliability of baseline functional connectivity does not eliminate the predictive gap. Furthermore, neither baseline functional connectivity nor functional connectivity change meaningfully predicts longitudinal change in cognitive ability. We also identify converging and diverging predictive network features across cross-sectional and longitudinal brain-cognition models – a multivariate twist on Simpson’s paradox – with clear sex-specific patterns. Overall, in early adolescence, stable individual differences in brain functional network organization play a more critical role than dynamic changes in shaping future cognitive outcomes.
Experimental asymmetric relativistic zero-knowledge proofs with unconditional security
Absolute quantification of enantiomeric purity of sorted carbon nanotubes by correlating hyperspectral fluorescence microscopy with ensemble chiroptical spectroscopy
Directing intermediate phase crystallographic orientation promotes carbon-based CsPbI3 perovskite solar cells to beyond 20% efficiency
An X-linked sex determination mechanism in cannabis and hop
Pathogenic variants in the autophagy-tethering factor EPG5 drive neurodegeneration through mitochondrial dysfunction and innate immune activation
Abstract The autophagy-tethering factor ectopic P-granule 5 autophagy protein (EPG5) plays a key role in autophagosome-lysosome fusion. Impaired autophagy associated with pathogenic variants in EPG5 causes a rare devastating multisystem disorder known as Vici syndrome, which features neurodevelopmental defects, severe progressive neurodegeneration and immunodeficiency. The pathophysiological mechanisms driving disease presentation and progression are only partially understood. In patient-derived fibroblasts and iPS cells differentiated to cortical neurons, we find that impaired mitophagy leads to mitochondrial bioenergetic dysfunction. Physiological cytosolic Ca 2+ transients result in unexpected mitochondrial Ca 2+ overload despite a decrease in mitochondrial membrane potential. This is attributed to downregulation of MICU1. Ca 2+ signals cause mitochondrial depolarisation, mtDNA release and activation of the cGAS-STING pathway, reversed by pharmacological inhibition of the mitochondrial permeability transition pore (mPTP) or of the STING pathway. Thus, we identify a pathophysiological cascade driving disease progression associated with EPG5 deficiency, including impaired mitochondrial bioenergetics, mitochondrial Ca 2+ overload, vulnerability to mPTP opening and activation of innate immune signalling, signposting multiple potential therapeutic targets.