Sulfur is a redox active element that may have helped mediate an electron flow that kickstarted life and which presently is an essential element for all life on Earth. Despite current uncertainties in global sulfur fluxes, modeling sulfur’s abiotic cycling through Earth’s deep history is important for understanding the impact of a planet-wide biosphere on sulfur’s geochemical cycling and availability and vice versa. 

We present here an open-source, dynamical box model for estimating global sulfur fluxes and concentrations among surface and deep Earth reservoirs over Earth history, allowing tracking and estimation of the sulfur distribution in planetary reservoirs over deep time in the absence of life. While the main model presented here does not take into account the abrupt evolution of redox-shunting biosynthetic pathways such as oxygenic photosynthesis, we also modeled the abiotic sulfur cycle before and after a Great Oxidation Event (GOE)-like transition on Earth-like planets. 

Our results suggest a considerably distinct chemical makeup of sulfur content in marine sediments in the absence of life on an Earth-like planet, leading to a marine sediment sulfate content two orders of magnitude larger than on present-day Earth and a marine sediment sulfide content 4 orders of magnitude lower than on present-day Earth, attributable to the lack of microbial sulfur metabolism. This model could be useful for understanding sulfur cycling on potentially habitable exoplanets. 

There is significant improvement in outcomes when acute type A aortic dissection (ATAAD) repairs are performed at high-volume centers, with both center and surgeon volumes contributing to improved survival. The aim of our study was to evaluate our own network and determine differences in ATAAD outcomes between our high- and low-volume aortic centers. 

This was an observational, multi-center retrospective study consisting of 205 cases of ATAAD repair within our institution across 3 hospitals within the region that perform cardiac surgery, from January 2017 to January 2025. Data were collected and stratified by center volume (high vs. low), then analyzed. 

There were 164 patients who presented to our high-volume center, while 41 presented to our low-volume centers. When stratified by center volume, there was no significant difference in preoperative characteristics. Cardiopulmonary bypass (CPB) [174 (137–218) versus 236.5 (195.5–288) min, p < 0.001], circulatory arrest [30 (22–45) versus 45 (33–67) min, p = 0.001], and cross clamp times [93 (72–127) versus 131 (94.5–194) min, p = 0.002] were significantly different between high–low volume centers, respectively. The univariable survival analysis did show a significant difference in survival at 3 years—81.5% versus 66.7% [p = 0.009]. The multivariable Cox regression model showed that having surgery at a high-volume center was associated with a significant difference in 3-year survival [p = 0.021]. 

Our study showed improved outcomes of type A aortic dissection when surgery was performed by surgeons with greater experience at comprehensive aortic centers. 

Through an examination of Epic v. Apple, this article defines and traces the project of metaverse engineering: a long-term, large-scale reorganization of the games industry at technical, organizational, and governmental scales. Metaverse engineering as a games industry project seeks to redefine regulatory and market landscapes to redefine what counts as a platform, as data ownership, and as games themselves. Epic Games′ goal of the platformization of gaming production software like Fortnite and the Unreal Engine will require more than just using game engines to develop financialized 3D worlds. It will require the production of enticing legal and monetization models to encourage content creation, and competing for influence in regulatory and governmental regimes. Gaming platformization is not only technical, it is ontopolitical: the material realities of platforms shape and are shaped by rhetorical, social, cultural, and institutional forces. Epic's court successes have already moved us into a post-metaverse world. 

Accurate real-time forecasting of cryogenic tank behavior is essential for the safe and efficient operation of propulsion and storage systems in future deep-space missions. While cryogenic fluid management (CFM) systems increasingly require autonomous capabilities, conventional simulation methods remain hindered by high computational cost, model imperfections, and sensitivity to unanticipated boundary condition changes. 

To address these limitations, this study proposes an Adaptive Real-Time Forecasting Framework for Cryogenic Propellant Management in Space Systems, featuring a lightweight, non-intrusive method named ARCTIC (Adaptive Real-time Cryogenic Tank Inference and Correction). ARCTIC integrates real-time sensor data with precomputed nodal simulations through a data-driven correction layer that dynamically refines forecast accuracy without modifying the underlying model. Two updating mechanisms, auto-calibration and observation-correction, enable continuous adaptation to evolving system states and transient disturbances. 

The method is first assessed through synthetic scenarios representing self-pressurization, sloshing, and periodic operations, then validated using experimental data from NASA’s Multipurpose Hydrogen Test Bed and K-Site facilities. Results demonstrate that ARCTIC significantly improves forecast accuracy under model imperfections, data noise, and boundary fluctuations, offering a robust real-time forecasting capability to support autonomous CFM operations. The framework’s compatibility with existing simulation tools and its low computational overhead make it especially suited for onboard implementation in space systems requiring predictive autonomy. 

Glycogen Synthase Kinase 3β (GSK-3β) is a key coordinator of neuronal development and maintenance; hyperactive GSK-3β is linked to neurodevelopmental and -degenerative diseases and therefore a promising therapeutic target. In neurons, GSK-3β coordinates the cytoskeleton by phosphorylating microtubule-binding proteins. 

In this study, we found that tight regulation of GSK-3β kinase activity is required for the maintenance of parallel microtubule bundles in Drosophila and rat axons. Up- or downregulation of GSK-3β led to axons forming pathological swellings in which microtubule bundles disintegrated into disorganized, curled microtubules. We identified the microtubule bundling proteins Shot and Tau as key GSK-3β targets and found that GSK-3β exerted its regulatory effect on microtubule bundling through them. GSK-3β regulates the ability of Shot and Tau to attach to microtubules and/or Eb1. Misregulation of GSK-3β leads to the loss of Eb1–Shot-mediated guidance of polymerizing microtubules into parallel bundles, thus causing disorganization. 

We propose that microtubule disorganization during both active and inactive states of GSK-3β links its hyperactivity to neurodegeneration and may explain why global GSK-3β inhibition has failed in clinical trials. 

Alcohol Use Disorder is a leading preventable cause of morbidity and mortality, yet knowledge of mechanisms driving ethanol-related neuroplasticity remains incomplete. While research has traditionally focused on neuronal signaling, emerging evidence implicates astrocytes in addiction-related adaptations. 

Here, we investigated the astrocyte-specific molecular consequences of chronic ethanol consumption in the prefrontal cortex and nucleus accumbens, two brain regions critical for executive control and reward processing. Using Translating Ribosome Affinity Purification RNA-seq and bulk RNA-seq in Aldh1l1-EGFP/Rpl10a mice, expressing an EGFP tag on astrocyte ribosomes, we identified hundreds of differentially translated astrocytic genes following chronic continuous two-bottle choice ethanol drinking. 

Sex-specific analyses revealed a higher number of astrocytic changes in the female PFC and male NAc. Pathway enrichment highlighted extracellular matrix remodeling, synaptic signaling, mitochondrial function, and immune-related pathways. Analyses of individual drinking levels further demonstrated distinct correlations between ethanol intake and astrocytic translation. The major components of the brain extracellular matrix are chondroitin sulfate proteoglycans, produced primarily by astrocytes and covalently bound to chondroitin sulfate glycosaminoglycan chains. Complementary mass spectrometry/liquid chromatography analyses of chondroitin sulfate, heparan sulfate, and hyaluronic acid glycosaminoglycan disaccharides revealed ethanol-induced alterations in chondroitin sulfate glycosaminoglycan sulfation patterns, with additional baseline differences identified between selectively bred high- and low-ethanol preference lines. 

Together, these findings indicate that astrocytes undergo profound sex- and region-specific adaptations to chronic ethanol, implicating extracellular matrix and glycosaminoglycan remodeling as key risk-factors for and mediators of chronic ethanol-related neuroplasticity.