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From fruit flies to football: Violent <i>Drosophila</i> provide novel ideas about CTE
Climate warming and atmospheric deposition jointly accelerate the Antarctic Peninsula atmosphere–glacier–land–ocean mercury loop
Mercury (Hg) is a toxic pollutant of global concern that threatens ecosystem and human health. Its cycle is being jointly reshaped by anthropogenic emissions and polar warming, yet the response of the Antarctic system remains poorly constrained. Here, we reconstruct the past 200 y of Hg source–sink dynamics in the Antarctic Peninsula (AP), Antarctica’s fastest-warming region with the most pronounced glacier melting, by combining geochemical and isotopic records from 16 sediment cores collected across the AP shelf, with a developed observation-constrained multimedia Hg budget model. We find that despite its remoteness from anthropogenic emission sources, the modern AP shelf exhibits an Hg accumulation rate of 93 ± 58 µg m −2 y −1 , twice the global shelf average. Since industrialization, this accumulation rate has increased by 160%, making the AP one of the major hotspots of marine Hg enrichment. The model further reveals that this acceleration is driven by two coupled mechanisms: 1) enhanced atmospheric deposition and expanding open water strengthen the direct uptake of atmospheric Hg by seawater within the atmosphere–ocean loop, and 2) ice melt and erosion activate the long-overlooked atmosphere–glacier–land–ocean loop, remobilizing legacy Hg stored on land. The coupling of these two loops has increased ice melt-driven terrestrial Hg release by 550% and air–sea exchange by 350%. Thus, climate warming is turning the large historical Hg reservoir in Antarctica into an active secondary pollution source, amplifying polar Hg pollution risk.
Counting birds while taking fire: Biodiversity monitoring in a war zone
Reply to Topaz and Bahl: Interpreting a post-2022 lexical shift in academic prose
Correction for Wu et al., Paramyxovirus infection driven by heteromultivalent sialoglycotope binding
Sterilization mechanism and material compatibility of low-pressure RF water plasma for spacecraft surface decontamination
Heat tolerance decreases and cold tolerance increases with elevation for a species-rich insect family on a tropical volcano
The climate crisis is moving the high ambient temperatures common in lower elevation tropical forests upslope into areas where they would not have occurred historically. Tropical invertebrates may be particularly vulnerable to such changes. Here, our goal was to understand whether the distribution of heat and cold tolerances along an elevational gradient in northwestern Costa Rica predicted by theory were present for a leaf-litter inhabiting insect community of rove beetles (Staphylinidae: Coleoptera). We found that heat tolerance decreased, and cold tolerance increased with elevation, supporting the predictions. High elevation communities may not be capable of tolerating the rising temperatures that come with climate change, while low elevation communities are already experiencing environmental temperatures that may meet or exceed their thermal limits. While the forests in the low elevation more frequently exhibit temperatures that meet or exceed the heat tolerances for the beetle community, the soil will offer a buffered refuge for some time. The decline in thermal tolerance that we show here is predicted by theory yet is inconsistent with the values for insect species in the thermal tolerance literature. This reinforces the need for a better understanding of the thermal tolerances of diverse assemblages of tropical species that are likely to experience complicated and negative impacts of climate change.
High-purity type I collagen wrap is associated with improved functional recovery after extensor tendon repair: a multicentre randomized trial
Abstract Extensor tendon repairs of the hand, particularly in zones VI–VIII, are frequently complicated by peritendinous adhesions, resulting in reduced tendon glide, extensor lag, and suboptimal functional recovery. This multicentre randomized controlled trial evaluated whether adjunctive high-purity type I collagen (HPTC) wrapping was associated with improved functional recovery and reduced adhesion-related morbidity following extensor tendon repair. In this multicentre randomized controlled trial, 60 adult patients with acute extensor tendon injuries in zones VI–VIII were randomized to undergo standard tendon repair with adjunctive HPTC wrap (n = 30) or standard repair alone (n = 30). Primary outcome was TAM at 8 weeks, with extended follow-up assessments at 3- and 5-months evaluating durability of functional recovery. Secondary outcomes included QuickDASH scores, extensor lag, grip strength, adhesion-related functional limitation, and complications. Outcomes were assessed by blinded evaluators. Statistical analysis was performed using intention-to-treat principles. At eight weeks, mean TAM was significantly higher in the HPTC group compared with controls (232.4 ± 21.6 vs. 201.3 ± 26.8 degrees; p < 0.001), with a large effect size (Cohen’s d = 1.30). The HPTC group demonstrated significantly lower QuickDASH scores, reduced extensor lag, and greater grip strength recovery (all p < 0.001). Adhesion-related functional limitation occurred in 6.7% of patients in the HPTC group versus 30.0% in controls ( p = 0.01). No collagen-related adverse events were observed. Extended follow-up demonstrated sustained functional benefit in the HPTC group through five months, including superior total active motion, lower QuickDASH disability scores, reduced extensor lag, greater grip strength recovery, and fewer secondary procedures related to adhesion formation. Adjunctive use of high-purity type I collagen wrap significantly improves early functional outcomes and reduces adhesion-related morbidity following extensor tendon repair. HPTC was associated with improved early and intermediate-term functional recovery and reduced adhesion-related morbidity, with longer follow-up with larger cohorts needed to confirm durability of these benefits.
PLCβs are recruited to the plasma membrane in macrophages by both Gβγ and Gα <sub>q</sub>
PLCβ enzymes cleave PIP2 from the plasma membrane, producing IP3 and DAG, which regulate intracellular Ca 2+ levels and protein kinase C activity, respectively. They are regulated by GPCR signaling through the G proteins Gβγ and Gα q and have been shown to function as coincidence detectors for dual stimulation of Gα q - and Gα i -coupled receptors via these G proteins. PLCβs are aqueous-soluble enzymes, but partition onto the membrane surface to access their lipid substrate. We previously demonstrated that membrane recruitment and orientation of the catalytic core on the membrane surface underlie Gβγ-dependent regulation of PLCβ enzymes. Using macrophages as a model system, where PLCβ signaling is essential for responses to infection and tissue injury, we investigated the contribution of Gβγ-dependent regulation and membrane recruitment of PLCβ in the context of endogenous signaling. By measuring Ca 2+ mobilization, we demonstrate that both Gα i - and Gα q -coupled receptors independently stimulate PLCβ activity. Using total internal reflection fluorescence and stimulated emission depletion microscopy, we demonstrate that most of the PLCβ3 in the cell is localized away from the plasma membrane at rest but is rapidly recruited to the plasma membrane upon stimulation by both Gα i - and Gα q -coupled receptors, illustrating that both Gβγ and Gα q recruit PLCβ to the plasma membrane. These results support an updated model for G protein–dependent regulation of PLCβ enzymes, where Gβγ-induced regulation in the absence of Gα q can occur and is apparently dictated by the local concentration of receptor, G proteins, and PLCβ.
Observational evaluation of children’s respirator donning ability in Indonesia and Nepal
Abstract Certified respirators, like KN95 N95, FFP2 and KF94, can offer strong protection against airborne particulates, but their effectiveness relies on proper fit and donning. This study evaluated how well children aged 6–13 years in Kathmandu, Nepal, and Bandung City, Indonesia, could independently don two child-marketed KN95-style respirators without guidance. Among 348 participants, only 21.8% met all seven essential donning criteria, though 79.6% successfully completed at least five steps. While this suggests a promising baseline, the most frequent mistake, improperly shaping the nose clip, could potentially compromise respirator effectiveness. Older children and girls generally performed better, and prior experience with KN95-style respirators was linked to greater confidence and improved technique. Respirator design also played a role in donning success. These findings reveal a critical gap between general mask-wearing familiarity and the specific skills needed for effective respirator use. The study highlights the urgent need for child-friendly respirator designs and accessible training materials, especially in regions where air pollution poses serious health risks.
When coordination is avoidable: A monotonicity analysis of organizational tasks
Organizations devote substantial resources to coordination, yet which tasks actually require it for correctness remains unclear. The problem is acute in multiagent AI systems, where coordination cost is directly measurable and can exceed the cost of the work itself. Distributed systems theory provides a precise criterion: Coordination is required when a task specification is nonmonotonic, meaning that as histories grow, new information can invalidate prior conclusions. Here we show that Thompson’s classic taxonomy of interdependence maps to that criterion, yielding a decision rule for when coordination is required for correctness. We formalize the correspondence in a bridge theorem, apply the rule to 65 workflows from the American Productivity & Quality Center (APQC), and (with a calibrated large language model (LLM), 13,417 Occupational Information Network (O*NET tasks), and illustrate it in multiagent AI simulations. Under our decompositions, 74% of workflows and 42% of O*NET tasks are monotonic, implying that up to 24 to 57% of coordination spending is unnecessary for correctness.
A large-scale in silico chimera-based strategy for engineering low-immunogenic L-asparaginase from Penicillium cerradense
Sources of technological innovation
Stress-induced cortisol clouds the gut feeling in decision-making: a randomized controlled study
Abstract The advice to “follow your gut” reflects the idea that instinctive feelings can guide decision-making. Indeed, anticipatory emotional bodily signals, such as skin conductance responses, have been shown to help people avoid risky choices. Yet, stress increases risk-taking, casting doubt on gut feelings’ reliability under stress and whether emotions are always beneficial to decision-making. In a study of 109 young adults (54 women), we randomly exposed half of the participants to a psychosocial stressor or a non-stressful control condition and assessed their cortisol reactivity levels. We then measured their performance on the Iowa Gambling Task alongside anticipatory skin conductance responses before each decision. We showed that stress-induced cortisol reactivity moderated the relationship between anticipatory skin conductance responses and risk-taking in the gambling task, but only in men. Greater anticipatory skin conductance responses were associated with increased risk-taking among men with low cortisol reactivity, whereas the opposite pattern emerged among men with high cortisol reactivity, suggesting that cortisol may alter the relationship between somatic signals and decision-making. Women showed no such effect and, on average, took more risks than men. These findings reveal a sex-specific pathway through which cortisol may impair the gut feeling that normally protects against risky decisions. [Study registration ID: NCT07702747; retrospectively registered on 2026-07-14; https://clinicaltrials.gov/study/NCT07702747 ]. .
Correction for Meng et al., Rethinking energy transition strategies for the European Union amid rising energy prices
Endemic Lilium ciliatum as a novel biogenic platform for microwave-assisted green synthesis of antioxidant and antimicrobial silver nanoparticles
Lexical change is not a calibrated measure of LLM prevalence or its determinants
5-Fluorouracil exacerbates oral mucositis through inflammation and fibroblast-mediated matrix imbalance
Abstract Oral mucositis (OM) is a critical complication of cancer chemotherapy that can lead to treatment interruption or discontinuation and adversely affect patient prognosis. Here, we established a 5-fluorouracil (5FU)-exacerbated OM model to elucidate the mechanism underlying chemotherapy-associated OM aggravation and evaluate the effects of a mouthwash (MW) containing antimicrobial (cetylpyridinium chloride) and anti-inflammatory components (glycyrrhizin, tranexamic acid, and Equisetum arvense extract). In this model, 5FU markedly enhanced subepithelial inflammation at the wound site, whereas MW treatment reduced inflammation and promoted mucosal healing. RNA sequencing and in vitro fibroblast analyses demonstrated that 5FU significantly upregulated Gremlin 1 ( Grem1 ), matrix metallopeptidase 3 ( Mmp3 ), and plasminogen activator, urokinase ( Plau ), while suppressing fibroblast growth factor 10 ( Fgf10 ). Scratch assays further revealed that 5FU impaired fibroblast migration and proliferation, which were restored by anti-inflammatory MW components, accompanied by normalization of Grem1 and Fgf10 expression. Collectively, these findings provide mechanistic insight into 5FU-exacerbated OM and suggest that modulation of fibroblast-associated inflammatory and regenerative pathways by MW may represent a promising strategy for OM management during chemotherapy.
speed-induced passive depth stabilization in a biomimetic underwater vehicle with a swim bladder
Abstract A nonlinear mathematical model describing the vertical motion of a biomimetic underwater vehicle equipped with a swim bladder is developed. For a passive bladder that changes its volume under hydrostatic pressure, the system can achieve depth stabilization through a speed-induced mechanism when the lever-arm geometry (relative positions of the swim bladder and lifting surfaces) is favorable; otherwise stabilization is not possible. Using the Routh–Hurwitz criterion, analytical stability conditions are obtained in closed form, revealing a lower onset speed that is set by a simple coupling between forward speed and geometry. Numerical simulations confirm the theoretical predictions and reveal the dominant loss-of-stability scenarios: loss of effective stiffness at the onset threshold and oscillatory instability when the mixed speed–geometry factor changes sign. The results demonstrate the feasibility of passive swim-bladder-based depth stabilization and provide practical guidelines for selecting the lever arms of the buoyancy and lift forces and operating speeds in autonomous underwater vehicles.
PLK1-mediated phosphorylation of PHGDH reprograms serine metabolism in advanced prostate cancer
Metabolic reprogramming is a hallmark of cancer, enabling tumor cells to meet their increased biosynthetic and energetic demands. Although cells possess the capacity for de novo serine biosynthesis, most transformed cancer cells preferentially rely on exogenous serine uptake to sustain their growth, yet the regulatory mechanisms driving this metabolic dependency remain poorly understood. Here, we uncover a mechanism by which Polo-like kinase 1 (PLK1), frequently overexpressed in prostate cancer, orchestrates a metabolic shift in serine and sphingolipid metabolism through phosphorylation of phosphoglycerate dehydrogenase (PHGDH), the rate-limiting enzyme of the serine synthesis pathway (SSP). Specifically, PLK1 directly phosphorylates PHGDH at S512, S513, and S517, leading to a marked reduction in its protein level and enzymatic activity. This downregulation of de novo serine biosynthesis forces cancer cells to increase their reliance on exogenous serine uptake via the ASCT2 transporter, which in turn fuels the biosynthesis of lipids, including sphingolipids essential for tumor growth and survival. Our findings suggest that targeting the SSP, serine uptake, or downstream lipid biosynthesis pathways may represent promising therapeutic strategies in advanced cancers characterized by PLK1 dysregulation.