npj Microgravity

Long-duration spaceflight may alter social cognition, yet the underlying biological mechanisms remain unclear. Emotion Recognition Task (ERT) performance remains stable during typical 6-month International Space Station (ISS) missions but declines markedly during the 340-day NASA Twins Study, suggesting duration-dependent vulnerability. Here, we propose the Von Economo Neuron (VEN) Fatigue Hypothesis, which posits that microgravity increases demand on VEN-associated social cognitive networks, eliciting adaptive myelination during shorter missions before compensatory mechanisms fail with prolonged exposure. To evaluate this hypothesis, we integrated evidence from rodent, human cortical organoid, astronaut plasma proteomic, and neuroimaging datasets. ISS-flown rodent frontal cortex demonstrated increased expression of myelination-related genes, while spaceflown cortical organoids exhibited changes consistent with oligodendrocyte remodeling. Astronaut plasma transcriptomics identified reproducible alterations in VEN-associated and myelination-related proteins across independent missions, and resting-state fMRI revealed transient changes in frontal insula connectivity following long-duration spaceflight. Together, these findings provide convergent evidence supporting the VEN Fatigue Hypothesis and identify adaptive myelination and VEN-associated network remodeling as candidate mechanisms underlying duration-dependent changes in social cognition during long-duration spaceflight.

Human deep-space missions face bone-kidney risks that cannot be extrapolated from six-month ISS data. We built a 12-state Ca-bone-urine-stone mechanistic ODE model and jointly calibrated its 11 physiological parameters on eight ISS targets by Bayesian identification (M0 base = 19-D; M1 extension adds a GCR-bone coupling term for parsimony testing only), then propagated the M0 posterior to four environments (ISS, Lunar subsurface, Lunar surface, Mars). Lumbar-lower BMD loss increases with mission duration and partial-gravity unloading (ISS 180 d -4.83% -> Mars 730 d -12.15%; 2^3 factorial: duration 82.9%, gravity 12.5%, GCR main effect ~ 0), whereas stone rate follows the opposite gradient (ISS 16.1 vs Mars 13.1 per 1000 person-years), reflecting weakened partial-gravity bone resorption alongside residual urinary chemistry changes. The dominant pathway thus shifts from bone-centric on the ISS to kidney-centric on Mars, where residual urinary-chemistry changes-not bone resorption-drive stone risk. The direct GCR-bone coupling term is unidentifiable at current ISS doses (DeltaWAIC = +0.0076 +/- 0.126 SE), so M0 is retained as the main inference model. Bisphosphonates provide >=84% BMD protection but leave a urinary-chemistry residual, so bisphosphonate monotherapy would underestimate Mars stone risk; potassium-magnesium-citrate combinations (RRR_RSS 51%) should therefore be added to deep-space countermeasures. A Lunar-surface 365-day mission is the earliest environment on the NASA roadmap to cross a composite RED threshold. That profile differs from the regolith-shielded 180-day case in both cumulative GCR (~69x) and duration (2x), so a shielding-specific effect cannot be isolated here; forcing the GCR coupling terms to zero leaves all four composite tiers unchanged (0/4, Supp S24), and the shielded 180-day profile is YELLOW rather than GREEN. Independent hold-out validation (Culliton 2025 60-day HDT-bedrest RCT, n=8 control arm of n=24 total) supports the M0 posterior predictive distribution on the lumbar-BMD sub-scope.

Space biology literature is growing exponentially. Existing infrastructure has not kept pace with organizing, synthesizing, and disseminating this knowledge. We present SpaceBio SpaceBio Knowledge Hub (www.spacebio.space), an integrated digital ecosystem that combines artificial intelligence, real-time data integration, and open-access infrastructure to advance research, education, and collaboration in microgravity, space biology and space exploration. The platform applies AI-driven approaches including natural language processing, machine learning, and automated content generation to construct a semantic atlas of the field. The atlas reveals the hierarchical thematic organization underlying microgravity-induced biological responses, space mission infrastructure, planetary science, and astrobiology. As part of this effort, SpaceBio is moving toward the construction of a LiteratOmics framework for microgravity, and space biology a systematic, AI-enabled approach to mining, integrating, and structuring the primary literature generated by omics-driven spaceflight research, treating the scientific literature itself as a navigable data layer alongside genomic, transcriptomic, and proteomic datasets. Built on a scalable, cloud-based architecture with a user-centered interface, SpaceBio supports literature exploration, data integration, and knowledge discovery for researchers, educators, students, industry partners, and citizen scientists. The platform also functions as a community-building ecosystem. It integrates hands-on research initiatives, AI-generated educational content, pilot data science projects, and social responsibility programs that broaden participation without compromising scientific rigor. AI-enabled digital environments can transform fragmented literature into a navigable knowledge landscape. SpaceBio accelerates research productivity, strengthens STEM education, and supports the global space life sciences community as human space exploration enters in the most ambitious era.

Current planetary protection approaches rely heavily on spore-based tests developed for Mars missions and may not adequately assess contamination risks for icy ocean worlds such as Europa. We developed a genome-based framework combining deep shotgun metagenomics and supervised machine learning to predict survival-relevant microbial traits in ESA JUICE launch-site cleanrooms. From 183 genome bins, 25 representative genomes were analyzed for traits including cryotolerance, desiccation tolerance, salt resilience, anaerobic metabolism, autotrophy, and sporulation. Several skin-associated microbes carried multiple relevant traits, and some appeared actively replicating. A broader meta-analysis of 1,868 genomes showed that trait profiles vary strongly within taxa, demonstrating that taxonomy alone is insufficient for risk assessment. This framework complements current planetary protection assays, helps to predict how microbes would survive in a new biotope, and supports functional, risk-informed contamination monitoring for future space missions.

Fungal contamination poses a growing threat to spacecraft integrity, crew health, and planetary protection efforts. We describe a scalable and interpretable pipeline for identifying fungi with adaptation potential to spaceflight-associated stress conditions such as extreme temperatures, radiation levels, etc., and pathogenicity risks. Starting with proteins known to confer stress resistance, we identify orthologs across over fifteen hundred fungal species and evaluate their contamination potential via comparative proteome analysis. Our pipeline integrates proteins with known functional inference, cross-database proteome matching, and identity-based scoring to generate a ranked list of fungal species of concern. We apply this approach to detections from spacecraft assembly facilities, highlighting species with combined stress-tolerance and pathogenic potential. This study establishes a foundation for future AI-based risk assessments that can scale to orders of magnitude more fungal species, thus laying the foundation for systematic identification and assessment of fungal contaminants with potential adaptation and pathogenicity risks in spaceflight environments, thereby supporting contamination control strategies for future space missions. We also present an interactive visual online tool for researchers to trivially check the contamination potential of species in their own samples.

Spaceflight imposes unique physiological stresses on mammals, including microgravity and cosmic radiation, which drive complex molecular adaptations. However, the systemic and temporal dynamics of space-induced epigenetic regulation remain poorly understood. We constructed a comprehensive DNA methylome BodyMap across 12 organs or tissues from mice exposed to long-duration spaceflight across three time points using Reduced Representation Bisulfite Sequencing (RRBS). We also performed RNA-seq for five organs and integrated with DNA methylome. We mapped the methylome and transcriptome landscapes and found that spaceflight induces limited but highly tissue-specific differentially methylated CpGs (DMCs). Most spaceflight-induced methylation changes were reverted toward baseline within one to six months of post-flight. Functional enrichment analysis of DMCs highlighted metabolic and mitochondrial dysregulation commonly across organs, while developmental responses in immune, reproductive, and structural tissues were tissue-specific. Transcriptome data revealed that spaceflight suppressed immune and increased inflammatory responses at the multi-organ level, triggering a phenomenon resembling aging. Our study provides a comprehensive DNA methylome BodyMap across 12 organs/tissues in spaceflight mice, elucidating the tissue specificity of epigenetic changes. These insights are essential for developing biomarkers and countermeasures to safeguard astronaut health during extended missions.

Spaceflight stressors may increase Parkinsons disease (PD) risk, but microgravitys specific contribution to human dopaminergic (DA) vulnerability remains undefined. Here, we exposed human iPSC-derived midbrain DA organoids and differentiated SH-SY5Y neurons to simulated microgravity for 72 hours. This exposure reduced neurite outgrowth, eroded DA identity, and activated familial-PD mitochondrial kinases without depleting extracellular dopamine. We observed severe mitochondrial dysfunction--including membrane potential loss and respiratory suppression--coupled with global translational repression. Furthermore, a sublethal, pre-degenerative state emerged, characterized by the selective release of mitochondrial cell-free DNA without apoptotic activation. Proteomic profiling revealed striking convergence with human PD transcriptomes and astronaut blood, highlighting shared suppression of mitochondrial metabolism, ribosomal translation, and altered RNA splicing. Together, these findings establish simulated microgravity as a sufficient, non-toxin trigger of early PD-like DA dysfunction, providing a robust human model for investigating prodromal neurodegeneration.

Despite extensive research on vestibular function in microgravity, particularly during orbital and parabolic flight exposure, several gaps remain regarding the spontaneous behavior of vestibular organs under non-terrestrial gravitoinertial conditions. In particular, semicircular canal function, typically assessed through vestibulo-ocular reflex (VOR) recordings, has yielded inconsistent findings, with reports describing either no effect or reduced performance in microgravity. Moreover, many of these studies are limited by methodological constraints that reduce the interpretability of their conclusions. To clarify these discrepancies, we evaluated horizontal and vertical VOR responses during parabolic flights to assess semicircular canal function under transient weightlessness. Participants were passively rotated at a constant frequency and amplitude during normogravity and microgravity phases, centered along the head vertical or inter-aural axis. Eye movements were recorded binocularly using infrared eye-tracking in darkness to eliminate visual influences, while participants were tightly restrained to minimize proprioceptive variability. Results show a reduction in VOR gain during microgravity in both axes, despite consistent rotational stimulation across gravity conditions. In addition, VOR gain remained reduced after parabolas in the horizontal plane, whereas vertical VOR performance was preserved. These are the first results to demonstrate an immediate alteration of semicircular canal function in weightlessness. Possible sources of the reduction in VOR performance in 0g are discussed. We also propose that the observed post-flight effects reflect a down-weighting of semicircular canal inputs during multisensory integration.

Mechanical cues are key regulators of bone formation, yet their potential as therapeutic stimuli remains incompletely explored in vivo. Nanovibrational stimulation, which delivers low-amplitude, high-frequency mechanical input, has been shown to promote osteogenic differentiation in vitro, and rodent studies have similarly demonstrated osteogenic effects. However, its impact on other cellular systems at the whole-organism level remains poorly understood. Here, we demonstrate that nanovibrational stimulation enhances myogenic differentiation in vitro before investigating its effects on skeletal development and tissue specificity in zebrafish. Larval zebrafish exposed to nanovibrational stimulation exhibited increased osteoblast numbers and enhanced bone formation relative to controls. In adult zebrafish, nanovibration increased the osteoblast response to a fracture-like injury, indicating enhanced osteogenic activity during repair. To assess tissue specificity, we examined additional cell types and systems relevant to skeletal regeneration, including cartilage, muscle, vasculature and innate immune cells. Although nanovibrational stimulation promoted myogenic differentiation of C2C12 cells in vitro, its effects on muscle and other non-skeletal tissues in zebrafish larvae were comparatively limited. These findings suggest that nanovibrational stimulation exerts a preferential effect on osteogenic processes in vivo. These findings demonstrate that nanovibrational stimulation preferentially enhances osteoblast-mediated bone formation and skeletal injury responses in zebrafish, without causing significant perturbations in other tissues. Our results establish zebrafish as a tractable in vivo model for investigating vibration-induced mechanobiological processes, providing a more physiologically relevant representation of tissue-level mechanotransduction than conventional two-dimensional culture systems. Furthermore, these findings highlight the potential of nanovibrational stimulation as a non-invasive strategy to promote bone regeneration and fracture repair.

To better understand how animals cope with increasingly variable and challenging environments, there is a need to study how prolonged exposure to elevated glucocorticoid hormones (i.e. one mediator of the stress response) affects their physiology. While glucocorticoid elevation is known to increase oxidative stress and accelerate cellular ageing, there is evidence that king penguins (Aptenodytes patagonicus) can prevent oxidative stress during acute stress exposure, suggesting that species may differ in their sensitivity to glucocorticoids downstream negative effects. As king penguins thrive in a seemingly harsh environment, we hypothesized that they may be able to limit the deleterious effects usually associated with chronic glucocorticoid elevation, either through resistance (i.e. prevention of downstream negative effect) or resilience (i.e. rapid recovery following transient negative effect). To test this hypothesis, we experimentally elevated corticosterone levels in incubating king penguins and quantified treatment effects on a suite of physiological traits at multiple time points across incubation and early chick-rearing, up to ca. 2 months after implantation. Corticosterone-treated individuals showed a prolonged increase in corticosterone and decrease in body condition, confirming our treatment likely mimicked sustained stress exposure. Heterophil-to-lymphocyte ratio was only increased transiently, and there was no clear evidence that treatment influenced oxidative stress or telomere length maintenance. Plasma energy metabolites were mainly affected early after implantation, with rapid recovery over time. Overall, our results suggest that adult king penguins show at least moderate resistance and resilience to chronic corticosterone elevation, especially in preventing cellular integrity loss, though at-sea physiological effects remain to be determined.

Personal light exposure is a modifiable determinant of circadian and neurobehavioural health, yet its everyday structure across populations remains poorly understood. We report a harmonised, multi-country field study of ocular light exposure in 191 adults across nine sites in Costa Rica, Germany, Ghana, the Netherlands, Spain, Sweden and Turkey, comprising 1,480 participant-days. Participants wore calibrated light loggers near the corneal plane and at chest level and completed repeated contextual assessments. Average daytime exposure remained below recommended melanopic levels, with adherence varying by site, daily phase and photoperiod. Exposure generally increased with latitude despite greater year-round sunlight at lower latitudes, suggesting behavioural filtering through shade-seeking, indoor living or heat avoidance. Individual and activity-level differences explained more variation than site. Daylight access, outdoor activity and micro-environment were the strongest exposure correlates, whereas demographic factors showed limited associations. This openly accessible dataset provides the first multi-site view of real-world ocular light exposure.

The present-day martian surface is generally considered inhospitable to life because of low atmospheric pressure, intense surface radiation, global desiccation, and oxidizing chemistry which has been increasing since the late Noachian. However, shallow martian subsurface regions where mineralogy has shown groundwater movement may include localized hypersaline environments capable of retaining liquid water and supporting microbial metabolism. Haloferax volcanii, a model halophilic archaeon, has previously been shown to survive under low-pressure martian conditions (24 mbar) and to grow anaerobically supported by the Mars-relevant oxyanions nitrate and perchlorate under high-salinity conditions. Here, we investigated whether H. volcanii could actively grow under a combination of environmental and chemical conditions relevant to potentially habitable shallow subsurface martian lacustrine settings. Cultures were incubated for 160 days under anoxic, CO2-enriched, low-pressure conditions (24 mbar) in hypersaline liquid media supplemented with nitrate or perchlorate. Growth was observed in all low-pressure treatments and was confirmed by increases in optical density and biological reduction of nitrate and perchlorate. Scanning electron microscopy revealed extensive biofilm formation in low-pressure cultures, and Raman spectroscopy demonstrated the persistence of carotenoid biosignatures after prolonged incubation under martian conditions. Water loss remained below 4% across all treatments, indicating long-term stability of hypersaline brines throughout the experiment. These results demonstrate for the first time that a halophilic archaeon is capable of active growth and metabolism under a Mars-relevant combination of low pressure, high salinity, anoxia, and oxidizing chemistry, providing experimental support for the potential habitability of localized shallow subsurface martian environments. ImportanceThe search for cellular life is a major objective of future Mars exploration. While many studies have examined whether microorganisms can survive under martian conditions, far fewer have demonstrated active growth and metabolism. Here, we document Haloferax volcanii as the first halophilic archaeon capable of active growth under a defined combination of Mars-relevant low atmospheric pressure, high salinity, anoxia, and oxidizing chemical conditions. These findings expand the current understanding of the environmental limits of microbial growth and provide experimental evidence that localized brine environments in the shallow martian subsurface could support active microbial metabolism, if suitable organics and liquid water are present. In addition, this study establishes a practical framework for cultivating halophilic microorganisms under low-pressure martian conditions and may help guide future efforts to detect, cultivate, and characterize potential extant life on Mars.

Despite the well-known health risks of neutron exposures, key gaps remain in understanding neutron-induced molecular responses and identifying reliable biodosimetric markers that distinguish neutrons from photon exposure. We provide the first genome-wide analysis of the human blood transcriptional response to an accelerator-derived fission-like spectrum of neutrons versus photons, evaluating transcriptomic relative biological effectiveness (RBE) and radiation quality-discriminating gene signatures. Whole blood from healthy donors was irradiated ex vivo with X-rays (140 kV, 0-4 Gy, n = 3) or neutrons (0.1-8 MeV, 0-1 Gy, n = 2), incubated for 6 h or 24 h, and processed for RNA sequencing from peripheral blood mononuclear cells (PBMCs). Neutrons were markedly more potent than X-rays at inducing differentially expressed genes (DEGs) at equal doses, showing a peak response 6 h post-irradiation followed by a decline. In contrast, X-rays caused a continuous increase in DEGs up to 24 h (neutrons vs. X-rays at 1 Gy: 1,449 vs. 121 DEGs at 6 h; 996 vs. 621 DEGs at 24 h). A universal p53-centered 34-gene signature, including FDXR, EDA2R, GADD45A, and ZMAT3, showed highly monotonic dose responses (Spearman correlation coefficient {approx} 1) across donors, radiation qualities, and timepoints. Additionally, difference-in-differences analysis identified radiation quality-discriminating genes only at 6 h, with transcriptional convergence observed by 24 h, suggesting a very narrow time window for biodosimetric differentiation. We identified a neutron-specific gene signature driven by cGAS-STING-NF-{kappa}B signaling (RELB, NFKB1, C3, MALAT1) and suppression of B-cell and myeloid identity genes (IGHD, TCL1A, CLEC7A, TLR2), defining a biologically coherent neutron quality index with distinct immunomodulatory effects. For the first time, we assessed neutron RBEs at the gene, pathway, and global transcriptomic levels in a human blood model, reporting a global transcriptomic neutron RBE of 1.30 (95% CI: 1.14-1.49) at 6 h and 1.21 (95% CI: 1.14-1.28) at 24 h, providing a valuable basis for biodosimetry in mixed-field exposure scenarios. Our findings advance the mechanistic understanding of neutron radiation responses and support the development of biodosimetric approaches for mixed-field exposure scenarios.

The formation of inert gas bubbles during decompression can lead to decompression sickness (DCS), a major operational risk for divers, compressed-gas workers, astronauts, and high-altitude aviators. In diving, DCS risk is typically inferred from post-dive ultrasound detection of venous gas emboli (VGE), precluding modification of decompression schedules based on real-time physiological feedback. Two-dimensional ultrasound imaging could provide additional insight into decompression-related physiological changes; however, its use in hyperbaric environments has been largely precluded by fire risk associated with elevated oxygen partial pressures (ppO2) in enclosed spaces. Here, we developed a workflow for operating a programmable ultrasound system under hyperbaric conditions and acquiring ultrasound data from the subclavian vein and calf muscle during decompression. A total of 42 dives were conducted by 26 individuals using a previously characterized dive profile to 132 feet seawater (FSW) for 20 min with 9 min of decompression. Three exposure conditions were evaluated: non-exercising, exercising, and a brief pause at 20 FSW during compression. Twelve dives included programmable ultrasound imaging during decompression. Post-dive VGE responses were consistent with prior reports while demonstrating substantial inter-individual variability and sensitivity to modest profile modifications. VGE were detected in the subclavian vein during decompression in two participants and subsequently confirmed by post-dive echocardiography. Calf muscle ultrasound brightness typically increased from pre-dive to decompression measurements, before decreasing below baseline in the 120 min post dive measurement period. These findings demonstrate the feasibility of programmable ultrasound imaging during human decompression and establish a practical framework for ultrasound operation under hyperbaric conditions. This approach may support future physiological studies and development of automated decompression monitoring technologies. New and NoteworthyThis study demonstrates the first use of a programmable ultrasound system to acquire and quantitatively analyze ultrasound data during human decompression. The approach enabled direct visualization of venous gas emboli during decompression and revealed calf muscle ultrasound signal changes, providing a new tool for investigating physiological responses during decompression that are not accessible through conventional post-dive monitoring.

Background: ERAS protocols reduce hospital stay by 1.88 days and complications by 29% globally, but their one-size-fits-all paradigm, validated at sea level, may fail at high altitude where chronic hypoxia and population-specific genetic adaptations remodel baseline physiology. No study has quantified ERAS effect weight shifts at high altitude or proposed a theoretical model to explain the gap. Objectives: To evaluate three dimensions of plateau ERAS remodeling: (i) risk factor weight shift, (ii) traditional marker failure, (iii) genetic background modification, and propose the PAERS (Plateau Adaptation-ERAS Remodeling Syndrome) risk stratification model tailored to altitude. Methods: Retrospective cohort of 612 adults undergoing elective laparoscopic cholecystectomy (2018-2023) at Qinghai Red Cross Hospital (2260 m). Three analytical tiers: (1) multivariable regression comparing risk factor coefficients against plain-altitude benchmarks; (2) restricted cubic spline and interaction modeling for Hb, SpO2, and LOS; (3) inferential genetic modifier analysis using population-level EPAS1 carrier rates. Primary outcomes: LOS and complication rate. Results: Three-dimensional shift was observed: (1) Weight Remodeling: BMI replaced sex as primary risk factor (OR = 1.86, P < .001), surgeon variability amplified (F = 6.33 vs plain benchmark 2-4, an ~58% increase in F-statistic ratio, P < .001); (2) Marker Failure: Hb showed J-type relationship with LOS (Hb x SpO2 interaction beta = -0.0095, P = .009), with effect reversal across SpO2 strata (Plateau Hemoglobin Paradox); (3) Genetic Modification (population-level inference): ~70% EPAS1 carrier rate (range 57-85% across studies) suggests HIF-2alpha pathway is a baseline modifier that must be accounted for. Three falsifiable predictions were proposed. Conclusions: High-altitude ERAS faces three challenges: effect weight remodeling, biomarker failure, and genetic background calibration. The PAERS hypothesis proposes an integrated risk stratification model, shifting from one-size-fits-all to altitude-aware, patient-specific protocols.

Prolonged low-temperature exposure may extend the preservation window of mammalian cells but can also disrupt cellular homeostasis and ultimately compromise cell viability. This study investigated the time-dependent phenotypic and transcriptomic responses of primary canine dermal fibroblasts to sustained hypothermic stress. Passage-three fibroblasts were continuously maintained at 15 for up to 15 days, with samples collected on Days 0, 3, 6, 9, 12, and 15. Cellular morphology, metabolic activity and viability, and apoptosis were evaluated using bright-field microscopy, Cell Counting Kit-8 assays, and Annexin V-FITC/propidium iodide flow cytometry, respectively. RNA sequencing was performed to characterize dynamic transcriptional changes throughout the exposure period. Early low-temperature exposure was associated with relatively preserved cellular morphology and viability, suggesting a transient adaptive response. With increasing exposure duration, fibroblasts exhibited progressive morphological deterioration, reduced metabolic activity, loss of adhesion, and increased apoptosis. Time-series transcriptomic analysis further revealed temporally coordinated and stage-dependent gene-expression programs associated with metabolic regulation, cellular stress responses, structural homeostasis, and cell survival. Integration of phenotypic and transcriptomic data demonstrated that the response of primary canine dermal fibroblasts to 15 was dynamic rather than linear, progressing from early adaptation to cumulative dysfunction during prolonged exposure. These findings provide a framework for defining the low-temperature tolerance of primary canine dermal fibroblasts and may inform the optimization of protocols for their short- to medium-term preservation and transportation.

Background: Hemoglobin (Hb) elevation is the hallmark of high-altitude adaptation, yet its effect on surgical outcomes may depend on arterial oxygen saturation (SpO2)--previously uninvestigated. Objectives: To explore whether preoperative Hb effect on postoperative length of stay (LOS) after laparoscopic cholecystectomy (LC) reverses across SpO2 strata. Methods: Retrospective single-center cohort of 612 adults undergoing elective LC (2018-2023) at Qinghai Red Cross Hospital, Xining, China (2260 m). Exposure: preoperative Hb (82-233 g/L) and SpO2 (86%-99%), stratified as low (<93%), mid (93%-95%), high (>=96%). Primary analysis: multivariable linear regression with Hb x SpO2 interaction, adjusted for BMI, age, sex, season. Results: Among 612 patients (65.8% female; mean age 43.5 [11.9] years; mean Hb 151.4 [20.7] g/L; mean SpO2 94.6% [2.3%]), the Hb x SpO2 interaction was significant (beta = -0.0095; P = .009). Hb effect reversed: in SpO2 >=93%, each 1 g/L Hb prolonged LOS by 0.003 days (P = .079); in SpO2 <93%, each 1 g/L reduced LOS by 0.006 days. In mid-SpO2 stratum (n = 251), Hb >=180 g/L had longer LOS (1.88 vs 1.62 days; P = .001; d = 0.54). Five computational robustness analyses confirmed the interaction (leave-one-out: 100% P < .05 across 612 iterations). Conclusions: In this exploratory cohort, we observed an SpO2-dependent reversal of the Hb effect on postoperative LOS, designated the "Plateau Hemoglobin Paradox." Given single-center design and achieved power of 0.754, findings require replication. If replicated, this pattern may inform future perioperative risk stratification at high altitude.

Plants emit substantial amounts of biogenic volatile organic compounds (VOCs) that link plant physiological activity to ecological interactions and atmospheric chemistry. However, the processes regulating VOC emissions within the forest air and at the interface directly above the canopy remain poorly characterized. In this study, we investigated forest-scale VOC dynamics in a cool-temperate deciduous forest dominated by Quercus crispula using high-time- and high-mass-resolution proton-transfer-reaction time-of-flight mass spectrometry (PTR-ToF-MS) integrated with positive matrix factorization (PMF). This non-targeted, process-oriented framework was applied to forest-interior and canopy-top atmospheres during rain-free summer days in 2024 and 2025 to extract dominant modes of VOC emissions. The PMF consistently resolved two recurring modes characterized by the daytime and nighttime enhancement patterns. The daytime mode was dominated by isoprene and its oxidation products and demonstrated strong light- and temperature-dependence, whereas the nighttime mode was enriched in mono- and sesquiterpenes. The daytime contribution exhibited a pronounced morning-afternoon asymmetry, indicating non-linear physiological and canopy-scale controls. These patterns were reproducible across the years. This study demonstrates that combining PTR-ToF-MS with PMF enables robust, top-down identification of recurring modes of forest VOC variability within and above forest canopies, linking leaf-level physiology and ecosystem-scale atmospheric exchange. HighlightForest-scale VOC emissions were resolved into recurring daytime and nighttime modes using a non-targeted PTR-ToF-MS and PMF framework.

A major barrier to scaling marine restoration and aquaculture is the lack of reliable tools to induce invertebrate larvae to settle and metamorphose when and where needed. Although microbial cues are known to induce metamorphosis in many invertebrates, existing methods rely on natural biofilms that are variable, difficult to standardize, and unsuitable for large-scale deployment. Here we introduce ReefTiles, a non-living bacterial coating that preserves inductive activity from metamorphosis-stimulating marine bacteria in a stable, reproducible format. Using both tubeworm and coral larvae, we show that dried and inactivated bacterial films retain full settlement-inducing capacity, matching or exceeding live biofilms while eliminating concerns associated with releasing viable microbes into the environment. Viability assays confirm inactivation, and the coating adheres reliably to common substrate materials. Because ReefTiles can be manufactured and stored at scale and tailored to different inductive strains, they provide a practical microbe-based biotechnology for enhancing larval settlement in reef restoration, sustainable aquaculture, and engineered marine infrastructure.

Introduction: High altitude is a physiologically stressful environment due to low barometric pressure and low oxygen availability. This hypoxic stress commonly leads to Acute Mountain Sickness (AMS) during high altitude travel. Additionally, among the physiological adaptations to sustained hypobaric hypoxia, ventilatory acclimatization is characterized by increases in the ventilatory chemoreflex responses to hypoxia and hypercapnia. This study aimed to determine how low-dose prophylactic use of Acetazolamide (ACZ), as utilized for recreational high-altitude travel, impacts these breathing reflexes. Methods: In a double-blind, randomized, placebo-controlled design, participants received 125 mg of ACZ taken twice daily (N=9) or placebo (N=9) starting 2 days prior to ascent to high-altitude (3801 m) and continued until departure. Ventilatory chemoreflex tests were performed at sea level prior to treatment and after 2 days at high altitude. Results: ACZ reduced AMS severity on the first two days at high altitude. ACZ also lowered end-tidal PCO2, indicating elevated baseline alveolar ventilation. Among the ventilatory chemoreflex characteristics, the ventilatory recruitment threshold was significantly lower at high altitude in both groups. We also found a highly significant three-way interaction between location, treatment, and PCO2 on the hypoxic ventilatory response (HVR), indicating that the relationship between PCO2 and the amplitude of the reflex increase in breathing in response to hypoxia is impacted by ACZ. Conclusions: ACZ may sensitize the interaction between the peripheral and central chemoreflex responses. This data provides insight into the mechanisms underlying the beneficial effects of ACZ on sleep quality and AMS symptoms at high altitude.