Source-specific organic matter modulates Anammox via humic-like DOM in mangrove sediments: Implications for eutrophication mitigation.

Endurance performance is regulated through dynamic interactions between physiological capacity, nutritional status, and psychological control processes. While traditional endurance models have emphasized metabolic and cardiorespiratory determinants, growing evidence indicates that energy availability also influences cognitive function, perceived effort, and decision-making during prolonged exercise. This narrative review synthesizes current literature on the interplay between nutritional strategies and psychological regulation in endurance sports, with particular emphasis on low energy availability, carbohydrate availability, mental fatigue, and pacing behavior. Acute and chronic reductions in energy availability are associated not only with endocrine and metabolic disturbances but also with amplified perceived exertion, impaired executive functioning, reduced effort tolerance, and altered risk-related decision-making, even in the absence of overt physiological failure. Carbohydrate availability emerges as a central modulator operating through both peripheral mechanisms (substrate supply and glycogen preservation) and central neurocognitive pathways influencing perception, motivation, and fatigue regulation. Hydration status, caffeine ingestion, and gastrointestinal tolerance further interact with perceptual and cognitive processes to shape real-time pacing and endurance sustainability. Integrating sport nutrition and sport psychology provides a unifying framework for understanding endurance regulation as a multilevel process linking metabolic state to perceptual experience and behavioral decision-making. From an applied perspective, optimizing endurance performance requires maintenance of adequate long-term energy availability, strategic carbohydrate periodization aligned with training demands, and systematic monitoring of perceived effort alongside physiological load. Future research should prioritize interdisciplinary, ecologically valid designs combining metabolic, perceptual, and cognitive measurements, supported by wearable and data-driven technologies capable of capturing real-time endurance regulation. Bridging nutritional and psychological mechanisms within a unified conceptual model offers a stronger scientific basis for improving performance sustainability while safeguarding athlete health in modern endurance sport.

Leaf dark respiration (Rdark) is often measured in artificially dark-adapted samples at a single time point during the day, with temperature-normalised rates often assumed to be constant throughout a 24-hour cycle. However, the extent to which the 24-hour cycle influences leaf Rdark and respiratory metabolic profile remains unclear, particularly in C4 plants. We quantified O2-based leaf Rdark and metabolites at six time points over a diel (i.e. 24-hour) cycle in leaves of four grass species (one C3 and three C4 species). We found that Rdark and leaf metabolites varied among species, and between dark-adapted day-sampled and night-sampled leaves. In general, C4 plants contained a relatively higher content of organic acids and soluble sugars than C3 plants. Across the four species, variations in Rdark were associated with changes in the abundance of metabolites involved in the mitochondrial tricarboxylic acid pathway (malate, fumarate, succinate and citrate), amino acid metabolism (alanine and asparagine) and sugar interconversion (lactose and mannose). Multivariate statistics suggested that Rdark of the examined species is influenced more by the relative contribution of multiple concurrent metabolic pathways across the diel cycle than by C3 and C4 photosynthetic types. We suggest that Rdark and metabolite profiles measured during daytime on dark-adapted leaves are not good surrogates for nighttime respiratory properties. Understanding how the supply of respiratory substrates varies during the diel cycle would lead to a more accurate prediction of Rdark over the course of a day.

Pilot-scale partial denitrification/anammox demonstration of concentrated circulating cooling water and municipal wastewater co-treatment.

Substrate supply, compartmentation, and utilization in hepatic de novo lipogenesis.

Side-stream fermentation drives partial denitrification/anammox for enhanced nitrogen removal and anaerobic ammonium oxidation bacteria enrichment in a flocs-based continuous-flow anaerobic/aerobic/anoxic system.

Novel incomplete nitritation-regulated multi-pathway anammox process for advanced nitrogen removal from real municipal wastewater.

Abstract Coastal sediments are globally significant sources and sinks of greenhouse gases (GHGs), yet their contributions to climate feedbacks of warming and ocean acidification remain uncertain, in part due to limited understanding of short‐term variability. Here, we use a fully factorial laboratory experiment to disentangle how diel light–dark and tidal inundation and exposure interact with warming and elevated p CO 2 to regulate benthic fluxes of CO 2 , CH 4 , and N 2 O in estuarine sediments, alongside concurrent changes in benthic oxygen exchange. While warming and p CO 2 exerted strong independent effects, their influence was shaped by diel and tidal fluctuations in redox conditions and oxygen availability, reflecting shifts in metabolic balance between primary production and respiration. Light consistently limited CO 2 , CH 4 , and N 2 O emissions through enhanced autotrophic uptake and oxygenation, while dark promoted anaerobic production pathways. N 2 O showed the greatest sensitivity to the combined effects of climate forcing and redox dynamics. Despite warming‐driven stimulation of benthic heterotrophy and the production of all GHGs, CO 2 remained the dominant greenhouse gas, with minimal CH 4 and N 2 O fluxes due to the limited organic matter availability within the sediment. This reflects the strong redox controls on CH 4 and N 2 O production, which relies on both oxygen depletion and organic substrate supply. Our findings emphasize that fine‐scale temporal variability can significantly shape both the magnitude and climate sensitivity of benthic GHG emissions. Capturing these fine‐scale controls is essential for accurately modeling the contributions of estuarine sediments to global GHG budgets and their feedbacks.

Climate warming is expected to stimulate soil nitrogen (N) transformations, thereby increasing the supply of available N to support plant growth and carbon (C) assimilation. However, it remains uncertain whether this stimulatory effect on soil N transformations can persist over time to sustain plant growth and N uptake. This study combines a global meta-analysis with a local warming experiment with 7 years to shed light on how soil N transformations respond to long-term warming and the underlying mechanisms, and how these transformations affect plant growth. We found that longer-term warming (≥ 6 years) did not stimulate gross soil N transformation rates, with gross nitrification and NO3 - immobilization rates being significantly inhibited. These responses of gross N mineralization and nitrification rates were primarily explained by biotic rather than abiotic factors. Altered substrate supply through N mineralization and nitrification influenced the responses of NH4 + and NO3 - immobilizations. Interestingly, despite the slower rate of soil N transformations, plant growth and N uptake (mainly NH4 + uptake) increased under warming, as the inhibition of NH4 + consumption by nitrifiers left more NH4 + for plants. The findings break the traditional views that warming has a positive effect on soil N cycling and thus contribute to plant N uptake and growth. The slower soil N transformations under longer-term warming and the changes in plant N uptake preference imply a coordination between soil and plant N cycling. Land management practices and C-N cycling simulations should incorporate this soil-plant N coordination and the slower soil N transformations under longer-term warming.

Post-COVID-19 condition (PCC) is characterized by fatigue, dyspnea, and muscle pain, with treatment including physical exercise and nutritional support. Creatine supplementation under these conditions may increase the total body creatine pool, thereby increasing muscular phosphocreatine availability and improving the energy substrate supply to sustain activity and reduce fatigue. This study investigated the efficacy of creatine supplementation in alleviating fatigue symptoms in patients with PCC, as well as its effects on quality of life, lung function, physical performance, body composition, and muscle strength. This randomized, single-blind, placebo-controlled pilot study assessed supplementation with either 6 g or 18 g of creatine per day or 6 g of maltodextrin (placebo) combined with physical activity three times a week over 4 weeks. Participants with PCC who experienced fatigue [score ≥4 on the revised Piper Fatigue Scale (PFS-R)] underwent physical examination; laboratory evaluation; pulmonary function tests; muscle ultrasound; respiratory and peripheral muscle strength assessments; body composition analysis; physical capacity tests; and questionnaires on quality of life, dyspnea, anxiety, and depression before and after the intervention. Difference-in-differences (DID) between these two time points were compared across the intervention groups and the control arm. Sixty-seven individuals were randomized. Participants were predominantly female (76.6%), with a mean age of 52 ± 12 years, body weight of 82.6 (73.1-93.4) kg, and height of 1.63 ± 0.07 m. A total of 58 completed the protocol: 21 in the 6 g/day group, 19 in the 18 g/day group, and 18 in the placebo arm. When the difference-in-differences (DiD) in the PFS-R before and after the intervention was assessed, a score change of -2.05 was observed in the 6 g/day arm [95% confidence interval (CI): -3.47 to -0.63; p = 0.005]. Additionally, this same group showed a significant increase in handgrip strength [mean difference (DiD estimate): 4.40 kgf; 95% CI: 0.27 to 8.52; p = 0.037]. Adverse events were minimal, transient, and did not require medical intervention. Creatine supplementation at 6 g/day was associated with improvements in fatigue and peripheral muscle strength in patients with PCC, with a favorable safety profile.

D-allulose is a rare low-calorie sugar with considerable health benefits and industrial potential. Compared with chemical synthesis and free enzyme catalysis, microbial production using engineered cells offers a low-cost and highly stable solution. Therefore, we investigated the reaction pathway underlying the synthesis of D-allulose from D-glucose. Specifically, the enhancement of glucose isomerase-catalyzed reactions and their role in D-allulose synthesis were evaluated. First, a mutant strain with significantly increased glucose isomerase from Anoxybacillus kamchatkensis G10 (AGGI) expression was obtained through ultraviolet mutagenesis combined with high-throughput flow cytometry. A 4.55-fold increase in AGGI activity and a D-fructose conversion yield of 51.2% were obtained. A dual-enzyme pathway was subsequently constructed by co-expressing AGGI and D-allulose 3-epimerase (DAEase) in the optimized host. After balancing the catalytic requirements of both enzymes through optimization of reaction conditions, CRISPR-associated transposase was employed to efficiently integrate the glucose transporter gene galP into the genome, further enhancing substrate supply. The final engineered Escherichia coli strain achieved a D-allulose conversion rate of 15% from 20 g/L D-glucose. This demonstrates the crucial role of glucose isomerase in microbial D-allulose production and advances the optimization and development of D-allulose synthesis strategies using D-glucose as a substrate.

Restriction of fetal substrate supply has an adverse effect on surfactant maturation in the lung and thus affects the transition from in utero placental oxygenation to pulmonary ventilation ex utero. However, the consequences of reduced fetal substrate supply are dependent on the timing of gestation, severity and duration. We hypothesise that maternal nutrient restriction (MNR) from early pregnancy negatively impacts fetal lung maturation. Female baboons of similar age and weight were randomly assigned to either a control diet (n=3F, 5M offspring) or MNR (n=4F, 4M offspring). On a weight-adjusted basis, MNR animals were fed 70% of the feed consumed by controls. Fetal lung tissue was collected at 0.9 gestation (term=184days). qRT-PCR and immunohistochemistry were utilised to measure expression of key molecules involved in surfactant maturation, reabsorption of lung liquid, vascularisation and immune cells. MNR decreased type II alveolar epithelial cell density and the mRNA expression of PCYT1A, the gene for choline-phosphate cytidylyltransferase A, the enzyme required for de novo surfactant phospholipid synthesis. However, MNR had no effect on the expression of surfactant proteins in the fetal lung. There was a reduced number of α-smooth muscle actin-stained vessels and presence of CD45+ immune cells within the lung of fetuses exposed to MNR. These data indicate that MNR from early pregnancy increases risk of neonatal respiratory complications at birth by impairing the capacity for surfactant maturation, reducing vascularisation within the fetal lung and impairing innate lung immunity.

Ischemic stroke (IS) features a dynamic collapse of neuronal mitochondrial metabolism. Current therapies fail to effectively address the sequential metabolic failures: ischemia disrupts the tricarboxylic acid cycle via substrate deprivation, while reperfusion impairs oxidative phosphorylation through ROS bursts. Inspired by the endosymbiotic metabolic loop between chloroplasts and mitochondria, we constructed a chloroplast-inspired nanoassembly via a membrane self-assembly strategy. This system compartmentalizes an energy module (nanothylakoids) and a catalytic module (CO2-fixing nanocatalysts) within a light-harvesting module (upconversion nanoparticles-functionalized platelet membrane nanomotors), mimicking natural chloroplast architecture and replicating its full "phototaxis, energy supply, and carbon fixation" functionality. Under near-infrared light, the light-harvesting module first achieves phototactic penetration through thrombi and the blood-brain barrier, enabling progressive targeting to damaged neurons. After entering the cell, the energy module generates O2/ATP/NADPH to reboot mitochondrial oxygen-carbon metabolism, while metabolic wastes (CO2/lactate/ROS) are reciprocally supplied to the catalytic module for carbon fixation, subsequently converting into CO to further activate oxidative phosphorylation. This process ultimately establishes a cross-kingdom oxygen-carbon metabolic loop for IS therapy. We further demonstrate the efficacy of the system in other ischemic models (myocardial and limb ischemia), showing its capacity for multimodal coordination in substrate supply and waste clearance to effectively remodel mitochondrial function in damaged cells, thereby providing a strategy for metabolic reprogramming in ischemic disease therapy.

Depending on the pregnancy complication, substrate delivery to a developing fetus can be reduced, changing the course of fetal growth below the genetically determined in utero growth potential, resulting in fetal growth restriction (FGR). FGR is linked to an increased risk of developing cardiovascular disease (CVD) in later life. When caused by placental insufficiency, FGR is characterized by fetal hypoxaemia and hypoglycaemia due to reduced substrate supply to the fetus. However, other common pregnancy complications exist, where fetal hypoxaemia or hypoglycaemia may or may not occur. It is therefore necessary to understand the independent and synergistic contributions of hypoxaemia and hypoglycaemia to the fetal origins of CVD. In doing so, this knowledge will aid in the development of intervention strategies. The aim of this review is to provide mechanistic insights by comparing findings across different paradigms of developmental programming using animal models of FGR, with consideration of the timing, duration, and severity of the insult, and the ventricles and fetal sex studied.

Members of the genus Streptomyces are major producers of a wide variety of secondary metabolites that serve as bioactive compounds. Many secondary metabolites are produced in response to environmental signals such as biotic and abiotic stresses. In this study, we identified salt supplementation as one of the stimuli activating secondary metabolism in the model Streptomyces species, Streptomyces coelicolor. Comparative metabolomics revealed overproduction of several known secondary metabolites, most notably undecylprodigiosin and coelimycin P1, in addition to their biosynthetic intermediates and derivatives, as well as many unknown metabolites. Transcriptomic analysis revealed activation of diverse biological processes including cation uptake, compatible solute production, and the phosphate limitation stress response through conserved and species-specific mechanisms, presumably to overcome the increased salinity. This response leads to activation of a variety of regulatory and metabolic pathways required for production of secondary metabolites including activation of conserved metabolic pathways for energy and substrate supply and species-specific secondary metabolite biosynthetic gene clusters. Furthermore, several promoter sequences contributing to upregulation of secondary metabolism induced by salt supplementation were identified. Overall, our data show how S. coelicolor copes with the increased salinity and tailors the cellular metabolism toward secondary metabolism in a conserved and species-specific manner.IMPORTANCEPrecise control of cellular metabolism is critical to ensure directing cellular resources toward metabolic pathways required for the environment. Many Streptomyces species activate production of secondary metabolites upon exposure to environmental stimuli. This study reveals dynamic reprogramming of cellular metabolism in Streptomyces coelicolor under increased salinity, which induces production of various secondary metabolites. Notably, this model biological system redirects cellular resources toward various metabolic pathways required for proper activation of secondary metabolite biosynthesis, including precursor and energy supply and posttranslational modification of biosynthetic enzymes. Interestingly, some pathways are activated by phosphate limitation stress, presumably caused as a result of increased salinity. Certain aspects of this metabolic reprogramming are likely common in many Streptomyces species and may be controlled by rather complex regulatory pathways. Overall, this study unveils how Streptomyces species tailor the cellular metabolism toward secondary metabolism and paves the way for understanding metabolic regulation.

This study examined how exogenous glutamate and cold stress enhance γ-aminobutyric acid (GABA) accumulation in germinated soybeans and regulate key enzymes of the GABA shunt. Treatment with 1.5 mmol L-1 glutamate or 2 h of cold stress (4 °C) increased GABA levels by 10.22 and 10.81%, respectively. Both interventions upregulated glutamate decarboxylase (GAD) while suppressing GABA transaminase. Glutamate directly activated GAD via substrate provision, whereas cold stress enhanced GABA synthesis through polyamine degradation. Metabolomics profiling revealed increased levels of amino acids, phenolic acid, and flavonoids in response to abiotic stress. Flavonoids drove antioxidant activity in glutamate-treated samples, while proline and arginine strongly correlated with antioxidants in cold-stressed groups. KEGG pathway analysis highlighted glutamate metabolism and polyamine degradation as core routes regulating GABA biosynthesis. These findings highlight distinct regulatory networks governing GABA accumulation under stress conditions, offering insights for optimizing bioactive compound production in functional foods.

Current therapeutic approaches for muscle reconstruction face considerable challenges, particularly in generating sufficiently dense cell aggregates and in establishing effective methods for reactivating the function of exogenous cells. Herein, we developed a pre-priming cell sheet therapy for volumetric muscle loss (VML) that leverages highly dense, electro-mechanically bioactive constructs. To achieve this goal, we fabricated a multifunctional cell culture platform based on a near-infrared (NIR)-responsive, wrinkle-patterned, conductive substrate. This system enables scalable preparation (>6 mm in diameter), non-invasive harvesting, and bioactive pre-priming of cell sheets for transplantation. Non-invasive harvesting of the sheets is achieved via a NIR-triggered release mechanism, in which dynamic changes in wrinkle morphology induce a sufficient shift in mechanical stress at the cell-substrate interface, thereby disrupting focal adhesions. Compared with conventional cell-suspension therapy, the microstructured electroactive surface demonstrated superior efficacy for VML repair, as evidenced by integrated in vitro electrophysiology, RNA sequencing, and in vivo analysis. This enhancement is attributed to the substrate's provision of combined electrical and mechanical priming cues, which collectively promote myogenic differentiation, growth, and pro-regenerative calcium signaling in C2C12 myoblasts. In conclusion, this work establishes that engineering interfacial dynamics—rather than relying solely on static material properties—is pivotal for the development of advanced cell therapies. The dynamic electroactive substrate offers a versatile strategy for fabricating pre-functionalized tissue constructs, with immediate promise for regenerating electroexcitable tissues and broad application prospects in regenerative medicine.

Temperature and substrate jointly shape significant anammox contributions to nitrogen removal in hot springs.

Complete and stable enhanced biological phosphorus removal at 30°C using glutamate and acetate as alternating carbon sources.

The use of peripheral blood mononuclear cells (PBMCs) in cardiovascular research is increasingly common. However, little is known regarding potential age-related changes in mitochondrial bioenergetics and oxidative stress in PBMCs, or whether such changes relate to endothelial function. We assessed mitochondrial bioenergetics and antioxidant buffering capacity (AoxBC) capacity in PBMCs from young (n = 18; 21 ± 2 yr) and older (n = 17, 66 ± 4 yr) adults. High-resolution respirometry and fluorometry measured mitochondrial respiration rate (JO2) and membrane potential (Δψm), respectively, in response to substrate provision (pyruvate, glutamate, malate, and succinate; PGMS) and a bioenergetic creatine kinase (CK) clamp at physiological ATP:ADP ratios (PCr1, PCr2, and PCr3). MtROS emission was measured as hydrogen peroxide (H2O2) emission, and H2O2 production was quantified using inhibitors of glutathione reductase and thioredoxin/peroxiredoxin. AoxBC was calculated as the percentage of H2O2 produced but not emitted. Endothelial function was assessed through flow-mediated dilation (FMD). JO2 was similar between groups at baseline (P = 0.08) and lower energetic states (PCr2, PCr3; P ≥ 0.09), but was lower in older adults at higher energetic states (PCr1: 14.05 ± 2.11 vs. 12.03 ± 2.98 pmol·s-1·106 cells-1, P = 0.03; PGMS: 20.61 ± 2.11 vs. 16.58 ± 3.56 pmol·s-1·106 cells-1; P = 0.0009). Δψm was hypopolarized in older compared with young adults at all energetic states (P ≤ 0.003). Although there were no statistical differences in H2O2 emission (P = 0.43) or production (P = 0.18), AoxBC was lower in older adults (52.59 ± 15.44% vs. 63.49 ± 10.30%; P = 0.03). Age-related changes in JO2 (PGMS, P = 0.02) and Δψm (PGMS, P = 0.0008; PCr2, P = 0.04; PCr3, P = 0.02) were related to FMD. These data demonstrate associations between altered PBMC mitochondrial bioenergetics and age-related vascular endothelial dysfunction.NEW & NOTEWORTHY The use of peripheral blood mononuclear cells (PBMCs) is increasingly common in cardiovascular research. However, relatively little is known regarding potential age-related changes in PBMC mitochondrial bioenergetics and oxidative stress, or whether age-related changes are related to endothelial (dys)function. We demonstrate altered mitochondrial bioenergetics (oxygen consumption rates and membrane potential) and antioxidant buffering capacity in PBMCs from older compared with young adults. We additionally demonstrate associations between mitochondrial bioenergetics and endothelial function (brachial-artery flow-mediated dilation).