Assessing stress in a mammal from plasma and feces: A nutritional mismatch between the diet needed and the food -available.

An evolutionary shift to prioritizing mating over care is associated with consistently high androgen levels in male threespine stickleback.

Soluble epoxide hydrolase deficiency rescues heart failure with preserved ejection fraction by targeting cytochrome P450 2E1.

Continuous loading with rotating principal stress axes using rotated dies

Impacts of phenanthrene on juveniles of dusky grouper, Epinephelus marginatus (Perciformes: Serranidae): Behavioral, endocrine and oxidative effects.

Growing evidence implicates the brain-gut axis in depression pathogenesis, though the underlying mechanisms remain elusive. This study investigated the antidepressant potential of rifaximin, a non-absorbable antibiotic, and its mechanisms via the brain-gut axis in a rat chronic unpredictable mild stress (CUMS) model. We found that CUMS induced anxiety- and depression-like behaviors, impaired colonic endocrine cell function, and downregulated neuropeptide Y (NPY) expression in both the colon and medial prefrontal cortex (mPFC). CUMS also altered neuronal activation and disrupted key neurotransmitter (GABA, Glu, 5-HT) balance in the mPFC. Rifaximin treatment ameliorated these behavioral deficits, restored colonic endocrine function, and increased NPY levels in both the colon and mPFC. Furthermore, it normalized CUMS-induced alterations in neuronal activation and neurotransmitter balance. Crucially, functional knockdown of NPY in the mPFC not only reduced colonic NPY expression in control rats but also abolished the anxiolytic effects of rifaximin in CUMS-treated rats. In summary, this study suggests that in the CUMS model, rifaximin can play an anxiolytic and antidepressant effect, and its mechanism may be related to the rifaximin’s regulation on NPY mediated gut-brain axis between colon and mPFC.Supplementary InformationThe online version contains supplementary material available at 10.1038/s41598-025-27826-9.

Classical studies of the ratcheting of pressure vessels under thermocyclic loading assume that the structural material is elastic-plastic without hardening (ideal plasticity). This allows for an analytical solution to the problem, which is typically presented in the form of a "Brie diagram" plotted on the axes of mechanical and thermal stresses. The actual behavior of a material under cyclic thermo-mechanical loading requires more complex mathematical models that consider isotropic, kinematic, or mixed isotropic-kinematic hardening effects. These additional factors significantly affect the adaptability characteristics of the structure. Modern Russian and international design standards (PNAE, GOST, ASME, RCC-MR) for nuclear power plant reactor installations (reactors using liquid metal coolants, high-temperature gas-cooled reactors, etc.) allow for the occurrence of plastic deformation in the material but limit the accumulation of these deformations over the lifespan of the structure. Specifically, these standards regulate the use of both a simplified method based on the classic Bree solution for perfectly plastic materials and a direct finite element analysis of the structural life cycle under conditions of plastic deformation and high-temperature creep. In this paper, we investigate the problem of thermal cycling of a pressure vessel using different hardening models. We have developed a numerical algorithm to construct and analyze the evolution of adaptation diagrams depending on the number of cycling loads. We perform a specific numerical calculation for the cyclic thermal force loading of a steel pressure vessel with known parameters for elastic-plastic deformation models. This is done in the context of predicting the design life based on current regulations and standards for the design of nuclear power plant equipment.

Bovine viral diarrhea virus (BVDV), the causative agent of bovine viral diarrhea-mucosal disease, is a major global threat to cattle health. BVDV employs sophisticated strategies to evade host defense and facilitate its replication. Understanding these mechanisms is crucial for developing effective vaccines and antiviral agents. Our study elucidates how cytopathic BVDV and non-cytopathic BVDV subvert the host's antiviral innate immune response by exploiting autophagy to inhibit the RIG-I-MAVS pathway. A key finding is that BECN1-mediated autophagy directly targets MAVS protein for degradation via a specific BECN1 and MAVS interaction. Furthermore, we demonstrate that BVDV activates autophagy through ROS-ER stress axis to promote its replication. These insights reveal a novel immune evasion mechanism of BVDV and highlight the therapeutic potential of autophagy inhibition in treating BVDV-related diseases.

High levels of stress and acute stress responses are significant predictors of chronic illnesses; however, specific stress response components of resilience and healthy coping are not well understood. To develop and assess a pain stress test (Yale Pain Stress Test - YPST) involving three uncontrollable and unpredictable consecutive 3-minute trials of pain-stress (0°C ice + water) or no pain-stress control (37°C warm water) hand immersion conditions, adapted from the Cold Pressor Task (CPT). Fifty men and women participated in a within-subjects experiment. Repeated autonomic [pulse, systolic and diastolic blood pressure (SBP/DBP)], hypothalamic pituitary adrenal (HPA) axis (cortisol, ACTH) and subjective stress (self-reported pain, anxiety) measures during the pre-stress baseline, acute reactivity and return to homeostasis/recovery time periods were collected. Behavioral pain tolerance per trial (in seconds) was also assessed. Robust multi-level stress responses were observed (p's < 0.009), with sex-specific interactions only for SBP, DBP and pain ratings. Greater reactivity in SBP, DBP, cortisol, and Cortisol/ACTH ratio predicted higher behavioral pain tolerance (p's < 0.038), and higher DBP predicted lower pain during recovery in the pain-stress condition (p < .028). Higher SBP, DBP, Cortisol, and ACTH reactivity in pain-stress but not control predicted lower basal anxiety during recovery (p's < 0.004). These findings indicate robust multi-level stress responses with YPST provocation, that were also significantly related to behavioral pain tolerance and subjective distress and recovery. The results suggest that acute physiological stress responses play a role in stress adaptability and resilient coping, but replication in larger samples and in individuals suffering from stress-related illnesses is warranted.

Sleep deprivation-induced cognitive impairment: Unraveling the role of neuroinflammation.

Attenuation of NF-κB/NLRP3 inflammasome axis and oxidative stress, and upregulation of Nrf2/HO-1 signaling mediate the protective effect of S-carboxymethylcysteine against cyclophosphamide-induced cardiotoxicity.

Psilocybin induces sex- and context-specific recruitment of the stress axis.

Strength and non-coaxiality behavior of warm frozen silt under inclined principal stress axes

Targeting TDP-43-activated GRP78/endoplasmic reticulum stress axis suppresses triple-negative breast cancer progression.

Bipolar disorder (BD) is a severe psychiatric illness characterized by recurrent mood episodes and significant psychosocial impairment. Emerging evidence supports a bidirectional link between diet and mental health, with growing interest in nutritional psychiatry. This narrative review examines the psychological and psychiatric impact of diet in BD, focusing on biological mechanisms (gut-brain axis, neuroinflammation, oxidative stress, neurotransmitter synthesis, and HPA axis dysregulation) and the role of specific dietary patterns, including Western, Mediterranean, ketogenic, and anti-inflammatory diets. Key micronutrients such as omega-3 fatty acids, B-vitamins, magnesium, and vitamin D are explored in relation to mood regulation. This review also addresses psychological factors, including emotional eating, disordered eating behaviors, and the symbolic meaning of food in BD. Furthermore, it highlights the integration of nutritional psychoeducation into psychotherapy, the impact of comorbidities (e.g., obesity, metabolic syndrome), and the role of lifestyle factors such as sleep and physical activity. Despite promising findings, current research is limited by methodological heterogeneity. Future perspectives should include interdisciplinary, personalized interventions that incorporate nutritional strategies into standard care for BD.

Neuroinflammation is a fundamental pathophysiological mechanism underlying various neurodegenerative diseases. This study investigated the therapeutic effects of quinacrine (QC), a phospholipase A2 (PLA2) inhibitor, in lipopolysaccharide (LPS)-induced neuroinflammation. Thirty-five male Sprague-Dawley rats were divided into five groups: control, QC alone, LPS, LPS + QC 10mg/kg, and LPS + QC 30mg/kg. QC was administered intraperitoneally for three consecutive days. LPS was administered two hours after the final QC dose, and the animals were euthanised six hours later. ELISA analyses revealed significant increases in IL-1β, IL-6, and PLA2 levels following LPS administration; however, QC pretreatment reduced these increases in a dose-dependent manner. Anti-inflammatory IL-10 levels were enhanced with QC pretreatment. The fact that QC is a direct PLA2 inhibitor is consistent with this mechanism. LPS increased MDA levels and decreased antioxidants such as GSH, GPx, CAT, and SOD. QC pretreatment normalized these parameters and reduced oxidative damage. LPS caused a significant drop in BDNF levels. Expressions of COX2, iNOS, and GFAP were notably increased in the LPS group, while pretreatment with QC pretreatment at 30mg/kg significantly lowered these glial and inflammatory markers. Western blot results showed that LPS-activated TLR4 and NF-κB protein levels were reduced dose-dependent manner by QC pretreatment. Overall, our results suggest that QC suppresses the proinflammatory response, decreases oxidative stress, and promotes neuroplasticity by targeting multiple pathways in the LPS-induced neuroinflammation model.

The formation and propagation of Lüders bands are important phenomena in the plastic deformation of some critical structural materials. The propagating Lüders front, which is structurally unstable, plays a key role in this process. Yet, the microstructural and stress states of the Lüders front are challenging to characterize and remain insufficiently understood. The present study utilized in-situ synchrotron-based high-energy X-ray diffraction on a fine-grained medium-Mn transformation-induced plasticity steel exhibiting typical Lüders banding behavior. Detailed analysis of evolving diffraction patterns was performed regarding peak intensity, full width at half maximum, and measured lattice strain. An abnormal measured lattice strain asymmetry was observed from the Debye rings that were collected when the Lüders front overlapped with the irradiated volume. This allows for a discussion of the local microstructural and stress states of the Lüders front, evidencing the possibility of a local shear stress component with a tilted principal stress axis. The work offers new insights into the micro-mechanisms of Lüders banding. It provides a practical and efficient analytical method for studying the dynamics of localized deformations, particularly when deformation is inhomogeneous within the characterized volume or inconsistent with macroscopic deformation.

Depression, often induced by chronic stress, results in significant behavioral and biochemical changes in the brain. Due to the limited effectiveness and potential side effects of traditional antidepressants, there is growing interest in exploring alternative therapies. Natural substances, particularly those found in foods with antioxidant and anti-inflammatory benefits, have emerged as promising candidates. Phoenix dactylifera (Ajwa date), rich in bioactive compounds like polyphenols and flavonoids, may help manage stress-induced depression. This study assessed the antidepressant and neuroprotective effects of Ajwa date seed powder extract (ADSP) and fruit pulp extract (AFP) in a chronic mild stress (CMS) mouse model. Male mice were treated with two doses of ADSP (400 and 800mg/kg) and AFP (500 and 1000mg/kg) daily for three weeks in their respective groups. To assess depressive-like behaviors, the study employed behavioral assessments such as the tail suspension test (TST) and the sucrose preference test (SPT). Biochemical analyses measured plasma corticosterone, nitrite levels, antioxidant enzyme activities (catalase, GSH, SOD, GPx), and cytokine levels (TNF-α, IFN-γ, IL-6, CRP, IL-10, TGF-β1). Administration of both ADSP and AFP led to a significant decrease in immobility time during the TST (p < 0.001) and a marked increase in sucrose preference in the SPT (p < 0.001), reflecting antidepressant-like activity. Additionally, both extracts significantly reduced plasma corticosterone and nitrite concentrations (p < 0.001), implying a modulatory effect on the HPA axis and oxidative stress. Antioxidant enzyme activities were elevated (p < 0.001), and pro-inflammatory cytokines (TNF-α, IFN-γ, IL-6, CRP) were reduced, while anti-inflammatory cytokines (IL-10, TGF-β1) were increased (p < 0.001). ADSP and AFP demonstrate notable antidepressant and neuroprotective properties, primarily attributed to their antioxidant and anti-inflammatory mechanisms. A comparison analysis revealed that AFP was more effective in reducing inflammation and enhancing behavioral outcomes. These results highlight the potential of food-based compounds, such as those found in Ajwa dates, as natural alternatives for addressing stress-related depression and neuroinflammation.

Alzheimer's Disease (AD) is a progressive and fatal neurodegenerative disorder (NDD), and the leading cause of dementia globally, with females being more susceptible than males. Existing animal models for AD are primarily pharmacologically induced or transgenic, yet many fail to recapitulate the full spectrum of human AD pathology and thereby elucidating its sex-based differences. This underscores the need for a cost-effective and robust experimental model that reliably mimics the multifactorial nature of AD taking into account the differences that arise due to sex. In recent years, the zebrafish (Danio rerio) has emerged as a promising model organism for studying central nervous system (CNS) disorders, including AD, owing to its high genetic and physiological homology to humans, transparent embryonic development, and amenability to high-throughput screening. This study aims to establish a novel chronic neurotoxicity induced ZF model, using AlCl3 as an inducing neurotoxic agent. The hypothesis centers on AlCl₃-induced oxidative stress, cholinergic pathway dysfunction, and gut pathophysiological changes as drivers of AD-like pathology. Adult zebrafish, of both sexes were exposed to chronic AlCl₃ treatment over a 28-day period. Post-treatment assessments included histopathological, biochemical, and behavioural analyses to evaluate changes in brain and gut tissues, oxidative stress biomarkers, and cognitive performance. Zebrafish exposed to AlCl₃ exhibited distinct pathological changes in both brain and gut tissues compared to controls. In the brain, hallmarks such as pyknotic neurons, neuronal vacuolisation, and neural tissue necrosis was observed. Gut tissue displayed significant abnormalities, including reduced villi number, epithelial cell loss, and fused or shortened villi. Biochemical analyses revealed elevated oxidative stress, evidenced by altered levels of catalase (CAT), glutathione (GSH), and lipid peroxidation (LPO). Additionally, disruption of the cholinergic system was evident. Behavioural analyses using locomotor tracking revealed marked cognitive deficits, including reduced average speed, decreased distance travelled, and increased immobility. Lastly, our sex specific differences revealed that females were more affected by the biochemical, histological and neurobehavioural parameters as compared to males, thereby indicating that females pose a greater susceptibility towards developing AD. The AlCl₃ -induced zebrafish model successfully replicates key features of human neurotoxicity, which may lead to AD like features including oxidative stress, cholinergic dysfunction, neurodegeneration, and gut-brain axis alterations. This novel and cost-effective model provides a comprehensive platform for exploring sex-mediated neurotoxicity experimental animal model and offers potential utility for screening therapeutic interventions and understanding disease-modifying mechanisms. Keywords: Alzheimer's Disease, Chronic Neurotoxicity, Gut-brain axis, Zebrafish, Sex differences, Alumnium chloride.

While contemporary cancer treatment strategies have significantly prolonged the lives of patients, therapeutic resistance remains a predominant cause of disease progression and cancer-related deaths. Cancer therapy often induces gene regulatory responses that promote cell survival in the face of this therapy. Herein, we sought to develop a stochastic model of the response to repeat therapeutic challenge. This model integrates reinforcement learning to account for environmental history-dependent cellular transitions and growth dynamics. When applied to prostate cancer, this memory-driven adaptive model successfully captures the experimentally-observed dynamics of drug-sensitive and drug-resistant LNCaP cells under varying dosing schedules of androgen receptor blockade with enzalutamide (enza), significantly outperforming traditional transition models that lack history dependence. This performance is especially evident in the ability of our approach to robustly predict stochastic fluctuations in cancer cell population sizes across the entire disease trajectory, including subtle, later-emerging responses following initial therapy. The model was further evaluated by predicting the control of resistant cells in an enza environment by modeling inhibition of the p38/MAPK pro-survival stress axis, which was then validated experimentally. Lastly, we developed and applied a patient-calibrated model using prostate-specific antigen (PSA) data from clinical patient cohorts undergoing intermittent androgen deprivation therapy. Our model accurately predicts the PSA dynamics under repeated treatment cycles and effectively distinguishing between patients who respond and those who do not respond to treatment, thereby providing quantitative insight into prostate cancer progression. We anticipate that such adaptive modeling frameworks will be broadly useful for predicting cancer treatment outcomes and developing optimized adaptive therapeutic strategies tailored to patient-specific disease dynamics in additional cancer contexts.