AdipoRon alleviates depression-like behaviors in mice by activating AdipoR2-JAK1-STAT3 pathway in microglia.

The Notch1 signalling pathway promotes Silicotic fibrosis by modulating macrophage polarization in response to crystalline silica.

Lipid peroxidation marker malondialdehyde is an independent determinant of hepatitis B vaccine response in hemodialysis patients.

Investigating the efficacy of propranolol in treating chronic stress combined with colorectal cancer in mice and its antitumor potential.

Establishment of a novel model of depression caused by olfactory dysfunction through intranasal administration of 3-methylindole.

Systemic inflammation and dorsolateral striatal activity converge to drive repetitive and compulsive-like behaviors caused by chronic stress.

Inhibition of the PDGFRβ/MMP-9 pathway attenuates CUMS-induced blood-brain barrier disruption, neuroinflammation, and depressive-like behaviors.

Injury-environment interaction: microglial priming by mTBI creates vulnerability to subsequent stress via the HMGB1-RAGE axis.

Standard laboratory housing (21°C) imposes chronic cold stress on mice, yet its fundamental impact on cardiac plasticity remains poorly defined. We systematically interrogated how environmental temperature dictates cardiac responses to endurance exercise, doxorubicin (DOX)-induced cardiotoxicity, and aging. Male mice were housed at standard room temperature (RT) or thermoneutrality (30°C, TN) and subjected to exercise, detraining, DOX treatment, or natural aging. Cardiac remodeling was evaluated by integrating physiological phenotyping (echocardiography, body composition) with comprehensive transcriptomic and proteomic profiling. Housing temperature fundamentally alters cardiac molecular baselines and adaptive trajectories. Exercise at TN elicited a coordinated, extracellular matrix (ECM)-focused transcriptional program, improving contractile function without inducing overt hypertrophy. Conversely, RT triggered a broad, uncoordinated stress response. Notably, while RT permitted classic regression of exercise-induced hypertrophy, detraining at TN revealed a unique cardiac structural economy, where cardiac mass significantly dropped below sedentary controls while maintaining enhanced functional efficiency. In pathological models, RT-induced compensatory survival pathways masked the true structural severity of DOX cardiotoxicity and paradoxically buffered against fibrosis. Furthermore, RT exacerbated cardiac aging phenotypes, inducing widespread fibrosis and upregulating senescence markers and specific microRNAs that remained quiescent under TN. Environmental temperature profoundly reshapes cardiac adaptive plasticity. The chronic thermal stress of standard housing distorts intrinsic molecular signaling, highlighting thermoneutrality as a crucial baseline for revealing true physiological adaptations and ensuring the translational validity of cardiovascular models.

Heat stress (HS) poses a significant threat to the global broiler industry by impairing growth performance and welfare of the birds. The metabolic adaptations to varying durations of heat exposure remain poorly understood. This study aimed to characterize the plasma metabolic profiles of broilers subjected to thermoneutral conditions (TN; 32-22°C, age depended), very short-term (8 h), intermediate (1 week), and long-term (5 weeks) cyclic heat stress (HS; 31°C on average), as well as a subsequent recovery (REC) phase after a 1-week period of HS. A total of 450 day-old male Cobb 500 broilers were randomly allocated to five treatments. Each treatment consisted of 6 replicate pens, with 15 birds per pen. The treatments were distributed in two environmentally controlled rooms based on their assigned climatic conditions (thermoneutral or heat stress). We evaluated growth performance, cloaca temperature, and performed liquid chromatography-mass spectrometry (LC-MS) based metabolomics on plasma from six broilers per treatment. As expected, exposure to heat stress for 1 week or longer significantly increased cloaca temperature (>1.5°C), reduced feed intake, and impaired growth performance. Metabolomic analysis revealed distinct, duration-dependent metabolic signatures. Very short-term (8 h) heat stress was uniquely characterized by elevated plasma uridine, suggesting an activation of nucleotide salvage pathways. In contrast, long-term (5 weeks) heat stress induced a catabolic phenotype, evidenced by increased plasma levels of kynurenine, creatinine, and argininosuccinate, reflecting muscle proteolysis and altered amino acid metabolism. Both short- and long-term heat stress suppressed de novo nucleotide synthesis, marked by decreased orotate and N-carbamoyl-aspartate. Notably, these metabolic alterations were largely reversible, with the profiles of recovery broilers returning to thermoneutral levels within 8 hours. Our findings demonstrate that the broilers' metabolic response to heat stress is a dynamic, duration-dependent process. The identified metabolites, particularly uridine and kynurenine, represent promising candidate biomarkers for distinguishing between acute and chronic heat stress, offering a valuable tool for improving welfare monitoring in poultry production.

Cytosolic PRDX1 acts as an extramitochondrial sink to set mitochondrial H2O2 levels and enable resilience to chronic mitochondrial oxidative stress.

Depression shows significant sex differences in prevalence and neurobiological underpinnings, yet preclinical research investigating the pathophysiology of depression and the efficacy of antidepressants has predominantly relied on male models. Here, we establish a novel female chronic social defeat stress paradigm by leveraging the natural aggression of parous CD1 females, co-housed with castrated males to induce aggression while eliminating confounding sexual behaviors and without hormonal or surgical manipulations. Selected aggressive females reliably displayed offensive behaviors toward C57BL/6NCrl intruders across repeated encounters. Defeated female mice exhibited pronounced depression-like behaviors, including social withdrawal, anhedonia, behavioral despair, and elevated anxiety-like responses. Biochemical analysis revealed elevated glutamate levels in Nucleus Accumbens (NAc) and caudate putamen (CPu). Alterations in EAAT1, GRIN2B, and Neurabin expression were observed in CPu, indicating excitotoxic stress and compromised synaptic integrity. Given the extensive literature on male CSDS and its established pathophysiology, we aimed and successfully developed female-specific replica model of traditional male CSDS, enabling direct comparison and elucidation of sex differences in depression pathophysiology.

Multi-omics analysis reveals CXCL14+ inhibitory neuron dysfunction in major depressive disorder.

This clinical report and its accompanying policy statement review the developmental challenges of young children in foster care under the age of 5years, including recent research on prenatal and postnatal environmental influences on early brain development, and the effects of severe or chronic stress on child development secondary to neglect, physical and sexual abuse. This report also highlights the impact of family disruption and child-parent attachment that occurs with foster care placement, the effects of structural and interpersonal racism, multigenerational poverty, and the more pervasive societal effects that are especially common among children in foster care. The report ends with a brief review of how interventions support resilience in the face of these challenges to child development.

Alteration of colonic circadian rhythm by gut microbiota dysbiosis and SCFA reduction links chronic stress-induced depressive-like behavior.

Cardiac arrhythmias affect 1%-5% of the global population, with atrial fibrillation (AF) being the most common and clinically relevant. While AF is traditionally linked to electrical and structural remodeling of the atria, growing evidence highlights a critical yet underexplored contributor: dysfunction of the autonomic nervous system (ANS). The ANS regulates heart rate and rhythm through sympathetic and parasympathetic inputs, and its imbalance can initiate and sustain AF by promoting ectopic activity, shortening refractory periods, and enhancing reentry circuits. Autonomic dysregulation is further impacted by lifestyle and environmental influences. Excessive alcohol intake, chronic stress, sleep deprivation, and extreme physical exertion have all been shown to modulate autonomic activity and elevate the risk of AF. Additionally, social determinants such as socioeconomic status and healthcare access indirectly influence AF susceptibility through chronic activation of neurocardiac stress pathways. Mechanistically, emerging research implicates sympathetic hyperinnervation, neuroinflammation, and dysfunction of intrinsic cardiac ganglionated plexi as key contributors to arrhythmogenic remodeling. However, current animal models often fail to capture the complexity of human neuro-cardiac interactions due to species-specific differences in cardiac anatomy, innervation patterns, and immune responses. Human induced pluripotent stem cell (iPSC)-derived models offer an alternative, patient-specific platform to study ANS-driven mechanisms in AF. This review focuses on the role of the ANS in AF pathophysiology, examining the cellular and molecular mechanisms by which autonomic dysregulation promotes arrhythmia. We explore current therapeutic interventions of autonomic-driven AF and discuss the potential of new models to improve mechanistic insight and therapeutic development.

This policy statement updates a previous statement to reflect advances in our understanding of both prenatal and postnatal environmental influences on early brain development, including the effects of alcohol and substance exposures prior to birth and the effects of severe or chronic stress on child development secondary to neglect, physical and sexual abuse, family disruption, poverty, and racism. The accompanying clinical report provides a detailed examination of the developmental challenges faced by children in foster care younger than 5years.

Dissociation in epilepsy: rethinking boundaries between psychiatry and neurology.

Examining the relation between empathy and hair cortisol levels.

Sensorimotor network hyperactivity and impaired psychomotor performance associated with cumulative occupational stress in firefighters.