Haemodynamic shear stress, sensed by vascular endothelial cells (ECs), is crucial for the functional integrity of ECs and the systemic benefits of exercise. Here, we observed that shear stress triggers the release of medium/large extracellular vesicles (m/lEVs), from ECs via activation of the mechanosensitive ion channel Piezo1. Endothelial Piezo1 activation induces Piezo1 translocation to the cell periphery, facilitating its trafficking from the vascular ECs to the smooth muscle cells in the splenic capsule. Within the splenic capsule, the translocated Piezo1 acts as a downstream effector of α1-adrenergic receptor, boosting exercise-induced spleen contraction and enhancing exercise endurance. Genetic or pharmacological inhibition of Piezo1 trafficking from ECs impaired spleen contraction during exercise and reduced exercise endurance in mice. Additionally, exercise-induced m/lEV release contributes to safeguard endothelial function through modulating intracellular Piezo1 homeostasis. Furthermore, positive correlations between exercise-induced increases in circulating Piezo1-enriched m/lEVs and the degree of spleen contraction were also observed in human volunteers. These findings unveil a vasculo-splenic axis during exercise, in which EC-derived m/lEVs shuttle Piezo1 to maintain endothelial function and exercise endurance, highlighting a novel role of Piezo1 in inter-organ communication.

Modulation of magnetic field strength may be a potential therapeutic strategy, particularly in the context of ageing and neurodegenerative disease. Research on magnetic fields (MFs) has been motivated by diverse factors, including interplanetary space travel, emissions from medical equipment, and the mechanisms underlying magnetoreception in migratory birds. The biochemistry of hypomagnetic field (HMFs; <5 μT) exposure has focused on healthy model organisms, leaving their therapeutic potential unexplored. We investigated the effects of HMF exposure in a neurodegenerative disease model. The Pink1 loss-of-function model recapitulates key features of early-onset Parkinson's disease, including mitochondrial dysfunction, locomotor impairment, dopaminergic neuron degeneration, and reduced lifespan. A MuMagnetic GA4 benchtop shielding apparatus (Magnetic Shields Limited, UK), was used to generate a uniform internal field of 5 nT, to effectively remove Earth's geomagnetic field (GMF; 25-60 μT). Wild-type W118 (WT) and Pink1B9/Y (Pink1⁻) D. melanogaster were exposed to HMF and assessed for survival, locomotor performance, mitochondrial respirometry and reactive oxygen species production. HMF exposure increased lifespan in Pink1⁻ D. melanogaster by 20%, with a paradoxical reduction in climbing ability. WT D. melanogaster had decreased lifespan and improved locomotor performance under HMF. Nitrogen-vacancy (NV) centre quantum diamond sensors, were used to detect elevated superoxide levels following HMF exposure. High-resolution respirometry showed increased mitochondrial complex II activity under HMF conditions. We demonstrate that hypomagnetic fields modulate mitochondrial physiology and reactive oxygen species production in D. melanogaster. This highlights the potential of HMF exposure as a novel, non-invasive approach for modulating mitochondrial dysfunction in neurodegenerative disease.

Energy metabolism matches adenosine triphosphate (ATP) resynthesis to hydrolysis even during abrupt transitions such as exercise onset. In 1984, Alois Mader proposed a mechanistic model that captures this regulation through 33 coupled differential equations linking oxidative phosphorylation, glycolysis, and the phosphocreatine shuttle via adenosine diphosphate (ADP), phosphate, and pH feedback. Despite its potential, broader adoption has been limited by closed-source implementations and key publications available only in German. Here, we present MetaboliSim, an open-source software tool that simulates muscle energy metabolism in a virtual human parameterized by four physiological inputs: V̇O2max (oxidative capacity), vLamax (glycolytic capacity), body mass, and active muscle mass. Using MetaboliSim, we test Mader's equations against 10 experimentally established phenomena of exercise metabolism, including ATP homeostasis under fatigue, transient pH alkalinization, glycogen-dependent lactate thresholds, intensity-dependent fat oxidation, the V̇O2 slow component, and work-rate-dependent exhaustion, without altering any equation or constant within the model. Mader's model qualitatively reproduces all 10 phenomena, generating similarly shaped response curves; absolute values depend on individual parameterization rather than being universally matched. The characteristic inverted-U of fat oxidation and the exercise intensity-dependent V̇O2 kinetics, for example, both emerge from the same equation system. A Sobol sensitivity analysis (S01) reveals a calibration hierarchy: V̇O2max and body mass drive power predictions; vLamax and buffer capacity drive metabolite predictions. That a compact, 40-year-old equation system accounts for this breadth of metabolic phenomena suggests that a small number of regulatory feedback loops may suffice to explain a wide range of metabolic responses to exercise. MetaboliSim is freely available to enable independent testing, empirical calibration, and refinement.

Since the enactment of the Affordable Care Act (ACA) in 2010, the Centers for Medicare & Medicaid Services (CMS) have embraced value-based care as the organizing principle of national payment reforms. Yet, after more than a decade, the value-based movement has, at best, generated modest returns and at worst increased costs on patients and negatively impacted access. Pursuant to its authority under the ACA, CMS proposed the Ambulatory Specialty Model (ASM) in the CY 2026 Physician Fee Schedule rulemaking and subsequently finalized the model, establishing the agency's first mandatory alternative payment model focused on ambulatory specialty care. ASM targets 2 high-cost, high-prevalence chronic conditions, heart failure, and low back pain (LBP) and will require eligible physicians in selected geographic regions to accept 2-sided financial risk beginning with performance year 1 in January 2027.This article summarizes the design of ASM, details how physicians are selected into the model and how payment adjustments are calculated (including how procedure mix and site of service, office versus ambulatory surgery center or hospital outpatient, affect episode-based cost scoring), enumerates the required quality measures and patient-reported outcome measures (PROMs), describes the Collaborative Care Arrangement requirements, compares ASM against traditional Merit-based Incentive Payment System (MIPS) and Advanced Alternative Payment Models (APM) such as Accountable Care Organizations (ACOs), weighs whether ASM functions as a carrot-and-stick or aversion-based policy and whether it represents innovation or limitation, and addresses whether performance is compared across specialty types (e.g., neurosurgery versus pain medicine). It then examines specific implications for interventional pain management (IPM) practices, situates IPM within the broader multispecialty landscape of LBP care, and closes with a practical action list and CMS reference links for IPM groups preparing for mandatory participation.

BackgroundThe rapid integration of Artificial Intelligence (AI) into healthcare and industry is often framed as a threat to human roles. Within rehabilitation and occupational health, this polarized discourse risks obscuring more nuanced possibilities for human-AI collaboration.ObjectiveThis article challenges the dominant automation narrative by arguing that AI is instead catalyzing a symbiotic shift within rehabilitation and return-to-work contexts. It aims to conceptualize how AI can augment human expertise to create more personalized, efficient, and equitable outcomes across the rehabilitation-to-work continuum.MethodsA structured literature exploration was conducted across PubMed/MEDLINE, IEEE Xplore, ACM Digital Library, PsycINFO, and Scopus. An initial search covered literature published between 2018 and March 2024, followed by an updated search conducted on 3 April 2026, which identified five additional relevant publications.ResultsThe analysis reveals three interconnected domains of AI application. First, in clinical rehabilitation, AI enables data-driven precision through personalized therapeutic programs, computer vision for objective movement analysis, and predictive analytics for prognostic forecasting. Second, AI facilitates safer and more sustainable return-to-work transitions through objective functional capacity evaluations and AI-assisted job coaching, as illustrated in a hypothetical scenario. Third, AI fosters inclusive workplace integration through intelligent accommodations and skills redeployment, supporting sustained employment for individuals with disabilities or chronic conditions. The review also identifies critical ethical imperatives, including data privacy, algorithmic bias, and equitable access, that must guide this integration to prevent the exacerbation of existing disparities.ConclusionWhen implemented ethically and collaboratively, AI does not replace human judgment but liberates rehabilitation professionals and workplace managers to focus on higher-order tasks of empathy, strategy, and complex decision-making. The future of work, therefore, lies not in automation alone, but in a human-AI partnership that builds a more adaptive, inclusive, and ultimately more humane environment. In this emerging paradigm, individuals are not simply returned to work but are empowered to thrive.

Based on the centuries-old ideology, caste is the core, structural organizing principle for Indians and Indian Americans, emphasizing graded hierarchical oppression. In the United States, caste functions at the intersection of race, immigration, gender, class, and religion, profoundly affecting the lived experiences of caste-oppressed people. This article theorizes caste critical race theory (CasteCRIT), grounded in Dalit feminist epistemology, and stands as an anticasteist, anti-racist, and anticolonial psychological theory. CasteCRIT builds on critical race theory as its necessary foundation, employing Caste × Race as the explanatory construct and drawing from the experiences of caste-oppressed individuals in the United States. This framework has four core tenets: (a) caste is a socioreligious construction based on graded hierarchical oppression; (b) caste is normal, pervasive, and deeply embedded versus rare or incidental; (c) caste dominant groups directly benefitted from the Civil Rights Movement; and (d) caste-oppressed people's testimonies are necessary counternarratives. The psychological applications of CasteCRIT are examined in relation to education, training, research, practice, and advocacy. (PsycInfo Database Record (c) 2026 APA, all rights reserved).

For most with Parkinson disease, a movement disorder, voice and speech are impaired at some point, which presents an opportunity to use digital recordings and sophisticated machine learning to assist objective clinical characterization of the condition. However, as highlighted by Shukla et al in their August 20, 2026 paper, ad-hoc observational datasets typically contain spurious causal associations that escape a purely statistical analysis. This commentary argues that causal inference, and ultimately, diagnostic clinical trials, are required to establish a direct mechanistic relationship between disease and algorithm predictions.

Nuclear medicine neuroimaging is becoming increasingly important for the diagnosis and differential diagnosis of Parkinson's disease, atypical parkinsonian syndromes and more rare neurological (movement) disorders. We report on a 46-year-old woman presented with frequent falls, a gradually progressive bipyramidal syndrome with gait ataxia, dysphagia, urinary urgency and -incontinence, low mood with disturbed emotional regulation and a mild asymmetric hypokinetic rigid syndrome. Additionally, she had a blurry vision, asymmetrical ptosis and abnormal vertical saccades. [18F]FDG PET/CT of the brain showed unspecific pattern of regional cortical hypometabolism and, more pronounced, striatal hypometabolism. [123I]FP-CIT SPECT showed a complete absence of on-target binding. Subsequent genetic testing revealed two variants in SPG7. The patient showed a modest favourable response on levodopa. This case illustrates profound neurodegeneration of the presynaptic dopaminergic nigrostriatal neurons in SPG7.

Perceiving social threats, especially expressions of anger, increases the speed of both action selection and execution. However, it remains unclear how individuals balance speed with achieving desirable outcomes, such as threat avoidance, under these conditions. To investigate this trade-off between decision speed and accuracy, we examined the kinematics of finger-reaching movements using a "go-before-you-know" paradigm. Participants chose between two empty outer chairs in a waiting room. Two central chairs were occupied by either two individuals with neutral expressions or one neutral individual and one threatening individual. The threatening individual expressed anger or fear at one of four intensity levels. The results showed that social threats generally invigorated action decision, as high-threat trials elicited faster movements, which correlated with more direct trajectories compared to neutral trials. However, when participants chose to avoid angry individuals, the most frequent response, movements followed more central trajectories, compared to when they approached angry individuals. These findings suggest that while social threats generally invigorate action selection and execution, it is possible that the accumulation of evidence for the decision can be temporarily prolonged to enhance the likelihood of a favorable outcome, such as threat avoidance. We discuss alternative interpretations and propose the integration of these results with recent models of action decisions under perceived urgency to advance the understanding of threat-related decision-making.