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Ketogenic diets (KDs) are gaining attention as a potential adjuvant therapy for cancer, but data are limited for KDs’ effects on quality of life. We hypothesized that the KD would (1) improve mental and physical function, including energy levels, (2) reduce hunger, and (3) diminish sweet and starchy food cravings in women with ovarian or endometrial cancer. Participants were randomized to a KD (70:25:5 energy from fat, protein, and carbohydrate) or the American Cancer Society diet (ACS: high-fiber, lower-fat). Questionnaires were administered at baseline and after 12 weeks on the assigned diet to assess changes in mental and physical health, perceived energy, appetite, and food cravings. We assessed both between-group differences and within-group changes using ANCOVA and paired t-tests, respectively. After 12 weeks, there was a significant between-group difference in adjusted physical function scores (p < 0.05), and KD participants not receiving chemotherapy reported a significant within-group reduction in fatigue (p < 0.05). There were no significant between-group differences in mental function, hunger, or appetite. There was a significant between-group difference in adjusted cravings for starchy foods and fast food fats at 12 weeks (p < 0.05 for both), with the KD group demonstrating less frequent cravings than the ACS. In conclusion, in women with ovarian or endometrial cancer, a KD does not negatively affect quality of life and in fact may improve physical function, increase energy, and diminish specific food cravings. This trial was registered at ClinicalTrials.gov as NCT03171506.

Physiological cardiac hypertrophy is a compensatory remodeling of the heart in response to stimuli such as exercise training or pregnancy that is reversible and well-tolerated. We previously described how the activating transcription factor 6 (ATF6) proteins, ATF6α and ATF6β, were required for pathological hypertrophy in response to hemodynamic stress. Here, we examine the functional roles of both ATF6 proteins in the context of exercise-induced physiological hypertrophy. After 20 days of swim training, we found differential roles: whole body gene-deleted mice lacking ATF6α had an attenuated hypertrophic response compared to wild-type mice but those lacking ATF6β did not. Additionally, mice lacking ATF6α displayed ventricular dilation and reduced fractional shortening after swimming. While we observed no differences in the expression of downstream UPR signaling between the exercise groups, mice lacking ATF6α showed enhanced phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2). Thus, in response to swim training, loss of ATF6β did not hinder the development of physiological hypertrophy, but loss of ATF6α resulted in significantly reduced cardiac fractional shortening.

Performance in many racing sports depends on the ability of the athletes to produce and maintain the highest possible work i.e., the highest power for the duration of the race. To model this energy production in an individualized way, an adaptation and a reinterpretation (including a physiological meaning of parameters) of the three-component Margaria–Morton model were performed. The model is applied to the muscles involved in a given task. The introduction of physiological meanings was possible thanks to the measurement of physiological characteristics for a given athlete. A method for creating a digital twin was therefore proposed and applied for national-level cyclists. The twins thus created were validated by comparison with field performance, experimental observations, and literature data. Simulations of record times and 3-minute all-out tests were consistent with experimental data. Considering the literature, the model provided good estimates of the time course of muscle metabolite concentrations (e.g., lactate and phosphocreatine). It also simulated the behavior of oxygen kinetics at exercise onset and during recovery. This methodology has a wide range of applications, including prediction and optimization of the performance of individually modeled athletes.

Type 2 diabetes mellitus (T2DM) is highly prevalent in the United States and represents a significant public health challenge. Telehealth interventions have shown promise for improving T2DM outcomes, but their effectiveness is often limited by disparities in digital literacy and access, especially in rural areas. To address this gap, we propose an innovative, individualized lifestyle modification intervention delivered via phone call to support glycemic control. This paper outlines the protocol for a pilot study designed to assess the feasibility and preliminary effectiveness of an artificial intelligence-assisted intervention for T2DM self-management in rural settings. The study uses the preparation phase of the MOST (Multiphase Optimization Strategy) framework to evaluate two components: (1) automated versus human health coaching and (2) fixed versus adapted gamified financial incentives, based on participants' daily engagement with automated monitoring calls. We aim to enroll 88 adults with T2DM and hemoglobin A (HbA ) levels between 6.5% and 11.5%. Participants receive daily interactive voice response calls tracking diet, physical activity, medication adherence, and blood glucose, and weekly coaching based on randomization. In the fixed-reward arm, participants earn US $0.60 per day; in the adaptive arm, rewards start at US $0.20 and increase weekly, with penalties for missed days. Primary outcomes include feasibility metrics and preliminary changes in HbA . Semistructured interviews will assess patient experience. This study was funded by the National Institute of Diabetes and Digestive and Kidney Diseases. As of October 2025, we have enrolled and completed data collection for 88 participants. We expect to complete the feasibility analysis by December 2025. This pilot and feasibility study evaluates a low-tech, artificial intelligence-assisted T2DM intervention designed to reduce digital barriers and inform a future MOST optimization trial. ClinicalTrials.gov NCT05344859; https://clinicaltrials.gov/study/NCT05344859. DERR1-10.2196/70271.

Background Intervention packages targeting obesity-related conditions often include multiple behavioral and pharmacological components, yet the independent and synergistic effects of these strategies on disease progression remain largely unexplored. Adaptive interventions offer a structured approach to tailoring treatments based on individual responses, but feasibility data in primary care settings are limited. The objective of this pilot Sequential Multiple Assignment Randomized Trial (SMART) was to investigate the feasibility of a 25-week adaptive biobehavioral intervention designed to improve insulin sensitivity among patients with stage 1 obesity. Methods Forty participants were initially randomized to either nutrition counseling (NC) or exercise counseling (EC), both employing a weight-neutral approach. At week 8, insulin sensitivity was reassessed using the Quantitative Insulin Sensitivity Check Index (QUICKI). Participants with a > 5% improvement were classified as responders, while non-responders were re-randomized to either augment their first-stage intervention with metformin or switch to weight loss counseling (WLC). Feasibility outcomes included recruitment and retention, adherence to intervention components, and preliminary treatment effect estimates. Results Findings support the overall feasibility of the SMART design, with high adherence to virtual counseling sessions and favorable participant retention. The study effectively differentiated responders from non-responders at week 8, with responders showing greater improvements in insulin sensitivity. Among non-responders, WLC and metformin provided a potential rescue effect, but overall insulin sensitivity remained lower than at of responders. While NC and WLC were preferred over EC and metformin, adherence to counseling sessions remained high across all interventions, regardless of preference. Metformin adherence posed challenges due to frequent gastrointestinal side effects and difficulties tracking usage. Conclusions This pilot study supports the feasibility of an adaptive biobehavioral intervention for improving insulin sensitivity among adults with obesity in a primary care setting. However, further refinement is needed to enhance clinical integration, optimize intervention messaging, and improve medication tracking. Findings from this study will inform a second pilot SMART, laying the foundation for a full-scale primary-care embedded intervention delivering personalized, adaptive strategies for improving cardiometabolic health. Trial registration NCT04392283 on April 19th, 2020.

In track cycling, performance in the team pursuit depends on the mechanical and physiological abilities of each member of the team, but also on the choice of racing strategy. Athletes must cover the 4000 m of the race, sharing the effort between them in successive relays. This raises the question of the optimum strategy. We propose a method for resolving this question by coupling a mechanical model of the race to physiological models (digital twins) of the athletes. The mechanical model enables one to predict a theoretical finishing time for a given strategy, while the physiological model enables one to determine whether or not a given strategy is feasible. By coupling the two models and using numerical optimization, an optimal strategy for a given team can then be predicted. Simplified team composition case studies are explored. For each case studied, an optimal strategy to maximize performance is obtained and composed of a set of three variables: relay lengths, power values for each relay, and the starting order of cyclists. The proposed method can be used for real athletes and extended to other disciplines.

Physiological cardiac hypertrophy is a compensatory remodeling of the heart in response to stimuli such as exercise training or pregnancy that is reversible and well-tolerated. We previously described how the activating transcription factor 6 (ATF6) proteins, ATF6[alpha] and ATF6[beta], were required for pathological hypertrophy in response to hemodynamic stress. Here, we examine the functional roles of both ATF6 proteins in the context of exercise-induced physiological hypertrophy. After 20 days of swim training, we found differential roles: whole body gene-deleted mice lacking ATF6[alpha] had an attenuated hypertrophic response compared to wild-type mice but those lacking ATF6[beta] did not. Additionally, mice lacking ATF6[alpha] displayed ventricular dilation and reduced fractional shortening after swimming. While we observed no differences in the expression of downstream UPR signaling between the exercise groups, mice lacking ATF6[alpha] showed enhanced phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2). Thus, in response to swim training, loss of ATF6[beta] did not hinder the development of physiological hypertrophy, but loss of ATF6[alpha] resulted in significantly reduced cardiac fractional shortening.

Enhancing endogenous cannabinoid (eCB) signaling has been considered as a potential strategy for the treatment of stress-related conditions. Fatty acid amide hydrolase (FAAH) represents the primary degradation enzyme of the eCB anandamide (AEA), oleoylethanolamide (OEA) and palmitoylethanolamide (PEA). This study describes a potent reversible FAAH inhibitor, SSR411298. The drug acts as a selective inhibitor of FAAH, which potently increases hippocampal levels of AEA, OEA and PEA in mice. Despite elevating eCB levels, SSR411298 did not mimic the interoceptive state or produce the behavioral side-effects (memory deficit and motor impairment) evoked by direct-acting cannabinoids. When SSR411298 was tested in models of anxiety, it only exerted clear anxiolytic-like effects under highly aversive conditions following exposure to a traumatic event, such as in the mouse defense test battery and social defeat procedure. Results from experiments in models of depression showed that SSR411298 produced robust antidepressant-like activity in the rat forced-swimming test and in the mouse chronic mild stress model, restoring notably the development of inadequate coping responses to chronic stress. This preclinical profile positions SSR411298 as a promising drug candidate to treat diseases such as post-traumatic stress disorder, which involves the development of maladaptive behaviors.