Exercise can powerfully influence the brain, but what if the same biological signals could be activated without physical movement?
Category: health
Exercise, nutrition, physical agent therapy in older adults with sarcopenic obesity: a systematic review and network meta-analysis
Sarcopenic obesity (SO) is characterized by the co-existence of excess adiposity and low muscle performance, with a high prevalence and poor prognosis in the geriatric population.
This systematic review and network meta-analysis (NMA) aims to assess the most effective non-pharmacological interventions for SO patients, including nutrition, exercise, and physical agent therapy.
A systematic search of six electronic databases was conducted from their inception until July 5, 2025, for randomized controlled trials. The NMA utilized a random-effects model, pooled mean difference (MD) and standardized mean difference (SMD), with 95% credible intervals (CrI), accounting for correlations within multi-arm trials. Subgroup analyses and sensitivity analyses were also performed.
Developmental reprogramming in melanocortin neurons modulates diet-induced obesity in mice
Reprogramming in melanocortin modulates diet-induced obesity.
Hypothalamic proopiomelanocortin (POMC) neurons promote satiety, while agouti-related peptide (AgRP) neurons drive hunger and maintain energy balance.
However, it is not clear how the system is diversified developmentally.
The researchers in this study show that transcription factor Otp act as a developmental ‘‘switch’’ in the hypothalamus and determines whether immature neurons become appetite suppressing (POMC) or appetite stimulating (AgRP).
Disrupting this switch reshapes feeding behavior and protects mice from obesity, revealing how early life programming shapes lifelong metabolic health. sciencenewshighlights ScienceMission https://sciencemission.com/melanocortin-neurons-modulates-diet-induced-obesity
Xu et al. show that a developmental “switch” in the hypothalamus determines whether immature neurons become appetite suppressing or appetite stimulating. Disrupting this switch reshapes feeding behavior and protects mice from obesity, revealing how early-life programming shapes lifelong metabolic health.
Patient Safety Begins With Access: Safety Events That Occur Before Meeting the Patient
💬 Viewpoint by Victor Hassid, MD, MBA, and Haytham Kaafarani, MD, MPH: Administrative delays and access failures introduce patient safety risks but are rarely treated as safety events in health systems.
More than 2 decades after To Err Is Human,1 health care has made substantial progress in defining, measuring, and mitigating clinical harm—by adopting high-reliability principles, implementing safety reporting systems, standardizing protocols, and embedding accountability instead of blame into clinical workflows. Yet access to care—despite being the gateway to all downstream clinical activity—remains largely outside this safety framework.
Delays in access are often discussed as throughput problems, capacity constraints, or scheduling inefficiencies. Rarely are they framed as patient safety issues. This distinction is consequential. When access failures are viewed as operational challenges, they are addressed as desk tasks—episodically and locally. When they are viewed as safety failures, they require immediate systematic analysis, leadership attention, and organizational accountability.
High-reliability organization principles provide a useful lens for reframing patient access to care as safety, even when accountability spans multiple stakeholders rather than a single organization.2 The preoccupation of high-reliability organization with failure requires attention to near misses, not just catastrophic outcomes. Reluctance to simplify acknowledges that access pathways are complex sociotechnical systems, not simplistic linear workflows. Sensitivity to operations requires understanding how delays in record retrieval, insurance authorization, or appointment scheduling propagate through the system and translate into patient harm. Deference to expertise elevates the voices of frontline access staff who understand when and where systems break down. Commitment to resilience requires learning from access failures and rapidly redesigning processes to prevent recurrence.
Brain-inspired device could lead to faster, more energy-efficient AI hardware
A team led by engineers at the University of California San Diego has developed a new brain-inspired hardware platform that could help computer hardware keep pace with the explosive growth of artificial intelligence. By combining memory and computation on the same chip—and allowing its components to interact collectively like neurons in the brain—the brain-inspired platform improved the speed, accuracy, and energy efficiency of pattern recognition in two simulated tasks: recognizing spoken digits and detecting epileptic seizures early from brain-wave recordings.
The approach could lead to the development of compact, energy-efficient hardware for smaller AI systems such as those used in wearable health monitors, smart sensors, and other autonomous devices.
The work, published on March 9 in Nature Nanotechnology, falls within the field of neuromorphic computing, which aims to build machines that mimic how the brain processes information. The researchers emphasize that the technology is brain-inspired, rather than brain-like; it draws ideas from how neural networks interact but does not attempt to replicate the brain itself.
DNA origami vaccine rivals mRNA shots while being easier to store and manufacture
The COVID-19 pandemic brought messenger RNA (mRNA) vaccines to the forefront of global health care. After their clinical trial stages, the first COVID-19 mRNA vaccine was administered on 8 December 2020 and mathematical models suggest that mRNA vaccines prevented at least 14.4 million deaths from COVID-19 in the first year alone.
Their extraordinary effectiveness in having softened the blow of the disease has led to the development of mRNA vaccines to also combat other infectious pathogens.
Clinical trials for influenza virus, Respiratory Syncytial Virus (RSV), HIV, Zika, Epstein-Barr virus, and tuberculosis bacteria are all on the way. Importantly, however, COVID-19 research has revealed shortcomings of mRNA vaccines that highlight the need for different approaches.
Should we target the mitochondria in systemic lupus erythematosus (SLE)?
In this Research Article, Denis Comte & team link defective mitochondrial recycling to impaired natural killer cell function in SLE and identify potential treatments to restore immune balance:
The image shows transmission electron microscopy of an NK cell from a patient with lupus showing mitochondrial structural alterations (false-colored red). Inset: healthy NK cell with preserved mitochondrial ultrastructure.
1Department of Medicine, Division of Immunology and Allergy, Lausanne University Hospital, University of Lausanne, Lausanne, Switzerland.
2Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
3Department of Immunobiology, University of Lausanne, Epalinges, Switzerland.
The Zero-Day Scramble is Avoidable: A Guide to Attack Surface Reduction
It also means carving out space for this work in how you prioritize. If strategic efforts like attack surface reduction are always competing against urgent patching, they will always lose. That might mean setting aside time each quarter to review and reduce exposure, or assigning clear ownership so someone is accountable for it — not just when a crisis hits, but routinely.
3. Continuous monitoring
Attack surface reduction isn’t a one-time exercise. Exposure changes constantly — a firewall rule gets edited, a new service gets deployed, a subdomain gets forgotten — and your team needs to detect those changes quickly.
How AI is integrated into clinical workflow lowers medical liability perception
Artificial intelligence (AI) is changing the field and practice of medicine, including legal liability and the perception of who is at fault when a patient experiences harm. “AI holds promise to improve the quality and safety of health care and to reduce errors and patient harm, but the risk of legal liability is a potential barrier for investment and development of this technology as well as the quality of care,” said Michael Bruno, professor of radiology and of medicine at Penn State College of Medicine.
Now, Bruno, working alongside a team of researchers from Brown University and Seton Hall University School of Law, found that the understanding of physician liability is influenced by the way in which AI is integrated into a clinician’s workflow. The study was published in the journal Nature Health.
The researchers presented mock jurors with a hypothetical malpractice case where a patient suffered irreversible brain damage because a radiologist didn’t detect a brain bleed from a computerized tomography (CT) scan, even though AI correctly identified the scan as abnormal.
The macroecology of immunity: predominant influence of climate on invertebrate immune response
https://vist.ly/4u8bp Macroecology Odonates Parasites
The immune system is the primary defense against parasites. With the ever-increasing rate of disease, epidemiologic models considering geographic variation in immune responses could prove useful. Despite increasing interest in the macroecology of parasitism and infectious diseases, we know little about the macroecology of immune responses (i.e. macroimmunology). Host characteristics, parasite exposure, and environmental factors can all affect immunity, but how these factors shape spatial variation in the strength of immune responses remains underexplored. We captured odonates (dragonflies and damselflies) and their conspicuous ectoparasitic mites from 42 sites spread across a geographic area spanning the temperate and boreal forest biomes in eastern Canada. We then conducted immune response bioassays on 1237 individuals from 63 odonate species. We used generalized additive models and structural equation models to relate immune responses to host body size, parasite load, pH, temperature and precipitation while accounting for spatial autocorrelation in immune ability and evolutionary relationships among host species. We found significant differences in the strength of immune response among host individuals, and this variation was best explained by climatic conditions, specifically strongly decreasing with precipitation. While host species significantly differed in immune response strength, we found no effect of host body size, evolutionary relationships among hosts, or parasitism on immune response. Our study investigating the drivers of immune response across dozens of species spread across two biomes is the most comprehensive to date. Climatic conditions have a strong influence on host immune response, regardless of host characteristics or parasitism rates. Strong immune responses were associated with low levels of annual precipitation, which could relate to the role of cuticular melanin content in desiccation resistance, and the melanin-based encapsulation response being a byproduct of this adaptation. A spatially explicit understanding of the biological processes affecting immunity could improve epidemiological models of disease risk that inform disease management globally.
Predicting parasite and pathogen spread is increasingly relevant and challenging in a highly connected world (Tsiotas and Tselios 2022), and an animal’s immune system is the first line of defense against attack by parasites and pathogens. Yet, the factors driving variation in immunity among individuals, populations, and species are poorly studied and rarely factored into epidemiologic models (Becker et al. 2019). Characteristics of the host, exposure to parasites or pathogens, and the abiotic environment can interact in complex ways to affect immunity (Sweeny and Albery 2022), but their interactions are challenging to elucidate (Johnson et al. 2019).
As the immune system is the primary line of defense against infection by parasites, pathogens, and disease, it is assumed to be costly in terms of fitness and should therefore lead to tradeoffs with life-history traits (e.g. fecundity, fertility, Albery et al. 2021). Although a plethora of studies have provided key evidence of immune variation due to such tradeoffs, most studies emphasize the role of biotic factors such as predation (Duong and McCauley 2016) and resource availability (Hasik et al. 2025a) without considering that of abiotic factors (Lazzaro and Little 2008). A relationship between immune response and temperature is expected in both invertebrate ectotherms (Mastore et al. 2019) and vertebrate endotherms (Butler et al. 2013), due to the thermal sensitivity of the enzymes involved in immune responses (Catalán et al. 2012). When one scales this temperature-dependent immunity to explore the effect of climate (specifically, temperature and humidity), then climate is expected to be a clear driver of geographic variation in immunity (Li et al. 2024).
Parasites are a leading cause of disease and death around the world and thus are drivers of life-history evolution via their effects on host fitness (Hasik and Siepielski 2022a) that have the potential to affect host macroevolutionary dynamics (Hasik et al. 2025b). The majority of organisms on earth are infected by at least one parasite (Price 1980), and yet, we have a very limited understanding of the multifarious factors governing the intensity of infection and, therefore, the health cost. Immune responses are necessary to defend organisms from the deleterious and fitness-reducing effects of parasites (and disease in general, Hasik and Siepielski 2022a). Although there is increasing interest in the macroecology of parasites and infectious diseases (Stephens et al. 2016), we know very little about macroimmunology (Becker et al. 2020). Both among-individual and interspecific variation in immune response surely plays a central role, but the factors regulating immunity in natural settings are poorly understood, which can interfere with the accuracy of predictive epidemiologic models. Environmental factors and local parasite pressure can independently drive differences in immunity across space, but they could also act in concert (Becker et al. 2020). Parasitism varies among host populations distributed across large-scale environmental gradients (LoScerbo et al. 2020, Hasik and Siepielski 2022b) and at fine spatial scales, within populations (Albery et al. 2019, Hasik et al. 2025a). To date, however, the focus on a limited set of taxa, specifically vertebrates (Becker et al. 2020), limits our ability to identify generalities regarding the relative influence of environmental conditions and parasitism on immune defenses that would apply across host–parasite systems (Rolff and Siva-Jothy 2003).