109 papers
Physiology explores how living systems function, from the microscopic signals inside a single cell to the complex rhythms of an entire organism. This field seeks to understand the mechanical, physical, and biochemical processes that keep life moving, offering crucial insights into health, disease, and the body's remarkable ability to adapt.
On Gist.Science, we process every new preprint in this category from bioRxiv to make these rapid discoveries accessible to everyone. For each study, we provide both a clear, plain-language explanation and a detailed technical summary, ensuring that whether you are a curious student or a seasoned researcher, you can grasp the latest findings without getting lost in jargon.
The papers listed below represent the newest physiological research recently shared on bioRxiv, ready for you to explore.
The paper introduces iMyocyte, an interactive web-based platform that utilizes a distributed cellular automaton model across student devices to enable real-time visualization and manipulation of cardiac excitation wave dynamics, thereby enhancing the teaching of arrhythmia mechanisms through improved engagement and conceptual clarity.
Macrophages autonomously generate heat in cold environments by increasing mitochondrial proton leak via the ADP/ATP carrier, a process that compromises their antibacterial function by suppressing antimicrobial peptide expression and thereby increasing susceptibility to infection.
By stratifying older adults based on functional status rather than chronological age, this study reveals that low-functioning individuals exhibit distinct, speed-independent gait impairments and instability-driven compensatory patterns, highlighting the value of combining functional assessments with quantitative gait profiling for early mobility decline detection.
This study demonstrates that Prader-Willi syndrome genes are expressed in the mouse placenta, where their reduced expression leads to a significant loss of fetal endothelial cells, suggesting that compromised placental function may contribute to the disorder's post-natal phenotypes.
This study demonstrates that transgenic expression of the senescence-inhibitory isoform Δ133p53α in a Hutchinson-Gilford progeria syndrome mouse model recapitulates its in vitro benefits by reducing cellular senescence and inflammation, preserving tissue integrity, and extending median lifespan, suggesting its potential as a broad therapeutic strategy for delaying aging.
The study demonstrates that the novel drug VC108, which selectively blocks the GPR39 receptor highly expressed in cardiomyocytes, significantly reduces no-reflow and infarct volumes in a rat model of acute myocardial infarction by inducing vasodilation and providing direct cardioprotection when administered before occlusion or prior to reperfusion.
This study demonstrates that local fatigue in either the plantar flexors or knee extensors does not increase the metabolic power of male runners, indicating that submaximal running energetics can be maintained despite significant local muscle fatigue through distinct neuromuscular activation strategies.
This study utilizes single-molecule FRET to reveal that ER calcium depletion triggers STIM1 activation by destabilizing the CC1 clamp and forcing the CAD to undergo a dramatic "fold-out" rearrangement to escape, a process that precedes the formation of the CC1 coiled-coil necessary for Orai1 channel opening.
This study reveals that myocardial infarction primes peripheral neutrophils to undergo terminal programming into a pro-fibrotic SiglecF+ state within the ischemic heart, a process that drives cardiac fibrosis through direct effects on fibroblasts and the recruitment of other immune cells.