Researchers at Touro University Nevada have discovered that tiny particles in the blood, called extracellular vesicles (EVs), are a major player in how a group of hormones are shuttled through the body. Physical exercise can stimulate this process.
The findings, published in the journal Proceedings of the National Academy of Sciences, open the door to deeper understanding of hormone circulation and access to the brain, how exercise may trigger changes in energy balance, mental health, and immune function, and circulation of certain drugs.
Blood and other body fluids are teeming with EVs—tiny particles that exist outside of cells. EVs transmit signals from cell-to-cell within tissues and a long distance across organ systems by delivering biological cargo such as proteins, lipids, and nucleic acids into cells. They also remove cell waste.
The leading cause of death due to injuries in war is excessive bleeding. A KAIST research team, in which an Army Major participated, has tackled this issue head-on. By developing a next-generation powder-type hemostatic agent that stops bleeding just by spraying it, they have presented an innovative technology that will change the paradigm of combatant survivability.
A joint research team led by Professor Steve Park from the Department of Materials Science and Engineering and Professor Sangyong Jon from the Department of Biological Sciences has developed a powder-type hemostatic agent that forms a powerful hydrogel barrier within approximately one second when sprayed on a wound.
The research was published in Advanced Functional Materials.
Encapsulated microbubbles (EMBs), tiny gas-filled bubbles coated in lipid or protein shells, play a central role in biomedical ultrasound. When exposed to ultrasound waves, EMBs contract, resulting in oscillations that enhance image contrast or deliver drugs directly by creating pores in cell membranes via sonoporation. However, while promising for biomedical applications, their behavior is far more complex.
Most existing theories on EMBs assume spherically symmetrical oscillations and only study them in simple Newtonian fluids. However, most biological fluids, such as blood, are viscoelastic (non-Newtonian) fluids. When inside the body, these fluid forces, pressure from vessel walls, and changing ultrasound pulses can influence the behavior of EMBs, affecting both imaging accuracy and treatment safety.
To better understand these effects, a multi-institutional research team has developed a comprehensive computational model that simulates the behavior of EMBs under real biological conditions. The team included Assistant Professor Haruki Furukawa and Professor Shuichi Iwata from Nagoya Institute of Technology (NITech), Japan, in collaboration with Emeritus Professor Tim N. Phillips, Dr. Michael J. Walters, and Reader Steven J. Lind from Cardiff University, Wales.
In a Science Immunology Review from earlier this year, researchers discuss how interactions between the nervous and immune systems could impact neurological disorders and allergy-related behaviors like food avoidance.
The nervous and type 2 immune systems regulate each other via cytokines and neurotransmitters, suggesting previously unidentified therapeutic avenues.
Liu et al. report chromosome-level genomes of 11 species across 10 Polygonaceae genera (including four previously published genomes), which encompass diverse habitats. Integrating genomic and transcriptomic analyses, this study provides insights into the evolutionary adaptation strategies of Polygonaceae to thrive in various habitats.
Vascular aging and genetic risk jointly shape coronary artery disease susceptibility across races and sexes.
BackgroundEstimated pulse wave velocity (ePWV), a noninvasive marker of arterial stiffness, reflects vascular aging and has been associated with increased coronary artery disease (CAD) risk. However, the interplay between ePWV and genetic factors, including polygenic risk score (PRS) and apolipoprotein E genotypes, in determining CAD susceptibility remains unclear.
This review examines some of the monogenic disorders that can masquerade as neuroinflammatory phenotypes.
A recent explosion in genomic testing has led to the identification of several genetic disorders that mimic CNS-specific autoimmune disorders. Such monogenic disorders, although rare, represent a diagnostic challenge because of their diverse phenotypes and overlapping features. Early recognition of these disorders is crucial not only to prevent overtreatment with immunotherapy but also to ensure that targeted treatments are available for many of these disorders. This review explores some of the monogenic disorders that can masquerade as neuroinflammatory phenotypes. These clinical vignettes are stratified according to neuroanatomical localization along the neuroaxis: supratentorial white matter, gray matter, brainstem, and spinal cord involvement.