Polymers from dietary fiber can control the aggregation of particulates in the murine small intestine in a manner qualitatively consistent with depletion interactions.

Stress sensors in the membrane of the endoplasmic reticulum respond to the accumulation of unfolded proteins by briefly forming small phosphorylation-competent oligomers and dissolving back into active dimers.

Globotriaosylcermide directly impacts neuronal integrity and ion channel function as potential mechanism underlying small fiber pathology in Fabry disease.

Light and X-ray scattering on the same primate and human brain samples cross-validate each other and enable accurate mapping of axonal trajectories in regions with uni- and multi-directional nerve fibers, which can be used to validate diffusion MRI.

By using structural methods to screen compounds for their ability to interact with amyloid beta, researchers have identified small molecules that stabilize amyloid fibers and reduce the toxic effect of smaller aggregates on cells.

Sensory nerve fiber ending ensheathment and connexin 43 contacts by keratinocytes at the neuro-cutaneous unit can be visualized and quantified at super-resolution in human skin.

Coarse-grained modeling of mammalian kinetochore-fiber shapes generated under microneedle manipulation reveals the need for lateral anchorage 1-3 μm from the kinetochore to robustly preserve their orientation in the spindle center, promoting mechanical integrity in the dynamic spindle.

Chaperones from different families and classes synergistically target different stages of tau aggregation, thus preventing pathological amyloid formation.

Pain behaviors in a Fabry mouse model are associated with the accumulation of a fat molecule that disrupts sodium ion channels in small fiber neurons.

Optogenetic experiments show that bridging microtubules buffer chromosome movements and promote their alignment through forces transferred to the associated kinetochore fibers, which rely on precise regulation of the overlap region.