Thinking on your feet: potentially enhancing phylogenetic tree learning accessibility through a kinaesthetic approach.

Background: Phylogenetics is one of the main methodologies to understand cross-cutting principles of evolution, such as common ancestry and speciation. Phylogenetic trees, however, are reportedly challenging to teach and learn. Furthermore, phylogenetics teaching methods traditionally rely solely on visual information, creating inaccessibility for people with visual impairment.

Towards Human Sensory Augmentation: A Cognitive Neuroscience Framework for Evaluating Integration of New Signals within Perception, Brain Representations, and Subjective Experience.

New wearable devices and technologies provide unprecedented scope to augment or substitute human perceptual abilities. However, the flexibility to reorganize brain processing to use novel sensory signals during early sensitive periods in infancy is much less evident at later ages, making integration of new signals into adults' perception a significant challenge. We believe that an approach informed by cognitive neuroscience is crucial for maximizing the true potential of new sensory technologies.

Oxytocin induces the formation of distinctive cortical representations and cognitions biased toward familiar mice.

Social recognition is essential for the formation of social structures. Many times, recognition comes with lesser exploration of familiar animals. This lesser exploration has led to the assumption that recognition may be a habituation memory.

DNMT3A clonal hematopoiesis-driver mutations induce cardiac fibrosis by paracrine activation of fibroblasts.

Hematopoietic mutations in epigenetic regulators like DNA methyltransferase 3 alpha (DNMT3A), play a pivotal role in driving clonal hematopoiesis of indeterminate potential (CHIP), and are associated with unfavorable outcomes in patients suffering from heart failure (HF). However, the precise interactions between CHIP-mutated cells and other cardiac cell types remain unknown. Here, we identify fibroblasts as potential partners in interactions with CHIP-mutated monocytes.