An aorta smooth muscle-on-a-chip model indicated that NOTCH1 insufficiency in HAoSMCs induced phenotypic switching from a contractile to a synthetic phenotype accompanied by an impairment of mitochondrial fusion, implying its potential role as a therapeutic target for BAV-TAA.

Point mutations in a ubiquitous human ATPase called p97/VCP deregulate inter-domain communication, resulting in impaired binding of an adaptor that recruits p97 to endosomal pathways and leading to a degenerative disease of bone, muscle and neurons.

Novel disease pathways underlie disease pathogenesis in Kelch-related nemaline myopathy through proteomic remodeling.

Wild-type human recombinant tau protein infused in presynaptic terminals newly assembled microtubules, which sequestered cytosolic dynamins, thereby blocking synaptic vesicle endocytosis and causing activity-dependent rundown of excitatory synaptic transmission in a slice model of mouse brainstem.

Integrated single-cell and spatial genomics provides the first molecular map of the human oral mucosa and reveals a novel pro-inflammatory fibroblast involved in disease progression.

Bulk whole genome sequencing data can be used to study the genetic variation present in pathogenic bacterial populations over the time-course of a single infection within a host.

COVID-19 severity, rather than sex or age, predicts SARS-CoV-2 kinetics, and SARS-CoV-2 viral load from lower respiratory tract specimens may predict severe disease days before clinical deterioration for COVID-19 patients.

Integrating over multiple forms of statistical uncertainty associated with serological surveys can improve serosurvey design while also enabling that uncertainty to be appropriately propagated through epidemiological models.

While predators can clearly reduce mosquito populations by consumption, they can also have non-consumptive effects on mosquito body size and oviposition behavior, and these effects on vector traits can influence infectious disease dynamics.

The factors which drive and control disease progression can be inferred from mathematical models that integrate measures of immune responses, data from tissue sampling and markers of infection dynamics.