Improving 10-year atherosclerotic cardiovascular disease estimation management using a Smartphrase for automated risk screening.

Background: Cardiovascular disease (CVD) is the most common cause of death in the United States, and 90% of cardiovascular events are preventable. The 2020 American College of Cardiology/American Heart Association Guidelines on the Primary Prevention of Cardiovascular Disease recommends 10-year atherosclerotic cardiovascular disease (ASCVD) risk estimates for 40- to 75-year-old adults with CVD risk indications to decrease the likelihood of cardiovascular events.

Local Problem: At the project site, the 10-year ASCVD risk estimates were rarely completed by providers.

Zic2 mutation causes holoprosencephaly via disruption of NODAL signalling.

The ZIC2 transcription factor is one of the genes most commonly mutated in Holoprosencephaly (HPE) probands. Studies in cultured cell lines and mice have shown a loss of ZIC2 function is the pathogenic mechanism but the molecular details of this ZIC2 requirement remain elusive. HPE arises when signals that direct morphological and fate changes in the developing brain and facial primordia are not sent or received.

Mouse strains for the ubiquitous or conditional overexpression of the Flii gene.

The gelsolin related actin binding protein, Flii, is able to regulate wound healing; mice with decreased Flii expression show improved wound healing whereas mice with elevated Flii expression exhibit impaired wound healing. In both mice and humans Flii expression increases with age and amelioration of FLII activity represents a possible therapeutic strategy for improved wound healing in humans. Despite analysis of Flii function in a variety of organisms we know little of the molecular mechanisms underlying Flii action.

Zic2-associated holoprosencephaly is caused by a transient defect in the organizer region during gastrulation.

The putative transcription factor ZIC2 is associated with a defect of forebrain development, known as Holoprosencephaly (HPE), in humans and mouse, yet the mechanism by which aberrant ZIC2 function causes classical HPE is unexplained. The zinc finger domain of all mammalian Zic genes is highly homologous with that of the Gli genes, which are transcriptional mediators of Shh signalling. Mutations in Shh and many other Hh pathway members cause HPE and it has been proposed that Zic2 acts within the Shh pathway to cause HPE.