Three-dimensional optical coherence tomography for guidance of percutaneous coronary intervention for coronary bifurcation disease: a review of current clinical applications.

Percutaneous coronary intervention (PCI) for coronary bifurcation disease remains one of the most challenging situations in interventional cardiology in terms of procedural success rates and long-term cardiac events. Optical coherence tomography (OCT), with a higher signal-to-noise ratio and the ability to distinguish plaque components, can display the true condition of bifurcation lesions without overlapping or shortening and achieve detailed visualization of vascular structures, which is superior to those of other imaging modalities. Three-dimensional (3D) reconstruction of OCT images (3D-OCT) helps to gain a more informed understanding of the geometry and morphology of bifurcation lesions and provide additive information on plaque distribution.

Assessing fall armyworm () allochronic behavior as a predictor of local strain composition in United States populations.

The fall armyworm, (J.E. Smith), is comprised of two genetically distinct strains that are morphologically identical yet exhibit differences in their behavior and physiology (C-strain and R-strain).

Assessment of fractal ratio of vessel diameters in coronary bifurcation lesions by angiography and intravascular ultrasound.

Physiological coronary branching at the bifurcation has a constant fractal ratio (FR) of the diameter of the mother vessel to the sum of daughter vessels on quantitative coronary angiography (QCA). We sought to investigate the FR of diseased coronary bifurcations using QCA and intravascular ultrasound (IVUS) and its impact on late lumen loss after percutaneous coronary intervention (PCI). In multicentre prospective studies of the J-REVERSE and 3D OCT Bifurcation Registry, 402 and 109 bifurcations treated with stenting that completed QCAs and IVUS examinations, respectively were analysed.

Bernard-Soulier syndrome caused by a novel GP1BB variant and 22q11.2 deletion.

Bernard-Soulier syndrome (BSS) is caused by defects in GP1BA, GP1BB, or GP9 genes. Patients with 22q11.2 deletion syndrome (22q11.