A computer model predicts different mechanisms of blood pressure regulation and effective hypertensive therapy for males and females, thereby serving as a foundational tool for improved treatment precision.

Genetic and molecular analyses show that FOXC1 and FOXC2 play a role in controlling lymphatic valve maintenance as key mediators of mechanotransduction to control cytoskeletal organization and RhoA/ROCK signaling.

Shigella flexneri, globally the most frequent cause of bacterial dysentery, is far more diverse, and has caused disease around the world for far longer than other Shigella species by persisting in local environments over extended timescales.

Arterial myocyte PKD2 channels are activated by vasoconstrictor stimuli, which increases blood pressure, are upregulated during hypertension and cell-specific knockout in vivo reduces both physiological blood pressure and hypertension.

The intestinal coelomic epithelium provides dedifferentiated precursor cell populations that drive the adult holothurian intestinal regeneration.

Genetic mouse models identify a critical mechanism of myogenic vasoconstriction and reveal the in vivo function of myogenic autoregulation in protecting from organ overperfusion and in maintaining vascular resistance.

A new pathway is described involving the estrogen receptor alpha in the acute response of small arteries to flow independent of the ligand (estrogen) and of the nuclear signaling.

EphrinB2/EphB4-mediated regulation of cytoskeletal contractility is a key homeostatic mechanism of lymphatic endothelial cell-cell junction maintenance, and provides a potential target for therapeutic modulation of lymphatic vessel permeability and function.

Notch signaling in human platelets functions in noncanonical juxtacrine manner to amplify platelet reactivity and thrombogenicity.