Independent regulation of Piezo1 activity by principal and intercalated cells of the collecting duct.

The renal collecting duct is continuously exposed to a wide spectrum of fluid flow rates and osmotic gradients. Expression of a mechanoactivated Piezo1 channel is the most prominent in the collecting duct. However, the status and regulation of Piezo1 in functionally distinct principal and intercalated cells (PCs and ICs) of the collecting duct remain to be determined.

TRPV4 functional status in cystic cells regulates cystogenesis in autosomal recessive polycystic kidney disease during variations in dietary potassium.

Mechanosensitive TRPV4 channel plays a dominant role in maintaining [Ca ] homeostasis and flow-sensitive [Ca ] signaling in the renal tubule. Polycystic kidney disease (PKD) manifests as progressive cyst growth due to cAMP-dependent fluid secretion along with deficient mechanosensitivity and impaired TRPV4 activity. Here, we tested how regulation of renal TRPV4 function by dietary K intake modulates the rate of cystogenesis and mechanosensitive [Ca ] signaling in cystic cells of PCK453 rats, a homologous model of human autosomal recessive PKD (ARPKD).

Development of technical skills in simulated cerebral aneurysm coiling.

Endovascular surgical procedures require visual-spatial coordination in workspaces with restricted motions and temporally limited imaging. The development of the skills needed for these procedures can be facilitated by 3D simulator-based training. Cerebral angiography (CA) has lagged behind in this training approach due to the lack of validated, realistic training models, relying strictly on clinical case exposure frequency ("number of hours logged") as a means of assessing proficiency.

of ClC-K2 Cl Channel in the Collecting Duct Intercalated Cells.

The renal collecting duct is known to play a critical role in many physiological processes, including systemic water-electrolyte homeostasis, acid-base balance, and the salt sensitivity of blood pressure. ClC-K2 (ClC-Kb in humans) is a Cl-permeable channel expressed on the basolateral membrane of several segments of the renal tubule, including the collecting duct intercalated cells. ClC-Kb mutations are causative for Bartters' syndrome type 3 manifested as hypotension, urinary salt wasting, and metabolic alkalosis.