Functional connectivity: studying nonlinear, delayed interactions between BOLD signals.

Correlation analysis has been widely used in the study of functional connectivity based on fMRI data. It assumes that the relevant information about the interactions of brain regions is reflected by a linear relationship between the values of two signals at the same time. However, this hypothesis has not been thoroughly investigated yet.

Endothelium-dependent blunted membrane potential responses to ATP-sensitive K+ channel modulators in aortae from rats with cirrhosis.

Background/aims: In vivo studies have shown that arterial vasodilation induced by synthetic openers of ATP-sensitive K+ (K(ATP)) channels is decreased in rats with cirrhosis. Since vasodilation induced by these substances is mediated by membrane potential hyperpolarization in arterial smooth muscle cells, membrane potential hyperpolarization in response to K(ATP) channel openers may be altered in cirrhotic smooth muscle cells. The aim of the present study was to investigate the effects of K(ATP) channel modulators (i.

In vitro and in vivo vascular responses to the L-type calcium channel activator, Bay K 8644, in rats with cirrhosis.

A substance which increases the entry of extracellular calcium into arterial smooth muscle may decrease cirrhosis-induced vasodilation. The aim of the present study was to measure the effects of the L-type Ca2+ channel activator, Bay K 8644, on the haemodynamics of rats with cirrhosis. Vascular reactivity to this substance was also investigated.

Effects of protein kinase C modulators on Na+/K+ adenosine triphosphatase activity and phosphorylation in aortae from rats with cirrhosis.

Protein kinase C (PKC) modulates the activity and phosphorylation of the catalytic alpha-subunit of sodium-potassium-adenosine triphosphatase (Na+/K+ ATPase) in normal arteries. Because PKC is altered in cirrhotic aortae, Na+/K+ ATPase may also be altered in these arteries. The aim of the present study was to investigate alpha-subunit activity and phosphorylation in aortae from normal and cirrhotic rats, under baseline conditions and during exposure to PKC modulators.