The results show that Kv3.1b/3.2 expression is differentially controlled by neuronal activity and neurotrophic factors. (C) 2008 IBRO. Published by Elsevier Ltd. All rights reserved.”
“Purpose: This study was conducted to determine the association between the characteristics of calf muscle hemoglobin oxygen saturation (StO(2)) and exercise performance in patients with intermittent claudication.

Methods: The study comprised 39 patients

with peripheral arterial disease limited by intermittent claudication. Patients were characterized GS-9973 mw oil calf muscle StO(2) before, during, and after a graded treadmill test, as well as oil demographic and cardiovascular AZD6738 nmr risk factors, ankle-brachial index (ABI), ischemic window, initial claudication distance (ICD), and absolute claudication distance (ACD).

Results: Calf muscle StO(2) decreased 72%, from 55% +/- 18% (mean +/- SD) saturation

at rest to the minimum value of 17%+/- 19% saturation attained 459 380 seconds after the initiation of exercise. After exercise, recovery half-time of calf muscle StO(2) was attained at 129 98 seconds, whereas full recovery to the resting value was reached it 225 +/- 140 seconds. After adjusting for sex, race, and grouping according to the initial decline constant in calf muscle StO(2) during exercise, the exercise time to minimum calf muscle StO(2) was correlated with the ischemic window (r = -0.493, P = .002), ICD (r = 0.339, P = .043), and ACD cAMP (r = 0.680, P < .001). After treadmill exercise, the

recover), half-time of calf muscle StO(2) was correlated with the ischemic window (r = 0.531, P < .001), ICD (r = -0.598, P < .001), and ACD (r = -0.491, P = .003).

Conclusion: In patients limited by intermittent claudication, shorter ICD and ACD values are associated with reaching a minimum value in calf muscle StO(2) sooner during treadmill exercise and with having a delayed recovery in calf muscle StO(2) after exercise.”
“Caffeine is a widely used psychostimulant freely crossing the placental barrier. At the doses usually absorbed, it acts as an antagonist of both A(1) and A(2A) adenosine receptors. Pregnant women are generally not advised to limit their caffeine consumption and thus expose their progeny to the drug during the whole of gestation and lactation. The possibility that such caffeine exposure may have long-term consequences on brain development has led to several behavioral investigations on animal models. Despite the crucial role played by adenosine receptor systems in neonatal breathing control, few studies in vitro have been concerned with the consequences of maternal caffeine absorption on breathing, and none in the unrestrained intact animal.