A naturally occurring membrane-anchored Gα variant, XLα, activates phospholipase Cβ4.

Extra-large stimulatory Gα (XLα) is a large variant of G protein α subunit (Gα) that uses an alternative promoter and thus differs from Gα at the first exon. XLα activation by G protein-coupled receptors mediates cAMP generation, similarly to Gα; however, Gα and XLα have been shown to have distinct cellular and physiological functions. For example, previous work suggests that XLα can stimulate inositol phosphate production in renal proximal tubules and thereby regulate serum phosphate levels.

Electrochemical Measurement of Dopamine Release and Uptake in Zebrafish Following Treatment with Carboplatin.

Post-chemotherapy cognitive impairment, also known as 'chemobrain,' is a neurological condition in which cognitive function is impaired as a result of cancer chemotherapy treatment. In this work, we used fast-scan cyclic voltammetry (FSCV) to measure electrically evoked dopamine release and uptake in whole brain preparations from zebrafish that have been treated with carboplatin, an agent associated with chemobrain. We administered carboplatin by addition to the fish's tank water or their food.

Acute altitude-induced hypoxia suppresses plasma glucose and leptin in healthy humans.

To examine the effects of acute altitude-induced hypoxia on the hormonal and metabolic response to ingested glucose, 8 young, healthy subjects (5 men and 3 women; age, 26 +/- 2 years; body mass index, 23.1 +/- 1.0 kg/m(2)) performed 2 randomized trials in a hypobaric chamber where a 75-g glucose solution was ingested under simulated altitude (ALT, 4300 m) or ambient (AMB, 362 m) conditions.

Venous but not skeletal muscle interstitial nitric oxide is increased during hypobaric hypoxia.

Systemic hypoxia leads to peripheral vasodilation that serves to counteract the decrease in peripheral oxygen (O(2)) delivery. Skeletal muscle vasodilation associated with hypoxia is due to release of vasodilator substances such as adenosine and/or nitric oxide (NO). We hypothesized that skeletal muscle may act as a source of NO during exposure to hypoxia.