5-HT1A receptor antagonist p-MPPI pretreatment (1 mg/kg i.p.) diminished hypothermia produced by centrally administered m-CPBG (40 nmol i.c.v.). The data suggest the cross-talk between 5-HT1A and 5-HT3 receptors in the mechanism of 5-HT-related hypothermia. (C) 2009 Elsevier Ireland Ltd. All rights reserved.”
“The sliding filament and crossbridge theories do not suffice to explain a number of muscle experiments. For example, from the entire muscle to myofibrils, predictions of these theories were shown to underestimate the force output during and after active tissue stretch. The converse applies to active tissue shortening.

In addition

to the crossbridge PRT062607 price cycle, we propose that another molecular mechanism is effective in sarcomere force generation. We suggest that, when

due to activation, myosin binding sites are available on actin, the giant protein titin’s PEVK region attaches itself to the actin filament at those sites. As a the molecular spring length is dramatically reduced. This leads to increased passive force when result, the sarcomere is stretched and to decreased or even negative passive force when the sarcomere shortens. Moreover, during shortening, the proposed mechanism interferes with active-force production by inhibiting selleck chemical crossbridges.

Incorporation of a simple ‘sticky-spring’ mechanism model into a Hill-type model of sarcomere dynamics offers explanations for several force-enhancement and Lonafarnib cell line force-depression effects. For example, the increase of the sarcomere force compared to the force predicted solely by the sliding filament and crossbridge theories depends on the stretch amplitude and on the working range. The same applies to the decrease of sarcomere force during and after

shortening. Using only literature data for its parameterization, the model predicts forces similar to experimental results. (C) 2009 Elsevier Ltd. All rights reserved.”
“Aims: To test the hypothesis that uridine 5′-triphosphate (UTP) had a protective effect on cerebral ischemia reperfusion (IR) injury in rats. Methods: Ischemia was induced by intraluminal suture of middle cerebral artery occlusion (MCAO). UTP solution was delivered through an indwelling tail venous catheter via microinfusion pump 30 min after the occlusion of MCA at a rate of 0.5 ml/100g/min. Neurological deficit score (NDS) and brain water content were determined 24 h after reperfusion. Infarct volume was determined by 2,3,5-triphenyl-tetrazolium chloride (TTC) staining and magnetic resonance imaging (MRI), and nerve cell death was studied under an electron microscope. Results: There was a dose-dependent relationship among 10, 30 and 90 mu g/kg UTP. The 90 mu g/kg UTP had the best protective effect among the 3 groups. We compared 90 mu g/kg UTP group with normal saline group and found that UTP had a protective effect on cerebral IR by the results of TTC staining (15.9% vs 30.5%, P < 0.01).