Influence of cardiovascular risk factors on infarct size and interaction with mechanical ischaemic postconditioning in ST-elevation myocardial infarction.

Objective: Previous studies have shown that mechanical postconditioning (PostC) significantly reduces infarct size (IS) in patients with acute myocardial infarction. Our objective was to assess the influence of traditional cardiovascular (CV) risk factors on IS and their interaction with ischaemic PostC in patients with acute ST-elevation myocardial infarction (STEMI).

Methods: The study population was constituted from the clinical database pooling of four previously published PostC prospective, multicentre, randomised, open-label controlled trials with identical inclusion criteria.

(1)H, (15)N and (13)C backbone resonance assignments of murine met-neuroglobin, free and in complex with cyanide.

Neuroglobin is a globin present in the brain and retina of mammals. This hexacoordinated hemoprotein binds small diatomic molecules, albeit with lower affinity compared with other globins. We report here the resonance assignment of murine met-Neuroglobine, free and in complex with cyanide.

Effect of cyclosporine on left ventricular remodeling after reperfused myocardial infarction.

Objectives: This study examined the effect of a single dose of cyclosporine administered at the time of reperfusion on left ventricular (LV) remodeling and function by cardiac magnetic resonance 5 days and 6 months after myocardial infarction.

Background: In a human study, administration of cyclosporine at the time of acute reperfusion was associated with a smaller infarct size.

Methods: Twenty-eight patients of the original cyclosporine study had an acute (at 5 days) and a follow-up (at 6 months) cardiac magnetic resonance study to determine LV volumes, mass, ejection fraction, myocardial wall thickness in infarcted and remote noninfarcted myocardium, and infarct size.

Towards the discovery of novel T-type calcium channel blockers.

Despite their presence in many tissues and their potential implication in various disease states, low-voltage activated T-type calcium channels (T-channels) have only recently become targets of interest. Unfortunately, the lack of selective T-channel blockers has hampered further characterisation of these channels. The recent availability of cloned T-channels, the Ca(V)3 proteins, facilitates identification of novel T-channel blockers.

Chemical determinants involved in anandamide-induced inhibition of T-type calcium channels.

Anandamide, originally described as an endocannabinoid, is the main representative molecule of a new class of signaling lipids including endocannabinoids and N-acyl-related molecules, eicosanoids, and fatty acids. Bioactive lipids regulate neuronal excitability by acting on G-protein-coupled receptors (such as CB1) but also directly modulate various ionic conductances including voltage-activated T-type calcium channels (T-channels). However, little is known about the properties and the specificity of this new class of molecules on their various targets.

Subunit-specific modulation of T-type calcium channels by zinc.

Zinc (Zn2+) functions as a signalling molecule in the nervous system and modulates many ionic channels. In this study, we have explored the effects of Zn2+ on recombinant T-type calcium channels (CaV3.1, CaV3.

Voltage-gated calcium channels in genetic diseases.

Voltage-gated calcium channels (VGCCs) mediate calcium entry into excitable cells in response to membrane depolarization. During the past decade, our understanding of the gating and functions of VGCCs has been illuminated by the analysis of mutations linked to a heterogeneous group of genetic diseases called "calcium channelopathies". Calcium channelopathies include muscular, neurological, cardiac and vision syndromes.

T-type calcium channels are inhibited by fluoxetine and its metabolite norfluoxetine.

Fluoxetine, a widely used antidepressant that primarily acts as a selective serotonin reuptake inhibitor, also inhibits various neuronal ion channels. Using the whole-cell patch-clamp technique, we have examined the effects of fluoxetine and norfluoxetine, its major active metabolite, on cloned low-voltage-activated T-type calcium channels (T channels) expressed in tsA 201 cells. Fluoxetine inhibited the three T channels Ca(V)3.