A constraint variational problem arising in stellar dynamics

We use the compactness result of A. Burchard and Y. Guo (cf. \cite{BuGu}) to analyze the reduced 'energy' functional arising naturally in the stability analysis of steady states of the Vlasov-Poisson system (cf. \cite{SaSo} and \cite{Ha}). We consider the associated variational problem and present a new proof that puts it in the general framework for tackling the variational problems of this type, given by Y. Guo and G. Rein (cf. \cite{Re1} and \cite{Re2})

Knowing what we count : a comment on Guo

Guo (2011) points to problems arising from different approaches to estimating the proportions of floras that are native or alien, specifically those across and within various regions. This results in inconsistency of numbers reported from internal administrative units by underestimating the numbers of species that are alien to the region and overestimating native species richness. Resulting species numbers and proportions for smaller units within large countries, or whole continents, can be seriously biased if only species alien to the larger unit as a whole are considered alien, while all other species are considered native

Guanosine-mediated anxiolytic-like effect: Interplay with adenosine a1 and a2a receptors

Acute or chronic administration of guanosine (GUO) induces anxiolytic-like effects, for which the adenosine (ADO) system involvement has been postulated yet without a direct experimental evidence. Thus, we aimed to investigate whether adenosine receptors (ARs) are involved in the GUO-mediated anxiolytic-like effect, evaluated by three anxiety-related paradigms in rats. First, we confirmed that acute treatment with GUO exerts an anxiolytic-like effect. Subsequently, we investigated the effects of pretreatment with ADO or A1R (CPA, CCPA) or A2AR (CGS21680) agonists 10 min prior to GUO on a GUO-induced anxiolytic-like effect. All the combined treatments blocked the GUO anxiolytic-like effect, whereas when administered alone, each compound was ineffective as compared to the control group. Interestingly, the pretreatment with nonselective antagonist caffeine or selective A1R (DPCPX) or A2AR (ZM241385) antagonists did not modify the GUO-induced anxiolytic-like effect. Finally, binding assay performed in hippocampal membranes showed that [3H]GUO binding became saturable at 100–300 nM, suggesting the existence of a putative GUO binding site. In competition experiments, ADO showed a potency order similar to GUO in displacing [3H]GUO binding, whereas AR selective agonists, CPA and CGS21680, partially displaced [3H]GUO binding, but the sum of the two effects was able to displace [3H]GUO binding to the same extent of ADO alone. Overall, our results strengthen previous data supporting GUO-mediated anxiolytic-like effects, add new evidence that these effects are blocked by A1R and A2AR agonists and pave, although they do not elucidate the mechanism of GUO and ADO receptor interaction, for a better characterization of GUO binding sites in ARs