A note on quadratic Poisson brackets on gl(n,R){\mathrm{gl}}(n,{\mathbb{R}}) related to Toda lattices

It is well known that the compatible linear and quadratic Poisson brackets of the full symmetric and of the standard open Toda lattices are restrictions of linear and quadratic $r$-matrix Poisson brackets on the associative algebra ${\mathrm{gl}}(n,{\mathbb{R}})$. We here show that the quadratic bracket on ${\mathrm{gl}}(n,{\mathbb{R}})$, corresponding to the $r$-matrix defined by the splitting of ${\mathrm{gl}}(n,{\mathbb{R}})$ into the direct sum of the upper triangular and orthogonal Lie subalgebras, descends by Poisson reduction from a quadratic Poisson structure on the cotangent bundle $T^*{\mathrm{GL}}(n,{\mathbb{R}})$. This complements the interpretation of the linear $r$-matrix bracket as a reduction of the canonical Poisson bracket of the cotangent bundle..Comment: 8 page

Isolation and Identification of Pyrene Mineralizing Mycobacterium spp. from Contaminated and Uncontaminated Sources

Copyright © 2011 Christopher W. M. Lease et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.Mycobacterium isolates obtained from PAH-contaminated and uncontaminated matrices were evaluated for their ability to degrade three-, four- and five-ring PAHs. PAH enrichment studies were prepared using pyrene and inocula obtained from manufacturing gas plant (MGP) soil, uncontaminated agricultural soil, and faeces from Macropus fuliginosus (Western Grey Kangaroo). Three pyrene-degrading microorganisms isolated from the corresponding enrichment cultures had broad substrate ranges, however, isolates could be differentiated based on surfactant, phenol, hydrocarbon and PAH utilisation. 16S rRNA analysis identified all three isolates as Mycobacterium sp. The Mycobacterium spp. could rapidly degrade phenanthrene and pyrene, however, no strain had the capacity to utilise fluorene or benzo[a]pyrene. When pyrene mineralisation experiments were performed, 70–79% of added 14C was evolved as 14CO2 after 10 days. The present study demonstrates that PAH degrading microorganisms may be isolated from a diverse range of environmental matrices. The present study demonstrates that prior exposure to PAHs was not a prerequisite for PAH catabolic activity for two of these Mycobacterium isolates

Synthesis, in silico and kinetics evaluation of N-(β-D-glucopyranosyl)-2-arylimidazole-4(5)-carboxamides and N-(β-D-glucopyranosyl)-4(5)-arylimidazole-2-carboxamides as glycogen phosphorylase inhibitors

Recently studied N-(β-D-glucopyranosyl)-3-aryl-1,2,4-triazole-5-carboxamides proved to be low micromolar inhibitors of glycogen phosphorylase (GP), a validated target for the treatment of type 2 diabetes mellitus. Since in other settings, the bioisosteric replacement of the 1,2,4-triazole moiety by imidazole resulted in significantly more efficient GP inhibitors, in silico calculations using Glide molecular docking along with unbound-state DFT calculations was performed on N-(β-D-glucopyranosyl)-arylimidazole-carboxamides revealing potential for strong GP inhibition. The syntheses of the target compounds involved formation of an amide bond between per-O-acetylated β-D-glucopyranosylamine and the corresponding arylimidazole-carboxylic acids. Kinetics experiments against rabbit muscle GPb revealed low micromolar inhibitors with the best inhibition constants (Kis) of ~ 3-4 µM obtained for 1- and 2-naphthyl substituted N-(β-D-glucopyranosyl)-imidazolecarboxamides, 2b-c. The predicted protein-ligand interactions responsible for the observed potencies are discussed and will facilitate the structure-based design of other inhibitors targeting this important therapeutic target. Meanwhile, the importance of careful consideration of ligand tautomeric states in binding calculations is highlighted, with the usefulness of DFT calculations in this regard proposed

Chronic venlafaxine treatment fails to alter the levels of galanin system transcripts in normal rats

It is widely accepted that efficacy and speed of current antidepressants' therapeutic effect are far from optimal. Thus, there is a need for the development of antidepressants with new mechanisms of action. The neuropeptide galanin and its receptors (GalR1, GalR2 and GalR3) are among the promising targets. However, it is not clear whether or not the galanin system is involved in the antidepressant effect exerted by the currently much used inhibitors of the reuptake of serotonin and/or noradrenaline. To answer this question we administered the selective serotonin and noradrenaline reuptake inhibitor (SNRI) venlafaxine (40mg/kg/day via osmotic minipumps) to normal rats and examined the levels of the transcripts for galanin and GalR1-3 after a 3-week venlafaxine treatment in the dorsal raphe, hippocampus and frontal cortex. These areas are known to be involved in the effects of antidepressants and in depression itself. Venlafaxine failed to alter the expression of any of the galanin system genes in these areas. Our results show that one of the most efficient, currently used SNRIs does not alter transcript levels of galanin or its three receptors in normal rats. These findings suggest that the pro- and antidepressive-like effects of galanin reported in animal experiments may employ a novel mechanism(s)

Transcriptional Evidence for the Role of Chronic Venlafaxine Treatment in Neurotrophic Signaling and Neuroplasticity Including also Glutatmatergic- and Insulin-Mediated Neuronal Processes.

OBJECTIVES: Venlafaxine (VLX), a serotonine-noradrenaline reuptake inhibitor, is one of the most commonly used antidepressant drugs in clinical practice for the treatment of major depressive disorder (MDD). Despite being more potent than its predecessors, similarly to them, the therapeutical effect of VLX is visible only 3-4 weeks after the beginning of treatment. Furthermore, recent papers show that antidepressants, including also VLX, enhance the motor recovery after stroke even in non depressed persons. In the present, transcriptomic-based study we looked for changes in gene expressions after a long-term VLX administration. METHODS: Osmotic minipumps were implanted subcutaneously into Dark Agouti rats providing a continuous (40 mg/kg/day) VLX delivery for three weeks. Frontal regions of the cerebral cortex were isolated and analyzed using Illumina bead arrays to detect genes showing significant chances in expression. Gene set enrichment analysis was performed to identify specific regulatory networks significantly affected by long term VLX treatment. RESULTS: Chronic VLX administration may have an effect on neurotransmitter release via the regulation of genes involved in vesicular exocytosis and receptor endocytosis (such as Kif proteins, Myo5a, Sv2b, Syn2 or Synj2). Simultaneously, VLX activated the expression of genes involved in neurotrophic signaling (Ntrk2, Ntrk3), glutamatergic transmission (Gria3, Grin2b and Grin2a), neuroplasticity (Camk2g/b, Cd47), synaptogenesis (Epha5a, Gad2) and cognitive processes (Clstn2). Interestingly, VLX increased the expression of genes involved in mitochondrial antioxidant activity (Bcl2 and Prdx1). Additionally, VLX administration also modulated genes related to insulin signaling pathway (Negr1, Ppp3r1, Slc2a4 and Enpp1), a mechanism that has recently been linked to neuroprotection, learning and memory. CONCLUSIONS: Our results strongly suggest that chronic VLX treatment improves functional reorganization and brain plasticity by influencing gene expression in regulatory networks of motor cortical areas. These results are consonant with the synaptic (network) hypothesis of depression and antidepressant-induced motor recovery after stroke