From Schritte and Wechsel to Coxeter Groups

The PLR-moves of neo-Riemannian theory, when considered as reflections on the edges of an equilateral triangle, define the Coxeter group $\widetilde S_3$. The elements are in a natural one-to-one correspondence with the triangles in the infinite Tonnetz. The left action of $\widetilde S_3$ on the Tonnetz gives rise to interesting chord sequences. We compare the system of transformations in $\widetilde S_3$ with the system of Schritte and Wechsel introduced by Hugo Riemann in 1880. Finally, we consider the point reflection group as it captures well the transition from Riemann's infinite Tonnetz to the finite Tonnetz of neo-Riemannian theory.Comment: 14 pages for the Mathematics and Computation in Music Conference in June 2019 in Madrid, the revised version extends the music theoretic discussio

Dopaminergic-cholinergic imbalance in movement disorders: a role for the novel striatal dopamine D2-muscarinic acetylcholine M1 receptor heteromer

The striatum is the primary input structure of the basal ganglia, which participates in motivational and goal-directed behaviors (Pisani et al., 2007). In physiological conditions, local cholinergic interneurons (ChIs) and dopaminergic afferents modulate basal ganglia output through striatal projection neurons, also called medium spiny neurons (MSNs). In general, the release of the neurotransmitters dopamine (DA) and acetylcholine (ACh) elicits contradictory effects on MSNs, which express their corresponding DA receptors (DARs) and muscarinic acetylcholine receptors (mAChRs), respectively (Ztaou and Amalric, 2019). Recently, we discovered a novel receptor-receptor interaction (i.e., heteromerization) between the dopamine D2 receptor (D2R) and the muscarinic acetylcholine M1 receptor (M1R), both expressed at striatopallidal MSNs (Crans et al., 2020). The putative striatal D2R-M1R complex coordinates a sophisticated interplay between the dopaminergic and cholinergic neurotransmission systems. Fuxe et al. (2012) foresaw that the existence of this heteromer within the striatum would mechanistically justify the use of anticholinergics in Parkinson's disease (PD) treatment, thus opening up the development of novel pharmacotherapeutic strategies for PD management. As a proof of concept, we demonstrated that an M1R-selective antagonist (i.e., VU0255035, 10 mg/kg, i.p.) potentiated the antiparkinsonian-like efficacy of an ineffective D2R-selective agonist dose (i.e., sumanirole, 3 mg/kg, i.p.) in a rodent model of experimental Parkinsonism (Crans et al., 2020). Overall, the novel D2R-M1R heteromer could serve as a specific drug target to alleviate motor deficits in PD, whereas it may avoid major adverse effects associated with traditional pharmacotherapies

Tetra-μ-aqua-octaaqua­bis(μ-4-chloro­pyridine-2,6-dicarboxyl­ato)bis­(4-chloro­pyridine-2,6-dicarboxyl­ato)tri­cobalt(II)disodium(I) bis­[triaqua­bis(4-chloro­pyridine-2,6-dicarboxyl­ato)cobalt(II)] hexa­hydrate

The title compound, [Co3Na2(C7H2ClNO4)4(H2O)12][Co(C7H2ClNO4)(H2O)3]2·6H2O, consists of a centrosymmetric dimer of [CoII(dipicCl)2]2− complex dianions [dipicCl is 4-chloro­pyridine-2,6-dicarboxyl­ate] bridged by an [Na2CoII(H2O)12]4+ tetra­cationic cluster, two independent [Co(dipicCl)(H2O)3] complexes, and six water mol­ecules of crystallization. The metals are all six-coordinate with distorted octahedral geometries. The [CoII(dipicCl)(H2O)3] complexes are neutral, with one tridentate ligand and three water molecules. The [CoII(dipicCl)2]2− complexes each have two tridentate ligands. The [Na2CoII(H2O)12]4+ cluster has a central CoII ion which is coordinated to six water molecules and lies on a crystallographic inversion center. Four of the water molecules bridge to two sodium ions, each of which have three other water molecules coordinated along with an O atom from the [CoII(dipicCl)2]2− complex. In the crystal structure, the various units are linked by O—H⋯O hydrogen bonds, forming a three-dimensional network. Two water molecules are disordered equally over two positions

Insulin-mimetic action of vanadium compounds on osteoblast-like cells in culture

Vanadium compounds mimic insulin actions in different cell types. The present study concerns the insulin-like effects of three vanadium(V) derivatives and one vanadium(IV) complex on osteoblast-like (UMR106 and MC3T3E1) cells in culture. The vanadium oxalate and vanadium citrate complexes hydrolyzed completely under the culture conditions, whereas more than 40% of the vanadium tartrate and nitrilotriacetate complexes remained. Vanadate, as well as vanadium oxalate, citrate, and tartrate complexes enhanced cell proliferation (as measured by the crystal violet assay), glucose consumption, and protein content in UMR106 and MC3T3E1 osteoblast-like cells. The vanadium nitrilotriacetate complex (the only peroxo complex tested) stimulated cell proliferation in UMR106 but not in MC3T3E1 cells. This derivative strongly transformed the morphology of the MC3T3E1 cells. All vanadium(V) compounds inhibited cell differentiation (alkaline phosphatase activity) in UMR106 cells. Our data are consistent with the interpretation that vanadium oxalate and citrate complexes hydrolyze to vanadate. Vanadium nitrilotriacetate would appear to be toxic for normal MC3T3E1 osteoblasts. In contrast, the vanadium tartrate complex induced a proliferative effect; however, it did not alter cell differentiation

Insulin-mimetic action of vanadium compounds on osteoblast-like cells in culture

Vanadium compounds mimic insulin actions in different cell types. The present study concerns the insulin-like effects of three vanadium(V) derivatives and one vanadium(IV) complex on osteoblast-like (UMR106 and MC3T3E1) cells in culture. The vanadium oxalate and vanadium citrate complexes hydrolyzed completely under the culture conditions, whereas more than 40% of the vanadium tartrate and nitrilotriacetate complexes remained. Vanadate, as well as vanadium oxalate, citrate, and tartrate complexes enhanced cell proliferation (as measured by the crystal violet assay), glucose consumption, and protein content in UMR106 and MC3T3E1 osteoblast-like cells. The vanadium nitrilotriacetate complex (the only peroxo complex tested) stimulated cell proliferation in UMR106 but not in MC3T3E1 cells. This derivative strongly transformed the morphology of the MC3T3E1 cells. All vanadium(V) compounds inhibited cell differentiation (alkaline phosphatase activity) in UMR106 cells. Our data are consistent with the interpretation that vanadium oxalate and citrate complexes hydrolyze to vanadate. Vanadium nitrilotriacetate would appear to be toxic for normal MC3T3E1 osteoblasts. In contrast, the vanadium tartrate complex induced a proliferative effect; however, it did not alter cell differentiation.Facultad de Ciencias Exacta

Insulin-mimetic action of vanadium compounds on osteoblast-like cells in culture

Vanadium compounds mimic insulin actions in different cell types. The present study concerns the insulin-like effects of three vanadium(V) derivatives and one vanadium(IV) complex on osteoblast-like (UMR106 and MC3T3E1) cells in culture. The vanadium oxalate and vanadium citrate complexes hydrolyzed completely under the culture conditions, whereas more than 40% of the vanadium tartrate and nitrilotriacetate complexes remained. Vanadate, as well as vanadium oxalate, citrate, and tartrate complexes enhanced cell proliferation (as measured by the crystal violet assay), glucose consumption, and protein content in UMR106 and MC3T3E1 osteoblast-like cells. The vanadium nitrilotriacetate complex (the only peroxo complex tested) stimulated cell proliferation in UMR106 but not in MC3T3E1 cells. This derivative strongly transformed the morphology of the MC3T3E1 cells. All vanadium(V) compounds inhibited cell differentiation (alkaline phosphatase activity) in UMR106 cells. Our data are consistent with the interpretation that vanadium oxalate and citrate complexes hydrolyze to vanadate. Vanadium nitrilotriacetate would appear to be toxic for normal MC3T3E1 osteoblasts. In contrast, the vanadium tartrate complex induced a proliferative effect; however, it did not alter cell differentiation.Facultad de Ciencias Exacta

Remote sensing and modeling of mosquito abundance and habitats in Coastal Virginia, USA

The increase in mosquito populations following extreme weather events poses a major threat to humans because of mosquitoes’ ability to carry disease-causing pathogens, particularly in low-lying, poorly drained coastal plains vulnerable to tropical cyclones. In areas with reservoirs of disease, mosquito abundance information can help to identify the areas at higher risk of disease transmission. Using a Geographic Information System (GIS), mosquito abundance is predicted across the City of Chesapeake, Virginia. The mosquito abundance model uses mosquito light trap counts, a habitat suitability model, and dynamic environmental variables (temperature and precipitation) to predict the abundance of the species Culiseta melanura, as well as the combined abundance of the ephemeral species, Aedes vexans and Psorophora columbiae, for the year 2003. Remote sensing techniques were used to quantify environmental variables for a potential habitat suitability index for the mosquito species. The goal of this study was to produce an abundance model that could guide risk assessment, surveillance, and potential disease transmission. Results highlight the utility of integrating field surveillance, remote sensing for synoptic landscape habitat distributions, and dynamic environmental data for predicting mosquito vector abundance across low-lying coastal plains. Limitations of mosquito trapping and multi-source geospatial environmental data are highlighted for future spatial modeling of disease transmission risk

Biological consequences of Vanadium effects on formation of reactive oxygen species and lipid peroxidation

Lipid peroxidation (LPO), a process that affects human health, can be induced by exposure to vanadium salts and compounds. LPO is often exacerbated by oxidation stress, with some forms of vanadium providing protective effects. The LPO reaction involves the oxidation of the alkene bonds, primarily in polyunsaturated fatty acids, in a chain reaction to form radical and reactive oxygen species (ROS). LPO reactions typically affect cellular membranes through direct effects on membrane structure and function as well as impacting other cellular functions due to increases in ROS. Although LPO effects on mitochondrial function have been studied in detail, other cellular components and organelles are affected. Because vanadium salts and complexes can induce ROS formation both directly and indirectly, the study of LPO arising from increased ROS should include investigations of both processes. This is made more challenging by the range of vanadium species that exist under physiological conditions and the diverse effects of these species. Thus, complex vanadium chemistry requires speciation studies of vanadium to evaluate the direct and indirect effects of the various species that are present during vanadium exposure. Undoubtedly, speciation is important in assessing how vanadium exerts effects in biological systems and is likely the underlying cause for some of the beneficial effects reported in cancerous, diabetic, neurodegenerative conditions and other diseased tissues impacted by LPO processes. Speciation of vanadium, together with investigations of ROS and LPO, should be considered in future biological studies evaluating vanadium effects on the formation of ROS and on LPO in cells, tissues, and organisms as discussed in this review.info:eu-repo/semantics/publishedVersio

Gauge Invariant Factorisation and Canonical Quantisation of Topologically Massive Gauge Theories in Any Dimension

Abelian topologically massive gauge theories (TMGT) provide a topological mechanism to generate mass for a bosonic p-tensor field in any spacetime dimension. These theories include the 2+1 dimensional Maxwell-Chern-Simons and 3+1 dimensional Cremmer-Scherk actions as particular cases. Within the Hamiltonian formulation, the embedded topological field theory (TFT) sector related to the topological mass term is not manifest in the original phase space. However through an appropriate canonical transformation, a gauge invariant factorisation of phase space into two orthogonal sectors is feasible. The first of these sectors includes canonically conjugate gauge invariant variables with free massive excitations. The second sector, which decouples from the total Hamiltonian, is equivalent to the phase space description of the associated non dynamical pure TFT. Within canonical quantisation, a likewise factorisation of quantum states thus arises for the full spectrum of TMGT in any dimension. This new factorisation scheme also enables a definition of the usual projection from TMGT onto topological quantum field theories in a most natural and transparent way. None of these results rely on any gauge fixing procedure whatsoever.Comment: 1+25 pages, no figure