2′-(3-Hydroxy­benzyl­idene)pyrazine-2-carbohydrazide monohydrate

The title compound, C12H10N4O2·H2O, was synthesized by the reaction of pyrazine-2-carboxylic acid hydrazide and 3-hydroxy­benzaldehyde in ethanol. In the crystal structure, the organic mol­ecules are linked into extended chains by inter­molecular N(amide)—H⋯O(hydr­oxy) hydrogen bonds. Additional hydrogen bonds between the water mol­ecule and three adjacent organic mol­ecules, as well as face-to-face π–π stacking inter­actions between the benzene and pyrazine rings [centroid-to-centroid separation = 3.669 (2) Å and offset = 1.362 Å], link the mol­ecules into a three-dimensional framework

Hypothalamic Vitamin D Improves Glucose Homeostasis and Reduces Weight

Despite clear associations between vitamin D deficiency and obesity and/or type 2 diabetes, a causal relationship is not established. Vitamin D receptors (VDRs) are found within multiple tissues, including the brain. Given the importance of the brain in controlling both glucose levels and body weight, we hypothesized that activation of central VDR links vitamin D to the regulation of glucose and energy homeostasis. Indeed, we found that small doses of active vitamin D, 1α,25-dihydroxyvitamin D3 (1,25D3) (calcitriol), into the third ventricle of the brain improved glucose tolerance and markedly increased hepatic insulin sensitivity, an effect that is dependent upon VDR within the paraventricular nucleus of the hypothalamus. In addition, chronic central administration of 1,25D3 dramatically decreased body weight by lowering food intake in obese rodents. Our data indicate that 1,25D3-mediated changes in food intake occur through action within the arcuate nucleus. We found that VDR colocalized with and activated key appetite-regulating neurons in the arcuate, namely proopiomelanocortin neurons. Together, these findings define a novel pathway for vitamin D regulation of metabolism with unique and divergent roles for central nervous system VDR signaling. Specifically, our data suggest that vitamin D regulates glucose homeostasis via the paraventricular nuclei and energy homeostasis via the arcuate nuclei

mGluR5 antagonism inhibits cocaine reinforcement and relapse by elevation of extracellular glutamate in the nucleus accumbens via a CB1 receptor mechanism.

Metabotropic glutamate receptor 5 (mGluR5) antagonism inhibits cocaine self-administration and reinstatement of drug-seeking behavior. However, the cellular and molecular mechanisms underlying this action are poorly understood. Here we report a presynaptic glutamate/cannabinoid mechanism that may underlie this action. Systemic or intra-nucleus accumbens (NAc) administration of the mGluR5 antagonist 2-methyl-6-(phenylethynyl)-pyridine (MPEP) dose-dependently reduced cocaine (and sucrose) self-administration and cocaine-induced reinstatement of drug-seeking behavior. The reduction in cocaine-taking and cocaine-seeking was associated with a reduction in cocaine-enhanced extracellular glutamate, but not cocaine-enhanced extracellular dopamine (DA) in the NAc. MPEP alone, when administered systemically or locally into the NAc, elevated extracellular glutamate, but not DA. Similarly, the cannabinoid CB1 receptor antagonist, rimonabant, elevated NAc glutamate, not DA. mGluR5s were found mainly in striatal medium-spiny neurons, not in astrocytes, and MPEP-enhanced extracellular glutamate was blocked by a NAc CB1 receptor antagonist or N-type Ca++ channel blocker, suggesting that a retrograde endocannabinoid-signaling mechanism underlies MPEP-induced glutamate release. This interpretation was further supported by our findings that genetic deletion of CB1 receptors in CB1-knockout mice blocked both MPEP-enhanced extracellular glutamate and MPEP-induced reductions in cocaine self-administration. Together, these results indicate that the therapeutic anti-cocaine effects of mGluR5 antagonists are mediated by elevation of extracellular glutamate in the NAc via an endocannabinoid-CB1 receptor disinhibition mechanism

U-Spin Symmetry in Charmless B Decays

We prove a general theorem about equal CP rate differences within pairs of U-spin related charmless $B$ and $B_s$ decays. Large deviations from equalities would be evidence for new physics. Six pairs of decays into two pseudoscalar mesons are identified where such relations hold. Ratios of corresponding rate differences and certain ratios of rates measure U-spin breaking. These processes provide useful information on the weak phase $\gamma={\rm Arg} V^*_{ub}$. Applications of U-spin symmetry to other decays are discussed.Comment: A few typos corrected, to appear in Phys. Lett.

Temperature Dependence of the Magnetic Penetration Depth in the Vortex State of the Pyrochlore Superconductor, Cd2Re2O7

We report transverse field and zero field muon spin rotation studies of the superconducting rhenium oxide pyrochlore, Cd2Re2O7. Transverse field measurements (H=0.007 T) show line broadening below Tc, which is characteristic of a vortex state, demonstrating conclusively the type-II nature of this superconductor. The penetration depth is seen to level off below about 400 mK (T/Tc~0.4), with a rather large value of lambda (T=0)~7500A. The temperature independent behavior below ~ 400 mK is consistent with a nodeless superconducting energy gap. Zero-field measurements indicate no static magnetic fields developing below the transition temperature.Comment: 4 pages, 4 figures, REVTEX 4, submitted to PR

N′-(4-Fluoro­benzyl­idene)-3,4,5-trimethoxy­benzohydrazide

The title compound, C17H17FN2O4, is of inter­est due to its potential pharmaceutical and agrochemical activity. All three meth­oxy groups are twisted with respect to the attached aromatic ring [C—C—O—C torsion angles = 10.43 (18), 97.38 (14), −19.34 (17)°] and the phenyl ring makes a dihedral angle of 40.6 (2)° with the plane through the remaining atoms in the mol­ecule. Inter­molecular N—H⋯O hydrogen bonds link the mol­ecules into chains running along the c axis

Grouping time series by pairwise measures of redundancy

A novel approach is proposed to group redundant time series in the frame of causality. It assumes that (i) the dynamics of the system can be described using just a small number of characteristic modes, and that (ii) a pairwise measure of redundancy is sufficient to elicit the presence of correlated degrees of freedom. We show the application of the proposed approach on fMRI data from a resting human brain and gene expression profiles from HeLa cell culture.Comment: 4 pages, 8 figure