Tetra­aqua­bis(3,5-di-4-pyridyl-1H-1,2,4-triazolido)cadmium(II) dihydrate

In the title compound, [Cd(C12H8N5)2(H2O)4]·2H2O, the CdII atom is located on an inversion center and is coordinated by the two N atoms [Cd—N = 2.278 (2) Å] and four O atoms [Cd—O = 2.304 (2)–2.322 (2) Å] in a distorted octa­hedral geometry. Inter­molecular O—H⋯O and O—H⋯N hydrogen bonds link the complex into a three-dimensional supra­molecular framework

Tetra­aqua­bis[3-(3-pyrid­yl)-5-(4-pyrid­yl)-1,2,4-triazolido]nickel(II) dihydrate

In the title compound, [Ni(C12H8N5)2(H2O)4]·2H2O, the NiII atom is coordinated by the two N atoms [Ni—N = 2.094 (3) Å] and four O atoms [Ni—O = 2.063 (3)–2.083 (2) Å] in a distorted octa­hedral geometry. The mol­ecule is centrosymmetric and the NiII atom is located on an inversion center. Inter­molecular O—H⋯N and O—H⋯O hydrogen bonds link the complex into a three-dimensional supra­molecular framework

Tetra­aqua­bis­(tetra­zolido-κN 1)magnesium

In the crystal structure of the title compound, [Mg(CHN4)2(H2O)4], the MgII atom is six-coordinated by two N atoms from two tetra­zolide anions and four O atoms from four coordinated water mol­ecules in a slightly distorted octa­hedral geometry. The Mg atom is located on centres of inversion whereas the tetra­zolide anion and the water mol­ecules occupy general positions. The crystal packing is stabilized by intermolecular O—H⋯N hydrogen bonding between the tetra­zolide anions and the coordinated water mol­ecules

Bis(μ-5-carboxyl­atotetra­zolido)bis­[aqua­(2,2′-bipyrid­yl)cadmium(II)]

In the title dinuclear CdII complex, [Cd2(C2N4O2)2(C10H8N2)2(H2O)2], each Cd atom is in a slightly distorted octa­hedral coordination by two N atoms and one O atom of two 1H-tetra­zole-5-carboxyl­ate (TZC) ligands, two N atoms of a 2,2′-bipyridyl ligand and one water O atom. The TZC ligand acts in a tridentate N,O-chelating N-bridging mode to two symmetry-equivalent CdII atoms. The complex reveals mol­ecular C i symmetry. Extensive O—H⋯O hydrogen bonding plays an important role in the crystal packing

Diaqua­bis­(3-nitro­benzoato-κO 1)bis­[1H-5-(3-pyrid­yl)-3-(4-pyrid­yl)-1H-1,2,4-triazole-κN 5]cobalt(II) dihydrate

In the centrosymmetric title compound, [Co(C7H4NO4)2(C12H9N5)2(H2O)2]·2H2O, the CoII atom, located on an inversion center, is coordinated by two N atoms [Co—N = 2.155 (3) Å] and four O atoms [Co—O = 2.099 (2)–2.117 (3) Å] in a distorted octa­hedral geometry. Inter­molecular N—H⋯O, O—H⋯N and O—H⋯O hydrogen bonds link the components into a three-dimensional supramolecular framework

Hippocampal PACAP signaling activation triggers a rapid antidepressant response

Background The development of ketamine-like rapid antidepressants holds promise for enhancing the therapeutic efcacy of depression, but the underlying cellular and molecular mechanisms remain unclear. Implicated in depres‑ sion regulation, the neuropeptide pituitary adenylate cyclase-activating polypeptide (PACAP) is investigated here to examine its role in mediating the rapid antidepressant response. Methods The onset of antidepressant response was assessed through depression-related behavioral paradigms. The signaling mechanism of PACAP in the hippocampal dentate gyrus (DG) was evaluated by utilizing site-directed gene knockdown, pharmacological interventions, or optogenetic manipulations. Overall, 446 mice were used for behavioral and molecular signaling testing. Mice were divided into control or experimental groups randomly in each experiment, and the experimental manipulations included: chronic paroxetine treatments (4, 9, 14 d) or a single treatment of keta‑ mine; social defeat or lipopolysaccharides-injection induced depression models; diferent doses of PACAP (0.4, 2, 4 ng/ site; microinjected into the hippocampal DG); pharmacological intra-DG interventions (CALM and PACAP6-38); intraDG viral-mediated PACAP RNAi; and opotogenetics using channelrhodopsins 2 (ChR2) or endoplasmic natronomonas halorhodopsine 3.0 (eNpHR3.0). Behavioral paradigms included novelty suppressed feeding test, tail suspension test, forced swimming test, and sucrose preference test. Western blotting, ELISA, or quantitative real-time PCR (RT-PCR) analysis were used to detect the expressions of proteins/peptides or genes in the hippocampus. Results Chronic administration of the slow-onset antidepressant paroxetine resulted in an increase in hippocam‑ pal PACAP expression, and intra-DG blockade of PACAP attenuated the onset of the antidepressant response. The levels of hippocampal PACAP expression were reduced in both two distinct depression animal models and intra-DG knockdown of PACAP induced depression-like behaviors. Conversely, a single infusion of PACAP into the DG region produced a rapid and sustained antidepressant response in both normal and chronically stressed mice. Optoge‑ netic intra-DG excitation of PACAP-expressing neurons instantly elicited antidepressant responses, while optoge‑ netic inhibition induced depression-like behaviors. The longer optogenetic excitation/inhibition elicited the more sustained antidepressant/depression-like responses. Intra-DG PACAP infusion immediately facilitated the signaling for rapid antidepressant response by inhibiting calcium/calmodulin-dependent protein kinase II (CaMKII)-eukaryotic elongation factor 2 (eEF2) and activating the mammalian target of rapamycin (mTOR). Pre-activation of CaMKII signaling within the DG blunted PACAP-induced rapid antidepressant response as well as eEF2-mTOR-brain-derivedneurotrophic factor (BDNF) signaling. Finally, acute ketamine treatment upregulated hippocampal PACAP expression, whereas intra-DG blockade of PACAP signaling attenuated ketamine’s rapid antidepressant response. Conclusions Activation of hippocampal PACAP signaling induces a rapid antidepressant response through the regu‑ lation of CaMKII inhibition-governed eEF2-mTOR-BDNF signaling

Diffractive Dijet Production at sqrt(s)=630 and 1800 GeV at the Fermilab Tevatron

We report a measurement of the diffractive structure function $F_{jj}^D$ of the antiproton obtained from a study of dijet events produced in association with a leading antiproton in $\bar pp$ collisions at $\sqrt s=630$ GeV at the Fermilab Tevatron. The ratio of $F_{jj}^D$ at $\sqrt s=630$ GeV to $F_{jj}^D$ obtained from a similar measurement at $\sqrt s=1800$ GeV is compared with expectations from QCD factorization and with theoretical predictions. We also report a measurement of the $\xi$ ($x$-Pomeron) and $\beta$ ($x$ of parton in Pomeron) dependence of $F_{jj}^D$ at $\sqrt s=1800$ GeV. In the region $0.035<\xi<0.095$, $|t|<1$ GeV$^2$ and $\beta<0.5$, $F_{jj}^D(\beta,\xi)$ is found to be of the form $\beta^{-1.0\pm 0.1} \xi^{-0.9\pm 0.1}$, which obeys $\beta$-$\xi$ factorization.Comment: LaTeX, 9 pages, Submitted to Phys. Rev. Letter

A Study of B0 -> J/psi K(*)0 pi+ pi- Decays with the Collider Detector at Fermilab

We report a study of the decays B0 -> J/psi K(*)0 pi+ pi-, which involve the creation of a u u-bar or d d-bar quark pair in addition to a b-bar -> c-bar(c s-bar) decay. The data sample consists of 110 1/pb of p p-bar collisions at sqrt{s} = 1.8 TeV collected by the CDF detector at the Fermilab Tevatron collider during 1992-1995. We measure the branching ratios to be BR(B0 -> J/psi K*0 pi+ pi-) = (8.0 +- 2.2 +- 1.5) * 10^{-4} and BR(B0 -> J/psi K0 pi+ pi-) = (1.1 +- 0.4 +- 0.2) * 10^{-3}. Contributions to these decays are seen from psi(2S) K(*)0, J/psi K0 rho0, J/psi K*+ pi-, and J/psi K1(1270)

Measurement of the branching fraction and CP content for the decay B(0) -> D(*+)D(*-)

This is the pre-print version of the Article. The official published version can be accessed from the links below. Copyright @ 2002 APS.We report a measurement of the branching fraction of the decay B0→D*+D*- and of the CP-odd component of its final state using the BABAR detector. With data corresponding to an integrated luminosity of 20.4  fb-1 collected at the Υ(4S) resonance during 1999–2000, we have reconstructed 38 candidate signal events in the mode B0→D*+D*- with an estimated background of 6.2±0.5 events. From these events, we determine the branching fraction to be B(B0→D*+D*-)=[8.3±1.6(stat)±1.2(syst)]×10-4. The measured CP-odd fraction of the final state is 0.22±0.18(stat)±0.03(syst).This work is supported by DOE and NSF (USA), NSERC (Canada), IHEP (China), CEA and CNRS-IN2P3 (France), BMBF (Germany), INFN (Italy), NFR (Norway), MIST (Russia), and PPARC (United Kingdom). Individuals have received support from the A.P. Sloan Foundation, Research Corporation, and Alexander von Humboldt Foundation

Measurement of D-s(+) and D-s(*+) production in B meson decays and from continuum e(+)e(-) annihilation at √s=10.6 GeV

This is the pre-print version of the Article. The official published version can be accessed from the links below. Copyright @ 2002 APSNew measurements of Ds+ and Ds*+ meson production rates from B decays and from qq̅ continuum events near the Υ(4S) resonance are presented. Using 20.8 fb-1 of data on the Υ(4S) resonance and 2.6 fb-1 off-resonance, we find the inclusive branching fractions B(B⃗Ds+X)=(10.93±0.19±0.58±2.73)% and B(B⃗Ds*+X)=(7.9±0.8±0.7±2.0)%, where the first error is statistical, the second is systematic, and the third is due to the Ds+→φπ+ branching fraction uncertainty. The production cross sections σ(e+e-→Ds+X)×B(Ds+→φπ+)=7.55±0.20±0.34pb and σ(e+e-→Ds*±X)×B(Ds+→φπ+)=5.8±0.7±0.5pb are measured at center-of-mass energies about 40 MeV below the Υ(4S) mass. The branching fractions ΣB(B⃗Ds(*)+D(*))=(5.07±0.14±0.30±1.27)% and ΣB(B⃗Ds*+D(*))=(4.1±0.2±0.4±1.0)% are determined from the Ds(*)+ momentum spectra. The mass difference m(Ds+)-m(D+)=98.4±0.1±0.3MeV/c2 is also measured.This work was supported by DOE and NSF (USA), NSERC (Canada), IHEP (China), CEA and CNRS-IN2P3 (France), BMBF (Germany), INFN (Italy), NFR (Norway), MIST (Russia), and PPARC (United Kingdom). Individuals have received support from the Swiss NSF, A. P. Sloan Foundation, Research Corporation, and Alexander von Humboldt Foundation