Benzil bis­(ketazine)

The title compound (systematic name: 1,1′,2,2′-tetra­phenyl-2,2′-azinodiethanone), C28H20N2O2, was obtained by the reaction of benzil monohydrazone with chromium(III) nitrate. The dibenzyl­idene hydrazine unit is nearly planar (r.m.s. deviation = 0.073 Å) and the two benzoyl units are oriented almost perpendicular to it [dihedral angle = 87.81 (2), 87.81 (2)°]. The mol­ecules are linked into chains along the c axis by C—H⋯O hydrogen bonds and the chains are cross-linked via C—H⋯π inter­actions involving the benzoyl phenyl rings

N,N′-Bis(4-pyridylmethyl­ene)octane-1,8-diamine

The complete molecule of the title compound, C20H26N4, is generated by a crystallographic centre of inversion and the central eight-carbon chain adopts a fully extended conformation. In the crystal, the molecules pack in layers parallel to (010)

Relating the Kick Velocities of Young Pulsars with Magnetic Field Growth Timescales Inferred From Braking Indices

A nascent neutron star may be exposed to fallback accretion soon after the proto-neutron star stage. This high accretion episode can submerge the magnetic field deep in the crust. The diffusion of the magnetic field back to the surface will take hundreds to millions of years depending on the amount of mass accreted and the consequent depth the field is buried. Neutron stars with large kick velocities will accrete less amount of fallback material leading to shallower submergence of their fields and shorter time-scales for the growth of their fields. We obtain the relation $\tau_{\rm Ohm} \propto v^{-1}$ between the space velocity of the neutron star and Ohmic time-scale for the growth of the magnetic field. We compare this with the relation between the measured transverse velocities, $v_{\perp}$ and the field growth time-scales, $\mu/\dot{\mu}$, inferred from the measured braking indices. We find that the observational data is consistent with the theoretical prediction though the small number of data precludes a strong conclusion. Measurement of the transverse velocities of pulsars B1509$-$58, J1846$-$0258, J1119$-$6127 and J1734$-$3333 would increase the number of the data and strongly contribute to understanding whether pulsar fields grow following fallback accretion.Comment: Accepted to MNRAS Letters. Title and abstract are change

Bacterial Metabolism During Biofilm Growth Investigated by 13C Tracing

This study investigated the metabolism of Pseudomonas aeruginosa PAO1 during its biofilm development via microscopy imaging, gene expression analysis, and 13C-labeling. First, dynamic labeling was employed to investigate glucose utilization rate in fresh biofilms (thickness 40∼60 micrometer). The labeling turnover time of glucose-6-P indicated biofilm metabolism was substantially slower than planktonic cells. Second, PAO1 was cultured in continuous tubular biofilm reactors or shake flasks. Then 13C-metabolic flux analysis of PAO1 was performed based on the isotopomer patterns of proteinogenic amino acids. The results showed that PAO1 biofilm cells during growth conserved the flux features as their planktonic mode. (1) Glucose could be degraded by two cyclic routes (the TCA cycle and the Entner-Doudoroff-Embden-Meyerhof-Parnas loop) that facilitated NAD(P)H supplies. (2) Anaplerotic pathways (including pyruvate shunt) increased flux plasticity. (3) Biofilm growth phenotype did not require significant intracellular flux rewiring (variations between biofilm and planktonic flux network, normalized by glucose uptake rate as 100%, were less than 20%). (4) Transcription analysis indicated that key catabolic genes in fresh biofilm cells had expression levels comparable to planktonic cells. Finally, PAO1, Shewanella oneidensis (as the comparing group), and their c-di-GMP transconjugants (with different biofilm formation capabilities) were 13C-labeled under biofilm reactors or planktonic conditions. Analysis of amino acid labeling variances from different cultures indicated Shewanella flux network was more flexibly changed than PAO1 during its biofilm formation

Endogenous Signaling by Omega-3 Docosahexaenoic Acid-derived Mediators Sustains Homeostatic Synaptic and Circuitry Integrity

The harmony and function of the complex brain circuits and synapses are sustained mainly by excitatory and inhibitory neurotransmission, neurotrophins, gene regulation, and factors, many of which are incompletely understood. A common feature of brain circuit components, such as dendrites, synaptic membranes, and other membranes of the nervous system, is that they are richly endowed in docosahexaenoic acid (DHA), the main member of the omega-3 essential fatty acid family. DHA is avidly retained and concentrated in the nervous system and known to play a role in neuroprotection, memory, and vision. Only recently has it become apparent why the surprisingly rapid increases in free (unesterified) DHA pool size take place at the onset of seizures or brain injury. This phenomenon began to be clarified by the discovery of neuroprotectin D1 (NPD1), the first-uncovered bioactive docosanoid formed from free DHA through 15-lipoxygenase-1 (15-LOX-1). NPD1 synthesis includes, as agonists, oxidative stress and neurotrophins. The evolving concept is that DHA-derived docosanoids set in motion endogenous signaling to sustain homeostatic synaptic and circuit integrity. NPD1 is anti-inflammatory, displays inflammatory resolving activities, and induces cell survival, which is in contrast to the pro-inflammatory actions of the many of omega-6 fatty acid family members. We highlight here studies relevant to the ability of DHA to sustain neuronal function and protect synapses and circuits in the context of DHA signalolipidomics. DHA signalolipidomics comprises the integration of the cellular/tissue mechanism of DHA uptake, its distribution among cellular compartments, the organization and function of membrane domains containing DHA phospholipids, and the precise cellular and molecular events revealed by the uncovering of signaling pathways regulated by docosanoids endowed with prohomeostatic and cell survival bioactivity. Therefore, this approach offers emerging targets for prevention, pharmaceutical intervention, and clinical translation involving DHA-mediated signaling

Enhancement of the superconducting transition temperature from the competition between electron-electron correlations and electron-phonon interactions

We uncover that the competition between electron-electron correlations and electron-phonon interactions gives rise to unexpectedly huge enhancement of the superconducting transition temperature, several hundreds percent larger ($\geq$ 200 K) than that of the case when only one of the two is taken into account ($\sim$ 30 K). Our renormalization group analysis claims that this mechanism for the enhancement of the critical temperature is not limited on superconductivity but applied to various Fermi surface instabilities, proposing an underlying universal structure, which turns out to be essentially identical to that of a recent study [Phys. Rev. Lett. {\bf 108}, 046601 (2012)] on the enhancement of the Kondo temperature in the presence of Rashba spin-orbit interactions. We also discuss the stability of superconductivity against nonmagnetic randomness

Docosahexaenoic Acid Therapy of Experimental Ischemic Stroke

We examined the neuroprotective efficacy of docosahexaenoic acid (DHA), an omega-3 essential fatty acid family member, in acute ischemic stroke; studied the therapeutic window; and investigated whether DHA administration after an ischemic stroke is able to salvage the penumbra. In each series described below, SD rats underwent 2 h of middle cerebral artery occlusion (MCAo). In series 1, DHA or saline was administered i.v. at 3, 4, 5, or 6 h after stroke. In series 2, MRI was conducted on days 1, 3 and 7. In series 3, DHA or saline was administered at 3 h, and lipidomic analysis was conducted on day 3. Treatment with DHA significantly improved behavior and reduced total infarct volume by a mean of 40% when administered at 3 h, by 66% at 4 h, and by 59% at 5 h. Total lesion volumes computed from T2-weighted images were reduced in the DHA group at all time points. Lipidomic analysis showed that DHA treatment potentiates neuroprotectin D1 (NPD1) synthesis in the penumbra 3 days after MCAo. DHA administration provides neurobehavioral recovery, reduces brain infarction and edema, and activates NPD1 synthesis in the penumbra when administered up to 5 h after focal cerebral ischemia in rats