Resonance Raman scattering studies in Br-2-adsorbed double-wall carbon nanotubes

ArticlePhysical Review B. 73(23):235413 (2006)journal articl

Conductance Fluctuations in Disordered Wires with Perfectly Conducting Channels

We study conductance fluctuations in disordered quantum wires with unitary symmetry focusing on the case in which the number of conducting channels in one propagating direction is not equal to that in the opposite direction. We consider disordered wires with $N+m$ left-moving channels and $N$ right-moving channels. In this case, $m$ left-moving channels become perfectly conducting, and the dimensionless conductance $g$ for the left-moving channels behaves as $g \to m$ in the long-wire limit. We obtain the variance of $g$ in the diffusive regime by using the Dorokhov-Mello-Pereyra-Kumar equation for transmission eigenvalues. It is shown that the universality of conductance fluctuations breaks down for $m \neq 0$ unless $N$ is very large.Comment: 6 pages, 2 figure

Asymptotic behavior of the conductance in disordered wires with perfectly conducting channels

We study the conductance of disordered wires with unitary symmetry focusing on the case in which $m$ perfectly conducting channels are present due to the channel-number imbalance between two-propagating directions. Using the exact solution of the Dorokhov-Mello-Pereyra-Kumar (DMPK) equation for transmission eigenvalues, we obtain the average and second moment of the conductance in the long-wire regime. For comparison, we employ the three-edge Chalker-Coddington model as the simplest example of channel-number-imbalanced systems with $m = 1$, and obtain the average and second moment of the conductance by using a supersymmetry approach. We show that the result for the Chalker-Coddington model is identical to that obtained from the DMPK equation.Comment: 20 pages, 1 figur

Conductance Distribution in Disordered Quantum Wires with a Perfectly Conducting Channel

We study the conductance of phase-coherent disordered quantum wires focusing on the case in which the number of conducting channels is imbalanced between two propagating directions. If the number of channels in one direction is by one greater than that in the opposite direction, one perfectly conducting channel without backscattering is stabilized regardless of wire length. Consequently, the dimensionless conductance does not vanish but converges to unity in the long-wire limit, indicating the absence of Anderson localization. To observe the influence of a perfectly conducting channel, we numerically obtain the distribution of conductance in both cases with and without a perfectly conducting channel. We show that the characteristic form of the distribution is notably modified in the presence of a perfectly conducting channel.Comment: 7 pages, 16 figure

In silico design of novel probes for the atypical opioid receptor MRGPRX2

The primate-exclusive MRGPRX2 G protein-coupled receptor (GPCR) has been suggested to modulate pain and itch. Despite putative peptide and small molecule MRGPRX2 agonists, selective nanomolar potency probes have not yet been reported. To identify a MRGPRX2 probe, we first screened 5,695 small molecules and found many opioid compounds activated MRGPRX2, including (−)- and (+)-morphine, hydrocodone, sinomenine, dextromethorphan and the prodynorphin-derived peptides, dynorphin A, dynorphin B, and α- and β-neoendorphin. We used these to select for mutagenesis-validated homology models and docked almost 4 million small molecules. From this docking, we predicted ZINC-3573, which represents a potent MRGPRX2-selective agonist, showing little activity against 315 other GPCRs and 97 representative kinases, and an essentially inactive enantiomer. ZINC-3573 activates endogenous MRGPRX2 in a human mast cell line inducing degranulation and calcium release. MRGPRX2 is a unique atypical opioid-like receptor important for modulating mast cell degranulation, which can now be specifically modulated with ZINC-3573

Genetic Ablation of Pannexin1 Protects Retinal Neurons from Ischemic Injury

Pannexin1 (Panx1) forms large nonselective membrane channel that is implicated in paracrine and inflammatory signaling. In vitro experiments suggested that Panx1 could play a key role in ischemic death of hippocampal neurons. Since retinal ganglion cells (RGCs) express high levels of Panx1 and are susceptible to ischemic induced injury, we hypothesized that Panx1 contributes to rapid and selective loss of these neurons in ischemia. To test this hypothesis, we induced experimental retinal ischemia followed by reperfusion in live animals with the Panx1 channel genetically ablated either in the entire mouse (Panx1 KO), or only in neurons using the conditional knockout (Panx1 CKO) technology. Here we report that two distinct neurotoxic processes are induced in RGCs by ischemia in the wild type mice but are inactivated in Panx1KO and Panx1 CKO animals. First, the post-ischemic permeation of RGC plasma membranes is suppressed, as assessed by dye transfer and calcium imaging assays ex vivo and in vitro. Second, the inflammasome-mediated activation of caspase-1 and the production of interleukin-1β in the Panx1 KO retinas are inhibited. Our findings indicate that post-ischemic neurotoxicity in the retina is mediated by previously uncharacterized pathways, which involve neuronal Panx1 and are intrinsic to RGCs. Thus, our work presents the in vivo evidence for neurotoxicity elicited by neuronal Panx1, and identifies this channel as a new therapeutic target in ischemic pathologies