Effective QCD Partition Function in Sectors with Non-Zero Topological Charge and Itzykson-Zuber Type Integral

It was conjectured by Jackson et.al. that the finite volume effective partition function of QCD with the topological charge $M-N$ coincides with the Itzyskon-Zuber type integral for $M\times N$ rectangular matrices. In the present article we give a proof of this conjecture, in which the original Itzykson-Zuber integral is utilized.Comment: 7pages, LaTeX2

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

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

Changes in Inflammatory Response after Endovascular Treatment for Type B Aortic Dissection

This present study aims to investigate the changes in the inflammatory markers after elective endovascular treatment of Type B aortic dissection with aneurysm, as related to different anatomical features of the dissection flap in the paravisceral perfusion. Consecutive patients with type B aortic dissections with elective endovascular stent graft repair were recruited and categorized into different groups. Serial plasma levels of cytokines (Interleukin-1β, -6, -8, -10, TNF-α), chemokines (MCP-1), and serum creatinine were monitored at pre-, peri- and post-operative stages. The length of stent graft employed in each surgery was retrieved and correlated with the change of all studied biochemical parameters. A control group of aortic dissected patients with conventional medication management was recruited for comparing the baseline biochemical parameters. In total, 22 endovascular treated and 16 aortic dissected patients with surveillance were recruited. The endovascular treated patients had comparable baseline levels as the non-surgical patients. There was no immediate or thirty day-mortality, and none of the surgical patients developed post-operative mesenteric ischaemia or clinically significant renal impairment. All surgical patients had detectable pro-inflammatory mediators, but none of the them showed any statistical significant surge in the peri-operative period except IL-1β and IL-6. Similar results were obtained when categorized into different groups. IL-1β and IL-6 showed maximal levels within hours of the endovascular procedure (range, 3.93 to 27.3 higher than baseline; p = 0.001), but returned to baseline 1 day post-operatively. The change of IL-1β and IL-6 at the stent graft deployment was statistically greater in longer stent graft (p>0.05). No significant changes were observed in the serum creatinine levels. In conclusion, elective endovascular repair of type B aortic dissection associated with insignificant changes in inflammatory mediators and creatinine. All levels fell toward basal levels post-operatively suggesting that thoracic endovascular aortic repair is rather less aggressive with insignificant inflammatory modulation

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

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