Critical points of the three-dimensional Bose-Hubbard model from on-site atom number fluctuations

We discuss how positions of critical points of the three-dimensional Bose-Hubbard model can be accurately obtained from variance of the on-site atom number operator, which can be experimentally measured. The idea that we explore is that the derivative of the variance, with respect to the parameter driving the transition, has a pronounced maximum close to critical points. We show that Quantum Monte Carlo studies of this maximum lead to precise determination of critical points for the superfluid-Mott insulator transition in systems with mean number of atoms per lattice site equal to one, two, and three. We also extract from such data the correlation-length critical exponent through the finite-size scaling analysis and discuss how the derivative of the variance can be reliably computed from numerical data for the variance. The same conclusions apply to the derivative of the nearest-neighbor correlation function, which can be obtained from routinely measured time-of-flight images.Comment: 15 pages, corrected typos, updated references, improvements in discussio

Regulation of the Endogenous Antioxidant Defense System in Diabetic Peripheral Neuropathy

Oxidative stress is implicated as a major contributor to the development of diabetes induced peripheral neuropathy. This debilitating condition significantly impacts the quality of life of patients, yet available treatment options are not optimal. They include tricyclic antidepressants, anticonvulsants, serotonin-norepinephrine reuptake inhibitors, selective serotonin reuptake inhibitors, and opiates. Unfortunately, these treatment options only reduce pain by 30-50%, and many patients discontinue use due to side effects. Furthermore, the current treatment options are focused on pain reduction, but not the protection of the peripheral nerves. Since oxidative stress driven by high glucose concentrations has been implicated as the key factor causing peripheral neuropathy, these studies focused on reducing or increasing protection against oxidative stress using dietary compounds with antioxidant properties to ameliorate diabetic peripheral neuropathy. Two dietary compounds with very different mechanisms of antioxidant protection were explored in detail, N-acetylcysteine (NAC) and 3H-1,2-dithiole-3-thione (D3T). To model diabetic peripheral neuropathy, differentiated SH-SY5Y cells were used and stressed with advanced glycation end products (AGE), which form as a result of high glucose concentrations in vivo and cause oxidative stress. In our initial studies, we showed that NAC conferred complete protection against AGE-induced neurite degeneration via a glutathione-mediated mechanism. These studies showed that maintenance of glutathione is critical for neurite structure, as inhibition of glutathione synthesis under non-stressed conditions resulted in significant neurite degeneration. Our next focus was on D3T, a potent nuclear factor (erythroid-derived 2)-like 2 (Nrf2) inducer. D3T generates its antioxidant effect though upregulation of endogenous cellular antioxidant defenses. Previous studies from our lab have shown that D3T treatment paradoxically exacerbates AGE-induced damage, and these prior results were confirmed in the present studies. The mechanism by which D3T potentiates damage was extensively studied. The results of the experiments indicated that D3T potentiates AGE-induced oxidative stress via two critical pathways in the cell-based system used. First, D3T upregulated the Nrf2 responsive gene glucose-6-phosphate dehydrogenase (G6PD), leading to increased G6PD protein expression. Increased expression of G6PD resulted in generation of reducing equivalents that are used by NADPH oxidases to generate superoxide. The oxidative stress damage caused by superoxide generation was then amplified by D3T-mediated reduction of glutathione reductase activity, which resulted in low cellular reduced glutathione concentrations and high oxidized glutathione concentrations. In this manner, D3T inhibited the effectiveness of the endogenous antioxidant defense system and led to disruption of the thiol redox state. In the final set of studies, we found that AGE-induced oxidative stress resulted in a significant increase of protein glutathionylation. Because D3T further disrupts the thiol redox state, it conferred no protection against AGE-induced protein glutathionylation. However, NAC, which was completely protective against AGE-induced neurite degeneration, was also able to fully protect against protein glutathionylation under challenged conditions. Based on the combined results, we conclude that maintenance of the thiol redox state is critical for maintaining neurite morphology, and antioxidants such as NAC that protect the thiol redox state will confer neurite protection in pro-oxidative conditions

Preparation and manipulation of a fault-tolerant superconducting qubit

We describe a qubit encoded in continuous quantum variables of an rf superconducting quantum interference device. Since the number of accessible states in the system is infinite, we may protect its two-dimensional subspace from small errors introduced by the interaction with the environment and during manipulations. We show how to prepare the fault-tolerant state and manipulate the system. The discussed operations suffice to perform quantum computation on the encoded state, syndrome extraction, and quantum error correction. We also comment on the physical sources of errors and possible imperfections while manipulating the system.Comment: Typo corrected, title changed as suggested by the editors of Phys. Rev. B, references adde

2-Aminopyrimidine-3,3,3-triphenyl- propanoic acid (1/1)

The title bimolecular compound, C4H5N3·C21H18O2, constructed from 2-aminopyrimidine and 3,3,3-triphenylpropanoic acid, forms a tetramolecular hydrogen-bonded motif via O—H...N, N—H...O and N—H...N contacts. This aggregate organizes to give crystal-packing motifs with hydrophilic and hydrophobic regions

The role of the mobile proton in fucose migration

Fucose migration reactions represent a substantial challenge in the analysis of fucosylated glycan structures by mass spectrometry. In addition to the well-established observation of transposed fucose residues in glycan-dissociation product ions, recent experiments show that the rearrangement can also occur in intact glycan ions. These results suggest a low-energy barrier for migration of the fucose residue and broaden the relevance of fucose migration to include other types of mass spectrometry experiments, including ion mobility-mass spectrometry and ion spectroscopy. In this work, we utilize cold-ion infrared spectroscopy to provide further insight into glycan scrambling in intact glycan ions. Our results show that the mobility of the proton is a prerequisite for the migration reaction. For the prototypical fucosylated glycans Lewis x and blood group antigen H-2, the formation of adduct ions or the addition of functional groups with variable proton affinity yields significant differences in the infrared spectra. These changes correlate well with the promotion or inhibition of fucose migration through the presence or absence of a mobile proton

Strange matter prospects within the string-flip model

In this contribution we extend the recently developed two-flavor quark-matter string-flip model by including strange quarks. We discuss implications for compact stars.Comment: 4 pages, 4 figures, proceedings to SQM201