Work and Quantum Phase Transitions: Is there Quantum Latency?

We study the physics of quantum phase transitions from the perspective of non-equilibrium thermodynamics. For first order quantum phase transitions, we find that the average work done per quench in crossing the critical point is discontinuous. This leads us to introduce the quantum latent work in analogy with the classical latent heat of first order classical phase transitions. For second order quantum phase transitions the irreversible work is closely related to the fidelity susceptibility for weak sudden quenches of the system Hamiltonian. We demonstrate our ideas with numerical simulations of first, second, and infinite order phase transitions in various spin chain models.Comment: accepted in PR

Charge transport and recombination of dye sensitized 1D nanostructured-TiO2 films prepared by reactive sputtering

Dye sensitized solar cells (DSCs) are governed by light absorption, charge injection, electron transport and recombination and electrolyte diffusion. One way to improve the efficiency of these devices is by the design of highly ordered nanostructured semiconductor materials.The advantages can be two-fold: Firstly charge transport within the metal-oxide can be enhanced and hence thicker films can be employed and secondly, the complete permeation with a solid-state hole-transport medium of the sensitized metal-oxide can be facilitated. Nanostructured materials should promote vectorial electron diffusion and have as few recombination sights as possible so as to further enhance electron lifetimes and electron collection efficiencies. These materials should also have a high surface area so as to allow for efficient dye-loading and hence light absorption. Highly ordered TiO2 nanostructured films were prepared by reactive sputtering and their charge transport characteristics evaluated in DSCs. These were compared to DSCs employing mesoporous TiO2 films prepared by doctor blade technique using commercial paste. Charge transport characteristics were evaluated by impedance spectroscopy (IS), incident photon to current conversion efficiencies (IPCE) and current-voltage (iV) curves under simulated AM1.5G irradiation. Film morphology and structural properties were evaluated by scanning electron microscopy (SEM) and X-ray diffraction (XRD), respectively

Initiation and evolution of phase separation in heteroepitaxial InAlAs films

We have investigated the initiation and evolution of phase separation in heteroepitaxial InAlAs films. In misfit-free InAlAs layers, cross-sectional scanning tunneling microscopy (XSTM) reveals the presence of isotropic nanometer-sized clusters. For lattice-mismatched InAlAs layers with 1.2% misfit, quasiperiodic contrast modulations perpendicular to the growth direction are apparent. Interestingly, these lateral modulations are apparently initiated within the first few bilayers of film growth, and both the amplitude and wavelength of the modulations increase with film thickness. The saturation value of the modulation wavelength determined from XSTM coincides with the lateral superlattice period determined from (002) x-ray reciprocal space maps, suggesting that the lateral modulation wavelength represents a periodic composition variation. Together, these results suggest that phase separation in the heteroepitaxial InAlAs thin-film system is a misfit-driven kinetic process initiated by random compositional nonuniformities, which later develop into coupled compositional and surface morphological variations. © 2002 American Institute of Physics.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/69359/2/APPLAB-80-18-3292-1.pd

Enterohemorrhagic Escherichia coli O157∶H7 Gene Expression Profiling in Response to Growth in the Presence of Host Epithelia

BACKGROUND: The pathogenesis of enterohemorrhagic Escherichia coli (EHEC) O157:H7 infection is attributed to virulence factors encoded on multiple pathogenicity islands. Previous studies have shown that EHEC O157:H7 modulates host cell signal transduction cascades, independent of toxins and rearrangement of the cytoskeleton. However, the virulence factors and mechanisms responsible for EHEC-mediated subversion of signal transduction remain to be determined. Therefore, the purpose of this study was to first identify differentially regulated genes in response to EHEC O157:H7 grown in the presence of epithelial cells, compared to growth in the absence of epithelial cells (that is, growth in minimal essential tissue culture medium alone, minimal essential tissue culture medium in the presence of 5% CO(2), and Penassay broth alone) and, second, to identify EHEC virulence factors responsible for pathogen modulation of host cell signal transduction. METHODOLOGY/PRINCIPAL FINDINGS: Overnight cultures of EHEC O157:H7 were incubated for 6 hr at 37 degrees C in the presence or absence of confluent epithelial (HEp-2) cells. Total RNA was then extracted and used for microarray analyses (Affymetrix E. coli Genome 2.0 gene chips). Relative to bacteria grown in each of the other conditions, EHEC O157:H7 cultured in the presence of cultured epithelial cells displayed a distinct gene-expression profile. A 2.0-fold increase in the expression of 71 genes and a 2.0-fold decrease in expression of 60 other genes were identified in EHEC O157:H7 grown in the presence of epithelial cells, compared to bacteria grown in media alone. CONCLUSION/SIGNIFICANCE: Microarray analyses and gene deletion identified a protease on O-island 50, gene Z1787, as a potential virulence factor responsible for mediating EHEC inhibition of the interferon (IFN)-gamma-Jak1,2-STAT-1 signal transduction cascade. Up-regulated genes provide novel targets for use in developing strategies to interrupt the infectious process

Design and Mechanism of (S)-3-Amino-4-(difluoromethylenyl)cyclopent-1-ene-1-carboxylic Acid, a Highly Potent γ-Aminobutyric Acid Aminotransferase Inactivator for the Treatment of Addiction

© 2018 American Chemical Society. γ-Aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the central nervous system. Inhibition of GABA aminotransferase (GABA-AT), a pyridoxal 5′-phosphate (PLP)-dependent enzyme that degrades GABA, has been established as a possible strategy for the treatment of substance abuse. The raised GABA levels that occur as a consequence of this inhibition have been found to antagonize the rapid release of dopamine in the ventral striatum (nucleus accumbens) that follows an acute challenge by an addictive substance. In addition, increased GABA levels are also known to elicit an anticonvulsant effect in patients with epilepsy. We previously designed the mechanism-based inactivator (1S,3S)-3-amino-4-difluoromethylenyl-1-cyclopentanoic acid (2), now called CPP-115, that is 186 times more efficient in inactivating GABA-AT than vigabatrin, the only FDA-approved drug that is an inactivator of GABA-AT. CPP-115 was found to have high therapeutic potential for the treatment of cocaine addiction and for a variety of epilepsies, has successfully completed a Phase I safety clinical trial, and was found to be effective in the treatment of infantile spasms (West syndrome). Herein we report the design, using molecular dynamics simulations, synthesis, and biological evaluation of a new mechanism-based inactivator, (S)-3-amino-4-(difluoromethylenyl)cyclopent-1-ene-1-carboxylic acid (5), which was found to be almost 10 times more efficient as an inactivator of GABA-AT than CPP-115. We also present the unexpected crystal structure of 5 bound to GABA-AT, as well as computational analyses used to assist the structure elucidation process. Furthermore, 5 was found to have favorable pharmacokinetic properties and low off-target activities. In vivo studies in freely moving rats showed that 5 was dramatically superior to CPP-115 in suppressing the release of dopamine in the corpus striatum, which occurs subsequent to either an acute cocaine or nicotine challenge. Compound 5 also attenuated increased metabolic demands (neuronal glucose metabolism) in the hippocampus, a brain region that encodes spatial information concerning the environment in which an animal receives a reinforcing or aversive drug. This multidisciplinary computational design to preclinical efficacy approach should be applicable to the design and improvement of mechanism-based inhibitors of other enzymes whose crystal structures and inactivation mechanisms are known