Equilibrium Statistical Mechanics of Fermion Lattice Systems

We study equilibrium statistical mechanics of Fermion lattice systems which require a different treatment compared with spin lattice systems due to the non-commutativity of local algebras for disjoint regions. Our major result is the equivalence of the KMS condition and the variational principle with a minimal assumption for the dynamics and without any explicit assumption on the potential. It holds also for spin lattice systems as well, yielding a vast improvement over known results. All formulations are in terms of a C*-dynamical systems for the Fermion (CAR) algebra with all or a part of the following assumptions: (I) The interaction is even with respect to the Fermion number. (Automatically satisfied when (IV) below is assumed.) (II) All strictly local elements of the algebra have the first time derivative. (III) The time derivatives in (II) determine the dynamics. (IV) The interaction is lattice translation invariant. A major technical tool is the conditional expectation from the total algebra onto the local subalgebra for any finite subset of the lattice, which induces a system of commuting squares. This technique overcomes the lack of tensor product structures for Fermion systems and even simplifies many known arguments for spin lattice systems.Comment: 103 pages, no figure. The Section 13 has become simpler and a problem in 14.1 is settled thanks to a referee. The format has been revised according to the suggestion of this and the other referee

The integral cohomology rings of some p-groups

We determine the integral cohomology rings of an infinite family of p-groups, for odd primes p, with cyclic derived subgroups. Our method involves embedding the groups in a compact Lie group of dimension one, and was suggested by P H Kropholler and J Huebschmann

Strongly thixotropic viscosity behavior of dimethylsulfoxide solution of polyrotaxane comprising alpha-cyclodextrin and low molecular weight poly(ethylene glycol)

ArticlePOLYMER. 48(24): 7139-7144 (2007)journal articl

Universal fermionization of bosons on permutative representations of the Cuntz algebra O2{\cal O}_{2}

Bosons and fermions are described by using canonical generators of Cuntz algebras on any permutative representation. We show a fermionization of bosons which universally holds on any permutative representation of the Cuntz algebra ${\cal O}_{2}$. As examples, we show fermionizations on the Fock space and the infinite wedge.Comment: 12 page

Bayesian Value-of-Information Analysis: An Application to a Policy Model of Alzheimer's Disease

A framework is presented which distinguishes the conceptually separate decisions of which treatment strategy is optimal from the question of whether more information is required to inform this choice in the future. The authors argue that the choice of treatment strategy should be based on expected utility and the only valid reason to characterise the uncertainty surrounding outcomes of interest is to establish the value of acquiring additional information. A Bayesian decision theoretic approach is demonstrated though a probabilistic analysis of a published policy model of Alzheimer’s disease. The expected value of perfect information is estimated for the decision to adopt a new pharmaceutical for the population of US Alzheimer’s disease patients. This provides an upper bound on the value of additional research. The value of information is also estimated for each of the model inputs. This analysis can focus future research by identifying those parameters where more precise estimates would be most valuable, and indicating whether an experimental design would be required. We also discuss how this type of analysis can also be used to design experimental research efficiently (identifying optimal sample size and optimal sample allocation) based on the marginal cost and marginal benefit of sample information. Value-of-information analysis can provide a measure of the expected payoff from proposed research, which can be used to set priorities in research and development. It can also inform an efficient regulatory framework for new health care technologies: an analysis of the value of information would define when a claim for a new technology should be deemed “substantiated” and when evidence should be considered “competent and reliable” when it is not cost-effective to gather anymore information.stochastic CEA; Bayesian decision theory; value of information.

Gorenstein duality for real spectra

Following Hu and Kriz, we study the C 2 -spectra BPℝ⟨n⟩hni and Eℝ(n) that refine the usual truncated Brown-Peterson and the Johnson-Wilson spectra. In particular, we show that they satisfy Gorenstein duality with a representation grading shift and identify their Anderson duals. We also compute the associated local cohomology spectral sequence in the cases n = 1 and 2

Identification of the protein kinases Pyk3 and Phg2 as regulators of the STATc-mediated response to hyperosmolarity

Cellular adaptation to changes in environmental osmolarity is crucial for cell survival. In Dictyostelium, STATc is a key regulator of the transcriptional response to hyperosmotic stress. Its phosphorylation and consequent activation is controlled by two signaling branches, one cGMP- and the other Ca(2+)-dependent, of which many signaling components have yet to be identified. The STATc stress signalling pathway feeds back on itself by upregulating the expression of STATc and STATc-regulated genes. Based on microarray studies we chose two tyrosine-kinase like proteins, Pyk3 and Phg2, as possible modulators of STATc phosphorylation and generated single and double knock-out mutants to them. Transcriptional regulation of STATc and STATc dependent genes was disturbed in pyk3(-), phg2(-), and pyk3(-)/phg2(-) cells. The absence of Pyk3 and/or Phg2 resulted in diminished or completely abolished increased transcription of STATc dependent genes in response to sorbitol, 8-Br-cGMP and the Ca(2+) liberator BHQ. Also, phospho-STATc levels were significantly reduced in pyk3(-) and phg2(-) cells and even further decreased in pyk3(-)/phg2(-) cells. The reduced phosphorylation was mirrored by a significant delay in nuclear translocation of GFP-STATc. The protein tyrosine phosphatase 3 (PTP3), which dephosphorylates and inhibits STATc, is inhibited by stress-induced phosphorylation on S448 and S747. Use of phosphoserine specific antibodies showed that Phg2 but not Pyk3 is involved in the phosphorylation of PTP3 on S747. In pull-down assays Phg2 and PTP3 interact directly, suggesting that Phg2 phosphorylates PTP3 on S747 in vivo. Phosphorylation of S448 was unchanged in phg2(-) cells. We show that Phg2 and an, as yet unknown, S448 protein kinase are responsible for PTP3 phosphorylation and hence its inhibition, and that Pyk3 is involved in the regulation of STATc by either directly or indirectly activating it. Our results add further complexities to the regulation of STATc, which presumably ensure its optimal activation in response to different environmental cues

Thermal Quantum Fields without Cut-offs in 1+1 Space-time Dimensions

We construct interacting quantum fields in 1+1 dimensional Minkowski space, representing neutral scalar bosons at positive temperature. Our work is based on prior work by Klein and Landau and Hoegh-KrohnComment: 48 page

Inactivation of mammalian Ero 1α is catalysed by specific protein disulfide isomerases

Disulfide formation within the endoplasmic reticulum is a complex process requiring a disulfide exchange protein such as protein disulfide isomerase and a mechanism to form disulfides de novo. In mammalian cells, the major pathway for de novo disulfide formation involves the enzyme Ero1α which couples oxidation of thiols to the reduction of molecular oxygen to form hydrogen peroxide. Ero1α activity is tightly regulated by a mechanism that requires the formation of regulatory disulfides. These regulatory disulfides are reduced to activate and reform to inactive the enzyme. To investigate the mechanism of inactivation we analysed regulatory disulfide formation in the presence of various oxidants under controlled oxygen concentration. Neither molecular oxygen, nor hydrogen peroxide was able to oxidise Ero1α efficiently to form the correct regulatory disulfides. However, specific members of the PDI family such as PDI or ERp46 were able to catalyse this process. Further studies showed that both active sites of PDI contribute to the formation of regulatory disulfides in Ero1α and that the PDI substrate binding domain is crucial to allow electron transfer between the two enzymes. These results demonstrate a simple feedback mechanism of regulation of mammalian Ero1α involving its primary substrate