Fermion Condensates of massless QED2QED_2 at Finite Density in non-trivial Topological Sectors

Vacuum expectation values of products of local bilinears $\bar\psi\psi$ are computed in massless $QED_2$ at finite density. It is shown that chiral condensates exhibit an oscillatory inhomogeneous behaviour depending on the chemical potential. The use of a path-integral approach clarifies the connection of this phenomenon with the topological structure of the theory.Comment: 16 pages, no figures, To be published in Phys.Rev.

Numerical study of the critical behavior of the Ashkin-Teller model at a line defect

We consider the Ashkin-Teller model on the square lattice, which is represented by two Ising models ($\sigma$ and $\tau$) having a four-spin coupling of strength, $\epsilon$, between them. We introduce an asymmetric defect line in the system along which the couplings in the $\sigma$ Ising model are modified. In the Hamiltonian version of the model we study the scaling behavior of the critical magnetization at the defect, both for $\sigma$ and for $\tau$ spins by density matrix renormalization. For $\epsilon>0$ we observe identical scaling for $\sigma$ and $\tau$ spins, whereas for $\epsilon<0$ one model becomes locally ordered and the other locally disordered. This is different of the critical behavior of the uncoupled model ($\epsilon=0$) and is in contradiction with the results of recent field-theoretical calculations.Comment: 6 pages, 4 figure

Multiflavor Correlation Functions in non-Abelian Gauge Theories at Finite Density in two dimensions

We compute vacuum expectation values of products of fermion bilinears for two-dimensional Quantum Chromodynamics at finite flavored fermion densities. We introduce the chemical potential as an external charge distribution within the path-integral approach and carefully analyse the contribution of different topological sectors to fermion correlators. We show the existence of chiral condensates exhibiting an oscillatory inhomogeneous behavior as a function of a chemical potential matrix. This result is exact and goes in the same direction as the behavior found in QCD_4 within the large N approximation.Comment: 28 pages Latex (3 pages added and other minor changes) to appear in Phys.Rev.

Renormalization of QCD_2

The low energy infrared scaling of the multi-color 2-dimensional quantum chromodynamics is determined in the framework of its bosonized model by using the functional renormalization group method with gliding sharp cut-off k in momentum space in the local potential approximation. The model exhibits a single phase with a superuniversal effective potential.Comment: 15 pages, 3 figures, final versio

Subjects With Early-Onset Type 2 Diabetes Show Defective Activation of the Skeletal Muscle PGC-1α/Mitofusin-2 Regulatory Pathway in Response to Physical Activity

Objective: Type 2 diabetes is associated with insulin resistance and skeletal muscle mitochondrial dysfunction. We have found that subjects with early-onset type 2 diabetes show incapacity to increase Vo2max in response to chronic exercise. This suggests a defect in muscle mitochondrial response to exercise. Here, we have explored the nature of the mechanisms involved. Research design and methods: Muscle biopsies were collected from young type 2 diabetic subjects and obese control subjects before and after acute or chronic exercise protocols, and the expression of genes and/or proteins relevant to mitochondrial function was measured. In particular, the regulatory pathway peroxisome proliferator-activated receptor gamma coactivator (PGC)-1alpha/mitofusin-2 (Mfn2) was analyzed. Results: At baseline, subjects with diabetes showed reduced expression (by 26%) of the mitochondrial fusion protein Mfn2 and a 39% reduction of the alpha-subunit of ATP synthase. Porin expression was unchanged, consistent with normal mitochondrial mass. Chronic exercise led to a 2.8-fold increase in Mfn2, as well as increases in porin, and the alpha-subunit of ATP synthase in muscle from control subjects. However, Mfn2 was unchanged after chronic exercise in individuals with diabetes, whereas porin and alpha-subunit of ATP synthase were increased. Acute exercise caused a fourfold increase in PGC-1alpha expression in muscle from control subjects but not in subjects with diabetes. Conclusions: Our results demonstrate alterations in the regulatory pathway that controls PGC-1alpha expression and induction of Mfn2 in muscle from patients with early-onset type 2 diabetes. Patients with early-onset type 2 diabetes display abnormalities in the exercise-dependent pathway that regulates the expression of PGC-1alpha and Mfn2.</p

QQˉQ{\bar Q} potential in the Schwinger model on curved space - time

We study the confining and screening aspects of the Schwinger model on curved static backgrounds.Comment: 14 pages, Latex. Typos corrected. Erratum submitte

Role of mitochondrial raft-like microdomains in the regulation of cell apoptosis

Lipid rafts are envisaged as lateral assemblies of specific lipids and proteins that dissociate and associate rapidly and form functional clusters in cell membranes. These structural platforms are not confined to the plasma membrane; indeed lipid microdomains are similarly formed at subcellular organelles, which include endoplasmic reticulum, Golgi and mitochondria, named raft-like microdomains. In addition, some components of raft-like microdomains are present within ER-mitochondria associated membranes. This review is focused on the role of mitochondrial raft-like microdomains in the regulation of cell apoptosis, since these microdomains may represent preferential sites where key reactions take place, regulating mitochondria hyperpolarization, fission-associated changes, megapore formation and release of apoptogenic factors. These structural platforms appear to modulate cytoplasmic pathways switching cell fate towards cell survival or death. Main insights on this issue derive from some pathological conditions in which alterations of microdomains structure or function can lead to severe alterations of cell activity and life span. In the light of the role played by raft-like microdomains to integrate apoptotic signals and in regulating mitochondrial dynamics, it is conceivable that these membrane structures may play a role in the mitochondrial alterations observed in some of the most common human neurodegenerative diseases, such as Amyotrophic lateral sclerosis, Huntington's chorea and prion-related diseases. These findings introduce an additional task for identifying new molecular target(s) of pharmacological agents in these pathologies

Production of D∗+(2010)D^{*+}(2010) mesons by high energy neutrinos from the Tevatron

Charged vector $D^{*+}(2010)$ meson production is studied in a high energy neutrino bubble chamber experiment with mean neutrino energy of 141 GeV. The $D^{*+}$ are produced in $(5.6 \pm 1.8)\%$ of the neutrino charged current interactions, indicating a steep increase of cross section with energy. The mean fractional hadronic energy of the $D^{*+}$ meson is $0.55 \pm 0.06$

A membrane-inserted structural model of the yeast mitofusin Fzo1

Mitofusins are large transmembrane GTPases of the dynamin-related protein family, and are required for the tethering and fusion of mitochondrial outer membranes. Their full-length structures remain unknown, which is a limiting factor in the study of outer membrane fusion. We investigated the structure and dynamics of the yeast mitofusin Fzo1 through a hybrid computational and experimental approach, combining molecular modelling and all-atom molecular dynamics simulations in a lipid bilayer with site-directed mutagenesis and in vivo functional assays. The predicted architecture of Fzo1 improves upon the current domain annotation, with a precise description of the helical spans linked by flexible hinges, which are likely of functional significance. In vivo site-directed mutagenesis validates salient aspects of this model, notably, the long-distance contacts and residues participating in hinges. GDP is predicted to interact with Fzo1 through the G1 and G4 motifs of the GTPase domain. The model reveals structural determinants critical for protein function, including regions that may be involved in GTPase domain-dependent rearrangements

The role of the mitochondria and the endoplasmic reticulum contact sites in the development of the immune responses

Abstract Mitochondria and endoplasmic reticulum (ER) contact sites (MERCs) are dynamic modules enriched in subset of lipids and specialized proteins that determine their structure and functions. The MERCs regulate lipid transfer, autophagosome formation, mitochondrial fission, Ca2+ homeostasis and apoptosis. Since these functions are essential for cell biology, it is therefore not surprising that MERCs also play a critical role in organ physiology among which the immune system stands by its critical host defense function. This defense system must discriminate and tolerate host cells and beneficial commensal microorganisms while eliminating pathogenic ones in order to preserve normal homeostasis. To meet this goal, the immune system has two lines of defense. First, the fast acting but unspecific innate immune system relies on anatomical physical barriers and subsets of hematopoietically derived cells expressing germline-encoded receptors called pattern recognition receptors (PRR) recognizing conserved motifs on the pathogens. Second, the slower but very specific adaptive immune response is added to complement innate immunity. Adaptive immunity relies on another set of specialized cells, the lymphocytes, harboring receptors requiring somatic recombination to be expressed. Both innate and adaptive immune cells must be activated to phagocytose and process pathogens, migrate, proliferate, release soluble factors and destroy infected cells. Some of these functions are strongly dependent on lipid transfer, autophagosome formation, mitochondrial fission, and Ca2+ flux; this indicates that MERCs could regulate immunity