Equilibrium states for the Bose gas

The generating functional of the cyclic representation of the CCR (Canonical Commutation Relations) representation for the thermodynamic limit of the grand canonical ensemble of the free Bose gas with attractive boundary conditions is rigorously computed. We use it to study the condensate localization as a function of the homothety point for the thermodynamic limit using a sequence of growing convex containers. The Kac function is explicitly obtained proving non-equivalence of ensembles in the condensate region in spite of the condensate density being zero locally.Comment: 21 pages, no figure

The N-terminal region of chromodomain helicase DNA-binding protein 4 (CHD4) is essential for activity and contains a high mobility group (HMG) box-like-domain that can bind poly(ADP-ribose)

Chromodomain Helicase DNA-binding protein 4 (CHD4) is a chromatin-remodeling enzyme that has been reported to regulate DNA-damage responses through its N-terminal region in a poly(ADP-ribose) polymerase-dependent manner. We have identified and determined the structure of a stable domain (CHD4-N) in this N-terminal region. The-fold consists of a four- -helix bundle with structural similarity to the high mobility group box, a domain that is well known as a DNA binding module. We show that the CHD4-N domain binds with higher affinity to poly(ADP-ribose) than to DNA. We also show that the N-terminal region of CHD4, although not CHD4-N alone, is essential for full nucleosome remodeling activity and is important for localizing CHD4 to sites of DNA damage. Overall, these data build on our understanding of how CHD4-NuRD acts to regulate gene expression and participates in the DNA-damage response

Accuracy in mineral identification: image spectral and spatial resolutions and mineral spectral properties

Problems related to airborne hyperspectral image data are reviewed and the requirements for data analysis applied to mineralogical (rocks and soils) interpretation are discussed. The variability of mineral spectral features, including absorption position, shape and depth is considered and interpreted as due to chemical composition, grain size effects and mineral association. It is also shown how this variability can be related to well defined geologic processes. The influence of sensor noise and diffuse atmospheric radiance in classification accuracy is also analyzed

The Varicella-Zoster Virus ORF47 Kinase Interferes with Host Innate Immune Response by Inhibiting the Activation of IRF3

The innate immune response constitutes the first line of host defence that limits viral spread and plays an important role in the activation of adaptive immune response. Viral components are recognized by specific host pathogen recognition receptors triggering the activation of IRF3. IRF3, along with NF-κB, is a key regulator of IFN-β expression. Until now, the role of IRF3 in the activation of the innate immune response during Varicella-Zoster Virus (VZV) infection has been poorly studied. In this work, we demonstrated for the first time that VZV rapidly induces an atypical phosphorylation of IRF3 that is inhibitory since it prevents subsequent IRF3 homodimerization and induction of target genes. Using a mutant virus unable to express the viral kinase ORF47p, we demonstrated that (i) IRF3 slower-migrating form disappears; (ii) IRF3 is phosphorylated on serine 396 again and recovers the ability to form homodimers; (iii) amounts of IRF3 target genes such as IFN-β and ISG15 mRNA are greater than in cells infected with the wild-type virus; and (iv) IRF3 physically interacts with ORF47p. These data led us to hypothesize that the viral kinase ORF47p is involved in the atypical phosphorylation of IRF3 during VZV infection, which prevents its homodimerization and subsequent induction of target genes such as IFN-β and ISG15

Pseudotumoural soft tissue lesions of the hand and wrist: a pictorial review

Mimickers of soft tissue tumours in the hand and wrist are more frequent than true neoplastic lesions. Pseudotumours belong to a large and heterogeneous group of disorders, varying from normal anatomical variants, cystic lesions, post-traumatic lesions, skin lesions, inflammatory and infectious lesions, non-neoplastic vascular lesions, metabolic disorders (crystal deposition disease and amyloidosis) and miscellaneous disorders. Although the imaging approach to pseudotumoural lesions is often very similar to the approach to “true” soft tissue tumoral counterparts, further management of these lesions is different. Biopsy should be performed only in doubtful cases, when the diagnosis is unclear. Therefore, the radiologist plays a pivotal role in the diagnosis of these lesions. Awareness of the normal anatomy and existence and common imaging presentation of these diseases, in combination with relevant clinical findings (clinical history, age, location and skin changes), enables the radiologist to make the correct diagnosis in most cases, thereby limiting the need for invasive procedures

Pseudotumoural soft tissue lesions of the foot and ankle: a pictorial review

In the foot and ankle region, benign neoplasms and pseudotumoural soft tissue lesions are significantly more frequent than malignant tumours. The pseudotumoural lesions constitute a heterogeneous group, with highly varied aetiology and histopathology. This article reviews the imaging features of the most common pseudotumours of the soft tissues in the foot and ankle. Although the imaging characteristics of several of the lesions discussed are non-specific, combining them with lesion location and clinical features allows the radiologist to suggest a specific diagnosis in most cases

A Gammaherpesvirus Cooperates with Interferon-alpha/beta-Induced IRF2 to Halt Viral Replication, Control Reactivation, and Minimize Host Lethality

The gammaherpesviruses, including Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV), establish latency in memory B lymphocytes and promote lymphoproliferative disease in immunocompromised individuals. The precise immune mechanisms that prevent gammaherpesvirus reactivation and tumorigenesis are poorly defined. Murine gammaherpesvirus 68 (MHV68) is closely related to EBV and KSHV, and type I (alpha/beta) interferons (IFNαβ) regulate MHV68 reactivation from both B cells and macrophages by unknown mechanisms. Here we demonstrate that IFNβ is highly upregulated during latent infection, in the absence of detectable MHV68 replication. We identify an interferon-stimulated response element (ISRE) in the MHV68 M2 gene promoter that is bound by the IFNαβ-induced transcriptional repressor IRF2 during latency in vivo. The M2 protein regulates B cell signaling to promote establishment of latency and reactivation. Virus lacking the M2 ISRE (ISREΔ) overexpresses M2 mRNA and displays uncontrolled acute replication in vivo, higher latent viral load, and aberrantly high reactivation from latency. These phenotypes of the ISREΔ mutant are B-cell-specific, require IRF2, and correlate with a significant increase in virulence in a model of acute viral pneumonia. We therefore identify a mechanism by which a gammaherpesvirus subverts host IFNαβ signaling in a surprisingly cooperative manner, to directly repress viral replication and reactivation and enforce latency, thereby minimizing acute host disease. Since we find ISREs 5′ to the major lymphocyte latency genes of multiple rodent, primate, and human gammaherpesviruses, we propose that cooperative subversion of IFNαβ-induced IRFs to promote latent infection is an ancient strategy that ensures a stable, minimally-pathogenic virus-host relationship

Rewriting DNA Methylation Signatures at Will:The Curable Genome Within Reach?

DNA methyltransferases are important enzymes in a broad range of organisms. Dysfunction of DNA methyltransferases in humans leads to many severe diseases, including cancer. This book focuses on the biochemical properties of these enzymes, describing their structures and mechanisms in bacteria, humans and other species, including plants, and also explains the biological processes of reading of DNA methylation and DNA demethylation. It covers many emerging aspects of the biological roles of DNA methylation functioning as an essential epigenetic mark and describes the role of DNA methylation in diseases. Moreover, the book explains modern technologies, like targeted rewriting of DNA methylation by designed DNA methyltransferases, as well as technological applications of DNA methyltransferases in DNA labelling. Finally, the book summarizes recent methods for the analysis of DNA methylation in human DNA. Overall, this book represents a comprehensive state-of-the-art- work and is a must-have for advanced researchers in the field of DNA methylation and epigenetics