The Bjorken sum rule with Monte Carlo and Neural Network techniques

Determinations of structure functions and parton distribution functions have been recently obtained using Monte Carlo methods and neural networks as universal, unbiased interpolants for the unknown functional dependence. In this work the same methods are applied to obtain a parametrization of polarized Deep Inelastic Scattering (DIS) structure functions. The Monte Carlo approach provides a bias--free determination of the probability measure in the space of structure functions, while retaining all the information on experimental errors and correlations. In particular the error on the data is propagated into an error on the structure functions that has a clear statistical meaning. We present the application of this method to the parametrization from polarized DIS data of the photon asymmetries $A_1^p$ and $A_1^d$ from which we determine the structure functions $g_1^p(x,Q^2)$ and $g_1^d(x,Q^2)$, and discuss the possibility to extract physical parameters from these parametrizations. This work can be used as a starting point for the determination of polarized parton distributions.Comment: 24 pages, 6 figure

Heme Oxygenase-1 Expression Affects Murine Abdominal Aortic Aneurysm Progression.

Heme oxygenase-1 (HO-1), the rate-limiting enzyme in heme degradation, is a cytoprotective enzyme upregulated in the vasculature by increased flow and inflammatory stimuli. Human genetic data suggest that a diminished HO-1 expression may predispose one to abdominal aortic aneurysm (AAA) development. In addition, heme is known to strongly induce HO-1 expression. Utilizing the porcine pancreatic elastase (PPE) model of AAA induction in HO-1 heterozygous (HO-1+/-, HO-1 Het) mice, we found that a deficiency in HO-1 leads to augmented AAA development. Peritoneal macrophages from HO-1+/- mice showed increased gene expression of pro-inflammatory cytokines, including MCP-1, TNF-alpha, IL-1-beta, and IL-6, but decreased expression of anti-inflammatory cytokines IL-10 and TGF-beta. Furthermore, treatment with heme returned AAA progression in HO-1 Het mice to a wild-type profile. Using a second murine AAA model (Ang II-ApoE-/-), we showed that low doses of the HMG-CoA reductase inhibitor rosuvastatin can induce HO-1 expression in aortic tissue and suppress AAA progression in the absence of lipid lowering. Our results support those studies that suggest that pleiotropic statin effects might be beneficial in AAA, possibly through the upregulation of HO-1. Specific targeted therapies designed to induce HO-1 could become an adjunctive therapeutic strategy for the prevention of AAA disease

Mean-Field Equations for Spin Models with Orthogonal Interaction Matrices

We study the metastable states in Ising spin models with orthogonal interaction matrices. We focus on three realizations of this model, the random case and two non-random cases, i.e.\ the fully-frustrated model on an infinite dimensional hypercube and the so-called sine-model. We use the mean-field (or {\sc tap}) equations which we derive by resuming the high-temperature expansion of the Gibbs free energy. In some special non-random cases, we can find the absolute minimum of the free energy. For the random case we compute the average number of solutions to the {\sc tap} equations. We find that the configurational entropy (or complexity) is extensive in the range T_{\mbox{\tiny RSB}}. Finally we present an apparently unrelated replica calculation which reproduces the analytical expression for the total number of {\sc tap} solutions.Comment: 22+3 pages, section 5 slightly modified, 1 Ref added, LaTeX and uuencoded figures now independent of each other (easier to print). Postscript available http://chimera.roma1.infn.it/index_papers_complex.htm

Loop Quantum Gravity: An Inside View

This is a (relatively) non -- technical summary of the status of the quantum dynamics in Loop Quantum Gravity (LQG). We explain in detail the historical evolution of the subject and why the results obtained so far are non -- trivial. The present text can be viewed in part as a response to an article by Nicolai, Peeters and Zamaklar [hep-th/0501114]. We also explain why certain no go conclusions drawn from a mathematically correct calculation in a recent paper by Helling et al [hep-th/0409182] are physically incorrect.Comment: 58 pages, no figure

Working Group Report on the Structure of the Proton

We summarize the developments on the structure of the proton that were studied at the Workshop on "HERA Physics" that was held in Durham in September 1995. We survey the latest structure function data; we overview the QCD interpretations of the measurements of the structure functions and of final state processes; we discuss charm production and the spin properties of the proton.Comment: 45 pages, latex file using epsfig and ioplppt macros. Figures included, but full resolution figure files and postscript file of the whole paper are available via anonymous ftp at ftp://cpt1.dur.ac.uk/pub/preprints/dtp96/dtp962

Chromatin Remodeling Pathways in Smooth Muscle Cell Differentiation, and Evidence for an Integral Role for p300

Phenotypic alteration of vascular smooth muscle cells (SMC) in response to injury or inflammation is an essential component of vascular disease. Evidence suggests that this process is dependent on epigenetic regulatory processes. P300, a histone acetyltransferase (HAT), activates crucial muscle-specific promoters in terminal (non-SMC) myocyte differentiation, and may be essential to SMC modulation as well.We performed a subanalysis examining transcriptional time-course microarray data obtained using the A404 model of SMC differentiation. Numerous chromatin remodeling genes (up to 62% of such genes on our array platform) showed significant regulation during differentiation. Members of several chromatin-remodeling families demonstrated involvement, including factors instrumental in histone modification, chromatin assembly-disassembly and DNA silencing, suggesting complex, multi-level systemic epigenetic regulation. Further, trichostatin A, a histone deacetylase inhibitor, accelerated expression of SMC differentiation markers in this model. Ontology analysis indicated a high degree of p300 involvement in SMC differentiation, with 60.7% of the known p300 interactome showing significant expression changes. Knockdown of p300 expression accelerated SMC differentiation in A404 cells and human SMCs, while inhibition of p300 HAT activity blunted SMC differentiation. The results suggest a central but complex role for p300 in SMC phenotypic modulation.Our results support the hypothesis that chromatin remodeling is important for SMC phenotypic switching, and detail wide-ranging involvement of several epigenetic modification families. Additionally, the transcriptional coactivator p300 may be partially degraded during SMC differentiation, leaving an activated subpopulation with increased HAT activity and SMC differentiation-gene specificity

Porphyromonas endodontalis in chronic periodontitis: a clinical and microbiological cross-sectional study

Although previous studies have shown the presence of Porphyromonas endodontalis in chronic periodontitis associated with periapical lesions, the occurrence of this pathogen in diseased periodontal sites without periapical lesions has been poorly investigated.The aims of this study were to quantify P. endodontalis in patients with chronic periodontitis without periapical lesions, to evaluate the potential correlation of P. endodontalis with Porphyromonas gingivalis and Tannerella forsythia, and to evaluate the ability of periodontal treatment to reduce these pathogens.Patients with generalized chronic periodontitis were selected by recording clinical attachment level (CAL), probing depth (PD), and bleeding on probing (BOP). Subgingival samples from 30 diseased nonadjacent sites (CAL ≥ 5 mm, PD between 5 and 7 mm and positive BOP) and 30 healthy nonadjacent sites (PD ≤ 3 mm and negative BOP) were collected and subjected to microbial analysis by quantitative polymerase chain reaction (qPCR) The variables of age, PD, CAL and BOP of all individuals were analyzed using the paired t-test (GrapPad Prism5®). Data of bacteria quantification were subjected to a normality test (D'Agostino-Pearson Test). For bacterial correlation analysis, the Spearman correlation was used.Our results showed that diseased sites had significantly higher levels of P. endodontalis compared to healthy sites, similar to the results obtained for P. gingivalis and T. forsythia. The numbers of all bacterial species were reduced significantly after mechanical periodontal treatment. P. endodontalis was significantly correlated with the presence of T. forsythia and P. gingivalis in the diseased group.Our results suggest that there is a high prevalence of P. endodontalis, P. gingivalis and T. forsythia in periodontitis sites and that mechanical periodontal treatment is effective at reducing the pathogens studied

Human pluripotent embryonal carcinoma NTERA2 cl.D1 cells maintain their typical morphology in an angiomyogenic medium

BACKGROUND: Pluripotent embryonal carcinomas are good potential models, to study, "in vitro," the mechanisms that control differentiation during embryogenesis. The NTERA2cl.D1 (NT2/D1) cell line is a well known system of ectodermal differentiation. Retinoic acid (RA) induces a dorsal pattern of differentiation (essentially neurons) and bone morphogenetic protein (BMP) or hexamethylenebisacetamide (HMBA) induces a more ventral (epidermal) pattern of differentiation. However, whether these human cells could give rise to mesoderm derivatives as their counterpart in mouse remained elusive. We analyzed the morphological characteristics and transcriptional activation of genes pertinent in cardiac muscle and endothelium differentiation, during the growth of NT2/D1 cells in an inductive angiomyogenic medium with or without Bone Morphogenetic Protein 2 (BMP2). RESULTS: Our experiments showed that NT2/D1 maintains their typical actin organization in angiomyogenic medium. Although the beta myosin heavy chain gene was never detected, all the other 15 genes analyzed maintained their expression throughout the time course of the experiment. Among them were early and late cardiac, endothelial, neuronal and teratocarcinoma genes. CONCLUSION: Our results suggest that despite the NT2/D1 cells natural tendency to differentiate into neuroectodermal lineages, they can activate genes of mesodermal lineages. Therefore, we believe that these pluripotent cells might still be a good model to study biological development of mesodermal derivatives, provided the right culture conditions are met

Epigenetic modifications in cardiovascular disease

Epigenetics represents a phenomenon of altered heritable phenotypic expression of genetic information occurring without changes in DNA sequence. Epigenetic modifications control embryonic development, differentiation and stem cell (re)programming. These modifications can be affected by exogenous stimuli (e.g., diabetic milieu, smoking) and oftentimes culminate in disease initiation. DNA methylation has been studied extensively and represents a well-understood epigenetic mechanism. During this process cytosine residues preceding a guanosine in the DNA sequence are methylated. CpG-islands are short-interspersed DNA sequences with clusters of CG sequences. The abnormal methylation of CpG islands in the promoter region of genes leads to a silencing of genetic information and finally to alteration of biological function. Emerging data suggest that these epigenetic modifications also impact on the development of cardiovascular disease. Histone modifications lead to the modulation of the expression of genetic information through modification of DNA accessibility. In addition, RNA-based mechanisms (e.g., microRNAs and long non-coding RNAs) influence the development of disease. We here outline the recent work pertaining to epigenetic changes in a cardiovascular disease setting