Built-up structure criticality

The built-up land represents an important type of overall landscape. In this paper the built-up land structure in the largest cities in the Czech Republic and selected cities in the U.S.A. is analysed using the framework of statistical physics. We calculate the variance of the built-up area and the number variance of built-up landed plots in discs. In both cases the variance as a function of a disc radius follows a power law. The obtained values of power law exponents are comparable through different cities. The study is based on cadastral data from the Czech Republic and building footprints from GIS data in the U.S.A.Comment: 14 pages, 11 figure

Chromosomal alterations in atherosclerotic plaques

Alterations of chromosomes 7 and 11 have been involved in the progression of atherosclerosis. Twenty-three carotid endarterectomy specimens were studied for the presence of alterations in chromosomes 7 and 11, and fibroblastic growth factor-3 (FGF-3) gene amplification. Besides classic histological stainings, immunophenotyping of cellular and vascular components and fluorescence in situ hybridization (FISH) were performed. At the caps, unstable plaques (n = 18) showed inflammatory infiltration of macrophages, smooth muscle cells, and T-lymphocytes. Specifically in these regions, the FISH showed varying percentages of trisomy (15/18) and tetrasomy (8/15) of chromosome 7. In four cases polisomy 7 was noted in some nuclei. Monosomy of chromosome 11 and gene amplification of FGF-3 gene was observed. The FISH of the five stable plaques and normal arterial walls showed no chromosome alterations; furthermore, chromosome 3, which is not involved in atherosclerotic progression, presented a normal ploidy of smooth muscle cells in stable and unstable plaques and normal arterial walls. In conclusion, chromosome 7 and 11 alterations and FGF-3 gene amplification are components of unstable plaques, and might contribute to the evolution of stable plaques into complicated plaques.Fil: Matturri, Luigi. Universidad de Buenos Aires. Facultad de Medicina; ArgentinaFil: Cazzullo, Alessandra. Universidad de Buenos Aires. Facultad de Medicina; ArgentinaFil: Turconi, Paola. Universidad de Buenos Aires. Facultad de Medicina; ArgentinaFil: Lavezzi, Anna Maria. Universidad de Buenos Aires. Facultad de Medicina; ArgentinaFil: Vandone, Pier Luigi. Universidad de Buenos Aires. Facultad de Medicina; ArgentinaFil: Gabrielli, Livio. Universidad de Buenos Aires. Facultad de Medicina; ArgentinaFil: Fernández Alonso, Graciela. Universidad de Buenos Aires. Facultad de Medicina; ArgentinaFil: Grana, Daniel Rodolfo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; ArgentinaFil: Milei, Jose. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentin

Application of a Machine Learning Technology in the Definition of Metabolically Healthy and Unhealthy Status: A Retrospective Study of 2567 Subjects Suffering from Obesity with or without Metabolic Syndrome.

The key factors playing a role in the pathogenesis of metabolic alterations observed in many patients with obesity have not been fully characterized. Their identification is crucial, and it would represent a fundamental step towards better management of this urgent public health issue. This aim could be accomplished by exploiting the potential of machine learning (ML) technology. In a single-centre study (n = 2567), we used an ML analysis to cluster patients with metabolically healthy (MHO) or metabolically unhealthy (MUO) obesity, based on several clinical and biochemical variables. The first model provided by ML was able to predict the presence/absence of MHO with an accuracy of 66.67% and 72.15%, respectively, and included the following parameters: HOMA-IR, upper body fat/lower body fat, glycosylated haemoglobin, red blood cells, age, alanine aminotransferase, uric acid, white blood cells, insulin-like growth factor 1 (IGF-1) and gamma-glutamyl transferase. For each of these parameters, ML provided threshold values identifying either MUO or MHO. A second model including IGF-1 zSDS, a surrogate marker of IGF-1 normalized by age and sex, was even more accurate with a 71.84% and 72.3% precision, respectively. Our results demonstrated high IGF-1 levels in MHO patients, thus highlighting a possible role of IGF-1 as a novel metabolic health parameter to effectively predict the development of MUO using ML technology

The QCD Chiral Condensate from the Lattice

We determine the chiral condensate from simulations of quenched lattice QCD with Wilson fermions. Our measurements have been obtained with high statistics at three values of the gauge coupling, corresponding to UV cutoffs in the range 2 - 4 GeV. Several improvements have been made with respect to earlier lattice computations. The most important are the non-perturbative renormalization of the condensate, the use of the tree-level improved Clover action and the reduction of the systematic error due to uncertainties in the lattice calibration. Our result for the chiral condensate in the \msbar scheme is (\bar\psi \psi)^{\msbar}(mu = 2 GeV) = - 0.0147(8)(16)(12) GeV^3 = - [245(4)(9)(7) MeV]^3 where the first error is statistical, the second is due to the non-perturbative renormalization and the third due to the lattice calibration.Comment: 34 pages, latex, no figures. Some references and the value of the chiral condensate at 1 GeV added, no conclusions change

Determination of the respiratory compensation point by detecting changes in intercostal muscles oxygenation by using near-infrared spectroscopy

This study aimed to evaluate if the changes in oxygen saturation levels at intercostal muscles (SmO2-m.intercostales) assessed by near-infrared spectroscopy (NIRS) using a wearable device could determine the respiratory compensation point (RCP) during exercise. Fifteen healthy competitive triathletes (8 male; 29±6 years; height 167.6±25.6 cm; weight 69.2±9.4 kg; V ̇O2-máx 58.4±8.1 mL·kg-1·min-1) were evaluated in a cycle ergometer during the maximal oxygen-uptake test (V ̇O2-máx), while lung ventilation (V ̇E), power output (watts, W) and SmO2-m.intercostales were measured. RCP was determined by visual method (RCPvisual: changes at ventilatory equivalents (V ̇E·V ̇CO2-1, V ̇E·V ̇O2-1) and end-tidal respiratory pressure (PetO2, PetCO2) and NIRS method (RCPNIRS: breakpoint of fall in SmO2-m.intercostales). During exercise, SmO2-m.intercostales decreased continuously showing a higher decrease when V ̇E increased abruptly. A good agreement between methods used to determine RCP was found (visual vs NIRS) at %V ̇O2-máx, V ̇O2, V ̇E, and W (Bland-Altman test). Correlations were found to each parameters analyzed (r=0.854; r=0.865; r=0.981; and r=0,968; respectively. p<0.001 in all variables, Pearson test), with no differences (p<0.001 in all variables, t-student test) between methods used (RCPvisual and RCPNIRS). We concluded that changes at SmO2-m.intercostales measured by NIRS could adequately determine RCP in triathletes

Targeted DNA oxidation by LSD1–SMAD2/3 primes TGF-β1/ EMT genes for activation or repression

Abstract The epithelial-to-mesenchymal transition (EMT) is a complex transcriptional program induced by transforming growth factor β1 (TGF-β1). Histone lysine-specific demethylase 1 (LSD1) has been recognized as a key mediator of EMT in cancer cells, but the precise mechanism that underlies the activation and repression of EMT genes still remains elusive. Here, we characterized the early events induced by TGF-β1 during EMT initiation and establishment. TGF-β1 triggered, 30–90 min post-treatment, a nuclear oxidative wave throughout the genome, documented by confocal microscopy and mass spectrometry, mediated by LSD1. LSD1 was recruited with phosphorylated SMAD2/3 to the promoters of prototypic genes activated and repressed by TGF-β1. After 90 min, phospho-SMAD2/3 downregulation reduced the complex and LSD1 was then recruited with the newly synthesized SNAI1 and repressors, NCoR1 and HDAC3, to the promoters of TGF-β1-repressed genes such as the Wnt soluble inhibitor factor 1 gene (WIF1), a change that induced a late oxidative burst. However, TGF-β1 early (90 min) repression of transcription also required synchronous signaling by reactive oxygen species and the stress-activated kinase c-Jun N-terminal kinase. These data elucidate the early events elicited by TGF-β1 and the priming role of DNA oxidation that marks TGF-β1-induced and -repressed genes involved in the EMT

Development of a Mass Sensitive Quartz Crystal Microbalance (QCM)-Based DNA Biosensor Using a 50 MHz Electronic Oscillator Circuit

This work deals with the design of a high sensitivity DNA sequence detector using a 50 MHz quartz crystal microbalance (QCM) electronic oscillator circuit. The oscillator circuitry is based on Miller topology, which is able to work in damping media. Calibration and experimental study of frequency noise are carried out, finding that the designed sensor has a resolution of 7.1 ng/cm2 in dynamic conditions (with circulation of liquid). Then the oscillator is proved as DNA biosensor. Results show that the system is able to detect the presence of complementary target DNAs in a solution with high selectivity and sensitivity. DNA target concentrations higher of 50 ng/mL can be detected

Nationwide genetic analysis of more than 600 families with inherited eye diseases in Argentina

This study corresponds to the first large-scale genetic analysis of inherited eye diseases (IED) in Argentina and describes the comprehensive genetic profile of a large cohort of patients. Medical records of 22 ophthalmology and genetics services throughout 13 Argentinian provinces were analyzed retrospectively. Patients with a clinical diagnosis of an ophthalmic genetic disease and a history of genetic testing were included. Medical, ophthalmological and family history was collected. A total of 773 patients from 637 families were included, with 98% having inherited retinal disease. The most common phenotype was retinitis pigmentosa (RP, 62%). Causative variants were detected in 379 (59%) patients. USH2A, RPGR, and ABCA4 were the most common disease-associated genes. USH2A was the most frequent gene associated with RP, RDH12 early-onset severe retinal dystrophy, ABCA4 Stargardt disease, PROM1 cone-rod dystrophy, and BEST1 macular dystrophy. The most frequent variants were RPGR c.1345 C > T, p.(Arg449*) and USH2A c.15089 C > A, p.(Ser5030*). The study revealed 156/448 (35%) previously unreported pathogenic/likely pathogenic variants and 8 possible founder mutations. We present the genetic landscape of IED in Argentina and the largest cohort in South America. This data will serve as a reference for future genetic studies, aid diagnosis, inform counseling, and assist in addressing the largely unmet need for clinical trials to be conducted in the region

An Upgraded Analysis of ϵ′/ϵ\epsilon\prime/\epsilon at the Next-to-Leading Order

An upgraded analysis of \ep, $x_d$ and \epp/\ep, using the latest determinations of the relevant experimental and theoretical parameters, is presented. Using the recent determination of the top quark mass, $m_t=(174 \pm 17)$ GeV, our best estimate is \epp/\ep= 3.1 \pm 2.5 , which lies in the range given by E731. We describe our determination of \epp/\ep and make a comparison with other similar studies. A detailed discussion of the matching of the full theory to the effective Hamiltonian, written in terms of lattice operators, is also given.Comment: LaTeX, 45 pages, 6 postscript figure