2,149 research outputs found
Dynamical epidemic suppression using stochastic prediction and control
We consider the effects of noise on a model of epidemic outbreaks, where the
outbreaks appear. randomly. Using a constructive transition approach that
predicts large outbreaks, prior to their occurrence, we derive an adaptive
control. scheme that prevents large outbreaks from occurring. The theory
inapplicable to a wide range of stochastic processes with underlying
deterministic structure.Comment: 14 pages, 6 figure
El derecho de acceso a información pública como mecanismo de control social: Análisis comparado en cinco países latinoamericanos
The following study seeks to review the states of policies and the institutional development of them in the area of Transparency and Right of Access to the information in the region, to, once within the pertinent conceptualization where diverse sources about Accountability are consulted, generate a comparison that, subsequently, allows to identify which the conditions would be for the tools present in each of the analyzed countries, according to their own legislation, to allow the exercise of Accountability and the configuration of access to information as a right in itself and a way of social control to public managementEl presente estudio busca revisar el estado y el desarrollo institucional de las políticas en materia de transparencia y derecho de acceso a la información presentes en la región. Una vez dentro de la conceptualización pertinente, donde se consultan diversas fuentes que tratan el Accountability, se realiza una comparación que permite identificar posteriormente las condiciones para que las herramientas presentes en cada uno de los países analizados, conforme a su propia legislación, permitan ejercer el Accountability y configurar el acceso a la información, tanto como derecho autónomo como medio efectivo de control social a la gestión públic
Edge-Based Compartmental Modeling for Infectious Disease Spread Part III: Disease and Population Structure
We consider the edge-based compartmental models for infectious disease spread
introduced in Part I. These models allow us to consider standard SIR diseases
spreading in random populations. In this paper we show how to handle deviations
of the disease or population from the simplistic assumptions of Part I. We
allow the population to have structure due to effects such as demographic
detail or multiple types of risk behavior the disease to have more complicated
natural history. We introduce these modifications in the static network
context, though it is straightforward to incorporate them into dynamic
networks. We also consider serosorting, which requires using the dynamic
network models. The basic methods we use to derive these generalizations are
widely applicable, and so it is straightforward to introduce many other
generalizations not considered here
Study of Tau-pair Production in Photon-Photon Collisions at LEP and Limits on the Anomalous Electromagnetic Moments of the Tau Lepton
Tau-pair production in the process e+e- -> e+e-tau+tau- was studied using
data collected by the DELPHI experiment at LEP2 during the years 1997 - 2000.
The corresponding integrated luminosity is 650 pb^{-1}. The values of the
cross-section obtained are found to be in agreement with QED predictions.
Limits on the anomalous magnetic and electric dipole moments of the tau lepton
are deduced.Comment: 20 pages, 9 figures, Accepted by Eur. Phys. J.
Energy dependence of Cronin momentum in saturation model for and collisions
We calculate dependence of Cronin momentum for and
collisions in saturation model. We show that this dependence is consistent with
expectation from formula which was obtained using simple dimentional
consideration. This can be used to test validity of saturation model (and
distinguish among its variants) and measure dependence of saturation
momentum from experimental data.Comment: LaTeX2e, 12 pages, 8 figure
CP asymmetry in in a general two-Higgs-doublet model with fourth-generation quarks
We discuss the time-dependent CP asymmetry of decay in an
extension of the Standard Model with both two Higgs doublets and additional
fourth-generation quarks. We show that although the Standard Model with
two-Higgs-doublet and the Standard model with fourth generation quarks alone
are not likely to largely change the effective from the decay of
, the model with both additional Higgs doublet and
fourth-generation quarks can easily account for the possible large negative
value of without conflicting with other experimental
constraints. In this model, additional large CP violating effects may arise
from the flavor changing Yukawa interactions between neutral Higgs bosons and
the heavy fourth generation down type quark, which can modify the QCD penguin
contributions. With the constraints obtained from processes
such as and , this model can lead to the
effective to be as large as in the CP asymmetry of .Comment: 13 pages, 5 figures, references added, to appear in Eur.Phys.J.
A Precise Measurement of the Tau Lifetime
The tau lepton lifetime has been measured with the e+e- -> tau+tau- events
collected by the DELPHI detector at LEP in the years 1991-1995. Three different
methods have been exploited, using both one-prong and three-prong tau decay
channels. Two measurements have been made using events in which both taus decay
to a single charged particle. Combining these measurements gave tau_tau (1
prong) = 291.8 +/- 2.3 (stat) +/- 1.5 (sys) fs. A third measurement using taus
which decayed to three charged particles yielded tau_tau (3 prong) = 288.6 +/-
2.4 (stat) +/- 1.3 (sys) fs. These were combined with previous DELPHI results
to measure the tau lifetime, using the full LEP1 data sample, to be tau_tau =
290.9 +/- 1.4 (stat) +/- 1.0 (sys) fs.Comment: 27 pages, 7 figure
A nonsynonymous mutation in PLCG2 reduces the risk of Alzheimer’s disease, dementia with Lewy bodies and frontotemporal dementia, and increases the likelihood of longevity
The genetic variant rs72824905-G (minor allele) in the PLCG2 gene was previously associated with a reduced Alzheimer’s disease risk (AD). The role of PLCG2 in immune system signaling suggests it may also protect against other neurodegenerative diseases and possibly associates with longevity. We studied the effect of the rs72824905-G on seven neurodegenerative diseases and longevity, using 53,627 patients, 3,516 long-lived individuals and 149,290 study-matched controls. We replicated the association of rs72824905-G with reduced AD risk and we found an association with reduced risk of dementia with Lewy bodies (DLB) and frontotemporal dementia (FTD). We did not find evidence for an effect on Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS) and multiple sclerosis (MS) risks, despite adequate sample sizes. Conversely, the rs72824905-G allele was associated with increased likelihood of longevity. By-proxy analyses in the UK Biobank supported the associations with both dementia and longevity. Concluding, rs72824905-G has a protective effect against multiple neurodegenerative diseases indicating shared aspects of disease etiology. Our findings merit studying the PLCγ2 pathway as drug-target.Fil: van der Lee, Sven J.. Vrije Universiteit Amsterdam; Países BajosFil: Conway, Olivia J.. Mayo Clinic Cancer Center; Estados UnidosFil: Jansen, Iris. Vrije Universiteit Amsterdam; Países BajosFil: Carrasquillo, Minerva M.. Mayo Clinic Cancer Center; Estados UnidosFil: Kleineidam, Luca. Universitat Bonn; Alemania. German Center for Neurodegenerative Diseases; Alemania. University Hospital Cologne; AlemaniaFil: van den Akker, Erik. Leiden University. Leiden University Medical Center; Países Bajos. Delft University of Technology; Países BajosFil: Hernández, Isabel. Universitat Internacional de Catalunya; España. Centro de Investigacion Biomedica en Red en Enfermedades Neurodegenerativas ; EspañaFil: van Eijk, Kristel R.. University of Utrecht; Países BajosFil: Stringa, Najada. Vrije Universiteit Amsterdam; Países BajosFil: Chen, Jason A.. University of California at Los Angeles; Estados UnidosFil: Zettergren, Anna. University of Gothenburg; SueciaFil: Andlauer, Till F. M.. Max Planck Institute of Psychiatry; Alemania. Universitat Technical Zu Munich; Alemania. German Competence Network Multiple Sclerosis; AlemaniaFil: Diez Fairen, Monica. University Hospital Mutua de Terrassa; España. Fundacio per la Recerca Biomedica I Social Mutua Terrassa; EspañaFil: Simon Sanchez, Javier. Deutsches Zentrum für Neurodegenerative Erkrankungen; Alemania. Eberhard Karls Universität Tübingen; AlemaniaFil: Lleó, Alberto. Universitat Autònoma de Barcelona; España. Centro de Investigacion Biomedica en Red en Enfermedades Neurodegenerativas ; EspañaFil: Zetterberg, Henrik. Sahlgrenska University Hospital; Suecia. University of Gothenburg; Suecia. University College London; Estados UnidosFil: Nygaard, Marianne. University of Southern Denmark; DinamarcaFil: Blauwendraat, Cornelis. National Institute of Neurological Disorders and Stroke; Estados UnidosFil: Savage, Jeanne E.. Vrije Universiteit Amsterdam; Países BajosFil: Mengel From, Jonas. University of Southern Denmark; DinamarcaFil: Moreno Grau, Sonia. Universitat Internacional de Catalunya; EspañaFil: Wagner, Michael. Universitat Bonn; Alemania. Deutsches Zentrum für Neurodegenerative Erkrankungen; AlemaniaFil: Fortea, Juan. Universitat Autònoma de Barcelona; España. Centro de Investigacion Biomedica en Red en Enfermedades Neurodegenerativas ; EspañaFil: Keogh, Michael J.. University of Newcastle; Reino Unido. University of Cambridge; Reino UnidoFil: Blennow, Kaj. Sahlgrenska University Hospital; Suecia. University of Gothenburg; SueciaFil: Skoog, Ingmar. University of Gothenburg; SueciaFil: Friese, Manuel A.. German Competence Network Multiple Sclerosis; Alemania. Universitätsklinikum Hamburg‐Eppendorf; AlemaniaFil: Pletnikova, Olga. University Johns Hopkins; Estados UnidosFil: Zulaica, Miren. Centro de Investigacion Biomedica en Red en Enfermedades Neurodegenerativas ; España. Instituto Biodonostia; EspañaFil: Dalmasso, Maria Carolina. University Hospital Cologne; Alemania. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentin
Unbound Plasma, Total Plasma, and Whole-Blood Tacrolimus Pharmacokinetics Early After Thoracic Organ Transplantation
Abstract: Therapeutic drug monitoring of tacrolimus whole-blood concentrations is standard care in thoracic organ transplantation. Nevertheless, toxicity may appear with alleged therapeutic concentrations possibly related to variability in unbound concentrations. However, pharmacokinetic data on unbound concentrations are not available. The objective of this study was to quantify the pharmacokinetics of whole-blood, total, and unbound plasma tacrolimus in patients early after heart and lung transplantation. Methods: Twelve-hour tacrolimus whole-blood, total, and unbound plasma concentrations of 30 thoracic organ recipients were analyzed with high-performance liquid chromatography–tandem mass spectrometry directly after transplantation. Pharmacokinetic modeling was performed using non-linear mixed-effects modeling. Results: Plasma concentration was < 1% of the whole-blood concentration. Maximum binding capacity of erythrocytes was directly proportional to hematocrit and estimated at 2700 pg/mL (95% confidence interval 1750–3835) with a dissociation constant of 0.142 pg/mL (95% confidence interval 0.087–0.195). The inter-individual variability in the binding constants was considerable (27% maximum binding capacity, and 29% for the linear binding constant of plasma). Conclusions: Tacrolimus association with erythrocytes was high and suggested a non-linear distribution at high concentrations. Monitoring hematocrit-corrected whole-blood tacrolimus concentrations might improve clinical outcomes in clinically unstable thoracic organ transplants. Clinical Trial Registration: NTR 3912/EudraCT 2012-001909-24
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