Kinetic Theory for the Interpretation of Measurements on Fluctuations in Radiation Distributions in Finite, Inhomogeneous Systems

A kinetic (transport) theory is presented for the first- and second-order (and, if necessary, higher) statistical moments of the number densities of the various particles and/or photons that describe the observable fluctuations in the radiation distribution from an emitting system. This treatment is particularly suitable for the analysis of finite, inhomogeneous systems that may be composed of detectors located outside of a radiating source. Because we are largely concerned with the utility of kinetic theory as a physical theory, considerable emphasis is placed upon an appropriate theoretical description of the actual observables of given experimental situations. The quantum Liouville equation is used to generate the coupled set of transport equations, and basic criteria for the applicability of transport and wave theories are discussed. Quantum-statistical effects are also quite naturally accounted for in cases where they are relevant. It is seen that fluctuation measurements are useful for inferring information relevant to the dynamic interactions within a given system. Such measurements often enjoy the feature of being passive with respect to the interacting system of interest. To illustrate the use of this spatially dependent form of kinetic theory on a system emitting optical radiation, we consider an example that interprets a fluctuation measurement on the radiation emergent from a finite nondispersive blackbody. We conclude by discussing the problems of statistical coupling between the radiation field and detector atom distributionsPeer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/86139/1/PhysRev.163.162-RKO.pd

Reactor Noise Analysis from Observations of the High Energy Radiation from the Reactor Core

US AEChttp://deepblue.lib.umich.edu/bitstream/2027.42/85749/1/UCRL-14719-T Gelinas+Osborn.PDF2

Interleukin-6 Contributes to Inflammation and Remodeling in a Model of Adenosine Mediated Lung Injury

Chronic lung diseases are the third leading cause of death in the United States due in part to an incomplete understanding of pathways that govern the progressive tissue remodeling that occurs in these disorders. Adenosine is elevated in the lungs of animal models and humans with chronic lung disease where it promotes air-space destruction and fibrosis. Adenosine signaling increases the production of the pro-fibrotic cytokine interleukin-6 (IL-6). Based on these observations, we hypothesized that IL-6 signaling contributes to tissue destruction and remodeling in a model of chronic lung disease where adenosine levels are elevated.We tested this hypothesis by neutralizing or genetically removing IL-6 in adenosine deaminase (ADA)-deficient mice that develop adenosine dependent pulmonary inflammation and remodeling. Results demonstrated that both pharmacologic blockade and genetic removal of IL-6 attenuated pulmonary inflammation, remodeling and fibrosis in this model. The pursuit of mechanisms involved revealed adenosine and IL-6 dependent activation of STAT-3 in airway epithelial cells.These findings demonstrate that adenosine enhances IL-6 signaling pathways to promote aspects of chronic lung disease. This suggests that blocking IL-6 signaling during chronic stages of disease may provide benefit in halting remodeling processes such as fibrosis and air-space destruction

Accounting information systems

xxx, 714 pages : illustrations ; 26 c

A genetic approach to the prediction of drug side effects: bleomycin induces concordant phenotypes in mice of the collaborative cross.

The antineoplastic drug bleomycin leads to the side effect of pulmonary fibrosis in both humans and mice. We challenged genetically diverse inbred lines of mice from the Collaborative Cross with bleomycin to determine the heritability of this phenotype. Sibling pairs of mice from 40 lines were treated with bleomycin. Lung disease was assessed by scoring lung pathology and by measuring soluble collagen levels in lavage fluid. Serum micro ribonucleic acids (miRNAs) were also measured. Inbred sibling pairs of animals demonstrated high coinheritance of the phenotypes of disease susceptibility or disease resistance. The plasma levels of one miRNA were clearly correlated in sibling mice. The results showed that, as in humans, the lines that comprise the Collaborative Cross exhibited wide genetic variation in response to this drug. This finding suggests that the genetically diverse Collaborative Cross animals may reveal drug effects that might be missed if a study were based on a conventional mouse strain

Provisional best practices guidelines for the evaluation of bulbar dysfunction in amyotrophic lateral sclerosis

Introduction: Universally established comprehensive clinical bulbar scales objectively assessing disease progression in amyotrophic lateral sclerosis (ALS) are currently lacking. The goal of this working group project is to design a best practice set of provisional bulbar ALS guidelines, available for immediate implementation within all ALS clinics. Methods: ALS specialists across multiple related disciplines participated in a series of clinical bulbar symposia, intending to identify and summarize the currently accepted best practices for the assessment and management of bulbar dysfunction in ALS Results: Summary group recommendations for individual speech, Augmentative and Alternative Communication (AAC), and swallowing sections were achieved, focusing on the optimal proposed level of care within each domain. Discussion: We have identified specific clinical recommendations for each of the 3 domains of bulbar functioning, available for incorporation within all ALS clinics. Future directions will be to establish a formal set of bulbar guidelines through a methodological and evidence-based approach. Muscle Nerve 59:531–531, 2019.Fil: Pattee, Gary L.. No especifíca;Fil: Plowman, Emily K.. University of Florida; Estados UnidosFil: Garand, Kendrea L.. University of Alabama at Birmingahm; Estados UnidosFil: Costello, John. No especifíca;Fil: Brooks, Benjamin Rix. No especifíca;Fil: Berry, James D.. No especifíca;Fil: Smith, Richard A.. No especifíca;Fil: Atassi, Nazem. No especifíca;Fil: Chapin, Jennifer L.. University of Florida; Estados UnidosFil: Yunusova, Yana. University of Toronto; CanadáFil: McIlduff, Courtney E.. No especifíca;Fil: Young, Eufrosina. No especifíca;Fil: Macklin, Eric A.. No especifíca;Fil: Locatelli, Eduardo R.. No especifíca;Fil: Silani, Vincenzo. Università degli Studi di Milano; ItaliaFil: Heitzman, Daragh. No especifíca;Fil: Wymer, James. University of Florida; Estados UnidosFil: Goutman, Stephen A.. No especifíca;Fil: Gelinas, Deborah F.. No especifíca;Fil: Perry, Bridget. No especifíca;Fil: Nalipinski, Paige. No especifíca;Fil: Stipancic, Kaila. Children's Hospital Boston; Estados UnidosFil: O'Brien, Meghan. Children's Hospital Boston; Estados UnidosFil: Sullivan, Stacey L.. No especifíca;Fil: Pioro, Erik P.. No especifíca;Fil: Gargiulo Monachelli, Gisella Mariana. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. CEMIC-CONICET. Centro de Educaciones Médicas e Investigaciones Clínicas "Norberto Quirno". CEMIC-CONICET; ArgentinaFil: Green, Jordan R.. No especifíca

Subcellular Dynamics of Type II PKA in Neurons

Summary Protein kinase A (PKA) plays multiple roles in neurons. The localization and specificity of PKA are largely controlled by A-kinase anchoring proteins (AKAPs). However, the dynamics of PKA in neurons and the roles of specific AKAPs are poorly understood. We imaged the distribution of type II PKA in hippocampal and cortical layer 2/3 pyramidal neurons in vitro and in vivo. PKA was concentrated in dendritic shafts compared to the soma, axons, and dendritic spines. This spatial distribution was imposed by the microtubule-binding protein MAP2, indicating that MAP2 is the dominant AKAP in neurons. Following cAMP elevation, catalytic subunits dissociated from the MAP2-tethered regulatory subunits and rapidly became enriched in nearby spines. The spatial gradient of type II PKA between dendritic shafts and spines was critical for the regulation of synaptic strength and long-term potentiation. Therefore, the localization and activity-dependent translocation of type II PKA are important determinants of PKA function