Theoretical study of the dynamic structure factor of superfluid 4He

We study the dynamic structure factor $S(\vec{q},\omega)$ of superfluid 4He at zero temperature in the roton momentum region and beyond using field-theoretical Green's function techniques. We start from the Gavoret-Nozi\`{e}res two-particle propagator and introduce the concept of quasiparticles. We treat the residual (weak) interaction between quasiparticles as being local in coordinate space and weakly energy dependent. Our quasiparticle model explicitly incorporates the Bose-Einstein condensate. A complete formula for the dynamic susceptibility, which is related to $S (\vec{q},\omega)$, is derived. The structure factor is numerically calculated in a self-consistent way in the special case of a momentum independent interaction between quasiparticles. Results are compared with experiment and other theoretical approaches.Comment: 17 pages, 16 figure

Infections with Avian Pathogenic and Fecal Escherichia coli Strains Display Similar Lung Histopathology and Macrophage Apoptosis

The purpose of this study was to compare histopathological changes in the lungs of chickens infected with avian pathogenic (APEC) and avian fecal (Afecal) Escherichia coli strains, and to analyze how the interaction of the bacteria with avian macrophages relates to the outcome of the infection. Chickens were infected intratracheally with three APEC strains, MT78, IMT5155, and UEL17, and one non-pathogenic Afecal strain, IMT5104. The pathogenicity of the strains was assessed by isolating bacteria from lungs, kidneys, and spleens at 24 h post-infection (p.i.). Lungs were examined for histopathological changes at 12, 18, and 24 h p.i. Serial lung sections were stained with hematoxylin and eosin (HE), terminal deoxynucleotidyl dUTP nick end labeling (TUNEL) for detection of apoptotic cells, and an anti-O2 antibody for detection of MT78 and IMT5155. UEL17 and IMT5104 did not cause systemic infections and the extents of lung colonization were two orders of magnitude lower than for the septicemic strains MT78 and IMT5155, yet all four strains caused the same extent of inflammation in the lungs. The inflammation was localized; there were some congested areas next to unaffected areas. Only the inflamed regions became labeled with anti-O2 antibody. TUNEL labeling revealed the presence of apoptotic cells at 12 h p.i in the inflamed regions only, and before any necrotic foci could be seen. The TUNEL-positive cells were very likely dying heterophils, as evidenced by the purulent inflammation. Some of the dying cells observed in avian lungs in situ may also be macrophages, since all four avian E. coli induced caspase 3/7 activation in monolayers of HD11 avian macrophages. In summary, both pathogenic and non-pathogenic fecal strains of avian E. coli produce focal infections in the avian lung, and these are accompanied by inflammation and cell death in the infected areas

Nucleon Polarizabilities from Deuteron Compton Scattering within a Green's-Function Hybrid Approach

We examine elastic Compton scattering from the deuteron for photon energies ranging from zero to 100 MeV, using state-of-the-art deuteron wave functions and NN-potentials. Nucleon-nucleon rescattering between emission and absorption of the two photons is treated by Green's functions in order to ensure gauge invariance and the correct Thomson limit. With this Green's-function hybrid approach, we fulfill the low-energy theorem of deuteron Compton scattering and there is no significant dependence on the deuteron wave function used. Concerning the nucleon structure, we use Chiral Effective Field Theory with explicit \Delta(1232) degrees of freedom within the Small Scale Expansion up to leading-one-loop order. Agreement with available data is good at all energies. Our 2-parameter fit to all elastic $\gamma d$ data leads to values for the static isoscalar dipole polarizabilities which are in excellent agreement with the isoscalar Baldin sum rule. Taking this value as additional input, we find \alpha_E^s= (11.3+-0.7(stat)+-0.6(Baldin)) x 10^{-4} fm^3 and \beta_M^s = (3.2-+0.7(stat)+-0.6(Baldin)) x 10^{-4} fm^3 and conclude by comparison to the proton numbers that neutron and proton polarizabilities are essentially the same.Comment: 47 pages LaTeX2e with 20 figures in 59 .eps files, using graphicx. Minor modifications; extended discussion of theoretical uncertainties of polarisabilities extraction. Version accepted for publication in EPJ

Hypertensive patients' perceptions of their physicians' knowledge about them: a cross-sectional study in Japan

<p>Abstract</p> <p>Background</p> <p>In order to evaluate the difference in quality of primary care provided by physicians between the types of medical institutions in Japan, we examined whether the physicians' comprehensive knowledge of their patients is perceived differently by the patients seen at clinics and hospitals.</p> <p>Methods</p> <p>Patients with prescriptions for hypertensive drugs were approached sequentially at 13 pharmacies, and were administered a questionnaire on their perception of their physician's knowledge about them. Data were obtained for 687 patients (362 from clinics and 325 from hospitals). A physician's knowledge of his or her patients was assessed according to six aspects: their medical history, their current medications, history of allergy, what worries patients most about their health, patients' values and beliefs on their health, and patients' roles and responsibilities at work, home, or school. Responses were scored from 1 through 6 (1: knows very well; 6: doesn't know at all).</p> <p>Results</p> <p>Patients treated in clinics were seen more frequently, for a longer period, and had fewer complications than the patients who were treated in hospitals. Among the six aspects of physicians' knowledge assessed, 79.3% of the patients reported that their physicians knew their complete list of medications "very well or well," while 28.3% reported the same about their roles and responsibilities at work, home, or school. Physicians in clinics were considered to know their patients' worries about their health (p = 0.004) and the roles and responsibilities of the patients at work, home, or school (p = 0.028) well. Multiple regression analysis showed that the type of medical institutions remained as a significant variable only for the aspect of patients' worries about their health. The factor that consistently affected the patients' perception of physicians' knowledge about them was the patients' age.</p> <p>Conclusions</p> <p>Hypertensive patients' perceptions of their physicians' knowledge about them did not differ significantly between clinics and hospitals in Japan for most of the aspects. In order to differentiate the roles of physicians in hospitals and clinics better and ensure the quality of primary care, the establishment of a standardized educational system to train primary care physicians better is recommended.</p

Evidence Use and the Institutions of the State: The Role of Parliament and the Judiciary

This chapter explores the role of parliaments and the judiciary in shaping evidence use in health policy making. Most analyses of the role of scientific evidence focus on the executive, i.e. national governments and ministries of health, as the key state actors in health policy and health system governance. This chapter shifts attention to the other two powers within the state, the legislative and the judiciary. Using the examples analysed in this book the chapter examines how parliaments can use evidence to inform legislative processes and to hold governments to account, although there are substantial differences between countries and political systems. However, there was little suggestion that such approaches were undertaken systematically. In cases in which policies are brought to court, judges may have to deal with scientific evidence within a country’s legal and constitutional framework, again with significant differences between national legal practices

Genetically Increasing Flux Through b-Oxidation in Skeletal Muscle Increases Mitochondrial Reductive Stress and Glucose Intolerance

Elevated mitochondrial hydrogen peroxide (H(2)O(2)) emission and an oxidative shift in cytosolic redox environment have been linked to high-fat-diet-induced insulin resistance in skeletal muscle. To test specifically whether increased flux through mitochondrial fatty acid oxidation, in the absence of elevated energy demand, directly alters mitochondrial function and redox state in muscle, two genetic models characterized by increased muscle β-oxidation flux were studied. In mice overexpressing peroxisome proliferator-activated receptor-α in muscle (MCK-PPARα), lipid-supported mitochondrial respiration, membrane potential (ΔΨ(m)), and H(2)O(2) production rate (JH(2)O(2)) were increased, which coincided with a more oxidized cytosolic redox environment, reduced muscle glucose uptake, and whole body glucose intolerance despite an increased rate of energy expenditure. Similar results were observed in lipin-1-deficient, fatty-liver dystrophic mice, another model characterized by increased β-oxidation flux and glucose intolerance. Crossing MCAT (mitochondria-targeted catalase) with MCK-PPARα mice normalized JH(2)O(2) production, redox environment, and glucose tolerance, but surprisingly, both basal and absolute insulin-stimulated rates of glucose uptake in muscle remained depressed. Also surprising, when placed on a high-fat diet, MCK-PPARα mice were characterized by much lower whole body, fat, and lean mass as well as improved glucose tolerance relative to wild-type mice, providing additional evidence that overexpression of PPARα in muscle imposes more extensive metabolic stress than experienced by wild-type mice on a high-fat diet. Overall, the findings suggest that driving an increase in skeletal muscle fatty acid oxidation in the absence of metabolic demand imposes mitochondrial reductive stress and elicits multiple counterbalance metabolic responses in an attempt to restore bioenergetic homeostasis. NEW & NOTEWORTHY Prior work has suggested that mitochondrial dysfunction is an underlying cause of insulin resistance in muscle because it limits fatty acid oxidation and therefore leads to the accumulation of cytotoxic lipid intermediates. The implication has been that therapeutic strategies to accelerate β-oxidation will be protective. The current study provides evidence that genetically increasing flux through β-oxidation in muscle imposes reductive stress that is not beneficial but rather detrimental to metabolic regulation

Reconstructing the Indian Origin and Dispersal of the European Roma: A Maternal Genetic Perspective

Previous genetic, anthropological and linguistic studies have shown that Roma (Gypsies) constitute a founder population dispersed throughout Europe whose origins might be traced to the Indian subcontinent. Linguistic and anthropological evidence point to Indo-Aryan ethnic groups from North-western India as the ancestral parental population of Roma. Recently, a strong genetic hint supporting this theory came from a study of a private mutation causing primary congenital glaucoma. In the present study, complete mitochondrial control sequences of Iberian Roma and previously published maternal lineages of other European Roma were analyzed in order to establish the genetic affinities among Roma groups, determine the degree of admixture with neighbouring populations, infer the migration routes followed since the first arrival to Europe, and survey the origin of Roma within the Indian subcontinent. Our results show that the maternal lineage composition in the Roma groups follows a pattern of different migration routes, with several founder effects, and low effective population sizes along their dispersal. Our data allowed the confirmation of a North/West migration route shared by Polish, Lithuanian and Iberian Roma. Additionally, eleven Roma founder lineages were identified and degrees of admixture with host populations were estimated. Finally, the comparison with an extensive database of Indian sequences allowed us to identify the Punjab state, in North-western India, as the putative ancestral homeland of the European Roma, in agreement with previous linguistic and anthropological studies

The fingerprint of the summer 2018 drought in Europe on ground-based atmospheric CO2 measurements

During the summer of 2018, a widespread drought developed over Northern and Central Europe. The increase in temperature and the reduction of soil moisture have influenced carbon dioxide (CO2) exchange between the atmosphere and terrestrial ecosystems in various ways, such as a reduction of photosynthesis, changes in ecosystem respiration, or allowing more frequent fires. In this study, we characterize the resulting perturbation of the atmospheric CO2 seasonal cycles. 2018 has a good coverage of European regions affected by drought, allowing the investigation of how ecosystem flux anomalies impacted spatial CO2 gradients between stations. This density of stations is unprecedented compared to previous drought events in 2003 and 2015, particularly thanks to the deployment of the Integrated Carbon Observation System (ICOS) network of atmospheric greenhouse gas monitoring stations in recent years. Seasonal CO2 cycles from 48 European stations were available for 2017 and 2018.The UK sites were funded by the UK Department of Business, Energy and Industrial Strategy (formerly the Department of Energy and Climate Change) through contracts TRN1028/06/2015 and TRN1537/06/2018. The stations at the ClimaDat Network in Spain have received funding from the ‘la Caixa’ Foundation, under agreement 2010-002624