Elastic and inelastic cross sections for low-energy electron collisions with pyrimidine

We present theoretical elastic and electronic excitation cross sections and experimental electronic excitation cross sections for electron collisions with pyrimidine. We use the R-matrix method to determine elastic integral and differential cross sections and integral inelastic cross sections for energies up to 15 eV. The experimental inelastic cross sections have been determined in the 15–50 eV impact energy range. Typically, there is quite reasonable agreement between the theoretical and experimental integral inelastic cross sections. Calculated elastic cross sections agree very well with prior results

Pancreatic β-Cell Death in Response to Pro-Inflammatory Cytokines Is Distinct from Genuine Apoptosis

A reduction in functional β-cell mass leads to both major forms of diabetes; pro-inflammatory cytokines, such as interleukin-1beta (IL-1β) and gamma-interferon (γ-IFN), activate signaling pathways that direct pancreatic β-cell death and dysfunction. However, the molecular mechanism of β-cell death in this context is not well understood. In this report, we tested the hypothesis that individual cellular death pathways display characteristic phenotypes that allow them to be distinguished by the precise biochemical and metabolic responses that occur during stimulus-specific initiation. Using 832/13 and INS-1E rat insulinoma cells and isolated rat islets, we provide evidence that apoptosis is unlikely to be the primary pathway underlying β-cell death in response to IL-1β+γ-IFN. This conclusion was reached via the experimental results of several different interdisciplinary strategies, which included: 1) tandem mass spectrometry to delineate the metabolic differences between IL-1β+γ-IFN exposure versus apoptotic induction by camptothecin and 2) pharmacological and molecular interference with either NF-κB activity or apoptosome formation. These approaches provided clear distinctions in cell death pathways initiated by pro-inflammatory cytokines and bona fide inducers of apoptosis. Collectively, the results reported herein demonstrate that pancreatic β-cells undergo apoptosis in response to camptothecin or staurosporine, but not pro-inflammatory cytokines. DOI: 10.1371/journal.pone.002248

Effect of adherence to self-monitoring of diet and physical activity on weight loss in a technology-supported behavioral intervention

Background: Examination of mediating behavioral factors could explain how an intervention works and thus provide guidance to optimize behavioral weight-loss programs. This study examined the mediating role of adherence to self-monitoring of diet and physical activity on weight loss in a behavioral weight-loss trial testing the use of personal digital assistants (PDA) for self-monitoring. Methods: Mediation analysis was conducted to examine the possible mediating role of adherence to self-monitoring of diet and physical activity between treatments using varying self-monitoring methods (paper record, PDA, and PDA with daily tailored feedback messages) and weight loss. Findings: The sample (N = 210) was predominantly white (78%) and female (85%). Compared to a paper record, using a PDA for self-monitoring diet (P = 0.027) and physical activity (P = 0.014) had significant direct effects on weight loss at 12 months, as well as a significant indirect effect on outcomes through improved adherence to self-monitoring (PS < 0.001). Receiving an automated daily feedback message via PDA only had a significant indirect effect on weight through self-monitoring adherence to diet (P = 0.004) and physical activity (P = 0.002). Conclusions: Adherence to self-monitoring of diet and physical activity is important as the underlying mechanism in this technology-supported behavioral weight-loss intervention. © 2012 Wang et al, publisher and licensee Dove Medical Press Ltd

An adenovirus-derived protein: A novel candidate for anti-diabetic drug development

© 2015 Elsevier B.V. and Société Française de Biochimie et Biologie Moléculaire (SFBBM). Aims Exposure to human adenovirus Ad36 is causatively and correlatively linked with better glycemic control in animals and humans, respectively. Although the anti-hyperglycemic property of Ad36 may offer some therapeutic potential, it is impractical to use an infectious agent for therapeutic benefit. Cell-based studies identified that Ad36 enhances cellular glucose disposal via its E4orf1 protein. Ability to improve glycemic control in vivo is a critical prerequisite for further investigating the therapeutic potential of E4orf1. Therefore, the aim of this study was to determine the ability of E4orf1 to improve glycemic control independent of insulin despite high fat diet. Materials & Methods 8-9wk old male C57BL/6J mice fed a high-fat diet (60% kcal) were injected with a retrovirus plasmid expressing E4orf1, or a null vector (Control). Glycemic control was determined by glucose and insulin tolerance test. Islet cell size, amount of insulin and glucagon were determined in formalin-fixed pancreas. Rat insulinoma cell line (832/13) was infected with E4orf1 or control to determine changes in glucose stimulated insulin secretion. Protein from flash frozen adipose tissue depots, liver and muscle was used to determine molecular signaling by western blotting. Results In multiple experiments, retrovirus-mediated E4orf1 expression in C57BL/6J mice significantly and reproducibly improved glucose excursion following a glucose load despite a high fat diet (60% energy). Importantly, E4orf1 improved glucose clearance without increasing insulin sensitivity, production or secretion, underscoring its insulin-independent effect. E4orf1 modulated molecular signaling in mice tissue, which included greater protein abundance of adiponectin, p-AKT and Glucose transporter Glu4. Conclusions This study provides the proof of concept for translational development of E4orf1 as a potential anti-diabetic agent. High fat intake and impaired insulin signaling are often associated with obesity, diabetes and insulin resistance. Hence, the ability of E4orf1 to improve glycemic control despite high fat diet and independent of insulin, is particularly attractive

Exoplanet Catalogues

One of the most exciting developments in the field of exoplanets has been the progression from 'stamp-collecting' to demography, from discovery to characterisation, from exoplanets to comparative exoplanetology. There is an exhilaration when a prediction is confirmed, a trend is observed, or a new population appears. This transition has been driven by the rise in the sheer number of known exoplanets, which has been rising exponentially for two decades (Mamajek 2016). However, the careful collection, scrutiny and organisation of these exoplanets is necessary for drawing robust, scientific conclusions that are sensitive to the biases and caveats that have gone into their discovery. The purpose of this chapter is to discuss and demonstrate important considerations to keep in mind when examining or constructing a catalogue of exoplanets. First, we introduce the value of exoplanetary catalogues. There are a handful of large, online databases that aggregate the available exoplanet literature and render it digestible and navigable - an ever more complex task with the growing number and diversity of exoplanet discoveries. We compare and contrast three of the most up-to-date general catalogues, including the data and tools that are available. We then describe exoplanet catalogues that were constructed to address specific science questions or exoplanet discovery space. Although we do not attempt to list or summarise all the published lists of exoplanets in the literature in this chapter, we explore the case study of the NASA Kepler mission planet catalogues in some detail. Finally, we lay out some of the best practices to adopt when constructing or utilising an exoplanet catalogue.Comment: 14 pages, 6 figures. Invited review chapter, to appear in "Handbook of Exoplanets", edited by H.J. Deeg and J.A. Belmonte, section editor N. Batalh