Hydrogen-atom Attack on Phenol and Toluene is \u3cem\u3eortho\u3c/em\u3e-directed

The reaction of H + phenol and H/D + toluene has been studied in a supersonic expansion after electric discharge. The (1 + 1′) resonance-enhanced multiphoton ionization (REMPI) spectra of the reaction products, at m/z = parent + 1, or parent + 2 amu, were measured by scanning the first (resonance) laser. The resulting spectra are highly structured. Ionization energies were measured by scanning the second (ionization) laser, while the first laser was tuned to a specific transition. Theoretical calculations, benchmarked to the well-studied H + benzene → cyclohexadienyl radical reaction, were performed. The spectrum arising from the reaction of H + phenol is attributed solely to the ortho-hydroxy-cyclohexadienyl radical, which was found in two conformers (syn and anti). Similarly, the reaction of H/D + toluene formed solely the ortho isomer. The preference for the ortho isomer at 100–200 K in the molecular beam is attributed to kinetic, not thermodynamic effects, caused by an entrance channel barrier that is ∼5 kJ mol−1 lower for ortho than for other isomers. Based on these results, we predict that the reaction of H + phenol and H + toluene should still favour the ortho isomer under elevated temperature conditions in the early stages of combustion (200–400 °C)

Investigation of the skeletal muscle transcriptome in lambs fed β adrenergic agonists and subjected to heat stress for 21 d

Dietary β-adrenergic agonists (β-AA) are used in livestock to increase muscle protein accretion and decrease adipose deposition during the last 20 to 40 d of the finishing period (Johnson et al., 2014). These β-AA act through specific seven transmembrane receptors and are classified by the receptor isoform to which they primarily bind (Mersmann, 1998). Two β-AA are approved for use in beef cattle in the United States: ractopamine HCl (RAC, β1 agonist) and zilpaterol HCl (ZH, β2 agonist) (Johnson et al., 2014). Supplementation of β-AA increases efficiency of the animal and results in a leaner carcass (Elam et al., 2009). However, the skeletal muscle’s genomic response to these treatments is not well understood. Heat stress (HS) has long been a major concern in the livestock industry. HS occurs when an animal’s body temperature rises above its thermoneutral zone, at which point the heat load exceeds the animal’s capacity for heat dissipation (Bernabucci et al., 2010), resulting in decreased feed intake and poor performance (Marai et al., 2007). Therefore, growth and production decrease during HS, affecting economically important carcass and reproductive traits. As a result, millions of dollars are lost each year due to HS (Renaudeau et al., 2012). Individually, HS and β-AA supplementation have antagonistic effects on muscle growth. However, there is a gap in understanding of the genomic mechanisms through which animals respond to these factors individually and in concert. The purpose of this study is to investigate the effects of β-AA, HS, and their interaction in skeletal muscle using transcriptomic analyses

Detection of stx1 and stx2 Genes in Pennsylvanian White-Tailed Deer

Shiga toxin-producing E. coli carrying the stx1 and/or stx2 genes can cause multi-symptomatic illness in humans. A variety of terrestrial and aquatic environmental reservoirs of stx have been described. Culture based detection of microbes in deer species have found a low percentage of samples that have tested positive for Stx-producing microbes, suggesting that while deer may contain these microbes, their overall abundance in deer is low. In this study, quantitative PCR (qPCR) was utilized to test for the presence of stx genes in white-tailed deer fecal matter in western Pennsylvania. In this culture independent screening, nearly half of the samples tested positive for the stx2 gene, with a bias towards samples that were concentrated with stx2. This study, while limited in scope, suggests that deer may be a greater reservoir for stx than was previously thought

The Detection and Characterization of cm Radio Continuum Emission from the Low-mass Protostar L1014-IRS

Observations by the Cores to Disk Legacy Team with the Spitzer Space Telescope have identified a low luminosity, mid-infrared source within the dense core, Lynds 1014, which was previously thought to harbor no internal source. Followup near-infrared and submillimeter interferometric observations have confirmed the protostellar nature of this source by detecting scattered light from an outflow cavity and a weak molecular outflow. In this paper, we report the detection of cm continuum emission with the VLA. The emission is characterized by a quiescent, unresolved 90 uJy 6 cm source within 0.2" of the Spitzer source. The spectral index of the quiescent component is $\alpha = 0.37\pm 0.34$ between 6 cm and 3.6 cm. A factor of two increase in 6 cm emission was detected during one epoch and circular polarization was marginally detected at the $5\sigma$ level with Stokes {V/I} $= 48 \pm 16$% . We have searched for 22 GHz H2O maser emission toward L1014-IRS, but no masers were detected during 7 epochs of observations between June 2004 and December 2006. L1014-IRS appears to be a low-mass, accreting protostar which exhibits cm emission from a thermal jet or a wind, with a variable non-thermal emission component. The quiescent cm radio emission is noticeably above the correlation of 3.6 cm and 6 cm luminosity versus bolometric luminosity, indicating more radio emission than expected. We characterize the cm continuum emission in terms of observations of other low-mass protostars, including updated correlations of centimeter continuum emission with bolometric luminosity and outflow force, and discuss the implications of recent larger distance estimates on the physical attributes of the protostar and dense molecular core.Comment: 14 pages. Accepted for publication in Ap

Enhancer Sequence Variants and Transcription-Factor Deregulation Synergize to Construct Pathogenic Regulatory Circuits in B-Cell Lymphoma

SummaryMost B-cell lymphomas arise in the germinal center (GC), where humoral immune responses evolve from potentially oncogenic cycles of mutation, proliferation, and clonal selection. Although lymphoma gene expression diverges significantly from GC B cells, underlying mechanisms that alter the activities of corresponding regulatory elements (REs) remain elusive. Here we define the complete pathogenic circuitry of human follicular lymphoma (FL), which activates or decommissions REs from normal GC B cells and commandeers enhancers from other lineages. Moreover, independent sets of transcription factors, whose expression was deregulated in FL, targeted commandeered versus decommissioned REs. Our approach revealed two distinct subtypes of low-grade FL, whose pathogenic circuitries resembled GC B or activated B cells. FL-altered enhancers also were enriched for sequence variants, including somatic mutations, which disrupt transcription-factor binding and expression of circuit-linked genes. Thus, the pathogenic regulatory circuitry of FL reveals distinct genetic and epigenetic etiologies for GC B-cell transformation

Low temperature electronic properties of Sr_2RuO_4 I: Microscopic model and normal state properties

Starting from the quasi one-dimensional kinetic energy of the d_{yz} and d_{zx} bands we derive a bosonized description of the correlated electron system in Sr_2RuO_4. At intermediate coupling the magnetic correlations have a quasi one-dimensional component along the diagonals of the basal plane of the tetragonal unit cell that accounts for the observed neutron scattering results. Together with two-dimensional correlations the model consistently accounts for the normal phase specific heat, cyclotron mass enhancement, static susceptibility, and Wilson ratio and implies an anomalous high temperature resistivity.Comment: 12 pages REVTEX, 6 figure

Pre-cooling for endurance exercise performance in the heat: a systematic review.

PMCID: PMC3568721The electronic version of this article is the complete one and can be found online at: http://www.biomedcentral.com/1741-7015/10/166. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.Endurance exercise capacity diminishes under hot environmental conditions. Time to exhaustion can be increased by lowering body temperature prior to exercise (pre-cooling). This systematic literature review synthesizes the current findings of the effects of pre-cooling on endurance exercise performance, providing guidance for clinical practice and further research

Expression of tumour-specific antigens underlies cancer immunoediting

Cancer immunoediting is a process by which immune cells, particularly lymphocytes of the adaptive immune system, protect the host from the development of cancer and alter tumour progression by driving the outgrowth of tumour cells with decreased sensitivity to immune attack1, 2. Carcinogen-induced mouse models of cancer have shown that primary tumour susceptibility is thereby enhanced in immune-compromised mice, whereas the capacity for such tumours to grow after transplantation into wild-type mice is reduced2, 3. However, many questions about the process of cancer immunoediting remain unanswered, in part because of the known antigenic complexity and heterogeneity of carcinogen-induced tumours4. Here we adapted a genetically engineered, autochthonous mouse model of sarcomagenesis to investigate the process of cancer immunoediting. This system allows us to monitor the onset and growth of immunogenic and non-immunogenic tumours induced in situ that harbour identical genetic and histopathological characteristics. By comparing the development of such tumours in immune-competent mice with their development in mice with broad immunodeficiency or specific antigenic tolerance, we show that recognition of tumour-specific antigens by lymphocytes is critical for immunoediting against sarcomas. Furthermore, primary sarcomas were edited to become less immunogenic through the selective outgrowth of cells that were able to escape T lymphocyte attack. Loss of tumour antigen expression or presentation on major histocompatibility complex I was necessary and sufficient for this immunoediting process to occur. These results highlight the importance of tumour-specific-antigen expression in immune surveillance, and potentially, immunotherapy.National Institutes of Health (U.S.) (Grant 1 U54 CA126515-01)National Cancer Institute (U.S.) (Cancer Center Support Grant P30-CA14051)Margaret A. Cunningham Immune Mechanisms in Cancer Research Fellowship AwardJohnD. Proctor FoundationDaniel K. Ludwig Schola