The Effects of Pre-Workout Meals High in Carbohydrates or Lipids on Muscle Fatigue during Resistance Exercise: A Pilot Study

Purpose: Pre-workout nutrition is important in exercise training and is often overlooked or misunderstood. The purpose of this study was to examine the effects of pre-workout meals high in carbohydrates or lipids on muscular endurance in lower body muscles and fatigue during a back squat exercise in physically active college students. Methods: All subjects (n = 8) reported to the lab 2 times, with 24-48 hours of rest between sessions. Subjects’ height, weight, and blood pressure were taken before each session. Subjects were led through a dynamic warm-up consisting of foam rolling, dynamic stretching, and barbell back squat warm-ups every session. Session one was for estimation of subjects’ back squat 1-repetition maximum (1RM) using a PUSH-Strength accelerometer-based velocity tool. During the second session, participants were instructed to consume a carbohydrate or lipid bar and wait 45 minutes for digestion. Subjects then completed the warm-up and performed one back squat set to failure using 75% of their predicted 1RM. Results: The carbohydrate group performed more repetitions and lifted for a longer time than the lipid group (p \u3c 0.05). Conclusion: Our data suggest that a carbohydrate-heavy meal immediately prior is beneficial to maximize muscular endurance in resistance training

Epstein-Barr virus IL-10 gene expression by a recombinant murine gammaherpesvirus in vivo enhances acute pathogenicity but does not affect latency or reactivation.

BackgroundMany viral genes affect cytokine function within infected hosts, with interleukin 10 (IL-10) as a commonly targeted mediator. Epstein-Barr virus (EBV) encodes an IL-10 homologue (vIL-10) expressed during productive (lytic) infection and induces expression of cellular IL-10 (cIL-10) during latency. This study explored the role of vIL-10 in a murine gammaherpesvirus (MHV) model of viral infection.MethodsThe EBV vIL-10 gene was inserted into MHV-76, a strain which lacks the ability to induce cIL-10, by recombination in transfected mouse cells. Mice were infected intranasally with the recombinant, vIL-10-containing MHV-76 or control virus strains and assayed at various days post infection for lung virus titer, spleen cell number, percentage of latently infected spleen cells and ability to reactivate virus from spleen cells.ResultsRecombinant murine gammaherpesvirus expressing EBV vIL-10 rose to significantly higher titers in lungs and promoted an increase in spleen cell number in infected mice in comparison to MHV strains lacking the vIL-10 gene. However, vIL-10 expression did not alter the quantity of latent virus in the spleen or its ability to reactivate.ConclusionsIn this mouse model of gammaherpesvirus infection, EBV vIL-10 appears to influence acute-phase pathogenicity. Given that EBV and MHV wild-type strains contain other genes that induce cIL-10 expression in latency (e.g. LMP-1 and M2, respectively), vIL-10 may have evolved to serve the specific role in acute infection of enlarging the permissive host cell population, perhaps to facilitate initial survival and dissemination of viral-infected cells

Epstein-Barr Virus Independent Dysregulation of UBP43 Expression Alters Interferon-Stimulated Gene Expression in Burkitt Lymphoma

Epstein-Barr virus (EBV) persists as a life-long latent infection within memory B cells, but how EBV may circumvent the innate immune response within this virus reservoir is unclear. Recent studies suggest that the latency-associated non-coding RNAs of EBV may actually induce type I (antiviral) interferon production, raising the question of how EBV counters the negative consequences this is likely to have on viral persistence. We addressed this by examining the type I interferon response in Burkitt lymphoma (BL) cell lines, the only in vitro model of the restricted program of EBV latency-gene expression in persistently infected B cells in vivo. Importantly, we observed no effect of EBV on interferon alpha-induced signaling or evidence of type I interferon production, suggesting that EBV in this latent state is silent to the cell's innate antiviral surveillance. We did uncover, however, a defect in the negative feedback control of interferon signaling in a subpopulation of BL lines as was revealed by prolonged interferon-stimulated gene transcription consistent with sustained tyrosine phosphorylation on STAT1 and STAT2. This was due to inadequate induction of expression of the ubiquitin-specific protease UBP43, which removes the ubiquitin-like ISG15 polypeptide conjugated to proteins (ISGylation) in response to type I interferons. Results here are consistent with previous findings in genetically engineered Ubp43−/− murine cells that UBP43 down-regulates interferon signaling, independent of its ISG15 isopeptidase activity, by precluding the protein kinase JAK1 from the interferon receptor. This natural deficiency in UBP43 expression may therefore provide a useful model to further probe the biological roles of UBP43 and ISGylation

The MAGIC of CINEMA: First in-flight science results from a miniaturised anisotropic magnetoresistive magnetometer

We present the first in-flight results from a novel miniaturised anisotropic magnetoresistive space magnetometer, MAGIC (MAGnetometer from Imperial College), aboard the first CINEMA (CubeSat for Ions, Neutrals, Electrons and MAgnetic fields) spacecraft in low Earth orbit. An attitude-independent calibration technique is detailed using the International Geomagnetic Reference Field (IGRF), which is temperature dependent in the case of the outboard sensor. We show that the sensors accurately measure the expected absolute field to within 2% in attitude mode and 1% in science mode. Using a simple method we are able to estimate the spacecraft's attitude using the magnetometer only, thus characterising CINEMA's spin, precession and nutation. Finally, we show that the outboard sensor is capable of detecting transient physical signals with amplitudes of ~ 20–60 nT. These include field-aligned currents at the auroral oval, qualitatively similar to previous observations, which agree in location with measurements from the DMSP (Defense Meteorological Satellite Program) and POES (Polar-orbiting Operational Environmental Satellites) spacecraft. Thus, we demonstrate and discuss the potential science capabilities of the MAGIC instrument onboard a CubeSat platform

VerdictDB: Universalizing Approximate Query Processing

Despite 25 years of research in academia, approximate query processing (AQP) has had little industrial adoption. One of the major causes of this slow adoption is the reluctance of traditional vendors to make radical changes to their legacy codebases, and the preoccupation of newer vendors (e.g., SQL-on-Hadoop products) with implementing standard features. Additionally, the few AQP engines that are available are each tied to a specific platform and require users to completely abandon their existing databases---an unrealistic expectation given the infancy of the AQP technology. Therefore, we argue that a universal solution is needed: a database-agnostic approximation engine that will widen the reach of this emerging technology across various platforms. Our proposal, called VerdictDB, uses a middleware architecture that requires no changes to the backend database, and thus, can work with all off-the-shelf engines. Operating at the driver-level, VerdictDB intercepts analytical queries issued to the database and rewrites them into another query that, if executed by any standard relational engine, will yield sufficient information for computing an approximate answer. VerdictDB uses the returned result set to compute an approximate answer and error estimates, which are then passed on to the user or application. However, lack of access to the query execution layer introduces significant challenges in terms of generality, correctness, and efficiency. This paper shows how VerdictDB overcomes these challenges and delivers up to 171$\times$ speedup (18.45$\times$ on average) for a variety of existing engines, such as Impala, Spark SQL, and Amazon Redshift, while incurring less than 2.6% relative error. VerdictDB is open-sourced under Apache License.Comment: Extended technical report of the paper that appeared in Proceedings of the 2018 International Conference on Management of Data, pp. 1461-1476. ACM, 201

The BHLF1 locus of Epstein-Barr virus contributes to viral latency and B-cell immortalization

Funding: U.S. Public Health Service grant AI110328 to J.T.S. and in part by Commonwealth Universal Research Enhancement (CURE) funds. L.N.L. received support from National Cancer Institute training grant T32 CA060395, and is a Lymphoma Research Foundation Grantee.The Epstein-Barr virus (EBV) BHLF1 gene encodes an abundant linear and several circular RNAs believed to perform non-coding functions during virus replication, though an open reading frame is retained among an unknown percentage of EBV isolates. Evidence suggests that BHLF1 is also transcribed during latent infection, which prompted us to investigate the contribution of this locus to latency. Analysis of transcripts transiting BHLF1 revealed its transcription is widespread among B-cell lines supporting the latency I or III program of EBV protein expression, and to be more complex than originally presumed. EBV-negative Burkitt lymphoma cell lines infected with either wild-type or two different BHLF1 mutant EBVs were initially indistinguishable in supporting latency III. However, cells infected with BHLF1- virus ultimately transitioned to the more restrictive latency I, whereas cells infected with wild-type virus either sustained latency III or transitioned more slowly to latency I. Upon infection of primary B cells, which require latency III for growth in vitro, both BHLF1- viruses exhibited variably reduced immortalization potential relative to wild-type virus. Finally, in transfection experiments, efficient protein expression from an intact BHLF1 ORF required the EBV post-transcriptional regulator protein SM, whose expression is limited to the replicative cycle. Thus, one way in which BHLF1 may contribute to latency is through a mechanism, possibly mediated or regulated by a long non-coding RNA, that supports latency III critical for the establishment of EBV latency and lifelong persistence within its host, whereas any retained protein-dependent function of BHLF1 may be restricted to the replication cycle. Importance. Epstein-Barr virus (EBV) has significant oncogenic potential that is linked to its latent infection of B lymphocytes, during which virus replication is not supported. Establishment of latent infection, which is life long and can precede tumor development by years, requires the concerted actions of nearly a dozen EBV proteins and numerous small non-protein-coding RNAs. Elucidation of how these EBV products contribute to latency is crucial to understanding EBV's role in specific malignancies, and ultimately to clinical intervention. Historically, EBV genes that contribute to virus replication have been excluded from consideration of a role in latency, primarily because of the general incompatibility between virus production and cell survival. However, here we provide evidence that the genetic locus containing one such gene, BHLF1, indeed contributes to key aspects of EBV latency, including its ability to promote continuous growth of B lymphocytes, thus providing significant new insight into EBV biology and oncogenic potential.PostprintPeer reviewe

Isospin breaking in the vector current of the nucleon

Extraction of the nucleon's strange form factors from experimental data requires a quantitative understanding of the unavoidable contamination from isospin violation. A number of authors have addressed this issue during the past decade, and their work is reviewed here. The predictions from early models are largely consistent with recent results that rely as much as possible on input from QCD symmetries and related experimental data. The resulting bounds on isospin violation are sufficiently precise to be of value to on-going experimental and theoretical studies of the nucleon's strange form factors.Comment: 5 pages, 3 figures. Presented at the International Workshop "From Parity Violation to Hadronic Structure and more...", Milos, Greece, 16-20 May 2006. Version 2 is only to update Refs. [21] and [25