544 research outputs found

    Ouachita graduate named Alpha Chi H.Y. Benedict Fellowship fourth alternate

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    Alpha Chi National College Honor Society named Sidney Salyers of Sugar Land, Texas, the $3,000 H.Y. Benedict Fellowship fourth alternate at the Alpha Chi National Convention in April. Salyers graduated summa cum laude with a Bachelor of Arts degree in communication sciences and disorders from Ouachita Baptist University in May. The H.Y. Benedict Fellowship is awarded to nominees for their first year of graduate study at any institution. Nominees must complete their undergraduate degree in the year of their application for the fellowship and must enroll in a full-time graduate or professional program for the following semester. Applicants for the fellowship are ranked according to overall academic performance within their area of study, service and extracurricular work, work within Alpha Chi and their submitted work samples

    WHY HAS THE PAPER ENTITLED "GREATWALL-PHOSPHORYLATED Α-ENDOSULFINE IS BOTH AN INHIBITOR AND A SUBSTRATE OF PP2A-B55 HETEROTRIMERS" BY WILLIAMS, M.C. ET AL. THAT WAS PUBLISHED IN ELIFE [WILLIAMS, B.C., FILTER, J.J., BLAKE-HODEK, K.A., FUDA, N.J., SHALLOWAY, D. AND GOLDBERG, M.L. (2014) ELIFE, DOI: 10.7554/ELIFE.01695 ] NOT BEEN RETRACTED?

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    The paper entitled "Greatwall-phosphorylated α-Endosulfine is both an inhibitor and a substrate of PP2A-B55 heterotrimers" authored by Williams, B.C. et al. [Williams, B.C., Filter, J.J., Blake-Hodek, K.A., Fuda, N.J., Shalloway, D. and Goldberg, M.L. and Published in the Journal eLife [eLife (2014) e01695, doi: 10.7554/elife.01695] was the subject of an investigative critique [Tung, H.Y.L. (2020) J. Invest. Cri. Pub. Sci. Articles, Vol. 1, pp193-200, DOI: 10.5281/zenodo.5115188]. It was previously reported that the paper by Williams, et al. was riddled with Dishonest Scientific Reported, Data Falsification and possibly Data Fabrication. After, contacting the Editor in Chief of eLife, Drs Michael B. Eisen, the author of this report was referred to the Managing Editor of eLife, Dr Wei Mun Chan who is not an expert in Enzymology by any stretch of imagination. The Managing Editor of eLife apparently obtained some response from Williams, et al. which was not only unsatisfactory scientifically but aggravated the seriousness of this case as it was revealed that Williams et al. obtained conclusions of their paper based on some experiments in which they were counting ~3 cpm of radioactivity above background. When the author of this report pointed the fantastical results that Williams et al. claimed they were able to obtain, the author of this Report received no sign of life from the Managing editor and the Editor in Chief of eLife. This Report provides further evidence that Williams, B.C. et al. committed Dishonest Scientific Reporting, Data Falsification and Data Fabrication in their paper

    WHAT IS THE PURPOSE OF SUBMITTING A PREPRINT ARTICLE TO BIORXIV AND CHEMRXIV: ARE BIORXIV AND CHEMRXIV ACTING AS MOB PEER REVIEW CENSORSHIP BOARD?

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    According to their websites of bioRxiv and chemRxiv do not perform peer reviews of preprint articles that are submitted to them and that they only screen submitted preprint articles for . The experience of this author is that bioRxiv and chemRxiv not only perform extensive reviews of submitted preprint articles, they also act a Mob Peer Review Censorship Board. The qualifications of the Mob Peer Reviewers of bioRxiv and chemRxiv are questionable. It is impossible to contact the persons who run bioRxiv and chemRxiv. It is quite disturbing and disgusting that the flow of scientific information in the "freest country of the world" is controlled by two outfits that acts as Mob Peer Review Censorship Board. The actions of bioRxiv and chemRxiv which operate with tax paper's largesse are selective, opaque, arbitrary and a violations of Fundamental Right of the United States citizens to write and publish

    Distinct contributions of metabolic dysfunction and genetic risk factors in the pathogenesis of non-alcoholic fatty liver disease

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    Funding Information: This study was supported by Academy of Finland Grant 309263 (H.Y.-J.) and Grant 138006 (J.P.), EU H2020 project ?Elucidating Pathways of Steatohepatitis? EPoS Grant 634413 (H.Y.-J.), H2020-JTI-IMI2 EU project 777377-2 Liver Investigation: Testing Marker Utility in Steatohepatitis (LITMUS) (H.Y.-J.), Government Funding (H.Y.-J.), Novo Nordisk Foundation (H.Y.-J., P.K.L., M.A.-K.), Ralph Gr?sbeck Scholarship of the Minerva Foundation (P.K.L.), Novo Nordisk Foundation (P.K.L.), Juho Vainio Foundation (J.P.), Finnish Medical Foundation (V.M.), British Heart Foundation Senior Research Fellowship in Basic Science (FS/15/56/31645) (L.H.) and Kuopio University Hospital Project grant (J.P., EVO/VTR grants 2005-2019). Funding Information: This study was supported by Academy of Finland Grant 309263 (H.Y.-J.) and Grant 138006 (J.P.), EU H2020 project ‘Elucidating Pathways of Steatohepatitis’ EPoS Grant 634413 (H.Y.-J.), H2020-JTI-IMI2 EU project 777377-2 Liver Investigation: Testing Marker Utility in Steatohepatitis (LITMUS) (H.Y.-J.), Government Funding (H.Y.-J.), Novo Nordisk Foundation (H.Y.-J., P.K.L., M.A.-K.), Ralph Gräsbeck Scholarship of the Minerva Foundation (P.K.L.), Novo Nordisk Foundation (P.K.L.), Juho Vainio Foundation (J.P.), Finnish Medical Foundation (V.M.), British Heart Foundation Senior Research Fellowship in Basic Science (FS/15/56/31645) (L.H.) and Kuopio University Hospital Project grant (J.P., EVO/VTR grants 2005-2019). Publisher Copyright: © 2021 The Author(s)Background & Aims: There is substantial inter-individual variability in the risk of non-alcoholic fatty liver disease (NAFLD). Part of which is explained by insulin resistance (IR) (‘MetComp’) and part by common modifiers of genetic risk (‘GenComp’). We examined how IR on the one hand and genetic risk on the other contribute to the pathogenesis of NAFLD. Methods: We studied 846 individuals: 492 were obese patients with liver histology and 354 were individuals who underwent intrahepatic triglyceride measurement by proton magnetic resonance spectroscopy. A genetic risk score was calculated using the number of risk alleles in PNPLA3, TM6SF2, MBOAT7, HSD17B13 and MARC1. Substrate concentrations were assessed by serum NMR metabolomics. In subsets of participants, non-esterified fatty acids (NEFAs) and their flux were assessed by D5-glycerol and hyperinsulinemic-euglycemic clamp (n = 41), and hepatic de novo lipogenesis (DNL) was measured by D2O (n = 61). Results: We found that substrate surplus (increased concentrations of 28 serum metabolites including glucose, glycolytic intermediates, and amino acids; increased NEFAs and their flux; increased DNL) characterized the ‘MetComp’. In contrast, the ‘GenComp’ was not accompanied by any substrate excess but was characterized by an increased hepatic mitochondrial redox state, as determined by serum β-hydroxybutyrate/acetoacetate ratio, and inhibition of hepatic pathways dependent on tricarboxylic acid cycle activity, such as DNL. Serum β-hydroxybutyrate/acetoacetate ratio correlated strongly with all histological features of NAFLD. IR and hepatic mitochondrial redox state conferred additive increases in histological features of NAFLD. Conclusions: These data show that the mechanisms underlying ‘Metabolic’ and ‘Genetic’ components of NAFLD are fundamentally different. These findings may have implications with respect to the diagnosis and treatment of NAFLD. Lay summary: The pathogenesis of non-alcoholic fatty liver disease can be explained in part by a metabolic component, including obesity, and in part by a genetic component. Herein, we demonstrate that the mechanisms underlying these components are fundamentally different: the metabolic component is characterized by hepatic oversupply of substrates, such as sugars, lipids and amino acids. In contrast, the genetic component is characterized by impaired hepatic mitochondrial function, making the liver less able to metabolize these substrates.Peer reviewe

    Dissolution characteristics of extrusion freeformed hydroxyapatite-tricalcium phosphate scaffolds

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    The dissolution behaviour of calcium phosphate filaments made by extrusion freeforming for hard tissue scaffolds was measured. The solubility of filaments with different HA/?-TCP ratios sintered at temperatures from 1,100 to 1,300°C was measured under simulated physiological conditions (tris buffer solution: tris(hydroxyl) methyl–aminomethane–HCl), pH 7.4, 37°C). Calcium and phosphate concentrations were measured separately by inductively coupled plasma (ICP) atomic emission spectroscopy. Surface morphologies and composition before and after immersion were analyzed by SEM and EDS. The results clearly show that as the ?-TCP content increased, the dissolution increased. Higher sintering temperatures, with consequent closure of surface pores, resulted in lower dissolution. Examination of the surface suggested dissolution on preferred sites by pitting. <br/

    Sintering behaviour of calcium phosphate filaments for use as hard tissue scaffolds

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    Lattices consisting of hydroxyapatite (HA) and ?-tricalcium phosphate (?-TCP) mixtures were prepared by extrusion freeforming to serve as bone substitute structures in which both shape and structural hierarchy are determined by computer control. Fine ceramic filaments were prepared from a non-aqueous, solvent-based, ceramic–polymer paste and sintered at temperatures from 1100 to 1300 °C. The characteristics of the sintered filaments were investigated because this determines the resulting microporosity and phase content while the higher levels of porosity are computer controlled. The effects of HA/?-TCP ratio and sintering temperature on the microstructure, density, shrinkage and final phase content were studied. These results provide a design reference for hard tissue engineering scaffolds built from these materials.<br/

    Extrusion pressure generated in high alumina content paste extrusion

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    Four different alumina pastes with various solvent volume fractions were processed by extrusion free forming and the pressures generated in the extrusion process were recorded and analyzed. The extrusion pressure increased as the solvent volume fraction decreased. Air bubbles and particle agglomeration influenced the final properties of the product and caused pressure to fluctuate. An aging process for the paste was introduced to obtain more even solvent distribution and hence deliver highly regular ceramic lattice structure

    Regulation of TMPRSS6 by BMP6 and iron in human cells and mice

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    Meynard, D., Vaja, V., Sun, C.C., Corradini, E., Chen, S., López-Otín, C., Grgurevic, L., Hong, C.C., Stirnberg, M., Gütschow, M., Vukicevic, S., Babitt, J.L., Lin, H.Y
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