414 research outputs found
Mechanism for serrated cathode dissolution in Cu/Sn/Cu interconnect under electron current stressing
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Critical Concerns in Soldering Reactions Arising from Space Confinement in 3-D IC Packages
No full textWHY 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J.J., BLAKE-HODEK, K.A., FUDA, N.J., SHALLOWAY, D. AND GOLDBERG, M.L. (2014) ELIFE, DOI: 10.7554/ELIFE.01695 ] NOT BEEN RETRACTED?
No full textThe 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?
No full textAccording 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
Full text linkFunding 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
Modeling biogas production from organic fraction of MSW co-digested with MSWI ashes in anaerobic bioreactors
No full textThis study aims at investigating the effects of MSW incinerator fly ash (FA) and bottom ash (BA) on the anaerobic co-digestion of OFMSW with FA or BA. It also simulates the biogas production from various dosed and control bioreactors. Results showed that suitable ashes addition (FA/MSW 10 and 20 g L?1 and BA/MSW 100 g L?1) could improve the MSW anaerobic digestion and enhance the biogas production rates. FA/MSW 20 g L?1 bioreactor had the higher biogas production and rate implying the potential option for MSW anaerobic co-digestion. Modeling studies showed that exponential plot simulated better for FA/MSW 10 g L?1 and control bioreactors while Gaussian plot was applicable for FA/MSW 20 g L?1 one. Linear and exponential plot of descending limb both simulated better for BA/MSW 100 g L?1 bioreactor. Modified Gompertz plot showed higher correlation of biogas accumulation than exponential rise to maximum plot for all bioreactor
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