Pulsed Electric Discharge in Active Metallic Grains for Water Purification Processes

Chemical reactions in electric metal pulse dispersion in the aqueous solutions of inorganic substance (НSiO[3]{–}, Ni{2+}, Н[2]AsO[4]{–}, Mn{2+}, Cr[2]O[7]{2–}) were determined through IR spectroscopy, X-ray phase, chemical, kinetic, and thermodynamic analyses. Under such conditions, both reduction and oxidation reactions occur, as well as, locally initiated by heating, hydrolysis and exchange reactions without changing the oxidation rate of the dissolved substance itself. Reduction and oxidation of dissolved substances is determined by the generation and activation of high dispersed Fe in an electric discharge. Physical and chemical processes which take place under the action of pulse electric discharges upon the layer of metallic grains in salt solution, containing НSiO[3]{–}, Ni{2+}, Н[2]AsO[4]{–}, Mn{2+}, Cr[2]O[7]{2–} ions were determined on the basis of product composition, obtained experimentally and the thermodynamic data. It was shown, that PED discharge in heterogeneous mediums can be used for waste and natural water purification

A signal from inside the peroxisome initiates its division by promoting the remodeling of the peroxisomal membrane

We define the dynamics of spatial and temporal reorganization of the team of proteins and lipids serving peroxisome division. The peroxisome becomes competent for division only after it acquires the complete set of matrix proteins involved in lipid metabolism. Overloading the peroxisome with matrix proteins promotes the relocation of acyl-CoA oxidase (Aox), an enzyme of fatty acid β-oxidation, from the matrix to the membrane. The binding of Aox to Pex16p, a membrane-associated peroxin required for peroxisome biogenesis, initiates the biosynthesis of phosphatidic acid and diacylglycerol (DAG) in the membrane. The formation of these two lipids and the subsequent transbilayer movement of DAG initiate the assembly of a complex between the peroxins Pex10p and Pex19p, the dynamin-like GTPase Vps1p, and several actin cytoskeletal proteins on the peroxisomal surface. This protein team promotes membrane fission, thereby executing the terminal step of peroxisome division

Chemical genetic screen identifies lithocholic acid as an anti-aging compound that extends yeast chronological life span in a TOR-independent manner, by modulating housekeeping longevity assurance processes

In chronologically aging yeast, longevity can be extended by administering a caloric restriction (CR) diet or some small molecules. These life-extending interventions target the adaptable target of rapamycin (TOR) and cAMP/protein kinase A (cAMP/PKA) signaling pathways that are under the stringent control of calorie availability. We designed a chemical genetic screen for small molecules that increase the chronological life span of yeast under CR by targeting lipid metabolism and modulating housekeeping longevity pathways that regulate longevity irrespective of the number of available calories. Our screen identifies lithocholic acid (LCA) as one of such molecules. We reveal two mechanisms underlying the life-extending effect of LCA in chronologically aging yeast. One mechanism operates in a calorie availability-independent fashion and involves the LCA-governed modulation of housekeeping longevity assurance pathways that do not overlap with the adaptable TOR and cAMP/PKA pathways. The other mechanism extends yeast longevity under non-CR conditions and consists in LCA-driven unmasking of the previously unknown anti-aging potential of PKA. We provide evidence that LCA modulates housekeeping longevity assurance pathways by suppressing lipid-induced necrosis, attenuating mitochondrial fragmentation, altering oxidation-reduction processes in mitochondria, enhancing resistance to oxidative and thermal stresses, suppressing mitochondria-controlled apoptosis, and enhancing stability of nuclear and mitochondrial DNA

Carbon isotopes, stratigraphy, and environmental change: the Middle–Upper Cambrian Positive Excursion (SPICE) in Port au Port Group, western Newfoundland, Canada

In many basins, Upper Cambrian carbonate successions display intervals with a positive carbon isotope excursion (CIE) of up to +5‰. In North America, this marks the boundary between the Sauk II–III super-sequences. A Steptoean positive carbon isotope excursion (SPICE) locality previously identified in the Port au Port peninsula, western Newfoundland, has been revisited and an additional potential SPICE locality found. In both locations, a CIE is found to be associated with a prominent bioherm and sandstone layer within a sequence of carbonate rocks. At March Point columnar stromatolites occur, whereas at Felix Cove thrombolites can be seen. In the latter, the sandstone immediately overlies the thrombolites coincident with the CIE, whereas at March Point a dolomitized grainstone occurs above the stromatolites. The sandstone at this locality post-dates the CIE. Although lower than the SPICE in some localities, a positive CIE is present in both sections: March Point (+1.1‰) and Felix Cove (+1.8‰). Additionally, δ13Corg rises from −30.0‰ to −22.0‰ at March Point and from −27‰ to −24.0‰ at Felix Cove and, in accordance with previously published work, we suggest that this could be the SPICE. Comparison of the stratigraphy and petrography between the two localities suggest that both depositional and diagenetic factors could have influenced the nature of the interpreted SPICE in Newfoundland. It is also possible that the local carbon isotopic signature may have been influenced by a semi-restricted depositional and early diagenetic environment related to the paleogeographic configuration rather than the global marine excursion

Nucleosynthetic molybdenum isotope anomalies in iron meteorites – new evidence for thermal processing of solar nebula material

publisher: Elsevier articletitle: Nucleosynthetic molybdenum isotope anomalies in iron meteorites – new evidence for thermal processing of solar nebula material journaltitle: Earth and Planetary Science Letters articlelink: https://doi.org/10.1016/j.epsl.2017.05.001 content_type: article copyright: © 2017 The Authors. Published by Elsevier B.V.© 2017 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/). https://doi.org/10.1016/j.epsl.2017.05.001

Chemical genetic screen identifies lithocholic acid as an anti-aging compound that extends yeast chronological life span in a TOR-independent manner, by modulating housekeeping longevity assurance processes

In chronologically aging yeast, longevity can be extended by administering a caloric restriction (CR) diet or some small molecules. These life-extending interventions target the adaptable target of rapamycin (TOR) and cAMP/protein kinase A (cAMP/PKA) signaling pathways that are under the stringent control of calorie availability. We designed a chemical genetic screen for small molecules that increase the chronological life span of yeast under CR by targeting lipid metabolism and modulating housekeeping longevity pathways that regulate longevity irrespective of the number of available calories. Our screen identifies lithocholic acid (LCA) as one of such molecules. We reveal two mechanisms underlying the life-extending effect of LCA in chronologically aging yeast. One mechanism operates in a calorie availability-independent fashion and involves the LCA-governed modulation of housekeeping longevity assurance pathways that do not overlap with the adaptable TOR and cAMP/PKA pathways. The other mechanism extends yeast longevity under non-CR conditions and consists in LCA-driven unmasking of the previously unknown anti-aging potential of PKA. We provide evidence that LCA modulates housekeeping longevity assurance pathways by suppressing lipid-induced necrosis, attenuating mitochondrial fragmentation, altering oxidation-reduction processes in mitochondria, enhancing resistance to oxidative and thermal stresses, suppressing mitochondria-controlled apoptosis, and enhancing stability of nuclear and mitochondrial DNA

Creative destruction in science

Drawing on the concept of a gale of creative destruction in a capitalistic economy, we argue that initiatives to assess the robustness of findings in the organizational literature should aim to simultaneously test competing ideas operating in the same theoretical space. In other words, replication efforts should seek not just to support or question the original findings, but also to replace them with revised, stronger theories with greater explanatory power. Achieving this will typically require adding new measures, conditions, and subject populations to research designs, in order to carry out conceptual tests of multiple theories in addition to directly replicating the original findings. To illustrate the value of the creative destruction approach for theory pruning in organizational scholarship, we describe recent replication initiatives re-examining culture and work morality, working parents\u2019 reasoning about day care options, and gender discrimination in hiring decisions. Significance statement It is becoming increasingly clear that many, if not most, published research findings across scientific fields are not readily replicable when the same method is repeated. Although extremely valuable, failed replications risk leaving a theoretical void\u2014 reducing confidence the original theoretical prediction is true, but not replacing it with positive evidence in favor of an alternative theory. We introduce the creative destruction approach to replication, which combines theory pruning methods from the field of management with emerging best practices from the open science movement, with the aim of making replications as generative as possible. In effect, we advocate for a Replication 2.0 movement in which the goal shifts from checking on the reliability of past findings to actively engaging in competitive theory testing and theory building. Scientific transparency statement The materials, code, and data for this article are posted publicly on the Open Science Framework, with links provided in the article

A framework for human microbiome research

A variety of microbial communities and their genes (the microbiome) exist throughout the human body, with fundamental roles in human health and disease. The National Institutes of Health (NIH)-funded Human Microbiome Project Consortium has established a population-scale framework to develop metagenomic protocols, resulting in a broad range of quality-controlled resources and data including standardized methods for creating, processing and interpreting distinct types of high-throughput metagenomic data available to the scientific community. Here we present resources from a population of 242 healthy adults sampled at 15 or 18 body sites up to three times, which have generated 5,177 microbial taxonomic profiles from 16S ribosomal RNA genes and over 3.5 terabases of metagenomic sequence so far. In parallel, approximately 800 reference strains isolated from the human body have been sequenced. Collectively, these data represent the largest resource describing the abundance and variety of the human microbiome, while providing a framework for current and future studies