82 research outputs found

    External mass transfer in a laser sintered structured reactor for continuous hydrogenation of alkynes

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    This work presents a study on the continuous operation of a structured reactor for alkyne hydrogenation in the field of Process Intensification. The reactor consists of a laser sintered metal structure characterized by a regular geometry, coated with a layer of ZnO/Al2O3 and impregnated with palladium nanoparticles. The partial hydrogenation of 2-methyl-3-butyn-2-ol with co-current gas-liquid upward flow was used as the test reaction system. A plug flow reactor model was applied to study the mass transfer phenomena under the reacting conditions. The reaction kinetics with the Pd/ZnO-based catalyst were simplified using a power rate law expression. The results in terms of the overall mass transfer coefficient Kov were modelled with a predictive Sherwood number correlation whose parameters were estimated by means of an optimization procedure. The structured reactor shows an overall mass transfer coefficient ranging between 0.2 and 1.2 s−1 depending on the operating conditions. The model is able to predict the impact of temperature (333–363 K), pressure (3.0–7.0 bar), gas velocity (0.005–0.024 m s−1) and liquid velocity (0.025–0.085 m s−1) on the overall mass transfer coefficient with a maximum deviation of 15%.</p

    Systems-level metabolism of the Altered Schaedler Flora, a complete gut microbiota

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    The Altered Schaedler Flora (ASF) is a model microbial community with both in vivo and in vitro relevance. Here we provide the first characterization of the ASF community in vitro, independent of a murine host. We compared the functional genetic content of the ASF to wild murine metagenomes and found that the ASF functionally represents wild microbiomes better than random consortia of similar taxonomic composition. We developed a chemically-defined medium that supported growth of seven of the eight ASF members. To elucidate the metabolic capabilities of these ASF species—including potential for interactions such as cross feeding—we performed a spent media screen and analyzed the results through dynamic growth measurements and non-targeted metabolic profiling. We found that cross-feeding is relatively rare (32 of 3 570 possible cases), but is enriched between Clostridium ASF356 and Parabacteroides ASF519. We identified many cases of emergent metabolism (856 of 3 570 possible cases). These data will inform efforts to understand ASF dynamics and spatial distribution in vivo, to design pre- and probiotics that modulate relative abundances of ASF members, and will be essential for validating computational models of ASF metabolism. Well-characterized, experimentally tractable microbial communities enable research that can translate into more effective microbiome-targeted therapies to improve human health

    Amber Valley Baseball Team

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    Photograph - Amber Valley baseball team in the Northern Alberta Baseball League, Athabasca, Alberta. Top row, left to right: Cliff Brown, Fordie Medlock, Horace Hinton, J.B. Brown, Alvin Brown, Alonzo Edwards and Ozzie Lipscombe. Front row, left to right: Booker Edwards, Arthur Saunders and Kenny Edward

    Protein- and zinc-deficient diets modulate the murine microbiome and metabolic phenotype

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    BACKGROUND: Environmental enteropathy, which is linked to undernutrition and chronic infections, affects the physical and mental growth of children in developing areas worldwide. Key to understanding how these factors combine to shape developmental outcomes is to first understand the effects of nutritional deficiencies on the mammalian system including the effect on the gut microbiota.OBJECTIVE: We dissected the nutritional components of environmental enteropathy by analyzing the specific metabolic and gut-microbiota changes that occur in weaned-mouse models of zinc or protein deficiency compared with well-nourished controls.DESIGN: With the use of a 1H nuclear magnetic resonance spectroscopy-based metabolic profiling approach with matching 16S microbiota analyses, the metabolic consequences and specific effects on the fecal microbiota of protein and zinc deficiency were probed independently in a murine model.RESULTS: We showed considerable shifts within the intestinal microbiota 14-24 d postweaning in mice that were maintained on a normal diet (including increases in Proteobacteria and striking decreases in Bacterioidetes). Although the zinc-deficient microbiota were comparable to the age-matched, well-nourished profile, the protein-restricted microbiota remained closer in composition to the weaned enterotype with retention of Bacteroidetes. Striking increases in Verrucomicrobia (predominantly Akkermansia muciniphila) were observed in both well-nourished and protein-deficient mice 14 d postweaning. We showed that protein malnutrition impaired growth and had major metabolic consequences (much more than with zinc deficiency) that included altered energy, polyamine, and purine and pyrimidine metabolism. Consistent with major changes in the gut microbiota, reductions in microbial proteolysis and increases in microbial dietary choline processing were observed.CONCLUSIONS: These findings are consistent with metabolic alterations that we previously observed in malnourished children. The results show that we can model the metabolic consequences of malnutrition in the mouse to help dissect relevant pathways involved in the effects of undernutrition and their contribution to environmental enteric dysfunction.</p

    Increased urinary trimethylamine N-oxide following cryptosporidium infection and protein malnutrition independent of microbiome effects

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    Cryptosporidium infections have been associated with growth stunting, even in the absence of diarrhea. Having previously detailed the effects of protein deficiency on both microbiome and metabolome in this model, we now describe the specific gut microbial and biochemical effects of Cryptosporidium infection. Protein-deficient mice were infected with Cryptosporidium parvum oocysts for 6-13 days and compared with uninfected controls. Following infection, there was an increase in the urinary excretion of choline- and amino-acid-derived metabolites. Conversely, infection reduced the excretion of the microbial-host cometabolite (3-hydroxyphenyl)propionate-sulfate and disrupted metabolites involved in the tricarboxylic acid (TCA) cycle. Correlation analysis of microbial and biochemical profiles resulted in associations between various microbiota members and TCA cycle metabolites, as well as some microbial-specific degradation products. However, no correlation was observed between the majority of the infection-associated metabolites and the fecal bacteria, suggesting that these biochemical perturbations are independent of concurrent changes in the relative abundance of members of the microbiota. We conclude that cryptosporidial infection in protein-deficient mice can mimic some metabolic changes seen in malnourished children and may help elucidate our understanding of long-term metabolic consequences of early childhood enteric infections.</p

    Inferring metabolic mechanisms of interaction within a defined gut microbiota

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    The diversity and number of species present within microbial communities create the potential for a multitude of interspecies metabolic interactions. Here, we develop, apply, and experimentally test a framework for inferring metabolic mechanisms associated with interspecies interactions. We perform pairwise growth and metabolome profiling of co-cultures of strains from a model mouse microbiota. We then apply our framework to dissect emergent metabolic behaviors that occur in co-culture. Based on one of the inferences from this framework, we identify and interrogate an amino acid cross-feeding interaction and validate that the proposed interaction leads to a growth benefit in vitro. Our results reveal the type and extent of emergent metabolic behavior in microbial communities composed of gut microbes. We focus on growth-modulating interactions, but the framework can be applied to interspecies interactions that modulate any phenotype of interest within microbial communities

    Substate regionalism: a study of coordination at the substate level

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    In the late 1960s, there was an increase in federal, state, and local interest in the concept of substate regionalism. This interest has led to the creation of substate district systems in at least thirty-eight states. Substate district systems generally provide for multi-county districts within which there are some sorts of voluntary councils of governments responsible for planning and coordination of activities on an area-, wide basis. Interest in substate regionalism was a product of several factors. Perhaps the major ones were: 1) local governments often found themselves without sufficient jurisdictional authority or financial resources, or both, with which to deal with areawide problems affecting them; 2) state governments found that the increasing complexity and expense in administering state programs required a uniform system through which all state activities could be planned and services delivered; and 3) the federal government began to emphasize much more strongly coordination of federal programs on an areawide basis with the passage of the Demonstration Cities and Metropolitan Development Act of 1966 and the Intergovernmental Cooperation Act of 1968. Significant power in the form of review authority over most federal grant-in-aid-applications (OMB Circular A-95) is granted to district councils of governments. The purpose of this study is to examine substate district systems in twelve states to determine their modes of establishment, their activities, their intergovernmental relations, and their likely futuie roles.Political Science, Department o

    Cross-modulation of pathogen-specific pathways enhances malnutrition during enteric co-infection with Giardia lamblia and enteroaggregative Escherichia coli.

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    Diverse enteropathogen exposures associate with childhood malnutrition. To elucidate mechanistic pathways whereby enteric microbes interact during malnutrition, we used protein deficiency in mice to develop a new model of co-enteropathogen enteropathy. Focusing on common enteropathogens in malnourished children, Giardia lamblia and enteroaggregative Escherichia coli (EAEC), we provide new insights into intersecting pathogen-specific mechanisms that enhance malnutrition. We show for the first time that during protein malnutrition, the intestinal microbiota permits persistent Giardia colonization and simultaneously contributes to growth impairment. Despite signals of intestinal injury, such as IL1α, Giardia-infected mice lack pro-inflammatory intestinal responses, similar to endemic pediatric Giardia infections. Rather, Giardia perturbs microbial host co-metabolites of proteolysis during growth impairment, whereas host nicotinamide utilization adaptations that correspond with growth recovery increase. EAEC promotes intestinal inflammation and markers of myeloid cell activation. During co-infection, intestinal inflammatory signaling and cellular recruitment responses to EAEC are preserved together with a Giardia-mediated diminishment in myeloid cell activation. Conversely, EAEC extinguishes markers of host energy expenditure regulatory responses to Giardia, as host metabolic adaptations appear exhausted. Integrating immunologic and metabolic profiles during co-pathogen infection and malnutrition, we develop a working mechanistic model of how cumulative diet-induced and pathogen-triggered microbial perturbations result in an increasingly wasted host
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