3,278 research outputs found

    FAIRNESS AND SHORT RUN PRICE ADJUSTMENT IN POSTED OFFER MARKETS

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    Questionnaire studies show that perceptions of fairness cause people to resist price increases following abrupt changes in conditions with no cost justification. We examine this hypothesis in posted-offer markets extending previous work. Consistent with the hypothesis, in the profit disclosure (fairness) treatment prices are initially below those in the cost and the no disclosure treatments. Over time prices converge in all treatments to the competitive surplus maximizing equilibrium. Fairness is thus interpreted as being a result of expectations that are not sustainable. Expectations adapt as the market converges to the predicted competitive equilibrium.

    Production of methyl ethyl ketone from biomass using a hybrid biochemical/catalytic approach

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    The recent demand for sustainable routes to fuels and chemicals has led to an increased amount of research in conversion of natural resources. A potential approach for conversion of biomass to fuels and chemicals is to combine biochemical and chemical processes. This research used microbial fermentation to produce 2,3-butanediol, which was then converted to methyl ethyl ketone by dehydration over a solid acid catalyst. The fermentation process was performed using the bacteria Klebsiella oxytoca (K.O). 2,3-butanediol then dehydrated to form methyl ethyl ketone on a solid acid catalyst, the proton form of ZSM-5, and heat. The goal was to determine the reaction kinetics of 2,3-butanediol dehydration over ZSM-5, and to demonstrate the hybrid biochemical/thermochemical approach for synthesizing chemicals from biomass. It was found that ZSM-5 produced methyl ethyl ketone with high selectivity (greater than 90%), and could convert fermentative 2,3-butanediol to methyl ethyl ketone. The reaction order of 2,3-butanediol dehydration was found to be slightly large than one, and an activation energy of 32.3 kJ/mol was measured

    Simplified CFD based Approach for Estimation of Heat Flux over Wedge Models in High Speed Plasma Flows

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    Analysis of plasma flows at hypersonic velocity over blunt bodies is quite complex and challenging as it involves complex flow physics and carries several uncertainties. Simultaneous simulation of all the parameters as existing in re-entry flight puts constraints on most of the ground based experiments. Numerical simulations, on the other hand, require modelling of ionisation and real gas effects and prove to be computationally costly. This paper highlights the development of unstructured, cell centred second order accurate parallel version of in-house computational fluid dynamics (CFD) solver where high temperature equivalent properties used from Hansen’s 7 species model and establishment of a simplified procedure for estimation of heat flux over wedge models tested in Plasma Wind Tunnel facility, Vikram Sarabhai Space Centre. Numerical simulations were carried out for Plasma tunnel initially to get the flow properties inside the tunnel when operated without any model. A simplified CFD based approach is established for computing the heat flux over the bodies tested inside the tunnel and compared with the measured data. The comparison of numerical and measured values shows that the proposed methodology captures the flow physics and various parameters with acceptable levels of accuracy

    SEAD Virtual Archive: Building a Federation of Institutional Repositories for Long Term Data Preservation

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    Major research universities are grappling with their response to the deluge of scientific data emerging through research by their faculty. Many are looking to their libraries and the institutional repository as a solution. Scientific data introduces substantial challenges that the document-based institutional repository may not be suited to deal with. The Sustainable Environment - Actionable Data (SEAD) Virtual Archive specifically addresses the challenges of “long tail” scientific data. In this paper, we propose requirements, policy and architecture to support not only the preservation of scientific data today using institutional repositories, but also its rich access and use into the future

    Calix[n]arene derivatives for gas storage

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    Abstract only availableThe calix[n]arenes are versatile inclusion compounds (Scheme 1) comprise of cyclic, polyphenolic compounds that can be tailored synthetically by altering X, Y, R and n. In solid state, we found simple calixarenes are quite interesting for example separation of hydrogen from mixture of gases so our attention turned into the closely related calixarenes for sorption studies. With this little back ground on calixarenes and their uses in solid state, we designed and synthesized tert-butylsulfonylcalix[4]arene and Tetra-p-tert-butyl-tetramethoxysulfonylcalix[4]arene from tert-butylthiacalix[4]arene by oxidizing in the presence H2O2 or NaBO3 in exceptional yield. Furthermore, asymmetric bridging of two calix[4]arene molecules to form a calixarene tubes with a larger and easily accessible cavity was also attempted to synthesize. Finally, H1NMR spectral and X- ray crystallographic modeling studies was done to reveal the conformational characteristics of the synthesized compounds.Stevens' Chemistry Progra

    Glucosamine prevents in vitro collagen degradation in chondrocytes by inhibiting advanced lipoxidation reactions and protein oxidation

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    Osteoarthritis (OA) affects a large segment of the aging population and is a major cause of pain and disability. At present, there is no specific treatment available to prevent or retard the cartilage destruction that occurs in OA. Recently, glucosamine sulfate has received attention as a putative agent that may retard cartilage degradation in OA. The precise mechanism of action of glucosamine is not known. We investigated the effect of glucosamine in an in vitro model of cartilage collagen degradation in which collagen degradation induced by activated chondrocytes is mediated by lipid peroxidation reaction. Lipid peroxidation in chondrocytes was measured by conjugated diene formation. Protein oxidation and aldehydic adduct formation were studied by immunoblot assays. Antioxidant effect of glucosamine was also tested on malondialdehyde (thiobarbituric acid-reactive substances [TBARS]) formation on purified lipoprotein oxidation for comparison. Glucosamine sulfate and glucosamine hydrochloride in millimolar (0.1 to 50) concentrations specifically and significantly inhibited collagen degradation induced by calcium ionophore-activated chondrocytes. Glucosamine hydrochloride did not inhibit lipid peroxidation reaction in either activated chondrocytes or in copper-induced oxidation of purified lipoproteins as measured by conjugated diene formation. Glucosamine hydrochloride, in a dose-dependent manner, inhibited malondialdehyde (TBARS) formation by oxidized lipoproteins. Moreover, we show that glucosamine hydrochloride prevents lipoprotein protein oxidation and inhibits malondialdehyde adduct formation in chondrocyte cell matrix, suggesting that it inhibits advanced lipoxidation reactions. Together, the data suggest that the mechanism of decreasing collagen degradation in this in vitro model system by glucosamine may be mediated by the inhibition of advanced lipoxidation reaction, preventing the oxidation and loss of collagen matrix from labeled chondrocyte matrix. Further studies are needed to relate these in vitro findings to the retardation of cartilage degradation reported in OA trials investigating glucosamine

    Assess the frequency and severity of adverse drug reactions due to errors in drug intake at a tertiary care hospital

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    Background: Drug-related problems are an important cause of morbidity and mortality and a significant burden on healthcare resources. There are few studies to account for errors in drug intake leading to adverse drug reactions (ADRs). This study was pursued with the objective of determining the frequency and severity of the ADRs resulting from erroneous drug intake, the expenses incurred in treating the same.Methods: The study was a prospective, cross-sectional, observational study. The study subjects were patients with ADRs due to errors in drug intake and from self-medication. All the information regarding the ADR were collected as per ADR reporting form issued by Central Drugs Standard Control Organization. Causality was assessed by both Naranjo and the WHO criteria for causality assessment. Direct cost of all the medications, hospital charges (admission, bed charges, consultations paid, treatment charges, investigations, and conveyance charges) were recorded to find the financial burden due to error in drug intake.Results: The study showed that nearly 30% of the ADRs were due to errors in drug intake and the major contributing factor is self-modification either by discontinuation or missed doses. Major drugs that are implicated in these ADRs were that of metformin and insulins among anti-diabetic drugs and amlodipine and atenolol among antihypertensives. These two groups contributed to 18 (62%) of the total 29 ADRs. Organ system commonly involved was central nervous system and that was followed by musculoskeletal system. The average direct cost incurred in the management of these ADRs was Rs. 5773 for non-serious adverse events (SAE’s) and Rs. 11,400 for SAE’s.Conclusion: Proper education about the importance of compliance and damaging consequences of self-modification of drug dosage in patients who are on treatment for chronic disorders like diabetes and hypertension will be an effective strategy to prevent many of these ADRs

    Heat shock-induced phosphorylation of TAR DNA-binding protein 43 (TDP-43) by MAPK/ERK kinase regulates TDP-43 function

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    TAR DNA-binding protein (TDP-43) is a highly conserved and essential DNA- and RNA-binding protein that controls gene expression through RNA processing, in particular, regulation of splicing. Intracellular aggregation of TDP-43 is a hallmark of amyotrophic lateral sclerosis and ubiquitin-positive frontotemporal lobar degeneration. This TDP-43 pathology is also present in other types of neurodegeneration including Alzheimer's disease. We report here that TDP-43 is a substrate of MEK, a central kinase in the MAPK/ERK signaling pathway. TDP-43 dual phosphorylation by MEK, at threonine 153 and tyrosine 155 (p-T153/Y155), was dramatically increased by the heat shock response (HSR) in human cells. HSR promotes cell survival under proteotoxic conditions by maintaining protein homeostasis and preventing protein misfolding. MEK is activated by HSR and contributes to the regulation of proteome stability. Phosphorylated TDP-43 was not associated with TDP-43 aggregation, and p-T153/Y155 remained soluble under conditions that promote protein misfolding. We found that active MEK significantly alters TDP-43-regulated splicing and that phosphomimetic substitutions at these two residues reduce binding to GU-rich RNA. Cellular imaging using a phospho-specific p-T153/Y155 antibody showed that phosphorylated TDP-43 was specifically recruited to the nucleoli, suggesting that p-T153/Y155 regulates a previously unappreciated function of TDP-43 in the processing of nucleolar-associated RNA. These findings highlight a new mechanism that regulates TDP-43 function and homeostasis through phosphorylation and, therefore, may contribute to the development of strategies to prevent TDP-43 aggregation and to uncover previously unexplored roles of TDP-43 in cell metabolism

    Transcriptomic comparison of Drosophila snRNP biogenesis mutants reveals mutant-specific changes in pre-mRNA processing: implications for spinal muscular atrophy

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    Survival motor neuron (SMN) functions in the assembly of spliceosomal small nuclear ribonucleoproteins (snRNPs) that catalyze pre-mRNA splicing. Here, we used disruptions in Smn and two additional snRNP biogenesis genes, Phax and Ars2, to classify RNA processing differences as snRNP-dependent or gene-specific in Drosophila. Phax and Smn mutants exhibited comparable reductions in snRNAs, and comparison of their transcriptomes uncovered shared sets of RNA processing changes. In contrast, Ars2 mutants displayed only small decreases in snRNA levels, and RNA processing changes in these mutants were generally distinct from those identified in Phax and Smn animals. Instead, RNA processing changes in Ars2 mutants support the known interaction of Ars2 protein with the cap-binding complex, as splicing changes showed a clear bias toward the first intron. Bypassing disruptions in snRNP biogenesis, direct knockdown of spliceosomal proteins caused similar changes in the splicing of snRNP-dependent events. However, these snRNP-dependent events were largely unaltered in three Smn mutants expressing missense mutations that were originally identified in human spinal muscular atrophy (SMA) patients. Hence, findings here clarify the contributions of Phax, Smn, and Ars2 to snRNP biogenesis in Drosophila, and loss-of-function mutants for these proteins reveal differences that help disentangle cause and effect in SMA model flies
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