Plasma Magnetohydrodynamics and Energy Conversion

Contains reports on seven research projects.U. S. Air Force (Aeronautical Systems Division) under Contract AF33 (615)-1083 with the Air Force Aero Propulsion Laboratory, Wright-Patterson Air Force Base, OhioNational Science Foundation (Grant GK-57

A Atuação da Renault S.A. no Brasil: circuitos espaciais produtivos e círculos de cooperação

TCC(graduação) - Universidade Federal de Santa Catarina. Centro de Filosofia e Ciências Humanas. GeografiaEsta pesquisa tem como principal objetivo analisar o circuito espacial produtivo e os círculos de cooperação da Renault S.A. na indústria automobilística brasileira, buscando identificar a formação dessa indústria e sua desconcentração pelo país, sempre trazendo à centralidade do debate a dialética terceiro-mundista entre Estado e mercado. A fundamentação teórica da pesquisa perpassa os conceitos de circuito espacial produtivo e círculos de cooperação, além de concepções marxistas a respeito da atividade produtiva e da acentuação dos fluxos internacionais, uma vez em que valorizamos tanto a impossibilidade de compreender a produção sem a análise das diversas etapas produtivas em sua realização concreta, quanto o papel central da união entre banco e indústria na intensificação dos fluxos estrangeiros. A metodologia da investigação conta com uma leitura sistemática da literatura produzida sobre o escopo temático, teórico e espaço-temporal, identificando uma linha de investigação focada na instalação da Renault S.A. na Grande Curitiba, além da pesquisa em fontes secundárias sobre a atuação da firma estrangeira no Brasil. Buscamos contribuir com a ciência geográfica ao aumentar o nível de compreensão a respeito da indústria automobilística instalada na Grande Curitiba e ao debater o processo de desconcentração industrial e busca por novas localizações da indústria automobilística. Finalizamos concluindo a impossibilidade de compreender os fluxos internacionais no Brasil sem centralizar a contradição entre Estado e mercado, ao mesmo tempo que compreendemos como, apesar da intensificação dos fluxos internacionais materializar firmas multinacionais pela periferia do capitalismo, seus centros de decisão são mantidos nos países centrais.This research's main objective is to analyse the spatial circuit of production and the cooperation circles of Renault SA in the brazilian automotive industry, intending to identify this industry's formation and its decentralization across the country, always bringing the dialectic between state and market in the Third World to the forefront of the discussion. The theoretical foundation of the research goes through the concepts of spatial circuit of production and cooperation circles, in addition of marxist conceptions of productive activity and the intensification of international capital flows, considering we acknowledge both the impossibility of understanding production without analysing the several steps that constitute the concrete process of production, and the primordial role of the industry-bank cooperation in the intensification of foreign capital flows. The investigation's methodology consists of a systematic reading of the literature produced on the thematic, theoric and temporal-spatial scope, identifying an investigation line focused on the installation of Renaut SA in the Greater Curitiba, along with secondary research sources about this foreign company operations in Brazil. We aim to contribute to the geographical sciences by increasing the extent of understanding of the automotive industry set up in the Greater Curitiba and by debating the industrial decentralization process and the automotive industry's search for new locations. We conclude that it's not possible to understand the international capital flows in Brazil without focusing on the contradiction between state and market; and we come to understand that, despite the intensification of international capital flows materializing multinational firms at the periphery of capitalism, their decision centers are kept in the central countries

Nicotinic acetylcholine receptors modulate osteoclastogenesis

Background: Our aim was to investigate the role of nicotinic acetylcholine receptors (nAChRs) in in-vitro osteoclastogenesis and in in-vivo bone homeostasis. Methods: The presence of nAChR subunits as well as the in-vitro effects of nAChR agonists were investigated by ex vivo osteoclastogenesis assays, real-time polymerase chain reaction, Western blot and flow cytometry in murine bone marrow-derived macrophages differentiated in the presence of recombinant receptor activator of nuclear factor kappa B ligand (RANKL) and macrophage colony-stimulating factor (M-CSF). The bone phenotype of mice lacking various nAChR subunits was investigated by peripheral quantitative computed tomography and histomorphometric analysis. Oscillations in the intracellular calcium concentration were detected by measuring the Fura-2 fluorescence intensity. Results: We could demonstrate the presence of several nAChR subunits in bone marrow-derived macrophages stimulated with RANKL and M-CSF, and showed that they are capable of producing acetylcholine. nAChR ligands reduced the number of osteoclasts as well as the number of tartrate-resistant acidic phosphatase-positive mononuclear cells in a dose-dependent manner. In vitro RANKL-mediated osteoclastogenesis was reduced in mice lacking α7 homomeric nAChR or β2-containing heteromeric nAChRs, while bone histomorphometry revealed increased bone volume as well as impaired osteoclastogenesis in male mice lacking the α7 nAChR. nAChR ligands inhibited RANKL-induced calcium oscillation, a well-established phenomenon of osteoclastogenesis. This inhibitory effect on Ca2+ oscillation subsequently led to the inhibition of RANKL-induced NFATc1 and c-fos expression after long-term treatment with nicotine. Conclusions: We have shown that the activity of nAChRs conveys a marked effect on osteoclastogenesis in mice. Agonists of these receptors inhibited calcium oscillations in osteoclasts and blocked the RANKL-induced activation of c-fos and NFATc1. RANKL-mediated in-vitro osteoclastogenesis was reduced in α7 knockout mice, which was paralleled by increased tibial bone volume in male mice in vivo. © 2016 Mandl et al

Diagnosing mucopolysaccharidosis IVA

Mucopolysaccharidosis IVA (MPS IVA; Morquio A syndrome) is an autosomal recessive lysosomal storage disorder resulting from a deficiency of N-acetylgalactosamine-6-sulfate sulfatase (GALNS) activity. Diagnosis can be challenging and requires agreement of clinical, radiographic, and laboratory findings. A group of biochemical genetics laboratory directors and clinicians involved in the diagnosis of MPS IVA, convened by BioMarin Pharmaceutical Inc., met to develop recommendations for diagnosis. The following conclusions were reached. Due to the wide variation and subtleties of radiographic findings, imaging of multiple body regions is recommended. Urinary glycosaminoglycan analysis is particularly problematic for MPS IVA and it is strongly recommended to proceed to enzyme activity testing even if urine appears normal when there is clinical suspicion of MPS IVA. Enzyme activity testing of GALNS is essential in diagnosing MPS IVA. Additional analyses to confirm sample integrity and rule out MPS IVB, multiple sulfatase deficiency, and mucolipidoses types II/III are critical as part of enzyme activity testing. Leukocytes or cultured dermal fibroblasts are strongly recommended for enzyme activity testing to confirm screening results. Molecular testing may also be used to confirm the diagnosis in many patients. However, two known or probable causative mutations may not be identified in all cases of MPS IVA. A diagnostic testing algorithm is presented which attempts to streamline this complex testing process

An update of the Worldwide Integrated Assessment (WIA) on systemic insecticides. Part 2: impacts on organisms and ecosystems

New information on the lethal and sublethal effects of neonicotinoids and fipronil on organisms is presented in this review, complementing the previous WIA in 2015. The high toxicity of these systemic insecticides to invertebrates has been confirmed and expanded to include more species and compounds. Most of the recent research has focused on bees and the sublethal and ecological impacts these insecticides have on pollinators. Toxic effects on other invertebrate taxa also covered predatory and parasitoid natural enemies and aquatic arthropods. Little, while not much new information has been gathered on soil organisms. The impact on marine coastal ecosystems is still largely uncharted. The chronic lethality of neonicotinoids to insects and crustaceans, and the strengthened evidence that these chemicals also impair the immune system and reproduction, highlights the dangers of this particular insecticidal classneonicotinoids and fipronil. , withContinued large scale – mostly prophylactic – use of these persistent organochlorine pesticides has the potential to greatly decreasecompletely eliminate populations of arthropods in both terrestrial and aquatic environments. Sublethal effects on fish, reptiles, frogs, birds and mammals are also reported, showing a better understanding of the mechanisms of toxicity of these insecticides in vertebrates, and their deleterious impacts on growth, reproduction and neurobehaviour of most of the species tested. This review concludes with a summary of impacts on the ecosystem services and functioning, particularly on pollination, soil biota and aquatic invertebrate communities, thus reinforcing the previous WIA conclusions (van der Sluijs et al. 2015)

A PBPK model recapitulates early kinetics of anti-PEG antibody-mediated clearance of PEG-liposomes

PEGylation is routinely used to extend the systemic circulation of various protein therapeutics and nanomedicines. Nonetheless, mounting evidence is emerging that individuals exposed to select PEGylated therapeutics can develop antibodies specific to PEG, i.e., anti-PEG antibodies (APA). In turn, APA increase both the risk of hypersensitivity to the drug as well as potential loss of efficacy due to accelerated blood clearance of the drug. Despite the broad implications of APA, the timescales and systemic specificity by which APA can alter the pharmacokinetics and biodistribution of PEGylated drugs remain not well understood. Here, we developed a physiologically based pharmacokinetic (PBPK) model designed to resolve APA's impact on both early- and late-phase pharmacokinetics and biodistribution of intravenously administered PEGylated drugs. Our model accurately recapitulates PK and biodistribution data obtained from PET/CT imaging of radiolabeled PEG-liposomes and PEG-uricase in mice with and without APA, as well as serum levels of PEG-uricase in humans. Our work provides another illustration of the power of high-resolution PBPK models for understanding the pharmacokinetic impacts of anti-drug antibodies and the dynamics with which antibodies can mediate clearance of foreign species

Management of Anticoagulant and Thrombolytic Agents in Deep Venous Thrombosis

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/68445/2/10.1177_153857448201600101.pd

The epithelial cholinergic system of the airways

Acetylcholine (ACh), a classical transmitter of parasympathetic nerve fibres in the airways, is also synthesized by a large number of non-neuronal cells, including airway surface epithelial cells. Strongest expression of cholinergic traits is observed in neuroendocrine and brush cells but other epithelial cell types—ciliated, basal and secretory—are cholinergic as well. There is cell type-specific expression of the molecular pathways of ACh release, including both the vesicular storage and exocytotic release known from neurons, and transmembrane release from the cytosol via organic cation transporters. The subcellular distribution of the ACh release machineries suggests luminal release from ciliated and secretory cells, and basolateral release from neuroendocrine cells. The scenario as known so far strongly suggests a local auto-/paracrine role of epithelial ACh in regulating various aspects on the innate mucosal defence mechanisms, including mucociliary clearance, regulation of macrophage function and modulation of sensory nerve fibre activity. The proliferative effects of ACh gain importance in recently identified ACh receptor disorders conferring susceptibility to lung cancer. The cell type-specific molecular diversity of the epithelial ACh synthesis and release machinery implies that it is differently regulated than neuronal ACh release and can be specifically targeted by appropriate drugs