990 resultados para Roth, Fedor


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We are witnessing a fundamental transformation in how Internet of Things (IoT) is having an impact on the experience users have with data-driven devices, smart appliances, and connected products. The experience of any place is commonly defined as the result of a series of user engagements with a surrounding place in order to carry out daily activities (Golledge, 2002). Knowing about users? experiences becomes vital to the process of designing a map. In the near future, a user will be able to interact directly with any IoT device placed in his surrounding place and very little is known on what kinds of interactions and experiences a map might offer (Roth, 2015). The main challenge is to develop an experience design process to devise maps capable of supporting different user experience dimensions such as cognitive, sensory-physical, affective, and social (Tussyadiah and Zach, 2012). For example, in a smart city of the future, the IoT devices allowing a multimodal interaction with a map could help tourists in the assimilation of their knowledge about points of interest (cognitive experience), their association of sounds and smells to these places (sensory-physical experience), their emotional connection to them (affective experience) and their relationships with other nearby tourists (social experience). This paper aims to describe a conceptual framework for developing a Mapping Experience Design (MXD) process for building maps for smart connected places of the future. Our MXD process is focussed on the cognitive dimension of an experience in which a person perceives a place as a "living entity" that uses and feeds through his experiences. We want to help people to undergo a meaningful experience of a place through mapping what is being communicated during their interactions with the IoT devices situated in this place. Our purpose is to understand how maps can support a person?s experience in making better decisions in real-time.

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Antecedentes: El potencial alergénico de las proteínas puede alterarse mediante modificaciones fisicoquímicas. El glutatión (GSH) es un agente reductor utilizado como antioxidante en productos alimentarios. Objetivo: Este estudio pretende caracterizar el plegamiento natural de las proteínas de melocotón y cuantificar la alergenicidad del alérgeno mayor del melocotón, Pru p 3, natural y reducido. Métodos: Para ello, se purificó Pru p 3 y se analizó su conformación mediante dicroismo circular (DC). Mediante el análisis con tiol fluorescente, se detectaron las proteínas reducidas en melocotones frescos. Pru p 3 reducido por GSH fue analizado mediante un ensayo in vitro de proliferación de células T e in vivo mediante prueba cutánea. Resultados: Pru p 3 reducido produjo reacciones variables en las pruebas cutáneas de los pacientes alérgicos a melocotón; sin embargo, su estabilidad a la digestión gastrointestinal fue similar a la de la forma natural. La respuesta proliferativa de las células mononucleares de los pacientes alérgicos frente a Pru p 3 reducido mostró una tendencia a ser inferior, mientras que la secreción de citocinas IFN?, IL5 e IL10 fue similar a la producida con la forma natural. La reducción alteró la unión de la IgE a Pru p 3 en un pool de sueros de pacientes alérgicos a melocotón. Conclusin: En conclusión, el glutatión es capaz de reducir Pru p 3, al menos de forma transitoria. En nuestro estudio, la reducción no afectó a la alergenicidad de Pru p 3, de forma que dicho aditivo no parece resolver el riesgo de alergia en pacientes alérgicos a melocotón. Palabras clave: GSH. Pru p 3. Alergia a melocotón. Agente reductor. Unión a IgE.

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We conclude that Bet v 1 and Bos d 5 not only structurally mimic human LCN2, but also functionally by their ability to bind iron via siderophores. The apo-forms promote Th2 cells, whereas the holo-forms appear to be immunosuppressive. These results provide for the first time a functional understanding on the principle of allergenicity of major allergens from entirely independent sources, like birch and milk.

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O objetivo deste estudo foi comparar as angulações e torques de braquetes de marcas comerciais distintas em relação à prescrição de Roth e também em relação aos valores preconizados pelo fabricante. Foram utilizados 150 braquetes metálicos de aço inoxidável, de caninos e incisivos superiores na respectiva prescrição, avaliadas por meio de um perfilômetro. Após a coleta dos dados e aplicação do tratamento estatístico, os resultados demonstraram que os valores de torque obtidos com a prescrição de Roth foram semelhantes entre os fabricantes. Na angulação, os caninos superiores apresentaram valores acima do proposto pelo autor para o fabricante Morelli, e para os dentes 21 e 22, a angulação foi maior para o fabricante Abzil. Na comparação dos valores de torque obtidos com os valores recomendados pelos fabricantes, a Unitek demonstrou maior fidedignidade no torque comparada às demais marcas. Conclui-se que as diferenças tanto de torque quanto de angulação quando comparados aos valores do autor e à prescrição dos fabricantes, se enquadram dentro de um grau de tolerância preconizada por um órgão regulador de peças ortodônticas alemãs.

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O objetivo deste estudo foi comparar as angulações e torques de braquetes de marcas comerciais distintas em relação à prescrição de Roth e também em relação aos valores preconizados pelo fabricante. Foram utilizados 150 braquetes metálicos de aço inoxidável, de caninos e incisivos superiores na respectiva prescrição, avaliadas por meio de um perfilômetro. Após a coleta dos dados e aplicação do tratamento estatístico, os resultados demonstraram que os valores de torque obtidos com a prescrição de Roth foram semelhantes entre os fabricantes. Na angulação, os caninos superiores apresentaram valores acima do proposto pelo autor para o fabricante Morelli, e para os dentes 21 e 22, a angulação foi maior para o fabricante Abzil. Na comparação dos valores de torque obtidos com os valores recomendados pelos fabricantes, a Unitek demonstrou maior fidedignidade no torque comparada às demais marcas. Conclui-se que as diferenças tanto de torque quanto de angulação quando comparados aos valores do autor e à prescrição dos fabricantes, se enquadram dentro de um grau de tolerância preconizada por um órgão regulador de peças ortodônticas alemãs.

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Estudo sobre as construções simbólicas e identitárias da mulher presentes na narrativa e na estrutura das personagens femininas do filme Malévola (2014) – produção dos estúdios Disney (EUA). A narrativa é inspirada no conto de fadas “A Bela Adormecida do Bosque” e distingue-se pela perspectiva feminina, modificando as possibilidades de interpretação, além de possibilitar a quebra do paradigma dicotômico relacionado ao Bem e ao Mal. A pesquisa tem por objetivo estudar a evolução das construções imaginárias da mulher no cinema e traçar paralelos entre as características arquetípicas das personagens de Malévola em relação à identidade da mulher na contemporaneidade. Para tal, será tomado como referencial teórico os estudos do imaginário social, com as obras de Gilbert Durand, Edgar Morin e, em especial, Michel Maffesoli; conceitos da psicanálise a partir dos trabalhos de C.G. Jung, Erich Neumann, Marie-Louise Von Franz e Clarissa Pinkola Estés; as teorias de Stuart Hall, Laura Mulvey e Gilles Lipovetsky relacionadas aos estudos culturais com ênfase em gênero; e também o ecofeminismo através dos trabalhos de autoras como Vandana Shiva e Maria Mies. Nosso referencial teórico-metodológico é a Hermenêutica de Profundidade (HP) visando à interpretação da estrutura simbólica de nosso objeto. Resultam desta pesquisa a verificação de um processo de saturação de padrões identitários e simbólicos provindos da modernidade e a evolução de novas dinâmicas nas narrativas presentes nas mídias e na comunicação

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Antigen presentation by major histocompatibility complex (MHC) class II molecules requires the participation of different proteases in the endocytic route to degrade endocytosed antigens as well as the MHC class II-associated invariant chain (Ii). Thus far, only the cysteine protease cathepsin (Cat) S appears essential for complete destruction of Ii. The enzymes involved in degradation of the antigens themselves remain to be identified. Degradation of antigens in vitro and experiments using protease inhibitors have suggested that Cat B and Cat D, two major aspartyl and cysteine proteases, respectively, are involved in antigen degradation. We have analyzed the antigen-presenting properties of cells derived from mice deficient in either Cat B or Cat D. Although the absence of these proteases provoked a modest shift in the efficiency of presentation of some antigenic determinants, the overall capacity of Cat B−/− or Cat D−/− antigen-presenting cells was unaffected. Degradation of Ii proceeded normally in Cat B−/− splenocytes, as it did in Cat D−/− cells. We conclude that neither Cat B nor Cat D are essential for MHC class II-mediated antigen presentation.

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The effects of insulin on the mammalian target of rapamycin, mTOR, were investigated in 3T3-L1 adipocytes. mTOR protein kinase activity was measured in immune complex assays with recombinant PHAS-I as substrate. Insulin-stimulated kinase activity was clearly observed when immunoprecipitations were conducted with the mTOR antibody, mTAb2. Insulin also increased by severalfold the 32P content of mTOR that was determined after purifying the protein from 32P-labeled adipocytes with rapamycin⋅FKBP12 agarose beads. Insulin affected neither the amount of mTOR immunoprecipitated nor the amount of mTOR detected by immunoblotting with mTAb2. However, the hormone markedly decreased the reactivity of mTOR with mTAb1, an antibody that activates the mTOR protein kinase. The effects of insulin on increasing mTOR protein kinase activity and on decreasing mTAb1 reactivity were abolished by incubating mTOR with protein phosphatase 1. Interestingly, the epitope for mTAb1 is located near the COOH terminus of mTOR in a 20-amino acid region that includes consensus sites for phosphorylation by protein kinase B (PKB). Experiments were performed in MER-Akt cells to investigate the role of PKB in controlling mTOR. These cells express a PKB-mutant estrogen receptor fusion protein that is activated when the cells are exposed to 4-hydroxytamoxifen. Activating PKB with 4-hydroxytamoxifen mimicked insulin by decreasing mTOR reactivity with mTAb1 and by increasing the PHAS-I kinase activity of mTOR. Our findings support the conclusion that insulin activates mTOR by promoting phosphorylation of the protein via a signaling pathway that contains PKB.

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The expression of alternatively spliced mRNAs from genes is an ubiquitous phenomenon in metazoa. A screen for trans-acting factors that alter the expression of alternatively spliced mRNAs reveals that the smg genes of Caenorhabditis elegans participate in this process. smg genes have been proposed to function in degradation of nonsense mutant mRNAs. Here we show that smg genes affect normal gene expression by modulating the levels of alternatively spliced SRp20 and SRp30b mRNAs. These SR genes contain alternatively spliced exons that introduce upstream stop codons. The effect of smg genes on SR transcripts is specific, because the gene encoding the catalytic subunit of the cAMP-dependent protein kinase, which also contains an alternatively spliced exon that introduces upstream stop codon, is not effected in a smg background. These results suggest that the levels of alternatively spliced mRNAs may, in part, be regulated by alternative mRNA stability.

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Peer reviewed

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The finding that ADP-ribosylation factor (ARF) can activate phospholipase D has led to debate as to whether ARF recruits coat proteins through direct binding or indirectly by catalytically increasing phosphatidic acid production. Here we test critical aspects of these hypotheses. We find that Golgi membrane phosphatidic acid levels do not rise—in fact they decline—during cell-free budding reactions. We confirm that the level of membrane-bound ARF can be substantially reduced without compromising coat assembly [Ktistakis, N. T., Brown, H. A., Waters, M. G., Sternweis, P. C. & Roth, M. G. (1996) J. Cell Biol. 134, 295–306], but find that under all conditions, ARF is present on the Golgi membrane in molar excess over bound coatomer. These results do not support the possibility that the activation of coat assembly by ARF is purely catalytic, and they are consistent with ARF forming direct interactions with coatomer. We suggest that ARF, like many other G proteins, is a multifunctional protein with roles in trafficking and phospholipid signaling.

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The amino acid sequence requirements of the transmembrane (TM) domain and cytoplasmic tail (CT) of the hemagglutinin (HA) of influenza virus in membrane fusion have been investigated. Fusion properties of wild-type HA were compared with those of chimeras consisting of the ectodomain of HA and the TM domain and/or CT of polyimmunoglobulin receptor, a nonviral integral membrane protein. The presence of a CT was not required for fusion. But when a TM domain and CT were present, fusion activity was greater when they were derived from the same protein than derived from different proteins. In fact, the chimera with a TM domain of HA and truncated CT of polyimmunoglobulin receptor did not support full fusion, indicating that the two regions are not functionally independent. Despite the fact that there is wide latitude in the sequence of the TM domain that supports fusion, a point mutation of a semiconserved residue within the TM domain of HA inhibited fusion. The ability of a foreign TM domain to support fusion contradicts the hypothesis that a pore is composed solely of fusion proteins and supports the theory that the TM domain creates fusion pores after a stage of hemifusion has been achieved.

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The accurate targeting of secretory vesicles to distinct sites on the plasma membrane is necessary to achieve polarized growth and to establish specialized domains at the surface of eukaryotic cells. Members of a protein complex required for exocytosis, the exocyst, have been localized to regions of active secretion in the budding yeast Saccharomyces cerevisiae where they may function to specify sites on the plasma membrane for vesicle docking and fusion. In this study we have addressed the function of one member of the exocyst complex, Sec10p. We have identified two functional domains of Sec10p that act in a dominant-negative manner to inhibit cell growth upon overexpression. Phenotypic and biochemical analysis of the dominant-negative mutants points to a bifunctional role for Sec10p. One domain, consisting of the amino-terminal two-thirds of Sec10p directly interacts with Sec15p, another exocyst component. Overexpression of this domain displaces the full-length Sec10 from the exocyst complex, resulting in a block in exocytosis and an accumulation of secretory vesicles. The carboxy-terminal domain of Sec10p does not interact with other members of the exocyst complex and expression of this domain does not cause a secretory defect. Rather, this mutant results in the formation of elongated cells, suggesting that the second domain of Sec10p is required for morphogenesis, perhaps regulating the reorientation of the secretory pathway from the tip of the emerging daughter cell toward the mother–daughter connection during cell cycle progression.

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Here we describe an association between α3β1 integrin and transmembrane-4 superfamily (TM4SF) protein CD151. This association is maintained in relatively stringent detergents and thus is remarkably stable in comparison with previously reported integrin–TM4SF protein associations. Also, the association is highly specific (i.e., observed in vitro in absence of any other cell surface proteins), and highly stoichiometric (nearly 90% of α3β1 associated with CD151). In addition, α3β1 and CD151 appeared in parallel on many cell lines and showed nearly identical skin staining patterns. Compared with other integrins, α3β1 exhibited a considerably higher level of associated phosphatidylinositol-4-kinase (PtdIns 4-kinase) activity, most of which was removed upon immunodepletion of CD151. Specificity for CD151 and PtdIns 4-kinase association resided in the extracellular domain of α3β1, thus establishing a novel paradigm for the specific recruitment of an intracellular signaling molecule. Finally, antibodies to either CD151 or α3β1 caused a ∼88–92% reduction in neutrophil motility in response to f-Met-Leu-Phe on fibronectin, suggesting an functionally important role of these complexes in cell migration.

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The number of neurons in the mammalian brain is determined by a balance between cell proliferation and programmed cell death. Recent studies indicated that Bcl-XL prevents, whereas Caspase-3 mediates, cell death in the developing nervous system, but whether Bcl-XL directly blocks the apoptotic function of Caspase-3 in vivo is not known. To examine this question, we generated bcl-x/caspase-3 double mutants and found that caspase-3 deficiency abrogated the increased apoptosis of postmitotic neurons but not the increased hematopoietic cell death and embryonic lethality caused by the bcl-x mutation. In contrast, caspase-3, but not bcl-x, deficiency changed the normal incidence of neuronal progenitor cell apoptosis, consistent with the lack of expression of Bcl-XL in the proliferative population of the embryonic cortex. Thus, although Caspase-3 is epistatically downstream to Bcl-XL in postmitotic neurons, it independently regulates apoptosis of neuronal founder cells. Taken together, these results establish a role of programmed cell death in regulating the size of progenitor population in the central nervous system, a function that is distinct from the classic role of cell death in matching postmitotic neuronal population with postsynaptic targets.