998 resultados para Bascom, H. B. (Henry Bidleman), 1796-1850.
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"The Anatomy of Man's Body" on page [3] is the only illustration.
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Proteolysis-inducing factor (PIF) is a sulphated glycoprotein produced by cachexia-inducing tumours, which initiates muscle protein degradation through an increased expression of the ubiquitin–proteasome proteolytic pathway. The role of kinase C (PKC) in PIF-induced proteasome expression has been studied in murine myotubes as a surrogate model of skeletal muscle. Proteasome expression induced by PIF was attenuated by 4alpha-phorbol 12-myristate 13-acetate (100 nM) and by the PKC inhibitors Ro31-8220 (10 muM), staurosporine (300 nM), calphostin C (300 nM) and Gö 6976 (200 muM). Proteolysis-inducing factor-induced activation of PKCalpha, with translocation from the cytosol to the membrane at the same concentration as that inducing proteasome expression, and this effect was attenuated by calphostin C. Myotubes transfected with a constitutively active PKCalpha (pCO2) showed increased expression of proteasome activity, and a longer time course, compared with their wild-type counterparts. In contrast, myotubes transfected with a dominant-negative PKCalpha (pKS1), which showed no activation of PKCalpha in response to PIF, exhibited no increase in proteasome activity at any time point. Proteolysis-inducing factor-induced proteasome expression has been suggested to involve the transcription factor nuclear factor-kappaB (NF-kappaB), which may be activated through PKC. Proteolysis-inducing factor induced a decrease in cytosolic I-kappaBalpha and an increase in nuclear binding of NF-kappaB in pCO2, but not in pKS1, and the effect in wild-type cells was attenuated by calphostin C, confirming that it was mediated through PKC. This suggests that PKC may be involved in the phosphorylation and degradation of I-kappaBalpha, induced by PIF, necessary for the release of NF-kappaB from its inactive cytosolic complex.
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Durante el siglo XIX diversos artistas europeos emprendieron el viaje hacia diferentes puntos del continente americano. Entre ellos, mucho se dedicaron a la litografía, logrando en ciertos casos un amplio éxito comercial. Este artículo examina la trayectoria de la artista ginebrina Andrienne Pauline Macaire (1796-1855), dueña junto a su esposo de un temprano emprendimiento litográfico en la ciudad de Buenos Aires. Macaire puede ser considerada la primera artista profesional de renombre activa en esa ciudad. En efecto, es posible diferenciar su trayectoria de las de otras artistas contemporáneas, de las cuales se dispone de menos información y de las que han sobrevivido menos obras. En una primera parte del texto se analiza su inscripción en la literatura artística nacional. A continuación, se describe su formación en Ginebra y se estudia su importante actividad en Buenos Aires, estableciendo conexiones con el panorama artístico local. A lo largo del artículo se presentan obras y fuentes inéditas, o insuficientemente exploradas, a fin de justipreciar su carrera artística y de brindar elementos para futuras investigaciones.
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This dissertation traces the ways in which nineteenth-century fictional narratives of white settlement represent “family” as, on the one hand, an abstract theoretical model for a unified and relatively homogenous British settler empire and on the other, a fundamental challenge to ideas about imperial integrity and transnational Anglo-Saxon racial identification. I argue that representations of transoceanic white families in nineteenth-century fictions about Australian settler colonialism negotiate the tension between the bounded domesticity of an insular English nation and the kind of kinship that spans oceans and continents as a result of mass emigration from the British isles to the United States, Canada, New Zealand, and the Australian colonies. As such, these fictions construct productive analogies between the familial metaphors and affective language in the political discourse of “Greater Britain”—-a transoceanic imagined community of British settler colonies and their “mother country” united by race and language—-and ideas of family, gender, and domesticity as they operate within specific bourgeois families. Concerns over the disruption of transoceanic families bear testament to contradictions between the idea of a unified imperial identity (both British and Anglo-Saxon), the proliferation of fractured local identities (such as settlers’ English, Irish Catholic, and Australian nationalisms), and the conspicuous absence of indigenous families from narratives of settlement. I intervene at the intersection of postcolonial literary criticism and gender theory by examining the strategic deployments of heteronormative kinship metaphors and metonymies in the rhetorical consolidation of settler colonial space. Settler colonialism was distinct from the “civilizing” domination of subject peoples in South Asia in that it depended on the rhetorical construction of colonial territory as empty space or as land occupied by nearly extinct “primitive” races. This dissertation argues that political rhetoric, travel narratives, and fiction used the image of white female bourgeois reproductive power and sentimental attachment as a technology for settler colonial success, embodying this technology both in the benevolent figure of the metropolitan “mother country” (the paternalistic female counter to the material realities of patriarchal and violent settler colonial practices) and in fictional juxtapositions of happy white settler fecund families with the solitary self-extinguishing figure of the black aboriginal “savage.” Yet even in the narratives where the continuity and coherence of families across imperial space is questioned—-and “Greater Britain” itself—-domesticity and heteronormative familial relations effectively rewrite settler space as white, Anglo-Saxon and bourgeois, and the sentimentalism of troubled European families masks the presence and genocide of indigenous aboriginal peoples. I analyze a range of novels and political texts, canonical and non-canonical, metropolitan and colonial. My introductory first chapter examines the discourse on a “Greater Britain” in the travel narratives of J.A. Froude, Charles Wentworth Dilke, and Anthony Trollope and in the Oxbridge lectures of Herman Merivale and J.R. Seeley. These writers make arguments for an imperial economy of affect circulating between Britain and the settler colonies that reinforces political connections, and at times surpasses the limits of political possibility by relying on the language of sentiment and feeling to build a transoceanic “Greater British community. Subsequent chapters show how metropolitan and colonial fiction writers, including Charles Dickens, Anthony Trollope, Marcus Clarke, Henry Kingsley, and Catherine Helen Spence, test the viability of this “Greater British economy of affect by presenting transoceanic family connections and structures straining under the weight of forces including the vast distances between colonies and the “mother country,” settler violence, and the transportation system.
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Phospholipases A2 (PLA2) are key enzymes for production of lipid mediators. We previously demonstrated that a snake venom sPLA2 named MT-III leads to prostaglandin (PG)E2 biosynthesis in macrophages by inducing the expression of cyclooxygenase-2 (COX-2). Herein, we explored the molecular mechanisms and signaling pathways leading to these MT-III-induced effects. Results demonstrated that MT-III induced activation of the transcription factor NF-κB in isolated macrophages. By using NF-κB selective inhibitors, the involvement of this factor in MT-III-induced COX-2 expression and PGE2 production was demonstrated. Moreover, MT-III-induced COX-2 protein expression and PGE2 release were attenuated by pretreatment of macrophages with SB202190, and Ly294002, and H-7-dihydro compounds, indicating the involvement of p38MAPK, PI3K, and PKC pathways, respectively. Consistent with this, MT-III triggered early phosphorylation of p38MAPK, PI3K, and PKC. Furthermore, SB202190, H-7-dihydro, but not Ly294002 treatment, abrogated activation of NF-κB induced by MT-III. Altogether, these results show for the first time that the induction of COX-2 protein expression and PGE2 release, which occur via NF-κB activation induced by the sPLA2-MT-III in macrophages, are modulated by p38MAPK and PKC, but not by PI3K signaling proteins.
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The 'dilution effect' (DE) hypothesis predicts that diverse host communities will show reduced disease. The underlying causes of pathogen dilution are complex, because they involve non-additive (driven by host interactions and differential habitat use) and additive (controlled by host species composition) mechanisms. Here, we used measures of complementarity and selection traditionally employed in the field of biodiversity-ecosystem function (BEF) to quantify the net effect of host diversity on disease dynamics of the amphibian-killing fungus Batrachochytrium dendrobatidis (Bd). Complementarity occurs when average infection load in diverse host assemblages departs from that of each component species in uniform populations. Selection measures the disproportionate impact of a particular species in diverse assemblages compared with its performance in uniform populations, and therefore has strong additive and non-additive properties. We experimentally infected tropical amphibian species of varying life histories, in single- and multi-host treatments, and measured individual Bd infection loads. Host diversity reduced Bd infection in amphibians through a mechanism analogous to complementarity (sensu BEF), potentially by reducing shared habitat use and transmission among hosts. Additionally, the selection component indicated that one particular terrestrial species showed reduced infection loads in diverse assemblages at the expense of neighbouring aquatic hosts becoming heavily infected. By partitioning components of diversity, our findings underscore the importance of additive and non-additive mechanisms underlying the DE.
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Staphylococcus aureus aggravates the allergic eosinophilic inflammation. We hypothesized that Staphylococcus aureus-derived enterotoxins directly affect eosinophil functions. Therefore, this study investigated the effects of Staphylococcal enterotoxins A and B (SEA and SEB) on human and mice eosinophil chemotaxis and adhesion in vitro, focusing on p38 MAPK phosphorylation and intracellular Ca(2+) mobilization. Eosinophil chemotaxis was evaluated using a microchemotaxis chamber, whereas adhesion was performed in VCAM-1 and ICAM-1-coated plates. Measurement of p38 MAPK phosphorylation and intracellular Ca(2+) levels were monitored by flow cytometry and fluorogenic calcium-binding dye, respectively. Prior incubation (30 to 240 min) of human blood eosinophils with SEA (0.5 to 3 ng/ml) significantly reduced eotaxin-, PAF- and RANTES-induced chemotaxis (P<0.05). Likewise, SEB (1 ng/ml, 30 min) significantly reduced eotaxin-induced human eosinophil chemotaxis (P<0.05). The reduction of eotaxin-induced human eosinophil chemotaxis by SEA and SEB was prevented by anti-MHC monoclonal antibody (1 μg/ml). In addition, SEA and SEB nearly suppressed the eotaxin-induced human eosinophil adhesion in ICAM-1- and VCAM-1-coated plates. SEA and SEB prevented the increases of p38 MAPK phosphorylation and Ca(2+) levels in eotaxin-activated human eosinophils. In separate protocols, we evaluated the effects of SEA on chemotaxis and adhesion of eosinophils obtained from mice bone marrow. SEA (10 ng/ml) significantly reduced the eotaxin-induced chemotaxis along with cell adhesion to both ICAM-1 and VCAM-1-coated plates (P<0.05). In conclusion, the inhibition by SEA and SEB of eosinophil functions (chemotaxis and adhesion) are associated with reductions of p38 MAPK phosphorylation and intracellular Ca(2+) mobilization.
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Solar radiation, especially ultraviolet A (UVA) and ultraviolet B (UVB), can cause damage to the human body, and exposure to the radiation may vary according to the geographical location, time of year and other factors. The effects of UVA and UVB radiation on organisms range from erythema formation, through tanning and reduced synthesis of macromolecules such as collagen and elastin, to carcinogenic DNA mutations. Some studies suggest that, in addition to the radiation emitted by the sun, artificial sources of radiation, such as commercial lamps, can also generate small amounts of UVA and UVB radiation. Depending on the source intensity and on the distance from the source, this radiation can be harmful to photosensitive individuals. In healthy subjects, the evidence on the danger of this radiation is still far from conclusive.
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Vitamin C stability and concentration was evaluated in isotonic beverages and B group vitamins (B1, B2, B3, B5 and B6) in power beverages. The amount of vitamins was found to be above of that declared on the labels, even after the shelf life had been exceeded. A small decrease in the amount of B group vitamins was observed during the shelf life of the products. In the case of vitamin C this decrease was slightly higher. The present research shows the need of increased quality control and inspection.
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The objective of this research was to determine the levels of enrichment of vitamins B1, B2, B6 and B3 in different types and brands of enriched cookies. The chromatographic separation was performed in a C18 column with gradient elution and UV detection at 254 and 287 nm. The results show that only 5 of the 24 brands evaluated are in accordance with the Brazilian legislation with respect to the vitamin content declared on the labels. However, consumption of approximately 100-150 g of most of the brands supplies the recommended dietary intake for children and adults of the vitamins evaluated.
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This work describes an overview of our synthesis of pteridic acids A and B and discloses some interesting results related to the lithium enolate-mediated aldol reaction used as key step to set up the C5-C15 fragment of these natural products. This first example, as far we know, of an aldol reaction between a chiral enolate of a (Z) enone and a chiral aldehyde has driven us to a series of experiments showing the remarkable relation between enolization selectivity and reaction conditions.
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PURPOSE: The objective of this paper is to report the clinical case of a patient who presented a chronic apical periodontitis, arising from internal inflammatory resorption followed by pulp necrosis, and a long-term success of a root canal therapy using calcium hydroxide as root canal dressing. CASE DESCRIPTION: A 20-year-old male patient presented for routine dental treatment. By radiographic examination we noted an extensive radioluscent area, laterally to the permanent maxillary right lateral incisor, with possibility of communication with the lateral periodontium, suggestive of a chronic apical periodontitis. Due to external root resorption detection, we used a calcium hydroxide root canal dressing, changed every 15 days, for a period of 2 months. Root canal filling was performed using gutta-percha cones by lateral condensation technique Radiographic follow up held after 19 years of treatment indicated a periodontium in conditions of normality, with the presence of lamina dura. CONCLUSION: Calcium hydroxide is a suitable material to be used as root canal dressing in teeth with apical periodontitis. Long-term evaluation demonstrated the satisfactory clinical outcome following root canal treatment.