990 resultados para right-side failure
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The use of famous and/or attractive models in brand marketing is ubiquitous yet little work, if any, has been carried out examining differences in their efficiency in driving subsequent consumer behaviour. Such brand platforms have an emotional selling proposition (ESP) that refers to the unique personality and image attributes that a particular endorsement generates. However, celebrity endorsers are also more than likely to be considered attractive and thus differences in the ESP (if any) would be very small. Such differences in an emotional response could be measured by a participant's electrodermal activity (EDA). This is a psychophysiological response, measurement of which is sensitive enough to detect differences engendered by a particular brand platform's ESP. In the present study, EDA measurements were recorded from participants who were shown advertisements containing a target product within four different types of endorsement platforms depicting models who were either famous/non-famous or attractive/average looking. The results showed that average looking celebrity endorsers produced a greater EDA response than any of the other conditions including the attractive looking celebrity endorsers. Furthermore, this effect was only revealed from recordings taken from the left hand side of the participants. Given that the right side of the brain would orchestrate any EDA responses recorded from the subjects' left side, the current results suggest a dedicated neural response for celebrity endorsed brand platforms. Future work examining the relationship between the specific EDA signature and consumer preferences is discussed.
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Relatório de Estágio apresentado para a obtenção do grau de Mestre em Desporto com especialização em Treino Desportivo
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Determining which marine species are sensitive to elevated CO2 and reduced pH, and which species tolerate these changes, is critical for predicting the impacts of ocean acidification on marine biodiversity and ecosystem function. Although adult fish are thought to be relatively tolerant to higher levels of environmental CO2, very little is known about the sensitivity of juvenile stages, which are usually much more vulnerable to environmental change. We tested the effects of elevated environmental CO2 on the growth, survival, skeletal development and otolith (ear bone) calcification of a common coral reef fish, the spiny damselfish Acanthochromis polyacanthus. Newly hatched juveniles were reared for 3 wk at 4 different levels of PCO2(seawater) spanning concentrations already experienced in near-reef waters (450 µatm CO2) to those predicted to occur over the next 50 to 100 yr in the IPCC A2 emission scenario (600, 725, 850 µatm CO2). Elevated PCO2 had no effect on juvenile growth or survival. Similarly, there was no consistent variation in the size of 29 different skeletal elements that could be attributed to CO2 treatments. Finally, otolith size, shape and symmetry (between left and right side of the body) were not affected by exposure to elevated PCO2, despite the fact that otoliths are composed of aragonite. This is the first comprehensive assessment of the likely effects of ocean acidification on the early life history development of a marine fish. Our results suggest that juvenile A. polyacanthus are tolerant of moderate increases in environmental CO2 and that further acidification of the ocean will not, in isolation, have a significant effect on the early life history development of this species, and perhaps other tropical reef fishes
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Using original data on 1,5000 mandibles, but mainly previously published data, I present a overview of the distribution characteristics of mandibular torus and a hypothesis concerning its cause. Pedigree studies have established that genetic factors influence torus development. Extrinsic factors are strongly implicated by other evidence: prevalence among Arctic peoples, effect of dietary change, age regression, preponderance in males and on the right side, effect of cranial deformation, concurrence with palatine torus and maxillary alveolar exostoses, and clinical evidence. I propose that the primary factor is masticatory stress. According to a mechanism suggested by orthodontic research, the horizontal component of bite force tips the lower canine, premolars and first molar so that their root apices exert pressure on the periodontal membrane, causing formation of new bone on the lingual cortical plate of the alveolar process. Thus formed, the hyperostosis is vulnerable to trauma and its periosteal covering becomes bruised causing additional deposition of bone. Genes influence torus indirectly through their effect on occlusion. A patern of increased expressivity with incidence suggests that a quasicontinuous model may provide a better fit to pedigree data than single locus models previously tested.
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Se realizó un estudio descriptivo- retrospectivo desde enero de 2007 a diciembre del 2011. El universo estuvo constituido por los pacientes de 18 años y más con diagnóstico de Neumotórax, internados en los departamentos de cirugía del Hospital Regional Vicente Corral Moscoso y Hospital Teófilo Dávila. Para el levantamiento de la información se utilizó un formulario previamente diseñado. Los datos se transcribieron de las historias clínicas a los formularios respectivos. Resultados: Se incluyeron 73 pacientes del HTD y 52 del HVCM, el neumotórax de mayor prevalencia fue el traumático con el 85.6% de los casos, izquierdo en el 54.4%; las características clínicas de mayor relevancia fueron: dolor moderado 40.8%; taquicardia 15.2%; desviación de la tráquea hacia la derecha 32.8%; distención de las venas del cuello 38.4%; hipersonoridad 76.8%; murmullo vesicular disminuido 80%; disnea 99.2%; cianosis 22.4%; los método diagnósticos presentaron la siguiente prevalencia: radiografía de tórax 100%; tomografía 27.2% y resonancia en el 0.8% de los casos; el tratamiento fue en el 16% toracocentesis con aspiración de aguja y en el 100% tubo de tórax. La media de días de hospitalización fue de 5 días y la mortalidad fue del 10.4%.- Conclusiones: Se registraron diferencias estadísticamente significativas entre ambas instituciones en las características clínicas en cuanto a la procedencia, intensidad del dolor, frecuencia cardiaca, murmullo vesicular disminuido y presentación de cianosis. Además se evidencia una alta mortalidad.au
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Wydział Biologii: Instytut Antropologii
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Relatório de Estágio apresentado para a obtenção do grau de Mestre em Desporto com especialização em Treino Desportivo
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Introdução: A aspiração de corpo estranho (ACE) é uma emergência pediátrica e uma causa importante de morte acidental na criança. A maioria dos casos ocorre com objetos orgânicos e inorgânicos de pequenas dimensões, sobretudo em idade pré-escolar. A ACE cursa com amplo espectro de manifestações e o seu diagnóstico representa muitas vezes um desafio. Caso clínico: Descrevemos o caso clínico de uma criança de dois anos que recorreu ao Serviço de Urgência por tosse, disfonia e disfagia. Ao exame objetivo apresentava acessos de tosse estridulosa, tiragem supra-esternal ligeira e auscultação pulmonar com sibilos inspiratórios/expiratórios e roncos dispersos bilateralmente. A telerradiografia do tórax evidenciava um reforço hilar bilateral, mais notável à direita. A avaliação por Otorrinolaringologia, incluindo a nasolaringofibroscopia, não de- mostrou alterações. A broncoscopia revelou a presença de corpo estranho vegetal condicionando obstrução superior a 50% do lúmen do brônquio principal direito. Conclusão: Pretendemos com este caso salientar a necessidade de manter alto índice de suspeição perante a possibilidade de ACE, pois o atraso no seu reconhecimento condiciona o seu tratamento e o eventual aparecimento de sequelas irreversíveis.
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International audience
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Depths shown by soundings.
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In 2013, a series of posters began appearing in Washington, DC’s Metro system. Each declared “The internet: Your future depends on it” next to a photo of a middle-aged black Washingtonian, and an advertisement for the municipal government’s digital training resources. This hopeful discourse is familiar but where exactly does it come from? And how are our public institutions reorganized to approach the problem of poverty as a problem of technology? The Clinton administration’s ‘digital divide’ policy program popularized this hopeful discourse about personal computing powering social mobility, positioned internet startups as the ‘right’ side of the divide, and charged institutions of social reproduction such as schools and libraries with closing the gap and upgrading themselves in the image of internet startups. After introducing the development regime that builds this idea into the urban landscape through what I call the ‘political economy of hope’, and tracing the origin of the digital divide frame, this dissertation draws on three years of comparative ethnographic fieldwork in startups, schools, and libraries to explore how this hope is reproduced in daily life, becoming the common sense that drives our understanding of and interaction with economic inequality and reproduces that inequality in turn. I show that the hope in personal computing to power social mobility becomes a method of securing legitimacy and resources for both white émigré technologists and institutions of social reproduction struggling to understand and manage the persistent poverty of the information economy. I track the movement of this common sense between institutions, showing how the political economy of hope transforms them as part of a larger development project. This dissertation models a new, relational direction for digital divide research that grounds the politics of economic inequality with an empirical focus on technologies of poverty management. It demands a conceptual shift that sees the digital divide not as a bug within the information economy, but a feature of it.
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Los índices mundialmente aplicados para la predicción de diámetros mesiodistales de caninos y premolares son los de Moyers y Tanaka – Johnston, actualmente, investigadores brasileros desarrollaron un nuevo método que emplea dos ecuaciones, una para hombres y otra para mujeres, e integra el tamaño del primer molar permanente mandibular. El presente estudio buscó determinar que método es más preciso para calcularlos. Fueron analizados 94 modelos de estudio, 41 de hombres y 53 de mujeres, en edades comprendidas entre los 12 y 31 años, la muestra fue elegida a conveniencia, se midieron todos los dientes desde el primer molar mandibular izquierdo permanente al primer molar mandibular derecho permanente con un calibrador Mitutuyo digital y se obtuvieron los valores de los dientes anteriormente referenciados. Se aplicó el test de Pearson y el test t de Student.. Los tres métodos analizados tuvieron una correlación positiva estadísticamente significativa con respecto al valor real (p=0,000), el sistema de Melgaҫo fue el que presentó el mayor grado de correlación (R=0,735). Los 3 índices muestran diferencias estadísticamente significativas al compararlos con el valor real (p=0,000),. No existió diferencia estadísticamente significativa entre el lado derecho e izquierdo (p= 0,6). Con referencia al sexo, no se encontró diferencia estadísticamente significativa en el lado derecho (p=0,15), mientras que en el lado izquierdo si se observó tal diferencia (p=0,04). Se concluyó que el Método de Melgaҫo es el más apegado a la realidad en nuestra población
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La hernia de Amyand es una entidad rara que se caracteriza por la presencia del apéndice vermiforme en el saco herniario de una hernia inguinal. La prevalencia es de aproximadamente el 1% y, por lo general, se presenta en hernias ubicadas al lado derecho; su diagnóstico habitual se realiza durante la intervención quirúrgica. En el presente caso se describe a un paciente de 67 años que acude al servicio de emergencia del Hospital Vicente Corral Moscoso presentando esta patología y su correspondiente manejo.
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SIN FINANCIACIÓN
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Pulmonary arterial hypertension (PAH) is a progressive disease of the small pulmonary arteries, characterised by pulmonary vascular remodelling due to excessive proliferation and resistance to apoptosis of pulmonary artery endothelial cells (PAECs) and pulmonary artery smooth muscle cells (PASMCs). The increased pulmonary vascular resistance and elevated pulmonary artery pressures result in right heart failure and premature death. Germline mutations of the bone morphogenetic protein receptor-2 (bmpr2) gene, a receptor of the transforming growth factor beta (TGF-β) superfamily, account for approximately 75%-80% of the cases of heritable form of PAH (HPAH) and 20% of sporadic cases or idiopathic PAH (IPAH). IPAH patients without known bmpr2 mutations show reduced expression of BMPR2. However only ~ 20% of bmpr2-mutation carriers will develop the disease, due to an incomplete penetrance, thus the need for a ‘second hit’ including other genetic and/or environmental factors is accepted. Diagnosis of PAH occurs most frequently when patients have reached an advanced stage of disease. Although modern PAH therapies can markedly improve a patient’s symptoms and slow the rate of clinical deterioration, the mortality rate from PAH remains unacceptably high. Therefore, the development of novel therapeutic approaches is required for the treatment of this multifaceted disease. Noncoding RNAs (ncRNAs) include microRNAs (miRNAs) and long noncoding RNAs (lncRNAs). MiRNAs are ~ 22 nucleotide long and act as negative regulators of gene ex-pression via degradation or translational inhibition of their target mRNAs. Previous studies showed extensive evidence for the role of miRNAs in the development of PAH. LncRNAs are transcribed RNA molecules greater than 200 nucleotides in length. Similar to classical mRNA, lncRNAs are translated by RNA polymerase II and are generally alternatively spliced and polyadenylated. LncRNAs are highly versatile and function to regulate gene expression by diverse mechanisms. Unlike miRNAs, which exhibit well-defined actions in negatively regulating gene expression via the 3’-UTR of mRNAs, lncRNAs play more diverse and unpredictable regulatory roles. Although a number of lncRNAs have been intensively investigated in the cancer field, studies of the role of lncRNAs in vascular diseases such as PAH are still at a very early stage. The aim of this study was to investigate the involvement of specific ncRNAs in the development of PAH using experimental animal models and cell culture. The first ncRNA we focused on was miR-143, which is up-regulated in the lung and right ventricle tissues of various animal models of PH, as well as in the lungs and PASMCs of PAH patients. We show that genetic ablation of miR-143 is protective against the development of chronic hypoxia induced PH in mice, assessed via measurement of right ventricular systolic pressure (RVSP), right ventricular hypertrophy (RVH) and pulmonary vascular remodelling. We further report that knockdown of miR-143-3p in WT mice via anti-miR-143-3p administration prior to exposure of mice to chronic hypoxia significantly decreases certain indices of PH (RVSP) although no significant changes in RVH and pulmo-nary vascular remodelling were observed. However, a reversal study using antimiR-143-3p treatment to modulate miR-143-3p demonstrated a protective effect on RVSP, RVH, and muscularisation of pulmonary arteries in the mouse chronic hypoxia induced PH model. In vitro experiments showed that miR-143-3p overexpression promotes PASMC migration and inhibits PASMC apoptosis, while knockdown miR-143-3p elicits the opposite effect, with no effects observed on cellular proliferation. Interestingly, miR-143-3p-enriched exosomes derived from PASMCs mediated cell-to-cell communication between PASMCs and PAECs, contributing to the pro-migratory and pro-angiogenic phenotype of PAECs that underlies the pathogenesis of PAH. Previous work has shown that miR-145-5p expression is upregulated in the chronic hypoxia induced mouse model of PH, as well as in PAH patients. Genetic ablation and pharmacological inhibition (subcutaneous injection) of miR-145-5p exert a protective against the de-velopment of PAH. In order to explore the potential for alternative, more lung targeted delivery strategies, miR-145-5p expression was inhibited in WT mice using intranasal-delivered antimiR-145-5p both prior to and post exposure to chronic hypoxia. The decreased expression of miR-145-5p in lung showed no beneficial effect on the development of PH compared with control antimiRNA treated mice exposed to chronic hypoxia. Thus, miR-143-3p modulated both cellular and exosome-mediated responses in pulmonary vascular cells, while the inhibition of miR-143-3p prevented the development of experimental pulmonary hypertension. We focused on two lncRNAs in this project: Myocardin-induced Smooth Muscle Long noncoding RNA, Inducer of Differentiation (MYOSLID) and non-annotated Myolnc16, which were identified from RNA sequencing studies in human coronary artery smooth muscle cells (HCASMCs) that overexpress myocardin. MYOSLID was significantly in-creased in PASMCs from patients with IPAH compared to healthy controls and increased in circulating endothelial progenitor cells (EPCs) from bmpr2 mutant PAH patients. Exposure of PASMCs to hypoxia in vitro led to a significant upregulation in MYOSLID expres-sion. MYOSLID expression was also induced by treatment of PASMC with BMP4, TGF-β and PDGF, which are known to be triggers of PAH in vitro. Small interfering RNA (siR-NA)-mediated knockdown MYOSLID inhibited migration and induced cell apoptosis without affecting cell proliferation and upregulated several genes in the BMP pathway in-cluding bmpr1α, bmpr2, id1, and id3. Modulation of MYOSLID also affected expression of BMPR2 at the protein level. In addition, MYOSLID knockdown affected the BMP-Smad and BMP-non-Smad signalling pathways in PASMCs assessed by phosphorylation of Smad1/5/9 and ERK1/2, respectively. In PAECs, MYOSLID expression was also induced by hypoxia exposure, VEGF and FGF2 treatment. In addition, MYOSLID knockdown sig-nificantly decreased the proliferation of PAECs. Thus, MYOSLID may be a novel modulator in pulmonary vascular cell functions, likely through the BMP-Smad and –non-Smad pathways. Treatment of PASMCs with inflammatory cytokines (IL-1 and TNF-α) significantly in-duced the expression of Myolnc16 at a very early time point. Knockdown of Myolnc16 in vitro decreased the expression of il-6, and upregulated the expression of il-1 and il-8 in PASMCs. Moreover, the expression levels of chemokines (cxcl1, cxcl6 and cxcl8) were sig-nificantly decreased with Myolnc16 knockdown. In addition, Myolnc16 knockdown decreased the MAP kinase signalling pathway assessed by phosphorylation of ERK1/2 and p38 MAPK and inhibited cell migration and proliferation in PASMCs. Thus, Myolnc16 may a novel modulator of PASMCs functions through anti-inflammatory signalling pathways. In summary, in this thesis we have demonstrated how miR-143-3p plays a protective role in the development of PH both in vivo animal models and patients, as well as in vitro cell cul-ture. Moreover, we have showed the role of two novel lncRNAs in pulmonary vascular cells. These ncRNAs represent potential novel therapeutic targets for the treatment of PAH with further work addressing to investigate the target genes, and the pathways modulated by these ncRNAs during the development of PAH.