959 resultados para Mouth Neoplasms
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Mode of access: Internet.
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Mode of access: Internet.
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Ernest G. Pretyman, chairman.
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Burning mouth syndrome (BMS) is characterized by a burning sensation of the oral mucosa in the absence of mucosal abnormality Various local, systemic and psychological factors are associated with BMS, but its aetiology is not fully understood. Recently, significant inroads have been made, producing a better understanding of this complex condition. The aim of the current paper is to explore the condition of BMS in an educational context with the specific outcome of increasing awareness of the condition.
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International and domestic tourism are sensitive to disastrous events which make areas inaccessible to visitors, less attractive or more dangerous. One form of tourism disaster is the outbreak of an exotic disease, of which Foot and Mouth Disease (FMD) is a prime case. It is now well documented that the 2001 FMD outbreak in the UK had a greater impact on tourism than on agriculture. It has been estimated than an FMD outbreak in Australia would impose a cost of about $13 million. The impact on tourism would be highly dependent on the extent and duration of an FMD outbreak, as well as on any management and containment restrictions imposed by the authorities in their attempt to control and eventually eradicate the disease. Public perception and thus the provision of accurate information and the way in which the media report disasters will also play an important role in determining the impact on the tourism industry. The economy of Tropical North Queensland relies heavily on international visitors, and an FMD outbreak in the region would impose a large cost to the regional economy, conservatively estimated here to be of the order of $200 million per year.
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Burning mouth syndrome is an oral dysaesthesia presenting as a burning sensation of the tongue and less frequently other oral and peri-oral sites. There may be other coincident symptoms and signs, but the defining feature is the absence of any obvious organic cause. Because of this the condition frequently remains unrecognized for extended periods with a variable progression of symptoms. The current paper describes the complex presentation of burning mouth syndrome with the major aim of increasing recognition.
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The present thesis encompasses the two researches projects I conducted during my PhD program in Molecular Biology and Pathology. The common thread is represented by the analysis of the signaling pathways implicated in the pathophysiology of the two most aggressive Philadelphia-negative myeloproliferative neoplasms, namely, atypical chronic myeloid leukemia (aCML) and primary myelofibrosis (PMF). In the last decade, since the description of the JAK2V617F mutation in 2005, the field of the molecular characterization of Philadelphia-negative myeloproliferative neoplasms has experienced an astonishing implementation that led to the discovery of 16 new mutations involving signal transduction, epigenetic modifiers, cell cycle regulators. Nevertheless, their pathogenetic relevance and whether they could represent good “druggable” candidates have to be proved yet. In the first section I provide the first report of the signaling cascade down-stream the rare cytogenetic lesion t(8;9)(p22;p24)/PCM1-JAK2 associated with aCML, finding that it selectively activates the ERK1/2 signaling without affecting JAK/STAT phosphorylation. In the second part, I investigated the implication of the ε isoform of novel Protein kinase Cs (PKCs) in the pathophysiology of the aberrant megakaryocytopoiesis in PMF, concluding that the over-expression of PKCε detains a crucial relevance in the aberrant behavior of PMF megakaryocytes and its inhibition is capable to restore their normal differentiation and abrogate the anti-apoptotic signaling. Both results are discussed in the view of their therapeutic implications. In case PCM1/JAK2-related hematologic neoplasms, ERK-inhibitors rather than JAK-inhibitors (i.e. ruxolitinib) should be considered as a “tailored” drugs. In case of PMF, PKCε-inhibitors (i.e. εV1-2 peptide) configure as an appealing strategy to re-direct the megakaryocytic neoplastic clone.