Conocer la propia mente

Revision of the theory of authority of first person enunciates which Cartesians imposed linking cognition study and philosophy and reasoning. Showing the limitation that diverse authors exposed, Davidson restates authority in first aperson enunciates’ use by language, also give the social factors in this use as well as other external elements such as cooperation and cultural features of speakers.Se recapitula la teoria de la autoridad de los enunciados en primera persona que el cartesianismo establecio ligando las bases del estudio de la cognicion con la filosofia y el razonamiento. Mostrando los limites que distintos autores han encontrado en esta tesis, el autor aboga de todos modos por la autoridad que el uso de la primera persona imprime a su lenguaje, tambien marcado por los factores sociales del lenguaje y otros elementos externos centrados en la cooperacion y rasgos culturales de los hablantes

O problema da objetividade

Desde Descartes a epistemologia tem se baseado no conhecimento de primeira pessoa. Devemos começar, de acordo com a história usual, com o que é mais certo: o conhecimento de nossas próprias sensações e pensamentos. De uma maneira ou outra, progredimos então, se pudermos, para o conhecimento de um mundo externo objetivo. Há por fim uma passagem tênue ao conhecimento das outras mentes. Defendo uma total revisão desse quadro. Todo pensamento proposicional, quer positivo ou cético, sobre o interior ou sobre o exterior, exige a posse do conceito de verdade objetiva, e esse conceito está acessível apenas a criaturas que estão em comunicação com outras. O conhecimento de outras mentes é, assim, básico para todo o pensamento. Mas esse conhecimento exige e supõe o conhecimento de um mundo compartilhado de objetos em um espaço e tempo comuns. Assim, a aquisição do conhecimento não é baseada em uma progressão do subjetivo para o objetivo; ele emerge holisticamente e é interpessoal desde o começo

Curriculum to fit the needs of the non-academic pupil in a small Vermont high school

Thesis (M.A.)--Boston University, 1941. This item was digitized by the Internet Archive

Lung disease in the cystic fibrosis mutant mouse

The discovery, in 1989, of the gene responsible for Cystic Fibrosis (CF), the cystic fibrosis transmembrane conductance regulator (CFTR), led to the development of mouse models of this disease. Such models were designed to facilitate the dissection of disease pathogenesis, to study the correlation between genotype and phenotype and to establish an invaluable resource for the development and evaluation of novel therapeutic agents. Fundamental to the success of such studies was the requirement that the mutant animals should develop the key phenotypic features of CF in humans. Initial characterisation of the first mouse models of CF demonstrated that they could be unequivocally distinguished from their wild type littermates and displayed many important disease features. However, the most important clinical consequence of CF, the development of chronic pulmonary infection with fibrotic lung damage, was not initially evident. In studies that preceded this thesis, we demonstrated an abnormal pulmonary phenotype in the Edinburgh CF mouse (Cftrᵗᵐ¹ᴴᵍᵘ /Cftrᵗᵐ¹ᴴᵍᵘ), on an outbred MF1 background, in response to repeated exposure to CF related respiratory pathogens. These observations established this mouse as an important model system for studies aimed at elucidating the mechanisms involved in the development of CF lung disease. The aims of this thesis were 1) to further characterise lung disease in mouse models of cystic fibrosis, and 2) to study the mechanisms underlying the development of this disease.Firstly, this thesis describes 1) the development and quantification of methods for the delivery of bacteria to the murine lung and 2) the analysis of the histopathological phenotype of mouse models of CF congenic on a C57B1/6N background, in response to such techniques. These studies were performed using a clinical strain of Staphylococcus aureus, a pathogen that is characteristic of the early stages of lung infection in CF. The experiments addressed the null hypothesis that there was no difference between the histopathological responses of 1) Cftrᵗᵐ¹ᴴᵍᵘ /Cftrᵗᵐ¹ᴴᵍᵘ mice or 2) Cftrᵗᵐ¹ᴴᵍᵘ/Cftrᵗᵐ¹ᵁⁿᶜ compound heterozygote mice, and non-CF littermates. The results led to the following conclusions; a) mouse models of CF (Cftrᵗᵐ¹ᴴᵍᵘ /Cftrᵗᵐ¹ᴴᵍᵘ and Cftrᵗᵐ¹ᴴᵍᵘ/Cftrᵗᵐ¹ᵁⁿᶜ) congenic on a C57B1/6N background developed lung pathology in response to repeated exposure to nebulised S. aureus, b) significantly more severe pathology was observed in CF mice compared to non-CF littermate controls, c) the spectrum of disease observed in CF mice and non-CF littermates congenic on a C57B1/6N background was narrowed in comparison to those on an outbred MF1 background, with wild type mice more severely affected, d) No difference was observed between the severity of disease in the Cftrᵗᵐ¹ᴴᵍᵘ/Cftrᵗᵐ¹ᵁⁿᶜ mice in comparison to the Cftrᵗᵐ¹ᴴᵍᵘ /Cftrᵗᵐ¹ᴴᵍᵘ mice, implying that the reduction in background levels of wild type CFTR did not have a major influence upon the observed response to pathogen exposure, and e) assessment of the histopathology suggested an exaggerated response rather than abnormality in any one aspect of this response.Until recently the mechanisms by which dysfunction of CF lR could lead to the development of characteristic CF lung pathology remained unclear. However, several compelling, and competing, hypotheses have been proposed, based largely on in vitro studies. This thesis also describes studies designed to complement the published research by utilising mouse models of CF and address the relevance of several of these theories in this model system.It has been proposed that CFTR interacts directly with P. aeruginosa to internalise these bacteria into airway epithelial cells. It is postulated that this process plays a role in lung defence and is compromised in CF. This thesis describes preliminary in vivo studies addressing this mechanism in mouse models of CF. Although internalisation of P. aeruginosa was observed, no difference was demonstrated between Cftrᵗᵐ¹ᴴᵍᵘ/Cftrᵗᵐ¹ᴴᵍᵘ mice and non-CF littermatesAirway surface liquid (ASL) from primary cultures of human airway epithelial cells has been shown to display salt sensitive antibacterial activity, the dysfunction of which has been implicated in the pathogenesis of CF lung disease. Airway Beta Defensins have been demonstrated to constitute an important component of this defence system. This thesis describes studies to characterise mouse Beta Defensin -1 (mBD1) and contrast it with human Beta Defensin-1 (hBD1) and concludes that a) synthetic hBD1 and mBD1 both display salt- sensitive antibacterial activity, b) hBD1 may play a role in determining the spectrum of lung pathogens that characterise CF and the predilection of P. aeruginosa for the human CF lung, c) dysfunction of mBD1 in Cftrᵗᵐ¹ᴴᵍᵘ/Cftrᵗᵐ¹ᴴᵍᵘ mice may contribute to the lung phenotype observed in response to S. aureus, and d) the differences demonstrated between mBD1 and hBD1 may result in species specific profiles of bacterial susceptibility secondary to CFTR dysfunction. In order to complement these studies by performing analysis of native murine ASL this thesis describes the development and characterisation of a primary culture model of differentiated mouse tracheal epithelium, grown at air/ liquid interface. This model demonstrates confluent, polarised epithelium, with differentiation to produce ciliated and secretory cells, expression of Cftr and murine Beta Defensin genes and a characteristic electrophysiological profile

A study of the effects of certain variables upon the attitudes and opinions of the citizens of a suburban community concerning their schools.

Thesis (Ed.D.)--Boston Universit

Understanding Periprosthetic Joint Infection

Prosthetic joint infection (PJI) is a serious complication of joint replacement surgery associated with morbidity, mortality, and socioeconomic cost. The aim of this thesis is to improve our understanding of PJI by assessing the problem at both the population and the microbiological scale. Bacteria can establish biofilms on all implant grade material and there is in vitro evidence that certain material characteristics are less attractive to bacteria and impede early biofilm formation. Clinical evidence that the choice of materials affects the risk of PJI at the population level is limited. In the first section of this thesis, a population level assessment was made to determine the influence of different implant materials on PJI using infective revision as a surrogate indicator. Propensity score matched (PSM) cohorts from 679,006 knee replacement patients demonstrated that antibiotic impregnated bone cement had no protective benefit at reducing infective revision over plain cement. Analysis using PSM cohorts demonstrated that oxidised zirconium and highly crosslinked polyethylene had a statistically insignificant trend towards decreased infective revision compared to cobalt chromium and conventional ultrahigh molecular weight polyethylene, respectively, but the analysis was likely under powered. In the second half of the thesis, at the microbial level, an in vitro model of PJI was established and modified to produce biofilms of either low or high mass and vitality depending on the incubation conditions. The model was then used to trial novel disclosure agents to demonstrate the presence of biofilm on implant material. Biofilm characterisation techniques were then trialled at the mesoscale and microscale and analysed using a novel computer program which was developed and successfully trialled. Finally, biofilm was cultivated on implant grade material, disclosed, and characterised at the macro-, meso- and microscale using a novel multimodal imaging protocol paving the way for a future ex vivo assessment