2,229 research outputs found
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
Effect of certain large organic cations on physico-colloidal properties related to soil stability
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
- …