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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Nuclear Science and Engineering, 2009., Cataloged from PDF version of thesis., Includes bibliographical references (p. 121-122)., Nuclear oil well logging tools utilizing radioisotope sources of photons are used ubiquitously in oilfields throughout the world. Because of safety and security concerns, there is renewed interest in shifting to electronically-switchable accelerator sources. Investigation of accelerator sources opens up the opportunity to study higher-energy sources. In this thesis, sources with a 10 MeV endpoint are examined, a several-fold increase over traditional techniques. The properties of high-energy photon transport are investigated for potential new or improved well logging measurements. Two obvious processes available with a high-energy photon source are pair production and photo neutron emission. A new measurement of formation density is proposed based on the annihilation radiation produced after the pair production of high-energy source photons in the rock formation. With a detector spacing of 55 cm, this measurement exhibits a sensitivity to density with a dynamic range of 10 across a typical range of formation density (2.0 - 3.0 g/cc), the same as traditional measurements. Increases in depth of investigation for these measurements can substantially improve the sampling of the formation and thus the quality and relevance of the measurement. Being distributed in angle and space throughout the formation, a measurement based on anni-hilation photons exhibits a greater depth of investigation than traditional methods. For a detector spacing of 39 cm (equivalent to a typical spacing for one detector in traditional approaches), this measurement has a depth of investigation of 8.0 cm while the traditional measurement has a depth of investigation of 3.6 cm., (cont.) For the 55 cm spacing, this depth is increased to 9.4 cm. Concerns remain for how to implement an accelerator source in which energy spectroscopy, essential for identifying an annihilation peak, is possible. Because pair production also depends on formation lithology, the effects of chemical composition on annihilation photon flux are small (<20 %) for the studied geometry. Additionally, lithology measurements based on attenuation at high energies show too small an effect to be likely to produce a useful measurement. Photoneutron production cross sections at this energy are too small to obtain a measurement based on this process., by Eric D. Johnson., Ph.D.

Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, 2008., Includes bibliographical references., The prion protein (PrP) is a conserved glycoprotein tethered to cell membranes by a glycosylphosphatidylinositol anchor. In mammals, PrP is expressed in many tissues, most abundantly in brain, heart, and muscle. Importantly, PrP is required for prion diseases, which are neurodegenerative diseases associated with misfolding and aggregation of PrP. PrP can adopt a self-perpetuating conformation that templates the misfolding of normal PrP molecules into its pathogenic conformation, termed PrPsC. The role of PrPSC in the pathogenesis of prion diseases, or transmissible spongiform encephalopathies, has been studied intensively yet the mechanism by which PrP misfolding in neurons leads to injury and death remains enigmatic. Much less attention has been focused on the role of PrP in normal physiology despite the possibility that deciphering PrP's normal function could help to understand prion diseases. My thesis work has spanned both the study of the normal function of PrP and the neurotoxic pathways that are involved in prion pathogenesis. Because prion disease and other neurodegenerative diseases share protein misfolding as the primary etiology, I aimed to determine whether PrP contributed to other neurodegenerative diseases apart from prion diseases. We deleted PrP from several well established transgenic mouse models of neurodegenerative disease, including Tauopathy, Parkinson's and Huntington's diseases. Deleting PrP did not substantially alter the disease phenotypes of the models that we tested, suggesting that PrP is not a major contributor to or protector against these disorders. In addition, in collaborative efforts we determined that PrP knockout mice have defects in hematopoiesis and neurogenesis., (cont.) Hematopoietic stem cells from PrP knockout mice have defects in self-renewal, as manifested during serial bone marrow transplantation or during the aging process. PrP knockout mice also display a slight reduction in cellular proliferation and/or neurogenesis in the adult brain. I also participated in the development of a video based behavior recognition system. We used this system to quantify the home cage behavioral changes in two mouse models of neurodegeneration, Huntington's disease and prion disease. Because studies of prion disease have been focused primary on the pathological level, I have attempted to elucidate the molecular pathways responsible for mediating neurotoxicity in a mouse model of infectious prion disease. In the first series of studies we tested whether apoptotoic cell death pathways are activated in prion disease. We inoculated mice deficient for Caspase-12 and Bax, both of which have been implicated in mediating prion toxicity, but did not observe any protection against disease in these mice. Also, neuronal overexpression of Bcl-2 did not protect against prion toxicity and instead, inhibition of apoptosis may have enhanced several aspects of disease (as did deletion of Bax). In a second attempt at determining pathways involved in prion toxicity, I determined that deletion of heat shock factor 1 (Hsfl), a stress responsive transcription factor, protects against prion toxicity. Mice that are deficient for Hsfl succumb to prion disease faster than controls, despite similar pathological and behavioral onset., by Andrew D. Steele., Ph.D.

Includes bibliographical references (p. 66-67)., Thesis (S.M. and S.B.)--Massachusetts Institute of Technology, Dept. of Nuclear Science and Engineering, 2006., (cont.) Further MCNP simulations of the neutron source impinging on cargo containers suggest that this technique can respond, as expected, qualitatively differently to containers containing SNM from containers that do not. Containers that contain small amounts of fissile isotopes as in the case of a few grams of uranium-235 in a kilogram of depleted uranium will also respond to this method but much more weakly. The system as proposed is viable and further simulation and experimental work will elucidate the behavior of this system under a wide range of cargo environments., The undeniable threat of nuclear terrorism presents an opportunity for innovation in developing active interrogation technology. The proposed system aims to detect the smuggling of special nuclear material (SNM) in maritime containers. Identifying the importation of SNM will be instrumental in protecting the American public from a nuclear terrorist attack made possible by the construction of a weapon with fissile material from abroad. The proposed system uses a directionally-biased beam of low-energy neutrons (60 - 100 keV) generated from a 7Li(p,n)7Be reaction run near threshold. These neutrons are directed towards a cargo container of unknown composition. If SNM is present in the container and the neutrons can reach it, high-energy fission neutrons will be detectable outside the cargo container. MCNP models indicate that even low-energy neutrons will be able to penetrate through reasonable amounts of material likely to be encountered in cargo environments. The only major exception is hydrogenous material, which could alter the radiation signature. The presence of shielding material may further alter these results. Small amounts of shielding that is hydrogenous will thermalize incident neutrons and raise the likelihood of generating fissions. An abundance of shielding material could mask the presence of fissile material but will also result in changes in the induced gamma energy spectrum and greatly increase the flux of thermal neutrons even outside the cargo container. Still, this material would not be resistant to other radiological techniques and the presence of an abundance of hydrogen will be evident and potentially raise suspicion in and of itself., by Erik D. Johnson., S.M.and S.B.

The purpose of this study was to search for the possible association between tooth alignment with the different dentornaxilar variables and to evaluate by means of causal models if tooth alignment is the product of variables conventionally described in the literature.; Fifty four patients ( 6.7 to 10.5 years of age) were studied. Study models and latera cephalometric radio graphs were taken on ah of them in order to evaluate 25 dentofacial variables. The causal model, which allows analysis of associations between variables withut assuming interdependence between then, vas used; the results reveal] that the dental crowding seems to have a multivariate origin and is not simply caused by a dento-skeletal discrepancy. Application of the causal model seerns to be a more logical approach when analyzing crowding. Given the dependence between involved variables. A slight association vas found that showed more crowding when there was a less favorable arch and tooth size realtion. However, it was not possible generalize concepts. New studies must consider new possible ethiological factors for crowding. Such as muscles, function. Age and genetics., El propósito de este estudio fue el de buscar una posible asociación entre el alineamiento dental y diferentes variables dentomaxilares: además, el de evaluar, por medio del método de modelos causales, si el alineamiento dental es producido por las variables convencionalmente descritas en la literatura.- Se estudiaron 54 pacientes de 6,7 a l05 años de edad. a los cuales se les tomaron modelos y radiografías cefálicas laterales para evaluar 25 variables dentolabiales. El método empleado permite analizar asociaciones entre variables sin asumir interdependencia entre ellas.- Los resultados indican que el apiñamiento dental parece tener un origen multivariable y que no se debe simplemente a una discrepancia dentó-esquelética. Una muy leve asociación mostró que mientras menos favorable sea la relación tamaño de arco/tamaño dental, más apiñamiento habrá. A pesar de lo anterior, no fue posible generalizar el concepto. Nuevos estudios deberían contemplar el papel de la musculatura, la función y la herencia entre las causas del apiñamiento.

The Princeton review. / Volume 1, 1880, Page(s) 88-104, (dlps) volume: acf4325.3-01.005, (dlps) article: acf4325.3-01.005:6, http://quod.lib.umich.edu/t/text/accesspolicy.html