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Passage of β-particles through matterWilliams, Evan James January 1929 (has links)
No description available.
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72 |
A biophysical study of amyloid-β aggregation and toxicity determinantsBolognesi, Benedetta Maria January 2011 (has links)
No description available.
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Single molecule studies of amyloid-β aggregationNarayan, Priyanka January 2012 (has links)
No description available.
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Microglial-mediated inflammatory responses and perturbed vasculature in an animal model of inflamed Alzheimer's disease brainRyu, Jae Kyu 05 1900 (has links)
Chronic inflammation in response to Aß peptide deposits is a pathological hallmark of Alzheimer's disease (AD). The inflammatory environment includes populations of reactive and proliferating microglia and astrocytes and perturbed vasculature. However, the association between activated glial cells and cerebrovascular dysfunction remain largely unknown. This study has used Aß1-42 intrahippocampal injection as an animal model of inflamed AD brain to characterize mechanisms of glial-vasculature responses as a basis for chronic inflammation.
Preliminary findings suggested Aß1-42-injected brain demonstrated vascular remodeling including evidence for formation of new blood vessels (angiogenesis). This result led to study of the effects of the anti-angiogenic/anti-inflammatory compound, thalidomide on activated glial cells and perturbations in the vasculature in an Aß1-42 peptide-injected rat model. First, Aß1-42 injection was found to cause perturbations in vasculature including new blood vessel formation and increased BBB leakiness. Second, thalidomide decreased the vascular perturbations and the glial reactivity and conferred neuroprotection. Overall, these results suggest that altered cerebral vasculature is integral to the overall inflammatory response induced by peptide.
Experiments then examined the level of parenchymal plasma proteins in brain tissue from AD and nondemented (ND) individuals. AD, but not ND, brain tissue demonstrated high levels of fibrinogen immunoreactivity (ir). Aß1_42 injection into the rat hippocampus increased the level of parenchymal fibrinogen, which was reduced by treatment with the defibrinogenating agent, ancrod. In addition, ancrod also attenuated microglial activation and prevented neuronal injury. Overall, these results demonstrate that extravasation of blood protein and a leaky BBB are important in promoting and amplifying inflammatory responses and causing neuronal damage in inflamed AD brain.
Microglial chemotactic responses to VEGF (vascular endothelial growth factor) receptor Flt-1 were next studied. Treatment with a monoclonal antibody to Flt-1 (anti-Flt-1 Ab) in the peptide-injected hippocampus diminished microglial reactivity and provided neuroprotection. Secondly, anti-Flt-1 Ab inhibited the AI3142-induced migration of human microglia. These results suggest critical functional roles for Flt-1 in mediating microglial chemotaxis and inflammatory responses in AD brain.
The overall conclusion from my work is that AP deposits induce microglial reactivity which subsequently causes vascular remodeling resulting in an amplified inflammatory microenvironment which is damaging to bystander neurons.
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Transverse polarization of beta particles in first forbidden beta decayWood, Robert Edgar 12 1900 (has links)
No description available.
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Transverse polarization of beta particles in the decay of Tm^;p170 ^;sand Eu^;p154^;sHungerford, E. V. (Ed Vernon) 12 1900 (has links)
No description available.
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Theoretical beta decay calculations employing the nilsson modelBrennan, John Joseph 05 1900 (has links)
No description available.
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Nuclear matrix elements in beta decay for spheriodal-shaped nucleiTuong, Nguyen Duc 08 1900 (has links)
No description available.
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Electron capture ratios of forbidden transitions in the decay of [superscript]81KR and [superscript]59NIChew, William Mahlon 08 1900 (has links)
No description available.
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Beta-ray spectroscopy using a superconducting solenoidRehfield, David Michael January 1977 (has links)
No description available.
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