Erosão dentária infantil e hábitos alimentares

Dissertação para obtenção do grau de Mestre no Instituto Superior de Ciências da Saúde Egas Moniz

An investigation of laminar heat transfer to slender cones in the hypersonic shock tunnel

"Contract no. AF-33(616)-6025. Project no. 7064. Task no. 70169. Aeronautical Research Laboratory, Air Force Research Division, Air Research and Development Command, United States Air Force, Wright-Patterson Air Force Base."

Implantation of a scaffold following bulbectomy induces laminar organization of regenerating olfactory axons

Primary olfactory axons expressing different odorant receptors are interspersed within the olfactory nerve. However, upon reaching the outer nerve fiber layer of the olfactory bulb they defasciculate, sort out, and refasciculate prior to targeting glomeruli in fixed topographic positions. While odorant receptors are crucial for the final targeting of axons to glomeruli, it is unclear what directs the formation of the nerve fiber and glomerular layers of the olfactory bulb. While the olfactory bulb itself may provide instructive cues for the development of these layers, it is also possible that the incoming axons may simply require the presence of a physical scaffold to establish the outer laminar cytoarchitecture. In order to begin to understand the underlying role of the olfactory bulb in development of the outer layers of the olfactory bulb, we physically ablated the olfactory bulbs in OMP-IRES-LacZ and P2-IRES-tau-LacZ neonatal mice and replaced them with artificial biological scaffolds molded into the shape of an olfactory bulb. Regenerating axons projected around the edge of the cranial cavity at the periphery of the artificial scaffold and were able to form an olfactory nerve fiber layer and, to some extent, a glomerular layer. Our results reveal that olfactory axons are able to form rudimentary cytoarchitectonic layers if they are provided with an appropriately shaped biological scaffold. Thus, the olfactory bulb does not appear to provide any tropic substance that either attracts regenerating olfactory axons into the cranial cavity or induces these axons to form a plexus around its outer surface. (c) 2006 Elsevier B.V. All rights reserved.

A bayesian artificial neural network method to characterise laminar defects using dynamic measurements

This paper reports on the development of an artificial neural network (ANN) method to detect laminar defects following the pattern matching approach utilizing dynamic measurement. Although structural health monitoring (SHM) using ANN has attracted much attention in the last decade, the problem of how to select the optimal class of ANN models has not been investigated in great depth. It turns out that the lack of a rigorous ANN design methodology is one of the main reasons for the delay in the successful application of the promising technique in SHM. In this paper, a Bayesian method is applied in the selection of the optimal class of ANN models for a given set of input/target training data. The ANN design method is demonstrated for the case of the detection and characterisation of laminar defects in carbon fibre-reinforced beams using flexural vibration data for beams with and without non-symmetric delamination damage.

Laminar distribution of neurofilament inclusions and swollen achromatic neurons in neurofilament inclusion disease (NID)

The laminar distribution of the neurofilament inclusions (NI) and swollen achromatic neurons (SN) was studied in gyri of the temporal cortex in four patients with neurofilament inclusion disease (NID). In 84% of gyri analysed, the density of the NI was maximal in the lower cortical laminae. The distribution of the SN was more variable than the NI. Density was maximal in the lower cortex in 46% of gyri, in the upper cortical laminae in 8% of gyri, and a bimodal distribution in 15% of gyri. In the remaining gyri, there was a more even distribution of SN with cortical depth. In 31% of gyri, the vertical density of the NI was positively correlated with that of the SN. The data suggest that cortical degeneration in the temporal lobe of NID initially affects neurons in the lower laminae. Subsequently, the pathology may spread to affect much of the cortical profile, the SN preceding the appearance of the NI.

Laminar distribution of the pathological changes in frontal and temporal cortex in 8 patients with progressive supranuclear palsy

OBJECTIVE: To determine the laminar distribution of the pathological changes in the cerebral cortex in progressive supranuclear palsy (PSP). METHOD: The distribution of the abnormally enlarged neurons (EN), surviving neurons, neurofibrillary tangles (NFT), glial inclusions (GI), tufted astrocytes (TA), and neuritic plaques (NP) were studied across the cortex in tau immunolabeled sections of frontal and temporal cortex in 8 cases of PSP. RESULTS: The distribution of the NFT was highly variable with no consistent pattern of laminar distribution. The GI were distributed either in the lower laminae or uniformly across the cortex. Surviving neurons exhibited either a density peak in the upper laminae or a bimodal distribution was present with density peaks in the upper and lower laminae. The EN and glial cell nuclei were distributed primarily in the lower cortical laminae. There were positive correlations between the densities of the EN and glial cell nuclei and negative correlations between the surviving neurons and glial cells. No correlations were present between the densities of the NFT and GI. CONCLUSION: Cortical pathology in PSP predominantly affects the lower laminae but may spread to affect the upper laminae in some cases. The NFT and GI may have different laminar distributions and gliosis occurs concurrently with neuronal enlargement.

Laminar distribution of β-amyloid deposits in dementia with Lewy bodies and in Alzheimer's disease

This study tested whether the laminar distribution of the β-amyloid (Aβ) deposits in dementia with Lewy bodies (DLB) cases with significant Alzheimer's disease (AD) pathology (DLB/AD) was similar to "pure" AD. In DLB/AD, the maximum density of the diffuse and primitive deposits occurred either in the upper laminae or a bimodal distribution was present with density peaks in the upper and lower laminae. A bimodal distribution of the classic Aβ deposits was also observed. Compared with AD, DLB/AD cases had fewer primitive deposits relative to the diffuse and classic deposits; the primitive deposits exhibited a bimodal distribution more frequently, and the diffuse deposits occurred more often in the upper laminae. These results suggest that Aβ pathology in DLB/AD may not simply represent the presence of associated AD. © 2006 Sage Publications.

Multiple system atrophy: laminar distribution of the pathological changes in frontal and temporal neocortex--a study in ten patients

OBJECTIVE: To determine the distribution of the pathological changes in the neocortex in multiple-system atrophy (MSA). METHOD: The vertical distribution of the abnormal neurons (neurons with enlarged or atrophic perikarya), surviving neurons, glial cytoplasmic inclusions (GCI) and neuronal cytoplasmic inclusions (NI) were studied in alpha-synuclein-stained material of frontal and temporal cortex in ten cases of MSA. RESULTS: Abnormal neurons exhibited two common patterns of distribution, viz., density was either maximal in the upper cortex or a bimodal distribution was present with a density peak in the upper and lower cortex. The NI were either located in the lower cortex or were more uniformly distributed down the cortical profile. The distribution of the GCI varied considerably between gyri and cases. The density of the glial cell nuclei was maximal in the lower cortex in the majority of gyri. In a number of gyri, there was a positive correlation between the vertical densities of the abnormal neurons, the total number of surviving neurons, and the glial cell nuclei. The vertical densities of the GCI were not correlated with those of the surviving neurons or glial cells but the GCI and NI were positively correlated in a small number of gyri. CONCLUSION: The data suggest that there is significant degeneration of the frontal and temporal lobes in MSA, the lower laminae being affected more significantly than the upper laminae. Cortical degeneration in MSA is likely to be secondary to pathological changes occurring within subcortical areas.

Quantification of the pathological changes with laminar depth in the cortex in sporadic Creutzfeldt-Jakob disease

The laminar distribution of the vacuolation ('spongiform change'), surviving neurons, glial cell nuclei, and prion protein (PrP) deposits was studied in the frontal, parietal and temporal cortex in 11 cases of sporadic Creutzfeldt-Jakob disease (CJD). The distribution of the vacuolation was mainly bimodal with peaks of density in the upper and lower cortical laminae. The density of surviving neurons was greatest in the upper cortex while glial cell nuclei were distributed largely in the lower cortex. PrP deposits exhibited either a bimodal distribution or reached a maximum density in the lower cortex. The vertical density of the vacuoles was positively correlated with the surviving neurons in 12/44 of cortical areas studied, with glial cell nuclei in 16/44 areas and with PrP deposition in 15/28 areas. PrP deposits were positively correlated with glial cell nuclei in 12/31 areas. These results suggest that in sporadic CJD: (1) the lower cortical laminae are the most affected by the pathological changes; (2) the development of the vacuolation may precede that of the extracellular PrP deposits and the glial cell reaction; and (3) the pathological changes may develop initially in the lower cortical laminae and spread to affect the upper cortical laminae. © 2001 Elsevier Science Ireland Ltd. All rights reserved.