El biotipo periodontal es considerado un factor significativo relacionado con el éxito en el resultado de los tratamientos odontológicos. El objetivo de este estudio es determinar la una posible relación entre el grosor gingival con respecto al grosor de la tabla ósea subyacente en los dientes incisivos y caninos maxilares y mandibulares. Material y Métodos Una muestra de 180 dientes anteriores (incisivos y caninos, 90 mandibulares y 90 maxilares) procedentes de 15 pacientes fueron incluidos en la muestra. El grosor gingival (GG) se midió usando la técnica de sondaje transgingival en tres posiciones: 1 mm apical al margen gingival (GGC), 1 mm coronal a la línea mucogingival (GGA), y un punto medio entre las dos posiciones anteriores (GGM). El espesor de la tabla ósea vestibular (GO) se midió haciendo uso de la tomografía computarizada en haz de cono(CBCT). Las mediciones fueron registradas en tres posiciones: 4mm apical a la unión amelo-cementaria (GOC), a nivel apical del diente (GOA), y un punto medio entre los dos anteriores (GOM). Además, el ancho inciso-apical de encía queratinizada (AEQ) y la profundidad de sondaje (PS) fueron registrados. Las mediciones clínicas y CBCT se compararon y se correlacionaron. Resultados. No se observó una relación estadísticamente significativa entre los valores de GG y el GO en cualquiera de las tres posiciones estudiadas. La media de GG a nivel crestal, medio y apical de los dientes superiores fue 1.01mm (± 0.58mm), 1.06mm (± 0.48mm) y 0.83mm (± 0,47 mm), respectivamente, y la media de GO correspondiente 1.24mm (± 0,90 mm ), 0.81mm (± 0,33 mm) y 2.78mm (± 1.62mm), respectivamente. Se observó una relación estadísticamente significativa entre el AEQ y el GOC (R = 0,007, P <0,05) . De igual manera se observó una relación similar entre la PS y el AEQ en los incisivos centrales superiores.(P = 0,01). Conclusiones: De acuerdo con nuestros resultados, el grosor del tejido gingival vestibular no está relacionado al grosor de la tabla ósea subyacente. Sin embargo, el AEQ parece correlacionarse con el grosor de la tabla ósea en el punto crestal. Estos resultados confirman la importancia de una adecuada evaluación del biotipo antes de establecer un plan de tratamiento

This study evaluated whether cortical reorganization occurs in response to macular degeneration (MD), a progressive disorder of the retina that results in central vision loss. Past research has observed the ability of V1 to adapt to retinal damage, demonstrating that deafferented cortex is activated by the stimulation of intact retinal areas. It is still unclear, however, if and to what degree cortical reorganization is associated with specific forms of macular degeneration. This study evaluated the retinal health of MD participants (both age-related and juvenile) as well age-matched controls with computerized microperimetry. Contrast-reversing stimuli were then presented to different parts of the visual field while participants were scanned with functional magnetic resonance imaging (fMRI). For MD participants, stimulation of peripheral retinal areas elicited activation in deafferented cortex. This activation occurred for retinal areas adapted for eccentric viewing (preferred retinal locations), but not in preserved retina at the same eccentricity. These findings add to the scientific knowledge of plasticity in sensory systems by supporting an experience driven understanding of cortical reorganization. They could also have a meaningful impact on how macular degeneration is treated by informing the design of therapeutic training regimes.

The cerebral cortex is gray matter tissue which covers cerebral hemispheres. In recent years, many studies reported that abnormal cortical thickness was found in several diseases of central neural system, such as multiple sclerosis, Alzheimer's diseases, and schizophrenia. Therefore, the whole-brain measurement of cortical thickness using the non-invasive magnetic resonance imaging becomes important. However, not many algorithms were reported in the past due to the extremely complex folding structure of human cortex. In this thesis, a voxel-based cortical thickness method proposed by Hutton et al was implemented using MATLAB to achieve automated measurement. Several crucial factors, including the definition of boundary condition, interpolation method, the step size of developing each streamline, and spatial resolution of imaging space, in the implementation were discussed. In addition, the analysis of stability, or precision, of our self-developed program was evaluated . Sixteen experiments of reproducibility were performed in two months on the same 24-year-old healthy volunteer repeatedly to obtain whole-brain 3D T1WI. Cortical thickness map was calculated independently and normalized to the same coordination. Mean, standard deviation, and normalized standard deviation of 16 measurements were calculated on every cortical voxel, along with whole-brain mean cortical thickness. Various sizes of 3D smoothing kernel were applied, and the results showed stronger smoothing might help higher precision by the cost of spatial resolution.

In adult rats, following unilateral stroke-like injury to the motor cortex, there is significant loss of function in the forelimb contralateral to the ischemic damage. In the remaining motor cortex, changes in neuronal activation patterns and connectivity are induced following motor learning and rehabilitation in the brains of adult animals. Rehabilitative training promotes functional recovery of the impaired forelimb following motor cortical strokes; however, its benefits are most efficacious when coupled with other rehabilitative treatments. Multiple lines of evidence suggest that focal cortical electrical stimulation (CS) enhances the effectiveness of rehabilitative training (RT) and promotes changes in neural activation and plasticity in the peri-lesion motor cortex. Specific examples of plastic events include increases in dendritic and synaptic density in the peri-lesion cortex following CS/RT compared to rehabilitative training alone. The objective of these studies was to investigate which conditions, such as timing and method of delivery of CS, when coupled with RT, are most efficacious in promoting neuronal plasticity and functional recovery of the impaired forelimb following ischemic cortical injury in adult animals. The central hypothesis of these dissertation studies is that, following unilateral stroke-like injury, CS improves the functional recovery of the impaired forelimb and promotes neural plasticity in remaining motor cortex when combined with RT. This hypothesis was tested in a series of experiments manipulating post-ischemic behavioral experience with the impaired forelimb. Adult rats were proficient in a motor skill (Single Pellet Retrieval Task) and received ischemic motor cortex lesion that caused impairments in the forelimb. Rats received daily rehabilitative training on a tray reaching task with or without concurrent cortical stimulation. Epidural cortical stimulation, when paired with rehabilitative training, resulted in enhanced reaching performance compared to RT alone when initiated 14 days after lesion. These results were found to be maintained well after the treatment period ended. Rats tested 9-10 months post-rehabilitative training on the single pellet retrieval task continued to have greater reaching performance compared to RT alone. However, delayed onset of rehabilitative training (3 months post-infarct) indicated that CS does not further improve forelimb function compared to RT along. It was further established that CS delivered over the intact skull (transcranial stimulation) of the lesioned motor cortex was not a beneficial adjunct to rehabilitative training. Together these dissertation studies provide insight into the effectiveness and limitations of CS on behavioral recovery. The findings in these studies are likely to be important for understanding how post-stroke behavioral interventions and adjunct therapies could be used to optimize brain reorganization and functional outcome. / text

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Cortical bone is a dynamic tissue which undergoes adaptive and pathological changes throughout life. An improved understanding of the spatio-temporal process of remodeling holds great promise for improving our understanding of bone development, maintenance and senescence. The use of micro-computed tomography (µCT) on living animals is relatively new and allows the three dimensional quantification of change in trabecular bone microarchitecture over time. The use of in vivo µCT is limited by the radiation dose created by the x-ray beam, with commercially available in vivo systems generally operating in the 10-20 um resolution range and delivering an absorbed dose between 0.5-1 Gy. Because dose scales to the power of four with resolution, in vivo imaging of the cortical canal network, which requires a higher resolution, has not been achieved. I hypothesized that using synchrotron propagation phase contrast µCT, cortical porosity could be imaged in vivo in rats at a dose on the same level as those used currently for trabecular bone analysis. Using the BMIT-BM beamline, I determined the optimal propagation distance and used ion chamber and lithium fluoride crystal thermoluminescent dosimetry to measure the absorbed dose of my in vivo protocol as well as several ex vivo protocols using synchrotron phase contrast µCT at 5 µm, 10 µm, and 11.8 µm and conventional desktop in vivo protocols using commercial µCT systems. Using synchrotron propagation phase contrast µCT, I scanned the forelimb of two adult Sprague-Dawley rats and measured an absorbed dose of 2.53 Gy. Using two commercial µCT system, I measured doses between 1.2-3.6 Gy for protocols at 18µm that are in common use. This thesis represents the first in vivo imaging of rat cortical porosity and demonstrates that an 11.8 µm resolution is enough to visualize cortical porosity in rats, with a dose within the scope of those used for imaging trabecular bone in vivo.

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Mitofusin 1 and 2 are outer-mitochondrial membrane proteins that have been shown to be involved in fusion. Mitofusin 2 has also been associated with apoptosis and development. When Mfn1 and Mfn2 were each conditionally knocked out from the cerebellum, Purkinje cells in Mfn2 deficient cerebellum during development had undergone neurodegeneration. Mutations in Mfn2 have also been associated with the Charcot Marie Tooth Type 2A (CMT2A). We want to asses the effect Mfn2 and Mfn1 might have on the development of other regions of the brain such as the telencephalon. We generated Mfn1 and Mfn2 conditional knockouts in the telencephalon by crossing them with Foxg1 Cre - a cre expressed in the telencephalon. We found that Mfn1 deficient mice have lost their corpus callosum at the midline, but survive over 6 months with a decrease in progenitor cells postnatally. Mfn2 deficient mice die between P9 and P12 with a decrease in progenitor cells postnatally and a decrease in number of neurons in the cortex. Therefore, our results suggest that Mfn1 and Mfn2 play a significant role in the development of the telencephalon.

Master of Philosophy (Medicine) / The actin cytoskeleton is important in many cellular processes such as motility, and establishing and maintaining cell morphology. Members of the tropomyosin protein family associate with the actin cytoskeleton along the major groove of actin filaments (F-actin), stabilising them and regulating actin-filament dynamics. To date over 40 non-muscle tropomyosin isoforms have been identified, which are encoded by 4 different genes (α, β, γ, δ). Individual tropomyosin isoforms define functionally distinct F-actin populations. Previous studies have shown that tropomyosins sort to distinct subcellular compartments at different stages of development in polarised cells. Neuronal growth cones are highly dynamic polarised structures, dependent on a constant reorganisation of the actin cytoskeleton. By eliminating tropomyosins in a knockout (KO) mouse model, we investigated the role of two tropomyosin isoforms, Tm5NM1 and Tm5NM2 (γTm gene products) in growth cone dynamics and neurite outgrowth. Growth cone protrusion rates were significantly increased in one day old Tm5NM1/2 KO hippocampal neurons compared to WT controls. Neuritogenesis was significantly affected by the elimination of Tm5NM1/2, with a slight decrease in neurite length and an increase in neuronal branching in neurons cultured for four days. At the molecular level, the depletion of Tm5NM1/2 had no impact on the protein levels and activity of ADF/cofilin in hippocampal neurons while in cortical neurons a subtle but significant increase in ADF/cofilin activity was observed. The subtle phenotype in the early stages of neuritogenesis observed from eliminating Tm5NM1/2 may be explained with functional compensation by other tropomyosin isoforms. Functional compensation for the loss of Tm5NM1/2 may be provided by isoforms Tm5a/5b, TmBr2 and Tm4 as they localise to the growth cones, structures where Tm5NM1/2 are normally found. These results suggest that Tm5NM1/2 may not be required for early stages of neuritogenesis but may still play a fine-tuning role for this process.