The main goal of this work is to evaluate the developed temperatures in bone tissue due to a drilling process, and verify the hypothesis of the thermal necrosis occurrence. Experimental methods were used in the laboratory based on the use of thermography and thermocouples during bone drilling in different materials. The follow-up of patients was also performed during the dental implants placement for data collecting from thermographic images.
Magnesium is an essential element for all living systems. The quantification of free intracellular Mg 2+ concentration () is of utmost importance since changes in its basal value may be an indication of different pathologies due to abnormalities of Mg 2+ metabolism. In this work we used 31 P NMR and fluorescence spectroscopy to determine the resting in bovine chromaffin cells, a neuron‐like cellular model, as well as confocal laser scanning microscopy to study the free Mg 2+ spatial distribution in these cells. 31 P NMR spectroscopy did not prove to be effective for the determination of in this particular case due to some special morphological and physiological properties of this cell type. A basal value of 0.551 ± 0.008 mM was found for these cells using fluorescence spectroscopy and the Mg 2+ ‐sensitive probe furaptra; this value falls in the concentration range reported in the literature for neurons from different sources. This technique proved to be an accurate and sensitive tool to determine the . lntraceilular free Mg 2+ seems to be essentially localized in the nucleus and around it, as shown by confocal microscopy with the Mg 2+ ‐sensitive probe Magnesium Green. It was not possible to derive any conclusion about free Mg 2+ localization inside the chromaffin granules and/or in the cytoplasm due to the lack of sufficient spatial resolution and to probe compartmentalization.
An overview of 13C nuclear magnetic resonance (NMR) spectroscopy methods and their applications in the study of the metabolism of brain cells in vitro and in the in vivo brain is presented as well as their implications for modern molecular imaging techniques. Various top- ics will be discussed, such as general properties of the 13C NMR spectrum, 13C NMR spectroscopy acquisition protocols, determination of fractional 13C enrichment, 13 C( 2 H) NMR methodologies, and the use of 13 C hyper-
Parkinson’s disease is an age-associated progressive neurodegenerative disorder that has gained crescent social and economic impact due to the aging of the western society. All current therapies are symptomatic and fail to reverse or halt the progression of dopaminergic neurons loss. The discovery of the capability of neurotrophic factors to protect these neurons lead numerous research groups to focus their efforts in developing therapies aiming at promoting the control of Parkinson´s disease through the delivery of neurotrophic factors to the brain or by boosting their endogenous levels. Both strategies were successful in inducing protection of dopaminergic neurons and motor recovery in preclinical models of the disease. Contrariwise, very limited success was obtained in clinical studies, where glial cell line-derived neurotrophic factor and neurturin were the neurotrophic factors of choice for Parkinson’s disease therapy. These drawbacks motivate the development of novel forms of delivery or the modification of the injected molecules aiming at providing a more stable and effective administration with improved diffusion in the target tissue, and without the immune responses observed in the earliest clinical studies. Although promising results were obtained with some of these new approaches performed in experimental models of the disease, they were not yet tested in human studies. In this review, we present the current knowledge on neurotrophic factors and their role in Parkinson’s disease, focusing on the strategies that have been developed to increase their levels in target areas of the brain to achieve protection of dopaminergic neurons and motor behaviour recovery. Keywords: Parkinson's disease, neurotrophic factors, dopaminergic neurons, BDNF, GDNF, neuroprotection, therapy.