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The role of type-1 astrocytes in the reconstruction of glial environments in the central nervous systemFranklin, Robin James Milroy January 1991 (has links)
No description available.
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Post-translational processing of microtubule protein during peripheral nerve regenerationMullins, Fraser Hewitt January 1993 (has links)
No description available.
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The study of the neurophysiology of high strain rate nerve injuryYang, In Hong 30 September 2004 (has links)
The study of the mechanism of traumatic brain injury (TBI) processes at the cellular level is vital to obtain characterization of nerve cell damage after mechanical deformation. This understanding is needed to find feasible therapeutic targets for mechanically damaged neurons. To study the cellular level of TBI damage, development of a new in vitro cellular model of TBI might be done to simulate in vivo cellular TBI.
In this research, two studies were performed: (1) the design and construction of an in vitro cell stretching device to mechanically injure cells and (2) the characterization of the molecular and cellular level of the TBI mechanism. The cell stretching device design allows for the precise control of cell strain and duration of stretching cells such that TBI can be mimicked. Analysis of the cellular and molecular level mechanisms of TBI in the proposed in vitro model might help in the design of therapeutic strategies for the treatment of TBI. Our proposed mechanism of injury due to TBI is as follows: after the cell is stretched, a cellular signaling molecule is released to activate the cellular signaling pathway. The activated cell signal may activate kinases which phosphorylate proteins and initiate new protein synthesis. Newly phosphorylated and synthesized proteins may activate the apoptotic process.
Using a variety of pharmacological agents, one could block steps in the hypothesized mechanism and examine the effect of those agents on downstream cellular processes and cell apoptosis. For example, the inhibitions of calcium transport, protein synthesis, and caspases were performed to examine the initial activation of the signaling pathway and the role of both in the apoptosis process. Proteomics of TBI may help the understanding of the mechanism of TBI related protein expression. This work will contribute to the discovery of new therapeutic targets and better treatments for TBI.
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A multiscale modeling approach to investigate traumatic brain injuryBakhtiarydavijani, Amirhamed 09 August 2019 (has links)
In the current study, mechanoporation-related neuronal injury as a result of mechanical loading has been studied using a multiscale approach. Injurious mechanical loads to the head induce strains in the brain tissue at the macroscale. As each length scale has its own unique morphology and heterogeneities, the strains have been scaled down from the macroscale brain tissue to the nanoscale neuronal components that result in mechanoporation of the neuronal membrane, while relevant neuronal membrane mechanoporation-related damage criteria have been scaled up to the macroscale. To achieve this, first, damage evolution equations has been developed and calibrated to molecular dynamics simulations of a representative neuronal membrane at the nanoscale. These damage evolution equations are strain rate and strain state dependent. The resulting damage evolution model has been combined with Nernst-Planck diffusion equations to analytically compare to intracellular ion concentration disruption through mechanical loading of in vitro neuron cell culture and found to agree well. Then, these damage evolution equations have been scaled up to the microscale for dynamic simulations of 3-dimensional reconstructed neurons of similar mechanical loads. It was found that the neuronal orientation significantly affects average damage accumulation on the neuron, while the morphology of neurons, for a given neuron type, had little effect on the average damage accumulation. At the mesoscale, finite element simulations of geometrical complexities of sulci and gyri, and the structural complexities of the gray and white matter and CSF on stress localization were studied. It was found that the brain convolutions, sulci, and gyri, along with the effects of impedance mismatch between the cerebrospinal fluid (CSF) and brain tissue localized shear stresses, at the depths of the sulcus end (near field effects) and in-between sulci (far field effects), that correlated well with the regions of tau protein accumulation that is observed in chronic traumatic encephalopathy (CTE). Further, sulcus length and orientation, with respect to impending stress waves, had a significant impact on the magnitude of stress localization in the brain tissue. Lastly, gray-white matter differentiation, pia matter, and brain-CSF interface interaction properties had minimal impact of the shear stress localization trends observed in these simulations.
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Molecular Characterization of Experimental Traumatic Brain InjuryIsraelsson, Charlotte January 2006 (has links)
Traumatic brain injury (TBI) is the most common cause of mortality and disability in the younger (<50 years) Swedish population with an incidence rate of 20,000 cases per year. This thesis aims to increase the understanding of brain injury mechanisms, especially in a molecular and cellular context. Bone morphogenetic protein (BMP) signalling was examined in three genetically modified mice (two “loss-of-function”, one “gain-of-function”) exposed to TBI (controlled cortical impact, CCI) with CaMKII used as promoter for Cre-driven recombination in postnatal forebrain neurons. The mice survived, developed normally and did not show any obvious phenotypes except for an upregulation in Mtap2 mRNA in mice with impaired BMP signalling. Reactive Gfap and Timp1 mRNA expression measured using quantitative RT-PCR (qRT-PCR) was reduced in the mice overexpressing BMP signals. The BMP signalling pathway was further studied in cultured PC12 cells with BMP4 and NGF added. Egr3 expression was substantially increased by these growth factors. Blocking Egr or Junb functions reduced neurite outgrowth. TBI-induced mRNA expression changes in 100 selected genes in C57BL/6J mouse neocortex and hippocampus were measured using qRT-PCR at different time points post-injury. Several distinct gene clusters with similar expression patterns were identified. GeneChip analysis (Affymetrix) of the injured mouse neocortex at three days revealed 146 transcripts significantly upregulated, confirming and extending the qRT-PCR results. The findings demonstrate marked increases after injury among chemokine transcripts and activation of many genes involved in inflammation. In conclusion, the present study has revealed transcriptional changes in specific signalling pathways after brain injury. The results may help to identify novel targets for neuroprotective interventions after traumatic brain injury.
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Ovlivní zvýšení tělesné teploty v průběhu epileptického statu u mláďat laboratorního potkana rozsah či charakter poškození hipokampu? / Will an increase in body temperature during status epilepticus in rat pups affect the extent and nature of damage to the hippocampus?Chott, Robert January 2012 (has links)
Febrile seizures are epileptic seizures, arising in connection with febrile conditions in children of prechool age. In adults with epilepsy is often present a history of febrile status epilepticus, seizure whose duration is longer than 20 minutes. To study the role of febrile status epilepticus (FSE) in the development of epilepsy and neuronal damage, it is necessary to have a relevant animal models. This work is focused on the morphological analysis of the new created model of febrile status epilepticus, using a combination of short-term hyperthermia and chemical induced status epilepticus at 10 days old rats. In adulthood, the animals were examined by video/EEG monitoring, and then morphometric analysis. The aim of this study was to determine the importance of short-term hyperthermia during SE for neuropathological changes using stereological measurements of hippocampal volume.
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Additiver Mikroglia-vermittelter Neuronenschaden durch β-Amyloid und bakterielle Toll-like-Rezeptor-Agonisten in primären murinen Mikroglia-Neuronen-Kokulturen. Entwicklung eines Auswertungsalgorithmus zur Quantifizierung des Neuronenschadens mit Hilfe einer Software zur objektorientierten Bildanalyse / Additive microglia-mediated neuronal injury caused by Amyloid-β and bacterial TLR agonists in primary murine neuron-microglia co-cultures. Developing a ruleset for quantifying the neuronal injury by an object-based image analysis software.Loleit, Tobias 20 June 2012 (has links)
No description available.
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