Articles by Nora Hlavac in JoVE
תא להתאמה אישי עבור נדידת תאים מדידות Aniqa N. Chowdhury1, Huu Tri Vo1, Sharon Olang1, Elliott Mappus1, Brian Peterson1, Nora Hlavac1, Tyler Harvey1, Delphine Dean1 1Department of Bioengineering, Clemson University פרוטוקול זה מפרט שיטה להתאמה אישית למדוד נדידת תאים בתגובת chemoattractants שעשוי לשמש גם כדי לקבוע את קצב הדיפוזיה של תרופה מתוך פולימר מטריקס.
Other articles by Nora Hlavac on PubMed
Two and Three-Dimensional in Vitro Models of Blast-Induced Neurotrauma Biomedical Sciences Instrumentation. 2015 | Pubmed ID: 25996750 Blast-induced neurotrauma (BINT) has become an increasingly significant concern in Veterans returning from warfare. Associated brain injury and cognitive deficits are difficult to diagnose as the nature of this injury is progressive. In order to better understand the mechanisms of BINT at the microscopic level, two- and three-dimensional models of astrocytes were studied. The 3-D model was developed using Matrigel® to embed the cells. Injury was induced by exposure to an overpressure of 20 psi (140 kPa) using a shock wave generator which simulates a free field blast profile. Cellular viability was measured by MTT assays conducted at 24 and 48 hours post-blast. Gene expression levels of glial-fibrillary acidic protein (GFAP), ß-actin, and vinculin were analyzed as potential structural biomarkers of injury at 48 and 72 hours post-blast. Results indicated that glial cells survived and became activated by 72 hours following exposure. Specifically, gene expression of GFAP was elevated in simulated blast cultures as compared to controls. Moreover, 2- and 3-D cultures were observed to have different time periods of activation. These activation markers may be useful when designing therapeutic targets to mitigate injury progression.
Role of Glia in Memory Deficits Following Traumatic Brain Injury: Biomarkers of Glia Dysfunction Frontiers in Integrative Neuroscience. 2016 | Pubmed ID: 26973475 Historically, glial cells have been recognized as a structural component of the brain. However, it has become clear that glial cells are intimately involved in the complexities of neural networks and memory formations. Astrocytes, microglia, and oligodendrocytes have dynamic responsibilities which substantially impact neuronal function and activities. Moreover, the importance of glia following brain injury has come to the forefront in discussions to improve axonal regeneration and functional recovery. The numerous activities of glia following injury can either promote recovery or underlie the pathobiology of memory deficits. This review outlines the pathological states of glial cells which evolve from their positive supporting roles to those which disrupt synaptic function and neuroplasticity following injury. Evidence suggests that glial cells interact extensively with neurons both chemically and physically, reinforcing their role as pivotal for higher brain functions such as learning and memory. Collectively, this mini review surveys investigations of how glial dysfunction following brain injury can alter mechanisms of synaptic plasticity and how this may be related to an increased risk for persistent memory deficits. We also include recent findings, that demonstrate new molecular avenues for clinical biomarker discovery.