Browsing by Subject "injury"
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Item Measurement of Traumatic Brain Injury (TBI) Inpatient Activity Levels Through Accelerometry(2017-05-01) Ramsey, Jeffrey T.; Patricia A. Gwirtz; J. Cameron Millar; Stephen O. MathewPurpose: The purpose of this study was to use retrospective analysis of actigraphy data to describe activity levels for patients undergoing inpatient rehabilitation. This study also examined the differences between activity levels of the different areas of therapy. The final aim of this study was to examine the affect of demographic factors, and injury characteristics on activity levels. Method: Fifty individuals with Traumatic Brain Injury (TBI) undergoing inpatient rehabilitation wore accelerometers. Activity Counts (ACs) were summarized in one-minute intervals. ACs, demographic and outcome variables were analyzed using descriptive statistics and general linear regression analysis. Results: During active therapy patients averaged 241.3 +/- 97.8 AC, which decreased to 142.2 +/- 74.1 during non-active therapy. Recreational time had an average of 112.8 +/- 59.5 AC, and sleep time had an average of 26.7 +/- 14.8 AC. Using predetermined definitions of physical activity, patients were determined to be inactive during therapy and sedentary/inactive for large portions of their stay. Linear regression analysis showed that the main factor with a negative association with physical activity is age. Discussion: The findings of this study demonstrate that patients undergoing inpatient rehabilitation are largely inactive or sedentary. Although age was determined to have the largest impact on physical activity, the other demographic and outcome measures analyzed by this study along with other confounders’ impact on physical activity require further study to determine the best way to safely increase patient activity.Item The Role of a Membrane Androgen Receptron in the Brain(2007-02-01) Gatson, John Wayne; Simpkins, James; Koulen, Peter; Basu, AlakanandaGatson, Joshua Wayne, The Role of a Membrane Androgen Receptor in the Brain. Doctor of Philosophy (Biomedical Sciences), February 2007, pp187, 34 illustrations. In the brain, depending on the insult type, androgens have been shown to protect from or exacerbate the levels of cell death. This discrepancy is partly due to the array of receptors that androgens may activate during injury. For example, activation of intracellular androgen receptors (AR) leads to the activation of pro-survival pathways and protects from various toxins such beta-amyloid. In contrast, previous studies have demonstrated that testosterone causes an increase in lesion size following stroke. The damaging effects of androgens in the brain may be mediated by a membrane-associated AR (mAR), since activation of mAR in peripheral tissue results in a decrease in cell growth and an increase in apoptotic cell death during serum deprivation. Here, I hypothesize that activation of a mAR in cortical astrocytes, suppresses the ERK and Akt signaling pathways and increases cell death in the presence of a metabolic and oxidative stressor. In this study, we found that glia express both isoforms of the AR (AR-B and AR-A) and that dihydrotestosterone (DHT) elicits ERK and Akt phosphorylation in rat glioma (C6) cells. The effect of DHT on the activation of these signaling pathways is AR dependent, since flutamide blocked this effect. In contrast to the intracellular receptor, we concluded that DHT-BSA (membrane impermeant form of DHT) binds to DHT displaceable sites on the plasma membrane. Also, treatment with DHT-BSA in the C6 cells resulted in a significant decrease in phosphor-ERK and Akt levels, suggesting the existence of two different pathways through which DHT can influence the activity of these signaling pathways. With respect to cell survival, the C6 cells and primary cortical astrocytes were treated with the metabolic and oxidative insult, iodoacetic acid (IAA), in the presence or absence of DHT, DHT-BSA, or estradiol. Following treatment, DHT and estradiol protected the glia from IAA-induced toxicity, whereas DHT-BSA caused a significant increase in cell death in the presence of a sublethal concentration of IAA. These results indicate that activation of the intracellular pathway is protective and activation of a membrane pathway is damage-inducing during injury, further supporting our results from the ERK and Akt signaling studies. To further characterize this mAR in the brain, we decided to look for indices of apoptosis such as caspase activation and TUNEL staining. It was found that DHT-BSA treatment in the presence of IAA, resulted in an increase in caspase-3/7 activation and increased TUNEL staining. In addition, PKC-delta mediated DHT-BSA-induced cell death, since antagonism of PKC-delta with rottlerin afforded protection. In conclusion, we have partially characterized a novel mAR in astrocytes during injury. Here, the damaging effects of androgens, at least in astrocytes, may in fact be mediated by a mAR, which may be a therapeutic target stroke or reperfusion injury.