Scientific and Technical Aerospace Reports Volume 39 April 6, 2001
Scientific and Technical Aerospace Reports Volume 39 April 6, 2001
Scientific and Technical Aerospace Reports Volume 39 April 6, 2001
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<strong>2001</strong>0025060 Ford (Henry) Hospital, Health Sciences Center, Detroit, MI USA<br />
Influence of Bone Remodeling Inhibition on the Development of Experimental Stress Fractures Annual Report, 1 Sep.<br />
1999-31 Aug. 2000<br />
Boyd, Robert D., Ford (Henry) Hospital, USA; Schaffler, Mitchell B., Ford (Henry) Hospital, USA; Sep. 2000; 6p; In English<br />
Contract(s)/Grant(s): DAMD17-98-1-8515<br />
Report No.(s): AD-A3848<strong>39</strong>; No Copyright; Avail: CASI; A01, Microfiche; A02, Hardcopy<br />
Stress fractures result from repetitive loading <strong>and</strong> have been regarded as a mechanical fatigue-driven process. However, histopathological<br />
data <strong>and</strong> experimental data from our laboratory suggests that increased remodeling precedes the occurrence of bone<br />
microdamage <strong>and</strong> stress fractures, suggesting a central role for increased intracortical remodeling in the pathogenesis of stress<br />
fractures. Thus, we propose that stress fracture occurs through a positive feedback mechanism, in which increased mechanical<br />
usage stimulates focal bone turnover, resulting in a locally increased in porosity. Microdamage accumulation <strong>and</strong> stress fractures<br />
result from continued cyclic loading of this transiently osteopenic bone. The proposed experiments test the hypothesis by pharmacologically<br />
inhibiting the bone remodeling response, the subsequent accumulation of microdamage <strong>and</strong> the severity of the stress<br />
fracture can be diminished. In the proposed experiments, this hypothesis is being tested experimentally in the rabbit tibial stress<br />
fracture model, which was developed in our laboratory. to test the hypothesis that reactive remodeling within the cortex drives<br />
the development of stress fractures, the effect of remodeling suppression using a bisphosphonate on the accumulation of bone<br />
microdamage <strong>and</strong> diminishing the severity of stress fracture will be examined. Outcomes of these experiments will be assessed<br />
using bone scintigraphy, histomorphometry <strong>and</strong> biomechanical approaches.<br />
DTIC<br />
Bone Demineralization; Fracturing; Histology; Biodynamics; Stress (Physiology); Pathogenesis<br />
<strong>2001</strong>0025061 Salk Inst. for Biological Studies, San Diego, CA USA<br />
Mechanisms of Resistance to Neurotoxins Annual Report, 1 Sep. 1999-31 Aug. 2000<br />
Schubert, David R., Salk Inst. for Biological Studies, USA; Sep. 2000; 102p; In English<br />
Contract(s)/Grant(s): DAMD17-99-1-9562<br />
Report No.(s): AD-A384832; No Copyright; Avail: CASI; A02, Microfiche; A06, Hardcopy<br />
Glutamic acid is both a neurotransmitter in the brain as well as a major neurotoxin, killing nerve cells during trauma <strong>and</strong> ischemia.<br />
Glutamate kills cells through receptor mediated excitotoxicity or via an oxidative stress pathway called oxidative glutamate<br />
toxicity. During the past year our laboratory has been studying the pathways which lead to glutamate induced cell death by the<br />
oxidative pathway. Using an expression cloning strategy, we have identified a protein, the translation initiation factor alpha IF2<br />
alpha, which acts as a central switch that determines whether cells live or die in response to oxidative stress. This appears to be<br />
done by the ability of eIF2 alpha to control the rate of glutathione synthesis by the translational regulation of the rate limiting<br />
enzyme in glutathione synthesis. An excellent model for glutamate excitotoxicity was also developed, <strong>and</strong> it was shown that oxidative<br />
glutamate toxicity is a component of the excitotoxicity cascade, a result which explains a great deal of confusing data on glutamate<br />
neurotoxicity. Finally, using Bax knock-out mice, we have ruled out the role of this classical death gene in the programmed<br />
cell death caused by both forms of glutamate toxicity.<br />
DTIC<br />
Neurotransmitters; Nervous System; Toxins <strong>and</strong> Antitoxins; Resistance; Glutamates; Cells (Biology)<br />
<strong>2001</strong>0025068 Catholic Univ. of America, Washington, DC USA<br />
A Computer-Based Decision Support System for Breast Cancer Diagnosis Annual Report, 1 Sep. 1998 - 31 Aug. 1999<br />
Luo, Lan, Catholic Univ. of America, USA; Sep. 1999; 11p; In English<br />
Contract(s)/Grant(s): DAMD17-98-1-8044<br />
Report No.(s): AD-A384615; No Copyright; Avail: CASI; A01, Microfiche; A03, Hardcopy<br />
The optimal goal of this project is to develop decision support systems for breast cancer diagnosis, treatment option, prognosis,<br />
<strong>and</strong> risk prediction. The primary goal for the first year is to develop visual presentation methods for the consultation system.<br />
We have developed an automated <strong>and</strong> intelligent procedure for generating the hierarchy of minimax entropy models <strong>and</strong> principal<br />
component visualization spaces for improving data explanation. The proposed model is both statistically principled <strong>and</strong> visually<br />
effective at revealing all of the interesting aspects of the data set. The methods involve multiple use of st<strong>and</strong>ard finite normal mixture<br />
models <strong>and</strong> probabilistic principal component projections, whose parameters are estimated using expectation-maximization<br />
algorithm <strong>and</strong> principal component neural networks under the information theoretic criteria.<br />
DTIC<br />
Computer Techniques; Diagnosis; Cancer; Mammary Gl<strong>and</strong>s; Algorithms<br />
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