NASA Scientific and Technical Aerospace Reports
NASA Scientific and Technical Aerospace Reports
NASA Scientific and Technical Aerospace Reports
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20040111748 Naval Research Lab., Stennis Space Center, MS<br />
Role of Microbes in the Smectite-to-Illite Reaction<br />
Kim, JinWook; Dong, Hailiang; Seabaugh, Jennifer; Newell, Steven; Eberl, Dennis D.; Dec. 24, 2003; 5 pp.; In English<br />
Report No.(s): AD-A425956; NRL/JA/7430-03-4; No Copyright; Avail: CASI; A01, Hardcopy<br />
Temperature, pressure, <strong>and</strong> time have been thought to control the smectite-to-illite (S-I) reaction, an important diagenetic<br />
process used for petroleum exploration. We demonstrated that microorganisms can promote the S-I reaction by dissolving<br />
smectite through reduction of structural Fe(III) at room temperature <strong>and</strong> I atmosphere within 14 days This reaction typically<br />
requires conditions of 300 to 35O C, 100 megapascals, <strong>and</strong> 4 to 5 months in the absence of microbial activity. These results<br />
challenge the conventional concept of the S-I reaction <strong>and</strong> of reaction kinetic models.<br />
DTIC<br />
Chemical Reactions; Illite; Microorganisms; Montmorillonite; Petroleum Products<br />
20040111749 Pittsburgh Univ., Pittsburgh, PA<br />
The Impact of Exercise on the Vulnerability of Dopamine Neurons to Cell Death in Animal Models of Parkinson’s<br />
Disease<br />
Sigmond, Michael J.; Jul. 2004; 10 pp.; In English<br />
Report No.(s): AD-A425957; No Copyright; Avail: CASI; A02, Hardcopy<br />
Parkinson’s disease (PD) results in part from the loss of dopamine (DA) neurons. We hypothesize that exercise reduces<br />
the vulnerability of DA neurons to neurotoxin exposure <strong>and</strong> have outlined experiments to test this hypothesis in rats treated<br />
with one of several neurotoxins, beginning with 6- hydroxydopamine (6-OHDA). Over the past year, we established a staff,<br />
the training, <strong>and</strong> most of the methodology needed to perform these studies. Subsequently, we have observed the following:<br />
(1) Casting protects against the effects of 6-OHDA administered along DA axons or in terminal fields. (2) This protection<br />
appears to result from the blockade of DA neuron degeneration. (3) There is little or no protection against the<br />
neuropathological <strong>and</strong> behavioral effects of 6-OHDA with treadmill running using the paradigms examined. (4) Exposure to<br />
very low levels of 6-OHDA results in significant protection against higher levels of 6-OHDA exposure. We have three primary<br />
objectives for the coming year: to complete our attempts to protect against 6-OHDA toxicity with treadmill running, explore<br />
other forms of exercise, <strong>and</strong> use an effective form of exercise to examine the relation between exercise duration <strong>and</strong> protection<br />
as well as the temporal relation between exercise, time of toxin exposure <strong>and</strong> protection.<br />
DTIC<br />
Death; Diseases; Dopamine; Exercise Physiology; Neurons; Physical Exercise; Veterinary Medicine; Vulnerability<br />
20040111750 Stanford Univ., Stanford, CA<br />
PTEN Regulates Beta-Catenin in Androgen Signaling: Implication in Prostate Cancer Progression<br />
Sun, Zijie; Mar. 2004; 9 pp.; In English; Original contains color illustrations<br />
Contract(s)/Grant(s): DAMD17-03-1-0090<br />
Report No.(s): AD-A425958; No Copyright; Avail: CASI; A02, Hardcopy<br />
Observations from <strong>and</strong>rogen ablation treatment of prostate cancer have shown that the <strong>and</strong>rogen-signaling pathway is<br />
important in the growth <strong>and</strong> progression of prostate cancer. The growth-promoting effects of <strong>and</strong>rogen are mediated mostly<br />
through the <strong>and</strong>rogen receptor (AR). P13K/Akt plays a critical role in prostate cancer cell growth <strong>and</strong> survival. It has been<br />
shown that the effect of P13K/Akt in prostate cells is mediated through <strong>and</strong>rogen signaling. The PI3K inhibitor, LY294002,<br />
<strong>and</strong> a tumor suppressor, PTEN, negatively regulate the PI3K/Akt pathway <strong>and</strong> repress AR activity. However, the molecular<br />
mechanisms whereby P13K/Akt <strong>and</strong> PTEN regulate the <strong>and</strong>rogen pathway are currently unclear. In this study, we will use<br />
several biological relevant experiments to test whether beta-catenin, an AR coactivator, is a major downstream effector of the<br />
PI3K/Akt <strong>and</strong> PTEN pathways in <strong>and</strong>rogen- mediated prostate cell growth <strong>and</strong> survival. Successful completion of the<br />
proposed study should provide fresh insight into the pathogenesis of prostate cancer that may help us to identify new pathways<br />
that can be targeted for prostate cancer treatment.<br />
DTIC<br />
Cancer; Hormones; Males; Prostate Gl<strong>and</strong><br />
20040111751 Chicago Univ., Chicago, IL<br />
Evaluation of the Role of the Metastasis- Suppressor Gene MKK4/SEK1 in Transgenic Models of Prostate Cancer<br />
Rinker-Schaeffer, Carrie W.; Jun. 2003; 9 pp.; In English<br />
Contract(s)/Grant(s): DAMD17-01-1-0700<br />
Report No.(s): AD-A425959; No Copyright; Avail: CASI; A02, Hardcopy<br />
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