Thruster configurations for maneuvering heavy payloads

The cargo transfer vehicle (CTV) will be required to perform six degree of freedom (6DOF) maneuvers while carrying a wide range of payloads varying from 100,000 lbm to no payload. The current baseline design configuration for the CTV uses a forward propulsion module (FPM) mounted in front of the payload and the CTV behind the payload so that the center of gravity (CG) of the combined stack is contained between the thruster sets. This allows for efficient rotation and translations of heavy payloads in all directions; however, the FPM is a costly item, so it is desirable to find design solutions which do not require the FPM. This presentation provides an overview of the work performed in analyzing the FPM requirements for the CTV. Specifically, key issues related to thruster configuration requirements for operating the CTV without the FPM, throughout the 100,000 lbm payload to no payload range, will be highlighted. In this study, only the reaction control system (RCS) thruster configurations are considered and the orbit adjust engines are not addressed. An important output of this study is the viable alternative thruster configurations which eliminate the need for the FPM. Initial results were derived using analytical techniques and simulation analysis tools. Results from the preliminary analysis were used as inputs for our 6DOF simulation. The 6DOF simulation was used to validate our design guidelines and to verify the performance of the thruster configurations

Mechanism of the mitogenic influence of hyperinsulinemia

Either endogenous or exogenous hyperinsulinemia in the setting of insulin resistance promotes phosphorylation and activation of farnesyltransferase, a ubiquitous enzyme that farnesylates Ras protein. Increased availability of farnesylated Ras at the plasma membrane enhances mitogenic responsiveness of cells to various growth factors, thus contributing to progression of cancer and atherosclerosis. This effect is specific to insulin, but is not related to the type of insulin used. Stimulatory effect of hyperinsulinemia on farnesyltransferase in the presence of insulin resistance represents one potential mechanism responsible for mitogenicity and atherogenicity of insulin

Math Anxiety in Fundamentals of Algebra Students

Thesis written by a student in the UNT Honors College discussing her experiences as a math tutor in math classes with traditionally high dropout rates. In addition, research into math anxiety is explored and evaluated

11 beta-hydroxysteroid dehydrogenase type 1 regulates glucocorticoid-induced insulin resistance in skeletal muscle

OBJECTIVE: Glucocorticoid excess is characterized by increased adiposity, skeletal myopathy, and insulin resistance, but the precise molecular mechanisms are unknown. Within skeletal muscle, 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) converts cortisone (11-dehydrocorticosterone in rodents) to active cortisol (corticosterone in rodents). We aimed to determine the mechanisms underpinning glucocorticoid-induced insulin resistance in skeletal muscle and indentify how 11beta-HSD1 inhibitors improve insulin sensitivity. \ud RESEARCH DESIGN AND METHODS: Rodent and human cell cultures, whole-tissue explants, and animal models were used to determine the impact of glucocorticoids and selective 11beta-HSD1 inhibition upon insulin signaling and action. \ud RESULTS: Dexamethasone decreased insulin-stimulated glucose uptake, decreased IRS1 mRNA and protein expression, and increased inactivating pSer$^{307}$ insulin receptor substrate (IRS)-1. 11beta-HSD1 activity and expression were observed in human and rodent myotubes and muscle explants. Activity was predominantly oxo-reductase, generating active glucocorticoid. A1 (selective 11beta-HSD1 inhibitor) abolished enzyme activity and blocked the increase in pSer$^{307}$ IRS1 and reduction in total IRS1 protein after treatment with 11DHC but not corticosterone. In C57Bl6/J mice, the selective 11beta-HSD1 inhibitor, A2, decreased fasting blood glucose levels and improved insulin sensitivity. In KK mice treated with A2, skeletal muscle pSer$^{307}$ IRS1 decreased and pThr$^{308}$ Akt/PKB increased. In addition, A2 decreased both lipogenic and lipolytic gene expression.\ud CONCLUSIONS: Prereceptor facilitation of glucocorticoid action via 11beta-HSD1 increases pSer$^{307}$ IRS1 and may be crucial in mediating insulin resistance in skeletal muscle. Selective 11beta-HSD1 inhibition decreases pSer$^{307}$ IRS1, increases pThr$^{308}$ Akt/PKB, and decreases lipogenic and lipolytic gene expression that may represent an important mechanism underpinning their insulin-sensitizing action

A 7-day high protein hypocaloric diet promotes cellular metabolic adaptations and attenuates lean mass loss in healthy males

Mitochondrial quantity and density are associated with increased oxidative metabolism. It has been demonstrated that a hypocaloric high fat/low carbohydrate (HF/LC) diet can up-regulate transcriptional markers of mitochondrial biogenesis; this was yet to be explored in vivo subsequent to a high protein/low carbohydrate (HP/LC) diet. Thus the aims of the study were to explore such diets on transcriptional markers or mitochondrial biogenesis, body composition and resting metabolic rate (RMR). Forty-five healthy male participants were randomly assigned one of four intervention diets: eucaloric high protein low carbohydrate (PRO-EM), hypocaloric high protein low carbohydrate (PRO-ER), eucaloric high carbohydrate (CHO-EM) or hypocaloric high carbohydrate (CHO-ER). The macronutrient ratio of the high protein diet and high carbohydrate diets was 40:30:30% and 10:60:30% (PRO:CHO:FAT) respectively. Energy intake for the hypocaloric diets were calculated to match resting metabolic rate. Participants visited the laboratory on 3 occasions each separated by 7 days. On each visit body composition, resting metabolic rate and a muscle biopsy from the vastus lateralis was collected. Prior to visit 1 and 2 habitual diet was consumed which was used as a control, between visit 2 and 3 the intervention diet was consumed continuously for 7-days. No group × time effect was observed, however in the PRO-ER group a significant increase in AMPK, PGC-1α, SIRT1 and SIRT3 mRNA expression was observed post diet intervention groups (p < 0.05). No change was observed in any of the transcriptional markers in the other 3 groups. Despite ∼30% reduction in calorie intake no difference in lean mass (LM) loss was observed between the PRO-ER and CHO-EM groups. The results from this study suggest that a 7-day a high protein low carbohydrate hypocaloric diet increased AMPK, SIRT1 and PGC-1 α mRNA expression at rest, and also suggest that increased dietary protein may attenuate LM mass loss in a hypocaloric stat

Math Anxiety in Fundamentals of Algebra Students

Thesis written by a student in the UNT Honors College discussing her experiences as a math tutor in math classes with traditionally high dropout rates. In addition, research into math anxiety is explored and evaluated

The public relations function in higher education

For too many decades, the function of public relations in higher education has been one of reaction rather than one of assertion. Regarded as merely a discretionary convenience for administrators to be used to combat poor images of the institution, or to extoll the V1rtues of its management, public relations was relegated to an innocuous post in the management construct. Contemporary crises in diminishing enrollments, financial shortfalls, identity losses and credibility gaps, have precipitated higher educational institutions to take a cue from business and industry and to consider exploiting the persuasive potentials of sound public relations programs. Becoming aware of social responsibility, higher education is beginning to recognize the fact that it owes the community in which it operates a profound obligation. It can no longer function under the archaic nineteenth century self-inflicted edict of "the public be damned." It is apparent that the public is its mainstay in society and it had better communicate with this constituent on a realistic basis. Institutional leadership and institutional identity have been challenged in recent years to the extent that many colleges and universities have been forced to introspectively analyze their positions. To combat these adversities, administrators are being forced to reevaluate the tools available to them. One such tool, public relations, this thesis maintains, offers an institution the channels for self-assertion through self-identity. The thesis also cites the history of educational public relations, the abuses to which the discipline has been subjected, and evolves an aggressive futuristic posture.California State University, Northridge. Department of Education.Includes bibliographical references (pages 131-132

Early responses of insulin signaling to high-carbohydrate and high-fat overfeeding

<p>Abstract</p> <p>Background</p> <p>Early molecular changes of nutritionally-induced insulin resistance are still enigmatic. It is also unclear if acute overnutrition alone can alter insulin signaling in humans or if the macronutrient composition of the diet can modulate such effects.</p> <p>Methods</p> <p>To investigate the molecular correlates of metabolic adaptation to either high-carbohydrate (HC) or high-fat (HF) overfeeding, we conducted overfeeding studies in 21 healthy lean (BMI < 25) individuals (10 women, 11 men), age 20-45, with normal glucose metabolism and no family history of diabetes. Subjects were studied first following a 5-day eucaloric (EC) diet (30% fat, 50% CHO, 20% protein) and then in a counter balanced manner after 5 days of 40% overfeeding of both a HC (20% fat, 60% CHO) diet and a HF (50% fat, 30% CHO) diet. At the end of each diet phase, <it>in vivo </it>insulin sensitivity was assessed using the hyperinsulinemic-euglycemic clamp technique. <it>Ex vivo </it>insulin action was measured from skeletal muscle tissue samples obtained 15 minutes after insulin infusion was initiated.</p> <p>Results</p> <p>Overall there was no change in whole-body insulin sensitivity as measured by glucose disposal rate (GDR, EC: 12.1 ± 4.7; HC: 10.9 ± 2.7; HF: 10.8 ± 3.4). Assessment of skeletal muscle insulin signaling demonstrated increased tyrosine phosphorylation of IRS-1 (p < 0.001) and increased IRS-1-associated phosphatidylinositol 3 (PI 3)-kinase activity (p < 0.001) following HC overfeeding. In contrast, HF overfeeding increased skeletal muscle serine phosophorylation of IRS-1 (p < 0.001) and increased total expression of p85α (P < 0.001).</p> <p>Conclusion</p> <p>We conclude that acute bouts of overnutrition lead to changes at the cellular level before whole-body insulin sensitivity is altered. On a signaling level, HC overfeeding resulted in changes compatible with increased insulin sensitivity. In contrast, molecular changes in HF overfeeding were compatible with a reduced insulin sensitivity.</p

Duffy antigen receptor for chemokines mediates chemokine endocytosis through a macropinocytosis-like process in endothelial cells

Background: The Duffy antigen receptor for chemokines (DARC) shows high affinity binding to multiple inflammatory CC and CXC chemokines and is expressed by erythrocytes and endothelial cells. Recent evidence suggests that endothelial DARC facilitates chemokine transcytosis to promote neutrophil recruitment. However, the mechanism of chemokine endocytosis by DARC remains unclear. Methodology/Principal Findings: We investigated the role of several endocytic pathways in DARC-mediated ligand internalization. Here we report that, although DARC co-localizes with caveolin-1 in endothelial cells, caveolin-1 is dispensable for DARC-mediated 125I-CXCL1 endocytosis as knockdown of caveolin-1 failed to inhibit ligand internalization. 125I-CXCL1 endocytosis by DARC was also independent of clathrin and flotillin-1 but required cholesterol and was, in part, inhibited by silencing Dynamin II expression. 125I-CXCL1 endocytosis was inhibited by amiloride, cytochalasin D, and the PKC inhibitor Gö6976 whereas Platelet Derived Growth Factor (PDGF) enhanced ligand internalization through DARC. The majority of DARC-ligand interactions occurred on the endothelial surface, with DARC identified along plasma membrane extensions with the appearance of ruffles, supporting the concept that DARC provides a high affinity scaffolding function for surface retention of chemokines on endothelial cells. Conclusions/Significance: These results show DARC-mediated chemokine endocytosis occurs through a macropinocytosis-like process in endothelial cells and caveolin-1 is dispensable for CXCL1 internalization. © 2011 Zhao et al