No description available.

No description available.

No description available.

No description available.

Information on the density of hydrocarbons at high pressures and temperatures is of great importance in many fields, such as the study of ultra-deep reservoirs up to ~240 MPa and 250°C. However, density data at such high pressures and temperatures are often not available in the literature. In this study, experimental densities are reported for n-pentane, n-octane, 2,2,4-trimethylpentane, cyclooctane, n-decane, and toluene to ~280 MPa and ~250°C. These experimental densities are in good agreement with available literature data, although the literature data for many of these fluids do not extend to the pressures and temperatures utilized in this study.

The purpose of the study was to examine the relationship and comparisons of athletic amenorrhea and bone mineral density in adolescent, cross-country runners. Subjects: Twenty-eight female adolescent cross-country runners (Mean Age + SD = 15.0 + 1.3 years); consisting of seventeen eumenorrheics & eleven amenorrheics. Design: The design consisted of a sixmonth longitudinal design in which the subjects were measured before and after cross-country season for height, weight, and lean tissue (LT), body fat (BF), bone mineral content (BMC), and bone mineral density (BMD) using whole-body scan densitiometry with a Lunar Dual-energy X-ray Absorptiometer (DXA). Run performance, weekly training volumes, menstrual dysfunction, menarchal age, nutritional information, and stress fractures were reported by the subjects. Statistical analyses consisted of Pearson product-moment and partial correlations to examine the associations of the variables, paired t-tests to measure seasonal body composition changes, multivariate analysis (MANOVA & MANCOVA) to investigate the subgroup differences of variables, and simple linear regression to determine the best body composition predictor variable for BMD. Results: The eumenorrheic subgroup's BMD was significantly greater than the amenorrheic subgroup's BMD (F(1, 54) = 16.22, p<.05, partial h² =.231). The eumenorrheic subgroup's bodyweight (F(1, 54) = 7.65, p<.05, partial h² =.124), BF (F(1, 54) = 8.56, p<.05, partial h² =.137), and BMC (F(1, 54) = 8.52, p<.05, partial h² =.136) were significantly greater than the amenorrheic subgroup. There was also a significant seasonal increase in BMD (t(27) = -4.01, p <.05) for the overall group. Bodyweight was the body composition component that best predicted BMD (F(1, 26) = 46.434, p<.05, R² =.641). There were no significant subgroup differences with respect to run performance, stress fractures, and nutritional supplementation. Conclusions: Athletic amenorrhea was highly associated with lower levels of BMD in adolescent, cross-country runners. Athletic amenorrhea was also highly associated with lower levels of bodyweight, BF, and BMC in adolescent cross-country runners. Finally, cross-country running was highly associated with increased BMD in adolescent athletes. Implications: The long-term implication of the study is that subjects with lower levels of BMD may be at a greater risk of osteoporosis. Recommendations: Educate and instruct runners to utilize proper training methods so the healthful benefits of crosscountry running, as well as improved performance, are obtained.

Noncovalent intermolecular interactions, widely found in molecular clusters and bio-molecules, play a key role in many important processes, such as phase changes, folding of proteins and molecular recognition. However, accurate calculation of interaction energies is a very difficult task because the interactions are normally very weak. Rigorous expressions for the electrostatic and polarization interaction energies between two molecules A and B, in term of the electronic densities, have been programmed: (see formula in document). Z is atomic charge, ρ0 is the electron density of the isolated molecule and Δρind is the electron density change of the molecule caused by polarization. With some approximations, procedures for electrostatic and polarization energy calculations were developed that involve numerical integration. Electrostatic and polarization energies for several bimolecular systems, some of which are hydrogen bonded, were calculated and the results were compared to other theoretical and experimental data. A second method for the computing of intermolecular interaction energies has also been developed. It involves a “supermolecule” calculation for the entire system, followed by a partitioning of the overall electric density into the two interacting components and then application of eq. (1) to find the interaction energy. In this approach, according to Feynman’s explanation to intermolecular interactions, all contributions are treated in a unified manner. The advantages of this method are that it avoids treating the supersystem and subsystems separately and no basis set superposition error (BSSE) correction is needed. Interaction energies for several hydrogen-bonded systems are calculated by this method. Compared with the result from experiment and high level ab initio calculation, the results are quite reliable.

Zellproliferation stellt einen integralen Bestandteil der Plaqueentstehung und somit der Atherosklerose dar. Zahlreiche Studien belegen, daß oxidativ verändertes LDL eine Schlüsselrolle in diesem Pathomechanismus spielt. Neben einer Reihe von proatherogenen Eigenschaften, vermag oxLDL die Zellzyklusregulation insbesondere über den Zyklinkinaseinhibitors p27kip1 zu beeinflussen. Als wichtigen Regulator der Zellproliferation wurde die kleine GTPase RhoA identifiziert. Vor diesem Hintergrund sollte in der vorliegenden Arbeit die oxLDL induzierte Expressionsminderung des Zyklinkinaseinhibitors p27kip1 sowie Zellproliferation über eine Aktivierung des RhoA/Rho-Kinase Signalwegs untersucht werden. Die Aktivierung von RhoA in HUVEC durch oxLDL sollte mittels immunhistochemischem Nachweisverfahren sichtbar gemacht werden. Weiterhin war interessant welche Rolle RhoA in der Signaltransduktion von oxLDL-Wirkungen spielt. Aus diesem Grund und um die Wirkung von RhoA analysieren zu können verwendeten wir die inaktive RhoA N19-Mutante und untersuchten sowohl die Auswirkung der RhoA-Hemmung auf die oxLDL induzierte Zellproliferation als auch auf die oxLDL induzierte p27kip1 Suppression. Zusätzlich sollten die Auswirkungen der Hemmung des nachgeschalteten Effektorproteins von RhoA nämlich Rho-Kinase mittels Y27632 auf die oxLDL-vermittelte Zellproliferation dargestellt werden. Es konnte gezeigt werden, daß oxLDL RhoA zu stimulieren vermag, indem die Translokation von RhoA aus dem Zytosol in die Plasmamembran, als Marker für die Aktivierung von RhoA nach oxLDL Stimulation sichtbar gemacht werden konnte. Die deutlichste Translokation von RhoA wurde nach 5 minütiger oxLDL Inkubation nachgewiesen. Die Hemmung der RhoA Aktivierung durch Transfektion einer dominant negativen RhoA N19 Mutante verdeutlichte, daß sowohl die oxLDL induzierte p27Kip1 Suppression in HUVEC als auch die oxLDL induzierte Proliferation auf die oxLDL vermittelte RhoA Aktivierung angewiesen sind. In Endothelzellen, welche nur mit dem Leervektor pcDNA3 transfiziert waren (Kontrolle), bestätigte sich nach einer vierstündigen oxLDL Inkubation wie in den früheren Untersuchungen eine signifikante Expressionsverminderung von p27Kip1 um ca. 66%. Im Gegensatz dazu konnte in Zellen, die mit der dominant-negativen RhoA N19 Mutante transfiziert waren keine p27Kip1 Suppression festgestellt werden. Ebenso zeigte sich in MTT-Assays bei Zellen mit der inaktiven RhoA N19 Mutante eine nahezu vollständig fehlende Proliferationsantwort. Im Anschluß daran, wurde in weiteren MTT-Assays die oxLDL induzierte Proliferation unter der Verwendung des Rho-Kinase Inhibitors Y27632 untersucht und eine signifikant reduzierte Proliferationsrate von 166 + 19 % im Vergleich zu Kontrollzellen 200 + 12 % nachgewiesen. Dieses Ergebnis könnte dadurch erklärt werden, daß neben dem nachgeschaltetem Effektorprotein Rho-Kinase, die Phosphatidylinositol 3-Kinase (PI3K) in der RhoA vermittelten p27Kip1 Suppression und Zellzyklusprogression eine zusätzliche Rolle zu spielen scheint. Zusammenfassend läßt sich sagen, daß sowohl die oxLDL induzierte Expressionsverminderung von p27Kip1 in HUVEC und somit die Zellprogression als auch die oxLDL induzierte Endothelproliferation auf die oxLDL vermittelte RhoA Aktivierung angewiesen ist. Diese Ergebnisse aus der vorliegenden Arbeit untermauern, daß der RhoA/Rho-Kinase Signalweg ein neuer therapeutischer bzw. medikamentöser Ansatz bei kardiovaskulären Erkrankungen sein könnte. / A typical feature of atherosclerotic plaques is increased cellular turnover, with the parallel existence of cell proliferation and cell death. Oxodized LDL plays a key role in its pathogenesis. Oxidized LDL induces proliferation in HUVEC. The influence of oxLDL on the cyclin-dependent kinase inhibitor p27Kip1, on the activity of small GTPase RhoA as a known regulator of p27Kip1, and on the resulting cell proliferation was studied. RhoA stimulation was assessed by means of its translocation from the cytosolic to the particulate fraction, an effect that is associated with RhoA activation. After oxLDL stimulation the translocation of RhoA to the cell membrane was visible after 1 min and peaked after 5 min of stimulation. We next investigated the influence of RhoA activation on oxLDL induced downregulation of p27Kip1 expression and proliferation. RhoA activity was inhibited in HUVEC by transfection with dominant inhibitory RhoA N19 mutant before stimulation with oxLDL. In cells that were transfected with dominant negative RhoA, the effect of oxLDL on p27Kip1 expression and on cellular proliferation was abolished. HUVEC that were preincubated with the Rho-kinase inhibitor Y27632 also showed a significantly decreased proliferative response to oxLDL stimulation. In summary, oxLDL induced cell-cycle progression via regulation of p27Kip1 expression, resulting in cellular proliferation, involving activation of RhoA. This results confirm, that the Rho/Rho signaling pathway could be a new target for the treatment of vascular disease.

Mahmood Ahmed. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1991. / Includes bibliographical references. / Title / Contents --- p.i-iii / Abstract --- p.2 / Introduction --- p.5 / Definitions : --- p.7 / Chapter - --- Bone --- p.7 / Chapter - --- Bone Cells --- p.9 / Chapter - --- Types of Bone & the Mineral Contents --- p.10 / Chapter - --- Composition of Bone Mass --- p.11 / Chapter - --- Bone Mass --- p.11 / Chapter - --- Factors Affecting The Bone Mass --- p.12 / Bone Minerals --- p.13 / Non Invasive Methods of Measurement of BMC : --- p.16 / Chapter - --- Radiograph --- p.16 / Chapter - --- Quantitative Morphometric --- p.16 / Chapter - --- Radiographic Photodensitometry --- p.16 / Chapter - --- Neutron Activation --- p.17 / Chapter - --- Quantitative Computed Tomography --- p.17 / Chapter - --- Bone Absorptiometery --- p.18 / Chapter - --- Transmission of Ultrasonics --- p.18 / Chapter - --- Dual Photon Absorptiometry --- p.19 / Chapter - --- Bone Scan --- p.19 / Chapter - --- Bone - Specific Biochemical Markers --- p.20 / Chapter - --- Summary --- p.20 / Effects of Drugs on Bone Mass: --- p.22 / Chapter - --- Alcohol --- p.22 / Chapter - --- Tetracycline --- p.22 / Chapter - --- Corticosteroid --- p.23 / Chapter - --- Antacids --- p.23 / Chapter - --- Estrogen --- p.24 / Chapter - --- Vitamins --- p.24 / Causes of Osteopenia in Children --- p.25 / Physical Activity and BMC --- p.28 / Bone Mineral Content - Reviews : --- p.30 / Chapter - --- In Neonates --- p.30 / Chapter - --- Normative Surveys in Children --- p.32 / Chapter - --- Skeletal Abnormalities --- p.35 / HK Chinese Children: / Chapter - --- A General View --- p.37 / Objectives of Study --- p.40 / Chapter - --- Determination of Normal Range --- p.40 / Chapter - --- Determination of Peak Bone Mass --- p.41 / Measurement of BMC : --- p.43 / Chapter - --- Material --- p.43 / Methods and Subjects --- p.46 / Chapter - --- Location of Scanning Site --- p.46 / Chapter - --- Recruitment of Subjects --- p.47 / Chapter - --- Statistical Analysis --- p.48 / Reproducibility of Measurement: --- p.56 / Chapter - --- The Means --- p.56 / Chapter - --- The Correlations --- p.57 / Results --- p.58 / Chapter - --- 6 months to 3 years --- p.58 / Chapter - --- 3 to 7 years --- p.60 / Chapter - --- 7 to 18 years --- p.61 / Chapter - --- 3 to 18 years --- p.62 / Chapter - --- Dual Energy X-Ray Absorptiometry versus Single Photon Absorptiometry --- p.66 / Graphs & Charts / Chapter - --- Age Distribution --- p.50 / Chapter - --- Dominance Distribution --- p.51 / Chapter - --- BMC from 0.6 to 2.9 years --- p.59 / Chapter - --- BMC Male & Female Difference --- p.63 / Chapter - --- BMC Dominance Difference --- p.64 / Chapter - --- BMC Predicted & Measured Value --- p.65 / Chapter - --- BMD by SPA vs DEXA --- p.67 / Discussions --- p.68 / Chapter - --- BMC & Total Body Calcium --- p.68 / Chapter - --- Age --- p.70 / Chapter - --- Handedness --- p.71 / Chapter - --- Bone Width --- p.72 / Chapter - --- Weight --- p.73 / Chapter - --- Sex --- p.73 / Chapter - --- Height --- p.74 / Chapter - --- "Nutritional Status, Calc. Intak" --- p.74 / Comparison --- p.75 / Chapter - --- BMC in Pathological Conditions --- p.75 / Chapter - --- Comparison with other series --- p.76 / Conclusion --- p.82 / Diagram --- p.45 / Chapter - --- Schematic Diagram of Equipment --- p.45 / Picture --- p.52 / Chapter - --- Single Photon Absorptiometry --- p.52 / Chapter - --- Dual Energy X-Ray Absorptiometry --- p.53 / Chapter - --- Single Photon Absorptiometry (Neonates) --- p.54 / Chapter - --- Photon Absorption Technique --- p.55 / Table --- p.78 / Chapter - --- Table I (Average yearly BMC & BMD) --- p.78 / Chapter - --- Table II(Average yearly Change in BMC) --- p.79 / Chapter - --- TableIII(BMC from 3 to 18 years) --- p.80 / Chapter - --- Table IV (Regression Analysis) --- p.81 / Appendix --- p.83 / Acknowledgements --- p.95 / References --- p.96-99

Understanding how energy flows through ecosystems reveals underlying ecological patterns that can drive processes such as growth and survival of organisms. To understand how energy is transferred through organisms, the energy content or energy density (ED) of both consumers and prey must be determined. To facilitate the ease of ED measurement across taxa, I developed a model to estimate the ED of organisms using percent ash-free dry weight (AFDW). Using data obtained from 11 studies with broad taxonomic, temporal and spatial coverage, I compared common predictors of ED using linear models. AFDW was determined to be the superior predictor of ED relative to previous metrics and was predictive for a broad range of taxonomic groups including aquatic invertebrates, aquatic vertebrates, aquatic plants and terrestrial invertebrates. This AFDW model enables measurement of ED with minimal cost and time investment, which allows ED to be more readily determined for diverse taxa. Next, I applied the AFDW method to the diet of a pelagic consumer, juvenile Chinook Salmon, to determine the effect of variable prey ED on growth. In 2017, I collected monthly zooplankton and fish samples of known importance in the diet of juvenile Chinook Salmon to look for fine-scale taxonomic, temporal and spatial differences in ED. Decapod zoeae and megalopae differed significantly from each other and showed family level variability in ED. Amphipods also showed significant species-level variability in ED. Temporal differences were observed, but did not reveal a consistent pattern among groups. Spatial variability was not significant. Using bioenergetics models, growth of juvenile Chinook Salmon was predicted to be greater when using fine-scale ED estimates. This difference was not substantial on average, but in some cases represented more than a two-fold difference in growth between coarse- and fine-scale estimates. These results suggest the need for higher resolution diet ED data when determining growth projections for juvenile Chinook Salmon. With the aid of the AFDW model presented in this thesis, the effort required to obtain these data is greatly reduced. / Graduate / 2020-03-25