18,366 research outputs found

    A large eddy simulation turbulence model for estuary using spline correction

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    2006-2007 > Academic research: refereed > Publication in refereed journalVersion of RecordPublishe

    Electronic measurement and control of spin transport in Silicon

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    The electron spin lifetime and diffusion length are transport parameters that define the scale of coherence in spintronic devices and circuits. Since these parameters are many orders of magnitude larger in semiconductors than in metals, semiconductors could be the most suitable for spintronics. Thus far, spin transport has only been measured in direct-bandgap semiconductors or in combination with magnetic semiconductors, excluding a wide range of non-magnetic semiconductors with indirect bandgaps. Most notable in this group is silicon (Si), which (in addition to its market entrenchment in electronics) has long been predicted a superior semiconductor for spintronics with enhanced lifetime and diffusion length due to low spin-orbit scattering and lattice inversion symmetry. Despite its exciting promise, a demonstration of coherent spin transport in Si has remained elusive, because most experiments focused on magnetoresistive devices; these methods fail because of universal impedance mismatch obstacles, and are obscured by Lorentz magnetoresistance and Hall effects. Here we demonstrate conduction band spin transport across 10 microns undoped Si, by using spin-dependent ballistic hot-electron filtering through ferromagnetic thin films for both spin-injection and detection. Not based on magnetoresistance, the hot electron spin-injection and detection avoids impedance mismatch issues and prevents interference from parasitic effects. The clean collector current thus shows independent magnetic and electrical control of spin precession and confirms spin coherent drift in the conduction band of silicon.Comment: Single PDF file with 4 Figure

    Smoking cessation and carotid atherosclerosis: The guangzhou biobank cohort studydCVD

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    Introduction Smoking has been shown to be associated with carotid atherosclerosis in cross-sectional and prospective studies in Western populations. However, few studies have examined the reversal of risk resulting from quitting smoking, and the results are conflicting. Methods 959 men aged 50e85 years were randomly selected from phase III (2006e2007) of the Guangzhou Biobank Cohort Study into this cross-sectional study. Common carotid artery intima-media thickness (CCAIMT) was measured by B-mode ultrasonography, and carotid artery plaques were identified. Major cardiovascular risk factors, including fasting triglyceride, low-density and high-density lipoprotein (LDL and HDL) cholesterol and glucose, and systolic and diastolic blood pressure, were assessed. Results CCA-IMT and the number of carotid plaque increased from never to former to current smokers (both p≤0.001). Among former smokers compared to current smokers, after adjustment for cigarette pack-years and other potential confounders, the adjusted ORs (95% CI) for quitting for 1-9, 10-19 and 20+ years were 0.77 (0.47 to 1.26), 0.45 (0.26 to 0.79) and 0.37 (0.17 to 0.77) for the presence of CCA atherosclerosis, and 0.69 (0.43 to 1.12), 0.47 (0.27 to 0.82) and 0.45 (0.23 to 0.96) for the presence of carotid plaques, respectively. Longer duration of quitting smoking was also significantly associated with decreasing risk of the severity of CCA atherosclerosis and carotid plaques (all p≤0.001). Conclusion Smoking cessation was beneficial in attenuating the risk of carotid atherosclerosis associated with cigarette smoking. The short duration of cessation in earlier studies is a likely explanation for the inconsistent results.published_or_final_versio

    Evaluation of recreational health risk in coastal waters based on enterococcus densities and bathing patterns.

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    We constructed a simulation model to compute the incidences of highly credible gastrointestinal illness (HCGI) in recreational bathers at two intermittently contaminated beaches of Orange County, California. Assumptions regarding spatial and temporal bathing patterns were used to determine exposure levels over a 31-month study period. Illness rates were calculated by applying previously reported relationships between enterococcus density and HCGI risk to the exposure data. Peak enterococcus concentrations occurred in late winter and early spring, but model results showed that most HCGI cases occurred during summer, attributable to elevated number of exposures. Approximately 99% of the 95,010 illness cases occurred when beaches were open. Model runs were insensitive to 0-10% swimming activity assumed during beach closure days. Comparable illness rates resulted under clustered and uniform bather distribution scenarios. HCGI attack rates were within federal guidelines of tolerable risk when averaged over the study period. However, tolerable risk thresholds were exceeded for 27 total days and periods of at least 6 consecutive days. Illness estimates were sensitive to the functional form and magnitude of the enterococcus density-HCGI relationships. The results of this study contribute to an understanding of recreational health risk in coastal waters

    Informative noncompliance in endpoint trials

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    Noncompliance with study medications is an important issue in the design of endpoint clinical trials. Including noncompliant patient data in an intention-to-treat analysis could seriously decrease study power. Standard methods for calculating sample size account for noncompliance, but all assume that noncompliance is noninformative, i.e., that the risk of discontinuation is independent of the risk of experiencing a study endpoint. Using data from several published clinical trials (OPTIMAAL, LIFE, RENAAL, SOLVD-Prevention and SOLVD-Treatment), we demonstrate that this assumption is often untrue, and we discuss the effect of informative noncompliance on power and sample size

    Activation of Human Stearoyl-Coenzyme A Desaturase 1 Contributes to the Lipogenic Effect of PXR in HepG2 Cells

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    The pregnane X receptor (PXR) was previously known as a xenobiotic receptor. Several recent studies suggested that PXR also played an important role in lipid homeostasis but the underlying mechanism remains to be clearly defined. In this study, we found that rifampicin, an agonist of human PXR, induced lipid accumulation in HepG2 cells. Lipid analysis showed the total cholesterol level increased. However, the free cholesterol and triglyceride levels were not changed. Treatment of HepG2 cells with rifampicin induced the expression of the free fatty acid transporter CD36 and ABCG1, as well as several lipogenic enzymes, including stearoyl-CoA desaturase-1 (SCD1), long chain free fatty acid elongase (FAE), and lecithin-cholesterol acyltransferase (LCAT), while the expression of acyl:cholesterol acetyltransferase(ACAT1) was not affected. Moreover, in PXR over-expressing HepG2 cells (HepG2-PXR), the SCD1 expression was significantly higher than in HepG2-Vector cells, even in the absence of rifampicin. Down-regulation of PXR by shRNA abolished the rifampicin-induced SCD1 gene expression in HepG2 cells. Promoter analysis showed that the human SCD1 gene promoter is activated by PXR and a novel DR-7 type PXR response element (PXRE) response element was located at -338 bp of the SCD1 gene promoter. Taken together, these results indicated that PXR activation promoted lipid synthesis in HepG2 cells and SCD1 is a novel PXR target gene. © 2013 Zhang et al

    A Biomimetic Approach toward Enhancing Angiogenesis: Recombinantly Expressed Domain V of Human Perlecan Is a Bioactive Molecule That Promotes Angiogenesis and Vascularization of Implanted Biomaterials

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    Abstract Angiogenic therapy involving delivery of pro-angiogenic growth factors to stimulate new blood vessel formation in ischemic disease is promising but has seen limited clinical success due to issues associated with the need to deliver supra-physiological growth factor concentrations. Bio-inspired growth factor delivery utilizing the native growth factor signaling roles of the extracellular matrix proteoglycans has the potential to overcome many of the drawbacks of angiogenic therapy. In this study, the potential of the recombinantly expressed domain V (rDV) of human perlecan is investigated as a means of promoting growth factor signaling toward enhanced angiogenesis and vascularization of implanted biomaterials. rDV is found to promote angiogenesis in established in vitro and in vivo angiogenesis assays by potentiating endogenous growth factor signaling via its glycosaminoglycan chains. Further, rDV is found to potentiate fibroblast growth factor 2 (FGF2) signaling at low concentrations that in the absence of rDV are not biologically active. Finally, rDV immobilized on 3D porous silk fibroin biomaterials promotes enhanced vascular ingrowth and integration of the implanted scaffolds with the surrounding tissue. Together, these studies demonstrate the important role of this biologically active perlecan fragment and its potential in the treatment of ischemia in both native and bioengineered tissues
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