Large-scale molecular dynamics simulation of magnetic properties of amorphous iron under pressure

Author name used in this publication: C. H. Woo2006-2007 > Academic research: refereed > Publication in refereed journalVersion of RecordPublishe

Influence of regional-scale anthropogenic emissions on CO2 distributions over the western North Pacific

We report here airborne measurements of atmospheric CO2 over the western North Pacific during the March-April 2001 Transport and Chemical Evolution over the Pacific (TRACE-P) mission. The CO2 spatial distributions were notably influenced by cyclogenesis-triggered transport of regionally polluted continental air masses. Examination of the CO2 to C2H2/CO ratio indicated rapid outflow of combustion-related emissions in the free troposphere below 8 km. Although the highest CO2 mixing ratios were measured within the Pacific Rim region, enhancements were also observed further east over the open ocean at locations far removed from surface sources. Near the Asian continent, discrete plumes encountered within the planetary boundary layer contained up to 393 ppmv of CO2. Coincident enhancements in the mixing ratios of C2Cl4, C2H2, and C2H4 measured concurrently revealed combustion and industrial sources. To elucidate the source distributions of CO2, an emissions database for Asia was examined in conjunction with the chemistry and 5-day backward trajectories that revealed the WNW/W sector of northeast Asia was a major contributor to these pollution events. Comparisons of NOAA/CMDL and JMA surface data with measurements obtained aloft showed a strong latitudinal gradient that peaked between 35° and 40°N. We estimated a net CO2 flux from the Asian continent of approximately 13.93 Tg C day-1 for late winter/early spring with the majority of the export (79%) occurring in the lower free troposphere (2-8 km). The apportionment of the flux between anthropogenic and biospheric sources was estimated at 6.37 Tg C day-1 and 7.56 Tg C day-1, respectively

IL-15Rα chaperones IL-15 to stable dendritic cell membrane complexes that activate NK cells via trans presentation

Natural killer (NK) cells are innate immune effectors that mediate rapid responses to viral antigens. Interleukin (IL)-15 and its high affinity IL-15 receptor, IL-15Rα, support NK cell homeostasis in resting animals via a novel trans presentation mechanism. To better understand how IL-15 and IL-15Rα support NK cell activation during immune responses, we have used sensitive assays for detecting native IL-15 and IL-15Rα proteins and developed an assay for detecting complexes of these proteins. We find that IL-15 and IL-15Rα are preassembled in complexes within the endoplasmic reticulum/Golgi of stimulated dendritic cells (DCs) before being released from cells. IL-15Rα is required for IL-15 production by DCs, and IL-15 that emerges onto the cell surface of matured DCs does not bind to neighboring cells expressing IL-15Rα. We also find that soluble IL-15–IL-15Rα complexes are induced during inflammation, but membrane-bound IL-15–IL-15Rα complexes, rather than soluble complexes, support NK cell activation in vitro and in vivo. Finally, we provide in vivo evidence that expression of IL-15Rα specifically on DCs is critical for trans presenting IL-15 and activating NK cells. These studies define an unprecedented cytokine–receptor biosynthetic pathway in which IL-15Rα serves as a chaperone for IL-15, after which membrane-bound IL-15Rα–IL-15 complexes activate NK cells via direct cell–cell contact

Influence of hyperhomocysteinemia on the cellular redox state - Impact on homocysteine-induced endothelial dysfunction

Hyperhomocysteinemia is an independent risk factor for the development of atherosclerosis. An increasing body of evidence has implicated oxidative stress as being contributory to homocysteines deleterious effects on the vasculature. Elevated levels of homocysteine may lead to increased generation of superoxide by a biochemical mechanism involving nitric oxide synthase, and, to a lesser extent, by an increase in the chemical oxidation of homocysteine and other aminothiols in the circulation. The resultant increase in superoxide levels is further amplified by homocysteinedependent alterations in the function of cellular antioxidant enzymes such as cellular glutathione peroxidase or extracellular superoxide dismutase. One direct clinical consequence of elevated vascular superoxide levels is the inactivation of the vasorelaxant messenger nitric oxide, leading to endothelial dysfunction. Scavenging of superoxide anion by either superoxide dismutase or 4,5-dihydroxybenzene 1,3-disulfonate (Tiron) reverses endothelial dysfunction in hyperhomocysteinemic animal models and in isolated aortic rings incubated with homocysteine. Similarly, homocysteineinduced endothelial dysfunction is also reversed by increasing the concentration of the endogenous antioxidant glutathione or overexpressing cellular glutathione peroxidase in animal models of mild hyperhomocysteinemia. Taken together, these findings strongly suggest that the adverse vascular effects of homocysteine are at least partly mediated by oxidative inactivation of nitric oxide

Quality of Care for Older Patients with Non-Cancer Diagnoses under the End-of-Life Care Program

Background: End-of-life (EOL) care is an important part of geriatric medicine in view of rapidly ageing populations in the world. Aim: We aimed to evaluate the quality of care for older patients with non-cancer terminal illnesses, who died in 2010, under the EOL care program of an academic medical unit in Hong Kong. This unit consisted of an acute hospital, Prince of Wales Hospital (PWH) and a convalescence hospital (Shatin Hospital, SH). Methods: This was a retrospective hospital-based audit of clinical effectiveness of the EOL service. We reviewed the quality of patient care during the final seven days of life. The quality of care was evaluated based on the compliance rates of five selected goals and the adoption of futile life-sustaining procedures and treatments. Results: Case records of 129 patients in the EOL care program were analyzed. Two goals, including minimization of regular monitoring of vital signs and no blood taking, achieved over 70% compliance at SH and 0% at PWH. The compliance rates of discontinuation of non-essential medications were 46.4% in SH and 47.1% in PWH; and the compliance rates of switching essential medications to non-oral routes were 63.4% in SH and 70.6% in PWH (not statistically significant). The compliance rates of using as-required intravenous or subcutaneous medications were extremely low (<2%) at both hospitals. All futile life-sustaining procedures and treatments were initiated at the PWH. Conclusions: We demonstrated significant differences in the quality of EOL care between the acute hospital and convalescence hospital. Greater emphasis on specialist training and education with allocation of resources may improve the EOL care in both settings.published_or_final_versio

Parallel algorithm for spin and spin-lattice dynamics simulations

Author name used in this publication: C. H. Woo2008-2009 > Academic research: refereed > Publication in refereed journalVersion of RecordPublishe

Electronic structure of the electron-doped cuprate superconductors

Within the framework of the kinetic energy driven d-wave superconductivity, the electronic structure of the electron doped cuprate superconductors is studied. It is shown that although there is an electron-hole asymmetry in the phase diagram, the electronic structure of the electron-doped cuprates in the superconducting-state is similar to that in the hole-doped case. With increasing the electron doping, the spectral weight in the $(\pi,0)$ point increases, while the position of the superconducting quasiparticle peak is shifted towards the Fermi energy. In analogy to the hole-doped case, the superconducting quasiparticles around the $(\pi,0)$ point disperse very weakly with momentum.Comment: 8 pages, 3 figures, accepted for publication in Phys. Lett.