9,613 research outputs found

    Ab initio diffusional potential energy surface for CO chemisorption on Pd{110} at high coverage: Coupled translation and rotation

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    [[abstract]]The ground statepotential energy surface for CO chemisorption across Pd{110} has been calculated using density functional theory with gradient corrections at monolayer coverage. The most stable site corresponds well with the experimental adsorption heat, and it is found that the strength of binding to sites is in the following order: pseudo-short-bridge>atop>long-bridge>hollow. Pathways and transition states for CO surfacediffusion, involving a correlation between translation and orientation, are proposed and discussed.[[notice]]č£œę­£å®Œē•¢[[journaltype]]國外[[booktype]]ē“™ęœ¬[[countrycodes]]US

    Fast measurement of SEP for monitoring spinal cord during scoliosis

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    Recently there has been considerable interest in the use of somatosensory evoked potential (SEP) for monitoring the functional integrity of the spinal cord during surgery such as scoliosis. This paper describes a monitoring system and signal processing algorithms, which consist of an artificial neural network filter and a wavelet signal enhancer developed to enhance the signal-to-noise ratio (SNR) of surface recorded SEP. Our system allows fast detection of change in SEP's peak latency, amplitude and signal waveform, which are the main parameters of interest during intra-operative procedures.published_or_final_versionThe 20th IEEE Engineering in Medicine and Biology Society Conference Proceedings, Hong Kong, China, 29 October - 1 November 1998, v. 4, p. 2239-224

    Quantitative characterization of mesenchymal cell aggregation process

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    Poster presentation - Theme 3: Development & stem cellsMesenchymal cell aggregation (or named ā€˜condensationā€™ in developmental biology) is a fundamental phenomenon in a wide variety of physiological and pathological processes. Although the mechanisms of mesenchymal cell condensation in kidney, vertebrate and limb bud development are still not clear yet, scientists have found ways to create the mesenchymal cell aggregates in vitro for tissue engineering applications. Mesenchymal cell aggregation with proper size and timing is key to the efficiency of subsequent differentiation and generation of functional cells. Nevertheless, there is still little ā€¦postprin

    SMAD3 prevents binding of NKX2.1 and FOXA1 to the SpB promoter through its MH1 and MH2 domains

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    Mechanisms of gene repression by transforming growth factor-beta (TGF-beta) are not well understood. TGF-beta represses transcription of pulmonary surfactant protein-B gene in lung epithelial cells. Repression is mediated by SMAD3 through interactions with NKX2.1 and FOXA1, two key transcription factors that are positive regulators of SpB transcription. In this study, we found that SMAD3 interacts through its MAD domains, MH1 and MH2 with NKX2.1 and FOXA1 proteins. The sites of interaction on NKX2.1 are located within the NH2 and COOH domains, known to be involved in transactivation function. In comparison, weaker interaction of FOXA1 winged helix, and the NH2-terminal domains was documented with SMAD3. Both in vitro studies and in vivo ChIP assays show that interaction of SMAD3 MH1 and MH2 domains with NKX2.1 and FOXA1 results in reduced binding of NKX2.1 and FOXA1 to their cognate DNA-binding sites, and diminished promoter occupancy within the SpB promoter. Thus, these studies reveal for the first time a mechanism of TGF-beta-induced SpB gene repression that involves interactions between specific SMAD3 domains and the corresponding functional sites on NKX2.1 and FOXA1 transcription factors

    Effects of maleimide-polyethylene glycol-modified human hemoglobin (MP4) on tissue necrosis in SKH1-hr hairless mice

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    <p>Abstract</p> <p>Objective</p> <p>Tissue hypoxia after blood loss, replantation and flap reperfusion remains a challenging task in surgery. Normovolemic hemodilution improves hemorheologic properties without increasing oxygen carrying capacity. Red blood cell transfusion is the current standard of treatment with its attendant risks. The aim of this study was to investigate the potential of the chemically modified hemoglobin, MP4, to reduce skin flap necrosis and its effect on selected blood markers and kidneys.</p> <p>Materials and methods</p> <p>Tissue ischemia was induced in the ear of hairless mice (n = 26). Hemodilution was performed by replacing one third of blood volume with the similar amount of MP4, dextran, or blood. The extent of non-perfused tissue was assessed by intravital fluorescent microscopy.</p> <p>Results</p> <p>Of all groups, MP4 showed the smallest area of no perfusion (in percentage of the ear Ā± SEM: 16.3% Ā± 2.4), the control group the largest (22.4% Ā± 3.5). Leukocytes showed a significant increase in the MP4 and dextran group (from 8.7 to 13.6 respectively 15.4*10<sup>9</sup>/l). On histology no changes of the kidneys could be observed.</p> <p>Conclusion</p> <p>MP4 causes an increase of leukocytes, improves the oxygen supply of the tissue and shows no evidence of renal impairment.</p

    Network Defence Using Attacker-Defender Interaction Modelling

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    Network security is still lacking an efficient system which selects a response action based on observed security events and which is capable of running autonomously. The main reason for this is the lack of an effective defence strategy. In this Ph.D., we endeavour to create such a defence strategy. We propose to model the interaction between an attacker and a defender to comprehend how the attackerā€™s goals affect his actions and use the model as a basis for a more refined network defence strategy. We formulate the research questions that need to be answered and we discuss, how the answers to these questions relate to the proposed solution. This research is at the initial phase and will contribute to a Ph.D. thesis in four years

    Laser Cooling of Optically Trapped Molecules

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    Calcium monofluoride (CaF) molecules are loaded into an optical dipole trap (ODT) and subsequently laser cooled within the trap. Starting with magneto-optical trapping, we sub-Doppler cool CaF and then load 150(30)150(30) CaF molecules into an ODT. Enhanced loading by a factor of five is obtained when sub-Doppler cooling light and trapping light are on simultaneously. For trapped molecules, we directly observe efficient sub-Doppler cooling to a temperature of 60(5)60(5) Ī¼K\mu\text{K}. The trapped molecular density of 8(2)Ɨ1078(2)\times10^7 cmāˆ’3^{-3} is an order of magnitude greater than in the initial sub-Doppler cooled sample. The trap lifetime of 750(40) ms is dominated by background gas collisions.Comment: 5 pages, 5 figure

    Effects of cyclooxygenase-1 and -2 gene disruption on Helicobacter pylori-induced gastric inflammation

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    Background. Cyclooxygenases (COXs) play important roles in inflammation and carcinogenesis. The present study aimed to determine the effects of COX-1 and COX-2 gene disruption on Helicobacter pylori-induced gastric inflammation. Methods. Wild-type (WT), COX-1 and COX-2 heterozygous (COX-1 +/- and COX-2 +/-), and homozygous COX-deficient (COX-1 -/- and COX-2 -/-) mice were inoculated with H. pylori strain TN2 and killed after 24 weeks of infection. Uninfected WT and COX-deficient mice were used as controls. Levels of gastric mucosal inflammation, epithelial cell proliferation and apoptosis, and cytokine expression were determined. Results. COX deficiency facilitated H. pylori-induced gastritis. In the presence of H. pylori infection, apoptosis was increased in both WT and COX-deficient mice, whereas cell proliferation was increased in WT and COX-1-deficient, but not in COX-2-deficient, mice. Tumor necrosis factor (TNF)-Ī± and interleukin-10 mRNA expression was elevated in H. pylori-infected mice, but only TNF-Ī± mRNA expression was further increased by COX deficiency. Prostaglandin E 2 levels were increased in infected WT and COX-2-deficient mice but were at very low levels in infected COX-1-deficient mice. Leukotriene (LT) B 4 and LTC 4 levels were increased to a similar extent in infected WT and COX-deficient mice. Conclusions. COX deficiency enhances H. pylori-induced gastritis, probably via TNF-Ī± expression. COX-2, but not COX-1, deficiency suppresses H. pylori-induced cell proliferation. Ā© 2006 by the Infectious Diseases Society of America. All rights reserved.published_or_final_versio
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