943 resultados para Online interaction
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Research Services Librarian, JCU and Paula Callan, Scholarly communications Librarian, QUT. Presented 16 September via Blackboard Collaborate as part of the QULOC Research Support for Library Liaison webinar series. This work is licensed under a Creative Commons
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RecJ exonuclease plays crucial roles in several DNA repair and recombination pathways, and its ubiquity in bacterial species points to its ancient origin and vital cellular function. RecJ exonuclease from Haemophilus influenzae is a 575-amino-acid protein that harbors the characteristic motifs conserved among RecJ homologs. The purified protein exhibits a process 5'-3' single-stranded-DNA-specific exonuclease activity. The exonuclease activity of H. influenzae RecJ (HiRecJ) was supported by Mg2+ or Mn2+ and inhibited by Cd2+ suggesting a different mode of metal binding in HiRecJ as compared to Escherichia coli RecJ (EcoRecJ). Site-directed mutagenesis of highly conserved residues in HiRecJ abolished enzymatic activity. Interestingly, substitution of alanine for aspartate 77 resulted in a catalytically inactive enzyme that bound to DNA with a significantly higher affinity as compared to the wild-type enzyme. Noticeably, steady-state kinetic studies showed that H. influenzae single-stranded DNA-binding protein (HiSSB) increased the affinity of HiRecJ for single-stranded DNA and stimulated its exonuclease activity. HiSSB, whose C-terminal tail had been deleted, failed to enhance RecJ exonuclease activity. More importantly, HiRecJ was found to directly associate with its cognate single-stranded DNA-binding protein (SSB), as demonstrated by various in vitro assays, Interaction studies carried out with the truncated variants of HiRecJ and HiSSB revealed that the two proteins interact via the C-terminus of SSB protein and the core-catalytic domain of RecJ. Taken together, these results emphasize direct interactio between RecJ and SSB, which confers functional cooperativity to these two proteins. In addition, these results implicate SSB as being involved in the recruitment of RecJ to DNA and provide insights into the interplay between these proteins in repair and recombination pathways.
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In this paper we explore some of the ethical issues associated with conducting Ethnographic Action Research (Tacchi, 2004; Tacchi et al., 2003) for understanding and facilitating distributed collaboration. Ethnography and action research are increasingly popular qualitative approaches to researching computer-supported collaboration and we are applying them together in a project within a distributed research centre. We identify ethical principles applied to the conduct of research in Australia and we briefly describe a number of ethical problems that arise due to the nature of Ethnographic Action Research.
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Maintaining intersubjectivity is crucial for accomplishing coordinated social action. Although conversational repair is a recognised defence of intersubjectivity and routinely used to address ostensible sources of trouble in social interaction, it is less clear how people address more equivocal trouble. This study uses conversation analysis to examine preschool classroom interaction, focusing on practices used to identify and address such trouble. Repair is found to be a recurrent frontline practice for addressing equivocal trouble, occasioning space for further information that might enable identifying a specific trouble source. Where further information is forthcoming, a range of strategies are subsequently employed to address the trouble. Where this is not possible or does not succeed, a secondary option is to progress a broader activity-in-progress. This allows for the possibility of another opportunity to identify and address the trouble. Given misunderstandings can jeopardise interactants’ ability to mutually accomplish courses of action, these practices defend intersubjectivity against the threat of equivocal trouble.
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Pt ions-CeO2 interaction in Ce1-xPtxO2-delta (x=0.02) has been studied for the first time by electrochemical method combined with x-ray diffraction and x-ray photoelectron spectroscopy. Working electrodes made of CeO2 and Ce0.98Pt0.02O2-delta mixed with 30% carbon are treated electrochemically between 0.0-1.2 V in potentiostatic (chronoamperometry) and potentiodynamic (cyclic voltametry) mode with reference to saturated calomel electrode. Reversible oxidation of Pt-0 to Pt2+ and Pt4+ state due to the applied positive potential is coupled to simultaneous reversible reduction of Ce4+ to Ce3+ state. CeO2 reduces to CeO2-y (y=0.35) after applying 1.2 V, which is not reversible; Ce0.98Pt0.02O2-delta reaches a steady state with Pt2+:Pt4+ in the ratio of 0.60:0.40 and Ce4+:Ce3+ in the ratio of 0.55:0.45 giving a composition Ce0.98Pt0.02O1.74 at 1.2 V, which is reversible. Composition of Pt ion substituted compound is reversible between Ce0.98Pt0.02O1.95 to Ce0.98Pt0.02O1.74 within the potential range of 0.0-1.2 V. Thus, Ce0.98Pt0.02O2-delta forms a stable electrode for oxidation of H2O to O-2 unlike CeO2. A linear relation between oxidation of Pt2+ to Pt4+ with simultaneous reduction in Ce4+ to Ce3+ is observed demonstrating Pt-CeO2 metal support interaction is due to reversible Pt-0/Pt2+/Pt4+ interaction with Ce4+/Ce3+ redox couple.
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The nicotinic Acetylcholine Receptor (nAChR) is the major class of neurotransmitter receptors that is involved in many neurodegenerative conditions such as schizophrenia, Alzheimer's and Parkinson's diseases. The N-terminal region or Ligand Binding Domain (LBD) of nAChR is located at pre- and post-synaptic nervous system, which mediates synaptic transmission. nAChR acts as the drug target for agonist and competitive antagonist molecules that modulate signal transmission at the nerve terminals. Based on Acetylcholine Binding Protein (AChBP) from Lymnea stagnalis as the structural template, the homology modeling approach was carried out to build three dimensional model of the N-terminal region of human alpha(7)nAChR. This theoretical model is an assembly of five alpha(7) subunits with 5 fold axis symmetry, constituting a channel, with the binding picket present at the interface region of the subunits. alpha-netlrotoxin is a potent nAChR competitive antagonist that readily blocks the channel resulting in paralysis. The molecular interaction of alpha-Bungarotoxin, a long chain alpha-neurotoxin from (Bungarus multicinctus) and human alpha(7)nAChR seas studied. Agonists such as acetylcholine, nicotine, which are used in it diverse array of biological activities, such as enhancements of cognitive performances, were also docked with the theoretical model of human alpha(7)nAChR. These docked complexes were analyzed further for identifying the crucial residues involved i interaction. These results provide the details of interaction of agonists and competitive antagonists with three dimensional model of the N-terminal region of human alpha(7)nAChR and thereby point to the design of novel lead compounds.
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Spectroscopic study on the interactions of trace elements Co, Mn, Mg and Al with d(GCGTACGC) indicated the following: Al and Mg did not alter T-m values. Mn enhanced T-m at lower concentration and decreased it at higher concentrations. Interestingly Co at higher concentration elevated the T-m. These studies also showed lower concentrations of Mn displaced EtBr, whereas Al could displace it at higher ionic strength. Mg and Co displaced EtBr fluorescence at moderate concentrations. The binding constant values and CD spectra clearly indicated strong binding of these elements to DNA.
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Interaction of tetrathiafulvalene (TTF) and tetracyanoethylene (TCNE) with few-layer graphene samples prepared by the exfoliation of graphite oxide (EG), conversion of nanodiamond (DG) and arc-evaporation of graphite in hydrogen (HG) has been investigated by Raman spectroscopy to understand the role of the graphene surface. The position and full-width at half maximum of the Raman G-band are affected on interaction with TTF and TCNE and the effect is highest with EG and least with HG. The effect of TTF and TCNE on the 2D-band is also maximum with EG. The magnitude of interaction between the donor/acceptor molecules varies in the same order as the surface areas of the graphenes. (C) 2009 Published by Elsevier B. V.
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Rupture of atherosclerotic plaque is a major cause of mortality. Plaque stress analysis, based on patient-specific multisequence in vivo MRI, can provide critical information for the understanding of plaque rupture and could eventually lead to plaque rupture prediction. However, the direct link between stress and plaque rupture is not fully understood. In the present study, the plaque from a patient who recently experienced a transient ischaemic attack (TIA) was studied using a fluid-structure interaction method to quantify stress distribution in the plaque region based on in vivo MR images. The results showed that wall shear stress is generally low in the artery with a slight increase at the plaque throat owing to minor luminal narrowing. The oscillatory shear index is much higher in the proximal part of the plaque. Both local wall stress concentrations and the relative stress variation distribution during a cardiac cycle indicate that the actual plaque rupture site is collocated with the highest rupture risk region in the studied patient.
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Atherosclerotic plaque rupture has been extensively considered as the leading cause of death in western countries. It is believed that high stresses within plaque can be an important factor on triggering the rupture of the plaque. Stress analysis in the coronary and carotid arteries with plaque have been developed by many researchers from 2D to 3-D models, from structure analysis only to the Fluid-Structure Interaction (FSI) models[1].
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It has been well accepted that over 50% of cerebral ischemic events are the result of rupture of vulnerable carotid atheroma and subsequent thrombosis. Such strokes are potentially preventable by carotid interventions. Selection of patients for intervention is currently based on the severity of carotid luminal stenosis. It has been, however, widely accepted that luminal stenosis alone may not be an adequate predictor of risk. To evaluate the effects of degree of luminal stenosis and plaque morphology on plaque stability, we used a coupled nonlinear time-dependent model with flow-plaque interaction simulation to perform flow and stress/strain analysis for stenotic artery with a plaque. The Navier-Stokes equations in the Arbitrary Lagrangian-Eulerian (ALE) formulation were used as the governing equations for the fluid. The Ogden strain energy function was used for both the fibrous cap and the lipid pool. The plaque Principal stresses and flow conditions were calculated for every case when varying the fibrous cap thickness from 0.1 to 2mm and the degree of luminal stenosis from 10% to 90%. Severe stenosis led to high flow velocities and high shear stresses, but a low or even negative pressure at the throat of the stenosis. Higher degree of stenosis and thinner fibrous cap led to larger plaque stresses, and a 50% decrease of fibrous cap thickness resulted in a 200% increase of maximum stress. This model suggests that fibrous cap thickness is critically related to plaque vulnerability and that, even within presence of moderate stenosis, may play an important role in the future risk stratification of those patients when identified in vivo using high resolution MR imaging.
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Background and Purpose Acute cerebral ischemic events are associated with rupture of vulnerable carotid atheroma and subsequent thrombosis. Factors such as luminal stenosis and fibrous cap thickness have been thought to be important risk factors for plaque rupture. We used a flow-structure interaction model to simulate the interaction between blood flow and atheromatous plaque to evaluate the effect of the degree of luminal stenosis and fibrous cap thickness on plaque vulnerability. Methods A coupled nonlinear time-dependent model with a flow-plaque interaction simulation was used to perform flow and stress/strain analysis in a stenotic carotid artery model. The stress distribution within the plaque and the flow conditions within the vessel were calculated for every case when varying the fibrous cap thickness from 0.1 to 2 mm and the degree of luminal stenosis from 10% to 95%. A rupture stress of 300 kPa was chosen to indicate a high risk of plaque rupture. A 1-sample t test was used to compare plaque stresses with the rupture stress. Results High stress concentrations were found in the plaques in arteries with >70% degree of stenosis. Plaque stresses in arteries with 30% to 70% stenosis increased exponentially as fibrous cap thickness decreased. A decrease of fibrous cap thickness from 0.4 to 0.2 mm resulted in an increase of plaque stress from 141 to 409 kPa in a 40% degree stenotic artery. Conclusions There is an increase in plaque stress in arteries with a thin fibrous cap. The presence of a moderate carotid stenosis (30% to 70%) with a thin fibrous cap indicates a high risk for plaque rupture. Patients in the future may be risk stratified by measuring both fibrous cap thickness and luminal stenosis.
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Abstract is not available.