Relevant bibliographies by topics / Activation barrier

Academic literature on the topic 'Activation barrier'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Activation barrier"

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Stepanov, A. V. "Activation process model: Einstein coefficients for activation barrier." Journal of Molecular Structure: THEOCHEM 805, no. 1-3 (March 2007): 87–90. http://dx.doi.org/10.1016/j.theochem.2006.10.021.

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Gessain, Grégoire, Yu-Huan Tsai, Laetitia Travier, Matteo Bonazzi, Solène Grayo, Pascale Cossart, Caroline Charlier, Olivier Disson, and Marc Lecuit. "PI3-kinase activation is critical for host barrier permissiveness to Listeria monocytogenes." Journal of Experimental Medicine 212, no. 2 (January 26, 2015): 165–83. http://dx.doi.org/10.1084/jem.20141406.

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Invasion of nonphagocytic cells, a critical property of Listeria monocytogenes (Lm) that enables it to cross host barriers, is mediated by the interaction of two bacterial surface proteins, InlA and InlB, with their respective receptors E-cadherin and c-Met. Although InlA–E-cadherin interaction is necessary and sufficient for Lm crossing of the intestinal barrier, both InlA and InlB are required for Lm crossing of the placental barrier. The mechanisms underlying these differences are unknown. Phosphoinositide 3-kinase (PI3-K) is involved in both InlA- and InlB-dependent pathways. Indeed, InlA-dependent entry requires PI3-K activity but does not activate it, whereas InlB–c-Met interaction activates PI3-K. We show that Lm intestinal target cells exhibit a constitutive PI3-K activity, rendering InlB dispensable for InlA-dependent Lm intestinal barrier crossing. In contrast, the placental barrier does not exhibit constitutive PI3-K activity, making InlB necessary for InlA-dependent Lm placental invasion. Here, we provide the molecular explanation for the respective contributions of InlA and InlB to Lm host barrier invasion, and reveal the critical role of InlB in rendering cells permissive to InlA-mediated invasion. This study shows that PI3-K activity is critical to host barrier permissiveness to microbes, and that pathogens exploit both similarities and differences of host barriers to disseminate.
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Bushuev, Mark B., Denis P. Pishchur, Elena B. Nikolaenkova, and Viktor P. Krivopalov. "Compensation effects and relation between the activation energy of spin transition and the hysteresis loop width for an iron(ii) complex." Physical Chemistry Chemical Physics 18, no. 25 (2016): 16690–99. http://dx.doi.org/10.1039/c6cp01892k.

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Wide thermal hysteresis loops for iron(ii) spin crossover complexes are associated with high activation barriers: the higher the activation barrier, the wider the hysteresis loop for a series of related spin crossover systems.
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Doering, Charles R., and Jonathan C. Gadoua. "Resonant activation over a fluctuating barrier." Physical Review Letters 69, no. 16 (October 19, 1992): 2318–21. http://dx.doi.org/10.1103/physrevlett.69.2318.

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de Jong, G. Theodoor, and F. Matthias Bickelhaupt. "Bond activation by group-11 transition-metal cations." Canadian Journal of Chemistry 87, no. 7 (July 2009): 806–17. http://dx.doi.org/10.1139/v09-009.

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We have computationally explored C–X bond activation by the group-11 transition-metal cations Cu+, Ag+, and Au+, and, for comparison, Pd, using relativistic density functional theory (DFT) at ZORA-BLYP/TZ2P. Oxidative insertion of the second-row transition-metal species Ag+ and Pd leads, for a given bond, to the highest overall reaction barriers. On the other hand, if we compare the different bonds oxidative insertion into the C–F bond is associated with (one of the) highest overall barriers whereas insertion into the C–Cl bond leads to the lowest overall barrier for any transition metal. The main trends in reactivity are rationalized using the activation strain model of chemical reactivity, which is an extension of the fragment approach to reaction profiles. In this model, the shape of the reaction profile ΔE(ζ) and the height of the overall reaction barrier ΔE≠ = ΔE(ζ=ζTS) are interpreted in terms of the strain energy ΔEstrain(ζ) associated with deforming the reactants along the reaction coordinate ζ plus the interaction energy ΔEint(ζ) between these deformed reactants: ΔE(ζ) = ΔEstrain(ζ) + ΔEint(ζ).
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Jiang, Heming, and Tian-Yu Sun. "The Activating Effect of Strong Acid for Pd-Catalyzed Directed C–H Activation by Concerted Metalation-Deprotonation Mechanism." Molecules 26, no. 13 (July 4, 2021): 4083. http://dx.doi.org/10.3390/molecules26134083.

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A computational study on the origin of the activating effect for Pd-catalyzed directed C–H activation by the concerted metalation-deprotonation (CMD) mechanism is conducted. DFT calculations indicate that strong acids can make Pd catalysts coordinate with directing groups (DGs) of the substrates more strongly and lower the C–H activation energy barrier. For the CMD mechanism, the electrophilicity of the Pd center and the basicity of the corresponding acid ligand for deprotonating the C–H bond are vital to the overall C–H activation energy barrier. Furthermore, this rule might disclose the role of some additives for C–H activation.
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Cheng, Chunyu, Yiming Zou, Jiahui Li, Amanda Jiamin Ong, Ronn Goei, Jingfeng Huang, Shuzhou Li, and Alfred Iing Yoong Tok. "Adsorption and Reaction Mechanisms of Direct Palladium Synthesis by ALD Using Pd(hfac)2 and Ozone on Si (100) Surface." Processes 9, no. 12 (December 13, 2021): 2246. http://dx.doi.org/10.3390/pr9122246.

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Palladium nanoparticles made by atomic layer deposition (ALD) normally involve formaldehyde or H2 as a reducing agent. Since formaldehyde is toxic and H2 is explosive, it is advantageous to remove this reducing step during the fabrication of palladium metal by ALD. In this work we have successfully used Pd(hfac)2 and ozone directly to prepare palladium nanoparticles, without the use of reducing or annealing agents. Density functional theory (DFT) was employed to explore the reaction mechanisms of palladium metal formation in this process. DFT results show that Pd(hfac)2 dissociatively chemisorbed to form Pd(hfac)* and hfac* on the Si (100) surface. Subsequently, an O atom of the ozone could cleave the C–C bond of Pd(hfac)* to form Pd* with a low activation barrier of 0.46 eV. An O atom of the ozone could also be inserted into the hfac* to form Pd(hfac-O)* with a lower activation barrier of 0.29 eV. With more ozone, the C–C bond of Pd(hfac-O)* could be broken to produce Pd* with an activation barrier of 0.42 eV. The ozone could also chemisorb on the Pd atom of Pd(hfac-O)* to form O3-Pd(hfac-O)*, which could separate into O-Pd(hfac-O)* with a high activation barrier of 0.83 eV. Besides, the activation barrier was 0.64 eV for Pd* that was directly oxidized to PdOx by ozone. Based on activation barriers from DFT calculations, it was possible to prepare palladium without reducing steps when ALD conditions were carefully controlled, especially the ozone parameters, as shown by our experimental results. The mechanisms of this approach could be used to prepare other noble metals by ALD without reducing/annealing agents.
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Winter, Michael C., Sandra S. Shasby, Dana R. Ries, and D. Michael Shasby. "PAR2 activation interrupts E-cadherin adhesion and compromises the airway epithelial barrier: protective effect of β-agonists." American Journal of Physiology-Lung Cellular and Molecular Physiology 291, no. 4 (October 2006): L628—L635. http://dx.doi.org/10.1152/ajplung.00046.2006.

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The airway epithelium is an important barrier between the environment and subepithelial tissues. The epithelium is also divided into functionally restricted apical and basolateral domains, and this restriction is dependent on the elements of the barrier. The protease-activated receptor-2 (PAR2) receptor is expressed in airway epithelium, and its activation initiates multiple effects including enhanced airway inflammation and reactivity. We hypothesized that activation of PAR2 would interrupt E-cadherin adhesion and compromise the airway epithelial barrier. The PAR2-activating peptide (PAR2-AP, SLIGRL) caused an immediate ∼50% decrease in the transepithelial resistance of primary human airway epithelium that persisted for 6–10 min. The decrease in resistance was accompanied by an increase in mannitol flux across the epithelium and occurred in cystic fibrosis transmembrane conductance receptor (CFTR) epithelium pretreated with amiloride to block Na and Cl conductances, confirming that the decrease in resistance represented an increase in paracellular conductance. In parallel experiments, activation of PAR2 interrupted the adhesion of E-cadherin-expressing L cells and of primary airway epithelial cells to an immobilized E-cadherin extracellular domain, confirming the hypothesis that activation of PAR2 interrupts E-cadherin adhesion. Selective interruption of E-cadherin adhesion with antibody to E-cadherin decreased the transepithelial resistance of primary airway epithelium by >80%. Pretreatment of airway epithelium or the E-cadherin-expressing L cells with the long-acting β-agonist salmeterol prevented PAR2 activation from interrupting E-cadherin adhesion and compromising the airway epithelial barrier. Activation of PAR2 interrupts E-cadherin adhesion and compromises the airway epithelial barrier.
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Stavenuiter, Fabian, and Laurent O. Mosnier. "Non-Canonical PAR3 Activation Induces Tie2-Dependent Endothelial Barrier Protective Effects." Blood 124, no. 21 (December 6, 2014): 2802. http://dx.doi.org/10.1182/blood.v124.21.2802.2802.

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Abstract Introduction: Endothelial barrier protective effects of activated protein C (APC) require the endothelial protein C receptor (EPCR), protease activated receptor 1 (PAR1), and PAR3. In contrast, PAR1 and PAR3 activation by thrombin results in barrier disruption. Non-canonical PAR1 and PAR3 activation by APC versus canonical activation by thrombin provide an explanation for the functional selectivity of these proteases. APC induces non-canonical PAR3 activation at Arg41 and synthetic peptides representing the tethered-ligand sequence of PAR3 after non-canonical cleavage (P3R) induce barrier protective effects in vitro and vascular integrity in vivo. However, signaling mechanisms employed by PAR3 remain undefined. To obtain better insights into the relation between coagulation proteases with endothelial barrier protective effects and canonical/non-canonical PAR1 and PAR3 activation, the PAR proteolysis analysis was extended to factor Xa (FXa). Similar to APC, FXa-mediates endothelial barrier protective effects that involve both PAR1 and EPCR. To date, however, no role for PAR3 in FXa-induced barrier integrity has been implicated. Results: In the presence of EPCR, FXa cleaved PAR1 at Arg41 similar to thrombin and not at Arg46 alike APC, whereas FXa cleaved PAR3 at the non-canonical Arg41 similar to APC but not at the canonical Lys38 corresponding to cleavage by thrombin. Surprisingly, changes in electric cell-substrate impedance sensing (ECIS) using the iCelligence system showed FXa induced an immediate drop in endothelial cell index (~60%) comparable to that induced by thrombin, indicating that FXa induced a loss of cell barrier function. Notwithstanding, after incubation of endothelial cells with FXa for 3 hours, FXa protected (~40%) against TRAP-induced loss of barrier function, similar to that induced by APC, confirming barrier protective effects of FXa. PAR1 blocking antibodies prevented the early FXa-mediated loss of barrier function, indicating that PAR1 cleavage at Arg41 was responsible for this.In contrast,a combinationofPAR1 and PAR2 blocking antibodies was needed to inhibit late (3h) FXa-mediated barrier protection. Blocking antibodies against PAR3 confirmed that canonical PAR3 activation enhanced PAR1-mediated barrier disruptive effects of thrombin (~15%). PAR3 blocking antibodies also significantly reduced the barrier protective effect of FXa (~15%), indicating a functional role for non-canonical PAR3 activation by FXa. Neither canonical (P3K) nor non-canonical (P3R) PAR3 tethered-ligand peptides directly induced significant phosphorylation of ERK1/2 or Akt in endothelial cells. The P3K however, but not the P3R peptide, enhanced TRAP induced ERK1/2 phosphorylation. No Akt phosphorylation was observed in endothelial cells treated with TRAP in the presence of either P3K or P3R. Interestingly, both APC and FXa but not thrombin induced prolonged activation of the endothelial cell specific Tie2 receptor, determined by phosphorylation of Y992 and S1119. Tie2 activation by FXa required PAR3 and EPCR with a partial contribution of PAR1 and PAR2. P3R induced potent activation of Tie2 achieving maximal activation at ~0.8 µM P3R, whereas P3K failed to do so. Additionally, neither (non-)canonical PAR1 nor PAR2 tethered-ligand peptides induced activation of Tie2. Activation of Tie2 by P3R was relatively fast and reached half-maximal activation in about 5 minutes. Blocking antibodies against Tie2 reduced FXa-mediated barrier protective effects by approximately 34%, whereas inhibition of Tie2 did not affect thrombin mediated barrier disruption. Immunohistochemistry indicated that Tie2 activation by FXa and P3R resulted in clustering of activated Tie2 at the cell borders. Accordingly, Tie2 activation by FXa and P3R resulted in changes in the cellular distribution of the tight-junction-associated protein zona occludens (ZO-1) in time. Conclusion: Here we identified a novel pathway for Tie2 activation by non-canonical PAR3 activation that promoted tight-junction formation and endothelial barrier protective effects. In contrast, canonical activation of PAR3 enhanced PAR1-mediated barrier disruptive effects by thrombin. These results exemplify the novel dimensions that non-canonical activation of PARs provides for the possible molecular mechanisms that are responsible for the functional selectivity of protease signaling. Disclosures No relevant conflicts of interest to declare.
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Carpenter, Chris. "Using Shale as a Barrier Simplifies Well Abandonment." Journal of Petroleum Technology 73, no. 01 (January 1, 2021): 62–63. http://dx.doi.org/10.2118/0121-0062-jpt.

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This article, written by JPT Technology Editor Chris Carpenter, contains highlights of paper SPE 199654, “Simplifying Well Abandonments Using Shale as a Barrier,” by Eric van Oort, SPE, and Maria Juenger, The University of Texas at Austin, and Munir Aldin, SPE, Metarock Laboratories, et al., prepared for the 2020 IADC/SPE International Drilling Conference and Exhibition, Galveston, Texas, 3-5 March. The paper has not been peer reviewed. The complete paper presents the results of an investigation into the creep behavior of North Sea shales and their ability to form effective annular barriers. The large-scale laboratory results show that Lark-Horda shales will form competent low-permeability annular barriers when left uncemented, as confirmed using pressure-pulse-decay measurements. Experimental conditions were found to influence the rate of barrier formation. Higher effective stress, higher temperature, and beneficial manipulation of annular fluid chemistry all have a significant effect. Introduction An alternative to traditional plug-and-abandonment techniques presented it-self more than a decade ago, with observations that formations such as mobile salts and shales could creep into uncemented annular spaces and form competent annular barriers that could be identified on sonic and ultrasonic bond logs and verified using pressure testing. Shale particularly has the necessary characteristics that several guidelines require of a good barrier, being largely impermeable, nonshrinking, ductile, and resistant to chemicals and substances, all of which help provide long-term integrity. Shales that appeared to be particularly well-suited to beneficial annular creep behavior were characterized by low strength and high ductility, high clay content with relatively high smectite content, low levels of quartz and carbonate cementation, relatively high porosity and low compressional wave velocity, and a tendency to yield wellbore instability problems while being drilled. Mechanisms other than creep were considered for the annular blockage behavior observed, but the mounting body of evidence indicates that the predominant mechanism is indeed creep (i.e., the viscoplastic behavior of argillaceous rocks). In the laboratory and field work published to date, stimulation of shale barriers through accelerated creep by pressure and temperature manipulation has received the most attention. The authors investigate barrier activation not only by temperature and pressure activation but also by chemical activation, because it offers practical advantages and reduces risks associated with temperature and pressure activation. Temperature has a significant effect on the viscoplastic behavior of shale, but heating a long shale section (with a minimum barrier length of 50 m) through casing with an effective downhole heater presents considerable practical challenges. Pressure reduction in the annulus through reduction of the hydrostatic head in the wellbore brings with it well-control concerns, particularly when no functional annular barrier is in place. By contrast, circulating a chemical solution in place in an annular space through casing perforations with a workstring and packer arrangement is relatively straightforward and is routine when practicing the perforate, wash, and cement technique in the field.
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Dissertations / Theses on the topic "Activation barrier"

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Pesic, Marija. "Visualizing T cell activation around the blood-brain barrier Dissertation." Diss., Ludwig-Maximilians-Universität München, 2013. http://nbn-resolving.de/urn:nbn:de:bvb:19-159898.

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T cells recognizing myelin auto-antigens penetrate into the CNS to induce inflammatory autoimmune disease following complex sequential interactions with individual components of the vascular blood-brain barrier (BBB), particularly endothelial cells, and perivascular phagocytes. To determine the functional consequences of these processes, two-photon intravital imaging was performed to compare the behavior of three myelin-specific GFP-expressing T cell lines with different potentials for transferring Experimental Autoimmune Encephalomyelitis. Imaging documented that, irrespective of their pathogenic potential, all T cell lines reached the CNS and interacted with vascular endothelial cells indistinguishably, crawling on the luminal surface, preferably against blood flow, before crossing the vessel wall. In striking contrast, after extravasation the T cell motility and their interactions with perivascular antigen presenting cells (APCs) varied dramatically. While highly encephalitogenic T cells showed a low motility, made stable contacts with local APCs and became activated, the corresponding contacts of weakly encephalitogenic T cells remained short, their motility high and their activation marginal. Supplying auto-antigen, via either local injection or by transfer of antigen-pulsed meningeal APCs, lowered their motility and prolonged the contact duration of weakly encephalitogenic T cells to values characteristic for highly pathogenic ones. Only after exogenous antigen supply, the weakly encephalitogenic T cells became activated, infiltrated the CNS parenchyma, and triggered clinical EAE, suggesting that the strength of the antigen-dependent signals received by immigrating effector T cells from leptomeningeal APCs is crucial for their pathogenic effect within the target tissue. To directly correlate the activation of encephalitogenic T cells with their dynamic behavior in the CNS, a truncated fluorescent derivative of nuclear factor of activated T cells (NFAT) was introduced as a real-time activation indicator. Two-photon imaging documented the activation of the auto-reactive T cells extravasated into the perivascular space, but not within the vascular lumen. Activation correlated with reduced T cell motility, and it was related to contacts with the local APCs. However, it did not necessarily lead to a long-lasting arrest, as individual, activated T cells SUMMARY 2 were able to sequentially contact other APCs. A spontaneous cytosol-nuclear translocation of the marker was noted only in T cells with a high pathogenic potential. The translocation implied the presentation of an auto-antigen, as the weakly pathogenic T cells, which remained silent in the untreated hosts, were activated upon the instillation of exogenous auto-antigen. It is proposed here that the presentation of local auto-antigen by BBB-associated APCs provides stimuli that guide autoimmune T cells to the CNS destination and enable them to attack the target tissue. In addition, a theoretical, physicist approach was used for modeling T cell activation in the leptomeningeal space. Assuming that T cells have evolved to gain their activation signal in a way that is energetically optimal for them, two possible scenarios for T cell activation were compared. The first one assumes that, after finding an APC presenting the epitope of interest, the T cell will stop and interact with the APC until it becomes fully activated. The second model considers the possibility that a T cell can accumulate activation signals from different APCs while scanning them without stopping, until a certain threshold is exceeded and the T cell becomes activated. Using this approach, it is proposed that the T cells in EAE are more likely to become activated following the first scenario. However, in a more natural environment such as a lymph node, the second scenario could give them some advantages
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Hussain, Imran [Verfasser]. "Insulin modulates the recovery of endothelial barrier function via Rac1 activation / Imran Hussain." Gießen : Universitätsbibliothek, 2016. http://d-nb.info/1112909990/34.

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Schwaiger, Christine S. "Voltage sensor activation and modulation in ion channels." Doctoral thesis, KTH, Beräkningsbiofysik, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-104742.

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Voltage-gated ion channels play fundamental roles in neural excitability, they are for instance responsible for every single heart beat in our bodies, and dysfunctional channels cause disease that can be even lethal. Understanding how the voltage sensor of these channels function is critical for drug design of compounds targeting neuronal excitability. The opening and closing of the pore in voltage-gated potassium (Kv) channels is caused by the arginine-rich S4 helix of the voltage sensor domain (VSD) moving in response to an external potential. In fact, VSDs are remarkably efficient at turning membrane potential into conformational changes, which likely makes them the smallest existing biological engines. Exactly how this is accomplished is not yet fully known and an area of hot debate, especially due to the lack of structures of the resting and intermediate states along the activation pathway. In this thesis I study how the VSD activation works and show how toxic compounds modulate channel gating through direct interaction with these quite unexplored drug targets. First, I show that a secondary structure transition from alpha- to 3(10)-helix in the S4 helix is an important part of the gating as this helix type is significantly more favorable compared to the -helix in terms of a lower free energy barrier. Second, I present new models for intermediate states along the whole voltage sensor cycle from closed to open and suggest a new gating model for S4, where it moves as a sliding 3(10)-helix. Interestingly, this 3(10)-helix is formed in the region of the single most conserved residue in Kv channels, the phenylalanine F233. Located in the hydrophobic core, it directly faces S4 and creates a structural barrier for the gating charges. Substituting this residue alters the deactivation free energy barrier and can either facilitate the relaxation of the voltage sensor or increase the free energy barrier, depending on the size of the mutant. These results are confirmed by new experimental data that supports that a rigid ring at the phenylalanine position is the rate-limiting factor for the deactivation gating process, while the activation is unaffected. Finally, we study how the activation can be modulated for pharmaceutical reasons. Neurotoxins such as hanatoxin and stromatoxin push S3b towards S4 helix limiting S4's flexibility. This makes it harder for the VSD to activate and might explain the stronger binding affinities in resting state. All these results are highly important both for the general topic of biological macromolecules undergoing functionally critical conformational transitions, as well as the particular case of voltage-gated ion channels where understanding of the gating process is probably the key step to explain the effects of mutations or drug interactions.

QC 20121115

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Pan, Yongping. "Characterization of Low Barrier Hydrogen Bonds in Enzyme Catalysis: an Ab Initio and DFT Investigation." Thesis, University of North Texas, 1999. https://digital.library.unt.edu/ark:/67531/metadc278586/.

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Hartree-Fock, Moller-Plesset, and density functional theory calculations have been carried out using 6-31+G(d), 6-31+G(d,p) and 6-31++G(d,p) basis sets to study the properties of low-barrier or short-strong hydrogen bonds (SSHB) and their potential role in enzyme-catalyzed reactions that involve proton abstraction from a weak carbon-acid by a weak base. Formic acid/formate anion, enol/enolate and other complexes have been chosen to simulate a SSHB system. These complexes have been calculated to form very short, very short hydrogen bonds with a very low barrier for proton transfer from the donor to the acceptor. Two important environmental factors including small amount of solvent molecules that could possibly exist at the active site of an enzyme and the polarity around the active site were simulated to study their energetic and geometrical influences to a SSHB. It was found that microsolvation that improves the matching of pK as of the hydrogen bond donor and acceptor involved in the SSHB will always increase the interaction of the hydrogen bond; microsolvation that disrupts the matching of pKas, on the other hand, will lead to a weaker SSHB. Polarity surrounding the SSHB, simulated by SCRF-SCIPCM model, can significantly reduce the strength and stability of a SSHB. The residual strength of a SSHB is about 10--11 kcal/mol that is still significantly stable compared with a traditional weak hydrogen bond that is only about 3--5 kcal/mol in any cases. These results indicate that SSHB can exist under polar environment. Possible reaction intermediates and transition states for the reaction catalyzed by ketosteroid isomerase were simulated to study the stabilizing effect of a SSHB on intermediates and transition states. It was found that at least one SSHB is formed in each of the simulated intermediate-catalyst complexes, strongly supporting the LBHB mechanism proposed by Cleland and Kreevoy. Computational results on the activation energy for catalyzed and uncatalyzed model reactions shows that strong hydrogen bonding between catalyst and the substrate at the transition state can significantly reduce the activation energy. This implies that LBHBs are possibly playing a crucial role in enzyme catalysis by supplying significant stabilizing energy to the reaction transition state.
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Pesic, Marija [Verfasser], and Mark [Akademischer Betreuer] Hübener. "Visualizing T cell activation around the blood-brain barrier Dissertation / Marija Pesic. Betreuer: Mark Hübener." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2013. http://d-nb.info/1038152488/34.

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Priori, Davide <1976&gt. "Diet Effects on Activation and Maturation of Feed Control over the Gastrointestinal Defence Barrier in Piglets." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2012. http://amsdottorato.unibo.it/4764/.

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Weaning is an important and complex step involving many stresses that interfere deeply with feed intake, gastro-intestinal tract (GIT) development and adaptation to the weaning diet in young pigs. The health of the pig at weaning, its nutrition in the immediate post-weaning period, and the physical, microbiological and psychological environment are all factors that interact to determine food intake and subsequent growth. GIT disorders, infections and diarrhoea increase at the time of weaning, in fact pathogens such as enterotoxigenic Escherichia coli (ETEC) are major causes of mucosal damage in post-weaning disease contributing to diarrhoea in suckling and post-weaned pigs. The European ban in 2006 put on antibiotic growth promoters (AGP) has stimulated research on the mechanisms of GIT disorders and on nutritional approaches for preventing or reducing such disturbances avoiding AGPs. Concerning these aspects here are presented five studies based on the interplay among nutrition, genomic, immunity and physiology with the aim to clarify some of these problematic issues around weaning period in piglets. The first three evaluate the effects of diets threonine or tryptophan enriched on gut defence and health as possible alternatives to AGP in the gut. The fourth is focused on the possible immunological function related with the development of the stomach. The fifth is a pilot study on the gastric sensing and orexygenic signal given by fasting or re-feeding conditions. Although some results are controversial, it appears that both tryptophan and threonine supplementation in weaning diets have a preventive role in E.coli PWD and favorable effects in the gut especially in relation to ETEC susceptible genotype. While the stomach is believed as almost aseptic organ, it shows an immune activity related with the mucosal maturation. Moreover it shows an orexygenic role of both oxyntic mucosa and pyloric mucosa, and its possible relation with nutrient sensing stimuli.
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Riaz, Muhammad Assad [Verfasser]. "Activation of AMP-activated kinase at reperfusion protects the endothelial barrier against reperfusion-induced failure / Muhammad Assad Riaz." Gießen : Universitätsbibliothek, 2012. http://d-nb.info/1069065315/34.

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Mohd, Nasir Mohd Hamzah. "Activation of endothelial cells and its potential involvement in blood-brain barrier damage in cerebral malaria : an in vitro study." Thesis, Keele University, 2015. http://eprints.keele.ac.uk/3252/.

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One of the severe complications of a Plasmodium falciparum infection is cerebral malaria (CM). CM is characterised by the accumulation of mature infected red blood cells (RBC) in the brain microvasculature. One of the consistent detrimental effects of sequestration is the breakdown of the blood-brain barrier (BBB), often with a fatal outcome in children in endemic areas. This study investigates the mechanisms underlying BBB breakdown secondary to sequestration, using immortalised human brain microvascular endothelial cells (tHBEC) as an in-vitro model of BBB and ITG-strain Plasmodium falciparum. First, the tHBEC monolayer was co-cultured with Plasmodium falciparum infected red blood cell (PRBC) or uninfected red blood cells (uRBC) control for 20 hours and the supernatant was recovered for subsequent analysis. The co-culture supernatants showed upregulation of inflammatory mediators (MCP-1 and IL-8) and a member of metalloproteases (ADAMTS-1, ADAMTS-4, MMP-2 and MMP-9) in the PRBC-tHBEC co-culture supernatants. The PRBC-tHBEC co-culture supernatants induced loss of endothelial cell monolayer integrity, represented by real time reduction in the transendothelial electrical resistance, measured using Electrical Cell-Substrate Impedance Sensing (ECIS™). The same supernatants also increased the permeability of tHBEC monolayer to the fluorescently labelled 40 kDa dextran showing leakage across the tHBEC monolayer. Interestingly, the loss of barrier function of tHBEC monolayer is partially inhibited by the addition of protease inhibitors GM6001 and rhTIMP-3. Prolonged exposure to PRBC-tHBEC co-culture supernatants reduced the level of vinculin. This study demonstrates that the interactions between PRBC and tHBEC induces activation of tHBEC and the release of proteases that contribute to BBB breakdown in CM, and could be a potential drug target for adjunct therapy in CM.
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Chaves, Catarina Alexandra da Silva. "Mechanisms of regulation of P-glycoprotein and breast cancer resistance protein at the blood-brain barrier : focus on the role of morphine, and P-glycoprotein activation." Thesis, Sorbonne Paris Cité, 2015. http://www.theses.fr/2015USPCB162/document.

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La barrière hémato-encéphalique (BHE) représente la principale interface d'échange moléculaire entre la circulation sanguine et le système nerveux central (SNC), où elle joue un rôle essentiel sur le contrôle du passage bidirectionnel de composés endogènes et exogènes. À la BHE, la P-glycoprotéine (P-gp) et Breast Cancer Resistance Protein (BCRP) sont les transporteurs d’efflux ABC les plus importants, empêchant l'entrée de composés toxiques, des médicaments et des xénobiotiques circulant dans le sang dans le cerveau. Il y a un intérêt croissant pour la compréhension des mécanismes moléculaires sous-jacents à la modulation de l’expression et de la fonction de la P-gp et BCRP, afin de pouvoir contrôler l'accumulation de substances neurotoxiques dans le SNC et de surmonter les phénomènes de pharmaco-résistance. Des études récentes ont montré que la morphine, elle-même un substrat de la P-gp, est impliquée dans l’augmentation de l'expression de la P-gp, qui peuvent contribuer à sa faible pénétration dans le cerveau et pour le développement de la tolérance. Cependant, le mécanisme sous-jacent à l’induction de la P-gp par la morphine, bien comme son rôle sur l'expression de BCRP était inconnu. Des rats ont été utilisés comme modèle animal pour l'étude de l'amplitude et la cinétique de la modulation de la P-gp et Bcrp à la BHE, après un traitement morphinique subchronique, en utilisant un protocole d’escalade de doses. Des microvaisseaux cérébraux isolés ont été utilisés comme modèle pour étudier la BHE, et les contenus en P-gp et Bcrp après le traitement in vivo, tandis que la lignée cellulaire hCMEC/D3 a parfois été utilisé pour des études complémentaires. Nos résultats ont montré qu’un régime subchronique de traitement à la morphine pendant 5 jours a induit la P-gp et Bcrp 12 à 24 heures après la dernière dose de morphine, un effet qui n'a pas été enregistrée lors des précédentes temps de sacrifices des animaux, ni avec une traitement aigue à la morphine. Le traitement des animaux avec un antagoniste de du récepteur glutamatergique NMDA, ou avec un inhibiteur de la COX-2 a aboli l’induction protéique de la P-gp et Bcrp par la morphine-subchronique, ce qui suggère que les deux facteurs sont impliqués dans l’up-régulation morphine-dépendante de la P-gp et BCRP. Sachant que l’induction a été enregistrée seulement à partir de 12h après la dernière dose de morphine, nous avons examiné si elle était un effet direct de l'exposition continue à la morphine, ou plutôt une conséquence du sevrage à la morphine développé après l'arrêt du traitement. Les rats ont été traités soit avec une perfusion constante de morphine (5 jours), soit avec deux schémas chroniques de morphine lorsque le sevrage a été précipité par l'administration de naloxone: un régime de doses croissantes (5 jours) ou un régime de doses constantes de morphine. La perfusion en continue de morphine n'a pas changé les niveaux de P-gp et Bcrp dans les microvaisseaux cérébraux de rat, et du coup n'a pas une conséquence directe sur la cascade de régulation de ces transporteurs à la BHE. Le sevrage provoqué par la naloxone a augmenté les niveaux d’ARNm pour le Mdr1a et Bcrp, mais l'expression et de l'activité protéiques sont restées inchangées après l'administration de naloxone. Cette disparité peut être dû soit à un effet de la régulation post-traductionnelle, soit à l’action de la naloxone dans des récepteurs non-opioïdes, qui peut entraver l’induction de la P-gp et Bcrp. Par la suite, on a fait un large screening de l'expression de plusieurs récepteurs de neurotransmetteurs chez la BHE de rat, beaucoup d'entre eux impliqués dans la signalisation inflammatoire, et qui peut jouer un rôle dans la modulation de ces transporteurs ABC. (...)
The blood-brain barrier (BBB) is the main interface of molecular exchange between the bloodstream and the central nervous system (CNS), where it plays an essential role on the control over the bi-directional passage of endogenous and exogenous compounds. At the BBB, P-glycoprotein (P-gp) and Breast Cancer Resistance Protein (BCRP) are the most important ABC drug efflux transporters preventing the entry into the brain of toxic compounds, drugs and xenobiotics circulating in the blood. There is increasing interest in understanding the molecular mechanisms underlying the modulation of P-gp and BCRP expression and function in order to control CNS accumulation of neurotoxicants and to overcome pharmacoresistance phenomena. Recent studies showed that morphine, itself a substrate of P-gp, is implicated in the up-regulation of P-gp expression, which may contribute to its poor brain penetration and tolerance. However, it was unknown the mechanism underlying P-gp induction by morphine and its role on BCRP expression. Rats were used as an animal model for the study of the amplitude and the kinetics of the modulation of P-gp and Bcrp expressions at the BBB following a subchronic morphine treatment, in an escalating morphine dose regimen. Freshly isolated rat brain microvessels were used as BBB model to study P-gp and Bcrp contents following the in vivo treatment, while the hCMEC/D3 cell line was occasionally used for complementary studies. Our results demonstrated that a 5-day subchronic morphine regimen up-regulated both P-gp and Bcrp 12 to 24h after the last dose of morphine, which was not registered at earlier time-points of animal sacrifice, nor with a single dose of morphine. The animal treatment with a glutamatergic NMDA receptor antagonist, or a COX-2 inhibitor abolished the subchronic morphine-induced P-gp and Bcrp protein up-regulation, 24h after the last dose of morphine, suggesting that both are implicated in the morphine-dependent P-gp and Bcrp up-regulation. Since the registered up-regulation only occurred from 12h after the last dose of morphine-onwards, we investigated whether it was a direct effect of continued exposure to morphine, or rather a consequence of the morphine withdrawal developed after discontinuation of treatment. Rats were treated either with a constant morphine infusion (5 days), or two chronic morphine regimens where withdrawal was precipitated by naloxone administration: an escalating dose (5 days) or a constant dose morphine regimen followed by a withdrawal period (2 days) and resume of the treatment for 3 additional days. Continuous i.v. morphine did not change P-gp and Bcrp levels in rat brain microvessels, it does not have a direct consequence on the cascade of regulation of these transporters at the BBB. Naloxone-precipitated withdrawal after escalating or chronic morphine dose regimen increased Mdr1a and Bcrp mRNA levels, but protein expression and activity remained unchanged after naloxone administration. This latter result discrepancy may be due to posttranslational regulation or naloxone action at non-opioid receptors hampering P-gp and Bcrp up-regulation. Subsequently, we did a large screening of the expression of several neurotransmitter receptors at the rat BBB, many of them implicated in the inflammatory cell-cell signaling, and which may have a role in the modulation of these ABC transporters. Also, we compared two different approaches of isolation of rat brain microvessels, mechanical dissection and enzymatic digestion, to assess which yield the purest microvessel fraction for the BBB study. The enzymatic digestion provided the highest enrichment of endothelial cells and pericytes, and the least contamination with astrocyte and neuron markers. (...)
A barreira hemato-encefálica (BHE) representa a principal interface entre a corrente sanguínea e o sistema nervoso central (SNC), desempenhando um papel essencial no controlo da passagem sangue-cérebro de diversos compostos endógenos e exógenos. A glicoproteina P (P-gp) e a proteína de resistência ao cancro da mama (BCRP) são os principais transportadores de efluxo da família ABC presentes ao nível da BHE, limitando a passagem cerebral de compostos tóxicos, fármacos e xenobióticos circulantes na corrente sanguínea. Actualmente, regista-se um crescente interesse na comunidade científica para a melhor compreensão dos mecanismos moleculares subjacentes à modulação quer da expressão quer da função da P-gp e BCRP, no sentido de desenvolver medidas mais eficazes quer para prevenção da acumulação de compostos neurotóxicos no SNC, quer para superar fenómenos de farmacorresistência associados à terapêutica. Estudos recentes evidenciam que a morfina, por si só um substrato da P-gp, está envolvida na indução da expressão da P-gp, o que poderá contribuir para a sua menor penetração cerebral, bem como para o desenvolvimento de tolerância. No entanto, não se conhece o mecanismo subjacente a tal indução da P-gp pela morfina, nem o seu eventual papel na expressão da BCRP. Com efeito, na condução da presente dissertação, realizamos um estudo da amplitude e a cinética da regulação da expressão da P-gp e BCRP ao nível da BHE na sequência de um tratamento subcrónico com morfina, em regime de doses crescentes, usando o rato como modelo animal. Para o efeito, foram isolados os capilares cerebrais dos animais sujeitos a tratamento, in vivo, enquanto que a linha celular hCMEC/D3 foi ocasionalmente utilizada para estudos complementares. Os nossos resultados demonstraram que um tratamento subcrónico com morfina (5 dias) foi capaz de induzir tanto a P-gp como a Bcrp 12 a 24 horas após a última dose de morfina administrada, mas não para tempos de sacrifício anteriores, bem como tal indução não foi registada quando a morfina foi administrada de forma aguda. O tratamento animal com um antagonista do receptor glutamatérgico NMDA, ou com um inibidor da COX-2 anulou este efeito de indução da P-gp e Bcrp pela administraçãosubcrónica de morfina, o que sugere o envolvimento destes dois componentes na indução da P-gp e Bcrp dependente da morfina. Uma vez que este aumento da expressão só surgiu a partir de 12h após a última dose de morfina, decidimos investigar se tal seria um efeito direto da exposição continuada à morfina, ou por outro lado, uma consequência do síndrome de abstinência à morfina, desenvolvido após a descontinuação do tratamento. Desta forma, os animais foram tratados por um lado com uma infusão contínua de morfina (5 dias), ou sujeitos a dois diferentes regimes de exposição crónica à morfina, após os quais o síndrome de abstinência foi provocado pela administração de naloxona. A administração de morfina em contínuo, via i.v., não alterou os níveis de P-gp e BCRP nos capilares cerebrais de rato, o que indica a ausência de uma consequência directa da morfina na cascata de regulação destes transportadores ao nível da BHE. O síndrome de abstinência opióide provocado pela naloxona aumentou os níveis de mRNA Mdr1a e Bcrp, mas tanto a expressão e atividade proteicas mantiveram-se inalteradas após a administração de naloxona. Esta discrepância de resultados pode-se dever ou a um regulamento pós-translacional, ou a uma acção inespecífica da naloxona em receptores não opiáceos, impedindo a indução da P-gp e Bcrp. Num outro estudo, foi feito um screening da expressão de vários receptores de neurotransmissores na BHE de rato, muitos deles envolvidos na sinalização célula-célula em processos inflamatórios, e que podem ter um papel na modulação destes transportadores ABC. (...)
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Chung, Charlotte Yuk-Yan. "Tight Junctions - The Link Between HIV-Associated Intestinal Barrier Dysfunction and Loss of Immune Homeostasis." Case Western Reserve University School of Graduate Studies / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=case1417822947.

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Books on the topic "Activation barrier"

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Cortese, R. A. Flame-powered trigger device for activating explosion suppression barrier. Washington, D.C: U.S. Dept. of the Interior, Bureau of Mines, 1991.

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Cortese, R. A. Flame powered trigger device for activating explosion suppression barrier. Washington, DC: U.S. Dept. of the Interior, Bureau of Mines, 1991.

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Magalhaes, Eric, Angelo Polito, Andréa Polito, and Tarek Sharshar. Sepsis-Associated Encephalopathy. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0032.

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Brain dysfunction is a major complication of sepsis and is characterized by alteration of consciousness, ranging from delirium to coma and marked electroencephalographic changes. It reflects a constellation of dynamic biological mechanisms, including neurotransmitter imbalance, macro- and microcirculatory dysfunction resulting in ischaemia, endothelial activation, alteration of the blood-brain barrier impairment with passage of neurotoxic mediators, activation of microglial cells within the central nervous system, cumulatively resulting in a neuroinflammatory state. Sepsis-associated brain dysfunction is associated with increased mortality and long-term cognitive decline, whose mechanisms might include microglial activation, axonopathy, or cerebral microinfarction. There is no specific treatment, other than the management of the underlying septic source, correction of physiological and metabolic abnormalities, and limiting the use of medications with neurotoxic effects.
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Henriksen, Niels Engholm, and Flemming Yssing Hansen. Microscopic Interpretation of Arrhenius Parameters. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198805014.003.0008.

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This chapter reviews the microscopic interpretation of the pre-exponential factor and the activation energy in rate constant expressions of the Arrhenius form. The pre-exponential factor of apparent unimolecular reactions is, roughly, expected to be of the order of a vibrational frequency, whereas the pre-exponential factor of bimolecular reactions, roughly, is related to the number of collisions per unit time and per unit volume. The activation energy of an elementary reaction can be interpreted as the average energy of the molecules that react minus the average energy of the reactants. Specializing to conventional transition-state theory, the activation energy is related to the classical barrier height of the potential energy surface plus the difference in zero-point energies and average internal energies between the activated complex and the reactants. When quantum tunnelling is included in transition-state theory, the activation energy is reduced, compared to the interpretation given in conventional transition-state theory.
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Bazzan, Anthony J., and Daniel A. Monti. Diet, Gut, and Brain: A New Horizon. Edited by Anthony J. Bazzan and Daniel A. Monti. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190690557.003.0001.

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There is growing data that dietary factors have profound effects on inflammation, the gut microbiome, intestinal permeability, and the blood–brain barrier; all of which impact brain health and psychological well-being. The Western diet in particular is deleterious for both physical and cognitive/emotional health. This occurs primarily by causing inflammation in the gut and an activation of the immune system along with causing impairment in the integrity of the gut lining. This allows many reactive molecules to enter the general circulation and even cross the blood–brain barrier. Recent research advances elucidate that understanding the harmful physiological effects of certain dietary behaviors is as important as knowing the role of critical nutrients for optimal brain health. This chapter reviews current knowledge regarding diet and nutrition in the context of psychiatric disorders and brain health. Information is reviewed regarding the most appropriate dietary and nutrition approaches to support optimum brain health.
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Dangayach, Neha S., Charles L. Francoeur, Stephan A. Mayer, and Tarek Sharshar. Neuroprotection in Sepsis and Acute Respiratory Distress Syndrome. Edited by David L. Reich, Stephan Mayer, and Suzan Uysal. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190280253.003.0013.

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Diffuse cerebral dysfunction in sepsis and acute respiratory distress syndrome (ARDS) patients is highly prevalent. Delirium and alterations in level of consciousness in septic patients are symptoms that constitute sepsis-associated encephalopathy (SAE), which is distinct from hypoxic encephalopathy. SAE is associated with substantial mortality and long-term cognitive impairment. The underlying pathophysiology of SAE is complex and poorly understood. The pathophysiology of SAE includes neuroinflammation, microglial activation, microcirculatory failure, autoregulation impairment, blood–brain barrier disruption, apoptosis, and development of microinfarcts and microhemorrhages. Apart from standard resuscitation techniques targeted at maintaining adequate cerebral perfusion and oxygenation, specific neuroprotective interventions are not currently available. Given the vast unmet need for improving functional outcome among survivors of SAE, it is a priority for the critical care community to better define, understand, and prevent this common and devastating form of neurological injury.
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De Souza, Jonathan. Sounding Actions. Oxford University Press, 2017. http://dx.doi.org/10.1093/acprof:oso/9780190271114.003.0003.

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When a musical instrument converts energy into sound, it makes aspects of the player’s action audible. This chapter analyzes this action-sound coupling in various instruments, drawing on ecological acoustics, organology, and cybernetics. It introduces a distinction between two aspects of sound production—“activation” and “control”—either of which may come from the player or the instrument. Pipe organs, for example, are activated by nonhuman power sources, though the pitches are controlled by the organist. Barrel organs, by contrast, are activated by human energy, but the pitches are preprogrammed. Instrumental sound production also involves distinctive combinations of sonic, visual, and tactile feedback. Moreover, by adapting Merleau-Ponty’s work on the body schema, this theory of action-sound coupling accounts for the feeling, often reported by performers, that an instrument is an extension of the body.
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Book chapters on the topic "Activation barrier"

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Persidsky, Yuri, and Howard E. Gendelman. "HIV-1 Encephalitis is a Consequence of Viral Infection and Neuroimmune Activation." In Biology and Physiology of the Blood-Brain Barrier, 365–67. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4757-9489-2_60.

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Marshall, G. R., M. L. Smythe, S. E. Huston, and R. D. Bindal. "The molten helix: low activation energy barrier for helix-helix transitions." In Peptides, 896–98. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-0683-2_301.

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Dore-Duffy, Paula, Roumen Balabanov, and Ruth Washington. "Recovery from Acute Experimental Autoimmune Encephalomyelitis (EAE) Characterized by Endothelial Cell Unresponsiveness to Cytokines and Pericyte Activation." In Biology and Physiology of the Blood-Brain Barrier, 347–51. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4757-9489-2_57.

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Rapoport, S. I., and P. J. Robinson. "Long-Chain Fatty Acid Transport at the Blood-Brain Barrier and Incorporation into Brain Phospholipids: A New In Vivo Method for Examining Neuroplasticity, and Brain Second Messenger Systems Involving Phospholipase A2 Activation." In New Concepts of a Blood—Brain Barrier, 119–40. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4899-1054-7_13.

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Schatz, George C. "Perspective on “Exchange reactions with activation energy. I. Simple barrier potential for (H, H2)”." In Theoretical Chemistry Accounts, 270–72. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-662-10421-7_31.

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Koenig, Harold, Jerome J. Trout, Alfred D. Goldstone, and Chung Y. Lu. "NMDA Receptors Mediate Activation of Polyamine Synthesis and Blood-Brain Barrier Breakdown after Cold Injury." In The Role of Neurotransmitters in Brain Injury, 279–83. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3452-5_42.

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Huegler, Nathalie, and Natasha Kersh. "Social Inclusion, Participation and Citizenship in Contexts of Neoliberalism: Examples of Adult Education Policy and Practice with Young People in the UK, The Netherlands and Ireland." In Young Adults and Active Citizenship, 57–78. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-65002-5_4.

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AbstractThis chapter focuses on contexts where public discourses regarding the education of young adults have been dominated by socio-economic perspectives, with a focus on the role of employment-related learning, skills and chances and with active participation in the labour market as a key concern for policy makers. A focus on ‘employability’ alone has been linked to narrow conceptualisations of participation, inclusion and citizenship, arising in the context of discourse shifts through neoliberalism which emphasise workfare over welfare and responsibilities over rights. A key critique of such contexts is that the focus moves from addressing barriers to participation to framing social inclusion predominantly as related to expectations of ‘activation’ and sometimes, assimilation. Key target groups for discourses of activation include young people not in education, employment or training (‘NEET’), while in- and exclusion of migrant and ethnic minority young people are often framed within the complex and contradictory interplay between discourses of assimilation and experiences of discrimination. These developments influence the field of adult education aimed at young people vulnerable to social exclusion. An alternative discourse to ‘activation’ is the promotion of young people’s skills and capabilities that enables them to engage in forms of citizenship activism, challenging structural barriers that lead to exclusion. Our chapter considers selected examples from EduMAP research in the UK, the Netherlands and Ireland which indicate that as well as framing the participation of young people as discourses of ‘activation’, adult education can also enable and facilitate skills related to more activist forms of citizenship participation.
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Wang, Z., and A. R. Crofts. "The Mechanism of Quinol Oxidation: Activation Barriers in UQH2:CYT C2 Oxidoreductase." In Current Research in Photosynthesis, 2197–200. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-0511-5_502.

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Whittington, Chris, John Latham, and Adam R. Offenbacher. "Tunneling through the Barriers: Resolving the Origins of the Activation of C-H Bonds Catalyzed by Enzymes." In ACS Symposium Series, 139–60. Washington, DC: American Chemical Society, 2020. http://dx.doi.org/10.1021/bk-2020-1357.ch007.

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Banks, William A. "Transport of Pituitary Adenylate Cyclase Activating Polypeptide Across the Blood–Brain Barrier: Consequences for Disease States and Therapeutic Effects." In Current Topics in Neurotoxicity, 423–32. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-35135-3_25.

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Conference papers on the topic "Activation barrier"

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Iwaniszewski, J. "On the resonant activation and inhibition of activation in fluctuating barrier problems." In Stochastic and chaotic dynamics in the lakes. AIP, 2000. http://dx.doi.org/10.1063/1.1302399.

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Lu, Q., G. Radin, J. Newton, and S. Rounds. "Pentostatin Enhances Endothelial Baseline Barrier Function through Rac-1 Activation." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a6117.

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Wang, Shengzhao, Dayong Huang, and Jianliang Qiao. "The evolution of GaN photocathode surface barrier before and after activation." In Optoelectronic Materials and Devices for Sensing and Imaging, edited by Mingbo Pu, Xue Feng, Yadong Jiang, Xiong Li, Xiaoliang Ma, and Bernard Kippelen. SPIE, 2019. http://dx.doi.org/10.1117/12.2505545.

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Wadgaonkar, Raj, Satish Gowda, and Fatima Anjum. "Essential Role Of Sphingomyelin Synthase Activation In Endotoxin Induced Barrier Dysfunction." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a1863.

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Soong, Grace, Jarin Chun, Francis Martin, Taylor S. Cohen, and Alice S. Prince. "Staphylococcal Activation Of EGFR Facilitates Invasion Across The Pulmonary Mucosal Barrier." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6777.

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Kristiansen, Tron Golder, Laurent Delabroy, Guillermo Andres Obando Palacio, Tonje Winther, Nils Andre Aarseth, Andreas Bauer, Karstein Hagenes, Anders Lindal, and Pål Tyberø. "Implementing a Strategy for Shale as Well Barrier in New Wells." In SPE/IADC International Drilling Conference and Exhibition. SPE, 2021. http://dx.doi.org/10.2118/204075-ms.

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Abstract Shale is an effective barrier material. It has a proven track record of acting as a seal (barrier) for oil and gas reservoirs for millions of years. Shale with high clay content and especially high smectite has low permeability, in the nanodarcy range, compared to standard class G laboratory cement that has permeability in the 10–20 microdarcy range. Weak ductile shales will also have a self-healing behavior should fractures be induced at some point. Shale is approved by regulators to be used as well barriers and part of permanent plug and abandonment (P&A) for oil and gas wells. Examples of regulations are Norsok D-010, 2013 in Norway and O&G UK, 2012. In Norsok D-010, one suggests the formation of shale barriers to happen due to creep in ductile shales. Creep occurs in many materials and is observed as deformation under constant load and is also well described in rock mechanics literature. In a previous paper (Kristiansen et al., 2018), it was discussed how shale can be activated as a barrier to form around the wellbore in some shale types. This can be done by inducing a pressure drop in the open annulus (rapid drawdown), by heating the shale by a couple of hundred degrees Celsius, or by chemical processes. In that paper, the process found most effective and practical at that time was demonstrated: the activation of shale barriers with a rapid pressure drop in the annulus. It was also shown that the barrier can be verified days after by standard verification methods used in the industry (pressure testing and bond logging). The shale barrier verification criteria are analogous to cement barriers. In this paper we share the experience from the implementation of a strategy to use shale as well barriers in new wells at Valhall and a second field, Ula, around 100 km away. The method used to activate the shale barriers has revealed some challenges from a well control point of view, but it has also shown that waiting a couple of weeks, or in some cases a couple of months, shale barriers are forming with the same quality as when they were activated or logged later as part of P&A. From this work it can be concluded that the shale barriers logged during P&A are, in some cases, in place only weeks or months after the wells have been drilled. The activation seems to induce an acceleration of time-dependent deformation that will naturally happen over longer time and is consistent with rock mechanics principles of time-dependent deformations in rocks (like creep and consolidation).
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Soskin, S. M. "Drastic Reduction of the Activation Barrier by a Moderately Weak Periodic Driving." In UNSOLVED PROBLEMS OF NOISE AND FLUCTUATIONS: UPoN 2002: Third International Conference on Unsolved Problems of Noise and Fluctuations in Physics, Biology, and High Technology. AIP, 2003. http://dx.doi.org/10.1063/1.1584916.

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Koehler, Andrew D., Travis J. Anderson, Marko J. Tadjer, Boris N. Feigelson, Karl D. Hobart, Francis J. Kub, Anindya Nath, and David I. Shahin. "Vertical GaN junction barrier schottky diodes by Mg implantation and activation annealing." In 2016 IEEE 4th Workshop on Wide Bandgap Power Devices and Applications (WiPDA). IEEE, 2016. http://dx.doi.org/10.1109/wipda.2016.7799965.

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Muscarella, Loreta, Eline Hutter, Francesca Wittmann, Young Won Woo, Young-Kwang Jung, Lucie McGovern, Jan Versluis, Aron Walsh, Huib Bakker, and Bruno Ehrler. "Lattice compression increases the activation barrier for phase segregation in mixed-halide perovskites." In International Conference on Impedance Spectroscopy and Related Techniques in Metal Halide Perovskites. València: Fundació Scito, 2020. http://dx.doi.org/10.29363/nanoge.perimped.2020.005.

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Pan, Mingqiang, Furong Yao, Jizhu Liu, Yangjun Wang, and Lining Sun. "Effect of Magnetic Field on Activation Performance of Silicon/Glass Dielectric Barrier Discharge." In 2018 19th International Conference on Electronic Packaging Technology (ICEPT). IEEE, 2018. http://dx.doi.org/10.1109/icept.2018.8480568.

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Reports on the topic "Activation barrier"

1

McGuinness, Seamus, Adele Whelan, Adele Bergin, and Judith Delaney. Profiling barriers to social inclusion in Ireland: the relative roles of individual characteristics and location. ESRI, July 2018. http://dx.doi.org/10.26504/rs71.

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Abstract:
The study uses data from participants in the Department of Rural and Community Development’s Social Inclusion and Community Activation Programme (SICAP), administered by Pobal, to examine who is most likely to experience at least one of five barriers to social inclusion. The barriers are (a) belonging to a jobless household, (b) being a lone parent, (c) having a disability, (d) being homeless or affected by housing exclusion and (e) belonging to an ethnic minority.
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2

Evans, Donald L., Avigdor Eldar, Liliana Jaso-Friedmann, and Herve Bercovier. Streptococcus Iniae Infection in Trout and Tilapia: Host-Pathogen Interactions, the Immune Response Towards the Pathogen and Vaccine Formulation. United States Department of Agriculture, February 2005. http://dx.doi.org/10.32747/2005.7586538.bard.

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Abstract:
The objectives of the BARD proposal were to determine the mechanisms of nonspecific cytotoxic cells (NCC) that are necessary to provide heightened innate resistance to infection and to identify the antigenic determinants in Streptococcus iniae that are best suited for vaccine development. Our central hypothesis was that anti-bacterial immunity in trout and tilapia can only be acquired by combining "innate" NCC responses with antibody responses to polysaccharide antigens. These Objectives were accomplished by experiments delineated by the following Specific Aims: Specific aim (SA) #1 (USA) "Clone and Identify the Apoptosis Regulatory Genes in NCC"; Specific aim #2 (USA)"Identify Regulatory Factors that Control NCC Responses to S. iniae"; Specific aim #3 (Israel) "Characterize the Biological Properties of the S. iniae Capsular Polysaccharide"; and Specific aim #4 (Israel) "Development of an Acellular Vaccine". Our model of S. iniae pathogenesis encompassed two approaches, identify apoptosis regulatory genes and proteins in tilapia that affected NCC activities (USA group) and determine the participation of S.iniae capsular polysaccharides as potential immunogens for the development of an acellular vaccine (Israel group). We previously established that it was possible to immunize tilapia and trout against experimental S. difficile/iniaeinfections. However these studies indicated that antibody responses in protected fish were short lived (3-4 months). Thus available vaccines were useful for short-term protection only. To address the issues of regulation of pathogenesis and immunogens of S. iniae, we have emphasized the role of the innate immune response regarding activation of NCC and mechanisms of invasiveness. Considerable progress was made toward accomplishing SA #1. We have cloned the cDNA of the following tilapia genes: cellular apoptosis susceptibility (CAS/AF547173»; tumor necrosis factor alpha (TNF / A Y 428948); and nascent polypeptide-associated complex alpha polypeptide (NACA/ A Y168640). Similar attempts were made to sequence the tilapia FasLgene/cDNA, however these experiments were not successful. Aim #2 was to "Identify Regulatory Factors that Control NCC Responses to S. iniae." To accomplish this, a new membrane receptor has been identified that may control innate responses (including apoptosis) of NCC to S. iniae. The receptor is a membrane protein on teleost NCC. This protein (NCC cationic antimicrobial protein-1/ncamp-1/AAQ99138) has been sequenced and the cDNA cloned (A Y324398). In recombinant form, ncamp-l kills S. iniae in vitro. Specific aim 3 ("Characterize the Biological Properties of the S.iniae Capsular Polysaccharide") utilized an in- vitro model using rainbow trout primary skin epithelial cell mono layers. These experiments demonstrated colonization into epithelial cells followed by a rapid decline of viable intracellular bacteria and translocation out of the cell. This pathogenesis model suggested that the bacterium escapes the endosome and translocates through the rainbow trout skin barrier to further invade and infect the host. Specific aim #4 ("Development of an Acellular Vaccine") was not specifically addressed. These studies demonstrated that several different apoptotic regulatory genes/proteins are expressed by tilapia NCC. These are the first studies demonstrating that such factors exist in tilapia. Because tilapia NCC bind to and are activated by S. iniae bacterial DNA, we predict that the apoptotic regulatory activity of S. iniae previously demonstrated by our group may be associated with innate antibacterial responses in tilapia.
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