The Experts below are selected from a list of 252 Experts worldwide ranked by ideXlab platform
Ozan Akca - One of the best experts on this subject based on the ideXlab platform.
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nitrous Oxide and risk of surgical wound infection a randomised trial
The Lancet, 2005Co-Authors: Edith Fleischmann, Rainer Lenhardt, Béla Fülesdi, Robert Greif, F Herbst, Daniel I Sessler, Andrea Kurz, Ozan AkcaAbstract:Summary Background Nitrous Oxide inactivates vitamin B12 and methionine synthase, thereby impairing DNA formation and, consequently, new cell formation. The gas also inhibits methionine production, which can reduce scar formation and depresses chemotactic migration by monocytes. Therefore, we assessed whether nitrous Oxide increases the incidence of surgical wound infection. Methods We recruited 418 patients aged 18–80 years, scheduled for colon resection that was expected to last more than 2 h, at three hospitals in Austria and Hungary. Patients were randomly assigned 65% intraoperative nitrous Oxide (n=208) or nitrogen (n=206), with remifentanil and isoflurane. The primary outcome was the incidence of clinical postoperative wound infection, analysed by intention to treat. Findings 206 patients in the nitrous Oxide Group and 202 in the nitrogen Group were included in the final analysis. Duration of surgery was longer in the nitrogen Group (3·4 h [1·5]) than in the nitrous Oxide Group (3·0 h [SD 1·3]) and arterial pressure (84 mm Hg [10] vs 81 mm Hg [9]), bispectral index values (53 [9] vs 44 [8]), and end-tidal isoflurane concentration (0·64% [0·14] vs 0·56% [0·13]) were greater in patients given nitrogen than in those given nitrous Oxide. Infection rate was 15% (31/206) in patients given nitrous Oxide and 20% (40/202) in those given nitrogen (p=0·205). Additionally, the ASEPSIS wound healing score, wound collagen deposition, number of patients admitted to critical care unit, time to first food ingestion, duration of hospital stay, and mortality did not differ between treatment Groups. Interpretation Nitrous Oxide does not increase the incidence of surgical wound infection.
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nitrous Oxide and risk of surgical wound infection a randomised trial
The Lancet, 2005Co-Authors: Edith Fleischmann, Rainer Lenhardt, Béla Fülesdi, Robert Greif, F Herbst, Daniel I Sessler, Andrea Kurz, Ozan AkcaAbstract:Summary Background Nitrous Oxide inactivates vitamin B12 and methionine synthase, thereby impairing DNA formation and, consequently, new cell formation. The gas also inhibits methionine production, which can reduce scar formation and depresses chemotactic migration by monocytes. Therefore, we assessed whether nitrous Oxide increases the incidence of surgical wound infection. Methods We recruited 418 patients aged 18–80 years, scheduled for colon resection that was expected to last more than 2 h, at three hospitals in Austria and Hungary. Patients were randomly assigned 65% intraoperative nitrous Oxide (n=208) or nitrogen (n=206), with remifentanil and isoflurane. The primary outcome was the incidence of clinical postoperative wound infection, analysed by intention to treat. Findings 206 patients in the nitrous Oxide Group and 202 in the nitrogen Group were included in the final analysis. Duration of surgery was longer in the nitrogen Group (3·4 h [1·5]) than in the nitrous Oxide Group (3·0 h [SD 1·3]) and arterial pressure (84 mm Hg [10] vs 81 mm Hg [9]), bispectral index values (53 [9] vs 44 [8]), and end-tidal isoflurane concentration (0·64% [0·14] vs 0·56% [0·13]) were greater in patients given nitrogen than in those given nitrous Oxide. Infection rate was 15% (31/206) in patients given nitrous Oxide and 20% (40/202) in those given nitrogen (p=0·205). Additionally, the ASEPSIS wound healing score, wound collagen deposition, number of patients admitted to critical care unit, time to first food ingestion, duration of hospital stay, and mortality did not differ between treatment Groups. Interpretation Nitrous Oxide does not increase the incidence of surgical wound infection.
Andrea Kurz - One of the best experts on this subject based on the ideXlab platform.
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nitrous Oxide and risk of surgical wound infection a randomised trial
The Lancet, 2005Co-Authors: Edith Fleischmann, Rainer Lenhardt, Béla Fülesdi, Robert Greif, F Herbst, Daniel I Sessler, Andrea Kurz, Ozan AkcaAbstract:Summary Background Nitrous Oxide inactivates vitamin B12 and methionine synthase, thereby impairing DNA formation and, consequently, new cell formation. The gas also inhibits methionine production, which can reduce scar formation and depresses chemotactic migration by monocytes. Therefore, we assessed whether nitrous Oxide increases the incidence of surgical wound infection. Methods We recruited 418 patients aged 18–80 years, scheduled for colon resection that was expected to last more than 2 h, at three hospitals in Austria and Hungary. Patients were randomly assigned 65% intraoperative nitrous Oxide (n=208) or nitrogen (n=206), with remifentanil and isoflurane. The primary outcome was the incidence of clinical postoperative wound infection, analysed by intention to treat. Findings 206 patients in the nitrous Oxide Group and 202 in the nitrogen Group were included in the final analysis. Duration of surgery was longer in the nitrogen Group (3·4 h [1·5]) than in the nitrous Oxide Group (3·0 h [SD 1·3]) and arterial pressure (84 mm Hg [10] vs 81 mm Hg [9]), bispectral index values (53 [9] vs 44 [8]), and end-tidal isoflurane concentration (0·64% [0·14] vs 0·56% [0·13]) were greater in patients given nitrogen than in those given nitrous Oxide. Infection rate was 15% (31/206) in patients given nitrous Oxide and 20% (40/202) in those given nitrogen (p=0·205). Additionally, the ASEPSIS wound healing score, wound collagen deposition, number of patients admitted to critical care unit, time to first food ingestion, duration of hospital stay, and mortality did not differ between treatment Groups. Interpretation Nitrous Oxide does not increase the incidence of surgical wound infection.
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nitrous Oxide and risk of surgical wound infection a randomised trial
The Lancet, 2005Co-Authors: Edith Fleischmann, Rainer Lenhardt, Béla Fülesdi, Robert Greif, F Herbst, Daniel I Sessler, Andrea Kurz, Ozan AkcaAbstract:Summary Background Nitrous Oxide inactivates vitamin B12 and methionine synthase, thereby impairing DNA formation and, consequently, new cell formation. The gas also inhibits methionine production, which can reduce scar formation and depresses chemotactic migration by monocytes. Therefore, we assessed whether nitrous Oxide increases the incidence of surgical wound infection. Methods We recruited 418 patients aged 18–80 years, scheduled for colon resection that was expected to last more than 2 h, at three hospitals in Austria and Hungary. Patients were randomly assigned 65% intraoperative nitrous Oxide (n=208) or nitrogen (n=206), with remifentanil and isoflurane. The primary outcome was the incidence of clinical postoperative wound infection, analysed by intention to treat. Findings 206 patients in the nitrous Oxide Group and 202 in the nitrogen Group were included in the final analysis. Duration of surgery was longer in the nitrogen Group (3·4 h [1·5]) than in the nitrous Oxide Group (3·0 h [SD 1·3]) and arterial pressure (84 mm Hg [10] vs 81 mm Hg [9]), bispectral index values (53 [9] vs 44 [8]), and end-tidal isoflurane concentration (0·64% [0·14] vs 0·56% [0·13]) were greater in patients given nitrogen than in those given nitrous Oxide. Infection rate was 15% (31/206) in patients given nitrous Oxide and 20% (40/202) in those given nitrogen (p=0·205). Additionally, the ASEPSIS wound healing score, wound collagen deposition, number of patients admitted to critical care unit, time to first food ingestion, duration of hospital stay, and mortality did not differ between treatment Groups. Interpretation Nitrous Oxide does not increase the incidence of surgical wound infection.
Jean-noël Jaubert - One of the best experts on this subject based on the ideXlab platform.
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Addition of the Sulfur DiOxide Group (SO2), the Oxygen Group (O-2), and the Nitric Oxide Group (NO) to the E-PPR78 Model
Industrial and engineering chemistry research, 2015Co-Authors: Romain Privat, Jean-noël JaubertAbstract:The E-PPR78 model is a predictive version of the widely used Peng-Robinson equation of state in which the binary interaction parameters are estimated by a Group-contribution method. With the 24 Groups available before the writing of this paper, such a model could be used to predict fluid phase equilibrium of systems containing hydrocarbons, permanent gases (CO2, N-2, H2S, H-2, CO, He, and Ar), mercaptans, alkenes, and water. During the process of the Carbon diOxide Capture and Storage (CCS), it is often necessary to know thermodynamic properties of mixtures containing carbon diOxide, water, hydrocarbons, and trace gases, such as nitrogen, argon, hydrogen, carbon monOxide, sulfur diOxide, oxygen, or nitric Oxide. Basically, except sulfur diOxide, oxygen, and nitric Oxide, most components encountered in systems regarding CCS processes could be modeled with the E-PPR78 model. So in order to predict the phase behavior and estimate energetic properties (e.g., enthalpy or heat capacity changes on mixing) of such systems, the applicability range of the E-PPR78 model is extended through the addition of three new Groups: "SO2," "O-2," and "NO.
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Addition of the Sulfur DiOxide Group (SO2), the Oxygen Group (O2), and the Nitric Oxide Group (NO) to the E-PPR78 Model
Industrial & Engineering Chemistry Research, 2015Co-Authors: Romain Privat, Jean-noël JaubertAbstract:The E-PPR78 model is a predictive version of the widely used Peng–Robinson equation of state in which the binary interaction parameters are estimated by a Group-contribution method. With the 24 Groups available before the writing of this paper, such a model could be used to predict fluid phase equilibrium of systems containing hydrocarbons, permanent gases (CO2, N2, H2S, H2, CO, He, and Ar), mercaptans, alkenes, and water. During the process of the Carbon diOxide Capture and Storage (CCS), it is often necessary to know thermodynamic properties of mixtures containing carbon diOxide, water, hydrocarbons, and trace gases, such as nitrogen, argon, hydrogen, carbon monOxide, sulfur diOxide, oxygen, or nitric Oxide. Basically, except sulfur diOxide, oxygen, and nitric Oxide, most components encountered in systems regarding CCS processes could be modeled with the E-PPR78 model. So in order to predict the phase behavior and estimate energetic properties (e.g., enthalpy or heat capacity changes on mixing) of such ...
Edith Fleischmann - One of the best experts on this subject based on the ideXlab platform.
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nitrous Oxide and risk of surgical wound infection a randomised trial
The Lancet, 2005Co-Authors: Edith Fleischmann, Rainer Lenhardt, Béla Fülesdi, Robert Greif, F Herbst, Daniel I Sessler, Andrea Kurz, Ozan AkcaAbstract:Summary Background Nitrous Oxide inactivates vitamin B12 and methionine synthase, thereby impairing DNA formation and, consequently, new cell formation. The gas also inhibits methionine production, which can reduce scar formation and depresses chemotactic migration by monocytes. Therefore, we assessed whether nitrous Oxide increases the incidence of surgical wound infection. Methods We recruited 418 patients aged 18–80 years, scheduled for colon resection that was expected to last more than 2 h, at three hospitals in Austria and Hungary. Patients were randomly assigned 65% intraoperative nitrous Oxide (n=208) or nitrogen (n=206), with remifentanil and isoflurane. The primary outcome was the incidence of clinical postoperative wound infection, analysed by intention to treat. Findings 206 patients in the nitrous Oxide Group and 202 in the nitrogen Group were included in the final analysis. Duration of surgery was longer in the nitrogen Group (3·4 h [1·5]) than in the nitrous Oxide Group (3·0 h [SD 1·3]) and arterial pressure (84 mm Hg [10] vs 81 mm Hg [9]), bispectral index values (53 [9] vs 44 [8]), and end-tidal isoflurane concentration (0·64% [0·14] vs 0·56% [0·13]) were greater in patients given nitrogen than in those given nitrous Oxide. Infection rate was 15% (31/206) in patients given nitrous Oxide and 20% (40/202) in those given nitrogen (p=0·205). Additionally, the ASEPSIS wound healing score, wound collagen deposition, number of patients admitted to critical care unit, time to first food ingestion, duration of hospital stay, and mortality did not differ between treatment Groups. Interpretation Nitrous Oxide does not increase the incidence of surgical wound infection.
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nitrous Oxide and risk of surgical wound infection a randomised trial
The Lancet, 2005Co-Authors: Edith Fleischmann, Rainer Lenhardt, Béla Fülesdi, Robert Greif, F Herbst, Daniel I Sessler, Andrea Kurz, Ozan AkcaAbstract:Summary Background Nitrous Oxide inactivates vitamin B12 and methionine synthase, thereby impairing DNA formation and, consequently, new cell formation. The gas also inhibits methionine production, which can reduce scar formation and depresses chemotactic migration by monocytes. Therefore, we assessed whether nitrous Oxide increases the incidence of surgical wound infection. Methods We recruited 418 patients aged 18–80 years, scheduled for colon resection that was expected to last more than 2 h, at three hospitals in Austria and Hungary. Patients were randomly assigned 65% intraoperative nitrous Oxide (n=208) or nitrogen (n=206), with remifentanil and isoflurane. The primary outcome was the incidence of clinical postoperative wound infection, analysed by intention to treat. Findings 206 patients in the nitrous Oxide Group and 202 in the nitrogen Group were included in the final analysis. Duration of surgery was longer in the nitrogen Group (3·4 h [1·5]) than in the nitrous Oxide Group (3·0 h [SD 1·3]) and arterial pressure (84 mm Hg [10] vs 81 mm Hg [9]), bispectral index values (53 [9] vs 44 [8]), and end-tidal isoflurane concentration (0·64% [0·14] vs 0·56% [0·13]) were greater in patients given nitrogen than in those given nitrous Oxide. Infection rate was 15% (31/206) in patients given nitrous Oxide and 20% (40/202) in those given nitrogen (p=0·205). Additionally, the ASEPSIS wound healing score, wound collagen deposition, number of patients admitted to critical care unit, time to first food ingestion, duration of hospital stay, and mortality did not differ between treatment Groups. Interpretation Nitrous Oxide does not increase the incidence of surgical wound infection.
J Penfold - One of the best experts on this subject based on the ideXlab platform.
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the formation of surface multilayers at the air water interface from sodium polyethylene glycol monoalkyl ether sulfate alcl 3 solutions the role of the size of the polyethylene Oxide Group
Langmuir, 2013Co-Authors: J Penfold, R K Thomas, Jordan T Petkov, I Tucker, John P R WebsterAbstract:Neutron reflectivity, NR, and surface tension, ST, have been used to study the surface adsorption properties at the air-water interface of the anionic surfactant sodium polyethylene glycol monododecyl ether sulfate (sodium lauryl ether sulfate, SLES) in the presence of Al(3+) multivalent counterions, by the addition of AlCl3. In the absence of AlCl3 and at low AlCl3 concentrations monolayer adsorption is observed. With increasing AlCl3 concentration, surface multilayer formation is observed, driven by SLES/Al(3+) complex formation. The onset of multilayer formation occurs initially as a single bilayer or a multilayer structure with a limited number of bilayers, N, ≤3, and ultimately at higher AlCl3 concentrations N is large, >20. The evolution in the surface structure is determined by the surfactant and AlCl3 concentrations, and the size of the polyethylene Oxide Group in the different SLES surfactants studied. From the NR data, approximate surface phase diagrams are constructed, and the evolution of the surface structure with surfactant and electrolyte concentration is shown to be dependent on the size of the polyethylene Oxide Group. As the polyethylene Oxide Group increases in size the multilayer formation requires increasingly higher surfactant and AlCl3 concentrations to promote the formation. This is attributed to the increased steric hindrance of the polyethylene Oxide Group disrupting SLES/Al(3+) complex formation.
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adsorption of polyelectrolyte surfactant mixtures at the air water interface modified poly ethyleneimine and sodium dodecyl sulfate
Langmuir, 2011Co-Authors: X L Zhang, R K Thomas, D J F Taylor, J PenfoldAbstract:The adsorption of surfactant/polyelectrolyte mixtures of sodium dodecyl sulfate (SDS) and different modified poly(ethyleneimine) (PEI) polyelectrolytes at the air-water interface has been studied using neutron reflectivity and surface tension. Modification of the PEI by the addition of short ethylene Oxide (EO) or propylene Oxide (PO) Groups is shown to have an impact upon the surface adsorption behavior. This is due to a modification of the polymer/surfactant interaction, an increase in the intrinsic surface activity of the modified polyelectrolyte, and changes in the relative importance of surface and solution complex formation. For the polyelectrolyte PEI, there is a marked change in the surface adsorption behavior between the addition of a single EO Group and that of the (EO)3 Group. The addition of a single EO or PO Group to the PEI results in an SDS concentration and solution pH adsorption dependence that is broadly similar in behavior to that of the unmodified PEI/SDS mixture. That is, there is strong surface complexation and adsorption down to low SDS concentrations, and there is evidence of a strong interaction at high pH in addition to the strong electrostatic attraction at low pH. The addition of a larger ethylene Oxide Group, triethylene Oxide (EO)3, results in a surface adsorption behavior that more closely resembles that of a neutral polymer/ionic surfactant mixture, similar to that observed for PEI with a larger ethylene Oxide Group, notably PEI-(EO)7. In that case, the adsorption of the polymer/surfactant complex is much less pronounced. The adsorption arises predominantly from competition between the polymer and surfactant and indicates a decrease in the polymer/surfactant interaction with increasing pH. That is, increasing the size of the ethylene Oxide Group induces a transition from a strong surface polymer/surfactant interaction to a weak polymer/surfactant interaction.
