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Experiments were carried out to determine the accuracy and validity of estimations of hepatic blood flow from systemic clearances of ethanol during very low dose (8 μmol∙min−1∙kg−1) infusions of ethanol in anesthetized cats. Systemic clearances were compared with directly measured hepatic blood flow using a hepatic venous long-circuit technique. This technique allowed direct measurement and alteration of hepatic blood flow and collection of arterial, portal, and hepatic venous blood samples without depletion of the animal's blood volume. In 18 cats, Vmax for ethanol was 93 ± 7 μmol∙min−1 per 100 g liver or 21 ± 2 μmol∙min−1∙kg·body weight−1 and Km was 144 ± 19 μM in terms of logarithmic mean sinusoidal concentration. At the dose of 8 μmol∙min−1∙kg body weight−1 used for estimation of hepatic blood flow, extraction was 0.95 ± 0.07 (mean ± SD). Systemic clearance of ethanol overestimated directly measured hepatic blood flow by 15 ± 16%. Hepatic blood flow changes expressed as percentages of the control level were accurately estimated from systemic ethanol clearance (100 ± 10%). Since 73 ± 12% of the infused ethanol was eliminated by the liver and 83 ± 11% was eliminated by the splanchnic bed, an extrasplanchnic uptake of 17% accounted for the overestimation of hepatic blood flow. Estimation of hepatic blood flow from systemic clearances of ethanol during very low dose infusions may have advantages over other clearance methods. Its use in cats was illustrated in a separate series of experiments and it was shown that surgery significantly reduced hepatic blood flow. The method may merit trial for estimation of hepatic blood flow in humans.

Molecular dynamics simulations have been performed to study photosystem II structure and function. Structural information obtained from simulations was combined with ab initio computations of chromophore excited states. In contrast to calculations based on the x-ray structure, the molecular-dynamics-based calculations accurately predicted the experimental absorbance spectrum. In addition, our calculations correctly assigned the energy levels of reaction-center (RC) chromophores, as well as the lowest-energy antenna chlorophyll. The primary and secondary quinone electron acceptors, Q(A) and Q(B), exhibited independent changes in position over the duration of the simulation. Q(B) fluctuated between two binding sites similar to the proximal and distal sites previously observed in light- and dark-adapted RC from purple bacteria. Kinetic models were used to characterize the relative influence of chromophore geometry, site energies, and electron transport rates on RC efficiency. The fluctuating energy levels of antenna chromophores had a larger impact on quantum yield than did their relative positions. Variations in electron transport rates had the most significant effect and were sufficient to explain the experimentally observed multi-component decay of excitation in photosystem II. The implications of our results are discussed in the context of competing evolutionary selection pressures for RC structure and function.

In a forward chemical equilibrium problem (FCEP), the state of minimum Gibbs energy for a chemical system is sought, in which temperature, pressure, elemental amounts, and thermodynamic model parameters are prescribed. We herein present a mathematical framework for characterizing and solving inverse chemical equilibrium problems (ICEP), a class of problems for which one or more of those prescribed conditions in a FCEP are unknown in advance. In an ICEP, complementary conditions must be imposed, which are referred to here as equilibrium constraints. Examples of ICEPs include those in which a certain property is known at equilibrium (e.g., volume is specified instead of pressure; enthalpy is specified instead of temperature; pH is specified instead of the amount of element H). The equilibrium constraints may also be specified by equations that govern the relationship between several equilibrium properties (e.g., the equations relating temperature, pressure, density, energy, and velocity of the gases produced during the detonation of an explosive). Chemical Engineering Science, 252 ISSN:0009-2509

Aims The aim of this study was to determine whether the sequential application of povidone iodine-alcohol (PVI) followed by chlorhexidine gluconate-alcohol (CHG) would reduce surgical wound contamination to a greater extent than PVI applied twice in patients undergoing spinal surgery. Patients and Methods A single-centre, interventional, two arm, parallel group randomised controlled trial was undertaken, involving 407 patients who underwent elective spinal surgery. For 203 patients, the skin was disinfected before surgery using PVI (10% [w/w (1% w/w available iodine)] in 95% industrial denatured alcohol, povidone iodine; Videne Alcoholic Tincture) twice, and for 204 patients using PVI once followed by CHG (2% [w/v] chlorhexidine gluconate in 70% [v/v] isopropyl alcohol; Chloraprep with tint). The primary outcome measure was contamination of the wound determined by aerobic and anaerobic bacterial growth from samples taken after disinfection. Results The detection of viable bacteria in any one of the samples taken after disinfection (culture-positive) was significantly lower in the group treated with both PVI and CHG than in the group treated with PVI alone (59 (29.1%) versus 85 (41.7%), p = 0.009; odds ratio 0.574; 95% confidence interval, 0.380 to 0.866). Conclusions Antisepsis of the skin with the sequential application of PVI and CHG more effectively reduces the contamination of a surgical wound than PVI alone. Cite this article: Bone Joint J 2017;99-B:1354–65.

Background and purpose:The contribution of endothelin‐1 (ET‐1) to vascular hyper‐reactivity associated with chronic ethanol intake, a major risk factor in several cardiovascular diseases, remains to be investigated.Experimental approach:The biphasic haemodynamic responses to ET‐1 (0.01–0.1 nmol kg−1, i.v.) or to the selective ETB agonist, IRL1620 (0.001–1.0 nmol kg−1, i.v.), with or without ETA or ETB antagonists (BQ123 (c(DTrp‐Dasp‐Pro‐Dval‐Leu)) at 1 and 2.5 mg kg−1 and BQ788 (N‐cis‐2,6‐dimethyl‐piperidinocarbonyl‐L‐γ‐methylleucyl1‐D‐1methoxycarbonyltryptophanyl‐D‐norleucine) at 0.25 mg kg−1, respectively) were tested in anaesthetized rats, after 2 weeks' chronic ethanol treatment. Hepatic parameters and ET receptor protein levels were also determined.Key results:The initial hypotensive responses to ET‐1 or IRL1620 were unaffected by chronic ethanol intake, whereas the subsequent pressor effects induced by ET‐1, but not by IRL1620, were potentiated. BQ123 at 2.5 but not 1 mg kg−1 reduced the pressor responses to ET‐1 in ethanol‐treated rats. Conversely, BQ788 (0.25 mg kg−1) potentiated ET‐1‐induced increases in mean arterial blood pressure in control as well as in ethanol‐treated rats. Interestingly, in the latter group, increases in heart rate, induced by ET‐1 at a dose of 0.025 mg kg−1 were enhanced following ETB receptor blockade. Finally, we observed higher levels of ETA receptor in the heart and mesenteric artery and a reduction of ETB receptor protein levels in the aorta and kidney from rats chronically treated with ethanol.Conclusions and implications:Increased vascular reactivity to ET‐1 and altered protein levels of ETA and ETB receptors could play a role in the pathogenesis of cardiovascular complications associated with chronic ethanol consumption.British Journal of Pharmacology (2008) 154, 971–981; doi:10.1038/bjp.2008.157; published online 12 May 2008

The fast decay in PEM fuel cells of a highly active, high performance, but unstable Fe/N/C catalyst like our NC_Ar + NH3 follows a chemical, not an electrochemical, demetallation mechanism for its ORR active FeN4 sites in the catalyst micropores.

In the present study, Tween 80, a non-ionic surfactant, has been used for enhanced hydrogen production by crude glycerol bioconversion using co-culture of Enterobacter aerogenes and Clostridium butyricum. The purpose of introducing the surfactant was to decrease the crude glycerol viscosity, so that apparent solubility and bioavailability of glycerol could be improved at the expenses of pretreatment steps. Experiments were planned using central composite design (CCD); crude glycerol and Tween 80 concentrations were optimized whereas, hydrogen production, glycerol utilization and viscosity of the media were considered as responses. The response surface for quadratic model showed, Tween 80 concentration had significant effect (p < 0.05) on all the three responses. Using the optimized conditions at 17.5 g/L crude glycerol and 15 mg/L Tween 80, hydrogen production reached a maximum of 32.1 ± 0.03 mmol/L of medium. The increase in hydrogen production was around 1.25-fold in presence of Tween 80 in comparison to its absence with 25.56 ± 0.91 mmol/L production. Selected optimum conditions were also validated against absence of crude glycerol (4.69 ± 0.76), with pretreated crude glycerol (20.06 ± 0.51) and across mono-culture system (15.43 ± 0.79 to 22.14 ± 0.94). Introduction of Tween 80 to the fermentation medium improved the glycerol utilization rate, resulting in increased hydrogen production and eliminated pretreatment steps.

We have previously demonstrated that adenylyl cyclase II (ACII) interacts with beta2-adrenergic receptors and heterotrimeric G proteins as part of a pre-assembled signalling complex. In this study, we further show that AC interacts with these proteins before it is targetted to the cell surface. Using a combination of approaches including bioluminescence resonance energy transfer (BRET) in concert with subcellular fractionation, we show that ACII and beta2AR initially interact in the ER. Further, dominant-negative Rab1 and Sar1 GTPases which block anterograde trafficking out of the ER have no effect on either ACII/receptor or ACII/Gbetagamma protein interactions. However, DN Rab1 and Sar1 constructs (but not DN Rabs 2, 6, 8 or 11) prevent the inclusion of Galpha subunits in ACII signalling complexes suggesting it assembles into the complex at a slightly later stage. Thus, like Kir3.1 inwardly rectifying potassium channels, signalosomes containing ACII are formed during their biosynthesis and not in response to agonist at the cell surface.