Introducing a variable speed of sound in single-component lattice Boltzmann simulations of isothermal fluid flows

To simulate the hydrodynamics and mixing characteristics of chemical reactors by means of a lattice Boltzmann method (LBM), it is essential to consider components with varying molecular weights (and therefore speeds of sound). This option requires modification of the standard equilibrium distribution function and the use of an extended velocity set. In this paper, we show that, for isothermal incompressible single-component non-reactive flows, tuning the speed of sound with a modified equilibrium distribution and an extended velocity set allows for reproducing the proper flow characteristics with strongly reduced errors (compared to LBM simulations on standard lattices). This is done for two isothermal benchmarks, viz. a damped standing pressure wave and a decaying viscous Taylor–Green Vortex. The convergence as a function of the number of lattice nodes used improves substantially for varying values of the speed of sound

Innovaties in de glasgroenteteelt : vergelijking van verschillende methoden voor het laten zakken van tomatenplanten = Innovations in horticulture : comparison of different working methods for lowering of tomato plants

In The Netherlands, the modern way of tomato production involves a high wire system. Here, metal hooks hold a rope that guides the growing tomato plant. Because the plants keep growing during the season, each rope is to be lowered periodically, which requires one-handed lifting. Because each plant weighs 4-6 kg and a complete cycle costs only 1-2 seconds, the task is considered to be strenuous and highly repetitive. Some alternative systems are available or under development, but their eventual load relieving effect is unknown. The present study considered some alternative systems from a theoretical viewpoint and investigated the effects of one particular alternative hook, the Tomguide. This hook eliminates most of the lifting part of the task because of application of a reel on which the rope is winded. The research involved seven experienced persons in six companies. All of the persons performed both tasks, i.e. the standard hook and the Tomguide. Muscular loading, experienced effort and working speed were measured during and after each task. Muscular loading was measured in four shoulder (trapezius and deltoid, left and right side) and two upper arm (biceps, left and right) muscles, applying electromyography (EMG). Static, median and peak load, relative to maximal activation, were calculated. Experienced effort was scored using a 10-point rating scale and a body diagram showing 14 body regions. EMG results showed a significant decrease in peak activity for both upper arm muscles when using the Tomguide. Median activity was reduced only for the right upper arm. If all 6 muscles were pooled, peak activity was reduced significantly, while median activity showed a tendency, without reaching significance. No difference was measured for any of the individual shoulder muscles measured. Experienced effort decreased significantly for the shoulder and upper arm regions, both left and right, in case of the Tomguide. It was observed that the Tomguide task lead to an increase in working time by 27%, compared to the standard hook, possibly partly due to insufficiently functioning of the mechanical brake on the reel. It is concluded that the Tomguide, and probably also comparable reel rope systems, contribute to a reduction of muscular load, in particular of the upper arm muscles, because lifting of the plants is strongly reduced. Because most workers copy their working height for the standard hook into the new situation, attention must be paid to instruction of the proper working height, in order to prevent unnecessarily high load of the shoulder muscles. Besides, final conclusions of the labour demand can only be drawn if the reel system applied is functioning well. The braking system of the Tomguide tested here did not allow for a relaxed working technique

Boundary conditions for surface reactions in lattice Boltzmann simulations

A surface reaction boundary condition in multicomponent lattice Boltzmann simulations is developed. The method is applied to a test case with nonlinear reaction rates and nonlinear density profiles. The results are compared to the corresponding analytical solution, which shows that the error of the method scales with the square of the lattice spacing.ChemE/Chemical EngineeringApplied Science

Long-term correction of bilirubin UDPglucuronyltransferase deficiency in rats by in utero lentiviral gene transfer

Long-term correction of bilirubin UDPglucuronyltransferase deficiency in rats by in utero lentiviral gene transfer.Seppen J, van der Rijt R, Looije N, van Til NP, Lamers WH, Oude Elferink RP.AMC Liver Center, S1-166, Meibergdreef 69, 1105 BK Amsterdam, The Netherlands. [email protected] is glucuronidated by bilirubin UDP-glucuronyltransferase (UGT1A1) before biliary excretion. Because bilirubin is toxic, patients with Crigler-Najjar type I (CN), who have no UGT1A1 activity, suffer severe brain damage early in childhood. The Gunn rat is the model for CN type 1. Gunn rat fetuses were injected with 10(7) transducing units of UGT1A1 lentiviral vector at the end of the third trimester on embryonic day 19. Serum bilirubin of injected Gunn rats was lowered by 45% compared to untreated controls. This decrease was highly significant (P < 10(6)) and was sustained for more than a year. In treated Gunn rats, bilirubin glucuronides were present in bile and UGT1A1 protein was detected in tissue. Liver, intestine, stomach, pancreas, and other organs were transduced and mostly contained 1% or less vector copies per genome. Tissue distribution was variable among experimental animals but high transduction levels were seen in pancreas and intestine in most animals. Immunohistochemistry of these organs revealed transduction of pancreatic acinar cells and intestinal epithelium. Injection of a lentiviral UGT1A1 vector into third-trimester Gunn rat fetuses corrects the metabolic deficiency and mediates a reduction of serum bilirubin levels that would be therapeutic in human

Disodium ascorbyl phytostanol phosphate (FM-VP4), a modified phytostanol, is a highly active hypocholesterolaemic agent that affects the enterohepatic circulation of both cholesterol and bile acids in mice

Disodium ascorbyl phytostanol phosphate (FM-VP4) is a synthetic compound derived from sitostanol and campestanol that has proved to be efficient as a cholesterol-lowering therapy in mice and human subjects. However, the mechanism of action of FM-VP4 remains unknown. The present study tests the ability of FM-VP4 to alter intestinal and liver cholesterol homeostasis in mice. Female C57BL/6J mice were fed either a control chow or a 2 % FM-VP4-enriched diet for 4 weeks. FM-VP4 reduced the in vivo net intestinal cholesterol absorption and plasma and liver cholesterol concentrations by 2.2-, 1.5- and 1.6-fold, respectively, compared with control mice. Furthermore, FM-VP4 also showed an impact on bile acid homeostasis. In FM-VP4 mice, liver and intestinal bile acid content was increased by 1.3- and 2.3-fold, respectively, whereas faecal bile acid output was 3.3-fold lower. FM-VP4 also increased the intestinal absorption of orally administered [H-3]taurocholic acid to small intestine in vivo. Inhibition of intestinal cholesterol absorption by FM-VP4 was not mediated via transcriptional increases in intestine liver X receptor (LXR)-alpha, adenosine triphosphate-binding cassette transporter (ABC)-A1, ABCG5/G8 nor to decreases in intestinal Niemann-Pick Cl-like 1 (NPC1L1) expression. In contrast, FM-VP4 up-regulated liver LXR alpha, ABCA1, ABCG5, scavenger receptor class BI (SR-BI) and hydroxymethylglutaryl coenzyme A reductase (HMGCoA-R) gene expression, whereas it down-regulated several farnesoid X receptor (FXR)-target genes such as cytochrome P450 family 7 subfamily A polypeptide I (CYP7AI) and Na+/taurocholate co-transporter polypeptide (NTCP). In conclusion, FM-VP4 reduced intestinal cholesterol absorption, plasma and liver cholesterol and affected bile acid homeostasis by inducing bile acid intestinal reabsorption and changed the liver expression of genes that play an essential role in cholesterol homeostasis. This is the first phytosterol or stanol that affects bile acid metabolism and lowers plasma cholesterol levels in normocholesterolaemic mice

Adenoviral overexpression of apolipoprotein A-V reduces serum levels of triglycerides and cholesterol in mice

Mice lacking ApoA-V, a novel HDL-associated apolipoprotein identified by our group and independently by Permacchio et al. [Science 294 (2001) 169], were recently shown to be hypertriglyceridemic. To study the role of ApoA-V in triglyceride homeostasis, we compared lipid profiles in mice expressing normal and highly elevated levels of ApoA-V. For this purpose, adenoviral vectors expressing sense or antisense ApoA-V cDNA were constructed. Treatment of mice with sense adenoviral constructs resulted in circa 20-fold higher serum ApoA-V levels compared with mice injected with either PBS or antisense adenoviral constructs. ApoA-V overexpressing mice had markedly decreased (-70%) serum triglyceride levels caused primarily by lowered triglyceride content of the VLDL fraction. Furthermore, in these mice cholesterol levels were found to be lowered in all lipoprotein fractions with the largest mass decrease in the HDL fraction. This resulted in a 40% drop of serum cholesterol content. These findings suggest a role of ApoA-V in regulating levels of circulating triglycerides and cholesterol. (C) 2002 Elsevier Science (USA). All rights reserve

A mouse genetic model for familial cholestasis caused by ATP8B1 mutations reveals perturbed bile salt homeostasis but no impairment in bile secretion

Mutations in ATP8B1, a broadly expressed P-type ATPase, result, through unknown mechanisms, in disorders of bile secretion. These disorders vary in severity from mild and episodic to progressive with liver failure. We generated Atp8b1(G308V/G308V) mutant mice, which carry a mutation orthologous to that present in homozygous form in patients from the Amish index kindred for severe ATP8B1 disease. In contrast to human patients, Atp8b1(G308V/G308V) mice had unimpaired bile secretion and no liver damage, but showed mild abnormalities including depressed weight at weaning and elevated serum bile salt levels. We challenged the hepatobiliary metabolism of Atp8b1(G308V/G308V) mice by administering exogenous bile salts. Upon bile salt feeding, Atp8b1(G308V/G308V) mice, but not wild-types, demonstrated serum bile salt accumulation, hepatic injury and expansion of the systemic bile salt pool. Unexpectedly, this failure of bile salt homeostasis occurred in the absence of any defect in hepatic bile secretion. Upon infusion of a hydrophobic bile salt, wild-type mice developed cholestasis while Atp8b1(G308V/G308V) mice maintained high biliary output and more extensively rehydroxylated the infused bile salt. Increased bile salt hydroxylation, which reduces bile salt toxicity, may explain the milder phenotype in Atp8b1(G308V/G308V) mice compared with humans with the equivalent mutation. These results demonstrate the key role of Atp8b1 in bile salt homeostasis and highlight the importance of bile salt hydroxylation in the prevention of cholestasis. The mouse phenotype reveals that loss of Atp8b1 disrupts bile salt homeostasis without impairment of canalicular bile secretion; in humans this process is likely to be obscured by early onset of severe liver diseas