Adsorption structures of phenol on the Si(001)-(2 \times 1) surface calculated using density functional theory

Several dissociated and two non-dissociated adsorption structures of the phenol molecule on the Si(001)-(2 \times 1) surface are studied using density functional theory with various exchange and correlation functionals. The relaxed structures and adsorption energies are obtained and it is found that the dissociated structures are energetically more favourable than the non-dissociated structures. However, the ground state energies alone do not determine which structure is obtained experimentally. To elucidate the situation core level shift spectra for Si 2p and C 1s states are simulated and compared with experimentally measured spectra. Several transition barriers were calculated in order to determine which adsorption structures are kinetically accessible. Based on these results we conclude that the molecule undergoes the dissociation of two hydrogen atoms on adsorption.Comment: 11 pages, 6 figure

The Origin And Loss Of Periodic Patterning In The Turtle Shell

The origin of the turtle shell over 200 million years ago greatly modified the amniote body plan, and the morphological plasticity of the shell has promoted the adaptive radiation of turtles. The shell, comprising a dorsal carapace and a ventral plastron, is a layered structure formed by basal endochondral axial skeletal elements (ribs, vertebrae) and plates of bone, which are overlain by keratinous ectodermal scutes. Studies of turtle development have mostly focused on the bones of the shell; however, the genetic regulation of the epidermal scutes has not been investigated. Here, we show that scutes develop from an array of patterned placodes and that these placodes are absent from a soft-shelled turtle in which scutes were lost secondarily. Experimentally inhibiting Shh, Bmp or Fgf signaling results in the disruption of the placodal pattern. Finally, a computational model is used to show how two coupled reaction-diffusion systems reproduce both natural and abnormal variation in turtle scutes. Taken together, these placodal signaling centers are likely to represent developmental modules that are responsible for the evolution of scutes in turtles, and the regulation of these centers has allowed for the diversification of the turtle shell

787-5 Systemic Effect of Ramipril on Endothelin, but not on Elcosanoid Levels in Patients with Coronary Artery Disease

Study aimNeurohumoral effects of ramipril (R) alone or in combination with isosorbide dinitrate (ISDN) compared to ISDN or placebo.Study designPlacebo-controlled double-blind parallel group trial.Methods32 patients with coronary artery disease (CAD) received placebo, R5mg, ISDN 20mg slow release b.i.d. or R+ISDN for one week. A 24 hour kinetic profile of ramipril and its metabolite, of ace activity (ACE-A) and of related hormones (renin and aldosterone), of endothelin and of prostaglandins (PG), thromboxane B2 (TXB2), PGF2a, 6-keto PGF1a, the stable metabolite of prostacyclin (PGI2-M) was studied after the first dose. Measurements were repeated after 8 days of treatment before and 3 hours after the morning dose.ResultsHormone measurements are presented as means of percent difference of patients treated with R (n=16) vs. those without ace-inhibitor (n=16).Time (hrs)0123468240–83–8Ramipril (mg/l)08543210.417Ramiprilat (mg/l)0611108751214ACE-A (%)-6-78-95-98-98-97-96-80-82-98Aldosteron (%)9-5-31-34-21-27-23-34--Renin (%)-9-771913175332--Endothelin (%)-17-13-25-19-16-15-40--TXB2 (%)41045-5012-3PGF2a (%)101700-8-22-9PGI2-M (%)70-38--59-1-713-=not done; significant differences are printed in italics (two-tailed t-test)A single oral dose of 5mg R reduced ACE activity (p<0.001), decreased aldosterone and increased renin (p<0.1). R did not influence plasma levels of the vasoconstricting (TXB2, PGF2a) or vasodilating (PGI2-M) eicosanoid mediators, but decreased endothelin (p<0.1).ConclusionR, in a dose that results in significant systemic inhibition of the renin angiotensin aldosteron system, does not induce measurable changes of circulating eicosanoid concentrations, but seems to diminish systemic release of endothelin

Polygenic and major-locus contributions to sexual maturation timing in Atlantic salmon

Sexual maturation timing is a life-history trait central to the balance between mortality and reproduction. Maturation may be triggered when an underlying compound trait, called liability, exceeds a threshold. In many different species and especially fishes, this liability is approximated by growth and body condition. However, environmental vs. genetic contributions either directly or via growth and body condition to maturation timing remain unclear. Uncertainty exists also because the maturation process can reverse this causality and itself affect growth and body condition. In addition, disentangling the contributions of polygenic and major loci can be important. In many fishes, males mature before females, enabling the study of associations between male maturation and maturation-unbiased female liability traits. Using 40 Atlantic salmon families, longitudinal common-garden experimentation, and quantitative genetic analyses, we disentangled environmental from polygenic and major locus (vgll3) effects on male maturation, and sex-specific growth and condition. We detected polygenic heritabilities for maturation, growth, and body condition, and vgll3 effects on maturation and body condition but not on growth. Longitudinal patterns for sex-specific phenotypic liability, and for genetic variances and correlations between sexes suggested that early growth and condition indeed positively affected maturation initiation. However, towards spawning time, causality appeared reversed for males whereby maturation affected growth negatively and condition positively via both the environmental and genetic effects. Altogether, the results indicate that growth and condition are useful traits to study liability for maturation initiation, but only until maturation alters their expression, and that vgll3 contributes to maturation initiation via condition.Peer reviewe

Maturation in Atlantic salmon (Salmo salar, Salmonidae) : a synthesis of ecological, genetic, and molecular processes

Over the past decades, Atlantic salmon (Salmo salar, Salmonidae) has emerged as a model system for sexual maturation research, owing to the high diversity of life history strategies, knowledge of trait genetic architecture, and their high economic value. The aim of this synthesis is to summarize the current state of knowledge concerning maturation in Atlantic salmon, outline knowledge gaps, and provide a roadmap for future work. We summarize the current state of knowledge: 1) maturation in Atlantic salmon takes place over the entire life cycle, starting as early as embryo development, 2) variation in the timing of maturation promotes diversity in life history strategies, 3) ecological and genetic factors influence maturation, 4) maturation processes are sex-specific and may have fitness consequences for each sex, 5) genomic studies have identified large-effect loci that influence maturation, 6) the brain-pituitary-gonadal axis regulates molecular and physiological processes of maturation, 7) maturation is a key component of fisheries, aquaculture, conservation, and management, and 8) climate change, fishing pressure, and other anthropogenic stressors likely have major effects on salmon maturation. In the future, maturation research should focus on a broader diversity of life history stages, including early embryonic development, the marine phase and return migration. We recommend studies combining ecological and genetic approaches will help disentangle the relative contributions of effects in different life history stages to maturation. Functional validation of large-effect loci should reveal how these genes influence maturation. Finally, continued research in maturation will improve our predictions concerning how salmon may adapt to fisheries, climate change, and other future challenges.Peer reviewe

Surface Nano-structured Coating for Improved Performance of Axial Piston Pumps

The work starts from the consideration that most of the power losses in a hydraulic pump is due to frictional losses made by the relative motion between moving parts. This fact is particularly true at low operating velocities, when the hydraulic lift effect must be able to maintain a minimum clearance in meatus to limit the volumetric losses. The potential of structured coatings at nanoscale, with super-hydrophobic and oleophobic characteristics, has never been exploited before in an industrial application. The work studies the potential application of nano-coating on piston slippers surface in a real industrial case. The aim is to develop a new industrial solution to increase the energetic efficiency of hydraulic pump used in earthmoving machines. The proposed solution is investigated using a dedicated test bench, designed to reproduce real working conditions of the pump. The results showa reduction of friction coefficient while changing working pressure and rotation velocity

Interfering with Glycolysis Causes Sir2-Dependent Hyper-Recombination of Saccharomyces cerevisiae Plasmids

Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is a key metabolic regulator implicated in a variety of cellular processes. It functions as a glycolytic enzyme, a protein kinase, and a metabolic switch under oxidative stress. Its enzymatic inactivation causes a major shift in the primary carbohydrate flux. Furthermore, the protein is implicated in regulating transcription, ER-to-Golgi transport, and apoptosis. We found that Saccharomyces cerevisiae cells null for all GAPDH paralogues (Tdh1, Tdh2, and Tdh3) survived the counter-selection of a GAPDH–encoding plasmid when the NAD+ metabolizing deacetylase Sir2 was overexpressed. This phenotype required a fully functional copy of SIR2 and resulted from hyper-recombination between S. cerevisiae plasmids. In the wild-type background, GAPDH overexpression increased the plasmid recombination rate in a growth-condition dependent manner. We conclude that GAPDH influences yeast episome stability via Sir2 and propose a model for the interplay of Sir2, GAPDH, and the glycolytic flux

Incorporation of enzyme concentrations into FBA and identification of optimal metabolic pathways

<p>Abstract</p> <p>Background</p> <p>In the present article, we propose a method for determining optimal metabolic pathways in terms of the level of concentration of the enzymes catalyzing various reactions in the entire metabolic network. The method, first of all, generates data on reaction fluxes in a pathway based on steady state condition. A set of constraints is formulated incorporating weighting coefficients corresponding to concentration of enzymes catalyzing reactions in the pathway. Finally, the rate of yield of the target metabolite, starting with a given substrate, is maximized in order to identify an optimal pathway through these weighting coefficients.</p> <p>Results</p> <p>The effectiveness of the present method is demonstrated on two synthetic systems existing in the literature, two pentose phosphate, two glycolytic pathways, core carbon metabolism and a large network of carotenoid biosynthesis pathway of various organisms belonging to different phylogeny. A comparative study with the existing extreme pathway analysis also forms a part of this investigation. Biological relevance and validation of the results are provided. Finally, the impact of the method on metabolic engineering is explained with a few examples.</p> <p>Conclusions</p> <p>The method may be viewed as determining an optimal set of enzymes that is required to get an optimal metabolic pathway. Although it is a simple one, it has been able to identify a carotenoid biosynthesis pathway and the optimal pathway of core carbon metabolic network that is closer to some earlier investigations than that obtained by the extreme pathway analysis. Moreover, the present method has identified correctly optimal pathways for pentose phosphate and glycolytic pathways. It has been mentioned using some examples how the method can suitably be used in the context of metabolic engineering.</p