Nucleation and growth of the electrodeposited iron layers in the presence of an external magnetic field

The effect of an uniform magnetic field with a flux density up to 1 T and different configurations relative to the electrode surface on the electrocrystallization of Fe on polycrystalline Au(1 1 1) from acidic sulphate electrolyte has been investigated. It was found, irrespective of the applied parameters, that the deposition proceeds through successive nucleation and growth steps. The first one related to 2D growth was followed by a second nucleation and 3D diffusion controlled growth. At potential of −1500 and −1550 mV_MSE nucleation proceeds via a progressive mode, while at −1650 mV_MSE it follows an instantaneous mode. A strong influence of the parallel-to-electrode magnetic field on the nucleation processes was found for the progressive mode, which leads to the increase of the growth rate and as a consequence to retardation of the nucleation rate of the 3D step. Additionally, in this configuration at a sufficiently high magnetic flux density a third nucleation step could be observed (3D), which was found to be also affected by a magnetic field. No effect of a perpendicular-to-electrode magnetic field on the nucleation has been observed. The effects of a magnetic field on the nucleation and growth processes are discussed with respect to the magnetohydrodynamic effect (MHD) and confirmed by rotating disc electrode (RDE) experiments.     

Chebyshev pseudospectral method of viscous flows with corner singularities

Chebyshev pseudospectral solutions of the biharmonic equation governing two-dimensional Stokes flow within a driven cavity converge poorly in the presence of corner singularities. Subtracting the strongest corner singularity greatly improves the rate of convergence. Compared to the usual stream function/ vorticity formulation, the single fourth-order equation for stream function used here has half the number of coefficients for equivalent spatial resolution and uses a simpler treatment of the boundary conditions. We extend these techniques to small and moderate Reynolds numbers.     

Bilaterally Microstructured Thin Polydimethylsiloxane Film Production

Thin PDMS films with complex microstructures are used in the manufacturing of dielectric electro active polymer (DEAP) actuators, sensors and generators, to protect the metal electrode from large strains and to assure controlled actuation. The current manufacturing process at Danfoss Polypower A/S produces films with a one-sided microstructured surface only. It would be advantageous to produce a film with both surfaces microstructured, as this increases the film’s performance efficiency. The new technique introduced herein produces bilaterally microstructured film by combining an embossing method with the existing manufacturing process. In employing the new technique, films with microstructures on both surfaces are successfully made with two different liquid silicone rubber (LSR) formulations: 1) pure XLR630 and 2) XLR630 with titanium dioxide (TiO₂). The LSR films (～70 µm) are cast on a carrier web substrate using a coating blade. The carrier web, which has a sinusoidal corrugation with wave height of 7 µm and a wave period of 7 µm on its surface, imparts corrugations to the bottom surface of the film. The elastomer film on the carrier web is preheated to the gel point, where the elastomer film can retain an imprint made on it. The preheated film at gel point is embossed between the rolls of a gravure lab coater, which corrugates the top surface of the film. The films are then heated, in order to cure completely. For the LSR systems used in this process, the optimum conditions for preheating are 110°C for 4–7 s, while for embossing the temperature is 110°C with 25 psi pressure between the rolls at a speed of 1.4 rpm. Scanning electron microscope (SEM) images confirm the formation of microstructures on both the surfaces of the film.     

The Chemical Biology of Phosphoinositide 3‐Kinases

Since its discovery in the late 1980s, phosphoinositide 3‐kinase (PI3K), and its isoforms have arguably reached the forefront of signal transduction research. Regulation of this lipid kinase, its functions, its effectors, in short its entire signaling network, has been extensively studied. PI3K inhibitors are frequently used in biochemistry and cell biology. In addition, many pharmaceutical companies have launched drug‐discovery programs to identify modulators of PI3Ks. Despite these efforts and a fairly good knowledge of the PI3K signaling network, we still have only a rudimentary picture of the signaling dynamics of PI3K and its lipid products in space and time. It is therefore essential to create and use novel biological and chemical tools to manipulate the phosphoinositide signaling network with spatial and temporal resolution. In this review, we discuss the current and potential future tools that are available and necessary to unravel the various functions of PI3K and its isoforms.     

Enhanced sensitivity of ubiquinone-deficient mutants of Saccharomyces cerevisiae to products of autoxidized polyunsaturated fatty acids

Coenzyme Q (ubiquinone or Q) plays a well known electron transport function in the respiratory chain, and recent evidence suggests that the reduced form of ubiquinone (QH2) may play a second role as a potent lipid-soluble antioxidant. To probe the function of QH2 as an antioxidant in vivo, we have made use of a Q-deficient strain of Saccharomyces cerevisiae harboring a deletion in the COQ3 gene [Clarke, C. F., Williams, W. & Teruya, J. H. (1991) J. Biol. Chem. 266, 16636-16644]. Q-deficient yeast and the wild-type parental strain were subjected to treatment with polyunsaturated fatty acids, which are prone to autoxidation and breakdown into toxic products. In this study we find that Q-deficient yeast are hypersensitive to the autoxidation products of linolenic acid and other polyunsaturated fatty acids. In contrast, the monounsaturated oleic acid, which is resistant to autoxidative breakdown, has no effect. The hypersensitivity of the coq3delta strains can be prevented by the presence of the COQ3 gene on a single copy plasmid, indicating that the sensitive phenotype results solely from the inability to produce Q. As a result of polyunsaturated fatty acid treatment, there is a marked elevation of lipid hydroperoxides in the coq3 mutant as compared with either wild-type or respiratory-deficient control strains. The hypersensitivity of the Q-deficient mutant can be rescued by the addition of butylated hydroxytoluene, alpha-tocopherol, or trolox, an aqueous soluble vitamin E analog. The results indicate that autoxidation products of polyunsaturated fatty acids mediate the cell killing and that QH2 plays an important role in vivo in protecting eukaryotic cells from these products.     

Ribonuclease A variants with potent cytotoxic activity

Select members of the bovine pancreatic ribonuclease A (RNase A) superfamily are potent cytotoxins. These cytotoxic ribonucleases enter the cytosol, where they degrade cellular RNA and cause cell death. Ribonuclease inhibitor (RI), a cytosolic protein, binds to members of the RNase A superfamily with inhibition constants that span 10 orders of magnitude. Here, we show that the affinity of a ribonuclease for RI plays an integral role in defining the potency of a cytotoxic ribonuclease. RNase A is not cytotoxic and binds RI with high affinity. Onconase, a cytotoxic RNase A homolog, binds RI with low affinity. To disrupt the RI-RNase A interaction, three RNase A residues (Asp-38, Gly-88, and Ala-109) that form multiple contacts with RI were replaced with arginine. Replacing Asp-38 and Ala-109 with an arginine residue has no effect on the RI-RNase interaction. In addition, these variants are not cytotoxic. In contrast, replacing Gly-88 with an arginine residue yields a ribonuclease (G88R RNase A) that retains catalytic activity in the presence of RI and is cytotoxic to a transformed cell line. Replacing Gly-88 with aspartate also yields a ribonuclease (G88D RNase A) with a decreased affinity for RI and cytotoxic activity. The cytotoxic potency of onconase, G88R RNase A, and G88D RNase A correlate with RI evasion. We conclude that ribonucleases that retain catalytic activity in the presence of RI are cytotoxins. This finding portends the development of a class of chemotherapeutic agents based on pancreatic ribonucleases.     

YC-1 potentiates nitric oxide- and carbon monoxide-induced cyclic GMP effects in human platelets

Nitric oxide (NO), the physiological activator of soluble guanylyl cyclase (sGC), induces inhibitory effects on platelet activation via elevation of cGMP levels and stimulation of the cGMP-dependent protein kinase. YC-1, a benzylindazole derivative, was shown to activate sGC in intact platelets, resulting in inhibition of platelet aggregation. In a previous study, we demonstrated that YC-1 not only stimulates purified sGC but also potentiates the stimulatory action of submaximally effective NO and carbon monoxide (CO) concentrations. Here, we investigated the potentiating effect of YC-1 in intact platelets. YC-1 together with NO or CO led to complete inhibition of platelet aggregation at concentrations that were ineffective by themselves. Maximally effective 2, 2-diethyl-1-nitroso-oxyhydrazine (3 microM) and YC-1 (100 microM) concentrations each elevated the cGMP levels in intact platelets approximately 13-fold, and administration of the two drugs together resulted in enormous potentiation of cGMP formation, which greatly exceeded the effect on the purified enzyme and yielded a >1300-fold increase in cGMP levels. Similar results were obtained using CO instead of NO. Furthermore, YC-1 not only stimulated sGC but also inhibited cGMP-hydrolyzing phosphodiesterases in platelets. The enormous elevation of cGMP levels led to enhanced phosphorylation of the cGMP-dependent protein kinase substrate vasodilator-stimulated phosphoprotein. Thus, by the combination of two effects (i.e., potentiation of NO-induced sGC stimulation and phosphodiesterase inhibition), YC-1-like substances are potent activators of the sGC/cGMP pathways and are therefore interesting candidates to act as modulators of cGMP-mediated effects, especially within the cardiovascular system.     

Reference values for height and weight in Prader-Willi syndrome based on 315 patients

The spontaneous growth of 315 patients (109 girls and 208 boys) with Prader-Willi syndrome (PWS) was analysed in a mixed longitudinal and cross-sectional manner. 33 patients were seen in the department between 1970 and 1994; height and weight of 76 patients from Germany were evaluated by means of a questionnaire with detailed measuring instructions, and 206 definite cases were added from the literature. Mean ( SD) length of newborn babies with PWS was 50.2+/-2.8 cm (145 boys) and 48.9 3.3 cm (79 girls). Mean weight at birth was 2945 570 g in boys and 2782+/-594 g in girls. During the 1st year, the children's growth was nearly normal, thereafter short stature was present in approximately 50% of PWS patients. Between 3 and 13 years of age, the 50th percentile for height in PWS is roughly identical with the 3rd percentile in healthy controls. Body weight was normal for all boys and girls during the first 2 years. Thereafter, a rapid weight gain occurred; after an age of 10 years weight-for-height index in nearly all patients exceeded the normal range. The extent of pubertal growth was reduced for the group. Mean adult height was 161.6+/-8.1 cm (23 males) and 150.2+/-5.5 cm (21 females). Head circumference for age was normal for boys and girls. CONCLUSION: Reference data on spontaneous development of growth and weight gain of children with Prader-Willi syndrome are described allowing a better counselling of patients and parents.