Hydrogen Evolution on Pyrolytic Graphite

The hydrogen evolution reaction from acid solutions was studied on highly oriented pyrolytic graphite at different surfaces obtained by cutting graphite under the various angles in respect to the basal plane. The experiments were done galvanostatically on the polished samples of desired orientation, in a cell which enabled the pretreatment of graphite at 1000° C in argon and use of prepurified Na2S04 + H2S04 solutions. Tafel lines with 2 RT/F slopes were obtained in all the experiments with i 0 varying from ca 10-9A/cm2 for cleavage plane to ca 10-8A/cm~ for edge plane. The transients show the considerable pseudo-capacitances of 250--500 μF/cm2 being larger at more negative potentials and edge surfaces. The experimental data are consistent with the slow discharge - electrochemical desorption mechanism with the limited number of sites of H adsorption but also with the coupled discharge - recombination reaction for hydrogen evolution

MEA Component Durability

Membrane electrode assembly (MEA) lifetime of greater than 40,000 hours remains a goal of the fuel cell industry. However, there is a lack of fundamental understanding of the mechanisms of MEA degradation. Specifically, the relationship between component physical property changes and MEA performance decay has not been established. We report preliminary data relating changes in gas diffusion layer (GDL) physical properties to fuel cell performance decay

Caveolin-1 and Altered Neuregulin Signaling Contribute to the Pathophysiological Progression of Diabetic Peripheral Neuropathy

Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.OBJECTIVE Evaluate if Erb B2 activation and the loss of caveolin-1 (Cav1) contribute to the pathophysiological progression of diabetic peripheral neuropathy (DPN). RESEARCH DESIGN AND METHODS Cav1 knockout and wild-type C57BL/6 mice were rendered diabetic with streptozotocin, and changes in motor nerve conduction velocity (MNCV), mechanical and thermal hypoalgesia, Erb B2 phosphorylation (pErb B2), and epidermal nerve fiber density were assessed. The contribution of Erb B2 to DPN was assessed using the Erb B2 inhibitors PKI 166 and erlotinib and a conditional bitransgenic mouse that expressed a constitutively active form of Erb B2 in myelinated Schwann cells (SCs). RESULTS Diabetic mice exhibited decreased MNCV and mechanical and thermal sensitivity, but the extent of these deficits was more severe in diabetic Cav1 knockout mice. Diabetes increased pErb B2 levels in both genotypes, but the absence of Cav1 correlated with a greater increase in pErb B2. Erb B2 activation contributed to the mechanical hypoalgesia and MNCV deficits in both diabetic genotypes because treatment with erlotinib or PKI 166 improved these indexes of DPN. Similarly, induction of a constitutively active Erb B2 in myelinated SCs was sufficient to decrease MNCV and induce a mechanical hypoalgesia in the absence of diabetes. CONCLUSIONS Increased Erb B2 activity contributes to specific indexes of DPN, and Cav1 may be an endogenous regulator of Erb B2 signaling. Altered Erb B2 signaling is a novel mechanism that contributes to SC dysfunction in diabetes, and inhibiting Erb B2 may ameliorate deficits of tactile sensitivity in DPN. Diabetic peripheral neuropathy (DPN) is a common complication of diabetes (1). Although hyperglycemia is the definitive cause of DPN (2), the vascular, glial, and neuronal damage that underlies the progressive axonopathy in DPN has a complex biochemical etiology involving oxidative stress (3,4), protein glycation (5), protein kinase C activation (6), polyol synthesis (7), and the hexosamine pathway (8). Altered neurotrophic support also contributes to sensory neuron dysfunction in DPN (9), but whether diabetes may alter growth factor signaling in Schwann cells (SCs), which also undergo substantial degeneration in diabetes, is poorly defined. Neuregulins are growth factors that control SC growth, survival, and differentiation via their interaction with Erb B receptors (10). Although Erb B2 signaling promotes developmental myelination and is clearly trophic for SCs, pharmacological evidence supports that pathologic activation of Erb B2 after axotomy (11) or infection with leprosy bacilli (12) is sufficient to induce SC dedifferentiation and demyelination. Additionally, genetic evidence supports that Erb B2 can promote the development of sensory neuropathies independent of diabetes because expression of a dominant-negative Erb B4 in nonmyelinating (13) or myelinating (14) SCs induced a temperature or mechanical sensory neuropathy, respectively. Given the contribution of Erb B2 to the degeneration of SCs, endogenous proteins that regulate Erb B2 activity may influence the development of certain aspects of sensory neuropathies. The interaction of Erb B2 with the protein caveolin-1 (Cav1) inhibits the intrinsic tyrosine kinase activity of the receptor (15). Cav1 is highly expressed in mature, myelinated SCs (16), and we have shown that prolonged hyperglycemia promoted the downregulation of Cav1 in SCs of sciatic nerve (17). Cav1 may regulate Erb B2 signaling in SCs because its forced downregulation was sufficient to enhance neuregulin-induced demyelination of SC–dorsal root ganglion (DRG) neuron cocultures (18). However, it is unknown whether an increase in Erb B2 activity may contribute to the pathophysiological development of DPN and if changes in Cav1 expression may alter Erb B2 activation in diabetic nerve. In the current study, we demonstrate that diabetic Cav1 knockout mice showed an increased activation of Erb B2 and developed greater motor nerve conduction velocity (MNCV) deficits relative to their wild-type counterparts. Inhibition of Erb B2 with two structurally diverse inhibitors corrected the MNCV deficits and mechanical hypoalgesia evident after 6 or 15 weeks of diabetes. Also, induction of a constitutively active Erb B2 in myelinated SCs of adult mice was sufficient to recapitulate the MNCV and mechanical sensitivity deficits observed in the diabetic mice. These studies provide the first evidence that activation of Erb B2 contributes to deficits associated with myelinated fiber function in diabetic nerve and suggest that Cav1 may serve as an endogenous regulator of Erb B2.This work was supported by grants from the Juvenile Diabetes Research Foundation and the National Institutes of Health (NS-054847 and DK-073594)

Copper corrosion in irradiated environments: The influence of H{sub 2}O{sub 2}on the electrochemistry of copper dissolution in HCl electrolyte

The anodic dissolution of copper was examined in deaerated, 0.1 M HCl aqueous solution in the presence of H{sub 2}O{sub 2}. Concentrations of H{sub 2}O{sub 2} up to 0.2 M were studied at a rotating copper disk-platinum ring electrode. The open circuit potential (OCP) of copper was found to depend on both peroxide concentration and rotation rate. The OCP shifts towards more positive values with increasing H{sub 2}O{sub 2} concentration (C) and decreasing rotation rate. The current-voltage curves for anodic dissolution of copper were also influenced by the presence of peroxide. The curves recorded with the potential scanned in the positive direction showed the expected 60 mV slope, but the reverse scans showed significant departures. At a given potential scan rate, hysteresis was observed which was larger for higher H{sub 2}O{sub 2} concentrations, lower rotation rates, and more positive anodic potential limits. Monitoring the cuprous ions at the outer Pt ring revealed that there was a complex set of events taking place at the copper surface, including film formation and the appearance of cupric ions. 13 refs., 7 figs

The effect of faradaic processes on the resonance of electrochemical cells

Electrolytic cells consisting of mercury electrodes immersed into pure aqueous sulphuric acid solution (ideally polarizable electrodes) and in the one containing Ti3+/Ti4+ redox couple (presence of a faradaic process) were shown to resonate with an induction coil connected in series when a.c. of appropriate frequency is applied across the circuit. The parameters of this faradaic resonance, ωr (resonance frequency) and Ar (amplification factor at resonance) depend on the properties of the system such as the concentration of the redox couple and the electrode potential, as well as on the amplitude of the applied a.c. Higher harmonics have been detected even with the lowest applied amplitude (1 mV). A detailed theoretical consideration has been given to the expected resonance properties of an electrode based on purely activation controlled electrode process as well as of the one in which some diffusional effects become significant, for overpotential changes in the linear domain. This was done in an attempt to assess the value of faradaic resonance measurements for studying kinetic properties of electrochemical cells

Photoelectrochemical microscopy of oxide films on metals: Ti/TiO2 interface

Thin electrochemically grown oxide films on polycrystalline titanium substrates were examined by photoelectrochemical and electron diffraction techniques. Photoelectrochemical microscopy, based on illumination by a focused laser beam, was used to measure the local photoresponse of the oxide films. For oxide films grown slowly (1 nm/h)if, by ramping the electrode potential at 0.1 mV/s, the oxide photoresponse was found to map the grain structure of the underlying substrate. As the oxide growth rate was increased the photoresponse became more homogeneous and the average photocurrent decreased. The photoresponse heterogeneities were associated with variations in the structure of the oxide film. Electron diffraction studies showed that for slowly grown films, an ordered oxide structure was present with a preferential growth direction of [110] occurring on some substrate grains. As the oxide growth rate was increased the film structure became more homogeneous and the average oxide crystalline size decreased. The decrease in oxide crystallinity with increase in oxide growth rate was also observed in photospectroscopy measurements as a loss of the 3.7 eV direct bandgap. For all oxide films studied here, rutile was the only identifiable phase

Local film thickness and photoresponse of thin anodic TiO2 films on polycrystalline titanium

Auger depth profiling was used to determine the local film thickness of a thin anodic oxide grown on a polycrystalline Ti substrate. The oxide thickness was studied as a function of substrate crystallography and final growth voltage. These results were related to local photocurrent measurements obtained using photoelectrochemical microscopy. Variations in the film thickness are too small to account for the non-uniform photocurrent response. The non-uniform photoresponse is instead attributed to variations in the defect density of the oxid