Contrasting Surface Behavior of Rh (111) and Pt (111) Electrodes

Low energy electron diffraction and voltammetric measurements of the Rh(lll) electrode were conducted and compared with the corresponding surface and electrochemical characteristics of Pt (111). Rhodium is unstable upon exposure to water vapor or liquid water, but retains its well-defined character after immersion to aqueous media. This is reflected in the voltammetric behavior of the clean surface, as well as the manner in which carbon monoxide and iodine are adsorbed from solution. That is, a monolayer of an oxygen-containing species, assembled into (2X2) surface structure, can either be reduced by the voltammetric treatment or replaced by adsorbing solution components without causing system disorder. The voltammetry of the Rh (111) electrode, while exhibiting the main features of several metallic single crystal surfaces, differs significantly from that of platinum electrodes normalized to the same 2D geometry. From the voltam- me\u27ric behavior, it is concluded that adsorption of high energy hydrogen is not taking place on Rh (111). Equally important, the packing density and the surface structure of the Rh(lll) — CO differs from its Pt(lll) — CO analog. While iodine chemisorption from the gas phase leads to the development of several surface structures known from the corresponding platinum work, preferential formation of the_Pt (111) (V3 X V3)R30°—I structure against the Pt(lll)(V7X V7)R19.1°—I was demonstrated. Both electronic and structural factors contribute to the contrasting surface behavior brought to focus in this work

Mitochondrial calcium uniporter complex modulation in cancerogenesis

Aberrations in mitochondrial Ca2+ homeostasis have been associated with different pathological conditions, including neurological defects, cardiovascular diseases, and, in the last years, cancer. With the recent molecular identification of the mitochondrial calcium uniporter (MCU) complex, the channel that allows Ca2+ accumulation into the mitochondrial matrix, alterations in the expression levels or functioning in one or more MCU complex members have been linked to different cancers and cancer-related phenotypes. In this review, we will analyze the role of the uniporter and mitochondrial Ca2+ derangements in modulating cancer cell sensitivity to death, invasiveness, and migratory capacity, as well as cancer progression in vivo. We will also discuss some critical points and contradictory results to highlight the consequence of MCU complex modulation in tumor development

Underpotential deposition of Cu on Au(111) in sulfate-containing electrolytes: a theoretical and experimental study

We study the underpotential deposition of Cu on single-crystal Au(111) electrodes in sulfate-containing electrolytes by a combination of computational statistical-mechanics based lattice-gas modeling and experiments. The experimental methods are in situ cyclic voltammetry and coulometry and ex situ Auger electron spectroscopy and low-energy electron diffraction. The experimentally obtained voltammetric current and charge densities and adsorbate coverages are compared with the predictions of a two-component lattice-gas model for the coadsorption of Cu and sulfate. This model includes effective, lateral interactions out to fourth-nearest neighbors. Using group-theoretical ground-state calculations and Monte Carlo simulations, we estimate effective electrovalences and lateral adsorbate--adsorbate interactions so as to obtain overall agreement with experiments, including both our own and those of other groups. In agreement with earlier work, we find a mixed R3xR3 phase consisting of 2/3 monolayer Cu and 1/3 monolayer sulfate at intermediate electrode potentials, delimited by phase transitions at both higher and lower potentials. Our approach provides estimates of the effective electrovalences and lateral interaction energies, which cannot yet be calculated by first-principles methods.Comment: 36 pages, 14 Postscript figures are in uufiles for

Melatonin as a master regulator of cell death and inflammation: molecular mechanisms and clinical implications for newborn care

Melatonin, more commonly known as the sleep hormone, is mainly secreted by the pineal gland in dark conditions and regulates the circadian rhythm of the organism. Its intrinsic properties, including high cell permeability, the ability to easily cross both the blood–brain and placenta barriers, and its role as an endogenous reservoir of free radical scavengers (with indirect extra activities), confer it beneficial uses as an adjuvant in the biomedical field. Melatonin can exert its effects by acting through specific cellular receptors on the plasma membrane, similar to other hormones, or through receptor-independent mechanisms that involve complex molecular cross talk with other players. There is increasing evidence regarding the extraordinary beneficial effects of melatonin, also via exogenous administration. Here, we summarize molecular pathways in which melatonin is considered a master regulator, with attention to cell death and inflammation mechanisms from basic, translational and clinical points of view in the context of newborn care