Spontaneous Oxidation of Ni Nanoclusters on MgO Monolayers Induced by Segregation of Interfacial Oxygen.

We report the study of Ni nanoclusters deposited on MgO/Ag(100) ultrathin films (one monolayer) at T = 200 K. We show by STM analysis and DFT calculations that in the limit of low Ni coverage the formation of nanoclusters of four to six atoms occurs and that these aggregates are flat rather than 3D, as expected for Ni tetramers, pentamers, or hexamers. Both the shape of the clusters and the interatomic distance between neighboring Ni atoms are indicative that the nanoparticles do not consist of pure metal atoms but that a NiyOx structure has formed thanks to the availability of atomic oxygen accumulated at the MgO/Ag interface, with Ni clusters acting as oxygen pumps. Besides being of relevance in view of the use of metal nanoclusters in catalysis and other applications, this finding gives a further proof of the peculiar behavior of ultrathin oxide films.

Positive inotropic effects of an ACTH analogue (ACTH 1-17) on myocardial performance.

The aim of the present investigation was to study the effects of a single 100-micrograms i.v. administration of the synthetic heptadecapeptide [beta-Ala1-Lys17]ACTH1-17-4-amino-N-butylamide (ACTH 1-17) on the left ventricular performance. The systolic time intervals (STI) were recorded in 20 healthy adult young subjects (10 treated with ACTH 1-17 and 10 receiving placebo) before as well as 20, 40, 60 and 80 min after the i.v. ACTH 1-17 or placebo infusion. The STI were recorded immediately after blood withdrawal for measuring cortisol, aldosterone, adrenaline and noradrenaline plasma levels. A highly significant statistical difference was demonstrated for preejection period (PEP) and preejection period/left ventricular ejection time (PEP/LVET) ratio between subjects treated with ACTH 1-17 and subjects receiving placebo. As expected, a significant increase of cortisol and aldosterone plasma levels was observed in subjects treated with ACTH 1-17. The difference of adrenaline and noradrenaline plasma levels was statistically highly significant between subjects treated with ACTH 1-17 and those receiving placebo. The lack of increase in PEP and PEP/LVET ratio recorded in subjects treated with ACTH 1-17 is consistent with an increased left ventricular contractile performance. An increased plasma catecholamine release is postulated as the mechanism of this improvement.

Evaluation of valproic acid fluoroimmunoassay and comparison with a gas liquid chromatographic method.

A method for monitoring valproic acid in serum with a fluoroimmunoassay is described. The evaluation was performed with run-to-run and within-run reproducibility, dilution, and recovery tests. The interferences of hemoglobin, bilirubin, and triglycerides were checked, and a comparison with a gas liquid chromatographic method was also performed. The between-run and within-run coefficients of variation were less than 5.2 and 2.6%, respectively. The method gave satisfactory results in dilution tests and a high correlation with a gas liquid chromatographic method (r = 0.98). The percentage of recovery was greater than 97%. No interference from hemolysis, bilirubin, or triglycerides was observed. The accuracy and simplicity of this method make it suitable for routine laboratory use.

Plasma catecholamines assay: comparison between fluorimetric and radioenzymatic methods.

Plasma catecholamines were simultaneously measured in duplicate plasma samples by the fluorimetric method of Renzini et al. (1970) Clin. Chim. Acta 39, 587-594) and by the radioenzymatic method of Da Prada & Zurcher ((1976) Life Sci. 19, 1161-1174). The correlation of noradrenaline and adrenaline plasma concentrations determined by the two methods were, respectively, r = 0.95 (p less than 0.001) and r = 0.75 (p less than 0.01). The fluorimetric method was less sensitive, but more economical and less time-consuming than the radioenzymatic method. The fluorimetric method is still of value for measuring plasma catecholamines in man.

Interrelationships between blood pressure, blood gases and plasma acetate concentrations during conventional hemodialysis.

To determine to what extent the intradialysis changes in blood pressure (BP) are related to the variations in blood gases and plasma acetate concentrations (plAc), 11 dialysed uremics were studied with measurement of plAc,pH, pCO2 and pO2 every 60' during a hemodialysis lasting 4 hrs. Dialysis resulted in significant decreases in the BP, pO2 and pCO2 and in significant increases in pH and plAc. Multiple regression analysis demonstrated that the delta % for the mean BP was closely related to plAc, pCO2 and delta-% of body weight (BW). Partial regression coefficient indicated the following rank order of correlation: plAc greater than pCO2 greater than or equal to delta-% BW greater than pO2 = O, thus demonstrating that the fall in blood pressure is related both to the increase in plAc and the decrease in pCO2. The physiological relevance of these relationships is discussed. The hypothesis is advanced that the pCO2 decrease during dialysis might contribute to the acetate-induced vascular instability.

[Effect of pretreatment with atenolol and propranolol on sympatho-adrenal and cardiovascular responses to acute insulin-induced hypoglycaemia in the hypertensive patient]. / Effetti del pretrattamento con atenololo o propranolol sulla risposta simpatosurrenalica e cardiovascolare all'ipoglicemia insulinica acuta nel paziente iperteso.

Plasma catecholamines and cardiovascular responses to acute insulin i.v. injection (0.12 U.I. per Kg of body weight) have been studied in eight patients with mild essential hypertension. The hypoglycaemia test was carried out before and after a week of atenolol treatment. In six patients the test was also repeated after propranolol treatment. Following insulin injection, blood sugar fell abruptly with a nadir at 30 m, diastolic blood pressure decreased, and systolic blood pressure and heart rate rose significantly. Atenolol treatment abolished almost completely these hemodynamic changes. By contrast, propranolol caused an increase in both systolic and diastolic blood pressures, leaving the heart rate unmodified. During hypoglycaemia, plasma adrenaline rose sharply in coincidence with the glycaemic nadir and declined thereafter during the glycaemic recovery. Plasma noradrenaline rose less markedly than adrenaline, but the increments were significant after 30 and 60 m. Neither atenolol, nor propranolol affected significantly these changes in plasma catecholamine concentration. These data indicate that beta-blockers do not alter the hypoglycaemia-induced adrenomedullary release of catecholamines. We conclude therefore that beta-blockers modify the pattern of the hemodynamic response to acute hypoglycaemia by interfering with the peripheral effects of circulating catecholamines in a way which depends on the degree of beta-1 selectivity of the drug used.