Superconducting imprint of magnetic textures in ferromagnets with perpendicular magnetic anisotropy.

Research on proximity effects in superconductor/ferromagnetic hybrids has most often focused on how superconducting properties are affected-and can be controlled-by the effects of the ferromagnet's exchange or magnetic fringe fields. The opposite, namely the possibility to craft, tailor and stabilize the magnetic texture in a ferromagnet by exploiting superconducting effects, has been more seldom explored. Here we show that the magnetic flux trapped in high-temperature superconducting YBa2Cu3O7-δ microstructures can be used to modify the magnetic reversal of a hard ferromagnet-a cobalt/platinum multilayer with perpendicular magnetic anisotropy-and to imprint unusual magnetic domain distributions in a controlled manner via the magnetic field history. The domain distributions imprinted in the superconducting state remain stable, in absence of an external magnetic field, even after increasing the temperature well above the superconducting critical temperature, at variance to what has been observed for soft ferromagnets with in-plane magnetic anisotropy. This opens the possibility of having non-trivial magnetic configuration textures at room temperature after being tailored below the superconducting transition temperature. The observed effects are well explained by micromagnetic simulations that demonstrate the role played by the magnetic field from the superconductor on the nucleation, propagation, and stabilization of magnetic domains.

Hepatic injury associated with amineptine therapy.

Cases are reported of two patients in whom acute hepatitis and cholestatic jaundice were induced by a tricyclic antidepressant, amineptine. A 29-year old woman received amineptine for 10 days before the onset of acute hepatitis. Slight jaundice and pruritus were preceded by fever, nausea and anorexia. The case is documented by a rapid return to normality of the liver function tests after amineptine was discontinued. We also report the case of a 55-year old woman to whom amineptine was administered for 4 weeks: she was admitted to our Department due to a 14-day history of pruritus and painless jaundice. Histological examination, in this case showed marked cholestasis without inflammatory infiltration. After suspending the treatment, it took 3 weeks for the liver function tests to return to normal. These observations, and the features of the cases published in the literature, suggest that amineptine can produce a wide spectrum of liver injuries, in different patients, taking the form of hepatocellular necrosis, cholestasis or a combination of both.

Role of gluconeogenesis from amino acids in determining fasting and absorptive levels of plasma ammonia in cirrhosis.

The aim of this study was to evaluate the contribution of gluconeogenesis from amino acids in the development of fasting and absorptive hyperammonemia in cirrhosis. Somatostatin (SRIF), which is known to inhibit the hepatic disposal of gluconeogenic amino acids, was administered in a continuous infusion (500 micrograms/h) for 90 min before and 5 h after a protein meal (240 g of meat) in 11 overnight fasting patients. Plasma glucagon, insulin, gluconeogenic amino acids (GAA: alanine, serine, glycine, and threonine) and ammonia (NH3) were evaluated before the infusion, immediately before, and at 1, 3, and 5 h after the meal. As control study, the same protocol was randomly repeated in a different day with saline infusion. During the latter, a direct correlation was found between fasting glucagon and ammonia (r = 0.68; p less than 0.05). Fasting glucagon, insulin, and NH3 did not change, whereas alanine (p less than 0.05) and the GAA sum decreased (p less than 0.01). When SRIF was infused, fasting glucagon (p less than 0.05), insulin (p less than 0.05), and NH3 (p less than 0.05) decreased. Alanine did not change, and GAA sum increased (p less than 0.02). No correlations were found by plotting changes in glucagon or GAA sum and NH3. After the meal, SRIF infusion abolished the plasma response of glucagon and markedly reduced that of insulin, so that their area under the curve (AUC0-5) were reduced (p less than 0.005, for both), with respect to control study. Moreover, the AUC0-5 of alanine (p less than 0.005) and GAA sum (p less than 0.005) were increased, suggesting a reduced disposal of these compounds. In spite of this, the meal-induced early increase and the AUC0-5 of plasma NH3 observed during SRIF and saline infusion did not differ. Our results do not confirm the importance of gluconeogenesis from alpha-amino-nitrogens in determining the fasting ammonemia of cirrhosis, and suggest that this metabolic pathway does not significantly influence the protein meal-induced exacerbation of plasma ammonia.