0 <= x <= 1.0, prepared by solid state reaction in air. All samples show the ORT-2 orthorhombic structure that suppresses the Jahn-Teller distortion, thus favoring a ferromagnetic (FM) superexchange interaction between Mn3+-O-Mn3+. For x = 0.0 the oxygen excess (y approximate to 0.09) produces vacancies in the

La and Mn sites and generates a fraction around 18% of Mn4+ ions and 82% of the usual Mn3+ ions, with possible double-exchange interaction between them. The Fe doping in this system is known to produce only stable Fe3+ ions. We find an evolution from a fairly strong FM phase with a Curie temperature T-C similar to 160 K, for x = 0.0, to an antiferromagnetic (AFM) phase with T-N = 790 K, for x = 1.0, accompanied by clear signatures of a cluster-glass Selleckchem Quisinostat behavior. For intermediate Fe contents a mixed-phase state occurs, with a gradual decrease (increase) in the FM (AFM) phase, accompanied by a systematic transition broadening for 0.2 < x < 0.7. A model based on the expected exchange interaction among the various magnetic-ion types accounts very well for the saturation magnetization (M-S) dependence on Fe doping. (C) 2009 American Institute of Physics. [DOI: 10.1063/1.3054323]“
“AMH is secreted by immature Sertoli cells (SC) and is responsible

for the regression of Mullerian ducts in the male fetus as part of the sexual differentiation process. AMH is also involved in testicular

development and function. AMHs are at their lowest levels in the first days after birth but increase after the first week, likely reflecting active SC proliferation. AMH rises rapidly AZD2014 in concentration in boys during the first month, reaching a peak level at about 6 months of age, and then slowly declines during childhood, falling to low levels in puberty. Basal and FSH-stimulated levels of AMH, might become a useful predictive marker of the spermatogenic response to gonadotropic treatment in young patients with hypogonadotropic hypogonadism. After puberty, AMH is released preferentially by the apical pole of the SC towards the lumen of the seminiferous tubules, resulting in higher concentrations in the seminal plasma than in the serum. Defects in AMH production and insensitivity MAPK Inhibitor Library concentration to AMH due to receptor defects result in the persistent Mullerian duct syndrome. A measurable value of AMH in a boy with bilateral cryptorchidism is predictive of undescended testes, while an undetectable value is highly suggestive of anorchia or ovaries, as would be the case in girls with female pseudohermaphroditism and pure gonadal dysgenesis. Lower serum AMH concentrations in otherwise healthy boys with cryptorchidism, who were compared with their age-matched counterparts with palpable testes, have been reported previously. AMH levels are higher in prepubertal patients with varicocele than in controls.