The objective was to evaluate the influence of the timing of hormonal induction, using gonadorelin or common carp pituitary extract (CPE), on the reproductive activity of female Astyanax bimaculatus. Fish (N = 44) were weighed, measured, and acclimatized to experimental conditions with a photoperiod of 12 h:12 h light:dark (L:D) for 10 days. Ovulation was induced with a single dose of CPE (6 mg/kg) or gonadorelin (80 μg/kg), given at 12:00 (halfway through the light phase (LP) or 24:00 (halfway through the dark phase (DP), in a 2 × 2 factorial design. The time of ovulation was calculated in degree hours and daily motor activity was recorded using a photocell. The fish were killed and the liver and gonads were weighed for calculation of gonadosomatic (GSI) and hepatosomatic (HSI) indexes, respectively. Absolute fecundity (AF), absolute fecundity relative to weight (AFRW) and length (AFRL), diameter of oocytes (mM), and percentage of oocytes with the germinal vesicle in a peripheral position (PPGV) were recorded. All females responded (ovulated). The female Astyanax bimaculatus had twilight motor activity rhythm. Females given CPE at 12:00 had a higher (P < 0.05) percentage of oocytes with the germinal vesicle in a peripheral position compared with the group that received gonadorelin in the same period (95 ± 6 vs. 79 ± 21%, mean ± SD). The absolute fecundity relative to weight was higher in groups induced at 12:00, regardless of the hormone used (LP: 805 ± 448 and 700 ± 214, for CPE and gonadorelin, respectively; dark phase: 580 ± 396 and 529 ± 105, P < 0.05). Both times used for hormonal induction with CPE and gonadorelin were suitable for inducing reproduction in lambari, although induction with CPE in LP had the best results.

Influence of nutritional status, hormones serum levels, and family history on breast cancer development

No abstract

No abstract

RESUMENLa enfermedad de Gaucher constituye una enfermedad lisosomal hereditaria que tiene su origen en un defecto a nivel del gen que codifica el enzima betaglucosidasa ácida, cuya deficiencia condiciona la acumulación de glucocerebrósidos en los lisosomas de macrófagos, causando las manifestaciones clínicas del cuadro. En el niño la forma más frecuente es la tipo 2 o variante neuropática, caracterizada por la presencia de visceromegalias, trastornos hematológicos y alteraciones óseas estructurales. A menudo, presenta mal pronóstico, especialmente cuando sólo se disponía de la esplenectomía y trasplante de medula ósea como únicas terapias. Representa la primera enfermedad en la que se ha utilizado terapia enzimática sustitutiva demostrando su seguridad y eficacia durante la última década, permitiendo mejorar la calidad de vida de los pacientes y disminuyendo su morbimortalidad. El objetivo de este trabajo ha sido mostrar una revisión actualizada acerca de la fisiopatología, diagnóstico y manejo clínico-terapéutico de este complejo proceso. Palabras clave. Enfermedad de Gaucher, Niño. ABSTRACT Gaucher's disease and its clinical management in the pediatric patientGaucher disease is an inherited lysosomal disease whose origin lies in a defect at the level of the gene encoding the enzyme acid betaglucosidasa, which deficiency affects the accumulation of glucocerebroside in lysosomes of macrophages, causing the clinical manifestations of the table In children, the most common form is type 2 or neuropathic variant characterized by the presence of visceromegalies, hematological disorders and structural bone changes. Often presents a poor prognosis, especially when they were available splenectomy and bone marrow transplantation as the only therapies. It represents the first disease in which enzyme replacement therapy has been used to demonstrate safety and efficacy over the last decade, enabling improved patients' quality of life and decreasing their morbidity and mortality. The aim of this study was to show an updated review about the pathophysiology, diagnosis and clinical management -treatment of this complex process.