Age and growth of Zapteryx brevirostris (Elasmobranchii: Rhinobatidae) in southern Brazil

Age and growth studies are fundamental to successful fisheries management. Zapteryx brevirostris (Muller & Henle, 1841) is distributed off the Brazilian continental shelf and this species is assessed as "Vulnerable" in the Red List of the International Union for the Conservation of Nature (IUCN). Thus, the objective of this study was to present previously unknown information about the age and growth of Z. brevirostris that can be used for its management, conservation, and fisheries. A total of 162 specimens were sampled, with total lengths (TL) varying between 35.7 cm and 56 cm. The vertebrae were embedded in resin, sectioned in cuts with 0.5 mm thickness and the growth bands of the vertebrae were read under a light microscope. In the studied area, Z. brevirostris ages were estimated from 4 to 10 years according to vertebrae patterns. The species reaches its maximum asymptotic size (Linf) around 56 cm (56 cm for females and 50.37 cm for males). This is the first estimate of age and growth for a species of the Zapteryx genus, and the results support the hypothesis that this ray requires future management conservation, particularly due to its slow growth rate and consequent susceptibility to overexploitation.Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES); Portuguese Foundation for Science and Technology (FCT, Fundacao para a Ciencia e Tecnologia) [IF/00253/2014

A prior history of binge-drinking increases sensitivity to the motivational valence of methamphetamine in female C57BL/6J mice.

Methamphetamine (MA) and alcohol use disorders exhibit a high degree of co-morbidity and sequential alcohol-MA mixing increases risk for co-abuse. Recently, we reported greater MA-conditioned reward in male C57BL/6J mice with a prior history of binge alcohol-drinking (14 days of 2-hour access to 5, 10, 20 and 40% alcohol). As female mice tend to binge-drink more alcohol than males and females tend to be more sensitive than males to the psychomotor-activating properties of MA, we first characterized the effects of binge-drinking upon MA-induced place-conditioning (four pairings of 0.25, 0.5, 1, 2, or 4 mg/kg IP) in females and then incorporated our prior data to analyze for sex differences in MA-conditioned reward. Prior binge-drinking history did not significantly affect locomotor hyperactivity or its sensitization in female mice. However, the dose-response function for place-conditioning was shifted to the left of water-drinking controls, indicating an increase in sensitivity to MA-conditioned reward. The examination of sex differences revealed no sex differences in alcohol intake, although females exhibited greater MA-induced locomotor stimulation than males, irrespective of their prior drinking history. No statistically significant sex difference was apparent for the potentiation of MA-conditioned reward produced by prior binge-drinking history. If relevant to humans, these data argue that both males and females with a prior binge-drinking history are similarly vulnerable to MA abuse and it remains to be determined whether or not the neural substrates underpinning this increased vulnerability reflect common or sex-specific adaptations in reward-related brain regions

Gene identification for the cblD defect of vitamin B12 metabolism

Background Vitamin B12 (cobalamin) is an essential cofactor in several metabolic pathways. Intracellular conversion of cobalamin to its two coenzymes, adenosylcobalamin in mitochondria and methylcobalamin in the cytoplasm, is necessary for the homeostasis of methylmalonic acid and homocysteine. Nine defects of intracellular cobalamin metabolism have been defined by means of somatic complementation analysis. One of these defects, the cblD defect, can cause isolated methylmalonic aciduria, isolated homocystinuria, or both. Affected persons present with multisystem clinical abnormalities, including developmental, hematologic, neurologic, and metabolic findings. The gene responsible for the cblD defect has not been identified. Methods We studied seven patients with the cblD defect, and skin fibroblasts from each were investigated in cell culture. Microcell-mediated chromosome transfer and refined genetic mapping were used to localize the responsible gene. This gene was transfected into cblD fibroblasts to test for the rescue of adenosylcobalamin and methylcobalamin synthesis. Results The cblD gene was localized to human chromosome 2q23.2, and a candidate gene, designated MMADHC (methylmalonic aciduria, cblD type, and homocystinuria), was identified in this region. Transfection of wild-type MMADHC rescued the cellular phenotype, and the functional importance of mutant alleles was shown by means of transfection with mutant constructs. The predicted MMADHC protein has sequence homology with a bacterial ATP-binding cassette transporter and contains a putative cobalamin binding motif and a putative mitochondrial targeting sequence. Conclusions Mutations in a gene we designated MMADHC are responsible for the cblD defect in vitamin B12 metabolism. Various mutations are associated with each of the three biochemical phenotypes of the disorder