Reproductive biology of Haemulon plumierii in the south-western Atlantic Ocean's most extensive reefs: implications for fisheries management.

The reproductive biology of the white grunt Haemulon plumierii was studied from 360 individuals obtained from artisanal fisheries landings in the Abrolhos Bank, Brazil, between August 2010 and March 2012. The overall sex-ratio did not differ significantly from 1:1, although males predominated in larger size classes. ß-Binomial modelling of historical sex-ratio data indicated that the catch rate of females has increased in recent years. Females reached maturity at a smaller total length (LT ; 214 mm) than males (235 mm LT ) and the LT at which 50% of all individuals are mature (L50 ) was 220 mm, corresponding to 41·5% of the maximum recorded LT . Variation in the gonado-somatic index and in the relative frequency of reproductive stages indicates that reproduction occurs year round, with increased activity during the austral spring and summer. Fecundity was not size dependent. The reproductive parameters provided here can support management measures focussed on seasonal closures during spawning peaks (September to November and February to March) and minimum sizes (>L50 ) for the capture of this important artisanal fisheries resource in Abrolhos, the region with the largest and most biodiverse coralline reefs in the South Atlantic Ocean.

Modulation of glutamatergic and GABAergic neurotransmission in glutaryl-CoA dehydrogenase deficiency.

Although the precise mechanisms underlying the CNS degeneration of patients with glutaryl-CoA dehydrogenase (GCDH) deficiency are still the subject of intense debate, many studies have highlighted that excitotoxicity plays a fundamental role in the neuropathology of this disease, particularly involving the N-methyl-D-aspartate receptor subtype of ionotropic glutamate receptors. Modulation of the glutamatergic system by these compounds involves an inhibition of glutamate uptake into synaptosomes and synaptic vesicles, and a decrease in glutamate binding. Furthermore, glutaric and 3-hydroxyglutaric acids inhibit glutamate decarboxylase, the key enzyme of GABA synthesis, and striatal GABAergic medium-spiny neurons are highly vulnerable to 3-hydroxyglutaric acid-induced neurotoxicity. In conclusion, glutaric acid and 3-hydroxyglutaric acid induce an imbalance in glutamatergic and GABAergic neurotransmission.

Plasmodium falciparum: use of a NANP19 antibody-test for the detection of infection in non-immune travellers.

Circumsporozoite (CS) antibodies are a reliable serological marker for the infection of Plasmodium falciparum. The purpose of this investigation was to construct and evaluate an enzyme-linked immunosorbent assay test for the detection of CS antibodies. While the sensitivity of the newly developed test reached 78%, the specificity was 99%. In addition, the optimized kit was used to test for infection with P. falciparum in 1903 travellers that were recruited from a prospective study for malaria chemoprophylaxis. Sixty-six of the 1903 patients (3.5%) showed elevated CS antigen antibody titres. However, seroconversion could only be demonstrated in 18 (0.95%) patients. Among those seroconverting, there was a significantly higher percentage of male travellers (1.28%) than female travellers (0.56%). Positive reactions were more frequent among returnees from West and East Africa (1.49 and 1.14%, respectively) than among those from other endemic areas, e.g. South America (n=0). Despite its limited sensitivity, this newly developed kit for CS antibody testing may be a valuable tool for the estimation of the risk for travellers in malarious regions to acquire an infection with P. falciparum. It may also be useful for the determination of the efficacy of malaria chemoprophylaxis for inhibiting outbreak of disease.

Intrastriatal administration of 3-hydroxyglutaric acid induces convulsions and striatal lesions in rats.

Glutaryl-CoA dehydrogenase deficiency is an inherited neurometabolic disease complicated by precipitation of acute encephalopathic crises during a vulnerable period of brain development. These crises result in bilateral striatal damage and subsequently a dystonic dyskinetic movement disorder. In previous in vitro studies neuronal damage in this disease has been linked to an excitotoxic mechanism mediated in particular by one of the accumulating metabolites, 3-hydroxyglutaric acid. However, nothing is known about the in vivo effects of this organic acid. In the present study, we used a stereotaxic intrastriatal injection technique to investigate the behavioral and neurotoxic effects of 3-hydroxyglutaric acid exposure in rats. Here, we report that 3-hydroxyglutaric acid induced an increase in convulsion frequency and duration as determined by open field measurement. Nissl-stained coronal sections from treated rats revealed a pale lesion in the striatum following 3-hydroxyglutaric acid exposure. N-methyl-D-aspartate (NMDA) receptor blockade by MK-801 and stimulation of GABA(A) receptors by muscimol prevented the induction of convulsions and striatal damage by 3-hydroxyglutaric acid, whereas blockade of non-NMDA receptors by 6,7-dinitroquinoxaline-2,3-dione (DNQX) was not protective. We conclude that 3-hydroxyglutaric acid induces convulsions and striatal damage via initiation of an imbalance in the excitatory glutamatergic and the inhibitory GABAergic neurotransmission, resulting in an enhanced excitatory input in striatal neurons. These results support the hypothesis of NMDA receptor-mediated excitotoxic cell damage in glutaryl-CoA dehydrogenase deficiency and represent the basis for the development of new neuroprotective treatment strategies.

Acute encephalopathy despite early therapy in a patient with homozygosity for E365K in the glutaryl-coenzyme A dehydrogenase gene.

A patient with glutaric aciduria type I had an acute encephalopathic crisis despite early treatment. This report indicates that current therapeutic strategies may be insufficient for some high-risk patients and stresses the demand for new approaches in glutaric aciduria type I.

Tyrosine hydroxylase deficiency with severe clinical course: clinical and biochemical investigations and optimization of therapy.

Tyrosine hydroxylase deficiency was diagnosed after determination of cerebrospinal fluid neurotransmitters and DNA analysis in a child with severe axial hypotonia and hypokinesia associated with dystonic and ballistic movements. L-dopa therapy was unsuccessful, whereas a combination with selegiline, a selective monoamine oxidase-beta inhibitor, with low-dose L-dopa markedly improved the severe clinical picture.

Modelo de Munich para trasplante óseo: infecciones y riesgos inmunológicos de trasplante óseo alogénico / Model of Munich for bone trasplantation infections and immunological risk of allogeneic bone trasplantation

El trasplante alogénico de hueso cortical y espongoso es un tema controvertido en la cirugía traumatológica y ortopédica. El trasplante óseo se realiza sin indicación vital en casi todos los casos; los argumentos biológicos e inmunológicos apoyan el transplantes de material autólogo siempre que esto sea técnicamente posible, el hueso artificial sintético aloplástico no cumple con todos los criterios requeridos para la sustitución de grandes defectos óseos hasta el momento. Aún existe el problema de la estabilidad geométrica y mecánica de estos materiales aloplásticos. Por lo tanto, en algunos casos no existe otra alternativa alotrasplante de fragmentos corticales estables y grandes. Por otra parte hay material aloplásticos sintéticos para la situación ósea que están libres de riesgos inmunológicos e higiénicos. En este contexto el valor de los injertos óseos alogénicos es discutido, considerando especialmente el problema del SIDA. Así, debe exigirse una seguridad higiénica óptima para los receptores de hueso alogénico. Se presentan los aspectos infecciosos y riesgos inmunológicos considerados por "Modelo de Munich" para trasplante óseo. (AU)

Modelo de Munich para trasplante óseo: infecciones y riesgos inmunológicos de trasplante óseo alogénico / Model of Munich for bone trasplantation infections and immunological risk of allogeneic bone trasplantation

El trasplante alogénico de hueso cortical y espongoso es un tema controvertido en la cirugía traumatológica y ortopédica. El trasplante óseo se realiza sin indicación vital en casi todos los casos; los argumentos biológicos e inmunológicos apoyan el transplantes de material autólogo siempre que esto sea técnicamente posible, el hueso artificial sintético aloplástico no cumple con todos los criterios requeridos para la sustitución de grandes defectos óseos hasta el momento. Aún existe el problema de la estabilidad geométrica y mecánica de estos materiales aloplásticos. Por lo tanto, en algunos casos no existe otra alternativa alotrasplante de fragmentos corticales estables y grandes. Por otra parte hay material aloplásticos sintéticos para la situación ósea que están libres de riesgos inmunológicos e higiénicos. En este contexto el valor de los injertos óseos alogénicos es discutido, considerando especialmente el problema del SIDA. Así, debe exigirse una seguridad higiénica óptima para los receptores de hueso alogénico. Se presentan los aspectos infecciosos y riesgos inmunológicos considerados por "Modelo de Munich" para trasplante óseo.

Severe hyperchloriduria-hyperkaliuria: a new congenital renal tubular abnormality?

A female infant, aged 5 weeks, had metabolic alkalosis associated with severe electrolyte disturbances. In addition to findings typically seen in patients with Bartter syndrome or hyperprostaglandin E syndrome, she had massive urinary excretion of prostaglandins E2 and E-M, normal calcium metabolism, hyperphosphaturia, and severe hyperchloriduria and hyperkaliuria with limited response to indomethacin. These findings may represent a new congenital renal tubular abnormality.

Enhanced urinary excretion of leukotriene E4 in patients with mevalonate kinase deficiency.

In patients with mevalonate kinase deficiency, urinary excretion of the leukotriene LTE4 was found to be elevated. A positive linear relationship between increased urinary excretion of mevalonate and LTE4 (n = 5) suggests that increased cysteinyl leukotriene synthesis is involved in the pathomechanisms of this disease.