Analysis of genetic structure of the red shrimp Aristeus antennatus from the Western Mediterranean employing two mitochondrial regions.

In this paper we addressed the phylogeographical genetic structure of the economically important red shrimp, Aristeus antennatus (Crustacea, Aristeidae) in the Western Mediterranean. Partial mitochondrial regions of the cytochrome c oxidase subunit I (514 bp) and ribosomal 16S subunit (547 bp) were sequenced in 137 individuals collected at three localities: Catalan Sea, Ligurian Sea and the southern Tyrrhenian Sea. Values of haplotypic diversity were h = 0.552-0.724, whereas those for nucleotide diversity were pi = 0.0012-0.0026. Among-sample genetic diversity was not significant and no geographical patterns in the distribution of haplotypes were apparent. Results of the present study are consistent with a past population expansion that occurred <2,000 years ago. Despite the current fishing pressure, genetic variability appears to be sufficiently high to keep A. antennatus populations stable over time. Dispersal-related life history traits may account for the shallow genetic structure. Our results are not in contrast with the hypothesis of sustainability of Western Mediterranean red shrimp fisheries predicted on the basis of previously obtained biological results.

Hiponatremia por pérdida renal de sal en paciente con diabetes insípida central / Hyponatremia due to renal salt wasting in a patient with partial central diabetes insipidus

La hiponatremia en el contexto de una diabetes insípida suele corresponder a un exceso en el uso de desmopresina; sin embargo, existen otras posibilidades. Se presenta el caso de un lactante de 18 meses, remitido por un cuadro de 2 meses de evolución de poliuria, polidipsia y pérdida ponderal. Los antecedentes, exploración física y exploraciones complementarias, incluida neuroimagen, eran normales, salvo la presencia de una poliuria hiposmolar de 3 litros que, tras dieta seca y administración de hormona antidiurética (ADH), se catalogó de diabetes insípida central parcial. Se inició tratamiento con desmopresina intranasal. Seis meses más tarde, ingresó en UCI por un cuadro de deshidratación hiponatrémica grave (sodio de 108 mEq/L), convulsiones y poliuria con fracción de excreción de sodio de 3 mL/100 mL de filtrado glomerular. Un mes más tarde, presentó otro cuadro similar, por lo que se inició la administración de sal por vía oral. A los cuatro meses, la poliuria-polidipsia mejoró. Ante la mejoría clinicoanalítica, se suspendió el tratamiento. El paciente permanece asintomático un año más tarde. El síndrome cerebral pierde sal se caracteriza por diuresis y natriuresis elevadas, hiponatremia y depleción del espacio extravascular. En su patogénesis, se baraja la acción de distintos péptidos natriuréticos; su desencadenante no es siempre una enfermedad intracraneal. En el caso descrito, se dudó de si se trataba de una verdadera diabetes insípida central parcial transitoria o bien de una polidipsia-poliuria primaria que desarrolló, posteriormente, un síndrome pierde sal por desajuste en el eje ADH-péptidos natriuréticos

Hyponatremia in association with diabetes insipidus usually corresponds to an overdose of desmopressin; nevertheless, there are other possibilities. We present the case of an 18-month-old boy who was referred to us with a 2-month history of polyuria, polydipsia and weight loss. His medical record and the results of physical examination and additional tests, including neuroimaging, were normal, except for the presence of hypo-osmolar polyuria (3 L). After dry diet and the administration of antidiuretic hormone (ADH), he was diagnosed as having partial central diabetes insipidus, and intranasal desmopressin therapy was begun. Six months later, he was admitted to the intensive care unit with severe dehydration associated with hyponatremia (Na: 108 mEq/L), seizures and polyuria, with fractional excretion of sodium of 3 mL/100 mL glomerular filtration rate (GFR). One month later, he presented a similar episode and oral salt supplementation was begun. Four months later, his polyuria and polydipsia had improved. Given the clinical and analytical improvement, the treatment was discontinued and the child remains asymptomatic one year later. Cerebral salt-wasting syndrome is characterized by marked diuresis and natriuresis, in the presence of hyponatremia and depletion of the extravascular space. Its pathogenesis has been attributed to the action of different natriuretic peptides, and it is not always triggered by an intracranial disease. In our case, we questioned whether the patient presented true transient partial central diabetes insipidus or, in contrast, primary polydipsia-polyuria with subsequent development of salt-wasting syndrome due to an imbalance in the ADH-natriuretic peptide axis

[Neuropathological findings in early-onset Alzheimer's disease (E280a-PS1 mutation)]. / Hallazgos neuropatológicos en la enfermedad de Alzheimer de inicio temprano (mutación E280A-PS1).

INTRODUCTION AND MATERIAL: Nine brains belonging to early onset Alzheimer disease (E280A-PS1 mutation) affected individuals from Antioquia, Colombia, were analyzed by neuropathological standard techniques. All individuals were ascertained from genealogies descendents from a common ancestor that shows a dominant autosomical pattern of inheritance. RESULTS: All cases analyzed were carriers to the E280A-PS1 mutation. This type of mutation produce beta-amyloid deposits of 42 aminoacids in the CNS. The mean of onset age was 48.4 years with an average of evolution time of 7.55 years and a mean of death age of 56.55. Although, all the cases showed symmetrical atrophy and them was more severe in the hippocampal region, a definitive anterior pattern (temporo-frontal) was showed. The higher the time of evolution of disease the lower the brain weight. CONCLUSIONS: All types of senile plaques and abundant neurofibrillary tanggles were found. In the stem, similar lesions were found but they were in lower number. Only the mesencephalic region showed a significative positive correlation between the number of senile plaques and the number of neurofibrillary tanggels (p < 0.05, r = 0.76). Only the parietal region showed a significant positive correlation between the number of senile plaques and the disease evolution time (p < 0.02, r = 0.74). Particularly, the cerebellum only showed senile plaques but neurofibrillary degeneration was not observed. With the exception of the Hirano bodies, all findings traditionally described were observed.