RESUMEN
The pattern and scale of the genetic structure of populations provides valuable information for the understanding of the spatial ecology of populations, including the spatial aspects of density fluctuations. In the present paper, the genetic structure of periodically fluctuating lemmings (Dicrostonyx groenlandicus) in the Canadian Arctic was analysed using mitochondrial DNA (mtDNA) control region sequences and four nuclear microsatellite loci. Low genetic variability was found in mtDNA, while microsatellite loci were highly variable in all localities, including localities on isolated small islands. For both genetic markers the genetic differentiation was clear among geographical regions but weaker among localities within regions. Such a pattern implies gene flow within regions. Based on theoretical calculations and population census data from a snap-trapping survey, we argue that the observed genetic variability on small islands and the low level of differentiation among these islands cannot be explained without invoking long distance dispersal of lemmings over the sea ice. Such dispersal is unlikely to occur only during population density peaks.
Asunto(s)
Arvicolinae/genética , Animales , Canadá , ADN Mitocondrial/análisis , ADN Mitocondrial/genética , Interpretación Estadística de Datos , Genética de Población , Haplotipos/genética , Región de Control de Posición/genética , Repeticiones de Microsatélite/genética , Dinámica PoblacionalRESUMEN
Although Apert syndrome has been characterized in the prenatal period and clinically described in the literature, postnatal echoencephalographic findings have not been reported. We present a case of Apert syndrome that shows bilateral periventricular cysts, unusual posterior downward curving of the lateral ventricles without evidence of hydrocephalus, along with a decreased anterior-posterior diameter of the cranial vault. Given that Apert syndrome, characterized by acrocephalosyndactyly, can give rise to numerous CNS abnormalities, echoencephalography could be used to further characterize Apert syndrome in the postnatal period.