We analysed the distribution of transposable elements (TEs) in 100 aligned pairs of orthologous intergenic regions from the mouse and human genomes. Within these regions, conserved segments of high similarity between the two species alternate with segments of low similarity. Identifiable TEs comprise 40-60% of segments of low similarity. Within such segments, a particular copy of a TE found in one species has no orthologue in the other. Overall, TEs comprise only approximately 20 % of conserved segments. However, TEs from two families, MIR and L2, are rather common within conserved segments. Statistical analysis of the distributions of TEs suggests that a majority of the MIR and L2 elements present in murine intergenic regions have human orthologues. These elements must have been present in the common ancestor of human and mouse and have remained under substantial negative selection that prevented their divergence beyond recognition. If so, recruitment of MIR- and L2-derived sequences to perform a function that increases host fitness is rather common, with at least two such events per host gene. The central part of the MIR consensus sequence is over-represented in conserved segments given its background frequency in the genome, suggesting that it is under the strongest selective constraint.

Background Full-endoscopic spinal surgery is an evolving technique. A laborious learning phase is inevitable due to the complexity of the orientation and instrumentation. The goal of the present study is to evaluate a single surgeon's learning curve and early outcomes in fullendoscopic resection of lumbar disc herniations. Methods This was a prospective non-controlled single-surgeon cohort study. In 54 patients with 57 herniations, 41 interlaminar and 16 transforaminal resections were performed. Surgery time, severity of adhesive process in the spinal canal, complication rates and clinical outcomes (VAS, ODI, custom questionnaire, recurrence and re-operation rate) were assessed.

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Genetic factors may play an important role in species extinction but their actual effect remains poorly understood, particularly because of a strong and potentially masking effect expected from ecological traits. We investigated the role of genetics in mammal extinction taking both ecological and genetic factors into account. As a proxy for the role of genetics we used the ratio of the rates of nonsynonymous (amino acid changing) to synonymous (leaving the amino acid unchanged) nucleotide substitutions, K a / K s . Because most nonsynonymous substitutions are likely to be slightly deleterious and thus selected against, this ratio is a measure of the inefficiency of selection: if large (but less than 1), it implies a low efficiency of selection against nonsynonymous mutations. As a result, nonsynonymous mutations may accumulate and thus contribute to extinction. As a proxy for the role of ecology we used body mass W, with which most extinction-related ecological traits strongly correlate. As a measure of extinction risk we used species' affiliation with the five levels of extinction threat according to the IUCN Red List of Threatened Species. We calculated K a / K s for mitochondrial protein-coding genes of 211 mammalian species, each of which was characterized by body mass and the level of threat. Using logistic regression analysis, we then constructed a set of logistic regression models of extinction risk on ln(K a / K s ) and lnW. We found that K a / K s and body mass are responsible for a 38% and a 62% increase in extinction risk, respectively. Given that the standard error of these values is 13%, the contribution of genetic factors to extinction risk in mammals is estimated to be one-quarter to one-half of the total of ecological and genetic effects. We conclude that the effect of genetics on extinction is significant, though it is almost certainly smaller than the effect of ecological traits.Mutation provides the material for evolution. However, most mutations that play a role in evolution are slightly deleterious and thus may contribute to extinction. We assess the role of mitochondrial DNA mutations in mammalian extinction risk and find it to be one-quarter to one-half of the total of mutation and body mass effects, where body mass represents an integral measure of extinction-related ecological traits. Genetic factors may be all the more important, because ecological traits associated with large body mass would both promote and protect from extinction, while mutation accumulation caused by low effective population size seems to have no counterbalance. Synthesis