Nutritional condition of elk in Rocky Mountain National Park

We tested the hypothesis that elk in Rocky Mountain National Park (RMNP) were at ecological carrying capacity by determining herd-specific levels of nutritional condition and fecundity. Ingesta-free body fat levels in adult cows that were lactating were 10.6% ( s = 1.7; range = 6.2-15.4) and 7.7% ( s = 0.5; range = 5.9-10.1) in November 2001 for the Horseshoe and Moraine Park herds, respectively. Cows that were not lactating were able to accrue significantly more body fat: 14.0% ( s = 1.1; range = 7.7-19.3) and 11.5% ( s = 0.8; range = 8.6-15.1) for the Horseshoe and Moraine Park herds, respectively. Cow elk lost most of their body fat over winter (April 2002 levels were 3.9% [ s = 0.4] and 2.9% [ s = 0.4] for the Horseshoe and Moraine Park herds, respectively). Nutritional condition indicated that both Horseshoe Park and Moraine Park elk were well below condition levels elk can achieve on very good-excellent nutrition (i.e., > 15% body fat; Cook et al. 2004) and were comparable to other free-ranging elk populations. However, condition levels were higher than those expected at a ""food-limited"" carrying capacity, and a proportion of elk in each herd were able to achieve condition levels indicative of very good-excellent nutrition. Elk in RMNP are likely regulated and/or limited by a complex combination of density-independent (including significant heterogeneity in forage conditions across RMNP's landscape) and density-dependent processes, as condition levels contradict a simple density-dependent model of a population at ecological carrying capacity.     

Dynamic receptive field plasticity in rat spinal cord dorsal horn following C-primary afferent input

The central terminals of cutaneous primary afferent neurons are spatially ordered in the dorsal horn in a highly organized fashion such that a point-to-point map represents the body surface. This afferent terminal somatotopic map correlates with the map of the receptive fields of the cells on which they terminate. The location, size and modality of the cutaneous receptive fields of dorsal horn neurons necessarily depend upon the anatomical presence of afferent nerve fibres which deliver information from the periphery, directly or indirectly, to the cells. However the receptive field size and modality of a cell do not depend only on anatomical connections. Excitatory and inhibitory interneurons, descending influences and facilitations or depressions of synaptic contacts can alter receptive field properties. Here we show that prolonged and substantial cutaneous receptive field changes can be produced by brief inputs from peripheral unmyelinated afferent fibres.     

Evidence for the nonhydrophobic interaction of aromatic,nitrogen-containing compounds with the coenzyme binding site of a NAD-linked D-lactate dehydrogenase

Summary Quantitative structure activity relationships suggest that the binding of quinoline and phenanthroline analogs to D-lactate dehydrogenase from the barnacle,Balanus nubilus Darwin, does not involve primarily hydrophobic effects. This phenomenon appears to exist also for other lactate dehydrogenases.We thank C. Hansch for advice regarding QSAR studies. Supported by U.S.P.H.S. (GM-22868-01) to GLL.     

Analysis of the DNA sequence and duplication history of human chromosome 15

Here we present a finished sequence of human chromosome 15, together with a high-quality gene catalogue. As chromosome 15 is one of seven human chromosomes with a high rate of segmental duplication, we have carried out a detailed analysis of the duplication structure of the chromosome. Segmental duplications in chromosome 15 are largely clustered in two regions, on proximal and distal 15q; the proximal region is notable because recombination among the segmental duplications can result in deletions causing Prader-Willi and Angelman syndromes. Sequence analysis shows that the proximal and distal regions of 15q share extensive ancient similarity. Using a simple approach, we have been able to reconstruct many of the events by which the current duplication structure arose. We find that most of the intrachromosomal duplications seem to share a common ancestry. Finally, we demonstrate that some remaining gaps in the genome sequence are probably due to structural polymorphisms between haplotypes; this may explain a significant fraction of the gaps remaining in the human genome.     

Editing-defective tRNA synthetase causes protein misfolding and neurodegeneration

Misfolded proteins are associated with several pathological conditions including neurodegeneration. Although some of these abnormally folded proteins result from mutations in genes encoding disease-associated proteins (for example, repeat-expansion diseases), more general mechanisms that lead to misfolded proteins in neurons remain largely unknown. Here we demonstrate that low levels of mischarged transfer RNAs (tRNAs) can lead to an intracellular accumulation of misfolded proteins in neurons. These accumulations are accompanied by upregulation of cytoplasmic protein chaperones and by induction of the unfolded protein response. We report that the mouse sticky mutation, which causes cerebellar Purkinje cell loss and ataxia, is a missense mutation in the editing domain of the alanyl-tRNA synthetase gene that compromises the proofreading activity of this enzyme during aminoacylation of tRNAs. These findings demonstrate that disruption of translational fidelity in terminally differentiated neurons leads to the accumulation of misfolded proteins and cell death, and provide a novel mechanism underlying neurodegeneration.