22 research outputs found

    Repeated evolution of limblessness and digging heads in worm lizards revealed by DNA from old bones.

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    The evolutionary relationships of the burrowing amphisbaenians ('worm lizards') have long been controversial for several reasons: the rarity of museum specimens available for study, highly derived morphological conditions that can confound comparative studies and difficulty in obtaining tissues for molecular phylogenetic studies because of their secretive habits in the wild. We present a phylogenetic analysis of two nuclear genes obtained from both fresh tissues and museum specimens of worm lizards. We achieved sufficient taxonomic sampling for analysis by extracting DNA from museum specimens using a modified forensics protocol. Results show the limbless Rhineuridae to be the most basal lineage, whereas the limbed Bipedidae occupy a more derived position as the sister-taxon to a Trogonophidae-Amphisbaenidae clade. This pattern of relationships indicates widespread morphological convergence within the group, including three independent incidences of limb loss. Convergence in skull shape and scalation is also prevalent. Mosaic evolution in the skull versus postcranial skeleton parallels that seen in snake evolution

    Recovery rates of bottlenose dolphin (\u3ci\u3eTursiops truncatus\u3c/i\u3e) carcasses estimated from stranding and survival rate data

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    Recovery of cetacean carcasses provides data on levels of human-caused mortality, but represents only a minimum count of impacts. Counts of stranded carcasses are negatively biased by factors that include at-sea scavenging, sinking, drift away from land, stranding in locations where detection is unlikely, and natural removal from beaches due to wave and tidal action prior to detection. We estimate the fraction of carcasses recovered for a population of coastal bottlenose dolphins (Tursiops truncatus), using abundance and survival rate data to estimate annual deaths in the population. Observed stranding numbers are compared to expected deaths to estimate the fraction of carcasses recovered. For the California coastal population of bottlenose dolphins, we estimate the fraction of carcasses recovered to be 0.25 (95% CI = 0.20– 0.33). During a 12 yr period, 327 animals (95% CI = 253–413) were expected to have died and been available for recovery, but only 83 carcasses attributed to this population were documented. Given the coastal habits of California coastal bottlenose dolphins, it is likely that carcass recovery rates of this population greatly exceed recovery rates of more pelagic dolphin species in the region

    Ethanol elevates physiological all-trans-retinoic acid levels in select loci through altering retinoid metabolism in multiple loci: a potential mechanism of ethanol toxicity

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    All-trans-retinoic acid (atRA) supports embryonic development, central nervous system function, and the immune response. atRA initiates neurogenesis and dendritic growth in the hippocampus and is required for spatial memory; superphysiological atRA inhibits neurogenesis, causes teratology and/or embryo toxicity, and alters cognitive function and behavior. Because abnormal atRA shares pathological conditions with alcoholism, inhibition of retinol (vitamin A) activation into atRA has been credited widely as a mechanism of ethanol toxicity. Here, we analyze the effects of ethanol on retinoid concentrations in vivo during normal vitamin A nutriture, using sensitive and analytically robust assays. Ethanol either increased or had no effect on atRA, regardless of changes in retinol and retinyl esters. Acute ethanol (3.5 g/kg) increased atRA in adult hippocampus (1.6-fold), liver (2.4-fold), and testis (1.5-fold). Feeding dams a liquid diet with 6.5% ethanol from embryonic day 13 (e13) to e19 increased atRA in fetal hippocampus (up to 20-fold) and cortex (up to 50-fold), depending on blood alcohol content. One-month feeding of the 6.5% ethanol diet increased atRA in adult hippocampus (20-fold), cortex (2-fold), testis (2-fold), and serum (10-fold). Tissue-specific increases in retinoid dehydrogenase mRNAs and activities, extrahepatic retinol concentrations, and atRA catabolism combined to produce site-specific effects. Because a sustained increase in atRA has deleterious effects on the central nervous system and embryo development, these data suggest that superphysiological atRA contributes to ethanol pathological conditions, including cognitive dysfunction and fetal alcohol syndrome.—Kane, M. A., Folias, A. E., Wang, C., Napoli, J. L. Ethanol elevates physiological all-trans-retinoic acid levels in select loci through altering retinoid metabolism in multiple loci: a potential mechanism of ethanol toxicity
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