3,654 research outputs found

    River Otter in Arkansas: I. Distribution and Harvest Trends

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    River otter (Lutra canadensis) management in Arkansas is hampered by a lack of information on population parameters. This initial study on the biology of Arkansas river otter is concerned with present distribution and harvest trends. Otter occur throughout Arkansas, except in the upper Ozark region. A distributional shift, apparently along the Arkansas River, has led to an increase in otter harvest in the Ouachita Mountain region. A dramatic increase in otter harvest over the past four years (1976-1979) is attributable, in part, to a pelt price increase. Additionally, nuisance level beaver (Castor canadensis) populations and an extended trapping season for beaver may have influenced the otter harvest

    River Otter in Arkansas: II. Indications of a Beaver-Facilitated Commensal Relationship

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    Dam building activities of beaver (Castor canadensis) create ponds that apparently augment habitat available to otter (Lutra canadensis). This paper considers possible effects of beaver activity and pond formation on distribution and populations of otter in Arkansas. Literature synthesis and analysis of harvest records were used to investigate the suspected relationship

    River Otter in Arkansas. IV. Winter Food Habits in Eastern Arkansas

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    Stomachs and intestines of 89 river otters (Lutra canadensis) collected in eastern Arkansas during the trapping seasons (December- January) of 1978-1983 were examined for food remains. Fish (primarily centrarchids, catostomids, and clupeids) dominated the diet (71.2%). The next most abundant prey was crayfish (18.3% of the diet). Other foods included gray squirrel (Sciurus carolinensis), wood duck (Aixsponsa), snakes (Thamnophis proximus), frogs (Ranidae and Hylidae), and beetles (Coleoptera)

    Rodenticidal Effects of Zinc Phosphide and Strychnine of Nontarget Species

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    When three rodenticide treatments—zinc phosphide (prebaited) and strychnine (both with and without prebait)were evaluated, zinc phosphide was the most effective in reducing active burrows of prairie dogs; but, it also resulted in a reduction in deer mouse densities. One month after treatment, counts of fecal pellets of eastern cottontails were greater on areas treated with strychnine without prebait than on sites treated with zinc phosphide. Eight months after treatment, no differences could be detected among rodenticides for either leporid. Horned lark densities were reduced 61% on sites treated with strychnine only

    Rodenticidal Effects of Zinc Phosphide and Strychnine of Nontarget Species

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    When three rodenticide treatments—zinc phosphide (prebaited) and strychnine (both with and without prebait)were evaluated, zinc phosphide was the most effective in reducing active burrows of prairie dogs; but, it also resulted in a reduction in deer mouse densities. One month after treatment, counts of fecal pellets of eastern cottontails were greater on areas treated with strychnine without prebait than on sites treated with zinc phosphide. Eight months after treatment, no differences could be detected among rodenticides for either leporid. Horned lark densities were reduced 61% on sites treated with strychnine only

    Effects of Noise Exposure on the Vestibular System: A Systematic Review

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    Despite our understanding of the impact of noise-induced damage to the auditory system, much less is known about the impact of noise exposure on the vestibular system. In this article, we review the anatomical, physiological, and functional evidence for noise-induced damage to peripheral and central vestibular structures. Morphological studies in several animal models have demonstrated cellular damage throughout the peripheral vestibular system and particularly in the otolith organs; however, there is a paucity of data on the effect of noise exposure on human vestibular end organs. Physiological studies have corroborated morphological studies by demonstrating disruption across vestibular pathways with otolith-mediated pathways impacted more than semicircular canal-mediated pathways. Similar to the temporary threshold shifts observed in the auditory system, physiological studies in animals have suggested a capacity for recovery following noise-induced vestibular damage. Human studies have demonstrated that diminished sacculo-collic responses are related to the severity of noise-induced hearing loss, and dose-dependent vestibular deficits following noise exposure have been corroborated in animal models. Further work is needed to better understand the physiological and functional consequences of noise-induced vestibular impairment in animals and humans

    Interleukin-17 Stimulates C-Reactive Protein Expression in Hepatocytes and Smooth Muscle Cells via p38 MAPK and ERK1/2-Dependent NF-κB and C/EBPβ Activation

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    Elevated systemic levels of the acute phase C-reactive protein (CRP) are predictors of future cardiovascular events. There is evidence that CRP may also play a direct role in atherogenesis. Here we determined whether the proinflammatory interleukin (IL)-17 stimulates CRP expression in hepatocytes (Hep3B cell line and primary hepatocytes) and coronary artery smooth muscle cells (CASMC). Our results demonstrate that IL-17 potently induces CRP expression in Hep3B cells independent of IL-1β and IL-6. IL-17 induced CRP promoter-driven reporter gene activity that could be attenuated by dominant negative IκBα or C/EBPβ knockdown and stimulated both NF-κB and C/EBP DNA binding and reporter gene activities. Targeting NF-κB and C/EBPβ activation by pharmacological inhibitors, small interfering RNA interference and adenoviral transduction of dominant negative expression vectors blocked IL-17-mediated CRP induction. Overexpression of wild type p50, p65, and C/EBPβ stimulated CRP transcription. IL-17 stimulated p38 MAPK and ERK1/2 activation, and SB203580 and PD98059 blunted IL-17-mediated NF-κB and C/EBP activation and CRP transcription. These results, confirmed in primary human hepatocytes and CASMC, demonstrate for the first time that IL-17 is a potent inducer of CRP expression via p38 MAPK and ERK1/2-dependent NF-κB and C/EBPβ activation and suggest that IL-17 may mediate chronic inflammation, atherosclerosis, and thrombosis
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