Relevant bibliographies by topics / Feral ferrets

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  1. Journal articles
  2. Dissertations / Theses
  3. Conference papers

Academic literature on the topic 'Feral ferrets'

Author: Grafiati
Published: 4 June 2021
Last updated: 19 February 2022

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Journal articles on the topic "Feral ferrets"

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Caley, Peter, L. M. McElrea, and Jim Hone. "Mortality rates of feral ferrets (Mustela furo) in New Zealand." Wildlife Research 29, no. 4 (2002): 323. http://dx.doi.org/10.1071/wr02004.

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Life-table data from feral ferret populations in New Zealand were analysed to estimate their mortality rates, and to test for any additive effect of Mycobacterium bovis infection on observed mortality rates. The observed instantaneous mortality rate was best estimated by modelling mortality as a 2-phase step model with different rates for juveniles (μ1 = 1.45 year–1, 95% C.I. 1.2–1.7 year–1) and adults (μ2 = 0.55 year–1, 95% C.I. 0.4–0.9 year–1). This corresponds to a survival probability of 0.25 during the first year of life, rising to 0.55 year–1 thereafter, and a life expectancy of 0.95 years. At a population level, no additional mortality due to M. bovis infection was observed, suggesting either that the rate of disease-induced mortality was negligible, or that it was compensatory with natural mortality.
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Medina‐Vogel, G., G. J. Hickling, and B. K. Clapperton. "Assessing spatial activity in captive feral ferrets,Mustela furoL. (Camivora: Mustelidae)." New Zealand Journal of Zoology 27, no. 2 (January 2000): 75–83. http://dx.doi.org/10.1080/03014223.2000.9518213.

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Byrom, Andrea E. "Dispersal and survival of juvenile feral ferrets Mustela furo in New Zealand." Journal of Applied Ecology 39, no. 1 (February 2002): 67–78. http://dx.doi.org/10.1046/j.1365-2664.2002.00689.x.

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Caley, P., J. Hone, and PE Cowan. "The relationship between prevalence ofMycobacterium bovisinfection in feral ferrets and possum abundance." New Zealand Veterinary Journal 49, no. 5 (October 2001): 195–200. http://dx.doi.org/10.1080/00480169.2001.36232.

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Henning, J., P. R. Davies, and J. Meers. "Seropositivity to rabbit haemorrhagic disease virus in non-target mammals during periods of viral activity in a population of wild rabbits in New Zealand." Wildlife Research 33, no. 4 (2006): 305. http://dx.doi.org/10.1071/wr03061.

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As part of a longitudinal study of the epidemiology of rabbit haemorrhagic disease virus (RHDV) in New Zealand, serum samples were obtained from trapped feral animals that may have consumed European rabbit (Oryctolagus cuniculus) carcasses (non-target species). During a 21-month period when RHDV infection was monitored in a defined wild rabbit population, 16 feral house cats (Felis catus), 11 stoats (Mustela erminea), four ferrets (Mustela furo) and 126 hedgehogs (Erinaceus europaeus) were incidentally captured in the rabbit traps. The proportions of samples that were seropositive to RHDV were 38% for cats, 18% for stoats, 25% for ferrets and 4% for hedgehogs. Seropositive non-target species were trapped in April 2000, in the absence of an overt epidemic of rabbit haemorrhagic disease (RHD) in the rabbit population, but evidence of recent infection in rabbits was shown. Seropositive non-target species were found up to 2.5 months before and 1 month after this RHDV activity in wild rabbits was detected. Seropositive predators were also trapped on the site between 1 and 4.5 months after a dramatic RHD epidemic in February 2001. This study has shown that high antibody titres can be found in non-target species when there is no overt evidence of RHDV infection in the rabbit population, although a temporal relationship could not be assessed statistically owning to the small sample sizes. Predators and scavengers might be able to contribute to localised spread of RHDV through their movements.
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Ogilvie, Shaun C., and Charles T. Eason. "Evaluation of iophenoxic acid and rhodamine B for marking feral ferrets(Mustela furo)." New Zealand Journal of Zoology 25, no. 2 (January 1998): 105–8. http://dx.doi.org/10.1080/03014223.1998.9518142.

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Gillies, Craig, and Matthew Brady. "Trialling monitoring methods for feral cats, ferrets and rodents in the Whangamarino wetland." New Zealand Journal of Zoology 45, no. 3 (July 3, 2018): 192–212. http://dx.doi.org/10.1080/03014223.2017.1418756.

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Byrom, AE, P. Caley, BM Paterson, and G. Nugent. "Feral ferrets (Mustela furo) as hosts and sentinels of tuberculosis in New Zealand." New Zealand Veterinary Journal 63, sup1 (March 10, 2015): 42–53. http://dx.doi.org/10.1080/00480169.2014.981314.

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Alterio, Nic. "Secondary poisoning of stoats (Mustela erminea), feral ferrets (Mustela furo),and feral house cats (Felis catus) by the anticoagulant poison, brodifacoum." New Zealand Journal of Zoology 23, no. 4 (January 1996): 331–38. http://dx.doi.org/10.1080/03014223.1996.9518092.

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Smith, G. P., J. R. Ragg, H. Moller, and K. A. Waldrup. "Diet of feral ferrets (Mustela furo) from pastoral habitats in Otago and Southland, New Zealand." New Zealand Journal of Zoology 22, no. 4 (January 1995): 363–69. http://dx.doi.org/10.1080/03014223.1995.9518054.

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Dissertations / Theses on the topic "Feral ferrets"

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Morley, Craig Gordon. "The ecology and behaviour of feral ferrets (Mustela furo) in Canterbury farmland, New Zealand." Thesis, University of Canterbury. Zoology, 1999. http://hdl.handle.net/10092/5824.

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Ferret (Mustela furo) control programs, especially those attempting to prevent the spread of Mycobacterium bovis (Tb), would greatly benefit from practical knowledge of ferret ecology and behaviour. This study had two main objectives: firstly, to investigate ferret ecology by examining ferret abundance, survival, trapping success, and diet; and, secondly, to investigate ferret behaviour and activity patterns by using an acoustically sensitive transmitter system (ASTS). Abundance and survival estimates of ferrets tagged with passive integrated transponders (PITs), showed a marked seasonal variation, and despite ferrets being controlled on one site, data from both sites showed that lagomorph numbers increased exponentially. A trapping success model (GLIM) showed that factors such as vegetation cover, rabbit sign, and animal tracks positively influenced capture rates. Although GPS technology provided accurate trap location data, trapping success also benefited from understanding the distribution signs of both predators and prey. GPS data further contributed to GIS models of animal movements, home range and site fidelity. As a result, trapping success was found to be affected by periods of low ferret abundance, fluctuations in trappability and possibly excess prey. It was found that, even though cats and ferrets use different hunting strategies, lagomorphs were their staple prey in North Canterbury. Unlike overseas habitats, New Zealand farmland lacks alternative suitable prey and this may explain the narrow diet of both predators. Even with the large increase in lagomorph numbers seen in North Canterbury in the second year of study, the diets of both predators remained the same, suggesting that these predators are unable to regulate lagomorphs once their numbers cross a certain threshold. By using ASTS technology to examine ferret behaviour and activity it was possible to identify a wider range of behaviours than previously documented using conventional radio tracking techniques. Despite using only one ferret, it was not only possible to document the time of an activity period, the length of each behaviour, as well as seasonal changes in activity, but also behaviours rarely recorded by researchers using more conventional techniques. Generally the ferret displayed an ultradian activity pattern, disputing the accepted nocturnal hypothesis. One implication for ferret control programs using baited traps was a documented decrease in eating behaviour during the breeding seasons. Nevertheless, this study provided as many questions as it did answers; however, with technology such as ASTS, further information about the behaviour and ecology of ferrets could advance future ferret control programs.
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Caley, Peter, and n/a. "Inference on the host status of feral ferrets (Mustela furo) in New Zealand for Mycobacterium bovis infection." University of Canberra. Resource, Environment & Heritage Studies, 2001. http://erl.canberra.edu.au./public/adt-AUC20050621.140940.

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This thesis is about making inference on the host status of feral ferrets in New Zealand for Mycobacterium bovis, the aetiological agent of bovine tuberculosis. The central question addressed is whether the rate of intra-specific transmission of M. bovis among ferrets is sufficient for the disease to persist in ferret populations in the absence of external, non-ferret sources of infection (inter-specific transmission). The question is tackled in three parts�firstly using model selection to identify suitable models for estimating the force of M. bovis infection in ferret populations; secondly applying statistical hypothesis testing to the results of planned manipulative field experiments to test the relationship between M. bovis infection in brushtail possums and that in ferrets; and thirdly using modelling to estimate intra-specific disease transmission rates and the basic reproductive rate (Ro) of M. bovis infection in ferrets. The model selection approach clearly identified the hypothesis of oral infection related to diet was, as modelled by a constant force of infection from the age of weaning, the best approximation of how M. bovis infection was transmitted to ferrets. No other form of transmission (e.g., during fighting, mating, or routine social interaction) was supported in comparison. The force of infection (λ) ranged from 0.14 yr-1 to 5.77 yr-1, and was significantly higher (2.2 times) in male than female ferrets. Statistical hypothesis testing revealed transmission of M. bovis to ferrets occurred from both brushtail possums and ferrets. The force of M. bovis infection in ferrets was reduced by 88% (λ=0.3 yr-1 vs. λ=2.5 yr-1) at sites with reductions in the population density of sympatric brushtail possum populations. A smaller decline in the force of infection resulting from the lethal cross-sectional sampling of the ferret populations was also demonstrated. The modelling approach estimated the basic reproductive rate (Ro) of M. bovis infection in ferrets in New Zealand to vary from 0.17 at the lowest population density (0.5 km-2) recorded to 1.6 at the highest population density (3.4 km-2) recorded. The estimates of Ro were moderately imprecise, with a coefficient of variation of 76%. Despite this imprecision, the Ro for M. bovis infection in ferrets was significantly less than unity for all North Island sites surveyed. Hence it is inferred ferrets are spillover hosts (0Kt), the rate of intra-specific transmission of M. bovis among ferrets is sufficient for the disease to establish in ferrets in the absence of interspecific transmission. In these areas, ferrets would be considered maintenance hosts for the disease. Active management (e.g., density reduction or vaccination) of ferrets would be required to eradicate M. bovis from ferret populations in these areas, in addition to the elimination of sources of inter-specific transmission, particularly brushtail possums.
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Paul, Arco P. "Overexpression of Serum Response Factor in Astrocytes Improves Neuronal Plasticity in a Model of Fetal Alcohol Spectrum Disorders." VCU Scholars Compass, 2012. http://scholarscompass.vcu.edu/etd/307.

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Neuronal plasticity deficits underlie many of the neurobehavioral problems seen in Fetal Alcohol Spectrum Disorders (FASD). Recently, we showed that third trimester alcohol exposure lead to a persistent disruption in ocular dominance (OD) plasticity. For instance, few days of monocular deprivation results in a robust reduction of cortical regions responsive to the deprived eye in normal animals, but not in ferrets exposed early to alcohol. This plasticity deficit can be reversed if alcohol-exposed animals are treated with a phosphodiesterase type 1 (PDE1) inhibitor during the period of monocular deprivation. PDE1 inhibition can increase cAMP and cGMP levels, activating transcription factors such as the cAMP response element binding protein (CREB) and the Serum response factor (SRF). SRF is important for many plasticity processes such as LTP, LTD, spine motility and axonal pathfinding. Here we attempt to rescue OD plasticity in alcohol-treated ferrets using a Sindbis viral vector to express a constitutively active form of SRF during the period of monocular deprivation. Using optical imaging of intrinsic signals and single unit recordings we observed that overexpression of a constitutively active form of SRF (Sindbis SRF+), but neither its dominant negative (SRF-) nor GFP, restored OD plasticity in alcohol-treated animals. Surprisingly, this restoration was observed throughout the extent of the primary visual cortex and most cells infected by the virus were positive for GFAP rather than NeuN. Hence, we further tested whether overexpression of SRF exclusively in astrocytes is sufficient to restore OD plasticity in alcohol-exposed ferrets. To accomplish that, first we exposed cultured astrocytes to the SRF+, SRF- or control GFP viruses. After 24h, these astrocytes were implanted in the visual cortex of alcohol-exposed animals or saline controls one day before MD. Optical imaging of intrinsic signals showed that alcohol-exposed animals that were implanted with astrocytes expressing SRF, but not SRF- or GFP, showed robust restoration of OD plasticity in all visual cortex. These findings suggest that overexpression of SRF exclusively in astrocytes can improve neuronal plasticity in FASD.
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Conference papers on the topic "Feral ferrets"

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Singh, S. K., and H. Ishiwara. "Bismuth ferrite Thin Films for Advanced FeRAM Devices." In 2005 International Conference on Solid State Devices and Materials. The Japan Society of Applied Physics, 2005. http://dx.doi.org/10.7567/ssdm.2005.h-8-3.

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Knutsen, Andrew K., Jason E. Hill, Jeffrey J. Neil, Terrie E. Inder, and Philip V. Bayly. "Quantification of Cortical Surface Convolution in the Developing Ferret and Human Infant." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-205716.

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The human cerebral cortex undergoes folding from the 5th fetal month into the first post-natal year. Disturbances of folding have serious and lasting consequences, but the mechanism is not well understood. Van Essen [1] has hypothesized that axonal tension between strongly interconnected regions draws them together and induces outward folds. However, no direct measurements have confirmed this theory. As measures of shape, cortical curvature and sulcal depth changes during development can help provide insight into underlying mechanisms of growth.
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Knutsen, Andrew K., Christopher D. Kroenke, Larry A. Taber, Jeffrey J. Neil, and Philip V. Bayly. "MRI Measurement of Surface Strain Due to Growth in the Developing Ferret Brain." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176010.

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The human cerebral cortex undergoes folding from the 5th fetal month into the first post-natal year. Disturbances of folding have serious and lasting consequences, but the mechanism is not well understood. Van Essen [1] has hypothesized that axonal tension between strongly interconnected regions draws them together and induces outward folds. However, no direct measurements have confirmed this theory. Experimental data are needed, beginning with a quantitative description of the kinematics of cortical growth during folding.
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