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This work was supported by United States Department of Agriculture (USDA) grants # 2008-51106-19463, 2012-36100-03618, and 2011-67012-30725. (Casey Cazer, 27 January 2014)

This work was supported by United States Department of Agriculture (USDA) grants # 2008-51106-19463, 2012-36100-03618, and 2011-67012-30725. read full comment

Comment on: Cazer et al. BMC Veterinary Research, 9:234

2 new papers using this technique (Markus Horning, 15 February 2012)

Predation on Steller sea lions detected by life-long implants: in PLoS ONE:
http://dx.plos.org/10.1371/journal.pone.0030173
and in Endang. Spec. Research:
http://www.int-res.com/abstracts/esr/v10/p135-143/ read full comment

Comment on: Horning et al. BMC Veterinary Research, 4:51

Incomplete antecedent reference impacting on claims (Malcolm Banks, 14 July 2010)

Thus is a useful piece of work that updates our knowledge on BoHV-1 prevalence in SW UK cattle herds. However, it is a real shame that the authors, for whatever reason, failed to consider the data in, or make any reference to the BoHV-1 antibody survey of 341 herds across England and Wales described by Paton et al (1998) [cf. only 114 herds confined to the SW of England in this paper]. Paton et al showed a UK prevalence of 69% to BoHV-1 antibodies at herd level, but with significant regional differences. Several of the other conclusions reached by Paton et al (1998) are common to this paper, but importantly, the failure to consider this earlier study, which is effectively another point on a temporal graph of BoHV-1 prevalence in UK cattle, inevitably detracts from the validity and... read full comment

Comment on: Woodbine et al. BMC Veterinary Research, 5:5

Effects of prion infection (Andrew Carmichael, 14 October 2008)

I refer to recent work in Alzheimer's showing that the damage is caused not by protein misfolding but by metabolic changes in the cells defending themselves by entombment of the HSV1 viral attacker in amyloid tangles. It is known that some people and some animals are immune to prion attack because they do not possess the gene PrPc. It seems possible that in those who do have this as PrPc+ or++ gene the cell may have its metabolism changed whilst forming defensive proteins incorporating and neutralising the prion. This may better explain the effects seen in vCJD which resemble a speeded up AD and/or PD. It also adds an interesting dimension to the hunt for other prions as possible causes of neurodegenerative disease. read full comment

Comment on: Jeffrey et al. BMC Veterinary Research, 4:38

Amendments/corrections from authors to "Is equine colic seasonal? Novel application of a model based approach" (Helen Clough, 28 September 2006)

Please note that the authors intended to include the following additional citations in the main manuscript, and, with apologies for any confusion, request that the reader makes the appropriate annotations to the text:Page 2, column 2, lines 2-5 (page 5, lines 8-10 in provisional pdf) should readOne possibility lies in the use of a Poisson distribution to model count data within a framework broadly analogous to that of generalised linear modelling (e.g. [17, 41-42]).On page 7 (page 14 in provisional pdf) there is a discussion of different types of dependence. An important reference in this area (observation versus parameter driven models), cited in [42], is:[51] Cox, D. R. (1981) Statistical analysis of time series, some recent developments. Scandinavian Journal of... read full comment

Comment on: Archer et al. BMC Veterinary Research, 2:27

re-Scrapie infectivity is quickly cleared in tissues of orally-infected farmed fish (Terry Singeltary, 20 June 2006)

>>>However, a few recipient mice were positive for PrPSc and spongiform lesions in the brain. We also showed a specific binding of PrPSc to the mucosal side of fish intestine in the absence of an active uptake of the prion protein through the intestinal wall. <<<WOULD this not be further evidence to show that the rendering of such product after ingesting TSE tainted product, would further expose species that consume such product, i.e. even if the fish do not contract a TSE, could not the intestines and the feed that may still be there further expose species eating those by-products ??? read full comment

Comment on: Ingrosso et al. BMC Veterinary Research, 2:21