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		<title>BMC Veterinary Research - Most viewed articles</title>
		<link>http://www.biomedcentral.com/bmcvetres/mostviewed/</link>
		<description>Most viewed articles in last 30 days from BMC Veterinary Research (ISSN 1746-6148) published by 
				
				BioMed Central
		</description>
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				    <rdf:li rdf:resource="http://www.biomedcentral.com/1746-6148/4/28"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1746-6148/4/32"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1746-6148/4/29"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1746-6148/4/27"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1746-6148/4/31"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1746-6148/2/12"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1746-6148/4/33"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1746-6148/4/22"/>			    
            
				    <rdf:li rdf:resource="http://www.biomedcentral.com/1746-6148/4/30"/>			    
            
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		<item rdf:about="http://www.biomedcentral.com/1746-6148/4/28">
            
            <title>First detection, isolation and molecular characterization of infectious salmon anaemia virus associated with clinical disease in farmed Atlantic salmon (Salmo salar) in Chile</title>
			<description>Background:
Infectious salmon anaemia (ISA) is a viral disease of marine-farmed Atlantic salmon (Salmo salar) caused by ISA virus (ISAV), which belongs to the genus Isavirus, family Orthomyxoviridae. The virus is considered to be carried by marine wild fish and for over 25 years has caused major disease outbreaks in marine-farmed Atlantic salmon in the Northern hemisphere. In the Southern hemisphere, ISAV was first detected in Chile in 1999 in marine-farmed Coho salmon (Oncorhynchus kisutch). In contrast to the classical presentation of ISA in Atlantic salmon, the presence of ISAV in Chile until now has only been associated with a clinical condition called Icterus Syndrome in Coho salmon and virus isolation has not always been possible. During the winter of 2007, unexplained mortalities were registered in market-size Atlantic salmon in a grow-out site located in Chilo&#233; in Region X of Chile. We report here the diagnostic findings of the first significant clinical outbreak of ISA in marine-farmed Atlantic salmon in Chile and the first characterization of the ISAV isolated from the affected fish.
Results:
In mid-June 2007, an Atlantic salmon marine farm site located in central Chilo&#233; Island in Region X of Chile registered a sudden increase in mortality following recovery from an outbreak of Pisciricketsiosis, which rose to a cumulative mortality of 13.6% by harvest time. Based on the clinical signs and lesions in the affected fish, and laboratory tests performed on the fish tissues, a confirmatory diagnosis of ISA was made; the first time ISA in its classical presentation and for the first time affecting farmed Atlantic salmon in Chile. Rapid sequencing of the virus-specific RT-PCR products amplified from the fish tissues identified the virus to belong to the European genotype (Genotype I) of the highly polymorphic region (HPR) group HPR 7b, but with an 11-amino acid insert in the fusion glycoprotein, and ability to cause cytopathic effects (CPE) in CHSE-214 cell line, characteristics which make it distinct from common European Genotype ISAV isolates from Europe and North America.
Conclusion:
In conclusion, the present work constitutes the first report of a case of ISA in farmed Atlantic salmon in Chile. The clinical signs and lesions are consistent with the classical descriptions of the disease in marine-farmed Atlantic salmon in the Northern hemisphere. The outbreak was caused by ISAV of European genotype (or Genotype I) of HPR 7b but distinct from common European Genotype ISAV isolates.</description>
			<link>http://www.biomedcentral.com/1746-6148/4/28</link>		
			<dc:creator>Marcos G Godoy, Alejandra Aedo, Molly JT Kibenge, David B Groman, Carmencita V Yason, Horts Grothusen, Angelica Lisperguer, Marlene Calbucura, Fernando Avenda&#241;o, Marcelo Imil&#225;n, Miguel Jarpa and Frederick SB Kibenge</dc:creator>
			<dc:source>BMC Veterinary Research 2008, 4:28</dc:source>
			<dc:subject>Number of accesses: 826</dc:subject>
			<dc:date>2008-08-04</dc:date>
			<dc:identifier>doi:10.1186/1746-6148-4-28</dc:identifier>
			
			
							
					<prism:publicationName>BMC Veterinary Research</prism:publicationName>
					
			
							
					<prism:issn>1746-6148</prism:issn>
					
			
							
					<prism:volume>4</prism:volume>
					
			
							
					<prism:startingPage>28</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-08-04</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1746-6148/4/32">
            
            <title>Evaluation of prognostic markers for canine mast cell tumors treated with vinblastine and prednisone</title>
			<description>Background:
Canine cutaneous mast cell tumor (MCT) is a common neoplastic disease associated with a variable biologic behavior. Surgery remains the primary treatment for canine MCT; however, radiation therapy (RT) and chemotherapy are commonly used to treat aggressive MCT. The goals of this study were to evaluate the prognostic utility of histologic grade, c-KIT mutations, KIT staining patterns, and the proliferation markers Ki67 and AgNORs in dogs postoperatively treated with vinblastine and prednisone +/- RT, and to compare the outcome of dogs treated with post-operative chemotherapy +/- RT to that of a prognostically matched group treated with surgery alone. Associations between prognostic markers and survival were evaluated. Disease-free intervals (DFI) and overall survival times (OS) of dogs with similar pretreatment prognostic indices postoperatively treated with chemotherapy were compared to dogs treated with surgery alone.
Results:
Histologic grade 3 MCTs, MCTs with c-KIT mutations, MCTs with increased cytoplasmic KIT, and MCTs with increased Ki67 and AgNOR values were associated with decreased DFI and OS. Dogs with histologic grade 3 MCT had significantly increased DFI and OS when treated with chemotherapy vs. surgery alone. Although not statistically significant due to small sample sizes, MCTs with c-KIT mutations had increased DFI and OS when treated with chemotherapy vs. surgery alone.Conclusion and clinical importanceThis study confirms the prognostic value of histologic grade, c-KIT mutations, KIT staining patterns, and proliferation analyses for canine MCT. Additionally, the results of this study further define the benefit of postoperative vinblastine and prednisone for histologic grade 3 MCTs.</description>
			<link>http://www.biomedcentral.com/1746-6148/4/32</link>		
			<dc:creator>Joshua D Webster, Vilma Yuzbasiyan-Gurkan, Douglas H Thamm, Elizabeth Hamilton and Matti Kiupel</dc:creator>
			<dc:source>BMC Veterinary Research 2008, 4:32</dc:source>
			<dc:subject>Number of accesses: 480</dc:subject>
			<dc:date>2008-08-13</dc:date>
			<dc:identifier>doi:10.1186/1746-6148-4-32</dc:identifier>
			
			
							
					<prism:publicationName>BMC Veterinary Research</prism:publicationName>
					
			
							
					<prism:issn>1746-6148</prism:issn>
					
			
							
					<prism:volume>4</prism:volume>
					
			
							
					<prism:startingPage>32</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-08-13</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1746-6148/4/29">
            
            <title>Gene expression profiles in liver of pigs with extreme high and low levels of androstenone</title>
			<description>Background:
Boar taint is the unpleasant odour and flavour of the meat of uncastrated male pigs that is primarily caused by high levels of androstenone and skatole in adipose tissue. Androstenone is a steroid and its levels are mainly genetically determined. Studies on androstenone metabolism have, however, focused on a limited number of genes. Identification of additional genes influencing levels of androstenone may facilitate implementation of marker assisted breeding practices. In this study, microarrays were used to identify differentially expressed genes and pathways related to androstenone metabolism in the liver from boars with extreme levels of androstenone in adipose tissue. 
Results:
Liver tissue samples from 58 boars of the two breeds Duroc and Norwegian Landrace, 29 with extreme high and 29 with extreme low levels of androstenone, were selected from more than 2500 individuals. The samples were hybridised to porcine cDNA microarrays and the 1 % most significant differentially expressed genes were considered significant. Among the differentially expressed genes were metabolic phase I related genes belonging to the cytochrome P450 family and the flavin-containing monooxygenase FMO1. Additionally, phase II conjugation genes including UDP-glucuronosyltransferases UGT1A5, UGT2A1 and UGT2B15, sulfotransferase STE, N-acetyltransferase NAT12 and glutathione S-transferase were identified. Phase I and phase II metabolic reactions increase the water solubility of steroids and play a key role in their elimination. Differential expression was also found for genes encoding 17beta-hydroxysteroid dehydrogenases (HSD17B2, HSD17B4, HSD17B11 and HSD17B13) and plasma proteins alpha-1-acid glycoprotein (AGP) and orosomucoid (ORM1). 17beta-hydroxysteroid dehydrogenases and plasma proteins regulate the availability of steroids by controlling the amount of active steroids accessible to receptors and available for metabolism. Differences in the expression of FMO1, NAT12, HSD17B2 and HSD17B13 were verified by quantitative real competitive PCR.
Conclusions:
A number of genes and pathways related to metabolism of androstenone in liver were identified, including new candidate genes involved in phase I oxidation metabolism, phase II conjugation metabolism, and regulation of steroid availability. The study is a first step towards a deeper understanding of enzymes and regulators involved in pathways of androstenone metabolism and may ultimately lead to the discovery of markers to reduce boar taint.</description>
			<link>http://www.biomedcentral.com/1746-6148/4/29</link>		
			<dc:creator>Maren Moe, Sigbjorn Lien, Christian Bendixen, Jakob Hedegaard, Henrik Hornshoj, Ingunn Berget, Theo HE Meuwissen and Eli Grindflek</dc:creator>
			<dc:source>BMC Veterinary Research 2008, 4:29</dc:source>
			<dc:subject>Number of accesses: 412</dc:subject>
			<dc:date>2008-08-06</dc:date>
			<dc:identifier>doi:10.1186/1746-6148-4-29</dc:identifier>
			
			
							
					<prism:publicationName>BMC Veterinary Research</prism:publicationName>
					
			
							
					<prism:issn>1746-6148</prism:issn>
					
			
							
					<prism:volume>4</prism:volume>
					
			
							
					<prism:startingPage>29</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-08-06</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1746-6148/4/27">
            
            <title>Contact structures in the poultry industry in Great Britain: Exploring transmission routes for a potential avian influenza virus epidemic</title>
			<description>Background:
The commercial poultry industry in United Kingdom (UK) is worth an estimated &#163;3.4 billion at retail value, producing over 174 million birds for consumption per year. An epidemic of any poultry disease with high mortality or which is zoonotic, such as avian influenza virus (AIV), would result in the culling of significant numbers of birds, as seen in the Netherlands in 2003 and Italy in 2000. Such an epidemic would cost the UK government millions of pounds in compensation costs, with further economic losses through reduction of international and UK consumption of British poultry. In order to better inform policy advisers and makers on the potential for a large epidemic in GB, we investigate the role that interactions amongst premises within the British commercial poultry industry could play in promoting an AIV epidemic, given an introduction of the virus in a specific part of poultry industry in Great Britain (GB).
Results:
Poultry premises using multiple slaughterhouses lead to a large number of premises being potentially connected, with the resultant potential for large and sometimes widespread epidemics. Catching companies can also potentially link a large proportion of the poultry population. Critical to this is the maximum distance traveled by catching companies between premises and whether or not between-species transmission could occur within individual premises. Premises closely linked by proximity may result in connections being formed between different species and or sectors within the industry.
Conclusion:
Even quite well-contained epidemics have the potential for geographically widespread dissemination, potentially resulting in severe logistical problems for epidemic control, and with economic impact on a large part of the country. Premises sending birds to multiple slaughterhouses or housing multiple species may act as a bridge between otherwise separate sectors of the industry, resulting in the potential for large epidemics. Investment into further data collection and analyses on the importance of industry structure as a determinant for spread of AIV would enable us to use the results from this study to contribute to policy on disease control.</description>
			<link>http://www.biomedcentral.com/1746-6148/4/27</link>		
			<dc:creator>Jennifer E Dent, Rowland R Kao, Istvan Z Kiss, Kieran Hyder and Mark Arnold</dc:creator>
			<dc:source>BMC Veterinary Research 2008, 4:27</dc:source>
			<dc:subject>Number of accesses: 366</dc:subject>
			<dc:date>2008-07-23</dc:date>
			<dc:identifier>doi:10.1186/1746-6148-4-27</dc:identifier>
			
			
							
					<prism:publicationName>BMC Veterinary Research</prism:publicationName>
					
			
							
					<prism:issn>1746-6148</prism:issn>
					
			
							
					<prism:volume>4</prism:volume>
					
			
							
					<prism:startingPage>27</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-07-23</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1746-6148/4/31">
            
            <title>Loop-mediated isothermal amplification as an emerging technology for detection of Yersinia ruckeri the causative agent of enteric red mouth disease in fish</title>
			<description>Background:
Enteric Redmouth (ERM) disease also known as Yersiniosis is a contagious disease affecting salmonids, mainly rainbow trout. The causative agent is the gram-negative bacterium Yersinia ruckeri. The disease can be diagnosed by isolation and identification of the causative agent, or detection of the Pathogen using fluorescent antibody tests, ELISA and PCR assays. These diagnostic methods are laborious, time consuming and need well trained personnel.
Results:
A loop-mediated isothermal amplification (LAMP) assay was developed and evaluated for detection of Y. ruckeri the etiological agent of enteric red mouth (ERM) disease in salmonids. The assay was optimised to amplify the yruI/yruR gene, which encodes Y. ruckeri quorum sensing system, in the presence of a specific primer set and Bst DNA polymerase at an isothermal temperature of 63degreesC for one hour. Amplification products were detected by visual inspection, agarose gel electrophoresis and by real-time monitoring of turbidity resulted by formation of LAMP amplicons. Digestion with HphI restriction enzyme demonstrated that the amplified product was unique. The specificity of the assay was verified by the absence of amplification products when tested against related bacteria. The assay had 10-fold higher sensitivity compared with conventional PCR and successfully detected Y. ruckeri not only in pure bacterial culture but also in tissue homogenates of infected fish.
Conclusions:
The ERM-LAMP assay represents a practical alternative to the microbiological approach for rapid, sensitive and specific detection of Y. ruckeri in fish farms. The assay is carried out in one hour and needs only a heating block or water bath as laboratory furniture. The advantages of the ERM-LAMP assay make it a promising tool for molecular detection of enteric red mouth disease in fish farms.</description>
			<link>http://www.biomedcentral.com/1746-6148/4/31</link>		
			<dc:creator>Mona Saleh, Hatem Soliman and Mansour El-Matbouli</dc:creator>
			<dc:source>BMC Veterinary Research 2008, 4:31</dc:source>
			<dc:subject>Number of accesses: 339</dc:subject>
			<dc:date>2008-08-12</dc:date>
			<dc:identifier>doi:10.1186/1746-6148-4-31</dc:identifier>
			
			
							
					<prism:publicationName>BMC Veterinary Research</prism:publicationName>
					
			
							
					<prism:issn>1746-6148</prism:issn>
					
			
							
					<prism:volume>4</prism:volume>
					
			
							
					<prism:startingPage>31</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-08-12</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1746-6148/2/12">
            
            <title>Degenerative suspensory ligament desmitis as a systemic disorder characterized by proteoglycan accumulation</title>
			<description>Background:
Degenerative suspensory ligament desmitis (DSLD) is a debilitating disorder thought to be limited to suspensory ligaments of Peruvian Pasos, Peruvian Paso crosses, Arabians, American Saddlebreds, American Quarter Horses, Thoroughbreds, and some European breeds. It frequently leads to persistent, incurable lameness and need to euthanize affected horses. The pathogenesis remains unclear, though the disease appears to run in families. Treatment and prevention are empirical and supportive, and not effective in halting the progression of the disease. Presently, the presumptive diagnosis of DSLD is obtained from patient signalment and history, clinical examination, and ultrasonographic examination of clinically affected horses, and is confirmed at post mortem examination. Presently, there are no reliable methods of diagnosing DSLD in asymptomatic horses. The goal of this study was to characterize and define the disorder in terms of tissue involvement at the macroscopic and microscopic levels.
Results:
We examined tissues and organs from 28 affected horses (22 Peruvian Pasos, 6 horses of other breeds) and from 8 control horses. Histopathological examination revealed the presence of excessive amounts of proteoglycans in the following tissues removed from DSLD-affected horses: suspensory ligaments, superficial and deep digital flexor tendons, patellar and nuchal ligaments, cardiovascular system, and sclerae. Electron microscopy demonstrated changes in diameters of collagen fibrils in the tendon, and in smooth muscle cells of the media of the aorta compatible with increased cell permeability in DSLD-affected cells. Separation of tendon extracts by gel chromatography revealed the presence of additional proteoglycan(s) in extracts from affected, but not control extracts.
Conclusion:
This study demonstrates for the first time that DSLD, a disease process previously thought to be limited to the suspensory ligaments of the distal limbs of affected horses, is in fact a systemic disorder involving tissues and organs with significant connective tissue component. Abnormal accumulation of proteoglycans between collagen and elastic fibers rather than specific collagen fibril abnormalities is the most prominent histological feature of DSLD. Because of this observation and because of the involvement of many other tendons and ligaments beside the suspensory ligament, and of non-ligamentous tissue we, therefore, propose that equine systemic proteoglycan accumulation or ESPA rather than DSLD is a more appropriate name for this condition.</description>
			<link>http://www.biomedcentral.com/1746-6148/2/12</link>		
			<dc:creator>Jaroslava Halper, Byoungjae Kim, Ahrar Khan, Jung Hae Yoon and PO Eric Mueller</dc:creator>
			<dc:source>BMC Veterinary Research 2006, 2:12</dc:source>
			<dc:subject>Number of accesses: 337</dc:subject>
			<dc:date>2006-04-12</dc:date>
			<dc:identifier>doi:10.1186/1746-6148-2-12</dc:identifier>
			
			
							
					<prism:publicationName>BMC Veterinary Research</prism:publicationName>
					
			
							
					<prism:issn>1746-6148</prism:issn>
					
			
							
					<prism:volume>2</prism:volume>
					
			
							
					<prism:startingPage>12</prism:startingPage>
					
			
							
					<prism:publicationDate>2006-04-12</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1746-6148/4/33">
            
            <title>A cross-sectional study to determine the seroprevalence of  Bluetongue virus serotype 8 in sheep and goats in 2006 and 2007 in the Netherlands </title>
			<description>Background:
In August 2006 a major epidemic of bluetongue virus serotype 8 (BTV8) started off in North-West Europe. In the course of 2007 it became evident that BTV8 survived the winter in North-West Europe, re-emerged and spread exponentially. Recently, the European Union decided to start vaccination against BTV8. In order to improve the understanding of the epidemiological situation, it is necessary to execute a cross-sectional serological study at the end of the BT vector season. Cattle were the target species for cross-sectional serological studies in Europe at the end of 2006 and 2007. However, with respect to goats and sheep there was no information on the BTV8-seroprevalence.
Results:
On the basis of a cross-sectional study, the estimated seroprevalence of BTV8-exposed locations in the Netherlands in 2006 was 0% for goats (95% confidence interval: 0 - 5.6%) and 7.0% for sheep (95% confidence interval: 3.5 - 12.9%). For 2007, it was 47% for goats (95% confidence interval: 36 - 58%) and 70% for sheep (95% confidence interval:  63 - 76%). There was a wide range in within-location  seroprevalence in locations with goats and sheep (1 - 100%). A gradient in seroprevalence was seen, with the highest level of seroprevalence in the southern Netherlands, the area where the epidemic started in 2006, and a decreasing seroprevalence when going in a northern direction.
Conclusions:
There is a much higher estimated seroprevalence of locations with goats exposed to BTV8 than can be inferred from the rather low number of reported  clinical outbreaks in goats. This is probably due to the fact that clinical signs in infected goats are far less obvious than in sheep. The wide range in within-location seroprevalence observed means that the proportion of animals protected in 2008 by a natural infection in 2006 and/or 2007 can differ highly between flocks. This should be taken into account when vaccinating animals.</description>
			<link>http://www.biomedcentral.com/1746-6148/4/33</link>		
			<dc:creator>Armin RW Elbers, Johan Popma, Sandra Oosterwolde, Piet A van Rijn, Piet Vellema and Eugene MA van Rooij</dc:creator>
			<dc:source>BMC Veterinary Research 2008, 4:33</dc:source>
			<dc:subject>Number of accesses: 323</dc:subject>
			<dc:date>2008-08-27</dc:date>
			<dc:identifier>doi:10.1186/1746-6148-4-33</dc:identifier>
			
			
							
					<prism:publicationName>BMC Veterinary Research</prism:publicationName>
					
			
							
					<prism:issn>1746-6148</prism:issn>
					
			
							
					<prism:volume>4</prism:volume>
					
			
							
					<prism:startingPage>33</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-08-27</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1746-6148/4/22">
            
            <title>Pregnancy success of lactating Holstein cows after a single administration of a sustained-release formulation of recombinant bovine somatotropin</title>
			<description>Background:
Results regarding the use of bovine somatotropin for enhancing fertility in dairy cattle are variable. Here, the hypothesis was tested that a single injection of a sustained-release preparation of bovine somatotropin (bST) during the preovulatory period would improve pregnancy success of lactating dairy cows at first service.
Results:
The first experiment was conducted in a temperate region of Mexico. Cows inseminated following natural estrus or timed artificial insemination were given a single injection of bST or a placebo injection at insemination (n = 100 cows per group). There was no significant difference between bST and control groups in the proportion of inseminated cows diagnosed pregnant (29 vs 31% pregnant). The second experiment was performed during heat stress in Florida. Cows were subjected to an ovulation synchronization regimen for first insemination. Cows treated with bST received a single injection at 3 days before insemination. Controls received no additional treatment. As expected, bST did not increase vaginal temperature. Treatment with bST did not significantly increase the proportion of inseminated cows diagnosed pregnant although it was numerically greater for the bST group (24.2% vs 17.8%, 124&#8211;132 cows per group). There was a tendency (p = 0.10) for a smaller percent of control cows to have high plasma progesterone concentrations (&#8805; 1 ng/ml) at Day 7 after insemination than for bST-treated cows (72.6 vs 81.1%). When only cows that were successfully synchronized were considered, the magnitude of the absolute difference in the percentage of inseminated cows that were diagnosed pregnant between bST and control cows was reduced (24.8 vs 22.4% pregnant for bST and control).
Conclusion:
Results failed to indicate a beneficial effect of bST treatment on fertility of lactating dairy cows.</description>
			<link>http://www.biomedcentral.com/1746-6148/4/22</link>		
			<dc:creator>A Bell, OA Rodr&#237;guez, LA de Castro e Paula, MB Padua, J Hern&#225;ndez-Cer&#243;n, CG Guti&#233;rrez, A De Vries and PJ Hansen</dc:creator>
			<dc:source>BMC Veterinary Research 2008, 4:22</dc:source>
			<dc:subject>Number of accesses: 290</dc:subject>
			<dc:date>2008-06-26</dc:date>
			<dc:identifier>doi:10.1186/1746-6148-4-22</dc:identifier>
			
			
							
					<prism:publicationName>BMC Veterinary Research</prism:publicationName>
					
			
							
					<prism:issn>1746-6148</prism:issn>
					
			
							
					<prism:volume>4</prism:volume>
					
			
							
					<prism:startingPage>22</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-06-26</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.biomedcentral.com/1746-6148/4/30">
            
            <title>Biomarkers for ragwort poisoning in horses: identification of protein targets</title>
			<description>Background:
Ingestion of the poisonous weed ragwort (Senecio jacobea) by horses leads to irreversible liver damage. The principal toxins of ragwort are the pyrrolizidine alkaloids that are rapidly metabolised to highly reactive and cytotoxic pyrroles, which can escape into the circulation and bind to proteins. In this study a non-invasive in vitro model system has been developed to investigate whether pyrrole toxins induce specific modifications of equine blood proteins that are detectable by proteomic methods.
Results:
One dimensional gel electrophoresis revealed a significant alteration in the equine plasma protein profile following pyrrole exposure and the formation of a high molecular weight protein aggregate. Using mass spectrometry and confirmation by western blotting the major components of this aggregate were identified as fibrinogen, serum albumin and transferrin.
Conclusion:
These findings demonstrate that pyrrolic metabolites can modify equine plasma proteins. The high molecular weight aggregate may result from extensive inter- and intra-molecular cross-linking of fibrinogen with the pyrrole. This model has the potential to form the basis of a novel proteomic strategy aimed at identifying surrogate protein biomarkers of ragwort exposure in horses and other livestock.</description>
			<link>http://www.biomedcentral.com/1746-6148/4/30</link>		
			<dc:creator>Rowan E Moore, Derek Knottenbelt, Jacqueline B Matthews, Robert J Beynon and Phillip D Whitfield</dc:creator>
			<dc:source>BMC Veterinary Research 2008, 4:30</dc:source>
			<dc:subject>Number of accesses: 281</dc:subject>
			<dc:date>2008-08-08</dc:date>
			<dc:identifier>doi:10.1186/1746-6148-4-30</dc:identifier>
			
			
							
					<prism:publicationName>BMC Veterinary Research</prism:publicationName>
					
			
							
					<prism:issn>1746-6148</prism:issn>
					
			
							
					<prism:volume>4</prism:volume>
					
			
							
					<prism:startingPage>30</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-08-08</prism:publicationDate>
					

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		<item rdf:about="http://www.biomedcentral.com/1746-6148/4/14">
            
            <title>Evidence of scrapie transmission via milk</title>
			<description>Background:
The risk of scrapie infection increases with increased duration and proximity of contact between sheep at lambing. Scrapie infectivity has not been detected in milk but cellular prion protein, the precursor of disease-associated prion protein PrPd, has been found in milk from ruminants. To determine whether milk is able to transmit scrapie, 18 lambs with a prion protein genotype associated with high susceptibility to scrapie (VRQ/VRQ) were fed milk from twelve scrapie-affected ewes of the same genotype, and 15 VRQ/VRQ sheep reared on scrapie-free dams served as controls.
Results:
Three lambs fed milk from scrapie-affected ewes were culled due to intercurrent diseases at 43, 44 and 105 days of age respectively, and PrPd was detected in the distal ileum of the first two lambs, whilst PrPd was not found in lymphoreticular tissues in the third lamb. A control lamb, housed in a separate pen and culled at 38 days of age, was also negative for PrPd in a range of tissues. Samples of recto-anal mucosa associated lymphoid tissue collected from the remaining 15 live lambs at seven months of age (between five to seven months after mixing) were positive for PrPd in the scrapie milk recipients, whereas PrPd was not detected in the remaining 14 controls at that time. A subsequent sample collected from control lambs revealed PrPd accumulation in two of five lambs eight months after mixing with scrapie milk recipients suggestive of an early stage of infection via lateral transmission. By contrast, the control sheep housed in the same building but not mixed with the scrapie milk recipients were still negative for PrPd.
Conclusion:
The presence of PrPd in distal ileum and rectal mucosa indicates transmission of scrapie from ewe to lamb via milk (or colostrum) although it is not yet clear if such cases would go on to develop clinical disease. The high level of infection in scrapie-milk recipients revealed by rectal mucosal testing at approximately seven months of age may be enhanced or supplemented by intra-recipient infection as these lambs were mixed together after feeding with milk from scrapie-affected ewes and we also observed lateral transmission from these animals to lambs weaned from scrapie-free ewes.</description>
			<link>http://www.biomedcentral.com/1746-6148/4/14</link>		
			<dc:creator>Timm Konold, S Jo Moore, Susan J Bellworthy and Hugh A Simmons</dc:creator>
			<dc:source>BMC Veterinary Research 2008, 4:14</dc:source>
			<dc:subject>Number of accesses: 217</dc:subject>
			<dc:date>2008-04-08</dc:date>
			<dc:identifier>doi:10.1186/1746-6148-4-14</dc:identifier>
			
			
							
					<prism:publicationName>BMC Veterinary Research</prism:publicationName>
					
			
							
					<prism:issn>1746-6148</prism:issn>
					
			
							
					<prism:volume>4</prism:volume>
					
			
							
					<prism:startingPage>14</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-04-08</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
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