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<title>Papers in Veterinary and Biomedical Science</title>
<copyright>Copyright (c) 2013 University of Nebraska - Lincoln All rights reserved.</copyright>
<link>http://digitalcommons.unl.edu/vetscipapers</link>
<description>Recent documents in Papers in Veterinary and Biomedical Science</description>
<language>en-us</language>
<lastBuildDate>Thu, 24 Jan 2013 23:44:31 PST</lastBuildDate>
<ttl>3600</ttl>








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<title>ENTERIC &lt;i&gt;STREPTOCOCCUS DURANS&lt;/i&gt;--AN ADHERING STREPTOCOCCUS AS A CAUSE OF DIARRHEA IN SUCKLING PIGLETS?</title>
<link>http://digitalcommons.unl.edu/vetscipapers/123</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/vetscipapers/123</guid>
<pubDate>Wed, 05 Dec 2012 06:32:20 PST</pubDate>
<description>
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	<p><em>Streptococcus durans</em> has been considered a normal part of the intestinal flora. We would contest that assumption in light of evidence from field case submissions and because of its ability to colonize intestinal mucosa and create pathologic changes in intestine of gnotobiotic pigs.</p>

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<author>Darrell D. Johnson</author>


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<title>Cellular Transcription Factors Induced in Trigeminal Ganglia during
Dexamethasone-Induced Reactivation from Latency Stimulate Bovine
Herpesvirus 1 Productive Infection and Certain Viral Promoters</title>
<link>http://digitalcommons.unl.edu/vetscipapers/122</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/vetscipapers/122</guid>
<pubDate>Mon, 13 Feb 2012 14:24:39 PST</pubDate>
<description>
	<![CDATA[
	<p>Bovine herpesvirus 1 (BHV-1), an alphaherpesvirinae subfamily member, establishes latency in sensory neurons. Elevated corticosteroid levels, due to stress, reproducibly triggers reactivation from latency in the field. A single intravenous injection of the synthetic corticosteroid dexamethasone (DEX) to latently infected calves consistently induces reactivation from latency. Lytic cycle viral gene expression is detected in sensory neurons within 6 h after DEX treatment of latently infected calves. These observations suggested that DEX stimulated expression of cellular genes leads to lytic cycle viral gene expression and productive infection. In this study, a commercially available assay—Bovine Gene Chip—was used to compare cellular gene expression in the trigeminal ganglia (TG) of calves latently infected with BHV-1 versus DEX-treated animals. Relative to TG prepared from latently infected calves, 11 cellular genes were induced more than 10-fold 3 h after DEX treatment. Pentraxin three, a regulator of innate immunity and neurodegeneration, was stimulated 35- to 63-fold after 3 or 6 h of DEXtreatment. Two transcription factors, promyelocytic leukemia zinc finger (PLZF) and Slug were induced more than 15-fold 3 h after DEX treatment. PLZF or Slug stimulated productive infection 20- or 5-fold, respectively, and Slug stimulated the late glycoprotein C promoter more than 10-fold. Additional DEX-induced transcription factors also stimulated productive infection and certain viral promoters. These studies suggest that DEX-inducible cellular transcription factors and/or signaling pathways stimulate lytic cycle viral gene expression, which subsequently leads to successful reactivation from latency in a small subset of latently infected neurons.</p>

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<author>Aspen M. Workman et al.</author>


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<title>A deletion mutation in bovine &lt;i&gt;SLC4A2&lt;/i&gt; is associated with osteopetrosis in Red Angus cattle</title>
<link>http://digitalcommons.unl.edu/vetscipapers/121</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/vetscipapers/121</guid>
<pubDate>Thu, 15 Sep 2011 12:37:42 PDT</pubDate>
<description>
	<![CDATA[
	<p>Background: Osteopetrosis is a skeletal disorder of humans and animals characterized by the formation of overly dense bones, resulting from a deficiency in the number and/or function of bone-resorbing osteoclast cells. In cattle, osteopetrosis can either be induced during gestation by viral infection of the dam, or inherited as a recessive defect. Genetically affected calves are typically aborted late in gestation, display skull deformities and exhibit a marked reduction of osteoclasts. Although mutations in several genes are associated with osteopetrosis in humans and mice, the genetic basis of the cattle disorder was previously unknown.</p>
<p>Results: We have conducted a whole-genome association analysis to identify the mutation responsible for inherited osteopetrosis in Red Angus cattle. Analysis of >54,000 SNP genotypes for each of seven affected calves and nine control animals localized the defective gene to the telomeric end of bovine chromosome 4 (BTA4). Homozygosity analysis refined the interval to a 3.4-Mb region containing the <em>SLC4A2</em> gene, encoding an anion exchanger protein necessary for proper osteoclast function. Examination of <em>SLC4A2</em> from normal and affected animals revealed a ~2.8-kb deletion mutation in affected calves that encompasses exon 2 and nearly half of exon 3, predicted to prevent normal protein function. Analysis of RNA from a proven heterozygous individual confirmed the presence of transcripts lacking exons 2 and 3, in addition to normal transcripts. Genotyping of additional animals demonstrated complete concordance of the homozygous deletion genotype with the osteopetrosis phenotype. Histological examination of affected tissues revealed scarce, morphologically abnormal osteoclasts displaying evidence of apoptosis.</p>
<p>Conclusions: These results indicate that a deletion mutation within bovine <em>SLC4A2</em> is associated with osteopetrosis in Red Angus cattle. Loss of <em>SLC4A2</em> function appears to induce premature cell death, and likely results in cytoplasmic alkalinization of osteoclasts which, in turn, may disrupt acidification of resorption lacunae.</p>

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<author>Stacey N. Meyers et al.</author>


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<title>Purification of maturation-promoting factor, an intracellular regulator of early mitotic events</title>
<link>http://digitalcommons.unl.edu/vetscipapers/120</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/vetscipapers/120</guid>
<pubDate>Thu, 15 Sep 2011 12:29:33 PDT</pubDate>
<description>
	<![CDATA[
	<p>Maturation-promoting factor causes germinal vesicle breakdown when injected into <em>Xenopus</em> oocytes and can induce metaphase in a cell-free system. The cell-free assay was used to monitor maturation-promoting factor during its purification from unfertilized <em>Xenopus</em> eggs. Ammonium sulfate precipitation and six chromatographic procedures resulted in a preparation purified >3000-fold that could induce germinal vesicle breakdown within 2 hr when injected into cycloheximide- treated oocytes. Proteins of 45 kDa and 32 kDa were correlated with fractions of highest activity in both assays. These fractions contained a protein kinase activity able to phosphorylate the endogenous 45-kDa protein, as well as histone Hi, phosphatase inhibitor 1, and casein. The highly purified preparations described here should help to identify the mechanism of action of maturation-promoting factor and to elucidate the role of protein kinases in the induction of metaphase.</p>

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<author>Manfred J. Lohka et al.</author>


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<title>Impairment of D-alanine biosynthesis in &lt;i&gt;Mycobacterium smegmatis&lt;/i&gt; determines decreased intracellular survival in human macrophages</title>
<link>http://digitalcommons.unl.edu/vetscipapers/119</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/vetscipapers/119</guid>
<pubDate>Fri, 12 Aug 2011 13:56:48 PDT</pubDate>
<description>
	<![CDATA[
	<p>D-alanine is a structural component of mycobacterial peptidoglycan. The primary route of d-alanine biosynthesis in eubacteria is the enantiomeric conversion from l-alanine, a reaction catalyzed by d-alanine racemase (Alr). <em>Mycobacterium smegmatis alr</em> insertion mutants are not dependent on d-alanine for growth and display a metabolic pattern consistent with an alternative pathway for d-alanine biosynthesis. In this study, we demonstrate that the <em>M. smegmatis alr</em> insertion mutant TAM23 can synthesize d-alanine at lower levels than the parental strain. The insertional inactivation of the alr gene also decreases the intracellular survival of mutant strains within primary human monocyte-derived macrophages. By complementation studies, we confirmed that the impairment of alr gene function is responsible for this reduced survival. Inhibition of superoxide anion and nitric oxide formation in macrophages suppresses the differential survival. In contrast, for bacteria grown in broth, both strains had approximately the same susceptibility to hydrogen peroxide, acidified sodium nitrite, low pH and polymyxin B. In contrast, TAM23 exhibited increased resistance to lysozyme. d-alanine supplementation considerably increased TAM23 viability in nutritionally deficient media and within macrophages. These results suggest that nutrient deprivation in phagocytic cells combined with killing mediated by reactive intermediates underlies the decreased survival of alr mutants. This knowledge may be valuable in the construction of mycobacterial auxotrophic vaccine candidates.</p>

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<author>Ofelia Barletta-Chacon et al.</author>


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<title>&lt;i&gt;Parelaphostrongylus tenuis&lt;/i&gt; in Captive Pronghorn Antelope (&lt;i&gt;Antilocapra americana&lt;/i&gt;) in Nebraska</title>
<link>http://digitalcommons.unl.edu/vetscipapers/118</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/vetscipapers/118</guid>
<pubDate>Wed, 07 Apr 2010 14:42:18 PDT</pubDate>
<description>
	<![CDATA[
	<p>Lesions in four captive pronghorn antelope (<i>Antilocapra americana</i>) naturally infected with <i>Parelaphostrongylus tenuis</i> in eastern Nebraska (USA) are described in this report. Animals were bright and alert with hind limb ataxia that progressed to sternal or lateral recumbency between July 28 and October 17, 1998. Animals were euthanized due to disease progression despite therapy. Multifocal decubital ulcers over bony prominences occurred in two animals and chronic unilateral otitis media was present in one animal. Histopathologic examination revealed severe Wallerian degeneration randomly scattered throughout the spinal cords of all four animals. Spinal cord sections from two animals contained adult nematode parasites consistent with <i>P. tenuis</i>. This is the first report of naturally occurring <i>P. tenuis</i> infection in pronghorn antelope. Pronghorn antelope should be considered susceptible to <i>P. tenuis</i> infection and contact with infected white-tailed deer as well as intermediate gastropod hosts of <i>P. tenuis</i> should be prevented in endemic areas.</p>

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<author>Heather A. Simmons et al.</author>


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<title>Serologic Survey of Select Infectious Diseases in Coyotes and Raccoons in Nebraska</title>
<link>http://digitalcommons.unl.edu/vetscipapers/117</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/vetscipapers/117</guid>
<pubDate>Wed, 07 Apr 2010 14:37:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>To obtain data about select zoonotic and other infectious diseases in free-ranging predators in five ecoregions in Nebraska, sera were collected from 67 coyotes (<i>Canis latrans</i>) and 63 raccoons (<i>Procyon lotor</i>)) from November 2002 through January 2003. For coyotes, antibodies were detected against canine distemper virus (CDV, 61%), <i>Francisella tularensis</i>) (32%), <i>Rickettsia rickettsi</i>) (13%), and flaviviruses (48%). None of the coyote sera had antibodies to <i>Borrelia burgdorferi, Brucella canis</i>), or six serovars of <i>Leptospira interrogans</i>). Because serologic cross-reactivity exists among flaviviruses, 14 sera from flavivirus-positive coyotes were also tested for St. Louis encephalitis virus (SLE) antibodies and two (14%) were positive, suggesting that up to 48% of coyotes tested had antibodies against West Nile virus (WNV). For raccoons, antibodies were detected against CDV (33%), <i>F. tularensis</i>) (38%), and three serovars of <i>L. interrogans</i>) (11%).</p>

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<author>Richard Bischof et al.</author>


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<title>Mouse × pig chimeric antibodies expressed in baculovirus retain the same properties of their parent antibodies</title>
<link>http://digitalcommons.unl.edu/vetscipapers/116</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/vetscipapers/116</guid>
<pubDate>Wed, 07 Apr 2010 14:32:38 PDT</pubDate>
<description>
	<![CDATA[
	<p>The development of hybridoma and recombinant DNA technologies has made it possible to use antibodies against cancer, autoimmune disorders, and infectious diseases in humans. These advances in therapy, as well as immunoprophylaxis, could also make it possible to use these technologies in agricultural species of economic importance such as pigs. Porcine reproductive and respiratory syndrome virus (PRRSV) is an arterivirus causing very important economic losses to the industry. Passive transfer of antibodies obtained by biotechnology could be used in the future to complement or replace vaccination against this and other pig pathogens. To this end, we constructed and studied the properties of chimeric mouse × pig anti-PRRSV antibodies. We cloned the constant regions of gamma-1 and gamma-2 heavy chains and the lambda light chain of pig antibodies in frame with the variable regions of heavy and light chains of mouse monoclonal antibody ISU25C1, which has neutralizing activity against PRRSV. The coding regions for chimeric IgG1 and IgG2 were expressed in a baculovirus expression system. Both chimeric antibodies recognized PRRSV in ELISA as well as in a Western-blot format and, more importantly, were able to neutralize PRRSV in the same fashion as the parent mouse monoclonal antibody ISU25C1. In addition, we show that both pig IgG1 and IgG2 antibodies could bind complement component C1q, with IgG2 being more efficient than IgG1 in binding C1q. Expressing chimeric pig antibodies with protective capabilities offers a new alternative strategy for infectious disease control in domestic pigs.</p>

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<author>Ana M. Jar et al.</author>


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<title>GP3 is a structural component of the PRRSV type II (US) virion</title>
<link>http://digitalcommons.unl.edu/vetscipapers/115</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/vetscipapers/115</guid>
<pubDate>Tue, 16 Feb 2010 11:52:10 PST</pubDate>
<description>
	<![CDATA[
	<p>Abstract Glycoprotein 3 (GP3) is a highly glycosylated PRRSV envelope protein which has been reported as being present in the virions of PRRSV type I, while missing in the type II PRRSV (US) virions. We herein present evidence that GP3 is indeed incorporated in the virus particles of a North American strain of PRRSV (FL12), at a density that is consistent with the minor structural role assigned to GP3 in members of the <i>Arterivirus</i> genus. Two 15aa peptides corresponding to two different immunodominant linear epitopes of GP3 derived from the North American strain of PRRSV (FL12) were used as antigen to generate a rabbit monospecific antiserum to this protein. The specificity of this anti-GP3 antiserum was confirmed by radioimmunoprecipitation (RIP) assay using BHK-21 cells transfected with GP3 expressing plasmid, MARC-145 cells infected with FL12 PRRSV, as well as by confocal microscopy on PRRSV-infected MARC-145 cells. To test if GP3 is a structural component of the virion, <sup>35</sup>S-labelled PRRSV virions were pelleted through a 30% sucrose cushion, followed by a second round of purification on a sucrose gradient (20–60%). Virions were detected in specific gradient fractions by radioactive counts and further confirmed by viral infectivity assay in MARC 145 cells. The GP3 was detected in gradient fractions containing purified virions by RIP using anti-GP3 antiserum. Predictably, the GP3 was less abundant in purified virions than other major structural envelope proteins such as GP5 and M. Further evidence of the presence of GP3 at the level of PRRSV FL12 envelope was obtained by immunogold staining of purified virions from the supernatant of infected cells with anti-GP3 antiserum. Taken together, these results indicate that GP3 is a minor structural component of the PRRSV type II (FL12 strain) virion, as had been previously described for PRRSV type I.</p>

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<author>M. de Lima et al.</author>


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<title>Viral Infections of Domestic Animals</title>
<link>http://digitalcommons.unl.edu/vetscipapers/114</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/vetscipapers/114</guid>
<pubDate>Wed, 13 Jan 2010 09:40:45 PST</pubDate>
<description>
	<![CDATA[
	<p>Contents <br />Health-Defined Animals  270 <br />Immunity in Health-Defined Animals 272 <br />Virus Infections During Gestation 275 <br />Respiratory Infections 279  <br />Influenza 279  <br />Ascariasis enhancement of respiratory infections  280  <br />Virus pneumonia of pigs 281  <br />Infectious atrophic rhinitis of swine 282  <br />Porcine inclusion body rhinitis  283  <br />Infectious bovine rhinotracheitis 283  <br />Bovine myxovirus parainfluenza  284  <br />Infectious bovine keratoconjunctivitis  284 <br />Enteric Infections  285  <br />Swine polio-encephalomyelitis viruses  285  <br />Transmissible gastroenteritis of swine 286  <br />Beran’s swine enterovirus 287  <br />Bovine virus diarrhea 287 <br />Systemic Diseases 288  <br />Hog cholera  288  <br />African swine fever  290  <br />Nebraska University disease  290  <br />Swine edema disease 291  <br />Exudative epidermitis of swine 292  <br />Foot-and-mouth disease and rinderpest 293</p>

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<author>George A. Young</author>


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<title>D-ALANINE RACEMASE MUTANTS OF MYCOBACTERIA AND USES THEREFORE: U.S. Patent No. US 6,929,799 B2</title>
<link>http://digitalcommons.unl.edu/vetscipapers/113</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/vetscipapers/113</guid>
<pubDate>Fri, 13 Nov 2009 12:45:03 PST</pubDate>
<description>
	<![CDATA[
	<p>The present invention is directed to D-alanine racemase mutants of mycobacterial species. The D-alanine racemase gene (alrA) is involved in the systhesis of D-alanine, a basic component of peptidoglycan that forms the backbone of the bacterial cell wall. The vresent invention is also directed to methods of making live-attenuated vaccines against pathogenic mycobacteria using such alrA mutants and to the vaccines made according to such methods. The present invention is further directed to use of alrA mutants in methods for screening antimycobacterial agents that are synergistic with peptidoglycan inhibitors. Finally, the present invention is directed to methods to identify new pathways of D-alanine biosynthesis for use in developing new drugs targeting peptidoglycan biosynthesis in mycobacteria and to identify vaccines useful against pathogenic mycobacteria.</p>

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<author>Raul G. Barletta et al.</author>


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<title>RECOMBINANT MYCOBACTERIA OVEREXPRESSING D-ALANINE LIGASE GENE AND USES THEREFORE: United States Patent No. US 7,371,571 B2</title>
<link>http://digitalcommons.unl.edu/vetscipapers/112</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/vetscipapers/112</guid>
<pubDate>Fri, 13 Nov 2009 12:42:25 PST</pubDate>
<description>
	<![CDATA[
	<p>Recombinant mycobacterial strains which overproduce essential biosynthetic enzymes of pathogenic mycobateria are provided. These strains overproduce enzymes involved in the synthesis and incorporation of D-alanine into mycobacterial peptidoglycan, the backbone of the mycobacterial cell wall. These overproducing strains may be used as reference strains in in vitro screening methods to identify antimycobacterial agents.</p>

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<author>Raul G. Barletta et al.</author>


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<title>LACTIC ACID BACTERIA CULTURES THAT INHIBIT FOOD-BORNE PATHOGENS: U.S. Patent No. US 7,323,166 B2</title>
<link>http://digitalcommons.unl.edu/vetscipapers/111</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/vetscipapers/111</guid>
<pubDate>Fri, 13 Nov 2009 12:37:47 PST</pubDate>
<description>
	<![CDATA[
	<p>The present invention provides methods and compositions for preventing or inhibiting human food-borne pathogens in animals, and methods for increasing feed efficiency in animals by administering to the animal effective amounts of probiotic lactic acid producing bacteria. Further provided are feed compositions comprising probiotic lactic acid producing bacteria. A preferred probiotic lactic acid producing bacteria is <i>Lactobacillus acidophilus</i> strain ATCC accession number PTA-5249. This bacterial strain inhibits nalidixic acid-resistant <i>Escherichia coli</i> 0157:H7.</p>

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<author>Mindy M. Brashears et al.</author>


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<title>Johne’s Disease, Inflammatory Bowel Disease, and &lt;i&gt;Mycobacterium paratuberculosis&lt;/i&gt;</title>
<link>http://digitalcommons.unl.edu/vetscipapers/110</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/vetscipapers/110</guid>
<pubDate>Wed, 14 Oct 2009 10:37:44 PDT</pubDate>
<description>
	<![CDATA[
	<p>Johne’s disease is a chronic diarrhea affecting all ruminants. Mycobacterium avium subsp. paratuberculosis (MAP), a slowly growing mycobacteria, is the etiologic agent. There is also a concern that MAP might be a causative agent of some cases of inflammatory bowel disease in humans, especially Crohn’s disease. Food products including pasteurized bovine milk have been suggested as potential sources of human infection. This review addresses microbial factors that may contribute to its pathogenicity. In addition, the experimental evidence defining MAP as the cause of Johne’s disease and the issues and controversies surrounding its potential pathogenic role in humans are discussed.</p>

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<author>Ofelia Barletta-Chacon et al.</author>


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<title>Premature Expression of the Latency-Related RNA Encoded by Bovine Herpesvirus Type 1 Correlates With Higher Levels of Beta Interferon RNA Expression in Productively Infected Cells</title>
<link>http://digitalcommons.unl.edu/vetscipapers/109</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/vetscipapers/109</guid>
<pubDate>Fri, 31 Jul 2009 08:08:47 PDT</pubDate>
<description>
	<![CDATA[
	<p>Bovine herpesvirus type 1 (BHV-1) is an important pathogen that can initiate bovine respiratory disease complex. Like other members of the subfamily <i>Alphaherpesvirinae</i>, BHV-1 establishes latency in sensory neurons. The latency-related (LR) gene expresses a family of alternatively spliced transcripts in infected sensory neurons that have the potential to encode several LR proteins. An LR mutant virus that contains three stop codons near the 5’ terminus of the first open reading frame in the LR gene does not express two LR proteins or reactivate from latency. In addition, the LR mutant virus induces higher levels of apoptosis in trigeminal ganglionic neurons and grows less efficiently in certain tissues of infected calves. In spite of the reduced pathogenesis, the LR mutant virus, wild-type BHV-1, and the LR rescued virus exhibit identical growth properties in cultured bovine cells. In this study, we demonstrated that during early phases of productive infection the LR mutant virus expressed higher levels of LR-RNA relative to the LR rescued virus or wt BHV-1. Bovine kidney cells infected with the LR mutant virus also induced higher levels of beta interferon RNA and interferon response genes. These results suggest that inappropriate expression of LR-RNA, in the absence of LR protein expression, may influence the latency-reactivation cycle and pathogenic potential of BHV-1.</p>

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<author>Sandra Perez et al.</author>


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<title>Factors Associated with the Presence of Coliforms in the Feed and Water of Feedlot Cattle</title>
<link>http://digitalcommons.unl.edu/vetscipapers/108</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/vetscipapers/108</guid>
<pubDate>Thu, 09 Jul 2009 08:07:49 PDT</pubDate>
<description>
	<![CDATA[
	<p>The objective of this study was to investigate coliform counts in feedlot cattle water and feed rations and their associations with management, climate, fecal material, and water <i>Escherichia coli</i> O157 using a cross-sectional study design. Coliform counts were performed on feed samples from 671 pens on 70 feedlots and on water samples from 702 pens on 72 feedlots in four U.S. states collected between May and August 2001. Management and climate factors were obtained by survey and observation. Month of sampling (higher in May and June), presence of corn silage in the ration (negative association), temperature of the feed 1 in. (ca. 2.5 cm) below the surface at the time of sampling (negative association), and wind velocity at the time of sampling (positive association) were significantly associated with log<sub>10</sub> coliform levels in feed. Month of sampling (lower in May versus June July and August), water pH (negative association), and water total solids (positive association) were significantly associated with log<sub>10</sub> water coliform levels. Coliform counts in feed and water were not associated with prevalence of <i>E. coli</i> O157 in cattle feces or water. Management risk factors must be interpreted with caution but the results reported here do not support the use of coliform counts as a marker for <i>E. coli </i>O157 contamination of feed or water.</p>

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<author>Michael W. Sanderson et al.</author>


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<title>Ileocolitis Associated with &lt;i&gt;Anaerobiospirillum&lt;/i&gt; in Cats</title>
<link>http://digitalcommons.unl.edu/vetscipapers/107</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/vetscipapers/107</guid>
<pubDate>Thu, 09 Jul 2009 08:03:16 PDT</pubDate>
<description>
	<![CDATA[
	<p>Ileocolitis associated with spiral bacteria identified as an <i>Anaerobiospirillum</i> sp. was found in six cats. Two cats had acute onset of gastrointestinal signs characterized by vomiting and diarrhea in one cat and vomiting in another cat, one cat had chronic diarrhea that was refractory to medical therapy; one cat had acute onset of anorexia and lethargy, and two cats had clinical signs that were not related to the gastrointestinal tract. The presence of an <i>Anaerobiospirillum</i> sp. was demonstrated on the basis of ultrastructural morphology of spiral bacteria associated with intestinal lesions and PCR amplification of a genus-specific 16S rRNA gene from affected tissues from each cat. The colons of three clinically healthy cats without lesions and one cat with mild colitis not associated with spiral bacteria were negative for <i>Anaerobiospirillum</i> spp. in the same assay. Comparative nucleotide sequence analysis of cloned PCR products from three affected cats further suggested that the spiral bacteria were closely related to <i>Anaerobiospirillum succiniciproducens</i>.</p>

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<author>H. E. V. De Cock et al.</author>


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<title>A Replicon &lt;i&gt;Trans&lt;/i&gt;-Packaging System Reveals the Requirement of Nonstructural Proteins for the Assembly of Bovine Viral Diarrhea Virus (BVDV) Virion</title>
<link>http://digitalcommons.unl.edu/vetscipapers/106</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/vetscipapers/106</guid>
<pubDate>Wed, 27 May 2009 09:47:30 PDT</pubDate>
<description>
	<![CDATA[
	<p>A selective <i>trans</i>-packaging system was developed to produce and isolate bovine viral diarrhea virus (BVDV) pseudo-particles with complementing reporter replicons and their packaging proteins expressed in trans with recombinant vaccinia virus. The encapsidation of replicon rNS3-5B was dependent not only on the <i>in trans</i> expression of structural proteins C, Erns, E1 and E2, but also the nonstructural proteins, p7 and contiguous precursor NS2-3-4A. Nonstructural p7, NS4B, NS5A or NS5B could be expressed <i>in cis</i> and <i>in trans</i> with precursor NS2-3-4A without significantly affecting virion assembly efficiency. NS2-3-4A was identified as an <i>in trans </i>functional precursor in virion assembly. BVDV genomes with mutant NS5B, which did not undergo active replication, were packaged 5-fold less efficiently than the intact genomes demonstrating the importance of replication in virion packaging. These results suggest that genome replication and assembly are closely associated, consistent with a model in which these two steps are coupled for maximum efficiency.</p>

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<author>Delin Liang et al.</author>


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<title>ATP Release by Infected Bovine Monocytes Increases the Intracellular Survival of &lt;i&gt;Mycobacterium avium&lt;/i&gt; Subsp. &lt;i&gt;paratuberculosis&lt;/i&gt;</title>
<link>http://digitalcommons.unl.edu/vetscipapers/105</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/vetscipapers/105</guid>
<pubDate>Wed, 13 May 2009 10:11:27 PDT</pubDate>
<description>
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	<p><i>Mycobacterium avium </i>subsp. <i>paratuberculosis</i> is the etiologic agent of Johne’s disease, a chronic intestinal infection in ruminants. Adenosine 5′-Triphosphate (ATP) has been reported to induce killing of several <i>Mycobacterium</i> species in human and murine macrophages. We investigated whether ATP secreted from <i>M. avium</i> subsp. <i>paratuberculosis</i>-infected bovine monocytes affects intracellular survival of the bacilli. Bovine monocytes constitutively secreted ATP during an 8-day incubation period in vitro; however, M. avium subsp. paratuberculosis infection did not enhance ATP release. Removal of extracellular ATP by the addition of apyrase increased the viability of infected monocytes, but surprisingly decreased the number of viable intracellular bacilli. In contrast to previous reports, addition of extracellular ATP (1 mM) increased intracellular survival of <i>M. avium</i> subsp. <i>paratuberculosis</i> in bovine monocytes. Neither apyrase nor ATP altered production of reactive oxygen intermediates (ROI) or reactive nitrogen intermediates (RNI) by bovine monocytes. These results suggest that ATP release from infected bovine monocytes improves, rather than decreases, the intracellular survival of <i>M. avium</i> subsp. <i>paratuberculosis</i>.</p>

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<author>Seng-Ryong Woo et al.</author>


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<title>What is the Point: Will Screening Mammography Save my Life?</title>
<link>http://digitalcommons.unl.edu/vetscipapers/104</link>
<guid isPermaLink="true">http://digitalcommons.unl.edu/vetscipapers/104</guid>
<pubDate>Wed, 29 Apr 2009 12:36:42 PDT</pubDate>
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	<p><b>Background: </b>We analyzed the claim "mammography saves lives" by calculating the life-saving absolute benefit of screening mammography in reducing breast cancer mortality in women ages 40 to 65. <br /> <b>Methods: </b>To calculate the absolute benefit, we first estimated the screen-free absolute death risk from breast cancer by adjusting the Surveillance, Epidemiology and End Results Program 15-year cumulative breast cancer mortality to account for the separate effects of screening mammography and improved therapy. We calculated the absolute risk reduction (reduction in absolute death risk), the number needed to screen assuming repeated screening, and the survival percentages without and with screening. We varied the relative risk reduction from 10%–30% based on the randomized trials of screening mammography. We developed additional variations of the absolute risk reduction for a screening intervention, including the average benefit of a single screen, as well as the life-saving proportion among patients with earlier cancer detection. <br /> <b>Results: </b>Because the screen-free absolute death risk is approximately 1% overall but rises with age, the relative risk reduction from repeated screening mammography is about 100 times the absolute risk reduction between the starting ages of 50 and 60. Assuming a base case 20% relative risk reduction, repeated screening starting at age 50 saves about 1.8 (overall range, 0.9–2.7) lives over 15 years for every 1000 women screened. The number needed to screen repeatedly is 1000/ 1.8, or 570. The survival percentage is 99.12% without and 99.29% with screening. The average benefit of a single screening mammogram is 0.034%, or 2970 women must be screened once to save one life. Mammography saves 4.3% of screen-detectable cancer patients' lives starting at age 50. This means 23 cancers must be found starting at age 50, or 27 cancers at age 40 and 21 cancers at age 65, to save one life. <br /> <b>Conclusion: </b>The life-saving absolute benefit of screening mammography increases with age as the absolute death risk increases. The number of events needed to save one life varies depending on the prospective screening subset or reference class. Less than 5% of women with screen-detectable cancers have their lives saved.</p>

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<author>James E. Keen et al.</author>


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