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<title>Veterinary Pathology</title>
<url>http://www.vetpathology.org/icons/banner/title.gif</url>
<link>http://www.vetpathology.org</link>
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<item rdf:about="http://www.vetpathology.org/cgi/content/full/45/3/285?rss=1">
<title><![CDATA[[IN MEMORIAM] Dr. Charles C. Capen An Enduring Legacy in Veterinary Pathology]]></title>
<link>http://www.vetpathology.org/cgi/content/full/45/3/285?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1354/vp.45-3-285</dc:identifier>
<dc:title><![CDATA[[IN MEMORIAM] Dr. Charles C. Capen An Enduring Legacy in Veterinary Pathology]]></dc:title>
<dc:publisher>American College of Veterinary Pathologists</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>45</prism:volume>
<prism:endingPage>285</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>285</prism:startingPage>
<prism:section>IN MEMORIAM</prism:section>
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<item rdf:about="http://www.vetpathology.org/cgi/content/full/45/3/287?rss=1">
<title><![CDATA[[EDITORIAL] Introducing the New "Diagnostic Exercise" Column]]></title>
<link>http://www.vetpathology.org/cgi/content/full/45/3/287?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Schoeb, T. R.]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1354/vp.45-3-287</dc:identifier>
<dc:title><![CDATA[[EDITORIAL] Introducing the New "Diagnostic Exercise" Column]]></dc:title>
<dc:publisher>American College of Veterinary Pathologists</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>45</prism:volume>
<prism:endingPage>287</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>287</prism:startingPage>
<prism:section>EDITORIAL</prism:section>
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<item rdf:about="http://www.vetpathology.org/cgi/content/full/45/3/288?rss=1">
<title><![CDATA[[ARTICLES] The Fetal Brain in Bovine Viral Diarrhea Virus-infected Calves: Lesions, Distribution, and Cellular Heterogeneity of Viral Antigen at 190 Days Gestation]]></title>
<link>http://www.vetpathology.org/cgi/content/full/45/3/288?rss=1</link>
<description><![CDATA[
<p>Previous studies have shown that the brain is a target of persistent infection with bovine viral diarrhea virus (BVDV) and have demonstrated viral tropism for neurons as well as other endogenous cell types in diverse brain areas. Apart from foci of mild residual inflammation in some postnatal calves, consistent brain lesions, per se, have not been reported. No similar comprehensive studies of the brain have been reported in bovine fetuses. In the current study, 12 BVDV-seronegative heifers were inoculated intranasally with a 2-ml 4.4 log<SUB>10</SUB> TCID<SUB>50</SUB>/ml dose of noncytopathic type 2 BVDV at 75 and 175&nbsp;days of gestation to create persistently and transiently infected fetuses, respectively. In only persistently infected fetuses, encephaloclastic lesions resulting in pseudocysts were observed in the subependymal zone in the region of the median eminence and adjacent corona radiata as well as in the region of the external capsule associated with lenticulostriate arteries. Additionally, areas of rarefaction in white matter were observed at the tips of cerebrocortical gyri and in the external capsule. The distribution of viral antigen was examined by immunohistochemical labeling using the 15C5 anti-BVDV monoclonal antibody. Viral antigen was detected only in calves inoculated at 75&nbsp;days of gestation, i.e., persistently infected. The pattern of BVDV immunolabeling revealed both similarities and differences compared with previous studies in postnatal calves, suggesting that viral infection in the brain is a dynamic and progressive rather than static process.</p>
]]></description>
<dc:creator><![CDATA[Montgomery, D. L., Van Olphen, A., Van Campen, H., Hansen, T. R.]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1354/vp.45-3-288</dc:identifier>
<dc:title><![CDATA[[ARTICLES] The Fetal Brain in Bovine Viral Diarrhea Virus-infected Calves: Lesions, Distribution, and Cellular Heterogeneity of Viral Antigen at 190 Days Gestation]]></dc:title>
<dc:publisher>American College of Veterinary Pathologists</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>45</prism:volume>
<prism:endingPage>296</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>288</prism:startingPage>
<prism:section>ARTICLES</prism:section>
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<item rdf:about="http://www.vetpathology.org/cgi/content/full/45/3/297?rss=1">
<title><![CDATA[[ARTICLES] Experimental Transmission of Chronic Wasting Disease (CWD) of Elk (Cervus elaphus nelsoni), White-tailed Deer (Odocoileus virginianus), and Mule Deer (Odocoileus hemionus hemionus) to White-tailed Deer by Intracerebral Route]]></title>
<link>http://www.vetpathology.org/cgi/content/full/45/3/297?rss=1</link>
<description><![CDATA[
<p>To compare clinical and pathologic findings of chronic wasting disease (CWD) in a natural host, 3 groups (<I>n</I>  =  5) of white-tailed deer (WTD) fawns were intracerebrally inoculated with a CWD prion of WTD, mule deer, or elk origin. Three other uninoculated fawns served as controls. Approximately 10&nbsp;months postinoculation (MPI), 1 deer from each of the 3 inoculated groups was necropsied and their tissues were examined for lesions of spongiform encephalopathy (SE) and for the presence of abnormal prion protein (PrP<sup>d</sup>) by immunohistochemistry (IHC) and Western blot (WB). The remaining deer were allowed to live until they developed clinical signs of the disease which began approximately 18 MPI. By 26 MPI, all deer were euthanatized on humane grounds. Obvious differences in clinical signs or the incubation periods were not observed between the 3 groups of deer given CWD. In 1 of 3 nonclinical deer euthanatized at 10 MPI, minimal microscopic lesions of SE were seen in the central nervous system (CNS) tissues, and PrP<sup>d</sup> was observed by IHC in tissues of all 3 deer. In the clinical deer, CNS lesions of SE and PrP<sup>d</sup> accumulations were more severe and extensive. It is concluded that the 3 sources of CWD prion did not induce significant differences in time to clinical disease or qualitative differences in signs or lesions in WTD. However, this observation does not imply that these CWD agents would necessarily behave similarly in other recipient species.</p>
]]></description>
<dc:creator><![CDATA[Hamir, A. N., Richt, J. A., Miller, J. M., Kunkle, R. A., Hall, S. M., Nicholson, E. M., O'Rourke, K. I., Greenlee, J. J., Williams, E. S.]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1354/vp.45-3-297</dc:identifier>
<dc:title><![CDATA[[ARTICLES] Experimental Transmission of Chronic Wasting Disease (CWD) of Elk (Cervus elaphus nelsoni), White-tailed Deer (Odocoileus virginianus), and Mule Deer (Odocoileus hemionus hemionus) to White-tailed Deer by Intracerebral Route]]></dc:title>
<dc:publisher>American College of Veterinary Pathologists</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>45</prism:volume>
<prism:endingPage>306</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>297</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://www.vetpathology.org/cgi/content/full/45/3/307?rss=1">
<title><![CDATA[[BRIEF COMMUNICATIONS AND CASE REPORTS] Aquaporin-4 in Acute Cerebral Edema Produced by Clostridium perfringens Type D Epsilon Toxin]]></title>
<link>http://www.vetpathology.org/cgi/content/full/45/3/307?rss=1</link>
<description><![CDATA[
<p>Sheep, particularly lambs, with high circulating levels of <I>Clostridium perfringens</I> type D epsilon toxin develop severe neurologic signs and often die suddenly. On microscopic examination, in the brain, there is microvascular endothelial injury and diffuse vasogenic edema. The aquaporin (AQP) family of membrane water-channel proteins, especially AQP-4, is important in the regulation of water balance in the brain and facilitates reabsorption of excess fluid. In rats given epsilon toxin, generalized cerebral edema was demonstrated by marked albumin extravasation and was correlated with widespread upregulation of AQP-4 in astrocytes. These results suggest that AQP-4 has a role in the clearance of edema fluid from brains damaged by this clostridial toxin.</p>
]]></description>
<dc:creator><![CDATA[Finnie, J. W., Manavis, J., Blumbergs, P. C.]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1354/vp.45-3-307</dc:identifier>
<dc:title><![CDATA[[BRIEF COMMUNICATIONS AND CASE REPORTS] Aquaporin-4 in Acute Cerebral Edema Produced by Clostridium perfringens Type D Epsilon Toxin]]></dc:title>
<dc:publisher>American College of Veterinary Pathologists</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>45</prism:volume>
<prism:endingPage>309</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>307</prism:startingPage>
<prism:section>BRIEF COMMUNICATIONS AND CASE REPORTS</prism:section>
</item>

<item rdf:about="http://www.vetpathology.org/cgi/content/full/45/3/310?rss=1">
<title><![CDATA[[BRIEF COMMUNICATIONS AND CASE REPORTS] Experimental Reproduction of Severe Bluetongue in Sheep]]></title>
<link>http://www.vetpathology.org/cgi/content/full/45/3/310?rss=1</link>
<description><![CDATA[
<p>Sheep inoculated with a virulent South African strain of bluetongue (BT) virus serotype 4 developed severe clinical signs and lesions characteristic of fulminant BT, including coronitis, hemorrhage and ulceration of the mucosal lining of the oral cavity and forestomaches, hemorrhage in the wall of the pulmonary artery, and focally extensive necrosis of skeletal muscle, especially of the neck. At necropsy, up to 14&nbsp;days after infection, the infected sheep exhibited striking pulmonary edema, edema of the subcutaneous tissues and fascial planes of the head and neck, and pleural and pericardial effusion of varying severity. A reliable model for experimental reproduction of fulminant BT in sheep will facilitate future studies to better characterize the pathogenesis of this disease, particularly as it regards the mechanisms responsible for the increased vascular permeability that characterizes BT and related orbiviral diseases such as African horse sickness.</p>
]]></description>
<dc:creator><![CDATA[MacLachlan, N. J., Crafford, J. E., Vernau, W., Gardner, I. A., Goddard, A., Guthrie, A. J., Venter, E. H.]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1354/vp.45-3-310</dc:identifier>
<dc:title><![CDATA[[BRIEF COMMUNICATIONS AND CASE REPORTS] Experimental Reproduction of Severe Bluetongue in Sheep]]></dc:title>
<dc:publisher>American College of Veterinary Pathologists</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>45</prism:volume>
<prism:endingPage>315</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>310</prism:startingPage>
<prism:section>BRIEF COMMUNICATIONS AND CASE REPORTS</prism:section>
</item>

<item rdf:about="http://www.vetpathology.org/cgi/content/full/45/3/316?rss=1">
<title><![CDATA[[ARTICLES] Regional Pulmonary Veno-occlusion: A Newly Identified Lesion of Equine Exercise-induced Pulmonary Hemorrhage]]></title>
<link>http://www.vetpathology.org/cgi/content/full/45/3/316?rss=1</link>
<description><![CDATA[
<p>Exercise-induced pulmonary hemorrhage (EIPH) is common in horses following intense exertion, occurring in up to 75% of racing Thoroughbreds and Standardbreds. In spite of this, the pathogenesis of EIPH is poorly understood. In 7 racing Thoroughbred horses with EIPH, 6 sections were collected from the left and right lung, representing the cranial, middle, and caudal region of the dorsal and ventral lung (84 sites total). Grossly, both right and left lungs had numerous dark brown to blue&ndash;black foci along the caudodorsal visceral pleura. Tissue sections were stained with hematoxylin-eosin, Masson's trichrome, and Prussian blue. Verhoeff Van Gieson and immunohistochemistry for -smooth muscle actin were used to assess the pulmonary vasculature. Histologic scores (HS  =  0&ndash;3) were assigned to each region/slide for the presence and severity of 5 findings: interstitial fibrosis, hemosiderin accumulation, pleural/interlobular septal thickness, arterial and venous wall thickness, and evidence of angiogenesis (maximum cumulative HS  =  15). Thirty-nine of the 84 (46%) sections were histologically normal (HS  =  0); 33/84 (39%) were mildly to moderately affected, with small amounts of hemosiderin and fibrosis (HS  =  1&ndash;9) while 12/84 (14%), primarily from the dorsocaudal lung, had severe vascular remodeling, fibrosis, and hemosiderin accumulation (HS  =  10&ndash;15). In the latter, veno-occlusive remodeling of the intralobular veins colocalized with hemosiderosis, fibrosis, hypertrophy of vessels within the pleura, and interlobular septa and bronchial neovascularization. We propose that regional veno-occlusive remodeling, especially within the caudodorsal lung fields, contributes to the pathogenesis of EIPH, with the venous remodeling leading to regional vascular congestion and hemorrhage, hemosiderin accumulation, fibrosis, and bronchial angiogenesis.</p>
]]></description>
<dc:creator><![CDATA[Williams, K. J., Derksen, F. J., de Feijter-Rupp, H., Pannirselvam, R. R., Steel, C. M., Robinson, N. E.]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1354/vp.45-3-316</dc:identifier>
<dc:title><![CDATA[[ARTICLES] Regional Pulmonary Veno-occlusion: A Newly Identified Lesion of Equine Exercise-induced Pulmonary Hemorrhage]]></dc:title>
<dc:publisher>American College of Veterinary Pathologists</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>45</prism:volume>
<prism:endingPage>326</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>316</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://www.vetpathology.org/cgi/content/full/45/3/327?rss=1">
<title><![CDATA[[ARTICLES] Photodamage in Feline Skin: Clinical and Histomorphometric Analysis]]></title>
<link>http://www.vetpathology.org/cgi/content/full/45/3/327?rss=1</link>
<description><![CDATA[
<p>The purpose of this study was to investigate clinical and histomorphometric features of cat skin under long-term solar exposure. Ear skin of 34 Domestic Shorthair cats that were chronically exposed to sun was classified as follows: group 0, normal (<I>n</I>  =  13); group 1, initial stage of photodamage (PD) (<I>n</I>  =  10); group 2, advanced stage of PD (<I>n</I>  =  11). Histologic sections were examined independently by 2 pathologists, and epidermal thickness, adnexal unit area, and dermal cellularity were assessed by morphometry. A positive correlation was obtained between age, degree of edema and sclerosis in the upper dermis, telangiectases, squamatization of basal keratinocytes, and epidermis thickness and the degree of PD. The area occupied by adnexal structures in the dermis diminished with increased PD. Dermal sclerosis and edema best separated the 3 groups. The results indicated a high level of skin hypersensitivity to sun rays in cats. The findings may be useful for clinical testing and in general veterinary pathology and dermatology.</p>
]]></description>
<dc:creator><![CDATA[Almeida, E. M. P., CaraCa, R. A., Adam, R. L., Souza, E. M., Metze, K., Cintra, M. L.]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1354/vp.45-3-327</dc:identifier>
<dc:title><![CDATA[[ARTICLES] Photodamage in Feline Skin: Clinical and Histomorphometric Analysis]]></dc:title>
<dc:publisher>American College of Veterinary Pathologists</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>45</prism:volume>
<prism:endingPage>335</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>327</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://www.vetpathology.org/cgi/content/full/45/3/336?rss=1">
<title><![CDATA[[ARTICLES] Necrotizing Meningoencephalitis in Five Chihuahua Dogs]]></title>
<link>http://www.vetpathology.org/cgi/content/full/45/3/336?rss=1</link>
<description><![CDATA[
<p>An acute to chronic idiopathic necrotizing meningoencephalitis was diagnosed in 5 Chihuahua dogs aged between 1.5 and 10&nbsp;years. Presenting neurologic signs included seizures, blindness, mentation changes, and postural deficits occurring from 5&nbsp;days to 5.5&nbsp;months prior to presentation. Cerebrospinal fluid analyses from 2 of 3 dogs sampled were consistent with an inflammatory disease. Magnetic resonance imaging of the brain of 2 dogs demonstrated multifocal loss or collapse of cortical gray/white matter demarcation hypointense on T1-weighted images, with T2-weighted hyperintensity and slight postcontrast enhancement. Multifocal asymmetrical areas of necrosis or collapse in both gray and white matter of the cerebral hemispheres was seen grossly in 4 brains. Microscopically in all dogs, there was a severe, asymmetrical, intensely cellular, nonsuppurative meningoencephalitis usually with cystic necrosis in subcortical white matter. There were no lesions in the mesencephalon or metencephalon except in 1 dog. Immunophenotyping defined populations of CD3, CD11d, CD18, CD20, CD45, CD45 RA, and CD79a immunoreactive inflammatory cells varying in density and location but common to acute and chronic lesions. In fresh frozen lesions, both CD1b,c and CD11c immunoreactive dendritic antigen-presenting cells were also identified. Immunoreactivity for canine distemper viral (CDV) antigen was negative in all dogs. The clinical signs, distribution pattern, and histologic type of lesions bear close similarities to necrotizing meningoencephalitis as described in series of both Pug and Maltese breed dogs and less commonly in other breeds.</p>
]]></description>
<dc:creator><![CDATA[Higgins, R. J., Dickinson, P. J., Kube, S. A., Moore, P. F., Couto, S. S., Vernau, K. M., Sturges, B. K., Lecouteur, R. A.]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1354/vp.45-3-336</dc:identifier>
<dc:title><![CDATA[[ARTICLES] Necrotizing Meningoencephalitis in Five Chihuahua Dogs]]></dc:title>
<dc:publisher>American College of Veterinary Pathologists</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>45</prism:volume>
<prism:endingPage>346</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>336</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://www.vetpathology.org/cgi/content/full/45/3/347?rss=1">
<title><![CDATA[[BRIEF COMMUNICATIONS AND CASE REPORTS] Noncongophilic Fibrillary Glomerulonephritis in a Cat]]></title>
<link>http://www.vetpathology.org/cgi/content/full/45/3/347?rss=1</link>
<description><![CDATA[
<p>This report describes an uncommon case of nonamyloidotic fibrillary glomerulonephritis. A 5-year-old female European cat was presented with nephrotic syndrome. Serum biochemistry and urinalysis revealed a mild increase in cholesterol, low total protein, severe hypoalbuminemia, and high proteinuria with a high protein-to-creatinine ratio. An histologic examination revealed an interstitial nephritis and a diffuse glomerulonephritis, with multifocal thickening of the Bowman's capsule. Transmission electron microscopy showed widespread fibrillary deposits in the glomerular basement membrane and in the mesangium. These fibrils ranged between 18 and 26&nbsp;nm in diameter and were Congo red negative, which allowed their differentiation from amyloid. Immunohistochemistry demonstrated expression for immunoglobulin M (IgM) and immunoglobulin G (IgG) within the mesangium. Renal deposits of Congo red&ndash;negative amyloid-like fibrils have been described in humans, horses, monkeys, and dogs. This is the first report of noncongophilic fibrillary glomerulopathy in a cat.</p>
]]></description>
<dc:creator><![CDATA[Cavana, P., Capucchio, M. T., Bovero, A., Ripanti, D., Catalano, D., Scaglione, F. E., Miller, J., Blunden, T., Farca, A. M.]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1354/vp.45-3-347</dc:identifier>
<dc:title><![CDATA[[BRIEF COMMUNICATIONS AND CASE REPORTS] Noncongophilic Fibrillary Glomerulonephritis in a Cat]]></dc:title>
<dc:publisher>American College of Veterinary Pathologists</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>45</prism:volume>
<prism:endingPage>351</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>347</prism:startingPage>
<prism:section>BRIEF COMMUNICATIONS AND CASE REPORTS</prism:section>
</item>

<item rdf:about="http://www.vetpathology.org/cgi/content/full/45/3/352?rss=1">
<title><![CDATA[[BRIEF COMMUNICATIONS AND CASE REPORTS] Cutaneous and Nasal Protothecosis in a Goat]]></title>
<link>http://www.vetpathology.org/cgi/content/full/45/3/352?rss=1</link>
<description><![CDATA[
<p>A case of protothecosis is reported in an adult goat with inspiratory dyspnea and stertor. Dermatitis with prominent ulcerated nodules up to 3&nbsp;cm in diameter was observed in the muzzle at the mucocutaneous junctions of nasal and lip skin, and in the border of the pinna. Histologic lesions were necrotizing pyogranulomatous dermatitis and rhinitis with myriads of walled sporangia, characteristic of <I>Prototheca wickerhamii.</I> This seems to be the first report of protothecosis in a goat.</p>
]]></description>
<dc:creator><![CDATA[Macedo, J. T. S. A., Riet-Correa, F., Dantas, A. F. M., Simoes, S. V. D.]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1354/vp.45-3-352</dc:identifier>
<dc:title><![CDATA[[BRIEF COMMUNICATIONS AND CASE REPORTS] Cutaneous and Nasal Protothecosis in a Goat]]></dc:title>
<dc:publisher>American College of Veterinary Pathologists</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>45</prism:volume>
<prism:endingPage>354</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>352</prism:startingPage>
<prism:section>BRIEF COMMUNICATIONS AND CASE REPORTS</prism:section>
</item>

<item rdf:about="http://www.vetpathology.org/cgi/content/full/45/3/355?rss=1">
<title><![CDATA[[BRIEF COMMUNICATIONS AND CASE REPORTS] Expression of Brain-derived Neurotrophic Factor and Tropomyosin-related Kinase-B in a Bovine Jejunal Nodular Ganglioneuroblastoma]]></title>
<link>http://www.vetpathology.org/cgi/content/full/45/3/355?rss=1</link>
<description><![CDATA[
<p>This report describes the morphologic, ultrastructural, and immunophenotypic features of a nodular ganglioneuroblastoma in the jejunum of a 13-month-old Holstein-Friesian heifer. On histologic examination, the mass was composed of clusters of neuroblasts and isolated ganglionic neurons in abundant neurophilic matrix that was surrounded by scanty Schwannian stroma. On ultrastructure examination, the large ganglionic neuron-like cells had unmyelinated neurites. Most ganglionic neuron-like tumor cells expressed neurofilament, neuron-specific enolase, chromogranin A, and S-100, whereas the Schwann-cell&ndash;like stromal cells expressed S-100 and vimentin. Both brain-derived neurotrophic factor (BDNF) and tropomyosin-related kinase-B (Trk-B) were expressed in ganglionic neuron-like tumor cells, which suggested the activation or reactivation of an embryonic autocrine BDNF/Trk-B pathway that could have prolonged cell survival and promoted differentiation with neurite formation.</p>
]]></description>
<dc:creator><![CDATA[Ulrich, R., Stan, A. C., Koch, A., Beineke, A.]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1354/vp.45-3-355</dc:identifier>
<dc:title><![CDATA[[BRIEF COMMUNICATIONS AND CASE REPORTS] Expression of Brain-derived Neurotrophic Factor and Tropomyosin-related Kinase-B in a Bovine Jejunal Nodular Ganglioneuroblastoma]]></dc:title>
<dc:publisher>American College of Veterinary Pathologists</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>45</prism:volume>
<prism:endingPage>360</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>355</prism:startingPage>
<prism:section>BRIEF COMMUNICATIONS AND CASE REPORTS</prism:section>
</item>

<item rdf:about="http://www.vetpathology.org/cgi/content/full/45/3/361?rss=1">
<title><![CDATA[[BRIEF COMMUNICATIONS AND CASE REPORTS] Primary Intimal Aortic Angiosarcoma in a Dog]]></title>
<link>http://www.vetpathology.org/cgi/content/full/45/3/361?rss=1</link>
<description><![CDATA[
<p>A primary intimal aortic angiosarcoma was diagnosed in a 4-year-old, spayed female German Shepherd that presented for complications of thromboembolic disease because of infarcts in multiple organs. On gross examination, aneurysmal dilatation of the aorta was associated with a friable, necrotic mass attached to the endothelial surface, which partially occluded the aortic lumen. On histologic examination, plump neoplastic spindle cells formed a plaque-like mass arising from the intima that merged with a large accumulation of fibrin and necrotic debris, and projected into the lumen. Neoplastic cells invaded periaortic vessels and were seen in some infarct-associated thromboemboli. Tumor cells expressed vimentin and CD31, with infrequent, patchy staining with factor VIII-related antigen; tumor cells were negative for cytokeratin and smooth-muscle actin. Aortic angiosarcoma is a rare malignancy in humans. This is the first description of a primary intimal aortic angiosarcoma in a dog, with immunohistochemical evidence of endothelial origin.</p>
]]></description>
<dc:creator><![CDATA[Ranck, R. S., Linder, K. E., Haber, M. D., Meuten, D. J.]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1354/vp.45-3-361</dc:identifier>
<dc:title><![CDATA[[BRIEF COMMUNICATIONS AND CASE REPORTS] Primary Intimal Aortic Angiosarcoma in a Dog]]></dc:title>
<dc:publisher>American College of Veterinary Pathologists</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>45</prism:volume>
<prism:endingPage>364</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>361</prism:startingPage>
<prism:section>BRIEF COMMUNICATIONS AND CASE REPORTS</prism:section>
</item>

<item rdf:about="http://www.vetpathology.org/cgi/content/full/45/3/365?rss=1">
<title><![CDATA[[BRIEF COMMUNICATIONS AND CASE REPORTS] Nasal Acinic Cell Carcinoma in a Cat]]></title>
<link>http://www.vetpathology.org/cgi/content/full/45/3/365?rss=1</link>
<description><![CDATA[
<p>This case report describes the clinical, magnetic resonance imaging (MRI)&ndash;related, and pathologic features of a nasal acinic cell carcinoma in a cat. A 16-year-old, castrated male, oriental shorthaired cat, weighing 3.8&nbsp;kg, was presented with history of sneezing, coughing, and nasal discharge persisting several months. Evaluation by MRI revealed an heterogeneous, space-occupying lesion that filled the left nasal cavity and was diagnosed by histopathologic examination as an acinic cell carcinoma arising from a minor salivary gland of the nasal cavity. Acinic cell carcinoma is a rare tumor in veterinary medicine. The tumor is composed mainly of cells resembling serous cells of salivary glands and originates from major or minor salivary glands. Clinicians and pathologists should be aware of the occurrence of acinic cell carcinoma in the sinonasal tract and include the tumor in the differential diagnosis of feline nasal diseases.</p>
]]></description>
<dc:creator><![CDATA[Psalla, D., Geigy, C., Konar, M., Marcal, V.C., Oevermann, A.]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1354/vp.45-3-365</dc:identifier>
<dc:title><![CDATA[[BRIEF COMMUNICATIONS AND CASE REPORTS] Nasal Acinic Cell Carcinoma in a Cat]]></dc:title>
<dc:publisher>American College of Veterinary Pathologists</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>45</prism:volume>
<prism:endingPage>368</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>365</prism:startingPage>
<prism:section>BRIEF COMMUNICATIONS AND CASE REPORTS</prism:section>
</item>

<item rdf:about="http://www.vetpathology.org/cgi/content/full/45/3/369?rss=1">
<title><![CDATA[[ARTICLES] An Outbreak of Fatal Herpesvirus Infection in Domestic Rabbits in Alaska]]></title>
<link>http://www.vetpathology.org/cgi/content/full/45/3/369?rss=1</link>
<description><![CDATA[
<p>A herpesvirus infection affecting mini Rex and crossbred meat rabbits was identified in a rabbitry in Alaska. Illness affected over half of the 55 rabbits on the premises, and 16 rabbits died or were euthanatized because of illness. Disease affected all ages from adults to nursing young and occurred over an approximately 2-month period. Clinical signs included conjunctivitis and periocular swelling, ulcerative dermatitis, progressive weakness, anorexia, respiratory distress, and abortion. Hemorrhagic dermatitis and panniculitis were associated with epidermal microvesicular degeneration, dermal and subcutaneous vascular necrosis, and thrombosis. Eosinophilic intranuclear inclusions consistent with herpesvirus were found within the epidermis and superficial follicular epithelium and within mesenchymal cells within the dermis and subcutis. Syncytial cells containing viral inclusions occurred within the epidermal and superficial follicular epithelium. Other findings were hemorrhagic necrosis of the myocardium with rare intranuclear inclusions within stromal cells, multifocal pulmonary hemorrhage, hemorrhage with sinus erythrophagocytosis in lymph nodes, and massive necrosis and fibrin deposition within red pulp of the spleen. A virus isolated from the skin produced syncytia, intranuclear inclusions, and cell lysis typical of herpesvirus in rabbit kidney cells in vitro. The viral isolate was characterized ultrastructurally as an enveloped virus with icosahedral nucleocapsids 100&nbsp;nm&nbsp;diameter, consistent with a herpesvirus.</p>
]]></description>
<dc:creator><![CDATA[Jin, L., Valentine, B. A., Baker, R. J., Lohr, C. V., Gerlach, R. F., Bildfell, R. J., Moerdyk-Schauwecker, M.]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1354/vp.45-3-369</dc:identifier>
<dc:title><![CDATA[[ARTICLES] An Outbreak of Fatal Herpesvirus Infection in Domestic Rabbits in Alaska]]></dc:title>
<dc:publisher>American College of Veterinary Pathologists</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>45</prism:volume>
<prism:endingPage>374</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>369</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://www.vetpathology.org/cgi/content/full/45/3/375?rss=1">
<title><![CDATA[[BRIEF COMMUNICATIONS AND CASE REPORTS] Non-gestational Malignant Placental Site Trophoblastic Tumor of the Ovary in a 4-Year-Old Rhesus Monkey]]></title>
<link>http://www.vetpathology.org/cgi/content/full/45/3/375?rss=1</link>
<description><![CDATA[
<p>We report a case of ovarian malignant intermediate-type trophoblastic tumor in a clinically normal, nonpregnant 4-year-old rhesus monkey (<I>Macaca mulatta</I>). A large solid lobulated mass replaced the right ovary and filled the pelvis. Multiple metastases were observed within the lungs and the liver. The tumor was histologically identified as predominantly composed of intermediate trophoblastic cells, without prominent hemorrhages and the classic bilaminar pattern of cyto- and syncytiotrophoblastic cells characteristic of choriocarcinoma. Immunohistochemical analysis showed the presence of placental lactogen hormone in many tumor cells and chorionic gonadotropin in a few multinucleated cells consistent with syncytiotrophoblastic differentiation. No other germ cell differentiation was identified in the pelvis mass nor in the metastases. In the absence of previous and present pregnancy, this neoplasm has to be considered as a nongestational malignant placental site trophoblastic tumor of the ovary.</p>
]]></description>
<dc:creator><![CDATA[Marbaix, E., Defrere, S., Duc, K. H. M., Lousse, J.-C, Dehoux, J.-P]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1354/vp.45-3-375</dc:identifier>
<dc:title><![CDATA[[BRIEF COMMUNICATIONS AND CASE REPORTS] Non-gestational Malignant Placental Site Trophoblastic Tumor of the Ovary in a 4-Year-Old Rhesus Monkey]]></dc:title>
<dc:publisher>American College of Veterinary Pathologists</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>45</prism:volume>
<prism:endingPage>378</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>375</prism:startingPage>
<prism:section>BRIEF COMMUNICATIONS AND CASE REPORTS</prism:section>
</item>

<item rdf:about="http://www.vetpathology.org/cgi/content/full/45/3/379?rss=1">
<title><![CDATA[[BRIEF COMMUNICATIONS AND CASE REPORTS] Ovarian Mucinous Cystadenoma with Smooth Muscle Proliferation in a Cynomolgus Monkey (Macaca fascicularis)]]></title>
<link>http://www.vetpathology.org/cgi/content/full/45/3/379?rss=1</link>
<description><![CDATA[
<p>An ovarian mucinous cystadenoma was found in a 5-year-old female cynomolgus monkey (<I>Macaca fascicularis</I>). The tumor was composed of various sizes of multilocular cystic glands lined by a single layer of mucin-filled epithelium. Each of these cystic glands was surrounded by a large amount of solid fibrous stroma resembling smooth muscle. The ovarian surface epithelium showed partial invagination into the ovarian cortex, and a transition was observed between the surface epithelium and the mucinous cyst-forming epithelium. Immunohistochemically, the stromal cells were positive for -smooth muscle actin and proliferating cell nuclear antigen. Ultrastructurally, the glandular epithelium had numerous mucinous secretory granules and microvilli. The stromal cells had numerous parallel microfibrils with focal density. It is rare to encounter evidence of a transition from the surface epithelium to the mucinous tumor epithelium and to show stromal smooth muscle proliferation in a mucinous cystadenoma.</p>
]]></description>
<dc:creator><![CDATA[Sato, J., Kokoshima, H., Tsuchitani, M.]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1354/vp.45-3-379</dc:identifier>
<dc:title><![CDATA[[BRIEF COMMUNICATIONS AND CASE REPORTS] Ovarian Mucinous Cystadenoma with Smooth Muscle Proliferation in a Cynomolgus Monkey (Macaca fascicularis)]]></dc:title>
<dc:publisher>American College of Veterinary Pathologists</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>45</prism:volume>
<prism:endingPage>382</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>379</prism:startingPage>
<prism:section>BRIEF COMMUNICATIONS AND CASE REPORTS</prism:section>
</item>

<item rdf:about="http://www.vetpathology.org/cgi/content/full/45/3/383?rss=1">
<title><![CDATA[[BRIEF COMMUNICATIONS AND CASE REPORTS] A Novel Immunohistochemical Marker of Normal and Neoplastic Melanocytes in Formalin-fixed, Paraffin-embedded Tissues of Albino Rats]]></title>
<link>http://www.vetpathology.org/cgi/content/full/45/3/383?rss=1</link>
<description><![CDATA[
<p>In albino rats, spontaneous occurrence of melanocytic tumors is rare, with diagnosis difficult. This study evaluated immunoreactivity for PNL2 in normal and neoplastic melanocytes in formalin-fixed and paraffin-embedded tissues of albino rats. The samples consisted of 11 (1.57%) amelanotic melanomas in 700 rats (2 studies), 23 non-melanocytic tumors, and a wide variety of normal tissues. In normal albino rats, PNL2 stained the melanocytes in the iris and choroid of the eyeball and the hair bulb and basal cell layers of the epidermis of the whole body. In amelanotic melanoma, the tumor cells consisted of spindle cells with eosinophilic cytoplasm without melanin granules. PNL2 consistently stained cytoplasm in all amelanotic melanoma cells. In contrast, the nonmelanocytic tumor cells were not labeled. Electron microscopically, neoplastic, and normal melanocytes showed numerous cytoplasmic premelanosomes (stage II melanosome). In conclusion, PNL2 is direct against a fixative- and decalcific-resistant melanocyte-associated antigen, and has high specificity against normal and neoplastic melanocytes of albino rats.</p>
]]></description>
<dc:creator><![CDATA[Kurotaki, T., Tomonari, Y., Kanno, T., Wako, Y., Tsuchitani, M.]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1354/vp.45-3-383</dc:identifier>
<dc:title><![CDATA[[BRIEF COMMUNICATIONS AND CASE REPORTS] A Novel Immunohistochemical Marker of Normal and Neoplastic Melanocytes in Formalin-fixed, Paraffin-embedded Tissues of Albino Rats]]></dc:title>
<dc:publisher>American College of Veterinary Pathologists</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>45</prism:volume>
<prism:endingPage>387</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>383</prism:startingPage>
<prism:section>BRIEF COMMUNICATIONS AND CASE REPORTS</prism:section>
</item>

<item rdf:about="http://www.vetpathology.org/cgi/content/full/45/3/388?rss=1">
<title><![CDATA[[ARTICLES] Harderian Gland Neoplasms in Captive, Wild-caught Beechey Ground Squirrels (Spermophilus beecheyi)]]></title>
<link>http://www.vetpathology.org/cgi/content/full/45/3/388?rss=1</link>
<description><![CDATA[
<p>Harderian gland neoplasms were identified in 18 aged, adult Beechey ground squirrels (<I>Spermophilus beecheyi</I>) from the records of 167 wild-caught captive animals that were necropsied. All but one animal had tumors that were classified as carcinomas, with infiltrative growth and frequent metastases. This is the first detailed report of Harderian gland neoplasia in wild Sciuridae, although this neoplasm has been described in other rodent species. Clinically, affected ground squirrels typically were inappetent and presented with weight loss and exophthalmos. The biologic behavior of Harderian gland neoplasia is variable among rodent species; in Beechey ground squirrels there was a high incidence of malignant behavior. Eleven of 17 tumor-bearing animals for which the gender was known were male, and 6 were female. Nine of 16 for which data were available were uninfected, and 7 had evidence of current or prior infection with ground squirrel hepatitis virus. Tumor development occurred in older animals; all but 2 were 5.5 years of age or older. The presence of metastasis was not related to gender or chronic ground squirrel hepatitis virus infection.</p>
]]></description>
<dc:creator><![CDATA[Ranck, R. S., Cullen, J. M., Waggie, K. S., Marion, P. L.]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1354/vp.45-3-388</dc:identifier>
<dc:title><![CDATA[[ARTICLES] Harderian Gland Neoplasms in Captive, Wild-caught Beechey Ground Squirrels (Spermophilus beecheyi)]]></dc:title>
<dc:publisher>American College of Veterinary Pathologists</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>45</prism:volume>
<prism:endingPage>392</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>388</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://www.vetpathology.org/cgi/content/full/45/3/393?rss=1">
<title><![CDATA[[ARTICLES] Amyloidosis in Black-footed Cats (Felis nigripes)]]></title>
<link>http://www.vetpathology.org/cgi/content/full/45/3/393?rss=1</link>
<description><![CDATA[
<p>A high prevalence of systemic amyloidosis was documented in the black-footed cat (<I>Felis nigripes</I>) based on a retrospective review of necropsy tissues (<I>n</I>  =  38) submitted as part of ongoing disease surveillance. Some degree of amyloid deposition was present in 33 of 38 (87%) of the examined cats, and amyloidosis was the most common cause of death (26/38, 68%). Amyloid deposition was most severe in the renal medullary interstitium (30/33, 91%) and glomeruli (21/33, 63%). Other common sites included the splenic follicular germinal centers (26/31, 84%), gastric lamina propria (9/23, 39%), and intestinal lamina propria (3/23, 13%). Amyloid in all sites stained with Congo red, and in 13 of 15 (87%) cats, deposits had strong immunoreactivity for canine AA protein by immunohistochemistry. There was no association with concurrent chronic inflammatory conditions (<I>P</I>  =  .51), suggesting that amyloidosis was not secondary to inflammation. Adrenal cortical hyperplasia, a morphologic indicator of stress that can predispose to amyloid deposition, was similarly not associated (<I>P</I>  =  .09) with amyloidosis. However, adrenals were not available from the majority of cats without amyloidosis; therefore, further analysis of this risk factor is warranted. Heritability estimation suggested that amyloidosis might be familial in this species. Additionally, tissues from a single free-ranging black-footed cat had small amounts of amyloid deposition, suggesting that there could be a predilection for amyloidosis in this species. Research to identify the protein sequence of serum amyloid A (SAA) in the black-footed cat is needed to further investigate the possibility of an amyloidogenic SAA in this species.</p>
]]></description>
<dc:creator><![CDATA[Terio, K. A., O'Brien, T., Lamberski, N., Famula, T. R., Munson, L.]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1354/vp.45-3-393</dc:identifier>
<dc:title><![CDATA[[ARTICLES] Amyloidosis in Black-footed Cats (Felis nigripes)]]></dc:title>
<dc:publisher>American College of Veterinary Pathologists</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>45</prism:volume>
<prism:endingPage>400</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>393</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://www.vetpathology.org/cgi/content/full/45/3/401?rss=1">
<title><![CDATA[[ARTICLES] Feather-picking Psittacines: Histopathology and Species Trends]]></title>
<link>http://www.vetpathology.org/cgi/content/full/45/3/401?rss=1</link>
<description><![CDATA[
<p>Histologic findings are described for 408 feather-picking or self-mutilating psittacines with the use of biopsies from clinically affected and unaffected skin. Inflammatory skin disease was diagnosed in 210 birds, and traumatic skin disease was diagnosed in 198 birds. Criteria used for the diagnosis of inflammatory skin disease included the presence of perivascular inflammation in the superficial or deep dermis of clinically affected and unaffected sites. The primary histologic criteria for the diagnosis of traumatic skin disease were superficial dermal scarring with or without inflammation in the affected sites and an absence of inflammation in the unaffected sites. The inflammatory cells associated with the lesions were typically lymphocytes and occasionally plasma cells, histiocytes, and granulocytes. A preponderance of inflammatory skin disease was seen in macaws (<I>Ara</I> spp.) and Amazon parrots (<I>Amazona</I> spp.). A preponderance of traumatic skin disease was seen in cockatoos (<I>Cacatua</I> spp.) and African grey parrots (<I>Psittacus erithacus</I>). The prevalence of each was approximately equal in several other species, including conures (<I>Aratinga</I> and <I>Pyrrhura</I> spp.), eclectus parrots (<I>Eclectus roratus</I>), quaker parrots (<I>Myiopsitta monachus</I>), cockatiels (<I>Nymphicus hollandicus</I>), parakeets (<I>Cyanorhamphus</I> and <I>Psittacula</I> spp.), and caiques (<I>Pionites</I> spp.). No geographic or gender-based trends were identified. These findings could be helpful for identifying and treating birds with feather-picking disorders.</p>
]]></description>
<dc:creator><![CDATA[Garner, M. M., Clubb, S. L., Mitchell, M. A., Brown, L.]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1354/vp.45-3-401</dc:identifier>
<dc:title><![CDATA[[ARTICLES] Feather-picking Psittacines: Histopathology and Species Trends]]></dc:title>
<dc:publisher>American College of Veterinary Pathologists</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>45</prism:volume>
<prism:endingPage>408</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>401</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://www.vetpathology.org/cgi/content/full/45/3/409?rss=1">
<title><![CDATA[[BRIEF COMMUNICATIONS AND CASE REPORTS] Trophoblast-like Cells in the Tissues of Porcupines (Erethizon dorsatum)]]></title>
<link>http://www.vetpathology.org/cgi/content/full/45/3/409?rss=1</link>
<description><![CDATA[
<p>During development and subsequent field evaluation of an oral vaccinia-rabies glycoprotein (V-RG) recombinant virus vaccine, 53 adult porcupines (<I>Erethizon dorsatum</I>; 38 females and 15 males) were examined. Microscopic examinations revealed the presence of giant epitheloid cells in various tissues (adrenal glands, spleen, liver, and lungs) of 4 (11%) female animals. These giant cells were approximately 20 times the size of the surrounding cells of the parenchyma. The cells were found singly and were not associated with any inflammatory cellular infiltrate and appeared to be located within vascular lumina. Morphologically these cells were typical of uterine epitheloid trophoblasts. This is the first record of the presence of trophoblast-like cells in nongenital tissues of porcupines.</p>
]]></description>
<dc:creator><![CDATA[Hamir, A. N., Rupprecht, C. E.]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1354/vp.45-3-409</dc:identifier>
<dc:title><![CDATA[[BRIEF COMMUNICATIONS AND CASE REPORTS] Trophoblast-like Cells in the Tissues of Porcupines (Erethizon dorsatum)]]></dc:title>
<dc:publisher>American College of Veterinary Pathologists</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>45</prism:volume>
<prism:endingPage>411</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>409</prism:startingPage>
<prism:section>BRIEF COMMUNICATIONS AND CASE REPORTS</prism:section>
</item>

<item rdf:about="http://www.vetpathology.org/cgi/content/full/45/3/412?rss=1">
<title><![CDATA[[BRIEF COMMUNICATIONS AND CASE REPORTS] Neuronal Migration Defect: A Case of Subcortical Heterotopia in a California Sea Lion]]></title>
<link>http://www.vetpathology.org/cgi/content/full/45/3/412?rss=1</link>
<description><![CDATA[
<p>A 2 and a half-year-old male California sea lion (<I>Zalophus californianus</I>) presented with a history of intermittent generalized seizures. Magnetic resonance imaging revealed a large focal mass occupying the right cerebral hemisphere with moderate dilatation of the contralateral lateral ventricle. At necropsy, the right cerebral hemispheric white matter was expanded by numerous irregularly shaped, pale pink nodules up to 10&nbsp;mm in diameter. The overlying cortex was characterized by increased numbers of small, poorly developed gyri with shallow, often indistinct, sulci (polymicrogyria). Microscopically, nodules were composed of neurons, oligodendroglia, microglia, and supporting neuropil and were well delineated from the surrounding white matter. The gross, histological, and immunohistochemical features of this lesion are consistent with a neuronal migration defect resulting in unilateral subcortical heterotopia.</p>
]]></description>
<dc:creator><![CDATA[Blankenship, B., Dold, C., Jensen, E., Smith, C., Van Bonn, W., Ridgway, S.]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1354/vp.45-3-412</dc:identifier>
<dc:title><![CDATA[[BRIEF COMMUNICATIONS AND CASE REPORTS] Neuronal Migration Defect: A Case of Subcortical Heterotopia in a California Sea Lion]]></dc:title>
<dc:publisher>American College of Veterinary Pathologists</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>45</prism:volume>
<prism:endingPage>416</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>412</prism:startingPage>
<prism:section>BRIEF COMMUNICATIONS AND CASE REPORTS</prism:section>
</item>

<item rdf:about="http://www.vetpathology.org/cgi/content/full/45/3/417?rss=1">
<title><![CDATA[[ARTICLES] Characterization of Melamine-containing and Calcium Oxalate Crystals in Three Dogs with Suspected Pet Food-induced Nephrotoxicosis]]></title>
<link>http://www.vetpathology.org/cgi/content/full/45/3/417?rss=1</link>
<description><![CDATA[
<p>The histomorphologic characteristics and chemical composition of the crystals associated with suspected pet food&ndash;induced nephrotoxicosis in 3 dogs are described. Kidney specimens from 2 dogs, a 3-year-old Parson Russell Terrier and a 3-year-old Bernese Mountain Dog, were examined. Both developed acute renal failure after eating canned pet food on the 2007 Menu Foods recall list. The third case was a kidney specimen from a 1-year-old mixed-breed dog from a similar 2004 outbreak of canine renal failure in Taiwan, which occurred after eating a commercial dog food. Hematoxylin and eosin (HE), 72-hour Oil Red O (ORO72h), Alizarin Red S (pH&nbsp;4.1&ndash;4.3), and Von Kossa stains; infrared (IR) spectroscopy; and scanning electron microscopy with energy dispersive X-ray analysis (SEM/EDXA) were performed to determine the histomorphologic characteristics and chemical composition of the crystals observed in each case. Histomorphologic findings in each case included acute, marked tubular degeneration and necrosis with many intratubular birefringent crystals, and lymphoplasmacytic interstitial nephritis. In each case, most of the crystals were rough, pale brown, and stained with ORO72h but did not stain with Alizarin Red S (pH&nbsp;4.1&ndash;4.3) or Von Kossa stains; these features were consistent with a plastic or lipid. IR spectroscopy and SEM/EDXA results were consistent with melamine-containing crystals. A second crystal type identified in each case was smooth and platelike with staining characteristics and IR spectroscopy and SEM/EDXA results consistent with calcium oxalate crystals. Melamine-containing crystals have distinct light microscopic, histochemical, and SEM/EDXA characteristics that facilitate their identification in tissue.</p>
]]></description>
<dc:creator><![CDATA[Thompson, M. E., Lewin-Smith, M. R., Kalasinsky, V. F., Pizzolato, K. M., Fleetwood, M. L., McElhaney, M. R., Johnson, T. O.]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1354/vp.45-3-417</dc:identifier>
<dc:title><![CDATA[[ARTICLES] Characterization of Melamine-containing and Calcium Oxalate Crystals in Three Dogs with Suspected Pet Food-induced Nephrotoxicosis]]></dc:title>
<dc:publisher>American College of Veterinary Pathologists</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>45</prism:volume>
<prism:endingPage>426</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>417</prism:startingPage>
<prism:section>ARTICLES</prism:section>
</item>

<item rdf:about="http://www.vetpathology.org/cgi/content/full/45/3/427?rss=1">
<title><![CDATA[[DIAGNOSTIC EXERCISE] Pneumonia in BALB/c Rag2-/- Mice Used in a CD45RB(high) T-Cell Transfer Model of Inflammatory Bowel Disease]]></title>
<link>http://www.vetpathology.org/cgi/content/full/45/3/427?rss=1</link>
<description><![CDATA[
<p>Six 3-month-old BALB/c Rag2&ndash;/&ndash; mice developed dyspnea 10 days after intravenous injection of wild type BALB/c CD45RB(high) lymphocytes to induce colitis as a model of inflammatory bowel disease. The lungs of all 6 mice were diffusely gray-purple and did not collapse completely. Microscopic findings were extensive coalescent patchy to diffuse alveolitis, characterized by macrophages and multinucleate giant cells, lymphocytes in alveolar lumina and septa, alveolar luminal of neutrophils, and alveolar proteinic material containing small black vesicular bodies characteristic of Pneumocystis sp. in methenamine silver stained sections. The morphologic diagnosis was diffuse granulomatous pneumonia with intra-alveolar organisms consistent with Pneumocystis sp., with an unusually aggressive inflammatory response related to the experimental procedure and possibly to the BALB/c genetic background.</p>
]]></description>
<dc:creator><![CDATA[Schoeb, T. R.]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1354/vp.45-3-427</dc:identifier>
<dc:title><![CDATA[[DIAGNOSTIC EXERCISE] Pneumonia in BALB/c Rag2-/- Mice Used in a CD45RB(high) T-Cell Transfer Model of Inflammatory Bowel Disease]]></dc:title>
<dc:publisher>American College of Veterinary Pathologists</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>45</prism:volume>
<prism:endingPage>429</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>427</prism:startingPage>
<prism:section>DIAGNOSTIC EXERCISE</prism:section>
</item>

<item rdf:about="http://www.vetpathology.org/cgi/content/full/45/3/430?rss=1">
<title><![CDATA[[BOOK REVIEWS] ]]></title>
<link>http://www.vetpathology.org/cgi/content/full/45/3/430?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Rush, L. J.]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1354/vp.45-3-430</dc:identifier>
<dc:title><![CDATA[[BOOK REVIEWS] ]]></dc:title>
<dc:publisher>American College of Veterinary Pathologists</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>45</prism:volume>
<prism:endingPage>430</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>430</prism:startingPage>
<prism:section>BOOK REVIEWS</prism:section>
</item>

<item rdf:about="http://www.vetpathology.org/cgi/content/full/45/3/430-a?rss=1">
<title><![CDATA[[BOOK REVIEWS] ]]></title>
<link>http://www.vetpathology.org/cgi/content/full/45/3/430-a?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Alves, D. A.]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1354/vp.45-3-430-a</dc:identifier>
<dc:title><![CDATA[[BOOK REVIEWS] ]]></dc:title>
<dc:publisher>American College of Veterinary Pathologists</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>45</prism:volume>
<prism:endingPage>431</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>430</prism:startingPage>
<prism:section>BOOK REVIEWS</prism:section>
</item>

<item rdf:about="http://www.vetpathology.org/cgi/content/full/45/3/431?rss=1">
<title><![CDATA[[BOOK REVIEWS] ]]></title>
<link>http://www.vetpathology.org/cgi/content/full/45/3/431?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Haschek-Hock, W.]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1354/vp.45-3-431</dc:identifier>
<dc:title><![CDATA[[BOOK REVIEWS] ]]></dc:title>
<dc:publisher>American College of Veterinary Pathologists</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>45</prism:volume>
<prism:endingPage>431</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>431</prism:startingPage>
<prism:section>BOOK REVIEWS</prism:section>
</item>

<item rdf:about="http://www.vetpathology.org/cgi/content/full/45/3/431-a?rss=1">
<title><![CDATA[[BOOK REVIEWS] ]]></title>
<link>http://www.vetpathology.org/cgi/content/full/45/3/431-a?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Uzal, F. A.]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1354/vp.45-3-431-a</dc:identifier>
<dc:title><![CDATA[[BOOK REVIEWS] ]]></dc:title>
<dc:publisher>American College of Veterinary Pathologists</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>45</prism:volume>
<prism:endingPage>432</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>431</prism:startingPage>
<prism:section>BOOK REVIEWS</prism:section>
</item>

<item rdf:about="http://www.vetpathology.org/cgi/content/full/45/3/432?rss=1">
<title><![CDATA[[BOOK REVIEWS] ]]></title>
<link>http://www.vetpathology.org/cgi/content/full/45/3/432?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Lohr, C. V.]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1354/vp.45-3-432</dc:identifier>
<dc:title><![CDATA[[BOOK REVIEWS] ]]></dc:title>
<dc:publisher>American College of Veterinary Pathologists</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>45</prism:volume>
<prism:endingPage>433</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>432</prism:startingPage>
<prism:section>BOOK REVIEWS</prism:section>
</item>

<item rdf:about="http://www.vetpathology.org/cgi/content/full/45/3/433?rss=1">
<title><![CDATA[[BOOK REVIEWS] ]]></title>
<link>http://www.vetpathology.org/cgi/content/full/45/3/433?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Tvedten, H.]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1354/vp.45-3-433</dc:identifier>
<dc:title><![CDATA[[BOOK REVIEWS] ]]></dc:title>
<dc:publisher>American College of Veterinary Pathologists</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>45</prism:volume>
<prism:endingPage>433</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>433</prism:startingPage>
<prism:section>BOOK REVIEWS</prism:section>
</item>

<item rdf:about="http://www.vetpathology.org/cgi/content/full/45/3/434?rss=1">
<title><![CDATA[[NOTEWORTHY] ]]></title>
<link>http://www.vetpathology.org/cgi/content/full/45/3/434?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Rush, L.]]></dc:creator>
<dc:date>2008-05-16</dc:date>
<dc:identifier>info:doi/10.1354/vp.45-3-434</dc:identifier>
<dc:title><![CDATA[[NOTEWORTHY] ]]></dc:title>
<dc:publisher>American College of Veterinary Pathologists</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>45</prism:volume>
<prism:endingPage>435</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>434</prism:startingPage>
<prism:section>NOTEWORTHY</prism:section>
</item>

</rdf:RDF>