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During meat inspections in pigs, dystrophinopathies are among the muscle lesions targeted for disposal. In this study, the authors examined the lesions and the distribution of dystrophin expression in 25 pigs with dystrophinopathy. In addition, complementary deoxyribonucleic acid (cDNA) sequencing and western blotting were performed in 6 of the 25 cases, all of which were characterized by degeneration, necrosis, and fat replacement of muscle fibers. Comparing the results of immunohistochemistry with anti-dystrophin antibodies that recognized at different sites in the protein, the authors noted that the loss of dystrophin expression was most pronounced in the C-terminus-recognizing antibody (19/25 cases). The authors detected 5 missense mutations and 3 types of shortened transcripts generated by the skipping of exons in the cDNA, which were associated with the pathogenesis. One missense mutation had been reported previously, whereas the remaining mutations identified had not been previously documented in pigs. In the cases with shortened transcripts, normal-sized transcripts were detected together with the defective transcripts, suggesting that these mutations were caused by splicing abnormalities. In addition, they were in-frame mutations, all of which have similar pathogeneses of Becker muscular dystrophy in humans. These cases were 6 months of age and exhibited macroscopic discoloration, fatty replacement, and muscle degeneration, suggesting that the effect of these mutations on skeletal muscle was significant. [ABSTRACT FROM AUTHOR]

We report a case of Becker muscular dystrophy in a 6-month-old, mixed-breed, castrated male pig detected with macroglossia at a meat inspection center. The pig presented a severely enlarged tongue extending outside its mouth. The tongue was firm and pale with discolored muscles. Histologically, there was severe fibrosis, fatty replacement, and myofiber necrosis, degeneration, and regeneration. Immunofluorescence showed focal and severely weak labeling for dystrophin at the sarcolemma of myocytes in the tongue. Analysis of dystrophin mRNA showed a 62 base pair insertion between exons 26 and 27. The insertion was derived from intron 26. Based on these findings, we diagnosed the case as Becker muscular dystrophy—the first known muscular dystrophy case induced by pseudoexon insertion in animals. [ABSTRACT FROM AUTHOR]

Malignant Leydig cell tumor (MLCT) is a rare testicular tumor in dogs. We report herein 2 dogs with MLCT and cutaneous metastasis. Grossly, marked enlargement and distortion of the involved testes were noted; on cut surface, the parenchyma was completely replaced by neoplastic tissue. In addition, these tumors had extensive necrosis and hemorrhage. Case 1 had a rapidly growing cutaneous mass in the left angle of the mouth; the lesion was well-circumscribed and had an indistinct lobular pattern. Case 2 had multiple cutaneous masses in the dorsal neck region, the thoracic back region, and the right hindlimb. Microscopically, the tumor lobules were composed of oval-to-polyhedral cells with eosinophilic cytoplasm and resembled testicular tumors. By immunohistochemistry, the neoplastic cells in both the testicular and cutaneous tumors were positive for inhibin-alpha and melan A. The mitotic counts of the primary tumors from cases 1 and 2 were 21 and 11 per 10 high-power fields, respectively. Based on these findings, the cases were diagnosed as MLCT with cutaneous metastasis. Ki-67 expression in the neoplastic cells of the 2 cases was higher than in benign Leydig cell tumors. Our findings may be helpful for the diagnosis of canine MLCT. [ABSTRACT FROM AUTHOR]

The authors previously investigated progressive glomerulonephropathy in 2- to 11-year-old common marmosets and characterized age-related changes of the renal glomeruli and development of tubulointerstitial lesions. In this study, immunoglobulin deposition and ultrastructural changes of the glomeruli were investigated in 5 young marmosets from 6 months to 3 years of age with pre-onset or early glomerulonephropathy. In all animals, the foot processes of podocytes were effaced, and IgM was deposited into the glomeruli. In glomeruli without glomerular basement membrane (GBM) alteration, IgM was the only immunoglobulin type deposited in the glomeruli. In cases with more advanced lesions of reticulation and thickening of GBM, IgA and IgG deposits were also observed. Therefore, the authors conclude that IgM may be the primary or earliest immunoglobulin deposited in this nephropathy, whereas IgA and IgG deposition may be connected to the progression of the glomerular lesions. IgM deposition and foot process effacement of podocytes occur early in the life of affected marmosets. [ABSTRACT FROM AUTHOR]

The authors describe a spontaneous case of amyloid A (AA) amyloidosis in an adult female Japanese quail (Coturnix japonica). The bird developed AA amyloidosis secondary to chronic peritonitis caused by a Gram-negative bacillus infection. Mild amyloid deposition was also identified in the intestinal tract of apparently healthy adult individuals, suggesting that quail may develop intestinal amyloidosis with age. Based on these observations, it was hypothesized that quail can develop AA amyloidosis following inflammatory stimulation with lipopolysaccharide (LPS). Therefore, adult quail were repeatedly injected with LPS and the development of AA amyloidosis was confirmed. The amyloid deposition in this model increased when quail amyloid was intravenously injected as an amyloid-enhancing factor. The experiments were repeated with young quail, but amyloid deposits were not observed following LPS injections. However, AA amyloidosis did develop when quail amyloid was injected in addition to LPS. These results indicated that adult quail develop AA amyloidosis after inflammatory stimulation with LPS. Furthermore, quail AA amyloidosis was shown to have transmissibility regardless of age. Interestingly, the authors found that administration of chicken amyloid fibrils also induced AA amyloidosis in young quail. This is the first report of cross-species transmission of avian AA amyloidosis. [ABSTRACT FROM AUTHOR]

Cutaneous epitheliotropic T-cell lymphoma (CETL) is characterized by neoplastic T-cell infiltration of the epidermis, adnexal structures, and oral mucosa. The objective of this report was to describe the pathological findings of a canine case of terminal-stage CETL. A 10-year-old, mixed-breed, neutered male dog was presented with erosion of the oral mucosa and mucocutaneous junction. The dog was diagnosed with CETL with no evidence of metastasis. Despite chemotherapy, the dog was re-presented with oral pain, vomiting, and diarrhea, and died 17 months after the first visit to the hospital. A complete autopsy was performed. Histologic examination of the primary lesion and systemic organs was performed. Gross examination revealed an advanced-stage oral lesion. Distinct tumor formation was not observed in the primary sites and systemic organs. Histologically, the primary oral lesion was characterized by massive intraepithelial infiltration of a large number of neoplastic lymphocytes. The neoplastic cells in the metastatic sites also showed exclusive epitheliotropic proliferation in organs, including the trachea, tonsils, esophagus, stomach, small intestine, colon, anal mucosa, liver, pancreas, kidneys, urinary bladder, prostate gland, ear canals, and auricular and ventral skin. Immunohistochemically, the neoplastic cells were positive for CD3 and negative for CD20 as well as CD79α, supporting a diagnosis of CETL with systemic dissemination. In canine CETL with systemic signs, systemic metastasis should be considered even without evident mass formation. Neoplastic lymphocytes of CETL showed distinct epitheliotropism even in the systemic metastatic sites. [ABSTRACT FROM AUTHOR]

The purpose of the present study was to estimate the relative contributions of degradation and brain-to-blood elimination processes to the clearance of microinjected human amyloid-β peptide(1-40) (hAβ(1-40)) from mouse cerebral cortex, using a solid-phase extraction method together with a newly developed ultraperformance liquid chromatography/tandem mass spectrometry (UPLC/MS/MS) quantitation method for intact hAβ(1-40). The clearance rate constant of hAβ(1-40) in mouse cerebral cortex was determined to be 3.21 × 10−2/min under conditions where the saturable brain-to-blood elimination process across the blood-brain barrier (BBB) was expected to be saturated. Thus, this clearance rate constant should mainly reflect degradation. The [125I]hAβ(1-40) elimination rate across the BBB under nonsaturating conditions was determined to be 1.48 × 10−2/min. Inhibition studies suggested that processes sensitive to insulin and phosphoramidon, which inhibit neprilysin, insulin-degrading enzyme, and endothelin-converting enzyme, are involved not only in degradation, but also in elimination of hAβ(1-40). In conclusion, our results suggest a dominant contribution of degradation to cerebral hAβ(1-40) clearance, and also indicate that a sequential process of degradation and elimination of degradation products is involved in cerebral hAβ(1-40) clearance. [ABSTRACT FROM AUTHOR]

An annular, reddened lesion with mild serosal hemorrhage and no tumorous mass formation was detected in the right uterine horn of a 37-week-old female Sprague-Dawley rat that had postpubertal vaginal bleeding. Histological examination revealed prominent proliferation of the endometrium, which occupied the uterine lumen. There were numerous aberrant vascular spaces filled with erythrocytes, proliferation of stromal cells, and inflammatory infiltrates including hemosiderin-laden macrophages in the endometrium. These vasculatures extended into the myometrium, and in a transverse section of the lesion, they were mostly distributed throughout the circumference of the uterus. They were irregular in shape and interconnected, forming a large vascular sinus and anastomosing reticular channels. In the area with serosal hemorrhage, the muscular layer covering the large irregular vascular space had undergone degeneration and necrosis. The lining cells of the vasculatures were often plump, and they protruded into the lumen and were arranged in a tombstone or hobnail manner. Immunostaining revealed that these cells were positive for von Willebrand factor and CD34. The aberrant vasculatures were not accompanied by pericytes or muscular layer, although a discontinuous muscular wall was present around some of them. From these results, the uterine lesion was diagnosed as a vascular hamartoma. [ABSTRACT FROM AUTHOR]

The article presents a case study of a 12-year-old neutered male Japanese domestic cat admitted to the veterinary hospital due to coughing, dysorexia, diarrhea and vomiting. The cat died after a month of its first visit to the hospital and researchers did an autopsy to determine the cause of his death. Moreover, results of ultrasonography revealed that the cat had malignant and metastasizing cardiac ganglioneuroma.

The article discusses a study which describes the case of a nine-year-old, female German Shepherd Dog that was diagnosed with a rare cutaneous hamartoma, accompanied by aberrant arteriovenous structures. The dog developed a firm, bulging lesion at the tip of the tail. Numerous poorly circumscribed clusters of vascular structures characterized the lesion. In the deep part of the lesion, large vessels that showed morphological aberrations were seen.

The article describes a complex canine mammary adenoma with a rare histological feature characterized by sebaceous differentiation of tumor cells. The tumor cells of a mixed breed, intact female dog were found to be positive for cytokeratin (CK) 14 while the myoepithelial cells were positive for α-smooth muscle actin and p63.