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- Author or Editor: Akinori Shimada x
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Abstract
Objective—To determine whether angiogenesis and microglial activation were related to seizure-induced neuronal death in the cerebral cortex of Shetland Sheepdogs with familial epilepsy.
Animals—Cadavers of 10 Shetland Sheepdogs from the same family (6 dogs with seizures and 4 dogs without seizures) and 4 age-matched unrelated Shetland Sheepdogs.
Procedures—Samples of brain tissues were collected after euthanasia and then fixed in neutral phosphate–buffered 10% formalin and routinely embedded in paraffin. The fixed samples were sectioned for H&E staining and immunohistochemical analysis.
Results—Evidence of seizure-induced neuronal death was detected exclusively in samples of cerebral cortical tissue from the dogs with familial epilepsy in which seizures had been observed. The seizure-induced neuronal death was restricted to tissues from the cingulate cortex and sulci surrounding the cerebral cortex. In almost the same locations as where seizure-induced neuronal death was identified, microvessels appeared longer and more tortuous and the number of microvessels was greater than in the dogs without seizures and control dogs. Occasionally, the microvessels were surrounded by oval to flat cells, which had positive immunohistochemical results for von Willebrand factor. Immunohistochemical results for neurons and glial cells (astrocytes and microglia) were positive for vascular endothelial growth factor, and microglia positive for ionized calcium–binding adapter molecule 1 were activated (ie, had swollen cell bodies and long processes) in almost all the same locations as where seizure-induced neuronal death was detected. Double-label immunofluorescence techniques revealed that the activated microglia had positive results for tumor necrosis factor-α, interleukin-6, and vascular endothelial growth factor receptor 1. These findings were not observed in the cerebrum of dogs without seizures, whether the dogs were from the same family as those with epilepsy or were unrelated to them.
Conclusions and Clinical Relevance—Signs of angiogenesis and microglial activation corresponded with seizure-induced neuronal death in the cerebral cortex of Shetland Sheepdogs with familial epilepsy. Microglial activation induced by vascular endothelial growth factor and associated proinflammatory cytokine production may accelerate seizure-induced neuronal death in dogs with epilepsy.
Abstract
Objective—To examine renal expression of α-smooth muscle actin (α-SMA) and fibronectin in cats with tubulointerstitial nephritis (TIN) for use in predicting progression to renal fibrosis.
Animals—19 cats with TIN and 9 cats without nephritis.
Procedure—Serum creatinine and BUN concentrations were measured. Indices for glomerular extra-cellular matrix (ECM), tubular injury (TI), and fibronectin were determined in renal specimens to quantify the extent of injury and fibrotic lesions. Expression of α-SMA in renal tissue was immunohistochemically detected, and correlations were evaluated between the α-SMA index and other histologic and clinical variables.
Results—The α-SMA index in tubulointerstitial areas (1.63 ± 0.78) was significantly higher in cats with TIN, especially in the periglomerular and peritubular areas, than in cats without nephritis (0.20 ± 0.14). The α-SMA index was significantly associated with the TI index (r 2 = 0.70), fibronectin index (r 2 = 0.95), BUN concentration (r 2 = 0.64), and serum creatinine concentration (r 2 = 0.66). Of special interest was that interstitial α-SMA expression appeared evident in the kidneys at an early stage of TIN, prior to the onset of ECM deposition.
Conclusion and Clinical Relevance—Analysis of results of histologic and clinical examinations revealed that interstitial α-SMA expression may have clinical importance and may be a useful early histologic marker for development of chronic renal failure in cats. An immunohistochemical examination for fibrogenic molecules (such as α-SMA expression) may provide fundamental information on the pathogenesis of early-stage renal disease and aid clinical management of cats with chronic renal failure, including TIN. (Am J Vet Res 2000;61:1080–1086)
SUMMARY
Objective
To examine whether Mycoplasma hyorhinis inoculated into the tympanic cavity can cause otitis media in pigs.
Animals
17- or 22-day-old specific-pathogen-free pigs.
Procedure
Histologic and bacteriologic examinations were performed on specimens from the tympanic cavity and auditory tube at 0, 7, 14, and 25 days after intratympanic inoculation of M hyorhinis (auditory tube cloning strain 14).
Results
In M hyorhinis-inoculated pigs, mild to moderate inflammation of the auditory tube and tympanic cavity first appeared at postinoculation day (PID) 7. In pigs euthanatized at PID 14, the degree of inflammation was aggravated. Immunohistochemical analysis revealed M hyorhinis antigens on the luminal surface of the auditory tube and tympanic cavity. By PID 25, lesions had lessened. By use of transmission and scanning electron microscopic examinations, mycoplasmal organisms were identified among the cilia in the auditory tubes at PID 14 but not at PID 25. Results of bacteriologic examination indicated that 104 to 106 color-changing units of M hyorhinis were isolated from the tympanic cavity at PID 0. Variable numbers of M hyorhinis were isolated at PID 7 and 14, and numbers were decreased at PID 25.
Conclusions
M hyorhinis inoculated into the tympanic cavity can cause a self-limiting otitis media in SPF pigs. (Am J Vet Res 1998;59:869–873)
