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A case of aspergillosis in a broiler breeder flock having respiratory and nervous system problems caused by Aspergillus fumigatus and Aspergillus niger is documented. Dyspnea, hyperpnea, blindness, torticollis, lack of equilibrium, and stunting were observed clinically. On postmortem examination of the affected birds, white to yellow caseous nodules were observed on lungs, thoracic air sacs, eyes, and cerebellum. Histopathologic examination of lungs and cerebellum revealed classic granulomatous inflammation and cerebellar lesions, necrotic meningoencephalitis, respectively. No lesions were noted in the cerebrum histopathologically. Aspergillus hyphae were observed in stained sections prepared from lesioned organs. Fungal spores and branched septate hyphae were observed in direct microscopy. Aspergillus fumigatus and A. niger were isolated from the inoculations prepared from the suspensions of organs showing lesions.

Clofibrate was a more potent inducer of PPARalpha expression than HFD in our rat fatty liver model. The finding of blunted peroxisomal enzyme response to clofibrate in fatty livers suggests that alterations in postreceptor events may exist and further contribute to liver steatosis. Clofibrate seems to stabilize glutathion content and this might contribute to the prevention of liver steatosis.

Abstract. The current study was designed to determine the changes of the cardiac troponin I (cTnI) expression in blood and tissue during the myocardial degeneration in calves with foot-and-mouth disease (FMD). Seventeen crossbred calves presenting pathological signs for FMD confirmed by viral analysis were studied. A biochemistry panel and immunohistochemistry were performed on 17 diseased calves and 7 calves used as controls. Creatine kinase (CK), CK-myocardial band (CK-MB), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) activities were analyzed for both groups. Cardiac troponin I levels were measured by a commercially available enzyme-linked immunosorbent assay kit. Mean cTnI (14.8 6 1.9 ng/ml) concentration and CK (573 6 407 U/l), CK-MB (238 6 37 U/l), AST (84 6 7), and LDH (298 6 29 U/l) activities were higher in FMD cases compared with controls. Immunohistochemistry revealed loss or depletion of cTnI expression in myocardium of all cases. None of the 7 controls showed loss of cTnI expression. Increased serum cTnI concentration correlated with myocardial injury and loss of cTnI immunolabeling in cardiomyocytes of calves with FMD.

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