Fifty canine lymphomas were classified cytomorphologically using the updated Kiel classification scheme. Aspirates of lymph nodes from dogs with lymphoma were stained using 5 canine-specific antibodies and 3 human-specific antibodies that cross-react with canine lymphocytes. The antibody-stained aspirates were analyzed by flow cytometry. A total of 32 (64%) of the 50 lymphomas were characterized as B-cell origin and 18 (36%) were of T-cell origin. B-cell lymphomas were identified in 12 females and 20 males with a mean age of 8.35 years. T-cell lymphomas were identified in 8 females and 10 males with a mean age of 7.9 years. A minority of the lymphomas were low-grade B-cell and T-cell lymphomas (6/50, 12% and 4/50, 8%, respectively). The most common morphologic types were high-grade centroblastic and unclassifiable plasmacytoid for B- and T-cell lymphomas (18/50, 36% and 7/50, 14%, respectively).

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.

FL grafts should be considered for repair of urethral defects in dogs.

The aim of this study was to investigate the effects of chronic ethanol intake and cigarette smoke exposure on rat kidney. The animals were divided into four experimental groups: (1) the control group (C), (2) the ethanol group (E), (3) the cigarette smoke group (CS), and (4) the cigarette smoke plus ethanol group (CS+E). Apart from the control group, these were treated with ethanol and/or cigarette smoke for 6 months. The animals were killed and the kidneys removed to determine the levels of reduced glutathione (GSH) and malondialdehyde (MDA) and for histopathological analysis. The levels of GSH/g wet tissue were 1.58+/-0.09 micro mol, 0.91+/-0.05 micro mol, 1.14+/-0.06 micro mol, and 0.82+/-0.04 micro mol for C, E, CS, and CS+E, respectively. In groups of E, CS, and CS+E, the GSH values were significantly lower than that of group C animals ( P<0.05). Although, we detected lower GSH levels in the CS+E than the CS group ( P<0.05), a significant difference in GSH levels between CS+E and E was not observed. The levels of MDA/g wet tissue were 40.1+/-3.4 nmol, 71.4+/-2.8 nmol, 64.0+/-3.6 nmol, and 76.5+/-4.3 nmol, for C, E, CS and CS+E, respectively. In E, CS, and CS+E, the MDA values were significantly higher than in group C ( P<0.05). The increase in MDA levels in CS+E were not significantly different from groups E or CS. Histopathological analysis of the kidney slices showed severe degeneration of the tissues. Advanced hydropic degeneration of kidney tubules was clearly observed in the CS group. In group E, advanced tubular and interstitial damage, mononuclear cell infiltration and tubular thyroidization were clearly visible. In group CS+E, an intense inflammatory cell infiltration was detected under the transitional epithelium. We conclude that chronic exposure to ethanol and cigarette smoke may cause an oxidative burst in rat kidney by increasing the formation of reactive oxygen species.

No abstract

Six colostrum-deprived, hysterotomy-derived calves were maintained under sterile conditions and fed a milk replacer diet. At five days of age, five of the calves were dosed orally with 10(9) cfu of Escherichia coli O157:H7 strain A84. They were killed after, one, two, six, 12 and 24 days, and samples were taken for bacteriological and pathological examination. The sixth uninfected control calf was killed at seven days of age and matched samples were taken for pathological comparison. The animals remained normal throughout the observation period. Bacteriological data indicated a heavy bacterial load of strain A84 throughout the gastrointestinal tract but the bacterium was not found in liver, kidney or muscle. No evidence of 'attaching and effacing' lesions in the small or large intestine was found although there was a mild inflammatory response in the intestinal tract, consisting mainly of infiltrating eosinophils.

The present study was conducted to investigate the effect of silymarin on experimental liver toxication induced by Fumonisin B1 (FB1) in BALB/c mice. The mice were divided into six groups (n = 15). Group 1 served as the control. Group 2 was the silymarin control (100 mg/kg by gavage). Groups 3 and 4 were treated with FB1 (Group 3, 1.5 mg/kg FB1, intraperitoneally; and Group 4, 4.5 mg/kg FB1). Group 5 received FB1 (1.5 mg/kg) and silymarin (100 mg/kg), and Group 6 was given a higher dose of FB1 (4.5 mg/kg FB1) with silymarin (100 mg/kg). Silymarin treatment significantly decreased (p < 0.0001) the apoptotic rate. FB1 administration significantly increased (p < 0.0001) proliferating cell nuclear antigen and Ki-67 expression. Furthermore, FB1 elevated the levels of caspase-8 and tumor necrosis factor-alpha mediators while silymarin significantly reduced (p < 0.0001) the expression of these factors. Vascular endothelial growth factor (VEGF) and fibroblast growth factor-2 (FGF-2) expressions were significantly elevated in Group 4 (p < 0.0001). Silymarin administration alleviated increased VEGF and FGF-2 expression levels (p < 0.0001). In conclusion, silymarin ameliorated toxic liver damage caused by FB1 in BALB/c mice.

Twenty-five bovine fetuses naturally infected with Brucella abortus were morphologically and immunohistochemically evaluated in association with bacteriologic culture. Histopathological changes were mainly bronchopneumonia in the lungs, lymphoid hyperplasia and lymphoreticular hyperplasia in the liver and spleen. Histopathologic changes in other organs and tissues revealed hematogenous spread of the infection. Immunoreactivity to Brucella abortus was detected in all the lungs (25 fetuses) examined. However, the antigen was not detected in any of the thymus examined. Intracellular antigenic localization was identified mainly in macrophages, neutrophils and hepatocytes. In addition, B. abortus strains were isolated from abomasal contents and lungs of 22 fetuses. Eighteen of the strains were biotype 1 and the remaining four were biotype 3. These findings indicate the usefulness of immunohistochemistry in suspected cases where bacteriologic culture is negative and in cases where serology is not possible or material fixed in formalin.