Experimental transmission of bovine leukosis virus by rectal palpation.
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Animals↗
Biomedical subjects
E Gruys
Publications and source records attributed to E Gruys.
Gastrointestinal AAPOAII and systemic AA-amyloidosis in aged C57BL/Ka mice. Amyloid-type dependent effect of long-term immunosuppressive treatment.
The light microscopic and immunohistochemical features of a novel localized senile amyloidosis in the gastrointestinal tract of C57BL/Ka mice are described. Senile gastrointestinal amyloidosis was predominantly found in the lamina propria of the ileum, cecum and stomach and infrequently in other segments of the gastrointestinal tract. The Congo red affinity of the senile amyloid was sensitive to potassium permanganate pretreatment. The amyloid did not react with anti-AA and anti-immunoglobulin antisera, but stained positively for apoAII, a major apolipoprotein of high density lipoproteins. A similar type of amyloid, termed AApoAII, has recently been described in a systemic form of senile amyloidosis in mice. In the present study, we investigated the effect of long-term immunosuppressive treatment on the incidence of systemic AA-amyloidosis and gastrointestinal AApoAII-amyloidosis in aged C57BL/Ka mice. Gastrointestinal amyloidosis occurred in 60% of the control mice, but significantly less in mice of the immunosuppressed groups. In contrast, systemic AA-immunoreactive amyloidosis was only found in mice that were given immunosuppressive treatment. There was no codeposition of AA and AApoAII-amyloid. These findings indicate that immunosuppressive drugs have a profound effect on the incidence as well as the type of amyloidosis in C57BL/Ka mice.
Aging↗
Hereditary necrotising myelopathy in Kooiker dogs.
A retrospective clinicopathological study of a neurological disorder in 22 Kooiker dogs (Dutch decoy dog) was made. The disease was found to occur equally in both sexes and clinical signs began at three to 12 months old. Physical examination revealed a progressive paresis of the hindlimbs. Post mortem examination showed symmetrical areas of malacia in the ventral, lateral and dorsal white matter of the spinal cord. In one dog dorsal white matter was spared. Cervical segments C4 to C8 were involved in all subjects. Rostral and caudal to these areas, Wallerian degeneration was prominent. The disease has much in common with similar myelopathies in the Afghan hound and the rottweiler. Indications of heritability were the similarity in clinical and pathological findings, the age of onset of the disease, and the significantly higher inbreeding coefficient in the patients than in the breed population (P = 0.001). All patients were descended from one pair. Segregation analysis suggested inheritance involving a simple autosomal recessive trait.
Animals↗
Recombinant human tumour necrosis factor-alpha (rhTNF-alpha) and rhTNF-alpha analogue enhance amyloid deposition in the Syrian hamster.
Tumour necrosis factor-alpha (TNF-alpha) is one of the cytokines that stimulate the production of serum amyloid A (SAA), the precursor of AA amyloid. The role of TNF-alpha in amyloidogenesis was investigated in experimental hamsters using purified recombinant human TNF-alpha (rhTNF-alpha) and rhTNF-alpha analogue different from the normal molecule by two amino acid substitutions. Daily injections of 1 microgram rhTNF-alpha resulted in elevated SAA levels but even in the presence of amyloid enhancing factor (AEF) no amyloid was deposited, indicating that apart from the AEF and one particular SAA stimulating factor an additional factor is needed to result in amyloid deposition. This factor is generated by repeated injections of E. coli lipopolysaccharide (LPS). A single intraperitoneal injection of 12.5 micrograms or more of rhTNF-alpha followed by seven daily subcutaneous injections of LPS resulted in enhanced amyloid deposition. Heat denaturation of rhTNF-alpha did abolish its AEF activity. The rhTNF-alpha analogue, having one-fifth of the cytotoxic activity of the normal rhTNF-alpha, showed a similar reduction in its SAA-inducing capacity and its amyloidogenicity. This suggests the AEF activity to be closely related to TNF-alpha activity. However, poly(I)-poly(C) (a potent inducer of IL-6) also showed AEF activity, suggesting that not a single cytokine but rather a certain combination of different cytokines could be decisive in AA amyloidogenesis.
Amyloid↗
Peripartum acute-phase protein serum amyloid-A concentration in plasma of cows and fetuses.
Concentration of the acute-phase protein serum amyloid-A (SAA) was measured by means of an indirect ELISA method, in plasma of 3 pregnant cows and in plasma taken by cannula from another 4 pregnant cows and, by separate cannula, from their fetuses. Blood samples were taken daily from approximately 72 hours before until 72 hours after parturition. After parturition, SAA concentration increased significantly (P < 0.05) in maternal plasma. In fetal plasma, only a nonsignificant increase was found at time of delivery. The concentration of maternal SAA started to increase within the first 24 hours after delivery, reaching a peak value between 24 and 48 hours after delivery. In the aforementioned plasma samples from the 4 pregnant cows and their fetuses, the concentration of maternally derived cortisol increased nonsignificantly after parturition. The concentration of fetally derived cortisol was significantly (P < 0.05) increased at parturition (t = 0), compared with the initial fetal cortisol concentration at 120 hours before delivery. Peripartum concentration of maternal SAA increased and maternal cortisol remained low, whereas fetal SAA concentration remained low and fetal cortisol concentration increased. These findings indicate possible suppressive action of fetal cortisol on fetal SAA production. However, it might be argued that the main cause of the difference in SAA concentration is the difference in tissue damage between cows and fetuses at parturition.
Acute-Phase Proteins↗
Hereditary Kooiker dog ataxia.
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Animals↗
[Mortality of cattle following feeding of moldy flower bulbs].
Five of eight meat cattle died suddenly without showing prior symptoms of disease. The sudden death occurred in connection with the feeding of mouldy tulip bulbs. A short review is given of the use of flower bulbs as cattle feed, the use of herbicides/fungicides in bulb cultivation, and the relevant legislation. Several toxicological aspects that should be taken into consideration when flower bulbs are used as cattle feed are discussed. Both the Central Veterinary Institute and the State Institute for Public Health and Environmental Hygiene showed, in experiments with mice, the presence of a toxin in extracts of the mouldy tulip bulbs. This toxin is probably produced by moulds present in the tulip bulbs. The death of the animals was probably caused by an as yet unidentified mycotoxin.
Animal Feed↗
Failure of adrenocorticotrophic hormone to release serum amyloid A in cattle.
The objective of this study was to determine whether adrenocorticotrophic hormone plays a direct role in the secretion of serum amyloid A (SAA) in cattle. Seven lactating Holstein-Friesian cows were given either saline or 25 iu adrenocorticotrophic hormone (ACTH) intravenously at 09.00 in a two factor crossover design. Plasma cortisol concentrations had increased significantly by one hour after the injection of ACTH, whereas the SAA level had not increased by 24 hours after injection. It is concluded that in cattle adrenocorticotrophic hormone has no direct influence on the release of SAA by the hepatocyte.
Adrenocorticotropic Hormone↗
Congenital tremor in Holstein Friesian-cattle.
In a female family line of Holstein-Friesian cattle a series of trembling calves was born within a period of ten years. All trembling animals were male; female calves appeared normal. At necropsy of one calf severe degenerative lesions of spinal cord and brain white matter were observed. Both myelin and axons were lost and some macrophages occurred within digestion chambers. Obviously degenerated neurones were not found. The lesion was interpreted as a single recessive sex-linked hereditary trait.
Animals↗
Subcutaneous tissue reaction to polyethylene terephtalate-covered electronic identification transponders in pigs.
Polyethylene terephtalate-covered identification transponders were injected in 4 week old piglets to examine clinically and histologically the reaction in the surrounding tissue after 4, 7 and 21 days and 6 months. Inflammatory signs at the injection site were clinically noticed from 2 days onwards and gradually decreased after day 3. A second series of inflammatory events occured in some animals around day 7. Swelling was observed thereafter in a few animals. In the pigs slaughtered at day 4, all samples showed a layer of exudate and debris surrounding the transponder. Afterwards a fibrous capsule developed. The mean thickness of reactive tissue decreased significantly (p < 0.01) between days 4 and 7 and days 14 and 21, and remained unchanged between day 21 and 6 months. The mean (+/- s.e.) capsule thickness was 0.32 +/- 0.12 mm after 6 months. It is concluded that PET-covered transponders are encapsulated in fibrous connective tissue within 3 weeks after injection at the base of the ear. After 6 months the capsule around the transponder revealed no or only minor signs of inflammation.
Animal Identification Systems↗
Total CK and CK-BB activity in serum from sheep with scrapie.
Total CK and iso-enzyme CK-BB activity was measured in serum from four sheep with scrapie and in serum from four healthy control sheep. Blood samples were taken weekly for about six months. There was a clear overlap between the total CK and CK-BB activity in serum from sheep with scrapie and that in serum from control sheep. Thus measurement of these enzymes does not aid the clinical diagnosis of scrapie.
Animals↗
Cytokine induction and therapeutic synergy with interleukin-2 against murine renal and colon cancers by xanthenone-4-acetic acid derivatives.
Derivatives of xanthenone-4-acetic acid (XAA) have been found to have similar activity to flavone-8-acetic acid against transplantable solid tumors. Some of these compounds were compared to flavone acetic acid (FAA) in their ability to induce cytokines as well as to mediate antitumor effects against murine renal cancer (Renca) and a mouse colon cancer (MCA-38). 5-Methyl-XAA and 5-chloro-XAA proved to be more potent than FAA on a mg/kg basis for induction of the genes for IFN alpha, IFN gamma, and TNF alpha, and for IFN and TNF activities in the sera of treated mice. These effects were sharply dose dependent. On the other hand, 7-methyl-XAA, which has no antitumor activity, did not induce these genes. In addition, 5-methyl-XAA and 5-chloro-XAA but not 7-methyl-XAA synergized with recombinant human interleukin-2 (rhIL-2) for the treatment of Renca and MCA-38. Doses of the active derivatives that failed to induce cytokines also exhibited no therapeutic synergy with rhIL-2. These results suggest that at least some of the antitumor effects of these XAA derivatives are related to their ability to induce cytokines.
Animals↗
Relationship between pathological findings and values of haematological and blood-chemistry variables in apparently healthy finishing pigs at slaughter.
The present study was performed to study possibilities of early decision making for appropriate conveyor-line at future slaughtering of normal, clinically healthy finishing pigs. Blood was collected at slaughter from barrows (n = 112). A meticulous examination for subclinical pathological lesions was performed, revealing 5 groups of subjects listed in order of increasing disease-activity: 1--no real disease-activity; 2--with mild subchronic lesions; 3--with subacute lesions; 4--with abscesses; and 5--with fibrinous-necrotic lesions. Significant differences for values of erythrocyte sedimentation rate (ESR), protein, albumin, globulins, and plasma viscosity appeared to occur in this series. It is suggested that measuring acute phase reactants in blood of slaughtered pigs in the near future may reveal appropriate modern tools for meat inspection and predicting slaughtered animal quality.
Abattoirs↗
Reversal of drug resistance in a human colon cancer xenograft expressing MDR1 complementary DNA by in vivo administration of MRK-16 monoclonal antibody.
One strategy to overcome multidrug resistance in neoplasia is to inhibit the gp170 glycoprotein (relative molecular mass, 170,000) that functions as a plasma membrane, energy-dependent, drug-efflux pump. The human colon cancer cell line HT-29, which grows as an ascitic tumor in athymic NCr-nu/nu nude mice, was made multidrug resistant by infection with an MDR1 (also known as PGY1) retrovirus. Referred to as HT-29mdr1, it was used to study reversal of drug resistance in vivo by the anti-P-glycoprotein monoclonal antibody MRK-16. Flow cytometry and radioimmunoassay demonstrated a marked increase in MRK-16 reactivity on HT-29mdr1 cells as compared with its reactivity on the parental, uninfected cell line (HT-29par). The 50% inhibitory concentrations (IC50) of vincristine on HT-29par and HT-29mdr1 cells were 2.5 and 15 ng/mL, respectively. The MRK-16 monoclonal antibody did not affect the vincristine sensitivity of the HT-29par cells. Pretreatment of HT-29mdr1 cells with 10 micrograms/mL MRK-16 in tissue culture partially restored the vincristine sensitivity (IC50 = 7 ng/mL). This modulation of vincristine sensitivity by MRK-16 was then tested in vivo. The median survival times of mice given intraperitoneal transplants of 5 x 10(6) HT-29par or HT-29mdr1 were 37 and 39 days, respectively. Treatment of mice with 1 mg/kg vincristine weekly for 3 weeks, beginning 10 days after tumor injection, resulted in a significant increase in the median survival time of the HT-29par tumor-bearing mice (68 days, P less than .0001), but it had no effect on the HT-29mdr1 tumor-bearing mice. However, treatment of mice bearing the HT-29mdr1 tumor with MRK-16 before vincristine therapy reversed the resistance to the drug (median survival time = 64 days, P less than .0001). The MRK-16 monoclonal antibody alone had no effect on the median survival time of mice given an injection of either HT-29par or HT-29mdr1 cells. These results suggest that strategies employing monoclonal antibody against gp170 may be clinically useful to reverse multidrug resistance.
ATP Binding Cassette Transporter, Subfamily B, Mem↗
Bovine laminitis: clinical aspects, pathology and pathogenesis with reference to acute equine laminitis.
This review deals with the features of clinical and subclinical laminitis in cattle. Prominent clinical signs of acute laminitis are a tender gait and arched back. The sole horn reveals red and yellowish discolourations within five days. In subacute and chronic cases clinical signs are less severe. In chronic laminitis the shape of the claws is altered. Laminitis is frequently followed by sole ulceration and white zone lesions. Blood tests showed no significant changes for laminitic animals. Arteriographic studies of claws affected by laminitis indicated that blood vessels had narrowed lumens. Gross pathology revealed congestion of the corium and rotation of the distal phalanx. Histopathologic studies indicate that laminitis is associated with changes of the vasculature. Peripartum management and nutrition are important factors in its aetiology. It is hypothesised that laminitis is evoked by disturbed digital circulation. In the pathogenesis of acute laminitis three factors are considered important: the occurrence of thrombosis, haemodynamic aspects of the corium, and endotoxins which trigger these pathologic events.
Animals↗
Fibril amyloid enhancing factor (FAEF)-accelerated amyloidosis in the hamster is not dependent on serine esterase activity and mononuclear phagocytosis.
Cells of the mononuclear phagocytic system (MPS) were described as playing a decisive role in amyloidogenesis. A relationship between the amyloid enhancing factor (AEF) and MPS cells was suggested and recently AEF activity was attributed to a serine esterase (SE) of leucocytic origin. In the present study, no correlation was found between the SE content and AEF activity in either peritoneal cell lysates or AEF preparations of different origin. Furthermore, pretreatment of fibril AEF (FAEF) with the SE inhibitor phenylmethylsulphonyl fluoride (PMSF) did not affect its activity in the hamster. Blockade of the MPS by dextran sulphate did not inhibit deposition of amyloid after intravenous injection of FAEF but amyloid deposition was inhibited when FAEF was administered intraperitoneally. These results suggest that MPS cells could be involved in transport of AEF, but that phagocytic activity of MPS cells is not essential in AA-amyloid fibrillogenesis. It is concluded that these results are not consistent with the previously suggested nature of the AEF or with the proposed central role of the MPS in amyloidogenesis.
Amyloidosis↗
Systemic alkalinization inhibits the ability of flavone acetic acid to augment natural killer activity, induce cytokine gene expression, and synergize with interleukin 2 for the treatment of murine renal cancer.
Flavone acetic acid (FAA) is an investigational drug that augments natural killer activity, induces the genes for alpha- and gamma-interferon (IFN) and tumor necrosis factor alpha, and synergizes with recombinant interleukin 2 for the successful treatment of murine renal cancer. However, in most clinical studies of FAA only minimal immunomodulatory effects have been reported. Most of the patients in these studies have also been given sodium bicarbonate to prevent possible nephrotoxicity. The current study was performed to determine whether alkalinization had any effects on FAA-induced immune modulation and therapeutic activity in mice. The results showed that alkalinization inhibited the treatment of murine renal cancer by FAA plus recombinant interleukin 2 such that the survival rate of 84% in nonalkalinized mice was reduced to 0 in mice that were alkalinized during treatment. Alkalinization also significantly inhibited the ability of FAA to augment both splenic and hepatic natural killer activity in a dose-dependent manner. In contrast, alkalinization did not inhibit the ability of polyinosinic:polycytidylic acid and poly-L-lysine stabilized in carboxymethyl cellulose, maleic anhydride divinyl ether, or Propionibacterium acnes to augment liver-associated natural killer activity. By Northern blot analysis, it was shown that the induction of mRNA for IFN-alpha, IFN-gamma, and tumor necrosis factor alpha by FAA in the spleen cells of mice was significantly reduced in alkalinized mice. Consistent with a reduction in the FAA-induced expression of the cytokine genes, alkalinization also resulted in a significant decrease in both the peak serum concentration and duration of detectable IFN activity following FAA treatment. Increasing the dose of FAA in alkalinized mice to 300 mg/kg overcame the deleterious effects of alkalinization for treatment of murine renal cancer by FAA plus recombinant interleukin 2. These results demonstrate that the process of alkalinization inhibits the immunomodulatory and immunotherapeutic effects of FAA in mice and suggest that alkalinization might have similar deleterious effects on FAA-induced immune stimulation in human clinical trials.
Adenocarcinoma↗