Oral pyogenic granulomas.

Pyogenic granulomas are benign growth occurring in various oral mucosal sites. They are thought to be caused by tissue response to non-specific irritation. Surgical excision and removal of irritants are the usual treatments, and recurrence is rare. The exception is the 'pregnancy epulis', where excision should only be considered if there is incomplete regression following childbirth.

Rapeseed induced liver haemorrhage, reticulolysis and biochemical changes in laying hens: the effects of feeding high and low glucosinolate meals.

Rapeseed meal hepatosis was produced by feeding high and low glucosinolate meals as a source of protein (about 200 g kg-1 diet) but could not be distinguished histologically from fatty liver-haemorrhagic syndrome which occurred in birds on the control diet. Both types of meal increased haemorrhage, reticulolysis and lymphoproliferation in the liver, reduced the packed cell volume and caused thyroid enlargement. Haemorrhages emanated from ruptured intrahepatic portal veins, capillaries and sinusoids and were associated with degenerative changes in vessel walls. Haemorrhage and reticulin scores were correlated. Parenchymal necrosis occurred only around large haematomas and caused increased aspartate transaminase activity in the plasma. Both meals also caused hyperglycaemia and reduced the plasma triglyceride content. Only the high glucosinolate meal decreased egg production, caused liver enlargement and reduced the plasma urate level. The addition of myrosinase enhanced its effects on egg production and packed cell volume but did not increase its hepatotoxicity.

Biochemical changes in layer and broiler chickens when fed on a high-glucosinolate rapeseed meal.

Diets containing 500 g high-glucosinolate rapeseed meal/kg or an equivalent amount of soybean meal as the only protein supplement were fed to layer-type chickens and two broiler strains from 1 to 56 d of age. Additional groups of the former were maintained on the diets until they were 16 and 28 d old. The rapeseed meal produced thyroid hypertrophy in all strains but reduced the growth rate of only one of the broiler strains. The livers of chickens fed on rapeseed meal were enlarged and DNA analysis indicated hyperplasia, but no macroscopic lesions were found. The activities of aspartate transaminase, lactate dehydrogenase and alkaline phosphatase in the plasma were increased by rapeseed meal, suggesting liver damage. In all strains, feeding rapeseed meal increased plasma total protein, albumin and cholesterol and decreased urate. Hyperglycaemia accompanied by a decrease in plasma triglycerides occurred in the layer strain. Through its extra-thyroidal toxicity (-)5-vinyl-oxazolidine-2-thione (goitrin) was probably responsible for most of these changes.

Effects of selective breeding and age on the ability of the domestic fowl (Gallus domesticus) to oxidize trimethylamine.

Groups of adults which were selected for low and high (normal) TMA oxidase activities produced chickens with a predominance of the same character showing that capacity for synthesizing the enzyme is strongly inherited. The low and high strains became homogenous in generations 2 and 3, respectively, demonstrating that the genetic factor that impairs the synthesis of TMA oxidase can be readily removed by selective breeding. There was a 7-fold difference in the hepatic TMA oxidase activities of the strains at the age of 1 day and a 26-fold difference at 22 days. The synthesis of the enzyme increased rapidly in the high strain between the ages of 8 and 36 days but did not alter significantly in the low strain. Sex had no effect on TMA oxidase synthesis. The high strain showed better feather development and laid eggs with paler shells. There was no difference in their growth rate, egg production or hatchability.

The effect of thionamides and related compounds on trimethylamine oxidase activity in hepatic microsomes isolated from chickens (Gallus domesticus).

1. Thiourea, ethylene thiourea, methimazole and (+) 5-vinyl-oxazolidine-2-thione (OZT) gave similar inhibition curves when added to the reaction mixture. A concentration of 20 microM reduced the activity by over 75%. Thioacetamide and thiobenzamide also behaved as potent inhibitors. 2. (-) OZT had less effect than the (+) isomer. 3. Microsomes from chickens with an inherently low capacity for synthesising TMA oxidase and enhanced susceptibility to the goitrogenic effects of OZT were more sensitive to this inhibition than those from a high TMA oxidase strain. 4. Inhibition by thiourea was competitive and the apparent K1 for low oxidase microsomes was 2.5 x 10(-6)M. 5. The inhibitory property of thionamides was lost when the S atom was replaced by O but was retained when it was oxidised to the sulphinic acid or sulphoxide. 6. Incubation of microsomes with sodium diethyldithiocarbamate reduced their TMA oxidase activity. 7. Sulphonium compounds, glucosinolates and antithyroid compounds with no thionamide group, including potassium thiocyanate, had no marked effect on the activity of the enzyme.

Bacterial endotoxins and the pathogenesis of fatty liver--haemorrhagic syndrome in the laying hen.

A high energy maize diet produced a higher incidence of fatty liver-haemorrhagic syndrome than a low energy barley diet when the diets were fed during the summer. The triglyceride content of the liver increased with the liver haemorrhage score and in hens with the highest scores there was evidence of hepatic hyperplasia. They also had high activities of aspartate transaminase and cholinesterase in the plasma and a low activity of sorbitol dehydrogenase. There was no increase in plasma endotoxin levels as the syndrome developed or any significant variation in these levels with the haemorrhage score, the triglyceride content of the liver or plasma enzyme activities. It was concluded that the steatosis does not impair the ability of the liver to inactivate endotoxins of enteric bacteria and that these toxins are not involved in the pathogenesis of the syndrome.

The influence of Escherichia coli O78 endotoxin on carbohydrate metabolism in the domestic fowl.

The injection of endotoxin isolated from a pathogenic avian strain of Escherichia coli (1 mg/kg intravenously) accelerated the depletion of liver glycogen in fasting nine- to 10-week-old chickens within the first hour and concurrently reduced their plasma inorganic phosphate levels. These changes were attributed to increased glycogenolysis and were followed by hypoglycaemia and a large increase in the lactate content of the plasma which appeared to be caused by enhanced glucose oxidation and reduced gluconeogenesis. The plasma glucose level returned to normal within three hours and simultaneous changes in the plasma urate and albumin content indicated that glucose was being synthesised from amino acids and that albumin was being catabolised to provide them.

Bacterial endotoxins and liver haemorrhage in the oestrogenised chicken.

Hepatic steatosis and haemorrhage in oestrogenised chickens were not associated with any increase in the endotoxin content of the plasma. The haemorrhage was not ameliorated by suppressing enteric bacteria with neomycin or exacerbated by the repeated injection of Escherichia coli O111 endotoxin and there were no relevant changes in plasma enzyme activities that are indicators of liver damage. These results therefore do not support the hypothesis that, as in the choline deficient rat, hepatic steatosis impairs the ability of the oestrogenised chicken to dispose of bacterial endotoxins and that these then damage the liver.

Effect of Escherichia coli O78 endotoxin on plasma lipids in the domestic fowl.

The injection of fasting nine- to 10-week-old chickens with endotoxin from a pathogenic avian strain of Escherichia coli (1 mg/kg iv) reduced the triglyceride, cholesterol and phospholipid content of the plasma 2 to 5 h afterwards. This effect was similar to that of an E coli infection and opposite to that produced in mammals. There was a transient rise in the cholesterol level within the first hour.

Response of caeruloplasmin to Escherichia coli endotoxins and adrenal hormones in the domestic fowl.

The injection of chickens with Escherichia coli endotoxins immediately produced a 50 per cent rise in plasma caeruloplasmin activity which was attributed to the release of the protein from liver cell. This was followed by a fall in activity, which was probably due to a fall in activity, which was probably due to a stabilising effect of adrenocortical hormones on the cell membranes, and then by a five-fold increase. The results of experiments with cycloheximide, adrenocorticotrophin, beta-methasone and reserpine indicated that the third phase of the response reflected increased synthesis in the liver which was partly induced by adrenal hormones. It increased with the dose and was not elicited by the particulate nature of the toxin preparation or by its lipid and polysaccharide components.

The effect of Escherichia coli endotoxins and adrenocortical hormones on plasma enzyme activities in the domestic fowl.

The intravenous injection of endotoxins isolated from Escherichia coli serogroups O111 and O78 (2 mg/kg) increased the activities of aspartate transaminase and lactate and sorbitol dehydrogenases in the plasma of six- to 11-week-old chickens during the next 24 h. These changes were compared with those produced by adrenocorticotrophic hormone and beta-methasone and were attributed to tissue damage involving the liver followed by increased enzyme synthesis which may have been induced partly by adrenocortical hormones. Further evidence of liver damage was provided by a fall in the activity of cholinesterase. The alkaline phosphatase activity gave no indication of cholestasis.