Characteristics of cytotoxic cells induced by Toxoplasma lysate antigen in mouse spleen.

Spleen cells from Toxoplasma lysate antigen (TLA)-sensitized BALB/c mice showed the strong cytotoxic activity against both natural killer (NK)-sensitive cells (YAC-1 and RL male-1) and NK-insensitive cells (P-815), when incubated with TLA or recombinant human IL-2 (rhIL-2). The increment of TLA concentration in culture medium increased the cytotoxic activity. Treatment of effector cells; spleen cells from TLA-sensitized mice incubated with TLA, with anti-asialo GM1 or anti-Thy-1 plus complement inhibited the cytotoxic activity of effector cells, whereas treatment with anti-mouse Lyt-2.2 serum plus complement had no effect on the cytotoxic activity. Treatment of spleen cells from TLA-sensitized mice with anti-asialo GM1 and/or anti-Thy-1 plus complement inhibited cytotoxic activities of effector cells. These results suggested that spleen cells sensitized with TLA both in vivo and in vitro were asialo GM1 positive and Thy-1 positive, and the majority of cytotoxic cells induced by TLA were similar to lymphokine-activated killer (LAK) cells induced by IL-2.     

Oxidative damage to the membrane of canine erythrocytes with inherited high Na, K-ATPase activity.

Oxidative damage to the membrane in canine erythrocytes with inherited high Na, K-ATPase activity (HK cells) was compared with that in normal canine cells (LK cells). When 30 mM beta-acetylphenylhydrazine (APH) was applied to HK and LK cells, lipid peroxidation and hemoglobin denaturation occurred. Lipid peroxidation determined from malondialdehyde (MDA) formation was significantly lower in HK than in LK cells so far as endogenous glutathione (GSH) concentration was maintained at appropriate levels. With the depletion of GSH, MDA formation was accelerated and difference between HK and LK cells was not significant. Denatured hemoglobin bound to the membrane protein was less in HK than in LK cells. During incubation with APH, osmotic fragility increased markedly in LK cells, while HK cells showed very little change. The amounts of total lipid, total and free cholesterol, glycolipid, phospholipid and fatty acids were essentially the same in both cell types. Fatty acid compositions showed very small differences. The membrane of HK cells thus appear to have greater protection against oxidative damage induced by APH, owing to the presence of excess GSH in HK cells. The capability of HK cells to withstand oxidative damage would not be due to differences in membrane lipid compositions.     

Prevention of estrus in the queen with chlormadinone acetate administered orally.

The possibility of estrus prevention in the queen by the oral administration of chlormadinone acetate was examined. The animals used were 29 mature and 15 immature queens. For 16 mature females, 4-12.5 mg was given daily by mouth for 7 days every 3 months. Ten of the 16 queens given this treatment came into estrus within 4 months of the first treatment. For 28 females including the immature, 2-12.5 mg was given once a week throughout the experiment. This treatment prevented estrous activity for at least 1 year. In the queens in this study, the side effects were not observed excepting an increase in body weight during treatment. Our results showed that oral administration of this drug weekly is safe and reliable for long-range prevention of estrus in queens.     

Dietary selenate versus selenite for cattle, sheep, and horses.

Food and Drug Administration regulations currently permit addition of .3 mg of Se per kilogram of diet for chickens, turkeys, ducks, swine, sheep, and cattle. However, field reports indicate that this level may not be adequate for ruminants in all situations. Because sodium selenite is the most common supplemental form and is known to be readily absorbed to particles or reduced to insoluble elemental Se or selenides in acid, anaerobic environments, studies were conducted with dairy cattle, sheep, and horses fed sodium selenate to determine whether Se from this source was more bioavailable than Se from sodium selenite. A 2-wk period of no Se supplementation was followed by 49 or 56 d of Se supplementation at .3 mg/kg of dietary DM. Serum Se concentrations and glutathione peroxidase (GSHPx) activities measured initially and periodically thereafter revealed no difference between Se forms in sheep and horses and only a small (P less than .05) advantage for selenate in supporting serum Se concentration in dairy cattle. Selenium concentrations in skeletal muscle and liver of sheep were not different between Se forms. Serum Se, but not GSHPx, increased with time, and .3 mg of supplemental Se per kilogram of dietary DM from either sodium selenate or sodium selenite supported normal serum Se concentrations in sheep, dairy cattle, and horses.     

Effect of sodium nitrite and sodium chloride on growth of lactic acid bacteria.

The effect of NaNO2 and NaCl on the growth of 24 lactic acid bacteria strains isolated from vacuum-packed cooked ring sausages were examined by analyzing different growth parameters with Bioscreen. NaNO2 had a very limited effect on the growth of lactic acid bacteria at 50 and 100 mg/l but at 400 mg/l a more pronounced inhibitory effect was found. Bacterial growth was enhanced by 1-2% (w/v) of added NaCl, while NaCl concentrations above 3% (w/v) had a clear inhibitory effect. Leuconostoc isolates seemed to be more sensitive to sodium nitrite and sodium chloride than homofermentative lactobacilli strains. Among homofermentative lactobacilli, the strains resembling Lactobacillus curvatus were more sensitive to NaCl than those resembling Lactobacillus sake.     

Impact of bovine somatotropin administration beginning at day 70 of lactation on serum metabolites, milk constituents, and production in cows previously exposed to exogenous somatotropin.

Metabolic and production responses are reported for 72 cows treated with bovine somatotropin (BST) for 30 days starting at day 70 of lactation. Of these 72 cows, 48 had been exposed in the preceding lactation to long-term treatment with BST at 3 dosages and 24 (controls) had not been given BST. Approximately half of the cows in each group were parity-2 cows, the rest were older. Comparisons between groups were made separately for parity-2, and older cows. Analyses, using pretreatment values of each variable as a covariate, indicated that older cows, but not parity-2 cows, significantly (P less than 0.05) increased milk production during treatment. Parity-2 cows, however, had a significantly higher milk fat percentage than controls following treatment. Cows treated with 51.6 or 86 mg BST/d in both parity groups had significantly higher serum-free fatty acids than controls. Estimated net energy balances were significantly lower for older treated cows, but did not significantly differ from controls for parity-2 treated cows. Older cows in the 86 mg of BST/d group tended to have higher concentrations of blood glucose than did older control-group cows. Treatment with BST did not significantly increase serum ketone concentrations in any group of animals, and none of the cows developed clinical ketosis during this period. Estimated net energy balance (ENEB) during treatment was a significant (P less than 0.05) covariate for free fatty acid concentrations in older cows and for milk fat percentage in parity-2 cows. Covariate adjusted analyses, using ENEB during treatment as a covariate, indicated that lipolytic stimuli already acting may be enhanced by treatment with BST, but a negative energy balance was not a necessary precondition for free fatty acid concentrations to increase following somatotropin treatment. Similarly, milk fat percentages for parity-2 treated cows were significantly (P less than 0.05) higher during treatment than controls when ENEB during treatment was used as a covariate. Increased milk fat concentrations in parity-2 treated cows were not associated with significant increases in the ratio of C18:C4-10 milk fatty acids, indicating that increased milk fat resulted from either an increase in incorporation of C18 fatty acids into milk fat coupled with an increase in de novo mammary synthesis of C4-10 milk fatty acids or an increase in C12-16 fatty acids that may arise either from increased tissue mobilization, from diet, or from de novo mammary synthesis.     

Use of autogenous cancellous bone graft for treatment of osteolytic defects in the phalanges of three cattle.

Osteolytic defects were detected radiographically in the distal sesamoid bone of a 16-month-old Bralers heifer, in the middle phalanx of a 14-month-old American Gray Brahman bull, and in the distal phalanx of a 3-year-old American Gray Brahman bull. The articular cartilage was damaged in each animal because of osteolysis or pathologic fracture. After each animal was anesthetized and positioned in lateral recumbency, the lesions were curetted and packed with cancellous bone harvested from the same animal's tuber coxae. Basic postoperative management involved stall rest and immobilization of the graft site with a fiberglass cast (42 to 79 days), after which a support bandage was used for approximately 2 weeks. Recurrence of lameness has not been observed in these animals for 60 months, 58 months, and 21 months, respectively. These cases exemplify the benefit of using an autogenous cancellous bone graft for treatment of severe osteolysis of a digit in cattle.     

Pathogenicity of Campylobacter jejuni for turkeys and chickens.

A Campylobacter jejuni isolate obtained from a turkey liver, designated C101, and a C. jejuni isolate obtained from the feces of a chicken, designated C111, were used to inoculate their respective hosts. Isolate C101 depressed weight gain by 20% when inoculated into newly hatched poults or 4-day-old poults. It also caused death, hepatic necrosis, and generalized hemorrhages in turkey embryos. The chicken-derived isolate, C111, did not reduce weight gain in newly hatched chicks, but it did induce mortality in chicken embryos. The supernatant of the cultures of both C. jejuni isolates also caused mortality in embryos.