Protein profiles of whole homogenates of anconeus (slow twitch) and biceps femoris (fast twitch) muscles of clinically normal dogs and of Labrador Retrievers with hereditary myopathy (HM) were resolved on flat bed polyacrylamide isoelectric-focusing gels. Three methods of sample solubilization were performed. The solubilization buffer, with high concentrations of urea, precipitated the zwitterionic detergent, but use of the buffer containing 3% NP-40, 9.2M urea, and 0.1M arginine resulted in better resolution and stability of pH gradient. Gels of anconeus muscle from clinically normal dogs contained 2 protein bands specific to anconeus muscle, whereas gels of biceps femoris muscle from clinically normal dogs contained 3 protein bands amplified in biceps femoris muscle that were barely detectable in anconeus muscle. The staining intensity of protein bands in biceps femoris muscles from Labrador Retrievers with HM was decreased, relative to controls. The quantitative analysis of peak height ratios of biceps femoris muscle revealed significant (P less than 0.05) differences between profiles of clinically normal dogs and Labrador Retrievers with HM.

Custom-designed Hall-effect strain sensors (HES) were implanted surgically onto the superficial digital flexor tendons of the forelimbs of 4 adult Thoroughbreds. Strains were recorded at various gaits, using a portable amplifer and FM cassette recorder. Strain calculations used the original length (L) as the HES position with the forelimb in the relaxed neutral position during anesthesia. A characteristic deflection in the strain cycle recording was confirmed to correspond to initial hoof contact with the ground (heel strike) by simultaneous recording of weight bearing via a footswitch. Heel strike was used as the reference point to determine the magnitude of strain change during weight bearing and nonweight bearing under various conditions. The weight-bearing strains (heel strike to maximal strain) recorded in 2 horses (with a rider) were 3.1% and 7.6% at the walk, 6.5% and 10.1% at the trot, and 11.5% and 16.6% at the gallop. Strain rate during tendon loading at the gallop was approximately 200%/s. The magnitude of strain change during nonweight bearing (minimal strain to heel strike) was smaller than during weight bearing, but also increased with faster gaits. In 3 horses led at the walk and trot, modest increases in hoof angle (baseline, 52%) resulted in small increases in the magnitude of strain change during weight bearing at the trot, but the magnitude of strain change at the walk was not affected. Results of the study indicated that the HES can be successfully adapted to provide continuous strain measurement without subjective signs of discomfort or lameness in horses during or after instrumentation.

Analysis of protein and antigen profiles of Tritrichomonas foetus isolates from cattle from 5 western states was accomplished sodium dodecyl sulfate polyacrylamide-gel electrophoresis, immunoblot, immunoprecipitation, and fluorography techniques. Total protein profiles of all isolates were compared by Coomassie brilliant blue staining of T foetus protein samples prepared by 4 protein-extraction methods. Antigenic tritrichomonas proteins were identified by immunoblot assay with polyclonal bovine or rabbit anti-T foetus serum. Additionally, [14C]glucosamine-labeled T foetus was used for total and antigenic glycoprotein analyses. Detectable differences in the composition of total proteins or antigenic tritrichomonal proteins were not observed among all isolates. However, intensity differences in some antigenic protein bands were apparent. Bovine and rabbit sera from immunized animals possessed antibodies to the same antigenic tritrichomonal proteins. Each T foetus isolate contained 4 to 7 molecular weight size classes of glycoprotein, which were labeled by [14C]glucosamine; however, only 3 to 4 glycoproteins were identified as antigens by bovine or rabbit antiserum.

Eighteen strains of Escherichia coli serogroup O115:K"V165" isolated from 1- to 8-week-old pigs with diarrhea were tested for toxigenicity, pathogenicity in pigs and mice, serum resistance, mannose-resistant hemagglutination (MRHA), F165 and other surface antigens, colicin V (Col V), aerobactin, and biotype. Twelve strains were positive for heat-stable enterotoxin (STb), MRHA-negative, and F165-negative; 5 strains were enterotoxin-negative, MRHA-positive, and F165-positive; and 1 strain was MRHA-positive, but F165- and enterotoxin-negative. Six of the 12 STb-positive strains moderately colonized the ileum of newborn colostrum-deprived pigs within 24 hours after inoculation. Two of the colonizing strains were able to induce watery diarrhea. All 12 STb-positive strains were nonpathogenic for adult mice and were serum-sensitive; 11 of 12 were Col V-negative, 9 of 12 did not produce aerobactin, and 10 of 12 belonged to biotypes other than 1 or 2. All 6 enterotoxin-negative strains colonized the small and large intestines, associated with peritoneal serosal surfaces, and induced septicemia and polyserositis in newborn colostrum-deprived pigs 1 to 2 days after inoculation. In contrast, 3 STb-positive strains poorly colonized the intestines and did not induce septicemia in pigs at 3 days after inoculation. All 6 enterotoxin-negative strains were Col V-positive, produced aerobactin, and belonged to biotype 1 or 2. Of the 5 enterotoxin-negative, F165-positive strains, only 4 were pathogenic for intraperitoneally inoculated adult mice and were serum-resistant. The enterotoxin-negative, F165-negative strain was neither serum-resistant nor mouse-pathogenic. O-agglutinable mutants of the mouse-pathogenic strains were, for the most part, no longer pathogenic for adult mice, although these strains remained unchanged for biotype and production of MRHA, F165, and Col V, and 3 of 4 mutant strains were serum-resistant. Thus, E coli strains of the same serogroup isolated from diarrheic pigs may cause either intestinal or extraintestinal disease upon reinoculation of pigs, depending on the virulence attributes produced by the strains.

Basal serum triiodothyronine (T3) and tetraiodothyronine (T4) concentrations have not been established for the llama (Lama glama). In addition, changes in T3 and T4 concentrations in response to thyroid-stimulating hormone (TSH) administration have not been determined, making clinical evaluation of problems referable to thyroid dysfunction difficult. In study 1, basal T3 and T4 concentrations were determined in serum samples collected from 132 clinically healthy llamas. The llamas were allotted to 3 groups: mature intact or neutered males (group I, n = 25), nonpregnant sexually mature females (group II, n = 21), and pregnant females (group III, n = 86). A mean concentration and a 95% confidence interval were computed for each group. An analysis of variance (ANOVA) indicated that a single confidence interval range (0.45 to 4.18, mean = 1.37 ng T3/ml) adequately defined the normal T3 concentrations for all groups. An ANOVA indicated that the T4 concentrations for the female populations (groups II and III) could be combined with a normal confidence interval range of 39 to 204 ng/ml (mean = 88 ng/ml), whereas a separate range (70 to 220 ng/ml, mean = 124 ng/ml) was determined for the male population. An ANOVA indicated that a single confidence interval range (0.0066 to 0.0321, mean = 0.0146) adequately defined the normal T3/T4 ratio for all groups. In study 2, T3 and T4 concentrations were evaluated in 10 healthy llamas immediately preceding and at 2, 4, 6, 8, and 24 hours after the IV administration of 3 IU of TSH/44 kg of body weight. The T3 and T4 concentrations were significantly higher by 2 hours after TSH administration in both groups. Peak T3 and T4 concentrations were observed at 4 and 8 hours, respectively, after TSH administration. When normalized with respect to serum T3 concentrations in samples collected immediately prior to TSH administration, the maximal increase in predicted T3 concentration was 4.06-fold (80% confidence interval range = 2.99- to 5.50-fold) at 4 hours after TSH administration. The maximal increase in predicted normalized T4 concentration was 2.32-fold (80% confidence interval range = 1.76- to 3.05-fold) at 8 hours after TSH administration. The TSH-stimulated increases in T3 and T4 concentrations at 4 hours were clearly distinguishable from values in samples obtained before TSH administration.

The possibility that the canine pancreas might have an important role in the physiologic absorption of cobalamin (vitamin B12) has been explored by determining the effect of exocrine pancreatic insufficiency on cobalamin absorption and by examining the subsequent influence of bovine pancreatic enzymes and canine pancreatic juice. Exocrine pancreatic insufficiency was induced by ligation of pancreatic ducts and confirmed by indirect assessment of exocrine pancreatic function. Cobalamin absorption was determined by oral administration of cyano[58Co]cobalamin and quantitation of radioactivity in blood, urine, and feces during 48 hours. Pancreatic duct ligation resulted in a significant (P less than 0.001) decrease in cobalamin absorption, which was not restored by oral administration of bovine pancreatic enzymes, despite considerable improvements in steatorrhea and in vivo proteolytic activities. In marked contrast, malabsorption of cobalamin was significantly (P less than 0.05) reversed by oral administration of canine pancreatic juice. These results indicate that pancreatic secretions have an important role in the normal absorption of cobalamin in the dog, a role that does not appear to be attributable to pancreatic enzymes, but is consistent with the existence of a pancreatic intrinsic factor in this species.

We studied 6 singly caged adult female rhesus monkeys to determine whether increased cage size had any effect on behavior or heart rate. Two monkeys at a time were placed in cages 40% larger than their standard cage for 1 week on 2 occasions, using a counter-balanced design. Direct behavioral observations were performed 75 minutes/week on each monkey. Heart rate and general activity were monitored 35 hours/week by a telemetry system. Statistically significant differences were not found in aggressive, submissive, abnormal, or self-abusive behavior, nor in time spent in the front half of the cage, duration of grooming, looking at the observer, or stereotyped or nonstereotyped locomotion. Vocalizations increased the first time in the larger cage, but not the second, and decreased upon the second return to the standard cage. Differences with respect to cage size were not found in heart rate or activity level, although there were significant variations at different times of day. We conclude that modest increases in cage size are unlikely to enrich the environment of singly caged laboratory primates.

Animals recovered from viral diseases represent an important model to study the host cellular and humoral immune responses to the etiologic agents. This is particularly important for African swine fever virus (ASFV) infections in which antibodies have little or no virus-neutralizing effect. Pigs surviving experimental infection with the naturally occurring low-virulent, nonhemadsorbing ASFV/NH/P68 (NHV) isolate did, however, exhibit virus-specific T-cell activities, as measured by a variety of assays. A strong virus-induced, antigen-specific blastogenic response was observed only with blood mononuclear cells (BMC) from ASF-recovered swine, whereas cells from recovered and naive swine responded similarly to the mitogens concanavalin A and phytohemagglutinin. The ASFV-induced blastogenesis was dependent on virus dose and on the presence of adherent cells. Blood mononuclear cells cultured with antigenically related hemadsorbing ASFV isolates of different virulence characteristics, the highly virulent L60 isolate and moderately virulent DRII isolate, exhibited a similar magnitude of blastogenesis to cells infected with the low-virulent NHV isolate. Virus-infected cells proved to be an efficient inducer of interleukin-2 (IL-2) activity to cells from recovered swine, but not from naive swine, whereas T-cell-specific lectins induced production of similar amounts of IL-2 activity from cells of naive and recovered swine. Correlated with the appearance of virus-induced IL-2 activity in the culture supernatant was the induction of promiscuous killing in cells exposed to prolonged (7 days) virus stimulation. This lymphokine-activated killing could be induced experimentally early in the virus stimulatory process (3 days) by the addition of exogenous lymphokines to the cultures. It was concluded that swine inoculated with low-virulent ASFV isolates are a useful model for identifying and characterizing ASFV immune mechanisms in vitro. Furthermore, this ASFV model implicates lymphokines as inducers of nonspecific cell-mediated immunity; in fact, lymphokine-activated killer type responses may contribute to recovery from this viral infection. More important, ASFV-specific blastogenic and cytotoxic T-cells are prime candidates for the cells inducing and/or conferring protective immunity against challenge ASFV infection.

To investigate the potential role of sympathetic nerves in preventing pronounced increases in cerebral blood flow, we evaluated the effects of abrupt hypertension on the cerebral circulation of newborn pigs with intact cerebral sympathetic innervation and after cerebral sympathetic denervation. Epinephrine infusion was used to induce abrupt increases in mean (+/- SEM) arterial pressure (innervated pigs, 62 +/- 3 mm of Hg to 115 +/- 3 mm of Hg; denervated pigs, 71 +/- 4 mm of Hg to 132 +/- 4 mm of Hg) that remained increased for the 3 minutes of the study. Abrupt hypertension increased blood flow to all brain regions. In denervated pigs, the increased flow to the cerebrum was prolonged, compared with that in pigs with intact sympathetic innervation. Differences between pigs of the innervated and denervated groups were not apparent, with respect to blood flow to any other region (caudate region, brain stem, cerebellum). In newborn pigs, sympathetic nerves may attenuate hypertension-induced increases in blood flow to the cerebrum, but do not appear to affect flow to the rest of the brain.

Bovine pulmonary artery cells in cell culture were exposed to lipopolysaccharide (LPS) purified from Pasteurella haemolytica serotype A1. This resulted in severe membrane damage, which caused a time- and dose-dependent release of lactate dehydrogenase that was first detected 4 hours after exposure and reached a maximal mean release of 67% after 24 hours of exposure to 1 microgram of LPS/ml. Mean release of 51chromium followed by a similar pattern and reached a maximum of 61% following 24 hours of exposure to 10 micrograms of LPS/ml. Morphologically, endothelial cells responded to LPS by marked cell membrane retraction, the formation of numerous cytoplasmic blebs, and ruffling of the cell membrane. Subsequently, the cells became round and detached. Cell detachment reached a mean of 95% following 8 hours of exposure to 1 microgram of LPS/ml. These studies demonstrated that P haemolytica LPS is capable of causing direct damage to bovine pulmonary arterial endothelial cells, which may be important in the pathogenesis of bovine pneumonic pasteurellosis.