During the breeding season, the effect of constant administration of an agonist analog of gonadotropin-releasing hormone (GnRH; goserelin acetate) on reproductive activity of mares was determined. Twenty-four mares undergoing estrous cycles were allocated at random to 6 groups (n = 4/group) and, on May 29 (day 0), received no treatment (group 1, controls), 120 micrograms (group 2), 360 micrograms (group 3), 600 micrograms (group 4), or 1,200 micrograms (group 5) of GnRH agonist/d for 28 days via a depot implanted subcutaneously. The final group of mares (group 6) was treated with 120 miocrograms of GnRH agonist/d for 84 days (3 occasions at 28-day intervals). During a pretreatment period (April 19 to May 29) and for 90 days after initiation of GnRH agonist treatment, follicular development and ovulation were monitored by transrectal ultrasonography of the reproductive tract at 2- to 3-day intervals. On each occasion a blood sample was collected for determination of luteinizing hormone (LH) and progesterone. Estrous behavior was monitored by teasing of mares with a stallion. Initiation of agonist treatment was random, relative to the stage of the estrous cycle, and all mares ovulated within 11 days before or after implantation. in 3 of 4 nontreated control mares, estrous cycles were observed throughout the study, with interovulatory intervals ranging from 18 to 26 days. In the remaining mare, concentration of progesterone was high after asynchronous double ovulation during the pretreatment period, suggestive of persistent corpus luteum. In group-2 mares, ovulation occurred in all mares 7 days before and 2 days after initiation of treatment; however, the next anticipated ovulation was delayed in 3 of 4 mares (interovulatory interval, 33 to 70 days). Estrous cycles were not disrupted in the remaining mare. At higher doses (groups 3-5), 1 mare each from groups 3 and 5 ovulated between days 0 and 2 of treatment initiation.

Sonographic observations were made of the image mean gray scale (MGS) of the flexor tendons and ligaments in the left and right metacarpal regions of each of 10 clinically normal horses. In images made in the dorsal and sagittal planes, the MGS was measured at multiple sites in the superficial digital flexor tendon (SDFT), deep digital flexor tendon (DDFT), accessory ligament (AL), and suspensory ligament (SL), and at single sites in the medial and lateral limbs of the SL, and the palmar ligament. Relative sonographic brightness of each tendon and ligament was calculated by dividing the value of its MGS by the mean value for the MGS of images of 3 soft tissue equivalent phantoms. When a multivariate repeated-measures of ANOVA of the relative brightness values was statistically significant (P < 0.05), Tukey's method of multiple comparisons was used to determine which values were significantly different from each other. In the dorsal plane, the SL was significantly brighter than the DDFT, SDFT, and AL; relative brightnesses of the DDFT and SDFT were similar, as were those of the SDFT and AL. In the sagittal plane, the SL again was the significantly brightest structure, followed by the Al, and similar brightnesses of the DDFT and SDFT. In dorsal images made 25 cm distal to the accessory carpal bone, relative brightnesses of the SDFT, DDFT, and the medial and lateral limbs of the SL were similar. In images made 30 cm distal to the accessory carpal bone, relative brightness of the palmar ligament was significantly (P < 0.05) less than that of the SDFT and DDFT in the dorsal plane, but not in the sagittal plane, where it was significantly greater. Relative brightness values represented a unique sonographic characteristic of each structure and, in the future, may provide further insights into tendon and ligament structure and function.

Infectious laryngotracheitis virus (ILTV) is the causative agent of a highly contagious upper respiratory tract infection in chickens. At present, ILTV vaccines are not satisfactory because of development of a latent carrier status in vaccinated birds. Development of recombinant virus vaccines has been hampered by the limited information available on the molecular level and organization of this virus. We isolated 3 assembly intermediates, designated A, B, and C from ILTV-infected cells. Analysis of [3H]thymidine- and [35S]methionine-labeled particles, and electron microscopic studies indicated that particle A was the empty capsid, particle B was the procapsid containing scaffolding protein, and particle C was the DNA-filled capsid. The ILTV procapsids could only be found in the nucleus, which indicated that procapsids could not translocate through the nuclear membrane until they packaged the DNA. The DNA-filled capsids migrated through the nuclear membrane and obtained an envelope from the inner membrane of the nucleus. The enveloped particles then migrated through the lumen of the endoplasmic reticulum into vacuoles in the cytoplasm. Infective virions were isolated from within the infected cells, indicating that budding through the cytoplasmic membrane is not a necessary step in ILTV maturation. Abundant arrays composed of tubules about 45 to 50 nm wide were found in the cytoplasm of chicken embryonic liver cells about 30 to 38 hours after infection. Comparison of the assembly intermediates and the DNA packaging pathway of ILTV with that of bacteriophage phi 29 indicates that similarity exists. A model for the pathway of ILTV assembly is proposed.

Genetically altered stable nonreverting aromatic-dependent (aro-) Salmonella dublin, strain SL5631, was administered orally to healthy colostrum-fed calves as vaccine. Twenty-six calves were allotted to 4 groups. There were 2 experiments, each with a vaccinated and nonvaccinated control group. Skin testing with 0.1 ml of sonicated S. dublin was performed 3 days prior to challenge exposure. The IgG and IgM titers to S. dublin lipopolysaccharide (LPS) antigen were determined by ELISA on sera before initial vaccination and at 1.5 to 2 weeks after each vaccination. In experiment 1, six calves received a dose of 1.7 X 10(10) colony-forming units (CFU) of aro(-) S. dublin SL5631 orally at 2 and 4 weeks of age. After the first vaccination, 2 of 6 calves developed fever, but all 6 calves continued to have normal appetite and mental attitude. Adverse changes were not observed after the second vaccination. At the time of challenge exposure at 6 weeks of age, all 12 calves were seronegative for IgG and IgM LPS-specific antibodies, and the difference in percentage increase in skin test reaction at 48 hours was not significant. At 6 weeks of age, the 6 vaccinates and 6 controls were orally challenge-exposed with 1.5 X 10(11) CFU of virulent S. dublin T2340. Protection from challenge was not evident, as 3 of 6 controls and 5 of 6 vaccinates died after challenge exposure. In experiment 2, eight calves received a dose of 5 X 10(11) CFU of aro(-)S dublin SL5631 orally at 2, 3.5, and 5 weeks of age. The vaccine dose and volume (300 ml) were 30 times that of experiment 1. After each vaccination, some calves (7, 6, and 2 calves for first, second, and third doses, respectively) developed fever, but all calves continued to have normal appetite and attitude. At 7 weeks of age, the 8 vaccinates and 6 controls were orally challenge-exposed with 1.5 X 10(11) CFU of virulent S. dublin T2340 (same dose as experiment 1).

We evaluated the biochemical and hemodynamic response to hypertonic saline solution plus dextran in isoflurane-anesthetized pigs infused IV with Escherichia coli endotoxin (5 micrograms/kg of body weight for 0 to 1 hour + 2 micrograms/kg for 1 to 4 hours). After 120 minutes of endotoxemia, pigs were treated with a bolus (4 ml/kg over 3 minutes) of either normal saline solution (NSS; 0.9% NaCl), or hypertonic saline solution plus dextran (HSSD; 7.5% NaCl + 6% dextran-70). Administration of HSSD significantly (P < 0.05) increased serum osmolality and concentrations of sodium and chloride for approximately 2 hours during endotoxemia. Plasma total protein concentration decreased significantly (P < 0.05) for 2 hours after treatment with HSSD, indicating hemodilution and increased plasma volume. Although HSSD transiently increased cardiac index (CI) for approximately 15 minutes, this effect was not sustained; however, the endotoxin-induced decrease in CI was ameliorated from 120 to 180 minutes. In pigs of the endotoxin + NSS group from 180 to 240 minutes, CI decreased significantly (P < 0.05), compared with baseline and control values. The endotoxin-induced increases in mean pulmonary arterial pressure and pulmonary vascular resistance were not attenuated by HSSD. At 135 minutes, total peripheral vascular resistance was transiently lower (for approx 15 minutes) in pigs treated with HSSD, compared with control pigs. The endotoxin-induced increase in plasma lactate concentration was not attenuated by HSSD, indicating continued peripheral O2 debt. We conclude that, despite sustained increases in serum osmolality and concentrations of sodium and chloride, HSSD has only transiently beneficial cardiopulmonary effects during endotoxemia in pigs.

Middle carpal cartilage explants from 4 horses with mild osteoarthritis involving that joint were maintained in tissue culture to test the effects of a polysulfated glycosaminoglycan (PSGAG) on proteoglycan synthesis and degradation. Cultures were exposed to 0.025 or 25 mg of PSGAG/ml for 48 hours, after which the medium was replaced with medium containing similar doses of PSGAG and 35S. Subsequently, the sulfated proteoglycan content of the medium and extracts of the explants was measured. Gel filtration chromatography was used to estimate the size and to purify the principal, large proteoglycan monomer, which was further characterized by digestion, using glycosidic enzymes. In a second experiment, explants were incubated with 35S for 48 hours, and were subsequently exposed to the same concentrations of the PSGAG for an additional 48 hours. The amount of remaining labeled proteoglycan was determined for culture medium and cartilage extracts. Gel filtration chromatography was used to assess the hydrodynamic size of the large proteoglycan monomer. Aliquots of proteoglycans from the second experiment were incubated in high-molecular weight hyaluronate and chromatographed to assess reaggregation. Polysulfated glycosaminoglycan caused a significant (P < 0.04) decrease in sulfated proteoglycan synthesis by cartilage explants. Radioactive proteoglycan content in explants labeled prior to exposure to PSGAG were similar. Large proteoglycan monomer size was similar in both experiments (median partition coefficient [K(AV)] = 0.40), and was not influenced by PSGAG treatment. Prelabeled explants exposed to hyaluronate and chromatographed under associative conditions had similar proportions of the radiolabel eluting as proteoglycan aggregate. Enzymatic digestion of newly synthesized large monomer revealed a mild dose-dependent increase in the proportion of keratan sulfate substitution on core protein. It was concluded that PSGAG in vitro, at the dosages evaluated, caused a decre.

Strength in bending was determined for inter. dental fixation apparatuses applied to hemimandibles obtained from 24 canine cadavers. Hemimandibles were osteotomized perpendicular to the long axis between the third and fourth premolars, and segments were stabilized with 1 of 5 interdental fixation apparatuses: Erich arch bar (EAB, n = 6); Stout loop (SL, n = 6); acrylic A, n = 6); Stout loop and acrylic (SLA, n = 24); and Erich arch bar and acrylic (EABA, n = 6). Ultimate strengths (mean +/- SEM) of EAB, SL, A, SLA, and EABA were 395 +/- 48; 523 t 57; 1,106 +/- 102; 1,306 +/- 156; and 2,707 +/- 504 N.m, respectively. Stiffness (mean +/- SEM) of EAB, SL, A, SLA, and EABA were 2,944 t 357; 6,322 +/- 2,201; 16,010 +/- 5,017; 15,777 +/- 1,026; and 27,079 +/- 5,576 N.m/ radian, respectively. Yield strengths (mean +/- SEM) Of EAB, SL, A, SIA, and EABA were 66 +/- 6; 264 +/- 19; 911 +/- 126; 1,114 +/- 159; and 1,855 +/- 401 N.m, respectively. There were no significant differences in acrylic weight, cross-sectional area of the acrylic, or area moment of inertia of acrylic at the osteotomy site among A, SIA, and EABA; and there were no significant differences in osteotomy surface area and area moment of inertia at the osteotomy site among all apparatuses (P > 0.05). The EABA apparatus had significantly higher mean ultimate strength, mean stiffness, and mean yield strength compared to other interdental fixation apparatuses. There were no significant differences in the mean ultimate strength, mean stiffness, or mean yield strength between EAB and SL (P > 0.05). Apparatuses that combine acrylic with metal reinforcement (SLA, EABA) were significantly stronger and stiffer than those that used metal alone (EAB, SL) or acrylic alone (A).

Fifteen isolates of Escherichia coli obtained from the blood and tissues of septic foals had plasmid DNA of size ranging from 2.5 to 93 megadaltons. These isolates grew in normal equine serum (serum resistant), a trait previously documented to be expressed by isolates obtained from blood and tissues of septic foals, but not by isolates obtained from the feces of clinically normal horses. Of these isolates, 3 contained conjugal plasmids that encoded resistance to multiple antimicrobial agents linked to serum resistance and, in 1 isolate, to production of aerobactin as well. Serum resistance and production of aerobactin are related to virulence of septicemic E coli from non-equine sources.

Two hundred ninety-six Eschericbia coli isolates from feces or intestines of calves with diarrhea were hybridized with 7 gene probes. One probe (the eae probe) was derived from the eae gene coding for a protein involved in the effacement of the enterocyte microvilli by the group of bacteria called attaching and effacing E coli (AEEC), and 2 probes were derived from genes coding for the Shiga-like toxins (SLT) 1 and 2 produced by the verocytotoxic E coli (VTEC). The other 4 probes were derived from DNA sequences associated with the adhesive properties of enteroadherent E coli (EAEC) to cultured cells (the EAF probe for the localized adherence pattern, probes F1845 and AIDA-1 for the diffuse adherence pattern, and the Agg probe for the aggregative adherence pattern). Hybridization results for the eae probe were in agreement, for all but 1 of the 8 isolates, with previously published phenotypic results of microvilli effacement. The latter was previously reported as effacing the microvilli of calf enterocytes, but was eae probe-negative. Two classes of isolates hybridized with the eae probe. Members of a first class (60 isolates) additionally produced a positive signal with 1 or both of the SLT probes (VTEC-AEEC isolates). Isolates hy- bridizing with the eae and the SLT1 probes were the most frequent: 56 isolates (ie, 93% of all VTEC-AEEC). Members of the second class (10 isolates) failed to hybridize with either SLT probe (non-VTEC-AEEC isolates). Most isolates of these 2 classes belong to only 4 serogroups: O5, O26, O111, and O118. In addition to these 2 AEEC classes, a VTEC class (20 isolates) was observed. Such isolates were positive with 1 or both SLT probes, but were negative with the eae probe. All but 1 isolate belonged to serogroups not found among the AEEC isolates. Only 7 of all AEEC and VTEC isolates were positive with the EAF, the F1845, or the AIDA-1 probe, and none were positive with the Agg probe. On the other hand, 32 non-VTEC, non-AEEC isolates were po.

An intramammary device (IMD) was adapted for use in ewes; this device was made of abraded poly. ethylene material (1.7 mm in diameter, 47 mm long) and formed a 15-mm-diameter loop in the gland cistern. The IMD was inserted in 1 gland in each of 43 ewes. A significant (P < 0.0001) increase in milk somatic cell count (SCC) was observed in glands provided with an IMD. This increase was attributable to an increase in neutrophil numbers and was observed during the first 12 weeks after insertion. The IMD had a protective effect against experimentally induced staphylococcal mastitis (Staphylococcus aureus and S epidermidis), although different milk SCC were required for protection from each bacterial species in most ewes (10(6) and 2 X 10(5) cells/ml, respectively). Histologic studies revealed that the IMD induced local squamous metaplasia in the glandular part of the lactiferous sinus. Erythrocytes were found in milk from glands provided with an IMD throughout the studied period (35 days of the 45-day lactation) and, in some cases, blood clots were observed during the first 2 weeks of lactation. Glands with IMD also had lower milk production and quality at 30 and 32 days of lactation. Eight ewes with IMD were studied throughout a subsequent lactation. Milk from the IMD-containing glands had an increase in SCC, as in the previous lactation period; did not contain blood clots or erythrocytes; and had normal composition (similar to that in glands without the IMD).