Estrogen and progesterone receptor status of mammary carcinomas and correlation with clinical outcome in dogs.

Estrogen and progesterone receptors (ER, PR) were measured in cytosol fractions from 18 primary canine mammary carcinomas by use of biochemical assays. One or both receptors were detected (> 10 fmol/mg of cytosol protein) in 11 tumors: 5 ER and PR; 2 ER only; 4 PR only. Mean cytoplasmic receptor concentrations (fmol/mg of cytosol protein) were 22.8 +/- 2.9 (SEM) for ER and 51.0 +/- 10.3 for PR in tumors containing ER and PR, 28.8 +/- 12.1 for ER in tumors containing only ER and 13.2 +/- 1.5 for PR in tumors containing only PR. Estrogen or progesterone receptors or both were identified in 6 of 9 tubular adenocarcinomas, 4 of 5 papillary adenocarcinomas, and 1 of 1 squamous cell carcinoma. These receptors were not identified in solid carcinomas (n = 2) or a single spindle cell carcinoma. Although the number of cases was limited, survival times of dogs tended to be longest in those with tumors containing ER alone or in combination with PR, intermediate in those with tumors containing only PR, and shortest in those with tumors without ER or PR. A correlation was not apparent between receptor status and age, presence of ovaries, tumor size, or histologic classification of the tumor. In the analysis of this series, the extent of surgery (mastectomy of the involved gland vs unilateral or bilateral mastectomy) did not appear to influence the outcome of the disease, and metastasis to regional lymph nodes did not appear to be a reliable prognostic indicator.     

In vitro nitroimidazole resistance of Trichomonas gallinae and successful therapy with an increased dosage of ronidazole in racing pigeons (Columba livia domestica)

Six out of eight different Trichomonas gallinae strains isolated from racing pigeons proved to be resistant to the nitroimidazole drugs ronidazole, carnidazole and metronidazole. The minimal cytocidal concentration of ronidazole was determined in in vitro experiments. Moreover, a therapeutic dose for ronidazole was determined for the control of trichomoniasis in pigeons from which the resistant T. gallinae strains were isolated. It was a 5-fold increase of the recommended ronidazole dosage which eliminated the infection in affected pigeons.     

Populations of Salmonella typhimurium in internal organs of experimentally infected carrier swine.

Experiments were conducted to determine comparative populations of Salmonella typhimurium in the most commonly infected body organs of long-term carrier swine. Naturally farrowed Salmonella-free pigs (n = 58) were orally exposed to S typhimurium when they were 47 days old. Necropsy of 3 to 5 randomly selected pigs was conducted at 3, 7, 10, 14, and 17 days and at 3, 4, 5, 6, 8, 12, 16, 20, 24, and 28 weeks after exposure. Mean populations (log10/g) of S typhimurium in palatine tonsils, ileum, cecum (wall and contents), ascending colon (wall and contents), and mandibular and ileocolic lymph nodes were estimated at each necropsy, using a most-probable-number method of bacteriologic examination. Populations of organisms in cecum and colon were similar to each other throughout the duration of the study. Mean populations (log10/g) associated with cecal and colonic walls decreased from 6.1 and 6.6, respectively, during the first postexposure (PE) week to less than or equal to 1.67 from PE weeks 4 to 28. Populations (log10/g) associated with cecal and colonic contents decreased from 5.6 and 5.5, respectively, at PE day 3 to 2.5 and 2.7, respectively, at PE week 4, and remained less than or equal to 2.8 until week 28. Populations (log10/g) associated with intestinal walls and contents were closely correlated during the study. Population (log10/g) in the ileum was greater than or equal to 5.3 from PE days 3 to 17, then varied between 5.4 and -0.4 up to PE week 28.(ABSTRACT TRUNCATED AT 250 WORDS)     

Xylazine and tiletamine-zolazepam anesthesia in horses

The cardiopulmonary and anesthetic effects of xylazine in combination with a 1:1 mixture of tiletamine and zolazepam were determined in 6 horses. Each horse was given xylazine IV or IM, as well as tiletamine-zolazepam IV on 4 randomized occasions. Anesthetics were administered at the rate of 1.1 mg of xylazine/kg of body weight, IV, 1.1 mg of tiletamine-zolazepam/kg, IV (treatment 1); 1.1 mg of xylazine/kg, IV, 1.65 mg of tiletamine-zolazepam/kg, IV (treatment 2); 1.1 mg of xylazine/kg, IV, 2.2 mg of tiletamine-zolazepam/kg, IV (treatment 3); and 2.2 mg of xylazine/kg, IM, 1.65 mg of tiletamine-zolazepam/kg, IV (treatment 4). Tiletamine-zolazepam doses were the sum of tiletamine plus zolazepam. Xylazine, when given IV, was given 5 minutes before tiletamine-zolazepam. Xylazine, when given IM, was given 10 minutes before tiletamine-zolazepam. Tiletamine-zolazepam induced recumbency in all horses. Duration of recumbency in group 1 was 31.9 +/- 7.2 (mean +/- 1 SD) minutes. Increasing the dosage of tiletamine-zolazepam (treatments 2 and 3) significantly (P less than 0.05) increased the duration of recumbency. Xylazine caused significant (P less than 0.05) decreases in heart rate and cardiac output and significant (P less than 0.05) increases in central venous pressure and mean pulmonary artery pressure 5 minutes after administration. Respiratory rate was decreased. Arterial blood pressures increased significantly (P less than 0.05) after xylazine was administered IV in treatments 1 and 3, but the increases were not significant in treatment 2. Xylazine administered IM caused significant (P less than 0.05) increases in central venous pressure and significant (P less than 0.05) decreases in cardiac output.(ABSTRACT TRUNCATED AT 250 WORDS)     

Flowering events in relation to smut susceptibility in pearl millet

In field experiments at ICRISAT, selected lines of pearl millet (Pennisetum glaucum) resistant and susceptible to smut (Tolyposporium penicillariae) were evaluated for the timing of flowering events. In smut-resistant lines, the time from the boot-leaf stage (inoculation) to stigma emergence varied in the range 46–120 h, from boot to anther emergence 105–190 h, and from stigma emergence to anther emergence (protogyny period) 59–131 h; in smut-susceptible lines, the corresponding periods were 62–140 h, 146–200 h and 44–120 h, respectively. There were no significant correlations between timing of events and smut severity. Three cytoplasmically male-sterile lines showed longer protogyny periods and higher smut severity than their corresponding maintainer lines. Four lines having short protogyny periods (22–52 h) and resistance to ergot (Claviceps fusiformis) also showed high resistance to smut. Resistance to smut in most ergot-susceptible lines was independent of the timing of flow ering events, but in ergot-resistant lines it could be closely related to flowering events.     

Systemic and pulmonary antibody responses of calves to Pasteurella haemolytica after intrapulmonary inoculation.

Systemic and pulmonary antibody responses of calves to Pasteurella haemolytica were evaluated by measuring immunoglobulin production in blood for 9 days and in pulmonary lavage fluid for 7 days after intrapulmonary inoculation. Clinical signs, pulmonary lesions, pulmonary and systemic inflammatory response, and amount of antigen in lavage fluid were used to evaluate the response of calves to challenge with P haemolytica. The pulmonary response consisted of production of IgG, IgE, and IgM antibodies to P haemolytica antigens and a 17- to 68-fold increase of cells in lavage fluid 8 hours after inoculation, with a gradual decrease toward normal. Antibodies of the IgM isotype to P haemolytica were demonstrated as early as 8 hours through 7 days after inoculation in 3 of 3 calves. Of the anti-P haemolytica isotypes, IgM was found in the highest concentration. In all of the inoculated calves, IgE was found 1 to 2 days after inoculation, and IgG was found in 2 of 3 inoculated calves from day 1 through 7 after inoculation. Detection of IgG correlated with smaller pulmonary lesions. Immunoglobulin A was not detected in lavage fluid. Serum was evaluated for IgG and IgM antibody response to P haemolytica. Specific IgM was detectable 5 days after inoculation, and IgG was detectable 7 days after inoculation. Pasteurella haemolytica antigens were not detected in serum or plasma. A transient increase in neutrophil count was found 8 hours after inoculation, with return to baseline values by 24 hours after inoculation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Relationship of common avian pathogen antibody titers in so-called chicken anemia agent (CAA)-antibody-positive chicks to titers in CAA-antibody-negative chicks.

Antibody titers for infectious bursal disease virus (IBDV), infectious bronchitis virus, Newcastle disease virus, and reovirus from chicks with chicken anemia agent (CAA) antibodies were compared with antibody titers from their CAA-antibody-negative counterparts. These comparisons were made in 396 chickens that were 1 day, 2 weeks, 8-9 weeks, 10 weeks, 17 weeks, or 29-32 weeks old. Only one serum sample was collected from any given chick or chicken. There were no significant differences between the antibody titers at any age for any antigen, with one exception: at 29-32 weeks, the IBDV titers were higher (t = 2.62, df = 142, P less than 0.01) in chickens with CAA antibody. Although not at all likely, we believe that the observation of high IBDV antibody titers in CAA-antibody-positive chicks could have been a spurious one.     

Biopsy of the bovine mammary gland.

A technique is described for biopsy of the bovine udder, employing sedation and local anaesthesia. Tissue samples of approximately 5 g were obtained by electrocautery from two quarters of the udder of a cow laterally recumbent. Care was taken to ensure complete haemostasis which was achieved by electrocoagulation and ligation. Postoperative recovery was rapid, and loss of yield was no greater in biopsied glands than in control glands of the same cow. Yield from all quarters returned to preoperative levels within 48 h.     

Monoclonal antibodies to bovine viral diarrhea virus: cross-reactivities to field isolates and hog cholera virus strains.

Monoclonal antibodies to bovine viral diarrhea virus (BVDV) were examined for binding with a large number of North American BVDV isolates and eight strains of the serologically related pestivirus, hog cholera virus (HCV). No single BVDV monoclonal antibody reacted with all BVDV isolates. The most cross-reactive monoclonal antibody was an anti-p80/p125 antibody which showed a positive reaction with 173 of 180 (96%) North American isolates. From a fewer number of isolates tested, one anti-gp53 monoclonal antibody also showed a high cross-reactivity (94%). All BVDV isolates showed a positive reaction with at least one of the seven monoclonal antibodies in the panel. Thus, the results indicated that a pool of these monoclonal antibodies may be used in place of polyclonal antisera for the detection of BVDV contamination of cell lines or for virus isolation. For HCV, all three anti-p80/p125 monoclonal antibodies reacted positively with all eight virus strains. In contrast, none of the anti-gp53 monoclonal antibodies were reactive to HCV strains. Thus, the anti-gp53 monoclonal antibodies may be useful for distinguishing between usually innocuous BVDV infections and the highly significant HCV infections in swine for foreign animal disease surveillance.     

5-bromo-2'-deoxyuridine blocks myogenesis by extinguishing expression of MyoD1

The pyrimidine analog 5-bromodeoxyuridine (BUdR) competes with thymidine for incorporation into DNA. Substitution of BUdR for thymidine does not significantly affect cell viability but does block cell differentiation in many different lineages. BUdR substitution in a mouse myoblast line blocked myogenic differentiation and extinguished the expression of the myogenic determination gene MyoD1. Forced expression of MyoD1 from a transfected expression vector in a BUdR-substituted myoblast overcame the block to differentiation imposed by BUdR. Activation of BUdR-substituted muscle structural genes and apparently normal differentiation were observed in transfected myoblasts. This shows that BUdR blocks myogenesis at the level of a myogenic regulatory gene, possibly MyoD1, not by directly inhibiting the activation of muscle structural genes. It is consistent with the idea that BUdR selectively blocks a class of regulatory genes, each member of which is important for the development of a different cell lineage.