Stranded seed displacement, migration, and loss after permanent prostate brachytherapy as estimated by Day 0 fluoroscopy and 4-month postimplant pelvic x-ray.

PURPOSE: The aim of the study was to determine the incidence of local displacement, distant seed migration to the chest, and seed loss after permanent prostate brachytherapy (PPB) with stranded seeds (SSs) using sequential two-dimensional fluoroscopic pelvic and chest x-rays. METHODS AND MATERIALS: Between October 2010 and April 2014, a total of 137 patients underwent PPB and 4-month followup pelvic and chest x-ray imaging. All patients had exclusively SSs placed and an immediate postimplant fluoroscopic image of the seed cluster. Followup x-ray images were evaluated for the number, location, and displacement of seeds in comparison to Day 0 fluoroscopic images. Significant seed displacement was defined as seed displacement >1 cm from the seed cluster. Followup chest x-rays were evaluated for seed migration to the chest. RESULTS: Seed migration to the chest occurred in 3 of the 137 patients (2%). Seed loss occurred in 38 of the 137 patients (28%), with median loss of one seed (range, 1-16), and total seeds loss of 104 of 10,088 (1.0%) implanted. Local seed displacement was seen in 12 of the 137 patients (8.8%), and total seeds displaced were 0.15% (15/10,088). CONCLUSIONS: SS placement in PPB is associated with low rates of substantial seed loss, local displacement, or migration to the chest. Comparing immediate postimplant fluoroscopic images to followup plain x-ray images is a straightforward method to supplement quality assurance in PPB and was found to be useful in identifying cases where seed loss was potentially of clinical significance.

Responses of pigs to a re-challenge with Actinobacillus pleuropneumoniae after being treated with different antimicrobials following their initial exposure.

Four groups of six specific pathogen-free (SPF) pigs were inoculated intranasally with Actinobacillus pleuropneumoniae serotype 2 and treated with either enrofloxacin, tetracycline or penicillin at the onset of clinical disease, or left untreated. A fifth group was left uninoculated. The inoculated control and the penicillin-treated groups developed severe disease, but the groups treated with enrofloxacin and tetracycline recovered rapidly. All the inoculated pigs, except those treated with enrofloxacin developed serum antibodies to A pleuropneumoniae. On day 28, all five groups were challenged with A pleuropneumoniae without any subsequent treatment. The previously uninoculated control group and the enrofloxacin-treated group developed severe disease, but the three seropositive groups remained unaffected.

Lectins inhibit the Aujeszky's disease virus-induced interferon-alpha production of porcine peripheral blood mononuclear cells.

The interaction between virus and peripheral blood mononuclear cells (PBMC) required to elicit the production of interferon-alpha (IFN-alpha) by the so-called natural interferon-producing cell is unknown. However, results from inhibition experiments suggest that viral glycoproteins are essential in this IFN induction process. We demonstrate here that cellular glycoproteins also appear to be involved in the initiation of IFN-alpha production. Lectins, that is, sugar binding glycoproteins, inhibited the Aujeszky's disease virus-induced IFN-alpha production of porcine PBMC by up to 99%. The level of inhibition varied with lectin used (concanavalin A, Galanthus nivalis lectin, Helix pomatia lectin, and lentil lectin). Preincubation experiments with porcine cells and concanavalin A (ConA) revealed that the lectin exerted its major effect directly on the PBMC. Although the IFN-alpha production in some cases was reduced by more than 90%, the PBMC were still able to proliferate in response to mitogenic lectins. The ConA-mediated inhibition of the IFN-alpha production was reduced if the lectin was added later than 6-8 h after the start of induction and was not mediated by soluble factors. Both orthovanadate and staurosporine inhibited the IFN-alpha production and did not relieve the ConA-mediated inhibition. Thus, ConA seems to interfere with the early events during IFN-alpha induction, but the mechanisms behind this interference could not be clarified.

Effect of vitamin E supplementation on weight gain, immune competence, and disease incidence in barley-fed beef cattle.

The aim of the study was to investigate whether vitamin E supplements in larger amounts than recommended could reduce incidence of disease, improve immune competence, and increase rate of weight gain of conventionally barley-fed beef cattle. Mean daily intake of vitamin E by individual calves in the experimental group was 200 mg during the first 2 mo, 400 mg during the next 2 mo, and 600 mg during the rest of the period. Corresponding daily intakes of vitamin E for the control group were 50, 100, and 150 mg. Mean plasma vitamin E of the experimental group increased from .49 mg/L at the start of the trial to 2.03 mg/L at the end, but that of the control group was lower at the end (.36 mg/L) than at the beginning (.53 mg/L). No significant differences were observed between the groups concerning incidence of disease or magnitude of lymphocyte stimulation. The results indicated that there was a surprisingly poor biological availability of the dietary vitamin. Therefore, a comparison in reality was made between calves with inadequate and normal vitamin E status. The differences in daily BW gain and time to reach slaughter weight thus probably were effects of the low vitamin E status rather than positive effects of additional vitamin in the diet.