Techniques of an "in vitro" method for determining toxigenicity of Corynebacterium diphtheriae strains.
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Biomedical subjects
Publications and source records attributed to J G Fox.
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Helicobacter mustelae, isolated from the stomachs of adult ferrets, appears to have a world-wide distribution. Ferrets are colonized with H. mustelae at a young age, usually 5-6 weeks; in our experience 100% of adult ferrets are colonized in both the antrum and the fundus. Gastric infection correlates with elevation of serum IgG antibodies to H. mustelae. In the oxyntic mucosa the presence of superficial gastritis coincides closely with the presence of H. mustelae. In the distal antrum the organism is associated with chronic inflammation occupying the full thickness of the mucosa. In addition to lesions seen in the distal antrum, focal glandular atrophy and regeneration are noted in the proximal antrum and transitional mucosa. Antibiotics used to eradicate Helicobacter pylori in humans are also effective in eliminating H. mustelae from ferrets. H. mustelae-free ferrets do not become colonized with H. pylori when challenged orally; however, sparse colonization follows oral inoculation with a related gastric organism, "Helicobacter felis." Controlled studies of the pathophysiology of gastroduodenal disease induced by Helicobacter species can be performed in H. mustelae-infected ferrets and their H. mustelae-negative counterparts.
Upper gastrointestinal examinations were performed in 11 unsedated ferrets and 4 ferrets sedated with ketamine and diazepam. Each animal received a 8-13 mL/kg body weight dosage of barium liquid (30% weight:volume). Radiographs were made immediately and at 5, 10, 20, 40, 60, 90, 120 and 150 min (mins) after the barium was administered. Gastric emptying began immediately. Mean total gastric emptying was longer in sedated ferrets (130 +/- 40 min versus 75 +/- 54 min); however, this difference was not statistically significant (p = 0.18). Small intestinal transit time was less than 2 h in all ferrets. The barium-filled small bowel was best visualized on the 20- and 40-min radiographs and did not exceed 5-7 mm in width. Flocculation of barium in the small intestine and adherence of barium to the stomach mucosa was seen in almost all animals. The longitudinal colonic mucosal folds in the colon were well visualized in the normal upper gastrointestinal study and aided in distinguishing small intestine from large intestine. The use of ketamine and diazepam sedation did not significantly affect the parameters evaluated in the upper gastrointestinal study series.
Since published results for the fast-neutron dose per x-ray rad from high-energy therapy installations have differed by as much as a factor of 300, we have measured the neutron production from our 25-MeV betatron. Fast-neutron activation of aluminum foils was the method used. The effect of photoneutron production in the detectors, which has affected some past work, has been eliminated. A major source of neutrons in the treatment field was the platinum target. The neutron spectra used in the calculations of fluence were obtained by interpolation between published energies and between neighboring elements. Fluences per rad of x rays without a phantom were largely independent of field size and energy in the range 18-23 MeV. At 100 cm SSD and 23 MeV a large beam flattener contributed 15% of the neutrons, the remainder coming equally from the target and background. A phantom increased the neutron fluence/rad of x rays by 0%-10% depending on the field size. At 23 MeV we estimated the neutron dose to a patient to be 2.2 X 10(-4) rad per rad of x rays inside the treatment field and 3 X 10(-5) at 20 cm outside the field. The uncertainty in these figures is believed to be +/- 50%. In the electron beam the neutron dose per rad was about 50 times smaller than in the x-ray beam. Estimates were made of neutron fluences at other energies and target thicknesses. We discuss our results in comparison with those of others.
An empirical formula has been developed to approximate the published axial depth doses of 60Co radiation with greater accuracy than available hitherto. With sets of nine constants, varying slightly with SSD, a total of 2100 percentage depth doses are reproduced with root-mean-square deviations ranging from 0.13 to 0.16 for four values of SSD from 50 to 100 cm.
The disease status of laboratory rodents should be clinically assessed before the animals are placed on toxicological bioassay programs. This is especially important when the stress of dietary or parenteral intake of toxic substances may trigger the clinical onset of latent diseases in research animals. In clinical evaluation of rodents, the environmental influence on biochemical, physiological and behavioral status of the animals must be continually monitored. Temperature, humidity, ventilation, lighting, and the microenvironment of the cage will all influence, independently or in consort, the response of the animal to various microbial or chemical insults. Unwanted variables in the diet can also markedly after the biological response of the animal and thus alter interpretation of experimental data. Adequately trained personnel, both professional and technical, must be available to provide daily care, clinical observation, and necessary treatment if signs of illness are noted in the laboratory rodent or bioassay experimentation. Clinical signs associated with commonly encountered diseases in laboratory rodents are briefly described. Clinical surveillance and assessment of rodents in part consists of recognition of and detailed recording of clinical signs, coupled with proper diagnostic resources to substantiate clinical observations. It is possible, with proper diagnosis, to evaluate the overall effect of a particular disease on the animal's health, the likelihood that the disease is jeopardizing the health of the other animals on test, and the effect of the disorder on interpretation of experimental results.