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Biomedical subjects

J G Fox

Publications and source records attributed to J G Fox.

At least 289 records · Page 16Linked to original sources
PubMed1987

Campylobacter jejuni infection in the ferret: an animal model of human campylobacteriosis.

Campylobacter infection in weanling ferrets (Mustela putorius furo) was studied as an animal model for enteric campylobacteriosis in persons. The screening of fecal cultures on selective campylobacter media showed that Campylobacter jejuni/coli was not present in the normal enteric flora. Intragastric feeding of a mixture of cat feed and 2.5 X 10(8) C jejuni isolated from ferrets with naturally occurring proliferative colitis was accomplished. All ferrets (n = 8) became infected on 3 days after they were inoculated, and at 5 to 7 days, they had bile-tinged, liquid feces with excessive mucus and blood. Ferrets gradually recovered from the diarrhea, and feces were normal 10 to 14 days after inoculation was done. Feces contained C jejuni at 14, 23, 28, 39, 46, 60, 91, 101, 109 and 144 days. In the second experiment, weanling ferrets initially were treated with 10% sodium bicarbonate, and 1 X 10(10) C jejuni organisms were administered in the cat feed. Diarrhea with fecal leukocytes and occult blood with occasional mucus appeared in almost all of the 21 ferrets from days 4 through 7. Campylobacter jejuni was isolated from the blood of 11 ferrets between 3 hours and 14 days after they were inoculated. Campylobacter jejuni bactericidal antibodies were present in serum samples at 14 days, with titers of 1:16 to 1:32. Intestinal lesions including cellular infiltration with mononuclear and polymorphonuclear leukocytes were in the lamina propria of the pyloric mucosa and small intestine of infected and control ferrets. The colon of 3 infected ferrets had small focal infiltrates of neutrophils on the lamina propria; one ferret had perivascular cuffing.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Single-step immunization using a controlled release, biodegradable polymer with sustained adjuvant activity.

The use of a biodegradable polymer for antigen delivery based on poly(CTTH-iminocarbonate) (IUPAC nomenclature: poly[oxyimidocarbonyloxy-p-phenylene [2-(hexyloxycarbonyl)ethylene]imino[2-[1-(benzyloxy)formamido]- 1-oxotrimethylene]-p-phenylene]) was investigated. This polymer was selected since its primary degradation product, N-benzyloxycarbonyl-L-tyrosyl-L-tyrosine hexyl ester (CTTH) was found to be as potent an adjuvant as complete Freund's adjuvant and muramyl dipeptide, when measuring the serum antibody response to bovine serum albumin (BSA) in male CD-1 mice over 56 weeks. BSA released from subcutaneously implanted polymeric antigen delivery devices made of poly(CTTH-iminocarbonate) resulted in significantly higher (P less than 0.006) anti-BSA antibody titers than devices made of poly(bisphenol A-iminocarbonate).

Adjuvants, Immunologic↗
PubMed1986

Proliferative colitis in a pet ferret.

A 4-month-old male ferret was examined because of mucus-laden diarrhea of several days' duration. The diarrhea became bloody and the ferret became progressively anorexic and lost weight. Treatment with antibiotics did not result in amelioration of clinical signs. A biopsy specimen was obtained from the colon, which was thick and turgid. Proliferative colitis associated with Campylobacter sp infection was diagnosed histologically. Because of the poor prognosis and potential zoonotic hazard associated with Campylobacter, the ferret was euthanatized.

Animals↗
PubMed1986

Chronic diarrhea associated with Campylobacter jejuni infection in a cat.

Campylobacter jejuni was isolated from a cat with chronic diarrhea. The diarrheic cat and another cat (which previously had diarrhea) in the same household had bactericidal antibody titers to the C jejuni. Clinical response to antibiotic therapy and not recovering Campylobacter sp from normal feces after treatment also supported the diagnosis of Campylobacter-associated diarrhea. Although the owner had a protracted episode of diarrhea, C jejuni was not isolated from the owner's feces, nor was a bactericidal antibody detected in the owner's serum.

Animals↗
PubMed1986

Excretion of radioactivity from rats and rabbits following cutaneous application of two 14C-labeled azo dyes.

A benzidine-derived azo dye, C.I. direct black 38 (DB38), and a p-phenylenediamine-derived dye, C.I. direct black 19 (DB19), labeled with carbon-14 in their aromatic amine moieties, were applied to the shaved dorsal skin of male Fischer-344 rats and New Zealand rabbits. Application sites were protected with nylon gauze and elastic bandage assemblies. Following application of measured amounts of radiolabeled dye in 0.1 M pH 10.2 carbonate buffer, serial urine and fecal samples were obtained from individual animals in metabolism cages at 24, 48, 72, 96, 120, and 144 h. Aliquots of urine and fecal homogenates were assayed for radioactivity by scintillation counting. Cumulative excretion of radioactivity from rats receiving DB38 was 0.05% of total dermal dose at 144 h in urine, and 0.16% of total dermal dose in feces. Cumulative excretion of radioactivity from DB38-treated rabbits at 144 h was 3.12% of total dermal dose in urine, and 5.12% in feces. From rats and rabbits receiving topical DB19, cumulative excretion of radioactivity at 144 h was less than that from DB38-treated animals. In rat urine, 0.04% of total dermal dose appeared; in rat feces, no radioactivity was recovered. In rabbit urine, 0.04% of dermal dose was found; 0.01% appeared in rabbit feces.

Animals↗
PubMed1986

Mechanisms for nitrite loss from the stomach.

Nitrite loss from the stomach was studied using dogs equipped with Thomas cannulas for direct access to the stomach lumen. Solutions containing sodium nitrite and non-absorbable volume marker (polyethylene glycol, PEG) were infused into the stomach, and samples were taken over 60 min to determine the concentration of 'total nitrite' (including NO2-, HNO2 and other species in equilibrium with NO2-) and rate of dilution of the stomach contents as a function of time. Changes in stomach volume were also measured. Nitrite loss was found to be very rapid, with total nitrite concentrations declining to less than half the initial levels in 10 min. The decay in total nitrite concentrations was due predominantly to gastric absorption, with small additional contributions from dilution of the stomach contents (inferred from PEG concentrations) and chemical reactions (from in vitro kinetic data). Results for initial nitrite concentrations varying over a range of 0.15-4.5 mM showed absorption to be first order in total nitrite. The permeability-area product for nitrite absorption (PA) was about 0.6 l/h, and was unaffected by the addition of 1 mM SCN- or Cl-. All of these results are consistent with nitrite absorption in the form of NO2- or HNO2. Buffering the infusate with HCO3- to increase luminal pH from approximately 2 to 7 caused a three-fold reduction in the apparent value of PA. When pentagastrin was used to stimulate acid secretion, nitrite absorption was only half as fast as when acid secretion was inhibited with cimetidine, or when no drug was given. This effect could not be explained by variations in luminal pH, and suggests that acid secretion either decreases PA or is accompanied by active secretion of nitrite. Based on these data, a mathematical model was developed to stimulate the physical and chemical factors governing nitrite concentrations in the stomach.

Animals↗
PubMed1986

Transport of dimethylamine, a precursor of nitrosodimethylamine, into stomach of ferret and dog.

Dimethylamine is important because it is a precursor of nitrosodimethylamine, a suspected carcinogen in man. Significant quantities of dimethylamine and nitrite are found in gastric fluid, and conditions in the stomach are favorable for nitrosodimethylamine formation. Little is known about the origins of dimethylamine in gastric fluid. Studies were performed to determine whether dimethylamine can be transported from blood to gastric fluid. There was no diurnal variation of the dimethylamine content in gastric fluid or blood from untreated dogs. We administered 50 mg/kg dimethylamine i.v. to dogs and ferrets and collected blood and gastric fluid samples at timed intervals. In both species we observed similar kinetics of dimethylamine distribution into biologic fluids. Dimethylamine concentrations in blood and gastric fluid rose rapidly during the first minutes after treatment. Blood dimethylamine concentrations peaked within 30 min after the dose (rising from 10 to 430 nmol/ml in the dogs, and from 30 to 430 nmol/ml in the ferrets). Dimethylamine concentrations in blood slowly decreased thereafter. Gastric fluid dimethylamine concentrations continued to rise for 3 h after the dose (from 40 to 540 nmol/ml in the dogs, and from 40 to 1056 nmol/ml in the ferrets). Gastric fluid dimethylamine remained elevated for more than 5 h. Between 1 h and 5 h after treatment, gastric fluid dimethylamine concentrations were significantly higher than blood dimethylamine concentrations (by greater than 2.5 X). In gastric fluid from control animals, dimethylamine concentration exceeded monomethylamine concentration, which in turn was higher than trimethylamine concentration. Administration of dimethylamine transiently increased gastric fluid monomethylamine content, but had little effect upon trimethylamine concentration. These data demonstrate that dimethylamine is efficiently transported from blood into gastric fluid.

Animals↗
PubMed1986

Surveillance of mice for antibodies to murine cytomegalovirus.

The sera of 256 mice from nine commercial sources were screened for antibodies to murine cytomegalovirus (MCMV) because a surveillance of this virus has not been reported in the literature for over a decade. Although no evidence of antibodies to MCMV were detected by complement fixation or nuclear anticomplement immunofluorescence, 54.7% of these sera did have antibodies that were detected by enzyme-linked immunosorbent assay. These data emphasize the need for proper containment of laboratory mice to prevent the potential outbreak of acute MCMV infection. Including MCMV antibody surveillance by enzyme-linked immunosorbent assay in routine health monitoring of mice and imparting these findings in an analysis of the role of MCMV on interpretation of experimental results is advised.

Animals↗
PubMed1986

Therapy with cyclosporine in experimental murine myocarditis with encephalomyocarditis virus.

To explain the progression from infectious viral myocarditis to congestive cardiomyopathy an infection/immune hypothesis has been proposed stating that the primary viral process incites an excessive or disordered immunologic response against the myocardium. To test whether one form of immunosuppressive therapy might ameliorate this process, we used cyclosporine in a murine preparation of infectious myocarditis (encephalomyocarditis [EMC] virus), which has been shown to result in a congestive cardiomyopathy pathologically similar to that seen in man. Eight-week-old male DBA-2 mice were infected with EMC virus and randomized to a treatment or control group. Cyclosporine (25 mg/kg/day) was administered subcutaneously for 3 weeks, starting (1) at 1 week after infection during viral replication, and (2) at 3 weeks after infection, after the period of active viral replication. In mice treated during viral replication there was a significantly higher mortality rate compared with that of control mice (15/21 vs 9/29, p = .01). There was no evident reduction in myocardial pathology (inflammation, necrosis, or calcification) in the treated compared with the control groups. In mice treated after the period of viral replication, there was no improvement in mortality (8/22 vs 2/19, NS) compared with control. Treated mice showed no reduction in myocardial histopathologic lesions. Furthermore, treated mice had significantly greater heart weight/body weight ratios (1.3 +/- 0.4% vs 1.0 +/- 0.3%, p less than .005), lung weight/body weight ratios (1.1 +/- 0.5% vs 0.8 +/- 0.3%, p less than .05), and liver weight/body weight ratios (6.0 +/- 0.8% vs 5.4 +/- 0.6%, p less than .005) than control mice, suggesting more severe myocardial failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Campylobacter-like organisms isolated from gastric mucosa of ferrets.

Campylobacter-like organisms (CLO) were isolated from gastric lesions in 1 ferret and gastric mucosa of 2 healthy ferrets. The organism was not isolated from biopsies of gastric mucosa of 14 other healthy ferrets, 1 of which had small gastric lesions located at the pylorus. Lesions from which CLO were isolated were located in the antrum of 1 ferret and were classified as inflammation with repair. Affected gastric tissue was highly vascularized with fibrous connective tissue surrounding irregularly shaped glands. Necrosis and ulceration of adjacent mucosa also were observed. Using Warthin-Starry stain, Campylobacter-like organisms were seen on and in the glandular epithelium of the ferret with gastric lesions from which CLO were isolated.

Animal Diseases↗
PubMed1986

Colonization of Syrian hamsters with streptomycin resistant Campylobacter jejuni.

A streptomycin resistant Campylobacter jejuni inoculated per os into two populations of Syrian hamsters (one endemically harboring C. jejuni, the other free of C. jejuni) established chronic colonization of the organism in both groups. Diet, steroid administration, age of hamsters or prior exposure to C. jejuni did not appreciably alter incidence of diarrhea or colonization of C. jejuni. The majority of hamsters sampled during the course of the experiment (1 to 22 weeks) shed streptomycin resistant C. jejuni in the feces. In four hamsters sampled at 14, 17, 19, and 22 weeks, post inoculation, streptomycin resistant C. jejuni were recovered in ileal, cecal, jejunal, duodenal and colonic contents (10(4) to 10(7) colony forming units/gram of intestinal content). The hamster appears to be a potentially useful model for the study of intestinal colonization of enteropathogenic C. jejuni. Hamsters shedding C. jejuni in their feces for extended periods of time should be considered a zoonotic threat to both pet owners and laboratory personnel.

Animals↗
PubMed1985

Endogenous formation of dimethylamine.

An understanding of the biosynthesis and metabolism of dimethylamine (DMA) is important because it is a precursor of dimethylnitrosamine (nitroso-DMA). DMA is the major short-chain aliphatic amine in human and rat urine. DMA is formed from trimethylamine (TMA), which, in turn, is a breakdown product of dietary choline. Enzymes within gut bacteria catalyse both of these reactions; it is not known whether mammalian cells can form DMA. To determine the relative importance of dietary choline, bacteria and other mechanisms for the formation of DMA, we measured DMA excretion in the urine of rats fed on a diet devoid of choline, and in urine of rats with no bacterial colonization of the intestines. We also describe an improved gas-chromatographic method for the measurement of methylamines in biological fluids. In control rats there were significant amounts of DMA within several biological fluids [urine, 54.2 +/- 3.0 mumol/kg body wt. per 24 h (556.2 +/- 37.5 nmol/ml); blood, 18.8 +/- 1.9 nmol/ml; gastric juice, 33.5 +/- 10.5 nmol/ml; means +/- S.E.M.]. Animals eating a diet containing no choline excreted as much MMA and DMA as did choline-supplemented rats (25-35 mumol/kg per 24 h), and they excreted slightly less TMA (2 versus 2.5 mumol/kg per 24 h). Rats with no gut bacteria excreted the same amount of DMA in their urine as did the control animals (45-55 mumol/kg per 24 h). They excreted much less MMA (16.3 +/- 1.5 versus 40.3 +/- 2.6 mumol/kg per 24 h; mean +/- S.E.M.; P less than 0.01), TMA (0.7 +/- 0.2 versus 2.5 +/- 0.5 mumol/kg per 24 h; mean +/- S.E.M.; P less than 0.01) and piperidine (2.0 +/- 0.3 versus 6.3 +/- 0.6 mumol/kg per 24 h; mean +/- S.E.M.; P less than 0.01) in their urine. From our studies we conclude that DMA is present in significant amounts within gastric fluid, an environment that is ideal for nitrosamine formation (under acidic conditions, nitroso-DMA is chemically formed by the reaction of nitrite with DMA). Results also indicate that dietary choline was not the sole precursor for DMA formation and that gut bacteria are not essential for the formation of DMA. Hence in mammals there must be endogenous pathways that are capable of forming DMA; however, these endogenous mechanisms remain unidentified.

Animals↗
PubMed1985

Laboratory animal medicine. Changes and challenges.

Less than three decades have elapsed since the specialty of laboratory animal medicine was first formally recognized. Tremendous progress and maturation has occurred in this short time frame due in large part to the foresight of early pioneers in the field, attention to the moral and ethical use of animals, and the recognition by the biomedical research community of the indispensable role played by the laboratory animal medicine specialist in forging new knowledge in the biomedical sciences. The ability of laboratory animal medicine specialists to properly balance their efforts in collaborative and independent research, clinical services and teaching, offers exciting challenges and opportunities for veterinarians entering the specialty. Undoubtedly, another challenge to the specialty, currently and in the foreseeable future, is the debate over animal rights which began to ferment in the late 1970's, after lying relatively dorment since the 1950's. A growing number of Americans, including some scientists, contend that animals have inherent rights to a full life, free of intentional pain, even when done in legitimate scientific pursuits; some ardent anti-vivisectionists state that the use of animals in experimental research is immoral. The laboratory animal medicine specialist will have to effectively deal with the administrators of institutions using research animals, the attendant federal and state guidelines and laws regulating their use, and defend the use of laboratory animals to a polarized public, while at the same time ensure the humane care and use of animals under their purview. Certainly, the specialty is squarely placed in a hotly debated dilemma, fraught with ethical, moral, medical, philosophical, religious, and political complexities. I believe the specialty has the vision and maturity, and is indeed ready, to successfully meet that challenge - to assuage public concern, implement new federal policy regarding animal care and use, and maintain the excellent progress in laboratory animal medicine realized in the last 75 years.

Animals↗
PubMed1985

Serum chemistry reference values in two strains of Syrian hamsters.

Blood samples were collected from 30 male and female hamsters (Mesocricetus auratus) from two sources. Serum was collected and analyzed for 17 biochemical values. The results were analyzed statistically and comparisons were made between males and females and between strains.

Animals↗
PubMed1985

Evaluation of ethylene-vinyl acetate copolymer as a non-inflammatory alternative to Freund's complete adjuvant in rabbits.

Ethylene-vinyl acetate copolymer (EVAc) was evaluated as an antigen delivery device in laboratory rabbits. Bovine serum albumin (BSA) was incorporated with EVAc in a pellet, which was implanted subcutaneously. Serum antibody titers to BSA in four implanted rabbits were equal to titers in four rabbits injected twice with BSA in complete Freund's adjuvant. Three of four rabbits implanted with EVAc displayed no inflammation or systemic illness in response to the pellet. The fourth rabbit repeatedly developed a small abscess at the implantation site, but the lesions were less severe than complete Freund's adjuvant injection sites. The EVAc pellet is recommended as a non-inflammatory alternative method to Freund's adjuvants for producing serum antibody in rabbits.

Adjuvants, Immunologic↗
PubMed1984

Nephrotic syndrome associated with renal amyloidosis in a colony of Syrian hamsters.

A 6% incidence of nephrotic syndrome was noted in a colony of 400 Syrian hamsters (Mesocricetus auratus) over a period of 2 years. Clinical findings consisted of severe ascites and anasarca, anorexia, cachexia, and papular dermatitis. Serum and urine chemical analysis revealed proteinuria and hypoalbuminemia in all animals tested; hypoproteinemia and high concentrations of serum cholesterol, triglycerides, and creatinine were detected in some of the affected hamsters. Demodex aurati was detected in skin scrapings from 4 of 8 hamsters. Necropsy findings included subcutaneous edema, ascites, and hydrothorax, as well as atrophic kidneys and testes. Extensive deposits of type AA amyloid were detected histologically in kidney, liver, spleen, and adrenal gland; smaller deposits were found in thyroid gland and intestine. Other histologic findings included periodontitis and hyalinization of the small arteries of the testes.

Amyloidosis↗