Search PubMed⌕ Search

Biomedical subjects

J G Fox

Publications and source records attributed to J G Fox.

At least 217 records · Page 12Linked to original sources
PubMed1992

Helicobacter muridarum sp. nov., a microaerophilic helical bacterium with a novel ultrastructure isolated from the intestinal mucosa of rodents.

Helical organisms with novel ultrastructural characteristics were isolated from the intestinal mucosa of rats and mice. These bacteria were characterized by the presence of 9 to 11 periplasmic fibers which appeared as concentric helical ridges on the surface of each cell. The cells were motile with a rapid corkscrewlike motion and had bipolar tufts of 10 to 14 sheathed flagella. The bacteria were microaerophilic, nutritionally fastidious, and physiologically similar to Helicobacter species and Wolinella succinogenes but could be differentiated from these organisms by their unique cellular ultrastructure. Using 16S rRNA sequencing, we found that strain ST1T (T = type strain) was related to previously described Helicobacter species, "Flexispira rappini," and W. succinogenes. The closest relatives of strain ST1T were Helicobacter mustelae and "F. rappini" (average similarity value, 96%). On the basis of phylogenetic data, strain ST1T (= ATCC 49282T) represents a new species of the genus Helicobacter, for which we propose the name Helicobacter muridarum.

Animals↗
PubMed1992

An ultrastructural study of Helicobacter mustelae and evidence of a specific association with gastric mucosa.

The ultrastructure of Helicobacter mustelae, a natural inhabitant of the ferret stomach, has been studied and compared with the human gastroduodenal pathogen H. pylori. H. mustelae is a short, slightly curved rod, 2 microns x 0.5 micron, with four or more sheathed flagella. The most common flagellar configuration is a single flagellum at one terminus, bipolar arrangement at the other end and a lateral flagellum. Dense inclusion bodies were observed below the flagellar insertion sites. It is suggested that this configuration is a specialised adaptation to motility in a viscous environment. On examination of the ferret gastric mucosa, similarities to H. pylori were observed such as adherence to gastric tissue and the formation of adhesion pedestals. However, unlike H. pylori, significant numbers of bacteria were intracellular. Furthermore, a much greater proportion of H. mustelae were attached to the mucosa with few bacteria lying free in the mucus, as is seen with H. pylori. It is concluded that the ferret is an important model for the study of adherence of bacteria to gastric mucosa and their possible role in peptic ulceration.

Animals↗
PubMed1992

Haemagglutination profiles of Helicobacter species that cause gastritis in man and animals.

Thirty-five Helicobacter pylori isolates, 21 H. mustelae isolates and four strains of H. felis were compared for their ability to agglutinate red blood cells (RBCs). Isolates were examined in a slide haemagglutination assay with RBCs from 11 animal species, including rodents, carnivores and primates, as well as man. RBCs were agglutinated by 65-90% of H. mustelae isolates and 16-57% of H. pylori isolates. Treatment of H. mustelae with pronase and heat inhibited haemagglutination (HA) whereas heating only of H. pylori inhibited HA. Treatment of all strains of H. mustelae with trypsin inhibited agglutination of human RBCs; 75% of the treated strains did not agglutinate ferret RBCs. These results suggested that protein(s) may be important haemagglutinins for these bacteria. Variable HA profiles together with varying results after treatment of RBCs with fetuin, D-mannose, and neuraminidase suggested that multiple receptors may be involved in HA reactions with H. pylori and H. mustelae. The observation that H. mustelae and H. pylori agglutinated RBCs of several species and closely adhered to gastric epithelium supported the hypothesis that adherence plays a role in the colonisation and pathogenicity of H. mustelae and H. pylori. H. felis did not adhere to gastric epithelium and did not agglutinate RBCs of any species; nevertheless, H. felis can readily colonise and produce gastritis in several mammals.

Animals↗
PubMed1992

Helicobacter mustelae isolation from feces of ferrets: evidence to support fecal-oral transmission of a gastric Helicobacter.

Helicobacter mustelae has been isolated from stomachs of ferrets with chronic gastritis and ulcers. When H. mustelae is inoculated orally into H. mustelae-negative ferrets, the animals become colonized and develop gastritis, a significant immune response, and a transient hypochlorhydria. All of these features mimic Helicobacter pylori-induced gastric disease in humans. Because the epidemiology of H. pylori infection is poorly understood and its route of transmission is unknown, the feces of weanling and adult ferrets were cultured for the presence of H. mustelae. H. mustelae was isolated from the feces of 11 of 36 ferrets by using standard helicobacter isolation techniques. H. mustelae was identified by biochemical tests, ultrastructural morphology, reactivity with specific DNA probes, and 16S rRNA sequencing. H. mustelae was not recovered from 20-week-old ferrets which had been H. mustelae positive as weanlings, nor was H. mustelae recovered from 1-year-old ferrets. Isolation of H. mustelae from feces may correspond to periods of transient hypochlorhydria, or H. mustelae may be shed in feces intermittently. The H. mustelae-colonized ferret provides an ideal model for studying the pathogenesis and transmission of H. pylori-induced gastric disease.

Animals↗
PubMed1992

Intestinal uptake and lymphatic absorption of beta-carotene in ferrets: a model for human beta-carotene metabolism.

To determine the appropriateness of the ferret as a model for human beta-carotene (beta-C) metabolism, we have perfused both 15,15'-beta-[14C]C and unlabeled beta-C through the upper 30-cm portion of the small intestine of ferrets in vivo. The effluents of a mesenteric lymph duct cannulation and a common bile duct cannulation, as well as portal vein blood periodically sampled via an indwelling catheter, were collected. Ten percent (9.5 +/- 0.06%) of the total administered beta-C was taken up by the intestine after a 4-h perfusion. Of the radioactivity taken up, 68.6 +/- 6.5% remained in the intestinal mucosa, 3.2 +/- 0.2% was recovered in the lymph, and 28.2 +/- 6.5% (calculated) was absorbed via the portal system. The total uptake/absorption of beta-C was 12.9 +/- 6.8 nmol.h-1.30 cm intestine-1. Large amounts of unchanged beta-C and relatively small amounts of both beta-apo-12'-carotenal and beta-apo-10'-carotenal were isolated in the intestinal mucosa after a 4-h perfusion with beta-C. Considerable amounts of metabolites more polar than retinol were formed and comprised 35% of the total radioactivity recovered in the intestinal mucosa. Polar metabolites were absorbed mostly into the portal venous system, whereas retinol and retinyl esters were absorbed mainly into the mesenteric lymph. Of the total absorbed radioactivity in lymph, 10 +/- 1.0% appeared as unchanged beta-C, with peak absorption occurring at 3 h after beginning the perfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗
PubMed1992

Eosinophilic gastroenteritis with Splendore-Hoeppli material in the ferret (Mustela putorius furo).

Eosinophilic gastroenteritis, focal or diffuse with eosinophilic infiltrations of the stomach or intestine, has been described in human beings, cats, dogs, and horses. In this paper, we describe infiltration of the gastrointestinal tract with eosinophils accompanied by a circulating eosinophilia in six ferrets (Mustela putorius furo). Clinical signs included chronic weight loss, anorexia, and diarrhea. The small intestines from five ferrets had diffuse infiltrates of eosinophils. This resulted in focal or multifocal loss of the muscular tunic in three ferrets. Two of these ferrets also had eosinophilic gastritis. Eosinophilic granulomas with Splendore-Hoeppli material were present in mesenteric lymph nodes in four ferrets. Two ferrets had multiple organ involvement; one had eosinophilic granulomas in the liver, mesentery, and choroid plexus as well as moderate parapancreatic segmental arteritis with infiltration of eosinophils and mural thrombosis. The second ferret had, in addition to moderate diffuse gastric and small intestinal eosinophilic mucosal infiltrations, interstitial eosinophilic pulmonary infiltrates. Examination of all tissues failed to reveal an infectious agent.

Animals↗
PubMed1992

Role of Helicobacter felis in chronic canine gastritis.

Five gnotobiotic Beagle dogs were orally inoculated with a pure culture of Helicobacter felis. The remaining two littermates served as contact controls. Thirty days after infection, all animals were euthanatized and specimens were collected for evaluation. In infected dogs, H. felis was recovered from all areas of the stomach. Colonization was heaviest in the fundus and antrum. H. felis was not cultured from any segment of the gastrointestinal tract distal to the duodenum. Two weeks after infection, all five infected dogs had detectable IgM and IgG serum antibody to H. felis, whereas control dogs had no measurable H. felis serum antibody throughout the study. Histopathologic changes in the stomachs of infected dogs included large numbers of lymphoid nodules throughout all regions of the gastric mucosa and were most numerous in the fundus and body. A mild, diffuse lymphocytic infiltrate with small numbers of plasma cells and eosinophils was also present in the subglandular region of all portions of the gastric mucosa. Electron microscopic examination revealed large numbers of spiral-shaped H. felis in gastric mucus adjacent to or superimposed over the areas of inflammation. Occasionally, however, H. felis was observed within the canaliculi of gastric parietal cells. Histopathologic changes in the stomachs of the contact control dogs were limited to focal infiltrates of eosinophils and small aggregates of lymphocytes in the subglandular portions of the gastric mucosa in one animal. Infection with H. felis is a likely cause of naturally occurring lymphofollicular gastritis.

Animals↗
PubMed1992

High prevalence and persistence of cytotoxin-positive Helicobacter pylori strains in a population with high prevalence of atrophic gastritis.

Helicobacter pylori is strongly associated with both chronic gastritis and duodenal ulcer. Certain strains of H. pylori produce a vacuolating cytotoxin in vitro. At New Orleans Charity Hospital, concentrated culture supernatants from 119 of 144 (83%) H. pylori strains isolated from 86 patients at high risk of developing gastric cancer, caused vacuolization in HeLa S3 cells. Cytotoxin activity was neutralized by acid (pH 4) and basic (pH 10) solutions and proteases, and was precipitable by (NH4)2SO4, which suggests that the cytotoxin is a protein. In 66 of 86 (76.7%) patients, the H. pylori strains isolated from single or multiple sequential gastric biopsies had a vacuolating cytotoxin. These cytotoxin-positive H. pylori strains were isolated from 69% of patients with diffuse antral gastritis and 89% of patients with chronic atrophic gastritis. The latter lesion is considered a precursor of gastric cancer. The cytotoxicity persisted in sequential biopsies over an interval of several months, indicating persistence of these strains in the gastric mucosa. Fifty-eight percent (7/12) of the sera from cytotoxin-positive H. pylori-infected patients neutralized cytotoxin activity, whereas 20% (1/5) of sera from patients with H. pylori cytotoxin-negative strains and none of five H. pylori-negative patients' sera neutralized cytotoxin activity. The relevance of this cytotoxin in the pathogenesis of H. pylori-induced gastritis requires further study.

Adult↗
PubMed1991

Successful use of cisplatin to treat metastatic seminoma during cisplatin-induced acute renal failure.

A chemotherapeutic regimen including cisplatin was administered to a man with extragonadal seminoma and cisplatin-induced acute renal failure. Three doses of cisplatin (30, 50, and 100 mg/m2) were given in conjunction with hemodialysis. Pharmacokinetic data for free and total plasma platinum were obtained. The patient also received one dose of carboplatin and a course of radiation therapy. Complete remission was achieved, and useful renal function returned. Cisplatin can be used successfully during acute renal failure.

Acute Kidney Injury↗
PubMed1991

Enzymatic conversion of beta-carotene into beta-apo-carotenals and retinoids by human, monkey, ferret, and rat tissues.

Whether the conversion of beta-carotene into retinoids involves an enzymatic excentric cleavage mechanism was examined in vitro with homogenates prepared from human, monkey, ferret, and rat tissue. Using high-performance liquid chromatography, significant amounts of beta-apo-12'-, -10'-, and -8'-carotenals, retinal, and retinoic acid were found after incubation of intestinal homogenates of the four different species with beta-carotene in the presence of NAD+ and dithiothreitol. No beta-apo-carotenals or retinoids were detected in control incubations done without tissue homogenates. The production of beta-apo-carotenals was linear for 30 min and up to tissue protein concentrations of 1.5 mg/ml. The rate of formation of beta-apo-carotenals from 2 microM beta-carotene was about 7- to 14-fold higher than the rate of retinoid formation in intestinal homogenates, and the rate of beta-apo-carotenal production was fivefold greater in primate intestine vs rat or ferret intestine (P less than 0.05). The amounts of beta-apo-carotenals and retinoids formed were markedly reduced when NAD+ was replaced by NADH, or when dithiothreitol and cofactors were deleted from the incubation mixture. Both beta-apo-carotenal and retinoid production from beta-carotene were inhibited completely by adding disulfiram, an inhibitor of sulfhydryl-containing enzymes. Incubation of beta-carotene with liver, kidney, lung, and fat homogenates from each species also resulted in the appearance of beta-apo-carotenals and retinoids. The identification of three unknown compounds which might be excentric cleavage products is ongoing. These data support the existence of an excentric cleavage mechanism for beta-carotene conversion.

Animals↗
PubMed1991

Management of duodenal injuries by proximal T-tube drainage.

Duodenal injuries may be caused by blunt or penetrating trauma. There is a high mortality rate with this type of injury, particularly when associated with pancreatic trauma. The surgical management of such injuries is difficult and a technique is described which may reduce postoperative morbidity, as illustrated by the two cases described.

Accidents, Traffic↗
PubMed1991

Transmission of Helicobacter spp. A challenge to the dogma of faecal-oral spread.

Faecal oral spread is claimed by many to be the mode of transmission of the gastric pathogen Helicobacter pylori. This idea is based not on experimental data but because the epidemiology of H. pylori infection resembles that of other pathogens known to be spread by the faecal-oral route. This is in spite of the observation that no-one has been successful in culturing H. pylori from human stool. In this study, a series of transmission experiments are reported on animals infected with the gastric spirilla, Helicobacter felis and 'Gastrospirillum hominis'. Germfree mice and rats infected with H. felis did not transmit their infection to uninoculated mice despite prolonged contact in the same cage nor could the bacterium be isolated from their intestinal contents. This was confirmed in specific pathogen free mice where infected dams did not pass the helicobacter to their progeny. Similarly, mice infected with a human isolate of 'Gastrospirillum hominis' did not transmit the infection while in close contact with uninoculated mice. In contrast, in a limited series of experiments, both H. pylori and H. felis were transmitted from infected gnotobiotic Beagle puppies to uninfected animals in the same enclosure. In addition, the gastric mucus from a cat with indigenous 'Gastrospirillum'-like organisms was infectious for mice, whereas faecal content from the same animal was not. It is suggested that the difference between the murine and canine experiments is that the dogs are more likely to have oral-oral contact than rodents. Unlike dogs, mice and rats do not vomit and are coprophagous. It is concluded that the case for faecal-oral spread of Helicobacter species is 'not proven' and that the inter-oral route is more likely.

Animals↗
PubMed1991

Phylogeny of Helicobacter felis sp. nov., Helicobacter mustelae, and related bacteria.

Strain CS1T (T = type strain) is a gram-negative, microaerophilic, urease-positive, spiral-shaped bacterium that was isolated from the gastric mucosa of a cat. Additional strains which possessed biochemical and ultrastructural characteristics similar to those of strain CS1T were isolated from the gastric mucosa of cats and dogs. The guanine-plus-cytosine content of the DNA of strain CS1T was 42.5 mol%. The 16S rRNA sequences of strain CS1T, strain DS3 (a spiral-shaped isolate from a dog), and Helicobacter mustelae were determined by direct RNA sequencing, using a modified Sanger method. These sequences were compared with the 16S rRNA sequences of Helicobacter pylori, "Flexispira rappini," Wolinella succinogenes, and 11 species of campylobacters. A dendrogram was constructed based upon sequence similarities. Strains CS1T and DS3 were very closely related (level of similarity, 99.3%). Two major phylogenetic groups were formed; one group consisted of strains CS1T and DS3, H. mustelae, H. pylori, "F. rappini," and W. succinogenes, and the other group contained the true campylobacters. The average level of similarity between members of these two groups was 84.9%. Within the first group, strains CS1T and DS3, H. pylori, and H. mustelae formed a cluster of organisms with an interspecies similarity level of 94.5%. The phylogenetic positions of W. succinogenes and "F. rappini" were just outside this cluster. On the basis of the results of this study, we believe that strains CS1T (= ATCC 49179T) and DS3 represent a new species of the genus Helicobacter, for which we propose the name Helicobacter felis.

Animals↗
PubMed1991

Inhibition of acid secretion from parietal cells by non-human-infecting Helicobacter species: a factor in colonization of gastric mucosa?

Helicobacter pylori has been shown to produce a protein that inhibits acid secretion from parietal cells. We have examined other non-human-infecting Helicobacter species for this property by measuring the uptake of [14C]aminopyrine into rabbit parietal cells as an indirect assessment of acid secretion. Helicobacter felis and an isolate from a rhesus monkey were shown to inhibit acid secretion. Isolates of Helicobacter mustelae gave variable responses. Whole bacteria and cell-free sonicates impaired the uptake of [14C]aminopyrine. We also tested other bacteria, including Escherichia coli, Proteus vulgaris, Klebsiella oxytoca, and Campylobacter jejuni. As whole organisms, these control bacteria had little effect on acid secretion, but sonicates caused pronounced inhibition that was partially heat labile. Pronase treatment of H. pylori destroyed its inhibitory effect. These results suggest that most Helicobacter species, but not all isolates, are able to inhibit acid secretion from rabbit parietal cells. This property may be a factor in the establishment of long-term infection by these species.

Aminopyrine↗
PubMed1991

Helicobacter felis gastritis in gnotobiotic rats: an animal model of Helicobacter pylori gastritis.

The gastric spirillum Helicobacter felis, originally isolated from the cat stomach, colonizes the stomachs of germfree rats. Studies were designed to examine the pathological and serological responses of germfree rats inoculated orally with H. felis. At 2 weeks postinoculation, the gastric mucosa of germfree rats had lymphocytes and eosinophils scattered in small foci throughout the subglandular region of the antrum. Small numbers of lymphocytes were present in the subglandular portion of the antral mucosa that focally extended through the lamina propria towards the luminal surface. Eight weeks postinoculation, the inflammation was confined to the antrum. It was characterized by increased numbers of lymphocytes and eosinophils in the subglandular areas, with focal aggregates of lymphocytes in the submucosa. Some lymphoid aggregates extended from the submucosa through the muscularis mucosa and lamina propria to the luminal surface. H. felis was demonstrated with the Warthin-Starry stain, bacterial culture, and urease assay, particularly in the antrum. H. felis also produced a significant immunoglobulin G antibody titer at 2, 4, and 8 weeks postinoculation as well as a transitory immunoglobulin M response at 2 to 4 weeks postinoculation. Contact control rats were not infected, inferring that fecal-oral spread of H. felis did not occur.

Animals↗
PubMed1991

Helicobacter mustelae-induced gastritis and elevated gastric pH in the ferret (Mustela putorius furo).

Helicobacter mustelae has been cultured from the stomachs of ferrets with chronic gastritis; the lesions in the stomach have many of the same histological features seen in H. pylori gastritis in humans. To determine whether H. mustelae-negative ferrets with normal gastric mucosa were susceptible to colonization and whether gastritis developed after infection, four H. mustelae-negative ferrets treated with cimetidine were inoculated orally on two successive days with 3 ml (1.5 x 10(8) CFU) of H. mustelae; eight age-matched H. mustelae-negative ferrets served as controls. All four ferrets became colonized; H. mustelae persisted through week 24 of the study, as determined by positive gastric culture, tissue urease, and Warthin-Starry staining of gastric tissue. Superficial gastritis developed in the oxyntic gastric mucosa, and a full-thickness gastritis, composed primarily of lymphocytes and plasma cells plus small numbers of neutrophils and eosinophils, was present in the antrum. The inflammation was accompanied by an elevation of immunoglobulin G antibody to H. mustelae. At 4 weeks post-inoculation, the four infected (experimental) ferrets developed an elevated gastric pH (4.0 to 5.2) for 2 weeks. The eight control ferrets did not have gastritis; H. mustelae could not be demonstrated in gastric tissue via culture, nor was there an immune response to the bacteria. In ferrets, H. mustelae readily colonizes the stomach and produces a gastritis, a significant immune response, and, like H. pylori infection in humans, a transient elevated gastric pH after Helicobacter infection.

Animals↗