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Biomedical subjects

J Rhodes

Publications and source records attributed to J Rhodes.

At least 253 records · Page 14Linked to original sources

Effect of compound 48/80 on canine gastric mucosa.

The effect of compound 48/80 on the mucosal barrier of the canine Heidenhain pouch and mast cell content of gastric mucosa has been studied. 48/80 was administered in increasing doses (0.5--2.0 mg/kg) over 5 days. 0.5 mg/kg produced signs of systemic histamine release and stimulation of acid secretion by the pouch; these effects being most marked on the 1st day and absent on the 5th. Subsequent exposure of the mucosa to sodium taurocholate produced damage to the barrier similar to that in untreated animals. Histological examination revealed no evidence of mucosal mast cell degranulation by 48/80. The results suggest that the effects of 48/80 on gastric mucosa are mediated by systemic release of histamine and that local mast cells are resistant to its action.

Animals↗

The role of histamine in changes which occur in the gastric mucosal barrier with bile damage.

H1 and H2 histamine receptor antagonists were used in dogs with Heidenhain pouches during experiments in which the mucosa was damaged with sodium taurocholate. In these experiments when both antagonists were used together the usual increase in hydrogen and sodium ion flux across the mucosa was not observed, but the usual fall in transmucosal potential difference occurred. The results suggest that mucosal histamine probably mediates the changes in ionic flux across gastric mucosa which follow exposure to bile. Attempts to establish the source of this histamine were made in both rats and dogs using compound 48/80 over a period to degranulate the mast cells. Treatment with this compound did not affect the change in ionic fluxes which followed exposure to bile acid, suggesting that the source of histamine mediating changes in ionic flux is probably from tissue sites other than mast cells.

Animals↗

Human macrophage function in cancer: systemic and local changes detected by an assay for Fc receptor expression.

The activity of human peripheral blood monocytes and pulmonary alveolar macrophages was examined with a rosette assay that detects changes in Fc receptor expression. Compared with peripheral blood monocytes from normal subjects, the peripheral blood monocytes of patients with carcinoma of the lung were found to be activated in this respect. In contrast, compared with pulmonary alveolar macrophages from normal subjects, carcinomas exhibited depressed function in terms of receptor alveolar macrophages from lungs bearing primary expression. Trypsinization of macrophages to remove bound immunoglobulin indicated that this depression of receptor activity was not due to blocking of receptors by immunoglobulin or immune complexes. In an in vitro study the expression of Fc receptors by cultured macrophages was shown to be depressed by a heat-stable, low-molecular-weight material in supernatants of cultured carcinoma tissue from the lung, breast, and urinary bladder.

Humans↗

The clinical significance of bile reflux.

Although bile reflux into the stomach has been a subject of major interest during the last 15 years, its role in gastric pathology is not fully understood. The simple technique of sampling gastric contents and measuring bile acids is probably the most useful and reliable method available. Whether the reflux always precedes ulceration or is caused in some way by the gastritis remains unresolved, for bile reflux is common in many clinical situations where gastritis is present. After gastric surgery bile has been blamed for the gastritis which occurs as well as symptoms of post prandial epigastric discomfort, heartburn and bile vomiting. This is probably the only clinical situation where further procedures have been examined which specifically divert bile away from the stomach with good results. Bile reflux is also very common in patients with heartburn suggesting that bile and acid are both necessary to produce oesophagitis and heartburn. This is borne out by clinical observations and experimental work in animals. With the exception of those patients who have had gastric surgery, we have little or no evidence of the consequences of bile exclusion from the stomach in other pathological situations.

Bile Acids and Salts↗

Inhibition of human monocyte Fc receptor and HLA-DR antigen expression by pregnancy alpha-2 glycoprotein.

The precise factor responsible for the altered immunological reactivity and diminished inflammatory responses occurring in pregnancy is unknown. Recent observations implicate the pregnancy-associated alpha-2 glycoprotein (PAG). Using rosette assays for the detection of cells carrying Fc receptors and for the demonstration of surface HLA-DR antigens, we demonstrate that a serum protein fraction rich in PAG inhibits these surface markers on human monocytes. Brief exposure of normal peripheral blood monocytes to physiological concentrations of PAG led to almost total loss of Fc receptor expression, an effect that was concentration-related. Using a monoclonal anti-HLA-DR antibody linked to red cells, physiological concentrations of PAG also significantly inhibited the detection of HLA-DR on monocytes. As controls, we used a protein fraction isolated in identical fashion from male sera devoid of PAG, and an alpha-2 macroglobulin isolate. These findings suggest that PAG, by masking monocyte surface markers, could be responsible for the suppression of some cell functions during pregnancy.

HLA-DR Antigens↗

Cysteine transport and sulfite reductase activity in a germination-defective mutant of Histoplasma capsulatum.

A mutant of the dimorphic, zoopathogenic fungus Histoplasma capsulatum, defective in the ability of its blastospores to germinate, was used to show that the nutritional requirement for cysteine and the expression of sulfite reductase activity are temperature dependent and not related to the growth form the fungus, whereas the kinetics of cysteine transport depend on both temperature and the form of the fungus.

Biological Transport↗

Agglutinins to bacteria in Crohn's disease.

Sera from patients with Crohn's disease were tested for antibodies against organisms which are thought to cause inflammatory bowel disease in animals, or have been implicated in human Crohn's disease. Control sera were collected from healthy individuals and patients with ulcerative colitis. Sera from Crohn's disease and controls failed to agglutinate Clostridium colinum or Campylobacter sputorum subsp. mucosalis and two strains of Mycobacterium paratuberculosis (M26 and M27). Most of the sera agglutinated a Citrobacter freundii variant, Mycobacterium paratuberculosis (M28) and Mycobacterium avium (M41) but Crohn's disease sera did not differ from controls. A complement fixation test against Chlamydia gave more positive reactions in patients with Crohn's disease and colitis than in healthy controls. There was a clear difference between the sera from patients with Crohn's disease and other sera, including ulcerative colitis, in agglutination tests with the commensal coccoid rods of the genera Eubacterium and Peptostreptococcus; in these tests 54% of sera from Crohn's disease were positive compared with 11% in ulcerative colitis and none of the sera from healthy controls. All the results were essentially negative with the exception of those from Eubacterium and Peptostreptococcus and these bacteria merit investigation.

Agglutination Tests↗

Crohn's disease in Wales, 1967-1976; an epidemiological survey based on hospital admissions.

One thousand and ninety-eight patients from Wales were treated in hospital for Crohn's disease between 1967 and 1976, which gave an overall 'period prevalence' for the disease of 40 cases/10(5) of the total population. The data were analysed for each of the 8 counties and for rural as well as urban populations of different sizes. The disease was significantly more common in the urban counties of Gwent and the 3 parts of Glamorgan compared with the remainder of Wales. The highest prevalence was in South Glamorgan (54 cases/10(5)) and the lowest in Dyfed (30/10(5)). There was a relatively small but highly significant difference in the prevalence for urban populations larger than 10 000 (47/10(5)) compared with smaller communities which were chiefly rural (34/10(5)).

Crohn Disease↗

Consumption of refined carbohydrate by patients with Crohn's disease in Tel-Aviv-Yafo.

In 27 patients with Crohn's disease living in Israel the current intake of refined carbohydrate (total sugars) and added sugar is significantly greater than in healthy controls. The dietary survey was retrospective and showed that patients with Crohn's disease ate 269 g of monosaccharides and disaccharides each day compared with 192 g by matched controls. Similar differences were also found at the onset of the symptoms, 314 g compared with 207 g. These findings were independent of the country of origin or cultural grouping. Several factors are discussed which suggest a secondary rather than causal relationship between sugar consumption and Crohn's disease.

Crohn Disease↗

Achalasia in the city of Cardiff from 1926 to 1977.

A retrospective study of 48 patients, living in the City of Cardiff, diagnosed as having achalasia between 1926 and 1977, was undertaken. The incidence of achalasia was 0.4/10(5)/year. One previous study in Rochester, Minn., of 11 patients had a comparable incidence of 0.6/10(5)/year. Our study failed to identify any aetiological factors.

Adolescent↗

Increased sugar consumption in Crohn's disease.

120 patients with Crohn's disease, 100 with ulcerative colitis and controls matched for age and sex were interviewed by questionnaire. Questions related to current and past sugar and milk intake and consumption of some breakfast cereals. Patients with Crohn's disease ate significantly more sugar than either controls or patients with ulcerative colitis at the time of interview. Their use of sugar had changed little since the onset of symptoms.

Adult↗

Mortality in Crohn's disease.

Two hundred and nineteen Cardiff residents were identified with Crohn's disease between 1934 and 1976, during which period 40 of them died. Young patients diagnosed under the age of 20 years had a significantly raised standardized mortality rate (SMR) which was 11. The risk of death was particularly high during the first two and a half years after diagnosis and again after the disease had been present for more than about 13 years. Case fatality has not diminished during the last 40 years despite changes in treatment.

Adolescent↗