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Biomedical subjects

R E Barry

Publications and source records attributed to R E Barry.

At least 19 recordsLinked to original sources
PubMed1995

Non-Hodgkin's lymphoma, coeliac disease, and Epstein-Barr virus: a study of 13 cases of enteropathy-associated T- and B-cell lymphoma.

A group of 166 patients with coeliac disease was followed for a period of up to 25 years. During this time, 17 patients developed intestinal tumours that were diagnosed as lymphoma, of which 15 cases were available for review. Eleven of the lymphomas were of T-cell type (enteropathy-associated T-cell lymphoma, EATL) and two were of B-cell type. Two cases were reclassified as undifferentiated carcinoma. The interval between the diagnosis of enteropathy and the onset of lymphoma varied from less than 2 months in four patients to more than 5 years in seven. Seven of the T-cell and both B-cell lymphomas were investigated for the presence of Epstein-Barr virus (EBV) by in situ hybridization (ISH) using probes against Epstein-Barr virus-encoded RNAs (EBERs) and by immunohistochemistry with EBV-specific monoclonal antibodies. All EATL cases were negative, suggesting that EBV is not an important factor in these cases. In one of the B-cell cases, EBV was detectable by ISH and immunohistochemistry in most tumour cells in the mesenteric lymph nodes, but not in any of the tumour cells in the primary ileal tumour, indicating that in this case EBV infection was a late event in the neoplastic process. These results show that lymphoma may develop any time after the onset of coeliac disease and that in our cases of EATL, EBV was not an important factor. In some cases of EBV-related neoplasia, virus infection may be a late event.

Adult↗
PubMed1990

Prenatal laboratory screening.

Expectations of the clinician are evolving in obstetric practice in regard to standards of performance, cost effectiveness, and outcomes for mother and child. Prenatal laboratory screening is shown to be an area where new developments are evident. The purpose of this article is to update information found in standard obstetrics textbooks.

Clinical Laboratory Techniques↗
PubMed1989

Individual and group hypnotherapy in treatment of refractory irritable bowel syndrome.

33 patients with refractory irritable bowel syndrome were treated with four 40-minute sessions of hypnotherapy over 7 weeks. 20 improved, 11 of whom lost almost all their symptoms. Short-term improvement was maintained for 3 months without further formal treatment. Hypnotherapy in groups of up to 8 patients was as effective as individual therapy.

Adult↗
PubMed1987

Serum amyloid A protein compared with C-reactive protein, alpha 1-antichymotrypsin and alpha 1-acid glycoprotein as a monitor of inflammatory bowel disease.

The serum concentrations of serum amyloid A protein (SAA), C-reactive protein (CRP), alpha 1-antichymotrypsin (alpha 1-ACT) and alpha 1-acid glycoprotein (alpha 1-AGP) have been measured in eighty-six patients with Crohn's disease, twenty-five patients with ulcerative colitis and twenty-two patients with the irritable bowel syndrome. In the Crohn's and ulcerative colitis group significant increases in concentration were observed in all four proteins, which parallelled disease severity as defined by other conventional laboratory parameters formulated into a simple activity index. In the irritable bowel group no significant changes were seen. Serum amyloid A and CRP concentrations were significantly lower in ulcerative colitis than in Crohn's disease when mild, but did not differ significantly when severe. Serum amyloid A correlated well with CRP (r = 0.83) and alpha 1-ACT (r = 0.80), but less well with alpha 1-AGP (r = 0.65). Serum amyloid A was the most sensitive protein (77%) but had the lowest specificity (74%). C-reactive protein was less sensitive (58%) than SAA but had greater specificity (100%). Alpha 1-ACT had a sensitivity and specificity similar to CRP and, therefore, provided little or no additional information. Alpha 1-AGP, although also 100% specific, had the lowest sensitivity (34%) and, therefore, is probably the least useful acute phase monitor of inflammatory bowel disease. The role, and associated problems, of SAA measurements are discussed.

Adolescent↗
PubMed1987

The detection of acetaldehyde/liver plasma membrane protein adduct formed in vivo by alcohol feeding.

In order to assess whether acetaldehyde adducts with liver plasma membrane proteins are formed in vivo during alcohol ingestion, liver plasma membranes were prepared from control rats and rats fed on 10% ethanol from weaning and the amino acid constituents of liver plasma membrane proteins were assessed by reversed phase liquid chromatography of an acid hydrolysate of the membranes. The retention time of acetaldehyde/lysine adduct after stabilisation through reduction was determined by chromatography of an acid hydrolysate of polylysine pretreated with acetaldehyde. The presence of a peak with identical retention time to the acetaldehyde/lysine adduct was detected in liver plasma membranes isolated from alcohol-fed rats indicating adduct formation in vivo. The adduct was detectable only when the membranes were prepared by a rapid (Percoll) method, suggesting that the adduct may be unstable. The findings are consistent with the hypothesis that the inflammation of acute alcoholic liver disease may be initiated by the product of acetaldehyde/membrane binding in vivo.

Acetaldehyde↗
PubMed1987

Free radical generation by neutrophils: a potential mechanism of cellular injury in acute alcoholic hepatitis.

Liver membrane vesicles were prepared from operative liver biopsies from six patient volunteers undergoing abdominal surgery for non-hepatic disease. Neutrophils were extracted from their blood. The liver membrane vesicles were exposed to 1 mmol/l acetaldehyde with or without reduction of the resultant adducts formed. The production of superoxide anion by the neutrophils upon exposure to the liver membrane vesicles prepared from the same patient was assessed by measuring the rate of cytochrome c reduction before and after the addition of superoxide dismutase. Preincubation with acetaldehyde significantly increased superoxide production in response to both the reduced (from 35.5 +/- 7.1 nmol O2-/10(8) cells/min to 128 +/- 25, mean +/- SEM, p less than 0.01) and the non-reduced liver cell membranes (from 17.2 +/- 4.3 to 81 +/- 17, p less than 0.01); 1 mmol/l acetaldehyde alone caused no superoxide production. Neutrophil free radical production in response to acetaldehyde altered hepatocyte membranes could be an important mechanism of cellular injury in acute alcoholic hepatitis.

Acetaldehyde↗
PubMed1986

Superoxide anion production and degranulation of rat neutrophils in response to acetaldehyde-altered liver cell membranes.

Rat liver membrane vesicles were exposed to acetaldehyde, with or without reduction of the resultant adducts formed. Superoxide anion production and degranulation of rat neutrophils, upon stimulation with the liver membrane vesicles, were measured by cytochrome c reduction before and after the addition of superoxide dismutase, and beta-glucuronidase release respectively. Preincubation with acetaldehyde significantly enhanced superoxide anion production by both the reduced and non-reduced membrane samples (1.7-fold and 4.4-fold, respectively). Preincubation with acetaldehyde significantly enhanced degranulation (1.5-fold) of neutrophils in response to the non-reduced membranes only. The reductive process itself caused a marked increase (2.4-fold) in the ability of the membrane vesicles to stimulate degranulation. Cytochalasin B, an inhibitor of phagocytosis, did not reduce degranulation, implying that it occurred as a consequence of cell surface stimulation. Neutrophil superoxide anion production and lysosomal enzyme release in response to acetaldehyde-altered liver cell membranes could be an important mechanism of hepatocyte injury in alcoholic liver disease.

Acetaldehyde↗
PubMed1985

Acetaldehyde alone may initiate hepatocellular damage in acute alcoholic liver disease.

Acetaldehyde may be the injurious agent in acute alcoholic liver disease. It has been suggested that the mechanism of liver injury in this situation may be immunologically mediated. In the present study acetaldehyde has been bound to human liver plasma membranes. The activation of C3 by the acetaldehyde/membrane product was measured by immunofixation of the separated C3 components. Activation of C3 by acetaldehyde exposed liver plasma membranes was increased to 16.4% compared with 6% by non-exposed membranes (p = 0.004). Human liver plasma membranes bound 212 +/- 18 nmol acetaldehyde per mg membrane protein. The binding constant was 439 +/- 81 microM. It is concluded that acetaldehyde bound to human liver plasma membranes activates the complement sequence and this may be the initial stage in the pathogenesis of acute alcoholic liver disease.

Acetaldehyde↗
PubMed1985

Studies on the pharmacokinetics of fluorescein and its dilaurate ester under the conditions of the fluorescein dilaurate test.

Some aspects of the pharmacokinetics of fluorescein have been studied under the conditions of the fluorescein dilaurate test (Pancreolauryl-Test) in healthy volunteers. Dependence of fluorescein excretion on urine volume was investigated in a retrospective study in 370 patients. For intravenously administered fluorescein mean Cmax was 10.9 micrograms/ml with a mean elimination half-life of 286 min. For orally administered fluorescein sodium mean Cmax was 3.5 micrograms/ml with a tmax of 120 min and a t 1/2 of 267 min. Bioavailability of fluorescein by oral administration was 99%. By contrast, fluorescein from fluorescein dilaurate showed a 56% bioavailability under the conditions of the test with a Cmax of 1.8 micrograms/ml, a tmax of 270 min and a tt 1/2 of 246 min. Following enteral absorption of fluorescein hepatic extraction and enterohepatic circulation via the bile occurs, but although the concentrations of fluorescein in the bile may exceed those in the urine the absolute amount is likely to be small. In spite of the enterohepatic circulation fluorescein cleared from the urine within 24 h indicating that no delay between Part 1 and Part 2 of the test seems necessary. However, an adequate urine flow must be maintained throughout the test since a renal clearance/urine flow relationship exists, with fluorescein excretion being increased with increasing urine volume.

Administration, Oral↗
PubMed1984

Acetaldehyde binds to liver cell membranes without affecting membrane function.

Acetaldehyde is a major metabolic product of ethanol and is found in high concentrations in the serum during alcohol abuse. The effects of acetaldehyde on isolated rat liver cells and on purified hepatocyte plasma membrane vesicles have been studied. In concentrations of 0-10 millimolar acetaldehyde has been shown to have no detectable effect on either hepatocyte metabolism or gross membrane function and is therefore unlikely to act as a direct metabolic poison. Acetaldehyde, however, is shown to bind to hepatocyte membranes via intermediary Schiff's base formation. The adduction of acetaldehyde to liver cell plasma membranes may have an effect on membrane structure. These findings are consistent with the hypothesis that any injurious effect of acetaldehyde on the liver may be mediated via the immune system rather than being a direct effect on cell metabolism.

Acetaldehyde↗