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Biomedical subjects

J Barker

Publications and source records attributed to J Barker.

At least 181 records · Page 10Linked to original sources
PubMed1972

Characteristics of some co-trimoxazole-resistant Enterobacteriaceae from infected patients.

Two isolates of Proteus mirabilis and four of Esch. coli which would not grow on commonly used commercial sensitivity test media are reported. These organisms appear to be resistant to co-trimoxazole, are exacting towards thymidine, and five of six were isolated from patients who had been treated with co-trimoxazole. A method for the detection of these strains is given and their significance in the laboratory and clinical practice discussed.

Aged↗
PubMed1971

Bacteria, bile salts, and intestinal monosaccharide malabsorption.

Intestinal monosaccharide transport was studied in a series of rats with a self-filling jejunal blind loop using 3mM arbutin (p-hydroxyphenyl-B-glucoside) or 1mM D-fructose as substrate in vitro and 10 mM arbutin or 5mM D-fructose in vivo. These results were compared with changes in the bacterial flora and state of conjugation of intraluminal bile salts in those animals. Observations were also made of the microscopic and ultrastructural appearances of the small-intestinal epithelium. In the small intestine of blind-loop rats intestinal monosaccharide transport is impaired, and in vitro is most marked in the blind loop, less so in the efferent jejunum, and not significantly altered in the afferent jejunum. A similar pattern of disturbed monosaccharide absorption was demonstrated by perfusions in vivo. The degree of the transport defect correlates closely with the luxuriance of the anaerobic flora, which averaged 10(8) per millilitre in the blind loop, 10(7) in the efferent jejunum, and 10(6) in the afferent jejunum. A similar pattern of abnormality of bile salt conjugation occurred. In the blind loop the ratio of free to conjugated bile salts was grossly abnormal; this disturbance was somewhat less marked in the efferent jejunum and considerably less in the intraluminal contents of the afferent jejunum. An irregularly distributed lesion, consisting of swelling and vacuolation of microvilli and intracellular organelles, was demonstrated in the small-intestinal epithelium of blind-loop animals. Impaired absorption of monosaccharides is a further consequence of bacterial contamination of the upper gut. It is suggested that this defect is caused by the presence of high levels of deconjugated bile salts produced by an abnormal anaerobic bacterial flora in the small intestine.

Anaerobiosis↗
PubMedDate not supplied

Closure of colostomy--a safe procedure?

A retrospective surgery of a series of 73 patients undergoing closure of colostomy has been carried out. Closure was complicated in 37.8 per cent of cases, and fecal fistulas occurred in 17.6 per cent. The overall mortality rate of the procedure was 2.7 per cent. The underlying disease (carcinoma or diverticulitis) did not influence the complication rate. Furthermore, intraperitoneal and ex-raperitoneal methods of closure appeared equally satisfactory. Closure of colostomy within a month of construction was associated with an unacceptably high incidence of fecal fistula of 33 per cent.

Adult↗
PubMedDate not supplied

Murine mucopolysaccharidosis VIL: impact of therapies on the phenotype, clinical course, and pathology in a model of a lysosomal storage disease.

The mucopolysaccharidoses are a group of lysosomal storage diseases caused by deficiency of an enzyme required for the normal degradation of glycosaminoglycans. Patients with mucopolysaccharidosis typically have widespread lysosomal storage, skeletal and central nervous system disease, and hepatosplenomegaly. Some patients with mucopolysaccharidosis may benefit from enzyme replacement therapy or bone marrow transplantation. Animal models of mucopolysaccharidosis have proven valuable for the evaluation of the effectiveness of potential treatments for patients with lysosomal storage disease. A murine model of MPS VII (Sly syndrome) has proven particularly useful because of its well-defined genetics and its well-characterized clinical, pathologic, and biochemical alterations, which resemble those seen in patients with mucopolysaccharidosis. Correction of these alterations forms the basis for evaluation of the effectiveness of novel treatments. A wide range of therapies have been tested using this model, including enzyme replacement therapy, bone marrow, stem cell, and neural progenitor cell transplantation, and a variety of viral-mediated gene therapies. The inferences drawn from these therapeutic studies using the murine MPS VII model are likely generalizable to other lysosomal storage diseases.

Animals↗