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Biomedical subjects
Publications and source records attributed to J Beckett.
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Resistant continuous ambulatory peritoneal dialysis (CAPD) peritonitis (recurrent or persistent infection) is traditionally treated by removal of the CAPD catheter and a period off peritoneal dialysis. In a pilot study we have treated 8 patients with recurrent staphylococcal peritonitis and 3 patients with persistent staphylococcal peritonitis by stopping CAPD for a 2-week period, the CAPD catheter being left in-situ. All 8 patients with recurrent peritonitis and 2 of the 3 patients with persistent peritonitis had resolution of their infection; the third patient required catheter removal to clear the infection. There were no acute problems associated with stopping CAPD, and there was no evidence of loss of peritoneal filtration capacity on restarting CAPD. This novel approach to the treatment of resistant CAPD peritonitis should reduce the number of CAPD catheters replaced and therefore diminish the risks and inconvenience to patients that such replacements entail.
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Changes in plasma histamine levels were studied in sixteen dogs under cardiopulmonary bypass (CPB) or bypass with the addition of prostacyclin (PGI2) infusion. In both groups, plasma histamine rose immediately after anaesthetic induction (median above pre-induction: 0.4 ng/ml) and following heparin infusion (median above pre-induction: 0.7 ng/ml). During CPB, plasma histamine levels were elevated throughout the 90 minute period of perfusion (median above pre-induction: 0.5-1.2 ng/ml). PGI2 infusion reduced the elevation in plasma histamine levels (median above preinduction: 0-0.7 ng/ml). These data support the hypothesis that histamine release occurs during CPB. Platelet aggregation in the extracorporeal circuit may be contributory since prostacyclin premedication reduces histamine release.
A series of human probes with unique sequences has been isolated from a recombinant phage library constructed with DNA obtained from a human-hamster hybrid cell line. This cell line contained the X chromosome as the only human component. For 18 of these probes, a human X-chromosome origin has been confirmed and they have been regionally assigned by a combination of techniques: dosage studies utilizing DNA from human fibroblasts carrying X-chromosome duplications and deletions; the presence or absence of hybridization to digested DNA from hybrid lines carrying fragments of the X chromosome; and in situ hybridization to metaphase chromosomes. The use of dosage as a means to regionally assign probes significantly improves resolution of the X chromosome.
A family is described in which Charcot-Marie-Tooth disease is inherited as an X-linked dominant mutation (CMT2). Ten DNA marker loci on the X chromosome were used to map the disease locus by linkage analysis. The DXYS1 sequence at Xq13 was found to be linked to the CMT2 locus at an estimated distance of 6 cM (Zmax = 2.87 at theta max = 0.06). The data also suggested close linkage of the CMT2 locus to PGK1 (Zmax = 1.51 at theta max = 0) which has also been mapped to Xq13. Another DNA locus (DXS3), in the Xq21.3----Xq22 region, did not show close linkage (Zmax = -2.231 at theta max = 0.01). We conclude that the CMT2 locus is probably in or close to band Xq13.
We have tested linkage between the locus for the fragile-X [fra(X)] syndrome at Xq27.3 and five polymorphic restriction sites identified by four DNA probes mapping distal to Xq26.1. A maximum distance of approximately 15 centimorgans (cM) between Xq27.3 and the marker loci mapping to this region was predicted based on the physical chromosome length. Close linkage between the disease and marker loci was excluded for probes DXS19 and DXS37 (theta = .05, Z = -2.94 and Z = -4.17, respectively). These marker loci were estimated to be less than five cM apart but approximately 40 cM proximal to the fragile site, indicating that there is a significantly greater frequency of recombination in this region of the X chromosome than expected from the physical length. Linkage results for the other marker loci and the fra(X) syndrome were inconclusive. However, the pX45d probe locus appears very closely linked to the factor IX locus (Z = 1.94 at theta = 0) and is approximately 20 cM proximal to Xq27.3. A relative map of the polymorphic restriction sites, fra(X) syndrome locus, and factor IX locus was constructed by maximizing lod scores over the Xq26.1----q27.3 region.
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