To investigate the safety and efficacy of postoperative autologous blood transfusion (AT) using the Shiley hardshell venous reservoir, a prospective, randomised, controlled study was carried out in two matched groups of twenty patients undergoing elective coronary artery bypass surgery. The mean volume of shed mediastinal blood reinfused in the first 6 h postoperatively was 371.7 +/- 63.23 ml. Use of homologous blood was reduced from 760.5 +/- 108.37 ml in the control patients to 466.25 +/- 87.44 ml in the AT patients, a reduction of 38.7% (p less than 0.05). There was no statistically significant difference in the clinical outcome, overall blood loss, use of platelets, fresh frozen plasma and colloids, haematological indices, renal and hepatic functions, or clotting mechanism, although there was a reduction in the fibrinogen level in the patients who received AT (p less than 0.05). Mediastinal blood did not clot and was defibrinogenated. It contained significant levels of haemoglobin (8.175 +/- 0.506 g/dl), platelets (96.55 +/- 10.39 per mm3 10(3)), protein (42.5 +/- 1.13 g/l), calcium (2.385 +/- 0.054 mmol/l) and was well oxygenated (PO2 = 20.46 +/- 0.81 kPa). No patients developed bacteraemia or had any AT-related infections. We conclude that postoperative autologous transfusion using the Shiley hardshell venous reservoir is a safe and efficient method for reducing postoperative homologous blood requirement after coronary artery bypass surgery.
suMMARY During the period 1970-81, 183 patients underwent mitral valve surgery for chordal rupture. Of these, 82 (45%) patients were treated by mitral valve repair and 101 (55%) by mitral valve replacement. Mean age at surgery was 57 years. The early mortality was nine of 183 (4.9%) patients, of whom five had undergone replacement and four repair. During the follow up period (mean 3-6 years, range 0-8-12-2 years) a further 27 patients died; 23 of these had undergone mitral valve replacement and four mitral valve repair. Cerebrovascular events accounted for 35% of the deaths after mitral valve replacement and none of those after mitral valve repair. In 11 patients repair was technically unsatisfactory, and mitral valve replacement was undertaken at the same operation; a further five patients required late replacement (mean 1.4 years) for pronounced mitral regurgitation. Actuarial curves predict a six year survival of 68+5 7% (mean+ SD) for all patients after mitral valve replacement compared with 88+6*9% (mean±+SD) after repair (p<001). Actuarial survival curves favour mitral valve repair as the procedure choice for chordal rupture, and in isolated posterior cusp repair breakdown of the repair is a rare occurrence.
INTRODUCTION: Deregulation of DNA methylation occurs early in neoplastic transformation. Increased cytosine methylation leads to chromatin compaction with gene inactivation, and hypermethylated DNA in condensed chromatin may be less susceptible to mutation and translocation. Cytosine methylation sites in non‐malignant cells are highly regulated, in contrast to the regional hyper‐ and global hypomethylation frequently found in lymphoid and other neoplasms. This preliminary study assessed the methylation status of BCL6 upstream from exon 1. BCL6 encodes a transcription factor essential for normal germinal centre formation and for B cell development after antigen stimulation. It is a repressor of gene transcription but its target genes are ill‐defined. In some categories of B cell non‐Hodgkin lymphoma (B‐NHL), somatic mutation and translocation of BCL6 are frequent. METHODS: DNA was extracted from 60 lymphoproliferative disorders (LPD) comprising 24 benign LPD, 30 B‐NHL (low and high grade) and 6 T cell neoplasms. The level of BCL6 methylation was assessed by Southern hybridization: DNA was digested with HpaII and MspI (methylation sensitive and insensitive respectively), and restricted BCL6 fragments were detected with a 32P‐dCTP radiolabelled 4 kb SacI BCL6 probe that hybridized to exon 1 and 5′ flanking sequences. Following autoradiography, the size and relative density of hybridized fragments was used to assign methylation status. RESULTS: HpaII digested DNA from benign LPDs was characterised by fragments of approximately 0.9 kb, 3.6 kb, 3.9 kb, 4.6 kb and 4.9 kb, and using GenBank sequence NT5962, 3 methylated MspI restriction sites were predicted. Of 22/24 (92%) HpaII digested DNA samples from benign LPDs, the 3.6 kb, 3.9 kb, 4.6 kb and 4.9 kb fragments all had either similar density, or the latter two fragment sizes had relatively greater density. 28/30 (93%) HpaII digested DNA samples from B‐NHL had a decrease in relative density of the 4.6 kb and 4.9 kb fragments compared to the 3.6 kb and 3.9 kb fragments, and one sample had a 3.3 kb fragment. Of the 6 HpaII digested DNA samples from T cell neoplasms, 3 samples had fragments larger than 4.9 kb, 1 sample had 4.6 kb and 4.9 kb fragments having less density than the 3.6 kb and 3.9 kb fragments, and 2 samples had findings indistinguishable from benign LPD samples. CONCLUSION: This study of the methylation status of the upstream flanking region of BCL6 indicates there may be alternative deregulatory mechanisms leading to hypomethylation in the majority of B‐NHL and hypermethylation in some T cell neoplasms. Whether hypomethylation of BCL6 in B‐NHL predisposes to somatic mutation and translocation of this gene remains to be investigated.
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