No abstract

The aim of the study was to carry out an audit of 283 hysterectomies performed for menstrual disorders over a one year period, and to determine the satisfaction of the women concerned towards their treatment. The medical records of these patients were examined, and they were each sent a questionnaire, 69% of which were completed and returned. The most common presenting symptoms were menorrhagia and dysmenorrhoea. In 53% of cases no clinical abnormality was postulated and in 31% of cases no pathological abnormality was found. The preoperative clinical and pathological diagnoses were in agreement for 59% of patients. Over 90% of women were satisfied with the management of their case by their GP and the gynaecology outpatient clinic. The use of patient-controlled analgesia systems was associated with better post-operative pain relief than intramuscular injections. Thirteen percent of patients required blood transfusion; 21% suffered some form of postoperative complication, most of which were minor. Ninety-four percent of the women were pleased that they had undergone hysterectomy, and 76% wished that they had had the operation sooner. It was concluded that hysterectomy is perceived positively by patients and should not necessarily be considered as a last resort treatment for menstrual disorders.

DNA ligase I is the key ligase for DNA replication in mammalian cells and has also been reported to be involved in a number of recombination and repair processes. Our previous finding that Lig1 knockout mouse embryos developed normally to mid-term before succumbing to a specific haematopoietic defect was difficult to reconcile with a report that DNA ligase I is essential for the viability of cultured mammalian cells. To address this issue, we generated a second Lig1 targeted allele and found that the phenotypes of our two Lig1 mutant mouse lines are identical. Widely different levels of Lig1 fusion transcripts were detected from the two targeted alleles, but we could not detect any DNA ligase I protein, and we believe both are effective Lig1 null alleles. Using foetal liver cells to repopulate the haematopoietic system of lethally irradiated adult mice, we demonstrate that the haematopoietic defect in DNA-ligase-I-deficient embryos is a quantitative deficiency relating to reduced proliferation rather than a qualitative block in any haematopoietic lineage. DNA ligase I null fibroblasts from Lig1 mutant embryos showed an accumulation of DNA replication intermediates and increased genome instability. In the absence of a demonstrable deficiency in DNA repair we postulate that, unusually, genome instability may result directly from the DNA replication defect. Lig1null mouse cells performed better in the survival and replication assays than a human LIG1 point mutant, and we suggest that the complete absence of DNA ligase I may make it easier for another ligase to compensate for DNA ligase I deficiency.