The aim of this study was to describe our experience in the management of bladder injuries occurring at intervesicovaginal dissection during the tension-free vaginal mesh (TVM) procedure. Seven hundred four patients were treated for prolapse by vaginal route using the TVM procedure. Bladder injury was diagnosed during the procedure in five patients. Polypropylene mesh was placed in the intervesicovaginal space after a careful repair of the bladder injury. Major postoperative complications were not diagnosed during the short-term follow up. We describe the occurrence and treatment of bladder injuries during the dissection phase in the TVM procedure. Such injuries can occur during the dissection. Placing an intervesicovaginal mesh is acceptable if cautious bladder repair is performed.
Formation and loss of methylated purines in DNA of various fetal and maternal tissues were measured up to 7 days following intravenous administration of N-[14C]methyl-N-nitrosourea to rats on the 21st day of gestation. Methylation products were detected in all tissues examined, the level in maternal liver being higher than in other tissues. The concentrations of 7-methylguanine and 3-methyladenine decreased faster in fetal than in corresponding maternal tissues, due to a higher rate of DNA synthesis in fetal tissues, as determined by incorporation of labelled thymidine. Removal of the promutagenic DNA lesion O6-methylguanine was most efficient in maternal and fetal liver; but it was very poorly repaired in kidney and brain. The persistence of O6-methylguanine relative to 7-methylguanine was highest in the DNA of fetal brain. The principal targets for the transplacental carcinogenic effect of N-methyl-N-nitrosourea under these experimental conditions were fetal neurogenic tissue and kidney; and malignant tumors developed at these sites in 31-34% and 15-16% of male and female descendants, respectively. These results support the concept that a complex interaction between DNA alkylation, repair and replication is the molecular basis of initiation of carcinogenesis by alkylating agents.
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