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Background Rectovaginal fistula (RVF) after low anterior resection for rectal cancer is troublesome and refractory. Although various surgical procedures have been previously described, no definitive procedure has shown a satisfactory outcome. We present two consecutive Japanese patients who underwent successful surgery for an RVF after low anterior resection. Case presentation The patients were two women (61-year-old and a 64-year-old). They were admitted to our hospital with a chief complaint of fecal discharge from the vagina after low anterior resection using the double-stapling technique for rectal cancer. They were diagnosed with RVF. Local surgical procedures, including diverting ileostomy, were unsuccessful in previous hospitals. Therefore, we performed laparoscopy-assisted repair of the RVF. In both patients, laparoscopically robust pelvic adhesions were dissected, and the sigmoid colon was transected at just oral side to the RVF. Thereafter, in combination with a perineal approach, the rectum, along with a previous anastomosis and fistula, were completely removed. Surgeries were completed after vaginal repair, redo coloanal anastomosis, and interposition of the dissected connective tissue. In both patients, the postoperative courses were uneventful. They complained of neither recurrence of any RVF nor fecal incontinence 1 year and 10 months after diverting stoma closure. Conclusions A laparoscopy-assisted procedure with reanastomosis and interposition of the perineal connective tissue can be an effective treatment for RVF after low anterior resection for rectal cancer.

HEPATOCYTE growth factor/scatter factor (HGF/SF) functions as a mitogen, motogen and morphogen for a variety of cultured cells1–7. The genes for HGF/SF and its receptor (the c-met protooncogene product8) are expressed in many tissues during the embryonic periods and in the adult9–14. HGF/SF is thought to mediate a signal exchange between the mesenchyme and epithelia during mouse development15. To examine the physiological role of HGF/SF, we generated mutant mice with a targeted disruption of the HGF/SF gene. Here we report that homozygous mutant embryos have severely impaired placentas with markedly reduced numbers of labyrinthine trophoblast cells, and die before birth. The growth of trophoblast cells was stimulated by HGF/SF in vitro, and the HGF/SF activity was released by allantois in primary culture of normal but not mutant embryos. These findings suggest that HGF/SF is an essential mediator of allantoic mesenchyme-trophoblastic epithelia interaction required for placental organogenesis.

A potent vasoactive peptide, bradykinin, is liberated from two distinct kininogens designated low molecular weight (LMW) and high molecular weight (HMW) kininogens1. We have recently cloned and sequenced cDNAs for bovine LMW prekininogens and indicated that LMW prekininogens are encoded by two very similar but distinct mRNAs2. This study concerns the structural basis for the relationship between HMW and LMW prekininogen mRNAs by examination of cDNA clones for bovine HMW prekininogens and a genomic clone. Two types of cDNAs for HMW prekininogens have been identified. The deduced sequences of these two mRNAs are identical with those of two LMW prekininogen mRNAs up to the regions preceding the sequences specifying the divergent C-terminal regions of HMW and LMW kininogens, with one-to-one correspondence. In genomic DNA, the sequence precisely corresponding to the divergent 3′-terminal region of LMW prekininogen mRNA is located after 87 nucleotides downstream from the sequence specifying the 3′-untranslated region of HMW prekininogen mRNA. Based on these findings, we conclude that HMW and LMW prekininogen mRNAs are transcribed from the same gene.

The renin-angiotensin and the kallikrein-kinin systems play important physiological roles including regulation of blood pressure and inflammation reactions. Our understanding of the structures, gene organizations and regulations of the enzymes and the peptide precursors in these systems has remarkably increased during the past few years. This article summarizes recent progress in the molecular and genetic studies of renin, angiotensinogen, kallikrein, and kininogens, and discusses some new aspects explored in these areas of research.

From the complete nucleotide sequence of the genome of the avian sarcoma virus Y73, we have predicted amino acid sequence of p90 gag-yes, the product of the transforming gene. Contrary to previous evidence from molecular hybridization studies p90 gag-yes was found to have much homology with the transforming gene product p60 src of Rous sarcoma virus, suggesting that the cellular counterparts of the two (c-yes and c-src) originated from a common prototype sequence.