The large plasmid-encoded outer membrane protein VirG (IcsA) of Shigella flexneri is essential for bacterial spreading by eliciting polar deposition of filamentous actin (F-actin) in the cytoplasm of epithelial cells. Recent studies have indicated that VirG is located at one pole on the surface of the bacterium and secreted into the culture supernatant and that in host cells it is localized along the length of the F-actin tail. The roles of these VirG phenotypes in bacterial spreading still remain to be elucidated. In this study, we examined the surfaceexposed portion of the VirG protein by limited trypsin digestion of S. flexneri YSH6000 and determined the sites for VirG processing during secretion into the culture supernatant. Our results indicated that the 85-kDa amino-terminal portion of VirG is located on the external side of the outer membrane, while the 37-kDa carboxy-terminal portion is embedded in it. The VirG cleavage required for release of the 85-kDa protein into the culture supernatant occurred at the Arg-Arg bond at positions 758 to 759. VirG-specific cleavage was observed in Shigella species and enteroinvasive Escherichia coli, which requires an as yet unidentified protease activity governed by the virB gene on the large plasmid. To investigate whether the VirG-specific cleavage occurring in extracellular and intracellular bacteria is essential for VirG function in bacterial spreading, the Arg-Arg cleavage site was modified to an Arg-Asp or Asp-Asp bond. The virG mutants thus constructed were capable of unipolar deposition of VirG on the bacterial surface but were unable to cleave VirG under in vitro or in vivo conditions. However, these mutants were still capable of eliciting aggregation of F-actin at one pole, spreading into adjacent cells, and giving rise to a positive Serény test. Therefore, the ability to cleave and secrete VirG in Shigella species is not a prerequisite for intracellular spreading.

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Clinical and histologic details of the two siblings with type 1a glycogen storage disease (GSD-1a) who developed hepatoblastoma are presented. The light microscopic studies on hepatic tumor in both siblings revealed fetal type of hepatoblastoma. Ultrastructural findings in Patient 2 showed markedly altered mitochondria, which were frequently surrounded by the rough endoplasmic reticulum. This is the first known occurrence with this association, and the third report on the familial occurrence of this neoplasm. Glycogen storage disease may increase the risk of hepatocellular carcinoma and hepatoblastoma.

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Morbidity, survival, and recurrence in 203 patients treated with curative low anterior resection (LAR) were compared with those in 100 patients treated with curative abdominoperineal resection (APR). The overall 5-year survival figures for the total number of, LAR and APR patients were 75.6 +/- 5.7%, 79.8 +/- 6.4% and 67.7 +/- 9.6%, respectively. The prognosis for cancers situated low enough in the rectum to involve the anal canal was poor even when managed by APR, as evidenced by a low survival at 5 years of 59.0 +/- 9.6% and a high pelvic recurrence rate of 34%. For all except these tumors, LAR proved at least equal to, or better than APR as a curative surgical method for middle and low rectal cancers, on the basis of 5-year survival being 79.8 +/- 6.4% vs 78.7 +/- 5.2%, operative mortality being 1.5% vs 1.0%, morbidity being 39.4% vs 59.0%, and the incidence of pelvic recurrence being 8.9% vs 13.5%. When deciding upon the most appropriate surgical procedure for rectal cancer, especially for middle or low rectal lesions, the patient should not simply be condemned to a permanent colostomy. Thus, we first attempt LAR for every lesion except those which are very advanced or those with anal canal involvement, if technically feasible and suitable for the individual patient.