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Bisphenol‐A (BP‐A), a monomer of plastics used in numerous consumer products and a xenoestrogen, induces cellular transformation and aneuploidy in Syrian hamster embryo (SHE) cells. In this study, the abilities of 4 other bisphenols to induce cellular transformation and genetic effects in SHE cells were examined and compared to BP‐A. Cellular growth was inhibited by all bisphenols in a concentration‐related manner. The growth inhibitory effect of the bisphenols ranked: BP‐5 > BP‐4 > BP‐3 > BP‐2 or BP‐A. Morphological transformation of SHE cells was induced by BP‐A, BP‐3, BP‐4 and BP‐5, and the induced‐transformation frequencies were highest with BP‐4. None of the bisphenols induced gene mutations at the Na+/K+ ATPase locus or the hprt locus, or chromosomal aberrations in SHE cells. By contrast, aneuploidy induction in the near‐diploid range was exhibited by BP‐A, BP‐3, BP‐4 or BP‐5, corresponding to the transforming activity of each compound. The results indicate that BP‐A, BP‐3, BP‐4 and BP‐5 exhibit transforming activity in SHE cells, while BP‐2 does not, and that aneuploidy induction may be a causal mechanism of the transforming activity. Int. J. Cancer 86:151–154, 2000. © 2000 Wiley‐Liss, Inc.

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Biopsy specimens of the antrum and corpus were obtained from four Helicobacter pylori-infected members of a family and from the same boy (son 1) in whom the infection reappeared after simultaneous successful eradication treatment of three family members, excluding the mother. A total of 18 to 60 H. pylori isolates were obtained from each specimen and subjected to rRNA gene restriction pattern analysis. The father's isolates and the initial isolates from son 1 showed the same HindIII type, which was divided into three HaeIII subtypes. Isolates from the mother and a brother (son 2) and posttreatment isolates from son 1 showed a distinct HindIII type (with one minor subtype), which was divided into six HaeIII subtypes. All subtypes of the initial isolates from son 1 were present in the father's isolates, and all subtypes of the posttreatment isolates from son 1 were present in the mother's isolates but not in son 2's. Electron microscopic analysis of the biopsy specimens demonstrated extremely high levels of H. pylori colonization in the father's gastric mucosa. H. pylori adherence with a ruffle formation was also demonstrated. The findings suggest that son 1 was infected initially with the H. pylori strain of the father and son 2 was infected with the H. pylori strain of the mother and that after eradication therapy son 1 was reinfected with the H. pylori strain of the mother, who did not undergo eradication therapy.Helicobacter pylori colonizes the gastric mucosa via an oral route, and around 60% of individuals worldwide are infected with H. pylori (5). Children are at high risk for H. pylori infections (21, 34). H. pylori infection may persist for years or be lifelong (30,35), although spontaneous clearance is also common in childhood (15,19). H. pylori infection is closely associated with gastritis and peptic ulcers (14, 25), and it is also a bacterial risk factor for gastric cancer (16) and mucosa-associated lymphoid tissue lymphoma (2).The precise mechanisms of H. pylori transmission are not yet known. Previous investigations by Drumm et al. in 1990 (8), Malaty et al. in 1991 (18), and Oderda et al. in 1991 (27) suggested intrafamilial clustering of H. pylori infections. Molecular DNA analyses of familial strains of H. pylori were then performed by Nwokolo et al. in 1992 (26) and by Bamford et al. in 1993 (1), demonstrating intrafamilial infections due to a single H. pylori strain (or a common source of infection within the family). Now, transmission among family members is considered to constitute the main route of H. pylori infection (6).In intrafamilial H. pylori infection, the infected parents, particularly infected mothers, have been considered likely to play a key role in the transmission of H. pylori (4, 28). In contrast, in developing countries, environmental factors may be more important than intrafamilial transmission (29, 32).Those epidemiological studies, however, are not based on molecular biological analysis of H. pylori strains. In this study, we investigated the molecular basis of H. pylor...

, in marked contrast to norfloxacin. Azithromycin decreased the tumor necrosis factor alpha (TNF-␣), interleukin-1␤ (IL-1␤), and IL-6 production from Stx-treated human peripheral mononuclear cells or monocytes to a greater extent than did clarithromycin. In Stx-injected mice, azithromycin significantly suppressed Stx-induced TNF-␣, IL-1␤, and IL-6 levels in serum and improved the outcome as assessed by survival rate. In the STEC oral infection experiment using immature mice immediately after weaning (weaned immaturemouse model), all mice died within 7 days postinfection. Azithromycin administration gave the mice 100% protection from killing, while ciprofloxacin administration gave them 67% protection. The data suggest that azithromycin (at least at higher concentrations) has a strong effect on Stx production by STEC and on the Stxinduced inflammatory host response and prevents death in mice. Azithromycin may have a beneficial effect on STEC-associated disease.