Aim To assess whether Epstein–Barr virus (EBV) reactivation is triggered by persistent apical periodontitis‐related microbes using in vitro and ex vivo methodologies. Methodology Surgically removed human periapical granulomas (n = 50) and healthy gingival tissues (n = 10) were analysed to determine the presence of EBV and seven persistent apical periodontitis‐related microbes. In addition, real‐time polymerase chain reaction was used to detect the mRNA expression of BZLF‐1, an immediate–early gene of EBV. Expression of latent membrane protein (LMP)‐1 and ZEBRA, an early lytic protein of EBV encoded by BZLF‐1, was also examined using triple‐colour immunofluorescence staining. n‐Butyric acid produced by the microbes was quantified, and luciferase assays were performed in association with bacterial lysates. In addition, Daudi cells were cultured with bacterial lysates, and the expression levels of BZLF‐1 mRNA and ZEBRA protein were determined. Results EBV DNA and BZLF‐1 mRNA were detected in 47 out of 50 periapical granulomas, but not in healthy gingival tissues. The EBV DNA copy number and the number of Fusobacterium nucleatum were significantly positively correlated with BZLF‐1 expression in periapical granulomas. The number of Prevotella intermedia was slightly correlated with BZLF‐1 expression; however, the other microbes were not. CD79a‐positive B cells in periapical granulomas, but not those in healthy gingival tissues, expressed both LMP‐1 and ZEBRA. n‐Butyric acid production was the highest in F. nucleatum and the lowest in P. intermedia. Enterococcus faecalis, Candida albicans and the other tested microbes did not produce n‐butyric acid. An F. nucleatum lysate exhibited significantly increased BZLF‐1‐luciferase activity in the same manner of commercial butyric acid, whereas P. intermedia did not. F. nucleatum also induced the expression of BZLF‐1 mRNA and ZEBRA protein by Daudi cells, indicating that EBV reactivation was induced. Conclusion Among the persistent apical periodontitis‐related bacteria that were tested, F. nucleatum most strongly reactivated latent EBV, whereas E. faecalis and C. albicans as well as the other microbes did not.
ABSTRACT. A pinealoma (benign) was found in a 61-week-old male Crj:CD (SD) IGS rat. The neoplasm was located between the cerebral hemispheres and the cerebellum. Histologically, the tumor cells consisted of two cell types: large, pale-staining cells and small darkstaining cells. A fibrovascular stroma divided the tumor cells into incomplete lobules or nest structures. Relatively numerous mitoses were noted in the tumor cells. Ultrastructurally, the tumor cells contained dense-cored vesicles, approximately 120 nm in diameter.-KEY WORDS: Crj:CD (SD) IGS, pinealoma (benign), pinealoma (spontaneous).
ABSTRACT. To examine the effect on cell population in hepatocytes of phenobarbital (PB) and other barbiturates, PB, allobarbital (ALB), barbital sodium (BS) and barbituric acid (BA) were given orally to male rats for 7 consecutive days. Although there was no apparent change in non-promoting BA, hepatomegaly was induced by PB, BS and ALB, which are promoters of hepatocarcinogenesis. In PB-and BS-treated livers, hepatomegaly was attributable to hepatocyte proliferation and enzyme induction. In ALB-treated liver, it was attributable to enzyme induction. The level of cell proliferation was reduced to less than the control values following withdrawal of PB, ALB and BS. It seemed that the degree of suppression of cell proliferation following withdrawal of these compounds correlated to the degree of cell proliferation (PB>BS>ALB) during treatment. In PB-treated liver, apoptosis was induced during treatment, serving to eliminate the excess of hepatocytes. This suggests that short-term administration of PB neither induced suppression of apoptosis nor disturbed homeostasis of hepatocyte populations.-KEY WORDS: apoptosis, cell proliferation, liver, phenobarbital, rat.
Background/Aim: S100A4 expression is associated with the pathology of chronic inflammatory diseases. In this study, we investigated the role of S100A4 and four inflammatory mediators IĸB, in human periapical granulomas (PGs). Materials and Methods: S100A4 expression in PGs obtained by apicoectomy was examined by immunohistochemistry. Further, the expression of S100A4 and four inflammatory mediators was compared between PGs and healthy gingival tissues (HGTs) using real-time PCR. Results: In the PGs, S100A4 was found to be expressed in endothelial cells and fibroblasts. Furthermore, real-time PCR revealed that the expression of S100A4 and IL-1β in PGs was significantly higher than that in HGTs. Although a correlation between the expression of S100A4 and IĸB or IL-10 was not detected, a positive correlation between the expression of S100A4 and IL-1β or TNF-α was observed. Conclusion: The expression of S100A4 correlates with the pathogenesis of PGs.
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