No abstract

Cells of the human promonocytic cell line U937 were found to be sensitive to hexadeeylphosphocholine (HPC), which is a potential anticancer drug. Induction of apoptosis was found in U937 cells after treatment with HPC for 24 to 48 hr. The apoptosis in U937 cells exposed to HPC was increased significantly in the presence of interferon‐gamma (IFN‐γ). The augmentation of HPC‐induced apoptosis by IFN‐γ is repressed in cells (U937‐MP) persistently infected with mumps virus. A persistently infected cell line, U937‐MP, showed poor induction of signal transducers and activators of transcription‐1α (STAT‐1α), STAT‐2, p48 and IFN‐regulatory factor‐1 (IRF‐1), which are closely correlated with interferon‐α (IFN‐α) and IFN‐γ signaling pathways. Expression of MHC class‐I or class‐II was augmented by IFN‐α or IFN‐γ in U937 cells, but not in persistently infected cells. Therefore, it is suggested that the IFN‐γ signaling pathway plays an important role in the augmentation of HPC‐induced apoptosis. Mumps virus can suppress the IFN‐γ signaling pathway and subsequent development of apoptosis.

The cluster of genes encoding the botulinum progenitor toxin and the upstream region including p21 and p47 were divided into three different gene arrangements (class I-III). To determine the gene similarity of the type E neurotoxin (BoNT/E) complex to other types, the gene organization in the upstream region of the nontoxic-nonhemagglutinin gene (ntnh) was investigated in chromosomal DNA from Clostridium botulinum type E strain Iwanai and C. butyricum strain BL6340. The gene cluster of type E progenitor toxin (Iwanai and BL6340) was similar to those of type F and type A (from infant botulism in Japan), but not to those of types A, B, and C. Though genes for the hemagglutinin component and P21 were not discovered, genes encoding P47, NTNH, and BoNT were found in type E strain Iwanai and C. butyricum strain BL6340. However, the genes of ORF-X1 (435 bp) and ORF-X2 (partially sequenced) were present just upstream of that of P47. The orientation of these genes was in inverted direction to that of p47. The gene cluster of type E progenitor toxin (Iwanai and BL6340) is, therefore, a specific arrangement (class IV) among the genes encoding components of the BoNT complex.

The purpose of this study was to assess the ability of serious periodontosis patients to regain satisfactory biting function, using the patients' own teeth, by regeneration of the alveolar bone. Twelve serious periodontosis patients whose alveolar bone was markedly absorbed and whose teeth were quite unstable were treated with replanting of their teeth and grafting of cancellous iliac bone and gingival flaps by the clinical team, which consisted of plastic surgeons and dentists. No patients developed postoperative complications (e.g., infections), and grafted iliac bone took in all patients. The total number of replanted teeth was 65, and only 4 of them fell off (92% take rate). Three to 4 months after surgery, the replanted teeth received prosthetic treatment so that the patients could begin biting. Ten patients were monitored for 5 months or longer, and they started to eat normal food after the fifth month. Regained biting function and satisfaction of having food were almost the same as before the periodontosis became severe in these 10 patients. Regeneration of alveolar bone was confirmed in later radiographs. To date, the maximum follow-up period is 2 years and 8 months (average = 1 year and 6 months). All patients have good biting function, and there have been no findings of absorption of reconstructed alveolar bone or of the root of replanted teeth. This treatment method would be quite useful for patients with serious periodontosis.

Verotoxin type 2 (VT2) produced by enterohemorrhagic Escherichia coli (EHEC) has been shown to have high cytotoxic potency toward several human B lymphoid cell lines with and without Epstein-Barr virus (EBV). Cell death, apoptosis induced by VT2, is closely correlated with the expression of receptor molecule Gb3/CD77, recognized by the toxin, but not with the infection or presence of EBV. Pretreatment of cells with interferon-alpha (IFN-alpha) for 24 h resulted in augmentation of apoptosis by VT2. Pretreatment within 8 h, however, was not effective. It has been reported that IFN-alpha-induced apoptosis is correlated with the induction of the 2',5'-OAS/RNase L system or dsRNA-activated protein kinase (PKR) or both. We have established persistent infection in both Akata and P3HR-1 cells with mumps virus. The persistently infected cell lines, P3HR-MP2 and Akata-MP2, showed poor induction of 2',5'-OAS and PKR in response to IFN-alpha. Augmentation of VT2-induced apoptosis by IFN-alpha was not found in the cell lines P3HR-MP2 and Akata-MP2. Therefore, these findings were interpreted to indicate that augmentation of VT2-induced apoptosis by IFN-alpha may be mediated by PKR and the 2',5'-OAS/RNaseL system. It is also suggested that mumps virus can suppress apoptosis and establish persistent infection.