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(A) Predicted secondary structure of mRNA at the vemP-secD2 VA intergenic region. The RNA sequence from the fifth last codon of vemP to the third codon of secD2 VA are shown with the secondary structure predicted by CentroidHomfold. The putative SD sequence and the start codon of secD2 VA are indicated by box and underline, respectively. The P site and the A site of the VemP-stalled ribosome (Fig. 4C) are shown schematically. To separate the VemP arrest point and the secondary structure-forming region, we inserted one or two copies of the 18 nucleotides encoding the last five amino acid residues of VemP followed by the termination codon, shown at the bottom. (B) Separation of the arrest point and the stem-loop-forming region impairs the regulation. E. coli cells carrying indicated vemP-secDF2 VA plasmids (with or without the insertion mutations shown in A) were induced with IPTG for 15 min at 37°C and treated with (+) or without (−) 3 mM NaN 3 for 5 min. Cells were then pulse-labeled for 1 min. Cell extracts of equivalent radioactivities were subjected to anti-VemP (upper gel) and anti-V. SecD2 (lower gel) immunoprecipitation. In the upper gel, "p" indicates the signal peptide unprocessed form of VemP, which included the polypeptide part of the elongation arrested VemP, whereas "m" indicates the signal peptide-processed mature form. Relative intensities of V.SecD2 are shown in the bottom graph, taking the value of lane 1 as unity (n = 3). Gray and black bars represent results obtained without and with NaN 3 treatment, respectively. (C) The insertion mutations do not affect translation arrest of VemP. E. coli cells carrying pBAD24-Δss-vemP-V.secDF2 with or without the insertion mutations were induced with 0.02% arabinose for 1 h at 37°C. The same amounts of proteins were separated by 10% wide-range gel electrophoresis, followed by immunodetection of VemP. (D) The secD2 VA -secF2 VA interval. The nucleotide sequence from the fourth last codon of secD2 VA to the fifth codon of secF2 VA is shown. The predicted SD sequence of secF2 VA is underlined.

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To elucidate the antibacterial activity of Gosyuyu, the crude extract from the fruit of Evodia rutaecarpa, a Chinese herbal medicine, has been fractionated chromatographically, and each fraction was assayed for antibacterial activity against Helicobacter pylori (H. pylori) in vitro. As the result, a single spot having marked antibacterial activity against H. pylori was obtained and the chemical structure was analyzed. The isolated compound was revealed to be a novel alkyl quinolone alkaloid based on the solubility, IR spectra, NMR analysis and mass spectrometric data after purification by TLC of silica. We compared the antimicrobial activity of this compound with that of other antimicrobial agents and examined susceptibility of various intestinal pathogens. As the result, the new quinolone compounds obtained from Gosyuyu extracts were found to be a mixture of two quinolone alkaloids, 1‐methyl‐2‐[(Z)‐8‐tridecenyl]‐4‐(1H)‐quinolone and 1‐methyl‐2‐[(Z)‐7‐tridecenyl]‐4‐(1H)‐quinolone (MW: 339), reported previously. The minimum inhibitory concentration (MIC) of these compounds against reference strains and clinically isolated H. pylori strains were less than 0.05 μg/ml, which was similar to the MIC of amoxicillin and clarithromycin that are used worldwide for the eradication of H. pylori, clinically. Furthermore, it was noted that the antimicrobial activity of these compounds was highly selective against H. pylori and almost non‐active against other intestinal pathogens. The above results showed that these alkyl methyl quinolone (AM quinolones) alkaloids were useful for the eradication of H. pylori without affecting other intestinal flora.

Background Little information is available on the longterm outcomes of endoscopic submucosal dissection (ESD) for early gastric cancer (EGC) in patients of advanced age (C80 years). Methods A multicenter study was conducted at 10 Japanese institutions concerning their results for ESD. Data on 440 patients of advanced age (C80 years) with EGC (470 lesions) were collected and reviewed. Early and long-term outcomes of ESD were assessed. We compared the overall survival rates between 3 patient groups, those with curative ESD, additional surgery after noncurative ESD, and nonsurgical follow-up after noncurative ESD.Results Bleeding and perforation rates were 3.2 and 2.8%, respectively. Curative ESD was achieved in 366 of the 470 lesions (77.9%). Of the 104 patients with noncurative ESD, 12 patients (11.5%) underwent additional surgery and 91 patients (87.5%) were followed without surgery. The 5-year survival rate in the patients with nonsurgical follow-up after noncurative ESD (66.7%) was significantly lower than that in the patients with curative ESD (80.3%, p = 0.0001). There was no significant -011-0067-8 difference in the 5-year survival rates between the patients with curative ESD and those with surgery after noncurative ESD (100%, p = 0.21), nor was there a difference in these rates between the patients with surgery after noncurative ESD and those with nonsurgical follow-up after noncurative ESD (p = 0.061). None of the patients developed cancer recurrence after curative ESD, and none developed cancer recurrence following the additional surgery after noncurative ESD. In the patients with curative ESD and in those with surgery after noncurative ESD, the cumulative observed survival was better than the expected survival for the general population of similar age and gender. Conclusions ESD is safe for the treatment of EGC in patients 80 years of age or older. Both curative ESD and additional surgery after noncurative ESD may contribute to the extension of life expectancy.123 Gastric Cancer (2012) 15:70-75 DOI 10.1007/s10120