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Research has been conducted on Escherichia coli prophage induction. The effects of RecE and RecT on illegitimate recombination during this induction have been investigated and the results indicate that spontaneous illegitimate recombination frequencies are enhanced by RecE and RecT proteins.

Research has been conducted on the DNA replication in UV-induced illegitimate recombination. The effect of temperature-sensitive dnaB mutations on the illegitimate recombination has been investigated and the results indicate that DNA replication is required for the UV-induced illegitimate recombination.

Research was conducted to show that illegitimate recombination is enhanced by the overexpression of the DnaB protein in Escherichia coli. The recombination enhanced by DnaB overexpression occurred between short regions of homology. A model for the initiation of illegitimate recombination in which DnaB overexpression may excessively unwind DNA at replication forks and induce double-strand breaks, causing illegitimate recombination.

DNA damage by oxidative stress is true of the causes of mutagenesis. However, whether or not DNA damage induces illegitimate recombination has not been determined. To study the effect of oxidative stress on illegitimate recombination, we examined the frequency of [Lambda]bio transducing phage in the presence of hydrogen peroxide and found that this reagent enhances illegitimate recombination. To clarify the types of illegitimate recombination, we examined the effect of mutations in mutM and related genes on the process. The frequency of [Lambda]bio transducing phage was 5- to 12-fold higher in the mutM mutant than in the wild type, while the frequency in the mutY and mutT mutants was comparable to that of the wild type. Because 7,8-dihydro-8-oxoguanine (8-oxoG) and formamido pyrimidine (Fapy) lesions can be removed from DNA by MutM protein, these lesions are thought to induce illegitimate recombination. Analysis of recombination junctions showed that the recombination at Hotspot I accounts for 22 or 4% of total [Lambda]bio transducing phages in the wild type or in the mutM mutant, respectively. The preferential increase of recombination at nonhotspot sites with hydrogen peroxide in the mutM mutant was discussed on the basis of a new model, in which 8-oxoG and/or Fapy residues may introduce double-strand breaks into DNA.

Abstract Background In 2005, the first disease-specific Helicobacter pylori virulence factor that induced duodenal ulcer and had a suppressive action on gastric cancer has been identified, and was named duodenal ulcer promoting gene (dupA). However, the importance of the dupA gene on clinical outcomes is conflicting in subsequent studies. The aim of this study was to estimate the magnitude of the risk for clinical outcomes associated with dupA gene. Methods A meta-analysis of case-control studies which provided raw data on the infection rates with the dupA-positive H. pylori detected by polymerase chain reaction was performed. Results Seventeen studies with a total of 2,466 patients were identified in the search. Infection with the dupA-positive H. pylori increased the risk for duodenal ulcer by 1.41-fold (95% confidence interval [CI], 1.12-1.76) overall. Subgroup analysis showed that the summary odds ratio (OR) was 1.57 (95% CI, 1.19-2.06) in Asian countries and 1.09 (95% CI, 0.73-1.62) in Western countries. There was no association between the presence of the dupA gene and gastric cancer and gastric ulcer. Publication bias did not exist. Conclusion Our meta-analysis confirmed the importance of the presence of the dupA gene for duodenal ulcer, especially in Asian countries.

Aims Cardiac hypertrophy is a compensatory response to pressure overload, leading to heart failure. Recent studies have demonstrated that Rho is immediately activated in left ventricles after pressure overload and that Rho signalling plays crucial regulatory roles in actin cytoskeleton rearrangement during cardiac hypertrophic responses. However, the mechanisms by which Rho and its downstream proteins control actin dynamics during hypertrophic responses remain not fully understood. In this study, we identified the pivotal roles of mammalian homologue of Drosophila diaphanous (mDia) 1, a Rho-effector molecule, in pressure overload-induced ventricular hypertrophy. Methods and results  Male wild-type (WT) and mDia1-knockout (mDia1KO) mice (10–12 weeks old) were subjected to a transverse aortic constriction (TAC) or sham operation. The heart weight/tibia length ratio, cardiomyocyte cross-sectional area, left ventricular wall thickness, and expression of hypertrophy-specific genes were significantly decreased in mDia1KO mice 3 weeks after TAC, and the mortality rate was higher at 12 weeks. Echocardiography indicated that mDia1 deletion increased the severity of heart failure 8 weeks after TAC. Importantly, we could not observe apparent defects in cardiac hypertrophic responses in mDia3-knockout mice. Microarray analysis revealed that mDia1 was involved in the induction of hypertrophy-related genes, including immediate early genes, in pressure overloaded hearts. Loss of mDia1 attenuated activation of the mechanotransduction pathway in TAC-operated mice hearts. We also found that mDia1 was involved in stretch-induced activation of the mechanotransduction pathway and gene expression of c-fos in neonatal rat ventricular cardiomyocytes (NRVMs). mDia1 regulated the filamentous/globular (F/G)-actin ratio in response to pressure overload in mice. Additionally, increases in nuclear myocardin-related transcription factors and serum response factor were perturbed in response to pressure overload in mDia1KO mice and to mechanical stretch in mDia1 depleted NRVMs. Conclusion  mDia1, through actin dynamics, is involved in compensatory cardiac hypertrophy in response to pressure overload. [ABSTRACT FROM AUTHOR]

We studied the role of DNA ligase in illegitimate recombination in Escherichia coli. A temperature-sensitive mutation in the liggene reduced the frequency with which 3, bio-transducing phages were generated to 10-14% of that of wild type under LTV irradiation. Reintroduction of the lig gene into this mutant restored the frequency of recombinant phage generation to that of wild type. Furthermore, overexpression of DNA ligase enhanced illegitimate recombination by 10-fold with or without LTV irradiation. In addition, when DNA ligase was present in only limited amounts, UV-induced or spontaneous illegitimate recombination occurred exclusively at hotspot sites that have relatively long sequences of homology (9 or 13 bp). However, when DNA ligase was overexpressed, most of the illegitimate recombination took place at nonhotspot sites having only short sequences of homology ([is less than] 4 bp). Thus, the level of ligase activity affects the frequency of illegitimate recombination, the length of sequence homology at the recombination sites, and the preference for recombination at hotspots, at least after UV irradiation. These observations support our hypothesis that the illegitimate recombination that generates [Lambda]bio-transducing phages is mediated by the DNA break-and-join mechanism.

Abstract: Aim: Constipation is a serious problem for persons with mental and physical disabilities in Japan. However, prophylaxis is extremely difficult because the major causes of constipation in these individuals are related to their mental and physical disabilities. Constipation can be successfully treated with glycerol enemas (GEs) and other aperients. As constipation is a lifetime issue for these persons, dietary regimens to prevent constipation can be important. Methods: This study evaluated the probiotic effects of kefir‐fermented milk for preventing constipation in 42 persons with mental and physical disabilities. The participants were administered 2 g of lyophilized kefir with each meal for 12 weeks and their bowel movements, the administration of GE and other aperients, and stool shape were recorded. Results: The intake of kefir significantly reduced constipation, compared with the baseline status. Some individuals showed complete relief of constipation, whereas others showed no effect. Conclusion: Despite individual variations, consuming kefir daily could prevent constipation. [ABSTRACT FROM AUTHOR]

Periodontal disease, an inflammatory disease, is caused by infection with periodontal pathogens. Long‐term periodontal disease increases the risk of oral carcinogenesis. Similar to other peptic cancers, oral carcinogenesis also requires multiple genome instabilities; however, the risk factors related to the accumulation of genome instabilities are poorly understood. Here, we suggested that specific periodontal pathogens may increase the risk of genome instability. Accordingly, we screened several periodontal pathogens based on the ability to induce DNA double‐strand breaks (DSBs) in host cells. We found that Aggregatibacter actinomycetemcomitans Y4 infection induced DSB formation in host cells. To assess whether DSB formation induced by infection with A. actinomycetemcomitans occurred through apoptotic chromosome fragmentation, cells were treated with a caspase inhibitor, Z‐VAD‐FMK. DSB accumulation induced by infection with A. actinomycetemcomitans was observed, even in the presence of Z‐VAD‐FMK, suggesting that this breakage occurred independently of apoptosis. These results suggested that some periodontal pathogens can increase the risk of genome instabilities in host cells and subsequently increase the risk of carcinogenesis. [ABSTRACT FROM AUTHOR]