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Herein, a DC and microwave performance of 2 μm gate length AlGaN/GaN high‐electron‐mobility transistor (HEMTs) on a Mn‐doped GaN substrate is demonstrated. The maximum drain current is 670 mA with a threshold voltage of −$-$2.5 V and with good pinch‐off characteristics. The breakdown voltage of the HEMT is ≈80 V. The HEMT shows Δ8% current collapse while referenced HEMT on a SiC substrates which is fabricated simultaneously shows large Δ30% current collapse. When the HEMT with a gate width of 100 μm is tuned for the maximum output power at 2.4 GHz with a drain voltage of 30 V, it delivers 500 mW (5 W mm−1) with the maximum drain efficiency of 54%. These output performances are in good agreement with ideal class‐A operation performance. Therefore, it is concluded that the HEMT on Mn‐doped GaN substrates is promising for future microwave and millimeter‐wave high‐power transistors. [ABSTRACT FROM AUTHOR]

Non-enzymatic spontaneous deamination of 5-methylcytosine, producing thymine, is the proposed etiology of cancer mutational signature 1, which is the most predominant signature in all cancers. Here, the proposed mutational process was reconstituted using synthetic DNA and purified proteins. First, single-stranded DNA containing 5-methylcytosine at CpG context was incubated at an elevated temperature to accelerate spontaneous DNA damage. Then, the DNA was treated with uracil DNA glycosylase to remove uracil residues that were formed by deamination of cytosine. The resulting DNA was then used as a template for DNA synthesis by yeast DNA polymerase δ. The DNA products were analyzed by next-generation DNA sequencing, and mutation frequencies were quantified. The observed mutations after this process were exclusively C>T mutations at CpG context, which was very similar to signature 1. When 5-methylcytosine modification and uracil DNA glycosylase were both omitted, C>T mutations were produced on C residues in all sequence contexts, but these mutations were diminished by uracil DNA glycosylase-treatment. These results indicate that the CpG>TpG mutations were produced by the deamination of 5-methylcytosine. Additional mutations, mainly C>G, were introduced by yeast DNA polymerase ζ on the heat-damaged DNA, indicating that G residues of the templates were also damaged. However, the damage on G residues was not converted to mutations with DNA polymerase δ or ε. [ABSTRACT FROM AUTHOR]

Replication protein-A (RPA) is involved in many processes of DNA metabolism, including DNA replication, repair, and recombination. Cells carrying a mutation in the largest subunit of RPA (rfa1-t11: K45E) have defects in meiotic recombination, mating-type switching, and survival after DNA damage caused by UV and methyl methanesulfonate, as well as increased genome instability; however, this mutant has no significant defect in DNA replication. We purified the RPA heterotrimer containing the rfa1-t11 substitution (RPA(rfa1-t11)). This mutant RPA binds single-stranded DNA (ssDNA) with the same site size, and the RPA(rfa1-t11).ssDNA complex shows a similar sensitivity to disruption by salt as the wild-type RPA.ssDNA complex. RPA(rfa1-t11)stimulates DNA strand exchange, provided that the Rad51 protein.ssDNA nucleoprotein complex is assembled prior to introduction of the mutant RPA. However, RPA(rfa1-t11) is displaced from ssDNA by Rad51 protein more slowly than wild-type RPA and, as a consequence, Rad51 protein-mediated DNA strand exchange is inhibited when the ssDNA is in a complex with RPA(rfa1-t11). Rad52protein can stimulate displacement of RPA(rfa1-t11) from ssDNA by Rad51 protein, but the rate of displacement remains slow compared with wild-type RPA. These in vitro results suggest that, in vivo, RPA is bound to ssDNA prior to Rad51 protein and that RPA displacement by Rad51 protein is a critical step in homologous recombination, which is impaired in the rfa1-t11 mutation.

Rad52 protein stimulates DNA strand exchange by targeting Rad51 protein to a complex of replication protein A (RPA) with single-stranded DNA. It appears that Rad52 protein facilitates the loading of Rad51 protein onto RPA-single stranded DNA. The activities of Rad52 protein are significant in double-strand DNA break repair and homologous recombination, but they cannot totally account for all the roles of RAD52 in these processes.

Identification and analysis of the region essential for autonomous replication of 15 Colicin E plasmids (ColE plasmids) that mediate Rep protein synthesis reveal that all the plasmids share a common pathway for activation and regulation of DNA replication. Four new IncB specificity types and 5 IncA specificity types are seen, with the plasmids of the four IncA specificity types containing nine-nucleotide sequences in the loop regions of stem-loop structures. Mutations of single or several nucleotides and of the C-terminal amino acid sequences of the Rep protein help determine the binding specificity of the Rep proteins.5

In this study, we determined the borders of the pathogenicity island in V. parahaemolyticus RIMD2210633 (Vp-PAI). Vp-PAI has features in common with Tn7 and other related elements at both terminal ends. Our findings indicate that the mobile element with a transposase which contains the DDE motif may have been involved in Vp-PAI formation.

The effects of surface treatments in H2, N2, and O2 on electron emission have been investigated for a ferroelectric electron emitter with a unique porous electrode. The electron emission was markedly enhanced after surface treatment in H2 at 90 kPa. The electron emission density was about 500 nC/cm2, 1.6 times higher than that of a nontreated emitter. On the other hand, electron emission after surface treatment in O2 at 90 kPa was decreased to about two-third of that of the nontreated emitter. These results indicate that electron emission can be significantly influenced by modification of the ferroelectric surface state. [ABSTRACT FROM AUTHOR]

Background: Pulmonary dysfunction often accompanies esophageal squamous cell carcinoma (SCC). Aims: This study examined the use of carbon dioxide (CO2) insufflation and its safety during esophageal endoscopic submucosal dissection (ESD) while under conscious sedation. Methods: ESD using CO2 insufflation (1.4 L/min) was performed in 102 consecutive esophageal SCC patients. Patients with a forced expiratory volume of 1.0 s/forced vital capacity (FEV1.0%) < 70% or a vital capacity < 80% were defined as having pulmonary dysfunction. Transcutaneous partial pressure of CO2 (PtcCO2) was recorded before, during, and after ESD. Results: A history of smoking was found in 90 patients (88%), while 43 patients (42%) had pulmonary dysfunction. No significant differences were found between the pulmonary dysfunction and normal groups for the baseline PtcCO2 before ESD, peak PtcCO2 during ESD, and median PtcCO2 after ESD. There was a significant correlation between the PtcCO2 elevation from baseline and the ESD procedure time (r = 0.32, p < 0.01), with the correlation for the pulmonary dysfunction group much stronger (r = 0.39, p < 0.05) than that for the normal group (r = 0.30, p < 0.01). Neither of the groups exhibited any differences for either the complication incidence or the hospital stay. Conclusions: Although the use of CO2 insufflation during esophageal ESD under conscious sedation is safe with regard to the risk of complications, longer procedure times can potentially induce CO2 retention in patients with obstructive lung disease. Thus, it is necessary to both shorten the procedure times and perform CO2 monitoring. [ABSTRACT FROM AUTHOR]