Unraveling the Nanoscale Segregation Mechanism in N-Doped Niobium for Enhanced SRF Performance.

The nitrogen doping (N-doping) treatment for niobium superconducting radio-frequency (SRF) cavities is one of the key enabling technologies that support the development of more efficient future large accelerators. However, the N-doping results have diverged due to a complex chemical profile under the nitrogen-doped surface. Particularly, under industrial-scale production conditions, it is difficult to understand the underlying mechanism thus hindering performance improvement. Herein, a combination of spatially resolved and surface-sensitive approaches is employed to establish the detailed near-surface phase composition of thermally processed niobium. The results show that intermediate phase segregations, particularly the nanometric carbon-rich phase, can impede the nitridation process and limit the interactions between nitrogen and the niobium sub-surface. In comparison, the removal of the carbon-rich layer at the Nb surface leads to enhanced nitrogen binding at the Nb surface. Combining the RF test results, it is shown that the complex uniformity and grain boundary penetrations of impurity elements have a direct correlation with the mid-field quench behavior in the N-doped Nb cavities. Therefore, proper control of the nanometric intermediate phase formation in discrete thermal steps is critical in improving the ultimate performance and production yield of the Nb cavities.

Ambient Pressure X-ray Photoelectron Spectroscopy Study of Oxidation Phase Transitions on Cu(111) and Cu(110).

The surface structure effect on the oxidation of Cu has been investigated by performing ambient-pressure X-ray photoelectron spectroscopy (APXPS) on Cu(111) and Cu(110) surfaces under oxygen pressures ranging from 10-8 to 1 mbar and temperatures from 300 to 750 K. The APXPS results show a subsequential phase transition from chemisorbed O/Cu overlayer to Cu2 O and then to CuO on both surfaces. For a given temperature, the oxygen pressure needed to induce initial formation of Cu2 O on Cu(110) is about two orders of magnitude greater than that on Cu(111), which is in contrast with the facile formation of O/Cu overlayer on clean Cu(110). The depth profile measurements during the initial stage of Cu2 O formation indicate the distinct growth modes of Cu2 O on the two surface orientations. We attribute these prominent effects of surface structure to the disparities in the kinetic processes, such as the dissociation and surface/bulk diffusion over O/Cu overlayers. Our findings provide new insights into the kinetics-controlled process of Cu oxidation by oxygen.

CO2 Activation on Ni(111) and Ni(110) Surfaces in the Presence of Hydrogen.

The structure sensitivity of CO2 activation in the presence of H2 has been identified by ambient-pressure X-ray photoelectron spectroscopy (APXPS) on Ni(111) and Ni(110) surfaces under identical reaction conditions. Based on the APXPS results and computer simulations, we propose that, around room temperature, the hydrogen-assisted activation of CO2 is the major reaction path on Ni(111), while the redox pathway of CO2 prevails on Ni(110). With increasing temperature, the two activation pathways are activated in parallel. While the Ni(111) surface is fully reduced to the metallic state at elevated temperatures, two stable Ni oxide species can be observed on Ni(110). Turnover frequency measurements indicate that the low-coordinated sites on Ni(110) promote the activity and selectivity of CO2 hydrogenation to methane. Our findings provide insights into the role of low-coordinated Ni sites in nanoparticle catalysts for CO2 methanation.

Clinical effect of laparoscopic cholecystectomy in the treatment of chronic cholecystitis with gallstones.

Chronic cholecystitis is a common disease that causes inflammation in the gallbladder and is usually associated with gallstones. Laparoscopic cholecystectomy has been widely used as a minimally invasive surgical technique to treat this condition. However, the clinical effect of laparoscopic cholecystectomy in the treatment of chronic cholecystitis with gallstones needs further investigation. This study aimed to investigate the clinical effect of laparoscopic cholecystectomy in treating chronic cholecystitis with gallstones. 90 patients with chronic cholecystitis and gallstones were randomly divided into control and research groups. The control group underwent traditional open cholecystectomy, while the research group received laparoscopic cholecystectomy. Perioperative indexes, oxidative stress indexes, serum inflammatory factors, liver function indexes and the incidence of complications were observed and compared. Results showed that laparoscopic cholecystectomy significantly reduced the operation time, blood loss, anal exhaust time, abdominal pain duration, and hospital stay compared to traditional open cholecystectomy (P < 0.05). Moreover, laparoscopic cholecystectomy significantly reduced the levels of oxidative stress indexes (GSH-Px), inflammatory factors (IL-6, TNF-α, and CRP), and liver function indexes (TBIL, AST, and ALT) compared to traditional open cholecystectomy. Moreover, the complication rate of the research group was significantly lower than that of the control group (P < 0.05). In conclusion, laparoscopic cholecystectomy for chronic cholecystitis with gallstones is a safe and effective procedure that reduces the perioperative stress response and promotes the rapid recovery of the postoperative body. The findings of this study provide a basis for the clinical promotion of laparoscopic cholecystectomy as the preferred surgical treatment for chronic cholecystitis with gallstones.

Correction: The lipogenic LXR-SREBF1 signaling pathway controls cancer cell DNA repair and apoptosis and is a vulnerable point of malignant tumors for cancer therapy.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

The lipogenic LXR-SREBF1 signaling pathway controls cancer cell DNA repair and apoptosis and is a vulnerable point of malignant tumors for cancer therapy.

Cancer cells are defective in DNA repair, so they experience increased DNA strand breaks, genome instability, gene mutagenesis, and tumorigenicity; however, multiple classic DNA repair genes and pathways are strongly activated in malignant tumor cells to compensate for the DNA repair deficiency and gain an apoptosis resistance. The mechanisms underlying this phenomenon in cancer are unclear. We speculate that a key DNA repair gene or signaling pathway in cancer has not yet been recognized. Here, we show that the lipogenic liver X receptor (LXR)-sterol response element binding factor-1 (SREBF1) axis controls the transcription of a key DNA repair gene polynucleotide kinase/phosphatase (PNKP), thereby governing cancer cell DNA repair and apoptosis. Notably, the PNKP levels were significantly reduced in 95% of human pancreatic cancer (PC) patients, particularly deep reduction for sixfold in all of the advanced-stage PC cases. PNKP is also deficient in three other types of cancer that we examined. In addition, the expression of LXRs and SREBF1 was significantly reduced in the tumor tissues from human PC patients compared with the adjacent normal tissues. The newly identified LXR-SREBF1-PNKP signaling pathway is deficient in PC, and the defect in the pathway contributes to the DNA repair deficiency in the cancer. Strikingly, further diminution of the vulnerable LXR-SREBF1-PNKP signaling pathway using a small molecule triptonide, a new LXR antagonist identified in this investigation, at a concentration of 8 nM robustly activated tumor-suppressor p53 and readily elevated cancer cell DNA strand breaks over an apoptotic threshold, and selectively induced PC cell apoptosis, resulting in almost complete elimination of tumors in xenograft mice without obvious complications. Our findings provide new insight into DNA repair and apoptosis in cancer, and offer a new platform for developing novel anticancer therapeutics.