Competitive Formation Mechanism for Bidentate Passivation of Halogen Vacancies in Perovskite Based on 6-Chloropurine.

For metal halide perovskite solar cells, bidentate passivation (BP) is highly effective, but currently, only passivation sites rather than molecular environments are being considered. Here, the authors report an effective approach for high-performance fully printable mesoscopic perovskite solar cells (FP-PSCs) through the BP strategy using the multidentate molecule 6-chloropurine (6-CP). By utilizing density functional theory (DFT) calculations, X-ray photoelectron spectroscopy (XPS), and Fourier transform infrared spectroscopy (FTIR) characterizations, the competition mechanism is identified of BP between the chlorine atom and neighboring nitrogen atom of the imidazole and pyrimidine rings. Through BP between the chlorine atom and adjacent nitrogen atom in imidazole, the power conversion efficiency (PCE) of the pristine samples is significantly enhanced from 16.25% to 17.63% with 6-CP. The formation of BP enhances interfacial hole selectivity and charge transfer, and suppresses nonradiative recombination, improving device stability under high humidity conditions. The competition mechanism of BP between two aromatic cycles provides a path for designing molecular passivants and selecting passivation pathways to approach theoretical limits.

Combination of berberine and ciprofloxacin reduces multi-resistant Salmonella strain biofilm formation by depressing mRNA expressions of luxS, rpoE, and ompR.

Bacterial biofilms have been demonstrated to be closely related to clinical infections and contribute to drug resistance. Berberine, which is the main component of Coptis chinensis, has been reported to have efficient antibacterial activity. This study aimed to investigate the potential effect of a combination of berberine with ciprofloxacin (CIP) to inhibit Salmonella biofilm formation and its effect on expressions of related genes (rpoE, luxS, and ompR). The fractional inhibitory concentration (FIC) index of the combination of berberine with CIP is 0.75 showing a synergistic antibacterial effect. The biofilm's adhesion rate and growth curve showed that the multi-resistant Salmonella strain had the potential to form a biofilm relative to that of strain CVCC528, and the antibiofilm effects were in a dose-dependent manner. Biofilm microstructures were rarely observed at 1/2 × MIC/FIC concentrations (MIC, minimal inhibition concentration), and the combination had a stronger antibiofilm effect than each of the antimicrobial agents used alone at 1/4 × FIC concentration. LuxS, rpoE, and ompR mRNA expressions were significantly repressed (p ＜ 0.01) at 1/2 × MIC/FIC concentrations, and the berberine and CIP combination repressed mRNA expressions more strongly at the 1/4 × FIC concentration. The results indicate that the combination of berberine and CIP has a synergistic effect and is effective in inhibiting Salmonella biofilm formation via repression of luxS, rpoE, and ompR mRNA expressions.

Evaluation of hepatoprotective activity of Syringa oblata leaves ethanol extract with the indicator of glutathione S-transferase A1

Abstract The leaves of Syringa oblata Lindl., Oleaceae, had been extensively used as a folk medicine to treat various infections, heal inflammations, icteric hepatitis and acute mastitis. The study was designed to evaluate the hepatoprotective activity of S. oblata leaves ethanol extract against CCl4-induced hepatotoxicity in primary hepatocytes and mice with the indicator of glutathione S-transferase alpha 1. The hepatoprotective effects of S. oblata leaves ethanol extract were evaluated on the basis of liver histopathology and biochemical parameters as well as hepatic oxidative stress markers. The results showed that CCl4 negatively modulated biochemical parameters and liver antioxidant activities. However, the use of S. oblata leaves ethanol extract restored altered-serum biochemical parameters and liver antioxidant activities in a dose-dependent manner. Importantly, the trends in S-transferase alpha 1 were similar to alanine aminotransferase and aspartate aminotransferase level, and S-transferase alpha 1 was suggested to be a marker for the evaluation of hepatoprotective activity of S. oblata leaves ethanol extract. Histopathological examination showed that CCl4 causes significant hepatic injury relative to control group. The above findings suggested that S. oblata leaves ethanol extract has hepatoprotective effects against CCl4-induced hepatic injury and S-transferase alpha 1 may be an indicator to evaluate the protective effects of S. oblata leaves ethanol extract.

Ultrasonic-assisted soldering of fine-grained 7034 aluminum alloy using Sn-Zn solders below 300°C.

The fine-grained Al alloys prefer to be soldered at as low as temperature to keep their mechanical properties. Solders of Sn-4Zn, Sn-9Zn, and Sn-20Zn alloys were used to solder fine-grained 7034 Al alloy pieces by ultrasonic-assisted soldering below 300°C in air. The joint using Sn-4Zn solder had the highest tensile strength of 201MPa and the fractures occurred in both ß-Sn and Sn-Zn eutectic phases. Such joint was much stronger than the 1060 Al joint using Sn-4Zn solder, and its strength had approached the strength of 7034 Al joint using Zn-5Al solder. The strength of the joints using Sn-9Zn and Sn-20Zn solders dropped to∼160MPa due to the appearance of weak interfaces between η-Zn and eutectic phases in the bond layers. All the joints using Sn-Zn solders had very strong interfacial bonding, and alumina interlayers were identified at all the interfaces. Al dissolved in the bond layer reacted with the O rapidly to form alumina interlayers at the interfaces under the ultrasonic action. Zn segregated at the interface and formed strong bonds with both the Al terminated surface of alumina and the bond layer, resulting in strong interfacial bonding between Sn-Zn solders and Al alloys.

Hepatoprotective effects of ethanol extracts from Folium Syringae against acetaminophen-induced hepatotoxicity in vitro and in vivo.

BACKGROUND: The leaves of Folium Syringae (FS) have been long used as a traditional Chinese folk medicine for their anti-inflammatory effect, utilized as an antibacterial and antiviral treatment. The purpose of this study was to investigate the potential hepatoprotective effects of FS on acetaminophen-induced hepatic injury in primary hepatocytes and mice. METHODS: Hepatocytes obtained by the inverse perfusion method were divided randomly into five groups. Prior to acetaminophen exposure, 3 different doses of FS ethanol extracts were given to hepatocytes and mice, respectively. Thereafter, transaminases, glutathione S-transferase A1 (GSTA1) and some hepatic indices were determined. RESULTS: FS ethanol extracts (200 µg/mL) pretreatment prevented all of the alterations, returning their levels to nearly those levels observed in the control group in vitro. Treatment with FS ethanol extracts (200 mg/kg) significantly reduced the toxicity induced by acetaminophen in vivo, which manifested as a decrease in transaminases, and the hepatoprotective effects of FS were similar to Silymarin (positive group). GSTA1 represented the same change trend as transaminases and hepatic indices, and at a dose of 100 µg/mL FS ethanol extracts in vitro and 100 mg/kg in vivo, GSTA1 content changed significantly (p < 0.01), but transaminases were insignificant (p > 0.05). CONCLUSION: The results of our investigation suggested that FS ethanol extracts possess significant protective effects against hepatotoxicity induced by acetaminophen both in vitro and in vivo. In addition, GSTA1 could be used as an indicator assessing the extents of hepatic injury, which is more sensitive than transaminases.

Glutathione S-transferase A1 (GSTA1) as a marker of acetaminophen-induced hepatocyte injury in vitro.

Acetaminophen (APAP) overdose causes serious hepatocyte injury, and new markers are needed to predict APAP-induced hepatic injury. Glutathione S-transferase A1 (GSTA1) plays a significant role in the metabolism of APAP. Primary mouse hepatocytes were isolated by a two-step perfusion in situ. An APAP-induced hepatocyte injury model was used to characterize GSTA1 in APAP treated cells and determine whether GSTA1 could be a prognostic marker in vitro. A significant increase (p < .05) in GSTA1 in cell culture supernatant was detected at 6 h after APAP treatment, while alanine aminotransferase (ALT), aspartate aminotransferase (AST), malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione (GSH) showed marked differences (p < .05) at 8 h after APAP exposure, 2 h later than GSTA1. Furthermore, GSTA1 increased in a dose-dependent manner with APAP treatment. GSTA1 increased significantly (p < .05) at a concentration of 5.0 mmol/L APAP, while the marked changes in ALT, AST and other indexes were undetectable until the concentration of APAP reached 7.5 mmol/L. These results suggest that increased GSTA1 can be more sensitive than ALT and other indexes as a marker of APAP-induced hepatic injury, which provide novel diagnostic index for APAP-induced hepatic injury and supply valuable information to further understand the pathogenesis of liver damage.

Ultrasonic-promoted rapid TLP bonding of fine-grained 7034 high strength aluminum alloys.

High strength aluminum alloys are extremely sensitive to the thermal cycle of welding. An ultrasonic-promoted rapid TLP bonding with an interlayer of pure Zn was developed to join fine-grained 7034 aluminum alloys at the temperature of lower 400°C. The oxide film could be successfully removed with the ultrasonic vibration, and the Al-Zn eutectic liquid phase generated once Al and Zn contacted with each other. Longer ultrasonic time can promote the diffusion of Zn into the base metal, which would shorten the holding time to complete isothermal solidification. The joints with the full solid solution of α-Al can be realized with the ultrasonic action time of 60s and holding time of only 3min at 400°C, and the shear strength of joints could reach 223MPa. The joint formation mechanism and effects of ultrasounds were discussed in details.

USP3 counteracts RNF168 via deubiquitinating H2A and γH2AX at lysine 13 and 15.

Histone ubiquitination plays a vital role in DNA damage response (DDR), which is important for maintaining genomic integrity in eukaryotic cells. In DDR, ubiquitination of histone H2A and γH2AX by the concerted action of ubiquitin (Ub) ligases, RNF168 and RNF8, generates a cascade of ubiquitination signaling. However, little is known about deubiquitinating enzymes (DUBs) that may catalyze the removal of Ub from these histones. This study demonstrated that USP3, an apparent DUB for mono-ubiquitinated H2A, is indeed the enzyme for deubiquitinating Ub conjugates of γH2AX and H2A from lysine sites, where the ubiquitination is initiated by RNF168. Here, we showed that ectopic expression of USP3 led to the deubiquitination of both H2A and γH2AX in response to UV-induced DNA damage. Moreover, ectopic USP3 expression abrogated FK2 antibody-reactive Ub-conjugate foci, which co-localize with damage-induced γH2AX foci. In addition, USP3 overexpression impaired the accumulation of downstream repair factors BRCA1 and 53BP1 at the damage sites in response to both UV and γ-irradiation. We further identified that the USP3 removes Ub at lysine 13 and 15 of H2A and γH2AX, as well as lysine 118 and 119 of H2AX in response to DNA damage. Taken together, the results suggested that USP3 is a negative regulator of ubiquitination signaling, counteracting RNF168- and RNF8-mediated ubiquitination.