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[Display omitted] • Both ion-sharing interface and directional doping are employed to construct a heterostructured HER electro-catalyst. • Electronic structure and coordination chemistry of Mo and Co centers are tailored to optimize adsorption/desorption of H ads and OH– intermediates for lowering the energy barriers. • Mo center with more coordination vacancies are main active sites responsible for rate-limiting step in the Volmer-Heyrovsky regime. • This catalyst presents an extremely low overpotential of 37 mV at 10 mA cm−2 in alkaline media, and excellent performance for overall water splitting. Interfacing and doping can effectively harmonize the electronic and coordination states of active centers in the electrocatalysts. Herein, we prepare heterostructured N-MoS 2 /Se-CoS 2 electrocatalyst with ion-sharing interfaces and directional doping to activate inert basal phases for hydrogen evolution reaction (HER). Based on experimental and theoretical results, their synergistic effects on electron redistribution, electronic structure and coordination chemistry are investigated; furthermore, roles of each component and bridged Mo-S-Co sites at the phase interfaces as active sites in optimizing the adsorption/desorption of essential reaction intermediates H* and OH–, as well as the free energies of unit reaction steps in the HER, are elucidated in depth. The N-MoS 2 /Se-CoS 2 catalyst needs only 37 mV to give current density of 10 mA cm−2 with a low Tafel slope of 49.4 mV dec−1; more importantly, the catalyst delivers a long-term durability for HER in alkaline condition and comparable performance with commercial RuO 2|| Pt/C system in a two-electrode assembled electrolyzer. This work provides more insights into the design and preparation of high-performance heterostructured electrocatalysts. [ABSTRACT FROM AUTHOR]

In the most primitive jawless vertebrate lamprey, the complement-dependent cytotoxicity regulated by variable lymphocyte receptors (VLRs) plays an important role in the adaptive immunity. Our previous studies have shown that the lamprey pore-forming protein (LPFP) acted as the terminal effector of VLR to lyse and kill the target cells. Here, the recombinant GST-LPFP protein was expressed and purified in prokaryotic expression system, and then used as the immunogen to produce mouse monoclonal antibody and rabbit polyclonal antibody. With these antibodies, we proved that LPFP existed as homodimers in the lamprey serum, and could be recruited to the membrane of target cells after stimulation. In conclusion, the antibodies we produced could specifically recognize the LPFP protein, which could be the useful tools to further study the pore-forming mechanism of LPFP. • LPFP protein was successfully expressed and purified via the prokaryotic expression system. • The rabbit polyclonal antibody and mouse monoclonal antibody with very high titers against LPFP were produced. • LPFP existed as a homodimer in the lamprey serum. • LPFP was recruited to the membrane of target cells to directly participate in the complement defense system in lamprey. [ABSTRACT FROM AUTHOR]

luxS-mediated autoinducer 2 (AI-2)-dependent quorum sensing (QS) has been demonstrated to affect many bacterial phenotypes, including virulence. Streptococcus agalactiae harbors a functional luxS gene required for the biosynthesis of AI-2. In this study, we investigated the regulation effect and mechanism of the luxS /AI-2 QS system in the pathogenicity of the piscine S. agalactiae strain GD201008-001. We found that inactivation of luxS caused a marked decrease in biofilm formation, hemolytic activity, antiphagocytosis and intracellular survival of S. agalactiae. Except for hemolytic activity, the altered phenotypes due to the luxS deletion were AI-2-independent. Further investigation indicated that high levels of the proinflammatory cytokines IL-1β and IL-6 could be induced in macrophages co-incubated with the luxS deletion mutant and synthetic AI-2, single or combined. Also, the results of tilapia infection showed that inactivation of luxS significantly decreased the virulence of S. agalactiae but upregulated the expression of cytokines in spleens and brains. Increased proinflammatory effects of the luxS mutant were restored in the luxS complemented strain but could not be restored by AI-2 addition. All the findings suggest that luxS is involved in virulence-associated phenotypes and immunological evasion of S. agalactiae , and furthermore, this involvement is mostly AI-2-independent. This study will provide valuable insights into our understanding of the role of the LuxS/AI-2 QS system in the pathogenesis of S. agalactiae. • Inactivation of luxS caused virulence decrease in the piscine S. agalactiae strain GD201008-001. • Both luxS deletion and AI-2 addition induced high expression levels of the proinflammatory cytokines in macrophages. • Most of altered phenotypes due to the luxS deletion were AI-2-independent. [ABSTRACT FROM AUTHOR]

The unfolded protein response (UPR) is widely activated in cancers. The mammalian UPR encompasses three signaling branches, namely inositol-requiring enzyme-1α (IRE1α), protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK) and activating transcription factor 6α (ATF6α). The functional significance of each branch in tumorigenesis is incompletely understood, especially in cancer stem cells (CSCs). Here, we report that inhibition and silencing of the three UPR sensors has differential effects on breast cancer growth and the CSC population. The levels of PERK and ATF6α strongly correlate with the expression of sex determining region Y (SRY)-box 2 (SOX2), a pluripotency regulator, in human breast cancer tissues. UPR activation is also elevated in the CSC-enriched mammospheres. Inhibition of the UPR sensors or excess ER stress markedly reduces the formation and maintenance of mammospheres, suggesting that an appropriate level of UPR activation is critical for the CSC survival. Mechanistically, transcription factors from UPR and pluripotency pathways interact and reciprocally influence each other. A transcription modulator, CCAAT-enhancer-binding protein delta (C/EBPδ), interacts with pluripotency regulator, SOX2, and UPR transcription factors, thus likely serving as a link to coordinate UPR and pluripotency maintenance in CSCs. Our findings demonstrate that UPR is critical for both cancer growth and pluripotency, and highlight the differential role and complexity of the three UPR branches in tumorigenesis. [ABSTRACT FROM AUTHOR]

Elucidating the generation mechanism of reactive oxygen species (ROS) is essential for advanced oxidation processes with respect to environmental and biological sciences. Herein, self-generation of ROS such as hydroxyl radicals (·OH), superoxide radicals (O 2 •-) and singlet oxygen (1O 2) from the interaction between multi-layered flowerlike MoS 2 nanosheets and H 2 O 2 is presented. The results demonstrate that H 2 O 2 can exfoliate multi-layered MoS 2 into quantum dots and promote a 2H to 1 T phase change accompanied by the dissolution of MoS 2 to produce H+, MoO 4 2− and SO 4 2−. Electron spin resonance (ESR) spectroscopy confirm the production of ·OH, superoxide radicals O 2 •- and 1O 2 in the MoS 2 /H 2 O 2 system. The calculation data based on density functional theory (DFT) indicate that the 1 T-MoS 2 can lower the free energy profiles for stepwise catalytic decomposition of H 2 O 2 to produce ROS as compared to 2H–MoS 2. • H 2 O 2 is decomposed into reactive oxygen species (ROS) over MoS 2. • MoS 2 is exfoliated and experiences a 2H to 1 T phase transition. • ·OH, O 2.•- and 1O 2 are the dominating ROS by the interaction between MoS 2 and H 2 O 2. • 1 T-MoS 2 can lower the free energy profiles for stepwise decomposition of H 2 O 2. • The degradation of methyl orange (MO) can probe the oxidation ability of ROS. [ABSTRACT FROM AUTHOR]