Carbon material is a promising electrocatalyst for the oxygen reduction reaction (ORR). Doping of heteroatoms, the most widely used modulating strategy, has attracted many efforts in the past decade. Despite all this, the catalytic activity of heteroatoms‐modulated carbon is hard to compare to that of metal‐based electrocatalysts. Here, a “double‐catalysts” (Fe salt, H3BO3) strategy is presented to directionally fabricate porous structure of crystal graphene nanoribbons (GNs)/amorphous carbon doped by pyridinic NB pairs. The porous structure and GNs accelerate ion/mass and electron transport, respectively. The N percentage in pyridinic NB pairs accounts for ≈80% of all N species. The pyridinic NB pair drives the ORR via an almost 4e− transfer pathway with a half‐wave potential (0.812 V vs reversible hydrogen electrode (RHE)) and onset potential (0.876 V vs RHE) in the alkaline solution. The ORR catalytic performance of the as‐prepared carbon catalysts approximates commercial Pt/C and outperforms most prior carbon‐based catalysts. The assembled Zn–air battery exhibits a high peak power density of 94 mW cm−2. Density functional theory simulation reveals that the pyridinic NB pair possesses the highest catalytic activity among all the potential configurations, due to the highest charge density at C active sites neighboring B, which enhances the interaction strength with the intermediates in the p‐band center.

Phenol HDO over bimetallic M@Ni(111) single-atom surface alloys was systematically investigated. For optimal phenolic-HDO performance, a balance of alloyed M's oxophilicity should be achieved.

Copper is a well-known metal for catalyzing the electrochemical CO 2 reduction reaction (CO 2 RR) toward valuable hydrocarbons and alcohols. Here, using a combined density functional theory and microkinetic modeling approach, we systematically investigated 11 bimetallic M@Cu(211) single-atom stepped surface alloys for their CO 2 RR activity. It is revealed that the stepped M edge is most likely to be the active site for CO 2 RR. The primary reaction pathway is identified as *COOH → *CO → *CHO with the potential-determining step of *CO + H + + e − → *CHO, leading to either CH 4 or CH 3 OH formation at more negative potential. Especially, Ru@Cu(211) and Fe@Cu(211) are both predicted to be most efficient in promoting CO 2 RR toward CH 4 owing to their breaking of the coupled scaling relations of key intermediates' binding at the active site. Furthermore, the binding strength of *CO and *OH can be used as a good descriptor for differentiating various M@ Cu(211) for CO 2 RR activity and selectivity, and specifically, the moderate oxophilic and carbophilic elements of M are preferred. Our study highlights the utmost importance of breaking the linear scaling relations of key intermediates' binding at the active site for boosting CO 2 RR performance.

Dihydroartemisinin is an effective antimalarial agent with multiple biological activities. In the present investigation, we elucidated its therapeutic potential and working mechanism on human tongue squamous cell carcinoma (TSCC). It was demonstrated that dihydroartemisinin could significantly inhibit cell growth in a dose- and time-dependent manner by the Cell Counting Kit-8 and colony formation assay in vitro. Meanwhile, autophagy was promoted in the Cal-27 cells treated by dihydroartemisinin, evidenced by increased LC3B-II level, increased autophagosome formation, and increased Beclin-1 level compared to dihydroartemisinin-untreated cells. Importantly, dihydroartemisinin caused DNA double-strand break with simultaneously increased γH2AX foci and oxidative stress; this inhibited the nuclear localization of phosphorylated signal transducer and activator of transcription 3 (p-STAT3), finally leading to autophagic cell death. Furthermore, the antitumor effect of dihydroartemisinin-monotherapy was confirmed with a mouse xenograft model, and no kidney injury associated with toxic effect was observed after intraperitoneal injection with dihydroartemisinin for 3 weeks in vivo. In the present study, it was revealed that dihydroartemisinin-induced DNA double-strand break promoted oxidative stress, which decreased p-STAT3 (Tyr705) nuclear localization, and successively increased autophagic cell death in the Cal-27 cells. Thus, dihydroartemisinin alone may represent an effective and safe therapeutic agent for human TSCC.

Playing six-a-side: Complex hexagonal prism Cu(1.94)S-ZnS heteronanostructures were synthesized by a colloidal route. Cu(1.94)S-ZnS, Cu(1.94)S-ZnS-Cu(1.94)S, and Cu(1.94)S-ZnS-Cu(1.94)S-ZnS-Cu(1.94)S structures are formed with screw-, dumbbell-, and sandwich-like shapes by using CuI and [Zn(S(2)CNEt(2))(2)] as precursors in oleylamine.

No abstract

Background: Photon (X-ray) radiotherapy (XRT) kills cells via DNA damage, however, how proton radiotherapy (PRT) causes cell death in head and neck squamous cell carcinoma (HNSCC) is unclear. We investigated mechanisms of HNSCC cell death after XRT versus PRT. Methods: We assessed type of death in 2 human papillomavirus (HPV)-positive and two HPV-negative cell lines: necrosis and apoptosis (Annexin-V fluorescein isothiocyanate [FITC]); senescence (β-galactosidase); and mitotic catastrophe (γ-tubulin and diamidino-phenylindole [DAPI]). Results: The XRT-induced or PRT-induced cellular senescence and mitotic catastrophe in all cell lines studied suggested that PRT caused cell death to a greater extent than XRT. After PRT, mitotic catastrophe peaked in HPV-negative and HPV-positive cells at 48 and 72 hours, respectively. No obvious differences were noted in the extent of cell necrosis or apoptosis after XRT versus PRT. Conclusion: Under the conditions and in the cell lines reported here, mitotic catastrophe and senescence were the major types of cell death induced by XRT and PRT, and PRT may be more effective. K E Y W O R D Scell death mechanisms, head and neck cancer, photon radiotherapy, proton radiotherapy, radiation-induced cell death

Exploiting a precise and reproducible phosphorescence tuning strategy is crucial to tailor-design carbon dots (CDs) for premium gradient anticounterfeiting applications. Toward this target, we designed a facile substrate engineering technique to manipulate the phosphorescence of F, O-codoped CDs. Applying phenolic compounds with different numbers of hydroxyl groups as precursors, the contents of the C–O–C groups in CDs are effectively regulated for gaining outstanding phosphorescence performance as well as the introduction of the F-dopant. After excitation using a UV lamp followed by turning it off, the CDs/polyvinyl alcohol matrix can emit bright yellow room-temperature phosphorescence, which may derive from the synergistic effect of C–F and C–O–C in F and O-codoped CDs. After O and F form a bond, many lone pairs of electrons are generated, which is conducive to the excitation of n → π* and promotes the supplementation of triplet excitons. The phosphorescence tuning of CDs is realized by mixing different substrates, which can provide various phosphorescence lifetimes and colors. Discovering the unique properties, F, O-codoped CDs/substrates can be applied in gradient anticounterfeiting applications. This substrate engineering technique, showing unique and reproducibility with high efficiency, may further facilitate the potential applications of CDs.