The present study reports an unprecedented protocol for the phosphonylation of unactivated C(sp(3))-H bonds. By utilizing 1 mol % 4DPAIPN (1,2,3,5-tetrakis(diphenylamino)-4,6-dicyanobenzene) as the catalyst, satisfactory yields of gamma-phosphonylated amides are obtained through a visible-light-induced reaction between N-((4-cyanobenzoyl)oxy)alkanamides and 9-fluorenyl o-phenylene phosphite at room temperature. This protocol demonstrates broad substrate scope and wide functional group compatibility.

Excellent mechanical properties are the fundamental requirement for the practical application of solid propellants. However, solid oxidant fillers such as hexahydro-1,3,5-trinitros triazine (RDX) seriously weaken the mechanical strength of the propellant due to poor adhesion with the binder matrix. In this work, novel cyclic borate ester (CBE) bonding agents with long-chain alkyl moiety were designed by the molecular dynamics (MD) method to improve the unfavorable interfacial bonding effect. The interface models, which consist of RDX substrate and binder matrix where hydroxyl-terminated polybutadiene (HTPB) crosslinked with curing agents, were constructed to reveal the interface enhancement mechanism by CBE bonding agents. The results indicate that the designed CBE bonding agents with appropriate solubility parameters (SPs) can migrate from the binder matrix to the RDX surface. Besides, CBE bonding agents exhibit strong interaction with RDX compared to the binder matrix due to the formation of hydrogen bonds. Finally, the simulated tensile tests with two tensile modes showed that CBE bonding agents can enhance the interfacial strength and reduce stress softening rates by the calculation of debonding work. Moreover, this improvement can be controlled by adjusting the chain length of CBE bonding agents. The results obtained in this work deepen the understanding of the interfacial strengthening mechanism of bonding agents for solid propellants and provide a framework for designing high-performance bonding agents based on the MD method.

The promoter region of proto-oncogene RET has continuous guanine -rich regions I-V, which form G-quadruplex (G4) structures. Reported RET20T G4 in the regions II-V has parallel folding in potassium -ion solutions; however, this G4 -DNA is not an ideal drug target, as its formation is limited to a low concentration potassium -ion solution. Here, we demonstrate that RET-21mer in the regions I-IV forms a mixed parallel/anti-parallel G4 in either 50 mM K + or 100 mM Na + solutions. It is stable, with a melting temperature of 74.3 degrees C in 100 mM Na + solution and 91.2 degrees C in 100 mM K + solution. A loop forms a special G center dot G base -pair plane in K + solution or an unconventional A center dot G center dot G plane in Na + solution, stacking with the 3 ' end G tetrad, stabilizing its conformation. We also show that RET21mer G4 could exist under physiological conditions. Therefore, RET-21mer G4s are likely a major G4 -DNA, providing a research direction for anti -cancer drug screening.

Here, we report a visible-light-mediated [2 + 2 + 1] cascade cyclization of 1,6-enynes with thiols, providing a new synthetic protocol for the rapid construction of sulfur-containing polycyclic derivatives in moderate to good yields along with a broad substrate scope. Mechanistic investigations were also performed through control experiments and Stern-Volmer analysis as well as DFT calculations, suggesting that this cascade cyclization reaction stems from a sulfur radical addition to the alkynyl moiety of 1,6-enyne along with a cascade cyclization with the alkenyl unit. Then, the formation of sulfur-containing polycyclic molecules can be achieved by homolytic SHi-type substitution at the thioether unit, stripping away a sulfur atom. Further transformations of the obtained product have also been disclosed. Here, we report a visible-light-mediated [2 + 2 + 1] cascade cyclization of 1,6-enynes with thiols, providing sulfur-containing polycyclic molecules in moderate to good yields.

Background Schizophrenia, a debilitating psychiatric disorder, displays considerable interindividual variation in clinical presentations. The ongoing debate revolves around whether this heterogeneity signifies a continuum of severity linked to a singular causative factor or a collection of distinct subtypes with unique origins. Within the realm of schizophrenia, the functional impairment of GluN2A, a subtype of the NMDA receptor, has been associated with an elevated risk. Despite GluN2A's expression across various neuronal types throughout the brain, its specific contributions to schizophrenia and its involvement in particular cell types or brain regions remain unexplored. Methods We generated age -specific, cell type -specific or brain region -specific conditional knockout mice targeting GluN2A and conducted a comprehensive analysis using tests measuring phenotypes relevant to schizophrenia. Findings Through the induction of germline ablation of GluN2A, we observed the emergence of numerous schizophrenia -associated abnormalities in adult mice. Intriguingly, GluN2A knockout performed at different ages, in specific cell types and within distinct brain regions, we observed overlapping yet distinct schizophrenia -related phenotypes in mice. Interpretation Our interpretation suggests that the dysfunction of GluN2A is sufficient to evoke heterogeneous manifestations associated with schizophrenia, indicating that GluN2A stands as a prominent risk factor and a potential therapeutic target for schizophrenia. Funding This project received support from the Shanghai Municipal Science and Technology Major Project (Grant No. 2019SHZDZX02) awarded to Y.C. and the Natural Science Foundation of Shanghai (Grant No. 19ZR1468600 and 201409003800) awarded to G.Y. Copyright (c) 2024 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY -NC -ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).