Surface in-situ reconstruction of LiNi 0.8 Co 0.1 Mn 0.1 O 2 cathode materials interacting with antimony compounds and the electrochemical performances

Abstract(#br)Interfacial stability is regarded as one of the greatest challenges in the commercialization of Ni-rich layered cathode materials for lithium battery. Surface modification can solve these issues to obtain superior electrochemical performances. Herein, LiNi 0.8 Co 0.1 Mn 0.1 O 2 (NCM811) cathode surface is reconstructed by a simple solid-state method using antimony oxides as modified agents. The modified mechanisms study show that the antimony oxides (Sb 2 O 5 ) can react with the surface lithium residues effectively and partial surface lattice lithium on the NCM811 surface to further construct the LiSbO 3 /Li–Sb– Me –O ( Me = Ni, Co, Mn) mixed coating layers. The uniform coating layer is mainly ascribed to the droplet spreading behaviors of the low smelting antimony oxides. The electrochemical measurements show that the Sb-modified NCM811 electrodes deliver 90.27% (180 mA g −1 ) and 96.07% (1440 mA g −1 ) capacity retentions over 3.0–4.3 V after 200 cycles, respectively, which are higher than 77.40 and 74.75% of the bare NCM811. The enhanced electrochemical performances are mainly benefitted to the enhanced the lithium transportation, the suppressed impedances increase and the more stable crystal structure

Enhanced biphasic reactions in amphiphilic silica mesopores

In this study, we investigated the effect of the pore volume and mesopore size of surface-active catalytic organosilicas on the genesis of particle-stabilized (Pickering) emulsions for the dodecanal/ethylene glycol system and their reactivity for the acid-catalyzed biphasic acetalization reaction. To this aim, we functionalized a series of fumed silica superparticles (size 100–300 nm) displaying an average mesopore size in the range of 11–14 nm and variable mesopore volume, with a similar surface density of octyl and propylsulfonic acid groups. The modified silica superparticles were characterized in detail using different techniques, including acid–base titration, thermogravimetric analysis, TEM, and dynamic light scattering. The pore volume of the particles impacts their self-assembly and coverage at the dodecanal/ethylene glycol (DA/EG) interface. This affects the stability and the average droplet size of emulsions and conditions of the available interfacial surface area for reaction. The maximum DA-EG productivity is observed for A200 super-SiNPs with a pore volume of 0.39 cm3·g–1 with an interfacial coverage by particles lower than 1 (i.e., submonolayer). Using dissipative particle dynamics and all-atom grand canonical Monte Carlo simulations, we unveil a stabilizing role of the pore volume of porous silica superparticles for generating emulsions and local micromixing of immiscible dodecanal and ethylene glycol, allowing fast and efficient solvent-free acetalization in the presence of Pickering emulsions. The micromixing level is interrelated to the adsorption energy of self-assembled particles at the DA/EG interface

Tumor‐derived exosomal PD-L1: a new perspective in PD-1/PD-L1 therapy for lung cancer

Exosomes play a crucial role in facilitating intercellular communication within organisms. Emerging evidence indicates that a distinct variant of programmed cell death ligand-1 (PD-L1), found on the surface of exosomes, may be responsible for orchestrating systemic immunosuppression that counteracts the efficacy of anti-programmed death-1 (PD-1) checkpoint therapy. Specifically, the presence of PD-L1 on exosomes enables them to selectively target PD-1 on the surface of CD8+ T cells, leading to T cell apoptosis and impeding T cell activation or proliferation. This mechanism allows tumor cells to evade immune pressure during the effector stage. Furthermore, the quantification of exosomal PD-L1 has the potential to serve as an indicator of the dynamic interplay between tumors and immune cells, thereby suggesting the promising utility of exosomes as biomarkers for both cancer diagnosis and PD-1/PD-L1 inhibitor therapy. The emergence of exosomal PD-L1 inhibitors as a viable approach for anti-tumor treatment has garnered significant attention. Depleting exosomal PD-L1 may serve as an effective adjunct therapy to mitigate systemic immunosuppression. This review aims to elucidate recent insights into the role of exosomal PD-L1 in the field of immune oncology, emphasizing its potential as a diagnostic, prognostic, and therapeutic tool in lung cancer

Knockdown of PLAC1 inhibits BCa growth and migration through upregulation of FOXO3a

Placenta-specific protein 1 (PLAC1) is considered to play a pivotal role in cancer progression. Here, we investigated the role of PLAC1 in the growth and motility of bladder cancer (BCa) cells. Database analysis and Immunoblot assays were conducted to determine PLAC1 expression in BCa tissues and its correlation with patient prognosis. Furthermore, wound healing, transwell and tube formation assays were performed to evaluate cell motility and angiogenic potential, and the underlying mechanism via which PLAC1 knockdown inhibits BCa progression in vitro was investigated. The data revealed that PLAC1 was obviously overexpressed in BCa tissues and was associated with poor patient prognoses. Additionally, silencing PLAC1 led to reduced viability, migratory capacity, invasion potential and angiogenesis of BCa cells, including T24 and UMUC3 cells. Further investigation showed that PLAC1 knockdown modulated the phosphoinositide 3-kinase/protein kinase B/forkhead box O3a (PI3K/Akt/FOXO3a) axis by enhancing the phosphorylation of FOXO3a while suppressing the phosphorylation of PI3K as well as Akt. Moreover, we demonstrated that the inhibition of BCa progression by PLAC1 knockdown was primarily mediated through the targeting of FOXO3a. In summary, these findings confirmed the potential of PLAC1 as a promising target for suppressing BCa growth by elevating FOXO3a levels and modulating the PI3K/Akt/FOXO3a signaling axis

Using bottleneck analysis to examine the implementation of standard precautions in hospitals.

BackgroundService providers are often inadequately compliant with standard precaution protocols. This study used bottleneck analysis to identify the weakest link in standard precaution implementation and its associated challenges in hospitals.MethodsBottleneck analysis was conducted in 12 hospitals in Fujian Province, China. In each hospital, a focus group was organized among the key informants to illustrate the sequential steps of standard precaution implementation graphically. The level of difficulty and the specific challenges associated with each step were discussed.ResultsThe sequential activities of standard precaution implementation generally start with making budget for personal protection equipment (PPE), followed by procurement, storage/inventory, in-hospital distribution, in-department distribution, usage/monitoring, and recycling of PPE. Service providers' improper use of PPE was the primary bottleneck. The reasons for improper use of PPE included high workload, time constraints, the sense of wearing PPE would interfere with clinical judgment, and various misconceptions. Making financial planning, recycling, and procurement of PPE were the secondary bottlenecks.ConclusionsBottleneck analysis is useful to illustrate workflow in healthcare systems and pinpoint constraints in standard precaution implementation. Institutional changes, including targeted provider training, adjustment of providers' workloads, and allocation of budget, are suggested strategies to address the identified bottlenecks in standard precaution

High‐mobility group box 1 emerges as a therapeutic target for asthma

Abstract High‐mobility group box 1 (HMGB1) is a highly conserved nonhistone nuclear protein found in the calf thymus and participates in a variety of intracellular processes such as DNA transcription, replication and repair. In the cytoplasm, HMGB1 promotes mitochondrial autophagy and is involved in in cellular stress response. Once released into the extracellular, HMGB1 becomes an inflammatory factor that triggers inflammatory responses and a variety of immune responses. In addition, HMGB1 binding with the corresponding receptor can activate the downstream substrate to carry out several biological effects. Meanwhile, HMGB1 is involved in various signaling pathways, such as the HMGB1/RAGE pathway, HMGB1/NF‐κB pathway, and HMGB1/JAK/STAT pathway, which ultimately promote inflammation. Moreover, HMGB1 may be involved in the pathogenesis of asthma by regulating downstream signaling pathways through corresponding receptors and mediates a number of signaling pathways in asthma, such as HMGB1/TLR4/NF‐κB, HMGB1/RAGE, HMGB1/TGF‐β, and so forth. Accordingly, HMGB1 emerges as a therapeutic target for asthma