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Background: Pesticide formulations based on nanotechnology can effectively improve the efficiency of pesticide utilization and reduce pesticide residues in the environment. In this study, mesoporous silica nanoparticles containing disulfide bonds were synthesized by the sol–gel method, carboxylated and adsorbed with lufenuron, and grafted with cellulose to obtain a lufenuron‐loaded nano‐controlled release formulation (Luf@MSNs‐ss‐cellulose). Results: The structure and properties of Luf@MSNs‐ss‐cellulose were characterized. The results showed that Luf@MSNs‐ss‐cellulose exhibits a regular spherical shape with 12.41% pesticide loading. The highest cumulative release rate (73.46%) of this pesticide‐loaded nanoparticle was observed at 7 days in the environment of glutathione and cellulase, which shows redox‐enzyme dual‐responsive performance. As a result of cellulose grafting, Luf@MSNs‐ss‐cellulose had a small contact angle and high adhesion work on corn leaves, indicating good wetting and adhesion properties. After 14 days of spraying with 20 mg L−1 formulations in the long‐term control efficacy experiment, the mortality of Luf@MSNs‐ss‐cellulose against Ostrinia furnacalis larvae (56.67%) was significantly higher than that of commercial Luf@EW (36.67%). Luf@MSNs‐ss‐cellulose is safer for earthworms and L02 cells. Conclusion: The nano‐controlled release formulation obtained in this study achieved intelligent pesticide delivery in time and space under the environmental stimulation of glutathione and cellulase, providing an effective method for the development of novel pesticide delivery systems. © 2023 Society of Chemical Industry. [ABSTRACT FROM AUTHOR]

The canonical Wnt signaling pathway is activated in numerous contexts, including normal and cancerous tissues. Here, we describe a synthetic cell‐based therapeutic strategy that inhibits aberrant Wnt activity in specific focuses without interfering with the normal tissues in vivo. As a proof of principle, we generated a triple transgenic zebrafish liver cancer model that conditionally expressed human MET and induced ectopic Wnt signaling in hepatocytes. Then, we generated a customized synthetic Notch receptor (synNotch) cascade to express Wnt inhibitor DKK1 in Jurkat T cells and human peripheral blood mononuclear cells (PBMCs) after recognizing MET as antigen. After that, the synNotch PBMCs were sorted and microinjected into different tissues of the zebrafish model. In MET‐expressing cancerous liver tissues, the injected cells expressed DKK1 and inhibited the local proliferation and Wnt activity; while in the yolk sac without MET, the injected cells remained inactive. Overall, our studies revealed the use of synthetic cells with antigen receptors to improve the spatiotemporal accuracy of anti‐Wnt therapy, and proposed that the genetically humanized zebrafish model may serve as a small‐scale and highly optically accessible platform for the functional evaluation of human synthetic cells. What's new? Aberrant regulation of the Wnt signaling pathway plays a critical role in cancer pathogenesis. Despite extensive knowledge of this pathway, however, drugs targeting Wnt and Wnt family proteins have shown limited promise. Here, using synthetic cells and a double‐humanized zebrafish model system, the authors generated MET‐targeting synthetic Notch cells expressing the negative Wnt regulator Dickkopf‐1 (DKK1). Upon injection into the hepatic region of zebrafish, synNotch‐modified peripheral blood mononuclear cells recognized MET antigens, leading to conditional DKK1 expression and Wnt repression. The findings demonstrate the successful application of synthetic cells and a small animal model to the design of Wnt‐targeting therapies. [ABSTRACT FROM AUTHOR]

Human hearing loss is a common neurosensory disorder about which many basic research and clinically relevant questions are unresolved. At least 50% of hearing loss are due to a genetic etiology. Although hundreds of genes have been reported, there are still hundreds of related deafness genes to be found. Clinical, genetic, and functional investigations were performed to identify the causative mutation in a distinctive Chinese family with postlingual nonsyndromic sensorineural hearing loss. Whole-exome sequencing (WES) identified lipoprotein receptor-related protein 5 ( LRP5), a member of the low-density lipoprotein receptor family, as the causative gene in this family. In the zebrafish model, lrp5 downregulation using morpholinos led to significant abnormalities in zebrafish inner ear and lateral line neuromasts and contributed, to some extent, to disabilities in hearing and balance. Rescue experiments showed that LRP5 mutation is associated with hearing loss. Knocking down lrp5 in zebrafish results in reduced expression of several genes linked to Wnt signaling pathway and decreased cell proliferation when compared with those in wild-type zebrafish. In conclusion, the LRP5 mutation influences cell proliferation through the Wnt signaling pathway, thereby reducing the number of supporting cells and hair cells and leading to nonsyndromic hearing loss in this Chinese family. [ABSTRACT FROM AUTHOR]

Background The pathogenesis and progression of branch atheromatous disease ( BAD), which differs from lipohyalinotic degeneration ( LD), remains controversial. Few studies have investigated the lipid indices and glycometabolism status factors for BAD in first-ever penetrating artery infarction ( PAI). Methods We retrospectively examined acute stroke patients with PAI admitted within 3 days after stroke. All patients underwent diffusion weight magnetic resonance imaging ( DWI) and magnetic resonance angiography ( MRA) and/or computed tomography angiography ( CTA). Progression was defined as an increase by 2 point or higher in the National Institutes of Health Stroke Scale score. The characteristics, clinical data were statistically analyzed. Results BAD and LD were diagnosed in 142 (57%) and 107 (43%) patients, respectively. Patients with BAD had higher low-density lipoprotein cholesterol ( LDL-C) compared with those with LD ( p = .013). Elevated LDL-C was related to early neurological deterioration in patients with BAD ( p = .045). The percentage of lenticulostriate arterial ( LSA) infarction was greater than that of the pontine penetrating arterial ( PPA) infarction in acute PAI (75.1% vs. 24.9%; p < .001). PPA infarction was more prevalent in the BAD group compared with the LD group (34.5% vs. 12.1%, p < .001). The PPA infarction had older age at onset and higher HbA1c concentrations than those with the LSA infarction ( p = .014, p = .036 respectively) in the BAD and LD patients, respectively. Conclusion LDL-C may be associated with both the pathogenesis and progression of intracranial BAD. The LSA infarction was the most frequently subtypes in PAI. Age at onset and HbA1c seem to be closely associated with the PPA infarction of first-ever PAI. [ABSTRACT FROM AUTHOR]

Activation of lymphatic cells is associated with changes in morphology, ultrastructure and adhesion force. We have investigated the activation efficiency of Staphylococcus aureus (SAC) on B-cell chronic lymphatic leukaemia (B-CLL) cells using atomic force microscopy (AFM), and found changes in the above properties. Cell viability and proliferation were measured using Cell Counting Kit-8 (CCK-8) and enzyme-linked immunosorbent assay (ELISA). AFM clearly showed that the volume and nuclear-cytoplasm ratio of cells increased significantly with activated time. It also showed that pseudopodia and immunological synapses began to appear at 24 h. In the activation process, nano-structures of the cell surface became aggregated, and adhesion increased. In conclusion, the results indicate a close relationship between membrane reconstruction and multiplication process of B-CLL cells. [ABSTRACT FROM AUTHOR]