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作者：范志阳，周 玥，张振宇 

白细胞介素-8（IL-8）；

肿瘤坏死因子－α（，ＴＮＦ－α）；

白细胞介素-8；

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作者：张玮晶，李文香，闫菁强，崔 伟，谭世通，李 辉

血清促卵泡素( FSH) ;

促黄体生成素( LH) ;

雌二醇( E ) 和孕酮水平;

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作者：顾宇、岳馨、韩翃、吴贤、罗文、徐涛    

乙酰胆碱；

5-羟色胺；

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Prostate-specific antigen (PSA) is a key marker for a
prostate cancer diagnosis. The low sensitivity of traditional lateralflow immunoassay (LFIA) methods makes them unsuitable forpoint-of-care testing. Herein, we designed a nanozyme by in situgrowth of Prussian blue (PB) within the pores of dendriticmesoporous silica (DMSN). The PB was forcibly dispersed into thepores of DMSN, leading to an increase in exposed active sites.Consequently, the atom utilization is enhanced, resulting insuperior peroxidase (POD)-like activity compared to that ofcubic PB. Antibody-modified DMSN@PB nanozymes serve asimmunological probes in an enzymatic-enhanced colorimetric andphotothermal dual-signal LFIA for PSA detection. After systematicoptimization, the LFIA based on DMSN@PB successfully achievesa 4-fold amplification of the colorimetric signal within 7 min through catalytic oxidation of the chromogenic substrate by POD-likeactivity. Moreover, DMSN@PB exhibits an excellent photothermal conversion ability under 808 nm laser irradiation. Accordingly,photothermal signals are introduced to improve the anti-interference ability and sensitivity of LFIA, exhibiting a wide linear range(1−40 ng mL−1) and a low PSA detection limit (0.202 ng mL−1), which satisfies the early detection level of prostate cancer. Thisresearch provides a more accurate and reliable visualization analysis methodology for the early diagnosis of prostate cancer.    

前列腺特异性抗原（PSA）；

PSA抗原；

PSA抗体；

山羊抗小鼠免疫球蛋白（IgG）；

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Acute lung injury (ALI) is characterized by pulmonary diffusion abnormalities that may progress to multiple- organ failure in severe cases. There are limited effective treatments for ALI, which makes the search for new therapeutic avenues critically important. Macrophages play a pivotal role in the pathogenesis of ALI. The degree of macrophage polarization is closely related to the severity and prognosis of ALI, and S100A9 promotes M1 polarization of macrophages. The present study assessed the effects of S100A9-gene deficiency on macrophage polarization and acute lung injury. Our cohort study showed that plasma S100A8/A9 levels had significant diagnostic value for pediatric pneumonia and primarily correlated with monocyte-macrophages and neutrophils. We established a lipopolysaccharide (LPS)-induced mouse model of acute lung injury and demonstrated that knockout of the S100A9 gene mitigated inflammation by suppressing the secretion of pro-inflammatory cyto-kines, reducing the number of inflammatory cells in the bronchoalveolar lavage fluid, and inhibiting cell apoptosis, which ameliorated acute lung injury in mice. The in vitro and in vivo mechanistic studies demon-strated that S100A9-gene deficiency inhibited macrophage M1 polarization and reduced the levels of pulmonary macrophage chemotactic factors and inflammatory cytokines by suppressing the TLR4/MyD88/NF-κB signaling pathway and reversing the expression of the NLRP3 pyroptosis pathway, which reduced cell death. In conclusion, S100A9-gene deficiency alleviated LPS-induced acute lung injury by inhibiting macrophage M1 polarization and pyroptosis via the TLR4/MyD88/NFκB pathway, which suggests a potential therapeutic strategy for the treat-ment of ALI.    

SYP-M0026；

小鼠白细胞介素1β(IL-1β)检测试剂盒；