This study proposes a medium optimal method based on DOE methodology and metabolomics of chicken embryo fibroblasts DF-1 cells.

The value of plasma fibronectin (pFN) in the diagnosis and prognosis of sepsis has not been fully established. Previous studies finding that pFN is significantly reduced in sepsis, however, whether reduced pFn affects the prognosis of sepsis has not been clarified. Here, we detected and analyzed pFN and other conventional inflammatory markers in advanced sepsis patients and performed correlation analysis with SOFA score. We also used Fn gene conditional knockout mice which were performed by cecum ligation and puncture (CLP) to investigate the effect of FN deficiency on sepsis prognosis. We found, compared with procalcitonin, c‐reactive protein, and interleukin‐6, pFN was more correlated with SOFA score in advanced sepsis patients ( r −.720, p < .001). In animal experiments, Fn gene knockout mice showed significantly greater mortality after CLP compared with the control group because of inhibited phagocytosis and bacterial clearance ability of macrophages, with double cytokine storm. Furthermore, FN can regulate macrophages through the integrin α5β1/Fak/Src signaling pathway. Overall, we found pFN can more accurately reflect the severity and prognosis of advanced sepsis. The absence of FN altered the cytokine storm and phagocytic function of macrophages, suggesting that FN could be a potential therapeutic target in sepsis.

A photoelectrochemical immunoassay was devised to detect CA-125 employing enzyme-catalyzed precipitation on hollow porous In ₂ O ₃ nanotubes with CdS nanoparticles.

A novel capacitance immunosensor based on DNAzyme concatemer-amplified signal-generation tags was developed for the sensitive detection of interleukin-6 (IL-6) on an interdigitated micro-comb electrode. To construct such an immunosensor, monoclonal mouse anti-human IL-6 antibodies were covalently conjugated onto a bovine serum albumin (BSA)-coated electrode using the glutaraldehyde cross-linker. Gold nanoparticles heavily functionalized with primer DNA (for the subsequent rolling cycle amplification; RCA) and polyclonal rabbit anti-human IL-6 antibodies were used for the development of a sandwich-type immunoassay on the modified interdigitated electrode in the presence of the target IL-6. Thereafter, the attached primer DNA with the immunocomplex triggered the RCA reaction for the formation of numerous DNAzyme concatemers with the assistance of hemins and G-rich DNA probes. DNAzyme concatemers catalyzed 4-chloro-1-naphthol into insoluble benzo-4-chlorohexadienone and were deposited onto the electrode, thus resulting in the local capacitance variation of the interdigitated micro-comb electrode. The performance and external factors affecting the analytical properties were studied in detail. Under optimum conditions, the capacitance variations of the immunosensor were proportional to the IL-6 concentration in the dynamic range of 1.0–1000 pg mL⁻¹ at a detection limit of 0.68 pg mL⁻¹. Good reproducibility, high specificity and acceptable storage stability were acquired for the analysis of the target IL-6. Moreover, the capacitance immunosensor was utilized to determine IL-6 in human serum specimens and gave well-matched analytical results in reference to the human IL-6 ELISA kit.

Most ovarian cancer (OC) tumors are P53-mutant with some mutant P53 proteins possesses an oncogenic activity in OC development. Glycogen synthase kinase 3β (GSK3β), an enzyme closely relates to OC development was found to regulate P53 abundance in several cancer cells, however, whether GSK3β regulates P53 protein expression in OC is unknown. We initially aimed to address this issue, which led to identify a novel signaling axis involved in DNA damage repair in OC cell lines. We found GSK3β reversely regulated P53 signaling across ovarian OC cell lines. Inhibition of GSK3β impeded the homogenous recombination (HR) signaling pathway for DNA damage repair thus caused DNA damage, which was responsible for the raised P53 expression in the HR-proficient OC cells. The raised P53, whether mutated or not, attenuated DNA damage caused by GSK3β inhibition. We further confirmed PLK1/Aurora A axis was governed by GSK3β. Inhibition of GSK3β activated PLK1 via Aurora A in ovarian cancer cells and activation of PLK1 related to DNA damage repair. Double inhibition of GSK3β and PLK1 had a synergistic effect on inducing DNA damage and cell apoptosis in OC cells, which stands as a promising therapeutic strategy for OC.