Development of Magnetic Molecularly Imprinted Polymer Coupled Nanospray Ion Source for Analysis of Cephalosporin Antibiotics in Food Samples.

A magnetic molecularly imprinted polymer (MMIP) coupled nanospray ion source was developed for analysis of cephalosporin antibiotics in food samples. MIP coated Fe3O4 nanospheres were prepared for magnetic solid-phase extraction (MSPE) of the antibiotics in the extract of samples and then integrated into the nanospray capillary for further desorption and mass spectrometry analysis. The developed device combines the advantages of high extraction efficiency of MSPE, unique selectivity of MIPs, and fast analysis speed of ambient ionization mass spectrometry (AIMS). Five cephalosporin antibiotics in milk, egg, and beef samples were analyzed using the developed methods. High sensitivities with limits of detection (LODs) from 0.3 to 0.5 µg kg-1 were achieved for cephalosporin antibiotics in milk, egg, and beef samples, respectively. Good linearity, determination coefficient values (R2 > 0.992), and precision (RSD < 15%) with recoveries ranging from 72.6% to 115.5% were obtained using the spiked milk, egg, and beef sample matrices.

Analysis of the impact of ERAS-based respiratory function training on older patients' ability to prevent pulmonary complications after abdominal surgery.

BACKGROUND: In China, as the population grows older, the number of elderly people who have died from respiratory problems has increased. AIM: To investigate whether enhanced recovery after surgery (ERAS)-based respiratory function training may help older patients who had abdominal surgery suffer fewer pulmonary problems, shorter hospital stays, and improved lung function. METHODS: The data of 231 elderly individuals having abdominal surgery was retrospectively analyzed. Based on whether ERAS-based respiratory function training was provided, patients were divided into ERAS group (n = 112) and control group (n = 119). Deep vein thrombosis (DVT), pulmonary embolism (PE), and respiratory tract infection (RTI) were the primary outcome variables. Secondary outcome variables included the Borg score Scale, FEV1/FVC and postoperative hospital stay. RESULTS: The percentage of 18.75% of ERAS group participants and 34.45% of control group participants, respectively, had respiratory infections (P = 0.007). None of the individuals experienced PE or DVT. The ERAS group's median postoperative hospital stay was 9.5 d (3-21 d) whereas the control groups was 11 d (4-18 d) (P = 0.028). The Borg score decreased on the 4th d following surgery in the ERAS group compared to the 2nd d prior (P = 0.003). The incidence of RTIs was greater in the control group than in the ERAS group among patients who spent more than 2 d in the hospital before surgery (P = 0.029). CONCLUSION: ERAS-based respiratory function training may reduce the risk of pulmonary complications in older individuals undergoing abdominal surgery.

Bergamottin alleviates LPS-induced acute lung injury by inducing SIRT1 and suppressing NF-κB.

Acute lung injury (ALI) is associated with a high mortality due to inflammatory cell infiltration and lung edema. The development of ALI commonly involves the activation of NF-κB. Since bergamottin is a natural furanocoumarin showing the ability to inhibit the activation of NF-κB, in this study we aimed to determine the effect of bergamottin on ALI. RAW264.7 mouse macrophages were pre-treated with bergamottin and then stimulated with LPS. Macrophage inflammatory responses were examined. Bergamottin (50 mg/kg body mass) was intraperitoneally administrated to mice 12 h before injection of LPS, and the effect of bergamottin on LPS-induced ALI was evaluated. Our results showed that LPS exposure led to increased production of TNF-α, IL-6, and monocyte chemoattractant protein-1 (MCP-1), which was impaired by bergamottin pre-treatment. In vivo studies confirmed that bergamottin pre-treatment suppressed LPS-induced lung inflammation and edema and reduced the levels of pro-inflammatory cytokines in lung tissues and bronchoalveolar lavage fluids. Mechanistically, bergamottin blocked LPS-induced activation of NF-κB signaling in lung tissues. Additionally, bergamottin treatment reduced NF-κB p65 protein acetylation, which was coupled with induction of SIRT1 expression. In conclusion, our results reveal the anti-inflammatory property of bergamottin in preventing ALI. Induction of SIRT1 and inhibition of NF-κB underlies the anti-inflammatory activity of bergamottin.

Mitofusion 2 Overexpression Decreased Proliferation of Human Embryonic Lung Fibroblasts in Acute Respiratory Distress Syndrome through Inhibiting RAS-RAF-1-ERK1/2 Pathway.

Acute respiratory distress syndrome (ARDS) is one of the most fatal diseases worldwide. Pulmonary fibrosis occurs early in ARDS, and its severity plays a crucial role in ARDS mortality rate. Some studies suggested that fibroproliferation is an essential mechanism in ARDS. Mitofusion2 (Mfn2) overexpression plays a role in inhibiting cell proliferation. However, the role and potential mechanism of Mfn2 on the proliferation of fibroblasts is still unknown. In this study, we aimed at exploring the effect of Mfn2 on the human embryonic lung fibroblasts (HELF) and discussed its related mechanism. The HELF were treated with the Mfn2 overexpressing lentivirus (adv-Mfn2). The cell cycle was detected by flow cytometry. MTT, PCR and Western blotting were used to investigate the effect of Mfn2 on the proliferation of the HELF, collagen expression, the RAS-RAF-1-ERK1/2 pathway and the expression of cycle-related proteins (p21, p27, Rb, Raf-1, p-Raf-1, Erk1/2 and p-Erk1/2). The co-immunoprecipitation assay was used to explore the interaction between Mfn2 and Ras. The results showed that the overexpression of Mfn2 inhibited the proliferation of the HELF and induced the cell cycle arrest at the G0/G1 phase. Meanwhile, Mfn2 also inhibited the expression of collagen I, p-Erk and p-Raf-1. In addition, an interaction between Mfn2 and Ras existed in the HELF. This study suggests that the overexpression of Mfn2 can decrease the proliferation of HELF in ARDS, which was associated with the inhibition of the RAS-RAF-1-ERK1/2 pathway. The results may offer a potential therapeutic intervention for patients with ARDS.