PPChain: A Blockchain for Pandemic Prevention and Control Assisted by Federated Learning.

Taking COVID-19 as an example, we know that a pandemic can have a huge impact on normal human life and the economy. Meanwhile, the population flow between countries and regions is the main factor affecting the changes in a pandemic, which is determined by the airline network. Therefore, realizing the overall control of airports is an effective way to control a pandemic. However, this is restricted by the differences in prevention and control policies in different areas and privacy issues, such as how a patient's personal data from a medical center cannot be effectively combined with their passenger personal data. This prevents more precise airport control decisions from being made. To address this, this paper designed a novel data-sharing framework (i.e., PPChain) based on blockchain and federated learning. The experiment uses a CPU i7-12800HX and uses Docker to simulate multiple virtual nodes. The model is deployed to run on an NVIDIA GeForce GTX 3090Ti GPU. The experiment shows that the relationship between a pandemic and aircraft transport can be effectively explored by PPChain without sharing raw data. This approach does not require centralized trust and improves the security of the sharing process. The scheme can help formulate more scientific and rational prevention and control policies for the control of airports. Additionally, it can use aerial data to predict pandemics more accurately.

Voluntary Exercise to Reduce Anxiety Behaviour in Traumatic Brain Injury Shown to Alleviate Inflammatory Brain Response in Mice.

Traumatic brain injury is a leading cause of neuroinflammation and anxiety disorders in young adults. Immune-targeted therapies have garnered attention for the amelioration of TBI-induced anxiety. A previous study has indicated that voluntary exercise intervention following TBI could reduce neuroinflammation. It is essential to determine the effects of voluntary exercise after TBI on anxiety via inhibiting neuroinflammatory response. Mice were randomly divided into four groups (sham, TBI, sham + voluntary wheel running (VWR), and TBI + VWR). One-week VWR was carried out on the 2nd day after trauma. The neurofunction of TBI mice was assessed. Following VWR, anxiety behavior was evaluated, and neuroinflammatory responses in the perilesional cortex were investigated. Results showed that after one week of VWR, neurofunctional recovery was enhanced, while the anxiety behavior of TBI mice was significantly alleviated. The level of pro-inflammatory factors decreased, and the level of anti-inflammatory factors elevated. Activation of nucleotide oligomerization domain-like thermal receptor protein domain associated protein 3 (NLRP3) inflammasome was inhibited significantly. All these alterations were consistent with reduced microglial activation at the perilesional site and positively correlated with the amelioration of anxiety behavior. This suggested that timely rehabilitative exercise could be a useful therapeutic strategy for anxiety resulting from TBI by targeting neuroinflammation.

C-Myc participates in ß-catenin-mediated drug resistance in A549/DDP lung adenocarcinoma cells.

The aim of this study was to investigate c-Myc and ß-catenin-mediated drug resistance in A549/DDP lung adenocarcinoma cells. Cisplatin sensitivity was determined by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) toxicity assay. ß-Catenin and c-Myc protein expression following cisplatin treatment were determined using western blotting and immunofluorescence. Flow cytometry was performed to detect cell cycle and apoptosis in A549, A549/DDP, and c-Myc small interfering RNA (siRNA)-transfected A549/DDP cells before and after treatment with different doses of cisplatin. The median inhibitory concentration (IC50 ) in cisplatin-treated A549 and A549/DDP cells was 5.769 ± 0.24 µmol/L and 28.373 ± 0.96 µmol/L, respectively; the cisplatin resistance of A549 cells was about five times that of A549/DDP cells. Endogenous ß-catenin and c-Myc expression in A549/DDP cells were higher than that in A549 cells, and were upregulated in A549/DDP cells (p < 0.05) and downregulated in A549 cells after 48 h cisplatin treatment (p < 0.05). ß-catenin localization transferred from membrane/cytoplasmic/nuclear to cytoplasmic/nuclear, and c-Myc localization transferred from cytoplasmic/nuclear to nuclear in both cell lines following cisplatin treatment. The rate of apoptosis increased in a dose-dependent manner with cisplatin. After 48-h transfection with c-myc siRNA, A549/DDP cells were blocked in the S phase, and G0/G1-phase cells increased. Simultaneously, the apoptotic rate was increased (p < 0.05) and the IC50 decreased significantly (p < 0.05). C-myc, the downstream target gene of ß-catenin, plays an important role in regulating cisplatin resistance in A549/DDP cells. C-Myc siRNA improved the sensitivity of A549/DDP cells to cisplatin.

Inhibition of cytoplasmic GSK-3ß increases cisplatin resistance through activation of Wnt/ß-catenin signaling in A549/DDP cells.

Cisplatin-based chemotherapy is recommended as the first-line therapy for advanced non-small cell lung cancer (NSCLC). However, acquired cisplatin resistance is ubiquitous in patients with NSCLC, but the molecular mechanism of such resistance remains ambiguous. The present study sought to examine the role of the Wnt/ß-catenin signaling pathway in cisplatin resistance by assessing the phosphorylation and subcellular distribution of GSK-3ß in a human lung adenocarcinoma cell line, A549, and its cisplatin-resistant subline, A549/DDP. Total GSK-3ß, phosphorylated GSK-3ß(ser9) and phosphorylated GSK-3ß(tyr216) in cytoplasmic and nuclear fractions of A549/DDP and A549 cells were examined by western blot analysis. The regulation of cisplatin resistance, apoptosis, ß-catenin and survivin protein expression by inhibition of cytoplasmic GSK-3ß were determined by MTT assay, flow cytometry analysis, immunofluorescence technique and western blot analysis. In the present study, cytoplasmic levels of p-GSK-3ß(ser9) were significantly increased in A549/DDP cells as compared with A549 cells (P<0.01), and these levels were further increased by cisplatin treatment in A549/DDP cells (P<0.01). In contrast, cytoplasmic levels of p-GSK-3ß(ser9) were reduced in A549 cells after treatment with cisplatin (P<0.01). However, cytoplasmic levels of p-GSK-3ß(tyr216) were significantly decreased in A549/DDP cells as compared with A549 cells (P<0.01), and these levels were further decreased by cisplatin treatment in A549/DDP cells (P<0.01). Conversely, cytoplasmic levels of p-GSK-3ß(tyr216) were raised in A549 cells after treatment with cisplatin (P<0.01). Analysis of downstream effectors of the Wnt/ß-catenin signaling pathway revealed upregulation of ß-catenin and survivin expression in A549/DDP cells treated with cisplatin as compared to untreated cells. In A549 cells, cisplatin treatment decreased the expression of ß-catenin and survivin. Furthermore, phosphorylation of GSK-3ß at serine 9 by LiCl and transient interference of GSK-3ß by siRNA increased ß-catenin and survivin protein expression in A549/DDP cells. Low exogenous and endogenous cytoplasmic GSK-3ß expression enhanced the IC50 and inhibited apoptosis. In conclusion, activation of the Wnt/ß-catenin signaling pathway and upregulated survivin expression due to cytoplasmic GSK-3ß inhibition might lead to cisplatin resistance in NSCLC.

Expression of ezrin correlates with malignant phenotype of lung cancer, and in vitro knockdown of ezrin reverses the aggressive biological behavior of lung cancer cells.

Ezrin, one of the ezrin-radixin-moesin proteins, is involved in the formation of cell membrane processes such as lamellipodia and filopodia and acts as a membrane-cytoskeleton linker. Its aberrant expression correlates with development and progression of several human cancers. However, the expression of ezrin and its role in lung cancer are currently unknown. In this study, we performed ezrin small interfering RNA transfection in two lung cancer cell lines and examined the effects on malignant phenotypes in cancer cells by using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, wound healing, and chamber transwell assays. Ezrin knockdown significantly reduced the proliferation, migration, and invasion of lung cancer cells in vitro. To address the possible mechanisms, we evaluated the expression of adhesion molecules E-cadherin and ß-catenin by Western blot and reverse transcriptase-polymerase chain reaction analyses. The results demonstrated that downregulation of ezrin reduced ß-catenin and increased E-cadherin at the protein level but had no effects on their mRNA levels, suggesting posttranscriptional regulation of these two adhesion molecules. Immunofluorescence assays revealed that ezrin knockdown restored membranous expression of E-cadherin and decreased cytoplasmic ß-catenin in lung cancer cells. In addition, ezrin expression was immunohistochemically evaluated on 135 normal and 183 lung cancer tissues. The expression of ezrin was significantly higher in cancer samples than paired autologous normal lung tissues. In normal bronchial epithelium, ezrin was mainly localized on the apical membrane, while in lung cancers and metastatic foci, ezrin was primarily distributed in cytoplasm. Among lung cancer tissues, expression of ezrin was higher in the invasive front of primary lesions and the highest in lymphatic metastasis. Statistical analysis demonstrated that ezrin expression correlated significantly with lymphatic metastasis and advanced TNM stage. Our data suggest that ezrin may play a crucial role in governing the biological behavior of lung cancer.

A method of extracting ginsenosides from Panax ginseng by pulsed electric field.

The objective of this study was to develop and optimize a pulsed electric field (PEF) extraction method. Various experimental conditions, including electric field intensity and frequency, were evaluated against extraction methods. The content of six major ginsenosides (Rg(1), Re, Rb(1), Rc, Rb(2), and Rd) were quantified by HPLC. The results indicated that the highest yield of the ginsenoside is 12.69 mg/g by PEF using the conditions of 20 kV/cm electric field intensity, 6000 Hz frequency, 70% ethanol-water solution, and 150 L/h velocity. The yield of the ginsenoside of PEF extraction method is higher than the other five methods, such as microwave-assisted extraction, heat reflux extraction, ultrasonic-assisted extraction, accelerated solvent extraction, and ultrahigh pressure extraction, The whole extraction process of PEF takes less than 1 s, which is much less than the heat reflux extraction method for 6 h and even newly used technique ultrahigh pressure extraction method of 2 min. The high efficiency, shorter extraction times, and lower energy cost of PEF extraction method can be applied in the industrial production of saponins from Panax ginseng. The PEF extraction method is a promising and constructive method to extract ginsenosides.