Anti-periodic solutions for a class of third-order nonlinear differential equations with a deviating argument

In this paper, we study a class of third-order nonlinear differential equations with a deviating argument and establish some sufficient conditions for the existence and exponential stability of anti-periodic solutions of the equation. These conditions are new and complement to previously known results

Real-time observation and control of optical chaos

Optical chaotic system is a central research topic due to its scientific importance and practical relevance in key photonic applications such as laser optics and optical communication. Because of the ultrafast propagation of light, all previous studies on optical chaos are based on either static imaging or spectral measurement, which shows only time-averaged phenomena. The ability to reveal real-time optical chaotic dynamics and, hence, control its behavior is critical to the further understanding and engineering of these systems. Here, we report a real-time spatial-temporal imaging of an optical chaotic system, using compressed ultrafast photography. The time evolution of the system’s phase map is imaged without repeating measurement. We also demonstrate the ability to simultaneously control and monitor optical chaotic systems in real time. Our work introduces a new angle to the study of nonrepeatable optical chaos, paving the way for fully understanding and using chaotic systems in various disciplines

Oxidative Degradation of Fentanyl in Aqueous Solutions of Peroxides and Hypochlorites

Fentanyl widely used in clinics as practices is potentially utilised as an incapacitant in countering terrorism and its analogues would be used as an addictive drug, so the degradation of these compounds need to be investigated for protecting environment and human health. In this work, the degradation of fentanyl was examined in a series of oxidant aqueous solutions. Meanwhile, the degradation pathways of fentanyl in the oxidant solution were discussed according to all products identified by GC/MS and LC/MS.Defence Science Journal, 2011, 61(1), pp.30-35, DOI:http://dx.doi.org/10.14429/dsj.61.6

Advances in genetic variation in metabolism-related fatty liver disease

Metabolism-related fatty liver disease (MAFLD) is the most common form of chronic liver disease in the world. Its pathogenesis is influenced by both environmental and genetic factors. With the upgrading of gene screening methods and the development of human genome project, whole genome scanning has been widely used to screen genes related to MAFLD, and more and more genetic variation factors related to MAFLD susceptibility have been discovered. There are genetic variants that are highly correlated with the occurrence and development of MAFLD, and there are genetic variants that are protective of MAFLD. These genetic variants affect the development of MAFLD by influencing lipid metabolism and insulin resistance. Therefore, in-depth analysis of different mechanisms of genetic variation and targeting of specific genetic variation genes may provide a new idea for the early prediction and diagnosis of diseases and individualized precision therapy, which may be a promising strategy for the treatment of MAFLD

FOXD1 Promotes Cell Growth and Metastasis by Activation of Vimentin in NSCLC

Background/Aims: Forkhead box D1 (FOXD1) has a well-established role in early embryonic development and organogenesis and functions as an oncogene in several cancers. However, the clinical significance and biological roles of FOXD1 in non-small cell lung cancer (NSCLC) remain largely unknown. Methods: A total of 264 primary NSCLC tissue samples were collected. The expression levels of FOXD1 in these samples were examined by immunohistochemical staining. The expression of FOXD1 was knocked down by lentiviral shRNA. The relative expression of FOXD1 was determined by qRT-PCR, Western blotting and immunofluorescence image. The functional roles of FOXD1 in NSCLC were demonstrated cell viability CCK-8 assay, colony formation, cell invasion and migration assays, and cell apoptosis assay in vitro. In vivo mouse xenograft and metastasis models were used to assess tumorigenicity and metastatic ability. The Chi-square test was used to assess the correlation between FOXD1 expression and the clinicopathological characteristics. Survival curves were estimated by Kaplan-Meier method and compared using the log-rank test. The Cox proportional hazards model was used for univariate and multivariate analyses. Results: We determined that higher levels of FOXD1 were present in NSCLC tissues, especially in metastatic NSCLC tissues. FOXD1 was also higher in all NSCLC cells compared with normal human bronchial epithelial cells. A higher expression level of FOXD1 was associated with malignant behavior and poor prognosis in NSCLC patients. Knockdown of FOXD1 significantly inhibited proliferation, migration, and invasion in vitro and tumor growth and metastasis in vivo, and it increased the apoptosis rates of NSCLC cells. Mechanistic analyses revealed that FOXD1 expressed its oncogenic characteristics through activating Vimentin in NSCLC. Multivariate Cox regression analysis indicated that FOXD1 was an independent prognostic factor both for overall survival (OS) and disease-free survival (DFS) in NSCLC patients. Conclusion: Our results indicated that FOXD1 might be involved in the development and progression of NSCLC as an oncogene, and thereby might be a potential therapeutic target for NSCLC patients

Distinct roles of the IRE1α arm and PERK arm of unfolded protein response in arachidonic acid-induced ferroptosis in hepatocytes

Ferroptosis is a distinct form of cell death that is driven by iron-dependent phospholipid peroxidation. Polyunsaturated fatty acids (PUFAs), particularly arachidonic acid (AA) and adrenal acid (AdA), are most prone to lipid peroxidation, which induces ferroptosis and affects the function of cell membranes. In this study, we discovered that AA induces ferritinophagy in hepatocytes, a selective form of autophagy that degrades ferritin, triggering unstable iron overload. Mechanistically, AA enhances cellular uptake of bound iron by up-regulating transferrin receptor 1 (TfR1). Additionally, AA induces endoplasmic reticulum stress (ER stress) and simultaneously activates two of its branches, pancreatic ER kinase (PERK) and inositol-requiring enzyme 1 (IRE1). Notably, PERK and IRE1 appear to play distinct roles in inducing ferritinophagy. Inhibition of PERK reduced the AA-induced increase of Fe2+ by alleviating ferritinophagy, while inhibition of IRE1 further exacerbated ferroptosis by activating ferritinophagy. Furthermore, there seems to be an interaction between the signaling pathways of ER stress, and inhibition of IRE1 exacerbates AA-induced ferritinophagy by further activating the PERK signaling pathway, thereby exacerbating the extent of cell death. Collectively, our findings suggest that iron overload is involved in AA-induced hepatocyte ferroptosis and that this process is regulated by ER stress-mediated ferritinophagy. This study suggests potential therapeutic strategies for treating liver diseases related to lipid metabolism disorders by intervening in the ferroptosis process