Ion-specific ice provides a facile approach for reducing ice friction.

HYPOTHESIS: Ice friction plays a crucial role in both basic study and practical use. Various strategies for controlling ice friction have been developed. However, one unsolved puzzle regarding ice friction is the effect of ion-ice interplay on its tribological properties. EXPERIMENTS AND SIMULATIONS: Here, we conducted ice friction experiments and summarized the specific effects of hydrated ions on ice friction. By selecting cations and anions, the coefficient of ice friction can be reduced by more than 70 percent. Experimental spectra, low-field nuclear magnetic resonance (LF-NMR), density functional theory (DFT) calculations, and Molecular dynamics (MD) simulations demonstrated that the addition of ions could break the H-bonds in water. FINDINGS: The link between the charge density of ions and the coefficients of ice friction was revealed. A part of the ice structure was changed from an ice-like to a liquid-like interfacial water structure with the addition of ions. Lower charge density ions led to weaker ionic forces with the water molecules in the immobilized water layer, resulting in free water molecules increasing in the lubricating layer. This study provides guidance for preparing ice-making solutions with low friction coefficients and a fuller understanding of the interfacial water structure at low temperatures.

Effect of the Molecular Structure of 1,3-Diketones on the Realization of Oil-Based Superlubricity on Steel/Steel Friction Pairs.

In this article, five kinds of 1,3-diketones and their chelates with different molecular structures were prepared, and their tribological properties were tested. The experimental results show that the running-in time and friction coefficient of the friction pairs lubricated by 1,3-diketones containing a benzene ring increased with the increase of the carbon chain length. In addition, only the friction pair lubricated by 1-(4-ethylphenyl)-butane-1,3-dione (0201) and 1-(4-ethylphenyl)-nonane-1,3-dione (0206) could achieve stable superlubricity. When the benzene ring was replaced with a carbon six-membered ring, it was found that although the friction pair lubricated by this lubricant could achieve superlubricity, the wear of the friction pair was severe, and obvious abrasive wear occurred. In addition, the lubricants prepared by mixing 1,3-diketones and the corresponding chelates in a ratio of 4:6 had greatly improved lubricating properties compared to 1,3-diketones. Through X-ray photoelectron spectroscopy (XPS) analysis of the surface of the friction pair after the test and Fourier transform infrared (FT-IR) and nuclear magnetic resonance (NMR) analyses of 1,3-diketones before and after the experiment, we found that the necessary conditions for the friction pair lubricated by 1,3-diketone to achieve superlubricity were formation of tribochemical adsorption films and the presence of chelates in solution.

Intercellular mitochondrial transfer in the brain, a new perspective for targeted treatment of central nervous system diseases.

AIM: Mitochondria is one of the important organelles involved in cell energy metabolism and regulation and also play a key regulatory role in abnormal cell processes such as cell stress, cell damage, and cell canceration. Recent studies have shown that mitochondria can be transferred between cells in different ways and participate in the occurrence and development of many central nervous system diseases. We aim to review the mechanism of mitochondrial transfer in the progress of central nervous system diseases and the possibility of targeted therapy. METHODS: The PubMed databank, the China National Knowledge Infrastructure databank, and Wanfang Data were searched to identify the experiments of intracellular mitochondrial transferrin central nervous system. The focus is on the donors, receptors, transfer pathways, and targeted drugs of mitochondrial transfer. RESULTS: In the central nervous system, neurons, glial cells, immune cells, and tumor cells can transfer mitochondria to each other. Meanwhile, there are many types of mitochondrial transfer, including tunneling nanotubes, extracellular vesicles, receptor cell endocytosis, gap junction channels, and intercellular contact. A variety of stress signals, such as the release of damaged mitochondria, mitochondrial DNA, or other mitochondrial products and the elevation of reactive oxygen species, can trigger the transfer of mitochondria from donor cells to recipient cells. Concurrently, a variety of molecular pathways and related inhibitors can affect mitochondrial intercellular transfer. CONCLUSION: This study reviews the phenomenon of intercellular mitochondrial transfer in the central nervous system and summarizes the corresponding transfer pathways. Finally, we propose targeted pathways and treatment methods that may be used to regulate mitochondrial transfer for the treatment of related diseases.

The driving mechanism and targeting value of mimicry between vascular endothelial cells and tumor cells in tumor progression.

The difficulty and poor prognosis of malignant tumor have always been a difficult problem to be solved. The internal components of solid tumor are complex, including tumor cells, stromal cells and immune cells, which play an important role in tumor proliferation, migration, metastasis and drug resistance. Hence, targeting of only the tumor cells will not likely improve survival. Various studies have reported that tumor cells and endothelial cells have high plasticity, which is reflected in the fact that they can simulate each other's characteristics by endothelial-mesenchymal transition (EndMT) and vasculogenic mimicry (VM). In this paper, this mutual mimicry concept was integrated and reviewed for the first time, and their similarities and implications for tumor development are discussed. At the same time, possible therapeutic methods are proposed to provide new directions and ideas for clinical targeted therapy and immunotherapy of tumor.

Insights on hematopoietic cell kinase: An oncogenic player in human cancer.

Hematopoietic cell kinase (Hck) is a member of the Src family and is expressed in hematopoietic cells. By regulating multiple signaling pathways, HCK can interact with multiple receptors to regulate signaling events involved in cell adhesion, proliferation, migration, invasion, apoptosis, and angiogenesis. However, aberrant expression of Hck in various hematopoietic cells and solid tumors plays a crucial role in tumor-related properties, including cell proliferation and epithelial-mesenchymal transition. In addition, Hck signaling regulates the function of immune cells such as macrophages, contributing to an immunosuppressive tumor microenvironment. The clinical success of various kinase inhibitors targeting the Src kinase family has validated the efficacy of targeting Src, and therapies with highly selective Hck kinase inhibitors are in clinical trials. This article reviews Hck inhibition as an emerging cancer treatment strategy, focusing on the expressions and functions of Hck in tumors and its impact on the tumor microenvironment. It also explores preclinical and clinical pharmacological strategies for Hck targeting to shed light on Hck-targeted tumor therapy.

Regulation of secretory pathway kinase or kinase-like proteins in human cancers.

Secretory pathway kinase or kinase-like proteins (SPKKPs) are effective in the lumen of the endoplasmic reticulum (ER), Golgi apparatus (GA), and extracellular space. These proteins are involved in secretory signaling pathways and are distinctive from typical protein kinases. Various reports have shown that SPKKPs regulate the tumorigenesis and progression of human cancer via the phosphorylation of various substrates, which is essential in physiological and pathological processes. Emerging evidence has revealed that the expression of SPKKPs in human cancers is regulated by multiple factors. This review summarizes the current understanding of the contribution of SPKKPs in tumorigenesis and the progression of immunity. With the epidemic trend of immunotherapy, targeting SPKKPs may be a novel approach to anticancer therapy. This study briefly discusses the recent advances regarding SPKKPs.

Secretory Pathway Kinase FAM20C, a Marker for Glioma Invasion and Malignancy, Predicts Poor Prognosis of Glioma.

PURPOSE: Glioblastoma (GBM) is the most lethal primary cancer in adult central nervous system, and new strategies are desperately needed. The secretory pathway kinase or kinase-like proteins (SPKKPs) have been shown to mediate multiple physiological functions by phosphorylating extracellular proteins and proteoglycans. However, their roles in cancers, especially GBM, remain poorly defined. METHODS: The least absolute shrinkage and selection operator (LASSO) regression was employed for establishing the SPKKPs signature for IDH wild type (wt) GBM prognosis. Integrative analyses with multiple datasets were employed to identify the core member of this gene family in glioma. The receiver operator characteristic (ROC) curves and immunohistochemistry were further used for evaluating its association with progressive malignancy in glioma and GBM patients' survival, respectively. Gene set enrichment analysis (GSEA) and Kyoto Encyclopedia of Genes and Genomes (KEGG) were used to interpret its functions in GBM, which were further verified in vitro. RESULTS: A SPKKPs classifier was constructed with 3 genes of this family. This signature could effectively distinguish IDH wt GBM survival. Family with sequence similarity 20 C (FAM20C) was further identified as the core member of this family in glioma. Elevated FAM20C expression was not only closely correlated with glioma malignancy progression and the mesenchymal subtype of GBM but also indicated unfavorable survival of GBM patients. FAM20C was also found to be associated with the disrupted immune response in GBM microenvironment and was required for the migration of glioma and immune cells. CONCLUSION: These data indicate that the potential of FAM20C serving as a predictive molecule and a therapeutic target for GBM.

Application of graphene derivatives and their nanocomposites in tribology and lubrication: a review.

Reducing friction and increasing lubrication are the goals that every tribologist pursues. Accordingly, layered graphene materials have attracted great research interest in tribology due to their anti-friction, anti-wear and excellent self-lubricating properties. However, recent studies have found that other forms of graphene derivatives not only perform better in tribological and lubricating applications, but also solve the problem of graphene being prone to agglomeration. Based on a large number of reports, herein, we review the research progress on graphene derivatives and their nanocomposites in tribology and lubrication. In the introduction, the topic of the article is introduced by highlighting the hazards and economic losses caused by frictional wear and the excellent performance of graphene materials in the field of lubrication. Then, by studying the classification of graphene materials, the research status of their applications in tribology and lubrication is introduced. The second chapter introduces the application of graphene derivatives in improving tribological properties. The main types of graphene are graphene oxide (GO), doped graphene (doped elements such as nitrogen, boron, phosphorus, and fluorine), graphene-based films, and graphene-based fibers. The third chapter summarizes the application of graphene-based nanocomposites in improving friction and anti-wear and lubrication properties. According to the different functional modifiers, they can be divided into three categories: graphene-inorganic nanocomposites (sulfides, metal oxides, nitrides, metal nanoparticles, and carbon-containing inorganic nanoparticles), graphene-organic nanocomposites (alkylation, amine functionalization, ionic liquids, and surface modifiers), and graphene-polymer nanocomposites (carbon chain polymers and heterochain polymers). Graphene not only exhibits an excellent performance in traditional processing and lubrication applications, but the fourth chapter proves that it has a good application prospect in the field of ultra-low friction and superlubricity. In the application part of the fifth chapter, the lubrication mechanism proposed by graphene as a nano-lubricant is introduced first; then, the main application research status is summarized, including micro-tribology applications, bio-tribology applications, and liquid lubrication additive applications. The last part is based on the following contents. Firstly, the advantages of graphene-based nanocomposites as lubricants and their current shortcomings are summarized. The challenges and prospects of the commercial applications of graphene-based nanocomposites in tribology and lubrication are further described.

Oxygen-glucose deprivation preconditioning protects neurons against oxygen-glucose deprivation/reperfusion induced injury via bone morphogenetic protein-7 mediated ERK, p38 and Smad signalling pathways.

Bone morphogenetic protein (BMP)-7 mediated neuroprotective effect of cerebral ischemic preconditioning (IPC) has been studied in an ischemic animal model, but the underlying cellular mechanisms have not been clearly clarified. In this study, primary cortical neurons and the SH-SY5Y cell line were used to investigate the role of BMP-7 and its downstream signals in the neuroprotective effects of oxygen-glucose deprivation preconditioning (OGDPC). Immunocytochemistry was used to detect the expression of neurofilament in neurons. MTT and lactate dehydrogenase activity assays were used to measure the cytotoxicity. Western blot was used to detect the protein expression of BMP-7 and downstream signals. BMP inhibitor, mitogen-activated protein kinase inhibitors, Smad inhibitor and siRNA of Smad 1 were used to investigate the role of corresponding signalling pathways in the OGDPC. Results showed that OGDPC-induced overexpression of BMP-7 in primary cortical neurons and SH-SY5Y cells. Both of endogenous and exogenous BMP-7 could replicate the neuroprotective effects seen in OGDPC pretreatment. In addition, extracellular regulated protein kinases, p38 and Smad signalling pathway were found to be involved in the neuroprotective effects mediated by OGDPC via BMP-7. This study primarily reveals the cellular mechanisms of the neuroprotection mediated by OGDPC, and provides evidence for better understanding of this intrinsic factor against ischemia.