Superlubricity of glycerol by self-sustained chemical polishing

International audienceAn impressive superlow coefficient of friction (CoF) as low as 0.004 (nearly equivalent to the rolling coefficient) was obtained by sliding a steel ball against a tetrahedral amorphous diamond-like carbon (ta-C) coating in glycerol under a boundary lubrication regime. X-ray photoelectron spectroscopy (XPS) and atomic force microscopy (AFM) revealed substantial changes in the surface chemistry and topography in the friction track. As shown by XPS analysis, a transfer of iron atoms from the steel ball to the ta-C layer occurred, forming iron oxy-hydroxide (FeOOH) termination on both surfaces. Between them, theoretical calculations show that a nanometre-thick fluid film consisting of glycerol and its degradation products prevents direct contact between the solid surfaces by nm-thick film EHL lubrication and results in the superlow friction, in agreement with the experiment. Furthermore, molecular dynamics (MD) simulations reveal that hydrogen atoms act as "low-friction brushes" between sliding layers of crystalline FeOOH, resulting also in low friction. A new model of sustainable green superlubricity is proposed. The tribo-formation of FeOOH with glycerol leads to a unique polishing process, which in turn leads to a self-sustained Elasto-Hydrodynamic Lubrication (EHL) regime until the very thin fluid film is no more than a few nanometres thick. At lower thicknesses, the hydroxide layer takes over. Wear of the ta-C coating is negligible, while wear on the steel ball is very moderate and acceptable for many practical applications, such as bio-tribology and the food industry, in which green lubrication is especially needed

Extracellular Release of HMGB1 as an Early Potential Biomarker for the Therapeutic Response in a Xenograft Model of Boron Neutron Capture Therapy

Boron neutron capture therapy (BNCT) is a non-invasive therapeutic technique for treating malignant tumors, however, methods to evaluate its therapeutic efficacy and adverse reactions are lacking. High mobility group box 1 (HMGB1) is an inflammatory molecule released during cell death. Therefore, we aimed to investigate HMGB1 as a biomarker for BNCT response, by examining the early responses of tumor cells to 10B-boronophenylalanine (BPA)-based BNCT in the Kyoto University Nuclear Reactor. Extracellular HMGB1 release was significantly increased in human squamous carcinoma SAS and melanoma A375 cells 24 h after neutron irradiation but not after γ-irradiation. At 3 days post-BPA-based BNCT irradiation in a SAS xenograft mouse model, plasma HMGB1 levels were higher than those in the non-irradiation control, and HMGB1 was detected in both nuclei and cytoplasm in tumor cells. Additionally, increased plasma HMGB1 levels post-BNCT irradiation were detected even when tumors decreased in size. Collectively, these results indicate that the extracellular HMGB1 release occurs at an early stage and is persistent when tumors are reduced in size; therefore, it is a potential biomarker for evaluating the therapeutic response during BNCT

A Computational Chemistry Study on Friction of h-MoS2. Part I. Mechanism of Single Sheet Lubrication

International audienceIn this work, we theoretically investigated the friction mechanism of hexagonal MoS2 (a well-known lamellar compound) using a computational chemistry method. First, we determined several parameters for molecular dynamics simulations via accurate quantum chemistry calculations and MoS2 and MoS2-xOx structures were successfully reproduced. We also show that the simulated Raman spectrum and peak shift on X-ray diffraction patterns were in good agreement with those of experiment. The atomic interactions between MoS2 sheets were studied by using a hybrid quantum chemical/classical molecular dynamics method. We found that the predominant interaction between two sulfur layers in different MoS2 sheets was Coulombic repulsion, which directly affects the MoS2 lubrication. MoS2 sheets adsorbed on a nascent iron substrate reduced friction further due to much larger Coulombic repulsive interactions. Friction for the oxygen-containing MoS2 sheets was influenced by not only the Coulomb repulsive interaction but also the atomic-scale roughness of the MoS2/MoS2 sliding interface

Extracellular Release of HMGB1 as an Early Potential Biomarker for the Therapeutic Response in a Xenograft Model of Boron Neutron Capture Therapy

SIMPLE SUMMARY: Boron neutron capture therapy (BNCT) is a non-invasive therapeutic technique for treating malignant tumors, however, there is a lack of methods to evaluate its therapeutic efficacy. Herein, we investigated whether high mobility group box 1 (HMGB1) is a potential biomarker of BNCT response in tumor cells and mice in combination with (10)B-p-boronophenylalanine in the Kyoto University Nuclear Reactor. We observed an increased extracellular HMGB1 release in cancer cells 24 h post-BNCT irradiation, compared to that observed with an equivalent dose of gamma-ray irradiation. High levels of plasma HMGB1 were observed on day 3 post-BNCT irradiation in a xenograft mouse model. These levels were stably detected even when the size of the tumor decreased, suggesting that HMGB1 is a potential biomarker for the therapeutic efficacy of BNCT. ABSTRACT: Boron neutron capture therapy (BNCT) is a non-invasive therapeutic technique for treating malignant tumors, however, methods to evaluate its therapeutic efficacy and adverse reactions are lacking. High mobility group box 1 (HMGB1) is an inflammatory molecule released during cell death. Therefore, we aimed to investigate HMGB1 as a biomarker for BNCT response, by examining the early responses of tumor cells to (10)B-boronophenylalanine (BPA)-based BNCT in the Kyoto University Nuclear Reactor. Extracellular HMGB1 release was significantly increased in human squamous carcinoma SAS and melanoma A375 cells 24 h after neutron irradiation but not after γ-irradiation. At 3 days post-BPA-based BNCT irradiation in a SAS xenograft mouse model, plasma HMGB1 levels were higher than those in the non-irradiation control, and HMGB1 was detected in both nuclei and cytoplasm in tumor cells. Additionally, increased plasma HMGB1 levels post-BNCT irradiation were detected even when tumors decreased in size. Collectively, these results indicate that the extracellular HMGB1 release occurs at an early stage and is persistent when tumors are reduced in size; therefore, it is a potential biomarker for evaluating the therapeutic response during BNCT