DataSheet1_A characterization method for equivalent elastic modulus of rock based on elastic strain energy.PDF

Energy is an internal variable during rock deformation and failure, and its dissipation and conversion law can reflect the rock’s internal damage and deterioration state. Analysis of rock deformation and failure process from the perspective of energy is helpful to deeply understand the mechanism of rock damage, fracture and instability failure, and has important theoretical and practical significance for the stability evaluation and support control of surrounding rock. In this study, through single cyclic loading and unloading (SCLU) experiments, cyclic triaxial loading and unloading (CTLU) experiments and conventional triaxial compression (CTC) experiments, the equivalent elastic modulus method based on elastic strain energy is proposed to analyze the energy conversion of rock. The results show that the error of the elastic strain energy calculated by the strain energy formula method is generally higher than 10% with the secant and tangent modulus of the loading and unloading curve as input parameters. Taking the equivalent elastic modulus proposed in this study as an input parameter, more accurate elastic strain energy can be obtained by the strain energy formula. During the rock failure process, the equivalent elastic modulus shows a three-stage characteristic of increase, steady and decrease. The equivalent elastic modulus can be estimated by the quadratic function between the equivalent elastic modulus and confining pressure and axial strain. Under the same deformation and deviatoric stress, the elastic strain energy stored in rock increases with increasing confining pressure. The local maximum energy dissipation rate corresponds to stress drop, and the peak energy dissipation rate appears near the peak strength. High energy dissipation mainly occurs in a short time after peak strength, and energy release and dissipation are more sudden and severe under high confining pressure.</p

Table1_A characterization method for equivalent elastic modulus of rock based on elastic strain energy.DOCX

Energy is an internal variable during rock deformation and failure, and its dissipation and conversion law can reflect the rock’s internal damage and deterioration state. Analysis of rock deformation and failure process from the perspective of energy is helpful to deeply understand the mechanism of rock damage, fracture and instability failure, and has important theoretical and practical significance for the stability evaluation and support control of surrounding rock. In this study, through single cyclic loading and unloading (SCLU) experiments, cyclic triaxial loading and unloading (CTLU) experiments and conventional triaxial compression (CTC) experiments, the equivalent elastic modulus method based on elastic strain energy is proposed to analyze the energy conversion of rock. The results show that the error of the elastic strain energy calculated by the strain energy formula method is generally higher than 10% with the secant and tangent modulus of the loading and unloading curve as input parameters. Taking the equivalent elastic modulus proposed in this study as an input parameter, more accurate elastic strain energy can be obtained by the strain energy formula. During the rock failure process, the equivalent elastic modulus shows a three-stage characteristic of increase, steady and decrease. The equivalent elastic modulus can be estimated by the quadratic function between the equivalent elastic modulus and confining pressure and axial strain. Under the same deformation and deviatoric stress, the elastic strain energy stored in rock increases with increasing confining pressure. The local maximum energy dissipation rate corresponds to stress drop, and the peak energy dissipation rate appears near the peak strength. High energy dissipation mainly occurs in a short time after peak strength, and energy release and dissipation are more sudden and severe under high confining pressure.</p

BP5 upregulated the expression of HO-1 protein in the LPS-induced DCs.

<p>DCs (1×10⁶ cells/ml) were treated with the indicated concentrations of BP5 for 2 h, and then incubated with or without LPS (100 ng/ml) for 22 h. (A) HO-1 levels were assessed by western blotting. (B) Quantification of the blots. (C-H) DCs were pretreatment with BP5 (100 μg/ml) in the presence or absence of Snpp (25 μM) or Copp (50 μM) for 2 h, and then incubated with or without LPS (100 ng/ml) for 22 h. (C) Supernatants were collected and NO production was measured using the Griess reagent. (D) TNF-α released from supernatants was measured by ELISA. DCs were harvested and the expressions of CD80 (E, G) and CD86 (F, H) were analyzed by FACS. Data shown are the means ± SD of three samples. *<i>P</i> < 0.05; **<i>P</i> < 0.01. All results are representative of three independent experiments.</p

MOESM1 of Associations between twelve common gene polymorphisms and susceptibility to hepatocellular carcinoma: evidence from a meta-analysis

Additional file 1: Figure S1. Forest plots of investigated polymorphisms

BP5 suppressed lipid peroxidation in the LPS-stimulated DCs.

<p>DCs (1×10⁶ cells/ml) were pretreated with or without BP5 for 2 h, and then exposed to LPS (100 ng/ml) or not for 22 h. The MDA contents in cell lysate supernatants were measured as described in Materials and Methods. Data shown are the means ± SD of three samples. *<i>P</i> < 0.05 in comparison with the LPS-only group; ^#<i>P</i> < 0.05 in comparison with the untreated group. All results are representative of three independent experiments.</p

BP5 suppressed the DC maturation in the LPS-stimulated ECs/DCs coculture system.

<p>Experimental setting to study the DC maturation in the ECs/DCs coculture system. (A) The scheme depicts: Caco-2 cells were grown on the filter to form a tight monolayer, and then DCs were cultured facing the basolateral side of Caco-2 cells on the bottom of the filter for 4 h. Pretreatment of BP5 on the basolateral DCs for 2 h, medium or LPS (300 ng/ml) was incubated on the apical side of the ECs for 22 h, then the basolateral DCs and culture supernatants were collected. (B) TEER was measured by a Millicell-ERS epithelial voltohmmeter (Millipore) at indicated time. (C-D) The filters were fixed with 4% paraformaldehyde and then processed to immunofluorescence stain for CLSM. Three-dimensional rendering of representative fields was obtained with Imaris 7.2 software, DCs (red, CD11c), tight junction of ECs (green, occludin). Submucosal DCs sent dendrites (arrows) to creep through ECs in response to LPS but not medium. (E-F) Supernatants were collected and NO production was measured using the Griess reagent. (G-H) TNF-α released from basolateral supernatants was measured by ELISA. (F, H) DCs stimulated with LPS before, at the same time as, or after BP5 (100 μg/ml) incubation. (I-L) The expressions of CD86 and MHCII on DCs were analyzed by FACS. Data shown are the means ± SD of three samples. *<i>P</i> < 0.05; **<i>P</i> < 0.01. SN, supernatants. To confirm the results, we repeated these experiments three times.</p

BP5 impaired the production of ROS by LPS-stimulated DCs.

<p>(A) DCs (1×10⁶ cells/ml) were incubated with the indicated concentrations of BP5 for 2 h, and then incubated with or without LPS (100 ng/ml) for 22 h, and then incubated with 10 μM DCFH-DA at 37°C for 20 min. ROS production was detected by fluorescence microplate reader. H₂O₂ (50 μM) was used as a positive control. (B-C) DCs stimulated with LPS before, at the same time as, or after BP5 (50 μg/ml) incubation. ROS production was detected by FACS. Data shown are the means ± SD of three samples. **<i>P</i> < 0.01, *<i>P</i> < 0.05 in comparison with the LPS-only group; ^#<i>P</i> < 0.05 in comparison with the untreated group. All results are representative of three independent experiments.</p

BP5 efficiently suppressed NO production in DCs.

<p>DCs (1×10⁶ cells/ml) were incubated with the indicated concentrations of BP5 for 2 h, and then incubated with or without LPS (100 ng/ml) for 22 h. Supernatants were collected and NO production was measured using the Griess reagent. Data shown are the means ± SD of three samples. *<i>P</i> < 0.05 in comparison with the LPS-only group; ^#<i>P</i> < 0.05 in comparison with the untreated group. All results are representative of three independent experiments.</p

BP5 enhanced the activities of antioxidant enzymes in the LPS-treated DCs.

<p>DCs (1×10⁶ cells/ml) were pretreated with BP5 for 2 h, followed by stimulation with or without LPS (100 ng/ml). After 22 h, Intracellular levels of (A) GPx, (B) CAT and (C) SOD were measured using commercial kits. Data shown are the means ± SD of three samples. *<i>P</i> < 0.05 in comparison with the LPS-only group; ^#<i>P</i> < 0.05 in comparison with the untreated group. All results are representative of three independent experiments.</p

BP5 modulated intracellular GSH, GSSG and the GSH/GSSG ratio in the LPS-stimulated DCs.

<p>DCs (1×10⁶ cells/ml) were pretreated with or without BP5. After 2 h, the cells were stimulated with LPS (100 ng/ml) or not for 22 h. The levels of (A) GSH, (B) GSSG and (C) GSH/GSSG ratio in the cells were measured as described in Materials and Methods. Data shown are the means ± SD of three samples. *<i>P</i> < 0.05 in comparison with the LPS-only group; ^#<i>P</i> < 0.05 in comparison with the untreated group. All results are representative of three independent experiments.</p