Journal: Scientific Reports

Article Title: Comparison of the specific energies of sinusoidal VCS cutter rings and CCS cutter rings in breaking rock-like materials based on the FEM

doi: 10.1038/s41598-024-58466-0

Figure Lengend Snippet: Compressive stress‒strain-damage constitutive relationships for a rock-like model.

Article Snippet: Abaqus provides a constitutive model for calculating rock tensile and compressive strength, 14 \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\upsigma_{{\text{t}}} = \upsigma_{{\text{t}}} \left( {\upvarepsilon_{{{\text{tp}}}} ,\;\upvarepsilon_{{{\text{tr}}}} } \right)$$\end{document} σ t = σ t ε tp , ε tr and 15 \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\upsigma_{{\text{c}}} = \upsigma_{{\text{c}}} \left( {\upvarepsilon_{{{\text{cp}}}} ,\;\upvarepsilon_{{{\text{cr}}}} } \right),$$\end{document} σ c = σ c ε cp , ε cr , where subscripts t and c refer to tension and compression, ε tp and ε cp are the equivalent plastic strains, and ε tr and ε cr are the equivalent plastic strain rates.

Techniques:

Journal: Scientific Reports

Article Title: Comparison of the specific energies of sinusoidal VCS cutter rings and CCS cutter rings in breaking rock-like materials based on the FEM

doi: 10.1038/s41598-024-58466-0

Figure Lengend Snippet: Tensile stress‒strain-damage constitutive relationships for a rock-like model.

Article Snippet: Abaqus provides a constitutive model for calculating rock tensile and compressive strength, 14 \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\upsigma_{{\text{t}}} = \upsigma_{{\text{t}}} \left( {\upvarepsilon_{{{\text{tp}}}} ,\;\upvarepsilon_{{{\text{tr}}}} } \right)$$\end{document} σ t = σ t ε tp , ε tr and 15 \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\upsigma_{{\text{c}}} = \upsigma_{{\text{c}}} \left( {\upvarepsilon_{{{\text{cp}}}} ,\;\upvarepsilon_{{{\text{cr}}}} } \right),$$\end{document} σ c = σ c ε cp , ε cr , where subscripts t and c refer to tension and compression, ε tp and ε cp are the equivalent plastic strains, and ε tr and ε cr are the equivalent plastic strain rates.

Techniques:

Journal: CNS Neuroscience & Therapeutics

Article Title: Deletion of glutamate carboxypeptidase II ( GCPII ), but not GCPIII , provided long‐term benefits in mice with traumatic brain injury

doi: 10.1111/cns.14299

Figure Lengend Snippet: Generation of GCPII, GCPIII, and GCPII/III gene knockout mice by CRISPR/Cas9‐mediated genome engineering. (A) Schematic of the strategy used to generate GCPII, GCPIII, and GCPII/III knockout mice. (B, C) Genotyping of GCPII, GCPIII, and GCPII/III knockout mice by RT–PCR analysis of tail DNA samples. (B) The molecular weight of the PCR product of GCPII was 1605 bp in wild‐type mice and GCPIII −/− mice and 808 bp in GCPII −/− and GCPII/III −/− mice (GCPII, P3 and P4 primers), while the molecular weight of the PCR product of GCPIII was 3796 bp in wild‐type and GCPII −/− mice and 758 bp in GCPII −/− and GCPII/III −/− mice (GCPIII, P3 and P4 primers). (C) The molecular weight of the PCR product of GCPII was 405 bp in wild‐type and GCPIII −/− mice (GCPII, P1 and P2 primers). No band was detected in GCPII −/− and GCPII/III −/− mice. The molecular weight of the PCR product of GCPIII was 423 bp in wild‐type mice and GCPII −/− mice (GCPIII, P1 and P2 primers). No band was detected in GCPIII −/− and GCPII/III −/− mice. (D) RT–PCR analysis of GCPII and GCPIII expression in the hippocampus of wild‐type, GCPII −/− , GCPIII −/− , and GCPII/III −/− mice. The molecular weight of the PCR product of GCPII was 405 bp in wild‐type and GCPIII −/− mice (GCPII, P1 and P2 primers). No band was detected in GCPII −/− and GCPII/III −/− mice. The molecular weight of the PCR product of GCPIII was 423 bp in wild‐type mice and GCPII −/− mice. No band was detected in GCPIII −/− and GCPII/III −/− mice (GCPIII, P1 and P2 primers). Gapdh was used as an endogenous reference gene. (E) Western blot analyses of GCPII expression in the hippocampus of wild‐type, GCPII −/− , GCPIII −/− , and GCPII/III −/− mice. A band over 100 kDa was detected in the wild‐type and GCPIII −/− mice, while no GCPII protein was detected in GCPII −/− and GCPII/III −/− mice. β‐Actin was used to control for loading. (F) Immunofluorescence, GCPII (green) in the hippocampus of wild‐type, GCPII −/− , GCPIII −/− , and GCPII/III −/− mice. Scale bar = 50 μm. (G) The expression levels of NEUN, GFAP, TNF‐α, and IBA1 in hippocampus of wild‐type, GCPII −/− , GCPIII −/− , and GCPII/III −/− mice were detected by immunoblotting, and β‐Actin was used to control for loading. The right panel (H) is the quantitative analysis of the protein bands ( n = 3 per group, one‐way ANOVA, p > 0.05 among all groups). The errors bars indicate the S.E.

Article Snippet: The study utilized male C57BL/6 mice aged 8–12 weeks, purchased from Shanghai SLAC Laboratory Animal Co., Ltd. Additionally, constitutive GCPII knockout (GCPII −/− ) mice and GCPIII knockout (GCPIII −/− ) mice were generated by Shanghai Model Organisms Center, Inc., using CRISPR/Cas9‐mediated gene editing on mice with a C57BL/6 background, where exon 2 was targeted for GCPII knockout and exons 3–5 were targeted for GCPIII knockout (Figure ).

Techniques: Gene Knockout, CRISPR, Knock-Out, Reverse Transcription Polymerase Chain Reaction, Molecular Weight, Expressing, Western Blot, Control, Immunofluorescence

Journal: CNS Neuroscience & Therapeutics

Article Title: Deletion of glutamate carboxypeptidase II ( GCPII ), but not GCPIII , provided long‐term benefits in mice with traumatic brain injury

doi: 10.1111/cns.14299

Figure Lengend Snippet: List of primer pairs used for RT–qPCR and real‐time RT–qPCR.

Article Snippet: The study utilized male C57BL/6 mice aged 8–12 weeks, purchased from Shanghai SLAC Laboratory Animal Co., Ltd. Additionally, constitutive GCPII knockout (GCPII −/− ) mice and GCPIII knockout (GCPIII −/− ) mice were generated by Shanghai Model Organisms Center, Inc., using CRISPR/Cas9‐mediated gene editing on mice with a C57BL/6 background, where exon 2 was targeted for GCPII knockout and exons 3–5 were targeted for GCPIII knockout (Figure ).

Techniques:

Journal: CNS Neuroscience & Therapeutics

Article Title: Deletion of glutamate carboxypeptidase II ( GCPII ), but not GCPIII , provided long‐term benefits in mice with traumatic brain injury

doi: 10.1111/cns.14299

Figure Lengend Snippet: Dynamic changes in glutamate carboxypeptidase expression after TBI. (A–D) Quantitative reverse transcription‐polymerase chain reaction (RT–PCR) was used to assess the mRNA expression levels of GCPII (A), GCPIII (B), GFAP (C), and IBA1 (D) in the injured hippocampus at 1, 3, and 7 days after TBI and in the same brain area in the Sham operation group ( n = 3 per group, one‐way ANOVA, *: versus WT‐Sham group). The mRNA expression of GCPII and GCPIII in the injured hippocampus gradually increased from day 3 after injury and remained elevated for at least 7 days after injury. (E, F) Representative immunoblots and quantification showing the protein expression levels of GCPII, GFAP, and IBA1 in the injured hippocampus at 1, 3, and 7 days after TBI and in the same brain area in the Sham operation group. The data are expressed as the fold change compared to the Sham operation group ( n = 3 per group, one‐way ANOVA, *: versus WT‐Sham group). (G) Representative images of GCPII, IBA1, and GFAP co‐staining in the injured hippocampus after TBI and in the same brain areas in the Sham operation group showing that GCPII was abundantly expressed in the plasma membrane of microglia and substantially upregulated in activated microglia following TBI (scale bar = 100 μm). The magnified regions are indicated by the boxes (scale bar = 20 μm). White arrows indicate cells clearly expressing GCPII. The errors bars indicate the S.E. *** p < 0.001, ** p < 0.01, and * p < 0.05.

Article Snippet: The study utilized male C57BL/6 mice aged 8–12 weeks, purchased from Shanghai SLAC Laboratory Animal Co., Ltd. Additionally, constitutive GCPII knockout (GCPII −/− ) mice and GCPIII knockout (GCPIII −/− ) mice were generated by Shanghai Model Organisms Center, Inc., using CRISPR/Cas9‐mediated gene editing on mice with a C57BL/6 background, where exon 2 was targeted for GCPII knockout and exons 3–5 were targeted for GCPIII knockout (Figure ).

Techniques: Expressing, Reverse Transcription, Polymerase Chain Reaction, Reverse Transcription Polymerase Chain Reaction, Western Blot, Staining, Clinical Proteomics, Membrane

Journal: CNS Neuroscience & Therapeutics

Article Title: Deletion of glutamate carboxypeptidase II ( GCPII ), but not GCPIII , provided long‐term benefits in mice with traumatic brain injury

doi: 10.1111/cns.14299

Figure Lengend Snippet: GCPII and GCPII/III knockout attenuated glutamate excitotoxicity. (A) The glutamate concentration (μmol/L) in the hippocampus was significantly increased in the injury group compared with the Sham group at 24 h post‐TBI, while the concentration of glutamate in the injured hippocampus was significantly decreased in GCPII −/− and GCPII/III −/− mice, but not GCPIII −/− mice, compared with the WT‐CCI group ( n = 6 per group, one‐way ANOVA, *: versus WT‐CCI group). (B–E) The mRNA expression of glutaminase, NR2A, NR2B, and TGF‐β were measured by RT‐qPCR. The mRNA levels of glutaminase and glutamate receptors (NR2A and NR2B) in the hippocampus were significantly increased in the injury group compared with the Sham group at 24 h post‐TBI and were decreased in GCPII −/− and GCPII/III −/− mice, but not GCPIII −/− mice, compared with the WT‐CCI group. (E) Compared with the injury group, GCPII −/− and GCPII/III −/− mice had significantly increased TGFβ‐1 mRNA expression ( n = 9 per group, one‐way ANOVA, *: versus WT‐CCI group). (F–H) 24 h post‐TBI, Nissl staining (G) and TUNEL (H) staining were used to analyze the number of neurons and apoptotic cells in hippocampal CA3 region of WT‐Sham, WT‐CCI, GCPII −/− ‐CCI, GCPIII −/− ‐CCI, and GCPII/III −/− ‐CCI mice (scale bar = 50 μm, n = 6 per group, one‐way ANOVA, *: versus WT‐CCI group). (I) 24 h post‐TBI, the expression levels of Caspase3, cleaved Caspase3, and Bax in the injured hippocampus were detected by Western blot. Gapdh was used as an internal control. The right panel (J) is a quantitative analysis of the Western blot bands ( n = 3 per group, one‐way ANOVA, *: versus WT‐CCI group). The error bars indicate the S.E. *** p < 0.001, ** p < 0.01, and * p < 0.05.

Article Snippet: The study utilized male C57BL/6 mice aged 8–12 weeks, purchased from Shanghai SLAC Laboratory Animal Co., Ltd. Additionally, constitutive GCPII knockout (GCPII −/− ) mice and GCPIII knockout (GCPIII −/− ) mice were generated by Shanghai Model Organisms Center, Inc., using CRISPR/Cas9‐mediated gene editing on mice with a C57BL/6 background, where exon 2 was targeted for GCPII knockout and exons 3–5 were targeted for GCPIII knockout (Figure ).

Techniques: Knock-Out, Concentration Assay, Expressing, Quantitative RT-PCR, Staining, TUNEL Assay, Western Blot, Control

Journal: CNS Neuroscience & Therapeutics

Article Title: Deletion of glutamate carboxypeptidase II ( GCPII ), but not GCPIII , provided long‐term benefits in mice with traumatic brain injury

doi: 10.1111/cns.14299

Figure Lengend Snippet: GCPII and GCPII/III knockout led to long‐term neuroprotective effects. To explore the microscopic changes in the brain of mice with different genotypes in the subacute stage of TBI (7 days after TBI). (A–D) RT‐qPCR was used to detect the mRNA expression of GCPII, GCPIII, GFAP, and IBA1 in the hippocampal CA3 region of the WT‐Sham, WT‐CCI, GCPII −/− ‐CCI, GCPIII −/− ‐CCI, and GCPII/III −/− ‐CCI mice ( n = 9 per group, one‐way ANOVA, *: versus WT‐CCI group). (E) The protein expression levels of GCPII, GFAP, and IBA1 in the injured hippocampus of each group were detected by Western blot. The right panel (F) is a quantitative analysis of the protein bands, suggesting decreased IBA protein expression in GCPII −/− ‐CCI and GCPII/III −/− ‐CCI mice ( n = 3 per group, one‐way ANOVA, *: versus WT‐CCI group). Immunohistochemical staining of IBA1 (G) and Nissl staining (I) were performed on the cortex around the injury site and the CA3 region of the hippocampus of each group mice, respectively (scale bar = 50 μm, n = 6 per group, one‐way ANOVA, *: versus WT‐CCI group), suggesting that GCPII −/− ‐CCI and GCPII/III −/− ‐CCI mice had reduced microglial activation (H) in the subacute phase of TBI, as did the number of dead neurons (J). The error bars indicate the S.E. *** p < 0.001, ** p < 0.01, and * p < 0.05.

Article Snippet: The study utilized male C57BL/6 mice aged 8–12 weeks, purchased from Shanghai SLAC Laboratory Animal Co., Ltd. Additionally, constitutive GCPII knockout (GCPII −/− ) mice and GCPIII knockout (GCPIII −/− ) mice were generated by Shanghai Model Organisms Center, Inc., using CRISPR/Cas9‐mediated gene editing on mice with a C57BL/6 background, where exon 2 was targeted for GCPII knockout and exons 3–5 were targeted for GCPIII knockout (Figure ).

Techniques: Knock-Out, Quantitative RT-PCR, Expressing, Western Blot, Immunohistochemical staining, Staining, Activation Assay

Journal: CNS Neuroscience & Therapeutics

Article Title: Deletion of glutamate carboxypeptidase II ( GCPII ), but not GCPIII , provided long‐term benefits in mice with traumatic brain injury

doi: 10.1111/cns.14299

Figure Lengend Snippet: Glutamate carboxypeptidase knockout affected global gene expression in the hippocampus after TBI. The hippocampus at the injured side were collected for whole‐transcriptome sequencing on the seventh day post‐TBI ( n = 4 per group, p‐value and q‐value were set at 0.05). (A) Differentially expressed genes among groups were screened based on “edgeR” algorithm. A total of 728 genes were significantly upregulated in the WT‐CCI group compared with the Sham group, while 164 genes were significantly downregulated in the GCPII −/− ‐CCI group compared with the WT‐CCI group. Volcano plot (B) showed that a large number of genes were significantly upregulated in the WT‐CCI group compared with the Sham group, while GCPII knockout (C) could significantly reverse the upregulation trend of many genes. In addition, there were many differentially expressed genes between GCPII −/− ‐CCI and GCPII/III −/− ‐CCI groups (D). GO analysis results were ranked from high to low by GeneRadio, and the top 10 enrichment results were selected. (E) Gene Ontology (GO) analysis of the upregulated genes between the WT‐CCI group and the Sham group indicated that immune‐related functions were significantly active. Part of these upregulated genes were selected to draw the heatmap (G) after the standardization of gene expression and k‐means clustering, and it was found that immune‐related chemokines, microglia, and astrocyte‐related genes were significantly upregulated. (F) GO analysis of downregulated genes between the GCPII −/− ‐CCI and the WT‐CCI group indicated the functions related to transmembrane transport and sodium ion transport. Some key genes were screened out to draw the heatmap (H, I), it was found that the expression of some solute carrier family 6 (Slc6) members was downregulated, and some functional genes such as Wnt6 and Kcne4 were also downregulated. The upregulated genes included not only some chemokines (Ccl2 and Ccl3) but also synaptic repair‐related gene Npas4. (J, K) GO analysis was performed on the differentially expressed genes between GCPII/III −/− ‐CCI group and GCPII −/− ‐CCI group. The result suggested that there may be differences in cell cycle, apoptosis regulation, and DNA damage response between these two genotypes mice.

Article Snippet: The study utilized male C57BL/6 mice aged 8–12 weeks, purchased from Shanghai SLAC Laboratory Animal Co., Ltd. Additionally, constitutive GCPII knockout (GCPII −/− ) mice and GCPIII knockout (GCPIII −/− ) mice were generated by Shanghai Model Organisms Center, Inc., using CRISPR/Cas9‐mediated gene editing on mice with a C57BL/6 background, where exon 2 was targeted for GCPII knockout and exons 3–5 were targeted for GCPIII knockout (Figure ).

Techniques: Knock-Out, Gene Expression, Sequencing, Expressing, Functional Assay

Journal: CNS Neuroscience & Therapeutics

Article Title: Deletion of glutamate carboxypeptidase II ( GCPII ), but not GCPIII , provided long‐term benefits in mice with traumatic brain injury

doi: 10.1111/cns.14299

Figure Lengend Snippet: Effects of glutamate carboxypeptidase knockout on the learning and memory of mice. (A) Representative heatmap images of the WT‐Sham, WT‐CCI, GCPII −/− ‐CCI, GCPIII −/− ‐CCI, and GCPII/III −/− ‐CCI groups in the acquisition trial. The longer the mice spent in each quadrant, the redder the image displayed. Conversely, a cooler color indicates a shorter duration. (B) Representative heatmap images of the WT‐Sham, WT‐CCI, GCPII −/− ‐CCI, GCPIII −/− ‐CCI, and GCPII/III −/− ‐CCI groups in the probe trial. (C) The latency to find the escape platform of the different groups was measured. After TBI, a significant memory deficit was observed in the WT‐CCI group compared with the Sham group. Notably, compared with the WT‐CCI group, the GCPII −/− ‐CCI group, and GCPII/III −/− ‐CCI group showed a significant improvement with reduced latency ( n = 11–14 per group, two‐way ANOVA, *: versus WT‐CCI group). (D) The time spent in four quadrants by different groups mice was measured. Mice in the WT‐Sham, GCPII −/− ‐CCI, and GCPII/III −/− ‐CCI groups showed spatial memory retention, as evidenced by their significantly higher percentage of time spent in the target quadrant (NW) than in all other quadrants. However, mice in the WT‐CCI and GCPIII −/− ‐CCI groups did not show a preference for the target quadrant compared with the other quadrants ( n = 11–14 per group, two‐way ANOVA, *: versus WT‐CCI group). The swimming speed of different group mice on all acquisition days (E) and in the probe trial (F) was measured. The error bars indicate the S.E. *** p < 0.001, ** p < 0.01, and * p < 0.05.

Article Snippet: The study utilized male C57BL/6 mice aged 8–12 weeks, purchased from Shanghai SLAC Laboratory Animal Co., Ltd. Additionally, constitutive GCPII knockout (GCPII −/− ) mice and GCPIII knockout (GCPIII −/− ) mice were generated by Shanghai Model Organisms Center, Inc., using CRISPR/Cas9‐mediated gene editing on mice with a C57BL/6 background, where exon 2 was targeted for GCPII knockout and exons 3–5 were targeted for GCPIII knockout (Figure ).

Techniques: Knock-Out