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Image Search Results
Journal: bioRxiv
Article Title: Mast Cells Enhance Myeloma Engraftment and Promote Bone Destruction in the NSG-hIL6 Patient Derived Xenograft Model
doi: 10.64898/2026.05.14.725220
Figure Lengend Snippet: Co-injection of human mast cells with primary CD138 MM cells leads to faster engraftment and bone destruction in the NSG-hIL6 MM PDX model.
Article Snippet: Fresh cells were subjected to
Techniques: Injection
Journal: Journal of Vascular Research
Article Title: Rivaroxaban as a Protector of Oxidative Stress-Induced Vascular Endothelial Glycocalyx Damage via the IQGAP1/PAR1-2/PI3K/Akt Pathway
doi: 10.1159/000542419
Figure Lengend Snippet: sCD138 release under oxidative stress and the effect of rivaroxaban in ECs. a sCD138 concentration in the culture supernatant of HUVECs 20 min after 1, 50, 100 m m H 2 O 2 stimulation ( n = 5 for each culture). b ECs viability in 20 min after 1, 50, 100 m m H 2 O 2 stimulation ( n = 4 for each culture). c FX levels measured in HUVEC cell lysates with or without 20 min H 2 O 2 treatment ( n = 2 for each culture). d sCD138 concentration in the 1 m m H 2 O 2 -stimulated HUVEC culture supernatant with or without rivaroxaban pretreatment ( n = 4 for each culture). Bar graph represents averaged data. Values are the mean +/−SE. * p < 0.05 versus control. Significance is assessed using one-way ANOVA, followed by Dunnett’s post hoc analysis. ECs, endothelial cells; sCD138, soluble CD138; HUVECs, human umbilical vein endothelial cells.
Article Snippet: The concentration of soluble
Techniques: Concentration Assay, Control
Journal: Journal of Vascular Research
Article Title: Rivaroxaban as a Protector of Oxidative Stress-Induced Vascular Endothelial Glycocalyx Damage via the IQGAP1/PAR1-2/PI3K/Akt Pathway
doi: 10.1159/000542419
Figure Lengend Snippet: Involvement PI3K pathway in the improvement of cell viability and sCD138 shedding by rivaroxaban. a The effect of rivaroxaban in ECs viability in 20 min of 1 m m H 2 O 2 stimulation with or without PI3K inhibitor LY29002 ( n = 5 for each culture). b The effect of rivaroxaban on sCD138 shedding from the cell surface was measured using HUVEC culture supernatant in 20 min of H 2 O 2 stimulation with or without LY29002 ( n = 5 for each culture). Bar graph represents averaged data. Values are the mean +/−SE. * p < 0.05. Significance is assessed using one-way ANOVA, followed by Dunnett’s post hoc analysis. ECs, endothelial cells; PI3K, phosphatidylinositol 3-kinase.
Article Snippet: The concentration of soluble
Techniques:
Journal: Arthritis and rheumatism
Article Title: Immunohistochemical analysis as a means to predict responsiveness to rituximab treatment.
doi: 10.1002/art.22967
Figure Lengend Snippet: Figure 1. B cells in peripheral blood, bone marrow, and synovium before and 12 weeks after rituximab treatment. A, CD20 and CD19 expression on CD3 lymphocytes in peripheral blood from a rheuma- toid arthritis (RA) patient (left). Numbers represent the percentages of total lymphocytes. Flow cytometric data on 24 individual RA patients are shown on the right. The broken line represents the detection limit. B, CD20 and CD19 expression on CD3 lymphocytes in bone marrow from the same RA patient (left). Flow cytometric data on 18 individual RA patients are shown on the right. C, Consecutive sections of synovium stained for cytoplasmic CD20 (CD20cy) and CD79a (top). Semiquantitative scoring of CD20cy, CD79a, and CD138 expression (0 no expression; 4 highest level of expression) in synovial specimens from 17 RA patients is shown at bottom. Values are the mean and SEM. Circles indicate outliers.
Article Snippet: The remainder of the serial sections were stained with mouse anti-human Ki-67 (clone MIB-1), mouse anti-human CD68 (clone KP1), rabbit anti-mouse Ig isotype control (code X0936) (all from Dako, Heverlee, Belgium), rabbit anti-human CD3 (clone SP7; NeoMarkers, Fremont, CA),
Techniques: Expressing, Staining
Journal: Arthritis and rheumatism
Article Title: Immunohistochemical analysis as a means to predict responsiveness to rituximab treatment.
doi: 10.1002/art.22967
Figure Lengend Snippet: Figure 3. Differences in baseline characteristics of good responders versus those with moderate or no response, as classified according to the European League Against Rheumatism response criteria. A, Expression of specific markers for B cells (cytoplasmic CD20 [CD20cy], CD79a), plasma cells (CD138), macrophages (CD68), T cells (CD3), proliferation (Ki-67), plasma cell counts, and total inflammation. B, Circulating titers of rheumatoid arthritis–specific autoantibod- ies ACPA IgG, IgM-RF, and ACPA IgM. Values are the mean and SEM. P 0.05; # P 0.10. NS not significant (see Figure 2 for other definitions).
Article Snippet: The remainder of the serial sections were stained with mouse anti-human Ki-67 (clone MIB-1), mouse anti-human CD68 (clone KP1), rabbit anti-mouse Ig isotype control (code X0936) (all from Dako, Heverlee, Belgium), rabbit anti-human CD3 (clone SP7; NeoMarkers, Fremont, CA),
Techniques: Expressing, Clinical Proteomics
Journal: Advanced science (Weinheim, Baden-Wurttemberg, Germany)
Article Title: Engineered Biomimetic Fibrillar Fibronectin Matrices Regulate Cell Adhesion Initiation, Migration, and Proliferation via α5β1 Integrin and Syndecan-4 Crosstalk.
doi: 10.1002/advs.202300812
Figure Lengend Snippet: Figure 3. Syndecan-4 crosstalks with 𝛼5𝛽1 integrin to sense the fibrillarity and mechanical stiffness of FN. a,b) Adhesion forces of pKO-𝛽1 fibroblasts to heparin-treated 2D globular FN substrates, 2.5D fibrillar FN matrices, and 3D fibrillar FN matrices a) without and b) with crosslinking. Reference adhesion forces of pKO-𝛽1 fibroblasts to non-treated FN substrates or matrices are given in gray. Bottom p values compare given and reference data. Middle p values compare 2.5D fibrillar or 3D fibrillar FN matrices with 2D globular FN substrates. Top p values compare 2.5D fibrillar and 3D fibrillar FN matrices. AS indicates the slope of a linear regression and s.e. of adhesion strengthening rate (pN s−1). c) Adhesion forces of pKO-𝛽1 fibroblasts depleted from syndecan-1 (SDC1 KO), syndecan-2 (SDC2 KO), syndecan-3 (SDC3 KO), or syndecan-4 (SDC4 KO) to 2D globular, 3D fibrillar, and crosslinked 3D fibrillar (3DX) FN substrates. Adhesion forces of pKO-𝛽1 fibroblasts to respective FN substrates are given in gray as reference. p values compare given and reference data. d) Adhesion forces of pKO-𝛽1 SDC4 KO fibroblasts rescued with syndecan-4 to 2D globular, 3D fibrillar, and crosslinked 3D fibrillar (3DX) FN substrates. Adhesion forces of pKO-𝛽1 fibroblasts to respective FN substrates are given in gray as reference. Bottom p values compare given and reference data. Middle p values compare 2.5D fibrillar or 3D fibrillar FN matrices with 2D globular FN substrates. Top p values compare 2.5D fibrillar and 3D fibrillar FN matrices. Dots represent adhesion forces of individual fibroblasts and red bars the median. n indicates the number of fibroblasts tested. p values were calculated using two-tailed Mann–Whitney test.
Article Snippet: The detached fibroblasts were resuspended in SCFS media with FBS (1% w/v) and recovered from detachment process at 37 °C for at least 30 min. After recovery, cells were pelleted and 106 fibroblasts were resuspended in flow cytometry buffer (100 μL, EDTA (2 mm) and BSA (2% w/v) in PBS) containing antibodies as follows; phycoerythrin (PE)-labeled integrin subunit β1 (1:6, BioLegend, 102 208),
Techniques: Two Tailed Test, MANN-WHITNEY
Journal: bioRxiv
Article Title: Single-cell sequencing reveals clonally expanded plasma cells during chronic viral infection produce virus-specific and cross-reactive antibodies
doi: 10.1101/2021.01.29.428852
Figure Lengend Snippet: Experimental overview of immunization schemes and antibody repertoire statistics. A. Serial immunization scheme with ovalbumin (OVA) and subsequent bone marrow plasma cell (BM PC) isolation using CD138+ magnetic beads. Subsequent antibody repertoire libraries were prepared using the 5’ single-cell immune profiling kit from 10X Genomics. B. Serial immunization scheme with the extracellular region of human tumor necrosis factor receptor 2 (TNFR2) and subsequent bone marrow plasma cell (BM PC) isolation using flow cytometry. BM PCs were sorted based on CD138 hi , TACI hi , B220 lo , CD19 lo . Subsequent antibody repertoire and transcriptome libraries were prepared using the 5’ single-cell immune profiling kit from 10X Genomics. C. The total number of cells recovered in each infected or immunized mouse. Only cells containing exactly one variable heavy (V H ) and variable light (V L ) chain were considered. D. The total number of clones recovered in each infected or immunized mouse. Clone was determined by grouping those B cells containing identical CDRH3+CDRL3 amino acid sequences. Only cells containing exactly one variable heavy (V H ) and variable light (V L ) chain were considered. E-F. Fraction of clones (E) and cells (F) corresponding to a given isotype in each infected or immunized mouse. Clone was determined by grouping those B cells containing identical CDRH3+CDRL3 amino acid sequences. Only cells containing exactly one variable heavy (V H ) and variable light (V L ) chain were considered.
Article Snippet: For the OVA immunized mouse, BM PCs were isolated using a
Techniques: Clinical Proteomics, Isolation, Magnetic Beads, Flow Cytometry, Infection, Clone Assay
Journal: bioRxiv
Article Title: Single-cell sequencing reveals clonally expanded plasma cells during chronic viral infection produce virus-specific and cross-reactive antibodies
doi: 10.1101/2021.01.29.428852
Figure Lengend Snippet: Differentially expressed genes between the bone marrow plasma cells from mice either chronically infected with LCMV or immunized with human TNFR2. (A) Normalized expression of plasma cell genes Sdc1 ( CD138 ), Tnfrsf13b ( TACI ), Slamf7 , and Ptprc ( B220 ) for either mice infected with LCMV or immunized with human TNFR2. (B) Uniform manifold approximation project (UMAP) plots showing normalized gene expression for selected genes.
Article Snippet: For the OVA immunized mouse, BM PCs were isolated using a
Techniques: Clinical Proteomics, Infection, Expressing, Gene Expression