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Revvity
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Image Search Results
Journal: Frontiers in Molecular Neuroscience
Article Title: Cohesive Regulation of Neural Progenitor Development by microRNA miR-26, Its Host Gene Ctdsp and Target Gene Emx2 in the Mouse Embryonic Cerebral Cortex
doi: 10.3389/fnmol.2018.00044
Figure Lengend Snippet: Ctdsp2 increases neural progenitor (NP) proliferation. (A–C) Overexpression of Ctdsp2 , but not the control construct pCAGIG, increased the proportion of cells expressing both proliferative marker bromodeoxyuridine + (BrdU + )/green fluorescence protein + (GFP + ) and radial glial cell (RGC) marker Pax6 + /GFP + , but not intermediate progenitor (IP) marker Tbr2 + /GFP + , in GFP-positive cells. (D–F) shRNA-mediated knockdown (sh Ctdsp2 ) of Ctdsp2 decreased the proportion of both BrdU + /GFP + cells and Pax6 + /GFP + cells, but not Tbr2 + /GFP + cells in GFP-positive cells, compared to the control construct pSilencer. Values represent mean ± SEM. n = 9 sections from at least three brains. ** P < 0.01; ns, not significant. ANOVA with post hoc test was used. Scale bar = 50 μm.
Article Snippet: Primary antibodies against the following antigens were used: BrdU (1:50, Developmental Studies Hybridoma Bank at University of Iowa (DSHB)), Ki67 (1:500, Abcam),
Techniques: Over Expression, Control, Construct, Expressing, Marker, Fluorescence, shRNA, Knockdown
Journal: Frontiers in Molecular Neuroscience
Article Title: Cohesive Regulation of Neural Progenitor Development by microRNA miR-26, Its Host Gene Ctdsp and Target Gene Emx2 in the Mouse Embryonic Cerebral Cortex
doi: 10.3389/fnmol.2018.00044
Figure Lengend Snippet: miR-26 promotes NP proliferation. (A,D,G) Overexpression of miR-26a, but not the control construct pCAGIG, proportion of cells expressing both proliferative marker BrdU + /GFP + and RGC marker Pax6 + /GFP + , but not IP marker Tbr2 + /GFP + , in GFP-positive cells. (B,E,H) miRNA sponge-mediated knockdown (miR-26-SP), but not the mutated sponge (miR-26-SPmut), decreased proportion of cells expressing both proliferative marker BrdU + /GFP + and RGC marker Pax6 + /GFP + in GFP-positive cells. (C,F,I) Ratio of BrdU + /GFP + , Pax6 + /GFP + or Tbr2 + /GFP + cells vs. GFP + cells in the electroporated cortex. Values represent mean ± SEM. n = 9 sections from at least three brains. * P < 0.05; ** P < 0.01; ns, not significant. ANOVA with post hoc test was used. Scale bar = 50 μm.
Article Snippet: Primary antibodies against the following antigens were used: BrdU (1:50, Developmental Studies Hybridoma Bank at University of Iowa (DSHB)), Ki67 (1:500, Abcam),
Techniques: Over Expression, Control, Construct, Expressing, Marker, Knockdown
Journal: Frontiers in Molecular Neuroscience
Article Title: Cohesive Regulation of Neural Progenitor Development by microRNA miR-26, Its Host Gene Ctdsp and Target Gene Emx2 in the Mouse Embryonic Cerebral Cortex
doi: 10.3389/fnmol.2018.00044
Figure Lengend Snippet: Emx2 is functionally inhibited by miR-26 in regulating NP proliferation. (A–F) Overexpression of Emx2 , but not the control construct pCAGIG, decreased the proportion of cells expressing both proliferative marker BrdU + /GFP + and RGC marker Pax6 + /GFP + , but not IP marker Tbr2 + /GFP + , in GFP-positive cells. short hairpin RNA (shRNA)-mediated knockdown (sh Emx2 ) of Emx2 increased the proportion of both BrdU + /GFP + cells and Pax6 + /GFP + cells, but not Tbr2 + /GFP + cells in GFP-positive cells, compared to the control construct pSilencer. (G–J) Emx2 expression suppressed the proportion of cells expressing both proliferative marker BrdU + /GFP + and RGC marker Pax6 + /GFP + in GFP-positive cells. Co-expressing Emx2 with miR-26, but not miR-26-mut, dramatically reversed the suppression. (K,L) Emx2 expression did not alter the proportion of cells expressing IP marker Tbr2 + /GFP + , in GFP-positive cells. Values represent mean ± SEM. n = 9 sections from at least three brains. ** P < 0.01; *** P < 0.001; ns, not significant. ANOVA with post hoc test was used. Scale bar = 50 μm.
Article Snippet: Primary antibodies against the following antigens were used: BrdU (1:50, Developmental Studies Hybridoma Bank at University of Iowa (DSHB)), Ki67 (1:500, Abcam),
Techniques: Over Expression, Control, Construct, Expressing, Marker, shRNA, Knockdown
Journal: Cell Reports Medicine
Article Title: LIFUS-driven engineered bacteria reprogram immunosuppressive niches via mechano-NOTCH signaling
doi: 10.1016/j.xcrm.2026.102658
Figure Lengend Snippet: Mechanical immunotherapy effect of LIFUS combined with VNP /ARG-GV for tumors (A) Schematic illustrating the five-cycle LIFUS + VNP /ARG-GVs treatment regimen over 21 days. (B and C) Repeated LIFUS activation of intratumoral VNP /ARG-GVs resulted in marked suppression of tumor growth compared with all control and monotherapy groups (∗∗∗∗ p < 0.0001; n = 6) (B). (D) Kaplan-Meier survival analysis demonstrating significantly prolonged survival in the combination group (median 47.5 days), with several mice surviving beyond 60 days. All control and monotherapy cohorts succumbed by days 30–40 (control and LIFUS alone: median 20 days, VNP /ARG: 27.5 days, VNP /ARG-GVs: 25 days, n = 10). (E and G) Flow cytometry analysis (E) showing differential immune remodeling across groups. The details of the flow cytometry gating strategy are shown in . LIFUS alone did not alter CD4 + /CD8 + infiltration. VNP /ARG monotherapy induced about 1.5-fold increase in CD8 + T cells. Combination treatment produced a pronounced expansion of cytotoxic CD8 + T cells (63.96% ± 4.90% vs. 14.31% ± 2.0% in control; ∗∗∗∗ p < 0.0001; n = 4) (G). (F and H) The combination group showed the strongest suppression of FOXP3 + Tregs (7.76% ± 1.60%), significantly lower than controls (28.38% ± 2.59%; ∗∗∗ p < 0.005; n = 4) (H). (I and J) ELISA quantification of effector cytokines. IFN-γ levels were highest in the combination group (37.4 ± 6.88 ng/mL), followed by LIFUS alone (12.1 ± 2.3 ng/mL) and control (5.6 ± 1.4 ng/mL) ( n = 4) (I). TNF-α expression followed a similar trend (1.37 ± 0.41 ng/mL vs. 0.42 ± 0.15 ng/mL and 0.18 ± 0.06 ng/mL) ( n = 4) (J). (K and L) Representative Ki67 and hematoxylin and eosin staining showing reduced proliferation and increased apoptosis across groups, with the strongest effects observed in the LIFUS + VNP /ARG-GVs cohort. Scale bars, 100 μm. Data are representative of three (B, D, I, and J) or two (G and H) independent experiments. Data are mean ± SD or chi-square (D). Statistical analysis was performed using one-way ANOVA (B and H–K), two-way ANOVA (G), or log rank test (D). See also .
Article Snippet:
Techniques: Activation Assay, Control, Flow Cytometry, Produced, Enzyme-linked Immunosorbent Assay, Expressing, Staining
Journal: International Journal of Nanomedicine
Article Title: Enhancement of Psoriasis Treatment by Phellodendri Chinensis Cortex Carbon Dots (PCC-CDs) Through Modulation of the HMGB1/TLR4/MAPK/NF-κB Pathway
doi: 10.2147/IJN.S578399
Figure Lengend Snippet: PCC-CDs spray regulate the HMGB1/TLR4/MAPK/NF-κB signaling pathway to ameliorate psoriasis-like dermatitis. ( A ) Serum levels of HMGB1, IFN-γ, and VEGF in mice. ( B ) Protein expression levels of HMGB1/TLR4/MAPK/NF-κB signaling pathway-related proteins in mouse skin tissues. Each group n = 3. Data were expressed as means ± standard deviation (SD). # P < 0.05, ## P < 0.01, ### P < 0.001 vs Control group; * P < 0.05, ** P < 0.01, *** P < 0.001vs Model group.
Article Snippet: The following antibodies were used: PCNA antibody (Cat. 10205-2-AP, Proteintech, Wuhan, China), Ki67 Polyclonal antibody (Cat. 28074-1-AP, Proteintech, Wuhan, China),
Techniques: Expressing, Standard Deviation, Control
Journal: International Journal of Nanomedicine
Article Title: Enhancement of Psoriasis Treatment by Phellodendri Chinensis Cortex Carbon Dots (PCC-CDs) Through Modulation of the HMGB1/TLR4/MAPK/NF-κB Pathway
doi: 10.2147/IJN.S578399
Figure Lengend Snippet: PCC-CDs alleviate M1 macrophage polarisation by modulating the HMGB1/TLR4/NF-κB signalling pathway. ( A ) Cytokine levels in cell supernatants, including HMGB1, TNF-α, IL-1β, IL-6 and IL-10. ( B ) The effects of PCC-CD intervention on HMGB1/TLR4/NF-κB protein expression in M1 macrophages (n = 3 per group). Data are expressed as mean ± standard deviation (SD). # P < 0.05, ## P < 0.01 compared with the control group; *P < 0.05, **P < 0.01 compared with the model group.
Article Snippet: The following antibodies were used: PCNA antibody (Cat. 10205-2-AP, Proteintech, Wuhan, China), Ki67 Polyclonal antibody (Cat. 28074-1-AP, Proteintech, Wuhan, China),
Techniques: Expressing, Standard Deviation, Control
Journal: International Journal of Nanomedicine
Article Title: Enhancement of Psoriasis Treatment by Phellodendri Chinensis Cortex Carbon Dots (PCC-CDs) Through Modulation of the HMGB1/TLR4/MAPK/NF-κB Pathway
doi: 10.2147/IJN.S578399
Figure Lengend Snippet: Schematic illustration of the therapeutic mechanism hypothesis of PCC-CDs spray in alleviating psoriatic inflammation via modulation of the HMGB1/TLR4/MAPK/NF-κB signaling pathway.
Article Snippet: The following antibodies were used: PCNA antibody (Cat. 10205-2-AP, Proteintech, Wuhan, China), Ki67 Polyclonal antibody (Cat. 28074-1-AP, Proteintech, Wuhan, China),
Techniques: