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New England Biolabs nebnext microbiome dna enrichment kit
Nebnext Microbiome Dna Enrichment Kit, supplied by New England Biolabs, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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UGO Basile S.R.L light dark box
Light Dark Box, supplied by UGO Basile S.R.L, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Chop 15204 1 Ap, supplied by Proteintech, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Proteintech anti fbxw7
Anti Fbxw7, supplied by Proteintech, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Micromanipulator Novarto, supplied by Sutter Instrument Company, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Rockland Immunochemicals pax6
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 <t>Pax6</t> + /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.
Pax6, supplied by Rockland Immunochemicals, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Proteintech anti foxp3 antibody
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 <t>FOXP3</t> + 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 .
Anti Foxp3 Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Rockland Immunochemicals concern methods n
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 <t>FOXP3</t> + 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 .
Concern Methods N, supplied by Rockland Immunochemicals, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/box/pmc07728777__41536_2020_109_MOESM2_ESM-25-29-51?v=Rockland+Immunochemicals
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93
Rockland Immunochemicals western blot assay
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 <t>FOXP3</t> + 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 .
Western Blot Assay, supplied by Rockland Immunochemicals, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/box/pmc03376858__emmm0004___0313___SD2-10-13-24?v=Rockland+Immunochemicals
Average 93 stars, based on 1 article reviews
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91
Revvity 96 well round bottom polypropylene plate
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 <t>FOXP3</t> + 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 .
96 Well Round Bottom Polypropylene Plate, supplied by Revvity, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/box/10__1038_slash_s41589___018___0031___6-442-11-15?v=Revvity
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93
Eppendorf AG l d100 buffer
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 <t>FOXP3</t> + 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 .
L D100 Buffer, supplied by Eppendorf AG, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Proteintech hmgb1 antibody
PCC-CDs spray regulate the <t>HMGB1/TLR4/MAPK/NF-κB</t> 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.
Hmgb1 Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


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.

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), Pax6 (1:500, Covance), Pax6 (1:15 DSHB), Tbr2 (1:500, Abcam), GFP (1:1000, Abcam, chicken), and GFP (1:1000, Rockland, rabbit).

Techniques: Over Expression, Control, Construct, Expressing, Marker, Fluorescence, shRNA, Knockdown

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.

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), Pax6 (1:500, Covance), Pax6 (1:15 DSHB), Tbr2 (1:500, Abcam), GFP (1:1000, Abcam, chicken), and GFP (1:1000, Rockland, rabbit).

Techniques: Over Expression, Control, Construct, Expressing, Marker, Knockdown

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.

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), Pax6 (1:500, Covance), Pax6 (1:15 DSHB), Tbr2 (1:500, Abcam), GFP (1:1000, Abcam, chicken), and GFP (1:1000, Rockland, rabbit).

Techniques: Over Expression, Control, Construct, Expressing, Marker, shRNA, Knockdown

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 .

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: Anti-FOXP3 antibody , Proteintech , Cat# 22228-1-AP; RRID: AB_11182376.

Techniques: Activation Assay, Control, Flow Cytometry, Produced, Enzyme-linked Immunosorbent Assay, Expressing, Staining

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.

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), HMGB1 antibody (Cat. 10829-1-AP, Proteintech, Wuhan, China), TLR4 antibody (Cat. 30400-1-AP, Proteintech, Wuhan, China), phospho-p38 MAPK (Thr180/Tyr182) Polyclonal antibody (Cat. 28796-1-AP, Proteintech, Wuhan, China), p38 MAPK Polyclonal antibody (Cat. 14064-1-AP, Proteintech, Wuhan, China), phospho-NF-κB p65 (Ser468) Recombinant antibody (Cat. 82335-1-AP, Proteintech, Wuhan, China), NF-κB p65 Polyclonal antibody (Cat. 10745-1-AP, Proteintech, Wuhan, China), GAPDH antibody (Cat. 60004-1-Ig, Proteintech, Wuhan, China), HRP-conjugated Goat Anti-Rabbit lgG (Cat. SA00001-2, Proteintech, Wuhan, China), HRP-conjugated Goat Anti-Mouse lgG (Cat. SA00001-1, Proteintech, Wuhan, China), Pentobarbital sodium salt (Cat. P3761, Sigma-Aldrich, St. Louis, MO,USA).

Techniques: Expressing, Standard Deviation, Control

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.

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), HMGB1 antibody (Cat. 10829-1-AP, Proteintech, Wuhan, China), TLR4 antibody (Cat. 30400-1-AP, Proteintech, Wuhan, China), phospho-p38 MAPK (Thr180/Tyr182) Polyclonal antibody (Cat. 28796-1-AP, Proteintech, Wuhan, China), p38 MAPK Polyclonal antibody (Cat. 14064-1-AP, Proteintech, Wuhan, China), phospho-NF-κB p65 (Ser468) Recombinant antibody (Cat. 82335-1-AP, Proteintech, Wuhan, China), NF-κB p65 Polyclonal antibody (Cat. 10745-1-AP, Proteintech, Wuhan, China), GAPDH antibody (Cat. 60004-1-Ig, Proteintech, Wuhan, China), HRP-conjugated Goat Anti-Rabbit lgG (Cat. SA00001-2, Proteintech, Wuhan, China), HRP-conjugated Goat Anti-Mouse lgG (Cat. SA00001-1, Proteintech, Wuhan, China), Pentobarbital sodium salt (Cat. P3761, Sigma-Aldrich, St. Louis, MO,USA).

Techniques: Expressing, Standard Deviation, Control

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.

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), HMGB1 antibody (Cat. 10829-1-AP, Proteintech, Wuhan, China), TLR4 antibody (Cat. 30400-1-AP, Proteintech, Wuhan, China), phospho-p38 MAPK (Thr180/Tyr182) Polyclonal antibody (Cat. 28796-1-AP, Proteintech, Wuhan, China), p38 MAPK Polyclonal antibody (Cat. 14064-1-AP, Proteintech, Wuhan, China), phospho-NF-κB p65 (Ser468) Recombinant antibody (Cat. 82335-1-AP, Proteintech, Wuhan, China), NF-κB p65 Polyclonal antibody (Cat. 10745-1-AP, Proteintech, Wuhan, China), GAPDH antibody (Cat. 60004-1-Ig, Proteintech, Wuhan, China), HRP-conjugated Goat Anti-Rabbit lgG (Cat. SA00001-2, Proteintech, Wuhan, China), HRP-conjugated Goat Anti-Mouse lgG (Cat. SA00001-1, Proteintech, Wuhan, China), Pentobarbital sodium salt (Cat. P3761, Sigma-Aldrich, St. Louis, MO,USA).

Techniques: