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93
Vector Laboratories fitc lectins
Fitc Lectins, supplied by Vector Laboratories, 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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ICONEUS functional ultrasound device
A) Representative images of the cerebral microvasculature recorded by functional <t>ultrasound</t> imaging resulting in the presented ultrasound localization microscopy images. Vascular density has been measured in the cortical (CX) and hippocampal (HIPP) areas of the mouse brain. B–C) Quantification of the cortical and hippocampal cerebral vascular density in young, aged, aged + FL-RSV and aged + ApoE-FL-RSV treated animals. D–E) Measurement of neurovascular coupling responses in the young, aged, aged + FL-RSV and aged + ApoE-FL-RSV treated mice. Note the significant differences between aged, aged + FL-RSV and aged + ApoE-FL-RSV. Data is shown in mean±SEM. *p<0.05, **p<0.01, ***p<0.001 with ANOVA, N≥8 for all groups. F) Single-cell RNA-seq analysis reveals restoration of endothelial heterogeneity with treatment. Stacked bar plots showing the proportional abundance of vascular cell populations across experimental groups. Aging markedly reduces angiogenic and proliferating endothelial subtypes, whereas FL-RSV and particularly APOE-FL-RSV treatment partially restores endothelial diversity and the presence of regenerative cell states, suggesting improved vascular maintenance capacity. G) Gene ontology enrichment indicates reduced endothelial senescence and improved barrier maintenance after APOE-FL-RSV treatment. Heatmap of endothelial GO term enrichment scores demonstrates that aging increased pathways associated with cellular senescence, endothelial stress, and barrier dysfunction, while APOE-FL-RSV shifted expression toward gene sets linked to blood–brain barrier integrity, lipid transport, and endothelial homeostasis. H-I) Measurement of learning and memory functions of the young, aged, aged + FL-RSV, aged + ApoE-FL-RSV treated animals and aged animals that have RSV per os . Young control and aged BL6 mice were subjected to vehicle, RSV per os , FL-RSV and ApoE-FL-RSV treatments and assessed for their spatial learning and memory using the Radial Arm Water Maze (RAWM). During the learning phase (days 2 to 6) and on probe (P), retrieval (R) and relearn (L) days aged mice displayed higher combined error rates compared to young mice. Treatment with FL-RSV and ApoE-FL-RSV significantly enhanced learning performance in aged mice relative to their untreated counterparts. The combined error rate was computed by adding one error for each incorrect arm entry plus an error for every 15 seconds of inactivity. Data are presented as mean±SEM (N=10–15 per group). Statistical significance indicated by *p<0.05, **p<0.01, ***p<0.001 using Repeated Measure ANOVA, demonstrating the beneficial effects of FL-RSV and ApoE-FL-RSV treatments on enhancing cognitive functions in aged mice, particularly in spatial learning, but less so in tasks requiring cognitive flexibility.
Functional Ultrasound Device, supplied by ICONEUS, 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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ICONEUS ultrasonic probe
A) Representative images of the cerebral microvasculature recorded by functional <t>ultrasound</t> imaging resulting in the presented ultrasound localization microscopy images. Vascular density has been measured in the cortical (CX) and hippocampal (HIPP) areas of the mouse brain. B–C) Quantification of the cortical and hippocampal cerebral vascular density in young, aged, aged + FL-RSV and aged + ApoE-FL-RSV treated animals. D–E) Measurement of neurovascular coupling responses in the young, aged, aged + FL-RSV and aged + ApoE-FL-RSV treated mice. Note the significant differences between aged, aged + FL-RSV and aged + ApoE-FL-RSV. Data is shown in mean±SEM. *p<0.05, **p<0.01, ***p<0.001 with ANOVA, N≥8 for all groups. F) Single-cell RNA-seq analysis reveals restoration of endothelial heterogeneity with treatment. Stacked bar plots showing the proportional abundance of vascular cell populations across experimental groups. Aging markedly reduces angiogenic and proliferating endothelial subtypes, whereas FL-RSV and particularly APOE-FL-RSV treatment partially restores endothelial diversity and the presence of regenerative cell states, suggesting improved vascular maintenance capacity. G) Gene ontology enrichment indicates reduced endothelial senescence and improved barrier maintenance after APOE-FL-RSV treatment. Heatmap of endothelial GO term enrichment scores demonstrates that aging increased pathways associated with cellular senescence, endothelial stress, and barrier dysfunction, while APOE-FL-RSV shifted expression toward gene sets linked to blood–brain barrier integrity, lipid transport, and endothelial homeostasis. H-I) Measurement of learning and memory functions of the young, aged, aged + FL-RSV, aged + ApoE-FL-RSV treated animals and aged animals that have RSV per os . Young control and aged BL6 mice were subjected to vehicle, RSV per os , FL-RSV and ApoE-FL-RSV treatments and assessed for their spatial learning and memory using the Radial Arm Water Maze (RAWM). During the learning phase (days 2 to 6) and on probe (P), retrieval (R) and relearn (L) days aged mice displayed higher combined error rates compared to young mice. Treatment with FL-RSV and ApoE-FL-RSV significantly enhanced learning performance in aged mice relative to their untreated counterparts. The combined error rate was computed by adding one error for each incorrect arm entry plus an error for every 15 seconds of inactivity. Data are presented as mean±SEM (N=10–15 per group). Statistical significance indicated by *p<0.05, **p<0.01, ***p<0.001 using Repeated Measure ANOVA, demonstrating the beneficial effects of FL-RSV and ApoE-FL-RSV treatments on enhancing cognitive functions in aged mice, particularly in spatial learning, but less so in tasks requiring cognitive flexibility.
Ultrasonic Probe, supplied by ICONEUS, 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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New England Biolabs phi29 polymerase amplification
A) Representative images of the cerebral microvasculature recorded by functional <t>ultrasound</t> imaging resulting in the presented ultrasound localization microscopy images. Vascular density has been measured in the cortical (CX) and hippocampal (HIPP) areas of the mouse brain. B–C) Quantification of the cortical and hippocampal cerebral vascular density in young, aged, aged + FL-RSV and aged + ApoE-FL-RSV treated animals. D–E) Measurement of neurovascular coupling responses in the young, aged, aged + FL-RSV and aged + ApoE-FL-RSV treated mice. Note the significant differences between aged, aged + FL-RSV and aged + ApoE-FL-RSV. Data is shown in mean±SEM. *p<0.05, **p<0.01, ***p<0.001 with ANOVA, N≥8 for all groups. F) Single-cell RNA-seq analysis reveals restoration of endothelial heterogeneity with treatment. Stacked bar plots showing the proportional abundance of vascular cell populations across experimental groups. Aging markedly reduces angiogenic and proliferating endothelial subtypes, whereas FL-RSV and particularly APOE-FL-RSV treatment partially restores endothelial diversity and the presence of regenerative cell states, suggesting improved vascular maintenance capacity. G) Gene ontology enrichment indicates reduced endothelial senescence and improved barrier maintenance after APOE-FL-RSV treatment. Heatmap of endothelial GO term enrichment scores demonstrates that aging increased pathways associated with cellular senescence, endothelial stress, and barrier dysfunction, while APOE-FL-RSV shifted expression toward gene sets linked to blood–brain barrier integrity, lipid transport, and endothelial homeostasis. H-I) Measurement of learning and memory functions of the young, aged, aged + FL-RSV, aged + ApoE-FL-RSV treated animals and aged animals that have RSV per os . Young control and aged BL6 mice were subjected to vehicle, RSV per os , FL-RSV and ApoE-FL-RSV treatments and assessed for their spatial learning and memory using the Radial Arm Water Maze (RAWM). During the learning phase (days 2 to 6) and on probe (P), retrieval (R) and relearn (L) days aged mice displayed higher combined error rates compared to young mice. Treatment with FL-RSV and ApoE-FL-RSV significantly enhanced learning performance in aged mice relative to their untreated counterparts. The combined error rate was computed by adding one error for each incorrect arm entry plus an error for every 15 seconds of inactivity. Data are presented as mean±SEM (N=10–15 per group). Statistical significance indicated by *p<0.05, **p<0.01, ***p<0.001 using Repeated Measure ANOVA, demonstrating the beneficial effects of FL-RSV and ApoE-FL-RSV treatments on enhancing cognitive functions in aged mice, particularly in spatial learning, but less so in tasks requiring cognitive flexibility.
Phi29 Polymerase Amplification, supplied by New England Biolabs, 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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Vector Laboratories biotinylated lectin ricinus communis agglutinin
Fig. 2. In situ hybridization analysis of miR-146a expression in hippocampal tissue of control rats and after induction of SE. (A, C, E, G) Control hippocampus showing neuronal miR-146a expression in the different hippocampal subfields, including pyramidal neurons of CA3 (C; insert in C) and CA1 (E; insert in E) regions, granule cells of the dentate gyrus (DG; G) and hilar neurons (G; insert in G: high-magnification of hilar neurons). gcl, granule cell layer. (B, D, F, H) Hippocampus 1 week post-SE showing increased miR-146a expression within the different hippocampal regions, including CA3 (D; insert in D: high-magnification of CA3), CA1 (F; insert in F: high-magnification of CA1) and DG (H). miR-146a expression was observed in both neuronal and glial cells; arrows in D, F (and insert in D) indicate positive pyramidal neurons of CA3 and CA1; positive glial cells (arrowheads in D, F and insert in D) were particularly abundant in regions of prominent gliosis (CA1, CA3 and the inner molecular layer, iml, of the DG). Insert in (H) shows a high-magnification of positive glial cells in the DG (iml). (I and J) In situ hybridization analysis of miR-146a expression in the hilar region of the hippocampus 1 week (I) and 3–4 months post-SE (J) showing increased expression in glial cells (arrows; insert in I). Sections are counterstained with haematoxylin. Inserts in (J): in situ hybridization and immunohistochemistry analysis showing in (a) absence of miR-146a (red) expression in <t>lectin-positive</t> microglial cells (blue) and in (b) colocalization with the astroglial marker glial fibrillary acidic protein (GFAP; purple) in astrocytes. Scale bars: 1250 lm (A and B); 70 lm (C–J); 35 lm (inserts in C, D, F and G); 20 lm (insert in E); 17 lm (inserts in H and I); 11 lm (insert in J). LT, long-term, 3–4 months after SE.
Biotinylated Lectin Ricinus Communis Agglutinin, supplied by Vector Laboratories, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/biotinylated lectin ricinus communis agglutinin/product/Vector Laboratories
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94
ICONEUS probe
Fig. 2. In situ hybridization analysis of miR-146a expression in hippocampal tissue of control rats and after induction of SE. (A, C, E, G) Control hippocampus showing neuronal miR-146a expression in the different hippocampal subfields, including pyramidal neurons of CA3 (C; insert in C) and CA1 (E; insert in E) regions, granule cells of the dentate gyrus (DG; G) and hilar neurons (G; insert in G: high-magnification of hilar neurons). gcl, granule cell layer. (B, D, F, H) Hippocampus 1 week post-SE showing increased miR-146a expression within the different hippocampal regions, including CA3 (D; insert in D: high-magnification of CA3), CA1 (F; insert in F: high-magnification of CA1) and DG (H). miR-146a expression was observed in both neuronal and glial cells; arrows in D, F (and insert in D) indicate positive pyramidal neurons of CA3 and CA1; positive glial cells (arrowheads in D, F and insert in D) were particularly abundant in regions of prominent gliosis (CA1, CA3 and the inner molecular layer, iml, of the DG). Insert in (H) shows a high-magnification of positive glial cells in the DG (iml). (I and J) In situ hybridization analysis of miR-146a expression in the hilar region of the hippocampus 1 week (I) and 3–4 months post-SE (J) showing increased expression in glial cells (arrows; insert in I). Sections are counterstained with haematoxylin. Inserts in (J): in situ hybridization and immunohistochemistry analysis showing in (a) absence of miR-146a (red) expression in <t>lectin-positive</t> microglial cells (blue) and in (b) colocalization with the astroglial marker glial fibrillary acidic protein (GFAP; purple) in astrocytes. Scale bars: 1250 lm (A and B); 70 lm (C–J); 35 lm (inserts in C, D, F and G); 20 lm (insert in E); 17 lm (inserts in H and I); 11 lm (insert in J). LT, long-term, 3–4 months after SE.
Probe, supplied by ICONEUS, 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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90
Addgene inc p2ct his mbp tev rccas13a
Fig. 2. In situ hybridization analysis of miR-146a expression in hippocampal tissue of control rats and after induction of SE. (A, C, E, G) Control hippocampus showing neuronal miR-146a expression in the different hippocampal subfields, including pyramidal neurons of CA3 (C; insert in C) and CA1 (E; insert in E) regions, granule cells of the dentate gyrus (DG; G) and hilar neurons (G; insert in G: high-magnification of hilar neurons). gcl, granule cell layer. (B, D, F, H) Hippocampus 1 week post-SE showing increased miR-146a expression within the different hippocampal regions, including CA3 (D; insert in D: high-magnification of CA3), CA1 (F; insert in F: high-magnification of CA1) and DG (H). miR-146a expression was observed in both neuronal and glial cells; arrows in D, F (and insert in D) indicate positive pyramidal neurons of CA3 and CA1; positive glial cells (arrowheads in D, F and insert in D) were particularly abundant in regions of prominent gliosis (CA1, CA3 and the inner molecular layer, iml, of the DG). Insert in (H) shows a high-magnification of positive glial cells in the DG (iml). (I and J) In situ hybridization analysis of miR-146a expression in the hilar region of the hippocampus 1 week (I) and 3–4 months post-SE (J) showing increased expression in glial cells (arrows; insert in I). Sections are counterstained with haematoxylin. Inserts in (J): in situ hybridization and immunohistochemistry analysis showing in (a) absence of miR-146a (red) expression in <t>lectin-positive</t> microglial cells (blue) and in (b) colocalization with the astroglial marker glial fibrillary acidic protein (GFAP; purple) in astrocytes. Scale bars: 1250 lm (A and B); 70 lm (C–J); 35 lm (inserts in C, D, F and G); 20 lm (insert in E); 17 lm (inserts in H and I); 11 lm (insert in J). LT, long-term, 3–4 months after SE.
P2ct His Mbp Tev Rccas13a, supplied by Addgene inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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86
Boston Scientific Corporation rca
Fig. 2. In situ hybridization analysis of miR-146a expression in hippocampal tissue of control rats and after induction of SE. (A, C, E, G) Control hippocampus showing neuronal miR-146a expression in the different hippocampal subfields, including pyramidal neurons of CA3 (C; insert in C) and CA1 (E; insert in E) regions, granule cells of the dentate gyrus (DG; G) and hilar neurons (G; insert in G: high-magnification of hilar neurons). gcl, granule cell layer. (B, D, F, H) Hippocampus 1 week post-SE showing increased miR-146a expression within the different hippocampal regions, including CA3 (D; insert in D: high-magnification of CA3), CA1 (F; insert in F: high-magnification of CA1) and DG (H). miR-146a expression was observed in both neuronal and glial cells; arrows in D, F (and insert in D) indicate positive pyramidal neurons of CA3 and CA1; positive glial cells (arrowheads in D, F and insert in D) were particularly abundant in regions of prominent gliosis (CA1, CA3 and the inner molecular layer, iml, of the DG). Insert in (H) shows a high-magnification of positive glial cells in the DG (iml). (I and J) In situ hybridization analysis of miR-146a expression in the hilar region of the hippocampus 1 week (I) and 3–4 months post-SE (J) showing increased expression in glial cells (arrows; insert in I). Sections are counterstained with haematoxylin. Inserts in (J): in situ hybridization and immunohistochemistry analysis showing in (a) absence of miR-146a (red) expression in <t>lectin-positive</t> microglial cells (blue) and in (b) colocalization with the astroglial marker glial fibrillary acidic protein (GFAP; purple) in astrocytes. Scale bars: 1250 lm (A and B); 70 lm (C–J); 35 lm (inserts in C, D, F and G); 20 lm (insert in E); 17 lm (inserts in H and I); 11 lm (insert in J). LT, long-term, 3–4 months after SE.
Rca, supplied by Boston Scientific Corporation, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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94
Vector Laboratories ricinus communis agglutinin i
Fig. 2. In situ hybridization analysis of miR-146a expression in hippocampal tissue of control rats and after induction of SE. (A, C, E, G) Control hippocampus showing neuronal miR-146a expression in the different hippocampal subfields, including pyramidal neurons of CA3 (C; insert in C) and CA1 (E; insert in E) regions, granule cells of the dentate gyrus (DG; G) and hilar neurons (G; insert in G: high-magnification of hilar neurons). gcl, granule cell layer. (B, D, F, H) Hippocampus 1 week post-SE showing increased miR-146a expression within the different hippocampal regions, including CA3 (D; insert in D: high-magnification of CA3), CA1 (F; insert in F: high-magnification of CA1) and DG (H). miR-146a expression was observed in both neuronal and glial cells; arrows in D, F (and insert in D) indicate positive pyramidal neurons of CA3 and CA1; positive glial cells (arrowheads in D, F and insert in D) were particularly abundant in regions of prominent gliosis (CA1, CA3 and the inner molecular layer, iml, of the DG). Insert in (H) shows a high-magnification of positive glial cells in the DG (iml). (I and J) In situ hybridization analysis of miR-146a expression in the hilar region of the hippocampus 1 week (I) and 3–4 months post-SE (J) showing increased expression in glial cells (arrows; insert in I). Sections are counterstained with haematoxylin. Inserts in (J): in situ hybridization and immunohistochemistry analysis showing in (a) absence of miR-146a (red) expression in <t>lectin-positive</t> microglial cells (blue) and in (b) colocalization with the astroglial marker glial fibrillary acidic protein (GFAP; purple) in astrocytes. Scale bars: 1250 lm (A and B); 70 lm (C–J); 35 lm (inserts in C, D, F and G); 20 lm (insert in E); 17 lm (inserts in H and I); 11 lm (insert in J). LT, long-term, 3–4 months after SE.
Ricinus Communis Agglutinin I, supplied by Vector Laboratories, 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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Fig. 2. In situ hybridization analysis of miR-146a expression in hippocampal tissue of control rats and after induction of SE. (A, C, E, G) Control hippocampus showing neuronal miR-146a expression in the different hippocampal subfields, including pyramidal neurons of CA3 (C; insert in C) and CA1 (E; insert in E) regions, granule cells of the dentate gyrus (DG; G) and hilar neurons (G; insert in G: high-magnification of hilar neurons). gcl, granule cell layer. (B, D, F, H) Hippocampus 1 week post-SE showing increased miR-146a expression within the different hippocampal regions, including CA3 (D; insert in D: high-magnification of CA3), CA1 (F; insert in F: high-magnification of CA1) and DG (H). miR-146a expression was observed in both neuronal and glial cells; arrows in D, F (and insert in D) indicate positive pyramidal neurons of CA3 and CA1; positive glial cells (arrowheads in D, F and insert in D) were particularly abundant in regions of prominent gliosis (CA1, CA3 and the inner molecular layer, iml, of the DG). Insert in (H) shows a high-magnification of positive glial cells in the DG (iml). (I and J) In situ hybridization analysis of miR-146a expression in the hilar region of the hippocampus 1 week (I) and 3–4 months post-SE (J) showing increased expression in glial cells (arrows; insert in I). Sections are counterstained with haematoxylin. Inserts in (J): in situ hybridization and immunohistochemistry analysis showing in (a) absence of miR-146a (red) expression in <t>lectin-positive</t> microglial cells (blue) and in (b) colocalization with the astroglial marker glial fibrillary acidic protein (GFAP; purple) in astrocytes. Scale bars: 1250 lm (A and B); 70 lm (C–J); 35 lm (inserts in C, D, F and G); 20 lm (insert in E); 17 lm (inserts in H and I); 11 lm (insert in J). LT, long-term, 3–4 months after SE.
Ricinus Communis Agglutinin I Agarose Resin, supplied by Vector Laboratories, 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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Vector Laboratories ricin
Fig. 2. In situ hybridization analysis of miR-146a expression in hippocampal tissue of control rats and after induction of SE. (A, C, E, G) Control hippocampus showing neuronal miR-146a expression in the different hippocampal subfields, including pyramidal neurons of CA3 (C; insert in C) and CA1 (E; insert in E) regions, granule cells of the dentate gyrus (DG; G) and hilar neurons (G; insert in G: high-magnification of hilar neurons). gcl, granule cell layer. (B, D, F, H) Hippocampus 1 week post-SE showing increased miR-146a expression within the different hippocampal regions, including CA3 (D; insert in D: high-magnification of CA3), CA1 (F; insert in F: high-magnification of CA1) and DG (H). miR-146a expression was observed in both neuronal and glial cells; arrows in D, F (and insert in D) indicate positive pyramidal neurons of CA3 and CA1; positive glial cells (arrowheads in D, F and insert in D) were particularly abundant in regions of prominent gliosis (CA1, CA3 and the inner molecular layer, iml, of the DG). Insert in (H) shows a high-magnification of positive glial cells in the DG (iml). (I and J) In situ hybridization analysis of miR-146a expression in the hilar region of the hippocampus 1 week (I) and 3–4 months post-SE (J) showing increased expression in glial cells (arrows; insert in I). Sections are counterstained with haematoxylin. Inserts in (J): in situ hybridization and immunohistochemistry analysis showing in (a) absence of miR-146a (red) expression in <t>lectin-positive</t> microglial cells (blue) and in (b) colocalization with the astroglial marker glial fibrillary acidic protein (GFAP; purple) in astrocytes. Scale bars: 1250 lm (A and B); 70 lm (C–J); 35 lm (inserts in C, D, F and G); 20 lm (insert in E); 17 lm (inserts in H and I); 11 lm (insert in J). LT, long-term, 3–4 months after SE.
Ricin, supplied by Vector Laboratories, 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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Fig. 2. In situ hybridization analysis of miR-146a expression in hippocampal tissue of control rats and after induction of SE. (A, C, E, G) Control hippocampus showing neuronal miR-146a expression in the different hippocampal subfields, including pyramidal neurons of CA3 (C; insert in C) and CA1 (E; insert in E) regions, granule cells of the dentate gyrus (DG; G) and hilar neurons (G; insert in G: high-magnification of hilar neurons). gcl, granule cell layer. (B, D, F, H) Hippocampus 1 week post-SE showing increased miR-146a expression within the different hippocampal regions, including CA3 (D; insert in D: high-magnification of CA3), CA1 (F; insert in F: high-magnification of CA1) and DG (H). miR-146a expression was observed in both neuronal and glial cells; arrows in D, F (and insert in D) indicate positive pyramidal neurons of CA3 and CA1; positive glial cells (arrowheads in D, F and insert in D) were particularly abundant in regions of prominent gliosis (CA1, CA3 and the inner molecular layer, iml, of the DG). Insert in (H) shows a high-magnification of positive glial cells in the DG (iml). (I and J) In situ hybridization analysis of miR-146a expression in the hilar region of the hippocampus 1 week (I) and 3–4 months post-SE (J) showing increased expression in glial cells (arrows; insert in I). Sections are counterstained with haematoxylin. Inserts in (J): in situ hybridization and immunohistochemistry analysis showing in (a) absence of miR-146a (red) expression in <t>lectin-positive</t> microglial cells (blue) and in (b) colocalization with the astroglial marker glial fibrillary acidic protein (GFAP; purple) in astrocytes. Scale bars: 1250 lm (A and B); 70 lm (C–J); 35 lm (inserts in C, D, F and G); 20 lm (insert in E); 17 lm (inserts in H and I); 11 lm (insert in J). LT, long-term, 3–4 months after SE.
Lectin, supplied by Vector Laboratories, 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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Image Search Results


A) Representative images of the cerebral microvasculature recorded by functional ultrasound imaging resulting in the presented ultrasound localization microscopy images. Vascular density has been measured in the cortical (CX) and hippocampal (HIPP) areas of the mouse brain. B–C) Quantification of the cortical and hippocampal cerebral vascular density in young, aged, aged + FL-RSV and aged + ApoE-FL-RSV treated animals. D–E) Measurement of neurovascular coupling responses in the young, aged, aged + FL-RSV and aged + ApoE-FL-RSV treated mice. Note the significant differences between aged, aged + FL-RSV and aged + ApoE-FL-RSV. Data is shown in mean±SEM. *p<0.05, **p<0.01, ***p<0.001 with ANOVA, N≥8 for all groups. F) Single-cell RNA-seq analysis reveals restoration of endothelial heterogeneity with treatment. Stacked bar plots showing the proportional abundance of vascular cell populations across experimental groups. Aging markedly reduces angiogenic and proliferating endothelial subtypes, whereas FL-RSV and particularly APOE-FL-RSV treatment partially restores endothelial diversity and the presence of regenerative cell states, suggesting improved vascular maintenance capacity. G) Gene ontology enrichment indicates reduced endothelial senescence and improved barrier maintenance after APOE-FL-RSV treatment. Heatmap of endothelial GO term enrichment scores demonstrates that aging increased pathways associated with cellular senescence, endothelial stress, and barrier dysfunction, while APOE-FL-RSV shifted expression toward gene sets linked to blood–brain barrier integrity, lipid transport, and endothelial homeostasis. H-I) Measurement of learning and memory functions of the young, aged, aged + FL-RSV, aged + ApoE-FL-RSV treated animals and aged animals that have RSV per os . Young control and aged BL6 mice were subjected to vehicle, RSV per os , FL-RSV and ApoE-FL-RSV treatments and assessed for their spatial learning and memory using the Radial Arm Water Maze (RAWM). During the learning phase (days 2 to 6) and on probe (P), retrieval (R) and relearn (L) days aged mice displayed higher combined error rates compared to young mice. Treatment with FL-RSV and ApoE-FL-RSV significantly enhanced learning performance in aged mice relative to their untreated counterparts. The combined error rate was computed by adding one error for each incorrect arm entry plus an error for every 15 seconds of inactivity. Data are presented as mean±SEM (N=10–15 per group). Statistical significance indicated by *p<0.05, **p<0.01, ***p<0.001 using Repeated Measure ANOVA, demonstrating the beneficial effects of FL-RSV and ApoE-FL-RSV treatments on enhancing cognitive functions in aged mice, particularly in spatial learning, but less so in tasks requiring cognitive flexibility.

Journal: bioRxiv

Article Title: Rejuvenation of the Aged Cerebrovascular System via Protein Corona–Guided Fusogenic Liposome Delivery

doi: 10.64898/2026.03.05.709925

Figure Lengend Snippet: A) Representative images of the cerebral microvasculature recorded by functional ultrasound imaging resulting in the presented ultrasound localization microscopy images. Vascular density has been measured in the cortical (CX) and hippocampal (HIPP) areas of the mouse brain. B–C) Quantification of the cortical and hippocampal cerebral vascular density in young, aged, aged + FL-RSV and aged + ApoE-FL-RSV treated animals. D–E) Measurement of neurovascular coupling responses in the young, aged, aged + FL-RSV and aged + ApoE-FL-RSV treated mice. Note the significant differences between aged, aged + FL-RSV and aged + ApoE-FL-RSV. Data is shown in mean±SEM. *p<0.05, **p<0.01, ***p<0.001 with ANOVA, N≥8 for all groups. F) Single-cell RNA-seq analysis reveals restoration of endothelial heterogeneity with treatment. Stacked bar plots showing the proportional abundance of vascular cell populations across experimental groups. Aging markedly reduces angiogenic and proliferating endothelial subtypes, whereas FL-RSV and particularly APOE-FL-RSV treatment partially restores endothelial diversity and the presence of regenerative cell states, suggesting improved vascular maintenance capacity. G) Gene ontology enrichment indicates reduced endothelial senescence and improved barrier maintenance after APOE-FL-RSV treatment. Heatmap of endothelial GO term enrichment scores demonstrates that aging increased pathways associated with cellular senescence, endothelial stress, and barrier dysfunction, while APOE-FL-RSV shifted expression toward gene sets linked to blood–brain barrier integrity, lipid transport, and endothelial homeostasis. H-I) Measurement of learning and memory functions of the young, aged, aged + FL-RSV, aged + ApoE-FL-RSV treated animals and aged animals that have RSV per os . Young control and aged BL6 mice were subjected to vehicle, RSV per os , FL-RSV and ApoE-FL-RSV treatments and assessed for their spatial learning and memory using the Radial Arm Water Maze (RAWM). During the learning phase (days 2 to 6) and on probe (P), retrieval (R) and relearn (L) days aged mice displayed higher combined error rates compared to young mice. Treatment with FL-RSV and ApoE-FL-RSV significantly enhanced learning performance in aged mice relative to their untreated counterparts. The combined error rate was computed by adding one error for each incorrect arm entry plus an error for every 15 seconds of inactivity. Data are presented as mean±SEM (N=10–15 per group). Statistical significance indicated by *p<0.05, **p<0.01, ***p<0.001 using Repeated Measure ANOVA, demonstrating the beneficial effects of FL-RSV and ApoE-FL-RSV treatments on enhancing cognitive functions in aged mice, particularly in spatial learning, but less so in tasks requiring cognitive flexibility.

Article Snippet: The ultrasonic probe (IcoPrime-4D MultiArray 15 MHz, ICONEUS, France) of the ICONEUS One functional ultrasound device (ICONEUS, France) was positioned directly above the cranial window and submerged in ultrasound gel (Gel de contact, Drexco Medical, France).

Techniques: Functional Assay, Imaging, Ultrasound Localization Microscopy, Single Cell, RNA Sequencing, Expressing, Control

Fig. 2. In situ hybridization analysis of miR-146a expression in hippocampal tissue of control rats and after induction of SE. (A, C, E, G) Control hippocampus showing neuronal miR-146a expression in the different hippocampal subfields, including pyramidal neurons of CA3 (C; insert in C) and CA1 (E; insert in E) regions, granule cells of the dentate gyrus (DG; G) and hilar neurons (G; insert in G: high-magnification of hilar neurons). gcl, granule cell layer. (B, D, F, H) Hippocampus 1 week post-SE showing increased miR-146a expression within the different hippocampal regions, including CA3 (D; insert in D: high-magnification of CA3), CA1 (F; insert in F: high-magnification of CA1) and DG (H). miR-146a expression was observed in both neuronal and glial cells; arrows in D, F (and insert in D) indicate positive pyramidal neurons of CA3 and CA1; positive glial cells (arrowheads in D, F and insert in D) were particularly abundant in regions of prominent gliosis (CA1, CA3 and the inner molecular layer, iml, of the DG). Insert in (H) shows a high-magnification of positive glial cells in the DG (iml). (I and J) In situ hybridization analysis of miR-146a expression in the hilar region of the hippocampus 1 week (I) and 3–4 months post-SE (J) showing increased expression in glial cells (arrows; insert in I). Sections are counterstained with haematoxylin. Inserts in (J): in situ hybridization and immunohistochemistry analysis showing in (a) absence of miR-146a (red) expression in lectin-positive microglial cells (blue) and in (b) colocalization with the astroglial marker glial fibrillary acidic protein (GFAP; purple) in astrocytes. Scale bars: 1250 lm (A and B); 70 lm (C–J); 35 lm (inserts in C, D, F and G); 20 lm (insert in E); 17 lm (inserts in H and I); 11 lm (insert in J). LT, long-term, 3–4 months after SE.

Journal: The European journal of neuroscience

Article Title: Expression pattern of miR-146a, an inflammation-associated microRNA, in experimental and human temporal lobe epilepsy.

doi: 10.1111/j.1460-9568.2010.07122.x

Figure Lengend Snippet: Fig. 2. In situ hybridization analysis of miR-146a expression in hippocampal tissue of control rats and after induction of SE. (A, C, E, G) Control hippocampus showing neuronal miR-146a expression in the different hippocampal subfields, including pyramidal neurons of CA3 (C; insert in C) and CA1 (E; insert in E) regions, granule cells of the dentate gyrus (DG; G) and hilar neurons (G; insert in G: high-magnification of hilar neurons). gcl, granule cell layer. (B, D, F, H) Hippocampus 1 week post-SE showing increased miR-146a expression within the different hippocampal regions, including CA3 (D; insert in D: high-magnification of CA3), CA1 (F; insert in F: high-magnification of CA1) and DG (H). miR-146a expression was observed in both neuronal and glial cells; arrows in D, F (and insert in D) indicate positive pyramidal neurons of CA3 and CA1; positive glial cells (arrowheads in D, F and insert in D) were particularly abundant in regions of prominent gliosis (CA1, CA3 and the inner molecular layer, iml, of the DG). Insert in (H) shows a high-magnification of positive glial cells in the DG (iml). (I and J) In situ hybridization analysis of miR-146a expression in the hilar region of the hippocampus 1 week (I) and 3–4 months post-SE (J) showing increased expression in glial cells (arrows; insert in I). Sections are counterstained with haematoxylin. Inserts in (J): in situ hybridization and immunohistochemistry analysis showing in (a) absence of miR-146a (red) expression in lectin-positive microglial cells (blue) and in (b) colocalization with the astroglial marker glial fibrillary acidic protein (GFAP; purple) in astrocytes. Scale bars: 1250 lm (A and B); 70 lm (C–J); 35 lm (inserts in C, D, F and G); 20 lm (insert in E); 17 lm (inserts in H and I); 11 lm (insert in J). LT, long-term, 3–4 months after SE.

Article Snippet: For the double-staining, combining immunocytochemistry with in situ hybridization, sections were first processed for immunocytochemistry as previously described (Aronica et al., 2001a, 2003) with glial fibrillary acidic protein (GFAP; polyclonal rabbit; DAKO, Glostrup, Denmark; 1 : 4000), neuronal nuclear protein (NeuN; mouse clone MAB377; Chemicon, Temecula, CA, USA; 1 : 2000), HLA-DR [anti-human leukocyte antigen (HLA)-DP, DQ, DR (mouse clone CR3 ⁄ 43); DAKO, Glostrup, Denmark; 1 : 400], CFH (polyclonal goat; Quidel, San Diego, CA, USA; 1 : 100) or the biotinylated lectin Ricinus Communis Agglutinin I (RCA 120; Vector Laboratories, Burlingame, CA, USA; 1 : 500, for the visualization of microglial cells on rat tissue), using Fast Blue B salt (St Louis, MO, USA) or Vector Blue substrate (Vector Laboratories) as chromogen.

Techniques: In Situ Hybridization, Expressing, Control, Immunohistochemistry, Marker