raybio® human vitronectin elisa kit Search Results


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Human Beta Ngf Elisa Kit, supplied by RayBiotech inc, 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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RayBiotech inc human il 4 elisa kit
Protein expression analysis of caspases and inflammatory markers in HCT116 cells treated with P. crispa Hex F. Protein levels were quantified using specific <t>ELISA</t> kits according to manufacturer's protocols. Cells were treated with 39.4 μg/mL Hex F for 48 h. After treatment with P. crispa Hex F, cell lysates were prepared, and enzymatic activities were measured by a colorimetric assay for A Caspase activity analysis showing significant activation of executioner caspases: caspase-3 (Casp3) (primary executioner caspase responsible for DNA fragmentation and apoptotic body formation) and caspase-7 (Casp7) (secondary executioner caspase with similar function to caspase-3). B Inflammatory marker analysis demonstrating anti-inflammatory response: IL-10 (an anti-inflammatory cytokine that suppresses inflammatory responses) and IL-4 (pro-inflammatory cytokine involved in Th2 immune responses). Data represent mean ± SD of three independent experiments performed in triplicate. Statistical significance: ** p < 0.005, and *** p < 0.001 compared to untreated control using independent t-test. Error bars represent standard deviation
Human Il 4 Elisa Kit, supplied by RayBiotech inc, 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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RayBiotech inc human leptin elisa kit
Protein expression analysis of caspases and inflammatory markers in HCT116 cells treated with P. crispa Hex F. Protein levels were quantified using specific <t>ELISA</t> kits according to manufacturer's protocols. Cells were treated with 39.4 μg/mL Hex F for 48 h. After treatment with P. crispa Hex F, cell lysates were prepared, and enzymatic activities were measured by a colorimetric assay for A Caspase activity analysis showing significant activation of executioner caspases: caspase-3 (Casp3) (primary executioner caspase responsible for DNA fragmentation and apoptotic body formation) and caspase-7 (Casp7) (secondary executioner caspase with similar function to caspase-3). B Inflammatory marker analysis demonstrating anti-inflammatory response: IL-10 (an anti-inflammatory cytokine that suppresses inflammatory responses) and IL-4 (pro-inflammatory cytokine involved in Th2 immune responses). Data represent mean ± SD of three independent experiments performed in triplicate. Statistical significance: ** p < 0.005, and *** p < 0.001 compared to untreated control using independent t-test. Error bars represent standard deviation
Human Leptin Elisa Kit, supplied by RayBiotech inc, 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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RayBiotech inc human tnf α elisa kit
Protein expression analysis of caspases and inflammatory markers in HCT116 cells treated with P. crispa Hex F. Protein levels were quantified using specific <t>ELISA</t> kits according to manufacturer's protocols. Cells were treated with 39.4 μg/mL Hex F for 48 h. After treatment with P. crispa Hex F, cell lysates were prepared, and enzymatic activities were measured by a colorimetric assay for A Caspase activity analysis showing significant activation of executioner caspases: caspase-3 (Casp3) (primary executioner caspase responsible for DNA fragmentation and apoptotic body formation) and caspase-7 (Casp7) (secondary executioner caspase with similar function to caspase-3). B Inflammatory marker analysis demonstrating anti-inflammatory response: IL-10 (an anti-inflammatory cytokine that suppresses inflammatory responses) and IL-4 (pro-inflammatory cytokine involved in Th2 immune responses). Data represent mean ± SD of three independent experiments performed in triplicate. Statistical significance: ** p < 0.005, and *** p < 0.001 compared to untreated control using independent t-test. Error bars represent standard deviation
Human Tnf α Elisa Kit, supplied by RayBiotech inc, 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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RayBiotech inc human rtk phosphorylation antibody array kit
Figure 5. PMI combined with ADR suppresses the <t>phosphorylation</t> of receptor tyrosine kinases in GC cell lines. (A and B) SGC7901 cells were treated with ADR (1.0 µM) or ADR (1.0 µM) combined with PMI (50.0 µM) and proteins were detected by the RayBio® Human <t>RTK</t> phosphorylation antibody array kit (chemilumi- nescent readout). 1, p-EGFR; 2, ACK1; 3, CsK; 4, EphA4; 5, EphA5; 6, EphA6; 7, EphA7; 8, EphB3; 9, FAK; 10, FER; 11, Fgr; 12, FRK; 13, LTK; 14, PDGFR-α; 15, ROS; 16, Tie-1; 17, Tie-2; 18, TyK2; 19, TYRO10. (C and D) Expression levels of p-EGFR, EGFR, p-FAK, FAK, cyclin D1 and cleaved (cl)-PARP were detected using western blotting. β-actin was used as a reference control. ADR, adriamycin; PMI, peiminine; *P<0.05, **P<0.01 compared with the ADR alone group.
Human Rtk Phosphorylation Antibody Array Kit, supplied by RayBiotech inc, 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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RayBiotech inc l series human antibody array 1000 glass slide kit
Figure 5. PMI combined with ADR suppresses the <t>phosphorylation</t> of receptor tyrosine kinases in GC cell lines. (A and B) SGC7901 cells were treated with ADR (1.0 µM) or ADR (1.0 µM) combined with PMI (50.0 µM) and proteins were detected by the RayBio® Human <t>RTK</t> phosphorylation antibody array kit (chemilumi- nescent readout). 1, p-EGFR; 2, ACK1; 3, CsK; 4, EphA4; 5, EphA5; 6, EphA6; 7, EphA7; 8, EphB3; 9, FAK; 10, FER; 11, Fgr; 12, FRK; 13, LTK; 14, PDGFR-α; 15, ROS; 16, Tie-1; 17, Tie-2; 18, TyK2; 19, TYRO10. (C and D) Expression levels of p-EGFR, EGFR, p-FAK, FAK, cyclin D1 and cleaved (cl)-PARP were detected using western blotting. β-actin was used as a reference control. ADR, adriamycin; PMI, peiminine; *P<0.05, **P<0.01 compared with the ADR alone group.
L Series Human Antibody Array 1000 Glass Slide Kit, supplied by RayBiotech inc, 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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RayBiotech inc ccl2 elisa kit
Fig. 4 BMAL1-mediated transcription of <t>CCL2</t> is altered in adipocyte precursors from obese patients. A–D ChIP analyses of BMAL1 and RNA POLII on CCL2 promoter in non-obese (blue) or obese (red) OAPs, either non-synchronized or harvested 27 h and 38 h post-synchronization. Mean ± SEM in fold enrichment over IgG; n = 6 independent cultures/group from three patients in each non-obese and obese group. E CCL2 gene expression in synchronized non-obese vs. obese OAPs. Mean ± SEM in mRNA RA, n = 8 (non-obese) and n = 7 (obese) independent cultures from four patients in each group. F Measurement of CCL2 secretion in synchronized non-obese vs. obese OAPs, between 27–33 h and 38–44 h post-synchronization. Mean ± SEM in pg/ ml; n = 4 patients/group. G ChIP analyses of BMAL1 in non-synchronized obese OAPs exposed to 10 μM JSH-23 (gray) vs. untreated (DMSO, Ctrl, red). Mean ± SEM in fold enrichment over IgG; n = 4 independent cultures from two patients. *p < 0.05, unpaired two-tailed t-test (A, B); **p < 0.01, paired two- tailed t-test (G); The effect of condition and time was tested by two-way ANOVA followed by post hoc Sidak’s test (C–F), *p < 0.05, **p < 0.01, ***p < 0.001 for unpaired measures (non-obese/obese), #p < 0.05, ##p < 0.01, ###p < 0.001 for paired measures (27 h vs. 38 h or 27–33 h and 38–44 h). H Proposed model of obesity linking circadian clock dysfunction in human omental fat and metabolic inflammation. The molecular clock is encoded by transcription–translation feedback loops composed of activators BMAL1 (B) and CLOCK (C) that induce the transcription of repressors, the most important being PER2. PER2 feeds back to inhibit the forward limb. This process generates a rhythm of ~24 h. In obesity, NF-κB activity is increased: increased NF-κB p65 binding prevents BMAL1 binding to PER2 E-box, thereby reducing BMAL1-mediated transcription of PER2 and inducing lengthening of the circadian period. The concomitant decreased BMAL1 binding to CCL2 leads to actively transcribed CCL2 and subsequent upregulated CCL2 secretion. In obesity, increased or decreased BMAL1 binding at other loci was associated with an altered production of the targets (“Other”; BMAL1 exerting a transactivator/ repressor role, see infra), contributing to metabolic inflammation and adipose remodeling (macrophages, purple; fibrosis, red). See also Supplementary Fig. 3.
Ccl2 Elisa Kit, supplied by RayBiotech inc, 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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RayBiotech inc tumors raybio human il 7 elisa kit ray biotech inc and quantikine elisa mouse il 12 p70 immunoassay r d systems respectively
Fig. 4 BMAL1-mediated transcription of <t>CCL2</t> is altered in adipocyte precursors from obese patients. A–D ChIP analyses of BMAL1 and RNA POLII on CCL2 promoter in non-obese (blue) or obese (red) OAPs, either non-synchronized or harvested 27 h and 38 h post-synchronization. Mean ± SEM in fold enrichment over IgG; n = 6 independent cultures/group from three patients in each non-obese and obese group. E CCL2 gene expression in synchronized non-obese vs. obese OAPs. Mean ± SEM in mRNA RA, n = 8 (non-obese) and n = 7 (obese) independent cultures from four patients in each group. F Measurement of CCL2 secretion in synchronized non-obese vs. obese OAPs, between 27–33 h and 38–44 h post-synchronization. Mean ± SEM in pg/ ml; n = 4 patients/group. G ChIP analyses of BMAL1 in non-synchronized obese OAPs exposed to 10 μM JSH-23 (gray) vs. untreated (DMSO, Ctrl, red). Mean ± SEM in fold enrichment over IgG; n = 4 independent cultures from two patients. *p < 0.05, unpaired two-tailed t-test (A, B); **p < 0.01, paired two- tailed t-test (G); The effect of condition and time was tested by two-way ANOVA followed by post hoc Sidak’s test (C–F), *p < 0.05, **p < 0.01, ***p < 0.001 for unpaired measures (non-obese/obese), #p < 0.05, ##p < 0.01, ###p < 0.001 for paired measures (27 h vs. 38 h or 27–33 h and 38–44 h). H Proposed model of obesity linking circadian clock dysfunction in human omental fat and metabolic inflammation. The molecular clock is encoded by transcription–translation feedback loops composed of activators BMAL1 (B) and CLOCK (C) that induce the transcription of repressors, the most important being PER2. PER2 feeds back to inhibit the forward limb. This process generates a rhythm of ~24 h. In obesity, NF-κB activity is increased: increased NF-κB p65 binding prevents BMAL1 binding to PER2 E-box, thereby reducing BMAL1-mediated transcription of PER2 and inducing lengthening of the circadian period. The concomitant decreased BMAL1 binding to CCL2 leads to actively transcribed CCL2 and subsequent upregulated CCL2 secretion. In obesity, increased or decreased BMAL1 binding at other loci was associated with an altered production of the targets (“Other”; BMAL1 exerting a transactivator/ repressor role, see infra), contributing to metabolic inflammation and adipose remodeling (macrophages, purple; fibrosis, red). See also Supplementary Fig. 3.
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Figure 2. Example of electrophoretic separation of PCR products for <t>VEGF-B,</t> MWM-molecular weight marker (50–500 bp); 1–6-samples (84 bp); 7-positive control; 8-negative control.
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Figure 2. Example of electrophoretic separation of PCR products for <t>VEGF-B,</t> MWM-molecular weight marker (50–500 bp); 1–6-samples (84 bp); 7-positive control; 8-negative control.
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Figure 2. Example of electrophoretic separation of PCR products for <t>VEGF-B,</t> MWM-molecular weight marker (50–500 bp); 1–6-samples (84 bp); 7-positive control; 8-negative control.
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Serum <t> BDNF </t> levels in stroke patients with and without type 2 diabetes mellitus
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Image Search Results


Protein expression analysis of caspases and inflammatory markers in HCT116 cells treated with P. crispa Hex F. Protein levels were quantified using specific ELISA kits according to manufacturer's protocols. Cells were treated with 39.4 μg/mL Hex F for 48 h. After treatment with P. crispa Hex F, cell lysates were prepared, and enzymatic activities were measured by a colorimetric assay for A Caspase activity analysis showing significant activation of executioner caspases: caspase-3 (Casp3) (primary executioner caspase responsible for DNA fragmentation and apoptotic body formation) and caspase-7 (Casp7) (secondary executioner caspase with similar function to caspase-3). B Inflammatory marker analysis demonstrating anti-inflammatory response: IL-10 (an anti-inflammatory cytokine that suppresses inflammatory responses) and IL-4 (pro-inflammatory cytokine involved in Th2 immune responses). Data represent mean ± SD of three independent experiments performed in triplicate. Statistical significance: ** p < 0.005, and *** p < 0.001 compared to untreated control using independent t-test. Error bars represent standard deviation

Journal: 3 Biotech

Article Title: Molecular mechanisms underlying the potential anticancer activity of Pulicaria crispa hexane fraction in HCT116 cancer cells

doi: 10.1007/s13205-025-04423-1

Figure Lengend Snippet: Protein expression analysis of caspases and inflammatory markers in HCT116 cells treated with P. crispa Hex F. Protein levels were quantified using specific ELISA kits according to manufacturer's protocols. Cells were treated with 39.4 μg/mL Hex F for 48 h. After treatment with P. crispa Hex F, cell lysates were prepared, and enzymatic activities were measured by a colorimetric assay for A Caspase activity analysis showing significant activation of executioner caspases: caspase-3 (Casp3) (primary executioner caspase responsible for DNA fragmentation and apoptotic body formation) and caspase-7 (Casp7) (secondary executioner caspase with similar function to caspase-3). B Inflammatory marker analysis demonstrating anti-inflammatory response: IL-10 (an anti-inflammatory cytokine that suppresses inflammatory responses) and IL-4 (pro-inflammatory cytokine involved in Th2 immune responses). Data represent mean ± SD of three independent experiments performed in triplicate. Statistical significance: ** p < 0.005, and *** p < 0.001 compared to untreated control using independent t-test. Error bars represent standard deviation

Article Snippet: On the other hand, inflammatory markers IL10 and IL4 were also measured in both treated and untreated HCT116 cells in triplicates using the kits (ab46034–IL-10 Human ELISA Kit, Abcam®, UK) and (RayBio® Human IL-4 ELISA Kit) respectively following the cytokine measurement protocols established by Bienvenu et al. ( ).

Techniques: Expressing, Enzyme-linked Immunosorbent Assay, Colorimetric Assay, Activity Assay, Activation Assay, Marker, Control, Standard Deviation

Figure 5. PMI combined with ADR suppresses the phosphorylation of receptor tyrosine kinases in GC cell lines. (A and B) SGC7901 cells were treated with ADR (1.0 µM) or ADR (1.0 µM) combined with PMI (50.0 µM) and proteins were detected by the RayBio® Human RTK phosphorylation antibody array kit (chemilumi- nescent readout). 1, p-EGFR; 2, ACK1; 3, CsK; 4, EphA4; 5, EphA5; 6, EphA6; 7, EphA7; 8, EphB3; 9, FAK; 10, FER; 11, Fgr; 12, FRK; 13, LTK; 14, PDGFR-α; 15, ROS; 16, Tie-1; 17, Tie-2; 18, TyK2; 19, TYRO10. (C and D) Expression levels of p-EGFR, EGFR, p-FAK, FAK, cyclin D1 and cleaved (cl)-PARP were detected using western blotting. β-actin was used as a reference control. ADR, adriamycin; PMI, peiminine; *P<0.05, **P<0.01 compared with the ADR alone group.

Journal: Oncology reports

Article Title: Peiminine serves as an adriamycin chemosensitizer in gastric cancer by modulating the EGFR/FAK pathway.

doi: 10.3892/or.2018.6184

Figure Lengend Snippet: Figure 5. PMI combined with ADR suppresses the phosphorylation of receptor tyrosine kinases in GC cell lines. (A and B) SGC7901 cells were treated with ADR (1.0 µM) or ADR (1.0 µM) combined with PMI (50.0 µM) and proteins were detected by the RayBio® Human RTK phosphorylation antibody array kit (chemilumi- nescent readout). 1, p-EGFR; 2, ACK1; 3, CsK; 4, EphA4; 5, EphA5; 6, EphA6; 7, EphA7; 8, EphB3; 9, FAK; 10, FER; 11, Fgr; 12, FRK; 13, LTK; 14, PDGFR-α; 15, ROS; 16, Tie-1; 17, Tie-2; 18, TyK2; 19, TYRO10. (C and D) Expression levels of p-EGFR, EGFR, p-FAK, FAK, cyclin D1 and cleaved (cl)-PARP were detected using western blotting. β-actin was used as a reference control. ADR, adriamycin; PMI, peiminine; *P<0.05, **P<0.01 compared with the ADR alone group.

Article Snippet: The RayBio® Human RTK phosphorylation antibody array kit was used to test the differential protein expression.

Techniques: Phospho-proteomics, Ab Array, Expressing, Western Blot, Control

Fig. 4 BMAL1-mediated transcription of CCL2 is altered in adipocyte precursors from obese patients. A–D ChIP analyses of BMAL1 and RNA POLII on CCL2 promoter in non-obese (blue) or obese (red) OAPs, either non-synchronized or harvested 27 h and 38 h post-synchronization. Mean ± SEM in fold enrichment over IgG; n = 6 independent cultures/group from three patients in each non-obese and obese group. E CCL2 gene expression in synchronized non-obese vs. obese OAPs. Mean ± SEM in mRNA RA, n = 8 (non-obese) and n = 7 (obese) independent cultures from four patients in each group. F Measurement of CCL2 secretion in synchronized non-obese vs. obese OAPs, between 27–33 h and 38–44 h post-synchronization. Mean ± SEM in pg/ ml; n = 4 patients/group. G ChIP analyses of BMAL1 in non-synchronized obese OAPs exposed to 10 μM JSH-23 (gray) vs. untreated (DMSO, Ctrl, red). Mean ± SEM in fold enrichment over IgG; n = 4 independent cultures from two patients. *p < 0.05, unpaired two-tailed t-test (A, B); **p < 0.01, paired two- tailed t-test (G); The effect of condition and time was tested by two-way ANOVA followed by post hoc Sidak’s test (C–F), *p < 0.05, **p < 0.01, ***p < 0.001 for unpaired measures (non-obese/obese), #p < 0.05, ##p < 0.01, ###p < 0.001 for paired measures (27 h vs. 38 h or 27–33 h and 38–44 h). H Proposed model of obesity linking circadian clock dysfunction in human omental fat and metabolic inflammation. The molecular clock is encoded by transcription–translation feedback loops composed of activators BMAL1 (B) and CLOCK (C) that induce the transcription of repressors, the most important being PER2. PER2 feeds back to inhibit the forward limb. This process generates a rhythm of ~24 h. In obesity, NF-κB activity is increased: increased NF-κB p65 binding prevents BMAL1 binding to PER2 E-box, thereby reducing BMAL1-mediated transcription of PER2 and inducing lengthening of the circadian period. The concomitant decreased BMAL1 binding to CCL2 leads to actively transcribed CCL2 and subsequent upregulated CCL2 secretion. In obesity, increased or decreased BMAL1 binding at other loci was associated with an altered production of the targets (“Other”; BMAL1 exerting a transactivator/ repressor role, see infra), contributing to metabolic inflammation and adipose remodeling (macrophages, purple; fibrosis, red). See also Supplementary Fig. 3.

Journal: Nature communications

Article Title: Circadian clock dysfunction in human omental fat links obesity to metabolic inflammation.

doi: 10.1038/s41467-021-22571-9

Figure Lengend Snippet: Fig. 4 BMAL1-mediated transcription of CCL2 is altered in adipocyte precursors from obese patients. A–D ChIP analyses of BMAL1 and RNA POLII on CCL2 promoter in non-obese (blue) or obese (red) OAPs, either non-synchronized or harvested 27 h and 38 h post-synchronization. Mean ± SEM in fold enrichment over IgG; n = 6 independent cultures/group from three patients in each non-obese and obese group. E CCL2 gene expression in synchronized non-obese vs. obese OAPs. Mean ± SEM in mRNA RA, n = 8 (non-obese) and n = 7 (obese) independent cultures from four patients in each group. F Measurement of CCL2 secretion in synchronized non-obese vs. obese OAPs, between 27–33 h and 38–44 h post-synchronization. Mean ± SEM in pg/ ml; n = 4 patients/group. G ChIP analyses of BMAL1 in non-synchronized obese OAPs exposed to 10 μM JSH-23 (gray) vs. untreated (DMSO, Ctrl, red). Mean ± SEM in fold enrichment over IgG; n = 4 independent cultures from two patients. *p < 0.05, unpaired two-tailed t-test (A, B); **p < 0.01, paired two- tailed t-test (G); The effect of condition and time was tested by two-way ANOVA followed by post hoc Sidak’s test (C–F), *p < 0.05, **p < 0.01, ***p < 0.001 for unpaired measures (non-obese/obese), #p < 0.05, ##p < 0.01, ###p < 0.001 for paired measures (27 h vs. 38 h or 27–33 h and 38–44 h). H Proposed model of obesity linking circadian clock dysfunction in human omental fat and metabolic inflammation. The molecular clock is encoded by transcription–translation feedback loops composed of activators BMAL1 (B) and CLOCK (C) that induce the transcription of repressors, the most important being PER2. PER2 feeds back to inhibit the forward limb. This process generates a rhythm of ~24 h. In obesity, NF-κB activity is increased: increased NF-κB p65 binding prevents BMAL1 binding to PER2 E-box, thereby reducing BMAL1-mediated transcription of PER2 and inducing lengthening of the circadian period. The concomitant decreased BMAL1 binding to CCL2 leads to actively transcribed CCL2 and subsequent upregulated CCL2 secretion. In obesity, increased or decreased BMAL1 binding at other loci was associated with an altered production of the targets (“Other”; BMAL1 exerting a transactivator/ repressor role, see infra), contributing to metabolic inflammation and adipose remodeling (macrophages, purple; fibrosis, red). See also Supplementary Fig. 3.

Article Snippet: CCL2 ELISA Kit (RayBio® Human MCP1 ELISA kit, #ELH-MCP1) was performed according to the manufacturer’s instructions.

Techniques: Gene Expression, Two Tailed Test, Activity Assay, Binding Assay

Figure 2. Example of electrophoretic separation of PCR products for VEGF-B, MWM-molecular weight marker (50–500 bp); 1–6-samples (84 bp); 7-positive control; 8-negative control.

Journal: Applied Sciences

Article Title: Systemic Antibiotic and Nonsteroidal Anti-Inflammatory Drug Treatment Decreases the Level of Endogenous Angiogenic Vascular Endothelial Growth Factor in Inflamed Human Periapical Tissues

doi: 10.3390/app11114976

Figure Lengend Snippet: Figure 2. Example of electrophoretic separation of PCR products for VEGF-B, MWM-molecular weight marker (50–500 bp); 1–6-samples (84 bp); 7-positive control; 8-negative control.

Article Snippet: In all the groups, VEGF levels were measured using a RayBio Human VEGF ELISA kit (RayBiotech Inc.) according to the manufacturer’s specifications.

Techniques: Molecular Weight, Marker, Positive Control, Negative Control

Figure 3. VEGF concentration in all groups of patients: group I (NSAIDs), group II (antibiotics), group II (NSAID and antibiotics) and control group (no drug treatment).

Journal: Applied Sciences

Article Title: Systemic Antibiotic and Nonsteroidal Anti-Inflammatory Drug Treatment Decreases the Level of Endogenous Angiogenic Vascular Endothelial Growth Factor in Inflamed Human Periapical Tissues

doi: 10.3390/app11114976

Figure Lengend Snippet: Figure 3. VEGF concentration in all groups of patients: group I (NSAIDs), group II (antibiotics), group II (NSAID and antibiotics) and control group (no drug treatment).

Article Snippet: In all the groups, VEGF levels were measured using a RayBio Human VEGF ELISA kit (RayBiotech Inc.) according to the manufacturer’s specifications.

Techniques: Concentration Assay, Control

Serum  BDNF  levels in stroke patients with and without type 2 diabetes mellitus

Journal: Journal of Family Medicine and Primary Care

Article Title: Diabetes mellitus type 2 impedes functional recovery, neuroplasticity and quality of life after stroke

doi: 10.4103/jfmpc.jfmpc_884_19

Figure Lengend Snippet: Serum BDNF levels in stroke patients with and without type 2 diabetes mellitus

Article Snippet: [ ] Serum concentration of BDNF was assessed by enzyme linked immunosorbent assay (ELISA) using double-sandwich human BDNF ELISA kit (Raybiomed, Boster).

Techniques:

Risk factors for poor improvement in  BDNF  levels and FIM scores 6 months after stroke

Journal: Journal of Family Medicine and Primary Care

Article Title: Diabetes mellitus type 2 impedes functional recovery, neuroplasticity and quality of life after stroke

doi: 10.4103/jfmpc.jfmpc_884_19

Figure Lengend Snippet: Risk factors for poor improvement in BDNF levels and FIM scores 6 months after stroke

Article Snippet: [ ] Serum concentration of BDNF was assessed by enzyme linked immunosorbent assay (ELISA) using double-sandwich human BDNF ELISA kit (Raybiomed, Boster).

Techniques:

Possible causes of reduced BDNF levels in diabetes

Journal: Journal of Family Medicine and Primary Care

Article Title: Diabetes mellitus type 2 impedes functional recovery, neuroplasticity and quality of life after stroke

doi: 10.4103/jfmpc.jfmpc_884_19

Figure Lengend Snippet: Possible causes of reduced BDNF levels in diabetes

Article Snippet: [ ] Serum concentration of BDNF was assessed by enzyme linked immunosorbent assay (ELISA) using double-sandwich human BDNF ELISA kit (Raybiomed, Boster).

Techniques: