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human interleukin 6 il 6 bt lab elisa kit  (Shanghai Korain Biotech Co Ltd)


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    Shanghai Korain Biotech Co Ltd human interleukin 6 il 6 bt lab elisa kit
    Human Interleukin 6 Il 6 Bt Lab Elisa Kit, supplied by Shanghai Korain Biotech Co Ltd, used in various techniques. Bioz Stars score: 95/100, based on 110 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/differentiation/Human+Interleukin+6/pmc13083175-101-0-4
    Average 95 stars, based on 110 article reviews
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    Enzyme-linked Immunosorbent Assay:

    Article Title: Cytokine profiles, genetic polymorphisms, and systemic inflammatory markers in type 1 diabetes patients with COVID-19: IL-18 a predictor of disease severity
    Article Snippet: .. Interleukin-6 (IL-6) and interleukin-10 (IL-10) levels were measured using ELISA kits from BT Laboratory (Shanghai, China; catalog numbers E0090Hu and E0102Hu, respectively). ..

    Article Title: PLA/BC/lard nanofiber composites as next-generation burn wound dressings
    Article Snippet: .. Human IL-6 and IL-17 ELISA kits (BT-Lab, Hangzhou, China) were employed according to the manufacturer's instructions. ..

    Article Title: Serum and gingival crevicular fluid asprosin levels in obese and normal-weight individuals with and without periodontitis: a cross-sectional study.
    Article Snippet: .. The sensitivity of the kits was as follows: Abcam Human Asprosin ELISA Kit (Catalog no: ab275108) – 0.92 ng/mL; BT Lab TNF-α ELISA Kit (Catalog no: E0082Hu) – 1.52 ng/L; BT Lab IL-6 ELISA Kit (Catalog no: E0090Hu) – 1.03 ng/L. ..

    Article Title: A prospective observational cohort study: neurotoxic processes associated with psychiatric symptoms in heroin use disorder: the kynurenine pathway and neopterin levels
    Article Snippet: .. Human Interleukin 6 (IL-6) BT Lab ELISA Kit (E0090Hu), Human Interferon Gamma (IFN-γ) BT Lab ELISA Kit (E0105Hu), Neopterin IBL ELISA Kit (RE59321), Human Tumor Necrosis Factor α (TNF-α) BT Lab ELISA Kit (E0082Hu) ( ). ..



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    Image Search Results


    RNA-seq profiling of human adipose-derived stem cells (hASCs) after 21 days of culture in myogenic differentiation medium. (a) Principal component analysis (PCA) based on transcriptome expression values (FPKM), showing clustering of biological replicates for Monolayer (2D), PCL, and Fibril conditions. (b) Venn diagram showing the overlap of detected genes among Monolayer, PCL, and Fibril groups (numbers indicate gene counts in each intersection). (c) Gene Ontology (GO) Biological Process (BP) over-representation analysis (ORA) for differentially expressed genes in 2D vs nFMBs (left) and PCL-mFiBs vs nFMBs (right); bars are plotted as −log10 (adjusted p value), with terms enriched among genes upregulated in the first condition shown to the right (red) and terms enriched among genes downregulated in nFMBs shown to the left (blue). (d) KEGG pathway enrichment analysis for differentially expressed genes between PCL-mFiBs and nFMBs groups; dot size represents the number of genes mapped to each pathway (Count), dot color indicates adjusted p value, and the x-axis denotes Gene Ratio. (e) Category network plot (CNP; category–gene network plot) for the PCL-mFiBs vs nFMBs comparison, visualizing representative enriched GO BP terms and their associated genes; gene nodes are colored by fold change and term nodes reflect enrichment significance. (f–i) Heatmaps of selected genes associated with representative GO terms: GO:0000280 (nuclear division), GO:0030198 (extracellular matrix organization), GO:0003012 (muscle system process), and GO:0007519 (skeletal muscle tissue development), respectively; expression patterns are shown across 2D, PCL-mFiBs, and nFMBs, with gene symbols listed alongside each heatmap.

    Journal: Bioactive Materials

    Article Title: Muscle-fiber-inspired nanofibrillar microbundles induce myogenic differentiation in human adipose-derived stem cells

    doi: 10.1016/j.bioactmat.2026.03.020

    Figure Lengend Snippet: RNA-seq profiling of human adipose-derived stem cells (hASCs) after 21 days of culture in myogenic differentiation medium. (a) Principal component analysis (PCA) based on transcriptome expression values (FPKM), showing clustering of biological replicates for Monolayer (2D), PCL, and Fibril conditions. (b) Venn diagram showing the overlap of detected genes among Monolayer, PCL, and Fibril groups (numbers indicate gene counts in each intersection). (c) Gene Ontology (GO) Biological Process (BP) over-representation analysis (ORA) for differentially expressed genes in 2D vs nFMBs (left) and PCL-mFiBs vs nFMBs (right); bars are plotted as −log10 (adjusted p value), with terms enriched among genes upregulated in the first condition shown to the right (red) and terms enriched among genes downregulated in nFMBs shown to the left (blue). (d) KEGG pathway enrichment analysis for differentially expressed genes between PCL-mFiBs and nFMBs groups; dot size represents the number of genes mapped to each pathway (Count), dot color indicates adjusted p value, and the x-axis denotes Gene Ratio. (e) Category network plot (CNP; category–gene network plot) for the PCL-mFiBs vs nFMBs comparison, visualizing representative enriched GO BP terms and their associated genes; gene nodes are colored by fold change and term nodes reflect enrichment significance. (f–i) Heatmaps of selected genes associated with representative GO terms: GO:0000280 (nuclear division), GO:0030198 (extracellular matrix organization), GO:0003012 (muscle system process), and GO:0007519 (skeletal muscle tissue development), respectively; expression patterns are shown across 2D, PCL-mFiBs, and nFMBs, with gene symbols listed alongside each heatmap.

    Article Snippet: For HSkMCs, myogenic differentiation was induced using Skeletal Muscle Differentiation Medium (ATCC, Manassas, USA).

    Techniques: RNA Sequencing, Derivative Assay, Cell Characterization, Expressing, Comparison

    Eight weeks of aerobic exercise improved the proliferation and migration capabilities of circulating EPC in both humans and rats with obesity through circulating exosomes. (A) Representative transmission electron microscopy image of exosomes derived from human peripheral blood. Scale bar = 200 nm. (B) Exosome characterization and identification. Exosomes derived from human peripheral blood express TSG101 and CD63. (C) Nanoparticle tracking analysis confirms the presence of exosomes with a peak diameter of 100 nm, characteristic of exosomal size. Quantitative analysis of exosomes derived from human peripheral blood revealed no statistically significant difference in the number of exosomes isolated from equal volumes of circulating blood between the control group and the exercise group ( n = 30 for each group). (D) Cell proliferation assay results showed that exosomes derived from the exercise group significantly enhanced the proliferative capacity of human EPC compared to those from the control group, as measured by the CCK-8 method ( n = 20 for each group). *** p < 0.001, Exercise vs . Control. (E) Scratch assay results showed that exosomes derived from the exercise group significantly promoted the migratory ability of human EPC compared to those from the control group ( n = 5 for each group). * p < 0.05, Exercise vs . Control. (F) Representative images of wound healing in the scratch assay, showcasing the migratory response of human EPC. (G) Characterization of circulating exosomes from rat peripheral blood. (H) Quantitative analysis of exosomes derived from rat peripheral blood revealed no statistically significant difference in the number of exosomes isolated from equal volumes of circulating blood among all groups ( n = 3 for each group). (I) Cell proliferation assays revealed that exosomes derived from the HC group exhibited a diminished capacity to promote EPC proliferation compared to those from the NC group in rats. In contrast, exosomes induced by 8 weeks of aerobic exercise significantly enhanced EPC proliferation ( n : 5–6 for each group). * p < 0.05, HC vs . NC; ## p < 0.01, HE vs . HC. (J) Scratch assays indicated that exosomes derived from the HC group exhibited a diminished capacity to enhance EPC migration rates compared to those from the NC group in rats. In contrast, exosomes induced by 8 weeks of aerobic exercise significantly enhanced EPC migration rates ( n = 4 for each group). ** p < 0.01, HC vs . NC; ## p < 0.01, HE vs . HC. (K) Representative images of wound healing in the scratch assay, showcasing the migratory response of rat EPC. CCK-8 = cell counting kit-8; CD63 = cluster of differentiation 63; EPC = endothelial progenitor cells; HC = the high-fat diet with sedentary group; HE = the high-fat diet with exercise group; NC = the normal diet with sedentary group; TSG101 = tumor susceptibility gene 101.

    Journal: Journal of Sport and Health Science

    Article Title: Long-term aerobic exercise enhances circulating exosomal miR-214-3p to promote endothelial progenitor cell-mediated repair of endothelial damage induced by obesity

    doi: 10.1016/j.jshs.2025.101094

    Figure Lengend Snippet: Eight weeks of aerobic exercise improved the proliferation and migration capabilities of circulating EPC in both humans and rats with obesity through circulating exosomes. (A) Representative transmission electron microscopy image of exosomes derived from human peripheral blood. Scale bar = 200 nm. (B) Exosome characterization and identification. Exosomes derived from human peripheral blood express TSG101 and CD63. (C) Nanoparticle tracking analysis confirms the presence of exosomes with a peak diameter of 100 nm, characteristic of exosomal size. Quantitative analysis of exosomes derived from human peripheral blood revealed no statistically significant difference in the number of exosomes isolated from equal volumes of circulating blood between the control group and the exercise group ( n = 30 for each group). (D) Cell proliferation assay results showed that exosomes derived from the exercise group significantly enhanced the proliferative capacity of human EPC compared to those from the control group, as measured by the CCK-8 method ( n = 20 for each group). *** p < 0.001, Exercise vs . Control. (E) Scratch assay results showed that exosomes derived from the exercise group significantly promoted the migratory ability of human EPC compared to those from the control group ( n = 5 for each group). * p < 0.05, Exercise vs . Control. (F) Representative images of wound healing in the scratch assay, showcasing the migratory response of human EPC. (G) Characterization of circulating exosomes from rat peripheral blood. (H) Quantitative analysis of exosomes derived from rat peripheral blood revealed no statistically significant difference in the number of exosomes isolated from equal volumes of circulating blood among all groups ( n = 3 for each group). (I) Cell proliferation assays revealed that exosomes derived from the HC group exhibited a diminished capacity to promote EPC proliferation compared to those from the NC group in rats. In contrast, exosomes induced by 8 weeks of aerobic exercise significantly enhanced EPC proliferation ( n : 5–6 for each group). * p < 0.05, HC vs . NC; ## p < 0.01, HE vs . HC. (J) Scratch assays indicated that exosomes derived from the HC group exhibited a diminished capacity to enhance EPC migration rates compared to those from the NC group in rats. In contrast, exosomes induced by 8 weeks of aerobic exercise significantly enhanced EPC migration rates ( n = 4 for each group). ** p < 0.01, HC vs . NC; ## p < 0.01, HE vs . HC. (K) Representative images of wound healing in the scratch assay, showcasing the migratory response of rat EPC. CCK-8 = cell counting kit-8; CD63 = cluster of differentiation 63; EPC = endothelial progenitor cells; HC = the high-fat diet with sedentary group; HE = the high-fat diet with exercise group; NC = the normal diet with sedentary group; TSG101 = tumor susceptibility gene 101.

    Article Snippet: The primary antibodies used included PI3K (SC-365290, 1:1000; Santa Cruz Biotechnology, Dallas, TX, USA), Akt1 (SC-5298, 1:1000; Santa Cruz), p-Akt (Ser473) (66444-1-lg, 1:1000; Proteintech Group, Rosemont, IL, USA), phosphatase and tensin homolog (PTEN) (60300-1-Ig, 1:1000; Proteintech), tumor susceptibility gene 101 (TSG101) (DF8427, 1:1000; Affinity Biosciences, Cincinnati, OH, USA), cluster of differentiation 63 (CD63) (AF5117, 1:1000; Affinity), and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) (GB15002-100, 1:4000; Servicebio).

    Techniques: Migration, Transmission Assay, Electron Microscopy, Derivative Assay, Isolation, Control, Proliferation Assay, CCK-8 Assay, Wound Healing Assay, Cell Counting