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fbm tm basal medium  (Lonza)


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    Structured Review

    Lonza fbm tm basal medium
    Conditions and resultant cells from PolA1 inhibitor treated human dermal <t>fibroblast</t> cells in iPSC reprogramming process . ( A ) EdU was pulsed for 20 minutes followed by quantification of EdU+ cells in human dermal fibroblast cells without and with different concentrations of PolA1 inhibitor. ( B ) Compared to the control (4.28±1.56%), no EdU+ cells were detected with PolA1 inhibitor treatment at high concentrations (10 µM, 1 µM, and 0.1 µM). In contrast, low concentrations of PolA1 treatment (0.02 µM: 4.95±1.09%, and 0.01 µM: 4.95±2.45%) show similar percentages of EdU+ cells: P =0.5368 (0.02 µM treatment vs. control) and P =0.8413 (0.01 µM treatment vs. control). All values = Average ±SEM, statistics was done using Mann Whitney test. ( C ) The NANOG and PDGFRα staining and at D4 and D10 during human iPSC reprogramming. ( D ) The live staining of TRA 1-60 in cells at D11 during reprogramming with and without PolA1 inhibitor. Ctrl: 17424±949.4; PolA1 treated: 26602±1137. **** P <10 -4 , Average ± SEM by Mann Whitney test. ( E ) Immunofluorescence staining of iPSCs (Passage 6) shows strong expression of pluripotency markers in both control and PolA1 inhibitor treated human iPSCs. The pluripotency markers NANOG, OCT4 and SOX2 were examined using immunostaining. Scale: 50 µm. ( F ) Feature plots show expression of NANOG, a well-known pluripotency stem cell marker in all samples. Two differentiation markers, PAX6 and SOX1, are detected in a very small subset of cells, due to a technical issue with high confluence of the cells .
    Fbm Tm Basal Medium, supplied by Lonza, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/fbm+tm+basal+medium/fbm+basal+medium/bio_rxiv__2024__09__19__613993-276-14-28
    Average 90 stars, based on 1 article reviews
    fbm tm basal medium - by Bioz Stars, 2026-10
    90/100 stars

    Images

    1) Product Images from "Modulating DNA Polα Enhances Cell Reprogramming Across Species"

    Article Title: Modulating DNA Polα Enhances Cell Reprogramming Across Species

    Journal: bioRxiv

    doi: 10.1101/2024.09.19.613993

    Conditions and resultant cells from PolA1 inhibitor treated human dermal fibroblast cells in iPSC reprogramming process . ( A ) EdU was pulsed for 20 minutes followed by quantification of EdU+ cells in human dermal fibroblast cells without and with different concentrations of PolA1 inhibitor. ( B ) Compared to the control (4.28±1.56%), no EdU+ cells were detected with PolA1 inhibitor treatment at high concentrations (10 µM, 1 µM, and 0.1 µM). In contrast, low concentrations of PolA1 treatment (0.02 µM: 4.95±1.09%, and 0.01 µM: 4.95±2.45%) show similar percentages of EdU+ cells: P =0.5368 (0.02 µM treatment vs. control) and P =0.8413 (0.01 µM treatment vs. control). All values = Average ±SEM, statistics was done using Mann Whitney test. ( C ) The NANOG and PDGFRα staining and at D4 and D10 during human iPSC reprogramming. ( D ) The live staining of TRA 1-60 in cells at D11 during reprogramming with and without PolA1 inhibitor. Ctrl: 17424±949.4; PolA1 treated: 26602±1137. **** P <10 -4 , Average ± SEM by Mann Whitney test. ( E ) Immunofluorescence staining of iPSCs (Passage 6) shows strong expression of pluripotency markers in both control and PolA1 inhibitor treated human iPSCs. The pluripotency markers NANOG, OCT4 and SOX2 were examined using immunostaining. Scale: 50 µm. ( F ) Feature plots show expression of NANOG, a well-known pluripotency stem cell marker in all samples. Two differentiation markers, PAX6 and SOX1, are detected in a very small subset of cells, due to a technical issue with high confluence of the cells .
    Figure Legend Snippet: Conditions and resultant cells from PolA1 inhibitor treated human dermal fibroblast cells in iPSC reprogramming process . ( A ) EdU was pulsed for 20 minutes followed by quantification of EdU+ cells in human dermal fibroblast cells without and with different concentrations of PolA1 inhibitor. ( B ) Compared to the control (4.28±1.56%), no EdU+ cells were detected with PolA1 inhibitor treatment at high concentrations (10 µM, 1 µM, and 0.1 µM). In contrast, low concentrations of PolA1 treatment (0.02 µM: 4.95±1.09%, and 0.01 µM: 4.95±2.45%) show similar percentages of EdU+ cells: P =0.5368 (0.02 µM treatment vs. control) and P =0.8413 (0.01 µM treatment vs. control). All values = Average ±SEM, statistics was done using Mann Whitney test. ( C ) The NANOG and PDGFRα staining and at D4 and D10 during human iPSC reprogramming. ( D ) The live staining of TRA 1-60 in cells at D11 during reprogramming with and without PolA1 inhibitor. Ctrl: 17424±949.4; PolA1 treated: 26602±1137. **** P <10 -4 , Average ± SEM by Mann Whitney test. ( E ) Immunofluorescence staining of iPSCs (Passage 6) shows strong expression of pluripotency markers in both control and PolA1 inhibitor treated human iPSCs. The pluripotency markers NANOG, OCT4 and SOX2 were examined using immunostaining. Scale: 50 µm. ( F ) Feature plots show expression of NANOG, a well-known pluripotency stem cell marker in all samples. Two differentiation markers, PAX6 and SOX1, are detected in a very small subset of cells, due to a technical issue with high confluence of the cells .

    Techniques Used: Control, MANN-WHITNEY, Staining, Immunofluorescence, Expressing, Immunostaining, Marker

    Related Articles

    Cell Culture:

    Article Title: Discrimination between NSIP- and IPF-Derived Fibroblasts Based on Multi-Parameter Characterization of Their Growth, Morphology and Physic-Chemical Properties
    Article Snippet: Normal human lung fibroblasts (NHLF) were purchased from Lonza (catalog number CC-2512), IPF-derived fibroblasts (LL97A) were purchased from ATCC (catalog number ATCC-CCL-191), and NSIP-derived fibroblasts (MN) were obtained from the patient sample, using the protocol described in the . .. All cell lines were cultured in a fibroblast-dedicated culture system containing FBM TM Basal Medium (Lonza, Basel, Switzerland, catalog number CC-3131), and FGM TM SingleQuots TM supplements (Lonza, catalog number CC-4126) in culture flasks, in a CO 2 incubator providing 95% air/5% CO 2 atmosphere. ..

    Article Title: Surface-Modified Inhaled Microparticle-Encapsulated Celastrol for Enhanced Efficacy in Malignant Pleural Mesothelioma
    Article Snippet: All mesothelioma cell lines were cultured in RPMI-1640 medium supplemented with 10% fetal bovine serum (FBS) (R&D Systems, Minneapolis, MN, USA), 1% sodium pyruvate, and 1% penicillin/streptomycin (Corning, NY, USA). .. NHLF cells were cultured in FBM TM basal medium supplemented with fibroblast growth medium (FGM TM )-2 SingleQuots TM supplements from Lonza. ..



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    Conditions and resultant cells from PolA1 inhibitor treated human dermal <t>fibroblast</t> cells in iPSC reprogramming process . ( A ) EdU was pulsed for 20 minutes followed by quantification of EdU+ cells in human dermal fibroblast cells without and with different concentrations of PolA1 inhibitor. ( B ) Compared to the control (4.28±1.56%), no EdU+ cells were detected with PolA1 inhibitor treatment at high concentrations (10 µM, 1 µM, and 0.1 µM). In contrast, low concentrations of PolA1 treatment (0.02 µM: 4.95±1.09%, and 0.01 µM: 4.95±2.45%) show similar percentages of EdU+ cells: P =0.5368 (0.02 µM treatment vs. control) and P =0.8413 (0.01 µM treatment vs. control). All values = Average ±SEM, statistics was done using Mann Whitney test. ( C ) The NANOG and PDGFRα staining and at D4 and D10 during human iPSC reprogramming. ( D ) The live staining of TRA 1-60 in cells at D11 during reprogramming with and without PolA1 inhibitor. Ctrl: 17424±949.4; PolA1 treated: 26602±1137. **** P <10 -4 , Average ± SEM by Mann Whitney test. ( E ) Immunofluorescence staining of iPSCs (Passage 6) shows strong expression of pluripotency markers in both control and PolA1 inhibitor treated human iPSCs. The pluripotency markers NANOG, OCT4 and SOX2 were examined using immunostaining. Scale: 50 µm. ( F ) Feature plots show expression of NANOG, a well-known pluripotency stem cell marker in all samples. Two differentiation markers, PAX6 and SOX1, are detected in a very small subset of cells, due to a technical issue with high confluence of the cells .
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    Conditions and resultant cells from PolA1 inhibitor treated human dermal <t>fibroblast</t> cells in iPSC reprogramming process . ( A ) EdU was pulsed for 20 minutes followed by quantification of EdU+ cells in human dermal fibroblast cells without and with different concentrations of PolA1 inhibitor. ( B ) Compared to the control (4.28±1.56%), no EdU+ cells were detected with PolA1 inhibitor treatment at high concentrations (10 µM, 1 µM, and 0.1 µM). In contrast, low concentrations of PolA1 treatment (0.02 µM: 4.95±1.09%, and 0.01 µM: 4.95±2.45%) show similar percentages of EdU+ cells: P =0.5368 (0.02 µM treatment vs. control) and P =0.8413 (0.01 µM treatment vs. control). All values = Average ±SEM, statistics was done using Mann Whitney test. ( C ) The NANOG and PDGFRα staining and at D4 and D10 during human iPSC reprogramming. ( D ) The live staining of TRA 1-60 in cells at D11 during reprogramming with and without PolA1 inhibitor. Ctrl: 17424±949.4; PolA1 treated: 26602±1137. **** P <10 -4 , Average ± SEM by Mann Whitney test. ( E ) Immunofluorescence staining of iPSCs (Passage 6) shows strong expression of pluripotency markers in both control and PolA1 inhibitor treated human iPSCs. The pluripotency markers NANOG, OCT4 and SOX2 were examined using immunostaining. Scale: 50 µm. ( F ) Feature plots show expression of NANOG, a well-known pluripotency stem cell marker in all samples. Two differentiation markers, PAX6 and SOX1, are detected in a very small subset of cells, due to a technical issue with high confluence of the cells .
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    Toxicity studies of KD1-Y11T/L17R-K COOH , aprotinin, EACA and TXA in primary endothelial cells or <t>fibroblasts.</t> ( A ) Cell viability in HUVEC and ( B ) in primary human skin fibroblasts. Cells were treated with KD1-Y11T/L17R-K COOH , aprotinin, EACA, or TXA for 24 h at the indicated concentrations. Fluorescence intensity is plotted against concentration of each antifibrinolytic inhibitor. Note that, fluorescence intensity is proportional to relative cell number. Data points represent means from three independent experiments ± SEM. In each case, cell viability appears to be not significantly different from the untreated cells ( p > 0.05). ( C ) Apoptosis in HUVEC cells. HUVEC cells were either untreated or treated with KD1-Y11T/L17R-K COOH , aprotinin, EACA or TXA for 24 h at increasing concentrations ( C1 – C4 ). Taxol was included as a positive control. Luminescence, displayed as relative light units (RLU), is proportional to caspase-3/7 activity. EACA and TXA, but not KD1-Y11T/L17R-K COOH or aprotinin show significantly increased caspase activity at concentrations used in C3 and C4 compared to the untreated cells. Data are mean ± SD from three experiments. (* p < 0.05, ** p < 0.01, *** p < 0.001). ( D ) Absence of cytotoxicity in HUVEC and ( E ) primary human skin fibroblasts with KD1-Y11T/L17R-K COOH . Cells were either untreated or treated with 30 µM KD1-Y11T/L17R-K COOH for 24 h. Taxol (0.05 µM) was included as positive control. FITC: CellTox green dye binds to DNA when membrane integrity has been compromised. Fluorescent signal indicates cytotoxicity. DAPI: nuclear stain, binds to all nuclei. Representative images of one of three independent experiments performed are shown. Graph depicts quantification of cytotoxicity assay. Percent of green cells out of all cells per field were calculated. Mean ± SD value of 4 fields per treatment group are displayed (** p < 0.01, **** p < 0.0001).
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    Conditions and resultant cells from PolA1 inhibitor treated human dermal fibroblast cells in iPSC reprogramming process . ( A ) EdU was pulsed for 20 minutes followed by quantification of EdU+ cells in human dermal fibroblast cells without and with different concentrations of PolA1 inhibitor. ( B ) Compared to the control (4.28±1.56%), no EdU+ cells were detected with PolA1 inhibitor treatment at high concentrations (10 µM, 1 µM, and 0.1 µM). In contrast, low concentrations of PolA1 treatment (0.02 µM: 4.95±1.09%, and 0.01 µM: 4.95±2.45%) show similar percentages of EdU+ cells: P =0.5368 (0.02 µM treatment vs. control) and P =0.8413 (0.01 µM treatment vs. control). All values = Average ±SEM, statistics was done using Mann Whitney test. ( C ) The NANOG and PDGFRα staining and at D4 and D10 during human iPSC reprogramming. ( D ) The live staining of TRA 1-60 in cells at D11 during reprogramming with and without PolA1 inhibitor. Ctrl: 17424±949.4; PolA1 treated: 26602±1137. **** P <10 -4 , Average ± SEM by Mann Whitney test. ( E ) Immunofluorescence staining of iPSCs (Passage 6) shows strong expression of pluripotency markers in both control and PolA1 inhibitor treated human iPSCs. The pluripotency markers NANOG, OCT4 and SOX2 were examined using immunostaining. Scale: 50 µm. ( F ) Feature plots show expression of NANOG, a well-known pluripotency stem cell marker in all samples. Two differentiation markers, PAX6 and SOX1, are detected in a very small subset of cells, due to a technical issue with high confluence of the cells .

    Journal: bioRxiv

    Article Title: Modulating DNA Polα Enhances Cell Reprogramming Across Species

    doi: 10.1101/2024.09.19.613993

    Figure Lengend Snippet: Conditions and resultant cells from PolA1 inhibitor treated human dermal fibroblast cells in iPSC reprogramming process . ( A ) EdU was pulsed for 20 minutes followed by quantification of EdU+ cells in human dermal fibroblast cells without and with different concentrations of PolA1 inhibitor. ( B ) Compared to the control (4.28±1.56%), no EdU+ cells were detected with PolA1 inhibitor treatment at high concentrations (10 µM, 1 µM, and 0.1 µM). In contrast, low concentrations of PolA1 treatment (0.02 µM: 4.95±1.09%, and 0.01 µM: 4.95±2.45%) show similar percentages of EdU+ cells: P =0.5368 (0.02 µM treatment vs. control) and P =0.8413 (0.01 µM treatment vs. control). All values = Average ±SEM, statistics was done using Mann Whitney test. ( C ) The NANOG and PDGFRα staining and at D4 and D10 during human iPSC reprogramming. ( D ) The live staining of TRA 1-60 in cells at D11 during reprogramming with and without PolA1 inhibitor. Ctrl: 17424±949.4; PolA1 treated: 26602±1137. **** P <10 -4 , Average ± SEM by Mann Whitney test. ( E ) Immunofluorescence staining of iPSCs (Passage 6) shows strong expression of pluripotency markers in both control and PolA1 inhibitor treated human iPSCs. The pluripotency markers NANOG, OCT4 and SOX2 were examined using immunostaining. Scale: 50 µm. ( F ) Feature plots show expression of NANOG, a well-known pluripotency stem cell marker in all samples. Two differentiation markers, PAX6 and SOX1, are detected in a very small subset of cells, due to a technical issue with high confluence of the cells .

    Article Snippet: During the early reprogramming stage, the 10-20 nM PolA1 inhibitor was added to the fibroblast growth medium: FBM TM Basal Medium with FGM TM -2 SingleQuots TM supplements (Lonza, CC-3131) until Day 7 and the fibroblast growth medium with PolA1 needs to be replaced daily.

    Techniques: Control, MANN-WHITNEY, Staining, Immunofluorescence, Expressing, Immunostaining, Marker

    Toxicity studies of KD1-Y11T/L17R-K COOH , aprotinin, EACA and TXA in primary endothelial cells or fibroblasts. ( A ) Cell viability in HUVEC and ( B ) in primary human skin fibroblasts. Cells were treated with KD1-Y11T/L17R-K COOH , aprotinin, EACA, or TXA for 24 h at the indicated concentrations. Fluorescence intensity is plotted against concentration of each antifibrinolytic inhibitor. Note that, fluorescence intensity is proportional to relative cell number. Data points represent means from three independent experiments ± SEM. In each case, cell viability appears to be not significantly different from the untreated cells ( p > 0.05). ( C ) Apoptosis in HUVEC cells. HUVEC cells were either untreated or treated with KD1-Y11T/L17R-K COOH , aprotinin, EACA or TXA for 24 h at increasing concentrations ( C1 – C4 ). Taxol was included as a positive control. Luminescence, displayed as relative light units (RLU), is proportional to caspase-3/7 activity. EACA and TXA, but not KD1-Y11T/L17R-K COOH or aprotinin show significantly increased caspase activity at concentrations used in C3 and C4 compared to the untreated cells. Data are mean ± SD from three experiments. (* p < 0.05, ** p < 0.01, *** p < 0.001). ( D ) Absence of cytotoxicity in HUVEC and ( E ) primary human skin fibroblasts with KD1-Y11T/L17R-K COOH . Cells were either untreated or treated with 30 µM KD1-Y11T/L17R-K COOH for 24 h. Taxol (0.05 µM) was included as positive control. FITC: CellTox green dye binds to DNA when membrane integrity has been compromised. Fluorescent signal indicates cytotoxicity. DAPI: nuclear stain, binds to all nuclei. Representative images of one of three independent experiments performed are shown. Graph depicts quantification of cytotoxicity assay. Percent of green cells out of all cells per field were calculated. Mean ± SD value of 4 fields per treatment group are displayed (** p < 0.01, **** p < 0.0001).

    Journal: Journal of Clinical Medicine

    Article Title: Enhanced Antifibrinolytic Efficacy of a Plasmin-Specific Kunitz-Inhibitor (60-Residue Y11T/L17R with C-Terminal IEK) of Human Tissue Factor Pathway Inhibitor Type-2 Domain1

    doi: 10.3390/jcm9113684

    Figure Lengend Snippet: Toxicity studies of KD1-Y11T/L17R-K COOH , aprotinin, EACA and TXA in primary endothelial cells or fibroblasts. ( A ) Cell viability in HUVEC and ( B ) in primary human skin fibroblasts. Cells were treated with KD1-Y11T/L17R-K COOH , aprotinin, EACA, or TXA for 24 h at the indicated concentrations. Fluorescence intensity is plotted against concentration of each antifibrinolytic inhibitor. Note that, fluorescence intensity is proportional to relative cell number. Data points represent means from three independent experiments ± SEM. In each case, cell viability appears to be not significantly different from the untreated cells ( p > 0.05). ( C ) Apoptosis in HUVEC cells. HUVEC cells were either untreated or treated with KD1-Y11T/L17R-K COOH , aprotinin, EACA or TXA for 24 h at increasing concentrations ( C1 – C4 ). Taxol was included as a positive control. Luminescence, displayed as relative light units (RLU), is proportional to caspase-3/7 activity. EACA and TXA, but not KD1-Y11T/L17R-K COOH or aprotinin show significantly increased caspase activity at concentrations used in C3 and C4 compared to the untreated cells. Data are mean ± SD from three experiments. (* p < 0.05, ** p < 0.01, *** p < 0.001). ( D ) Absence of cytotoxicity in HUVEC and ( E ) primary human skin fibroblasts with KD1-Y11T/L17R-K COOH . Cells were either untreated or treated with 30 µM KD1-Y11T/L17R-K COOH for 24 h. Taxol (0.05 µM) was included as positive control. FITC: CellTox green dye binds to DNA when membrane integrity has been compromised. Fluorescent signal indicates cytotoxicity. DAPI: nuclear stain, binds to all nuclei. Representative images of one of three independent experiments performed are shown. Graph depicts quantification of cytotoxicity assay. Percent of green cells out of all cells per field were calculated. Mean ± SD value of 4 fields per treatment group are displayed (** p < 0.01, **** p < 0.0001).

    Article Snippet: Primary human dermal skin fibroblasts were obtained from LONZA and maintained in Fibroblast Basal Medium (FBM TM , LONZA, Basel, Switzerland), supplemented with a cocktail of growth factors, fetal bovine serum and antibiotics (FGM TM -2 SingleQuots TM , LONZA).

    Techniques: Fluorescence, Concentration Assay, Positive Control, Activity Assay, CellTox Assay, Membrane, Staining, Cytotoxicity Assay