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c18 (plasm)-18  (Croda International Plc)

 
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    Structured Review

    Croda International Plc c18 (plasm)-18
    C18 (Plasm) 18, supplied by Croda International Plc, used in various techniques. Bioz Stars score: 94/100, based on 38 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/pe+850759c/pm41987289-168-16-19?v=Croda+International+Plc
    Average 94 stars, based on 38 article reviews
    c18 (plasm)-18 - by Bioz Stars, 2026-07
    94/100 stars

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    Experimental kinetics of amyloid‐β (Aβ) aggregation in the presence of C18(Plasm)‐20:4 <t>phosphatidylethanolamine</t> (PE). (A) Molecular structure of lipids of C18(Plasm)‐20:4 PE, C18(Plasm)‐18:1 PE, 16:0‐20:4 PE, and 16:0‐18:1 PE. (B‐E) Experimental kinetics for Aβ40 and Aβ42 aggregation under varying concentrations of C18(Plasm)‐20:4 PE. (B and D) Aggregation kinetics of Aβ40 and Aβ42 in the presence of serially diluted C18(Plasm)‐20:4 PE (0.1‐100 mM), using the thioflavin T (ThT) fluorescence assay. Fluorescence intensity is shown as relative fluorescence units (RFU) at Ex/Em = 440/484 nm. Positive control: Aβ40 or Aβ42 + ThT; negative control: Aβ40 or Aβ42 + ThT + phenol red + morin. (C,E) Quantification of aggregation kinetics by calculating the area under the fluorescence curve (AUC) for each concentration. AUC values reflect the extent of Aβ40/ Aβ42 fibrillization. Asterisks (*) and hash symbols (#) indicate statistical significance compared to the Positive control group. Statistical approach consistent with Methods Section , with significance thresholds as follows: *, increase; # , decrease; p > 0.05 (ns), p < 0.05 (* /# ), p < 0.01 (** /## ), p < 0.001 (*** /### ), and p < 0.0001 (**** /#### ).
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    Experimental kinetics of amyloid‐β (Aβ) aggregation in the presence of C18(Plasm)‐20:4 <t>phosphatidylethanolamine</t> (PE). (A) Molecular structure of lipids of C18(Plasm)‐20:4 PE, C18(Plasm)‐18:1 PE, 16:0‐20:4 PE, and 16:0‐18:1 PE. (B‐E) Experimental kinetics for Aβ40 and Aβ42 aggregation under varying concentrations of C18(Plasm)‐20:4 PE. (B and D) Aggregation kinetics of Aβ40 and Aβ42 in the presence of serially diluted C18(Plasm)‐20:4 PE (0.1‐100 mM), using the thioflavin T (ThT) fluorescence assay. Fluorescence intensity is shown as relative fluorescence units (RFU) at Ex/Em = 440/484 nm. Positive control: Aβ40 or Aβ42 + ThT; negative control: Aβ40 or Aβ42 + ThT + phenol red + morin. (C,E) Quantification of aggregation kinetics by calculating the area under the fluorescence curve (AUC) for each concentration. AUC values reflect the extent of Aβ40/ Aβ42 fibrillization. Asterisks (*) and hash symbols (#) indicate statistical significance compared to the Positive control group. Statistical approach consistent with Methods Section , with significance thresholds as follows: *, increase; # , decrease; p > 0.05 (ns), p < 0.05 (* /# ), p < 0.01 (** /## ), p < 0.001 (*** /### ), and p < 0.0001 (**** /#### ).
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    pe 16 0 20 4 avanti polar lipids  (Croda International Plc)
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    Experimental kinetics of amyloid‐β (Aβ) aggregation in the presence of C18(Plasm)‐20:4 <t>phosphatidylethanolamine</t> (PE). (A) Molecular structure of lipids of C18(Plasm)‐20:4 PE, C18(Plasm)‐18:1 PE, 16:0‐20:4 PE, and 16:0‐18:1 PE. (B‐E) Experimental kinetics for Aβ40 and Aβ42 aggregation under varying concentrations of C18(Plasm)‐20:4 PE. (B and D) Aggregation kinetics of Aβ40 and Aβ42 in the presence of serially diluted C18(Plasm)‐20:4 PE (0.1‐100 mM), using the thioflavin T (ThT) fluorescence assay. Fluorescence intensity is shown as relative fluorescence units (RFU) at Ex/Em = 440/484 nm. Positive control: Aβ40 or Aβ42 + ThT; negative control: Aβ40 or Aβ42 + ThT + phenol red + morin. (C,E) Quantification of aggregation kinetics by calculating the area under the fluorescence curve (AUC) for each concentration. AUC values reflect the extent of Aβ40/ Aβ42 fibrillization. Asterisks (*) and hash symbols (#) indicate statistical significance compared to the Positive control group. Statistical approach consistent with Methods Section , with significance thresholds as follows: *, increase; # , decrease; p > 0.05 (ns), p < 0.05 (* /# ), p < 0.01 (** /## ), p < 0.001 (*** /### ), and p < 0.0001 (**** /#### ).
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    Image Search Results


    Experimental kinetics of amyloid‐β (Aβ) aggregation in the presence of C18(Plasm)‐20:4 phosphatidylethanolamine (PE). (A) Molecular structure of lipids of C18(Plasm)‐20:4 PE, C18(Plasm)‐18:1 PE, 16:0‐20:4 PE, and 16:0‐18:1 PE. (B‐E) Experimental kinetics for Aβ40 and Aβ42 aggregation under varying concentrations of C18(Plasm)‐20:4 PE. (B and D) Aggregation kinetics of Aβ40 and Aβ42 in the presence of serially diluted C18(Plasm)‐20:4 PE (0.1‐100 mM), using the thioflavin T (ThT) fluorescence assay. Fluorescence intensity is shown as relative fluorescence units (RFU) at Ex/Em = 440/484 nm. Positive control: Aβ40 or Aβ42 + ThT; negative control: Aβ40 or Aβ42 + ThT + phenol red + morin. (C,E) Quantification of aggregation kinetics by calculating the area under the fluorescence curve (AUC) for each concentration. AUC values reflect the extent of Aβ40/ Aβ42 fibrillization. Asterisks (*) and hash symbols (#) indicate statistical significance compared to the Positive control group. Statistical approach consistent with Methods Section , with significance thresholds as follows: *, increase; # , decrease; p > 0.05 (ns), p < 0.05 (* /# ), p < 0.01 (** /## ), p < 0.001 (*** /### ), and p < 0.0001 (**** /#### ).

    Journal: Alzheimer's & Dementia

    Article Title: Decoding adipose–brain crosstalk: Distinct lipid cargo in human adipose‐derived extracellular vesicles modulates amyloid aggregation in Alzheimer's disease

    doi: 10.1002/alz.70603

    Figure Lengend Snippet: Experimental kinetics of amyloid‐β (Aβ) aggregation in the presence of C18(Plasm)‐20:4 phosphatidylethanolamine (PE). (A) Molecular structure of lipids of C18(Plasm)‐20:4 PE, C18(Plasm)‐18:1 PE, 16:0‐20:4 PE, and 16:0‐18:1 PE. (B‐E) Experimental kinetics for Aβ40 and Aβ42 aggregation under varying concentrations of C18(Plasm)‐20:4 PE. (B and D) Aggregation kinetics of Aβ40 and Aβ42 in the presence of serially diluted C18(Plasm)‐20:4 PE (0.1‐100 mM), using the thioflavin T (ThT) fluorescence assay. Fluorescence intensity is shown as relative fluorescence units (RFU) at Ex/Em = 440/484 nm. Positive control: Aβ40 or Aβ42 + ThT; negative control: Aβ40 or Aβ42 + ThT + phenol red + morin. (C,E) Quantification of aggregation kinetics by calculating the area under the fluorescence curve (AUC) for each concentration. AUC values reflect the extent of Aβ40/ Aβ42 fibrillization. Asterisks (*) and hash symbols (#) indicate statistical significance compared to the Positive control group. Statistical approach consistent with Methods Section , with significance thresholds as follows: *, increase; # , decrease; p > 0.05 (ns), p < 0.05 (* /# ), p < 0.01 (** /## ), p < 0.001 (*** /### ), and p < 0.0001 (**** /#### ).

    Article Snippet: For the lipid details, sodium oleate (Sigma, #07501), sodium palmitate (Sigma, #P9767), Brain SM (Avanti, #860062P), egg SM (Avanti, #860061P), milk SM (Avanti, #860063P), egg lysophosphatidylcholine (LPC) (Lyso PC; Avanti, #830071P), 18:0 LPC (Lyso PC; Avanti, #855775), 16:0‐20:4 phosphatidylethanolamine (PE) (Avanti, #850759C), 16:0‐18:1 PE (Avanti, #850757P), C18(Plasm)‐18:1 PE (Avanti, #852758P), and C18(Plasm)‐20:4 PE in ethanol (Cayman, #37137).

    Techniques: Fluorescence, Positive Control, Negative Control, Concentration Assay