| evidence-b2-doi-10-1016-j-jma-2023-05-007-1 | KF1: Exosome-associated coating and particle characteristics were documented using material-level tests. | Exosome identity-related Western blot complete images were cited as missing Figure S1; no conclusion requires interpretation of that unavailable supplement. | Exosome-associated coating and particle characteristics were documented using material-level tests. Alloy: Mg-Zn-Y-Nd modified with MgF2 and PDA/exosome; Particle size from NTA: Reported 50–150 nm distribution; Source completeness: Full Western-blot Figure S1 supplement unavailable; excluded from validated findings | Exosome identity-related Western blot complete images were cited as missing Figure S1; no conclusion requires interpretation of that unavailable supplement. | Exosome identity-related Western blot complete images were cited as missing Figure S1; no conclusion requires interpretation of that unavailable supplement. | Publisher VOR PDF: Abstract and Results §3.1 Exosome characterization, PDF pp.1,6 (printed pp.4988,4993); main Figure 2. The full Western blot is referred to as Figure S1 and was not available in the source pack. | KF1 |
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| evidence-b2-doi-10-1016-j-jma-2023-05-007-2 | KF2: The modified surface showed different corrosion characteristics from bare magnesium alloy in laboratory immersion/electrochemical tests. | Corrosion outcomes reflect specified HBSS and bench-test conditions, not confirmed long-term human implant degradation or clinical durability. | The modified surface showed different corrosion characteristics from bare magnesium alloy in laboratory immersion/electrochemical tests. Test domain: Electrochemical behavior, pH, hydrogen evolution and weight loss; Material comparison: Bare Mg alloy, MgF2, MgF2–PDA and MgF2–PDA/exosome; Result direction: Article reports improved resistance with modified coating | Corrosion outcomes reflect specified HBSS and bench-test conditions, not confirmed long-term human implant degradation or clinical durability. | Corrosion outcomes reflect specified HBSS and bench-test conditions, not confirmed long-term human implant degradation or clinical durability. | Publisher VOR PDF: Methods §2.4 Corrosion resistance, Results §3.3 Corrosion resistance; Figures 3–5; PDF pp.3–9 (printed 4990–4996). | KF2 |
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| evidence-b2-doi-10-1016-j-jma-2023-05-007-3 | KF3: MgF2–PDA/exosome surfaces were associated with improved cultured endothelial readouts. | Bench-cell observations are surrogate readouts relevant to endothelialization, not a measurement of human-stent clinical restenosis or healing. | MgF2–PDA/exosome surfaces were associated with improved cultured endothelial readouts. Endothelial assays: Adhesion, CCK-8 growth proxy, CD31 staining, NO release and migration; Reported 3-day surface cell density: Approximately 1.8×10^5 cells/cm² on coated surface versus 2×10^4 on bare alloy (article-described comparison); Figure-level replicates: Figure 8B/C: n=6; Figure 8D: n=3 | Bench-cell observations are surrogate readouts relevant to endothelialization, not a measurement of human-stent clinical restenosis or healing. | Bench-cell observations are surrogate readouts relevant to endothelialization, not a measurement of human-stent clinical restenosis or healing. | Publisher VOR PDF: Methods §§2.8–2.10, Results §3.7 vascular endothelial cell responses; Figure 8A–H; PDF pp.4–5 and 10–12 (printed 4991–4992 and 4997–4999). | KF3 |
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| evidence-b2-doi-10-1016-j-jma-2023-05-007-4 | KF4: Inflammatory and smooth-muscle cell readouts differed under the coated-material conditions. | Macrophage TNF-α/CD206 or smooth-muscle α-SMA/OPN expression is not a directly tested causal anti-restenosis mechanism in human vessels. | Inflammatory and smooth-muscle cell readouts differed under the coated-material conditions. Macrophage assessment: TNF-α, CD206 and reactive oxygen species in extract-solution culture; Smooth-muscle assessment: α-SMA, osteopontin and cell competition assays; Model domain: In-vitro phenotype and compatibility metrics | Macrophage TNF-α/CD206 or smooth-muscle α-SMA/OPN expression is not a directly tested causal anti-restenosis mechanism in human vessels. | Macrophage TNF-α/CD206 or smooth-muscle α-SMA/OPN expression is not a directly tested causal anti-restenosis mechanism in human vessels. | Publisher VOR PDF: Results §§3.6–3.8, Figures 7, 9 and 10; PDF pp.9–14 (printed 4996–5001). | KF4 |
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| evidence-b2-doi-10-1016-j-jma-2023-05-007-5 | KF5: Exosome-associated signals were observed in cultured endothelial uptake and release assays. | Fluorescence overlap with cellular organelles indicates reported localization, not a proven cargo-mediated causal pathway or controlled therapeutic dose. | Exosome-associated signals were observed in cultured endothelial uptake and release assays. Release window: Approximately 5–7 days in the tested coating system; Cellular colocalization: Reported overlap with lysosomal and mitochondrial fluorescent markers; Interpretation: Exploratory uptake/localization observations | Fluorescence overlap with cellular organelles indicates reported localization, not a proven cargo-mediated causal pathway or controlled therapeutic dose. | Fluorescence overlap with cellular organelles indicates reported localization, not a proven cargo-mediated causal pathway or controlled therapeutic dose. | Publisher VOR PDF: Methods §§2.10–2.11, Results §3.8 Release and uptake of exosomes, Figure 11; PDF pp.5–6 and 14–15 (printed 4992–4993 and 5001–5002). | KF5 |
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| evidence-b2-doi-10-1016-j-jma-2023-05-007-6 | KF6: A short rat aortic wire-implant experiment showed descriptive vessel-wall histological differences. | The animal intervention used wires rather than clinical coronary stents; the presented H&E sections do not independently establish quantitative lumen patency, thrombosis prevention or long-term safety. | A short rat aortic wire-implant experiment showed descriptive vessel-wall histological differences. Rodent design: 15 SD rats; bare-Mg, MgF2 and MgF2–PDA/exosome wire groups, n=5 each; Site and time: Rat abdominal aorta; 21-day histology; Endpoint limitation: Qualitative H&E representative sections only in Figure 12 | The animal intervention used wires rather than clinical coronary stents; the presented H&E sections do not independently establish quantitative lumen patency, thrombosis prevention or long-term safety. | The animal intervention used wires rather than clinical coronary stents; the presented H&E sections do not independently establish quantitative lumen patency, thrombosis prevention or long-term safety. | Publisher VOR PDF: Methods §2.12 The SD rat experiment, PDF p.6 (printed 4993); Results and Figure 12, PDF pp.15–16 (printed 5002–5003). | KF6 |
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