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Background: Wound healing monitoring and timely decision‐making are critical for wound classification. Tryptophan (Tr) intrinsic fluorescence, detected at 295/340 nm, provides a noninvasive approach for wound assessment. Our previous work demonstrated that this autofluorescence is associated with keratinocytes in a highly proliferative state in vitro. Objective: We investigated the correlation between Tr fluorescence and key wound healing parameters, including re‐epithelialization, fibrosis, neovascularization, and acute and chronic inflammation, using a rabbit model. Methods: Seven rabbits underwent wound healing assessment over a 15‐day period. We employed histological analysis from central and marginal biopsies, and UV fluorescence imaging captured by a monochromatic near‐UV sensitive camera equipped with a passband optical filter (340 nm/12 nm). Excitation was achieved using a 295 nm LEDs ring lamp. Normalized fluorescence values were correlated with histological measurements using Pearson correlation. Results: The UV fluorescence strongly exhibited a strong correlation with re‐epithelization (r = 0.8) at the wound edge, with peak intensity observed between the sixth and ninth days. Notably, wound‐healing dynamics differed between the wound center and edge, primarily attributed to variations in re‐epithelialization, neovascularization, and chronic inflammation. Conclusion: Our findings highlight the presence of autofluorescence at 295/340 nm during wound healing, demonstrating a robust association with re‐epithelialization. This excitation/emission signal holds promise as a valuable noninvasive strategy for monitoring wound closure, re‐epithelialization, and other biological processes where Tr plays a pivotal role. [ABSTRACT FROM AUTHOR]

We have recently reported that serum concentrations of α-carotene (AC) and β-carotene (BC) are under strong genetic influences and were correlated with obesity and other cardio-metabolic traits in Mexican American (MA) children. Our previously developed Pediatric Metabolic Index (PMI) correlates with insulin resistance (IR) after adjusting for age and sex using lipid and adiposity data from Mexican children. A PMI score > 2.0 predicts metabolic abnormalities including IR (i.e., HOMA-IR). Yet data on other MA children with PMI > 2 with normal IR and PMI < 2 with high IR, suggest a role for additional factors in determining insulin sensitivity (IS). In this study, we aimed to assess interactions between carotenoids and the PMI in predicting IS as measured by Matsuda index using the surface-response analysis (SRA). Four different carotenoids, namely, AC, BC, lycopene (Lyc), and β-cryptoxanthin (CX) from ∼590 children enrolled in the San Antonio Family Assessment of Metabolic Risk Indicators in Youth (SAFARI) study were measured by mass spectrometry. Glucose and insulin levels were measured after oral glucose tolerance test and IS index (ISI) was calculated using Matsuda method. SRA was used to determine two-way interactions of serum carotenoids and PMI on ISI. The computer programs SOLAR and STATISTICA 7.0 were used for statistical analysis. The SRA showed an increase in ISI in children with PMI scores between 2 to 4. This effect was modified in the presence of lower serum AC and BC levels; and, interactions between these two carotenoids and PMI had maximal effect on ISI. Conversely, MA children with moderate PMI scores can have substantial improvement in their IS with higher serum AC and BC levels. In contrast, there was a minimal surface response to Lyc and CX serum levels. Notably, despite an optimal PMI, children with lower concentrations of AC and BC showed less IS. In summary, we found that interactions between carotenoids with PMI may predict IS in MA children. Disclosure: S. Mummidi: None. J. Hernandez-Ruiz: None. V.S. Farook: None. L. Reddivari: None. A. Diaz-Badillo: None. S.P. Fowler: None. R.G. Resendez: None. F. Akhtar: None. D. Lehman: None. C. Jenkinson: None. R. Arya: None. J.L. Lynch: Board Member; Self; American Academy of Pediatrics. Consultant; Self; Novo Nordisk Inc. Research Support; Self; Daiichi Sankyo Company, Limited, National Institutes of Health, Novo Nordisk Inc., Pediatric Diabetes Consortium. R.A. DeFronzo: Advisory Panel; Self; AstraZeneca, Boehringer Ingelheim Pharmaceuticals, Inc., Elcelyx Therapeutics, Inc., Intarcia Therapeutics, Inc., Janssen Pharmaceuticals, Inc., Novo Nordisk Inc. Research Support; Self; AstraZeneca, Boehringer Ingelheim Pharmaceuticals, Inc., Janssen Pharmaceuticals, Inc., Merck & Co., Inc. Speaker's Bureau; Self; AstraZeneca, Novo Nordisk Inc. D.E. Hale: None. J. Blangero: None. J.C. Lopez-Alvarenga: None. R. Duggirala: None. J.K. Vanamala: None. Funding: National Institutes of Health (R01HD049051, R01AI119131, HD049051-5S1, HD041111, DK053889, DK042273, DK047482, P01HL45522, MH59490, M01-RR-01346), U.S. Department of Veterans Affairs; Max and Minnie Tomerlin Voelcker Fund; National Institute of Food and Agriculture (2009-55200-05197) [ABSTRACT FROM AUTHOR]