Browsing by Author "Li, Kelvin"

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    Factors Associated with MASLD Resilience in Type 2 Diabetes: A Prospective Study Integrating Longitudinal MRI/MRE Imaging and Stable Isotope Tracing
    (2026) Tavaglione, Federica; Ajmera, Veeral; Díaz Piga, Luis Antonio; Li, Kelvin; Madamba, Egbert; Bettencourt, Ricki; Richards, Lisa; Hellerstein, Marc; Loomba, Rohit
    Background & Aims Type 2 diabetes is one of the strongest factors contributing to the development and progression of metabolic dysfunction-associated steatotic liver disease (MASLD). In this study, we aimed to identify factors associated with MASLD resilience in a prospective cohort of individuals with type 2 diabetes.MethodsThis is a prospective study including 148 individuals with type 2 diabetes who underwent advanced liver phenotyping using MRI and MRE techniques at baseline and 2-year follow-up. MASLD resilience was defined by imaging absence of hepatic steatosis (MRI-PDFF < 5%) and significant fibrosis (MRE < 3 kPa) at both time points. Factors associated with MASLD resilience were assessed using Firth’s penalized logistic regression. Regularized logistic regression models were fitted as complementary analyses.ResultsThe mean (SD) age and body mass index (BMI) were 65 (8) years and 30.4 (4.3) kg/m2, respectively. After a median follow-up of 2 (1.5–2.4) years, 27 (18%) individuals demonstrated MASLD resilience. Across all modeling approaches, lower BMI (odds ratio [OR] 0.81, 95% CI 0.64–0.98; p=0.029), lower HOMA-IR (OR 0.59, 95% CI 0.39–0.83; p=8.6e-4), and lower circulating triglycerides (OR 0.986, 95% CI 0.973–0.997; p=0.011) emerged as the strongest predictors of MASLD resilience. An exploratory analysis of 11 individuals with type 2 diabetes from an independent cohort, with hepatic de novo lipogenesis (DNL) quantified by stable isotope tracing, revealed lower hepatic DNL in those free from MASLD.
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    Oxidized phospholipid and transcriptomic signatures of THC-related vaping associated lung injury
    (NATURE PORTFOLIO, 2024) Suber, Tomeka L.; Tabary, Mohammadreza; Bain, William; Olonisakin, Tolani; Lockwood, Karina; Xiong, Zeyu; Zhang, Yingze; Kohli, Naina; Furguiele, Lauren; Peñaloza Cerda, Hernán Felipe; Mcverry, Bryan J.; Rose, Jason J.; Shah, Faraaz; Methe, Barbara; Li, Kelvin; Mallampalli, Rama K.; Chen, Kong; Fan, Li; Morris, Alison; Tyurin, Vladimir A.; Samovich, Svetlana N.; Bayir, Hulya; Tyurina, Yulia Y.; Kagan, Valerian; Lee, Janet S.
    E-cigarette/vaping-associated lung injury (EVALI) is strongly associated with vitamin E acetate and often occurs with concomitant tetrahydrocannabinol (THC) use. To uncover pathways associated with EVALI, we examined cytokines, transcriptomic signatures, and lipidomic profiles in bronchoalveolar lavage fluid (BALF) from THC-EVALI patients. At a single center, we prospectively enrolled mechanically ventilated patients with EVALI from THC-containing products (N = 4) and patients with non-vaping acute lung injury and airway controls (N = 5). BALF samples were analyzed by Luminex multiplex assay, RNA sequencing, and mass spectrometry. After treating BEAS-2B lung epithelial cells with vaping and non-vaping BALF, LDH release was quantified. THC-EVALI BALF had significant increases in IFN gamma, CCL2, CXCL5, and MMP2 relative to non-vaping patients. RNA sequencing showed enrichment for biological oxidation, glucuronidation, and fatty acid metabolism pathways. Oleic acid and arachidonic acid metabolites were increased in THC-EVALI, as were oxidized phosphatidylethanolamines (PE) such as PE(38:4). THC-EVALI BALF induced more LDH release compared to BALF from non-vaping patients. Thus, THC-EVALI is characterized by altered phospholipid composition, accumulation of lipid oxidation products, and increased pro-inflammatory mediators that may contribute to epithelial cell death. These findings serve as a framework to study novel oxidized phospholipids implicated in the pathogenesis of EVALI.
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    Oxidized phospholipid and transcriptomic signatures of THC-related vaping associated lung injury
    (2024) Suber, Tomeka L.; Tabary, Mohammadreza; Bain, William; Olonisakin, Tolani; Lockwood, Karina; Xiong, Zeyu; Zhang, Yingze; Kohli, Naina; Furguiele, Lauren; Peñaloza Cerda, Hernán Felipe; Mcverry, Bryan J.; Rose, Jason J.; Shah, Faraaz; Methe, Barbara; Li, Kelvin; Mallampalli, Rama K.; Chen, Kong; Fan, Li; Morris, Alison; Tyurin, Vladimir A.; Samovich, Svetlana N.; Bayir, Hulya; Tyurina, Yulia Y.; Kagan, Valerian; Lee, Janet S.
    E-cigarette/vaping-associated lung injury (EVALI) is strongly associated with vitamin E acetate and often occurs with concomitant tetrahydrocannabinol (THC) use. To uncover pathways associated with EVALI, we examined cytokines, transcriptomic signatures, and lipidomic profiles in bronchoalveolar lavage fluid (BALF) from THC-EVALI patients. At a single center, we prospectively enrolled mechanically ventilated patients with EVALI from THC-containing products (N = 4) and patients with non-vaping acute lung injury and airway controls (N = 5). BALF samples were analyzed by Luminex multiplex assay, RNA sequencing, and mass spectrometry. After treating BEAS-2B lung epithelial cells with vaping and non-vaping BALF, LDH release was quantified. THC-EVALI BALF had significant increases in IFN gamma, CCL2, CXCL5, and MMP2 relative to non-vaping patients. RNA sequencing showed enrichment for biological oxidation, glucuronidation, and fatty acid metabolism pathways. Oleic acid and arachidonic acid metabolites were increased in THC-EVALI, as were oxidized phosphatidylethanolamines (PE) such as PE(38:4). THC-EVALI BALF induced more LDH release compared to BALF from non-vaping patients. Thus, THC-EVALI is characterized by altered phospholipid composition, accumulation of lipid oxidation products, and increased pro-inflammatory mediators that may contribute to epithelial cell death. These findings serve as a framework to study novel oxidized phospholipids implicated in the pathogenesis of EVALI.