Browsing by Author "Lin, Emily"

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    Change in Systemic Arterial Pulsatility index (SAPi) during heart failure hospitalization is associated with improved outcomes
    (Elsevier, 2023-03) Lin, Emily; Boadu, Akua; Skeiky, Natalie; Mehta, Nishaki; Kwon, Younghoon; Breathett, Khadijah; Ilonze, Onyedika; Lamp, Josephine; Bilchick, Kenneth C.; Mazimba, Sula; Medicine, School of Medicine
    Study objective: To identify Change in Systemic Arterial Pulsatitlity index (∆SAPi) as a novel hemodynamic marker associated with outcomes in heart failure (HF). Design: The ESCAPE trial was a randomized controlled trial. Setting: The ESCAPE trial was conducted at 26 sites. Participants: 134 patients were analyzed (mean age 56.8 ± 13.4 years, 29 % female). Interventions: We evaluated the change in SAPi, (systemic pulse pressure/pulmonary artery wedge pressure) obtained at baseline and at the final hemodynamic measurement in the ESCAPE trial. Main outcome measures: Change in SAPi, (∆SAPi), was analyzed for the primary outcomes of death, heart transplant, left ventricular assist device (DTxLVAD) or hospitalization, (DTxLVADHF) and secondary outcome of DTxLVAD using Cox proportional hazards regression. Results: Median change in SAPi was 0.81 (IQR 0.20–1.68). ∆SAPi in uppermost quartile was associated with reductions in DTxLVADHF (HR 0.55 [95 % CI 0.32, 0.93]). ∆SAPi in the uppermost and lowermost quartiles combined was similarly associated with significant reductions in DTxLVADHF (HR 0.62 [95 % CI 0.41, 0.94]). ∆SAPi higher than 1.17 was associated with improved DTxLVADHF. ∆SAPi was also associated with troponin levels at discharge (regression coefficient p = 0.001) and trended with 6-minute walk at discharge (Spearman correlation r = 0.179, p = 0.058). Conclusion: ∆SAPi was strongly associated with improved HF clinical profile and adverse outcomes. These findings support further exploration of ∆ SAPi in the risk stratification of HF.
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    Kupffer Cells: Inflammation Pathways and Cell-Cell Interactions in Alcohol-Associated Liver Disease
    (Elsevier, 2020) Slevin, Elise; Baiocchi, Leonardo; Wu, Nan; Ekser, Burcin; Sato, Keisaku; Lin, Emily; Ceci, Ludovica; Chen, Lixian; Lorenzo, Sugeily R.; Xu, Wenjuan; Kyritsi, Konstantina; Meadows, Victoria; Zhou, Tianhao; Kundu, Debiyoti; Han, Yuyan; Kennedy, Lindsey; Glaser, Shannon; Francis, Heather; Alpini, Gianfranco; Meng, Fanyin; Surgery, School of Medicine
    Chronic alcohol consumption is linked to the development of alcohol-associated liver disease (ALD). This disease is characterized by a clinical spectrum ranging from steatosis to hepatocellular carcinoma. Several cell types are involved in ALD progression, including hepatic macrophages. Kupffer cells (KCs) are the resident macrophages of the liver involved in the progression of ALD by activating pathways that lead to the production of cytokines and chemokines. In addition, KCs are involved in the production of reactive oxygen species. Reactive oxygen species are linked to the induction of oxidative stress and inflammation in the liver. These events are activated by the bacterial endotoxin, lipopolysaccharide, that is released from the gastrointestinal tract through the portal vein to the liver. Lipopolysaccharide is recognized by receptors on KCs that are responsible for triggering several pathways that activate proinflammatory cytokines involved in alcohol-induced liver injury. In addition, KCs activate hepatic stellate cells that are involved in liver fibrosis. Novel strategies to treat ALD aim at targeting Kupffer cells. These interventions modulate Kupffer cell activation or macrophage polarization. Evidence from mouse models and early clinical studies in patients with ALD injury supports the notion that pathogenic macrophage subsets can be successfully translated into novel treatment options for patients with this disease.