Browsing by Author "Huang, Ying"

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    Metabolomic Analysis Uncovers Energy Supply Disturbance as an Underlying Mechanism of the Development of Alcohol‐Associated Liver Cirrhosis
    (Wiley, 2021-03-08) Huang, Ying; Niu, Ming; Jing, Jing; Zhang, Zi-teng; Zhao, Xu; Chen, Shuai-shuai; Li, Shan-shan; Shi, Zhu; Huang, Ang; Zou, Zheng-Sheng; Yu, Yue-cheng; Xiao, Xiao-he; Liangpunsakul, Suthat; Wang, Jia-bo; Medicine, School of Medicine
    Alcohol-associated liver disease (ALD) is caused by alcohol metabolism's effects on the liver. The underlying mechanisms from a metabolic view in the development of alcohol-associated liver cirrhosis (ALC) are still elusive. We performed an untargeted serum metabolomic analysis in 14 controls, 16 patients with ALD without cirrhosis (NC), 27 patients with compensated cirrhosis, and 79 patients with decompensated ALC. We identified two metabolic fingerprints associated with ALC development (38 metabolites) and those associated with hepatic decompensation (64 metabolites) in ALC. The cirrhosis-associated fingerprint (eigenmetabolite) showed a better capability to differentiate ALC from NC than the aspartate aminotransferase-to-platelet ratio index score. The eigenmetabolite associated with hepatic decompensation showed an increasing trend during the disease progression and was positively correlated with the Model for End-Stage Liver Disease score. These metabolic fingerprints belong to the metabolites in lipid metabolism, amino acid pathway, and intermediary metabolites in the tricarboxylic acid cycle. Conclusion: The metabolomic fingerprints suggest the disturbance of the metabolites associated with cellular energy supply as an underlying mechanism in the development and progression of alcoholic cirrhosis.
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    Myocardial injury and coronary microvascular disease in sickle cell disease
    (Ferrata Storti Foundation, 2021-07) Kaur, Kiranveer; Huang, Ying; Raman, Subha V.; Kraut, Eric; Desai, Payal; Medicine, School of Medicine
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    Phase II randomized, double-blind, placebo-controlled study of tivantinib in men with asymptomatic or minimally symptomatic metastatic castration-resistant prostate cancer (mCRPC)
    (Springer Nature, 2018-10) Monk, Paul; Liu, Glenn; Stadler, Walter M.; Geyer, Susan; Huang, Ying; Wright, John; Villalona-Calero, Miguel; Wade, James; Szmulewitz, Russell; Gupta, Shilpa; Mortazavi, Amir; Dreicer, Robert; Pili, Roberto; Dawson, Nancy; George, Saby; Garcia, Jorge A.; Medicine, School of Medicine
    Background Tivantinib is a non-ATP competitive inhibitor of c-MET receptor tyrosine kinase that may have additional cytotoxic mechanisms including tubulin inhibition. Prostate cancer demonstrates higher c-MET expression as the disease progresses to more advanced stages and to a castration resistant state. Methods 80 patients (pts) with asymptomatic or minimally symptomatic mCRPC were assigned (2:1) to either tivantinib 360 mg PO BID or placebo (P). The primary endpoint was progression free survival (PFS). Results Of the 80 pts. enrolled, 78 (52 tivantinib, 26 P) received treatment and were evaluable. Median follow up is 8.9 months (range: 2.3 to 19.6 months). Patients treated with tivantinib had significantly better PFS vs. those treated with placebo (medians: 5.5 mo vs 3.7 mo, respectively; HR = 0.55, 95% CI: 0.33 to 0.90; p = 0.02). Grade 3 febrile neutropenia was seen in 1 patient on tivantinib while grade 3 and 4 neutropenia was recorded in 1 patient each on tivantinib and placebo. Grade 3 sinus bradycardia was recorded in two men on the tivantinib arm. Conclusions Tivantinib has mild toxicity and improved PFS in men with asymptomatic or minimally symptomatic mCRPC.