Publications by authors named "T H Chen"

Purpose: This study aims to harness machine learning techniques, particularly the Random Survival Forest (RSF) model, to assess the impact of depression on cardiovascular disease (CVD) mortality among hypertensive patients. A key objective is to elucidate the interplay between mental health, lifestyle, and physical activity while comparing the effectiveness of the RSF model against the traditional Cox proportional hazards model in predicting CVD mortality.

Methods: Data from the National Health and Nutrition Examination Survey (NHANES) spanning 2007 to 2014 were used for comprehensive depression screening.

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Several potent carcinogenic nitrosamines, including N-nitrosodiethylamine (NDEA) and N-nitrosodimethylamine (NDMA), induce micronuclei in the micronucleated hepatocyte (MNHEP) assay but not in the micronucleated reticulocyte (MNRET) assay. However, the MNHEP assay is not as frequently used as the MNRET assay for evaluating in vivo genotoxicity. The present study evaluated MN formation in the liver of Big Blue transgenic rats exposed to four small-molecule nitrosamines, NDMA, N-nitrosodiisopropylamine (NDIPA), N-nitrosoethylisoporpylamine (NEIPA), and N-nitrosomethylphenylamine (NMPA), using a repeat-dose protocol typically used for in vivo mutagenicity studies.

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We report the application of organoiridium complexes as catalytic agents for the detoxification of biogenic reactive aldehyde species (RASP), which are implicated in the pathogenesis of neurodegenerative disorders. We show that Ir complexes functionalized with phosphonium cations localize selectively in the mitochondria and have better cellular retention compared to that of their parent Ir species. In a cell model for Parkinsonism, the mitochondria-targeted iridium catalysts exhibited superior cell protecting abilities and longer-lasting effects (up to 6 d) than conventional RASP scavengers, which failed to be effective beyond 24 h.

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Background: The development of resistance to oxaliplatin is a multifaceted process, often involving modifications in drug transport, DNA repair mechanisms, and the ability of cells to evade drug-induced apoptosis.

Objective: To evaluate whether knocking down RFC3 promotes the sensitivity of colorectal cancer (CRC) cells to oxaliplatin, potentially offering a new approach to combat drug resistance.

Methods: siRNA-mediated knockdown of RFC3 was employed in colorectal cancer cell lines to assess the impact on oxaliplatin responsiveness.

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