Background: Ethanol metabolism is intimately linked with the physiological and behavioral aspects of ethanol consumption. Ethanol is mainly oxidized by alcohol dehydrogenase (ADH) to acetaldehyde and further to acetate via aldehyde dehydrogenases (ALDHs). Understanding how ethanol and its metabolites work together to initiate and drive continued ethanol consumption is crucial for identifying interventions for alcohol use disorder (AUD).
View Article and Find Full Text PDFAlcohol Clin Exp Res (Hoboken)
May 2025
Background: Ethanol metabolism is intimately linked with the physiological and behavioral aspects of ethanol consumption. Ethanol is mainly oxidized by alcohol dehydrogenase (ADH) to acetaldehyde and further to acetate via aldehyde dehydrogenases (ALDHs). Understanding how ethanol and its metabolites work together to initiate and drive continued ethanol consumption is crucial for identifying interventions for alcohol use disorder (AUD).
View Article and Find Full Text PDFAlcohol use disorder (AUD) affects millions of people worldwide, causing extensive morbidity and mortality with limited pharmacological treatments. The liver is considered as the principal site for the detoxification of ethanol metabolite, acetaldehyde (AcH), by aldehyde dehydrogenase 2 (ALDH2) and as a target for AUD treatment, however, our recent data indicate that the liver only plays a partial role in clearing systemic AcH. Here we show that a liver-gut axis, rather than liver alone, synergistically drives systemic AcH clearance and voluntary alcohol drinking.
View Article and Find Full Text PDFThe liver plays an important role in both metabolism and immunity. Disruption of the hepatic immune microenvironment is closely associated with various liver diseases. To gain a better understanding of how different types of immune cells contribute to the progression of liver diseases, it is crucial to thoroughly characterize hepatic immune cells.
View Article and Find Full Text PDFThe liver can fully regenerate after partial resection, and its underlying mechanisms have been extensively studied. The liver can also rapidly regenerate after injury, with most studies focusing on hepatocyte proliferation; however, how hepatic necrotic lesions during acute or chronic liver diseases are eliminated and repaired remains obscure. Here, we demonstrate that monocyte-derived macrophages (MoMFs) were rapidly recruited to and encapsulated necrotic areas during immune-mediated liver injury and that this feature was essential in repairing necrotic lesions.
View Article and Find Full Text PDFObjective: The current treatment for hepatocellular carcinoma (HCC) to block angiogenesis and immunosuppression provides some benefits only for a subset of patients with HCC, thus optimised therapeutic regimens are unmet needs, which require a thorough understanding of the underlying mechanisms by which tumour cells orchestrate an inflamed tumour microenvironment with significant myeloid cell infiltration. MicroRNA-223 (miR-223) is highly expressed in myeloid cells but its role in regulating tumour microenvironment remains unknown.
Design: Wild-type and miR-223 knockout mice were subjected to two mouse models of inflammation-associated HCC induced by injection of diethylnitrosamine (DEN) or orthotopic HCC cell implantation in chronic carbon tetrachloride (CCl)-treated mice.
Guang Pu Xue Yu Guang Pu Fen Xi
May 2010
In this research, hemicellulose contents of 78 wood meal samples of Acacia spp trees grown in Guangxi and another 33 wood meal samples of Acacia spp trees grown in Fujian were measured by wet chemistry. NIR spectra were also collected by a Bruker MPA spectrometer within 4 000-12 500 cm(-1) of wavenumbers using a standard sample cup. Equations were developed using partial least squares (PLS) regression and cross validation for multivariate calibration in this study.
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