The study objective is to establish the role of light hepatocytes (Kraevsky cells) for forensic histological diagnosis of glycogen depletion in the liver due to various conditions, including shock. A standard histological examination of liver samples of persons who died from various causes was performed; routine staining with hematoxylin and eosin and additional staining by the PAS method was used. Histotopographic comparison of cross sections was performed to clarify the localization of light hepatocytes with different PAS staining results. It was shown that light hepatocytes have different morphological features, localization, and results of PAS staining, regardless of the cause of death, and are not related to glycogen depletion in them. Light hepatocytes (Kraevski cells) cannot be used as a sign of glycogen depletion and/or shock.
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http://dx.doi.org/10.17116/sudmed20236601155 | DOI Listing |
J Biomed Sci
January 2025
Graduate Institute of Microbiology, National Taiwan University College of Medicine, Taipei, Taiwan.
Background: In regions with a high prevalence of chronic hepatitis B virus (HBV) and hepatitis C virus (HCV) infections, coinfected patients face a heightened risk of developing hepatocellular carcinoma (HCC), termed HBV/HCV-related HCC (HBCV-HCC). We aimed to investigate the contribution of preexisting chronic hepatitis B (CHB) and subsequent chronic hepatitis C (CHC) to the development of HBCV-HCC.
Methods: We examined HBV's involvement in 93 HBCV-HCC cases by analyzing HBV DNA integration as an indicator of HCC originating from HBV-infected hepatocytes, compared with 164 HBV-HCCs and 56 HCV-HCCs as controls.
Metabolism
December 2024
Translational Nuclear Receptor Research, UGent Department of Biomolecular Medicine, VIB Center for Medical Biotechnology, Ghent, Belgium. Electronic address:
Background And Aims: Metabolic dysfunction-associated steatotic liver disease (MASLD), the most prevalent liver disease worldwide, continues to rise. More effective therapeutic strategies are urgently needed. We investigated how targeting two key nuclear receptors involved in hepatic energy metabolism, peroxisome proliferator-activated receptor alpha (PPARα) and estrogen-related receptor alpha (ERRα), ameliorates MASLD.
View Article and Find Full Text PDFJ Diabetes Res
January 2025
Department of Endocrinology and Metabolism, The First Affiliated Hospital of Jinan University, Guangzhou, China.
Diabetic liver injury is a serious complication due to the lack of effective treatments and the unclear pathogenesis. Ferroptosis, a form of cell death involving reactive oxygen species (ROS)-dependent lipid peroxidation (LPO), is closely linked to autophagy and diabetic complications. Therefore, this study is aimed at investigating the role of autophagy in regulating ferroptosis by modulating the degradation of acyl-CoA synthetase long-chain family member 4 (ACSL4) in diabetic hepatocytes and its potential impact on diabetic liver injury.
View Article and Find Full Text PDFCurr Issues Mol Biol
December 2024
Department of Functional Morphology, Meiji Pharmaceutical University, 2-522-1 Noshio, Kiyose 204-8588, Japan.
Hepatitis, a significant medical concern owing to its potential to cause acute and chronic liver disease, necessitates early intervention. In this study, we aimed to elucidate the histopathological features of lipopolysaccharide-induced hepatitis in mice, focusing on tissue alterations. The results demonstrated that hepatocytes exhibited decreased eosin staining, indicating cellular shrinkage, whereas sinusoids were swollen with blood cells.
View Article and Find Full Text PDFAutophagy
January 2025
Life Sciences Institute, University of Michigan, Ann Arbor, MI, USA.
Lipophagy is a selective type of autophagy where lipid droplets are targeted to the lysosome/vacuole for degradation. Even though lipophagy has been reported in various species, many questions remain unaddressed. How are the lipid droplets sequestered to the lysosome? What is the lipophagy receptor? How is this receptor regulated at a posttranslational level? A new collaborative study among several universities conducted on mouse and human hepatocytes sheds light on these questions, deciphering the lipophagy mechanism in the liver.
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