Background/Aims: An increase in intracellular lipid droplet formation and hepatic triglyceride (TG) content usually results in nonalcoholic fatty liver disease. However, the mechanisms underlying the regulation of hepatic TG homeostasis remain unclear. Methods: Oil red O staining and TG measurement were performed to determine the lipid content. miRNA expression was evaluated by quantitative PCR. A luciferase assay was performed to validate the regulation of Yin Yang 1 (YY1) by microRNA (miR)-122. The effects of miR-122 expression on YY1 and its mechanisms involving the farnesoid X receptor and small heterodimer partner (FXR-SHP) pathway were evaluated by quantitative PCR and Western blot analyses. Results: miR-122 was downregulated in free fatty acid (FFA)-induced steatotic hepatocytes, and streptozotocin and high-fat diet (STZ-HFD) induced nonalcoholic steatohepatitis (NASH) in mice. Transfection of hepatocytes with miR-122 mimics before FFA induction inhibited lipid droplet formation and TG accumulation in vitro. These results were verified by overexpressing miR-122 in the livers of STZ-HFD-induced NASH mice. The 3’-untranslated region (3’UTR) of YY1 mRNA is predicted to contain an evolutionarily conserved miR-122 binding site. In silico searches, a luciferase reporter assay and quantitative PCR analysis confirmed that miR-122 directly bound to the YY1 3’UTR to negatively regulate YY1 mRNA in HepG2 and Huh7 cells. The (FXR-SHP) signaling axis, which is downstream of YY1, may play a key role in the mechanism of miR-122-regulated lipid homeostasis. YY1-FXR-SHP signaling, which is negatively regulated by FFA, was enhanced by miR-122 overexpression. This finding was also confirmed by overexpression of miR-122 in the livers of NASH mice. Conclusions: The present results indicate that miR-122 plays an important role in lipid (particularly TG) accumulation in the liver by reducing YY1 mRNA stability to upregulate FXR-SHP signaling.

Background: The use of alpha‐fetoprotein (AFP) testing for the surveillance, diagnosis, and prognosis of hepatocellular carcinoma (HCC) remains controversial. Here, we compared AFP testing rates, elevated AFP rates, factors associated with elevated AFP levels, and prognostic factors associated with overall survival (OS) in HCC patients from different ethnic groups.Methods: Patients with HCC were identified from the Surveillance, Epidemiology, and End Results registries. Race was categorized as white, black, and others. AFP testing rates and elevated AFP rates were analyzed. Multivariable logistic regression and Cox regression analyses were used to identify independent factors associated with elevated AFP levels and prognosis, respectively. All statistical tests were two sided.Results: A proportion of 79.2% of total HCC patients had AFP testing reports; 77.3% of white, 79.7% of black, and 81.2% of other races underwent AFP testing. Compared with white and other races, black HCC patients had a higher rate of elevated AFP levels among all patients and the early‐stage HCC patient cohort. Elevated AFP level was a significant prognostic factor for all HCC patients in different race groups. Factors associated with elevated AFP level and prognostic factors associated with OS varied significantly by race.Conclusions: AFP testing, elevated AFP rates, predictors of elevated AFP level, and prognostic factors associated with OS differed significantly according to race after adjusting for AFP levels among the three groups. AFP testing for the surveillance, diagnosis, and prognosis of HCC patients is strongly recommended, although racial disparities need to be considered.

Current International Standards Organization (ISO) for testing antimicrobial materials often lack regulatory approval for clinical use because they do not accurately reflect real-world environmental conditions. In this study, we systematically evaluated the effects of temperature (4°C–37°C) and humidity (15%–100% relative humidity) on microbial survival ( Staphylococcus aureus , Escherichia coli , HCoV-OC43, and influenza virus) and the efficacy of various antimicrobial surfaces (stainless steel, copper, polyethylene terephthalate [PET], and Cu₂O@ZrP-modified PET) using established ISO standards, including ISO 21702, 18184, 22196, and 20743. We found that pathogen survival declined sharply with increasing temperature, while the effects of humidity varied by material. Copper and Cu₂O@ZrP-PET surfaces achieved greater than 99% viral and bacterial inactivation within 60 min; however, their activity was delayed by two to threefold at 4°C. The effects of humidity were material-dependent. Non-porous copper maintained consistent efficacy across humidity levels, whereas PET/Cu₂O@ZrP exhibited enhanced antibacterial activity under low humidity. Mechanistically, reactive oxygen species generation correlated with efficacy changes across conditions. We advocate revising ISO protocols to include dynamic environmental parameters and propose a tiered classification of antimicrobial efficiency that aligns with clinical demands. This framework addresses the discrepancy between laboratory tests and real-world performance, enabling the robust evaluation of antimicrobial materials for clinical and public health applications. IMPORTANCE: This study addresses a critical gap in our understanding of how real-world environmental conditions affect the performance of antimicrobial materials. Current International Standards Organization (ISO) testing standards fail to adequately account for temperature and humidity variations, leading to discrepancies between laboratory results and real-world effectiveness. Our findings demonstrate that both temperature and humidity significantly impact pathogen survival and antimicrobial efficacy, with important implications for material selection in healthcare, public spaces, and pandemic preparedness. By systematically evaluating these environmental factors across different material types, we provide evidence-based recommendations for revising international testing protocols. This work is essential for ensuring that antimicrobial materials perform as expected when deployed in actual environments, potentially saving lives by improving the reliability of these critical defense mechanisms against infectious diseases.

Renal ischemia-reperfusion injury (IRI), a common complication following kidney transplantation and partial nephrectomy, is the leading cause of renal dysfunction with limited treatment. Excessive cellular iron accumulation drives lipid peroxidation and activates pathways associated with ferroptosis, which has been implicated in renal IRI. However, the regulatory mechanisms of cellular iron metabolism and its relationship with ferroptosis during ischemia-reperfusion (IR) remain unclear. In this study, in vitro OGSD-R (oxygen, glucose, and serum deprivation-restoration) models and in vivo IR models were employed to investigate alterations in iron metabolism, ferroptosis, and the underlying molecular mechanisms using immunofluorescence, immunoblotting and biochemical testing. We identified glucose deprivation-restoration (GD-R) as a key trigger of cellular iron overload under renal IR condition. Mechanistically, GD-R-induced iron overload is driven by the dysfunction of vacuolar ATPase (V-ATPase)-mammalian target of rapamycin (mTOR) pathway. Inactivation of mTOR results in lysosomal iron releases via two-pore channel 2 (TPC2) and ferritin degradation through ferritinophagy. This process elevates intracellular iron levels, thereby promoting ferroptosis in renal IRI. Targeting cellular iron metabolism effectively alleviates renal IRI. These findings highlight the critical role of glucose metabolism and V-ATPase-mTOR pathway in the regulation of iron homeostasis and ferroptosis during renal IRI, and establish a mechanistic link among glucose metabolism, iron overload and ferroptosis, providing potential therapeutic targets for renal IRI.

SARS-CoV-2 has high infectivity and some of its variants have higher transmissibility. To explore the high infectivity mechanism, the charge distributions of SARS-CoV, SARS-CoV-2, and variants of concern were calculated through a series of net charge calculation formulas. The results showed that the SARS-CoV-2 spike protein had more positive charges than that of SARS-CoV. Further results showed that the variants had similar but higher positive charges than preexisting SARS-CoV-2. In particular, the Delta variant had the greatest increase in positive charges in S₁ resulting in the highest infectivity. In particular, the S₁ positive charge increased greatly in the Delta variant. The S₁ positive charge increased, and due to the large negative charge of angiotensin-converting enzyme-2 (ACE2), this resulted in a large increase in Coulomb’s force between S₁ and ACE2. This finding agrees with the expectation that the positive charges in the spike protein result in more negative charges on SARS-CoV-2 antibodies than that of SARS-CoV. Thus, the infectivity of a novel SARS-CoV-2 variant may be evaluated preliminarily by calculating the charge distribution.