To investigate the effects of airborne fine particle on cell viability and inflammation in human bronchial epithelial cells. Methods: Atmospheric PM2.5 samples were collected by PM2.5 sampler. PM2.5 morphology was observed by scanning electron microscope (SEM). Human bronchial epithelial cells (BEAS-2B) were treated with PM2.5 at different concentrations (0, 50, 100, 200, 400, 800 μg/mL) for 12, 24 or 48 hours, and the cell activity were evaluated by cell counting kit-8 (CCK-8). The mRNA expression levels of (granulocyte-macrophage colony stimulating factor,GM-CSF) and TNF-α were detected by quantitative real-time PCR (qRT-PCR). Western blot was used to detect the protein expressions of GM-CSF and TNF-α. Results: According to SEM, the shape of PM2.5 varied, and the diameter was different and mostly equal to or less than 2.5 μm. CCK-8 assay showed that different concentrations of PM2.5 exposure for 12 hours, 24 hours and 48 hours resulted in loss of cell viability of BEAS-2B cells (P<0.05). Different concentrations of PM2.5 increased the mRNA and protein expression of GM-CSF and TNF-α, and the higher concentration of PM2.5 induced higher expression, which have statistical significant difference between the groups (P<0.05). Conclusion: Atmospheric PM2.5 can cause inflammatory response in human bronchial epithelial cells. They can reduce cell viability, which may be related to the PM2.5 trigger and aggravation of bronchopulmonary inflammatory diseases.
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http://dx.doi.org/10.11817/j.issn.1672-7347.2017.09.008 | DOI Listing |
Hepatology
January 2025
Division of Gastroenterology and Hepatology, University of California, San Francisco, San Francisco, CA.
Background Aims: Patients with hepatocellular carcinoma (HCC) meeting UNOS-downstaging (DS) criteria have excellent post-liver transplantation (LT) outcomes. Studies on HCC beyond UNOS-DS criteria ("All-comers" (AC)) have been limited by small sample size and short follow-up time, prompting this analysis.
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Blood
January 2025
H. Lee Moffitt Cancer Center, Tampa, Florida, United States.
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January 2025
Universitätsklinikum Heidelberg, Med. Klinik V, GMMG-Studygroup, Heidelberg, Germany.
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View Article and Find Full Text PDFBioconjug Chem
January 2025
Department of Biochemistry, Faculty of Biological and Veterinary Sciences, Nicolaus Copernicus University in Torun, ul. Lwowska 1, 87-100 Torun, Poland.
l-Asparaginase (l-ASNase) catalyzes the hydrolysis of l-asparagine, leading to its depletion and subsequent effects on the cellular proliferation and survival. In contrast to normal cells, malignant cells that lack asparagine synthase are extremely susceptible to asparagine deficiency. l-ASNase has been successfully employed in treating pediatric leukemias and non-Hodgkin lymphomas; however, its usage in adult patients and other types of cancer is limited due to significant side effects and drug resistance.
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