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Rationale: Current research on antiviral treatment in children is relatively limited, especially in children under 1 year old.

Patient Concerns: Liu XX, an 8-month-old infant (case number: 3001120473), presented to the hospital in August 2016 with a chief complaint of being "hepatitis B surface antigen positive for 8 months and experiencing abnormal liver function for 5 months."

Diagnoses: The patient was diagnosed as chronic hepatitis B cirrhosis (G3S3-4) with active compensatory phase.

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A ferroptosis amplifier based on triple-enhanced lipid peroxides accumulation strategy for effective pancreatic cancer therapy.

Biomaterials

September 2024

School of Chemical Science and Engineering, Department of Oncology, East Hospital Affiliated to Tongji University, School of Medicine, Tongji University, Shanghai, 200092, PR China. Electronic address:

As an iron dependent regulatory cell death process driven by excessive lipid peroxides (LPO), ferroptosis is recognized as a powerful weapon for pancreatic cancer (PC) therapy. However, the tumor microenvironment (TME) with hypoxia and elevated glutathione (GSH) expression not only inhibits LPO production, but also induces glutathione peroxidase 4 (GPX4) mediated LPO clearance, which greatly compromise the therapeutic outcomes of ferroptosis. To address these issues, herein, a novel triple-enhanced ferroptosis amplifier (denoted as Zal@HM-PTBC) is rationally designed.

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Hypertriglyceridemia is the third cause of acute pancreatitis after lithiasis and alcohol. When triglycerides are >2000 mg/dL the risk increases to 20%. Acute pancreatitis is an important cause of morbidity in patients infected with human immunodeficiency virus (HIV), especially in those treated with lamivudine, due to hypertriglyceridemia.

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Pancreatic cancer tends to be highly resistant to current therapy and remains one of the great challenges in biomedicine with very low 5-year survival rates. Here, we report that zalcitabine, an antiviral drug for human immunodeficiency virus infection, can suppress the growth of primary and immortalized human pancreatic cancer cells through the induction of ferroptosis, an iron-dependent form of regulated cell death. Mechanically, this effect relies on zalcitabine-induced mitochondrial DNA stress, which activates the STING1/TMEM173-mediated DNA sensing pathway, leading to macroautophagy/autophagy-dependent ferroptotic cell death via lipid peroxidation, but not a type I interferon response.

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