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| http://dx.doi.org/10.1073/pnas.1402097111 | DOI Listing |
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A Single Early Life Acetaminophen Exposure Causes Persistent Abnormalities in the Murine Lung.
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University of Colorado Denver School of Medicine, Aurora, Colorado, United States;
Whether early life acetaminophen (APAP) exposures injure the developing lung is controversial. We sought to correlate murine pulmonary developmental expression profiles of to susceptibility to APAP exposure. P14 C57BL/6 mice were exposed to APAP (140 mg/kg x 1, IP) and assessed for evidence of a histologic, metabolic, functional, and/or transcriptional pulmonary response.
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Department of Gastroenterology, Xinhua Hospital of zhejiang Province: The Second Affiliated Hospital of Zhejiang Chinese Medical University, Zhejiang, China. Electronic address:
Non-alcoholic fatty liver disease (NAFLD), now recognized as metabolic dysfunction-associated steatotic liver disease (MASLD), represents a significant and escalating global health challenge. Its prevalence is intricately linked to obesity, insulin resistance, and other components of the metabolic syndrome. As our comprehension of MASLD deepens, it has become evident that this condition extends beyond the liver, embodying a complex, multi-systemic disease with hepatic manifestations that mirror the broader metabolic landscape.
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Sepsis associated acute lung injury (SALI) is a common complication in patients with severe sepsis and a disease with high morbidity and mortality in ICU patients. The main mechanism of SALI is pulmonary hypoperfusion due to hypotension and shock caused by sepsis, which leads to ischemic necrosis of alveolar endothelial cells and eventually lung failure. At present, SALI therapy mainly includes antibiotic therapy, fluid resuscitation, transfusion products and vasoactive drugs, but these strategies are not satisfactory.
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J Pharm Pharmacol
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Department of Pharmacy, Birla Institute of Technology and Science, Pilani, Pilani Campus, 333031, Rajasthan, India.
Objectives: Chronic kidney disease (CKD) is a serious health issue with rising morbidity and mortality rates. Despite advances in understanding its pathophysiology, effective therapeutic options are limited, necessitating innovative treatment approaches. Also, current frontline treatments that are available against CKD are not uniformly effective and often come with significant side effects.
View Article and Find Full Text PDFAcid-Triggered Cascaded Responsive Supramolecular Peptide Alleviates Myocardial Ischemia‒Reperfusion Injury by Restoring Redox Homeostasis and Protecting Mitochondrial Function.
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Department of Cardiology, Laboratory of Heart Center, Zhujiang Hospital, Southern Medical University, Guangzhou, 510280, P. R. China.
Redox imbalance, including excessive production of reactive oxygen species (ROS) caused by mitochondrial dysfunction and insufficient endogenous antioxidant capacity, is the primary cause of myocardial ischemia‒reperfusion (I/R) injury. In the exploration of reducing myocardial I/R injury, it is found that protecting myocardial mitochondrial function after reperfusion not only reduces ROS bursts but also inhibits cell apoptosis triggered by the release of cytochrome c. Additionally, nuclear factor erythroid 2-related factor 2 (Nrf2) is considered a potential therapeutic target for treating myocardial I/R injury by enhancing the cellular antioxidant capacity through the induction of endogenous antioxidant enzymes.
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