Publications by authors named "M G Mennuni"

Pulmonary embolism (PE) is a life-threatening medical condition caused by the thrombotic occlusion of one or more branches of the lung vasculature, which represents the third most common cause of cardiovascular mortality after myocardial infarction and stroke. PE treatment requires a tailored approach based on accurate risk stratification and personalized treatment decision-making. Anticoagulation is the cornerstone of PE management, yet patients at higher clinical risk may require more rapid reperfusion therapies.

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  • Pulmonary embolism (PE) after childbirth poses serious risks to both mothers and infants, requiring careful management.
  • The case report highlights a patient with intermediate-high risk PE who experienced hemodynamic instability, complicating treatment.
  • This situation emphasizes the need for updated clinical practices to effectively handle PE in post-partum patients.
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  • Lung adenocarcinoma is a serious cancer that is a major cause of death globally, and this study examines how mitochondrial DNA (mtDNA) copy number impacts tumor growth in mice.
  • Increased mtDNA levels were found in lung tumors caused by KRAS expression, leading to larger tumors in mice with higher mtDNA and reduced growth when mtDNA was depleted.
  • The findings suggest mtDNA copy number is critical for lung cancer progression and could pave the way for new cancer treatments, while immune responses in the lung remained unaffected by mtDNA levels.
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Background: Several repair strategies emerged as possible treatment for severe mitral regurgitation (MR). A systematic review and meta-analysis was performed to compare the different percutaneous mitral valve repair approaches.

Methods: PubMed and Scopus electronic databases were scanned for eligible studies until December 11th, 2023.

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  • The oxidative phosphorylation system in mitochondria is crucial for converting energy from food and can adapt its metabolism based on the body's needs or diseases.
  • Oral treatment with an inhibitor of mitochondrial transcription (IMT) shifts metabolism in male mice towards burning fatty acids, leading to reduced body weight and improved liver and glucose health on a high-fat diet.
  • The treatment causes a decrease in oxidative phosphorylation but increases fatty acid oxidation in the liver, suggesting a potential drug strategy for obesity and related health issues.
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