Publications by authors named "M Detrait"

Introduction: Primary refractory disease affects 30-40% of patients diagnosed with DLBCL and is a significant challenge in disease management due to its poor prognosis. Predicting refractory status could greatly inform treatment strategies, enabling early intervention. Various options are now available based on patient and disease characteristics.

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Article Synopsis
  • Obstructive sleep apnea (OSA) impacts nearly 1 billion people globally, causing chronic intermittent hypoxia (CIH) that leads to organ damage, especially affecting the heart and visceral white adipose tissue (WAT).
  • The study aimed to explore if CIH causes premature senescence in visceral WAT, which in turn may trigger changes in heart structure and function.
  • Results showed that CIH caused significant changes in WAT and early signs of heart damage, but these effects could be mitigated through surgical removal of fat tissue or deletion of specific genes, highlighting visceral WAT senescence as a promising target for combating OSA-related issues.
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Unlike classical protein kinase A, with separate catalytic and regulatory subunits, EPACs are single chain multi-domain proteins containing both catalytic and regulatory elements. The importance of cAMP-Epac-signaling as an energy provider has emerged over the last years. However, little is known about Epac1 signaling in chronic kidney disease.

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Background: Cardiac hypertrophy is an intermediate stage in the development of heart failure. The structural and functional processes occurring in cardiac hypertrophy include extensive gene reprogramming, which is dependent on epigenetic regulation and chromatin remodeling. However, the chromatin remodelers and their regulatory functions involved in the pathogenesis of cardiac hypertrophy are not well characterized.

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Doxorubicin (Dox) is an effective anticancer molecule, but its clinical efficacy is limited by strong cardiotoxic side effects. Lysosomal dysfunction has recently been proposed as a new mechanism of Dox-induced cardiomyopathy. However, to date, there is a paucity of therapeutic approaches capable of restoring lysosomal acidification and function in the heart.

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