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Article Synopsis
  • The study assessed left ventricular ultrasound parameters in postmenopausal breast cancer patients undergoing anti-cancer therapy, focusing on cardiac dysfunction.
  • A total of 74 patients were monitored over two years, and 36.5% developed cardiac issues (CTRCD), with no signs of symptomatic heart failure reported.
  • Key findings indicated that global longitudinal strain (GLS) and ejection fraction (EF) declined in patients with CTRCD, while certain measurements remained normal in those without cardiac dysfunction.
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Cancer chemotherapy induces cell stress in rapidly dividing cancer cells to trigger their growth arrest and apoptosis. However, adverse effects related to cardiotoxicity underpinned by a limited regenerative potential of the heart limits clinical application: In particular, chemotherapy with doxorubicin (DOXO) causes acute heart injury that can transition to persisting cardiomyopathy (DOXO-CM). Here, we tested if MuRF1 inhibition ("MuRFi") was able to attenuate DOXO-CM.

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Real-time electro-mechanical profiling of dynamically beating human cardiac organoids by coupling resistive skins with microelectrode arrays.

Biosens Bioelectron

January 2025

Department of Chemical & Biological Engineering, Monash University, Clayton, Victoria, 3800, Australia; The Melbourne Centre for Nanofabrication, Clayton, Victoria, 3800, Australia. Electronic address:

Cardiac organoids differentiated from induced pluripotent stem cells are emerging as a promising platform for pre-clinical drug screening, assessing cardiotoxicity, and disease modelling. However, it is challenging to simultaneously measure mechanical contractile forces and electrophysiological signals of cardiac organoids in real-time and in-situ with the existing methods. Here, we present a biting-inspired sensory system based on a resistive skin sensor and a microelectrode array.

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Doxorubicin, the most prescribed chemotherapeutic drug, causes dose-dependent cardiotoxicity and heart failure. However, our understanding of the immune response elicited by doxorubicin is limited. Here we show that an aberrant CD8 T cell immune response following doxorubicin-induced cardiac injury drives adverse remodeling and cardiomyopathy.

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