Publications by authors named "A Zarzycki"

Article Synopsis
  • Human pericardial fluid (PF) contains biologically active markers that have significant effects on heart-related cellular activities.
  • PF can enhance the activity of cardiac fibroblasts, which are important for heart tissue repair, through a specific biological pathway known as the transforming growth factor-β pathway.
  • In patients with coronary artery disease, the PF possesses a higher capacity to promote fibrosis compared to those without the disease, indicating a potential area for clinical attention.
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Direct magnetic writing of ferromagnetic nanoscale elements provides an alternative pathway for potential application in data storage or spintronic devices. Magnetic patterning due to local chemical disordering of FeAl thin films results in adjacent nanoscale regions that possess two different phases, a low-magnetization and high-coercive chemically ordered phase (non-irradiated ferromagnetic area, NIFM) and a high-magnetization and low-coercive chemically disordered phase (irradiated ferromagnetic area, IMF). Depending on the volume of NIFM and IFM phases, different interaction mechanisms were revealed.

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Background: Pericardial fluid (PF) contains cells, proteins, and inflammatory mediators, such as cytokines, chemokines, growth factors, and matrix metalloproteinases. To date, we lack an adequate understanding of the inflammatory response that acute injury elicits in the pericardial space.

Objective: To characterize the inflammatory profile in the pericardial space acutely after ischemia/reperfusion.

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Cardiac fibrosis is a significant driver of congestive heart failure, a syndrome that continues to affect a growing patient population globally. Cardiac fibrosis results from a constellation of complex processes at the transcription, receptor, and signaling axes levels. Various mediators and signaling cascades, such as the transformation growth factor-beta pathway, have been implicated in the pathophysiology of cardiac tissue fibrosis.

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Cardiac fibrosis is a significant contributor to heart failure, a condition that continues to affect a growing number of patients worldwide. Various cardiovascular comorbidities can exacerbate cardiac fibrosis. While fibroblasts are believed to be the primary cell type underlying fibrosis, recent and emerging data suggest that other cell types can also potentiate or expedite fibrotic processes.

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