Publications by authors named "U Trahtemberg"
Article Synopsis
- Researchers created a heart-on-a-chip model that includes immune cells to study the effects of SARS-CoV-2 on heart inflammation.
- This model demonstrated that infection leads to increased inflammation, impaired heart function, and elevated levels of mitochondrial damage markers.
- The study found that using exosomes from endothelial cells could reverse heart function issues, regulate calcium levels, lower inflammatory markers, and decrease mitochondrial damage.
Article Synopsis
- ARDS (Acute Respiratory Distress Syndrome) is a critical condition linked mainly to infections like COVID-19, influenza, and bacterial pneumonia, and research is focused on its mechanisms and treatment options.
- The study aims to compare metabolic profiles of ARDS caused by COVID-19, H1N1 influenza, and bacterial pneumonia to understand their unique metabolic pathways.
- Results showed distinct metabolic differences based on the infection type, indicating different underlying mechanisms in ARDS associated with each infectious cause.
Introduction: Severe COVID-19 and non-COVID-19 pulmonary sepsis share pathophysiological, immunological, and clinical features, suggesting that severe COVID-19 is a form of viral sepsis. Our objective was to identify shared gene expression trajectories strongly associated with eventual mortality between severe COVID-19 patients and contemporaneous non-COVID-19 sepsis patients in the intensive care unit (ICU) for potential therapeutic implications.
Methods: Whole blood was drawn from 20 COVID-19 patients and 22 non-COVID-19 adult sepsis patients at two timepoints: ICU admission and approximately a week later.
The COVID-19 pandemic has created an urgency to study the host gene response that leads to variable clinical presentations of the disease, particularly the critical illness response. miRNAs have been implicated in the mechanism of host immune dysregulation and thus hold potential as biomarkers and/or therapeutic agents with clinical application. Hence, further analyses of their altered expression in COVID-19 is warranted.
View Article and Find Full Text PDFCardiovascular disease continues to take more human lives than all cancer combined, prompting the need for improved research models and treatment options. Despite a significant progress in development of mature heart-on-a-chip models of fibrosis and cardiomyopathies starting from induced pluripotent stem cells (iPSCs), human cell-based models of myocardial inflammation are lacking. Here, we bioengineered a vascularized heart-on-a-chip system with circulating immune cells to model SARS-CoV-2-induced acute myocarditis.
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