Publications by authors named "J C Schippers"

Clinical monitoring of pulmonary edema due to vascular hyperpermeability in acute respiratory distress syndrome (ARDS) poses significant clinical challenges. Presently, no biological or radiological markers are available for quantifying pulmonary edema. Our aim was to phenotype pulmonary edema and pulmonary vascular permeability in patients with coronavirus disease 2019 (COVID-19) ARDS.

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Article Synopsis
  • Life evolved in a reducing environment but faced challenges from reactive oxygen species (ROS) during the great oxidation event (GOE), leading to the development of copper-zinc superoxide dismutases (CuZnSODs) in some plants.
  • The chemical inhibitor lung cancer screen 1 (LCS-1) was used to study the effects of CuZnSOD inhibition on plant growth, transcription, and metabolism across different species, including bryophytes and vascular plants.
  • The results showed that LCS-1 caused oxidative stress and a core physiological response related to glutathione balance in all species, but varying metabolic responses were observed based on the number and types of CuZnSOD isoforms present in each plant.
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Flooding impairs plant growth through oxygen deprivation, which activates plant survival and acclimation responses. Transcriptional responses to low oxygen are generally associated with the activation of group VII ETHYLENE-RESPONSE FACTOR (ERFVII) transcription factors. However, the exact mechanisms and molecular components by which ERFVII factors initiate gene expression are not fully elucidated.

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The Wilms' tumor protein 1 (WT1) is a well-known and prioritized tumor-associated antigen expressed in numerous solid and blood tumors. Its abundance and immunogenicity have led to the development of different WT1-specific immune therapies. The driving player in these therapies, the WT1-specific T-cell receptor (TCR) repertoire, has received much less attention.

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Truncating variants in TTN (TTNtv) are present in 15-25 % of patients with idiopathic dilated cardiomyopathy. Interestingly, the pathogenicity of TTNtv seems to be linked to their location within the gene. More proximal I-band TTNtv (TTNtvI) harbour less pathogenic potential than distant A-band TTNtv (TTNtvA).

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