Publications by authors named "D Janszen"

Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous in the environment as components of fossil fuels and by-products of combustion. These multi-ring chemicals differentially activate the aryl hydrocarbon receptor (AHR) in a structurally dependent manner, and induce toxicity via both AHR-dependent and -independent mechanisms. PAH exposure is known to induce developmental malformations in zebrafish embryos, and recent studies have shown cardiac toxicity induced by compounds with low AHR affinity.

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Article Synopsis
  • The aryl hydrocarbon receptor (AHR) is crucial for understanding the toxic effects of compounds like TCDD, and research continues to explore its various roles in cellular signaling.
  • A mutant zebrafish line, ahr2(hu3335), was created to study AHR functionality, revealing that this variant is non-functional and helps analyze the toxicity mechanisms of TCDD through different AHR paralogues.
  • Additionally, in silico modeling and in vivo studies indicated that while AHR1A is a pseudogene and does not interact with TCDD, it may still bind to leflunomide, showing the complexity of AHR functionality in toxicological responses during development.
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Sodium and potassium cyanide are highly toxic, produced in large amounts by the chemical industry, and linked to numerous high-profile crimes. The U.S.

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The recent advances in high-throughput data acquisition have driven a revolution in the study of human disease and determination of molecular biomarkers of disease states. It has become increasingly clear that many of the most important human diseases arise as the result of a complex interplay between several factors including environmental factors, such as exposure to toxins or pathogens, diet, lifestyle, and the genetics of the individual patient. Recent research has begun to describe these factors in the context of networks which describe relationships between biological components, such as genes, proteins and metabolites, and have made progress towards the understanding of disease as a dysfunction of the entire system, rather than, for example, mutations in single genes.

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