Publications by authors named "L T Tram"

Background: Arteriovenous malformations (AVMs) within the mediastinum are rare vascular anomalies. With the increasing number of coronary angiographies being performed, the number of incidentally found cases is rising. This presents challenges in terms of determining the appropriate treatment strategy.

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The development of electrophilic ligands that rapidly modify specific lysine residues remains a major challenge. Salicylaldehyde-based inhibitors have been reported to form stable imine adducts with the catalytic lysine of protein kinases. However, the targeted lysine in these examples is buried in a hydrophobic environment.

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Article Synopsis
  • Sonodynamic therapy (SDT) offers a noninvasive way to target deep tumors using ultrasound and special sonosensitizers, but the process faces challenges due to sonosensitizers' low stability and poor uptake in cells.
  • This study explores the use of non-ionic polysorbate (Tween 80, T80) to create micelles that enhance the delivery of a mitochondria-targeting sonosensitizer (T-Ce6) combined with a pro-oxidant (piperlongumine, PL) for better treatment effectiveness.
  • The T80 micelles significantly improved the internalization of T-Ce6, leading to increased production of reactive oxygen species in cancer cells and triggering cancer-specific
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Spontaneous epidural haematoma (SEDH) is a rare complication of sickle cell disease (SCD). To our knowledge, 38 cases of patients with SEDH associated with SCD have been reported in the literature. In this case report we describe the first Danish paediatric case with SCD and SEDH.

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Dysregulated iron homeostasis underlies diverse pathologies, from ischemia-reperfusion injury to epithelial-mesenchymal transition and drug-tolerant "persister" cancer cell states. Here, we introduce ferrous iron-activatable luciferin-1 (FeAL-1), a small-molecule probe for bioluminescent imaging of the labile iron pool (LIP) in luciferase-expressing cells and animals. We find that FeAL-1 detects LIP fluctuations in cells after iron supplementation, depletion, or treatment with hepcidin, the master regulator of systemic iron in mammalian physiology.

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