Publications by authors named "S M Timmermans"

Article Synopsis
  • Thrombotic microangiopathy (TMA) syndromes can lead to serious kidney issues like acute kidney injury and end-stage disease, often marked by low platelet counts and hemolytic anemia.
  • A study examined different types of kidney-limited TMA and their outcomes, finding that a significant portion (66%) of patients had this particular form, with distinct characteristics in those with complement-related TMA compared to other types.
  • Results showed that treatments like eculizumab were beneficial for kidney-limited complement-mediated TMA, emphasizing the importance of kidney biopsies for early detection and the need to assess for complement issues to guide treatment options.
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Annexin A1, a protein released by neutrophils, is a potent regulator of inflammation in the intact form, but loses this activity when cleaved. The presence of autoantibodies to this protein can impact its function. An immunoassay, developed to measure autoantibodies to Annexin A1 in plasma or serum, has been developed and performances are reported.

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Sepsis remains a huge unmet medical need for which no approved drugs, besides antibiotics, are on the market. Despite the clinical impact of sepsis, its molecular mechanism remains inadequately understood. Recent insights have shown that profound hepatic transcriptional reprogramming, leading to fatal metabolic abnormalities, might open a new avenue to treat sepsis.

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The small intestinal crypts harbor secretory Paneth cells (PCs) which express bactericidal peptides that are crucial for maintaining intestinal homeostasis. Considering the diverse environmental conditions throughout the course of the small intestine, multiple subtypes of PCs are expected to exist. We applied single-cell RNA-sequencing of PCs combined with deep bulk RNA-sequencing on PC populations of different small intestinal locations and discovered several expression-based PC clusters.

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In sepsis, limited food intake and increased energy expenditure induce a starvation response, which is compromised by a quick decline in the expression of hepatic PPARα, a transcription factor essential in intracellular catabolism of free fatty acids. The mechanism upstream of this PPARα downregulation is unknown. We found that sepsis causes a progressive hepatic loss-of-function of HNF4α, which has a strong impact on the expression of several important nuclear receptors, including PPARα.

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