Publications by authors named "R W Heilig"
Article Synopsis
- - Sepsis is a severe response to infection that causes life-threatening organ dysfunction, highlighting the need for better understanding and new treatments for this global health issue.
- - Researchers utilized high-throughput tandem mass spectrometry to analyze the plasma proteins of sepsis patients compared to other groups, collecting extensive data from over 2,600 samples to identify specific protein changes and disease features.
- - The findings offer insights into the immune response to sepsis, helping to pinpoint subtypes of the condition, potential biomarkers for diagnosis, and paving the way for personalized treatment strategies.
Article Synopsis
- Mutations in the Nuclear factor I/X (NFIX) gene are linked to two skeletal disorders, Marshall-Smith syndrome (MSS) and Malan syndrome (MAL), affecting gene expression in nervous tissue.
- Researchers analyzed fibroblast cell lines from MSS patients and controls, discovering that certain frameshift mutations produced truncated NFIX proteins while not significantly impacting other gene expressions.
- Further studies involving RNA sequencing revealed 191 misregulated transcripts and 815 proteins in affected cells, identifying specific genes like cellular retinoic acid binding protein 2 and vascular cell adhesion molecule 1 as potential targets for drug development.
Background: The widespread use of the antifibrinolytic agent, tranexamic acid (TXA), interferes with the quantification of fibrinolysis by dynamic laboratory assays such as clot lysis, making it difficult to measure fibrinolysis in many trauma patients. At the final stage of coagulation, factor (F)XIIIa catalyzes the formation of fibrin-fibrin and fibrin-α-antiplasmin (αAP) cross-links, which increases clot mechanical strength and resistance to fibrinolysis.
Objectives: Here, we developed a method to quantify fibrin-fibrin and fibrin-αAP cross-links that avoids the challenges posed by TXA in determining fibrinolytic resistance in conventional assays.
Mitochondrial outer membrane permeabilisation (MOMP) is often essential for apoptosis, by enabling cytochrome c release that leads to caspase activation and rapid cell death. Recently, MOMP has been shown to be inherently pro-inflammatory with emerging cellular roles, including its ability to elicit anti-tumour immunity. Nonetheless, how MOMP triggers inflammation and how the cell regulates this remains poorly defined.
View Article and Find Full Text PDFMutations within viral epitopes can result in escape from T cells, but the contribution of mutations in flanking regions of epitopes in SARS-CoV-2 has not been investigated. Focusing on two SARS-CoV-2 nucleoprotein CD8 epitopes, we investigated the contribution of these flanking mutations to proteasomal processing and T cell activation. We found decreased NP-B*27:05 CD8 T cell responses to the NP-Q7K mutation, likely due to a lack of efficient epitope production by the proteasome, suggesting immune escape caused by this mutation.
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