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Portal hypertension is a complication of children with biliary atresia. It results from progression of liver scarring (fibrosis) and can lead to gastrointestinal bleeding and accumulation of fluid in the abdomen (also known as ascites). In this study, investigations from the Childhood Liver Disease Research Network analyzed the blood of patients to identify protein that increase in children with portal hypertension. Investigators analyzed over 1,000 proteins using an assay known as proteomics. Among the proteins that increased in babies with portal hypertension they found that semaphorin 6B (SEMA6B) alone and three other protein combinations (SEMA6B+SFRP3, SEMA6B+COMMD7, and VCAM1+BMX) had high accuracy to identify portal hypertension. Analyzing liver biopsies, the new protein biomarkers showed increased expression in liver vascular cells (endothelial cells), bile duct epithelium (cholangiocytes), and immune cells within portal triads.
Conclusion
Large-scale proteomics identified SEMA6B, SFRP3, COMMD7, BMX, and VCAM1 as biomarkers highly associated with clinical portal hypertension in children with biliary atresia. The expression of the biomarkers in liver epithelial, endothelial, and immune cells support their potential role in the mechanisms that cause portal hypertension.
Arbor Research Collaborative for Health (Arbor Research) is pleased to announce its successful award of a position in a new subgroup within the General Services Administration (GSA) Schedule Contract focusing on Program Evaluation Services. The establishment of this subgroup will streamline the federal procurement process. Program evaluation is a crucial aspect of federal initiatives, providing […]
Arbor Research will engage with stakeholders across the health care system to identify, develop, and pilot web-based competency training for health care professionals in best practices for quality and safety. November 6, 2023 – Ann Arbor, MI – Arbor Research Collaborative for Health is excited to be collaborating with Reveal Global Consulting in the initiation […]
Individuals with BSEP deficiency with one p.E297G or p.D482G mutation and one PPTM have a similarly severe disease course and low responsiveness to siEHC as those with two PPTMs.
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