Publications by authors named "R Almaas"
Background: Cholestasis causes accumulation of bile acids (BAs) and changes the circulating bile acid profile. Quantification of circulating BAs in dried bloodspots (DBS) may demonstrate obstruction of bile flow and altered bile acid metabolism in the liver. High sample throughput enables rapid screening of cholestatic diseases.
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- * Key findings reveal that expression of aquaporins (AQP8 and AQP9) increases during cell differentiation, but AQP8 protein levels decrease post-hypoxia despite increased mRNA levels after reoxygenation.
- * The research indicates that post-transcriptional mechanisms, rather than transcription changes, lead to reduced AQP8 protein concentration after hypoxia and reoxygenation events in liver cells.
Article Synopsis
- The study focuses on using parenteral nutrition (PN) for premature newborns, who are at risk for liver disease associated with PN, and aims to develop predictive models for this condition.
- Researchers utilized liver organoids derived from induced pluripotent stem cells to simulate the liver environment and assess the effects of different lipid treatments used in PN.
- Results indicated that both lipid treatments led to lipid accumulation in liver cells and decreased liver function markers, suggesting that liver organoids could serve as a useful platform for testing new, less harmful PN solutions.
The prevailing concept is that gestational alloimmune liver disease (GALD) is caused by maternal antibodies targeting a currently unknown antigen on the liver of the fetus. This leads to deposition of complement on the fetal hepatocytes and death of the fetal hepatocytes and extensive liver injury. In many cases, the newborn dies.
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