Publications by authors named "L Semendric"
Article Synopsis
- The study focuses on the differentiation of embryonic stem (ES) cells into primitive ectoderm-like (EPL) cells, which is crucial for developing cell therapies, using a specific biological factor in the conditioned medium called MEDII.
- Through fractionation of MEDII, researchers identified that l-proline, a low-molecular-weight amino acid, is essential for the differentiation of ES cells into EPL cells, as blocking l-proline uptake inhibited this process.
- Additionally, while the mTOR signaling pathway is involved in the activity of l-proline, it alone does not suffice to change the phenotype of ES cells, highlighting a unique role of l-proline in regulating pluripotency and differentiation.
The interactions between hepatitis C virus (HCV) and alcohol metabolism are not well understood. To determine the effect that alcohol metabolism has on HCV replication and the antiviral action of interferon (IFN), Huh-7 cells that harbor HCV replication and metabolize ethanol via the introduced expression of cytochrome P450 2E1 (Cyp2e1) were treated with ethanol and IFN-alpha. Treatment of these cells with ethanol (0-100 mmol/L) significantly increased HCV replication.
View Article and Find Full Text PDFInterferon (IFN) alpha inhibits hepatitis C virus (HCV) replication both clinically and in vitro; however, the complete spectrum of interferon-stimulated genes (ISGs) expressed in the HCV-infected liver or the genes responsible for control of HCV replication have not been defined. To better define ISG expression in the chronically infected HCV liver, DNA microarray analysis was performed on 9 individuals with chronic hepatitis C (CHC). A total of 232 messenger RNAs were differentially regulated in CHC compared with nondiseased liver controls.
View Article and Find Full Text PDFBackground: Long-term persistence of C. burnetii in infected animals was established in the 1950s and 60s, but the implications for human Q fever are not fully explored.
Aim: To compare the prevalence of markers of infection in a cohort of Q fever patients in Australia (up to 5 years after infection) with those in the 1989 Birmingham cohort (12 years after infection).