Lipoprotein apheresis: present and future uses.
Kansas City, United States. In Curr Opin Lipidol, Dec 2015
RECENT FINDINGS: Lipoprotein apheresis lowers not only plasma levels of apolipoprotein B lipoproteins but also markers of vascular inflammation and blood rheology.
Meta-analysis of lipid-traits in Hispanics identifies novel loci, population-specific effects, and tissue-specific enrichment of eQTLs.
Houston, United States. In Sci Rep, Dec 2015
Genome-wide significant signals were observed in or near CELSR2, ZNF259/APOA5, KANK2/DOCK6 and NCAN/MAU2 for total cholesterol, LPL, ABCA1, ZNF259/APOA5, LIPC and CETP for HDL cholesterol, CELSR2, APOB and NCAN/MAU2 for LDL cholesterol, and GCKR, TRIB1, ZNF259/APOA5 and NCAN/MAU2 for triglycerides.
[Position of lipoprotein apheresis in present].
In Vnitr Lek, Nov 2015
These compounds act either by reducing low density lipoprotein (LDL) cholesterol production by inhibiting apolipoprotein B synthesis with an antisense oligonucleotide (mipomersen), or by inhibiting microsomal triglyceride transfer protein (lomitapid), or by enhancing LDL catabolism via monoclonal antibody-mediated inhibition of the activity of proprotein convertase subtilisin/kexin 9 (PCSK9 - alirocumab, evolocumab etc).
Hypermutation in human cancer genomes: footprints and mechanisms.
More papers using
In Nat Rev Cancer, 2014
This major expansion of cancer mutation data sets has provided unprecedented statistical power for the analysis of mutation spectra, which has confirmed several classical sources of mutation in cancer, highlighted new prominent mutation sources (such as apolipoprotein B mRNA editing enzyme catalytic polypeptide-like (APOBEC) enzymes) and empowered the search for cancer drivers.