3,593 research outputs found
Effects of physiological environments on the hydration behavior of mineral trioxide aggregate.
Application of highly sensitive, modified glass substrate-based immuno-PCR on the early detection of nasopharyngeal carcinoma
Tissue engineering-based cartilage repair with allogenous chondrocytes and gelatin–chondroitin–hyaluronan tri-copolymer scaffold: A porcine model assessed at 18, 24, and 36 weeks
FH through the retrospectoscope
After training as a gastroenterologist in the UK, the author became interested in lipidology while he was a research fellow in the USA and switched careers after returning home. Together with Nick Myant, he introduced the use of plasma exchange to treat familial hypercholesterolemia (FH) homozygotes and undertook non-steady state studies of LDL kinetics, which showed that the fractional catabolic rate of LDL remained constant irrespective of pool size. Subsequent steady-state turnover studies showed that FH homozygotes had an almost complete lack of receptor-mediated LDL catabolism, providing in vivo confirmation of the Nobel Prize-winning discovery by Goldstein and Brown that LDL receptor dysfunction was the cause of FH. Further investigation of metabolic defects in FH revealed that a significant proportion of LDL in homozygotes and heterozygotes was produced directly via a VLDL-independent pathway. Management of heterozygous FH has been greatly facilitated by statins and proprotein convertase subtilisin/kexin type 9 inhibitors but remains dependent upon lipoprotein apheresis in homozygotes. In a recent analysis of a large cohort treated with a combination of lipid-lowering measures, survival was markedly enhanced in homozygotes in the lowest quartile of on-treatment serum cholesterol. Emerging therapies could further improve the prognosis of homozygous FH; whereas in heterozygotes, the current need is better detection
Chondrogenesis from immortalized human mesenchymal stem cells: Comparison between collagen gel and pellet culture methods
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