2009 - Fellow of the American Association for the Advancement of Science (AAAS)
Jonathan D. Smith focuses on Internal medicine, Endocrinology, Cholesterol, Apolipoprotein E and Apolipoprotein B. His work deals with themes such as Lesion, Antioxidant and In vivo, which intersect with Internal medicine. His Endocrinology study incorporates themes from Inflammation and Transgene.
Jonathan D. Smith works mostly in the field of Cholesterol, limiting it down to concerns involving Trimethylamine N-oxide and, occasionally, Gut flora. His work carried out in the field of Apolipoprotein E brings together such families of science as Pathogenesis, Aorta, Ratón, Monocyte and Alzheimer's disease. The study incorporates disciplines such as Endocytosis, Lipoprotein particle and Losartan, Angiotensin II receptor antagonist in addition to Apolipoprotein B.
His primary areas of study are Internal medicine, Endocrinology, Cholesterol, Apolipoprotein E and Biochemistry. Internal medicine is often connected to Cardiology in his work. His Endocrinology research integrates issues from Inflammation, Immunology, Macrophage and In vivo.
His Cholesterol research is multidisciplinary, relying on both Efflux and Myeloperoxidase. His research integrates issues of Lesion, Genetically modified mouse, Transgene, Molecular biology and Alzheimer's disease in his study of Apolipoprotein E. His Reverse cholesterol transport research includes elements of ABCA1 and High-density lipoprotein.
The scientist’s investigation covers issues in Atrial fibrillation, Internal medicine, Gene, Bioinformatics and In vitro. Jonathan D. Smith works mostly in the field of Atrial fibrillation, limiting it down to topics relating to Mitochondrion and, in certain cases, Heart failure, Oxidative phosphorylation, Sinus rhythm and Sirtuin. His Internal medicine research incorporates elements of Endocrinology and Cardiology.
His studies examine the connections between Endocrinology and genetics, as well as such issues in Proteomics, with regards to Inflammation. Jonathan D. Smith focuses mostly in the field of In vitro, narrowing it down to topics relating to Genetic enhancement and, in certain cases, Cholesterol. He works in the field of Cholesterol, focusing on Apolipoprotein B in particular.
His main research concerns 2019-20 coronavirus outbreak, Spike Protein, Angiotensin II Receptor Blockers, Severe acute respiratory syndrome coronavirus 2 and Bioinformatics. His 2019-20 coronavirus outbreak research includes elements of In patient and In vitro.
This overview was generated by a machine learning system which analysed the scientist’s body of work. If you have any feedback, you can contact us here.
Gut flora metabolism of phosphatidylcholine promotes cardiovascular disease
Zeneng Wang;Elizabeth Klipfell;Brian J. Bennett;Robert A. Koeth.
Intestinal microbiota metabolism of L-carnitine, a nutrient in red meat, promotes atherosclerosis
Robert A Koeth;Zeneng Wang;Bruce S Levison;Jennifer A Buffa.
Nature Medicine (2013)
Severe hypercholesterolemia and atherosclerosis in apolipoprotein E-deficient mice created by homologous recombination in ES cells
Andrew S. Plump;Jonathan D. Smith;Tony Hayek;Katriina Aalto-Setälä.
Targeted disruption of the class B scavenger receptor CD36 protects against atherosclerotic lesion development in mice
Maria Febbraio;Eugene A. Podrez;Jonathan D. Smith;David P. Hajjar.
Journal of Clinical Investigation (2000)
Apolipoprotein E allele-specific antioxidant activity and effects on cytotoxicity by oxidative insults and beta-amyloid peptides.
Masaaki Miyata;Jonathan D. Smith.
Nature Genetics (1996)
Decreased atherosclerosis in mice deficient in both macrophage colony-stimulating factor (op) and apolipoprotein E
Jonathan D. Smith;Eugene Trogan;Michael Ginsberg;Claire Grigaux.
Proceedings of the National Academy of Sciences of the United States of America (1995)
Apolipoprotein A-I is a selective target for myeloperoxidase-catalyzed oxidation and functional impairment in subjects with cardiovascular disease
Lemin Zheng;Benedicta Nukuna;Marie Luise Brennan;Mingjiang Sun.
Journal of Clinical Investigation (2004)
ApoE Promotes the Proteolytic Degradation of Aβ
Qingguang Jiang;C.Y. Daniel Lee;Shweta Mandrekar;Brandy Wilkinson.
Meta-analysis identifies six new susceptibility loci for atrial fibrillation
Patrick T Ellinor;Kathryn L Lunetta;Christine M Albert;Christine M Albert;Nicole L Glazer.
Nature Genetics (2012)
Common variants in KCNN3 are associated with lone atrial fibrillation
Patrick T. Ellinor;Kathryn L. Lunetta;Kathryn L. Lunetta;Nicole L. Glazer;Arne Pfeufer.
Nature Genetics (2010)
If you think any of the details on this page are incorrect, let us know.
We appreciate your kind effort to assist us to improve this page, it would be helpful providing us with as much detail as possible in the text box below: