J
Jose C. Florez
Researcher at Harvard University
Publications - 414
Citations - 58686
Jose C. Florez is an academic researcher from Harvard University. The author has contributed to research in topics: Type 2 diabetes & Diabetes mellitus. The author has an hindex of 87, co-authored 357 publications receiving 50750 citations. Previous affiliations of Jose C. Florez include George Washington University & University of California, Davis.
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Journal ArticleDOI
1723-P: Genetic Risk Scores Predict Glycemic Traits and Response to Glipizide Treatment in the Study to Understand the Genetics of the Acute Response to Metformin and Glipizide in Humans (SUGAR-MGH)
Posted ContentDOI
Genome-wide meta-analysis and omics integration identifies novel genes associated with diabetic kidney disease
Niina Sandholm,Joanne B. Cole,Joanne B. Cole,Joanne B. Cole,Viji Nair,Xin Sheng,Hongbo Liu,Emma Ahlqvist,Natalie R. van Zuydam,Natalie R. van Zuydam,Emma H. Dahlström,Damian Fermin,Laura Smyth,Rany M. Salem,Carol Forsblom,Erkka Valo,Valma Harjutsalo,Eoin P. Brennan,Gareth J. McKay,Darrell Andrews,Ross Doyle,Helen C. Looker,Robert G. Nelson,Colin N. A. Palmer,Amy Jayne McKnight,Catherine Godson,Alexander P. Maxwell,Alexander P. Maxwell,Leif Groop,Mark I. McCarthy,Matthias Kretzler,Katalin Susztak,Joel N. Hirschhorn,Joel N. Hirschhorn,Joel N. Hirschhorn,Jose C. Florez,Per-Henrik Groop +36 more
TL;DR: In this article, the authors performed genome-wide association study (GWAS) meta-analyses using ten different phenotypic definitions of diabetic kidney disease (DKD), including nearly 27,000 individuals with diabetes, and integrated the results with various kidney omics datasets.
Journal ArticleDOI
Extending precision medicine tools to populations at high risk of type 2 diabetes
Shivani Misra,Jose C. Florez +1 more
TL;DR: In this Perspective, Shivani Misra and Jose C Florez discuss the application of precision medicine tools in under-represented populations and suggest ways to improve the quality of care in these populations.
Identification of a novel proinsulin-associated SNP and demonstration that proinsulin is unlikely to be a causal factor in subclinical vascular remodelling using Mendelian randomisation
Rona J. Strawbridge,Angela Silveira,Marcel den Hoed,Stefan Gustafsson,Jian'an Luan,Denis Rybin,Josée Dupuis,Ruifang Li-Gao,Maryam Kavousi,Abbas Dehghan,Kadri Haljas,Jari Lahti,Jesper R. Gådin,Alexandra Bäcklund,Ulf de Faire,Karl Gertow,P. Giral,Anuj Goel,Steve E. Humphries,Sudhir Kurl,Claudia Langenberg,Lars Lannfelt,Lars Lind,Cecilia M. Lindgren,Elmo Mannarino,Dennis O. Mook-Kanamori,Andrew P. Morris,Renée de Mutsert,Rainer Rauramaa,Peter Saliba-Gustafsson,Bengt Sennblad,Andries J. Smit,Ann-Christine Syvänen,Elena Tremoli,Fabrizio Veglia,Björn Zethelius,Hanna M. Björck,Johan G. Eriksson,Albert Hofman,Oscar H. Franco,Hugh Watkins,J. Wouter Jukema,Jose C. Florez,Nicholas J. Wareham,James B. Meigs,Erik Ingelsson,Damiano Baldassarre,Anders Hamsten +47 more
TL;DR: It is demonstrated that whilst proinsulin levels are associated with cIMT measures, proins insulin per se is unlikely to have a causative effect on cIMTs, and a novel Proinsulin-associated locus is identified.
Journal ArticleDOI
Common variation in PPARGC1A/B and progression to diabetes or change in metabolic traits following preventive interventions: the Diabetes Prevention Program.
Paul W. Franks,Costas A. Christophi,Kathleen A. Jablonski,Linda M. Delahanty,Edward S. Horton,W. C. Knowler,Jose C. Florez,Jose C. Florez +7 more
TL;DR: Findings provide some novel and confirmatory insights into the roles of PPARGC1A/B variation in type 2 diabetes and related metabolic traits and a range of relevant metabolic quantifiable traits.