Zobrazeno 1 - 10
of 13
pro vyhledávání: '"Siobhan I. Davis"'
Publikováno v:
BMJ military health. 166(6)
Disease non-battle injury has plagued British expeditionary forces through the ages. While in recent years significant mortality has reduced, it has had a large impact on operational effectiveness, at times leading to closure of major medical treatme
Autor:
Harika Boztepe, Siobhan I. Davis, Kenneth E. White, Fatemehsadat Esteghamat, Refik Tanakol, Seyed Mohammad Javad Mortazavi, Mahdi Malekpour, Holly J. Garringer
Publikováno v:
American Journal of Medical Genetics Part A. :2390-2396
Familial tumoral calcinosis (TC) is characterized by elevated serum phosphate concentrations, normal or elevated 1,25(OH)2 vitamin D, as well as periarticular and vascular calcifications. Recessive mutations in the mucin-like glycosyltransferase GalN
Autor:
Shubin Zhang, Marc K. Drezner, Shiguang Liu, Yongbo Lu, Frank Rauch, Baozhi Yuan, Siobhan I. Davis, Hector F. Rios, Leanne M Ward, Lynda F. Bonewald, Jian Q. Feng, Xijie Yu, L. Darryl Quarles, Yixia Xie, Kenneth E. White
Publikováno v:
Nature Genetics. 38:1310-1315
The osteocyte, a terminally differentiated cell comprising 90%–95% of all bone cells1,2, may have multiple functions, including acting as a mechanosensor in bone (re)modeling3. Dentin matrix protein 1 (encoded by DMP1) is highly expressed in osteoc
Autor:
Bhaskar Dasgupta, Mohamad S. Draman, Holly J. Garringer, Daniel L. Koller, Niamh Conlon, Siobhan I. Davis, Neal S. Fedarko, Alka Jain, Kenneth E. White, Corinne Fisher, M. J. Cullen, Tobias E. Larsson
Publikováno v:
The Journal of Clinical Endocrinology & Metabolism. 91:4037-4042
Context: Familial tumoral calcinosis (TC) results from disruptions in phosphate metabolism and is characterized by high serum phosphate with normal or elevated 1,25 dihydroxyvitamin vitamin D concentrations and ectopic and vascular calcifications. Re
Autor:
Siobhan I. Davis, Fuming Zhang, Moosa Mohammadi, Regina Goetz, Kenneth E. White, Xijie Yu, David M. Ornitz, Omar A. Ibrahimi, Robert J. Linhardt, Holly J. Garringer
Publikováno v:
Endocrinology. 146:4647-4656
Fibroblast growth factor (FGF)-23 has emerged as an endocrine regulator of phosphate and of vitamin D metabolism. It is produced in bone and, unlike other FGFs, circulates in the bloodstream to ultimately regulate phosphate handling and vitamin D pro
Publikováno v:
ResearcherID
Fibroblast growth factor-23 (FGF23) is a circulating factor that plays critical roles in phosphate and vitamin D metabolism. The goal of our studies was to dissect the pathways directing the vitamin D-phosphate-FGF23 homeostatic axis. To test the rol
Autor:
Siobhan I. Davis, Tobias E. Larsson, Xijie Yu, Mohamad S. Draman, M. J. Cullen, Kenneth E. White, Sean D. Mooney
Publikováno v:
The Journal of Clinical Endocrinology & Metabolism. 90:2424-2427
Gain-of-function mutations in fibroblast growth factor-23 (FGF23) are responsible for autosomal dominant hypophosphatemic rickets, a disorder of isolated renal phosphate wasting. Patients with the disorder display hypophosphatemia with normocalcemia
Autor:
Leo Mascarenhas, Emily G. Farrow, Pisit Pitukcheewanont, Yvonne Gutierrez, Peter Beighton, Siobhan I. Davis, Sean D. Mooney, Kenneth E. White
Publikováno v:
American Journal of Medical Genetics Part A. :537-539
Publikováno v:
Journal of the American Society of Nephrology : JASN. 20(5)
Fibroblast growth factor-23 (FGF23), a hormone central to phosphate and vitamin D metabolism, reduces renal absorption of phosphate by downregulating the sodium-phosphate cotransporter Npt2a. However, the mechanisms of FGF23 action in the kidney are
Autor:
Emily G. Farrow, Mahdi Malekpour, Dan E. Arking, Kenneth E. White, Fatemehsadat Esteghamat, Seyed Mohammad Javad Mortazavi, Xijie Yu, Holly J. Garringer, Siobhan I. Davis, Harry C. Dietz
Publikováno v:
American journal of physiology. Endocrinology and metabolism. 295(4)
Fibroblast growth factor 23 (FGF23) is a hormone required for normal renal phosphate reabsorption. FGF23 gain-of-function mutations result in autosomal dominant hypophosphatemic rickets (ADHR), and FGF23 loss-of-function mutations cause familial hype