Results 61 to 70 of about 2,952,556 (266)

Conditional Deletion of Murine Fgf23: Interruption of the Normal Skeletal Responses to Phosphate Challenge and Rescue of Genetic Hypophosphatemia [PDF]

open access: yes, 2016
The transgenic and knockout (KO) animals involving Fgf23 have been highly informative in defining novel aspects of mineral metabolism, but are limited by shortened lifespan, inability of spatial/temporal FGF23 control, and infertility of the global KO ...
Allen, Matthew R.   +6 more
core   +1 more source

Dietary phosphate restriction normalizes biochemical and skeletal abnormalities in a murine model of tumoral calcinosis [PDF]

open access: yes, 2011
Mutations in the GALNT3 gene cause tumoral calcinosis characterized by ectopic calcifications due to persistent hyperphosphatemia. We recently developed Galnt3 knockout mice in a mixed background, which had hyperphosphatemia with increased bone mineral ...
Allen, Matthew R.   +4 more
core   +2 more sources

Tumoral calcinosis

open access: yesJournal of British Surgery, 1983
Abstract Tumoral calcinosis is an uncommon, usually solitary, tumour-like mass characterized by soft tissue calcification for no apparent reason. Nearly all cases have occurred in negroes, including 2 previously recorded in this country.
S A, Knowles, G, Declerck, P P, Anthony
openaire   +2 more sources

The Case | Ectopic calcifications in a child [PDF]

open access: yes, 2015
The case A nine year old boy, born of third degree consanguinity, presented with a hard left scapular swelling for 6 months. There was no history of fever, trauma or weight loss. There was no pain, redness or discharge. This mass was excised but recurred
Econs, Michael J.   +6 more
core   +2 more sources

Risk factors associated with calcinosis of juvenile dermatomyositis [PDF]

open access: yes, 2008
OBJETIVO: Identificar fatores de risco associados à calcinose em crianças e adolescentes com dermatomiosite juvenil. MÉTODOS: Prontuários de 54 pacientes com dermatomiosite juvenil foram estudados.
AIKAWA, Nádia E.   +6 more
core   +3 more sources

FGF23 Deficiency Leads to Mixed Hearing Loss and Middle Ear Malformation in Mice [PDF]

open access: yes, 2014
Fibroblast growth factor 23 (FGF23) is a circulating hormone important in phosphate homeostasis. Abnormal serum levels of FGF23 result in systemic pathologies in humans and mice, including renal phosphate wasting diseases and hyperphosphatemia. We sought
Caruso, Paul   +7 more
core   +12 more sources

Tumoral Calcinosis: An Uncommon Cause for a Mass in a Reconstructed Breast [PDF]

open access: yes, 2016
This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited.
Dean, Nicola Ruth   +2 more
core   +1 more source

A novel FGF23 mutation in hyperphosphatemic familial tumoral calcinosis and its deleterious effect on protein O-glycosylation

open access: yesFrontiers in Endocrinology, 2022
Background Hyperphosphatemic familial tumoral calcinosis (HFTC) is a rare disease characterized by hyperphosphatemia and ectopic calcification, predominantly at periarticular locations.
Q. Zuo   +8 more
semanticscholar   +1 more source

Resolution of uremic tumoral calcinosis in a patient on peritoneal dialysis with long-term low-calcium dialysate treatment

open access: yesKidney Research and Clinical Practice, 2014
Tumoral calcinosis is a rare complication in uremic patients. An in-depth review of published literature suggests that most patients with uremic tumoral calcinosis do not respond to medical treatment.
Yaerim Kim, Eunah Hwang, Sungbae Park
doaj   +1 more source

Therapeutic Management of Symptomatic Calcification in a Patient With Normophosphatemic Tumoral Calcinosis

open access: yesAnnals of Internal Medicine: Clinical Cases, 2023
Tumoral calcinosis is a rare autosomal recessive disorder marked by lobulated soft tissue calcifications not associated with physiologic osteogenesis but rather phosphate metabolism dysregulation.
Derek T. Clar   +2 more
doaj   +1 more source

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