craniosynostoses/protease

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Multisuture Craniosynostosis and Papilledema in Pycnodysostosis: A Paradox?

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Pycnodysostosis (PYCD) is a rare autosomal-recessive skeletal disorder that typically presents with osteosclerosis of the majority of the postcranial skeleton and osteolysis of the calvarium, manifesting as persistent open cranial fontanelles and widely spaced cranial sutures. Craniosynsostosis in

Craniosynostosis in pycnodysostosis: broadening the spectrum of the cranial flat bone abnormalities.

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Pycnodysostosis is a rare autosomal recessive skeletal dysplasia caused by the absence of active cathepsin K, which is a lysosomal cysteine protease that plays a role in degrading the organic matrix of bones, acting in bone resorption and bone remodeling. The disease is primarily characterized by

Spondyloepimetaphyseal Dysplasia With Elevated Plasma Lysosomal Enzymes Caused by Homozygous Variant in MBTPS1

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Variants in MBTPS1 (membrane-bound transcription factor peptidase, site 1) encoding the protein convertase site-1 protease (S1P) were recently reported in a single individual with skeletal dysplasia and elevated plasma lysosomal enzymes. Here, we report the second individual with this newly

[Prophylactic use of tranexamic acid in noncardiac surgery : Update 2017].

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BACKGROUND Minimising perioperative bleeding is a key goal of "patient blood management" programs. One component of respective strategies includes preventive inhibition of fibrinolysis using protease inhibitors, such as tranexamic acid (TXA). TXA inhibits plasminogen activation and plasmin-induced

P253R fibroblast growth factor receptor-2 mutation induces RUNX2 transcript variants and calvarial osteoblast differentiation.

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Unregulated fibroblast growth factor 2 (FGF2) signaling caused by mutations in the fibroblast growth factor receptor (FGFR2) leads to human craniosynostosis such as the Apert syndrome. In an in vitro control model of calvarial osteoblasts from Apert patients carrying the FGFR2 P253R mutation, we

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