6 results match your criteria: "University of Washington and Center for Developmental Biology[Affiliation]"

Hyaluronic acid is required for palatal shelf movement and its interaction with the tongue during palatal shelf elevation.

Dev Biol

January 2020

Division of Craniofacial Medicine, Department of Pediatrics, University of Washington and Center for Developmental Biology and Regenerative Medicine, Seattle Children's Research Institute, Seattle, WA, 98101, USA. Electronic address:

Palatal shelf elevation is an essential morphogenetic process that results from palatal shelf movement caused by an intrinsic elevating force. The nature of the elevating force remains unclear, but the accumulation of hyaluronic acid (HA) in the extracellular matrix (ECM) of the palatal shelves may play a pivotal role in developing the elevating force. In mammals, HA is synthesized by hyaluronic acid synthases (HAS) that are encoded by three genes (Has1-3).

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In Vitro Analysis of Palatal Shelf Elevation During Secondary Palate Formation.

Anat Rec (Hoboken)

September 2019

Division of Craniofacial Medicine, Department of Pediatrics, University of Washington and Center for Developmental Biology and Regenerative Medicine, Seattle Children's Research Institute, Seattle, Washington.

Palatal shelf elevation is an essential morphogenetic process during secondary palate formation. It has been proposed that shelf elevation results from an intrinsic elevating force and is regulated by extrinsic factors that are associated with development of other orofacial structures. Although dynamic palate culture is a common in vitro approach for studying shelf elevation, it requires the tongue or the tongue and mandible to be removed before culture, which prevents any determination of the role of the extrinsic factors in regulating shelf elevation.

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Geometric morphometrics reveal altered corpus callosum shape in pyridoxine-dependent epilepsy.

Neurology

July 2018

From the Division of Pediatric Neurology (G.O., S.M.G.), Departments of Neurology and Pediatrics, University of Washington, and Seattle Children's Hospital; Division of Craniofacial Medicine (A.M.M.), Department of Pediatrics, University of Washington and Center for Developmental Biology and Regenerative Medicine, Seattle Children's Research Institute; Department of Radiology (S.D.F., S.L.P., C.B.B., J.N.W.), Seattle Children's Hospital, WA; and Department of Pediatrics (L.A.B.), Máxima Medical Center, Veldhoven, the Netherlands.

Objective: To evaluate the features and maturational changes in overall callosal shape in patients with pyridoxine-dependent epilepsy (PDE).

Methods: Measurements were conducted through landmark-based geometric morphometrics applied on cerebral MRIs of patients with PDE and age-matched control subjects. The outline of the corpus callosum was manually traced in the midsagittal plane.

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Fibroblast growth factor (FGF) signaling is important for skeletal development; however, cell-specific functions, redundancy and feedback mechanisms regulating bone growth are poorly understood. FGF receptors 1 and 2 (Fgfr1 and Fgfr2) are both expressed in the osteoprogenitor lineage. Double conditional knockout mice, in which both receptors were inactivated using an osteoprogenitor-specific Cre driver, appeared normal at birth; however, these mice showed severe postnatal growth defects that include an ∼50% reduction in body weight and bone mass, and impaired longitudinal bone growth.

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Background: Palatal shelf elevation is an essential morphogenetic process during secondary palate closure and failure or delay of palatal shelf elevation is a common cause of cleft palate, one of the most common birth defects in humans. Here, we studied the role of mesenchymal fibroblast growth factor receptor (FGFR) signaling during palate development by conditional inactivation of Fgfrs using a mesenchyme-specific Dermo1-Cre driver.

Results: We showed that Fgfr1 is expressed throughout the palatal mesenchyme and Fgfr2 is expressed in the medial aspect of the posterior palatal mesenchyme overlapping with Fgfr1.

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At reproductive onset the marine green alga Acetabularia acetabulum (L.) P.C.

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