Effects of the histamine H1 antagonist chlorcyclizine on rat fetal palate development

2010 ◽  
Vol 89 (6) ◽  
pp. 474-484 ◽  
Author(s):  
Brian P. Enright ◽  
Yi-Zhong Gu ◽  
Ronald D. Snyder ◽  
Ravi R. Dugyala ◽  
Leslie A. Obert ◽  
...  
Keyword(s):  
Palate Development ◽  
H1 Antagonist

The histamine H1-antagonist chlorpheniramine facilitates learning in aged rats

1997 ◽  
Vol 229 (2) ◽  
pp. 89-92 ◽  
Author(s):  
Christian Frisch ◽  
Rüdiger U. Hasenöhrl ◽  
Joseph P. Huston
Keyword(s):  
Aged Rats ◽  
H1 Antagonist

Mesenchymal Smad4 mediated signaling is essential for palate development

2010 ◽  
Vol 36 (6) ◽  
pp. 460 ◽  
Author(s):  
Chi-Young Yoon ◽  
Jin-A Baek ◽  
Eui-Sic Cho ◽  
Seung-O Ko
Keyword(s):  
Palate Development

Palate development: Mechanisms and malformations

1987 ◽  
Vol 156 (11) ◽  
pp. 309-315 ◽  
Author(s):  
M. W. J. Ferguson
Keyword(s):  
Palate Development

Morphological and molecular changes associated with Pitchfork during mouse palate development

2014 ◽  
Vol 358 (2) ◽  
pp. 385-393 ◽  
Author(s):  
Chengri Jin ◽  
Jong-Min Lee ◽  
Qinghuang Tang ◽  
Liwen Li ◽  
Min-Jung Lee ◽  
...  
Keyword(s):  
Molecular Changes ◽  
Palate Development

scholarly journals Onset of the acquired potentiality for fusion in the palatal shelves of rats

Development ◽  
1966 ◽  
Vol 16 (1) ◽  
pp. 171-182
Author(s):  
M. Pourtois
Keyword(s):  
Oral Cavity ◽  
Cleft Palate ◽  
Horizontal Plane ◽  
Horizontal Position ◽  
Palate Development

This paper is concerned with that phase of palate development in rats leading to fusion of the shelves in the midline. Previous experimentation in palate development in mammals has encompassed both the earlier phase of assumption of the horizontal position of the palatal shelves, and the subsequent approximation and fusion of the shelves. Since the two processes do not occur simultaneously and can theoretically be studied separately, it was possible and feasible to confine the experiment to the later fusion phase. The present research was designed to eliminate the possible confounding effects of palate rotation in vitro on the fusion of the shelves by approximation of the explanted palatal shelves in the same horizontal plane, irrespective of their original positions in the oral cavity. Current theories of cleft palate pathogenesis hold that either the palatal shelves fail to assume (rotate to) the horizontal position, or, that having done so, they fail to fuse.

Palate Development: In Vitro Procedures

2003 ◽  
pp. 267-274
Author(s):  
M. Michele Pisano ◽  
Robert M. Greene
Keyword(s):  
Palate Development ◽  
Development In Vitro

A Novel Pathogenic Variant in the MN1 Gene in a Patient Presenting with Rhombencephalosynapsis and Craniofacial Anomalies, Expanding MN1 C-terminal Truncation Syndrome

2021 ◽  
Author(s):  
Carmen Palma ◽  
Pérez Mohand Patricia ◽  
José M. Lezana ◽  
Jaime Cruz ◽  
Juan F. Quesada ◽  
...  
Keyword(s):  
De Novo ◽  
Pathogenic Variant ◽  
Craniofacial Anomalies ◽  
Osteoblast Proliferation ◽  
Terminal Portion ◽  
Transcription Activator ◽  
Palate Development ◽  
Partial Rhombencephalosynapsis ◽  
And Function ◽  
Craniofacial Defects

AbstractMeningioma-1 is a transcription activator that regulates mammalian palate development and is required for appropriate osteoblast proliferation, motility, differentiation, and function. Microdeletions involving the MN1 gene have been linked to syndromes including craniofacial anomalies, such as Toriello–Carey syndrome. Recently, truncating variants in the C-terminal portion of the MN1 transcriptional factor have been linked to a characteristic and distinct phenotype presenting with craniofacial anomalies and partial rhombencephalosynapsis, a rare brain malformation characterized by midline fusion of the cerebellar hemispheres with partial or complete loss of the cerebellar vermis. It has been called MN1 C-terminal truncation (MCTT) syndrome or CEBALID (Craniofacial defects, dysmorphic Ears, Brain Abnormalities, Language delay, and Intellectual Disability) and suggested to be caused by dominantly acting truncated protein MN1 instead of haploinsufficiency. As a proto-oncogene, MN1 is also involved in familial meningioma. In this study, we present a novel case of MCTT syndrome in a female patient presenting with craniofacial anomalies and rhombencephalosynapsis, harboring a de novo pathogenic variant in the MN1 gene: c.3686_3698del, p.(Met1229Argfs*87).

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