Education about crying in normal infants is associated with a reduction in pediatric emergency room visits for crying complaints.

Objective: The primary aim of this study was to determine whether there was any change in visits of 0- to 5-month old infants to the medical emergency room (MER) of a metropolitan pediatric hospital after province-wide implementation of a public health prevention program that teaches new parents about the properties of early crying in normal infants.

Methods: Free-text descriptions of Presenting Complaint and Final Diagnosis on electronic MER clinic visit files were used to classify infants as cases of infant crying not due to disease. Annual crying case visits as a percent of MER visits were analyzed pre- and post-introduction of the prevention program.

Perspectives of expectant women and health care providers on birth plans.

Objective: A birth plan is a document detailing a woman's preferences and expectations related to labour and delivery. Empirical research exploring the value of birth plans has shown conflicting findings about whether birth plans have a positive or negative effect on labour and delivery, suggesting a need for further study. This study aimed to understand the perspectives of women, health care providers, and support persons regarding the use of birth plans.

Expression of Wnt5a in tooth germs and the related signal transduction analysis.

Objective: Wnt5a is generally considered a non-canonical Wnt family member and plays an important role in the development of several tissues through regulation of cell fate, proliferation, migration, polarity and death. This study investigates its expression mode in human tooth development and the involved cell signal transduction pathways, as they remain unclear.

Design: The expression of Wnt5a was analyzed by immunohistochemistry method.

A large X-chromosomal deletion is associated with microphthalmia with linear skin defects (MLS) and amelogenesis imperfecta (XAI).

A female patient is described with clinical symptoms of both microphthalmia with linear skin defects (MLS or MIDAS) and dental enamel defects, having an appearance compatible with X-linked amelogenesis imperfecta (XAI). Genomic DNA was purified from the patient's blood and semiquantitative multiplex PCR revealed a deletion encompassing the amelogenin gene (AMELX). Because MLS is also localized to Xp22, genomic DNA was subjected to array comparative genomic hybridization, and a large heterozygous deletion was identified.

The leucine-rich amelogenin peptide alters the amelogenin null enamel phenotype.

Introduction: The amelogenin proteins secreted by ameloblasts during dental enamel development are required for normal enamel structure. Amelx null (KO) mice have hypoplastic, disorganized enamel similar to that of human patients with mutations in the AMELX gene, and provide a model system for studies of the enamel defect amelogenesis imperfecta. Because many amelogenin proteins are present in developing enamel due to RNA alternative splicing and proteolytic processing, understanding the function of individual amelogenins has been challenging.

Partial rescue of the amelogenin null dental enamel phenotype.

The amelogenins are the most abundant secreted proteins in developing dental enamel. Enamel from amelogenin (Amelx) null mice is hypoplastic and disorganized, similar to that observed in X-linked forms of the human enamel defect amelogenesis imperfecta resulting from amelogenin gene mutations. Both transgenic strains that express the most abundant amelogenin (TgM180) have relatively normal enamel, but strains of mice that express a mutated amelogenin (TgP70T), which leads to amelogenesis imperfecta in humans, have heterogeneous enamel structures.

Comparison of body weight and gene expression in amelogenin null and wild-type mice.

Amelogenin (AmelX) null mice develop hypomineralized enamel lacking normal prism structure, but are healthy and fertile. Because these mice are smaller than wild-type mice prior to weaning, we undertook a detailed analysis of the weight of mice and analyzed AmelX expression in non-dental tissues. Wild-type mice had a greater average weight each day within the 3-wk period.

Effects of sodium fluoride on the actin cytoskeleton of murine ameloblasts.

Fluoride is associated with a decrease in the incidence of dental caries, but excess fluoride can lead to enamel fluorosis, a defect that occurs during tooth enamel formation. In fibroblasts, the Arhgap gene encodes a RhoGAP, which regulates the small G protein designated RhoA. Fluoride treatment of fibroblasts inactivates RhoGAP, thereby activating RhoA, which leads to elevation of filamentous actin (F-actin).