Loss of BMP2 and BMP4 Signaling in the Dental Epithelium Causes Defective Enamel Maturation and Aberrant Development of Ameloblasts.

BMP signaling is crucial for differentiation of secretory ameloblasts, the cells that secrete enamel matrix. However, whether BMP signaling is required for differentiation of maturation-stage ameloblasts (MA), which are instrumental for enamel maturation into hard tissue, is hitherto unknown. To address this, we used an in vivo genetic approach which revealed that combined deactivation of the and genes in the murine dental epithelium causes development of dysmorphic and dysfunctional MA.

Distinct and Overlapping Expression Patterns of the Homer Family of Scaffolding Proteins and Their Encoding Genes in Developing Murine Cephalic Tissues.

In mammals Homer1, Homer2 and Homer3 constitute a family of scaffolding proteins with key roles in Ca signaling and Ca transport. In rodents, Homer proteins and mRNAs have been shown to be expressed in various postnatal tissues and to be enriched in brain. However, whether the Homers are expressed in developing tissues is hitherto largely unknown.

Sonic Hedgehog Signaling Is Required for Cyp26 Expression during Embryonic Development.

Deciphering how signaling pathways interact during development is necessary for understanding the etiopathogenesis of congenital malformations and disease. In several embryonic structures, components of the Hedgehog and retinoic acid pathways, two potent players in development and disease are expressed and operate in the same or adjacent tissues and cells. Yet whether and, if so, how these pathways interact during organogenesis is, to a large extent, unclear.

Cell fate specification in the lingual epithelium is controlled by antagonistic activities of Sonic hedgehog and retinoic acid.

The interaction between signaling pathways is a central question in the study of organogenesis. Using the developing murine tongue as a model, we uncovered unknown relationships between Sonic hedgehog (SHH) and retinoic acid (RA) signaling. Genetic loss of SHH signaling leads to enhanced RA activity subsequent to loss of SHH-dependent expression of Cyp26a1 and Cyp26c1.

"Better safe than sorry"-Reasons for consulting care due to decreased fetal movements.

Background: Experience of reduced fetal movements is a common reason for consulting health care in late pregnancy. There is an association between reduced fetal movements and stillbirth.

Aim: To explore why women decide to consult health care due to reduced fetal movements at a specific point in time and investigate reasons for delaying a consultation.

To be taken seriously and receive rapid and adequate care - Womens' requests when they consult health care for reduced fetal movements.

Background: decreased fetal movement is a reason for women to seek health care in late pregnancy.

Objective: to examine what pregnant women who present with decreased fetal movements want to communicate to health care professionals and to other women in the same situation.

Design: a qualitative descriptive study.

Fetal movement in late pregnancy - a content analysis of women's experiences of how their unborn baby moved less or differently.

Background: Pregnant women sometimes worry about their unborn baby's health, often due to decreased fetal movements. The aim of this study was to examine how women, who consulted health care due to decreased fetal movements, describe how the baby had moved less or differently.

Methods: Women were recruited from all seven delivery wards in Stockholm, Sweden, during 1/1 - 31/12 2014.

Women's Experiences of Fetal Movements before the Confirmation of Fetal Death--Contractions Misinterpreted as Fetal Movement.

Background: Decreased fetal movement often precedes a stillbirth. The objective of this study was to describe women's experiences of fetal movement before the confirmation of fetal death.

Methods: Data were collected through a Web-based questionnaire.

Expression patterns and subcellular localization of carbonic anhydrases are developmentally regulated during tooth formation.

Carbonic anhydrases (CAs) play fundamental roles in several physiological events, and emerging evidence points at their involvement in an array of disorders, including cancer. The expression of CAs in the different cells of teeth is unknown, let alone their expression patterns during odontogenesis. As a first step towards understanding the role of CAs during odontogenesis, we used immunohistochemistry, histochemistry and in situ hybridization to reveal hitherto unknown dynamic distribution patterns of eight CAs in mice.

Developmental changes in cellular and extracellular structural macromolecules in the secondary palate and in the nasal cavity of the mouse.

The aim of this study was to analyse the hitherto largely unknown expression patterns of some specific cellular and extracellular molecules during palate and nasal cavity development. We showed that epithelia of the developing palate and the vomerine epithelium express similar sets of structural proteins. With the exception of keratin 15, which becomes barely detectable in the elevated palatal shelves, nearly all of these proteins become upregulated at the presumptive areas of fusion and in the adhering epithelia of the palate and nasal septum.

Expression patterns of the Tmem16 gene family during cephalic development in the mouse.

Tmem16a, Tmem16c, Tmem16f, Tmem16h and Tmem16k belong to the newly identified Tmem16 gene family encoding eight-pass transmembrane proteins. We have analyzed the expression patterns of these genes during mouse cephalic development. In the central nervous system, Tmem16a transcripts were abundant in the ventricular neuroepithelium, whereas the other Tmem16 family members were readily detectable in the subventricular zone and differentiating fields.

Abnormal hair development and apparent follicular transformation to mammary gland in the absence of hedgehog signaling.

We show that removing the Shh signal tranducer Smoothened from skin epithelium secondarily results in excess Shh levels in the mesenchyme. Moreover, the phenotypes we observe reflect decreased epithelial Shh signaling, yet increased mesenchymal Shh signaling. For example, the latter contributes to exuberant hair follicle (HF) induction, while the former depletes the resulting follicular stem cell niches.

Expression of Pit2 sodium-phosphate cotransporter during murine odontogenesis is developmentally regulated.

Different sodium-dependent inorganic phosphate (P(i)) uptake mechanisms play a major role in cellular P(i) homeostasis. The function and detailed distribution patterns of the type III Na(+)-phosphate cotransporter, PiT-2, in different organs during development are still largely unknown. We therefore examined the temporospatial expression patterns of Pit2 during murine odontogenesis.

Fate-mapping of the epithelial seam during palatal fusion rules out epithelial-mesenchymal transformation.

During palatogenesis, fusion of the palatine shelves is a crucial event, the failure of which results in the birth defect, cleft palate. The fate of the midline epithelial seam (MES), which develops transiently upon contact of the two palatine shelves, is still strongly debated. Three major mechanisms underlying the regression of the MES upon palatal fusion have been proposed: (1) apoptosis has been evidenced by morphological and molecular criteria; (2) epithelial-mesenchymal transformation has been suggested based on ultrastructural and lipophilic dye cell labeling observations; and (3) migration of MES cells toward the oral and nasal areas has been proposed following lipophilic dye cell labeling.

Shh signaling within the dental epithelium is necessary for cell proliferation, growth and polarization.

Sonic hedgehog (Shh), a member of the mammalian Hedgehog (Hh) family, plays a key role during embryogenesis and organogenesis. Tooth development, odontogenesis, is governed by sequential and reciprocal epithelial-mesenchymal interactions. Genetic removal of Shh activity from the dental epithelium, the sole source of Shh during tooth development, alters tooth growth and cytological organization within both the dental epithelium and mesenchyme of the tooth.

Effects of ECL cell extracts and granule/vesicle-enriched fractions from rat oxyntic mucosa on cAMP and IP(3) in rat osteoblast-like cells.

The existence of an osteotropic hormone (referred to as gastrocalcin) in the ECL cells of the gastric mucosa has been suggested. Both gastrin and an extract of the oxyntic mucosa lower blood Ca(2+) and stimulate Ca(2+) uptake into bone. The ECL cells are known to operate under gastrin control and, conceivably, gastrin lowers blood Ca(2+) indirectly by releasing the hypothetical ECL cell hormone.

Osteopromotion: A Soft-Tissue Exclusion Principle Using a Membrane for Bone Healing and Bone Neogenesis.

The research reviewed in this paper constitutes a series of investigations intended to develop and evaluate a new membrane technique, which provides improved conditions for osteogenesis during healing of bone defects and restitution of earlier existing bone. The technique has also been shown to aid in bone grafting as well as having the capacity to create new bone for reconstructive purposes. According to this methodology, membranes are utilized to create a space in the tissue in which osteogenesis can occur relatively unimpeded.