Pneumovirus in Dogs with Acute Respiratory Disease

To determine which respiratory viruses circulate among confined dogs, we analyzed nasal and pharyngeal swab specimens from shelter dogs with acute respiratory disease. An unknown virus was isolated. Monoclonal antibody testing indicated that it was probably a pneumovirus. PCR and sequence analysis indicated that it was closely related to murine pneumovirus

The role of amelogenin during enamel-crystallite growth and organization in vivo: Amelogenin and enamel-crystallite formation

Amelogenin is critical for enamel formation and human AMELX gene mutations cause hypoplastic and/or hypomaturation enamel phenotypes. The Amelx null (AKO) mouse has a severe hypoplastic phenotype. This study evaluated the effect of amelogenin loss on enamel formation and crystallite morphology. Enamel from AKO and wild type (WT) mice was used. AKO mice were mated with transgenic mice expressing the most abundant known amelogenin isoform TgM180-87 to rescue (KOM180-87) the enamel crystallite phenotype. Molar enamel was embedded, sectioned with a diamond microtome and photographed using transmission electron microscopy. Crystallite sizes from multiple sections were measured using Image J. Crystallite mean thicknesses were (WT = 26 nm, AKO = 16 nm, KOm180-87 = 25 nm) and the mean widths were (WT = 96 nm, AKO = 59 nm, KOm180-87 = 85 nm). Despite a complete loss of amelogenin in AKO mice, a mineralized enamel layer with well-defined and organized crystallites forms. Enamel crystallites forming in the absence of amelogenin were reduced in thickness and width. For the first time we show that introduction of the m180 amelogenin isoform into the AKO mouse through crossbreeding rescues the crystallite phenotype. We conclude that amelogenin is essential for the development of normal crystallite size

Communication, Decision Making, and Cancer: What African Americans Want Physicians to Know

To explore and identify communication and decision making with health care providers for African Americans living with cancer and for their families

Rescue of the murine amelogenin null phenotype with two amelogenin transgenes

The amelogenin proteins are required for normal enamel development; the most abundant amelogenins expressed from alternatively spliced mRNAs are M180 and leucine rich amelogenin protein (LRAP). The Amelx null (KO) mouse has an enamel defect similar to human X-linked amelogenesis imperfecta. The disorganized enamel layer in KO mice is 10–20% the thickness of wild-type (WT) enamel and lacks prismatic structures. When the KO mice were mated with mice that express TgM180-87, partial rescue of the phenotype was observed such that enamel thickness, volume and density increased. A second transgene was introduced by mating the TgM180KO mice with TgLRAP mice, and male offspring were characterized for genotype and tooth phenotype was evaluated by SEM. TgM180LRAPKO molar enamel thickness further increased, and the structure was improved, with a more defined decussation pattern compared to singly rescued mice. We conclude that TgM180 provides significant rescue of the KO phenotype. Although the effectiveness of TgLRAP to rescue by itself is less obvious, the addition of TgLRAP to TgM180 in KO enamel leads to added improvement in both amount and structure and thus these transgenes function in a complementary manner. Together the two most abundant amelogenins lead to formation of obvious enamel decussation patterns

Mouse Genetic Background Influences the Dental Phenotype

Dental enamel covers the crown of the vertebrate tooth and is considered to be the hardest tissue in the body. Enamel develops during secretion of an extracellular matrix by ameloblast cells in the tooth germ, prior to eruption of the tooth into the oral cavity. Secreted enamel proteins direct mineralization patterns during the maturation stage of amelogenesis as the tooth prepares to erupt. The amelogenins are the most abundant enamel proteins, and are required for normal enamel development. Phenotypic differences were observed between incisors from individual Amelx (Amelogenin) null mice that had a mixed 129xC57BL/6J genetic background, and between inbred wld-type (WT) mice with different genetic backgrounds (C57BL/6J, C3H/HEJ, FVB/NJ). We hypothesized this could be due to modifier genes, as human patients with a mutation in an enamel protein gene causing the enamel defect amelogenesis imperfecta (AI) also can have varied appearance of dentitions within a kindred. Enamel density measurements varied for all WT inbred strains midway during incisor development. Enamel thickness varied between some WT strains and, unexpectedly, dentin density varied extensively between incisors and molars of all WT and Amelx null strains studied. WT FVB/NJ incisors were more similar to Amelx null than to the other WT strains in incisor height/weight ratio and pattern of enamel mineralization. Strain-specific differences led to the conclusion that modifier genes may be implicated in determining both normal development and severity of enamel appearance in AI mouse models and may in future studies be related to phenotypic heterogeneity within human AI kindreds reported in the literature

The Leucine-Rich Amelogenin Peptide Alters the Amelogenin Null Enamel Phenotype

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

The \u27Healthy Parks-Healthy People\u27 Movement in Canada: Progress, Challenges, and an Emerging Knowledge and Action Agenda

In this article, we outline progress and challenges in establishing effective health promotion tied to visitor experiences provided by protected and conserved areas in Canada. Despite an expanding global evidence base, case studies focused on aspects of health and well-being within Canada’s protected and conserved areas remain limited. Data pertaining to motivations, barriers and experiences of visitors are often not collected by governing agencies and, if collected, are not made generally available or reported on. There is an obvious, large gap in research and action focused on the needs and rights of groups facing systemic barriers related to a variety of issues including, but not limited to, access, nature experiences, and needs with respect to health and well-being outcomes. Activation of programmes at the site level continue to grow, and Park Prescription programmes, as well as changes to the Accessible Canada Act, represent significant, positive examples of recent cross-sector policy integration. Evaluations of outcomes associated with HPHP programmes have not yet occurred but will be important to adapting interventions and informing cross-sector capacity building. We conclude by providing an overview of gaps in evidence and practice that, if addressed, can lead to more effective human health promotion vis-à-vis nature contact in protected and conserved areas in Canada

Parent-of-origin-specific allelic associations among 106 genomic loci for age at menarche.

Age at menarche is a marker of timing of puberty in females. It varies widely between individuals, is a heritable trait and is associated with risks for obesity, type 2 diabetes, cardiovascular disease, breast cancer and all-cause mortality. Studies of rare human disorders of puberty and animal models point to a complex hypothalamic-pituitary-hormonal regulation, but the mechanisms that determine pubertal timing and underlie its links to disease risk remain unclear. Here, using genome-wide and custom-genotyping arrays in up to 182,416 women of European descent from 57 studies, we found robust evidence (P < 5 × 10(-8)) for 123 signals at 106 genomic loci associated with age at menarche. Many loci were associated with other pubertal traits in both sexes, and there was substantial overlap with genes implicated in body mass index and various diseases, including rare disorders of puberty. Menarche signals were enriched in imprinted regions, with three loci (DLK1-WDR25, MKRN3-MAGEL2 and KCNK9) demonstrating parent-of-origin-specific associations concordant with known parental expression patterns. Pathway analyses implicated nuclear hormone receptors, particularly retinoic acid and γ-aminobutyric acid-B2 receptor signalling, among novel mechanisms that regulate pubertal timing in humans. Our findings suggest a genetic architecture involving at least hundreds of common variants in the coordinated timing of the pubertal transition