Quantitative Measurement of the Improvement Derived From a 10-Mo Progressive Exercise Program to Improve Balance and Function in Women at Increased Risk for Fragility Fractures.

Introduction/background: Osteoporosis is a common disorder and is associated with an increased risk of bone fracture. Falls are a proximate cause of a high proportion of medical costs and mortality. Improving balance can reduce the risk of falls and improve health outcomes, especially for the at-risk population of people with osteoporosis and osteopenia.

Accelerating efforts to prevent childhood obesity: spreading, scaling, and sustaining healthy eating and physical activity.

During the past decade, progress has been made in addressing childhood obesity through policy and practice changes that encourage increased physical activity and access to healthy food. With the implementation of these strategies, an understanding of what works to prevent childhood obesity is beginning to emerge. The task now is to consider how best to spread, scale, and sustain promising childhood obesity prevention strategies.

The role of SHIP in the development and activation of mouse mucosal and connective tissue mast cells.

Although SHIP is a well-established suppressor of IgE plus Ag-induced degranulation and cytokine production in bone marrow-derived mast cells (BMMCs), little is known about its role in connective tissue (CTMCs) or mucosal (MMCs) mast cells. In this study, we compared SHIP's role in the development as well as the IgE plus Ag and TLR-induced activation of CTMCs, MMCs, and BMMCs and found that SHIP delays the maturation of all three mast cell subsets and, surprisingly, that it is a positive regulator of IgE-induced BMMC survival. We also found that SHIP represses IgE plus Ag-induced degranulation of all three mast cell subsets and that TLR agonists do not trigger their degranulation, whether SHIP is present or not, nor do they enhance IgE plus Ag-induced degranulation.

Tyrosine phosphorylation of SHIP promotes its proteasomal degradation.

Objective: The activity of the SH2-containing-phosphatidylinositol-5'-phosphatase (SHIP, also known as SHIP1), a critical hematopoietic-restricted negative regulator of the PI3 kinase (PI3K) pathway, is regulated in large part via its protein levels. We sought to determine the mechanism(s) involved in its downregulation by BCR-ABL and by interleukin (IL)-4.

Materials And Methods: We used Ba/F3(p210-tetOFF) cells to study the downregulation of SHIP by BCR-ABL and bone marrow-derived macrophages to study SHIP's downregulation by IL-4.