Communities for healthy living (CHL) - A family-centered childhood obesity prevention program integrated into Head Start services: Study protocol for a pragmatic cluster randomized trial.

Background: Childhood obesity is highly prevalent and carries substantial health consequences. Childhood obesity interventions have had mixed results, which may be partially explained by the absence of theory that incorporates broader family context and methods that address implementation challenges in low-resource settings. Communities for Healthy Living (CHL) is an obesity prevention program for Head Start preschools designed with careful focus on theory and implementation.

Autoreactive T cells induce neurotrophin production by immune and neural cells in injured rat optic nerve: implications for protective autoimmunity.

Accumulating evidence suggests that activation of the immune system in the central nervous system (CNS) after trauma protects the CNS from damage propagation and facilitates regeneration. Studies by our group have shown that passive transfer of autoimmune T cells specific to myelin basic protein (T(MBP)) can protect injured neurons in the rat CNS from secondary degeneration. In this study, we investigated the effects of T(MBP) treatment on the local immune response (by B cells and macrophages) and on the expression of neurotrophic factors after crush injury of the rat optic nerve.

Vaccination with a Nogo-A-derived peptide after incomplete spinal-cord injury promotes recovery via a T-cell-mediated neuroprotective response: comparison with other myelin antigens.

The myelin-associated protein Nogo-A has received more research attention than any other inhibitor of axonal regeneration in the injured central nervous system (CNS). Circumvention of its inhibitory effect, by using antibodies specific to Nogo-A, has been shown to promote axonal regrowth. Studies in our laboratory have demonstrated that active or passive immunization of CNS-injured rats or mice with myelin-associated peptides induces a T-cell-mediated protective autoimmune response, which promotes recovery by reducing posttraumatic degeneration.

Nerve growth factor regulates TNF-alpha production in mouse macrophages via MAP kinase activation.

In this study, we examined the expression of nerve growth factor (NGF) and its receptors in mouse macrophages and the mechanisms involved in the effect of NGF on tumor necrosis factor (TNF)-alpha production. Macrophages expressed NGF and the NGF receptors TrkA and p75. Treatment of J744 cells or peritoneal macrophages with NGF induced a large increase in the production of TNF-alpha.

Self-Protective mechanism awakened by glutamate in retinal ganglion cells.

The progression of degeneration in chronic optic neuropathies or in animal models of optic nerve injury is thought to be caused, at least in part, by an increase in glutamate to abnormally high concentrations. We show here that glutamate, when injected in subtoxic amounts into the vitreal body of the rat eye, transduces a self-protecting signal that renders the retinal ganglion cells resistant to further toxicity, whether glutamate-derived or not. This neuroprotective effect is attained within 24 h and lasts at least 4 days.