Niños Sanos, Familia Sana: Mexican immigrant study protocol for a multifaceted CBPR intervention to combat childhood obesity in two rural California towns.

BACKGROUND: Overweight and obese children are likely to develop serious health problems. Among children in the U.S., Latino children are affected disproportionally by the obesity epidemic. Niños Sanos, Familia Sana (Healthy Children, Healthy Family) is a five-year, multi-faceted intervention study to decrease the rate of BMI growth in Mexican origin children in California's Central Valley. This paper describes the methodology applied to develop and launch the study. METHODS/DESIGN: Investigators use a community-based participatory research approach to develop a quasi-experimental intervention consisting of four main components including nutrition, physical activity, economic and art-community engagement. Each component's definition, method of delivery, data collection and evaluation are described. Strategies to maintain engagement of the comparison community are reported as well. DISCUSSION: We present a study methodology for an obesity prevention intervention in communities with unique environmental conditions due to rural and isolated location, limited infrastructure capacity and limited resources. This combined with numerous cultural considerations and an unstable population with limited exposure to researcher expectations necessitates reassessment and adaptation of recruitment strategies, intervention delivery and data collection methods. Trial registration # NCT01900613. TRIAL REGISTRATION: NCT01900613.

Regulation of the cAMP-elevating effects of isoproterenol and forskolin in cardiac myocytes by treatments that cause increases in cAMP.

Regulation of the cAMP-elevating effects of isoproterenol and forskolin in cardiac myocytes by treatments that cause increases in cAMP. We have found that elevations in cyclic AMP (cAMP) have long-term effects on both the beta-adrenergic receptor and adenylyl cyclase in cultured chick ventricular myocytes. Pretreatment with isoproterenol for 15min markedly reduced the cAMP-elevating effect of a subsequent treatment with isoproterenol 18h later. Responses to isoproterenol were similarly reduced after overnight treatments with forskolin or phosphodiesterase inhibitors. Furthermore, these same treatments also markedly blunted the cAMP-elevating effect of forskolin, a direct activator of adenylyl cyclase. The blunting of the isoproterenol effect was greater than that of the forskolin effect, at least partially because the pretreatments caused a decrease in the number of beta-adrenergic receptors as well as a net decrease in adenylyl cyclase activity. Experiments with a recombinant adenovirus to express luciferase under the control of cAMP responsive elements (CREs) showed that the same treatments elevated cAMP sufficiently to drive the transcription of a gene with CREs in its promoter. The blunting of both the isoproterenol and forskolin responses was blocked by the inhibition of protein synthesis or by infecting cells with a recombinant adenovirus that expresses rabbit muscle cAMP-dependent protein kinase inhibitor (PKI). It is hypothesized that one or more adenylyl cyclase isozymes responsible for the generation of cAMP in the myocytes, along with other proteins previously reported to regulate beta-adrenergic receptors and perhaps adenylyl cyclase, are negatively regulated by cAMP, most likely at the level of gene expression, and that this regulation may have therapeutic consequences in the treatment of cardiac diseases.