A communications tool to recruit policymakers to a CBPR partnership for childhood obesity prevention.

The purpose of this paper is to describe a process and technical requirements for the development of a video and related communications strategy that CBPR partnerships can use to recruit policymakers to participatory research. Policymakers play a critical role in social change agendas, yet are often difficult to engage for a variety of reasons, including limited availability and multiple, competing demands and constituencies. This paper draws on the experience of the Healthy Jacksonville Childhood Obesity Prevention Coalition, a 10-year-old partnership with a large membership and strong community roots in Duval County, Florida.

Changes in circulating satiety hormones in obese children: a randomized controlled physical activity-based intervention study.

The aims of this study are to examine in children: (i) obesity-related alterations in satiety factors such as leptin, ghrelin, and obestatin; (ii) the link between satiety factors and cardiometabolic risk factors; and (iii) the impact of a physical activity-based lifestyle intervention on the levels of these satiety factors in the obese. We studied a total of 21 adolescents (BMI percentile, 99.0 +/- 0.

Association analyses of adrenergic receptor polymorphisms with obesity and metabolic alterations.

Genes involved in the regulation of catecholamine function may be important in obesity because of the role catecholamines play in energy expenditure and lipolysis. To determine if common single nucleotide polymorphisms (SNPs) in beta(1)-adrenergic receptor (ADRB1), beta(2)-adrenergic receptor (ADRB2), beta(3)-adrenergic receptor (ADRB3), and alpha(2)-adrenergic receptor (ADRA2A) genes associate with obesity and metabolic alterations, we recruited 74 healthy African American and 161 white men and women (age, 18-49 years) to participate in this case-control genetic association study. Genotypes were determined by polymerase chain reaction and restriction fragment length polymorphism.

Physician-diagnosed asthma and acute chest syndrome: associations with NOS polymorphisms.

The main objectives of this paper were to test the hypothesis that polymorphisms in NOS1 and NOS3 genes associate with ACS in SCD patients and to characterize the association between physician-diagnosed asthma and acute chest syndrome (ACS). Case-control study of sickle cell disease patients >or=5 years old with ACS (cases; n=86) and those without ACS (controls; n=48) was carried out. Associations between ACS and the AAT repeat in intron 13 (formerly intron 20) of the NOS1, and with NOS3 T-786C polymorphism were explored.

The C523A beta2 adrenergic receptor polymorphism associates with markers of asthma severity in African Americans.

Our goal was to explore associations between ss2 adrenergic receptor polymorphisms and markers of asthma severity in African American and Caucasian patients with asthma. Polymorphisms at loci -1023, -654, -47, 46, 79, 491, and 523 were genotyped and haplotypes were imputed in 143 African Americans and 336 Caucasians. C523A genotype associated with percentage of African Americans (but not of Caucasians) having an asthma exacerbation: AA, AC, and CC genotypes were 17, 29, and 40%, respectively (p = 0.

Influence of sex and beta2 adrenergic receptor haplotype on resting and terbutaline-stimulated whole body lipolysis.

beta 2 adrenergic receptors ( beta 2 ARs) are important mediators of lipolysis. The beta 2 AR gene is highly polymorphic. To determine the contribution of beta 2 AR polymorphisms to variability in whole body lipolysis, we compared basal and terbutaline-stimulated lipolytic rates (Ra) using tracer techniques in 14 healthy, non-obese males (n=7) and females (n=7) who were homozygous for Cys-19/Arg16/Gln27 or Arg-19/Gly16/Glu27 haplotypes.

Modeling the metabolic effects of terbutaline in beta2-adrenergic receptor diplotypes.

Objective: Our objective was to determine whether beta(2)-adrenergic receptor polymorphisms influence terbutaline-stimulated changes in glucose, insulin, and potassium concentrations in healthy adults.

Methods: Seven healthy adults homozygous for the Arg-19/Gly16/Glu27 haplotype (RGE) and seven homozygous for the Cys-19/Arg16/Gln27 haplotype (CRQ) volunteered to receive a 1-hour infusion of terbutaline (0.01 mg/kg).

Growth factor regulation of human growth plate chondrocyte proliferation in vitro.

Linear growth occurs as the result of growth plate chondrocytes undergoing proliferative and hypertrophic phases. Paracrine feedback loops that regulate the entry of chondrocytes into the hypertrophic phase have been shown and similar pathways likely exist for the proliferative phase. Human long-bone growth plate chondrocytes were cultured in vitro.

Mitochondrial ribosomal proteins: candidate genes for mitochondrial disease.

Most of the energy requirement for cell growth, differentiation, and development is met by the mitochondria in the form of ATP produced by the process of oxidative phosphorylation. Human mitochondrial DNA encodes a total of 13 proteins, all of which are essential for oxidative phosphorylation. The mRNAs for these proteins are translated on mitochondrial ribosomes.

Effect of montelukast on time-course of exhaled nitric oxide in asthma: influence of LTC4 synthase A(-444)C polymorphism.

Leukotrienes (LT) mediate inflammation in asthma. The fraction of exhaled nitric oxide (FE(NO)) is thought to be a sensitive and reproducible method for assessing airway inflammation in asthmatics and the anti-inflammatory effects of drugs. A number of factors are known to contribute to intrapatient variation in FE(NO) which can confound interpretation.

Using real-time, quantitative PCR for rapid genotyping of the steroid 21-hydroxylase gene in a north Florida population.

The most common cause of congenital adrenal hyperplasia is steroid 21-hydroxylase deficiency. The molecular genetics of this disease are such that genotyping is a potentially useful tool in its diagnosis. An assay was developed using real-time, quantitative PCR to detect deletions of the steroid 21-hydroxylase gene (CYP21A2).