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The transcription factor AP1 which regulates expression of collagenase in response to various extracellular signals is a multimeric complex composed of members of the Jun- and Fos families. To examine the biological role of the various components in signal transduction we analyzed the expression of two of them (cJun, JunB) and collagenase in response to phorbol esters, cAMP and TGF-beta. While all three genes are induced by phorbol ester and TGF-beta only JunB is induced by cAMP. In contrast expression of cJun and collagenase is reduced by cAMP indicating that cJun and JunB are not coordinately regulated. In addition JunB is not an efficient activator of the cJun and collagenase promoters although both cJun and JunB exhibit similar DNA binding properties, indicating that the differences in biological activity is due to differences in their activation domains. Our results imply that enhanced expression of collagenase (and cJun) depends on the activation of cJun. Expression of cJun and collagenase is inhibited under certain conditions of high levels of JunB. This suggests a negative regulatory function of JunB which greatly expands the potential of the Jun protein family in changing the transcription of specific genes involved in triggering complex biological processes.

It is believed that families are important influences on the development of health habits, and the purpose of the present study was to examine the familial

The purpose of the present study was to determine the extent to which intervention process measures are useful in predicting changes in cardiovascular disease (CVD) risk factors among subjects exposed to interventions. Subjects were 99 adult and 105 children who participated in an 18 session, family-based diet and exercise change program. During the intervention, each participant self-monitonally, diet and exercise for 12 weeks. Additinally, attendance, session evaluation, confidence to achieve goals and goal achievement data were collected each week. The intervention was successful in changing diet, blood pressure and cholesterol levels, but did not produce significant changes in exercise or body mass index. Stepwise multiple regression analyses were conducted for each outcome variable at the 1 and 2 year follow-ups. Ethnicity and sex were first forced into each regression. None of the process measures consistently predicted multiple outcomes in adults and children. The pattern of results provides limited support for the hypothesis that intervention process variables such as attendance, adherence to self–monitoring, achievement of goals and attitude toward sessions partially mediate intervention effects. It is concluded that process measures should be collected in health behavior change programs so that process-outcome relation ships can be further explored.

(1995). Review of Behavioral Research for Cardiopulmonary Health: Emphasis on Youth, Gender, and Ethnicity. Journal of Health Education: Vol. 26, Cardiopulmonary Health Behavior Research: Focus on Youth, Gender, and Ethnicity, pp. S9-S17.

Inflammation is thought to underlie the pathogenesis of many chronic diseases. It is now established that obesity results in a state of chronic low-grade inflammation thought to contribute to several metabolic disorders, including insulin resistance and pancreatic islet dysfunction. The protein kinases JNK1 and IKKbeta have been found to serve as critical molecular links between obesity, metabolic inflammation, and disorders of glucose homeostasis. The precise mechanisms of these linkages are still being investigated. However, as we discuss here, JNK1 and IKKbeta are activated by almost all forms of metabolic stress that have been implicated in insulin resistance or islet dysfunction. Furthermore, both JNK1 and IKKbeta are critically involved in the promotion of diet-induced obesity, metabolic inflammation, insulin resistance, and beta-cell dysfunction. Understanding the molecular mechanisms by which JNK1 and IKKbeta mediate obesity-induced metabolic stress is likely to be of importance for the development of new treatments for a variety of obesity-associated diseases.

Utilization of a community mental health center was found to be extremely low in a “high risk” segment of its catchment area. To test the hypot

Clinical studies have shown that obstructive sleep apnea (OSA) increases atherosclerosis risk. The inflammation, especially mediated by the macrophages via nuclear factor-κB (NF-κB), has been speculated to contribute to atherogenicity in OSA patients. Inhibitor of NF-κB kinase-β (IKKβ) is an essential element of the NF-κB pathway and is linked to atherosclerosis. We previously reported that atherosclerosis was accelerated in pulmonary artery (PA) but not in aorta when low-density lipoprotein receptor knockout (<i>Ldlr^-/-</i>) mice were exposed to intermittent hypoxia/hypercapnia (IHH), a surrogate for recurrent upper-airway obstruction. Therefore, we hypothesized that IKKβ-dependent NF-κB activation in monocytes and macrophages plays a role in IHH-induced PA atherosclerosis. To test this hypothesis, myeloid restricted IKKβ deletion (<i>Ikkβ^ΔMye</i>) or control (<i>Ikkβ^F/F</i>) mice were crossed with <i>Ldlr^-/-</i> mice to generate double-knockout mice. Then, the mice were exposed to IHH or room air (Air) on high-fat diet for 8 or 16 wk. Lesions of PA and aorta were examined in <i>Ikkβ^ΔMye</i>;<i>Ldlr^-/-</i> and <i>Ikkβ^F/F</i>;<i>Ldlr^-/-</i> male mice under IHH vs. Air. The results revealed that IKKβ deletion abolished IHH-induced PA atherosclerosis after 8-wk exposure but not after 16-wk exposure (8 wk: <i>Ikkβ^F/F</i>;<i>Ldlr^-/-</i>, IHH 13.5 ± 1.4 vs. Air 5.7 ± 0.7%, <i>P</i> < 0.01; <i>Ikkβ^ΔMye</i>;<i>Ldlr^-/-</i>, IHH 7.4 ± 1.9% vs. Air 4.6 ± 1.3%, <i>P</i> = 0.24). Both IKKβ deletion and IHH had no effects on atherosclerosis in the aorta. Our findings demonstrate that IKKβ-dependent NF-κB activity in myeloid-lineage cells plays a critical role in IHH-induced PA atherosclerosis at the early stage.

MCKENZIE, T. L., J. F. SALLIS, J. J. PROCHASKA, T. L. CONWAY, S. J. MARSHALL, and P. ROSENGARD. Evaluation of a Two-Year Middle-School Physical Education Intervention: M-SPAN. Med. Sci. Sports Exerc., Vol. 36, No. 8, pp. 1382–1388, 2004. Purpose: School physical education (PE) is highly recommended as a means of promoting physical activity, and randomized studies of health-related PE interventions in middle schools have not been reported. We developed, implemented, and assessed an intervention to increase physical activity during middle-school PE classes. Methods: Twenty-four middle schools (approximately 25,000 students, 45% nonwhite) in Southern California participated in a randomized trial. Schools were assigned to intervention (N = 12) or control (N = 12) conditions, and school was the unit of analysis. A major component of the intervention was a 2-yr PE program, which consisted of curricular materials, staff development, and on-site follow-up. Control schools continued usual programs. Student activity and lesson context were observed in 1849 PE lessons using a validated instrument during baseline and intervention years 1 and 2. Results: The intervention significantly (P = 0.02) improved student moderate to vigorous physical activity (MVPA) in PE, by approximately 3 min per lesson. Effects were cumulative; by year 2 intervention schools increased MVPA by 18%. Effect sizes were greater for boys (d = 0.98; large) than girls (d = 0.68; medium). Conclusions: A standardized program increased MVPA in middle schools without requiring an increase in frequency or duration of PE lessons. Program components were well received by teachers and have the potential for generalization to other schools. Additional strategies may be needed for girls.