Correlates of e-cigarette use among active duty US military personnel: implications for cessation policy.

BACKGROUND: Electronic cigarette (or e-cigarette) use has grown substantially since its US market introduction in 2007. Although marketed as a safer alternative to traditional cigarettes, studies have shown they can also be a gateway to their use. The purpose of this investigation is to identify factors associated with different patterns of tobacco use among active duty military personnel. METHODS: A secondary analysis was conducted using the 2014 Defense Health Agency Health Related Behaviors survey data. Results are based on 45 986 US military respondents, weighted to 1 251 606. Both univariate and regression analyses were conducted to identify correlates. RESULTS: In 2014, approximately 7.8% of respondents reported using e-cigarettes at least once in the past year. Among e-cigarette users, 49% reported exclusive e-cigarette use. Prevalence of exclusive use is highest among white people (58%), Navy (33%), men (83%) and persons with income ≤$45 000 (65%). Regression comparing exclusive cigarette with exclusive e-cigarette users revealed higher odds of being Air Force (OR=2.19; CI 1.18 to 4.06) or Navy (OR=2.25; CI 1.14 to 4.41) personnel and being male (OR=1.72; CI 1.12 to 2.64), and more likely to not receive smoking cessation messaging from healthcare providers in the last 12 months (OR=2.88; CI 1.80 to 4.62). When comparing exclusive e-cigarette users with poly-tobacco users, e-cigarette users had higher odds of being Hispanic (OR=2.20; CI 1.02 to 4.78), college educated (OR=4.25; CI 1.22 to 14.84) and not receiving tobacco prevention/cessation messaging (OR=4.80; CI 2.79 to 8.27). CONCLUSION: The results demonstrate that exclusive e-cigarette users in the military have unique characteristics when compared with groups of other/mixed tobacco users. Findings can inform cessation and prevention efforts to improve both the overall health and combat readiness of active duty military personnel.

Efficacy and safety of mirikizumab (LY3074828) in the treatment of moderate-to-severe plaque psoriasis: results from a randomized phase II study.

BACKGROUND: Inhibiting interleukin (IL)-23 in patients with psoriasis has demonstrated high levels of skin clearance. OBJECTIVES: To investigate, in a phase II (AMAF; NCT02899988), multicentre, double-blind trial, the efficacy and safety of three doses of mirikizumab (LY3074828), a p19-directed IL-23 antibody, vs. placebo in patients with moderate-to-severe plaque psoriasis. METHODS: Adult patients were randomized 1 : 1 : 1 : 1 to receive placebo (n = 52), mirikizumab 30 mg (n = 51), mirikizumab 100 mg (n = 51) or mirikizumab 300 mg (n = 51) subcutaneously at weeks 0 and 8. The primary objective was to evaluate the superiority of mirikizumab over placebo in achieving a 90% improvement in the Psoriasis Area and Severity Index (PASI 90) response at week 16. Comparisons were done using logistic regression analysis with treatment, geographical region and previous biological therapy in the model. Missing data were imputed as nonresponses. RESULTS: Ninety-seven per cent of patients completed the first 16 weeks of the study. The primary end point was met for all mirikizumab dose groups vs. placebo, with PASI 90 response rates at week 16 of 0%, 29% (P = 0·009), 59% (P < 0·001) and 67% (P < 0·001) for patients receiving placebo, and mirikizumab 30 mg, 100 mg and 300 mg, respectively. There were two (1%) serious adverse events in mirikizumab-treated patients vs. one (2%) in a placebo-group patient. CONCLUSIONS: At week 16, 67% of patients treated with mirikizumab 300 mg at 8-week intervals achieved PASI 90. The percentage of patients reporting at least one treatment-emergent adverse event was similar among patients treated with placebo or mirikizumab.

Leukocyte Hsp72 mRNA transcription does not differ between males and females during heat acclimation.

Purpose: Thermotolerance is an acquired state of increased cytoprotection achieved following single or repeated exposures to heat stress, in part characterized by changes in the intracellular 72 kda heat shock protein (HSP72; HSPA1A). Females have demonstrated reduced exercise induced HSP72 in comparison to males. This study examined sex differences in heat shock protein 72 messenger ribonucleic acid (Hsp72 mRNA) transcription during heat acclimation (HA) to identify whether sex differences were a result of differential gene transcription. Methods: Ten participants (5M, 5F) performed 10, 90 min controlled hyperthermia [rectal temperature (Tre) ≥ 38.5°C] HA sessions over 12 d. Leukocyte Hsp72 mRNA was measured pre and post D1, D5, and D10, via Reverse transcription polymerase chain reaction (RT-QPCR). Results: HA was evidenced by a reduction in resting Tre (-0.4 ± 0.5°C) and resting heart rate [(HR); -13 ± 7 beats.min-1] following HA (p ≤ 0.05). During HA no difference (p > 0.05) was observed in ΔTre between males (D1 = 1.5 ± 0.2°C; D5 = 1.6 ± 0.4°C; D10 = 1.8 ± 0.3°C) and females (D1 = 1.5 ± 0.5°C; D5 = 1.4 ± 0.2°C; D10 = 1.8 ± 0.3°C). This was also true of mean Tre demonstrating equality of thermal stimuli for mRNA transcription and HA. There were no differences (p > 0.05) in Hsp72 mRNA expression between HA sessions or between males (D1 = +1.8 ± 1.5-fold; D5 = +2.0 ± 1.0 fold; D10 = +1.1 ± 0.4-fold) and females (D1 = +2.6 ± 1.8-fold; D5 = +1.8 ± 1.4-fold; D10 = +0.9 ± 1.9-fold). Conclusions: This experiment demonstrates that there is no difference in Hsp72 mRNA increases during HA between sexes when controlled hyperthermia HA is utilised. Gender specific differences in exercise-induced HSP72 reported elsewhere likely result from post-transcriptional events.

Isothermic and fixed-intensity heat acclimation methods elicit equal increases in Hsp72 mRNA.

Thermotolerance, to which heat shock protein-72 (Hsp72) contributes, is an acquired state achieved following heat acclimation (HA), eliciting cellular adaption and protection against thermal stress. Optimal HA methods achieving the greatest heat shock response (HSR) are equivocal; therefore, investigation of methods provoking the greatest sustained HSR is required to optimize cellular adaptation. Twenty-four males performed short-term HA (STHA; five sessions) and long-term HA (LTHA; STHA plus further five sessions) utilizing fixed-intensity (FIXED; workload = 50% V ˙ O 2 p e a k ), continuous isothermic HA [ISOCONT ; target rectal temperature (Trec ) = 38.5 °C], or progressive isothermic HA (ISOPROG ; target Trec = 38.5 °C for STHA then target Trec = 39.0 °C for LTHA). Leukocyte Hsp72 mRNA was measured pre- and post day 1, day 5, and day 10 of HA via reverse transcription quantitative polymerase chain reaction to determine the HSR. Hsp72 mRNA increased (P < 0.05) pre- to post day 1, pre- to post day 5, and pre to post day 10 in FIXED, ISOCONT , and ISOPROG , but no differences were observed between methods (P > 0.05). The equal Hsp72 mRNA increases occurring from consistent, reduced, or increased endogenous strain following STHA and LTHA suggest that transcription occurs following attainment of sufficient endogenous criteria. These data give confidence that all reported HA methods increase Hsp72 mRNA and are capable of eliciting adaptations toward thermotolerance.

Surveillance for severe community-associated methicillin-resistant Staphylococcus aureus infection.

Community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) has rapidly emerged in the USA as a cause of severe infections in previously healthy persons without traditional risk factors. We describe the epidemiology of severe CA-MRSA disease in the state of Georgia, USA and analyse the risk of death associated with three different clinical syndromes of CA-MRSA disease - pneumonia, invasive disease, and skin and soft-tissue infections (SSTIs). A total of 1670 cases of severe CA-MRSA disease were reported during 2005-2007. The case-fatality rate was 3.4%; sex and race of fatal and non-fatal cases did not differ significantly. While CA-MRSA pneumonia and invasive disease were less common than SSTIs, they were about 15 times more likely to result in death [risk ratio 16.69, 95% confidence interval (CI) 10.28-27.07 and 13.98, 95% CI 7.74-25.27, respectively]. When controlling for age and the presence of other clinical syndromes the odds of death in patients manifesting specific severe CA-MRSA syndromes was highest in those with pneumonia (odds ratio 11.34). Possible risk factors for severe CA-MRSA SSTI and pneumonia included the draining of lesions without medical assistance and an antecedent influenza-like illness.

Immersed membrane bioreactor (IMBR) for treatment of combined domestic and dairy wastewater in an isolated farm.

In many regions dairy farms and milk processing industries discharge large quantities of their wastes to the surroundings posing serious environmental risks. This problem is mostly faced in small dairy farms and isolated communities lacking both central collection and conventional wastewater treatment systems. Dairy wastewater is characterized by high concentrations of organic matter, solids, nutrients, as well as fractions of dissolved inorganic pollutants, exceeding those levels considered typical for high strength domestic wastewaters. With the purpose of treating the combined dairy and domestic wastewater from a small dairy farm in the Negev Desert of Israel, the use of a recent emerging technology of Immersed Membrane BioReactor (IMBR) was evaluated over the course of 500 test hours, under a variety of wastewater feed quality conditions (during the test periods, the feed BOD5 ranged from 315 ppm up to 4,170 ppm). The overall performance of a pilot-scale Ultrafiltration (UF) IMBR process for a combined domestic and dairy wastewater was analyzed based on the Data Envelopment Analysis (DEA) method. The IMBR performance in terms of membrane performance (permeate flux, transmembrane pressure, and organic removal) and DEA model (Technical Efficiency) was acceptable. DEA is an empirically based methodology and the research approach has been found to be effective in the depiction and analysis for complex systems, where a large number of mutual interacting variables are involved.

Reduced perivascular PO2 increases nitric oxide release from endothelial cells.

Many studies have suggested that endothelial cells can act as "oxygen sensors" to large reductions in oxygen availability by increasing nitric oxide (NO) production. This study determined whether small reductions in oxygen availability enhanced NO production from in vivo intestinal arterioles, venules, and parenchymal cells. In vivo measurements of perivascular NO concentration ([NO]) were made with NO-sensitive microelectrodes during normoxic and reduced oxygen availability. During normoxia, intestinal first-order arteriolar [NO] was 397 +/- 26 nM (n = 5), paired venular [NO] was 298 +/- 34 nM (n = 5), and parenchymal cell [NO] was 138 +/- 36 nM (n = 3). During reduced oxygen availability, arteriolar and venular [NO] significantly increased to 695 +/- 79 nM (n = 5) and 534 +/- 66 nM (n = 5), respectively, whereas parenchymal [NO] remained unchanged at 144 +/- 34 nM (n = 4). During reduced oxygenation, arteriolar and venular diameters increased by 15 +/- 3% and 14 +/- 5%, respectively: NG-nitro-L-arginine methyl ester strongly suppressed the dilation to lower periarteriolar Po2. Micropipette injection of a CO2 embolus into arterioles significantly attenuated arteriolar dilation and suppressed NO release in response to reduced oxygen availability. These results indicated that in rat intestine, reduced oxygen availability increased both arteriolar and venular NO and that the main site of NO release under these conditions was from endothelial cells.

Histological and neurotrophic changes triggered by varying models of bladder inflammation.

PURPOSE: We determined whether bladder inflammation causes elevated expression of nerve growth factor by bladder parenchymal cells, leading to alterations in neurons innervating the bladder. To answer this question biochemical, histological and neuronal size data were obtained in rats following various experimental models of bladder inflammation. MATERIALS AND METHODS: Chemical (2.5% formalin), immune (lipopolysaccharide 2 x 104 cfu/ml.) and mechanical (chromic catgut) inflammation was evaluated at various times and compared to control bladders. Hematoxylin and eosin, and Giemsa staining was done to characterize inflammation and quantify mast cells in the bladder. Nerve growth factor protein and messenger RNA were assayed in the bladder and major pelvic ganglion using 2-site enzyme-linked immunosorbent assay and reverse transcriptase-polymerase chain reaction, respectively. Retrograde axonal tracing was done to size bladder neurons in the major pelvic and dorsal root ganglia. RESULTS: All forms of inflammation increased bladder weight and produced diffuse hyperplasia, intramural edema, acute and chronic inflammatory cells, infiltration and mastocytosis. Generally bladder inflammation resulted in a 50% increase in nerve growth factor and 52% to 58% enlargement of peripheral neurons. CONCLUSIONS: Inflammation results in altered nerve growth factor content of the bladder, and morphological changes in sensory and motor neurons innervating the bladder. Such neuroplasticity may be a possible explanation for the association of bladder inflammation with long-term symptoms and pain after inflammation subsides.

Shear level influences resistance artery remodeling: wall dimensions, cell density, and eNOS expression.

The magnitude of shear stimulus has been shown to determine the level of growth factor expression in cell culture. However, little is known regarding what effect shear level has on specific arterial wall remodeling events in vivo. We have hypothesized that the rate of luminal diameter change and specific remodeling events within the arterial wall layers are dependent on shear level. Selective ligations were made to alter the number of microvascular perfusion units of mesenteric arteries within the same animal to approximately 50%, 200%, and 400% of control. Arterial blood flow and wall shear rate were correlated with the degree of alteration in perfusion units. Luminal diameters were decreased in 50% arteries by day 2 and increased approximately 17% and 33% respectively, in 200% and 400% arteries at day 7. The rate of diameter change was greatest in 50% and 400% arteries. Wall areas (medial +37%; intimal +18% at day 2) and cell densities (intimal +26%; adventitial +44% at day 2) were altered only in the 400% arteries. A positive correlation existed by day 2 between endothelial staining for endothelial nitric oxide synthase and shear level. The results demonstrate that shear level influences the rate of luminal expansion, specific remodeling events within each wall layer, and the degree of endothelial gene expression. A greater understanding of how shear level influences specific remodeling events within each wall layer should aid in the development of targeted therapies to manipulate the remodeling process in health and disease.

Nitric oxide release during alpha1-adrenoceptor-mediated constriction of arterioles.

We examined endothelial modulation of norepinephrine (NE)-mediated constriction in isolated, cannulated, first-order arterioles from skeletal muscle of rats. Acute arteriolar constrictor responses to NE (10(-9) to 10(-7) M) were significantly (P < 0.05) enhanced after either endothelial denudation or inhibition of nitric oxide synthase with NG-monomethyl-L-arginine (10(-4) M, 30 min). In contrast, arteriolar constrictions to NE were not different after treatment with either the cyclooxygenase inhibitor diclofenac (10(-6) M, 30 min) or the K+-channel blocker tetrabutylammonium (5 x 10(-5) M, 30 min). We also measured arteriolar responses to the vasoconstrictor PGF2alpha; responses were not altered by any of the experimental treatments, which indicates that this phenomenon is not ubiquitous to all vasoconstricting agents. Mechanistically, we examined vascular smooth muscle (VSM) and endothelial cell calcium. Both NE and PGF2alpha significantly increased VSM cell calcium measurements; however, endothelial cell calcium was significantly increased with NE or phenylephrine (an alpha1-adrenergic agonist) but not with PGF2alpha or UK-14304 (an alpha2-adrenergic agonist). Together these findings suggest that in rat cremaster first-order arterioles, NE stimulates an increase in VSM calcium via adrenergic receptors with subsequent increase in endothelial cell calcium, possibly via stimulation of alpha1-adrenergic receptors on the arteriolar endothelium. The burst in endothelial cell calcium may then lead to the production of nitric oxide, which diffuses to the VSM, attenuates constriction, and maintains at least some minimal level of blood flow.

Chronic reduction in complex I function alters calcium signaling in SH-SY5Y neuroblastoma cells.

Sporadic, non-familial Parkinson's disease is characterized by a 15-30% reduction in complex I activity of the electron transport chain. A pharmacological model of reduced complex I activity was created by prolonged treatment of SH-SY5Y cells with low doses (5-20 nM) of rotenone, a selective inhibitor of complex I. Short-term (less than 2 week) exposure to rotenone did not influence calcium signaling, production of reactive oxygen species, or mitochondrial morphology. However, following 2 weeks of rotenone exposure, SH-SY5Y cells showed unusual calcium dynamics, specifically multiple calcium responses to carbachol, a muscarinic agonist. These secondary calcium responses were not seen in control SH-SY5Y cells and were dependent upon calcium influx. Mitochondrial membrane potential was also reduced in low dose rotenone-treated cells. These results demonstrate that a chronic, partial reduction in complex I activity, such as that seen in Parkinson's disease, can alter cell signaling events and perhaps increase the susceptibility of cells to calcium overload and subsequent cell death.

Activation of the transcription factors nuclear factor-kappaB and activator protein-1 in bladder smooth muscle exposed to outlet obstruction and mechanical stretching.

PURPOSE: Transcriptional control of bladder genes in response to outlet obstruction, growth factors and mechanical force is poorly understood. We analyzed the effects of bladder obstruction, mechanical stretching and platelet derived growth factor on the activation of the major growth controlling transcription factors nuclear factor-kappaB and activator protein-1. MATERIALS AND METHODS: Complete outlet obstruction was created in female rats by proximal urethral ligation and bladders were harvested 3, 6 and 24 hours later, respectively. Bladder cells were grown in culture and stimulated with 10 ng./ml. platelet derived growth factor or 10 cycles per minute of mechanical stretching for 0.5 to 4 hours. Nuclear proteins were high salt extracted and incubated with 32phosphorus double strand oligonucleotides containing a consensus binding sequence for activator protein-1 or nuclear factor-kappaB. The resulting DNA protein complexes were analyzed by electrophoretic mobility shift assay. RESULTS: Nuclear extract isolated from obstructed bladders showed intense activator protein-1 binding activity 3, 6 and 24 hours after obstruction as well as increased nuclear factor-kappaB binding activity after 6 and 24 hours. Binding activity was absent or minimal in sham operated rats. Cultured cells exposed to mechanical stretching for 2 and 4 hours showed increased activator protein-1 and nuclear factor-kappaB DNA binding compared with unstretched cells. Likewise stimulation with platelet derived growth factor caused a consistent increase in activator protein-1 and nuclear factor-kappaB binding activity. The binding of nuclear proteins was abolished by a 40-fold excess of an unlabeled specific oligonucleotide but not by excess irrelevant oligonucleotide. Thus, the assays were specific for the factors involved. CONCLUSIONS: Bladder obstruction and mechanical stretching cause the formation of activator protein-1 and nuclear factor-kappaB DNA complexes, consistent with a role of these transcription factors in the control of hypertrophy associated gene activation.

In vivo and in vitro investigation of the effects of sildenafil on rat cavernous smooth muscle.

PURPOSE: We investigated the effect of sildenafil on rat erectile tissues in vivo and in vitro. MATERIALS AND METHODS: Intracavernous pressure was recorded in pentobarbital anesthetized, male Sprague-Dawley rats and we studied the effect of 100 or 200 microg/kg(-1) sildenafil given intravenously. In an isolated endothelin-1 contracted strip preparation of rat corpus cavernosum we also assessed the effect of sildenafil on the response to electrical field stimulation of the nerves. RESULTS: Electrical stimulation of the cavernous nerve induced a frequency dependent increase in intracavernous pressure of a mean plus or minus standard error of mean 55 +/- 3 mm Hg at 20 Hz, corresponding to a mean of 47% +/- 2% of mean arterial pressure. The 100 microg/kg(-1) dose did not increase intracavernous pressure but significantly increased mean decay time of the pressure response from 16 +/- 3 to 35 +/- 3 seconds (p <0.001). In vitro sildenafil significantly enhanced the amplitude and duration of the relaxation induced by the electrical stimulation of corpus cavernosum strips in a concentration dependent fashion. CONCLUSIONS: In anesthestized rats sildenafil significantly prolonged the decay period of the intracavernous pressure response induced by electrical stimulation of the cavernous nerve but it did not increase the amplitude. Sildenafil enhanced the amplitude and duration of the relaxant response to electrical field stimulation in isolated corpus cavernosum tissue.

Treatment of aged rat sensory neurons in short-term, serum-free culture with nerve growth factor reverses the effect of aging on neurite outgrowth, calcium currents, and neuronal survival.

Impaired NGF production and release has been documented in aged animals, suggesting that decreased NGF receptor stimulation may be one factor contributing to neuronal dysfunction with aging. Other studies have suggested that aging may be associated with impaired intracellular responses to NGF. Because aging-associated neuronal dysfunction contributes to morbidity and mortality in the geriatric population, it is important to determine whether the effects of aging on sensory neuron function and survival are reversible. In the present study, we observed significantly decreased neurite outgrowth and neuronal survival in short-term cultures (0-96 h) of dorsal root ganglion (DRG) neurons from aged (>22 months) Fisher 344 x Brown Norway F1 hybrid rats, compared to young (4-6 month) and middle-aged (14 month) animals. From 24 to 96 h in culture, diminished survival of aged neurons appeared to be due to an increased rate of apoptotic cell death. DRG neurons from aged animals also exhibited significantly decreased whole cell, high-threshold voltage-dependent calcium currents, with a larger proportion of L-type current, compared to youthful and middle-aged animals. Treatment of aged DRG neurons with NGF restored neurite outgrowth, neuronal survival and calcium current amplitude and subtype distribution to those observed in youthful DRG neurons.

Altered neural control of micturition in the aged F344 rat.

The purpose of this study was to determine whether micturition reflexes are altered in aged rats. Voiding frequencies and awake cystometrograms (CMGs) were measured in young (3-5 months old) and aged (24 months) F344 male rats. Bladder contractions induced by subcutaneous apomorphine and intravesical capsaicin stimulation were measured using awake CMGs. Urodynamic parameters were compared. Aged rats voided less frequently (4.1 vs 6.9 times/18 h, P = 0.006), with a higher volume per void (1.1 vs 0.7 ml, P = 0.02) and had a higher micturitional threshold pressure (8.7 vs 4.6 mmHg, P = 0.0001) than the young rats. Apomorphine induced a higher frequency of bladder contractions in aged animals compared to young animals (5.5 vs 3.1 contractions/min, P = 0.03). Intravesical capsaicin caused a lower pressure bladder response in the aged rats (38.5 vs 70.6 mmHg, P = 0.01) compared to the young rats. Bladder afferents and central micturition pathways may be altered in aged rats. Impaired bladder contractility in the elderly may be exacerbated by reduced sensory input, whereas the propensity for detrusor instability could result from altered central processing. This study demonstrated the utility of the F344 animal model to study micturitional changes resulting from aging.

Stretch-activated signaling of nerve growth factor secretion in bladder and vascular smooth muscle cells from hypertensive and hyperactive rats.

Elevated vascular (VSMC) and bladder smooth muscle (BSMC) NGF are associated with altered visceral innervation in the spontaneously hypertensive rat (SHR: hypertensive, behaviorally hyperactive) compared with control Wistar-Kyotos (WKYs). Stretch stimulates increased NGF production in BSMCs. To elucidate whether stretch induces NGF synthesis in VSMCs, and to determine if disturbances in stretch-mediated NGF production contribute to the elevated tissue levels of NGF in SHRs, we subjected VSMCs and BSMCs cultured from four established inbred rat strains (WKY, WKHA: hyperactive; SHR and WKHT: hypertensive) to several stretch paradigms. For VSMCs, acute and cyclic stretch affected cells derived from hypertensive rats (80-100% increase over control) but not from normotensive strains. For BSMCs, cyclic and static stretch increased NGF secretion in all four strains, but had a two- to threefold greater effect in cells from SHRs and WKHTs (increase up to 600%) at early time points. At later time points of a 24-h experimental period, stretch increased NGF output up to 400% in SHR and WKHA cultures. Thus, defects that influence early induction of stretch-mediated SHR NGF secretion cosegregate with the hypertensive phenotype. Stretch-gated ion channel inhibitors, voltage-gated ion channel inhibitors, and protease inhibitors failed to affect stretch-induced BSMC NGF secretion. In contrast, gene transcription, intracellular calcium, protein kinase C (PKC), and autocrine release of an unknown factor may play a role in the elevated NGF secretion observed in smooth muscle from hypertensive animals. Altered stretch-induced smooth muscle NGF secretion may contribute to the augmented vascular and bladder NGF content associated with high blood pressure and hyperactive voiding in SHRs.

Teen Club: a nursing intervention for reducing risk-taking behavior and improving well-being in female African American adolescents.

This article describes a nursing intervention called Teen Club that was designed to reduce risk-taking behavior and improve well-being in female African American adolescents. Participants were referred to Teen Club by their nurse practitioners, physicians, and a community health nurse who were working at an urban neighborhood health center's teen clinic. Referrals were based on factors such as parental substance abuse, lack of social and family support, and other characteristics thought to increase vulnerability to risk-taking behavior. The 2-year intervention included weekly group meetings co-led by a European American female community health nurse and a Latino American male community worker, supplemented by case management and home visits by both these persons. Findings from a retrospective group interview conducted with 11 of the 12 original participants are presented. This is the first step in a series of pilot studies designed to refine the Teen Club intervention in anticipation of a future prospective, randomized investigation of this health promotion and disease prevention model of nursing care.