Translational Potential of High-Resistance Inspiratory Muscle Strength Training.

Age-associated cardiovascular (CV) dysfunction increases the risk for CV diseases. Aerobic exercise training can improve CV function, but only a minority of adults meet aerobic exercise guidelines. High-resistance inspiratory muscle strength training is a time-efficient lifestyle intervention that may promote adherence and improve CV function. However, further investigation is needed to translate inspiratory muscle strength training into the public health domain.

Novel BAG3 Variants in African American Patients With Cardiomyopathy: Reduced ß-Adrenergic Responsiveness in Excitation-Contraction.

BACKGROUND: We reported 3 novel nonsynonymous single nucleotide variants of Bcl2-associated athanogene 3 (BAG3) in African Americans with heart failure (HF) that are associated with a 2-fold increase in cardiac events (HF hospitalization, heart transplantation, or death). METHODS AND RESULTS: We expressed BAG3 variants (P63A, P380S, and A479V) via adenovirus-mediated gene transfer in adult left ventricular myocytes isolated from either wild-type (WT) or cardiac-specific BAG3 haploinsufficient (cBAG3+/-) mice: the latter to simulate the clinical situation in which BAG3 variants are only found on 1 allele. Compared with WT myocytes, cBAG3+/- myocytes expressed approximately 50% of endogenous BAG3 levels and exhibited decreased [Ca2+]i and contraction amplitudes after isoproterenol owing to decreased L-type Ca2+ current. BAG3 repletion with WT BAG3 but not P380S, A479V, or P63A/P380S variants restored contraction amplitudes in cBAG3+/- myocytes to those measured in WT myocytes, suggesting excitation-contraction abnormalities partly account for HF in patients harboring these mutants. Because P63A is near the WW domain (residues 21-55) and A479V is in the BAG domain (residues 420-499), we expressed BAG3 deletion mutants (Δ1-61 and Δ421-575) in WT myocytes and demonstrated that the BAG but not the WW domain was involved in enhancement of excitation-contraction by isoproterenol. CONCLUSIONS: The BAG3 variants contribute to HF in African American patients partly by decreasing myocyte excitation-contraction under stress, and that both the BAG and PXXP domains are involved in mediating ß-adrenergic responsiveness in myocytes.

Developing educational modules to enhance care of aged and dying inmates: Set-up phase.

The purpose of this article is to explain the strategies used in the "Set-up" phase of developing computer-based education on the care and management of incarcerated people who are older and/or dying. Public health nurses have an opportunity to support efforts in educating corrections staff to enhance health care for older and dying inmates. Such endeavors can promote social justice through inmates receiving evidence-based care that parallels that received by the community at large. "Set-up" is the first of four phases in the Institute for Healthcare Improvement's Framework for Going to Full Scale. Our design approach was threefold and included an environmental scan, a modified Delphi survey, and a usability study. An expert advisory board was consulted throughout the Set-up Phase. Participants for the Delphi Survey had expertise in geriatrics and corrections health care. Usability testing was conducted at two State Correctional Institutions. The Delphi Survey consisted of three Qualtrics surveys. Usability testing examined navigability; detected problems; observed time spent solving problems; identified problem severity; and developed recovery strategies. The Set-up established proof of concept, three prototype modules, and a specifications document to guide future programming. In addition, a Technology Niche Analyses® provided a preliminary commercialization plan (NIH, 2017). The Set-up phase has been instrumental in exposing the available infrastructure for dissemination of an educational product within corrections and may be a first step in addressing public health concerns on issues in aging. Commercial feasibility of the program and the need for continued research for Developing the Scalable Unit were established.

Haplo-insufficiency of Bcl2-associated athanogene 3 in mice results in progressive left ventricular dysfunction, ß-adrenergic insensitivity, and increased apoptosis.

Bcl2-associated athanogene 3 (BAG3) is a 575 amino acid protein that is found predominantly in the heart, skeletal muscle, and many cancers. Deletions and truncations in BAG3 that result in haplo-insufficiency have been associated with the development of dilated cardiomyopathy. To study the cellular and molecular events attributable to BAG3 haplo-insufficiency we generated a mouse in which one allele of BAG3 was flanked by loxP recombination sites (BAG3fl/+ ). Mice were crossed with α-MHC-Cre mice in order to generate mice with cardiac-specific haplo-insufficiency (cBAG3+/-) and underwent bi-weekly echocardiography to assess their cardiac phenotype. By 10 weeks of age, cBAG3+/- mice demonstrated increased heart size and diminished left ventricular ejection fraction when compared with non-transgenic littermates (Cre-/- BAG3fl/+ ). Contractility in adult myocytes isolated from cBAG3+/- mice were similar to those isolated from control mice at baseline, but showed a significantly decreased response to adrenergic stimulation. Intracellular calcium ([Ca2+ ]i ) transient amplitudes in myocytes isolated from cBAG3+/- mice were also similar to myocytes isolated from control mice at baseline but were significantly lower than myocytes from control mice in their response to isoproterenol. BAG3 haplo-insufficiency was also associated with decreased autophagy flux and increased apoptosis. Taken together, these results suggest that mice in which BAG3 has been deleted from a single allele provide a model that mirrors the biology seen in patients with heart failure and BAG3 haplo-insufficiency.

BAG3 regulates contractility and Ca(2+) homeostasis in adult mouse ventricular myocytes.

Bcl2-associated athanogene 3 (BAG3) is a 575 amino acid anti-apoptotic protein that is constitutively expressed in the heart. BAG3 mutations, including mutations leading to loss of protein, are associated with familial cardiomyopathy. Furthermore, BAG3 levels have been found to be reduced in end-stage non-familial failing myocardium. In contrast to neonatal myocytes in which BAG3 is found in the cytoplasm and involved in protein quality control and apoptosis, in adult mouse left ventricular (LV) myocytes BAG3 co-localized with Na(+)-K(+)-ATPase and L-type Ca(2+) channels in the sarcolemma and t-tubules. BAG3 co-immunoprecipitated with ß1-adrenergic receptor, L-type Ca(2+) channels and phospholemman. To simulate decreased BAG3 protein levels observed in human heart failure, we targeted BAG3 by shRNA (shBAG3) in adult LV myocytes. Reducing BAG3 by 55% resulted in reduced contraction and [Ca(2+)]i transient amplitudes in LV myocytes stimulated with isoproterenol. L-type Ca(2+) current (ICa) and sarcoplasmic reticulum (SR) Ca(2+) content but not Na(+)/Ca(2+) exchange current (INaCa) or SR Ca(2+) uptake were reduced in isoproterenol-treated shBAG3 myocytes. Forskolin or dibutyryl cAMP restored ICa amplitude in shBAG3 myocytes to that observed in WT myocytes, consistent with BAG3 having effects upstream and at the level of the receptor. Resting membrane potential and action potential amplitude were unaffected but APD50 and APD90 were prolonged in shBAG3 myocytes. Protein levels of Ca(2+) entry molecules and other important excitation-contraction proteins were unchanged in myocytes with lower BAG3. Our findings that BAG3 is localized at the sarcolemma and t-tubules while modulating myocyte contraction and action potential duration through specific interaction with the ß1-adrenergic receptor and L-type Ca(2+) channel provide novel insight into the role of BAG3 in cardiomyopathies and increased arrhythmia risks in heart failure.

Vasopressin type 1A receptor deletion enhances cardiac contractility, ß-adrenergic receptor sensitivity and acute cardiac injury-induced dysfunction.

Vasopressin type 1A receptor (V1AR) expression is elevated in chronic human heart failure (HF) and contributes to cardiac dysfunction in animal models, in part via reduced ß-adrenergic receptor (ßAR) responsiveness. Although cardiac V1AR overexpression and V1AR stimulation are each sufficient to decrease ßAR activity, it is unknown whether V1AR inhibition conversely augments ßAR responsiveness. Further, although V1AR has been shown to contribute to chronic progression of HF, its impact on cardiac function following acute ischaemic injury has not been reported. Using V1AR knockout (V1AR KO) mice we assessed the impact of V1AR deletion on cardiac contractility at baseline and following ischaemic injury, ßAR sensitivity and cardiomyocyte responsiveness to ßAR stimulation. Strikingly, baseline cardiac contractility was enhanced in V1AR KO mice and they experienced a greater loss in contractile function than control mice following acute ischaemic injury, although the absolute levels of cardiac dysfunction and survival rates did not differ. Enhanced cardiac contractility in V1AR KO mice was associated with augmented ß-blocker sensitivity, suggesting increased basal ßAR activity, and indeed levels of left ventricular cAMP, as well as phospholamban (PLB) and cardiac troponin I (cTnI) phosphorylation were elevated compared with control mice. At the cellular level, myocytes isolated from V1AR KO mice demonstrated increased responsiveness to ßAR stimulation consistent with the finding that acute pharmacological V1AR inhibition enhanced ßAR-mediated contractility in control myocytes. Therefore, although V1AR deletion does not protect the heart from the rapid development of cardiac dysfunction following acute ischaemic injury, its effects on ßAR activity suggest that acute V1AR inhibition could be utilized to promote myocyte contractile performance.

ß-adrenergic receptor-mediated cardiac contractility is inhibited via vasopressin type 1A-receptor-dependent signaling.

BACKGROUND: Enhanced arginine vasopressin levels are associated with increased mortality during end-stage human heart failure, and cardiac arginine vasopressin type 1A receptor (V1AR) expression becomes increased. Additionally, mice with cardiac-restricted V1AR overexpression develop cardiomyopathy and decreased ß-adrenergic receptor (ßAR) responsiveness. This led us to hypothesize that V1AR signaling regulates ßAR responsiveness and in doing so contributes to development of heart failure. METHODS AND RESULTS: Transaortic constriction resulted in decreased cardiac function and ßAR density and increased cardiac V1AR expression, effects reversed by a V1AR-selective antagonist. Molecularly, V1AR stimulation led to decreased ßAR ligand affinity, as well as ßAR-induced Ca(2+) mobilization and cAMP generation in isolated adult cardiomyocytes, effects recapitulated via ex vivo Langendorff analysis. V1AR-mediated regulation of ßAR responsiveness was demonstrated to occur in a previously unrecognized Gq protein-independent/G protein receptor kinase-dependent manner. CONCLUSIONS: This newly discovered relationship between cardiac V1AR and ßAR may be informative for the treatment of patients with acute decompensated heart failure and elevated arginine vasopressin.

BAG3: a new player in the heart failure paradigm.

BAG3 is a cellular protein that is expressed predominantly in skeletal and cardiac muscle but can also be found in the brain and in the peripheral nervous system. BAG3 functions in the cell include: serving as a co-chaperone with members of the heat-shock protein family of proteins to facilitate the removal of misfolded and degraded proteins, inhibiting apoptosis by interacting with Bcl2 and maintaining the structural integrity of the Z-disk in muscle by binding with CapZ. The importance of BAG3 in the homeostasis of myocytes and its role in the development of heart failure was evidenced by the finding that single allelic mutations in BAG3 were associated with familial dilated cardiomyopathy. Furthermore, significant decreases in the level of BAG3 have been found in end-stage failing human heart and in animal models of heart failure including mice with heart failure secondary to trans-aortic banding and in pigs after myocardial infarction. Thus, it becomes relevant to understand the cellular biology and molecular regulation of BAG3 expression in order to design new therapies for the treatment of patients with both hereditary and non-hereditary forms of dilated cardiomyopathy.

Decreased levels of BAG3 in a family with a rare variant and in idiopathic dilated cardiomyopathy.

The most common cause of dilated cardiomyopathy and heart failure (HF) is ischemic heart disease; however, in a third of all patients the cause remains undefined and patients are diagnosed as having idiopathic dilated cardiomyopathy (IDC). Recent studies suggest that many patients with IDC have a family history of HF and rare genetic variants in over 35 genes have been shown to be causative of disease. We employed whole-exome sequencing to identify the causative variant in a large family with autosomal dominant transmission of dilated cardiomyopathy. Sequencing and subsequent informatics revealed a novel 10-nucleotide deletion in the BCL2-associated athanogene 3 (BAG3) gene (Ch10:del 121436332_12143641: del. 1266_1275 [NM 004281]) that segregated with all affected individuals. The deletion predicted a shift in the reading frame with the resultant deletion of 135 amino acids from the C-terminal end of the protein. Consistent with genetic variants in genes encoding other sarcomeric proteins there was a considerable amount of genetic heterogeneity in the affected family members. Interestingly, we also found that the levels of BAG3 protein were significantly reduced in the hearts from unrelated patients with end-stage HF undergoing cardiac transplantation when compared with non-failing controls. Diminished levels of BAG3 protein may be associated with both familial and non-familial forms of dilated cardiomyopathy.

Psychosocial predictors of weight regain in the weight loss maintenance trial.

This study's purpose was to identify psychosocial predictors of weight loss maintenance in a multi-site clinical trial, following a group-based weight loss program. Participants (N = 1025) were predominately women (63%) and 38% were Black (mean age = 55.6 years; SD = 8.7). At 12 months, higher SF-36 mental health composite scores were associated with less weight regain (p < .01). For Black participants, an interaction existed between race and friends' encouragement for exercise, where higher exercise encouragement was related to more weight regain (p < .05). At 30 months, friends' encouragement for healthy eating was associated with more weight regain (p < .05), whereas higher SF-36 mental health composite scores were related to less weight regain (p < .0001). Perceived stress and select health-related quality of life indices were associated with weight regain; this relationship varied across gender, race, and treatment conditions. Temporal changes in these variables should be investigated for their impact on weight maintenance.

Resistance of Akt kinases to dephosphorylation through ATP-dependent conformational plasticity.

Phosphorylation of a threonine residue (T308 in Akt1) in the activation loop of Akt kinases is a prerequisite for deregulated Akt activity frequently observed in neoplasia. Akt phosphorylation in vivo is balanced by the opposite activities of kinases and phosphatases. Here we describe that targeting Akt kinase to the cell membrane markedly reduced sensitivity of phosphorylated Akt to dephosphorylation by protein phosphatase 2A. This effect was amplified by occupancy of the ATP binding pocket by either ATP or ATP-competitive inhibitors. Mutational analysis revealed that R273 in Akt1 and the corresponding R274 in Akt2 are essential for shielding T308 in the activation loop against dephosphorylation. Thus, occupancy of the nucleotide binding pocket of Akt kinases enables intramolecular interactions that restrict phosphatase access and sustain Akt phosphorylation. This mechanism provides an explanation for the "paradoxical" Akt hyperphosphorylation induced by ATP-competitive inhibitor, A-443654. The lack of phosphatase resistance further contributes insight into the mechanism by which the human Akt2 R274H missense mutation may cause autosomal-dominant diabetes mellitus.

Arginine vasopressin enhances cell survival via a G protein-coupled receptor kinase 2/ß-arrestin1/extracellular-regulated kinase 1/2-dependent pathway in H9c2 cells.

Circulating levels of arginine vasopressin (AVP) are elevated during hypovolemia and during cardiac stress. AVP activates arginine vasopressin type 1A (V(1A))/Gα(q)-coupled receptors in the heart and vasculature and V(2)/Gα(s)-coupled receptors in the kidney. However, little is known regarding the signaling pathways that influence the effects of V(1A) receptor (V(1A)R) activation during cellular injury. Using hypoxia-reoxygenation (H/R) as a cell injury model, we evaluated cell survival and caspase 3/7 activity in H9c2 myoblasts after treatment with AVP. Pretreatment of H9c2 cells with AVP significantly reduced H/R-induced cell death and caspase 3/7 activity, effects that were blocked via both selective V(1A)R inhibition and mitogen-activated protein kinase (MEK1/2) inhibition. AVP increased extracellular-regulated kinase 1/2 (ERK1/2) phosphorylation in a concentration-dependent manner that was sensitive to MEK1/2 inhibition and V(1A)R inhibition, but not V(1B)R or V(2)R inhibition. Discrete elements of the V(1A)/Gα(q)-protein kinase C (PKC) and V(1A)/G protein-coupled receptor kinase (GRK)/ß-arrestin signaling cascades were inhibited to dissect the pathways responsible for the protective effects of V(1A)R signaling: Gα(q) (overexpression of Gq-I-ires-green fluorescent protein), PKC (administration of Ro 31-82425; 2-[8-(aminomethyl)-6,7,8,9-tetrahydropyrido[1,2-a]indol-3-yl]-3-(1-methyl-1H-indol-3-yl)maleimide, HCl, bisindolylmaleimide X, HCl), GRK2 [C-terminal GRK2 peptide overexpression and small interfering RNA (siRNA) knockdown], GRK5 (siRNA knockdown), and ß-arrestin1 (siRNA knockdown). These studies demonstrated that both Gα(q)/PKC- and GRK2/ß-arrestin1-dependent V(1A)R signaling were capable of inducing ERK1/2 phosphorylation in response to AVP stimulation. However, AVP-mediated protection against H/R was elicited only via GRK2- and ß-arrestin1-dependent signaling. These results suggest that activation of the V(1A)R in H9c2 cells mediates protective signaling via a GRK2/ß-arrestin1/ERK1/2-dependent mechanism that leads to decreased caspase 3/7 activity and enhanced survival under conditions of ischemic stress.

Weight loss history as a predictor of weight loss: results from Phase I of the weight loss maintenance trial.

Past studies have suggested that weight loss history is associated with subsequent weight loss. However, questions remain whether method and amount of weight lost in previous attempts impacts current weight loss efforts. This study utilized data from the Weight Loss Maintenance Trial to examine the association between weight loss history and weight loss outcomes in a diverse sample of high-risk individuals. Multivariate regression analysis was conducted to determine which specific aspects of weight loss history predict change in weight during a 6-month weight loss intervention. Greater weight loss was predicted by fewer previous weight loss attempts with assistance (p = 0.03), absence of previous dietary/herbal weight loss supplement use (p = 0.01), and greater maximum weight loss in previous attempts (p < 0.001). Future interventions may benefit from assessment of weight loss history and tailoring of interventions based on past weight loss behaviors and outcomes.

Cancer survival through lifestyle change (CASTLE): a pilot study of weight loss.

BACKGROUND: Excess weight is a strong predictor of incident breast cancer (BC) and survivorship. A limited number of studies comparing strategies for promoting successful weight loss in women with remitted BC exist. PURPOSE: CASTLE was a pilot study comparing the effectiveness/feasibility of in-person and telephonic behavioral-based lifestyle weight loss interventions in BC survivors. METHOD: Fifty-two overweight/obese women (BMI = 25-45 kg/m(2)) with remitted BC (stages I-IIIa) who recently completed cancer treatment were assigned to either an in-person group (n = 24) or an individual telephone-based condition (n = 11). Both interventions focused on increasing physical activity and reducing caloric intake. The phase I intervention lasted 6 months. The in-person condition received 16 group-based sessions, and the telephone condition received intervention calls approximately weekly. Phase II lasted 6 months (e.g., months 6-12), and all participants received monthly intervention calls via telephone. RESULTS: Participants were predominately Caucasian (80 %) with a mean age of 52.8 (8.0) years and BMI of 31.9 (5.4) kg/m(2). Mixed models ANOVAs showed significant within group weight loss after 6 months for both the in-person (-3.3 kg ± 4.4, p = 0.002) and the telephonic (-4.0 kg ± 6.0, p = 0.01) conditions with no between group differences. During phase II, the in-person group demonstrated significant weight regain (1.3 kg ± 1.7, p = 0.009). CONCLUSION: Our pilot study findings demonstrated that telephone-based behavioral weight loss programs are effective and feasible in BC survivors and that telephonic programs may have advantages in promoting weight loss maintenance.

Bag3 Regulates Mitochondrial Function and the Inflammasome Through Canonical and Noncanonical Pathways in the Heart.

B-cell lymphoma 2-associated athanogene-3 (Bag3) is expressed in all animal species, with Bag3 levels being most prominent in the heart, the skeletal muscle, the central nervous system, and in many cancers. Preclinical studies of Bag3 biology have focused on animals that have developed compromised cardiac function; however, the present studies were performed to identify the pathways perturbed in the heart even before the occurrence of clinical signs of dilatation and failure of the heart. These studies show that hearts carrying variants that knockout one allele of BAG3 have significant alterations in multiple cellular pathways including apoptosis, autophagy, mitochondrial homeostasis, and the inflammasome.

Controlled and cardiac-restricted overexpression of the arginine vasopressin V1A receptor causes reversible left ventricular dysfunction through Gαq-mediated cell signaling.

BACKGROUND: [Arg8]-vasopressin (AVP) activates 3 G-protein-coupled receptors: V1A, V2, and V1B. The AVP-V1A receptor is the primary AVP receptor in the heart; however, its role in cardiac homeostasis is controversial. To better understand AVP-mediated signaling in the heart, we created a transgenic mouse with controlled overexpression of the V1A receptor. METHODS AND RESULTS: The V1A receptor transgene was placed under the control of the tetracycline-regulated, cardiac-specific α-myosin heavy chain promoter (V1A-TG). V1A-TG mice had a normal cardiac function phenotype at 10 weeks of age; however, by 24 weeks of age, tetracycline-transactivating factor/V1A-TG mouse hearts had reduced cardiac function, cardiac hypertrophy, and dilatation of the ventricular cavity. Contractile dysfunction was also observed in isolated adult cardiac myocytes. When V1A receptor transgene was induced to be expressed in adult mice (V1A-TG(Ind)), left ventricular dysfunction and dilatation were also seen, albeit at a later time point. Because the V1A receptor mediates cell signaling through Gα(q) protein, we blocked Gα(q) signaling by crossing tetracycline-transactivating factor/V1A mice with transgenic mice that expressed a small inhibitory peptide against Gα(q). Gα(q) blockade abrogated the development of the heart failure phenotype in tetracycline-transactivating factor/V1A-TG mice. The heart failure phenotype could be reversed by administration of doxycycline. CONCLUSIONS: Our results demonstrate a role for V1A-mediated signaling in the development of heart failure and support a role for V1A blockade in the treatment of patients with elevated levels of vasopressin.

Actual medical and pharmacy costs for bariatric surgery: 6-year follow-up.

OBJECTIVE: To determine the change in total medical expenditures, total pharmacy expenditures, and subcategories of medical and pharmacy expenditures in obese individuals following weight loss surgery (WLS), and to compare these costs with expenditures in obese individuals not receiving WLS. METHODS: Louisiana Office of Group Benefits (OGB), the state-managed health insurer, invited members to be evaluated for insurance-covered WLS. Of 951 obese members who provided written consent to begin the WLS screening process, 40 were selected for surgery. Medical and pharmaceutical claims cost data of the 911 patients who did not have surgery and the 39 individuals who completed surgery were compared over a 2-year presurgical and 6-year postsurgical period. RESULTS: Total nonpharmacy medical costs were lower for WLS patients compared with non-WLS patients beginning 4 years postsurgery and lasting through 6 years postsurgery. No differences were found between WLS and non-WLS patients in expenditures for most medical subcategories examined, including emergency department, physical and occupational therapy, office visits, and laboratory/pathology; whereas sleep facility and all remaining medical expenditures not represented by a subcategory were lower for WLS patients during some postsurgery years. Total pharmacy costs were lower for WLS participants at 2 and 3 years postsurgery, but these lower costs were not maintained; however, costs remained lower for antidiabetic agents, antihypertensive agents, and dyslipidemic agents through all 6 postsurgery years under study. CONCLUSIONS: The cost of WLS may begin to be recouped within the first 4 years postsurgery with continued effects 6 years postsurgery.

Training the next generation of behavioral medicine scientists to accelerate digital health.

We trace the evolution of digital health industry careers for behavioral medicine specialists. We discuss the current misalignment of career opportunities in the private sector with the predominant graduate education training model that emphasizes the pursuit of academic positions. We describe the potential risks to the profession and public health if the field does not adapt professional training models to be inclusive of private sector industry roles. Finally, we offer a series of recommendations aimed at trainees, faculty advisors, and training programs to better prepare trainees for meaningful careers in industry.

This commentary focuses on the career paths available for behavioral medicine scientists in the private sector digital health industry. Although this field has exciting and impactful career options, graduate training models have been slow to adapt to prepare graduates for these opportunities. We describe many actionable steps that trainees, advisors, and graduate programs can take to help training programs to evolve to prepare graduate for more diverse career paths.

Large-scale evaluation of a computer-based learning program to increase prison staff knowledge on geriatric and end-of-life care.

PURPOSE: The purpose of this study is to continue research and development of the ECAD-P learning system with an emphasis on developing a scalable unit for testing in a larger number of more diverse correctional settings. There are almost 2.3 million US persons incarcerated. Geriatric and end-of-life (EOL) care in corrections is not as equitable as care in the free world. Technological delivery of geriatric training to staff through computer-based learning (CBL) offers a novel approach to improve care and reduce disparities among those who are most vulnerable during confinement. DESIGN/METHODOLOGY/APPROACH: This mixed methods study built an interactive CBL for multidisciplinary staff to address EOL and geriatric issues in prisons. The CBL was iteratively built and tested prior to launching a full-scale evaluation using a pre/post-intervention design. FINDINGS: Evaluation of the CBL occurred at 7 sites (i.e. 6 state prisons and 1 prison health-care vendor). A total of 241 staff were recruited with 173 completing post-tests. Outcomes were knowledge acquisition regarding care for aging and dying incarcerated persons (i.e. cognitive measure) and attitudes, motivations and values for providing care (i.e. affective measure). Cognitive and affective post-tests were significantly better than at pre-test (all ps < 0.01). ANCOVAs revealed no significant differences for sex or ethnicity. ORIGINALITY/VALUE: Outcomes reveal that the CBL is acceptable, feasible and usable in corrections. Staff improved their knowledge after receiving the training. Correctional settings face increasing pressures to better address the health care and management needs of aged, chronically ill and dying incarcerated persons. This e-learning holds promise to contribute to better preparation of corrections staff to effectively care for these populations.

A Pilot Study of a Tablet-Based Emotion Regulation Intervention for Early Adolescents.

OBJECTIVE: This study examined the feasibility, acceptability, and preliminary outcomes of internet-based Talking About Risk and Adolescent Choices (iTRAC), a tablet intervention designed to promote emotion regulation (ER) skills among middle schoolers as a strategy for reducing risk behaviors. METHODS: Adolescents (12-14 years) were recruited from 3 urban US schools for advisory groups (n = 15), acceptability testing (n = 11), and pilot testing (n = 85). Youth advisory boards and expert panels tailored content, resulting in an animated intervention of instructional videos, games, and activities designed to teach ER strategies to young adolescents. Eighty-five adolescents were randomized to the 4-module digital iTRAC intervention or a wait-list control group. Adolescents and 1 parent completed baseline and 3-month follow-up questionnaires examining ER attitudes and behaviors; adolescents also completed behavioral tasks related to distress tolerance. RESULTS: Among those randomized to iTRAC, 88% completed all modules. Moderate effect sizes ( d ≥ 0.36) were found from baseline to follow-up on adolescents' beliefs in the controllability of emotions, awareness of emotions, self-efficacy for managing emotions, perceived access to ER strategies, and use of ER strategies. Parent measures of adolescent regulation showed mixed results. CONCLUSION: A digital intervention to enhance ER skills for youth in early adolescence was feasible and demonstrated promising indicators of impact on emotional competence. Increasing adolescents' awareness of and access to ER strategies could reduce decisions driven by transient emotions, which in turn may reduce engagement in risk behaviors and resultant negative health outcomes. This brief tablet-based intervention has the potential to be self-administered and used to increase emotional competency.