Adopting Sustainable Menu Practices in Healthcare Institutions: Perceived Barriers and Facilitators.

Purpose: The healthcare sector is an important area for sustainable food initiatives, given its inherent mission to heal and its substantial impact on the food system. Foodservice managers can take part in these initiatives by using sustainable menu practices (SMPs). This study aimed to explore managerial perceptions of barriers and facilitators to adopting SMPs in Québec healthcare institutions.Methods: Seventeen foodservice managers were recruited through purposeful sampling to participate in a qualitative semi-structured interview. The Diffusion of Innovations theory was used to assess the main determinants of the diffusion of an innovation (SMPs) through a complex social system (healthcare organization).Results: Participants reported more barriers than facilitators. Lack of support at many levels was recognized as a major hindrance to SMP adoption, as were shortfalls in political directives. Increased collaboration between all food system actors and better communication in healthcare were perceived as needed for increased SMP adoption.Conclusions: This research contributes to an in-depth understanding of managerial experiences in SMP adoption in various regional and healthcare settings. Findings suggest the need for support and strategies that would remove important barriers for foodservice managers and contributed to the development of a guide to support foodservice managers in implementing SMPs.

Hearts lacking plasma membrane KATP channels display changes in basal aerobic metabolic substrate preference and AMPK activity.

Cardiac ATP-sensitive K+ (KATP) channels couple changes in cellular metabolism to membrane excitability and are activated during metabolic stress, although under basal aerobic conditions, KATP channels are thought to be predominately closed. Despite intense research into the roles of KATP channels during metabolic stress, their contribution to aerobic basal cardiac metabolism has not been previously investigated. Hearts from Kir6.2+/+ and Kir6.2-/- mice were perfused in working mode, and rates of glycolysis, fatty acid oxidation, and glucose oxidation were measured. Changes in activation/expression of proteins regulating metabolism were probed by Western blot analysis. Despite cardiac mechanical function and metabolic efficiency being similar in both groups, hearts from Kir6.2-/- mice displayed an approximately twofold increase in fatty acid oxidation and a 0.45-fold reduction in glycolytic rates but similar glucose oxidation rates compared with hearts from Kir6.2+/+ mice. Kir6.2-/- hearts also possessed elevated levels of activated AMP-activated protein kinase (AMPK), higher glycogen content, and reduced mitochondrial density. Moreover, activation of AMPK by isoproterenol or diazoxide was significantly blunted in Kir6.2-/- hearts. These data indicate that KATP channel ablation alters aerobic basal cardiac metabolism. The observed increase in fatty acid oxidation and decreased glycolysis before any metabolic insult may contribute to the poor recovery observed in Kir6.2-/- hearts in response to exercise or ischemia-reperfusion injury. Therefore, KATP channels may play an important role in the regulation of cardiac metabolism through AMPK signaling.NEW & NOTEWORTHY In this study, we show that genetic ablation of plasma membrane ATP-sensitive K+ channels results in pronounced changes in cardiac metabolic substrate preference and AMP-activated protein kinase activity. These results suggest that ATP-sensitive K+ channels may play a novel role in regulating metabolism in addition to their well-documented effects on ionic homeostasis during periods of stress.

Burden of treatment for chronic illness: a concept analysis and review of the literature.

CONTEXT: Treatment burden, the burden associated with the treatment and management of chronic illness, has not yet been well articulated. OBJECTIVE: Using Rodgers' (1989, Journal of Advanced Nursing, 14, 330-335) method of concept analysis, this review describes the ways in which treatment burden has been conceptualized to define the concept and to develop a framework for understanding its attributes, antecedents and consequences. METHODS: Leading databases were searched electronically between the years 2002 and 2011. To ensure the review focused on actual observations of the concept of interest, articles that did not measure treatment burden (either qualitatively or quantitatively) were excluded. An inductive approach was used to identify themes related to the concept of treatment burden. MAIN RESULTS: Thirty articles, identified from 1557 abstracts, were included in the review. The attributes of treatment burden include burden as a dynamic process, as a multidimensional concept, and comprising of both subjective and objective elements. Prominent predisposing factors (antecedents) include the person's age and gender, their family circumstances, possible comorbidity, high use of medications, characteristics of treatment and their relationship with their health-care provider. The most dominant consequences are poor health and well-being, non-adherence to treatment, ineffective resource use and burden on significant others. Furthermore, many of these consequences can also become antecedents, reflecting the cyclic and dynamic nature of treatment burden. CONCLUSION: The findings underscore the need for researchers and health-care professionals to engage in collaborative discussions and make cooperative efforts to help alleviate treatment burden and tailor treatment regimens to the realities of people's daily lives.

Ischemia induced peroxynitrite dependent modifications of cardiomyocyte MLC1 increases its degradation by MMP-2 leading to contractile dysfunction.

Damage to cardiac contractile proteins during ischemia followed by reperfusion is mediated by reactive oxygen species such as peroxynitrite (ONOO(-)), resulting in impairment of cardiac systolic function. However, the pathophysiology of systolic dysfunction during ischemia only, before reperfusion, remains unclear. We suggest that increased ONOO(-) generation during ischemia leads to nitration/nitrosylation of myosin light chain 1 (MLC1) and its increased degradation by matrix metalloproteinase-2 (MMP-2), which leads to impairment of cardiomyocyte contractility. We also postulate that inhibition of ONOO(-) action by use of a ONOO(-) scavenger results in improved recovery from ischemic injury. Isolated rat cardiomyocytes were subjected to 15 and 60 min. of simulated ischemia. Intact MLC1 levels, measured by 2D gel electrophoresis and immunoblot, were shown to decrease with increasing duration of ischemia, which correlated with increasing levels of nitrotyrosine and nitrite/nitrate. In vitro degradation of human recombinant MLC1 by MMP-2 increased after ONOO(-) exposure of MLC1 in a concentration-dependent manner. Mass spectrometry analysis of ischemic rat cardiomyocyte MLC1 showed nitration of tyrosines 78 and 190, as well as of corresponding tyrosines 73 and 185 within recombinant human cardiac MLC1 treated with ONOO(-). Recombinant human cardiac MLC1 was additionally nitrosylated at cysteine 67 and 76 corresponding to cysteine 81 of rat MLC1. Here we show that increased ONOO(-) production during ischemia induces MLC1 nitration/nitrosylation leading to its increased degradation by MMP-2. Inhibition of MLC1 nitration/nitrosylation during ischemia by the ONOO(-) scavenger FeTPPS (5,10,15,20-tetrakis-[4-sulfonatophenyl]-porphyrinato-iron[III]), or inhibition of MMP-2 activity with phenanthroline, provides an effective protection of cardiomyocyte contractility.

Molecular determinants of ATP-sensitive potassium channel MgATPase activity: diabetes risk variants and diazoxide sensitivity.

ATP-sensitive K(+) (KATP) channels play an important role in insulin secretion. KATP channels possess intrinsic MgATPase activity that is important in regulating channel activity in response to metabolic changes, although the precise structural determinants are not clearly understood. Furthermore, the sulfonylurea receptor 1 (SUR1) S1369A diabetes risk variant increases MgATPase activity, but the molecular mechanisms remain to be determined. Therefore, we hypothesized that residue-residue interactions between 1369 and 1372, predicted from in silico modelling, influence MgATPase activity, as well as sensitivity to the clinically used drug diazoxide that is known to increase MgATPase activity. We employed a point mutagenic approach with patch-clamp and direct biochemical assays to determine interaction between residues 1369 and 1372. Mutations in residues 1369 and 1372 predicted to decrease the residue interaction elicited a significant increase in MgATPase activity, whereas mutations predicted to possess similar residue interactions to wild-type (WT) channels elicited no alterations in MgATPase activity. In contrast, mutations that were predicted to increase residue interactions resulted in significant decreases in MgATPase activity. We also determined that a single S1369K substitution in SUR1 caused MgATPase activity and diazoxide pharmacological profiles to resemble those of channels containing the SUR2A subunit isoform. Our results provide evidence, at the single residue level, for a molecular mechanism that may underlie the association of the S1369A variant with type 2 diabetes. We also show a single amino acid difference can account for the markedly different diazoxide sensitivities between channels containing either the SUR1 or SUR2A subunit isoforms.

Calreticulin induces dilated cardiomyopathy.

BACKGROUND: Calreticulin, a Ca(2+)-buffering chaperone of the endoplasmic reticulum, is highly expressed in the embryonic heart and is essential for cardiac development. After birth, the calreticulin gene is sharply down regulated in the heart, and thus, adult hearts have negligible levels of calreticulin. In this study we tested the role of calreticulin in the adult heart. METHODOLOGY/PRINCIPAL FINDINGS: We generated an inducible transgenic mouse in which calreticulin is targeted to the cardiac tissue using a Cre/loxP system and can be up-regulated in adult hearts. Echocardiography analysis of hearts from transgenic mice expressing calreticulin revealed impaired left ventricular systolic and diastolic function and impaired mitral valve function. There was altered expression of Ca(2+) signaling molecules and the gap junction proteins, Connexin 43 and 45. Sarcoplasmic reticulum associated Ca(2+)-handling proteins (including the cardiac ryanodine receptor, sarco/endoplasmic reticulum Ca(2+)-ATPase, and cardiac calsequestrin) were down-regulated in the transgenic hearts with increased expression of calreticulin. CONCLUSIONS/SIGNIFICANCE: We show that in adult heart, up-regulated expression of calreticulin induces cardiomyopathy in vivo leading to heart failure. This is due to an alternation in changes in a subset of Ca(2+) handling genes, gap junction components and left ventricle remodeling.

The experiences of leaders of self-management courses in Queensland: exploring Health Professional and Peer Leaders' perceptions of working together.

This paper describes the experiences of volunteers who have been trained to deliver the Stanford Chronic Disease Self-Management Program course. In Queensland, Australia, Leaders usually work in pairs (a Health Professional Leader (HPL) and a Peer Leader (PL)). Qualitative data were collected to explore volunteers' experiences as Leaders and their opinions about working together to deliver self-management courses. The data were collected from September 2005 to December 2005. In-depth, semistructured telephone interviews were conducted with a purposive sample of 34 Leaders (17 PL, 17 HPLs). Thematic analysis revealed two core themes that described Leaders' perceptions and experiences of working relationships between HPLs and PLs: (i) The Value of Working Together and (2) Relationship Tensions. Both HPLs and PLs believed that working together represented 'the best of both worlds' and that the combination of peers and health professionals enhanced the sustainability of the approach. However, a number of tensions were revealed that undermined the development and sustainability of these working relationships. From HPLs' perspective, the benefits of working with volunteer PLs did not always justify the 'burden'. Finding the 'right person' for the PL role was difficult and a higher value was often placed on the contribution of professionals. The tensions that were most prominent for PLs were grounded in the disparity between their status and that of HPLs, their lack of ownership over courses coupled with lack of a strong voice in the co-Leader relationship, and the absence of connection and engagement among Leaders. Working relationships between HPLs and PLs have potential to deliver positive outcomes for people with chronic disease, but the current study has highlighted the necessity of developing a culture of mutual respect and a system that values both forms of knowledge and expertise (i.e. experiential and professional).

Distinct early signaling events resulting from the expression of the PRKAG2 R302Q mutant of AMPK contribute to increased myocardial glycogen.

BACKGROUND: Humans with an R302Q mutation in AMPKgamma(2) (the PRKAG2 gene) develop a glycogen storage cardiomyopathy characterized by a familial form of Wolff-Parkinson-White syndrome and cardiac hypertrophy. This phenotype is recapitulated in transgenic mice with cardiomyocyte-restricted expression of AMPKgamma(2)R302Q. Although considerable information is known regarding the consequences of harboring the gamma(2)R302Q mutation, little is known about the early signaling events that contribute to the development of this cardiomyopathy. METHODS AND RESULTS: To distinguish the direct effects of gamma(2)R302Q expression from later compensatory alterations in signaling, we used transgenic mice expressing either the wild-type AMPKgamma(2) subunit (TGgamma(2)WT) or the mutated form (TGgamma(2)R302Q), in combination with acute expression of these proteins in neonatal rat cardiomyocytes. Although acute expression of gamma(2)R302Q induces AMPK activation and upregulation of glycogen synthase and AS160, with an associated increase in glycogen content, AMPK activity, glycogen synthase activity, and AS160 expression are reduced in hearts from TGgamma(2)R302Q mice, likely in response to the existing 37-fold increase in glycogen. Interestingly, gamma(2)WT expression has similar, yet less marked effects than gamma(2)R302Q expression in both cardiomyocytes and hearts. CONCLUSIONS: Using acute and chronic models of gamma(2)R302Q expression, we have differentiated the direct effects of the gamma(2)R302Q mutation from eventual compensatory modifications. Our data suggest that expression of gamma(2)R302Q induces AMPK activation and the eventual increase in glycogen content, a finding that is masked in hearts from transgenic adult mice. These findings are the first to highlight temporal differences in the effects of the PRKAG2 R302Q mutation on cardiac metabolic signaling events.