Interprofessional partnerships in chronic illness care: a conceptual model for measuring partnership effectiveness

Introduction: Interprofessional health and social service partnerships (IHSSP) are internationally acknowledged as integral for comprehensive chronic illness care. However, the evidence-base for partnership effectiveness is lacking. This paper aims to clarify partnership measurement issues, conceptualize IHSSP at the front-line staff level, and identify tools valid for group process measurement. <br><br> Theory and methods: A systematic literature review utilizing three interrelated searches was conducted. Thematic analysis techniques were supported by NVivo 7 software. Complexity theory was used to guide the analysis, ground the new conceptualization and validate the selected measures. Other properties of the measures were critiqued using established criteria. <br><br> Results: There is a need for a convergent view of what constitutes a partnership and its measurement. The salient attributes of IHSSP and their interorganizational context were described and grounded within complexity theory. Two measures were selected and validated for measurement of proximal group outcomes. <br><br> Conclusion: This paper depicts a novel complexity theory-based conceptual model for IHSSP of front-line staff who provide chronic illness care. The conceptualization provides the underpinnings for a comprehensive evaluative framework for partnerships. Two partnership process measurement tools, the PSAT and TCI are valid for IHSSP process measurement with consideration of their strengths and limitations

Qualitative methods: are you enchanted or are you alienated?

Copyright © 2007 SAGE Publications. Author's draft version; post-print. Final version published by Sage available on Sage Journals Online http://online.sagepub.com/Since the last report on qualitative methods (Crang, 2005), many of the practical procedures of doing qualitative research remain the same. Human geographers continue to study texts, to conduct interviews, to convene focus groups and to engage in ethnography. Indeed, it is hard, though perhaps not impossible, to imagine what a radically new form of qualitative research practice might look like. So, for the time being, this suite of methods remains the backbone of qualitative research in human geography. Yet we would like to contend that, while these activities continue as before, there are changes in the way they are being conceived and carried out, and related to this there are transformations in the way these methods are being used to make claims to understanding and intervening in the world. In the first of our three reports, it is this link between qualitative methodologies and interpretative strategies we would like to reflect on

Examining Committed Action in Chronic Pain:Further Validation and Clinical Utility of the Committed Action Questionnaire

Psychosocial treatments for chronic pain conditions, such as Acceptance and Commitment Therapy, have highlighted minimizing pain avoidance behaviors and increasing engagement in valued activities as key treatment targets. In terms of salient processes within Acceptance and Commitment Therapy, committed action is considered essential to the pursuit of a meaningful life, as it entails a flexible persistence over time in living consistently with one's values. To date, however, only 1 study has examined the association between measures of committed action and important aspects of pain-related functioning. The purpose of the present study was to analyze the reliability of the Committed Action Questionnaire (CAQ) in a sample of 149 chronic pain patients, perform a confirmatory analysis of its factor structure, and examine how CAQ scores uniquely account for variance in functioning. Confirmatory factor analyses provided support for a 2-factor model, and regression analyses, which examined the cross-sectional direct effects of the 2 subscales on health-related functioning, indicated that the CAQ accounted for significant variance in functioning after controlling for relevant covariates. Overall, these findings provide further support for the CAQ as a measure of adaptive functioning in those with longstanding pain. PERSPECTIVE: This article presents additional evidence for the reliability and validity of the CAQ with chronic pain patients. Confirmatory factor analyses provided support for the 2-factor model, with both subscales demonstrating significant associations with multiple facets of health- and pain-related functioning

Metabolic State Determines Sensitivity to Cellular Stress in Huntington Disease: Normalization by Activation of PPARγ

Impairments in mitochondria and transcription are important factors in the pathogenesis of Huntington disease (HD), a neurodegenerative disease caused by a polyglutamine expansion in the huntingtin protein. This study investigated the effect of different metabolic states and peroxisome proliferator-activated receptor γ (PPARγ) activation on sensitivity to cellular stressors such as H2O2 or thapsigargin in HD. Striatal precursor cells expressing wild type (STHdhQ7) or mutant huntingtin (STHdhQ111) were prepared in different metabolic conditions (glucose vs. pyruvate). Due to the fact that STHdhQ111 cells exhibit mitochondrial deficits, we expected that in the pyruvate condition, where ATP is generated primarily by the mitochondria, there would be greater differences in cell death between the two cell types compared to the glucose condition. Intriguingly, it was the glucose condition that gave rise to greater differences in cell death. In the glucose condition, thapsigargin treatment resulted in a more rapid loss of mitochondrial membrane potential (ΔΨm), a greater activation of caspases (3, 8, and 9), and a significant increase in superoxide/reactive oxygen species (ROS) in STHdhQ111 compared to STHdhQ7, while both cell types showed similar kinetics of ΔΨm-loss and similar levels of superoxide/ROS in the pyruvate condition. This suggests that bioenergetic deficiencies are not the primary contributor to the enhanced sensitivity of STHdhQ111 cells to stressors compared to the STHdhQ7 cells. PPARγ activation significantly attenuated thapsigargin-induced cell death, concomitant with an inhibition of caspase activation, a delay in ΔΨm loss, and a reduction of superoxide/ROS generation in STHdhQ111 cells. Expression of mutant huntingtin in primary neurons induced superoxide/ROS, an effect that was significantly reduced by constitutively active PPARγ. These results provide significant insight into the bioenergetic disturbances in HD with PPARγ being a potential therapeutic target for HD

Recommendations for the analysis of individually randomised controlled trials with clustering in one arm - a case of continuous outcomes

BACKGROUND: In an individually randomised controlled trial where the treatment is delivered by a health professional it seems likely that the effectiveness of the treatment, independent of any treatment effect, could depend on the skill, training or even enthusiasm of the health professional delivering it. This may then lead to a potential clustering of the outcomes for patients treated by the same health professional, but similar clustering may not occur in the control arm. Using four case studies, we aim to provide practical guidance and recommendations for the analysis of trials with some element of clustering in one arm. METHODS: Five approaches to the analysis of outcomes from an individually randomised controlled trial with clustering in one arm are identified in the literature. Some of these methods are applied to four case studies of completed randomised controlled trials with clustering in one arm with sample sizes ranging from 56 to 539. Results are obtained using the statistical packages R and Stata and summarised using a forest plot. RESULTS: The intra-cluster correlation coefficient (ICC) for each of the case studies was small (<0.05) indicating little dependence on the outcomes related to cluster allocations. All models fitted produced similar results, including the simplest approach of ignoring clustering for the case studies considered. CONCLUSIONS: A partially clustered approach, modelling the clustering in just one arm, most accurately represents the trial design and provides valid results. Modelling homogeneous variances between the clustered and unclustered arm is adequate in scenarios similar to the case studies considered. We recommend treating each participant in the unclustered arm as a single cluster. This approach is simple to implement in R and Stata and is recommended for the analysis of trials with clustering in one arm only. However, the case studies considered had small ICC values, limiting the generalisability of these results

Effect of Hydrocortisone on Mortality and Organ Support in Patients With Severe COVID-19: The REMAP-CAP COVID-19 Corticosteroid Domain Randomized Clinical Trial.

Importance: Evidence regarding corticosteroid use for severe coronavirus disease 2019 (COVID-19) is limited. Objective: To determine whether hydrocortisone improves outcome for patients with severe COVID-19. Design, Setting, and Participants: An ongoing adaptive platform trial testing multiple interventions within multiple therapeutic domains, for example, antiviral agents, corticosteroids, or immunoglobulin. Between March 9 and June 17, 2020, 614 adult patients with suspected or confirmed COVID-19 were enrolled and randomized within at least 1 domain following admission to an intensive care unit (ICU) for respiratory or cardiovascular organ support at 121 sites in 8 countries. Of these, 403 were randomized to open-label interventions within the corticosteroid domain. The domain was halted after results from another trial were released. Follow-up ended August 12, 2020. Interventions: The corticosteroid domain randomized participants to a fixed 7-day course of intravenous hydrocortisone (50 mg or 100 mg every 6 hours) (n = 143), a shock-dependent course (50 mg every 6 hours when shock was clinically evident) (n = 152), or no hydrocortisone (n = 108). Main Outcomes and Measures: The primary end point was organ support-free days (days alive and free of ICU-based respiratory or cardiovascular support) within 21 days, where patients who died were assigned -1 day. The primary analysis was a bayesian cumulative logistic model that included all patients enrolled with severe COVID-19, adjusting for age, sex, site, region, time, assignment to interventions within other domains, and domain and intervention eligibility. Superiority was defined as the posterior probability of an odds ratio greater than 1 (threshold for trial conclusion of superiority >99%). Results: After excluding 19 participants who withdrew consent, there were 384 patients (mean age, 60 years; 29% female) randomized to the fixed-dose (n = 137), shock-dependent (n = 146), and no (n = 101) hydrocortisone groups; 379 (99%) completed the study and were included in the analysis. The mean age for the 3 groups ranged between 59.5 and 60.4 years; most patients were male (range, 70.6%-71.5%); mean body mass index ranged between 29.7 and 30.9; and patients receiving mechanical ventilation ranged between 50.0% and 63.5%. For the fixed-dose, shock-dependent, and no hydrocortisone groups, respectively, the median organ support-free days were 0 (IQR, -1 to 15), 0 (IQR, -1 to 13), and 0 (-1 to 11) days (composed of 30%, 26%, and 33% mortality rates and 11.5, 9.5, and 6 median organ support-free days among survivors). The median adjusted odds ratio and bayesian probability of superiority were 1.43 (95% credible interval, 0.91-2.27) and 93% for fixed-dose hydrocortisone, respectively, and were 1.22 (95% credible interval, 0.76-1.94) and 80% for shock-dependent hydrocortisone compared with no hydrocortisone. Serious adverse events were reported in 4 (3%), 5 (3%), and 1 (1%) patients in the fixed-dose, shock-dependent, and no hydrocortisone groups, respectively. Conclusions and Relevance: Among patients with severe COVID-19, treatment with a 7-day fixed-dose course of hydrocortisone or shock-dependent dosing of hydrocortisone, compared with no hydrocortisone, resulted in 93% and 80% probabilities of superiority with regard to the odds of improvement in organ support-free days within 21 days. However, the trial was stopped early and no treatment strategy met prespecified criteria for statistical superiority, precluding definitive conclusions. Trial Registration: ClinicalTrials.gov Identifier: NCT02735707

Discussion of "Probabilistic Index Models," by Thas, O., de Neve, J., Lieven, C. and Ottoy., J.-P.

We present a semiparametric statistical model for the probabilistic index which can be defined as P (Y \u3c-Y*) where Y and Y* are independent random response variables associated with covariate patterns X and X* respectively. A link function defines the relationship between the probabilistic index and a linear predictor. Asymptotic normality of the estimators and consistency of the covariance matrix estimator are established through semiparametric theory. The model is illustrated with several examples, and the estimation theory is validated in a simulation study

Genetic contributions to two special factors of neuroticism are associated with affluence, higher intelligence, better health, and longer life

Higher scores on the personality trait of neuroticism, the tendency to experience negative emotions, are associated with worse mental and physical health. Studies examining links between neuroticism and health typically operationalize neuroticism by summing the items from a neuroticism scale. However, neuroticism is made up of multiple heterogeneous facets, each contributing to the effect of neuroticism as a whole. A recent study showed that a 12-item neuroticism scale described one broad trait of general neuroticism and two special factors, one characterizing the extent to which people worry and feel vulnerable, and the other characterizing the extent to which people are anxious and tense. This study also found that, although individuals who were higher on general neuroticism lived shorter lives, individuals whose neuroticism was characterized by worry and vulnerability lived longer lives. Here, we examine the genetic contributions to the two special factors of neuroticism—anxiety/tension and worry/vulnerability—and how they contrast with that of general neuroticism. First, we show that, whereas the polygenic load for neuroticism is associated with the genetic risk of coronary artery disease, lower intelligence, lower socioeconomic status (SES), and poorer self-rated health, the genetic variants associated with high levels of anxiety/tension, and high levels of worry/vulnerability are associated with genetic variants linked to higher SES, higher intelligence, better self-rated health, and longer life. Second, we identify genetic variants that are uniquely associated with these protective aspects of neuroticism. Finally, we show that different neurological pathways are linked to each of these neuroticism phenotypes.</p