Engagement with eHealth Self-Monitoring in a Primary Care-Based Weight Management Intervention

Background

While eHealth approaches hold promise for improving the reach and cost-effectiveness of behavior change interventions, they have been challenged by declining participant engagement over time, particularly for self-monitoring behaviors. These are significant concerns in the context of chronic disease prevention and management where durable effects are important for driving meaningful changes.

Purpose

“Be Fit, Be Well” was an eHealth weight loss intervention that allowed participants to self-select a self-monitoring modality (web or interactive voice response (IVR)). Participants could change their modality. As such, this study provides a unique opportunity to examine the effects of intervention modality choice and changing modalities on intervention engagement and outcomes.

Methods

Intervention participants, who were recruited from community health centers, (n = 180) were expected to self-monitor health behaviors weekly over the course of the 24-month intervention. We examined trends in intervention engagement by modality (web, IVR, or changed modality) among participants in the intervention arm.

Results

The majority (61%) of participants chose IVR self-monitoring, while 39% chose web. 56% of those who selected web monitoring changed to IVR during the study versus no change in those who initially selected IVR. Self-monitoring declined in both modalities, but completion rates were higher in those who selected IVR. There were no associations between self-monitoring modality and weight or blood pressure outcomes.

Conclusions

This is the first study to compare web and IVR self-monitoring in an eHealth intervention where participants could select and change their self-monitoring modality. IVR shows promise for achieving consistent engagement.     

Metacaspase involvement in programmed cell death of the marine cyanobacterium Trichodesmium

Metacaspases are cysteine specific proteases implicated in cell-signalling, stress acclimation and programmed cell death (PCD) pathways in plants, fungi, protozoa, bacteria and algae. We investigated metacaspase-like gene expression and biochemical activity in the bloom-forming, N₂-fixing, marine cyanobacterium Trichodesmium, which undergoes PCD under low iron and high-light stress. We examined these patterns with respect to in-silico analyses of protein domain architectures that revealed a diverse array of regulatory domains within Trichodesmium metacaspases-like (TeMC) proteins. Experimental manipulations of laboratory cultures and oceanic surface blooms of Trichodesmium from the South Pacific Ocean triggered PCD under Fe-limitation and high light along with enhanced TeMC activity and upregulated expression of diverse TeMC representatives containing different regulatory domains. Furthermore, TeMC activity was significantly and positively correlated with caspase-like activity, which has been routinely observed to increase with PCD induction in Trichodesmium. Although both TeMC and caspase-like activities were stimulated upon PCD induction, inhibitor treatments of these proteolytic activities provided further evidence of largely distinct substrate specificities, even though some inhibitory crossover was observed. Our findings are the first results linking metacaspase expression and activity in PCD induced mortality in Trichodesmium. Yet, the role/s and specific activities of these different proteins remain to be elucidated.     

Inhibition of Astrocyte Glutamine Production by α-Ketoisocaproic Acid

Abstract: We have evaluated the effect of α-ketoisocaproic acid (KIC), the ketoacid of leucine, on the production of glutamine by cultured astrocytes. We used ¹⁵NH₄Cl as a metabolic tracer to measure the production of both [5-¹⁵N]glutamine, reflecting amidation of glutamate via glutamine synthetase, and [2-¹⁵N]glutamine, representing the reductive amination of 2-oxoglutarate via glutamate dehydrogenase and subsequent conversion of [¹⁵N]-glutamate to [2-¹⁵N]glutamine. Addition of KIC (1 mM) to the medium diminished the production of [5-¹⁵N]glutamine and stimulated the formation of [2-¹⁵N]glutamine with the overall result being a significant inhibition of net glutamine synthesis. An external KIC concentration as low as 0.06 mM inhibited synthesis of [5-¹⁵N]glutamine and a level as low as 0.13 mM enhanced labeling (atom% excess) of [2-¹⁵N]glutamine. Higher concentrations of KIC in the medium had correspondingly larger effects. The presence of KIC in the medium did not affect flux through glutaminase, which was measured using [2-¹⁵N]glutamine as a tracer. Nor did KIC inhibit the activity of glutamine synthetase that was purified from sheep brain. Addition of KIC to the medium caused no increased release of lactate dehydrogenase from the astrocytes, suggesting that the ketoacid was not toxic to the cells. KIC treatment was associated with an approximately twofold increase in the formation of ¹⁴CO₂ from [U-¹⁴C]glutamate, indicating that transamination of glutamate with KIC increases intraastrocytic α-ketoglutarate, which is oxidized in the tricarboxylic acid cycle. KIC inhibited glutamine synthesis more than any other ketoacid tested, with the exception of hydroxypyruvate. The data indicate that KIC diminishes flux through glutamine synthetase by lowering the intraastrocytic glutamate concentration below the K_m of glutamine synthetase for glutamate, which we determined to be ～7 mM.     

Freeze-fracturing and surface labelling of embryonic neural retina cells

Freeze-fracturing of dissociated and aggregating neural retina cells from 7-day chick embryos revealed on the inner faces (PF) of the cell membrane numerous particles 6–20 nm in size. In contrast, the PF faces of blebs and some of the lobopodia that project from the cell surface were practically devoid of such particles. However, the elongated filopodia that abound on these cells showed numerous particles on their PF faces. These regional differences in the distribution of particles on PF faces of these cells are interpreted as reflecting membrane activity that leads to the formation of blebs and lobopodia. The frequent presence of “pits” at the basis of blebs and lobopodia is described. It is suggested that the “pits” are associated with the formation of these membrane projections; they may represent anchoring sites for microfilaments and for microtubules involved in the dynamic structure of the cell surface. ConA-binding sites on these cells were studied by scanning electron microscopy, using labeling with hemocyanin. The distribution of these sites on different regions of the cell surface coincided with the regional differences in the distribution of the inner membrane particles.     

Regulation of osteoblast and adipocyte differentiation from human mesenchymal stem cells by conjugated linoleic acid

Conjugated linoleic acid (CLA) describes a group of isomers of linoleic acid and has variable effects on bone formation and adiposity in vivo and in vitro. The variability may be due to individual effects of the predominant bioactive 9cis,11trans (9,11) and 10trans,12cis (10,12) CLA isomers. Osteoblasts and adipocytes are derived from mesenchymal stem cells (MSCs), and bone loss is accompanied by an increase in marrow adiposity. Osteoblast differentiation from MSCs requires activation of Wnt/β-catenin signaling by Wnt10b, which inhibits adipocyte differentiation by suppressing CCAAT/enhancer-binding protein (C/EBP) α. The objective of this study was to determine if 9,11 and 10,12 CLA affect osteoblast and adipocyte differentiation from MSCs and to determine whether any effects are associated with changes in Wnt10b and C/EBPα expression. Osteoblast differentiation was assessed by calcium deposition, alkaline phosphatase (ALP) activity, and the expression of Wnt10b, runx2 and osteocalcin. Adipocyte differentiation was assessed by oil red O staining and C/EBPα, PPARγ and FABP4 expression. Compared to vehicle, 9,11 CLA decreased calcium deposition (～15%), increased oil red O staining (～21-28%) and increased FABP4 (AP2) expression (～58-75%). In contrast, 10,12 CLA increased calcium deposition (～12-60%), ALP activity (～2.1-fold) and the expression of Wnt10b (～60-80%) and osteocalcin (～90%), but decreased oil red O staining (～30%) and the expression of C/EBPα (～24-38%) and PPARγ (～60%) (P<.05). Thus, our findings demonstrate isomer-specific effects of CLA on MSC differentiation, and suggest that 10,12 CLA may be a useful therapeutic agent to promote osteoblast differentiation from MSCs.     

A mutation in SNAP29, coding for a SNARE protein involved in intracellular trafficking, causes a novel neurocutaneous syndrome characterized by cerebral dysgenesis, neuropathy, ichthyosis, and palmoplantar keratoderma

Neurocutaneous syndromes represent a vast, largely heterogeneous group of disorders characterized by neurological and dermatological manifestations, reflecting the common embryonic origin of epidermal and neural tissues. In the present report, we describe a novel neurocutaneous syndrome characterized by cerebral dysgenesis, neuropathy, ichthyosis, and keratoderma (CEDNIK syndrome). Using homozygosity mapping in two large families, we localized the disease gene to 22q11.2 and identified, in all patients, a 1-bp deletion in SNAP29, which codes for a SNARE protein involved in vesicle fusion. SNAP29 expression was decreased in the skin of the patients, resulting in abnormal maturation of lamellar granules and, as a consequence, in mislocation of epidermal lipids and proteases. These data underscore the importance of vesicle trafficking regulatory mechanisms for proper neuroectodermal differentiation.