Examining dietary self-talk content and context for discretionary snacking behaviour: a qualitative interview study.

Background: Consuming discretionary snack foods high in calories, salt, sugar or fat in between regular meals can have a negative impact on weight management and health. Despite the intention to refrain from discretionary snacking, individuals often report feeling tempted by snack foods. A cognitive process to resolve food choice related tension may be dietary self-talk which is one's inner speech around dietary choice. This study aimed to understand the content and context of dietary self-talk before consuming discretionary snack foods. Methods: Qualitative semi-structured interviews based on Think-Aloud methods were conducted remotely. Participants answered open-ended questions and were presented with a list of 37 dietary self-talk items. Interview transcripts were analyzed thematically. Results: Interviews (n = 18, age: 19-54 years, 9 men, 9 women) confirmed the frequent use of dietary self-talk with all 37 content items endorsed. Reported use was highest for the self-talk items: 'It is a special occasion'; 'I did physical activity/exercise today'; and 'I am hungry'. Three new items were developed, eight items were refined. Identified key contextual themes were: 'reward', 'social', 'convenience', 'automaticity', and 'hunger'. Conclusions: This study lists 40 reasons people use to allow themselves to consume discretionary snack foods and identifies contextual factors of dietary-self talk. All participants reported using dietary self-talk, with variation in content, frequency and degree of automaticity. Recognising and changing dietary self-talk may be a promising intervention target for changing discretionary snacking behaviour.

Mitochondrial Metabolism in Astrocytes Regulates Brain Bioenergetics, Neurotransmission and Redox Balance.

In the brain, mitochondrial metabolism has been largely associated with energy production, and its dysfunction is linked to neuronal cell loss. However, the functional role of mitochondria in glial cells has been poorly studied. Recent reports have demonstrated unequivocally that astrocytes do not require mitochondria to meet their bioenergetics demands. Then, the question remaining is, what is the functional role of mitochondria in astrocytes? In this work, we review current evidence demonstrating that mitochondrial central carbon metabolism in astrocytes regulates overall brain bioenergetics, neurotransmitter homeostasis and redox balance. Emphasis is placed in detailing carbon source utilization (glucose and fatty acids), anaplerotic inputs and cataplerotic outputs, as well as carbon shuttles to neurons, which highlight the metabolic specialization of astrocytic mitochondria and its relevance to brain function.

The Complete Care Model and Glycemic Control in California State Prisons.

Since integrating the chronic care theory in 2008 and the complete care model (CCM) in 2015, the California Department of Corrections and Rehabilitation (CDCR) has seen steady improvement in health care-related mortality. However, comparing glycated hemoglobin (HbA1c) levels for the 2 years pre- and the 2 years post-CCM shows the glycemic control for diabetes patients has not significantly changed. Findings suggest that additional components of the theory will need to be incorporated into the CCM to achieve CDCR's progressive goal of 90% of their diabetes patients having HbA1c levels less than 8%. Authors recommend specific direction for further research and development of the CCM in order to reach patient care goals associated with the full adoption of the chronic care theory.

Evaluating the immediate effect of forearm and wrist orthoses on pain and function in individuals with lateral elbow tendinopathy: A systematic review.

BACKGROUND: Lateral elbow tendinopathy is associated with pain during gripping, with forearm/wrist orthoses prescribed for treatment. OBJECTIVES: To investigate the immediate effects of forearm and/or wrist orthoses on outcome measures of pain and function in individuals with lateral elbow tendinopathy. DESIGN: Systematic review METHODS: Four electronic databases were searched to identify randomised controlled trials reporting the immediate effects of forearm and/or wrist orthoses on pain and function in individuals with lateral elbow tendinopathy. The quality of evidence was rated from high to very low, using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) for the primary outcomes. Where possible, standardised mean difference (SMD) and 95% confidence intervals were calculated to compare post measures between forearm and/or wrist orthoses and control/placebo conditions. RESULTS: The search revealed 1965 studies, of which, seven randomised crossover trials were included. Using the GRADE approach there was low quality evidence revealing a significant decrease in pain during contraction (SMD range -0.65 to -0.83) with forearm orthoses compared to a control/placebo condition. Low quality evidence revealed improvements in pain-free grip strength with the use of a forearm orthosis (SMD range 0.24-0.38), but not maximal grip strength (SMD range 0.14-0.15). Low quality evidence revealed a static wrist orthosis did not improve pain-free grip strength (SMD -0.08) or maximal grip strength (SMD -0.22). CONCLUSION: There is low quality evidence that forearm orthoses can immediately reduce pain during contraction and improve pain-free grip strength but not maximal grip strength in individuals with lateral elbow tendinopathy.

Survival Mechanisms and Xenobiotic Susceptibility of Keratinocytes Exposed to Metal-Derived Nanoparticles.

Metal-derived nanoparticles (Mt-NPs) are increasingly used in cosmetology due to their ultraviolet shielding (titanium dioxide [TiO2]), antioxidant (cerium dioxide [CeO2]), and biocidal (silver [Ag]) properties. In the absence of overt toxicity (i.e., cell death), Mt-NPs are considered safe for cosmetic applications. However, there is little understanding about the mechanisms involved in the survival of keratinocytes exposed to subtoxic levels of Mt-NPs. Human keratinocytes (HaCaT) were exposed subacutely to subtoxic concentrations (≤30 µg/mL, 48-72 h) of rutile (r) TiO2 (cylindrical), CeO2 (cubic) and Ag (spherical) with a core/hydrodynamic size of <50/<100 nm and >98% purity. Mt-NP uptake was indirectly quantified by changes in the light side scatter, where the kinetics (time/dose-response) suggested that the three types of Mt-NPs were similarly uptaken by keratinocytes. rTiO2 and CeO2, but not Ag-NPs, increased autophagy, whose inhibition prompted cell death. No increase in the steady-state levels of reactive oxygen species (ROS) was induced by exposure to any of the Mt-NPs tested. Interestingly, intracellular Ag-NP aggregates observed an increased far-red autofluorescence (≥740 nm em), which has been ascribed to their binding to thiol molecules such as glutathione (GSH). Accordingly, inhibition of GSH synthesis, but not the impairment of oxidized GSH recycling, sensitized keratinocytes to Ag-NPs suggesting that GSH homeostasis, and its direct scavenging of Ag-NPs, but not ROS, is essential for keratinocyte survival upon exposure to Ag-NP. rTiO2 and Ag, but not CeO2-NPs, compromised metabolic flux (glycolysis and respiration), but ATP levels were unaltered. Finally, we also observed that exposure to Mt-NPs sensitized keratinocytes to non-UV xenobiotic exposure (arsenite and paraquat). Our results demonstrate the differential contribution of autophagy and GSH homeostasis to the survival of human keratinocytes exposed to subtoxic concentrations of Mt-NPs and highlight the increased susceptibility of keratinocytes exposed to Mt-NPs to a second xenobiotic insult.

Shotgun metagenomic analysis of microbial communities from the Loxahatchee nature preserve in the Florida Everglades.

BACKGROUND: Currently, much is unknown about the taxonomic diversity and the mechanisms of methane metabolism in the Florida Everglades ecosystem. The Loxahatchee National Wildlife Refuge is a section of the Florida Everglades that is almost entirely unstudied in regard to taxonomic profiling. This short report analyzes the metagenome of soil samples from this Refuge to investigate the predominant taxa, as well as the abundance of genes involved in environmentally significant metabolic pathways related to methane production (nitrogen fixation and dissimilatory sulfite reduction). METHODS: Shotgun metagenomic sequencing using the Illumina platform was performed on 17 soil samples from four different sites within the Loxahatchee National Wildlife Refuge, and underwent quality control, assembly, and annotation. The soil from each sample was tested for water content and concentrations of organic carbon and nitrogen. RESULTS: The three most common phyla of bacteria for every site were Actinobacteria, Acidobacteria, and Proteobacteria; however, there was variation in relative phylum composition. The most common phylum of Archaea was Euryarchaeota for all sites. Alpha and beta diversity analyses indicated significant congruity in taxonomic diversity in most samples from Sites 1, 3, and 4 and negligible congruity between Site 2 and the other sites. Shotgun metagenomic sequencing revealed the presence of biogeochemical biomarkers of particular interest (e.g., mrcA, nifH, and dsrB) within the samples. The normalized abundances of mcrA, nifH, and dsrB exhibited a positive correlation with nitrogen concentration and water content, and a negative correlation with organic carbon concentration. CONCLUSION: This Everglades soil metagenomic study allowed examination of wetlands biological processes and showed expected correlations between measured organic constituents and prokaryotic gene frequency. Additionally, the taxonomic profile generated gives a basis for the diversity of prokaryotic microbial life throughout the Everglades.

Metabolomics Analyses from Tissues in Parkinson's Disease.

Metabolomics has been successfully applied to study neurological and neurodegenerative disorders including Parkinson's disease for (1) the identification of potential biomarkers of onset and disease progression; (2) the identification of novel mechanisms of disease progression; and (3) the assessment of treatment prognosis and outcome. Reproducible and efficient extraction of metabolites is imperative to the success of any metabolomics investigation. Unlike other omics techniques, the composition of the metabolome can be negatively impacted by the preparation, processing, and handling of these samples. The proper choice of data collection, preprocessing, and processing protocols is similarly important to the design of an effective metabolomics experiment. Likewise, the correct application of univariate and multivariate statistical methods is essential for providing biologically relevant insights. In this chapter, we have outlined a detailed metabolomics workflow that addresses all of these issues. A step-by-step protocol from the preparation of neuronal cells and metabolomic tissue samples to their metabolic analyses using nuclear magnetic resonance, mass spectrometry, and chemometrics is presented.

Assessing the generality and durability of interview-informed functional analyses and treatment.

Due to the limited research demonstrating socially valid outcomes of function-based treatments in ecologically relevant environments (Santiago, Hanley, Moore, & Jin, 2016), we replicated and extended the effects of the interview-informed functional analysis and skill-based treatment procedure described by Hanley, Jin, Vanselow, and Hanratty (2014) with two children diagnosed with autism in a home setting. The assessment and treatment was implemented by a home-based service provider and treatment was extended to the participants' parents. Following the interview-informed functional analyses, we taught the participants functional communication responses and to engage in less-preferred activities when functional communication outcomes were delayed. We observed large reductions in problem behavior following the introduction of the function-based treatment. The effects extended to novel settings, stimuli, and caregivers and the results maintained at 6-week follow-ups.

Mitochondrial dysfunction in glial cells: Implications for neuronal homeostasis and survival.

Mitochondrial dysfunction is central to the pathogenesis of neurological disorders. Neurons rely on oxidative phosphorylation to meet their energy requirements and thus alterations in mitochondrial function are linked to energy failure and neuronal cell death. Furthermore, in neurons, dysfunctional mitochondria are reported to increase the steady-state levels of reactive oxygen species derived from the leakage of electrons from the electron transport chain. Research aimed at understanding mitochondrial dysfunction and its role in neurological disorders has been primarily geared towards neurons. In contrast, the effects of mitochondrial dysfunction in glial cells' function and its implication for neuronal homeostasis and brain function has been largely understudied. Unlike neurons and oligodendrocytes, astrocytes and microglia do not degenerate upon the impairment of mitochondrial function, as they rely primarily on glycolysis to produce energy and have a higher antioxidant capacity than neurons. However, recent evidence highlights the role of mitochondrial metabolism and signaling in glial cell function. In this work, we review the functional role of mitochondria in glial cells and the evidence regarding its potential role regulating neuronal homeostasis and disease progression.

Genomic epidemiology of multidrug-resistant Mycobacterium tuberculosis during transcontinental spread.

The transcontinental spread of multidrug-resistant (MDR) tuberculosis is poorly characterized in molecular epidemiologic studies. We used genomic sequencing to understand the establishment and dispersion of MDR Mycobacterium tuberculosis within a group of immigrants to the United States. We used a genomic epidemiology approach to study a genotypically matched (by spoligotype, IS6110 restriction fragment length polymorphism, and mycobacterial interspersed repetitive units-variable number of tandem repeat signature) lineage 2/Beijing MDR strain implicated in an outbreak of tuberculosis among refugees in Thailand and consecutive cases within California. All 46 MDR M. tuberculosis genomes from both Thailand and California were highly related, with a median difference of 10 single-nucleotide polymorphisms (SNPs). The Wat Tham Krabok (WTK) strain is a new sequence type distinguished from all known Beijing strains by 55 SNPs and a genomic deletion (Rv1267c) associated with increased fitness. Sequence data revealed a highly prevalent MDR strain that included several closely related but distinct allelic variants within Thailand, rather than the occurrence of a single outbreak. In California, sequencing data supported multiple independent introductions of WTK with subsequent transmission and reactivation within the state, as well as a potential super spreader with a prolonged infectious period. Twenty-seven drug resistance-conferring mutations and 4 putative compensatory mutations were found within WTK strains. Genomic sequencing has substantial epidemiologic value in both low- and high-burden settings in understanding transmission chains of highly prevalent MDR strains.

Beijing sublineages of Mycobacterium tuberculosis differ in pathogenicity in the guinea pig.

The Beijing family of Mycobacterium tuberculosis strains is part of lineage 2 (also known as the East Asian lineage). In clinical studies, we have observed that isolates from the sublineage RD207 of lineage 2 were more readily transmitted among humans. To investigate the basis for this difference, we tested representative strains with the characteristic Beijing spoligotype from four of the five sublineages of lineage 2 in the guinea pig model and subjected these strains to comparative whole-genome sequencing. The results of these studies showed that all of the clinical strains were capable of growing and causing lung pathology in guinea pigs after low-dose aerosol exposure. Differences between the abilities of the four sublineages to grow in the lungs of these animals were not overt, but members of RD207 were significantly more pathogenic, resulting in severe lung damage. The RD207 strains also induced much higher levels of markers associated with regulatory T cells and showed a significant loss of activated T cells in the lungs over the course of the infections. Whole-genome sequencing of the strains revealed mutations specific for RD207 which may explain this difference. Based on these data, we hypothesize that the sublineages of M. tuberculosis are associated with distinct pathological and clinical phenotypes and that these differences influence the transmissibility of particular M. tuberculosis strains in human populations.