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Nature contact has associations with emotional ill-being and well-being. However, the mechanisms underlying these associations are not fully understood. We hypothesised that increased adaptive and decreased maladaptive emotion regulation strategies would be a pathway linking nature contact to ill-being and well-being. Using data from a survey of 600 U.S.-based adults administered online in 2022, we conducted structural equation modelling to test our hypotheses. We found that (1) frequency of nature contact was significantly associated with lesser emotional ill-being and greater emotional well-being, (2) effective emotion regulation was significantly associated with lesser emotional ill-being and greater emotional well-being, and (3) the associations of higher frequency of nature contact with these benefits were partly explained via emotion regulation. Moreover, we found a nonlinear relationship for the associations of duration of nature contact with some outcomes, with a rise in benefits up to certain amounts of time, and a levelling off after these points. These findings support and extend previous work that demonstrates that the associations of nature contact with emotional ill-being and well-being may be partly explained by changes in emotion regulation. [ABSTRACT FROM AUTHOR]

Beliefs about the controllability and usefulness of emotions may influence successful emotion regulation across multiple emotional disorders and could thus be influential mechanisms in long-term mental health outcomes. However, to date there has been little empirical work in this area. Our aim was to fill this gap, by examining the links between emotion beliefs and common emotional disorder symptoms. Specifically, we examined whether emotion beliefs can account for significant variance in depression, anxiety, and stress symptoms, and explored which profiles of emotion beliefs might characterise each of these symptom categories. A sample of 948 Australian university students completed self-report measures of emotion beliefs and emotional disorder symptoms. A path analysis indicated that emotion beliefs accounted for a modest but significant 11%, 12%, and 9% of the variance in depression, anxiety, and stress symptoms, respectively (ps <.001). A latent profile analysis revealed six different profiles of combinations of emotion beliefs and emotional disorder symptom levels, collectively reinforcing the transdiagnostic relevance of emotion beliefs across each symptom category. Overall, our results indicate the importance of considering emotion beliefs in conceptualisations of depression, anxiety, and stress, and suggest that emotion beliefs may be a useful assessment and treatment target. What is already known about this topic: Ford and Gross's (2018, 2019) theoretical framework of emotion beliefs posits that believing positive and negative emotions are uncontrollable and useless is detrimental for emotion regulation efforts and mental health outcomes. Beliefs about emotions being uncontrollable are associated with increased emotional disorder symptoms. The limited research examining beliefs about the usefulness of emotions indicates that believing emotions are useless is also associated with increased emotional disorder symptoms. What this topic adds: This study is the first to comprehensively examine controllability and usefulness beliefs across the negative and positive valence domains. We systematically mapped the emotion belief profiles characterising depression, anxiety, and stress symptoms, and found profiles with stronger maladaptive emotion beliefs tended to have greater emotional disorder symptoms. We found that both belief categories across both valence domains are relevant to emotional disorder symptoms, but beliefs about the controllability of negative emotion were particularly important. [ABSTRACT FROM AUTHOR]

Background: People with alcohol use disorder (AUD) have an increased risk of developing pneumonia and pulmonary diseases. Alveolar macrophages (AMs) are immune cells of the lower respiratory tract that are necessary for clearance of pathogens. However, alcohol causes AM oxidative stress, mitochondrial damage and dysfunction, and diminished phagocytic capacity, leading to lung injury and immune suppression. Methods: AMs were isolated by bronchoalveolar lavage from people with AUD and male and female C57BL/6J mice given chronic ethanol (20% w/v, 12 weeks) in drinking water. The peroxisome proliferator‐activated receptor γ ligand, pioglitazone, was used to treat human AMs ex vivo (10 μM, 24 h) and mice in vivo by oral gavage (10 mg/kg/day). Levels of AM mitochondrial superoxide and hypoxia‐inducible factor‐1 alpha (HIF‐1α) mRNA, a marker of oxidative stress, were measured by fluorescence microscopy and RT‐qPCR, respectively. Mouse AM phagocytic ability was determined by internalized Staphylococcus aureus, and mitochondrial capacity, dependency, and flexibility for glucose, long‐chain fatty acid, and glutamine oxidation were measured using an extracellular flux analyzer. In vitro studies used a murine AM cell line, MH‐S (±0.08% ethanol, 72 h) to investigate mitochondrial fuel oxidation and ATP‐linked respiration. Results: Pioglitazone treatment decreased mitochondrial superoxide in AMs from people with AUD and ethanol‐fed mice and HIF‐1α mRNA in ethanol‐fed mouse lungs. Pioglitazone also reversed mouse AM glutamine oxidation and glucose or long‐chain fatty acid flexibility to meet basal oxidation needs. In vitro, ethanol decreased the rate of AM mitochondrial and total ATP production, and pioglitazone improved changes in glucose and glutamine oxidation. Conclusions: Pioglitazone reversed chronic alcohol‐induced oxidative stress in human AM and mitochondrial substrate oxidation flexibility and superoxide levels in mouse AM. Decreased ethanol‐induced AM HIF‐1α mRNA with pioglitazone suggests that this pathway may be a focus for metabolic‐targeted therapeutics to improve morbidity and mortality in people with AUD. [ABSTRACT FROM AUTHOR]

Systems Engineering has demonstrated significant value and has become increasingly necessary. However, this has increased challenges in the quest to build next gen systems tailored to changing customer needs and evolving industry requirements. Many systems engineering practices have evolved catering to these challenges, leading to development of model‐based systems engineering approaches. This paper describes leveraging MBSE and systems thinking application in medical device industry to adapt with changing customer needs, comply with regulatory constraints and advance towards sustainability. [ABSTRACT FROM AUTHOR]

Alcohol use disorder (AUD) is a significant public health concern and people with AUD are more likely to develop severe acute respiratory distress syndrome (ARDS) in response to respiratory infections. To examine whether AUD was a risk factor for more severe outcome in response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, we examined early responses to infection using cultured differentiated bronchial epithelial cells derived from brushings obtained from people with AUD or without AUD. RNA-seq analysis of uninfected cells determined that AUD cells were enriched for expression of epidermal genes as compared with non-AUD cells. Bronchial epithelial cells from patients with AUD showed a significant decrease in barrier function 72 h postinfection, as determined by transepithelial electrical resistance. In contrast, barrier function of non-AUD cells was enhanced 72 h after SARS-CoV-2 infection. AUD cells showed claudin-7 that did not colocalize with zonula occludens-1 (ZO-1), indicative of disorganized tight junctions. However, both AUD and non-AUD cells showed decreased β-catenin expression following SARS-CoV-2 infection. To determine the impact of AUD on the inflammatory response to SARS-CoV-2 infection, cytokine secretion was measured by multiplex analysis. SARS-CoV-2-infected AUD bronchial cells had enhanced secretion of multiple proinflammatory cytokines including TNFα, IL-1β, and IFNγ as opposed to non-AUD cells. In contrast, secretion of the barrier-protective cytokines epidermal growth factor (EGF) and granulocyte macrophage-colony stimulating factor (GM-CSF) was enhanced for non-AUD bronchial cells. Taken together, these data support the hypothesis that AUD is a risk factor for COVID-19, where alcohol primes airway epithelial cells for increased inflammation and increased barrier dysfunction and increased inflammation in response to infection by SARS-CoV-2. NEW & NOTEWORTHY Alcohol use disorder (AUD) is a significant risk factor for severe acute respiratory distress syndrome. We found that AUD causes a phenotypic shift in gene expression in human bronchial epithelial cells, enhancing expression of epidermal genes. AUD cells infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) had higher levels of proinflammatory cytokine secretion and barrier dysfunction not present in infected non-AUD cells, consistent with increased early COVID-19 severity due to AUD. [ABSTRACT FROM AUTHOR]

Among the many organ systems affected by harmful alcohol use, the lungs are particularly susceptible to infections and injury. The mechanisms responsible for rendering people with alcohol use disorder (AUD) [...]

Alexithymia is a key transdiagnostic risk factor for emotion-based psychopathologies. Conceptual models specify that this is because alexithymia impairs emotion regulation. However, the extent of these putative emotion regulation impairments remains underexplored. Our aim in this study was to begin to address this gap by examining whether people with high, average, or low levels of alexithymia differ in the types of emotion regulation strategies they typically use. General community adults from the United States (N = 501) completed a battery of alexithymia and emotion regulation measures. Participants were grouped into high, average, and low alexithymia quantiles. After controlling for demographics and current levels of distress, the high, average, and low alexithymia groups differed in their use of cognitive and behavioral emotion regulation strategies. Compared to the other groups, the high alexithymia group reported lesser use of generally adaptive regulation strategies (cognitive reappraisal, approaching problems, and seeking social support) and greater use of generally maladaptive regulation strategies (expressive suppression, behavioral withdrawal, ignoring). Our data were cross-sectional and from self-report questionnaires. Future work in other cultural groups would be beneficial. Our results support the view that alexithymia is associated with impaired emotion regulation. In particular, people with high alexithymia seem to exhibit a less adaptive profile of emotion regulation strategies. Direct targeting of these emotion regulation patterns in psychotherapy may therefore be a useful pathway for the treatment of emotional disorder symptoms in people with high alexithymia. • The process model predicts that alexithymia should impair emotion regulation • We examined the emotion regulation strategy use profiles characterizing alexithymia • Alexithymia was characterized by a less adaptive emotion regulation profile: • Less use of cognitive reappraisal, approaching problems, and seeking social support. • More use of expressive suppression, behavioural withdrawal, and ignoring. [ABSTRACT FROM AUTHOR]