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Improving dietary reporting among people living with obesity is challenging as many factors influence reporting accuracy. Reactive Reporting may occur in response to dietary recording, but little is known about how image-based methods influence this process. Using a 4-d image-based mobile food record (mFRTM), this study aimed to identify demographic and psychosocial correlates of measurement error and reactivity bias, among adults with BMI 25–40 kg/m2. Participants (n 155, aged 18–65 years) completed psychosocial questionnaires and kept a 4-d mFRTM. Energy expenditure (EE) was estimated using ≥ 4 d of hip-worn accelerometer data, and energy intake (EI) was measured using mFRTM. EI:EE ratios were calculated, and participants in the highest tertile were considered to have Plausible Intakes. Negative changes in EI according to regression slopes indicated Reactive Reporting. Mean EI was 72 % (sd = 21) of estimated EE. Among participants with Plausible Intakes, mean EI was 96 % (sd = 13) of estimated EE. Higher BMI (OR 0·81, 95 % CI 0·72, 0·92) and greater need for social approval (OR 0·31, 95 % CI 0·10, 0·96) were associated with lower likelihood of Plausible Intakes. Estimated EI decreased by 3 % per d of recording (interquartile range − 14 %,6 %) among all participants. The EI of Reactive Reporters (n 52) decreased by 17 %/d (interquartile range − 23 %,–13 %). A history of weight loss (> 10 kg) (OR 3·4, 95 % CI 1·5, 7·8) and higher percentage of daily energy from protein (OR 1·1, 95 % CI 1·0, 1·2) were associated with greater odds of Reactive Reporting. Identification of reactivity to measurement, as well as Plausible Intakes, is recommended in community-dwelling studies to highlight and address sources of bias.

Reducing individual fossil fuel use is an important component of climate change mitigation, but motivating behaviour change to achieve this is difficult. Protection motivation theory (PMT) is a psychological framework that outlines the conditions under which people are more likely to be persuaded to take a specific response or action. This experimental study investigated the impact six different protection motivation theory-based messages had on intention to reduce fossil fuel use in a sample 3803 US adults recruited via Amazon Mechanical (MTurk). Only messages targeting self-efficacy and response efficacy increased intention to reduce fossil fuel use relative to the control message. However, only the self-efficacy message had an impact on its target construct (i.e. self-efficacy). As such, the mechanism for action for the response efficacy message is unclear. Furthermore, while the current study demonstrates that many of the PMT-related messages did not achieve changes in intention, this it is still possible that messages targeting these constructs could still lead to changes in intention in other modalities and when other message content is used. Given the urgency of responding to climate change, the potential for additive benefits of combining effective PMT-based messages should be considered irrespective of their mechanism as should research focused on how to effectively target other key PMT constructs.

Demographic and psychosocial factors concerning dietary assessment error have been explored, but few studies have investigated the perceived problems experienced when completing dietary recalls. The aim of this research was to (i) compare the perceived problems encountered in two commonly used self-administered 24-hour dietary recall (24HR) programs (INTAKE24© and ASA24

Many aspects of society changed due to the COVID-19 pandemic. As a result, many individuals experienced the introduction of travel bans and restrictions, COVID-19 related anxiety, greater risk to their health and an increased need for adaptive coping. Research has shown health-related quality of life was negatively affected during the time. However, the influence that these restrictions and experiences had on other various quality of life domains (physical, psychological, environmental, and social) is not yet known. Therefore, we aimed to examine the relationships between COVID-19-related variables, health variables, psychological variables and five domains of quality of life in Australian adults. Data was collected via cross-sectional online surveys from 264 Australian participants (Mage = 29.76 years, SD = 12.40). Five hierarchical multiple regression analyses were conducted. The findings showed better adaptive coping, decreased COVID-19 anxiety, and lower perceived health risk were all associated with better quality of life during this time. Neither having travel plans during 2020–2021 nor engaging in compensatory behaviours were associated with quality of life. During times of uncertainty, such as pandemics, natural disasters or war, providing anxiety-reducing coping strategies may be beneficial for reducing the negative impacts on quality of life. In line with these findings and similar research, we have provided several directions and recommendations for governments and media organisations for when future events, similar to COVID-19, occur.

Improving dietary reporting among people living with obesity is challenging as many factors influence reporting accuracy. Reactive reporting may occur in response to dietary recording but little is known about how image-based methods influence this process. Using a 4-day image-based mobile food record (mFRTM), this study aimed to identify demographic and psychosocial correlates of measurement error and reactivity bias, among adults with BMI 25-40kg/m2. Participants (n=155, aged 18-65y) completed psychosocial questionnaires, and kept a 4-day mFRTM. Energy expenditure (EE) was estimated using ≥4 days of hip-worn accelerometer data, and energy intake (EI) was measured using mFRTM. Energy intake: energy expenditure ratios were calculated, and participants in the highest tertile were considered to have Plausible Intakes. Negative changes in EI according to regression slopes indicated Reactive Reporting. Mean EI was 72% (SD=21) of estimated EE. Among participants with Plausible Intakes, mean EI was 96% (SD=13) of estimated EE. Higher BMI (OR 0.81, 95%CI 0.72-0.92) and greater need for social approval (OR 0.31, 95% CI 0.10-0.96), were associated with lower likelihood of Plausible Intakes. Estimated EI decreased by 3% per day of recording (IQR -14%,6%) among all participants. The EI of Reactive Reporters (n=52) decreased by 17%/day (IQR -23%,-13%). A history of weight loss (10kg) (OR 3.4, 95% CI 1.5-7.8), and higher percentage of daily energy from protein (OR 1.1, 95%CI 1.0-1.2) were associated with greater odds of Reactive Reporting. Identification of reactivity to measurement, as well as Plausible Intakes, is recommended in community-dwelling studies to highlight and address sources of bias.

To date, few interventions have been developed to target pre-drinking specifically. An online, theory-based intervention by Caudwell et al. (2018) showed reductions in pre-drinking alcohol consumption and alcohol-related harm, albeit independent of the intervention component/s used. Information about feasibility and acceptability of pre-drinking interventions may therefore be an important point of focus in refining and developing effective interventions. The present manuscript investigates how participants (N = 117) in Caudwell et al. (2018) rated the intervention in terms of feasibility and acceptability. A feasibility and acceptability measure was factor analysed and investigated in relation to participant scores on theory-based measures (e.g., attitude, goal self-concordance), as well as demographic and alcohol consumption variables measured at baseline. Results indicate participants with higher scores on theory-based measures related to behaviour change and goal self-concordance at baseline rated the intervention more positively at follow-up. The findings indicate future intervention research should consider stages of change, with broader alcohol policy and public health strategy focused on changing attitudes toward pre-drinking, which remains a popular health-risk behaviour.

Structural models of psychopathology have emerged as an alternative to traditional categorical approaches. The bifactor model, which incorporates a general p-factor, has become the preferred structure. The p-factor is claimed to represent a substantive construct or property of the system; however, recent evidence suggests that it may be without substantive meaning. If a universal substantive p, and associated specific factors, is to be developed they not only must be applicable and consistent between populations but also must be applicable and consistent within subgroups of a population. This consistency needs to include not only factor loadings but also factor correlates. We used a simulated data approach to explore the applicability and consistency of four popular models of psychopathology to a range of heterogeneous subgroups and examined the consistency of their neurocognitive correlates. We found that only eight out of sixty-three subgroups fitted any of the models with all significant loadings, no negative loadings, no non-positive-definite identification issues, and no negative variance. All eight of these subgroups fit the correlated factors model, none fit the original bifactor model, four subgroups fit the revised bifactor model, and one subgroup fit the single-factor model. Correlates of the factors also varied substantially between the subgroups fitted to the same model. We discuss the implications of the findings, including the implications for the development of universal substantive factors of psychopathology.

Acid pneumonitis is a major cause of sterile acute lung injury (ALI) in humans. Acid pneumonitis spans the clinical spectrum from asymptomatic to acute respiratory distress syndrome (ARDS), characterized by neutrophilic alveolitis, and injury to both alveolar epithelium and vascular endothelium. Clinically, ARDS is defined by acute onset of hypoxemia, bilateral patchy pulmonary infiltrates and non-cardiogenic pulmonary edema. Human studies have provided us with valuable information about the physiological and inflammatory changes in the lung caused by ARDS, which has led to various hypotheses about the underling mechanisms. Unfortunately, difficulties determining the etiology of ARDS, as well as a wide range of pathophysiology have resulted in a lack of critical information that could be useful in developing therapeutic strategies. Translational animal models are valuable when their pathogenesis and pathophysiology accurately reproduce a concept proven in both in vitro and clinical settings. Although large animal models (e.g., sheep) share characteristics of the anatomy of human trachea-bronchial tree, murine models provide a host of other advantages including: low cost; short reproductive cycle lending itself to greater data acquisition; a well understood immunologic system; and a well characterized genome leading to the availability of a variety of gene deletion and transgenic strains. A robust model of low pH induced ARDS requires a murine ALI that targets mainly the alveolar epithelium, secondarily the vascular endothelium, as well as the small airways leading to the alveoli. Furthermore, a reproducible injury with wide differences between different injurious and non-injurious insults is important. The murine gastric acid aspiration model presented here using hydrochloric acid employs an open tracheostomy and recreates a pathogenic scenario that reproduces the low pH pneumonitis injury in humans. Additionally, this model can be used to examine interaction of a low pH insult with other pulmonary injurious entities (e.g., food particles, pathogenic bacteria).

Background Gastric aspiration is a significant cause of acute lung injury and acute respiratory distress syndrome. Environmental risk factors, such as a diet high in pro-inflammatory advanced glycation end-products (AGEs), may render some patients more susceptible to lung injury after aspiration. We hypothesized that high dietary AGEs increase its pulmonary receptor, RAGE, producing an amplified pulmonary inflammatory response in the presence of high mobility group box 1 (HMGB1), a RAGE ligand and an endogenous signal of epithelial cell injury after aspiration.

Recruitment of neutrophils and release of reactive oxygen species are considered to be major pathogenic components driving acute lung injury (ALI). However, NADPH oxidase, the major source of reactive oxygen species in activated phagocytes, can paradoxically limit inflammation and injury. We hypothesized that NADPH oxidase protects against ALI by limiting neutrophilic inflammation and activating Nrf2, a transcriptional factor that induces antioxidative and cytoprotective pathways. Our objective was to delineate the roles of NADPH oxidase and Nrf2 in modulating acute lung inflammation and injury in clinically relevant models of acute gastric aspiration injury, a major cause of ALI. Acid aspiration caused increased ALI (as assessed by bronchoalveolar lavage fluid albumin concentration) in both NADPH oxidase–deficient mice and Nrf2−/− mice compared with wild-type mice. NADPH oxidase reduced airway neutrophil accumulation, but Nrf2 decreased ALI without affecting neutrophil recovery. Acid injury resulted in a 120-fold increase in mitochondrial DNA, a proinflammatory and injurious product of cellular necrosis, in cell-free bronchoalveolar lavage fluid. Pharmacologic activation of Nrf2 by the triterpenoid 1-[2-cyano-3-,12-dioxooleana-1,9 (11)-dien-28-oyl]imidazole limited aspiration-induced ALI in wild-type mice and reduced endothelial cell injury caused by mitochondrial extract–primed human neutrophils, leading to the conclusion that NADPH oxidase and Nrf2 have coordinated, but distinct, functions in modulating inflammation and injury. These results also point to Nrf2 as a therapeutic target to limit ALI by attenuating neutrophil-induced cellular injury.

AGEs are a heterogeneous group of molecules formed from the nonenzymatic reaction of reducing sugars with free amino groups of proteins, lipids, and/or nucleic acids. AGEs have been shown to play a role in various conditions including cardiovascular disease and diabetes. In this study, we hypothesized that AGEs play a role in the “multiple hit hypothesis” of nonalcoholic fatty liver disease (NAFLD) and contribute to the pathogenesis of hepatosteatosis. We measured the effects of various mouse chows containing high or low AGE in the presence of high or low fat content on mouse weight and epididymal fat pads. We also measured the effects of these chows on the inflammatory response by measuring cytokine levels and myeloperoxidase activity levels on liver supernatants. We observed significant differences in weight gain and epididymal fat pad weights in the high AGE-high fat (HAGE-HF) versus the other groups. Leptin, TNF-α, IL-6, and myeloperoxidase (MPO) levels were significantly higher in the HAGE-HF group. We conclude that a diet containing high AGEs in the presence of high fat induces weight gain and hepatosteatosis in CD-1 mice. This may represent a model to study the role of AGEs in the pathogenesis of hepatosteatosis and steatohepatitis.

It is not clear why some patients with aspiration advance to acute lung injury or acute respiratory distress syndrome, whereas others do not. The Western diet is high in advanced glycation end-products (AGEs), which have been found to be proinflammatory. We hypothesize that dietary AGEs exaggerate the pulmonary inflammatory response following gastric aspiration. CD-1 mice were randomized to receive either a low-AGE (LAGE) or a high-AGE (HAGE) diet for 4 weeks. Five hours after intratracheal instillation of acidified small gastric particles, pulmonary function was determined. Polymorphonuclear neutrophil counts, albumin, cytokine/chemokine, and tumor necrosis factor soluble receptor II concentrations in the bronchoalveolar lavage and lung myeloperoxidase activity were measured. Compared with LAGE-fed animals, those fed a HAGE diet had increased lung tissue resistance (P = 0.017), bronchoalveolar lavage albumin concentration (P < 0.05), pulmonary polymorphonuclear neutrophil counts (P = 0.0045), and lung myeloperoxidase activity (P = 0.002) following aspiration. In addition, the plasma levels of tumor necrosis factor soluble receptor II were significantly elevated (P < 0.05), whereas paradoxically levels of keratinocyte chemoattractant and monocyte chemoattractant protein 1 were decreased in mice with HAGE diet. In conclusion, a diet high in AGEs exacerbates acute lung injury following gastric aspiration as evidenced by increases in neutrophil infiltration, airway albumin leakage, and decreased pulmonary compliance. This is the first evidence implicating exacerbation of acute inflammatory lung injury by dietary AGEs. Targeting AGEs in the circulatory system may offer a therapeutic strategy for limiting lung injury following gastric aspiration.

Increased reactive oxidant intermediates (ROIs) from primed leukocytes have been implicated in the pathogenesis of acid aspiration lung injury. To evaluate the specific role of the phagocyte NADPH oxidase-derived ROIs in acid lung injury, the p47phox−/−knockout mouse model of chronic granulomatous disease was used. p47phox−/−mice developed a significantly greater alveolar neutrophilic leukocytosis compared with wild-type mice at all time points after acid injury, with the difference between genotypes being most marked at 48 h. In contrast, the p47phox−/−mice had a decreased number of macrophages in bronchoalveolar lavage (BAL) compared with wild-type at 48 h after acid or saline aspiration. Albumin concentration in BAL reflecting capillary leak was also greater in p47phox−/−compared with wild-type mice. BAL concentrations of proinflammatory cytokines and chemokines were greater in p47phox−/−compared with wild-type mice. These findings suggest that NADPH oxidase, directly or indirectly, plays a role in attenuating the acute neutrophilic response after acid lung injury. We speculate that this downmodulating effect may be mediated by promoting the transition from production of cytokines and chemokines involved in neutrophilic infiltration to a less injurious, chronic inflammatory response.

Background: To minimize the risk of pneumonia, many anesthesiologists delay anesthesia-requiring procedures when patients exhibit signs of viral upper respiratory tract infection. Postinfluenza secondary bacterial pneumonias (SBPs) are a major cause of morbidity and mortality. An increased host susceptibility to SBP postinfluenza has been attributed to physical damage to the pulmonary epithelium, but flu-induced effects on the immune system are being shown to also play an important role. The authors demonstrate that halothane mitigates the risk of SBP postflu through modulation of the effects of type I interferon (IFN). Methods: Mice (n = 6 to 15) were exposed to halothane or ketamine and treated with influenza and Streptococcus pneumoniae. Bronchoalveolar lavage and lung homogenate were procured for the measurement of inflammatory cells, cytokines, chemokines, albumin, myeloperoxidase, and bacterial load. Results: Halothane exposure resulted in decreased bacterial burden (7.9 ± 3.9 × 105vs. 3.4 ± 1.6 × 108 colony-forming units, P < 0.01), clinical score (0.6 ± 0.2 vs. 2.3 ± 0.2, P < 0.0001), and lung injury (as measured by bronchoalveolar lavage albumin, 1.5 ± 0.7 vs. 6.8 ± 1.6 mg/ml, P < 0.01) in CD-1 mice infected with flu for 7 days and challenged with S. pneumoniae on day 6 postflu. IFN receptor A1 knockout mice similarly infected with flu and S. pneumoniae, but not exposed to halothane, demonstrated a reduction of lung bacterial burden equivalent to that achieved in halothane-exposed wild-type mice. Conclusion: These findings indicate that the use of halogenated volatile anesthetics modulates the type I IFN response to influenza and enhance postinfection antibacterial immunity.

Matrix metalloproteinases (MMPs) modulate development, inflammation, and repair in lungs. Tissue inhibitors of MMPs (TIMPs) interact with MMPs, controlling the intensity and nature of the response to injury. Absence of MMP-9, -2, and -8 activities is associated with altered lung inflammation during allergic sensitization. To test the hypothesis that the absence of TIMP-1 enhances allergic lung inflammation, airway hyperreactivity (AHR), and lung remodeling in asthma, we studied TIMP-1 null (TIMP-1 KO) mice and their WT controls using an ovalbumin (OVA) asthma model. TIMP-1 KO mice, compared to WT controls, developed an asthma phenotype characterized by AHR, pronounced cellular lung infiltrates, greater reduction in lung compliance, enhanced Th2 cytokine mRNA and protein expression, and altered collagen lung content associated with enhanced MMP-9 activity. Our findings support the hypothesis that TIMP-1 plays a protective role by preventing AHR and modulating inflammation, remodeling, and cytokine expression in an animal model of asthma.

A model of aspiration lung injury was developed in WT C57BL/6 mice to exploit genetically modified animals on this background, i.e., MCP-1(−/−) mice. Mice were given intratracheal hydrochloric acid (ACID, pH 1.25), small nonacidified gastric particles (SNAP), or combined acid plus small gastric particles (CASP). As reported previously in rats, lung injury in WT mice was most severe for “two-hit” aspiration from CASP (40 mg/ml particulates) based on the levels of albumin, leukocytes, TNF-α, IL-1β, IL-6, MCP-1, KC, and MIP-2 in bronchoalveolar lavage (BAL) at 5, 24, and 48 h. MCP-1(−/−) mice given 40 mg/ml CASP had significantly decreased survival compared with WT mice (32% vs. 80% survival at 24 h and 0% vs. 72% survival at 48 h). MCP-1(−/−) mice also had decreased survival compared with WT mice for CASP aspirates containing reduced particulate doses of 10–20 mg/ml. MCP-1(−/−) mice given 5 mg/ml CASP had survival similar to WT mice given 40 mg/ml CASP. MCP-1(−/−) mice also had differing responses from WT mice for several inflammatory mediators in BAL (KC or IL-6 depending on the particle dose of CASP and time of injury). Histopathology of WT mice with CASP (40 mg particles/ml) showed microscopic areas of compartmentalization with prominent granuloma formation by 24 h, whereas lung tissue from MCP-1(−/−) mice had severe diffuse pneumonia without granulomas. These results indicate that MCP-1 is important for survival in murine aspiration pneumonitis and appears to act partly to protect uninjured lung regions by promoting isolation and compartmentalization of tissue with active inflammation.

It is generally accepted that long term chronic ethanol consumption by young rats will lead to significant losses of cerebellar granule neurons (GN). A recent study in this laboratory showed, however, that 40 weeks of chronic ethanol consumption had no effect on the total numbers of GN in aged Fischer 344 rats (F344). The goals of the present study were to determine whether F344 GN were resistant to ethanol toxicity only in aged rats and whether resistance of GN in aged rats to ethanol toxicity occurred only in the F344 strain. To accomplish those goals, young and aged adult F344 and Wistar-Kyoto (WKY) rats were treated chronically with ethanol for 40 weeks during the first or second half of their life span. In each rat the total numbers of GN were estimated with the optical fractionator and the volumes of the GN layer were estimated according to Cavalieri's theorem. After the 40 weeks of ethanol, there were significant age-related differences in the total numbers of GN in the F344 rats. There were also significant strain-related differences in the total numbers of GN and volumes of the GN layer. There were no significant ethanol-related differences, however, in numbers of cerebellar GN or volumes of the GN layer in F344 rats or WKY rats. The results presented here show that consumption of ethanol over long periods of time had no effect on the total numbers of cerebellar GN or the granular layer volumes in young or aged F344 or WKY rats.