Endomucin selectively regulates vascular endothelial growth factor receptor-2 endocytosis through its interaction with AP2.

The endothelial glycocalyx, located at the luminal surface of the endothelium, plays an important role in the regulation of leukocyte adhesion, vascular permeability, and vascular homeostasis. Endomucin (EMCN), a component of the endothelial glycocalyx, is a mucin-like transmembrane glycoprotein selectively expressed by venous and capillary endothelium. We have previously shown that knockdown of EMCN impairs retinal vascular development in vivo and vascular endothelial growth factor 165 isoform (VEGF165)-induced cell migration, proliferation, and tube formation by human retinal endothelial cells in vitro and that EMCN is essential for VEGF165-stimulated clathrin-mediated endocytosis and signaling of VEGF receptor 2 (VEGFR2). Clathrin-mediated endocytosis is an essential step in receptor signaling and is of paramount importance for a number of receptors for growth factors involved in angiogenesis. In this study, we further investigated the molecular mechanism underlying EMCN's involvement in the regulation of VEGF-induced endocytosis. In addition, we examined the specificity of EMCN's role in angiogenesis-related cell surface receptor tyrosine kinase endocytosis and signaling. We identified that EMCN interacts with AP2 complex, which is essential for clathrin-mediated endocytosis. Lack of EMCN did not affect clathrin recruitment to the AP2 complex following VEGF stimulation, but it is necessary for the interaction between VEGFR2 and the AP2 complex during endocytosis. EMCN does not inhibit VEGFR1 and FGFR1 internalization or their downstream activities since EMCN interacts with VEGFR2 but not VEGFR1 or FGFR1. Additionally, EMCN also regulates VEGF121-induced VEGFR2 phosphorylation and internalization.

Artificial intelligence in myopia in children: current trends and future directions.

PURPOSE OF REVIEW: Myopia is one of the major causes of visual impairment globally, with myopia and its complications thus placing a heavy healthcare and economic burden. With most cases of myopia developing during childhood, interventions to slow myopia progression are most effective when implemented early. To address this public health challenge, artificial intelligence has emerged as a potential solution in childhood myopia management. RECENT FINDINGS: The bulk of artificial intelligence research in childhood myopia was previously focused on traditional machine learning models for the identification of children at high risk for myopia progression. Recently, there has been a surge of literature with larger datasets, more computational power, and more complex computation models, leveraging artificial intelligence for novel approaches including large-scale myopia screening using big data, multimodal data, and advancing imaging technology for myopia progression, and deep learning models for precision treatment. SUMMARY: Artificial intelligence holds significant promise in transforming the field of childhood myopia management. Novel artificial intelligence modalities including automated machine learning, large language models, and federated learning could play an important role in the future by delivering precision medicine, improving health literacy, and allowing the preservation of data privacy. However, along with these advancements in technology come practical challenges including regulation and clinical integration.

Development and External Validation of Machine Learning Models for Diabetic Microvascular Complications: Cross-Sectional Study With Metabolites.

BACKGROUND: Diabetic kidney disease (DKD) and diabetic retinopathy (DR) are major diabetic microvascular complications, contributing significantly to morbidity, disability, and mortality worldwide. The kidney and the eye, having similar microvascular structures and physiological and pathogenic features, may experience similar metabolic changes in diabetes. OBJECTIVE: This study aimed to use machine learning (ML) methods integrated with metabolic data to identify biomarkers associated with DKD and DR in a multiethnic Asian population with diabetes, as well as to improve the performance of DKD and DR detection models beyond traditional risk factors. METHODS: We used ML algorithms (logistic regression [LR] with Least Absolute Shrinkage and Selection Operator and gradient-boosting decision tree) to analyze 2772 adults with diabetes from the Singapore Epidemiology of Eye Diseases study, a population-based cross-sectional study conducted in Singapore (2004-2011). From 220 circulating metabolites and 19 risk factors, we selected the most important variables associated with DKD (defined as an estimated glomerular filtration rate <60 mL/min/1.73 m2) and DR (defined as an Early Treatment Diabetic Retinopathy Study severity level ≥20). DKD and DR detection models were developed based on the variable selection results and externally validated on a sample of 5843 participants with diabetes from the UK biobank (2007-2010). Machine-learned model performance (area under the receiver operating characteristic curve [AUC] with 95% CI, sensitivity, and specificity) was compared to that of traditional LR adjusted for age, sex, diabetes duration, hemoglobin A1c, systolic blood pressure, and BMI. RESULTS: Singapore Epidemiology of Eye Diseases participants had a median age of 61.7 (IQR 53.5-69.4) years, with 49.1% (1361/2772) being women, 20.2% (555/2753) having DKD, and 25.4% (685/2693) having DR. UK biobank participants had a median age of 61.0 (IQR 55.0-65.0) years, with 35.8% (2090/5843) being women, 6.7% (374/5570) having DKD, and 6.1% (355/5843) having DR. The ML algorithms identified diabetes duration, insulin usage, age, and tyrosine as the most important factors of both DKD and DR. DKD was additionally associated with cardiovascular disease history, antihypertensive medication use, and 3 metabolites (lactate, citrate, and cholesterol esters to total lipids ratio in intermediate-density lipoprotein), while DR was additionally associated with hemoglobin A1c, blood glucose, pulse pressure, and alanine. Machine-learned models for DKD and DR detection outperformed traditional LR models in both internal (AUC 0.838 vs 0.743 for DKD and 0.790 vs 0.764 for DR) and external validation (AUC 0.791 vs 0.691 for DKD and 0.778 vs 0.760 for DR). CONCLUSIONS: This study highlighted diabetes duration, insulin usage, age, and circulating tyrosine as important factors in detecting DKD and DR. The integration of ML with biomedical big data enables biomarker discovery and improves disease detection beyond traditional risk factors.

Postoperative vasoplegia in lung transplantation: incidence and relation to outcome in a single-centre retrospective study.

BACKGROUND: The incidence and clinical importance of vasoplegia after lung transplantation remains poorly studied. We describe the incidence of vasoplegia and its association with complications after lung transplantation. METHODS: Perioperative data of 279 lung transplant recipients operated on from 2015 to 2020 in a UK hospital were analysed retrospectively. RESULTS: Vasoplegia occurred in 41.6% of patients after lung transplantation (mild, 31.0%; moderate, 55.2%; severe, 13.8%). Compared with non-vasoplegic patients, vasoplegic patients had a higher incidence of any acute kidney injury, defined by Kidney Disease Improving Global Outcomes (KDIGO) criteria (78.5% vs 65%, P=0.015), renal replacement therapy (47.4% vs 24.5%, P<0.001), and delayed chest closure (18.4% vs 9.2%, P=0.025); were ventilated longer (70 [32-368] vs 34 [19-105] h, P<0.001); and stayed longer in the ICU (12.9 [5-30] vs 6.8 [3-20] days, P<0.001). Mortality at 30 days and 1 yr was higher in patients with vasoplegia (11.2% vs 5.5% and 20.7% vs 11.7%, P=0.039, respectively). Severe vasoplegia represented a predictor of longer-term mortality (hazard ratio=1.65, P=0.008). Underlying infectious disease, increased BMI, higher preoperative pulmonary artery systolic pressure and bilirubin levels, lower glomerular filtration rate, and increased fresh frozen plasma transfusion were predictors of vasoplegia severity. Neutrophilia, leucocytosis, and increased C-reactive protein were associated with vasoplegia, but release of the neutrophil activation markers myeloperoxidase and heparin-binding protein was similar between groups. CONCLUSIONS: Influenced by preoperative status as well as procedural factors and inflammatory response, vasoplegia is a common and critical condition after lung transplantation with worse short-term outcomes and long-term survival.

Novel engineered, membrane-tethered VEGF-A variants promote formation of filopodia, proliferation, survival, and cord or tube formation by endothelial cells via persistent VEGFR2/ERK signaling and activation of CDC42/ROCK pathways.

Therapeutic angiogenesis would be clinically valuable in situations such as peripheral vascular disease in diabetic patients and tissue reperfusion following ischemia or injury, but approaches using traditional isoforms of vascular endothelial growth factor-A (VEGF) have had little success. The isoform VEGF165 is both soluble and matrix-associated, but can cause pathologic vascular changes. Freely diffusible VEGF121 is not associated with pathologic angiogenesis, but its failure to remain in the vicinity of the targeted area presents therapeutic challenges. In this study, we evaluate the cellular effects of engineered VEGF variants that tether extracellular VEGF121 to the cell membrane with the goal of activating VEGF receptor 2 (VEGFR2) in a sustained, autologous fashion in endothelial cells. When expressed by primary human retinal endothelial cells (hRECs), the engineered, membrane-tethered variants eVEGF-38 and eVEGF-53 provide a lasting VEGF signal that induces cell proliferation and survival, increases endothelial permeability, promotes the formation of a cord/tube network, and stimulates the formation of elongated filopodia on the endothelial cells. The engineered VEGF variants activate VEGFR2, MAPK/ERK, and the Rho GTPase mediators CDC42 and ROCK, activities that are required for the formation of the elongated filopodia. The sustained, pro-angiogenic activities induced by eVEGF-38 and eVEGF-53 support the potential of engineered VEGF variants-overexpressing endothelial cells as a novel combination of gene and cell-based therapeutic strategy for stimulating endothelial cell-autologous therapeutic angiogenesis.

The impact of complete versus partial preservation of the sub-valvular apparatus on left ventricular function in mitral valve replacement.

INTRODUCTION: In mitral valve replacement (MVR), sudden increases in afterload and disruption of the annular-chordal-papillary-left-ventricular wall causes left ventricular (LV) dysfunction in the early postoperative period. Preservation of the posterior mitral leaflet apparatus (MVR-P) has a favorable outcome on LV function. However, there is paucity of data on the impact of complete preservation of the sub-valvular apparatus (MVR-C). OBJECTIVE: We investigated the impact of MVR-P and MVR-C on baseline and 3-months postoperative LV ejection fraction (EF) and global longitudinal strain (GLS). METHODS: We retrospectively analyzed a cohort of 29 MVR-P and 19 MVR-C patients with complete echocardiography data at our unit, who were operated between 2008 and 2017. Between-group changes in LVEF and GLS were compared using independent sample T-test. RESULTS: Median age was 59 years (IQR 50-69 years). Baseline LVEF was 58% (51%- 60%). Baseline GLS was -18.4 (-21.2 to -15.5). There were no significant between-group differences between all baseline demographics and echocardiographic markers. There was significantly higher absolute postoperative LVEF in MVR-C patients (p = 0.029). There was also significant worsening in LVEF (p = 0.0121) and GLS (p < 0.0001) after MVR-P and not MVR-C, suggesting no reduction in LV function post-MVR-C but a reduction post-MVR-P. There was significantly less postoperative worsening of GLS per patient in MVR-C group as compared to the MVR-P group (p = 0.023), indicating better preservation of LV function. There was also a smaller decline in LVEF per patient in the MVR-C as compared to the MVR-P group, although not statistically significant (p = 0.23). CONCLUSION: MVR with complete preservation of the sub-valvular apparatus shows a favorable impact on the longitudinal function of the heart at 3 months. Further studies with larger patient numbers are indicated to investigate the long-term results of this surgical approach.

ADAM10 and ADAM17 proteases mediate proinflammatory cytokine-induced and constitutive cleavage of endomucin from the endothelial surface.

Contact between inflammatory cells and endothelial cells (ECs) is a crucial step in vascular inflammation. Recently, we demonstrated that the cell-surface level of endomucin (EMCN), a heavily O-glycosylated single-transmembrane sialomucin, interferes with the interactions between inflammatory cells and ECs. We have also shown that, in response to an inflammatory stimulus, EMCN is cleared from the cell surface by an unknown mechanism. In this study, using adenovirus-mediated overexpression of a tagged EMCN in human umbilical vein ECs, we found that treatment with tumor necrosis factor α (TNF-α) or the strong oxidant pervanadate leads to loss of cell-surface EMCN and increases the levels of the C-terminal fragment of EMCN 3- to 4-fold. Furthermore, treatment with the broad-spectrum matrix metalloproteinase inhibitor batimastat (BB94) or inhibition of ADAM metallopeptidase domain 10 (ADAM10) and ADAM17 with two small-molecule inhibitors, GW280264X and GI254023X, or with siRNA significantly reduced basal and TNFα-induced cell-surface EMCN cleavage. Release of the C-terminal fragment of EMCN by TNF-α treatment was blocked by chemical inhibition of ADAM10 alone or in combination with ADAM17. These results indicate that cell-surface EMCN undergoes constitutive cleavage and that TNF-α treatment dramatically increases this cleavage, which is mediated predominantly by ADAM10 and ADAM17. As endothelial cell-surface EMCN attenuates leukocyte-EC interactions during inflammation, we propose that EMCN is a potential therapeutic target to manage vascular inflammation.

Obesity and risk of age-related eye diseases: a systematic review of prospective population-based studies.

BACKGROUND: Obesity is a public health challenge worldwide. The relationship between obesity and age-related eye diseases including cataract, glaucoma, age-related macular degeneration (AMD) and diabetic retinopathy (DR) have remained elusive. DESIGN AND METHODS: We conducted a systematic review of three electronic databases for longitudinal population-based studies that described associations between measures of obesity including body mass index (BMI), waist-circumference (WC), and waist-to-hip ratio (WHR), and age-related eye diseases. RESULTS: Our search yielded 1731 articles, of which 14, 10, 16 and 8 articles met our eligibility criteria for cataract, glaucoma, AMD and DR, respectively. BMI-defined obesity was positively associated with incident cataract, incident AMD and incident DR in Western populations, but in Asian populations associations for incident AMD were not significant and associations for incident DR were inverse. WC-defined obesity was associated with incident glaucoma in non-Western populations. WHR-defined obesity but not BMI-defined obesity was associated with the incidence or progression of AMD in two Western studies. CONCLUSIONS: Overall, we found strong evidence supporting associations between obesity and age-related eye diseases. Further research on the association of abdominal obesity and effect of weight loss and physical activity on age-related eye diseases is warranted to support clinical and public health recommendations.

Glycocalyx regulation of vascular endothelial growth factor receptor 2 activity.

We have previously shown that knockdown of endomucin (EMCN), an integral membrane glycocalyx glycoprotein, prevents VEGF-induced proliferation, migration, and tube formation in vitro and angiogenesis in vivo. In the endothelium, VEGF mediates most of its angiogenic effects through VEGF receptor 2 (VEGFR2). To understand the role of EMCN, we examined the effect of EMCN depletion on VEGFR2 endocytosis and activation. Results showed that although VEGF stimulation promoted VEGFR2 internalization in control endothelial cells (ECs), loss of EMCN prevented VEGFR2 endocytosis. Cell surface analysis revealed a decrease in VEGFR2 following VEGF stimulation in control but not siRNA directed against EMCN-transfected ECs. EMCN depletion resulted in heightened phosphorylation following VEGF stimulation with an increase in total VEGFR2 protein. These results indicate that EMCN modulates VEGFR2 endocytosis and activity and point to EMCN as a potential therapeutic target.-LeBlanc, M. E., Saez-Torres, K. L., Cano, I., Hu, Z., Saint-Geniez, M., Ng, Y.-S., D'Amore, P. A. Glycocalyx regulation of vascular endothelial growth factor receptor 2 activity.

Indications of sole lift and foot orthoses in the management of mild idiopathic scoliosis-a review.

[Purpose] Leg length discrepancy is common among patients with scoliosis. Some studies reported reduced functional scoliosis curves with correction of leg length discrepancy. Others, however, have shown that induced leg length discrepancy has little effects on spinal deformities. Also, small number of studies assessed the use of foot orthoses in patients with faulty foot biomechanics and their impact on idiopathic scoliosis. In this context, a review of the literature is needed to determine the current evidence for the appropriate use of sole lift and foot orthoses in a context of scoliosis. [Methods] A literature review was performed. [Results] It appeared that sole lifts are indicated for functional lumbar scoliosis when the level of the sacrum is parallel to that of the hips. Sole lifts may not be indicated for patients with structural scoliosis, seemingly inducing a compensatory curve. Custom foot orthoses were found to reduce spinal curves in juvenile patients with mild idiopathic scoliosis and concomitant abnormal foot biomechanics. [Conclusion] Sole lift appeared to be indicated in the presence of certain types of functional scoliosis. Custom foot orthoses can be considered in the management of mild idiopathic scoliosis in juvenile patients. Evidence, however, is low and quality studies are needed to validate these findings.

A Proinflammatory Function of Toll-Like Receptor 2 in the Retinal Pigment Epithelium as a Novel Target for Reducing Choroidal Neovascularization in Age-Related Macular Degeneration.

Current treatments for choroidal neovascularization, a major cause of blindness for patients with age-related macular degeneration, treat symptoms but not the underlying causes of the disease. Inflammation has been strongly implicated in the pathogenesis of choroidal neovascularization. We examined the inflammatory role of Toll-like receptor 2 (TLR2) in age-related macular degeneration. TLR2 was robustly expressed by the retinal pigment epithelium in mouse and human eyes, both normal and with macular degeneration/choroidal neovascularization. Nuclear localization of NF-κB, a major downstream target of TLR2 signaling, was detected in the retinal pigment epithelium of human eyes, particularly in eyes with advanced stages of age-related macular degeneration. TLR2 antagonism effectively suppressed initiation and growth of spontaneous choroidal neovascularization in a mouse model, and the combination of anti-TLR2 and antivascular endothelial growth factor receptor 2 yielded an additive therapeutic effect on both area and number of spontaneous choroidal neovascularization lesions. Finally, in primary human fetal retinal pigment epithelium cells, ligand binding to TLR2 induced robust expression of proinflammatory cytokines, and end products of lipid oxidation had a synergistic effect on TLR2 activation. Our data illustrate a functional role for TLR2 in the pathogenesis of choroidal neovascularization, likely by promoting inflammation of the retinal pigment epithelium, and validate TLR2 as a novel therapeutic target for reducing choroidal neovascularization.

Phytoremediation capabilities of Spirodela polyrhiza, Salvinia molesta and Lemna sp. in synthetic wastewater: A comparative study.

Macrophytes have been used to mitigate eutrophication and upgrade effluent quality via their nutrient removal capability. However, the available data are influenced by factors such as microbial activities, weather, and wastewater quality, making comparison between nutrient removal performance of different macrophytes almost impossible. In this study, phytoremediation by Spirodela polyrhiza, Salvinia molesta and Lemna sp. were carried out axenically in synthetic wastewater under controlled condition to precisely evaluate nutrient removal efficiency of NO3--N, PO43-, NH3-N, COD and pH in the water sample. The results showed that ammonia removal was rapid, significant for S. polyrhiza and Lemna sp., with efficiency of 60% and 41% respectively within 2 days. S. polyrhiza was capable of reducing 30% of the nitrate. Lemna sp. achieved the highest phosphate reduction of 86% at day 12 to mere 1.07 mg/L PO43--P. Correlation was found between COD and TC, suggesting the release of organic substances by macrophytes into the medium. All the macrophytes showed biomass increment. S. polyrhiza outperformed other macrophytes in nutrient removal despite lower biomass production. The acquired nutrient removal profiles can serve as a guideline for the selection of suitable macrophytes in wastewater treatment and to evaluate microbial activity in non-aseptic phytoremediation system.

Canine and feline cutaneous screw-worm myiasis in Malaysia: clinical aspects in 76 cases.

BACKGROUND: Cutaneous screw-worm myiasis in companion animals either due to the New World screw-worm, Cochliomyia hominivorax or the Old World screw-worm, Chrysomya bezziana, has been reported particularly in tropical and subtropical regions of the world. Although treatment of screw-worm myiasis in dogs has been described, few studies have been conducted regarding its clinical and epidemiological aspects in companion animals. OBJECTIVES: To describe clinical and epidemiological aspects of canine and feline screw-worm myiasis. ANIMALS: Naturally infested dogs and cats, presented to five veterinary clinics in four Malaysian states from September 2017 to February 2018. METHODS AND MATERIALS: Cutaneous screw-worm myiasis was diagnosed based on clinical signs and visual examination of burrowing larvae within lesion. Age, breed, gender, anatomical site of infestation and suspected underlying predisposing causes were investigated. RESULTS: A total of 55 dogs and 21 cats were included in the study. Intact male mixed breed dogs (mean age 58 months) and intact male domestic short hair cats (mean age 24 months) with suspected fight-related wounds were most commonly presented with exudative and ulcerative lesions associated with screw-worm myiasis. The most common anatomical sites of infestation in the dogs were the external ear canals, followed by the perineum and medial canthus. For the cats, the most commonly affected areas were paws and tail. Five cats with screw-worm myiasis were concurrently infected with sporotrichosis. CONCLUSION AND CLINICAL RELEVANCE: Aggression between unneutered animals is a likely underlying cause for cutaneous screw-worm myiasis in both cats and dogs. Sporotrichosis was also a potential predisposing cause for screw-worm myiasis in cats.

Novel CCR3 Antagonists Are Effective Mono- and Combination Inhibitors of Choroidal Neovascular Growth and Vascular Permeability.

Choroidal neovascularization (CNV) is a defining feature of wet age-related macular degeneration. We examined the functional role of CCR3 in the development of CNV in mice and primates. CCR3 was associated with spontaneous CNV lesions in the newly described JR5558 mice, whereas CCR3 ligands localized to CNV-associated macrophages and the retinal pigment epithelium/choroid complex. Intravitreal injection of neutralizing antibodies against vascular endothelial growth factor receptor 2, CCR3, CC chemokine ligand 11/eotaxin-1, and CC chemokine ligand 24/eotaxin-2 all reduced CNV area and lesion number in these mice. Systemic administration of the CCR3 antagonists GW766994X and GW782415X reduced spontaneous CNV in JR5558 mice and laser-induced CNV in mouse and primate models in a dose-dependent fashion. Combination treatment with antivascular endothelial growth factor receptor 2 antibody and GW766994X yielded additive reductions in CNV area and hyperpermeability in mice. Interestingly, topical GW766994X and intravitreal anti-CCR3 antibody yielded strong systemic effects, reducing CNV in the untreated, contralateral eye. Contrarily, ocular administration of GW782415X in primates failed to substantially elevate plasma drug levels or to reduce the development of grade IV CNV lesions. These findings suggest that CCR3 signaling may be an attractive therapeutic target for CNV, utilizing a pathway that is at least partly distinct from that of vascular endothelial growth factor receptor. The findings also demonstrate that systemic exposure to CCR3 antagonists may be crucial for CNV-targeted activity.

Killer cell immunoglobulin receptor profile on CD4(+) CD28(-) T cells and their pathogenic role in non-dialysis-dependent and dialysis-dependent chronic kidney disease patients.

There is a progressive increase in cardiovascular disease with declining renal function, unexplained by traditional risk factors. A CD4(+) T-cell subpopulation (CD4(+)  CD28(-) ), activated by human heat-shock protein 60 (hHSP 60), expands in patients with acute coronary syndrome and is associated with vascular damage. These cells exhibit cytotoxicity via expression of activating killer cell-immunoglobulin-like receptor KIR2DS2, mainly in the absence of inhibitory KIR2DL3. We investigated expansion of these cells and the pathogenic role of the KIR in non-dialysis-dependent chronic kidney disease (NDD-CKD) and end-stage haemodialysis-dependent renal disease (HD-ESRD) patients. CD4(+)  CD28(-) cells were present in 27% of the NDD-CKD and HD-ESRD patients (8-11% and 10-11% of CD4(+) compartment, respectively). CD4(+)  CD28(-) cells were phenotyped for KIR and DAP12 expression. Cytotoxicity was assessed by perforin and pro-inflammatory function by interferon-γ expression on CD4(+)  CD28(-) clones (NDD-CKD n = 97, HD-ESRD n = 262). Thirty-four per cent of the CD4(+)  CD28(-) cells from NDD-CKD expressed KIR2DS2 compared with 56% in HD-ESRD patients (P = 0·03). However, 20% of clones expressed KIR2DL3 in NDD-CKD compared with 7% in HD-ESRD patients (P = 0·004). DAP12 expression in CD28(-)  2DS2(+) clones was more prevalent in HD-ESRD than NDD-CKD (92% versus 60%; P < 0·001). Only 2DS2(+)  2DL3(-)  DAP12(+) clones were cytotoxic in response to hHSP 60. CD4(+)  CD28(-) cells exhibited increased KIR2DS2, reduced KIR2DL3 and increased DAP12 expression in HD-ESRD compared with NDD-CKD patients. These findings suggest a gradual loss of expression, functionality and protective role of inhibitory KIR2DL3 as well as increased cytotoxic potential of CD4(+)  C28(-) cells with progressive renal impairment. Clonal expansion of these T cells may contribute to heightened cardiovascular events in HD-ESRD.

Why don't poor men eat fruit? Socioeconomic differences in motivations for fruit consumption.

BACKGROUND: Those of lower socioeconomic status (SES) tend to have less healthy diets than those of higher SES. This study aimed to assess whether differences in motivations for particular foods might contribute to socioeconomic differences in consumption. METHODS: Participants (n = 732) rated their frequency of consumption and explicit liking of fruit, cake and cheese. They reported eating motivations (e.g., health, hunger, price) and related attributes of the investigated foods (healthiness, expected satiety, value for money). Participants were randomly assigned to an implicit liking task (Single Category Implicit Association Task) for one food category. Analyses were conducted separately for different SES measures (income, education, occupational group). RESULTS: Lower SES and male participants reported eating less fruit, but no SES differences were found for cheese or cake. Analyses therefore focused on fruit. In implicit liking analyses, results (for income and education) reflected patterning in consumption, with lower SES and male participants liking fruit less. In explicit liking analyses, no differences were found by SES. Higher SES participants (all indicators) were more likely to report health and weight control and less likely report price as motivators of food choices. For perceptions of fruit, no SES-based differences were found in healthiness whilst significant interactions (but not main effects) were found (for income and education) for expected satiety and value for money. Neither liking nor perceptions of fruit were found to mediate the relationship between SES and frequency of fruit consumption. CONCLUSIONS: There is evidence for social patterning in food motivation, but differences are modified by the choice of implicit or explicit measures. Further work should clarify the extent to which these motivations may be contributing to the social and gender patterning in diet.

Priming healthy eating. You can't prime all the people all of the time.

OBJECTIVE: In the context of a food purchasing environment filled with advertising and promotions, and an increased desire from policy makers to guide individuals toward choosing healthier foods, this study tests whether priming methods that use healthy food adverts to increase preference for healthier food generalize to a representative population. METHODS: In two studies (Study 1 n = 143; Study 2 n = 764), participants were randomly allocated to a prime condition, where they viewed fruit and vegetable advertisements, or a control condition, with no advertisements. A subsequent forced choice task assessed preference between fruits and other sweet snacks. Additional measures included current hunger and thirst, dietary restraint, age, gender, education and self-reported weight and height. RESULTS: In Study 1, hunger reduced preferences for fruits (OR (95% CI) = 0.38 (0.26-0.56), p <0.0001), an effect countered by the prime (OR (95% CI) = 2.29 (1.33-3.96), p = 0.003). In Study 2, the effect of the prime did not generalize to a representative population. More educated participants, as used in Study 1, chose more fruit when hungry and primed (OR (95% CI) = 1.42 (1.13-1.79), p = 0.003), while less educated participants' fruit choice was unaffected by hunger or the prime. CONCLUSION: This study provides preliminary evidence that the effects of adverts on healthy eating choices depend on key individual traits (education level) and states (hunger), do not generalize to a broader population and have the potential to increase health inequalities arising from food choice.