Study on consumers' motivation to buy green food based on meta-analysis

IntroductionThere exists a noticeable gap between consumers' willingness to purchase green food and their actual purchase behavior. However, the awareness of green development is a crucial factor influencing this purchase behavior and acts as an internal driving force promoting green consumption. Consumers' green development awareness is shaped by various psychological motivations, including environmental concern, health consciousness, knowledge, norms, and price considerations. The existing literature often focuses on specific regions or groups, lacking comprehensive cross-regional and multivariate evaluations, and frequently overlooks the potential impact of moderating variables such as economic development level, product type, and behavior type.MethodsTo clarify the overall effect of each motivational factor on green food purchase behavior, this study conducted a meta-analysis. We selected eight causal variables and three moderating variables that significantly influence consumers' green food purchase behavior. The analysis included 132 independent effect values from 45 research papers.ResultsThe meta-analysis revealed that: Consumers' green food purchase behavior is significantly positively correlated with eight motivational factors: environmental awareness, health awareness, green attitude, green knowledge, subjective norms, price awareness, perceived behavior control, and perceived usefulness. Economic development level, product type, and behavior type significantly affect consumers' green food purchase behavior. The impact of motivational factors on actual purchase behavior is weaker than on purchase intention, suggesting that interventions should focus on converting purchase intentions into actual purchase behavior. The findings indicate that environmental responsibility, government policies, and marketing strategies can influence consumers' psychological motives, guiding them toward more responsible consumption choices.DiscussionEnhancing consumers' environmental and health awareness is essential, and policy support and marketing strategies can effectively promote green food consumption. These insights underscore the importance of targeted interventions to bridge the gap between green purchase intention and behavior

Coronary artery disease as an independent predictor of short-term and long-term outcomes in patients with type-B aortic dissection undergoing thoracic endovascular repair

Background and aimsPrevious studies reported a high prevalence of concomitant coronary artery disease (CAD) in patients with Type B aortic dissection (TBAD). However, there is too limited data on the impact of CAD on prognosis in patients with TBAD. The present study aimed to assess the short-term and long-term impact of CAD on patients with acute or subacute TBAD undergoing thoracic endovascular aortic repair (TEVAR).MethodsWe retrospectively evaluated 463 patients with acute or subacute TBAD undergoing TEVAR from a prospectively maintained database from 2010 to 2017. CAD was defined before TEVAR by coronary angiography. Multivariable logistic and cox regression analyses were performed to evaluate the relationship between CAD and the short-term as well as long-term outcomes.ResultsAccording to the results of coronary angiography, the 463 patients were divided into the following two groups: CAD group (N = 148), non-CAD group (N = 315). In total, 12 (2.6%) in-hospital deaths and 54 (12%) all-cause deaths following a median follow-up of 48.1 months were recorded. Multivariable analysis revealed that CAD was an independent predictor of in-hospital major adverse clinical events (MACE) (odd ratio [OR], 2.33; 95% confidence interval [CI], 1.07–5.08; p = 0.033), long-term mortality [hazard ratio (HR), 2.11, 95% CI, 1.19–3.74, P = 0.011] and long-term MACE (HR, 1.95, 95% CI, 1.26–3.02, P = 0.003). To further clarify the relationship between the severity of CAD and long-term outcomes, we categorized patients into three groups: zero-vessel disease, single-vessel disease and multi-vessel disease. The long-term mortality (9.7 vs. 14.4 vs. 21.2%, P = 0.045), and long-term MACE (16.8 vs. 22.2 vs. 40.4%, P = 0.001) increased with the number of identified stenosed coronary vessels. Multivariable analysis indicated that, multi-vessel disease was independently associated with long-term mortality (HR, 2.38, 95% CI, 1.16–4.89, P = 0.018) and long-term MACE (HR, 2.79, 95% CI, 1.65–4.73, P = 0.001), compared with zero-vessel disease.ConclusionsCAD was associated with short-term and long-term worse outcomes in patients with acute or subacute TBAD undergoing TEVAR. Furthermore, the severity of CAD was also associated with worse long-term prognosis. Therefore, CAD could be considered as a useful independent predictor for pre-TEVAR risk stratification in patients with TBAD

A simple prediction model to estimate obstructive coronary artery disease

BackgroundA simple noninvasive model to predict obstructive coronary artery disease (OCAD) may promote risk stratification and reduce the burden of coronary artery disease (CAD). This study aimed to develop pre-procedural, noninvasive prediction models that better estimate the probability of OCAD among patients with suspected CAD undergoing elective coronary angiography (CAG).MethodsWe included 1262 patients, who had reliable Framingham risk variable data, in a cohort without known CAD from a prospective registry of patients referred for elective CAG. We investigated pre-procedural OCAD (&ge;50% stenosis in at least one major coronary vessel based on CAG) predictors.ResultsA total of 945 (74.9%) participants had OCAD. The final modified Framingham scoring (MFS) model consisted of anemia, high-sensitivity C-reactive protein, left ventricular ejection fraction, and five Framingham factors (age, sex, total and high-density lipoprotein cholesterol, and hypertension). Bootstrap method (1000 times) revealed that the model demonstrated a good discriminative power (c statistic, 0.729&thinsp;&plusmn;&thinsp;0.0225; 95% CI, 0.69&ndash;0.77). MFS provided adequate goodness of fit (P&thinsp;=&thinsp;0.43) and showed better performance than Framingham score (c statistic, 0.703 vs. 0.521; P&thinsp;&lt;&thinsp;0.001) in predicting OCAD, thereby identifying patients with high risks for OCAD (risk score&thinsp;&ge;&thinsp;27) with &ge;70% predictive value in 68.8% of subjects (range, 37.2&ndash;87.3% for low [&le;17] and very high [&ge;41] risk scores).ConclusionOur data suggested that the simple MFS risk stratification tool, which is available in most primary-level clinics, showed good performance in estimating the probability of OCAD in relatively stable patients with suspected CAD; nevertheless, further validation is needed.<br /

Characterisation of fibroblast-like synoviocytes from a murine model of joint inflammation

INTRODUCTION: Fibroblast-like synoviocytes (FLS) play a central role in defining the stromal environment in inflammatory joint diseases. Despite a growing use of FLS isolated from murine inflammatory models, a detailed characterisation of these cells has not been performed. METHODS: In this study, FLS were isolated from inflamed joints of mice expressing both the T cell receptor transgene KRN and the MHC class II molecule Ag7 (K/BxN mice) and their purity in culture determined by immunofluorescence and real-time reverse transcription polymerase chain reaction (real-time RT-PCR). Basal expression of proinflammatory genes was determined by real-time RT-PCR. Secreted interleukin 6 (IL-6) was measured by enzyme-linked immunosorbent assay (ELISA), and its regulation by tumor necrosis factor-alpha (TNF-α and corticosterone (the major glucocorticoid in rodents) measured relative to other mesenchymal cell populations. RESULTS: Purity of FLS culture was identified by positive expression of fibronectin, prolyl 4-hydroxylase, cluster of differentiation 90.2 (CD90.2) and 248 (CD248) in greater than 98% of the population. Cultured FLS were able to migrate and invade through matrigel, a process enhanced in the presence of TNF-α. FLS isolated from K/BxN mice possessed significantly greater basal expression of the inflammatory markers IL-6, chemokine ligand 2 (CCL-2) and vascular cell adhesion molecule 1 (VCAM-1) when compared to FLS isolated from non-inflamed tissue (IL-6, 3.6 fold; CCL-2, 11.2 fold; VCAM-1, 9 fold; P < 0.05). This elevated expression was abrogated in the presence of corticosterone at 100 nmol/l. TNF-α significantly increased expression of all inflammatory markers to a much greater degree in K/BxN FLS relative to other mesenchymal cell lines (K/BxN; IL-6, 40.8 fold; CCL-2, 1343.2 fold; VCAM-1, 17.8 fold; ICAM-1, 13.8 fold; P < 0.05), with secreted IL-6 mirroring these results (K/BxN; con, 169 ± 29.7 versus TNF-α, 923 ± 378.8 pg/ml/1 × 10(5 )cells; P < 0.05). Dose response experiments confirmed effective concentrations between 10 and 100 nmol/l for corticosterone and 1 and 10 ng/ml for TNF-α, whilst inflammatory gene expression in FLS was shown to be stable between passages four and seven. CONCLUSIONS: This study has established a well characterised set of key inflammatory genes for in vitro FLS culture, isolated from K/BxN mice and non-inflamed wild-type controls. Their response to both pro- and anti-inflammatory signalling has been assessed and shown to strongly resemble that which is seen in human FLS culture. Additionally, this study provides guidelines for the effective characterisation, duration and treatment of murine FLS culture

LIS1 determines cleavage plane positioning by regulating actomyosin-mediated cell membrane contractility

Heterozygous loss of human PAFAH1B1 (coding for LIS1) results in the disruption of neurogenesis and neuronal migration via dysregulation of microtubule (MT) stability and dynein motor function/localization that alters mitotic spindle orientation, chromosomal segregation, and nuclear migration. Recently, human induced pluripotent stem cell (iPSC) models revealed an important role for LIS1 in controlling the length of terminal cell divisions of outer radial glial (oRG) progenitors, suggesting cellular functions of LIS1 in regulating neural progenitor cell (NPC) daughter cell separation. Here we examined the late mitotic stages NPCs in vivo and mouse embryonic fibroblasts (MEFs) in vitro from Pafah1b1-deficient mutants. Pafah1b1-deficient neocortical NPCs and MEFs similarly exhibited cleavage plane displacement with mislocalization of furrow-associated markers, associated with actomyosin dysfunction and cell membrane hyper-contractility. Thus, it suggests LIS1 acts as a key molecular link connecting MTs/dynein and actomyosin, ensuring that cell membrane contractility is tightly controlled to execute proper daughter cell separation

An Id-like molecule, HHM, is a synexpression group-restricted regulator of TGF-β signalling

Transforming growth factor (TGF)-β induces various cellular responses principally through Smad-dependent transcriptional regulation. Activated Smad complexes cooperate with transcription factors in regulating a group of target genes. The target genes controlled by the same Smad-cofactor complexes are denoted a synexpression group. We found that an Id-like helix-loop-helix protein, human homologue of Maid (HHM), is a synexpression group-restricted regulator of TGF-β signalling. HHM suppressed TGF-β-induced growth inhibition and cell migration but not epithelial–mesenchymal transition. In addition, HHM inhibited TGF-β-induced expression of plasminogen activator inhibitor-type 1 (PAI-1), PDGF-B, and p21WAF, but not Snail. We identified a basic-helix-loop-helix protein, Olig1, as one of the Smad-binding transcription factors affected by HHM. Olig1 interacted with Smad2/3 in response to TGF-β stimulation, and was involved in transcriptional activation of PAI-1 and PDGF-B. HHM, but not Id proteins, inhibited TGF-β signalling-dependent association of Olig1 with Smad2/3 through physical interaction with Olig1. HHM thus appears to regulate a subset of TGF-β target genes including the Olig1-Smad synexpression group. HHM is the first example of a cellular response-selective regulator of TGF-β signalling with clearly determined mechanisms

DISC1 genetics, biology and psychiatric illness

Psychiatric disorders are highly heritable, and in many individuals likely arise from the combined effects of genes and the environment. A substantial body of evidence points towards DISC1 being one of the genes that influence risk of schizophrenia, bipolar disorder and depression, and functional studies of DISC1 consequently have the potential to reveal much about the pathways that lead to major mental illness. Here, we review the evidence that DISC1 influences disease risk through effects upon multiple critical pathways in the developing and adult brain

Correlation of left ventricular longitudinal strain and E/e’ ratio in primary hypertension patients

Objectives: The aim of this study is to explore and compare the relationships of both global longitudinal strain (GLS) and strain (SR) with E/e’ ratio in a population of asymptomatic patients with systemic hypertension. Methods: Retrospectively included 210 cases of essential hypertension patients. Dynamic images were analyzed for left ventricular myocardial systolic global longitudinal strain (GLS), left ventricular longitudinal peak systolic strain rate (SRs), early diastolic peak strain rate (SRe), late diastolic peak strain rate (SRa). According to the 2012 baseline E/e’ ratio, the population was divided into three groups, group A (E/e’14). Results: Systolic function parameters left ventricular ejection fraction (LVEF) remained at normal rage and no different, but patients with elevated E/e’ ratio had significantly lower GLS, lower early diastolic strain rate(SRe), lower ratio of early diastolic strain rate to late diastolic strain rate (SRe/a) and higher E/SRe. Positive relationships were observed between GLS, E/SRe and E/e’ ratio, inverse relationships were observed between SRe, SRe/a and E/e’ ratio. E/SRe >0.73 had a sensitivity of 87.7% and a specificity of 38.2% for predicting an elevated E/e’ ratio (E/e’>14). In multivariable analysis, IVS-e’ <7 cm/s showed almost 2.5-fold increased risk for decreased GLS (OR 2.48[95% CI 1.36–4.53]; p = 003). Conclusions: Our current study demonstrated that hypertensive patients with preserved LVEF and elevated E/e’ ratio have systolic and diastolic abnormalities in longitudinal directions as detected by speckle imaging. E/SRe correlates well with E/e’ and predicted elevated left ventricular filling pressure

A comprehensive review of an unmet public health issue: resistant hypertension

Resistant hypertension is an intractable problem to patients and physicians. In recent decades, a substantial amount of basic and epidemiological studies provide us a vast number of valuable evidence and information about this once elusive disease. Better understanding about this entity could help physicians improve diagnostic and therapeutic accuracy. In present review, therefore, we first will detail the definition and diagnosis of resistant hypertension between cardiology societies, and followed by the information of prevalence of resistant hypertension around the world, and then briefly discuss currently used different nomenclature of resistant hypertension, and finally present diagnostic and therapeutic strategies of resistant hypertension