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This review addresses the issues of low consumer engagement and market development difficulties in intangible cultural heritage (ICH) products. Dietary ICH products are selected as research materials to discover contemporary commercial survival paths for ICH through the psychological effects of advertising. Firstly, this study examines the respective advantages of rational and emotional ICH advertisement in terms of emotional responses, cognitive responses, attitudes, recall, and recognition. Then, it explores the effects of different ICH advertisement types (rational advertisement, emotional advertisement) and different degrees of situational involvement (purchasing for oneself, purchasing gifts for others) on the advertising effectiveness, aiming to identify factors influencing the psychological effects of ICH advertisement. Through statistical analysis, the main conclusions are as follows: (1) Rational ICH advertisement prompts consumers to consider the actual attributes of ICH products, leading to a more positive purchasing attitude. (2) Emotional ICH advertisement is more effective in eliciting positive emotions from consumers and enhancing brand memory. (3) Under the scenario of purchasing a gift for others, emotional ICH advertisement has a more positive impact on consumers' attitudes towards advertising. (4) Under different degrees of situational involvement, rational ICH advertisement has a more positive impact on consumers' purchasing attitudes. This study not only provides guidance for optimizing ICH advertising strategies but also offers new directions for market expansion, contributing valuable insights into cultural heritage preservation, as well as the development and protection of ICH. [ABSTRACT FROM AUTHOR]

Aims Vascular peroxidase 1 (VPO1) is a newly identified haem-containing peroxidase that catalyses the oxidation of a variety of substrates by hydrogen peroxide (H2O2). Considering the well-defined effects of H2O2 on the vascular remodelling during hypertension, and that VPO1 can utilize H2O2 generated from co-expressed NADPH oxidases to catalyse peroxidative reactions, the aims of this study were to determine the potential role of VPO1 in vascular remodelling during hypertension. Methods and results The vascular morphology and the expression of VPO1 in arterial tissues of spontaneously hypertensive rats and Wistar–Kyoto rats were assessed. The VPO1 expression was significantly increased concomitantly with definite vascular remodelling assessed by evaluating the media thickness, lumen diameter, media thickness-to-lumen diameter ratio and mean nuclear area in artery media in spontaneously hypertensive rats. In addition, in cultured rat aortic smooth muscle cells we found that the angiotensin II-mediated cell proliferation was inhibited by knockdown of VPO1 using small hairpin RNA. Moreover, the NADPH oxidase inhibitor, apocynin, and the hydrogen peroxide scavenger, catalase, but not the ERK1/2 inhibitor, PD98059, attenuated angiotensin II-mediated up-regulation of VPO1 and generation of hypochlorous acid. Conclusion VPO1 is a novel regulator of vascular smooth muscle cell proliferation via NADPH oxidase–H2O2–VPO1–hypochlorous acid–ERK1/2 pathways, which may contribute to vascular remodelling in hypertension. [ABSTRACT FROM PUBLISHER]

Abstract: Seizure is one kind of severe side effects during clozapine (Clo) treatment. However, the mechanism of seizure associated with Clo therapy is not completely clear. Strychnine-sensitive glycine receptors (GlyRs) play an important role in regulating the excitability in the hippocampus. In the present study, we investigated the effect of Clo on GlyRs in cultured hippocampal neurons of rats. Clo reversibly inhibited the glycine-induced chloride currents (I Gly) in a concentration-dependent manner. The half-maximal effect concentration (EC50) for glycine alone was 25.6±0.7 μM with the Hill coefficient 1.5±0.1; in the presence of Clo, the EC50 and the Hill coefficient were 28.9±6.3 μM and 1.2±0.3 respectively, which were not significantly affected by Clo. In addition, Clo inhibition of I Gly was not influenced by blocking D1 and D2 dopamine receptors with haloperidol (Hal). Taken together, these results suggest that Clo is a non-competitive antagonist of GlyR independent of its activation of dopamine receptors, which may contribute to seizure associated with Clo therapy. [Copyright &y& Elsevier]

Abstract: LOX-1, a cell surface lectin-like receptor, is upregulated by oxidized low-density lipoprotein (ox-LDL) and angiotensin II (Ang II), and plays an important role in host defense. The specific C-type lectin domain on LOX-1 is essential for ox-LDL binding and internalization, generation of oxidant species and eliciting immune response. Here, we show that LOX-1 deletion alters genes that relate to immune response. Microarray (and qPCR) analysis of cardiac tissues showed downregulated expression of several immunoglobulins (Igk-V8, Igk-C, Igh-6, Igj, Ighg, Igh, and Igl-V1) in the LOX-1 knockout (KO) mice [p <0.05 vs. the wild-type (WT) mice]. The expression of these immunoglobulins was upregulated several-fold in the LOX-1 KO mice hearts when these mice were infused with Ang II (p <0.05, vs. WT mice). Importantly, cultured mouse HL-1 cardiomyocytes expressed these immunoglobulins, and pretreatment of cardiomyocytes with a specific anti-LOX-1 antibody enhanced the generation of immunoglobulins upon subsequent exposure to Ang II. These observations mirrored the data obtained from WT and LOX-1 KO mice hearts in the resting state and following Ang II infusion. This study provides first set of data on immunoglobulin expression in cardiac tissues of WT and LOX-1 KO mice and in cultured HL-1 cardiomyocytes, and demonstrates that LOX-1 inactivation leads to upregulation of immunoglobulins in cardiomyocytes upon challenge with Ang II. [Copyright &y& Elsevier]

Abstract: Atherogenesis is associated with inflammation and oxidative stress. Activation of renin-angiotensin system with generation of angiotensin II and type 1 receptor (AT1R) stimulation has been amply reported in atherosclerosis. Since angiotensin II type 2 receptor (AT2R) activity is purported to oppose the effects of AT1R, we hypothesized that AT2R (agtr2) over-expression would inhibit atherogenesis. We prepared recombinant adeno-associated virus type-2 (AAV) carrying AT2R cDNA (AAV/AT2R), and homozygous LDLR-deficient (KO) mice were given AAV/AT2R, AAV/Neo or saline. All mice were placed on a high cholesterol diet. After 18 weeks, AT2R was found to be over-expressed systemically in AAV/AT2R-treated mice. Atherogenesis in aorta was reduced in the AAV/AT2R group by ≈50% compared to other LDLR KO mice groups. Expression of NADPH oxidase, nitrotyrosine and NF-κB was increased in aortic tissues of the LDLR KO mice given saline or AAV/Neo, but not in mice with AT2R upregulation. Expression of endothelial nitric oxide synthase (eNOS) and heme-oxygenase-1 (HO-1) was decreased and that of the lectin-like oxidized-LDL receptor (LOX-1) increased in the LDLR KO mice, but not in the mice with AT2R over-expression. Further, Akt-1 phosphorylation was reduced in the LDLR KO mice, but not in the mice with AT2R over-expression. Thus, AT2R upregulation can reduce atherogenesis, possibly by modulating oxidative stress and the pro-inflammatory cascade, mediated via Akt-1. Over-expression of AT2R may be an important therapeutic approach in atherosclerosis. [Copyright &y& Elsevier]

Aims: Collagen, as a component of the extracellular matrix, has been linked to atherosclerotic plaque formation and stability. Activation of LOX-1, a lectin-like oxidized low-density lipoprotein (LDL) receptor-1, exerts a significant role in collagen formation. We examine the hypothesis that LOX-1 deletion may inhibit collagen accumulation in atherosclerotic arteries in LDL receptor (LDLR) knockout (KO) mice. [ABSTRACT FROM PUBLISHER]

Abstract: LOX-1 is a newly described lectin-like receptor for oxidized-LDL (ox-LDL), which is over-expressed in the ischemic myocardium. To examine the pathogenic role of LOX-1 in the determination of ischemia–reperfusion (I–R) injury to the heart, we developed LOX-1 knockout (KO) mice, and subjected these mice to 60 min of left coronary artery occlusion followed by 60 min of reperfusion. I–R in the LOX-1 KO mice resulted in a significant reduction in myocardial injury as well as in accumulation of inflammatory cells in the I–R myocardium and lipid peroxidation (P <0.01 vs. wild-type mice). Concomitantly, there was significant preservation of cardiac function in the LOX-1 KO mice despite I–R (P <0.01 vs. the wild-type mice). The phosphorylation of oxidative stress-sensitive mitogen-activated protein kinase (p38MAPK) and protein kinase B/Akt-1, expression of nitrotyrosine and inducible nitric oxide synthase (iNOS), and superoxide dismutase activity were enhanced during I–R in the wild-type mice. These alterations in p38MAPK, Akt-1 and iNOS were much less pronounced in the LOX-1 KO mice. The superoxide dismutase activity increased further in the LOX-1 KO mice. These observations provide compelling evidence that LOX-1 may be a key modulator of myocardial I–R injury, and its effect is mediated by pro-oxidant signals. LOX-1 may be a potential target for therapy of myocardial ischemic injury. [Copyright &y& Elsevier]

Abstract: Objective: Chronic ischemia is associated with alterations in genes that result in myocardial remodeling. An important biochemical basis of cardiac remodeling is generation of reactive oxygen species (ROS). A few studies have suggested that acute ischemia triggers signals for remodeling. We examined the hypothesis that targeted deletion of lectin-like oxidized-LDL receptor (LOX-1) may inhibit signals related to cardiac remodeling. Methods and results: We generated LOX-1 knockout (KO) mice on C57BL/6 (wild-type mice) background, and subjected wild-type and KO mice to ischemia–reperfusion (I–R). The wild-type mice developed a marked reduction in left ventricular systolic pressure and ±dp/dtmax and an increase in left ventricular end-diastolic pressure following I–R, and this change was much less in the LOX-1 KO mice, indicating preservation of left ventricular function with LOX-1 deletion. There was evidence for marked oxidative stress (NADPH oxidase expression, malondialdehyde and 8-isoprostane) following I–R in the wild-type mice, much less so in the LOX-1 KO mice (P <0.01). In concert, collagen deposition (Masson''s trichrome and Picro-sirius red staining) increased dramatically in the wild-type mice, but only half as much in the LOX-1 KO mice (P <0.01). Collagen staining data was corroborated with procollagen-I expression. Further, fibronectin and osteopontin expression increased in the wild-type mice, but to a much smaller extent in the LOX-1 KO mice (P <0.01). Conclusions: These findings provide compelling evidence that LOX-1 is a key modulator of cardiac remodeling which starts immediately following I–R. [Copyright &y& Elsevier]

By comparing the usage of structural equation model (SEM) and tetra-class model (TCM) in the model structure, data analysis method, and result presentation when evaluating Chinese academic libraries, this study aims to illustrate the strategies in evaluating satisfaction of academic library services. The study sample consists of 353 academic library users who are asked to evaluate 27 Chinese typical academic library service elements. The findings show that SEM could reveal the influence relations among constructs by path coefficients, while TCM focuses on the visual classification and comparison of specific service elements based on their contributions to user satisfaction. These two models are complementary to each other. They can be used for comprehensively showing the influence factors and current situation of service satisfaction, which are valuable and instructive for improving the service quality of a digital library. The results also indicate that a digital library needs to ensure the quality of retrieval service elements and to improve the service capability of information-organizing service elements. Meanwhile, the developments of characteristic resources and library community are critical to the promotion of user satisfaction of academic library service. [ABSTRACT FROM AUTHOR]

Highlights: [•] Most of macrophage accumulation in atherosclerotic tissues is on the adventitial and subendothelial regions of the artery. [•] Macrophage accumulation increases until 12weeks of high cholesterol feeding to mice and then begins to decline. [•] LOX-1 deletion reduces macrophage accumulation by reducing migration potential of these cells. [Copyright &y& Elsevier]

Background: The serum surfactant protein D (SP-D) level is suggested to be a useful biomarker for acute lung injuries and acute respiratory distress syndrome. Whether the serum SP-D level could identify the severity of coronavirus disease 2019 (COVID-19) in the early stage has not been elucidated.Methods: We performed an observational study on 39 laboratory-confirmed COVID-19 patients from The Fourth People's Hospital of Yiyang, Hunan, China. Receiver operating characteristic (ROC) curve analysis, correlation analysis, and multivariate logistic regression model analysis were performed.Results: In the acute phase, the serum levels of SP-D were elevated significantly in severe COVID-19 patients than in mild cases (mean value ± standard deviation (SD), 449.7 ± 125.8 vs 245.9 ± 90.0 ng/mL, P<0.001), while the serum levels of SP-D in the recovery period were decreased dramatically than that in the acute phase (mean value ± SD, 129.5 ± 51.7 vs 292.9 ± 130.7 ng/ml, P<0.001), and so were for the stratified patients. The chest CT imaging scores were considerably higher in the severe group compared with those in the mild group (median value, 10.0 vs 9.0, P = 0.011), while markedly lower in the recovery period than those in the acute phase (median value, 2.0 vs 9.0, P<0.001), and so were for the stratified patients. ROC curve analysis revealed that areas under the curve of lymphocyte counts (LYM), C-reaction protein (CRP), erythrocyte sedimentation rate (ESR), interleukin-6 (IL-6), and SP-D for severe COVID-19 were 0.719, 0.833, 0.817, 0.837, and 0.922, respectively. Correlation analysis showed that the SP-D levels were negatively correlated with LYM (r = - 0.320, P = 0.047), while positively correlated with CRP (r = 0.658, P<0.001), IL-6 (r = 0.471, P = 0.002), the duration of nucleic acid of throat swab turning negative (r = 0.668, P<0.001), chest CT imaging score on admission (r = 0.695, P<0.001) and length of stay (r = 0.420, P = 0.008). Multivariate logistic regression model analysis showed that age (P = 0.041, OR = 1.093) and SP-D (P = 0.008, OR = 1.018) were risk factors for severe COVID-19.Conclusions: Elevated serum SP-D level was a potential biomarker for the severity of COVID-19; this may be useful in identifying patients whose condition worsens at an early stage. [ABSTRACT FROM AUTHOR]

[Display omitted] • g-C 3 N 4 /GO was designed as a metal-free electrocatalyst for uric acid and dopamine. • g-C 3 N 4 /GO showed good electrocatalytic performance for the oxidation of uric acid and dopamine. • The sensor achieved the simultaneous determination of uric acid and dopamine at nanomolar level. • The sensor showed satisfactory reproducibility, selectivity and stability. Graphitic-like carbon nitride/graphene oxide composite nanosheets (g-C 3 N 4 /GO) were synthesized for simultaneous determination of uric acid (UA) and dopamine (DA). The surface features and electrochemical properties of the g-C 3 N 4 /GO were investigated by scanning electron microscopy, X-ray diffraction, cyclic voltammetry and electrochemical impedance spectra. The voltammetric responses of UA and DA were determinated by cyclic voltammetry and differential pulse voltammetry. g-C 3 N 4 /GO had significantly improved electrical conductivity, selective oxidation capacity and electrocatalytic activity. The proposed g-C 3 N 4 /GO modified glassy carbon electrode (GCE) consequently displayed excellent electrocatalytic activity for UA and DA, with a broad linear detection range (0.03–30 μM) and extremely low detection limits (UA 4.6 nM; DA 5.4 nM). The proposed g-C 3 N 4 /GO/GCE also demonstrated excellent reproducibility, selectivity and stability. The levels of UA and DA in human serum were measured by the g-C 3 N 4 /GO/GCE, and then the known concentrations of UA and DA were spiked to the samples, which proved that the recoveries were good. [ABSTRACT FROM AUTHOR]

In pulmonary hypertension (PH), pulmonary arterial smooth muscle cells (PASMCs) are dedifferentiated, undergoing a contractile-to-synthetic phenotypic switching. Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) plays diverse roles in the cardiovascular system, but its contribution to PH remains to be fully defined. The present study was undertaken to explore the role of LOX-1 in PASMCs dedifferentiation in hypoxia-induced pulmonary vascular remodeling and PH. In a rat model of hypoxic PH, pulmonary vascular remodeling was accompanied by increased expression of LOX-1 in pulmonary arteries. In primary rat PASMCs, hypoxia-induced PASMCs dedifferentiation occurred concomitantly with LOX-1 upregulation. Inhibition of LOX-1 by either siRNA knockdown or neutralizing antibody significantly ameliorated PASMCs dedifferentiation. Mechanistically, LOX-1 promotes PASMCs dedifferentiation under hypoxic conditions via ERK1/2-Elk-1/MRTF-A/SRF signaling pathway. In conclusion, our data uncovers an important role of LOX-1 in the maintenance of PASMCs phenotype. Therapeutic targeting of LOX-1/ERK1/2-Elk-1/MRTF-A/SRF signaling axis would be exploited to treat hypoxic PH. [ABSTRACT FROM AUTHOR]

Mulberry leaf, an important traditional Chinese medicine, possesses many biological activities, including effects of anti-obesity. However, which constituents of mulberry leaf are responsible for its anti-adipogenic action is unclear. This study primarily investigated the chemical constituents from mulberry leaf and their bioactivity on the proliferation and differentiation of 3T3-L1 preadipocytes. A new flavane derivative, (2 S )-4′-hydroxy-7-methoxy-8-prenylflavan ( 1 ), together with twelve known compounds including three flavanes ( 2 – 4 ), three chalcones ( 5 – 7 ), two flavones ( 8 – 9 ), two benzofurans ( 10 – 11 ) and two coumarin ( 12 – 13 ) was isolated from mulberry leaf. The structure of the new compound was elucidated by various spectroscopic methods including UV, HR-ESI-MS, 1 H and 13 C NMR and CD. The results of activity screening showed that compound 2 , 6 and 7 inhibited the proliferation and differentiation of 3T3-L1 preadipocytes. [ABSTRACT FROM AUTHOR]

Highlights: [•] VPO1 was over-expressed in hypertensive SHRs as compared to WKY rats. [•] VPO1 over-expression was accompanied by increased oxidative stress. [•] VPO1 over-expression was found to be related to impaired endothelial function. [ABSTRACT FROM AUTHOR]

It is assumed that acute myocardial infarction affects renal function. To study the mechanism, we used mice following permanent ligation of their left coronary artery that results in extensive myocardial infarction. Soon after ligation, there was a marked rise in circulating pro-inflammatory cytokines and malondialdehyde (thiobarbituric acid-positive evidence of lipid peroxidation). Renal function had significantly declined by the third day in association with mild fibrosis, and swelling of glomeruli and tubules. There was a significant increase in the expression of the lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1), interelukin-1β, vascular cell adhesion molecule-1, and thiobarbituric acid-reactive substances in the kidney. Renal function showed some recovery by Day 21; however, there was progressive fibrosis of the kidneys. LOX-1 knockout mice had significantly diminished increases in systemic and renal pro-inflammatory cytokines, malondialdehyde, structural alterations, and decline in renal function than the wild-type mice following ligation of the left coronary artery. Cardiac function and survival rates were also significantly better in the LOX-1 knockout mice than in the wild-type mice. Hence, severe myocardial ischemia results in renal dysfunction and histological abnormalities suggestive of acute renal injury. Thus, LOX-1 is a key modulator among multiple mechanisms underlying renal dysfunction following extensive myocardial infarction. [ABSTRACT FROM AUTHOR]

It is assumed that acute myocardial infarction affects renal function. To study the mechanism, we used mice following permanent ligation of their left coronary artery that results in extensive myocardial infarction. Soon after ligation, there was a marked rise in circulating pro-inflammatory cytokines and malondialdehyde (thiobarbituric acid-positive evidence of lipid peroxidation). Renal function had significantly declined by the third day in association with mild fibrosis, and swelling of glomeruli and tubules. There was a significant increase in the expression of the lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1), interelukin-1β, vascular cell adhesion molecule-1, and thiobarbituric acid-reactive substances in the kidney. Renal function showed some recovery by Day 21; however, there was progressive fibrosis of the kidneys. LOX-1 knockout mice had significantly diminished increases in systemic and renal pro-inflammatory cytokines, malondialdehyde, structural alterations, and decline in renal function than the wild-type mice following ligation of the left coronary artery. Cardiac function and survival rates were also significantly better in the LOX-1 knockout mice than in the wild-type mice. Hence, severe myocardial ischemia results in renal dysfunction and histological abnormalities suggestive of acute renal injury. Thus, LOX-1 is a key modulator among multiple mechanisms underlying renal dysfunction following extensive myocardial infarction. [ABSTRACT FROM AUTHOR]

Abstract: Previous studies have indicated that GABAergic disinhibition contributes to cognitive deficits mediated by NMDA receptor hypofunction in schizophrenia model of rats. However, the underlying mechanism of GABAergic disinhibition in schizophrenia remains elusive. In this study, we found that the maintenance of long term potentiation (LTP) was impaired in the hippocampus of rats with MK-801-induced cognitive impairments. The impairment of LTP maintenance was significantly reversed by picrotoxinin, a specific GABAA receptor-chloride channel blocker and furosemide, a K+–Cl− cotransporter 2 (KCC2) blocker, respectively. Furthermore, immunoblotting results indicated KCC2 expression in hippocampal CA1 of MK-801-treated rats was lower than that of normal rats before LTP induction. Additionally, LTP-accompanied downregulation of KCC2 was prevented in MK-801-treated rats during LTP induction. Our results suggested that KCC2 expression in hippocampal CA1 of MK-801-treated rats was not further decreased by LTP induction because of its low expression caused by MK-801 treatment. Accordingly, GABAergic inhibition was not further decreased during LTP induction due to the depressed basal GABAergic tone in MK-801-treated rats, Therefore, GABAergic disinhibition in MK-801-treated rats restricts the further downregulation of KCC2 during LTP induction and contributes to the stable GABAergic inhibition and the impaired LTP expression. Our results thus reveal the mechanism that GABAergic disinhibition contributes to cognitive deficits. [Copyright &y& Elsevier]

Continuous recruitment and inappropriate activation of platelets in pulmonary arteries contribute to pulmonary vascular remodeling in pulmonary hypertension (PH). Our previous study has demonstrated that lectin like oxidized low-density lipoprotein receptor-1 (LOX-1) regulates the proliferation of pulmonary arterial smooth muscle cells (PASMCs). Phosphatidylserine exposed on the surface of activated platelets is a ligand for LOX-1. However, whether hypoxia-activated platelets stimulate the proliferation and migration of PASMCs by phosphatidylserine/LOX-1 signaling-impelled intercellular communication remains unclear. The present study found that rats treated with hypoxia (10% O 2) for 21 days revealed PH with the activation of platelets and the recruitment of platelets in pulmonary arteries, and LOX-1 knockout inhibited hypoxia-induced PH and platelets activation. Notably, co-incubation of PASMCs with hypoxic PH rats-derived platelets up-regulated LOX-1 expression in PASMCs leading to the proliferation and migration of PASMCs, which was inhibited by the phosphatidylserine inhibitor annexin V or the LOX-1 neutralizing antibody. LOX-1 knockout led to decreased proliferation and migration of PASMCs stimulated by hypoxia-activated platelets. In rats, hypoxia up-regulated the phosphorylation of signal transducer and activator of transcription 3 (Stat3) and the expression of Pim-1 in pulmonary arteries. Hypoxia-activated platelets also up-regulated the phosphorylation of Stat3 and the expression of Pim-1 in PASMCs, which was inhibited by annexin V, the LOX-1 neutralizing antibody, the protein kinase C inhibitor and LOX-1 knockout. In conclusion, we for the first time demonstrated that hypoxia-activated platelets stimulated the proliferation and migration of PASMCs by phosphatidylserine/LOX-1/PKC/Stat3/Pim-1 signaling-impelled intercellular communication, thereby potentially contributing to hypoxic pulmonary vascular remodeling. • Continuous recruitment and inappropriate activation of platelets in PAs contribute to pulmonary vascular remodeling in PH. • Phosphatidylserine (PS) exposed on the surface of activated platelets is a ligand for LOX-1. • PS/LOX-1 signaling-impelled intercellular communication mediating the interaction between platelets and PASMCs is unclear. • Hypoxia-activated platelets stimulated the proliferation and migration of PASMCs by PS/LOX-1/PKC/Stat3/Pim-1signaling. [ABSTRACT FROM AUTHOR]