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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]

Pulmonary hypertension (PH) can cause breathing difficulty, a rapid decline of exercise capacity, heart failure, and eventually death of the patients. The latest epidemiological study demonstrates that PH has a much higher incidence than previously thought. PH is still a highly fatal disease due to the many disadvantages of the current drugs, such as short half-life, lack of targeting, and potent side effects. The PH pathological features offer great opportunities for nanomedicines for PH. Recently, emerging nanomedicines demonstrated great advantages in the therapeutic effect of PH by enhancing the accumulation of drugs in PH lesion, optimizing drug efficacy, and minimizing drug side effects. However, this promising field of cross-cutting research is far from being widely explored due to the huge professional barriers. To solve this problem, we provide a comprehensive review for the latest progresses of nanomedicines in the treatment of PH. Firstly, we systematical summarized the PH pathological features and the current clinical drug treatment of PH. The advantages of nanomedicines are also deeply discussed in the treatment of PH. Subsequently, we focused on the research progresses of nanomedicines in PH through three aspects: advanced nano-drug delivery system for traditional drugs and new target drugs, gene therapy-based nanomedicines, and other nanomedicines for the treatment of PH. Finally, we also discussed the prospects and challenges for the clinical application of nanomedicines in PH, and provided directions for the research and development of nanomedicines for PH treatment in the future. [ABSTRACT FROM AUTHOR]

This paper describes the introduction of an open-access preprint server in China covering 43 disciplines. The system includes mandatory deposit for state-funded research and reports on the repository and its effectiveness and outlines a novel process of peer-review of preprints in the repository, which can be incorporated into the established system of promotion and tenure. This state-initiated innovation is considered to have been well incorporated into the established scientific communication system despite the sociological differences between the various disciplines served by the repository. (Contains 3 figures and 2 tables.)

Purpose: Sentiment lexicon is an essential resource for sentiment analysis of user reviews. By far, there is still a lack of domain sentiment lexicon with large scale and high accuracy for Chinese book reviews. This paper aims to construct a large-scale sentiment lexicon based on the ultrashort reviews of Chinese books. Design/methodology/approach: First, large-scale ultrashort reviews of Chinese books, whose length is no more than six Chinese characters, are collected and preprocessed as candidate sentiment words. Second, non-sentiment words are filtered out through certain rules, such as part of speech rules, context rules, feature word rules and user behaviour rules. Third, the relative frequency is used to select and judge the polarity of sentiment words. Finally, the performance of the sentiment lexicon is evaluated through experiments. Findings: This paper proposes a method of sentiment lexicon construction based on ultrashort reviews and successfully builds one for Chinese books with nearly 40,000 words based on the Douban book. Originality/value: Compared with the idea of constructing a sentiment lexicon based on a small number of reviews, the proposed method can give full play to the advantages of data scale to build a corpus. Moreover, different from the computer segmentation method, this method helps to avoid the problems caused by immature segmentation technology and an imperfect N-gram language model. [ABSTRACT FROM AUTHOR]

Atherosclerotic cardiovascular disease is a major cause of morbidity and mortality in the Western world. Despite tremendous strides in understandings its pathogenesis, it still remains a challenge because of gaps in our understanding of its initiation, progression and complications leading to the clinical syndromes of angina, acute coronary syndrome, cerebrovascular disease and peripheral vascular disease. Recent studies have provided impetus on the shift from models of atherosclerosis based on cellular interactions to models where the important role of extracellular matrix is recognized. Proteoglycans, especially those belonging to the small leucine-rich proteoglycan family of which decorin is a representative example, have come under close scrutiny for their role in atherogenesis. There is evidence from in vitro and in vivo animal models as well as humans to suggest an important role of decorin in attenuating progression of atherosclerosis. Decorin distribution in different blood vessels has been shown to inversely correlate with the tendency to develop atherosclerosis. Decorin seems to interact closely with different cellular components of the plaque milieu, thereby suggesting its role in influencing atherogenesis at different steps. Here we review the current understanding of the role of decorin in the pathogenesis of atherosclerosis. [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]

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]

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]

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]

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]