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Platelet over-activation is one of the important mechanisms of atherosclerosis （AS） in diabetes mellitus. Dietary nutrient intervention plays an important role in the primary prevention and treatment of diabetes mellitus combined with AS. Studies have shown that the antiplatelet factor in tomato extract can inhibit platelet aggregation and activation in different environments. Its bioactive ingredient are nucleosides and derivatives and phenolic compounds， which retard the pathological progress of diabetes mellitus complicated with AS. This review aims to explore the mechanism of the antiplatelet effect of tomato extract， and to provide a theoretical basis for the prevention and treatment of diabetes mellitus complicated with AS.

Lung cancer progression relies on angiogenesis, which is a response to hypoxia typically coordinated by hypoxia- inducible transcription factors (HIFs), but growing evidence indicates that transcriptional programs beyond HIFs control tumor angiogenesis. Here, we show that the redox-sensitive transcription factor BTB and CNC homology 1 (BACH1) controls the transcription of a broad range of angiogenesis genes. BACH1 is stabilized by lowering ROS levels; consequently, angiogenesis gene expression in lung cancer cells, tumor organoids, and xenograft tumors increased substantially following administration of vitamins C and E and N-acetylcysteine in a BACH1-dependent fashion under normoxia. Moreover, angiogenesis gene expression increased in endogenous BACH1-overexpressing cells and decreased in SACH7-knockout cells in the absence of antioxidants. BACH1 levels also increased upon hypoxia and following administration of prolyl hydroxylase inhibitors in both HfF7A-knockout and WT cells. BACH1 was found to be a transcriptional target of HIF1[alpha], but BACH1's ability to stimulate angiogenesis gene expression was HIF1[alpha] independent. Antioxidants increased tumor vascularity in vivo in a BACH1- dependent fashion, and overexpressing BACH1 rendered tumors sensitive to antiangiogenesis therapy. BACH1 expression in tumor sections from patients with lung cancer correlated with angiogenesis gene and protein expression. We conclude that BACH1 is an oxygen- and redox-sensitive angiogenesis transcription factor., Introduction Lung tumor growth and metastasis requires angiogenesis--the formation of new blood vessels (1, 2). Angiogenesis is typically triggered by hypoxia, which stabilizes hypoxia-inducible transcription factors (HIFs) including HIF1[alpha] and [...]

The bond–slip behavior of concrete pile–cemented soil interface is crucial for load transfer analysis of stiffened deep cement mixing piles, which is greatly influenced by ground temperature and age during long-term curing. However, the thermal–temporal effect on the frictional characteristics of this interface remains unclear. In this paper, an element-scale specimen of concrete pile–cemented soil interface was first designed. Then interfacial shear tests were performed on batches of samples subjected to varied curing temperatures (T) and ages (t) to obtain interfacial bond–slip (τ‒s) curves. The test results showed that the interfacial peak shear strength (τu) increased with the growth of T and t. Based on the experimental observations, a strength development model for τu considering the thermal effect was established. Subsequently, a disturbed state concept (DSC)-based constitutive model incorporating the thermal–temporal effect was proposed for the investigated interface. Both prepeak and postpeak stages of the τ‒s curves can be effectively described by the developed DSC model, exhibiting robust performance in fitting and predicting experimental results. Finally, the DSC model was cross-validated by the interfacial τ‒s data sets collected from reported experimental publications. Across all data sets, the coefficient of determination (R2) exceeded 0.9, and the mean absolute percentage error of τu remained below 10% when comparing predictions with measurements, which strongly highlights the generalization capability of the DSC model. [ABSTRACT FROM AUTHOR]

The experiment aims to determine the nutritional components of reed mushroom foot waste and evaluate its nutritional value. The conventional feed nutrient determination method was used to measure the content of crude protein, crude fat, moisture, crude ash, and main trace elements in reed mushroom foot waste. The internationally accepted non-biological evaluation method was used to assess the nutritional value of protein. The results showed that the reed mushroom foot waste contained 24.76% crude protein, 0.29% crude fat, 11.78% moisture and 7.46% crude ash, the content of main mineral elements in reed mushroom foot waste was Cu 57 mg/kg, Fe 212 mg/kg, Mn 31 mg/kg and Zn 66 mg/kg. A total of 17 kinds of amino acids were detected in reed mushroom foot waste. The ratio of essential amino acids (EAA) to the total amino acids (TAA) was 0.40, and the ratio of non-essential amino acids (NEAA) to TAA was 0.60. The results of AAS showed that the first limiting amino acid was valine, the second limiting amino acid was methionine, and the third limiting amino acid was methionine + cystine. The EAARR score of reed mushroom foot waste was 66.5%, and the GRG method score was 0.78. The study indicates that reed mushroom foot waste can be used as a high quality protein feed raw material, which has the value of development and application. [ABSTRACT FROM AUTHOR]

Accurate and sensitive near‐infrared (NIR) luminescent lateral flow immunoassay (LFIA) has attracted considerable attention in the field of point‐of‐care testing (POCT). However, the detection accuracy and sensitivity are often compromised by the low fluorescence quantum efficiency (<10%) of the NIR fluorescent probe. Herein, ultrabright NIR AIEgen nanoparticles (PS@AIE830NPs) composed of polystyrene (PS) nanoparticles and NIR aggregation‐induced emission luminogen (AIEgen) with the maximum emission at 830 nm (AIE830) is reported, and its potential to promote an accurate and sensitive detection of complex samples by LFIA is described. The relative quantum yield (QY) of the PS@AIE830NPs was 14.76%, which was superior to that of the polymer embedding method and indocyanine green (ICG)‐based NIR nanoparticles. The PS@AIE830NPs immunolabeled‐LFIA combined with laboratory‐built NIR‐LFIA portable quantitative instruments (detected light range > 800 nm) completely eliminated background interference and allowed highly accurate and sensitive detection without any pre‐treatment steps. The limits of detection (LODs) for aflatoxin B1 (AFB1) in soy sauce, alpha hemolysin (Hla) of Staphylococcus aureus biomarker in joint fluid, and C‐reactive protein (CRP) in human haemolysed samples were 0.01 ng mL−1, 0.02 µg mL−1, and 0.156 mg L−1, respectively, commensurating with those of the corresponding gold standard assays and covering the detection range of interests. It is anticipated that the ultrabright NIR AIEgen nanoparticles will serve as a universally applicable signal probe for NIR‐LFIA diagnostics, promising to expand the range of applications for quantitative detection of complex samples. [ABSTRACT FROM AUTHOR]

This paper provides evidence of confirmation bias by sell-side analysts in their earnings forecasts. We show that analysts tend to put higher weight on public information when the current forecast consensus is more consistent with their previous forecasts. We further find that analysts with better past forecasting performance, longer firm-specific experience, or forecasting earlier, tend to be more subject to confirmation bias, consistent with some of the existing cognitive and social psychology theories. The results remain significant after controlling for analyst incentives. Finally, we distinguish evidence of confirmation bias from that of other important behavioral biases such as conservative bias. [ABSTRACT FROM AUTHOR]

BACKGROUND Increased reactive oxygen species (ROS) and oxidative stress response lead to cardiomyocyte hypertrophy and apoptosis, which play crucial roles in the pathogenesis of heart failure. The purpose of current research was to explore the role of antioxidant N -acetylcysteine (NAC) on cardiomyocyte dysfunction and the underlying molecular mechanisms. METHODS AND RESULTS Compared with control group without NAC treatment, NAC dramatically inhibited the cell size of primary cultured neonatal rat cardiomyocytes (NRCMs) tested by immunofluorescence staining and reduced the expression of representative markers associated with hypertrophic, fibrosis and apoptosis subjected to phenylephrine administration examined by reverse transcription-polymerase chain reaction (RT-PCR) and western blot. Moreover, enhanced ROS expression was attenuated, whereas activities of makers related to oxidative stress response examined by individual assay Kits, including total antioxidation capacity (T-AOC), glutathione peroxidase (GSH-Px), and primary antioxidant enzyme Superoxide dismutase (SOD) were induced by NAC treatment in NRCMs previously treated with phenylephrine. Mechanistically, we noticed that the protein expression levels of phosphorylated phosphatidylinositol 3-kinase (PI3K) and AKT were increased by NAC stimulation. More importantly, we identified that the negative regulation of NAC in cardiomyocyte dysfunction was contributed by PI3K/AKT signaling pathway through further utilization of PI3K/AKT inhibitor (LY294002) or agonist (SC79). CONCLUSIONS Collected, NAC could attenuate cardiomyocyte dysfunction subjected to phenylephrine, partially by regulating the ROS-induced PI3K/AKT-dependent signaling pathway. [ABSTRACT FROM AUTHOR]

Background: Frailty appears to be associated with unfavorable prognosis after stroke in observational studies, but the causality remains largely unknown. Aims: The aim of this study is to investigate the potential causal effect of frailty on functional outcome at 3 months after ischemic stroke using the Mendelian randomization (MR) framework. Methods: Genetic instruments for frailty index were identified in a genome-wide association study meta-analysis including 175,226 individuals of European descent. Corresponding genetic association estimates for functional outcome after ischemic stroke at 90 days were taken from the Genetic of Ischemic Stroke Functional Outcome (GISCOME) network of 6021 patients. We performed inverse-variance weighted MR as the main analyses, followed by several alternate methods and sensitivity analyses. Results: In univariable MR, we found evidence that genetically predicted higher frailty index (odds ratio (OR) = 5.12; 95% confidence interval (CI) = 1.31–20.09; p = 0.019) was associated with worse functional outcome (modified Rankin Scale score ⩾3) after ischemic stroke. In further multivariable MR adjusting for potential confounding traits including body mass index, C-reactive protein, inflammatory bowel disease, and smoking initiation, the overall patterns between genetic liability to frailty and poor functional outcome status remained. Sensitivity analyses with complementary methods and with model unadjusted for baseline stroke severity (OR = 4.19; 95% CI = 1.26–13.90; p = 0.019) yielded broadly concordant results. Conclusions: The present MR study suggested a possible causal effect of frailty on poor functional outcome after ischemic stroke. Frailty might represent a potential target for intervention to improve recovery after ischemic stroke. [ABSTRACT FROM AUTHOR]

Recently macrophage polarization has emerged as playing an essential role in the oathogenesis of atherosclerosis, which is the most important underlying process in many types of cardiovascular diseases. Although Nek6 has been reported to be involved in various cellular processes, the effect of Nek6 on macrophage polarization remains unknown. Macrophages exposed to lipopolysaccharide (LPS) or IL‐4 were used to establish an in vitro model for the study of regulation of classically (M1) or alternatively (M2) activated macrophage. Bone marrow‐derived macrophages (BMDMs) transfected with short hairpin RNA‐targeting Nek6 were then in functional studies. We observed that Nek6 expression was decreased in both peritoneal macrophages (PMs) and BMDMs stimulated by LPS. This effect was seen at both mRNA and protein level. The opposite results were obtained after administration of IL‐4. Macrophage‐specific Nek6 knockdown significantly exacerbated pro‐inflammatory M1 polarized macrophage gene expression in response to LPS challenge, but the anti‐inflammatory response gene expression that is related to M2 macrophages was attenuated by Nek6 silencing followed by treatment with IL‐4. Mechanistic studies exhibited that Nek6 knockdown inhibited the phosphorylated STAT3 expression that mediated the effect on macrophage polarization regulated by AdshNek6. Moreover, decreased Nek6 expression was also observed in atherosclerotic plaques. Collectively, these evidences suggested that Nek6 acts as a crucial site in macrophage polarization, and that this operates in a STAT3‐dependent manner. [ABSTRACT FROM AUTHOR]