Optimizing Parametric Factors in CIELAB and CIEDE2000 Color-Difference Formulas for 3D-Printed Spherical Objects.

The current color-difference formulas were developed based on 2D samples and there is no standard guidance for the color-difference evaluation of 3D objects. The aim of this study was to test and optimize the CIELAB and CIEDE2000 color-difference formulas by using 42 pairs of 3D-printed spherical samples in Experiment I and 40 sample pairs in Experiment II. Fifteen human observers with normal color vision were invited to attend the visual experiments under simulated D65 illumination and assess the color differences of the 82 pairs of 3D spherical samples using the gray-scale method. The performances of the CIELAB and CIEDE2000 formulas were quantified by the STRESS index and F-test with respect to the collected visual results and three different optimization methods were performed on the original color-difference formulas by using the data from the 42 sample pairs in Experiment I. It was found that the optimum parametric factors for CIELAB were kL = 1.4 and kC = 1.9, whereas for CIEDE2000, kL = 1.5. The visual data of the 40 sample pairs in Experiment II were used to test the performance of the optimized formulas and the STRESS values obtained for CIELAB/CIEDE2000 were 32.8/32.9 for the original formulas and 25.3/25.4 for the optimized formulas. The F-test results indicated that a significant improvement was achieved using the proposed optimization of the parametric factors applied to both color-difference formulas for 3D-printed spherical samples.

Spectral Reconstruction Using an Iteratively Reweighted Regulated Model from Two Illumination Camera Responses.

An improved spectral reflectance estimation method was developed to transform captured RGB images to spectral reflectance. The novelty of our method is an iteratively reweighted regulated model that combines polynomial expansion signals, which was developed for spectral reflectance estimation, and a cross-polarized imaging system, which is used to eliminate glare and specular highlights. Two RGB images are captured under two illumination conditions. The method was tested using ColorChecker charts. The results demonstrate that the proposed method could make a significant improvement of the accuracy in both spectral and colorimetric: it can achieve 23.8% improved accuracy in mean CIEDE2000 color difference, while it achieves 24.6% improved accuracy in RMS error compared with classic regularized least squares (RLS) method. The proposed method is sufficiently accurate in predicting the spectral properties and their performance within an acceptable range, i.e., typical customer tolerance of less than 3 DE units in the graphic arts industry.

Age-related and gender-stratified differences in the association between high triglyceride and risk of hyperuricemia.

BACKGROUND: Elevated serum uric acid is commonly associated with high triglyceride. However, the relation of triglyceride and hyperuricemia in different gender and age groups is currently not well understood. This study aimed to evaluate age- and gender-related association of high triglyceride with hyperuricemia in a subgroup of Chinese population. METHODS: We retrospectively analyzed physical examination data of 24,438 subjects (12,557 men and 11,881 women) in Kaifeng, China. The alanine aminotransferase, γ-glutamyl transpeptidase, serum creatinine, blood urea nitrogen, total cholesterol, high-density lipoprotein cholesterol, triglyceride and serum uric acid were measured in all subjects. The triglyceride was categorized into < 1.21, 1.21 ~, 1.7 ~, 2.83 ~ and >  5.6 mmol/L subgroups, and odds ratio (OR) and 95% confidence interval (CI) of hyperuricemia were calculated by logistic regression analysis. RESULTS: Univariate and age-adjusted analyses showed that high triglyceride was positively associated with hyperuricemia (p <  0.01). Further age-stratified analysis showed that the positive association was significant in the 20 ~, 30 ~, 40 ~, 50 ~, 60 ~ and 80 ~ age groups in men. In women, no statistically significant was found in 60 ~ and 70 ~ age groups. CONCLUSION: High triglyceride is positively associated with hyperuricemia in both men and women, and this association is age-related, especially in women.

Retracted Article: MicroRNA-135a alleviates lipid accumulation and inflammation of atherosclerosis through targeting lipoprotein lipase.

MicroRNAs (miRNAs) have recently attracted increasing attention for their involvement in atherosclerosis (AS). The purpose of this study was to further explore the function and underlying mechanism of miR-135a in AS progression. The expression levels of miR-135a and lipoprotein lipase (LPL) mRNA were detected by qRT-PCR, and LPL protein expression was measured by western blotting. The levels of blood lipids and inflammatory cytokines, and LPL activity were assessed using corresponding Assay Kits, and an HPLC assay was used to determine the levels of free cholesterol (FC), total cholesterol (TC) and cholesterol ester (CE). A Dil-oxLDL binding assay was performed to evaluate the ability of cholesterol uptake. The direct interaction between miR-135a and LPL was confirmed by a dual-luciferase reporter assay and RNA immunoprecipitation assay. Our data indicated that miR-135a was downregulated in serum samples of AS patients and mice. Upregulation of miR-135a alleviated lipid metabolic disorders and inflammation in AS mice. Moreover, miR-135a negatively regulated lipid accumulation and inflammation in ox-LDL-treated THP-1 macrophages. Mechanistically, miR-135a directly targeted LPL and repressed LPL expression. LPL mediated the regulatory effect of miR-135a on lipid accumulation and inflammation in ox-LDL-treated THP-1 macrophages. In conclusion, our study indicated that miR-135a upregulation ameliorated lipid accumulation and inflammation at least partly by targeting LPL in THP-1 macrophages, highlighting miR-135a as a potential antiatherogenic agent.

MicroRNA-30c-5p inhibits NLRP3 inflammasome-mediated endothelial cell pyroptosis through FOXO3 down-regulation in atherosclerosis.

Atherosclerosis is a chronic inflammatory disease involved in endothelial dysfunction. Pyroptosis is a pro-inflammatory form of cell death and plays pivotal roles in atherosclerosis. MicroRNAs (miRNAs) are implicated in atherosclerosis, however the mechanisms that underlie miR-30c-5p is required for endothelial cell pyroptosis remain elusive. In the present study, we probed the interaction of miR-30c-5p with forkhead box O3 (FOXO3) and investigated the effect of miR-30c-5p and FOXO3 on NLRP3 inflammasome and endothelial cell pyroptosis. Introduction of oxidized low density lipoprotein (ox-LDL) dose-dependently increased lactate dehydrogenase (LDH) release as well as pyroptosis in human aortic endothelial cells (HAECs). On the basis of ox-LDL treatment, we found the expression of miR-30c-5p was impaired and enrichment of miR-30c-5p protected HAECs from ox-LDL-induced pyroptosis. Moreover, addition of miR-30c-5p inhibited ox-LDL-activated NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome, which was associated with HEACs pyroptosis. Nevertheless, miR-30c-5p failed to show efficacy of Toll-like receptor (TLR) signaling of NLRP3 inflammasome activation. Intriguingly, FOXO3 was suggested to be targeted by miR-30c-5p and addition of miR-30c-5p blocked FOXO3 expression, whereas miR-30c-5p depletion showed opposite effects. Furthermore, silencing of FOXO3 inhibited NLRP3-mediated pyroptosis and reversed anti-miR-30c-5p-induced activation of NLRP3 inflammasome and pyroptosis in HEACs with ox-LDL treatment. Our finding suggested that miR-30c-5p might play essential role in NLRP3 inflammasome-modulated cell pyroptosis by targeting FOXO3 in HAECs, providing a novel therapeutic avenue for atherosclerosis treatment.

Downregulation of microRNA­34a inhibits oxidized low­density lipoprotein­induced apoptosis and oxidative stress in human umbilical vein endothelial cells.

Oxidized low­density lipoprotein (ox­LDL) promotes endothelial cell dysfunction, which is a primary risk factor for the development of atherosclerosis. A previous study reported that microRNA (miRNA/miR)­34a is upregulated in atherosclerotic samples. However, its function and underlying mechanisms remain to be fully elucidated. In the present study, miRNA microarray analysis was performed to investigate the miRNA expression profile in atherosclerotic plaque tissues and examine the role of miR­34a in ox­LDL­induced apoptosis of human umbilical vein endothelial cells (HUVECs). Cell viability, apoptosis and protein expression was determined by a cell counting kit­8 assay, flow cytometry and western blot analysis, respectively. It was observed that miR­34a was upregulated in atherosclerotic plaque tissues and that ox­LDL treatment significantly increased the levels of miR­34a in a dose­dependent manner in the HUVECs. The knockdown of miR­34a increased the protein expression of B­cell lymphoma 2 (Bcl­2) and cell viability, improved mitochondrial membrane potential, and decreased the activity of caspase­3, number of apoptotic cells and release of cytochrome c from mitochondria in the ox­LDL­treated HUVECs. The results also demonstrated that the knockdown of miR­34a suppressed the levels of ox­LDL­induced reactive oxygen species (ROS) in HUVECs. Additionally, it was found that Bcl­2 was a target of miR­34a in HUVECs, and that silencing Bcl­2 abrogated the protective effects of the downregulation of miR­34a on ox­LDL­induced apoptosis. These data indicated that the knockdown of miR­34a protected against ox­LDL apoptosis and ROS in HUVECs via inhibiting the mitochondrial apoptotic pathway, suggesting it may offer potential as a biomarker in the clinical diagnosis and as a target for the treatment of atherosclerosis.

H19 knockdown suppresses proliferation and induces apoptosis by regulating miR-148b/WNT/ß-catenin in ox-LDL -stimulated vascular smooth muscle cells.

BACKGROUND: Long non-coding RNAs (lncRNAs) have been identified as critical regulators in the development of atherosclerosis (AS). Here, we focused on discussing roles and molecular mechanisms of lncRNA H19 in vascular smooth muscle cells (VSMCs) progression. METHODS: RT-qPCR assay was used to detect the expression patterns of H19 and miR-148b in clinical samples and cells. Cell proliferative ability was evaluated by CCK-8 and colony formation assays. Cell apoptotic capacity was assessed by apoptotic cell percentage and the caspase-3 activity. Bioinformatics analysis, luciferase and RNA immunoprecipitation (RIP) assays were employed to demonstrate cell percentage and the relationship among H19, miR-148b and wnt family member 1 (WNT1). Western blot assay was performed to determine expressions of proliferating cell nuclear antigen (PCNA), ki-67, Bax, Bcl-2, WNT1, ß-catenin, C-myc and E-cadherin. RESULTS: The level of H19 was increased and miR-148b expression was decreased in human AS patient serums and oxidized low-density lipoprotein (ox-LDL)-stimulated human aorta vascular smooth muscle cells (HA-VSMCs). H19 knockdown suppressed proliferation and promoted apoptosis in HA-VSMCs following the treatment of ox-LDL. H19 inhibited miR-148b expression by direct interaction. Moreover, miR-148b inhibitor could reverse the effects of H19 depletion on proliferation and apoptosis in ox-LDL-stimulated HA-VSMCs. Further mechanical explorations showed that WNT1 was a target of miR-148b and H19 acted as a competing endogenous RNA (ceRNA) of miR-148b to enhance WNT1 expression. Furthermore, miR-148 inhibitor exerted its pro-proliferation and anti-apoptosis effects through activating WNT/ß-catenin signaling in ox-LDL-stimulated HA-VSMCs. CONCLUSION: H19 facilitated proliferation and inhibited apoptosis through modulating WNT/ß-catenin signaling pathway via miR-148b in ox-LDL-stimulated HA-VSMCs, implicating the potential values of H19 in AS therapy.

TUG1 knockdown ameliorates atherosclerosis via up-regulating the expression of miR-133a target gene FGF1.

BACKGROUND: Long non-coding RNAs (lncRNAs) have been revealed to participate in the pathological events associated with atherosclerosis. However, the exact role of lncRNA taurine-up-regulated gene 1 (TUG1) and its possible molecular mechanism in atherosclerosis remain unidentified. METHODS: High-fat diet (HFD)-treated ApoE-/- mice were used as an in vivo model of atherosclerosis. Ox-LDL-induced macrophages and vascular smooth muscle cells (VSMCs) were employed as cell models of atherosclerosis. qRT-PCR was performed to detect the expression of TUG1 and miR-133a. Serum levels of total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) were analyzed by commercially available enzyme kits. Oil red O and hematoxylin and eosin (H&E) staining were conducted to examine atherosclerotic lesion. Luciferase reporter assay combined with RNA immunoprecipitation (RIP) was applied to confirm the interaction between TUG1, miR-133a and FGF1. Cell proliferation ability was determined by Cell Counting Kit-8 (CCK-8) assay and trypan blue dye exclusion test. Cell apoptosis was evaluated with TUNEL assay. Expression and production of inflammatory cytokines was measured with western blot and ELISA analysis. RESULTS: TUG1 expression was up-regulated in HFD-treated ApoE-/- mice, as well as in ox-LDL-induced RAW264.7 and MOVAS cells. TUG1 knockdown inhibited hyperlipidemia, decreased inflammatory response, and attenuated atherosclerotic lesion in HFD-treated ApoE-/- mice. TUG1 could function as a molecular sponge of miR-133a to suppress its expression. TUG1 overexpression accelerated cell growth, improved inflammatory factor expression, and inhibited apoptosis in ox-LDL-stimulated RAW264.7 and MOVAS cells, while this effect was abated after transfection with miR-133 mimic. Moreover, fibroblast growth factor 1 (FGF1) was identified as a direct target of miR-133a. Restored expression of FGF1 overturned the effect of miR-133a on cell proliferation, inflammatory factor secretion and apoptosis in ox-LDL-treated RAW264.7 and MOVAS cells. Finally, TUG1 was revealed to up-regulate FGF1 expression by sponging miR-133a. CONCLUSION: TUG1 knockdown ameliorates atherosclerosis by modulating FGF1 via miR-133a, raising the possibility of targeting TUG1 as an atheroprotective therapeutic strategy.

MIAT promotes proliferation and hinders apoptosis by modulating miR-181b/STAT3 axis in ox-LDL-induced atherosclerosis cell models.

BACKGROUND: Plenty of lncRNAs and microRNAs have been identified to be critical mediators in the progression of atherosclerosis (AS). Myocardial infarction-associated transcript (MIAT) were aberrantly high expressed and closely associated with the pathogenesis of AS. However, its molecular mechanism has not been well characterized. METHODS: The expression patterns of MIAT and microRNA-181b (miR-181b) in clinical samples and cells were measured by RT-qPCR assays. Luciferase reporter assay and RIP assays were used to manifest the potential interaction between MIAT, miR-181b and signal transducer and activator of transcription 3 (STAT3). Cell Counting Kit-8 (CCK-8), Propidium Iodide (PI) staining, Terminal dexynucleotidyl transferase(TdT)-mediated dUTP nick end labeling (TUNEL) and western blot assays were carried out to detect cell proliferation, cell cycle distribution, apoptosis, and STAT3 protein level, respectively. RESULTS: MIAT expression was up-regulated and miR-181b expression was down-regulated in AS patients serum and oxidized low-density lipoprotein (ox-LDL) induced AS cells model. MIAT facilitated cell proliferation, accelerated cell cycle progression and inhibited apoptosis in ox-LDL-induced AS cell lines, while this effect was partly reversed by miR-181b overexpression. Moreover, MIAT enhanced STAT3 expression through sequestering miR-181b as a molecular sponge. Furthermore, MiR-181b hindered cell growth, induced cell cycle arrest and promoted apoptosis by directly targeting STAT3. CONCLUSION: MIAT performed as an induction factor of AS by regulating miR-181b/STAT3 axis in ox-LDL-induced AS cell lines, offering a new insight into the potential application of MIAT in AS treatment.

Inflammatory potential of diet and risk of cardiovascular disease or mortality: A meta-analysis.

Inconsistent findings have reported on the inflammatory potential of diet and cardiovascular disease (CVD) and mortality risk. The aim of this meta-analysis was to investigate the association between the inflammatory potential of diet as estimated by the dietary inflammatory index (DII) score and CVD or mortality risk in the general population. A comprehensive literature search was conducted in PubMed and Embase databases through February 2017. All prospective observational studies assessing the association of inflammatory potential of diet as estimated by the DII score with CVD and all-cause, cancer-related, cardiovascular mortality risk were included. Nine prospective studies enrolling 134,067 subjects were identified. Meta-analyses showed that individuals with the highest category of DII (maximal pro-inflammatory) was associated with increased risk of all-cause mortality (hazard risk [HR] 1.22; 95% confidence interval [CI] 1.06-1.41), cardiovascular mortality (RR 1.24; 95% CI 1.01-1.51), cancer-related mortality (RR 1.28; 95% CI 1.04-1.58), and CVD (RR 1.32; 95% CI 1.09-1.60) than the lowest DII score. More pro-inflammatory diets, as estimated by the higher DII score are independently associated with an increased risk of all-cause, cardiovascular, cancer-related mortality, and CVD in the general population, highlighting low inflammatory potential diet may reduce mortality and CVD risk.

AT1 Receptor Modulator Attenuates the Hypercholesterolemia-Induced Impairment of the Myocardial Ischemic Post-Conditioning Benefits.

BACKGROUND AND OBJECTIVES: Ischemic post-conditioning (PostC) has been demonstrated as a novel strategy to harness nature's protection against myocardial ischemia-reperfusion (I/R). Hypercholesterolemia (HC) has been reported to block the effect of PostC on the heart. Angiotensin II type-1 (AT1) modulators have shown benefits in myocardial ischemia. The present study investigates the effect of a novel inhibitor of AT1, azilsartan in PostC of the heart of normocholesterolemic (NC) and HC rats. MATERIALS AND METHODS: HC was induced by the administration of high-fat diet to the animals for eight weeks. Isolated Langendorff's perfused NC and HC rat hearts were exposed to global ischemia for 30 min and reperfusion for 120 min. I/R-injury had been assessed by cardiac hemodynamic parameters, myocardial infarct size, release of tumor necrosis factor-alpha troponin I, lactate dehydrogenase, creatine kinase, nitrite in coronary effluent, thiobarbituric acid reactive species, a reduced form of glutathione, superoxide anion, and left ventricle collagen content in normal and HC rat hearts. RESULTS: Azilsartan post-treatment and six episodes of PostC (10 sec each) afforded cardioprotection against I/R-injury in normal rat hearts. PostC protection against I/R-injury was abolished in HC rat hearts. Azilsartan prevented the HC-mediated impairment of the beneficial effects of PostC in I/R-induced myocardial injury, which was inhibited by L-N5-(1-Iminoethyl)ornithinehydrochloride, a potent inhibitor of endothelial nitric oxide synthase (eNOS). CONCLUSION: Azilsartan treatment has attenuated the HC-induced impairment of beneficial effects of PostC in I/R-injury of rat hearts, by specifically modulating eNOS. Azilsartan may be explored further in I/R-myocardial injury, both in NC and HC conditions, with or without PostC.

Hs-CRP and all-cause, cardiovascular, and cancer mortality risk: A meta-analysis.

BACKGROUND AND AIMS: Inconsistent findings have been reported on the association between high-sensitivity C-reactive protein (hs-CRP) and mortality risk. The objective of this meta-analysis was to investigate the association of elevated baseline hs-CRP levels with all-cause, cardiovascular, and cancer mortality risk in the general population. METHODS: PubMed and Embase were systematically searched for studies published from inception to October 2016. Prospective observational studies were eligible if they reported the effects of elevated baseline hs-CRP levels on cancer-related, cardiovascular or all-cause mortality in the general population. The pooled adjusted risk ratio (RR) with 95% confidence interval (CI) comparing the highest to the lowest category of hs-CRP levels was used as association measures. RESULTS: A total of 83,995 participants from 14 studies were identified. When comparing the highest to the lowest category of hs-CRP levels, the pooled RR was 1.25 (95% CI 1.13-1.38) for cancer-related mortality, 2.03 (95% CI 1.65-2.50) for cardiovascular mortality, and 1.75 (1.55-1.98) for all-cause mortality, respectively. Subgroup analysis showed that the effect of elevated hs-CRP levels on cancer-related mortality was observed in men (RR 1.26; 95% CI 1.11-1.43) but not in women (RR 1.03; 95% CI 0.83-1.27). CONCLUSIONS: Elevated hs-CRP levels can independently predict risk of all-cause, cardiovascular mortality in the general population. However, the gender differences in the predictive role of hs-CRP on cancer mortality should to be further investigated.

Effects of different routes of tirofiban injection on the left ventricular function and prognosis of patients with myocardial infarction treated with percutaneous coronary intervention.

The aim of this study was to investigate the effect of different routes of tirofiban injection on the function of the left ventricle and the prognosis of patients with myocardial infarction (MI) treated with percutaneous coronary intervention (PCI). Ninety-five patients with MI treated with PCI were divided into two groups [coronary (n=49) and intravenous (n=46)] according to the injection route. A comparison of the left ventricular function and prognosis was made between the two groups following PCI. The success rate of PCI in the coronary group was 97.96%, which was higher than that in the intravenous group (P<0.05). No significant differences were identified in the platelet count (PLT) and platelet aggregation rate (PAR) between the two groups prior to the tirofiban injection. Following the tirofiban injection, the PLT decreased markedly in both groups, with no significant differences between them. The PAR also decreased significantly in the two groups; however, the value in the coronary group was lower than that in the intravenous group (P<0.05). The improvements in the thrombolysis in MI grades, left ventricular ejection fraction and left ventricular diastolic function were greater in the coronary group than those in the intravenous group (P<0.05). All patients received follow-up for 30 days and the incidence of bleeding in the coronary group was lower than that in the intravenous group (P<0.05). No significant differences were recorded in the recurrence rates of MI, arrhythmia, myocardial ischemia, thrombocytopenia and mortality between the two groups. In conclusion, the administration of tirofiban into the coronary artery could effectively improve the blood flow, left ventricular function and prognosis of patients with MI treated with PCI.

Robust and highly sensitive fluorescence approach for point-of-care virus detection based on immunomagnetic separation.

In this work, robust approach for a highly sensitive point-of-care virus detection was established based on immunomagnetic nanobeads and fluorescent quantum dots (QDs). Taking advantage of immunomagnetic nanobeads functionalized with the monoclonal antibody (mAb) to the surface protein hemagglutinin (HA) of avian influenza virus (AIV) H9N2 subtype, H9N2 viruses were efficiently captured through antibody affinity binding, without pretreatment of samples. The capture kinetics could be fitted well with a first-order bimolecular reaction with a high capturing rate constant k(f) of 4.25 × 10(9) (mol/L)(-1) s(-1), which suggested that the viruses could be quickly captured by the well-dispersed and comparable-size immunomagnetic nanobeads. In order to improve the sensitivity, high-luminance QDs conjugated with streptavidin (QDs-SA) were introduced to this assay through the high affinity biotin-streptavidin system by using the biotinylated mAb in an immuno sandwich mode. We ensured the selective binding of QDs-SA to the available biotin-sites on biotinylated mAb and optimized the conditions to reduce the nonspecific adsorption of QDs-SA to get a limit of detection low up to 60 copies of viruses in 200 µL. This approach is robust for application at the point-of-care due to its very good specificity, precision, and reproducibility with an intra-assay variability of 1.35% and an interassay variability of 3.0%, as well as its high selectivity also demonstrated by analysis of synthetic biological samples with mashed tissues and feces. Moreover, this method has been validated through a double-blind trial with 30 throat swab samples with a coincidence of 96.7% with the expected results.