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Myocardial infarction (MI) is an acute coronary syndrome that refers to tissue infarction of the myocardium. This study aimed to investigate the effect of long intergenic non-protein-coding RNA (lincRNA) ATPase plasma membrane Ca2+ transporting 1 antisense RNA 1 (ATP2B1-AS1) against MI by targeting nuclear factor-kappa-B inhibitor alpha (NFKBIA) and mediating the nuclear factor-kappa-B (NF-κB) signalling pathway. An MI mouse model was established and idenepsied by cardiac function evaluation. It was determined that ATP2B1-AS1 was highly expressed, while NFKBIA was poorly expressed and NF-κB signalling pathway was activated in MI mice. Cardiomyocytes were extracted from mice and introduced with a series of mouse ATP2B1-AS1 vector, NFKBIA vector, siRNA-mouse ATP2B1-AS1 and siRNA-NFKBIA. The expression of NF-κBp50, NF-κBp65 and IKKß was determined to idenepsy whether ATP2B1-AS1 and NFKBIA affect the NF-κB signalling pathway, the results of which suggested that ATP2B1-AS1 down-regulated the expression of NFKBIA and activated the NF-κB signalling pathway in MI mice. Based on the data from assessment of cell viability, cell cycle, apoptosis and levels of inflammatory cytokines, either silencing of mouse ATP2B1-AS1 or overexpression of NFKBIA was suggested to result in reduced cardiomyocyte apoptosis and expression of inflammatory cytokines, as well as enhanced cardiomyocyte viability. Our study provided evidence that mouse ATP2B1-AS1 silencing may have the potency to protect against MI in mice through inhibiting cardiomyocyte apoptosis and inflammation, highlighting a great promise as a novel therapeutic target for MI.
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Infarto del Miocardio/genética , Inhibidor NF-kappaB alfa/genética , ATPasas Transportadoras de Calcio de la Membrana Plasmática/genética , ARN Largo no Codificante/genética , Animales , Apoptosis/genética , Modelos Animales de Enfermedad , Silenciador del Gen , Humanos , Ratones , Infarto del Miocardio/patología , Miocardio/metabolismo , Miocardio/patología , Miocitos Cardíacos/metabolismo , Miocitos Cardíacos/patología , FN-kappa B/genética , Transducción de Señal/genética , Factor de Transcripción ReIA/genéticaRESUMEN
OBJECTIVE: Over the years, the roles of microRNAs (miRNAs) and histone deacetylase 3 (HDAC3) in human diseases have been investigated. This study focused on the effect of miR-19a-3p and HDAC3 in myocardial ischemia-reperfusion (I/R) injury (MIRI) by targeting cyclin-dependent kinase 2 (CDK2). METHODS: The I/R rat models were established by coronary artery ligation, which were then treated with RGFP966 (an inhibitor of HDAC3), miR-19a-3p agomir or antagomir, or silenced CDK2 to explore their roles in the cardiac function, pathological changes of myocardial tissues, myocardial infarction area, inflammatory factors and oxidative stress factors in rats with MIRI. The expression of miR-19a-3p, HDAC3, and CDK2 was determined by RT-qPCR and western blot assay, and the interaction among which was also verified by online prediction, luciferase activity assay and ChIP assay. RESULTS: The results indicated that HDAC3 and CDK2 were upregulated while miR-19a-3p was downregulated in myocardial tissues of I/R rats. The inhibited HDAC3/CDK2 or elevated miR-19a-3p could promote cardiac function, attenuate pathological changes, inflammatory reaction, oxidative stress, myocardial infarction area and apoptosis of myocardial tissues. HDAC3 mediates miR-19a-3p and CDK2 is targeted by miR-19a-3p. CONCLUSION: Inhibited HDAC3 ameliorates MIRI in a rat model by elevating miR-19a-3p and reducing CDK2, which may contribute to the treatment of MIRI.
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Quinasa 2 Dependiente de la Ciclina/antagonistas & inhibidores , Regulación de la Expresión Génica , Histona Desacetilasas/química , MicroARNs/genética , Daño por Reperfusión Miocárdica/prevención & control , Animales , Apoptosis , Masculino , Daño por Reperfusión Miocárdica/etiología , Daño por Reperfusión Miocárdica/metabolismo , Daño por Reperfusión Miocárdica/patología , Miocitos Cardíacos/fisiología , Estrés Oxidativo , Ratas , Ratas Sprague-DawleyRESUMEN
Most face recognition methods employ single-bit binary descriptors for face representation. The information from these methods is lost in the process of quantization from real-valued descriptors to binary descriptors, which greatly limits their robustness for face recognition. In this study, we propose a novel weighted feature histogram (WFH) method of multi-scale local patches using multi-bit binary descriptors for face recognition. First, to obtain multi-scale information of the face image, the local patches are extracted using a multi-scale local patch generation (MSLPG) method. Second, with the goal of reducing the quantization information loss of binary descriptors, a novel multi-bit local binary descriptor learning (MBLBDL) method is proposed to extract multi-bit local binary descriptors (MBLBDs). In MBLBDL, a learned mapping matrix and novel multi-bit coding rules are employed to project pixel difference vectors (PDVs) into the MBLBDs in each local patch. Finally, a novel robust weight learning (RWL) method is proposed to learn a set of robust weights for each patch to integrate the MBLBDs into the final face representation. In RWL, a codebook is first constructed by clustering MBLBDs on each local patch to extract a feature histogram. Then, considering that different parts of the face have different degrees of robustness to local changes, a set of weights is learned to concatenate the feature histograms of all local patches into the final representation of a face image. In addition, to further improve the performance for heterogeneous face recognition, a coupled WFH (C-WFH) method is proposed. C-WFH maintains the similarity of the corresponding MBLBDs and feature histograms for a pair of heterogeneous face images by means of a novel coupled feature learning (CFL) method to reduce the modality gap. A series of experiments are conducted on widely used face datasets to analyze the performance of WFH and C-WFH. Extensive experimental results show that WFH and C-WFH outperform state-of-the-art face recognition methods.
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OBJECTIVE: To investigate the association of serum uric acid levels with in-hospital heart failure (HF) in patients with acute myocardial infarction (AMI) who are undergoing percutaneous coronary intervention (PCI). METHODS: Two hundred sixteen patients with AMI who were treated with PCI were enrolled in our study. Univariate and multivariate logistic regression analyses were performed to estimate the associations between uric acid levels and the risk of in-hospital HF in AMI patients. Analyses of the areas under the receiver operating characteristic (ROC) curve were performed to determine the accuracy of uric acid levels in predicting in-hospital HF. RESULTS: A dose-response relationship was found for the incidence of in-hospital HF and levels of uric acid, showing increased HF from the lowest to the highest tertile of uric acid. Compared with subjects in the bottom tertile, the adjusted odds ratio for in-hospital HF was 1.92 (95% CI 0.70-5.24) and 3.33 (95% CI 1.18-9.46) in the second tertile group and the third tertile group, respectively. Every 1 mg/dl increase in the serum uric acid level was associated with a 1.60-fold increased risk of incident in-hospital HF (OR, 1.60; 95% CI 1.22-2.11; P = 0.001). ROC curve analysis showed that the optimal cut-off value of uric acid to predict in-hospital HF was 5.75 mg/dl with a sensitivity of 69.2% and specificity of 56.3%. CONCLUSIONS: Our study showed that the serum uric acid level on admission is an independent predictor of in-hospital heart failure in patients with AMI.
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Insuficiencia Cardíaca/metabolismo , Infarto del Miocardio/metabolismo , Intervención Coronaria Percutánea , Ácido Úrico/metabolismo , Anciano , Femenino , Humanos , Masculino , Persona de Mediana Edad , Infarto del Miocardio/cirugía , Estudios ProspectivosRESUMEN
OBJECTIVE: To observe the outcome of percutaneous balloon mitral valvuloplasty (PBMV) in patients with rheumatic mitral valve stenosis. METHODS: From April 1992 to November 2008, 1768 patients underwent PBMV in our hospital.Clinical and echocardiographic follow up data were analyzed in 426 patients from April 1992 to August 1998. Left atrial pressure and the mitral valve gradient (MVG) were measured before and immediately after PBMV in all patients. RESULTS: PBMV was successful in 1748 out of 1768 patients (98.86%). Left atrial pressure decreased from (38 +/- 7) mm Hg (1 mm Hg = 0.133 kPa) to (12 +/- 4) mm Hg (P < 0.001), MVG decreased from (28 +/- 6) mm Hg to (8 +/- 3) mm Hg (P < 0.001) and the area of the mitral valve increased from (0.98 +/- 0.26) cm(2) to (1.97 +/- 0.39) cm(2) (P < 0.001) post PBMV. The main complications included death (n = 2), acute pericardial effusion (n = 1), severe mitral regurgitation (n = 12), cerebral embolism (n = 2) and pulmonary edema (n = 1). Ten years follow up was finished in 426 patients and 288 patients (67.6%) were still in NYHA class Ior II without mitral valve replace operation or repeated PBMV, restenosis was evidenced in 140 patients (33.3%) and 31 patients dead (7.5%). CONCLUSION: PBMV was an effective therapy option for patients with rheumatic mitral valve stenosis.
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Cateterismo , Estenosis de la Válvula Mitral/terapia , Cardiopatía Reumática/terapia , Cateterismo/efectos adversos , Ecocardiografía , Estudios de Seguimiento , Humanos , Resultado del TratamientoRESUMEN
Almost all conventional template-matching methods employ low-level image features to measure the similarity between a template image and a scene image using similarity measures such as pixel intensity and pixel gradient. Although these methods have been widely used in many applications, they cannot simultaneously address all types of robustness challenges. In this study, with the goal of simultaneously addressing the various challenges, we present a robust semantic template-matching approach (RSTM). Inspired by the local binary descriptor, we propose a novel superpixel region binary descriptor (SRBD) to construct a multilevel semantic fusion feature vector for RSTM. SRBD uses a new kernel-distance-based simple linear iterative clustering (KD-SLIC) method to extract the stable superpixels from the template image; Then, based on the average intensity difference between each superpixel region and its neighbors, the dominant gradient orientation of each superpixel can be obtained, and the semantic features of each superpixel can be described as the dominant orientation difference vector, which is coded as the rotation-invariant SRBD. In the off-line matching phase, the fusion semantic feature vector of RSTM combines the multilevel SRBD features with different numbers of superpixels. In the online matching phase, to cope with rotation invariance, a marginal probability model is proposed and applied to locate the positions of template images in the scene image. Moreover, to accelerate computation, an image pyramid is employed. We conduct a series of experiments on a large dataset randomly selected from the MS COCO dataset to fully analyze the robustness of this approach. The experimental results show that RSTM simultaneously addresses rotation changes, scale changes, noise, occlusions, blur, nonlinear illumination changes and deformation with high time efficiency while also outperforming previous stateof- the-art template-matching methods.
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The present study aimed to measure the levels of microRNA-381 (miR-381) in the plaque tissues, peripheral blood mononuclear cells (PBMCs) and serum of patients with coronary atherosclerosis. In addition, the regulatory mechanisms of miR-381 and cyclooxygenase (COX)-2 in coronary atherosclerosis were investigated. A total of 36 patients with coronary atherosclerosis who received coronary endarterectomy at Linyi People's Hospital and Junan Hospital of Traditional Chinese Medicine (Linyi, China) between January 2013 and June 2016 were enrolled into the present study, while 39 healthy subjects were included as the control group. Peripheral blood was collected form all patients and healthy subjects. Plaque tissues were resected from patients with coronary atherosclerosis and adjacent artery intimal tissues were resected as the control tissues. Using quantitative polymerase chain reaction, the levels of miR-381 and COX-2 mRNA in the plaque tissues, PBMCs and serum were determined. In addition, COX-2 protein expression in the plaque tissues and PBMCs was measured by western blotting, while enzyme-linked immunosorbent assay was utilized to examine the protein content in the serum. To identify the direct interaction between miR-381 and COX-2 mRNA, dual-luciferase reporter assay was also conducted. The levels of COX-2 mRNA and protein in the plaque tissues, PBMCs and serum of patients with coronary atherosclerosis were significantly elevated compared with those in the corresponding control groups. However, the expression of miR-381 was significantly reduced in the coronary atherosclerosis patients. Dual-luciferase reporter assay revealed that miR-381 was able to directly target the 3'-untranslated region of COX-2 mRNA to regulate the expression of COX-2. Therefore, the present study demonstrated that enhanced levels of COX-2 expression in patients with coronary atherosclerosis are associated with the downregulation of miR-381 expression, while miR-381 may regulate the occurrence and immune responses of coronary atherosclerosis via COX-2.