RESUMO
Ischemic stroke (IS) is a severe cerebrovascular disease that seriously endangers human health. Gut microbiota plays a key role as an intermediate mediator in bidirectional regulation between the brain and the intestine. In recent years, trimethylamine N-oxide (TMAO) as a gut microbiota metabolite has received widespread attention in cardiovascular diseases. Elevated levels of TMAO may increase the risk of IS by affecting IS risk factors such as atherosclerosis, atrial fibrillation, hypertension, and type 2 diabetes. TMAO exacerbates neurological damage in IS patients, increases the risk of IS recurrence, and is an independent predictor of post-stroke cognitive impairment (PSCI) in patients. Current research suggests that the mechanisms of TMAO action include endothelial dysfunction, promoting of foam cell formation, influence on cholesterol metabolism, and enhancement of platelet reactivity. Lowering plasma TMAO levels through the rational use of traditional Chinese medicine, dietary management, vitamins, and probiotics can prevent and treat IS.
Assuntos
Microbioma Gastrointestinal , AVC Isquêmico , Metilaminas , Metilaminas/metabolismo , Metilaminas/sangue , Humanos , Microbioma Gastrointestinal/fisiologia , AVC Isquêmico/metabolismo , Fatores de RiscoRESUMO
[This retracts the article DOI: 10.3892/etm.2019.7644.].
RESUMO
Gene expression sample data, which usually contains massive expression profiles of genes, is commonly used for disease related gene analysis. The selection of relevant genes from huge amount of genes is always a fundamental process in applications of gene expression data. As more and more genes have been detected, the size of gene expression data becomes larger and larger; this challenges the computing efficiency for extracting the relevant and important genes from gene expression data. In this paper, we provide a novel Bi-dimensional Principal Feature Selection (BPFS) method for efficiently extracting critical genes from big gene expression data. It applies the principal component analysis (PCA) method on sample and gene domains successively, aiming at extracting the relevant gene features and reducing redundancies while losing less information. The experimental results on four real-world cancer gene expression datasets show that the proposed BPFS method greatly reduces the data size and achieves a nearly double processing speed compared to the counterpart methods, while maintaining better accuracy and effectiveness.
Assuntos
Expressão GênicaRESUMO
In this work, two macrocyclic hosts, named hydroxylatopillar[6]arene and dihydroxylatopillar[6]arene (HP6, 2HP6), are proposed. We found that the reduction of Au3+ to Au0 can success by using HP6 or 2HP6 as a reductant and stabilizing agent. At the end of HP6/2HP6, hydroxyl (-OH) groups were used as a reductant to reduce Au3+ to Au0. At the same time, -OH on HP6/2HP6 was oxidized to -COOH, and then the formed -COOH can be used as the stabilizer to prevent the infinite growth of AuNPs. The cellulose nanocrystals (CNCs) prepared by a clean and nonpolluting method were used as carriers to load AuNPs on them. The CNCs were applied for the adsorption of methylene blue (MB), and then the MB was catalytically degraded by HP6/2HP6-AuNPs-CNC. Besides, the HP6/2HP6-AuNPs-CNC showed remarkable catalytic performance for reducing nitro to the amino group in 4-nitrophenol. The advantages of clean and green synthesis make the HP6/2HP6-AuNPs-CNC a hybrid material and its application sustainable.
RESUMO
Malignant melanoma (MM) is the most aggressive form of skin cancer originating from melanocytes with increased proliferative and metastatic ability. Previous studies have revealed that microRNA-338-3p (miR-338-3p) functions as a tumor suppressor in several types of cancer, including cervical cancer, renal cell carcinoma and thyroid cancer. However, the function and mechanism underlying the action of miR-383-3p in MM remain unclear. In the study, aberrant downregulation of miR-338-3p was observed in 60 pairs of MM and adjacent non-tumor tissue using quantitative polymerase chain reaction assay. Decreased miR-383-3p expression was associated with advanced clinical stage (P<0.05) and lymph node metastasis (P<0.001). The overexpression of miR-338-3p in A375 and G361 cells suppressed cell proliferation and migration using MTT, colony formation, wound healing and transwell assays. Mechanistically, MACC1 was identified as a direct target for miR-338-3p using bioinformatics prediction and dual-luciferase assays. Furthermore, MACC1 expression was significantly increased and inversely correlated with the levels of miR-338-3p in MM tissues. More importantly, restoration of MACC1 resulted in reversed the inhibitory effects of miR-338-3p overexpression on MM cells by altering the expression levels of PCNA and epithelial-mesenchymal transition (EMT)-associated proteins. These results suggest that miR-338-3p functions as a novel tumor suppressor, at least in part, via targeting MACC1 and suggest that miR-338-3p may serve as a potential target for treatment of MM patients.
RESUMO
Fibulin-5, a multifunctional extracellular matrix protein, is up-regulated in response to mechanical injury and can promote dermal wound healing. This study aimed to explore the role and mechanism of Fibulin-5 in the pathogenesis of post-burn inflammation in thermally-injured mice. Here, we found that Fibulin-5 was up-regulated in the dorsal root ganglion (DRG) of burn-injured mice. After nociceptive behavioral testing, DRG was isolated and cultured to detect the mechanism of Fibulin-5 in thermal injury models by recombinant adenovirus overexpressing Fibulin-5, RT-qPCR, Western Blot, ELISA, AP20187 (an activator of one kind of kinase phosphorylating the α subunit of eukaryotic initiation factor 2, eIF2α), capsaicin (an agonist of transient receptor potential vanilloid (TRPV)-1), and an anti-CGRP neutralizing antibody. Also, the pathological state of skin tissues and the expression of cyclooxygenase 2 and myeloperoxidase were examined by Hematoxylin-Eosin staining and immunohistochemistry, respectively. We found that overexpression of Fibulin-5 attenuated the pain, inhibited the inflammatory response, and improved the pathologic condition induced by burn injury. Fibulin-5 overexpression significantly down-regulated the phosphorylation level of eIF2α and subsequently inhibited the TRPV1 channel and CREB/CGRP signaling. Additionally, anti-CGRP neutralizing antibody dramatically suppressed the inflammatory response induced by burn injury. The results suggest that overexpression of Fibulin-5 attenuates thermal inflammation via suppressing TRPV1/CGRP pathway. This may provide a potential therapy target to alleviate excessive inflammation in burn patients.