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Antibody indexes throughout COVID-19 convalescent lcd contributor: Un answered questions.
Hyperlipidemia is a major risk factor for cardiovascular diseases. Simvastatin (SV), a cholesterol‑lowering agent, has been widely used in the treatment of hyperlipidemia. Gut microbiota is known to influence drug response, including that to statins. However, the effect of SV on the gut microbiota of hyperlipidemic rats is not fully understood. To investigate the influence of SV on gut microbiota in hyperlipidemic rats, the molecular characterization of gut microbiota and the potential functions of genes involved in the downstream metabolic pathways were analyzed using high‑throughput sequencing technology and the Phylogenetic Investigation of Communities by Reconstruction of Unobserved States approach. The results revealed that SV treatment could reduce the gut microbial diversity and drive marked remodeling of the fecal bacterial community composition. At the phylum level, the relative abundance of Firmicutes and Actinobacteria was decreased following SV therapy, whereas that of Bacteroidetes was elevated. At the genus level, the percentage of the genera Bacteroides, Sutterella and Phascolarctobacterium was significantly increased, but that of Bifidobacterium, Ruminococcaceae_NK4A214, Ruminococcaceae_UCG‑009, Intestinimonas and Tyzzerella was significantly decreased. Additionally, functional prediction analysis indicated that in the SV‑associated microbiota, genes involved in energy, carbohydrate, amino acid and nucleotide metabolism likely exhibited enrichment. Briefly, to the best of our knowledge, the present study was the first to establish a profound and comprehensive association between the SV‑induced alterations of the gut flora and the consequent influences of downstream metabolic pathways by gut microbiota. These findings suggested that the gut microbiota may contribute to the SV hypolipidemic efficacy in the progression of hyperlipidemia, which could provide insights for the prevention and treatment of hyperlipidemia.Thrombospondin (TSP)‑1 and TSP‑2 are matricellular proteins in the extracellular matrix (ECM), which serve a significant role in the pathological processes of various cardiovascular diseases (CVDs). The multiple effects of TSP‑1 and TSP‑2 are due to their ability to interact with various ligands, such as structural components of the ECM, cytokines, cellular receptors, growth factors, proteases and other stromal cell proteins. TSP‑1 and TSP‑2 regulate the structure and activity of the aforementioned ligands by interacting directly or indirectly with them, thereby regulating the activity of different types of cells in response to environmental stimuli. The pathological processes of numerous CVDs are associated with the degradation and remodeling of ECM components, and with cell migration, dysfunction and apoptosis, which may be regulated by TSP‑1 and TSP‑2 through different mechanisms. Therefore, investigating the role of TSP‑1 and TSP‑2 in different CVDs and the potential signaling pathways they are associated with may provide a new perspective on potential therapies for the treatment of CVDs. In the present review, the current understanding of the roles TSP‑1 and TSP‑2 serve in various CVDs were summarized. In addition, the interacting ligands and the potential pathways associated with these thrombospondins in CVDs are also discussed.Sepsis is a systemic inflammatory response syndrome that can cause multiple‑organ damage, including acute kidney injury (AKI). Studies have shown that the long non‑coding RNA cancer susceptibility candidate 2 (CASC2) is involved in the occurrence and development of multiple human diseases, although its expression and role in AKI has not yet been reported. The present study demonstrated that the expression of CASC2 was significantly decreased in the serum of patients with sepsis compared with healthy subjects. In addition, the CASC2 level was negatively associated with the severity of AKI. Further experiments revealed that CASC2 promoted cell viability and inhibited inflammatory factor secretion, apoptosis and oxidative stress in lipopolysaccharide‑stimulated human renal tubular epithelial HK‑2 cells. Importantly, the current study observed that CASC2 was negatively associated with a pro‑inflammatory microRNA (miR)‑155. In addition, the upregulation of CASC2 significantly suppressed the nuclear factor κB (NF‑κB) signaling pathway. In conclusion, the results of the present study suggested that CASC2 may serve as a potential target for treating sepsis‑induced AKI by inhibiting the miR‑155 and NF‑κB pathway‑mediated inflammation.Lung adenocarcinoma (LUAD) is one of the most common types of lung cancer and its poor prognosis largely depends on the tumor pathological stage. Critical roles of microRNAs (miRNAs) have been reported in the tumorigenesis and progression of lung cancer. However, whether the differential expression pattern of miRNAs could be used to distinguish early‑stage (stage I) from mid‑late‑stage (stages II‑IV) LUAD tumors is still unclear. In this study, clinical information and miRNA expression profiles of patients with LUAD were downloaded from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus databases. TCGA‑LUAD (n=470) dataset was used for model training and validation, and the GSE62182 (n=94) and GSE83527 (n=36) datasets were used as external independent test datasets. The diagnostic model was created through miRNA feature selection followed by SVM classifier and was confirmed by 5‑fold cross‑validation. A receiver operating characteristic curve was calculated to evaluate the accuracy and robustness of the model. Using the DX score and LIBSVM tool, a 16‑miRNA signature that could distinguish LUAD pathological stages was identified. The area under the curve rates were 0.62 [95% confidence interval (CI) 0.56‑0.67], 0.66 (95% CI 0.54‑0.76) and 0.63 (95% CI 0.43‑0.82) in TCGA‑LUAD internal validation dataset, the GSE62182 external validation dataset, and the GSE83527 external validation dataset, respectively. Kyoto Encyclopedia of Genes and Genomes and Gene Ontology enrichment analyses suggested that the target genes of the 16‑miRNA signature were mainly involved in metabolic pathways. The present findings demonstrate that a 16‑miRNA signature could serve as a promising diagnostic biomarker for pathological staging in LUAD.Adipose tissue‑derived stem cells (ASCs) are beneficial for myocardial regeneration. The physiological oxygen content of human organs is estimated to range between 1 and 11%. However, in the majority of previous in vitro studies with cultured ASCs, the O2 concentration was artificially set to 21%. The present study aimed to compare the protective effects of rat ASCs on neonatal rat ventricular myocytes (NRVMs) under normoxic (21% O2) and physioxic (5% O2) conditions. Rat NRVMs cultured under normoxia or physioxia were treated with H2O2 or left untreated, and further co‑cultured with ASCs in 21% or 5% O2. The apoptosis of NRVMs was evaluated by Annexin V staining and quantitating the protein levels of Bcl‑2 and Bax by western blotting. The oxidative stress of NRVMs was determined by a glutathione/oxidized glutathione assay kit. The concentrations of secreted vascular endothelium growth factor (VEGF), insulin like growth factor‑1 (IGF‑1) and basic fibroblast growth factor (bFGF) in the culture medium were quantified by enzyme‑linked immunosorbent assay. Under both normoxia and physioxia, co‑culture with ASCs protected H2O2‑exposed NRVMs from apoptosis and significantly alleviated the oxidative stress in NRVMs. Endocrinology antagonist The protective effects of ASCs were associated with increased secretion of VEGF, IGF‑1 and bFGF. ASCs cultured in 5% O2 exhibited certain cardioprotective effects against H2O2 stress. The results of the present study suggested that O2 concentrations influenced the cardioprotective effects of ASCs. VEGF, IGF‑1 and bFGF may serve a role in the myocardial regeneration mediated by transplanted ASCs.The synthesis and secretion of surfactant proteins (SPs) is an important sign of lung maturation. Furthermore, the morbidity of lung developmental diseases, including respiratory distress syndrome and bronchopulmonary dysplasia which are mainly caused by immature lung development and lack of SPs, is increasing. As is well known, multiple microRNAs (miRs/miRNAs) are able to influence lung development via numerous different signaling pathways. However, few studies examine the association between the miRNAs and lung developmental diseases. A previous study has demonstrated that miR‑431 was significantly (F=33.49; P less then 0.001) downregulated in the lung tissues of Sprague‑Dawley rats at 3 time points, embryonic day 19, embryonic day 21 and postnatal day 3. The present study reported that the regulation of miR‑431 may influence the expression of SPs. Thus, the further potential mechanisms of miR‑431 in negatively regulating lung development were examined in the present study. Stable A549 cell lines overexpressing or knocking down SMAD family member 4 (SMAD4) transfected with miR‑431 overexpressed or knocked down, and their control groups were established. Subsequently, the expression of bone morphogenetic protein 4 (BMP4), SMAD4 and SPs (SP‑A, SP‑B and SP‑C) at the RNA and protein levels were validated respectively by reverse transcription quantitative PCR and western blotting. miR‑431 exhibited a decreased expression, while BMP4 and SPs exhibited increased expression at the mRNA and protein levels in the SMAD4 knockdown group. Meanwhile, the expression of SPs were reduced in the SMAD4‑knockdown group via overexpressing miR‑431 and increased in the SMAD4‑overexpression group via inhibiting miR‑431. The present results indicate that SMAD4 negatively regulates the expression of SPs, and that miR‑431 negatively regulates the expression of SPs through inhibiting the BMP4/activin/transforming growth factor‑β signaling pathway by targeting SMAD4.The aim of the present study was to identify potential serum biomarkers for insulin resistance (IR) in patients with polycystic ovary syndrome (PCOS) by comparing the differences in serum protein expression levels between PCOS patients with and without IR. PCOS patients aged from 18 to 35 years were recruited at Guangdong Women and Children's Hospital from January, 2013 to February, 2014. A total of 218 PCOS patients were enrolled and divided into the insulin resistance (PCOS‑IR) and non‑insulin resistance (PCOS‑NIR) groups according to their homeostasis model assessment of insulin resistance. Two‑dimensional difference gel electrophoresis (2D‑DIGE) and matrix‑assisted laser desorption/ionization time‑of‑flight mass spectrometry (MALDI‑TOF‑MS/MS) techniques were used to identify differences in protein expression levels between the PCOS‑IR and PCOS‑NIR groups. The present study demonstrated that the total cholesterol (TCH), triglycerides (TG), low‑density lipoprotein (LDL), fasting plasma glucose (FPG), 3‑h blood glucose (3hBG) and uric acid (UA) levels in the PCOS‑IR group were higher than those in the PCOS‑NIR group (P less then 0.05). Between the PCOS‑IR and PCOS‑NIR groups, a total of 20 differentially expressed protein spots were detected by 2D‑DIGE. Among these, 4 proteins, namely afamin, serotransferrin, complement C3 and apolipoprotein C3 (APOC3), were also identified by MALDI‑TOF‑MS/MS. The alteration of APOC3 was further confirmed by western blot analysis and enzyme‑linked immunosorbent assay (ELISA). The present study also confirmed that the expression level of APOC3 was positively associated with the homeostasis model assessment of insulin resistance (HOMA‑IR). On the whole, the data indicate that APOC3 may be a potential diagnostic marker for PCOS‑IR patients.
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