Δευτέρα 24 Ιανουαρίου 2022

Electrochemical monitoring of bronchial inflammation in pediatric athletes: A prospective study

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Exp Ther Med. 2022 Feb;23(2):180. doi: 10.3892/etm.2021.11103. Epub 2021 Dec 28.

ABSTRACT

The assessment of inflammation by accessible, reproducible and especially non-invasive methods is one of the main goals for numerous medical specialties. One variable for assessment is the fraction of nitric oxide in exhaled air (FeNO), which correlates with the inflammatory syndrome of the airways. The objective of the present study was the biochemical evaluation of FeNO in children practicing sports in Oltenia, Romania. Between January and December 2018, children practicing sports (football, track and field, judo, fencing, handball, volleyball and basketball) were enrolled in the study. The FeNO values were compared with the asthma history and with the spirometric evaluation. A total of 23 children without a previous asthma diagnosis exhibited positive spirometry results. The prevalence of the disease was 3.6% in the cohort, and FeNO dosing show ed higher values in the group at risk in children diagnosed with asthma, compared with that in children without this diagnosis. The children who performed outdoor sports (soccer, and track and field) had higher electrochemical levels of nitric oxide compared with those who performed indoor sports (mean, 29.70 vs. 20.56; P<0.0005), which led to the hypothesis that these children had an increased risk of developing bronchospasm. FeNO dosing can thus be a useful and easy-to-use tool in practice for assessing bronchial inflammation in children practicing various types of sports. The spirometric data of undiagnosed asthma patients from the present study may indicate that the disease is still underdiagnosed within Romania.

PMID:3506 9861 | PMC:PMC8764892 | DOI:10.3892/etm.2021.11103

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p-Coumaric acid suppresses reactive oxygen species-induced senescence in nucleus pulposus cells

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Exp Ther Med. 2022 Feb;23(2):183. doi: 10.3892/etm.2021.11106. Epub 2021 Dec 30.

ABSTRACT

p-Coumaric acid (PCA) is a phenolic acid that is widely present in numerous plants and human diets. Studies have demonstrated the antioxidant and anti-senescence effects of PCA in different cell types. However, the anti-senescence effects of PCA in nucleus pulposus (NP) cells have remained to be determined. In the present study, reverse transcription-quantitative PCR was used to measure the gene expression of Cyclooxygenase-2 (Cox-2), inducible nitric oxide synthase (iNOS), p53, p16, aggrecan and collagen-2 in NP cells. Immunofluorescence staining was used to evaluate the protein expression of p53, p16 and collagen-2 in NP cells. In addition, cell cycle of NP cells was measured by flow cytometry. β-galactosidase staining were used to investigate the senescence of NP cells. Preliminary results indicated that PCA suppressed ROS-induced senescence i n NP cells via both the p16 and p53 pathways. NP cells were pretreated with PCA at a concentration of 10 or 50 µg/ml prior to stimulation with 200 µM hydrogen peroxide (H2O2). Pretreatment with PCA significantly inhibited H2O2-induced cell cycle arrest in a dose-dependent manner. PCA also reduced the gene expression of Cox-2, iNOS, p53 and p16 induced by H2O2. By contrast, aggrecan and collagen-2 expression in NP cells was upregulated after PCA treatment. Furthermore, PCA suppressed H2O2-induced changes in the protein expression of p16, p53 and collagen-2. H2O2 stimulation of NP cells increased senescence-associated β-galactosidase (SA-β-gal) activities, while PCA treatment markedly reversed these SA-β-gal activities. Collectively, the present results indicated that PCA attenuated H2O2-induced oxidative stress and cellular senescence, suggesting a potential therapeutic utility of PCA in intervertebral disc degeneration.

PMID:35069864 | PMC:PMC8764901 | DOI:10.3892/etm.2021.11106

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Portal vein reconstruction with interposition of cryopreserved aortic graft: A case report and literature review

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Exp Ther Med. 2022 Feb;23(2):184. doi: 10.3892/etm.2021.11107. Epub 2021 Dec 30.

ABSTRACT

Pancreatic cancer is one of the most aggressive malignancies with poor rates of survival especially in the event radical procedures are not feasible. However, improvements in surgical techniques have led to the successful association of vascular resection followed by reconstruction without a significant increase in the rates of postoperative complications. In the present article, we present the case of a 49-year-old patient diagnosed with pancreatic head cancer invading the portal vein. After discussing with the patient the risks and the benefits of the surgical procedure, the patient was submitted to pancreatoduodenectomy en bloc with portal vein resection while the continuity of the portal vein was reestablished by using a cadaveric graft originating from the abdominal aorta. The postoperative outcome was uneventful. In conclusion, in selected c ases, arterial cadaveric grafts may be used in order to establish the continuity of the portal vein with good results. However, it should be emphasized that these are demanding procedures which should be carefully analyzed before deciding upon the opportunity for performing them.

PMID:35069865 | PMC:PMC8764900 | DOI:10.3892/etm.2021.11107

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KDM2B overexpression prevents myocardial ischemia-reperfusion injury in rats through regulating inflammatory response via the TLR4/NF-κB p65 axis

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Exp Ther Med. 2022 Feb;23(2):154. doi: 10.3892/etm.2021.11077. Epub 2021 Dec 17.

ABSTRACT

Histone modifier lysine-specific demethylase 2B (KDM2B) has been previously reported to activate the inflammatory response by transcription initiation of the IL-6 gene. However, the effects of KDM2B on the inflammatory response during myocardial ischemia-reperfusion (I/R) injury and corresponding mechanisms remain poorly understood. The present study aimed to investigate the role and mechanism of KDM2B in myocardial I/R injury. Therefore, a myocardial I/R injury model was established in rats through coronary artery ligation. Adeno-associated virus-encoding KDM2B and small interfering RNA-KDM2B were designed to determine the effects of KDM2B on myocardial I/R injury using H&E staining and a TUNEL assay in the myocardial tissues. Reverse transcription-quantitative PCR and western blotting were performed to detect the mRNA and protein expr ession levels of KDM2B, toll-like receptor 4 (TLR4), NF-κB p65 and NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3). ELISA was used to detect the levels of TNF-α, IL-6 and IL-1β in the peripheral blood samples. Pathological analysis demonstrated that the cells in the model group were disordered, with a large area of necrosis and neutrophil infiltration. Knocking down KDM2B expression significantly upregulated the mRNA and protein expression levels of TLR4, NLRP3, NF-κB p65 and the ratio of phosphorylated (p)-p65 to p65. KDM2B knockdown also significantly increased the levels of IL-1β, IL-6 and TNF-α in the peripheral blood, which aggravated myocardial injury and promoted the apoptosis of myocardial cells. However, overexpression of KDM2B downregulated the mRNA and protein expression levels of TLR4, NLRP3, NF-κB P65, the ratio of p-p65 to p65 whilst reducing the levels of IL-1β, IL-6 and TNF-α in the peripheral blood, which markedly improved myocardial injury and sig nificantly inhibited the apoptosis of cells in myocardial tissue. In conclusion, the results indicated that overexpression of KDM2B may prevent myocardial I/R injury in rats by reducing the inflammatory response through regulation of the TLR4/NF-κB p65 axis.

PMID:35069835 | PMC:PMC8753960 | DOI:10.3892/etm.2021.11077

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Potential biomarkers of acute myocardial infarction based on co-expression network analysis

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Exp Ther Med. 2022 Feb;23(2):162. doi: 10.3892/etm.2021.11085. Epub 2021 Dec 21.

ABSTRACT

Acute myocardial infarction (AMI) is a common cause of death in numerous countries. Understanding the molecular mechanisms of the disease and analyzing potential biomarkers of AMI is crucial. However, specific diagnostic biomarkers have thus far not been fully established and candidate regulatory targets for AMI remain to be determined. In the present study, the AMI gene chip dataset GSE48060 comprising blood samples from control subjects with normal cardiac function (n=21) and patients with AMI (n=26) was downloaded from Gene Expression Omnibus. The differentially expressed genes (DEGs) between the AMI and control groups were identified with the online tool GEO2R. The co-expression network of DEGs was analyzed by calculating the Pearson correlation coefficient of all gene pairs, mutual rank screening and cutoff threshold screening. Subsequently, the Gene Ontology (GO) database was used to analyze the genes' functions and pathway enrichment of genes in the most important modules was performed. Kyoto Encyclopedia of Genes and Genomes (KEGG) Disease and BioCyc were used to analyze the hub genes in the module to determine important sub-pathways. In addition, the expression of hub genes was confirmed by reverse transcription-quantitative PCR in AMI and control specimens. In the present study, 52 DEGs, including 26 upregulated and 26 downregulated genes, were identified. As key hub genes, three upregulated genes (AKR1C3, RPS24 and P2RY12) and three downregulated genes (ACSL1, B3GNT5 and MGAM) were identified from the co-expression network. Furthermore, GO enrichment analysis of all AMI co-expression network genes revealed functional enrichment mainly in 'RAGE receptor binding' and 'negative regulation of T cell cytokine production'. In addition, KEGG Disease and BioCyc analysis indicated functional enrichment of the genes RPS24 a nd P2RY12 in 'cardiovascular diseases', of AKR1C3 in 'cardenolide biosynthesis', of MGAM in 'glycogenolysis', of B3GNT5 in 'glycosphingolipid biosynthesis' and of ACSL1 in 'icosapentaenoate biosynthesis II'. In conclusion, the hub genes AKR1C3, RPS24, P2RY12, ACSL1, B3GNT5 and MGAM are potential markers of AMI, and have potential application value in the diagnosis of AMI.

PMID:35069843 | PMC:PMC8753964 | DOI:10.3892/etm.2021.11085

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Systematic review of the role of indocyanine green near-infrared fluorescence in safe laparoscopic cholecystectomy (Review)

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Exp Ther Med. 2022 Feb;23(2):187. doi: 10.3892/etm.2021.11110. Epub 2021 Dec 30.

ABSTRACT

With the widespread introduction of laparoscopic cholecystectomy, the incidence of iatrogenic main bile duct lesions has significantly increased, with incidences ranging from 0.2 to 1.5% according to current studies. Although there are studies regarding the use of indocyanine green (ICG) for improved visualization of the biliary anatomy, there is no consensus on the dose, timing and optimal mode of administration, or the indications in which ICG provides a real benefit through increased safety in laparoscopic cholecystectomy (LC). A systematic review was performed on articles in English published until March 2021, which were identified on PubMed, Springer Nature, Elsevier and Scopus via specific mesh terms: 'Indocyanine green'/'near-infrared fluorescence' and 'laparoscopic cholecystitis'. The most used method of administration of ICG was intraveno usly, only one study evaluated the efficiency of a near-infrared cholangiogram (NIRC) when ICG was administered directly in the gallbladder. The majority of the studies included in the review used 2.5 mg of ICG administered within 1 h before imaging. The intensity of the NIRC fluorescence signal was revealed to depend on several factors, with obesity and inflammation as the most clinically significant. NIRC was reported to be a simple, feasible, safe and cost-effective procedure, which may improve safety in difficult cases of LC. NIRC use in combination with white light has been demonstrated to be superior to white light alone in identifying extrahepatic biliary anatomy, thus decreasing the risk of intraoperative bile duct injuries (BDI). For its large-scale use, data on a higher number of patients to confirm its clinical value and specific indications is required.

PMID:35069868 | PMC:PMC8764893 | DOI:10.3892/etm.2021.11110

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MicroRNA-126 and VEGF enhance the function of endothelial progenitor cells in acute myocardial infarction

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Exp Ther Med. 2022 Feb;23(2):142. doi: 10.3892/etm.2021.11065. Epub 2021 Dec 14.

ABSTRACT

Previous studies have found that microRNA-126 (miR-126) overexpression can exert beneficial effects on endothelial function and angiogenesis. The role of miR-126 was previously reported to be by directly limiting the activities of negative regulators of the vascular endothelial growth factor (VEGF) pathway, such as PI3K regulation subunit 2 (PIK3R2). The aim of the present study was to investigate the role of the miR-126/PIK3R2/VEGF axis in endothelial progenitor cells (EPCs) under hypoxic conditions. An in vitro hypoxia model in EPCs was established by exposing EPCs to hypoxia (O2/N2/CO2, 1/94/5) for 72 h, before reverse transcription-quantitative PCR (RT-qPCR) and western blot analyzes were used to measure miR-126 and PIK3R2 expression in EPCs. The proliferation, migration and tube-forming ability of the t ransfected cells were measured using MTT, Transwell and tube formation assays, respectively. miR-126 expression was found to be lower in EPCs in the hypoxia group compared with that in the control group (P<0.01). The expression of PIK3R2, a direct target gene of miR-126, was found to be higher in the hypoxia group compared with that in the control group (P<0.01). miR-126 mimic and VEGF-plasmid co-transfection improved the proliferation, migration, tube-forming ability and restored the phosphorylation of AKT in EPCs under hypoxic conditions (all P<0.01). In addition, the effects of miR-126 mimic on hypoxia-induced EPCs were reversed by PIK3R2-plasmid co-transfection, whilst the effects of VEGF-plasmid were enhanced further by co-transfection with the miR-126 mimic. In conclusion, miR-126 promoted the functions of EPCs under hypoxic conditions by negatively targeting PIK3R2, whilst the combined overexpression of miR-126 and VEGF enhanced these aforementioned effects.

PM ID:35069823 | PMC:PMC8756429 | DOI:10.3892/etm.2021.11065

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