Abstract Background Recent seasonal epidemics of influenza have been caused by human influenza A viruses of the H1N1 and H3N2 subtypes and influenza B viruses. Annual vaccination is recommended to prevent infection; however, how annual influenza vaccination influences vaccine effectiveness is largely unknown. Methods To investigate the impact of repeated vaccination on immune and protective effect, we performed a prospective seroepidemiologic study. Participants with or without prior vaccination (2018–2019) were enrolled during the 2019–2020 influenza season. Inactivated quadrivalent influenza vaccine (IIV4) was administered through the intramuscular route, and venous blood samples were collected regularly to test hemagglutination inhibition (HAI) titers. Results The geometric mean titers and proportion with titers ≥40 against the influenza vaccine components peaked at 30 days post‐vaccination. At Day 30, the geometric mean titer and proportion with titers ≥40 in participants who had been previously vaccinated were higher for H3N2 but similar for both B lineages (Victoria and Yamagata) as compared with participants vaccinated for the first time. As for H1N1, the geometric mean titer was lower in repeated vaccinated participants, but the proportion with titers ≥40 was consistent in both groups. Conclusions Repeated vaccination provides similar or enhanced protection as compared with single vaccination in first‐time vaccinees.
Abstract Silicon carbide (SiC) is regarded as a promising semiconductor owing to its wide band gap and high thermal conductivity. Meanwhile, it possesses issues such as interface properties, which may affect the performance of SiC substrate power devices (e.g. MOSFET), especially when compared with similarly structured silicon appliances. Given that the development of SiC semiconductor devices has a number of commonalities with conventional silicon-based semiconductors, titanium dioxide (TiO 2 ), a material that has a great track record in Si-based semiconductor devices, has been chosen for investigation in this work. Although TiO 2 is not capable of being a gate dielectric alone on the SiC substrate because of its relatively narrow band gap, it can be adopted into composite or multilayer gate dielectrics to reach satisfying characteristics. As such, the interfacial state and heterostructure between TiO 2 and SiC remain worthy being researched. In the present study, the properties of atomic layer deposited (ALD) TiO 2 films on silicon substrates were compared with those on 4H-SiC substrates via x-ray photoelectron spectroscopy, atomic force microscopy, and x-ray reflectometry. It is shown that the interface state between ALD TiO 2 film and both types of substrates as-deposited have similar chemical conditions, whereby TiO 2 layer barely react with substrates, containing great amount of oxygen vacancies. According to band alignment calculations, heterostructure of both samples are type-II heterojunctions with negatively shifted conduction band. Although the large bandwidth of 4H-SiC hinders the use of TiO 2 as a gate dielectric in power devices, this structure has the potential for other semiconductor products.
Acute lung injury (ALI) is the leading cause of death in sepsis patients. Exosomes participate in the occurrence and development of ALI by regulating endothelial cell inflammatory response, oxidative stress and apoptosis, causing serious pulmonary vascular leakage and interstitial edema. The current study investigated the effect of exosomal miRNAs on endothelial cells during sepsis. We found a significant increase in miR-1-3p expression in cecal ligation and puncture (CLP) rats exosomes sequencing and sepsis patients' exosomes, and lipopolysaccharide (LPS)-stimulated human umbilical vein endothelial cells (HUVECs) in vitro. However, the specific biological function of miR-1-3p in ALI remains unknown. Therefore, mimics or inhibitors of miR-1-3p were transfected to modulate its expression in HUVECs. Cell proliferation, apoptosis, contraction, permeability, and membrane injury were examined via cell counting kit-8 (CCK-8), flow cytometry, phalloidin staining, Transwell assay, lactate dehydrogenase (LDH) activity, and Western blotting. The miR-1-3p target gene was predicted with miRNA-related databases and validated by luciferase reporter. Target gene expression was blocked by siRNA to explore the underlying mechanisms. The results illustrated increased miR-1-3p and decreased stress-associated endoplasmic reticulum protein 1 (SERP1) expression both in vivo and in vitro. SERP1 was a direct target gene of miR-1-3p. Up-regulated miR-1-3p inhibits cell proliferation, promotes apoptosis and cytoskeleton contraction, increases monolayer endothelial cell permeability and membrane injury by targeting SERP1, which leads to dysfunction of endothelial cells and weakens vascular barrier function involved in the development of ALI. MiR-1-3p and SERP1 may be promising therapeutic candidates for sepsis-induced lung injury.
A fire-fighting control system, which is usually implemented through programmable logic controllers, is a typical type of safety-critical cycle physical system. It has been widely used in currently complex industrial applications. So it is significant for a fire-fighting control system to conduct safety checking. There have been many methods to check safety of a fire-fighting control system so far, but they all ignore the effect of communication networks which are important for data transmission. In this paper, considering communication networks, we propose to model a fire-fighting control system with timed automata and describe system requirements with computation tree logic (CTL) formulas. A real dock fire fighting control system illustrates the method. And some safety properties are verified in the model checking tool Uppaal, and verified results show the effectiveness of the method.
Presenting the best practices, experimental protocols, and the latest understanding of regulations, this book offers a comprehensive review of LC–MS bioanalysis of small molecules and macromolecules. It not only addresses the needs of bioanalytical scientists working on routine projects, but also explores advanced and emerging technologies such as high–resolution mass spectrometry and dried blood spot microsampling.
Drug repositioning identifies novel therapeutic potentials for existing drugs and is considered an attractive approach due to the opportunity for reduced development timelines and overall costs. Prior computational methods usually learned a drug's representation from an entire graph of drug-disease associations. Therefore, the representation of learned drugs representation are static and agnostic to various diseases. However, for different diseases, a drug's mechanism of actions (MoAs) are different. The relevant context information should be differentiated for the same drug to target different diseases. Computational methods are thus required to learn different representations corresponding to different drug-disease associations for the given drug. In view of this, we propose an end-to-end partner-specific drug repositioning approach based on graph convolutional network, named PSGCN. PSGCN firstly extracts specific context information around drug-disease pairs from an entire graph of drug-disease associations. Then, it implements a graph convolutional network on the extracted graph to learn partner-specific graph representation. As the different layers of graph convolutional network contribute differently to the representation of the partner-specific graph, we design a layer self-attention mechanism to capture multi-scale layer information. Finally, PSGCN utilizes sortpool strategy to obtain the partner-specific graph embedding and formulates a drug-disease association prediction as a graph classification task. A fully-connected module is established to classify the partner-specific graph representations. The experiments on three benchmark datasets prove that the representation learning of partner-specific graph can lead to superior performances over state-of-the-art methods. In particular, case studies on small cell lung cancer and breast carcinoma confirmed that PSGCN is able to retrieve more actual drug-disease associations in the top prediction results. Moreover, in comparison with other static approaches, PSGCN can partly distinguish the different disease context information for the given drug.
Abstract. On August 8, 2017, a strong magnitude 7.0 earthquake occurred in Jiuzhaigou, Sichuan Province, China. To assess pre-earthquake anomalies, we utilized variational mode decomposition to preprocess borehole strain observation data and combined it with a graph wavenet graph neural network model to process data from multiple stations. We obtained one-year data from four stations near the epicenter as the training dataset and data from January 1 to August 10, 2017, as the test dataset. For the prediction results of the variational mode decomposition-graph wavenet model, the anomalous days were extracted using statistical methods, and the results of anomalous day accumulation at multiple stations showed that an increase in the number of anomalous days occurred 15–32 days before the earthquake. The acceleration effect of anomalous accumulation was most obvious in the 20-day period before the earthquake, and an increase in the number of anomalous days also occurred in the one to three days post-earthquake. We tentatively deduce that the pre-earthquake anomalies are caused by the diffusion of strain energy near the epicenter during the accumulation process, which can be used as a signal of pro-seismic anomalies, whereas the post-earthquake anomalies are caused by the frequent occurrence of aftershocks.
Plasma UII has been observed to be raised in patients with acute myocardial infarction, a lower UII response is associated with more severe injury of myocardium, suggesting a possible cardioprotective role for this peptide. In the present study, we studied plasma UII concentration of thirty patients admitted to the Cardiology Department with acute myocardial infartion.The results showed that plasma UII was sharply increased in patients compared to that in health control within one week after admission. We then explore whether UII could protect cardiomyocytes from injury induced by oxidative stress. Cultured cardiomyocyte were treated with H2O2 to induce oxidative stress, and the influence of UII on H2O2-induced apoptosis was observed. The results showed that UII pretreatment significantly reduced the number of TUNEL-positive cardiomyocytes induced by H2O2, and it partly abolished the upregulation of pro-apoptotic protein Bax and the down-regulation of anti-apoptotic protein Bcl-2. siRNA targeted to urotensin receptor (UT) greatly inhibited these effects. H2S has been reported to exert protective effect on cardiomyocytes, we detected the effect of UII on H2S production and CSE (Major H2S-producing enzyme) expressions in cardiomyocytes exposed to H2O2.The present data revealed that UII increased the H2S production by enhancing the expression of CSE by activating the ERK signaling in cardiomyocytes exposed to H2O2. Si-CSE or ERK inhibitor not only greatly inhibited the upregulation of CSE or the phosphorylation of ERK induced by UII but also reversed UII-induced-upregulation of H2S production and anti-apoptosis in cadiomyocytes exposed to H2O2. In conclusion, UII rapidly promoted the phosphorylation of ERK, increased CSE exression and induced H2S production, which in turn enhanced the p-ERK level to protect cardiomyocytes from apoptosis under ischemic or oxidative stress. The increased plasma UII level in patients may be critical for cardiac protection in patients at early-phase of acute myocardial infarction.
In previous studies on glucose metabolism during in vitro maturation, intact cumulus-oocyte complexes (COCs) were treated with enzyme inhibitors/activators. Because inhibitors/activators may have non-specificity and/or toxicity, and culture of COCs cannot differentiate whether glucose metabolism of cumulus cells (CCs) or that of the oocyte supports oocyte maturation, results from the previous studies must be verified by silencing genes in either CCs or cumulus-denuded oocytes (DOs). In this study, RNAi was adopted to specify the effects of glucose metabolism in CCs or DOs on oocyte maturation. Although silencing either glyceraldehyde 3-phosphate dehydrogenase (GAPDH) or glucose-6-phosphate dehydrogenase (G6PD) genes in CCs significantly decreased competence of the cocultured DOs, silencing G6PD impaired competence to a greater extent. While silencing G6PD or GAPDH of CCs decreased glutathione and ATP contents of cocultured DOs to similar extents, silencing G6PD increased oxidative stress as well. Analysis on metabolite contents and oxidative stress index and culture of DOs in medium conditioned with gene-silenced CCs indicated that CCs supported oocyte maturation by releasing glucose metabolites. Silencing mitochondrial pyruvate carrier 1 or NADH dehydrogenase (ubiquintone) flavoprotein 1 of DOs significantly impaired their maturation. The results have unequivocally confirmed that CCs promote oocyte maturation by releasing glucose metabolites from both pentose phosphate pathway (PPP) and glycolysis. Pyruvate is transferred into DOs by mitochondrial pyruvate carrier (MPC) and utilized through mitochondrial electron transport to support maturation.
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