881 research outputs found
Event-Triggered Robust Cooperative Output Regulation for a Class of Linear Multi-Agent Systems with an Unknown Exosystem
This paper investigates the robust cooperative output regulation problem for
a class of heterogeneous uncertain linear multi-agent systems with an unknown
exosystem via event-triggered control (ETC). By utilizing the internal model
approach and the adaptive control technique, a distributed adaptive internal
model is constructed for each agent. Then, based on this internal model, a
fully distributed ETC strategy composed of a distributed event-triggered
adaptive output feedback control law and a distributed dynamic event-triggering
mechanism is proposed, in which each agent updates its control input at its own
triggering time instants. It is shown that under the proposed ETC strategy, the
robust cooperative output regulation problem can be solved without requiring
either the global information associated with the communication topology or the
bounds of the uncertain or unknown parameters in each agent and the exosystem.
A numerical example is provided to illustrate the effectiveness of the proposed
control strategy.Comment: 13 pages, 8 figure
MiR-541-3p suppresses gastric cancer via negative regulation of HSF1
Purpose: To explore the effects of miR-541-3P on the expression of heat shock transcription factor 1 (HSF1) in gastric cancer cells (GC).Methods: The MicroRNA Target Prediction Database was used to predict whether miR-541-3p interacts with HSF1. Interaction was assessed by dual-luciferase reporter assays. Furthermore, miR-541-3p mRNA levels in GC cell lines were determined by qRT-PCR. Human GC cell lines MKN45 and NCI-N87 were transfected with miR-541-3p mimic. Cell apoptosis, proliferation, invasion, and migration were evaluated using flow cytometry, apoptosis assays, Edu assays, CCK-8 assays, and transwell assays, respectively. Caspase-3, Bcl-2, and cleaved caspase-3 expression levels were determined by western blot.Results: Expression of miR-541-3p was significantly down-regulated in GC cells. Functionally, miR-541-3p mimic inhibited GC cell proliferation, migration, and invasion and induced apoptosis in vitro (p <0.01). Mechanistically, miR-541-3p interacted with HSF1 and inhibited its expression. Overexpression of HSF1 counteracted the effects of miR-541-3p mimic in GC cells.Conclusion: These results indicate that miR-541-3p suppresses the development of GC by targeting HSF1 and thus, is a possible strategy for for the management of GC
Credit default swaps and corporate innovation
We show that credit default swap (CDS) trading on a firm’s debt positively influences its technological innovation output measured by patents and patent citations. This positive effect is more pronounced in firms relying more on debt financing or being more subject to continuous monitoring by lenders prior to CDS trade initiation. Moreover, after CDS trade initiation, firms pursue more risky and original innovations and generate patents with higher economic value. Further analysis suggests that CDSs improve borrowing firms’ innovation output by enhancing lenders’ risk tolerance and borrowers’ risk taking in the innovation process rather than by increasing R&D investment. Taken together, our findings reveal the real effects of CDSs on companies’ investments and technological progress
Insights into distinct regulatory modes of nucleosome positioning
<p>Abstract</p> <p>Background</p> <p>The nucleosome is the fundamental unit of eukaryotic genomes. Experimental evidence suggests that the genomic DNA sequence and a variety of protein factors contribute to nucleosome positioning <it>in vivo</it>. However, how nucleosome positioning is determined locally is still largely unknown.</p> <p>Results</p> <p>We found that transcription factor binding sites (TFBSs) with particular nucleosomal contexts show a preference to reside on specific chromosomes. We identified four typical gene classes associated with distinct regulatory modes of nucleosome positioning, and further showed that they are distinguished by transcriptional regulation patterns. The first mode involves the cooperativity between chromatin remodeling and stable transcription factor (TF)-DNA binding that is linked to high intrinsic DNA binding affinities, evicting nucleosomes from favorable DNA sequences. The second is the DNA-encoded low nucleosome occupancy that is associated with high gene activity. The third is through chromatin remodeling and histone acetylation, sliding nucleosomes along DNA. This mode is linked to more cryptic sites for TF binding. The last consists of the nucleosome-enriched organization driven by other factors that overrides nucleosome sequence preferences. In addition, we showed that high polymerase II (Pol II) occupancy is associated with high nucleosome occupancy around the transcription start site (TSS).</p> <p>Conclusions</p> <p>We identified four different regulatory modes of nucleosome positioning and gave insights into mechanisms that specify promoter nucleosome location. We suggest two distinct modes of recruitment of Pol II, which are selectively employed by different genes.</p
Genome-wide analysis of interactions between ATP-dependent chromatin remodeling and histone modifications
<p>Abstract</p> <p>Background</p> <p>ATP-dependent chromatin remodeling and the covalent modification of histones play central roles in determining chromatin structure and function. Although several specific interactions between these two activities have been elaborated, the global landscape remains to be elucidated.</p> <p>Results</p> <p>In this paper, we have developed a computational method to generate the first genome-wide landscape of interactions between ATP-dependent chromatin remodeling and the covalent modification of histones in <it>Saccharomyces cerevisiae</it>. Our method succeeds in identifying known interactions and uncovers many previously unknown interactions between these two activities. Analysis of the genome-wide picture revealed that transcription-related modifications tend to interact with more chromatin remodelers. Our results also demonstrate that most chromatin remodeling-modification interactions act via interactions of remodelers with both histone-modifying enzymes and histone residues. We also found that the co-occurrence of both modification and remodeling has significantly different influences on multiple gene features (e.g. nucleosome occupancy) compared with the presence of either one.</p> <p>Conclusion</p> <p>We gave the first genome-wide picture of ATP-dependent chromatin remodeling-histone modification interactions. We also revealed how these two activities work together to regulate chromatin structure and function. Our results suggest that distinct strategies for regulating chromatin activity are selectively employed by genes with different properties.</p
Genome-wide analysis of the effect of histone modifications on the coexpression of neighboring genes in Saccharomyces cerevisiae
<p>Abstract</p> <p>Background</p> <p>Neighboring gene pairs in the genome of <it>Saccharomyces cerevisiae </it>have a tendency to be expressed at the same time. The distribution of histone modifications along chromatin fibers is suggested to be an important mechanism responsible for such coexpression. However, the extent of the contribution of histone modifications to the coexpression of neighboring genes is unclear.</p> <p>Results</p> <p>We investigated the similarity of histone modification between neighboring genes using autocorrelation analysis and composite profiles. Our analysis showed that neighboring genes had similar levels or changes of histone modifications, especially those transcribed in the same direction. The similarities, however, were restricted to 1 or 2 neighboring genes. Moreover, the expression of a gene was significantly correlated with histone modification of its neighboring gene(s), but this was limited to only 1 or 2 neighbors. Using a hidden Markov model (HMM), we found more than 2000 chromatin domains with similar acetylation changes as the cultures changed and a considerable number of these domains covered 2-4 genes. Gene pairs within domains exhibited a higher level of coexpression than random pairs and shared similar functions.</p> <p>Conclusions</p> <p>The results of this study suggest that similar histone modifications occur within only a small local chromatin region in yeast. The modifications generally have an effect on coexpression with only 1 or 2 neighboring genes. Some blocking mechanism(s) might strictly restrain the distribution of histone modifications in yeast.</p
Two distinct modes of nucleosome modulation associated with different degrees of dependence of nucleosome positioning on the underlying DNA sequence
<p>Abstract</p> <p>Background</p> <p>The nucleosome is the fundamental unit of eukaryotic genomes. Its positioning plays a central role in diverse cellular processes that rely on access to genomic DNA. Experimental evidence suggests that the genomic DNA sequence is one important determinant of nucleosome positioning. Yet it is less clear whether the role of the underlying DNA sequence in nucleosome positioning varies across different promoters. Whether different determinants of nucleosome positioning have characteristic influences on nucleosome modulation also remains to be elucidated.</p> <p>Results</p> <p>We identified two typical promoter classes in yeast associated with high or low dependence of nucleosome positioning on the underlying DNA sequence, respectively. Importantly, the two classes have low or high intrinsic sequence preferences for nucleosomes, respectively. The two classes are further distinguished by multiple promoter features, including nucleosome occupancy, nucleosome fuzziness, H2A.Z occupancy, changes in nucleosome positions before and after transcriptional perturbation, and gene activity. Both classes have significantly high turnover rates of histone H3, but employ distinct modes of nucleosome modulation: The first class is characterized by hyperacetylation, whereas the second class is highly regulated by ATP-dependent chromatin remodelling.</p> <p>Conclusion</p> <p>Our results, coupled with the known features of nucleosome modulation, suggest that the two distinct modes of nucleosome modulation selectively employed by different genes are linked with the intrinsic sequence preferences for nucleosomes. The difference in modes of nucleosome modulation can account for the difference in the contribution of DNA sequence to nucleosome positioning between both promoter classes.</p
Dietary L-Tryptophan Modulates the Hematological Immune and Antibacterial Ability of the Chinese Mitten Crab, Eriocheir sinensis, Under Cheliped Autotomy Stress
In pond cultures of juvenile Eriocheir sinensis, limb autotomy stress seriously affects and restricts the quality and economic benefits of aquaculture. This study was designed to evaluate the effects of dietary supplementation of L-tryptophan on E. sinensis under the cheliped autotomy stress. In the present study, 252 crabs were divided into four groups: dietary L-trp supplementation with 0.28, 0.40, 0.53, and 0.70%, and their hematological immunity, antioxidant capacity, anti-stress, and antibacterial ability were evaluated after 14 days of using biochemical analysis, flow cytometry, and molecular biology techniques. First, we counted the mortality after 14 days of feeding and found that compared with other treatments, dietary supplementation of 0.53 and 0.70% L-trp significantly lowered the mortality of E. sinensis. Moreover, the total hemocyte count (THC), hemocyanin, and glutathione (GSH) content, and glutathione peroxidase (GSH-Px) activity significantly increased at 7 and 14 d with dietary supplementation of 0.53 and 0.70% L-trp, in contrast with the significant decrease in malondialdehyde (MDA) content at 14 d in the same dietary groups (P<0.05). Next, the bacterial challenge test after 14 days of feeding showed that the THC levels, phagocytic rate, and acid phosphatase (ACP) and alkaline phosphatase (ALP) activity were significantly higher with dietary supplementation of 0.53 and 0.70% L-trp after 12 and 24 h of Aeromonas hydrophila injection, along with a significant improvement in the antioxidant capacity (P<0.05). Further, we measured the expression of antibacterial-related protein genes (EslecB and HSP 90) and found that they were significant up-regulated in the hepatopancreas, hemocytes, intestine, and gill in the groups with dietary supplementation of 0.53% and 0.70% L-trp after 12 h or 24 h of A. hydrophila injection (P<0.05). Taken together, the observations in this study indicate that dietary supplementation of L-trp can enhance the antioxidant capacity and improve the hematological immune status and antibacterial ability of E. sinensis under the cheliped autotomy stress, thereby increasing the survival rate of E. sinensis under cheliped autotomy stress
CAD increases the long noncoding RNA PUNISHER in small extracellular vesicles and regulates endothelial cell function via vesicular shuttling
Long noncoding RNAs (lncRNAs) have emerged as biomarkers and regulators of cardiovascular disease. However, the expression pattern of circulating extracellular vesicle (EV)-incorporated lncRNAs in patients with coronary artery disease (CAD) is still poorly investigated. A human lncRNA array revealed that certain EV-lncRNAs are significantly dysregulated in CAD patients. Circulating small EVs (sEVs) from patients with (n = 30) or without (n = 30) CAD were used to quantify PUNISHER (also known as AGAP2-antisense RNA 1 [AS1]), GAS5, MALAT1, and H19 RNA levels. PUNISHER (p = 0.002) and GAS5 (p = 0.02) were significantly increased in patients with CAD, compared to non-CAD patients. Fluorescent labeling and quantitative real-time PCR of sEVs demonstrated that functional PUNISHER was transported into the recipient cells. Mechanistically, the RNA-binding protein, heterogeneous nuclear ribonucleoprotein K (hnRNPK), interacts with PUNISHER, regulating its loading into sEVs. Knockdown of PUNISHER abrogated the EV-mediated effects on endothelial cell (EC) migration, proliferation, tube formation, and sprouting. Angiogenesis-related gene profiling showed that the expression of vascular endothelial growth factor A (VEGFA) RNA was significantly increased in EV recipient cells. Protein stability and RNA immunoprecipitation indicated that the PUNISHER-hnRNPK axis regulates the stability and binding of VEGFA mRNA to hnRNPK. Loss of PUNISHER in EVs abolished the EV-mediated promotion of VEGFA gene and protein expression. Intercellular transfer of EV-incorporated PUNISHER promotes a pro-angiogenic phenotype via a VEGFA-dependent mechanism
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