A further specification of the effects of font emphasis on reading comprehension: Evidence from event-related potentials and neural oscillations.

The attention hypothesis, which assumes that font emphasis captures readers' attention, is usually used to explain the mechanism by which such emphasis operates. This study further delineates the attention hypothesis by investigating the ways in which font emphasis captures attention and its effects on the integration of emphasized information into the previous context. We computed event-related potentials and frequency band-specific electroencephalographic power changes occurring while participants read sentences containing critical words that were either emphasized (i.e., displayed in a color different from the other words in the sentence) or not (i.e., shown in the same color as the rest of the sentence) and semantically congruent with prior words or not. The results showed that the emphasized words (as compared to control words) elicited a reduced N1 and increased P2, indicating that font emphasis reduced familiarity-based visuo-orthographic processing and instead increased controlled attentional processing. We also observed greater P300 and power decreases in the alpha and beta frequency range in response to critical words in the emphasized condition, suggesting that font emphasis enhances focal attention to promote a fuller integration of information into the sentence context. Furthermore, relative to the control condition, the emphasized condition induced delta and theta power increases for the incongruent words. These results suggest that font emphasis increases the efficiency of glyph processing, which facilitates lexical access.

Profiling analysis reveals the potential contribution of long non-coding RNAs to preterm white matter injury.

AIMS: The aim of this study was to investigate the molecular mechanism underlying preterm white matter injury (WMI) via the identification and functional analysis of differentially expressed long non-coding RNAs (lncRNAs) and mRNAs. MAIN METHODS: A neonatal rat model of preterm WMI was established by ligating the common carotid artery and hypoxia induction. RNA sequencing was performed to analyze gene expression profiles of brain samples. Gene Ontology (GO) and Kyoto Encyclopedia of Genes (KEGG) analyses were performed to evaluate functions of target mRNAs. A co-expression network was generated to explore regulatory mechanisms. KEY FINDINGS: In total, 210 lncRNAs and 619 mRNAs were differentially expressed between the preterm WMI group and the sham group. Based on GO and KEGG analyses, enriched pathways included the apoptotic signaling pathway, vascular endothelial growth factor (VEGF) signaling pathway, natural killer cell-mediated cytotoxicity pathway, and the autophagy pathway. SIGNIFICANCE: Differentially expressed lncRNAs and mRNAs in the brain tissues of preterm WMI model were identified, and the biological processes were closely associated with the development of preterm WMI, thus being considered potential targets for future studies.

Profile analysis reveals endogenous RNAs regulate necrotizing enterocolitis progression.

Necrotizing enterocolitis (NEC) is one of the most common and devastating gastrointestinal diseases in preterm newborns, and its underlying mechanisms remain unclear. Non-coding RNAs (ncRNAs) play critical roles in intestinal diseases; however, little is known about their roles in the development of NEC. To gain a deeper understanding of the pathophysiological mechanism of NEC, long non-coding RNAs (lncRNAs), microRNAs (miRNAs) and mRNAs were detected in an NEC rat model. In total, 1820 lncRNAs, 118 miRNAs and 929 mRNAs were differentially expressed in NEC group. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis indicated that these molecules were enriched in apoptosis, autophagic cell death, TLR4 signaling pathway, Notch signaling pathway, and mTOR signaling pathway. These pathways are thought to be closely associated with NEC. Furthermore, a lncRNA-miRNA interaction network was constructed, and four of the novel, differentially expressed lncRNAs with large changes were randomly verified using quantitative polymerase chain reaction (qPCR). The GO and KEGG pathway analysis of these four lncRNAs showed that they were associated with the negative regulation of TLR4 signaling pathway and Notch signaling pathway. In conclusion, our study revealed that these differentially expressed lncRNAs may participate in the development of NEC via interactions with miRNAs and may serve as possible biomarkers and target genes in NEC.

Peptidomics analysis of umbilical cord blood reveals potential preclinical biomarkers for neonatal respiratory distress syndrome.

AIMS: The purpose of this study was to investigate the pathophysiology and discover novel predictors of neonatal respiratory distress syndrome (NRDS) from a peptidomics perspective. MAIN METHODS: Comparative profiling of umbilical cord blood from NRDS and control patients was performed by liquid chromatography tandem mass spectrometry technology. The underlying biological functions of the differentially expressed peptides (DEPs) were predicted by Gene Ontology (GO) and KEGG pathway analyses. The interactions of DEPs and their precursor proteins were explored by ingenuity pathway analysis (IPA). The sources and stability of DEPs were determined by online databases, including UniProt, SMART and ProtParam tool. KEY FINDINGS: A total of 251 DEPs were identified, of which 139 peptides were upregulated, and 112 peptides were downregulated (fold change ≥2.0, P < 0.05). These DEPs were predicted to be associated with respiratory failure, atelectasis, and morphogenesis of endothelial cells. These processes indicated that DEPs may play a role in NRDS. Among them, eleven stable DEPs might be used as preclinical biomarkers. SIGNIFICANCE: Our findings improve our understanding of NRDS and facilitate the discovery of candidate diagnostic biomarkers for NRDS from the perspective of peptidomics.