Table_1_Conventionality matters in Chinese metaphor but not simile comprehension: evidence from event-related potentials.XLSX

Metaphor and simile, two prevalent forms of figurative language widely employed in daily communication, serve as significant research subjects in linguistics. The Career of Metaphor Theory in cognitive linguistics posits that as conventionality increases, the cognitive mechanisms of metaphor comprehension shift from “comparison” to “categorization.” In line with this notion, prior electrophysiological investigations have revealed that novel metaphors elicit a stronger N400 brain response compared to conventional metaphors. However, the observed N400 difference between conventional and novel metaphors may merely stem from the familiarity contrast between them, as conventional metaphors are typically more familiar than novel ones. To address this dichotomy, the present study not only compared the N400 responses between conventional and novel metaphors but also between conventional and novel similes. While conventional and novel similes differ in familiarity, similar to conventional and novel metaphors, both are processed via “comparison” mechanisms. The results revealed that novel metaphors elicited larger N400 amplitudes compared to conventional metaphors, aligning with previous findings. In contrast, no significant N400 differences were observed between conventional and novel similes, suggesting that familiarity disparity is unlikely to account for N400 distinctions. Our findings imply that conventional and novel metaphors undergo distinct cognitive processing mechanisms (“comparison” versus “categorization”), thereby providing further empirical validation for the Career of Metaphor Theory.</p

Sea Surface Temperature Prediction With Memory Graph Convolutional Networks

No description supplie

MiR-223 promoted TRAIL-induced cell death by down-regulating HAX-1 expression in TNBCSCs.

(A) The transfection efficiency of HAX-1 siRNA and HAX-1 vector in MDA-MB-231 CSCs and MDA-MB-435 CSCs was evaluated by western blot analysis. *Pvs. the siRNA-NC group, t test, #Pvs. the miR-NC group, t test, &Pvs. the miR-223 group, t test. (B) MDA-MB-231 CSCs and MDA-MB-435 CSCs were transfected with miR-223 mimics, HAX-1 siRNA, and HAX-1 vector. Twenty-four hours after transfection, the cells were treated with TRAIL (10 ng/ml) for 48 h. Relative cell viability was determined by MTT assay. *Pvs. the TRAIL+miR-NC group, #Pvs. the TRAIL+miR-223 group, t test.</p

MicroRNA-223 Increases the Sensitivity of Triple-Negative Breast Cancer Stem Cells to TRAIL-Induced Apoptosis by Targeting HAX-1

<div><p>Drug resistance remains a significant challenge in the treatment of triple-negative breast cancer (TNBC). Recent studies have demonstrated that this drug resistance is associated with a group of cells known as cancer stem cells (CSCs), which are believed to determine the sensitivity of tumor cells to cancer treatment. MicroRNAs (miRNAs) are small, non-coding RNAs that play significant roles in normal and cancer cells. MiR-223 reportedly acts as a tumor suppressor in a range of cancers. However, the role of miR-223 in TNBC, especially in triple-negative breast cancer stem cells (TNBCSCs), remains unknown. Here, we found that miR-223 expression was down-regulated in CD44⁺CD24^-/low TNBCSCs compared with non-CSCs. Furthermore, we found that miR-223 overexpression resensitized TNBCSCs to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis. The HAX-1 gene, which is located in the mitochondria and functions as an anti-apoptotic protein, was found to be directly regulated by miR-223 in MDA-MB-231 cells. We demonstrated that miR-223 overexpression promoted TRAIL-induced apoptosis through the mitochondria/ROS pathway. In conclusion, our results suggest that miR-223 increases the sensitivity of TNBCSCs to TRAIL-induced apoptosis by targeting HAX-1. Our findings have improved our understanding of the role of miR-223 in TNBC and may contribute to TNBC treatment.</p></div

MiR-223 promoted TRAIL-induced apoptosis through the mitochondria/ROS pathway.

<p>(A) The mitochondrial membrane potential (ΔΨ_m) of MDA-MB-231 CSCs and MDA-MB-435 CSCs cells treated with miR-223 and TRAIL was detected using JC-1 staining and flow cytometry. (B) ROS generation was detected using DHE staining and flow cytometry. (C) MDA-MB-231 CSCs and MDA-MB-435 CSCs cells were treated with miR-223 and TRAIL (10 ng/ml) in the presence or absence of 5 mM NAC. Cell viability was then detected by MTT assay. *<i>P</i><0.05 <i>vs</i>. the TRAIL+miR-NC group, ^&<i>P</i><0.05 <i>vs</i>. the TRAIL group, ^#<i>P</i><0.05 <i>vs</i>. the TRAIL+miR-223 group, t test.</p

MiR-223 expression levels in breast cancer cell lines.

<p>(A) QRT-PCR analysis showed that the decrease of miR-223 expression was more significant in TNBC cell lines (MDA-MB-231 and MDA-MB-435) than the non-TNBC cell lines (MCF-7 and SKBR3). *<i>P</i><0.05 <i>vs</i>. MCF-10A cells, t test, **<i>P</i><0.01 <i>vs</i>. MCF-10A cells, t test. (B) MiR-223 expression was significantly down-regulated in both MDA-MB-231 CSCs and MDA-MB-435 CSCs compared with their parental cells. *<i>P</i><0.05, t test, **<i>P</i><0.01, t test.</p

Expression stability values (M) and ranking of candidate reference genes as calculated by NormFinder.

<p>Expression stability values (M) and ranking of candidate reference genes as calculated by NormFinder.</p

Globally Accurate Potential Energy Surface for BH₂⁺2(1³A′) Using the Switching Function Formalism

A great number of ab initio energy points are calculated using the aug-cc-pV­(Q,5)­Z basis sets at the multireference configuration interaction level and extrapolated to the complete basis set limit. An exact three-dimensional potential energy surface of the ground-state BH2+ is obtained. A switching function is developed to model the transition of B+(3P) to B+(1S) to guarantee the reliable behavior at B+(3P) + H2(X1∑g+) and BH+(X2∑+) + H­(2S) dissociation limits. The various topographic features of the new global potential energy surface are discussed in detail, showing a good agreement with the previous results from the theory. The quasi-classical trajectory method is utilized to calculate the integral cross sections of the B+(3P) + H2(X1∑g+) (v = 0, j = 0) → BH+(X2∑+) + H­(2S) reaction, which can provide another support for reliability of the title potential energy surface

HAX-1 is the target of miR-223 in TNBCSCs.

<p>(A) HAX-1 was predicted to be a target of miR-223 by the TargetScan database. (B) HAX-1 expression in MDA-MB-231 CSCs, MDA-MB-231 non-CSCs, MDA-MB-435 CSCs, MDA-MB-435 non-CSCs, and MCF-10A cells was evaluated by western blot analysis. *<i>P</i><0.05 <i>vs</i>. the MCF-10A, t test, ^#<i>P</i><0.05 <i>vs</i>. the MDA-MB-231-non-CSCs, t test, ^&<i>P</i><0.05 <i>vs</i>. the MDA-MB-435-non-CSCs, t test. (C) MDA-MB-231 CSCs or MDA-MB-231-non-CSCs were cotransfected with the wildtype/mutant 3’-UTR of HAX-1 and miR-223 mimics as indicated. Forty-eight hours post-transfection, luciferase activity was detected using a dual-luciferase reporter assay system, according to the manufacturer’s instructions. *<i>P</i><0.05, t test. (D) Luciferase assays in MDA-MB-435 CSCs or MDA-MB-231-non-CSCs. *<i>P</i><0.05, t test. (E) Western blot analysis showed that transfection of miR-223 mimics down-regulated HAX-1 expression in TNBCSCs. *<i>P</i><0.05, t test.</p

MiR-223 enhances the anti-tumor effect of doxorubicin and cisplatin in TNBCSCs.

<p>(A) MDA-MB-231 CSCs and MDA-MB-435 CSCs were transfected with miR-223 mimics and HAX-1 vector. Twenty-four hours after transfection, the cells were treated with doxorubicin (2 μg/ml) for 48 h. Relative cell viability was determined by MTT assay. *<i>P</i><0.05 <i>vs</i>. the doxorubicin+miR-NC group, t test, ^#<i>P</i><0.05 <i>vs</i>. the doxorubicin+miR-223 group, t test. (B) MDA-MB-231 CSCs and MDA-MB-435 CSCs were transfected with miR-223 mimics and HAX-1 vector. Twenty-four hours after transfection, the cells were treated with cisplatin (2 μM) for 48 h. Relative cell viability was determined by MTT assay. *<i>P</i><0.05 <i>vs</i>. the cisplatin+miR-NC group, t test, ^#<i>P</i><0.05 <i>vs</i>. the cisplatin+miR-223 group, t test.</p