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Although the data-driven static voltage stability problems have been widely studied, most of the classical algorithms focus more on improving the accuracy of the system prediction, ignoring the error classification errors generated during the prediction process. Furthermore, current research ignores the utilization of data-driven voltage stability assessment of energy storage systems. Therefore, this paper proposes a static voltage stability assessment method for photovoltaic energy storage systems based on considering the error classification constraint algorithm using Neyman-Pearson umbrella algorithms. Firstly, the Spearman Correlation Coefficient is employed in the feature selection phase. Secondly, an updated voltage stability assessment (VSA) model is proposed. Compared with the existing data-driven prediction of system static voltage stability in the literature, it can realize voltage stability assessment more quickly. Furthermore, on the basis of rapid voltage stability assessment, the umbrella NP classifier can also effectively limit the first-class error and attenuate the effect of error classification by mirroring the control of the number of cycle splits and the type I classification error threshold. Finally, the simulation and experimental results show that the effectiveness and robustness of the scheme proposed in this paper in grid-connected photovoltaic energy farms.

This study assesses the impact of simulated sea level rise (SLR) on mercury distribution and migration in an urban mangrove wetland on the northern coast of Maluan Bay, Xiamen City, Fujian Province, China. Two adjacent Kandelia obovata mangrove plots with elevations representing current sea level and a 40-cm SLR were examined. Total mercury (THg), methylmercury (MeHg), and mercury isotopes in sediments from different elevations were analyzed to reveal the geochemical behavior of mercury under a simulated 100-year SLR scenario. THg and MeHg distribution in sediments mirrored patterns of biogenic elements (carbon, nitrogen, and phosphorus), suggesting adsorption onto organic matter as the primary entry mechanism. Low-elevation plots showed significantly higher concentrations of THg, MeHg, total organic carbon (TOC), total nitrogen (TN), and total phosphorus (TP) compared to high-elevation plots. Mercury isotope characteristics indicated that the primary mercury source was anthropogenic emissions from surrounding lands, entering the wetland from both landward and seaward directions. The study highlights the crucial role of mangrove wetlands in mercury pollution control and nutrient cycling under SLR conditions. Results suggest that SLR enhances the retention capacity of mangrove wetlands for THg, MeHg, and nutrients. This research provides a scientific basis for mangrove conservation and restoration, offering new insights into the geochemical behavior of mercury in vegetated intertidal ecosystems in the context of climate change.

Vitamins are dietary components necessary for cellular metabolic balance, especially redox homeostasis; deficient or excessive supply may give rise to symptoms of psychiatric disorders. Exploring the nutritional and metabolic pathways of vitamins could contribute to uncovering the underlying pathogenesis of ferroptosis-associated diseases. This mini-review aims to provide insights into vitamins closely linked to the regulation of ferroptosis from the perspective of cellular reactive oxygen species biology. The mainstream reprogramming mechanisms of ferroptosis are overviewed, focusing on unique biological processes of iron metabolism, lipid metabolism, and amino acid metabolism. Moreover, recent breakthroughs in therapeutic interventions targeting ferroptosis via fully utilizing vitamin-based pharmacological tools were overviewed, covering vitamins (B, C, E, and K). Finally, mechanism insight related to vitamin-associated nutrient signaling was provided, highlighting the pharmacological benefits of metabolically reprogramming ferroptosis-associated diseases.

Alzheimer’s disease (AD) is one of the most common chronic neurodegenerative diseases. Hyperphosphorylated tau plays an indispensable role in neuronal dysfunction and synaptic damage in AD. Proteolysis-targeting chimeras (PROTACs) are a novel type of chimeric molecule that can degrade target proteins by inducing their polyubiquitination. This approach has shown promise for reducing tau protein levels, which is a potential therapeutic target for AD. Compared with traditional drug therapies, the use of PROTACs to reduce tau levels may offer a more specific and efficient strategy for treating AD, with fewer side effects. In the present study, we designed and synthesized a series of small-molecule PROTACs to knock down tau protein. Of these, compound C8 was able to lower both total and phosphorylated tau levels in HEK293 cells with stable expression of wild-type full-length human tau (termed HEK293-htau) and htau-overexpressed mice. Western blot findings indicated that C8 degraded tau protein through the ubiquitin–proteasome system in a time-dependent manner. In htau-overexpressed mice, the results of both the novel object recognition and Morris water maze tests revealed that C8 markedly improved cognitive function. Together, our findings suggest that the use of the small-molecule PROTAC C8 to degrade phosphorylated tau may be a promising therapeutic strategy for AD.

As the highest altitude and the longest plateau railway line, the Qinghai–Tibet railway passes through a large area of continuous permafrost. As the key position of the combination of roadbed and bridge, the stability and strength of the bridge approach directly affect the smoothness of the whole line. Through an indoor model test, the distribution pattern of space temperature field and the change law of temperature measuring points in the bridge approach of gravel sandwich are studied. With the increase in the depth from the subgrade surface, the influence of the temperature change in the upper atmosphere decreases gradually at the 2.5-m platform back of the subgrade center section, resulting in an obvious lag in the subgrade. By comparing the temperature measurement data of different bridge approaches of the gravel interlayer road bridge and the bridge approach of the U-shaped block gravel road bridge, it is shown that the U-shaped structure not only has a better overall cooling effect, but also the cooling effect gradually increases with the increase in the distance from the abutment back. The influence range of the road–bridge transition section on the spatial temperature field is approximately 14 m in the back of the abutment, and the influence range at 7.5 m is the most severe. The research results have important practical significance and engineering application value for the operation and maintenance of the Qinghai–Tibet railway.

Porcine epidemic diarrhea (PED) is a highly contagious intestinal infection primarily affecting pigs. It is caused by the porcine epidemic diarrhea virus (PEDV). PEDV targets the villus tissue cells in the small intestine and mesenteric lymph nodes, resulting in shortened intestinal villi and, in extreme cases, causing necrosis of the intestinal lining. Moreover, PEDV infection can disrupt the balance of the intestinal microflora, leading to an overgrowth of harmful bacteria like Escherichia coli. Exosomes, tiny membrane vesicles ranging from 30 to 150 nm in size, contain a complex mixture of RNA and proteins. MicroRNA (miRNA) regulates various cell signaling, development, and disease progression processes. This study extracted exosomes from both groups and performed high-throughput miRNA sequencing and bioinformatics techniques to investigate differences in miRNA expression within exosomes isolated from PEDV-infected porcine small intestine tissue compared to healthy controls. Notably, two miRNA types displayed upregulation in infected exosomes, while 12 exhibited downregulation. These findings unveil abnormal miRNA regulation patterns in PEDV-infected intestinal exosomes, shedding light on the intricate interplay between PEDV and its host. This will enable further exploration of the relationship between these miRNA changes and signaling pathways, enlightening PEDV pathogenesis and potential therapeutic targets.

ObjectivesA retrospective analysis of the clinical outcomes of personalized interventions for type 2 diabetes mellitus (T2DM) in an interdisciplinary team.MethodsUnder the guidance of an interdisciplinary team, 40 patients with T2DM underwent a systematic examination at the beginning of the intervention, 3 months after the intervention, and 3 months of follow-up at the end of the intervention (i.e., at 6 months). Key indicators such as fasting plasma glucose (FPG), 2-hour postprandial glucose (2hPG), fasting insulin level (FINS), glycated hemoglobin (HbA1c), blood lipids, and body mass index (BMI) were measured.ResultsAfter the 3-month intervention, participants’ BMI, FPG, 2hPG, FINS, and HbA1c improved significantly, with statistically significant differences (P

Background and aims: Obesity is one of the most prevalent diseases worldwide with less ideal approved agents in clinic. Activating the HSF1/PGC-1α axis in adipose tissues has been reported to induce thermogenesis in mice, which presents a promising therapeutic avenue for obesity treatment. The present study aimed to identified novel natural HSF1 activator and evaluated the therapeutic effects of the newly discovered compound on obesity-associated metabolic disorders and the molecular mechanisms of these effects.Methods: Our previous reported HSF1/PGC-1α activator screening system was used to identify novel natural HSF1 activator. The PGC-1α luciferase activity, immunoblot, protein nuclear-translocation, immunofluorescence, chromatin immunoprecipitation assays were used to evaluate the activity of compound HN-001 in activating HSF1. The experiments of mitochondrial number measurement, TG assay and imaging, cellular metabolic assay, gene assays, and CRISPR/Cas 9 were applied for investigating the metabolic effect of HN-001 in C3H10-T1/2 adipocytes. The in vivo anti-obesity efficacies and beneficial metabolic effects of HN-001 were evaluated by performing body and fat mass quantification, plasma chemical analysis, GTT, ITT, cold tolerance test, thermogenesis analysis.Results: HN-001 dose- and time-dependently activated HSF1 and induced HSF1 nuclear translocation, resulting in an enhancement in binding with the gene Pgc-1α. This improvement induced activation of adipose thermogenesis and enhancement of mitochondrial oxidation capacity, thus inhibiting adipocyte maturation. Deletion of HSF1 in adipocytes impaired mitochondrial oxidation and abolished the above beneficial metabolic effects of HN-001, including adipocyte browning induction, improvements in mitogenesis and oxidation capacity, and lipid-lowering ability. In mice, HN-001 treatment efficiently alleviated diet-induced obesity and metabolic disorders. These changes were associated with increased body temperature in mice and activation of the HSF1/PGC-1α axis in adipose tissues. UCP1 expression and mitochondrial biogenesis were increased in both white and brown adipose tissues of HN-001-treated mice.Conclusion: These data indicate that HN-001 may have therapeutic potential for obesity-related metabolic diseases by increasing the capacity of energy expenditure in adipose tissues through a mechanism involving the HSF1/PGC-1α axis, which shed new light on the development of novel anti-obesity agents derived from marine sources.

Faculty members' research performance holds great significance for the development of a university. The primary objective of this study is to examine the influences of researchers' personalities on their research performance within universities, as well as the mediating role of research engagement in this relationship. The study encompassed 189 faculty members from a university and employed descriptive statistics, correlation analysis, measurement, and structural equation modeling as the analytical procedures. The results obtained from structural equation modeling reveal significant effects of faculty members' personalities on their objective research performance rather than self-reported performance. Specifically, conscientiousness and openness to experience exhibit a positive correlation with research performance. On the contrary, the neuroticism and social attributes of personality (the integration of extraversion and agreeableness) exhibit a negative correlation with research performance. Furthermore, research engagement mediates the effects of openness to experience and neuroticism on research performance. This study carries significant implications for the training and recruitment selection of faculty members in universities and enhances our understanding of how different personalities lead to a variance in research engagement and performance.

The activation of anti-tumor immunity is critical in treating cancers. Recent studies indicate that several chemotherapy agents can stimulate anti-tumor immunity by inducing immunogenic cell death and durably eradicate tumors. This suggests that immunogenic chemotherapy holds great potential for improving response rates. However, chemotherapy in practice has only had limited success in inducing long-term survival or cure of cancers when used either alone or in combination with immunotherapy. We think that this is because the importance of dose, schedule, and tumor model dependence of chemotherapy-activated anti-tumor immunity is under-appreciated. Here, we review immune modulation function of representative chemotherapy agents and propose a model of immunogenic chemotherapy-induced long-lasting responses that rely on synergetic interaction between killing tumor cells and inducing anti-tumor immunity. We comb through several chemotherapy treatment schedules, and identify the needs for chemotherapy dose and schedule optimization and combination therapy with immunotherapy when chemotherapy dosage or immune responsiveness is too low. We further review tumor cell intrinsic factors that affect the optimal chemotherapy dose and schedule. Lastly, we review the biomarkers indicating responsiveness to chemotherapy and/or immunotherapy treatments. A deep understanding of how chemotherapy activates anti-tumor immunity and how to monitor its responsiveness can lead to the development of more effective chemotherapy or chemo-immunotherapy, thereby improving the efficacy of cancer treatment.

While hippocampal atrophy and its regional susceptibility to Alzheimer’s disease (AD) are well reported at late stages of AD, studies of the asymptomatic stage of AD are limited but could elucidate early stage pathophysiology as well as provide predictive biomarkers. In this study, we performed multi-modal magnetic resonance imaging (MRI) to estimate morphometry, functional connectivity, and tissue microstructure of hippocampal subfields in cognitively normal adults including those with asymptomatic AD. High-resolution resting-state functional, diffusion and structural MRI, cerebral spinal fluid (CSF), and neuropsychological evaluations were performed in healthy young adults (HY: n = 40) and healthy older adults with negative (HO−: n = 47) and positive (HO+ : n = 25) CSF biomarkers of AD. Morphometry, functional connectivity, and tissue microstructure were estimated from the structural, functional, and diffusion MRI images, respectively. Our results indicated that normal aging affected morphometry, connectivity, and microstructure in all hippocampal subfields, while the subiculum and CA1-3 demonstrated the greatest sensitivity to asymptomatic AD pathology. Tau, rather than amyloid-β, was closely associated with imaging-derived synaptic and microstructural measures. Microstructural metrics were significantly associated with neuropsychological assessments. These findings suggest that the subiculum and CA1-3 are the most vulnerable in asymptomatic AD and tau level is driving these early changes.

The purpose of this study was to assess spatially remote effects of hemodynamic impairment on functional network topology contralateral to unilateral anterior circulation steno-occlusive disease (SOD) using resting-state blood oxygen level-dependent (BOLD) imaging, and to investigate the relationships between network connectivity and cerebrovascular reactivity (CVR), a measure of hemodynamic stress. Twenty patients with unilateral, chronic anterior circulation SOD and 20 age-matched healthy controls underwent resting-state BOLD imaging. Five-minute standardized baseline BOLD acquisition was followed by acetazolamide infusion to measure CVR. The BOLD baseline was used to analyze network connectivity contralateral to the diseased hemispheres of SOD patients. Compared to healthy controls, reduced network degree (z-score = −1.158 ± 1.217, P < 0.001, false discovery rate (FDR) corrected), local efficiency (z-score = −1.213 ± 1.120, P < 0.001, FDR corrected), global efficiency (z-score = −1.346 ± 1.119, P < 0.001, FDR corrected), and enhanced modularity (z-score = 1.000 ± 1.205, P = 0.002, FDR corrected) were observed in the contralateral, normal hemispheres of SOD patients. Network degree (P = 0.089, FDR corrected; P = 0.027, uncorrected) and nodal efficiency (P = 0.089, FDR corrected; P = 0.045, uncorrected) showed a trend toward a positive association with CVR. The results indicate remote abnormalities in functional connectivity contralateral to the diseased hemispheres in patients with unilateral SOD, despite the absence of macrovascular disease or demonstrable hemodynamic impairment. The clinical impact of remote functional disruptions requires dedicated investigation but may portend far reaching consequence for even putatively unilateral cerebrovascular disease.

The relationship between bilingual language control and domain-general cognitive control has been a hot topic in the research field of bilingualism. Previous studies mostly examined the correlation between performances of bilinguals in language control tasks and that in domain-general cognitive control tasks and came to the conclusions that they overlap, partially overlap, or are qualitatively different. These contradictory conclusions are possibly due to the neglect of the moderating effect of second language (L2) proficiency, that is, the relationship between bilingual language control and domain-general cognitive control might vary with the L2 proficiency of bilinguals. To examine this hypothesis, we recruited 36 unbalanced Chinese-English bilinguals to perform the Simon task (to assess domain-general cognitive control), Oxford Placement Test (to assess L2 proficiency), and picture naming tasks in single-and dual-language contexts (to evoke local and global language control). We find that Simon scores positively predicted switching costs in bilinguals with low L2 proficiency, but not in bilinguals with high L2 proficiency. Furthermore, Simon scores positively predicted mixing costs in bilinguals with high L2 proficiency, but not in bilinguals with low L2 proficiency. These results verify the moderating effect of L2 proficiency on the relationship between bilingual language control and domain-general cognitive control, that is, bilinguals with more proficient L2 rely on domain-general cognitive control less for local language control and more for global language control. This may imply a shift from local to global for the dependency of bilingual language control on domain-general cognitive control during the L2 development of bilinguals.

BackgroundThe 5-year survival rate of patients with lung cancer in China is less than 20% and predicting their prognosis is challenging. We investigated the association between a common non-synonymous single nucleotide polymorphism (SNP), rs7214723, in the Ca2+/calmodulin-dependent protein kinase kinase 1 (CAMKK1) gene and the prognosis of patients with lung cancer.MethodsGenomic DNA was extracted from the blood samples of 839 patients with lung cancer, recruited from Changhai Hospital (n = 536) and Taizhou Institute of Health Sciences (n = 352), and genotyped using the SNPscan technique. The association between patient prognosis and the genotypic data for CAMKK1 was analyzed using a multivariate Cox proportional hazards model adjusted for multiple potential confounders. The CRISPR/Cas9 gene-editing system was used to introduce point mutations in the CAMKK1 rs7214723 of A549 and NCI-H358 cells. Subsequently, Cell proliferation and migration ability were assessed with the Cell Counting Kit-8 and scratch assay. The Annexin V-FITC apoptosis detection kit was used to detect cell apoptosis.ResultsThe CAMKK1 rs7214723 recessive CC genotype conferred significantly better overall survival (CC vs. TT + TC: adjusted hazard ratio = 0.78, 95% confidence interval [CI], 0.61-1.00, P = 0.049) than the TT + TC genotypes. Stratified analysis showed that the CAMKK1 rs7214723 CC genotype and recessive CC genotype conferred a significantly decreased risk of death in patients who were male, had a smoking history, or had stage III + IV cancer, compared with the TT and TT + TC genotypes. Relative to the TT + TC genotypes, the rs7214723 recessive CC genotype was also associated with a decreased risk of death in patients aged < 60 years (CC vs. TT + TC: adjusted hazard ratio = 0.59, 95% CI, 0.37-0.93, P = 0.024) and patients with squamous cell carcinoma (CC vs. TT + TC: adjusted hazard ratio = 0.65, 95% CI, 0.44-0.98, P = 0.038). Remarkably, CRISPR/Cas9-guided single nucleotide editing demonstrated that CAMKK1 rs7214723 T > C mutation significantly inhibits cell proliferation and migration and promotes cell apoptosis.ConclusionsCAMKK1 SNP rs7214723 may be a significant prognostic factor for the risk of death among patients with lung cancer.

Metronomic chemotherapy can drastically enhance immunogenic tumor cell death. However, the mechanisms responsible are still incompletely understood. Here, we develop a mathematical model to elucidate the underlying complex interactions between tumor growth, immune system activation, and therapy-mediated immunogenic cell death. Our model is conceptually simple, yet it provides a surprisingly excellent fit to empirical data obtained from a GL261 SCID mouse glioma model treated with cyclophosphamide on a metronomic schedule. The model includes terms representing immune recruitment as well as the emergence of drug resistance during prolonged metronomic treatments. Strikingly, a single fixed set of parameters, adjusted neither for individuals nor for drug schedule, recapitulates experimental data across various drug regimens remarkably well, including treatments administered at intervals ranging from 6 to 12 days. Additionally, the model predicts peak immune activation times, rediscovering experimental data that had not been used in parameter fitting or in model construction. Notably, the validated model suggests that immunostimulatory and immunosuppressive intermediates are responsible for the observed phenomena of resistance and immune cell recruitment, and thus for variation of responses with respect to different schedules of drug administration.

The genetic control of plant architecture in crops is critical for agriculture and understanding morphological evolution. This study showed that an open reading frame (ORF) of the rice domestication gene PROG1 appeared 3.4–3.9 million years ago (Mya). Subsequently, it acquired a novel protein-coding gene function in the genome of O. rufipogon (~0.3–0.4 Mya). This extremely young gene and its paralogous C2H2 genes located nearby define the prostrate architecture of O. rufipogon and, thus, are of adaptive significance for wild rice in swamp and water areas. However, selection for dense planting and high yield during rice domestication silenced the PROG1 gene and caused the loss of the RPAD locus containing functional C2H2 paralogs; hence, domesticated lines exhibit an erect plant architecture. Analysis of the stepwise origination process of PROG1 and its evolutionary genetics revealed that this zinc-finger coding gene may have rapidly evolved under positive selection and promoted the transition from non- or semi-prostrate growth to prostrate growth. A transgenic assay showed that PROG1 from O. rufipogon exerts a stronger function compared with PROG1 sequences from other Oryza species. However, the analysis of the expression levels of PROG1 in different Oryza species suggests that the transcriptional regulation of PROG1 has played an important role in its evolution. This study provides the first strong case showing how a fundamental morphological trait evolved in Oryza species driven by a gene locus.

Interactions between the brain networks and subnetworks are crucial for active and resting cognitive states. Whether a subnetwork can restore the adequate function of the parent network whenever a disease state affects the parent network is unclear. Investigations suggest that the control of the anterior insula-based network (AIN) over the default-mode network (DMN) and central-executive network (CEN) is decreased in individuals with mild cognitive impairment (MCI). Here, we hypothesized that the posterior insula-based network (PIN) attempts to compensate for this decrease. To test this, we compared a group of MCI and normal cognitive individuals. A dynamical causal modeling method has been employed to investigate the dynamic network controls/modulations. We used the resting state functional MRI data, and assessed the interactions of the AIN and of the PIN, respectively, over the DMN and CEN. We found that the greater control of AIN than that of DMN (Wilcoxon rank sum: Z = 1.987; p = 0.047) and CEN (Z = 3.076; p = 0.002) in normal group and the lower (impaired) control of AIN than that of CEN (Z = 8.602; p = 7.816 × 10-18). We further revealed that the PIN control was significantly higher than that of DMN (Z = 6.608; p = 3.888 × 10-11) and CEN (Z = 6.429; p = 1.278 × 10-10) in MCI group where the AIN was impaired, but that control was significantly lower than of DMN (Z = 5.285; p = 1.254 × 10-7) and CEN (Z = 5.404; p = 6.513 × 10-8) in normal group. Finally, the global cognitive test score assessed using Montreal cognitive assessment and the network modulations were correlated (Spearman’s correlation: r = 0.47; p = 3.76 × 10-5 and r = -0.43; p = 1.97 × 10-4). These findings might suggest the flexible functional profiles of AIN and PIN in normal aging and MCI.

Hypertensive African–Americans have a greater risk of cognitive impairment than hypertensive Caucasian–Americans. The neural basis of this increased risk is yet unknown. Neuroimaging investigations suggest that the normal neural activity comprises complex interactions between brain networks. Recent studies consistently demonstrate that the insula, part of the salience network, provides modulation effects (information flow) over the default-mode and central-executive networks in cognitively normal subjects, and argue that the modulation effect is declined in cognitive impairment. The purpose of this study is to examine the information flow at the nodes of three networks using resting state functional magnetic resonance imaging (MRI) data in cognitively impaired hypertensive individuals with the African–Americans and the Caucasian–Americans races, and to compare the thickness of impaired node between two racial groups. Granger causality methodology was used to calculate information flow between networks using resting state functional MRI data, and FreeSurfer was used to measure cortical thickness from T1-weighted structural images. We found that negative information flow of the insula in both African–Americans and Caucasian–Americans, which was in contrast with previously reported positive information flow in this region of normal individuals. Also, significantly greater negative information flow in insula was found in African–Americans than Caucasian–Americans (Wilcoxon rank sum; Z = 2.06; p < 0.05). Significantly, lower insula thickness was found in African–Americans compared with Caucasian–Americans (median = 2.797 mm vs. 2.897 mm) (Wilcoxon rank sum; Z = 2.09; p < 0.05). Finally, the insula thickness correlated with the global cognitive testing measured by Montreal cognitive assessment (Spearman’s correlation; r = 0.30; p < 0.05). These findings suggest that the insula is a potential biomarker for the racial disparity in cognitive impairment of hypertensive individuals.

Ambiguous words are hard to learn, yet little is known about what causes this difficulty. The current study aimed to investigate the relationship between the representations of new and prior meanings of ambiguous words in second language (L2) learning, and to explore the function of inhibitory control on L2 ambiguous word learning at the initial stage of learning. During a 4-day learning phase, Chinese–English bilinguals learned 30 novel English words for 30 min per day using bilingual flashcards. Half of the words to be learned were unambiguous (had one meaning) and half were ambiguous (had two semantically unrelated meanings learned in sequence). Inhibitory control was introduced as a subject variable measured by a Stroop task. The semantic representations established for the studied items were probed using a cross-language semantic relatedness judgment task, in which the learned English words served as the prime, and the targets were either semantically related or unrelated to the prime. Results showed that response latencies for the second meaning of ambiguous words were slower than for the first meaning and for unambiguous words, and that performance on only the second meaning of ambiguous words was predicted by inhibitory control ability. These results suggest that, at the initial stage of L2 ambiguous word learning, the representation of the second meaning is weak, probably interfered with by the representation of the prior learned meaning. Moreover, inhibitory control may modulate learning of the new meanings, such that individuals with better inhibitory control may more effectively suppress interference from the first meaning, and thus learn the new meaning more quickly.

Interactions between the brain networks and subnetworks are crucial for active and resting cognitive states. Whether a subnetwork can restore the adequate function of the parent network whenever a disease state affects the parent network is unclear. Investigations suggest that the control of the anterior insula-based network (AIN) over the default-mode network (DMN) and central-executive network (CEN) is decreased in individuals with mild cognitive impairment (MCI). Here, we hypothesized that the posterior insula-based network (PIN) attempts to compensate for this decrease. To test this, we compared a group of MCI and normal cognitive individuals. A dynamical causal modeling method has been employed to investigate the dynamic network controls/modulations. We used the resting state functional MRI data, and assessed the interactions of the AIN and of the PIN, respectively, over the DMN and CEN. We found that the greater control of AIN than that of DMN (Wilcoxon rank sum: Z = 1.987; p = 0.047) and CEN (Z = 3.076; p = 0.002) in normal group and the lower (impaired) control of AIN than that of CEN (Z = 8.602; p = 7.816 1018). We further revealed that the PIN control was significantly higher than that of DMN (Z = 6.608; p = 3.888 10 11) and CEN (Z = 6.429; p = 1.278 1010) in MCI group where the AIN was impaired, but that control was significantly lower than of DMN (Z = 5.285; p = 1.254 107) and CEN (Z = 5.404; p = 6.513 10 8) in normal group. Finally, the global cognitive test score assessed using Montreal cognitive assessment and the network modulations were correlated (Spearman's correlation: r = 0.47; p = 3.76 10 5 and r = 0.43; p = 1.97 104). These findings might suggest the flexible functional profiles of AIN and PIN in normal aging and MCI. [ABSTRACT FROM AUTHOR]

The article discusses the problems of studying ambiguous words in the second language. Particular focus is given to the function of inhibitory control in word learning and the significance of semantics. Other topics addressed include the relation between semantics and ambiguous words and the lexical representation of words.