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Prior work decoding linguistic meaning from imaging data has been largely limited to concrete nouns, using similar stimuli for training and testing, from a relatively small number of semantic categories. Here we present a new approach for building a brain decoding system in which words and sentences are represented as vectors in a semantic space constructed from massive text corpora. By efficiently sampling this space to select training stimuli shown to subjects, we maximize the ability to generalize to new meanings from limited imaging data. To validate this approach, we train the system on imaging data of individual concepts, and show it can decode semantic vector representations from imaging data of sentences about a wide variety of both concrete and abstract topics from two separate datasets. These decoded representations are sufficiently detailed to distinguish even semantically similar sentences, and to capture the similarity structure of meaning relationships between sentences. Previous work decoding linguistic meaning from imaging data has generally been limited to a small number of semantic categories. Here, authors show that a decoder trained on neuroimaging data of single concepts sampling the semantic space can robustly decode meanings of semantically diverse new sentences with topics not encountered during training.

PurposeAmblyopia is a leading cause of vision impairment among children and young adults. Individual studies showed significant variations in the prevalence of amblyopia in different regions and age groups. This study is to estimate the global prevalence of amblyopia by pooling its prevalence from the previous studies and to project the number of people affected through 2040.MethodsWe performed a systematic review and meta-analysis on the prevalence of amblyopia using data published before 20 October 2018. We estimated the prevalence rate of amblyopia and its 95% CI globally and by subgroups (eg, region and age). The prevalence data were applied to United Nations World Population Prospects to derive the projected number with amblyopia through 2040.ResultsA meta-analysis of 60 studies (1 859 327 subjects) showed that the pooled prevalence rate of amblyopia was 1.44% (95% CI 1.17% to 1.78%). Prevalences in Europe (2.90%) and North America (2.41%) were higher than in Asia (1.09%) and Africa (0.72%). The highest prevalence was found in subjects over 20 years old (3.29%). There was no difference in the prevalence between genders. We estimated 99.2 (95% CI 71.7 to 146.1) million people with amblyopia in 2019 worldwide, increasing to 175.2 (95% CI 81.3 to 307.8) million by 2030 and 221.9 (95% CI 83.7 to 429.2) million by 2040.ConclusionsThe amblyopia is becoming a significant vision problem worldwide. It is of great importance to design and implement amblyopia screening, treatment and related public health strategies.

Arsenic poisoning is a global health problem. Chronic exposure to arsenic has been associated with the development of a wide range of diseases and health problems in humans. Arsenic exposure induces the generation of intracellular reactive oxygen species (ROS), which mediate multiple changes to cell behavior by altering signaling pathways and epigenetic modifications, or cause direct oxidative damage to molecules. Antioxidants with the potential to reduce ROS levels have been shown to ameliorate arsenic-induced lesions. However, emerging evidence suggests that constructive activation of antioxidative pathways and decreased ROS levels contribute to chronic arsenic toxicity in some cases. This review details the pathways involved in arsenic-induced redox imbalance, as well as current studies on prophylaxis and treatment strategies using antioxidants.

Due to the high content of polycyclic aromatic hydrocarbons and solid powders in catalytic slurry, its utilization value is currently low. However, the fragrant components in it are high-quality raw materials for the preparation of carbon materials such as mesophase pitch. Therefore, in this study, mesophase pitch was prepared from the extracted oil of the petrochemical catalytic slurry by a direct thermal condensation reaction. Elemental analysis, mass spectrometry, and polarizing microscopy were used to characterize the mesophase pitch. The effects of temperature and pressure on the softening point, H/C atomic ratio, mesophase content, and microstructure of the mesophase pitch were investigated. The results showed that the optimal conditions for thermal condensation to extract oil from a catalytic slurry were 430 °C, 2 MPa, and 8 hours. The mesophase pitch, possessing a softening point of 275 °C and a mesophase content of 98.5%, with a wide-area optical structure, could be prepared under optimal conditions. This study effectively utilized the aromatic components of oil slurry, providing crucial theoretical guidance for achieving high-value utilization of oil slurry.

Quercetin, a flavone, is multifaceted, having anti-oxidative, anti-inflammatory, and anticancer properties. In the present study, we explored the effects of quercetin on the epithelial-mesenchymal transition (EMT) and invasion of pancreatic cancer cells and the underlying mechanisms. We noted that quercetin exerted pronounced inhibitory effects in PANC-1 and PATU-8988 cells. Moreover, quercetin inhibited EMT and decreased the secretion of matrix metalloproteinase (MMP). Meanwhile, we determined the activity of STAT3 after quercetin treatment. STAT3 phosphorylation decreased following treatment with quercetin. We also used activating agent of STAT3, IL-6, to induce an increase in cell malignancy and to observe the effects of treatment with quercetin. As expected, the EMT and MMP secretion increased with activation of the STAT3 signaling pathway, and quercetin reversed IL-6-induced EMT, invasion, and migration. Therefore, our results demonstrate that quercetin triggers inhibition of EMT, invasion, and metastasis by blocking the STAT3 signaling pathway, and thus, quercetin merits further investigation.

Backgrouds and Objective Keloids are defined as overrepairing products that develop after skin lesions. Keloids are characterized by the proliferation of fibroblasts and the overaccumulation of extracellular matrix components (mainly collagen), leading to a locally hypoxic microenvironment. Hence, this article was aimed to review hypoxia in pathogenesis of keloids. Methods We reviewed and summarized the relevant published studies. Results Hypoxia results in the accumulation of hypoxia‐inducible factor 1α (HIF‐1α) in keloids, contributing to overactivation of the fibrotic signaling pathway, epithelial–mesenchymal transition, and changes in metabolism, eventually leading to aggravated fibrosis, infiltrative growth, and radiotherapy resistance. Conclusion It is, therefore, essential to understand the role of HIF‐1α in the pathogenic mechanisms of keloids in order to develop new therapeutic approaches.

Maintaining oxygen homeostasis is a basic cellular process for adapting to physiological oxygen variations in which the oxygen‐sensing pathway plays a critical role, especially in tumour progression. Little is known about the activity of the oxygen‐sensing pathway in keloid tissue. In this study, key features of the oxygen‐sensing pathway and its downstream effects were evaluated and compared between normal skin tissue and keloid tissue. Keloid tissue showed increased oxygen‐sensing pathway activation and a higher expression of key downstream factors such as tumour necrosis factor‐1α (TNF‐α) and vascular endothelial growth factor (VEGF). In addition, the effects of 2‐methoxyestradiol on the oxygen‐sensing pathway in both hypoxic and normoxic keloid fibroblasts were evaluated. Our results suggest that 2‐methoxyestradiol could be used to inhibit keloid fibroblast activity by inhibiting the oxygen‐sensing pathway and its downstream effectors.

The MAPK/Erk signaling pathway is a classic pathway in cell proliferation. Our former study showed that keloid tissue revealed a higher proliferation level than physiological scars and normal skin. As a natural metabolite of estradiol, 2-methoxyestradiol (2ME2) showed an inhibition proliferation effect on tumor cells. In this study, the treatment effect of 2ME2 and its potential mechanisms are explored. Six keloid patients and six non-keloid patients were randomly selected from the Department of Plastic Surgery at our hospital during June 2021 to December 2021. Six groups were established: normal skin fibroblasts (N); keloid fibroblasts (K); keloid fibroblasts treated with 2ME2 (K + 2ME2); keloid fibroblasts treated with dimethyl sulfoxide (DMSO) (K + DMSO); keloid fibroblasts treated with doramapimod (K + IN); keloid fibroblasts treated with doramapimod (p38 inhibitor) and 2ME2 (K + IN+2ME2). The fibroblast activity and key factor expression of the MAPK/Erk signaling pathway were measured. In the results, 2ME2 significantly inhibited keloid fibroblast activity and key factor expression (except STAT1). The proliferation levels were reduced by both the p38 inhibitor and 2ME2, indicating 2ME2 may achieve an antiproliferation effect by targeting p38 in keloid fibroblasts.

Background Gastric cancer (GC) is associated with high mortality and heterogeneity and poses a great threat to humans. Gene therapies for the receptor tyrosine kinase RON and its spliceosomes are attracting increasing amounts of attention due to their unique characteristics. However, little is known about the mechanism involved in the formation of the RON mRNA alternative spliceosome RONΔ160. Methods Fourteen human GC tissue samples and six normal gastric tissue samples were subjected to label-free relative quantitative proteomics analysis, and MAGOH was identified as a candidate protein for subsequent studies. The expression of MAGOH in clinical specimens was verified by quantitative real-time PCR and western blotting. We then determined the biological function of MAGOH in GC through in vitro and in vivo experiments. RNA pulldown, RNA sequencing and RNA immunoprecipitation (RIP) were subsequently conducted to uncover the underlying mechanism by which MAGOH regulated the formation of RONΔ160. Results Proteomic analysis revealed that MAGOH, which is located at key nodes and participates in RNA processing and mRNA splicing, was upregulated in GC tissue and GC cell lines and was associated with poor prognosis. Functional analysis showed that MAGOH promoted the proliferation, migration and invasion of GC cells in vitro and in vivo. Mechanistically, MAGOH inhibited the expression of hnRNPA1 and reduced the binding of hnRNPA1 to RON mRNA, thereby promoting the formation of RONΔ160 to activate the PI3K/AKT signaling pathway and consequently facilitating GC progression. Conclusions Our study revealed that MAGOH could promote the formation of RONΔ160 and activate the PI3K/AKT signaling pathway through the inhibition of hnRNPA1 expression. We elucidate a novel mechanism and potential therapeutic targets for the growth and metastasis of GC based on the MAGOH-RONΔ160 axis, and these findings have important guiding significance and clinical value for the future development of effective therapeutic strategies for GC.

Pre-stimulus α power has been shown to correlate with the behavioral accuracy of perceptual decisions. In most cases, these correlations have been observed by comparing α power for different behavioral outcomes (e.g. correct vs incorrect trials). In this paper we investigate such covariation within the context of behaviorally-latent fluctuations in task-relevant post-stimulus neural activity. Specially we consider variations of pre-stimulus α power with post-stimulus EEG components in a two alternative forced choice visual discrimination task. EEG components, discriminative of stimulus class, are identified using a linear multivariate classifier and only the variability of the components for correct trials (regardless of stimulus class, and for nominally identical stimuli) are correlated with the corresponding pre-stimulus α power. We find a significant relationship between the mean and variance of the pre-stimulus α power and the variation of the trial-to-trial magnitude of an early post-stimulus EEG component. This relationship is not seen for a later EEG component that is also discriminative of stimulus class and which has been previously linked to the quality of evidence driving the decision process. Our results suggest that early perceptual representations, rather than temporally later neural correlates of the perceptual decision, are modulated by pre-stimulus state. •Task-related EEG components are identified using a linear multivariate classifier.•Prestimulus alpha variability correlates with an early poststimulus component.•No correlation is seen with a later component linked to evidence accumulation.•We conclude prestimulus alpha modulates sensory encoding during perceptual decisions.