Explore the vast range of titles available.

Time series analysis plays a critical role in informed decision-making across domains like energy management, transportation systems, and financial markets. Real-world time series data are inherently characterized by nonlinear dynamics and multi-scale temporal features. Nevertheless, existing methods face challenges such as insufficient nonlinear modeling, incomplete multi-scale feature separation, and ineffective time-frequency domain fusion. To tackle these issues, we put forward the WTConv-iKransformer framework. By incorporating the Kolmogorov-Arnold Network (KAN) into an improved nonlinear attention mechanism (KAN-attention), its nonlinear modeling capacity is enhanced. At the same time, the framework uses wavelet-based multi-frequency decomposition to clearly divide signals into trend, periodic, and noise components, and enhances feature representation via frequency-domain specific convolutions. Lastly, a gating network dynamically balances temporal and frequency-domain features to achieve cross-domain information integration. Experimental results show that the WTConv-iKransformer achieves an additional 3% error reduction compared with individual enhanced models and realizes an average 25% error decrease over mainstream methods (e.g., Informer, LSTM) on ETTh1, ETTm1, Electricity, and Traffic datasets.

Power gives people the ability to control themselves and their environment, and this control is considered a fundamental human need. We investigated whether experiencing powerlessness induces the experience of self-dehumanization using three methods: priming, role-playing, and cueing. People in a position of low power viewed themselves (Experiments 1-3) as less human relative to people in a position of high power; furthermore, people with low power believed that they were viewed as less human by others as well (Experiments 2-3). In all of the experiments, human nature traits were most negatively affected by powerlessness in self-perception judgments, and uniquely human traits were most negatively affected by powerlessness in meta-perception judgments. Furthermore, the powerless believed they were viewed as less human not only by the powerful people but also the outside observers of the power dynamic. Self-dehumanization also appears to be a consequence of powerlessness rather than an incidental result of a change in mood or a negative self-view. Our findings are an important extension of previous work on the adverse effects of powerlessness and dehumanization.

Silicon–glass anode bonding is the key technology in the process of wafer-level packaging for MEMS sensors. During the anodic bonding process, the device may experience adhesion failure due to the influence of electric field forces. A common solution is to add a metal shielding layer between the glass substrate and the device. In order to solve the problem of device failure caused by the electrostatic attraction phenomenon, this paper designed a double-ended solidly supported cantilever beam parallel plate capacitor structure, focusing on the study of the critical size of the window opening in the metal layer for the electric field shielding effect. The metal shield consists of 400 Å of Cr and 3400 Å of Au. Based on theoretical calculations, simulation analysis, and experimental testing, it was determined that the critical size for an individual opening in the metal layer is 180 μm × 180 μm, with the movable part positioned 5 μm from the bottom, which does not lead to failure caused by stiction due to electrostatic pull-in of the detection structure. It was proven that the metal shielding layer is effective in avoiding suction problems in secondary anode bonding.

Glioblastoma Multiforme (GBM) is a highly malignant brain cancer with limited effective therapies. Neurodevelopmental pathways have been implicated in glioma formation, with key neurodevelopmental regulators being re-expressed or co-opted during glioma tumorigenesis. Here we identified a serine/threonine kinase, NUAK family kinase 2 (NUAK2), as a fetal oncogene in mouse and human brains. We found robust expression of NUAK2 in the embryonic brain that decreases throughout postnatal stages and then is re-expressed in malignant gliomas. However, the role of NUAK2 in GBM tumorigenesis remains unclear. We demonstrate that CRIPSR-Cas9 mediated NUAK2 deletion in GBM cells results in suppression of proliferation, while overexpression leads to enhanced cell growth in both in vitro and in vivo models. Further investigation of the downstream biological processes dysregulated in the absence of NUAK2 reveals that NUAK2 modulates extracellular matrix (ECM) components to facilitate migratory behavior. Lastly, we determined that pharmaceutical inhibition of NUAK2 is sufficient to impede the proliferation and migration of malignant glioma cells. Our results suggest that NUAK2 is an actionable therapeutic target for GBM treatment. Synopsis NUAK2 was found to be re-expressed in glioblastoma and function as a fetal oncogene that promotes tumor growth and migration. GBM progression was suppressed by targeting NUAK2 through genetic or pharmacological means, identifying it as a promising therapeutic target. NUAK2 was revealed to be highly expressed in the embryonic brain, downregulated postnatally, and reactivated in malignant gliomas. GBM cell proliferation was reduced by CRISPR-mediated knockout of NUAK2, while tumor growth was enhanced by its overexpression. Extracellular matrix components were regulated by NUAK2 to promote glioma cell migration. Both proliferation and migration of GBM cells were decreased by pharmacological inhibition of NUAK2. NUAK2 was found to be re-expressed in glioblastoma and function as a fetal oncogene that promotes tumor growth and migration. GBM progression was suppressed by targeting NUAK2 through genetic or pharmacological means, identifying it as a promising therapeutic target.

Migraine with brainstem aura (MBA) constitutes a rare subtype of migraine, characterized by aura symptoms including vertigo, dysarthria, diplopia, tinnitus, ataxia, and impaired consciousness. Patients with MBA have been reported to exhibit abnormal electroencephalograms (EEGs) featuring diffuse slow-wave activity and bilateral slowing of the posterior head activity. Notably, there have been no documented reports of abnormal discharges specifically localized in the anterior head. The presence of abnormal EEG discharges in MBA patients who experience loss of consciousness may lead to potential misdiagnosis, especially as epilepsy, in the early stages. This study describes three patients who were ultimately diagnosed with MBA, offering a retrospective analysis of their clinical features, electroencephalographic manifestations, and diagnostic procedures. In the three cases described, all patients were female, aged 16–21, and had been admitted to the hospital due to recurrent loss of consciousness. They exhibited a consistent EEG pattern, characterized by paroxysmal moderate-to-high amplitude theta activity in the anterior head, interspersed with spikes and sharp waves. Laboratory tests and imaging studies yielded unremarkable results. They all received a diagnosis of epilepsy and were treated with antiseizure medication, which proved ineffective. After evaluation by an epilepsy specialist, they received a final diagnosis of MBA. Following flunarizine administration, all three patients demonstrated improvement, with no subsequent occurrences of loss of consciousness during the follow-up period. This study describes the pattern of abnormal discharges that may be observed in the interictal EEGs of these MBA patients, which is characterized by a predominantly anterior head pattern. Recognizing this specific condition constitutes a crucial element in the differential diagnosis of epilepsy, with the aim of preventing misdiagnosis. Concurrently, we investigate their pathophysiological origins.

Background Ferroptosis, is characterized by lipid peroxidation of fatty acids in the presence of iron ions, which leads to cell apoptosis. This leads to the disruption of metabolic pathways, ultimately resulting in liver dysfunction. Although ferroptosis is linked to nonalcoholic steatohepatitis (NASH), understanding the key ferroptosis-related genes (FRGs) involved in NASH remains incomplete. NASH may be targeted therapeutically by identifying the genes responsible for ferroptosis. Methods To identify ferroptosis-related genes and develop a ferroptosis-related signature (FeRS), 113 machine-learning algorithm combinations were used. Results The FeRS constructed using the Generalized Linear Model Boosting algorithm and Gradient Boosting Machine algorithms exhibited the best prediction performance for NASH. Eight FRGs, with ZFP36 identified by the algorithms as the most crucial, were incorporated into in FeRS. ZFP36 is significantly enriched in various immune cell types and exhibits significant positive correlations with most immune signatures. Conclusion ZFP36 is a key FRG involved in NASH pathogenesis.

Background The marine crustacean Oratosquilla oratoria is economically significant in seafood and aquaculture industries. However, the lack of high-quality genome assembly has hindered our understanding of O. oratoria , particularly the mechanisms underlying its developed visual system. Results We generated a chromosome-level genome assembly for O. oratoria (2.97 Gb, 44 pseudo-chromosomes) using combination sequencing strategies. Our analysis revealed that more than half of the genome was covered by repeat sequences, and LINE elements showed significant expansion. Furthermore, phylogenetic analysis revealed a close relationship of O. oratoria with Dendrobranchiata and Pleocyemata. In addition, the evolutionary rate of O. oratoria was slightly faster than that of Dendrobranchiata and slower than that of Pleocyemata. Interestingly, we observed the significant expansion of middle-wavelength-sensitive (MWS) opsins in the O. oratoria genome by tandem duplication, partially contributing to their unique visual capabilities. Compared with other crustaceans, O. oratoria has evolved a thicker cornea that was possibly driven by visual adaptations and ecological requirements. Employing comparative transcriptome analysis, we identified a tandemly duplicated cuticle protein (CP) cluster that was specifically expanded and expressed in the ocular tissues of O. oratoria , potentially contributing to the thick cornea of O. oratoria . Conclusions Our study established the first chromosome-level genome for Stomatopoda species, providing a valuable genomic resource for studying the molecular mechanisms underlying the developed visual system of O. oratoria .

Background Certain dental diseases in pediatric patients may disturb their sleep, affect their oral health‐related quality of life, and result in a negative influence on cognition and behavior. On the other hand, sleep disturbances may also increase the risk or participate in development and progression of dental diseases. Objective This narrative review aimed to overview of the bidirectional relationship between common dental diseases and sleep disturbances, as well as the potential mechanisms behind. Material and Methods PubMed, Web of Science, and Google Scholar were searched using the keywords “dental disease,” “sleep disturbances,” and “children,” and only articles published in English were included. Results Evidence provided by previous studies has indicated that common dental diseases, including dental caries, temporomandibular disorders, and dentofacial deformities, induced sleep disturbances in children and adolescents. On the other hand, common sleep disturbances such as sleep disordered breathing, obstructive sleep apnea, as well as other sleep problems, including sleep bruxism and sleep profile impairments, have a strong link to oral health conditions in pediatric patients. Alteration of oral microorganism colonization, impairment in the immune system, persistent inflammation, and chronic pain have contributed to sleep disorders triggered by these dental diseases. Conclusion Upon identification of dental caries, gingivitis, periodontitis, as well as other dental problems, a checkup on a child's sleep is important, as this may subsequently affect his/her initiation, maintenance, duration, and quality of sleep. Dentists and orthodontists could play a critical role in early detection, prevention, and intervention of the dental health‐related sleep disturbances.

Obesity has become one of the major threats to human health across the globe. The rhizomes of Polygonatum sibiricum have shown promising anti-obesity effect. However, the metabolic and genetic basis mediating this beneficial effect are not fully resolved. It is well known that older rhizomes of P. sibiricum exert stronger pharmacological effects. Here, we performed high-resolution metabolome profiling of P. sibiricum rhizomes at different growth stages, and identified that three candidate anti-obesity metabolites, namely phloretin, linoleic acid and α-linolenic acid, accumulated more in adult rhizomes. To elucidate the genetic basis controlling the accumulation of these metabolites, we performed transcriptome profiling of rhizomes from juvenile and adult P. sibiricum . Through third-generation long-read sequencing, we built a high-quality transcript pool of P. sibiricum , and resolved the genetic pathways involved in the biosynthesis and metabolism of phloretin, linoleic acid and α-linolenic acid. Comparative transcriptome analysis revealed altered expression of the genetic pathways in adult rhizomes, which likely lead to higher accumulation of these candidate metabolites. Overall, we identified several metabolic and genetic signatures related to the anti-obesity effect of P. sibiricum . The metabolic and transcriptional datasets generated in this work could also facilitate future research on other beneficial effects of this medicinal plant.

Background Evidence suggests that hepatocyte mitochondrial dysfunction leads to abnormal lipid metabolism, redox imbalance, and programmed cell death, driving the onset and progression of non-alcoholic steatohepatitis (NASH). Identifying hub mitochondrial genes linked to NASH may unveil potential therapeutic targets. Methods Mitochondrial hub genes implicated in NASH were identified via analysis using 134 algorithms. Results The Random Forest algorithm (RF), the most effective among the 134 algorithms, identified three genes: Aldo–keto reductase family 1 member B10 ( AKR1B10 ), thymidylate synthase ( TYMS ), and triggering receptor expressed in myeloid cell 2 ( TREM2 ). They were upregulated and positively associated with genes promoting inflammation, genes involved in lipid synthesis, fibrosis, and nonalcoholic steatohepatitis activity scores in patients with NASH. Moreover, using these three genes, patients with NASH were accurately categorized into cluster 1, exhibiting heightened disease severity, and cluster 2, distinguished by milder disease activity. Conclusion These three genes are pivotal mitochondrial genes implicated in NASH progression.