FACT-Net: a Frequency Adapter CNN with Temporal-periodicity Inception for Fast and Accurate MI-EEG Decoding.

Motor imagery brain-computer interface (MI-BCI) based on non-invasive electroencephalogram (EEG) signals is a typical paradigm of BCI. However, existing decoding methods face significant challenges in terms of signal decoding accuracy, real-time processing, and deployment. To overcome these challenges, we propose FACT-Net, an innovative deep-learning network for the fast and accurate decoding of MI-EEG signals.

Study on the influence of soil properties on fluorescence intensity of polycyclic aromatic hydrocarbons.

The properties of soil matrix have an impact on the fluorescence intensity of polycyclic aromatic hydrocarbons (PAHs), which restricts the application of fluorescence spectral technology in detecting PAHs in soil. The present study explored the mechanism of the influence of soil matrix properties on the fluorescence intensity of PAHs from the perspective of specific surface area (SSA). A three-factor three-level experimental design was adopted for investigating the relationship between soil matrix properties, PAH fluorescence intensity, and soil SSA.

Identification of Oral Bioavailable Coumarin Derivatives as Potential AR Antagonists Targeting Prostate Cancer.

Androgen receptor (AR) is a crucial driver of prostate cancer (PCa), but acquired resistance to AR antagonists significantly undermines their clinical efficacy. We previously discovered coumarin derivative , which is capable of disrupting AR ligand-binding domain dimers, offering the potential for overcoming resistance. However, its poor oral bioavailability limited further development.

Integrating Prior Chemical Knowledge into the Graph Transformer Network to Predict the Stability Constants of Chelating Agents and Metal Ions.

The latest advancements in nuclear medicine indicate that radioactive isotopes and associated metal chelators play crucial roles in the diagnosis and treatment of diseases. The development of metal chelators mainly relies on traditional trial-and-error methods, lacking rational guidance and design. In this study, we propose the structure-aware transformer (SAT) combined with molecular fingerprint (SATCMF), a novel graph transformer network framework that incorporates prior chemical knowledge to construct coordination edges and learns the interactions between chelating agents and metal ions.

Reduced mesencephalic astrocyte-derived neurotrophic factor expression by mutant androgen receptor contributes to neurodegeneration in a model of spinal and bulbar muscular atrophy pathology.

JOURNAL/nrgr/04.03/01300535-202509000-00027/figure1/v/2024-11-05T132919Z/r/image-tiff Spinal and bulbar muscular atrophy is a neurodegenerative disease caused by extended CAG trinucleotide repeats in the androgen receptor gene, which encodes a ligand-dependent transcription factor. The mutant androgen receptor protein, characterized by polyglutamine expansion, is prone to misfolding and forms aggregates in both the nucleus and cytoplasm in the brain in spinal and bulbar muscular atrophy patients.

TRIM37 is a primate-specific E3 ligase for Huntingtin and accounts for the striatal degeneration in Huntington's disease.

Huntington's disease (HD) is an autosomal dominant neurodegenerative disease characterized by preferential neuronal loss in the striatum. The mechanism underlying striatal selective neurodegeneration remains unclear, making it difficult to develop effective treatments for HD. In the brains of nonhuman primates, we examined the expression of Huntingtin (), the gene responsible for HD.

HAP40 modulates mutant Huntingtin aggregation and toxicity in Huntington's disease mice.

Huntington's disease (HD) is a monogenic neurodegenerative disease, caused by the CAG trinucleotide repeat expansion in exon 1 of the Huntingtin (HTT) gene. The HTT gene encodes a large protein known to interact with many proteins. Huntingtin-associated protein 40 (HAP40) is one that shows high binding affinity with HTT and functions to maintain HTT conformation in vitro.

M-FANet: Multi-Feature Attention Convolutional Neural Network for Motor Imagery Decoding.

Motor imagery (MI) decoding methods are pivotal in advancing rehabilitation and motor control research. Effective extraction of spectral-spatial-temporal features is crucial for MI decoding from limited and low signal-to-noise ratio electroencephalogram (EEG) signal samples based on brain-computer interface (BCI). In this paper, we propose a lightweight Multi-Feature Attention Neural Network (M-FANet) for feature extraction and selection of multi-feature data.

Aberrant splicing of mutant huntingtin in Huntington's disease knock-in pigs.

Huntington's disease (HD) is an autosomal-dominant inherited neurodegenerative disease caused by a CAG repeat expansion in exon1 of the huntingtin gene (HTT). This expansion leads to the production of N-terminal mutant huntingtin protein (mHtt) that contains an expanded polyglutamine tract, which is toxic to neurons and causes neurodegeneration. While the production of N-terminal mHtt can be mediated by proteolytic cleavage of full-length mHtt, abnormal splicing of exon1-intron1 of mHtt has also been identified in the brains of HD mice and patients.

Pharmacophore-Based Virtual Screening and Structural Modification of Novel Benzamide Derivatives as HBV Capsid Assembly Modulators.

Hepatitis B virus (HBV) infection is the most common cause of death from liver disease worldwide. The use of capsid assembly modulators is considered a prominent strategy for the development of novel anti-HBV therapies. We performed a pharmacophore-based virtual screening strategy, and a benzamide scaffold hit, WAI-5, was chosen for further structural optimization.

CRISPR-Based Genome-Editing Tools for Huntington's Disease Research and Therapy.

Huntington's disease (HD) is an autosomal dominantly-inherited neurodegenerative disease, which is caused by CAG trinucleotide expansion in exon 1 of the Huntingtin (HTT) gene. Although HD is a rare disease, its monogenic nature makes it an ideal model in which to understand pathogenic mechanisms and to develop therapeutic strategies for neurodegenerative diseases. Clustered regularly-interspaced short palindromic repeats (CRISPR) is the latest technology for genome editing.

AMPK activation induced in pemetrexed-treated cells is associated with development of drug resistance independently of target enzyme expression.

Pemetrexed (PEM) inhibits DNA and RNA synthesis and is currently one of the first-line agents for mesothelioma. PEM suppresses the activities of several enzymes involved in purine and pyrimidine synthesis, and elevated activity of these enzymes in tumors is often linked with resistance to PEM. The agent also stimulates AMP-activated protein kinase (AMPK) and consequently influences the mammalian target of rapamycin complex 1 (mTORC1) pathways.

Construction of a human monoclonal antibody against bFGF for suppression of NSCLC.

Compelling evidence implicates that overexpression of basic fibroblast growth factor (bFGF) and fibroblast growth factor receptor 1 (FGFR1) in non-small cell lung cancer (NSCLC) drives tumor progression, can serve as prognostic biomarkers or therapeutic targets for NSCLC patients. But at present, we still lack of effective drugs for bFGF. The preparation of monoclonal antibodies against bFGF or to understand its mechanism of action is urgently need.

Augmented expression of cardiac ankyrin repeat protein is induced by pemetrexed and a possible marker for the pemetrexed resistance in mesothelioma cells.

Background: Pemetrexed (PEM) is an anti-cancer agent targeting DNA and RNA synthesis, and clinically in use for mesothelioma and non-small cell lung carcinoma. A mechanism of resistance to PEM is associated with elevated activities of several enzymes involved in nucleic acid metabolism.

Methods: We established two kinds of PEM-resistant mesothelioma cells which did not show any increase of the relevant enzyme activities.

Production of bFGF monoclonal antibody and its inhibition of metastasis in Lewis lung carcinoma.

Basic fibroblast growth factor (bFGF) and fibroblast growth factor receptor 1 (FGFR1) are associated with drug resistance in lung cancer. In the present study, mouse monoclonal antibodies (mAb) against human bFGF, targeting the binding site of bFGF with FGFR1 were produced, and the antitumor activity and inhibition of metastasis was studied in Lewis lung carcinoma (LLC). A total of four hybridoma cell strains that stably secreted bFGF mAb were obtained.

[Functional Analysis of DNA Damage Repair Factor WDR70 and Its Mutation in Ovarian Cancer].

Objectives: To analyze the cellular function of the newly discovered DNA damage repair factor WDR70, and investigate the mutation in ovarian cancer to verify if function loss of the gene was associated with ovarian cancer.

Methods: The gene was silenced by using siRNA technique or overexpressed its wild and mutation type by with lentivirus and plasmid in hunman cells. The subcellular localization and biochemical function of WDR70 was analyzes by indirect immunofluorescence and immunoblotting.

Ganglioside GD1a suppresses LPS-induced pro-inflammatory cytokines in RAW264.7 macrophages by reducing MAPKs and NF-κB signaling pathways through TLR4.

Gangliosides, sialic acid-containing glycosphingolipids, have been considered to be involved in the development, differentiation, and function of nervous systems in vertebrates. However, the mechanisms for anti-inflammation caused by gangliosides are not clear. In this paper, we investigated the anti-inflammation effects of ganglioside GD1a by using RAW264.