106 research outputs found
Linear codes with few weights from non-weakly regular plateaued functions
Linear codes with few weights have significant applications in secret sharing
schemes, authentication codes, association schemes, and strongly regular
graphs. There are a number of methods to construct linear codes, one of which
is based on functions. Furthermore, two generic constructions of linear codes
from functions called the first and the second generic constructions, have
aroused the research interest of scholars. Recently, in \cite{Nian}, Li and
Mesnager proposed two open problems: Based on the first and the second generic
constructions, respectively, construct linear codes from non-weakly regular
plateaued functions and determine their weight distributions.
Motivated by these two open problems, in this paper, firstly, based on the
first generic construction, we construct some three-weight and at most
five-weight linear codes from non-weakly regular plateaued functions and
determine the weight distributions of the constructed codes. Next, based on the
second generic construction, we construct some three-weight and at most
five-weight linear codes from non-weakly regular plateaued functions belonging
to (defined in this paper) and determine the weight
distributions of the constructed codes. We also give the punctured codes of
these codes obtained based on the second generic construction and determine
their weight distributions. Meanwhile, we obtain some optimal and almost
optimal linear codes. Besides, by the Ashikhmin-Barg condition, we have that
the constructed codes are minimal for almost all cases and obtain some secret
sharing schemes with nice access structures based on their dual codes.Comment: 52 pages, 34 table
A Further Study of Vectorial Dual-Bent Functions
Vectorial dual-bent functions have recently attracted some researchers'
interest as they play a significant role in constructing partial difference
sets, association schemes, bent partitions and linear codes. In this paper, we
further study vectorial dual-bent functions , where , denotes an
-dimensional vector space over the prime field . We give new
characterizations of certain vectorial dual-bent functions (called vectorial
dual-bent functions with Condition A) in terms of amorphic association schemes,
linear codes and generalized Hadamard matrices, respectively. When , we
characterize vectorial dual-bent functions with Condition A in terms of bent
partitions. Furthermore, we characterize certain bent partitions in terms of
amorphic association schemes, linear codes and generalized Hadamard matrices,
respectively. For general vectorial dual-bent functions with and , we give a necessary and sufficient condition on constructing
association schemes. Based on such a result, more association schemes are
constructed from vectorial dual-bent functions
A Further Study of Vectorial Dual-Bent Functions
Vectorial dual-bent functions have recently attracted some researchers\u27 interest as they play a significant role in constructing partial difference sets, association schemes, bent partitions and linear codes. In this paper, we further study vectorial dual-bent functions , where , denotes an -dimensional vector space over the prime field . We give new characterizations of certain vectorial dual-bent functions (called vectorial dual-bent functions with Condition A) in terms of amorphic association schemes, linear codes and generalized Hadamard matrices, respectively. When , we characterize vectorial dual-bent functions with Condition A in terms of bent partitions. Furthermore, we characterize certain bent partitions in terms of amorphic association schemes, linear codes and generalized Hadamard matrices, respectively. For general vectorial dual-bent functions with and , we give a necessary and sufficient condition on constructing association schemes. Based on such a result, more association schemes are constructed from vectorial dual-bent functions
TANGO: Time-Reversal Latent GraphODE for Multi-Agent Dynamical Systems
Learning complex multi-agent system dynamics from data is crucial across many
domains, such as in physical simulations and material modeling. Extended from
purely data-driven approaches, existing physics-informed approaches such as
Hamiltonian Neural Network strictly follow energy conservation law to introduce
inductive bias, making their learning more sample efficiently. However, many
real-world systems do not strictly conserve energy, such as spring systems with
frictions. Recognizing this, we turn our attention to a broader physical
principle: Time-Reversal Symmetry, which depicts that the dynamics of a system
shall remain invariant when traversed back over time. It still helps to
preserve energies for conservative systems and in the meanwhile, serves as a
strong inductive bias for non-conservative, reversible systems. To inject such
inductive bias, in this paper, we propose a simple-yet-effective
self-supervised regularization term as a soft constraint that aligns the
forward and backward trajectories predicted by a continuous graph neural
network-based ordinary differential equation (GraphODE). It effectively imposes
time-reversal symmetry to enable more accurate model predictions across a wider
range of dynamical systems under classical mechanics. In addition, we further
provide theoretical analysis to show that our regularization essentially
minimizes higher-order Taylor expansion terms during the ODE integration steps,
which enables our model to be more noise-tolerant and even applicable to
irreversible systems. Experimental results on a variety of physical systems
demonstrate the effectiveness of our proposed method. Particularly, it achieves
an MSE improvement of 11.5 % on a challenging chaotic triple-pendulum systems
PP2A Inhibitors Arrest G2/M Transition Through JNK/Sp1-Dependent Down-Regulation of CDK1 and Autophagy-Dependent Up-Regulation of p21
Protein phosphatase 2A (PP2A) plays an important role in the control of the cell cycle. We previously reported that the PP2A inhibitors, cantharidin and okadaic acid (OA), efficiently repressed the growth of cancer cells. In the present study, we found that PP2A inhibitors arrested the cell cycle at the G2 phase through a mechanism that was dependent on the JNK pathway. Microarrays further showed that PP2A inhibitors induced expression changes in multiple genes that participate in cell cycle transition. To verify whether these expression changes were executed in a PP2A-dependent manner, we targeted the PP2A catalytic subunit (PP2Ac) using siRNA and evaluated gene expression with a microarray. After the cross comparison of these microarray data, we identified that CDK1 was potentially the same target when treated with either PP2A inhibitors or PP2Ac siRNA. In addition, we found that the down-regulation of CDK1 occurred in a JNK-dependent manner. Luciferase reporter gene assays demonstrated that repression of the transcription of CDK1 was executed through the JNK-dependent activation of the Sp1 transcription factor. By constructing deletion mutants of the CDK1 promoter and by using ChIP assays, we identified an element in the CDK1 promoter that responded to the JNK/Sp1 pathway after stimulation with PP2A inhibitors. Cantharidin and OA also up-regulated the expression of p21, an inhibitor of CDK1, via autophagy rather than PP2A/JNK pathway. Thus, this present study found that the PP2A/JNK/Sp1/CDK1 pathway and the autophagy/p21 pathway participated in G2/M cell cycle arrest triggered by PP2A inhibitors
Nucleocapsid Protein as Early Diagnostic Marker for SARS
Serum samples from 317 patients with patients with severe acute respiratory syndrome (SARS) were tested for the nucleocapsid (N) protein of SARS-associated coronavirus, with sensitivities of 94% and 78% for the first 5 days and 6–10 days after onset, respectively. The specificity was 99.9%. N protein can be used as an early diagnostic maker for SARS
Artificial Intelligence Framework Identifies Candidate Targets for Drug Repurposing in Alzheimer’s Disease
Background: Genome-wide association studies (GWAS) have identified numerous susceptibility loci for Alzheimer’s disease (AD). However, utilizing GWAS and multi-omics data to identify high-confidence AD risk genes (ARGs) and druggable targets that can guide development of new therapeutics for patients suffering from AD has heretofore not been successful. Methods: To address this critical problem in the field, we have developed a network-based artificial intelligence framework that is capable of integrating multi-omics data along with human protein–protein interactome networks to accurately infer accurate drug targets impacted by GWAS-identified variants to identify new therapeutics. When applied to AD, this approach integrates GWAS findings, multi-omics data from brain samples of AD patients and AD transgenic animal models, drug-target networks, and the human protein–protein interactome, along with large-scale patient database validation and in vitro mechanistic observations in human microglia cells. Results: Through this approach, we identified 103 ARGs validated by various levels of pathobiological evidence in AD. Via network-based prediction and population-based validation, we then showed that three drugs (pioglitazone, febuxostat, and atenolol) are significantly associated with decreased risk of AD compared with matched control populations. Pioglitazone usage is significantly associated with decreased risk of AD (hazard ratio (HR) = 0.916, 95% confidence interval [CI] 0.861–0.974, P = 0.005) in a retrospective case-control validation. Pioglitazone is a peroxisome proliferator-activated receptor (PPAR) agonist used to treat type 2 diabetes, and propensity score matching cohort studies confirmed its association with reduced risk of AD in comparison to glipizide (HR = 0.921, 95% CI 0.862–0.984, P = 0.0159), an insulin secretagogue that is also used to treat type 2 diabetes. In vitro experiments showed that pioglitazone downregulated glycogen synthase kinase 3 beta (GSK3β) and cyclin-dependent kinase (CDK5) in human microglia cells, supporting a possible mechanism-of-action for its beneficial effect in AD. Conclusions: In summary, we present an integrated, network-based artificial intelligence methodology to rapidly translate GWAS findings and multi-omics data to genotype-informed therapeutic discovery in AD
Dub3 Inhibition Suppresses Breast Cancer Invasion and Metastasis by Promoting Snail1 Degradation
Snail1, a key transcription factor of epithelial–mesenchymal transition (EMT), is subjected to ubiquitination and degradation, but the mechanism by which Snail1 is stabilized in tumours remains unclear. We identify Dub3 as a bona fide Snail1 deubiquitinase, which interacts with and stabilizes Snail1. Dub3 is overexpressed in breast cancer; knockdown of Dub3 resulted in Snail1 destabilization, suppressed EMT and decreased tumour cell migration, invasion, and metastasis. These effects are rescued by ectopic Snail1 expression. IL-6 also stabilizes Snail1 by inducing Dub3 expression, the specific inhibitor WP1130 binds to Dub3 and inhibits the Dub3-mediating Snail1 stabilization in vitroand in vivo. Our study reveals a critical Dub3–Snail1 signalling axis in EMT and metastasis, and provides an effective therapeutic approach against breast cancer
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