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Abstract The purpose of epilepsy detection is to determine whether epilepsy has occurred by analysing the patient's electroencephalogram (EEG) signals. Compared to traditional methods, epilepsy detection methods based on deep learning have achieved significant improvements in detection accuracy. However, when the number of training samples is limited, the model's detection performance often significantly declines. To address this issue, here a sample enhancement method based on electroencephalogram signal channel swapping is proposed. This method generates new electroencephalogram samples by exchanging electroencephalogram sequences from different channels, thereby expanding the training set and improving epilepsy detection accuracy in few‐shot scenarios. Experiments using the Children's Hospital Boston and the Massachusetts Institute of Technology (CHB‐MIT) dataset show that for training sets with 100, 500, and 1000 samples, detection accuracy improves from 0.6797 to 0.7789, 0.6952 to 0.8210, and 0.7273 to 0.8517, respectively. Compared to the sliding window method, the proposed method demonstrates higher accuracy in extreme low sample sizes. Combining both methods can further enhances detection performance, showing an improvement of approximately 8% across various configurations.

The precise and automated detection of epileptic seizures has become a focal point of research due to its potential to alleviate the severe consequences experienced by patients. Recent advancements in deep learning-based detection techniques utilizing electroencephalogram (EEG) signals have yielded state-of-the-art performance. However, these methods typically require a large number of training samples to effectively train the deep neural networks. Consequently, their performance can be compromised in scenarios where only a limited number of samples are available. This paper presents two novel approaches that aim to improve seizure detection accuracy in situations with a scarcity of data by harnessing the power of empirical mode decomposition (EMD) applied to EEG signals. Specifically, in both methods, the EMD of EEG signals and the power spectral density (PSD) of the resulting EMD components are employed as inputs for subsequent neural networks. Multiple convolutional neural networks (CNNs) are purposefully designed to perform seizure detection using these inputs. Experimental results demonstrate that our proposed methods achieve superior detection accuracy compared to traditional deep learning-based detection methods that do not incorporate EMD in few-shot scenarios. In particular, when the number of training samples is reduced to 10%, our method shows an improvement of 23%, 19%, and 26% in accuracy, sensitivity, and specificity, respectively, compared to the original EEG input across different networks.

Background: There is a paucity of systematic reviews on the associated factors of mortality among ST-elevation myocardial infarction (STEMI) patients after percutaneous coronary intervention (PCI). This meta-analysis was designed to synthesize available evidence on the prevalence and associated factors of mortality after PCI for adult patients with STEMI. Materials and Methods: Databases including the Cochrane Library, PubMed, Web of Science, Embase, Ovid, Scopus, ProQuest, MEDLINE, and CINAHL Complete were searched systematically to identify relevant articles published from January 2008 to March 2020 on factors affecting mortality after PCI in STEMI patients. Meta-analysis was conducted using Stata 12.0 software package. Results: Our search yielded 91 cohort studies involving a total of 199, 339 participants. The pooled mortality rate for STEMI patients after PCI was 10%. After controlling for grouping criteria or follow-up time, the following 17 risk factors were significantly associated with mortality for STEMI patients after PCI: advanced age (odds ratio [OR] = 3.89), female (OR = 2.01), out-of-hospital cardiac arrest (OR = 5.55), cardiogenic shock (OR = 4.83), renal dysfunction (OR = 3.50), admission anemia (OR = 3.28), hyperuricemia (OR = 2.71), elevated blood glucose level (OR = 2.00), diabetes mellitus (OR = 1.8), chronic total occlusion (OR = 2.56), Q wave (OR = 2.18), without prodromal angina (OR = 2.12), delay in door-to-balloon time (OR = 1.72), delay in symptom onset-to-balloon time (OR = 1.43), anterior infarction (OR = 1.66), ST-segment resolution (OR = 1.40), and delay in symptom onset-to-door time (OR = 1.29). Conclusion: The pooled prevalence of mortality after PCI for STEMI patients was 10%, and 17 risk factors were significantly associated with mortality for STEMI patients after PCI.

Abstract Background A recently discovered tea [Camellia sinensis (L.) O. Kuntze] cultivar can generate tender shoots in winter. We performed comparative proteomics to analyze the differentially accumulated proteins between winter and spring tender shoots of this clonal cultivar to reveal the physiological basis of its evergrowing character during winter. Results We extracted proteins from the winter and spring tender shoots (newly formed two leaves and a bud) of the evergrowing tea cultivar “Dongcha11” respectively. Thirty-three differentially accumulated high-confidence proteins were identified by matrix-assisted laser desorption ionization time of flight mass spectrometry (MALDI-TOF / TOF MS). Among these, 24 proteins had increased abundance while nine showed were decreased abundance in winter tender shoots as compared with the spring tender shoots. We categorized the differentially accumulated proteins into eight critical biological processes based on protein function annotation including photosynthesis, cell structure, protein synthesis & destination, transporters, metabolism of sugars and polysaccharides, secondary metabolism, disease/defense and proteins with unknown functions. Proteins with increased abundance in winter tender shoots were mainly related to the processes of photosynthesis, cytoskeleton and protein synthesis, whereas those with decreased abundance were correlated to metabolism and the secondary metabolism of polyphenolic flavonoids. Biochemical analysis showed that the total contents of soluble sugar and amino acid were higher in winter tender shoots while tea polyphenols were lower as compared with spring tender shoots. Conclusions Our study suggested that the simultaneous increase in the abundance of photosynthesis-related proteins rubisco, plastocyanin, and ATP synthase delta chain, metabolism-related proteins eIF4 and protease subunits, and the cytoskeleton-structure associated proteins phosphatidylinositol transfer protein and profilin may be because of the adaptation of the evergrowing tea cultivar “Dongcha11” to low temperature and light conditions. Histone H4, Histone H2A.1, putative In2.1 protein and protein lin-28 homologs may also regulate the development of winter shoots and their response to adverse conditions.

Alzheimer's disease (AD) is a leading cause of dementia in the elderly. Mitogen-activated protein kinase phosphatase 1 (MKP-1) plays a neuroprotective role in AD. However, the molecular mechanisms underlying the effects of MKP-1 on AD have not been extensively studied. MicroRNAs (miRNAs) regulate gene expression at the post-transcriptional level, thereby repressing mRNA translation. Here, we reported that the microRNA-429-3p (miR-429-3p) was significantly increased in the brain of APP23/PS45 AD model mice and N2AAPP AD model cells. We further found that miR-429-3p could downregulate MKP-1 expression by directly binding to its 3′-untranslated region (3′ UTR). Inhibition of miR-429-3p by its antagomir (A-miR-429) restored the expression of MKP-1 to a control level and consequently reduced the amyloidogenic processing of APP and Aβ accumulation. More importantly, intranasal administration of A-miR-429 successfully ameliorated the deficits of hippocampal CA1 long-term potentiation and spatial learning and memory in AD model mice by suppressing extracellular signal-regulated kinase (ERK1/2)-mediated GluA1 hyperphosphorylation at Ser831 site, thereby increasing the surface expression of GluA1-containing α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs). Together, these results demonstrate that inhibiting miR-429-3p to upregulate MKP-1 effectively improves cognitive and synaptic functions in AD model mice, suggesting that miR-429/MKP-1 pathway may be a novel therapeutic target for AD treatment.

Abstract Background The nucleotide-binding oligomeric domain (NOD)-like receptor protein 3 (NLRP3) inflammasome is believed to be a key mediator of neuroinflammation and subsequent secondary brain injury induced by ischemic stroke. However, the role and underlying mechanism of the NLRP3 inflammasome in neonates with hypoxic-ischemic encephalopathy (HIE) are still unclear. Methods The protein expressions of the NLRP3 inflammasome including NLRP3, cysteinyl aspartate specific proteinase-1 (caspase-1) and interleukin-1β (IL-1β), the α-amino-3-hydroxy-5-methyl-4-isoxazole-propionicacid receptor (AMPAR) subunit, and the ATPase valosin-containing protein (VCP/p97), were determined by Western blotting. The interaction between p97 and AMPA glutamate receptor 1 (GluA1) was determined by co-immunoprecipitation. The histopathological level of hypoxic-ischemic brain damage (HIBD) was determined by triphenyltetrazolium chloride (TTC) staining. Polymerase chain reaction (PCR) and Western blotting were used to confirm the genotype of the knockout mice. Motor functions, including myodynamia and coordination, were evaluated by using grasping and rotarod tests. Hippocampus-dependent spatial cognitive function was measured by using the Morris-water maze (MWM). Results We reported that the NLRP3 inflammasome signaling pathway, such as NLRP3, caspase-1 and IL-1β, was activated in rats with HIBD and oxygen-glucose deprivation (OGD)-treated cultured primary neurons. Further studies showed that the protein level of the AMPAR GluA1 subunit on the hippocampal postsynaptic membrane was significantly decreased in rats with HIBD, and it could be restored to control levels after treatment with the specific caspase-1 inhibitor AC-YVAD-CMK. Similarly, in vitro studies showed that OGD reduced GluA1 protein levels on the plasma membrane in cultured primary neurons, whereas AC-YVAD-CMK treatment restored this reduction. Importantly, we showed that OGD treatment obviously enhanced the interaction between p97 and GluA1, while AC-YVAD-CMK treatment promoted the dissociation of p97 from the GluA1 complex and consequently facilitated the localization of GluA1 on the plasma membrane of cultured primary neurons. Finally, we reported that the deficits in motor function, learning and memory in animals with HIBD, were ameliorated by pharmacological intervention or genetic ablation of caspase-1. Conclusion Inhibiting the NLRP3 inflammasome signaling pathway promotes neurological recovery in animals with HIBD by increasing p97-mediated surface GluA1 expression, thereby providing new insight into HIE therapy.

Disrupting the balance of neuronal excitation and inhibition (E/I) is an important pathogenic mechanism of anxiety and depression. Interferon regulatory factor 3 (IRF3) plays a key role in the innate immune response, and activation of IRF3 triggers the expression of type I interferons and downstream interferon-stimulated genes, which are associated with anxiety and depression. However, whether IRF3 participates in the pathogenesis of anxiety/depression by regulating E/I balance remains poorly understood. Here, we reported that global knockout (KO) of IRF3 (IRF3−/−) significantly increased anxiety/depression-like behaviors, but did not affect normal spatial learning and memory. Compared with wild type (WT) control mice, the E/I balance was disrupted, as reflected by enhanced glutamatergic transmission and decreased GABAergic transmission in the neurons of hippocampal CA1 and medial prefrontal cortex (mPFC) in IRF3-KO mice. Importantly, genetic rescue of IRF3 expression by adeno-associated virus (AAV) was sufficient to alleviate anxiety/depression-like behaviors and restore the neuronal E/I balance in IRF3-KO mice. Taken together, our results indicate that IRF3 is critical in maintaining neuronal E/I balance, thereby playing an essential role in ensuring emotional stability.

Abstract The imbalance between neuronal excitation and inhibition (E/I) in neural circuit has been considered to be at the root of numerous brain disorders. We recently reported a novel feedback crosstalk between the excitatory neurotransmitter glutamate and inhibitory γ‐aminobutyric acid type A receptor (GABAAR)‐glutamate allosteric potentiation of GABAAR functions through a direct binding of glutamate to the GABAAR itself. Here, we investigated the physiological significance and pathological implications of this cross‐talk by generating the β3E182G knock‐in (KI) mice. We found that β3E182G KI, while had little effect on basal GABAAR‐mediated synaptic transmission, significantly reduced glutamate potentiation of GABAAR‐mediated responses. These KI mice displayed lower thresholds for noxious stimuli, higher susceptibility to seizures and enhanced hippocampus‐related learning and memory. Additionally, the KI mice exhibited impaired social interactions and decreased anxiety‐like behaviors. Importantly, hippocampal overexpression of wild‐type β3‐containing GABAARs was sufficient to rescue the deficits of glutamate potentiation of GABAAR‐mediated responses, hippocampus‐related behavioral abnormalities of increased epileptic susceptibility, and impaired social interactions. Our data indicate that the novel crosstalk among excitatory glutamate and inhibitory GABAAR functions as a homeostatic mechanism in fine‐tuning neuronal E/I balance, thereby playing an essential role in ensuring normal brain functioning.