A Deep Multi-Task Learning Approach for Bioelectrical Signal Analysis

Deep learning is a promising technique for bioelectrical signal analysis, as it can automatically discover hidden features from raw data without substantial domain knowledge. However, training a deep neural network requires a vast amount of labeled samples. Additionally, a well-trained model may be sensitive to the study object, and its performance may deteriorate sharply when transferred to other study objects. We propose a deep multi-task learning approach for bioelectrical signal analysis to address these issues. Explicitly, we define two distinct scenarios, the consistent source-target scenario and the inconsistent source-target scenario based on the motivation and purpose of the tasks. For each scenario, we present methods to decompose the original task and dataset into multiple subtasks and sub-datasets. Correspondingly, we design the generic deep parameter-sharing neural networks to solve the multi-task learning problem and illustrate the details of implementation with one-dimension convolutional neural networks (1D CNN), vanilla recurrent neural networks (RNN), recurrent neural networks with long short-term memory units (LSTM), and recurrent neural networks with gated recurrent units (GRU). In these two scenarios, we conducted extensive experiments on four electrocardiogram (ECG) databases. The results demonstrate the benefits of our approach, showing that our proposed method can improve the accuracy of ECG data analysis (up to 5.2%) in the MIT-BIH arrhythmia database

Phage Therapy as a Promising New Treatment for Lung Infection Caused by Carbapenem-Resistant Acinetobacter baumannii in Mice

Carbapenem-resistant Acinetobacter baumannii (CRAB) which is noted as a major pathogen associated with healthcare-associated infections has steadily developed beyond antibiotic control. Lytic bacteriophages with the characteristics of infecting and lysing specific bacteria have been used as a potential alternative to traditional antibiotics to solve multidrug-resistant bacterial infections. Here, we isolated A. baumannii-specific lytic phages and evaluated their potential therapeutic effect against lung infection caused by CRAB clinical strains. The combined lysis spectrum of four lytic phages’ ranges was 87.5% (42 of 48) against CRAB clinical isolates. Genome sequence and analysis indicated that phage SH-Ab15519 is a novel phage which does not contain the virulence or antibiotic resistance genes. In vivo study indicated that phage SH-Ab15519 administered intranasally can effectively rescue mice from lethal A. baumannii lung infection without deleterious side effects. Our work explores the potential use of phages as an alternative therapeutic agent against the lung infection caused by CRAB strains

Caenorhabditis elegans Extracts Stimulate IAA Biosynthesis in Arthrobacter pascens ZZ21 via the Indole-3-pyruvic Acid Pathway

Inter-organismal metabolites play important roles in regulating organism behavior and the communication between organisms. Nematodes, the most abundant animals on earth, are crucial participants in soil ecosystems through their interactions with microbes. For example, bacterial-feeding nematodes increase the activity of indole-3-acetic acid (IAA)-producing bacteria and the IAA content in soil. However, the way in which these nematodes interact with bacteria and affect IAA biosynthesis is not well understood. Here, using the model nematode Caenorhabditis elegans and the plant-beneficial bacterium Arthrobacter pascens ZZ21, we examined the effects of nematode excretions or extracts on bacterial IAA biosynthesis. To explore the underlying regulatory mechanism in more detail, we performed transcriptome sequencing and metabolomic analysis. Our findings suggest that C. elegans extracts promote IAA biosynthesis in A. pascens ZZ21 by increasing the expression of genes and the abundance of intermediates involved in the indole-3-pyruvic acid (IPyA) pathway. C. elegans extracts also significantly influenced biosynthetic and metabolic activity in A. pascens ZZ21. Treatment with C. elegans extracts promoted pyruvate metabolism, the citrate cycle (TCA) cycle and the production of some TCA-cycle-related amino acids and inhibited oxidative phosphorylation, which induced the accumulation of reduced nicotinamide adenine dinucleotide (NADH). We propose that the extracts altered the metabolism of A. pascens ZZ21 to help the bacteria resist stress caused by their predator. Our findings indicate that bacterial-feeding nematodes mediate the interaction between nematodes and bacteria via their extracts, providing insights into the ecological function of C. elegans in soil

Impairments of GABAergic transmission in hippocampus mediate increased susceptibility of epilepsy in the early stage of Alzheimer’s disease

Abstract Background Patients with Alzheimer’s disease (AD) are often co-morbid with unprovoked seizures, making clinical diagnosis and management difficult. Although it has an important role in both AD and epilepsy, abnormal γ-aminobutyric acid (GABA)ergic transmission is recognized only as a compensative change for glutamatergic damage. Neuregulin 1 (NRG1)-ErbB4 signaling can promote GABA release and suppress epileptogenesis, but its effects on cognition in AD are still controversial. Methods Four-month-old APPswe/PS1dE9 mice (APP mice) were used as animal models in the early stage of AD in this study. Acute/chronic chemical-kindling epilepsy models were established with pentylenetetrazol. Electroencephalogram and Racine scores were performed to assess seizures. Behavioral tests were used to assess cognition and emotion. Electrophysiology, western blot and immunofluorescence were performed to detect the alterations in synapses, GABAergic system components and NRG1-ErbB4 signaling. Furthermore, NRG1 was administrated intracerebroventricularly into APP mice and then its antiepileptic and cognitive effects were evaluated. Results APP mice had increased susceptibility to epilepsy and resulting hippocampal synaptic damage and cognitive impairment. Electrophysiological analysis revealed decreased GABAergic transmission in the hippocampus. This abnormal GABAergic transmission involved a reduction in the number of parvalbumin interneurons (PV+ Ins) and decreased levels of GABA synthesis and transport. We also found impaired NRG1-ErbB4 signaling which mediated by PV+ Ins loss. And NRG1 administration could effectively reduce seizures and improve cognition in four-month-old APP mice. Conclusion Our results indicated that abnormal GABAergic transmission mediated hippocampal hyperexcitability, further excitation/inhibition imbalance, and promoted epileptogenesis in the early stage of AD. Appropriate NRG1 administration could down-regulate seizure susceptibility and rescue cognitive function. Our study provided a potential direction for intervening in the co-morbidity of AD and epilepsy

Microfluidic antibody affinity profiling of alloantibody-HLA interactions in human serum.

Antibody profiling is a fundamental component of understanding the humoral response in a wide range of disease areas. Most currently used approaches operate by capturing antibodies onto functionalised surfaces. Such measurements of surface binding are governed by an overall antibody titre, while the two fundamental molecular parameters, antibody affinity and antibody concentration, are challenging to determine individually from such approaches. Here, by applying microfluidic diffusional sizing (MDS), we show how we can overcome this challenge and demonstrate reliable quantification of alloantibody binding affinity and concentration of alloantibodies binding to Human Leukocyte Antigens (HLA), an extensively used clinical biomarker in organ transplantation, both in buffer and in crude human serum. Capitalising on the ability to vary both serum and HLA concentrations during MDS, we show that both affinity and concentration of HLA-specific antibodies can be determined directly in serum when neither of these parameters is known. Finally, we provide proof of principle in clinical transplant patient sera that our assay enables differentiation of alloantibody reactivity against HLA proteins of highly similar structure, providing information not attainable through currently available techniques. These results outline a path towards detection and in-depth profiling of humoral immunity and may enable further insights into the clinical relevance of antibody reactivity in clinical transplantation and beyond

Bulk spin torque driven perpendicular magnetization switching in L1 0 FePt

International audienceModern information technology demands advanced storage material and efficient data writing scheme. Inherent with a superior perpendicular magnetocrystalline anisotropy, the FePt in L1 0 phase envisions magnetic storage with ultrahigh capacity. However, reversing FePt magnetic state and therefore the encoded information has been proven to be extremely difficult. Here, we demonstrate that an electric current is capable to exert a large spin torque on a L1 0 FePt magnet, which ultimately leads to reversible magnetization switching through domain nucleation and expansion in an efficient and simple manner

Bulk Spin Torque‐Driven Perpendicular Magnetization Switching in L

International audienceModern information technology demands advanced storage material and efficient data writing scheme. Inherent with a superior perpendicular magnetocrystalline anisotropy, the FePt in L1 0 phase envisions magnetic storage with ultrahigh capacity. However, reversing FePt magnetic state and therefore the encoded information has been proven to be extremely difficult. Here, we demonstrate that an electric current is capable to exert a large spin torque on a L1 0 FePt magnet, which ultimately leads to reversible magnetization switching through domain nucleation and expansion in an efficient and simple manner

Additional file 2 of Impairments of GABAergic transmission in hippocampus mediate increased susceptibility of epilepsy in the early stage of Alzheimer’s disease

Supplementary Material 2

Additional file 1 of Impairments of GABAergic transmission in hippocampus mediate increased susceptibility of epilepsy in the early stage of Alzheimer’s disease

Supplementary Material 1