Compare More Nuanced:Pairwise Alignment Bilinear Network For Few-shot Fine-grained Learning

The recognition ability of human beings is developed in a progressive way. Usually, children learn to discriminate various objects from coarse to fine-grained with limited supervision. Inspired by this learning process, we propose a simple yet effective model for the Few-Shot Fine-Grained (FSFG) recognition, which tries to tackle the challenging fine-grained recognition task using meta-learning. The proposed method, named Pairwise Alignment Bilinear Network (PABN), is an end-to-end deep neural network. Unlike traditional deep bilinear networks for fine-grained classification, which adopt the self-bilinear pooling to capture the subtle features of images, the proposed model uses a novel pairwise bilinear pooling to compare the nuanced differences between base images and query images for learning a deep distance metric. In order to match base image features with query image features, we design feature alignment losses before the proposed pairwise bilinear pooling. Experiment results on four fine-grained classification datasets and one generic few-shot dataset demonstrate that the proposed model outperforms both the state-ofthe-art few-shot fine-grained and general few-shot methods.Comment: ICME 2019 Ora

ApoE and Aβ in Alzheimer’s Disease: Accidental Encounters or Partners?

Among the three human apolipoprotein E (apoE) isoforms, apoE4 increases the risk of Alzheimer’s disease (AD). While transporting cholesterol is a primary function, apoE also regulates amyloid-β (Aβ) metabolism, aggregation, and deposition. Although earlier work suggests that different affinities of apoE isoforms to Aβ might account for their effects on Aβ clearance, recent studies indicate that apoE also competes with Aβ for cellular uptake through apoE receptors. Thus, several factors probably determine the variable effects apoE has on Aβ. In this Review, we examine biochemical, structural, and functional studies and propose testable models that address the complex mechanisms underlying apoE-Aβ interaction and how apoE4 may increase AD risk and also serve as a target pathway for therapy

Zoom in on neurodegeneration

Despite the existence of several scientific journals that publish research papers and reviews related to neurodegenerative diseases, a journal specifically devoted to the molecular and cellular aspects of disease mechanisms is lacking. Molecular Neurodegeneration is an open-access, peer-reviewed, online journal created to publish original research articles that address i) the mechanisms of neurodegeneration at the cellular, subcellular and molecular levels and ii) potential therapeutic interventions for neurodegenerative diseases. Through publication of reviews, editorial commentaries, and meeting reports, Molecular Neurodegeneration will also provide a forum to enhance the exchange of ideas and promote debate that is essential for scientific progress. Molecular Neurodegeneration will enable scientists to rapidly communicate their important research discoveries to their colleagues around the world

Masked Cross-image Encoding for Few-shot Segmentation

Few-shot segmentation (FSS) is a dense prediction task that aims to infer the pixel-wise labels of unseen classes using only a limited number of annotated images. The key challenge in FSS is to classify the labels of query pixels using class prototypes learned from the few labeled support exemplars. Prior approaches to FSS have typically focused on learning class-wise descriptors independently from support images, thereby ignoring the rich contextual information and mutual dependencies among support-query features. To address this limitation, we propose a joint learning method termed Masked Cross-Image Encoding (MCE), which is designed to capture common visual properties that describe object details and to learn bidirectional inter-image dependencies that enhance feature interaction. MCE is more than a visual representation enrichment module; it also considers cross-image mutual dependencies and implicit guidance. Experiments on FSS benchmarks PASCAL-$5^i$ and COCO-$20^i$ demonstrate the advanced meta-learning ability of the proposed method.Comment: conferenc

Notch Signaling Mediates TNF-α-Induced IL-6 Production in Cultured Fibroblast-Like Synoviocytes from Rheumatoid Arthritis

It has been reported that Notch family proteins are expressed in synovium tissue and involved in the proliferation of synoviocyte from rheumatoid arthritis (RA). The aim of this paper was to investigate whether Notch signaling mediated TNF-α-induced cytokine production of cultured fibroblast-like synoviocytes (FLSs) from RA. Exposure of RA FLSs to TNF-α (10 ng/ml) led to increase of Hes-1, a target gene of Notch signaling, and a marked upregulation of Notch 2, Delta-like 1, and Delta-like 3 mRNA levels. Blockage of Notch signaling by a γ-secretase inhibitor (DAPT) inhibited IL-6 secretion of RA FLSs in response to TNF-α while treatment with recombinant fusion protein of Notch ligand Delta-like 1 promoted such response. TNF-α stimulation also induced IL-6 secretion in OA FLSs; however, the Hes-1 level remained unaffected. Our data confirm the functional involvement of Notch pathway in the pathophysiology of RA FLSs which may provide a new target for RA therapy

Insufficient ER-stress response causes selective mouse cerebellar granule cell degeneration resembling that seen in congenital disorders of glycosylation

BACKGROUND: Congenital disorders of glycosylation (CDGs) are inherited diseases caused by glycosylation defects. Incorrectly glycosylated proteins induce protein misfolding and endoplasmic reticulum (ER) stress. The most common form of CDG, PMM2-CDG, is caused by deficiency in the cytosolic enzyme phosphomannomutase 2 (PMM2). Patients with PMM2-CDG exhibit a significantly reduced number of cerebellar Purkinje cells and granule cells. The molecular mechanism underlying the specific cerebellar neurodegeneration in PMM2-CDG, however, remains elusive. RESULTS: Herein, we report that cerebellar granule cells (CGCs) are more sensitive to tunicamycin (TM)-induced inhibition of total N-glycan synthesis than cortical neurons (CNs). When glycan synthesis was inhibited to a comparable degree, CGCs exhibited more cell death than CNs. Furthermore, downregulation of PMM2 caused more CGCs to die than CNs. Importantly, we found that upon PMM2 downregulation or TM treatment, ER-stress response proteins were elevated less significantly in CGCs than in CNs, with the GRP78/BiP level showing the most significant difference. We further demonstrate that overexpression of GRP78/BiP rescues the death of CGCs resulting from either TM-treatment or PMM2 downregulation. CONCLUSIONS: Our results indicate that the selective susceptibility of cerebellar neurons to N-glycosylation defects is due to these neurons’ inefficient response to ER stress, providing important insight into the mechanisms of selective neurodegeneration observed in CDG patients

Genotyping of Salmonella enterica serovar Typhi strains isolated from 1959 to 2006 in China and analysis of genetic diversity by genomic microarray

Aim To determine the genotype of Salmonella enterica serovar Typhi (S. Typhi) strains in China and analyze their genetic diversity. Methods We collected S. Typhi strains from 1959 to 2006 in five highly endemic Chinese provinces and chose 40 representative strains. Multilocus sequence typing was used to determine the genotypes or sequence types (ST) and microarray-based comparative genomic hybridization (M-CGH) to investigate the differences in gene content among these strains. Results Forty representative S. Typhi strains belonged to 4 sequence types (ST1, ST2, ST890, and ST892). The predominant S. Typhi genotype (31/40) was ST2 and it had a diverse geographic distribution. We discovered two novel STs – ST890 and ST892. M-CGH showed that 69 genes in these two novel STs were divergent from S. Typhi Ty2, which belongs to ST1. In addition, 5 representative Typhi strains of ST2 isolated from Guizhou province showed differences in divergent genes. Conclusion We determined two novel sequence types, ST890 and ST892, and found that ST2 was the most prevalent genotype of S. Typhi in China. Genetic diversity was present even within a highly clonal bacterial population

Compensatory Mechanisms Modulate the Neuronal Excitability in a Kainic Acid-Induced Epilepsy Mouse Model

Epilepsy is one of the most common neurological disorders affecting millions of people. Due to the complicated and unclear mechanisms of epilepsy, still a significant proportion of epilepsy patients remain poorly controlled. Epilepsy is characterized by convulsive seizures that are caused by increased excitability. In this study, by using kainic acid (KA)-induced epilepsy mice, we investigated the neuronal activities and revealed the neuronal compensatory mechanisms after KA-induced toxic hyperexcitability. The results indicate that both phasic inhibition induced by enhanced inhibitory synaptic activity and tonic inhibition mediated by activated astrocytes participate in the compensatory mechanisms. Compensatory mechanisms were already found in various neuronal disorders and were considered important in protecting nervous system from toxic hyperexcitability. This study hopefully will provide valuable clues in understanding the complex neuronal mechanisms of epilepsy, and exploring potential clinical treatment of the disease