Estimates on the first two buckling eigenvalues on spherical domains

In this paper, we study the first two eigenvalues of the buckling problem on spherical domains. We obtain an estimate on the second eigenvalue in terms of the first eigenvalue, which improves one recent result obtained by Wang-Xia in [7].Comment: This article has been submitted for publication on 2009-04-2

GCN-Based Linkage Prediction for Face Clustering on Imbalanced Datasets: An Empirical Study

In recent years, benefiting from the expressive power of Graph Convolutional Networks (GCNs), significant breakthroughs have been made in face clustering. However, rare attention has been paid to GCN-based clustering on imbalanced data. Although imbalance problem has been extensively studied, the impact of imbalanced data on GCN-based linkage prediction task is quite different, which would cause problems in two aspects: imbalanced linkage labels and biased graph representations. The problem of imbalanced linkage labels is similar to that in image classification task, but the latter is a particular problem in GCN-based clustering via linkage prediction. Significantly biased graph representations in training can cause catastrophic overfitting of a GCN model. To tackle these problems, we evaluate the feasibility of those existing methods for imbalanced image classification problem on graphs with extensive experiments, and present a new method to alleviate the imbalanced labels and also augment graph representations using a Reverse-Imbalance Weighted Sampling (RIWS) strategy, followed with insightful analyses and discussions. The code and a series of imbalanced benchmark datasets synthesized from MS-Celeb-1M and DeepFashion are available on https://github.com/espectre/GCNs_on_imbalanced_datasets.Comment: 7 page

Metabolic Profiling Analysis of the Alleviation Effect of Treatment with Baicalin on Cinnabar Induced Toxicity in Rats Urine and Serum

Objectives: Baicalin is the main bioactive flavonoid constituent isolated from Scutellaria baicalensis Georgi. The mechanisms of protection of liver remain unclear. In this study, 1H NMR-based metabonomics approach has been used to investigate the alleviation effect of Baicalin.Method:1H NMR metabolomics analyses of urine and serum from rats, was performed to illuminate the alleviation effect of Baicalin on mineral medicine (cinnabar)-induced liver and kidney toxicity.Results: The metabolic profiles of groups receiving Baicalin at a dose of 80 mg/kg were remarkably different from cinnabar, and meanwhile, the level of endogenous metabolites returned to normal compared to group cinnabar. PLS-DA scores plots demonstrated that the variation tendency of control and Baicalein are apart from Cinnabar. The metabolic profiles of group Baicalein were similar to those of group control. Statistics results were confirmed by the histopathological examination and biochemical assay.Conclusion: Baicalin have the alleviation effect to the liver and kidney damage induced by cinnabar. The Baicalin could regulate endogenous metabolites associated with the energy metabolism, choline metabolism, amino acid metabolism, and gut flora

Magnetoelectric coupling induced by interfacial orbital reconstruction

The magnetoelectric coupling effect with profound physics and enormous potential applications has provoked a great number of research activities in materials science. Here, we report that the reversible orbital reconstruction driven by ferroelectric polarization modulates the magnetic performance of ferroelectric ferromagnetic heterostructure. Mn in plane orbital occupancy and related interfacial exotic magnetic state are enhanced and weakened by the negative and positive electric field, respectively. Our findings thus not only present a broad opportunity to fill the missing member, orbital in the mechanism of magnetoelectric coupling, but also make the orbital degree of freedom straight forward to the application in microelectronic device.Comment: 26 pages, 5 figures, Accepted by Advanced Material

Inhibition of ERK-DLP1 signaling and mitochondrial division alleviates mitochondrial dysfunction in Alzheimer's disease cybrid cell

Mitochondrial dysfunction is an early pathological feature of Alzheimer’s disease (AD). The underlying mechanisms and strategies to repair it remain unclear. Here, we demonstrate for the first time the direct consequences and potential mechanisms of mitochondrial functional defects associated with abnormal mitochondrial dynamics in AD. Using cytoplasmic hybrid (cybrid) neurons with incorporated platelet mitochondria from AD and age-matched non-AD human subjects into mitochondrial DNA (mtDNA)-depleted neuronal cells, we observed that AD cybrid cells had significant changes in morphology and function; such changes associate with altered expression and distribution of dynamin-like protein (DLP1) and mitofusin 2 (Mfn2). Treatment with antioxidant protects against AD mitochondria-induced extracellular signal-regulated kinase (ERK) activation and mitochondrial fission-fusion imbalances. Notably, inhibition of ERK activation not only attenuates aberrant mitochondrial morphology and function but also restores the mitochondrial fission and fusion balance. These effects suggest a role of oxidative stress-mediated ERK signal transduction in modulation of mitochondrial fission and fusion events. Further, blockade of the mitochondrial fission protein DLP1 by a genetic manipulation with a dominant negative DLP1 (DLP1K38A), its expression with siRNA-DLP1, or inhibition of mitochondrial division with mdivi-1 attenuates mitochondrial functional defects observed in AD cybrid cells. Our results provide new insights into mitochondrial dysfunction resulting from changes in the ERK-fission/fusion (DLP1) machinery and signaling pathway. The protective effect of mdivi-1 and inhibition of ERK signaling on maintenance of normal mitochondrial structure and function holds promise as a potential novel therapeutic strategy for AD

Inhibition of ERK-DLP1 signaling and mitochondrial division alleviates mitochondrial dysfunction in Alzheimer's disease cybrid cell

Mitochondrial dysfunction is an early pathological feature of Alzheimer’s disease (AD). The underlying mechanisms and strategies to repair it remain unclear. Here, we demonstrate for the first time the direct consequences and potential mechanisms of mitochondrial functional defects associated with abnormal mitochondrial dynamics in AD. Using cytoplasmic hybrid (cybrid) neurons with incorporated platelet mitochondria from AD and age-matched non-AD human subjects into mitochondrial DNA (mtDNA)-depleted neuronal cells, we observed that AD cybrid cells had significant changes in morphology and function; such changes associate with altered expression and distribution of dynamin-like protein (DLP1) and mitofusin 2 (Mfn2). Treatment with antioxidant protects against AD mitochondria-induced extracellular signal-regulated kinase (ERK) activation and mitochondrial fission-fusion imbalances. Notably, inhibition of ERK activation not only attenuates aberrant mitochondrial morphology and function but also restores the mitochondrial fission and fusion balance. These effects suggest a role of oxidative stress-mediated ERK signal transduction in modulation of mitochondrial fission and fusion events. Further, blockade of the mitochondrial fission protein DLP1 by a genetic manipulation with a dominant negative DLP1 (DLP1K38A), its expression with siRNA-DLP1, or inhibition of mitochondrial division with mdivi-1 attenuates mitochondrial functional defects observed in AD cybrid cells. Our results provide new insights into mitochondrial dysfunction resulting from changes in the ERK-fission/fusion (DLP1) machinery and signaling pathway. The protective effect of mdivi-1 and inhibition of ERK signaling on maintenance of normal mitochondrial structure and function holds promise as a potential novel therapeutic strategy for AD