Multi-Modal Multi-Scale Deep Learning for Large-Scale Image Annotation

Image annotation aims to annotate a given image with a variable number of class labels corresponding to diverse visual concepts. In this paper, we address two main issues in large-scale image annotation: 1) how to learn a rich feature representation suitable for predicting a diverse set of visual concepts ranging from object, scene to abstract concept; 2) how to annotate an image with the optimal number of class labels. To address the first issue, we propose a novel multi-scale deep model for extracting rich and discriminative features capable of representing a wide range of visual concepts. Specifically, a novel two-branch deep neural network architecture is proposed which comprises a very deep main network branch and a companion feature fusion network branch designed for fusing the multi-scale features computed from the main branch. The deep model is also made multi-modal by taking noisy user-provided tags as model input to complement the image input. For tackling the second issue, we introduce a label quantity prediction auxiliary task to the main label prediction task to explicitly estimate the optimal label number for a given image. Extensive experiments are carried out on two large-scale image annotation benchmark datasets and the results show that our method significantly outperforms the state-of-the-art.Comment: Submited to IEEE TI

Tetra­aqua­bis[2-(2,4-dichloro­phen­oxy)acetato]nickel(II)

In the title complex, [Ni(C8H5Cl2O3)2(H2O)4], the NiII atom (site symmetry ) adopts a slightly distorted NiO6 octa­hedral coordination. An intra­molecular O—H⋯O hydrogen bond helps to establish the conformation. In the crystal, further O—H⋯O hydrogen bonds link the mol­ecules

ent-Kaurane diterpenoids from the plant Wedelia trilobata

Four new ent-kaurane diterpenoids, namely, 3α-tigloyloxypterokaurene L(3) (1), ent-17-hydroxy-kaura-9(11),15-dien-19-oic acid (2), and wedelobatins A (3) and B (4), together with 11 known ent-kaurane diterpenoids (5-15), were isolated from the ethanol extract of Wedelia trilobata. All the structures of 1–15 were elucidated on the basis of spectroscopic studies. [Image: see text] ELECTRONIC SUPPLEMENTARY MATERIAL: Supplementary material is available for this article at 10.1007/s13659-013-0029-4 and is accessible for authorized users

Dexmedetomidine post-treatment attenuates cardiac ischaemia/reperfusion injury by inhibiting apoptosis through HIF-1α signalling.

Hypoxia-inducible factor 1α (HIF-1α) plays a critical role in the apoptotic process during cardiac ischaemia/reperfusion (I/R) injury. This study aimed to investigate whether post-treatment with dexmedetomidine (DEX) could protect against I/R-induced cardiac apoptosis in vivo and in vitro via regulating HIF-1α signalling pathway. Rat myocardial I/R was induced by occluding the left anterior descending artery for 30 minutes followed by 6-hours reperfusion, and cardiomyocyte hypoxia/reoxygenation (H/R) was induced by oxygen-glucose deprivation for 6 hours followed by 3-hours reoxygenation. Dexmedetomidine administration at the beginning of reperfusion or reoxygenation attenuated I/R-induced myocardial injury or H/R-induced cell death, alleviated mitochondrial dysfunction, reduced the number of apoptotic cardiomyocytes, inhibited the activation of HIF-1α and modulated the expressions of apoptosis-related proteins including BCL-2, BAX, BNIP3, cleaved caspase-3 and cleaved PARP. Conversely, the HIF-1α prolyl hydroxylase-2 inhibitor IOX2 partly blocked DEX-mediated cardioprotection both in vivo and in vitro. Mechanistically, DEX down-regulated HIF-1α expression at the post-transcriptional level and inhibited the transcriptional activation of the target gene BNIP3. Post-treatment with DEX protects against cardiac I/R injury in vivo and H/R injury in vitro. These effects are, at least in part, mediated via the inhibition of cell apoptosis by targeting HIF-1α signalling

Exploration and Practice of Blended Teaching Model Based Flipped Classroom and SPOC in higher University

SPOC is characterized by improving teaching effectiveness. Currently open teaching mode is the popular trend, which is mainly related to several aspects: how to carry out teaching practice by using MOOC proprietary, high-quality online teaching resources in open education, that is, deep integration of curriculum resources and teaching design. On the basis of SPOC development, combined with open education analysis of SPOC with instructional design theory and philosophy from flipped classroom as a guide, the present research try to propose instructional design model based on flipped classroom, including design of teaching content system, design of personalized learning strategies, design of teaching activities and teaching evaluation system. Four designs above contribute to the effective implementation of the open teaching activities based on the blended model of flipped classroom and SPOC teaching, so as to enhance the quality of education. Keywords: Teaching design model; SPOC; Teaching methods; Flipped classroo

Geometric density of states of electronic structures for local responses: Phase information from the amplitudes of STM measurement

Electronic band structures underlie the physical properties of crystalline materials, their geometrical exploration renovates the conventional cognition and brings about novel applications. Inspired by geometry phases, we introduce a geometric amplitude named as the geometric density of states (GDOS) dictated by the differential curvature of the constant-energy contour. The GDOS determines the amplitude of the real-space Green's function making it attain the ultimate expression with transparent physics. The local responses of crystalline materials are usually formulated by the real-space Green's function, so the relevant physics should be refreshed by GDOS. As an example of local responses, we suggest using scanning tunneling microscopy (STM) to characterize the surface states of three-dimensional topological insulator under an in-plane magnetic field. The GDOS favors the straightforward simulation of STM measurement without resorting to Fourier transform of the real-space measurement, and also excavates the unexplored potential of STM measurement to extract the phase information of wavefunction through its amplitude, i.e., the spin and curvature textures. Therefore, the proposed GDOS deepens the understanding of electronic band structures and is indispensable in local responses, and it should be universal for any periodic systems.Comment: 6 pages, 2 figure

Heat Shock Protein 70 Protects the Heart from Ischemia/Reperfusion Injury through Inhibition of p38 MAPK Signaling.

BackgroundHeat shock protein 70 (Hsp70) has been shown to exert cardioprotection. Intracellular calcium ([Ca2+]i) overload induced by p38 mitogen-activated protein kinase (p38 MAPK) activation contributes to cardiac ischemia/reperfusion (I/R) injury. However, whether Hsp70 interacts with p38 MAPK signaling is unclear. Therefore, this study investigated the regulation of p38 MAPK by Hsp70 in I/R-induced cardiac injury.MethodsNeonatal rat cardiomyocytes were subjected to oxygen-glucose deprivation for 6 h followed by 2 h reoxygenation (OGD/R), and rats underwent left anterior artery ligation for 30 min followed by 30 min of reperfusion. The p38 MAPK inhibitor (SB203580), Hsp70 inhibitor (Quercetin), and Hsp70 short hairpin RNA (shRNA) were used prior to OGD/R or I/R. Cell viability, lactate dehydrogenase (LDH) release, serum cardiac troponin I (cTnI), [Ca2+]i levels, cell apoptosis, myocardial infarct size, mRNA level of IL-1β and IL-6, and protein expression of Hsp70, phosphorylated p38 MAPK (p-p38 MAPK), sarcoplasmic/endoplasmic reticulum Ca2+-ATPase2 (SERCA2), phosphorylated signal transducer and activator of transcription3 (p-STAT3), and cleaved caspase3 were assessed.ResultsPretreatment with a p38 MAPK inhibitor, SB203580, significantly attenuated OGD/R-induced cell injury or I/R-induced myocardial injury, as evidenced by improved cell viability and lower LDH release, resulted in lower serum cTnI and myocardial infarct size, alleviation of [Ca2+]i overload and cell apoptosis, inhibition of IL-1β and IL-6, and modulation of protein expressions of p-p38 MAPK, SERCA2, p-STAT3, and cleaved-caspase3. Knockdown of Hsp70 by shRNA exacerbated OGD/R-induced cell injury, which was effectively abolished by SB203580. Moreover, inhibition of Hsp70 by quercetin enhanced I/R-induced myocardial injury, while SB203580 pretreatment reversed the harmful effects caused by quercetin.ConclusionsInhibition of Hsp70 aggravates [Ca2+]i overload, inflammation, and apoptosis through regulating p38 MAPK signaling during cardiac I/R injury, which may help provide novel insight into cardioprotective strategies