5,271 research outputs found

    The roles of endoglin gene in cerebrovascular diseases.

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    Endoglin (ENG, also known as CD105) is a transforming growth factor β (TGFβ) associated receptor and is required for both vasculogenesis and angiogenesis. Angiogenesis is important in the development of cerebral vasculature and in the pathogenesis of cerebral vascular diseases. ENG is an essential component of the endothelial nitric oxide synthase activation complex. Animal studies showed that ENG deficiency impairs stroke recovery. ENG deficiency also impairs the regulation of vascular tone, which contributes to the pathogenesis of brain arteriovenous malformation (bAVM) and vasospasm. In human, functional haploinsufficiency of ENG gene causes type I hereditary hemorrhagic telangiectasia (HHT1), an autosomal dominant disorder. Compared to normal population, HHT1 patients have a higher prevalence of AVM in multiple organs including the brain. Vessels in bAVM are fragile and tend to rupture, causing hemorrhagic stroke. High prevalence of pulmonary AVM in HHT1 patients are associated with a higher incidence of paradoxical embolism in the cerebral circulation causing ischemic brain injury. Therefore, HHT1 patients are at risk for both hemorrhagic and ischemic stroke. This review summarizes the possible mechanism of ENG in the pathogenesis of cerebrovascular diseases in experimental animal models and in patients

    Theoretical analysis of direct CPCP violation and differential decay width in D±π±π+πD^\pm\to \pi^\pm \pi^+\pi^- in phase space around the resonances ρ0(770)\rho^0(770) and f0(500)f_0(500)

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    We perform a theoretical study on direct CPCP violation in D±π±π+πD^\pm\to \pi^\pm \pi^+\pi^- in phase space around the intermediate states ρ0(770)\rho^0(770) and f0(500)f_0(500). The possible interference between the amplitudes corresponding to the two resonances is taken into account, and the relative strong phase of the two amplitudes is treated as a free parameter. Our analysis shows that by properly chosen the strong phase, both the CPCP violation strength and differential decay width accommodate to the experimental results.Comment: 15 pages, 5 figure

    SIRT3 Protects Rotenone-induced Injury in SH-SY5Y Cells by Promoting Autophagy through the LKB1-AMPK-mTOR Pathway.

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    SIRT3 is a class III histone deacetylase that modulates energy metabolism, genomic stability and stress resistance. It has been implicated as a potential therapeutic target in a variety of neurodegenerative diseases, including Parkinson's disease (PD). Our previous study demonstrates that SIRT3 had a neuroprotective effect on a rotenone-induced PD cell model, however, the exact mechanism is unknown. In this study, we investigated the underlying mechanism. We established a SIRT3 stable overexpression cell line using lentivirus infection in SH-SY5Y cells. Then, a PD cell model was established using rotenone. Our data demonstrate that overexpression of SIRT3 increased the level of the autophagy markers LC3 II and Beclin 1. After addition of the autophagy inhibitor 3-MA, the protective effect of SIRT3 diminished: the cell viability decreased, while the apoptosis rate increased; α-synuclein accumulation enhanced; ROS production increased; antioxidants levels, including SOD and GSH, decreased; and MMP collapsed. These results reveal that SIRT3 has neuroprotective effects on a PD cell model by up-regulating autophagy. Furthermore, SIRT3 overexpression also promoted LKB1 phosphorylation, followed by activation of AMPK and decreased phosphorylation of mTOR. These results suggest that the LKB1-AMPK-mTOR pathway has a role in induction of autophagy. Together, our findings indicate a novel mechanism by which SIRT3 protects a rotenone-induced PD cell model through the regulation of autophagy, which, in part, is mediated by activation of the LKB1-AMPK-mTOR pathway

    What aspects of the home literacy environment differentiate Chinese children at risk for reading difficulties from their not at risk controls?

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    We examined what aspects of the home literacy environment (formal home literacy activities, informal home literacy activities, access to literacy resources, age of onset of literacy instruction, child’s interest in reading, and parents’ expectations) differentiate Chinese children at risk for reading difficulties from their not-at-risk controls. Eighteen children from Jining, China, who were at risk for reading difficulties and 32 not-at-risk controls participated in the study. Their parents also participated in the study by filling out a home literacy questionnaire, by recording the daily parent-child reading activities (diary), and by completing the Children’s Title Recognition Checklist. Group comparisons revealed significant differences only in items measuring children’s access to literacy resources and reading interest. Results of discriminant function analyses further showed that the home literacy environment variables could discriminate well between the children at risk for reading difficulties and their controls. Taken together, our findings suggest that to the extent environment plays a role in reading difficulties in Chinese, this should be traced to factors such as child’s interest in reading and access to literacy resources.

    Towards Few-Shot Open-Set Object Detection

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    Open-set object detection (OSOD) aims to detect the known categories and identify unknown objects in a dynamic world, which has achieved significant attentions. However, previous approaches only consider this problem in data-abundant conditions, while neglecting the few-shot scenes. In this paper, we seek a solution for the few-shot open-set object detection (FSOSOD), which aims to quickly train a detector based on few samples while detecting all known classes and identifying unknown classes. The main challenge for this task is that few training samples induce the model to overfit on the known classes, resulting in a poor open-set performance. We propose a new FSOSOD algorithm to tackle this issue, named Few-shOt Open-set Detector (FOOD), which contains a novel class weight sparsification classifier (CWSC) and a novel unknown decoupling learner (UDL). To prevent over-fitting, CWSC randomly sparses parts of the normalized weights for the logit prediction of all classes, and then decreases the co-adaptability between the class and its neighbors. Alongside, UDL decouples training the unknown class and enables the model to form a compact unknown decision boundary. Thus, the unknown objects can be identified with a confidence probability without any pseudo-unknown samples for training. We compare our method with several state-of-the-art OSOD methods in few-shot scenes and observe that our method improves the recall of unknown classes by 5%-9% across all shots in VOC-COCO dataset setting

    Lifshitz transitions in a heavy-Fermion liquid driven by short-range antiferromagnetic correlations in the two-dimensional Kondo lattice model

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    The heavy-Fermion liquid with short-range antiferromagnetic correlations is carefully considered in the two-dimensional Kondo-Heisenberg lattice model. As the ratio of the local Heisenberg superexchange JHJ_{H} to the Kondo coupling JKJ_{K} increases, Lifshitz transitions are anticipated, where the topology of the Fermi surface (FS) of the heavy quasiparticles changes from a hole-like circle to four kidney-like pockets centered around (π,π)(\pi ,\pi). In-between these two limiting cases, a first-order quantum phase transition is identified at JH/JK=0.1055J_{H}/J_{K}=0.1055 where a small circle begins to emerge within the large deformed circle. When JH/JK=0.1425J_{H}/J_{K}=0.1425, the two deformed circles intersect each other and then decompose into four kidney-like Fermi pockets via a second-order quantum phase transition. As JH/JKJ_{H}/J_{K} increases further, the Fermi pockets are shifted along the direction (π,π\pi,\pi) to (π/2,π/2\pi/2,\pi/2), and the resulting FS is consistent with the FS obtained recently using the quantum Monte Carlo cluster approach to the Kondo lattice system in the presence of the antiferrmagnetic order.Comment: 4 pages, 5 figure

    (Z)-1-Phenyl-3-(3-pyridyl­meth­ylamino)­but-2-en-1-one

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    The reaction of 3-C5H4NCH2NH2 and C6H5COCH2COCH3 affords the title compound, C16H16N2O. The O=C—C=C—N portion is essentially planar [maximum deviation = 0.046 (2) Å] and is aligned at dihedral angles of 22.6 (1) and 78.9 (1)° to the phenyl and pyridyl rings, respectively. The N—H and O=C groups are linked by an intra­molecular hydrogen bond. In the crystal, C—H⋯O hydrogen bonds and C—H⋯π inter­actions occur
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