Shanghai Jiao Tong University

About: Shanghai Jiao Tong University is a education organization based out in Shanghai, Shanghai, China. It is known for research contribution in the topics: Population & Cancer. The organization has 157524 authors who have published 184620 publications receiving 3451038 citations. The organization is also known as: Shanghai Communications University & Shanghai Jiaotong University.

Compressive data gathering for large-scale wireless sensor networks

Abstract: This paper presents the first complete design to apply compressive sampling theory to sensor data gathering for large-scale wireless sensor networks. The successful scheme developed in this research is expected to offer fresh frame of mind for research in both compressive sampling applications and large-scale wireless sensor networks. We consider the scenario in which a large number of sensor nodes are densely deployed and sensor readings are spatially correlated. The proposed compressive data gathering is able to reduce global scale communication cost without introducing intensive computation or complicated transmission control. The load balancing characteristic is capable of extending the lifetime of the entire sensor network as well as individual sensors. Furthermore, the proposed scheme can cope with abnormal sensor readings gracefully. We also carry out the analysis of the network capacity of the proposed compressive data gathering and validate the analysis through ns-2 simulations. More importantly, this novel compressive data gathering has been tested on real sensor data and the results show the efficiency and robustness of the proposed scheme.

APPL1 binds to adiponectin receptors and mediates adiponectin signalling and function

Abstract: Adiponectin, also known as Acrp30, is an adipose tissue-derived hormone with anti-atherogenic, anti-diabetic and insulin sensitizing properties. Two seven-transmembrane domain-containing proteins, AdipoR1 and AdipoR2, have recently been identified as adiponectin receptors, yet signalling events downstream of these receptors remain poorly defined. By using the cytoplasmic domain of AdipoR1 as bait, we screened a yeast two-hybrid cDNA library derived from human fetal brain. This screening led to the identification of a phosphotyrosine binding domain and a pleckstrin homology domain-containing adaptor protein, APPL1 (adaptor protein containing pleckstrin homology domain, phosphotyrosine binding (PTB) domain and leucine zipper motif). APPL1 interacts with adiponectin receptors in mammalian cells and the interaction is stimulated by adiponectin. Overexpression of APPL1 increases, and suppression of APPL1 level reduces, adiponectin signalling and adiponectin-mediated downstream events (such as lipid oxidation, glucose uptake and the membrane translocation of glucose transport 4 (GLUT4)). Adiponectin stimulates the interaction between APPL1 and Rab5 (a small GTPase) interaction, leading to increased GLUT4 membrane translocation. APPL1 also acts as a critical regulator of the crosstalk between adiponectin signalling and insulin signalling pathways. These results demonstrate a key function for APPL1 in adiponectin signalling and provide a molecular mechanism for the insulin sensitizing function of adiponectin.

Immunoregulatory mechanisms of mesenchymal stem and stromal cells in inflammatory diseases.

Abstract: Mesenchymal stem cells (MSCs; also referred to as mesenchymal stromal cells) have attracted much attention for their ability to regulate inflammatory processes. Their therapeutic potential is currently being investigated in various degenerative and inflammatory disorders such as Crohn’s disease, graft-versus-host disease, diabetic nephropathy and organ fibrosis. The mechanisms by which MSCs exert their therapeutic effects are multifaceted, but in general, these cells are thought to enable damaged tissues to form a balanced inflammatory and regenerative microenvironment in the presence of vigorous inflammation. Studies over the past few years have demonstrated that when exposed to an inflammatory environment, MSCs can orchestrate local and systemic innate and adaptive immune responses through the release of various mediators, including immunosuppressive molecules, growth factors, exosomes, chemokines, complement components and various metabolites. Interestingly, even nonviable MSCs can exert beneficial effects, with apoptotic MSCs showing immunosuppressive functions in vivo. Because the immunomodulatory capabilities of MSCs are not constitutive but rather are licensed by inflammatory cytokines, the net outcomes of MSC activation might vary depending on the levels and the types of inflammation within the residing tissues. Here, we review current understanding of the immunomodulatory mechanisms of MSCs and the issues related to their therapeutic applications.

Ultralow-loading platinum-cobalt fuel cell catalysts derived from imidazolate frameworks.

Abstract: Achieving high catalytic performance with the lowest amount of platinum is critical in fuel cell cost reduction. We describe a method of preparing highly active yet stable electrocatalysts containing ultralow Pt content using Co or Co/Zn zeolitic imidazolate frameworks as precursors. Synergistic catalysis between strained Pt-Co core-shell nanoparticles over a platinum-group-metal-free (PGM-free) catalytic substrate led to excellent fuel cell performance under 1 atmosphere of O 2 or air at both high voltage and high current domains. Two catalysts achieved the oxygen reduction reaction (ORR) mass activities of 1.08 A mg Pt −1 /1.77 A mg Pt −1 and retained 64%/15% of initial values after 30,000 voltage cycles in fuel cell. Computational modeling reveals that the interaction between Pt-Co and PGM-free sites improves ORR activity and durability.

The gut microbiota and obesity: from correlation to causality

Abstract: The gut microbiota has been linked with chronic diseases such as obesity in humans. However, the demonstration of causality between constituents of the microbiota and specific diseases remains an important challenge in the field. In this Opinion article, using Koch's postulates as a conceptual framework, I explore the chain of causation from alterations in the gut microbiota, particularly of the endotoxin-producing members, to the development of obesity in both rodents and humans. I then propose a strategy for identifying the causative agents of obesity in the human microbiota through a combination of microbiome-wide association studies, mechanistic analysis of host responses and the reproduction of diseases in gnotobiotic animals.