Institution
Tongji University
Education•Shanghai, China•
About: Tongji University is a education organization based out in Shanghai, China. It is known for research contribution in the topics: Population & Adsorption. The organization has 76116 authors who have published 81176 publications receiving 1248911 citations. The organization is also known as: Tongji & Tóngjì Dàxué.
Topics: Population, Adsorption, Cancer, Finite element method, Lung cancer
Papers published on a yearly basis
Papers
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TL;DR: It was found that pretreating sludge at pH 10 caused the greatest sludge hydrolysis, acidification, soluble C:N and C:P ratios, and Fe(3+) concentration with a suitable short-chain fatty acids composition in the first stage, which resulted in the highest microorganism activity (ATP) and methane production in the second phase.
Abstract: During two-phase sludge anaerobic digestion, sludge is usually hydrolyzed and acidified in the first phase, then methane is produced in the second stage. To get more methane from sludge, most studies in literature focused on the increase of sludge hydrolysis. In this paper a different sludge pretreatment method, i.e., pretreating sludge at pH 10 for 8 d is reported, by which both waste activated sludge hydrolysis and acidification were increased, and the methane production was significantly improved. First, the effect of different sludge pretreatment methods on methane yield was compared. The pH 10 pretreated sludge showed the highest accumulative methane yield (398 mL per g of volatile suspended solids), which was 4.4-, 3.5-, 3.1-, and 2.3-fold of the blank (unpretreated), ultrasonic, thermal, and thermal-alkaline pretreated sludge, respectively. Nevertheless, its total time involved in the first (hydrolysis and acidification) and second (methanogenesis) stages was 17 (8 + 9) d, which was almost the same...
204 citations
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TL;DR: In this article, a composite adsorbent, hydroxyapatite/magnetite (HAp/Fe 3 O 4 ), has been prepared for the purpose of removing lead ions from aqueous solution.
204 citations
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TL;DR: It was showed that the MDD groups with and without childhood neglect exhibited overlapping and segregated functional connectivity patterns in the whole‐brain networks, providing empirical evidence for the contribution of early life stress to the pathophysiology of MDD.
Abstract: Many studies have suggested that childhood maltreatment increase risk of adulthood major depressive disorder (MDD) and predict its unfavorable treatment outcome, yet the neural underpinnings associated with childhood maltreatment in MDD remain poorly understood. Here, we seek to investigate the whole-brain functional connectivity patterns in MDD patients with childhood maltreatment. Resting-state functional magnetic resonance imaging was used to explore intrinsic or spontaneous functional connectivity networks of 18 MDD patients with childhood neglect, 20 MDD patients without childhood neglect, and 20 healthy controls. Whole-brain functional networks were constructed by measuring the temporal correlations of every pairs of brain voxels and were further analyzed by using graph-theory approaches. Relative to the healthy control group, the two MDD patient groups showed overlapping reduced functional connectivity strength in bilateral ventral medial prefrontal cortex/ventral anterior cingulate cortex. However, compared with MDD patients without a history of childhood maltreatment, those patients with such a history displayed widespread reduction of functional connectivity strength primarily in brain regions within the prefrontal-limbic-thalamic-cerebellar circuitry, and these reductions significantly correlated with measures of childhood neglect. Together, we showed that the MDD groups with and without childhood neglect exhibited overlapping and segregated functional connectivity patterns in the whole-brain networks, providing empirical evidence for the contribution of early life stress to the pathophysiology of MDD.
204 citations
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TL;DR: It is shown that in diabetic mouse models, β-arrestin-2 is severely downregulated, and this provides new insight into the molecular pathogenesis of insulin resistance, and implicate new preventive and therapeutic strategies against insulin resistance and type 2 diabetes.
Abstract: The insulin resistance characteristic of type 2 diabetes and obesity is caused by the failure of insulin to stimulate receptor signalling. Defining the cellular mechanisms of this defect is critical to understanding these disorders. Experiments in type 2 diabetes clinical samples and mouse models now show that the scaffold protein β-arrestin-2 is necessary for efficient insulin signalling, linking the downstream kinases Akt and Src to the insulin receptor. β-arrestin-2 is downregulated both in diabetic mice and in patients. Without β-arrestin-2, insulin resistance develops, and reinstating its expression restores insulin sensitivity in mice. This suggests possible new therapeutic targets in insulin resistance and its related disorders. Beta-arrestin-2, an adaptor protein, is necessary for efficient insulin signalling by scaffolding downstream kinases, Akt and Src, to the insulin receptor. Without beta-arrestin-2 insulin resistance develops. Insulin resistance, a hallmark of type 2 diabetes, is a defect of insulin in stimulating insulin receptor signalling1,2, which has become one of the most serious public health threats. Upon stimulation by insulin, insulin receptor recruits and phosphorylates insulin receptor substrate proteins3, leading to activation of the phosphatidylinositol-3-OH kinase (PI(3)K)–Akt pathway. Activated Akt phosphorylates downstream kinases and transcription factors, thus mediating most of the metabolic actions of insulin4,5,6. β-arrestins mediate biological functions of G-protein-coupled receptors by linking activated receptors with distinct sets of accessory and effecter proteins, thereby determining the specificity, efficiency and capacity of signals7,8,9,10,11. Here we show that in diabetic mouse models, β-arrestin-2 is severely downregulated. Knockdown of β-arrestin-2 exacerbates insulin resistance, whereas administration of β-arrestin-2 restores insulin sensitivity in mice. Further investigation reveals that insulin stimulates the formation of a new β-arrestin-2 signal complex, in which β-arrestin-2 scaffolds Akt and Src to insulin receptor. Loss or dysfunction of β-arrestin-2 results in deficiency of this signal complex and disturbance of insulin signalling in vivo, thereby contributing to the development of insulin resistance and progression of type 2 diabetes. Our findings provide new insight into the molecular pathogenesis of insulin resistance, and implicate new preventive and therapeutic strategies against insulin resistance and type 2 diabetes.
204 citations
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TL;DR: It is demonstrated that cytotoxicity, permeability, and inflammation in vascular endothelial cells following exposure to metal oxide nanoparticles depended on particle composition, concentration, and exposure time.
Abstract: Wide applications and extreme potential of metal oxide nanoparticles (NPs) increase occupational and public exposure and may yield extraordinary hazards for human health. Exposure to NPs has a risk for dysfunction of the vascular endothelial cells. The objective of this study was to assess the cytotoxicity of six metal oxide NPs to human cardiac microvascular endothelial cells (HCMECs) in vitro. Metal oxide NPs used in this study included zinc oxide (ZnO), iron(III) oxide (Fe2O3), iron(II,III) oxide (Fe3O4), magnesium oxide (MgO), aluminum oxide (Al2O3), and copper(II) oxide (CuO). The cell viability, membrane leakage of lactate dehydrogenase, intracellular reactive oxygen species, permeability of plasma membrane, and expression of inflammatory markers vascular cell adhesion molecule-1, intercellular adhesion molecule-1, macrophage cationic peptide-1, and interleukin-8 in HCMECs were assessed under controlled and exposed conditions (12–24 h and 0.001–100 μg/ml of exposure). The results indicated that Fe2O3, Fe3O4, and Al2O3 NPs did not have significant effects on cytotoxicity, permeability, and inflammation response in HCMECs at any of the concentrations tested. ZnO, CuO, and MgO NPs produced the cytotoxicity at the concentration-dependent and time-dependent manner, and elicited the permeability and inflammation response in HCMECs. These results demonstrated that cytotoxicity, permeability, and inflammation in vascular endothelial cells following exposure to metal oxide nanoparticles depended on particle composition, concentration, and exposure time.
204 citations
Authors
Showing all 76610 results
Name | H-index | Papers | Citations |
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Gang Chen | 167 | 3372 | 149819 |
Yang Yang | 164 | 2704 | 144071 |
Georgios B. Giannakis | 137 | 1321 | 73517 |
Jian Li | 133 | 2863 | 87131 |
Jianlin Shi | 127 | 859 | 54862 |
Zhenyu Zhang | 118 | 1167 | 64887 |
Ju Li | 109 | 623 | 46004 |
Peng Wang | 108 | 1672 | 54529 |
Qian Wang | 108 | 2148 | 65557 |
Yan Zhang | 107 | 2410 | 57758 |
Richard B. Kaner | 106 | 557 | 66862 |
Han-Qing Yu | 105 | 718 | 39735 |
Wei Zhang | 104 | 2911 | 64923 |
Fabio Marchesoni | 104 | 607 | 74687 |
Feng Li | 104 | 995 | 60692 |