Recovery of ammonium-nitrogen from landfill leachate as a multi-nutrient fertilizer

Author name used in this publication: X. Z. Li2002-2003 > Academic research: refereed > Publication in refereed journalAccepted ManuscriptPublishe

Inhibition of microbial activity of activated sludge by ammonia in leachate

Author name used in this publication: X. L. LiAccepted ManuscriptPublishe

Map precipitation from landfill leachate and seawater bittern waste

Author name used in this publication: X. Z. Li2002-2003 > Academic research: refereed > Publication in refereed journalAccepted ManuscriptPublishe

On-site treatment of dyeing wastewater by a bio-photoreactor system

Author name used in this publication: X. Z. LiAccepted ManuscriptPublishe

Degradation of 2,4-dichlorophenol in aqueous solution by a hybrid oxidation process

Author name used in this publication: X. Z. LiAuthor name used in this publication: B. X. ZhaoAuthor name used in this publication: P. Wang2007-2008 > Academic research: refereed > Publication in refereed journalAccepted ManuscriptPublishe

Ammonium removal from landfill leachate by chemical precipitation

Accepted ManuscriptPublishe

Efficiency of biological treatment affected by high strength of ammonium-nitrogen in leachate and chemical precipitation of ammonium-nitrogen as pretreatment

Author name used in this publication: X. Z. Li2000-2001 > Academic research: refereed > Publication in refereed journalAccepted ManuscriptPublishe

CD36 Senses Dietary Lipids and Regulates Lipids Homeostasis in the Intestine

Dietary lipids absorbed in the intestine are closely related to the development of metabolic syndrome. CD36 is a multi-functional scavenger receptor with multiple ligands, which plays important roles in developing hyperlipidemia, insulin resistance, and metabolic syndrome. In the intestine, CD36 is abundant on the brush border membrane of the enterocytes mainly localized in proximal intestine. This review recapitulates the update and current advances on the importance of intestinal CD36 in sensing dietary lipids and regulating intestinal lipids uptake, synthesis and transport, and regulating intestinal hormones secretion. However, further studies are still needed to demonstrate the complex interactions between intestinal CD36 and dietary lipids, as well as its importance in diet associated metabolic syndrome

Paradoxical effect of rapamycin on inflammatory stress-induced insulin resistance in vitro and in vivo

Insulin resistance is closely related to inflammatory stress and the mammalian target of rapamycin/S6 kinase (mTOR/S6K) pathway. The present study investigated whether rapamycin, a specific inhibitor of mTOR, ameliorates inflammatory stress-induced insulin resistance in vitro and in vivo. We used tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) stimulation in HepG2 hepatocytes, C2C12 myoblasts and 3T3-L1 adipocytes and casein injection in C57BL/6J mice to induce inflammatory stress. Our results showed that inflammatory stress impairs insulin signaling by reducing the expression of total IRS-1, p-IRS-1 (tyr632), and p-AKT (ser473); it also activates the mTOR/S6K signaling pathway both in vitro and in vivo. In vitro, rapamycin treatment reversed inflammatory cytokine-stimulated IRS-1 serine phosphorylation, increased insulin signaling to AKT and enhanced glucose utilization. In vivo, rapamycin treatment also ameliorated the impaired insulin signaling induced by inflammatory stress, but it induced pancreatic β-cell apoptosis, reduced pancreatic β-cell function and enhanced hepatic gluconeogenesis, thereby resulting in hyperglycemia and glucose intolerance in casein-injected mice. Our results indicate a paradoxical effect of rapamycin on insulin resistance between the in vitro and in vivo environments under inflammatory stress and provide additional insight into the clinical application of rapamycin