| 11. |
- Tang, Jinfeng, 1984, et al.
(författare)
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Optimizing critical metals recovery and correlative decontamination from MSWI fly ash: Evaluation of an integrating two-step leaching hydrometallurgical process
- 2022
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Ingår i: Journal of Cleaner Production. - : Elsevier BV. - 0959-6526. ; 368
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Tidskriftsartikel (refereegranskat)abstract
- While municipal solid waste incineration (MSWI) fly ash is classified as hazardous waste, it can also serve as an urban mining source for numerous precious metals. Of particular interest are antimony (Sb) and zinc (Zn); the former of which is a strategic and critical metal that is being rapidly depleted, putting society at high risk for supply shortages. In this work, a two-step leaching method for recovering Sb and Zn from MSWI fly ash is proposed. Furthermore, the leaching behavior and adsorption mechanism of Sb in the MSWI fly ash waste stream were also investigated. Results from the first constant pH leaching tests (CPLT) showed that under diluted acidic condition, the maximum amount of Sb released from fly ash was ∼20%. In addition, at pH 4.0, 67% of the fly ash was dissolved, while 79.3% and 12.1% of the Zn and Sb, respectively, were recovered. After optimizing and executing a second Sb leaching procedure (6 M HCl solution at 60 °C), >80% of the Sb was recovered. Thus, the proposed two-step leaching process, consisting of extraction followed by decontamination using a magnetic HAP@CoFe2O4 adsorbent, can eliminate the Sb in fly ash effluent with a removal efficiency >95%. Moreover, this process produces less toxic products and lowers the effluent residue concentration. As such, the two-step process described herein is suggested for Sb and Zn recovery from fly ash; as it not only enables precious metal recovery, but also aids in treating secondary waste streams produced from urban mining.
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| 12. |
- Turpaev, Kyril, et al.
(författare)
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The protein synthesis inhibitor brusatol normalizes high-fat diet-induced glucose intolerance in male C57BL/6 mice : role of translation factor eIF5A hypusination
- 2019
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Ingår i: The FASEB Journal. - : FEDERATION AMER SOC EXP BIOL. - 0892-6638 .- 1530-6860. ; 33:3, s. 3510-3522
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Tidskriftsartikel (refereegranskat)abstract
- The naturally occurring quassinoid compound brusatol improves the survival of insulin-producing cells when exposed to the proinflammatory cytokines IL-1b and IFN-g in vitro. The aim of the present study was to investigatewhetherbrusatol also promotes beneficial effects inmice fed a high-fat diet (HFD), and if so, to study the mechanisms by which brusatol acts. In vivo, we observed that the impaired glucose tolerance of HFD-fed male C57BL/ 6micewas counteracted by a 2wk treatmentwith brusatol. Brusatol treatment improvedbothb-cell function and peripheral insulin sensitivity of HFD-fed mice. In vitro, brusatol inhibited b-cell total protein and proinsulin biosynthesis, withanED50 of 40nM. In linewith this, brusatol blocked cytokine-inducediNOSprotein expression via inhibition of iNOS mRNA translation. Brusatol may have affected protein synthesis, at least in part, via inhibition of eukaryotic initiation factor 5A (eIF5A) hypusination, as eIF5A spermidine association and hypusinationin RIN-5AHcellswas reducedinadose-andtime-dependentmanner. The eIF5AhypusinationinhibitorGC7 promoted a similar effect. Both brusatol and GC7 protected rat RIN-5AH cells against cytokine-induced cell death. Brusatol reduced eIF5A hypusination and cytokine-induced cell death in EndoC-bH1 cells as well. Finally, hypusinated eIF5A was reduced in vivo by brusatol in islet endocrine and endothelial islet cells of mice fed anHFD. The results of the present study suggest that brusatol improves glucose intolerance in mice fed an HFD, possibly by inhibiting protein biosynthesis and eIF5A hypusination.-Turpaev, K., Krizhanovskii, C., Wang, X., Sargsyan, E., Bergsten, P., Welsh, N. The protein synthesis inhibitor brusatol normalizes high-fat diet-induced glucose intolerance in male C57BL/ 6 mice: role of translation factor eIF5A hypusination. FASEB J. 33, 3510-3522 (2019). www.fasebj.org
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| 13. |
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| 14. |
- Wang, Xuan, 1984-, et al.
(författare)
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Knock-down of ZBED6 in insulin-producing cells promotes N-cadherin junctions between beta-cells and neural crest stem cells in vitro
- 2016
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Ingår i: Scientific Reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 6
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Tidskriftsartikel (refereegranskat)abstract
- The role of the novel transcription factor ZBED6 for the adhesion/clustering of insulin-producing mouse MIN6 and βTC6 cells was investigated. Zbed6-silencing in the insulin producing cells resulted in increased three-dimensional cell-cell clustering and decreased adhesion to mouse laminin and human laminin 511. This was paralleled by a weaker focal adhesion kinase phosphorylation at laminin binding sites. Zbed6-silenced cells expressed less E-cadherin and more N-cadherin at cell-to-cell junctions. A strong ZBED6-binding site close to the N-cadherin gene transcription start site was observed. Three-dimensional clustering in Zbed6-silenced cells was prevented by an N-cadherin neutralizing antibody and by N-cadherin knockdown. Co-culture of neural crest stem cells (NCSCs) with Zbed6-silenced cells, but not with control cells, stimulated the outgrowth of NCSC processes. The cell-to-cell junctions between NCSCs and βTC6 cells stained more intensely for N-cadherin when Zbed6-silenced cells were co-cultured with NCSCs. We conclude that ZBED6 decreases the ratio between N- and E-cadherin. A lower N- to E-cadherin ratio may hamper the formation of three-dimensional beta-cell clusters and cell-to-cell junctions with NCSC, and instead promote efficient attachment to a laminin support and monolayer growth. Thus, by controlling beta-cell adhesion and cell-to-cell junctions, ZBED6 might play an important role in beta-cell differentiation, proliferation and survival.
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| 15. |
- Wang, Xuan, 1984-
(författare)
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Study of the Proliferation, Function and Death of Insulin-Producing Beta-Cells in vitro: Role of the Transcription Factor ZBED6
- 2014
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- A thorough understanding of beta-cell proliferation, function, death and regeneration under normal condition as well as in the progression of diabetes is crucial to the conquest of this disease. The work presented in this thesis aimed to investigate the expression and role of a novel transcription factor, Zinc finger BED domain-containing protein 6 (ZBED6), in beta-cells.ZBED6 was present in mouse βTC-6 cells and human islets as a double nuclear band at 115/120 kDa and as a single cytoplasmic band at 95-100 kDa, which lacked N-terminal nuclear localization signals. Lentiviral shRNA-mediated stable silencing of ZBED6 in βTC-6 cells resulted in altered morphology, decreased proliferation, a partial S/G2 cell cycle arrest, increased expression of beta-cell specific genes, and higher rates of apoptosis. ChIP sequencing of human islets showed that ZBED6 binding was preferentially to genes that control transcription, macromolecule biosynthesis and apoptosis. We proposed that ZBED6 supported proliferation and survival of beta-cells, possibly at the expense of specialized beta-cell function, i.e. insulin production.To further investigate the role of ZBED6 in beta-cells, ChIP sequencing and whole transcriptome analysis were performed using MIN6 cells. More than 4000 putative target genes of ZBED6 were identified, including Pdx1, MafA and Nkx6.1. ZBED6-silencing resulted in differential expression of more than 700 genes, which was paralleled by an increase in the content and release of insulin in response to a high glucose concentration. Altered morphology/growth patterns as indicated by increased cell clustering were observed in ZBED6 silenced cells. We found also that ZBED6 decreased the ratio between N- and E-cadherin. A lower N- to E-cadherin ratio may hamper the formation of three-dimensional beta-cell clusters and cell-to-cell junctions with neural crest stem cells, and instead promote efficient attachment to a laminin support and monolayer growth. Thus, by controlling beta-cell adhesion and cell-to-cell junctions, ZBED6 might play an important role in beta-cell differentiation, proliferation and survival.
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| 16. |
- Wang, Xuan, 1984-, et al.
(författare)
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The novel NADPH oxidase 4 selective inhibitor GLX7013114 counteracts human islet cell death in vitro
- 2018
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Ingår i: PLOS ONE. - : PUBLIC LIBRARY SCIENCE. - 1932-6203. ; 13:9
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Tidskriftsartikel (refereegranskat)abstract
- It has been proposed that pancreatic beta-cell dysfunction in type 2 diabetes is promoted by oxidative stress caused by NADPH oxidase (Nox) over-activity. The aim of the present study was to evaluate the efficacy of novel Nox inhibitors as protective agents against cytokine- or high glucose + palmitate-induced human beta-cell death. The Nox2 protein was present mainly in the cytoplasm and was induced by cytokines. Nox4 protein immunoreactivity, with some nuclear accumulation, was observed in human islet cells, and was not affected by islet culture in the presence of cytokines or high glucose + palmitate. Nox inhibitors with partial or no isoform selectivity (DPI, dapsone, GLX351322, and GLX481372) all reduced ROS production of human islet cells exposed to high glucose + palmitate. This was paralleled by improved viability and reduced caspase 3 activation. The Nox1 selective inhibitor ML171 failed to reduce human islet cell death in response to both cytokines and high glucose + palmitate. The selective Nox2 inhibitor Phox-12 also failed to protect against cytokines, but protected partially against high glucose + palmitate-induced cellular death. The highly selective Nox4 inhibitor GLX7013114 protected islet cells against both cytokines and high glucose + palmitate. However, as no osmotic control for high glucose was used, we cannot exclude the possibility that the high glucose effect was due to osmosis. It is concluded that Nox4 may participate in stress-induced islet cell death in human islets in vitro. We propose that Nox4 mediates pro-apoptotic effects in intact islets under stressful conditions and that selective Nox4-inhibition may be a therapeutic strategy in type 2 diabetes.
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| 17. |
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| 18. |
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| 19. |
- Wang, Xuan, 1984-, et al.
(författare)
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ZBED6 negatively regulates insulin production, neuronal differentiation, and cell aggregation in MIN6 cells
- 2019
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Ingår i: The FASEB Journal. - : FEDERATION AMER SOC EXP BIOL. - 0892-6638 .- 1530-6860. ; 33:1, s. 88-100
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Tidskriftsartikel (refereegranskat)abstract
- Zinc finger BED domain containing protein 6 (Zbed6) has evolved from a domesticated DNA transposon and encodes a transcription factor unique to placental mammals. The aim of the present study was to investigate further the role of ZBED6 in insulin-producing cells, using mouse MIN6 cells, and to evaluate the effects of Zbed6 knockdown on basal -cell functions, such as morphology, transcriptional regulation, insulin content, and release. Zbed6-silenced cells and controls were characterized with a range of methods, including RNA sequencing, chromatin immunoprecipitation sequencing, insulin content and release, subplasma membrane Ca2+ measurements, cAMP determination, and morphologic studies. More than 700 genes showed differential expression in response to Zbed6 knockdown, which was paralleled by increased capacity to generate cAMP, as well as by augmented subplasmalemmal calcium concentration and insulin secretion in response to glucose stimulation. We identified >4000 putative ZBED6-binding sites in the MIN6 genome, with an enrichment of ZBED6 sites at upregulated genes, such as the -cell transcription factors v-maf musculoaponeurotic fibrosarcoma oncogene homolog A and Nk6 homeobox 1. We also observed altered morphology/growth patterns, as indicated by increased cell clustering, and in the appearance of axon-like Neurofilament, medium polypeptide and tubulin 3, class III-positive protrusions. We conclude that ZBED6 acts as a transcriptional regulator in MIN6 cells and that its activity suppresses insulin production, cell aggregation, and neuronal-like differentiation.Wang, X., Jiang, L., Wallerman, O., Younis, S., Yu, Q., Klaesson, A., Tengholm, A., Welsh, N., Andersson, L. ZBED6 negatively regulates insulin production, neuronal differentiation, and cell aggregation in MIN6 cells.
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| 20. |
- Wu, Yuan, et al.
(författare)
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A Comparison of Functional Features in Chinese and US Mobile Apps for Diabetes Self-Management : A Systematic Search in App Stores and Content Analysis
- 2019
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Ingår i: JMIR mhealth and uhealth. - : JMIR PUBLICATIONS, INC. - 2291-5222. ; 7:8
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Tidskriftsartikel (refereegranskat)abstract
- Background: Mobile health interventions are widely used for self-management of diabetes, which is one of the most burdensome noncommunicable chronic diseases worldwide. However, little is known about the distribution of characteristics and functions of in-store mobile apps for diabetes. Objective: This study aimed to investigate the distribution of characteristics and functions of the in-store mobile apps for self-management of diabetes in the United States and China using a predefined functional taxonomy, which was developed and published in our previous study. Methods: We identified apps by searching diabetes in English or Chinese in the Apple iTunes Store and Android Markets (both in the United States and China) and included apps for diabetes self-management. We examined the validity and reliability of the predefined functional taxonomy with 3 dimensions: clinical module, functional module, and potential risk. We then classified all functions in the included apps according to the predefined taxonomy and compared the differences in the features of these apps between the United States and China. Results: We included 171 mobile diabetes apps, with 133 from the United States and 38 from China. Apps from both countries faced the challenges of evidence-based information, proper risk assessment, and declaration, especially Chinese apps. More Chinese apps provide app-based communication functions (general communication: Chinese vs US apps, 39%, 15/38 vs 18.0%, 24/133; P=.006 and patient-clinician communication: Chinese vs US apps, 68%, 26/38 vs 6.0%, 8/133; P<.001), whereas more US apps provide the decision-making module (Chinese vs US apps, 0%, 0/38 vs 23.3%, 31/133; P=.001), which is a high-risk module. Both complication prevention (Chinese vs US apps, 8%, 3/38 vs 3.8%, 5/133; P=.50) and psychological care (Chinese vs US apps, 0%, 0/38 vs 0.8%, 1/133; P>.99) are neglected by the 2 countries. Conclusions: The distribution of characteristics and functions of in-store mobile apps for diabetes self-management in the United States was different from China. The design of in-store diabetes apps needs to be monitored closely.
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