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1.
J Environ Manage ; 129: 586-92, 2013 Nov 15.
Artigo em Inglês | MEDLINE | ID: mdl-24036091

RESUMO

In this study, vitrification was applied to treat Ni-Cu electroplating sludge. The sludge was mixed with additives (limestone:cullet = 4:6) and then heated to 1450 °C. The cooled product could be separated into slag and ingot. An atomic absorption spectrometer was used to determine the metal levels of specimens and toxicity characteristic leaching procedure (TCLP) tests, whereas the crystalline and surface characteristics were examined using quantitative X-ray diffraction (XRD) analysis and scanning electron microscopy, respectively. With a glassy structure, the slag was mainly composed of Ca, Si, and Mg. The TCLP results of slags met the Taiwan regulated standards, suggesting that slag can be used for recycling purposes. With the aid of additives, the crystalline phase of slag was transformed form CaMgSiO4 into CsSiO3. The ingots were mainly composed of Ni (563,000-693,800 mg/kg), Cu (79,900-87,400 mg/kg), and Fe (35,000-43,600 mg/kg) (target metals) due the gravity separation during vitrification. At appropriate additives/sludge ratios (>0.2), >95% of target metals gathered in the ingot as a recoverable form (Ni-Fe alloy). The high Ni level of slag suggests that the ingot can be used as the raw materials for smelters or the additives for steel making. Therefore, the vitrification approach of this study is a promising technology to recover valuable metals from Ni-Cu electroplating sludge.


Assuntos
Galvanoplastia , Resíduos Industriais/análise , Metais Pesados/química , Reciclagem/métodos , Esgotos/química , Vitrificação , Gerenciamento de Resíduos/métodos , Microscopia Eletrônica de Varredura , Oxirredução , Relação Estrutura-Atividade , Taiwan , Difração de Raios X
2.
Mol Pharmacol ; 62(2): 297-303, 2002 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-12130681

RESUMO

Glucocorticoids are potent anti-inflammatory and immunosuppressant agents. However, they also produce serious side effects that limit their usage. It has been proposed that anti-inflammatory properties of glucocorticoids are caused mostly by repression of activator protein 1- and nuclear factor kappabeta-stimulated synthesis of inflammatory mediators, whereas most of their adverse effects are associated with trans-activation of genes involved with metabolic processes. Our laboratories have sought to discover novel glucocorticoid receptor (GR) ligands that have high repression but low trans-activation activities. We describe here cellular properties of 2,5-dihydro-9-hydroxy-10-methoxy-2,2,4-trimethyl-5-(1-methylcyclohexen-3-y1)-1H-[1]benzopyrano[3,4-f]quinoline (A276575) and its four enantiomers. Similar to dexamethasone, A276575 exhibited high affinity for GR and potently repressed interleukin (IL) 1beta-stimulated IL-6 production in human skin fibroblasts, prostaglandin (PG) E(2) production in A549 human lung epithelial cells, and concanavalin A-induced monocyte proliferation. In contrast to dexamethasone, A276575 caused smaller induction of aromatase activity in human skin fibroblasts and antagonized dexamethasone-induced activation of an mouse mammary tumor virus-glucocorticoid-response element (GRE) reporter gene construct. Among the four enantiomers of A276575, the two (-)-enantiomers showed 10- to 30-fold higher affinities for GR than their respective (+)-enantiomers. Both (-)-Syn and (-)-Anti enantiomers of A276575 were potent inhibitors of IL-1beta-stimulated PGE2 production in A549 lung epithelial cells; unexpectedly, however, only the (-)-Anti enantiomer inhibited regulated on T-cell activation, normal T-cell expressed and secreted (RANTES) production in A549 cells. In summary, A276575 is a novel, nonsteroidal GR ligand that possesses high repression activities against inflammatory mediator production but has lower GRE trans-activation activities than traditional steroids. Differential repression of RANTES and PGE2 production in a cell by the two (-)-enantiomers of A276575 illustrates the complexity of repression by GR.


Assuntos
Benzopiranos/farmacologia , Inativação Gênica/efeitos dos fármacos , Quinolinas/farmacologia , Receptores de Glucocorticoides/antagonistas & inibidores , Ativação Transcricional/efeitos dos fármacos , Aromatase/metabolismo , Benzopiranos/química , Divisão Celular/efeitos dos fármacos , Quimiocina CCL5/metabolismo , Concanavalina A/farmacologia , Dinoprostona/metabolismo , Interações Medicamentosas , Fibroblastos/efeitos dos fármacos , Fibroblastos/enzimologia , Humanos , Interleucina-1/farmacologia , Interleucina-6/metabolismo , Leucócitos Mononucleares/citologia , Vírus do Tumor Mamário do Camundongo/genética , Quinolinas/química , Receptores de Glucocorticoides/agonistas , Receptores de Glucocorticoides/química , Receptores de Glucocorticoides/genética , Receptores de Progesterona/agonistas , Receptores de Progesterona/antagonistas & inibidores , Pele/efeitos dos fármacos , Pele/enzimologia , Estereoisomerismo , Transfecção
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