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Soleyman Sahebi - One of the best experts on this subject based on the ideXlab platform.
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enhanced dynamic cu ii ion removal using hot pressed chitosan poly vinyl alcohol electrospun nanofibrous affinity membrane ENAM
Process Safety and Environmental Protection, 2020Co-Authors: Mostafa Managheb, Soheil Zarghami, Toraj Mohammadi, Amir Atabak Asadi, Soleyman SahebiAbstract:Abstract Different Multilayer electrospun nanofibrous membranes were synthesized to study the effects of potentially important steps and parameters including hot-pressing and chitosan / poly (vinyl alcohol) (CTS/PVA) solutions on the membranes performance in Cu(II) ions removal. Due to the importance of continuous adsorption process, in this research, dynamic removal from synthetic wastewater of Cu(II) ions was discussed. Five ENAMs were prepared using different chitosan / poly (vinyl alcohol) (CTS/PVA) solutions. A bead free, smooth ENAM with uniform interconnected porous structure was obtained using 3 % wt./vol CTS solution with CTS/PVA weight ratio of 50/50. The average fiber diameter, porosity and average pore diameter of the as synthesized ENAM were 99.1 nm, 50.6 %, and 0.189 µm, respectively. Multilayer ENAMs were prepared with steady state pure water fluxes of 237 to 706 LMH/bar as well as time dependent rejections up to 98.6 %. Considering the slight (3%) reduction of multilayer ENAMs rejection, as well as their high (80%) flux recovery ratio (FRR) after two regeneration cycles, it can be concluded that the membranes are definitely reusable.
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Enhanced dynamic Cu(II) ion removal using hot-pressed chitosan / poly (vinyl alcohol) electrospun nanofibrous affinity membrane (ENAM)
Process Safety and Environmental Protection, 1Co-Authors: Mostafa Managheb, Soheil Zarghami, Toraj Mohammadi, Amir Atabak Asadi, Soleyman SahebiAbstract:Abstract Different Multilayer electrospun nanofibrous membranes were synthesized to study the effects of potentially important steps and parameters including hot-pressing and chitosan / poly (vinyl alcohol) (CTS/PVA) solutions on the membranes performance in Cu(II) ions removal. Due to the importance of continuous adsorption process, in this research, dynamic removal from synthetic wastewater of Cu(II) ions was discussed. Five ENAMs were prepared using different chitosan / poly (vinyl alcohol) (CTS/PVA) solutions. A bead free, smooth ENAM with uniform interconnected porous structure was obtained using 3 % wt./vol CTS solution with CTS/PVA weight ratio of 50/50. The average fiber diameter, porosity and average pore diameter of the as synthesized ENAM were 99.1 nm, 50.6 %, and 0.189 µm, respectively. Multilayer ENAMs were prepared with steady state pure water fluxes of 237 to 706 LMH/bar as well as time dependent rejections up to 98.6 %. Considering the slight (3%) reduction of multilayer ENAMs rejection, as well as their high (80%) flux recovery ratio (FRR) after two regeneration cycles, it can be concluded that the membranes are definitely reusable.
James P. Simmer - One of the best experts on this subject based on the ideXlab platform.
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human and mouse ENAMel phenotypes resulting from mutation or altered expression of amel ENAM mmp20 and klk4
Cells Tissues Organs, 2009Co-Authors: Timothy J Wright, Darrin Simmons, Cynthia Suggs, Bill Daley, J C C Hu, Suzanne P Hart, John D. Bartlett, Thomas C. Hart, James P. Simmer, Yong LiAbstract:Amelogenesis imperfecta (AI) is caused by AMEL, ENAM, MMP20 and KLK4 gene mutations. Mice lacking expression of the AmelX, ENAM and Mmp20 genes have been generated. These mouse models provide tools for understanding ENAMel formation and AI pathogenesis. This study describes the AI phenotypes and relates them to their mouse model counterparts. Human AI phenotypes were determined in a clinical population of AI families and published cases. Human and murine teeth were evaluated using light and electron microscopy. A total of 463 individuals from 54 families were evaluated and mutations in the AMEL, ENAM and KLK4 genes were identified. The majority of human mutations for genes coding ENAMel nonproteinase proteins (AMEL and ENAM) resulted in variable hypoplasia ranging from local pitting to a marked, generalized ENAMel thinning. Specific AMEL mutations were associated with abnormal mineralization and maturation defects. Amel and ENAM null murine models displayed marked ENAMel hypoplasia and a complete loss of prism structure. Human mutations in genes coding for the ENAMel proteinases (MMP20 and KLK4) cause variable degrees of hypomineralization. The murine Mmp20 null mouse exhibits both hypoplastic and hypomineralized defects. The currently available Amel and ENAM mouse models for AI exhibit ENAMel phenotypes (hypoplastic) that are generally similar to those seen in humans. Mmp20 null mice have a greater degree of hypoplasia than humans with MMP20 mutations. Mice lacking expression of the currently known genes associated with the human AI conditions provide useful models for understanding the pathogenesis of these conditions.
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Identifying Promoter Elements Necessary for ENAMelin Tissue-Specific Expression
Cells Tissues Organs, 2008Co-Authors: Petros Papagerakis, Jerry Q. Feng, James P. SimmerAbstract:ENAMel development requires the strictly regulated spatiotemporal expression of genes encoding ENAMel matrix proteins. The mechanisms orchestrating the initiation and termination of gene transcription at each specific stage of amelogenesis are unknown. In this study, we identify cis- regulatory regions necessary for normal ENAMelin (ENAM) expression. Sequence analysis of the ENAM promoter 5′-noncoding region identified potentially important cis-regulatory elements located within 5.2 kb upstream of the ENAM translation initiation site. DNA constructs containing 5.2 or 3.9 kb upstream of the ENAM translation initiation site were linked to an LacZ reporter gene and used to generate transgenic mice. The 3.9-kb ENAM-LacZ transgenic lines showed no expression in ameloblasts, but ectopic LacZ staining was detected in osteoblasts. In contrast, the 5.2-kb ENAM-LacZ construct was sufficient to mimic the endogenous ENAM ameloblast-specific expression pattern. Our study provides new insights into the molecular control of ENAM cell- and stage-specific expression.
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ENAMel defects and ameloblast specific expression in ENAM knock out lacz knock in mice
Journal of Biological Chemistry, 2008Co-Authors: Charles E. Smith, Timothy J Wright, Petros Papagerakis, Jerry Q. Feng, Marc D. Mckee, Yasuo Yamakoshi, Graeme K. Hunter, Fumiko Yamakoshi, James P. SimmerAbstract:Next Section Abstract ENAMelin is critical for proper dental ENAMel formation, and defects in the human ENAMelin gene cause autosomal dominant amelogenesis imperfecta. We used gene targeting to generate a knock-in mouse carrying a null allele of ENAMelin (ENAM) that has a lacZ reporter gene replacing the ENAM translation initiation site and gene sequences through exon 7. Correct targeting of the transgene was confirmed by Southern blotting and PCR analyses. No ENAMelin protein could be detected by Western blotting in the ENAM-null mice. Histochemical 5-bromo-4-chloro-3-indolyl-β-d-galactopyranoside (X-gal) staining demonstrated ameloblast-specific expression of ENAMelin. The ENAMel of the ENAM+/- mice was nearly normal in the maxillary incisors, but the mandibular incisors were discolored and tended to wear rapidly where they contacted the maxillary incisors. The ENAM-/- mice showed no true ENAMel. Radiography, microcomputed tomography, and light and scanning electron microscopy were used to document changes in the ENAMel of ENAM-/- mice but did not discern any perturbations of bone, dentin, or any other tissue besides the ENAMel layer. Although a thick layer of ENAMel proteins covered normal-appearing dentin of unerupted teeth, von Kossa staining revealed almost a complete absence of mineral formation in this protein layer. However, a thin, highly irregular, mineralized crust covered the dentin on erupted teeth, apparently arising from the formation and fusion of small mineralization foci (calcospherites) in the deeper part of the accumulated ENAMel protein layer. These results demonstrate ameloblast-specific expression of ENAMelin and reveal that ENAMelin is essential for proper ENAMel matrix organization and mineralization.
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Distal cis-regulatory elements are required for tissue-specific expression of ENAMelin (ENAM).
European Journal of Oral Sciences, 2008Co-Authors: Petros Papagerakis, Jerry Q. Feng, James P. SimmerAbstract:ENAMel formation is orchestrated by the sequential expression of genes encoding ENAMel matrix proteins; however, the mechanisms sustaining the spatio-temporal order of gene transcription during amelogenesis are poorly understood. The aim of this study was to characterize the cis-regulatory sequences necessary for normal expression of ENAMelin (ENAM). Several ENAMelin transcription regulatory regions, showing high sequence homology among species, were identified. DNA constructs containing 5.2 or 3.9 kb regions upstream of the ENAMelin translation initiation site were linked to a LacZ reporter and used to generate transgenic mice. Only the 5.2-ENAM-LacZ construct was sufficient to recapitulate the endogenous pattern of ENAMelin tooth-specific expression. The 3.9-ENAM-LacZ transgenic lines showed no expression in dental cells, but ectopic beta-galactosidase activity was detected in osteoblasts. Potential transcription factor-binding sites were identified that may be important in controlling ENAMelin basal promoter activity and in conferring ENAMelin tissue-specific expression. Our study provides new insights into regulatory mechanisms governing ENAMelin expression.
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a nonsense mutation in the ENAMelin gene causes local hypoplastic autosomal dominant amelogenesis imperfecta aih2
Human Molecular Genetics, 2002Co-Authors: Carina Karrman Mardh, Birgitta Backman, Gosta Holmgren, Jan C C Hu, James P. Simmer, Kristina ForsmansembAbstract:: Amelogenesis imperfecta (AI) is an inherited tooth disorder affecting tooth ENAMel formation only. A gene for autosomal dominant AI, the local hypoplastic form, has been localized to a 4 Mb region on chromosome 4q (AIH2). The ENAMelin gene (ENAM ), has been mapped to chromosome 4q21, to the same region as AIH2, and was recently shown to be mutated in patients with smooth and thin hypoplastic autosomal dominant AI (ADAI). In this study, we describe an ENAM mutation causing the local hypoplastic form of ADAI, a phenotype that accounts for 27% of the autosomally inherited cases in Northern Sweden. This nonsense mutation in the ENAMelin gene results in a truncated peptide of 52 amino acids as compared with 1142 amino acids of the normal protein. Our results show that while a splice site mutation is associated with smooth and thin hypoplastic AI, a base substitution resulting in a shorter peptide causes local hypoplasia of the ENAMel, a milder form of AI. These findings support ENAM as a disease gene, and shed new light on the molecular mechanism of the disease and to the function of the ENAMelin protein in ENAMel formation.
Amir Atabak Asadi - One of the best experts on this subject based on the ideXlab platform.
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enhanced dynamic cu ii ion removal using hot pressed chitosan poly vinyl alcohol electrospun nanofibrous affinity membrane ENAM
Process Safety and Environmental Protection, 2020Co-Authors: Mostafa Managheb, Soheil Zarghami, Toraj Mohammadi, Amir Atabak Asadi, Soleyman SahebiAbstract:Abstract Different Multilayer electrospun nanofibrous membranes were synthesized to study the effects of potentially important steps and parameters including hot-pressing and chitosan / poly (vinyl alcohol) (CTS/PVA) solutions on the membranes performance in Cu(II) ions removal. Due to the importance of continuous adsorption process, in this research, dynamic removal from synthetic wastewater of Cu(II) ions was discussed. Five ENAMs were prepared using different chitosan / poly (vinyl alcohol) (CTS/PVA) solutions. A bead free, smooth ENAM with uniform interconnected porous structure was obtained using 3 % wt./vol CTS solution with CTS/PVA weight ratio of 50/50. The average fiber diameter, porosity and average pore diameter of the as synthesized ENAM were 99.1 nm, 50.6 %, and 0.189 µm, respectively. Multilayer ENAMs were prepared with steady state pure water fluxes of 237 to 706 LMH/bar as well as time dependent rejections up to 98.6 %. Considering the slight (3%) reduction of multilayer ENAMs rejection, as well as their high (80%) flux recovery ratio (FRR) after two regeneration cycles, it can be concluded that the membranes are definitely reusable.
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Enhanced dynamic Cu(II) ion removal using hot-pressed chitosan / poly (vinyl alcohol) electrospun nanofibrous affinity membrane (ENAM)
Process Safety and Environmental Protection, 1Co-Authors: Mostafa Managheb, Soheil Zarghami, Toraj Mohammadi, Amir Atabak Asadi, Soleyman SahebiAbstract:Abstract Different Multilayer electrospun nanofibrous membranes were synthesized to study the effects of potentially important steps and parameters including hot-pressing and chitosan / poly (vinyl alcohol) (CTS/PVA) solutions on the membranes performance in Cu(II) ions removal. Due to the importance of continuous adsorption process, in this research, dynamic removal from synthetic wastewater of Cu(II) ions was discussed. Five ENAMs were prepared using different chitosan / poly (vinyl alcohol) (CTS/PVA) solutions. A bead free, smooth ENAM with uniform interconnected porous structure was obtained using 3 % wt./vol CTS solution with CTS/PVA weight ratio of 50/50. The average fiber diameter, porosity and average pore diameter of the as synthesized ENAM were 99.1 nm, 50.6 %, and 0.189 µm, respectively. Multilayer ENAMs were prepared with steady state pure water fluxes of 237 to 706 LMH/bar as well as time dependent rejections up to 98.6 %. Considering the slight (3%) reduction of multilayer ENAMs rejection, as well as their high (80%) flux recovery ratio (FRR) after two regeneration cycles, it can be concluded that the membranes are definitely reusable.
Peter M Snyder - One of the best experts on this subject based on the ideXlab platform.
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acetylation stimulates the epithelial sodium channel by reducing its ubiquitination and degradation
Journal of Biological Chemistry, 2015Co-Authors: Phillip L Butler, Alexander Staruschenko, Peter M SnyderAbstract:Abstract The epithelial Na+ channel (ENaC) functions as a pathway for Na+ absorption in the kidney and lung, where it is crucial for Na+ homeostasis and blood pressure regulation. ENaC is regulated in part through signaling pathways that control the ubiquitination state of ENaC lysines. A defect in ubiquitination causes Liddle syndrome, an inherited form of hypertension. Here we determined that α-, β-, and γENaC are also substrates for lysine acetylation. Trichostatin A (TSA), a histone deacetylase inhibitor, enhanced ENaC acetylation and increased ENaC abundance in the total cell lysate and at the cell surface. Moreover, TSA increased ENaC current in Fischer rat thyroid and kidney collecting duct epithelia. We found that HDAC7 is expressed in the kidney collecting duct, supporting a potential role for this histone deacetylase in ENaC regulation. HDAC7 overexpression reduced ENaC abundance and ENaC current, whereas ENaC abundance and current were increased by silencing of HDAC7. ENaC and HDAC7 form a complex, as detected by coimmunoprecipitation. We observed a reciprocal relationship between acetylation and ubiquitination; TSA reduced ENaC ubiquitination, whereas HDAC7 increased ubiquitination. By reducing ENaC ubiquitination, TSA decreased the rate of ENaC degradation. Thus, acetylation increases epithelial Na+ absorption by antagonizing ENaC ubiquitination. This stabilizes ENaC, and hence, increases its abundance at the cell surface.
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ubiquitin specific peptidase 8 usp8 regulates endosomal trafficking of the epithelial na channel
Journal of Biological Chemistry, 2013Co-Authors: Ruifeng Zhou, Phillip L Butler, Vivian R. Tomkovicz, Luis A. Ochoa, Zerubbabel J. Peterson, Peter M SnyderAbstract:Ubiquitination plays a key role in trafficking of the epithelial Na+ channel (ENaC). Previous work indicated that ubiquitination enhances ENaC endocytosis and sorting to lysosomes for degradation. Moreover, a defect in ubiquitination causes Liddle syndrome, an inherited form of hypertension. In this work, we identified a role for USP8 in the control of ENaC ubiquitination and trafficking. USP8 increased ENaC current in Xenopus oocytes and collecting duct epithelia and enhanced ENaC abundance at the cell surface in HEK 293 cells. This resulted from altered endocytic sorting; USP8 abolished ENaC degradation in the endocytic pathway, but it had no effect on ENaC endocytosis. USP8 interacted with ENaC, as detected by co-immunoprecipitation, and it deubiquitinated ENaC. Consistent with a functional role for deubiquitination, mutation of the cytoplasmic lysines of ENaC reduced the effect of USP8 on ENaC cell surface abundance. In contrast to USP8, USP2-45 increased ENaC surface abundance by reducing endocytosis but not degradation. Thus, USP8 and USP2-45 selectively modulate ENaC trafficking at different steps in the endocytic pathway. Together with previous work, the data indicate that the ubiquitination state of ENaC is critical for the regulation of epithelial Na+ absorption.
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Ubiquitin Specific Peptidase 8 (USP8) Regulates Endosomal Trafficking of the Epithelial Na+ Channel
Journal of Biological Chemistry, 2013Co-Authors: Ruifeng Zhou, Phillip L Butler, Vivian R. Tomkovicz, Luis A. Ochoa, Zerubbabel J. Peterson, Peter M SnyderAbstract:Ubiquitination plays a key role in trafficking of the epithelial Na+ channel (ENaC). Previous work indicated that ubiquitination enhances ENaC endocytosis and sorting to lysosomes for degradation. Moreover, a defect in ubiquitination causes Liddle syndrome, an inherited form of hypertension. In this work, we identified a role for USP8 in the control of ENaC ubiquitination and trafficking. USP8 increased ENaC current in Xenopus oocytes and collecting duct epithelia and enhanced ENaC abundance at the cell surface in HEK 293 cells. This resulted from altered endocytic sorting; USP8 abolished ENaC degradation in the endocytic pathway, but it had no effect on ENaC endocytosis. USP8 interacted with ENaC, as detected by co-immunoprecipitation, and it deubiquitinated ENaC. Consistent with a functional role for deubiquitination, mutation of the cytoplasmic lysines of ENaC reduced the effect of USP8 on ENaC cell surface abundance. In contrast to USP8, USP2-45 increased ENaC surface abundance by reducing endocytosis but not degradation. Thus, USP8 and USP2-45 selectively modulate ENaC trafficking at different steps in the endocytic pathway. Together with previous work, the data indicate that the ubiquitination state of ENaC is critical for the regulation of epithelial Na+ absorption.
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extracellular chloride regulates the epithelial sodium channel
Journal of Biological Chemistry, 2009Co-Authors: Daniel M Collier, Peter M SnyderAbstract:Abstract The extracellular domain of the epithelial sodium channel ENaC is exposed to a wide range of Cl− concentrations in the kidney and in other epithelia. We tested whether Cl− alters ENaC activity. In Xenopus oocytes expressing human ENaC, replacement of Cl− with SO42−, H2PO4−, or SCN− produced a large increase in ENaC current, indicating that extracellular Cl− inhibits ENaC. Extracellular Cl− also inhibited ENaC in Na+-transporting epithelia. The anion selectivity sequence was SCN− < SO42− < H2PO4− < F− < I− < Cl− < Br−. Crystallization of ASIC1a revealed a Cl− binding site in the extracellular domain. We found that mutation of corresponding residues in ENaC (αH418A and βR388A) disrupted the response to Cl−, suggesting that Cl− might regulate ENaC through an analogous binding site. Maneuvers that lock ENaC in an open state (a DEG mutation and trypsin) abolished ENaC regulation by Cl−. The response to Cl− was also modulated by changes in extracellular pH; acidic pH increased and alkaline pH reduced ENaC inhibition by Cl−. Cl− regulated ENaC activity in part through enhanced Na+ self-inhibition, a process by which extracellular Na+ inhibits ENaC. Together, the data indicate that extracellular Cl− regulates ENaC activity, providing a potential mechanism by which changes in extracellular Cl− might modulate epithelial Na+ absorption.
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liddle s syndrome mutations increase na transport through dual effects on epithelial na channel surface expression and proteolytic cleavage
Proceedings of the National Academy of Sciences of the United States of America, 2006Co-Authors: Kristin K. Knight, Ruifeng Zhou, Diane R. Olson, Peter M SnyderAbstract:Liddle’s syndrome, an inherited form of hypertension, is caused by mutations that delete or disrupt a C-terminal PY motif in the epithelial Na+ channel (ENaC). Previous work indicates that these mutations increase expression of ENaC at the cell surface by disrupting its binding to Nedd4-2, an E3 ubiquitin–protein ligase that targets ENaC for degradation. However, it remains uncertain whether this mechanism alone is responsible; increased activity of ENaC channels could also contribute to excessive Na+ transport in Liddle’s syndrome. ENaC activity is controlled in part by its cleavage state; proteolytic cleavage produces channels with a high open-state probability, whereas uncleaved channels are inactive. Here, we found that Liddle’s syndrome mutations have two distinct effects of ENaC surface expression, both of which contribute to increased Na+ transport. First, these mutations increased ENaC expression at the cell surface; second, they increased the fraction of ENaC at the cell surface that was cleaved (active). This disproportionate increase in cleavage was reproduced by expression of a dominant-negative Nedd4-2 or mutation of ENaC ubiquitination sites, interventions that disrupt ENaC endocytosis and lysosomal degradation. Conversely, overexpression of Nedd4-2 had the opposite effect, decreasing the fraction of cleaved ENaC at the cell surface. Thus, the data not only suggest that Nedd4-2 regulates epithelial Na+ transport in part by controlling the relative expression of cleaved and uncleaved ENaC at the cell surface but also provide a mechanism by which Liddle’s syndrome mutations alter ENaC activity.
Mostafa Managheb - One of the best experts on this subject based on the ideXlab platform.
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enhanced dynamic cu ii ion removal using hot pressed chitosan poly vinyl alcohol electrospun nanofibrous affinity membrane ENAM
Process Safety and Environmental Protection, 2020Co-Authors: Mostafa Managheb, Soheil Zarghami, Toraj Mohammadi, Amir Atabak Asadi, Soleyman SahebiAbstract:Abstract Different Multilayer electrospun nanofibrous membranes were synthesized to study the effects of potentially important steps and parameters including hot-pressing and chitosan / poly (vinyl alcohol) (CTS/PVA) solutions on the membranes performance in Cu(II) ions removal. Due to the importance of continuous adsorption process, in this research, dynamic removal from synthetic wastewater of Cu(II) ions was discussed. Five ENAMs were prepared using different chitosan / poly (vinyl alcohol) (CTS/PVA) solutions. A bead free, smooth ENAM with uniform interconnected porous structure was obtained using 3 % wt./vol CTS solution with CTS/PVA weight ratio of 50/50. The average fiber diameter, porosity and average pore diameter of the as synthesized ENAM were 99.1 nm, 50.6 %, and 0.189 µm, respectively. Multilayer ENAMs were prepared with steady state pure water fluxes of 237 to 706 LMH/bar as well as time dependent rejections up to 98.6 %. Considering the slight (3%) reduction of multilayer ENAMs rejection, as well as their high (80%) flux recovery ratio (FRR) after two regeneration cycles, it can be concluded that the membranes are definitely reusable.
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Enhanced dynamic Cu(II) ion removal using hot-pressed chitosan / poly (vinyl alcohol) electrospun nanofibrous affinity membrane (ENAM)
Process Safety and Environmental Protection, 1Co-Authors: Mostafa Managheb, Soheil Zarghami, Toraj Mohammadi, Amir Atabak Asadi, Soleyman SahebiAbstract:Abstract Different Multilayer electrospun nanofibrous membranes were synthesized to study the effects of potentially important steps and parameters including hot-pressing and chitosan / poly (vinyl alcohol) (CTS/PVA) solutions on the membranes performance in Cu(II) ions removal. Due to the importance of continuous adsorption process, in this research, dynamic removal from synthetic wastewater of Cu(II) ions was discussed. Five ENAMs were prepared using different chitosan / poly (vinyl alcohol) (CTS/PVA) solutions. A bead free, smooth ENAM with uniform interconnected porous structure was obtained using 3 % wt./vol CTS solution with CTS/PVA weight ratio of 50/50. The average fiber diameter, porosity and average pore diameter of the as synthesized ENAM were 99.1 nm, 50.6 %, and 0.189 µm, respectively. Multilayer ENAMs were prepared with steady state pure water fluxes of 237 to 706 LMH/bar as well as time dependent rejections up to 98.6 %. Considering the slight (3%) reduction of multilayer ENAMs rejection, as well as their high (80%) flux recovery ratio (FRR) after two regeneration cycles, it can be concluded that the membranes are definitely reusable.
