11 research outputs found

    Recent Advancements in Chitosan-based Adsorbents for Hexavalent Chromium Removal from Aqueous Media

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    Contamination of aqueous environments by Cr(VI) has become a matter of concern owing to its detrimental impacts on human health with its long-term exposure. Thus, effective treatment of adulterated aqueous media is critical in terms of the health and safety of humans together with flora and fauna. Currently, chitosan is considered an excellent adsorptive material for theremediation of Cr(VI) contamination owing primarily to its biodegradability, non-toxicity, abundance, and ability to modify its microstructure. The present review focuses on the up-to-date progression of chitosan-based sorbents that can be utilized in the mitigation of Cr(VI) oxyanions from aqueous media. This paper provides an overview of pristine chitosan along with recentadvancements and insights into structurally and chemically modified chitosan. Chitosan has been chemically modified through cross-linking, grafting, and/or combination with other adsorptive materials to enhance its performance in Cr(VI) removal. Structurally modified chitosan-based hybrid materials that are commonly used in Cr(VI) removal include magnetic adsorbents,hydrogels, aerogels, and nano/microparticles. The sorption capacities of chitosan-based hybrid materials have varied from 27.25 - 357.14 mg g-1 depending on the type of adsorbent, dosage, initial Cr(VI) concentration, pH, and type of modification. Also, beneficial information through a compare-and-contrast of the effectiveness of the stated sorbent materials and their variants in themitigation of Cr(VI) is provided. Furthermore, mechanisms of Cr(VI) removal by chitosan-based sorbents accentuating the main governing mechanism, electrostatic interactions are described and discussed. Desorption and regeneration studies are presented to assess the reusability of the chitosan-based adsorptive materials utilized in the mitigation of Cr(VI) contamination. Desorptionstudies reveal that sorption of Cr(VI) onto most of the chitosan-based adsorbents are fairly reversible with desorbed percentages above 60% with the usage of an efficient stripping agent. Through the literature survey of approximately 100 recently published papers, it could be evinced that chitosan-based adsorbents have proved to be an outstanding sorbent even if some challengesremain. Keywords: Adsorption, chitosan, Cr(VI), hybrid materials, mechanis

    Endophilin, Lamellipodin, and Mena cooperate to regulate F-actin-dependent EGF-receptor endocytosis

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    The epidermal growth factor receptor (EGFR) plays an essential role during development and diseases including cancer. Lamellipodin (Lpd) is known to control lamellipodia protrusion by regulating actin filament elongation via Ena/VASP proteins. However, it is unknown whether this mechanism supports endocytosis of the EGFR. Here, we have identified a novel role for Lpd and Mena in clathrin-mediated endocytosis (CME) of the EGFR. We have discovered that endogenous Lpd is in a complex with the EGFR and Lpd and Mena knockdown impairs EGFR endocytosis. Conversely, overexpressing Lpd substantially increases the EGFR uptake in an F-actin-dependent manner, suggesting that F-actin polymerization is limiting for EGFR uptake. Furthermore, we found that Lpd directly interacts with endophilin, a BAR domain containing protein implicated in vesicle fission. We identified a role for endophilin in EGFR endocytosis, which is mediated by Lpd. Consistently, Lpd localizes to clathrin-coated pits (CCPs) just before vesicle scission and regulates vesicle scission. Our findings suggest a novel mechanism in which Lpd mediates EGFR endocytosis via Mena downstream of endophilin

    F-Actin Interactome Reveals Vimentin as a Key Regulator of Actin Organization and Cell Mechanics in Mitosis.

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    Most metazoan cells entering mitosis undergo characteristic rounding, which is important for accurate spindle positioning and chromosome separation. Rounding is driven by contractile tension generated by myosin motors in the sub-membranous actin cortex. Recent studies highlight that alongside myosin activity, cortical actin organization is a key regulator of cortex tension. Yet, how mitotic actin organization is controlled remains poorly understood. To address this, we characterized the F-actin interactome in spread interphase and round mitotic cells. Using super-resolution microscopy, we then screened for regulators of cortex architecture and identified the intermediate filament vimentin and the actin-vimentin linker plectin as unexpected candidates. We found that vimentin is recruited to the mitotic cortex in a plectin-dependent manner. We then showed that cortical vimentin controls actin network organization and mechanics in mitosis and is required for successful cell division in confinement. Together, our study highlights crucial interactions between cytoskeletal networks during cell division

    Trend and variability of rainfall in two river basins in Sri Lanka: an analysis of meteorological data and farmers’ perceptions

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    Selected rainfall characteristics derived by analyzing observed rainfall data in two Sri Lankan river basins (Malwathu Oya and Kalu Ganga) were compared with the perceptions of farmers. The rainfall characteristics used for this analysis are trends, onset and cessation dates, length of the growing period, number of rainy days, and length of the dry spell. Farmers’ perceptions of changes in those characteristics were collected through household surveys. The majority of farmers in both river basins failed to recognize the long-term upward trend in annual rainfall. They also failed to describe the adaptation measures they were currently practising

    Lamellipodin and the Scar/WAVE complex cooperate to promote cell migration in vivo

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    Cell migration is essential for development, but its deregulation causes metastasis. The Scar/WAVE complex is absolutely required for lamellipodia and is a key effector in cell migration, but its regulation in vivo is enigmatic. Lamellipodin (Lpd) controls lamellipodium formation through an unknown mechanism. Here, we report that Lpd directly binds active Rac, which regulates a direct interaction between Lpd and the Scar/WAVE complex via Abi. Consequently, Lpd controls lamellipodium size, cell migration speed, and persistence via Scar/WAVE in vitro. Moreover, Lpd knockout mice display defective pigmentation because fewer migrating neural crest-derived melanoblasts reach their target during development. Consistently, Lpd regulates mesenchymal neural crest cell migration cell autonomously in Xenopus laevis via the Scar/WAVE complex. Further, Lpd’s Drosophila melanogaster orthologue Pico binds Scar, and both regulate collective epithelial border cell migration. Pico also controls directed cell protrusions of border cell clusters in a Scar-dependent manner. Taken together, Lpd is an essential, evolutionary conserved regulator of the Scar/WAVE complex during cell migration in vivo

    Endophilin, Lamellipodin, and Mena cooperate to regulate F-actin-dependent EGF-receptor endocytosis

    No full text
    The epidermal growth factor receptor (EGFR) plays an essential role during development and diseases including cancer. Lamellipodin (Lpd) is known to control lamellipodia protrusion by regulating actin filament elongation via Ena/VASP proteins. However, it is unknown whether this mechanism supports endocytosis of the EGFR. Here, we have identified a novel role for Lpd and Mena in clathrin-mediated endocytosis (CME) of the EGFR. We have discovered that endogenous Lpd is in a complex with the EGFR and Lpd and Mena knockdown impairs EGFR endocytosis. Conversely, overexpressing Lpd substantially increases the EGFR uptake in an F-actin-dependent manner, suggesting that F-actin polymerization is limiting for EGFR uptake. Furthermore, we found that Lpd directly interacts with endophilin, a BAR domain containing protein implicated in vesicle fission. We identified a role for endophilin in EGFR endocytosis, which is mediated by Lpd. Consistently, Lpd localizes to clathrin-coated pits (CCPs) just before vesicle scission and regulates vesicle scission. Our findings suggest a novel mechanism in which Lpd mediates EGFR endocytosis via Mena downstream of endophilin
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