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Biodiesel manufacturing from waste cooking oil has emerged as a potential alternative in the search of sustainable energy. This process helps mitigate environmental pollution and reduces reliance on fossil fuels. This research examines the catalytic efficiency of environmentally friendly catalysts in this process, with a specific emphasis on catalysts based on enzymes. It assesses their effectiveness in terms of the production of biodiesel, the rate of the chemical reactions, cost efficiency, and their influence on the environment. Experimental evidence demonstrates that enzyme-based catalysts have enhanced catalytic activity, leading to an average biodiesel production of 90%, outperforming traditional catalysts such as solid acids, bases, and heterogeneous metal catalysts. Moreover, enzyme catalysts exhibit enhanced reaction rates due to their unique enzymatic activity and gentle reaction conditions. The cost study shows that the manufacturing costs for enzyme catalysts are competitive, with an average total cost of $800, which is equivalent to traditional catalysts. Environmental impact evaluation emphasizes the sustainability of enzyme catalysts by demonstrating their lower energy consumption, waste production, and greenhouse gas emissions compared to traditional alternatives. The results highlight the capacity of green catalysts, namely enzyme- based catalysts, to enhance sustainable biodiesel production methods, hence promoting a more eco-friendly and robust energy framework.

This research article explores the viability of biodegradable nanomaterials for sustainable food packaging applications. The study involves a thorough analysis of the materials, including material characterisation, mechanical testing, barrier testing, and biodegradation tests. The material characterisation demonstrates a consistent distribution of nanoparticles throughout the polymer matrix, as validated by SEM and TEM examination. XRD analysis also indicates the presence of crystalline phases in the nanomaterials. FTIR spectroscopy is a technique that can identify specific functional groups and chemical bonds in a substance, allowing us to get knowledge about its composition and compatibility. Ongoing research and development are crucial to enhance the efficiency and economic feasibility of packaging materials made from biodegradable nanomaterials. This will help advance the sustainability of the food packaging sector.

In order to tackle the worldwide problems of water pollution and shortage, this work explores the green synthesis of nanocomposite membranes for sustainable water filtering. Graphene oxide, cellulose nanocrystals, and silver nanoparticles were used as nanofillers in the fabrication of nanocomposite membranes, which were made using renewable polymer matrix (PES, PVDF, PAN). By including different polymer matrices and nanofillers, the composition analysis demonstrated the adaptability of nanocomposite membrane manufacturing, enabling the customization of membrane characteristics. Improved membrane shape and structural integrity were shown to result from the homogeneous dispersion of nanofillers inside the polymer matrix, according to characterization tests. Nanocomposite membranes demonstrated high flux rates and rejection rates for different pollutants, confirming their excellent performance in filtration experiments. The membranes' improved fouling resistance also increased their service life and decreased the frequency of maintenance needs. Supporting the eco-friendliness of nanocomposite membrane production, an environmental impact evaluation found that it used less energy and generated less trash than traditional techniques. All things considered, nanocomposite membranes have shown great promise as long- term water treatment solutions due to their superior performance, durability, and environmental friendliness, as well as their effective production and characterisation. More study is needed to perfect membrane characteristics and solve the remaining problems that prevent their broad use in water treatment systems.

This research examines the characteristics and ecological viability of polymer matrix nanocomposites used in sustainable packaging. Nanocomposites were produced by combining varied proportions of polymer and nanofiller material. Through mechanical testing, it was determined that nanocomposite formulation 3 had the maximum tensile strength of 55 MPa, as well as a Young's modulus of 3.5 GPa, showing greater stiffness in comparison to the other formulations. The evaluation of barrier qualities revealed that nanocomposite formulation 2 exhibited the most minimal oxygen permeability at a rate of 8 cc/m2/day and the lowest water vapor transmission rate at 4.5 g/m2/day, showing very efficient performance in preventing the passage of gases and moisture. The environmental impact study showed that nanocomposite formulation 3 had the most efficient energy consumption during manufacture, with a rate of 1.8 kWh/kg. It also had the lowest waste creation, with just 0.08 kg/kg, and the lowest CO2 emissions, with only 0.4 kg/kg. Nanocomposite formulation 3 demonstrated substantial improvements in mechanical characteristics, barrier properties, and environmental impact indicators when compared to the reference formulations, as shown by the percentage change analysis. In summary, this study showcases the capabilities of polymer matrix nanocomposites, specifically formulation 3, as environmentally friendly packaging materials that offer improved mechanical properties, effective barrier performance, and reduced ecological footprint. These findings contribute to the development of sustainable packaging solutions across different industries.

CCAAT/enhancer‐binding protein α (C/EBPα), a key myeloid transcription factor, drives myeloid differentiation from blast cells by regulating the expression of granulocyte colony stimulating factor receptor and C/EBPε as required for promoting granulocyte differentiation. Here, we show that serine/threonine‐protein kinase NLK, also known as Nemo‐like kinase, physically associates with C/EBPα and phosphorylates it at multiple sites, including Ser21, Thr226, Thr230 and S234, leading to its ubiquitin‐mediated degradation. Individual phospho‐point mutants of C/EBPα could be phosphorylated by NLK, but a mutant with all phosphorylatable residues replaced by alanine resisted phosphorylation and degradation by NLK, as did the single point mutants. Furthermore, although ectopic expression of NLK enhanced phosphorylation of C/EBPα levels, it markedly inhibited total C/EBPα protein levels. Conversely, NLK depletion inhibited endogenous C/EBPα phosphorylation but enhanced its total protein levels in several acute myeloid leukemia (AML) cell lines and in peripheral blood mononuclear cells isolated from number of AML patient samples. Importantly, NLK depletion in peripheral blood mononuclear cells from primary AML patients not only restored C/EBPα protein levels, but also induced myeloid differentiation, suggesting that NLK could be therapeutically targeted to restore C/EBPα to resolve differentiation arrest in AML. [ABSTRACT FROM AUTHOR]

Imparting epithelial to mesenchymal transition (EMT) during cellular transformation, a major driving force behind tumor progression, is one of the notorious oncogenic activities of transforming growth factor β (TGFβ); however, the secretary factors released during TGFβ‐induced EMT that may have role in potentiating EMT and tumor progression are poorly known. This study was undertaken to identify such secreted protein factors from TGFβ‐induced A549 cells cultured in serum‐free chemically defined medium (FreestyleTM) using Matrix Assisted Laser Desorption Ionization‐Time of flight/Time of flight (MALDI‐TOF/TOF) mass spectrometry. We identified some of the potential factors such as ESR, ANXA2, ALDH1A, TGFβ‐induced protein ig‐h3, and PAI‐1 that were not only secreted but some were also elevated in TGFβ‐induced A549 cells. Interestingly, these factors are widely reported to play crucial role in EMT induction and progression, which not only validates our findings but also opens avenues for further investigation, if upon secretion they act exogenously through certain receptors to potentiate cellular signaling involved in EMT induction and tumor progression. [ABSTRACT FROM AUTHOR]

Glycogen synthase kinase 3β (GSK3β), an ubiquitously expressed serine/threonine kinase is reported to be overexpressed and hyperactivated in cancers including acute myeloid leukemia (AML) where it promotes self-renewal, growth, and survival of AML cells. Therefore, GSK3β inhibition results in AML cell growth inhibition and myeloid differentiation. Here we identified master transcription factor PU.1 of monocyte-macrophage differentiation pathway as potential GSK3β target. We demonstrate that GSK3β phosphorylates PU.1 at Ser41 and Ser140 leading to its recognition and subsequent ubiquitin-mediated degradation by E3 ubiquitin ligase FBW7. This GSK3-dependent degradation of PU.1 by FBW7 inhibited monocyte-macrophage differentiation. We further showed that a phospho-deficient PU.1 mutant (PU.1-S41, S140A) neither bound to FBW7 nor was degraded by it. Consequently, PU.1-S41, S140A retained its transactivation, DNA-binding ability and promoted monocyte-macrophage differentiation of U937 cells even without phorbol 12-myristate 13-acetate (PMA) treatment. We further showed that FBW7 overexpression inhibited both PMA as well as M-CSF-induced macrophage differentiation of myeloid cell lines and peripheral blood mononuclear cells (PBMC) from healthy volunteers, respectively. Contrarily, FBW7 depletion promoted differentiation of these cells even without any inducer suggesting for a robust role of GSK3β-FBW7 axis in negatively regulating myeloid differentiation. Furthermore, we also recapitulated these findings in PBMCs isolated from patients with leukemia where FBW7 overexpression markedly inhibited endogenous PU.1 protein levels. In addition, PBMCs also showed enhanced differentiation when treated with M-CSF and GSK3 inhibitor (SB216763) together compared with M-CSF treatment alone. IMPLICATIONS: Our data demonstrate a plausible mechanism behind PU.1 restoration and induction of myeloid differentiation upon GSK3β inhibition and further substantiates potential of GSK3β as a therapeutic target in AML., (©2020 American Association for Cancer Research.)