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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]

Ormeloxifene (ORM) (3,4‐trans‐2,2‐dimethyl‐3‐phenyl‐4‐p‐(β‐pyrrolidinoethoxy) phenyl‐7‐methoxychroman), world's first nonsteroidal selective estrogen receptor modulator approved for contraception in India has been shown to have potential anticancer activities. Here, we show that ORM can induce megakaryocyte and myeloid (granulocytic) but not erythroid differentiation in multipotent human myeloid leukemia cell line K562. We show that ORM at an IC50 of 7.5 µM can induce morphological changes similar to megakaryocytes in K562 cells. ORM led to increase in levels of megakaryocytic differentiation markers (CD41 and CD61) as well as key transcription factors GATA1 and AML1. We further show that ORM induces megakaryocytic differentiation in K562 cells through ERK activation and induction of autophagy in a fashion similar to other known inducers of megakaryocytic differentiation such as phorbol esters. In addition, as shown earlier, we yet again observed that ORM led to activation of caspases since their inhibition through pan‐caspase inhibitor mitigated megakaryocytic differentiation as they led to significant decrease in CD41 and CD61. Because induction of megakaryocytic differentiation in K562 involves growth arrest and exit from cell cycle, we also observed an increase in levels of p21 and p27 with decrease in c‐Myc protein levels in K562 cells treated with 7.5 µM ORM for 24 and 48 h, respectively. Taken together, these findings indicate that ORM can markedly induce megakaryocytic differentiation in K562 cells. [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]

Triple‐negative breast cancers (TNBC) are highly aggressive and drug resistant accounting for majority of cases with poor outcome. Purified natural compounds display substantial anticancer activity with reduced cytotoxicity providing a new avenue to combat TNBC. Chebulinic acid (CA), a polyphenol derived from the fruits of various medicinal plants has potent anticancer activity. Here, we demonstrate that CA shows significant cytotoxicity against triple negative MDA‐MB‐231 cells. CA exhibited cytotoxicity to MDA‐MB‐231 cells in 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide assay. Further, CA mitigated MDA‐MB‐231 cells viability and proliferation as shown by reduced live cell count, crystal violet staining, colony formation assay, soft agar assay and cell cycle analysis. Wound healing assay and trans‐well migration assay demonstrated that CA significantly inhibited migration of MDA‐MB‐231 cells. Also reduced MMP9 expression was observed in CA‐treated cells by gelatin zymography. CA negatively regulated mesenchymal characteristics of MDA‐MB‐231 cells demonstrated by F‐actin staining and reduced expression of N‐cadherin by confocal microscopy and western blot analysis. Annexin V/propidium iodide (PI) and active caspase‐3 staining showed that CA was able to induce apoptosis in MDA‐MB‐231 cells but did not activate caspase‐3. Two‐dimensional gel electrophoresis based proteomic analysis demonstrated that CA regulated proteins belonging to the oxidative stress pathway, apoptotic pathway and proteins with antiproliferative activity. Western blot analysis analysis revealed that CA negatively regulated superoxide dismutase 1 (SOD1) and enhanced oxidative stress in MDA‐MB‐231 cells. SOD1 in‐gel activity assay also showed reduced SOD1 activity upon CA treatment. Overexpression studies with GFP‐LC3 and tandem tagged RFP‐GFP‐LC‐3 also demonstrated enhanced autophagy upon CA treatment. [ABSTRACT FROM AUTHOR]

E6AP (E6 associated protein) is a HECT domain containing protein having dual E3 ligase and ERα coactivation activity in breast cancer cells. Although E6AP is known to possess antitumorigenic activity, the underlying molecular mechanism is poorly understood. In the present study, we applied nano‐LC based proteomics approach to identify E6AP‐interacting proteins where we performed GST‐pull down using GST‐E6AP from whole cell extracts of MCF7 cells, resolved the differentially interacting proteins on 1D‐SDS‐PAGE, excised the gel bands that were trypsin digested followed by fractionation and spotting on MALDI‐TOF/TOF plate through Nano‐LC MALDI spotter. Subsequently, fractionated and spotted peptides were identified using MALDI‐TOF/TOF. We identified several E6AP interacting proteins including previously reported such as HSP70 and new ones such as Enolase‐1. We further confirmed that E6AP and Enolase1 interacted and colocalized more in the cytoplasmic periphery in breast cancer cells and further demonstrated that E6AP also targeted ENO1 for ubiquitin‐mediated degradation in these cells. [ABSTRACT FROM AUTHOR]

Epithelial ovarian cancer (EOC) is the leading cause of death among all gynecologic cancers around the world. This is so because women diagnosed with early-stage disease have a better prognosis and hence better chances of survival. Cancer antigen (CA)-125 is a high-molecular-mass glycoprotein produced both by ovarian cancer cells and also by the normal cells of tissues derived from coelomic epithelium. This study explores the significance of CA-125 for patients with ovarian cancer residing near rivers. The medical records of 80 patients treated at the Mahavir Cancer Institute and Research Centre for ovarian cancer between 2005 and 2007 with preoperative serum CA-125 levels were reviewed. Study reveals that the patients residing in the Gangetic region have the lowest mean CA-125 level (82.09 IU/mL), whereas the ovarian cancer not patients residing in the Gangetic zone have a higher mean CA-125 level (353.37 IU/mL). Although CA-125 is the best available single marker for ovarian cancer, its sensitivity and specificity might not be sufficient for the screening of patients from Bihar residing in the Gangetic zone who have epithelial ovarian cancer. [ABSTRACT FROM AUTHOR]

Tamoxifen-mediated endocrine therapy has been standard treatment for ER+ breast cancers; however, majority of them acquire resistance leading to disease relapse. Although numerous substrates of E3 ligase FBW7 are known, only a handful of factors that regulate FBW7 expression and function are reported. In particular, there remains a lack of in-depth understanding of FBW7 transcriptional regulation. Luciferase reporter assay was performed after cloning full length and truncated FBW7 promoters followed by Chromatin immunoprecipitation assay to validate binding of SOX4 on FBW7 promoter. Transcriptional regulation of FBW7 by SOX4 and their biological consequences with respect to ER+ breast cancer was then evaluated using immunoblotting and other cell based assays. SOX4 positively regulates FBW7 at transcriptional level by binding to three putative SOX4 biding sites within 3.1 kb long FBW7 promoter. Analysis of publicly available RNAseq datasets also showed a positive correlation between SOX4 and FBW7 mRNA in cancer cell lines and patient samples. qPCR and Immunoblotting confirmed that transiently or stably expressed SOX4 induced both endogenous FBW7 mRNA and protein levels. Our findings further demonstrated that increased levels of SOX4 and FBW7 in MCF7 mammospheres promoted cancer stemness and tumor cell dormancy. We further showed that both MCF7 mammospheres and MCFTAMR cells had elevated SOX4 levels which apparently enhanced FBW7 to potentiate GATA3 degradation leading to enhanced stemness, tumor dormancy and Tamoxifen resistance in MCF7TAMR as well as patients with ER+ breast cancers. Targeting SOX4-FBW7-GATA3 axis may overcome tamoxifen resistance in ER+ breast cancers. Graphical model depicts that SOX4 positively regulates FBW7 levels in ER+ breast cancers where it promotes stemness, tumor dormancy and TAM resistance by targeting GATA3 and c-Myc. [Display omitted] [ABSTRACT FROM AUTHOR]