Biosorption and Chemical Precipitation of Lead Using Biomaterials, Molecular Sieves, and Chlorides, Carbonates, and Sulfates of Na &Ca

Lead, a heavy metal, is a well known contaminant in water and has been reported to cause serious health implications to humans, animals, and plants. One of the processes for heavy metal remediation of contaminated water is chemical precipitation. In this present work, chemical precipitation of lead from a contaminated aqueous matrix by chlorides, carbonates, and sulfates of sodium and calcium was compared to lead removal by molecular sieves and biomaterials (fishbone, grape and spinach). The order of lead removal from 1400 ppm of lead solution is sodium chloride (31%) < calcium chloride (62%) burnt grape (83%) < charred spinach (92.3%) < sodium phosphate (95.8%) < sodium carbonate (97%) < molecular sieve sphere (98.7%) < sodium sulfate (99.3%) s ground (99.71%) < fishbone (99.87%)

Hepatic transcriptome profiling reveals early signatures associated with disease transition from non-alcoholic steatosis to steatohepatitis

Background and aim:Non-alcoholic fatty liver disease(NAFLD)is becoming a leading cause of chronic liver disease worldwide.The molecular events that influence disease progression from non-alcoholic fatty liver(NAFL)to aggressive non-alcoholic steatohepatitis(NASH)remain incompletely understood,leading to lack of mechanism-based targeted treatment options for NASH.This study aims to identify early signatures associated with disease progression from NAFL to NASH in mice and humans.Materials and methods:Male C57BL/6J mice were fed a high-fat,-cholesterol,and-fructose(HFCF)diet for up to 9 months.The extent of steatosis,inflammation,and fibrosis was evaluated in liver tissues.Total RNA sequencing(RNA-seq)was conducted to determine liver transcriptomic changes.Results:After being fed the HFCF diet,mice sequentially developed steatosis,early steatohepatitis,steatohepatitis with fibrosis,and eventually spontaneous liver tumor.Hepatic RNA-seq revealed that the key signatures during steatosis progression to early steatohepatitis were pathways related to extracel-lular matrix organization and immune responses such as T cell migration,arginine biosynthesis,C-type lectin receptor signaling,and cytokine-cytokine receptor interaction.Genes regulated by transcription factors forkhead box M1(FOXM1)and negative elongation factor complex member E(NELFE)were significantly altered during disease progression.This phenomenon was also observed in patients with NASH.

Role of early growth response 1 in liver metabolism and liver cancer

The liver is an essential organ for nutrient and drug metabolism - possessing the remarkable ability to sense environmental and metabolic stimuli and provide an optimally adaptive response. Early growth response 1 (Egr1), an immediate early transcriptional factor which acts as a coordinator of the complex response to stress, is induced during liver injury and controls the expression of a wide range of genes involved in metabolism, cell proliferation, and inflammation. In support of an important role of Egr1 in liver injury and repair, deficiency of Egr1 delays liver regeneration process. The known upstream regulators of Egr1 include, but are not limited to, growth factors (e.g. transforming growth factor β1, platelet-derived growth factor, epidermal growth factor, hepatocyte growth factor), nuclear receptors (e.g. hepatocyte nuclear factor 4α, small heterodimer partner, peroxisome proliferator-activated receptor-γ), and other transcription factors (e.g. Sp1, E2F transcription factor 1). Research efforts using various animal models such as fatty liver, liver injury, and liver fibrosis contribute greatly to the elucidation of Egr1 function in the liver. Hepatocellular carcinoma (HCC) represents the second leading cause of cancer mortality worldwide due to the heterogeneity and the late stage at which cancer is generally diagnosed. Recent studies highlight the involvement of Egr1 in HCC development. The purpose of this review is to summarize current studies pertaining to the role of Egr1 in liver metabolism and liver diseases including liver cancer.

Decoding the role of extracellular vesicles in liver diseases

Cell-to-cell communication is a fascinating process that is essential for maintaining tissue and wholebody homeostasis.Extracellular vesicles(EVs)are cell-derived membrane-bound nanoparticles that are a means of communication between cells.Accumulating evidence indicates that EVs can render either beneficial or harmful outcomes,depending on the specific cargos(e.g.,proteins,lipids,RNAs)transferred between cells.EVs also have great value as diagnostic and prognostic markers of disease because they are present in a variety of biological fluids and carry bioactive molecules from their cells or tissues of origin.Liver cells can both release and receive EVs derived from other cells and emerging evidence indicates that liver EVs play important roles in the pathogenesis of various liver diseases,including liver cancer,viral hepatitis,non-alcoholic fatty liver disease,and alcoholic liver disease.This review provides an overview of the biogenesis and secretion of EVs and summarizes the most recent advances in understanding the role of EVs in liver physiology and diseases.Additionally,we discuss potential applications of liver EVs as biomarkers and in therapeutic approaches to treat liver diseases.