Zero-valent aluminum based trimetallic particles comprising a combination of catalytically effective amounts (1 wt%) of palladium and zero-valent iron on the aluminum surface were synthesized and tested for the dechlorination of chlorinated methanes in batch reactors. XRD analysis indicated the trimetallic particles present in zero-valent form of all three components. Trimetallic Pd/Fe/Al particles showed a very rapid degradation of carbon tetrachloride leading to a surface normalized rate constant (k(SA)) of approximately 0.03 L/h/m(2), two orders of magnitude higher than that of reported data on zero-valent iron particles under near neutral pH conditions. Hydrocarbons including methane and ethane were the major products that accounted for about 38% and 27% of the carbon tetrachloride lost, respectively. Repetitive addition of carbon tetrachloride showed no loss of activity of Pd/Fe/Al particles for more than 20 cycles. In the absence of palladium, the degradation rate decreased by a factor of 10 suggesting palladium serves as a catalyst. Analysis of anions in the solution revealed that the chloride accounted for 75% of the carbon tetrachloride lost. Metallic ions for aluminum and iron were determined to be about 0.02 and 20 mg/L, respectively at the end of the experiment. No palladium ion was measured.
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http://dx.doi.org/10.2166/wst.2010.303 | DOI Listing |
Eur J Med Chem
January 2025
State Key Laboratory of Natural Medicines, Jiangsu Key Laboratory of Drug Discovery for Metabolic Diseases, Center of Advanced Pharmaceuticals and Biomaterials, China Pharmaceutical University, Nanjing, 211198, PR China. Electronic address:
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View Article and Find Full Text PDFSci Rep
January 2025
Institute of Comparative Molecular Endocrinology, Ulm University, 89081, Ulm, Germany.
Hepatocellular carcinoma (HCC) remains the most prevalent type of primary liver cancer worldwide. p53 is one of the most frequently mutated tumor-suppressor genes in HCC and its deficiency in hepatocytes triggers tumor formation in mice. To investigate iron metabolism during liver carcinogenesis, we employed a model of chronic carbon tetrachloride injections in liver-specific p53-deficient mice to induce liver fibrosis, cirrhosis and subsequent carcinogenesis.
View Article and Find Full Text PDFBioorg Chem
January 2025
State Key Laboratory of Phytochemistry and Plant Resources in West China, Kunming Institute of Botany, Chinese Academy of Sciences, Kunming 650201 China; University of Chinese Academy of Sciences, Beijing 100049 China. Electronic address:
Non-alcoholic fatty liver disease (NAFLD), also known as metabolic dysfunction- associated with fatty liver disease (MAFLD), is one of the most prevalent chronic liver diseases globally. NAFLD is characterized by the accumulation of liver fat unrelated to excessive alcohol consumption. Non-alcoholic steatohepatitis (NASH) is the disease progression of NAFLD and could develop into cirrhosis and hepatocellular carcinoma.
View Article and Find Full Text PDFAnat Cell Biol
January 2025
Department of Human and Clinical Anatomy, College of Medicine and Health Sciences, Sultan Qaboos University, Muscat, Sultanate of Oman.
Liver regeneration is intricate, involves many cells, and necessitates extended research. This study aimed to investigate the response of liver oval cells (bipotent liver progenitors) to the epigenetic modifier trichostatin A (TSA), an HDAC1 inhibitor, and to develop a scoring system for assessing the response of these cells. Three groups of equally divided rats (n=24) were selected: control (A, dimethyl sulfoxide treated); oval cell induction (B, acetylaminofluorene [2-AAF] to block hepatocyes/carbon tetrachloride [CCL4] to induce oval cell response); and epigenetic modulation (C, TSA post 2-AAF/CCL4 injury).
View Article and Find Full Text PDFZhongguo Zhong Yao Za Zhi
December 2024
School of Medicine, Jianghan University Wuhan 430056, China.
This study aims to investigate the mechanism of tanshinone Ⅱ_A(Tan Ⅱ_A) in protecting mice from diethylinitrosamine(DEN)/carbon tetrachloride(CCl_4)/ethanol(C_2H_5OH)-induced hepatocellular carcinoma(HCC) and HepG2 cells from hydrogen peroxide(H_2O_2)-induced oxidative damage via the phosphoinositide 3-kinase(PI3K)/protein kinase B(Akt) and nuclear factor E2-related factor 2(Nrf2)/heme oxygenase 1(HO-1) signaling pathways. Sixty male C57BL/6J mice were grouped as follows: control, model, low, medium, and high-dose(10, 20, 40 mg·kg~(-1), respectively) Tan Ⅱ_A, and colchicine(0.2 mg·kg~(-1)), with 10 mice in each group.
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