Minia University

About: Minia University is a education organization based out in Minya, Egypt. It is known for research contribution in the topics: Population & Medicine. The organization has 4967 authors who have published 8986 publications receiving 108384 citations.

Thermal decomposition and creation of reactive solid surfaces

Abstract: Three chromia precursors, namely CrO3, (NH4)2Cr2O7 and chromia gel, were subjected to thorough thermal analysis by means of TG and DTA. The thermal decomposition products obtained by calcination of these precursors at various temperatures (150–500°) for 5 h were investigated by infrared and X-ray techniques. The results obtained allowed a thorough physicochemical characterization of the intermediate steps and products throughout the thermal decomposition.

A novel mechanism of action of ketoconazole: inhibition of the NorA efflux pump system and biofilm formation in multidrug-resistant Staphylococcus aureus .

Abstract: Background: The rapid emergence of antimicrobial resistance among Gram-positive organisms, especially staphylococci, has become a serious clinical challenge. Efflux machinery and biofilm formation are considered two of the main causes of antimicrobial resistance and therapy failure. Aim: Our study aims to evaluate the antibiofilm and efflux pump inhibitory activity of the antifungal ketoconazole against multidrug-resistant (MDR) Staphylococcus aureus. Methods: Ketoconazole was tested for its effect on the following: minimum inhibitory concentrations (MICs) of ciprofloxacin, norfloxacin, levofloxacin, and ethidium bromide (EtBr) by the broth microdilution method, the efflux of EtBr by NorA-positive MDR S. aureus, and the relative expression of NorA, NorB, and NorC efflux pump genes. Docking studies of ketoconazole were performed using 1PW4 (glycerol-3-phosphate transporter from Escherichia coli which was the representative structure from the major facilitator superfamily). Results: Ketoconazole significantly decreased the MICs of levofloxacin, ciprofloxacin, norfloxacin, and EtBr (a substrate for efflux pump) by 8 to 1024-fold (P<0.01) and decreased the efflux of EtBr. Furthermore, a time-kill assay revealed that combinations of levofloxacin with ketoconazole or carbonyl cyanide m-chlorophenylhydrazone showed no growth for the tested strains after 24 h in comparison to the effect of levofloxacin alone. Docking studies and the ability of ketoconazole to diminish the relative expression of NorA gene in comparison to control (untreated strains) confirmed its action as an efflux pump inhibitor. Conclusion: The findings showed that the antifungal ketoconazole has no antibacterial activity but can potentiate the activity of the fluroquinolones against MDR S. aureus via inhibiting efflux pump and biofilm formation in vitro.

Design, Synthesis, and Biological Evaluation of Novel 1,3,4-Thiadiazole Derivatives as Potential Antitumor Agents against Chronic Myelogenous Leukemia: Striking Effect of Nitrothiazole Moiety

Abstract: In an attempt to develop potent antitumor agents, new 1,3,4-thiadiazole derivatives were synthesized and evaluated for their cytotoxic effects on multiple human cancer cell lines, including the K562 chronic myelogenous leukemia cell line that expresses the Bcr-Abl tyrosine kinase. N-(5-Nitrothiazol-2-yl)-2-((5-((4-(trifluoromethyl)phenyl)amino)-1,3,4-thiadiazol-2-yl)thio)acetamide (2) inhibited the Abl protein kinase with an IC50 value of 7.4 µM and showed selective activity against the Bcr-Abl positive K562 cell line. Furthermore, a Bcr-Abl-compound 2 molecular modelling simulation highlighted the anchoring role of the nitrothiazole moiety in bonding and hydrophobic interaction with the key amino acid residues. These results provide promising starting points for further development of novel kinase inhibitors.

Reversibility and heritability of liver fibrosis: Implications for research and therapy

Abstract: Liver fibrosis continues to be a major health problem worldwide due to lack of effective therapy. If the etiology cannot be eliminated, liver fibrosis progresses to cirrhosis and eventually to liver failure or malignancy; both are associated with a fatal outcome. Liver transplantation, the only curative therapy, is still mostly unavailable. Liver fibrosis was shown to be a reversible process; however, complete reversibility remains debatable. Recently, the molecular markers of liver fibrosis were shown to be transmitted across generations. Epigenetic mechanisms including DNA methylation, histone posttranslational modifications and noncoding RNA have emerged as major determinants of gene expression during liver fibrogenesis and carcinogenesis. Furthermore, epigenetic mechanisms have been shown to be transmitted through mitosis and meiosis to daughter cells and subsequent generations. However, the exact epigenetic regulation of complete liver fibrosis resolution and inheritance has not been fully elucidated. This communication will highlight the recent advances in the search for delineating the mechanisms governing resolution of liver fibrosis and the potential for multigenerational and transgenerational transmission of fibrosis markers. The fact that epigenetic changes, unlike genetic mutations, are reversible and can be modulated pharmacologically underscores the unique opportunity to develop effective therapy to completely reverse liver fibrosis, to prevent the development of malignancy and to regulate heritability of fibrosis phenotype.