Enhanced photoelectric properties of PbSnSe thin films via quick oxygen ion-implantation sensitization

Journal of Materials Science - Although chalcogenide materials continue to generate considerable interest due to great potentials for various optoelectronic devices, annealing for a long time in...     

Editorial: the March 2022 cover paper

Journal of Materials Science -     

Torque Transfer to a Conducting Particle Using the Lorentz Force

Semiconductors - In this work, we discuss for the first time the principle of rotation in the constant electric field of a conducting particle with participation of the Lorentz force, which ensures...     

Comparison of the Parameters of UWB Signals for Comparing the Characteristics of the Human Visual System and Matrix Receivers

Journal of Communications Technology and Electronics - A quantitative comparison of the spectral characteristics of the human visual system and matrix photodetectors is carried out. Criteria for a...     

Neoagarooligosaccharide Protects against Hepatic Fibrosis via Inhibition of TGF-β/Smad Signaling Pathway

Hepatic fibrosis occurs when liver tissue becomes scarred from repetitive liver injury and inflammatory responses; it can progress to cirrhosis and eventually to hepatocellular carcinoma. Previously, we reported that neoagarooligosaccharides (NAOs), produced by the hydrolysis of agar by β-agarases, have hepatoprotective effects against acetaminophen overdose-induced acute liver injury. However, the effect of NAOs on chronic liver injury, including hepatic fibrosis, has not yet been elucidated. Therefore, we examined whether NAOs protect against fibrogenesis in vitro and in vivo. NAOs ameliorated PAI-1, α-SMA, CTGF and fibronectin protein expression and decreased mRNA levels of fibrogenic genes in TGF-β-treated LX-2 cells. Furthermore, downstream of TGF-β, the Smad signaling pathway was inhibited by NAOs in LX-2 cells. Treatment with NAOs diminished the severity of hepatic injury, as evidenced by reduction in serum alanine aminotransferase and aspartate aminotransferase levels, in carbon tetrachloride (CCl₄)-induced liver fibrosis mouse models. Moreover, NAOs markedly blocked histopathological changes and collagen accumulation, as shown by H&E and Sirius red staining, respectively. Finally, NAOs antagonized the CCl₄-induced upregulation of the protein and mRNA levels of fibrogenic genes in the liver. In conclusion, our findings suggest that NAOs may be a promising candidate for the prevention and treatment of chronic liver injury via inhibition of the TGF-β/Smad signaling pathway.     

Use of Nuclear Energy in Outer-Space Systems

Atomic Energy - The history and direction of further development of space nuclear energetics are examined. The functional diagram and principle of operation of a promising, powerful,...     

A Hybrid Analytic Model for the Effective Prediction of Different Stages in Chronic Kidney Ailments

Wireless Personal Communications - Chronic kidney disease (CKD) is a gradual loss of kidney function over the period of time and it is irrevocable once functionality reaches the critical state....