The role and mechanism of hydrogen sulfide in liver fibrosis.

Hydrogen sulfide (H2S) is the third new gas signaling molecule in the human body after the discovery of NO and CO. Similar to NO, it has the functions of vasodilation, anti-inflammatory, antioxidant, and regulation of cell formation. Enzymes that can produce endogenous H2S, such as CSE, CSB, and 3-MST, are common in liver tissues and are important regulatory molecules in the liver. In the development of liver fibrosis, H2S concentration and expression of related enzymes change significantly, which makes it possible to use exogenous gases to treat liver diseases. This review summarizes the role of H2S in liver fibrosis and its complications induced by NAFLD and CCl4, and elaborates on the anti-liver fibrosis effect of H2S through the mechanism of reducing oxidative stress, inhibiting inflammation, regulating autophagy, regulating glucose and lipid metabolism, providing theoretical reference for further research on the treatment of liver fibrosis with H2S.

Room-temperature weak ferromagnetism induced by point defects in alpha-Fe2O3.

Unusual room-temperature weak ferromagnetism alpha-Fe(2)O(3) was prepared by heating the mixture of commercial alpha-Fe(2)O(3) (as raw material) and tartaric acid at a mild temperature of 250 degrees C. This reaction involves a fast heating and cooling process resulting from the self-catalyzed oxidation of tartaric acid. Careful chemical analyses confirmed that no any ferromagnetic impurities, such as Fe, Fe(3)O(4), amorphous iron oxide and gamma-Fe(2)O(3,) were present in the treated sample. The unusual weak ferromagnetism was then attributed to the formation of a large amount of point defects in the treated sample during the peculiar synthetic process. Such a mechanism is supported by the result of annealing, which reduces the amount of point defects and thereby reestablishes the original antiferromagnetism in alpha-Fe(2)O(3).