Streptococcus pyogenes, also known as group A streptococcus (GAS), causes a wide variety of acute infections, ranging from localized purulent infections to severe, even fatal, invasive disease. Systemic spread is usually caused by bacterial penetration of the epithelial barrier of the pharynx or damaged skin and, if not well controlled, can lead to blood and soft tissue invasion. Superficial colonization and invasive infection of GAS depend on secreted GAS virulence factors, of which cysteine protease exotoxin (SpeB) is the key. SpeB is initially an inactive zymogen that is proteolytically converted to a mature catalytically active enzyme. SpeB contributes to epidermal localization and systemic spread, but the underlying mechanisms are unknown.

In the previous issues, we introduced various formulations and strategies for drug dissolution. Among them, DMSO, which is not recommended, also has a place as a co-solvent, but it is quite controversial. The use of this solvent, which is restricted by the FDA, is widely spread and is highly toxic. How toxic is it, and how do we use it in our experiments? Today we will reveal to you the correct use of "universal solvent" DMSO in cell and animal experiments.

There are various modes of administration in animal experimental studies, such as oral, intraperitoneal, intravenous, intracerebral injection, etc. However, we often choose a certain drug delivery method commonly used in the laboratory without knowing the reason. For example, our laboratory often chooses intraperitoneal injection, but do not know why. In fact, there is a lot of knowledge included! In this case, from the perspective of pharmacology and pharmacokinetics, we will popularize the principles of choosing the mode of administration.

Ferroptosis is a newly discovered form of cell death in recent years, and its essence is the peroxidative death caused by the accumulation of lipid reactive oxygen species (L-ROS) in cells, which is iron ion-dependent. Erastin, as a potent inducer of ferroptosis, can mediate ferroptosis through multiple molecules such as cystine-glutamate transport receptors, voltage-dependent anion channels, and p53. More importantly, Erastin can enhance the sensitivity of cancer cells to chemotherapy and radiotherapy, so it can be used as a new type of anticancer drug. This article reviews the discovery of Erastin, the ferroptosis pathway, the action pathway of Erastin and its anti-tumor characteristics, as well as the latest research progress at home and abroad.