Pyroptosis: the dawn of a new era in endometrial cancer treatment.

Endometrial cancer (EC) is a malignancy of the inner epithelial lining of the uterus. While early-stage EC is often curable through surgery, the management of advanced, recurrent and metastatic EC poses significant challenges and is associated with a poor prognosis. Pyroptosis, an emerging form of programmed cell death, is characterized by the cleavage of gasdermin proteins, inducing the formation of extensive gasdermin pores in the cell membrane and the leakage of interleukin-1ß (IL-1ß) and interleukin-18 (IL-18), consequently causing cell swelling, lysis and death. It has been found to be implicated in the occurrence and progression of almost all tumors. Recent studies have demonstrated that regulating tumor cells pyroptosis can exploit synergies function with traditional tumor treatments. This paper provides an overview of the research progress made in molecular mechanisms of pyroptosis. It then discusses the role of pyroptosis and its components in initiation and progression of endometrial cancer, emphasizing recent insights into the underlying mechanisms and highlighting unresolved questions. Furthermore, it explores the potential value of pyroptosis in the treatment of endometrial cancer, considering its current application in tumor radiotherapy, chemotherapy, targeted therapy and immunotherapy.

2-Bromo-2-methyl-1-[4-(methyl-sulfan-yl)phen-yl]propan-1-one.

In the title compound, C(11)H(13)BrOS, the thio-ether unit and the phenyl ring adopt an essentially planar conformation, with a maximum deviation of 0.063 Å. In the crystal, mol-ecules are linked by C-H⋯O hydrogen bonds, extending in zigzag chains along the b axis. A weak intra-molecular C-H⋯Br hydrogen bond is also observed, which forms an S(6) ring motif.

Jinkui Shenqi Pills Ameliorate Asthma with "Kidney Yang Deficiency" by Enhancing the Function of the Hypothalamic-Pituitary-Adrenal Axis to Regulate T Helper 1/2 Imbalance.

The aim of the study was to investigate the effects and underlying mechanism of JKSQP in a rat model of asthma with kidney-yang deficiency (KYD). Materials and Methods. Hydrocortisone (HYD) was used to establish the rat model of KYD; rats were then sensitized and challenged with ovalbumin (OVA). JKSQP was administered to OVA-challenged rats, and the changes in signs and symptoms of KYD were observed. The leukocyte number and subpopulations in bronchoalveolar lavage fluid (BALF) were counted and the cells were stained with Wright-Giemsa dye. Serum adrenocorticotropic hormone (ACTH), corticosterone (CORT), corticotropin-releasing hormone (CRH), total immunoglobulin E (IgE), and OVA-specific IgE levels were determined using relevant enzyme-linked immunosorbent assays (ELISA) kits. Results. JKSQP not only reversed the phenomenon of KYD but also significantly inhibited the number of leukocyte and eosinophils in the BALF, increasing the level of interferon (IFN)-γ and decreasing the levels of interleukin-4 (IL-4) and IgE in the serum compared with the OVA-challenged groups. Conclusions. Taken together, the antiasthma effects of JKSQP were likely mediated by the enhancement of the function of the hypothalamic-pituitary-adrenal axis and the reversal of T helper 1/2 imbalance.