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Sepsis is a life-threatening systemic inflammatory response syndrome caused by the host imbalanced response to infection. Lung injury is the most common complication of sepsis and one of the leading causes of patient death. Pyroptosis is a specific programmed cell death characterized by the release of inflammatory cytokines. Appropriate pyroptosis can reduce tissue damage and exert a protective effect against infection during sepsis. However, overactivated pyroptosis results in massive cell death, leading to septic shock, multiple organ dysfunction syndrome, and even an increased risk of secondary infection. Recent studies suggest that pyroptosis can interact with and cross-regulate other types of cell death programs to establish a complex network of cell death, which participates in the occurrence and development of septic lung injury. This review will focus on the interactions between pyroptosis and other types of cell death, including apoptosis, necroptosis, PANoptosis, NETosis, autophagy, and ferroptosis, to summarize the role of pyroptosis in sepsis-induced lung injury, and will discuss the potential therapeutic strategies of targeting pyroptosis during sepsis treatment.

Vacuum pair production under intense electromagnetic fields is an intriguing prediction in quantum electrodynamics (QED), and has become a topic of considerable interest with the rapid advancements in laser technologies. The pair production efficiency can be enhanced using chirped electric fields. In this study, the effects of electric field chirping on electron–positron pair production in different oscillating electric fields were investigated using the Dirac–Heisenberg–Wigner (DHW) formalism. We primarily considered quadratic and sinusoidal chirped electric fields. The results revealed that chirping significantly influences the momentum spectra of the generated particles in an electric field dominated by low-frequency tunneling effects, resulting in pronounced oscillations of the momentum spectrum, particularly in a sinusoidal chirped field. However, multiphoton processes gradually emerge as the chirp parameter increases. Consequently, in a high-frequency electric field dominated by multiphoton processes, the number density of the generated particles increases with the chirping parameter in a quadratic chirped field, whereas the momentum distribution remains relatively symmetric. However, in a sinusoidal chirped electric field, introducing a chirp parameter immediately alters the momentum distribution and enhances pair production rate. Moreover, there exists an optimal chirp parameter and the total particle number is enhanced approximately more than an order of magnitude with optimal chirping in a sinusoidal chirped electric field. These findings provide valuable insights into the intricate dynamics of pair production under the influence of chirping in different oscillating electric fields, and offer potential directions for future research in this domain.

Osteosarcoma (OS) is the most malignant bone tumor which mainly occurs in childhood or adolescence. The previous studies indicated that OS is difficult to treat. KIAA1429 is one of the components of m6A complex that regulating the process of m6A modification, which plays a crucial role in tumorigenesis. But the mechanism of KIAA1429 regulating OS cell identity was not entirely clear, which needs further investigate. RT-qPCR and western blotting were applied to determine KIAA1429 expression station in OS cells and tissues. To further detect the KIAA1429 function in OS cells, the ability of proliferation, migration and invasion were analyzed by Edu, wound-healing and transwell experiments respectively. Besides, RNA sequencing was also used to further find the downstream of KIAA1429 regulation and small molecule inhibitor was added to explore the specific role of signaling pathway. Our data found that KIAA1429 is up-regulated in human OS cell lines compared to the human osteoblast cells. Meanwhile, the deletion of KIAA1429 significantly decreased cell proliferation, migration, and invasion. Interestingly, the JAK2/STAT3 signal pathway was involved in KIAA1429 regulation on OS cell characters. The KIAA1429 eliminated OS cells exhibited a decreased activity of JAK2/STAT3 signal. And the addition of JAK2/STAT3 stimulator (colivelin) could distinctly rescue the decreased OS cells’ proliferation, migration, and invasion upon KIAA1429 knockdown. In summary, these data demonstrated that KIAA1429/JAK2/STAT3 axis may a new target for OS therapy.