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Background/aims: Bruise is the extravasation of blood that may be mild or severe. Bone marrow mesenchymal stem cells (BM-MSCs) are one of the most promising cells used in regenerative medicine for treating many disorders. We aimed to evaluate the efficiency of BM-MSCs in treating cutaneous bruises.

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Sepsis-induced acute lung injury (ALI) is a common acute and severe reason of death in the intensive care unit. Although the pathogenesis is complicated and multifactorial, elevated inflammation and oxidative stress are considered as fundamental mechanisms for the progression of ALI. Anemonin is a natural compound with diverse biological properties including anti-inflammatory and anti-oxidative effects.

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Parthenolide improves sepsis-induced coagulopathy by inhibiting mitochondrial-mediated apoptosis in vascular endothelial cells through BRD4/BCL-xL pathway.

J Transl Med

January 2025

Department of Anesthesiology, Daping Hospital, Army Medical University, No.10, Changjiang Road, Yuzhong District, Chongqing, 400042, China.

Background: Sepsis is a systemic inflammatory syndrome that can cause coagulation abnormalities, leading to damage in multiple organs. Vascular endothelial cells (VECs) are crucial in the development of sepsis-induced coagulopathy (SIC). The role of Parthenolide (PTL) in regulating SIC by protecting VECs remains unclear.

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Purpose: Cardiomyocyte death is a major cytopathologic response in acute myocardial infarction (AMI) and involves complex inflammatory interactions. Although existing reports indicating that mixed lineage kinase domain-like protein (MLKL) is involved in macrophage necroptosis and inflammasome activation, the downstream mechanism of MLKL in necroptosis remain poorly characterized in AMI.

Methods: MLKL knockout mice (MLKL), RIPK3 knockout mice (RIPK3), and macrophage-specific MLKL conditional knockout mice (MLKL) were established.

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Background: As a member of the tumor necrosis factor (TNF) superfamily, tumor necrosis factor superfamily member 4 (TNFSF4) is expressed on antigen-presenting cells and activated T cells by binding to its receptor TNFRSF4. However, tumorigenicity of TNFSF4 has not been studied in pan-cancer. Therefore, comprehensive bioinformatics analysis of pan-cancer was performed to determine the mechanisms through which TNFSF4 regulates tumorigenesis.

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