Deletion of stimulator of interferons genes aggravated cardiac dysfunction in physiological aged mice.

Background: Stimulator of interferons genes (STING) is crucial for innate immune response. It has been demonstrated that cGAS-STING pathway was the driver of aging-related inflammation. However, whether STING is involved in cardiac dysfunction during the physiological aging process remains unclear.

A deep belief rule base-based fault diagnosis method for complex systems.

Complex systems are prone to faults due to their intricate structures, potentially impacting system stability. Therefore, fault diagnosis has become crucial for maintaining stable operation. In the field of complex systems, the combinatorial explosion problem in belief rule base (BRB) has attracted significant attention.

Multilocular thymic cysts can be easily misdiagnosed as malignant tumor on computer tomography: A case report.

Background: Multilocular thymic cyst (MTC) is a rare mediastinal lesion which is considered to occur in the process of acquired inflammation. It is usually characterized by well-defined cystic density and is filled with transparent liquid.

Case Summary: We report on a 39-year-old male with a cystic-solid mass in the anterior mediastinum.

Deficiency of S100A8/A9 attenuates pulmonary microvascular leakage in septic mice.

Background: We have reported a positive correlation between S100 calcium-binding protein (S100) A8/S100A9 and sepsis-induced lung damage before. However, limited knowledge exists concerning the biological role of S100A8/A9 in pulmonary vascular endothelial barrier dysfunction, as well as the diagnostic value of S100A8/A9 in sepsis.

Methods: Sepsis was induced in C57BL/6J mice and S100A9-knockout (KO) mice through the cecal ligation and puncture (CLP).

iNOS aggravates pressure overload-induced cardiac dysfunction via activation of the cytosolic-mtDNA-mediated cGAS-STING pathway.

Sterile inflammation contributes to the pathogenesis of cardiac dysfunction caused by various conditions including pressure overload in hypertension. Mitochondrial DNA (mtDNA) released from damaged mitochondria has been implicated in cardiac inflammation. However, the upstream mechanisms governing mtDNA release and how mtDNA activates sterile inflammation in pressure-overloaded hearts remain largely unknown.

Deficiency of S100 calcium binding protein A9 attenuates vascular dysfunction in aged mice.

Background: S100 calcium-binding protein A9 (S100A9) is a danger-associated molecular pattern molecule that mediates the inflammatory response. Inflammation is essential in aging-related cardiovascular diseases. However, less is known regarding the role of S100A9 in vascular aging.

S100A9 blockade prevents lipopolysaccharide-induced lung injury via suppressing the NLRP3 pathway.

Background: S100 calcium binding protein A9 (S100A9) is a pro-inflammatory alarmin associated with several inflammation-related diseases. However, the role of S100A9 in lung injury in sepsis has not been fully investigated. Therefore, the present study aimed to determine the role of S100A9 in a lipopolysaccharide (LPS)-induced lung injury murine model and its underlying molecular mechanisms.

Quenching of the electrochemiluminescence of tris(2,2'-bipyridine)-ruthenium(II) by sodium diphenylamine-4-sulfonate.

Efficient quenching electrochemiluminescence (ECL) of the tris(2,2'-bipyridine)ruthenium(II)/tripropylamine (Ru(bpy)(3)(2+)/TPrA) system by a novel quencher, sodium diphenylamine-4-sulfonate (SDS), has been investigated. The quenching behaviors can be observed with a 100-fold excess of SDS over Ru(bpy)(3)(2+). The mechanism of quenching is believed to involve energy transfer from the excited-state Ru(bpy)(3)(2+*) to the dimer of SDS, which was formed after the electrochemical oxidation of SDS at the electrode surface.