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Snake venom-secreted phospholipases A (svPLAs) are critical, highly toxic enzymes present in almost all snake venoms. Upon snakebite envenomation, svPLAs hydrolyze cell membrane phospholipids and induce pathological effects such as paralysis, myonecrosis, inflammation, or pain. Despite its central importance in envenomation, the chemical mechanism of svPLAs is poorly understood, with detrimental consequences for the design of small-molecule snakebite antidotes, which is highly undesirable given the gravity of the epidemiological data that ranks snakebite as the deadliest neglected tropical disease.

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Metabolic reprogramming occurs in cardiomyopathy and heart failure contributing to progression of the disease. Activation of cardiac Hippo pathway signaling has been implicated in mediating mitochondrial dysfunction and metabolic reprogramming in cardiomyopathy, albeit influence of Hippo pathway on lipid profile is unclear. Using a dual-omics approach, we determined alterations of cardiac lipids in a mouse model of cardiomyopathy due to enhanced Hippo signaling and explored molecular mechanisms.

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Cyanogenic glycosides are plant-derived, nitrogen-containing secondary metabolites that release toxic cyanide ions upon hydrolysis by glycosidic enzymes. Therefore, consuming food items enriched with such compounds without proper remediation can cause acute cyanide intoxication. Thus, in this work, we utilize cyanide-responsive oxidized bisindole-based chromogenic probes to detect cyanogenic glycosides, such as amygdalin and linamarin (LOD: 0.

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