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Nitric oxide-sensitive guanylyl cyclase (NO-GC) is a heterodimeric enzyme with an α- and a β-subunit. In its active form as an αβ-heterodimer, NO-GC produces cyclic guanosine-3',5'-monophophate (cGMP) to regulate vasodilation and proliferation of vascular smooth muscle cells (VSMCs). In contrast to VSMCs, only a few studies reported on the expression of the NO-GC αβ-heterodimer in human pericytes.

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The diversity and heterogeneity of biomarkers has made the development of general methods for single-step quantification of analytes difficult. For individual biomarkers, electrochemical methods that detect a conformational change in an affinity binder upon analyte binding have shown promise. However, because the conformational change must operate within a nanometer-scale working distance, an entirely new sensor, with a unique conformational change, must be developed for each analyte.

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Endocannabinoids have been shown to play a complex role in the pathophysiology of a number of cardiovascular disorders. In the present study, the effects of the two major endocannabinoids anandamide (AEA) and 2-arachidonoylglycerol (2-AG) were investigated in human coronary artery smooth muscle cells (HCASMC) and human coronary artery endothelial cells (HCAEC) with regard to potential atheroprotective and anti-inflammatory effects. In HCASMC, AEA showed an inhibitory effect on platelet-derived growth factor-induced migration, but not proliferation, independent of major cannabinoid-activatable receptors (CB, CB, TRPV1), while 2-AG left both responses unaffected.

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With the ongoing rise in the incidence of inflammatory bowel disease (IBD), its extraintestinal manifestations have garnered significant attention. IBD-related arthritis is notable for its insidious onset and unpredictability, presenting considerable challenges for clinical diagnosis and management. Factors such as gut microbiota, plasma proteins, inflammatory proteins, and biomarkers found in blood and urine may be closely associated with IBD-related arthritis.

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Objective: As a reversible condition at its early stages, liver fibrosis can progress to cirrhosis and hepatocellular carcinoma, underscoring the importance of early detection for preventing severe outcomes and improving prognosis. To address this issue, we developed a platelet-derived growth factor receptor β (PDGFRβ)-targeted nanoscale phase-change contrast agent to target activated hepatic stellate cells (aHSC) and enable ultrasound imaging as a foundation for the early evaluation of liver fibrosis.

Methods: PDGFR-β antibody-modified phase-change contrast agents (PPCAs) were synthesized utilizing film hydration and ultrasonic emulsification with perfluoropentane (PFP) encapsulated.

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