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Ultra‐high field (UHF) magnetic resonance imaging (MRI) has emerged as a focal point of interest in the field of cancer diagnosis. Despite the ability of current paramagnetic or superparamagnetic smart MRI contrast agents to selectively enhance tumor signals in low‐field MRI, their effectiveness at UHF remains inadequate due to inherent magnetism. Here, we report a ligand‐mediated magnetism‐conversion nanoprobe (MCNP) composed of 3‐mercaptopropionic acid ligand‐coated silver‐gadolinium bimetallic nanoparticles. The MCNP exhibits a pH‐dependent magnetism conversion from ferromagnetism to diamagnetism, facilitating tunable nanomagnetism for pH‐activatable UHF MRI. Under neutral pH, the thiolate (−S−) ligands lead to short τ′m and increased magnetization of the MCNPs. Conversely, in the acidic tumor microenvironment, the thiolate ligands are protonated and transform into thiol (−SH) ligands, resulting in prolonged τ′m and decreased magnetization of the MCNP, thereby enhancing longitudinal relaxivity (r1) values at UHF MRI. Notably, under a 9 T MRI field, the pH‐sensitive changes in Ag−S binding affinity of the MCNP lead to a remarkable (>10‐fold) r1 increase in an acidic medium (pH 5.0). In vivo studies demonstrate the capability of MCNPs to amplify MRI signal of hepatic tumors, suggesting their potential as a next‐generation UHF‐tailored smart MRI contrast agent. [ABSTRACT FROM AUTHOR]

Ultra-high field (UHF) magnetic resonance imaging (MRI) has emerged as a focal point of interest in the field of cancer diagnosis. Despite the ability of current paramagnetic or superparamagnetic smart MRI contrast agents to selectively enhance tumor signals in low-field MRI, their effectiveness at UHF remains inadequate due to inherent magnetism. Here, we report a ligand-mediated magnetism-conversion nanoprobe (MCNP) composed of 3-mercaptopropionic acid ligand-coated silver-gadolinium bimetallic nanoparticles. The MCNP exhibits a pH-dependent magnetism conversion from ferromagnetism to diamagnetism, facilitating tunable nanomagnetism for pH-activatable UHF MRI. Under neutral pH, the thiolate (-S - ) ligands lead to short τ' m and increased magnetization of the MCNPs. Conversely, in the acidic tumor microenvironment, the thiolate ligands are protonated and transform into thiol (-SH) ligands, resulting in prolonged τ' m and decreased magnetization of the MCNP, thereby enhancing longitudinal relaxivity (r1) values at UHF MRI. Notably, under a 9 T MRI field, the pH-sensitive changes in Ag-S binding affinity of the MCNP lead to a remarkable (>10-fold) r1 increase in an acidic medium (pH 5.0). In vivo studies demonstrate the capability of MCNPs to amplify MRI signal of hepatic tumors, suggesting their potential as a next-generation UHF-tailored smart MRI contrast agent., (© 2024 Wiley-VCH GmbH.)

Objective: To establish a stable and feasible rabbit model of cardiopulmonary bypass (CPB) in acute cerebral embolism phase for studying the effects of CPB on brain tissues and the timing of surgical intervention of acute cerebral embolism., Methods: Fifty-four rabbits were randomized into group A (n=18) to receive CPB without middle cerebral artery occlusion (MCAO) and group B to undergo CPB at 24 h (group B1, n=18) or 1 week (group B2, n=18) after MCAO. Through a supraorbital margin approach, electrocoagulation was carried out to occlude the main stem of the left MCA under direct vision to establish MCAO. Magnetic resonance imaging (MRI) was performed at both 24 h and 1 week after MCAO, and the severity of cerebral embolization was evaluated. CPB was established by cannulation of the ascending aorta and the right atrium through a median sternotomy incision. MRI was performed at 2 h after CPB to observe the brain tissues., Results: MCAO was successfully established in groups B1 and B2, and all the rabbits survived after MCAO. In both groups A and B, MRI examination detected no cerebral hemorrhage or new embolism 2 h after CPB., Conclusions: We have established a stable and feasible CPB model in rabbits with acute cerebral embolism to allow study of the mechanisms of CPB-related organ damage and its interventions.