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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]

Unsatisfactory post‐stroke recovery has long been a negative factor in the prognosis of ischemic stroke due to the lack of pharmacological treatments. Mesenchymal stem cells (MSCs)‐based therapy has recently emerged as a promising strategy redefining stroke treatment; however, its effectiveness has been largely restricted by insufficient therapeutic gene expression and inadequate cell numbers in the ischemic cerebrum. Herein, a non‐viral and magnetic field‐independent gene transfection approach is reported, using magnetosome‐like ferrimagnetic iron oxide nanochains (MFIONs), to genetically engineer MSCs for highly efficient post‐stroke recovery. The 1D MFIONs show efficient cellular uptake by MSCs, which results in highly efficient genetic engineering of MSCs to overexpress brain‐derived neurotrophic factor for treating ischemic cerebrum. Moreover, the internalized MFIONs promote the homing of MSCs to the ischemic cerebrum by upregulating CXCR4. Consequently, a pronounced recovery from ischemic stroke is achieved using MFION‐engineered MSCs in a mouse model. [ABSTRACT FROM AUTHOR]