Traditional diagnosis relies on identifying anatomical abnormality, which offers a stage for various anatomical imaging techniques, such as X-ray computed tomography (CT), ultrasonic imaging, and magnetic resonance imaging (MRI). The good capacity of providing anatomical details, especially for soft tissues, popularizes the clinical use of MRI. However, as the understanding of various diseases reaches the molecular level, it is gradually accepted that molecular anomaly often precedes anatomical abnormality. Therefore, molecular imaging, which is aimed at gathering various molecular information in organisms via imaging, starts to gain momentum. Unfortunately, traditional MRI is not capable of molecular imaging. As a result, there is an urgent demand for probes that enable MRI to "see" molecules. A promising design strategy for these probes is to elicit a signal change triggered by the presence of molecular targets, i.e. activation. Benefiting from the rapid development of nanotechnology, a number of nanoparticle-based activatable MRI probes have been developed for molecular imaging. This review summarizes recent advances of activatable MRI nanoprobes for imaging pathological characteristics of cancer, inflammation, and neurodegenerative diseases, with a focus on the design strategies and applications of these probes. In addition, the prospects and challenges of activatable MRI nanoprobes are also discussed.

Objective: To study the clinical efficacy of Dapagliflozin in patients with coronary heart disease (CHD) combined with Heart Failure with Reduced Ejection Fraction (HFrEF) and type 2 diabetes mellitus (T2DM) who have CHD. Methods: A retrospective analysis of 202 patients with CHD and T2DM who were hospitalized in our department of cardiovascular medicine and underwent PCI treatment from November 2019 to November 2022 was conducted. Patients were divided into two groups according to whether they received Dapagliflozin treatment: the Dapagliflozin group (n=100) and the control group (n=102). A subgroup analysis was performed on the 80 HFrEF patients in the total population, which was also divided into two groups: the Dapagliflozin group (n=44) and the control group (n=36). The incidence of major adverse cardiovascular events (MACE) during hospitalization and the median follow-up period (224.5 days) was recorded and analyzed in both the total population and the subgroup. Results: The results of the analysis of the total patient population showed no statistical differences between the two groups in baseline data and related clinical treatment conditions (P>0.05). The follow-up period event analysis showed that the overall MACE event rate in the Dapagliflozin group was lower than that in the control group (6.00% vs. 17.65%), but not statistically significant (P=0.071). The COX regression analysis of MACE events showed that the use of Dapagliflozin was an independent protective factor for MACE events [HR=0.166, 95% CI (0.026-0.953), P=0.047]. In the HFrEF subgroup analysis, there was no significant difference between the two groups in the baseline data analysis (P>0.05). The COX regression analysis in the subgroup analysis showed that the use of Dapagliflozin was a strong protective factor for the HFrEF subgroup during the follow-up period [HR=0.250, 95% CI (0.017-0.518), P<0.001]. Further analysis using the Kaplan-Meier method showed that the event rate in the Dapagliflozin group was significantly lower than that in the control group. Conclusion: The use of Dapagliflozin in patients with CHD combined with HFrEF and T2DM may be effective in reducing the incidence of MACE.

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