Nanobubbles, which have the potential for ultrasonic targeted imaging and treatment in tumors, have been a research focus in recent years. With the current methods, however, the prepared uniformly sized nanobubbles either undergo post-formulation manipulation, such as centrifugation, after the mixture of microbubbles and nanobubbles, or require the addition of amphiphilic surfactants. These processes influence the nanobubble stability, possibly create material waste and complicate the preparation process. In the present work, we directly prepared uniformly sized nanobubbles by modulating the thickness of a phospholipid film without the purification processes or the addition of amphiphilic surfactants. The fabricated nanobubbles from the optimal phospholipid film thickness exhibited optimal physical characteristics, such as uniform bubble size, good stability and low toxicity. We also evaluated the enhanced imaging ability of the nanobubbles both in vitro and in vivo. The in vivo enhancement intensity in the tumor was stronger than that of SonoVue after injection (UCA; 2 min: 162.47 ± 8.94 dB vs. 132.11 ± 5.16 dB, P < 0.01; 5 min: 128.38.47 ± 5.06 dB vs. 68.24 ± 2.07 dB, P < 0.01). Thus, the optimal phospholipid film thickness can lead to nanobubbles that are effective for tumor imaging.

Background: Several cardiovascular risk factors have been suggested to be associated with anthracycline-induced cardiotoxicity, but their quantitative effects have not reached a consensus.Methods: We searched PubMed, EMBASE, and Cochrane Library databases for manuscripts published from inception to February 2021, which reported the results of cardiotoxicity due to anthracycline chemotherapy without trastuzumab. Cardiotoxicity defined by any reduction of left ventricular eject fraction (LVEF) to below 50% or a >10% reduction from baseline was defined as the primary endpoint. Odd ratios (OR) with 95% confidence intervals (CI) were calculated using a random-effects model meta-analysis.Results: A total of 7,488 patients receiving anthracycline chemotherapy without trastuzumab were included, who had at least one risk factor at baseline. Hypertension (OR: 1.99; 95% CI: 1.43–2.76), diabetes mellitus (OR: 1.74; 95% CI: 1.11–2.74), and obesity (OR: 1.72; 95% CI: 1.13–2.61) were associated with increased risk of cardiotoxicity. In addition, the relative reduction of global longitudinal strain (GLS) from baseline after anthracycline treatment could significantly improve the detection ability of cardiotoxicity (28.5%, 95% CI: 22.1–35.8% vs. 16.4%, 95% CI: 13.4–19.9%) compared with LVEF. The early detection rate of anthracycline-induced cardiotoxicity (3 months after chemotherapy) by GLS was 30.2% (95% CI: 24.9–36.1%), which is similar with the overall result of GLS.Conclusions: Hypertension, diabetes mellitus, and obesity are associated with increased risk of anthracycline-induced cardiotoxicity, which indicates that corresponding protective strategies should be used during and after anthracycline treatment. The findings of higher detection rate and better early detection ability for cardiotoxicity than LVEF added new proofs for the advantages of GLS in detection of AIC.

Background: Clearance of apoptotic cells by efferocytosis is crucial for prevention of atherosclerosis progress, and impaired efferocytosis contributes to the aggravated atherosclerosis. Results: In this study, we found that diabetic ApoE^–/– mice showed aggravated atherosclerosis as hyperglycemia damaged the efferocytosis capacity at least partially due to decreased expression of Mer tyrosine kinase (MerTK) on macrophages. To locally restore MerTK in the macrophages in the plaque, hybrid membrane nanovesicles (HMNVs) were thus developed. Briefly, cell membrane from MerTK overexpressing RAW264.7 cell and transferrin receptor (TfR) overexpressing HEK293T cell were mixed with DOPE polymers to produce nanovesicles designated as HMNVs. HMNVs could fuse with the recipient cell membrane and thus increased MerTK in diabetic macrophages, which in turn restored the efferocytosis capacity. Upon intravenous administration into diabetic ApoE^–/– mice, superparamagnetic iron oxide nanoparticles (SMN) decorated HMNVs accumulated at the aorta site significantly under magnetic navigation, where the recipient macrophages cleared the apoptotic cells efficiently and thus decreased the inflammation. Conclusions: Our study indicates that MerTK decrease in macrophages contributes to the aggravated atherosclerosis in diabetic ApoE^–/– mice and regional restoration of MerTK in macrophages of the plaque via HMNVs could be a promising therapeutic approach. Graphic

Objective: Whether arterial elasticity is reduced in pre‐eclampsia has been investigated only rarely. This study aimed to characterize in vivo the carotid arterial intima–media thickness (IMT) and mechanical properties in women with pre‐eclampsia by employing a radiofrequency ultrasound technique.Methods: We included 22 late‐onset pre‐eclamptic pregnant women and 28 normotensive pregnant women who were matched for age (29 ± 6 vs 27 ± 3, P = 0.09) and gestational age (36.0 ± 3.2 vs 35.8 ± 2.4 weeks, P = 0.802). All women were nulliparous with singleton pregnancy. The pre‐eclamptic women had a significantly higher arterial pressure than did the normotensive women (P < 0.0001). All women underwent right common carotid arterial measurements with an ultrasound machine equipped with automatic Quality IMT (QIMT) and Quality Arterial Stiffness (QAS) capability. At follow‐up examination 18 months after parturition, measurements were repeated in 10 of the pre‐eclamptic women and 11 of the normotensive women.Results: In pre‐eclamptic compared with normotensive pregnancy, carotid arterial IMT (459 ± 95 vs 351 ± 85 µm, P = 0.0001), internal diameter (7.8 ± 0.5 vs 7.2 ± 0.4 mm, P < 0.0001), pulse wave velocity (7.1 ± 1.7 vs 6.0 ± 1.5 m/s, P = 0.007), augmentation index (7.9 ± 9.2 vs −5.0 ± 5.6%, P < 0.0001) and arterial wall tension (55.0 ± 6.5vs 38.6 ± 4.9 mmHg/cm, P < 0.0001) were significantly greater, and the distensibility coefficient (0.020 ± 0.009 vs 0.029 ± 0.011 1/kPa, P = 0.006) was significantly smaller, remaining so after adjusting for body mass index and carotid arterial pressure. Eighteen months after parturition, carotid arterial internal diameter, pressure and wall tension remained greater in the pre‐eclamptic group.Conclusion: Carotid arterial remodeling, including changes in arterial internal diameter and wall thickness, and arterial stiffening occur in pre‐eclampsia but this may reverse, to some extent, postpartum. QIMT and QAS techniques together could provide a comprehensive assessment of carotid arterial remodeling. Copyright © 2013 ISUOG. Published by John Wiley & Sons Ltd.