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Magnetic nanomotors (MNMs), powered by a magnetic field, are ideal platforms to achieve versatile biomedical applications in a collective and spatio­temporal fashion. Although the programmable swarm of MNMs that mimics the highly ordered behaviors of living creatures has been extensively studied at the microscale, it is of vital importance to manipulate MNM swarms at the nanoscale for on-demand tasks at the cellular level. In this work, a Cy5-tagged caspase-3-specific peptide-modified MNM is designed, and the adaptive control behaviors of MNM swarms are revealed in lysosomes to induce the cancer cell apoptosis under a rotating magnetic field (RMF). A magneto-programmed vortex is predicted to occur with swarms under RMF by the finite element method model and verified in vitro. According to the dynamic model and numerical simulation, the critical rotating frequency under which MNMs are out of step is strongly correlated to their assembling and swarming properties. The adaptivity of swarms maximizes the synchronous rotation to achieve an optimal energy conversion rate. The frequency-adapted controllability of MNM swarms for cancer cell apoptosis is observed in real time in vitro and in vivo. This work provides theoretical and experimental insights to adaptively control MNM swarms for cancer treatment.

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Code-switching has become a common linguistic phenomenon. Comparing to monolingual ASR tasks, insufficient data is a major challenge for code-switching speech recognition. In this paper, we propose an approach to compositionally employ the Bidirectional Encoder Representations from Transformers (Bert) model and Generative Adversarial Net (GAN) model for code-switching text data generation. It improves upon previous work by (1) applying Bert as a masked language model to predict the mixed-in foreign words and (2) basing on the GAN framework with Bert for both the generator and discriminator to further assure the generated sentences similar enough to the natural examples. We evaluate the effectiveness of the generated data by its contribution to ASR. Experiments show our approach can reduce the English word error rate by 1.5% with the Mandarin-English code-switching spontaneous speech corpus OC16-CE80.

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Implantation of leadless pacemaker is efficacy and safety compared with the traditional pacemaker in structurally normal hearts. However, delivery experience of leadless pacemaker in patients with severe right heart enlargement remains limited. We present the rare case of a patient with giant right heart and moderate to severe tricuspid regurgitation implanted with a leadless Micra transcatheter pacemaker system. The extension of the Micra delivery catheter can be improved by using a single‐loop snare on the catheter proximal to appropriate right ventricle (RV) pacing position. The snare‐kissing‐catheter technique can aid in successful deployment in the setting of challenging right heart enlargement.

Purpose Macrophage apoptosis coupled with a defective phagocytic clearance of the apoptotic cells promotes plaque necrosis in advanced atherosclerosis, which causes acute atherothrombotic vascular disease. Nonsteroidal anti-inflammatory drug sulindac derivative K-80003 treatment was previously reported to dramatically attenuate atherosclerotic plaque progression and destabilization. However, the underlying mechanisms are not fully understood. This study aimed to determine the role of K-80003 on macrophage apoptosis and elucidate the underlying mechanism. Methods The mouse model of vulnerable carotid plaque in ApoE−/− mice was developed in vivo. Consequently, mice were randomly grouped into two study groups: the control group and the K-80003 group (30 mg/kg/day). Samples of carotid arteries were collected to determine atherosclerotic necrotic core area, cellular apoptosis, and oxidative stress. The effects of K-80003 on RAW264.7 macrophage apoptosis, oxidative stress, and autophagic flux were also examined in vitro. Results K-80003 significantly suppressed necrotic core formation and inhibited cellular apoptosis of vulnerable plaques. K-80003 can also inhibit 7-ketocholesterol-induced macrophage apoptosis in vitro. Furthermore, K-80003 inhibited intraplaque cellular apoptosis mainly through the suppression of oxidative stress, which is a key cause of advanced lesional macrophage apoptosis. Mechanistically, K-80003 prevented 7-ketocholesterol-induced impairment of autophagic flux in macrophages, evidenced by the decreased LC3II and SQSTM1/p62 expression, GFP-RFP-LC3 cancellation upon K-80003 treatment. Conclusion Inhibition of macrophage apoptosis and necrotic core formation by autophagy-mediated reduction of oxidative stress is one mechanism of the suppression of plaque progression and destabilization by K-80003.

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