The objective of this study is to map the global scientific competitive landscape in the field of artificial intelligence (AI) medical devices using scientific data. A bibliometric analysis was conducted using the Web of Science Core Collection to examine global research trends in AI-based medical devices. As of the end of 2023, a total of 55 147 relevant publications were identified worldwide, with 76.6% published between 2018 and 2024. Research in this field has primarily focused on AI-assisted medical image and physiological signal analysis. At the national level, China (17 991 publications) and the United States (14 032 publications) lead in output. China has shown a rapid increase in publication volume, with its 2023 output exceeding twice that of the U.S.; however, the U.S. maintains a higher average citation per paper (China: 16.29; U.S.: 35.99). At the institutional level, seven Chinese institutions and three U.S. institutions rank among the global top ten in terms of publication volume. At the researcher level, prominent contributors include Acharya U Rajendra, Rueckert Daniel and Tian Jie, who have extensively explored AI-assisted medical imaging. Some researchers have specialized in specific imaging applications, such as Yang Xiaofeng (AI-assisted precision radiotherapy for tumors) and Shen Dinggang (brain imaging analysis). Others, including Gao Xiaorong and Ming Dong, focus on AI-assisted physiological signal analysis. The results confirm the rapid global development of AI in the medical device field, with "AI + imaging" emerging as the most mature direction. China and the U.S. maintain absolute leadership in this area-China slightly leads in publication volume, while the U.S., having started earlier, demonstrates higher research quality. Both countries host a large number of active research teams in this domain.
Artificial Intelligence ; Bibliometrics ; Humans ; China ; Equipment and Supplies ; United States ; Biomedical Research

ObjectiveTo explore the intervention effect and mechanism of Buzhong Yiqiwan （BZYQ） on colitis mice. MethodSixty-four C57BL/6 mice were randomly divided into 2 weeks blank group， 2 weeks model group， 2 weeks high-dose BZYQ （12 g·kg^-1） group， 2 weeks low-dose BZYQ （6 g·kg^-1） group， 4 weeks blank group， 4 weeks model group， 4 weeks high-dose BZYQ （12 g·kg^-1） group， and 4 weeks low-dose BZYQ （6 g·kg^-1） group. The colitis model was induced in mice by feeding 3% dextran sodium sulfate （DSS） for 7 days. The mice received BZYQ （12 and 6 g·kg^-1） by gavage on the 8^th day after modeling， once per day， and sacrificed on the 2^nd and 4^th weeks， correspondingly. The colon length and weight of mice in each group were measured. Hematoxylin-eosin （HE） staining was used for pathological observation and colonic mucosal inflammation was scored. The mRNA and protein expression of NOD-like receptor thermoprotein domain 3 （NLRP3）， apoptosis-associated speck-like protein containing a CARD （ASC）， and cysteinyl aspartate-specific protease-1 （Caspase-1） was detected by real-time quantitative polymerase chain reaction （Real-time PCR） and Western blot， respectively. Enzyme-linked immunosorbent assay （ELISA） was used to detect the content of inflammatory cytokines， such as interleukin （IL）-1β， IL-18， and IL-33 in colonic tissues. ResultCompared with the 2 weeks blank group， the 2 weeks model group showed shortened colon length， increased colon weight （P<0.05）， loss of epithelial cells， destruction of gland structure， infiltration of a large number of inflammatory cells in mucosa and submucosa， local crypt abscess， and increase in mucosal inflammation score （P<0.01） as revealed by light microscopy， elevated levels of IL-1β， IL-18， and IL-33 in colonic tissues （P<0.05）， and increased mRNA and protein expression of NLRP3， ASC， and Caspase-1 （P<0.05）. The intervention of BZYQ （12 g·kg^-1） restored colon length， alleviated mucosal injury （P<0.05）， down-regulated the content of IL-18 （P<0.05）， reduced the mRNA expression of NLRP3 and ASC as well as the protein expression of ASC and Caspase-1 compared with the conditions in the 2 weeks model group. Compared with the 4 weeks blank group， the 4 weeks model group showed decreased colon length， increased colon weight （P<0.05）， decreased glands in the mucosal layer， expansion of glandular cavity， atrophy of crypt， local connective tissue hyperplasia and lymphocyte infiltration， increased inflammation score （P<0.01） as revealed by the light microscopy， increased expression of IL-1β， IL-18， and IL-33 （P<0.05）， and elevated mRNA and expression of NLRP3 inflammasome complex （P<0.05）. Compared with the conditions in the 4 weeks model group， the intervention of BZYQ （12 and 6 g·kg^-1） could improve colon length and weight （P<0.05）， and the intervention of BZYQ （12 g·kg^-1） could also improve the inflammation score of the colon （P<0.05）. Different from the acute stage， the intervention of BZYQ （12 and 6 g·kg^-1） increased the content of IL-33 in the intestinal mucosa and up-regulated the mRNA and protein expression of NLRP3 inflammasome complexes ASC and Caspase-1 （P<0.05）. ConclusionBZYQ can relieve the injury of colitis induced by DSS in mice. The mechanism is related to the regulation of intestinal immune response mediated by NLRP3 inflammasome， and it has different regulatory effects in acute and chronic inflammation stages.

Despite considerable progresses in cancer treatment, tumor metastasis is still a thorny issue, which leads to majority of cancer-related deaths. In hematogenous metastasis, the concept of "seed and soil" suggests that the crosstalk between cancer cells (seeds) and premetastatic niche (soil) facilitates tumor metastasis. Considerable efforts have been dedicated to inhibit the tumor metastatic cascade, which is a highly complicated process involving various pathways and biological events. Nonetheless, satisfactory therapeutic outcomes are rarely observed, since it is a great challenge to thwart this multi-phase process. Recent advances in nanotechnology-based drug delivery systems have shown great potential in the field of anti-metastasis, especially compared with conventional treatment methods, which are limited by serious side effects and poor efficacy. In this review, we summarized various factors involved in each phase of the metastatic cascade ranging from the metastasis initiation to colonization. Then we reviewed current approaches of targeting these factors to stifle the metastatic cascade, including modulating primary tumor microenvironment, targeting circulating tumor cells, regulating premetastatic niche and eliminating established metastasis. Additionally, we highlighted the multi-phase targeted drug delivery systems, which hold a better chance to inhibit metastasis. Besides, we demonstrated the limitation and future perspectives of nanomedicine-based anti-metastasis strategies.