An artificial intelligence model based on the American College of Radiology Thyroid Imaging Reporting and Data System was developed to differentiate between malignant and benign nodules as well as ... Background US-based diagnosis of thyroid nodules is subjective and influenced by radiologists’ experience levels. Purpose To develop an artificial intelligence model based on American College of Ra...

Stem cell-based tissue engineering has provided a promising platform for repairing of bone defects. However, the use of exogenous bone marrow mesenchymal stem cells (BMSCs) still faces many challenges such as limited sources and potential risks. It is important to develop new approach to effectively recruit endogenous BMSCs and capture them for in situ bone regeneration. Here, we designed an acoustically responsive scaffold (ARS) and embedded it into SDF-1/BMP-2 loaded hydrogel to obtain biomimetic hydrogel scaffold complexes (BSC). The SDF-1/BMP-2 cytokines can be released on demand from the BSC implanted into the defected bone via pulsed ultrasound (p-US) irradiation at optimized acoustic parameters, recruiting the endogenous BMSCs to the bone defected or BSC site. Accompanied by the daily p-US irradiation for 14 days, the alginate hydrogel was degraded, resulting in the exposure of ARS to these recruited host stem cells. Then another set of sinusoidal continuous wave ultrasound (s-US) irradiation was applied to excite the ARS intrinsic resonance, forming highly localized acoustic field around its surface and generating enhanced acoustic trapping force, by which these recruited endogenous stem cells would be captured on the scaffold, greatly promoting them to adhesively grow for in situ bone tissue regeneration. Our study provides a novel and effective strategy for in situ bone defect repairing through acoustically manipulating endogenous BMSCs.

Rationale: Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic inflammation and damage to articular tissues that can lead to irreversible joint damage and progressive disability. The multipotent mesenchymal stem cells (MSCs) play an important role in immune disorders and tissue regeneration. However, their immunosuppressive effects and the underlying mechanisms are largely unclear due to the lack of tools for real-time imaging of MSCs in vivo. Gas vesicles (GVs) are biosynthetic nanobubbles that are ejected from aquatic microbes, such as bacteria and archaea, and have an excellent ultrasound imaging capacity.

Previous studies showed that radiofrequency ablation (RFA) has a favorable treatment efficacy for hepatocellular carcinoma (HCC) or colorectal liver metastases (CRLMs). Palliative RFA (pRFA) resulting from larger HCC or multiple CRLMs further accelerated the progression of potential residual tumor, yet its mechanism was still unknown. This study investigated the influence of myeloid-derived suppressor cells (MDSCs) on T-cell immune responses and tumor recurrence after pRFA. CT26 tumor models were used. The percentage of MDSCs in peripheral blood was analyzed by flow cytometry after pRFA. The level of Th1 and Th2 cytokines were measured by ELISA through different treatments (n = 4/group). The tumor-infiltrating MDSCs, dendritic cells, and intracellular cytokines level were analyzed by IHC staining after different treatments. The functional CD8⁺ T cells were confirmed by the co-localization immunofluorescence staining. The long-term outcomes were also evaluated through CT26 and 4T1 tumor models. The results showed that tumor models treated with pRFA displayed significant increases in the percentage of MDSCs of peripheral blood and tumor infiltration. The expression level of TGF-β and IL-6 after pRFA was higher than that before pRFA by ELISA and IHC staining. After depleting MDSCs by combining with Abs, the pRFA + Abs group achieved a higher level of Th1 cytokines and greatly enhanced the percentage of tumor-infiltrating functional CD8⁺ T cells when compared with pRFA alone. The depletion of MDSCs through combination with Abs also resulted in tumor regression. In conclusion, pRFA accelerates the residual tumor progression through increasing tumor-infiltrating MDSCs and reducing T-cell-mediated anti-tumor immune responses, which could provide a potential approach for delaying tumor recurrence caused by pRFA.