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Background and Purpose: Colorectal cancer (CRC) ranks second in mortality worldwide and requires effective and affordable remedies. Cyclovirobuxine D (CVB‐D) is the main effective component of Huangyangning tablet, an approved traditional patent medicine, which is mainly used for cardiovascular treatment. As a multibioactive natural compound, CVB‐D possesses underlying anticancer activities. Experimental Approach: Cell viability and clone‐forming ability were determined in human CRC lines. Western blot, immunofluorescence assay, transmission electron microscopy and senescence‐associated β‐galactosidase (SA‐β‐Gal) staining were utilized to investigate cell autophagy and senescence. The molecular mechanisms were explored by virtual prediction and experimental validation. Patient‐derived xenograft (PDX), dextran sulfate sodium salt (DSS), and azomethane (AOM)/DSS mouse models were employed for in vivo studies. Key Results: CVB‐D inhibited the growth and development of advanced CRC cells / mice by inducing autophagic and senescent activities through the chaperonin containing TCP1 subunit 3 (CCT3)/yes‐associated protein (YAP) axis. CVB‐D acted as a promising inhibitor of CCT3 by interacting with its ATP site. In PDX tumours, CVB‐D showed potential therapeutic effects by targeting CCT3. Treatment with CVB‐D alleviated the mouse model of colitis induced by DSS and attenuated AOM/DSS‐induced formation of adenomatous polyps by its action on CCT3. Conclusions and Implications: Our study has provided a scientific basis for the suggestion that CVB‐D may be recognized as a prospective drug candidate for the therapy of CRC in patients. [ABSTRACT FROM AUTHOR]

Cardiovascular and cerebrovascular diseases (CCVDs) significantly contribute to global mortality and morbidity due to their complex pathogenesis involving multiple biological processes. Ferroptosis is an important physiological process in CCVDs, manifested by an abnormal increase in intracellular iron concentration. MiRNAs, a key class of noncoding RNA molecules, are crucial in regulating CCVDs through pathways like glutathione–glutathione peroxidase 4, glutamate/cystine transport, iron metabolism, lipid metabolism, and other oxidative stress pathways. This article summarizes the progress of miRNAs' regulation on CCVDs, aiming to provide insights for the diagnosis and treatment of CCVDs. [ABSTRACT FROM AUTHOR]

Cardiac cine magnetic resonance imaging (MRI) is one of the important means to assess cardiac functions and vascular abnormalities. Mitigating artifacts arising during image reconstruction and accelerating cardiac cine MRI acquisition to obtain high‐quality images is important. A novel end‐to‐end deep learning network is developed to improve cardiac cine MRI reconstruction. First, a U‐Net is adopted to obtain the initial reconstructed images in k‐space. Further to remove the motion artifacts, the motion‐guided deformable alignment (MGDA) module with second‐order bidirectional propagation is introduced to align the adjacent cine MRI frames by maximizing spatial–temporal information to alleviate motion artifacts. Finally, the multi‐resolution fusion (MRF) module is designed to correct the blur and artifacts generated from alignment operation and obtain the last high‐quality reconstructed cardiac images. At an 8× acceleration rate, the numerical measurements on the ACDC dataset are structural similarity index (SSIM) of 78.40% ± 4.57%, peak signal‐to‐noise ratio (PSNR) of 30.46 ± 1.22 dB, and normalized mean squared error (NMSE) of 0.0468 ± 0.0075. On the ACMRI dataset, the results are SSIM of 87.65% ± 4.20%, PSNR of 30.04 ± 1.18 dB, and NMSE of 0.0473 ± 0.0072. The proposed method exhibits high‐quality results with richer details and fewer artifacts for cardiac cine MRI reconstruction on different accelerations. [ABSTRACT FROM AUTHOR]

Left ventricular hypertrophy (LVH) is a common clinical manifestation associated with cardiovascular adverse events. Relying solely on the subjective judgment, it is challenging to promptly and accurately diagnose mild LVH. Quantitatively measuring the interventricular septum and left ventricular posterior wall to diagnose mild LVH is a time‐consuming and labor‐intensive process that is prone to errors. To propose a novel method for rapid and automatic end‐to‐end diagnosis of mild LVH. We propose a novel end‐to‐end automated method for detecting mild LVH. This method achieves rapid end‐to‐end detection of mild LVH in echocardiographic videos without the need for quantitative measurements. Initially, representative frames are extracted from echocardiographic videos, and these frames are then automatically diagnosed by the proposed network to detect LVH. The network architecture primarily consists of three key components: a feature extractor, bidirectional LSTM, and attention module. The Vit‐b model achieved 88% video classification accuracy in the experiment where 32 frames are extracted, and the ViT‐l model achieves 92% video classification accuracy in the experiment where 16 frames are extracted. It is shown experimentally that extracting fewer video frames can diagnose LVH more accurately. The experiments illustrate the superior performance and competitiveness of this method compared to other approaches, potentially applicable to the clinic. [ABSTRACT FROM AUTHOR]

Controlling the collective behavior of micro/nanomotors with ultrasound may enable new functionality in robotics, medicine, and other engineering disciplines. Currently, various collective behaviors of nanomotors, such as assembly, reconfiguration, and disassembly, have been explored by using acoustic fields with a fixed frequency, while regulating their collective behaviors by varying the ultrasound frequency still remains challenging. In this work, we designed an ultrasound manipulation methodology that allows nanomotors to exhibit different collective behaviors by regulating the applied ultrasound frequency. The experimental results and FEM simulations demonstrate that the secondary ultrasonic waves produced from the edge of the sample cell lead to the formation of complex acoustic pressure fields and microfluidic patterns, which causes these collective behaviors. This work has important implications for the design of artificial actuated nanomotors and optimize their performances. [ABSTRACT FROM AUTHOR]

Dermal fibroblasts (dFBs) defend against deep bacterial skin infections by differentiating into preadipocytes (pAds) that produce the antimicrobial peptide cathelicidin; this differentiation is known as the dermal reactive adipogenesis response. However, the role of dFBs in fungal infection remains unknown. Here, we found that cathelicidin-producing pAds were present in high numbers in skin lesions from patients with cutaneous Candida granulomas. Second, we showed that dermal Candida albicans (C. albicans) infection in mice robustly triggered the dermal reactive adipogenesis response and induced cathelicidin expression, and inhibition of adipogenesis with pharmacological inhibitors of peroxisome proliferator–activated receptor γ (PPARγ) impaired skin resistance to C. albicans. In vitro, C. albicans products induced cathelicidin expression in pAds, and differentiating pAds markedly suppressed the growth of C. albicans by producing cathelicidin. Finally, we showed that C. albicans induced an antimicrobial response in pAds through the FGFR-MEK-ERK pathway. Together, our data reveal a previously unknown role of dFBs in the defense against skin infection caused by C. albicans. Author summary: Candida albicans (C. albicans) is the pathogen that most commonly causes human fungal infections. It normally inhabits the skin surface, genital and/or intestinal mucosa of almost 30–70% healthy individuals. In certain instances, such as impairment of skin barrier integrity or immunosuppression, C. albicans can cause mucosal and cutaneous candidiasis. Here, we demonstrated the protective role of dermal fibroblasts against C. albicans skin infection, which is previously unknown. Firstly, we found that the number of cathelicidin-producing preadipocytes (pAds) increased in both human and mouse skin lesions infected with C. albicans, indicating that C. albicans infection triggers a dermal reactive adipogenesis response. Furthermore, we found inhibiting adipogenesis by administration of pharmacological inhibitors of peroxisome proliferator–activated receptor γ, or suppressing cathelicidin expression, impaired skin resistance to C. albicans. Finally, we showed that pAds produced cathelicidin through the FGFR-MEK-ERK pathway in response to C. albicans infection. Our results could provide new therapeutic strategies for the treatment of deep cutaneous candidiasis. [ABSTRACT FROM AUTHOR]