Implementation and Evaluation of Spatial Attention Mechanism in Apricot Disease Detection Using Adaptive Sampling Latent Variable Network.

In this study, an advanced method for apricot tree disease detection is proposed that integrates deep learning technologies with various data augmentation strategies to significantly enhance the accuracy and efficiency of disease detection. A comprehensive framework based on the adaptive sampling latent variable network (ASLVN) and the spatial state attention mechanism was developed with the aim of enhancing the model's capability to capture characteristics of apricot tree diseases while ensuring its applicability on edge devices through model lightweighting techniques. Experimental results demonstrated significant improvements in precision, recall, accuracy, and mean average precision (mAP). Specifically, precision was 0.92, recall was 0.89, accuracy was 0.90, and mAP was 0.91, surpassing traditional models such as YOLOv5, YOLOv8, RetinaNet, EfficientDet, and DEtection TRansformer (DETR). Furthermore, through ablation studies, the critical roles of ASLVN and the spatial state attention mechanism in enhancing detection performance were validated. These experiments not only showcased the contributions of each component for improving model performance but also highlighted the method's capability to address the challenges of apricot tree disease detection in complex environments. Eight types of apricot tree diseases were detected, including Powdery Mildew and Brown Rot, representing a technological breakthrough. The findings provide robust technical support for disease management in actual agricultural production and offer broad application prospects.

Unveiling the Impact of Hemodynamics on Endothelial Inflammation-Mediated Hepatocellular Carcinoma Metastasis Using a Biomimetic Vascular Flow Model.

Hepatocellular carcinoma (HCC) hematogenous dissemination is a leading cause of HCC-related deaths. The inflammatory facilitates this process by promoting the adhesion and invasion of tumor cells in the circulatory system. But the contribution of hemodynamics to this process remains poorly understood due to the lack of a suitable vascular flow model for investigation. This study develops a vascular flow model to examine the impact of hemodynamics on endothelial inflammation-mediated HCC metastasis. This work finds the increasing shear stress will reduce the recruitment of HCC cells by disturbing adhesion forces between endothelium and HCC cells. However, this reduction will be restored by the inflammation. When applying high FSS (4-6 dyn cm-2) to the inflammatory endothelium, there will be a 4.8-fold increase in HCC cell adhesions compared to normal condition. Nevertheless, the increase fold of cell adhesions is inapparent, around 1.5-fold, with low and medium FSS. This effect can be attributed to the FSS-induced upregulation of ICAM-1 and VCAM-1 of the inflammatory endothelium, which serve to strengthen cell binding forces. These findings indicate that hemodynamics plays a key role in HCC metastasis during endothelial inflammation by regulating the expression of adhesion-related factors.

[Extracellular Matrix Stiffness Induces Mitochondrial Morphological Heterogeneity via AMPK Activation]. / 细胞外基质硬度通过AMPK调控干细胞线粒体的形态异质性.

Objective: To investigate the mechanical responses of mitochondrial morphology to extracellular matrix stiffness in human mesenchymal stem cells (hMSCs) and the role of AMP-activated protein kinase (AMPK) in the regulation of mitochondrial mechanoresponses. Methods: Two polyacrylamide (PAAm) hydrogels, a soft one with a Young's modulus of 1 kPa and a stiff one of 20 kPa, were prepared by changing the monomer concentrations of acrylamide and bis-acrylamide. Then, hMSCs were cultured on the soft and stiff PAAm hydrogels and changes in mitochondrial morphology were observed using a laser confocal microscope. Western blot was performed to determine the expression and activation of AMPK, a protein associated with mitochondrial homeostasis. Furthermore, the activation of AMPK was regulated on the soft and stiff matrixes by AMPK activator A-769662 and the inhibitor Compound C, respectively, to observe the morphological changes of mitochondria. Results: The morphology of the mitochondria in hMSCs showed heterogeneity when there was a change in gel stiffness. On the 1 kPa soft matrix, 74% mitochondria exhibited a dense, elongated filamentous network structure, while on the 20 kPa stiff matrix, up to 63.3% mitochondria were fragmented or punctate and were sparsely distributed. Western blot results revealed that the phosphorylated AMPK (p-AMPK)/AMPK ratio on the stiff matrix was 1.6 times as high as that on the soft one. Immunofluorescence assay results revealed that the expression of p-AMPK was elevated on the hard matrix and showed nuclear localization, which indicated that the activation of intracellular AMPK increased continuously along with the increase in extracellular matrix stiffness. When the hMSCs on the soft matrix were treated with A-769662, an AMPK activator, the mitochondria transitioned from a filamentous network morphology to a fragmented morphology, with the ratio of filamentous network decreasing from 74% to 9.5%. Additionally, AMPK inhibition with Compound C promoted mitochondrial fusion on the stiff matrix and significantly reduced the generation of punctate mitochondria. Conclusion: Extracellular matrix stiffness regulates mitochondrial morphology in hMSCs through the activation of AMPK. Stiff matrix promotes the AMPK activation, resulting in mitochondrial fission and the subsequent fragmentation of mitochondria. The impact of matrix stiffness on mitochondrial morphology can be reversed by altering the level of AMPK phosphorylation.

AnnexinA6: a potential therapeutic target gene for extracellular matrix mineralization.

The mineralization of the extracellular matrix (ECM) is an essential and crucial process for physiological bone formation and pathological calcification. The abnormal function of ECM mineralization contributes to the worldwide risk of developing mineralization-related diseases; for instance, vascular calcification is attributed to the hyperfunction of ECM mineralization, while osteoporosis is due to hypofunction. AnnexinA6 (AnxA6), a Ca2+-dependent phospholipid-binding protein, has been extensively reported as an essential target in mineralization-related diseases such as osteoporosis, osteoarthritis, atherosclerosis, osteosarcoma, and calcific aortic valve disease. To date, AnxA6, as the largest member of the Annexin family, has attracted much attention due to its significant contribution to matrix vesicles (MVs) production and release, MVs-ECM interaction, cytoplasmic Ca2+ influx, and maturation of hydroxyapatite, making it an essential target in ECM mineralization. In this review, we outlined the recent advancements in the role of AnxA6 in mineralization-related diseases and the potential mechanisms of AnxA6 under normal and mineralization-related pathological conditions. AnxA6 could promote ECM mineralization for bone regeneration in the manner described previously. Therefore, AnxA6 may be a potential osteogenic target for ECM mineralization.

ML323, a USP1 inhibitor triggers cell cycle arrest, apoptosis and autophagy in esophageal squamous cell carcinoma cells.

Esophageal squamous cell carcinoma (ESCC) is a common digestive cancer with high mortality rate due to late diagnosis and drug resistance. It is important to identify new molecular target and develop new anticancer strategy. ML323 is a novel USP1 inhibitor and exhibits anticancer activity against several cancers. Herein, we investigated whether ML323 has some cytotoxity effect on ESCC cells and explored the underlying mechanisms. Results revealed that ML323 impeded esophageal cancer cell viability and colony formation. Meanwhile, ML323 blocked cells at G0/G1 phase concomitant with the reduced protein level of c-Myc, cyclin D1, CDK4 and CDK6. ML323 treatment also triggered DNA damage and active p53. Then, ML323 induced apoptosis by p53-Noxa. Additionally, it stimulated protective autophagy. Co-treatment with CQ or BafA1, two classical autophagy inhibitors, enhanced the cytotoxity of ML323. These findings suggested that USP1 inhibitor (ML323) could be used as a viable anti-ESCC approach.

Expert consensus workshop report: Guidelines for thermal ablation of thyroid tumors (2019 edition).

As a treatment option for cancer, thermal ablation has satisfactory effects on many types of solid tumors (such as liver and renal cancers). However, its clinical applications for the treatment of thyroid nodules and metastatic cervical lymph nodes are still under debate both in China and abroad. In 2015, the "Zhejiang Expert consensus on thermal ablation for thyroid benign nodules, microcarcinoma, and metastatic cervical lymph nodes (2015 edition)," was released by the Thyroid Cancer Committee of Zhejiang Anti-Cancer Association, China. To further standardize the application of thermal ablation for thyroid tumors, the Thyroid Tumor Ablation Experts Group of Chinese Medical Doctor Association has organized many seminars and finally produced a consensus to formulate the "Expert consensus workshop report: Guidelines for thermal ablation of thyroid tumors (2019 edition)."

[The effect of nuclear transcription factor-kappaB decoy oligodeoxynucleotides on the intimal hyperplasia in vein graft].

OBJECTIVE: To investigate the effect of nuclear transcription factor-kappaB decoy oligodeoxynucleotides (NFkappaB decoyODNs) on the intimal hyperplasia (IH) in vein graft in rats. METHODS: Autogenous vein graft model for 72 Wistar rats was established, and the interior jugular vein was transplanted to common jugular artery by microsurgical technique. The rats were divided into 6 groups according to different processing methods, including NFkappaB decoyODNs 50 microg and 200 microg, scramble decoyODNs 50 microg and 200 microg, control and lipofectin + pluronic teams. Vein graft samples were harvested in 1 or 2 weeks after surgery and ICAM-1 mRNA were measured by RT-PCR. Western blotting and immunohistochemistry methods were also employed to detect the expression of p65 and ICAM-1. IH was compared at the same time. RESULTS: The intimal hyperplasia was evident in 1 or 2 weeks after vein graft, and ameliorated by 50 microg of NFkappaB decoyODNs with inhibition rate from 22% to 31%, 200 microg of NFkappaB decoyODNs had a higher inhibition rate from 41% to 53%. However, no effect was found in the other teams. The expression of ICAM-1 mRNA was also inhibited significantly by NFkappaB decoyODNs and more obvious in 2 weeks after surgery. Expression of ICAM-1 and p65 decreased greatly in NFkappaB decoyODNs team, which has a inhibition rate from 30% to 57%. CONCLUSION: Transfection of NFkappaB decoyODNs can inhibit the IH after vein graft, which may be accomplished by the inhibition of gene expression of ICAM-1.