RingMo-lite: A Remote Sensing Multi-task Lightweight Network with CNN-Transformer Hybrid Framework

In recent years, remote sensing (RS) vision foundation models such as RingMo have emerged and achieved excellent performance in various downstream tasks. However, the high demand for computing resources limits the application of these models on edge devices. It is necessary to design a more lightweight foundation model to support on-orbit RS image interpretation. Existing methods face challenges in achieving lightweight solutions while retaining generalization in RS image interpretation. This is due to the complex high and low-frequency spectral components in RS images, which make traditional single CNN or Vision Transformer methods unsuitable for the task. Therefore, this paper proposes RingMo-lite, an RS multi-task lightweight network with a CNN-Transformer hybrid framework, which effectively exploits the frequency-domain properties of RS to optimize the interpretation process. It is combined by the Transformer module as a low-pass filter to extract global features of RS images through a dual-branch structure, and the CNN module as a stacked high-pass filter to extract fine-grained details effectively. Furthermore, in the pretraining stage, the designed frequency-domain masked image modeling (FD-MIM) combines each image patch's high-frequency and low-frequency characteristics, effectively capturing the latent feature representation in RS data. As shown in Fig. 1, compared with RingMo, the proposed RingMo-lite reduces the parameters over 60% in various RS image interpretation tasks, the average accuracy drops by less than 2% in most of the scenes and achieves SOTA performance compared to models of the similar size. In addition, our work will be integrated into the MindSpore computing platform in the near future

Disulfiram/Cu Kills and Sensitizes <i>BRAF</i>-Mutant Thyroid Cancer Cells to <i>BRAF</i> Kinase Inhibitor by ROS-Dependently Relieving Feedback Activation of MAPK/ERK and PI3K/AKT Pathways

BRAFV600E, the most common genetic alteration, has become a major therapeutic target in thyroid cancer. Vemurafenib (PLX4032), a specific inhibitor of BRAFV600E kinase, exhibits antitumor activity in patients with BRAFV600E-mutated thyroid cancer. However, the clinical benefit of PLX4032 is often limited by short-term response and acquired resistance via heterogeneous feedback mechanisms. Disulfiram (DSF), an alcohol-aversion drug, shows potent antitumor efficacy in a copper (Cu)-dependent way. However, its antitumor activity in thyroid cancer and its effect on cellular response to BRAF kinase inhibitors remain unclear. Antitumor effects of DSF/Cu on BRAFV600E-mutated thyroid cancer cells and its effect on the response of these cells to BRAF kinase inhibitor PLX4032 were systematically assessed by a series of in vitro and in vivo functional experiments. The molecular mechanism underlying the sensitizing effect of DSF/Cu on PLX4032 was explored by Western blot and flow cytometry assays. DSF/Cu exhibited stronger inhibitory effects on the proliferation and colony formation of BRAFV600E-mutated thyroid cancer cells than DSF treatment alone. Further studies revealed that DSF/Cu killed thyroid cancer cells by ROS-dependent suppression of MAPK/ERK and PI3K/AKT signaling pathways. Our data also showed that DSF/Cu strikingly increased the response of BRAFV600E-mutated thyroid cancer cells to PLX4032. Mechanistically, DSF/Cu sensitizes BRAF-mutant thyroid cancer cells to PLX4032 by inhibiting HER3 and AKT in an ROS-dependent way and subsequently relieving feedback activation of MAPK/ERK and PI3K/AKT pathways. This study not only implies potential clinical use of DSF/Cu in cancer therapy but also provides a new therapeutic strategy for BRAFV600E-mutated thyroid cancers

Disulfiram/Cu Kills and Sensitizes BRAF-Mutant Thyroid Cancer Cells to BRAF Kinase Inhibitor by ROS-Dependently Relieving Feedback Activation of MAPK/ERK and PI3K/AKT Pathways

BRAFV600E, the most common genetic alteration, has become a major therapeutic target in thyroid cancer. Vemurafenib (PLX4032), a specific inhibitor of BRAFV600E kinase, exhibits antitumor activity in patients with BRAFV600E-mutated thyroid cancer. However, the clinical benefit of PLX4032 is often limited by short-term response and acquired resistance via heterogeneous feedback mechanisms. Disulfiram (DSF), an alcohol-aversion drug, shows potent antitumor efficacy in a copper (Cu)-dependent way. However, its antitumor activity in thyroid cancer and its effect on cellular response to BRAF kinase inhibitors remain unclear. Antitumor effects of DSF/Cu on BRAFV600E-mutated thyroid cancer cells and its effect on the response of these cells to BRAF kinase inhibitor PLX4032 were systematically assessed by a series of in vitro and in vivo functional experiments. The molecular mechanism underlying the sensitizing effect of DSF/Cu on PLX4032 was explored by Western blot and flow cytometry assays. DSF/Cu exhibited stronger inhibitory effects on the proliferation and colony formation of BRAFV600E-mutated thyroid cancer cells than DSF treatment alone. Further studies revealed that DSF/Cu killed thyroid cancer cells by ROS-dependent suppression of MAPK/ERK and PI3K/AKT signaling pathways. Our data also showed that DSF/Cu strikingly increased the response of BRAFV600E-mutated thyroid cancer cells to PLX4032. Mechanistically, DSF/Cu sensitizes BRAF-mutant thyroid cancer cells to PLX4032 by inhibiting HER3 and AKT in an ROS-dependent way and subsequently relieving feedback activation of MAPK/ERK and PI3K/AKT pathways. This study not only implies potential clinical use of DSF/Cu in cancer therapy but also provides a new therapeutic strategy for BRAFV600E-mutated thyroid cancers

Effect of surface roughness on the anomalous Hall effect in Fe thin films

International audienceSurface roughness plays an important role on the magnetotransport properties of thin films, especially in ultrathin films. In this work, we prepared Fe thin films with various surface roughness by using different seed layers and studied the electrical transport and anomalous Hall effect. By tuning surface roughness scattering, the longitudinal resistivity (ρ xx) measured at 5 K increases by one order of magnitude and the corresponding anomalous Hall resistivity (ρ AHE) increases by three times with increasing roughness. The intrinsic, skewscattering, and side-jump contributions to ρ AHE were separated from our data. The anomalous Hall angle depends on the surface roughness, which may be of importance to the material engineering for achieving large spin Hall angle

ACAT2 Is a Novel Negative Regulator of Pig Intramuscular Preadipocytes Differentiation

Intramuscular fat (IMF) is considered as the fat deposited between muscle fibers. The extracellular matrix microenvironment of adipose tissue is of critical importance for the differentiation, remodeling and function of adipocytes. Therefore, in this study we extracted the muscle tissue centrifugal fluid (MTF) of the longissimus dorsi of Erhualian pigs to mimic the microenvironment of intramuscular pre-adipocytes. MTF of pigs with low intramuscular fat level can inhibit pig intramuscular pre-adipocytes differentiation. Then, proteomics technology (iTRAQ) was used to analyze the MTF with different IMF content, and it was found that individuals with high IMF had low ACAT2 (Acyl-CoA: cholesterol acyltransferases 2) levels, while individuals with low IMF had high ACAT2 levels. Significant changes took place in the pathways involved in coenzyme A, which are closely related to fat and cholesterol metabolism. Therefore, we speculate that ACAT2, as an important element involved in cholesterol metabolism, may become a potential molecular marker for the mechanism of pig intramuscular preadipocytes differentiation. Overexpression of ACAT2 in pig intramuscular pre-adipocytes can inhibit their differentiation, while adding ACAT2 inhibitor avasimibe can rescue the process. Knockdown of srebp2 or ldlr, which are two key genes closely related to ACAT2 and cholesterol metabolism, can inhibit pig intramuscular pre-adipocytes differentiation. Overall, our results suggest that ACAT2 is a novel negative regulator of intramuscular adipocyte differentiation through regulation of pparγ, cebpα signaling and srebp2/ldlr signaling involved in cholesterol metabolism