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The main challenges faced when detecting targets captured by UAVs include small target image size, dense target distribution, and uneven category distribution.In addition, the hardware limitations of UAVs impose constraints on the size and complexity of the model, which may lead to poor detection accuracy of the model. In order to solve these problems, a small target detection method based on the improved YOLOv8 algorithm for UAV viewpoint is proposed. The following improvements are made to the YOLOv8n model. Firstly, a bi-directional feature pyramid network (BiFPN) is introduced to enhance the fusion capability of the features. This improvement leads to better detection of small targets. Secondly, in the head part of the model, the original C2f module is replaced with the C3Ghost module. This change maintains the model's performance while significantly reducing the computational load. Lastly, the detection head adds a channel attention mechanism. This mechanism helps in filtering out unimportant information and enhancing the recognition of key features. The MPDIoU (Minimum Point Distance based IoU) loss function is improved, and the idea of inner-IoU loss function is adopted as a way to improve the model's learning ability for difficult samples. Experimental results on the VisDrone dataset show that the YOLOv8n model with these improvements improves 17.2%, 10.5%, and 16.2% in mean accuracy (mAP), precision (P), and recall (R), respectively, and these improvements significantly improve the performance of small target detection from the UAV viewpoint. [ABSTRACT FROM AUTHOR]

The thalassemia of Hemoglobin H-Constant Spring disease (HbH-CS) is the most common type of Thalassemia in non-transfusion thalassemia. Interestingly, the clinical manifestations of the same genotype of thalassemia can be vastly different, likely due to epigenetic regulation. Here, we used microarray technology to reveal the epigenetic regulation of m6A in modifiable diseases and demonstrated a role of BCL2A1 in disease regulation. In this study, we revealed that methylating enzyme writers including METTL16, WTAP, CBLL1, RBM15B, and ZC3H13 displayed low expression and the demethylating enzyme ALKBH5, along with reader proteins including IGF2BP2 and YTHDF3 exhibited high expression. In addition, BCL2A1 was hypo-methylated and showed low expression. We also revealed that the BCL2A1 methylation level and IGF2BP2 expression were negatively correlated. Additionally, the mRNAs expression between ALKBH5 and IGF2BP2 were positively correlated. In HbH-CS, most genes were hypo-methylated. This included BCL2A1, which may play an important role in the process of red blood cell differentiation and development of HbH-CS. Moreover, the mRNA-M6A methylation status may be regulated by the demethylating enzyme ALKBH5 via IGF2BP2. [ABSTRACT FROM AUTHOR]

A translocator protein 18 kDa targeted radiotracer, N,N-diethyl-2-(2-(4-[18F]fluorophenyl)-5,7-dimethylpyrazolo[1,5-a] pyrimidin-3-yl) acetamide ([18F]FDPA), was automated synthetized and evaluated for cardiac inflammation imaging. Various reaction conditions for an automated synthesis were systematically optimized. MicroPET/CT imaging were performed on normal rats and rats with myocardial infarction (MI). Normalized SUV ratios of [18F]FDPA to [13N]NH3 (NSRs) in different regions were calculated to normalize the uptake of [18F]FDPA to perfusion. The amount of TBAOMs and the volume/proportion of water were crucial for synthesis. After optimization, the total synthesis time was 68 min. The non-decay corrected radiochemical yields (RCYs) and molar activities were 19.9 ± 1.7% and 169.7 ± 46.5 GBq/μmol, respectively. In normal rats, [18F]FDPA showed a high and stable cardiac uptake and fast clearance from other organs. In MI rats, NSRs in the peri-infarct and infarct regions, which were infiltrated with massive inflammatory cells revealed by pathology, were higher than that in the remote region (1.20 ± 0.01 and 1.08 ± 0.10 vs. 0.89 ± 0.05, respectively). [18F]FDPA was automated synthesized with high RCYs and molar activities. It showed a high uptake in inflammation regions and offered a wide time window for cardiac imaging, indicating it could be a potential cardiac inflammation imaging agent. [ABSTRACT FROM AUTHOR]

Live-imaging techniques are at the forefront of biology research to explore behaviour and function from sub-cellular to whole organism scales. These methods rely on intracellular fluorescent probes to label specific proteins, which are commonly assumed to only introduce artefacts at concentrations far-exceeding routine use. Lifeact, a small peptide with affinity for actin microfilaments has become a gold standard in live cell imaging of the cytoskeleton. Nevertheless, recent reports have raised concerns on Lifeact-associated artefacts at the molecular and whole organism level. We show here that Lifeact induces dose-response artefacts at the cellular level, impacting stress fibre dynamics and actin cytoskeleton architecture. These effects extend to the microtubule and intermediate filament networks as well as the nucleus, and ultimately lead to altered subcellular localization of YAP, reduced cell migration and abnormal mechanical properties. Our results suggest that reduced binding of cofilin to actin filaments may be the underlying cause of the observed Lifeact-induced cellular artefacts. [ABSTRACT FROM AUTHOR]

Accelerated repopulation has been observed in various tumors. This study was aimed to evaluate the potential of 3′-deoxy-3′-18F-fluorothymidine (18F-FLT) uptake and Computed Tomography Number (CTN) in monitoring tumor responses to radiotherapy compared with tumor volume (TV) changes. Tumor bearing nude mice were assigned to either irradiated daily or every second day group and then randomized to 6 sub-groups to receive 0Gy, 6Gy, 12Gy, 18Gy, 24Gy, 36Gy irradiation, respectively. TV was measured every 3 days. 18F-FLT micro-PET/CT scans were performed after irradiation being completed. Tumor sections were stained to calculate the immunohistochemical (Ki-67) labeling index (LI). Comparison analysis between FLT uptake parameters, CTNs, VTs and Ki-67 LI results were conducted to determine the correlation. Ki-67 LI increased significantly after 6 times of irradiation at irradiated daily group and after 3 times at irradiated every second day group, suggesting accelerated repopulation. No shrinkage of TV was noticed at two groups during irradiation delivery. Both 18F-FLT uptake and CTN increased significantly after irradiation of 12Gy/6f/6d and 6Gy/3f/6d. Comparison analysis found a significant relationship between Ki-67 LI and 18F-FLT uptake parameters as well as CTN. Both 18F-FLT PET and CT have the potential to reflect the tumor proliferative response during radiation delivery. [ABSTRACT FROM AUTHOR]

Accelerated repopulation has been observed in various tumors. This study was aimed to evaluate the potential of 3'-deoxy-3'- 18 F-fluorothymidine ( 18 F-FLT) uptake and Computed Tomography Number (CTN) in monitoring tumor responses to radiotherapy compared with tumor volume (TV) changes. Tumor bearing nude mice were assigned to either irradiated daily or every second day group and then randomized to 6 sub-groups to receive 0Gy, 6Gy, 12Gy, 18Gy, 24Gy, 36Gy irradiation, respectively. TV was measured every 3 days. 18 F-FLT micro-PET/CT scans were performed after irradiation being completed. Tumor sections were stained to calculate the immunohistochemical (Ki-67) labeling index (LI). Comparison analysis between FLT uptake parameters, CTNs, VTs and Ki-67 LI results were conducted to determine the correlation. Ki-67 LI increased significantly after 6 times of irradiation at irradiated daily group and after 3 times at irradiated every second day group, suggesting accelerated repopulation. No shrinkage of TV was noticed at two groups during irradiation delivery. Both 18 F-FLT uptake and CTN increased significantly after irradiation of 12Gy/6f/6d and 6Gy/3f/6d. Comparison analysis found a significant relationship between Ki-67 LI and 18 F-FLT uptake parameters as well as CTN. Both 18 F-FLT PET and CT have the potential to reflect the tumor proliferative response during radiation delivery.