16 research outputs found
YOLO-Drone:Airborne real-time detection of dense small objects from high-altitude perspective
Unmanned Aerial Vehicles (UAVs), specifically drones equipped with remote
sensing object detection technology, have rapidly gained a broad spectrum of
applications and emerged as one of the primary research focuses in the field of
computer vision. Although UAV remote sensing systems have the ability to detect
various objects, small-scale objects can be challenging to detect reliably due
to factors such as object size, image degradation, and real-time limitations.
To tackle these issues, a real-time object detection algorithm (YOLO-Drone) is
proposed and applied to two new UAV platforms as well as a specific light
source (silicon-based golden LED). YOLO-Drone presents several novelties: 1)
including a new backbone Darknet59; 2) a new complex feature aggregation module
MSPP-FPN that incorporated one spatial pyramid pooling and three atrous spatial
pyramid pooling modules; 3) and the use of Generalized Intersection over Union
(GIoU) as the loss function. To evaluate performance, two benchmark datasets,
UAVDT and VisDrone, along with one homemade dataset acquired at night under
silicon-based golden LEDs, are utilized. The experimental results show that, in
both UAVDT and VisDrone, the proposed YOLO-Drone outperforms state-of-the-art
(SOTA) object detection methods by improving the mAP of 10.13% and 8.59%,
respectively. With regards to UAVDT, the YOLO-Drone exhibits both high
real-time inference speed of 53 FPS and a maximum mAP of 34.04%. Notably,
YOLO-Drone achieves high performance under the silicon-based golden LEDs, with
a mAP of up to 87.71%, surpassing the performance of YOLO series under ordinary
light sources. To conclude, the proposed YOLO-Drone is a highly effective
solution for object detection in UAV applications, particularly for night
detection tasks where silicon-based golden light LED technology exhibits
significant superiority
MicroRNAâ215â5p promotes proliferation, invasion, and inhibits apoptosis in liposarcoma cells by targeting MDM2
Abstract Background Liposarcoma (LPS) is one of the most common soft tissue malignancies in adults, and it is characterized by dysregulation of multiple signaling pathways, including MDM2 protoâoncogene (MDM2) amplification. MicroRNA (miRNA) regulates gene expression through incomplete complementary pairing with the 3' untranslated region of mRNAs involved in tumor progression. Methods In this study, bioinformatics analysis, RTâqPCR, dualâluciferase reporter gene, MTT, flow cytometry, cell scratches, chamber migration, colony formation, FISH, WB, and CCK8 were used. Results RTâqPCR showed that the expression of MDM2 was increased when miRâ215â5p was overexpressed compared with the control group. The dualâluciferase reporter gene showed that the Renilla ratio firefly fluorescence intensity was decreased in the overexpression group compared with the control group. Cell phenotype experiments revealed that the overexpression group had increased cell proliferation rate, increased apoptosis rate, increased colony formation rate, increased cell healing area ratio, and increased number of cell invasions. FISH revealed increased MDM2 expression in the overexpression group. WB suggested decreased Bax expression, increased PCNA, Bclâ2, and MDM2 expression, and decreased P53 and P21 expression in the overexpression group. Conclusions In this study, we suggest that miRâ215â5p can target and promote MDM2 expression, promote the proliferation and invasion of LPS cells SWâ872, and inhibit apoptosis.Targeting miRâ215â5p may be a novel therapeutic strategy for the treatment of LPS
Genomic Profiles in Stage I Primary Non Small Cell Lung Cancer Using Comparative Genomic Hybridization Analysis of cDNA Microarrays
To investigate the genomic aberrations that are involved in lung tumorigenesis and therefore may be developed as biomarkers for lung cancer diagnosis, we characterized the genomic copy number changes associated with individual genes in 14 tumors from patients with primary non small cell lung cancer (NSCLC). Six squamous cell carcinomas (SQCAs) and eight adenocarcinomas (ADCAs) were examined by high-resolution comparative genomic hybridization (CGH) analysis of cDNA microarray. The SQCAs and ADCAs shared common frequency distributions of recurrent genomic gains of 63 genes and losses of 72 genes. Cluster analysis using 57 genes defined the genomic differences between these two major histologic types of NSCLC. Genomic aberrations from a set of 18 genes showed distinct difference of primary ADCAs from their paired normal lung tissues. The genomic copy number of four genes was validated by fluorescence in situ hybridization of 32 primary NSCLC tumors, including those used for cDNA microarray CGH analysis; a strong correlation with cDNA microarray CGH data emerged. The identified genomic aberrations may be involved in the initiation and progression of lung tumorigenesis and, most importantly, may be developed as new biomarkers for the early detection and classification of lung cancer
Angiopoietinâ2 Promotes Mechanical Stressâinduced Extracellular Matrix Degradation in Annulus Fibrosus Via the HIFâ1α/NFâÎșB Signaling Pathway
Objective Mechanical stress is an important risk factor for intervertebral disc degeneration (IVDD). Angiopoietinâ2 (ANGâ2) is regulated by mechanical stress and is widely involved in the regulation of extracellular matrix metabolism. In addition, the signaling cascade between HIFâ1α and NFâÎșB is critical in matrix degradation. This study aims to investigate the role and molecular mechanism of ANGâ2 in regulating the degeneration of annulus fibrosus (AF) through the HIFâ1α/NFâÎșB signaling pathway. Methods The bipedal standing mice IVDD model was constructed, and histological experiments were used to evaluate the degree of IVDD and the expression of ANGâ2 in the AF. Mouse primary AF cells were extracted in vitro and subjected to mechanical stretching experiments. Western blot assay was used to detect the effect of mechanical stress on ANGâ2, and the role of the ANGâ2âmediated HIFâ1α/NFâÎșB pathway in matrix degradation. In addition, the effect of inhibiting ANGâ2 expression by siRNA or monoclonal antibody on delaying IVDD was investigated at in vitro and in vivo levels. Oneâway ANOVA with the least significant difference method was used for pairwise comparison of the groups with homogeneous variance, and Dunnett's method was used to compare the groups with heterogeneous variance. Results In IVDD, the expressions of catabolic biomarkers (mmpâ13, ADAMTSâ4) and ANGâ2 were significantly increased in AF. In addition, p65 expression was increased while HIFâ1α expression was significantly decreased. The results of western blot assay showed mechanical stress significantly upâregulated the expression of ANGâ2 in AF cells, and promoted matrix degradation by regulating the activity of HIFâ1α/NFâÎșB pathway. Exogenous addition of Bay117082 and CoCl2 inhibited matrix degradation caused by mechanical stress. Moreover, injection of neutralizing antibody or treatment with siRNA to inhibit the expression of ANGâ2 improved the matrix metabolism of AF and inhibited IVDD progression by regulating the HIFâ1α/NFâÎșB signaling pathway. Conclusion In IVDD, mechanical stress could regulate the HIFâ1α/NFâÎșB signaling pathway and matrix degradation by mediating ANGâ2 expression in AF degeneration
Photoemission evidence for dilute k-doped phase KxCïŒ60ïŒ with x<0.2
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Adsorption of oxygen on KxCïŒ60ïŒ studied by photoelectron spectroscopy
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