LiDAR point clouds are widely adopted in robotics to precisely depict the surrounding environment. However, dense point cloud acquisition significantly increases data processing costs. To address the extensive memory demands of dense 3D maps, compression techniques are crucial for efficient storage and transmission. Traditional point cloud compression methods overlook local structural information and contextual relationships among point clouds. To tackle this issue, we propose a kernel-based attention network, which employs the attention mechanism to capture contextual information. Our novel deep convolutional encoder directly operates on the point cloud, avoiding structural information loss caused by voxelization. Furthermore, we introduce a self-attention feature aggregation module for extracting features and obtaining more robust representations. We evaluate our method on KITTI and nuScenes datasets. Experimental results show that our compression network achieves superior reconstruction compared to other state-of-the-art approaches at the same bit-rate.
The scope of the surrounding rock loosening and its mechanical properties can significantly affect the analysis of the excavation loosening range, stress–strain state partitioning, and surrounding rock mass stability. Investigating the mechanical properties and failure modes of the surrounding rock mass is of significant engineering value for optimizing support design and ensuring the safety of tunnel construction and. Therefore, the tests on loose circle and mechanical properties of the rock mass were conducted, yielding the following results. (1) The sonic wave testing method and ground penetrating radar (GPR) detection were more suitable for loose circle testing of extremely thin-layered phyllite than the True Reflection Tomography (TRT) method and borehole camera method. (2) The loose circle ranges for the test sections were 4.9 m and 6.8 m, respectively. (3) The cohesion and internal friction angle of the test sections were less than 0.3276 MPa and 19.0°, respectively. The test results were consistent with the predominant phyllite composition of the surrounding rock. This study combined in situ tests and site conditions to analyze the causes of tunnel deformation and instability, offering recommendations for tunnel support. These findings served as valuable guidance for similar tunnel support design and construction, and play a crucial role in ensuring constructor safety.
Here we investigated Brahma-related gene 1 (BRG1) expression in aortic smooth muscle cells (SMCs) and its role in the regulation of the pathological changes in aortic SMCs of thoracic arotic dissection (TAD). BRG1, matrix metalloproteinase 2 (MMP2), and MMP9 mRNA and protein expression in human aortic specimens were examined by qPCR and western blot, respectively. The percentage of apoptotic and contractile SMCs in aortic specimens were determined by TUNEL assay and α-SMA immunohistochemical staining, respectively. The role of BRG1 in MMP2 and MMP9 expression, cell apoptosis, and phenotype transition in aortic SMCs were investigated using a human aortic SMC line via adenovirus mediated gene transfer. MMPs mRNA and protein levels were analyzed by qPCR and western blot, respectively. The percentage of apoptotic and contractile cells were determined through flow cytometry analysis. The expression level of BRG1 in the aortic walls (adventitia-removed) was significantly higher in the TAD than the normal group. BRG1 expression was positively correlated to expression of MMP2 and MMP9 and SMC apoptosis, but was negatively correlated to the percentage of contractile aortic SMCs in TAD specimens. In human aortic SMC line, BRG1 transfection led to significant upregulation of MMP2 and MMP9 expression and a concomitant increase in SMC apoptosis as well as a decrease in the percentage of contractile phenotype of cells. BRG1 is significantly upregulated in the aortic SMCs of TAD, and its overexpression might promote the development of TAD by increasing MMP2 and MMP9 expression, inducing SMC apoptosis and the transition from contractile to synthetic phenotype.
Abstract Esophageal squamous cell carcinoma (ESCC) is a malignant disease with poor prognosis. Because of early metastasis prior to diagnosis and therapeutic resistance, ESCC has become one of the leading causes of cancer‐related death. Here, we investigated the clinicopathological significance of the association of octamer‐binding transcription factor 4 (OCT4) with lymphoid enhancer‐binding factor 1 (LEF1) expression and the potential molecular mechanism in the epithelial‐mesenchymal transition (EMT), invasion, and migration of ESCC. The expression of OCT4 and LEF1 was detected via immunohistochemistry analysis. High levels of LEF1 expression were observed in 95 ESCC specimens and were obviously associated with aberrant clinicopathological features and poor patient prognosis. Our previous study showed that OCT4 expression level is elevated in ESCC, and statistical analysis showed that the elevated expression of OCT4 and LEF1 in ESCC was significantly associated with histologic grade, lymph node metastasis, TNM stage, and poor patient prognosis. The specific inhibition of OCT4 expression via a lentivirus encoding OCT4‐shRNA (LV‐shOCT4) in Eca109 cells led to decreased levels of OCT4 and LEF1 in vitro. Additionally, we applied a rescue strategy by infecting LV‐shOCT4 Eca109 cells with a LEF1 overexpression plasmid (p‐LEF1) and detected changes in EMT, migration, and invasion. Unsurprisingly, the p‐LEF1 group exhibited greater EMT, invasion, and migration than did the LV‐shOCT4 and negative control groups. This study demonstrates for the first time the relationship between OCT4 and LEF1 expression. The combination of high expression of OCT4 and LEF1 was associated with clinicopathological features of atypical patients, and this combination might be an ideal prognostic factor in ESCC. OCT4 positively regulated LEF1 expression, and LEF1 mediated the effects of OCT4 in cancer cell EMT, invasion, and migration. The data presented here suggest that the inhibition of OCT4‐LEF1 signaling may be a new therapeutic target for the treatment of ESCC.
By analyzing 482 pb$^{-1}$ of $e^+e^-$ collision data collected at the center-of-mass energy $\sqrt s=4.009$ GeV with the BESIII detector, we measure the %absolute branching fractions for the semi-leptonic decays $D_{s}^{+}\to \phi e^{+}\nu_{e}$, $\phi \mu^{+}\nu_{\mu}$, $\eta \mu^{+}\nu_{\mu}$ and $\eta'\mu^{+}\nu_{\mu}$ to be ${\mathcal B}(D_{s}^{+}\to\phi e^{+}\nu_{e})=(2.26\pm0.45\pm0.09)$\%, ${\mathcal B}(D_{s}^{+}\to\phi \mu^{+}\nu_{\mu})=(1.94\pm0.53\pm0.09)$\%, ${\mathcal B}(D_{s}^{+}\to\eta \mu^{+}\nu_{\mu})=(2.42\pm0.46\pm0.11)$\% and ${\mathcal B}(D_{s}^{+}\to\eta'\mu^{+} \nu_{\mu}) = (1.06\pm0.54\pm0.07)$\%, where the first and second uncertainties are statistical and systematic, respectively. The branching fractions for the three semi-muonic decays $D_s^+\to\phi \mu^+\nu_\mu, \eta \mu^+\nu_\mu$ and $\eta' \mu^+\nu_\mu$ are determined for the first time and that of $D^+_s\to \phi e^+\nu_e$ is consistent with the world average value within uncertainties.
Abstract Background Prenylated Rab acceptor 1 domain family member 3 (PRAF3) is involved in the regulation of many cellular processes including apoptosis, migration and invasion. This study was conducted to investigate the effect of PRAF3 on apoptosis, migration and invasion in human esophageal squamous cell carcinoma (ESCC). Methods The expression of PRAF3 mRNA and protein in primary ESCC and the matched normal tissues (57cases) was determined by quantitative RT-PCR and Western blot. Immunohistochemical analysis of PRAF3 expression was carried out in paraffin-embedded sections of ESCC and correlated with clinical features. The role of PRAF3 in apoptosis, migration and invasion was studied in ESCC cell lines of Eca109 and TE-1 through the adenovirus mediated PRAF3 gene transfer. The effect of PRAF3 on apoptosis was analyzed by annexin V-FITC assay. The regulation of PRAF3 on migration was determined by transwell and wounding healing assay, while the cellular invasion was analyzed by matrigel-coated transwell assay. Results We found that the expression of PRAF3 was significantly down-regulated in ESCC tissue compared with the matched normal tissue and was correlated with the clinical features of pathological grade, tumor stage and lymph node metastasis. Moreover, overexpression of PRAF3 induced cell apoptosis through both caspase-8 and caspase-9 dependent pathways, and inhibited cell migration and invasion by suppressing the activity of both MMP-2 and MMP-9 in human ESCC cell lines. Conclusions Our data suggest that PRAF3 plays an important role in the regulation of tumor progression and metastasis and serves as a tumor suppressor in human ESCC. We propose that PRAF3 might be used as a potential therapeutic agent for human ESCC.
With the data samples taken at center-of-mass energies from 2.00 to 3.08 GeV with the BESIII detector at the BEPCII collider, a partial wave analysis on the e+e−→π+π−π0 process is performed. The Born cross sections for e+e−→π+π−π0 and its intermediate processes e+e−→ρπ and ρ(1450)π are measured as functions of s. The results for e+e−→π+π−π0 are consistent with previous results measured with the initial state radiation method within one standard deviation, and improve the uncertainty by a factor of ten. By fitting the line shapes of the Born cross sections for the e+e−→ρπ and e+e−→ρ(1450)π, a structure with mass M=2119±11±15MeV/c2 and width Γ=69±30±5MeV is observed with a significance of 5.9σ, where the first uncertainties are statistical and the second ones are systematic. This structure can be interpreted as an excited ω state. Published by the American Physical Society 2024
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