Self-Attention Mechanism-Based Head Pose Estimation Network with Fusion of Point Cloud and Image Features.

Head pose estimation serves various applications, such as gaze estimation, fatigue-driven detection, and virtual reality. Nonetheless, achieving precise and efficient predictions remains challenging owing to the reliance on singular data sources. Therefore, this study introduces a technique involving multimodal feature fusion to elevate head pose estimation accuracy. The proposed method amalgamates data derived from diverse sources, including RGB and depth images, to construct a comprehensive three-dimensional representation of the head, commonly referred to as a point cloud. The noteworthy innovations of this method encompass a residual multilayer perceptron structure within PointNet, designed to tackle gradient-related challenges, along with spatial self-attention mechanisms aimed at noise reduction. The enhanced PointNet and ResNet networks are utilized to extract features from both point clouds and images. These extracted features undergo fusion. Furthermore, the incorporation of a scoring module strengthens robustness, particularly in scenarios involving facial occlusion. This is achieved by preserving features from the highest-scoring point cloud. Additionally, a prediction module is employed, combining classification and regression methodologies to accurately estimate head poses. The proposed method improves the accuracy and robustness of head pose estimation, especially in cases involving facial obstructions. These advancements are substantiated by experiments conducted using the BIWI dataset, demonstrating the superiority of this method over existing techniques.

Kaposi's sarcoma-associated herpesvirus infection promotes proliferation of SH-SY5Y cells by the Notch signaling pathway.

BACKGROUND: The cancer caused by Kaposi's sarcoma-associated herpesvirus (KSHV) infection is one of the major causes of death in AIDS patients. Some patients have neurological symptoms, which appear to be associated with KSHV infection, based on the neurotropic tendency of this virus in recent years. The objectives of this study were to investigate the effects of KSHV infection on neuronal SH-SY5Y cells and to identify differentially expressed genes. METHODS: KSHV was collected from islk.219 cells. Real-time PCR was used to quantify KSHV copy numbers. KSHV was used to infect SH-SY5Y cells. The KSHV copy number in the supernatants and mRNA levels of latency-associated nuclear antigen (LANA), ORF26, K8.1 A, and replication and transcriptional activator (RTA) were detected by real-time PCR. Proteins were detected by immunohistochemistry. The effect of KSHV infection on cell proliferation was detected by MTT and Ki-67 staining. Cell migration was evaluated by Transwell and wound healing assays. The cell cycle was analyzed by flow cytometry. The expression of CDK4, CDK5, CDK6, cyclin D1, and p27 were measured by western blotting. The levels of cell cycle proteins were re-examined in LANA-overexpressing SH-SY5Y cells. Transcriptome sequencing was used to identify differentially expressed genes in KSHV-infected cells. The levels of Notch signaling pathway proteins were measured by western blotting. RNA interference was used to silence Notch1 and proliferation were analyzed again. RESULTS: SH-SY5Y cells were successfully infected with KSHV, and they maintained the ability to produce virions. KSHV-infected SH-SY5Y expressed LANA, ORF26, K8.1 A, and RTA. After KSHV infection, cell proliferation was enhanced, but cell migration was suppressed. KSHV infection accelerated the G0/G1 phase. CDK4, CDK5, CDK6, and cyclin D1 expression was increased, whereas p27 expression was decreased. After LANA overexpression, CDK4, CDK6 and cyclin D1 expression was increased. Transcriptome sequencing showed that 11,258 genes were upregulated and 1,967 genes were downregulated in KSHV-infected SH-SY5Y. The Notch signaling pathway played a role in KSHV infection in SH-SY5Y, and western blots confirmed that Notch1, NICD, RBP-Jĸ and Hes1 expression was increased. After silencing of Notch1, the related proteins and cell proliferation ability were decreased. CONCLUSIONS: KSHV infected SH-SY5Y cells and promoted the cell proliferation. KSHV infection increased the expression of Notch signaling pathway proteins, which may have been associated with the enhanced cell proliferation.

miR-769-3p inhibits cellular proliferation of KSHV-infected SH-SY5Y cells through targeting mTOR.

The infection by Kaposi's sarcoma-associated herpesvirus (KSHV) is one of the most common causes of death in AIDS patients. Our studies have found that KSHV can infect SH-SY5Y cells (named SK-RG) in vivo and mTOR was up-regulated, which results in remarkable enhancement of cell proliferation, migration. But the regulatory role of mTOR in KSHV infected neurons has not yet been fully elucidated. Here, we find that miR-769-3p is decreased in SK-RG cells, which can exert anti-KSHV effect through negatively regulating the expression of mTOR. The knockdown of mTOR or overexpress of miR-769-3p decreased the proliferation, migration ability and cell cycle related protein of SK-RG cells, and the expression of KSHV related genes. In contrast, activating mTOR function by 3BDO treatment weakened the cellular behaviors of miR-769-3p overexpressing cells. Meanwhile, overexpressed miR-769-3p and rapamycin showed a shared inhibition trend in the effects on cell proliferation and motility. Our data indicated that miR-769-3p can inhibit cell proliferation and migration by down regulating mTOR in KSHV infected SH-SY5Y cells, and can be a candidate molecule for anti-KSHV therapy.

miR-34a-5p inhibits the malignant progression of KSHV-infected SH-SY5Y cells by targeting c-fos.

Background: We aimed to investigate the effects of miR-34a-5p on c-fos regulation mediating the malignant behaviors of SH-SY5Y cells infected with Kaposi's sarcoma-associated herpesvirus (KSHV). Methods: The KSHV-infected (SK-RG) and uninfected SH-SY5Y parent cells were compared for differentially expressed miRNAs using transcriptome sequencing. Then miR-34a-5p was upregulated in SK-RG cells by the miRNA mimics transfection. Cell proliferation ability was determined by MTT and plate clone assays. The cell cycle was assessed by flow cytometry analysis, and CDK4, CDK6, cyclin D1 levels were determined by Western blot analysis. The migration behavior was detected by wound healing and transwell assays. The protein levels of MMP2 and MMP9 were measured by Western blot analysis. The regulation of c-fos by miR-34a-5p was detected by the dual-luciferase reporter gene assay. Rescue assays were carried out by upregulating c-fos in miR-34a-5p-overexpressing SK-RG cells. KSHV DNA copy numbers and relative virus gene expressions were detected. Xenograft tumor experiments and immunohistochemistry assays were further used to detect the effects of miR-34a-5p. Results: miR-34a-5p was lower in SK-RG cells. Restoration of miR-34a-5p decreased cell proliferation and migration, leading to a G1 cell cycle arrest and down-regulation of CDK4/6, cyclin D1, MMP2, MMP9. KSHV copy number and expression of virus gene including latency-associated nuclear antigen (LANA), replication and transcription activator (RTA), open reading frame (K8.1), and KSHV G protein-coupled receptor (v-GPCR) were also reduced. Furthermore, c-fos is the target of miR-34a-5p, while enhanced c-fos weakened cellular behaviors of miR-34a-5p-overexpressing cells. Xenograft experiments and immunohistochemistry assays showed that miR-34a-5p inhibited tumor growth and virus gene expression. Conclusion: Upregulated miR-34a-5p in KSHV-infected SH-SY5Y cells suppressed cell proliferation and migration through down-regulating c-fos. miR-34a-5p was a candidate molecular drug for KSHV-infected neuronal cells.

[Effects of biochar covering on the release of pollutants from sediment].

In order to study the effects of biochar on the release of pollutants from sediment, Arundo donax, Phragmites australis, Arachis hypogaea and Zea mays were pyrolyzed into biochar. Biochar was used to cover the contaminated sediment in the simulated reactors. Concentrations of NH4(+) -N, NO3(-) -N, NO2(-) -N, COD and P4(3-) -P were continuously monitored, and the cumulative release amount and release rate were calculated. Besides that, the release amount of water-soluble NH4(+) -N and PO4(3-) -P from biochars were determined. In the blank control group, which was not covered with any kinds of biochar, the ammonia-nitrogen concentration of the overlying water reached a maximum value of 4.27 mg x L(-1) on the twenty-fifth day, and then stabilized at about 4.02 mg x L(-1). Ammonia-nitrogen concentrations of the treatment groups with the four kinds of biochar all maintained below 0.3 mg x L(-1) after 25 days. Particularly, the Phragmites australis treatment group showed the best ability to inhibit ammonia-nitrogen release, and the cumulative release amount of ammonia-nitrogen was reduced by 85.61%. The cumulative release amount of COD was reduced by 28.83% to 30%. Phosphate concentration of the Zea mays group was higher than that of the blank group. On the contrary, Arundo donax and Phragmites australis groups showed a great potential in the inhibition of phosphate release. Biochar released the majority of NH4(+) -N and PO4(3-) -P in the first 3 days. The release amount of NH4(+) -N from Arachis hypogaea group was larger than those of the other three groups, reaching 36.79 mg x kg(-1). Similarly, Zea mays group had the largest release of PO4(3-) -P, which was 70.64 mg x kg(-1). All suggest that biochar is a potential in-situ capping material to reduce the release of NH4(+) -N, COD and PO4(3-) -P in polluted sediments, and has the ability of applying to the remediation of sediment in the polluted water.