Robust Multiple-View Geometry Estimation Based on GMM

Given three partially overlapping views of the scene from which a set of point or line correspondences have been extracted, 3D structure and camera motion parameters can be represented by the trifocal tensor, which is the key to many problems of computer vision on three views. Unlike in conventional typical methods, the residual value is the only rule to eliminate outliers with large value, we build a Gaussian mixture model assuming that the residuals corresponding to the inliers come from Gaussian distributions different from that of the residuals of outliers. Then Bayesian rule of minimal risk is employed to classify all the correspondences using the parameters computed from GMM. Experiments with both synthetic data and real images show that our method is more robust and precise than other typical methods because it can efficiently detect and delete the bad corresponding points, which include both bad locations and false matches

PRL-3 promotes the motility, invasion, and metastasis of LoVo colon cancer cells through PRL-3-integrin β1-ERK1/2 and-MMP2 signaling

<p>Abstract</p> <p>Background</p> <p>Phosphatase of regenerating liver-3 (PRL-3) plays a causative role in tumor metastasis, but the underlying mechanisms are not well understood. In our previous study, we observed that PRL-3 could decrease tyrosine phosphorylation of integrin β1 and enhance activation of ERK1/2 in HEK293 cells. Herein we aim to explore the association of PRL-3 with integrin β1 signaling and its functional implications in motility, invasion, and metastasis of colon cancer cell LoVo.</p> <p>Methods</p> <p>Transwell chamber assay and nude mouse model were used to study motility and invasion, and metastsis of LoVo colon cancer cells, respectively. Knockdown of integrin β1 by siRNA or lentivirus were detected with Western blot and RT-PCR. The effect of PRL-3 on integrin β1, ERK1/2, and MMPs that mediate motility, invasion, and metastasis were measured by Western blot, immunofluorencence, co-immunoprecipitation and zymographic assays.</p> <p>Results</p> <p>We demonstrated that PRL-3 associated with integrin β1 and its expression was positively correlated with ERK1/2 phosphorylation in colon cancer tissues. Depletion of integrin β1 with siRNA, not only abrogated the activation of ERK1/2 stimulated by PRL-3, but also abolished PRL-3-induced motility and invasion of LoVo cells in vitro. Similarly, inhibition of ERK1/2 phosphorylation with U0126 or MMP activity with GM6001 also impaired PRL-3-induced invasion. In addition, PRL-3 promoted gelatinolytic activity of MMP2, and this stimulation correlated with decreased TIMP2 expression. Moreover, PRL-3-stimulated lung metastasis of LoVo cells in a nude mouse model was inhibited when integrin β1 expression was interfered with shRNA.</p> <p>Conclusion</p> <p>Our results suggest that PRL-3's roles in motility, invasion, and metastasis in colon cancer are critically controlled by the integrin β1-ERK1/2-MMP2 signaling.</p

Self-assembly of hydrofluorinated Janus graphene monolayer:a versatile route for designing novel Janus nanoscrolls

With remarkably interesting surface activities, two-dimensional Janus materials arouse intensive interests recently in many fields. We demonstrate by molecular dynamic simulations that hydrofluorinated Janus graphene (J-GN) can self-assemble into Janus nanoscroll (J-NS) at room temperature. The van der Waals (vdW) interaction and the coupling of C-H/π/C-F interaction and π/π interaction are proven to offer the continuous driving force of self-assembly of J-GN. The results show that J-GN can self-assemble into various J-NSs structures, including arcs, multi-wall J-NS and arm-chair-like J-NS by manipulating its original geometry (size and aspect ratio). Moreover, we also investigated self-assembly of hydrofluorinated J-GN and Fe nanowires (NWs), suggesting that Fe NW is a good alternative to activate J-GN to form J-NS. Differently, the strong vdW interaction between J-GN and Fe NW provides the main driving force of the self-assembly. Finally, we studied the hydrogen sorption over the formed J-NS with a considerable interlayer spacing, which reaches the US DOE target, indicating that J-NS is a promising candidate for hydrogen storage by controlling the temperature of system. Our theoretical results firstly provide a versatile route for designing novel J-NS from 2D Janus nanomaterials, which has a great potential application in the realm of hydrogen storage/separation

Synuclein gamma predicts poor clinical outcome in colon cancer with normal levels of carcinoembryonic antigen

<p>Abstract</p> <p>Background</p> <p>Synuclein gamma (SNCG), initially identified as a breast cancer specific gene, is aberrantly expressed in many different malignant tumors but rarely expressed in matched nonneoplastic adjacent tissues. In this study, we investigated the prognostic potential of SNCG in colon cancer particularly in the patients with normal carcinoembryonic antigen (CEA) levels.</p> <p>Methods</p> <p>SNCG levels were assessed immunohistochemically in cancer tissues from 229 colon adenocarcinoma patients with a mean follow-up of 44 months. Correlations between SNCG levels and clinicopathologic features, preoperative serum CEA level, and clinical outcome were analyzed statistically using SPSS.</p> <p>Results</p> <p>SNCG levels in colon adenocarcinoma were closely associated with intravascular embolus and tumor recurrence but independent of preoperative serum CEA levels. SNCG expression was an independent prognostic factor of a shorter disease-free survival (DFS) and overall survival (OS) (<it>P </it>< 0.0001). Multivariate analysis revealed that both tissue SNCG and serum CEA were independent prognostic factors of DFS (<it>P </it>= 0.001, <0.0001, respectively) for 170 patients with colon adenocarcinomas. Importantly, SNCG remained a prognostic determinant of DFS and OS (<it>P </it>= 0.001, 0.002) for 97 patients with normal preoperative serum CEA level.</p> <p>Conclusions</p> <p>Our results suggest for the first time that SNCG is a new independent predicator for poor prognosis in patients with colon adenocarcinoma, including those with normal CEA levels. Combination of CEA with SNCG improves prognostic evaluation for patients with colon adenocarcinoma.</p

A Differential Evolution-Based Routing Algorithm for Environmental Monitoring Wireless Sensor Networks

The traditional Low Energy Adaptive Cluster Hierarchy (LEACH) routing protocol is a clustering-based protocol. The uneven selection of cluster heads results in premature death of cluster heads and premature blind nodes inside the clusters, thus reducing the overall lifetime of the network. With a full consideration of information on energy and distance distribution of neighboring nodes inside the clusters, this paper proposes a new routing algorithm based on differential evolution (DE) to improve the LEACH routing protocol. To meet the requirements of monitoring applications in outdoor environments such as the meteorological, hydrological and wetland ecological environments, the proposed algorithm uses the simple and fast search features of DE to optimize the multi-objective selection of cluster heads and prevent blind nodes for improved energy efficiency and system stability. Simulation results show that the proposed new LEACH routing algorithm has better performance, effectively extends the working lifetime of the system, and improves the quality of the wireless sensor networks

Transcriptomic analysis reveals the functions of H2S as a gasotransmitter independently of Cys in Arabidopsis

Numerous studies have revealed the gasotransmitter functions of hydrogen sulfide (H2S) in various biological processes. However, the involvement of H2S in sulfur metabolism and/or Cys synthesis makes its role as a signaling molecule ambiguous. The generation of endogenous H2S in plants is closely related to the metabolism of Cys, which play roles in a variety of signaling pathway occurring in various cellular processes. Here, we found that exogenous H2S fumigation and Cys treatment modulated the production rate and content of endogenous H2S and Cys to various degrees. Furthermore, we provided comprehensive transcriptomic analysis to support the gasotransmitter role of H2S besides as a substrate for Cys synthesis. Comparison of the differentially expressed genes (DEGs) between H2S and Cys treated seedlings indicated that H2S fumigation and Cys treatment caused different influences on gene profiles during seedlings development. A total of 261 genes were identified to respond to H2S fumigation, among which 72 genes were co-regulated by Cys treatment. GO and KEGG enrichment analysis of the 189 genes, H2S but not Cys regulated DEGs, indicated that these genes mainly involved in plant hormone signal transduction, plant-pathogen interaction, phenylpropanoid biosynthesis, and MAPK signaling pathway. Most of these genes encoded proteins having DNA binding and transcription factor activities that play roles in a variety of plant developmental and environmental responses. Many stress-responsive genes and some Ca2+ signal associated genes were also included. Consequently, H2S regulated gene expression through its role as a gasotransmitter, rather than just as a substrate for Cys biogenesis, and these 189 genes were far more likely to function in H2S signal transduction independently of Cys. Our data will provide insights for revealing and enriching H2S signaling networks

RANKL/RANK promotes the migration of gastric cancer cells by interacting with EGFR

BACKGROUND: The incidence and mortality rates of gastric cancer (GC) rank in top five among all malignant tumors. Chemokines and their receptor-signaling pathways reportedly play key roles in the metastasis of malignant tumor cells. Receptor activator of nuclear factor κB ligand (RANKL) is a member of the tumor necrosis factor family, with strong chemokine-like effects. Some studies have pointed out that the RANKL/RANK pathway is vital for the metastasis of cancer cells, but the specific mechanisms in GC remain poorly understood. RESULTS: This study reports original findings in cell culture models and in patients with GC. Flow cytometry and western blotting analyses showed that RANK was expressed in BGC-823 and SGC-7901 cells in particular. Chemotaxis experiments and wound healing assay suggested that RANKL spurred the migration of GC cells. This effect was offset by osteoprotegerin (OPG), a decoy receptor for RANKL. RANKL contributed to the activation of human epidermal growth factor receptor (HER) family pathways. The lipid raft core protein, caveolin 1 (Cav-1), interacted with both RANK and human epidermal growth factor receptor-1(EGFR). Knockdown of Cav-1 blocked the activation of EGFR and cell migration induced by RANKL. Moreover, RANK-positive GC patients who displayed higher levels of EGFR expression had poor overall survival. CONCLUSIONS: In summary, we confirmed that with the promotion of RANKL, RANK and EGFR can form complexes with the lipid raft core protein Cav-1, which together promote GC cell migration. The formation of the RANK-Cav-1-EGFR complex provides a novel mechanism for the metastasis of GC. These observations warrant confirmation in independent studies, in vitro and in vivo. They also inform future drug target discovery research and innovation in the treatment of GC progression

TfR1 binding with H-ferritin nanocarrier achieves prognostic diagnosis and enhances the therapeutic efficacy in clinical gastric cancer

H-ferritin (HFn) nanocarrier is emerging as a promising theranostic platform for tumor diagnosis and therapy, which can specifically target tumor cells via binding transferrin receptor 1 (TfR1). This led us to investigate the therapeutic function of TfR1 in GC. The clinical significance of TfR1 was assessed in 178 GC tissues by using a magneto-HFn nanoparticle-based immunohistochemistry method. The therapeutic effects of doxorubicin-loaded HFn nanocarriers (HFn-Dox) were evaluated on TfR1-positive GC patient-derived xenograft (GC-PDX) models. The biological function of TfR1 was investigated through in vitro and in vivo assays. TfR1 was upregulated (73.03%) in GC tissues, and reversely correlated with patient outcome. TfR1-negative sorted cells exhibited tumor-initiating features, which enhanced tumor formation and migration/invasion, whereas TfR1-positive sorted cells showed significant proliferation ability. Knockout of TfR1 in GC cells also enhanced cell invasion. TfR1-deficient cells displayed immune escape by upregulating PD-L1, CXCL9, and CXCL10, when disposed with IFN-γ. Western blot results demonstrated that TfR1-knockout GC cells upregulated Akt and STAT3 signaling. Moreover, in TfR1-positive GC-PDX models, the HFn-Dox group significantly inhibited tumor growth, and increased mouse survival, compared with that of free-Dox group. TfR1 could be a potential prognostic and therapeutic biomarker for GC: (i) TfR1 reversely correlated with patient outcome, and its negative cells possessed tumor-aggressive features; (ii) TfR1-positive cells can be killed by HFn drug nanocarrier. Given the heterogeneity of GC, HFn drug nanocarrier combined with other therapies toward TfR1-negative cells (such as small molecules or immunotherapy) will be a new option for GC treatment

Quantitatively assessing ecological stress of urbanization on natural ecosystems by using a landscape-adjacency index

Urban spatial expansion poses a threat to regional ecosystems and biodiversity directly through altering the size, shape, and interconnectivity of natural landscapes. Monitoring urban spatial expansion using traditional area-based metrics from remote sensing provides a feasible way to quantify this regional ecological stress. However, variation in landscape-adjacency relationships (i.e., the adjacency between individual landscape classes) caused by urban expansion is often overlooked. In this study, a novel edge-based index (landscape-adjacency index, LAdI) was proposed based on the spatial-adjacency relationship between landscape patches to measure the regional ecological stress of urban expansion on natural landscapes. Taking the entire Yangtze River Delta Urban Agglomerations (YRD) as a study area, we applied the LAdI for individual landscape classes (Vi) and landscape level (LV) to quantitatively assess change over time in the ecological stress of YRD from 1990 to 2015 at two spatial scales: municipal scale and 5 km-grid scale. The results showed that the vulnerable zones (LV ≥ 0.6) were mainly distributed in the north of the YRD, and cultivated land was the most vulnerable natural landscape (Vi ≥ 0.6) at the 5 km-grid scale. The most vulnerable landscape at the municipal scale was cultivated land in 19 of 26 cities in each period, and that in the remaining 7 cities varied at distinct urbanization stages. We used scatter diagrams and Pearson correlation analysis to compare the edge-based LAdI with an area-based index (percent of built-up area, PB) and found that: LV and PB had a significant positive correlation at both the municipal scale and 5 km-grid scale. But there were multiple LVs with different values corresponding to one PB with the same value at the 5 km-grid scale. Both indexes could represent the degree of urban expansion; however, the edge-based metric better quantified ecological stress under different urban-sprawl patterns sharing the same percent of built-up area. As changes in land use affect both the size and edge effect among landscape patches, the area-based PB and the edge-based LAdI should be applied together when assessing the ecological stress caused by urbanization

The role of APOBEC3C in modulating the tumor microenvironment and stemness properties of glioma: evidence from pancancer analysis

BackgroundIt is now understood that APOBEC3 family proteins (A3s) are essential in tumor progression, yet their involvement in tumor immunity and stemness across diverse cancer types remains poorly understood.MethodsIn the present study, comprehensive genome-wide statistical and bioinformatic analyses were conducted to elucidate A3 family expression patterns, establishing clinically relevant correlations with prognosis, the tumor microenvironment(TME), immune infiltration, checkpoint blockade, and stemness across cancers. Different experimental techniques were applied, including RT–qPCR, immunohistochemistry, sphere formation assays, Transwell migration assays, and wound-healing assays, to investigate the impact of A3C on low-grade glioma (LGG) and glioblastoma multiforme (GBM), as well as its function in glioma stem cells(GSCs).ResultsDysregulated expression of A3s was observed in various human cancer tissues. The prognostic value of A3 expression differed across cancer types, with a link to particularly unfavorable outcomes in gliomas. A3s are associated with the the TME and stemness in multiple cancers. Additionally, we developed an independent prognostic model based on A3s expression, which may be an independent prognostic factor for OS in patients with glioma. Subsequent validation underscored a strong association between elevated A3C expression and adverse prognostic outcomes, higher tumor grades, and unfavorable histology in glioma. A potential connection between A3C and glioma progression was established. Notably, gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses implicated A3C in immune system-related diseases, with heightened A3C levels contributing to an immunosuppressive tumor microenvironment (TME) in glioma. Furthermore, in vitro experiments substantiated the role of A3C in sustaining and renewing glioma stem cells, as A3C deletion led to diminished proliferation, invasion, and migration of glioma cells.ConclusionThe A3 family exhibits heterogeneous expression across various cancer types, with its expression profile serving as a predictive marker for overall survival in glioma patients. A3C emerges as a regulator of glioma progression, exerting its influence through modulation of the tumor microenvironment and regulation of stemness