DCLRE1B promotes tumor progression and predicts immunotherapy response through METTL3-mediated m6A modification in pancreatic cancer.

BACKGROUND: DCLRE1B is a 5'-to-3' exonuclease, which is involved in repairing ICL-related DNA damage. DCLRE1B has been reported to cause poor prognosis in a variety of cancers. Nonetheless, there is no research on DCLRE1B's biological role in pan-cancer datasets. Thus, ascertaining the processes via which DCLRE1B modulates tumorigenesis was the goal of the extensive bioinformatics investigation of pan-cancer datasets in the present research. METHODS: In our research, employing internet websites and databases including TIMER, GEPIA, TISIDB, Kaplan-Meier Plotter, SangerBox, cBioPortal, and LinkedOmics, DCLRE1B-related data in numerous tumors were extracted. To ascertain the association among DCLRE1B expression, prognosis, genetic changes, and tumor immunity, the pan-cancer datasets were examined. The DCLRE1B's biological roles in pancreatic cancer cells were ascertained by employing wound healing, in vitro CCK-8, and MeRIP-qPCR assays. RESULT: According to the pan-cancer analysis, in numerous solid tumors, DCLRE1B upregulation was observed. Expression of DCLRE1B was found to be substantially related to the cancer patients' prognoses. Similarly, expression of DCLRE1B exhibited substantial association with immune cells in several cancer types. DCLRE1B expression correlated with immune checkpoint (ICP) gene expression and impacted immunotherapy sensitivity. According to in vitro trials, DCLRE1B promoted PC cells' proliferation and migration capacities. Also, according to GSEA enrichment analysis, DCLRE1B might participate in the JAK-STAT signaling pathway, which was confirmed by western blotting. In addition, we also found that the downregulation of DCLRE1B may be regulated by METTL3-mediated m6A modification. CONCLUSIONS: In human cancer, the overexpression of DCLRE1B was generally observed, which aided cancer onset and advancement via a variety of processes comprising control of the immune cells' tumor infiltration. According to this study's findings, in a few malignant tumors, DCLRE1B is a candidate immunotherapeutic and prognostic biomarker.

HairStyle Editing via Parametric Controllable Strokes.

In this work, we propose a stroke-based hairstyle editing network, dubbed HairstyleNet, allowing users to conveniently change the hairstyles of an image in an interactive fashion. Different from previous works, we simplify the hairstyle editing process where users can manipulate local or entire hairstyles by adjusting the parameterized hair regions. Our HairstyleNet consists of two stages: a stroke parameterization stage and a stroke-to-hair generation stage. In the stroke parameterization stage, we firstly introduce parametric strokes to approximate the hair wisps, where the stroke shape is controlled by a quadratic Bézier curve and a thickness parameter. Since rendering strokes with thickness to an image is not differentiable, we opt to leverage a neural renderer to construct the mapping from stroke parameters to a stroke image. Thus, the stroke parameters can be directly estimated from hair regions in a differentiable way, enabling us to flexibly edit the hairstyles of input images. In the stroke-to-hair generation stage, we design a hairstyle refinement network that first encodes coarsely composed images of hair strokes, face, and background into latent representations and then generates high-fidelity face images with desirable new hairstyles from the latent codes. Extensive experiments demonstrate that our HairstyleNet achieves state-of-the-art performance and allows flexible hairstyle manipulation.

Hypoxia-induced Long Non-coding RNA LSAMP-AS1 Regulates ceRNA Network to Predict Prognosis for Pancreatic Cancer.

BACKGROUND: The limited efficacy of chemotherapy and immunotherapy for pancreatic cancer is thought to be largely influenced by the surrounding cancer microenvironment. The hypoxic microenvironment caused by insufficient local blood supply is very important. However, the method to assess the level of hypoxia in the microenvironment of pancreatic cancer (PC) remains unclear. METHODS: In our research, we downloaded transcriptomic and clinicopathological data from the Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO). A prognostic model was developed using univariate and multivariate Cox regression. The ConsensuClusterPlus R package was used to consistently cluster PC samples through unsupervised clustering. Gene set variation analysis (GSVA) was performed to identify the different functional phenotypes. The CIBERSORT evaluated the infiltration status of immune cells. qRT-PCR was performed to detect the expression of genes in PC cells and tissues. RESULTS: A preliminary risk model was developed to reflect the hypoxic environment of pancreatic cancer. We found that a high hypoxia risk score indicated poor long-term survival and the presence of an immunosuppressive microenvironment. In addition, based on prognostic hypoxia-related genes, 177 PC samples were divided into two subtypes. Compared with cluster 2, cluster 1 was defined as the "hypoxic subgroup". The infiltration of CD8 T cells, activated memory CD4 T cells, naive B cells, memory B cells, plasma cells, and neutrophils were lower in cluster 1, suggesting that there was significant immunosuppression in cluster 1. Beyond that, we constructed a ceRNA regulatory network composed of differentially expressed lncRNA, miRNA, and mRNA. LSAMPAS1/ hsa-miR-129-5p/S100A2 has been identified as a key ceRNA network that regulates the hypoxic environment and the prognosis of PC. Notably, in our study, qRT-PCR revealed the relative expression of LSAMP-AS1 and S100A2 was significantly upregulated in PC cells and tissue. CONCLUSION: The hypoxia-related prognostic risk model and core ceRNA network established in our study will provide a new perspective for exploring the carcinogenic mechanism and potential therapeutic targets of pancreatic cancer.

Molecular subtyping based on TRP family and prognostic assessment for TRP-associated lncRNAs in pancreatic adenocarcinoma.

BACKGROUND: Transient receptor potential (TRP) channels have high permeability to Ca2+ ions because they are non-selective ion channels. TRP channels have been implicated in tumor onset and progression, proliferation, and migration in recent years. However, the prognostic value of genes related to TRP and their specific mechanism in pancreatic adenocarcinoma (PAAD) are yet to be understood. METHODS: Public databases such as TCGA and GEO were used to retrieve data on gene expression and clinical information of patients with pancreatic adenocarcinoma for our study. ConsensusClusterPlus package was used for unsupervised clustering analysis. The microenvironment cell population (MCP)-counter approach was employed to measure the immune cells infiltration status. The Pearson correlation was performed to identify TRP-associated lncRNAs. RESULTS: Initially, we separated PAAD patients into three clusters depending on TRP-related genes, and of the three clusters, cluster B showed the least immune cell infiltration, which was correlated with poor prognosis. Moreover, GSVA enrichment analysis further revealed that cluster A was subjected to a considerable enrichment in carcinogenic signaling pathways, whereas cluster C was enriched in immune-related pathways. Then, using TRP-associated lncRNAs as a starting point, we constructed a prognostic risk model for PAAD patients that could efficiently predict their prognosis. Further, GSEA revealed that cancer-related pathways, for instance, the cell cycle, p53 signaling pathway, etc. were considerably enriched in the high-risk group. In addition, we looked into the link between the prognostic model and the immunological microenvironment. Lower cytotoxic lymphocytes, NK cells, CD8 T cells, and endothelial cells infiltration were found to be associated with high risk using the MCP-counter algorithm. The expression of CD274, POLE2, MCM6, and LOXL2 was also found to be higher in the high-risk group. TMB was also considerably greater in high-risk individuals, indicating that immune checkpoint inhibitors (ICIs) therapy may benefit them more. Lastly, qRT-PCR further confirmed the differential expression of these prognostic TRP-associated lncRNAs, indicating that these lncRNAs play an imperative role in PAAD tumorigenesis. CONCLUSION: TRP family genes may represent a new class of candidate molecular markers of the occurrence and progression of PAAD. Risk models based on TRP-associated lncRNAs could provide important new references for immunotargeted therapy of pancreatic adenocarcinoma.

Identification of CKS1B as a prognostic indicator and a predictive marker for immunotherapy in pancreatic cancer.

As a regulatory subunit of cyclin kinase, CKS1B promotes cancer development and is associated with poor prognosis in multiple cancer patients. However, the intrinsic role of CKS1B in pancreatic cancer remains elusive. In our research, CKS1B expression in pancreatic tumor tissue was higher than that in normal tissue by TCGA, Oncomine and CPTAC databases analysis. Similar result was verified in our center tissues by qRT-PCR. CKS1B expression was closely relevant to histologic grading, prognosis, and TMB. GSEA showed that CKS1B mainly participated in the regulation of autophagy and T cell receptor signaling pathway. Furthermore, CIBERSORT analysis showed that there was a strong correlation between CKS1B expression and tumor immune cells infiltration. Drug sensitivity analysis showed that patients with high CKS1B expression appeared to be more sensitive to gemcitabine, 5-fluorouracil, and paclitaxel. We then investigated cell viability and migratory ability by CCK8 and transwell assay, respectively. Results indicated that CKS1B knockdown by short hairpin RNA significantly reduced pancreatic cancer cell viability and invasion via regulating PD-L1 expression. In conclusion, our research further demonstrates the role of CKS1B in pancreatic cancer and the signaling pathways involved. The association of CKS1B with immune infiltration and immune checkpoint may provide a new direction for immunotherapy of pancreatic cancer.

Robotic Taj Mahal Hepatectomy for Hilar Cholangiocarcinoma.

Hilar cholangiocarcinoma is the most common malignant tumor of the biliary tract. Radical surgical resection is the only effective treatment option. In this study, a 32-year-old male patient with Bismuth Type IVa hilar cholangiocarcinoma underwent radical robotic resection of hepatic S4b, S5, and S1 (Taj Mahal hepatectomy) combined with regional lymphadenectomy, hilar bile duct reconstruction, and hepaticojejunostomy by the robotic surgical system. Postoperative pathological examination showed moderately-differentiated adenocarcinoma of the hilar bile duct. The surgical margins of the liver and bile ducts were negative. Recovery was smooth and the patient was discharged on the 17th postoperative day. The robotic surgical system and associated multiple instruments along with flexible and precise movements is suitable for the local hepatectomy around the porta hepatis, and delicate reconstruction of the hilar bile duct with a smaller diameter. This first clinical application study found that robotic Taj Mahal hepatectomy for hilar cholangiocarcinoma is safe and feasible and needs more experience for the evaluation of its long-term outcomes.

Analysis of Pyroptosis-Related Signature for Predicting Prognosis and Tumor Immune Microenvironment in Pancreatic Cancer.

Pancreatic cancer (PC) has a poor prognosis, which is attributable to its high aggressiveness and lack of effective therapies. Although immunotherapy has been used for the treatment of various tumor, its efficacy in pancreatic cancer is not satisfactory. As a caspase-1-dependent programmed cell death, pyroptosis s involved in the pathological process of many tumors. Nevertheless, the vital role of the pyroptosis-related gene (PRG) in PC remains unknown. In this study, univariate COX regression was performed for 33 pyroptosis-related genes. Based on these prognosis-related PRGs, all PC patients in the Cancer Genome Atlas (TCGA) database were divided into four subtypes. Then, pyroptosis score (PP-score) was established to quantify pyroptosis level for individual PC patients using principal component analysis (PCA) algorithms. Assessment of pyroptosis level within individual PC patients may predict tumor classification and patient prognosis. Finally, a signature was constructed in TCGA and verified in ICGC. In addition, immunocheckpoint analysis revealed the possibility that the low-risk group would benefit more from immunocheckpoint therapy. Taken together, pyroptosis-related genes play a significant role in tumor immunotherapy and can be utilized to predict the prognosis of PC patients.

PIWIL4 and SUPT5H combine to predict prognosis and immune landscape in intrahepatic cholangiocarcinoma.

BACKGROUND: Intrahepatic cholangiocarcinoma (ICC) is a fatal primary liver cancer, and its long-term survival rate remains poor. RNA-binding proteins (RBPs) play an important role in critical cellular processes, failure of any one or more processes can lead to the development of multiple cancers. This study aimed to explore pivotal biomarkers and corresponding mechanisms to predict the prognosis of patients with ICC. METHODS: The transcriptomic and clinical information of patients were collected from The Cancer Genome Atlas and Gene Expression Omnibus databases. Bioinformatic methods were used to identify survival-related and differentially-expressed biomarkers. Quantitative real-time PCR (qRT-PCR) and immunohistochemistry were used to detect the expression levels of key biomarkers in independent real-world cohorts. Subsequently, a prognostic signature was constructed that effectively distinguished patients in the high- and low-risk groups. Independent prognosis analysis was used to verify the signature's independent predictive capabilities, and two nomograms were developed to predict survival. RESULTS: PIWIL4 and SUPT5H were identified and considered as pivotal biomarkers, and the same expression trends of upregulation in ICC were also validated via qRT-PCR and immunohistochemistry in the separate real-world sample cohorts. The prognostic signature showed good predictive capabilities according to the area under the curve. The correlation of the biomarkers with the tumour microenvironment suggested that the high riskScore was positively related to the enrichment of resting natural killer cells and activated memory CD4 + T cells. CONCLUSION: In the present study, we demonstrated that PIWIL4 and SUPT5H could be used as novel prognostic biomarkers to develop a prognostic signature. This study provides potential biomarkers of prognostic value for patients with intrahepatic cholangiocarcinoma.

Up-regulation of S100P predicts the poor long-term survival and construction of prognostic signature for survival and immunotherapy in patients with pancreatic cancer.

Pancreatic cancer is associated with a high mortality rate, and the prognosis is positively related to immune status. In this study, we constructed a prognostic signature from survival- and immune-related genes (IRGs) to guide treatment and assess prognosis of patients with pancreatic cancer. The transcriptomic data were obtained from The Cancer Genome Atlas (TCGA) database, and IRGs were extracted from the ImmPort database. Univariate and LASSO regression analysis were used to obtain survival-related IRGs. Finally, the prognostic signature was constructed using multivariate regression analysis. The laboratory experiments were conducted to verify the key IRG expression. Immune cells infiltration was analyzed using the CIBERSORT algorithm and TIMER database. Prognostic signature containing four IRGs (ADA2, TLR1, PTPN6, S100P) was constructed with good predictive performance; in particular, S100P played a significant role in the immune microenvironment, and tumorigenesis of pancreatic cancer. Moreover, we found that CD8+ T cell and activated CD4+ memory T cell tumor infiltration was lower in the high-risk group, while high-risk score correlated positively with higher tumor mutational burden, and the higher half inhibitory centration 50 of chemotherapeutic agents Docetaxel and Sunitinib. In summary, this study identified and constructed an immune-related prognostic signature that can predict overall survival, besides suggests that S100P was a novel immune-related biomarker. We hope that this signature will aid the identification of new biomarkers for the individualized immunotherapy of pancreatic cancer.

A metabolism-related 4-lncRNA prognostic signature and corresponding mechanisms in intrahepatic cholangiocarcinoma.

BACKGROUND: Long non-coding RNA (lncRNA) plays a critical role in the malignant progression of intrahepatic cholangiocarcinoma (iCCA). This study aimed to establish a 4-lncRNA prognostic signature and explore corresponding potential mechanisms in patients with iCCA. METHODS: The original lncRNA-seq and clinical data were collected from the TCGA and GEO databases. Overlapping and differentially expressed lncRNAs (DE-lncRNAs) were further identified from transcriptome data. Univariate regression analysis was performed to screen survival-related DE-lncRNAs, which were further selected to develop an optimal signature to predict prognosis using multivariate regression analysis. The Kaplan-Meier survival curve visualized the discrimination of the signature on overall survival (OS). The area under the curve (AUC) and C-index were used to verify the predictive accuracy of the signature. Combined with clinical data, multivariate survival analysis was used to reveal the independent predictive capability of the signature. In addition, a prognostic nomogram was constructed. Finally, the common target genes of 4 lncRNAs were predicted by the co-expression method, and the corresponding functions were annotated by GO and KEGG enrichment analysis. Gene set enrichment analysis (GSEA) was also performed to explore the potential mechanism of the signature. Quantitative real-time PCR was used to evaluated the expression of 4 lncRNAs in an independent cohort. RESULTS: We identified and constructed a 4-lncRNA (AC138430.1, AGAP2-AS1, AP001783.1, and AP005233.2) prognostic signature using regression analysis, and it had the capability to independently predict prognosis. The AUCs were 0.952, 0.909, and 0.882 at 1, 2, and 3 years, respectively, and the C-index was 0.808, which showed good predictive capability. Subsequently, combined with clinical data, we constructed a nomogram with good clinical application. Finally, 252 target genes of all four lncRNAs were identified by the co-expression method, and functional enrichment analysis showed that the signature was strongly correlated with metabolism-related mechanisms in tumourigenesis. The same results were also validated via GSEA. CONCLUSION: We demonstrated that a metabolism-related 4-lncRNA prognostic signature could be a novel biomarker and deeply explored the target genes and potential mechanism. This study will provide a promising therapeutic strategy for patients with intrahepatic cholangiocarcinoma.

Integrative Analysis of MicroRNAs and mRNAs in LPS-Induced Macrophage Inflammation Based on Adipose Tissue Stem Cell Therapy.

Severe inflammation can lead to multiple organ dysfunction syndrome, which has high mortality. Adipose-derived stem cells have been shown to affect the inflammatory response of macrophages. However, the molecular mechanism of the anti-inflammatory capacity of adipose-derived stem cells (ADSCs) remains to be understood. In the present study, a macrophage inflammation model was established by LPS, and treated with different volumes of ADSC supernatant. Then, we investigated the key genes in the LPS group and treatment group by RT-PCR, RNA sequencing technology, and bioinformatics analysis. A total of 26 miRNAs and 11,882 mRNAs were differentially expressed between them. The expression of 15 of the miRNAs (9 upregulated and 6 downregulated) was confirmed by RT-PCR. GO and KEGG pathway analyses of the targets of the 9 significantly upregulated miRNAs showed that they were related to immune system process, inflammatory response, lipopolysaccharide, and TNF-α, NF-κB, Toll-like receptor, and MAPK signaling pathways. Moreover, a miRNA-mRNA network also revealed 8 important genes (Mapkapk2, Sepp1, Cers6, Snn, ZfP568, Ccdc93, Pofut1, Pik3cd). We finally confirmed the expression of these 8 targeted genes by performing the RT-PCR analysis. This study may provide a new understanding of the molecular mechanism of ADSCs in the inflammatory response related to multiple miRNAs and mRNAs.

Extracellular Vesicles From Adipose Tissue-Derived Stem Cells Affect Notch-miR148a-3p Axis to Regulate Polarization of Macrophages and Alleviate Sepsis in Mice.

Extracellular vesicles (EVs) from adipose tissue-derived stem cells have been reported to attenuate lipopolysaccharide (LPS) induced inflammation and sepsis while the specific mechanism is unclear. This study explored the underlying molecular mechanisms of EVs from adipose tissue-derived stem cells in reducing inflammation. LPS- induced macrophage models and mice model were established to mimic inflammation in vitro and in vivo. EVs were extracted from adipose tissue-derived stem cells and identified. It was found that proinflammatory cytokines, including IL-1ß, IL-6, and TNF-α, substantially decreased after EVs were applied to LPS-stimulated macrophages and mice, and thus, LPS induced M1 polarization was inhibited and sepsis was strongly alleviated. In the LPS induced macrophages, the expression of Notch signaling molecules and the activation of the NF-κB pathway were substantially decreased after the administration of EVs. Then, RBP-J-/- mice and macrophages were used. It was found that the miR-148a-3p level was significantly lower in the RBP-J-/- macrophages than in the wildtype macrophages. In the LPS induced macrophages, the increasing of miR-148a-3p was milder in the RBP-J-/- macrophages than in the wild type macrophages. Then, miR-148a-3p was overexpressed in macrophages and mice, and we found that the expression of proinflammatory cytokines was increased both in vivo and in vitro. The protective effect of EVs in LPS induced sepsis was diminished by the overexpression of miR-148a-3p. In conclusion, we proved that EVs could attenuate inflammation and further protect organ function by regulating the Notch-miR148a-3p signaling axis and then decreasing macrophage polarization to M1.

Highly Efficient Adsorption and Reduction of Cr(VI) Ions by a Core-Shell Fe3O4@UiO-66@PANI Composite.

Herein, we reported a simple solvothermal and chemical oxidation method to synthesize a magnetic core-shell composite (Fe3O4@UiO-66@PANI) for Cr(VI) removal from wastewater. Due to the porosity and stability of UiO-66 and stability, high acid resistance, and multiple active (reducing and chelating) groups of polyaniline (PANI), Fe3O4@UiO-66@PANI exhibited excellent efficiency, regeneration, and reusability performance for Cr(VI) removal. Its maximum adsorption capacity and removal rate were 474.42 mg·g-1 and 99.90%, respectively. The effects of initial pH values, contact time, and initial Cr(VI) concentration on Cr(VI) removal were investigated. The fitted data showed that the adsorption process was consistent with the pseudo-second-order kinetic model and Langmuir isothermal model. The study of the mechanism shows that the excellent efficiency of Fe3O4@UiO-66@PANI is due to the electrostatic adsorption and reduction of Cr(VI) and the chelation of Cr3+. The results demonstrate that Fe3O4@UiO-66@PANI is a promising adsorbent for the Cr(VI) removal.

Research progress on SIRT1 and sepsis.

SIRT1, a member of the sirtuin family, belongs to the NAD⁺-dependent class III histone deacetylase. SIRT1 can regulate gene expression by catalyzing non-histone and histone lysine residues deacetylation. SIRT1 also plays important roles in glucose and lipid metabolism, cell aging, tumorigenesis and inflammation. Recent studies indicate that SIRT1 can inhibit the inflammatory responses via regulating several inflammatory signaling pathways. It is closely related to the occurrence and development of sepsis and other inflammatory diseases. Research has been done on relevant signaling pathways of SIRT1 as well as its target genes during inflammation. SIRT1 is a hot spot in uncontrolled inflammatory response research. This article focuses on the role of SIRT1 in inflammation, especially its targets and involved signaling pathways in sepsis, and tries to provide more convincing evidence for the clinical treatment of sepsis and other inflammatory diseases.

A novel superparamagnetic micro-nano-bio-adsorbent PDA/Fe3O4/BC for removal of hexavalent chromium ions from simulated and electroplating wastewater.

In order to improve the adsorption efficiency of the adsorbent and solve the problem of separation difficulty, a novel superparamagnetic micro-nano-bio-adsorbent (PDA/Fe3O4/BC) was prepared by in situ self-assembly of polydopamine (PDA). The results of scanning electron microscope (SEM), X-ray diffraction (XRD), Fourier transform infrared spectrometer (FT-IR), X-ray photoelectron spectrometer (XPS), and vibrating sample magnetometer (VSM) characterization showed that the size of bio-adsorbent was about 200 nm. PDA and Fe3O4 modifications increased the specific surface area of adsorbent, changed the surface functional group of biochar (BC), and made the adsorbent have super-high magnetization (294.76 emu g-1). PDA/Fe3O4/BC was applied to treat Cr wastewater. The results show that the adsorption of Cr by PDA/Fe3O4/BC includes single-layer and multilayer adsorption. The adsorption follows the pseudo-second-order kinetic model. The adsorption is spontaneous and endothermic, and its maximum adsorption capacity and activation energy are 25.25 mg g-1 at 318 K and 23.108 kJ mol-1, respectively. After adsorption treatment, PDA/Fe3O4/BC still possesses high magnetization (233.04 emu g-1). PDA/Fe3O4/BC can treat actual electroplating wastewater with Cr(VI) concentration from 20 mg L-1 to less than 0.2 mg L-1, which met the PRC discharge standard (GB/21900-2008) of electroplating pollutants. Graphical abstract.

Inhibition of SIRT1 by microRNA-9, the key point in process of LPS-induced severe inflammation.

Severe inflammation may lead to multiple organs dysfunction syndrome, which has a high mortality. MicroRNA is found participated in this process. In this study we developed a lipopolysaccharide-induced inflammation cell model on macrophages and a lipopolysaccharide-induced inflammation mouse model. It was found that during inflammation, microRNA-9 was increased, accompanied with the up-regulation of pro-inflammatory cytokines and anti-inflammatory cytokines. Down-regulation of microRNA-9 inhibited the up-regulation of inflammatory cytokines, promoted the up-regulation of anti-inflammatory cytokines and induced the remission of organ damage, showing a protective effect in inflammation. Bioinformatics analysis combined with luciferase reporter assay showed that SIRT1 was the target gene of microRNA-9. Transfection of microRNA-9 inhibitor could increase the level of SIRT1 and decrease the activation of NF-κB pathway in macrophages. Myeloid specific sirt1 knockout mice were included and we found that lack of SIRT1 in mice macrophages led to aggravated inflammation, cell apoptosis and organ injury, and eliminated the protective property of microRNA-9 inhibitor. In conclusion, we demonstrated that inhibition of microRNA-9 could alleviate inflammation through the up-regulation of SIRT1 and then suppressed the activation of NF-κB pathway. This is a meaningful explore about the specific mechanism of microRNA-9 in inflammation.

3D cost aggregation with multiple minimum spanning trees for stereo matching.

Cost aggregation is one of the key steps in the stereo matching problem. In order to improve aggregation accuracy, we propose a cost-aggregation method that can embed minimum spanning tree (MST)-based support region filtering into PatchMatch 3D label search rather than aggregating on fixed size patches. However, directly combining PatchMatch label search and MST filtering is not straightforward, due to the extremely high complexity. Thus, we develop multiple MST structures for cost aggregation on plenty of 3D labels, and design the tree-level random search strategy to find possible 3D labels of each pixel. Extensive experiments show that our method reaches higher accuracy than the other existing cost-aggregation and global-optimization methods such as the 1D MST, the PatchMatch and the PatchMatch Filter, and currently ranks first on the Middlebury 3.0 benchmark.