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Spatial-temporal graph modeling plays an important role in the fields of transportation, meteorology, and social networks. Traffic flow prediction is a classic spatial-temporal modeling task. Existing methods usually do not take into account the asynchronous spatial-temporal correlation in traffic data. In addition, due to the complexity and variability of traffic data, long-term traffic forecasting is highly challenging. In order to solve the above problems, this paper proposes a new deep learning-based Asynchronous Dilation Graph Convolution Network (ADGCN) to model the spatial-temporal graphs. We mine the asynchronous spatial-temporal correlation in the traffic network, and propose the Asynchronous Spatial-Temporal Graph Convolution (ASTGC) operation to extract this special relationship. Furthermore, we extend the dilated 1D causal convolution to a graph convolution. The receptive field of the model increases exponentially with the increase of the network depth. Experiments are conducted on three public traffic datasets, and the results show that the prediction performance of ADGCN is better than the existing counterpart methods, especially in longterm prediction tasks.

In wireless sensor networks (WSNs), data anomalies/faults often occur due to the limited resources and unreliability of sensor nodes. Many traditional anomaly detection methods are designed in a batch manner, but for the nature of streaming data in WSNs, continuous anomaly detection method is preferred. Existing methods often detect only a single type of faults but cannot detect multiple types of faults that actually are more common in the sensor data. Therefore, this paper provides a Hypergrid based Adaptive Detection of Faults (HADF) method, which adopts hypergrid and statistical analysis to recognize three types of faults in the sensor data, including outliers, stuck-at faults, and noisy faults. HADF is a distributed method running on sensor nodes, which can reduce the influence of concept drift in unstable streaming data through combining both lazy leaning and continuous learning to adaptively update its normal profile. In the experimental study, we have manually inserted different types of faults into two real-world datasets, and the results demonstrate that HADF achieves higher accuracy with reasonable efficiency for detecting the data faults than four counterpart methods.

Data missing problems often occur on the Internet-of-Things domains. This article proposes a missing type-aware interpolation framework (IMA) for data loss problems in city-wide environmental monitoring systems that contain many scattered stations. To interpolate data as accurately as possible, IMA considers three aspects of information, i.e., spatiotemporal, all attributes of one measurement, and all values and accordingly develop three methods to estimate the missing data. First, we develop an improved multiviewer method, which uses the spatiotemporal correlation of data from neighbor stations to estimate random missing values. Second, we propose a new multi-eXtreme Gradient Boosting (multi-XGBoost) method that uses the values of the co-occurring and correlated correct attributes to predict the value of the missing attribute. Third, we take advantage of matrix factorization to estimate the missing parts if the data of the interpolation matrix are not all missing. To avoid the influence of uncorrelated data, IMA calculates Pearson’s correlation coefficient between data of each station and uses those data from its top $k$ highest correlation neighbors to form an interpolation matrix. Furthermore, due to the complexity of missing cases, IMA uses confidence levels in each of the three data prediction methods. For example, if the multiviewer method fails, IMA weights all valid results with confidence levels. We conduct our experiments on two real-world datasets from air quality monitoring stations in Beijing. Both datasets contain numerous missing measurements. Experimental results show that IMA outperforms other counterpart methods in interpolating the missing measurements, in terms of accuracy and effectiveness. Compared with the most related method, IMA improves the interpolation accuracy from 0.818 to 0.849 in a small dataset and from 0.214 to 0.759 in a large one.

Background In clinical practice, the cases with bacterial infection caused by titanium implants and bacterial biofilm formation on the surface of titanium materials implanted into human body can often be observed. Thus, this study aimed to demonstrate whether the mixed biofilm of Staphylococcus aureus/Escherichia coli can be formed on the surface of titanium material through in vitro experiments and its formation rules. Methods The titanium plates were put into the well containing S aureus or/and E coli. Bacterial adhesion and biofilm formation were analyzed by crystal violet, XTT method, confocal laser scanning microscopy, and scanning electron microscopy. Results The results of bacterial adhesion in each group at 6‐72 hours showed that the number of bacterial adhesion in each group was increased with the extension of time and reached to the highest level at 72 hours. Moreover, the biofilm structure in the S aureus‐E coli group was significantly more complex than that of the simple S aureus group or E coli group, and the number of bacteria was also significantly increased in the S aureus‐E coli group. Conclusion Those data provide a laboratory basis for the prevention and treatment of mixed infection of subsequent biological materials.

Objective To explore the molecular mechanism of Res in regulation of pulmonary fibrosis (PF). Methods Rats were injected with bleomycin (BLM) to establish a PF model and treated with resveratrol (Res) and/or miR-21 agomir. After 14 days, lung tissues were collected for Hematoxylin-eosin and Masson’s staining, and real-time quantitative polymerase chain reaction and Western blot were performed to detect fibrosis-related protein expression and the activation of the TGF-β1/Smad pathway. In vitro, MRC-5 cells were pretreated with TGF-β1, Res, and/or miR-21 agomir. After 48 h, total soluble collagen was detected with a Sircol Soluble Collagen Assay. Subsequently, a miR-21 mimic was transfected into MRC-5 cells, and a luciferase reporter assay was employed to verify whether miR-21 targeted Smad7. Results Res reversed the increased levels of miR-21 induced by BLM and alleviated serious PF symptoms, but agomiR-21 treatment effectively impaired the above manifestations. In vivo, miR-21 inhibited the decreases of TGF-β1 and p-Smad2/3 that were induced by Res. In vitro, miR-21 significantly disrupted the positive effect of Res on TGF-β-induced collagen deposition, as well as the levels of Fn, α-SMA, p-Smad2, and Smad7. In addition, Smad7 was found to be a direct target of miR-21-5p. TGF-β stimulation led to an enormous increase in p-c-Jun, c-Jun, and c-Fos, which were significantly reduced by Res. Finally, miR-21 sharply reduced the increased phosphorylation levels of ERK, JNK and p38 that were induced by Res. Conclusion Res inhibits BLM-induced PF by regulating miR-21 through MAPK/AP-1 pathways.

Carboxyl-terminal binding protein 1 (CtBP1), a well-known transcriptional co-repressor, is highly expressed in a number of cancer types. However, it is still absent in osteosarcoma cells. Here, we found that CtBP1, but not CtBP2, is overexpressed in invasive osteosarcoma tissues and cells. The overexpressed CtBP1 in turn represses its downstream targets, such as the pro-apoptotic regulators Bax, Bim and p53 upregulated modulator of apoptosis (PUMA), cell adhesion molecule E-cadherin, and the cell cycle regulators p16, p21 and phosphatase and tensin homolog (PTEN). To explore the molecular mechanism of CtBP1 overexpression, we subjected three independent clinical samples to miRNA microarray analysis and found that miR-485-3p could specifically bind to the 3'-untranslated region (3'-UTR) of CtBP1, thereby negatively controlling CtBP1 expression. The overexpression of miR-485-3p in osteosarcoma cells significantly repressed CtBP1 levels and inhibited cell proliferation, colony formation, cell migration and sphere formation. Further analysis indicated that DNA hypermethylation in the promoter region of miR-485-3p caused the downregulation of miR-485-3p. Treatment with the DNA methylation inhibitor 5-aza-2'-deoxycytidine (AZA) resulted in the upregulation of miR-485-3p and the downregulation of CtBP1 as well as inhibited osteosarcoma cell growth. This study provides evidence that CtBP1 is also overexpressed in osteosarcoma cells and demonstrates the underlying mechanism regarding its overexpression. Thus, therapeutically targeting CtBP1 may represent an effective strategy for osteosarcoma therapy.

Objective Osteosarcoma is a common malignancy with high rate of metastasis. miR-10b has been reported to be expressed in many types of tumors abnormally and be associated with cancer carcinogenesis and progression. But the function of miR-10b in osteosarcoma is still unknown. So this study was aimed to investigate the role of miR-10b in osteosarcoma development. Methods miR-10b expression in osteosarcoma tissues and osteosarcoma cells were detected using real time PCR. The effects of miR-10b on osteosarcoma cells proliferation, apoptosis, migration and invasion were detected using CCK-8 assay, flow cytometry, wound-healing assay and transwell assay, respectively. The relationship between miR-10b and KLF4 was evaluated using dual-luciferase assay, correlation analysis. Results miR-10b was highly expressed in osteosarcoma tissues and osteosarcoma cells. Furthermore, inhibition of miR-10b in osteosarcoma cells depressed the cells proliferation, migration and invasion but promoted cells apoptosis. In addition, KLF4 was down-regulated by miR-10b and miR-10b expression was negatively related to KLF4 expression in osteosarcoma tissue, miR-10b participated in the process of osteosarcoma cells invasion by regulating KLF4 expression. Conclusion miR-10b is overexpressed in osteosarcoma and KLF4 is the direct target gene of miR-10b. Furthermore, miR-10b promotes osteosarcoma cells progression by downregulating KLF4 expression. These results suggest that miR-10b functions as an oncomiR and play an important role in osteosarcoma cellular processes at least partially through regulating KLF4; miR-10b may be a therapeutic target for osteosarcoma treatment.

The miRNA miR-124 has been reported to be a promising target for the repair of spinal cord injury (SCI), which is a devastating neurological condition. This study aimed to investigate the underlying molecular mechanisms of miR-124-mediated SCI repair. We established miR-124 SCI model rats and further treated them with agomiR-124 for 14 days. After that, their spinal cords were sectioned, and levels of NeuN, GFAP, and NF-200 were measured via immunofluorescence or via immunohistochemistry. In addition, the spinal dorsal horns were collected for sequencing of total RNA. Differentially expressed (DE) mRNAs were then profiled and a number of these were further verified with qPCR. Gene ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were performed to predict the potential functions of the DE mRNAs. AgomiR-124 was found to significantly inhibit the decrease of neurons and the activation of astrocytes, while promoting NF-200 expression in the dorsal horn. At fourteen days after agomiR-124 treatment, a total of 85 mRNAs were upregulated and 80 mRNAs were downregulated. We focused our analysis of the DE mRNAs on the top 20 most DE mRNAs, and found four upregulated genes (Nploc4, Yme1l1, LOC103693564, and Aspa) and four downregulated genes (Epb41l2, LOC100911685, LOC100910833, and Smarcc1), which are likely to be of interest to SCI researchers. In addition, we noted that Tal1 is a potential target gene of miR-124, and that a low level of this gene promoted the proliferation of neuronal precursor cells and inhibited their differentiation. In conclusion, miR-124 was able to mediate SCI repair by altering the expression of various mRNAs in rats. The miR-124/Tal1 axis may participate in the treatment of SCI by agomiR-124 by repopulating neural stem cells.

Altered expression of miRNA-98 (miR-98) has been reported in osteoarthritis (OA) patients, while its role and underlying mechanisms remain elusive. In the present study, a rat model of OA was established using modified Hulth method, and the expression level of miR-98 and its effect on cartilage degradation and cell apoptosis in OA rats were examined. The results showed that up-regulated miR-98 was observed in OA rats, and knockdown of miR-98 in OA rats resulted in an inhibitory effect on cartilage degradation and chondrocyte apoptosis. Then the potential apoptosis associated genes regulated by miR-98 were screened and examined in cartilage tissues. The target gene of miR-98 was validated by luciferase reporter assay. The data showed that the increased miR-98 was accompanied with a reduced expression of Bcl-2 at both mRNA and protein levels. Furthermore, the silencing of miR-98 in OA rats prevented the down-regulation of Bcl-2 in cartilage tissues. Finally, the luciferase reporter assay validated that Bcl-2 was the target gene of miR-98. In this study, we found that miR-98 might promote chondrocyte apoptosis and cartilage degradation by down-regulating Bcl-2 expression in the pathogenesis of OA, suggesting that miR-98 can be a potential target for the treatment of OA.

Background: MiR-126 is likely to be closely associated with the threatening disease deep venous thrombosis (DVT). Aim: This study aims to investigate the influence of aberrantly expressed miR-126 on vascular endothelial cell (VEC) apoptosis during DVT and explore how miR-126 functions in it. Methods: MiR-126 inhibition and overexpression in vivo were respectively performed with antagomir and agomir of miR-126. Using a rat traumatic femoral DVT model, VEC apoptosis and miR-126 expression were detected by TUNEL assay and qRT-PCR before thrombogenesis and at different time phases of thrombogenesis. Protein levels of MMPs, Akt, Bcl-2, Bad, and caspase-9 in vascular tissue were measured by western blotting. In vitro, miR-126 interference, and overexpression were performed on human umbilical vein endothelial cells (HUVECs) using miR-126 inhibitor and mimics. After HUVECs were pretreated with CoCl2, cell apoptosis was analyzed using flow cytometry, and RNA/protein levels of miR-126, PIK3R2, PTEN, and phosphorylated Akts were measured with qRT-PC/western blotting. Results: The apoptosis of VECs was increased by miR-126 inhibition and obviously rescued by miR-126 overexpression. PI3K/Akt signal transduction was suppressed by miR-126 inhibition and evidently enhanced by miR-126 overexpression. Consistent with these findings, the downstream proteins (Bcl-2, Bad, and cleaved caspase-9) in PI3K/Akt pathway and the MMPs were remarkably changed by inhibition or overexpression of miR-126. In vitro experiments also showed that PI3K/Akt signaling was strengthened when miR-126 expression was upregulated or inhibited when miR-126 was knockdown. Conclusion: Overexpressed miR-126 inhibits apoptosis of VECs and DVT through targeting the anti-apoptotic pathway PI3K/Akt via PIK3R2. General significance: These findings may provide a new target for the therapy of DVT.

Carboxyl-terminal binding protein 1 (

Background Spinal osteochondroma is a rare but recognized cause of myelopathy. Brown-Sequard syndrome is a form of severe myelopathy characterized by a clinical picture of hemisection of the spinal cord. Brown-Sequard syndrome caused by osteochondroma is extremely rare, calling for individualized surgical procedures. Case Description We report a 16-year-old girl with hereditary multiple exostoses and a rare case of thoracic osteochondroma causing partial Brown-Sequard syndrome. Customized surgical procedures were designed to avoid iatrogenic spinal cord injury. The patient underwent neural decompression and tumor excision through a transpedicular approach. The surgical procedure consisted of 4 consecutive steps: 1) laminectomy, 2) costotransversectomy and pediculectomy, 3) extracavitary removal of the mass, and 4) pedicular fixation with fusion. Total resection of the tumor was achieved macroscopically without intraoperative spinal cord injury. The postoperative recovery was uneventful, and the patient returned to a normal life without evidence of recurrence at 24-month follow-up. Conclusions For patients with hereditary multiple exostosis and new onset of neurologic symptoms, the possibility of a spinal osteochondroma should be considered. In the situation of an intraspinal exostosis protruding from the lateral side, customized surgical procedures with a transpedicular approach may be a valid way to minimize intraoperative neural injury and achieve a satisfactory outcome.

This study was aimed to explore the role of miR‐29b‐3p and PGRN in chondrocyte apoptosis and the initiation and progress of osteoarthritis (OA). Both miR‐29b‐3p and PGRN were up‐regulated in cartilage tissue from patients with OA. Transfection of miR‐29b‐3p mimic into rat primary chondrocytes and SW1353 chondrosarcoma cells significantly suppressed PGRN expression and release, induced apoptosis, inhibited proliferation and scratch wound closure. By contrast, transfection of miR‐29b‐3p inhibitor exhibited the opposite effects. Moreover, the expression and secretion of cartilaginous degeneration‐related molecules were also altered by miR‐29b‐3p. Luciferase reporter gene assay showed rat GRN mRNA is directly targeted and repressed by miR‐29b‐3p. The fact that recombinant PGRN or shPGRN‐mediated PGRN interference abolished miR‐29b‐3p mimic‐induced cell apoptosis and growth inhibition suggested miR‐29b‐3p affect the cellular functions of chondrocyte through regulating PGRN expression. In vivo, joint cavity injection of miR‐29b‐3p antagomir prior to surgical induction of OA significantly suppressed the upregulation of miR‐29b‐3p, whereas further promoted the increased expression of PGRN. Articular chondrocytes apoptosis and cartilage loss in the knee joint of surgically induced OA rats were also ameliorated by the injection of miR‐29b‐3p antagomir, demonstrated by TUNEL and safranin O‐fast green staining. This work showed miR‐29b‐3p facilitates chondrocyte apoptosis and OA by targeting PGRN, and miR‐29b‐3p or PGRN may be the potential target for OA treatments.

In order to figure out the negative effect on groundwater environment caused by weathered granite tunnel construction with mining method, the influence factors were considered comprehensively to establish the evaluation index system and classification standard for negative effect on groundwater environment. The fuzzy comprehensive evaluation and analytic hierarchy process were used to quantify the evaluation indexes and determine the weight of indexes. The system to evaluate the negative effect caused by tunnel construction with mining method on groundwater environment was developed based on GIS and was applied to a tunnel section of Guangzhou Metro line 21. The research results show that: the permeability of rock, the grouting effect and the waterproof and drainage are the major influence factors. The negative effects of DK25+984.0 ∼ DK26+000.0 and DK26+000.0 ∼ DK26+434.0 mileage sections are strong and medium, respectively, which coincided with the actual situation. This research can provide a scientific approach to evaluate the negative effect caused by tunnel construction with mining method on groundwater environment.

In Guangzhou Metro line 21 tunnel construction process, weathered granite shows diversification in strength, deformation characteristics and permeability characteristics. The rock mass permeability coefficient is the core parameter necessary in the construction, and the definition of its value directly affects the accuracy of the calculation in design of tunnel anti-drainage structure and the negative effect evaluation of groundwater environment. With on-site and indoor tests, theoretical calculations, microstructure observations and mineral analysis, the permeability characteristics of granites in different degrees of weathering is studied. The variation of the final permeability characteristics is described. The permeability of granite does not increase unidirectionally as the degree of weathering deepens.

Mood disorders are a severe health burden but molecular mechanisms underlying mood dysfunction remain poorly understood. Here, we show that wild-type p53-induced phosphatase 1 (Wip1) negatively responds to the stress-induced negative mood-related behaviors. Specifically, we show that Wip1 protein but not its mRNA level was downregulated in the hippocampus but not in the neocortex after 4 weeks of chronic unpredictable mild stress (CUMS) in mice. Moreover, the CUMS-responsive WIP1 downregulation in the hippocampus was restored by chronic treatment of fluoxetine (i.p. 20 mg/kg) along with the CUMS procedure. In addition, Wip1 knockout mice displayed decreased exploratory behaviors as well as increased anxiety-like and depression-like behaviors in mice without impaired motor activities under the non-CUMS condition. Furthermore, the Wip1 deficiency-responsive anxiety-like but not depression-like behaviors were further elevated in mice under CUMS. Although limitations like male-alone sampling and multiply behavioral testing exist, the present study suggests a potential protective function of Wip1 in mood stabilization. Refereed/Peer-reviewed

Cardiovascular disease (CVD) is recognized as a major and increasing health problem affected older subjects in China, and clopidogrel has been widely used for treatment of CVD patients such as atherosclerosis, myocardial infarction, and myocardial ischaemia–reperfusion damage. However, the molecular mechanisms of clopidogrel for treatment of CVD are only partially understood. This study investigated the effects of clopidogrel on palmitic acid-induced damage of human vascular endothelial cells (HUVECs), and the molecular mechanisms of LncRNA HIF1A-AS1 in regulating the proliferation and apoptosis of HUVECs in vitro. We firstly established a damage model of HUVECs through palmitic acid (PA) treatment. And the effect of clopidogrel reducing PA-induced apoptosis of HUVECs was observed by the flow cytometric measurement. To further understand the molecular mechanism of clopidogrel rescues PA-induced apoptosis, we used human LncRNA PCR array to compare the LncRNA expression profile difference between clopidogrel-treated cells and control cells. The expression of LncRNA HIF 1 alpha-antisense RNA 1 (HIF1A-AS1) was significantly altered in clopidogrel-treated cells. We further proved that suppression of HIF1A-AS1 by siRNA reduce PA-induced apoptosis and promote proliferation of HUVECs. Furthermore, we also demonstrated inhibition apoptosis effect by HIF1A-AS1 is related to mitochondrial apoptosis pathway. Hence, our results suggest that clopidogrel rescues apoptosis and promotes proliferation of PA-induced damage model of HUVECs through inhibiting the mediator LncRNA HIF1A-AS1. These findings indicate that LncRNA HIF1A-AS1 may play an important role in the pathogenesis of CVD, and provide a novel molecular mechanism of clopidogrel for treatment of CVD.