Instance Consistency Regularization for Semi-Supervised 3D Instance Segmentation.

Large-scale datasets with point-wise semantic and instance labels are crucial to 3D instance segmentation but also expensive. To leverage unlabeled data, previous semi-supervised 3D instance segmentation approaches have explored self-training frameworks, which rely on high-quality pseudo labels for consistency regularization. They intuitively utilize both instance and semantic pseudo labels in a joint learning manner. However, semantic pseudo labels contain numerous noise derived from the imbalanced category distribution and natural confusion of similar but distinct categories, which leads to severe collapses in self-training. Motivated by the observation that 3D instances are non-overlapping and spatially separable, we ask whether we can solely rely on instance consistency regularization for improved semi-supervised segmentation. To this end, we propose a novel self-training network InsTeacher3D to explore and exploit pure instance knowledge from unlabeled data. We first build a parallel base 3D instance segmentation model DKNet, which distinguishes each instance from the others via discriminative instance kernels without reliance on semantic segmentation. Based on DKNet, we further design a novel instance consistency regularization framework to generate and leverage high-quality instance pseudo labels. Experimental results on multiple large-scale datasets show that the InsTeacher3D significantly outperforms prior state-of-the-art semi-supervised approaches.

Antisymmetric planar Hall effect in rutile oxide films induced by the Lorentz force.

The conventional Hall effect is linearly proportional to the field component or magnetization component perpendicular to a film. Despite the increasing theoretical proposals on the Hall effect to the in-plane field or magnetization in various special systems induced by the Berry curvature, such an unconventional Hall effect has only been experimentally reported in Weyl semimetals and in a heterodimensional superlattice. Here, we report an unambiguous experimental observation of the antisymmetric planar Hall effect (APHE) with respect to the in-plane magnetic field in centrosymmetric rutile RuO2 and IrO2 single-crystal films. The measured Hall resistivity is found to be linearly proportional to the component of the applied in-plane magnetic field along a particular crystal axis and to be independent of the current direction or temperature. Both the experimental observations and theoretical calculations confirm that the APHE in rutile oxide films is induced by the Lorentz force. Our findings can be generalized to ferromagnetic materials for the discovery of anomalous Hall effects and quantum anomalous Hall effects induced by in-plane magnetization. In addition to significantly expanding knowledge of the Hall effect, this work opens the door to explore new members in the Hall effect family.

Circular RNA circARPC1B functions as a stabilisation enhancer of Vimentin to prevent high cholesterol-induced articular cartilage degeneration.

BACKGROUND: Osteoarthritis (OA) is a prevalent and debilitating condition, that is, directly associated with cholesterol metabolism. Nevertheless, the molecular mechanisms of OA remain largely unknown, and the role of cholesterol in this process has not been thoroughly investigated. This study aimed to investigate the role of a novel circular RNA, circARPC1B in the relationship between cholesterol and OA progression. METHODS: We measured total cholesterol (TC) levels in the synovial fluid of patients with or without OA to determine the diagnostic role of cholesterol in OA. The effects of cholesterol were explored in human and mouse chondrocytes in vitro. An in vivo OA model was also established in mice fed a high-cholesterol diet (HCD) to explore the role of cholesterol in OA. RNAseq analysis was used to study the influence of cholesterol on circRNAs in chondrocytes. The role of circARPC1B in the OA development was verified through circARPC1B overexpression and knockdown. Additionally, RNA pulldown assays and RNA binding protein immunoprecipitation were used to determine the interaction between circARPC1B and Vimentin. CircARPC1B adeno-associated virus (AAV) was used to determine the role of circARPC1B in cholesterol-induced OA. RESULTS: TC levels in synovial fluid of OA patients were found to be elevated and exhibited high sensitivity and specificity as predictors of OA diagnosis. Moreover, elevated cholesterol accelerated OA progression. CircARPC1B was downregulated in chondrocytes treated with cholesterol and played a crucial role in preserving the extracellular matrix (ECM). Mechanistically, circARPC1B is competitively bound to the E3 ligase synoviolin 1 (SYVN1) binding site on Vimentin, inhibiting the proteasomal degradation of Vimentin. Furthermore, circARPC1B AAV infection alleviates Vimentin degradation and OA progression caused by high cholesterol. CONCLUSIONS: These findings indicate that the cholesterol-circARPC1B-Vimentin axis plays a crucial role in OA progression, and circARPC1B gene therapy has the opportunity to provide a potential therapeutic approach for OA.

An inducible long noncoding RNA, LncZFHX2, facilitates DNA repair to mediate osteoarthritis pathology.

Cartilage homeostasis is essential for chondrocytes to maintain proper phenotype and metabolism. Because adult articular cartilage is avascular, chondrocytes must survive in low oxygen conditions, and changing oxygen tension can significantly affect metabolism and proteoglycan synthesis in these cells. However, whether long noncoding RNA participate in cartilage homeostasis under hypoxia has not been reported yet. Here, we first identified LncZFHX2 as a lncRNA upregulated under physiological hypoxia in cartilage, specifically by HIF-1α. LncZFHX2 knockdown simultaneously accelerated cellular senescence, targeted multiple components of extracellular matrix metabolism, and increased DNA damage in chondrocytes. Through a series of in vitro and in vivo experiments, we identified that LncZFHX2 performed a novel function that regulated RIF1 expression through forming a transcription complex with KLF4 and promoting chondrocyte DNA repair. Moreover, chondrocyte-conditional knockout of LncZFHX2 accelerated injury-induced cartilage degeneration in vivo. In conclusion, we identified a hypoxia-activated DNA repair pathway that maintains matrix homeostasis in osteoarthritis cartilage.

USP7 Inhibits Osteoclastogenesis via Dual Effects of Attenuating TRAF6/TAK1 Axis and Stimulating STING Signaling.

Ubiquitination is a reversible post-translational modification implicated in cell differentiation, homeostasis, and organ development. Several deubiquitinases (DUBs) decrease protein ubiquitination through the hydrolysis of ubiquitin linkages. However, the role of DUBs in bone resorption and formation is still unclear. In this study, we identified DUB ubiquitin-specific protease 7 (USP7) as a negative regulator of osteoclast formation. USP7 combines with tumor necrosis factor receptor-associated factor 6 (TRAF6) and inhibits its ubiquitination by impairing the Lys63-linked polyubiquitin chain. Such impairment leads to the suppression of receptor activator of NF-κB ligand (RANKL)-mediated nuclear factor-κB (NF-κB) and mitogen-activated protein kinases (MAPKs) activation without affecting TRAF6 stability. USP7 also protects the stimulator of interferon genes (STING) against degradation, inducing interferon-ß (IFN-ß) expression in osteoclast formation, thereby inhibiting osteoclastogenesis cooperatively with the classical TRAF6 pathway. Furthermore, USP7 inhibition accelerates osteoclast differentiation and bone resorption both in vitro and in vivo. Contrarily, USP7 overexpression impairs osteoclast differentiation and bone resorption in vitro and in vivo. Additionally, in ovariectomy (OVX) mice, USP7 levels are lower than those in sham-operated mice, suggesting that USP7 plays a role in osteoporosis. Altogether, our data reveal the dual effect of USP7-mediated TRAF6 signal transduction and USP7-mediated protein degradation of STING in osteoclast formation.

Metabolite asymmetric dimethylarginine (ADMA) functions as a destabilization enhancer of SOX9 mediated by DDAH1 in osteoarthritis.

Osteoarthritis (OA) is a degenerative disease with a series of metabolic changes accompanied by many altered enzymes. Here, we report that the down-regulated dimethylarginine dimethylaminohydrolase-1 (DDAH1) is accompanied by increased asymmetric dimethylarginine (ADMA) in degenerated chondrocytes and in OA samples. Global or chondrocyte-conditional knockout of ADMA hydrolase DDAH1 accelerated OA development in mice. ADMA induces the degeneration and senescence of chondrocytes and reduces the extracellular matrix deposition, thereby accelerating OA progression. ADMA simultaneously binds to SOX9 and its deubiquitinating enzyme USP7, blocking the deubiquitination effects of USP7 on SOX9 and therefore leads to SOX9 degradation. The ADMA level in synovial fluids of patients with OA is increased and has predictive value for OA diagnosis with good sensitivity and specificity. Therefore, activating DDAH1 to reduce ADMA level might be a potential therapeutic strategy for OA treatment.

Nanoengineered Spintronic-Metasurface Terahertz Emitters Enable Beam Steering and Full Polarization Control.

The demand for emerging applications at the terahertz frequencies motivates the development of novel and multifunctional devices for the generation and manipulation of terahertz waves. In this work, we report the realization of multifunctional spintronic-metasurface emitters, which allow simultaneous beam-steering and full polarization control over a broadband terahertz beam. This is achieved through engineering individual meta-atoms with nanoscale magnetic heterostructures and, thus, implementing microscopical control over the laser-induced spin and charge dynamics. By arranging the spintronic meta-atoms in the metagrating geometry, the generated terahertz beam can be flexibly steered in space between different orders of diffraction. Furthermore, we demonstrate a simultaneous control over the terahertz polarization states at different emission angles and show that the two control capabilities are mutually independent of each other. The nanoengineered multifunctional terahertz emitter demonstrated in this work can provide a solution to the challenge associated with a growing variety of applications of terahertz technology.

Silicon-Based Metastructure Optical Scattering Multiply-Accumulate Computation Chip.

Optical neural networks (ONN) have become the most promising solution to replacing electronic neural networks, which have the advantages of large bandwidth, low energy consumption, strong parallel processing ability, and super high speed. Silicon-based micro-nano integrated photonic platforms have demonstrated good compatibility with complementary metal oxide semiconductor (CMOS) processing. Therefore, without completely changing the existing silicon-based fabrication technology, optoelectronic hybrid devices or all-optical devices of better performance can be achieved on such platforms. To meet the requirements of smaller size and higher integration for silicon photonic computing, the topology of a four-channel coarse wavelength division multiplexer (CWDM) and an optical scattering unit (OSU) are inversely designed and optimized by Lumerical software. Due to the random optical power splitting ratio and incoherency, the intensities of different input signals from CWDM can be weighted and summed directly by the subsequent OSU to accomplish arbitrary multiply-accumulate (MAC) operations, therefore supplying the core foundation for scattering ONN architecture.

Exchange-Torque-Triggered Fast Switching of Antiferromagnetic Domains.

The antiferromagnet is considered to be a promising hosting material for the next generation of magnetic storage due to its high stability and stray-field-free property. Understanding the switching properties of the antiferromagnetic (AFM) domain state is critical for developing AFM spintronics. By utilizing the magneto-optical birefringence effect, we experimentally demonstrate the switching rate of the AFM domain can be enhanced by more than 2 orders of magnitude through applying an alternating square-wave field on a single crystalline Fe/CoO bilayer. The observed extraordinary speed can be much faster than that triggered by a constant field with the same amplitude. The effect can be understood as the efficient suppression of the pinning of AFM domain walls by the strong exchange torque triggered by the reversal of the Fe magnetization, as revealed by spin dynamics simulations. Our finding opens up new opportunities to design the antiferromagnet-based spintronic devices utilizing the ferromagnet-antiferromagnet heterostructure.

Reversible writing/deleting of magnetic skyrmions through hydrogen adsorption/desorption.

Magnetic skyrmions are topologically nontrivial spin textures with envisioned applications in energy-efficient magnetic information storage. Toggling the presence of magnetic skyrmions via writing/deleting processes is essential for spintronics applications, which usually require the application of a magnetic field, a gate voltage or an electric current. Here we demonstrate the reversible field-free writing/deleting of skyrmions at room temperature, via hydrogen chemisorption/desorption on the surface of Ni and Co films. Supported by Monte-Carlo simulations, the skyrmion creation/annihilation is attributed to the hydrogen-induced magnetic anisotropy change on ferromagnetic surfaces. We also demonstrate the role of hydrogen and oxygen on magnetic anisotropy and skyrmion deletion on other magnetic surfaces. Our results open up new possibilities for designing skyrmionic and magneto-ionic devices.

Mechanical force promotes dimethylarginine dimethylaminohydrolase 1-mediated hydrolysis of the metabolite asymmetric dimethylarginine to enhance bone formation.

Mechanical force is critical for the development and remodeling of bone. Here we report that mechanical force regulates the production of the metabolite asymmetric dimethylarginine (ADMA) via regulating the hydrolytic enzyme dimethylarginine dimethylaminohydrolase 1 (Ddah1) expression in osteoblasts. The presence of -394 4 N del/ins polymorphism of Ddah1 and higher serum ADMA concentration are negatively associated with bone mineral density. Global or osteoblast-specific deletion of Ddah1 leads to increased ADMA level but reduced bone formation. Further molecular study unveils that mechanical stimulation enhances TAZ/SMAD4-induced Ddah1 transcription. Deletion of Ddah1 in osteoblast-lineage cells fails to respond to mechanical stimulus-associated bone formation. Taken together, the study reveals mechanical force is capable of down-regulating ADMA to enhance bone formation.

Circular RNA circRHOBTB3 represses metastasis by regulating the HuR-mediated mRNA stability of PTBP1 in colorectal cancer.

Background: Tumor metastasis of colorectal cancer (CRC) is the main cause of death in most patients and the major difficulty in comprehensive CRC treatment. Circular RNAs (circRNAs) affect many biological functions in solid tumors. However, their mechanisms in CRC metastasis remain unclear. Methods: RNA sequencing (RNA-seq) and quantitative real-time PCR were performed to screen differentially expressed circRNAs between CRC tissues and adjacent normal tissues. CCK-8, cell migration and wound healing assays were performed to determine the functions of circRHOBTB3 in cell proliferation and metastasis. RNA pulldown and RNA immunoprecipitation assays were performed to verify the interaction between circRHOBTB3 and the HuR (ELAVL1) protein. Further RNA-seq and rescue experiments were applied to search for the downstream target. We also conducted a mouse xenograft model to elucidate the effect of circRHOBTB3 on cancer metastasis in vivo. Results: We identified circRHOBTB3 which is markedly downregulated in CRC tissues and cell lines. Furthermore, lower circRHOBTB3 levels were significantly associated with advanced clinical stages and greater risk of metastases. Overexpression of circRHOBTB3 suppresses tumor metastasis in CRC cells. Mechanistically, circRHOBTB3 binds to HuR, which is a ubiquitously expressed and functional RNA-binding protein (RBP) in CRC development, and promotes ß-Trcp1-mediated ubiquitination of HuR. Normally, HuR binds to the 3'UTR of target mRNAs to facilitate their stabilization, whereas the interaction between circRHOBTB3 and HuR degrades HuR to reduce the expression level of the downstream target PTBP1. Furthermore, overexpressed circRHOBTB3 suppresses lung metastases in vivo, and this effect can be partly reversed by PTBP1 overexpression. In addition, the transcription of circRHOBTB3 can be improved by both FUS and ADARB2 in CRC cells. Conclusions: Our findings indicate that circRHOBTB3 exerts suppressive effects on CRC aggressiveness through the HuR/PTBP1 axis.

CircSLC7A2 protects against osteoarthritis through inhibition of the miR-4498/TIMP3 axis.

OBJECTIVES: Circular RNAs (circRNAs) are noncoding RNAs that compete against other endogenous RNA species, such as microRNAs, and have been implicated in many diseases. In this study, we investigated the role of a new circRNA (circSLC7A2) in osteoarthritis (OA). MATERIALS AND METHODS: The relative expression of circSLC7A2 was significantly lower in OA tissues than it was in matched controls, as shown by real-time quantitative polymerase chain reaction (RT-qPCR). Western blotting, RT-qPCR and immunofluorescence experiments were employed to evaluate the roles of circSLC7A2, miR-4498 and TIMP3. The in vivo role and mechanism of circSLC7A2 were also conformed in a mouse model. RESULTS: circSLC7A2 was decreased in OA model and the circularization of circSLC7A2 was regulated by FUS. Loss of circSLC7A2 reduced the sponge of miR-4498 and further inhibited the expression of TIMP3, subsequently leading to an inflammatory response. We further determined that miR-4498 inhibitor reversed circSLC7A2-knockdown-induced OA phenotypes. Intra-articular injection of circSLC7A2 alleviated in vivo OA progression in a mouse model of anterior cruciate ligament transection (ACLT). CONCLUSIONS: The circSLC7A2/miR-4498/TIMP3 axis of chondrocytes catabolism and anabolism plays a critical role in OA development. Our results suggest that circSLC7A2 may serve as a new therapeutic target for osteoarthritis.

Effects of Vehicle Load on Emissions of Heavy-Duty Diesel Trucks: A Study Based on Real-World Data.

Vehicle loads have significant impacts on the emissions of heavy-duty trucks, even in the same traffic conditions. Few studies exist covering the differences in emissions of diesel semi-trailer towing trucks (DSTTTs) with different loads, although these vehicles have a wide load range. In this context, the operating modes and emission rates of DSTTTs were analyzed under varying loads scenarios to understand the effect of vehicle loads on emission factors. First, second-by-second field speed data and emission data of DSTTTs with different loads were collected. Then, the methods for calculating the scaled tractive power (STP) and the emissions model for DSTTTs were proposed to evaluate the effect of different loading scenarios. The STP distributions, emission rate distributions, and emission factor characteristics of different loaded trucks were analyzed and compared. The results indicated that the STP distributions of DSTTTs that under the unloaded state were more narrow than those under fully loaded or overloaded conditions. The emission rates of carbon dioxide (CO2), carbon monoxide (CO) and total hydrocarbon (THC) for DSTTTs under a fully loaded state were significantly higher than those under an unloaded state. However, due to the influence of exhaust temperature, the emission rates of nitrogen oxides (NOx) among fully loaded trucks were lower than those under the unloaded state when STP bin was above 4 kW/ton. The emission factors of CO2, CO, THC, and NOx for fully loaded trucks demonstrated the largest increases at low-speed intervals (0-30 km/h), which rose by 96.2%, 47.9%, 27.8%, and 65.2%, respectively.

Circular RNA circPDE4D Protects against Osteoarthritis by Binding to miR-103a-3p and Regulating FGF18.

Osteoarthritis (OA) is a common, age-related, and painful disease characterized by cartilage destruction, osteophyte formation, and synovial hyperplasia. This study revealed that circPDE4D, a circular RNA derived from human linear PDE4D, plays a critical role in maintaining the extracellular cellular matrix (ECM) during OA progression. circPDE4D was significantly downregulated in OA cartilage tissues and during stimulation with inflammatory cytokines. The knockdown of circPDE4D predominantly contributed to Aggrecan loss and the upregulation of matrix catabolic enzymes, including MMP3, MMP13, ADAMTS4, and ADAMTS5, but not proliferation or apoptosis. In a murine model of destabilization of the medial meniscus (DMM), the intraarticular injection of circPDE4D alleviated DMM-induced cartilage impairments. Mechanistically, we found that circPDE4D exerted its effect by acting as a sponge for miR-103a-3p and thereby regulated FGF18 expression, which is a direct target of miR-103a-3p. In conclusion, our findings highlight a novel protective role of circPDE4D in OA pathogenesis and indicate that the targeting of the circPDE4D-miR-103a-3p-FGF18 axis might provide a potential and promising approach for OA therapy.

Oxidative stress abrogates the degradation of KMT2D to promote degeneration in nucleus pulposus.

Nucleus pulposus (NP) degeneration plays pivotal roles in intervertebral disc degeneration. The effect and mechanism of oxidative stress and epigenetics in NP degeneration is still unclear. We performed this study to evaluate the function of oxidative stress in NP and to explore the potential mechanism of ROS induced expression of matrix metalloproteinases (MMPs). We tested four methyltransferases, KMT2A, KMT2B, KMT2C and KMT2D in human NP samples, only KMT2D was significantly up-regulated in the severe degeneration samples. Knockdown of Kmt2d by siRNA significantly down-regulated the expression levels of catabolic enzymes including Mmp3, Mmp9 and Mmp13. Moreover, an interaction between KMT2D and ubiquitination was confirmed, and the application of H2O2 abrogated this process. Co-IP assay confirmed that H2O2 induced the phosphorylation of KMT2D to block the ubiquitination degradation, which was mainly mediated by phosphorylation of p38/MAPK. Further investigation suggested that ROS induced the alteration in levels of methylation is linked to H3K4me1 and H3K4me2, but not me3. However, usage of OICR-9429 (OICR) also suppressed the expression levels of Mmp3, Mmp9 and Mmp13. In an ex vivo model, application of OICR-9429 (OICR) also attenuated the degeneration of NP according to the H&E and Safranin-O/Fast Green staining assay, and the protein levels of MMP3, MMP9 and MMP13 were down-regulated, as well. In conclusion, we approved that oxidative stress induced ROS production promote the process of NP degeneration by enhancing KMT2D mediated transcriptional regulation of matrix degeneration related genes during NP degeneration.

TGFß attenuates cartilage extracellular matrix degradation via enhancing FBXO6-mediated MMP14 ubiquitination.

OBJECTIVES: FBXO6, a component of the ubiquitin E3 ligases, has been shown to bind high mannose N-linked glycoproteins and act as ubiquitin ligase subunits. Most proteins in the secretory pathway, such as matrix metalloproteinases, are modified with N-glycans and play important roles in the development of osteoarthritis (OA). However, whether FBXO6 exerts regulatory effects on the pathogenesis of OA remains undefined. METHODS: The expression of FBXO6 was examined in the cartilage of human and multiple mouse OA models. The role of FBXO6 in cartilage degeneration was analysed with global FBXO6-/- mice, transgenic Col2a1-CreERT2;FBXO6f/f mice. The FBXO6 interacting partner MMP14 and its regulatory transcriptional factor SMAD2/3 were identified and validated in different pathological models as well as SMAD2-/- mice. RESULTS: The expression of FBXO6 decreased in the cartilage from human OA samples, anterior cruciate ligament transaction (ACLT) -induced OA samples, spontaneous OA STR/ort samples and aged mice samples. Global knockout or conditional knockout of FBXO6 in cartilage promoted experimental OA process. The molecular mechanism study revealed that FBXO6 decreased MMP14 by ubiquitination and degradation, leading to inhibited proteolytic activation of MMP13. Interestingly, FBXO6 expression is regulated by transforming growth factor ß (TGFß)-SMAD2/3 signalling pathway. Therefore, the overexpression of FBXO6 protected mice from post-injury OA development. CONCLUSIONS: TGFß-SMAD2/3 signalling pathway suppressed MMP13 activation by upregulating of FBXO6 transcription and consequently promoting MMP14 proteasomal degradation. Inducement of FBXO6 expression in OA cartilage might provide a promising OA therapeutic strategy.

Correction to: CircMYO10 promotes osteosarcoma progression by regulating miR-370-3p/RUVBL1 axis to enhance the transcriptional activity of ß-catenin/LEF1 complex via effects on chromatin remodeling.

Following the publication of the original paper [1], one corresponding author was inadvertently missed.

CircMYO10 promotes osteosarcoma progression by regulating miR-370-3p/RUVBL1 axis to enhance the transcriptional activity of ß-catenin/LEF1 complex via effects on chromatin remodeling.

BACKGROUND: CircMYO10 is a circular RNA generated by back-splicing of gene MYO10 and is upregulated in osteosarcoma cell lines, but its functional role in osteosarcoma is still unknown. This study aimed to clarify the mechanism of circMYO10 in osteosarcoma. METHODS: CircMYO10 expression in 10 paired osteosarcoma and chondroma tissues was assessed by quantitative reverse transcription polymerase chain reaction (PCR). The function of circMYO10/miR-370-3p/RUVBL1 axis was assessed regarding two key characteristics: proliferation and endothelial-mesenchymal transition (EMT). Bioinformatics analysis, western blotting, real-time PCR, fluorescence in situ hybridization, immunoprecipitation, RNA pull-down assays, luciferase reporter assays, chromatin immunoprecipitation, and rescue experiments were used to evaluate the mechanism. Stably transfected MG63 cells were injected via tail vein or subcutaneously into nude mice to assess the role of circMYO10 in vivo. RESULTS: CircMYO10 was significantly upregulated, while miR-370-3p was downregulated, in osteosarcoma cell lines and human osteosarcoma samples. Silencing circMYO10 inhibited cell proliferation and EMT in vivo and in vitro. Mechanistic investigations revealed that miR-370-3p targets RUVBL1 directly, and inhibits the interaction between RUVBL1 and ß-catenin/LEF1 complex while circMYO10 showed a contrary effect via the inhibition of miR-370-3p. RUVBL1 was found to be complexed with chromatin remodeling and histone-modifying factor TIP60, and lymphoid enhancer factor-1 (LEF1) to promote histone H4K16 acetylation (H4K16Ac) in the vicinity of the promoter region of gene C-myc. Chromatin immunoprecipitation methods showed that miR-370-3p sponge promotes H4K16Ac in the indicated region, which is partially abrogated by RUVBL1 small hairpin RNA (shRNA) while circMYO10 showed a contrary result via the inhibition of miR-370-3p. Either miR-370-3p sponge or ShRUVBL1 attenuated circMYO10-induced phenotypes in osteosarcoma cell lines. MiR-370-3p inhibition abrogated the inhibition of proliferation, EMT of osteosarcoma cells in vitro and in vivo seen upon circMYO10 suppression via Wnt/ß-catenin signaling. CONCLUSIONS: CircMYO10 promotes osteosarcoma progression by regulating miR-370-3p/RUVBL1 axis to promote chromatin remodeling and thus enhances the transcriptional activity of ß-catenin/LEF1 complex, which indicates that circMYO10 may be a potential therapeutic target for osteosarcoma treatment.

The Impact of Activity-Based Mobility Pattern on Assessing Fine-Grained Traffic-Induced Air Pollution Exposure.

Quantifying the air pollution and health impacts of transportation plans provides decision makers with valuable information that can help to target interventions. However, a large number of environmental epidemiological research assumes exposures of static populations at residential locations and does not consider the human activity patterns, which may lead to significant estimation errors. This study uses an integrated modeling framework to predict fine-grained air pollution exposures occurring throughout residents' activity spaces. We evaluate concentrations of fine particulate matter (PM2.5) under a regional transportation plan for Sacramento, California, using activity-based travel demand model outputs, vehicle emission, and air dispersion models. We use predicted air pollution exposures at the traffic analysis zone (TAZ) level to estimate residents' exposure accounting for their movements throughout the day to assess the impact of activity-based mobility pattern on air pollution exposure. Results of PM2.5 exposures estimated statically (at residential locations) versus dynamically (over residents' activity-based mobility) demonstrates that the two methods yield statistically significant different results (p < 0.05). In addition, the comparison conducted in different age groups shows that the difference between these two approaches is greater among youth and working age residents, whereas seniors show a similar pattern using both approaches due to their lower rates of travel activity.