Immediate Pose Recovery Method for Untracked Frames in Feature-Based SLAM.

In challenging environments, feature-based visual SLAM encounters frequent failures in frame tracking, introducing unknown poses to robotic applications. This paper introduces an immediate approach for recovering untracked camera poses. Through the retrieval of key information from elapsed untracked frames, lost poses are efficiently restored with a short time consumption. Taking account of reconstructed poses and map points during local optimizing, a denser local map is constructed around ambiguous frames to enhance the further SLAM procedure. The proposed method is implemented in a SLAM system, and monocular experiments are conducted on datasets. The experimental results demonstrate that our method can reconstruct the untracked frames in nearly real time, effectively complementing missing segments of the trajectory. Concurrently, the accuracy and robustness for subsequent tracking are improved through the integration of recovered poses and map points.

A Ferroptosis-Inducing Arsenene-Iridium Nanoplatform for Synergistic Immunotherapy in Pancreatic Cancer.

Due to multidrug resistance and the high risk of recurrence, effective and less toxic alternative pancreatic cancer treatments are urgently needed. Pancreatic cancer cells are highly resistant to apoptosis but sensitive to ferroptosis. In this study, an innovative nanoplatform (AsIr@PDA) was developed by electrostatic adsorption of a cationic iridium complex (IrFN) onto two-dimensional (2D) arsenene nanosheets. This nanoplatform exhibits superior ferroptosis-inducing effects with high drug loading capacity and, importantly, excellent anti-cancer immune activation function, leading to efficient elimination of pancreatic tumors with no observable side effects. Interestingly, AsIr@PDA significantly prevents the recurrence of pancreatic cancer in vivo when compared with a cisplatin-loaded nanoplatform. This designed nanoplatform demonstrated superior therapeutic efficacy by synergistic ferroptosis-induced chemotherapy with immunotherapy via an all-in-one strategy, providing new insights for future pancreatic cancer therapy.

Protein arginine methyltransferase 1 in the generation of immune megakaryocytes: A perspective review.

Megakaryocytes (Mks) in bone marrow are heterogeneous in terms of polyploidy. They not only produce platelets but also support the self-renewal of hematopoietic stem cells and regulate immune responses. Yet, how the diverse functions are generated from the heterogeneous Mks is not clear at the molecular level. Advances in single-cell RNA seq analysis from several studies have revealed that bone marrow Mks are heterogeneous and can be clustered into 3 to 4 subpopulations: a subgroup that is adjacent to the hematopoietic stem cells, a subgroup expressing genes for platelet biogenesis, and a subgroup expressing immune-responsive genes, the so-called immune Mks that exist in both humans and mice. Immune Mks are predominantly in the low-polyploid (≤8 N nuclei) fraction and also exist in the lung. Protein arginine methyltransferase 1 (PRMT1) expression is positively correlated with the expression of genes involved in immune response pathways and is highly expressed in immune Mks. In addition, we reported that PRMT1 promotes the generation of low-polyploid Mks. From this perspective, we highlighted the data suggesting that PRMT1 is essential for the generation of immune Mks via its substrates RUNX1, RBM15, and DUSP4 that we reported previously. Thus, we suggest that protein arginine methylation may play a critical role in the generation of proinflammatory platelet progeny from immune Mks, which may affect many immune, thrombotic, and inflammatory disorders.

All-fiber orthogonal-polarized white-noise-modulated laser for short-coherence dynamic interferometry.

An all-fiber orthogonal-polarized white-noise-modulated laser (AOWL) for short-coherence dynamic interferometry is proposed. Short-coherence laser is achieved by current modulating of a laser diode with the band-limited white noise. A pair of orthogonal-polarized lights with adjustable delay for short-coherence dynamic interferometry are output by the all-fiber structure. In the non-common-path interferometry, the AOWL can significantly suppress the interference signal clutter with 73% side lobe suppression ratio, that improves the positioning accuracy of zero optical path difference. The wavefront aberrations of a parallel plate are measured with the AOWL in the common-path dynamic interferometers, avoiding the fringe crosstalk.

Altered expression of the L-arginine/nitric oxide pathway in ovarian cancer: metabolic biomarkers and biological implications.

MOTIVATION: Ovarian cancer (OC) is a highly lethal gynecological malignancy. Extensive research has shown that OC cells undergo significant metabolic alterations during tumorigenesis. In this study, we aim to leverage these metabolic changes as potential biomarkers for assessing ovarian cancer. METHODS: A functional module-based approach was utilized to identify key gene expression pathways that distinguish different stages of ovarian cancer (OC) within a tissue biopsy cohort. This cohort consisted of control samples (n = 79), stage I/II samples (n = 280), and stage III/IV samples (n = 1016). To further explore these altered molecular pathways, minimal spanning tree (MST) analysis was applied, leading to the formulation of metabolic biomarker hypotheses for OC liquid biopsy. To validate, a multiple reaction monitoring (MRM) based quantitative LCMS/MS method was developed. This method allowed for the precise quantification of targeted metabolite biomarkers using an OC blood cohort comprising control samples (n = 464), benign samples (n = 3), and OC samples (n = 13). RESULTS: Eleven functional modules were identified as significant differentiators (false discovery rate, FDR < 0.05) between normal and early-stage, or early-stage and late-stage ovarian cancer (OC) tumor tissues. MST analysis revealed that the metabolic L-arginine/nitric oxide (L-ARG/NO) pathway was reprogrammed, and the modules related to "DNA replication" and "DNA repair and recombination" served as anchor modules connecting the other nine modules. Based on this analysis, symmetric dimethylarginine (SDMA) and arginine were proposed as potential liquid biopsy biomarkers for OC assessment. Our quantitative LCMS/MS analysis on our OC blood cohort provided direct evidence supporting the use of the SDMA-to-arginine ratio as a liquid biopsy panel to distinguish between normal and OC samples, with an area under the ROC curve (AUC) of 98.3%. CONCLUSION: Our comprehensive analysis of tissue genomics and blood quantitative LC/MSMS metabolic data shed light on the metabolic reprogramming underlying OC pathophysiology. These findings offer new insights into the potential diagnostic utility of the SDMA-to-arginine ratio for OC assessment. Further validation studies using adequately powered OC cohorts are warranted to fully establish the clinical effectiveness of this diagnostic test.

Highly Strong and Tough Supramolecular Polymer Networks Enabled by Cryptand-Based Host-Guest Recognition.

Supramolecular polymer networks (SPNs) demonstrate great potential in the development of smart materials owing to their attractive dynamic properties. However, as they suffer from the inherent weak bonding of most noncovalent cross-links, it remains a significant challenge to construct SPNs with outstanding mechanical performance. Herein, we exploit the cryptand/paraquat host-guest recognition motifs as cross-links to prepare a class of highly strong and tough SPNs. Unlike those supramolecular cross-links with relatively weak binding abilities, the cryptand-based host-guest interactions have a high association constant and steady complexing structure, which effectively stabilizes the network and resists mechanical deformation under external force. Such favorable structural stability endows our SPNs with greatly enhanced mechanical performance, compared with the control-1 cross-linked by the weakly complexed crown ether/secondary ammonium salt motif (tensile strength: 21.1±0.5 vs 2.8±0.1 MPa; Young's modulus: 102.6±4.8 vs 2.1±0.3 MPa; toughness: 90.4±2.0 vs 10.8±0.6 MJ m-3 ). Moreover, our SPNs also retain abundant dynamic properties including good abilities in energy dissipation, reprocessability, and stimuli-responsiveness. These findings provide novel insights into the preparation of SPNs with enhanced mechanical properties, and promote the development of high-performance intelligent supramolecular materials.

The macromolecular complexes of histones affect protein arginine methyltransferase activities.

Histone arginine methylation is a key post-translational modification that mediates epigenetic events that activate or repress gene transcription. Protein arginine methyltransferases (PRMTs) are the driving force for the process of arginine methylation, and the core histone proteins have been shown to be substrates for most PRMT family members. However, previous reports of the enzymatic activities of PRMTs on histones in the context of nucleosomes seem contradictory. Moreover, what governs nucleosomal substrate recognition of different PRMT members is not understood. We sought to address this key biological question by examining how different macromolecular contexts where the core histones reside may regulate arginine methylation catalyzed by individual PRMT members (i.e., PRMT1, PRMT3, PRMT4, PRMT5, PRMT6, PRMT7, and PRMT8). Our results demonstrated that the substrate context exhibits a huge impact on the histone arginine methylation activity of PRMTs. Although all the tested PRMTs methylate multiple free histones individually, they show a preference for one particular histone substrate in the context of the histone octamer. We found that PRMT1, PRMT3, PRMT5, PRMT6, PRMT7, and PRMT8 preferentially methylate histone H4, whereas PRMT4/coactivator-associated arginine methyltransferase 1 prefers histone H3. Importantly, neither reconstituted nor cell-extracted mononucleosomes could be methylated by any PRMTs tested. Structural analysis suggested that the electrostatic interaction may play a mechanistic role in priming the substrates for methylation by PRMT enzymes. Taken together, this work expands our knowledge on the molecular mechanisms of PRMT substrate recognition and has important implications for understanding cellular dynamics and kinetics of histone arginine methylation in regulating gene transcription and other chromatin-templated processes.

Carbon Dots Mediated In Situ Confined Growth of Bi Clusters on g-C3 N4 Nanomeshes for Boosting Plasma-Assisted Photoreduction of CO2.

Synthesis of high-efficiency, cost-effective, and stable photocatalysts has long been a priority for sustainable photocatalytic CO2 reduction reactions (CRR), given its importance in achieving carbon neutrality goals under the new development philosophy. Fundamentally, the sluggish interface charge transportation and poor selectivity of products remain a challenge in the CRR progress. Herein, this work unveils a synergistic effect between high-density monodispersed Bi/carbon dots (CDs) and ultrathin graphite phase carbon nitride (g-C3 N4 ) nanomeshes for plasma-assisted photocatalytic CRR. The optimal g-C3 N4 /Bi/CDs heterojunction displays a high selectivity of 98% for CO production with a yield up to 22.7 µmol g-1 without any sacrificial agent. The in situ confined growth of plasmonic Bi clusters favors the production of more hot carriers and improves the conductivity of g-C3 N4 . Meanwhile, a built-in electric field driving force modulates the directional injection photogenerated holes from plasmonic Bi clusters and g-C3 N4 photosensitive units to adjacent CDs reservoirs, thus promoting the rapid separation and oriented transfer in the CRR process. This work sheds light on the mechanism of plasma-assisted photocatalytic CRR and provides a pathway for designing highly efficient plasma-involved photocatalysts.

Hierarchical Assembly of Flexible Biopolymer Polyphosphate-Manganese into Nanosheets.

Polyphosphate (polyP) is one of the most compact inorganic polyanionic biopolymers that participates in various physiological processes. However, the development of polyP-based nanomaterials is still in its infancy. Here, biocompatible polyphosphate-manganese nanosheets are designed and synthesized by a hierarchical assembly strategy. The thickness and the lateral size of the resulting polyP-Mn nanosheets (PMNSs) are 5 nm and 120-130 nm, respectively. Molecular dynamics simulations suggested that the polyP-hexadecyl trimethyl ammonium bromide flat structure possesses a strong aggregating capacity and serves as the template for the 2D assembly of polyP-Mn. The PMNSs can activate the inflammatory response of macrophages resulting in the recovery of innate immunological functions to inhibit tumor proliferation. This work has initiated a new direction in constructing layered polyP-based nanomaterials and provides guidance for biocompatible and biodegradable biopolymer-based materials in the regulation of innate responses.

Transcriptional Programming in Arteriosclerotic Disease: A Multifaceted Function of the Runx2 (Runt-Related Transcription Factor 2).

Despite successful therapeutic strategies in the prevention and treatment of arteriosclerosis, the cardiovascular complications remain a major clinical and societal issue worldwide. Increased vascular calcification promotes arterial stiffness and accelerates cardiovascular morbidity and mortality. Upregulation of the Runx2 (Runt-related transcription factor 2), an essential osteogenic transcription factor for bone formation, in the cardiovascular system has emerged as an important regulator for adverse cellular events that drive cardiovascular pathology. This review discusses the regulatory mechanisms that are critical for Runx2 expression and function and highlights the dynamic and complex cross talks of a wide variety of posttranslational modifications, including phosphorylation, acetylation, ubiquitination, and O-linked ß-N-acetylglucosamine modification, in regulating Runx2 stability, cellular localization, and osteogenic transcriptional activity. How the activation of an array of signaling cascades by circulating and local microenvironmental factors upregulates Runx2 in vascular cells and promotes Runx2-mediated osteogenic transdifferentiation of vascular smooth muscle cells and expression of inflammatory cytokines that accelerate macrophage infiltration and vascular osteoclast formation is summarized. Furthermore, the increasing appreciation of a new role of Runx2 upregulation in promoting vascular smooth muscle cell phenotypic switch, and Runx2 modulated by O-linked ß-N-acetylglucosamine modification and Runx2-dependent repression of smooth muscle cell-specific gene expression are discussed. Further exploring the regulation of this key osteogenic transcription factor and its new perspectives in the vasculature will provide novel insights into the transcriptional regulation of vascular smooth muscle cell phenotype switch, reprograming, and vascular inflammation that promote the pathogenesis of arteriosclerosis.

Robust and Dynamic Polymer Networks Enabled by Woven Crosslinks.

Crosslinking plays a crucial role in determining mechanical properties of polymer materials. Although various crosslinks based on covalent or noncovalent bonds have been adopted, it remains an enormous challenge to develop a crosslink which could endow corresponding polymer network with robust yet dynamic properties. Herein, we report a crosslink simultaneously having dynamic property and woven geometry, and the polymer network with woven crosslinks (WPN) could integrate the merits of covalent polymer network (CPN) and supramolecular polymer network (SPN). In specific, the WPN not only exhibits comparable stiffness, strength, elastic recovery, and anti-fatigue property to those of CPN, but also possesses decent mechanical adaptivity and ductility, similar to those of SPN. Particularly, its toughness and puncture resistance are much superior to those of the others. Besides, the dynamicity of woven crosslink also imparts good performances of self-healing and processability to WPN.

Muscle-Mimetic Synergistic Covalent and Supramolecular Polymers: Phototriggered Formation Leads to Mechanical Performance Boost.

A thin filament stimulated by Ca2+ to combine with myosin is the structural basis to achieve filament sliding and muscle contraction. Though a large variety of artificial materials has been developed by mimicking muscle, the on-demand combination of the actin filament and myosin has never been precisely reproduced in polymeric systems. Herein, we show that both the combination process and the combined structure of actin filament and myosin have been mimicked to construct synergistic covalent and supramolecular polymers (CSPs). Specifically, photoirradiation as a stimulus induces the independently formed covalent polymers (CPs) and supramolecular polymers (SPs) to interact with each other through activated quadruple H-bonding. The resultant CSPs possess a unique network structure which not only facilitates the synergistic effect of CPs and SPs to afford stiff, strong, yet tough materials but also provides efficient pathways to dissipate energy with the damping capacity of the representative material being higher than 95%. Furthermore, muscle functions, for example, by becoming stiff during contraction and self-growth by training, are imitated well in our system via in situ phototriggered formation of CSP in the solid state. We hope that the fundamental understanding gained from this work will promote the development of synergistic CSP systems with emergent functions and applications by mimicking the principle of muscle movements.

PRMT1-mediated FLT3 arginine methylation promotes maintenance of FLT3-ITD+ acute myeloid leukemia.

The presence of FMS-like receptor tyrosine kinase-3 internal tandem duplication (FLT3-ITD) mutations in patients with acute myeloid leukemia (AML) is associated with poor clinical outcome. FLT3 tyrosine kinase inhibitors (TKIs), although effective in kinase ablation, do not eliminate primitive FLT3-ITD+ leukemia cells, which are potential sources of relapse. Thus, understanding the mechanisms underlying FLT3-ITD+ AML cell persistence is essential to devise future AML therapies. Here, we show that expression of protein arginine methyltransferase 1 (PRMT1), the primary type I arginine methyltransferase, is increased significantly in AML cells relative to normal hematopoietic cells. Genome-wide analysis, coimmunoprecipitation assay, and PRMT1-knockout mouse studies indicate that PRMT1 preferentially cooperates with FLT3-ITD, contributing to AML maintenance. Genetic or pharmacological inhibition of PRMT1 markedly blocked FLT3-ITD+ AML cell maintenance. Mechanistically, PRMT1 catalyzed FLT3-ITD protein methylation at arginine 972/973, and PRMT1 promoted leukemia cell growth in an FLT3 methylation-dependent manner. Moreover, the effects of FLT3-ITD methylation in AML cells were partially due to cross talk with FLT3-ITD phosphorylation at tyrosine 969. Importantly, FLT3 methylation persisted in FLT3-ITD+ AML cells following kinase inhibition, indicating that methylation occurs independently of kinase activity. Finally, in patient-derived xenograft and murine AML models, combined administration of AC220 with a type I PRMT inhibitor (MS023) enhanced elimination of FLT3-ITD+ AML cells relative to AC220 treatment alone. Our study demonstrates that PRMT1-mediated FLT3 methylation promotes AML maintenance and suggests that combining PRMT1 inhibition with FLT3 TKI treatment could be a promising approach to eliminate FLT3-ITD+ AML cells.

Arterial Stiffness: A Focus on Vascular Calcification and Its Link to Bone Mineralization.

This review focuses on the association between vascular calcification and arterial stiffness, highlighting the important genetic factors, systemic and local microenvironmental signals, and underlying signaling pathways and molecular regulators of vascular calcification. Elevated oxidative stress appears to be a common procalcification factor that induces osteogenic differentiation and calcification of vascular cells in a variety of disease conditions such as atherosclerosis, diabetes mellitus, and chronic kidney disease. Thus, the role of oxidative stress and oxidative stress-regulated signals in vascular smooth muscle cells and their contributions to vascular calcification are highlighted. In relation to diabetes mellitus, the regulation of both hyperglycemia and increased protein glycosylation, by AGEs (advanced glycation end products) and O-linked ß-N-acetylglucosamine modification, and its role in enhancing intracellular pathophysiological signaling that promotes osteogenic differentiation and calcification of vascular smooth muscle cells are discussed. In the context of chronic kidney disease, this review details the role of calcium and phosphate homeostasis, parathyroid hormone, and specific calcification inhibitors in regulating vascular calcification. In addition, the impact of the systemic and microenvironmental factors on respective intrinsic signaling pathways that promote osteogenic differentiation and calcification of vascular smooth muscle cells and osteoblasts are compared and contrasted, aiming to dissect the commonalities and distinctions that underlie the paradoxical vascular-bone mineralization disorders in aging and diseases.

Development and validation of a preoperative nomogram for predicting patients with impacted ureteral stone: a retrospective analysis.

BACKGROUND: To develop and validate a practical nomogram for predicting the probability of patients with impacted ureteral stone. METHODS: Between June 2020 to March 2021, 214 single ureteral stones received ureteroscopy lithotripsy (URSL) were selected in development group. While 82 single ureteral stones received URSL between April 2021 to May 2021 were included in validation group. Independent factors for predicting impacted ureteral stone were screened by univariate and multivariate logistic regression analysis. The relationship between preoperative factors and stone impaction was modeled according to the regression coefficients. Discrimination and calibration were estimated by area under the receiver operating characteristic (AUROC) curve and calibration curve respectively. Clinical usefulness of the nomogram was evaluated by decision curve analysis. RESULTS: Age, ipsilateral stone treatment history, hydronephrosis and maximum ureteral wall thickness (UWTmax) at the portion of stone were identified as independent predictors for impacted stone. The AUROC curve of development and validation group were 0.915 and 0.882 respectively. Calibration curve of two groups showed strong concordance between the predicted and actual probabilities. Decision curve analysis showed that the predictive nomogram had a superior net benefit than UWTmax for all examined probabilities. CONCLUSIONS: We developed and validated an individualized model to predict impacted ureteral stone prior to surgery. Through this prediction model, urologists can select an optimal treatment method and decrease intraoperative and postoperative complications for patients with impacted ureteral calculus.

Prevalence and risk factors for antibiotic utilization in Chinese children.

BACKGROUND: Antibiotic resistance poses a significant threat to public health globally. Irrational utilization of antibiotics being one of the main reasons of antibiotic resistant. Children as a special group, there's more chance of getting infected. Although most of the infection is viral in etiology, antibiotics still are the most frequently prescribed medications for children. Therefore, high use of antibiotics among children raises concern about the appropriateness of antibiotic prescribing. This systematic review aims to measuring prevalence and risk factors for antibiotic utilization in children in China. METHODS: English and Chinese databases were searched to identify relevant studies evaluating the prevalence and risk factors for antibiotic utilization in Chinese children (0-18 years), which were published between 2010 and July 2020. A Meta-analysis of prevalence was performed using random effect model. The Agency for Healthcare Research and Quality (AHRQ) and modified Jadad score was used to assess risk of bias of studies. In addition, we explored the risk factors of antibiotic utilization in Chinese children using qualitative analysis. RESULTS: Of 10,075 studies identified, 98 eligible studies were included after excluded duplicated studies. A total of 79 studies reported prevalence and 42 studies reported risk factors for antibiotic utilization in children. The overall prevalence of antibiotic utilization among outpatients and inpatients were 63.8% (35 studies, 95% confidence interval (CI): 55.1-72.4%), and 81.3% (41 studies, 95% CI: 77.3-85.2%), respectively. In addition, the overall prevalence of caregiver's self-medicating of antibiotics for children at home was 37.8% (4 studies, 95% CI: 7.9-67.6%). The high prevalence of antibiotics was associated with multiple factors, while lacking of skills and knowledge in both physicians and caregivers was the most recognized risk factor, caregivers put pressure on physicians to get antibiotics and self-medicating with antibiotics at home for children also were the main factors attributed to this issue. CONCLUSION: The prevalence of antibiotic utilization in Chinese children is heavy both in hospitals and home. It is important for government to develop more effective strategies to improve the irrational use of antibiotic, especially in rural setting.

Regulation of pancreatic cancer TRAIL resistance by protein O-GlcNAcylation.

TRAIL-activating therapy is promising in treating various cancers, including pancreatic cancer, a highly malignant neoplasm with poor prognosis. However, many pancreatic cancer cells are resistant to TRAIL-induced apoptosis despite their expression of intact death receptors (DRs). Protein O-GlcNAcylation is a versatile posttranslational modification that regulates various biological processes. Elevated protein O-GlcNAcylation has been recently linked to cancer cell growth and survival. In this study, we evaluated the role of protein O-GlcNAcylation in pancreatic cancer TRAIL resistance, and identified higher levels of O-GlcNAcylation in TRAIL-resistant pancreatic cancer cells. With gain- and loss-of-function of the O-GlcNAc-adding enzyme, O-GlcNActransferase (OGT), we determined that increasing O-GlcNAcylation rendered TRAIL-sensitive cells more resistant to TRA-8-induced apoptosis, while inhibiting O-GlcNAcylation promoted TRA-8-induced apoptosis in TRAIL-resistance cells. Furthermore, we demonstrated that OGT knockdown sensitized TRAIL-resistant cells to TRA-8 therapy in a mouse model in vivo. Mechanistic studies revealed direct O-GlcNAc modifications of DR5, which regulated TRA-8-induced DR5 oligomerization. We further defined that DR5 O-GlcNAcylation was independent of FADD, the adapter protein for the downstream death-inducing signaling. These studies have demonstrated an important role of protein O-GlcNAcylation in regulating TRAIL resistance of pancreatic cancer cells; and uncovered the contribution of O-GlcNAcylation to DR5 oligomerization and thus mediating DR-inducing signaling.

Metabolic Stress and Cardiovascular Disease in Diabetes Mellitus: The Role of Protein O-GlcNAc Modification.

Mammalian cells metabolize glucose primarily for energy production, biomass synthesis, and posttranslational glycosylation; and maintaining glucose metabolic homeostasis is essential for normal physiology of cells. Impaired glucose homeostasis leads to hyperglycemia, a hallmark of diabetes mellitus. Chronically increased glucose in diabetes mellitus promotes pathological changes accompanied by impaired cellular function and tissue damage, which facilitates the development of cardiovascular complications, the major cause of morbidity and mortality of patients with diabetes mellitus. Emerging roles of glucose metabolism via the hexosamine biosynthesis pathway (HBP) and increased protein modification via O-linked ß-N-acetylglucosamine (O-GlcNAcylation) have been demonstrated in diabetes mellitus and implicated in the development of diabetic cardiovascular complications. This review will discuss the biological outcomes of the glucose metabolism via the hexosamine biogenesis pathway and protein O-GlcNAcylation in regulating cellular homeostasis, and highlight the regulations and contributions of elevated O-GlcNAcylation to the pathogenesis of diabetic cardiovascular disease.

A New Cycle Slip Detection and Repair Method Using a Single Receiver's Single Station B1 and L1 Frequencies in Ground-Based Positioning Systems.

The detection and repair of the cycle slip is a key step for high precision navigation and positioning in indoor environments. Different methods have been developed to detect and repair cycle slips for carrier phase processing. However, most approaches are designed to eliminate the effects of the ionosphere in an outdoor environment, and many of them use pseudorange (code) information that is no longer suitable for indoor multipath environments. In this paper, a method based on the geometry-free combination without the pseudorange data is proposed to detect and fix cycle slips. A ground-based navigation system is built for data collection. Unlike the traditional dual-frequency cycle slip detection method, the Beidou B1, GPS L1 carrier phase combination is used instead of the B1, B2, or L1, L2 carrier phase combination, Ublox is used for data collecting. For fixing the cycle slips quickly, an improved adaptive Particle Swarm Optimization (PSO) algorithm is employed. We compared the performance of the new method with the existing two methods using simulated data in different conditions. The results show that the proposed method has better performance than other methods.

Characterization of iPSCs derived from low grade gliomas revealed early regional chromosomal amplifications during gliomagenesis.

INTRODUCTION: IDH1 mutation has been identified as an early genetic event driving low grade gliomas (LGGs) and it has been proven to exerts a powerful epigenetic effect. Cells containing IDH1 mutation are refractory to epigenetical reprogramming to iPSC induced by expression of Yamanaka transcription factors, a feature that we employed to study early genetic amplifications or deletions in gliomagenesis. METHODS: We made iPSC clones from freshly surgically resected IDH1 mutant LGGs by forced expression of Yamanaka transcription factors. We sequenced the IDH locus and analyzed the genetic composition of multiple iPSC clones by array-based comparative genomic hybridization (aCGH). RESULTS: We hypothesize that the primary cell pool isolated from LGG tumor contains a heterogeneous population consisting tumor cells at various stages of tumor progression including cells with early genetic lesions if any prior to acquisition of IDH1 mutation. Because cells containing IDH1 mutation are refractory to reprogramming, we predict that iPSC clones should originate only from LGG cells without IDH1 mutation, i.e. cells prior to acquisition of IDH1 mutation. As expected, we found that none of the iPSC clones contains IDH1 mutation. Further analysis by aCGH of the iPSC clones reveals that they contain regional chromosomal amplifications which are also present in the primary LGG cells. CONCLUSIONS: These results indicate that there exists a subpopulation of cells harboring gene amplification but without IDH1 mutation in the LGG primary cell pool. Further analysis of TCGA LGG database demonstrates that these regional chromosomal amplifications are also present in some cases of low grade gliomas indicating they are reoccurring lesions in glioma albeit at a low frequency. Taken together, these data suggest that regional chromosomal alterations may exist prior to the acquisition of IDH mutations in at least some cases of LGGs.