62 research outputs found

    A distance measure of interval-valued belief structures

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    Interval-valued belief structures are generalized from belief function theory, in terms of basic belief assignments from crisp to interval numbers. The distance measure has long been an essential tool in belief function theory, such as conflict evidence combinations, clustering analysis, belief function and approximation. Researchers have paid much attention and proposed many kinds of distance measures. However, few works have addressed distance measures of interval-valued belief structures up. In this paper, we propose a method to measure the distance of interval belief functions. The method is based on an interval-valued one-dimensional Hausdorff distance and Jaccard similarity coefficient. We show and prove its properties of non-negativity, non-degeneracy, symmetry and triangle inequality. Numerical examples illustrate the validity of the proposed distance

    Voltage-Controlled Enzyme-Catalyzed Glucose–Gluconolactone Conversion Using A Field-Effect Enzymatic Detector

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    The field-effect enzymatic detection (FEED) technique was used to control the kinetics of the enzymatic conversion of glucose to gluconolactone. The glucose–gluconolactone conversion occurring at an enzyme-immobilized electrode, a well-studied process, was confirmed using mass spectrometry. Electrochemical studies showed that the glucose oxidation current depends on the gating voltage VG and the ion concentration of the sample solution. Additionally, the depletion of glucose in the sample also showed a dependence on VG. FEED was used to detect H2O2 on the zepto-molar level in order to show the ultrasensitive detection capability of the technique. These results, while providing evidence for the proposed mechanism of FEED, indicate that VG controls the conversion process. The effect of VG on the glucose–gluconolactone conversion was demonstrated by the observed VG-dependent kinetic parameters of the conversion process

    Povezanost polimorfizma pojedinačnog nukleotida gena ARID4A i kvalitete sperme kineskog vodenog bivola

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    ARID4A (AT-rich interaction domain 4A) is closely related to animal sperm quality traits. In the present study, the association between ARID4A gene polymorphisms of Chinese water buffalo (Bubalus bubalis) with sperm quality traits was examined, including ejaculate volume, sperm concentration, post-thaw sperm motility, and sperm abnormality of buffalo semen. Seven single-nucleotide polymorphisms (SNPs) of ARID4A gene were detected in 156 Chinese water buffaloes by Sanger sequencing and identifying overlap peaks. Among the SNPs, six were associated with at least one sperm quality trait. In brief, g.21192G>C, g.21285C>G, and g.21364A>G could be used as potential markers for selecting semen with low sperm abnormality, high ejaculate volume, sperm concentration, and sperm motility. Furthermore, 10 haplotypes (H1: -CTCGG, H2: GTGGCA, H3: GCGGCA, H4: GCTGCA, H5: GCTCGA, H6: GTGGGG, H7: GCTCCG, H8: -CGGGA, H9: GCGGCG, and H10: GTTGCA) were formed by the six SNPs through linkage disequilibrium analysis, and then 14 different combined haplotypes were collected. Correlation analysis showed that the combined H1H2 haplotype had the highest genotype frequency. Notably, the combined H1H2 haplotype had low sperm concentration, low sperm motility, and high sperm abnormality. The combined H2H3 haplotype could be used as a potential molecular marker for selecting semen with high sperm motility. In general, we illustrated a significant correlation between SNPs in ARID4A and sperm quality traits of Chinese water buffalo, which may be useful in the marker-assisted selection of buffalo breeding. This study was the first to analyze the genetic polymorphisms of ARID4A and association with sperm qualities of Chinese buffalo.Gen ARID4A (engl AT-rich interaction domain 4A) usko je povezan s kvalitetom sperme. U ovom je radu istraživana povezanost polimorfizma gena ARID4A u kineskih vodenih bivola (Bubalus bubalis) s kvalitetom sperme, uključujući volumen ejakulata, koncentraciju sperme, pokretljivost spermija nakon odmrzavanja i abnormalnost spermija u sjemenu bivola. U 156 kineskih vodenih bivola otkriveno je sedam polimorfizama pojedinačnog nukleotida (SNPs) gena ARID4A Sangerovim sekvenciranjem i identifikacijom preklopljenih vrhova. Među SNP-ovima njih je šest bilo povezano s barem jednim svojstvom kvalitete spermija. Ukratko, g. 21192G>C, g. 21285C>G i g. 21364A>G mogu se upotrijebiti kao potencijalni markeri za selekciju sjemena s niskom abnormalnošću spermija, većim volumenom ejakulata, većom koncentracijom i pokretljivošću spermija. Nadalje, šest SNP-ova formiralo je 10 haplotipova (H1: -CTCGG, H2: GTGGCA, H3: GCGGCA, H4: GCTGCA, H5: GCTCGA, H6: GTGGGG, H7: GCTCCG, H8: -CGGGA, H9: GCGGCG i H10: GTTGCA) analizom povezanosti nepodudarnosti te je ustanovljeno 14 različitih kombiniranih haplotipova. Analiza korelacije pokazala je da kombinirani haplotip H1H2 ima najveću učestalost. Kombinirani haplotip H1H2 imao je najmanju koncentraciju sperme, slabu pokretljivost seprmija i znatnu abnormalnost spermija. Kombinirani haplotip H2H3 može se upotrijebiti kao potencijalni molekularni marker za odabir sjemena s većom pokretljivošću. Općenito je pokazana znakovita korelacija između SNP-ova u ARID4A i kvalitete sperme kineskog vodenog bivola, što može biti korisno u selekciji bivola potpomognutoj markerima. Ovo je prvo istraživanje koje je analiziralo genske polimorfizme ARID4A i njihovu povezanost s kvalitetom sjemena kineskih vodenih bivola

    Efficient Deformable ConvNets: Rethinking Dynamic and Sparse Operator for Vision Applications

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    We introduce Deformable Convolution v4 (DCNv4), a highly efficient and effective operator designed for a broad spectrum of vision applications. DCNv4 addresses the limitations of its predecessor, DCNv3, with two key enhancements: 1. removing softmax normalization in spatial aggregation to enhance its dynamic property and expressive power and 2. optimizing memory access to minimize redundant operations for speedup. These improvements result in a significantly faster convergence compared to DCNv3 and a substantial increase in processing speed, with DCNv4 achieving more than three times the forward speed. DCNv4 demonstrates exceptional performance across various tasks, including image classification, instance and semantic segmentation, and notably, image generation. When integrated into generative models like U-Net in the latent diffusion model, DCNv4 outperforms its baseline, underscoring its possibility to enhance generative models. In practical applications, replacing DCNv3 with DCNv4 in the InternImage model to create FlashInternImage results in up to 80% speed increase and further performance improvement without further modifications. The advancements in speed and efficiency of DCNv4, combined with its robust performance across diverse vision tasks, show its potential as a foundational building block for future vision models.Comment: Tech report; Code: https://github.com/OpenGVLab/DCNv

    Loss of Asxl1 leads to myelodysplastic syndrome-like disease in mice

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    ASXL1 is mutated/deleted with high frequencies in multiple forms of myeloid malignancies, and its alterations are associated with poor prognosis. De novo ASXL1 mutations cause Bohring-Opitz syndrome characterized by multiple congenital malformations. We show that Asxl1 deletion in mice led to developmental abnormalities including dwarfism, anophthalmia, and 80% embryonic lethality. Surviving Asxl1(-/-) mice lived for up to 42 days and developed features of myelodysplastic syndrome (MDS), including dysplastic neutrophils and multiple lineage cytopenia. Asxl1(-/-) mice had a reduced hematopoietic stem cell (HSC) pool, and Asxl1(-/-) HSCs exhibited decreased hematopoietic repopulating capacity, with skewed cell differentiation favoring granulocytic lineage. Asxl1(+/-) mice also developed mild MDS-like disease, which could progress to MDS/myeloproliferative neoplasm, demonstrating a haploinsufficient effect of Asxl1 in the pathogenesis of myeloid malignancies. Asxl1 loss led to an increased apoptosis and mitosis in Lineage(-)c-Kit(+) (Lin(-)c-Kit(+)) cells, consistent with human MDS. Furthermore, Asxl1(-/-) Lin(-)c-Kit(+) cells exhibited decreased global levels of H3K27me3 and H3K4me3 and altered expression of genes regulating apoptosis (Bcl2, Bcl2l12, Bcl2l13). Collectively, we report a novel ASXL1 murine model that recapitulates human myeloid malignancies, implying that Asxl1 functions as a tumor suppressor to maintain hematopoietic cell homeostasis. Future work is necessary to clarify the contribution of microenvironment to the hematopoietic phenotypes observed in the constitutional Asxl1(-/-) mice

    ShenQiWan ameliorates renal injury in type 2 diabetic mice by modulating mitochondrial fusion and endoplasmic reticulum stress

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    Background: ShenQiWan is commonly used in traditional Chinese medicine for the treatment of diabetic nephropathy, which is closely related to mitochondrial fusion and endoplasmic reticulum stress. This study aimed to investigate the intervention effect and molecular mechanisms of ShenQiWan on renal injury in KKAy mice.Methods: C57BL/6J mice (11 weeks old) were fed a regular diet upon arrival, while KKAy mice (11 weeks old) were fed a high-fat diet upon arrival. At 12 weeks of age, KKAy mice with random blood glucose ≥13.9 mmol/L were identified as diabetic mice and randomly divided into the model group (n = 30) and the treatment group (n = 30), while C57BL/6J mice of 12 weeks old (n = 30) served as the control group. The treatment group received daily aqueous decoction of ShenQiWan (13.5 g/kg), while the control group and model group received daily equal amounts of saline from 12 weeks old to 24 weeks old. The general status of mice was observed regularly, and fasting blood glucose and 24-hour urine microalbumin were measured. Ten mice were euthanized in each group at the age of 16, 20, and 24 weeks, serum samples were used for biochemical indexes and kidney tissues were used for morphological studies. GRP78, OPA1, MFN1, MFN2 mRNA and protein expression were detected by Real-time PCR, immunohistochemistry and Western blot.Results: The mice in the model group exhibited symptoms of lethargy, slow movement, obesity, polyuria and proteinuria. Morphological observation revealed pathological changes, including thickening of the glomerular basement membrane and interstitial fibrosis. After treatment with ShenQiWan, the fasting blood glucose level of KKAy mice was significantly reduced, urinary albuminuria was decreased, serum biochemical indexes were improved, renal tissue pathological changes were significantly alleviated. The results also showed a significant reduction in the expression of endoplasmic reticulum stress-related factor GRP78 and an increase in the expression of mitochondrial fusion-related factors OPA1, MFN1 and MFN2 after treatment with ShenQiWan.Conclusion: ShenQiWan can protect diabetic mice from renal damage by modulating mitochondrial fusion and alleviating endoplasmic reticulum stress, exerting its protective effects

    Tet2 loss leads to hypermutagenicity in haematopoietic stem/progenitor cells

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    TET2 is a dioxygenase that catalyses multiple steps of 5-methylcytosine oxidation. Although TET2 mutations frequently occur in various types of haematological malignancies, the mechanism by which they increase risk for these cancers remains poorly understood. Here we show that Tet2?/? mice develop spontaneous myeloid, T- and B-cell malignancies after long latencies. Exome sequencing of Tet2?/? tumours reveals accumulation of numerous mutations, including Apc, Nf1, Flt3, Cbl, Notch1 and Mll2, which are recurrently deleted/mutated in human haematological malignancies. Single-cell-targeted sequencing of wild-type and premalignant Tet2?/? Lin?c-Kit+ cells shows higher mutation frequencies in Tet2?/? cells. We further show that the increased mutational burden is particularly high at genomic sites that gained 5-hydroxymethylcytosine, where TET2 normally binds. Furthermore, TET2-mutated myeloid malignancy patients have significantly more mutational events than patients with wild-type TET2. Thus, Tet2 loss leads to hypermutagenicity in haematopoietic stem/progenitor cells, suggesting a novel TET2 loss-mediated mechanism of haematological malignancy pathogenesis

    Hyperactive transforming growth factor-β1 signaling potentiates skeletal defects in a neurofibromatosis type 1 mouse model

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    Dysregulated transforming growth factor beta (TGF-β) signaling is associated with a spectrum of osseous defects as seen in Loeys-Dietz syndrome, Marfan syndrome, and Camurati-Engelmann disease. Intriguingly, neurofibromatosis type 1 (NF1) patients exhibit many of these characteristic skeletal features, including kyphoscoliosis, osteoporosis, tibial dysplasia, and pseudarthrosis; however, the molecular mechanisms mediating these phenotypes remain unclear. Here, we provide genetic and pharmacologic evidence that hyperactive TGF-β1 signaling pivotally underpins osseous defects in Nf1(flox/-) ;Col2.3Cre mice, a model which closely recapitulates the skeletal abnormalities found in the human disease. Compared to controls, we show that serum TGF-β1 levels are fivefold to sixfold increased both in Nf1(flox/-) ;Col2.3Cre mice and in a cohort of NF1 patients. Nf1-deficient osteoblasts, the principal source of TGF-β1 in bone, overexpress TGF-β1 in a gene dosage-dependent fashion. Moreover, Nf1-deficient osteoblasts and osteoclasts are hyperresponsive to TGF-β1 stimulation, potentiating osteoclast bone resorptive activity while inhibiting osteoblast differentiation. These cellular phenotypes are further accompanied by p21-Ras-dependent hyperactivation of the canonical TGF-β1-Smad pathway. Reexpression of the human, full-length neurofibromin guanosine triphosphatase (GTPase)-activating protein (GAP)-related domain (NF1 GRD) in primary Nf1-deficient osteoblast progenitors, attenuated TGF-β1 expression levels and reduced Smad phosphorylation in response to TGF-β1 stimulation. As an in vivo proof of principle, we demonstrate that administration of the TGF-β receptor 1 (TβRI) kinase inhibitor, SD-208, can rescue bone mass deficits and prevent tibial fracture nonunion in Nf1(flox/-) ;Col2.3Cre mice. In sum, these data demonstrate a pivotal role for hyperactive TGF-β1 signaling in the pathogenesis of NF1-associated osteoporosis and pseudarthrosis, thus implicating the TGF-β signaling pathway as a potential therapeutic target in the treatment of NF1 osseous defects that are refractory to current therapie

    Tet2 loss leads to hypermutagenicity in haematopoietic stem/progenitor cells

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    TET2 is a dioxygenase that catalyses multiple steps of 5-methylcytosine oxidation. Although TET2 mutations frequently occur in various types of haematological malignancies, the mechanism by which they increase risk for these cancers remains poorly understood. Here we show that Tet2-/- mice develop spontaneous myeloid, T- and B-cell malignancies after long latencies. Exome sequencing of Tet2-/- tumours reveals accumulation of numerous mutations, including Apc, Nf1, Flt3, Cbl, Notch1 and Mll2, which are recurrently deleted/mutated in human haematological malignancies. Single-cell-targeted sequencing of wild-type and premalignant Tet2-/- Lin-c-Kit+ cells shows higher mutation frequencies in Tet2-/- cells. We further show that the increased mutational burden is particularly high at genomic sites that gained 5-hydroxymethylcytosine, where TET2 normally binds. Furthermore, TET2-mutated myeloid malignancy patients have significantly more mutational events than patients with wild-type TET2. Thus, Tet2 loss leads to hypermutagenicity in haematopoietic stem/progenitor cells, suggesting a novel TET2 loss-mediated mechanism of haematological malignancy pathogenesis
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