31 research outputs found

    Association Analysis of NLRP3 Inflammation-Related Gene Promotor Methylation as Well as Mediating Effects on T2DM and Vascular Complications in a Southern Han Chinese Population

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    Objective: To explore the association between the methylation levels in the promoter regions of the NLRP3, AIM2, and ASC genes and T2DM and its vascular complications in a Southern Han Chinese population and further analyze their interaction and mediating effects with environmental factors in T2DM.Methods: A case-control study was used to determine the association between population characteristics, the methylation level in the promoter region of the NLRP3, AIM2, and ASC genes and T2DM and vascular complications. A mediating effect among genes-environment-T2DM and the interaction of gene-gene or gene-environment factors was explored.Results: In the logistic regression model with adjusted covariants, healthy people with lower total methylation levels in the AIM2 promoter region exhibited a 2.29-fold [OR: 2.29 (1.28~6.66), P = 0.011] increased risk of developing T2DM compared with higher-methylation individuals. T2DM patients without any vascular complications who had lower methylation levels (<methylation median) in NLRP3 CpG2 and AIM2 total methylation had 6.45 (OR: 6.45, 95% CI: 1.05~39.78, P = 0.011) and 9.48 (OR: 9.48, 95% CI: 1.14~79.00, P = 0.038) times higher risks, respectively, of developing diabetic microvascular complications than T2DM patients with higher methylation. Similar associations were also found between the lower total methylation of the NLRP3 and AIM2 promoter regions and macrovascular complication risk (NLRP3 OR: 36.03, 95% CI: 3.11~417.06, P = 0.004; AIM2 OR: 30.90, 95% CI: 2.59~368.49, P = 0.007). Lower NLRP3 promoter total methylation was related to a 17.78-fold increased risk of micro-macrovascular complications (OR: 17.78, 95% CI: 2.04~155.28, P = 0.009). Lower ASC CpG1 or CpG3 methylation levels had significant partial mediating effects on T2DM vascular complications caused by higher age (ASC CpG1 explained approximately 52.8% or 32.9% of the mediating effect of age on macrovascular or macro-microvascular complications; ASC CpG3 explained approximately 38.9% of the mediating effect of age on macrovascular complications). No gene-gene or gene-environment interaction was identified in T2DM.Conclusion: Lower levels of AIM2 promoter total methylation might increase the risk of T2DM. NLRP3, AIM2, and ASC promoter total methylation or some CpG methylation loss might increase the risk of T2DM vascular complications, which merits further study to support the robustness of these findings

    3D-Heisenberg ferromagnetic characteristics in a La

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    We conducted a study of critical exponents to investigate the nature of paramagnetic to ferromagnetic phase transition in a La0.67_{\mathrm{0.67}}Ba0.33_{\mathrm{0.33}}MnO3_{\mathrm{3}} (LBMO) film deposited on SrTiO3_{\mathrm{3}}. To this end, we performed dc magnetization M (H, T) measurements around the Curie temperature (TC∌T_{\mathrm{C}}\sim 276.5 K) within a temperature range that includes the critical region ∣Δ∣|\varepsilon |==∣T−TC∣|T-T_{\mathrm{C}}|/TC<0.05T_{\mathrm{C}} < 0.05. We found that the transition is a second-order transition. Three main critical exponents, namely ÎČ\beta (0.387), Îł\gamma (1.309) and ÎŽ\delta (4.634), and the critical temperature TC=T_{\mathrm{C}} = 276.6 K are derived from the modified Arrott plots. These exponents obey the Widom relation ÎŽ=\delta = 1+Îł+\gamma /ÎČ\beta and are able to collapse a bunch of isothermal magnetization data into two branches below and above TCT_{\mathrm{C}} based on the single scaling equation M(H,Δ{H, \varepsilon })Δ−ÎČ=f±(HΔ(−ÎČ+Îł))\varepsilon ^{-\beta } = {f}_{\pm }({H} \varepsilon ^{({-\beta +\gamma })}). The critical behavior in LBMO film is close to a 3D Heisenberg model, although certain long-range interactions still exist. Compared to a polycrystalline bulk sample, the long-range interactions are greatly suppressed, which may be attributed to the reduced dimensionality

    Reducing Emitter Clogging in Drip Fertigation Systems by Magnetization Technology

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    The issue of emitter clogging is a common phenomenon in drip fertigation systems, which causes uneven irrigation and fertilization. However, efficient and environmentally friendly methods are scarcely available for alleviating clogging. In the present study, we investigated the anti-fouling efficacy of three magnetic field strength levels (0, 0.4 T and 0.6 T) on emitter clogging in drip fertigation systems. Our results show that magnetized water treatment could effectively relieve emitter clogging and delay the occurrence time of clogging, which increased the average discharge variation rate (Dra) by 37.00–61.64% and decreased the dry weight (DW) by 53.00–69.29% compared with non-magnetized water treatments. X-rays were used to estimate the compositions of the main clogging substances, and the results show that phosphates were the dominant substances that induced emitter clogging. In addition, magnetized water treatment effectively reduced the contents of chemical and particulate fouling, as exhibited by a decrease in phosphates, silicate and quartz by 53.17–69.58%, 47.22–61.95% and 43.18–74.80%, respectively. In comparison, the higher strength of magnetized water treatment (0.6 T) was better in clogging control, which increased Dra and the Christiansen of uniformity (CU) by 24.64% and 43.96%, respectively, and the DW was reduced by 34.67% compared with that of 0.4 T. This study proves that magnetized water treatment is an effective, chemical-free treatment method with great potential for fouling control technology, and it is helpful for the further promotion of drip fertigation technology

    Compact Scheduling for Task Graph Oriented Mobile Crowdsourcing

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    International audienceWith the proliferation of increasingly powerful mobile devices and wireless networks, mobile crowdsourcing has emerged as a novel service paradigm. It enables crowd workers to take over outsourced location-dependent tasks, and has attracted much attention from both research communities and industries. In this paper, we consider a mobile crowdsourcing scenario, where a mobile crowdsourcing task is too complex (e.g., post-earthquake recovery, citywide package delivery) but can be divided into a number of easier subtasks, which have interdependency between them. Under this scenario, we investigate an important problem, namely task graph scheduling in mobile crowdsourcing (TGS-MC), which seeks to optimize a compact scheduling, such that the task completion time (i.e., makespan) and overall idle time are simultaneously minimized with the consideration of worker reliability. We analyze the complexity and NP-complete of the TGS-MC problem, and propose two heuristic approaches, including BFS-based dynamic priority scheduling BFSPriD algorithm, and an evolutionary multitasking-based EMTTSch algorithm, to solve our problem from local and global optimization perspective, respectively. We conduct extensive evaluation using two real-world data sets, and demonstrate superiority of our proposed approaches

    Clinical and genetic characteristics of Chinese patients with familial or sporadic pediatric cataract

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    Abstract Background Pediatric cataract is a clinically and genetically heterogeneous disease which is a significant cause of lifelong visual impairment and treatable blindness. Our study aims to investigate the genotype spectrum in a group of Chinese patients with pediatric cataract. Methods We enrolled 39 families with pediatric cataract from October 2015 to April 2016. DNA samples of the probands were analyzed by target next-generation sequencing. Variants were validated using Sanger sequencing in the probands and available family members. Results In our cohort of 39 cases with different types of pediatric cataract, 23 cases were found to harbor putative pathogenic variants in 15 genes: CRYAA, CRYBA1, CRYBA4, CRYBB1, CRYGC, CRYGD, MIP, GCNT2, IARS2, NHS, BCOR, BFSP2, FYCO1, MAF, and PAX6. The mutation detection rates in the familial and sporadic cases were 75 and 47.8%, respectively. Of the 23 causative variants, over half were novel. Conclusions This is a rare report of systematic mutation screening analysis of pediatric cataract in a comparably large cohort of Chinese patients. Our observations enrich the mutation spectrum of pediatric cataract. Next-generation sequencing provides significant diagnostic information for pediatric cataract cases, especially when considering sporadic and subtle syndromal cases

    Bioinspired artificial visual system based on 2D WSe₂ synapse array

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    Machine vision systems that capture images for visual inspection and recognition tasks must be able to perceive, memorize, and compute any color scene. To achieve this, most of the current visual systems use circuits and algorithms which may reduce efficiency and increase complexity. Herein, a 2D semiconductor tungsten diselenide (WSe2)-based phototransistor that successfully demonstrates an artificial vision system integrating the processing capability of visual information sensing memory, is reported. Furthermore, based on a 6 × 6 fabricated retinal perception array, artificial visual information sensing memory and processing system are proposed to perform image recognition tasks, which can avoid the time delay and energy consumption caused by data conversion and movement. On the other hand, highly linear symmetric synaptic plasticity can be achieved based on the modulation of carrier types in WSe2 transistors with different thicknesses, facilitating the high level of training and inference accuracy for artificial neural networks. Last, through training and inference simulations, the feasibility of the hybrid synapses for optical neural networks (ONN) is demonstrated.This research was supported by the NSFC Program (grant nos. 62122055, 62074104, 62104154, 61974093, and 62001307), the Guangdong Basic and Applied Basic Research Foundation (Grant Nos. 2023A1515012479 and 2021A1515012569), the Science and Technology Innovation Commission of Shenzhen (Grant Nos. RCYX20200714114524157, JCYJ20220818100206013, and 20210324095207020), and the NTUT-SZU Joint Research Program

    Image_1_Autophagy and senescence of rat retinal precursor cells under high glucose.tif

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    BackgroundsDiabetic retinopathy (DR) is a common diabetic ocular disease characterized by retinal ganglion cell (RGC) changes. An abnormal environment, hyperglycemia, may progressively alter the structure and function of RGCs, which is a primary pathological feature of retinal neurodegeneration in DR. Accumulated studies confirmed autophagy and senescence play a vital role in DR; however, the underlying mechanisms need to be clarified.MethodsThis study included the microarray expression profiling dataset GSE60436 from Gene Expression Omnibus (GEO) to conduct the bioinformatics analysis. The R software was used to identify autophagy-related genes (ARGs) that were differentially expressed in fibrovascular membranes (FVMs) and normal retinas. Co-expression and tissue-specific expression were elicited for the filtered genes. The genes were then analyzed by ontology (GO) enrichment analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis and Gene Set Enrichment Analysis (GSEA). R28 cells were cultured with high glucose, detected by reverse transcription-quantitative (RT-qPCR) and stained by apoptosis kit.ResultsIn the retina, 31 differentially expressed ARGs (24 up-regulated genes) were discovered and enriched. The enrichment results revealed that differentially expressed ARGs were significantly enriched in autophagy, apoptosis, aging, and neural function. Four hub genes (i.e., TP53, CASP1, CCL2, and CASP1) were significantly up-regulated. Upregulation of cellular autophagy and apoptosis level was detected in the hyperglycemia model in vitro.ConclusionsOur results provide evidence for the autophagy and cellular senescence mechanisms involved in retinal hyperglycemia injury, and the protective function of autophagy is limited. Further study may favour understanding the disease progression and neuroprotection of DR.</p

    Table_1_Autophagy and senescence of rat retinal precursor cells under high glucose.docx

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    BackgroundsDiabetic retinopathy (DR) is a common diabetic ocular disease characterized by retinal ganglion cell (RGC) changes. An abnormal environment, hyperglycemia, may progressively alter the structure and function of RGCs, which is a primary pathological feature of retinal neurodegeneration in DR. Accumulated studies confirmed autophagy and senescence play a vital role in DR; however, the underlying mechanisms need to be clarified.MethodsThis study included the microarray expression profiling dataset GSE60436 from Gene Expression Omnibus (GEO) to conduct the bioinformatics analysis. The R software was used to identify autophagy-related genes (ARGs) that were differentially expressed in fibrovascular membranes (FVMs) and normal retinas. Co-expression and tissue-specific expression were elicited for the filtered genes. The genes were then analyzed by ontology (GO) enrichment analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis and Gene Set Enrichment Analysis (GSEA). R28 cells were cultured with high glucose, detected by reverse transcription-quantitative (RT-qPCR) and stained by apoptosis kit.ResultsIn the retina, 31 differentially expressed ARGs (24 up-regulated genes) were discovered and enriched. The enrichment results revealed that differentially expressed ARGs were significantly enriched in autophagy, apoptosis, aging, and neural function. Four hub genes (i.e., TP53, CASP1, CCL2, and CASP1) were significantly up-regulated. Upregulation of cellular autophagy and apoptosis level was detected in the hyperglycemia model in vitro.ConclusionsOur results provide evidence for the autophagy and cellular senescence mechanisms involved in retinal hyperglycemia injury, and the protective function of autophagy is limited. Further study may favour understanding the disease progression and neuroprotection of DR.</p

    Recent Progress in Multiterminal Memristors for Neuromorphic Applications

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    Abstract The essential step for developing neuromorphic systems is to construct more biorealistic elementary devices with rich spatiotemporal dynamics to exhibit highly separable responses in dynamic environmental circumstances. Unlike transistor‐based devices and circuits with zeroth‐order complexity, memristors intrinsically express some simple biomimetic functions. However, with only two‐terminal structure, precise control of operation principles to ensure large dynamic space, improved linearity and symmetry, multimodal operation as well as high‐order complexity is hard to achieve in a traditional memristor owing to its limited degree of freedom. Therefore, multiterminal memristors including both concrete terminals and virtual terminals (light, pressure, gas, ferroelectric polarity, etc.) have been proposed to obtain precise modulation of memristive characteristics. This review focuses on the recent progress in multiterminal memristors and their neuromorphic applications. The operation principle, application of multiterminal memristor on neuromorphic computing in different scenarios, existing challenges and future prospects are discussed

    Table_2_Autophagy and senescence of rat retinal precursor cells under high glucose.xlsx

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    BackgroundsDiabetic retinopathy (DR) is a common diabetic ocular disease characterized by retinal ganglion cell (RGC) changes. An abnormal environment, hyperglycemia, may progressively alter the structure and function of RGCs, which is a primary pathological feature of retinal neurodegeneration in DR. Accumulated studies confirmed autophagy and senescence play a vital role in DR; however, the underlying mechanisms need to be clarified.MethodsThis study included the microarray expression profiling dataset GSE60436 from Gene Expression Omnibus (GEO) to conduct the bioinformatics analysis. The R software was used to identify autophagy-related genes (ARGs) that were differentially expressed in fibrovascular membranes (FVMs) and normal retinas. Co-expression and tissue-specific expression were elicited for the filtered genes. The genes were then analyzed by ontology (GO) enrichment analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis and Gene Set Enrichment Analysis (GSEA). R28 cells were cultured with high glucose, detected by reverse transcription-quantitative (RT-qPCR) and stained by apoptosis kit.ResultsIn the retina, 31 differentially expressed ARGs (24 up-regulated genes) were discovered and enriched. The enrichment results revealed that differentially expressed ARGs were significantly enriched in autophagy, apoptosis, aging, and neural function. Four hub genes (i.e., TP53, CASP1, CCL2, and CASP1) were significantly up-regulated. Upregulation of cellular autophagy and apoptosis level was detected in the hyperglycemia model in vitro.ConclusionsOur results provide evidence for the autophagy and cellular senescence mechanisms involved in retinal hyperglycemia injury, and the protective function of autophagy is limited. Further study may favour understanding the disease progression and neuroprotection of DR.</p
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