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Graphitic carbon nitride (g-CN) is an attractive electrochemiluminescence (ECL) luminophore. However, g-CN with wavelength-tunable ECL emission is still limited, which limits its application in multicolor ECL sensing and imaging analysis. In this study, porous g-CN (PCN) with nitrogen defects was synthesized through the condensation of melamine by using

Hydrogel beads exhibit good biocompatibility, high stability, and monodispersity. However, hydrogel beads possessing intensive and multicolor chemiluminescence (CL) have not been reported. In this work, two kinds of multifunctionalized hydrogel beads, one consisting of chitosan (CS), Co

As an advanced downhole instrument in drilling engineering, drilling fluid continuous wave generator (DFCWG) has great application prospects. The large load torque is one of the key problems that hinder the development of DFCWG. In this paper, based on the design theory of rotary valve and finite element method, the structure of rotary valve is designed and the load torque characteristics is analyzed and points out that the load torque has strong alternating characteristics. It is pointed out that the load torque has the characteristics of strong alternating. According to the characteristics of the load torque, the "fluid-magnetic" collaborative compensation method is proposed. The load compensation turbine and magnetic compensation device are used to compensate the DC and AC components of the load torque respectively, and the load compensation device is designed. The rationality of the design of the load compensation device is verified by simulation. Finally, the comprehensive compensation effect is analyzed by the finite element method. According to the analysis results, the "fluid-magnetic" collaborative compensation method can effectively reduce the load torque. The research results can provide technical support for DFCWG design.

Chemiluminescence (CL) reagent luminol was loaded into the porous structure of cobalt-imidazole metal-organic framework (MOF) ZIF-67 to obtain luminol-functionalized ZIF-67 (luminol@ZIF-67) with CL property. The morphology, composition, CL property, and CL mechanism of luminol@ZIF-67 were carefully investigated. The obtained luminol@ZIF-67 exhibited strong, stable, and visible CL emission that reacted with H2O2, attributed to the strong catalytic effect of ZIF-67 combined with the shortened diffusion distance between luminol and the catalytic center. The CL intensity of luminol@ZIF-67 was more than 550 times higher than that of luminol. Catechol can effectively quench the CL emission of luminol@ZIF-67 that reacted with H2O2. Then, a simple paper-based CL imaging detection method was developed for the detection of catechol by using a smartphone as a portable detector. The linear calibration curve of the developed CL assay for catechol ranged from 5 to 100 mg/L with detection limit of 1.1 mg/L (S/N = 3δ). The strong CL emission of luminol@ZIF-67 combined with the effective quench ability of catechol guaranteed high sensitivity of the detection method. The practical application ability of the developed CL assay was tested by the determination of catechol in tea and tap water samples, resulting in acceptable results. This work provides an effective paper-based CL detection method for catechol and enriches the species of the chemiluminescent MOF material.

In order to improve the prediction performance of the existing nonlinear grey Bernoulli model and extend its applicable range, an improved nonlinear grey Bernoulli model is presented by using a grey modeling technique and optimization methods. First, the traditional whitening equation of nonlinear grey Bernoulli model is transformed into its linear formulae. Second, improved structural parameters of the model are proposed to eliminate the inherent error caused by the leap jumping from the differential equation to the difference one. As a result, an improved nonlinear grey Bernoulli model is obtained. Finally, the structural parameters of the model are calculated by the whale optimization algorithm. The numerical results of several examples show that the presented model’s prediction accuracy is higher than that of the existing models, and the proposed model is more suitable for these practical cases.

The hydropower plays a key role in electricity system owing to its renewability and largest share of clean electricity generation that promotes sustainable development of national economy. Developing a proper forecasting model for the quarterly hydropower generation is crucial for associated energy sectors, which could assist policymakers in adjusting corresponding schemes for facing with sustained demands. For this purpose, this paper presents a fractional nonlinear grey Bernoulli model (abbreviated as FANGBM(1,1)) coupled seasonal factor and Particular Swarm Optimization (PSO) algorithm, namely PSO algorithm-based FASNGBM(1,1) model. In the proposed method, the moving average method that eliminates the seasonal fluctuations is introduced into FANGBM(1,1), then in which the structure parameters of FASNGBM(1,1) are determined by PSO. Based on hydropower generation of China from the first quarter of 2011 to the final quarter of 2018 (2011Q1-2018Q4), the numerical results show that the proposed model has a better performance than that of other benchmark models. Eventually, the quarterly hydropower generation of China from 2019 to 2020 are forecasted by the proposed model, according to results, the hydropower generation of China will reach 11287.14 × 108 Kwh in 2020.

The negative pulsed downlink communication system is used to send surface control commands to the downhole rotary steering tool at thousands of meters, which is a significant part of the current rotary steering technology. At present, the transmission efficiency of negative pulsed downlink communication is very low, and only simple control commands can be transmitted in a few minutes, which limits the development of rotary steering technology with complex control functions. To improve the transmission rate of the downlink system, the downlink pulse width needs to be shortened. However, due to the influence of signal transmission characteristics, the waveform of a narrow pulse width signal will be severely distorted, which increases the difficulty of decoding the downlink signal. Therefore, a decoding method based on pattern recognition for negative pulsed downlink signal with narrow pulse width is proposed in this paper, which establishes a Euclidean distance matrix model between similar characteristic signal segments on the rising or falling edge of the downlink signal, the pulse coding timing of among the signal segment with each rising or falling edge is analyzed, the decoding and recognition of the downlink instruction are achieved, which solves the problem of large timing deviation in decoding the downlink signal with a current threshold method. The experimental results show that the method proposed in this paper can achieve accurate decoding of the 6 s pulse width downlink signal. Compared with the threshold method, it can be seen that the decoding accuracy of the method proposed in this paper can be greatly improved, and the smaller the signal pulse width, the more significant the advantage.

Drilling fluid continuous wave(DFCW) generator is an advanced downhole instrument and has broad application prospects. The load torque acting on the DFCW generator has a great impact on the performance on the DFCW generator, and there is a lack of theory describing the load torque because of the irregularity of the rotary valve. In this paper, the drilling fluid flow area is divided into the curve flow area, the radial flow area and the axial flow area. The flow area of each part is divided into several meshes based on finite element theory, then the load torque acting on each part is calculated based on the fluid momentum conservation theory. The theoretical model is verified by combining the simulation and the experiment, and the effects of the discharge and the axial gap on the load torque are analyzed. The research results show that:(1) the theoretical model can be used to determine the load torque, (2) the amplitude of the load torque reduces as the gap decreases and increases rapidly as the discharge increases. The results can provide the theoretical guidance for the structure design of the rotary valve and the control system design of the drilling fluid continuous wave generator.

Low back pain (LBP) is the leading cause of disability in the elderly population and is strongly associated with intervertebral disc degeneration (IVDD). However, the precise molecular mechanisms regulating IVDD remain elusive. This study aimed to investigate the role of differentially expressed miRNAs in the pathogenesis of IVDD.We analysed miRNA microarray datasets to identify differentially expressed miRNAs in IVDD progression and conducted qRT-PCR (quantitative real-time PCR) and fluorescence in situ hybridization (FISH) analysis to further confirm the differential expression of miR-4478 in NP tissues of patients diagnosed with IVDD. Using public databases of miRNA-mRNA interactions, we predicted the target genes of miR-4478, and subsequent flow cytometry and western blot analyses demonstrated the effect of MTH1 in H2O2-induced NPCs apoptosis. Finally, miR-4478 inhibitor was injected into NP tissues of IVDD mouse model to explore the effect of miR-4478 in vivo.miR-4478 was upregulated in NP tissues from IVDD patients. Silencing of miR-4478 inhibits H2O2-induced NPCs apoptosis. MTH1 was identified as a target gene for miR-4478, and miR-4478 regulates H2O2-induced NPCs apoptosis by modulating MTH1. Additionally, downregulation of miR-4478 alleviated IVDD in a mouse model.In summary, our study provides evidence that miR-4478 may aggravate IVDD through its target gene MTH1 by accelerating oxidative stress in NPCs and demonstrates that miR-4478 has therapeutic potential in IVDD treatment.

Backgroud: Pompe disease is a rare metabolic disorder with available enzymatic replacement therapy. Contrasting with the classic infantile form, the others subtypes have a heterogeneous presentation that makes an early and accurate diagnosis difficulty. A multicenter observational study was aimed to assess the prevalence of late-onset Pompe disease (LOPD) in high-risk population, using dried blood spot (DBS) as a main screening tool.Methods: 20 Chinese neuromuscular centers were involved in the early LOPD screening study. Inclusion criteria were: (1) age ≥1 years, (2) either one of a) persistent hyperCKemia; or b) muscle weakness of axial and/or limb-girdle muscles; or c) unexplained restrictive respiratory insufficiency. Enzymatic activity of acid α-glucosidase (GAA) was measured on DBS by tandem mass spectrometry (MS/MS) assay. For the final diagnosis genotype was assessed by next-generation sequencing.Result: In a 9-month period, we studied 492 cases: 26 positive samples (5.3%) were detected by DBS screening. Molecular studies finally confirmed LOPD diagnosis in 8 cases (1.6%). The GAA activities in individuals bearing pseudodeficiency alleles were well separated from those in LOPD patients by MS/MS assay. The median interval from the onset of symptoms to diagnosis was 5 years. Besides axial/proximal muscle weakness, all patients showed respiratory insufficiency with a mean forced vital capacity of predicted of 48%. The level of creatine kinase ranged from normal to no more than 5-fold of upper normal limit. LOPD with isolated hyperCKemia was not identified.Conclusions: This study confirms that DBS test is a reliable method for screening for LOPD. Respiratory insufficiency is earlier and more severe among Chinese LOPD patients. LOPD presented with paucisymptomatic hyperCKemia. Therefore, a prompt diagnosis is critical to prognosis.

This paper aims to further increase the prediction accuracy of the grey model based on the existing discrete grey model, DGM(1,1). Herein, we begin by studying the connection between forecasts and the first entry of the original series. The results comprehensively show that the forecasts are independent of the first entry in the original series. On this basis, an effective method of inserting an arbitrary number in front of the first item of the original series to extract messages is applied to produce a novel grey model, which is abbreviated as FDGM(1,1) for simplicity. Incidentally, the proposed model can even forecast future data using only three historical data. To demonstrate the effectiveness of the proposed model, two classical examples of the tensile strength and life of the product are employed in this paper. The numerical results indicate that FDGM(1,1) has a better prediction performance than most commonly used grey models.

Two cases of F2-lacuna and their simultaneous ionospheric convection and TEC variations were presented to further understand F2-lacuna formation mechanism. Both cases of F2-lacuna are accompanied by decreased electron density and increased plasma flow. Through analyzing the role of convection electric field in the formation of F2-lacuna, an explanation for F2-lacuna formation was provided. The joule heating and frictional heating ascribed to the strengthened electric field causes the increase of electron and ion temperature, which subsequently, causes the enhancements of the recombination rate and the upflow of the O+ density resulting in decreased O+ density in F2 region.

Truncating variants in TTN (TTNtv), coding for the largest structural protein in the sarcomere, contribute to the largest portion of familial and ambulatory dilated cardiomyopathy (DCM). TTN haploinsufficiency caused by TTNtv is suggested as the disease mechanism. However, it is unclear whether TTN insufficiency causes DCM. Moreover, it is unknown whether modulation of downstream pathways serves as a therapeutic strategy for DCM caused by TTN insufficiency. Here, we show that reduction of cardiac Ttn expression by adeno-associated virus mediated shRNA (Ttn shRNA) generated DCM in mouse, demonstrating impaired cardiac performance, enlarged left ventricle (LV) and reduced LV wall thickness. A screen of 10 dysregulated and selected genes identified that Yin Yang 1 (Yy1) significantly suppressed DCM caused by Ttn shRNA. Gene profiling by RNAseq showed Yy1 modulated cell growth related genes. Ttn insufficiency activated cardiomyocyte cell cycle reentry by upregulating of Ccnd1 and Ccnd2. Cardiomyocytes activated by Ttn insufficiency did not advance to S phase by EdU incorporation assay. Yy1 promoted cardiomyocyte cell cycle by further enhancing Ccnd1 and Ccnd2 and increasing DNA replication without undergoing cell division. Importantly, upregulation of Ccnd1 and Ccnd2 suppressed DCM caused by Ttn insufficiency. Our findings demonstrate that DCM caused by Ttn insufficiency can be treated by therapeutically promoting cardiac cell cycle.

Rationale: Pathogenic variations in the lamin gene ( LMNA ) cause familial dilated cardiomyopathy (DCM). LMNA insufficiency caused by LMNA pathogenic variants is believed to be the basic mechanism underpinning LMNA -related DCM. Objective: To assess whether silencing of cardiac Lmna causes DCM and investigate the role of Yin Yang 1 ( Yy1 ) in suppressing Lmna DCM. Methods and Results: We developed a Lmna DCM mouse model induced by cardiac-specific Lmna short hairpin RNA. Silencing of cardiac Lmna induced DCM with associated cardiac fibrosis and inflammation. We demonstrated that upregulation of Yy1 suppressed Lmna DCM and cardiac fibrosis by inducing Bmp7 expression and preventing upregulation of Ctgf . Knockdown of upregulated Bmp7 attenuated the suppressive effect of Yy1 on DCM and cardiac fibrosis. However, upregulation of Bmp7 alone was not sufficient to suppress DCM and cardiac fibrosis. Importantly, upregulation of Bmp7 together with Ctgf silencing significantly suppressed DCM and cardiac fibrosis. Mechanistically, upregulation of Yy1 regulated Bmp7 and Ctgf reporter activities and modulated Bmp7 and Ctgf gene expression in cardiomyocytes. Downregulation of Ctgf inhibited TGF-β (transforming growth factor-β)/Smad signaling in DCM hearts. Regulation of both Bmp7 and Ctgf further suppressed TGFβ/Smad signaling. In addition, co-modulation of Bmp7 and Ctgf reduced CD3+ T cell numbers in DCM hearts. Conclusions: Our findings demonstrate that upregulation of Yy1 or co-modulation of Bmp7 and Ctgf offer novel therapeutic strategies for the treatment of DCM caused by LMNA insufficiency.

Background: The human genome folds in 3 dimensions to form thousands of chromatin loops inside the nucleus, encasing genes and cis -regulatory elements for accurate gene expression control. Physical tethers of loops are anchored by the DNA-binding protein CTCF and the cohesin ring complex. Because heart failure is characterized by hallmark gene expression changes, it was recently reported that substantial CTCF-related chromatin reorganization underpins the myocardial stress–gene response, paralleled by chromatin domain boundary changes observed in CTCF knockout. Methods: We undertook an independent and orthogonal analysis of chromatin organization with mouse pressure-overload model of myocardial stress (transverse aortic constriction) and cardiomyocyte-specific knockout of Ctcf . We also downloaded published data sets of similar cardiac mouse models and subjected them to independent reanalysis. Results: We found that the cardiomyocyte chromatin architecture remains broadly stable in transverse aortic constriction hearts, whereas Ctcf knockout resulted in ≈99% abolition of global chromatin loops. Disease gene expression changes correlated instead with differential histone H3K27-acetylation enrichment at their respective proximal and distal interacting genomic enhancers confined within these static chromatin structures. Moreover, coregulated genes were mapped out as interconnected gene sets on the basis of their multigene 3D interactions. Conclusions: This work reveals a more stable genome-wide chromatin framework than previously described. Myocardial stress–gene transcription responds instead through H3K27-acetylation enhancer enrichment dynamics and gene networks of coregulation. Robust and intact CTCF looping is required for the induction of a rapid and accurate stress response.

With the rapid development of the Internet of Things, VANETs (Vehicular Ad-Hoc Networks) have become an attractive ad-hoc network that brings convenience into people’s lives. Vehicles can be informed of the position, direction, speed and other real-time information of nearby vehicles to avoid traffic jams and accidents. However, VANET environments could be dangerous in the absence of security protection. Because of the open nature and self-organization of VANETs, there are plenty of malicious pathways. To guarantee vehicle security, the research aims to provide an effective VANET security mechanism that can track malicious vehicles as necessary. Therefore, this work focuses on malicious vehicles and proposes an anonymous authentication scheme in VANETs based on the Fair Blind Signature to protect vehicle security.

BackgroundDrug abuse has many negative effects not only on individuals but also on society. Nowadays, researchers pay a lot of attention to the quality of life of drug-dependent persons. However, there are few scales available to measure the quality of life of people with substance-abuse disorders. A quality of life scale for patients with drug addiction/dependence (QLICD-DA) developed in China according to their actual situation could be used to measure the quality of life of drug abusers. It has good validity and reliability and is sensitive to the quality of life of drug-dependent persons. MethodsWe selected 192 drug-dependent persons as participants and they all completed the general information questionnaire and the QLICD-DA. We used a t-test to compare the scores of the quality of life of the participants with the norm in different domains, then we used one-way ANOVA to screen for variables. A stepwise regression method was applied to explore the influencing factors of the quality of life of the participants.ResultsThe quality of life of the participants was lower than the norm in the physiological domain, psychological domain, social domain, and common general domain, and the differences were statistically significant (p

Background Drug abuse has many negative effects not only on individuals but also on society. Nowadays, researchers pay a lot of attention to quality of life of drug addicts. However, there are few scales available to measure quality of life of drug addicts. The scale QLICD-DA (quality of life instrument for chronic diseases-drug addition) developed by modular approach could be used to measure quality of life of drug addicts with good validity, reliability and sensitivity. Objective This study is aimed to understand the quality of life status and influencing factors in drug addicts by suitable sensitively scale, with the hypothesis of the quality of life in drug addicts being different from that of other peoples and possibly being influenced by many factors. Methods By cluster random sampling method, 192 drug addicts at Kunming compulsory drug rehabilitation center were recruited to take part in the investigation. All participants completed the general information questionnaire and the scale QLICD-DA. We used a t-test to compare the scores of the quality of life of the participants with the norm (QOL scores from 1953 patients of 10 chronic diseases). A stepwise regression method was applied to explore the influencing factors of the quality of life in drug addicts. Results 192 participants ranged in age from 19 to 59 with an average age of 34.86. Most of them were male (70.3%), high school education level (67.7%) and of Han nationality (82.8%). The quality of life of drug addicts was lower than the norm in the physical domain, psychological domain, social domain, and general module, and the differences were statistically significant (p p = 0.006) and specific module (p = 0.019). Past family atmosphere and the mode of drug abuse were the influencing factors in the general module (p = 0.027, p = 0.037). Conclusion The quality of life of drug addicts was worse than that of patients with other chronic diseases, and the influencing factors of the quality of life of drug abusers were sex, mode of drug abuse, and past family atmosphere.

The coagulation protein tissue factor (TF) regulates inflammation and angiogenesis via its cytoplasmic domain in infection, cancer and diabetes. While TF is highly abundant in the heart and is implicated in cardiac pathology, the contribution of its cytoplasmic domain to post-infarct myocardial injury and adverse left ventricular (LV) remodeling remains unknown.Methods: Myocardial infarction was induced in wild-type mice or mice lacking the TF cytoplasmic domain (TF increment CT) by occlusion of the left anterior descending coronary artery. Heart function was monitored with echocardiography. Heart tissue was collected at different time-points for histological, molecular and flow cytometry analysis.Results: Compared with wild-type mice, TF increment CT had a higher survival rate during a 28-day follow-up after myocardial infarction. Among surviving mice, TF increment CT mice had better cardiac function and less LV remodeling than wild-type mice. The overall improvement of post-infarct cardiac performance in TF increment CT mice, as revealed by speckle-tracking strain analysis, was attributed to reduced myocardial deformation in the peri-infarct region. Histological analysis demonstrated that TF increment CT hearts had in the infarct area greater proliferation of myofibroblasts and better scar formation. Compared with wild-type hearts, infarcted TF increment CT hearts showed less infiltration of proinflammatory cells with concomitant lower expression of protease-activated receptor-1 (PAR1) -Rac1 axis. In particular, infarcted TF increment CT hearts displayed markedly lower ratios of inflammatory M1 macrophages and reparative M2 macrophages (M1/M2). In vitro experiment with primary macrophages demonstrated that deletion of the TF cytoplasmic domain inhibited macrophage polarization toward the M1 phenotype. Furthermore, infarcted TF increment CT hearts presented markedly higher peri-infarct vessel density associated with enhanced endothelial cell proliferation and higher expression of PAR2 and PAR2-associated pro-angiogenic pathway factors. Finally, the overall cardioprotective effects observed in TF increment CT mice could be abolished by subcutaneously infusing a cocktail of PAR1-activating peptide and PAR2-inhibiting peptide via osmotic minipumps.Conclusions: Our findings demonstrate that the TF cytoplasmic domain exacerbates post-infarct cardiac injury and adverse LV remodeling via differential regulation of inflammation and angiogenesis. Targeted inhibition of the TF cytoplasmic domain-mediated intracellular signaling may ameliorate post-infarct LV remodeling without perturbing coagulation.

Introduction: The mammalian hearts including humans have a limited regenerative capacity. Activation of proliferation or related signaling pathways has been shown to reinstate cell renewal capacity of cardiomyocytes (CM) which is believed to ameliorate heart failure (HF). However, whether new CM are generated underlying cardiac regeneration in adult mammalian hearts upon damage is elusive. It is also unknown whether and by what mechanisms activation of CM proliferation benefits HF besides cardiac regeneration. Hypothesis: The protective role of cardiac cell cycle activation for damaged hearts could be independent of heart regeneration. Methods and Results: We show that cardiac specific activation of YAP1 , the terminal effector of the Hippo signaling pathway, suppressed HF and cardiac fibrosis induced by Lmna insufficiency ( Lmna HF). Although activation of YAP1 promoted G1 and S phase of cardiac cell cycle in disease hearts, CM did not undergo mitotic phase, a critical step for heart regeneration. RNAseq followed by signaling pathway analysis and validation showed that Fanconi anemia (FA) DNA repair pathway was activated by YAP1 . Cardiac DNA damage in Lmna HF was suppressed by YAP1 activation. Importantly, reduction of Fancd2 compromised the suppressive role of YAP1 in Lmna HF. Mechanistically, YAP1 promoted mono-ubiquitination of FANCD2 (ub-FANCD2) through promoting cell cycle. Conclusions: Our findings demonstrate that promoting cardiac DNA repair becomes a new therapeutic strategy against HF.