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Nanofiltration (NF) has the potential to achieve precise ion-ion separation at the subnanometer scale, which is necessary for resource recovery and a circular water economy. Fabricating NF membranes for selective ion separation is highly desirable but represents a substantial technical challenge. Dipole-dipole interaction is a mechanism of intermolecular attractions between polar molecules with a dipole moment due to uneven charge distribution, but such an interaction has not been leveraged to tune membrane structure and selectivity. Herein, we propose a novel strategy to achieve tunable surface charge of polyamide membrane by introducing polar solvent with a large dipole moment during interfacial polymerization, in which the dipole-dipole interaction with acyl chloride groups of trimesoyl chloride (TMC) can successfully intervene in the amidation reaction to alter the density of surface carboxyl groups in the polyamide selective layer. As a result, the prepared positively charged (PEI-TMC)-NH2 and negatively charged (PEI-TMC)-COOH composite membranes, which show similarly high water permeance, demonstrate highly selective separations of cations and anions in engineering applications, respectively. Our findings, for the first time, confirm that solvent-induced dipole-dipole interactions are able to alter the charge type and density of polyamide membranes and achieve tunable surface charge for selective and efficient ion separation.

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Stable communication technologies in complex waters are a prerequisite for underwater operations. Underwater acoustic communication is susceptible to multipath interference, while underwater optical communication is susceptible to environmental impact. The underwater electric field communication established based on the weak electric fish perception mechanism is not susceptible to environmental interference, and the communication is stable. It is a new type of underwater communication technology. To address issues like short communication distances and high bit error rates in existing underwater electric field communication systems, this study focuses on underwater electric field communication systems based on direct sequence spread spectrum (DSSS) and binary phase shift keying (BPSK) modulation techniques. To verify the feasibility of the established spread spectrum electric field communication system, static communication experiments were carried out in a swimming pool using the DSSS-based system. The experimental results show that in fresh water with a conductivity of 739 µS/cm, the system can achieve underwater current electric field communication within a 11.2 m range with 10-6 bit errors. This paper validates the feasibility of DSSS BPSK in short-range underwater communication, and compact communication devices are expected to be deployed on underwater robots for underwater operations.

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The oxygenation membrane, a core material of extracorporeal membrane oxygenation (ECMO), is facing challenges in balancing anti-plasma leakage, gas exchange efficiency, and hemocompatibility. Here, inspired by the asymmetric structural features of alveolus pulmonalis, a novel triple-functional membrane for blood oxygenation with a Janus architecture is proposed, which is composed of a hydrophobic polydimethylsiloxane (PDMS) layer to prevent plasma leakage, an ultrathin polyamide layer to enhance gas exchange efficiency with a CO2 :O2 permeance ratio of ≈10.7, and a hydrophilic polyzwitterionic layer to improve the hemocompatibility. During the simulated ECMO process, the Janus oxygenation membrane exhibits excellent performance in terms of thrombus formation and plasma leakage prevention, as well as adequate O2 transfer rate (17.8 mL min-1 m-2 ) and CO2 transfer rate (70.1 mL min-1 m-2 ), in comparison to the reported oxygenation membranes. This work presents novel concepts for the advancement of oxygenation membranes and demonstrates the application potential of the asymmetric triple-functional Janus oxygenation membrane in ECMO.

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Positively charged nanofiltration (NF) membranes offer enormous potential for lithium-magnesium separation, hard water softening, and heavy metal removal. However, fundamental performance limitations for these applications exist in conventional polyamide-based NF membranes due to the negatively charged surface and low ion-ion selectivity. We hereby innovatively develop an advanced positively charged polyamine-based NF membrane built by the nucleophilic substitution of bromine and amine groups for precise ion-ion separation. Specifically, polyethylenimine (PEI) and 1,3,5-tris(bromomethyl)benzene (TBB) are interfacially polymerized to generate an amine-linked PEI-TBB selective layer with an ultrathin thickness of ∼95 nm, an effective pore size of 6.5 Å, and a strong positively charged surface with a zeta potential of +20.9 mV at pH 7. The PEI-TBB composite membrane achieves a water permeance of 4.2 L·m-2·h-1·bar-1, various divalent salt rejections above 90%, and separation factors above 15 for NaCl/MgCl2 and LiCl/MgCl2 mixed solutions. A three-stage NF process is implemented to achieve a Mg2+/Li+ mass ratio sharply decreasing from 50 to 0.11 with a total separation factor (SLi,Mg) of 455. Furthermore, the polyamine-based NF membrane exhibits excellent operational stability under continuous filtration and high operational pressure, demonstrating great application potential for precise ion-ion separation.

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The inverse finite element method (iFEM) based on fiber grating sensors has been demonstrated as a shape sensing method for health monitoring of large and complex engineering structures. However, the existing optimization algorithms cause the local optima and low computational efficiency for high-dimensional strain sensor layout optimization problems of complex antenna truss models. This paper proposes the improved adaptive large-scale cooperative coevolution (IALSCC) algorithm to obtain the strain sensors deployment on iFEM, and the method includes the initialization strategy, adaptive region partitioning strategy, and gbest selection and particle updating strategies, enhancing the reconstruction accuracy of iFEM for antenna truss structure and algorithm efficiency. The strain sensors optimization deployment on the antenna truss model for different postures is achieved, and the numerical results show that the optimization algorithm IALSCC proposed in this paper can well handle the high-dimensional sensor layout optimization problem.

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Spatiotemporal clustering of vehicle emissions, which reveals the evolution pattern of air pollution from road traffic, is a challenging representation learning task due to the lack of supervision. Some recent work building upon graph convolutional network (GCN) models the intrinsic spatiotemporal correlations among the nodes in road networks as graph representations for clustering. However, these existing methods ignore the interactions between spatial and temporal variations in vehicle emissions, resulting in incomplete descriptions and inaccurate detection of the evolution pattern of air pollution. To address this issue, this article proposes a two-way self-supervised spatiotemporal representation learning scheme, in which the temporal and spatial features are progressively learned in a mutually reinforced manner. Our proposed method is based on the observation that though the variation in vehicle emissions in the road network is consistent in the spatial and temporal domains, its expression is more distinct in temporal sequences. To this end, the input emission data are first projected into an initial temporal representation space spanned by the captured features from a pretrained BiLSTM network. Then the generated distribution of temporal features is used to construct an objective constraint for high-purity clustering through a two-way self-supervised mechanism, which is leveraged as a constraint for the feature clustering of a GCN. Furthermore, to eliminate the initial errors, a joint optimization scheme is presented to generate the decoupled clustering results through the progressive refinement of representation and clustering. Our proposed method is evaluated on the traffic emission dataset of Xian city in 2020, and the experimental results have demonstrated the superiority against the state-of-the-art.

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The inverse finite element method (iFEM) is a novel method for reconstructing the full-field displacement of structures by discrete measurement strain. In practical engineering applications, the accuracy of iFEM is reduced due to the positional offset of strain sensors during installation and errors in structural installation. Therefore, a coarse and fine two-stage calibration (CFTSC) method is proposed to enhance the accuracy of the reconstruction of structures. Firstly, the coarse calibration is based on a single-objective particle swarm optimization algorithm (SOPSO) to optimize the displacement-strain transformation matrix related to the sensor position. Secondly, as selecting different training data can affect the training effect of self-constructed fuzzy networks (SCFN), this paper proposes to screen the appropriate training data based on residual analysis. Finally, the experiments of the wing-integrated antenna structure verify the efficiency of the method on the reconstruction accuracy of the structural body displacement field.

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INTRODUCTION: Postnatal cardiomyocytes respond to stress signals by hypertrophic growth and fetal gene reprogramming, which involves epigenetic remodeling mediated by histone methyltransferase polycomb repressive complex 2 (PRC2) and histone deacetylases (HDACs). However, it remains unclear to what extent these histone modifiers contribute to the development of cardiomyocyte hypertrophy. METHODS: Neonatal rat ventricular myocytes (NRVMs) were stimulated by phenylephrine (PE; 50µM) to induce hypertrophy in the presence or absence of the PRC2 inhibitor GSK126 or the HDACs inhibitor Trichostatin A (TSA). Histone methylation and acetylation were measured by Western blot. Cell size was determined by wheat germ agglutinin (WGA) staining. Cardiac hypertrophy markers were quantified by quantitative reverse transcription polymerase chain reaction (qRT-PCR). RESULTS: PE treatment induced the expression of cardiac hypertrophy markers, including natriuretic peptide A (Nppa), natriuretic peptide B (Nppb), and myosin heavy chain 7 (Myh7), in a time-dependent manner in NRVMs. Histone modifications, including H3K27me3, H3K9ac, and H3K27ac, were dynamically altered after PE treatment. Treatment with TSA and GSK126 dose-dependently repressed histone acetylation and methylation, respectively. While TSA reversed the PE-induced cell size enlargement in a wide range of concentrations, cardiomyocyte hypertrophy was only inhibited by GSK126 at a higher dose (1µM). Consistently, TSA dose-dependently suppressed the induction of Nppa, Nppb, and Myh7/Myh6 ratio, while these indexes were only inhibited by GSK126 at 1µM. However, TSA, but not GSK126, caused pro-hypertrophic expression of pathological genes at the basal level. CONCLUSION: Our data demonstrate diversified effects of TSA and GSK126 on PE-induced cardiomyocyte hypertrophy, and shed light on epigenetic reprogramming in the pathogenesis of cardiac hypertrophy.

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Root-associated microorganisms are widely recognized as playing an important role in mitigating stress-induced damage to plants, but the responses of rhizosphere microbial communities after inoculation and their relationship with plant responses remain unclear. In this study, the bacterium Providencia vermicola BR68 and the fungus Sarocladium kiliense FS18 were selected from among 91 strains isolated from the halophyte Suaeda salsa to interact with maize seedlings under salt stress. The results showed that compared with NaCl-only treatment, inoculation with strains BR68 and FS18 significantly improved the growth, net photosynthetic rate, and antioxidant enzyme activities of maize; significantly reduced proline content and generation rate of reactive oxygen species (ROS); and alleviated oxidative stress and osmotic stress. Moreover, inoculation with these two strains increased the activities of soil microbiome enzymes such as sucrase, catalase, and fluorescein diacetate hydrolase, which improved maize physiologies and promoted maize growth under salt stress. In addition, these inoculated strains significantly affected the abundance of certain genera, and the correlation trends for these genera with soil properties and maize physiologies were similar to those of these inoculated strains. Strain BR68 was indirectly associated with bacterial communities through BR-specific biomarkers, and bacterial communities and soil properties explained most of the variation in maize physiologies and growth. Inoculation of strain FS18 was directly associated with variations in soil properties and maize physiologies. The two strains improved maize growth under salt stress and alleviated stress damage in maize in different ways. The links among salt-tolerant microorganisms, soil, and plants established in this study can inform strategies for improving crop cultivation in salinized lands. IMPORTANCE This study demonstrates that halophyte root-associated microorganisms can promote crop tolerance to salt stress and clarify the mechanism by which the strains work in rhizosphere soil. The links among salt-tolerant microorganisms, soil, and plants established in this study can inform strategies for improving crop cultivation in salinized lands.

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Extracellular vesicles (EVs), including exosomes and microvesicles, emerge to be crucial mediators of cell-to-cell communication in multiple organs. Non-coding RNAs loaded inside EVs contribute as one major mechanism for remote information transfer among different cell types or organs. Increasing evidence suggests that EV-associated non-coding RNAs derived from cardiovascular or non-cardiac cells regulate cardiovascular pathophysiology in heart development and diseases. The functional relevance of the EV-associated ncRNAs in heart diseases provides an avenue to develop novel diagnostic tools and therapies for heart diseases. In this review, we summarize the recent advancement of EV-associated ncRNAs in different cardiovascular diseases, including myocardial infarction, arrhythmias, cardiac hypertrophy, and heart failure, with an emphasis on the underlying molecular mechanisms.

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Zinc dyshomeostasis has been involved in the pathogenesis of cardiac hypertrophy; however, the dynamic regulation of intracellular zinc and its downstream signaling in cardiac hypertrophy remain largely unknown. Using Zincpyr1 staining, we found a significant decrease of intracellular Zinc concentration in phenylephrine (PE)-induced hypertrophy of neonatal rat ventricular myocytes (NRVMs). We then screened SLC39 family members responsible for zinc uptake and identified Slc39a2 as the only one altered by PE treatment. Slc39a2 knockdown in NRVMs reduced the intracellular Zinc level, and exacerbated the hypertrophic responses to PE treatment. In contrast, adenovirus-mediated Slc39a2 overexpression enhanced zinc uptake and suppressed PE-induced Nppb expression. RNA sequencing analysis showed a pro-hypertrophic transcriptome reprogramming after Slc39a2 knockdown. Interestingly, the innate immune signaling pathways, including NOD signaling, TOLL-like receptor, NFκB, and IRFs, were remarkably enriched in the Slc39a2-regulated genes. Slc39a2 deficiency enhanced the phosphorylation of P65 NFκB and STAT3, and reduced the expression of IκBα. Finally, the expression of IRF7 was significantly increased by Slc39a2 knockdown, which was in turn suppressed by IRF7 knockdown. Our data demonstrate that zinc homeostasis mediated by a Slc39a2/IRF7 regulatory circuit contributes to the alteration of innate immune signaling in cardiomyocyte hypertrophy.

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Pathological growth of cardiomyocytes during hypertrophy is characterized by excess protein synthesis; however, the regulatory mechanism remains largely unknown. Using a neonatal rat ventricular myocytes (NRVMs) model, here we find that the expression of nucleosome assembly protein 1 like 5 (Nap1l5) is upregulated in phenylephrine (PE)-induced hypertrophy. Knockdown of Nap1l5 expression by siRNA significantly blocks cell size enlargement and pathological gene induction after PE treatment. In contrast, Adenovirus-mediated Nap1l5 overexpression significantly aggravates the pro-hypertrophic effects of PE on NRVMs. RNA-seq analysis reveals that Nap1l5 knockdown reverses the pro-hypertrophic transcriptome reprogramming after PE treatment. Whereas, immune response is dominantly enriched in the upregulated genes, oxidative phosphorylation, cardiac muscle contraction and ribosome-related pathways are remarkably enriched in the down-regulated genes. Although Nap1l5-mediated gene regulation is correlated with PRC2 and PRC1, Nap1l5 does not directly alter the levels of global histone methylations at K4, K9, K27 or K36. However, puromycin incorporation assay shows that Nap1l5 is both necessary and sufficient to promote protein synthesis in cardiomyocyte hypertrophy. This is attributable to a direct regulation of nucleolus hypertrophy and subsequent ribosome assembly. Our findings demonstrate a previously unrecognized role of Nap1l5 in translation control during cardiac hypertrophy.

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BACKGROUND: Rheumatoid arthritis (RA) is a systemic disease characterized by chronic synovial infiltration and proliferation, cartilage destruction, and joint injury. Ginkgolide B (GB) is an extract of the leaves of Ginkgo biloba, and pharmacological studies have shown that it has anti-inflammatory and anti-apoptotic activities. The purpose of this study was to investigate the anti-RA properties of GB. METHODS: In vivo, we established a collagen II-induced arthritis (CIA) mouse model. Mice were divided into five groups (n=10): sham, CIA, GB (10 µM), GB (20 µM), and GB (40 µM). We measured arthritis score, synovial histopathological change, and peripheral blood cytokine levels. In vitro, we used lipopolysaccharide (LPS)-induced-fibroblast-like synoviocytes (RA-FLSs) as the study subject. Cell viability, apoptosis, and inflammatory cytokines levels were detected by 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di-phenytetrazoliumromide (MTT) assay, flow cytometry, and quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR), respectively. Finally, the protein expression of wingless-type family member 5A (Wnt5a), c-Jun N-terminal kinase (JNK), and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) p65 were detected by Western blot. RESULTS: Arthritis scores, synovial hyperplasia, and cartilage and bone destruction were significantly ameliorated by GB. Additionally, GB decreased the serum levels of interleukin (IL)-1ß, IL-6, monocyte chemoattractant protein-1 (MCP-1), and tumor necrosis factor alpha (TNF-α), matrix metalloproteinase (MMP)-3 and MMP-13, and increased IL-10. In vitro, we found that GB remarkably inhibited RA-FLSs viability at 24 or 48 h in a concentration-dependent manner. The apoptotic ratio was reduced by GB, and it increased the expression of cleaved-Caspase-3 and Bax while decreasing Bcl-2 expression in RA-FLSs. Furthermore, GB attenuated the progression of inflammation by mediating inflammatory cytokine release and MMPs gene expression. Meanwhile, GB inactivated the expression levels of Wnt5a, phosphorylated (p)-JNK, and p-P65 in the synovial tissues and RA-FLSs. CONCLUSIONS: This study was the first to demonstrate that the anti-RA effect of GB is related to reducing articular cartilage and bone destruction, inducing RA-FLSs apoptosis, and regulating inflammatory cytokine release and the Wnt5a/JNK/NF-κB axis. All the findings highlight that GB might provide a novel treatment approach for RA.

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OBJECTIVE: To investigate the effects of high dose vitamin C on proliferation and apoptosis of acute myeloid leukemia (AML) cell lines including HL-60, U937 and primary CD34+ leukemia cells in AML. METHODS: CD34+ cells were sorted by using immunomagnetic cell sorting system, then the primary CD34+ leukemia cells, including HL-60 and U937 cell lines were cultured in vitro. Cells in each group were treated with different concentrations of vitamin C, the survival rate of cells was determined by MTT assay, the apoptosis rate of cells was evaluated by Annexin V/PI double staining, the expression of apoptotic proteins-including cleaved caspase 3, cleaved caspase-9 and cleaved PARP were detected by Western blot. RESULTS: The proliferation of HL-60 and U937 cells could be inhibited by high dose vitamin C, which showed a concentration-dependent manner (r=-0.9664; r=-0.9796). HL-60 and U937 cells were treated with different concentrations of vitamin C (8 and 20 mmol/L) for 24 hours, respectively, it was found that with the increasing of vitamin C concentration, cell apoptosis rate was significantly increased (r=0.9905; r=0.9971), and the expression of apoptosis related proteins including cleaved caspase 3, cleaved caspase-9 and cleaved PARP was aslo significantly increased with the increasing of concentration. In addition, it was found that with or without the mutation of TET2, high dose vitamin C could inhibit the proliferation (r=-0.9719; r=-0.9699) and promote the apoptosis (r=0.9998; r=0.9901) of primary CD34+ leukemia cells in AML, which showed a dose-dependent manner, but it showed no effect on the proliferation (r=-0.2032) and apoptosis (r=0.1912) of normal CD34+ cells. CONCLUSION: High dose vitamin C can inhibit the proliferation and promote the apoptosis of acute myeloid leukemia cells, and selectively kill primary CD34+ leukemia cells in AML.

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Triptolide (TPL), the main active ingredient in Tripterygium glycosides, has been reported to exert anti-inflammation and anti-tumor effects. The present study was designed to investigate the effects of TPL on rheumatoid arthritis (RA) and explore the underlying mechanisms. By using human synoviocyte MH7A cells, TPL was proven to significantly impede migration and invasion of MH7A cells, and also inhibited MMP-2 and MMP-9 expression. Moreover, TPL was found to increase SOD, CAT, GSH-Px activities while decrease MDA activity, indicating that TPL maintained redox balance in MH7A cells. TPL could down-regulate the number of LC3+ puncta, Beclin1 expression and LC3 II/I ratio in a concentration-dependent manner, indicating that TPL inhibited autophagy in MH7A cells. Activation of autophagy was found to counteract the effects of TPL on MH7A cells while inhibition of autophagy had the opposite effects. Our data demonstrated that TPL suppressed cell mobility and maintained redox balance through inhibiting autophagy in MH7A cells. Finally, our data revealed that TPL increased p-AKT/AKT ratio significantly and inhibition of PI3K/AKT signaling pathway activated autophagy in MH7A cells, suggesting that TPL suppressed autophagy through activating AKT signaling pathway in MH7A cells. Taken together, our present study revealed that TPL inhibited cell mobility and maintained redox balance in human synoviocyte MH7A cells through autophagy inhibition. Our findings suggested the potential clinical application of TPL on RA treatment.

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Hyaluronan synthase 2 (HAS2)-AS1 (natural antisense transcript of HAS2) functions as oncogenic long noncoding RNA (lncRNA) in oral squamous cell carcinoma, breast cancer, and osteosarcoma. The role of HAS2-AS1 in glioma remains unknown. In our research, HAS2-AS1 expression was elevated in glioma tissues compared with normal brain tissues. Moreover, high levels of HAS2-AS1 expression was observed in patients with glioma with high WHO grade (III-IV) or large tumor size ( > 4 cm). The survival analysis from The Cancer Genome Atlas showed glioma cases with high HAS2-AS1 expression that had shorter disease-free survival time and overall survival time than those with low HAS2-AS1 expression. In vitro studies suggested that knocking down HAS2-AS1 expression inhibited glioma cell viability, migration, and invasion through phosphoinositide 3-kinase/protein kinase B signaling pathway. In conclusion, HAS2-AS1 may be considered as a predictor for clinical outcome and a potential therapeutic target in glioma.

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IKBKE is increased in several types of cancers and is associated with tumour malignancy. In this study, we confirmed that IKBKE promoted glioma proliferation, migration and invasion in vitro. Then, we further discovered that IKBKE increased Yes-associated protein 1 (YAP1) and TEA domain family member 2 (TEAD2), two important Hippo pathway downstream factors, to induce an epithelial-mesenchymal transition (EMT), thus contributing to tumour invasion and metastasis. We also testified that YAP1 and TEAD2 promoted epithelial-mesenchymal transition (EMT) in malignant glioma. Furthermore, we constructed nude mouse subcutaneous and intracranial models to verify that IKBKE could attenuate U87-MG tumourigenicity in vivo. Collectively, our results suggest that IKBKE plays a pivotal role in regulating cell proliferation, invasion and epithelial-mesenchymal transition of malignant glioma cells in vitro and in vivo by impacting on the Hippo pathway. Therefore, targeting IKBKE may become a new strategy to treat malignant glioma.

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OBJECTIVE: To investigate the expression levels of 2', 5'-oligoadenylate synthetase-like (OASL) and interferon induced protein with tetratricopeptide repeats 2 (IFIT2) genes in the peripheral blood leukocyte of patients with systemic lupus erythematosus (SLE), and to evaluate the relations between these gene expression levels and disease activity. METHODS: The clinical data of 50 SLE patients, 25 non-SLE patients with rheumatic diseases, and 25 normal controls were collected. Specimens of peripheral blood were collected; total RNA was extracted and transcribed into cDNA. SYBR green dye based real-time quantitative PCR method was applied to compare the expression levels (indicated as deltaCT value) of OASL and IFIT2 in patients with SLE and those in the controls. RESULTS: The deltaCT value of OASL expression level of the SLE patients was (4.83 +/- 0.41), significantly higher than those of the non-SLE patients (3.26 +/- 0.47) and normal controls (3.07 +/- 0.54, both P < 0.05), The deltaCT value of IFIT2 expression level of the SLE patients was (2.85 +/- 0.41), significantly higher than those of the non-SLE patients (1.19 +/- 0.52) and normal controls (1.07 +/- 0.47, both P < 0.05). The deltaCT value of OASL is related with the SLEDAI scores and immunoglobulin A. (Both P < 0.05). The deltaCT value of IFIT2 is related with the SLEDAI scores and IgA, white blood cell (both P < 0.05). CONCLUSION: The value of IFIT2 and OASL expression level of the SLE patients is up-regulation, the real time expression levels of OASL and IFIT2 genes are associated with SLE disease activity. To inhibit the expression of OASL and IFIT2 may become a novel therapeutic approach for SLE.

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OBJECTIVE: To investigate the expression of myxovirus resistance 1(MX1) and 2'5'-oligoadenylate synthetase 1(OAS1) genes in the peripheral blood leukocyte of patients with systemic lupus erythematosus (SLE), and to evaluated the relations between these genes expression levels and disease activity. METHODS: In this study, there were 50 SLE petients, 20 non-SLE patients with rheumatic dieases, and 25 normal controls. The peripheral blood samples of these patients were collected, and the expression levels (indicated as delta Ct value) of MX1 and OAS1 were measured by Sybr green dye based real-time quantitative PCR method. RESULTS: The deltaCt value of MX1 expression in SLE patients was 3.55 +/- 1.39, which was significantly higher than those of non-SLE patients (2.31 +/- 0.52, P = 0.000) and normal controls (2.23 +/- 1.05, P = 0.000). (2) The deltaCt value of OAS1 expression in SLE patients was 4.45 +/- 1.56, which also was significantly higher than those of non-SLE patients (3.03 +/- 0.76, P = 0.000) and normal controls (2.75 +/- 0.64, P = 0.000). (3) The deltaCt value of OAS1 was correlated with the SLEDAI scores (r = 0.338, P = 0.019) and serum IgA level. (4) The ACt value of MX1 was not correlated with the SLEDAI scores (r = 0.064, P = 0.661), but correlated with the serum levels of triglyceride (TG), cholesterol (TC), low density lipoprotein (LDL), albuminuria of 24 hours (r = 0.428, P = 0.003 r = 0.383, P = 0.009 r = 0.394, P = 0.007; r = 0.316, P = 0.025); (5) The deltaCt values of MX1 and OAS1 in the SLE patients with arthritis were significantly higher than those in non-arthritis SLE patients (3.04 +/- 1.42, P = 0.004; 3.89 +/- 1.49, P = 0.006). CONCLUSION: The expression levels of both MX1 and OAS1 in SLE patients are up-regulated, the expression levels of OAS1 genes are associated with SLE disease activity. As IFN-induced genes, MX1 and OAS1 play their respective role in SLE.

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To search for a new method of determining, we developed a new flow injection analyzer, applied to the atomic absorption spectrophotometer, relying on it without flame in place of visible spectrophotometer, and studied the appropriate condition for the determination of aluminum in sediments, thus built up a kind of new analytical test technique. Three peak and two valley absorption values (A1, A2, A3, A4 and A5) can be continuously obtained simultaneously that all can be used for quantitative analysis, then we discussed its theory and experiment technique. Based on the additivity of absorbance (A = A1+A2+A3+A4+ A5), the sensitivity of FIA is enhanced, and its precision and linear relation are also good, raising the efficiency of AAS. The simple method has been applied to determining Al in sediments, and the results are satisfactory.