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The development of cracks in reinforced concrete structures can accelerate structural deterioration and reduce service life. A numerical model was established to analyse steel bar corrosion in chloride-contaminated concrete with transverse cracks. In the model, the dynamic distinction between anode and cathode regions on the steel surface is considered by introducing an empirical formula for the anodic Tafel slope related to chloride concentration. The time-dependent characteristics of the corroded region were examined using the proposed corrosion prediction model and the corrosion process of steel bars in cracked concrete was revealed. The effects of crack width and crack spacing on steel corrosion were analysed in detail in terms of the corrosion area and corrosion rate. The results showed a variation in the corrosion area adjacent to cracks over time and a positive correlation between corrosion area and the square root of time. According to the micro-cell and macro-cell contributions to the corrosion rate, the process of steel bar corrosion was determined to occur in three stages. The effects of transverse cracks on the corrosion rate were found to vary with exposure time and to depend on the control steps of the micro- or macro-cells.

Introduction/objectivesTo seek significant features of systemic lupus erythematosus (SLE) by utilizing bioinformatics analysis.MethodLiquid chromatography-tandem mass spectrometry (LC–MS/MS) was used to quantify lysine crotonylation (Kcr) and lysine 2-hydroxyisobutyrylation (Khib) in peripheral blood mononuclear cells (PBMCs) of systemic lupus erythematosus (SLE) patients and normal controls.ResultsSeventy-six differentially modified proteins (DMPs) dually modified by Kcr and Khib were identified between SLE patients and healthy people. GO enrichment analysis prompted significant enrichment of seventy-six DMPs in MHC class II protein complex binding and leukocyte migration. KEGG pathways were enriched in antigen processing and presentation pathway and leukocyte transendothelial migration pathway. Six DMPs (CLTC, HSPA1B, HSPA8, HSP90AB1, HSPD1, and PDIA3) were identified in antigen processing and presentation pathway, of which HSPA8 was the core protein. Significant changes of Kcr and Khib in HSPA8 may increase ATP hydrolysis and promote antigen binding to MHC II molecule. In leukocyte transendothelial migration pathway, 7 DMPs (ACTN1, ACTN4, EZR, MSN, RAC1, RHOA, and VCL) were identified. MSN was the protein with the most modification sites in this pathway. In amino terminal ferm region of MSN, Kcr and Khib expression change may lead to the adhesion between leukocytes and endothelial cells, which was an important step of leukocyte migration.ConclusionKcr and Khib may promote the antigen presentation and jointly regulate the tissue damage mediated by leukocyte migration in SLE patients, which may play key roles in the pathogenesis of SLE probably.Key Points• Antigen processing and presentation and leukocyte transendothelial migration may play key roles in the pathogenesis of SLE.

The construction of advanced metering infrastructure and the rapid evolution of artificial intelligence bring opportunities to quickly search for the optimal dispatching strategy for reactive power optimization by mining existing prior knowledge and massive data without explicitly constructing physical models. Therefore, a novel data-driven-based approach is proposed for reactive power optimization of distribution networks using capsule networks (CapsNet). The convolutional layers with strong feature extraction ability are used to project the power loads to the feature space to realize the automatic extraction of key features. Furthermore, the complex relationship between input features and dispatching strategies is captured accurately by capsule layers. The back propagation algorithm is utilized to complete the training process of the CapsNet. Case studies show that the accuracy and robustness of the CapsNet are better than those of popular baselines (e.g., convolutional neural network, multi-layer perceptron and case-based reasoning). Besides, the computing time is much lower than the traditional heuristic methods, such as genetic algorithm, which can meet the real-time demand of reactive power optimization in distribution networks.

Cisplatin is an effective chemotherapeutic agent in facilitating the inhibition of proliferation, migration, and invasion in cancerous cells. However, the detailed mechanism of the regulation by cisplatin of human breast cancer cells is still unclear. This study aimed to investigate the mechanism of kruppel-like factor 2 (KLF2) transcription factor in cisplatin therapy for breast cancer. RT-qPCR was performed to quantify the expression of KLF2 and WEE1 in clinical tissue samples from breast cancer patients and in MDA-MB-231 cells. ChIP assay and dual-luciferase reporter assay were used to analyze the potential-binding sites of KLF2 and WEE1 promoter. Gain- or loss-of-function approaches were used to manipulate KLF2 and WEE1 in cisplatin-treated MDA-MB-231 cells, and the mechanism of KLF2 in breast cancer was evaluated both via CCK-8 assay, flow cytometry, Transwell assay, and Western blot. Further validation of the KLF2 was performed on nude mouse models. Breast cancer tissues and cells showed a relative decline of KLF2 expression and abundant WEE1 expression. Cisplatin inhibited the proliferation, migration, and invasion of MDA-MB-231 cells. Overexpression of KLF2 enhanced the inhibitory effect of cisplatin on the malignant characteristics of MDA-MB-231 cells in vitro. KLF2 targeted WEE1 and negatively regulated its expression, thus enhancing the sensitivity to cisplatin of breast cancer cells as well as tumor-bearing mice. Overall, these results suggest that KLF2 can potentially inhibit WEE1 expression and sensitize breast cancer cells to cisplatin, thus presenting a promising adjunct treatment.

Interleukin-17A is a proinflammatory cytokine that is produced by TH17 cells, and plays a dual role in tumor progression, infectious diseases, and autoimmune disorders. Interleukin-17A is induced during colorectal tumorigenesis and angiogenesis, although some studies have reported an anti-tumor effect as well. The aim of our study was to assess the prognostic role of interleukin-17A in colorectal cancer and determine the potential mechanisms.The GEO database was searched using the keyword "colorectal cancer", and 10 datasets were identified that included interleukin-17A mRNA expression and survival data of several colorectal cancer patient cohorts. The patients were stratified into the interleukin-17Ahigh and interleukin-17Alow groups based on the median expression level.Higher interleukin-17A mRNA levels were associated with better overall survival rates and the early tumor stage, indicating a protective role of interleukin-17A in colorectal cancer. Furthermore, interleukin-17A mRNA expression also correlated positively with that of TNFS11, CCR6, and CCL20, indicating that the anti-tumor effect of interleukin-17A is likely mediated by enhancing tumor antigen presentation by dendritic cells and recruiting the activated tumor-specific CD8+ cytotoxic T lymphocytes. The IL-23 and STAT3 mRNA levels were also significantly higher in the interleukin-17Ahigh group, which points to an upstream regulatory role of IL-23/STAT3 axis. Finally, the immune checkpoints PDCD1 (PD-1) and CD274 (PDL-1) were also positively correlated with interleukin-17A mRNA expression, indicating that interleukin-17A is a promising predictor of the immunotherapeutic outcome of PD-1/PDL-1 blockade in colorectal cancer.Interleukin-17A mRNA is a protective factor in colorectal cancer and a promising biomarker for assessing the prognosis and immunotherapeutic response.

Introduction. The modification of lysine crotonylation (Kcr) is another biological function of histone in addition to modification of lysine acetylation (Kac), which may play a specific regulatory role in diseases. Objectives. This study compared the expression levels of Kcr and proteome between patients with chronic obstructive pulmonary disease (COPD) combined with type II respiratory failure (RF) to study the relationship between Kcr, proteome, and COPD. Methods. We tested the Kcr and proteome of COPD combined with type II RF and normal control (NC) using croton acylation enrichment technology and liquid chromatography tandem mass spectrometry (LC-MS/MS) with high resolution. Results. We found that 32 sites of 23 proteins were upregulated and 914 sites of 295 proteins were downregulated. We performed Kyoto Encyclopedia of Genes and Genomes (KEGG), protein domain, and Gene Ontology (GO) analysis on crotonylated protein. In proteomics research, we found that 190 proteins were upregulated and 151 proteins were downregulated. Among them, 90 proteins were both modified by differentially expressed crotonylation sites and differentially expressed in COPD combined with type II RF and NC. Conclusion. Differentially expressed crotonylation sites may be involved in the development of COPD combined with type II RF. 90 proteins modified by crotonylation and differentially expressed in COPD combined with type II RF can be used as markers for the study of the molecular pathogenesis of COPD combined with type II RF.

A water freeze-thaw cycle and sulfate freeze-thaw coupling cycle were explored experimentally to evaluate the durability of recycled concrete with lithium slag (LS). The damage-deterioration law was studied from the aspects of mass-change rate, relative dynamic modulus of elasticity, and cube’s compressive strength. Based on the relative dynamic modulus of elasticity, the damage-degree equation of the concrete was fitted, and a mechanical-attenuation model related to this parameter and the cube’s compressive strength was established and verified. The damage mechanism under the action of the sulfate freeze-thaw cycle was revealed through scanning electron microscopy (SEM). The combination of recycled coarse aggregate (RCA) and LS was beneficial to the anti-deterioration ability of the concrete. During the cycle experiments, the mass and relative dynamic modulus of elasticity increased initially and then decreased, while the cube’s compressive strength declined continually. The concrete with a 30 % RCA substitution rate and 20 % LS exhibited the optimal comprehensive durability, and specimens with excessive LS showed more susceptibility to sulfate erosion. The residual compressive strength of concrete structures can be evaluated by measuring the relative dynamic modulus of elasticity as the two parameters are ideally correlated.

In this study, a new electrochemical aptasensor with specific identification and quantitative analysis of glypican-3 (GPC3) was constructed using reduced graphene oxide-chitosan-ferrocene deposition of Pt–Pd bimetallic nanoparticles (RGO-CS-Fc/Pt–Pd BNPs) as biosensing platform and GPC3 aptamer (GPC3apt) as recognition molecule. The GPC3apt could react specifically with GPC3 present in the experimental samples, resulting in the formation of GPC3-aptamer complexes on the biosensing platform, which would increase the electron transfer impedance and reduce the redox current of ferrocene. The electrochemical aptasensor was characterized by scanning electron microscopy (SEM), cyclic voltammetry (CV), electrochemical impedance spectrometry (EIS), and Raman spectroscopy. Under the optimal experimental conditions, the response redox current was linearly related to the concentration of GPC3 in the range from 0.001 to 10 µg mL−1 with good linear correlation coefficient (R2 of 0.9929), and had a low detection limit of 3.67 ng mL−1 (S/N = 3), high sensitivity of 0.149 µA µM−1 cm−2. In addition, the aptasensor showed long stability, good specificity, acceptable reproducibility and satisfactory recoveries (101.1–105.6%) in the detection of clinical serum samples, which developed a new research method for early clinical diagnosis.

Glypican-3 (GPC3) is a potential hepatocellular carcinoma (HCC) serum marker with good sensitivity and specificity. Herein, a label-free electrochemical aptasensor for the detection of GPC3 was developed using a reduced graphene oxide–hemin–chitosan (RGO–H–CS) nanocomposite-modified screen-printed electrode (SPE) as a biosensing platform and GPC3 aptamer as the recognition element. When GPC3 was present, the aptamer could specifically bind with the target GPC3 by specific recognition reaction and form GPC3–aptamer conjugations on the sensing surface, which could alter the electrochemical redox signal of hemin (Fe(III)/hemin(Fe(II))) in the RGO–H–CS nanocomposite recorded by differential pulse voltammetry (DPV). The electrochemical GPC3 aptasensor was characterized via scanning electron microscopy (SEM), Raman spectroscopy, cyclic voltammetry (CV) and electrochemical impedance spectroscopy (EIS). Under optimal conditions, currents originating from the oxidation of hemin had a linear relationship with the concentration of GPC3 in the range of 0.01 µg mL−1 to 10.0 µg mL−1 with a detection limit of 7.9 ng mL−1 (S/N = 3). The developed aptasensor was applied to detect the GPC3 level in the human serum samples with the recovery rate of 101.04–104.9%. Moreover, the label-free aptasensor exhibited considerable anti-interfering ability, acceptable stability and good reproducibility. Therefore, this study provides a reliable and objective analysis method to achieve high screening for the early diagnosis of HCC.

The under-deposit corrosion behavior and mechanism of aluminum brass (HAl77-2) were investigated in artificial seawater with a custom double electrolytic cell. The experiments included linear polarization, electrochemical impedance spectroscopy, and multielectrode arrays analysis. The electrochemical results revealed a pronounced effect of temperature on the under-deposit corrosion behavior of HAl77-2. The corrosion of HAl77-2 inside the CaCO3 scale is aggravated with increasing temperature. However, the increasing frequency of the corrosion rate of HAl77-2 gradually decreased after 333 K. Moreover, in the desalination of artificial seawater, the corrosion rate of HAl77-2 in the occulated area initially increased and subsequently decreased with increasing Cl− concentration. The scanning electron microscopy and energy dispersive spectrometry analysis showed a remarkable appearance of selective localized corrosion on the surface of HAl77-2.

Transplantation is currently the best treatment for patients with end-stage renal disease. However, acute rejection (AR) is the major source of failure in renal transplantation. The current best practice for the diagnosis of AR involves renal biopsy, but it is invasive, time-consuming, costly and inconvenient. Sensitive and less invasive detection of AR episodes in renal transplant patients is essential to preserve allograft function. The present study applied isobaric tags for relative and absolute quantitation (iTRAQ) mass spectrometry to analyze serum protein expression in patients with AR and healthy controls. Overall, 1,399 proteins were identified. Using a cut-off of Q1.2 for the variation in expression, 109 proteins were identified to be differentially expressed between the AR and control groups, 72 of which were upregulated and 37 were downregulated. Several proteins, including properdin, keratin 1, lipoprotein(a) and vitamin D-binding protein, may have roles in the pathogenesis of AR. The present study focused on iTRAQ-based proteomic profiling of serum samples in AR. Insight from the present study may help advance the understanding of the molecular mechanisms of AR and identify potential novel biomarkers of AR for further characterization.

TOX high mobility group box family member 3 (TOX3) can function as tumor suppressor or oncogene in different tumors, while ras homolog family member B (RhoB) is a well-known tumor suppressor. The expression and role of TOX3 in colorectal cancer (CRC) are unknown. This study aimed to investigate the expression of TOX3 in CRC and the role of TOX3/mitogen-activated protein kinase (MAPK)/RhoB signaling in the proliferation and apoptosis of CRC cells. We showed that TOX3 messenger RNA (mRNA) and protein expression levels were significantly upregulated in CRC tissues and cell lines. High TOX3 expression was associated with high T stage, nodal invasion, and advanced tumor stage. Disease-free survival (DFS) was shortened for CRC patients with high expression of TOX3, while overall survival showed no significant difference. TOX3 promoted proliferation, inhibited apoptosis, and decreased the sensitivity to oxaliplatin of CRC cells. In addition, the inhibition of TOX3 led to the upregulation of RhoB, and RhoB overexpression suppressed the proliferation and promoted apoptosis of CRC cells. Moreover, TOX3 overexpression upregulated MAPK signaling, while MAPK signaling inhibitor U0126 induced CRC cell proliferation arrest or apoptosis, and attenuated the inhibition of RhoB in TOX3 overexpression cells. In addition, the overexpression of TOX3 increased tumor volume in nude mice. In conclusion, TOX3 may be an oncogene in CRC and can predict DFS in CRC patients. TOX3/MAPK/RhoB signaling plays an important role in the modulation of proliferation and apoptosis of CRC cells.

Ultra-high performance geopolymer concrete (UHPGC) has been favored due to its excellent sustainability and outstanding mechanical properties. This study was conducted to explore the mechanical and durability properties of slag/metakaolin-based UHPGC with steel fibers reinforcement. The uniaxial compression test and rapid chloride migration test were conducted to measure the compressive strength and chloride penetration resistance of UHPGC. A total of nine groups of mixture proportions were designed and tested to investigate the influences of steel fiber dosage and sodium hydroxide (NaOH) solution concentration. The results showed that an increased steel fiber dosage and alkali concentration can improve compressive strength, and the maximum compressive strength can reach more than 140 MPa. In addition, the rapid chloride migration test showed that the chloride penetration resistance of the slag/metakaolin-based concrete was moderate, with a non-steady chloride migration coefficient ranging from 6.5 × 10−12 m2/s to 14.1 × 10−12 m2/s. The increase in steel fiber volume content slightly enlarged chloride penetration depth, while the higher concentration of sodium hydroxide solution was beneficial as it improved chloride penetration resistance. The results suggest that although ultra-high compressive strength can be achieved, the durability issues of steel fiber reinforced slag/metakaolin-based geopolymer concrete still need considerable attention.

The morbidity and mortality associated with acute kidney injury (AKI) remain obstinately high. Early diagnosis is urgently required and should be pursued in at-risk populations. Recently, a newly validated biomarker, matrix metalloproteinase-7 (MMP-7), was reported as a novel indicator for early AKI prediction and a noninvasive surrogate biomarker of kidney function. Monitoring urinary MMP-7 (uMMP-7) levels fills the gaps in early diagnosis of AKI at early onset. However, the lack of available reagents for its rapid detection limits its use. Herein, we established an ultrasensitive and rapid immunomagnetic microparticles-based time-resolved fluoroimmunoassay to measure urinary MMP-7 in AKI patients. The assay time is 30 min. The calibration curve showed high linear correlation (r = 0.9998) with a linearity of detection of 0.063–150 ng mL−1 and lower limit of detection of 0.039 ng mL−1. The coefficient variation of the intra- and inter-assay lower than 5.17%, and the analytical recovery was 99.06%–105.60%. Testing of clinical samples using the proposed assay and a DUOSET@ ELISA kit showed good correlations in the comparison of uMMP-7 levels (r = 0.9541) and uMMP-7/uCreatinine (r = 0.9595). The proposed assay has satisfactory analytical performance and may serve as a promising tool for early diagnosis of AKI.

Background: Chromosome 22q11.2 deletion (CH22qD) syndrome is the most common human deletion syndrome. Competing endogenous RNAs (ceRNAs) have miRNA binding sites that are capable of competitively binding miRNAs and inhibiting miRNA regulation of target genes. Results: We identified differently expressed miRNAs, circRNAs, lncRNAs and mRNAs of CH22qD, and we analysed the results by using GO analysis, KEGG pathway analysis and network regulation analysis. Conclusions: These analyses may predict the effects of chromosomal microdeletions.

Objective: LncRNAs are a class of competing for endogenous RNAs (ceRNAs) with no coding ability and have miRNA binding sites that competitively bind to miRNAs and inhibit miRNA-mediated regulation of target genes. In recent years, an increasing number of studies have recognized the biological functions of lncRNAs.Methods: Illumina RNA-Seq technology was used to analyze the cord blood with Patau syndrome (PS) fetal and the peripheral blood of pregnant women to obtain differential expression profiles of lncRNAs, miRNAs, and mRNAs. Further, Combined with bioinformatics analysis of the biological functions of differentially expressed lncRNAs (DElncRNAs). Results: The results showed that 467 DElncRNAs, 8512 differentially expressed mRNAs (DEmRNAs), and 18 differentially expressed miRNAs (DEmiRNAs) were found to be co-expressed in cord blood and peripheral blood. The hsa-miR-15a-5p is located on chromosome 13. We constructed the ceRNA network with hsa-miR-15a-5p, lncRNAs as the bait, and mRNAs as the targe. Conclusion: We consider that the DElncRNAs may indirectly regulate the target gene CLASRP or KARS by binding hsa-miR-15a-5p to participate in the occurrence of PS.

Systemic lupus erythematosus (SLE) is a complex autoimmune disease that affects multiple organs, the pathogenic mechanism is related to many factors, but the specific pathogenic mechanism has not been clarified yet. Protein lysine modifications play important roles in gene regulation, transcription, metabolism and other biological processes. The lysine 2-hydroxyisobutyrylation(K hib ) histone mark has recently been discovered as a novel protein modification. In this study, patients in the active SLE group were examined (N=8), while the control group was healthy (N=20).Utilizing antibody-based affinity enrichment and nano-HPLC/MS/MS analyses of K hib peptides, we identified 156 upregulated proteins(fold change>1.5),124 downregulated proteins(fold change

The aim of this study was to identify novel genetic variants affecting tacrolimus trough blood concentrations. We analyzed the association between 58 single nucleotide polymorphisms (SNPs) across the CYP3A gene cluster and the log-transformed tacrolimus concentration/dose ratio (log (C0/D)) in 819 renal transplant recipients (Discovery cohort). Multivariate linear regression was used to test for associations between tacrolimus log (C0/D) and clinical factors. Luciferase reporter gene assays were used to evaluate the functions of select SNPs. Associations of putative functional SNPs with log (C0/D) were further tested in 631 renal transplant recipients (Replication cohort). Nine SNPs were significantly associated with tacrolimus log (C0/D) after adjustment for CYP3A5*3 and clinical factors. Dual luciferase reporter assays indicated that the rs4646450 G allele and rs3823812 T allele were significantly associated with increased normalized luciferase activity ratios (p

Liver cirrhosis of hepatitis B is an immune-related disease in which liver cells die during the body’s immune system activation to clear the virus, and the progress is closely related to T lymphocytes. T lymphocyte cells recognise antigens, specifically by major histocompatibility complex (MHC), through a membrane protein T cell receptor (TCR). Here, we used high throughput immune repertoire sequencing technique to study the characteristics and diversity of the TCR repertoire between patients who underwent liver transplantation and healthy controls (NC). We sequenced the TCR β-chain complementary-determining region 3 (CDR3) repertoire in peripheral blood mononuclear cells (PBMCs) from 6 liver transplantation patients before transplantation (Pre) and on the first (Post1) and seventh days (Post7) after transplantation along with 6 NC. We observed that the distributions of CDR3, VD indel, and DJ indel lengths were similar among the Pre, Post1, Post7 and NC groups. We found that the TCR repertoire diversity of transplantation groups was relatively lower compared to NC group. The Pre-group had more highly expanded T cell clones compared to Post1, Post7 and NC groups, and the diversity of the T cell repertoire of the Post7 group was significantly decreased compared to the Pre, Post1 and NC groups. In addition, we found our results also show that various TRBV expression increased and some public sequences at different time points after liver transplantation, and the expression levels of 3 TRBV segments and 2 TRBJ segments were also significantly different in Pre, Post1, Post7 and NC groups. Moreover, 1 aa sequence shared by all liver transplantation patients and 2 aa sequences shared by at least two groups, which may serve as biomarkers to monitor the immune status of liver transplant patients.

Recent studies have shown that circular RNAs (circRNAs) exhibit differential expression in certain diseases. However, to the best of our knowledge, maternal fetal-derived circRNAs and mRNAs associated with Down's syndrome (DS) have not yet been investigated. A total of 12 umbilical cord blood samples were collected from pregnant women, including six women carrying fetuses with DS (diagnosed by G-banding karyotype analysis), and six women carrying fetuses without DS. In addition, 12 peripheral blood samples were obtained from children, including six children with DS and six children without DS. Gene chip technology was used to screen for differentially expressed circRNAs and mRNAs in the cord blood samples, and were subsequently verified by reverse transcription-quantitative polymerase chain reaction in peripheral blood from the children to identify potential biomarkers. Furthermore, circRNA/microRNA (miRNA) interactions were predicted using Arraystar miRNA target prediction software. There was a significant difference in the expression of hsa_circRNA_103127, hsa_circRNA_103112 and hsa_circRNA_104907 between cord blood obtained from the women carrying fetuses with and without DS, and between peripheral blood obtained from children with and without DS (P

Early diagnosis of diabetes yields significant clinical benefits. The serum level of 1,5‑anhydroglucitol (1,5‑AG) has been a new biochemical marker for postprandial hyperglycemia. In this study, a simple colorimetric method for 1,5‑AG detection has been designed based on highly efficient peroxidase mimetic activity of GQDs and enzyme-catalyzed reaction. By the catalytic action of pyranose oxidase (PROD), the 1,5‑AG was oxidized to 1,5‑anhydrofuctose and H2O2. The GQDs in the presence of H2O2 exhibited highly efficient catalytic activity toward the oxidation of 3, 3', 5, 5'‑tetramethylbenzidine (TMB) to a blue colored product. The influence of relevant experimental variables was optimized. A linear relationship of optical signal with the concentration of 1,5‑AG in the range of 20.0-100.0μg/mL with the regression correlation coefficient of 0.9985 was obtained which could be monitored by colorimetry detection. The limit of detection (LOD) for 1,5‑AG detection was approximately 0.144μg/mL. All in all, the proposed 1,5‑AG detection system based on GQDs and PROD-catalyzed reaction showed better performances with simple operation, low-cost, higher selectivity.

The aim of the present study was to screen gastric cancer (GC) tissue and adjacent tissue for differences in mRNA and circular (circRNA) expression, to analyze the differences in circRNA and mRNA expression, and to investigate the circRNA expression in gastric carcinoma and its mechanism. circRNA and mRNA differential expression profiles generated using Agilent microarray technology were analyzed in the GC tissues and adjacent tissues. qRT-PCR was used to verify the differential expression of circRNAs and mRNAs according to the interactions between circRNAs and miRNAs as well as the possible existence of miRNA and mRNA interactions. We found that: i) the circRNA expression profile revealed 1,285 significant differences in circRNA expression, with circRNA expression downregulated in 594 samples and upregulated in 691 samples via interactions with miRNAs. The qRT-PCR validation experiments showed that hsa_circRNA_400071, hsa_circRNA_000543 and hsa_circRNA_001959 expression was consistent with the microarray analysis results. ii) 29,112 genes were found in the GC tissues and adjacent tissues, including 5,460 differentially expressed genes. Among them, 2,390 differentially expressed genes were upregulated and 3,070 genes were downregulated. Gene Ontology (GO) analysis of the differentially expressed genes revealed these genes involved in biological process classification, cellular component classification and molecular function classification. Pathway analysis of the differentially expressed genes identified 83 significantly enriched genes, including 28 upregulated genes and 55 downregulated genes. iii) 69 differentially expressed circRNAs were found that might adsorb specific miRNAs to regulate the expression of their target gene mRNAs. The conclusions are: i) differentially expressed circRNAs had corresponding miRNA binding sites. These circRNAs regulated the expression of target genes through interactions with miRNAs and might become new molecular biomarkers for GC in the future. ii) Differentially expressed genes may be involved in the occurrence of GC via a variety of mechanisms. iii) CD44, CXXC5, MYH9, MALAT1 and other genes may have important implications for the occurrence and development of GC through the regulation, interaction, and mutual influence of circRNA-miRNA-mRNA via different mechanisms.

Hepatocellular carcinoma (HCC) is one of the most lethal malignancies that is closely associated with the Hepatitis B virus (HBV). HBV integration into host genomes can induce instability and the aberrant expression of human genomic DNA. To directly assess HBV integration breakpoints at whole genome level, four small sequencing libraries were constructed and the HBV integration profiles of four patients with HCC were characterized. In total, the current study identified 11,800,974, 11,216,998, 11,026,546 and 11,607,842 clean reads for patients 1-3 and 4, respectively, of which 92.82, 95.95, 97.21 and 97.29% were properly aligned to the hybrid reference genome. In addition, 220 HBV integration events were detected from the tumor tissues of four patients with HCC and an average of 55 breakpoints per sample was calculated. The results indicated that HBV integration events may be implicated in HCC physiologies and diseases. The results acquired may also provide insight into the pathogenesis of HCC, which may be valuable for future HCC therapy.

Full proteomic analysis methods. (DOCX 21 kb)

Down syndrome (DS) is caused by trisomy of human chromosome 21 and is associated with a number of deleterious phenotypes. To investigate the role of microRNA (miRNA) in the regulation of DS, high-throughput Illumina sequencing technology and isobaric tagging for relative and absolute protein quantification analysis were utilized for simultaneous expression profiling of miRNA and protein in fetuses with DS and normal fetuses. A total of 344 miRNAs were associated with DS. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses were used to investigate the proteins found to be differentially expressed. Functionally important miRNAs were determined by identifying enriched or depleted targets in the transcript and the protein expression levels were consistent with miRNA regulation. The results indicated that GRB2, TMSB10, RUVBL2, the hsa-miR-329 and hsa-miR-27b, hsa-miR-27a targets, and MAPK1, PTPN11, ACTA2 and PTK2 or other differentially expressed proteins were connected with each other directly or indirectly. Integrative analysis of miRNAs and proteins provided an expansive view of the molecular signaling pathways in DS.

Mucopolysaccharidosis VII (MPS VII) is a rare, genetic disease that is usually inherited as an autosomal-recessive trait. Genetic mutations affect mental retardation, skeletal deformities, corneal clouding, hepatosplenomegaly and intelligence. To date, several genes have been found in related to patients with MPS VII. Here, we used whole-exome sequencing to identify a mutation (NC_000007.13:g. 65444706G>A) in GUSB gene in an eight year old boy with MPS VII. Subsequently, we speculated that the variant of GUSB gene is critical for the proper function of GUSB, and might had led to an absence of the β-glucuronidase or reduce activity of the enzyme.

Objective: The objective of this study was to measure the 3′-untranslated region (3′-UTR) polymorphism lengths in peripheral blood mononuclear cells (PBMCs) from uremia patients.Method: We sequenced the alternative polyadenylation sites in the 3′-UTR of PBMCs from 10 uremic patients and 10 healthy people to detect different gene expression levels between uremia patients and healthy controls. Quantitative reverse transcription polymerase chain reaction was used as validation. Result: Compared with the healthy control group, 691 genes in uremic patients had significantly different 3′-UTR lengths. Of these genes, 475 genes showed shortened 3′-UTRs, and the 3′-UTRs of 216 genes were lengthened. The verification results matched the original sequencing results. Conclusion: There were significant differences in 3′-UTR lengths between uremic patients and healthy controls, and analysis of the differential genes may contribute to the understanding of uremia pathogenesis.

Systemic lupus erythematosus (SLE) is a chronic, potentially fatal systemic autoimmune disease characterized by the production of autoantibodies against a wide range of self-antigens. To investigate the role of the 5-hmC DNA modification with regard to the onset of SLE, we compared the levels 5-hmC between SLE patients and normal controls. Whole blood was obtained from patients, and genomic DNA was extracted. Using the hMeDIP-chip analysis and validation by quantitative RT-PCR (RT-qPCR), we identified the differentially hydroxymethylated regions that are associated with SLE. There were 1,701 genes with significantly different 5-hmC levels at the promoter region in the SLE patients compared with the normal controls. The CpG islands of 3,826 genes showed significantly different 5-hmC levels in the SLE patients compared with the normal controls. Out of the differentially hydroxymethylated genes, three were selected for validation, including TREX1, CDKN1A and CDKN1B. The hydroxymethylation levels of the three genes were confirmed by RT-qPCR. The results suggested that there were significant alterations of 5-hmC in SLE patients. Thus, these differentially hydroxymethylated genes may contribute to the pathogenesis of SLE. These findings show the significance of 5-hmC as a potential biomarker or promising target for epigenetic-based SLE therapies.

The global usage of veterinary antibiotics is significant. These antibiotics can be released into the aquatic environment and exert toxic effects on non-target organisms. To explore the physiological effects of tetracycline antibiotics on aquatic life, the growth characteristics of and toxin release from the cyanobacterium Microcystis aeruginosa (M. aeruginosa) were studied. Results showed that the toxicity order of the three target antibiotics was TC (tetracycline) > CTC (chlortetracycline hydrochloride) > OTC (oxytetracycline) in terms of inhibition occurrence time and the EC10 and EC25 values. Further, the target antibiotics regulated the production of MC-LR (microcystin-LR) to different degrees. CTC destroyed the M. aeruginosa cells and resulted in a decreased MC-LR release but stimulated the ability to synthesise MC-LR. OTC had a relatively weaker toxicity compared with CTC, while TC was the most toxic among the three antibiotics. Therefore, TC is friendly to the aquatic environment because it simultaneously reduced the intracellular and extracellular MC-LR content. These results aid our understanding of the effects of tetracycline antibiotics on Microcystis aeruginosa, which is important for environmental evaluation and protection. These results are also helpful for guiding the application of veterinary antibiotics in agricultural settings.

Interferon‑induced transmembrane protein 3 (IFITM3) has been recently identified as a potential molecular marker. IFITM3 has been reported to be upregulated in various human diseases, including colon and breast cancer, astrocytoma, as well as ulcerative colitis. However, the clinical significance and underlying mechanisms of IFITM3 dysregulated expression in gastric cancer (GC) remain to be determined. The present study aimed to evaluate the expression of IFITM3 in human gastric tumor cells and specimens and investigate the effects of IFITM3 knockdown in the regulation of GC growth and its potential mechanism. IFITM3 expression was significantly overexpressed in the GC cell lines and GC tissues compared with corresponding normal controls by RT‑qPCR, western blot analysis and immunohistochemistry, and this overexpression was correlated with tumor differentiation, lymph node and distant metastasis, and advanced tumor node metastasis stages. Furthermore, knockdown of IFITM3 expression suppressed tumor cell migration, invasion and proliferation significantly in vitro, arrested tumor cells at the G0/G1 phase and reduced the cell numbers in the S phase of the cell cycle. We preliminarily confirmed that IFITM3 can be mediated by the activities of Wnt/β-catenin signaling. Further investigation revealed that silencing of IFITM3 effectively reversed the epithelial-to-mesenchymal transition (EMT) phenotype and reduced the activities of MMP-2 and MMP-9 expression. Taken together, these data suggested that IFITM3 is a potential therapeutic target for GC.

Immunoglobulin (Ig) A nephropathy (IgAN) is the most common form of glomerulonephritis. In clinical practice, it is difficult to monitor the repeating relapse in patients suffering from IgAN, which usually occurs within 10 years of end-stage renal disease. In order to identify and quantify the total protein content in the renal tissue of patients with IgAN, isobaric tags for relative and absolute quantification (iTRAQ) technology was performed. iTRAQ coupled with multiple chromatographic fractionation and tandem mass spectrometry was used to analyze the total protein of normal renal tissue in IgAN and healthy patients. The individual proteins were identified by the Mascot search engine and any that were differentially expressed were monitored. A total of 574 different proteins were identified, and 287 proteins were up- or downregulated by >1 fold alteration in levels. The results showed that iTRAQ-based quantitative proteomic technology for the identification and relative quantitation of the renal tissue proteome is efficiently applicable. The differential expression of the proteome profiles for IgAN patients was determined. Further studies using large cohorts of patient samples with long-term clinical follow-up data should be conducted to evaluate the usefulness of the pathogenesis and novel biomarker candidates of IgAN, which may develop a novel technique for the diagnosis of IgAN.

Long non-coding RNAs (lncRNAs) are recently identified regulators in tumorigenesis and tumour progression. BRAF-activated lncRNA (BANCR) is overexpressed in melanoma and has a potential functional role in melanoma cell migration. However, little is known concerning the role of BANCR in the development of colorectal cancer (CRC). The current study examined BANCR expression in 60 pairs of CRC and matched adjacent normal tissues. The quantitative polymerase chain reaction results showed that BANCR was frequently overexpressed in cancer tissues and this overexpression was found to significantly correlate with lymph node metastasis and tumour stage. The ectopic expression of BANCR contributed to the migration of human CRC Caco-2 cells, whereas knockdown of BANCR inhibited the migration of the HCT116 cells in vitro. Further investigation into the underlying mechanisms responsible for the migratory effects revealed that BANCR induced the epithelial-mesenchymal transition (EMT) through an MEK/extracellular signal-regulated kinase-dependent mechanism as treatment with the MEK inhibitor, U0126 decreased migration and reversed the EMT in the BANCR-overexpressed HCT116 cells. These results revealed the significance of BANCR in the molecular etiology of CRC and implied the potential application of BANCR in the therapeutic treatment of CRC.

Treatment of uremia is now dominated by dialysis; in some cases, patients are treated with dialysis for decades, but overall outcomes are disappointing. A number of studies have confirmed the relevance of several experimental insights to the pathogenesis of uremia, but the specific biomarkers of uremia have not been fully elucidated. To date, our knowledge about the alterations in DNA 5-hydroxymethylcytosine (5-hmC) in uremia is unclear, to investigate the role of DNA 5-hmC in the onset of uremia, we performed hMeDIP-chip between the uremia patients and the normal controls from the experiment to identify differentially expressed 5-hmC in uremia-associated samples.Extract genomic DNA, using hMeDIP-chip technology of Active Motif companies for the analysis of genome-wide DNA 5-hmC, and quantitative real-time PCR confirmation to identify differentially expressed 5-hmC level in uremia-associated samples.There were 1875 genes in gene Promoter, which displayed significant 5-hmC differences in uremia patients compared with normal controls. Among these genes, 960 genes displayed increased 5-hmC and 915 genes decreased 5-hmC. 4063 genes in CpG Islands displayed significant 5-hmC differences in uremia patients compared with normal controls. Among these genes, 1780 genes displayed increased 5-hmC and 2283 genes decreased 5-hmC. Three positive genes, HMGCR, THBD, and STAT3 were confirmed by quantitative real-time PCR.Our studies indicate the significant alterations of 5-hmC. There is a correlation of gene modification 5-hmC in uremia patients. Such novel findings show the significance of 5-hmC as a potential biomarker or promising target for epigenetic-based uremia therapies.

Acute rejection remains a problem in renal transplantation. To further illustrate the mechanism of rejection, we integrated protein array-based proteomics and RNA microarray-based genomics to investigate the transcription factor, microRNA and long noncoding RNA of biopsies of three patients with acute rejections and a control group. 99 transcription factors were identified in acute rejection biopsies compared to normal renal tissue. We correlated transcription factor data with microRNA and long noncoding RNA data sets and reported the expression of 5 transcription factors (AP-1, AP-4, STATx, c-Myc and p53), 12 miRNAs and 32 lncRNAs in acute rejection biopsies. Pathway analysis demonstrated that over-presentation of transcription factor pathway plays a critical role in acute rejection. This is the first study to comprehensively report the acute rejection transcription factor pathway. Integrative analysis of the transcription factor, microRNA and long noncoding RNA provided an expansive view of molecular signaling pathways in acute rejection after renal transplantation.

Systemic lupus erythematosus (SLE) is an autoimmune disease that is characterized by multi-organ involvement leading to significant morbidity and mortality in predominantly young women. The underlying pathogenesis involves the emergence of autoreactive T and B lymphocytes, production of autoantibodies, formation and deposition of immune complexes in various tissues leading to inflammation and organ damage. Recently, growing evidence suggests that the functions of hematopoietic stem cells (HSCs) and mesenchymal stem cells (MSCs) are disrupted in SLE pathology. And HSC or MSC transplantation (HSCT/MSCT) can offer an effective and safe therapy for the severe SLE patients, resulting in disease clinical remission and improvement of organ dysfunction. In this article, we provide a brief overview of current research of autologous or allogeneic HSCT/MSCT in SLE and describe our current understanding of the mechanisms by which it plays a part in treating SLE, for better understanding of the pathogenesis, diagnosis and treatment for SLE.

Renal transplant success is closely tied to the ability to monitor transplant recipients. However, transplant monitoring still depends on relatively dated technologies. Thus, we applied a novel method of proton nuclear magnetic resonance (NMR)-based metabolomics to investigate the altered metabolic pattern in serum, seeking to identify biomarkers involved to different periods of renal transplant patients. Serum was obtained from 28 healthy controls (class 4) and from 20 renal transplant patients in different periods: pretransplant (class 1) and on the 1st (class 2) and the 7th day (class 3) after transplantation. After performing proton NMR spectroscopy, multivariate pattern recognition was applied to cluster the groups and establish disease-specific metabolite biomarker profiles. Compared with class 4, 19 different peaks and 10 potential biomarkers were identified in class 1, class 2, and class 3 (p0.0001). Nevertheless, there was no obvious difference between class 1, class 2, and class 3 (p0.05). Partial least squares-discriminant analysis models were able to identify patients with sensitivity and specificity of 98.7% and 95.4%, respectively. These results not only indicate that this novel method has sufficient sensitivity to distinguish renal transplant patients from controls but also identify biomarkers to monitor graft function, which could be developed to a clinically useful diagnostic tool.

In this study, persimmon tannin was extracted from Diospyros kaki L.f. using ultrasound-assisted extraction and purified by D101 macroporous resin column chromatography and polysulfone ultrafiltration membrane. The tannin content of the final persimmon tannin extracts was attained to 39.56% calculated as catechin equivalents. Also, the radioprotective effects of persimmon tannin for HEK 293T cells proliferation and apoptosis after Gamma irradiation were investigated by CCK-8, Hoechst 33258 staining, flow cytometry assay and intracellular reactive oxygen species assay (ROS). Persimmon tannin was pre-incubated with HEK 293T cells for 12 h prior to Gamma irradiation. It was found that pretreatment with persimmon tannin increased cell viability and inhibited generation of Gamma-radiation induced ROS in HEK 293T cells exposed to 8 Gy Gamma-radiation. The percentage of apoptotic cells were only 6.7% when the radiation dose was 8 Gy and pretreated with 200 μg/ml of persimmon tannin. All these results indicated that persimmon tannin offered a potent radioprotective effect on cell vitality and cell apoptosis of Gamma-radiation exposure in HEK 293T cells. This study would serve as a pre-clinical evaluation of persimmon tannin for use in people with radiation protection.

Background: Long noncoding RNAs (lncRNAs) are transcripts longer than ~200 nucleotides with little or no protein-coding capacity. There is evidence that the lncRNAs are involved in a variety of biological functions and are associated with human diseases. The aim of this study was to reveal any potential lncRNA regulatory mechanism in uremia. Methods: Blood samples were obtained from 20 uremic patients not on dialysis and 20 healthy volunteers. The genome-wide analysis of lncRNA expression in peripheral blood mononuclear cells was completed by microarray assay and validated by quantitative real-time reverse transcriptase polymerase chain reaction (real-time qRT-PCR) analysis. Differentially expressed lncRNAs and mRNAs were identified through fold-change filtering. Gene ontology analysis and pathway analysis were performed with the standard enrichment computation method. The relationship between lncRNAs and adjacent protein-coding genes was determined by complex transcriptional loci analysis. Results: We identified thousands of lncRNAs and mRNA that were differentially expressed in uremic patients. Some lncRNAs are transcribed in complex loci with overlapping and antisense patterns relative to adjacent protein-coding genes. Differential expression of ZAP70 and BC133674 (ZAP70-ncRNA) was confirmed by RT-PCR. Conclusions: Some lncRNAs and their associated protein-coding genes are closely related and may be part of a potential regulatory mechanism of uremia, and lncRNAs will provide additional opportunities to advance our understanding of the basic biology of uremia.

microRNAs are a type of small non-coding RNAs which play important roles in post-transcriptional gene regulation, and the characterization of microRNA expression profiling in peripheral blood mononuclear cells (PBMCs) from patients with Klinefelter syndrome requires further investigation. In this study, PBMCs were obtained from patients with Klinefelter syndrome and normal controls. After preparation of small RNA libraries, the two groups of samples were sequenced simultaneously using next generation high-throughput sequencing technology, and novel and known microRNAs were analyzed. A total of 9,772,392 and 9,717,633 small RNA reads were obtained; 8,014,466 (82.01%) and 8,104,423 (83.40%) genome-matched reads, 64 and 49 novel microRNAs were identified in the library of Klinefelter syndrome and the library of healthy controls, respectively. There were 71 known microRNAs with differential expression levels between the two libraries. Clustering of over-represented gene ontology (GO) classes in predicted targets of novel microRNAs in the Klinefelter syndrome library showed that the most significant GO terms were genes involved in the endomembrane system, nucleotide binding and kinase activity. Our data revealed that there are a large number of microRNAs deregulated in PBMCs taken from patients with Klinefelter syndrome, of which certain novel and known microRNAs may be involved in the pathological process of Klinefelter syndrome. Further studies are necessary to determine the roles of microRNAs in the pathological process of Klinefelter syndrome in the future.

Background Mesangial proliferative glomerulonephritis (MePGN) is characterized by excessive mesangial cell proliferation and mesangial matrix expansion, which lead to glomerular sclerosis and obliteration and, in turn, to deteriorating renal function. To identify and quantify the total proteins in renal tissues of MePGN patients, we used isobaric tags for relative and absolute quantification (iTRAQ) technology, and then looked for differentially expressed proteome profiles in MePGN patients. Methods Eight-plex iTRAQ coupled with multiple chromatographic fractionation and tandem mass spectrometry was used to analyze total proteins in renal tissues of MePGN patients. Proteins were identified using Mascot, compared to show any differential expression. Results Among 512 distinct proteins identified, 113 proteins were up-regulated or down-regulated with a onefold or more alteration in levels across groups. Among of them, there was significant variation in our present iTRAQ study, which contains lamin A, actin, profilin-1, annexin-A1 and A2 up-regulated, and antiquitin and aldolase B down-regulated. Conclusion iTRAQ-based quantitative proteomic technology is efficiently applicable for protein identification and relative quantitation of proteomes of renal tissue. Differentially expressed proteome profiles of MePGN patients are determined. Further investigation of the molecular mechanism of the involved proteins may help to better understand the pathogenesis of MePGN and to discover novel biomarker candidates, which may enable the development of new approaches to diagnosis of MePGN.

Background Transcription factors (TFs) play a central role in regulating gene expression and in providing interconnecting regulatory networks between related pathway elements. Systemic lupus erythematosus (SLE) is an organ-nonspecific autoimmune disorder characterized by the production of autoantibodies against a host of nuclear antigens. Aim The pathogenesis of lupus is incompletely understood. Understanding the mechanisms that contribute to SLE and finding effect biomarkers to anticipate SLE will be of great value. Method To investigate possible mechanisms, we describe a comparison of TF activity profiles between SLE and controls. Through TF assay analysis and electrophoretic mobility shift assay (EMSA) confirmation, we identified different activities of TFs in SLE. Results Three hundred and forty-five TFs were detected in both groups, with 92 of them differentially expressed by TF array in which 78 TFs up-regulated and 14 TFs down-regulated in SLE compared with the control group, while 253 TFs showed no significant expression levels. The array data was consistent with the EMSA verification results. Conclusion Our data indicated that TFs may be potentially involved in the pathogenesis of SLE, and can help to diagnose, treat and prevent SLE. The method could simplify the assay of multiple TFs and may facilitate high-throughput profiling of large numbers of TFs.

Proteomics is one of the emerging techniques for biomarker discovery. Biomarkers can be used for early noninvasive diagnosis and prognosis of diseases and treatment efficacy evaluation. In the present study, the well-established research systems of ClinProt Micro solution incorporated unique magnetic bead sample preparation technology, which, based on matrix-assisted laser desorption ionization time-of-flight mass spectrometry (MALDI-TOF MS), have become very successful in bioinformatics due to its outstanding performance and reproducibility for discovery disease-related biomarker. We collected fasting blood samples from patients with biopsy-confirmed acute renal allograft rejection (n = 12), chronic rejection (n = 12), stable graft function (n = 12) and also from healthy volunteers (n = 13) to study serum peptidome patterns. Specimens were purified with magnetic bead-based weak cation exchange chromatography and analyzed with a MALDI-TOF mass spectrometer. The results indicated that 18 differential peptide peaks were selected as potential biomarkers of acute renal allograft rejection, and 6 differential peptide peaks were selected as potential biomarkers of chronic rejection. A Quick Classifier Algorithm was used to set up the classification models for acute and chronic renal allograft rejection. The algorithm models recognize 82.64% of acute rejection and 98.96% of chronic rejection episodes, respectively. We were able to identify serum protein fingerprints in small sample sizes of recipients with renal allograft rejection and establish the models for diagnosis of renal allograft rejection. This preliminary study demonstrated that proteomics is an emerging tool for early diagnosis of renal allograft rejection and helps us to better understand the pathogenesis of disease process.

This study investigated the gain of the human telomerase RNA gene TERC at 3q26 in patients with uterine cervix disease in the southern part of China and assessed the relationship between TERC gain and cervical pathological findings. One hundred ten cervical specimens, which were collected from patients with various kinds of uterine cervix disease that was subsequently diagnosed as chronic cervicitis and with examination results negative for intraepithelial lesion or malignancy (NILM, n = 23), mild dysplasia (cervical intraepithelial neoplasia type 1 [CIN1], n = 37), moderate dysplasia (CIN2, n = 12), severe dysplasia (CIN3, n = 10), and squamous cell carcinoma (SCA, n = 28) confirmed by histologic diagnosis, were analyzed for the proportion of abnormal cells with TERC gain using a commercially available 2-color fluorescence in situ hybridization (FISH) probe. The cases with a higher proportion of abnormal cells than the threshold evaluated by NILM were recorded as positive TERC gain. The chi and Kruskal-Wallis tests were used to assess the associations between FISH findings and diagnoses. The incidence of positive TERC gain in the cases diagnosed as NILM or CIN1 was significantly lower than that in cases diagnosed as CIN2, CIN3, or SCA (P0.01). In addition, a significantly higher proportion of abnormal cells with TERC gain was found as a pathological change from CIN1 to SCA (P0.01). We conclude that the TERC gain seems to be an important associated genetic event in CIN and carcinoma; FISH is a potential tool for the diagnoses of uterine cervix disease.

Systemic lupus erythematosus (SLE) is a multifactorial autoimmune disease which affects different organs and systems that, has a complex genetic inheritance, and is affected by both epigenetic and environmental risk factors. Previous studies on SLE have lacked the statistical power and genetic resolution to fully determine the influence of major histocompatibility complex (MHC) on SLE. In this study, in order to determine this influence, a total of 15 patients with SLE and 15 healthy controls were enrolled. MHC region capture technology, hMeDIP-chip, transcribed ultra-conserved region (T-UCR) microarray and bioinformatics analysis were utilized for both groups. The results revealed methylated CpG enrichment at 6 loci in the MHC segment of SLE. We found 4 single-nucleotide polymorphisms (SNPs) in the CpG promoter of human leukocyte antigen-B (HLA-B) and 2 SNPs in chr6:29521110‑29521833. No significant GO term or KEGG pathway enrichment was noted for an immune-correlated process in the SLE patients for the corresponding CpG-methylated genes. In this study, T-UCR was not discovered in the MHC segment. The analysis of SNPs (rs1050683, rs12697943, rs17881210, rs1065378, rs17184255 and rs16895070) and gene expression in peripheral blood lymphocytes indicated that these SNPs were associated with the occurrence of SLE. Further studies are warranted to examine the roles of these SNPs in the pathogenesis of SLE. Integrative analysis technology provided a view of the molecular signaling pathways in SLE.