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Xiangrui Meng - Top 30 Publications

Brain MR image segmentation based on an improved active contour model.

It is often a difficult task to accurately segment brain magnetic resonance (MR) images with intensity in-homogeneity and noise. This paper introduces a novel level set method for simultaneous brain MR image segmentation and intensity inhomogeneity correction. To reduce the effect of noise, novel anisotropic spatial information, which can preserve more details of edges and corners, is proposed by incorporating the inner relationships among the neighbor pixels. Then the proposed energy function uses the multivariate Student's t-distribution to fit the distribution of the intensities of each tissue. Furthermore, the proposed model utilizes Hidden Markov random fields to model the spatial correlation between neigh-boring pixels/voxels. The means of the multivariate Student's t-distribution can be adaptively estimated by multiplying a bias field to reduce the effect of intensity inhomogeneity. In the end, we reconstructed the energy function to be convex and calculated it by using the Split Bregman method, which allows our framework for random initialization, thereby allowing fully automated applications. Our method can obtain the final result in less than 1 second for 2D image with size 256 × 256 and less than 300 seconds for 3D image with size 256 × 256 × 171. The proposed method was compared to other state-of-the-art segmentation methods using both synthetic and clinical brain MR images and increased the accuracies of the results more than 3%.

Nature, Nurture, and Cancer Risks: Genetic and Nutritional Contributions to Cancer.

It is speculated that genetic variants are associated with differential responses to nutrients (known as gene-diet interactions) and that these variations may be linked to different cancer risks. In this review, we critically evaluate the evidence across 314 meta-analyses of observational studies and randomized controlled trials of dietary risk factors and the five most common cancers (breast, lung, prostate, colorectal, and stomach). We also critically evaluate the evidence across 13 meta-analyses of observational studies of gene-diet interactions for the same cancers. Convincing evidence for association was found only for the intake of alcohol and whole grains in relation to colorectal cancer risk. Three nutrient associations had highly suggestive evidence and another 15 associations had suggestive evidence. Among the examined gene-diet interactions, only one had moderately strong evidence.

Comprehensive Study of the Flow Control Strategy in a Wirelessly Charged Centrifugal Microfluidic Platform with Two Rotation Axes.

Centrifugal microfluidics has been widely applied in the sample-in-answer-out systems for the analyses of nucleic acids, proteins, and small molecules. However, the inherent characteristic of unidirectional fluid propulsion limits the flexibility of these fluidic chips. Providing an extra degree of freedom to allow the unconstrained and reversible pumping of liquid is an effective strategy to address this limitation. In this study, a wirelessly charged centrifugal microfluidic platform with two rotation axes has been constructed and the flow control strategy in such platform with two degrees of freedom was comprehensively studied for the first time. Inductively coupled coils are installed on the platform to achieve wireless power transfer to the spinning stage. A micro servo motor is mounted on both sides of the stage to alter the orientation of the device around a secondary rotation axis on demand during stage rotation. The basic liquid operations on this platform, including directional transport of liquid, valving, metering, and mixing, are comprehensively studied and realized. Finally, a chip for the simultaneous determination of hexavalent chromium [Cr(VI)] and methanal in water samples is designed and tested based on the strategy presented in this paper, demonstrating the potential use of this platform for on-site environmental monitoring, food safety testing, and other life science applications.

Socioeconomic status and prevalence of type 2 diabetes in mainland China, Hong Kong and Taiwan: a systematic review.

China is estimated to have had the largest number of people with diabetes in the world in 2015, with extrapolation of existing data suggesting that this situation will continue until at least 2030. Type 2 diabetes has been reported to be more prevalent among people with low socioeconomic status (SES) in high-income countries, whereas the opposite pattern has been found in studies from low- and middle-income countries. We conducted a systematic review to describe the cross-sectional association between SES and prevalence of type 2 diabetes in Chinese in mainland China, Hong Kong and Taiwan.

Serum uric acid levels and multiple health outcomes: umbrella review of evidence from observational studies, randomised controlled trials, and Mendelian randomisation studies.

Objective To map the diverse health outcomes associated with serum uric acid (SUA) levels.Design Umbrella review.Data sources Medline, Embase, Cochrane Database of Systematic Reviews, and screening of citations and references.Eligibility criteria Systematic reviews and meta-analyses of observational studies that examined associations between SUA level and health outcomes, meta-analyses of randomised controlled trials that investigated health outcomes related to SUA lowering treatment, and Mendelian randomisation studies that explored the causal associations of SUA level with health outcomes.Results 57 articles reporting 15 systematic reviews and144 meta-analyses of observational studies (76 unique outcomes), 8 articles reporting 31 meta-analyses of randomised controlled trials (20 unique outcomes), and 36 articles reporting 107 Mendelian randomisation studies (56 unique outcomes) met the eligibility criteria. Across all three study types, 136 unique health outcomes were reported. 16 unique outcomes in meta-analyses of observational studies had P<10(-6), 8 unique outcomes in meta-analyses of randomised controlled trials had P<0.001, and 4 unique outcomes in Mendelian randomisation studies had P<0.01. Large between study heterogeneity was common (80% and 45% in meta-analyses of observational studies and of randomised controlled trials, respectively). 42 (55%) meta-analyses of observational studies and 7 (35%) meta-analyses of randomised controlled trials showed evidence of small study effects or excess significance bias. No associations from meta-analyses of observational studies were classified as convincing; five associations were classified as highly suggestive (increased risk of heart failure, hypertension, impaired fasting glucose or diabetes, chronic kidney disease, coronary heart disease mortality with high SUA levels). Only one outcome from randomised controlled trials (decreased risk of nephrolithiasis recurrence with SUA lowering treatment) had P<0.001, a 95% prediction interval excluding the null, and no large heterogeneity or bias. Only one outcome from Mendelian randomisation studies (increased risk of gout with high SUA levels) presented convincing evidence. Hypertension and chronic kidney disease showed concordant evidence in meta-analyses of observational studies, and in some (but not all) meta-analyses of randomised controlled trials with respective intermediate or surrogate outcomes, but they were not statistically significant in Mendelian randomisation studies.Conclusion Despite a few hundred systematic reviews, meta-analyses, and Mendelian randomisation studies exploring 136 unique health outcomes, convincing evidence of a clear role of SUA level only exists for gout and nephrolithiasis.

miR-202 Promotes Cell Apoptosis in Esophageal Squamous Cell Carcinoma by Targeting HSF2.

Esophageal squamous cell carcinoma (ESCC) is one of the most common malignant cancers with high mortality around the world. However, the regulatory mechanism of ESCC carcinogenesis is not completely known. Here we demonstrate the novel role of miR-202 in regulating ESCC cell apoptosis. The analysis of data obtained from the GEO database showed that the expression of miR-202 is aberrantly decreased in tumor tissue from ESCC patients and cultured ESCC cell lines. After transfection with miR-202 mimic or inhibitor, the apoptotic capacity of ESCC cells was significantly increased by miR-202 overexpression but reduced by miR-202 repression. We then identified HSF2 as a direct target of miR-202 with the binding site on the 3'-UTR of HSF2 mRNA in ESCC cells. The apoptosis of ESCC cells induced by the miR-202 mimic could be repressed by HSF2 overexpression. Further studies indicated that HSF2 overexpression strongly upregulated the expression of Hsp70 at both the mRNA and protein levels. In addition, HSF2/Hsp70 suppressed ESCC cell apoptosis by preventing caspase 3 activation. In conclusion, miR-202 is a potential tumor suppressor in human ESCC and acts by regulating the apoptosis of ESCC cells by targeting HSF2, in which caspase 3 activation is involved. This might provide a novel therapeutic target for human ESCC.

Suberoyl bis-hydroxamic acid activates Notch1 signaling and induces apoptosis in anaplastic thyroid carcinoma through p53.

Anaplastic thyroid cancer (ATC), usually derived from well-differentiated thyroid cancers is one of the most lethal human endocrine malignancies. In the present study, we report that in human ATC tumor tissue samples exist undetectable Notch1 and the active Notch1 intracellular domain could not be detected in ATC-CAL-62 cells. Interesting, suberoyl bis-hydroxamic acid (SBHA) administration could induce Notch1 intracellular domain levels in a dose-dependent manner, coupled with the increase of p53 and p21. Furthermore, ectopic expression of Notch1 or deletion of p53 with small-interfering RNA was able to abolish the effects of SBHA to elevation of Notch1 and p53 in ATC cells. As a result, SBHA treatment efficiently induced ATC cell apoptosis. These results indicate that SBHA may play antitumor functions via regulating Notch1/p53 signals, and highlight that SBHA could have clinical potential to benefit the therapy of ATC patients.

Physical activity and sedentary behavior can modulate the effect of the PNPLA3 variant on childhood NAFLD: a case-control study in a Chinese population.

The patatin like phospholipase containing domain 3 gene (PNPLA3) rs738409 C > G polymorphism, one of the most important gene polymorphisms involved in hepatic steatosis, has been reported to interact with different nutrients and dietary patterns on Non-Alcoholic Fatty Liver Disease (NAFLD), but no studies have focused on its interaction with physical activity or sedentary behavior. Therefore, this study aims at determining whether physical activity or sedentary behavior could modulate the effect of the PNPLA3 variant on childhood NAFLD.

miR-10a inhibits cell proliferation and promotes cell apoptosis by targeting BCL6 in diffuse large B-cell lymphoma.

The BCL6 (B-Cell Lymphoma 6) gene is a proto-oncogene that is often expressed in diffuse large B-cell lymphomas (DLBCLs). BCL6 loss of function can kill DLBCL cells, demonstrating that BCL6 is necessary for the survival of DLBCL cells and could be a therapeutic target. In this study, we found that BCL6 protein levels were consistently upregulated in DLBCL tissues, whereas its mRNA levels varied randomly in tissues, suggesting that a post-transcriptional mechanism was involved in BCL6 regulation. We used bioinformatics analysis to search for miRNAs, which potentially target BCL6, and identified specific targeting sites for miR-10a in the 3'-untranslated region (3'-UTR) of BCL6. We further identified an inverse correlation between miR-10a levels and BCL6 protein levels, but not mRNA levels, in DLBCL tumor tissue samples. By overexpressing or knocking down miR-10a in DLBCL cells, we experimentally validated that miR-10a directly recognizes the 3'-UTR of the BCL6 transcript and regulated BCL6 expression. Furthermore, we demonstrated that negatively regulating BCL6 by miR-10a suppressed the proliferation and promoted apoptosis of DLBCL cells.

Systematic meta-analyses and field synopsis of genetic and epigenetic studies in paediatric inflammatory bowel disease.

We provide a comprehensive field synopsis of genetic and epigenetic associations for paediatric Inflammatory Bowel Disease (IBD). A systematic review was performed and included 84 genetic association studies reporting data for 183 polymorphisms in 71 genes. Meta-analyses were conducted for 20 SNPs in 10 genes of paediatric Crohn's disease (CD) and for 8 SNPs in 5 genes of paediatric ulcerative colitis (UC). Five epigenetic studies were also included, but formal meta-analysis was not possible. Venice criteria and Bayesian false discovery probability test were applied to assess the credibility of associations. Nine SNPs in 4 genes were considered to have highly credible associations with paediatric CD, of which four variants (rs2066847, rs12521868, rs26313667, rs1800629) were not previously identified in paediatric GWAS. Differential DNA methylation in NOD2 and TNF-α, dysregulated expression in let-7 and miR-124 were associated with paediatric IBD, but not as yet replicated. Highly credible SNPs associated with paediatric IBD have also been implicated in adult IBD, with similar magnitudes of associations. Early onset and distinct phenotypic features of paediatric IBD might be due to distinct epigenetic changes, but these findings need to be replicated. Further progress identifying genetic and epigenetic susceptibility of paediatric IBD will require international collaboration, population diversity and harmonization of protocols.

MicroRNA-202 inhibits tumor progression by targeting LAMA1 in esophageal squamous cell carcinoma.

Esophageal squamous cell carcinoma (ESCC) is one of the most aggressive malignancies in the gastrointestinal tract. Emerging studies have indicated that microRNAs (miRNAs) are strongly implicated in the development and progression of ESCC. Here, we focused on the function and the underlying molecular mechanism of miR-202 in ESCC. The results showed that miR-202 was significantly down-regulated in ESCC tissues and cell lines. Overexpression of miR-202 in ECa-109 and KYSE-510 cells markedly suppressed cell proliferation and cell migration, and induced cell apoptosis. Furthermore, laminin α1 (LAMA1) expression was frequently positive in ESCC tissues and inversely correlated with miR-202 expression. Then we demonstrated that miR-202 targeted 3'-untranslated region (UTR) of LAMA1 and inhibited its protein expression. Additionally, LAMA1 overexpression rescued the proliferation inhibition and cell apoptosis elevation induced by miR-202. MiR-202 also inhibited the protein expression of p-FAK and p-Akt, which were all reversed by LAMA1 overexpression. Taken together, these findings suggest that miR-202 may function as a novel tumor suppressor in ESCC by repressing cell proliferation and migration, and its biological effects may attribute the inhibition of LAMA1-mediated FAK-PI3K-Akt signaling.

miR-367 promotes proliferation and invasion of hepatocellular carcinoma cells by negatively regulating PTEN.

MicroRNAs play important roles in the carcinogenesis of many types of cancers by inhibiting gene expression at posttranscriptional level. However, the roles of microRNAs in hepatocellular carcinoma, are still unclear. Here, we identified that miR-367 promotes hepatocellular carcinoma (HCC) cell proliferation by negatively regulates its target gene PTEN. The expression of miR-367 and PTEN are significantly inverse correlated in 35 HCC patients. In HCC cell line, CCK-8 proliferation assay indicated that the cell proliferation was promoted by miR-367, while miR-367 inhibitor significantly inhibited the cell proliferation. Transwell assay showed that miR-367 mimics significantly promoted the migration and invasion of HCC cells, whereas miR-367 inhibitors significantly reduced cell migration and invasion. Luciferase assays confirmed that miR-367 directly bound to the 3'untranslated region of PTEN, and western blotting showed that miR-367 suppressed the expression of PTEN at the protein levels. This study indicated that miR-367 negatively regulates PTEN and promotes proliferation and invasion of HCC cells. Thus, miR-367 may represent a potential therapeutic target for HCC intervention.

The androgen receptor cytosine-adenine-guanine repeat length contributes to the development of epithelial ovarian cancer.

Ovarian cancer is the main cause of death among women with gynecological malignancies. Androgen and its receptors play an important role in ovarian cancer pathogenesis. Here, We aim to evaluate the relationship between AR CAG and GGN repeat length polymorphisms and Epithelial Ovarian Cancer (EOC) risk in a two-stage, case-control study among Chinese women. The repeat length was analyzed as a categorical variable for CAG_A and GGN_A (average allele), CAG-S and GGN_S (shorter allele), CAG-L and GGN_L (longer allele), respectively. The median value of the repeat length among the controls was used as the cutoff point. Women with longer AR CAG repeats had a decreased risk of developing EOC. The results was replicated in an independent samples. Compared to those with shorter (<22) CAG_A repeat length, women with longer (≥22) CAG_A repeats length had a 31% decreased EOC risk (OR = 0.69, 95% CI: 0.62-0.77, P = 5.06 × 10-11). For CAG_S and CAG_L, the results remain consistent. However, we didn't detected any significant associations for GGN_A, GGN_S, and GGN_L. This should be the first study to examine the association between AR repeat length polymorphisms and ovarian cancer risk in a relatively large group of Asian women.

MicroRNA-24 induces cisplatin resistance by targeting PTEN in human tongue squamous cell carcinoma.

miR-24 is one of the most significantly up-regulated miRNAs in tongue squamous cell carcinoma (TSCC). PTEN plays an important role in the cell survival and cisplatin resistance of multiple cancers. However, it remains unclear what role does function and mechanism of miR-24 and PTEN play in TSCC.

Determination of 16 pesticide residues in fruits and vegetables by QuEChERS-liquid chromatography-tandem mass spectrometry.

A sensitive and convenient liquid chromatography-tandem mass spectrometric method was developed for the determination of 16 pesticides such as imidacloprid, prochloraz, difenoconazole, azoxystrobin, and thiamethoxam in fruits and vegetables. After compared with methanol and acetone-cyclohexane (1:2, v/v), acetonitrile was chosen as the extraction solvent. The samples were extracted by acetonitrile in high-speed homogenization. The extraction solution was cleaned up by liquid-liquid extraction, and the supernatant was collected. In this work, QuEChERS exhibited much higher efficiency than Carbon-NH2 solid-phase extraction in purification. The pigments and organic acids were removed by purge line (150 mg primary secondary amine (PSA) sorbent and 900 mg absolute magnesium sulfate), leading to the decrease of the background interferences. The average recoveries of the 16 pesticides were almost in the range of 75%-111% at the three spiked levels, and the relative standard deviations were less than 16%. The qualitative analysis and quantitative analysis were investigated by LC-MS/MS and matrix-matched calibration curves. The results showed that the method of QuEChERS combined with LC-MS/MS is rapid, accurate and sensitive for the determination of the 16 pesticide residues in fruits and vegetables.

Positive MACC1 expression correlates with invasive behaviors and postoperative liver metastasis in colon cancer.

Metastasis-associated in colon cancer-1 (MACC1), a new gene associated with primary and metastatic colon cancer, promotes tumor cell growth as well as the development of distant metastasis. The aim of this study is to investigate the expression of MACC1 protein in colon cancer and its association with clinicopathological parameters and postoperative liver metastasis.


We describe a parallel iterative least squares solver named LSRN that is based on random normal projection. LSRN computes the min-length solution to min x∈ℝ (n) ‖Ax - b‖2, where A ∈ ℝ (m × n) with m ≫ n or m ≪ n, and where A may be rank-deficient. Tikhonov regularization may also be included. Since A is involved only in matrix-matrix and matrix-vector multiplications, it can be a dense or sparse matrix or a linear operator, and LSRN automatically speeds up when A is sparse or a fast linear operator. The preconditioning phase consists of a random normal projection, which is embarrassingly parallel, and a singular value decomposition of size ⌈γ min(m, n)⌉ × min(m, n), where γ is moderately larger than 1, e.g., γ = 2. We prove that the preconditioned system is well-conditioned, with a strong concentration result on the extreme singular values, and hence that the number of iterations is fully predictable when we apply LSQR or the Chebyshev semi-iterative method. As we demonstrate, the Chebyshev method is particularly efficient for solving large problems on clusters with high communication cost. Numerical results show that on a shared-memory machine, LSRN is very competitive with LAPACK's DGELSD and a fast randomized least squares solver called Blendenpik on large dense problems, and it outperforms the least squares solver from SuiteSparseQR on sparse problems without sparsity patterns that can be exploited to reduce fill-in. Further experiments show that LSRN scales well on an Amazon Elastic Compute Cloud cluster.

Transcriptional regulatory networks in human lung adenocarcinoma.

Lung adenocarcinoma (AC) is the most common histological subtype of lung cancer worldwide and its absolute incidence is increasing markedly. Transcriptional regulation is one of the most fundamental processes in lung AC development. However, high-throughput functional analyses of multiple transcription factors and their target genes in lung AC are rare. Thus, the objective of our study was to interpret the mechanisms of human AC through the regulatory network using the GSE2514 microarray data. Our results identified the genes peroxisome proliferator activated receptor-γ (PPARG), CCAAT/enhancer binding protein β (CEBPB), ets variant 4 (ETV4), Friend leukemia virus integration 1 (FLI1), T-cell acute lymphocytic leukemia 1 (TAL1) and nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 (NFKB1) as hub nodes in the transcriptome network. Among these genes, it appears that: PPARG promotes the PPAR signaling pathway via the upregulation of lipoprotein lipase (LPL) expression, but suppresses the cell cycle pathway via downregulation of growth arrest and DNA-damage-inducible, γ (GADD45G) expression; ETV4 stimulates matrix metallopeptidase 9 (MMP9) expression to induce the bladder cancer pathway; FLI upregulates transforming growth factor, β receptor II (TGFBR2) expression to activate TGF-β signaling and upregulates cyclin D3 (CCND3) expression to promote the cell cycle pathway; NFKB1 upregulates interleukin 1, β (IL-1B) expression and initiates the prostate cancer pathway; CEBPB upregulates IL-6 expression and promotes pathways in cancer; and TAL1 promotes kinase insert domain receptor (KDR) expression to promote the TGF-β signaling pathway. This transcriptional regulation analysis may provide an improved understanding of the molecular mechanisms and potential therapeutic targets in the treatment of lung AC.