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Articles by G Li
Total Records ( 17 ) for G Li
  J Huang , J Gao , X Lv , G Li , D Hao , X Yao , L Zhou , D Liu and R. Wang

Glioma-specific transcription of tumor-killing genes has been exploited as a promising gene therapeutic modality in glioma patients. Musashi1 (Msi1) and GFAP gene promoters are both cancer-specific promoters. Optimized HIF-binding site (optHBS) sequence was newly found as efficient as EPO HREs used as enhancer in cancer gene therapy. We constructed 4optHBS-Msi1/GFAP promoters and tested their ability to mediate BAX expression to induce apoptosis in glioma cell lines. Our results demonstrated that 4optHBS-Msi1/GFAP promoters are apparently strong and glioma-selective promoters with potential application in targeted glioma gene therapy, and 4optHBS-Msi1/GFAP-BAX are valuable tools for glioma gene therapy.

  R. B Schnabel , T Aspelund , G Li , L. M Sullivan , A Suchy Dicey , T. B Harris , M. J Pencina , R. B D'Agostino , D Levy , W. B Kannel , T. J Wang , R. A Kronmal , P. A Wolf , G. L Burke , L. J Launer , R. S Vasan , B. M Psaty , E. J Benjamin , V Gudnason and S. R. Heckbert

Background  We sought to validate a recently published risk algorithm for incident atrial fibrillation (AF) in independent cohorts and other racial groups.

Methods  We evaluated the performance of a Framingham Heart Study (FHS)-derived risk algorithm modified for 5-year incidence of AF in the FHS (n = 4764 participants) and 2 geographically and racially diverse cohorts in the age range 45 to 95 years: AGES (the Age, Gene/Environment Susceptibility-Reykjavik Study) (n = 4238) and CHS (the Cardiovascular Health Study) (n = 5410, of whom 874 [16.2%] were African Americans). The risk algorithm included age, sex, body mass index, systolic blood pressure, electrocardiographic PR interval, hypertension treatment, and heart failure.

Results  We found 1359 incident AF events in 100 074 person-years of follow-up. Unadjusted 5-year event rates differed by cohort (AGES, 12.8 cases/1000 person-years; CHS whites, 22.7 cases/1000 person-years; and FHS, 4.5 cases/1000 person-years) and by race (CHS African Americans, 18.4 cases/1000 person-years). The strongest risk factors in all samples were age and heart failure. The relative risks for incident AF associated with risk factors were comparable across cohorts and race groups. After recalibration for baseline incidence and risk factor distribution, the Framingham algorithm, reported in C statistic, performed reasonably well in all samples: AGES, 0.67 (95% confidence interval [CI], 0.64-0.71); CHS whites, 0.68 (95% CI, 0.66-0.70); and CHS African Americans, 0.66 (95% CI, 0.61-0.71). Risk factors combined in the algorithm explained between 47.0% (AGES) and 63.6% (FHS) of the population-attributable risk.

Conclusions  Risk of incident AF in community-dwelling whites and African Americans can be assessed reliably by routinely available and potentially modifiable clinical variables. Seven risk factors accounted for up to 64% of risk.

  G Li and D. Majumdar

Sufficient conditions are established for the locally D$-optimal design for a nonlinear model to have a minimal number of support points. The conditions are applied to obtain locally D-optimal designs for a one-compartment pharmacokinetic model and a Poisson regression model.

  L. M Chen , G Li , L. R Reitzel , K. B Pytynia , M. E Zafereo , Q Wei and E. M. Sturgis

It is unknown whether population-level racial or ethnic disparities in mortality from squamous cell carcinoma of the head and neck (SCCHN) also occur in the setting of standardized multidisciplinary-team directed care. Therefore, we conducted a matched-pair study that controlled for several potentially confounding prognostic variables to assess whether a difference in survival exists for African American or Hispanic American compared with non-Hispanic white American SCCHN patients receiving similar care. Matched pairs were 81 African American case and 81 non-Hispanic white control patients and 100 Hispanic American cases and 100 matched non-Hispanic white controls selected from 1,833 patients of a prospective epidemiologic study of incident SCCHN within a single, large multidisciplinary cancer center. Matching variables included age (±10 years), sex, smoking status (never versus ever), site, tumor stage (T1-2 versus T3-4), nodal status (negative versus positive), and treatment. Cases and controls were not significantly different in proportions of comorbidity score, alcohol use, subsite distribution, overall stage, or tumor grade. Matched-pair and log-rank analyses showed no significant differences between cases and controls in recurrence-free, disease-specific, or overall survival. Site-specific analyses suggested that more aggressive oropharyngeal cancers occurred more frequently in minority than in non-Hispanic white patients. We conclude that minority and non-Hispanic white SCCHN patients receiving similar multidisciplinary-team directed care at a tertiary cancer center have similar survival results overall. These results encourage reducing health disparities in SCCHN through public-health efforts to improve access to multidisciplinary oncologic care (and to preventive measures) and through individual clinician efforts to make the best multidisciplinary cancer treatment choices available for their minority patients. The subgroup finding suggests a biologically based racial/ethnic disparity among oropharyngeal patients and that prevention and treatment strategies should be tailored to different populations of these patients.

  Z Liu , G Li , S Wei , J Niu , L. E Wang , E. M Sturgis and Q. Wei

Single-nucleotide polymorphisms (SNPs) of TERT-rs2736098 (C > T) and CLPTM1L-rs401681(C > T) at the 5p15.33 locus are significantly associated with cancer risk as reported in genome-wide association studies (GWAS), but there are no reported studies for squamous cell carcinoma of the head and neck (SCCHN). In a case–control study of 1079 SCCHN cases and 1115 cancer-free controls of non-Hispanic whites who were frequency matched by age and sex, we genotyped for these two SNPs and assessed their associations with SCCHN risk. Compared with the CC genotypes of each polymorphism, the associations of a slightly reduced risk of SCCHN with the variant genotypes of CT + TT of both polymorphisms were approaching statistical significance [Odds ratio (OR) = 0.90, 95% confidence interval (CI) = 0.76–1.08 for TERT-rs2736098 and OR = 0.86, 95% CI = 0.71–1.04 for CLPTM1L-rs401681, respectively]. When the two SNPs were combined, the variant genotypes of the two SNPs were significantly associated a moderately reduced risk of SCCHN (OR = 0.82, 95% CI = 0.67–0.99), and the number of variant genotypes was associated with a significantly reduced risk in a dose–response manner (P = 0.028). Furthermore, the reduced risk was more pronounced in ever smokers, ever drinkers and patients with oropharyngeal cancer. Our results suggested that these two SNPs at the 5p15.33 locus may be associated with a reduced risk of SCCHN, particularly for their combined effect. Although we added additional evidence for the association of the two SNPs with cancer risk as reported in GWAS, additional studies are needed to replicate our findings.

  W Zhang , L Wang , Y Liu , J Xu , G Zhu , H Cang , X Li , M Bartlam , K Hensley , G Li , Z Rao and X. C. Zhang

Eukaryotic lanthionine synthetase C-like protein 1 (LanCL1) is homologous to prokaryotic lanthionine cyclases, yet its biochemical functions remain elusive. We report the crystal structures of human LanCL1, both free of and complexed with glutathione, revealing glutathione binding to a zinc ion at the putative active site formed by conserved GxxG motifs. We also demonstrate by in vitro affinity analysis that LanCL1 binds specifically to the SH3 domain of a signaling protein, Eps8. Importantly, expression of LanCL1 mutants defective in Eps8 interaction inhibits nerve growth factor (NGF)-induced neurite outgrowth, providing evidence for the biological significance of this novel interaction in cellular signaling and differentiation.

  S Kaneko , G Li , J Son , C. F Xu , R Margueron , T. A Neubert and D. Reinberg

Ezh2 functions as a histone H3 Lys 27 (H3K27) methyltransferase when comprising the Polycomb-Repressive Complex 2 (PRC2). Trimethylation of H3K27 (H3K27me3) correlates with transcriptionally repressed chromatin. The means by which PRC2 targets specific chromatin regions is currently unclear, but noncoding RNAs (ncRNAs) have been shown to interact with PRC2 and may facilitate its recruitment to some target genes. Here we show that Ezh2 interacts with HOTAIR and Xist. Ezh2 is phosphorylated by cyclin-dependent kinase 1 (CDK1) at threonine residues 345 and 487 in a cell cycle-dependent manner. A phospho-mimic at residue 345 increased HOTAIR ncRNA binding to Ezh2, while the phospho-mimic at residue 487 was ineffectual. An Ezh2 domain comprising T345 was found to be important for binding to HOTAIR and the 5' end of Xist.

  L Laurent , E Wong , G Li , T Huynh , A Tsirigos , C. T Ong , H. M Low , K. W Kin Sung , I Rigoutsos , J Loring and C. L. Wei

DNA methylation is a critical epigenetic regulator in mammalian development. Here, we present a whole-genome comparative view of DNA methylation using bisulfite sequencing of three cultured cell types representing progressive stages of differentiation: human embryonic stem cells (hESCs), a fibroblastic differentiated derivative of the hESCs, and neonatal fibroblasts. As a reference, we compared our maps with a methylome map of a fully differentiated adult cell type, mature peripheral blood mononuclear cells (monocytes). We observed many notable common and cell-type-specific features among all cell types. Promoter hypomethylation (both CG and CA) and higher levels of gene body methylation were positively correlated with transcription in all cell types. Exons were more highly methylated than introns, and sharp transitions of methylation occurred at exon–intron boundaries, suggesting a role for differential methylation in transcript splicing. Developmental stage was reflected in both the level of global methylation and extent of non-CpG methylation, with hESC highest, fibroblasts intermediate, and monocytes lowest. Differentiation-associated differential methylation profiles were observed for developmentally regulated genes, including the HOX clusters, other homeobox transcription factors, and pluripotence-associated genes such as POU5F1, TCF3, and KLF4. Our results highlight the value of high-resolution methylation maps, in conjunction with other systems-level analyses, for investigation of previously undetectable developmental regulatory mechanisms.

  W Zheng , W Wen , Y. T Gao , Y Shyr , Y Zheng , J Long , G Li , C Li , K Gu , Q Cai , X. O Shu and W. Lu

Most of the genetic variants identified from genome-wide association studies of breast cancer have not been validated in Asian women. No risk assessment model that incorporates both genetic and clinical predictors is currently available to predict breast cancer risk in this population.


We analyzed 12 single-nucleotide polymorphisms (SNPs) identified in recent genome-wide association studies mostly of women of European ancestry as being associated with the risk of breast cancer in 3039 case patients and 3082 control subjects who participated in the Shanghai Breast Cancer Study. All participants were interviewed in person to obtain information regarding known and suspected risk factors for breast cancer. The c statistic, a measure of discrimination ability with a value ranging from 0.5 (random classification) to 1.0 (perfect classification), was estimated to evaluate the contribution of genetic and established clinical predictors of breast cancer to a newly established risk assessment model for Chinese women. Clinical predictors included in the model were age at menarche, age at first live birth, waist-to-hip ratio, family history of breast cancer, and a previous diagnosis of benign breast disease. The utility of the models in risk stratification was evaluated by estimating the proportion of breast cancer patients in the general population that could be accounted for above a given risk threshold as predicted by the models. All statistical tests were two-sided.


Eight SNPs (rs2046210, rs1219648, rs3817198, rs8051542, rs3803662, rs889312, rs10941679, and rs13281615), each of which reflected a genetically independent locus, were found to be associated with the risk of breast cancer. A dose–response association was observed between the risk of breast cancer and the genetic risk score, which is an aggregate measure of the effect of these eight SNPs (odds ratio for women in the highest quintile of genetic risk score vs those in the lowest = 1.85, 95% confidence interval = 1.58 to 2.18, Ptrend = 2.5 x 10–15). The genetic risk score, the waist-to-hip ratio, and a previous diagnosis of benign breast disease were the top three predictors of the risk of breast cancer, each contributing statistically significantly (P < .001) to the full risk assessment model. The model, with a c statistic of 0.6295 after adjustment for overfitting, showed promise for stratifying women into different risk groups; women in the top 30% risk group accounted for nearly 50% of the breast cancers diagnosed in the general population.


A risk assessment model that includes both genetic markers and clinical predictors may be useful to classify Asian women into relevant risk groups for cost-efficient screening and other prevention programs.

  Z Xiao , G Li , Y Chen , M Li , F Peng , C Li , F Li , Y Yu , Y Ouyang and Z. Chen

Formalin-fixed, paraffin-embedded (FFPE) tissue specimens represent a potentially valuable resource for protein biomarker investigations. In this study, proteins were extracted by a heat-induced antigen retrieval technique combined with a retrieval solution containing 2% SDS from FFPE tissues of normal nasopharyngeal epithelial tissues (NNET) and three histological types of nasopharyngeal carcinoma (NPC) with diverse differentiation degrees. Then two-dimensional liquid chromatography-tandem mass spectrometry coupled with isobaric tags for relative and absolute quantification (iTRAQ) labeling was employed to quantitatively identify the differentially expressed proteins among the types of NPC FFPE tissues. Our study resulted in the identification of 730 unique proteins, the distributions of subcellular localizations and molecular functions of which were similar to those of the proteomic database of human NPC and NNET that we had set up based on the frozen tissues. Additionally, the relative expression levels of cathepsin D, keratin8, SFN, and stathmin1 identified and quantified in this report were consistent with the immunohistochemistry results acquired in our previous study. In conclusion, we have developed an effective approach to identifying protein changes in FFPE NPC tissues utilizing iTRAQ technology in conjunction with an economical and easily accessible sample preparation method. (J Histochem Cytochem 58:517–527, 2010)

  G Li , A. M Thomas , S. N Hart , X Zhong , D Wu and G. L. Guo

As a unique nuclear receptor with only ligand-binding but no DNA-binding domain, small heterodimer partner (SHP) interacts with many transcription factors to inhibit their function. However, the regulation of SHP expression is not well understood. SHP is highly expressed in the liver, and previous studies have shown farnesoid X receptor (FXR) highly induces SHP by binding to a FXR response element (FXRRE) in the promoter of the Nr0b2 gene, which encodes SHP. The FXR-SHP pathway is critical in maintaining bile acid and fatty acid homeostasis. After genome-wide FXR binding by chromatin immunoprecipitation (ChIP) coupled to massively parallel sequencing (ChIP-seq), a novel FXRRE was found in the 3'-enhancer region of the Nr0b2 gene. This downstream inverted repeat separated by one nucleotide is highly conserved throughout mammalian species. We hypothesized that this downstream FXRRE is functional and may mediate a head-to-tail chromatin looping by interacting with the proximal promoter FRXRE to increase SHP transcription efficiency. In the current study, a ChIP-quantitative PCR assay revealed FXR strongly bound to this downstream FXRRE in mouse livers. The downstream FXRRE is important for FXR-mediated transcriptional activation revealed by luciferase gene transcription activation, as well as by deletion and site-directed mutagenesis. The chromatin conformation capture assay was used to detect chromatin looping, and the result confirmed the two FXRREs located in the Nr0b2 promoter and downstream enhancer interacted to form a head-to-tail chromatin loop. To date, the head-to-tail chromatin looping has not been reported in the liver. In conclusion, our results suggest a mechanism by which activation of FXR efficiently induces SHP transcription is through head-to-tail chromatin looping.

  J. M Alpert , M Kozanek , G Li , B. T Kelly and P. D. Asnis

Hip pain in patients with normal bony anatomy and anterior labral injury may be related to compression of the iliopsoas tendon across the anterior capsulolabral complex. No attempts to characterize the 3-dimensional anatomy of the iliopsoas tendon and its relationship to the acetabular labrum have been reported to date.


The iliopsoas tendon directly overlies the capsulolabral complex. Contribution of the muscle belly and tendon to the overall circumference at the level of the labrum is approximately the same.

Study Design

Descriptive laboratory study.

Materials and Methods

Eight hip joints were dissected and cross-sectional measurements of the iliopsoas muscle-tendon complex were performed using digital calipers and image analysis software.


The iliopsoas tendon in all specimens was located directly anterior to the anterosuperior capsulolabral complex at the 2 to 3 o’clock position. The overall length of the iliopsoas tendon from the lesser trochanter to the acetabular labrum was 75.4 ± 0.9 mm. The circumference of the iliopsoas tendon at the lesser trochanter was 25.5 ± 2.6 mm, the iliopsoas tendon at the level of the labrum was 28.4 ± 2.8 mm, and the iliopsoas tendon–muscle belly complex at the level of the labrum was 63.8 ± 7.4 mm. At the level of the labrum, the iliopsoas is composed of 44.5% tendon and 55.5% muscle belly.


The close anatomic relationship of the iliopsoas tendon to the anterior capsulolabral complex suggests that iliopsoas pathologic changes at this level may lead to labral injury. Additionally, these data suggest that at the level of the labrum, 45% of the tendon–muscle belly complex should be released to release the entire tendinous portion.

Clinical Relevance

Knowledge of the cross-sectional anatomy of the iliopsoas tendon and its relationship to the acetabular labrum will better assist surgeons in treating lesions associated with iliopsoas injury.

  E. K Song , L. S Oh , T. J Gill , G Li , H. R Gadikota and J. K. Seon

The intent of double-bundle anterior cruciate ligament reconstruction is to reproduce the normal anterior cruciate ligament anatomy and improve knee joint rotational stability. However, no consensus has been reached on the advantages of this technique over the single-bundle technique.


We hypothesized that double-bundle anterior cruciate ligament reconstruction could provide better intraoperative stability and clinical outcome than single-bundle reconstruction.

Type of study

Cohort study; Level of evidence, 2.


Forty patients with anterior cruciate ligament injury in one knee were recruited; 20 were allocated to a double-bundle anterior cruciate ligament reconstruction group and 20 to a single-bundle anterior cruciate ligament reconstruction group. Intraoperative stabilities at 30° of knee flexion were compared between the 2 groups using a navigation system. Clinical outcomes including Lysholm knee scores, Tegner activity scores, Lachman and pivot-shift test results, and radiographic stabilities were also compared between the 2 groups after a minimum of 2 years of follow-up.


Intraoperative anterior and rotational stabilities after anterior cruciate ligament reconstruction in the double-bundle group were significantly better than those in single-bundle group (P = .020 and P < .001, respectively). Nineteen patients (95%) in each group were available at a minimum 2-year follow-up. Clinical outcomes including Lysholm knee and Tegner activity scores were similar in the 2 groups at 2-year follow-up (P > .05). Furthermore, stability results of the Lachman and pivot-shift tests, and radiologic findings at 2-year follow-up failed to reveal any significant intergroup differences (P > .05).


Although double-bundle anterior cruciate ligament reconstruction produces better intraoperative stabilities than single-bundle anterior cruciate ligament reconstruction, the 2 modalities were found to be similar in terms of clinical outcomes and postoperative stabilities after a minimum of 2 years of follow-up.

  J Zhu , X Wu , S Goel , N. M Gowda , S Kumar , G Krishnegowda , G Mishra , R Weinberg , G Li , M Gaestel , T Muta and D. C. Gowda

Proinflammatory responses induced by Plasmodium falciparum glycosylphosphatidylinositols (GPIs) are thought to be involved in malaria pathogenesis. In this study, we investigated the role of MAPK-activated protein kinase 2 (MK2) in the regulation of tumor necrosis factor- (TNF-) and interleukin (IL)-12, two of the major inflammatory cytokines produced by macrophages stimulated with GPIs. We show that MK2 differentially regulates the GPI-induced production of TNF- and IL-12. Although TNF- production was markedly decreased, IL-12 expression was increased by 2–3-fold in GPI-stimulated MK2–/– macrophages compared with wild type (WT) cells. MK2–/– macrophages produced markedly decreased levels of TNF- than WT macrophages mainly because of lower mRNA stability and translation. In the case of IL-12, mRNA was substantially higher in MK2–/– macrophages than WT. This enhanced production is due to increased NF-B binding to the gene promoter, a markedly lower level expression of the transcriptional repressor factor c-Maf, and a decreased binding of GAP-12 to the gene promoter in MK2–/– macrophages. Thus, our data demonstrate for the first time the role of MK2 in the transcriptional regulation of IL-12. Using the protein kinase inhibitors SB203580 and U0126, we also show that the ERK and p38 pathways regulate TNF- and IL-12 production, and that both inhibitors can reduce phosphorylation of MK2 in response to GPIs and other toll-like receptor ligands. These results may have important implications for developing therapeutics for malaria and other infectious diseases.

  G Li , M Mongillo , K. T Chin , H Harding , D Ron , A. R Marks and I. Tabas

CHOP turns on ERO1- to release calcium via IP3R and trigger cell death in response to ER stress.

  C. A Kunder , A. L St. John , G Li , K. W Leong , B Berwin , H. F Staats and S. N. Abraham

During infection, signals from the periphery are known to reach draining lymph nodes (DLNs), but how these molecules, such as inflammatory cytokines, traverse the significant distances involved without dilution or degradation remains unclear. We show that peripheral mast cells, upon activation, release stable submicrometer heparin-based particles containing tumor necrosis factor and other proteins. These complexes enter lymphatic vessels and rapidly traffic to the DLNs. This physiological drug delivery system facilitates communication between peripheral sites of inflammation and remote secondary lymphoid tissues.

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