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Articles by X Guo
Total Records ( 7 ) for X Guo
  R Ning , X Zhang , X Guo and Q. Li
 

Nuclear factor kappa B (NF-B) plays a prominent role in the pathogenesis of infectious diseases. Staphylococcus aureus (S. aureus), which can attach to and invade human osteoblasts, is the most common causative agent of osteomyelitis. To determine whether S. aureus can activate NF-B in human osteoblasts and explore the possible factors of activation in response to infection, we used flow cytometry, enzyme-linked immunosorbent assay, immunoblots, and electrophoretic mobility shift assays to quantify the invasion of bacteria, to measure the interleukin-6 (IL-6) of culture supernatants, and to investigate the IB degradation and NF-B activation in human osteoblasts. Moreover, we explored the possible factors responsible for the activation of NF-B by preventing S. aureus from physically touching human osteoblasts or inhibiting the invasion of S. aureus into human osteoblasts under co-culture conditions, by incubating proteinase K-treated or ultraviolet-killed S. aureus with human osteoblasts and by treating human osteoblasts with peptidoglycan (PGN) or lipoteichoic acid (LTA). We found that S. aureus induced the IB degradation and NF-B activation, which could regulate IL-6 secretion in the culture supernatants of human osteoblasts in response to infection. In addition, the maximal IB degradation and NF-B activation in human osteoblasts occurred prior to the maximal invasion of S. aureus. It was the attachment not invasion or the secreted soluble factor(s), PGN, LTA of S. aureus, that could induce the IB degradation and NF-B activation in human osteoblasts. These results indicated that S. aureus can activate NF-B in human osteoblasts and that the attachment of S. aureus is required for this activation in response to infection.

  X Guo , X Xiao , S Li , P Wang , X Jia and Q. Zhang
 

Objective  To identify the genetic locus for X-linked nonsyndromic high myopia in a large Chinese family.

Methods  Phenotypic information and DNA samples were collected from 19 individuals in a Chinese family; 7 had high myopia and 12 were unaffected. We performed a linkage scan on the X chromosome and sequenced several candidate genes.

Results  High myopia in this family, presenting since early childhood and ranging from –6.00 to –15.00 diopters of sphere, is consistent with an X-linked recessive trait. The presence of a normal optic disc and the absence of color visual defects and other systemic abnormalities indicated that high myopia in this family is nonsyndromic. Our linkage analysis mapped the disease locus to Xq28, a 6.1-cM region between DXS8069 and Xqter, with 2-point logarithm of odds scores greater than 2.0 for 5 markers and a maximum logarithm of odds score of 3.59 at  = 0 for 2 markers. Sequence analysis of coding and adjacent intronic regions of GPR50, PRRG3, CNGA2, and BGN did not identify any potential causative mutation.

Conclusions  Nonsyndromic high myopia in a Chinese family was mapped to the MYP1 region, which confirmed and refined this region for high myopia. In addition, our results suggest that color visual defects and optic disc hypoplasia are not necessary signs of high myopia attributed to the MYP1 region.

Clinical Relevance  MYP1 is a common and the best locus for positional cloning of the gene responsible for high myopia. Our results suggest that MYP1 is also responsible for nonsyndromic high myopia.

  X Guo and A. J. Hartemink
 

Motivation: Recent advances in high-throughput experimental techniques have yielded a large amount of data on protein–protein interactions (PPIs). Since these interactions can be organized into networks, and since separate PPI networks can be constructed for different species, a natural research direction is the comparative analysis of such networks across species in order to detect conserved functional modules. This is the task of network alignment.

Results: Most conventional network alignment algorithms adopt a node-then-edge-alignment paradigm: they first identify homologous proteins across networks and then consider interactions among them to construct network alignments. In this study, we propose an alternative direct-edge-alignment paradigm. Specifically, instead of explicit identification of homologous proteins, we directly infer plausibly alignable PPIs across species by comparing conservation of their constituent domain interactions. We apply our approach to detect conserved protein complexes in yeast–fly and yeast–worm PPI networks, and show that our approach outperforms two recent approaches in most alignment performance metrics.

Availability: Supplementary material and source code can be found at http://www.cs.duke.edu/~amink/.

Contact: xinguo@cs.duke.edu

  L Johansson , X Guo , M Waern , S Ostling , D Gustafson , C Bengtsson and I. Skoog
 

The number of people with dementia has increased dramatically with global ageing. Nevertheless, the pathogeneses of these diseases are not sufficiently understood. The present study aims to analyse the relationship between psychological stress in midlife and the development of dementia in late-life. A representative sample of females (n = 1462) aged 38–60 years were examined in 1968–69 and re-examined in 1974–75, 1980–81, 1992–93 and 2000–03. Psychological stress was rated according to a standardized question in 1968, 1974 and 1980. Dementia was diagnosed according to Diagnostic and Statistical Manual of Mental Disorders criteria based on information from neuropsychiatric examinations, informant interviews, hospital records and registry data. During the 35-year follow-up, 161 females developed dementia (105 Alzheimer’s disease, 40 vascular dementia and 16 other dementias). We found that the risk of dementia (hazard ratios, 95% confidence intervals) was increased in females reporting frequent/constant stress in 1968 (1.60, 1.10–2.34), in 1974 (1.65, 1.12–2.41) and in 1980 (1.60, 1.01–2.52). Frequent/constant stress reported in 1968 and 1974 was associated with Alzheimer’s disease. Reporting stress at one, two or three examinations was related to a sequentially higher dementia risk. Compared to females reporting no stress, hazard ratios (95% confidence intervals) for incident dementia were 1.10 (0.71–1.71) for females reporting frequent/constant stress at one examination, 1.73 (1.01–2.95) for those reporting stress at two examinations and 2.51 (1.33–4.77) at three examinations. To conclude, we found an association between psychological stress in middle-aged women and development of dementia, especially Alzheimer’s disease. More studies are needed to confirm our findings and to study potential neurobiological mechanisms of these associations.

  X Guo
  Objective:

This study aims to investigate the association between mode of transportation to work and dyslipidaemia.

Methods:

During the period between January and February 2006, telephone interviews were conducted with 2506 randomly selected urban residents aged 18 years or older in the 8 districts of Beijing, using a multiple stratified random sampling technique. Of the selected individuals, 1024 (40.86%) members of the workforce were subsequently tested for biomarkers (ie, total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C)). Multiple logistic regression modelling was used, adjusted for potential confounders.

Results:

The probability of dyslipidaemia in workers who travel to work by bus, car or taxi is higher than that of workers who walk to work, with prevalence odds ratios (PORs) of 1.99 (95% CI 1.33 to 2.97) and 2.21 (95% CI 1.28 to 3.84), respectively. There is no significant difference in the risk of experiencing dyslipidaemia when workers who ride bicycles are compared with those who walk to work (POR = 1.22, 95% CI 0.83 to 1.78).

Conclusions:

These findings indicate that modes of transportation to work are significantly associated with the prevalence of dyslipidaemia. Prevention education should be emphasised among higher-risk people who usually go to work by car, bus or taxi.

  M McGeachie , R. L. B Ramoni , J. C Mychaleckyj , K. L Furie , J. M Dreyfuss , Y Liu , D Herrington , X Guo , J. A Lima , W Post , J. I Rotter , S Rich , M Sale and M. F. Ramoni
 

Background— Many different genetic and clinical factors have been identified as causes or contributors to atherosclerosis. We present a model of preclinical atherosclerosis based on genetic and clinical data that predicts the presence of coronary artery calcification in healthy Americans of European descent 45 to 84 years of age in the Multi-Ethnic Study of Atherosclerosis (MESA).

Methods and Results— We assessed 712 individuals for the presence or absence of coronary artery calcification and assessed their genotypes for 2882 single-nucleotide polymorphisms. With the use of these single-nucleotide polymorphisms and relevant clinical data, a Bayesian network that predicts the presence of coronary calcification was constructed. The model contained 13 single-nucleotide polymorphisms (from genes AGTR1, ALOX15, INSR, PRKAB1, IL1R2, ESR2, KCNK1, FBLN5, PPARA, VEGFA, PON1, TDRD6, PLA2G7, and 1 ancestry informative marker) and 5 clinical variables (sex, age, weight, smoking, and diabetes mellitus) and achieved 85% predictive accuracy, as measured by area under the receiver operating characteristic curve. This is a significant (P<0.001) improvement on models that use just the single-nucleotide polymorphism data or just the clinical variables.

Conclusions— We present an investigation of joint genetic and clinical factors associated with atherosclerosis that shows predictive results for both cases, as well as enhanced performance for their combination.

 
 
 
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