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Articles by X Jia
Total Records ( 5 ) for X Jia
  L Zhang , X Jia , X Peng , Q Ou , Z Zhang , C Qiu , Y Yao , F Shen , H Yang , F Ma , J Wang and Z. Yuan

This paper presents an liquid chromatography (LC)/mass spectrometry (MS)-based metabonomic platform that combined the discovery of differential metabolites through principal component analysis (PCA) with the verification by selective multiple reaction monitoring (MRM). These methods were applied to analyze plasma samples from liver disease patients and healthy donors. LC–MS raw data (about 1000 compounds), from the plasma of liver failure patients (n = 26) and healthy controls (n = 16), were analyzed through the PCA method and a pattern recognition profile that had significant difference between liver failure patients and healthy controls (P < 0.05) was established. The profile was verified in 165 clinical subjects. The specificity and sensitivity of this model in predicting liver failure were 94.3 and 100.0%, respectively. The differential ions with m/z of 414.5, 432.0, 520.5, and 775.0 were verified to be consistent with the results from PCA by MRM mode in 40 clinical samples, and were proved not to be caused by the medicines taken by patients through rat model experiments. The compound with m/z of 520.5 was identified to be 1-Linoleoylglycerophosphocholine or 1-Linoleoylphosphatidylcholine through exact mass measurements performed using Ion Trap–Time-of-Flight MS and METLIN Metabolite Database search. In all, it was the first time to integrate metabonomic study and MRM relative quantification of differential peaks in a large number of clinical samples. Thereafter, a rat model was used to exclude drug effects on the abundance of differential ion peaks. 1-Linoleoylglycerophosphocholine or 1-Linoleoylphosphatidylcholine, a potential biomarker, was identified. The LC/MS-based metabonomic platform could be a powerful tool for the metabonomic screening of plasma biomarkers.

  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.

  E. G McFarland , J Garzon Muvdi , X Jia , P Desai and S. A. Petersen

The shoulder is one of the most complex joints in the human body and, as such, presents an evaluation and diagnostic challenge. The first steps in its evaluation are obtaining an accurate history and physical examination and evaluating conventional radiography. The use of other imaging modalities (eg, ultrasound, magnetic resonance imaging and computed tomography) should be based on the type of additional information needed. The goals of this study were to review the current limitations of evidence-based medicine with regard to shoulder examination and to assess the rationale for and against the use of diagnostic physical examination tests.

  E Basch , X Jia , G Heller , A Barz , L Sit , M Fruscione , M Appawu , A Iasonos , T Atkinson , S Goldfarb , A Culkin , M. G Kris and D. Schrag

In cancer treatment trials, the standard source of adverse symptom data is clinician reporting by use of items from the National Cancer Institute’s Common Terminology Criteria for Adverse Events (CTCAE). Patient self-reporting has been proposed as an additional data source, but the implications of such a shift are not understood.


Patients with lung cancer receiving chemotherapy and their clinicians independently reported six CTCAE symptoms and Karnofsky Performance Status longitudinally at sequential office visits. To compare how patient's vs clinician's reports relate to sentinel clinical events, a time-dependent Cox regression model was used to measure associations between reaching particular CTCAE grade severity thresholds with the risk of death and emergency room visits. To measure concordance of CTCAE reports with indices of daily health status, Kendall tau rank correlation coefficients were calculated for each symptom with EuroQoL EQ-5D questionnaire and global question scores. Statistical tests were two-sided.


A total of 163 patients were enrolled for an average of 12 months (range = 1–28 months), with a mean of 11 visits and 67 (41%) deaths. CTCAE reports were submitted by clinicians at 95% of visits and by patients at 80% of visits. Patients generally reported symptoms earlier and more frequently than clinicians. Statistically significant associations with death and emergency room admissions were seen for clinician reports of fatigue (P < .001), nausea (P = .01), constipation (P = .038), and Karnofsky Performance Status (P < .001) but not for patient reports of these items. Higher concordance with EuroQoL EQ-5D questionnaire and global question scores was observed for patient-reported symptoms than for clinician-reported symptoms.


Longitudinally collected clinician CTCAE assessments better predict unfavorable clinical events, whereas patient reports better reflect daily health status. These perspectives are complementary, each providing clinically meaningful information. Inclusion of both types of data in treatment trial results and drug labels appears to be warranted.

  F Sheng , X Jia , A Yep , J Preiss and J. H. Geiger

Escherichia coli glycogen synthase (EcGS, EC is a retaining glycosyltransferase (GT) that transfers glucose from adenosine diphosphate glucose to a glucan chain acceptor with retention of configuration at the anomeric carbon. EcGS belongs to the GT-B structural superfamily. Here we report several EcGS x-ray structures that together shed considerable light on the structure and function of these enzymes. The structure of the wild-type enzyme bound to ADP and glucose revealed a 15.2° overall domain-domain closure and provided for the first time the structure of the catalytically active, closed conformation of a glycogen synthase. The main chain carbonyl group of His-161, Arg-300, and Lys-305 are suggested by the structure to act as critical catalytic residues in the transglycosylation. Glu-377, previously thought to be catalytic is found on the -face of the glucose and plays an electrostatic role in the active site and as a glucose ring locator. This is also consistent with the structure of the EcGS(E377A)-ADP-HEPPSO complex where the glucose moiety is either absent or disordered in the active site.

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