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Articles by X Sun
Total Records ( 8 ) for X Sun
  H Cheng , N Sun , X Sun , B Chen , F Li , J Feng , L Cheng and Y. Cao

Platinum-based chemotherapeutics are the most common regimens for advanced non-small-cell lung cancer (NSCLC) patients. However, it is difficult to identify platinum resistance in clinical treatment. Genetic factors are thought to represent important determinants of drug efficacy. In this study, we investigated whether single-nucleotide polymorphisms (SNPs) in human mutS homolog 2 (hMSH2) and the human mutL homolog 1 (hMLH1) were associated with the tumor response in advanced NSCLC patients received platinum-based chemotherapy in Chinese population. Totally, 96 patients with advanced NSCLC were routinely treated with cisplatin- or carboplatin-based chemotherapy. The three-dimensional (3D), polyacrylamide gel-based DNA microarray method was used to evaluate the genotypes of hMSH2 gIVS12-6T/C and hMLH1-1151T/A with peripheral lymphocytes. We found that there was a significantly increased chance of treatment response to platinum-based chemotherapy with the hMSH2 gIVS12-6T/C polymorphism. The 3D polyacrylamide gel-based DNA microarray method is accurate, high-throughput, and inexpensive, especially suitable for a large scale of SNP genotyping in population.

  Y. P Tabak , X Sun , R. S Johannes , V Gupta and A. F. Shorr

Background  Acute exacerbations of chronic obstructive pulmonary disease (AECOPDs) often require hospitalization, may necessitate mechanical ventilation, and can be fatal. We sought to develop a simple risk score to determine its severity.

Methods  We analyzed 88 074 subjects admitted with an AECOPD between 2004 and 2006. We used recursive partition to create risk classifications for in-hospital mortality. Need for mechanical ventilation served as a secondary end point. We internally validated the model via 1000 bootstrapping on half of patients and externally validated it on the remaining patients. We assessed predictive ability using the area under the receiver operating curve (AUROC).

Results  The in-hospital mortality rate was 2%. Three variables had high discrimination of outcomes: serum urea nitrogen level greater than 25 mg/dL (to convert to millimoles per liter, multiply by 0.357); acute mental status change, and pulse greater than 109/min. For those without any of the 3 factors, age 65 years or younger further differentiated the lowest-risk group. In those with all 3 factors, the mortality rates were 13.1% (131 in 1000) and 14.6% (146 in 1000) in the derivation and validation cohorts, respectively, compared with 0.3% (3 in 1000) in both cohorts among patients without any of the 3 factors and age 65 years or younger (P < .001). The AUROC for mortality in the 2 cohorts were 0.72 (95% confidence interval [CI], 0.70-0.74) and 0.71 (95% CI, 0.70-0.73), respectively. For mechanical ventilation, the AUROCs were 0.77 (95% CI, 0.75-0.79) for both cohorts.

Conclusions  A simple risk class based on clinical variables easily obtained at presentation predicts mortality and need for mechanical ventilation. It may facilitate the triage and care of patients with AECOPD.

  X Pan , N Gong , J Zhao , Z Yu , F Gu , J Chen , X Sun , L Zhao , M Yu , Z Xu , W Dong , Y Qin , G Fei , C Zhong and T. L. Xu

Reduction of glucose metabolism in brain is one of the main features of Alzheimer’s disease. Thiamine (vitamin B1)-dependent processes are critical in glucose metabolism and have been found to be impaired in brains from patients with Alzheimer’s disease. However, thiamine treatment exerts little beneficial effect in these patients. Here, we tested the effect of benfotiamine, a thiamine derivative with better bioavailability than thiamine, on cognitive impairment and pathology alterations in a mouse model of Alzheimer’s disease, the amyloid precursor protein/presenilin-1 transgenic mouse. We show that after a chronic 8 week treatment, benfotiamine dose-dependently enhanced the spatial memory of amyloid precursor protein/presenilin-1 mice in the Morris water maze test. Furthermore, benfotiamine effectively reduced both amyloid plaque numbers and phosphorylated tau levels in cortical areas of the transgenic mice brains. Unexpectedly, these effects were not mimicked by another lipophilic thiamine derivative, fursultiamine, although both benfotiamine and fursultiamine were effective in increasing the levels of free thiamine in the brain. Most notably, benfotiamine, but not fursultiamine, significantly elevated the phosphorylation level of glycogen synthase kinase-3 and -3β, and reduced their enzymatic activities in the amyloid precursor protein/presenilin-1 transgenic brain. Therefore, in the animal Alzheimer’s disease model, benfotiamine appears to improve the cognitive function and reduce amyloid deposition via thiamine-independent mechanisms, which are likely to include the suppression of glycogen synthase kinase-3 activities. These results suggest that, unlike many other thiamine-related drugs, benfotiamine may be beneficial for clinical Alzheimer’s disease treatment.

  X Sun , C Li , C Zhuang , W. C Gilmore , E Cobos , Y Tao and Z. Dai

Abl interactor 1 (Abi1) is a key regulator of actin polymerization/depolymerization. The involvement of Abi1 in the development of abnormal cytoskeletal functions of cancer cells has recently been reported. It remains unclear, however, how Abi1 exerts its effects in tumor cells and whether it contributes to tumor progression in vivo. We report here a novel function for Abi1 in the regulation of invadopodia formation and Src-inhibitor of differentiation protein 1 (Id1)-matrix metalloproteinase (MMP)-9 pathway in MDA-MB-231 human breast cancer cells. Abi1 is found in the invadopodia of MDA-MB-231 cells. Epigenetic silencing of the Abi1 gene by short hairpin RNA in MDA-MB-231 cells impaired the formation of invadopodia and resulted in downregulation of the Src activation and Id1/MMP-9 expression. The decreased invadopodia formation and MMP-9 expression correlate with a reduction in the ability of these cells to degrade extracellular matrix. Remarkably, the knockdown of Abi1 expression inhibited tumor cell proliferation and migration in vitro and slowed tumor growth in vivo. Taken together, these results indicate that the Abi1 signaling plays a critical role in breast cancer progression and suggest that this pathway may serve as a therapeutic target for the treatment of human breast cancer.

  X Sun , J. j Liu , Y. s Wang , L Wang , G. r Yang , Z. b Zhou , Y. q Li , Y. b Liu and T. y. Li

To evaluate roles of preoperative lymphoscintigraphy for sentinel lymph node biopsy in breast cancer patients.


Five hundred and sixty-five consecutive breast cancer patients were prospectively randomized into groups with or without preoperative lymphoscintigraphy.


In a group with lymphoscintigraphy, 238 patients had sentinel lymph nodes spotted in lymphoscintigram. The visualization of sentinel lymph nodes in lymphoscintigram was not associated with patients' age, primary tumor size and location, histopathologic type and time interval from injection of radiocolloid to lymphoscintigraphy. However, patients with axillary metastasis had a lower identification rate of sentinel lymph nodes by lymphoscintigraphy than those without metastasis (P = 0.003). The identification rate of axillary sentinel lymph nodes was 99.3% in the group and the rate was similar whether there was sentinel lymph nodes spotted in axillary in lymphoscintigram or not (99.6% vs. 98.1%, P = 0.327). The false-negative rate in this group was 4.2%. While in a group without lymphoscintigraphy, the identification rate and the false-negative rate were 99.6% and 4.8%, respectively. There was no significant difference between the two groups in the identification rate of axillary sentinel lymph nodes (P = 0.594) and in the false-negative rate (P = 1.00).


Preoperative lymphoscintigraphy could neither improve the identification rate nor reduce the false-negative rate of breast cancer sentinel lymph node biopsy, and it is not necessary for sentinel lymph node biopsy in breast cancer patients.

  Z Zhen , X Sun , Y Xia , J Ling , Y Cai , J Wang and Z. Guan

Thymic regrowth following chemotherapy has typical clinical and imaging manifestations that can be used to diagnose it prior to pathological diagnosis. We investigated methods for diagnosing thymic regrowth following chemotherapy with non-invasive methods.


Our study included 26 children and adolescents with thymic regrowth following chemotherapy for malignant lymphoma. Computed tomography scans were routinely performed for follow-up observations. After the emergence of new mediastinal masses, patients either underwent Fluorine-18 fluorodeoxyglucose-positron emission tomography scans to identify the characteristics of the mass, or were closely followed up.


Thymic regrowth occurred 1–12 months after the last chemotherapy (mean, 4 months). Computed tomography mostly revealed diffusely enlarged thymic parenchymatous tissues that maintained normal thymic morphology. Computed tomography values were 36.72 ± 9.48 Hu and increased by 5.56 ± 2.62 Hu in contrast enhancement. The mean volume of the mass was 19.2 cm3. Twenty patients underwent positron emission tomography; among them, five (25%) showed no intake of Fluorine-18 fluorodeoxyglucose in the anterior mediastinal mass, and 15 (75%) showed radioactivity distribution in the mass with a mean standardized uptake value of 2.7; the shape was regular and radioactivity distribution was uniform. The mean follow-up duration was 40 months and all patients achieved disease-free survival.


In the absence of pathological diagnosis, thymic regrowth following chemotherapy can be diagnosed by clinical features combined with characteristic manifestations in computed tomography and positron emission tomography scans.

  H Amlal , S Petrovic , J Xu , Z Wang , X Sun , S Barone and M. Soleimani

The anion exchanger Pendrin, which is encoded by SLC26A4 (human)/Slc26a4 (mouse) gene, is localized on the apical membrane of non-acid-secreting intercalated (IC) cells in the kidney cortical collecting duct (CCD). To examine its role in the mediation of bicarbonate secretion in vivo and the apical Cl/HCO3 exchanger in the kidney CCD, mice with genetic deletion of pendrin were generated. The mutant mice show the complete absence of pendrin expression in their kidneys as assessed by Northern blot hybridization, Western blot, and immunofluorescence labeling. Pendrin knockout (KO) mice display significantly acidic urine at baseline [pH 5.20 in KO vs. 6.01 in wild type (WT); P < 0.0001] along with elevated serum HCO3 concentration (27.4 vs. 24 meq/l in KO vs. WT, respectively; P < 0.02), consistent with decreased bicarbonate secretion in vivo. The urine chloride excretion was comparable in WT and KO mice. For functional studies, CCDs were microperfused and IC cells were identified by their ability to trap the pH fluorescent dye BCECF. The apical Cl/HCO3 exchanger activity in B-IC and non-A, non-B-IC cells, as assessed by intracellular pH monitoring, was significantly reduced in pendrin-null mice. The basolateral Cl/HCO3 exchanger activity in A-IC cells and in non-A, non-B-IC cells, was not different in pendrin KO mice relative to WT animals. Urine NH4+ (ammonium) excretion increased significantly, consistent with increased trapping of NH3 in the collecting duct in pendrin KO mice. We conclude that Slc26a4 (pendrin) deletion impairs the secretion of bicarbonate in vivo and reduces apical Cl/HCO3 exchanger activity in B-IC and non-A, non-B-IC cells in CCD. Additional apical Cl/HCO3 exchanger(s) is (are) present in the CCD.

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