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Articles by X Zhong
Total Records ( 5 ) for X Zhong
  K Kroenke , X Zhong , D Theobald , J Wu , W Tu and J. S. Carpenter

Background  The adverse impact of a high somatic symptom burden is well established for primary care and other noncancer populations with chronic medical disorders.

Methods  This study examines the impact of somatic symptom burden on disability and health care use in patients with cancer experiencing pain, depression, or both. We performed secondary analyses of baseline data from 405 patients with cancer enrolled in a telecare management trial for pain or depression. Somatic symptom burden was measured using a 22-item scale. Multivariable models were conducted to determine the association of somatic symptom burden with the Sheehan Disability Scale (SDS) score, the number of self-reported disability days in the past 3 months, and health care use. Models were adjusted for sociodemographic characteristics, medical comorbidity, and depression and pain severity.

Results  Somatic symptoms were highly prevalent, with 15 of the 22 symptoms reported by more than 50% of patients. The somatic symptom burden was similar across different types and phases of cancer. The mean SDS score (scored 0-10 [not at all disabled to unable to carry out any activities]) was 5.4, and the mean number of self-reported disability days in the past 4 weeks was 16.9. In multivariable models, somatic symptom burden was associated with SDS score (P < .001) and the likelihood of at least 14 disability days in the past 4 weeks (odds ratio, 1.51; 95% confidence interval, 1.19-1.92) but not with increased health care use.

Conclusions  The somatic symptom burden is high in patients with cancer who experience pain or depression. Given the strong association with disability and the high prevalence of many types of symptoms, recognizing and managing somatic symptoms may be important in improving quality of life and functional status regardless of type or phase of cancer.

Trial Registration Identifier: NCT00313573

  H Wang , A Zhao , L Chen , X Zhong , J Liao , M Gao , M Cai , D. H Lee , J Li , D Chowdhury , Y. g Yang , G. P Pfeifer , Y Yen and X. Xu

Human Rap1-interacting protein 1 (RIF1) contributes to the ataxia telangiectasia, mutated-mediated DNA damage response against the dexterous effect of DNA lesions and plays a critical role in the S-phase checkpoint. However, the molecular mechanisms by which human RIF1 conquers DNA aberrations remain largely unknown. We here showed that inhibition of RIF1 expression by small interfering RNA led to defective homologous recombination-mediated DNA double-strand break repair and sensitized cancer cells to camptothecin or staurosporine treatment. RIF1 underwent caspase-dependent cleavage upon apoptosis. We further found that RIF1 was highly expressed in human breast tumors, and its expression status was positively correlated with differentiation degrees of invasive ductal carcinoma of the breast. Our results suggest that RIF1 encodes an anti-apoptotic factor required for DNA repair and is a potential target for cancer treatment.

  J Luan , J Yuan , X Li , S Jin , L Yu , M Liao , H Zhang , C Xu , Q He , B Wen , X Zhong , X Chen , H. L.Y Chan , J. J.Y Sung , B Zhou and C. Ding

Background: Variations in the hepatitis B virus (HBV) genome may develop spontaneously or under selective pressure from antiviral therapy. Such variations may confer drug resistance or affect virus replication capacity, resulting in failure of antiviral therapy.

Methods: A duplex PCR was used to amplify the region of the reverse transcriptase gene, the precore promoter, and the basal core promoter of the HBV genome. Four multiplex primer-extension reactions were used to interrogate 60 frequently observed HBV variants during antiviral therapy. Automated MALDI-TOF mass spectrometry (MS) was used for mutation detection. Capillary sequencing was used to confirm the MS results.

Results: The limit of quantification was 1000 HBV copies/mL for multiplex detection of HBV variants. Fifty-three variants (88.3%) were analyzed successfully in at least 90% of the sera from 88 treatment-naive patients and 80 patients with virologic breakthrough. MS was able to detect twice as many minor variants as direct sequencing while achieving close to full automation. MS and direct sequencing showed only 0.1% discordance in variant calls.

Conclusions: This platform based on multiplex primer extension and MALDI-TOF MS was able to detect 60 HBV variants in 4 multiplex reactions with accuracy and low detection limits.

  X Zhong and S. Z. Ozdemir

Continual increase in the complexity of technologies and innovations has resulted in actors, i.e. individuals or organizations, becoming more dependent on other actor’s knowledge and skills to complement their own skills in the innovation process. As a result, networks have become more and more prominent in affecting the innovation process. Conceptualizing innovation as a search and learning process that results in a successful product, we introduce a two-phase model of collective innovation that accounts for the deliberateness of the innovation process. Using agent-based modeling, we explore how interaction structure among a group of actors affects the speed at which the group can collectively innovate. In addition, we present results from counterfactual simulations to highlight the importance of deliberate search and changing realized connections in modeling collective innovation process. Moreover, we discuss the effects of the structure under different mechanisms of learning and different levels of actor’s learning capabilities.

  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.

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