Daiming Fan

Fourth Military Medical University, Xi’an, Liaoning, China

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Publications (427)1788.56 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Acute variceal bleeding is the most common lethal complication of liver cirrhosis. A meta-analysis was conducted to compare the outcomes of transjugular intrahepatic portosystemic shunt (TIPS) to those of medical/endoscopic therapy for acute variceal bleeding in cirrhotic patients.
    Journal of clinical gastroenterology. 08/2014;
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    ABSTRACT: AbstactBackground and AimThe gut microbiota plays a pivotal role in the intestinal diseases. Fecal microbiota transplantation (FMT) might be a rescue therapy for refractory inflammatory bowel disease. This study aimed to evaluate the safety, feasibility and efficacy of FMT through mid-gut for refractory Crohn's disease (CD).Methods We established standardized laboratory protocol and clinical work flow for FMT. Only refractory CD patients with Harvey-Bradshaw Index (HBI) score ≥ 7 were enrolled for this study. All included patients were treated with single FMT through mid-gut and assessed during follow-up.ResultsMetagenomics analysis showed a high concordance between feces sample and purified fecal microbiota from same donors. Standardized fecal microbiota preparation and clinical flow significantly simplified the practical aspects of FMT. Totally 30 patients were qualified for the present analysis. The rate of clinical improvement and remission based on clinical activity at the first month was 86.7 % (26/30) and 76.7 % (23/30) respectively, which was higher than other assessment points within 15-month follow-up. Patients’ body weight increased after FMT, and the lipid profile improved as well. FMT also showed a fast and continuous significant effect in relieving the sustaining abdominal pain associated with sustaining CD.Conclusions This is a pilot study with the largest sample of patients with refractory CD underwent single FMT. The results demonstrated that FMT through mid-gut might be a safe, feasible, and efficient rescue therapy for refractory CD.
    Journal of Gastroenterology and Hepatology 08/2014; · 3.33 Impact Factor
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    ABSTRACT: Dysregulation of transcription factors (TFs) is associated with tumor progression, but little is known about TF expression patterns in the context of gastric cancer (GC) metastasis. Using array-based profile analysis, we found that 22 TFs showed differential activities between GC cell lines with low- and high-metastatic potential. Of this group of TFs, serum response factor (SRF) was significantly upregulated in metastatic GC cells. SRF expression was frequently elevated in a panel of metastatic GC cells and tissues, and high-level expression of SRF was significantly associated with a more aggressive phenotype and poor prognosis in patients with GC. In GC cell lines, overexpression of SRF potently promoted cell migration and invasion in vitro as well as the formation of intrahepatic and pulmonary metastases in vivo, whereas loss of SRF inhibited GC cell invasion and metastasis. We also performed a microRNA microarray to screen for transcriptional targets of SRF and found that SRF transactivates miR-199a-5p and miR-199a-3p by directly binding to their promoters. We further determined that overexpression of miR-199a-5p, but not miR-199a-3p, increased GC cell invasion and metastasis. In contrast, inhibition of miR-199a-5p impaired the metastatic potential of GC cells in vitro and in vivo, and E-cadherin was identified as a direct and functional target of miR-199a-5p in GC cells. Specifically, our results showed that SRF promotes GC metastasis and the epithelial to mesenchymal transition (EMT) though miR-199a-5p-mediated downregulation of E-cadherin. The present study thus provides insight into the specific biological behavior of SRF in GC metastasis. As increased activity of the SRF/miR-199a-5p/E-cadherin pathway appears to promote GC cell EMT and metastasis, these regulators may therefore be developed as therapeutic targets or biomarkers for GC progression.Cell Death and Differentiation advance online publication, 1 August 2014; doi:10.1038/cdd.2014.109.
    Cell death and differentiation. 08/2014;
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    ABSTRACT: Context.-The expression of membrane-bound complement regulatory proteins (mCRPs) that inhibit the complement system in normal tissues is essential for self-protection against an autologous immune reaction. However, the expression patterns of mCRPs, including CD46, CD55, and CD59, are inconsistent in different types of cancer cells. Objectives.-To determine whether CD46, CD55, and CD59 are differentially expressed in neoplastic and adjacent normal colon tissues and to assess their clinical significance. Design.-Immunohistochemistry was performed on tissue microarrays of cancerous and adjacent normal colon tissues. Results.-The expression levels of CD46, CD55, and CD59 were significantly higher in colon cancer tissues compared with the normal adjacent colon tissues. We found that the expression levels of CD55 and CD59 correlated with the grade of differentiation in colon cancers. In addition, the expression of CD55 and CD59 was greater in stage III and stage IV colon cancers than in stage I and stage II cancers according to staging by the TNM classification. Conclusions.-CD46, CD55, and CD59 are up-regulated in colon cancer. Specifically, CD55 and CD59 are of clinical relevance to differentiation and TNM staging of colon cancer. These data suggest that CD46, CD55, and CD59 have the potential to be used for molecular staging diagnoses and for colon cancer therapies.
    Archives of pathology & laboratory medicine 07/2014; 138(7):910-919. · 2.78 Impact Factor
  • Lina Cui, Yongquan Shi, Ying Han, Daiming Fan
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    ABSTRACT: Unbalanced immune cell populations or immune cell infiltration of the liver can disrupt the immune-privileged state of the liver, resulting in liver injury or fibrosis. Therefore, the treatment for liver diseases involves not only hepatic regeneration but also immunological regulation. Recent studies demonstrated that stem cells, especially mesenchymal stem cells, have the capacity for not only hepatic differentiation but also immunomodulation. In this respect, stem cell therapy could be a realistic aim for liver diseases by modulating the liver regenerative processes and down-regulating immune-mediated liver damage. In this review, we discuss in detail the importance of immune cells in liver injury and repair; the mechanism by which stem cells demonstrate an immune-tolerant phenotype that can be used for allogeneic transplantation; the effect of stem cell transplantation on immune-mediated diseases, especially liver diseases; and the mechanism by which stem cells improve the hepatic microenvironment.
    Expert Review of Clinical Immunology 06/2014; · 2.89 Impact Factor
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    ABSTRACT: Multidrug resistance (MDR) is the most common cause of chemotherapy failure in gastric cancer (GC) treatment; however, the underlying molecular mechanisms remain elusive. Long non-coding RNAs (lncRNAs) can be involved in carcinogenesis, but the effects of lncRNAs on MDR are poorly understood. We show herein that the lncRNA, MRUL (MDR-related and up-regulated lncRNA), located 400 kb downstream of ABCB1 (ATP-binding cassette, sub-family B, member 1), was significantly up-regulated in two multidrug-resistant GC cell sublines, SGC7901/ADR and SGC7901/VCR. Furthermore, the relative expression levels of MRUL in GC tissues were negatively correlated with in vitro growth inhibition rates of GC specimens treated with chemotherapy drugs and indicated a poor prognosis for GC patients. MRUL knockdown in SGC7901/ADR and SGC7901/VCR cells led to increased rates of apoptosis, increased accumulation, and reduced Adriamycin release in the presence of Adriamycin or vincristine. Moreover, MRUL depletion reduced ABCB1 mRNA levels in a dose- and time-dependent manner. Heterologous luciferase reporter assays demonstrated that MRUL might positively affect ABCB1 expression in an orientation- and position-independent manner. Our findings indicate that MRUL plays a positive role in the regulation of ABCB1 expression and is a potential target to reverse the MDR phenotype of GC MDR cell sublines.
    Molecular and cellular biology. 06/2014;
  • X Qi, S Hu, W Hou, J Jia, G Han, D Fan
    Journal of Gastroenterology and Hepatology 06/2014; 29(6). · 3.33 Impact Factor
  • X. Qi, D. Fan, G. Han
    Alimentary Pharmacology & Therapeutics 06/2014; 39(12). · 4.55 Impact Factor
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    ABSTRACT: FOXO4, a member of the FOXO family of transcription factors, is currently the focus of intense study. Its role and function in gastric cancer have not been fully elucidated. The present study was aimed to investigate the expression profile of FOXO4 in gastric cancer and the effect of FOXO4 on cancer cell growth and metastasis.
    BMC Cancer 05/2014; 14(1):378. · 3.33 Impact Factor
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    ABSTRACT: Ran, a member of the RasGTPase family, has been showed to function in diverse cellular processes of cancer. In the present study, we examined the effects of Ran on the cell motility in pancreatic cancer cells and explored the possible mechanism of Ran's function in the metastasis of pancreatic cancer. We demonstrated that the expression of Ran was remarkably higher in lymph lode metastases than in primary pancreatic cancer tissues. In the functional studies, stable knockdown of Ran by shRNA could efficiently inhibit the migration and invasion of pancreatic cancer cells both in vitro and in vivo. By PCR array, we analyzed the differences in the expression levels of metastasis-associated genes before and after the downregulation of Ran, and it was showed that the regulation of pancreatic cancer metastasis by Ran was partially mediated by AR and CXCR4. We further confirmed that AR and CXCR4 were significantly decreased following knockdown of Ran. These data indicated that Ran could regulate the invasion and metastasis of pancreatic cancer cells through AR and CXCR4.
    Cancer biology & therapy 05/2014; 15(8). · 3.29 Impact Factor
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    ABSTRACT: FOXJ1 is a member of the forkhead transcription factor family, which has been mostly studied for its role in the development of ciliated epithelium and immunology. However, the role of FOXJ1 in tumorigenesis remains largely unknown or even conflicting. We thus investigated FOXJ1 expression in gastric cancer and analyzed its correlations with tumor progression and prognosis. The expression of FOXJ1 was detected by immunohistochemistry in 105 gastric cancer samples and adjacent noncancerous tissues. Staining evaluation was conducted to assess clinicopathological parameters and the survival rate. In addition, the relation between FOXJ1 and metastasis was investigated in another 40 pairs of primary lesions and corresponding lymph node metastases. Furthermore, cell proliferation, migration, and invasion were confirmed in vitro. Decreased FOXJ1 expression was significantly correlated with clinic stage, lymph node metastasis, and distant metastasis, and lower FOXJ1 expression independently predicted shorter survival time in gastric carcinoma. Moreover, the positive incidence of FOXJ1 decreased significantly in metastatic lymph nodes compared with that in the primary lesions. Consistently, FOXJ1 overexpression significantly weakened cell proliferation, motility, migration, and invasion, while FOXJ1 knockdown induced the opposite effects. Decreased expression of FOXJ1 is an independent prognostic predictor for gastric cancer and is critical to disease progression. FOXJ1 may be an attractive therapeutic target for the treatment of gastric cancer.
    Annals of Surgical Oncology 05/2014; · 4.12 Impact Factor
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    ABSTRACT: Surgical treatment does not cure Crohn's disease, and postoperative recurrence is a feature of the clinical course of the disease. Ileocolonoscopy remains the gold standard for the surveillance of recurrent Crohn's disease and should be performed 6-12 months after an operation. Many other non-invasive techniques are also useful and complement endoscopy for the early diagnosis of postoperative recurrence. Anti-TNF agents show great efficacy for the prevention of postoperative recurrence, and long-term use can maintain remission. It remains undetermined whether early treatment after postoperative endoscopic recurrence is ultimately as efficacious as prophylactic therapy.
    Expert review of gastroenterology & hepatology 05/2014;
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    ABSTRACT: This study aimed to test the exact functions and potential mechanisms of miR-17-5p in gastric cancer. Using real-time PCR, miR-17-5p was found to be expressed more highly in gastric cancer compared with-normal tissues. Gain- and loss-of-function assays demonstrated that miR-17-5p increased the proliferation and growth of gastric cancer cells in vitro and in vivo. Through reporter gene and western blot assays, SOCS6 was shown to be a direct target of miR-17-5p, and proliferative assays confirmed that SOCS6 exerted opposing function to that of miR-17-5p in gastric cancer. In short, miR-17-5p might function as a pro-proliferative factor by repressing SOCS6 in gastric cancer.
    FEBS letters 05/2014; · 3.54 Impact Factor
  • European journal of gastroenterology & hepatology 05/2014; 26(5):576-7. · 1.66 Impact Factor
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    ABSTRACT: Background Use of TIPSS is associated with increases in ammonia concentration and hepatic encephalopathy (HE) risk. l-ornithine-l-aspartate (LOLA) is effective in reducing ammonia concentration.AimTo evaluate the effects of LOLA on venous ammonia concentration after TIPSS.Methods The included patients were randomised to receive LOLA or no-LOLA treatment for 7 days. Fasting and post-prandial venous ammonia levels were the primary outcomes. Psychometric performance, post-TIPSS HE, and liver and renal function were assessed as secondary outcomes.ResultsOf 133 cirrhotic patients who received successful TIPSS between November 2011 and June 2012, 40 met the inclusion criteria and were randomised to the LOLA (n = 21) or control (n = 19) groups. Change in fasting ammonia significantly favoured the LOLA group at days 4 (P = 0.001) and 7 (P = 0.003). Changes in post-prandial ammonia concentration significantly favoured the LOLA group at days 1, 4 and 7 as well. During the study period, patients in the LOLA group had better improvement in psychometric tests than those in the control group. Overt HE during treatment was observed in one patient in the LOLA group and three patients in the control group (P = 0.331). There were no differences in complications, adverse events or mortality between the two groups.Conclusions Prophylactic use of LOLA infusion after TIPSS is safe and effective in significantly reducing the increase of venous ammonia concentration, and can benefit the patient's mental status as well.
    Alimentary Pharmacology & Therapeutics 05/2014; · 4.55 Impact Factor
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    ABSTRACT: We conducted a systematic review and meta-analysis to evaluate the associations of the coagulation factor V (encoded by F5) Leiden (FVL) or prothrombin (encoded by F2) G20210A mutation with Budd-Chiari syndrome or portal vein thrombosis (PVT). Relevant articles were identified in searches of the PubMed, EMBASE, Cochrane Library, and ScienceDirect databases. The prevalence of the FVL and prothrombin G20210A mutations were compared between patients with Budd-Chiari syndrome or PVT without cirrhosis and healthy individuals (controls) and between patients with cirrhosis, with and without PVT. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated. We initially identified 869 articles, and included 27 in our final analysis. Compared with controls, patients with Budd-Chiari syndrome had a significantly higher prevalence of the FVL mutation (OR=6.21; 95% CI, 3.93-9.79) and a similar prevalence of the prothrombin G20210A mutation (OR=1.90; 95% CI, 0.69-5.23); patients with PVT without cirrhosis had a significantly higher prevalence of the FVL mutation (OR=1.85, 95%CI: 1.09-3.13) or the prothrombin G20210A mutation (OR=5.01; 95% CI, 3.03-8.30). Compared to patients with cirrhosis without PVT, patients with cirrhosis and PVT had a significantly higher prevalence of the FVL mutation (OR=2.55; 95% CI, 1.29-5.07). We observed a trend toward a higher prevalence of the prothrombin G20210A mutation in patients with cirrhosis and PVT, but the difference was not statistically significant (OR=2.93; 95% CI, 0.94-9.07). Based on a meta-analysis, the FVL mutation is associated with an increased risk of Budd-Chiari syndrome, PVT without cirrhosis, and PVT in liver cirrhosis. The prothrombin G20210A mutation is associated with PVT, but not Budd-Chiari syndrome. Studies are needed to confirm these findings in different racial and ethnic groups.
    Clinical gastroenterology and hepatology: the official clinical practice journal of the American Gastroenterological Association 04/2014; · 5.64 Impact Factor
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    ABSTRACT: Understanding the mechanism underlying multidrug resistance and identifying effective targets that can overcome it is of critical importance. In this study, mRNA and miRNA expression profiling of the drug resistant sublines, SGC7901/VCR and SGC7901/ADR, and their parental gastric cancer cell line SGC7901 were performed. A significant number of genes and a limited subset of miRNAs were commonly dysregulated, which were further validated using qRT-PCR. GO and KEGG pathway analyses of the commonly dysregulated genes indicated that the MAPK signalling pathway may be involved in multidrug resistance, which was further validated using immunoblotting and MTT assay. Finally a primary multidrug resistance network in gastric cancer, consisting of the commonly dysregulated genes and miRNAs, was established and functional miRNA-mRNA pairs were identified. The commonly dysregulated genes and miRNAs identified in this study may represent good therapeutic targets and further study of these targets may increase our understanding of the mechanisms underlying multidrug resistance.
    Cancer letters 04/2014; · 4.86 Impact Factor
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    ABSTRACT: Introduction: Although chemotherapy is an important therapeutic strategy for gastrointestinal cancer, its clinical effect remains unsatisfied due to drug resistance. Drug resistance is a complex multistep process resulting from deregulated expression of many molecules, including tumor suppressor genes, oncogenes and microRNAs (miRNAs). A better understanding of drug resistance-related miRNAs may eventually lead to optimized therapeutic strategies for cancer patients. Areas covered: This review summarizes the recent advances of drug resistance-related miRNAs in esophageal, gastric and colorectal cancer. Furthermore, this study envisages future developments toward the clinical applications of these miRNAs to cancer therapy. Expert opinion: Drug resistance-related miRNAs may be potentially predicting biomarkers that help guide individualized chemotherapy. Specific miRNAs and their target genes can be used as therapeutic targets by reversing drug resistance. More investigations should be performed to promote the translational bridging of the latest research into clinical application.
    Expert opinion on biological therapy 04/2014; · 3.22 Impact Factor
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    Xingshun Qi, Guohong Han, Daiming Fan
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    ABSTRACT: Portal vein thrombosis (PVT) is a fairly common complication of liver cirrhosis. Importantly, occlusive PVT might influence the prognosis of patients with cirrhosis. Evidence from a randomized controlled trial has shown that anticoagulation can prevent the occurrence of PVT in patients with cirrhosis without prior PVT. Evidence from several case series has also demonstrated that anticoagulation can achieve portal vein recanalization in patients with cirrhosis and PVT. Early initiation of anticoagulation therapy and absence of previous portal hypertensive bleeding might be positively associated with a high rate of portal vein recanalization after anticoagulation. However, the possibility of spontaneous resolution of partial PVT questions the necessity of anticoagulation for the treatment of partial PVT. In addition, a relatively low recanalization rate of complete PVT after anticoagulation therapy suggests its limited usefulness in patients with complete PVT. Successful insertion of a transjugular intrahepatic portosystemic shunt (TIPS) not only recanalizes the thrombosed portal vein, but also relieves the symptomatic portal hypertension. However, the technical difficulty of TIPS potentially limits its widespread application, and the risk and benefits should be fully balanced. Notably, current recommendations regarding the management of PVT in liver cirrhosis are insufficient owing to low-quality evidence.
    Nature Reviews Gastroenterology &#38 Hepatology 04/2014; · 10.43 Impact Factor
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    ABSTRACT: AimsA systematic review and meta-analysis were conducted to explore the role of the methylenetetrahydrofolate reductase (MTHFR) C677T gene mutation and hyperhomocysteinemia in patients with Budd-Chiari syndrome (BCS) and portal vein thrombosis (PVT).Methods PubMed, EMBASE, Cochrane library, and ScienceDirect databases were searched. Eligible studies should compare the prevalence of the MTHFR C677T mutation or hyperhomocysteinemia or the homocysteine levels between BCS or non-cirrhotic PVT patients and healthy controls or between cirrhotic patients with and without PVT. A pooled odds ratio (OR) or weighted mean difference (WMD) with 95% confidence interval (CI) was calculated.ResultsOf the 484 articles retrieved, 20 were included. BCS and non-cirrhotic PVT patients had a higher prevalence of homozygous MTHFR mutation than healthy controls. The difference was statistically significant in BCS patients (OR=2.01, 95%CI:1.12-3.61), but not in non-cirrhotic PVT patients (OR=1.72, 95%CI:0.90-3.29). BCS and non-cirrhotic PVT patients had a significantly higher prevalence of hyperhomocysteinemia (BCS: OR=2.57, 95%CI:1.19-5.51; PVT: OR=4.21, 95%CI:1.01-17.54) and homocysteine level (BCS: WMD=3.30, 95%CI:0.94-5.66; PVT: WMD=2.40, 95%CI:0.17-4.63) than healthy controls. Cirrhotic patients with PVT had a significantly higher prevalence of homozygous MTHFR mutation (OR=2.44, 95%CI:1.58-3.76) than those without PVT. But the association between homocysteine level and PVT in cirrhotic patients was inconsistent among three studies.Conclusion Homozygous MTHFR mutation and hyperhomocysteinemia might be associated with the occurrence of BCS and non-cirrhotic PVT. In addition, homozygous MTHFR mutation might increase the risk of PVT in cirrhotic patients. However, the current evidence failed to support the association of hyperhomocysteinemia with PVT in cirrhotic patients.
    Hepatology Research 04/2014; · 2.07 Impact Factor

Publication Stats

5k Citations
1,788.56 Total Impact Points


  • 2000–2014
    • Fourth Military Medical University
      • • State Key Laboratory of Cancer Biology
      • • Department of Gastroenterology
      Xi’an, Liaoning, China
    • Virginia Commonwealth University
      • School of Medicine
      Richmond, VA, United States
  • 2009–2011
    • State Key Laboratory of Medical Genetics of China
      Ch’ang-sha-shih, Hunan, China
  • 1998–2010
    • Xi'an Jiaotong University
      • • School of Science
      • • Department of Gastroenterology
      Xi’an, Shaanxi Sheng, China
  • 2008
    • Logistical College of Chinese People's Armed Police Force
      T’ien-ching-shih, Tianjin Shi, China
  • 2004
    • Huazhong University of Science and Technology
      Wu-han-shih, Hubei, China
  • 2002
    • General Hospital of Jinan Military Region
      Chi-nan-shih, Shandong Sheng, China
  • 2001–2002
    • Southern Medical University
      Shengcheng, Guangdong, China
  • 1997–2001
    • Emory University
      • Department of Internal Medicine
      Atlanta, GA, United States