Yi Miao

Nanjing Medical University, Nan-ching, Jiangsu, China

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Publications (115)325.12 Total impact

  • J. Wei · X. Liu · Y. Fu · W. Gao · K. Jiang · Z. Zhang · Y. Miao

    No preview · Article · Jan 2016 · Pancreatology
  • B. Xiao · K. Jiang · J. Wu · W. Gao · J. Chen · J. Wei · F. Guo · Z. Lu · Y. Miao

    No preview · Article · Jan 2016 · Pancreatology
  • K. Jiang · J. Wu · W. Gao · J. Chen · J. Wei · F. Guo · Z. Lu · P. Wu · Y. Miao

    No preview · Article · Jan 2016 · Pancreatology
  • J. Wei · B. Chen · X. Liu · W. Xu · Z. Lu · J. Chen · F. Guo · K. Jiang · C. Dai · Y. Miao

    No preview · Article · Jan 2016 · Pancreatology
  • D. Huang · Q. Li · C. Dai · K. Jiang · J. Wu · W. Gao · J. Wei · J. Chen · F. Guo · Z. Lu · Y. Miao

    No preview · Article · Jan 2016 · Pancreatology
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    ABSTRACT: Pancreatic adenocarcinoma (PDAC) and chronic pancreatitis (CP) are characterized by a desmoplastic reaction involving activated pancreatic stellate cells (PSCs). However, the mechanisms of PSC activation remain poorly understood. We examined whether the epithelial-mesenchymal transition (EMT) process might play a role in PSC activation. PSCs were isolated from a rat pancreas and characterized using immunofluorescence and immunocytochemistry. We evaluated changes in cell motility and in the expression levels of a panel of EMT-related genes during the PSC activation process. Activation of PSCs occurred after 48 h of in vitro culture, as indicated by a morphological change to a myofibroblastic shape and a decrease in the number of cytoplasmic lipid droplets. After activation, PSCs showed enhanced cell migration ability compared to quiescent cells. In addition, the expression of epithelial markers (E-cadherin, BMP7 and desmoplakin) decreased, while expression of mesenchymal markers (N-cadherin, vimentin, fibronectin1, collagen1α1 and S100A4) increased in activated PSCs. EMT-related transcription factors (Snail and Slug) were also upregulated after PSC activation. The concurrent increase in cell migration ability and alterations in EMT-related gene expression suggests that the activation of PSCs involves an EMT-like process. The knowledge that PSC activation involves an EMT‑like process may help to identify potential new therapeutic targets to alleviate pancreatic fibrosis in diseases like CP and PDAC.
    No preview · Article · Dec 2015 · International Journal of Oncology
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    ABSTRACT: Background: Delayed gastric emptying (DGE) is one of the most troublesome complications after classical pancreaticoduodenectomy (PD) or pylorus-preserving PD. Whether the route of gastroenteric reconstruction has any influence on DGE remains controversial. The aim of this study was to investigate the influence of different types of gastroenteric anastomosis on DGE after PD/PPPD. Methods: A systematic search of literature databases (Cochrane Library, PubMed, EMBASE, and Web of Science) was performed to identify eligible studies. Cochrane collaboration's tool for assessing risk of bias was utilized to evaluate the quality of included studies. The primary outcome was DGE incidence rate. Further outcomes included mortality, morbidity, and other operation related events. Random-effect or fix-effect models were used as appropriate. Results: Five randomized controlled trials (RCTs) including a total of 530 patients were identified and included in the analysis. Based on these studies, no difference was found in DGE incidence between antecolic and retrocolic groups (relative risk [RR], 0.82; 95% confidence interval [CI], 0.51-1.32; P = 0.41). Mortality, morbidity, and operation related events were not significantly different between groups. Conclusions: Results of the meta-analysis reveal that DGE occurrence is not affected by route of gastroenteric anastomosis. Anastomosis approach should be chosen according to the surgeons' preference.
    No preview · Article · Dec 2015 · Pancreatology
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    ABSTRACT: Objective: To identify potential risk factors associated with pancreatic infection in severe acute pancreatisis (SAP) patients, thus providing evidence for clinical prediction and treatment. Methods: A total of 42 patients with SAP collected in our hospital from January 2013 to July 2014 were divided into two groups according to the presence or absence of pancreatic infection and retrospectively analyzed. Clinical characteristics and laboratory examine results of the two groups including age, sex, APACHE II score, serum amylase, serum calcium, blood glucose, ALT, AST, hyoxemia, serum albumin, serum creatinine and blood urea nitrogen were investigated for their relevance to pancreatic infection. Results: The overall occurrence of secondary pancreatic infection of the 42 patients was 52.38%. A significantly positive correlation was revealed between the incidence rate of the secondary pancreatic infection and the factors including hyoxemia, blood creatinine and urea nitrogen in SAP patients (P < 0.05 or P < 0.01). Meanwhile, the level of serum albumin was negatively correlated with the rate of secondary infection in SAP patients (P < 0.01). The rest factors showed no significant correlation (P > 0.05). Conclusion: Hyoxemia, blood creatinine and urea nitrogen are potential factors leading to pancreatic infection in SAP patients, while an increase of serum albumin may reduce the incidence of infection.
    No preview · Article · Nov 2015 · International Journal of Clinical and Experimental Medicine
  • D. Huang · Q. Li · C. Dai · K. Jiang · J. Wu · W. Gao · J. Wei · J. Chen · F. Guo · Z. Lu · Y. Miao

    No preview · Article · Nov 2015 · Pancreas
  • W. Gao · K. Jiang · J. Wu · Q. Li · F. Guo · J. Chen · J. Wei · Z. Lu · M. Tu · X. Dai · C. Dai · Y. Miao

    No preview · Article · Nov 2015 · Pancreas
  • J. Chen · N. Lv · K. Jiang · C. Dai · W. Gao · Q. Li · J. Wu · J. Wei · F. Guo · Z. Lu · Y. Miao

    No preview · Article · Nov 2015 · Pancreas
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    ABSTRACT: The abnormal change of octamer transcription factor 4 (OCT4) is associated with tumor progression; however, its effect on hepatocellular carcinoma (HCC) behavior remains unclear. The purpose of this study was to determine the correlation between HCC and OCT4. In the present study, IHC, western blot analysis, and QRT-PCR were performed to identify differentially expressed OCT4 in a series of HCC tissues and adjacent non-cancerous tissues. In addition, the functions of OCT4 on HCC progression were studied in vitro. Silencing of OCT4 with siRNA was performed in HCC cell lines, and the impact on proliferation, migration, and the EMT marker of HCC was analyzed. Our results found that OCT4 levels were significantly higher in HCC tissues compared with the adjacent non-cancerous tissues. Furthermore, OCT4 siRNA significantly reduced the proliferation rate of SMMC-7721 and HepG2 cells, inhibited the migration and inversion, and could reverse EMT in HCC cells, indicating that OCT4 plays a critical role in HCC progression. Our data suggest that the pathogenesis of human HCC may be mediated by OCT4, and thus, OCT4 could represent selective targets for the molecularly targeted treatments of HCC.
    No preview · Article · Oct 2015 · Tumor Biology

  • No preview · Article · Oct 2015 · Journal of the American College of Surgeons

  • No preview · Article · Oct 2015 · Journal of the American College of Surgeons
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    ABSTRACT: The safety of vascular closure devices (VCDs) is still debated. The emergence of more related randomized controlled trials (RCTs) and newer VCDs makes it necessary to further evaluate the safety of VCDs. Relevant RCTs were identified by searching PubMed, EMBASE, Google Scholar and the Cochrane Central Register of Controlled Trials electronic databases updated in December 2014. Traditional and network meta-analyses were conducted to evaluate the rate of combined adverse vascular events (CAVEs) and haematomas by calculating the risk ratios and 95% confidence intervals. Forty RCTs including 16868 patients were included. Traditional meta-analysis demonstrated that there was no significant difference in the rate of CAVEs between all the VCDs and manual compression (MC). Subgroup analysis showed that FemoSeal and VCDs reported after the year 2005 reduced CAVEs. Moreover, the use of VCDs reduced the risk of haematomas compared with MC. Network meta-analysis showed that AngioSeal, which might be the best VCD among all the included VCDs, was associated with reduced rates of both CAVE and haematomas compared with MC. In conclusion, the use of VCDs is associated with a decreased risk of haematomas, and FemoSeal and AngioSeal appears to be better than MC for reducing the rate of CAVEs.
    Preview · Article · Sep 2015 · Scientific Reports
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    ABSTRACT: Background/aims: Primary biliary cirrhosis (PBC), an autoimmune disease of the liver, is marked by slow progressive destruction of bile ducts. These patients with PBC often undergo orthotopic liver transplantation (OLT). Ischemic bile duct lesion (IBDL) is a major source of morbidity and even mortality after OLT. Cirrhosis of the liver has a higher tolerance to ischemia than a normal liver, but the mechanism remains unknown. Angiogenesis and proliferation of bile duct often responses in bile duct ischemia, which may enhance ischemic tolerance in patients with cirrhosis. Methodology: To test the hypothesis, a rat model with cirrhosis was established. Biochemical indexes of ischemic severity were measured including total bilirubin (TBIL) and direct bilirubin (DBIL). Immunohistochemical assay was performed for Ki67 (a biomarker for the proliferation of bile duct) and CD34 (a biomarker of angiogenesis). Results: The levels were lower for TBIL and DBIL in the bile duct from rat model with cirrhosis than that from a normal rat after ischemic surgery (P < 0.05). The levels were higher for Ki67 and CD34 from a rat model with cirrhosis than that from a normal rat after ischemic surgery (P < 0.05). Conclusions: The results suggest that a liver with cirrhosis has a better ischemic tolerance than a normal liver. Angiogenesis and proliferation of bile duct enhances ischemic tolerance in rats with cirrhosis. More research on the pathogenesis of IBDLs is needed for developing more specific preventive or therapeutic strategies.
    No preview · Article · Aug 2015 · International Journal of Clinical and Experimental Medicine
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    ABSTRACT: As a member of the vasohibin (VASH2) family, VASH2 is localized intracellularly as a nuclear and cytoplasmic type. Cytoplasmic VASH2 is associated with carcinoma angiogenesis and malignant transformation and promotes cancer growth. However, the function of nuclear VASH2 has yet to be investigated. The aim of the present study was to detect the nuclear VASH2 expression profile in human organs and tissues by protein microarray technique. To examine the function of nuclear VASH2, we analyzed the relationship between nuclear VASH2 and Ki-67, and stably constructed VASH2 overexpression and knockdown in LO2 and HepG2 cell lines, based on a previous study in hepatic cells. The study was conducted using bromodeoxyuridine, immunofluorescent staining, western blot analysis and flow cytometry. Nuclear VASH2 was highly expressed in actively dividing cells in normal and cancer tissues. There was a significant positive correlation between nuclear VASH2 and Ki-67, indicating that nuclear VASH2 positively correlated with cell proliferation in normal and cancer tissues. The bromodeoxyuridine (BrdU) proliferation test showed that nuclear VASH2 increased the S-phase population and promoted cell proliferation, while VASH2 knockdown reduced BrdU absorbance. Cell cycle analysis revealed that nuclear VASH2 overexpression increased the S-phase population in LO2 and HepG2 cells, while nuclear VASH2 knockdown reduced the S-phase population and increased the G0/G1 population. The findings of this study challenge the classic view of VASH2, which was previously reported as an angiogenesis factor. Furthermore, to the best of our knowledge, these results are the first clinical data indicating that nuclear VASH2, but not cytoplasmic VASH2, promotes cell proliferation by driving the cell cycle from the G0/G1 to S phase.
    No preview · Article · Jul 2015 · Oncology Reports
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    ABSTRACT: SATB1 plays an important role in human malignant progression, inducing cancer cell proliferation and metastasis by regulating downstream gene expressions. However, little is known about the underlying mechanisms in which SATB1 promotes pancreatic cancer tumorigenesis. To investigate SATB1 expression levels and its biological functions in promoting pancreatic cancer growth and invasion. SATB1 expression levels were detected in seven human pancreatic cancer cell lines and 16 pairs of normal pancreatic/pancreatic cancer tissues using RT-PCR and western blot. SW1990 or Capan-1 cells stably knockdown (shRNA) or transiently knockdown (siRNA) SATB1 cells, and PANC-1 stably overexpressing SATB1 cells were investigated with MTT, EdU assay, flow cytometry, and transwell invasion assay for cell proliferation and invasion activity. The binding of SATB1 to MYC promoter region was examined using reporter assay. Expression of SATB1 in 68 pancreatic cancer samples was studied by immunohistochemical staining and scoring. SATB1 was overexpressed in pancreatic cancer tissues samples, showing strong correlation with pancreatic cancer invasion depth and tumor staging. SATB1 induced MYC mRNA and protein expression; promoted pancreatic cancer cell growth; increased cell population in S phase; and enhanced pancreatic cancer cell invasion in vitro. On the other hand, SATB1 knockdown showed opposite effects. Furthermore, MYC blocking in SATB1-overexpressing cells attenuated the promotion of pancreatic cancer cell growth and invasion. Our data also indicated that SATB1 bound to specific promoter region of MYC. SATB1 is overexpressed in pancreatic cancer, promoting cancer cell proliferation and invasion through the activation of MYC.
    Preview · Article · Jun 2015 · Digestive Diseases and Sciences
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    ABSTRACT: Postoperative pancreatic fistula (POPF) is a major source of morbidity after pancreaticoduodenectomy (PD). The purpose of this retrospective study comparing one-layer pancreaticojejunostomy (PJ) with two-layer PJ after PD was to evaluate whether the one-layer duct-to-mucosa PJ after PD can reduce the incidence of POPF.A total of 194 consecutive patients who underwent PD by one surgeon (Y. Miao) from January 2011 to February 2014 were included in this study. Among those patients, 104 underwent one-layer PJ (one-layer group) and 90 patients underwent two-layer PJ (two-layer group), respectively. Preoperative clinicopathologic features, intraoperative parameters, postoperative morbidity with focus on POPF, were compared between the two groups.The overall incidence of POPF was 19.6% (38/194), and clinically relevant grade B/C POPF rates were 8.6% (16/194) and 3.1% (6/194), respectively. There were no differences in patients' demographics and operation related factors between the two groups. However, the incidence of POPF in the one-layer group was significantly lower than in two-layer group (13.5% [14/104 patients] and 26.7% [24/90 patients] respectively; p=0.021). The median postoperative hospital stay was also significantly lower in the one-layer group compared to the two-layer group (13 days vs. 15 days, p=0.035). One patient in two-layer group died due to postoperative hemorrhage.One-layer duct-to-mucosa pancreaticojejunostomy is a simple and easy technique for pancreaticojejunal anastomosis after PD, and can reduce the POPF rate in comparison to the two-layer technique.
    No preview · Article · Jun 2015 · International surgery
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    ABSTRACT: Necrolytic migratory erythema (NME), diabetes mellitus and glucagon-secreting tumors form the hallmarks of glucagonoma syndrome, and represent the major clinical manifestations of glucagonoma. NME is usually presented as the initial complaint of patients. Due to the rare incidence of glucagonoma, its diagnosis is often delayed, which leads to its progression. Here, we report a case of NME with a typical skin rash, which was misdiagnosed and treated with corticosteroids for two years. Removal of the tumor in the pancreatic body led to the rapid relief of the symptoms. The aim of the present study is to demonstrate the typical characteristics of glucagonoma syndrome to clinicians in order to improve its diagnosis and treatment.
    No preview · Article · May 2015 · Oncology letters

Publication Stats

791 Citations
325.12 Total Impact Points

Institutions

  • 1999-2015
    • Nanjing Medical University
      • • Department of General Surgery
      • • Department of Surgery
      • • The Affiliated Huai’an First Hospital
      Nan-ching, Jiangsu, China
  • 2010
    • Nanjing General Hospital
      Nan-ching, Jiangsu Sheng, China
  • 2007
    • Soochow University (PRC)
      Wu-hsien, Jiangsu Sheng, China