Publications by authors named "Zhong Sheng Xia"

Background: Intraductal papillary mucinous neoplasm (IPMN) is a cystic tumor of the pancreas arising from abnormal papillary proliferation of ductal epithelial cells, and is a precancerous lesion of pancreatic malignancy. This study aimed to evaluate associations between acute pancreatitis (AP) and histologic subtypes of IPMN.

Methods: In the clinical study, patients with IPMN confirmed by surgical resection specimens at our institute between 2009 and 2021 were eligible for inclusion.

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Objectives: Embryonic stem cells (ESCs)-derived pancreatic precursor cells have great potential for pancreas repair. Expression of pancreatic duodenal homeobox 1 (Pdx1) in definitive endoderm (DE) cells is the premise that DE cells differentiate into pancreatic cells. To achieve the required number of Pdx1-expressing DE cells for cell transplantation therapy, a valid model must be established.

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Colorectal cancer (CRC) is the most common form of gastrointestinal malignancies. A growing number of reports focusing on oxaliplatin (OXA) resistance in CRC treatment have revealed that drug resistance is an urgent issue in clinical applications, especially for finding effective therapeutic targets. Recently, microRNAs (miRNAs) are reported to play a critical role in tumor progressions and multi-drug resistance.

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Aberrant expression of SNHG8 has been observed in some types of cancers. However, whether SNHG8 was aberrantly expressed in colorectal cancer and whether it could exert any function on the development of colorectal cancer remains largely elusive. In this study, we first investigated the expression pattern and biological function of SNHG8 in colorectal cancer.

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Butyrate is widely accepted as a proliferation inhibitor in colon cancer but less thoroughly characterized in the colonic epithelium of objects with type 2 diabetes mellitus. The present study investigated the regulatory effect of butyrate on proliferation, the related molecule high-mobility group box 1 (HMGB1) and the receptor for advanced glycation end products (RAGE) in the colon of db/db type 2 diabetic model mice and non-cancerous NCM460 colon cells. Proliferation and the expression of HMGB1 and RAGE were increased and could be partially reversed by butyrate treatment in the colon of db/db mice, which were consistent in NCM460 cells under a high glucose state.

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Colon cancer is one of the most common cancers in the world. Multidrug resistance is one of the main reasons for failure of therapy in patients with advanced colon cancer. In previous studies, multiple methods were investigated to reverse the multidrug resistance of colon cancer cells.

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Induced differentiation of definitive endoderm (DE) from embryonic stem cells (ESCs) has been the recent focus of studies investigating regeneration and transplantation of organs of the digestive system. Poor cell survival is the most important challenge to DE differentiation from ESCs. This study aimed to optimize culture conditions to promote the differentiation of mouse ESCs into DE, and to investigate the roles of the Wnt and Nodal signaling pathways in the DE differentiation.

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Background: Distinctive structures called crypts harbor intestinal epithelial stem cells (IESCs) which generate progenitor and terminally differentiated cells in the intestinal epithelium. Mammalian IESCs and their daughter cells require the participation of DNA methylation and the transcription factor Sox9 for proliferation and differentiation. However, the association between Sox9 and DNA methylation in this process remains elusive.

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Diabetes mellitus (DM) is a group of metabolic diseases characterised by insulin deficiency/resistance and hyperglycaemia. We previously reported the presence of an impaired tight junction and decreased expression of occludin (Ocln) and zonula occludens-1 (ZO-1) in the intestinal epithelial cells (IECs) of type 1 DM mice, but the exact mechanism remains unclear. In this study, we investigated the role of microRNAs (miRNAs) in impairing the tight junction in IECs of DM mice.

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BACKGROUND Type 1 diabetes mellitus (T1DM) is associated with increased risks of enteric infection. Paneth cells constitute the first line of the gut defense. Little is known about the impact of T1DM on the bactericidal function of intestinal Paneth cells.

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Objectives: Depression of the Notch/Hes1 pathway has been reported to play a role in abnormal differentiation of intestinal epithelial cells (IECs) in diabetes mellitus (DM). However, the mechanism by which this pathway influences IEC differentiation has remained unclear. In this study, we have investigated the role of microRNAs (miRNAs) in regulating the Notch/Hes1 pathway in IECs of DM mice.

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In previous studies, we have reported the abnormal proliferation and differentiation of intestinal epithelial cells (IECs) in diabetes mellitus (DM) mice. The insulin receptor (IR) and its downstream mitogen-activated protein kinase kinase (MAPKK also known as MEK)/extracellular-regulated protein kinase (ERK) pathway is a classic pathway associated with cell proliferation and differentiation. The purpose of the present study is to investigate the role of the MEK/ERK pathway in abnormal proliferation and differentiation of IECs in DM mice.

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Objective: Recent studies proved that patients with diabetes were at significantly higher risk of developing colorectal cancer. However, the association between diabetes mellitus and the risk of colorectal adenoma remains undefined. Thus we conducted an updated meta-analysis to identify the association between diabetes mellitus and the risk of colorectal neoplasia including adenoma and cancer.

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Background: The effect of rebamipide on repairing intestinal mucosal damage induced by nonsteroidal anti-inflammatory drugs and its mechanism remain unclear. In this study, we sought to explore the mechanism whereby rebamipide could promote the regeneration of aspirin-induced intestinal mucosal damage.

Methods: BALB/c mice were administered aspirin (200 mg/kg/d) for 5 days to induce acute small intestinal injury (SII).

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Intestinal epithelial stem cells (IESCs) can differentiate into all types of intestinal epithelial cells (IECs) and Leucine-rich repeat-containing G protein-coupled receptor 5 (Lgr5) is a marker for IESC. Previous studies reported enhanced proliferation of IECs in diabetic mice. In this study, the in vitro differentiation of Lgr5 positive IESCs sorted from diabetic mice was further investigated.

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Treatments for pancreatic injuries have been significantly improved recently, but full recovery of pancreatic function remains difficult. Embryonic stem cells have great potentialities for self-renewal and multiple differentiations. In this study, we explored an approach to induce the differentiation of pancreatic progenitor cells from embryonic stem cells in vitro.

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Background: Autoimmune pancreatitis (AIP) is a distinct type of pancreatitis associated with a presumed autoimmune mechanism. The aim of this study was to analyze the clinical features and expressions of forkhead box P3 (Foxp3) and interleukin-17 (IL-17) in type 1 AIP in China and to identify factors for differentiation of AIP from non-AIP chronic pancreatitis (CP).

Material And Methods: We retrospectively reviewed pancreatic specimens with diagnosis of type 1 AIP and non-AIP CP at Sun Yat-Sen Memorial Hospital in China from January 2000 to December 2013.

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Pancreatic cancer (PC) is a highly lethal disease and notoriously difficult to treat. Only a small proportion of PC patients are eligible for surgical resection, whilst conventional chemoradiotherapy only has a modest effect with substantial toxicity. Gene therapy has become a new widely investigated therapeutic approach for PC.

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Article Synopsis
  • The study investigates the relationship between β-catenin accumulation and the proliferation of colorectal epithelium in patients with type 2 diabetes mellitus (DM).
  • Colorectal samples from DM patients showed significantly higher proliferative indexes and altered Wnt/β-catenin signaling compared to non-DM patients and control groups.
  • The findings indicate that increased proliferation in diabetic patients' colorectal epithelium is linked to β-catenin changes, suggesting a connection between diabetes and cancer proliferation.
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Colon cancer is one of the most common cancers in the world. Multidrug resistance is related to poor prognosis of advanced colon cancer. The side population plays an important role in multiple drug resistance (MDR) of colon cancer.

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Identifying predictive biomarkers for colorectal cancer would facilitate diagnosis and treatment of the disease. This study aimed to investigate the association of the serological biomarkers CEA, CA19-9, CA125, CYFRA21-1 and CA72-4 with patient characteristics and disease outcomes in colorectal cancer. Patients (N = 373) with colorectal cancer were evaluated for the association of CEA, CA19-9, CA125, CYFRA21-1, and CA72-4 pre and post-surgery and at disease recurrence with demographics, disease characteristics including pathological types, degree of differentiation, invasion depth, abdominal lymph node metastasis, TMN stage, Dukes stage, location of cancer and metastasis, and disease outcomes.

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Background: Insulin-like growth factor-II mRNA-binding protein 3 (IMP3) is a newly identified mRNA-binding protein that is involved in embryogenesis and carcinogenesis of some malignant tumors. The aim of this study was to detect the expression of IMP3 protein in gastric adenocarcinoma (GAC) and the correlation with clinicopathological features.

Methods: IMP3 protein in 92 samples of GAC was evaluated by immunohistochemical method.

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Aim: To investigate the expression of Erythropoietin (Epo) and its receptor (EpoR) in gastric adenocarcinoma (GAC) and the correlation with angiogenesis and clinicopathological features.

Methods: The expressions of Epo, EpoR and vascular endothelial growth factor (VEGF), as well as microvessel density were evaluated in 172 GAC biopsies by immunohistochemical staining. The correlations between these parameters and patient's clinicopathological features were analyzed statistically.

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Msi1 (Musashi 1) is regarded as a marker for neural and intestinal epithelial stem cells. However, it is still unclear whether Msi1-positive cells derived from mouse embryonic stem cells have the ability to differentiate into neural or intestinal epithelial cells. A pMsi1-GFP (green fluorescent protein) reporter plasmid was constructed in order to sort Msi1-positive cells out of the differentiated cell population.

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