Institute of Digestive Diseases

Baotou, China

Institute of Digestive Diseases

Baotou, China

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Haag S.,University of Duisburg - Essen | Andrews J.M.,University of Adelaide | Gapasin J.,University of Adelaide | Gapasin J.,Institute of Digestive Diseases | And 4 more authors.
Alimentary Pharmacology and Therapeutics | Year: 2011

Aliment Pharmacol Ther 2011; 33: 722-729 Summary Background Previous data collected in separate studies using various different survey instruments have suggested some variability in the prevalence of symptoms between nations. However, there is a lack of studies which assess and compare the prevalence of upper gastrointestinal symptoms contemporaneously in various countries using a uniform, standardised method. Aim To determine the prevalence of upper gastrointestinal (UGI) symptoms in 13 European countries, and the association between socioeconomic factors and symptoms using a standardised method. Methods A representative age- and gender-stratified sample of 23 163 subjects (aged 18-69 years) was surveyed. Results The prevalence of UGI symptoms was 38%. UGI symptoms were most prevalent in Hungary [45%, 95% confidence interval (CI): 42.2-48.4] and lowest in the Netherlands (24%, 95% CI: 21.0-26.2). UGI symptoms were more prevalent in women (39%, 95% CI: 38.4-39.6) vs. men (37%, 95% CI: 36.4-37.6). Heartburn (24%, 95% CI: 23.4-24.6) and acidic reflux (14%, 95% CI: 13.6-14.4) were most common. With age, the prevalence of UGI symptoms decreased (e.g. 18-29 years: 43%, 95% CI: 41.4-44.3 vs. 50-69 years: 33%, 95% CI: 32.3-34.4); in contrast, the frequency of symptom episodes/year increased with age (e.g. 18-29 years: 11.3 episodes per years, 95% CI: 10.5-12.1 vs. 50-69 years: 21.8, 95% CI: 20.7-22.9). Socioeconomic status as measured by gross domestic product was inversely associated with symptoms and in total, socioeconomic factors, gender, body mass index, smoking habits and alcohol consumption explained 83% of the variance of UGI symptoms. Conclusions There are marked differences in the country specific prevalence of upper gastrointestinal complaints. Socioeconomic factors are closely associated with the prevalence of upper gastrointestinal symptoms. © 2011 Blackwell Publishing Ltd.


Stankovic M.N.,University of Belgrade | Mladenovic D.,University of Belgrade | Ninkovic M.,Medical Military Academy | Crossed D Signuricic I.,University of Belgrade | And 5 more authors.
Journal of Medicinal Food | Year: 2014

Development of nonalcoholic fatty liver disease (NAFLD) occurs through initial steatosis and subsequent oxidative stress. The aim of this study was to examine the effects of α-lipoic acid (LA) on methionine-choline deficient (MCD) diet-induced NAFLD in mice. Male C57BL/6 mice (n=21) were divided into three groups (n=7 per group): (1) control fed with standard chow, (2) MCD2 group -fed with MCD diet for 2 weeks, and (3) MCD2+LA group -2 weeks on MCD receiving LA i.p. 100 mg/kg/day. After the treatment, liver samples were taken for pathohistology, oxidative stress parameters, antioxidative enzymes, and liver free fatty acid (FFA) composition. Mild microvesicular hepatic steatosis was found in MCD2 group, while it was reduced to single fat droplets evident in MCD2+LA group. Lipid peroxidation and nitrosative stress were increased by MCD diet, while LA administration induced a decrease in liver malondialdehyde and nitrates+nitrites level. Similary, LA improved liver antioxidative capacity by increasing total superoxide dismutase (tSOD), manganese SOD (MnSOD), and copper/zinc-SOD (Cu/ZnSOD) activity as well as glutathione (GSH) content. Liver FFA profile has shown a significant decrease in saturated acids, arachidonic, and docosahexaenoic acid (DHA), while LA treatment increased their proportions. It can be concluded that LA ameliorates lipid peroxidation and nitrosative stress in MCD diet-induced hepatic steatosis through an increase in SOD activity and GSH level. In addition, LA increases the proportion of palmitic, stearic, arachidonic, and DHA in the fatty liver. An increase in DHA may be a potential mechanism of anti-inflammatory and antioxidant effects of LA in MCD diet-induced NAFLD. © Copyright 2014, Mary Ann Liebert, Inc. and Korean Society of Food Science and Nutrition 2014.


Stankovic M.N.,University of Belgrade | Mladenovic D.R.,University of Belgrade | Duricic I.,University of Belgrade | Sobajic S.S.,University of Belgrade | And 6 more authors.
Archives of Medical Research | Year: 2014

Background and Aims: Methionine-choline deficient (MCD) diet duration necessary for development of non-alcoholic fatty liver disease (NAFLD) and the dynamic of lipid profile and fatty acids are not completely established. The study examined dynamics and association between liver free fatty acids (FFA), serum lipid profile and liver morphological changes on MCD diet-induced NAFLD in mice. Methods: Male C57BL/6 mice (n= 28) were divided into four groups (n= 7 per group): control: fed with standard chow, MCD diet-fed groups: 2, 4 or 6 weeks. After treatment, liver and blood samples were taken for histopathology, serum lipid profile, and liver FFA composition. Results: Hepatic FFA profile showed a decrease in saturated acids, arachidonic and docosahexaenoic acid, whereas proportions of docosapentaenoic, oleic and linoleic acid were increased. Total cholesterol, HDL and triglycerides progressively decreased, whereas LDL level progressively increased. Focal fatty change in the liver appeared after 2 weeks, whereas diffuse fatty change with severe inflammation and ballooned hepatocytes were evident after 6 weeks. Conclusions: Six-week diet model may be appropriate for investigation of the role of lipotoxicity in the progression of NAFLD. Therefore, supplementation with n-3 polyunsaturated acid like DHA, rather than DPA, especially in the initial stage of fatty liver disease, may potentially have preventive effects and alleviate development of NAFLD/NASH and may also potentially reduce cardiovascular risk by moderating dyslipidemia. © 2014 IMSS.


PubMed | University of Belgrade and Institute of Digestive Diseases
Type: Journal Article | Journal: Veterinary parasitology | Year: 2015

The main objective of our research was to examine the role and immunophenotypic characteristics of myofibroblasts in sheep liver naturally infected by the lancet liver fluke (Dicrocoelium dendriticum). In the reported study we analyzed liver samples from 20 adult sheep, 14 infected animals and 6 controls. The liver samples were fixed in 10% buffered formalin, and routinely processed and stained using hematoxylin eosin, the periodic acid-Schiff and Masson-Goldner trichrome methods. The immunohistochemical examination was carried out by the streptavidin biotin (LSAB2) method, using antibodies for -smooth muscle actin (-SMA), desmin and vimentin. The histopathological examination revealed liver fibrosis in 6 out of 14 (42.9%) analyzed samples, while different forms of cholangitis were observed in the remaining 8 out of 14 (57.1%). The expression of -SMA was proven in perisinusoidal hepatic stellate cells, portal/septal myofibroblasts, and interface myofibroblasts. The degree of -SMA expression and the number of -SMA immunopositive cells were the most intensive in the liver with fibrosis. Desmin expression in all liver samples of infected sheep was confirmed in hepatic stellate cells and smooth muscle cells. The hepatic stellate cells, portal/septal myofibroblasts, and interface myofibroblasts reacted as vimentin positive cells. In the liver without fibrotic changes hepatic stellate cells and smooth muscle cells were desmin positive. The obtained results suggest that all populations of myofibroblasts, especially hepatic stellate cells, play an important role in the increased extracellular matrix formation during parasitic liver fibrosis in sheep naturally infected with D. dendriticum.


Wedd J.,University of Colorado at Denver | Bambha K.M.,University of Colorado at Denver | Stotts M.,Saint Louis University | Laskey H.,University of Colorado at Denver | And 4 more authors.
Liver Transplantation | Year: 2014

The Model for End-Stage Liver Disease (MELD) score has reduced predictive ability in patients with cirrhosis and MELD scores ≤20. We aimed to assess whether a 5-stage clinical model could identify liver transplantation (LT) candidates with low MELD scores who are at increased risk for death. We conducted a case-control study of subjects with cirrhosis and MELD scores≤20 who were awaiting LT at a single academic medical center between February 2002 and May 2011. Conditional logistic regression was used to evaluate the risk of liver-related death according to the cirrhosis stage. We identified 41 case subjects who died from liver-related causes with MELD scores≤20 within 90 days of death while they were waiting for LT. The cases were matched with up to 3 controls (66 controls in all) on the basis of the listing year, age, sex, liver disease etiology, presence of hepatocellular carcinoma, and MELD score. The cirrhosis stage was assessed for all subjects: (1) no varices or ascites, (2) varices, (3) variceal bleeding, (4) ascites, and (5) ascites and variceal bleeding. The MELD scores were similar for cases and controls. Clinical states contributing to death in cases were: sepsis 49%, spontaneous bacterial peritonitis 15%, variceal bleeding 24%, and hepatorenal syndrome 22%. In a univariate analysis, variceal bleeding [odds ratio (OR)=5.6, P=0.003], albumin (OR=0.5, P=0.041), an increasing cirrhosis stage (P=0.003), reaching cirrhosis stage 2, 3, or 4 versus lower stages (OR=3.6, P=0.048; OR=7.4, P<0.001; and OR=4.1, P=0.008), a sodium level<135 mmol/L (OR=3.4, P=0.006), and hepatic encephalopathy (OR=2.3, P=0.082) were associated with liver-related death. In a multivariate model including the cirrhosis stage, albumin, sodium, and hepatic encephalopathy, an increasing cirrhosis stage (P=0.010) was independently associated with liver-related death. In conclusion, assessing the cirrhosis stage in patients with low MELD scores awaiting LT may help to select candidates for more aggressive monitoring or for living or extended criteria donation. © 2014 AASLD.


Culafic D.M.,Institute of Digestive Diseases | Kerkez M.D.,Institute of Digestive Diseases | Mijac D.D.,Institute of Digestive Diseases | Lekic N.S.,Institute of Digestive Diseases | And 3 more authors.
Scandinavian Journal of Gastroenterology | Year: 2010

Aim: The aim of our study was to demonstrate clinical manifestations and diagnostic methods of splenic echinococcosis and suggest surgical approach. Methods: The study involved 20 patients of previously diagnosed spleen echinococcosis. A diagnosis was made for each patient, based on medical history, biochemical and serological tests, physical examination and abdominal ultrasonography. All the patients received a CT scan of the abdomen. These patients had undergone the following surgery procedures: total splenectomy 13 (60%), and spleen-preserving surgery 7 (35%) patients. Histological examination confirmed the spleen echinoccocosis in all the patients. Results: Nonspecific left upper abdominal pain was present in 10 (50%) cases, while 5 (25%) patients presented with the right upper abdominal pain with dyspepsia and five patients (25%) were asymptomatic. Postoperative complications developed in 2/13 (15.4 %) patients who underwent total splenectomy, while there were no complications after spleen-preserving surgery. Conclusion: Spleen-preserving surgery should be undertaken if possible in patients with spleen echinococcosis, and total splenectomy is reserved for the patients with large cysts located centrally or near the hilus.


Wu W.K.K.,Institute of Digestive Diseases | Sakamoto K.M.,Mattel Childrens Hospital UCLA | Milani M.,Growth Factor Group | Aldana-Masankgay G.,Mattel Childrens Hospital UCLA | And 6 more authors.
Drug Resistance Updates | Year: 2010

Macroautophagy and the ubiquitin-proteasome system are two complementary pathways for protein degradation. The former degrades long-lived proteins and damaged organelles while the later degrades short-lived proteins. Recent findings indicate that suppression of the ubiquitin-proteasome system by proteasome inhibitors induces macroautophagy through multiple pathways, including (1) accumulation of ubiquitinated proteins and activation of HDAC6; (2) activation of the IRE1-JNK pathway; (3) proteasomal stabilization of ATF4; (4) inhibition of mTOR complex 1 signaling; (5) reduced proteasomal degradation of LC3. Induction of macroautophagy attenuates the antitumor effect of proteasome inhibitors in various types of cancer. These findings suggest that inhibition of macroautophagy may represent a novel strategy to enhance cellular sensitivity to proteasome inhibition. © 2010 Elsevier Ltd. All rights reserved.


Zhang S.,Institute of Digestive Diseases | Wang C.,Institute of Digestive Diseases
Chinese Journal of Gastroenterology | Year: 2015

Functional dyspepsia (FD) is a group of clinical syndromes presented as upper abdominal pain, epigastric burning sensation, postprandial fullness, satiety and other symptoms, but lack of organic disease causing these symptoms. Eosinophils (EOS) in gastrointestinal tract play an important role in preventing pathogen invasion and maintaining intestinal epithelial homeostasis. In recent years, many studies have shown a significant increase of duodenal EOS in patients with FD. This article reviewed the expression and significance of duodenal EOS in patients with FD. Copyright © 2015 by Editorial Office of Chinese Journal of Gastroenterology.


Peng K.,Huazhong University of Science and Technology | Xu W.,Institute of Digestive Diseases | Zheng J.,Huazhong University of Science and Technology | Huang K.,Huazhong University of Science and Technology | And 12 more authors.
Nucleic Acids Research | Year: 2013

Disease and Gene Annotations database (DGA, http://dga.nubic.northwestern. edu) is a collaborative effort aiming to provide a comprehensive and integrative annotation of the human genes in disease network context by integrating computable controlled vocabulary of the Disease Ontology (DO version 3 revision 2510, which has 8043 inherited, developmental and acquired human diseases), NCBI Gene Reference Into Function (GeneRIF) and molecular interaction network (MIN). DGA integrates these resources together using semantic mappings to build an integrative set of disease-to-gene and gene-to-gene relationships with excellent coverage based on current knowledge. DGA is kept current by periodically reparsing DO, GeneRIF, and MINs. DGA provides a user-friendly and interactive web interface system enabling users to efficiently query, download and visualize the DO tree structure and annotations as a tree, a network graph or a tabular list. To facilitate integrative analysis, DGA provides a web service Application Programming Interface for integration with external analytic tools. © The Author(s) 2012.


Shin V.Y.,University of Hong Kong | Jin H.,Zhejiang University | Ng E.K.O.,University of Hong Kong | Cheng A.S.L.,Institute of Digestive Diseases | And 10 more authors.
Carcinogenesis | Year: 2011

Cigarette smoke is one of the risk factors for gastric cancer and nicotine has been reported to promote tumor growth. Deregulation of microRNA (miRNA) and cyclooxygenase-2 (COX-2) expressions are hallmarks of many cancers including gastric cancer. Here, we used an miRNA array platform covering a panel of 95 human miRNAs to examine the expression profile in nicotine-treated gastric cancer cells. We found that miR-16 and miR-21 were upregulated upon nicotine stimulation, transfection with anti-miR-16 or anti-miR-21 significantly abrogated cell proliferation. In contrast, ectopic miR-16 or miR-21 expression exhibited a similar stimulatory effect on cell proliferation as nicotine. Nicotine-mediated IkappaBα degradation and nuclear factor-kappa B (NF-κB) translocation dose-dependently. Knockdown of NF-κB by short interfering RNA (siRNA) or specific inhibitor (Bay-11-7085) markedly suppressed nicotine-induced cell proliferation and upregulation of miR-16 and miR-21. Interestingly, NF-κB-binding sites were located in both miR-16 and miR-21 gene transcriptional elements and we showed that nicotine enhanced the binding of NF-κB to the promoters of miR-16 and miR-21. Furthermore, activation of COX-2/prostaglandin E2 (PGE2) signaling in response to nicotine was mediated by the action of prostaglandin E receptors (EP2 and EP4). EP2 or EP4 siRNA or antagonists impaired the nicotine-mediated NF-κB activity, upregulation of miR-16 and miR-21 and cell proliferation. Taken together, these results suggest that miR-16 and miR-21 are directly regulated by the transcription factor NF-κB and yet nicotine-promoted cell proliferation is mediated via EP2/4 receptors. Perhaps this study may shed light on the development of anticancer drugs to improve the chemosensitivity in smokers. © The Author 2010. Published by Oxford University Press. All rights reserved.

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