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
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. Source
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
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. Source
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
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. Source
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.
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. Source
Cheung K.-F.,Chinese University of Hong Kong |
Lam C.N.Y.,Chinese University of Hong Kong |
Wu K.,Institute of Digestive Diseases |
Ng E.K.O.,Chinese University of Hong Kong |
And 6 more authors.
Background: By using genome-wide methylation screening, the authors identified ring finger protein 180 (RNF180) as preferentially methylated in cancer. This study was undertaken to clarify its structure and functional role in gastric cancer. Methods: The transcription start site and core functional promoter region of RNF180 were revealed by 5â rapid amplification of cDNA ends and luciferase activity assays. Promoter methylation was detected by combined bisulfite restriction analysis and bisulfite genomic sequencing. Cell growth was detected by colony formation assay, apoptosis by annexin V assay, and RNF180 target genes by cDNA microarray. Results: The authors revealed the transcription start site of RNF180 gene and identified the functional core promoter region (-202/+372) in the CpG island, which could be silenced by in vitro methylation assay. RNF180 was silenced in 6 of 7 gastric cancer cell lines and significantly down-regulated in primary gastric cancers compared with adjacent normal tissues (P =.001). Loss of gene expression was associated with promoter methylation. Re-expression of RNF180 suppressed cell growth (P <.001) and induced apoptosis (P <.05), which were mediated by up-regulating the antiproliferation regulators MTSS1 and CDKN2A and the proapoptotic mediator TIMP3. Promoter methylation of RNF180 was detected in 76% (150 of 198) of primary gastric cancers and 55% (11 of 20) of intestinal metaplasia, but in none of 23 normal gastric tissues. Methylated RNF180 DNA was detected in the plasma of 56% of gastric cancer patients, but not in healthy controls (P =.003). Patients with low or loss of RNF180 expression had significantly poorer overall survival. Conclusions: RNF180 is a novel potential tumor suppressor in gastric carcinogenesis and has potential clinical utility as a biomarker for gastric cancer patients. © 2011 American Cancer Society. Source