Database : MEDLINE
Search on : liver and cirrhosis [Words]
References found : 105260 [refine]
Displaying: 1 .. 10   in format [Detailed]

page 1 of 10526 go to page                         

  1 / 105260 MEDLINE  
              next record last record
select
to print
Photocopy
Full text

[PMID]: 29515105
[Au] Autor:Rani B; Malfettone A; Dituri F; Soukupova J; Lupo L; Mancarella S; Fabregat I; Giannelli G
[Ad] Address:School of Medicine, University of Bari, Bari, Italy.
[Ti] Title:Galunisertib suppresses the staminal phenotype in hepatocellular carcinoma by modulating CD44 expression.
[So] Source:Cell Death Dis;9(3):373, 2018 Mar 07.
[Is] ISSN:2041-4889
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Cancer stem cells (CSCs) niche in the tumor microenvironment is responsible for cancer recurrence and therapy failure. To better understand its molecular and biological involvement in hepatocellular carcinoma (HCC) progression, one can design more effective therapies and tailored then to individual patients. While sorafenib is currently the only approved drug for first-line treatment of advanced stage HCC, its role in modulating the CSC niche is estimated to be small. By contrast, transforming growth factor (TGF)-ß pathway seems to influence the CSC and thus may impact hallmarks of HCC, such as liver fibrosis, cirrhosis, and tumor progression. Therefore, blocking this pathway may offer an appealing and druggable target. In our study, we have used galunisertib (LY2157299), a selective ATP-mimetic inhibitor of TGF-ß receptor I (TGFßI/ALK5) activation, currently under clinical investigation in HCC patients. Because the drug resistance is mainly mediated by CSCs, we tested the effects of galunisertib on stemness phenotype in HCC cells to determine whether TGF-ß signaling modulates CSC niche and drug resistance. Galunisertib modulated the expression of stemness-related genes only in the invasive (HLE and HLF) HCC cells inducing a decreased expression of CD44 and THY1. Furthermore, galunisertib also reduced the stemness-related functions of invasive HCC cells decreasing the formation of colonies, liver spheroids and invasive growth ability. Interestingly, CD44 loss of function mimicked the galunisertib effects on HCC stemness-related functions. Galunisertib treatment also reduced the expression of stemness-related genes in ex vivo human HCC specimens. Our observations are the first evidence that galunisertib effectiveness overcomes stemness-derived aggressiveness via decreased expression CD44 and THY1.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1038/s41419-018-0384-5

  2 / 105260 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29231189
[Au] Autor:Lai JC; Covinsky KE; McCulloch CE; Feng S
[Ad] Address:Division of Gastroenterology and Hepatology, Department of Medicine, University of California-San Francisco, San Francisco, California, USA.
[Ti] Title:The Liver Frailty Index Improves Mortality Prediction of the Subjective Clinician Assessment in Patients With Cirrhosis.
[So] Source:Am J Gastroenterol;113(2):235-242, 2018 Feb.
[Is] ISSN:1572-0241
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVES: Frailty, a critical determinant of health outcomes, is most commonly assessed in patients with cirrhosis by general clinician assessment that is limited by its subjectivity. We aimed to compare the objective Liver Frailty Index (LFI), consisting of three performance-based tests (grip, chair stands, balance), with a subjective hepatologist assessment. METHODS: Outpatients with cirrhosis awaiting liver transplantation (LT) underwent: (1) objective measurement using the LFI and (2) subjective clinician assessment. Spearman's correlation assessed associations between the LFI and clinician assessment; Cox regression with waitlist mortality (death/delisting for sickness); discriminative ability with Concordance(C) statistics. The net reclassification index evaluated the percentage of patients correctly reclassified by adding the LFI to the clinician assessment. RESULTS: Of the 529 patients with cirrhosis, median LFI was 3.8 (range 1.0-7.0) and clinician assessment was 3 (range 0-5). Correlation between LFI and the clinician assessment was modest (ρ=0.38) with high variability by hepatologist (ρ=0.26-0.70). At a median of 11 months, 102 (19%) died/were delisted. Both the LFI (hazard ratio (HR) 2.2, 95% confidence interval (CI) 1.7-2.9) and clinician assessment (HR 1.6, 95% CI 1.3-1.9) were associated with adjusted waitlist mortality risk (P<0.01). The addition of the LFI to the clinician assessment significantly improved mortality prediction over the clinician assessment alone (0.74 vs. 0.68; P=0.02). Compared with the clinician assessment alone, the addition of the LFI correctly reclassified 34% (95% CI 8-53%) of patients to their correct survival status. CONCLUSION: The subjective clinician assessment can predict waitlist mortality in patients with cirrhosis but is subjective and variable by hepatologist. The addition of the LFI to the subjective clinician assessment significantly improved mortality risk prediction, reclassifying 34% of patients. Our data strongly support the incorporation of the objective LFI to anchor our assessments of patients with cirrhosis to enhance our decision-making.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1038/ajg.2017.443

  3 / 105260 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29194969
[Au] Autor:Cullaro G; Sarkar M; Lai JC
[Ad] Address:Department of Medicine, University of California, San Francisco, CA, USA.
[Ti] Title:Sex-based disparities in delisting for being "too sick" for liver transplantation.
[So] Source:Am J Transplant;, 2017 Dec 01.
[Is] ISSN:1600-6143
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Women with cirrhosis awaiting liver transplantation (LT) experience higher rates of waitlist mortality than men; it is unknown whether practices surrounding delisting for being "too sick" for LT contribute to this disparity beyond death alone. We conducted an analysis of patients listed for LT in the United Network for Organ Sharing/Organ Procurement and Transplantation Network not receiving exception points from May 1, 2007 to July 1, 2014 with a primary outcome of delisting with removal codes of "too sick" or "medically unsuitable." A total of 44 388 patients were included; 4458 were delisted for being "too sick" for LT. Delisting was more frequent in women (11% vs 9%, P < .001). Compared to delisted men, delisted women differed in age (58 vs 57), non-hepatitis C virus listing diagnoses (69% vs 56%), hepatic encephalopathy (36% vs 31%), height (161.9 vs 177.0 cm), private insurance (47% vs 52%), and Karnofsky performance status (60 vs 70) (P < .001 for all). There were no differences in Model for End-Stage Liver Disease including serum sodium and Child Pugh Scores. A competing risk analysis demonstrated that female sex was independently associated with a 10% (confidence interval 2%-18%) higher risk of delisting when accounting for rates of death and transplantation and adjusting for confounders. This study demonstrates a significant disparity in delisting practices by sex, highlighting the need for better assessments of sickness, particularly in women.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher
[do] DOI:10.1111/ajt.14608

  4 / 105260 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29524121
[Au] Autor:Xue J; Feng R; Fu H; Jiang Q; Jiang H; Lu J; Liu H; Wang J; Niu T; Wang X; Xie Y; Wang H; Xu L; Liu K; Huang X; Zhang X
[Ad] Address:Peking University People's Hospital, Peking University Institute of Hematology, Beijing Key Laboratory of Hematopoietic Stem Cell Transplantation, Collaborative Innovation Center of Hematology, Peking University, Beijing, 100044, China.
[Ti] Title:Combined prednisone and levothyroxine improve treatment of severe thrombocytopenia in hepatitis B with compensatory cirrhosis accompanied by subclinical and overt hypothyroidism.
[So] Source:Sci China Life Sci;, 2018 Mar 08.
[Is] ISSN:1869-1889
[Cp] Country of publication:China
[La] Language:eng
[Ab] Abstract:The aim of the present study was to investigate the relationship between hypothyroidism and thrombocytopenia in hepatitis Brelated compensatory liver cirrhosis and to determine whether treatment with levothyroxine and prednisone is superior in a multicenter, open-label, observational study in China. In total, 125 consecutive hepatitis B-related compensated liver cirrhosis patients with severe thrombocytopenia accompanied by hypothyroidism were included. The patients were divided into four groups according to treatment strategy: a control group (n=29), a prednisone group (n=25), a levothyroxine group (n=32) and a prednisone plus levothyroxine group (n=39). Severe thrombocytopenia was more prevalent in hepatitis B-associated compensatory liver cirrhosis patients with hypothyroidism than in euthyroid patients (29.6% vs. 14.7%, P<0.05). Combination treatment with prednisone and levothyroxine decreased the risk of bleeding and improved platelet recovery compared to control treatment and treatment with either prednisone or levothyroxine alone. The platelet count before therapy, serum thyroid stimulating hormone and combination treatment with prednisone and levothyroxine were associated with bleeding events. Therefore, the present study suggests that hypothyroidism is associated with severe thrombocytopenia in hepatitis B-associated compensatory liver cirrhosis. Treatment with prednisone plus levothyroxine may present a novel approach in these patients.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1007/s11427-017-9250-1

  5 / 105260 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29523470
[Au] Autor:El-Koofy N; Fouad HM; Fahmy ME; Helmy H; Shaker O; El-Karaksy HM; Mohsen N
[Ad] Address:Department of Paediatrics, Cairo University, Cairo, Egypt.
[Ti] Title:Copper concentrations in Egyptian infants with cholestasis: A single center study.
[So] Source:Arab J Gastroenterol;, 2018 Mar 06.
[Is] ISSN:2090-2387
[Cp] Country of publication:Egypt
[La] Language:eng
[Ab] Abstract:BACKGROUND AND STUDY AIMS: Hepatobiliary cholestatic disorders produce excess copper (Cu) retention in the liver, which is toxic and may cause hepatitis, fulminant hepatic failure, cirrhosis and death. In this study, we measured hepatic Cu and tested its correlation with serum Cu (S. Cu) and serum ceruloplasmin (S. ceruloplasmin) in cholestatic infants. PATIENTS AND METHODS: 41 cholestatic infants were enrolled as cases and 11 healthy infants as control subjects. S. Cu and S. ceruloplasmin were done for all infants and hepatic Cu was measured in the liver specimen in cases. RESULTS: Cases were 63.5% males with their age ranging between 1 and 7 months, while control subjects were 45.5% males with an age range between 3 and 18 months. Among cases, 41.5% had biliary atresia and 58.5% had intrahepatic cholestasis. Cholestatic infants had significantly higher levels of S. Cu and S. ceruloplasmin than control subjects and their hepatic Cu concentration was significantly higher than literature control. Infants with biliary atresia showed higher levels of Cu indices, with no statistical significance. Serum and hepatic Cu levels positively correlated with each other and with S. ceruloplasmin. Results of ROC curve showed that S. Cu was highly sensitive and specific for predicting hepatic Cu concentration at cut-off 181 µg/dl. CONCLUSION: Serum and hepatic Cu concentrations were markedly elevated in patients with cholestasis and positively correlated with each other and with S. ceruloplasmin. S. Cu level can predict hepatic Cu concentration.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  6 / 105260 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29523305
[Au] Autor:Thomsen KL; De Chiara F; Rombouts K; Vilstrup H; Andreola F; Mookerjee RP; Jalan R
[Ad] Address:UCL Institute for Liver and Digestive Health, University College London, United Kingdom; Department of Hepatology & Gastroenterology, Aarhus University Hospital, Denmark.
[Ti] Title:Ammonia: A novel target for the treatment of non-alcoholic steatohepatitis.
[So] Source:Med Hypotheses;113:91-97, 2018 Apr.
[Is] ISSN:1532-2777
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Non-alcoholic fatty liver disease (NAFLD) is a spectrum of liver diseases ranging from steatosis, through non-alcoholic steatohepatitis (NASH) to cirrhosis. The development of fibrosis is the most important factor contributing to NASH-associated morbidity and mortality. Hepatic stellate cells (HSCs) are responsible for extracellular matrix deposition in conditions of frank hepatocellular injury and are key cells involved in the development of fibrosis. In experimental models and patients with NASH, urea cycle enzyme gene and protein expression is reduced resulting in functional reduction in the in vivo capacity for ureagenesis and subsequent hyperammonemia at a pre-cirrhotic stage. Ammonia has been shown to activate HSCs in vivo and in vitro. Hyperammonemia in the context of NASH may therefore favour the progression of fibrosis and the disease. We therefore hypothesise that ammonia is a potential target for prevention of fibrosis progression of patients with NASH.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Process

  7 / 105260 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29523186
[Au] Autor:Zhang Y; Li Y; Zhang L; Li J; Zhu C
[Ad] Address:Department of Infectious Disease, the First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
[Ti] Title:Mesenchymal stem cells: potential application for the treatment of hepatic cirrhosis.
[So] Source:Stem Cell Res Ther;9(1):59, 2018 Mar 09.
[Is] ISSN:1757-6512
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Nowadays, orthotopic liver transplantation is considered the most efficient approach to the end stage of chronic hepatic cirrhosis. Because of the limitations of orthotopic liver transplantation, stem cells are an attractive therapeutic option. Mesenchymal stem cells (MSCs) especially show promise as an alternative treatment for hepatic cirrhosis in animal models and during clinical trials. Nevertheless, the homing of transplanted MSCs to the liver occurs in limited numbers. Therefore, we review the strategies for enhancing the homing of MSCs, mainly via the delivery routes, optimizing cell culture conditions, stimulating the target sites, and genetic modification.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Data-Review
[do] DOI:10.1186/s13287-018-0814-4

  8 / 105260 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29425759
[Au] Autor:Lu JG; Nguyen L; Samadzadeh S; Masouminia M; Mendoza A; Sweeney O; Tillman B; Afifyan N; Morgan T; French BA; French SW
[Ad] Address:Harbor UCLA Medical Center, 1000 W Carson St., Torrance, CA 90502, United States.
[Ti] Title:Expression of proteins upregulated in hepatocellular carcinoma in patients with alcoholic hepatitis (AH) compared to non-alcoholic steatohepatitis (NASH): An immunohistochemical analysis of candidate proteins.
[So] Source:Exp Mol Pathol;104(2):125-129, 2018 Feb 06.
[Is] ISSN:1096-0945
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Both non-alcoholic steatohepatitis (NASH) and alcoholic hepatitis (AH) can lead to cirrhosis and hepatocellular carcinoma. However, the rate of progression to cirrhosis and tumorigenesis in AH is greater than that in NASH. We asked whether there are differences between the two conditions in the expression levels of proteins involved in the pathogenesis of hepatocellular carcinoma. The proteins tested were presented at the 2017 American Association for the Study of Liver Diseases (AASLD) Liver Meeting as overexpressed in hepatocellular carcinoma: KLF4, SCL19A1, FANCG, HRH-1, DNMT1, DNMT3B, TNFR2, DUSP4, EGFR, Integrin α6, HDACII, PDE3A, BCL-XL, and MTCO2. The expression of these proteins was measured in liver biopsy sections from NASH and AH patients using immunohistochemical staining with fluorescent antibodies and then quantifying the fluorescence intensity morphometrically. In AH patients, levels of all tested proteins except HRH-1 were elevated compared to normal patients. In NASH patients, KLF4, SCL19A1, FANCG, HDACII, BCL-XL levels were increased compared to normal controls while HRH-1, DNMT1 and PDE3A levels were decreased. The relative expression of all proteins studied except BCL-XL was significantly higher in AH compared to NASH. In conclusion, proteins involved in hepatocellular cancer development are more highly expressed in AH compared to NASH and normal liver, which corresponds with the higher rate of tumorigenesis in AH patients compared to NASH patients.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  9 / 105260 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29408622
[Au] Autor:Zeng Y; Shen Z; Gu W; Wu M
[Ad] Address:Department of Medical Oncology, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, Jiangsu 210009, China; The First Clinical Medical College, Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210023, China. Ele
[Ti] Title:Inhibition of hepatocellular carcinoma tumorigenesis by curcumin may be associated with CDKN1A and CTGF.
[So] Source:Gene;651:183-193, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:This study aimed to explore crucial genes, transcription factors (TFs), and microRNAs (miRNAs) associated with the effects of curcumin against hepatocellular carcinoma (HCC). We downloaded data (GSE59713) from Gene Expression Omnibus to analyze differentially expressed genes (DEGs) between curcumin-treated and untreated HCC cell lines. Then, we identified the disease ontology (DO) and functional enrichment analysis of these DEGs and analyzed their protein-protein interactions (PPIs). Additionally, we constructed TF-target gene and miRNA-target gene regulatory networks and explored the potential functions of these DEGs. Finally, we detected the expression of CDKN1A, CTGF, LEF1 TF and MIR-19A regulated by curcumin in PLC/PRF/5 cells using RT-PCR. In total, 345 upregulated and 212 downregulated genes were identified. The main enriched pathway of upregulated genes was the TNF signaling pathway. The downregulated genes were significantly enriched in TGF-beta signaling pathway. In addition, most DEGs were significantly enriched in DO terms such as liver cirrhosis, hepatitis, hepatitis C and cholestasis (eg., CTGF). In the constructed PPI network, CDKN1A and CTGF were the key proteins. Moreover, LEF1, CDKN1A, and miR-19A that regulated CTGF were highlighted in the regulatory networks. Furthermore, the expression of CDKN1A, CTGF, LEF1 TF and miR-19A regulated by curcumin in PLC/PRF/5 cells was consistent with the aforementioned bioinformatics analysis results. To conclude, curcumin might exert its protective effects against HCC tumorigenesis by downregulating LEF1 and downregulating CTGF regulated by MIR-19A and upregulating CDKN1A expression.
[Mh] MeSH terms primary: Carcinogenesis/drug effects
Carcinoma, Hepatocellular/drug therapy
Connective Tissue Growth Factor/genetics
Curcumin/therapeutic use
Cyclin-Dependent Kinase Inhibitor p21/genetics
[Mh] MeSH terms secundary: Carcinoma, Hepatocellular/genetics
Cell Line, Tumor
Databases, Genetic
Gene Expression Regulation, Neoplastic/drug effects
Humans
Liver Neoplasms/genetics
Lymphoid Enhancer-Binding Factor 1/genetics
MicroRNAs/genetics
Neoplasm Proteins/genetics
Protein Interaction Maps
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (CDKN1A protein, human); 0 (CTGF protein, human); 0 (Cyclin-Dependent Kinase Inhibitor p21); 0 (LEF1 protein, human); 0 (Lymphoid Enhancer-Binding Factor 1); 0 (MIRN19 microRNA, human); 0 (MicroRNAs); 0 (Neoplasm Proteins); 139568-91-5 (Connective Tissue Growth Factor); IT942ZTH98 (Curcumin)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180207
[St] Status:MEDLINE

  10 / 105260 MEDLINE  
              first record previous record
select
to print
Photocopy
Full text

[PMID]: 29408309
[Au] Autor:Mohamed DI; Nabih ES; El-Waseef DAA; El-Kharashi OA; Abd El Samad AA
[Ad] Address:Department of Pharmacology, Faculty of Medicine, Ain Shams University, Cairo, Egypt.
[Ti] Title:The protective effect of pentoxifylline versus silymarin on the pancreas through increasing adenosine by CD39 in a rat model of liver cirrhosis: Pharmacological, biochemical and histological study.
[So] Source:Gene;651:9-22, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Impaired glucose homoeostasis due to insulin resistance and decrease sensitivity of pancreatic ß-cells is a feature of liver disease and results into hepatogenous diabetes. Decrease expression of CD39 was linked to inflammation and occurrence of diabetes. Therefore, we performed this study to explore the protective effect of pentoxifylline (PTX) and silymarin administration on the ß-cells of the pancreas in a rat model of thioacetamide induced liver cirrhosis. Biochemical, histological and immunohistochemistry studies of the liver and pancreas were performed and provided an evidence on the protective effect of PTX to pancreatic ß-cells compared to silymarin. Also, silymarin induced a significant improvement of liver cirrhosis compared to PTX. In conclusion, the potential protective effect of PTX against ß-cells deterioration could be attributed to increasing pancreatic CD39 expression and the subsequent increase of adenosine.
[Mh] MeSH terms primary: Adenosine/metabolism
Antigens, CD/metabolism
Apyrase/metabolism
Liver Cirrhosis, Experimental/drug therapy
Pancreas/drug effects
Pentoxifylline/therapeutic use
Protective Agents/therapeutic use
Silymarin/therapeutic use
[Mh] MeSH terms secundary: Amylases/blood
Animals
Disease Models, Animal
Insulin-Secreting Cells/drug effects
Liver/pathology
Liver Cirrhosis, Experimental/metabolism
Liver Cirrhosis, Experimental/pathology
Liver Function Tests
Male
Pancreas/pathology
Rats
Rats, Wistar
Transforming Growth Factor beta1/metabolism
[Pt] Publication type:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Name of substance:0 (Antigens, CD); 0 (Protective Agents); 0 (Silymarin); 0 (Transforming Growth Factor beta1); EC 3.2.1.- (Amylases); EC 3.6.1.5 (Apyrase); EC 3.6.1.5 (CD39 antigen); K72T3FS567 (Adenosine); SD6QCT3TSU (Pentoxifylline)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180207
[St] Status:MEDLINE


page 1 of 10526 go to page                         
   


Refine the search
  Database : MEDLINE Advanced form   

    Search in field  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/PAHO/WHO - Latin American and Caribbean Center on Health Sciences Information