scholarly journals IN VIVO AND IN VITRO EXPRESSIONS OF CCR1 AND CCR5 IN PATIENTS WITH ACTIVE SCHISTOSOMIASIS AND CHRONIC LIVER DISEASE

2010 ◽  
Vol 6 (1) ◽  
pp. 45-68
Author(s):  
Samir A. El-Masry ◽  
Mona S. Gouida ◽  
Khalid M. El-azab ◽  
Mahmoud E Nasr
Keyword(s):  
Liver Disease ◽  
Chronic Liver Disease ◽  
Chronic Liver

scholarly journals Initiation of hepatic stellate cell activation extends into chronic liver disease

2021 ◽  
Vol 12 (12) ◽  
Author(s):  
Vincent De Smet ◽  
Nathalie Eysackers ◽  
Vincent Merens ◽  
Mina Kazemzadeh Dastjerd ◽  
Georg Halder ◽  
...  
Keyword(s):  
Liver Disease ◽  
Chronic Liver Disease ◽  
Cell Activation ◽  
Stellate Cell ◽  
Chronic Liver ◽  
Cell Level ◽  
Two Phases ◽  
Druggable Targets

AbstractActivated hepatic stellate cells (aHSC) are the main source of extra cellular matrix in liver fibrosis. Activation is classically divided in two phases: initiation and perpetuation. Currently, HSC-based therapeutic candidates largely focus on targeting the aHSCs in the perpetuation phase. However, the importance of HSC initiation during chronic liver disease (CLD) remains unclear. Here, we identified transcriptional programs of initiating and activated HSCs by RNA sequencing, using in vitro and in vivo mouse models of fibrosis. Importantly, we show that both programs are active in HSCs during murine and human CLD. In human cirrhotic livers, scar associated mesenchymal cells employ both transcriptional programs at the single cell level. Our results indicate that the transcriptional programs that drive the initiation of HSCs are still active in humans suffering from CLD. We conclude that molecules involved in the initiation of HSC activation, or in the maintenance of aHSCs can be considered equally important in the search for druggable targets of chronic liver disease.

scholarly journals Albumin in patients with liver disease shows an altered conformation

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Margret Paar ◽  
Vera H. Fengler ◽  
Daniel J. Rosenberg ◽  
Angelika Krebs ◽  
Rudolf E. Stauber ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Liver Disease ◽  
Chronic Liver Disease ◽  
Chronic Liver ◽  
X Ray Scattering ◽  
Pathological Conditions ◽  
Healthy Donors ◽  
Relevant Variables ◽  
End Stage

AbstractHuman serum albumin (HSA) constitutes the primary transporter of fatty acids, bilirubin, and other plasma compounds. The binding, transport, and release of its cargos strongly depend on albumin conformation, which is affected by bound ligands induced by physiological and pathological conditions. HSA is both highly oxidized and heavily loaded with fatty acids and bilirubin in chronic liver disease. By employing small-angle X-ray scattering we show that HSA from the plasma of chronic liver disease patients undergoes a distinct opening compared to healthy donors. The extent of HSA opening correlates with clinically relevant variables, such as the model of end-stage liver disease score, bilirubin, and fatty acid levels. Although the mild oxidation of HSA in vitro does not alter overall structure, the alteration of patients’ HSA correlates with its redox state. This study connects clinical data with structural visualization of albumin dynamicity in solution and underlines the functional importance of albumin’s inherent flexibility.

Rifaximin in Chronic Liver Disease-induced Hepatic Encephalopathy: An In Vivo Longitudinal Study of Brain Metabolism on BDL Rats

2017 ◽  
Vol 7 ◽  
pp. S55-S56
Author(s):  
Emmanuelle Flatt ◽  
Cristina Cudalbu ◽  
Olivier Braissant ◽  
Stefan Mitrea ◽  
Dario Sessa ◽  
...  
Keyword(s):  
Liver Disease ◽  
Longitudinal Study ◽  
Hepatic Encephalopathy ◽  
Chronic Liver Disease ◽  
Brain Metabolism ◽  
Chronic Liver

P: 36 Antibiotic Rifaximin for Treatment of Chronic Liver Disease-Induced HE: A Longitudinal In Vivo 1H-MRS Study of Brain Metabolism on BDL Rats

2019 ◽  
Vol 114 (1) ◽  
pp. S18-S19
Author(s):  
Emmanuelle Flatt ◽  
Olivier Braissant ◽  
Stefanita Mitrea ◽  
Dario Sessa ◽  
Rolf Gruetter ◽  
...  
Keyword(s):  
Liver Disease ◽  
Chronic Liver Disease ◽  
Brain Metabolism ◽  
Chronic Liver ◽  
1H Mrs

In vivo, high-field, 3-Tesla 1H MR spectroscopic assessment of liver fibrosis in HCV-correlated chronic liver disease

2008 ◽  
Vol 113 (2) ◽  
pp. 289-299 ◽  
Author(s):  
A. Orlacchio ◽  
F. Bolacchi ◽  
M. Angelico ◽  
A. Mancini ◽  
V. Cozzolino ◽  
...  
Keyword(s):  
Liver Disease ◽  
Liver Fibrosis ◽  
Chronic Liver Disease ◽  
High Field ◽  
Chronic Liver ◽  
3 Tesla

High adiponectin in chronic liver disease and cholestasis suggests biliary route of adiponectin excretion in vivo

2005 ◽  
Vol 42 (5) ◽  
pp. 666-673 ◽  
Author(s):  
Frank Tacke ◽  
Torsten Wüstefeld ◽  
Rüdiger Horn ◽  
Tom Luedde ◽  
Annavarapu Srinivas Rao ◽  
...  
Keyword(s):  
Liver Disease ◽  
Chronic Liver Disease ◽  
Chronic Liver

Different mechanisms responsible for in vitro cell-mediated cytotoxicity to autologous hepatocytes in children with autoimmune and HbsAg-positive chronic liver disease

1985 ◽  
Vol 106 (6) ◽  
pp. 899-906 ◽  
Author(s):  
Mario Mondelli ◽  
Giorgina Mieli-Vergani ◽  
Flavia Bortolotti ◽  
Paolo Cadrobbi ◽  
Bernard Portmann ◽  
...  
Keyword(s):  
Liver Disease ◽  
Chronic Liver Disease ◽  
Chronic Liver

scholarly journals Functional Foods for the Management of Non-Alcoholic Fatty Liver Disease

2021 ◽  
Author(s):  
Venkateish V. Palanisamy ◽  
Nivya Vijayan ◽  
Vani Vijay ◽  
Baskaran Vallikannan ◽  
Madan Kumar Perumal
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Functional Foods ◽  
Chronic Liver ◽  
Alcoholic Fatty Liver ◽  
Sedentary Life Style ◽  
Alcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease (NAFLD) is increasingly evolving and a critical public health concern, raising the likelihood of liver cirrhosis, type 2 diabetes and cardiac problems. Existing epidemics of obesity and sedentary life style have lead to NAFLD’s elevated prevalence. In recent years there is profound change in the diet pattern, particularly the hypercaloric fat and carbohydrates for preventing or treating chronic liver disorders such as NASH and NAFLD. Functional and nutritional foods have contributed significantly to NAFLDimprovement and management. The justification for exploring functional foods as anti-NAFLD candidates for the chronic liver disease prevention is derived knowledge from in vitro and in vivo models. The findings from the in vitro and in vivo studies confirmed that these compounds are healthy, efficient, reversible inhibitors, when sufficiently consumed over a lifetime without severe toxicity, suitable for clinical trials and potentially becoming low-cost medication.

scholarly journals Acquired Dysfibrinogenemia in Acute and Chronic Liver Disease

1977 ◽  
Author(s):  
D.A. Lane ◽  
V.V. Kakkar ◽  
I.L. Woolf ◽  
R. Williams
Keyword(s):  
Liver Disease ◽  
Chronic Liver Disease ◽  
Polypeptide Chain ◽  
Degradation Products ◽  
Polyacrylamide Gel Electrophoresis ◽  
Sodium Dodecyl ◽  
Chronic Liver ◽  
Polypeptide Chains ◽  
Fibrin Monomers

Recent work with the thrombin-like snake venom Reptilase has suggested that the incidence of dysfibrinogenemia in liver disease may be much higher than has been recognised previously. In the present study, nine patients with fulminant hepatic failure and three with chronic liver disease, all exhibiting prolonged thrombin and ancrod clotting times, were examined for evidence of dysfibrinogenemia with a variety of physiochemical and clotting techniques. Sodium dodecyl sulphate Polyacrylamide gel electrophoresis revealed normal fibrinogen polypeptide chains, polypeptide chain crosslinking by Factor XIII, and in vitro generated plasmin degradation products of fibrinogen (FDP) in the plasma of these patients. Isolated and purified fibrin monomers were prepared by clotting plasma with Reptilase (Reptilase monomer) and thrombin (thrombin monomers). This enabled fibrin monomer polymerisation to be studied free of interference from plasma inhibitors such as FDP, and independent of any abnormal fibrinopeptide release. Delayed polymerisation of both Reptilase and thrombin monomers was demonstrated, providing an explanation for the observed prolonged clotting times. These results confirm that an abnormal fibrinogen may be produced during acute and chronic liver disease.

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