scholarly journals Advances on liver cell‐derived exosomes in liver diseases

2020 ◽  
Author(s):  
Yan Jiao ◽  
Ping Xu ◽  
Honglin Shi ◽  
Dexi Chen ◽  
Hongbo Shi
Keyword(s):  
Liver Cell ◽  
Liver Diseases

Death by association: BH3 domain-only proteins and liver injury

2005 ◽  
Vol 289 (6) ◽  
pp. G987-G990 ◽  
Author(s):  
E. S. Baskin-Bey ◽  
G. J. Gores
Keyword(s):  
Cell Death ◽  
Liver Injury ◽  
Mitochondrial Dysfunction ◽  
Liver Cell ◽  
Liver Diseases ◽  
Chronic Liver Diseases ◽  
Concise Review ◽  
Bh3 Domain ◽  
A Cell

Apoptosis, a prominent form of cell death, is a prime feature of many acute and chronic liver diseases. Apoptosis requires mitochondrial dysfunction, which is regulated by proteins of the Bcl-2 family. Whether or not a cell should live or die is controlled by the interaction of multidomain Bcl-2 proteins with proapoptotic BH3 domain-only proteins of this family. Current models suggest multidomain, antiapoptotic Bcl-2 proteins prevent mitochondrial dysfunction by sequestering and/or preventing activation of its proapoptotic relatives. BH3-only proteins initiate cell death by neutralizing and or ligating multidomain prosurvival Bcl-2 proteins. Thus BH3 domain-only proteins are paramount in the apoptotic process as exemplified by the role of the BH3 domain-only protein Bid in liver injury. In this concise review, we will focus on how these BH3 domain-only proteins are regulated in the cell, their association with the Bcl-2 family of proteins, and finally, current information regarding their involvement in liver cell apoptosis and injury.

scholarly journals Hyperasialoglycoproteinemia in patients with chronic liver diseases and/or liver cell carcinoma

1984 ◽  
Vol 87 (6) ◽  
pp. 1217-1221 ◽  
Author(s):  
T. Sawamura ◽  
H. Nakada ◽  
H. Hazama ◽  
Y. Shiozaki ◽  
Y. Sameshima ◽  
...  
Keyword(s):  
Cell Carcinoma ◽  
Liver Cell ◽  
Liver Diseases ◽  
Chronic Liver ◽  
Chronic Liver Diseases ◽  
Liver Cell Carcinoma

scholarly journals Complex Assessment of Functional Activity of Chang Liver Cell Culture in Blood Serum of Patients with Liver Diseases of Various Etiology

2015 ◽  
Vol 7 (2) ◽  
pp. 16-24
Author(s):  
E.I. Cherkasova ◽  
M.S. Murtazaliyeva ◽  
T.N. Gorshkova ◽  
I.L. Novozhilov ◽  
A.V. Meleshina ◽  
...  
Keyword(s):  
Cell Culture ◽  
Blood Serum ◽  
Liver Cell ◽  
Functional Activity ◽  
Liver Diseases ◽  
Chang Liver Cell ◽  
Liver Cell Culture ◽  
Chang Liver

scholarly journals IMMUNOCYTOCHEMICAL STUDY OF GAMMA GLOBULIN IN LIVER IN HEPATITIS AND POSTNECROTIC CIRRHOSIS

1960 ◽  
Vol 111 (2) ◽  
pp. 285-294 ◽  
Author(s):  
Seymour Cohen ◽  
Goroku Ohta ◽  
Edward J. Singer ◽  
Hans Popper
Keyword(s):  
Lymph Nodes ◽  
Liver Cell ◽  
Liver Diseases ◽  
Gamma Globulin ◽  
Plasma Cells ◽  
Fluorescence Technique ◽  
Immunocytochemical Study ◽  
Postnecrotic Cirrhosis ◽  
Spleen And Lymph Nodes ◽  
Cell Breakdown

Gamma globulin was demonstrated by immunocytochemical fluorescence technique in many reticuloendothelial cells of the hepatic sinusoids and of the fibrous tracts in various forms of hepatitis and in postnecrotic cirrhosis. In other liver diseases and in normal livers, even in the presence of hypergammaglobulinemia, few if any gamma globulin-containing cells were found. In contrast, spleen and lymph nodes showed no difference between postnecrotic cirrhosis or hepatitis and other types of cirrhosis or non-hepatic hypergammaglobulinemias. The gamma globulin-containing cells in the liver are on cytologic grounds considered reticuloendothelial cells showing transition to plasma cells and exhibiting little or no phagocytosis of tissue breakdown products. These cells are assumed to form rather than engulf gamma globulin. The possibility that the gamma globulin formed represents antibody to liver cell breakdown products is discussed.

Inter-Relationships of dysfibrinogenaemia, Fetal Fibrinogen and Liver Cell Growth

1979 ◽  
Author(s):  
R.D. Barr ◽  
M.M. Clause ◽  
M.A. Johnston
Keyword(s):  
Cell Growth ◽  
Embryonic Development ◽  
Umbilical Cord ◽  
Liver Cell ◽  
Liver Diseases ◽  
Young Patients ◽  
Alpha Fetoprotein ◽  
Similar Data ◽  
Plasma Samples ◽  
Chronic Liver Diseases

When operationally defined as an excess of immunoassayable fibrinogen (IAF) over thrombin-clottable fibrinogen (TCF) of ≥ 1 g per L, dysfibrinogenaemia (DF) is demonstrable in more than 1/3 of patients with chronic liver diseases (CLD)1. Some features of this protein suggest a similarity to fetal fibrinogen.2 To further pursue these investigations, it was deemed necessary to identify a population of very young patients who were synthesizing fibrinogen rapidly. Twenty (2C Infected neonates, of gestational ages 24-41 weeks, were selected for study on the basic of TCF levels ≥5 g per L, Using antisera raised in sheep and rabbits, there was no demonstrable excess of IAF in the same plasma samples. Similar data were obtained fron assays in an unselected aeries of umbilical cord plasmas. These findings suggest either thet DF in CLD is not due to the renewed synthesis of fetal fibrinogen, or that fetal fibrinogen, like alpha-fetoprotein and fetal pre-albumin,3 is physiologically I evident only during early embryonic development.1. Barr, R.D. et al. J. Clin. Path. (1978) 31, 89.2. Barr, R.D. Blomedlcine (1979) in press.3. Tatarinov, Y, S. et al. Lancet (1978) 2, 1122.

Detection and clinical significance of acetoneinsoluble liver cell membrane antigen in sera of patients with chronic active liver diseases

1985 ◽  
Vol 20 (1) ◽  
pp. 37-47 ◽  
Author(s):  
Takao Tsuji ◽  
Kenji Takahashi ◽  
Masahiko Sawahara ◽  
Eiji Matsuura ◽  
Itaru Yamamoto
Keyword(s):  
Cell Membrane ◽  
Clinical Significance ◽  
Liver Cell ◽  
Liver Diseases ◽  
Liver Cell Membrane ◽  
Cell Membrane Antigen
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