scholarly journals Mediation of inflammatory ascites formation induced by macromolecules in mice

2018 ◽  
Vol 65 (2) ◽  
pp. 151-162
Author(s):  
Károly Baintner
Keyword(s):  
Ascites Formation

THE ROLE OF ALDOSTERONE IN THE MECHANISM OF EXPERIMENTAL ASCITES FORMATION IN DOGS

1967 ◽  
Vol 56 (1_Suppl) ◽  
pp. S91
Author(s):  
G. S. Chudnovsky ◽  
A. G. Rummel ◽  
R. A. Samsonenko ◽  
I. S. Sterental
Keyword(s):  
Ascites Formation

Dynamics of ascites formation in rats with experimental cirrhosis

1980 ◽  
Vol 238 (5) ◽  
pp. F353-F357 ◽  
Author(s):  
J. M. Lopez-Novoa ◽  
M. A. Rengel ◽  
L. Hernando
Keyword(s):  
Renal Function ◽  
Glomerular Filtration Rate ◽  
Plasma Flow ◽  
Filtration Rate ◽  
Hepatic Cirrhosis ◽  
Renal Plasma Flow ◽  
Sodium Balance ◽  
Partial Removal ◽  
Experimental Cirrhosis ◽  
Ascites Formation

Renal function, sodium balance, and ascites formation were observed during induction in rats of experimental cirrhosis. The same variables were studied after partial removal of the ascites in rats with experimental cirrhosis. Glomerular filtration rate (GFR) and effective renal plasma flow (RPF) did not change during hepatic cirrhosis development. Positive sodium balance significantly higher than that observed in controls preceded the appearance of ascites for a period of about 2 wk. When the ascites was removed, GFR, RPF and positive Na balance did not change if Na intake remained constant. Ascites reformation rate was largely dependent on sodium balance. These data strongly support the "overflow" theory of ascites formation and are difficult to reconcile with the classical "underfilling" theory.

Temporal relationship between hyperaldosteronism, sodium retention and ascites formation in rats with experimental cirrhosis

Hepatology ◽  
1985 ◽  
Vol 5 (2) ◽  
pp. 245-250 ◽  
Author(s):  
Wladimiro Jiménez ◽  
Antonio Martinez-Pardo ◽  
Vicente Arroyo ◽  
Jordi Bruix ◽  
Antoni Rimola ◽  
...  
Keyword(s):  
Temporal Relationship ◽  
Sodium Retention ◽  
Experimental Cirrhosis ◽  
Ascites Formation

scholarly journals LY2157299 Monohydrate, a TGF-βR1 Inhibitor, Suppresses Tumor Growth and Ascites Development in Ovarian Cancer

Cancers ◽  
2018 ◽  
Vol 10 (8) ◽  
pp. 260 ◽  
Author(s):  
Qing Zhang ◽  
Xiaonan Hou ◽  
Bradley Evans ◽  
Jamison VanBlaricom ◽  
Saravut Weroha ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Tumor Growth ◽  
Cell Lines ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Migration And Invasion ◽  
Ascites Formation ◽  
Tgf Β1

Transforming growth factor beta (TGF-β) signaling has pleiotropic functions regulating cancer initiation, development, and metastasis, and also plays important roles in the interaction between stromal and cancer cells, making the pathway a potential therapeutic target. LY2157299 monohydrate (LY), an inhibitor of TGF-β receptor I (TGFBRI), was examined for its ability to inhibit ovarian cancer (OC) growth both in high-grade serous ovarian cancer (HGSOC) cell lines and xenograft models. Immunohistochemistry, qRT-PCR, and Western blot were performed to study the effect of LY treatment on expression of cancer- and fibroblast-derived genes. Results showed that exposure to TGF-β1 induced phosphorylation of SMAD2 and SMAD3 in all tested OC cell lines, but this induction was suppressed by pretreatment with LY. LY alone inhibited the proliferation, migration, and invasion of HGSOC cells in vitro. TGF-β1-induced fibroblast activation was blocked by LY. LY also delayed tumor growth and suppressed ascites formation in vivo. In addition, independent of tumor inhibition, LY reduces ascites formation in vivo. Using OVCAR8 xenograft specimens we confirmed the inhibitory effect of LY on TGF-β signaling and tumor stromal expression of collagen type XI chain 1 (COL11A1) and versican (VCAN). These observations suggest a role for anti-TGF-β signaling-directed therapy in ovarian cancer.

scholarly journals Evolution of sarcoma 180 in mice infected with Trypanosoma cruzi

1983 ◽  
Vol 78 (3) ◽  
pp. 237-244
Author(s):  
Fausto Edmundo Lima Pereira ◽  
William Assad Sassine ◽  
Dimith Chequer Bouhabib ◽  
Elton de Almeida Lucas
Keyword(s):  
Weight Gain ◽  
Trypanosoma Cruzi ◽  
Tumor Cells ◽  
Ascitic Fluid ◽  
Tumor Development ◽  
Sarcoma 180 ◽  
Tumor Inoculation ◽  
Time Intervals ◽  
Tumor Challenge ◽  
Ascites Formation

Mice infected with Trypanosoma cruzi were challenged with 2x10[raised to the power of 6] cells of sarcoma 180 (ascite tumor) by i.p. route, on day seven post infection. Tumor development was followed by evaluation of weight gain, by measurement of ascitic fluid produced and enumeration of tumor cells in ascitic fluid. Infected mice were more resitant to tumor development as demonstrated by reduction in ascites formation and by reduction in the number of tumor cells in ascitic fluid, at different time intervals after tumor challenge. The number of peritoneal cells exsudated after tumor inoculation was greater in infected mice than in controls. This increased resitance of mice infected with T. cruzi to tumor development could be due to the action of macrophages activated by the infection and by the action of endotoxins absorbed from the gut or produced by the own parasite.

scholarly journals Managing portal hypertension in patients with liver cirrhosis

F1000Research ◽  
2018 ◽  
Vol 7 ◽  
pp. 533 ◽  
Author(s):  
Tilman Sauerbruch ◽  
Robert Schierwagen ◽  
Jonel Trebicka
Keyword(s):  
Portal Hypertension ◽  
Viral Infections ◽  
Current Knowledge ◽  
Beta Blockers ◽  
Recurrent Bleeding ◽  
The Past ◽  
Ascites Formation ◽  
Inflammatory Stimuli ◽  
Impact On Survival ◽  
Initiating Factors

Portal hypertension is one cause and a part of a dynamic process triggered by chronic liver disease, mostly induced by alcohol or incorrect nutrition and less often by viral infections and autoimmune or genetic disease. Adequate staging - continuously modified by current knowledge - should guide the prevention and treatment of portal hypertension with defined endpoints. The main goals are interruption of etiology and prevention of complications followed, if necessary, by treatment of these. For the past few decades, shunts, mostly as intrahepatic stent bypass between portal and hepatic vein branches, have played an important role in the prevention of recurrent bleeding and ascites formation, although their impact on survival remains ambiguous. Systemic drugs, such as non-selective beta-blockers, statins, or antibiotics, reduce portal hypertension by decreasing intrahepatic resistance or portal tributary blood flow or by blunting inflammatory stimuli inside and outside the liver. Here, the interactions among the gut, liver, and brain are increasingly examined for new therapeutic options. There is no general panacea. The interruption of initiating factors is key. If not possible or if not possible in a timely manner, combined approaches should receive more attention before considering liver transplantation.

Abdominal pseudocysts and ascites formation after ventriculoperitoneal shunt procedures

1975 ◽  
Vol 43 (4) ◽  
pp. 476-480 ◽  
Author(s):  
S. Walton Parry ◽  
John F. Schuhmacher ◽  
Raeburn C. Llewellyn
Keyword(s):  
Cerebrospinal Fluid ◽  
Ventriculoperitoneal Shunt ◽  
Signs And Symptoms ◽  
Late Complications ◽  
Neurological Symptoms ◽  
Shunt Malfunction ◽  
Content Type ◽  
Ventriculoperitoneal Shunts ◽  
Ascites Formation ◽  
Fine Print

✓The authors report three patients with abdominal pseudocysts and one with cerebrospinal fluid ascites as late complications of ventriculoperitoneal shunts. The presenting signs and symptoms were those of an intraabdominal abnormality, with no neurological symptoms suggestive of shunt malfunction.

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