Disease relevance of Ascites

• Epithelial cells in culture often express vimentin as well as cytokeratins, but co-expression in vivo, as reported for pleomorphic adenomas of the parotid gland and metastatic carcinoma cells in ascites or pleural fluid, is still controversial [1].
• Patients with edema, ascites, or both had significantly greater elevation of plasma aldosterone levels compared to nonedematous patients; these patients also demonstrated a substantial degree of hepatic dysfunction as evidenced by lower serum albumin levels and higher bilirubin and alkaline phosphatase levels [2].
• The alloantigenic phenotype of these MuLV+ and MuLV- cell lines was H-2D+, H-2K+, Thy-1.2+ or -, PC.1+ or -, Lyt-1.2-, Lyt-2.2-, Ia.7-, and TL.2-. A unique antigen was defined on the BALB/c ascites sarcoma Meth A with antisera prepared in BALB/c or (BALB/c X C57BL/6)F1 mice [3].
• Guinea pig hepatoma cells (line-10) growing as ascites were studied for the presence of immunoglobulin, C4, and C3 (components of complement) on their surfaces [4].
• Rats with carbon tetrachloride-induced cirrhosis and ascites were investigated using balance studies [5].

Psychiatry related information on Ascites

• The analysis showed that a poor prognosis was associated with a low prothrombin index, marked ascites, GI bleeding, high age, high daily alcohol consumption, high bilirubin and alkaline phosphatase and low albumin values, little liver connective tissue inflammation, and poor nutritional status [6].

High impact information on Ascites

• Treatment failure was defined as a doubling of bilirubin levels to more than 70 mumol per liter or the occurrence of a severe complication (ascites or variceal bleeding) or an adverse reaction [7].
• We report here that administration of ATP in combination with diethylmaleate and X-rays leads to complete regression of 95% of Ehrlich ascites tumours in mice [8].
• Histone exchange in chromatin of hydroxyurea-blocked Ehrlich ascites tumour cells [9].
• Substitution of guanine for a specific base in tRNA by extracts of Ehrlich ascites tumour cells [10].
• Tumor cells secrete a vascular permeability factor that promotes accumulation of ascites fluid [11].

Chemical compound and disease context of Ascites

• Such treatment with tocopherol does not, however, alter the magnitude or duration of the adriamycin-induced suppression of DNA synthesis in P388 ascites tumor, nor does it diminish the antitumor responsiveness of P388 ascites tumor [12].
• An optimal diuretic regimen for cirrhotic ascites. A controlled trial evaluating safety and efficacy of spironolactone and furosemide [13].
• These results suggest that the galactosyltransferase from the ascites of ovarian cancer patients catalyzes the transfer of galactose to N-acetylglucosamine, irrespective of whether it is a part of an N-glycan or an O-glycan [14].
• Metabolic fate on 1-hexylcarbamoyl-5-fluorouracil and 5-fluorouracil in mice bearing ascites sarcoma 180 [15].
• Peritoneal macrophages exposed in vivo for 7-21 d to ascites fluid derived from plasma containing sixfold elevations of lipoproteins did not accumulate unesterified or esterified cholesterol [16].

Biological context of Ascites

• A major cell-surface glycoprotein of the TA3-Ha ascites mammary adenocarcinoma diminished during transfer from ascites growth to cell growth in suspension culture [17].
• Thromboxane-receptor blockade increases water diuresis in cirrhotic patients with ascites [18].
• Patients with ascites (n = 9) had significantly increased total blood volume, cardiac output, pulse rate, plasma renin activity, and plasma norepinephrine concentration, as well as decreased systemic vascular resistance and arterial blood pressure compared with patients without ascites (n = 8) [19].
• METHODS: Arterial pressure, cardiac output, and total peripheral resistance were measured before and after the administration of a cannabinoid CB1 receptor antagonist to cirrhotic rats with ascites and to control rats [20].
• Cardiac output (thermodilution; n = 8), mean circulatory filling pressure (balloon technique; n = 6), and blood volume (Evans blue dye; n = 7) were investigated in a rat model of liver cirrhosis without ascites induced by a 12-week individualized CCl4/phenobarbital treatment [21].

Anatomical context of Ascites

• Tissue localization of a human pancreas cancer-associated antigen (PCAA) and carcinoembryonic antigen (CEA) was studied in a homologous pancreatic tumoral xenograft, a human pancreatic cancer line established from ascites (AsPC-1), with the use of the indirect immunofluorescence technique with specific anti-PCAA and anti-CEA antisera [22].
• METHODS: NO2- accumulation produced by macrophages from control rats and cirrhotic rats with ascites was determined. iNOS messenger RNA and protein expression were analyzed by Northern and Western blot and immunocytochemical analysis [23].
• The aim of this study was to investigate the lipoxygenase pathway of arachidonic acid metabolism and its influence in leukocyte trafficking in patients with cirrhosis and ascites [24].
• METHODS: Neutrophils (polymorphonuclear leukocytes [PMN]) were isolated from patients with cirrhosis and ascites and healthy subjects, and 5-lipoxygenase (5-LO) messenger RNA levels and 5-LO-derived products were measured [24].
• Two patients with cirrhosis and ascites complicated by extensive unilateral pleural transudates refractory to therapy with dietary sodium restriction, diuretics, and repeated thoracentesis were successfully managed by tetracycline-induced pleural symphysis [25].

Gene context of Ascites

• The formation of ascites was directly associated with expression of VEGF/ VPF, and survival was inversely associated with expression of IL-8 [26].
• Human MCP-1 protein was also detected in culture supernatants from cell lines and in ascites from human ovarian tumor xenografts which induce a peritoneal monocytosis in nude mice [27].
• After adjustment for presence of more than 1-L ascites or age more than 50 years, nuclear p53 staining did not retain independent prognostic significance in stage III/IV tumors [28].
• The mean volume of ascites, number of tumor cells in ascites, and the peritoneal capillary permeability were significantly suppressed by VEGF-A nAb and KDR/Flk-1 nAb treatment [29].
• When ascites tumor cells were cultured for 7 days, TNF-alpha expression ceased but could be reinduced by treatment with TNF-alpha or IL-1 beta [30].
• Tumor cell monitoring revealed a reduction of EpCAM-positive malignant cells in ascites by up to 5 log [31].

Analytical, diagnostic and therapeutic context of Ascites

• In vivo chemotherapy of mice bearing TA3 ascites tumors was most effective with respect to tumor growth inhibition and animal survival when GlcN and FUrd were combined [32].
• When ovarian tumor cells, freshly isolated from carcinomatous ascites or surgical specimens, were used as target cells in the cytotoxicity assay, 8 of 14 PBLs and 5 of 7 TAL preparations lysed the autologous tumor after treatment with IL-2, while no spontaneous reactivity was observed in any of the 14 patients tested [33].
• METHODS: Changes in plasma renin, aldosterone, and norepinephrine, and in systemic and hepatic hemodynamics were assessed 1 hour and 6 days after complete mobilization of ascites in 37 patients treated by total paracentesis plus intravenous dextran-70 infusion [34].
• Fibronectin determination in ascites in combination with other parameters suitable for exclusion of infectious or pancreatic origin of ascites may prove useful in the differential diagnosis of ascites [35].
• Human atrial natriuretic factor (ANF) levels were measured before and after peritoneovenous shunt implantation in 10 cirrhotic patients with ascites, in whom sodium retention is a major clinical problem [36].

References