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[Studies on fibrinolysis and ascites accumulation associated with peritonitis carcinomatosa--inducer of plasminogen activator (IPA) in malignant ascites tumor].

This study was undertaken to investigate the mechanism for hyperfibrinolysis in the ascites associated with peritonitis carcinomatosa. Various combinations of mouse MM2 ascites tumor (MAT) and mouse peritoneum (Mpr) and plasminogen (Plg) were incubated in medium 199 and the fibrinolytic activity of each preparation was assayed. 1) Among the preparations, the preparation of MAT plus Mpr plus Plg showed particularly high fibrinolytic activity. This suggests that plasminogen activator (PA) production is initiated by MAT together with Mpr. 2) Equal volumes of the ultrafiltrate and the concentrate of supernatant from MAT were each separately treated with a Mpr plus Plg preparation and incubated. The fibrinolytic activity of the ultrafiltrate was 10 times as great as that of the concentrate. 3) The ultrafiltrate of MAT was extracted in turn with petroleum ether, ether and hexane. The fibrinolytic activity of the petroleum ether and hexane extracts was higher than that of the ether extracts. These results suggest that MAT has a low polarity, low molecular weight, and lipid like substance (inducer of PA,IPA), which stimulates the Mpr to release PA.

Animals↗

[Eosinophilic gastroenteritis simulating ascites (eosinophilic ascites). Presentation of a case and review of the literature].

Eosinophilic gastroenteritis is an uncommon disorder of unknown etiology characterized by recurrent episodes of infiltration of the gastrointestinal wall with eosinophils and peripheral eosinophilia. The Authors report a patient in which ascites with eosinophilia in the ascitic fluid was the cardinal feature of the disease. A low E.S.R. in the acute phase of illness was found. Steroids are indicated in patients presenting obstructive symptoms or malabsorption. In our case the treatment was not necessary because of the spontaneous remission of the symptoms.

Adult↗

Flux of free fatty acids among host tissues, ascites fluid, and Ehrlich ascites carcinoma cells.

The role of plasma free fatty acids (FFA) in the transport of fatty acids from host tissues to Ehrlich ascites carcinoma in mice was studied. [9,10-(3)H] Palmitate complexed to mouse serum (albumin) was injected either intraperitoneally or intravenously into unanesthetized tumor-bearing mice. The incorporation of radioactivity into tumor extracellular fluid FFA, tumor cell FFA, neutral lipid, phospholipid, water-soluble material in cells and fluid, plasma FFA, host carcass total lipid fatty acids, and water-soluble (i.e., nonlipid) material was measured. In addition, the quantity of fatty acid in each of the above lipid fractions was determined. The data were analyzed by multicompartmental analysis (SAAM) using a digital computer, and fractional rate constants of FA movement within and out of the host-tumor system were calculated. These rate constants and pool size measurements were used to estimate the corresponding fluxes. Although FFA in the tumor's extracellular fluid were replaced rapidly, almost none of the newly formed fluid FFA was derived from plasma FFA. Moreover, the transfer of FFA from the tumor extracellular fluid FFA to plasma FFA was virtually negligible. We suggest that the net amount of FFA required to replace the fluid FFA utilized for tumor energy and growth may be derived from direct transfer of FFA from host tissues to the ascitic fluid and that plasma FFA is not an intermediate in this transport process. The transport of FFA from the host to tumor cell lipids through the tumor extracellular fluid was about 26-fold greater than that required to account for net lipid accumulation during growth.

Animals↗

Cell free ascitic fluid prevents loss of cell surface sialic acid from Zajdela Ascitic Hepatoma cells in culture.

In the Zajdela Ascitic Hepatoma (ZAH), a rat tumor, high levels of cell surface sialic acid residues are present which masked the immunogenicity of the cells. We have shown here that cell surface sialic acid level goes down rapidly when ZAH cells are put in culture. The reduction in surface sialic acid levels is due to a decrease in sialic acid residues on the major sialylated glycoprotein, gp 120, as well as a decrease in gp 120 polypeptide. The loss of sialic acid from the cultured cells is reduced if the cells are cultured in the presence of cell free ascitic fluid from ZAH tumor.

Animals↗

Glycoproteins from ascitic fluid of Ehrlich ascites tumor. Isolation and chemical characterization.

Three glycoprotein bands were identified by polyacrylamide disc gel electrophoresis in the perchloric acid soluble fraction of ascitic fluid of Ehrlich ascites tumor in mice. The three proteins were first separated by a new discontinuous preparative electrophoresis apparatus described previously [1]. They were further purified on Sephadex G-100 and then were subjected to chemical characterization. These glycoproteins were rich in glutamic and aspartic acids and contained the sugar moieties galactose, mannose, fucose, N-acetyl-D-glucosamine and sialic acid. The percent sugar composition ranged from 17.7-37.3% of the total weights of these glycoproteins.

Amino Acids↗

Physical studies on glycoproteins from ascitic fluid of Ehrlich ascites tumor.

Three glycoproteins, designated as F, M and S glycoproteins were identified in the HCIO4-soluble fraction of ascitic fluid of Ehrlich ascites tumor by 8% polyacrylamide disc gel electrophoresis. They were separated and purified as described previously (Reznick, A.Z. and Winzler, R.J. (1973) Fed. Proc. 32, 368 and Reznick, A.Z., Allen, H.J. and Winzler, R.J. (1973) Anal. Biochem. 52, 395-401) and subjected to physical characterization. Several physical properties such as molecular weights, sedimentation and diffusion coefficients, partial specific volumes, Stoke's radii and frictional ratios were determined. The physical parameters of F and S glycoproteins resemble data that have been reported for orosomucoid and haptoglobin-like glycoproteins, respectively. Properties of M glycoprotein could not be associated with a known glycoprotein.

Animals↗

Purification of ornithine decarboxylase-inducing factor from cell-free ascites fluid of Ehrlich ascites tumor and its characteristics.

The ornithine decarboxylase-inducing factor (ODC factor) was purified about 1,000-fold in 42% yield from the ascites fluids of an Ehrlich ascites tumor by a combination of centrifugation and concanavalin A (ConA) treatment. A single ip injection of 0.5 micrograms of the purified factor per mouse resulted in half-maximum induction of liver ODC. The factor was found to be a trypsin- and chymotrypsin-resistant, acidic glycoprotein (pI about 4.43) with a minimum molecular weight of about 70 kilodaltons, containing a disulfide bond(s) in its functional domain. It did not react with ConA. This factor induced retrodifferentiation of liver function, causing a marked increase of prototype M2 isozyme of pyruvate kinase. It reduced liver catalase activity, and also modified thyroid hormone metabolism, reducing the serum levels of T4 and T3. These results suggest that the ODC factor is multifunctional and induces many of the changes observed in a tumor-bearing host.

Animals↗

Ascitic versus solid growth of Ehrlich ascites tumor influenced by immunological factors.

A certain number of CBA mice injected intraperitoneally with 1 X 10(6) or fewer Ehrlich ascites tumor (EAT) cells did not develop ascites tumors but solid tumors at the inoculation site. The incidence of solid tumors proved dependent on the level of immunological reactivity of recipients, being increased in mice with increased immunological potency and absent in mice in which this potency was reduced. Mice bearing solid tumors had increased level of cytotoxic antitumor antibodies in serum. Possible reasons for a greater immune resistance of cells growing in subcutaneous tissue, than in the abdominal cavity, are discussed.

Animals↗

Targeting of peritoneum by the small numbers of isogeneic and allogeneic ascites carcinoma cells that infiltrate or attach to peritoneum during ascites growth.

In the course of development of an in vivo invasion model, sublines of a series of allogenic and isogeneic carcinoma cell lines have been selected that show enhanced invasion of the peritoneum. It was found that, during the proliferation of tumor cell lines in ascitic form in the abdominal cavity, small numbers of cells infiltrated or firmly adhered to the peritoneum in at least 8/12 of the tumor-host combinations tried. After thorough washing of the peritoneum it was disaggregated by an enzyme mixture, and the resulting mixture of normal and tumor cells was inoculated intraperitoneally. Peritoneal isolations were made serially for 3 to 12 times. In 6 of 8 cases where the isolation produced a stable ascites, the cells showed enhanced peritoneal invasion compared with the parent cell line. The invasion of some of the cell lines was tested in another invasion model consisting of cultured mouse buccal mucosa (9/10 cell lines invaded the explant). In 3/3 cell lines showing enhanced peritoneum invasion in vivo, there was no enhanced invasion of the buccal mucosa. The enhanced peritoneum invasion appears to be tissue specific rather than a general increase in invasion potential. Pairs of high- and low-invasive cell lines were obtained that should be useful for screening for invasion modulating agents using the mouse ascites/peritoneum in vivo model. It is suggested that the method might be generalized to produce various tumor cell lines that target for the normal tissues that are adjacent to proliferating solid or circulating tumors.

9,10-Dimethyl-1,2-benzanthracene↗

Electron microscopic evidence of surface immunoglobulins in Yoshida ascites sarcomas and ascites hepatomas.

Yoshida ascties sarcoma and its variants and several azo dye-induced ascites hepatomas of rats were examined by an immuno-peroxidase technique to demonstrate surface immunoglobulins. More than 60% of the tumor cells in 8 ascites tumors showed positive surface staining (Group A), whereas the other 9 tumors were less than 15% positive (Group B). One tumor showed 34% positive reaction. The staining did not show capping. Six of the 8 Group-A tumors were single cell type, while 5 of the 9 Group-B tumors were island type. Intravenous transplantation rate was very low (less than 10%) in 2 of the 6 Group-B tumors, but only 1 of the 7 Group-A tumors showed moderately low (40%) intravenous transplantation rate. All of the 8 Group-A tumors showed survival period of less than 35 days after intraperitoneal transplantation, while the survival period was more than 45 days in 3 out of the 9 Group-B tumors.

Animals↗

[DNA-bound lipids of the cells of Zajdela ascites hepatoma and of Ehrlich ascites cancer].

DNA-bound neutral lipids (NL) and phospholipids (PL) were isolated and characterized from the Zajdel ascites hepatoma (ZAH) and Ehrlich ascites carcinoma (EAC) cells. The lipids are represented by light- and tightly bound components. It was shown, that the tumour DNA contained minor amount of NL (25, 17 micrograms and 16.87 micrograms per mg DNA, respectively) and of PL (4.54 micrograms and 5.36 micrograms per mg DNA, respectively, for ZAH and EAC). The composition of the tumour DNA-bound lipids was shown to differ from that of DNA-bound lipids of liver and thymus of intact rats by the next parameters: NL/PL ratio is much more than one; increased content of FC; equal values of the three basic ratios--CE/FC, NL/PL, cholesterol/PL, presence of mono- and triglycerides.

Animals↗

Temporal aspects of O-glycosylation and cell surface expression of ascites sialoglycoprotein-1, the major cell surface sialomucin of 13762 mammary ascites tumor cells.

We have investigated the biosynthesis and cell surface expression of the major cell surface sialomucin (ascites sialoglycoprotein-1 (ASGP-1] of 13762 rat mammary ascites tumor cells by pulse or pulse-chase metabolic labeling combined with precipitation with peanut agglutinin and alkaline borohydride elimination or proteolytic fragmentation. The minimum time for initial glycosylation was estimated from the time required for the protein to acquire the ability to bind to peanut agglutinin to be less than 5 min. Moreover, when cells were labeled with threonine for 5 min and the ASGP-1 isolated by peanut agglutinin precipitation, 3% of the labeled threonine could be converted to 2-aminobutyric acid by alkaline borohydride elimination of the carbohydrate, indicating that at least 3% of the threonines of ASGP-1 are O-glycosylated within 5 min of polypeptide synthesis. The minimum time between the final glycosylation reactions in the cell and appearance of ASGP-1 at the cell surface was determined by trypsinizing galactose- or glucosamine-labeled cells at timed intervals after labeling to occur within 5-10 min of labeling. Both labeled glucosamine and galactosamine appeared in ASGP-1 fragments within 5 min, but the amount of labeled galactosamine was less than the amount of labeled glucosamine until after 20 min, when the 1:1 equilibrium ratio was reached. The half-time for appearance of glucosamine-labeled ASGP-1 at the cell surface was found to be greater than 4 h. The minimum time required from synthesis of the ASGP-1 polypeptide to appearance at the cell surface was determined by leucine labeling and proteolysis to be 70-80 min. These combined studies suggest a continuum of O-linked oligosaccharide initiation events extending over most of the period of ASGP-1 biosynthesis and transit from the endoplasmic reticulum to the cell surface.

Adenocarcinoma↗

[Treatment of ascites with reinfusion of ascitic fluid concentrate].

Ascites which is refractory to common therapeutical measures is a great problem. It deteriorates patient's life and is a sign of poor prognosis. Different methods of peritoneal fluid reinfusion belong to effective non-pharmaceutical therapeutic approaches. Main target of this study was to analyse the effectiveness and safety of peritoneal fluid reinfusion and to compare two methods of its administration (i.v. reinfusion and intraperitoneal reinfusion). During three years we have performed 97 reinfusions in 4 patients (2 women and 2 men; mean age 56 years). I.v. reinfusion was administered 68 times and intraperitoneal ewinfusion was performed 28 times. Usually we evacuated 8000 ml of ultrafiltrate. The most common complications were haemoperitoneum (6x) and short-term chills (2x). We didn't have any complications such as coagulopathy, peritonitis or circulation collapse. Intraperitoneal administration seems to be more advantageous when compared with i.v. application, because of less frequent detection of fibrin degradation products and D-dimers after the procedure and higher diuresis during the following days. (Tab. 2, Fig. 5, Ref. 13.).

Ascites↗

[Therapy-induced formation of ascites and pleural effusion during initial chemotherapy in a patient with non-Hodgkin's lymphoma. Ascites and pleural effusion during initial chemotherapy].

We report on a 16-year old boy with non-Hodgkin's lymphoma who acquired a therapy-induced ascites and pleural effusion during initial chemotherapy. This life-threatening condition could be controlled by intensive care measures including pleural tap and drainage. Chemotherapy could then be continued. The patient has been in continuous complete remission for 18 months.

Adolescent↗

[Polymorphism of a tumor cell population and selective processes. II. Change in the correlation of the numbers of 2 subpopulations of Ehrlich-Ich Ph ascites tumor cells in mice under the action of cell-free ascitic fluid and its fractions].

After repeated injections to mice of cell-free fluid the inhibition of growth of ascitic cell number was noticed already on the 5th day after transplantation of tumor. It was found that the inhibition of growth was due to the death of cells having 45 chromosomes, and containing A + B + 2C- and A + D + 2C-markers.

Animals↗

Translation of ascites and mengovirus RNA in fractionated cell-free systems from uninfected and mengovirus-infected Ehrlich-ascites-tumor cells.

We have prepared homologous, fractionated, cell-free translational systems from uninfected and mengovirus-infected Ehrlich ascites tumor cells in order to determine what alterations occur following virus infection in the translational machinery of the host cell. Two major differences distinguish the system developed from infected cells. First, it has a 40% lower rate of protein synthesis, primarily a consequence of the rate of chain elongation, which is depressed to 60 amino acids/min from 90 amino acids/min in the system from uninfected cells. Second, at supraoptimal concentrations of Mg2+ and K+ the system from virus-infected cells supports the translation of mengovirus RNA but not host mRNA. These differences between the two systems may reflect specific changes which are responsible for the selective translation of mengovirus RNA in the infected cell. In both systems the optimal concentrations of polyamines, monovalent and divalent cations, mRNA, and ribosomal subunits are the same for the translation of either host or viral RNA. This uniformity is useful in experiments, designed to investigate the selective translation of viral RNA, where various components of the two systems are interchanged.

Animals↗

[Abortive myxovirus infection of Ehrlich ascites carcinoma cells. Analysis of virus-specific structures in the ascitic fluid].

In the course of classical fowl plague virus reproduction in Ehrlich ascites carcinoma cells both hemagglutinins and S-antigen accumulate and titers of the infectious activity increase. However virus reproduction does not terminate in formation of virus, and subviral structures are found in the liquid fraction of the infected cells. Analysis of these structures has shown them to have a sedimentation coefficient of 350-370S and buovant density 1.29 g/ml. The rapidly sedimenting structure has complement-fixing hemagglutinating activity but bow infectivity.

Amino Acids↗

[Thymidine transport and its incorporation into the cellular DNA of Ehrlich ascites cancer and Zajdela's ascitic hepatoma in the presence of thiophosphamide and thiophosphamide-modified DNA].

Antitumour agents, thiotepa and alkylated DNA, inhibit the transport of thymidine in the cells within the first minutes of incubation. Penetration of the exogenous DNA in the Ehrlich ascites tumour cells and stimulation of this process with dimethylsulfoxide are shown. The possible mechanism of the antitumour effect of alkylated DNA is discussed.

Alkylation↗