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  • 1
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 34 (1956), S. 765-767 
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 34 (1956), S. 163-166 
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 37 (1959), S. 774-779 
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-1440
    Keywords: Ascites ; Liver cirrhosis ; Plasminogen ; Antiproteases ; Fibrinolysis ; Dexamethasone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Fibrinolysis induced by the infusion of plasminogen activators into the circulation has been shown to cause coagulation disorders in ascites retransfusion. Dexamethasone is known to inhibit the synthesis of plasminogen activators by peritoneal macrophages. We therefore assessed its potential in preventing the occurrence of fibrinolysis by injecting 16 mg dexamethasone intraperitoneally in 10 patients 24 h before ascites retransfusion was performed. In addition, the effect of dexamethasone upon the activity or concentration of several proteases and antiproteases related to coagulation in plasma and ascites was analyzed on 15 occasions. An increase of the activity of plasminogen, α2-antiplasmin, and antithrombin III, and in the concentration of α1-protease inhibitor in ascites was induced by the dexamethasone injection. However, the reaction was not identical in all patients. Those patients having an increase of plasminogen activities of 0.6 CTA U/ml or more did not show signs of fibrinolysis during retransfusion. The results obtained indicate that intraperitoneal injection of dexamethasone decreases the concentration of plasminogen activators in ascites and thereby reduces the risk of coagulation disorders during retransfusion procedures. Since the effect is variable and not sustained, assessment of preoperative plasminogen concentrations is mandatory in order to prevent complications.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-1440
    Keywords: Plasminogen ; Fibronectin ; Antiproteases ; Ascites ; Liver cirrhosis ; Tumors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The concentrations of several proteases and antiproteases known to be present in ascites were tested in plasma and ascitic fluid with regard to their ability to separate ascites according to malignant or nonmalignant disease. Seventeen patients with proven malignant ascites and 37 with ascites due to liver cirrhosis were included. Activities of plasminogen,α 2-antiplasmin, antithrombin-III, and factor V, and the concentration ofα 1-protease inhibitor were significantly higher in the plasma of patients with malignant ascites than in cirrhotic patients. Fibronectin, plasminogen,α 2-macroglobulin,α 1-protease inhibitor, antithrombin-III, and albumin revealed higher concentrations or activities in malignant ascites than in cirrhotic ascites. Due to a wide variation of most parameters, only fibronectin, antithrombin III, andα 1-protease inhibitor in ascites had a sensitivity and specificity higher than 90% for malignant ascites. When the specific protein/albumin ratio was used, only the accuracy of fibronectin was increased reaching a sensitivity and specificity of 100%. The plasma/ascites gradients of the proteins assessed differed significantly, that of fibronectin being much higher (22±7) than that of all other proteins. In malignant ascites fibronectin concentration was only correlated withα 1-protease inhibitor concentration but not with the concentration or activity of all other proteins, while in cirrhotic ascites most proteins revealed a positive correlation. The determination of the fibronectin concentration or the fibronectin/albumin ratio in ascites can differentiate malignant and nonmalignant ascites. All other proteases and antiproteases assessed are of lesser value for this purpose, although most are significantly increased in ascites and plasma of patients with malignant disorders.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 65 (1987), S. 726-726 
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-1238
    Keywords: Transthoracic electrical impedance ; Acute respiratory failure ; Pulmonary interstitial edema ; Intrathoracic fluid volume
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The alteration (ΔZ 0 ) of transthoracic electrical impedance (TEI) during extracorporeal hemodialysis (EHD) was investigated in two Groups of patients with acute renal and acute respiratory failure, that differed with respect to the severity of respiratory insufficiency. Group I had moderate respiratory failure (Fi O 2 0.31±0.10, Pa 0 2 84±14 mmHg), and Group II had severe respiratory failure (Fi 0 2 0.75±0.17, Pa O O 77±14 mmHg). There was a significant correlation between increase in TEI (ΔZ0) and decrease in body weight (ΔBW) in each individual patient, but the slope of regression lines was remarkably flattened in Group II. In Group I, ΔTEI was 1.9±0.9 Ω, the calculated TEI for 500 gr decrease in BW (ΔZ0–500 gr) was 0.59±0.21 Ω, and a significant correlation existed between pooled data of ΔZ0 and ΔBW. In Group II TEI increased less significantly, ΔTEI was 0.6±0.3 Ω (P〈0.001), ΔZ0–500 gr was 0.26±0.27 Ω (P〈0.01), and there was no correlation between pooled data of ΔZ0 and ΔBW. Increase of TEI in Group II could be completely attributed to increase in hematocrit. It is concluded that patients of Group I with acute renal failure and moderate respiratory failure lost intrathoracic fluid during EHD, whereas patients of Group II with severe respiratory failure did not. TEI during EHD may serve as a test for detection of fixed fluid within the pulmonary interstitium indicating a poor prognosis of the acute respiratory failure.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Intensive care medicine 7 (1981), S. 77-87 
    ISSN: 1432-1238
    Keywords: Burn toxins ; Immunotherapy ; Liver damage
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Modern intensive care combined with current improvements in the specific, systemic and local therapy of burns has delayed the mortal effects of severe burns. Nor has there been any significant improvement in this mortality during the last decade. The occurrence of uncontrollable infection and sepsis due to gram-negative bacteria or fungi as the basic cause of death was not a satisfactory explanation. So, progress should only be expected from a new concept in burn treatment. This new concept should be to view the burn disease as being caused by toxic factors induced by thermal injury to the skin. Electron-microscope studies in mice and rats have revealed similar mitochondrial alterations in hepatocytes after either a sublethal controlled burn injury or an intraperiotoneal application of an equivalent dose, of a cutaneous burn toxin. The intraperitoneal injection of different amounts of the burn toxin indicated, that the extent of the mitochondrial changes correlated directly with the dose of toxin. Investigations of liver metabolism suggested an inhibition of the oxygenation chain. The incubation of isolated liver cells together with the burn toxin demonstrated by scanning electron microscopy a direct cytotoxic effect of the burn toxin. In animal tests the pathogenic effect of the burn toxin could be prevented by treatment with an antitoxic IgG generated in sheep. The fatal sepsis of severely burned patients is the consequence of a decreased host defence against infections, which is caused by a primary and general toxic alteration of the whole organism. One important aspect of treatment should therefore be the elimination of burn toxins. To achieve this management should include primary excision of the burns, local application of nonabsorbable protein-complex-binding substances and specific passive immuno-therapy with an antitoxic IgG.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1435-2451
    Keywords: Isolated rat hepatocytes ; Burnt skin ; Toxic effect of a burn toxin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Die Existenz von bei der Verbrennung in der Haut entstehenden toxischen Substanzen und deren Bedeutung für die Pathogenese der Verbrennungskrankheit wird heute weithin als wahrscheinlich angesehen. In der vorliegenden Arbeit wurde der Stoffwechsel isolierter Hepatocyten sowie deren Ultrastruktur unter dem direkten Einfluß sowie nach systemischer Applikation eines aus verbrannter Menschen- und Mäusehaut isolierten hochgereinigten toxischen Faktors untersucht. Unbehandelte Zellen sowie solche, die mit der physiologischen, nicht toxischen Vorstufe des Toxins behandelt wurden, dienten als Kontrolle. Direkt mit dem Toxin inkubierte Zellen wiesen keine Veränderung der Gluconeogenese, eine deutliche Verringerung der Harnstoffsynthese und eine noch deutlichere Reduktion der Glykogenbildung aus den meisten der angebotenen Prekursoren auf. Rasterelektronenmikroskopisch fanden sich deutliche Schädigungen der Zelloberfläche. Zellen von zuvor mit Toxin behandelten Tieren zeigten Einschränkungen aller Syntheseleistungen und wesentlich geringere Membranschäden. Ein direkter zelltoxischer Effekt des Toxins konnte somit gezeigt werden.
    Notes: Summary The existence of a burn toxin which could be responsible for the late burn disease has become increasingly accepted. The present study investigates both metabolism and ultrastructure of isolated rat hepatocytes both under the influence of a burn toxin isolated from burnt mouse and human skin and of its native nontoxic precursor. Cells from rats treated with toxin systematically were also investigated. The cells directly incubated with toxin showed no alterations of gluconeogenesis, but a reduced urea — and glycogensynthesis from most precursors used. Cells of pretreated rats were reduced in all functions and showed more distinct ultrastructural damage, while those incubated directly were significantly more altered. The results prove a direct toxic effect of a burn toxin on isolated liver cells.
    Type of Medium: Electronic Resource
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