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  • 1
    Keywords: CANCER ; CELLS ; EXPRESSION ; carcinoma ; Germany ; SITE ; GENES ; PROTEIN ; PROTEINS ; TISSUE ; CARCINOGENESIS ; PHOSPHORYLATION ; antibodies ; MOUSE ; LESIONS ; PROGRESSION ; immunohistochemistry ; CERVIX ; CELL-LINE ; REGION ; REGIONS ; CARCINOMAS ; INTERCELLULAR COMMUNICATION ; STRATIFIED EPITHELIUM ; JUNCTION ; premalignant ; gap junction ; cell communication
    Abstract: Connexins are proteins that form the connexons, gap junction structures, which allow cells to communicate. Phosphorylation of connexins has been found to impair this communication. Using an antibody specifically recognizing the S279/S282-phosphorylated form of connexin43 (Cx43) for immunohistochemistry, we have analysed Cx43 phosphorylation in normal epithelium, CIN III lesions, and carcinomas of the cervix. We found that in normal epithelium the basal layer was devoid of staining and most of the protein was localized in stratum spinosum and stratum granulosum. In pre-malignant CIN-III lesions Cx43 was strongly phosphorylated, but the basal layer was still negative. In squamous carcinomas, the cells were intensely stained. In these tumours, sites of strong staining were adjacent to less stained regions, suggesting that the tumours are intrinsically heterogeneous. Immunoblotting of proteins extracted from carcinomas with the specific antibody showed the classical pattern of multiple reacting bands, with the appearance of low migrating forms of the protein. Our results suggest that increased S279/S282 phosphorylation of Cx43 is the result of altered tissue structure rather than of cell malignization. (c) 2005 Elsevier Ireland Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 15958277
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  • 2
    Keywords: ACTIN-BINDING ; skin tumors ; keratinocyte ; LOCALIZATION ; tumor ; TUMORS ; INDUCTION ; KERATINOCYTES ; SKIN ; PROTEIN
    Type of Publication: Meeting abstract published
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  • 3
    Keywords: APOPTOSIS ; CANCER ; EXPRESSION ; GROWTH ; tumor ; CELL ; Germany ; human ; PROSTATE ; DISEASE ; GENE ; PROTEIN ; TUMORS ; ACCURACY ; MARKER ; REDUCTION ; CELL-CYCLE ; PHOSPHORYLATION ; ASSOCIATION ; chromosome ; BREAST-CANCER ; score ; PROGRESSION ; immunohistochemistry ; prostate cancer ; PROSTATE-CANCER ; MARKERS ; VARIABILITY ; LOCALIZATION ; Jun ; FREQUENT ; p27 ; NUCLEAR-LOCALIZATION ; MITOSIS ; P27(KIP1) ; BINDS ; CELL-GROWTH ; TUMOR-SUPPRESSOR ; HUMAN CANCER ; GRADE ; 3-KINASE/AKT PATHWAY ; INHIBITOR P27(KIP1) ; needle biopsy ; prostatic carcinoma ; PTEN/MMAC1 ; RADICAL PROSTATECTOMY
    Abstract: The extreme variability of prostate cancer implies latent disease with missing clinical symptoms in some cases. Tumor suppressors PTEN (phosphatase and tensin homolog deleted on chromosome ten) and p27(kip1) are frequently mutated in various human cancers. PTEN negatively influences cell growth and induces apoptosis, while p27(kip1) binds to cyclin-E-Cdk2 and counteracts mitosis. This study investigated the expression of PTEN and p27(kip1) in prostatectomies and needle biopsies in order to determine whether protein localization or expression levels are correlated with tumor grade and whether PTEN and p27(kip1) expression in biopsies are valuable predictive tumor markers. Analysis of PTEN demonstrated that weak expression levels were significantly more prevalent in high-grade tumors. Analysis of p27(kip1) revealed that high-grade tumors had a higher percentage of cytoplasmic localization of the protein than low-grade tumors, where nuclear localization was more frequent. Furthermore, this study indicated a positive association between PTEN and p27(kip1) levels. An increase of high-grade tumors corresponded to a progressive loss of both tumor suppressors in needle biopsies and prostatectomies. p27(kip1) and PTEN did not show a higher predictive accuracy of the tumor grade in the surgical specimen than the Gleason score. However, p27(kip1) had the same predictive value as the Gleason score in needle biopsies
    Type of Publication: Journal article published
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  • 4
    Keywords: CANCER ; EXPRESSION ; INVASION ; tumor ; TUMOR-CELLS ; BLOOD ; Germany ; PROSTATE ; COMMON ; MORTALITY ; TISSUE ; TUMORS ; PATIENT ; ACTIVATION ; SERA ; MARKER ; CONTRAST ; ASSOCIATION ; FREQUENCY ; FREQUENCIES ; NO ; STAGE ; PROGRESSION ; immunohistochemistry ; MALIGNANCIES ; TUMOR PROGRESSION ; METASTASIS ; MEN ; prostate cancer ; PROSTATE-CANCER ; RATES ; BENIGN ; Jun ; CANCER-PATIENTS ; adenocarcinoma ; intraepithelial neoplasia ; western blot ; CANCER PATIENTS ; MMP ; INHIBITORS ; SERUM ; MATRIX ; MALIGNANCY ; TUMOR INVASION ; collagen ; IV ; MATRIX METALLOPROTEINASES ; GRADE ; prostatic carcinoma ; RADICAL PROSTATECTOMY ; CORE ; gelatin zymography ; GELATINASE-A ; IV COLLAGENASES ; MMP-2
    Abstract: Prostate cancer is the most common cancer in men and second in the cancer-related frequency of mortality. Matrix metalloproteinases (MMPs) are involved in tumor invasion and metastasis in various malignancies. MMP-2 and MMP-9 are capable of digesting collagen type IV. Numerous studies have demonstrated an association between increased MMP-2 and -9 expression and tumor progression in various tumors. In this study, the expression and activities of MMP-2 and -9 were assessed in serum probes and tumor tissue from core needle biopsies and radical prostatectomies of 97 patients. MMP-2 and -9 serum expression was analyzed in a subgroup of 31 patients. MMP-9 serum expression was significantly increased in tumor patients and correlated with tumor grade. In contrast, the MMP-9 tissue expression and activity revealed no significant correlations to tumor stage or grade. The MMP-2 activity, however, showed a positive correlation for MMP-2 with tumor stage. Increased activity was predominantly detected in advanced tumor stages. Immunohistochemical analysis of MMP-2 expression demonstrated a positive association with tumor grade in prostatectomy specimens. The relative expression rates in biopsies matched in 65% with those of the prostatectomies. Detection of MMP-2 in core needle biopsies seems not to be a helpful marker for diagnostic purposes
    Type of Publication: Journal article published
    PubMed ID: 15088144
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  • 5
    Keywords: CANCER ; CELLS ; GROWTH ; GROWTH-FACTOR ; tumor ; carcinoma ; Germany ; human ; MICROSCOPY ; DIAGNOSIS ; PROTEIN ; PROTEINS ; TUMORS ; COMPLEX ; COMPLEXES ; INDUCTION ; KERATINOCYTES ; SKIN ; ASSOCIATION ; immunohistochemistry ; skin cancer ; CARCINOMA-CELLS ; LOCALIZATION ; ADHESION ; intermediate filaments ; CARCINOMAS ; INVOLVEMENT ; squamous cell carcinoma ; beta-catenin ; epidermis ; human hair follicle ; HUMAN EPIDERMIS ; SKIN-CANCER ; CATENIN ; basal cell carcinoma ; HUMAN SKIN ; EPIDERMAL-GROWTH-FACTOR ; INNER-ROOT-SHEATH ; RE ; keratinocyte ; TUMORIGENESIS ; HAIR FOLLICLE ; SKIN CANCERS ; cell adhesion ; hair ; INTERCELLULAR-JUNCTIONS ; BCC ; DESMOSOMAL PLAQUE PROTEINS ; ADHERENS JUNCTIONS ; CELL-CARCINOMA ; E-CADHERIN EXPRESSION ; actin-binding protein ; INTERCELLULAR-ADHESION
    Abstract: Isoform E2 of drebrin, an actin-binding protein originally identified in neuronal cells, has recently been identified in diverse non-neuronal cells, mostly in association with cell processes and intercellular junctions. Here, we report on the presence of drebrin in normal human skin, epithelial skin cancers, and cultured keratinocytes. Keratinocytes of normal epidermis contain almost no drebrin but the protein is readily seen in hair follicles. By immunohistochemistry and immunoblot, basal cell carcinomas (BCC) are rich in drebrin, and confocal laser scanning and immunoelectron microscopy show accumulation at adhering junctions, in co-localization with actin and partially with plaque proteins. In squamous cell carcinomas, keratoacanthomas, and in epidermal precancers, drebrin is heterogeneously distributed, appearing as mosaics. Primary keratinocyte cultures contain significant amounts of drebrin enriched at adhering junctions. When epithelium-derived cells devoid of drebrin are transfected with drebrin-enhanced green fluorescent protein, constructs accumulate in the cell periphery, and immunoprecipitation shows complexes with actin. During epidermal growth factor induced formation of cell processes, drebrin retains this junction association, as observed by live cell microscopy. Our results suggest novel functions of drebrin such as an involvement in cell-cell adhesion and tumorigenesis and a potential value in diagnosis of BCC
    Type of Publication: Journal article published
    PubMed ID: 16185277
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  • 6
    ISSN: 1432-1076
    Keywords: Intravascular Coagulation ; Neonatal Thrombosis ; Perinatal Consumption Coagulopathia ; Shock (Inadequate Capillary Perfusion) ; Perinatal Death
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Bei drei Neugeborenen fand sich eine Thrombose der peripheren Extremitätengefäße als morphologisches Teilsymptom einer generalisierten plasmatischen Hyperkoagulabilität und disseminierten intravasalen Gerinnung der Neonati unter der Geburt und in der Perinatalperiode. Fibrinreiche intravasale Mikrothromben in den Extremitätengefäßen können morphologisches Äquivalent einer intrauterin eingeleiteten plasmatischen Hyperkoagulabilität und bereits intrauterin nachfolgenden disseminierten intravasalen Gerinnung darstellen. Eine disseminierte intravasale Gerinnung post natum kann daneben im Verlauf einer intrauterin begonnenen, perinatal fortbestehenden generalisierten plasmatischen Hyperkoagulabilität in der unmittelbaren Perinatalperiode auftreten und durch den hypoxämieprovozierenden Einfluß eines Membranensyndroms perpetuiert und intensiviert werden. Hypoxämie und Acidose können nach rezidivierendem Atemstillstand auch unabhängig von asphyxieprovozierenden Geburtskomplikationen eine generalisierte plasmatische Hyperkoagulabilität und nachfolgende disseminierte intravasale Gerinnung induzieren. An Hand der drei vorliegenden Fälle werden die pathogenetischen Beziehungen zwischen den Faktoren Hypoxämie und Acidose in der Blutbahn der Nascituri und Neonati, plasmatische Hyperkoagulabilität unter Thrombocytopenie und Verbauch von Gerinnungsfaktoren in utero, hämorrhagische Diathese unter der Geburt, extravasale Polymerisation der intravasal entstehenden Fibrinmonomere zu perinatalen pulmonalen hyalinen Membranen einerseits und der intravasalen Polymerisation der Monomere zu perinatalen disseminierten intravasalen Gerinnseln mit Thrombose peripherer Extremitätengefäße andererseits diskutiert.
    Notes: Abstract Three out of four newborn infants (premature twins, one case of prolonged delivery and one case of relapsing respiratory arrest) showed microthrombi in the vessels of the extremities as morphological symptoms of a generalized plasmatic hypercoagulability, consumption of clotting factors, and disseminated intravascular coagulation which takes place in the newborns during birth and during the perinatal period. The thrombi in the extremities are regarded as clinical manifestation of a generalized microthrombosis which involves the vascular system of many organs, i.e. liver, lungs, spleen, intestine, suprarenal glands, and kidneys. Fibrin-rich intravascular microthrombi in the vessels of the extremities are considered as morphological equivalents of a generalized hypercoagulability and subsequent disseminated intravascular coagulation. They are already initiated in utero following intra-uterine asphyxia with hypoxemia and acidosis in the capillary microcirculation (inadequate capillary perfusion). Disseminated intravascular coagulation can also occur in the immediate perinatal period due to a generalized hypercoagulability of the plasma, which had been initiated in utero and persisted during the perinatal time without having been already converted in utero into a disseminated intravascular microthrombosis. Hypercoagulability can be perpetuated and intensified by a membrane syndrome in newborn infants with respiratory distress syndrome. The pathogenetic relations between hypoxemia and acidosis in the microcirculation of nascituri and newborns, hypercoagulability of plasma with thrombocytopenia and with consumption of clotting factors in utero, hemorrhagic diathesis during birth, disseminated intravascular coagulation in stillbirths and in newborn infants, and the respiratory distress syndrome with hyaline membranes of the lung are discussed.
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  • 7
    ISSN: 1432-2307
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Eine 24jährige Erstgebärende mit dichorialer, diamniotischer Zwillingsschwangerschaft erkrankte während der Ausstoßung eines nach vorzeitigem Blasensprungeiner Fruchtblase und aufsteigender Infektion mit Escherichia coli intrauterin abgestorbenen Kindes im 5. Schwangerschaftsmonat unter den Zeichen eines septischen Zustandsbildes und einer beginnenden Verbrauchskoagulopathie. Bei der feingeweblichen Untersuchung zeigte der intrauterin abgestorbene Zwilling eine Chorionamnionitis und eine generalisierte Gerinnung in den fetalen Organgefäßen. Ein nach Sprengung der Fruchtblase zunächst überlebender zweiter Zwilling ließ nur ausgedehnte placentare Zottenhämorrhagien und Zottennekrosen erkennen. Die intravasale Gerinnung in den fetalen Organen des ersten (totgeborenen) Zwillings wird als morphologischer Ausdruck eines generalisierten Sanarelli-Shwartzman-Äquivalentes nach Endotoxineinschwenimung von der chorialen Deckplatte in die fetalen Deckplattengefäße und damit in die fetale Blutbahn gewertet. Die placentaren Zottenhämorrhagien und -nekrosen in der Placenta des 2. Zwillings werden dagegen als Symptom eines lokalen Sanarelli-Shwartzman-Äquivalentes nach Einbruch des Endotoxins von der Choriondeckplatte der 1. Placenta in das mütterliche Intervillum, Endotoxinpassage des mütterlichen Organismus und hämatogener Endotoxineinschwemmung in das Intervillum der 2. Placenta verständlich. Das simultan auftretende lokale und generalisierte fetale Sanarelli-Shwartzman-Phänomen haben in dieser Beobachtung gleiche ätiologische Wurzeln — das Endotoxin gramnegativer Bakterien — und dokumentieren nur den unterschiedlichen (extravasalen und intravasalen) pathogenetischen Effekt des Endotoxins bei dichorialer, diamniotischer Zwillingsschwangerschaft.
    Notes: Summary A 24 year old primigravida with a dichorial, diamniotic twin pregnancy became ill in the fifth month of pregnancy during the delivery of a stillborn infant which followed premature rupture of the membranes and an infection with Escherichia coli. Clinical signs of sepsis and a beginning consumption of clotting factors were noted. Histologically the stillborn infant (#1) revealed a chorioamnionitis and a generalized clotting within its visceral vessels. The placenta of the second live-born infant showed only hemorrhages and necroses of villi. The intravascular clotting in the fetal organs of the stillborn (# 1) is regarded as a morphologic equivalent of a generalized Sanarelli-Shwartzman-reaction caused by endotoxin permeating from the chorionic plate through into fetal vessels and hence into the fetal circulation. In contrast, the hemorrhages and necroses of the placental villi of infant # 2 are looked upon as evidence of a local Sanarelli-Shwartzman-reaction brought about by endotoxin penetrating through the chorionic plate of the first placenta into the maternal intervillus spaces with a generalized spread throughout the mother and by hematogenous route into the intervillus spaces of the placenta of infant# 2. The local and generalized fetal Sanarelli-Shwartzman phenomena occurring simultaneously here have a common etiology — the endotoxin-producing gram negative bacteria. The results demonstrate well the various (extravascular and intravascular) pathogenic effects of endotoxin in dichorial, diamniotic twin pregnancy.
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  • 8
    ISSN: 1432-2307
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Bei zwei Fällen von vorzeitiger Placentarlösung mit Störungen der mütterlichen Hämostase ohne Fibrino- bzw. Fibrinogenolyse-Symptomatik ließen sich in den fetalen Organen disseminierte intravasale Gerinnsel als morphologisches Indiz einer gleichzeitigen perinatalen fetalen Hämostase-Störung nachweisen. Bei einem dritten Fall, in dem mütterlichen Blut im clot-observation-test eine Fibrinolyse beobachtet wurde, fehlten dagegen auch in den fetalen Organen disseminierte intravasale Gerinnsel. Die formal gleichsinnigen Hämostase-Veränderungen erlauben bislang nicht ohne weiteres auch die Annahme identischer pathogenetischer Vorgänge bei Mutter und Kind. Die disseminierte intravasale Gerinnung im fetalen Organismus kann in utero auftreten, obwohl der mütterliche Organismus nur sehr diskrete Zeichen einer vorzeitigen Lösung der Placenta und einer Verbrauchsreaktion aufweist. Die Bedeutung einer möglichen Freisetzung thromboplastischer Aktivitäten aus der Placenta, die Bedeutung eines hämorrhagischen Schocks nach transplacentarer Blutung und die Bedeutung des im Gefolge einer utero-placentaren Insuffizienz nach vorzeitiger Placentarlösung auftretenden Schocks mit respiratorischer und metabolischer Acidose für die Auslösung einer disseminierten intravasalen Gerinnung mit bzw. ohne sekundäre Fibrinolyse im fetalen Organismus werden diskutiert.
    Notes: Summary Two cases of premature separation of the placenta are described in which disturbances in maternal hemostasis developed without evidence of fibrinolysis or fibrinogenolysis. A disseminated intravascular coagulation in the fetal organs served as evidence that fetal hemostasis (perinatal) also was disturbed at the same time. In a third case the clot observation test showed fibrinolytic activity in the maternal blood. The organs of the infant failed to disclose intravascular coagulation. Although the structural changes in the hemostasis may be similar, they do not allow one to assume that pathogenic processes in mother and infant are identical. Disseminated intravascular coagulation in the fetus may develop in utero, although the mother may show only slight evidence of premature separation of the placenta and of disseminated intravascular coagulation. The following pathogenetic mechanisms causing disseminated intravascular coagulation in the fetus are discussed: the possible release of thromboplastin (activity) from the placenta, the role of shock after transplacental hemorrhage, and the importance of shock after uteroplacental insufficiency from premature separation of the placenta, resulting in respiratory and metabolic acidosis.
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  • 9
    ISSN: 1432-2307
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung 1. Disseminierte intravasale Gerinnsel werden als Ausdruck einer generalisierten plasmatischen Gerinnungsaktivierung im Obduktionsgut operativ korrigierter und nicht korrigierter connataler cyanotischer Vitien (49 Fälle) außerordentlich häufig sichtbar. 20 der operierten Fälle mit angeborenen cyanotischen Herzfehlern und 10 der nicht operierten Fälle zeigten in einem oder in mehreren der untersuchten Organe fibrinreiche intravasale Mikrothromben, nicht selten kombiniert mit einer ausgeprägten Makrothrombose. 2. Die Häufigkeit disseminierter intravasaler Gerinnsel im Obduktionsgut angeborener Herzfehler mit Blausucht entspricht der Häufigkeit, mit der Mikrothromben bei Schockfällen verschiedenster Ätiologie, die mit einer generalisierten Hypercoagulabilität einhergehen, sichtbar werden. Acidose und Hypoxämie in der terminalen Strombahn begünstigen bei connatalen cyanotischen Vitien die Ausbildung einer derartigen generalisierten Hypercoagulabilität und disseminierten intravasalen Gerinnung. Durch Operationen im EKK mit per- und postoperativer Hypotension und Hypozirkulation wird die präexistente chronische generalisierte Hypercoagulabilität bei derartigen Vitien überdies akzentuiert und der Verbrauch von Gerinnungsfaktoren akzeleriert. 3. Die Träger angeborener cyanotischer Vitien mit generalisierter plasmatischer Hypercoagulabilität versterben häufig unter dem pathoanatomischen Bild pulmonaler hyaliner Membranen und der klinischen Symptomatik eines Atemnotsyndroms. 18 der Fälle mit dissemininierter intravasaler Gerinnung zeigten pathoanatomisch gleichzeitig pulmonale hyaline Membranen In 85% der Fälle mit pulmonalen hyalinen Membranen fanden sich andererseits disseminierte intravasale Gerinnsel in der terminalen Strombahn der Organe. Pulmonale hyaline Membranen treten sowohl bei nicht operativ korrigierten als auch bei operativ korrigierten cyanotischen Herzmißbildungen auf. 4. Pulmonale hyaline Membranen sind wie disseminierte intravasale Gerinnsel morphologisches Äquivalent einer voraufgegangenen plasmatischen Hypercoagulabilität und Verbrauchscoagulopathie. Die bei angeborenen Herzfehlern mit Cyanose als Ausdruck der subakuten oder chronischen generalisierten Hypercoagulabilität mit Verbrauch von Gerinnungsfaktoren im Blute kreisenden Fibrinmonomeren können nicht nur intravasal zu disseminierten intravasalen Gerinnseln, sondern nach Extravasation in den Alveolarraum extravasal auch zu pulmonalen hyalinen Membranen polymerisieren. Der Tod an einem klinisch fast unbeeinflußbaren Atemnotsyndrom ist eine der häufigsten Spätkomplikationen dieser generalisierten plasmatischen Hypercoagulabilität bei connatalen Vitien. Auf die Bedeutung der Extravasation plasmatischer Fibrinmonomere für die Aktivität des sog. Antiatelektasefaktors wird verwiesen.
    Notes: Summary 1. Disseminated intravascular coagulation as evidence of generalized activation of plasmatic hypercoagulation is commonly seen in the autopsy material of surgically corrected and unoperated cyanotic congenital heart disease (49 cases). Twenty of the operated cases and ten of the non-operated ones showed in one or several of the organs examined fibrinous intravascular microthrombi, sometimes combined with extensive macrothrombi. 2. Besides the increase of hematocrit and blood viscosity, the hemolysis, acidosis, and hypoxemia in the terminal bloodstream are conditions that favour generalized hypercoagulability and disseminated intravascular coagulation in cases of congenital cyanotic heart disease. The generalized hypercoagulability, which may occur even pre-operatively, can be intensified and the consumption of coagulation factors can be accelerated by operations employing the open heart bypass with hypotension and hypoperfusion during and after the operation. 3. Cases of cyanotic congenital heart disease with generalized plasmatic hypercoagulability often die with anatomical evidence of pulmonary hyaline membranes; clinically they often show symptoms of respiratory distress. In 18 cases with disseminated intravascular coagulation there were pulmonary hyaline membranes. On the other hand disseminated intravascular coagulation in the terminal bloodstream of other organs was found in 85% of the cases with pulmonary hyaline membranes. Pulmonary hyaline membranes are found both in unoperated and in surgically corrected cyanotic congenital heart disease. 4. Both the pulmonary hyaline membranes and disseminated intravascular microthrombi represent morphological equivalents of a recent plasmatic hypercoagulability and consumption coagulopathia. Fibrinmonomers, which appear in cases with cyanotic congenital heart disease as an expression of an acute or chronic generalized hypercoagulability with consumption of coagulation factors, may polymerize not only intravascularly into disseminated intravascular microthrombi but may also polymerize extravascularly as pulmonary hyaline membranes. 5. The main terminal complication of generalized plasmatic hypercoagulability caused by cyanotic congenital heart disease is respiratory distress which clinically is almost incurable. The importance of extravasation of plasmatic fibrin-monomers for the activity of the socalled surfactant is discussed.
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  • 10
    ISSN: 1432-2307
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Thirty-two rabbits were exposed to normobaric hyperoxia (100% oxygen at 1 ata) for 30 to 85 hours. A disseminated microthrombosis (DIC) representing a generalized intravascular activation of coagulation was first seen after 33 hours. The microthrombi were found mainly in the form of hyaline globules in the terminal vessels of the kidney, less often in other organs. The formation of pulmonary hyaline membranes (PHM) was observed only after oxygen exposure in excess of 54 hours. These findings support that the PHM following oxygen exposure in animal experiments, as PHM in the newborn and the adult, may be considered to be the expression and result of an intravascular coagulation activation.
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