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J Kappelmayer

Publications and source records attributed to J Kappelmayer.

34 records · Page 2Linked to original sources
PubMed1995

Prognostic value of assessing contact system activation and factor V in systemic inflammatory response syndrome.

OBJECTIVE: To test if serially sampled determinations of the contact system proteins and factor V have prognostic value for death in patients who develop the systemic inflammatory response syndrome. DESIGN: Prospective, observational study with sequential measurements in an inception cohort. SETTING: Medical intensive care unit (ICU) in a community hospital. PATIENTS: Over a 1-yr period, a population base sample of 23 patients was selected from all ICU admissions who met established criteria for the systemic inflammatory response syndrome. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Components of the contact system, factor XII, prekallikrein, high-molecular-weight kininogen, factor XI, alpha 2-macroglobulin-kallikrein complexes and factor V values were measured in plasma samples collected serially (day of admission, and at 2, 12, 24, 48 and/or 72 hrs or at discharge). Data were analyzed to determine if admission values or serially obtained values within 48 hrs were useful in predicting outcome. Fourteen patients survived and nine died. At admission, in all patients, assay values indicated that prekallikrein, high-molecular-weight kininogen, and factor V were significantly lower than normal (as observed in a range of 20 to 23 healthy adults), alpha 2-macroglobulin-kallikrein complexes were higher than normal, while concentrations of factor XII and factor XI were in the normal range. No differences were detected in the admission values between survivors and nonsurvivors, nor between patients with positive or negative blood cultures. However, subsequent values demonstrated a difference in values between survivors and nonsurvivors. Survivors showed improvement in high molecular weight kininogen values and higher than normal factor V values, as compared with nonsurvivors. CONCLUSIONS: Low or persistently low serial factor XII, high-molecular-weight kininogen and factor V values are associated with a poor prognosis, whereas high or increasing values of factor XII, high-molecular-weight kininogen, prekallikrein, and factor V all correlate with a favorable outcome.

Aged↗
PubMed1994

Onset and distribution of factor XIII-containing cells in the mesenchyme of chorionic villi during early phase of human placentation.

To learn more about the distribution and possible function of factor XIII (FXIII)-containing cells of human placenta, paraffin embedded and frozen sections of placenta samples from the first trimester of pregnancies--terminated by legal abortions--were studied by single and double labelling immunomorphological techniques. It was observed that at the fifth gestational week in the chorionic mesenchyme, FXIII-containing small mononuclear, round shaped cells start to appear. The relative amount of the FXIII-containing cells rapidly increased up to the seventh gestational week, reaching nearly 30 per cent of all mesenchymal cells. Simultaneously these cells differentiated into large stellate cells having numerous vacuoles in their cytoplasm. These cells were characterized in double labelling experiments and proved to be macrophages (CD 14+, KiM7+, labelled with antimacrophage monoclonal antibody). In the fifth-seventh weeks of gestation, these cells were homogenously scattered in the immature mesenchymal connective tissue, but from the eight gestational week they tended to accumulate in the peripheral part of chorionic villi while the central mesenchyme showed intense fibrotic changes. The abundance and characteristic distribution of the FXIII-positive macrophages in the chorionic mesenchyme during the first trimester of pregnancy suggest that these cells may have an active role in the formation of connective tissue in the early phase of placentation.

Chorionic Villi↗
PubMed1993

Characterization of monocyte-associated factor V.

We demonstrate that in addition to possessing binding sites for intact factor V (FV), unstimulated peripheral blood monocytes also express activated factor V (FVa) on their surfaces. FVa was identified on the monocyte surface by monoclonal antibody B38 recognizing FVa light chain and by human oligoclonal antibodies H1 (to FVa light chain) and H2 (to FVa heavy chain) using immunofluorescence microscopy and flow cytometry. On Western blots, partially cleaved FV could be identified as a 220 kDa band in lysates of monocytes. In addition to surface expression of FVa, monocytes also contain intracellular FV as detected only after permeabilization by Triton X-100 by monoclonal antibody B10 directed specifically to the Cl domain not present in FVa. We sought to determine whether the presence of FV in peripheral blood monocytes is a result of de novo synthesis. Using in situ hybridization, no FV mRNA could be detected in monocytes, while in parallel control studies, factor V mRNA was detectable in Hep G2 cells and CD18 mRNA in monocytes. In addition, using reverse transcriptase and the polymerase chain reaction, no FV mRNA was detected in mononuclear cells or in U937 cells, but mRNA for factor V was present in Hep G2 cells using the same techniques. These data suggest that FV is present in human monocytes, presumably acquired by binding of plasma FV, and that the presence of this critical coagulation factor is not due to de novo synthesis.

Antibodies, Monoclonal↗
PubMed1993

Tissue factor is expressed on monocytes during simulated extracorporeal circulation.

Certain forms of extracorporeal circulation exemplified by cardiopulmonary bypass require continuous high-dose anticoagulation to prevent thromboembolic complications. We hypothesized that monocytes may be stimulated to express tissue factor (TF) during prolonged simulated extracorporeal circulation. TF was identified both by flow cytometry by using three TF-specific monoclonal antibodies and functional assay of procoagulant activity (PCA). TF significantly increased between 2 and 6 hours of simulated extracorporeal circulation by both analyses. Relative fluorescence on monocytes increased from a control value of 100 to 313 +/- 79 on cells from the simulated extracorporeal circuit (p < 0.05). PCA increased from 21 +/- 8 to 775 +/- 326 pg TF/10(6) monocytes (p < 0.05) and was blocked 99.6% by preincubation of cells with a mixture of monoclonal antibodies to TF. By 6 hours, the number of leukocytes in the circuit was decreased by 43%. The cells were recovered from the oxygenator membrane by washing with EDTA. Compared with initial values, by 6 hours, both TF antigen at 378 +/- 90 (p < 0.05) and PCA at 1,357 +/- 280 pg TF/10(6) monocytes (p < 0.01) were highest in the recovered cells. Cells incubated for 6 hours and not subjected to simulated extracorporeal circulation did not increase TF. Examination of monocytes for the adhesive receptor CD11b/18 (Mac-1) paralleled TF expression, providing an additional putative receptor for the coagulant proteins, factor X and fibrinogen or fibrin.(ABSTRACT TRUNCATED AT 250 WORDS)

Antigens, CD↗
PubMed1993

Upregulation of Mac-1 surface expression on neutrophils during simulated extracorporeal circulation.

The leukocyte integrin Mac-1 (alpha m beta 2, CD11b/18 CR3, MO1), in addition to binding iC3b, has been shown to be the receptor for the coagulation proteins fibrinogen, factor X, and high molecular weight kininogen. Mac-1 is known to be upregulated by agonists that stimulate neutrophils or monocytes. Previous studies from this laboratory have documented neutrophil activation during cardiopulmonary bypass. We therefore used an experimental model for cardiopulmonary bypass, a simulated extracorporeal circulation, to study the surface expression of Mac-1 on peripheral blood leukocytes by immunofluorescence flow cytometry. The number of Mac-1 receptors in polymorphonuclear leukocytes had increased 2.2 times and 2.9 times baseline by 2 hours at 37 degrees C and 28 degrees C, respectively (p < 0.001). Neutrophil elastase-alpha 1-proteinase inhibitor complexes (a measure of neutrophil degranulation) increased more than sixfold from 41 micrograms/L to 256 micrograms/L after 2 hours at 28 degrees C. The number of Mac-1 receptors expressed on polymorphonuclear leukocytes correlated with polymorphonuclear leukocyte elastase complexes (r = 0.93). Mac-1--bearing lymphocytes did not display any change in receptor number in the simulated extracorporeal circulation. By 2 hours, monocytes at 37 degrees C showed only insignificant increase; at 28 degrees C they displayed a 1.6 times increase (p < 0.05). By maintaining a temperature-matched standing control samples, we could prove that, unlike the Mac-1 in polymorphonuclear leukocytes, this increase in monocyte Mac-1 is not from bypass but is rather an effect of temperature. These data suggest that a receptor for procoagulant proteins on circulating polymorphonuclear leukocytes (Mac-1) is upregulated during simulated extracorporeal circulation.

Adult↗
PubMed1989

Factors of the extrinsic pathway of blood coagulation in tumour associated macrophages.

Despite the growing evidence implicating intratumoural fibrin formation in the progression of malignant tumours, the origin of coagulation factors that participate in extravascular clotting has not been elucidated. Using immunohistochemical methods we attempted to detect and localize clotting factors of extrinsic pathway in different human malignant tumours. Coagulation factors II, V, VII and X (FII, FV, FVII and FX) were detected in a huge number of cells showing spindle-shaped or stellate morphology. By double immunohistochemical labellings it was demonstrated that cells containing these clotting factors express monocyte/macrophage differentiation marker antigens recognized by Leu M3, Ki M7 and DAKO-macrophage monoclonal antibodies, i.e. they represent monocyte-derived, phagocytic tumour associated macrophages (TAMs). These findings suggest that TAMs can be viewed as clot cells, which in addition to the initiation of extravascular clotting by expressing procoagulant activity can also provide all the components necessary for the extrinsic thrombin formation.

Animals↗
PubMed1989

Factors of the extrinsic pathway of blood coagulation in fetal placental macrophages.

Term human placentae were examined to identify and localize the factors contributing to extravascular fibrin formation. In addition to blood vessels, components of the extrinsic coagulation cascade were also demonstrated in intracellular localization. These cells in double and treble labeling systems expressed macrophage marker antigens, recognized by DAKO antimacrophage, RFD7, Amersham antimacrophage, and KiM7 monoclonal antibodies and showed positivity for alpha-naphthyl-acetate-esterase (ANAE). The fact that factors of the extrinsic coagulation system can be demonstrated in fetal macrophages of the chorionic stroma suggests that their role is not restricted to cellular defense and phagocytosis, but they may be involved in extravascular intraplacental fibrin formation as well.

Antibodies, Monoclonal↗
PubMed1989

Characterization of rapidly adhering amniotic fluid cells by combined immunofluorescence and phagocytosis assays.

Culture of human amniotic-fluid cells from cases of fetal neural tube defects produces a population of rapidly adhering cells that were initially thought to be macrophages and later interpreted to be of neural origin. In this study double and triple labeling systems for the simultaneous detection of glial and macrophage differentiation marker antigens have been used to demonstrate that rapidly adhering cells cannot be considered a homogeneous population but instead represent two distinct cell types. One of these cell populations is of glial origin and shows specific staining for glial fibrillary acidic protein, while the other population is monocyte-derived macrophages which express marker antigens recognized by Leu M3, KiM7, and Dako antimacrophage monoclonal antibodies.

Amniotic Fluid↗
PubMed1988

Platelet vinculin: a substrate of activated factor XIII.

In addition to plasma, Factor XIII of blood coagulation (FXIII) is also present in the cytosol of platelets, monocytes and macrophages. However, its intracellular function has not yet been revealed. Activated Factor XIII (FXIIIa) is a transglutaminase (protein-glutamine: amine gamma-glutamyltransferase, EC 2.3.2.13) of highly restricted substrate specificity with only a few known protein substrates. In this report, we showed that FXIIIa can link dansylcadaverine, radiolabelled histamine and putrescine to vinculin. Quantitative determinations revealed that in the vinculin molecule a single glutamine residue can serve as acyl donor for the incorporation of small-molecular-weight amines. Vinculin could not be crosslinked to another vinculin molecule. It could be covalently bound, however, to fibrinogen, which indicates that the acyl donor glutamine residue can be engaged in an epsilon-(gamma-glutamyl)lysyl crosslink formation. Since it has been shown that platelet actin and myosin, two main components of cytoskeleton, are also substrates for FXIIIa, and that vinculin is associated to the cytoskeleton during platelet activation, the involvement of FXIII in the stabilization of cytoskeleton at certain phases of cellular function is a likely possibility.

Animals↗
PubMedDate not supplied

Cerebrovascular reactivity and reserve capacity in type II diabetes mellitus.

The aim of the study was to test the hypothesis that cerebrovascular reserve capacity and cerebrovascular reactivity are impaired in patients suffering from non insulin-dependent diabetes mellitus. We also intended to investigate factors which may influence resting cerebral blood flow velocity and cerebrovascular reserve capacity. A total of 28 patients suffering from type II diabetes mellitus and 20 healthy control subjects were studied. Based on diabetes duration patients were divided into two groups: subjects with > 10 years and those with < or = 10 years disease duration. Middle cerebral artery mean blood flow velocities were measured at rest and after intravenous administration of 1g acetazolamide. Cerebrovascular reactivity and reserve capacity were calculated. Blood glucose, insulin, glycosylated hemoglobin, hemostatic factors (fibrinogen, alpha-2 macroglobulin and von Willebrand factor antigen) were determined. Cerebrovascular reactivity and reserve capacity values were compared between the two diabetic subgroups and controls. Correlations between laboratory parameters and cerebrovascular reserve were investigated by linear regression analysis. Resting cerebral blood flow velocity was similar in controls and in the two diabetic subgroups. Cerebrovascular reactivity was elevated for a shorter time in patients with > 10 years disease duration than in controls and short-term diabetic patients. Cerebrovascular reserve capacity was lower in the long-term diabetes group (means +/- SD: 39.6 +/- 20.7%) than in patients with < or = 10 years disease duration (63.3 +/- 17.4%, p < 0.02 after Bonferroni correction). Cerebrovascular reserve capacity was inversely related to the duration of the disease (R = 0.53, p < 0.003). None of the determined laboratory factors had any relation with resting cerebral blood flow and cerebrovascular reserve capacity. The vasodilatory ability of cerebral arterioles is diminished in long-standing type II diabetes mellitus.

Aged↗
PubMedDate not supplied

Monocytes express tissue factor in young patients with cerebral ischemia.

Activation of blood coagulation and fibrinolysis has previously been detected in stroke patients. It is unknown, however, what factors contribute to the acceleration of coagulation reactions, especially in cases where no obvious predisposing factors exist. We therefore postulated and tested the hypothesis that in such patients monocytes may trigger the pathway leading to thrombosis by expressing tissue factor (TF). TF antigen was determined in 48 patients and 40 controls by flow cytometry using an indirect immunofluorescent technique. TF antigen expression was significantly increased on monocytes in young stroke patients in both the acute (p < 0.01) and chronic (p < 0.05) phases of the disease. The TF antigen also possessed functional activity, quantitated by a one-stage clotting assay. TF expression on monocytes was not associated with an elevation in C-reactive protein values. In both acute and chronic phases, blood coagulation activation markers, e.g. the thrombin-antithrombin complex and F1 + 2 fragments, were significantly elevated. However, in the acute phase D-dimer levels were similar to those in controls and were only elevated in the chronic phase of the disease (p < 0.05). In conclusion, in cerebral ischemia TF expression on monocytes suggests enhanced activation of blood coagulation and subsequent fibrinolysis.

Adolescent↗
PubMedDate not supplied

Evaluation of hemostatic changes and blood antioxidant capacity in acute and chronic pancreatitis.

BACKGROUND/AIMS: We examined changes in hemostasis, in levels of total antioxidant capacity, and pancreatic enzymes (amylase, lipase) in patients with pancreatitis 1, 3 and 7 days after admission to the clinic, in order to evaluate the inflammatory processes in acute and chronic pancreatitis and to identify new prognostic markers. METHODOLOGY: The rate of CD62 expression--a marker of platelet hyperactivity--and the rate of platelet-leukocyte aggregates were measured by flow cytometry. The connection between the parameters measured and the severity of pancreatitis and also the differences of the parameters in acute and chronic pancreatitis were investigated. RESULTS: On the basis of previous studies it was assumed, that there is a connection between the level of parameters measured and the inflammatory process in the pancreas, and also between the defending processes of the body against free radicals. CONCLUSIONS: Based on our results, we suggest to extend the laboratory measurements to the investigation of hemostatic parameters. The measurement of plasma level of fibrinogen, von Willebrand factor and the rate of platelet activation is especially important.

Acute Disease↗