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Biomedical subjects

G Schmer

Publications and source records attributed to G Schmer.

At least 37 records · Page 2Linked to original sources
PubMed1985

Fibrinogen Seattle II: defective release of fibrinopeptide A in a slow clotting fibrinogen.

A functionally abnormal fibrinogen was detected in a 27-year-old woman with no prior history of bleeding. Investigation of the defect revealed abnormal release of fibrinopeptide A and incomplete polymerization of fibrin monomers. Crosslinking of polymerized fibrin by Factor XIII was normal. To further characterize the dysfibrinogen, the increase in mechanical impedance during clot development was measured. Fibrinogen Seattle II showed several differences from normal fibrinogen: delayed onset of clotting, decreased rate of clot formation, and lower final clot impedance. Taken cumulatively, these data are consistent with an amino acid substitution at or near residue 16 in one of the A alpha chains, the point at which thrombin cleaves.

Adult↗
PubMed1985

Hemodynamic measurements in a sheep model with a hollow fiber artificial kidney containing modified cellulose.

HFAK-RC caused pronounced leukopenia, increase in TXB2 levels in plasma and hemodynamic pressure changes as a reflection of complement activation during EC in sheep. In contrast no increase in TXB2 levels and no changes in hemodynamics are observed with HFAK-MC. The leukopenia and granulocytopenia in the latter is much less pronounced and probably reflects the phenomenon "frustrated phagocytosis".

Animals↗
PubMed1984

Isolation, characterization, and propagation in vitro of human glomerular endothelial cells.

Human glomerular endothelial cells have been isolated, cloned, and characterized. They appeared as the first outgrowth from human glomeruli in the presence of platelet-derived growth factor, which was also a requirement for continuous growth. By phase microscopy they appeared as monolayers of polygonal cells. Von Willebrand's factor (VWF) was detected in the cytoplasm of all clones. Their intermediate filaments differed antigenically from that present in human umbilical vein endothelial cells. Like other endothelial cells, they demonstrated high levels of membrane-associated angiotensin-converting enzyme (ACE).

Cell Division↗
PubMed1984

Application of mechanical impedance measurements to the study of dysfibrinogens.

Most techniques of clot detection do not give information about the mechanical properties of the forming clot. A procedure was developed by which the dynamic loss modulus, or mechanical impedance, of a solution of fibrinogen could be continuously monitored during clot development. This method was then applied to the analysis of purified preparations of normal fibrinogen and two dysfibrinogens. Both thrombin and reptilase were used as clotting agents, and unique tracings of clot impedance vs. time were generated for each dysfibrinogen. The functional defect was known in each case, and the clot impedance tracings were able to distinguish between abnormalities in the release of fibrinopeptides A and B. Mechanical impedance measurements were shown to complement other types of analyses now used in the characterization of dysfibrinogens. In particular, they distinguished between dysfibrinogens that appeared similar by more conventional laboratory methods.

Batroxobin↗
PubMed1983

Fibrinogen Seattle releases half the normal amount of fibrinopeptide B.

Fibrinogen Seattle, a clinically silent, slow-clotting dysfibrinogen, releases 50% of the normal amount of fibrinopeptide B as assessed by amino acid analysis. The reduced dysfibrin exhibited equal quantities of chains with B beta- and beta-charge mobility on polyacrylamide gel electrophoresis in 2 M urea at low pH. By these same techniques, the release of fibrinopeptide A was normal. Clots formed by repolymerizing the thrombin and batroxobin dysfibrin monomers showed a maximal turbidity that was lower than normal. Fibrinogen Seattle was indistinguishable from normal fibrinogen by radial immunodiffusion and immunoelectrophoresis. Degradation by plasmin and transamination by factor XIIIa were normal. The characteristics of fibrinopeptide release by fibrinogen Seattle distinguish it from other reported dysfibrinogens.

Amino Acids↗
PubMed1983

Successful long-term use of a plasmapheresis reactor system in dogs with lymphoma.

The successful long-term use of asparaginase-glutaminase reactor in dogs with lymphoma is described. The limitations of the system consisting of an activation of enzymes leading to rapid neosynthesis of asparagine and glutamine are outlined. The possible beneficial effect of future combination therapy with amino acid analogues is discussed.

Animals↗
PubMed1982

Immunohistochemical identification of mast cells in paraffin- and epon-embedded tissues using platelet factor 41.

An immunoperoxidase method has been developed for staining heparin in the granules of mast cells. The method employs human platelet factor 4 (or anti-heparin) and a rabbit antiserum to this polypeptide. Platelet factor 4 binds to mast cell heparin and provides the basis for immunoperoxidase staining using the rabbit antiserum. Preliminary studies of mast cells in various tissues indicate that the stain is quite specific for the content of mast cell granules, presumably heparin and possibly other glycosaminoglycans.

Blood Coagulation Factors↗
PubMed1982

Successful in vivo experiments in sheep using a new nonhydrolyzable enzyme reactor resistant against tryptic digestion.

Blockage of E-amino groups of asp-ase bound to cellulose by succinylation results in a greatly enhanced resistance against tryptic digestion by "plasma enzymes." Plasmapheresis in sheep by plasma filters connected to asp-ase Cellulose cartridges led to decrease of asp-NH2 and glut-NH2 in plasma over 21 hrs with undetectable enzyme leakage from the solid phase.

Animals↗
PubMed1981

A method for monitoring antifibrinolytic therapy in patients with ruptured intracranial aneurysms.

A rapid fluorometric assay technique has been utilized to assess the degree of fibrinolytic inhibition in 20 patients with ruptured intracranial aneurysms treated with epsilon-aminocaproic acid (EACA). This method quantitates the available plasminogen activity (APA) of plasma, and has proven to be a reliable means of monitoring antifibrinolytic therapy. Determination of the plasma APA also permits correlation of the level of fibrinolytic activity with putative complications of EACA therapy. Normal control plasma APA was 3.1 +/- 0.7 CTA units/ml, but in patients with subarachnoid hemorrhage (SAH), pretreatment fibrinolytic activity was supranormal at 3.78 +/- 0.88 CTA units/ml. During continuous intravenous administration of EACA (1.5 gm/hr) in patients with SAH, the plasma fibrinolytic activity was decreased to 0.9 +/- 0.31 CTA units/ml. A case described which examplifies the use of this assay. In addition, an approach to monitoring antifibrinolytic therapy using the plasma APA is proposed.

Aminocaproates↗
PubMed1981

The bio-artificial organ: review and progress report.

A definition and a review is given for the bioartificial organ. In addition new developments are reported with the successful lyophilization of enzyme filled RCG with cryoprotective polyethylene glycol (PEG). The successful use of an enzyme reactor consisting of crosslinked fibrin with asparaginase covalently attached is reported in sheep. The small organ (0.4 m2) removes 70% of the animal's asparagine in 6 hours. No enzyme leakage down to 10(-5) units per ml. plasma could be found. The highly preserved substrate affinity of insolubilized asparaginase as well as its high activity and stability when bound to fibrin are additional outstanding features of this system.

Animals↗
PubMed1980

Successful use of two new reactor types in sheep.

The new enzyme reactor types based on the use of biogenic material (red cell ghosts and crosslinked fibrin) were tested in vitro and in vivo (sheep). The main characteristics of the reactors were highly maintained substrate affinity, high enzyme activity per unit surface and good physicochemical stability.

Animals↗
PubMed1979

Induction of hypothermia in mice by semi-artificial cells containing indolyl-3-alkane alpha-hydroxylase.

The administration of red cell ghost encapsulated indolyl-3-alkane alpha-hydroxylase (an enzyme which destroys tryptophan by oxidation of the side chains) in CD-1 female mice causes effective tryptophan depletion in plasma and brain and induces hypothermia by probably decreasing the serotonin concentration in brain by decreasing the concentration of its precursor, L-tryptophan.

Alkanes↗
PubMed1979

Molecular engineering of the L-tryptophan-depleting enzyme indolyl-3-alkane alpha-hydroxylase.

Polymaleic acid and polyacrylic acid polymers have been covalently linked to indolyl-3-alkane alpha-hydroxylase with a shift of the pH optimum from 3.5 to between 5.0 and 5.5. In addition, the specific activity of the modified enzyme was increased approximately threefold at pH 7.0. The Km values of the polymer-bound enzyme preparations are essentially the same as that of the native enzyme. The plasma half-life was shortened from 6-7 hours with the native enzyme to 2-4 hours with the modified enzymes. The degree of L-tryptophan depletion in the circulation of mice, however, was the same during a 24-hour period after injection of native or modified enzymes.

Animals↗