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1,396 results on '"Scharrer, Inge"'

7. Clinical Trials of Recombinant Factor VIII

Author

White, Gilbert C., II, McMillan, Campbell W., Gomperts, Edward D., Addiego, Joseph E., Jr., Brackmann, Hans H., Brettler, Doreen B., Gill, Joan C., Goldsmith, Jonathon C., Hoots, W. Keith, Kessler, Craig M., Kisker, C. Thomas, Laurian, Y., Lewis, B., Lusher, Jeanne M., Mannucci, Piero M., Morfini, Messimo, Scharrer, Inge, Schulman, Sam, Lee, Martin L., Courter, Suzanne G., Kingdon, Henry S., Roberts, Harold R., Hoyer, Leon W., editor, and Drohan, William N., editor

Published
1991
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14. No Evidence for Classic Thrombotic Microangiopathy in COVID-19

Author

Falter, Tanja, primary, Rossmann, Heidi, additional, Menge, Philipp, additional, Goetje, Jan, additional, Groenwoldt, Steffen, additional, Weinmann, Arndt, additional, Sivanathan, Visvakanth, additional, Schulz, Andreas, additional, Lemmermann, Niels A.W., additional, Danckwardt, Sven, additional, Lackner, Karl J., additional, Galle, Peter R., additional, Scharrer, Inge, additional, Lämmle, Bernhard, additional, and Sprinzl, Martin F., additional

Published
2021
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19. Mutations in VKORC1 cause warfarin resistance and multiple coagulation factor deficiency type 2

Author

Rost, Simone, Fregin, Andreas, Ivaskevicius, Vytautas, Conzelmann, Ernst, Hortnagel, Konstanze, Pelz, Hans-Joachim, Lappegard, Knut, Seifried, Erhard, Scharrer, Inge, Tuddenham, Edward G. D., Muller, Clemens R., Strom, Tim M., and Oldenburg, Johannes

Subjects
Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Author(s): Simone Rost [1, 2, 10]; Andreas Fregin [1, 10]; Vytautas Ivaskevicius [3]; Ernst Conzelmann [4]; Konstanze Hörtnagel [2]; Hans-Joachim Pelz [5]; Knut Lappegard [6]; Erhard Seifried [3]; Inge Scharrer [...]

Published
2004
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25. Von Willebrand factor-cleaving protease in thrombotic thrombocytopenic purpura and the hemolytic-uremic syndrome

Author

Furlan, Miha, Robles, Rodolfo, Galbusera, Miriam, Remuzzi, Giuseppe, Kyrle, Paul A., Brenner, Brigitte, Krause, Manuela, Scharrer, Inge, Aumann, Volker, Mittler, Uwe, Solenthaler, Max, and Lammle, Bernhard

Subjects
Thrombocytopenic purpura -- Causes of, Proteases -- Health aspects, Hemolytic-uremic syndrome -- Causes of
Abstract

An absence of von Willebrand factor-cleaving protein or its inhibition may be a factor in thrombotic thrombocytopenic purpura and hemolytic-uremic syndrome. These diseases are both bleeding disorders. Researchers analyzed blood samples from 53 patients with either condition for the presence of a protease that breaks down clumps of von Willebrand factor. These clumps could bind to platelets and prevent blood clot formation. All 30 patients with thrombotic thrombocytopenic purpura had low levels of the protease, and in many cases, an antibody was inhibiting the protease.

Published
1998

37. Human recombinant DNA-derived antihemophilic factor (factor VIII) in the treatment of hemophilia

Author

Schwartz, Richard S., Abildgaard, Charles F., Aledort, Louis M., Arkin, Steven, Bloom, Arthur L., Brackmann, Hans H., Brettler, Doreen B., Fukui, Hiromu, Hilgartner, Margaret W., Inwood, Martin J., Kasper, Carol K., Kernoff, Peter B.A., Levine, Peter H., Lusher, Jeanne M., Mannucci, Pier M., Scharrer, Inge, MacKenzie, Mary A., Pancham, Nazreen, Kuo, Harng S., and Allred, Randy U.

Subjects
Blood coagulation factor VIII -- Health aspects, Hemophilia -- Drug therapy
Abstract

Hemophilia A is a relatively common genetic disorder that affects the blood clotting process, resulting in an tendency to hemorrhage. As an X-linked disorder, it occurs predominantly in men, affecting about 1 in 10,000 males. In its most severe form, it is a life-threatening illness. Patients with hemophilia A do not possess adequate activity of clotting factor VIII. The introduction of factor VIII treatment has resulted in a better quality of life and longer life expectancy for hemophilia patients. However, since the factor VIII has been obtained from blood, hemophilia patients have always been at higher risk for viral hepatitis and immunization against alloantigens. More recently, AIDS has been added as one of the diseases hemophiliacs may contract from contaminated factor VIII. This has provided an incentive to develop recombinant factor VIII, produced by bacteria using the human factor VIII gene. Since recombinant factor VIII does not come from human blood, the opportunity for the transmission of viral diseases is effectively eliminated. Two research groups have reported success with the cloning of factor VIII, one of the largest molecules cloned to date. Now, investigation of the effectiveness of recombinant factor VIII in treating 107 hemophiliacs has revealed that the new substance is safe and effective. The new recombinant factor VIII was no less effective or long-lasting in the blood than the traditional preparations. Furthermore, the new preparation proved to be no more antigenic than blood-derived factor VIII. As is the case with insulin and other protein factors, one of the major impediments to continued use of a factor VIII preparation is the development of antibodies. A small fraction of patients with hemophilia develop antibodies against factor VIII, which not only bind to the molecule, but inhibit its function. Such inhibitor antibodies developed in eight of the patients; the antibodies were strong in only one. This is comparable to the incidence of inhibitor antibodies seen using blood-derived factor VIII. (Consumer Summary produced by Reliance Medical Information, Inc.)

Published
1990

43. Mice deficient in the anti-haemophilic coagulation factor VIII show increased von Willebrand factor plasma levels

Author

Kiouptsi, Klytaimnistra, Grill, Alexandra, Mann, Amrit, Döhrmann, Mareike, Lillich, Maren, Jäckel, Sven, Malinarich, Frano, Formes, Henning, Manukyan, Davit, Subramaniam, Saravanan, Khandagale, Avinash, Karwot, Cornelia, Thal, Serge C., Bosmann, Markus, Scharrer, Inge, Jurk, Kerstin, and Reinhardt, Christoph

Subjects
Heredity, Physiology, Genetic Linkage, 610 Medizin, lcsh:Medicine, Cardiovascular Medicine, Pathology and Laboratory Medicine, Biochemistry, Vascular Medicine, Mice, Animal Cells, hemic and lymphatic diseases, 610 Medical sciences, Medicine and Health Sciences, lcsh:Science, Immune Response, Thrombin, Animal Models, Hematology, Body Fluids, Blood, Experimental Organism Systems, Cardiovascular Diseases, X-Linked Traits, Sex Linkage, Blood Coagulation Tests, Anatomy, Cellular Types, Research Article, Platelets, congenital, hereditary, and neonatal diseases and abnormalities, Immunology, Mouse Models, Hemorrhage, Enzyme-Linked Immunosorbent Assay, Research and Analysis Methods, Hemophilia A, Real-Time Polymerase Chain Reaction, Blood Plasma, Model Organisms, Signs and Symptoms, Diagnostic Medicine, von Willebrand Factor, Genetics, Animals, Hemophilia, Blood Coagulation, Inflammation, Clinical Genetics, Blood Cells, Coagulation Disorders, lcsh:R, Biology and Life Sciences, Proteins, Cell Biology, Mice, Inbred C57BL, lcsh:Q
Abstract

Von Willebrand factor (VWF) is the carrier protein of the anti-haemophilic Factor VIII (FVIII) in plasma. It has been reported that the infusion of FVIII concentrate in haemophilia A patients results in lowered VWF plasma levels. However, the impact of F8-deficiency on VWF plasma levels in F8-/y mice is unresolved. In order to avoid confounding variables, we back-crossed F8-deficient mice onto a pure C57BL/6J background and analysed VWF plasma concentrations relative to C57BL/6J WT (F8+/y) littermate controls. F8-/y mice showed strongly elevated VWF plasma concentrations and signs of hepatic inflammation, as indicated by increased TNF-α, CD45, and TLR4 transcripts and by elevated macrophage counts in the liver. Furthermore, immunohistochemistry showed that expression of VWF antigen was significantly enhanced in the hepatic endothelium of F8-/y mice, most likely resulting from increased macrophage recruitment. There were no signs of liver damage, as judged by glutamate-pyruvate-transaminase (GPT) and glutamate-oxalacetate-transaminase (GOT) in the plasma and no signs of systemic inflammation, as white blood cell subsets were unchanged. As expected, impaired haemostasis was reflected by joint bleeding, prolonged in vitro clotting time and decreased platelet-dependent thrombin generation. Our results point towards a novel role of FVIII, synthesized by the liver endothelium, in the control of hepatic low-grade inflammation and VWF plasma levels.

Published
2017
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46. Relapse Rate in Survivors of Acute Autoimmune Thrombotic Thrombocytopenic Purpura Treated with or without Rituximab

Author

Falter, Tanja, additional, Herold, Stephanie, additional, Weyer-Elberich, Veronika, additional, Scheiner, Carina, additional, Schmitt, Veronique, additional, von Auer, Charis, additional, Messmer, Xavier, additional, Wild, Philipp, additional, Lackner, Karl, additional, Lämmle, Bernhard, additional, and Scharrer, Inge, additional

Published
2018
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48. Mice deficient in the anti-haemophilic coagulation factor VIII show increased von Willebrand factor plasma levels

Author

Kiouptsi, Klytaimnistra, primary, Grill, Alexandra, additional, Mann, Amrit, additional, Döhrmann, Mareike, additional, Lillich, Maren, additional, Jäckel, Sven, additional, Malinarich, Frano, additional, Formes, Henning, additional, Manukyan, Davit, additional, Subramaniam, Saravanan, additional, Khandagale, Avinash, additional, Karwot, Cornelia, additional, Thal, Serge C., additional, Bosmann, Markus, additional, Scharrer, Inge, additional, Jurk, Kerstin, additional, and Reinhardt, Christoph, additional

Published
2017
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