World's Best Scientists 2026 revealed!

Research.com Recognitions

  • 1996 - Fellow of the American Association for the Advancement of Science (AAAS)
  • Member of the Association of American Physicians

Overview

Harry S. Jacob is affiliated with the University of Minnesota in the United States. Their research primarily spans the field of Biochemistry, Genetics and Molecular Biology, with specific focus on subfields such as Molecular Biology, Pathology and Forensic Medicine, Cell Biology, Immunology, and Genetics.

The main topics covered in their work include:

  • Heme Oxygenase-1 and Carbon Monoxide
  • Alcohol Consumption and Health Effects
  • Hemoglobin structure and function
  • Immunodeficiency and Autoimmune Disorders
  • Blood disorders and treatments
  • Streptococcal Infections and Treatments

Jacob has contributed to several publications, with recent papers including:

  • "Heme cytotoxicity is the consequence of endoplasmic reticulum stress in atherosclerotic plaque progression," 2021, published in Scientific Reports
  • "Case report of an unusual presentation of Staphylococcus aureus induced toxic shock syndrome/hyperimmunoglobulinemia E syndrome," 2020, published in Medicine
  • "Das große "Ja, aber"," 2020, published in VDI nachrichten
  • "Steuerungstechnik gewinnt an Vielfalt," 2021, published in VDI nachrichten

Frequent co-authors in their research include:

  • Dávid Pethő
  • Zoltán Hendrik
  • Annamária Nagy
  • Lívia Beke
  • Andreas Patsalos

The scientist has published repeatedly in venues such as VDI nachrichten, Scientific Reports, and Medicine.

Among honors received, Harry S. Jacob was named a Fellow of the American Association for the Advancement of Science (AAAS) in 1996 and is a member of the Association of American Physicians.

Best Publications

  • Oxygen radicals mediate endothelial cell damage by complement-stimulated granulocytes. An in vitro model of immune vascular damage.

    Thomas Sacks;Charles F. Moldow;Philip R. Craddock;Timothy K. Bowers

  • Ferritin: a cytoprotective antioxidant strategem of endothelium.

    György Balla;Harry S. Jacob;József Balla;M. Rosenberg

  • Hemodialysis leukopenia. Pulmonary vascular leukostasis resulting from complement activation by dialyzer cellophane membranes.

    P R Craddock;J Fehr;A P Dalmasso;K L Brighan

  • Complement and Leukocyte-Mediated Pulmonary Dysfunction in Hemodialysis

    Philip R. Craddock;Philip R. Craddock;Jorg Fehr;Jorg Fehr;Kenneth L. Brigham;Kenneth L. Brigham;Richard S. Kronenberg;Richard S. Kronenberg

  • C-reactive protein induces human peripheral blood monocytes to synthesize tissue factor

    Jaroslav Cermak;Nigel S. Key;Ronald R. Bach;Jozsef Balla

  • Complement (C5-a)-induced granulocyte aggregation in vitro. A possible mechanism of complement-mediated leukostasis and leukopenia.

    P R Craddock;D Hammerschmidt;J G White;A P Dalmosso

  • Induction of heme oxygenase is a rapid, protective response in rhabdomyolysis in the rat

    Karl A. Nath;Gyorgy Balla;Gregory M. Vercellotti;Jozsef Balla

  • ASSOCIATION OF COMPLEMENT ACTIVATION AND ELEVATED PLASMA-C5a WITH ADULT RESPIRATORY DISTRESS SYNDROME. Pathophysiological Relevance and Possible Prognostic Value

    Dale E Hammerschmidt;Leonard D. Hudson;L. Jean Weaver;Philip R. Craddock

  • Complement-induced granulocyte aggregation: an unsuspected mechanism of disease.

    Harry S. Jacob;Philip R. Craddock;Dale E. Hammerschmidt;Charles F. Moldow

  • Endothelial-cell heme uptake from heme proteins: induction of sensitization and desensitization to oxidant damage.

    Jozsef Balla;Harry S. Jacob;Gyorgy Balla;Karl Nath

  • Abnormal Adherence of Sickle Erythrocytes to Cultured Vascular Endothelium: POSSIBLE MECHANISM FOR MICROVASCULAR OCCLUSION IN SICKLE CELL DISEASE

    Robert P. Hebbel;Osamu Yamada;Charles F. Moldow;Harry S. Jacob

  • Hemin: a possible physiological mediator of low density lipoprotein oxidation and endothelial injury.

    G. Balla;Harry S Jacob;J. W. Eaton;John D Belcher

  • Complement activation and neutropenia occurring during cardiopulmonary bypass

    Dale E. Hammerschmidt;David F. Stroncek;Timothy K. Bowers;Carol J. Lammi-Keefe

  • EFFECTS OF SULFHYDRYL INHIBITION ON RED BLOOD CELLS. I. MECHANISM OF HEMOLYSIS

    Harry S. Jacob;James H. Jandl

  • Fat embolism prophylaxis with corticosteroids. A prospective study in high-risk patients.

    Steven A. Schonfeld;Yongyudh Ploysongsang;Ralph DiLISIO;John D. Crissman

  • Elevated erythrocyte calcium in sickle cell disease.

    John W. Eaton;Harry S. Jacob;T. D. Skelton;Harold S. Swofford

  • Acquired phagocyte dysfunction. A complication of the hypophosphatemia of parenteral hyperalimentation

    P. R. Craddock;Y. Yawata;L. Vansanten;S. Gilberstadt

  • Exposure of endothelial cells to free heme potentiates damage mediated by granulocytes and toxic oxygen species.

    G Balla;G M Vercellotti;U Muller-Eberhard;J Eaton

  • Corticosteroids inhibit complement-induced granulocyte aggregation. A possible mechanism for their efficacy in shock states.

    Dale E Hammerschmidt;J. G. White;P. R. Craddock;Harry S Jacob

  • Activation of plasma complement by perfluorocarbon artificial blood: probable mechanism of adverse pulmonary reactions in treated patients and rationale for corticosteroids prophylaxis

    Gregory M. Vercellotti;Dale E. Hammerschmidt;Philip R. Craddock;Harry S. Jacob

Frequent Co-Authors

Gregory M. Vercellotti
Gregory M. Vercellotti University of Minnesota
John W. Eaton
John W. Eaton University of Louisville
Daniel J. Weisdorf
Daniel J. Weisdorf University of Minnesota
Karl A. Nath
Karl A. Nath Mayo Clinic
James G. White
James G. White University of Minnesota
David F. Stroncek
David F. Stroncek National Institutes of Health
Robert P. Hebbel
Robert P. Hebbel University of Minnesota
Leo T. Furcht
Leo T. Furcht University of Minnesota
John R. Hoidal
John R. Hoidal University of Utah
Nigel S. Key
Nigel S. Key University of North Carolina at Chapel Hill

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