In order to accurately and reliably quantitate HLE on the plasma membranes of the lymphocytes and mononuclear phagocytes, a test sample containing the lymphocytes and mononuclear phagocytes is initially treated with a first antiserum specific for CD4 receptors on the plasma membrane or with a second antiserum specific for chemokine receptors on the plasma membrane. Once the CD4 or chemokine receptors have been rendered non-reactive (competitive) relative to the HLE receptors (also “binding sites”) on the plasma membrane, the test sample is contacted with an immunoreagent specific for interaction with one or more of the HLE receptors on the plasma membranes of the lymphocytes and mononuclear phagocytes. The immunoreagent forms a complex with the HLE binding sites and produces a characteristic physical change in the lymphocytes and mononuclear phagocytes that can be monitored by anyone of a number of standard techniques, (e. g. , confocal laser scanning microscopy and flow cytometry).
Detection Of Surface-Associated Human Leukocyte Elastase
In order to accurately and reliably quantitate HLE on the plasma membranes of the lymphocytes and mononuclear phagocytes, a test sample containing the lymphocytes and mononuclear phagocytes is initially treated with a first antiserum specific for CD4 receptors on the plasma membrane or with a second antiserum specific for chemokine receptors on the plasma membrane. Once the CD4 or chemokine receptors have been rendered non-reactive (competitive) relative to the HLE receptors (also “binding sites”) on the plasma membrane, the test sample is contacted with an immunoreagent specific for interaction with one or more of the HLE receptors on the plasma membranes of the lymphocytes and mononuclear phagocytes. The immunoreagent forms a complex with the HLE binding sites and produces a characteristic physical change in the lymphocytes and mononuclear phagocytes that can be monitored by any one of a number of standard techniques, (e.g., confocal laser scanning microscopy and flow cytometry).
Therapeutic Administration Of A Modified Alpha1 Proteinase Inhibitor
A method for the treatment of asymtomatic HIV seropositive individuals to inhibit onset of an AIDS infection and, for suppression of propagation of HIV infections in individuals with a fully developed AIDS infection. The method consists of administering a therapeutic effective amount of a modified {acute over ()}Proteinase Inhibitor (m{acute over ()}PI) to an individual within the effected population so as to inhibit and/or prevent {acute over ()} PI facilitated HIV entry into healthy/uninfected cells.
Modulation Of Plasma Membrane Human Leukocyte Elastase
A method for modulation of plasma membrane associated Human Leukocyte Elastase (HLE) to inflammatory states by interaction of HLE with an antagonist to inhibit HLE and thereby interruption in plasma associated events (e.g. HIV disease progression, bacterial infections and autoimmune diseases), which are responsive/sensitive to such inflammation. The antagonist suitable for use in this invention is designed to interact with each of the catalytic triad of the HLE plasma membranes protein and the lipid interactive amino acids of the HLE plasma membrane protein.
Modulation Of Plasma Membrane Human Leukocyte Elastase
A method for modulation of plasma membrane associated Human Leukocyte Elastase (HLE) to inflammatory states by interaction of HLE with an antagonist to inhibit HLE and thereby interruption in plasma associated events (e.g. HIV disease progression, bacterial infections and autoimmune diseases), which are responsive/sensitive to such inflammation. The antagonist suitable for use in this invention is designed to interact with each of the catalytic triad of the HLE plasma membranes protein and the lipid interactive amino acids of the HLE plasma membrane protein.
Detection Of Surface-Associated Human Leukocyte Elastase
In order to accurately and reliably quantitate HLE on the plasma membranes of the lymphocytes and mononuclear phagocytes, a test sample containing the lymphocytes and mononuclear phagocytes is initially treated with a first antiserum specific for CD4 receptors on the plasma membrane or with a second antiserum specific for chemokine receptors on the plasma membrane. Once the CD4 or chemokine receptors have been rendered non-reactive (competitive) relative to the HLE receptors (also “binding sites”) on the plasma membrane, the test sample is contacted with an immunoreagent specific for interaction with one or more of the HLE receptors on the plasma membranes of the lymphocytes and mononuclear phagocytes. The immunoreagent forms a complex with the HLE binding sites and produces a characteristic physical change in the lymphocytes and mononuclear phagocytes that can be monitored by any one of a number of standard techniques, (e.g., confocal laser scanning microscopy and flow cytometry).
Modulation Of Plasma Membrane Human Leukocyte Elastase
A method for modulation of plasma membrane associated Human Leukocyte Elastase (HLE) to inflammatory states by interaction of HLE with an antagonist to inhibit HLE and thereby interruption in plasma associated events (e.g. HIV disease progression, bacterial infections and autoimmune diseases), which are responsive/sensitive to such inflammation. The antagonist suitable for use in this invention is designed to interact with each of the catalytic triad of the HLE plasma membranes protein and the lipid interactive amino acids of the HLE plasma membrane protein.
Therapeutic Use For Alpha1 Proteinase Inhibitor In Hematopoiesis
A previously unrecognized fundamental property of αPI is to regulate the phenotypic composition of circulating and tissue-associated cells derived from hematopoietic stem cells. The present invention comprises screening for various unmodified and modified αPI's which are useful in the treatment of abnormalities in the number of cells of myeloid or lymphoid lineage that are associated with HIV-1 infection, microbial infection, leukemia, solid tumor cancers, atherosclerosis, autoimmunity, stem cell transplantation, organ transplantation, and other diseases affected by cells of the immune system. The interaction of αPI with its receptors, HLEand LRP, influences the level of cells of different lineages. Genetic and proteolytic modification of αPI is used to target these receptors to increase or decrease specific cell populations, as needed, in the various disease states.
Resumes
Chief Science Officer At Alpha-1 Biologics Corporation
Chief Science Officer at Alpha-1 Biologics Corporation, Director of Research at Institute for Human Genetics and Biochemistry
Location:
United States
Industry:
Research
Work:
Alpha-1 Biologics Corporation - Stony Brook, NY since May 2011
Chief Science Officer
Institute for Human Genetics and Biochemistry since 2003
Director of Research
Weill Cornell Medical College 2009 - 2012
Asst Prof, Dept of Medicine, Div Hematology/Med Oncology
Mount Sinai School of Medicine 2004 - 2008
Asst Prof, Dept of Medicine
The Rockefeller University 2001 - 2002
Res Assoc
Education:
Medical University of South Carolina 1979 - 1986
MS,PhD, Basic and Clinical Immunology and Microbiology
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