KENNETH E. BERNSTEIN, M.D.
Medical Practice at Woodruff Cir, Atlanta, GA
License number
Georgia 030010
Category
Medical Practice
Type
Anatomic Pathology
Address
Address
101 Woodruff Cir BUILDING MEMORIAL, Atlanta, GA 30322
Phone
(404) 727-3134
(404) 727-8540 (Fax)
(404) 727-8540 (Fax)
Professional information
See more information about KENNETH E. BERNSTEIN at trustoria.com
Dr. Kenneth E Bernstein, Los Angeles CA - MD (Doctor of Medicine)
Dr. Kenneth E Bernstein, Los Angeles CA - MD (Doctor of Medicine)
Specialties:
Anatomic Pathology
Address:
8700 Beverly Blvd SUITE 2021, Los Angeles 90048
(310) 423-5431 (Phone), (310) 423-3539 (Fax)
101 Woodruff Cir SUITE 7107A, Atlanta 30322
(404) 727-3134 (Phone), (404) 727-8540 (Fax)
CEDARS-SINAI PATHOLOGY DEPT
8700 Beverly Blvd SUITE 4711, Los Angeles 90048
(310) 423-5471 (Phone), (310) 423-0122 (Fax)
(310) 423-5431 (Phone), (310) 423-3539 (Fax)
101 Woodruff Cir SUITE 7107A, Atlanta 30322
(404) 727-3134 (Phone), (404) 727-8540 (Fax)
CEDARS-SINAI PATHOLOGY DEPT
8700 Beverly Blvd SUITE 4711, Los Angeles 90048
(310) 423-5471 (Phone), (310) 423-0122 (Fax)
Certifications:
Anatomic Pathology, 1985
Awards:
Healthgrades Honor Roll
Languages:
English
Education:
Medical School
New York University
Graduated: 1978
New York University
Graduated: 1978
Methods And Compositions For Modulating The Activity Of Peptidases In Macrophage And Macrophage-Like Cells
Methods And Compositions For Modulating The Activity Of Peptidases In Macrophage And Macrophage-Like Cells
US Patent:
2009021, Aug 27, 2009
Filed:
May 18, 2006
Appl. No.:
11/914881
Inventors:
Kenneth Bernstein - Atlanta GA, US
Xiao Shen - Los Angeles CA, US
Xiao Shen - Los Angeles CA, US
Assignee:
Emory University - Atlanta GA
International Classification:
A01K 67/00, C12N 15/00, C12N 5/00, A61K 35/12, A61K 39/00, C12N 15/63
US Classification:
800 18, 435455, 435325, 424 9321, 4241841, 800 13, 4353201
Abstract:
Methods and compositions are provided for modulating the activity of macrophage and macrophage-like cells, particularly by modulating the peptidase activity of such cells. In certain aspects, methods are provided for enhancing or suppressing the immune function of a host by increasing or decreasing, respectively, expression of a target peptidase in host macrophage and macrophage-like cells. Such methods for enhancing or suppressing the immune function of a host by increasing or inhibiting (suppressing or silencing) expression of a target peptidase in host macrophage and macrophage-like cells find use in methods for treating and/or preventing a number of diseases and conditions, including cancer, viral and/or bacterial infection, Alzheimer's disease, tissue transplant rejection, autoimmune diseases, and chronic inflammatory diseases. The invention also provides compositions and research tools related to these methods, including vectors for increasing or inhibiting the expression of a peptidase in macrophage and macrophage-like cells, macrophage and macrophage-like cells transfected with these vectors, genetically modified mice that over-express a target peptidase or in which expression of a target peptidase has been disrupted, and selective modulators of peptidase activity in macrophages as well as methods for identifying and using such modulators.
Self-Induced Deletion Of Dna
Self-Induced Deletion Of Dna
US Patent:
2008029, Nov 27, 2008
Filed:
Jun 7, 2007
Appl. No.:
11/759574
Inventors:
Kirk R. Thomas - Salt Lake City UT, US
Kenneth E. Bernstein - Atlanta GA, US
Michaeline Bunting - Salt Lake City UT, US
Joy Greer - Salt Lake City UT, US
Mario Capecchi - Salt Lake City UT, US
Kenneth E. Bernstein - Atlanta GA, US
Michaeline Bunting - Salt Lake City UT, US
Joy Greer - Salt Lake City UT, US
Mario Capecchi - Salt Lake City UT, US
Assignee:
UNIVERSITY OF UTAH - Salt Lake City UT
International Classification:
A01K 67/027, C07H 21/04, C12N 15/63
US Classification:
800 18, 536 231, 435440
Abstract:
The present invention is directed to a method for deleting DNA sequences in a tissue specific manner. In one embodiment, DNA sequences are specifically deleted in germline tissue. In a second embodiment, DNA sequences are specifically deleted in desired somatic tissue. The present invention is further directed to a nucleic acid molecule for use in the method. More specifically, a nucleic acid molecule is provide by the present invention which comprises (a) a recombinase site, (b) a tissue-specific promoter, (c) a recombinase gene, (d) a foreign DNA, and (e) a recombinase site. The nucleic acid molecule may further comprise a gene which is desired to be incorporated into and expressed in a transgenic organism. The method can be used in both plants and animals, and has many applications as described herein.