JOHN D MOUNTZ
Pilots at Vestavia Frst Pl, Birmingham, AL
License number
Alabama A1346435
Issued Date
Apr 2015
Expiration Date
Apr 2017
Category
Airmen
Type
Authorized Aircraft Instructor
Address
Address
2800 Vestavia Forest Pl, Birmingham, AL 35216
Organization information
See more information about JOHN D MOUNTZ at bizstanding.comJohn D Mountz MD
1825 University Blvd, Birmingham, AL 35233
Categories:
Internal Medicine Physicians & Surgeons
Phone:
(205) 975-5196 (Phone)
Professional information
Program Director At Clear Channel Radio
Position:
Program Director at Clear Channel Radio
Location:
Birmingham, Alabama Area
Industry:
Broadcast Media
Work:
Clear Channel Radio
- Birmingham, Alabama Area since Dec 2012
-
Program Director
Sun Broadcasting
Aug 2010 - Dec 2012
-
Program Director 92.5 Fox News
Cumulus Media
Aug 2004 - Aug 2010
-
APD
Cumulus Broadcasting
- Huntsville, Alabama Area Jul 2003 - Aug 2004
-
Program Director
Clear Channel Radio
1996 - 2003
-
Producer
Ameron Broadcasting, Inc.
1996 - 1998
-
Producer
Education:
University of Alabama at Birmingham 1996 - 2000
BA, Communication Management
BA, Communication Management
Human Fas Gene Promoter Region
US Patent:
5888764, Mar 30, 1999
Filed:
Jan 20, 1995
Appl. No.:
8/377522
Inventors:
John D. Mountz - Birmingham AL
Jianhua Cheng - Alabaster AL
William J. Koopman - Indian Springs AL
Tong Zhou - W. Stonebrook Pl. AL
Jianhua Cheng - Alabaster AL
William J. Koopman - Indian Springs AL
Tong Zhou - W. Stonebrook Pl. AL
Assignee:
UAB Research Foundation - Birmingham AL
International Classification:
C12N 121, C12N 510, C12N 1511, C12P 2100
US Classification:
435 691
Abstract:
Disclosed is a 5' flanking sequence of the human fas gene containing a promoter region. This sequence also contains at least three transcription initiation sites, as well as consensus sequences for AP-1, GF-1, NY-Y, CP-2, EB20, and c-myb. Also disclosed are methods of altering senescence of the immune system by modifying Fas activity in cells to increase or decrease apoptosis. Fas expression and function on T cells from old (22-26-month-old) mice is also compared to young (2-month-old) mice and old CD2-fas transgenic mice. Fas expression and ligand-induced apoptosis was decreased on T cells from old mice compared to young mice. In 26-month-old CD2-fas transgenic mice, Fas and CD44 expression, Fas-induced apoptosis, T cell proliferation and cytokine production were comparable to that of the young mice. These results suggest that T cell senescence with age is associated with defective apoptosis and that the CD2-fas transgene allows the maintenance of Fas apoptosis function and T cell function in aged mice comparable to that of young mice.
Professor Of Medicine At University Of Alabama At Birmingham
Position:
Professor of Medicine at University of Alabama at Birmingham
Location:
Birmingham, Alabama Area
Industry:
Higher Education
Work:
University of Alabama at Birmingham
-
Professor of Medicine
John Mountz, Birmingham AL
Work:
Dept of Med/Rheumatology Div Univ of Alabama-Birmingham
1825 University Blvd, Birmingham, AL 35233
1825 University Blvd, Birmingham, AL 35233
Controlling Immune Response To Specific Antigens
US Patent:
6689605, Feb 10, 2004
Filed:
Jan 2, 2000
Appl. No.:
09/424281
Inventors:
John D. Mountz - Birmingham AL
David T. Curiel - Birmingham AL
David T. Curiel - Birmingham AL
Assignee:
UAB Research Foundation - Birmingham AL
International Classification:
C12N 1563
US Classification:
4353201, 435455, 435325, 424 932, 424 9321, 4241991
Abstract:
One major problem with adenovirus gene therapy has been the T-cell mediated immune response elicited by inoculation of adenovirus, which leads to rapid clearance of the virus and loss of transgene expression. In the instant invention, the immune response to a virus is prevented by pre-treatment with adenovirus, adenoassociated virus or herpes virus infected antigen-presenting cell (APC) expressing Fas ligand with induced T-cell tolerance. Administration of AdCMVLacZ after tolerance resulted in prolonged expression of LacZ in tolerized animals compared to control treated animals. In control, but not tolerized animals, there was proliferation of CD3 T-cell in the spleen in response to AdCMVLacZ treatment. Tolerance induction is also indicated by decreased production of interferon- and IL-2 by peripheral T-cells isolated from treated animals after stimulation with the adenovirus infected APCs. T-cell tolerance is specific for the virus as the T-cell responses to an irrelative virus, mouse cytomegalovirus (MCMV) remained unimpaired.
Methods Of Producing High Titer Recombinant Adeno-Associated Virus
US Patent:
6383794, May 7, 2002
Filed:
Aug 24, 1999
Appl. No.:
09/379841
Inventors:
John D. Mountz - Birmingham AL
Assignee:
UAB Research Foundation - Birmingham AL
International Classification:
C12N 701
US Classification:
4352351, 4353201
Abstract:
The present invention discloses a method of producing large-scale recombinant adeno-associated virus stocks by infection of cells with at least one recombinant adenovirus vector(s). The vector(s) encode a therapeutic gene flanked by the terminal repeat ends of adeno-associated virus and the adeno-associated virus rep and cap genes. Transfection with two recombinant adenovirus vector(s) instead of two plasmids plus adenovirus results in the large scale, high titer production of recombinant adeno-associated virus with little to no contaminating adenovirus present.
Controlling Immune Response To Specific Antigens
US Patent:
2004015, Aug 12, 2004
Filed:
Feb 10, 2004
Appl. No.:
10/776119
Inventors:
John Mountz - Birmingham AL, US
David Curiel - Birmingham AL, US
David Curiel - Birmingham AL, US
International Classification:
A61K048/00
US Classification:
514/044000, 424/093210
Abstract:
One major problem with adenovirus gene therapy has been the T-cell mediated immune response elicited by inoculation of adenovirus, which leads to rapid clearance of the virus and loss of transgene expression. In the instant invention, the immune response to a virus is prevented by pre-treatment with adenovirus, adenoassociated virus or herpes virus infected antigen-presenting cell (APC) expressing Fas ligand with induced T-cell tolerance. Administration of AdCMVLacZ after tolerance resulted in prolonged expression of LacZ in tolerized animals compared to control treated animals. In control, but not tolerized animals, there was proliferation of CD3T-cell in the spleen in response to AdCMVLacZ treatment. Tolerance induction is also indicated by decreased production of interferon- and IL-2 by peripheral T-cells isolated from treated animals after stimulation with the adenovirus infected APCs. T-cell tolerance is specific for the virus as the T-cell responses to an irrelative virus, mouse cytomegalovirus (MCMV) remained unimpaired. The instant invention utilizes virus specific T-cell tolerance, which is induced by APCs that co-express Fas ligand and virus antigens. The instant invention involves novel vectors and methods to induce tolerance to a viral vector gene therapy and prolong expression of a transgene in a viral host.
Akt And Regulation Of Ra Synovial Fibroblast Apoptosis
US Patent:
2006010, May 18, 2006
Filed:
Nov 16, 2004
Appl. No.:
10/989722
Inventors:
John Mountz - Birmingham AL, US
Hui-Chen Hsu - Birmingham AL, US
Hui-Chen Hsu - Birmingham AL, US
International Classification:
A61K 48/00, A61K 31/366
US Classification:
424093200, 514044000, 514453000
Abstract:
The administration of an Akt inhibitor in a suitable carrier to a rheumatoid arthritis synovial fibroblast affords a process for inducing rheumatoid arthritis synovial fibroblast apoptosis. The Akt inhibitor is administered either as an active molecule or as a gene sequence expressible within rheumatoid arthritis synovial fibroblast cells. The gene sequence can be encompassed within a gene vector such as an adenovirus. A process for assaying rheumatoid arthritis drug candidates for apoptosis affect includes exposing a culture of rheumatoid arthritis synovial fibroblast cells to a drug candidate and monitoring apoptosis in the culture in the presence of the drug candidate. Apoptosis in the culture is compared to apoptosis induced in a duplicate culture in the presence of a known Akt inhibitor.
Fas Ligand Expressing Antigen Presenting Cells For Tolerance Induction
US Patent:
2002004, Apr 25, 2002
Filed:
May 15, 1998
Appl. No.:
09/079834
Inventors:
JOHN D. MOUNTZ - BIRMINGHAM AL, US
TONG ZHOU - BIRMINGHAM AL, US
TONG ZHOU - BIRMINGHAM AL, US
International Classification:
A61M001/00, A01N063/00, A01N065/00, A61K035/26, A61K035/28
US Classification:
604/028000, 424/577000, 424/578000
Abstract:
The present invention provides a method of inducing systemic tolerance to an antigen in an individual in need of such treatment, comprising the step of: administering antigen presenting cells to said individual, wherein said cells express Fas ligand and said antigen.
.Delta.nur77 Transgenic Mouse
US Patent:
5981829, Nov 9, 1999
Filed:
May 6, 1997
Appl. No.:
8/852173
Inventors:
John D. Mountz - Birmingham AL
Tong Zhou - Birmingham AL
Jianhua Cheng - Alabaster AL
Tong Zhou - Birmingham AL
Jianhua Cheng - Alabaster AL
Assignee:
UAB Research Foundation - Birmingham AL
International Classification:
C12N 500, C12N 1500, C12N 1509, C12N 1563
US Classification:
800 18
Abstract:
The present invention provides a transgenic mouse containing a transgene, said transgene comprising a truncated Nur77 (. DELTA. Nur77) gene. Also provided is a double transgenic mouse, wherein said double transgenic mouse comprises the. DELTA. Nur77 transgenic mouse backcrossed with the D. sup. b /HY T cell receptor transgenic mouse.