Debra A Hullett

6352857, Mar 5, 2002

Mar 28, 2000

09/537696

Tausif Alam - Madison WI
Debra A. Hullett - Madison WI
Hans W. Sollinger - Madison WI

Wisconsin Alumni Research Foundation - Madison WI

C12N 1500

4353201, 536 241, 536 235

Disclosed is a method for obtaining glucose-regulated expression of active insulin in the cells of a mammalian subject. The method involves delivering into the subject a genetic construct comprising a coding sequence for a human proinsulin operably connected a promoter functional in the host cells. The construct includes a glucose responsive regulatory module having at least one glucose inducible regulatory element comprising a pair of CACGTG motifs linked by a five base nucleotide sequence, which confers glucose inducible expression of the proinsulin coding sequence. To ensure proper processing of the proinsulin to active insulin, the coding sequence was modified to direct the synthesis of a mutant proinsulin polypeptide having amino acid sequences that can be cleaved to mature insulin in suitable host cells, such as hepatocytes.

6933133, Aug 23, 2005

Nov 12, 2001

10/013032

Tausif Alam - Madison WI, US
Debra A. Hullett - Madison WI, US
Hans W. Sollinger - Madison WI, US

Wisconsin Alumni Research Foundation - Madison WI

C12P021/04
C12P021/06
C12N015/74
C12N015/87
C12N005/00
C12N048/00

435 691, 435 696, 4353201, 435325, 435455, 514 44, 424 932, 424 9321

Disclosed is a method for obtaining glucose-regulated expression of active insulin in the cells of a mammalian subject. The method involves delivering into the subject a genetic construct comprising a coding sequence for a human proinsulin operably connected a promoter functional in the host cells. The construct includes a glucose responsive regulatory module having at least one glucose inducible regulatory element comprising a pair of CACGTG motifs linked by a five base nucleotide sequence, which confers glucose inducible expression of the proinsulin coding sequence. To ensure proper processing of the proinsulin to active insulin, the coding sequence was modified to direct the synthesis of a mutant proinsulin polypeptide having amino acid sequences that can be cleaved to mature insulin in suitable host cells, such as hepatocytes.

7425443, Sep 16, 2008

May 12, 2005

11/127629

Tausif Alam - Madison WI, US
Debra A. Hullett - Madison WI, US
Hans W. Sollinger - Madison WI, US

Wisconsin Alumni Research Foundation - Madison WI

C12N 15/00
A01N 63/00

4353201, 424 932, 424 9321, 536 235, 536 241

Disclosed is a method for obtaining glucose-regulated expression of active insulin in the cells of a mammalian subject. The method involves delivering into the subject a genetic construct comprising a coding sequence for a human proinsulin operably connected a promoter functional in the host cells. The construct includes a glucose responsive regulatory module having at least one glucose inducible regulatory element comprising a pair of CACGTG motifs linked by a five base nucleotide sequence, which confers glucose inducible expression of the proinsulin coding sequence. To ensure proper processing of the proinsulin to active insulin, the coding sequence was modified to direct the synthesis of a mutant proinsulin polypeptide having amino acid sequences that can be cleaved to mature insulin in suitable host cells, such as hepatocytes.

20030225045, Dec 4, 2003

Mar 13, 2003

10/240029

Hector Deluca - Deerfield WI, US
Bryan Becker - Verona WI, US
Hans Sollinger - Madison WI, US
Debra Hullett - Oregon WI, US

A61K031/59

514/167000

A method of stabilizing kidney function in transplant patients is disclosed. In one embodiment, the method comprises the steps of kidney transplant patient, wherein the transplant patient is undergoing immunosuppressive therapy, with a sufficient amount of vitamin D compound whereby the kidney function stabilizes.

20050282877, Dec 22, 2005

Apr 12, 2005

11/104165

Bryan Becker - Verona WI, US
Lynn Jacobson - Madison WI, US
Debra Hullett - Oregon WI, US
Jon Weidanz - Amarillo TX, US
Vaughan Wittman - Amarillo TX, US

A61K031/4184

514381000

Disclosed is a method of inhibiting production of IFN-Γ in patients having a transplanted organ. The method involves administering to the patient an amount of an angiotensin receptor-blocking compound, the amount being effective to inhibit production of IFN-Γ by T cells. The method can be used to treat inflammation involving an allograft, to treat chronic allograft nephropathy, and to treat other pathologies associated with allograft rejection.

20070280908, Dec 6, 2007

Aug 23, 2004

10/923924

Tausif Alam - Madison WI, US
Debra Hullett - Madison WI, US
Hans Sollinger - Madison WI, US

A61K 35/76
A61K 31/7052
A61P 3/08
C12N 15/63
C12N 15/86
C12N 5/08
C12N 7/01

424093600, 435235100, 435320100, 435370000, 435455000, 435456000, 514044000

Disclosed is a method for obtaining glucose-regulated expression of active insulin in the cells of a mammalian subject. The method involves delivering into the subject a genetic construct comprising a coding sequence for a human proinsulin operably connected a promoter functional in the host cells. The construct includes a glucose responsive regulatory module having at least one glucose inducible regulatory element comprising a pair of CACGTG motifs linked by a five base nucleotide sequence, which confers glucose inducible expression of the proinsulin coding sequence. To ensure proper processing of the proinsulin to active insulin, the coding sequence was modified to direct the synthesis of a mutant proinsulin polypeptide having amino acid sequences that can be cleaved to mature insulin in suitable host cells, such as hepatocytes.

20080021002, Jan 24, 2008

Jun 20, 2007

11/765947

Hector DeLuca - Deerfield WI, US
Bryan Becker - Verona WI, US
Hans Sollinger - Madison WI, US
Debra Hullett - Oregon WI, US

A61K 31/59
A61P 13/12

514167000

A method of stabilizing kidney function in transplant patients is disclosed. In one embodiment, the method comprises the steps of kidney transplant patient, wherein the transplant patient is undergoing immunosuppressive therapy, with a sufficient amount of vitamin D compound whereby the kidney function stabilizes and wherein the development of interstitial fibrosis is decreased.

20130338021, Dec 19, 2013

Mar 15, 2013

13/838428

Hans Sollinger - Madison WI, US
Debra A. Hullett - Oregon WI, US

Wisconsin Alumni Research Foundation - Madison WI

G01N 33/50

506 9, 435 29, 435 792, 435 71

The present disclosure provides methods and compositions for determining the presence of or predisposition to insulin resistance, diabetes, and complications of diabetes in a subject. The methods relate to measuring the capacity of a subject's peripheral blood mononuclear cells (PBMCs) to induce physiological and/or morphological changes characteristic of fibrosis in cultured.