JAY EDELBERG, MD
Osteopathic Medicine at 70 St, New York, NY

6437215, Aug 20, 2002

Jun 28, 2000

09/606324

Monty Krieger - Needham MA
Jay M. Edelberg - New York NY
Bernardo Trigatti - Arlington MA

Massachusetts Institute of Technology - Cambridge MA

A01K 67027

800 18, 800 3, 800 9

Transgenic animals that do not express functional SR-BI and ApoE develop severe atherosclerosis, by age four weeks in transgenic mice. Moreover, these animals exhibit progressive heart block by age four weeks, and die by age nine weeks. Pathology shows extensive fibrosis of the heart and occlusion of coronary arteries. The occlusion appears to be due to clotting, since fat deposition is in the walls. These animals are good models for the following diseases, and for screening of drugs useful in the treatment and/or prevention of these disorders: cardiac fibrosis, myocardial infarction, defects in electrical conductance, atherosclerosis, unstable plaque, and stroke. In contrast to other known models for atherosclerosis, these animals do not have to be fed extreme diets for long periods before developing atherosclerosis. No other known model for heart attacks and stroke is known.

2002010, Aug 8, 2002

Sep 13, 2001

09/951936

Monty Krieger - Needham MA, US
Jay Edelberg - New York NY, US
Bernardo Trigatti - Hamilton, CA

A01K067/027, A61K049/00

800/003000, 800/014000, 800/018000, 800/009000, 424/009200

Transgenic animals that do not express functional SR-BI and ApoE develop severe atherosclerosis, by age four weeks in transgenic mice. Moreover, these animals exhibit progressive heart block by age four weeks, and die by age nine weeks. Pathology shows extensive fibrosis of the heart and occlusion of coronary arteries. The occlusion appears to be due to clotting, since fat deposition is in the walls. These animals are good models for the following diseases, and for screening of drugs useful in the treatment and/or prevention of these disorders: cardiac fibrosis, myocardial infarction, defects in electrical conductance, atherosclerosis, unstable plaque, and stroke. In contrast to other known models for atherosclerosis, these animals do not have to be fed extreme diets for long periods before developing atherosclerosis. No other known model for heart attacks and stroke is known.

6776987, Aug 17, 2004

Jul 12, 2000

09/614326

Jay M. Edelberg - New York NY
Robert D. Rosenberg - Boston MA

Massachusetts Institute of Technology - Cambridge MA

A01N 6300

424 9321, 424 931, 424 932, 514 44

Molecularly-mediated and cellular-based -adrenergic receptor-dependent biological pacemakers are disclosed. Methods of using these compositions to improve cardiac chrontropic responsiveness by upregulating heart rate and altering cardiac rhythm are also disclosed.

6650919, Nov 18, 2003

May 3, 2001

09/848064

Jay M. Edelberg - New York NY
David J. Christini - Brooklyn NY

Cornell Research Foundation, Inc. - Ithaca NY

A61B 505

600345, 600300, 600365, 600373, 20440301, 435176

The present invention provides implantable physiological or pathophysiological biosensors. The subject biosensors comprise tissue or cells capable of carrying out a physiological or pathophysiological function, which can be used to monitor a chemical, physiological or pathophysiological variable associated with the physiological or pathophysiological function. In one embodiment, the tissue or cells are coupled via an electrical interface to an electronic measuring device or an electronic amplifying device. In another embodiment, the tissue or cells are coupled via an electrical interface to endogenous tissue or cells, including the blood. Preferably, the tissue or cells are excitable tissue or cells such as cardiac tissue or cells and neuronal tissue or cells. The subject biosensors may be placed, inserted or implanted in any animal including but not limited to a mouse, rat, rabbit, pig, cat, dog, cattle, horse, sheep or human. The present invention also provides various methods which employ a biosensor of the present invention.

2004013, Jul 15, 2004

Oct 21, 2003

10/690798

Jay Edelberg - New York NY, US
David Christini - Brooklyn NY, US

Cornell Research Foundation, Inc.

A61K048/00, C12N005/08

435/368000, 424/093210

The present invention provides implantable physiological or pathophysiological biosensors. The subject biosensors comprise tissue or cells capable of carrying out a physiological or pathophysiological function, which can be used to monitor a chemical, physiological or pathophysiological variable associated with the physiological or pathophysiological function. In one embodiment, the tissue or cells are coupled via an electrical interface to an electronic measuring device or an electronic amplifying device. In another embodiment, the tissue or cells are coupled via an electrical interface to endogenous tissue or cells, including the blood. Preferably, the tissue or cells are excitable tissue or cells such as cardiac tissue or cells and neuronal tissue or cells. The subject biosensors may be placed, inserted or implanted in any animal including but not limited to a mouse, rat, rabbit, pig, cat, dog, cattle, horse, sheep or human. The present invention also provides various methods which employ a biosensor of the present invention. Such methods include a method of monitoring physiological or pathophysiological function, a method of regulating output of a signal to a subject, and a method for controlling heart function.

7135171, Nov 14, 2006

Feb 13, 2003

10/367639

Jay Edelberg - New York NY, US
Shahin Rafii - Great Neck NY, US
Mun Hong - New York NY, US
Robert P. Lanza - Clinton MA, US
Michael D. West - Southborough MA, US

Cornell Research Foundation, Inc. - Ithaca NY

A01N 63/00, A61K 48/00, A01N 43/04, C12P 21/06, C12N 5/00, C12N 16/63

424 931, 424 932, 424 9321, 424 937, 514 44, 435 691, 435325, 435455

The invention provides methods of treating and preventing loss of tissue vascularization that can occur, for example, upon aging.

2006017, Aug 3, 2006

Jan 23, 2006

11/337981

Jay Edelberg - New York NY, US
Victoria Ballard - New York NY, US

A61K 38/17

514012000

The invention relates to Tenascin-C and peptides that bind thereto. According to the invention, Tenascin-C or peptides and antibodies that bind thereto can be used to treat or prevent vascular diseases, either alone or in combination with therapeutic agents or cells that have cardioplastic potential.

7910694, Mar 22, 2011

Sep 18, 2003

10/527832

Jay M. Edelberg - New York NY, US
Dong Qing Cai - Guangzhou, CN
Barbara L. Hempstead - New York NY, US

Cornell Research Foundation, Inc. - Ithaca NY

A61K 38/04, A61K 38/00, A61K 51/00

530329, 530300, 530324, 514 11, 424 169

The present invention relates to peptides which selectively or preferentially home to areas of a heart. The invention further relates to conjugates of the homing peptides and uses thereof.