DR. JOSHUA M HARE, MD, FACC, FAHA
Osteopathic Medicine at 12 Ave, Miami, FL

8507433, Aug 13, 2013

Oct 28, 2010

12/914023

Andrew V. Schally - Miami Beach FL, US
Norman L Block - Hollywood FL, US
Joshua Hare - Miami Beach FL, US
Rosemeire Miyuki Kanashiro Takeuchi - Miami FL, US

University of Miami - Miami FL
The United States of America, represented by the Deptartment of Veterans Affairs - Washington DC

A61K 38/25, C07K 14/60, A61P 9/10

514 112, 514 151, 514 213, 530324, 930120

Whether the growth hormone (GH)/Insulin-like growth factor 1(IGF-I) axis exerts cardioprotective effects remains controversial; and the underlying mechanism(s) for such actions are unclear. Here we tested the hypothesis that growth-hormone releasing hormone (GHRH) directly activates cellular reparative mechanisms within the injured heart, in a GH/IGF-I independent fashion. Following experimental myocardial infarction (MI), rats were randomly assigned to receive, during a 4 week period, either placebo (n=14), rat recombinant GH (rrGH, n=8) or JI-38 (n=8; 50 μg/Kg/day), a potent GHRH-agonist. JI-38 did not elevate serum levels of GH or IGF-I, but markedly attenuated the degree of cardiac functional decline and remodeling after injury. In contrast, GH administration markedly elevated body weight, heart weight, circulating GH and IGF-I, but did not offset the decline in cardiac structure and function. Whereas, both JI-38 and GH augmented levels of cardiac precursor cell proliferation, only JI-38 increased anti-apoptotic gene expression.

2014005, Feb 27, 2014

Jul 22, 2013

13/947800

Joshua M. Hare - Miami Beach FL, US

United States of America, Represented by The Department of Veterans Affairs - Washington DC
University of Miami - Miami FL

A61K 38/25

514 112

Disclosed herein are methods demonstrating that growth-hormone releasing hormone (GHRH) directly activates cellular reparative mechanisms within the injured heart, in a GH/IGF-I independent fashion. Following experimental myocardial infarction (MI), rats were randomly assigned to receive, during a 4 week period, either placebo (n=14), rat recombinant GH (rrGH, n=8) or JI-38 (n=8; 50 μg/Kg/day), a potent GHRH-agonist. JI-38 did not elevate serum levels of GH or IGF-I, but markedly attenuated the degree of cardiac functional decline and remodeling after injury. In contrast, GH administration markedly elevated body weight, heart weight, circulating GH and IGF-I, but did not offset the decline in cardiac structure and function. Whereas, both JI-38 and GH augmented levels of cardiac precursor cell proliferation, only JI-38 increased anti-apoptotic gene expression. Collectively, these findings demonstrate that within the heart, GHRH-agonists can activate cardiac repair following MI.

2010026, Oct 14, 2010

Mar 31, 2010

12/751445

Joshua Hare - Miami Beach FL, US
Konstantinos Chatzistergos - Kos, GR

UNIVERSITY OF MIAMI - Miami FL

A61K 35/28, A61K 35/12, C07K 14/52, C07K 16/24, A61P 9/00, C12N 5/0775

424 937, 530350, 5303892, 435347, 435366

Compositions comprising stem cells delivered into infarcted myocardium by endocardial injection, engraft and differentiate into myocytes, endothelial cells, and vascular smooth muscle, and do so without the requirement for survival enhancing modification. These cells engraft whether injected acutely (days) or late (months) after myocardial infarction, and the efficiency of engraftment correlates with the functional recovery of the heart. The stem cells also recruit endogenous cardiac precursor cells, reconstitute myocardial stem cell niches, and enhance endogenous cell differentiation into myocytes.

2010011, May 6, 2010

Nov 2, 2009

12/610529

Joshua M. Hare - Miami Beach FL, US
Bettina Heidecker - Miami FL, US

University Of Miami - Miami FL

C12Q 1/68, C12N 5/00, C12N 15/63, C40B 40/06, C07K 16/00, C07H 21/00

435 6, 435325, 4353201, 506 16, 5303871, 536 231

A novel transcriptomic biomarker for prognosis in heart failure has a direct clinical application in prediction of prognosis in new onset heart failure, heart disease, heart disorders and associated heart conditions. This approach should improve individualization of cardiac care and help identify patients at highest risk for circulatory collapse within the first years of presentation with heart failure.

2014002, Jan 23, 2014

Aug 29, 2011

13/819154

Joshua M. Hare - Miami Beach FL, US
Ian K. McNiece - Coral Gables FL, US

University of Miami - Miami FL

A61K 35/28

424 937

Methods for the isolation of CD271 stem cell populations are important in the prevention or treatment of cardio-vascular diseases and repair of cardiac tissue. The methods are applicable to stem cells from different sources and can be used to treat or prevent diseases or repair of tissues elsewhere in the organism's body.

2012014, Jun 7, 2012

Jun 2, 2010

13/376046

Joshua M. Hare - Miami Beach FL, US
Bettina Heidecker - Miami FL, US

University of Miami - Miami FL

C40B 30/00, G01N 33/566, C12N 5/10, C07H 21/00, C40B 40/06, C40B 40/10, C07K 14/00, C12Q 1/68, C12N 15/63

506 7, 435 612, 435 792, 435325, 4353201, 436501, 506 16, 506 18, 530350, 536 231

Molecular signatures that function as very sensitive diagnostic biomarker for myocarditis, heart disease and disorders thereof, are identified.

2009027, Nov 5, 2009

May 4, 2009

12/434833

Karen Young - Miami FL, US
Cleide Suguihara - Miami FL, US
Joshua M. Hare - Miami Beach FL, US

University Of Miami - Miami FL

A61K 31/7088, A61K 38/02, A61K 39/395, A61P 11/00, C12N 5/00, C12Q 1/02

4241301, 514 44 R, 514 2, 435375, 435 29

Blockade of stromal derived factor-1 (SDF-1), a stem cell mobilizer and/or its receptor, chemokine receptor 4 (CXCR4) attenuates and reverses hypoxia-induced cardiopulmonary remodeling in vivo. Compositions for treating hypoxia-induced cardiovascular disorders modulate the SDF-1/CXCR4 axis.

2010019, Jul 29, 2010

Oct 30, 2009

12/609194

Joshua M. Hare - Miami Beach FL, US
Bettina Heidecker - Miami FL, US

Univrsity of Miami - Miami FL

C40B 30/00, C07K 14/00, G01N 33/50, C12Q 1/68, G01N 33/53, C07H 21/00, C07K 16/00, C40B 40/06, C12N 15/74, C12N 5/071

506 7, 530350, 436 86, 435 6, 435 71, 536 231, 5303871, 506 16, 4353201, 435325

Molecular signatures that function as very sensitive diagnostic biomarker for myocarditis, heart disease and disorders thereof, are identified.