University of Miami

The United States Government As Represented by the Department of Veterans Affairs

Dresden University of Technology

Other

The State University of New York

Norman L Block

Andrew V Schally

Lorne M Golub

Thomas F McNamara

Joshua Hare

Nungavaram S Ramamurthy

Sanford R Simon

Hsi-Ming Lee

Balakrishna L Lokeshwar

Marie G Selzer

Eugene C Eckstein

Barbara Ludwig

Stefan Bornstein

Rosemeire M Kanashiro-Takeuchi

Samirah Gomes

Leonard Pinchuk

Rosemeire Miyuki Kanashiro Takeuchi

Jacob Kline

Samirah A Gomes

Disclosed herein are compositions of GHRH agonists and peptides, and methods to treat disorders, such as ischemia and reperfusion injury. In one embodiment, a method of treating a reperfusion injury in a subject in need may involve administering a therapeutically effective amount of at least one GHRH agonist peptide to the subject. In additional embodiment, a method of promoting vasculogenesis in a mammal may involve administering a therapeutically effective amount of at least one GHRH agonist peptide to the subject. In a further embodiment, a method of promoting differentiation of mesenchymal stem cells into endothelial cells may involve contacting mesenchymal stem cells with at least one GHRH agonist peptide.

GHRH agonists for the treatment of ischemic disorders

Disclosed herein are compositions of GHRH agonists and peptides, and methods to treat diabetes. In one embodiment, a method of promoting survival of grafted cells and/or tissues may involve exposing the cells and/or tissues to an effective amount of at least one agonist of GHRH. In some embodiments, the grafted cells and/or tissues may be pancreatic cells. In some embodiments, the grafted cells may be islet cells co-cultured with non-pancreatic cells. In a further embodiment, a method of treating a patient diagnosed with diabetes involves transplanting and/or grafting the islet cells and/or tissues comprising islet cells into a patient, and administering a therapeutically effective amount of at least one agonist of GHRH to the patient. In some embodiments, the islet cells and/or tissues comprising islet cells may be optionally exposed to GHRH and/or at least one agonist of GHRH prior to transplantation into a patient. In some embodiments, the at least one agonist of GHRH is administered pre-transplantation, concurrently with transplantation, post-transplantation or any combinations thereof.

GHRH agonists for islet cell transplantation and function and the treatment of diabetes

Agonists of growth hormone releasing hormone promote islet graft growth and proliferation in patients. Methods of treating patients comprise the use of these agonists.

Agonists of growth hormone releasing hormone as effectors for survival and proliferation of pancreatic islets

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 &#x3bc;g/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. The receptor for GHRH was detectable on myocytes supporting direct activation of cardiac signal transduction. Collectively, these findings demonstrate that within the heart GHRH-agonists can activate cardiac repair following MI, suggesting the existence of a potential signaling pathway based on GHRH in the heart. The phenotypic profile of the response to a potent GHRH agonist has therapeutic implications.

Cardioprotective effects of GHRH agonists

The invention is a method of inhibiting a sarcoma, such as Kaposi's sarcoma, in a mammal. The method employs 6-demethyl-6-deoxy-4-de(dimethylamino)tetracycline (CMT-3.)

Method of inhibiting cancer growth

The invention is a method of inhibiting cancer growth, by inhibiting cellular proliferation, invasiveness, or metastasis, or by inducing cytotoxicity against cancer in mammals. The method employs 6-demethyl-6-deoxy-4-de(dimethylamino)tetracycline (CMT-3) and other functionally related chemically modified, preferably non-antibacterial, tetracycline compounds to inhibit cancer growth. The method is particularly effective to inhibit the establishment, growth, and metastasis of solid tumors, such as tumors derived from colon cancer cells, breast cancer cells, melanoma cells, prostatic carcinoma cells, or lung cancer cells.

The invention is a method of inhibiting cancer growth, including cellular proliferation, invasiveness, or metastasis in mammals. The method employs 6-demethyl-6-deoxy-4-dedimethylaminotetracycline (CMT-3) and other functionally related chemically modified, preferably non-antibacterial, tetracycline compounds to inhibit cancer growth. The method is particularly effective to inhibit the establishment, growth, and metastasis of solid tumors, such as tumors derived from colon cancer cells, breast cancer cells, melanoma cells, prostatic carcinoma cells, or lung cancer cells.

An anastomotic method for connecting a biological duct, such as the ureter, to a man-made device. The method involves connecting the duct to the prosthesis via an intermediate tissue so there is no direct connection between the ureter and the prosthesis. The method includes securing the resected duct to a remote living tissue, such as the peritoneum or omentum, and then securing that tissue to the prosthesis so that the duct drains into the prosthesis.

Method and device for connecting biological duct to a prosthesis

Disclosed is a urological device comprising a polymeric prosthesis coated on its surface by a grafted or interpenetrated hydrogel copolymer comprising 2-hydroxyethyl methacrylate, methacrylic acid, and a crosslinking agent, wherein each constituent of said copolymer is present in an amount selected from a defined range of mole fraction %. The hydrogel exhibits a shrink/swell behavior which varies with changing urine composition such that the polymer undergoes swelling and collapse in rapid response to said change and thereby prevents calcium encrustation. Also disclosed is a method for making the device.

Growing community of inventors

Miami, FL, United States of America

Norman L Block