Abstract: A medical device for approximating and securing tissue without requiring knots includes a lock-head, a strap section, distal protuberance, and a leader section. The device also includes a transition section between the leader and the strap section and a stiffening section proximal to the protuberance. The leader section is used to draw the strap section into the body through small apertures in tissue and the transition section provides a gradual transition in stiffness and size between the leader and the strap section.

Abstract: A medical device for approximating and securing tissue without requiring knots includes a lock-head, a strap section, distal protuberance, and a leader section. The device also includes a transition section between the leader and the strap section and a stiffening section proximal to the protuberance. The leader section is used to draw the strap section into the body through small apertures in tissue and the transition section provides a gradual transition in stiffness and size between the leader and the strap section.

Abstract: A medical device for approximating and securing tissue without requiring knots includes a lock-head, a strap section, distal protuberance, and a leader section. The device also includes a transition section between the leader and the strap section and a stiffening section proximal to the protuberance. The leader section is used to draw the strap section into the body through small apertures in tissue and the transition section provides a gradual transition in stiffness and size between the leader and the strap section.

Abstract: Methods to treat or prevent acute kidney injury and chronic kidney injury in subjects using CXCR4 antagonists are disclosed.

Abstract: The disclosure relates to methods of ameliorating nephrotoxic side effects of immunosuppressive agents whose immunosuppressive activity is mediated via upregulation of TGF-? such as, for example, cyclosporine (CsA). The disclosure provides treatment modalities for use in patients that require immunosuppression, e.g., patients at risk of transplant rejection or having an autoimmune disease. In the methods of the invention, a TGF-? antagonist, e.g., an anti-TGF-? antibody, is administered to a patient treated with an immunosuppressive agent. Such a TGF-? antagonist is administered in a therapeutically effective amount sufficient to alleviate the nephrotoxic effects of the immunosuppressive agent without substantially interfering with immunosuppressive activity of the agent.

Abstract: The disclosure relates to methods of ameliorating nephrotoxic side effects of immunosuppressive agents whose immunosuppressive activity is mediated via upregulation of TGF-? such as, for example, cyclosporine (CsA). The disclosure provides treatment modalities for use in patients that require immunosuppression, e.g., patients at risk of transplant rejection or having an autoimmune disease. In the methods of the invention, a TGF-? antagonist, e.g., an anti-TGF-? antibody, is administered to a patient treated with an immunosuppressive agent. Such a TGF-? antagonist is administered in a therapeutically effective amount sufficient to alleviate the nephrotoxic effects of the immunosuppressive agent without substantially interfering with immunosuppressive activity of the agent.

Abstract: The present invention relates to antibody molecules, in particular antibody molecules that bind Transforming Growth Factor beta (TGF?), and uses thereof. More particularly, the invention relates to antibody molecules that bind and preferably neutralise TGF?1, TGF?2 and TGF?3, so-called “pan-specific” antibody molecules, and uses of such antibody molecules. Preferred embodiments within the present invention are antibody molecules, whether whole antibody (e.g. IgG, such as IgG1 or IgG4) or antibody fragments (e.g. scFv, Fab, dAb).

Abstract: The present invention relates to antibody molecules, in particular antibody molecules that bind Transforming Growth Factor beta (TGF?), and uses thereof. More particularly, the invention relates to antibody molecules that bind and preferably neutralise TGF?1, TGF?2 and TGF?3, so-called “pan-specific” antibody molecules, and uses of such antibody molecules. Preferred embodiments within the present invention are antibody molecules, whether whole antibody (e.g. IgG, such as IgG1 or IgG4) or antibody fragments (e.g. scFv, Fab, dAb).

Abstract: The disclosure provides methods for treating, preventing, and reducing risk of occurrence of renal insufficiency in mammals. The disclosed methods include administering to a subject susceptible to, or afflicted with, renal disorder therapeutically effective amounts of a TGF-? antagonist and a renin-angiotensin-aldosterone system (RAAS) antagonist so as to maintain desirable levels of renal function. The populations treated by the methods of the invention include but are not limited to patients suffering or at risk for the development of renal insufficiency, such as those afflicted with type I or type II diabetes, hypertension, (auto)immune disease, systemic fibrosis, etc.

Abstract: The present invention relates to antibody molecules, in particular antibody molecules that bind Transforming Growth Factor beta (TGF?), and uses thereof. More particularly, the invention relates to antibody molecules that bind and preferably neutralise TGF?1, TGF?2 and TGF?3, so-called “pan-specific” antibody molecules, and uses of such antibody molecules. Preferred embodiments within the present invention are antibody molecules, whether whole antibody (e.g. IgG, such as IgG1 or IgG4) or antibody fragments (e.g. scFv, Fab, dAb).