Abstract: An autonomously controllable pull wire injection 5 catheter 1 and a method for operating the same are provided. The catheter 1 includes an outer catheter guide 2, 33 having an outer catheter guide casing 39 and an inner operating catheter 3, 31 having an inner operating catheter casing 16, wherein the inner operating catheter 3, 31 includes a catheter handle 30, a catheter tip 10, at least one needle 5 that is connected to at least one source of medicinal solution via at least one needle 10 channel 4, 26, at least one contact force sensor 9a-f, 25, at least one electrode 7, 24, at least four actuator driven pull wires 12-15, 20-23 for moving the tip 10 of the inner operating catheter 3, 31.

Abstract: An autonomously controllable pull wire injection 5 catheter 1 and a method for operating the same are provided. The catheter 1 includes an outer catheter guide 2, 33 having an outer catheter guide casing 39 and an inner operating catheter 3, 31 having an inner operating catheter casing 16, wherein the inner operating catheter 3, 31 includes a catheter handle 30, a catheter tip 10, at least one needle 5 that is connected to at least one source of medicinal solution via at least one needle 10 channel 4, 26, at least one contact force sensor 9a-f, 25, at least one electrode 7, 24, at least four actuator driven pull wires 12-15, 20-23 for moving the tip 10 of the inner operating catheter 3, 31.

Abstract: Embodiments of the present invention include methods and systems for designing inhibitors of amyloidosis in humans, domesticated animals, and wild animals as well as inhibitors of amyloidosis designed by the methods and systems. Methods and systems for designing inhibitors of amyloidosis are largely computational, in nature, and are directed to designing various types of polymers, small-molecule organic compounds, organometallic compounds, or non-chemical physical processes that can target the extended-?-strand and ?-sheet regions of amyloidogenic protein and polypeptide intermediates in order to prevent aggregation of those intermediates into protofibrils and fibrils that, in turn, recruit additional native-conformation proteins and polypeptides into amyloidogenic intermediates and that additionally aggregate to form higher-order structures, such as plaques observed in the brains of patients suffering from the various spongiform encephalopathies.

Abstract: Embodiments of the present invention include methods and systems for designing inhibitors of amyloidosis in humans, domesticated animals, and wild animals as well as inhibitors of amyloidosis designed by the methods and systems. Methods and systems for designing inhibitors of amyloidosis are largely computational, in nature, and are directed to designing various types of polymers, small-molecule organic compounds, organometallic compounds, or non-chemical physical processes that can target the extended-?-strand and ?-sheet regions of amyloidogenic protein and polypeptide intermediates in order to prevent aggregation of those intermediates into protofibrils and fibrils that, in turn, recruit additional native-conformation proteins and polypeptides into amyloidogenic intermediates and that additionally aggregate to form higher-order structures, such as plaques observed in the brains of patients suffering from the various spongiform encephalopathies.

Abstract: Embodiments of the present invention include methods and systems for designing inhibitors of amyloidosis in humans, domesticated animals, and wild animals as well as inhibitors of amyloidosis designed by the methods and systems. Methods and systems for designing inhibitors of amyloidosis are largely computational, in nature, and are directed to designing various types of polymers, small-molecule organic compounds, organometallic compounds, or non-chemical physical processes that can target the extended-?-strand and ?-sheet regions of amyloidogenic protein and polypeptide intermediates in order to prevent aggregation of those intermediates into protofibrils and fibrils that, in turn, recruit additional native-conformation proteins and polypeptides into amyloidogenic intermediates and that additionally aggregate to form higher-order structures, such as plaques observed in the brains of patients suffering from the various spongiform encephalopathies.

Abstract: Bioengineering the regenerative heart or other body organ in need of greater muscle mass or improved blood perfusion provides a novel treatment for organ weakness or failure. In the case of cardiac failure treatment, on May 14, 2002, a 55-year-old man suffering ischemic myocardial infarction received 25 injections carrying 465 million cGMP-produced pure myoblasts into his myocardium after coronary artery bypass grafting. Three myogenesis mechanisms were elucidated with 17 human/porcine xenografts using cyclosporine as immunosuppressant. Some myoblasts developed to become cardiomyocytes. Others transferred their nuclei into host cardiomyocytes through natural cell fusion. As yet others formed skeletal myofibers with satellite cells. De novo production of contractile filaments augmented heart contractility. Human myoblasts transduced with VEGF165 gene produced six times more capillaries in porcine myocardium than placebo.

Abstract: Bioengineering the regenerative heart provides a novel treatment for heart failure. On May 14, 2002, a 55-year-old man suffering ischemic myocardial infarction received 25 injections carrying 465 million cGMP-produced pure myoblasts into his myocardium after coronary artery bypass grafting. Three myogenesis mechanisms were elucidated with 17 human/porcine xenografts using cyclosporine as immunosuppressant. Some myoblasts developed to become cardiomyocytes. Others transferred their nuclei into host cardiomyocytes through natural cell fusion. As yet others formed skeletal myofibers with satellite cells. De novo production of contractile filaments augmented heart contractility. Human myoblasts transduced with VEGF165 gene produced six times more capillaries in porcine myocardium than placebo. Xenograft rejection was not observed for up to 20 weeks despite cyclosporine discontinuation at 6 weeks.

Abstract: Muscle cell materials and methods are provided for refurbishing skin. Skin surfaces are prepared by removing dead cells and myoblasts are added in a cell-nutritive solution. An embodiment provides autologous human myoblast cells from the individual to be treated, serum from the individual, and an angiogenesis factor for stimulation of vascularization. Large 6 chondroitin sulfate may be used for controlled rapid cell fusion of the myoblasts. Foreskin fibroblast cell suspensions also may be used singly or in combination with myoblasts. In yet another embodiment non-immunogenic cells from another animal such as a pig with a double knockout mutation that affects foreign recognition may be added to cell surfaces.

Abstract: Myoblast cells obtained by culturing, particularly from satellite cells or other progenitor cells, are transplanted into tissue such as diseased heart tissue to form healthy repair tissue and reverse disease. This technique can be carried out in various ways and preferably includes a cellular integration factor to assist cellular survival, integration and longevity into the treated organ. Angiogenesis factors such as vascular endothelial growth factor are particularly preferred and may be transgenically expressed by the transplanted cell. Other factors that may be used to augment the procedure include migratory and scaffolding molecules. The methods and materials are particularly useful in combination with an automated cell processor and an automated catheter delivery system. The materials and methods for their use may be applied to the prophylaxis and therapy of damaged hearts, using cells originally obtained from the patient, another human, or another animal.

Abstract: Catheters and methods for their use are presented that provide automated delivery of cells to structures in the body such as degenerative or weak muscle. The catheters contain one or more sensing components and a system for delivery of cells such as autologous myogenic cells. The sensing component(s) triggers automatic discharge of the cells upon detection of a body surface that needs repair. The discharge of cells may occur through an automated lancing mechanism that alleviates operator error from manual injection timing. During use, an operator can position the catheter end to a structure in need of cellular repair, and the device can automatically discharge cells at a location and time as determined by conditions sensed at the catheter end. A catheter and system is particularly useful for repair of degenerative and or weak heart muscle, such as that found after a myocardial infarct.