58 results about "Cardiac repair" patented technology

A pharmacological delivery implement for use with cardiac repair devices. The pharmacological delivery implement comprises a porous member defining an outer surface, an internal channel configured to selectively house a pharmacological agent, and a plurality of release holes each extending from the outer surface to the internal channel. Following implantation of the pharmacological delivery implement, at least a portion of the pharmacological agent exits the internal channel through the plurality of release holes.

Structurally supportive material is implanted or injected into cardiac veins as discrete masses at various sites in the cardiac venous system to reinforce the myocardium for the purpose of preventing, moderating, stopping or reversing negative cardiac remodeling due to various adverse cardiac conditions, both acute and chronic, or for the purpose of treating localize anomalies of the heart, or for both purposes. The sites may be arranged in a pattern about one or more chambers of the heart such that the masses cooperatively reduce stress in the chamber wall and reduce chamber size. Some patterns also cause a beneficial global reshaping of the chamber. These changes occur quickly and are sustainable, and have a rapid and sustainable therapeutic effect on cardiac function. Patterns of distribution of discrete masses in the heart for global resizing and reshaping may also be used as is or augmented by supplemental patterns to treat localized conditions such as myocardial infarctions and overt aneurysm of the ventricular wall as typically forms in response to large transmural myocardial infarctions. These techniques may also be used to treat localized conditions that may not yet have progressed to cardiomyopathy.

A method for treating a subject afflicted with a cardiac disorder, in vivo, comprising (i) producing a solution comprising media conditioned from the culture of cells, in vitro, and (ii) administering the solution of step (i) to the subject, thereby treating the cardiac disorder in the subject. Methods for determining whether an agent stimulates or inhibits myocyte proliferation.

A method for treating a subject afflicted with a cardiac disorder, in vivo, comprises (i) inducing differentiation of a progenitor cell, in vitro, to a cardiogenic cell; and (ii) administering a therapeutically effective amount of the cardiogenic cell of step (i) to the subject, thereby treating the cardiac disorder in the subject. This invention further provides related articles of manufacture and methods.

The present invention provides LIFR and FGFR3 as cell surface markers for isolating human cardiomyogenic ventricular progenitor cells, in particular progenitor cells that preferentially differentiate into cardiac ventricular muscle cells. Thus, the invention provides human ventricular progenitor (HVP) cells. The invention provides in vitro methods of the separation of Islet 1+ LIFR+ ventricular progenitor cells and/or Islet 1+/FGFR3+ ventricular progenitor cells and/or Islet 1+/LIFR+/FGFR3+ ventricular progenitor cells, and the large scale expansion and propagation thereof. Large clonal populations of isolated LIFR+ and/or FGFR3+ ventricular progenitor cells are also provided. Methods of in vivo use of LIFR+ and/or FGFR3+ ventricular progenitor cells for cardiac repair or to improve cardiac function are also provided. Methods of using the LIFR+ and/or FGFR3+ ventricular progenitor cells for cardiac toxicity screening of test compounds are also provided.

The present invention provides Jagged 1 and Frizzled 4 as cell surface markers for isolating human cardiomyogenic ventricular progenitor cells, in particular progenitor cells that preferentially differentiate into cardiac ventricular muscle cells. Thus, the invention provides human ventricular progenitor (HVP) cells. The invention provides in vitro methods of the separation of Islet 1+ Jagged 1+ ventricular progenitor cells and/or Islet 1+/Frizzled 4+ ventricular progenitor cells and/or Islet 1+/Jagged 1+/Frizzled 4+ ventricular progenitor cells, and the large scale expansion and propagation thereof. Large clonal populations of isolated Jagged 1+ and/or Frizzled 4+ventricular progenitor cells are also provided. Methods of in vivo use of Jagged 1+ and/or Frizzled 4+ ventricular progenitor cells for cardiac repair or to improve cardiac function are also provided. Methods of using the Jagged 1+ and/or Frizzled 4+ ventricular progenitor cells for cardiac toxicity screening of test compounds are also provided.

The present invention is directed to proteins in which a heparin binding peptide is fused to a growth factor that promotes cell growth and survival. The compound thus formed is bound to the surface of cells which are then administered to damaged tissue. The growth factor is thereby maintained at the site of administration where it promotes repair.

The invention relates to a biologic patch material and concretely relates to a biologic patch material for cardiac repair. The biologic patch material comprises (i) at least two porous structural layers that are compounded together, wherein the porous structural layer comprises a first structural layer for preventing repairing cell loss and a second structural layer for loading (or accommodating) cardiac repairing cells and the repairing cells are selected from cardiac stem cells, cardiac progenitor (precursor) cells or their composition (derived from embryonic stem cells, induced pluripotent stem cells, heart tissue stem cells, bone marrow and peripheral blood), and (ii) repairing cells loaded on the second structural layer, wherein at least a part of or all the repairing cells are located in gaps of the second structural layer. The biologic patch material can load growing of repairing cells and has very good biocompatibility and mechanical strength.

The present invention provides methods for isolating human cardiac ventricular progenitor cells (HVPs), wherein cultures of day 5-7 cardiac progenitor cells are negatively selected for one or more first markers expressed on human pluripotent stem cells, such as TRA-1-60, to thereby isolate HVPs. The methods can further include positive selection for expression of a second marker selected from the group consisting of JAG1, FZD4, LIFR, FGFR3 and TNFSF9. Large populations, including clonal populations, of isolated HVPs that are first marker negative/second marker positive are also provided. Methods of in vivo use of the HVPs for cardiac repair or to improve cardiac function are also provided. Methods of using the HVPs for cardiac toxicity screening of test compounds are also provided.

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. 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.

The invention discloses an acellular dermis matrix enhanced thermally-induced phase separation nanofiber small-bore tubular stent and a preparation method thereof. The preparation method comprises the following steps: performing decellularization treatment on aorta of healthy animals; placing the matrix obtained by decellularization on a watch glass, dropwise adding ultrapure water to submerge all the matrix, and placing in a refrigerator for freezing; spinning nanofibers onto stainless steel shaft core of a mold, putting whole nanofiber and the shaft core into a vacuum drying oven for drying; sheathing the outer layer of the nanofiber with the tubular matrix as a mechanical reinforcing layer; and assembling the compounded double-layer stent together with the shaft core into the mold, and performing solution casting and treatment to obtain the tubular stent. The prepared tubular stent has good mechanical performance, bursting strength and biocompatibility, has no hypersensitivity on a human body in transplanting operation, and has affinity with the blood and peripheral tissues in a human body, thus having good application prospects in cardiovascular and cardiac repair surgeries.

A method for treating a subject afflicted with a cardiac disorder, in vivo, comprising (i) producing a solution comprising media conditioned from the culture of cells, in vitro, and (ii) administering the solution of step (i) to the subject, thereby treating the cardiac disorder in the subject. Methods for determining whether an agent stimulates or inhibits myocyte proliferation.

The invention belongs to the animal cell culture techniques and relates to a method for sorting cardiac fibroblast CD90<+> subsets of mice and application of the cardiac fibroblast CD90<+> subsets. The method comprises the following steps: carrying out recovery and enlarged culture on mice cardiac fibroblast cell strains; sorting cardiac fibroblast CD90<+> subsets by virtue of a PE-marked CD90 antibody; collecting the sorted cardiac fibroblast CD90<+> subsets, carrying out centrifugation to remove supernatant so as to obtain precipitates, inoculating the precipitates into a culture bottle, carrying out enlarged culture, so as to finish the sorting of the cardiac fibroblast CD90<+> subsets of the mice. The sorted cardiac fibroblast CD90<+> subsets are taken as preponderant subsets for sorting cardiac fibroblasts and are used for triggering the myocardium repair potential of the cardiac fibroblasts, so that the experimental basis and theoretical support are provided for the efficient utilization of the cardiac fibroblasts.

The present invention features compositions comprising a modified RNA encoding a Yes-associated protein (YAP) polypeptide and methods of using such compositions for cardiac repair. In particular embodiments, a modified RNA encoding a YAP polypeptide is administered in combination with an agent that reduces YAP degradation, such as a small molecule E64d.

The present invention relates to the discovery of the role of Wnt1 in multiple cardiovascular processes, including cardiac repair, angiogenesis, and stimulation of endothelial progenitor cells. This discovery provides methods of using Wnt1 to treat cardiovascular disorders and injuries.

The invention discloses an application of a TNFR2 activating agent to preparing a drug for promoting activation, migration and survival of cardiac stem cells. The TNFR2 activating agent has the effect of promoting activation of the cardiac stem cells and cardiac repair. The activated TNFR2-Bmx can enhance expression and the activity of Nkx2.5+/Gata4+, and mediate activation, migration and survival of c-Kit+ endogenous cardiac stem cells (eCSCs). In addition, the activation of the TNFR2 increases the differentiation of cardiac cells of a hESC/hiPSC source. The TNFR2 activating agent activates the TNFR2 through the specificity so that the TNFR2 is beneficial to repairing of myocardial infarction, and a new strategy can be provided for human heart disease treatment.