Patents by Inventor Eduardo Marbán
Eduardo Marbán has filed for patents to protect the following inventions. This listing includes patent applications that are pending as well as patents that have already been granted by the United States Patent and Trademark Office (USPTO).
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Publication number: 20110245772Abstract: Disclosed is an invention for focally modulating the activity of a calcium channel in a mammal. In one aspect, the invention features a method that includes contacting a pre-determined tissue or organ region with a nucleic acid sequence encoding a GEM protein or a variant thereof to express the GEM protein or variant within the region. Typical methods further include expressing the GEM protein or variant so as to modulate the activity of the calcium channel. The invention has a wide spectrum of useful applications including treating a medical condition associated with unsuitable calcium channel activity.Type: ApplicationFiled: December 27, 2010Publication date: October 6, 2011Applicant: THE JOHN HOPKINS UNIVERSITYInventors: Eduardo MARBAN, Mitsushige MURATA
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Patent number: 8003618Abstract: Disclosed is an invention for focally modulating the activity of a calcium channel in a mammal. In one aspect, the invention features a method that includes contacting a pre-determined tissue or organ region with a nucleic acid sequence encoding a GEM protein or a variant thereof to express the GEM protein or variant within the region. Typical methods further include expressing the GEM protein or variant so as to modulate the activity of the calcium channel. The invention has a wide spectrum of useful applications including treating a medical condition associated with unsuitable calcium channel activity.Type: GrantFiled: October 2, 2003Date of Patent: August 23, 2011Assignee: The John Hopkins UniversityInventors: Eduardo Marban, Mitsushige Murata
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Publication number: 20110110488Abstract: A computed tomography system has a support stage constructed and arranged to support a subject while under observation, an x-ray illumination system arranged proximate the support stage to illuminate the subject with x-rays, an x-ray detection system arranged proximate the support stage to detect x-rays after they pass through the subject and to provide signals based on the detected x-rays, and a data processing system in communication with the x-ray detection system to receive the signals from the x-ray detection system. The computed tomography system has a dynamic mode of operation and a scanning mode of operation. The data processing system extracts information concerning a dynamic process of the subject based on signals from both the dynamic mode and the scanning mode of operation.Type: ApplicationFiled: September 29, 2008Publication date: May 12, 2011Applicant: THE JOHNS HOPKINS UNIVERSITYInventors: Albert Clark Lardo, Richard T. George, Joao A.C. Lima, Eduardo Marban
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Publication number: 20100124740Abstract: The present invention relates to somatic cell gene transfer methods for mimicking one or more effects of a drug candidate compound. In one aspect, the methods mimic the effect of a drug candidate compound with potential to potentiate or suppress activity of a selected target molecule. In another aspect, the methods provide means of identifying a molecular target for the drug candidate compound. The present methods have a variety of uses including providing identified molecular targets for use in drug screens.Type: ApplicationFiled: May 13, 2009Publication date: May 20, 2010Applicant: The Johns Hopkins UniversityInventor: Eduardo Marban
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Publication number: 20100111909Abstract: Dedifferentiation is a mechanism whereby specialized cells regain properties of their ancestors, including, in the extreme, stemness. We found that highly-purified cardiomyocytes isolated from adult mammalian hearts dedifferentiated rapidly when cultured in mitogen-rich medium. Such myocytes reentered the cell cycle and proliferated, expressing stem cell surface markers such as c-kit and early cardiac transcription factors including GATA and NKx2.5. These myocyte-derived cells (MDC) were capable of re-differentiating into myocytes and endothelial cells. Contrary to prevailing dogma, cardiomyocyte dedifferentiation yields proliferative cells expressing stem cell markers and capable of multilineage differentiation. Cardiomyocyte dedifferentiation is a potential source of endogenous stem cells in the adult heart.Type: ApplicationFiled: January 11, 2010Publication date: May 6, 2010Applicant: THE JOHNS HOPKINS UNIVERSITYInventor: EDUARDO MARBAN
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Publication number: 20100112694Abstract: Dedifferentiation is a mechanism whereby specialized cells regain properties of their ancestors, including, in the extreme, stemness. We found that highly-purified cardiomyocytes isolated from adult mammalian hearts dedifferentiated rapidly when cultured in mitogen-rich medium. Such myocytes reentered the cell cycle and proliferated, expressing stem cell surface markers such as c-kit and early cardiac transcription factors including GATA and NKx2.5. These myocyte-derived cells (MDC) were capable of re-differentiating into myocytes and endothelial cells. Contrary to prevailing dogma, cardiomyocyte dedifferentiation yields proliferative cells expressing stem cell markers and capable of multilineage differentiation. Cardiomyocyte dedifferentiation is a potential source of endogenous stem cells in the adult heart.Type: ApplicationFiled: January 11, 2010Publication date: May 6, 2010Applicant: THE JOHNS HOPKINS UNIVERSITYInventor: EDUARDO MARBAN
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Publication number: 20100093089Abstract: Dedifferentiation is a mechanism whereby specialized cells regain properties of their ancestors, including, in the extreme, stemness. We found that highly-purified cardiomyocytes isolated from adult mammalian hearts dedifferentiated rapidly when cultured in mitogen-rich medium. Such myocytes reentered the cell cycle and proliferated, expressing stem cell surface markers such as c-kit and early cardiac transcription factors including GATA and NKx2.5. These myocyte-derived cells (MDC) were capable of re-differentiating into myocytes and endothelial cells. Contrary to prevailing dogma, cardiomyocyte dedifferentiation yields proliferative cells expressing stem cell markers and capable of multilineage differentiation. Cardiomyocyte dedifferentiation is a potential source of endogenous stem cells in the adult heart.Type: ApplicationFiled: November 9, 2007Publication date: April 15, 2010Inventor: Eduardo Marban
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Publication number: 20100068811Abstract: Human cardiac stem cells can be isolated from endomyocardial biopsies. Such cells mediate cardiac regeneration and improve heart function in a mouse infarct model. The cells can be used for autologous, allogeneic, syngeneic, or xenogeneic therapeutic applications in patients. The stem cells can be genetically modified to enhance their therapeutic activity.Type: ApplicationFiled: November 19, 2009Publication date: March 18, 2010Applicant: The Johns Hopkins UniversityInventors: Eduardo Marban, Maria Roselle Abraham, Rachel R. Smith
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Publication number: 20100061966Abstract: Human cardiac stem cells can be isolated from endomyocardial biopsies. Such cells mediate cardiac regeneration and improve heart function in a mouse infarct model. The cells can be used for autologous, allogeneic, syngeneic, or xenogeneic therapeutic applications in patients. The stem cells can be genetically modified to enhance their therapeutic activity.Type: ApplicationFiled: November 19, 2009Publication date: March 11, 2010Applicant: The Johns Hopkins UniversityInventors: Eduardo Marban, Maria Roselle Abraham, Rachel R. Smith
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Publication number: 20090304588Abstract: As an alternative strategy to electronic pacemaker devices, we explored the feasibility of converting normally-quiescent ventricular myocytes into pacemakers by somatic cell fusion. The idea is to create chemically-induced fusion between myocytes and syngeneic fibroblasts engineered to express HCN1 pacemaker ion channels (HCN1 fibroblasts), in normally-quiescent myocardium. HCN1-expressing fibroblasts formed stable heterokaryons with myocytes, generating spontaneously-oscillating action potentials as well as ventricular pacemaker activity in vivo and provides a platform for an autologous, non-viral, adult somatic cell therapy. We also converted a depolarization-activated potassium-selective channel, Kv1.4, into a hyperpolarization-activated non-selective channel by site-directed mutagenesis (R447N, L448A, and R453I in S4 and G528S in the pore).Type: ApplicationFiled: October 16, 2006Publication date: December 10, 2009Applicant: THE JOHNS HOPKINS UNIVERSITYInventor: Eduardo Marban
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Publication number: 20090291068Abstract: The present invention relates to novel compositions and methods to induce, and/or modulate bio-electrical rhythms (e.g. in cardiac, neuronal and pancreatic cells) by fine-tuning the activity of HCN-encoded pacemaker channels via a novel protein- and genetic-engineering approach to augment or attenuate the associated physiological responses (e.g. heart beat, neuronal firing, insulin secretion, etc) for achieving various therapeutic purposes (e.g. sick sinus syndrome, epilepsy, neuropathic pain, diabetes, etc).Type: ApplicationFiled: February 2, 2007Publication date: November 26, 2009Applicant: The Johns Hopkins UniversityInventors: Eduardo Marban, Ronald A. Li, Suk-Ying Tsang, Hee Cheol Cho, Tian Xue
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Publication number: 20090233990Abstract: Compositions and methods for enhancing hyperpolarization-activated cation inward current and disrupting inwardly rectifying potassium current of cells are described. The compositions and methods may be employed to cause the cells to become biological pacemaker cells, e.g. to become more like SA node cells, and to undergo spontaneous oscillating action potentials.Type: ApplicationFiled: October 31, 2008Publication date: September 17, 2009Inventors: Hee Cheol Cho, Eduardo Marban, Daniel Sigg
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Publication number: 20090233991Abstract: Compositions and methods for enhancing hyperpolarization-activated cation inward current and disrupting inwardly rectifying potassium current of cells are described. The compositions and methods may be employed to cause the cells to become biological pacemaker cells, e.g. to become more like SA node cells, and to undergo spontaneous oscillating action potentials.Type: ApplicationFiled: October 31, 2008Publication date: September 17, 2009Inventors: Hee Cheol Cho, Eduardo Marban, Daniel Sigg
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Publication number: 20090175790Abstract: Disclosed are methods of preventing or treating cardiac arrhythmia. In one embodiment, the methods include administering to an amount of at least one polynucleotide that modulates an electrical property of the heart. The methods have a wide variety of important uses including treating cardiac arrhythmia. Also disclosed are methods and systems for modulating electrical behavior of cardiac cells. Preferred methods include administering a polynucleotide or cell-based composition that can modulate cardiac contraction to desired levels, e.g., the administered composition functions as a biological pacemaker.Type: ApplicationFiled: February 21, 2008Publication date: July 9, 2009Applicant: THE JOHNS HOPKINS UNIVERSITYInventor: Eduardo Marban
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Publication number: 20090012422Abstract: A bioptome (1) includes a flexible catheter (2) which can be remotely steered. Two handles (6,7) coupled to a proximal end of the catheter are used to actuate a pair of jaws (4,5) coupled to a distal end of the catheter. A separate control handle (8) includes a rotatable knob (16). Rotation of the knob in one direction causes a distal end of the catheter to bend in a first direction. Rotation of the knob in an opposite direction causes the catheter to bend in a second direction. The control knob may be coupled to the distal catheter end by steering wires (42,43) that move within lumens (44,45) of the catheter in response to knob rotation. The jaws or other operating members) at the distal catheter end may be replaceable (80A, 80B).Type: ApplicationFiled: November 8, 2005Publication date: January 8, 2009Inventor: Eduardo Marban
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Publication number: 20080318893Abstract: Knock-down of L-type calcium channel beta subunit (LTCC?) attenuates the hypertrophic response both in vitro and in vivo without compromising systolic performance. Knock-down can be accomplished by administration of a vector encoding a short hairpin RNA which specifically modulates expression of LTCC?. Suppression of the LTCC? expression represents a therapeutic modality for cardiac hypertrophy.Type: ApplicationFiled: October 26, 2006Publication date: December 25, 2008Applicant: THE JOHNS HOPKINS UNIVERSITYInventor: Eduardo Marban
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Publication number: 20080267921Abstract: Human cardiac stem cells can be isolated from endomyocardial biopsies. Such cells mediate cardiac regeneration and improve heart function in a mouse infarct model. The cells can be used for autologous, allogeneic, syngeneic, or xenogeneic therapeutic applications in patients. The stem cells can be genetically modified to enhance their therapeutic activity.Type: ApplicationFiled: November 8, 2005Publication date: October 30, 2008Applicant: Johns Hopkins UniversityInventors: Eduardo Marban, Maria Roselle Abraham, Rachel R. Smith
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Publication number: 20080260705Abstract: Skeletal myoblasts are an attractive cell type for transplantation since they are autologous and resistant to ischemia. However, clinical trials of myoblasts transplantation in heart failure have been plagued by ventricular tachy-arrhythmias and sudden cardiac death. The pathogenesis of these arrhythmias is poorly understood, but may be related to the fact that skeletal muscle cells, unlike heart cells, are electrically isolated by the absence of gap junctions. An in vitro model of myoblasts transplantation into cardiomyocyte monolayers can be used to investigate the mechanisms of transplant-associated arrhythmias. Co-cultures of human skeletal myoblasts and rat cardiomyocytes result in reentrant arrhythmias (spiral waves) that reproduce the features of ventricular tachycardia seen in patients receiving myoblasts transplants. These arrhythmias can be terminated by nitrendipine, an L-type calcium channel Mocker, but not by the Na channel blocker lidocaine.Type: ApplicationFiled: March 22, 2005Publication date: October 23, 2008Applicant: The Johns Hopkins UniversityInventors: Eduardo Marban, Maria Roselle Abraham
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Publication number: 20080181871Abstract: Disclosed is an invention for focally modulating the activity of a calcium channel in a mammal. In one aspect, the invention features a method that includes contacting a pre-determined tissue or organ region with a nucleic acid sequence encoding a GEM protein or a variant thereof to express the GEM protein or variant within the region. Typical methods further include expressing the GEM protein or variant so as to modulate the activity of the calcium channel. The invention has a wide spectrum of useful applications including treating a medical condition associated with unsuitable calcium channel activity.Type: ApplicationFiled: October 3, 2007Publication date: July 31, 2008Applicant: The Johns Hopkins UniversityInventors: Eduardo Marban, Mitsushige Murata
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Publication number: 20070259343Abstract: The present invention relates to somatic cell gene transfer methods for mimicking one or more effects of a drug candidate compound. In one aspect, the methods mimic the effect of a drug candidate compound with potential to potentiate or suppress activity of a selected target molecule. In another aspect, the methods provide means of identifying a molecular target for the drug candidate compound. The present methods have a variety of uses including providing identified molecular targets for use in drug screens.Type: ApplicationFiled: April 3, 2006Publication date: November 8, 2007Applicant: The Johns Hopkins UniversityInventor: Eduardo Marban