Professor of Medicine, University Wash
Cardiology
Dr. David A. Dichek, MD
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David Dichek is an expert in the field of Cardiology. He went to medical school at David Geffen School of Medicine at UCLA. David Geffen School of Medicine at UCLA is one of the top medical schools in the US. David Geffen School of Medicine at UCLA is ranked 13 in research and 7 in primary care medicine He has 1 awards "America's Top Doctors". David Dichek has written publications. He has 90 publications published with PubMed. The lastest paper is: 'Lipoprotein clearance mechanisms in LDL receptor-deficient "Apo-B48-only" and "Apo-B100-only" mice.' He is registered with Medicare and accepts Medicare payments.
Publications
- Postnatal Deletion of the Type II Transforming Growth Factor-β Receptor in Smooth Muscle Cells Causes Severe Aortopathy in Mice.
- Reduction of mouse atherosclerosis by urokinase inhibition or with a limited-spectrum matrix metalloproteinase inhibitor.
- Efficient Gene Transfer and Durable Transgene Expression in Grafted Rabbit Veins.
- Improved Animal Models for Testing Gene Therapy for Atherosclerosis.
- Overexpression of eNOS Improves Endothelium-Dependent Vasodilation in Arteries Infused with Helper-Dependent Adenovirus.
- Transforming growth factor-? signaling in myogenic cells regulates vascular morphogenesis, differentiation, and matrix synthesis.
- Expression of Apolipoprotein A-I in Rabbit Carotid Endothelium Protects Against Atherosclerosis.
- Mechanisms of urokinase plasminogen activator (uPA)-mediated atherosclerosis: role of the uPA receptor and S100A8/A9 proteins.
- Helper-Dependent Adenoviral Vector Achieves Prolonged, Stable Expression of Interleukin-10 in Rabbit Carotid Arteries but Does Not Limit Early Atherogenesis.
- Helper-Dependent Adenovirus Is Superior to First-Generation Adenovirus for Expressing Transgenes in Atherosclerosis-Prone Arteries.
- Helper-dependent adenoviral vectors are superior in vitro to first-generation vectors for endothelial cell-targeted gene therapy.
- Overexpression of urokinase by plaque macrophages causes histological features of plaque rupture and increases vascular matrix metalloproteinase activity in aged apoli...
- Level of macrophage uPA expression is an important determinant of atherosclerotic lesion growth in Apoe-/- mice.
- TGF-[beta]1 limits plaque growth, stabilizes plaque structure, and prevents Aortic dilation in apolipoprotein E-null mice.
- Plasminogen mediates the atherogenic effects of macrophage-expressed urokinase and accelerates atherosclerosis in apoE-knockout mice.
- Targeted rearrangement of floxed alleles in smooth muscle cells in vivo.
- Mechanisms of TGF-beta1-induced intimal growth: plasminogen-independent activities of plasminogen activator inhibitor-1 and heterogeneous origin of intimal cells.
- Mechanisms of cardiac fibrosis induced by urokinase plasminogen activator.
- Transforming growth factor beta 1 induces neointima formation through plasminogen activator inhibitor-1-dependent pathways.
- Regulated transgene expression in vascular smooth muscle.
- Overexpression of urokinase by macrophages or deficiency of plasminogen activator inhibitor type 1 causes cardiac fibrosis in mice.
- Improved vascular gene transfer with a helper-dependent adenoviral vector.
- Macrophage-targeted overexpression of urokinase causes accelerated atherosclerosis, Coronary artery occlusions, and premature death.
- Increased expression of urokinase during atherosclerotic lesion development causes arterial constriction and lumen loss, and accelerates lesion growth.
- Identification of intracellular pathways through which TGF-beta1 upregulates PAI-1 expression in endothelial cells.
- Smooth muscle cells give rise to osteochondrogenic precursors and chondrocytes in calcifying arteries.
- In vivo expression of a conditional TGF-beta1 transgene: no evidence for TGF-beta1 transgene expression in SM22alpha-tTA transgenic mice.
- A critical developmental role for tgfbr2 in myogenic cell lineages is revealed in mice expressing SM22-Cre, not SMMHC-Cre.
- Constriction of Carotid arteries by urokinase-type plasminogen activator requires catalytic activity and is independent of NH(2)-terminal domains.
- Construction of a novel expression cassette for increasing transgene expression in vivo in endothelial cells of large blood vessels.
- Control of clot lysis by gene transfer.
- Angiosarcoma of the Heart: three-year survival and follow-up by nuclear magnetic resonance imaging.
- A genetic therapy for familial hypercholesterolemia.
- Seeding of intravascular stents with genetically engineered endothelial cells.
- Overexpression of transforming growth factor beta1 in arterial endothelium causes hyperplasia, apoptosis, and cartilaginous metaplasia.
- Adenoviral gene transfer in arteries of hypercholesterolemic nonhuman primates.
- Adhesion of monocytes to vascular cell adhesion molecule-1-transduced human endothelial cells: implications for atherogenesis.
- Cationic liposomes enhance adenovirus entry via a pathway independent of the fiber receptor and alpha(v)-integrins.
- Gene therapy for restenosis: are we ready?
- Gene therapy for arterial thrombosis.
- Regional variability in the time course of TGF-beta 1 expression, cellular proliferation and extracellular matrix expansion following arterial injury.
- Fas ligand expression in islets of Langerhans does not confer immune privilege and instead targets them for rapid destruction.
- Intravascular stent endothelialization. A goal worth pursuing?
- Established immunity precludes adenovirus-mediated gene transfer in rat Carotid arteries. Potential for immunosuppression and vector engineering to overcome barriers o...
- Adhesion of memory lymphocytes to vascular cell adhesion molecule-1-transduced human vascular endothelial cells under simulated physiological flow conditions in vitro.
- Identification of a cis-acting sequence in the human plasminogen activator inhibitor type-1 gene that mediates transforming growth factor-beta1 responsiveness in endot...
- Adenovirus-mediated gene transfer into normal rabbit arteries results in prolonged vascular cell activation, inflammation, and neointimal hyperplasia.
- Seeding of vascular grafts with genetically modified endothelial cells. Secretion of recombinant TPA results in decreased seeded cell retention in vitro and in vivo.
- Unesterified long chain fatty acids inhibit the binding of single chain urokinase to the urokinase receptor.
- Local adenoviral-mediated expression of recombinant hirudin reduces neointima formation after arterial injury.
- Enhanced in vivo antithrombotic effects of endothelial cells expressing recombinant plasminogen activators transduced with retroviral vectors.
- Transduced endothelial cells expressing high levels of tissue plasminogen activator have an unaltered phenotype in vitro.
- In vivo adenoviral vector-mediated gene transfer into balloon-injured rat Carotid arteries.
- Characterization of plasminogen activation by glycosylphosphatidylinositol-anchored urokinase.
- Anatomic barriers influence the distribution of in vivo gene transfer into the arterial wall. Modeling with microscopic tracer particles and verification with a recomb...
- Gene transfer in the treatment of thrombosis.
- Characterization of recombinant plasminogen activator production by primate endothelial cells transduced with retroviral vectors.
- Optimization of recombinant t-PA secretion from seeded vascular grafts.
- Adenoviral vector-mediated gene transfer into sheep arteries using a double-balloon catheter.
- In vivo gene transfer into injured carotid arteries. Optimization and evaluation of Acute toxicity.
- In vivo adenovirus-mediated gene transfer via the pulmonary Artery of rats.
- Endothelium-specific in vivo gene transfer.
- Enhancement of the fibrinolytic activity of sheep endothelial cells by retroviral vector-mediated gene transfer.
- Quantification of vascular graft seeding by use of computer-assisted image analysis and genetically modified endothelial cells.
- Retroviral vector-mediated gene transfer into endothelial cells.
- Genetically engineered endothelial cells remain adherent and viable after stent deployment and exposure to flow in vitro.
- Retroviral vector-mediated in vivo expression of low-density-lipoprotein receptors in the Watanabe heritable hyperlipidemic rabbit.
- Low level in vivo gene transfer into the arterial wall through a perforated balloon catheter.
- Expression of an anchored urokinase in the apical endothelial cell membrane. Preservation of enzymatic activity and enhancement of cell surface plasminogen activation.
- Molecular cloning and nucleotide sequence of cDNA encoding a functional murine low-density-lipoprotein receptor.
- Optimization of retroviral vector-mediated gene transfer into endothelial cells in vitro.
- inclusion of the E3 region in an adenoviral vector decreases inflammation and neointima formation after arterial gene transfer.
- Plasminogen activator inhibitor type 1 increases neointima formation in balloon-injured rat Carotid arteries.
- Germline incorporation of a replication-Defective adenoviral vector in mice does not alter immune responses to adenoviral vectors.
- Receptor-mediated regulation of plasminogen activator function: plasminogen activation by two directly membrane-anchored forms of urokinase.
- Second-generation adenoviral vectors do not prevent rapid loss of transgene expression and vector DNA from the arterial wall.
- A non-cleavable mutant of Fas ligand does not prevent neutrophilic destruction of islet transplants.
- Cardiovascular overexpression of transforming growth factor-beta(1) causes abnormal yolk sac vasculogenesis and early embryonic death.
- Expression of Fas ligand in arteries of hypercholesterolemic rabbits accelerates atherosclerotic lesion formation.
- A mouse model of arterial gene transfer: antigen-specific immunity is a minor determinant of the early loss of adenovirus-mediated transgene expression.
- Retroviral vector-mediated expression of hirudin by human vascular endothelial cells: implications for the design of retroviral vectors expressing biologically active ...
- Optimizing vascular gene transfer of plasminogen activator inhibitor 1.
- Seeding of intraCoronary stents with endothelial cells: current status and future prospects.
- Adventitial delivery minimizes the proinflammatory effects of adenoviral vectors.
- Lipoprotein clearance mechanisms in LDL receptor-deficient "Apo-B48-only" and "Apo-B100-only" mice.
- IgG1 is the predominant subclass of in vivo- and in vitro- produced anti-tetanus toxoid antibodies and also serves as the membrane IgG molecule for delivering inhibito...
- Thrombin regulation of mRNA levels of tissue plasminogen activator and plasminogen activator inhibitor-1 in cultured human umbilical vein endothelial cells.
- Drug delivery by genetically engineered cell implants.
- Variability in messenger RNA levels in human umbilical vein endothelial cells of different lineage and time in culture.
Schools
University of California At Los Angeles
Massachusetts General Hospital
Johns Hopkins Hospital
Mass Genl Hospital
Procedures Preformed
- Cardiac Imaging
- Cardiac MRI (Magnetic Resonance Imaging) of Heart or Chest
- Cardiac Myocardial Perfusion Imaging
- Cardioversion, Elective
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Conditions Treated
- Angina and Acute Coronary Syndrome
- Aortic Aneurysm
- Aortic Valve Disease
- Arrhythmias (incl. Atrial Fibrillation)
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Doctors Specialties
- Cardiology
Accepted Insurances
Awards
- America's Top Doctors
Education
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Massachusetts General Hospital -
David Geffen School of Medicine at UCLA
Hospital
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University of Washington Medical Center
Drug Facts
| NPI NUMBER | 1922198878 | |
| NPPES Provider LastName | DICHEK | |
| NPPES Provider FirstName | DAVID | |
| NPPES Provider ZIPCode | 981956043 | |
| NPPES Provider State | WA | |
| Specialty Description | Cardiology | |
| Total Claim Count | 161.0 | |
| Distinct Opioid Count | 0.0 | |
| Opioid Claim Count | 0.0 | |
| Percent Opioid Claims | 0.0 |
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1922198878 |
| Last Name Of The Provider | DICHEK |
| First Name Of The Provider | DAVID |
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