5 results on '"András Bratincsák"'
Search Results
2. Improvement in Pulmonary Function After Closure of Atrial Septal Defect in a Patient With Cystic Fibrosis
- Author
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Abdulfattah Saidi, Anwar Tandar, Elisa Rhee, András Bratincsák, William Van Alstine, Lindsay Koren, Kimberly Stoughton, José Negrón-Garcia, Anthony Ragheb, Hannah El-Sabrout, John W. Moore, Howaida el-Said, John P. Breinholt, Jason P. Glotzbach, Frederick G.P. Welt, Vikas Sharma, Kelsee Browning, Craig H. Selzman, David A. Bull, and Holly Carveth
- Subjects
medicine.medical_specialty ,business.industry ,Closure (topology) ,Medicine ,business ,medicine.disease ,Cystic fibrosis ,Pulmonary function testing ,Surgery - Published
- 2017
3. Transforming growth factor α induces angiogenesis and neurogenesis following stroke
- Author
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Eva Mezey, András Bratincsák, Tal Shahar, Ildiko Szalayova, Ronen R. Leker, Riccardo Cassiani-Ingoni, and Zsuzsanna E. Tóth
- Subjects
medicine.medical_specialty ,TGF alpha ,Angiogenesis ,business.industry ,General Neuroscience ,medicine.medical_treatment ,Neurogenesis ,medicine.disease ,Neuroprotection ,Neovascularization ,chemistry.chemical_compound ,Cytokine ,Endocrinology ,chemistry ,Internal medicine ,Immunology ,medicine ,medicine.symptom ,business ,Stroke ,Bromodeoxyuridine - Abstract
The cytokine transforming growth factor alpha (TGF alpha) has proangiogenic and proneurogenic effects and can potentially reduce infarct volumes. Therefore, we administered TGF alpha or vehicle directly into the area surrounding the infarct in female mice that received gender-mismatched bone marrow transplants from green fluorescent protein (GFP)-expressing males prior to undergoing permanent middle cerebral artery occlusion. Newborn cells were tracked with bromodeoxyuridine (BrdU) labeling and immunohistochemistry at 90 days after stroke onset. We also studied the ingress of bone marrow-derived cells into the ischemic brain to determine whether such cells contribute to angiogenesis or neurogenesis. Infarct volumes were measured at 90 days poststroke. The results show that TGF alpha led to significant increments in the number of newborn neurons and glia in the ischemic hemisphere. TGF alpha also led to significant increments in the number of bone marrow-derived cells entering into the ischemic hemisphere. Most of these cells did not label with BrdU and represented endothelial cells that incorporated into blood vessels in the infarct border zone. Our results also show that infarct size was significantly reduced in animals treated with TGF alpha compared with controls. These results suggest that TGF alpha can induce angiogenesis, neurogenesis and neuroprotection after stroke. At least part of the pro-angiogenic effect appears to be secondary to the incorporation of bone marrow-derived endothelial cells into blood vessels in the infarct border zone.
- Published
- 2009
4. Disease Progression After Bone Marrow Transplantation in a Model of Multiple Sclerosis Is Associated With Chronic Microglial and Glial Progenitor Response
- Author
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Larry S. Sherman, Riccardo Cassiani-Ingoni, Tal Shahar, Jacqueline A. Quandt, Roland Martin, Tim Magnus, András Bratincsák, Mahendra S. Rao, Mark P. Mattson, Paolo A. Muraro, Jens Schmidt, Jaebong Huh, Susan Reichert-Scrivner, and Fabrizio Eusebi
- Subjects
Encephalomyelitis, Autoimmune, Experimental ,Multiple Sclerosis ,Nerve Tissue Proteins ,Pathology and Forensic Medicine ,Mice ,Cellular and Molecular Neuroscience ,Antigens, CD ,Glial Fibrillary Acidic Protein ,Basic Helix-Loop-Helix Transcription Factors ,Animals ,Medicine ,Neuroinflammation ,Bone Marrow Transplantation ,Cell Proliferation ,Glycoproteins ,Microglia ,business.industry ,Stem Cells ,Experimental autoimmune encephalomyelitis ,Brain ,General Medicine ,Oligodendrocyte Transcription Factor 2 ,Flow Cytometry ,medicine.disease ,Peptide Fragments ,Mice, Inbred C57BL ,Disease Models, Animal ,medicine.anatomical_structure ,Spinal Cord ,Neurology ,Gliosis ,Immunology ,Disease Progression ,Neuroglia ,Myelin-Oligodendrocyte Glycoprotein ,Neurology (clinical) ,Bone marrow ,Stem cell ,medicine.symptom ,business ,Astrocyte - Abstract
Multiple sclerosis (MS), the most common nontraumatic cause of neurologic disability in young adults in economically developed countries, is characterized by inflammation, gliosis, demyelination, and neuronal degeneration in the CNS. Bone marrow transplantation (BMT) can suppress inflammatory disease in a majority of patients with MS but retards clinical progression only in patients treated in the early stages of the disease. Here, we applied BMT in a mouse model of neuroinflammation, experimental autoimmune encephalomyelitis (EAE), and investigated the kinetics of reconstitution of the immune system in the periphery and in the CNS using bone marrow cells isolated from syngeneic donors constitutively expressing green fluorescent protein. This approach allowed us to dissect the contribution of donor cells to the turnover of resident microglia and to the pathogenesis of observed disease relapses after BMT. BMT effectively blocked or delayed EAE development when mice were treated early in the course of the disease but was without effect in mice with chronic disease. We found that there is minimal overall replacement of host microglia with donor cells in the CNS and that newly transplanted cells do not appear to contribute to disease progression. In contrast, EAE relapses are accompanied by the robust activation of endogenous microglial and macroglial cells, which further involves the maturation of endogenous Olig2 glial progenitor cells into reactive astrocytes through the cytoplasmic translocation of Olig2 and the expression of CD44 on the cellular membrane. The observed maturation of large numbers of reactive astrocytes from glial progenitors and the chronic activation of host microglial cells have relevance for our understanding of the resident glial response to inflammatory injury in the CNS. Our data indicate that reactivation of a local inflammatory process after BMT is sustained predominantly by endogenous microglia/macrophages.
- Published
- 2007
5. The combination of granulocyte colony-stimulating factor and stem cell factor significantly increases the number of bone marrow-derived endothelial cells in brains of mice following cerebral ischemia
- Author
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Tal Shahar, Krisztián Németh, András Bratincsák, Ildiko Szalayova, Ronen R. Leker, Balázs Mayer, Brook Asemenew, Zsuzsanna E. Tóth, Alissa Parmelee, Sandra Pastorino, Sharon Key, and Eva Mezey
- Subjects
Pathology ,medicine.medical_specialty ,Hematopoiesis and Stem Cells ,Angiogenesis ,medicine.medical_treatment ,Immunology ,Green Fluorescent Proteins ,Neovascularization, Physiologic ,Stem cell factor ,Biochemistry ,Brain Ischemia ,Mice ,Granulocyte Colony-Stimulating Factor ,medicine ,Animals ,Bone Marrow Transplantation ,Stem Cell Factor ,business.industry ,Endothelial Cells ,Infarction, Middle Cerebral Artery ,Cell Biology ,Hematology ,Recovery of Function ,Granulocyte colony-stimulating factor ,Endothelial stem cell ,Mice, Inbred C57BL ,Haematopoiesis ,Cytokine ,medicine.anatomical_structure ,Cancer research ,Drug Therapy, Combination ,Female ,Bone marrow ,Stem cell ,business ,Cell Division - Abstract
Granulocyte colony-stimulating factor (G-CSF) induces proliferation of bone marrow–derived cells. G-CSF is neuroprotective after experimental brain injury, but the mechanisms involved remain unclear. Stem cell factor (SCF) is a cytokine important for the survival and differentiation of hematopoietic stem cells. Its receptor (c-kit or CD117) is present in some endothelial cells. We aimed to determine whether the combination of G-CSF/SCF induces angiogenesis in the central nervous system by promoting entry of endothelial precursors into the injured brain and causing them to proliferate there. We induced permanent middle cerebral artery occlusion in female mice that previously underwent sex-mismatched bone marrow transplantation from enhanced green fluorescent protein (EGFP)–expressing mice. G-CSF/SCF treatment reduced infarct volumes by more than 50% and resulted in a 1.5-fold increase in vessel formation in mice with stroke, a large percentage of which contain endothelial cells of bone marrow origin. Most cells entering the brain maintained their bone marrow identity and did not transdifferentiate into neural cells. G-CSF/SCF treatment also led to a 2-fold increase in the number of newborn cells in the ischemic hemisphere. These findings suggest that G-CSF/SCF treatment might help recovery through induction of bone marrow–derived angiogenesis, thus improving neuronal survival and functional outcome.
- Published
- 2008
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