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| 1 | Hematological disorders and pulmonary hypertension显示文摘Pulmonary hypertension(PH),a serious disorder with a high morbidity and mortality rate,is known to occur in a number of unrelated systemic diseases.Several hematological disorders such as sickle cell disease,thalassemia and myeloproliferative diseases develop PH which worsens the prognosis.Associated oxidant injury and vascular inflammation cause endothelial damage and dysfunction.Pulmonary vascular endothelial damage/dysfunction is an early event in PH resulting in the loss of vascular reactivity,activation of proliferative and antiapoptotic pathways leading to vascular remodeling,elevated pulmonary artery pressure,right ventricular hypertrophy and premature death.Hemolysis observed in hematological disorders leads to free hemoglobin which rapidly scavenges nitric oxide(NO),limiting its bioavailability,and leading to endothelial dysfunction.In addition,hemolysis releases arginase into the circulation which converts L-arginine to ornithine,thus bypassing NO production.Furthermore,treatments for hematological disorders such as immunosuppressive therapy,splenectomy,bone marrow transplantation,and radiation have been shown to contribute to the development of PH.Recent studies have shown deregulated iron homeostasis in patients with cardiopulmonary diseases including pulmonary arterial hypertension(PAH).Several studies have reported low iron levels in patients with idiopathic PAH,and iron deficiency is an important risk factor.This article reviews PH associated with hematological disorders and its mechanism:and iron homeostasis and its relevance to PH. | Rajamma Mathew Jing Huang Joseph M Wu John T Fallon Michael H Gewitz | 2016 | World Journal of Cardiology2016，8，12： | 6 |
| 2 | Update on Cardiovascular Implantable Electronic Device Infections and Their Management: A Scientific Statement From the American Heart Association显示文摘 | Larry M. Baddour Andrew E. Epstein Christopher C. Erickson Bradley P. Knight Matthew E. Levison Peter B. Lockhart Frederick A. Masoudi Eric J. Okum Walter R. Wilson Lee B. Beerman Ann F. Bolger N A. Mark Estes Michael Gewitz Jane W. Newburger Eleanor B. S | 2010 | Circulation2010，，3： | 4 |
| 3 | Diagnosis, Treatment, and Long-Term Management of Kawasaki Disease: A Statement for Health Professionals From the Committee on Rheumatic Fever, Endocarditis and Kawasaki Disease, Council on Cardiovascular Disease in the Young, American Heart Association显示文摘 | Jane W. Newburger Masato Takahashi Michael A. Gerber Michael H. Gewitz Lloyd Y. Tani Jane C. Burns Stanford T. Shulman Ann F. Bolger Patricia Ferrieri Robert S. Baltimore Walter R. Wilson Larry M. Baddour Matthew E. Levison Thomas J. Pallasch Donald A. Fa | 2004 | Circulation2004，，17： | 2 |
| 4 | Enhanced caveolin-1 expression in smooth muscle cells: Possible prelude to neointima formation显示文摘AIM: To study the genesis of neointima formation in pulmonary hypertension(PH), we investigated the role of caveolin-1 and related proteins. METHODS: Male Sprague Dawley rats were given monocrotaline(M, 40 mg/kg) or subjected to hypobaric hypoxia(H) to induce PH. Another group was given M and subjected to H to accelerate the disease process(M + H). Right ventricular systolic pressure, right ventricular hypertrophy, lung histology for medial hypertrophy and the presence of neointimal lesions were examined at 2 and 4 wk. The expression of caveolin-1 and its regulatory protein peroxisome proliferator-activated receptor(PPAR) γ, caveolin-2, proliferative and antiapoptotic factors(PY-STAT3, p-Erk, Bcl-x L), endothelial nitric oxide synthase(e NOS) and heat shock protein(HSP) 90 in the lungs were analyzed, and the results from M + H group were compared with the controls, M and H groups. Double immunofluorescence technique was used to identify the localization of caveolin-1 in pulmonary arteries in rat lungs and in human PH lung tissue. RESULTS: In the M + H group, PH was more severe compared with M or H group. In the 4 wk M+H group, several arteries with reduced caveolin-1 expression in endothelial layer coupled with an increased expression in smooth muscle cells(SMC), exhibited neointimal lesions. Neointima was present only in the arteries exhibiting enhanced caveolin-1 expression in SMC. Lung tissue obtained from patients with PH also revealed neointimal lesions only in the arteries exhibiting endothelial caveolin-1 loss accompanied by an increased caveolin-1 expression in SMC. Reduction in e NOS and HSP90 expression was present in the M groups(2 and 4 wk), but not in the M + H groups. In both M groups and in the M + H group at 2 wk, endothelial caveolin-1 loss was accompanied by an increase in PPARγ expression. In the M + H group at 4 wk, increase in caveolin-1 expression was accompanied by a reduction in the PPARγ expression. In the H group, there was neither a loss of endothelial caveolin-1, eNOS or HSP 90, nor an increase in SMC caveolin-1 expression; or any alteration in PPARγ expression. Proliferative pathways were activated in all experimental groups. CONCLUSION: Enhanced caveolin-1 expression in SMC follows extensive endothelial caveolin-1 loss with subsequent neointima formation. Increased caveolin-1 expression in SMC, thus, may be a prelude to neointima formation. | Jing Huang John H Wolk Michael H Gewitz James E Loyd James West Eric D Austin Rajamma Mathew | 2015 | World Journal of Cardiology2015，7，10： | 2 |
| 5 | Orthostatic intolerancein adolescent chronic fatigue syndrome 显示文摘 | Stewart JM Gewitz MH Weldon A | 1999 | Pediatrics1999，103，1： | 1 |
| 6 | Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group显示文摘 | Wilson W Taubert KA Gewitz M | 2007 | Circulation2007，116，15： | 1 |
| 7 | Prevention of Infective Endocarditis Guidelines From the American Heart Association: A Guideline From the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group显示文摘 | Wilson W Taubert KA Gewitz M | 2007 | Circulation2007，116，15： | 1 |
| 8 | Three-dimensional crystals of ribosomes and their subunits from en-and archaebacteria 显示文摘 | Glotz C Mussig J Gewitz HS | 1987 | Biochem lnt1987，15，5： | 1 |
| 9 | Prevention of infective endocarditis:guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever,Endocarditis,and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology,Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group显示文摘 | Wilson W Taubert KA Gewitz M | 2007 | Circulation2007，116，15： | 1 |
| 10 | Characterization and crystallization of ribosomal particles from Halobacterium rnarismortui 显示文摘 | SHEVACK A GEWITZ H S HENNEMANN B | 1985 | FEBS Lett1985，184，： | 1 |
| 11 | Three-dimensional crystals of ribosomes and their subunits from eu-and archaebacteria显示文摘 | GLOTZ C MUSSIG J GEWITZ H S | 1987 | Biochem Int1987，15，： | 1 |
| 12 | Treatment of pulmonary hy- pertension in children with chronic lung disease with newer oral therapies显示文摘 | Krishnan U Krishnan S Gewitz M | 2008 | Pediatr Cardiol2008，29，6： | 1 |
| 13 | Diagnosis, treatment, and long-term management of Kawasaki disease: a statement for health professionals from the Committee on Rheumatic Fever, Endocarditis and Kawasaki Disease, Council on Cardiovascular Disease in the Young, American Heart Association 显示文摘 | Newburger J W Takahashi M Gerber M A Gewitz M H Tani L Y Burns J C | 2004 | Circulation2004，110，： | 1 |
| 14 | Patterns of orthostatic intole- rance:the orthostatic tachycardia syndrome and adolescent chronic fa- tigue显示文摘 | Stewart JM Gewitz MH Weldon A | 1999 | J Pediatr1999，135，21： | 1 |
| 15 | Diagnosis treatment, and long-term management of Kawasaki disease: a statement for health professi-onals from the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease, Council on CardiovascularDisease in the Young, American Heart Association显示文摘 | Newburger JW Takahashi M Gerber MA Gewitz MH Tani LY Burns JC | 2004 | Pediatrics2004，114，： | 1 |
| 16 | Prevention of infective endocarditis: Guidelines from the American Heart Association显示文摘 | Wilson W Taubert KA Gewitz M | 2007 | Crculation2007，116，15： | 1 |
| 17 | Diagnosis, treatment, and long-term management of Kawasaki disease: a statement for health professionals from the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease, Council on Cardiovascular Disease in the Young, American Heart Association 显示文摘 | Newburger JW Takahashi M Gerber MA Gewitz MH Tani LY Burns JC | 2004 | Pediatrics2004，114，6： | 1 |
| 18 | Echocardiographic cha-racteristics of premature infants with patent ductus arteriosus显示文摘 | Johnson GL Breart GL Gewitz MH | 1983 | Pediatrics1983，72，： | 1 |
| 19 | Kawasaki disease Di- agnosis management and long - term inplications 显示文摘 | Satou GM Giamelli J Gewitz MH | 2007 | Cardiol Rev2007，15，4： | 1 |
| 20 | Diagnosis,treatment, and long-term management of Kawasaki disease : a statement for health professionals from the Committee on Rheumatic Fever, Endocarditis and Kawasaki Disease, Council on Cardiovascular Disease in the Young, American Heart Association 显示文摘 | Newburger JW Takahashi M Gerber MA Gewitz MH Tani LY Burns JC | 2004 | Circulation2004，110，17： | 1 |
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