Correlation between the functional impairment of bone marrow-derived circulating progenitor cells and the extend of coronary artery disease
Background Bone marrow-derived circulating progenitor cells (BM-CPCs) in patients with coronary heart disease are impaired with respect to number and functional activity. However, the relation between the functional activity of BM-CPCs and the number of diseased coronary arteries is yet not known. W...
Ausführliche Beschreibung
Autor*in: |
Bozdag-Turan, Ilkay [verfasserIn] |
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E-Artikel |
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Sprache: |
Englisch |
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2012 |
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Anmerkung: |
© Bozdag-Turan et al.; licensee BioMed Central Ltd. 2012 |
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Übergeordnetes Werk: |
Enthalten in: Journal of translational medicine - London : BioMed Central, 2003, 10(2012), 1 vom: 09. Juli |
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Übergeordnetes Werk: |
volume:10 ; year:2012 ; number:1 ; day:09 ; month:07 |
Links: |
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DOI / URN: |
10.1186/1479-5876-10-143 |
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Katalog-ID: |
SPR028942655 |
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100 | 1 | |a Bozdag-Turan, Ilkay |e verfasserin |4 aut | |
245 | 1 | 0 | |a Correlation between the functional impairment of bone marrow-derived circulating progenitor cells and the extend of coronary artery disease |
264 | 1 | |c 2012 | |
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520 | |a Background Bone marrow-derived circulating progenitor cells (BM-CPCs) in patients with coronary heart disease are impaired with respect to number and functional activity. However, the relation between the functional activity of BM-CPCs and the number of diseased coronary arteries is yet not known. We analyzed the influence of the number of diseased coronary arteries on the functional activity of BM-CPCs in peripheral blood (PB) in patients with ischemic heart disease (IHD). Methods The functional activity of BM-CPCs was measured by migration assay and colony forming unit in 120 patients with coronary 1 vessel (IHD1, n = 40), coronary 2 vessel (IHD2, n = 40), coronary 3 vessel disease (IHD3, n = 40) and in a control group of healthy subjects (n = 40). There was no significant difference of the total number of cardiovascular risk factors between IHD groups, beside diabetes mellitus (DM), which was significantly higher in IHD3 group compared to IHD2 and IHD1. Results The colony-forming capacity (CFU-E: p < 0.001, CFU-GM: p < 0.001) and migratory response to stromal cell-derived factor 1 (SDF-1: p < 0.001) as well as vascular endothelial growth factor (VEGF: p < 0001) of BM-CPCs were reduced in the group of patients with IHD compared to control group. The functional activity of BM-CPCs was significantly impaired in patients with IHD3 as compared to IHD1 (VEGF: p < 0.01, SDF-1: p < 0.001; CFU-E: p < 0.001, CFU-GM: p < 0.001) and to IHD2 (VEGF: p = 0.003, SDF-1: p = 0.003; CFU-E: p = 0.001, CFU-GM: p = 0.001). No significant differences were observed in functional activity of BM-CPCs between patients with IHD2 and IHD1 (VEGF: p = 0.8, SDF-1: p = 0.9; CFU-E: p = 0.1, CFU-GM: p = 0.1). Interestingly, the levels of haemoglobin AIc (HbAIc) correlated inversely with the functional activity of BM-CPCs (VEGF: p < 0.001, r = −0.8 SDF-1: p < 0.001, r = −0.8; CFU-E: p = 0.001, r = −0.7, CFU-GM: p = 0.001, r = −0.6) in IHD patients with DM. Conclusions The functional activity of BM-CPCs in PB is impaired in patients with IHD. This impairment increases with the number of diseased coronary arteries. Moreover, the regenerative capacity of BM-CPCs in ischemic tissue further declines in IHD patients with DM. Furthermore, monitoring the level of BM-CPCs in PB may provide new insights in patients with IHD. | ||
650 | 4 | |a Circulating progenitor cells |7 (dpeaa)DE-He213 | |
650 | 4 | |a Migration capacity |7 (dpeaa)DE-He213 | |
650 | 4 | |a Colony forming capacity |7 (dpeaa)DE-He213 | |
650 | 4 | |a Ischemic heart disease |7 (dpeaa)DE-He213 | |
650 | 4 | |a Diabetes |7 (dpeaa)DE-He213 | |
650 | 4 | |a Coronary artery disease |7 (dpeaa)DE-He213 | |
700 | 1 | |a Turan, R Goekmen |4 aut | |
700 | 1 | |a Paranskaya, Lylia |4 aut | |
700 | 1 | |a Arsoy, Nicole S |4 aut | |
700 | 1 | |a Turan, C Hakan |4 aut | |
700 | 1 | |a Akin, Ibrahim |4 aut | |
700 | 1 | |a Kische, Stephan |4 aut | |
700 | 1 | |a Ortak, Jasmin |4 aut | |
700 | 1 | |a Schneider, H |4 aut | |
700 | 1 | |a Ludovicy, S |4 aut | |
700 | 1 | |a Hermann, Tina |4 aut | |
700 | 1 | |a D’Ancona, Giuseppe |4 aut | |
700 | 1 | |a Durdu, Serkan |4 aut | |
700 | 1 | |a Akar, A Ruchan |4 aut | |
700 | 1 | |a Ince, Hueseyin |4 aut | |
700 | 1 | |a Nienaber, Christoph A |4 aut | |
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10.1186/1479-5876-10-143 doi (DE-627)SPR028942655 (SPR)1479-5876-10-143-e DE-627 ger DE-627 rakwb eng Bozdag-Turan, Ilkay verfasserin aut Correlation between the functional impairment of bone marrow-derived circulating progenitor cells and the extend of coronary artery disease 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Bozdag-Turan et al.; licensee BioMed Central Ltd. 2012 Background Bone marrow-derived circulating progenitor cells (BM-CPCs) in patients with coronary heart disease are impaired with respect to number and functional activity. However, the relation between the functional activity of BM-CPCs and the number of diseased coronary arteries is yet not known. We analyzed the influence of the number of diseased coronary arteries on the functional activity of BM-CPCs in peripheral blood (PB) in patients with ischemic heart disease (IHD). Methods The functional activity of BM-CPCs was measured by migration assay and colony forming unit in 120 patients with coronary 1 vessel (IHD1, n = 40), coronary 2 vessel (IHD2, n = 40), coronary 3 vessel disease (IHD3, n = 40) and in a control group of healthy subjects (n = 40). There was no significant difference of the total number of cardiovascular risk factors between IHD groups, beside diabetes mellitus (DM), which was significantly higher in IHD3 group compared to IHD2 and IHD1. Results The colony-forming capacity (CFU-E: p < 0.001, CFU-GM: p < 0.001) and migratory response to stromal cell-derived factor 1 (SDF-1: p < 0.001) as well as vascular endothelial growth factor (VEGF: p < 0001) of BM-CPCs were reduced in the group of patients with IHD compared to control group. The functional activity of BM-CPCs was significantly impaired in patients with IHD3 as compared to IHD1 (VEGF: p < 0.01, SDF-1: p < 0.001; CFU-E: p < 0.001, CFU-GM: p < 0.001) and to IHD2 (VEGF: p = 0.003, SDF-1: p = 0.003; CFU-E: p = 0.001, CFU-GM: p = 0.001). No significant differences were observed in functional activity of BM-CPCs between patients with IHD2 and IHD1 (VEGF: p = 0.8, SDF-1: p = 0.9; CFU-E: p = 0.1, CFU-GM: p = 0.1). Interestingly, the levels of haemoglobin AIc (HbAIc) correlated inversely with the functional activity of BM-CPCs (VEGF: p < 0.001, r = −0.8 SDF-1: p < 0.001, r = −0.8; CFU-E: p = 0.001, r = −0.7, CFU-GM: p = 0.001, r = −0.6) in IHD patients with DM. Conclusions The functional activity of BM-CPCs in PB is impaired in patients with IHD. This impairment increases with the number of diseased coronary arteries. Moreover, the regenerative capacity of BM-CPCs in ischemic tissue further declines in IHD patients with DM. Furthermore, monitoring the level of BM-CPCs in PB may provide new insights in patients with IHD. Circulating progenitor cells (dpeaa)DE-He213 Migration capacity (dpeaa)DE-He213 Colony forming capacity (dpeaa)DE-He213 Ischemic heart disease (dpeaa)DE-He213 Diabetes (dpeaa)DE-He213 Coronary artery disease (dpeaa)DE-He213 Turan, R Goekmen aut Paranskaya, Lylia aut Arsoy, Nicole S aut Turan, C Hakan aut Akin, Ibrahim aut Kische, Stephan aut Ortak, Jasmin aut Schneider, H aut Ludovicy, S aut Hermann, Tina aut D’Ancona, Giuseppe aut Durdu, Serkan aut Akar, A Ruchan aut Ince, Hueseyin aut Nienaber, Christoph A aut Enthalten in Journal of translational medicine London : BioMed Central, 2003 10(2012), 1 vom: 09. Juli (DE-627)369084136 (DE-600)2118570-0 1479-5876 nnns volume:10 year:2012 number:1 day:09 month:07 https://dx.doi.org/10.1186/1479-5876-10-143 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2012 1 09 07 |
spelling |
10.1186/1479-5876-10-143 doi (DE-627)SPR028942655 (SPR)1479-5876-10-143-e DE-627 ger DE-627 rakwb eng Bozdag-Turan, Ilkay verfasserin aut Correlation between the functional impairment of bone marrow-derived circulating progenitor cells and the extend of coronary artery disease 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Bozdag-Turan et al.; licensee BioMed Central Ltd. 2012 Background Bone marrow-derived circulating progenitor cells (BM-CPCs) in patients with coronary heart disease are impaired with respect to number and functional activity. However, the relation between the functional activity of BM-CPCs and the number of diseased coronary arteries is yet not known. We analyzed the influence of the number of diseased coronary arteries on the functional activity of BM-CPCs in peripheral blood (PB) in patients with ischemic heart disease (IHD). Methods The functional activity of BM-CPCs was measured by migration assay and colony forming unit in 120 patients with coronary 1 vessel (IHD1, n = 40), coronary 2 vessel (IHD2, n = 40), coronary 3 vessel disease (IHD3, n = 40) and in a control group of healthy subjects (n = 40). There was no significant difference of the total number of cardiovascular risk factors between IHD groups, beside diabetes mellitus (DM), which was significantly higher in IHD3 group compared to IHD2 and IHD1. Results The colony-forming capacity (CFU-E: p < 0.001, CFU-GM: p < 0.001) and migratory response to stromal cell-derived factor 1 (SDF-1: p < 0.001) as well as vascular endothelial growth factor (VEGF: p < 0001) of BM-CPCs were reduced in the group of patients with IHD compared to control group. The functional activity of BM-CPCs was significantly impaired in patients with IHD3 as compared to IHD1 (VEGF: p < 0.01, SDF-1: p < 0.001; CFU-E: p < 0.001, CFU-GM: p < 0.001) and to IHD2 (VEGF: p = 0.003, SDF-1: p = 0.003; CFU-E: p = 0.001, CFU-GM: p = 0.001). No significant differences were observed in functional activity of BM-CPCs between patients with IHD2 and IHD1 (VEGF: p = 0.8, SDF-1: p = 0.9; CFU-E: p = 0.1, CFU-GM: p = 0.1). Interestingly, the levels of haemoglobin AIc (HbAIc) correlated inversely with the functional activity of BM-CPCs (VEGF: p < 0.001, r = −0.8 SDF-1: p < 0.001, r = −0.8; CFU-E: p = 0.001, r = −0.7, CFU-GM: p = 0.001, r = −0.6) in IHD patients with DM. Conclusions The functional activity of BM-CPCs in PB is impaired in patients with IHD. This impairment increases with the number of diseased coronary arteries. Moreover, the regenerative capacity of BM-CPCs in ischemic tissue further declines in IHD patients with DM. Furthermore, monitoring the level of BM-CPCs in PB may provide new insights in patients with IHD. Circulating progenitor cells (dpeaa)DE-He213 Migration capacity (dpeaa)DE-He213 Colony forming capacity (dpeaa)DE-He213 Ischemic heart disease (dpeaa)DE-He213 Diabetes (dpeaa)DE-He213 Coronary artery disease (dpeaa)DE-He213 Turan, R Goekmen aut Paranskaya, Lylia aut Arsoy, Nicole S aut Turan, C Hakan aut Akin, Ibrahim aut Kische, Stephan aut Ortak, Jasmin aut Schneider, H aut Ludovicy, S aut Hermann, Tina aut D’Ancona, Giuseppe aut Durdu, Serkan aut Akar, A Ruchan aut Ince, Hueseyin aut Nienaber, Christoph A aut Enthalten in Journal of translational medicine London : BioMed Central, 2003 10(2012), 1 vom: 09. Juli (DE-627)369084136 (DE-600)2118570-0 1479-5876 nnns volume:10 year:2012 number:1 day:09 month:07 https://dx.doi.org/10.1186/1479-5876-10-143 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2012 1 09 07 |
allfields_unstemmed |
10.1186/1479-5876-10-143 doi (DE-627)SPR028942655 (SPR)1479-5876-10-143-e DE-627 ger DE-627 rakwb eng Bozdag-Turan, Ilkay verfasserin aut Correlation between the functional impairment of bone marrow-derived circulating progenitor cells and the extend of coronary artery disease 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Bozdag-Turan et al.; licensee BioMed Central Ltd. 2012 Background Bone marrow-derived circulating progenitor cells (BM-CPCs) in patients with coronary heart disease are impaired with respect to number and functional activity. However, the relation between the functional activity of BM-CPCs and the number of diseased coronary arteries is yet not known. We analyzed the influence of the number of diseased coronary arteries on the functional activity of BM-CPCs in peripheral blood (PB) in patients with ischemic heart disease (IHD). Methods The functional activity of BM-CPCs was measured by migration assay and colony forming unit in 120 patients with coronary 1 vessel (IHD1, n = 40), coronary 2 vessel (IHD2, n = 40), coronary 3 vessel disease (IHD3, n = 40) and in a control group of healthy subjects (n = 40). There was no significant difference of the total number of cardiovascular risk factors between IHD groups, beside diabetes mellitus (DM), which was significantly higher in IHD3 group compared to IHD2 and IHD1. Results The colony-forming capacity (CFU-E: p < 0.001, CFU-GM: p < 0.001) and migratory response to stromal cell-derived factor 1 (SDF-1: p < 0.001) as well as vascular endothelial growth factor (VEGF: p < 0001) of BM-CPCs were reduced in the group of patients with IHD compared to control group. The functional activity of BM-CPCs was significantly impaired in patients with IHD3 as compared to IHD1 (VEGF: p < 0.01, SDF-1: p < 0.001; CFU-E: p < 0.001, CFU-GM: p < 0.001) and to IHD2 (VEGF: p = 0.003, SDF-1: p = 0.003; CFU-E: p = 0.001, CFU-GM: p = 0.001). No significant differences were observed in functional activity of BM-CPCs between patients with IHD2 and IHD1 (VEGF: p = 0.8, SDF-1: p = 0.9; CFU-E: p = 0.1, CFU-GM: p = 0.1). Interestingly, the levels of haemoglobin AIc (HbAIc) correlated inversely with the functional activity of BM-CPCs (VEGF: p < 0.001, r = −0.8 SDF-1: p < 0.001, r = −0.8; CFU-E: p = 0.001, r = −0.7, CFU-GM: p = 0.001, r = −0.6) in IHD patients with DM. Conclusions The functional activity of BM-CPCs in PB is impaired in patients with IHD. This impairment increases with the number of diseased coronary arteries. Moreover, the regenerative capacity of BM-CPCs in ischemic tissue further declines in IHD patients with DM. Furthermore, monitoring the level of BM-CPCs in PB may provide new insights in patients with IHD. Circulating progenitor cells (dpeaa)DE-He213 Migration capacity (dpeaa)DE-He213 Colony forming capacity (dpeaa)DE-He213 Ischemic heart disease (dpeaa)DE-He213 Diabetes (dpeaa)DE-He213 Coronary artery disease (dpeaa)DE-He213 Turan, R Goekmen aut Paranskaya, Lylia aut Arsoy, Nicole S aut Turan, C Hakan aut Akin, Ibrahim aut Kische, Stephan aut Ortak, Jasmin aut Schneider, H aut Ludovicy, S aut Hermann, Tina aut D’Ancona, Giuseppe aut Durdu, Serkan aut Akar, A Ruchan aut Ince, Hueseyin aut Nienaber, Christoph A aut Enthalten in Journal of translational medicine London : BioMed Central, 2003 10(2012), 1 vom: 09. Juli (DE-627)369084136 (DE-600)2118570-0 1479-5876 nnns volume:10 year:2012 number:1 day:09 month:07 https://dx.doi.org/10.1186/1479-5876-10-143 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2012 1 09 07 |
allfieldsGer |
10.1186/1479-5876-10-143 doi (DE-627)SPR028942655 (SPR)1479-5876-10-143-e DE-627 ger DE-627 rakwb eng Bozdag-Turan, Ilkay verfasserin aut Correlation between the functional impairment of bone marrow-derived circulating progenitor cells and the extend of coronary artery disease 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Bozdag-Turan et al.; licensee BioMed Central Ltd. 2012 Background Bone marrow-derived circulating progenitor cells (BM-CPCs) in patients with coronary heart disease are impaired with respect to number and functional activity. However, the relation between the functional activity of BM-CPCs and the number of diseased coronary arteries is yet not known. We analyzed the influence of the number of diseased coronary arteries on the functional activity of BM-CPCs in peripheral blood (PB) in patients with ischemic heart disease (IHD). Methods The functional activity of BM-CPCs was measured by migration assay and colony forming unit in 120 patients with coronary 1 vessel (IHD1, n = 40), coronary 2 vessel (IHD2, n = 40), coronary 3 vessel disease (IHD3, n = 40) and in a control group of healthy subjects (n = 40). There was no significant difference of the total number of cardiovascular risk factors between IHD groups, beside diabetes mellitus (DM), which was significantly higher in IHD3 group compared to IHD2 and IHD1. Results The colony-forming capacity (CFU-E: p < 0.001, CFU-GM: p < 0.001) and migratory response to stromal cell-derived factor 1 (SDF-1: p < 0.001) as well as vascular endothelial growth factor (VEGF: p < 0001) of BM-CPCs were reduced in the group of patients with IHD compared to control group. The functional activity of BM-CPCs was significantly impaired in patients with IHD3 as compared to IHD1 (VEGF: p < 0.01, SDF-1: p < 0.001; CFU-E: p < 0.001, CFU-GM: p < 0.001) and to IHD2 (VEGF: p = 0.003, SDF-1: p = 0.003; CFU-E: p = 0.001, CFU-GM: p = 0.001). No significant differences were observed in functional activity of BM-CPCs between patients with IHD2 and IHD1 (VEGF: p = 0.8, SDF-1: p = 0.9; CFU-E: p = 0.1, CFU-GM: p = 0.1). Interestingly, the levels of haemoglobin AIc (HbAIc) correlated inversely with the functional activity of BM-CPCs (VEGF: p < 0.001, r = −0.8 SDF-1: p < 0.001, r = −0.8; CFU-E: p = 0.001, r = −0.7, CFU-GM: p = 0.001, r = −0.6) in IHD patients with DM. Conclusions The functional activity of BM-CPCs in PB is impaired in patients with IHD. This impairment increases with the number of diseased coronary arteries. Moreover, the regenerative capacity of BM-CPCs in ischemic tissue further declines in IHD patients with DM. Furthermore, monitoring the level of BM-CPCs in PB may provide new insights in patients with IHD. Circulating progenitor cells (dpeaa)DE-He213 Migration capacity (dpeaa)DE-He213 Colony forming capacity (dpeaa)DE-He213 Ischemic heart disease (dpeaa)DE-He213 Diabetes (dpeaa)DE-He213 Coronary artery disease (dpeaa)DE-He213 Turan, R Goekmen aut Paranskaya, Lylia aut Arsoy, Nicole S aut Turan, C Hakan aut Akin, Ibrahim aut Kische, Stephan aut Ortak, Jasmin aut Schneider, H aut Ludovicy, S aut Hermann, Tina aut D’Ancona, Giuseppe aut Durdu, Serkan aut Akar, A Ruchan aut Ince, Hueseyin aut Nienaber, Christoph A aut Enthalten in Journal of translational medicine London : BioMed Central, 2003 10(2012), 1 vom: 09. Juli (DE-627)369084136 (DE-600)2118570-0 1479-5876 nnns volume:10 year:2012 number:1 day:09 month:07 https://dx.doi.org/10.1186/1479-5876-10-143 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2012 1 09 07 |
allfieldsSound |
10.1186/1479-5876-10-143 doi (DE-627)SPR028942655 (SPR)1479-5876-10-143-e DE-627 ger DE-627 rakwb eng Bozdag-Turan, Ilkay verfasserin aut Correlation between the functional impairment of bone marrow-derived circulating progenitor cells and the extend of coronary artery disease 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Bozdag-Turan et al.; licensee BioMed Central Ltd. 2012 Background Bone marrow-derived circulating progenitor cells (BM-CPCs) in patients with coronary heart disease are impaired with respect to number and functional activity. However, the relation between the functional activity of BM-CPCs and the number of diseased coronary arteries is yet not known. We analyzed the influence of the number of diseased coronary arteries on the functional activity of BM-CPCs in peripheral blood (PB) in patients with ischemic heart disease (IHD). Methods The functional activity of BM-CPCs was measured by migration assay and colony forming unit in 120 patients with coronary 1 vessel (IHD1, n = 40), coronary 2 vessel (IHD2, n = 40), coronary 3 vessel disease (IHD3, n = 40) and in a control group of healthy subjects (n = 40). There was no significant difference of the total number of cardiovascular risk factors between IHD groups, beside diabetes mellitus (DM), which was significantly higher in IHD3 group compared to IHD2 and IHD1. Results The colony-forming capacity (CFU-E: p < 0.001, CFU-GM: p < 0.001) and migratory response to stromal cell-derived factor 1 (SDF-1: p < 0.001) as well as vascular endothelial growth factor (VEGF: p < 0001) of BM-CPCs were reduced in the group of patients with IHD compared to control group. The functional activity of BM-CPCs was significantly impaired in patients with IHD3 as compared to IHD1 (VEGF: p < 0.01, SDF-1: p < 0.001; CFU-E: p < 0.001, CFU-GM: p < 0.001) and to IHD2 (VEGF: p = 0.003, SDF-1: p = 0.003; CFU-E: p = 0.001, CFU-GM: p = 0.001). No significant differences were observed in functional activity of BM-CPCs between patients with IHD2 and IHD1 (VEGF: p = 0.8, SDF-1: p = 0.9; CFU-E: p = 0.1, CFU-GM: p = 0.1). Interestingly, the levels of haemoglobin AIc (HbAIc) correlated inversely with the functional activity of BM-CPCs (VEGF: p < 0.001, r = −0.8 SDF-1: p < 0.001, r = −0.8; CFU-E: p = 0.001, r = −0.7, CFU-GM: p = 0.001, r = −0.6) in IHD patients with DM. Conclusions The functional activity of BM-CPCs in PB is impaired in patients with IHD. This impairment increases with the number of diseased coronary arteries. Moreover, the regenerative capacity of BM-CPCs in ischemic tissue further declines in IHD patients with DM. Furthermore, monitoring the level of BM-CPCs in PB may provide new insights in patients with IHD. Circulating progenitor cells (dpeaa)DE-He213 Migration capacity (dpeaa)DE-He213 Colony forming capacity (dpeaa)DE-He213 Ischemic heart disease (dpeaa)DE-He213 Diabetes (dpeaa)DE-He213 Coronary artery disease (dpeaa)DE-He213 Turan, R Goekmen aut Paranskaya, Lylia aut Arsoy, Nicole S aut Turan, C Hakan aut Akin, Ibrahim aut Kische, Stephan aut Ortak, Jasmin aut Schneider, H aut Ludovicy, S aut Hermann, Tina aut D’Ancona, Giuseppe aut Durdu, Serkan aut Akar, A Ruchan aut Ince, Hueseyin aut Nienaber, Christoph A aut Enthalten in Journal of translational medicine London : BioMed Central, 2003 10(2012), 1 vom: 09. Juli (DE-627)369084136 (DE-600)2118570-0 1479-5876 nnns volume:10 year:2012 number:1 day:09 month:07 https://dx.doi.org/10.1186/1479-5876-10-143 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2012 1 09 07 |
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Enthalten in Journal of translational medicine 10(2012), 1 vom: 09. Juli volume:10 year:2012 number:1 day:09 month:07 |
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Circulating progenitor cells Migration capacity Colony forming capacity Ischemic heart disease Diabetes Coronary artery disease |
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Bozdag-Turan, Ilkay @@aut@@ Turan, R Goekmen @@aut@@ Paranskaya, Lylia @@aut@@ Arsoy, Nicole S @@aut@@ Turan, C Hakan @@aut@@ Akin, Ibrahim @@aut@@ Kische, Stephan @@aut@@ Ortak, Jasmin @@aut@@ Schneider, H @@aut@@ Ludovicy, S @@aut@@ Hermann, Tina @@aut@@ D’Ancona, Giuseppe @@aut@@ Durdu, Serkan @@aut@@ Akar, A Ruchan @@aut@@ Ince, Hueseyin @@aut@@ Nienaber, Christoph A @@aut@@ |
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However, the relation between the functional activity of BM-CPCs and the number of diseased coronary arteries is yet not known. We analyzed the influence of the number of diseased coronary arteries on the functional activity of BM-CPCs in peripheral blood (PB) in patients with ischemic heart disease (IHD). Methods The functional activity of BM-CPCs was measured by migration assay and colony forming unit in 120 patients with coronary 1 vessel (IHD1, n = 40), coronary 2 vessel (IHD2, n = 40), coronary 3 vessel disease (IHD3, n = 40) and in a control group of healthy subjects (n = 40). There was no significant difference of the total number of cardiovascular risk factors between IHD groups, beside diabetes mellitus (DM), which was significantly higher in IHD3 group compared to IHD2 and IHD1. Results The colony-forming capacity (CFU-E: p < 0.001, CFU-GM: p < 0.001) and migratory response to stromal cell-derived factor 1 (SDF-1: p < 0.001) as well as vascular endothelial growth factor (VEGF: p < 0001) of BM-CPCs were reduced in the group of patients with IHD compared to control group. The functional activity of BM-CPCs was significantly impaired in patients with IHD3 as compared to IHD1 (VEGF: p < 0.01, SDF-1: p < 0.001; CFU-E: p < 0.001, CFU-GM: p < 0.001) and to IHD2 (VEGF: p = 0.003, SDF-1: p = 0.003; CFU-E: p = 0.001, CFU-GM: p = 0.001). No significant differences were observed in functional activity of BM-CPCs between patients with IHD2 and IHD1 (VEGF: p = 0.8, SDF-1: p = 0.9; CFU-E: p = 0.1, CFU-GM: p = 0.1). Interestingly, the levels of haemoglobin AIc (HbAIc) correlated inversely with the functional activity of BM-CPCs (VEGF: p < 0.001, r = −0.8 SDF-1: p < 0.001, r = −0.8; CFU-E: p = 0.001, r = −0.7, CFU-GM: p = 0.001, r = −0.6) in IHD patients with DM. Conclusions The functional activity of BM-CPCs in PB is impaired in patients with IHD. This impairment increases with the number of diseased coronary arteries. Moreover, the regenerative capacity of BM-CPCs in ischemic tissue further declines in IHD patients with DM. 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Bozdag-Turan, Ilkay |
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Bozdag-Turan, Ilkay misc Circulating progenitor cells misc Migration capacity misc Colony forming capacity misc Ischemic heart disease misc Diabetes misc Coronary artery disease Correlation between the functional impairment of bone marrow-derived circulating progenitor cells and the extend of coronary artery disease |
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Correlation between the functional impairment of bone marrow-derived circulating progenitor cells and the extend of coronary artery disease Circulating progenitor cells (dpeaa)DE-He213 Migration capacity (dpeaa)DE-He213 Colony forming capacity (dpeaa)DE-He213 Ischemic heart disease (dpeaa)DE-He213 Diabetes (dpeaa)DE-He213 Coronary artery disease (dpeaa)DE-He213 |
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Bozdag-Turan, Ilkay Turan, R Goekmen Paranskaya, Lylia Arsoy, Nicole S Turan, C Hakan Akin, Ibrahim Kische, Stephan Ortak, Jasmin Schneider, H Ludovicy, S Hermann, Tina D’Ancona, Giuseppe Durdu, Serkan Akar, A Ruchan Ince, Hueseyin Nienaber, Christoph A |
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correlation between the functional impairment of bone marrow-derived circulating progenitor cells and the extend of coronary artery disease |
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Correlation between the functional impairment of bone marrow-derived circulating progenitor cells and the extend of coronary artery disease |
abstract |
Background Bone marrow-derived circulating progenitor cells (BM-CPCs) in patients with coronary heart disease are impaired with respect to number and functional activity. However, the relation between the functional activity of BM-CPCs and the number of diseased coronary arteries is yet not known. We analyzed the influence of the number of diseased coronary arteries on the functional activity of BM-CPCs in peripheral blood (PB) in patients with ischemic heart disease (IHD). Methods The functional activity of BM-CPCs was measured by migration assay and colony forming unit in 120 patients with coronary 1 vessel (IHD1, n = 40), coronary 2 vessel (IHD2, n = 40), coronary 3 vessel disease (IHD3, n = 40) and in a control group of healthy subjects (n = 40). There was no significant difference of the total number of cardiovascular risk factors between IHD groups, beside diabetes mellitus (DM), which was significantly higher in IHD3 group compared to IHD2 and IHD1. Results The colony-forming capacity (CFU-E: p < 0.001, CFU-GM: p < 0.001) and migratory response to stromal cell-derived factor 1 (SDF-1: p < 0.001) as well as vascular endothelial growth factor (VEGF: p < 0001) of BM-CPCs were reduced in the group of patients with IHD compared to control group. The functional activity of BM-CPCs was significantly impaired in patients with IHD3 as compared to IHD1 (VEGF: p < 0.01, SDF-1: p < 0.001; CFU-E: p < 0.001, CFU-GM: p < 0.001) and to IHD2 (VEGF: p = 0.003, SDF-1: p = 0.003; CFU-E: p = 0.001, CFU-GM: p = 0.001). No significant differences were observed in functional activity of BM-CPCs between patients with IHD2 and IHD1 (VEGF: p = 0.8, SDF-1: p = 0.9; CFU-E: p = 0.1, CFU-GM: p = 0.1). Interestingly, the levels of haemoglobin AIc (HbAIc) correlated inversely with the functional activity of BM-CPCs (VEGF: p < 0.001, r = −0.8 SDF-1: p < 0.001, r = −0.8; CFU-E: p = 0.001, r = −0.7, CFU-GM: p = 0.001, r = −0.6) in IHD patients with DM. Conclusions The functional activity of BM-CPCs in PB is impaired in patients with IHD. This impairment increases with the number of diseased coronary arteries. Moreover, the regenerative capacity of BM-CPCs in ischemic tissue further declines in IHD patients with DM. Furthermore, monitoring the level of BM-CPCs in PB may provide new insights in patients with IHD. © Bozdag-Turan et al.; licensee BioMed Central Ltd. 2012 |
abstractGer |
Background Bone marrow-derived circulating progenitor cells (BM-CPCs) in patients with coronary heart disease are impaired with respect to number and functional activity. However, the relation between the functional activity of BM-CPCs and the number of diseased coronary arteries is yet not known. We analyzed the influence of the number of diseased coronary arteries on the functional activity of BM-CPCs in peripheral blood (PB) in patients with ischemic heart disease (IHD). Methods The functional activity of BM-CPCs was measured by migration assay and colony forming unit in 120 patients with coronary 1 vessel (IHD1, n = 40), coronary 2 vessel (IHD2, n = 40), coronary 3 vessel disease (IHD3, n = 40) and in a control group of healthy subjects (n = 40). There was no significant difference of the total number of cardiovascular risk factors between IHD groups, beside diabetes mellitus (DM), which was significantly higher in IHD3 group compared to IHD2 and IHD1. Results The colony-forming capacity (CFU-E: p < 0.001, CFU-GM: p < 0.001) and migratory response to stromal cell-derived factor 1 (SDF-1: p < 0.001) as well as vascular endothelial growth factor (VEGF: p < 0001) of BM-CPCs were reduced in the group of patients with IHD compared to control group. The functional activity of BM-CPCs was significantly impaired in patients with IHD3 as compared to IHD1 (VEGF: p < 0.01, SDF-1: p < 0.001; CFU-E: p < 0.001, CFU-GM: p < 0.001) and to IHD2 (VEGF: p = 0.003, SDF-1: p = 0.003; CFU-E: p = 0.001, CFU-GM: p = 0.001). No significant differences were observed in functional activity of BM-CPCs between patients with IHD2 and IHD1 (VEGF: p = 0.8, SDF-1: p = 0.9; CFU-E: p = 0.1, CFU-GM: p = 0.1). Interestingly, the levels of haemoglobin AIc (HbAIc) correlated inversely with the functional activity of BM-CPCs (VEGF: p < 0.001, r = −0.8 SDF-1: p < 0.001, r = −0.8; CFU-E: p = 0.001, r = −0.7, CFU-GM: p = 0.001, r = −0.6) in IHD patients with DM. Conclusions The functional activity of BM-CPCs in PB is impaired in patients with IHD. This impairment increases with the number of diseased coronary arteries. Moreover, the regenerative capacity of BM-CPCs in ischemic tissue further declines in IHD patients with DM. Furthermore, monitoring the level of BM-CPCs in PB may provide new insights in patients with IHD. © Bozdag-Turan et al.; licensee BioMed Central Ltd. 2012 |
abstract_unstemmed |
Background Bone marrow-derived circulating progenitor cells (BM-CPCs) in patients with coronary heart disease are impaired with respect to number and functional activity. However, the relation between the functional activity of BM-CPCs and the number of diseased coronary arteries is yet not known. We analyzed the influence of the number of diseased coronary arteries on the functional activity of BM-CPCs in peripheral blood (PB) in patients with ischemic heart disease (IHD). Methods The functional activity of BM-CPCs was measured by migration assay and colony forming unit in 120 patients with coronary 1 vessel (IHD1, n = 40), coronary 2 vessel (IHD2, n = 40), coronary 3 vessel disease (IHD3, n = 40) and in a control group of healthy subjects (n = 40). There was no significant difference of the total number of cardiovascular risk factors between IHD groups, beside diabetes mellitus (DM), which was significantly higher in IHD3 group compared to IHD2 and IHD1. Results The colony-forming capacity (CFU-E: p < 0.001, CFU-GM: p < 0.001) and migratory response to stromal cell-derived factor 1 (SDF-1: p < 0.001) as well as vascular endothelial growth factor (VEGF: p < 0001) of BM-CPCs were reduced in the group of patients with IHD compared to control group. The functional activity of BM-CPCs was significantly impaired in patients with IHD3 as compared to IHD1 (VEGF: p < 0.01, SDF-1: p < 0.001; CFU-E: p < 0.001, CFU-GM: p < 0.001) and to IHD2 (VEGF: p = 0.003, SDF-1: p = 0.003; CFU-E: p = 0.001, CFU-GM: p = 0.001). No significant differences were observed in functional activity of BM-CPCs between patients with IHD2 and IHD1 (VEGF: p = 0.8, SDF-1: p = 0.9; CFU-E: p = 0.1, CFU-GM: p = 0.1). Interestingly, the levels of haemoglobin AIc (HbAIc) correlated inversely with the functional activity of BM-CPCs (VEGF: p < 0.001, r = −0.8 SDF-1: p < 0.001, r = −0.8; CFU-E: p = 0.001, r = −0.7, CFU-GM: p = 0.001, r = −0.6) in IHD patients with DM. Conclusions The functional activity of BM-CPCs in PB is impaired in patients with IHD. This impairment increases with the number of diseased coronary arteries. Moreover, the regenerative capacity of BM-CPCs in ischemic tissue further declines in IHD patients with DM. Furthermore, monitoring the level of BM-CPCs in PB may provide new insights in patients with IHD. © Bozdag-Turan et al.; licensee BioMed Central Ltd. 2012 |
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However, the relation between the functional activity of BM-CPCs and the number of diseased coronary arteries is yet not known. We analyzed the influence of the number of diseased coronary arteries on the functional activity of BM-CPCs in peripheral blood (PB) in patients with ischemic heart disease (IHD). Methods The functional activity of BM-CPCs was measured by migration assay and colony forming unit in 120 patients with coronary 1 vessel (IHD1, n = 40), coronary 2 vessel (IHD2, n = 40), coronary 3 vessel disease (IHD3, n = 40) and in a control group of healthy subjects (n = 40). There was no significant difference of the total number of cardiovascular risk factors between IHD groups, beside diabetes mellitus (DM), which was significantly higher in IHD3 group compared to IHD2 and IHD1. Results The colony-forming capacity (CFU-E: p < 0.001, CFU-GM: p < 0.001) and migratory response to stromal cell-derived factor 1 (SDF-1: p < 0.001) as well as vascular endothelial growth factor (VEGF: p < 0001) of BM-CPCs were reduced in the group of patients with IHD compared to control group. The functional activity of BM-CPCs was significantly impaired in patients with IHD3 as compared to IHD1 (VEGF: p < 0.01, SDF-1: p < 0.001; CFU-E: p < 0.001, CFU-GM: p < 0.001) and to IHD2 (VEGF: p = 0.003, SDF-1: p = 0.003; CFU-E: p = 0.001, CFU-GM: p = 0.001). No significant differences were observed in functional activity of BM-CPCs between patients with IHD2 and IHD1 (VEGF: p = 0.8, SDF-1: p = 0.9; CFU-E: p = 0.1, CFU-GM: p = 0.1). Interestingly, the levels of haemoglobin AIc (HbAIc) correlated inversely with the functional activity of BM-CPCs (VEGF: p < 0.001, r = −0.8 SDF-1: p < 0.001, r = −0.8; CFU-E: p = 0.001, r = −0.7, CFU-GM: p = 0.001, r = −0.6) in IHD patients with DM. Conclusions The functional activity of BM-CPCs in PB is impaired in patients with IHD. This impairment increases with the number of diseased coronary arteries. Moreover, the regenerative capacity of BM-CPCs in ischemic tissue further declines in IHD patients with DM. Furthermore, monitoring the level of BM-CPCs in PB may provide new insights in patients with IHD.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Circulating progenitor cells</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Migration capacity</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Colony forming capacity</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Ischemic heart disease</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Diabetes</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Coronary artery disease</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Turan, R Goekmen</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Paranskaya, Lylia</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Arsoy, Nicole S</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Turan, C Hakan</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Akin, Ibrahim</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kische, Stephan</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Ortak, Jasmin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Schneider, H</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Ludovicy, S</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Hermann, Tina</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">D’Ancona, Giuseppe</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Durdu, Serkan</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Akar, A Ruchan</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Ince, Hueseyin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Nienaber, Christoph A</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">Journal of translational medicine</subfield><subfield code="d">London : BioMed Central, 2003</subfield><subfield code="g">10(2012), 1 vom: 09. 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7.401827 |