Platelet Response to Serotonin in Patients With Stable Coronary Heart Disease
Patients with heart disease and depression have an increased mortality rate. Both behavioral and biologic factors have been proposed as potential etiologic mechanisms. Given that the pathophysiology of depression is considered to involve disruption in brain serotonergic signaling, we investigated pl...
Ausführliche Beschreibung
Autor*in: |
Kim, Dan A. [verfasserIn] |
---|
Format: |
E-Artikel |
---|---|
Sprache: |
Englisch |
Erschienen: |
2014transfer abstract |
---|
Umfang: |
6 |
---|
Übergeordnetes Werk: |
Enthalten in: PI simultaneous stabilization and set-point output regulation of Port-Hamiltonian systems - Zhang, Meng ELSEVIER, 2017, official journal of the American College of Cardiology, Amsterdam [u.a.] |
---|---|
Übergeordnetes Werk: |
volume:114 ; year:2014 ; number:2 ; day:15 ; month:07 ; pages:181-186 ; extent:6 |
Links: |
---|
DOI / URN: |
10.1016/j.amjcard.2014.04.023 |
---|
Katalog-ID: |
ELV01792877X |
---|
LEADER | 01000caa a22002652 4500 | ||
---|---|---|---|
001 | ELV01792877X | ||
003 | DE-627 | ||
005 | 20230625123049.0 | ||
007 | cr uuu---uuuuu | ||
008 | 180602s2014 xx |||||o 00| ||eng c | ||
024 | 7 | |a 10.1016/j.amjcard.2014.04.023 |2 doi | |
028 | 5 | 2 | |a GBVA2014019000017.pica |
035 | |a (DE-627)ELV01792877X | ||
035 | |a (ELSEVIER)S0002-9149(14)01037-6 | ||
040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
041 | |a eng | ||
082 | 0 | |a 610 | |
082 | 0 | 4 | |a 610 |q DE-600 |
082 | 0 | 4 | |a 510 |q VZ |
084 | |a 31.80 |2 bkl | ||
100 | 1 | |a Kim, Dan A. |e verfasserin |4 aut | |
245 | 1 | 0 | |a Platelet Response to Serotonin in Patients With Stable Coronary Heart Disease |
264 | 1 | |c 2014transfer abstract | |
300 | |a 6 | ||
336 | |a nicht spezifiziert |b zzz |2 rdacontent | ||
337 | |a nicht spezifiziert |b z |2 rdamedia | ||
338 | |a nicht spezifiziert |b zu |2 rdacarrier | ||
520 | |a Patients with heart disease and depression have an increased mortality rate. Both behavioral and biologic factors have been proposed as potential etiologic mechanisms. Given that the pathophysiology of depression is considered to involve disruption in brain serotonergic signaling, we investigated platelet response to serotonin stimulation in patients with stable coronary artery disease (CAD). We enrolled 92 patients with stable CAD. Platelet response to increasing concentrations of serotonin (5-HT), epinephrine-augmented 5-HT, and adenosine diphosphate (ADP) was measured by optical aggregation and flow cytometry. As concentrations of 5-HT and ADP increased, so did the activation and aggregation of the platelets. However, on addition of the highest concentration of 5-HT (30 μM), a significant decrease in platelet activation (p = 0.005) was detected by flow cytometry. This contrasts the increase in platelet activation seen with the addition of the highest concentration of ADP. In conclusion, we found increased platelet activation and aggregation with increased concentrations of ADP; however, when platelets are stimulated with a high concentration of 5-HT (30 μM), there is decreased platelet activation. The data demonstrate unique patterns of platelet activation by 5-HT in patients with stable CAD. The cause of this phenomenon is unclear. Our study sheds light on the in vitro response of platelet function to serotonin in patients with stable CAD, which may further the mechanistic understanding of heart disease and depression. | ||
520 | |a Patients with heart disease and depression have an increased mortality rate. Both behavioral and biologic factors have been proposed as potential etiologic mechanisms. Given that the pathophysiology of depression is considered to involve disruption in brain serotonergic signaling, we investigated platelet response to serotonin stimulation in patients with stable coronary artery disease (CAD). We enrolled 92 patients with stable CAD. Platelet response to increasing concentrations of serotonin (5-HT), epinephrine-augmented 5-HT, and adenosine diphosphate (ADP) was measured by optical aggregation and flow cytometry. As concentrations of 5-HT and ADP increased, so did the activation and aggregation of the platelets. However, on addition of the highest concentration of 5-HT (30 μM), a significant decrease in platelet activation (p = 0.005) was detected by flow cytometry. This contrasts the increase in platelet activation seen with the addition of the highest concentration of ADP. In conclusion, we found increased platelet activation and aggregation with increased concentrations of ADP; however, when platelets are stimulated with a high concentration of 5-HT (30 μM), there is decreased platelet activation. The data demonstrate unique patterns of platelet activation by 5-HT in patients with stable CAD. The cause of this phenomenon is unclear. Our study sheds light on the in vitro response of platelet function to serotonin in patients with stable CAD, which may further the mechanistic understanding of heart disease and depression. | ||
700 | 1 | |a McClure, Willie G. |4 oth | |
700 | 1 | |a Neighoff, Jordan B. |4 oth | |
700 | 1 | |a Vaidya, Dhananjay |4 oth | |
700 | 1 | |a Williams, Marlene S. |4 oth | |
773 | 0 | 8 | |i Enthalten in |n Elsevier |a Zhang, Meng ELSEVIER |t PI simultaneous stabilization and set-point output regulation of Port-Hamiltonian systems |d 2017 |d official journal of the American College of Cardiology |g Amsterdam [u.a.] |w (DE-627)ELV000623679 |
773 | 1 | 8 | |g volume:114 |g year:2014 |g number:2 |g day:15 |g month:07 |g pages:181-186 |g extent:6 |
856 | 4 | 0 | |u https://doi.org/10.1016/j.amjcard.2014.04.023 |3 Volltext |
912 | |a GBV_USEFLAG_U | ||
912 | |a GBV_ELV | ||
912 | |a SYSFLAG_U | ||
912 | |a SSG-OPC-MAT | ||
936 | b | k | |a 31.80 |j Angewandte Mathematik |q VZ |
951 | |a AR | ||
952 | |d 114 |j 2014 |e 2 |b 15 |c 0715 |h 181-186 |g 6 | ||
953 | |2 045F |a 610 |
author_variant |
d a k da dak |
---|---|
matchkey_str |
kimdanamcclurewilliegneighoffjordanbvaid:2014----:ltltepneoeooiiptetwtsalc |
hierarchy_sort_str |
2014transfer abstract |
bklnumber |
31.80 |
publishDate |
2014 |
allfields |
10.1016/j.amjcard.2014.04.023 doi GBVA2014019000017.pica (DE-627)ELV01792877X (ELSEVIER)S0002-9149(14)01037-6 DE-627 ger DE-627 rakwb eng 610 610 DE-600 510 VZ 31.80 bkl Kim, Dan A. verfasserin aut Platelet Response to Serotonin in Patients With Stable Coronary Heart Disease 2014transfer abstract 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Patients with heart disease and depression have an increased mortality rate. Both behavioral and biologic factors have been proposed as potential etiologic mechanisms. Given that the pathophysiology of depression is considered to involve disruption in brain serotonergic signaling, we investigated platelet response to serotonin stimulation in patients with stable coronary artery disease (CAD). We enrolled 92 patients with stable CAD. Platelet response to increasing concentrations of serotonin (5-HT), epinephrine-augmented 5-HT, and adenosine diphosphate (ADP) was measured by optical aggregation and flow cytometry. As concentrations of 5-HT and ADP increased, so did the activation and aggregation of the platelets. However, on addition of the highest concentration of 5-HT (30 μM), a significant decrease in platelet activation (p = 0.005) was detected by flow cytometry. This contrasts the increase in platelet activation seen with the addition of the highest concentration of ADP. In conclusion, we found increased platelet activation and aggregation with increased concentrations of ADP; however, when platelets are stimulated with a high concentration of 5-HT (30 μM), there is decreased platelet activation. The data demonstrate unique patterns of platelet activation by 5-HT in patients with stable CAD. The cause of this phenomenon is unclear. Our study sheds light on the in vitro response of platelet function to serotonin in patients with stable CAD, which may further the mechanistic understanding of heart disease and depression. Patients with heart disease and depression have an increased mortality rate. Both behavioral and biologic factors have been proposed as potential etiologic mechanisms. Given that the pathophysiology of depression is considered to involve disruption in brain serotonergic signaling, we investigated platelet response to serotonin stimulation in patients with stable coronary artery disease (CAD). We enrolled 92 patients with stable CAD. Platelet response to increasing concentrations of serotonin (5-HT), epinephrine-augmented 5-HT, and adenosine diphosphate (ADP) was measured by optical aggregation and flow cytometry. As concentrations of 5-HT and ADP increased, so did the activation and aggregation of the platelets. However, on addition of the highest concentration of 5-HT (30 μM), a significant decrease in platelet activation (p = 0.005) was detected by flow cytometry. This contrasts the increase in platelet activation seen with the addition of the highest concentration of ADP. In conclusion, we found increased platelet activation and aggregation with increased concentrations of ADP; however, when platelets are stimulated with a high concentration of 5-HT (30 μM), there is decreased platelet activation. The data demonstrate unique patterns of platelet activation by 5-HT in patients with stable CAD. The cause of this phenomenon is unclear. Our study sheds light on the in vitro response of platelet function to serotonin in patients with stable CAD, which may further the mechanistic understanding of heart disease and depression. McClure, Willie G. oth Neighoff, Jordan B. oth Vaidya, Dhananjay oth Williams, Marlene S. oth Enthalten in Elsevier Zhang, Meng ELSEVIER PI simultaneous stabilization and set-point output regulation of Port-Hamiltonian systems 2017 official journal of the American College of Cardiology Amsterdam [u.a.] (DE-627)ELV000623679 volume:114 year:2014 number:2 day:15 month:07 pages:181-186 extent:6 https://doi.org/10.1016/j.amjcard.2014.04.023 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-MAT 31.80 Angewandte Mathematik VZ AR 114 2014 2 15 0715 181-186 6 045F 610 |
spelling |
10.1016/j.amjcard.2014.04.023 doi GBVA2014019000017.pica (DE-627)ELV01792877X (ELSEVIER)S0002-9149(14)01037-6 DE-627 ger DE-627 rakwb eng 610 610 DE-600 510 VZ 31.80 bkl Kim, Dan A. verfasserin aut Platelet Response to Serotonin in Patients With Stable Coronary Heart Disease 2014transfer abstract 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Patients with heart disease and depression have an increased mortality rate. Both behavioral and biologic factors have been proposed as potential etiologic mechanisms. Given that the pathophysiology of depression is considered to involve disruption in brain serotonergic signaling, we investigated platelet response to serotonin stimulation in patients with stable coronary artery disease (CAD). We enrolled 92 patients with stable CAD. Platelet response to increasing concentrations of serotonin (5-HT), epinephrine-augmented 5-HT, and adenosine diphosphate (ADP) was measured by optical aggregation and flow cytometry. As concentrations of 5-HT and ADP increased, so did the activation and aggregation of the platelets. However, on addition of the highest concentration of 5-HT (30 μM), a significant decrease in platelet activation (p = 0.005) was detected by flow cytometry. This contrasts the increase in platelet activation seen with the addition of the highest concentration of ADP. In conclusion, we found increased platelet activation and aggregation with increased concentrations of ADP; however, when platelets are stimulated with a high concentration of 5-HT (30 μM), there is decreased platelet activation. The data demonstrate unique patterns of platelet activation by 5-HT in patients with stable CAD. The cause of this phenomenon is unclear. Our study sheds light on the in vitro response of platelet function to serotonin in patients with stable CAD, which may further the mechanistic understanding of heart disease and depression. Patients with heart disease and depression have an increased mortality rate. Both behavioral and biologic factors have been proposed as potential etiologic mechanisms. Given that the pathophysiology of depression is considered to involve disruption in brain serotonergic signaling, we investigated platelet response to serotonin stimulation in patients with stable coronary artery disease (CAD). We enrolled 92 patients with stable CAD. Platelet response to increasing concentrations of serotonin (5-HT), epinephrine-augmented 5-HT, and adenosine diphosphate (ADP) was measured by optical aggregation and flow cytometry. As concentrations of 5-HT and ADP increased, so did the activation and aggregation of the platelets. However, on addition of the highest concentration of 5-HT (30 μM), a significant decrease in platelet activation (p = 0.005) was detected by flow cytometry. This contrasts the increase in platelet activation seen with the addition of the highest concentration of ADP. In conclusion, we found increased platelet activation and aggregation with increased concentrations of ADP; however, when platelets are stimulated with a high concentration of 5-HT (30 μM), there is decreased platelet activation. The data demonstrate unique patterns of platelet activation by 5-HT in patients with stable CAD. The cause of this phenomenon is unclear. Our study sheds light on the in vitro response of platelet function to serotonin in patients with stable CAD, which may further the mechanistic understanding of heart disease and depression. McClure, Willie G. oth Neighoff, Jordan B. oth Vaidya, Dhananjay oth Williams, Marlene S. oth Enthalten in Elsevier Zhang, Meng ELSEVIER PI simultaneous stabilization and set-point output regulation of Port-Hamiltonian systems 2017 official journal of the American College of Cardiology Amsterdam [u.a.] (DE-627)ELV000623679 volume:114 year:2014 number:2 day:15 month:07 pages:181-186 extent:6 https://doi.org/10.1016/j.amjcard.2014.04.023 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-MAT 31.80 Angewandte Mathematik VZ AR 114 2014 2 15 0715 181-186 6 045F 610 |
allfields_unstemmed |
10.1016/j.amjcard.2014.04.023 doi GBVA2014019000017.pica (DE-627)ELV01792877X (ELSEVIER)S0002-9149(14)01037-6 DE-627 ger DE-627 rakwb eng 610 610 DE-600 510 VZ 31.80 bkl Kim, Dan A. verfasserin aut Platelet Response to Serotonin in Patients With Stable Coronary Heart Disease 2014transfer abstract 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Patients with heart disease and depression have an increased mortality rate. Both behavioral and biologic factors have been proposed as potential etiologic mechanisms. Given that the pathophysiology of depression is considered to involve disruption in brain serotonergic signaling, we investigated platelet response to serotonin stimulation in patients with stable coronary artery disease (CAD). We enrolled 92 patients with stable CAD. Platelet response to increasing concentrations of serotonin (5-HT), epinephrine-augmented 5-HT, and adenosine diphosphate (ADP) was measured by optical aggregation and flow cytometry. As concentrations of 5-HT and ADP increased, so did the activation and aggregation of the platelets. However, on addition of the highest concentration of 5-HT (30 μM), a significant decrease in platelet activation (p = 0.005) was detected by flow cytometry. This contrasts the increase in platelet activation seen with the addition of the highest concentration of ADP. In conclusion, we found increased platelet activation and aggregation with increased concentrations of ADP; however, when platelets are stimulated with a high concentration of 5-HT (30 μM), there is decreased platelet activation. The data demonstrate unique patterns of platelet activation by 5-HT in patients with stable CAD. The cause of this phenomenon is unclear. Our study sheds light on the in vitro response of platelet function to serotonin in patients with stable CAD, which may further the mechanistic understanding of heart disease and depression. Patients with heart disease and depression have an increased mortality rate. Both behavioral and biologic factors have been proposed as potential etiologic mechanisms. Given that the pathophysiology of depression is considered to involve disruption in brain serotonergic signaling, we investigated platelet response to serotonin stimulation in patients with stable coronary artery disease (CAD). We enrolled 92 patients with stable CAD. Platelet response to increasing concentrations of serotonin (5-HT), epinephrine-augmented 5-HT, and adenosine diphosphate (ADP) was measured by optical aggregation and flow cytometry. As concentrations of 5-HT and ADP increased, so did the activation and aggregation of the platelets. However, on addition of the highest concentration of 5-HT (30 μM), a significant decrease in platelet activation (p = 0.005) was detected by flow cytometry. This contrasts the increase in platelet activation seen with the addition of the highest concentration of ADP. In conclusion, we found increased platelet activation and aggregation with increased concentrations of ADP; however, when platelets are stimulated with a high concentration of 5-HT (30 μM), there is decreased platelet activation. The data demonstrate unique patterns of platelet activation by 5-HT in patients with stable CAD. The cause of this phenomenon is unclear. Our study sheds light on the in vitro response of platelet function to serotonin in patients with stable CAD, which may further the mechanistic understanding of heart disease and depression. McClure, Willie G. oth Neighoff, Jordan B. oth Vaidya, Dhananjay oth Williams, Marlene S. oth Enthalten in Elsevier Zhang, Meng ELSEVIER PI simultaneous stabilization and set-point output regulation of Port-Hamiltonian systems 2017 official journal of the American College of Cardiology Amsterdam [u.a.] (DE-627)ELV000623679 volume:114 year:2014 number:2 day:15 month:07 pages:181-186 extent:6 https://doi.org/10.1016/j.amjcard.2014.04.023 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-MAT 31.80 Angewandte Mathematik VZ AR 114 2014 2 15 0715 181-186 6 045F 610 |
allfieldsGer |
10.1016/j.amjcard.2014.04.023 doi GBVA2014019000017.pica (DE-627)ELV01792877X (ELSEVIER)S0002-9149(14)01037-6 DE-627 ger DE-627 rakwb eng 610 610 DE-600 510 VZ 31.80 bkl Kim, Dan A. verfasserin aut Platelet Response to Serotonin in Patients With Stable Coronary Heart Disease 2014transfer abstract 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Patients with heart disease and depression have an increased mortality rate. Both behavioral and biologic factors have been proposed as potential etiologic mechanisms. Given that the pathophysiology of depression is considered to involve disruption in brain serotonergic signaling, we investigated platelet response to serotonin stimulation in patients with stable coronary artery disease (CAD). We enrolled 92 patients with stable CAD. Platelet response to increasing concentrations of serotonin (5-HT), epinephrine-augmented 5-HT, and adenosine diphosphate (ADP) was measured by optical aggregation and flow cytometry. As concentrations of 5-HT and ADP increased, so did the activation and aggregation of the platelets. However, on addition of the highest concentration of 5-HT (30 μM), a significant decrease in platelet activation (p = 0.005) was detected by flow cytometry. This contrasts the increase in platelet activation seen with the addition of the highest concentration of ADP. In conclusion, we found increased platelet activation and aggregation with increased concentrations of ADP; however, when platelets are stimulated with a high concentration of 5-HT (30 μM), there is decreased platelet activation. The data demonstrate unique patterns of platelet activation by 5-HT in patients with stable CAD. The cause of this phenomenon is unclear. Our study sheds light on the in vitro response of platelet function to serotonin in patients with stable CAD, which may further the mechanistic understanding of heart disease and depression. Patients with heart disease and depression have an increased mortality rate. Both behavioral and biologic factors have been proposed as potential etiologic mechanisms. Given that the pathophysiology of depression is considered to involve disruption in brain serotonergic signaling, we investigated platelet response to serotonin stimulation in patients with stable coronary artery disease (CAD). We enrolled 92 patients with stable CAD. Platelet response to increasing concentrations of serotonin (5-HT), epinephrine-augmented 5-HT, and adenosine diphosphate (ADP) was measured by optical aggregation and flow cytometry. As concentrations of 5-HT and ADP increased, so did the activation and aggregation of the platelets. However, on addition of the highest concentration of 5-HT (30 μM), a significant decrease in platelet activation (p = 0.005) was detected by flow cytometry. This contrasts the increase in platelet activation seen with the addition of the highest concentration of ADP. In conclusion, we found increased platelet activation and aggregation with increased concentrations of ADP; however, when platelets are stimulated with a high concentration of 5-HT (30 μM), there is decreased platelet activation. The data demonstrate unique patterns of platelet activation by 5-HT in patients with stable CAD. The cause of this phenomenon is unclear. Our study sheds light on the in vitro response of platelet function to serotonin in patients with stable CAD, which may further the mechanistic understanding of heart disease and depression. McClure, Willie G. oth Neighoff, Jordan B. oth Vaidya, Dhananjay oth Williams, Marlene S. oth Enthalten in Elsevier Zhang, Meng ELSEVIER PI simultaneous stabilization and set-point output regulation of Port-Hamiltonian systems 2017 official journal of the American College of Cardiology Amsterdam [u.a.] (DE-627)ELV000623679 volume:114 year:2014 number:2 day:15 month:07 pages:181-186 extent:6 https://doi.org/10.1016/j.amjcard.2014.04.023 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-MAT 31.80 Angewandte Mathematik VZ AR 114 2014 2 15 0715 181-186 6 045F 610 |
allfieldsSound |
10.1016/j.amjcard.2014.04.023 doi GBVA2014019000017.pica (DE-627)ELV01792877X (ELSEVIER)S0002-9149(14)01037-6 DE-627 ger DE-627 rakwb eng 610 610 DE-600 510 VZ 31.80 bkl Kim, Dan A. verfasserin aut Platelet Response to Serotonin in Patients With Stable Coronary Heart Disease 2014transfer abstract 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Patients with heart disease and depression have an increased mortality rate. Both behavioral and biologic factors have been proposed as potential etiologic mechanisms. Given that the pathophysiology of depression is considered to involve disruption in brain serotonergic signaling, we investigated platelet response to serotonin stimulation in patients with stable coronary artery disease (CAD). We enrolled 92 patients with stable CAD. Platelet response to increasing concentrations of serotonin (5-HT), epinephrine-augmented 5-HT, and adenosine diphosphate (ADP) was measured by optical aggregation and flow cytometry. As concentrations of 5-HT and ADP increased, so did the activation and aggregation of the platelets. However, on addition of the highest concentration of 5-HT (30 μM), a significant decrease in platelet activation (p = 0.005) was detected by flow cytometry. This contrasts the increase in platelet activation seen with the addition of the highest concentration of ADP. In conclusion, we found increased platelet activation and aggregation with increased concentrations of ADP; however, when platelets are stimulated with a high concentration of 5-HT (30 μM), there is decreased platelet activation. The data demonstrate unique patterns of platelet activation by 5-HT in patients with stable CAD. The cause of this phenomenon is unclear. Our study sheds light on the in vitro response of platelet function to serotonin in patients with stable CAD, which may further the mechanistic understanding of heart disease and depression. Patients with heart disease and depression have an increased mortality rate. Both behavioral and biologic factors have been proposed as potential etiologic mechanisms. Given that the pathophysiology of depression is considered to involve disruption in brain serotonergic signaling, we investigated platelet response to serotonin stimulation in patients with stable coronary artery disease (CAD). We enrolled 92 patients with stable CAD. Platelet response to increasing concentrations of serotonin (5-HT), epinephrine-augmented 5-HT, and adenosine diphosphate (ADP) was measured by optical aggregation and flow cytometry. As concentrations of 5-HT and ADP increased, so did the activation and aggregation of the platelets. However, on addition of the highest concentration of 5-HT (30 μM), a significant decrease in platelet activation (p = 0.005) was detected by flow cytometry. This contrasts the increase in platelet activation seen with the addition of the highest concentration of ADP. In conclusion, we found increased platelet activation and aggregation with increased concentrations of ADP; however, when platelets are stimulated with a high concentration of 5-HT (30 μM), there is decreased platelet activation. The data demonstrate unique patterns of platelet activation by 5-HT in patients with stable CAD. The cause of this phenomenon is unclear. Our study sheds light on the in vitro response of platelet function to serotonin in patients with stable CAD, which may further the mechanistic understanding of heart disease and depression. McClure, Willie G. oth Neighoff, Jordan B. oth Vaidya, Dhananjay oth Williams, Marlene S. oth Enthalten in Elsevier Zhang, Meng ELSEVIER PI simultaneous stabilization and set-point output regulation of Port-Hamiltonian systems 2017 official journal of the American College of Cardiology Amsterdam [u.a.] (DE-627)ELV000623679 volume:114 year:2014 number:2 day:15 month:07 pages:181-186 extent:6 https://doi.org/10.1016/j.amjcard.2014.04.023 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-MAT 31.80 Angewandte Mathematik VZ AR 114 2014 2 15 0715 181-186 6 045F 610 |
language |
English |
source |
Enthalten in PI simultaneous stabilization and set-point output regulation of Port-Hamiltonian systems Amsterdam [u.a.] volume:114 year:2014 number:2 day:15 month:07 pages:181-186 extent:6 |
sourceStr |
Enthalten in PI simultaneous stabilization and set-point output regulation of Port-Hamiltonian systems Amsterdam [u.a.] volume:114 year:2014 number:2 day:15 month:07 pages:181-186 extent:6 |
format_phy_str_mv |
Article |
bklname |
Angewandte Mathematik |
institution |
findex.gbv.de |
dewey-raw |
610 |
isfreeaccess_bool |
false |
container_title |
PI simultaneous stabilization and set-point output regulation of Port-Hamiltonian systems |
authorswithroles_txt_mv |
Kim, Dan A. @@aut@@ McClure, Willie G. @@oth@@ Neighoff, Jordan B. @@oth@@ Vaidya, Dhananjay @@oth@@ Williams, Marlene S. @@oth@@ |
publishDateDaySort_date |
2014-01-15T00:00:00Z |
hierarchy_top_id |
ELV000623679 |
dewey-sort |
3610 |
id |
ELV01792877X |
language_de |
englisch |
fullrecord |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV01792877X</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230625123049.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180602s2014 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.amjcard.2014.04.023</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBVA2014019000017.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV01792877X</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S0002-9149(14)01037-6</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2=" "><subfield code="a">610</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">510</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">31.80</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Kim, Dan A.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Platelet Response to Serotonin in Patients With Stable Coronary Heart Disease</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2014transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">6</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Patients with heart disease and depression have an increased mortality rate. Both behavioral and biologic factors have been proposed as potential etiologic mechanisms. Given that the pathophysiology of depression is considered to involve disruption in brain serotonergic signaling, we investigated platelet response to serotonin stimulation in patients with stable coronary artery disease (CAD). We enrolled 92 patients with stable CAD. Platelet response to increasing concentrations of serotonin (5-HT), epinephrine-augmented 5-HT, and adenosine diphosphate (ADP) was measured by optical aggregation and flow cytometry. As concentrations of 5-HT and ADP increased, so did the activation and aggregation of the platelets. However, on addition of the highest concentration of 5-HT (30 μM), a significant decrease in platelet activation (p = 0.005) was detected by flow cytometry. This contrasts the increase in platelet activation seen with the addition of the highest concentration of ADP. In conclusion, we found increased platelet activation and aggregation with increased concentrations of ADP; however, when platelets are stimulated with a high concentration of 5-HT (30 μM), there is decreased platelet activation. The data demonstrate unique patterns of platelet activation by 5-HT in patients with stable CAD. The cause of this phenomenon is unclear. Our study sheds light on the in vitro response of platelet function to serotonin in patients with stable CAD, which may further the mechanistic understanding of heart disease and depression.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Patients with heart disease and depression have an increased mortality rate. Both behavioral and biologic factors have been proposed as potential etiologic mechanisms. Given that the pathophysiology of depression is considered to involve disruption in brain serotonergic signaling, we investigated platelet response to serotonin stimulation in patients with stable coronary artery disease (CAD). We enrolled 92 patients with stable CAD. Platelet response to increasing concentrations of serotonin (5-HT), epinephrine-augmented 5-HT, and adenosine diphosphate (ADP) was measured by optical aggregation and flow cytometry. As concentrations of 5-HT and ADP increased, so did the activation and aggregation of the platelets. However, on addition of the highest concentration of 5-HT (30 μM), a significant decrease in platelet activation (p = 0.005) was detected by flow cytometry. This contrasts the increase in platelet activation seen with the addition of the highest concentration of ADP. In conclusion, we found increased platelet activation and aggregation with increased concentrations of ADP; however, when platelets are stimulated with a high concentration of 5-HT (30 μM), there is decreased platelet activation. The data demonstrate unique patterns of platelet activation by 5-HT in patients with stable CAD. The cause of this phenomenon is unclear. Our study sheds light on the in vitro response of platelet function to serotonin in patients with stable CAD, which may further the mechanistic understanding of heart disease and depression.</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">McClure, Willie G.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Neighoff, Jordan B.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Vaidya, Dhananjay</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Williams, Marlene S.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier</subfield><subfield code="a">Zhang, Meng ELSEVIER</subfield><subfield code="t">PI simultaneous stabilization and set-point output regulation of Port-Hamiltonian systems</subfield><subfield code="d">2017</subfield><subfield code="d">official journal of the American College of Cardiology</subfield><subfield code="g">Amsterdam [u.a.]</subfield><subfield code="w">(DE-627)ELV000623679</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:114</subfield><subfield code="g">year:2014</subfield><subfield code="g">number:2</subfield><subfield code="g">day:15</subfield><subfield code="g">month:07</subfield><subfield code="g">pages:181-186</subfield><subfield code="g">extent:6</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.amjcard.2014.04.023</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OPC-MAT</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">31.80</subfield><subfield code="j">Angewandte Mathematik</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">114</subfield><subfield code="j">2014</subfield><subfield code="e">2</subfield><subfield code="b">15</subfield><subfield code="c">0715</subfield><subfield code="h">181-186</subfield><subfield code="g">6</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">610</subfield></datafield></record></collection>
|
author |
Kim, Dan A. |
spellingShingle |
Kim, Dan A. ddc 610 ddc 510 bkl 31.80 Platelet Response to Serotonin in Patients With Stable Coronary Heart Disease |
authorStr |
Kim, Dan A. |
ppnlink_with_tag_str_mv |
@@773@@(DE-627)ELV000623679 |
format |
electronic Article |
dewey-ones |
610 - Medicine & health 510 - Mathematics |
delete_txt_mv |
keep |
author_role |
aut |
collection |
elsevier |
remote_str |
true |
illustrated |
Not Illustrated |
topic_title |
610 610 DE-600 510 VZ 31.80 bkl Platelet Response to Serotonin in Patients With Stable Coronary Heart Disease |
topic |
ddc 610 ddc 510 bkl 31.80 |
topic_unstemmed |
ddc 610 ddc 510 bkl 31.80 |
topic_browse |
ddc 610 ddc 510 bkl 31.80 |
format_facet |
Elektronische Aufsätze Aufsätze Elektronische Ressource |
format_main_str_mv |
Text Zeitschrift/Artikel |
carriertype_str_mv |
zu |
author2_variant |
w g m wg wgm j b n jb jbn d v dv m s w ms msw |
hierarchy_parent_title |
PI simultaneous stabilization and set-point output regulation of Port-Hamiltonian systems |
hierarchy_parent_id |
ELV000623679 |
dewey-tens |
610 - Medicine & health 510 - Mathematics |
hierarchy_top_title |
PI simultaneous stabilization and set-point output regulation of Port-Hamiltonian systems |
isfreeaccess_txt |
false |
familylinks_str_mv |
(DE-627)ELV000623679 |
title |
Platelet Response to Serotonin in Patients With Stable Coronary Heart Disease |
ctrlnum |
(DE-627)ELV01792877X (ELSEVIER)S0002-9149(14)01037-6 |
title_full |
Platelet Response to Serotonin in Patients With Stable Coronary Heart Disease |
author_sort |
Kim, Dan A. |
journal |
PI simultaneous stabilization and set-point output regulation of Port-Hamiltonian systems |
journalStr |
PI simultaneous stabilization and set-point output regulation of Port-Hamiltonian systems |
lang_code |
eng |
isOA_bool |
false |
dewey-hundreds |
600 - Technology 500 - Science |
recordtype |
marc |
publishDateSort |
2014 |
contenttype_str_mv |
zzz |
container_start_page |
181 |
author_browse |
Kim, Dan A. |
container_volume |
114 |
physical |
6 |
class |
610 610 DE-600 510 VZ 31.80 bkl |
format_se |
Elektronische Aufsätze |
author-letter |
Kim, Dan A. |
doi_str_mv |
10.1016/j.amjcard.2014.04.023 |
dewey-full |
610 510 |
title_sort |
platelet response to serotonin in patients with stable coronary heart disease |
title_auth |
Platelet Response to Serotonin in Patients With Stable Coronary Heart Disease |
abstract |
Patients with heart disease and depression have an increased mortality rate. Both behavioral and biologic factors have been proposed as potential etiologic mechanisms. Given that the pathophysiology of depression is considered to involve disruption in brain serotonergic signaling, we investigated platelet response to serotonin stimulation in patients with stable coronary artery disease (CAD). We enrolled 92 patients with stable CAD. Platelet response to increasing concentrations of serotonin (5-HT), epinephrine-augmented 5-HT, and adenosine diphosphate (ADP) was measured by optical aggregation and flow cytometry. As concentrations of 5-HT and ADP increased, so did the activation and aggregation of the platelets. However, on addition of the highest concentration of 5-HT (30 μM), a significant decrease in platelet activation (p = 0.005) was detected by flow cytometry. This contrasts the increase in platelet activation seen with the addition of the highest concentration of ADP. In conclusion, we found increased platelet activation and aggregation with increased concentrations of ADP; however, when platelets are stimulated with a high concentration of 5-HT (30 μM), there is decreased platelet activation. The data demonstrate unique patterns of platelet activation by 5-HT in patients with stable CAD. The cause of this phenomenon is unclear. Our study sheds light on the in vitro response of platelet function to serotonin in patients with stable CAD, which may further the mechanistic understanding of heart disease and depression. |
abstractGer |
Patients with heart disease and depression have an increased mortality rate. Both behavioral and biologic factors have been proposed as potential etiologic mechanisms. Given that the pathophysiology of depression is considered to involve disruption in brain serotonergic signaling, we investigated platelet response to serotonin stimulation in patients with stable coronary artery disease (CAD). We enrolled 92 patients with stable CAD. Platelet response to increasing concentrations of serotonin (5-HT), epinephrine-augmented 5-HT, and adenosine diphosphate (ADP) was measured by optical aggregation and flow cytometry. As concentrations of 5-HT and ADP increased, so did the activation and aggregation of the platelets. However, on addition of the highest concentration of 5-HT (30 μM), a significant decrease in platelet activation (p = 0.005) was detected by flow cytometry. This contrasts the increase in platelet activation seen with the addition of the highest concentration of ADP. In conclusion, we found increased platelet activation and aggregation with increased concentrations of ADP; however, when platelets are stimulated with a high concentration of 5-HT (30 μM), there is decreased platelet activation. The data demonstrate unique patterns of platelet activation by 5-HT in patients with stable CAD. The cause of this phenomenon is unclear. Our study sheds light on the in vitro response of platelet function to serotonin in patients with stable CAD, which may further the mechanistic understanding of heart disease and depression. |
abstract_unstemmed |
Patients with heart disease and depression have an increased mortality rate. Both behavioral and biologic factors have been proposed as potential etiologic mechanisms. Given that the pathophysiology of depression is considered to involve disruption in brain serotonergic signaling, we investigated platelet response to serotonin stimulation in patients with stable coronary artery disease (CAD). We enrolled 92 patients with stable CAD. Platelet response to increasing concentrations of serotonin (5-HT), epinephrine-augmented 5-HT, and adenosine diphosphate (ADP) was measured by optical aggregation and flow cytometry. As concentrations of 5-HT and ADP increased, so did the activation and aggregation of the platelets. However, on addition of the highest concentration of 5-HT (30 μM), a significant decrease in platelet activation (p = 0.005) was detected by flow cytometry. This contrasts the increase in platelet activation seen with the addition of the highest concentration of ADP. In conclusion, we found increased platelet activation and aggregation with increased concentrations of ADP; however, when platelets are stimulated with a high concentration of 5-HT (30 μM), there is decreased platelet activation. The data demonstrate unique patterns of platelet activation by 5-HT in patients with stable CAD. The cause of this phenomenon is unclear. Our study sheds light on the in vitro response of platelet function to serotonin in patients with stable CAD, which may further the mechanistic understanding of heart disease and depression. |
collection_details |
GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-MAT |
container_issue |
2 |
title_short |
Platelet Response to Serotonin in Patients With Stable Coronary Heart Disease |
url |
https://doi.org/10.1016/j.amjcard.2014.04.023 |
remote_bool |
true |
author2 |
McClure, Willie G. Neighoff, Jordan B. Vaidya, Dhananjay Williams, Marlene S. |
author2Str |
McClure, Willie G. Neighoff, Jordan B. Vaidya, Dhananjay Williams, Marlene S. |
ppnlink |
ELV000623679 |
mediatype_str_mv |
z |
isOA_txt |
false |
hochschulschrift_bool |
false |
author2_role |
oth oth oth oth |
doi_str |
10.1016/j.amjcard.2014.04.023 |
up_date |
2024-07-06T17:32:46.197Z |
_version_ |
1803851835584282624 |
fullrecord_marcxml |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV01792877X</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230625123049.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180602s2014 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.amjcard.2014.04.023</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBVA2014019000017.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV01792877X</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S0002-9149(14)01037-6</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2=" "><subfield code="a">610</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">510</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">31.80</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Kim, Dan A.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Platelet Response to Serotonin in Patients With Stable Coronary Heart Disease</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2014transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">6</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Patients with heart disease and depression have an increased mortality rate. Both behavioral and biologic factors have been proposed as potential etiologic mechanisms. Given that the pathophysiology of depression is considered to involve disruption in brain serotonergic signaling, we investigated platelet response to serotonin stimulation in patients with stable coronary artery disease (CAD). We enrolled 92 patients with stable CAD. Platelet response to increasing concentrations of serotonin (5-HT), epinephrine-augmented 5-HT, and adenosine diphosphate (ADP) was measured by optical aggregation and flow cytometry. As concentrations of 5-HT and ADP increased, so did the activation and aggregation of the platelets. However, on addition of the highest concentration of 5-HT (30 μM), a significant decrease in platelet activation (p = 0.005) was detected by flow cytometry. This contrasts the increase in platelet activation seen with the addition of the highest concentration of ADP. In conclusion, we found increased platelet activation and aggregation with increased concentrations of ADP; however, when platelets are stimulated with a high concentration of 5-HT (30 μM), there is decreased platelet activation. The data demonstrate unique patterns of platelet activation by 5-HT in patients with stable CAD. The cause of this phenomenon is unclear. Our study sheds light on the in vitro response of platelet function to serotonin in patients with stable CAD, which may further the mechanistic understanding of heart disease and depression.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Patients with heart disease and depression have an increased mortality rate. Both behavioral and biologic factors have been proposed as potential etiologic mechanisms. Given that the pathophysiology of depression is considered to involve disruption in brain serotonergic signaling, we investigated platelet response to serotonin stimulation in patients with stable coronary artery disease (CAD). We enrolled 92 patients with stable CAD. Platelet response to increasing concentrations of serotonin (5-HT), epinephrine-augmented 5-HT, and adenosine diphosphate (ADP) was measured by optical aggregation and flow cytometry. As concentrations of 5-HT and ADP increased, so did the activation and aggregation of the platelets. However, on addition of the highest concentration of 5-HT (30 μM), a significant decrease in platelet activation (p = 0.005) was detected by flow cytometry. This contrasts the increase in platelet activation seen with the addition of the highest concentration of ADP. In conclusion, we found increased platelet activation and aggregation with increased concentrations of ADP; however, when platelets are stimulated with a high concentration of 5-HT (30 μM), there is decreased platelet activation. The data demonstrate unique patterns of platelet activation by 5-HT in patients with stable CAD. The cause of this phenomenon is unclear. Our study sheds light on the in vitro response of platelet function to serotonin in patients with stable CAD, which may further the mechanistic understanding of heart disease and depression.</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">McClure, Willie G.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Neighoff, Jordan B.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Vaidya, Dhananjay</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Williams, Marlene S.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier</subfield><subfield code="a">Zhang, Meng ELSEVIER</subfield><subfield code="t">PI simultaneous stabilization and set-point output regulation of Port-Hamiltonian systems</subfield><subfield code="d">2017</subfield><subfield code="d">official journal of the American College of Cardiology</subfield><subfield code="g">Amsterdam [u.a.]</subfield><subfield code="w">(DE-627)ELV000623679</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:114</subfield><subfield code="g">year:2014</subfield><subfield code="g">number:2</subfield><subfield code="g">day:15</subfield><subfield code="g">month:07</subfield><subfield code="g">pages:181-186</subfield><subfield code="g">extent:6</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.amjcard.2014.04.023</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OPC-MAT</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">31.80</subfield><subfield code="j">Angewandte Mathematik</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">114</subfield><subfield code="j">2014</subfield><subfield code="e">2</subfield><subfield code="b">15</subfield><subfield code="c">0715</subfield><subfield code="h">181-186</subfield><subfield code="g">6</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">610</subfield></datafield></record></collection>
|
score |
7.397807 |