Putniković, Biljana

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  • Putniković, Biljana (7)
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Author's Bibliography

Influence of glycaemia and HbA1C levels at admission of insulin-independent diabetes patients on the length and outcome of hospitalization due to NSTEMI/STEMI

Kovačević, Pejka; Gluvić, Zoran; Putniković, Biljana; Zarić, Božidarka; Radenković, Saša; Resanović, Ivana; Isenović, Esma R.

(2018)

TY  - JOUR
AU  - Kovačević, Pejka
AU  - Gluvić, Zoran
AU  - Putniković, Biljana
AU  - Zarić, Božidarka
AU  - Radenković, Saša
AU  - Resanović, Ivana
AU  - Isenović, Esma R.
PY  - 2018
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10155
AB  - This study aims to examine the influence of admission glycaemia and glycosylated haemoglobin (HbA1C) levels on the length of hospitalization and its outcome in insulin-independent diabetes mellitus (DM) patients suffering from ST-Segment Elevation Myocardial Infarction (STEMI)/Non-STEMI (NSTEMI). This cross-sectional study included 103 subjects with a history of insulin-independent DM, currently hospitalized due to acute myocardial infarction (AMI). Out of 103 subjects, 59 (57%) were men and 66 (64.1%) of them suffered from STEMI. Mean age of study population was 67±9 years. The following parameters were monitored: demographic, coronary, cardiovascular and DM risk factors history, as well as laboratory, clinical, echocardiography and angiography parameters. DM mean duration was 7 (1-30) months, and it influenced the length of hospitalization (r=0.232, p<0.05), but not the outcome (r=0.174, p>0.05). Mean length of hospitalization was 8 and 8.5 days in STEMI and NSTEMI patients respectively, with no difference between groups (log-rank ch2= 0.476, p>0.05). HbA1C values influenced the length of hospitalization (r=0.213, p<0.05), opposite to admission glycaemia (r=0.148, p>0.05). Duration of DM and the level of HbA1C prolong the length of hospitalization, but do not influence the clinical outcome of AMI patients suffering from insulin-independent DM.
AB  - Cilj prikazane studije je izučavanje uticaja glikemije i glikoziliranog hemoglobina (HbA1C) pri prijemu u bolnicu na dužinu trajanja hospitalizacije, kao i njen ishod kod kod obolelih od insulin-nezavisnog dijabetesa sa NSTEMI/STEMI. Materijal i metode: Ova studija je uključila 103 ispitanika, od kojih su 59 (57%) ispitanici muškog pola, a 66 (64.1%) ispitanika imalo STEMI. Prosečna životna dob ispitivane populacije je bila 67±9 godina. Praćeni su sledeći parametri: demografske karakteristike, anamneza o koronarnim, kardiovaskularnim i rizičnim faktorima za dijabetes, kao i laboratorijski, klinički, ehokardiografski parametri. Rezultati: Prosečno trajanje dijabetesa kod osoba uključenih u studiju je bilo 7 (1-30) meseci i imalo je uticaj na dužinu hospitalizacije (r=0.232, p<0.05), ali ne i na njen krajnji ishod (r=0.174, p>0.05). Prosečno trajanje hospitalizacije je bilo 8 i 8.5 dana kod ispitanika sa STEMI i NSTEMI i nije se razlikovalo među grupama ispitanika (log-rank ch2= 0.476, p>0.05). Nivoi HbA1C su uticali na dužinu trajanja hospitalizacije (r=0.213, p<0.05), što nije bio slučaj sa glikemijom pri prijemu u bolnicu (r=0.148, p>0.05). Zaključak: Dužina trajanja DM i nivo HbA1C produžavaju dužinu hospitalizacije, ali ne utiču na klinički ishod ispitanika sa insulin-nezavisnim dijabetesom koji su doživeli AIM.
T2  - Medicinska istraživanja
T1  - Influence of glycaemia and HbA1C levels at admission of insulin-independent diabetes patients on the length and outcome of hospitalization due to NSTEMI/STEMI
T1  - Uticaj glikemije i nivoa HbA1C na prijemu na dužinu i ishod hospitalizacije kod obolelih od insulin-nezavisnog dijabetesa sa NSTEMI/STEMI
VL  - 52
IS  - 3
SP  - 1
EP  - 6
DO  - 10.5937/MedIst1801001K
ER  - 
@article{
author = "Kovačević, Pejka and Gluvić, Zoran and Putniković, Biljana and Zarić, Božidarka and Radenković, Saša and Resanović, Ivana and Isenović, Esma R.",
year = "2018",
abstract = "This study aims to examine the influence of admission glycaemia and glycosylated haemoglobin (HbA1C) levels on the length of hospitalization and its outcome in insulin-independent diabetes mellitus (DM) patients suffering from ST-Segment Elevation Myocardial Infarction (STEMI)/Non-STEMI (NSTEMI). This cross-sectional study included 103 subjects with a history of insulin-independent DM, currently hospitalized due to acute myocardial infarction (AMI). Out of 103 subjects, 59 (57%) were men and 66 (64.1%) of them suffered from STEMI. Mean age of study population was 67±9 years. The following parameters were monitored: demographic, coronary, cardiovascular and DM risk factors history, as well as laboratory, clinical, echocardiography and angiography parameters. DM mean duration was 7 (1-30) months, and it influenced the length of hospitalization (r=0.232, p<0.05), but not the outcome (r=0.174, p>0.05). Mean length of hospitalization was 8 and 8.5 days in STEMI and NSTEMI patients respectively, with no difference between groups (log-rank ch2= 0.476, p>0.05). HbA1C values influenced the length of hospitalization (r=0.213, p<0.05), opposite to admission glycaemia (r=0.148, p>0.05). Duration of DM and the level of HbA1C prolong the length of hospitalization, but do not influence the clinical outcome of AMI patients suffering from insulin-independent DM., Cilj prikazane studije je izučavanje uticaja glikemije i glikoziliranog hemoglobina (HbA1C) pri prijemu u bolnicu na dužinu trajanja hospitalizacije, kao i njen ishod kod kod obolelih od insulin-nezavisnog dijabetesa sa NSTEMI/STEMI. Materijal i metode: Ova studija je uključila 103 ispitanika, od kojih su 59 (57%) ispitanici muškog pola, a 66 (64.1%) ispitanika imalo STEMI. Prosečna životna dob ispitivane populacije je bila 67±9 godina. Praćeni su sledeći parametri: demografske karakteristike, anamneza o koronarnim, kardiovaskularnim i rizičnim faktorima za dijabetes, kao i laboratorijski, klinički, ehokardiografski parametri. Rezultati: Prosečno trajanje dijabetesa kod osoba uključenih u studiju je bilo 7 (1-30) meseci i imalo je uticaj na dužinu hospitalizacije (r=0.232, p<0.05), ali ne i na njen krajnji ishod (r=0.174, p>0.05). Prosečno trajanje hospitalizacije je bilo 8 i 8.5 dana kod ispitanika sa STEMI i NSTEMI i nije se razlikovalo među grupama ispitanika (log-rank ch2= 0.476, p>0.05). Nivoi HbA1C su uticali na dužinu trajanja hospitalizacije (r=0.213, p<0.05), što nije bio slučaj sa glikemijom pri prijemu u bolnicu (r=0.148, p>0.05). Zaključak: Dužina trajanja DM i nivo HbA1C produžavaju dužinu hospitalizacije, ali ne utiču na klinički ishod ispitanika sa insulin-nezavisnim dijabetesom koji su doživeli AIM.",
journal = "Medicinska istraživanja",
title = "Influence of glycaemia and HbA1C levels at admission of insulin-independent diabetes patients on the length and outcome of hospitalization due to NSTEMI/STEMI, Uticaj glikemije i nivoa HbA1C na prijemu na dužinu i ishod hospitalizacije kod obolelih od insulin-nezavisnog dijabetesa sa NSTEMI/STEMI",
volume = "52",
number = "3",
pages = "1-6",
doi = "10.5937/MedIst1801001K"
}
Kovačević, P., Gluvić, Z., Putniković, B., Zarić, B., Radenković, S., Resanović, I.,& Isenović, E. R.. (2018). Influence of glycaemia and HbA1C levels at admission of insulin-independent diabetes patients on the length and outcome of hospitalization due to NSTEMI/STEMI. in Medicinska istraživanja, 52(3), 1-6.
https://doi.org/10.5937/MedIst1801001K
Kovačević P, Gluvić Z, Putniković B, Zarić B, Radenković S, Resanović I, Isenović ER. Influence of glycaemia and HbA1C levels at admission of insulin-independent diabetes patients on the length and outcome of hospitalization due to NSTEMI/STEMI. in Medicinska istraživanja. 2018;52(3):1-6.
doi:10.5937/MedIst1801001K .
Kovačević, Pejka, Gluvić, Zoran, Putniković, Biljana, Zarić, Božidarka, Radenković, Saša, Resanović, Ivana, Isenović, Esma R., "Influence of glycaemia and HbA1C levels at admission of insulin-independent diabetes patients on the length and outcome of hospitalization due to NSTEMI/STEMI" in Medicinska istraživanja, 52, no. 3 (2018):1-6,
https://doi.org/10.5937/MedIst1801001K . .

Effects of beta-blocker therapy on hs-CRP levels in elderly patients with ischemic and non-ischemic heart failure: Results from the CIBIS-ELD trail

Duengen, Hans-Dirk; Putniković, Biljana; Milićević, Predrag; Radenović, Sara; Trippel, T.; Tahirović, Elvis; Von Heahling, S.; Edelmann, Frank; Pieske, B.; Isenović, Esma R.

(2016)

TY  - CONF
AU  - Duengen, Hans-Dirk
AU  - Putniković, Biljana
AU  - Milićević, Predrag
AU  - Radenović, Sara
AU  - Trippel, T.
AU  - Tahirović, Elvis
AU  - Von Heahling, S.
AU  - Edelmann, Frank
AU  - Pieske, B.
AU  - Isenović, Esma R.
PY  - 2016
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1100
C3  - European Journal of Heart Failure
T1  - Effects of beta-blocker therapy on hs-CRP levels in elderly patients with ischemic and non-ischemic heart failure: Results from the CIBIS-ELD trail
VL  - 18
IS  - SI
SP  - 106
EP  - 106
UR  - https://hdl.handle.net/21.15107/rcub_vinar_1100
ER  - 
@conference{
author = "Duengen, Hans-Dirk and Putniković, Biljana and Milićević, Predrag and Radenović, Sara and Trippel, T. and Tahirović, Elvis and Von Heahling, S. and Edelmann, Frank and Pieske, B. and Isenović, Esma R.",
year = "2016",
journal = "European Journal of Heart Failure",
title = "Effects of beta-blocker therapy on hs-CRP levels in elderly patients with ischemic and non-ischemic heart failure: Results from the CIBIS-ELD trail",
volume = "18",
number = "SI",
pages = "106-106",
url = "https://hdl.handle.net/21.15107/rcub_vinar_1100"
}
Duengen, H., Putniković, B., Milićević, P., Radenović, S., Trippel, T., Tahirović, E., Von Heahling, S., Edelmann, F., Pieske, B.,& Isenović, E. R.. (2016). Effects of beta-blocker therapy on hs-CRP levels in elderly patients with ischemic and non-ischemic heart failure: Results from the CIBIS-ELD trail. in European Journal of Heart Failure, 18(SI), 106-106.
https://hdl.handle.net/21.15107/rcub_vinar_1100
Duengen H, Putniković B, Milićević P, Radenović S, Trippel T, Tahirović E, Von Heahling S, Edelmann F, Pieske B, Isenović ER. Effects of beta-blocker therapy on hs-CRP levels in elderly patients with ischemic and non-ischemic heart failure: Results from the CIBIS-ELD trail. in European Journal of Heart Failure. 2016;18(SI):106-106.
https://hdl.handle.net/21.15107/rcub_vinar_1100 .
Duengen, Hans-Dirk, Putniković, Biljana, Milićević, Predrag, Radenović, Sara, Trippel, T., Tahirović, Elvis, Von Heahling, S., Edelmann, Frank, Pieske, B., Isenović, Esma R., "Effects of beta-blocker therapy on hs-CRP levels in elderly patients with ischemic and non-ischemic heart failure: Results from the CIBIS-ELD trail" in European Journal of Heart Failure, 18, no. SI (2016):106-106,
https://hdl.handle.net/21.15107/rcub_vinar_1100 .

Effects of beta-blocker therapy on hs-CRP levels in elderly patients with ischemic and non-ischemic heart failure: Results from the CIBIS-ELD trail

Duengen, Hans-Dirk; Putniković, Biljana; Milićević, Predrag; Tahirović, Elvis; Trippel, T.; Radenović, Sara; Vesković, Jovan; Von Haehling, Stephan; Edelmann, Frank; Wachter, Rolf; Pieske, B.; Isenović, Esma R.

(2016)

TY  - CONF
AU  - Duengen, Hans-Dirk
AU  - Putniković, Biljana
AU  - Milićević, Predrag
AU  - Tahirović, Elvis
AU  - Trippel, T.
AU  - Radenović, Sara
AU  - Vesković, Jovan
AU  - Von Haehling, Stephan
AU  - Edelmann, Frank
AU  - Wachter, Rolf
AU  - Pieske, B.
AU  - Isenović, Esma R.
PY  - 2016
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1031
AB  - C reactive protein (CRP) is a biomarker indicating systemic inflammation. Elevated levels of this biomarker are associated with increased rates of cardiovascular disease, including chronic heart failure (HF). High‐sensitivity CRP assays were developed in order to measure lower levels of CRP, down to 0.3mg/l (hs‐CRP). Up to now, very little is known about the effects of beta‐blocker titration on hs‐CRP levels in ischemic and non‐ischemic HF patients. Also, little is known if this effect differs between selective and unselective blockers. Purpose: This research explored the trajectories of hs‐CRP before and after beta‐blocker (carvedilol vs bisoprolol) titration in elderly HF patients depending on the type of beta‐blocker used and the etiology of the disease (ischemic vs non‐ischemic). Methods: We measured plasma levels of hs‐CRP and NT‐proBNP in 520 HF patients ≥ 65 years (72.06±5.24 years, 38%f, LVEF 41.8±13.8%; ischemic n=243; nonischemic n=277) of the Cardiac Insufficiency Bisoprolol Study in ELDerly (CIBIS‐ELD). In this trial, patients were randomized to bisoprolol vs. carvedilol and doses were uptitrated to the target or maximally tolerated dose. hs‐CRP and NT‐proBNP levels were assessed at baseline (BL) and at follow‐up (FU), after 12 weeks. Results: In patients with ischemic HF, hs‐CRP levels decreased in the bisoprolol group (BL=0.60±0.94 mg/ dl, n=166; FU=0.43±0.694mg/dl, n=131; p=0.010), and were without a change in the carvedilol group (BL=0.60±1.69mg/dl, n=181; FU=0.57±0.982mg/ dl, n=136; p=0.731). There was also no change of hs‐CRP levels in non‐ischemic HF patients in both groups (bisoprolol: BL=0.64±1.175 mg/dl, n=197; FU=0.470±0.81mg/dl, n=152, p=0.069; carvedilol: BL=0.45±0.78mg/dl, n=198; FU=0.41±0.701 mg/ dl, n=152, p=0.420). Plasma levels of NT‐proBNP decreased in ischemic patients treated with bisoprolol, (BL=1594±2146 pg/ml, n=169; FU=1468±2110pg/ ml, n=133, p=0.04), while changes in the carvedilol group were not significant (BL=1648±1991 pg/ml, n=188; FU=1567±2119pg/ml, n=135, p=0.556). In the non‐ischemic group NT‐pro levels did not change significantly in the carvedilol group, while there was an increase in non‐ischemic patients in the bisoprolol group (BL=1427±3113 pg/ml, n=208; FU=1533±5385 pg/ml, n=166, p=0.017). Conclusion: Results indicate that bisoprolol might be associated with a decrease of hs‐CRP and NT‐proBNP levels only in ischemic HF patients, while in nonischemic HF patients there was no change of hs‐CRP and an increase of NT‐proBNP levels. In carvedilol treated patients no significant changes were shown in neither group.
C3  - European Journal of Cardiovascular Nursing
T1  - Effects of beta-blocker therapy on hs-CRP levels in elderly patients with ischemic and non-ischemic heart failure: Results from the CIBIS-ELD trail
VL  - 15
SP  - S21
EP  - S21
DO  - 10.1177/1474515116634263
ER  - 
@conference{
author = "Duengen, Hans-Dirk and Putniković, Biljana and Milićević, Predrag and Tahirović, Elvis and Trippel, T. and Radenović, Sara and Vesković, Jovan and Von Haehling, Stephan and Edelmann, Frank and Wachter, Rolf and Pieske, B. and Isenović, Esma R.",
year = "2016",
abstract = "C reactive protein (CRP) is a biomarker indicating systemic inflammation. Elevated levels of this biomarker are associated with increased rates of cardiovascular disease, including chronic heart failure (HF). High‐sensitivity CRP assays were developed in order to measure lower levels of CRP, down to 0.3mg/l (hs‐CRP). Up to now, very little is known about the effects of beta‐blocker titration on hs‐CRP levels in ischemic and non‐ischemic HF patients. Also, little is known if this effect differs between selective and unselective blockers. Purpose: This research explored the trajectories of hs‐CRP before and after beta‐blocker (carvedilol vs bisoprolol) titration in elderly HF patients depending on the type of beta‐blocker used and the etiology of the disease (ischemic vs non‐ischemic). Methods: We measured plasma levels of hs‐CRP and NT‐proBNP in 520 HF patients ≥ 65 years (72.06±5.24 years, 38%f, LVEF 41.8±13.8%; ischemic n=243; nonischemic n=277) of the Cardiac Insufficiency Bisoprolol Study in ELDerly (CIBIS‐ELD). In this trial, patients were randomized to bisoprolol vs. carvedilol and doses were uptitrated to the target or maximally tolerated dose. hs‐CRP and NT‐proBNP levels were assessed at baseline (BL) and at follow‐up (FU), after 12 weeks. Results: In patients with ischemic HF, hs‐CRP levels decreased in the bisoprolol group (BL=0.60±0.94 mg/ dl, n=166; FU=0.43±0.694mg/dl, n=131; p=0.010), and were without a change in the carvedilol group (BL=0.60±1.69mg/dl, n=181; FU=0.57±0.982mg/ dl, n=136; p=0.731). There was also no change of hs‐CRP levels in non‐ischemic HF patients in both groups (bisoprolol: BL=0.64±1.175 mg/dl, n=197; FU=0.470±0.81mg/dl, n=152, p=0.069; carvedilol: BL=0.45±0.78mg/dl, n=198; FU=0.41±0.701 mg/ dl, n=152, p=0.420). Plasma levels of NT‐proBNP decreased in ischemic patients treated with bisoprolol, (BL=1594±2146 pg/ml, n=169; FU=1468±2110pg/ ml, n=133, p=0.04), while changes in the carvedilol group were not significant (BL=1648±1991 pg/ml, n=188; FU=1567±2119pg/ml, n=135, p=0.556). In the non‐ischemic group NT‐pro levels did not change significantly in the carvedilol group, while there was an increase in non‐ischemic patients in the bisoprolol group (BL=1427±3113 pg/ml, n=208; FU=1533±5385 pg/ml, n=166, p=0.017). Conclusion: Results indicate that bisoprolol might be associated with a decrease of hs‐CRP and NT‐proBNP levels only in ischemic HF patients, while in nonischemic HF patients there was no change of hs‐CRP and an increase of NT‐proBNP levels. In carvedilol treated patients no significant changes were shown in neither group.",
journal = "European Journal of Cardiovascular Nursing",
title = "Effects of beta-blocker therapy on hs-CRP levels in elderly patients with ischemic and non-ischemic heart failure: Results from the CIBIS-ELD trail",
volume = "15",
pages = "S21-S21",
doi = "10.1177/1474515116634263"
}
Duengen, H., Putniković, B., Milićević, P., Tahirović, E., Trippel, T., Radenović, S., Vesković, J., Von Haehling, S., Edelmann, F., Wachter, R., Pieske, B.,& Isenović, E. R.. (2016). Effects of beta-blocker therapy on hs-CRP levels in elderly patients with ischemic and non-ischemic heart failure: Results from the CIBIS-ELD trail. in European Journal of Cardiovascular Nursing, 15, S21-S21.
https://doi.org/10.1177/1474515116634263
Duengen H, Putniković B, Milićević P, Tahirović E, Trippel T, Radenović S, Vesković J, Von Haehling S, Edelmann F, Wachter R, Pieske B, Isenović ER. Effects of beta-blocker therapy on hs-CRP levels in elderly patients with ischemic and non-ischemic heart failure: Results from the CIBIS-ELD trail. in European Journal of Cardiovascular Nursing. 2016;15:S21-S21.
doi:10.1177/1474515116634263 .
Duengen, Hans-Dirk, Putniković, Biljana, Milićević, Predrag, Tahirović, Elvis, Trippel, T., Radenović, Sara, Vesković, Jovan, Von Haehling, Stephan, Edelmann, Frank, Wachter, Rolf, Pieske, B., Isenović, Esma R., "Effects of beta-blocker therapy on hs-CRP levels in elderly patients with ischemic and non-ischemic heart failure: Results from the CIBIS-ELD trail" in European Journal of Cardiovascular Nursing, 15 (2016):S21-S21,
https://doi.org/10.1177/1474515116634263 . .
2

Effects of beta-blocker therapy on hs-CRP levels in elderly patients with ischemic and non-ischemic heart failure: results from the CIBIS-ELD trail

Duengen, Hans-Dirk; Isenović, Esma R.; Putniković, Biljana; Milićević, Predrag; Radenović, Sara; Tahirović, Elvis; Loncar, G.; Fritschka, M.; Trippel, T.; Edelmann, Frank; Competence Network Heart Failure

(2015)

TY  - CONF
AU  - Duengen, Hans-Dirk
AU  - Isenović, Esma R.
AU  - Putniković, Biljana
AU  - Milićević, Predrag
AU  - Radenović, Sara
AU  - Tahirović, Elvis
AU  - Loncar, G.
AU  - Fritschka, M.
AU  - Trippel, T.
AU  - Edelmann, Frank
AU  - Competence Network Heart Failure
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/7076
C3  - European Heart Journal
T1  - Effects of beta-blocker therapy on hs-CRP levels in elderly patients with ischemic and non-ischemic heart failure: results from the CIBIS-ELD trail
VL  - 36
SP  - 1004
EP  - 1004
UR  - https://hdl.handle.net/21.15107/rcub_vinar_7076
ER  - 
@conference{
author = "Duengen, Hans-Dirk and Isenović, Esma R. and Putniković, Biljana and Milićević, Predrag and Radenović, Sara and Tahirović, Elvis and Loncar, G. and Fritschka, M. and Trippel, T. and Edelmann, Frank and Competence Network Heart Failure",
year = "2015",
journal = "European Heart Journal",
title = "Effects of beta-blocker therapy on hs-CRP levels in elderly patients with ischemic and non-ischemic heart failure: results from the CIBIS-ELD trail",
volume = "36",
pages = "1004-1004",
url = "https://hdl.handle.net/21.15107/rcub_vinar_7076"
}
Duengen, H., Isenović, E. R., Putniković, B., Milićević, P., Radenović, S., Tahirović, E., Loncar, G., Fritschka, M., Trippel, T., Edelmann, F.,& Competence Network Heart Failure. (2015). Effects of beta-blocker therapy on hs-CRP levels in elderly patients with ischemic and non-ischemic heart failure: results from the CIBIS-ELD trail. in European Heart Journal, 36, 1004-1004.
https://hdl.handle.net/21.15107/rcub_vinar_7076
Duengen H, Isenović ER, Putniković B, Milićević P, Radenović S, Tahirović E, Loncar G, Fritschka M, Trippel T, Edelmann F, Competence Network Heart Failure. Effects of beta-blocker therapy on hs-CRP levels in elderly patients with ischemic and non-ischemic heart failure: results from the CIBIS-ELD trail. in European Heart Journal. 2015;36:1004-1004.
https://hdl.handle.net/21.15107/rcub_vinar_7076 .
Duengen, Hans-Dirk, Isenović, Esma R., Putniković, Biljana, Milićević, Predrag, Radenović, Sara, Tahirović, Elvis, Loncar, G., Fritschka, M., Trippel, T., Edelmann, Frank, Competence Network Heart Failure, "Effects of beta-blocker therapy on hs-CRP levels in elderly patients with ischemic and non-ischemic heart failure: results from the CIBIS-ELD trail" in European Heart Journal, 36 (2015):1004-1004,
https://hdl.handle.net/21.15107/rcub_vinar_7076 .

Uloga trombina u proliferaciji glatkih mišićnih ćelija krvnih sudova (VSMCs) i aterosklerozi

Smiljanić, Katarina; Zafirović, Sonja; Obradović, Milan M.; Gluvić, Zoran; Stokić, Edita; Putniković, Biljana; Isenović, Esma R.

(2012)

TY  - JOUR
AU  - Smiljanić, Katarina
AU  - Zafirović, Sonja
AU  - Obradović, Milan M.
AU  - Gluvić, Zoran
AU  - Stokić, Edita
AU  - Putniković, Biljana
AU  - Isenović, Esma R.
PY  - 2012
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10324
AB  - Glatke mišićne ćelije krvnih sudova (VSMCs) su od vitalnog značaja, kako za strukturu tako i za funkcionisanje i dinamiku krvnih sudova. Proliferacija i abnormalna akumulacija VSMCs su među ključnim događajima u nastanku raznih vaskularnih oboljenja, uključujući aterosklerozu i hipertenziju. Kardiovaskularne bolesti su vodeći uzrok smrtnosti ljudske populacije u čijoj osnovi u najvećoj meri dominira ateroskleroza kao patološka komponenta. Ateroskleroza jedan je od glavnih uzroka infarkta miokarda, moždanog udara i perifernih vaskularnih bolesti, koji čine približno polovinu svih smrtnih slučajeva u razvijenim zemljama. Ona uključuje orkestrirane procese endotelijalne disfunkcije, inflamacije, proliferacije VSMCs i reorganizaciju ekstracelularnog matriksa. Dediferencijacija i proliferacija VSMCs predstavljaju ključne događaje u nastanku aterosklerotskih lezija, postangioplastične restenoze i odbacivanja kalema pri bajpasu krvnih sudova. Trombin je moćni modulator mnogih procesa kao što su regulisanje tonusa i propustljivosti krvnog suda, migracije i proliferacije VSMCs, privlačenja monocita u aterosklerotske lezije i raznih proinflamatornih markera, a sve ovo, takođe, doprinosi progresiji kardiovaskularnih oboljenja.
AB  - Vascular smooth muscle cells (VSMCs) are vital to the structure, functioning and dynamics of blood vessels. Proliferation and abnormal accumulation of VSMCs are among the key events in the development of various vascular diseases including atherosclerosis and hypertension. Cardiovascular diseases are the leading cause of mortality in human population which is based largely dominated by atherosclerosis as a pathological component. Atherosclerosis is a major cause of myocardial infarction, stroke and peripheral vascular disease, which constitute approximately half of all deaths in developed countries. It involves orchestrated processes of endothelial dysfunction, inflammation, proliferation of VSMCs and extracellular matrix reorganization. Dedifferentiation and proliferation of VSMCs is a key event in the development of atherosclerotic lesions, postangioplastic restenosis and rejection of the bypass graft vessels. Thrombin is a potent modulator of many processes such as regulation of muscle tone and permeability of the blood vessel, migration and proliferation of VSMCs, attracting monocytes into atherosclerotic lesions and a variety of inflammatory markers, and all this also contributes to the progression of cardiovascular disease.
T2  - Medicinska istraživanja
T1  - Uloga trombina u proliferaciji glatkih mišićnih ćelija krvnih sudova (VSMCs) i aterosklerozi
T1  - The role of thrombin in the proliferation of vascular smooth muscle cells (VSMCs) and atherosclerosis
VL  - 46
IS  - 2
SP  - 44
EP  - 53
UR  - https://hdl.handle.net/21.15107/rcub_vinar_10324
ER  - 
@article{
author = "Smiljanić, Katarina and Zafirović, Sonja and Obradović, Milan M. and Gluvić, Zoran and Stokić, Edita and Putniković, Biljana and Isenović, Esma R.",
year = "2012",
abstract = "Glatke mišićne ćelije krvnih sudova (VSMCs) su od vitalnog značaja, kako za strukturu tako i za funkcionisanje i dinamiku krvnih sudova. Proliferacija i abnormalna akumulacija VSMCs su među ključnim događajima u nastanku raznih vaskularnih oboljenja, uključujući aterosklerozu i hipertenziju. Kardiovaskularne bolesti su vodeći uzrok smrtnosti ljudske populacije u čijoj osnovi u najvećoj meri dominira ateroskleroza kao patološka komponenta. Ateroskleroza jedan je od glavnih uzroka infarkta miokarda, moždanog udara i perifernih vaskularnih bolesti, koji čine približno polovinu svih smrtnih slučajeva u razvijenim zemljama. Ona uključuje orkestrirane procese endotelijalne disfunkcije, inflamacije, proliferacije VSMCs i reorganizaciju ekstracelularnog matriksa. Dediferencijacija i proliferacija VSMCs predstavljaju ključne događaje u nastanku aterosklerotskih lezija, postangioplastične restenoze i odbacivanja kalema pri bajpasu krvnih sudova. Trombin je moćni modulator mnogih procesa kao što su regulisanje tonusa i propustljivosti krvnog suda, migracije i proliferacije VSMCs, privlačenja monocita u aterosklerotske lezije i raznih proinflamatornih markera, a sve ovo, takođe, doprinosi progresiji kardiovaskularnih oboljenja., Vascular smooth muscle cells (VSMCs) are vital to the structure, functioning and dynamics of blood vessels. Proliferation and abnormal accumulation of VSMCs are among the key events in the development of various vascular diseases including atherosclerosis and hypertension. Cardiovascular diseases are the leading cause of mortality in human population which is based largely dominated by atherosclerosis as a pathological component. Atherosclerosis is a major cause of myocardial infarction, stroke and peripheral vascular disease, which constitute approximately half of all deaths in developed countries. It involves orchestrated processes of endothelial dysfunction, inflammation, proliferation of VSMCs and extracellular matrix reorganization. Dedifferentiation and proliferation of VSMCs is a key event in the development of atherosclerotic lesions, postangioplastic restenosis and rejection of the bypass graft vessels. Thrombin is a potent modulator of many processes such as regulation of muscle tone and permeability of the blood vessel, migration and proliferation of VSMCs, attracting monocytes into atherosclerotic lesions and a variety of inflammatory markers, and all this also contributes to the progression of cardiovascular disease.",
journal = "Medicinska istraživanja",
title = "Uloga trombina u proliferaciji glatkih mišićnih ćelija krvnih sudova (VSMCs) i aterosklerozi, The role of thrombin in the proliferation of vascular smooth muscle cells (VSMCs) and atherosclerosis",
volume = "46",
number = "2",
pages = "44-53",
url = "https://hdl.handle.net/21.15107/rcub_vinar_10324"
}
Smiljanić, K., Zafirović, S., Obradović, M. M., Gluvić, Z., Stokić, E., Putniković, B.,& Isenović, E. R.. (2012). Uloga trombina u proliferaciji glatkih mišićnih ćelija krvnih sudova (VSMCs) i aterosklerozi. in Medicinska istraživanja, 46(2), 44-53.
https://hdl.handle.net/21.15107/rcub_vinar_10324
Smiljanić K, Zafirović S, Obradović MM, Gluvić Z, Stokić E, Putniković B, Isenović ER. Uloga trombina u proliferaciji glatkih mišićnih ćelija krvnih sudova (VSMCs) i aterosklerozi. in Medicinska istraživanja. 2012;46(2):44-53.
https://hdl.handle.net/21.15107/rcub_vinar_10324 .
Smiljanić, Katarina, Zafirović, Sonja, Obradović, Milan M., Gluvić, Zoran, Stokić, Edita, Putniković, Biljana, Isenović, Esma R., "Uloga trombina u proliferaciji glatkih mišićnih ćelija krvnih sudova (VSMCs) i aterosklerozi" in Medicinska istraživanja, 46, no. 2 (2012):44-53,
https://hdl.handle.net/21.15107/rcub_vinar_10324 .

Effects of carvedilol on nitric oxide (NO) activity/expression in patient with chronic heart failure (CHF)

Dobutović, Branislava; Trpković, Andreja; Putniković, Biljana; Gluvić, Zoran; Isenović, Esma R.

(2008)

TY  - JOUR
AU  - Dobutović, Branislava
AU  - Trpković, Andreja
AU  - Putniković, Biljana
AU  - Gluvić, Zoran
AU  - Isenović, Esma R.
PY  - 2008
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10330
AB  - Previous studies have reported increased myocardial inducible nitric oxide synthase (iNOs) expression and activity in chronic heart failure (ChF). Nitric oxide (NO) is a free radical which reacts with various molecules to cause multiple biological effects. Carvedilol is a α1-, β1-, and β2-adrenergic antagonist, used in therapy of hypertension and ChF. recently, it has been shown that carvedilol has an effect as NO quenching agent. Carvedilol presents several other mechanisms of action that converge to improve the symptomatology of hypertension and CHF. In addition to the adrenergic antagonism, carvedilol is also an antioxidant and endothelin suppressor. The molecular mechanism for the NO quenching potency of carvedilol remains to be determined. In cardiac cells the major pathway responsible for the regulation of iNOS activity/expression involves the activation of phosphatidylinositol 3-kinase (PI3K) and protein kinase B (Akt). Thus, in our current ongoing and future studies, we will test the hypothesis that in disease states such as CHF where the PI3K/Akt pathway is interrupted, the regulation of iNOS activity/expression will be abolished. as a corollary of this primary hypothesis, we postulate that in CHF carvedilol stimulates cardiovascular iNOS via a mechanism involving activation of PI3K/akt cascade and further amplifies iNOS activity/expression. Moreover, since the PI3K/akt pathway have been acknowledged as a critically important mediator of cardiac iNOS regulation, PI3K/akt are identified as one of key targets for novel therapeutic interventions to minimize irreversible tissue damage associated with CHF and hypertension. A safer technology to regulate in vivo synthesis of PI3K/akt by generic manipulation would be a welcome work.
AB  - Azot oksid (NO) je slobodni radikal čije reakcije dovode do različitih bioloških dejstava. Karvedilol je antagonist α1-, β1-,i β2 adrenergičkih receptora koji se koristi u terapiji hipertenzije i nedavno je pokazano da hemijski reaguje sa NO. Pored adrenergičke blokade karvedilol doprinosi poboljšanju hipertenzije i HSI drugim mehanizmima. Takođe, pokazano je da karvedilol ima ulogu antioksidansa i ulogu u supresiji endotelina. Precizan mehanizam interakcije karvedilola i NO do sada nije u potpunosti razjašnjen. aktivnost/ekspresija inducibilne azot oksid sintetaze (iNOS) u kardiomiocitima dominantno je regulisana aktivacijom fosfatidilinozitol 3-kinaze (PI3K) i protein kinaze B (akt). U našim tekućim i planiranim istraživanjima, polazimo od hipoteze da je u HSI poremećen PI3K/akt signalni put, a time konsekventno i smanjena aktivnost/ekspresija iNOS-a. Takođe, naša hipoteza se bazira na pretpostavci da karvedilol u HSI stimuliše iNOS u kardiovaskularnom sistemu preko aktivacije PI3K/Akt kaskade. U zaključku, regulacija PI3K/Akt signalnog puta ima veoma bitnu ulogu u regulaciji iNOS-a u stanjima HSI. S obzirom da PI3K/Akt signalni put ima biološku ulogu kao kritično-važni signalni put u delovanju adrenergičkih lekova, kao što je karvedilol, to ga čini ključnim za terapeutske intervencije u cilju minimalizacije ireverzibilnih tkivnih i ćelijskih oštećenja koja su asocirana sa HSI i hipertenzijom.
T2  - Materia medica
T1  - Effects of carvedilol on nitric oxide (NO) activity/expression in patient with chronic heart failure (CHF)
T1  - Efekti karvedilola na aktivnost/ekspresiju inducibilne azot oksid sintetaze (iNOS) kod bolesnika sa hroničnom srčanom insuficijencijom (HSI)
VL  - 24
IS  - 1
SP  - 21
EP  - 25
UR  - https://hdl.handle.net/21.15107/rcub_vinar_10330
ER  - 
@article{
author = "Dobutović, Branislava and Trpković, Andreja and Putniković, Biljana and Gluvić, Zoran and Isenović, Esma R.",
year = "2008",
abstract = "Previous studies have reported increased myocardial inducible nitric oxide synthase (iNOs) expression and activity in chronic heart failure (ChF). Nitric oxide (NO) is a free radical which reacts with various molecules to cause multiple biological effects. Carvedilol is a α1-, β1-, and β2-adrenergic antagonist, used in therapy of hypertension and ChF. recently, it has been shown that carvedilol has an effect as NO quenching agent. Carvedilol presents several other mechanisms of action that converge to improve the symptomatology of hypertension and CHF. In addition to the adrenergic antagonism, carvedilol is also an antioxidant and endothelin suppressor. The molecular mechanism for the NO quenching potency of carvedilol remains to be determined. In cardiac cells the major pathway responsible for the regulation of iNOS activity/expression involves the activation of phosphatidylinositol 3-kinase (PI3K) and protein kinase B (Akt). Thus, in our current ongoing and future studies, we will test the hypothesis that in disease states such as CHF where the PI3K/Akt pathway is interrupted, the regulation of iNOS activity/expression will be abolished. as a corollary of this primary hypothesis, we postulate that in CHF carvedilol stimulates cardiovascular iNOS via a mechanism involving activation of PI3K/akt cascade and further amplifies iNOS activity/expression. Moreover, since the PI3K/akt pathway have been acknowledged as a critically important mediator of cardiac iNOS regulation, PI3K/akt are identified as one of key targets for novel therapeutic interventions to minimize irreversible tissue damage associated with CHF and hypertension. A safer technology to regulate in vivo synthesis of PI3K/akt by generic manipulation would be a welcome work., Azot oksid (NO) je slobodni radikal čije reakcije dovode do različitih bioloških dejstava. Karvedilol je antagonist α1-, β1-,i β2 adrenergičkih receptora koji se koristi u terapiji hipertenzije i nedavno je pokazano da hemijski reaguje sa NO. Pored adrenergičke blokade karvedilol doprinosi poboljšanju hipertenzije i HSI drugim mehanizmima. Takođe, pokazano je da karvedilol ima ulogu antioksidansa i ulogu u supresiji endotelina. Precizan mehanizam interakcije karvedilola i NO do sada nije u potpunosti razjašnjen. aktivnost/ekspresija inducibilne azot oksid sintetaze (iNOS) u kardiomiocitima dominantno je regulisana aktivacijom fosfatidilinozitol 3-kinaze (PI3K) i protein kinaze B (akt). U našim tekućim i planiranim istraživanjima, polazimo od hipoteze da je u HSI poremećen PI3K/akt signalni put, a time konsekventno i smanjena aktivnost/ekspresija iNOS-a. Takođe, naša hipoteza se bazira na pretpostavci da karvedilol u HSI stimuliše iNOS u kardiovaskularnom sistemu preko aktivacije PI3K/Akt kaskade. U zaključku, regulacija PI3K/Akt signalnog puta ima veoma bitnu ulogu u regulaciji iNOS-a u stanjima HSI. S obzirom da PI3K/Akt signalni put ima biološku ulogu kao kritično-važni signalni put u delovanju adrenergičkih lekova, kao što je karvedilol, to ga čini ključnim za terapeutske intervencije u cilju minimalizacije ireverzibilnih tkivnih i ćelijskih oštećenja koja su asocirana sa HSI i hipertenzijom.",
journal = "Materia medica",
title = "Effects of carvedilol on nitric oxide (NO) activity/expression in patient with chronic heart failure (CHF), Efekti karvedilola na aktivnost/ekspresiju inducibilne azot oksid sintetaze (iNOS) kod bolesnika sa hroničnom srčanom insuficijencijom (HSI)",
volume = "24",
number = "1",
pages = "21-25",
url = "https://hdl.handle.net/21.15107/rcub_vinar_10330"
}
Dobutović, B., Trpković, A., Putniković, B., Gluvić, Z.,& Isenović, E. R.. (2008). Effects of carvedilol on nitric oxide (NO) activity/expression in patient with chronic heart failure (CHF). in Materia medica, 24(1), 21-25.
https://hdl.handle.net/21.15107/rcub_vinar_10330
Dobutović B, Trpković A, Putniković B, Gluvić Z, Isenović ER. Effects of carvedilol on nitric oxide (NO) activity/expression in patient with chronic heart failure (CHF). in Materia medica. 2008;24(1):21-25.
https://hdl.handle.net/21.15107/rcub_vinar_10330 .
Dobutović, Branislava, Trpković, Andreja, Putniković, Biljana, Gluvić, Zoran, Isenović, Esma R., "Effects of carvedilol on nitric oxide (NO) activity/expression in patient with chronic heart failure (CHF)" in Materia medica, 24, no. 1 (2008):21-25,
https://hdl.handle.net/21.15107/rcub_vinar_10330 .

Regulation of sodium pump by estradiol in vascular smooth muscle cells

Trpković, Andreja; Putniković, Biljana; Sudar, Emina; Velebit, Jelena; Gluvić, Zoran; Ilić, Želmira; Đurić, Jovanka; Isenović, Esma R.

(2007)

TY  - JOUR
AU  - Trpković, Andreja
AU  - Putniković, Biljana
AU  - Sudar, Emina
AU  - Velebit, Jelena
AU  - Gluvić, Zoran
AU  - Ilić, Želmira
AU  - Đurić, Jovanka
AU  - Isenović, Esma R.
PY  - 2007
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10333
AB  - The effects of estradiol involve the activation of multiple signaling cascades, including and p42/44 mitogen-activated protein kinase. In addition, some of the effects of estradiol have been linked to activity of cytosolic phospholipase. The mechanisms of estradiol action on the cardiovascular system can be divided into two broad categories: effects on systemic cardiovascular risk factors, and direct effects on vascular cells. A number of direct vascular effects of estradiol have been reported, including its impact on the regulation of sodium pump activity and vasomotor tone. The sodium pump is a ubiquitous plasma membrane- bound enzyme that plays an essential role in regulatory vasomotion. The association between reduced sodium pump expression and the development and/or pathogenesis of several disease states including hypertension, congestive heart failure, chronic renal failure and diabetes underscores the importance of the sodium pump. We hypothesize that estradiol stimulates the vascular smooth muscle cell sodium pump via a mechanism involving phosphatydil inositol-3 kinase-dependent activation of cytosolic phospholipase and release of arachidonic acid , which activates the p42/44 mitogen-activated protein kinase cascade and further increases cytosolic phospholipase activity. Furthermore, we postulate that in a disease state such as hypertension (as in spontaneously hypertensive rat ), the resulting overproduction of Angiotensin II will interfere with estradiol regulation of the sodium pump.
AB  - Estradiol aktivira multipne kaskadne signalne reakcije u kojima su ukljuceni i enzimi, kinaze, kao sto su fosfatidil inozitol-3 kinaza i p42/44 mitogenom aktivirana kinaza. Takođe, se smatra da su pojedini efekti estradiola posledica aktivnosti citosolne fosfolipaze 2. Uticaj estradiola na kardiovaskularni sistem je dvojak: pored direktnog efekta na vaskularne ćelije, estradiol utiče i na sistemske faktore rizika koji dovode do pojave kardiovaskularne bolesti. Poznati su brojni direktni uticaji estradiola na vaskularni sistem, uključujući i ulogu estradiola u regulaciji aktivnosti natrijumove pumpe i vazomotornog tonusa. Natrijumova pumpa je ubikvitaran enzim lokalizovan u ćelijskoj membrani i ima značajnu ulogu u regulaciji vazomotornog tonusa. Poremecaj u regulaciji aktivnosti (npr. smanjena aktivnost), natrijumove pumpe je posebno izražena u nastanku i/ili patogenezi pojedinih oboljenja kao što su: hipertenzija, kongestivna srčana slabost, hronična bubrežna slabost i šećerna bolest. U nasem radu polazimo od hipoteze da estradiol stimuliše aktivnost/sintezu natrijumove pumpe u vaskularnim glatkim mišićnim ćelijama putem fosfatidil inozitol-3 kinazne-zavisne aktivacije citosolne fosfolipaze 2, nakon cega oslobođena arahidonska kiselina, indukuje aktivaciju p42/44 mitogenom aktiviriranu kinaznu kaskadnu reakciju sto dodatno doprinosi aktivnosti citosolne fosfolipaze 2.Takođe, smatramo da se u oboljenjima kao što je hipertenzija, povećana sinteza angiotenzina II ometa estradiolom regulisanu aktivnost/sintezu natrujumove pumpe.
T2  - Materia medica
T1  - Regulation of sodium pump by estradiol in vascular smooth muscle cells
T1  - Uloga estradiola u regulaciji netrijumove pumpe u vaskularnim glatkim mišićnim ćelijama
VL  - 23
IS  - 3
SP  - 32
EP  - 36
UR  - https://hdl.handle.net/21.15107/rcub_vinar_10333
ER  - 
@article{
author = "Trpković, Andreja and Putniković, Biljana and Sudar, Emina and Velebit, Jelena and Gluvić, Zoran and Ilić, Želmira and Đurić, Jovanka and Isenović, Esma R.",
year = "2007",
abstract = "The effects of estradiol involve the activation of multiple signaling cascades, including and p42/44 mitogen-activated protein kinase. In addition, some of the effects of estradiol have been linked to activity of cytosolic phospholipase. The mechanisms of estradiol action on the cardiovascular system can be divided into two broad categories: effects on systemic cardiovascular risk factors, and direct effects on vascular cells. A number of direct vascular effects of estradiol have been reported, including its impact on the regulation of sodium pump activity and vasomotor tone. The sodium pump is a ubiquitous plasma membrane- bound enzyme that plays an essential role in regulatory vasomotion. The association between reduced sodium pump expression and the development and/or pathogenesis of several disease states including hypertension, congestive heart failure, chronic renal failure and diabetes underscores the importance of the sodium pump. We hypothesize that estradiol stimulates the vascular smooth muscle cell sodium pump via a mechanism involving phosphatydil inositol-3 kinase-dependent activation of cytosolic phospholipase and release of arachidonic acid , which activates the p42/44 mitogen-activated protein kinase cascade and further increases cytosolic phospholipase activity. Furthermore, we postulate that in a disease state such as hypertension (as in spontaneously hypertensive rat ), the resulting overproduction of Angiotensin II will interfere with estradiol regulation of the sodium pump., Estradiol aktivira multipne kaskadne signalne reakcije u kojima su ukljuceni i enzimi, kinaze, kao sto su fosfatidil inozitol-3 kinaza i p42/44 mitogenom aktivirana kinaza. Takođe, se smatra da su pojedini efekti estradiola posledica aktivnosti citosolne fosfolipaze 2. Uticaj estradiola na kardiovaskularni sistem je dvojak: pored direktnog efekta na vaskularne ćelije, estradiol utiče i na sistemske faktore rizika koji dovode do pojave kardiovaskularne bolesti. Poznati su brojni direktni uticaji estradiola na vaskularni sistem, uključujući i ulogu estradiola u regulaciji aktivnosti natrijumove pumpe i vazomotornog tonusa. Natrijumova pumpa je ubikvitaran enzim lokalizovan u ćelijskoj membrani i ima značajnu ulogu u regulaciji vazomotornog tonusa. Poremecaj u regulaciji aktivnosti (npr. smanjena aktivnost), natrijumove pumpe je posebno izražena u nastanku i/ili patogenezi pojedinih oboljenja kao što su: hipertenzija, kongestivna srčana slabost, hronična bubrežna slabost i šećerna bolest. U nasem radu polazimo od hipoteze da estradiol stimuliše aktivnost/sintezu natrijumove pumpe u vaskularnim glatkim mišićnim ćelijama putem fosfatidil inozitol-3 kinazne-zavisne aktivacije citosolne fosfolipaze 2, nakon cega oslobođena arahidonska kiselina, indukuje aktivaciju p42/44 mitogenom aktiviriranu kinaznu kaskadnu reakciju sto dodatno doprinosi aktivnosti citosolne fosfolipaze 2.Takođe, smatramo da se u oboljenjima kao što je hipertenzija, povećana sinteza angiotenzina II ometa estradiolom regulisanu aktivnost/sintezu natrujumove pumpe.",
journal = "Materia medica",
title = "Regulation of sodium pump by estradiol in vascular smooth muscle cells, Uloga estradiola u regulaciji netrijumove pumpe u vaskularnim glatkim mišićnim ćelijama",
volume = "23",
number = "3",
pages = "32-36",
url = "https://hdl.handle.net/21.15107/rcub_vinar_10333"
}
Trpković, A., Putniković, B., Sudar, E., Velebit, J., Gluvić, Z., Ilić, Ž., Đurić, J.,& Isenović, E. R.. (2007). Regulation of sodium pump by estradiol in vascular smooth muscle cells. in Materia medica, 23(3), 32-36.
https://hdl.handle.net/21.15107/rcub_vinar_10333
Trpković A, Putniković B, Sudar E, Velebit J, Gluvić Z, Ilić Ž, Đurić J, Isenović ER. Regulation of sodium pump by estradiol in vascular smooth muscle cells. in Materia medica. 2007;23(3):32-36.
https://hdl.handle.net/21.15107/rcub_vinar_10333 .
Trpković, Andreja, Putniković, Biljana, Sudar, Emina, Velebit, Jelena, Gluvić, Zoran, Ilić, Želmira, Đurić, Jovanka, Isenović, Esma R., "Regulation of sodium pump by estradiol in vascular smooth muscle cells" in Materia medica, 23, no. 3 (2007):32-36,
https://hdl.handle.net/21.15107/rcub_vinar_10333 .