Unić-Stojanović, Dragana R.

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Authority KeyName Variants
6992a7b5-7196-4b11-bf37-c946c2fe84be
  • Unić-Stojanović, Dragana R. (3)
  • Unić-Stojanović, Dragana (2)
  • Stojanović, Dragana (1)
Projects

Author's Bibliography

Toxicity assessment of mesoporous silica nanoparticles under different extraction procedures

Filipović Tričković, Jelena G.; Kokunešoski, Maja; Momić, Tatjana; Jovanović, Ivan G.; Anastasov, Marina; Stojanović, Dragana; Valenta Šobot, Ana

(2023)

TY  - CONF
AU  - Filipović Tričković, Jelena G.
AU  - Kokunešoski, Maja
AU  - Momić, Tatjana
AU  - Jovanović, Ivan G.
AU  - Anastasov, Marina
AU  - Stojanović, Dragana
AU  - Valenta Šobot, Ana
PY  - 2023
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/11409
C3  - 13th international congress of the Serbian society of toxicology & 1st toxSEE regional conference : abstract book
T1  - Toxicity assessment of mesoporous silica nanoparticles under different extraction procedures
T1  - Procena toksičnosti mezoporoznih nanočestica silicijum dioksida pri različitim postupcima ekstrakcije
UR  - https://hdl.handle.net/21.15107/rcub_vinar_11409
ER  - 
@conference{
author = "Filipović Tričković, Jelena G. and Kokunešoski, Maja and Momić, Tatjana and Jovanović, Ivan G. and Anastasov, Marina and Stojanović, Dragana and Valenta Šobot, Ana",
year = "2023",
journal = "13th international congress of the Serbian society of toxicology & 1st toxSEE regional conference : abstract book",
title = "Toxicity assessment of mesoporous silica nanoparticles under different extraction procedures, Procena toksičnosti mezoporoznih nanočestica silicijum dioksida pri različitim postupcima ekstrakcije",
url = "https://hdl.handle.net/21.15107/rcub_vinar_11409"
}
Filipović Tričković, J. G., Kokunešoski, M., Momić, T., Jovanović, I. G., Anastasov, M., Stojanović, D.,& Valenta Šobot, A.. (2023). Toxicity assessment of mesoporous silica nanoparticles under different extraction procedures. in 13th international congress of the Serbian society of toxicology & 1st toxSEE regional conference : abstract book.
https://hdl.handle.net/21.15107/rcub_vinar_11409
Filipović Tričković JG, Kokunešoski M, Momić T, Jovanović IG, Anastasov M, Stojanović D, Valenta Šobot A. Toxicity assessment of mesoporous silica nanoparticles under different extraction procedures. in 13th international congress of the Serbian society of toxicology & 1st toxSEE regional conference : abstract book. 2023;.
https://hdl.handle.net/21.15107/rcub_vinar_11409 .
Filipović Tričković, Jelena G., Kokunešoski, Maja, Momić, Tatjana, Jovanović, Ivan G., Anastasov, Marina, Stojanović, Dragana, Valenta Šobot, Ana, "Toxicity assessment of mesoporous silica nanoparticles under different extraction procedures" in 13th international congress of the Serbian society of toxicology & 1st toxSEE regional conference : abstract book (2023),
https://hdl.handle.net/21.15107/rcub_vinar_11409 .

Carotid Restenosis Rate After Stenting for Primary Lesions Versus Restenosis After Endarterectomy With Creation of Risk Index

Tanasković, Slobodan; Sagić, Dragan Ž.; Radak, Đorđe J.; Antonić, Želimir; Kovačević, Vladimir; Vuković, Mira; Aleksić, Nikola; Radak, Sandra; Nenezić, Dragoslav; Cvetković, Slobodan M.; Isenović, Esma R.; Vučurević, Goran; Lozuk, Branko; Babić, Aleksandar; Babić, Srđan; Matić, Predrag; Gajin, Predrag; Unić-Stojanović, Dragana; Ilijevski, Nenad

(2022)

TY  - JOUR
AU  - Tanasković, Slobodan
AU  - Sagić, Dragan Ž.
AU  - Radak, Đorđe J.
AU  - Antonić, Želimir
AU  - Kovačević, Vladimir
AU  - Vuković, Mira
AU  - Aleksić, Nikola
AU  - Radak, Sandra
AU  - Nenezić, Dragoslav
AU  - Cvetković, Slobodan M.
AU  - Isenović, Esma R.
AU  - Vučurević, Goran
AU  - Lozuk, Branko
AU  - Babić, Aleksandar
AU  - Babić, Srđan
AU  - Matić, Predrag
AU  - Gajin, Predrag
AU  - Unić-Stojanović, Dragana
AU  - Ilijevski, Nenad
PY  - 2022
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10259
AB  - Purpose: Carotid artery stenting (CAS) is an option for carotid restenosis (CR) treatment with favorable outcomes. However, CAS has also emerged as an alternative to carotid endarterectomy (CEA) for the management of patients with primary carotid stenosis. This study aimed to report CR rates after CAS was performed in patients with primary lesions versus restenosis after CEA, to identify predictors of CR, and to report both neurological and overall outcomes.Materials and methods:From January 2000 to September 2018, a total of 782 patients were divided into 2 groups: The CAS (prim) group consisted of 440 patients in whom CAS was performed for primary lesions, and the CAS (res) group consisted of 342 patients with CAS due to restenosis after CEA. Indications for CAS were symptomatic stenosis/restenosis >70% and asymptomatic stenosis/restenosis >85%. A color duplex scan (CDS) of carotid arteries was performed 6 months after CAS, after 1 year, and annually afterward. Follow-up ranged from 12 to 88 months, with a mean follow-up of 34.6±18.0 months.Results:There were no differences in terms of CR rate between the patients in the CAS (prim) and CAS (res) groups (8.7% vs 7.2%, ?2=0.691, p=0.406). The overall CR rate was 7.9%, whereas significant CR (>70%) rate needing re-intervention was 5.6%, but there was no difference between patients in the CAS (prim) and CAS (res) groups (6.4% vs 4.7%, p=0.351). Six independent predictors for CR were smoking, associated previous myocardial infarction and angina pectoris, plaque morphology, spasm after CAS, the use of FilterWire or Spider Fx cerebral protection devices, and time after stenting. A carotid restenosis risk index (CRRI) was created based on these predictors and ranged from ?7 (minimal risk) to +10 (maximum risk); patients with a score >?4 were at increased risk for CR. There were no differences in terms of neurological and overall morbidity and mortality between the 2 groups.Conclusions:There was no difference in CR rate after CAS between the patients with primary stenosis and restenosis after CEA. A CRRI score >?4 is a criterion for identifying high-risk patients for post-CAS CR that should be tested in future randomized trials.
T2  - Journal of Endovascular Therapy
T1  - Carotid Restenosis Rate After Stenting for Primary Lesions Versus Restenosis After Endarterectomy With Creation of Risk Index
SP  - 15266028221091895
DO  - 10.1177/15266028221091895
ER  - 
@article{
author = "Tanasković, Slobodan and Sagić, Dragan Ž. and Radak, Đorđe J. and Antonić, Želimir and Kovačević, Vladimir and Vuković, Mira and Aleksić, Nikola and Radak, Sandra and Nenezić, Dragoslav and Cvetković, Slobodan M. and Isenović, Esma R. and Vučurević, Goran and Lozuk, Branko and Babić, Aleksandar and Babić, Srđan and Matić, Predrag and Gajin, Predrag and Unić-Stojanović, Dragana and Ilijevski, Nenad",
year = "2022",
abstract = "Purpose: Carotid artery stenting (CAS) is an option for carotid restenosis (CR) treatment with favorable outcomes. However, CAS has also emerged as an alternative to carotid endarterectomy (CEA) for the management of patients with primary carotid stenosis. This study aimed to report CR rates after CAS was performed in patients with primary lesions versus restenosis after CEA, to identify predictors of CR, and to report both neurological and overall outcomes.Materials and methods:From January 2000 to September 2018, a total of 782 patients were divided into 2 groups: The CAS (prim) group consisted of 440 patients in whom CAS was performed for primary lesions, and the CAS (res) group consisted of 342 patients with CAS due to restenosis after CEA. Indications for CAS were symptomatic stenosis/restenosis >70% and asymptomatic stenosis/restenosis >85%. A color duplex scan (CDS) of carotid arteries was performed 6 months after CAS, after 1 year, and annually afterward. Follow-up ranged from 12 to 88 months, with a mean follow-up of 34.6±18.0 months.Results:There were no differences in terms of CR rate between the patients in the CAS (prim) and CAS (res) groups (8.7% vs 7.2%, ?2=0.691, p=0.406). The overall CR rate was 7.9%, whereas significant CR (>70%) rate needing re-intervention was 5.6%, but there was no difference between patients in the CAS (prim) and CAS (res) groups (6.4% vs 4.7%, p=0.351). Six independent predictors for CR were smoking, associated previous myocardial infarction and angina pectoris, plaque morphology, spasm after CAS, the use of FilterWire or Spider Fx cerebral protection devices, and time after stenting. A carotid restenosis risk index (CRRI) was created based on these predictors and ranged from ?7 (minimal risk) to +10 (maximum risk); patients with a score >?4 were at increased risk for CR. There were no differences in terms of neurological and overall morbidity and mortality between the 2 groups.Conclusions:There was no difference in CR rate after CAS between the patients with primary stenosis and restenosis after CEA. A CRRI score >?4 is a criterion for identifying high-risk patients for post-CAS CR that should be tested in future randomized trials.",
journal = "Journal of Endovascular Therapy",
title = "Carotid Restenosis Rate After Stenting for Primary Lesions Versus Restenosis After Endarterectomy With Creation of Risk Index",
pages = "15266028221091895",
doi = "10.1177/15266028221091895"
}
Tanasković, S., Sagić, D. Ž., Radak, Đ. J., Antonić, Ž., Kovačević, V., Vuković, M., Aleksić, N., Radak, S., Nenezić, D., Cvetković, S. M., Isenović, E. R., Vučurević, G., Lozuk, B., Babić, A., Babić, S., Matić, P., Gajin, P., Unić-Stojanović, D.,& Ilijevski, N.. (2022). Carotid Restenosis Rate After Stenting for Primary Lesions Versus Restenosis After Endarterectomy With Creation of Risk Index. in Journal of Endovascular Therapy, 15266028221091895.
https://doi.org/10.1177/15266028221091895
Tanasković S, Sagić DŽ, Radak ĐJ, Antonić Ž, Kovačević V, Vuković M, Aleksić N, Radak S, Nenezić D, Cvetković SM, Isenović ER, Vučurević G, Lozuk B, Babić A, Babić S, Matić P, Gajin P, Unić-Stojanović D, Ilijevski N. Carotid Restenosis Rate After Stenting for Primary Lesions Versus Restenosis After Endarterectomy With Creation of Risk Index. in Journal of Endovascular Therapy. 2022;:15266028221091895.
doi:10.1177/15266028221091895 .
Tanasković, Slobodan, Sagić, Dragan Ž., Radak, Đorđe J., Antonić, Želimir, Kovačević, Vladimir, Vuković, Mira, Aleksić, Nikola, Radak, Sandra, Nenezić, Dragoslav, Cvetković, Slobodan M., Isenović, Esma R., Vučurević, Goran, Lozuk, Branko, Babić, Aleksandar, Babić, Srđan, Matić, Predrag, Gajin, Predrag, Unić-Stojanović, Dragana, Ilijevski, Nenad, "Carotid Restenosis Rate After Stenting for Primary Lesions Versus Restenosis After Endarterectomy With Creation of Risk Index" in Journal of Endovascular Therapy (2022):15266028221091895,
https://doi.org/10.1177/15266028221091895 . .
1

Hypothesis related to the regulation of inducible nitric oxide synthase during carotid endarterectomy

Obradović, Milan M.; Bogdanović, Nikola; Stanimirović, Julijana; Unić-Stojanović, Dragana R.; Radak, Đorđe J.; Isenović, Esma R.

(2019)

TY  - JOUR
AU  - Obradović, Milan M.
AU  - Bogdanović, Nikola
AU  - Stanimirović, Julijana
AU  - Unić-Stojanović, Dragana R.
AU  - Radak, Đorđe J.
AU  - Isenović, Esma R.
PY  - 2019
UR  - https://linkinghub.elsevier.com/retrieve/pii/S0306987718308302
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/7930
AB  - Sudden occlusion of an artery caused by a thrombus or emboli is the most frequent cause of acute brain ischemia (ABI). Carotid endarterectomy (CEA) represents the gold standard for preventing strokes of carotid origin. However, neuronal damage caused by ischemia and/or reperfusion may contribute to a poor clinical outcome after CEA. In response to shear stress caused by hypoxic-ischemic conditions in patients undergoing CEA, stimulation of the hypothalamic-pituitaryadrenal axis leads to biological responses known as hypermetabolic stress, characterized by hemodynamic, metabolic, inflammatory and immunological changes. These changes maintain homeostasis and assist recovery, but an unregulated inflammatory response could lead to further tissue damage and death of neurons. Nitric oxide (NO) is an important signaling molecule involved in several physiological and pathological processes, including ABI. However, an excess of NO could have detrimental effects. We hypothesized that the hypoxic-ischemic state induced by carotid clamping leads to overexpression of inducible NO synthase and that uncontrolled production of NO could adversely affect outcome after CEA. © 2018 Elsevier Ltd
T2  - Medical Hypotheses
T1  - Hypothesis related to the regulation of inducible nitric oxide synthase during carotid endarterectomy
VL  - 122
SP  - 16
EP  - 18
DO  - 10.1016/j.mehy.2018.10.011
ER  - 
@article{
author = "Obradović, Milan M. and Bogdanović, Nikola and Stanimirović, Julijana and Unić-Stojanović, Dragana R. and Radak, Đorđe J. and Isenović, Esma R.",
year = "2019",
abstract = "Sudden occlusion of an artery caused by a thrombus or emboli is the most frequent cause of acute brain ischemia (ABI). Carotid endarterectomy (CEA) represents the gold standard for preventing strokes of carotid origin. However, neuronal damage caused by ischemia and/or reperfusion may contribute to a poor clinical outcome after CEA. In response to shear stress caused by hypoxic-ischemic conditions in patients undergoing CEA, stimulation of the hypothalamic-pituitaryadrenal axis leads to biological responses known as hypermetabolic stress, characterized by hemodynamic, metabolic, inflammatory and immunological changes. These changes maintain homeostasis and assist recovery, but an unregulated inflammatory response could lead to further tissue damage and death of neurons. Nitric oxide (NO) is an important signaling molecule involved in several physiological and pathological processes, including ABI. However, an excess of NO could have detrimental effects. We hypothesized that the hypoxic-ischemic state induced by carotid clamping leads to overexpression of inducible NO synthase and that uncontrolled production of NO could adversely affect outcome after CEA. © 2018 Elsevier Ltd",
journal = "Medical Hypotheses",
title = "Hypothesis related to the regulation of inducible nitric oxide synthase during carotid endarterectomy",
volume = "122",
pages = "16-18",
doi = "10.1016/j.mehy.2018.10.011"
}
Obradović, M. M., Bogdanović, N., Stanimirović, J., Unić-Stojanović, D. R., Radak, Đ. J.,& Isenović, E. R.. (2019). Hypothesis related to the regulation of inducible nitric oxide synthase during carotid endarterectomy. in Medical Hypotheses, 122, 16-18.
https://doi.org/10.1016/j.mehy.2018.10.011
Obradović MM, Bogdanović N, Stanimirović J, Unić-Stojanović DR, Radak ĐJ, Isenović ER. Hypothesis related to the regulation of inducible nitric oxide synthase during carotid endarterectomy. in Medical Hypotheses. 2019;122:16-18.
doi:10.1016/j.mehy.2018.10.011 .
Obradović, Milan M., Bogdanović, Nikola, Stanimirović, Julijana, Unić-Stojanović, Dragana R., Radak, Đorđe J., Isenović, Esma R., "Hypothesis related to the regulation of inducible nitric oxide synthase during carotid endarterectomy" in Medical Hypotheses, 122 (2019):16-18,
https://doi.org/10.1016/j.mehy.2018.10.011 . .
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Copeptin Levels Do Not Correlate With Cross-Clamping Time in Patients Undergoing Carotid Endarterectomy Under General Anesthesia

Unić-Stojanović, Dragana R.; Isenović, Esma R.; Jovic, Miomir; Maravić-Stojković, Vera; Miljković, Milica; Gojković, Tamara; Milicic, Biljana; Bogdanović, Nikola; Radak, Đorđe J.

(2016)

TY  - JOUR
AU  - Unić-Stojanović, Dragana R.
AU  - Isenović, Esma R.
AU  - Jovic, Miomir
AU  - Maravić-Stojković, Vera
AU  - Miljković, Milica
AU  - Gojković, Tamara
AU  - Milicic, Biljana
AU  - Bogdanović, Nikola
AU  - Radak, Đorđe J.
PY  - 2016
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1285
AB  - Copeptin is a sensitive and more stable surrogate marker for arginine vasopressin. In this study, we evaluated copeptin levels in carotid endarterectomy (CEA) patients, perioperatively, to determine whether copeptin levels can be related to carotid artery cross clamping (CC) time and to postoperative neurological outcomes. Copeptin, interleukin 6, C-reactive protein, cortisol, and brain natriuretic peptide were measured preoperatively (T1) and 3 hours postoperatively (T3) as well as intraoperatively (T2). We recruited 77 patients. Values of copeptin rose gradually over the observed times: T1 = 7.9 (6.4-9.6), T2 = 12.6 (9.3-16.8), and T3 = 72.3 (49.1-111.2) pmol/L. There was a significant difference for repeated measurement (P = .000, P = .000, and P = .000). Duration of carotid artery CC during CEA does not affect postoperative copeptin level (CC 13 minutes: 106.8 +/- 93.6 pmol/L, CC GT 13 minutes: 96.7 +/- 89.1 pmol/L; P = .634). Preoperative copeptin level was significantly higher in patients with ulcerated plaque morphology. Activation of the stress axis in patients undergoing CEA results in copeptin elevation. Duration of CC during CEA does not affect postoperative copeptin levels.
T2  - Angiology
T1  - Copeptin Levels Do Not Correlate With Cross-Clamping Time in Patients Undergoing Carotid Endarterectomy Under General Anesthesia
VL  - 67
IS  - 10
SP  - 951
EP  - 960
DO  - 10.1177/0003319716629322
ER  - 
@article{
author = "Unić-Stojanović, Dragana R. and Isenović, Esma R. and Jovic, Miomir and Maravić-Stojković, Vera and Miljković, Milica and Gojković, Tamara and Milicic, Biljana and Bogdanović, Nikola and Radak, Đorđe J.",
year = "2016",
abstract = "Copeptin is a sensitive and more stable surrogate marker for arginine vasopressin. In this study, we evaluated copeptin levels in carotid endarterectomy (CEA) patients, perioperatively, to determine whether copeptin levels can be related to carotid artery cross clamping (CC) time and to postoperative neurological outcomes. Copeptin, interleukin 6, C-reactive protein, cortisol, and brain natriuretic peptide were measured preoperatively (T1) and 3 hours postoperatively (T3) as well as intraoperatively (T2). We recruited 77 patients. Values of copeptin rose gradually over the observed times: T1 = 7.9 (6.4-9.6), T2 = 12.6 (9.3-16.8), and T3 = 72.3 (49.1-111.2) pmol/L. There was a significant difference for repeated measurement (P = .000, P = .000, and P = .000). Duration of carotid artery CC during CEA does not affect postoperative copeptin level (CC 13 minutes: 106.8 +/- 93.6 pmol/L, CC GT 13 minutes: 96.7 +/- 89.1 pmol/L; P = .634). Preoperative copeptin level was significantly higher in patients with ulcerated plaque morphology. Activation of the stress axis in patients undergoing CEA results in copeptin elevation. Duration of CC during CEA does not affect postoperative copeptin levels.",
journal = "Angiology",
title = "Copeptin Levels Do Not Correlate With Cross-Clamping Time in Patients Undergoing Carotid Endarterectomy Under General Anesthesia",
volume = "67",
number = "10",
pages = "951-960",
doi = "10.1177/0003319716629322"
}
Unić-Stojanović, D. R., Isenović, E. R., Jovic, M., Maravić-Stojković, V., Miljković, M., Gojković, T., Milicic, B., Bogdanović, N.,& Radak, Đ. J.. (2016). Copeptin Levels Do Not Correlate With Cross-Clamping Time in Patients Undergoing Carotid Endarterectomy Under General Anesthesia. in Angiology, 67(10), 951-960.
https://doi.org/10.1177/0003319716629322
Unić-Stojanović DR, Isenović ER, Jovic M, Maravić-Stojković V, Miljković M, Gojković T, Milicic B, Bogdanović N, Radak ĐJ. Copeptin Levels Do Not Correlate With Cross-Clamping Time in Patients Undergoing Carotid Endarterectomy Under General Anesthesia. in Angiology. 2016;67(10):951-960.
doi:10.1177/0003319716629322 .
Unić-Stojanović, Dragana R., Isenović, Esma R., Jovic, Miomir, Maravić-Stojković, Vera, Miljković, Milica, Gojković, Tamara, Milicic, Biljana, Bogdanović, Nikola, Radak, Đorđe J., "Copeptin Levels Do Not Correlate With Cross-Clamping Time in Patients Undergoing Carotid Endarterectomy Under General Anesthesia" in Angiology, 67, no. 10 (2016):951-960,
https://doi.org/10.1177/0003319716629322 . .
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Anesthetics and Cerebral Protection in Patients Undergoing Carotid Endarterectomy

Jovic, Miomir; Unić-Stojanović, Dragana R.; Isenović, Esma R.; Manfredi, Rizzo; Cekić, Olivera; Ilijevski, Nenad; Babić, Srđan; Radak, Đorđe J.

(2015)

TY  - JOUR
AU  - Jovic, Miomir
AU  - Unić-Stojanović, Dragana R.
AU  - Isenović, Esma R.
AU  - Manfredi, Rizzo
AU  - Cekić, Olivera
AU  - Ilijevski, Nenad
AU  - Babić, Srđan
AU  - Radak, Đorđe J.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/397
T2  - Journal of Cardiothoracic and Vascular Anesthesia
T1  - Anesthetics and Cerebral Protection in Patients Undergoing Carotid Endarterectomy
VL  - 29
IS  - 1
SP  - 178
EP  - 184
DO  - 10.1053/j.jvca.2014.05.019
ER  - 
@article{
author = "Jovic, Miomir and Unić-Stojanović, Dragana R. and Isenović, Esma R. and Manfredi, Rizzo and Cekić, Olivera and Ilijevski, Nenad and Babić, Srđan and Radak, Đorđe J.",
year = "2015",
journal = "Journal of Cardiothoracic and Vascular Anesthesia",
title = "Anesthetics and Cerebral Protection in Patients Undergoing Carotid Endarterectomy",
volume = "29",
number = "1",
pages = "178-184",
doi = "10.1053/j.jvca.2014.05.019"
}
Jovic, M., Unić-Stojanović, D. R., Isenović, E. R., Manfredi, R., Cekić, O., Ilijevski, N., Babić, S.,& Radak, Đ. J.. (2015). Anesthetics and Cerebral Protection in Patients Undergoing Carotid Endarterectomy. in Journal of Cardiothoracic and Vascular Anesthesia, 29(1), 178-184.
https://doi.org/10.1053/j.jvca.2014.05.019
Jovic M, Unić-Stojanović DR, Isenović ER, Manfredi R, Cekić O, Ilijevski N, Babić S, Radak ĐJ. Anesthetics and Cerebral Protection in Patients Undergoing Carotid Endarterectomy. in Journal of Cardiothoracic and Vascular Anesthesia. 2015;29(1):178-184.
doi:10.1053/j.jvca.2014.05.019 .
Jovic, Miomir, Unić-Stojanović, Dragana R., Isenović, Esma R., Manfredi, Rizzo, Cekić, Olivera, Ilijevski, Nenad, Babić, Srđan, Radak, Đorđe J., "Anesthetics and Cerebral Protection in Patients Undergoing Carotid Endarterectomy" in Journal of Cardiothoracic and Vascular Anesthesia, 29, no. 1 (2015):178-184,
https://doi.org/10.1053/j.jvca.2014.05.019 . .
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Uloga azot-monoksid sintaza u stanjima ishemije mozga tokom karotidne endarterektomije

Bogdanović, Nikola; Obradović, Milan M.; Jasnić, Nebojša; Spremo-Potparević, Biljana; Unić-Stojanović, Dragana; Radak, Đorđe J.; Isenović, Esma R.

(2015)

TY  - JOUR
AU  - Bogdanović, Nikola
AU  - Obradović, Milan M.
AU  - Jasnić, Nebojša
AU  - Spremo-Potparević, Biljana
AU  - Unić-Stojanović, Dragana
AU  - Radak, Đorđe J.
AU  - Isenović, Esma R.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10318
AB  - Prema podacima Svetske zdravstvene organizacije, 15 miliona ljudi godišnje doživi moždani udar. Najčešći uzročnik moždanog udara je ishemija mozga, koja se dešava u skoro 85% slučajeva. Moždana ishemija izazvana tromboembolijskim događajima definiše se kao trajno ili prolazno smanjenje cirkulacije krvi, što za posledicu ima nedostatak kiseonika, glukoze i ostalih važnih nutritijenata, dovodeći postepeno do metaboličkih promena i apoptoze ćelija. Tokom operativnih zahvata kao što je karotidna endarterektomija (CEA) može doći do hipoksično-ishemičnog stanja mozga ili akutne ishemije mozga (ABI), kao i do samog moždanog udara. Glavni uzrok ABI u toku CEA je cerebralna hipoperfuzija koja je uzrokovana klemovanjem karotidne arterije, pri čemu dolazi do hipoksije, što može predstavljati jedan od okidača za niz fizioloških odgovora organizma, među kojima je oslobađanje različitih medijatora inflamacije. Jedan od medijatora inflamacije je i azot monoksid (NO), slobodni radikal koji pored mnogobrojnih fizioloških efekata ima važnu ulogu i u samom imunom odgovoru organizma. Međutim, NO može biti veoma štetan i svojim delovanjem dovesti do oštećenja ćelija i tkiva. Nedostatak podataka u literaturi o ulozi endotelne NOS (eNOS) i inducibilne NOS (iNOS) tokom CEA, kao i mehanizama njihove regulacije u stanjima ishemije, ukazuju na pravac kojim treba da se usmere buduća istraživanja. Poznavanje molekularnih mehanizama regulacije aktivnosti i ekspresije iNOS, svakako će pomoći razvoju novih terapijskih strategija u tretmanu štetnih efekata produkcije slobodnih radikala, pre svega nekontrolisane produkcije NO.
AB  - According to the World Health Organization, 15 million people per year are affected by stroke. The most common cause of stroke is brain ischemia, which occurs in almost 85% of cases. Ischemia caused by thromboembolism is defined as permanently or temporarily decreased blood flow which prevents an adequate delivery of oxygen, glucose and other important nutrients, leading progressively to metabolic changes and cell apoptosis. Carotid endarterectomy (CEA) can cause hypoxic - ischemic states of the brain or acute brain ischemia (ABI) leading eventually to stroke. The main cause of ABI as a result of CEA is cerebral hypoperfusion caused by clamping of carotid arteries, when hypoxia occurs.. Hypoxia per se is one of the triggers of complex physiological responses in the body, including the release of various mediators of inflammation. One of these inflammatory mediators is nitric oxide (NO), a free radical which has numerous physiological effects and also plays an important role in the immune response of the organism. However, NO may be very harmful and cause cell and tissue damage. The lack of literature data on the role of endothelial NOS (eNOS) and inducible NOS (iNOS) during CEA, as well as the mechanisms of their regulation in ischemic conditions, suggest that intensifying future research in this field is very important. An insight into molecular mechanisms of iNOS activity and expression regulation will certainly help to develop new therapeutic strategies for treating harmful effects of free radicals, especially uncontrolled production of NO.
T2  - Medicinska istraživanja
T1  - Uloga azot-monoksid sintaza u stanjima ishemije mozga tokom karotidne endarterektomije
T1  - The role of the nitric oxide synthases in brain ischemia during carotid endarterectomy
VL  - 49
IS  - 1
SP  - 40
EP  - 46
DO  - 10.5937/MedIst1501040B
ER  - 
@article{
author = "Bogdanović, Nikola and Obradović, Milan M. and Jasnić, Nebojša and Spremo-Potparević, Biljana and Unić-Stojanović, Dragana and Radak, Đorđe J. and Isenović, Esma R.",
year = "2015",
abstract = "Prema podacima Svetske zdravstvene organizacije, 15 miliona ljudi godišnje doživi moždani udar. Najčešći uzročnik moždanog udara je ishemija mozga, koja se dešava u skoro 85% slučajeva. Moždana ishemija izazvana tromboembolijskim događajima definiše se kao trajno ili prolazno smanjenje cirkulacije krvi, što za posledicu ima nedostatak kiseonika, glukoze i ostalih važnih nutritijenata, dovodeći postepeno do metaboličkih promena i apoptoze ćelija. Tokom operativnih zahvata kao što je karotidna endarterektomija (CEA) može doći do hipoksično-ishemičnog stanja mozga ili akutne ishemije mozga (ABI), kao i do samog moždanog udara. Glavni uzrok ABI u toku CEA je cerebralna hipoperfuzija koja je uzrokovana klemovanjem karotidne arterije, pri čemu dolazi do hipoksije, što može predstavljati jedan od okidača za niz fizioloških odgovora organizma, među kojima je oslobađanje različitih medijatora inflamacije. Jedan od medijatora inflamacije je i azot monoksid (NO), slobodni radikal koji pored mnogobrojnih fizioloških efekata ima važnu ulogu i u samom imunom odgovoru organizma. Međutim, NO može biti veoma štetan i svojim delovanjem dovesti do oštećenja ćelija i tkiva. Nedostatak podataka u literaturi o ulozi endotelne NOS (eNOS) i inducibilne NOS (iNOS) tokom CEA, kao i mehanizama njihove regulacije u stanjima ishemije, ukazuju na pravac kojim treba da se usmere buduća istraživanja. Poznavanje molekularnih mehanizama regulacije aktivnosti i ekspresije iNOS, svakako će pomoći razvoju novih terapijskih strategija u tretmanu štetnih efekata produkcije slobodnih radikala, pre svega nekontrolisane produkcije NO., According to the World Health Organization, 15 million people per year are affected by stroke. The most common cause of stroke is brain ischemia, which occurs in almost 85% of cases. Ischemia caused by thromboembolism is defined as permanently or temporarily decreased blood flow which prevents an adequate delivery of oxygen, glucose and other important nutrients, leading progressively to metabolic changes and cell apoptosis. Carotid endarterectomy (CEA) can cause hypoxic - ischemic states of the brain or acute brain ischemia (ABI) leading eventually to stroke. The main cause of ABI as a result of CEA is cerebral hypoperfusion caused by clamping of carotid arteries, when hypoxia occurs.. Hypoxia per se is one of the triggers of complex physiological responses in the body, including the release of various mediators of inflammation. One of these inflammatory mediators is nitric oxide (NO), a free radical which has numerous physiological effects and also plays an important role in the immune response of the organism. However, NO may be very harmful and cause cell and tissue damage. The lack of literature data on the role of endothelial NOS (eNOS) and inducible NOS (iNOS) during CEA, as well as the mechanisms of their regulation in ischemic conditions, suggest that intensifying future research in this field is very important. An insight into molecular mechanisms of iNOS activity and expression regulation will certainly help to develop new therapeutic strategies for treating harmful effects of free radicals, especially uncontrolled production of NO.",
journal = "Medicinska istraživanja",
title = "Uloga azot-monoksid sintaza u stanjima ishemije mozga tokom karotidne endarterektomije, The role of the nitric oxide synthases in brain ischemia during carotid endarterectomy",
volume = "49",
number = "1",
pages = "40-46",
doi = "10.5937/MedIst1501040B"
}
Bogdanović, N., Obradović, M. M., Jasnić, N., Spremo-Potparević, B., Unić-Stojanović, D., Radak, Đ. J.,& Isenović, E. R.. (2015). Uloga azot-monoksid sintaza u stanjima ishemije mozga tokom karotidne endarterektomije. in Medicinska istraživanja, 49(1), 40-46.
https://doi.org/10.5937/MedIst1501040B
Bogdanović N, Obradović MM, Jasnić N, Spremo-Potparević B, Unić-Stojanović D, Radak ĐJ, Isenović ER. Uloga azot-monoksid sintaza u stanjima ishemije mozga tokom karotidne endarterektomije. in Medicinska istraživanja. 2015;49(1):40-46.
doi:10.5937/MedIst1501040B .
Bogdanović, Nikola, Obradović, Milan M., Jasnić, Nebojša, Spremo-Potparević, Biljana, Unić-Stojanović, Dragana, Radak, Đorđe J., Isenović, Esma R., "Uloga azot-monoksid sintaza u stanjima ishemije mozga tokom karotidne endarterektomije" in Medicinska istraživanja, 49, no. 1 (2015):40-46,
https://doi.org/10.5937/MedIst1501040B . .