TY  - JOUR
AU  - Lukić, Nikola
AU  - Mačvanin, Mirjana T.
AU  - Gluvić, Zoran
AU  - Rizzo, Manfredi
AU  - Radak, Đorđe
AU  - Suri, Jasjit S.
AU  - Isenović, Esma R.
PY  - 2023
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/12022
AB  - Type 2 diabetes mellitus (T2DM) has become a worldwide concern in recent years, primarily in highly developed Western societies. T2DM causes systemic complications, such as atherosclerotic heart disease, ischemic stroke, peripheral artery disease, kidney failure, and diabetes-related maculopathy and retinopathy. The growing number of T2DM patients and the treatment of long-term T2DM-related complications pressurize and exhaust public healthcare systems. As a result, strategies for combating T2DM and developing novel drugs are critical global public health requirements. Aside from preventive measures, which are still the most effective way to prevent T2DM, novel and highly effective therapies are emerging. In the spotlight of next-generation T2DM treatment, sodium-glucose co-transporter 2 (SGLT-2) inhibitors are promoted as the most efficient perspective therapy. SGLT-2 inhibitors (SGLT2i) include phlorizin derivatives, such as canagliflozin, dapagliflozin, empagliflozin, and ertugliflozin. SGLT-2, along with SGLT-1, is a member of the SGLT family of proteins that play a role in glucose absorption via active transport mediated by Na+ /K+ ATPase. SGLT-2 is only found in the kidney, specifically the proximal tubule, and is responsible for more than 90% glucose absorption. Inhibition of SGLT-2 reduces glucose absorption, and consequently increases urinary glucose excretion, decreasing blood glucose levels. Thus, the inhibition of SGLT-2 activity ultimately alleviates T2DM-related symptoms and prevents or delays systemic T2DM-associated chronic complications. This review aimed to provide a more detailed understanding of the effects of SGLT2i responsible for the acute improvement in blood glucose regulation, a prerequisite for T2DM-associated cardiovascular complications control.
T2  - Current Medicinal Chemistry
T1  - SGLT-2 Inhibitors: The Next-generation Treatment for Type 2 Diabetes Mellitus
VL  - 31
DO  - 10.2174/0109298673251493231011192520
ER  - 

@article{
author = "Lukić, Nikola and Mačvanin, Mirjana T. and Gluvić, Zoran and Rizzo, Manfredi and Radak, Đorđe and Suri, Jasjit S. and Isenović, Esma R.",
year = "2023",
abstract = "Type 2 diabetes mellitus (T2DM) has become a worldwide concern in recent years, primarily in highly developed Western societies. T2DM causes systemic complications, such as atherosclerotic heart disease, ischemic stroke, peripheral artery disease, kidney failure, and diabetes-related maculopathy and retinopathy. The growing number of T2DM patients and the treatment of long-term T2DM-related complications pressurize and exhaust public healthcare systems. As a result, strategies for combating T2DM and developing novel drugs are critical global public health requirements. Aside from preventive measures, which are still the most effective way to prevent T2DM, novel and highly effective therapies are emerging. In the spotlight of next-generation T2DM treatment, sodium-glucose co-transporter 2 (SGLT-2) inhibitors are promoted as the most efficient perspective therapy. SGLT-2 inhibitors (SGLT2i) include phlorizin derivatives, such as canagliflozin, dapagliflozin, empagliflozin, and ertugliflozin. SGLT-2, along with SGLT-1, is a member of the SGLT family of proteins that play a role in glucose absorption via active transport mediated by Na+ /K+ ATPase. SGLT-2 is only found in the kidney, specifically the proximal tubule, and is responsible for more than 90% glucose absorption. Inhibition of SGLT-2 reduces glucose absorption, and consequently increases urinary glucose excretion, decreasing blood glucose levels. Thus, the inhibition of SGLT-2 activity ultimately alleviates T2DM-related symptoms and prevents or delays systemic T2DM-associated chronic complications. This review aimed to provide a more detailed understanding of the effects of SGLT2i responsible for the acute improvement in blood glucose regulation, a prerequisite for T2DM-associated cardiovascular complications control.",
journal = "Current Medicinal Chemistry",
title = "SGLT-2 Inhibitors: The Next-generation Treatment for Type 2 Diabetes Mellitus",
volume = "31",
doi = "10.2174/0109298673251493231011192520"
}

Lukić, N., Mačvanin, M. T., Gluvić, Z., Rizzo, M., Radak, Đ., Suri, J. S.,& Isenović, E. R.. (2023). SGLT-2 Inhibitors: The Next-generation Treatment for Type 2 Diabetes Mellitus. in Current Medicinal Chemistry, 31.
https://doi.org/10.2174/0109298673251493231011192520

Lukić N, Mačvanin MT, Gluvić Z, Rizzo M, Radak Đ, Suri JS, Isenović ER. SGLT-2 Inhibitors: The Next-generation Treatment for Type 2 Diabetes Mellitus. in Current Medicinal Chemistry. 2023;31.
doi:10.2174/0109298673251493231011192520 .

Lukić, Nikola, Mačvanin, Mirjana T., Gluvić, Zoran, Rizzo, Manfredi, Radak, Đorđe, Suri, Jasjit S., Isenović, Esma R., "SGLT-2 Inhibitors: The Next-generation Treatment for Type 2 Diabetes Mellitus" in Current Medicinal Chemistry, 31 (2023),
https://doi.org/10.2174/0109298673251493231011192520 . .

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 . .

TY  - JOUR
AU  - Joksić, Gordana
AU  - Radak, Đorđe J.
AU  - Sudar-Milovanović, Emina
AU  - Obradović, Milan M.
AU  - Radovanović, Jelena V.
AU  - Isenović, Esma R.
PY  - 2021
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/9407
AB  - Background: Gentiana lutea (GL), commonly known as yellow gentian, bitter root, and bit-terwort, belongs to family Gentianaceae. GL belongs to genus Gentiana, which is a rich natural source of iridoids, secoiridoids, xantones, flavonoids, triterpenoids, and carbohydrates. Medicinal plants from Gentiana species have anti-oxidant, anti-inflammatory, anti-mitogenic, anti-proliferative, and lipid-lowering effects, as well as a cardioprotective, hypotensive, vasodilator and anti-platelet activities. Objective: We reviewed the recent literature related to the effects of Gentiana species, and their active components on vascular diseases. Methods: Data used for this review were obtained by searching the electronic database [PUB-MED/MEDLINE 1973-February 2020]. The primary data search terms of interest were: Gentiana lutea, Gentienacea family, phytochemistry, vascular diseases, treatment of vascular diseases, anti-oxidant, anti-inflammatory, anti-atherogenic. Conclusion: Gentiana species and their constituents affect many different factors related to vascular disease development and progression. Therefore, Gentiana-based therapeutics represent potentially use-ful drugs for the management of vascular diseases. © 2021 Bentham Science Publishers.
T2  - Current Vascular Pharmacology
T1  - Effects of Gentiana lutea Root on Vascular Diseases
VL  - 19
IS  - 4
SP  - 359
EP  - 369
DO  - 10.2174/1570161118666200529111314
ER  - 

@article{
author = "Joksić, Gordana and Radak, Đorđe J. and Sudar-Milovanović, Emina and Obradović, Milan M. and Radovanović, Jelena V. and Isenović, Esma R.",
year = "2021",
abstract = "Background: Gentiana lutea (GL), commonly known as yellow gentian, bitter root, and bit-terwort, belongs to family Gentianaceae. GL belongs to genus Gentiana, which is a rich natural source of iridoids, secoiridoids, xantones, flavonoids, triterpenoids, and carbohydrates. Medicinal plants from Gentiana species have anti-oxidant, anti-inflammatory, anti-mitogenic, anti-proliferative, and lipid-lowering effects, as well as a cardioprotective, hypotensive, vasodilator and anti-platelet activities. Objective: We reviewed the recent literature related to the effects of Gentiana species, and their active components on vascular diseases. Methods: Data used for this review were obtained by searching the electronic database [PUB-MED/MEDLINE 1973-February 2020]. The primary data search terms of interest were: Gentiana lutea, Gentienacea family, phytochemistry, vascular diseases, treatment of vascular diseases, anti-oxidant, anti-inflammatory, anti-atherogenic. Conclusion: Gentiana species and their constituents affect many different factors related to vascular disease development and progression. Therefore, Gentiana-based therapeutics represent potentially use-ful drugs for the management of vascular diseases. © 2021 Bentham Science Publishers.",
journal = "Current Vascular Pharmacology",
title = "Effects of Gentiana lutea Root on Vascular Diseases",
volume = "19",
number = "4",
pages = "359-369",
doi = "10.2174/1570161118666200529111314"
}

Joksić, G., Radak, Đ. J., Sudar-Milovanović, E., Obradović, M. M., Radovanović, J. V.,& Isenović, E. R.. (2021). Effects of Gentiana lutea Root on Vascular Diseases. in Current Vascular Pharmacology, 19(4), 359-369.
https://doi.org/10.2174/1570161118666200529111314

Joksić G, Radak ĐJ, Sudar-Milovanović E, Obradović MM, Radovanović JV, Isenović ER. Effects of Gentiana lutea Root on Vascular Diseases. in Current Vascular Pharmacology. 2021;19(4):359-369.
doi:10.2174/1570161118666200529111314 .

Joksić, Gordana, Radak, Đorđe J., Sudar-Milovanović, Emina, Obradović, Milan M., Radovanović, Jelena V., Isenović, Esma R., "Effects of Gentiana lutea Root on Vascular Diseases" in Current Vascular Pharmacology, 19, no. 4 (2021):359-369,
https://doi.org/10.2174/1570161118666200529111314 . .

TY  - JOUR
AU  - Gluvić, Zoran
AU  - Obradović, Milan M.
AU  - Sudar-Milovanović, Emina
AU  - Zafirović, Sonja
AU  - Radak, Đorđe J.
AU  - Essack, Magbubah
AU  - Bajić, Vladimir B.
AU  - Gojobori, Takashi
AU  - Isenović, Esma R.
PY  - 2020
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8474
AB  - Hypothyroidism is a common endocrine disorder that predominantly occurs in females. It is associated with an increased risk of cardiovascular diseases (CVD), but the molecular mechanism is not known. Disturbance in lipid metabolism, the regulation of oxidative stress, and inflammation characterize the progression of subclinical hypothyroidism. The initiation and progression of endothelial dysfunction also exhibit these changes, which is the initial step in developing CVD. Animal and human studies highlight the critical role of nitric oxide (NO) as a reliable biomarker for cardiovascular risk in subclinical and clinical hypothyroidism. In this review, we summarize the recent literature findings associated with NO production by the thyroid hormones in both physiological and pathophysiological conditions. We also discuss the levothyroxine treatment effect on serum NO levels in hypothyroid patients. © 2020 The Authors
T2  - Biomedicine and Pharmacotherapy
T1  - Regulation of nitric oxide production in hypothyroidism
VL  - 124
SP  - 109881
DO  - 10.1016/j.biopha.2020.109881
ER  - 

@article{
author = "Gluvić, Zoran and Obradović, Milan M. and Sudar-Milovanović, Emina and Zafirović, Sonja and Radak, Đorđe J. and Essack, Magbubah and Bajić, Vladimir B. and Gojobori, Takashi and Isenović, Esma R.",
year = "2020",
abstract = "Hypothyroidism is a common endocrine disorder that predominantly occurs in females. It is associated with an increased risk of cardiovascular diseases (CVD), but the molecular mechanism is not known. Disturbance in lipid metabolism, the regulation of oxidative stress, and inflammation characterize the progression of subclinical hypothyroidism. The initiation and progression of endothelial dysfunction also exhibit these changes, which is the initial step in developing CVD. Animal and human studies highlight the critical role of nitric oxide (NO) as a reliable biomarker for cardiovascular risk in subclinical and clinical hypothyroidism. In this review, we summarize the recent literature findings associated with NO production by the thyroid hormones in both physiological and pathophysiological conditions. We also discuss the levothyroxine treatment effect on serum NO levels in hypothyroid patients. © 2020 The Authors",
journal = "Biomedicine and Pharmacotherapy",
title = "Regulation of nitric oxide production in hypothyroidism",
volume = "124",
pages = "109881",
doi = "10.1016/j.biopha.2020.109881"
}

Gluvić, Z., Obradović, M. M., Sudar-Milovanović, E., Zafirović, S., Radak, Đ. J., Essack, M., Bajić, V. B., Gojobori, T.,& Isenović, E. R.. (2020). Regulation of nitric oxide production in hypothyroidism. in Biomedicine and Pharmacotherapy, 124, 109881.
https://doi.org/10.1016/j.biopha.2020.109881

Gluvić Z, Obradović MM, Sudar-Milovanović E, Zafirović S, Radak ĐJ, Essack M, Bajić VB, Gojobori T, Isenović ER. Regulation of nitric oxide production in hypothyroidism. in Biomedicine and Pharmacotherapy. 2020;124:109881.
doi:10.1016/j.biopha.2020.109881 .

Gluvić, Zoran, Obradović, Milan M., Sudar-Milovanović, Emina, Zafirović, Sonja, Radak, Đorđe J., Essack, Magbubah, Bajić, Vladimir B., Gojobori, Takashi, Isenović, Esma R., "Regulation of nitric oxide production in hypothyroidism" in Biomedicine and Pharmacotherapy, 124 (2020):109881,
https://doi.org/10.1016/j.biopha.2020.109881 . .

TY  - JOUR
AU  - Obradović, Milan M.
AU  - Zafirović, Sonja
AU  - Essack, Magbubah
AU  - Dimitrov, Jelena
AU  - Živković, Lada
AU  - Spremo-Potparević, Biljana
AU  - Radak, Đorđe J.
AU  - Bajić, Vladimir B.
AU  - Isenović, Esma R.
PY  - 2020
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8487
AB  - To remedy carotid artery stenosis and prevent stroke surgical intervention is commonly used, and the gold standard being carotid endarterectomy (CEA). During CEA cerebrovascular hemoglobin oxygen saturation decreases and when this decrease reaches critical levels it leads to cerebral hypoxia that causes neuronal damage. One of the proposed mechanism that affects changes during CEA and contribute to acute brain ischemia (ABI) is oxidative stress. The increased production of reactive oxygen species and reactive nitrogen species during ABI may cause an unregulated inflammatory response and further lead to structural and functional injury of neurons. Antioxidant activity are involved in the protection against neuronal damage after cerebral ischemia. We hypothesized that neuronal injury and poor outcomes in patients undergoing CEA may be results of oxidative stress that disturbed function of antioxidant enzymes and contributed to the DNA damage in lymphocytes. © 2019 The Authors
PB  - Churchill Livingstone
T2  - Medical Hypotheses
T1  - Antioxidant enzymes expression in lymphocytes of patients undergoing carotid endarterectomy
VL  - 134
SP  - 109419
DO  - 10.1016/j.mehy.2019.109419
ER  - 

@article{
author = "Obradović, Milan M. and Zafirović, Sonja and Essack, Magbubah and Dimitrov, Jelena and Živković, Lada and Spremo-Potparević, Biljana and Radak, Đorđe J. and Bajić, Vladimir B. and Isenović, Esma R.",
year = "2020",
abstract = "To remedy carotid artery stenosis and prevent stroke surgical intervention is commonly used, and the gold standard being carotid endarterectomy (CEA). During CEA cerebrovascular hemoglobin oxygen saturation decreases and when this decrease reaches critical levels it leads to cerebral hypoxia that causes neuronal damage. One of the proposed mechanism that affects changes during CEA and contribute to acute brain ischemia (ABI) is oxidative stress. The increased production of reactive oxygen species and reactive nitrogen species during ABI may cause an unregulated inflammatory response and further lead to structural and functional injury of neurons. Antioxidant activity are involved in the protection against neuronal damage after cerebral ischemia. We hypothesized that neuronal injury and poor outcomes in patients undergoing CEA may be results of oxidative stress that disturbed function of antioxidant enzymes and contributed to the DNA damage in lymphocytes. © 2019 The Authors",
publisher = "Churchill Livingstone",
journal = "Medical Hypotheses",
title = "Antioxidant enzymes expression in lymphocytes of patients undergoing carotid endarterectomy",
volume = "134",
pages = "109419",
doi = "10.1016/j.mehy.2019.109419"
}

Obradović, M. M., Zafirović, S., Essack, M., Dimitrov, J., Živković, L., Spremo-Potparević, B., Radak, Đ. J., Bajić, V. B.,& Isenović, E. R.. (2020). Antioxidant enzymes expression in lymphocytes of patients undergoing carotid endarterectomy. in Medical Hypotheses
Churchill Livingstone., 134, 109419.
https://doi.org/10.1016/j.mehy.2019.109419

Obradović MM, Zafirović S, Essack M, Dimitrov J, Živković L, Spremo-Potparević B, Radak ĐJ, Bajić VB, Isenović ER. Antioxidant enzymes expression in lymphocytes of patients undergoing carotid endarterectomy. in Medical Hypotheses. 2020;134:109419.
doi:10.1016/j.mehy.2019.109419 .

Obradović, Milan M., Zafirović, Sonja, Essack, Magbubah, Dimitrov, Jelena, Živković, Lada, Spremo-Potparević, Biljana, Radak, Đorđe J., Bajić, Vladimir B., Isenović, Esma R., "Antioxidant enzymes expression in lymphocytes of patients undergoing carotid endarterectomy" in Medical Hypotheses, 134 (2020):109419,
https://doi.org/10.1016/j.mehy.2019.109419 . .

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 . .

TY  - JOUR
AU  - Radak, Đorđe J.
AU  - Nešković, Mihailo
AU  - Otašević, Petar
AU  - Isenović, Esma R.
PY  - 2019
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8038
AB  - Abdominal Aortic Aneurysm (AAA) is a degenerative disease of the aortic wall with potentially fatal complications. Open Repair (OR) was considered the gold standard, until the emergence of Endovascular Aneurysm Repair (EVAR), which is less invasive and equally (if not more) effective. As the popularity of endovascular procedures grows, related complications become more evident, with kidney damage being one of them. Although Acute Kidney Injury (AKI) following EVAR is relatively common, its true incidence is still uncertain. Also, there is insufficient data concerning long-term renal outcomes after EVAR, especially with repeated contrast agent exposure. Despite the lack of firm evidence on the effectiveness of individual strategies, it is evident that prevention of AKI following EVAR requires a multifactorial approach. This review focuses on recent findings based on human studies regarding the current evidence of renal impairment after EVAR, its quantification and strategies for its prevention. © 2019 Bentham Science Publishers.
T2  - Current Vascular Pharmacology
T1  - Renal Dysfunction Following Elective Endovascular Aortic Aneurysm Repair
VL  - 17
IS  - 2
SP  - 133
EP  - 140
DO  - 10.2174/1570161115666171116163203
ER  - 

@article{
author = "Radak, Đorđe J. and Nešković, Mihailo and Otašević, Petar and Isenović, Esma R.",
year = "2019",
abstract = "Abdominal Aortic Aneurysm (AAA) is a degenerative disease of the aortic wall with potentially fatal complications. Open Repair (OR) was considered the gold standard, until the emergence of Endovascular Aneurysm Repair (EVAR), which is less invasive and equally (if not more) effective. As the popularity of endovascular procedures grows, related complications become more evident, with kidney damage being one of them. Although Acute Kidney Injury (AKI) following EVAR is relatively common, its true incidence is still uncertain. Also, there is insufficient data concerning long-term renal outcomes after EVAR, especially with repeated contrast agent exposure. Despite the lack of firm evidence on the effectiveness of individual strategies, it is evident that prevention of AKI following EVAR requires a multifactorial approach. This review focuses on recent findings based on human studies regarding the current evidence of renal impairment after EVAR, its quantification and strategies for its prevention. © 2019 Bentham Science Publishers.",
journal = "Current Vascular Pharmacology",
title = "Renal Dysfunction Following Elective Endovascular Aortic Aneurysm Repair",
volume = "17",
number = "2",
pages = "133-140",
doi = "10.2174/1570161115666171116163203"
}

Radak, Đ. J., Nešković, M., Otašević, P.,& Isenović, E. R.. (2019). Renal Dysfunction Following Elective Endovascular Aortic Aneurysm Repair. in Current Vascular Pharmacology, 17(2), 133-140.
https://doi.org/10.2174/1570161115666171116163203

Radak ĐJ, Nešković M, Otašević P, Isenović ER. Renal Dysfunction Following Elective Endovascular Aortic Aneurysm Repair. in Current Vascular Pharmacology. 2019;17(2):133-140.
doi:10.2174/1570161115666171116163203 .

Radak, Đorđe J., Nešković, Mihailo, Otašević, Petar, Isenović, Esma R., "Renal Dysfunction Following Elective Endovascular Aortic Aneurysm Repair" in Current Vascular Pharmacology, 17, no. 2 (2019):133-140,
https://doi.org/10.2174/1570161115666171116163203 . .

TY  - JOUR
AU  - Radak, Đorđe J.
AU  - Nešković, Mihailo
AU  - Otašević, Petar
AU  - Isenović, Esma R.
PY  - 2019
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8040
AB  - Abdominal Aortic Aneurysm (AAA) is a degenerative disease of the aortic wall with potentially fatal complications. Open Repair (OR) was considered the gold standard, until the emergence of Endovascular Aneurysm Repair (EVAR), which is less invasive and equally (if not more) effective. As the popularity of endovascular procedures grows, related complications become more evident, with kidney damage being one of them. Although Acute Kidney Injury (AKI) following EVAR is relatively common, its true incidence is still uncertain. Also, there is insufficient data concerning long-term renal outcomes after EVAR, especially with repeated contrast agent exposure. Despite the lack of firm evidence on the effectiveness of individual strategies, it is evident that prevention of AKI following EVAR requires a multifactorial approach. This review focuses on recent findings based on human studies regarding the current evidence of renal impairment after EVAR, its quantification and strategies for its prevention. © 2019 Bentham Science Publishers.
T2  - Current Vascular Pharmacology
T1  - Renal Dysfunction Following Elective Endovascular Aortic Aneurysm Repair
VL  - 17
IS  - 2
SP  - 133
EP  - 140
DO  - 10.2174/1570161115666171116163203
ER  - 

@article{
author = "Radak, Đorđe J. and Nešković, Mihailo and Otašević, Petar and Isenović, Esma R.",
year = "2019",
abstract = "Abdominal Aortic Aneurysm (AAA) is a degenerative disease of the aortic wall with potentially fatal complications. Open Repair (OR) was considered the gold standard, until the emergence of Endovascular Aneurysm Repair (EVAR), which is less invasive and equally (if not more) effective. As the popularity of endovascular procedures grows, related complications become more evident, with kidney damage being one of them. Although Acute Kidney Injury (AKI) following EVAR is relatively common, its true incidence is still uncertain. Also, there is insufficient data concerning long-term renal outcomes after EVAR, especially with repeated contrast agent exposure. Despite the lack of firm evidence on the effectiveness of individual strategies, it is evident that prevention of AKI following EVAR requires a multifactorial approach. This review focuses on recent findings based on human studies regarding the current evidence of renal impairment after EVAR, its quantification and strategies for its prevention. © 2019 Bentham Science Publishers.",
journal = "Current Vascular Pharmacology",
title = "Renal Dysfunction Following Elective Endovascular Aortic Aneurysm Repair",
volume = "17",
number = "2",
pages = "133-140",
doi = "10.2174/1570161115666171116163203"
}

Radak, Đ. J., Nešković, M., Otašević, P.,& Isenović, E. R.. (2019). Renal Dysfunction Following Elective Endovascular Aortic Aneurysm Repair. in Current Vascular Pharmacology, 17(2), 133-140.
https://doi.org/10.2174/1570161115666171116163203

Radak ĐJ, Nešković M, Otašević P, Isenović ER. Renal Dysfunction Following Elective Endovascular Aortic Aneurysm Repair. in Current Vascular Pharmacology. 2019;17(2):133-140.
doi:10.2174/1570161115666171116163203 .

Radak, Đorđe J., Nešković, Mihailo, Otašević, Petar, Isenović, Esma R., "Renal Dysfunction Following Elective Endovascular Aortic Aneurysm Repair" in Current Vascular Pharmacology, 17, no. 2 (2019):133-140,
https://doi.org/10.2174/1570161115666171116163203 . .

TY  - JOUR
AU  - Radak, Đorđe J.
AU  - Atanasijević, Igor
AU  - Nešković, Mihailo
AU  - Isenović, Esma R.
PY  - 2019
UR  - http://www.eurekaselect.com/159661/article
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8098
AB  - Chronic venous disease (CVeD) is a highly prevalent condition in the general population, and it has a significant impact on quality of life. While it is usually manifested by obvious signs, such as varicose veins and venous ulcers, other symptoms of the disease are less specific. Among the other symptoms, which include heaviness, swelling, muscle cramps and restless legs, pain is the symptom that most frequently compels CVeD patients to seek medical aid. However, there is a substantial discrepancy between pain severity and clinically detectable signs of CVeD, questioned by several opposing studies. Further evaluation is needed to clarify this subject, and to analyse whether pain development predicts objective CVeD progression. General management of CVeD starts with advising lifestyle changes, such as lowering body mass index and treating comorbidities. However, the mainstay of treatment is compression therapy, with the additional use of pharmacological substances. Venoactive drugs proved to be the drugs of choice for symptom alleviation and slowing the progression of CVeD, with micronized purified flavonoid fraction being the most effective one. Interventional therapy is reserved for advanced stages of the disease.
T2  - Current Vascular Pharmacology
T1  - The Significance of Pain in Chronic Venous Disease and its Medical Treatment
VL  - 17
IS  - 3
SP  - 291
EP  - 297
DO  - 10.2174/1570161116666180209111826
ER  - 

@article{
author = "Radak, Đorđe J. and Atanasijević, Igor and Nešković, Mihailo and Isenović, Esma R.",
year = "2019",
abstract = "Chronic venous disease (CVeD) is a highly prevalent condition in the general population, and it has a significant impact on quality of life. While it is usually manifested by obvious signs, such as varicose veins and venous ulcers, other symptoms of the disease are less specific. Among the other symptoms, which include heaviness, swelling, muscle cramps and restless legs, pain is the symptom that most frequently compels CVeD patients to seek medical aid. However, there is a substantial discrepancy between pain severity and clinically detectable signs of CVeD, questioned by several opposing studies. Further evaluation is needed to clarify this subject, and to analyse whether pain development predicts objective CVeD progression. General management of CVeD starts with advising lifestyle changes, such as lowering body mass index and treating comorbidities. However, the mainstay of treatment is compression therapy, with the additional use of pharmacological substances. Venoactive drugs proved to be the drugs of choice for symptom alleviation and slowing the progression of CVeD, with micronized purified flavonoid fraction being the most effective one. Interventional therapy is reserved for advanced stages of the disease.",
journal = "Current Vascular Pharmacology",
title = "The Significance of Pain in Chronic Venous Disease and its Medical Treatment",
volume = "17",
number = "3",
pages = "291-297",
doi = "10.2174/1570161116666180209111826"
}

Radak, Đ. J., Atanasijević, I., Nešković, M.,& Isenović, E. R.. (2019). The Significance of Pain in Chronic Venous Disease and its Medical Treatment. in Current Vascular Pharmacology, 17(3), 291-297.
https://doi.org/10.2174/1570161116666180209111826

Radak ĐJ, Atanasijević I, Nešković M, Isenović ER. The Significance of Pain in Chronic Venous Disease and its Medical Treatment. in Current Vascular Pharmacology. 2019;17(3):291-297.
doi:10.2174/1570161116666180209111826 .

Radak, Đorđe J., Atanasijević, Igor, Nešković, Mihailo, Isenović, Esma R., "The Significance of Pain in Chronic Venous Disease and its Medical Treatment" in Current Vascular Pharmacology, 17, no. 3 (2019):291-297,
https://doi.org/10.2174/1570161116666180209111826 . .

TY  - JOUR
AU  - Bajić, Vladan P.
AU  - Van Neste, Christophe
AU  - Obradović, Milan M.
AU  - Zafirović, Sonja
AU  - Radak, Đorđe J.
AU  - Bajić, Vladimir B.
AU  - Essack, Magbubah
AU  - Isenović, Esma R.
PY  - 2019
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8375
AB  - More people die from cardiovascular diseases (CVD) than from any other cause. Cardiovascular complications are thought to arise from enhanced levels of free radicals causing impaired “redox homeostasis,” which represents the interplay between oxidative stress (OS) and reductive stress (RS). In this review, we compile several experimental research findings that show sustained shifts towards OS will alter the homeostatic redox mechanism to cause cardiovascular complications, as well as findings that show a prolonged antioxidant state or RS can similarly lead to such cardiovascular complications. This experimental evidence is specifically focused on the role of glutathione, the most abundant antioxidant in the heart, in a redox homeostatic mechanism that has been shifted towards OS or RS. This may lead to impairment of cellular signaling mechanisms and elevated pools of proteotoxicity associated with cardiac dysfunction.
T2  - Oxidative Medicine and Cellular Longevity
T1  - Glutathione “Redox Homeostasis” and Its Relation to Cardiovascular Disease
VL  - 2019
SP  - 5028181
DO  - 10.1155/2019/5028181
ER  - 

@article{
author = "Bajić, Vladan P. and Van Neste, Christophe and Obradović, Milan M. and Zafirović, Sonja and Radak, Đorđe J. and Bajić, Vladimir B. and Essack, Magbubah and Isenović, Esma R.",
year = "2019",
abstract = "More people die from cardiovascular diseases (CVD) than from any other cause. Cardiovascular complications are thought to arise from enhanced levels of free radicals causing impaired “redox homeostasis,” which represents the interplay between oxidative stress (OS) and reductive stress (RS). In this review, we compile several experimental research findings that show sustained shifts towards OS will alter the homeostatic redox mechanism to cause cardiovascular complications, as well as findings that show a prolonged antioxidant state or RS can similarly lead to such cardiovascular complications. This experimental evidence is specifically focused on the role of glutathione, the most abundant antioxidant in the heart, in a redox homeostatic mechanism that has been shifted towards OS or RS. This may lead to impairment of cellular signaling mechanisms and elevated pools of proteotoxicity associated with cardiac dysfunction.",
journal = "Oxidative Medicine and Cellular Longevity",
title = "Glutathione “Redox Homeostasis” and Its Relation to Cardiovascular Disease",
volume = "2019",
pages = "5028181",
doi = "10.1155/2019/5028181"
}

Bajić, V. P., Van Neste, C., Obradović, M. M., Zafirović, S., Radak, Đ. J., Bajić, V. B., Essack, M.,& Isenović, E. R.. (2019). Glutathione “Redox Homeostasis” and Its Relation to Cardiovascular Disease. in Oxidative Medicine and Cellular Longevity, 2019, 5028181.
https://doi.org/10.1155/2019/5028181

Bajić VP, Van Neste C, Obradović MM, Zafirović S, Radak ĐJ, Bajić VB, Essack M, Isenović ER. Glutathione “Redox Homeostasis” and Its Relation to Cardiovascular Disease. in Oxidative Medicine and Cellular Longevity. 2019;2019:5028181.
doi:10.1155/2019/5028181 .

Bajić, Vladan P., Van Neste, Christophe, Obradović, Milan M., Zafirović, Sonja, Radak, Đorđe J., Bajić, Vladimir B., Essack, Magbubah, Isenović, Esma R., "Glutathione “Redox Homeostasis” and Its Relation to Cardiovascular Disease" in Oxidative Medicine and Cellular Longevity, 2019 (2019):5028181,
https://doi.org/10.1155/2019/5028181 . .

TY  - JOUR
AU  - Veljković, Nevena V.
AU  - Zarić, Božidarka
AU  - Đurić, Ilona
AU  - Obradović, Milan M.
AU  - Sudar-Milovanović, Emina
AU  - Radak, Đorđe J.
AU  - Isenović, Esma R.
PY  - 2018
UR  - http://www.mdpi.com/1010-660X/54/3/36
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/7878
AB  - Coronary artery disease (CAD) and myocardial infarction (MI) are recognized as leading causes of mortality in developed countries. Although typically associated with behavioral risk factors, such as smoking, sedentary lifestyle, and poor dietary habits, such vascular phenotypes have also long been recognized as being related to genetic background. We review the currently available data concerning genetic markers for CAD in English and non-English articles with English abstracts published between 2003 and 2018. As genetic testing is increasingly available, it may be possible to identify adequate genetic markers representing the risk profile and to use them in a clinical setting. © 2018 by the authors. Licensee MDPI, Basel, Switzerland.
T2  - Medicina
T1  - Genetic Markers for Coronary Artery Disease
VL  - 54
IS  - 3
SP  - 36
DO  - 10.3390/medicina54030036
ER  - 

@article{
author = "Veljković, Nevena V. and Zarić, Božidarka and Đurić, Ilona and Obradović, Milan M. and Sudar-Milovanović, Emina and Radak, Đorđe J. and Isenović, Esma R.",
year = "2018",
abstract = "Coronary artery disease (CAD) and myocardial infarction (MI) are recognized as leading causes of mortality in developed countries. Although typically associated with behavioral risk factors, such as smoking, sedentary lifestyle, and poor dietary habits, such vascular phenotypes have also long been recognized as being related to genetic background. We review the currently available data concerning genetic markers for CAD in English and non-English articles with English abstracts published between 2003 and 2018. As genetic testing is increasingly available, it may be possible to identify adequate genetic markers representing the risk profile and to use them in a clinical setting. © 2018 by the authors. Licensee MDPI, Basel, Switzerland.",
journal = "Medicina",
title = "Genetic Markers for Coronary Artery Disease",
volume = "54",
number = "3",
pages = "36",
doi = "10.3390/medicina54030036"
}

Veljković, N. V., Zarić, B., Đurić, I., Obradović, M. M., Sudar-Milovanović, E., Radak, Đ. J.,& Isenović, E. R.. (2018). Genetic Markers for Coronary Artery Disease. in Medicina, 54(3), 36.
https://doi.org/10.3390/medicina54030036

Veljković NV, Zarić B, Đurić I, Obradović MM, Sudar-Milovanović E, Radak ĐJ, Isenović ER. Genetic Markers for Coronary Artery Disease. in Medicina. 2018;54(3):36.
doi:10.3390/medicina54030036 .

Veljković, Nevena V., Zarić, Božidarka, Đurić, Ilona, Obradović, Milan M., Sudar-Milovanović, Emina, Radak, Đorđe J., Isenović, Esma R., "Genetic Markers for Coronary Artery Disease" in Medicina, 54, no. 3 (2018):36,
https://doi.org/10.3390/medicina54030036 . .

TY  - JOUR
AU  - Gluvić, Zoran
AU  - Zarić, Božidarka
AU  - Resanović, Ivana
AU  - Obradović, Milan M.
AU  - Mitrović, Aleksandar
AU  - Radak, Đorđe J.
AU  - Isenović, Esma R.
PY  - 2017
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1470
AB  - Metabolic syndrome (MetS) is a leading public health and clinical challenge worldwide. MetS represents a group of interrelated risk factors that predict cardiovascular diseases (CVD) and diabetes mellitus (DM). Its prevalence ranges between 10 and 84%, depending on the geographic region, urban or rural environment, individual demographic characteristics of the population studied (sex, age, racial and ethnic origin), as well as the criteria used to define MetS. Persons with MetS have higher mortality rate when compared with people without MetS, primarily caused by progressive atherosclerosis, accelerated by pro-inflammatory and pro-coagulation components of MetS. Considering the high prevalence of metabolic disorders (glucose metabolism disorder, hypertension, dyslipidaemia, obesity etc.), preventive healthcare should focus on changing lifestyle in order to reduce obesity and increase physical activity. This narrative review considers the available evidence from clinical and experimental studies dealing with MetS, and current treatment options for patients with insulin resistance and MetS.
T2  - Current Vascular Pharmacology
T1  - Link between Metabolic Syndrome and Insulin Resistance
VL  - 15
IS  - 1
SP  - 30
EP  - 39
DO  - 10.2174/1570161114666161007164510
ER  - 

@article{
author = "Gluvić, Zoran and Zarić, Božidarka and Resanović, Ivana and Obradović, Milan M. and Mitrović, Aleksandar and Radak, Đorđe J. and Isenović, Esma R.",
year = "2017",
abstract = "Metabolic syndrome (MetS) is a leading public health and clinical challenge worldwide. MetS represents a group of interrelated risk factors that predict cardiovascular diseases (CVD) and diabetes mellitus (DM). Its prevalence ranges between 10 and 84%, depending on the geographic region, urban or rural environment, individual demographic characteristics of the population studied (sex, age, racial and ethnic origin), as well as the criteria used to define MetS. Persons with MetS have higher mortality rate when compared with people without MetS, primarily caused by progressive atherosclerosis, accelerated by pro-inflammatory and pro-coagulation components of MetS. Considering the high prevalence of metabolic disorders (glucose metabolism disorder, hypertension, dyslipidaemia, obesity etc.), preventive healthcare should focus on changing lifestyle in order to reduce obesity and increase physical activity. This narrative review considers the available evidence from clinical and experimental studies dealing with MetS, and current treatment options for patients with insulin resistance and MetS.",
journal = "Current Vascular Pharmacology",
title = "Link between Metabolic Syndrome and Insulin Resistance",
volume = "15",
number = "1",
pages = "30-39",
doi = "10.2174/1570161114666161007164510"
}

Gluvić, Z., Zarić, B., Resanović, I., Obradović, M. M., Mitrović, A., Radak, Đ. J.,& Isenović, E. R.. (2017). Link between Metabolic Syndrome and Insulin Resistance. in Current Vascular Pharmacology, 15(1), 30-39.
https://doi.org/10.2174/1570161114666161007164510

Gluvić Z, Zarić B, Resanović I, Obradović MM, Mitrović A, Radak ĐJ, Isenović ER. Link between Metabolic Syndrome and Insulin Resistance. in Current Vascular Pharmacology. 2017;15(1):30-39.
doi:10.2174/1570161114666161007164510 .

Gluvić, Zoran, Zarić, Božidarka, Resanović, Ivana, Obradović, Milan M., Mitrović, Aleksandar, Radak, Đorđe J., Isenović, Esma R., "Link between Metabolic Syndrome and Insulin Resistance" in Current Vascular Pharmacology, 15, no. 1 (2017):30-39,
https://doi.org/10.2174/1570161114666161007164510 . .

TY  - JOUR
AU  - Radak, Đorđe J.
AU  - Katsiki, Niki
AU  - Resanović, Ivana
AU  - Jovanović, Aleksandra
AU  - Sudar, Emina
AU  - Zafirović, Sonja
AU  - Mousa, Shaker A.
AU  - Isenović, Esma R.
PY  - 2017
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1521
AB  - Apoptosis may contribute to a significant proportion of neuron death following acute brain ischemia (ABI), but the underlying mechanisms are still not fully understood. Brain ischemia may lead to stroke, which is one of the main causes of long-term morbidity and mortality in both developed and developing countries. Therefore, stroke prevention and treatment is clinically important. There are two important separate areas of the brain during ABI: the ischemic core and the ischemic penumbra. The ischemic core of the brain experiences a sudden reduction of blood flow, just minutes after ischemic attack with irreversible injury and subsequent cell death. On the other hand, apoptosis within the ischemic penumbra may occur after several hours or days, while necrosis starts in the first hours after the onset of ABI in the ischemic core. ABI is characterized by key molecular events that initiate apoptosis in many cells, such as overproduction of free radicals, Ca2+ overload and excitotoxicity. These changes in cellular homeostasis may trigger either necrosis or apoptosis, which often depends on cell type, cell age, and location in the brain. Apoptosis results in DNA fragmentation, degradation of cytoskeletal and nuclear proteins, cross-linking of proteins, formation of apoptotic bodies, expression of ligands for phagocytic cell receptors and finally uptake by phagocytic cells. This review focuses on recent findings based on animal and human studies regarding the apoptotic mechanisms of neuronal death following ABI and the development of potential neuroprotective agents that reduce morbidity. The effects of statins on stroke prevention and treatment as well as on apoptotic mediators are also considered.
T2  - Current Vascular Pharmacology
T1  - Apoptosis and Acute Brain Ischemia in Ischemic Stroke
VL  - 15
IS  - 2
SP  - 115
EP  - 122
DO  - 10.2174/1570161115666161104095522
ER  - 

@article{
author = "Radak, Đorđe J. and Katsiki, Niki and Resanović, Ivana and Jovanović, Aleksandra and Sudar, Emina and Zafirović, Sonja and Mousa, Shaker A. and Isenović, Esma R.",
year = "2017",
abstract = "Apoptosis may contribute to a significant proportion of neuron death following acute brain ischemia (ABI), but the underlying mechanisms are still not fully understood. Brain ischemia may lead to stroke, which is one of the main causes of long-term morbidity and mortality in both developed and developing countries. Therefore, stroke prevention and treatment is clinically important. There are two important separate areas of the brain during ABI: the ischemic core and the ischemic penumbra. The ischemic core of the brain experiences a sudden reduction of blood flow, just minutes after ischemic attack with irreversible injury and subsequent cell death. On the other hand, apoptosis within the ischemic penumbra may occur after several hours or days, while necrosis starts in the first hours after the onset of ABI in the ischemic core. ABI is characterized by key molecular events that initiate apoptosis in many cells, such as overproduction of free radicals, Ca2+ overload and excitotoxicity. These changes in cellular homeostasis may trigger either necrosis or apoptosis, which often depends on cell type, cell age, and location in the brain. Apoptosis results in DNA fragmentation, degradation of cytoskeletal and nuclear proteins, cross-linking of proteins, formation of apoptotic bodies, expression of ligands for phagocytic cell receptors and finally uptake by phagocytic cells. This review focuses on recent findings based on animal and human studies regarding the apoptotic mechanisms of neuronal death following ABI and the development of potential neuroprotective agents that reduce morbidity. The effects of statins on stroke prevention and treatment as well as on apoptotic mediators are also considered.",
journal = "Current Vascular Pharmacology",
title = "Apoptosis and Acute Brain Ischemia in Ischemic Stroke",
volume = "15",
number = "2",
pages = "115-122",
doi = "10.2174/1570161115666161104095522"
}

Radak, Đ. J., Katsiki, N., Resanović, I., Jovanović, A., Sudar, E., Zafirović, S., Mousa, S. A.,& Isenović, E. R.. (2017). Apoptosis and Acute Brain Ischemia in Ischemic Stroke. in Current Vascular Pharmacology, 15(2), 115-122.
https://doi.org/10.2174/1570161115666161104095522

Radak ĐJ, Katsiki N, Resanović I, Jovanović A, Sudar E, Zafirović S, Mousa SA, Isenović ER. Apoptosis and Acute Brain Ischemia in Ischemic Stroke. in Current Vascular Pharmacology. 2017;15(2):115-122.
doi:10.2174/1570161115666161104095522 .

Radak, Đorđe J., Katsiki, Niki, Resanović, Ivana, Jovanović, Aleksandra, Sudar, Emina, Zafirović, Sonja, Mousa, Shaker A., Isenović, Esma R., "Apoptosis and Acute Brain Ischemia in Ischemic Stroke" in Current Vascular Pharmacology, 15, no. 2 (2017):115-122,
https://doi.org/10.2174/1570161115666161104095522 . .

TY  - JOUR
AU  - Radak, Đorđe J.
AU  - Đukić, Nenad
AU  - Tanasković, Slobodan
AU  - Obradović, Milan M.
AU  - Cenić-Milošević, Desanka
AU  - Isenović, Esma R.
PY  - 2017
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1522
AB  - Endovascular surgery represents a minimally invasive procedure for the treatment of occlusive and aneurysmal arterial disease. However, it is followed by inflammatory response, with a rise in specific inflammatory biomarkers, such as C-reactive protein, serum amyloid A and fibrinogen. Shear stress during balloon inflation and vascular injury represents triggering events for the inflammatory process, stimulating the production of proinflammatory molecules and activation of circulating monocytes. The current literature indicates that stent implantation induces more prominent inflammatory reaction. Additionally, it has been shown that muscular arteries of femoropopliteal segment react to a greater extent to stent implantation, compared with elastic carotid or iliac arteries. The endovascular treatment of thoracic and abdominal aortic aneurysm is frequently followed with post-implantation inflammatory syndrome. Most recent findings point out that stent graft material plays a significant role in the inflammatory response, representing a challenge for clinicians. Future studies should consider the pathophysiology of the inflammatory response associated with endovascular procedures as well as predictors and risk factors including preventive strategies and therapeutic algorithms. Although the potential role of anti-inflammatory drugs after endovascular procedures has been observed, it needs to be validated in upcoming trials. The Neutrophil Lymphocyte Ratio, platelet count, Platelet-to-Lymphocyte Ratio and other biomarkers should be considered in future trials to assess the inflammatory response after endovascular procedures. Inflammatory markers may also become therapeutic targets.
T2  - Current Vascular Pharmacology
T1  - Should We be Concerned About the Inflammatory Response to Endovascular Procedures?
VL  - 15
IS  - 3
SP  - 230
EP  - 237
DO  - 10.2174/1570161115666170105121900
ER  - 

@article{
author = "Radak, Đorđe J. and Đukić, Nenad and Tanasković, Slobodan and Obradović, Milan M. and Cenić-Milošević, Desanka and Isenović, Esma R.",
year = "2017",
abstract = "Endovascular surgery represents a minimally invasive procedure for the treatment of occlusive and aneurysmal arterial disease. However, it is followed by inflammatory response, with a rise in specific inflammatory biomarkers, such as C-reactive protein, serum amyloid A and fibrinogen. Shear stress during balloon inflation and vascular injury represents triggering events for the inflammatory process, stimulating the production of proinflammatory molecules and activation of circulating monocytes. The current literature indicates that stent implantation induces more prominent inflammatory reaction. Additionally, it has been shown that muscular arteries of femoropopliteal segment react to a greater extent to stent implantation, compared with elastic carotid or iliac arteries. The endovascular treatment of thoracic and abdominal aortic aneurysm is frequently followed with post-implantation inflammatory syndrome. Most recent findings point out that stent graft material plays a significant role in the inflammatory response, representing a challenge for clinicians. Future studies should consider the pathophysiology of the inflammatory response associated with endovascular procedures as well as predictors and risk factors including preventive strategies and therapeutic algorithms. Although the potential role of anti-inflammatory drugs after endovascular procedures has been observed, it needs to be validated in upcoming trials. The Neutrophil Lymphocyte Ratio, platelet count, Platelet-to-Lymphocyte Ratio and other biomarkers should be considered in future trials to assess the inflammatory response after endovascular procedures. Inflammatory markers may also become therapeutic targets.",
journal = "Current Vascular Pharmacology",
title = "Should We be Concerned About the Inflammatory Response to Endovascular Procedures?",
volume = "15",
number = "3",
pages = "230-237",
doi = "10.2174/1570161115666170105121900"
}

Radak, Đ. J., Đukić, N., Tanasković, S., Obradović, M. M., Cenić-Milošević, D.,& Isenović, E. R.. (2017). Should We be Concerned About the Inflammatory Response to Endovascular Procedures?. in Current Vascular Pharmacology, 15(3), 230-237.
https://doi.org/10.2174/1570161115666170105121900

Radak ĐJ, Đukić N, Tanasković S, Obradović MM, Cenić-Milošević D, Isenović ER. Should We be Concerned About the Inflammatory Response to Endovascular Procedures?. in Current Vascular Pharmacology. 2017;15(3):230-237.
doi:10.2174/1570161115666170105121900 .

Radak, Đorđe J., Đukić, Nenad, Tanasković, Slobodan, Obradović, Milan M., Cenić-Milošević, Desanka, Isenović, Esma R., "Should We be Concerned About the Inflammatory Response to Endovascular Procedures?" in Current Vascular Pharmacology, 15, no. 3 (2017):230-237,
https://doi.org/10.2174/1570161115666170105121900 . .

TY  - JOUR
AU  - Jovanović, Aleksandra
AU  - Sudar, Emina
AU  - Obradović, Milan M.
AU  - Pitt, Samantha J.
AU  - Stewart, Alan J.
AU  - Zafirović, Sonja
AU  - Stanimirović, Julijana
AU  - Radak, Đorđe J.
AU  - Isenović, Esma R.
PY  - 2017
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1678
AB  - Background: Overexpression of inducible nitric oxide synthase (iNOS) is a key link between high-fat (HF) diet induced obesity and cardiovascular disease. Oestradiol has cardioprotective effects that may be mediated through reduction of iNOS activity/expression. Methods: In the present study, female Wistar rats were fed a standard diet or a HF diet (42% fat) for 10 weeks. iNOS gene and protein expressions were measured in heart tissue. HF-fed rats exhibited a significant increase in cardiac iNOS mRNA by 695% (p LT 0.05), iNOS protein level by 248% (p LT 0.01), without changes in nitrate/nitrite levels. Expression of CD36 protein in plasma membranes was increased by 37% (p LT 0.05), while the concentration of free fatty acids (FFA) was reduced by 25% (p LT 0.01) in HF-fed rats. Expression of the p50 subunit of nuclear factor-kappa B (NF kappa B-p50) in heart was increased by 77% (p LT 0.01) in HF-fed rats. Expression of protein kinase B (Akt) and extracellular signal-regulated kinases 1/2 (ERK1/2) were unchanged between the groups. There was a significant increase in the ratio of phospho-Akt/total Akt but not for phospho-ERK1/2/total ERK1/2 in HF-fed rats. Estrogen receptor-levels (by 50%; p LT 0.05) and serum oestradiol concentrations (by 35%; p LT 0.05) were shown to be significantly reduced in HF-fed rats. Results and Conclusion: Our results revealed that a HF diet led to increased iNOS expression, most likely via a mechanism involving Akt and NF kappa B-p50 proteins. Decreased levels of oestradiol and ER protein in the HF-fed group, in combination with increased iNOS levels are consistent with the hypothesis that oestradiol has a cardioprotective effect through its ability to regulate iNOS expression.
T2  - Current Vascular Pharmacology
T1  - Influence of a High-fat Diet on Cardiac iNOS in Female Rats
VL  - 15
IS  - 5
SP  - 491
EP  - 500
DO  - 10.2174/1570161114666161025101303
ER  - 

@article{
author = "Jovanović, Aleksandra and Sudar, Emina and Obradović, Milan M. and Pitt, Samantha J. and Stewart, Alan J. and Zafirović, Sonja and Stanimirović, Julijana and Radak, Đorđe J. and Isenović, Esma R.",
year = "2017",
abstract = "Background: Overexpression of inducible nitric oxide synthase (iNOS) is a key link between high-fat (HF) diet induced obesity and cardiovascular disease. Oestradiol has cardioprotective effects that may be mediated through reduction of iNOS activity/expression. Methods: In the present study, female Wistar rats were fed a standard diet or a HF diet (42% fat) for 10 weeks. iNOS gene and protein expressions were measured in heart tissue. HF-fed rats exhibited a significant increase in cardiac iNOS mRNA by 695% (p LT 0.05), iNOS protein level by 248% (p LT 0.01), without changes in nitrate/nitrite levels. Expression of CD36 protein in plasma membranes was increased by 37% (p LT 0.05), while the concentration of free fatty acids (FFA) was reduced by 25% (p LT 0.01) in HF-fed rats. Expression of the p50 subunit of nuclear factor-kappa B (NF kappa B-p50) in heart was increased by 77% (p LT 0.01) in HF-fed rats. Expression of protein kinase B (Akt) and extracellular signal-regulated kinases 1/2 (ERK1/2) were unchanged between the groups. There was a significant increase in the ratio of phospho-Akt/total Akt but not for phospho-ERK1/2/total ERK1/2 in HF-fed rats. Estrogen receptor-levels (by 50%; p LT 0.05) and serum oestradiol concentrations (by 35%; p LT 0.05) were shown to be significantly reduced in HF-fed rats. Results and Conclusion: Our results revealed that a HF diet led to increased iNOS expression, most likely via a mechanism involving Akt and NF kappa B-p50 proteins. Decreased levels of oestradiol and ER protein in the HF-fed group, in combination with increased iNOS levels are consistent with the hypothesis that oestradiol has a cardioprotective effect through its ability to regulate iNOS expression.",
journal = "Current Vascular Pharmacology",
title = "Influence of a High-fat Diet on Cardiac iNOS in Female Rats",
volume = "15",
number = "5",
pages = "491-500",
doi = "10.2174/1570161114666161025101303"
}

Jovanović, A., Sudar, E., Obradović, M. M., Pitt, S. J., Stewart, A. J., Zafirović, S., Stanimirović, J., Radak, Đ. J.,& Isenović, E. R.. (2017). Influence of a High-fat Diet on Cardiac iNOS in Female Rats. in Current Vascular Pharmacology, 15(5), 491-500.
https://doi.org/10.2174/1570161114666161025101303

Jovanović A, Sudar E, Obradović MM, Pitt SJ, Stewart AJ, Zafirović S, Stanimirović J, Radak ĐJ, Isenović ER. Influence of a High-fat Diet on Cardiac iNOS in Female Rats. in Current Vascular Pharmacology. 2017;15(5):491-500.
doi:10.2174/1570161114666161025101303 .

Jovanović, Aleksandra, Sudar, Emina, Obradović, Milan M., Pitt, Samantha J., Stewart, Alan J., Zafirović, Sonja, Stanimirović, Julijana, Radak, Đorđe J., Isenović, Esma R., "Influence of a High-fat Diet on Cardiac iNOS in Female Rats" in Current Vascular Pharmacology, 15, no. 5 (2017):491-500,
https://doi.org/10.2174/1570161114666161025101303 . .

TY  - JOUR
AU  - Sudar-Milovanović, Emina
AU  - Obradović, Milan M.
AU  - Jovanović, Aleksandra
AU  - Zarić, Božidarka
AU  - Zafirović, Sonja
AU  - Panić, Anastasija
AU  - Radak, Đorđe J.
AU  - Isenović, Esma R.
PY  - 2016
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/829
AB  - The amino acid, L-Arginine (L-Arg) plays an important role in the cardiovascular system. Data from the literature show that L-Arg is the only substrate for the production of nitric oxide (NO), from which L-Arg develops its effects on the cardiovascular system. As a free radical, NO is synthesized in all mammalian cells by L-Arg with the activity of NO synthase (NOS). In states of hypertension, diabetes, hypercholesterolemia and vascular inflammation a disorder occurs in the metabolic pathway of the synthesis of NO from L-Arg which all together bring alterations of blood vessels. Experimental results obtained on animals, as well as clinical studies show that L-Arg has an effect on thrombocytes, on the process of coagulation and on the fibrolytic system. This mini review represents a summary of the latest scientific animal and human studies related to L-Arg and its mechanisms of actions with a focus on the role of L-Arg via NO pathway in cardiovascular disorders. Moreover, here we present data from recent animal and clinical studies suggesting that L-Arg could be one of the possible therapeutic molecules for improving the treatment of different cardiovascular disorders.
PB  - Bentham Science Publishers
T2  - Mini Reviews in Medicinal Chemistry
T1  - Benefits of L-Arginine on Cardiovascular System
VL  - 16
IS  - 2
SP  - 94
EP  - 103
DO  - 10.2174/1389557515666151016125826
ER  - 

@article{
author = "Sudar-Milovanović, Emina and Obradović, Milan M. and Jovanović, Aleksandra and Zarić, Božidarka and Zafirović, Sonja and Panić, Anastasija and Radak, Đorđe J. and Isenović, Esma R.",
year = "2016",
abstract = "The amino acid, L-Arginine (L-Arg) plays an important role in the cardiovascular system. Data from the literature show that L-Arg is the only substrate for the production of nitric oxide (NO), from which L-Arg develops its effects on the cardiovascular system. As a free radical, NO is synthesized in all mammalian cells by L-Arg with the activity of NO synthase (NOS). In states of hypertension, diabetes, hypercholesterolemia and vascular inflammation a disorder occurs in the metabolic pathway of the synthesis of NO from L-Arg which all together bring alterations of blood vessels. Experimental results obtained on animals, as well as clinical studies show that L-Arg has an effect on thrombocytes, on the process of coagulation and on the fibrolytic system. This mini review represents a summary of the latest scientific animal and human studies related to L-Arg and its mechanisms of actions with a focus on the role of L-Arg via NO pathway in cardiovascular disorders. Moreover, here we present data from recent animal and clinical studies suggesting that L-Arg could be one of the possible therapeutic molecules for improving the treatment of different cardiovascular disorders.",
publisher = "Bentham Science Publishers",
journal = "Mini Reviews in Medicinal Chemistry",
title = "Benefits of L-Arginine on Cardiovascular System",
volume = "16",
number = "2",
pages = "94-103",
doi = "10.2174/1389557515666151016125826"
}

Sudar-Milovanović, E., Obradović, M. M., Jovanović, A., Zarić, B., Zafirović, S., Panić, A., Radak, Đ. J.,& Isenović, E. R.. (2016). Benefits of L-Arginine on Cardiovascular System. in Mini Reviews in Medicinal Chemistry
Bentham Science Publishers., 16(2), 94-103.
https://doi.org/10.2174/1389557515666151016125826

Sudar-Milovanović E, Obradović MM, Jovanović A, Zarić B, Zafirović S, Panić A, Radak ĐJ, Isenović ER. Benefits of L-Arginine on Cardiovascular System. in Mini Reviews in Medicinal Chemistry. 2016;16(2):94-103.
doi:10.2174/1389557515666151016125826 .

Sudar-Milovanović, Emina, Obradović, Milan M., Jovanović, Aleksandra, Zarić, Božidarka, Zafirović, Sonja, Panić, Anastasija, Radak, Đorđe J., Isenović, Esma R., "Benefits of L-Arginine on Cardiovascular System" in Mini Reviews in Medicinal Chemistry, 16, no. 2 (2016):94-103,
https://doi.org/10.2174/1389557515666151016125826 . .

TY  - JOUR
AU  - Kolaković, Ana
AU  - Stanković, Aleksandra
AU  - Đurić, Tamara
AU  - Živković, Maja
AU  - Končar, Igor
AU  - Davidović, Lazar
AU  - Radak, Đorđe J.
AU  - Alavantić, Dragan
PY  - 2016
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1123
AB  - Background: The angiotensin II type 2 receptor (AT2R) - 1332 A/G polymorphism has been denoted as functional and associated with certain cardiovascular disease phenotypes. However, there are no studies considering the association of this gene polymorphism with carotid atherosclerosis (CA) and cerebrovascular events. Therefore, the aim of our study was to investigate a possible association of the AT2R - 1332 A/G polymorphism with the occurrence of carotid plaques (CPs) and history of cerebrovascular insult (CVI) in advanced CA. Methods: The study group included 381 controls and 509 patients with CA consecutively admitted for endarterectomy. Genotyping was determined by polymerase chain reaction-restriction fragment length polymorphism method. The association was analyzed separately for males and females because the AT2R gene is located on the X chromosome. Results: The AT2R - 1332 GG genotype was associated with the advanced CA in the female study group (recessive model of inheritance, AA+AG versus GG; adjusted odds ratio [OR] = 2.25; 95% confidence interval [CI] 1.17-4.33; P=.01). In the male subgroup of patients with CA, the significant overrepresentation of G/- hemizygote was detected in patients with CVI compared to male patients without this event (crude OR = 2.05, 95% CI 1.20-3.50, P=.008). Conclusions: This study suggests a gender-specific association between the AT2R -1332 A/G polymorphism and the occurrence of CP and the history of CVI in advanced CA, but further replication studies are needed. (C) 2016 National Stroke Association. Published by Elsevier Inc. All rights reserved.
T2  - Journal of Stroke and Cerebrovascular Diseases
T1  - Gender-Specific Association between Angiotensin II Type 2 Receptor-1332 A/G Gene Polymorphism and Advanced Carotid Atherosclerosis
VL  - 25
IS  - 7
SP  - 1622
EP  - 1630
DO  - 10.1016/j.jstrokecerebrovasdis.2016.03.011
ER  - 

@article{
author = "Kolaković, Ana and Stanković, Aleksandra and Đurić, Tamara and Živković, Maja and Končar, Igor and Davidović, Lazar and Radak, Đorđe J. and Alavantić, Dragan",
year = "2016",
abstract = "Background: The angiotensin II type 2 receptor (AT2R) - 1332 A/G polymorphism has been denoted as functional and associated with certain cardiovascular disease phenotypes. However, there are no studies considering the association of this gene polymorphism with carotid atherosclerosis (CA) and cerebrovascular events. Therefore, the aim of our study was to investigate a possible association of the AT2R - 1332 A/G polymorphism with the occurrence of carotid plaques (CPs) and history of cerebrovascular insult (CVI) in advanced CA. Methods: The study group included 381 controls and 509 patients with CA consecutively admitted for endarterectomy. Genotyping was determined by polymerase chain reaction-restriction fragment length polymorphism method. The association was analyzed separately for males and females because the AT2R gene is located on the X chromosome. Results: The AT2R - 1332 GG genotype was associated with the advanced CA in the female study group (recessive model of inheritance, AA+AG versus GG; adjusted odds ratio [OR] = 2.25; 95% confidence interval [CI] 1.17-4.33; P=.01). In the male subgroup of patients with CA, the significant overrepresentation of G/- hemizygote was detected in patients with CVI compared to male patients without this event (crude OR = 2.05, 95% CI 1.20-3.50, P=.008). Conclusions: This study suggests a gender-specific association between the AT2R -1332 A/G polymorphism and the occurrence of CP and the history of CVI in advanced CA, but further replication studies are needed. (C) 2016 National Stroke Association. Published by Elsevier Inc. All rights reserved.",
journal = "Journal of Stroke and Cerebrovascular Diseases",
title = "Gender-Specific Association between Angiotensin II Type 2 Receptor-1332 A/G Gene Polymorphism and Advanced Carotid Atherosclerosis",
volume = "25",
number = "7",
pages = "1622-1630",
doi = "10.1016/j.jstrokecerebrovasdis.2016.03.011"
}

Kolaković, A., Stanković, A., Đurić, T., Živković, M., Končar, I., Davidović, L., Radak, Đ. J.,& Alavantić, D.. (2016). Gender-Specific Association between Angiotensin II Type 2 Receptor-1332 A/G Gene Polymorphism and Advanced Carotid Atherosclerosis. in Journal of Stroke and Cerebrovascular Diseases, 25(7), 1622-1630.
https://doi.org/10.1016/j.jstrokecerebrovasdis.2016.03.011

Kolaković A, Stanković A, Đurić T, Živković M, Končar I, Davidović L, Radak ĐJ, Alavantić D. Gender-Specific Association between Angiotensin II Type 2 Receptor-1332 A/G Gene Polymorphism and Advanced Carotid Atherosclerosis. in Journal of Stroke and Cerebrovascular Diseases. 2016;25(7):1622-1630.
doi:10.1016/j.jstrokecerebrovasdis.2016.03.011 .

Kolaković, Ana, Stanković, Aleksandra, Đurić, Tamara, Živković, Maja, Končar, Igor, Davidović, Lazar, Radak, Đorđe J., Alavantić, Dragan, "Gender-Specific Association between Angiotensin II Type 2 Receptor-1332 A/G Gene Polymorphism and Advanced Carotid Atherosclerosis" in Journal of Stroke and Cerebrovascular Diseases, 25, no. 7 (2016):1622-1630,
https://doi.org/10.1016/j.jstrokecerebrovasdis.2016.03.011 . .

TY  - JOUR
AU  - Radak, Đorđe J.
AU  - Tanasković, Slobodan
AU  - Katsiki, Niki
AU  - Isenović, Esma R.
PY  - 2016
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1005
AB  - An inverse association between diabetes mellitus (DM) and abdominal aortic aneurysm (AAA) risk have been reported. Apart from a lower AAA prevalence among patients with vs without DM, there are data showing that DM may exert a protective role on aneurysmal growth in patients with small AAAs, thus decreasing the risk of rupture. As atherosclerosis has almost the same risk factors as aneurysms, the decreased AAA prevalence in patients with DM may indicate that atherosclerosis is an associated feature and not a cause of the aneurysms. Alternatively, DM may be associated with factors that influence AAA formation. In this narrative review, we discuss the inverse association between DM and AAA. We also comment on underlying cellular and genetic pathophysiological mechanisms of DM, AAA and atherosclerosis. The effects of drugs, commonly prescribed in DM patients, on AAA development and growth are also considered.
T2  - Current Vascular Pharmacology
T1  - Protective Role of Diabetes Mellitus on Abdominal Aortic Aneurysm Pathogenesis: Myth or Reality?
VL  - 14
IS  - 2
SP  - 196
EP  - 200
DO  - 10.2174/1570161113666150529125127
ER  - 

@article{
author = "Radak, Đorđe J. and Tanasković, Slobodan and Katsiki, Niki and Isenović, Esma R.",
year = "2016",
abstract = "An inverse association between diabetes mellitus (DM) and abdominal aortic aneurysm (AAA) risk have been reported. Apart from a lower AAA prevalence among patients with vs without DM, there are data showing that DM may exert a protective role on aneurysmal growth in patients with small AAAs, thus decreasing the risk of rupture. As atherosclerosis has almost the same risk factors as aneurysms, the decreased AAA prevalence in patients with DM may indicate that atherosclerosis is an associated feature and not a cause of the aneurysms. Alternatively, DM may be associated with factors that influence AAA formation. In this narrative review, we discuss the inverse association between DM and AAA. We also comment on underlying cellular and genetic pathophysiological mechanisms of DM, AAA and atherosclerosis. The effects of drugs, commonly prescribed in DM patients, on AAA development and growth are also considered.",
journal = "Current Vascular Pharmacology",
title = "Protective Role of Diabetes Mellitus on Abdominal Aortic Aneurysm Pathogenesis: Myth or Reality?",
volume = "14",
number = "2",
pages = "196-200",
doi = "10.2174/1570161113666150529125127"
}

Radak, Đ. J., Tanasković, S., Katsiki, N.,& Isenović, E. R.. (2016). Protective Role of Diabetes Mellitus on Abdominal Aortic Aneurysm Pathogenesis: Myth or Reality?. in Current Vascular Pharmacology, 14(2), 196-200.
https://doi.org/10.2174/1570161113666150529125127

Radak ĐJ, Tanasković S, Katsiki N, Isenović ER. Protective Role of Diabetes Mellitus on Abdominal Aortic Aneurysm Pathogenesis: Myth or Reality?. in Current Vascular Pharmacology. 2016;14(2):196-200.
doi:10.2174/1570161113666150529125127 .

Radak, Đorđe J., Tanasković, Slobodan, Katsiki, Niki, Isenović, Esma R., "Protective Role of Diabetes Mellitus on Abdominal Aortic Aneurysm Pathogenesis: Myth or Reality?" in Current Vascular Pharmacology, 14, no. 2 (2016):196-200,
https://doi.org/10.2174/1570161113666150529125127 . .

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 . .

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 . .

TY  - JOUR
AU  - Trpković, Andreja
AU  - Resanović, Ivana
AU  - Stanimirović, Julijana
AU  - Radak, Đorđe J.
AU  - Mousa, Shaker A.
AU  - Cenić-Milošević, Desanka
AU  - Jevremovic, Danimir
AU  - Isenović, Esma R.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/635
AB  - Atherosclerosis is a life-long illness that begins with risk factors, which in turn contribute to the development of subclinical disease, followed by the establishment of overt cardiovascular disease (CVD). Thrombotic-occlusive complications of atherosclerosis are among the most widespread and costly health problems. Oxidized low-density lipoprotein (OxLDL) plays an important role in atherogenesis by promoting an inflammatory environment and lipid deposition in the arterial wall. As cardiovascular events occur in individuals without common risk factors, there is a need for additional tools that may help in CVD risk assessment and management. The use of biomarkers has improved diagnostic, therapeutic and prognostic outcome in cardiovascular medicine. This review elaborates on the value of circulating OxLDL as a biomarker of CVD. Three enzyme-linked immunosorbent assays (4E6, DLH3 and E06) using murine monoclonal antibodies for determination of OxLDL blood levels have been developed. However, none of these assays are currently approved for routine clinical practice. We identified studies investigating OxLDL in CVD (measured by 4E6, DLH3 or E06 assay) by searching the PubMed database. Circulating OxLDL was found to be associated with all stages of atherosclerosis, from early atherogenesis to hypertension, coronary and peripheral arterial disease, acute coronary syndromes and ischemic cerebral infarction. The results of studies investigating the usefulness of OxLDL for CVD prediction were also summarized. Furthermore, OxLDL was found to be associated with pathologic conditions linked to CVD, including diabetes mellitus, obesity and metabolic syndrome (MetS). In addition, we have addressed the mechanisms by which OxLDL promotes atherogenesis, and the effects of antiatherogenic treatments on circulating OxLDL. Finally, we highlight the evidence suggesting that lipoprotein (a) [ Lp(a)] is the preferential carrier of oxidized phospholipids (OxPL) in human plasma. A strong association between OxPLapoB level (representing the content of OxPL on apolipoprotein B-100 particles, measured by E06 assay) and Lp(a) has been determined.
T2  - Critical Reviews in Clinical Laboratory Sciences
T1  - Oxidized low-density lipoprotein as a biomarker of cardiovascular diseases
VL  - 52
IS  - 2
SP  - 70
EP  - 85
DO  - 10.3109/10408363.2014.992063
ER  - 

@article{
author = "Trpković, Andreja and Resanović, Ivana and Stanimirović, Julijana and Radak, Đorđe J. and Mousa, Shaker A. and Cenić-Milošević, Desanka and Jevremovic, Danimir and Isenović, Esma R.",
year = "2015",
abstract = "Atherosclerosis is a life-long illness that begins with risk factors, which in turn contribute to the development of subclinical disease, followed by the establishment of overt cardiovascular disease (CVD). Thrombotic-occlusive complications of atherosclerosis are among the most widespread and costly health problems. Oxidized low-density lipoprotein (OxLDL) plays an important role in atherogenesis by promoting an inflammatory environment and lipid deposition in the arterial wall. As cardiovascular events occur in individuals without common risk factors, there is a need for additional tools that may help in CVD risk assessment and management. The use of biomarkers has improved diagnostic, therapeutic and prognostic outcome in cardiovascular medicine. This review elaborates on the value of circulating OxLDL as a biomarker of CVD. Three enzyme-linked immunosorbent assays (4E6, DLH3 and E06) using murine monoclonal antibodies for determination of OxLDL blood levels have been developed. However, none of these assays are currently approved for routine clinical practice. We identified studies investigating OxLDL in CVD (measured by 4E6, DLH3 or E06 assay) by searching the PubMed database. Circulating OxLDL was found to be associated with all stages of atherosclerosis, from early atherogenesis to hypertension, coronary and peripheral arterial disease, acute coronary syndromes and ischemic cerebral infarction. The results of studies investigating the usefulness of OxLDL for CVD prediction were also summarized. Furthermore, OxLDL was found to be associated with pathologic conditions linked to CVD, including diabetes mellitus, obesity and metabolic syndrome (MetS). In addition, we have addressed the mechanisms by which OxLDL promotes atherogenesis, and the effects of antiatherogenic treatments on circulating OxLDL. Finally, we highlight the evidence suggesting that lipoprotein (a) [ Lp(a)] is the preferential carrier of oxidized phospholipids (OxPL) in human plasma. A strong association between OxPLapoB level (representing the content of OxPL on apolipoprotein B-100 particles, measured by E06 assay) and Lp(a) has been determined.",
journal = "Critical Reviews in Clinical Laboratory Sciences",
title = "Oxidized low-density lipoprotein as a biomarker of cardiovascular diseases",
volume = "52",
number = "2",
pages = "70-85",
doi = "10.3109/10408363.2014.992063"
}

Trpković, A., Resanović, I., Stanimirović, J., Radak, Đ. J., Mousa, S. A., Cenić-Milošević, D., Jevremovic, D.,& Isenović, E. R.. (2015). Oxidized low-density lipoprotein as a biomarker of cardiovascular diseases. in Critical Reviews in Clinical Laboratory Sciences, 52(2), 70-85.
https://doi.org/10.3109/10408363.2014.992063

Trpković A, Resanović I, Stanimirović J, Radak ĐJ, Mousa SA, Cenić-Milošević D, Jevremovic D, Isenović ER. Oxidized low-density lipoprotein as a biomarker of cardiovascular diseases. in Critical Reviews in Clinical Laboratory Sciences. 2015;52(2):70-85.
doi:10.3109/10408363.2014.992063 .

Trpković, Andreja, Resanović, Ivana, Stanimirović, Julijana, Radak, Đorđe J., Mousa, Shaker A., Cenić-Milošević, Desanka, Jevremovic, Danimir, Isenović, Esma R., "Oxidized low-density lipoprotein as a biomarker of cardiovascular diseases" in Critical Reviews in Clinical Laboratory Sciences, 52, no. 2 (2015):70-85,
https://doi.org/10.3109/10408363.2014.992063 . .

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 . .

TY  - JOUR
AU  - Sudar-Milovanović, Emina
AU  - Obradović, Milan M.
AU  - Bajić, Vladan P.
AU  - Bogdanović, Nikola
AU  - Radak, Đorđe J.
AU  - Isenović, Esma R.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10319
AB  - Esencijalna aminokiselina, L-Arginin (L-Arg) ima veoma važnu ulogu u kardiovaskularnom sistemu. Podaci iz literature pokazuju da je L-Arg jedini supstrat za produkciju azot-monoksida (NO), preko koga L-Arg i ostvaruje svoje efekte na kardiovaskularni sistem. Kao slobodni radikal, NO se sintetiše u svim ćelijama sisara od L-Arg uz aktivnost enzima NO sintaze (NOS). U stanjima hipertenzije, dijabetesa, hiperholesterolemije i vaskularne inflamacije dolazi do poremećaja metaboličkog puta sinteze NO od L-Arg, što sve zajedno dovodi do oštećenja krvnih sudova. Kliničke studije ukazuju da L-Arg može imati efekte na trombocite, proces koagulacije kao i na fibrinolitički sistem. U okviru ovog preglednog članka sumirani su najnoviji podaci iz literature koji sugerišu da bi L-Arg mogao biti jedan od bitnih terapeutskih molekula u poboljšanju lečenja kardiovaskularnih poremećaja.
AB  - The essential amino acid, L-Arginine (L-Arg) has an important role in the cardiovascular system. Literature data show that L-Arg is the only substrate for the production of nitric oxide (NO), from which L-Arg develops its effects on the cardiovascular system. As a free radical, NO is synthesized in all mammal cells by L-Arg with the activity of NO synthase (NOS). In the states of hypertension, diabetes, hypercholesterolemia and vascular inflammation, a disorder occurs in the metabolic pathway of the synthesis of NO from L-Arg which all together bring alterations to blood vessels. Clinical studies show that L-Arg has an effect on thrombocytes, the process of coagulation and the fibrolytic system. All the new data summarized in this review suggest that L-Arg could be one of important therapeutic molecules for improving cardiovascular disorders.
T2  - Medicinska istraživanja
T1  - Uloga L-Arginina u kardiovaskularnom sistemu
T1  - The role of L-Arginine in cardiovascular system
VL  - 49
IS  - 1
SP  - 36
EP  - 39
DO  - 10.5937/MedIst1501036S
ER  - 

@article{
author = "Sudar-Milovanović, Emina and Obradović, Milan M. and Bajić, Vladan P. and Bogdanović, Nikola and Radak, Đorđe J. and Isenović, Esma R.",
year = "2015",
abstract = "Esencijalna aminokiselina, L-Arginin (L-Arg) ima veoma važnu ulogu u kardiovaskularnom sistemu. Podaci iz literature pokazuju da je L-Arg jedini supstrat za produkciju azot-monoksida (NO), preko koga L-Arg i ostvaruje svoje efekte na kardiovaskularni sistem. Kao slobodni radikal, NO se sintetiše u svim ćelijama sisara od L-Arg uz aktivnost enzima NO sintaze (NOS). U stanjima hipertenzije, dijabetesa, hiperholesterolemije i vaskularne inflamacije dolazi do poremećaja metaboličkog puta sinteze NO od L-Arg, što sve zajedno dovodi do oštećenja krvnih sudova. Kliničke studije ukazuju da L-Arg može imati efekte na trombocite, proces koagulacije kao i na fibrinolitički sistem. U okviru ovog preglednog članka sumirani su najnoviji podaci iz literature koji sugerišu da bi L-Arg mogao biti jedan od bitnih terapeutskih molekula u poboljšanju lečenja kardiovaskularnih poremećaja., The essential amino acid, L-Arginine (L-Arg) has an important role in the cardiovascular system. Literature data show that L-Arg is the only substrate for the production of nitric oxide (NO), from which L-Arg develops its effects on the cardiovascular system. As a free radical, NO is synthesized in all mammal cells by L-Arg with the activity of NO synthase (NOS). In the states of hypertension, diabetes, hypercholesterolemia and vascular inflammation, a disorder occurs in the metabolic pathway of the synthesis of NO from L-Arg which all together bring alterations to blood vessels. Clinical studies show that L-Arg has an effect on thrombocytes, the process of coagulation and the fibrolytic system. All the new data summarized in this review suggest that L-Arg could be one of important therapeutic molecules for improving cardiovascular disorders.",
journal = "Medicinska istraživanja",
title = "Uloga L-Arginina u kardiovaskularnom sistemu, The role of L-Arginine in cardiovascular system",
volume = "49",
number = "1",
pages = "36-39",
doi = "10.5937/MedIst1501036S"
}

Sudar-Milovanović, E., Obradović, M. M., Bajić, V. P., Bogdanović, N., Radak, Đ. J.,& Isenović, E. R.. (2015). Uloga L-Arginina u kardiovaskularnom sistemu. in Medicinska istraživanja, 49(1), 36-39.
https://doi.org/10.5937/MedIst1501036S

Sudar-Milovanović E, Obradović MM, Bajić VP, Bogdanović N, Radak ĐJ, Isenović ER. Uloga L-Arginina u kardiovaskularnom sistemu. in Medicinska istraživanja. 2015;49(1):36-39.
doi:10.5937/MedIst1501036S .

Sudar-Milovanović, Emina, Obradović, Milan M., Bajić, Vladan P., Bogdanović, Nikola, Radak, Đorđe J., Isenović, Esma R., "Uloga L-Arginina u kardiovaskularnom sistemu" in Medicinska istraživanja, 49, no. 1 (2015):36-39,
https://doi.org/10.5937/MedIst1501036S . .

TY  - JOUR
AU  - Obradović, Milan M.
AU  - Bogdanović, Nikola
AU  - Radak, Đorđe J.
AU  - Isenović, Esma R.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/534
T2  - Current Vascular Pharmacology
T1  - Editorial: Oxidative Stress in Pathophysiological Conditions
VL  - 13
IS  - 2
SP  - 226
EP  - 228
DO  - 10.2174/1570161113999150311153109
ER  - 

@article{
author = "Obradović, Milan M. and Bogdanović, Nikola and Radak, Đorđe J. and Isenović, Esma R.",
year = "2015",
journal = "Current Vascular Pharmacology",
title = "Editorial: Oxidative Stress in Pathophysiological Conditions",
volume = "13",
number = "2",
pages = "226-228",
doi = "10.2174/1570161113999150311153109"
}

Obradović, M. M., Bogdanović, N., Radak, Đ. J.,& Isenović, E. R.. (2015). Editorial: Oxidative Stress in Pathophysiological Conditions. in Current Vascular Pharmacology, 13(2), 226-228.
https://doi.org/10.2174/1570161113999150311153109

Obradović MM, Bogdanović N, Radak ĐJ, Isenović ER. Editorial: Oxidative Stress in Pathophysiological Conditions. in Current Vascular Pharmacology. 2015;13(2):226-228.
doi:10.2174/1570161113999150311153109 .

Obradović, Milan M., Bogdanović, Nikola, Radak, Đorđe J., Isenović, Esma R., "Editorial: Oxidative Stress in Pathophysiological Conditions" in Current Vascular Pharmacology, 13, no. 2 (2015):226-228,
https://doi.org/10.2174/1570161113999150311153109 . .

TY  - JOUR
AU  - Trpković, Andreja
AU  - Stanimirović, Julijana
AU  - Resanović, Ivana
AU  - Otasevic, Petar
AU  - Jevremovic, Danimir
AU  - Radak, Đorđe J.
AU  - Isenović, Esma R.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/312
AB  - It is now recognized that inflammatory processes regulate all stages of atherosclerosis, from disease initiation to thrombotic complications. C-reactive protein (CRP) is a plasmatic protein used as a general marker of inflammation. The high sensitivity C-reactive protein (hsCRP) refers to the measurement of CRP in blood samples using assays with sufficient sensitivity to quantify low (baseline) levels of this biomarker. Low-grade chronic inflammatory processes are linked to atherosclerosis and may be screened with the use of hsCRP, thus providing additional information in cardiovascular risk prediction. This review elaborates the role of CRP in atherogenesis and the value of hsCRP as a biomarker in cardiovascular risk prediction in both primary and secondary prevention setting.
T2  - Current Pharmaceutical Analysis
T1  - High Sensitivity C-reactive Protein and Cardiovascular Risk Prediction
VL  - 11
IS  - 1
SP  - 60
EP  - 65
DO  - 10.2174/1573412910666140822003911
ER  - 

@article{
author = "Trpković, Andreja and Stanimirović, Julijana and Resanović, Ivana and Otasevic, Petar and Jevremovic, Danimir and Radak, Đorđe J. and Isenović, Esma R.",
year = "2015",
abstract = "It is now recognized that inflammatory processes regulate all stages of atherosclerosis, from disease initiation to thrombotic complications. C-reactive protein (CRP) is a plasmatic protein used as a general marker of inflammation. The high sensitivity C-reactive protein (hsCRP) refers to the measurement of CRP in blood samples using assays with sufficient sensitivity to quantify low (baseline) levels of this biomarker. Low-grade chronic inflammatory processes are linked to atherosclerosis and may be screened with the use of hsCRP, thus providing additional information in cardiovascular risk prediction. This review elaborates the role of CRP in atherogenesis and the value of hsCRP as a biomarker in cardiovascular risk prediction in both primary and secondary prevention setting.",
journal = "Current Pharmaceutical Analysis",
title = "High Sensitivity C-reactive Protein and Cardiovascular Risk Prediction",
volume = "11",
number = "1",
pages = "60-65",
doi = "10.2174/1573412910666140822003911"
}

Trpković, A., Stanimirović, J., Resanović, I., Otasevic, P., Jevremovic, D., Radak, Đ. J.,& Isenović, E. R.. (2015). High Sensitivity C-reactive Protein and Cardiovascular Risk Prediction. in Current Pharmaceutical Analysis, 11(1), 60-65.
https://doi.org/10.2174/1573412910666140822003911

Trpković A, Stanimirović J, Resanović I, Otasevic P, Jevremovic D, Radak ĐJ, Isenović ER. High Sensitivity C-reactive Protein and Cardiovascular Risk Prediction. in Current Pharmaceutical Analysis. 2015;11(1):60-65.
doi:10.2174/1573412910666140822003911 .

Trpković, Andreja, Stanimirović, Julijana, Resanović, Ivana, Otasevic, Petar, Jevremovic, Danimir, Radak, Đorđe J., Isenović, Esma R., "High Sensitivity C-reactive Protein and Cardiovascular Risk Prediction" in Current Pharmaceutical Analysis, 11, no. 1 (2015):60-65,
https://doi.org/10.2174/1573412910666140822003911 . .