Bogdanović, Nikola

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orcid::0000-0002-8640-4027
  • Bogdanović, Nikola (9)
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Author's Bibliography

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

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

(2019)

TY  - JOUR
AU  - Obradović, Milan M.
AU  - Bogdanović, Nikola
AU  - Stanimirović, Julijana
AU  - Unić-Stojanović, Dragana R.
AU  - Radak, Đorđe J.
AU  - Isenović, Esma R.
PY  - 2019
UR  - https://linkinghub.elsevier.com/retrieve/pii/S0306987718308302
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/7930
AB  - Sudden occlusion of an artery caused by a thrombus or emboli is the most frequent cause of acute brain ischemia (ABI). Carotid endarterectomy (CEA) represents the gold standard for preventing strokes of carotid origin. However, neuronal damage caused by ischemia and/or reperfusion may contribute to a poor clinical outcome after CEA. In response to shear stress caused by hypoxic-ischemic conditions in patients undergoing CEA, stimulation of the hypothalamic-pituitaryadrenal axis leads to biological responses known as hypermetabolic stress, characterized by hemodynamic, metabolic, inflammatory and immunological changes. These changes maintain homeostasis and assist recovery, but an unregulated inflammatory response could lead to further tissue damage and death of neurons. Nitric oxide (NO) is an important signaling molecule involved in several physiological and pathological processes, including ABI. However, an excess of NO could have detrimental effects. We hypothesized that the hypoxic-ischemic state induced by carotid clamping leads to overexpression of inducible NO synthase and that uncontrolled production of NO could adversely affect outcome after CEA. © 2018 Elsevier Ltd
T2  - Medical Hypotheses
T1  - Hypothesis related to the regulation of inducible nitric oxide synthase during carotid endarterectomy
VL  - 122
SP  - 16
EP  - 18
DO  - 10.1016/j.mehy.2018.10.011
ER  - 
@article{
author = "Obradović, Milan M. and Bogdanović, Nikola and Stanimirović, Julijana and Unić-Stojanović, Dragana R. and Radak, Đorđe J. and Isenović, Esma R.",
year = "2019",
abstract = "Sudden occlusion of an artery caused by a thrombus or emboli is the most frequent cause of acute brain ischemia (ABI). Carotid endarterectomy (CEA) represents the gold standard for preventing strokes of carotid origin. However, neuronal damage caused by ischemia and/or reperfusion may contribute to a poor clinical outcome after CEA. In response to shear stress caused by hypoxic-ischemic conditions in patients undergoing CEA, stimulation of the hypothalamic-pituitaryadrenal axis leads to biological responses known as hypermetabolic stress, characterized by hemodynamic, metabolic, inflammatory and immunological changes. These changes maintain homeostasis and assist recovery, but an unregulated inflammatory response could lead to further tissue damage and death of neurons. Nitric oxide (NO) is an important signaling molecule involved in several physiological and pathological processes, including ABI. However, an excess of NO could have detrimental effects. We hypothesized that the hypoxic-ischemic state induced by carotid clamping leads to overexpression of inducible NO synthase and that uncontrolled production of NO could adversely affect outcome after CEA. © 2018 Elsevier Ltd",
journal = "Medical Hypotheses",
title = "Hypothesis related to the regulation of inducible nitric oxide synthase during carotid endarterectomy",
volume = "122",
pages = "16-18",
doi = "10.1016/j.mehy.2018.10.011"
}
Obradović, M. M., Bogdanović, N., Stanimirović, J., Unić-Stojanović, D. R., Radak, Đ. J.,& Isenović, E. R.. (2019). Hypothesis related to the regulation of inducible nitric oxide synthase during carotid endarterectomy. in Medical Hypotheses, 122, 16-18.
https://doi.org/10.1016/j.mehy.2018.10.011
Obradović MM, Bogdanović N, Stanimirović J, Unić-Stojanović DR, Radak ĐJ, Isenović ER. Hypothesis related to the regulation of inducible nitric oxide synthase during carotid endarterectomy. in Medical Hypotheses. 2019;122:16-18.
doi:10.1016/j.mehy.2018.10.011 .
Obradović, Milan M., Bogdanović, Nikola, Stanimirović, Julijana, Unić-Stojanović, Dragana R., Radak, Đorđe J., Isenović, Esma R., "Hypothesis related to the regulation of inducible nitric oxide synthase during carotid endarterectomy" in Medical Hypotheses, 122 (2019):16-18,
https://doi.org/10.1016/j.mehy.2018.10.011 . .
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Regulation of Na+/K+-ATPase by Estradiol and IGF-1 in Cardio-Metabolic Diseases

Obradović, Milan M.; Stanimirović, Julijana; Panić, Anastasija; Bogdanović, Nikola; Sudar, Emina; Cenić-Milošević, Desanka; Isenović, Esma R.

(2017)

TY  - JOUR
AU  - Obradović, Milan M.
AU  - Stanimirović, Julijana
AU  - Panić, Anastasija
AU  - Bogdanović, Nikola
AU  - Sudar, Emina
AU  - Cenić-Milošević, Desanka
AU  - Isenović, Esma R.
PY  - 2017
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1581
AB  - Background: The sodium/potassium- adenosine- triphosphatase (Na+/K+-ATPase) is an important mediator in vasculature tone and contractility, and its abnormal regulation has been implicated in many diseases such as obesity, insulin resistance, diabetes, and hypertension. Decreased Na+/K+-ATPase abundance and its altered isoform expression induce cardiomyocytes death and cardiac dysfunction, possibly leading to the development of myocardial dilation and heart failure. Therefore, the regulation of Na+/K+-ATPase activity/expression could be important in treatment and possible prevention of cardio-metabolic diseases. A number of hormones and environmental factors regulate the function of Na+/K+-ATPase in response to changing cellular requirements. Estradiol and insulin like growth factor-1 (IGF-1) are among potent hormones that positively regulate Na+/K+-ATPase activity or de novo synthesis of alpha -and beta -subunits. Both estradiol and IGF-1 have a huge therapeutic potential in treatment of vasculopathy in cardio-metabolic diseases. Methods: We searched the MEDLINE and PUBMED databases for all English and non-English articles with an English abstract from April 1978 to May 2016. The main data search terms were: Na+/K+-ATPase; estradiol and Na+/K+-ATPase; estradiol, Na+/K+-ATPase and CVS; estradiol, Na+/K+-ATPase and CVD; estradiol, Na+/K+-ATPase and obesity; estradiol, Na+/K+-ATPase and diabetes; estradiol, Na+/K+-ATPase and hypertension; IGF-1; IGF-1 and Na+/K+-ATPase; IGF-1, Na+/K+-ATPase and CVS; IGF-1, Na+/K+-ATPase and CVD; IGF-1, Na+/K+-ATPase and obesity; IGF-1, Na+/K+-ATPase and diabetes; IGF-1, Na+/K+-ATPase and hypertension. Results: The present review discusses the latest data from animal and human studies which focus on the effects of estradiol and IGF-1 on Na+/K+-ATPase regulation in physiological and pathophysiological conditions in cardiovascular system. Conclusion: Understanding the molecular mechanisms of estradiol and IGF-1 action on Na+/K+-ATPase in humans, may help resolving outstanding issues and developing new strategies for the protection and treatment of cardiovascular diseases.
T2  - Current Pharmaceutical Design
T1  - Regulation of Na+/K+-ATPase by Estradiol and IGF-1 in Cardio-Metabolic Diseases
VL  - 23
IS  - 10
SP  - 1551
EP  - 1561
DO  - 10.2174/1381612823666170203113455
ER  - 
@article{
author = "Obradović, Milan M. and Stanimirović, Julijana and Panić, Anastasija and Bogdanović, Nikola and Sudar, Emina and Cenić-Milošević, Desanka and Isenović, Esma R.",
year = "2017",
abstract = "Background: The sodium/potassium- adenosine- triphosphatase (Na+/K+-ATPase) is an important mediator in vasculature tone and contractility, and its abnormal regulation has been implicated in many diseases such as obesity, insulin resistance, diabetes, and hypertension. Decreased Na+/K+-ATPase abundance and its altered isoform expression induce cardiomyocytes death and cardiac dysfunction, possibly leading to the development of myocardial dilation and heart failure. Therefore, the regulation of Na+/K+-ATPase activity/expression could be important in treatment and possible prevention of cardio-metabolic diseases. A number of hormones and environmental factors regulate the function of Na+/K+-ATPase in response to changing cellular requirements. Estradiol and insulin like growth factor-1 (IGF-1) are among potent hormones that positively regulate Na+/K+-ATPase activity or de novo synthesis of alpha -and beta -subunits. Both estradiol and IGF-1 have a huge therapeutic potential in treatment of vasculopathy in cardio-metabolic diseases. Methods: We searched the MEDLINE and PUBMED databases for all English and non-English articles with an English abstract from April 1978 to May 2016. The main data search terms were: Na+/K+-ATPase; estradiol and Na+/K+-ATPase; estradiol, Na+/K+-ATPase and CVS; estradiol, Na+/K+-ATPase and CVD; estradiol, Na+/K+-ATPase and obesity; estradiol, Na+/K+-ATPase and diabetes; estradiol, Na+/K+-ATPase and hypertension; IGF-1; IGF-1 and Na+/K+-ATPase; IGF-1, Na+/K+-ATPase and CVS; IGF-1, Na+/K+-ATPase and CVD; IGF-1, Na+/K+-ATPase and obesity; IGF-1, Na+/K+-ATPase and diabetes; IGF-1, Na+/K+-ATPase and hypertension. Results: The present review discusses the latest data from animal and human studies which focus on the effects of estradiol and IGF-1 on Na+/K+-ATPase regulation in physiological and pathophysiological conditions in cardiovascular system. Conclusion: Understanding the molecular mechanisms of estradiol and IGF-1 action on Na+/K+-ATPase in humans, may help resolving outstanding issues and developing new strategies for the protection and treatment of cardiovascular diseases.",
journal = "Current Pharmaceutical Design",
title = "Regulation of Na+/K+-ATPase by Estradiol and IGF-1 in Cardio-Metabolic Diseases",
volume = "23",
number = "10",
pages = "1551-1561",
doi = "10.2174/1381612823666170203113455"
}
Obradović, M. M., Stanimirović, J., Panić, A., Bogdanović, N., Sudar, E., Cenić-Milošević, D.,& Isenović, E. R.. (2017). Regulation of Na+/K+-ATPase by Estradiol and IGF-1 in Cardio-Metabolic Diseases. in Current Pharmaceutical Design, 23(10), 1551-1561.
https://doi.org/10.2174/1381612823666170203113455
Obradović MM, Stanimirović J, Panić A, Bogdanović N, Sudar E, Cenić-Milošević D, Isenović ER. Regulation of Na+/K+-ATPase by Estradiol and IGF-1 in Cardio-Metabolic Diseases. in Current Pharmaceutical Design. 2017;23(10):1551-1561.
doi:10.2174/1381612823666170203113455 .
Obradović, Milan M., Stanimirović, Julijana, Panić, Anastasija, Bogdanović, Nikola, Sudar, Emina, Cenić-Milošević, Desanka, Isenović, Esma R., "Regulation of Na+/K+-ATPase by Estradiol and IGF-1 in Cardio-Metabolic Diseases" in Current Pharmaceutical Design, 23, no. 10 (2017):1551-1561,
https://doi.org/10.2174/1381612823666170203113455 . .
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Copeptin Levels Do Not Correlate With Cross-Clamping Time in Patients Undergoing Carotid Endarterectomy Under General Anesthesia

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

(2016)

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

Bajić, Vladan P.; Sudar, Emina; Spremo-Potparević, Biljana; Živković, Lada; Milićević, Zorka T.; Stanimirović, Julijana; Bogdanović, Nikola; Isenović, Esma R.

(Bentham Science Publishers, 2016)

TY  - JOUR
AU  - Bajić, Vladan P.
AU  - Sudar, Emina
AU  - Spremo-Potparević, Biljana
AU  - Živković, Lada
AU  - Milićević, Zorka T.
AU  - Stanimirović, Julijana
AU  - Bogdanović, Nikola
AU  - Isenović, Esma R.
PY  - 2016
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1039
AB  - Alzheimers disease (AD) is a complex and progressive neurodegenerative disorder, and represents the most common form of dementia. The number of people affected by AD is estimated to be doubled by the year of 2050, and more than 100 million people worldwide will be affected by this disease. Still, there is no reliable diagnostic test which would indicate pre-symptomatic conditions or an increased risk of developing AD. The only drugs approved by the FDA belong to the cholinesterase inhibitors (ChEI) group, such as donepezil, rivastigmine, galantamine and memantine that belongs to a class of drugs named receptor NMDA antagonists. Most mainstream pharmacotherapeutic approaches act by slowing the progression of the condition rather than to treat or prevent the cause of AD. In this review we are presenting literature data from recent research related to new avenues in the classical approach to prevention and treatment of AD.
PB  - Bentham Science Publishers
T2  - Current Pharmaceutical Analysis
T1  - Treatment of Alzheimers Disease: Classical Therapeutic Approach
VL  - 12
IS  - 2
SP  - 82
EP  - 90
DO  - 10.2174/1573412911666150611184740
ER  - 
@article{
author = "Bajić, Vladan P. and Sudar, Emina and Spremo-Potparević, Biljana and Živković, Lada and Milićević, Zorka T. and Stanimirović, Julijana and Bogdanović, Nikola and Isenović, Esma R.",
year = "2016",
abstract = "Alzheimers disease (AD) is a complex and progressive neurodegenerative disorder, and represents the most common form of dementia. The number of people affected by AD is estimated to be doubled by the year of 2050, and more than 100 million people worldwide will be affected by this disease. Still, there is no reliable diagnostic test which would indicate pre-symptomatic conditions or an increased risk of developing AD. The only drugs approved by the FDA belong to the cholinesterase inhibitors (ChEI) group, such as donepezil, rivastigmine, galantamine and memantine that belongs to a class of drugs named receptor NMDA antagonists. Most mainstream pharmacotherapeutic approaches act by slowing the progression of the condition rather than to treat or prevent the cause of AD. In this review we are presenting literature data from recent research related to new avenues in the classical approach to prevention and treatment of AD.",
publisher = "Bentham Science Publishers",
journal = "Current Pharmaceutical Analysis",
title = "Treatment of Alzheimers Disease: Classical Therapeutic Approach",
volume = "12",
number = "2",
pages = "82-90",
doi = "10.2174/1573412911666150611184740"
}
Bajić, V. P., Sudar, E., Spremo-Potparević, B., Živković, L., Milićević, Z. T., Stanimirović, J., Bogdanović, N.,& Isenović, E. R.. (2016). Treatment of Alzheimers Disease: Classical Therapeutic Approach. in Current Pharmaceutical Analysis
Bentham Science Publishers., 12(2), 82-90.
https://doi.org/10.2174/1573412911666150611184740
Bajić VP, Sudar E, Spremo-Potparević B, Živković L, Milićević ZT, Stanimirović J, Bogdanović N, Isenović ER. Treatment of Alzheimers Disease: Classical Therapeutic Approach. in Current Pharmaceutical Analysis. 2016;12(2):82-90.
doi:10.2174/1573412911666150611184740 .
Bajić, Vladan P., Sudar, Emina, Spremo-Potparević, Biljana, Živković, Lada, Milićević, Zorka T., Stanimirović, Julijana, Bogdanović, Nikola, Isenović, Esma R., "Treatment of Alzheimers Disease: Classical Therapeutic Approach" in Current Pharmaceutical Analysis, 12, no. 2 (2016):82-90,
https://doi.org/10.2174/1573412911666150611184740 . .
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Effects of altered hepatic lipid metabolism on regulation of hepatic iNOS

Stanimirović, Julijana; Obradović, Milan M.; Zafirović, Sonja; Resanović, Ivana; Bogdanović, Nikola; Gluvić, Zoran; Mousa, Shaker A.; Isenović, Esma R.

(2015)

TY  - JOUR
AU  - Stanimirović, Julijana
AU  - Obradović, Milan M.
AU  - Zafirović, Sonja
AU  - Resanović, Ivana
AU  - Bogdanović, Nikola
AU  - Gluvić, Zoran
AU  - Mousa, Shaker A.
AU  - Isenović, Esma R.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/511
AB  - An altered hepatic lipid metabolism involves multifactorial pathologies such as hepatic inflammation, insulin resistance and oxidative stress. Immunity has an essential role in the regulation of glucose and lipid metabolism in the liver. Inducible nitric oxide (NO) synthase (iNOS) has been proposed as an important factor that interplays between immunity and energy metabolism and also in the pathogenesis of obesity-linked insulin resistance. In the liver, locally produced NO plays a protective role during inflammation, and the balance of NO protective and cytotoxic effects is very important. This review is focused on understanding the molecular mechanisms of iNOS regulation in the state of altered hepatic lipid metabolism, which is critical for developing new strategies for treatment of hepatic disorders.
T2  - Clinical Lipidology
T1  - Effects of altered hepatic lipid metabolism on regulation of hepatic iNOS
VL  - 10
IS  - 2
SP  - 167
EP  - 175
DO  - 10.2217/CLP.15.8
ER  - 
@article{
author = "Stanimirović, Julijana and Obradović, Milan M. and Zafirović, Sonja and Resanović, Ivana and Bogdanović, Nikola and Gluvić, Zoran and Mousa, Shaker A. and Isenović, Esma R.",
year = "2015",
abstract = "An altered hepatic lipid metabolism involves multifactorial pathologies such as hepatic inflammation, insulin resistance and oxidative stress. Immunity has an essential role in the regulation of glucose and lipid metabolism in the liver. Inducible nitric oxide (NO) synthase (iNOS) has been proposed as an important factor that interplays between immunity and energy metabolism and also in the pathogenesis of obesity-linked insulin resistance. In the liver, locally produced NO plays a protective role during inflammation, and the balance of NO protective and cytotoxic effects is very important. This review is focused on understanding the molecular mechanisms of iNOS regulation in the state of altered hepatic lipid metabolism, which is critical for developing new strategies for treatment of hepatic disorders.",
journal = "Clinical Lipidology",
title = "Effects of altered hepatic lipid metabolism on regulation of hepatic iNOS",
volume = "10",
number = "2",
pages = "167-175",
doi = "10.2217/CLP.15.8"
}
Stanimirović, J., Obradović, M. M., Zafirović, S., Resanović, I., Bogdanović, N., Gluvić, Z., Mousa, S. A.,& Isenović, E. R.. (2015). Effects of altered hepatic lipid metabolism on regulation of hepatic iNOS. in Clinical Lipidology, 10(2), 167-175.
https://doi.org/10.2217/CLP.15.8
Stanimirović J, Obradović MM, Zafirović S, Resanović I, Bogdanović N, Gluvić Z, Mousa SA, Isenović ER. Effects of altered hepatic lipid metabolism on regulation of hepatic iNOS. in Clinical Lipidology. 2015;10(2):167-175.
doi:10.2217/CLP.15.8 .
Stanimirović, Julijana, Obradović, Milan M., Zafirović, Sonja, Resanović, Ivana, Bogdanović, Nikola, Gluvić, Zoran, Mousa, Shaker A., Isenović, Esma R., "Effects of altered hepatic lipid metabolism on regulation of hepatic iNOS" in Clinical Lipidology, 10, no. 2 (2015):167-175,
https://doi.org/10.2217/CLP.15.8 . .
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Uloga azot-monoksid sintaza u stanjima ishemije mozga tokom karotidne endarterektomije

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

(2015)

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

Uloga L-Arginina u kardiovaskularnom sistemu

Sudar-Milovanović, Emina; Obradović, Milan M.; Bajić, Vladan P.; Bogdanović, Nikola; Radak, Đorđe J.; Isenović, Esma R.

(2015)

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 . .

Osnove apoptoze

Resanović, Ivana; Sudar-Milovanović, Emina; Bogdanović, Nikola; Jovanović, Aleksandra; Zafirović, Sonja; Panić, Anastasija; Isenović, Esma R.

(2015)

TY  - JOUR
AU  - Resanović, Ivana
AU  - Sudar-Milovanović, Emina
AU  - Bogdanović, Nikola
AU  - Jovanović, Aleksandra
AU  - Zafirović, Sonja
AU  - Panić, Anastasija
AU  - Isenović, Esma R.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10316
AB  - Apoptoza je evolutivno očuvan mehanizam programirane ćelijske smrti, koji ima važnu ulogu u fiziološkim procesima, kao što su embrionalno razviće, hromonima regulisana ćelijska smrt, funkcionisanje imunog sistema i uklanjanje oštećenih ćelija. Dva osnovna puta indukcije apoptoze su unutrašnji i spoljašnji. Dok unutrašnji put apoptoze može pokrenuti unutarćeljska akumulacija Ca 2+ jona, koja je praćena permeabilizacijom membrane mitohondrija i oslobađanjem pro-apoptotskih proteina iz mitohondrija u citoplazmu, spoljašnji put uključuje aktivaciju membransih receptora za TNF-a (engl. Tumor Necrosis Factor-a), kao što su TNFR-1 (engl. Tumor Necrosis Factor receptor 1), Fas, i TRAIL-R (engl. TNF-related apoptosis-inducing ligand receptors). Pored toga, postoji i perforin-granzim put koji uključuje aktivaciju citotoksičnih T-limfocita. Sva tri puta rezultiraju fragmentacijom DNK, degradacijom citoskeleta i nuklearnih proteina, unakrsnim povezivanjem proteina, formiranjem apoptotskih tela, ekspresijom liganada za receptore na fagocitima i na kraju fagocitozom. U ovoj reviji su objedinjeni podaci iz nedavno objavljenih studija koje su fokusirane na proteine uključene u proces apoptoze i molekularne mehanizme apoptoze. Razumevanje mehanizama apoptoze može da pruži korisne informacije i nove pristupe u prevenciji i razvoju novih terapija za različite bolesti.
AB  - Apoptosis is evolutionary conserved, programmed pattern of cell death with an essential role in various physiological processes, such as normal cell turnover and embryonic development, hormone-regulated cell demise, aging, immune system functioning and development and removal of defective and harmful cells. There are two general pathways for activation of apoptosis: the intrinsic and extrinsic pathways. While the intrinsic apoptotic pathway can be triggered by a cytotoxic accumulation of intracellular Ca 2+ , followed permeabilization of mitochondrial membrane and release of pro-apoptotic proteins into the cytosol from mitochondria, the extrinsic mechanisms of apoptosis include the participation of death receptors of tumor necrosis factor-a (TNF-a), receptor superfamily such as TNFR-1, Fas, and TNF-related apoptosis-inducing ligand receptors (TRAIL-R) located on the plasma membrane. There is also the perforin-granzyme pathway that involves T-cell mediated cytotoxicity. All three pathways converge on the same execution pathway, resulting 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. In this review we summarize data from recent studies focusing on apoptotic proteins that have been identified and molecular mechanisms of apoptosis. Understanding apoptotic mechanism might provide useful information and a new approach to prevention and development of new therapies for variety of diseases.
T2  - Medicinska istraživanja
T1  - Osnove apoptoze
T1  - Fundamentals of apoptosis
VL  - 49
IS  - 2
SP  - 42
EP  - 45
DO  - 10.5937/MedIst1502042R
ER  - 
@article{
author = "Resanović, Ivana and Sudar-Milovanović, Emina and Bogdanović, Nikola and Jovanović, Aleksandra and Zafirović, Sonja and Panić, Anastasija and Isenović, Esma R.",
year = "2015",
abstract = "Apoptoza je evolutivno očuvan mehanizam programirane ćelijske smrti, koji ima važnu ulogu u fiziološkim procesima, kao što su embrionalno razviće, hromonima regulisana ćelijska smrt, funkcionisanje imunog sistema i uklanjanje oštećenih ćelija. Dva osnovna puta indukcije apoptoze su unutrašnji i spoljašnji. Dok unutrašnji put apoptoze može pokrenuti unutarćeljska akumulacija Ca 2+ jona, koja je praćena permeabilizacijom membrane mitohondrija i oslobađanjem pro-apoptotskih proteina iz mitohondrija u citoplazmu, spoljašnji put uključuje aktivaciju membransih receptora za TNF-a (engl. Tumor Necrosis Factor-a), kao što su TNFR-1 (engl. Tumor Necrosis Factor receptor 1), Fas, i TRAIL-R (engl. TNF-related apoptosis-inducing ligand receptors). Pored toga, postoji i perforin-granzim put koji uključuje aktivaciju citotoksičnih T-limfocita. Sva tri puta rezultiraju fragmentacijom DNK, degradacijom citoskeleta i nuklearnih proteina, unakrsnim povezivanjem proteina, formiranjem apoptotskih tela, ekspresijom liganada za receptore na fagocitima i na kraju fagocitozom. U ovoj reviji su objedinjeni podaci iz nedavno objavljenih studija koje su fokusirane na proteine uključene u proces apoptoze i molekularne mehanizme apoptoze. Razumevanje mehanizama apoptoze može da pruži korisne informacije i nove pristupe u prevenciji i razvoju novih terapija za različite bolesti., Apoptosis is evolutionary conserved, programmed pattern of cell death with an essential role in various physiological processes, such as normal cell turnover and embryonic development, hormone-regulated cell demise, aging, immune system functioning and development and removal of defective and harmful cells. There are two general pathways for activation of apoptosis: the intrinsic and extrinsic pathways. While the intrinsic apoptotic pathway can be triggered by a cytotoxic accumulation of intracellular Ca 2+ , followed permeabilization of mitochondrial membrane and release of pro-apoptotic proteins into the cytosol from mitochondria, the extrinsic mechanisms of apoptosis include the participation of death receptors of tumor necrosis factor-a (TNF-a), receptor superfamily such as TNFR-1, Fas, and TNF-related apoptosis-inducing ligand receptors (TRAIL-R) located on the plasma membrane. There is also the perforin-granzyme pathway that involves T-cell mediated cytotoxicity. All three pathways converge on the same execution pathway, resulting 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. In this review we summarize data from recent studies focusing on apoptotic proteins that have been identified and molecular mechanisms of apoptosis. Understanding apoptotic mechanism might provide useful information and a new approach to prevention and development of new therapies for variety of diseases.",
journal = "Medicinska istraživanja",
title = "Osnove apoptoze, Fundamentals of apoptosis",
volume = "49",
number = "2",
pages = "42-45",
doi = "10.5937/MedIst1502042R"
}
Resanović, I., Sudar-Milovanović, E., Bogdanović, N., Jovanović, A., Zafirović, S., Panić, A.,& Isenović, E. R.. (2015). Osnove apoptoze. in Medicinska istraživanja, 49(2), 42-45.
https://doi.org/10.5937/MedIst1502042R
Resanović I, Sudar-Milovanović E, Bogdanović N, Jovanović A, Zafirović S, Panić A, Isenović ER. Osnove apoptoze. in Medicinska istraživanja. 2015;49(2):42-45.
doi:10.5937/MedIst1502042R .
Resanović, Ivana, Sudar-Milovanović, Emina, Bogdanović, Nikola, Jovanović, Aleksandra, Zafirović, Sonja, Panić, Anastasija, Isenović, Esma R., "Osnove apoptoze" in Medicinska istraživanja, 49, no. 2 (2015):42-45,
https://doi.org/10.5937/MedIst1502042R . .

Editorial: Oxidative Stress in Pathophysiological Conditions

Obradović, Milan M.; Bogdanović, Nikola; Radak, Đorđe J.; Isenović, Esma R.

(2015)

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 . .
2
3