TY  - JOUR
AU  - Alamri, Hasan S.
AU  - Mufti, Rana
AU  - Sabir, Deema Kamal
AU  - Abuderman, Abdulwahab A.
AU  - Dawood, Amal F.
AU  - ShamsEldeen, Asmaa M.
AU  - Haidara, Mohamed A.
AU  - Isenović, Esma R.
AU  - El-Bidawy, Mahmoud H.
PY  - 2023
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/11457
AB  - The first-generation antihistamine chlorpheniramine (CPA) is believed to have both anxiolytic and antidepressant properties. The current study sought to assess the mechanisms behind the antidepressant and anxiolytic effects of CPA therapy concerning oxidative stress, inflammation, and nuclear factor p45 for erythroid 2-Brain-derived neurotrophic factor (Nrf2-BDNF) signaling pathway in forced swimming-induced depressive-like behavior and anxiety. Eighteen male Wistar rats (180–200 gm) rats were separated into three groups (n = 6): a stressed group (acute stress) that underwent the forced swimming test (FST) and a stressed group that received pretreatment with CPA (10 mg/kg body weight) for 3 weeks (CPA + acute stress). Animals were subsequently put through the following behavioral tests after undergoing a forced swim test (FST) for 5 min: an immobility test, open field test, and elevated plus maze test. Serum cortisol levels were measured when the rats were euthanized at the end of the experiments. Brain neurotransmitters (cortisol, serotonin, and noradrenaline), oxidative stress (SOD and MDA), inflammatory (IL-6 and IL-1) biomarkers, and the Nrf2-BDNF signaling pathway in the hippocampus and cerebral cortex tissues was determined. CPA prevented stress-induced increases in cortisol levels (p < 0.0001), decreased brain neurotransmitters, and increased oxidative stress and inflammation. CPA also upregulated the Nrf2-BDNF signaling pathway. Thus, CPA mitigates depressive-like behavior and anxiety by inhibiting oxidative stress and inflammation and upregulating the Nrf2-BDNF signaling pathway in the brain tissues.
T2  - Current Issues in Molecular Biology
T1  - Forced Swimming-Induced Depressive-like Behavior and Anxiety Are Reduced by Chlorpheniramine via Suppression of Oxidative and Inflammatory Mediators and Activating the Nrf2-BDNF Signaling Pathway
VL  - 45
IS  - 8
SP  - 6449
EP  - 6465
DO  - 10.3390/cimb45080407
ER  - 

@article{
author = "Alamri, Hasan S. and Mufti, Rana and Sabir, Deema Kamal and Abuderman, Abdulwahab A. and Dawood, Amal F. and ShamsEldeen, Asmaa M. and Haidara, Mohamed A. and Isenović, Esma R. and El-Bidawy, Mahmoud H.",
year = "2023",
abstract = "The first-generation antihistamine chlorpheniramine (CPA) is believed to have both anxiolytic and antidepressant properties. The current study sought to assess the mechanisms behind the antidepressant and anxiolytic effects of CPA therapy concerning oxidative stress, inflammation, and nuclear factor p45 for erythroid 2-Brain-derived neurotrophic factor (Nrf2-BDNF) signaling pathway in forced swimming-induced depressive-like behavior and anxiety. Eighteen male Wistar rats (180–200 gm) rats were separated into three groups (n = 6): a stressed group (acute stress) that underwent the forced swimming test (FST) and a stressed group that received pretreatment with CPA (10 mg/kg body weight) for 3 weeks (CPA + acute stress). Animals were subsequently put through the following behavioral tests after undergoing a forced swim test (FST) for 5 min: an immobility test, open field test, and elevated plus maze test. Serum cortisol levels were measured when the rats were euthanized at the end of the experiments. Brain neurotransmitters (cortisol, serotonin, and noradrenaline), oxidative stress (SOD and MDA), inflammatory (IL-6 and IL-1) biomarkers, and the Nrf2-BDNF signaling pathway in the hippocampus and cerebral cortex tissues was determined. CPA prevented stress-induced increases in cortisol levels (p < 0.0001), decreased brain neurotransmitters, and increased oxidative stress and inflammation. CPA also upregulated the Nrf2-BDNF signaling pathway. Thus, CPA mitigates depressive-like behavior and anxiety by inhibiting oxidative stress and inflammation and upregulating the Nrf2-BDNF signaling pathway in the brain tissues.",
journal = "Current Issues in Molecular Biology",
title = "Forced Swimming-Induced Depressive-like Behavior and Anxiety Are Reduced by Chlorpheniramine via Suppression of Oxidative and Inflammatory Mediators and Activating the Nrf2-BDNF Signaling Pathway",
volume = "45",
number = "8",
pages = "6449-6465",
doi = "10.3390/cimb45080407"
}

Alamri, H. S., Mufti, R., Sabir, D. K., Abuderman, A. A., Dawood, A. F., ShamsEldeen, A. M., Haidara, M. A., Isenović, E. R.,& El-Bidawy, M. H.. (2023). Forced Swimming-Induced Depressive-like Behavior and Anxiety Are Reduced by Chlorpheniramine via Suppression of Oxidative and Inflammatory Mediators and Activating the Nrf2-BDNF Signaling Pathway. in Current Issues in Molecular Biology, 45(8), 6449-6465.
https://doi.org/10.3390/cimb45080407

Alamri HS, Mufti R, Sabir DK, Abuderman AA, Dawood AF, ShamsEldeen AM, Haidara MA, Isenović ER, El-Bidawy MH. Forced Swimming-Induced Depressive-like Behavior and Anxiety Are Reduced by Chlorpheniramine via Suppression of Oxidative and Inflammatory Mediators and Activating the Nrf2-BDNF Signaling Pathway. in Current Issues in Molecular Biology. 2023;45(8):6449-6465.
doi:10.3390/cimb45080407 .

Alamri, Hasan S., Mufti, Rana, Sabir, Deema Kamal, Abuderman, Abdulwahab A., Dawood, Amal F., ShamsEldeen, Asmaa M., Haidara, Mohamed A., Isenović, Esma R., El-Bidawy, Mahmoud H., "Forced Swimming-Induced Depressive-like Behavior and Anxiety Are Reduced by Chlorpheniramine via Suppression of Oxidative and Inflammatory Mediators and Activating the Nrf2-BDNF Signaling Pathway" in Current Issues in Molecular Biology, 45, no. 8 (2023):6449-6465,
https://doi.org/10.3390/cimb45080407 . .

TY  - JOUR
AU  - Zarić, Božidarka
AU  - Obradović, Milan M.
AU  - Bajić, Vladan P.
AU  - Haidara, Mohamed A.
AU  - Jovanović, Miloš
AU  - Isenović, Esma R.
PY  - 2019
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8485
AB  - Homocysteine (Hcy) is a thiol group containing the amino acid, which naturally occurs in all humans. Hcy is degraded in the body through two metabolic pathways, while a minor part is excreted through kidneys. The chemical reactions that are necessary for degradation of Hcy require the presence of folic acid, vitamins B6 and B12. Consequently, the level of the total Hcy in the serum is influenced by the presence or absence of these vitamins. An elevated level of the Hcy, hyperhomocysteinemia (HHcy) and homocystinuria is connected with occlusive artery disease, especially in the brain, the heart, and the kidney, in addition to venous thrombosis, chronic renal failure, megaloblastic anemia, osteoporosis, depression, Alzheimer's disease, pregnancy problems, and others. Elevated Hcy levels are connected with various pathologies both in adult and child population. Causes of HHcy include genetic mutations and enzyme deficiencies in 5, 10-methylenetetrahydrofolate reductase (MTHFR) methionine synthase (MS), and cystathionine β-synthase (CβS). HHcy can be caused by deficiencies in the folate, vitamin B12 and to a lesser extent, deficiency in B6 vitamin what influences methionine metabolism. Additionally, HHcy can be caused by the rich diet and renal impairment. This review presents literature data from recent research related to Hcy metabolism and the etiology of the Hcy blood level disorder. In addition, we also described various pathological mechanisms induced by hereditary disturbances or nutritional influences and their association with HHcy induced pathology in adults and children and treatment of these metabolic disorders. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.
T2  - Current Medicinal Chemistry
T1  - Homocysteine and Hyperhomocysteinaemia
VL  - 26
IS  - 16
SP  - 2948
EP  - 2961
DO  - 10.2174/0929867325666180313105949
ER  - 

@article{
author = "Zarić, Božidarka and Obradović, Milan M. and Bajić, Vladan P. and Haidara, Mohamed A. and Jovanović, Miloš and Isenović, Esma R.",
year = "2019",
abstract = "Homocysteine (Hcy) is a thiol group containing the amino acid, which naturally occurs in all humans. Hcy is degraded in the body through two metabolic pathways, while a minor part is excreted through kidneys. The chemical reactions that are necessary for degradation of Hcy require the presence of folic acid, vitamins B6 and B12. Consequently, the level of the total Hcy in the serum is influenced by the presence or absence of these vitamins. An elevated level of the Hcy, hyperhomocysteinemia (HHcy) and homocystinuria is connected with occlusive artery disease, especially in the brain, the heart, and the kidney, in addition to venous thrombosis, chronic renal failure, megaloblastic anemia, osteoporosis, depression, Alzheimer's disease, pregnancy problems, and others. Elevated Hcy levels are connected with various pathologies both in adult and child population. Causes of HHcy include genetic mutations and enzyme deficiencies in 5, 10-methylenetetrahydrofolate reductase (MTHFR) methionine synthase (MS), and cystathionine β-synthase (CβS). HHcy can be caused by deficiencies in the folate, vitamin B12 and to a lesser extent, deficiency in B6 vitamin what influences methionine metabolism. Additionally, HHcy can be caused by the rich diet and renal impairment. This review presents literature data from recent research related to Hcy metabolism and the etiology of the Hcy blood level disorder. In addition, we also described various pathological mechanisms induced by hereditary disturbances or nutritional influences and their association with HHcy induced pathology in adults and children and treatment of these metabolic disorders. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.",
journal = "Current Medicinal Chemistry",
title = "Homocysteine and Hyperhomocysteinaemia",
volume = "26",
number = "16",
pages = "2948-2961",
doi = "10.2174/0929867325666180313105949"
}

Zarić, B., Obradović, M. M., Bajić, V. P., Haidara, M. A., Jovanović, M.,& Isenović, E. R.. (2019). Homocysteine and Hyperhomocysteinaemia. in Current Medicinal Chemistry, 26(16), 2948-2961.
https://doi.org/10.2174/0929867325666180313105949

Zarić B, Obradović MM, Bajić VP, Haidara MA, Jovanović M, Isenović ER. Homocysteine and Hyperhomocysteinaemia. in Current Medicinal Chemistry. 2019;26(16):2948-2961.
doi:10.2174/0929867325666180313105949 .

Zarić, Božidarka, Obradović, Milan M., Bajić, Vladan P., Haidara, Mohamed A., Jovanović, Miloš, Isenović, Esma R., "Homocysteine and Hyperhomocysteinaemia" in Current Medicinal Chemistry, 26, no. 16 (2019):2948-2961,
https://doi.org/10.2174/0929867325666180313105949 . .

TY  - JOUR
AU  - Haidara, Mohamed A.
AU  - Assiri, Abdullah S.
AU  - Yassin, Hanaa Z.
AU  - Ammar, Hania I.
AU  - Obradović, Milan M.
AU  - Isenović, Esma R.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/716
AB  - Cardiovascular disease (CVD) is among the most major causes of morbidity and mortality worldwide. Great progress has been made in the management of CVD which has been influenced by the use of experimental animal models. These models provided information at cellular and molecular levels and allowed the development of treatment strategies. CVD models have been developed in many species, including large animals (e.g. pigs and dogs) and small animals (e.g. rats and mice). Although, no model can solely reproduce clinical HF, simulations of heart failure (HF) are available to experimentally tackle certain queries not easily resolved in humans. Induced HF may also be produced experimentally through myocardial infarction (MI), pressure loading, or volume loading. Volume loading is useful to look at hormone and electrolyte disturbances, while pressure loading models is helpful to study ventricular hypertrophy, cellular imbalance and vascular changes in HF. Coronary heart disease is assessed in MI animal models. In this review we describe various experimental models used to study the pathophysiology of HF.
T2  - Current Vascular Pharmacology
T1  - Heart Failure Models: Traditional and Novel Therapy
VL  - 13
IS  - 5
SP  - 658
EP  - 669
DO  - 10.2174/1570161113666150212151506
ER  - 

@article{
author = "Haidara, Mohamed A. and Assiri, Abdullah S. and Yassin, Hanaa Z. and Ammar, Hania I. and Obradović, Milan M. and Isenović, Esma R.",
year = "2015",
abstract = "Cardiovascular disease (CVD) is among the most major causes of morbidity and mortality worldwide. Great progress has been made in the management of CVD which has been influenced by the use of experimental animal models. These models provided information at cellular and molecular levels and allowed the development of treatment strategies. CVD models have been developed in many species, including large animals (e.g. pigs and dogs) and small animals (e.g. rats and mice). Although, no model can solely reproduce clinical HF, simulations of heart failure (HF) are available to experimentally tackle certain queries not easily resolved in humans. Induced HF may also be produced experimentally through myocardial infarction (MI), pressure loading, or volume loading. Volume loading is useful to look at hormone and electrolyte disturbances, while pressure loading models is helpful to study ventricular hypertrophy, cellular imbalance and vascular changes in HF. Coronary heart disease is assessed in MI animal models. In this review we describe various experimental models used to study the pathophysiology of HF.",
journal = "Current Vascular Pharmacology",
title = "Heart Failure Models: Traditional and Novel Therapy",
volume = "13",
number = "5",
pages = "658-669",
doi = "10.2174/1570161113666150212151506"
}

Haidara, M. A., Assiri, A. S., Yassin, H. Z., Ammar, H. I., Obradović, M. M.,& Isenović, E. R.. (2015). Heart Failure Models: Traditional and Novel Therapy. in Current Vascular Pharmacology, 13(5), 658-669.
https://doi.org/10.2174/1570161113666150212151506

Haidara MA, Assiri AS, Yassin HZ, Ammar HI, Obradović MM, Isenović ER. Heart Failure Models: Traditional and Novel Therapy. in Current Vascular Pharmacology. 2015;13(5):658-669.
doi:10.2174/1570161113666150212151506 .

Haidara, Mohamed A., Assiri, Abdullah S., Yassin, Hanaa Z., Ammar, Hania I., Obradović, Milan M., Isenović, Esma R., "Heart Failure Models: Traditional and Novel Therapy" in Current Vascular Pharmacology, 13, no. 5 (2015):658-669,
https://doi.org/10.2174/1570161113666150212151506 . .

TY  - JOUR
AU  - Obradović, Milan M.
AU  - Bjelogrlic, Predrag
AU  - Rizzo, Manfredi
AU  - Katsiki, Niki
AU  - Haidara, Mohamed A.
AU  - Stewart, Alan J.
AU  - Jovanović, Aleksandra
AU  - Isenović, Esma R.
PY  - 2013
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5672
AB  - Obesity is associated with aberrant sodium/potassium-ATPase (Na+/K+-ATPase) activity, apparently linked to hyperglycemic hyperinsulinemia, which may repress or inactivate the enzyme. The reduction of Na+/K+-ATPase activity in cardiac tissue induces myocyte death and cardiac dysfunction, leading to the development of myocardial dilation in animal models; this has also been documented in patients with heart failure (HF). During several pathological situations (cardiac insufficiency and HF) and in experimental models (obesity), the heart becomes more sensitive to the effect of cardiac glycosides, due to a decrease in Na+/K+-ATPase levels. The primary female sex steroid estradiol has long been recognized to be important in a wide variety of physiological processes. Numerous studies, including ours, have shown that estradiol is one of the major factors controlling the activity and expression of Na+/K+-ATPase in the cardiovascular (CV) system. However, the effects of estradiol on Na+/K+-ATPase in both normal and pathological conditions, such as obesity, remain unclear. Increasing our understanding of the molecular mechanisms by which estradiol mediates its effects on Na+/K+-ATPase function may help to develop new strategies for the treatment of CV diseases. Herein, we discuss the latest data from animal and clinical studies that have examined how pathophysiological conditions such as obesity and the action of estradiol regulate Na+/K+-ATPase activity.
T2  - Journal of Endocrinology
T1  - Effects of obesity and estradiol on Na+/K+-ATPase and their relevance to cardiovascular diseases
VL  - 218
IS  - 3
SP  - R13
EP  - R23
DO  - 10.1530/JOE-13-0144
ER  - 

@article{
author = "Obradović, Milan M. and Bjelogrlic, Predrag and Rizzo, Manfredi and Katsiki, Niki and Haidara, Mohamed A. and Stewart, Alan J. and Jovanović, Aleksandra and Isenović, Esma R.",
year = "2013",
abstract = "Obesity is associated with aberrant sodium/potassium-ATPase (Na+/K+-ATPase) activity, apparently linked to hyperglycemic hyperinsulinemia, which may repress or inactivate the enzyme. The reduction of Na+/K+-ATPase activity in cardiac tissue induces myocyte death and cardiac dysfunction, leading to the development of myocardial dilation in animal models; this has also been documented in patients with heart failure (HF). During several pathological situations (cardiac insufficiency and HF) and in experimental models (obesity), the heart becomes more sensitive to the effect of cardiac glycosides, due to a decrease in Na+/K+-ATPase levels. The primary female sex steroid estradiol has long been recognized to be important in a wide variety of physiological processes. Numerous studies, including ours, have shown that estradiol is one of the major factors controlling the activity and expression of Na+/K+-ATPase in the cardiovascular (CV) system. However, the effects of estradiol on Na+/K+-ATPase in both normal and pathological conditions, such as obesity, remain unclear. Increasing our understanding of the molecular mechanisms by which estradiol mediates its effects on Na+/K+-ATPase function may help to develop new strategies for the treatment of CV diseases. Herein, we discuss the latest data from animal and clinical studies that have examined how pathophysiological conditions such as obesity and the action of estradiol regulate Na+/K+-ATPase activity.",
journal = "Journal of Endocrinology",
title = "Effects of obesity and estradiol on Na+/K+-ATPase and their relevance to cardiovascular diseases",
volume = "218",
number = "3",
pages = "R13-R23",
doi = "10.1530/JOE-13-0144"
}

Obradović, M. M., Bjelogrlic, P., Rizzo, M., Katsiki, N., Haidara, M. A., Stewart, A. J., Jovanović, A.,& Isenović, E. R.. (2013). Effects of obesity and estradiol on Na+/K+-ATPase and their relevance to cardiovascular diseases. in Journal of Endocrinology, 218(3), R13-R23.
https://doi.org/10.1530/JOE-13-0144

Obradović MM, Bjelogrlic P, Rizzo M, Katsiki N, Haidara MA, Stewart AJ, Jovanović A, Isenović ER. Effects of obesity and estradiol on Na+/K+-ATPase and their relevance to cardiovascular diseases. in Journal of Endocrinology. 2013;218(3):R13-R23.
doi:10.1530/JOE-13-0144 .

Obradović, Milan M., Bjelogrlic, Predrag, Rizzo, Manfredi, Katsiki, Niki, Haidara, Mohamed A., Stewart, Alan J., Jovanović, Aleksandra, Isenović, Esma R., "Effects of obesity and estradiol on Na+/K+-ATPase and their relevance to cardiovascular diseases" in Journal of Endocrinology, 218, no. 3 (2013):R13-R23,
https://doi.org/10.1530/JOE-13-0144 . .

TY  - JOUR
AU  - Haidara, Mohamed A.
AU  - Mikhailidis, Dimitri P.
AU  - Yassin, Hanaa Z.
AU  - Dobutović, Branislava
AU  - Smiljanić, Katarina
AU  - Soskić, Sanja S.
AU  - Mousa, Shaker A.
AU  - Rizzo, Manfredi
AU  - Isenović, Esma R.
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4662
AB  - The metabolic syndrome (MetS) is common, and its associated risk burdens of diabetes and cardiovascular disease (CVD) are a major public health problem. The hypothesis that main constituent parameters of the MetS share common pathophysiologic mechanisms provides a conceptual framework for the future research. Exercise and weight loss can prevent insulin resistance and reduce the risk of diseases associated with the MetS. Interrupting intracellular and extracellular reactive oxygen species (ROS) overproduction could also contribute to normalizing the activation of metabolic pathways leading to the onset of diabetes, endothelial dysfunction, and cardiovascular (CV) complications. On the other hand, it is difficult to counteract the development of CV complications by using conventional antioxidants. Indeed, interest has focused on strategies that enhance the removal of ROS using either antioxidants or drugs that enhance endogenous antioxidant defense. Although these strategies have been effective in laboratory experiments, several clinical trials have shown that they do not reduce CV events, and in some cases antioxidants have actually worsened the outcome. More research is needed in this field.
T2  - Current Pharmaceutical Design
T1  - Evaluation of the Possible Contribution of Antioxidants Administration in Metabolic Syndrome
VL  - 17
IS  - 33
SP  - 3699
EP  - 3712
DO  - 10.2174/138161211798220882
ER  - 

@article{
author = "Haidara, Mohamed A. and Mikhailidis, Dimitri P. and Yassin, Hanaa Z. and Dobutović, Branislava and Smiljanić, Katarina and Soskić, Sanja S. and Mousa, Shaker A. and Rizzo, Manfredi and Isenović, Esma R.",
year = "2011",
abstract = "The metabolic syndrome (MetS) is common, and its associated risk burdens of diabetes and cardiovascular disease (CVD) are a major public health problem. The hypothesis that main constituent parameters of the MetS share common pathophysiologic mechanisms provides a conceptual framework for the future research. Exercise and weight loss can prevent insulin resistance and reduce the risk of diseases associated with the MetS. Interrupting intracellular and extracellular reactive oxygen species (ROS) overproduction could also contribute to normalizing the activation of metabolic pathways leading to the onset of diabetes, endothelial dysfunction, and cardiovascular (CV) complications. On the other hand, it is difficult to counteract the development of CV complications by using conventional antioxidants. Indeed, interest has focused on strategies that enhance the removal of ROS using either antioxidants or drugs that enhance endogenous antioxidant defense. Although these strategies have been effective in laboratory experiments, several clinical trials have shown that they do not reduce CV events, and in some cases antioxidants have actually worsened the outcome. More research is needed in this field.",
journal = "Current Pharmaceutical Design",
title = "Evaluation of the Possible Contribution of Antioxidants Administration in Metabolic Syndrome",
volume = "17",
number = "33",
pages = "3699-3712",
doi = "10.2174/138161211798220882"
}

Haidara, M. A., Mikhailidis, D. P., Yassin, H. Z., Dobutović, B., Smiljanić, K., Soskić, S. S., Mousa, S. A., Rizzo, M.,& Isenović, E. R.. (2011). Evaluation of the Possible Contribution of Antioxidants Administration in Metabolic Syndrome. in Current Pharmaceutical Design, 17(33), 3699-3712.
https://doi.org/10.2174/138161211798220882

Haidara MA, Mikhailidis DP, Yassin HZ, Dobutović B, Smiljanić K, Soskić SS, Mousa SA, Rizzo M, Isenović ER. Evaluation of the Possible Contribution of Antioxidants Administration in Metabolic Syndrome. in Current Pharmaceutical Design. 2011;17(33):3699-3712.
doi:10.2174/138161211798220882 .

Haidara, Mohamed A., Mikhailidis, Dimitri P., Yassin, Hanaa Z., Dobutović, Branislava, Smiljanić, Katarina, Soskić, Sanja S., Mousa, Shaker A., Rizzo, Manfredi, Isenović, Esma R., "Evaluation of the Possible Contribution of Antioxidants Administration in Metabolic Syndrome" in Current Pharmaceutical Design, 17, no. 33 (2011):3699-3712,
https://doi.org/10.2174/138161211798220882 . .

TY  - JOUR
AU  - Al-Hashem, Fahaid
AU  - Ibrahim, Ibrahim
AU  - Bastawy, Nermeen
AU  - Rateb, Moshira
AU  - Haidara, Mohamed A.
AU  - Dallak, Mohammed
AU  - Soskić, Sanja S.
AU  - Bin-Jaliah, Ismaeel
AU  - Isenović, Esma R.
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4472
AB  - The present study was designed to investigate the effect of insulin on insulin resistance (IR), plasma adiponectin level and expression of adiponectin receptors 1 (AdipoR1) in obese and streptozotocin-induced type 2 diabetic rats. Male Sprague-Dowley rats were randomized to control group and 3 obese experimental groups. Type 2 diabetic mellitus was induced in the 3(rd) and 4(th) experimental groups by given 30 mg/kg of a single dose streptozotocin via intraperitoneal injection (i.p.). Fourth group was treated with i.p. 1 IU insulin/kg/day for 6 days before end of the experiment which lasts for 8 weeks while same amount of normal saline was i.p. given to other group. At the end of the study (8 weeks), plasma levels of adiponectin, triglycerides (TO), cholesterol, fasting blood glucose and insulin were measured. Obesity index (01) and IR were calculated. AdipoR1 mRNA levels in the soleus muscle tissue were semi-quantitated. Hyperlipidemia, hyperinsulinemia and hyperglycemia were observed ill both obese and diabetic rats, which were accompanied by hypoadiponectinemia and down regulation of AdipoR1 expression as compared to the control rats. Adiponectin was negatively correlated with all the biochemical parameters assessed. Insulin treatment significantly improved these metabolic abnormalities and effectively restored adiponectin and AdipoR1 to the control level. In conclusion, adiponectin and its receptor-associated cascade may be aberrantly regulated in both obesity and type 2 diabetes and targeting adiponectin and its receptors may offer a novel therapy against obesity and type 2 diabetes.
T2  - Journal of Health Science
T1  - Effect of Insulin on Adiponectin and Adiponectin Receptor-1 Expression in Rats with Streptozotocin-induced Type 2 Diabetes
VL  - 57
IS  - 4
SP  - 334
EP  - 340
DO  - 10.1248/jhs.57.334
ER  - 

@article{
author = "Al-Hashem, Fahaid and Ibrahim, Ibrahim and Bastawy, Nermeen and Rateb, Moshira and Haidara, Mohamed A. and Dallak, Mohammed and Soskić, Sanja S. and Bin-Jaliah, Ismaeel and Isenović, Esma R.",
year = "2011",
abstract = "The present study was designed to investigate the effect of insulin on insulin resistance (IR), plasma adiponectin level and expression of adiponectin receptors 1 (AdipoR1) in obese and streptozotocin-induced type 2 diabetic rats. Male Sprague-Dowley rats were randomized to control group and 3 obese experimental groups. Type 2 diabetic mellitus was induced in the 3(rd) and 4(th) experimental groups by given 30 mg/kg of a single dose streptozotocin via intraperitoneal injection (i.p.). Fourth group was treated with i.p. 1 IU insulin/kg/day for 6 days before end of the experiment which lasts for 8 weeks while same amount of normal saline was i.p. given to other group. At the end of the study (8 weeks), plasma levels of adiponectin, triglycerides (TO), cholesterol, fasting blood glucose and insulin were measured. Obesity index (01) and IR were calculated. AdipoR1 mRNA levels in the soleus muscle tissue were semi-quantitated. Hyperlipidemia, hyperinsulinemia and hyperglycemia were observed ill both obese and diabetic rats, which were accompanied by hypoadiponectinemia and down regulation of AdipoR1 expression as compared to the control rats. Adiponectin was negatively correlated with all the biochemical parameters assessed. Insulin treatment significantly improved these metabolic abnormalities and effectively restored adiponectin and AdipoR1 to the control level. In conclusion, adiponectin and its receptor-associated cascade may be aberrantly regulated in both obesity and type 2 diabetes and targeting adiponectin and its receptors may offer a novel therapy against obesity and type 2 diabetes.",
journal = "Journal of Health Science",
title = "Effect of Insulin on Adiponectin and Adiponectin Receptor-1 Expression in Rats with Streptozotocin-induced Type 2 Diabetes",
volume = "57",
number = "4",
pages = "334-340",
doi = "10.1248/jhs.57.334"
}

Al-Hashem, F., Ibrahim, I., Bastawy, N., Rateb, M., Haidara, M. A., Dallak, M., Soskić, S. S., Bin-Jaliah, I.,& Isenović, E. R.. (2011). Effect of Insulin on Adiponectin and Adiponectin Receptor-1 Expression in Rats with Streptozotocin-induced Type 2 Diabetes. in Journal of Health Science, 57(4), 334-340.
https://doi.org/10.1248/jhs.57.334

Al-Hashem F, Ibrahim I, Bastawy N, Rateb M, Haidara MA, Dallak M, Soskić SS, Bin-Jaliah I, Isenović ER. Effect of Insulin on Adiponectin and Adiponectin Receptor-1 Expression in Rats with Streptozotocin-induced Type 2 Diabetes. in Journal of Health Science. 2011;57(4):334-340.
doi:10.1248/jhs.57.334 .

Al-Hashem, Fahaid, Ibrahim, Ibrahim, Bastawy, Nermeen, Rateb, Moshira, Haidara, Mohamed A., Dallak, Mohammed, Soskić, Sanja S., Bin-Jaliah, Ismaeel, Isenović, Esma R., "Effect of Insulin on Adiponectin and Adiponectin Receptor-1 Expression in Rats with Streptozotocin-induced Type 2 Diabetes" in Journal of Health Science, 57, no. 4 (2011):334-340,
https://doi.org/10.1248/jhs.57.334 . .

TY  - JOUR
AU  - Trpković, Andreja
AU  - Stokić, Edita
AU  - Radak, Đorđe J.
AU  - Gluvić, Zoran
AU  - Haidara, Mohamed A.
AU  - Mikhailidis, Dimitri P.
AU  - Isenović, Esma R.
PY  - 2010
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4208
AB  - The role of hepatitis C virus (HCV) infection in the development of vascular disease is controversial. Insulin resistance (IR) is a recognized risk factor for cardiovascular disease (CVD) and is associated with chronic hepatitis C (CHC). Thus, IR may promote atherosclerosis and vascular disease in CHC patients. HCV-associated IR may also cause hepatic steatosis and resistance to antiviral treatment. In addition, HCV may contribute a direct, proatherogenetic action on the vascular wall. This review considers the impact of IR on interferon-based therapy of HCV infection and the role of insulin-sensitizing agents on the response to antiviral treatment and prevention of IR complications, including CVD.
T2  - Current Pharmaceutical Design
T1  - Chronic Hepatitis C, Insulin Resistance and Vascular Disease
VL  - 16
IS  - 34
SP  - 3823
EP  - 3829
DO  - 10.2174/138161210794455067
ER  - 

@article{
author = "Trpković, Andreja and Stokić, Edita and Radak, Đorđe J. and Gluvić, Zoran and Haidara, Mohamed A. and Mikhailidis, Dimitri P. and Isenović, Esma R.",
year = "2010",
abstract = "The role of hepatitis C virus (HCV) infection in the development of vascular disease is controversial. Insulin resistance (IR) is a recognized risk factor for cardiovascular disease (CVD) and is associated with chronic hepatitis C (CHC). Thus, IR may promote atherosclerosis and vascular disease in CHC patients. HCV-associated IR may also cause hepatic steatosis and resistance to antiviral treatment. In addition, HCV may contribute a direct, proatherogenetic action on the vascular wall. This review considers the impact of IR on interferon-based therapy of HCV infection and the role of insulin-sensitizing agents on the response to antiviral treatment and prevention of IR complications, including CVD.",
journal = "Current Pharmaceutical Design",
title = "Chronic Hepatitis C, Insulin Resistance and Vascular Disease",
volume = "16",
number = "34",
pages = "3823-3829",
doi = "10.2174/138161210794455067"
}

Trpković, A., Stokić, E., Radak, Đ. J., Gluvić, Z., Haidara, M. A., Mikhailidis, D. P.,& Isenović, E. R.. (2010). Chronic Hepatitis C, Insulin Resistance and Vascular Disease. in Current Pharmaceutical Design, 16(34), 3823-3829.
https://doi.org/10.2174/138161210794455067

Trpković A, Stokić E, Radak ĐJ, Gluvić Z, Haidara MA, Mikhailidis DP, Isenović ER. Chronic Hepatitis C, Insulin Resistance and Vascular Disease. in Current Pharmaceutical Design. 2010;16(34):3823-3829.
doi:10.2174/138161210794455067 .

Trpković, Andreja, Stokić, Edita, Radak, Đorđe J., Gluvić, Zoran, Haidara, Mohamed A., Mikhailidis, Dimitri P., Isenović, Esma R., "Chronic Hepatitis C, Insulin Resistance and Vascular Disease" in Current Pharmaceutical Design, 16, no. 34 (2010):3823-3829,
https://doi.org/10.2174/138161210794455067 . .

TY  - JOUR
AU  - Isenović, Esma R.
AU  - Kedees, Mamdouh H.
AU  - Haidara, Mohamed A.
AU  - Trpković, Andreja
AU  - Mikhailidis, Dimitri P.
AU  - Marche, Pierre
PY  - 2010
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/3984
AB  - It is well recognized that the proliferation of vascular smooth muscle cells (VSMCs) is a key event in the pathogenesis of various vascular diseases, including atherosclerosis and hypertension. We have previously shown that among extracellular signal-regulated protein kinases (ERKs), the 42- and 44-kDa isoforms (ERK1/2)participate in the cellular mitogenic machinery triggered by several VSMCs activators, including insulin (INS) and thrombin (Thr). However, understanding of the intracellular signal transduction pathways involved is incomplete. This review considers the recent findings in INS and Thr signaling mechanisms that modulate the proliferation of VSMCs with particular emphasis on the ERK1/2 signaling pathway, an important mediator of VSMCs hypertrophy and vascular disease. Moreover, because the ERK1/2 pathway have been acknowledged as an important mediator of VSMCs hypertrophy, ERK1/2 is identified as a key target for novel therapeutic interventions to minimize irreversible tissue damage associated with hypertension and atherosclerosis.
T2  - Angiology
T1  - Involvement of ERK1/2 Kinase in Insulin- and Thrombin-Stimulated Vascular Smooth Muscle Cell Proliferation
VL  - 61
IS  - 4
SP  - 357
EP  - 364
DO  - 10.1177/0003319709358693
ER  - 

@article{
author = "Isenović, Esma R. and Kedees, Mamdouh H. and Haidara, Mohamed A. and Trpković, Andreja and Mikhailidis, Dimitri P. and Marche, Pierre",
year = "2010",
abstract = "It is well recognized that the proliferation of vascular smooth muscle cells (VSMCs) is a key event in the pathogenesis of various vascular diseases, including atherosclerosis and hypertension. We have previously shown that among extracellular signal-regulated protein kinases (ERKs), the 42- and 44-kDa isoforms (ERK1/2)participate in the cellular mitogenic machinery triggered by several VSMCs activators, including insulin (INS) and thrombin (Thr). However, understanding of the intracellular signal transduction pathways involved is incomplete. This review considers the recent findings in INS and Thr signaling mechanisms that modulate the proliferation of VSMCs with particular emphasis on the ERK1/2 signaling pathway, an important mediator of VSMCs hypertrophy and vascular disease. Moreover, because the ERK1/2 pathway have been acknowledged as an important mediator of VSMCs hypertrophy, ERK1/2 is identified as a key target for novel therapeutic interventions to minimize irreversible tissue damage associated with hypertension and atherosclerosis.",
journal = "Angiology",
title = "Involvement of ERK1/2 Kinase in Insulin- and Thrombin-Stimulated Vascular Smooth Muscle Cell Proliferation",
volume = "61",
number = "4",
pages = "357-364",
doi = "10.1177/0003319709358693"
}

Isenović, E. R., Kedees, M. H., Haidara, M. A., Trpković, A., Mikhailidis, D. P.,& Marche, P.. (2010). Involvement of ERK1/2 Kinase in Insulin- and Thrombin-Stimulated Vascular Smooth Muscle Cell Proliferation. in Angiology, 61(4), 357-364.
https://doi.org/10.1177/0003319709358693

Isenović ER, Kedees MH, Haidara MA, Trpković A, Mikhailidis DP, Marche P. Involvement of ERK1/2 Kinase in Insulin- and Thrombin-Stimulated Vascular Smooth Muscle Cell Proliferation. in Angiology. 2010;61(4):357-364.
doi:10.1177/0003319709358693 .

Isenović, Esma R., Kedees, Mamdouh H., Haidara, Mohamed A., Trpković, Andreja, Mikhailidis, Dimitri P., Marche, Pierre, "Involvement of ERK1/2 Kinase in Insulin- and Thrombin-Stimulated Vascular Smooth Muscle Cell Proliferation" in Angiology, 61, no. 4 (2010):357-364,
https://doi.org/10.1177/0003319709358693 . .

TY  - JOUR
AU  - Bin-Jaliah, Ismaeel
AU  - Ammar, Hania I.
AU  - Mikhailidis, Dimitri P.
AU  - Dallak, Mohammed A.
AU  - Al-Hashem, Fahaid H.
AU  - Haidara, Mohamed A.
AU  - Yassin, Hanaa Z.
AU  - Bahnasi, Abeer A.
AU  - Rashed, Laila A.
AU  - Isenović, Esma R.
PY  - 2010
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/3883
AB  - The role of vascular endothelial growth factor (VEGF) and erythropoietin (EPO) in mediating hypoxic preconditioning under the acute intermittent hypoxic condition (AIH) was investigated in this study. Male Wistar rats were randomly assigned and kept in normoxic conditions, (Nx) or in AIH conditions and subjected to brief cycles hypoxia/reoxygenation. Hearts were isolated, perfused, and subjected to in vitro global ischemia followed by reperfusion. During and at the end of reperfusion, left ventricular developed pressure (LVDP); LV end diastolic pressure (LVEDP); rate pressure product (RPP); peak left ventricular pressure rise (Delta P/Delta t(max)) and heart rate (HR) were measured. Hearts subjected to AIH displayed a significant higher LVDP (P LT .001), RPP (P LT .001), and Delta P/Delta t(max) (P LT .001). Expression of VEGF and EPO were significantly increased at 3, 8, and 24 hours after AIH. Hypoxic training could provide a new approach to enhance endogenous cardioprotective mechanisms.
T2  - Angiology
T1  - Cardiac Adaptive Responses After Hypoxia in an Experimental Model
VL  - 61
IS  - 2
SP  - 145
EP  - 156
DO  - 10.1177/0003319709352486
ER  - 

@article{
author = "Bin-Jaliah, Ismaeel and Ammar, Hania I. and Mikhailidis, Dimitri P. and Dallak, Mohammed A. and Al-Hashem, Fahaid H. and Haidara, Mohamed A. and Yassin, Hanaa Z. and Bahnasi, Abeer A. and Rashed, Laila A. and Isenović, Esma R.",
year = "2010",
abstract = "The role of vascular endothelial growth factor (VEGF) and erythropoietin (EPO) in mediating hypoxic preconditioning under the acute intermittent hypoxic condition (AIH) was investigated in this study. Male Wistar rats were randomly assigned and kept in normoxic conditions, (Nx) or in AIH conditions and subjected to brief cycles hypoxia/reoxygenation. Hearts were isolated, perfused, and subjected to in vitro global ischemia followed by reperfusion. During and at the end of reperfusion, left ventricular developed pressure (LVDP); LV end diastolic pressure (LVEDP); rate pressure product (RPP); peak left ventricular pressure rise (Delta P/Delta t(max)) and heart rate (HR) were measured. Hearts subjected to AIH displayed a significant higher LVDP (P LT .001), RPP (P LT .001), and Delta P/Delta t(max) (P LT .001). Expression of VEGF and EPO were significantly increased at 3, 8, and 24 hours after AIH. Hypoxic training could provide a new approach to enhance endogenous cardioprotective mechanisms.",
journal = "Angiology",
title = "Cardiac Adaptive Responses After Hypoxia in an Experimental Model",
volume = "61",
number = "2",
pages = "145-156",
doi = "10.1177/0003319709352486"
}

Bin-Jaliah, I., Ammar, H. I., Mikhailidis, D. P., Dallak, M. A., Al-Hashem, F. H., Haidara, M. A., Yassin, H. Z., Bahnasi, A. A., Rashed, L. A.,& Isenović, E. R.. (2010). Cardiac Adaptive Responses After Hypoxia in an Experimental Model. in Angiology, 61(2), 145-156.
https://doi.org/10.1177/0003319709352486

Bin-Jaliah I, Ammar HI, Mikhailidis DP, Dallak MA, Al-Hashem FH, Haidara MA, Yassin HZ, Bahnasi AA, Rashed LA, Isenović ER. Cardiac Adaptive Responses After Hypoxia in an Experimental Model. in Angiology. 2010;61(2):145-156.
doi:10.1177/0003319709352486 .

Bin-Jaliah, Ismaeel, Ammar, Hania I., Mikhailidis, Dimitri P., Dallak, Mohammed A., Al-Hashem, Fahaid H., Haidara, Mohamed A., Yassin, Hanaa Z., Bahnasi, Abeer A., Rashed, Laila A., Isenović, Esma R., "Cardiac Adaptive Responses After Hypoxia in an Experimental Model" in Angiology, 61, no. 2 (2010):145-156,
https://doi.org/10.1177/0003319709352486 . .

TY  - JOUR
AU  - Haidara, Mohamed A.
AU  - Yassin, Hanaa Z.
AU  - Žakula, Zorica
AU  - Mikhailidis, Dimitri P.
AU  - Isenović, Esma R.
PY  - 2010
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4112
AB  - Numerous studies have shown that increased oxidative stress (OxS) is present in diabetic patients. There is evidence that this OxS can be increased before complications associated with diabetes mellitus (DM) occur. However, the role and influence of OxS in the initiation and progression of DM remains the subject of debate. It has been suggested that in DM, OxS is caused by increased production of reactive oxygen species (ROS), and associated with reduction in antioxidant defenses and altered cellular redox status. Acute and chronic OxS which could enhance the development of complications associated with DM. This review considers recent findings on the role of antioxidants in controlling OxS and the incidence of DM with emphasis on animal and human studies.
T2  - Current Vascular Pharmacology
T1  - Diabetes and Antioxidants: Myth or Reality?
VL  - 8
IS  - 5
SP  - 661
EP  - 672
UR  - https://hdl.handle.net/21.15107/rcub_vinar_4112
ER  - 

@article{
author = "Haidara, Mohamed A. and Yassin, Hanaa Z. and Žakula, Zorica and Mikhailidis, Dimitri P. and Isenović, Esma R.",
year = "2010",
abstract = "Numerous studies have shown that increased oxidative stress (OxS) is present in diabetic patients. There is evidence that this OxS can be increased before complications associated with diabetes mellitus (DM) occur. However, the role and influence of OxS in the initiation and progression of DM remains the subject of debate. It has been suggested that in DM, OxS is caused by increased production of reactive oxygen species (ROS), and associated with reduction in antioxidant defenses and altered cellular redox status. Acute and chronic OxS which could enhance the development of complications associated with DM. This review considers recent findings on the role of antioxidants in controlling OxS and the incidence of DM with emphasis on animal and human studies.",
journal = "Current Vascular Pharmacology",
title = "Diabetes and Antioxidants: Myth or Reality?",
volume = "8",
number = "5",
pages = "661-672",
url = "https://hdl.handle.net/21.15107/rcub_vinar_4112"
}

Haidara, M. A., Yassin, H. Z., Žakula, Z., Mikhailidis, D. P.,& Isenović, E. R.. (2010). Diabetes and Antioxidants: Myth or Reality?. in Current Vascular Pharmacology, 8(5), 661-672.
https://hdl.handle.net/21.15107/rcub_vinar_4112

Haidara MA, Yassin HZ, Žakula Z, Mikhailidis DP, Isenović ER. Diabetes and Antioxidants: Myth or Reality?. in Current Vascular Pharmacology. 2010;8(5):661-672.
https://hdl.handle.net/21.15107/rcub_vinar_4112 .

Haidara, Mohamed A., Yassin, Hanaa Z., Žakula, Zorica, Mikhailidis, Dimitri P., Isenović, Esma R., "Diabetes and Antioxidants: Myth or Reality?" in Current Vascular Pharmacology, 8, no. 5 (2010):661-672,
https://hdl.handle.net/21.15107/rcub_vinar_4112 .

TY  - JOUR
AU  - Haidara, Mohamed A.
AU  - Morsy, Mohamed D.
AU  - Abdel-Razek, Hesham A.
AU  - Mikhailidis, Dimitri P.
AU  - Isenović, Esma R.
PY  - 2010
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4145
AB  - Septicemia leads to oxidative stress with overproduction of reactive-oxygen species (ROS) and consumption of endogenous antioxidant enzymes. We tested a twofold hypothesis: (1) does oxidative stress (OxS) induced by sepsis acting alone or in concert with augmented inflammatory processes contributes to sepsis-related vascular dysfunction, and, (2) whether ozone (O(3)) and L-canavanine (CAV) mitigate the negative impact of the aforementioned phenomena. We investigated the relative impact of treatment with CAV and/or O(3) on vascular OxS associated vascular functional changes in septicemic rats. For this study, 60 male Sprague-Dawley rats were used and divided into six experimental groups (n=10): control group (C), sham-operated (Sham), septicemic rats (S), S rats treated with CAV (100 mg/kg. i.p; S+CAV), S rats treated with O(3) (1.2 mg/kg, i.p.; S+O(3)) and S rats treated with both O(3) and CAV (S+O(3)+CAV). After 22 h, the mean arterial blood pressure (MAP), the aortic ring vascular reactivity to phenylephrine, abdominal aortic blood flow (AABF), serum tumor necrosis factor-alpha (TNF-alpha) and plasma nitrite/nitrate (NOx) concentration were measured. In addition, hepatic antioxidant enzyme activities sodium dismutase (SOD) and glutathione peroxidase (GSH-Px) were estimated. Septicemia caused significant elevation of serum TNF-alpha (p LT 0.001) and plasma NOx (p LT 0.001) and significant (p LT 0.001) reduction of AABF (p LT 0.001), aortic vascular response to phenylephrine (p LT 0.001), MAP (p LT 0.001) and hepatic SOD and GSH-Px activity (p LT 0.001) compared with the C group, while treatment with O(3) and/or CAV induced significant amelioration of all those increases. Abnormalities were attenuated to a similar extent with treatment with both O(3) and CAV. These results suggested that concomitant administration of O(3) and CAV alleviated the compromised vascular reactivity in septicemic conditions and prevent its progression into septic shock compared with each alone.
T2  - Journal of Physiology and Biochemistry
T1  - Effects of L-Canavanine and ozone on vascular reactivity in septicemic rats
VL  - 66
IS  - 3
SP  - 255
EP  - 264
DO  - 10.1007/s13105-010-0034-6
ER  - 

@article{
author = "Haidara, Mohamed A. and Morsy, Mohamed D. and Abdel-Razek, Hesham A. and Mikhailidis, Dimitri P. and Isenović, Esma R.",
year = "2010",
abstract = "Septicemia leads to oxidative stress with overproduction of reactive-oxygen species (ROS) and consumption of endogenous antioxidant enzymes. We tested a twofold hypothesis: (1) does oxidative stress (OxS) induced by sepsis acting alone or in concert with augmented inflammatory processes contributes to sepsis-related vascular dysfunction, and, (2) whether ozone (O(3)) and L-canavanine (CAV) mitigate the negative impact of the aforementioned phenomena. We investigated the relative impact of treatment with CAV and/or O(3) on vascular OxS associated vascular functional changes in septicemic rats. For this study, 60 male Sprague-Dawley rats were used and divided into six experimental groups (n=10): control group (C), sham-operated (Sham), septicemic rats (S), S rats treated with CAV (100 mg/kg. i.p; S+CAV), S rats treated with O(3) (1.2 mg/kg, i.p.; S+O(3)) and S rats treated with both O(3) and CAV (S+O(3)+CAV). After 22 h, the mean arterial blood pressure (MAP), the aortic ring vascular reactivity to phenylephrine, abdominal aortic blood flow (AABF), serum tumor necrosis factor-alpha (TNF-alpha) and plasma nitrite/nitrate (NOx) concentration were measured. In addition, hepatic antioxidant enzyme activities sodium dismutase (SOD) and glutathione peroxidase (GSH-Px) were estimated. Septicemia caused significant elevation of serum TNF-alpha (p LT 0.001) and plasma NOx (p LT 0.001) and significant (p LT 0.001) reduction of AABF (p LT 0.001), aortic vascular response to phenylephrine (p LT 0.001), MAP (p LT 0.001) and hepatic SOD and GSH-Px activity (p LT 0.001) compared with the C group, while treatment with O(3) and/or CAV induced significant amelioration of all those increases. Abnormalities were attenuated to a similar extent with treatment with both O(3) and CAV. These results suggested that concomitant administration of O(3) and CAV alleviated the compromised vascular reactivity in septicemic conditions and prevent its progression into septic shock compared with each alone.",
journal = "Journal of Physiology and Biochemistry",
title = "Effects of L-Canavanine and ozone on vascular reactivity in septicemic rats",
volume = "66",
number = "3",
pages = "255-264",
doi = "10.1007/s13105-010-0034-6"
}

Haidara, M. A., Morsy, M. D., Abdel-Razek, H. A., Mikhailidis, D. P.,& Isenović, E. R.. (2010). Effects of L-Canavanine and ozone on vascular reactivity in septicemic rats. in Journal of Physiology and Biochemistry, 66(3), 255-264.
https://doi.org/10.1007/s13105-010-0034-6

Haidara MA, Morsy MD, Abdel-Razek HA, Mikhailidis DP, Isenović ER. Effects of L-Canavanine and ozone on vascular reactivity in septicemic rats. in Journal of Physiology and Biochemistry. 2010;66(3):255-264.
doi:10.1007/s13105-010-0034-6 .

Haidara, Mohamed A., Morsy, Mohamed D., Abdel-Razek, Hesham A., Mikhailidis, Dimitri P., Isenović, Esma R., "Effects of L-Canavanine and ozone on vascular reactivity in septicemic rats" in Journal of Physiology and Biochemistry, 66, no. 3 (2010):255-264,
https://doi.org/10.1007/s13105-010-0034-6 . .

TY  - JOUR
AU  - Fouad, Hanan H.
AU  - Al-Dera, Husain
AU  - Bakhoum, Sameh W.
AU  - Rashed, Laila A.
AU  - Sayed, Rehab H.
AU  - Rateb, Moshira A.
AU  - Haidara, Mohamed A.
AU  - Soskić, Sanja S.
AU  - Isenović, Esma R.
PY  - 2010
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4039
AB  - We determined the serum levels of soluble CD40 ligand (sCD4OL) in patients with chronic coronary artery disease (CAD) and acute coronary syndrome (ACS). Patients with unstable angina (UA) and myocardial infarction (MI) showed significantly higher levels (P LT .001) of sCD4OL compared with patients with stable angina (SA) and controls; particularly, high levels occurred in patients with UA (UA: 9.23 +/- 2.92, MI: 7.38 +/- 1.05, SA: 4.42 +/- 1.08; control: 4.01 +/- 0.87 ng/mL). There was no significant difference in sCD4OL levels between patients with UA and MI or between patients with SA and controls. Levels of sCD4OL did not show any significant correlation with peak creatine kinase (CK), CK-MB isoenzyme activity in patients with MI, troponin T serum levels in patients with UA or with culprit vessel (CV) complexity score (CVCS), type of CV lesion, or vessel score in patients with UA or MI. These results suggest that CD40L plays a pathogenic role in triggering ACS.
T2  - Angiology
T1  - Levels of sCD40 Ligand in Chronic and Acute Coronary Syndromes and its Relation to Angiographic Extent of Coronary Arterial Narrowing
VL  - 61
IS  - 6
SP  - 567
EP  - 573
DO  - 10.1177/0003319709356785
ER  - 

@article{
author = "Fouad, Hanan H. and Al-Dera, Husain and Bakhoum, Sameh W. and Rashed, Laila A. and Sayed, Rehab H. and Rateb, Moshira A. and Haidara, Mohamed A. and Soskić, Sanja S. and Isenović, Esma R.",
year = "2010",
abstract = "We determined the serum levels of soluble CD40 ligand (sCD4OL) in patients with chronic coronary artery disease (CAD) and acute coronary syndrome (ACS). Patients with unstable angina (UA) and myocardial infarction (MI) showed significantly higher levels (P LT .001) of sCD4OL compared with patients with stable angina (SA) and controls; particularly, high levels occurred in patients with UA (UA: 9.23 +/- 2.92, MI: 7.38 +/- 1.05, SA: 4.42 +/- 1.08; control: 4.01 +/- 0.87 ng/mL). There was no significant difference in sCD4OL levels between patients with UA and MI or between patients with SA and controls. Levels of sCD4OL did not show any significant correlation with peak creatine kinase (CK), CK-MB isoenzyme activity in patients with MI, troponin T serum levels in patients with UA or with culprit vessel (CV) complexity score (CVCS), type of CV lesion, or vessel score in patients with UA or MI. These results suggest that CD40L plays a pathogenic role in triggering ACS.",
journal = "Angiology",
title = "Levels of sCD40 Ligand in Chronic and Acute Coronary Syndromes and its Relation to Angiographic Extent of Coronary Arterial Narrowing",
volume = "61",
number = "6",
pages = "567-573",
doi = "10.1177/0003319709356785"
}

Fouad, H. H., Al-Dera, H., Bakhoum, S. W., Rashed, L. A., Sayed, R. H., Rateb, M. A., Haidara, M. A., Soskić, S. S.,& Isenović, E. R.. (2010). Levels of sCD40 Ligand in Chronic and Acute Coronary Syndromes and its Relation to Angiographic Extent of Coronary Arterial Narrowing. in Angiology, 61(6), 567-573.
https://doi.org/10.1177/0003319709356785

Fouad HH, Al-Dera H, Bakhoum SW, Rashed LA, Sayed RH, Rateb MA, Haidara MA, Soskić SS, Isenović ER. Levels of sCD40 Ligand in Chronic and Acute Coronary Syndromes and its Relation to Angiographic Extent of Coronary Arterial Narrowing. in Angiology. 2010;61(6):567-573.
doi:10.1177/0003319709356785 .

Fouad, Hanan H., Al-Dera, Husain, Bakhoum, Sameh W., Rashed, Laila A., Sayed, Rehab H., Rateb, Moshira A., Haidara, Mohamed A., Soskić, Sanja S., Isenović, Esma R., "Levels of sCD40 Ligand in Chronic and Acute Coronary Syndromes and its Relation to Angiographic Extent of Coronary Arterial Narrowing" in Angiology, 61, no. 6 (2010):567-573,
https://doi.org/10.1177/0003319709356785 . .

TY  - JOUR
AU  - El Barbary, Magdy A.
AU  - Saad, Alaa Eldin M.
AU  - Attia, Fadia M.
AU  - Mandour, Magda I.
AU  - Haidara, Mohamed A.
AU  - Dallak, Mohammad M.
AU  - Isenović, Esma R.
PY  - 2010
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/3932
AB  - A total of 30 patients with chronic hepatitis C (HCV) thrombocytopenia (TP) and 20 healthy controls were studied. Both groups were subjected to complete medical history, clinical examination in addition to assessment of hepatitis markers: level of thrombopoietin (Tpo), Geimsa-stained bone marrow smears, and in vitro short-term megakaryocytic progenitors culture (CFU-MK). Serum Tpo level was significantly elevated in patients with TP HCV. Short-term CFU-MK showed an evident depression in the colony-forming unit-megakaryocyte (CFU-meg). There is a positive correlation between the number of CFU-meg and the platelet count and between serum Tpo level and prothrombin time, transaminase, albumin, and the Child Pugh score of liver disease; a negative correlation between serum Tpo level and the number of CFU-meg and between serum Tpo level and the platelet count. Thus, the level of Tpo could be an indicator of intact functional response of the hepatocytes.
T2  - Angiology
T1  - Thrombocytopenia in Patients With Chronic Hepatitis C: A Possible Role of HCV on Platelet Progenitor Cell Maturation
VL  - 61
IS  - 3
SP  - 304
EP  - 313
DO  - 10.1177/0003319709343178
ER  - 

@article{
author = "El Barbary, Magdy A. and Saad, Alaa Eldin M. and Attia, Fadia M. and Mandour, Magda I. and Haidara, Mohamed A. and Dallak, Mohammad M. and Isenović, Esma R.",
year = "2010",
abstract = "A total of 30 patients with chronic hepatitis C (HCV) thrombocytopenia (TP) and 20 healthy controls were studied. Both groups were subjected to complete medical history, clinical examination in addition to assessment of hepatitis markers: level of thrombopoietin (Tpo), Geimsa-stained bone marrow smears, and in vitro short-term megakaryocytic progenitors culture (CFU-MK). Serum Tpo level was significantly elevated in patients with TP HCV. Short-term CFU-MK showed an evident depression in the colony-forming unit-megakaryocyte (CFU-meg). There is a positive correlation between the number of CFU-meg and the platelet count and between serum Tpo level and prothrombin time, transaminase, albumin, and the Child Pugh score of liver disease; a negative correlation between serum Tpo level and the number of CFU-meg and between serum Tpo level and the platelet count. Thus, the level of Tpo could be an indicator of intact functional response of the hepatocytes.",
journal = "Angiology",
title = "Thrombocytopenia in Patients With Chronic Hepatitis C: A Possible Role of HCV on Platelet Progenitor Cell Maturation",
volume = "61",
number = "3",
pages = "304-313",
doi = "10.1177/0003319709343178"
}

El Barbary, M. A., Saad, A. E. M., Attia, F. M., Mandour, M. I., Haidara, M. A., Dallak, M. M.,& Isenović, E. R.. (2010). Thrombocytopenia in Patients With Chronic Hepatitis C: A Possible Role of HCV on Platelet Progenitor Cell Maturation. in Angiology, 61(3), 304-313.
https://doi.org/10.1177/0003319709343178

El Barbary MA, Saad AEM, Attia FM, Mandour MI, Haidara MA, Dallak MM, Isenović ER. Thrombocytopenia in Patients With Chronic Hepatitis C: A Possible Role of HCV on Platelet Progenitor Cell Maturation. in Angiology. 2010;61(3):304-313.
doi:10.1177/0003319709343178 .

El Barbary, Magdy A., Saad, Alaa Eldin M., Attia, Fadia M., Mandour, Magda I., Haidara, Mohamed A., Dallak, Mohammad M., Isenović, Esma R., "Thrombocytopenia in Patients With Chronic Hepatitis C: A Possible Role of HCV on Platelet Progenitor Cell Maturation" in Angiology, 61, no. 3 (2010):304-313,
https://doi.org/10.1177/0003319709343178 . .