TY  - CONF
AU  - Krstić, Dragana Ž.
AU  - Ilić, Radovan
AU  - Jovanović, Aleksandra
AU  - Nikezić, Dragoslav
AU  - Jeremić, Marija
AU  - Nikolić, Nebojša
AU  - Mihajlović, Jasmina
PY  - 2019
UR  - https://plus.sr.cobiss.net/opac7/bib/279687436
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8719
AB  - U radu je prikazano poređenje apsorbovanih doza u brahiterapijskim planovima i Monte Karlo simulacijama u brahiterapiji pacijentkinja sa karcinomom grlića materice. U Odeljenju za brahiterapiju u Kliničkom centru Kragujevac primenjuje se mikroSelektron za intrakavitarnu brahiterapiju u HDR režimu. Ovaj uređaj koristi minijaturni radioaktivni izvor 192Ir u obliku cilindra, aktivnih dimenzija 0,6 mm × 3,5 mm, i visoke početne aktivnosti od 370 GBq.Pre terapije, vrši se kompjutersko planiranje, koje predstavlja kompjutersku rekonstruk-ciju položaja vodiča izvora u pacijentu na osnovu dva radiografska snimka, i izodozno planiranje u odnosu na željene dozimetrijske tačke. Osnovni podaci planiranja su dnevna doza, koja iznosi 700 cGy i broj frakcija; dnevna doza se isporučuje se u tri frakcije jednom nedeljno. Monte Karlo simulacije su obavljene korišćenjem MCNP6 softvera verzije 2.0 kako bi se procenila raspodela doze u materici i kritičnim organima od rizika (bešika i debelo crevo). MCNP F6 tally (MeV/g) je izabran zbog lakog konvertovanja deponovane energije u apsorbovanu dozu. Za pripremu ulaznih datoteka koje simuliraju brahi-terapiju korišćeni su matematički ORNL i voksel fantomi. Upoređivanjem izmerenih i izračunatih vrednosti može se videti da su Monte Carlo tehnike moćno sredstvo za primenu u planiranju brahiterapije.
AB  - This paper presents the comparison of absorbed doses in brachytherapy plans and Monte Carlo simulation for brachytherapy treatment of a female patient with cervix carcinoma. At the Department of Brachytherapy at the Clinical Center Kragujevac, the microSelectron after loading deviceis used for intracavitary brachytherapy in the HDR regime. This device uses a miniature radioactive source 192Ir in the form of a cylinder, active dimensions of 0.6 mm × 3.5 mm, and a high initial activity of about 370 GBq. Before therapy, computer planning is performed, which represents a computer reconstruction of the position of the source guide in the patient based on two radiographic images, and isodose planning in relation to the desired dosimetry points. Essential planning data are the daily dose and number of fractions. In this case, the daily dose is 700 cGy and is delivered in three fractions once a week. This means that the duration of this brachytherapy treatment will be a total of three weeks. Monte Carlo simulations by using MCNP6 code version 2.0 were applied for brachytherapy treatment to estimate the dose distribution in uterus and several critical organs at risk (bladder and colon). The MCNP tally f6 (MeV/g) was chosen due to easy convert energy deposition toabsorbed dose. The computational ORNL and voxel phantoms were used to prepare input files which simulate brachytherapy.By comparing measured and calculated values, it can be seen that Monte Carlo techniques are a powerful tool for application in brachytherapy planning.
PB  - Београд : Институт за нуклеарне науке "Винча" : Друштво за заштиту од зрачења Србије и Црне Горе
C3  - 30. симпозијум ДЗЗСЦГ : зборник радова
T1  - Monte Carlo dozimetrija u brahiterapiji kancera cerviksa
T1  - Monte Carlo dosimetry for brachytherapy of cervical cancer
SP  - 483
EP  - 488
UR  - https://hdl.handle.net/21.15107/rcub_vinar_8719
ER  - 

@conference{
author = "Krstić, Dragana Ž. and Ilić, Radovan and Jovanović, Aleksandra and Nikezić, Dragoslav and Jeremić, Marija and Nikolić, Nebojša and Mihajlović, Jasmina",
year = "2019",
abstract = "U radu je prikazano poređenje apsorbovanih doza u brahiterapijskim planovima i Monte Karlo simulacijama u brahiterapiji pacijentkinja sa karcinomom grlića materice. U Odeljenju za brahiterapiju u Kliničkom centru Kragujevac primenjuje se mikroSelektron za intrakavitarnu brahiterapiju u HDR režimu. Ovaj uređaj koristi minijaturni radioaktivni izvor 192Ir u obliku cilindra, aktivnih dimenzija 0,6 mm × 3,5 mm, i visoke početne aktivnosti od 370 GBq.Pre terapije, vrši se kompjutersko planiranje, koje predstavlja kompjutersku rekonstruk-ciju položaja vodiča izvora u pacijentu na osnovu dva radiografska snimka, i izodozno planiranje u odnosu na željene dozimetrijske tačke. Osnovni podaci planiranja su dnevna doza, koja iznosi 700 cGy i broj frakcija; dnevna doza se isporučuje se u tri frakcije jednom nedeljno. Monte Karlo simulacije su obavljene korišćenjem MCNP6 softvera verzije 2.0 kako bi se procenila raspodela doze u materici i kritičnim organima od rizika (bešika i debelo crevo). MCNP F6 tally (MeV/g) je izabran zbog lakog konvertovanja deponovane energije u apsorbovanu dozu. Za pripremu ulaznih datoteka koje simuliraju brahi-terapiju korišćeni su matematički ORNL i voksel fantomi. Upoređivanjem izmerenih i izračunatih vrednosti može se videti da su Monte Carlo tehnike moćno sredstvo za primenu u planiranju brahiterapije., This paper presents the comparison of absorbed doses in brachytherapy plans and Monte Carlo simulation for brachytherapy treatment of a female patient with cervix carcinoma. At the Department of Brachytherapy at the Clinical Center Kragujevac, the microSelectron after loading deviceis used for intracavitary brachytherapy in the HDR regime. This device uses a miniature radioactive source 192Ir in the form of a cylinder, active dimensions of 0.6 mm × 3.5 mm, and a high initial activity of about 370 GBq. Before therapy, computer planning is performed, which represents a computer reconstruction of the position of the source guide in the patient based on two radiographic images, and isodose planning in relation to the desired dosimetry points. Essential planning data are the daily dose and number of fractions. In this case, the daily dose is 700 cGy and is delivered in three fractions once a week. This means that the duration of this brachytherapy treatment will be a total of three weeks. Monte Carlo simulations by using MCNP6 code version 2.0 were applied for brachytherapy treatment to estimate the dose distribution in uterus and several critical organs at risk (bladder and colon). The MCNP tally f6 (MeV/g) was chosen due to easy convert energy deposition toabsorbed dose. The computational ORNL and voxel phantoms were used to prepare input files which simulate brachytherapy.By comparing measured and calculated values, it can be seen that Monte Carlo techniques are a powerful tool for application in brachytherapy planning.",
publisher = "Београд : Институт за нуклеарне науке "Винча" : Друштво за заштиту од зрачења Србије и Црне Горе",
journal = "30. симпозијум ДЗЗСЦГ : зборник радова",
title = "Monte Carlo dozimetrija u brahiterapiji kancera cerviksa, Monte Carlo dosimetry for brachytherapy of cervical cancer",
pages = "483-488",
url = "https://hdl.handle.net/21.15107/rcub_vinar_8719"
}

Krstić, D. Ž., Ilić, R., Jovanović, A., Nikezić, D., Jeremić, M., Nikolić, N.,& Mihajlović, J.. (2019). Monte Carlo dozimetrija u brahiterapiji kancera cerviksa. in 30. симпозијум ДЗЗСЦГ : зборник радова
Београд : Институт за нуклеарне науке "Винча" : Друштво за заштиту од зрачења Србије и Црне Горе., 483-488.
https://hdl.handle.net/21.15107/rcub_vinar_8719

Krstić DŽ, Ilić R, Jovanović A, Nikezić D, Jeremić M, Nikolić N, Mihajlović J. Monte Carlo dozimetrija u brahiterapiji kancera cerviksa. in 30. симпозијум ДЗЗСЦГ : зборник радова. 2019;:483-488.
https://hdl.handle.net/21.15107/rcub_vinar_8719 .

Krstić, Dragana Ž., Ilić, Radovan, Jovanović, Aleksandra, Nikezić, Dragoslav, Jeremić, Marija, Nikolić, Nebojša, Mihajlović, Jasmina, "Monte Carlo dozimetrija u brahiterapiji kancera cerviksa" in 30. симпозијум ДЗЗСЦГ : зборник радова (2019):483-488,
https://hdl.handle.net/21.15107/rcub_vinar_8719 .

TY  - THES
AU  - Jovanović, Aleksandra
PY  - 2019
UR  - http://nardus.mpn.gov.rs/handle/123456789/11023
UR  - http://eteze.bg.ac.rs/application/showtheses?thesesId=6735
UR  - https://fedorabg.bg.ac.rs/fedora/get/o:19580/bdef:Content/download
UR  - https://plus.sr.cobiss.net/opac7/bib/1025214130
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8726
AB  - Gojaznost je oboljenje povezano sa nizom patoloških stanja kao što su: rezistencija na insulin (IR), kardiovaskularne bolesti (KVB) i Diabetes Mellitus tipa 2 (DMT2). Povećana ekspresija i aktivnost inducibilne azot-monoksid-sintaze (iNOS; engl. Inducible Nitric Oxide Synthase) u srcu u stanju gojaznosti, moţe dovesti do apoptoze kardiomiocita i hipertrofije srca, dok sa druge strane gojaznost zdruţena sa IR doprinosi smanjenoj aktivnosti Na+/K+-ATPaze, što dovodi do smanjenja kontraktilnosti vaskulature i razvoja sistemske hipertenzije. Endogeni estradiol svojim delovanjem sprečava nastanak IR i hiperglikemije i ostvaruje pozitivne efekte na kardiovaskularni sistem (KVS), ali sinteza i kardioprotektivni uticaj estradiola mogu biti smanjeni usled razvoja gojaznosti.Estradiol ostvaruje kardioprotektivne tako što utiče na smanjenje ekspresije i aktivnosti iNOS, kao i povećanje ekspresije i aktivnosti Na+/K+-ATPaze, posredstvom različitih signalnih molekula i kinaza, kao što su: supstrat receptora za insulin 1 (IRS-1; engl. Insulin Receptor Substrate)/ fosfatidil-inozitol-3-kinaza (PI3K; engl. Phosphatidylinositide 3-Kinase)/ protein kinaza B (Akt; engl. Protein Kinase B), ekstracelularnim signalima regulisane kinaze 1 i 2 (ERK1/2; engl. Extracellular Signal-Regulated Protein Kinases 1 i 2) kao i RhoA (engl. Ras homolog gene family, member A)/ROCK (engl. Rho-associated protein kinase). Pored direktnog efekta na srce, estradiol posredno reguliše i njegovu funkciju tako sto utiče na metabolizam i transport glukoze i SMK, preko transportera glukoze (GLUT; engl. Glucose Transporters) i translokaze masnih kiselina (FAT; CD36 ; engl. Fatty Acid Translocase).Za izradu ove doktorske disertacije je korišćeno 16 adultnih ţenki pacova soja Wistar, podeljenih u dve eksperimentalne grupe. Prva grupa pacova je tokom 10 nedelja hranjena standardnom laboratorijskom hranom za pacove, dok je druga grupa pacova tokom 10 nedelja hranjena standardnom laboratorijskom hranom obogaćenom sa 42% masti (HF reţim ishrane). Nakon 10 nedelja pacovi su ţrtvovani, sakupljena je krv i izolovan je serum, a srca su ekstrahovana i delovi tkiva su korišćeni za izolovanje proteina i RNK. U serumu pacova je odreĎivana koncentracija estradiola, dok su u lizatu srca pacova odreĎivane koncentracije L-Arginina (L-Arg), NO i slobodnih masnih kiselina (SMK). Metodom qRT-PCR odreĎivan je nivo iRNK iNOS u srcu pacova...
AB  - Obesity is associated with several pathological conditions such as: insulin resistance (IR), cardiovascular disease (CVD) and Diabetes Mellitus type 2 (DMT2). Obesity related inducible nitric oxide synthase (iNOS) overexpression could lead to cardiac hypertrophy, while on the other hand obesity induced IR contributes to the reduced Na+/K+-ATPase activity, leading to vascular contractility impairment and development of systemic hypertension. Endogenous estradiol prevents IR and hyperglycaemia and has protective effects on the cardiovascular system (CVS), but the synthesis and cardioprotective effect of estradiol can be reduced due to the development of obesity. Estradiol exerts cardioprotective effects by reducing the expression and activity of iNOS, as well as by increasing the expression of Na+/K+-ATPase activity by regulating the activity of signaling molecules and kinases, such as: insulin receptor substrate 1 (IRS-1)/phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt, PKB), extracellular signal regulated kinase 1 and 2 (ERK1/2) as well as RhoA (Ras homolog gene family, member A)/ROCK (Rho-associated protein kinase). Additionally, estradiol indirectly regulates CVS function by influencing the metabolism and transport of glucose and free fatty acids (FFA), through glucose transporter (GLUT) and FAT; CD36 (Fatty Acid Translocase). In this doctoral dissertation 16 adult female Wistar rats were used and divided into two experimental groups. The first group of rats was fed a standard chow for laboratory rats for 10 weeks, while the second group of rats was fed a standard chow for laboratory rats enriched with 42% fat (HF diet) for 10 weeks. After 10 weeks, the rats were sacrificed, blood was collected and the serum isolated, the hearts were collected, and its tissue fragments were used to isolate proteins and RNA. The concentration of estradiol was measured in serum, while concentrations of L-Arginine (L-Arg), NO and free fatty acids (FFA) were measured in the heart lysates. qRT-PCR method was used to measure the level of iNOS mRNA in rats’ hearts. Na+/K+-ATPase was measured in plasma membranes of rats’ hearts. Western blot was used to measure the level of the following proteins: iNOS, NFkB-p50, ERα, p85 and p110 subunits of PI3K, NDRG2, RhoA, ROCK1 and ROCK2 in heart lysates. The level of phosphorylation and expression of Akt and ERK1/2 kinases, as well as the IRS-1/PI3K associations, were determined in heart lysates...
PB  - Универзитет у Београду, Биолошки факултет
T2  - Универзитет у Београду
T1  - Signalni putevi estradiola uključeni u regulaciju ekspresije i aktivnosti inducibilne azot-monoksid-sintaze i natrijum-kalijum adenozintrifosfataze u srcu gojaznih ženki pacova
UR  - https://hdl.handle.net/21.15107/rcub_nardus_11023
ER  - 

@phdthesis{
author = "Jovanović, Aleksandra",
year = "2019",
abstract = "Gojaznost je oboljenje povezano sa nizom patoloških stanja kao što su: rezistencija na insulin (IR), kardiovaskularne bolesti (KVB) i Diabetes Mellitus tipa 2 (DMT2). Povećana ekspresija i aktivnost inducibilne azot-monoksid-sintaze (iNOS; engl. Inducible Nitric Oxide Synthase) u srcu u stanju gojaznosti, moţe dovesti do apoptoze kardiomiocita i hipertrofije srca, dok sa druge strane gojaznost zdruţena sa IR doprinosi smanjenoj aktivnosti Na+/K+-ATPaze, što dovodi do smanjenja kontraktilnosti vaskulature i razvoja sistemske hipertenzije. Endogeni estradiol svojim delovanjem sprečava nastanak IR i hiperglikemije i ostvaruje pozitivne efekte na kardiovaskularni sistem (KVS), ali sinteza i kardioprotektivni uticaj estradiola mogu biti smanjeni usled razvoja gojaznosti.Estradiol ostvaruje kardioprotektivne tako što utiče na smanjenje ekspresije i aktivnosti iNOS, kao i povećanje ekspresije i aktivnosti Na+/K+-ATPaze, posredstvom različitih signalnih molekula i kinaza, kao što su: supstrat receptora za insulin 1 (IRS-1; engl. Insulin Receptor Substrate)/ fosfatidil-inozitol-3-kinaza (PI3K; engl. Phosphatidylinositide 3-Kinase)/ protein kinaza B (Akt; engl. Protein Kinase B), ekstracelularnim signalima regulisane kinaze 1 i 2 (ERK1/2; engl. Extracellular Signal-Regulated Protein Kinases 1 i 2) kao i RhoA (engl. Ras homolog gene family, member A)/ROCK (engl. Rho-associated protein kinase). Pored direktnog efekta na srce, estradiol posredno reguliše i njegovu funkciju tako sto utiče na metabolizam i transport glukoze i SMK, preko transportera glukoze (GLUT; engl. Glucose Transporters) i translokaze masnih kiselina (FAT; CD36 ; engl. Fatty Acid Translocase).Za izradu ove doktorske disertacije je korišćeno 16 adultnih ţenki pacova soja Wistar, podeljenih u dve eksperimentalne grupe. Prva grupa pacova je tokom 10 nedelja hranjena standardnom laboratorijskom hranom za pacove, dok je druga grupa pacova tokom 10 nedelja hranjena standardnom laboratorijskom hranom obogaćenom sa 42% masti (HF reţim ishrane). Nakon 10 nedelja pacovi su ţrtvovani, sakupljena je krv i izolovan je serum, a srca su ekstrahovana i delovi tkiva su korišćeni za izolovanje proteina i RNK. U serumu pacova je odreĎivana koncentracija estradiola, dok su u lizatu srca pacova odreĎivane koncentracije L-Arginina (L-Arg), NO i slobodnih masnih kiselina (SMK). Metodom qRT-PCR odreĎivan je nivo iRNK iNOS u srcu pacova..., Obesity is associated with several pathological conditions such as: insulin resistance (IR), cardiovascular disease (CVD) and Diabetes Mellitus type 2 (DMT2). Obesity related inducible nitric oxide synthase (iNOS) overexpression could lead to cardiac hypertrophy, while on the other hand obesity induced IR contributes to the reduced Na+/K+-ATPase activity, leading to vascular contractility impairment and development of systemic hypertension. Endogenous estradiol prevents IR and hyperglycaemia and has protective effects on the cardiovascular system (CVS), but the synthesis and cardioprotective effect of estradiol can be reduced due to the development of obesity. Estradiol exerts cardioprotective effects by reducing the expression and activity of iNOS, as well as by increasing the expression of Na+/K+-ATPase activity by regulating the activity of signaling molecules and kinases, such as: insulin receptor substrate 1 (IRS-1)/phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt, PKB), extracellular signal regulated kinase 1 and 2 (ERK1/2) as well as RhoA (Ras homolog gene family, member A)/ROCK (Rho-associated protein kinase). Additionally, estradiol indirectly regulates CVS function by influencing the metabolism and transport of glucose and free fatty acids (FFA), through glucose transporter (GLUT) and FAT; CD36 (Fatty Acid Translocase). In this doctoral dissertation 16 adult female Wistar rats were used and divided into two experimental groups. The first group of rats was fed a standard chow for laboratory rats for 10 weeks, while the second group of rats was fed a standard chow for laboratory rats enriched with 42% fat (HF diet) for 10 weeks. After 10 weeks, the rats were sacrificed, blood was collected and the serum isolated, the hearts were collected, and its tissue fragments were used to isolate proteins and RNA. The concentration of estradiol was measured in serum, while concentrations of L-Arginine (L-Arg), NO and free fatty acids (FFA) were measured in the heart lysates. qRT-PCR method was used to measure the level of iNOS mRNA in rats’ hearts. Na+/K+-ATPase was measured in plasma membranes of rats’ hearts. Western blot was used to measure the level of the following proteins: iNOS, NFkB-p50, ERα, p85 and p110 subunits of PI3K, NDRG2, RhoA, ROCK1 and ROCK2 in heart lysates. The level of phosphorylation and expression of Akt and ERK1/2 kinases, as well as the IRS-1/PI3K associations, were determined in heart lysates...",
publisher = "Универзитет у Београду, Биолошки факултет",
journal = "Универзитет у Београду",
title = "Signalni putevi estradiola uključeni u regulaciju ekspresije i aktivnosti inducibilne azot-monoksid-sintaze i natrijum-kalijum adenozintrifosfataze u srcu gojaznih ženki pacova",
url = "https://hdl.handle.net/21.15107/rcub_nardus_11023"
}

Jovanović, A.. (2019). Signalni putevi estradiola uključeni u regulaciju ekspresije i aktivnosti inducibilne azot-monoksid-sintaze i natrijum-kalijum adenozintrifosfataze u srcu gojaznih ženki pacova. in Универзитет у Београду
Универзитет у Београду, Биолошки факултет..
https://hdl.handle.net/21.15107/rcub_nardus_11023

Jovanović A. Signalni putevi estradiola uključeni u regulaciju ekspresije i aktivnosti inducibilne azot-monoksid-sintaze i natrijum-kalijum adenozintrifosfataze u srcu gojaznih ženki pacova. in Универзитет у Београду. 2019;.
https://hdl.handle.net/21.15107/rcub_nardus_11023 .

Jovanović, Aleksandra, "Signalni putevi estradiola uključeni u regulaciju ekspresije i aktivnosti inducibilne azot-monoksid-sintaze i natrijum-kalijum adenozintrifosfataze u srcu gojaznih ženki pacova" in Универзитет у Београду (2019),
https://hdl.handle.net/21.15107/rcub_nardus_11023 .

TY  - JOUR
AU  - Resanović, Ivana
AU  - Gluvić, Zoran
AU  - Zarić, Božidarka
AU  - Sudar-Milovanović, Emina
AU  - Jovanović, Aleksandra
AU  - Milačić, Davorka
AU  - Isaković, Radmilo
AU  - Isenović, Esma R.
PY  - 2019
UR  - https://www.hindawi.com/journals/ije/2019/2328505/
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8209
AB  - This study aimed at examining the early effects of hyperbaric oxygen therapy (HBOT) on inducible nitric oxide synthase (iNOS) activity/expression in lymphocytes of type 1 diabetes mellitus (T1DM) patients. A group of 19 patients (mean age: 63 ± 2.1) with T1DM and with the peripheral arterial disease were included in this study. Patients were exposed to 10 sessions of HBOT in the duration of 1 h to 100% oxygen inhalation at 2.4 ATA. Blood samples were collected for the plasma C-reactive protein (CRP), plasma free fatty acid (FFA), serum nitrite/nitrate, and serum arginase activity measurements. Expression of iNOS and phosphorylation of p65 subunit of nuclear factor- κ B (NF κ B-p65), extracellular-regulated kinases 1/2 (ERK1/2), and protein kinase B (Akt) were examined in lymphocyte lysates by Western blot. After exposure to HBOT, plasma CRP and FFA were significantly decreased ( p < 0.001 ). Protein expression of iNOS and serum nitrite/nitrate levels were decreased ( p < 0.01 ), while serum arginase activity was increased ( p < 0.05 ) versus before exposure to HBOT. Increased phosphorylation of NF κ B-p65 at Ser 536 ( p < 0.05 ) and decreased level of NF κ B-p65 protein ( p < 0.001 ) in lymphocytes of T1DM patients were observed after HBOT. Decreased phosphorylation of ERK1/2 ( p < 0.05 ) and Akt ( p < 0.05 ) was detected after HBOT. Our results indicate that exposure to HBO decreased iNOS activity/expression via decreasing phosphorylation of ERK1/2 and Akt followed by decreased activity of NF κ B.
T2  - International Journal of Endocrinology
T1  - Early Effects of Hyperbaric Oxygen on Inducible Nitric Oxide Synthase Activity/Expression in Lymphocytes of Type 1 Diabetes Patients: A Prospective Pilot Study
VL  - 2019
SP  - 1
EP  - 12
DO  - 10.1155/2019/2328505
ER  - 

@article{
author = "Resanović, Ivana and Gluvić, Zoran and Zarić, Božidarka and Sudar-Milovanović, Emina and Jovanović, Aleksandra and Milačić, Davorka and Isaković, Radmilo and Isenović, Esma R.",
year = "2019",
abstract = "This study aimed at examining the early effects of hyperbaric oxygen therapy (HBOT) on inducible nitric oxide synthase (iNOS) activity/expression in lymphocytes of type 1 diabetes mellitus (T1DM) patients. A group of 19 patients (mean age: 63 ± 2.1) with T1DM and with the peripheral arterial disease were included in this study. Patients were exposed to 10 sessions of HBOT in the duration of 1 h to 100% oxygen inhalation at 2.4 ATA. Blood samples were collected for the plasma C-reactive protein (CRP), plasma free fatty acid (FFA), serum nitrite/nitrate, and serum arginase activity measurements. Expression of iNOS and phosphorylation of p65 subunit of nuclear factor- κ B (NF κ B-p65), extracellular-regulated kinases 1/2 (ERK1/2), and protein kinase B (Akt) were examined in lymphocyte lysates by Western blot. After exposure to HBOT, plasma CRP and FFA were significantly decreased ( p < 0.001 ). Protein expression of iNOS and serum nitrite/nitrate levels were decreased ( p < 0.01 ), while serum arginase activity was increased ( p < 0.05 ) versus before exposure to HBOT. Increased phosphorylation of NF κ B-p65 at Ser 536 ( p < 0.05 ) and decreased level of NF κ B-p65 protein ( p < 0.001 ) in lymphocytes of T1DM patients were observed after HBOT. Decreased phosphorylation of ERK1/2 ( p < 0.05 ) and Akt ( p < 0.05 ) was detected after HBOT. Our results indicate that exposure to HBO decreased iNOS activity/expression via decreasing phosphorylation of ERK1/2 and Akt followed by decreased activity of NF κ B.",
journal = "International Journal of Endocrinology",
title = "Early Effects of Hyperbaric Oxygen on Inducible Nitric Oxide Synthase Activity/Expression in Lymphocytes of Type 1 Diabetes Patients: A Prospective Pilot Study",
volume = "2019",
pages = "1-12",
doi = "10.1155/2019/2328505"
}

Resanović, I., Gluvić, Z., Zarić, B., Sudar-Milovanović, E., Jovanović, A., Milačić, D., Isaković, R.,& Isenović, E. R.. (2019). Early Effects of Hyperbaric Oxygen on Inducible Nitric Oxide Synthase Activity/Expression in Lymphocytes of Type 1 Diabetes Patients: A Prospective Pilot Study. in International Journal of Endocrinology, 2019, 1-12.
https://doi.org/10.1155/2019/2328505

Resanović I, Gluvić Z, Zarić B, Sudar-Milovanović E, Jovanović A, Milačić D, Isaković R, Isenović ER. Early Effects of Hyperbaric Oxygen on Inducible Nitric Oxide Synthase Activity/Expression in Lymphocytes of Type 1 Diabetes Patients: A Prospective Pilot Study. in International Journal of Endocrinology. 2019;2019:1-12.
doi:10.1155/2019/2328505 .

Resanović, Ivana, Gluvić, Zoran, Zarić, Božidarka, Sudar-Milovanović, Emina, Jovanović, Aleksandra, Milačić, Davorka, Isaković, Radmilo, Isenović, Esma R., "Early Effects of Hyperbaric Oxygen on Inducible Nitric Oxide Synthase Activity/Expression in Lymphocytes of Type 1 Diabetes Patients: A Prospective Pilot Study" in International Journal of Endocrinology, 2019 (2019):1-12,
https://doi.org/10.1155/2019/2328505 . .

TY  - JOUR
AU  - Sudar, Emina
AU  - Zafirović, Sonja
AU  - Jovanović, Aleksandra
AU  - Trebaljevac, Jovana
AU  - Obradović, Milan M.
AU  - Cenić-Milošević, Desanka
AU  - Isenović, Esma R.
PY  - 2017
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1580
AB  - Background: Nitric oxide (NO) is a potential biochemical, cardio-metabolic risk marker. The production of NO is catalyzed by different isoforms of enzymes, NO synthases (NOS). An altered NO level is associated with obesity, insulin resistance (IR), diabetes and cardiovascular diseases (CVD). Activity of NOS and NO production are regulated by various hormones under physiological and pathophysiological condition. Methods: Data used for this review were obtained by searching the electronic database [PUBMED/MEDLINE 1984 - May 2016]. Additionally, abstracts from national and international diabetes and cardiovascular related meetings were searched. The main data search terms were: nitric oxide, nitric oxide synthase, cardio-metabolic risk, obesity, diabetes, cardiovascular disease, estradiol and insulin-like growth factor-1. Results: In this review, we summarize the recent literature data related to the regulation of endothelial NOS (eNOS), inducible (iNOS) activity/expression, and thereby NO production by the hormones: estradiol (E2), and insulin-like growth factor-1 (IGF-1). Conclusion: Understanding the regulation of NO production by different hormones such as E2, and IGF-1 may provide novel and useful knowledge regarding how endothelial dysfunction (ED) is linked with cardio-metabolic alterations and diseases.
T2  - Current Pharmaceutical Design
T1  - Hormonal Regulation of Nitric Oxide (NO) in Cardio-metabolic Diseases
VL  - 23
IS  - 10
SP  - 1427
EP  - 1434
DO  - 10.2174/1381612823666170124124855
ER  - 

@article{
author = "Sudar, Emina and Zafirović, Sonja and Jovanović, Aleksandra and Trebaljevac, Jovana and Obradović, Milan M. and Cenić-Milošević, Desanka and Isenović, Esma R.",
year = "2017",
abstract = "Background: Nitric oxide (NO) is a potential biochemical, cardio-metabolic risk marker. The production of NO is catalyzed by different isoforms of enzymes, NO synthases (NOS). An altered NO level is associated with obesity, insulin resistance (IR), diabetes and cardiovascular diseases (CVD). Activity of NOS and NO production are regulated by various hormones under physiological and pathophysiological condition. Methods: Data used for this review were obtained by searching the electronic database [PUBMED/MEDLINE 1984 - May 2016]. Additionally, abstracts from national and international diabetes and cardiovascular related meetings were searched. The main data search terms were: nitric oxide, nitric oxide synthase, cardio-metabolic risk, obesity, diabetes, cardiovascular disease, estradiol and insulin-like growth factor-1. Results: In this review, we summarize the recent literature data related to the regulation of endothelial NOS (eNOS), inducible (iNOS) activity/expression, and thereby NO production by the hormones: estradiol (E2), and insulin-like growth factor-1 (IGF-1). Conclusion: Understanding the regulation of NO production by different hormones such as E2, and IGF-1 may provide novel and useful knowledge regarding how endothelial dysfunction (ED) is linked with cardio-metabolic alterations and diseases.",
journal = "Current Pharmaceutical Design",
title = "Hormonal Regulation of Nitric Oxide (NO) in Cardio-metabolic Diseases",
volume = "23",
number = "10",
pages = "1427-1434",
doi = "10.2174/1381612823666170124124855"
}

Sudar, E., Zafirović, S., Jovanović, A., Trebaljevac, J., Obradović, M. M., Cenić-Milošević, D.,& Isenović, E. R.. (2017). Hormonal Regulation of Nitric Oxide (NO) in Cardio-metabolic Diseases. in Current Pharmaceutical Design, 23(10), 1427-1434.
https://doi.org/10.2174/1381612823666170124124855

Sudar E, Zafirović S, Jovanović A, Trebaljevac J, Obradović MM, Cenić-Milošević D, Isenović ER. Hormonal Regulation of Nitric Oxide (NO) in Cardio-metabolic Diseases. in Current Pharmaceutical Design. 2017;23(10):1427-1434.
doi:10.2174/1381612823666170124124855 .

Sudar, Emina, Zafirović, Sonja, Jovanović, Aleksandra, Trebaljevac, Jovana, Obradović, Milan M., Cenić-Milošević, Desanka, Isenović, Esma R., "Hormonal Regulation of Nitric Oxide (NO) in Cardio-metabolic Diseases" in Current Pharmaceutical Design, 23, no. 10 (2017):1427-1434,
https://doi.org/10.2174/1381612823666170124124855 . .

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

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

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

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

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

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

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

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

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

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

TY  - JOUR
AU  - Zafirović, Sonja
AU  - Obradović, Milan M.
AU  - Sudar-Milovanović, Emina
AU  - Jovanović, Aleksandra
AU  - Stanimirović, Julijana
AU  - Stewart, Alan J.
AU  - Pitt, Samantha J.
AU  - Isenović, Esma R.
PY  - 2017
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1520
AB  - The aim of this study was to investigate the in vivo effects of 17 beta-estradiol (E-2) on myocardial metabolism and inducible nitric oxide synthase (iNOS) expression/activity in obese rats. Male Wistar rats were fed with a normal or a high fat (HF) diet (42% fat) for 10 weeks. Half of the HF fed rats were treated with a single dose of E-2 while the other half were placebo-treated. 24 h after treatment animals were sacrificed. E-2 reduced cardiac free fatty acid (FFA) (p LT 0.05), L-arginine (p LT 0.01), iNOS mRNA (p LT 0.01), and protein (p LT 0.05) levels and translocation of the FFA transporter (CD36) (p LT 0.01) to the plasma membrane (PM) in HF fed rats. In contrast, Akt phosphorylation at Thr308 (p LT 0.05) and translocation of the glucose transporter GLUT4 (p LT 0.05) to the PM increased after E-2 treatment in HF rats. Our results indicate that E-2 acts via the PI3K/Akt signalling pathway to partially protect myocardial metabolism by attenuating the detrimental effects of increased iNOS expression/activity in HF fed rats. (C) 2017 Elsevier B.V. All rights reserved.
T2  - Molecular and Cellular Endocrinology
T1  - 17 beta-Estradiol protects against the effects of a high fat diet on cardiac glucose, lipid and nitric oxide metabolism in rats
VL  - 446
IS  - C
SP  - 12
EP  - 20
DO  - 10.1016/j.mce.2017.02.001
ER  - 

@article{
author = "Zafirović, Sonja and Obradović, Milan M. and Sudar-Milovanović, Emina and Jovanović, Aleksandra and Stanimirović, Julijana and Stewart, Alan J. and Pitt, Samantha J. and Isenović, Esma R.",
year = "2017",
abstract = "The aim of this study was to investigate the in vivo effects of 17 beta-estradiol (E-2) on myocardial metabolism and inducible nitric oxide synthase (iNOS) expression/activity in obese rats. Male Wistar rats were fed with a normal or a high fat (HF) diet (42% fat) for 10 weeks. Half of the HF fed rats were treated with a single dose of E-2 while the other half were placebo-treated. 24 h after treatment animals were sacrificed. E-2 reduced cardiac free fatty acid (FFA) (p LT 0.05), L-arginine (p LT 0.01), iNOS mRNA (p LT 0.01), and protein (p LT 0.05) levels and translocation of the FFA transporter (CD36) (p LT 0.01) to the plasma membrane (PM) in HF fed rats. In contrast, Akt phosphorylation at Thr308 (p LT 0.05) and translocation of the glucose transporter GLUT4 (p LT 0.05) to the PM increased after E-2 treatment in HF rats. Our results indicate that E-2 acts via the PI3K/Akt signalling pathway to partially protect myocardial metabolism by attenuating the detrimental effects of increased iNOS expression/activity in HF fed rats. (C) 2017 Elsevier B.V. All rights reserved.",
journal = "Molecular and Cellular Endocrinology",
title = "17 beta-Estradiol protects against the effects of a high fat diet on cardiac glucose, lipid and nitric oxide metabolism in rats",
volume = "446",
number = "C",
pages = "12-20",
doi = "10.1016/j.mce.2017.02.001"
}

Zafirović, S., Obradović, M. M., Sudar-Milovanović, E., Jovanović, A., Stanimirović, J., Stewart, A. J., Pitt, S. J.,& Isenović, E. R.. (2017). 17 beta-Estradiol protects against the effects of a high fat diet on cardiac glucose, lipid and nitric oxide metabolism in rats. in Molecular and Cellular Endocrinology, 446(C), 12-20.
https://doi.org/10.1016/j.mce.2017.02.001

Zafirović S, Obradović MM, Sudar-Milovanović E, Jovanović A, Stanimirović J, Stewart AJ, Pitt SJ, Isenović ER. 17 beta-Estradiol protects against the effects of a high fat diet on cardiac glucose, lipid and nitric oxide metabolism in rats. in Molecular and Cellular Endocrinology. 2017;446(C):12-20.
doi:10.1016/j.mce.2017.02.001 .

Zafirović, Sonja, Obradović, Milan M., Sudar-Milovanović, Emina, Jovanović, Aleksandra, Stanimirović, Julijana, Stewart, Alan J., Pitt, Samantha J., Isenović, Esma R., "17 beta-Estradiol protects against the effects of a high fat diet on cardiac glucose, lipid and nitric oxide metabolism in rats" in Molecular and Cellular Endocrinology, 446, no. C (2017):12-20,
https://doi.org/10.1016/j.mce.2017.02.001 . .

TY  - JOUR
AU  - Jovanović, Aleksandra
AU  - Obradović, Milan M.
AU  - Sudar-Milovanović, Emina
AU  - Stewart, Alan J.
AU  - Pitt, Samantha J.
AU  - Alavantić, Dragan
AU  - Aleksić, Ema
AU  - Isenović, Esma R.
PY  - 2017
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1812
AB  - The aim of this study was to investigate whether the presence of endogenous estradiol alters the effects of a high-fat (HF) diet on activity/expression of the cardiac Na+/K+-ATPase, via PI3K/IRS and RhoA/ROCK signalling cascades in female rats. For this study, female Wistar rats (8 weeks old, 150-200 g) were fed a standard diet or a HF diet (balanced diet for laboratory rats enriched with 42% fat) for 10 weeks. The results show that rats fed a HF diet exhibited a decrease in phosphorylation of the alpha(1) subunit of Na+/K+-ATPase by 30% (p LT 0.05), expression of total alpha(1) subunit of Na+/K+-ATPase by 31% (p LT 0.05), and association of IRS1 with p85 subunit of PI3K by 42% (p LT 0.05), while the levels of cardiac RhoA and ROCK2 were significantly increased by 84% (p LT 0.01) and 62% (p LT 0.05), respectively. Our results suggest that a HF diet alters cardiac Na+/K+-ATPase expression via molecular mechanisms involving RhoA/ROCK and IRS-1/PI3K signalling in female rats.
T2  - Molecular and Cellular Biochemistry
T1  - Changes in cardiac Na+/K+-ATPase expression and activity in female rats fed a high-fat diet
VL  - 436
IS  - 1-2
SP  - 49
EP  - 58
DO  - 10.1007/s11010-017-3077-y
ER  - 

@article{
author = "Jovanović, Aleksandra and Obradović, Milan M. and Sudar-Milovanović, Emina and Stewart, Alan J. and Pitt, Samantha J. and Alavantić, Dragan and Aleksić, Ema and Isenović, Esma R.",
year = "2017",
abstract = "The aim of this study was to investigate whether the presence of endogenous estradiol alters the effects of a high-fat (HF) diet on activity/expression of the cardiac Na+/K+-ATPase, via PI3K/IRS and RhoA/ROCK signalling cascades in female rats. For this study, female Wistar rats (8 weeks old, 150-200 g) were fed a standard diet or a HF diet (balanced diet for laboratory rats enriched with 42% fat) for 10 weeks. The results show that rats fed a HF diet exhibited a decrease in phosphorylation of the alpha(1) subunit of Na+/K+-ATPase by 30% (p LT 0.05), expression of total alpha(1) subunit of Na+/K+-ATPase by 31% (p LT 0.05), and association of IRS1 with p85 subunit of PI3K by 42% (p LT 0.05), while the levels of cardiac RhoA and ROCK2 were significantly increased by 84% (p LT 0.01) and 62% (p LT 0.05), respectively. Our results suggest that a HF diet alters cardiac Na+/K+-ATPase expression via molecular mechanisms involving RhoA/ROCK and IRS-1/PI3K signalling in female rats.",
journal = "Molecular and Cellular Biochemistry",
title = "Changes in cardiac Na+/K+-ATPase expression and activity in female rats fed a high-fat diet",
volume = "436",
number = "1-2",
pages = "49-58",
doi = "10.1007/s11010-017-3077-y"
}

Jovanović, A., Obradović, M. M., Sudar-Milovanović, E., Stewart, A. J., Pitt, S. J., Alavantić, D., Aleksić, E.,& Isenović, E. R.. (2017). Changes in cardiac Na+/K+-ATPase expression and activity in female rats fed a high-fat diet. in Molecular and Cellular Biochemistry, 436(1-2), 49-58.
https://doi.org/10.1007/s11010-017-3077-y

Jovanović A, Obradović MM, Sudar-Milovanović E, Stewart AJ, Pitt SJ, Alavantić D, Aleksić E, Isenović ER. Changes in cardiac Na+/K+-ATPase expression and activity in female rats fed a high-fat diet. in Molecular and Cellular Biochemistry. 2017;436(1-2):49-58.
doi:10.1007/s11010-017-3077-y .

Jovanović, Aleksandra, Obradović, Milan M., Sudar-Milovanović, Emina, Stewart, Alan J., Pitt, Samantha J., Alavantić, Dragan, Aleksić, Ema, Isenović, Esma R., "Changes in cardiac Na+/K+-ATPase expression and activity in female rats fed a high-fat diet" in Molecular and Cellular Biochemistry, 436, no. 1-2 (2017):49-58,
https://doi.org/10.1007/s11010-017-3077-y . .

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

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

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

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

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

TY  - JOUR
AU  - Stanimirović, Julijana
AU  - Obradović, Milan M.
AU  - Jovanović, Aleksandra
AU  - Sudar, Emina
AU  - Zafirović, Sonja
AU  - Pitt, Samantha J.
AU  - Stewart, Alan J.
AU  - Isenović, Esma R.
PY  - 2016
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1004
AB  - Men and women differ substantially with regard to the severity of insulin resistance (IR) but the underlying mechanism(s) of how this occurs is poorly characterized. We investigated whether a high fat (HF) diet resulted in sex-specific differences in nitrite/nitrate production and lipid metabolism and whether these variances may contribute to altered obesity-induced IR. Male and female Wistar rats were fed a standard laboratory diet or a HF diet for 10 weeks. The level of plasma nitrite/nitrate, as well as free fatty acid (FFA), in both plasma and liver lysates were assessed. The levels of inducible nitric oxide (NO) synthase (iNOS), p65 subunit of NF kappa B, total and phosphorylated forms of Akt, mTOR and PDK-1 in lysates, and the levels of glucose transporter 2 (Glut-2) and fatty acid translocase/cluster of differentiation 36 (FAT/CD36) in plasma membrane fractions of liver were assessed. HF-fed male rats exhibited a significant increase in plasma nitrite/nitrate, and hepatic FFA and FAT/CD36 levels compared with controls. They also displayed a relative decrease in iNOS and Glut-2 levels in the liver. Phosphorylation of Akt (at Ser(473) and Thr(308)), mTOR and PDK-1 was also reduced. HF-fed female rats exhibited increased levels of NF kappa B-p65 in liver compared with controls, while levels of Glut-2, FAT/CD36 and Akt phosphorylation at Thr(308) and PDK-1 were decreased. Our results reveal that altered lipid and glucose metabolism in obesity, lead to altered iNOS expression and nitrite/nitrate production. It is likely that this mechanism contributes to sex-specific differences in the development of IR. (C) 2016 Elsevier Inc. All rights reserved.
PB  - Elsevier
T2  - Nitric Oxide: Biology and Chemistry
T1  - A high fat diet induces sex-specific differences in hepatic lipid metabolism and nitrite/nitrate in rats
VL  - 54
SP  - 51
EP  - 59
DO  - 10.1016/j.niox.2016.02.007
ER  - 

@article{
author = "Stanimirović, Julijana and Obradović, Milan M. and Jovanović, Aleksandra and Sudar, Emina and Zafirović, Sonja and Pitt, Samantha J. and Stewart, Alan J. and Isenović, Esma R.",
year = "2016",
abstract = "Men and women differ substantially with regard to the severity of insulin resistance (IR) but the underlying mechanism(s) of how this occurs is poorly characterized. We investigated whether a high fat (HF) diet resulted in sex-specific differences in nitrite/nitrate production and lipid metabolism and whether these variances may contribute to altered obesity-induced IR. Male and female Wistar rats were fed a standard laboratory diet or a HF diet for 10 weeks. The level of plasma nitrite/nitrate, as well as free fatty acid (FFA), in both plasma and liver lysates were assessed. The levels of inducible nitric oxide (NO) synthase (iNOS), p65 subunit of NF kappa B, total and phosphorylated forms of Akt, mTOR and PDK-1 in lysates, and the levels of glucose transporter 2 (Glut-2) and fatty acid translocase/cluster of differentiation 36 (FAT/CD36) in plasma membrane fractions of liver were assessed. HF-fed male rats exhibited a significant increase in plasma nitrite/nitrate, and hepatic FFA and FAT/CD36 levels compared with controls. They also displayed a relative decrease in iNOS and Glut-2 levels in the liver. Phosphorylation of Akt (at Ser(473) and Thr(308)), mTOR and PDK-1 was also reduced. HF-fed female rats exhibited increased levels of NF kappa B-p65 in liver compared with controls, while levels of Glut-2, FAT/CD36 and Akt phosphorylation at Thr(308) and PDK-1 were decreased. Our results reveal that altered lipid and glucose metabolism in obesity, lead to altered iNOS expression and nitrite/nitrate production. It is likely that this mechanism contributes to sex-specific differences in the development of IR. (C) 2016 Elsevier Inc. All rights reserved.",
publisher = "Elsevier",
journal = "Nitric Oxide: Biology and Chemistry",
title = "A high fat diet induces sex-specific differences in hepatic lipid metabolism and nitrite/nitrate in rats",
volume = "54",
pages = "51-59",
doi = "10.1016/j.niox.2016.02.007"
}

Stanimirović, J., Obradović, M. M., Jovanović, A., Sudar, E., Zafirović, S., Pitt, S. J., Stewart, A. J.,& Isenović, E. R.. (2016). A high fat diet induces sex-specific differences in hepatic lipid metabolism and nitrite/nitrate in rats. in Nitric Oxide: Biology and Chemistry
Elsevier., 54, 51-59.
https://doi.org/10.1016/j.niox.2016.02.007

Stanimirović J, Obradović MM, Jovanović A, Sudar E, Zafirović S, Pitt SJ, Stewart AJ, Isenović ER. A high fat diet induces sex-specific differences in hepatic lipid metabolism and nitrite/nitrate in rats. in Nitric Oxide: Biology and Chemistry. 2016;54:51-59.
doi:10.1016/j.niox.2016.02.007 .

Stanimirović, Julijana, Obradović, Milan M., Jovanović, Aleksandra, Sudar, Emina, Zafirović, Sonja, Pitt, Samantha J., Stewart, Alan J., Isenović, Esma R., "A high fat diet induces sex-specific differences in hepatic lipid metabolism and nitrite/nitrate in rats" in Nitric Oxide: Biology and Chemistry, 54 (2016):51-59,
https://doi.org/10.1016/j.niox.2016.02.007 . .

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 . .

TY  - JOUR
AU  - Gluvić, Zoran
AU  - Sudar, Emina
AU  - Tica, Jelena
AU  - Jovanović, Aleksandra
AU  - Zafirović, Sonja
AU  - Tomasevic, Ratko
AU  - Isenović, Esma R.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/459
AB  - The aim of this study was to investigate the effect of levothyroxine (LT4) replacement therapy during three months on some parameters of metabolic syndrome and atherosclerosis in patients with increased thyroid-stimulating hormone (TSH) level. This study included a group of 30 female patients with TSH level GT 4mIU/L and 15 matched healthy controls. Intima media complex thickness (IMCT) and peak systolic flow velocity (PSFV) of superficial femoral artery were determined by Color Doppler scan. In hypothyroid subjects, BMI, SBP, DBP, and TSH were significantly increased versus controls and decreased after LT4 administration. FT4 was significantly lower in hypothyroid subjects compared with controls and significantly higher by treatment. TC, Tg, HDLC, and LDL-C were similar to controls at baseline but TC and LDL-C were significantly decreased by LH4 treatment. IMCT was significantly increased versus controls at baseline and significantly reduced by treatment. PSFV was similar to controls at baseline and significantly decreased on treatment. In this study, we have demonstrated the effects of LT4 replacement therapy during three months of treatment on correction of risk factors of metabolic syndrome and atherosclerosis.
T2  - International Journal of Endocrinology
T1  - Effects of Levothyroxine Replacement Therapy on Parameters of Metabolic Syndrome and Atherosclerosis in Hypothyroid Patients: A Prospective Pilot Study
DO  - 10.1155/2015/147070
ER  - 

@article{
author = "Gluvić, Zoran and Sudar, Emina and Tica, Jelena and Jovanović, Aleksandra and Zafirović, Sonja and Tomasevic, Ratko and Isenović, Esma R.",
year = "2015",
abstract = "The aim of this study was to investigate the effect of levothyroxine (LT4) replacement therapy during three months on some parameters of metabolic syndrome and atherosclerosis in patients with increased thyroid-stimulating hormone (TSH) level. This study included a group of 30 female patients with TSH level GT 4mIU/L and 15 matched healthy controls. Intima media complex thickness (IMCT) and peak systolic flow velocity (PSFV) of superficial femoral artery were determined by Color Doppler scan. In hypothyroid subjects, BMI, SBP, DBP, and TSH were significantly increased versus controls and decreased after LT4 administration. FT4 was significantly lower in hypothyroid subjects compared with controls and significantly higher by treatment. TC, Tg, HDLC, and LDL-C were similar to controls at baseline but TC and LDL-C were significantly decreased by LH4 treatment. IMCT was significantly increased versus controls at baseline and significantly reduced by treatment. PSFV was similar to controls at baseline and significantly decreased on treatment. In this study, we have demonstrated the effects of LT4 replacement therapy during three months of treatment on correction of risk factors of metabolic syndrome and atherosclerosis.",
journal = "International Journal of Endocrinology",
title = "Effects of Levothyroxine Replacement Therapy on Parameters of Metabolic Syndrome and Atherosclerosis in Hypothyroid Patients: A Prospective Pilot Study",
doi = "10.1155/2015/147070"
}

Gluvić, Z., Sudar, E., Tica, J., Jovanović, A., Zafirović, S., Tomasevic, R.,& Isenović, E. R.. (2015). Effects of Levothyroxine Replacement Therapy on Parameters of Metabolic Syndrome and Atherosclerosis in Hypothyroid Patients: A Prospective Pilot Study. in International Journal of Endocrinology.
https://doi.org/10.1155/2015/147070

Gluvić Z, Sudar E, Tica J, Jovanović A, Zafirović S, Tomasevic R, Isenović ER. Effects of Levothyroxine Replacement Therapy on Parameters of Metabolic Syndrome and Atherosclerosis in Hypothyroid Patients: A Prospective Pilot Study. in International Journal of Endocrinology. 2015;.
doi:10.1155/2015/147070 .

Gluvić, Zoran, Sudar, Emina, Tica, Jelena, Jovanović, Aleksandra, Zafirović, Sonja, Tomasevic, Ratko, Isenović, Esma R., "Effects of Levothyroxine Replacement Therapy on Parameters of Metabolic Syndrome and Atherosclerosis in Hypothyroid Patients: A Prospective Pilot Study" in International Journal of Endocrinology (2015),
https://doi.org/10.1155/2015/147070 . .

TY  - JOUR
AU  - Obradović, Milan M.
AU  - Zafirović, Sonja
AU  - Jovanović, Aleksandra
AU  - Sudar, Emina
AU  - Mousa, Shaker A.
AU  - Labudović-Borović, Milica
AU  - Isenović, Esma R.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/803
AB  - The aim of this study was to investigate in vivo effects of estradiol on Na+/K+-ATPase activity/expression in high fat (HF) diet fed rats. Adult male Wistar rats were fed normally (Control, n = 7) or with a HF diet (Obese, n = 14) for 10 weeks. After 10 weeks, half of the obese rats were treated with estradiol (Obese + Estradiol, n = 7, 40 mu g/kg, i.p.) as a bolus injection and 24 h after treatment all the rats were sacrificed. Estradiol in vivo in obese rats in comparison with obese non-treated rats led to a statistically significant increase in concentration of serum Na+ (p LT 0.05), Na+/K+-ATPase activity (p LT 0.01), expression of alpha 1 (p LT 0.01) and alpha 2 (p LT 0.05) subunit of Na+/K+-ATPase, both PI3K subunits p85 (p LT 0.01), p110 (p LT 0.05), and association of IRS-1 with p85 (p LT 0.05), while significantly decrease expression of AT1 (p LT 0.05) and Rho A (p LT 0.01) proteins. Our results suggest that estradiol in vivo in pathophysiological conditions, such as obesity accompanied with insulin resistance stimulates activity and expression of Na+/K+-ATPase by a mechanism that involves the participation of IRS-1/PI3K/Akt signaling. In addition, the decreasing level of AT1 and Rho A proteins estradiol probably attenuates the detrimental effect of obesity to decreased IRS-1/P13K association and consequently reduce Na+/K+-ATPase activity/expression. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
PB  - Elsevier
T2  - Molecular and Cellular Endocrinology
T1  - Effects of 17 beta-estradiol on cardiac Na+/K+-ATPase in high fat diet fed rats
VL  - 416
IS  - C
SP  - 46
EP  - 56
DO  - 10.1016/j.mce.2015.08.020
ER  - 

@article{
author = "Obradović, Milan M. and Zafirović, Sonja and Jovanović, Aleksandra and Sudar, Emina and Mousa, Shaker A. and Labudović-Borović, Milica and Isenović, Esma R.",
year = "2015",
abstract = "The aim of this study was to investigate in vivo effects of estradiol on Na+/K+-ATPase activity/expression in high fat (HF) diet fed rats. Adult male Wistar rats were fed normally (Control, n = 7) or with a HF diet (Obese, n = 14) for 10 weeks. After 10 weeks, half of the obese rats were treated with estradiol (Obese + Estradiol, n = 7, 40 mu g/kg, i.p.) as a bolus injection and 24 h after treatment all the rats were sacrificed. Estradiol in vivo in obese rats in comparison with obese non-treated rats led to a statistically significant increase in concentration of serum Na+ (p LT 0.05), Na+/K+-ATPase activity (p LT 0.01), expression of alpha 1 (p LT 0.01) and alpha 2 (p LT 0.05) subunit of Na+/K+-ATPase, both PI3K subunits p85 (p LT 0.01), p110 (p LT 0.05), and association of IRS-1 with p85 (p LT 0.05), while significantly decrease expression of AT1 (p LT 0.05) and Rho A (p LT 0.01) proteins. Our results suggest that estradiol in vivo in pathophysiological conditions, such as obesity accompanied with insulin resistance stimulates activity and expression of Na+/K+-ATPase by a mechanism that involves the participation of IRS-1/PI3K/Akt signaling. In addition, the decreasing level of AT1 and Rho A proteins estradiol probably attenuates the detrimental effect of obesity to decreased IRS-1/P13K association and consequently reduce Na+/K+-ATPase activity/expression. (C) 2015 Elsevier Ireland Ltd. All rights reserved.",
publisher = "Elsevier",
journal = "Molecular and Cellular Endocrinology",
title = "Effects of 17 beta-estradiol on cardiac Na+/K+-ATPase in high fat diet fed rats",
volume = "416",
number = "C",
pages = "46-56",
doi = "10.1016/j.mce.2015.08.020"
}

Obradović, M. M., Zafirović, S., Jovanović, A., Sudar, E., Mousa, S. A., Labudović-Borović, M.,& Isenović, E. R.. (2015). Effects of 17 beta-estradiol on cardiac Na+/K+-ATPase in high fat diet fed rats. in Molecular and Cellular Endocrinology
Elsevier., 416(C), 46-56.
https://doi.org/10.1016/j.mce.2015.08.020

Obradović MM, Zafirović S, Jovanović A, Sudar E, Mousa SA, Labudović-Borović M, Isenović ER. Effects of 17 beta-estradiol on cardiac Na+/K+-ATPase in high fat diet fed rats. in Molecular and Cellular Endocrinology. 2015;416(C):46-56.
doi:10.1016/j.mce.2015.08.020 .

Obradović, Milan M., Zafirović, Sonja, Jovanović, Aleksandra, Sudar, Emina, Mousa, Shaker A., Labudović-Borović, Milica, Isenović, Esma R., "Effects of 17 beta-estradiol on cardiac Na+/K+-ATPase in high fat diet fed rats" in Molecular and Cellular Endocrinology, 416, no. C (2015):46-56,
https://doi.org/10.1016/j.mce.2015.08.020 . .

TY  - JOUR
AU  - Obradović, Milan M.
AU  - Trpković, Andreja
AU  - Bajić, Vladan P.
AU  - Soskić, Sanja S.
AU  - Jovanović, Aleksandra
AU  - Stanimirović, Julijana
AU  - Panic, Milos
AU  - Isenović, Esma R.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/281
AB  - C-reactive protein (CRP) is a marker of inflammation. Atherosclerosis is now recognized as inflammatory disease, and it seems that CRP directly contributes to atherogenesis. Oxidation of low-density lipoprotein (LDL) molecule increases the uptake of lipid products by macrophages leading to cholesterol accumulation and subsequent foam cell formation. The elevated levels of high sensitivity CRP (hsCRP) and oxidized LDL (OxLDL) in the blood were found to be associated with cardiovascular diseases (CVD). In this review, we highlighted the evidence that CRP and OxLDL are involved in interrelated (patho) physiological pathways. The findings on association between hsCRP and OxLDL in the clinical setting will be also summarized.
T2  - Clinical Chemistry and Laboratory Medicine
T1  - Interrelatedness between C-reactive protein and oxidized low-density lipoprotein
VL  - 53
IS  - 1
SP  - 29
EP  - 34
DO  - 10.1515/cclm-2014-0590
ER  - 

@article{
author = "Obradović, Milan M. and Trpković, Andreja and Bajić, Vladan P. and Soskić, Sanja S. and Jovanović, Aleksandra and Stanimirović, Julijana and Panic, Milos and Isenović, Esma R.",
year = "2015",
abstract = "C-reactive protein (CRP) is a marker of inflammation. Atherosclerosis is now recognized as inflammatory disease, and it seems that CRP directly contributes to atherogenesis. Oxidation of low-density lipoprotein (LDL) molecule increases the uptake of lipid products by macrophages leading to cholesterol accumulation and subsequent foam cell formation. The elevated levels of high sensitivity CRP (hsCRP) and oxidized LDL (OxLDL) in the blood were found to be associated with cardiovascular diseases (CVD). In this review, we highlighted the evidence that CRP and OxLDL are involved in interrelated (patho) physiological pathways. The findings on association between hsCRP and OxLDL in the clinical setting will be also summarized.",
journal = "Clinical Chemistry and Laboratory Medicine",
title = "Interrelatedness between C-reactive protein and oxidized low-density lipoprotein",
volume = "53",
number = "1",
pages = "29-34",
doi = "10.1515/cclm-2014-0590"
}

Obradović, M. M., Trpković, A., Bajić, V. P., Soskić, S. S., Jovanović, A., Stanimirović, J., Panic, M.,& Isenović, E. R.. (2015). Interrelatedness between C-reactive protein and oxidized low-density lipoprotein. in Clinical Chemistry and Laboratory Medicine, 53(1), 29-34.
https://doi.org/10.1515/cclm-2014-0590

Obradović MM, Trpković A, Bajić VP, Soskić SS, Jovanović A, Stanimirović J, Panic M, Isenović ER. Interrelatedness between C-reactive protein and oxidized low-density lipoprotein. in Clinical Chemistry and Laboratory Medicine. 2015;53(1):29-34.
doi:10.1515/cclm-2014-0590 .

Obradović, Milan M., Trpković, Andreja, Bajić, Vladan P., Soskić, Sanja S., Jovanović, Aleksandra, Stanimirović, Julijana, Panic, Milos, Isenović, Esma R., "Interrelatedness between C-reactive protein and oxidized low-density lipoprotein" in Clinical Chemistry and Laboratory Medicine, 53, no. 1 (2015):29-34,
https://doi.org/10.1515/cclm-2014-0590 . .

TY  - JOUR
AU  - Sudar, Emina
AU  - Jovanović, Aleksandra
AU  - Misirkić-Marjanović, Maja
AU  - Vučićević, Ljubica
AU  - Janjetović, Kristina D.
AU  - Isenović, Esma R.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/832
AB  - The aim of this study was to examine the effects of ghrelin on regulation of cardiac inducible nitric oxide synthase (iNOS) activity/expression in high fat (HF), obese rats. For this study, male Wistar rats fed with HF diet (30 % fat) for 4 weeks were injected every 24 h for 5 days intracerebroventriculary (ICV) with ghrelin (0.3 nmol/5 mu l) or with an equal volume of phosphate buffered saline (PBS). Control rats were ICV injected with an equal volume of PBS. Glucose, insulin and nitric oxide (NO) concentrations were measured in serum, while arginase activity and citrulline concentrations were measured in heart lysate. Protein iNOS and regulatory subunit of nuclear factor-kappa B (NF kappa B-p65), phosphorylation of enzymes protein kinase B (Akt) at Ser(473), and extracellular signal-regulated kinases 1/2 (ERK1/2) at Tyr(202)/Tyr(204) were determined in heart lysate by Western blot. For gene expression of iNOS qRT-PCR was used. Results show significantly (p LT 0.01) higher serum NO production in ghrelin treated HF rats compared with HF rats. Ghrelin significantly reduced citrulline concentration (p LT 0.05) and arginase activity (p LT 0.01) in HF rats. In ghrelin treated HF rats, gene and protein expression of iNOS and NF kappa B-p65 levels were significantly (p LT 0.05) increased compared with HF rats. Increased phosphorylation of Akt (p LT 0.01) and decreased (p LT 0.05) ERK1/2 phosphorylation were detected in HF ghrelin treated rats compared with HF rats hearts. Results from this study indicate that exogenous ghrelin induces expression and activity of cardiac iNOS via Akt phosphorylation followed by NF kappa B activation in HF rats.
PB  - Georg Thieme Verlag KG
T2  - Experimental and Clinical Endocrinology and Diabetes
T1  - Effects of Intracerebroventricularly (ICV) Injected Ghrelin on Cardiac Inducible Nitric Oxide Synthase Activity/Expression in Obese Rats
VL  - 123
IS  - 10
SP  - 581
EP  - 588
DO  - 10.1055/s-0035-1559758
ER  - 

@article{
author = "Sudar, Emina and Jovanović, Aleksandra and Misirkić-Marjanović, Maja and Vučićević, Ljubica and Janjetović, Kristina D. and Isenović, Esma R.",
year = "2015",
abstract = "The aim of this study was to examine the effects of ghrelin on regulation of cardiac inducible nitric oxide synthase (iNOS) activity/expression in high fat (HF), obese rats. For this study, male Wistar rats fed with HF diet (30 % fat) for 4 weeks were injected every 24 h for 5 days intracerebroventriculary (ICV) with ghrelin (0.3 nmol/5 mu l) or with an equal volume of phosphate buffered saline (PBS). Control rats were ICV injected with an equal volume of PBS. Glucose, insulin and nitric oxide (NO) concentrations were measured in serum, while arginase activity and citrulline concentrations were measured in heart lysate. Protein iNOS and regulatory subunit of nuclear factor-kappa B (NF kappa B-p65), phosphorylation of enzymes protein kinase B (Akt) at Ser(473), and extracellular signal-regulated kinases 1/2 (ERK1/2) at Tyr(202)/Tyr(204) were determined in heart lysate by Western blot. For gene expression of iNOS qRT-PCR was used. Results show significantly (p LT 0.01) higher serum NO production in ghrelin treated HF rats compared with HF rats. Ghrelin significantly reduced citrulline concentration (p LT 0.05) and arginase activity (p LT 0.01) in HF rats. In ghrelin treated HF rats, gene and protein expression of iNOS and NF kappa B-p65 levels were significantly (p LT 0.05) increased compared with HF rats. Increased phosphorylation of Akt (p LT 0.01) and decreased (p LT 0.05) ERK1/2 phosphorylation were detected in HF ghrelin treated rats compared with HF rats hearts. Results from this study indicate that exogenous ghrelin induces expression and activity of cardiac iNOS via Akt phosphorylation followed by NF kappa B activation in HF rats.",
publisher = "Georg Thieme Verlag KG",
journal = "Experimental and Clinical Endocrinology and Diabetes",
title = "Effects of Intracerebroventricularly (ICV) Injected Ghrelin on Cardiac Inducible Nitric Oxide Synthase Activity/Expression in Obese Rats",
volume = "123",
number = "10",
pages = "581-588",
doi = "10.1055/s-0035-1559758"
}

Sudar, E., Jovanović, A., Misirkić-Marjanović, M., Vučićević, L., Janjetović, K. D.,& Isenović, E. R.. (2015). Effects of Intracerebroventricularly (ICV) Injected Ghrelin on Cardiac Inducible Nitric Oxide Synthase Activity/Expression in Obese Rats. in Experimental and Clinical Endocrinology and Diabetes
Georg Thieme Verlag KG., 123(10), 581-588.
https://doi.org/10.1055/s-0035-1559758

Sudar E, Jovanović A, Misirkić-Marjanović M, Vučićević L, Janjetović KD, Isenović ER. Effects of Intracerebroventricularly (ICV) Injected Ghrelin on Cardiac Inducible Nitric Oxide Synthase Activity/Expression in Obese Rats. in Experimental and Clinical Endocrinology and Diabetes. 2015;123(10):581-588.
doi:10.1055/s-0035-1559758 .

Sudar, Emina, Jovanović, Aleksandra, Misirkić-Marjanović, Maja, Vučićević, Ljubica, Janjetović, Kristina D., Isenović, Esma R., "Effects of Intracerebroventricularly (ICV) Injected Ghrelin on Cardiac Inducible Nitric Oxide Synthase Activity/Expression in Obese Rats" in Experimental and Clinical Endocrinology and Diabetes, 123, no. 10 (2015):581-588,
https://doi.org/10.1055/s-0035-1559758 . .

TY  - JOUR
AU  - Smiljanić, Katarina
AU  - Obradović, Milan M.
AU  - Jovanović, Aleksandra
AU  - Đorđević, Jelena D.
AU  - Dobutović, Branislava
AU  - Jevremovic, Danimir
AU  - Marche, Pierre
AU  - Isenović, Esma R.
PY  - 2014
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/134
AB  - In this study, the role of epidermal growth factor receptor (EGFR), extracellular signal-regulated kinase (ERK1/2), heparin-binding EGF-like growth factor (HB-EGF), general metalloproteinases, matrix metalloproteinases-2 (MMP-2) in mediating the mitogenic action of thrombin in rat vascular smooth muscle cells (VSMC) was investigated. The incubation of rat VSMC with thrombin (1 U/ml) for 5 min resulted in significant (p LT 0.001) increase of ERK1/2 phosphorylation by 8.7 +/- A 0.9-fold, EGFR phosphorylation by 8.5 +/- A 1.3-fold (p LT 0.001) and DNA synthesis by 3.6 +/- A 0.4-fold (p LT 0.001). Separate 30-min pretreatments with EGFR tyrosine kinase irreversible inhibitor, 10 A mu M PD169540 (PD), and 20 A mu M anti-HB-EGF antibody significantly reduced thrombin-stimulated EGFR and ERK1/2 phosphorylation by 81, 72 % and by 48 and 61 %, respectively. Furthermore, the same pretreatments with PD or anti-HB-EGF antibody reduced thrombin-induced VSMC proliferation by 44 and 45 %, respectively. In addition, 30-min pretreatments with 10 A mu M specific MMP-2 inhibitor significantly reduced thrombin-stimulated phosphorylation of both EGFR and ERK1/2 by 25 %. Moreover, the same pretreatment with MMP-2 inhibitor reduced thrombin-induced VSMC proliferation by 45 %. These results show that the thrombin-induced DNA synthesis correlates with the level of ERK1/2 activation rather than EGFR activation. These results further suggest that thrombin acts through EGFR and ERK 1/2 signaling pathways involving MMP-2 to upregulate proliferation of VSMC.
T2  - Molecular and Cellular Biochemistry
T1  - Thrombin stimulates VSMC proliferation through an EGFR-dependent pathway: involvement of MMP-2
VL  - 396
IS  - 1-2
SP  - 147
EP  - 160
DO  - 10.1007/s11010-014-2151-y
ER  - 

@article{
author = "Smiljanić, Katarina and Obradović, Milan M. and Jovanović, Aleksandra and Đorđević, Jelena D. and Dobutović, Branislava and Jevremovic, Danimir and Marche, Pierre and Isenović, Esma R.",
year = "2014",
abstract = "In this study, the role of epidermal growth factor receptor (EGFR), extracellular signal-regulated kinase (ERK1/2), heparin-binding EGF-like growth factor (HB-EGF), general metalloproteinases, matrix metalloproteinases-2 (MMP-2) in mediating the mitogenic action of thrombin in rat vascular smooth muscle cells (VSMC) was investigated. The incubation of rat VSMC with thrombin (1 U/ml) for 5 min resulted in significant (p LT 0.001) increase of ERK1/2 phosphorylation by 8.7 +/- A 0.9-fold, EGFR phosphorylation by 8.5 +/- A 1.3-fold (p LT 0.001) and DNA synthesis by 3.6 +/- A 0.4-fold (p LT 0.001). Separate 30-min pretreatments with EGFR tyrosine kinase irreversible inhibitor, 10 A mu M PD169540 (PD), and 20 A mu M anti-HB-EGF antibody significantly reduced thrombin-stimulated EGFR and ERK1/2 phosphorylation by 81, 72 % and by 48 and 61 %, respectively. Furthermore, the same pretreatments with PD or anti-HB-EGF antibody reduced thrombin-induced VSMC proliferation by 44 and 45 %, respectively. In addition, 30-min pretreatments with 10 A mu M specific MMP-2 inhibitor significantly reduced thrombin-stimulated phosphorylation of both EGFR and ERK1/2 by 25 %. Moreover, the same pretreatment with MMP-2 inhibitor reduced thrombin-induced VSMC proliferation by 45 %. These results show that the thrombin-induced DNA synthesis correlates with the level of ERK1/2 activation rather than EGFR activation. These results further suggest that thrombin acts through EGFR and ERK 1/2 signaling pathways involving MMP-2 to upregulate proliferation of VSMC.",
journal = "Molecular and Cellular Biochemistry",
title = "Thrombin stimulates VSMC proliferation through an EGFR-dependent pathway: involvement of MMP-2",
volume = "396",
number = "1-2",
pages = "147-160",
doi = "10.1007/s11010-014-2151-y"
}

Smiljanić, K., Obradović, M. M., Jovanović, A., Đorđević, J. D., Dobutović, B., Jevremovic, D., Marche, P.,& Isenović, E. R.. (2014). Thrombin stimulates VSMC proliferation through an EGFR-dependent pathway: involvement of MMP-2. in Molecular and Cellular Biochemistry, 396(1-2), 147-160.
https://doi.org/10.1007/s11010-014-2151-y

Smiljanić K, Obradović MM, Jovanović A, Đorđević JD, Dobutović B, Jevremovic D, Marche P, Isenović ER. Thrombin stimulates VSMC proliferation through an EGFR-dependent pathway: involvement of MMP-2. in Molecular and Cellular Biochemistry. 2014;396(1-2):147-160.
doi:10.1007/s11010-014-2151-y .

Smiljanić, Katarina, Obradović, Milan M., Jovanović, Aleksandra, Đorđević, Jelena D., Dobutović, Branislava, Jevremovic, Danimir, Marche, Pierre, Isenović, Esma R., "Thrombin stimulates VSMC proliferation through an EGFR-dependent pathway: involvement of MMP-2" in Molecular and Cellular Biochemistry, 396, no. 1-2 (2014):147-160,
https://doi.org/10.1007/s11010-014-2151-y . .

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  - Sudar, Emina
AU  - Zafirović, Sonja
AU  - Obradović, Milan M.
AU  - Soskić, Sanja S.
AU  - Jovanović, Aleksandra
AU  - Stokić, Edita
AU  - Gluvić, Zoran
AU  - Isenović, Esma R.
PY  - 2012
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10322
AB  - Gojaznost se definiše kao prekomerno prisustvo masnog tkiva u organizmu koje može dovesti do mnogih zdravstvenih komplikacija koje pogoršavaju kvalitet života i skraćuju životni vek. Gojaznost je rezultat fizioloških odgovora organizma u situaciji kada je kalorijski unos veći od stvarnih energetskih potreba organizma u dužem vremenskom periodu, bez adekvatnog utroška energije. Prema podacima Svetske zdravstvene organizacije (WHO) gojaznost zauzima peto mesto u paleti vodećih uzroka smrti na globalnom nivou i može se definisati kao hroničan poremećaj metabolizma koji je udružen sa kardiovaskularnim oboljenjima (CVD) kao i sa povećanom stopom morbiditeta i mortaliteta. Danas je prihvaćeno mišljenje da je gojaznost usko povezana sa razvojem rezistencije na insulin (IR). Metaboličke i hormonske promene, koje su posledica pre svega visceralne gojaznosti karakteristične za metabolički sindrom, dovode vremenom do pojave IR u adipoznom tkivu, jetri i mišićnom tkivu. Pretpostavlja se da IR koja se javlja usled gojaznosti predstavlja prvi korak u razvoju CVD. Delimično, IR povećava rizik za nastanak nekih CVD zbog hipertenzije i dislipidemije, kao i promena u adipocitokinima, koje vode inflamaciji krvnih sudova. Osim toga, gojaznost nepovoljno utiče kako na hemodinamiku, tako i na strukturu i funkciju kardiovaskularnog sistema (CVS). Kardiovaskularne komplikacije koje su povezane sa gojaznošću doprinose visokoj stopi morbiditeta i mortaliteta. Usled porasta broja gojaznih osoba, kao i prisustva IR i CVD kod ovih osoba, izučavanje masnog tkiva i njegovog uticaja na razvoj različitih patofizioloških stanja kao što su IR i CVD predstavljaju veoma važno polje biomedicinskih istraživanja, rezultati kojih bi zasigurno omogućili nove terapeutske pristupe u lečenju ovih poremećaja. Takođe, u cilju sprečavanja razvoja gojaznosti, a samim tim i oboljenja koja nastaju kao posledica ovog poremećaja, veoma veliki značaj imaju prevencija i edukacija o mogućim aspektima koje prekomerna akumulacija masnog tkiva može imati na normalno funkcionisanje organizma.
AB  - Obesity is defined as abnormal or excessive fat tissue accumulation that may impair health and well-being and also increases death risk. Obesity occurs as a result of physiological responses of the organism in situations when the caloric intake is greater than energy expenditure/ consumption over an extended period of time, resulting in energy conservation. According to the World Health Organization (WHO) overweight and obesity are the fifth of the leading risk factors for global deaths and they could be defined as a chronic metabolic disorder associated with cardiovascular diseases (CVD) and increased risk of morbidity and mortality. Today, it is accepted that obesity is closely related to insulin resistance (IR). Metabolic and hormonal changes occurring first of all with increased visceral obesity which is a characteristic of metabolic syndrome, lead to IR development in adipose, liver and muscle tissue. It is assumed that IR, which occurs due to obesity, represents the first step in CVD development. Partly, IR increases the risk for CVD development due to the presence of multiple risk factors as hypertension and dyslipidemia, and changes in adipocytokines lead to blood vessel inflammation. Besides that, obesity adversely affects hemodynamic, structure and function of cardiovascular system (CVS). Cardiovascular complications associated with obesity greatly contribute to increased risk of morbidity and mortality. Due to the rising number of obese patients and also presence of IR and CVD in these patients, the study of adipose tissue and its effects on the development of various pathophysiological states as IR and CVD represents a very important area of biomedical research which would lead to new therapeutic approaches in these conditions. Also, in order to prevent obesity development and associated disorders, prevention and education are of great importance.
T2  - Medicinska istraživanja
T1  - Gojaznost, rezistencija na insulin i kardiovaskularna oboljenja
T1  - Obesity, insulin resistance and cardiovascular disease
VL  - 46
IS  - 2
SP  - 54
EP  - 59
UR  - https://hdl.handle.net/21.15107/rcub_vinar_10322
ER  - 

@article{
author = "Sudar, Emina and Zafirović, Sonja and Obradović, Milan M. and Soskić, Sanja S. and Jovanović, Aleksandra and Stokić, Edita and Gluvić, Zoran and Isenović, Esma R.",
year = "2012",
abstract = "Gojaznost se definiše kao prekomerno prisustvo masnog tkiva u organizmu koje može dovesti do mnogih zdravstvenih komplikacija koje pogoršavaju kvalitet života i skraćuju životni vek. Gojaznost je rezultat fizioloških odgovora organizma u situaciji kada je kalorijski unos veći od stvarnih energetskih potreba organizma u dužem vremenskom periodu, bez adekvatnog utroška energije. Prema podacima Svetske zdravstvene organizacije (WHO) gojaznost zauzima peto mesto u paleti vodećih uzroka smrti na globalnom nivou i može se definisati kao hroničan poremećaj metabolizma koji je udružen sa kardiovaskularnim oboljenjima (CVD) kao i sa povećanom stopom morbiditeta i mortaliteta. Danas je prihvaćeno mišljenje da je gojaznost usko povezana sa razvojem rezistencije na insulin (IR). Metaboličke i hormonske promene, koje su posledica pre svega visceralne gojaznosti karakteristične za metabolički sindrom, dovode vremenom do pojave IR u adipoznom tkivu, jetri i mišićnom tkivu. Pretpostavlja se da IR koja se javlja usled gojaznosti predstavlja prvi korak u razvoju CVD. Delimično, IR povećava rizik za nastanak nekih CVD zbog hipertenzije i dislipidemije, kao i promena u adipocitokinima, koje vode inflamaciji krvnih sudova. Osim toga, gojaznost nepovoljno utiče kako na hemodinamiku, tako i na strukturu i funkciju kardiovaskularnog sistema (CVS). Kardiovaskularne komplikacije koje su povezane sa gojaznošću doprinose visokoj stopi morbiditeta i mortaliteta. Usled porasta broja gojaznih osoba, kao i prisustva IR i CVD kod ovih osoba, izučavanje masnog tkiva i njegovog uticaja na razvoj različitih patofizioloških stanja kao što su IR i CVD predstavljaju veoma važno polje biomedicinskih istraživanja, rezultati kojih bi zasigurno omogućili nove terapeutske pristupe u lečenju ovih poremećaja. Takođe, u cilju sprečavanja razvoja gojaznosti, a samim tim i oboljenja koja nastaju kao posledica ovog poremećaja, veoma veliki značaj imaju prevencija i edukacija o mogućim aspektima koje prekomerna akumulacija masnog tkiva može imati na normalno funkcionisanje organizma., Obesity is defined as abnormal or excessive fat tissue accumulation that may impair health and well-being and also increases death risk. Obesity occurs as a result of physiological responses of the organism in situations when the caloric intake is greater than energy expenditure/ consumption over an extended period of time, resulting in energy conservation. According to the World Health Organization (WHO) overweight and obesity are the fifth of the leading risk factors for global deaths and they could be defined as a chronic metabolic disorder associated with cardiovascular diseases (CVD) and increased risk of morbidity and mortality. Today, it is accepted that obesity is closely related to insulin resistance (IR). Metabolic and hormonal changes occurring first of all with increased visceral obesity which is a characteristic of metabolic syndrome, lead to IR development in adipose, liver and muscle tissue. It is assumed that IR, which occurs due to obesity, represents the first step in CVD development. Partly, IR increases the risk for CVD development due to the presence of multiple risk factors as hypertension and dyslipidemia, and changes in adipocytokines lead to blood vessel inflammation. Besides that, obesity adversely affects hemodynamic, structure and function of cardiovascular system (CVS). Cardiovascular complications associated with obesity greatly contribute to increased risk of morbidity and mortality. Due to the rising number of obese patients and also presence of IR and CVD in these patients, the study of adipose tissue and its effects on the development of various pathophysiological states as IR and CVD represents a very important area of biomedical research which would lead to new therapeutic approaches in these conditions. Also, in order to prevent obesity development and associated disorders, prevention and education are of great importance.",
journal = "Medicinska istraživanja",
title = "Gojaznost, rezistencija na insulin i kardiovaskularna oboljenja, Obesity, insulin resistance and cardiovascular disease",
volume = "46",
number = "2",
pages = "54-59",
url = "https://hdl.handle.net/21.15107/rcub_vinar_10322"
}

Sudar, E., Zafirović, S., Obradović, M. M., Soskić, S. S., Jovanović, A., Stokić, E., Gluvić, Z.,& Isenović, E. R.. (2012). Gojaznost, rezistencija na insulin i kardiovaskularna oboljenja. in Medicinska istraživanja, 46(2), 54-59.
https://hdl.handle.net/21.15107/rcub_vinar_10322

Sudar E, Zafirović S, Obradović MM, Soskić SS, Jovanović A, Stokić E, Gluvić Z, Isenović ER. Gojaznost, rezistencija na insulin i kardiovaskularna oboljenja. in Medicinska istraživanja. 2012;46(2):54-59.
https://hdl.handle.net/21.15107/rcub_vinar_10322 .

Sudar, Emina, Zafirović, Sonja, Obradović, Milan M., Soskić, Sanja S., Jovanović, Aleksandra, Stokić, Edita, Gluvić, Zoran, Isenović, Esma R., "Gojaznost, rezistencija na insulin i kardiovaskularna oboljenja" in Medicinska istraživanja, 46, no. 2 (2012):54-59,
https://hdl.handle.net/21.15107/rcub_vinar_10322 .