TY  - CONF
AU  - Martinović, Tamara
AU  - Ćirić, Darko
AU  - Pantić, Igor
AU  - Lalić, Katarina
AU  - Rasulić, Iva
AU  - Despotović, Sanja
AU  - Lalić, Ivana
AU  - Đuričić, Danica
AU  - Vučićević, Ljubica
AU  - Misirkić Marjanović, Maja
AU  - Trajković, Vladimir
AU  - Bumbaširević, Vladimir
AU  - Kravić-Stevović, Tamara
PY  - 2019
UR  - https://klinbiolabmed.rs/wp-content/uploads/2022/05/Knjiga-sazetka-Kongresa.pdf
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6662
AB  - Uvod: Osobine tip 2 dijabetes melitusa (T2DM) su insulinska rezistencija, poremećena sekrecija insulina i hiperglikemija. Kao početna terapija T2DM koristi se metformin. Novija istraživanja su pokazala da u T2DM dolazi do morfoloških promena u izgledu nukleusa u vidu nepravilnosti oblika i binukelacije nukleusa.
Cilj: Cilj istraživanja je da se analiziraju ultrastrukturne karakteristike nukleusa limfocita periferne krvi kod pacijenata sa T2DM pomoću kompjuterizovane analize slike, fraktalne i teksturalne analize, kao i utvrđivanje efekta metformina na karakteristike nukleusa.
Metodologija: Mononuklearne ćelije izolovane iz periferne krvi novootkrivenih T2DM bolesnika, bolesnika lečenih metforminom i zdravih ispitanika analizirane su na transmisionom elektronskom mikroskopu (TEM). Primenom ImageJ programa analizirani su oblik i procenat heterohromatina, kao i fraktalna i teksturalna analiza nukleusa limfocita.
Rezultati: Limfociti zdravih osoba su imali okrugle, predominantno heterohromatične nukleuse i malu količinu citoplazme sa retko prisutnim organelama, dok su limfociti T2DM bolesnika imali euhromatične nukleu uz povećanje strukturnih praznina kod T2DM bolesnika. Nivo glukoze našte i HbA1c koreliraju sa fraktalnom dimenzijom i sa parametrima oblika nukleusa. Postoji korelacija između nivoa triglicerida u krvi i fraktalne dimenzije nukleusa.
Zaključak: Nukleusi limfocita bolesnika sa T2DM su nepravilnog oblika i sa većom količinom euhromatina, a promena njihovog izgleda je u vezi sa nivoom glikemije.
PB  - Beograd: Srpsko lekarsko društvo, Sekcija kliničke biohemije
C3  - Knjiga sažetaka: 1. kongres kliničkih biohemičara i specijalista laboratorijske medicine Srbije sa međunarodnim učešćem;  2019 Nov 27-29; Belgrade, Serbia
T1  - Uticaj glikemije i lipidnog statusa na morfološke karakteristike nukleusa kod pacijenata sa tip 2 dijabetes melitusom
SP  - 58
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_6662
ER  - 

@conference{
author = "Martinović, Tamara and Ćirić, Darko and Pantić, Igor and Lalić, Katarina and Rasulić, Iva and Despotović, Sanja and Lalić, Ivana and Đuričić, Danica and Vučićević, Ljubica and Misirkić Marjanović, Maja and Trajković, Vladimir and Bumbaširević, Vladimir and Kravić-Stevović, Tamara",
year = "2019",
abstract = "Uvod: Osobine tip 2 dijabetes melitusa (T2DM) su insulinska rezistencija, poremećena sekrecija insulina i hiperglikemija. Kao početna terapija T2DM koristi se metformin. Novija istraživanja su pokazala da u T2DM dolazi do morfoloških promena u izgledu nukleusa u vidu nepravilnosti oblika i binukelacije nukleusa.
Cilj: Cilj istraživanja je da se analiziraju ultrastrukturne karakteristike nukleusa limfocita periferne krvi kod pacijenata sa T2DM pomoću kompjuterizovane analize slike, fraktalne i teksturalne analize, kao i utvrđivanje efekta metformina na karakteristike nukleusa.
Metodologija: Mononuklearne ćelije izolovane iz periferne krvi novootkrivenih T2DM bolesnika, bolesnika lečenih metforminom i zdravih ispitanika analizirane su na transmisionom elektronskom mikroskopu (TEM). Primenom ImageJ programa analizirani su oblik i procenat heterohromatina, kao i fraktalna i teksturalna analiza nukleusa limfocita.
Rezultati: Limfociti zdravih osoba su imali okrugle, predominantno heterohromatične nukleuse i malu količinu citoplazme sa retko prisutnim organelama, dok su limfociti T2DM bolesnika imali euhromatične nukleu uz povećanje strukturnih praznina kod T2DM bolesnika. Nivo glukoze našte i HbA1c koreliraju sa fraktalnom dimenzijom i sa parametrima oblika nukleusa. Postoji korelacija između nivoa triglicerida u krvi i fraktalne dimenzije nukleusa.
Zaključak: Nukleusi limfocita bolesnika sa T2DM su nepravilnog oblika i sa većom količinom euhromatina, a promena njihovog izgleda je u vezi sa nivoom glikemije.",
publisher = "Beograd: Srpsko lekarsko društvo, Sekcija kliničke biohemije",
journal = "Knjiga sažetaka: 1. kongres kliničkih biohemičara i specijalista laboratorijske medicine Srbije sa međunarodnim učešćem;  2019 Nov 27-29; Belgrade, Serbia",
title = "Uticaj glikemije i lipidnog statusa na morfološke karakteristike nukleusa kod pacijenata sa tip 2 dijabetes melitusom",
pages = "58",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_6662"
}

Martinović, T., Ćirić, D., Pantić, I., Lalić, K., Rasulić, I., Despotović, S., Lalić, I., Đuričić, D., Vučićević, L., Misirkić Marjanović, M., Trajković, V., Bumbaširević, V.,& Kravić-Stevović, T.. (2019). Uticaj glikemije i lipidnog statusa na morfološke karakteristike nukleusa kod pacijenata sa tip 2 dijabetes melitusom. in Knjiga sažetaka: 1. kongres kliničkih biohemičara i specijalista laboratorijske medicine Srbije sa međunarodnim učešćem;  2019 Nov 27-29; Belgrade, Serbia
Beograd: Srpsko lekarsko društvo, Sekcija kliničke biohemije., 58.
https://hdl.handle.net/21.15107/rcub_ibiss_6662

Martinović T, Ćirić D, Pantić I, Lalić K, Rasulić I, Despotović S, Lalić I, Đuričić D, Vučićević L, Misirkić Marjanović M, Trajković V, Bumbaširević V, Kravić-Stevović T. Uticaj glikemije i lipidnog statusa na morfološke karakteristike nukleusa kod pacijenata sa tip 2 dijabetes melitusom. in Knjiga sažetaka: 1. kongres kliničkih biohemičara i specijalista laboratorijske medicine Srbije sa međunarodnim učešćem;  2019 Nov 27-29; Belgrade, Serbia. 2019;:58.
https://hdl.handle.net/21.15107/rcub_ibiss_6662 .

Martinović, Tamara, Ćirić, Darko, Pantić, Igor, Lalić, Katarina, Rasulić, Iva, Despotović, Sanja, Lalić, Ivana, Đuričić, Danica, Vučićević, Ljubica, Misirkić Marjanović, Maja, Trajković, Vladimir, Bumbaširević, Vladimir, Kravić-Stevović, Tamara, "Uticaj glikemije i lipidnog statusa na morfološke karakteristike nukleusa kod pacijenata sa tip 2 dijabetes melitusom" in Knjiga sažetaka: 1. kongres kliničkih biohemičara i specijalista laboratorijske medicine Srbije sa međunarodnim učešćem;  2019 Nov 27-29; Belgrade, Serbia (2019):58,
https://hdl.handle.net/21.15107/rcub_ibiss_6662 .

TY  - JOUR
AU  - Harhaji-Trajković, Ljubica
AU  - Vilimanovich, Urosh
AU  - Kravić-Stevović, Tamara
AU  - Bumbaširević, Vladimir
AU  - Trajković, Vladimir
PY  - 2009
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6547
AB  - The role of autophagy in cisplatin anticancer action was investigated using human U251 glioma, rat C6 glioma and mouse L929 fibrosarcoma cell lines. A dose- and time-dependent induction of autophagy was observed in tumour cells following cisplatin treatment, as demonstrated by up-regulation of autophagy-inducing protein beclin-1 and subsequent appearance of acridine orange-stained acidic autophagic vesicles. The presence of autophagosomes in cisplatin-treated cells was also confirmed by electron microscopy. Inhibition of autophagy with lysosomal inhibitors bafilomycin A1 and chloroquine, or a PI3 kinase inhibitor wortmannin, markedly augmented cisplatin-triggered oxidative stress and caspase activation, leading to an increase in DNA fragmentation and apoptotic cell death. The mechanisms underlying the protective effect of autophagy apparently involved the interference with cisplatin-induced modulation of Bcl-2 family proteins, as inhibition of autophagy potentiated cisplatin-mediated up-regulation of proapoptotic Bax and down-regulation of anti-apoptotic Bcl-2. Autophagy induction in cisplatin-treated cells was preceded by activation of adenosine monophosphate-activated protein kinase (AMPK) and concomitant down-regulation of mammalian target of rapamycin (mTOR)-mediated phosphorylation of p70S6 kinase. The ability of cisplatin to trigger autophagy was reduced by small interfering RNA (siRNA)-mediated AMPK silencing, while transfection with mTOR siRNA was sufficient to trigger autophagy in tumour cells. Finally, siRNA-mediated AMPK down-regulation and AMPK inhibitor compound C increased cisplatin-induced tumour cell death, while mTOR siRNA and AMPK activator metformin protected tumour cells from cisplatin. Taken together, these data suggest that cisplatin-triggered activation of AMPK and subsequent suppression of mTOR activity can induce an autophagic response that protects tumour cells from cisplatin-mediated apoptotic death.
PB  - Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd
T2  - Journal of Cellular and Molecular Medicine
T1  - AMPK-mediated autophagy inhibits apoptosis in cisplatin-treated tumour cells
IS  - 9B
VL  - 13
DO  - 10.1111/j.1582-4934.2009.00663.x
SP  - 3644
EP  - 3654
ER  - 

@article{
author = "Harhaji-Trajković, Ljubica and Vilimanovich, Urosh and Kravić-Stevović, Tamara and Bumbaširević, Vladimir and Trajković, Vladimir",
year = "2009",
abstract = "The role of autophagy in cisplatin anticancer action was investigated using human U251 glioma, rat C6 glioma and mouse L929 fibrosarcoma cell lines. A dose- and time-dependent induction of autophagy was observed in tumour cells following cisplatin treatment, as demonstrated by up-regulation of autophagy-inducing protein beclin-1 and subsequent appearance of acridine orange-stained acidic autophagic vesicles. The presence of autophagosomes in cisplatin-treated cells was also confirmed by electron microscopy. Inhibition of autophagy with lysosomal inhibitors bafilomycin A1 and chloroquine, or a PI3 kinase inhibitor wortmannin, markedly augmented cisplatin-triggered oxidative stress and caspase activation, leading to an increase in DNA fragmentation and apoptotic cell death. The mechanisms underlying the protective effect of autophagy apparently involved the interference with cisplatin-induced modulation of Bcl-2 family proteins, as inhibition of autophagy potentiated cisplatin-mediated up-regulation of proapoptotic Bax and down-regulation of anti-apoptotic Bcl-2. Autophagy induction in cisplatin-treated cells was preceded by activation of adenosine monophosphate-activated protein kinase (AMPK) and concomitant down-regulation of mammalian target of rapamycin (mTOR)-mediated phosphorylation of p70S6 kinase. The ability of cisplatin to trigger autophagy was reduced by small interfering RNA (siRNA)-mediated AMPK silencing, while transfection with mTOR siRNA was sufficient to trigger autophagy in tumour cells. Finally, siRNA-mediated AMPK down-regulation and AMPK inhibitor compound C increased cisplatin-induced tumour cell death, while mTOR siRNA and AMPK activator metformin protected tumour cells from cisplatin. Taken together, these data suggest that cisplatin-triggered activation of AMPK and subsequent suppression of mTOR activity can induce an autophagic response that protects tumour cells from cisplatin-mediated apoptotic death.",
publisher = "Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd",
journal = "Journal of Cellular and Molecular Medicine",
title = "AMPK-mediated autophagy inhibits apoptosis in cisplatin-treated tumour cells",
number = "9B",
volume = "13",
doi = "10.1111/j.1582-4934.2009.00663.x",
pages = "3644-3654"
}

Harhaji-Trajković, L., Vilimanovich, U., Kravić-Stevović, T., Bumbaširević, V.,& Trajković, V.. (2009). AMPK-mediated autophagy inhibits apoptosis in cisplatin-treated tumour cells. in Journal of Cellular and Molecular Medicine
Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd., 13(9B), 3644-3654.
https://doi.org/10.1111/j.1582-4934.2009.00663.x

Harhaji-Trajković L, Vilimanovich U, Kravić-Stevović T, Bumbaširević V, Trajković V. AMPK-mediated autophagy inhibits apoptosis in cisplatin-treated tumour cells. in Journal of Cellular and Molecular Medicine. 2009;13(9B):3644-3654.
doi:10.1111/j.1582-4934.2009.00663.x .

Harhaji-Trajković, Ljubica, Vilimanovich, Urosh, Kravić-Stevović, Tamara, Bumbaširević, Vladimir, Trajković, Vladimir, "AMPK-mediated autophagy inhibits apoptosis in cisplatin-treated tumour cells" in Journal of Cellular and Molecular Medicine, 13, no. 9B (2009):3644-3654,
https://doi.org/10.1111/j.1582-4934.2009.00663.x . .