TY  - JOUR
AU  - Spector, Novera Herbert
AU  - Jovanova-Nešić, Katica
AU  - Gertz, A.M.
PY  - 2013
UR  - http://intor.torlakinstitut.com/handle/123456789/379
AB  - First, the latest scientific and clinical reports will be evaluated to separate the wheat from the chaff, that is, good data versus merely anecdotal evidence. Thus, the famous (infamous) Stromboli Cocktail will be brought up to date. Second, longevity statistics will be reviewed: Why do the most scientifically advanced countries have such low (comparatively) life expectancies? Scientific knowledge expands exponentially each decade, whereas there have been no significant advances in our knowledge, government, economics, politics, anti-corruption, and so forth since the dawn of history. What can we expect in the future? Will the human species outlive the cockroach? Can we expect to get closer to that theoretical asymptote of 120 years of human life? Will this ceiling ever be lifted? Finally, we offer two vital challenges to scientists of today.
T2  - Current Aging Science
T1  - Aging, cancer, and longevity: The uncertain road
EP  - 91
IS  - 1
SP  - 86
VL  - 6
DO  - 10.2174/1874609811306010011
ER  - 

@article{
author = "Spector, Novera Herbert and Jovanova-Nešić, Katica and Gertz, A.M.",
year = "2013",
abstract = "First, the latest scientific and clinical reports will be evaluated to separate the wheat from the chaff, that is, good data versus merely anecdotal evidence. Thus, the famous (infamous) Stromboli Cocktail will be brought up to date. Second, longevity statistics will be reviewed: Why do the most scientifically advanced countries have such low (comparatively) life expectancies? Scientific knowledge expands exponentially each decade, whereas there have been no significant advances in our knowledge, government, economics, politics, anti-corruption, and so forth since the dawn of history. What can we expect in the future? Will the human species outlive the cockroach? Can we expect to get closer to that theoretical asymptote of 120 years of human life? Will this ceiling ever be lifted? Finally, we offer two vital challenges to scientists of today.",
journal = "Current Aging Science",
title = "Aging, cancer, and longevity: The uncertain road",
pages = "91-86",
number = "1",
volume = "6",
doi = "10.2174/1874609811306010011"
}

Spector, N. H., Jovanova-Nešić, K.,& Gertz, A.M.. (2013). Aging, cancer, and longevity: The uncertain road. in Current Aging Science, 6(1), 86-91.
https://doi.org/10.2174/1874609811306010011

Spector NH, Jovanova-Nešić K, Gertz A. Aging, cancer, and longevity: The uncertain road. in Current Aging Science. 2013;6(1):86-91.
doi:10.2174/1874609811306010011 .

Spector, Novera Herbert, Jovanova-Nešić, Katica, Gertz, A.M., "Aging, cancer, and longevity: The uncertain road" in Current Aging Science, 6, no. 1 (2013):86-91,
https://doi.org/10.2174/1874609811306010011 . .

TY  - JOUR
AU  - Jovanova-Nešić, Katica
AU  - Shoenfeld, Yehuda
AU  - Spector, Novera Herbert
PY  - 2012
UR  - http://intor.torlakinstitut.com/handle/123456789/345
AB  - In the central nervous system (CNS) microglia are crucial for the defense of the brain against invading microorganisms, formation of tumors, and damage following trauma [1]. However, uncontrolled activation of these cells may have deleterious outcomes [2] through activation of Fcγ and the complement 3 receptors and the induction of an adaptive immune reaction [3]. Proteins contributing to this reaction are the intercellular adhesion molecule-1 (ICAM-1) [3] and CD3 molecules, among others. Both can be expressed on the glia cells before cytokine release and may facilitate an autoimmune inflammatory reaction in the brain. Round microglial cells among the pyramidal cells of the hippocampus with increased expression of CD32+ (FcγIIa) and near the site of injection of aluminum were detected immunohistochemically and indicate microglial activation at the site of aluminum injury. ICAM-1+ immunoreactivity significantly increased in the hippocampus and in the choroids plexus, indicating increased inflammation in the brain as well as increased CD3ε+ expression in the hippocampus and non-MHC-restricted T cytotoxicity after aluminum injection. The pattern of expression of CD32+ (FcγIIa receptor) near the site of aluminum injection indicates that microglia may play a phagocytic role at the site of aluminum-induced excitotoxicity in the brain. Significant expression of ICAM-1+ and CD3ε + immunoreactive cells with the clusters of ICAM-1+ in the choroid plexus suggests a consequently neurotoxic autoimmune reaction induced by microglial hyperactivation in the injured brain.
T2  - Current Aging Science
T1  - Aluminum excytotoxicity and neuroautotoimmunity: The role of the brain expression of CD32+ (FcγRIIa), ICAM-1+ and CD3ε in aging
EP  - 217
IS  - 3
SP  - 209
VL  - 5
DO  - 10.2174/1874609811205030007
ER  - 

@article{
author = "Jovanova-Nešić, Katica and Shoenfeld, Yehuda and Spector, Novera Herbert",
year = "2012",
abstract = "In the central nervous system (CNS) microglia are crucial for the defense of the brain against invading microorganisms, formation of tumors, and damage following trauma [1]. However, uncontrolled activation of these cells may have deleterious outcomes [2] through activation of Fcγ and the complement 3 receptors and the induction of an adaptive immune reaction [3]. Proteins contributing to this reaction are the intercellular adhesion molecule-1 (ICAM-1) [3] and CD3 molecules, among others. Both can be expressed on the glia cells before cytokine release and may facilitate an autoimmune inflammatory reaction in the brain. Round microglial cells among the pyramidal cells of the hippocampus with increased expression of CD32+ (FcγIIa) and near the site of injection of aluminum were detected immunohistochemically and indicate microglial activation at the site of aluminum injury. ICAM-1+ immunoreactivity significantly increased in the hippocampus and in the choroids plexus, indicating increased inflammation in the brain as well as increased CD3ε+ expression in the hippocampus and non-MHC-restricted T cytotoxicity after aluminum injection. The pattern of expression of CD32+ (FcγIIa receptor) near the site of aluminum injection indicates that microglia may play a phagocytic role at the site of aluminum-induced excitotoxicity in the brain. Significant expression of ICAM-1+ and CD3ε + immunoreactive cells with the clusters of ICAM-1+ in the choroid plexus suggests a consequently neurotoxic autoimmune reaction induced by microglial hyperactivation in the injured brain.",
journal = "Current Aging Science",
title = "Aluminum excytotoxicity and neuroautotoimmunity: The role of the brain expression of CD32+ (FcγRIIa), ICAM-1+ and CD3ε in aging",
pages = "217-209",
number = "3",
volume = "5",
doi = "10.2174/1874609811205030007"
}

Jovanova-Nešić, K., Shoenfeld, Y.,& Spector, N. H.. (2012). Aluminum excytotoxicity and neuroautotoimmunity: The role of the brain expression of CD32+ (FcγRIIa), ICAM-1+ and CD3ε in aging. in Current Aging Science, 5(3), 209-217.
https://doi.org/10.2174/1874609811205030007

Jovanova-Nešić K, Shoenfeld Y, Spector NH. Aluminum excytotoxicity and neuroautotoimmunity: The role of the brain expression of CD32+ (FcγRIIa), ICAM-1+ and CD3ε in aging. in Current Aging Science. 2012;5(3):209-217.
doi:10.2174/1874609811205030007 .

Jovanova-Nešić, Katica, Shoenfeld, Yehuda, Spector, Novera Herbert, "Aluminum excytotoxicity and neuroautotoimmunity: The role of the brain expression of CD32+ (FcγRIIa), ICAM-1+ and CD3ε in aging" in Current Aging Science, 5, no. 3 (2012):209-217,
https://doi.org/10.2174/1874609811205030007 . .

TY  - JOUR
AU  - Jovanova-Nešić, Katica
AU  - Jovičić, S.
AU  - Sovilj, M.
AU  - Spector, Novera Herbert
PY  - 2009
UR  - http://intor.torlakinstitut.com/handle/123456789/280
AB  - We are most thankful to Prof. Yehuda Shoenfeld, head of Autoimmunity Center, Sheba Hospital at Tel Aviv, University in Israel, for critical and constructive comments on the manuscript. Thanks to Prof. B. Reljin and N. Stepanic, School of Informational Technology, Universirty of Belgrade for contribution in molecular images and computing analysis. Authors gratefully acknowledge the repeated gifts of the magnetic beads for magnetic brain stimulation of rats presented by Institute for Nuclear Physics, Vincha, Belgrade. Clinical signs appearance and significant increases of ICAM-1 and MMP-2 expressions with the clusters of VCAM-1(+) immunoreactivity in the choroids plexus epithelium to transferred anti-myelin oligodendroglial antibodies into the third brain ventricle, indicate important role of choroids plexus in the induction of acute experimental autoimmune encephalomyelitis (EAE). Magnetic brain stimulation with AKMA micro-magnet flux density of 60 miliTesla, 5 mm in diameter, implanted upon the pineal gland (PG), immediately after antibody injection, significantly decreases the expression of MMP-2 and ICAM-1 in the choroids plexus of the rat brain and abruptly suppresses the induction of acute EAE.
PB  - Taylor & Francis Ltd, Abingdon
T2  - International Journal of Neuroscience
T1  - Magnetic brain stimulation upregulates adhesion and prevents EAE: MMP-2, ICAM-1, and VCAM-1 in the choroid plexus as a target
EP  - 1418
IS  - 9
SP  - 1399
VL  - 119
DO  - 10.1080/00207450802324564
ER  - 

@article{
author = "Jovanova-Nešić, Katica and Jovičić, S. and Sovilj, M. and Spector, Novera Herbert",
year = "2009",
abstract = "We are most thankful to Prof. Yehuda Shoenfeld, head of Autoimmunity Center, Sheba Hospital at Tel Aviv, University in Israel, for critical and constructive comments on the manuscript. Thanks to Prof. B. Reljin and N. Stepanic, School of Informational Technology, Universirty of Belgrade for contribution in molecular images and computing analysis. Authors gratefully acknowledge the repeated gifts of the magnetic beads for magnetic brain stimulation of rats presented by Institute for Nuclear Physics, Vincha, Belgrade. Clinical signs appearance and significant increases of ICAM-1 and MMP-2 expressions with the clusters of VCAM-1(+) immunoreactivity in the choroids plexus epithelium to transferred anti-myelin oligodendroglial antibodies into the third brain ventricle, indicate important role of choroids plexus in the induction of acute experimental autoimmune encephalomyelitis (EAE). Magnetic brain stimulation with AKMA micro-magnet flux density of 60 miliTesla, 5 mm in diameter, implanted upon the pineal gland (PG), immediately after antibody injection, significantly decreases the expression of MMP-2 and ICAM-1 in the choroids plexus of the rat brain and abruptly suppresses the induction of acute EAE.",
publisher = "Taylor & Francis Ltd, Abingdon",
journal = "International Journal of Neuroscience",
title = "Magnetic brain stimulation upregulates adhesion and prevents EAE: MMP-2, ICAM-1, and VCAM-1 in the choroid plexus as a target",
pages = "1418-1399",
number = "9",
volume = "119",
doi = "10.1080/00207450802324564"
}

Jovanova-Nešić, K., Jovičić, S., Sovilj, M.,& Spector, N. H.. (2009). Magnetic brain stimulation upregulates adhesion and prevents EAE: MMP-2, ICAM-1, and VCAM-1 in the choroid plexus as a target. in International Journal of Neuroscience
Taylor & Francis Ltd, Abingdon., 119(9), 1399-1418.
https://doi.org/10.1080/00207450802324564

Jovanova-Nešić K, Jovičić S, Sovilj M, Spector NH. Magnetic brain stimulation upregulates adhesion and prevents EAE: MMP-2, ICAM-1, and VCAM-1 in the choroid plexus as a target. in International Journal of Neuroscience. 2009;119(9):1399-1418.
doi:10.1080/00207450802324564 .

Jovanova-Nešić, Katica, Jovičić, S., Sovilj, M., Spector, Novera Herbert, "Magnetic brain stimulation upregulates adhesion and prevents EAE: MMP-2, ICAM-1, and VCAM-1 in the choroid plexus as a target" in International Journal of Neuroscience, 119, no. 9 (2009):1399-1418,
https://doi.org/10.1080/00207450802324564 . .

TY  - JOUR
AU  - Jovanova-Nešić, Katica
AU  - Erić-Jovičić, Milena
AU  - Spector, Novera Herbert
PY  - 2006
UR  - http://intor.torlakinstitut.com/handle/123456789/207
AB  - This article reports here on the influence of the static magnetic fields ( MFs), locally applied to the brain area, on Na, K-ATPase activity in the rat with lesioned nucleus basalis magnocellularis ( NBM) by intracerebral injection of 5 mu l, 1% AlCl3 into the nucleus. Two AKMA micromagnets ( M) flux density of 60 miliTesla, 5 mm in diameter, were bilaterally implanted with "N" polarity facing down to the cranial bones in the vicinity of the pineal gland ( PG), immediately after the lesioning of NBM, during the same operation procedure. Ten days after the lesions of NBM, Na, K-ATPase activity on the erythrocyte membranes in the peripheral blood, measured spectrophotometrically, was completely inhibited. Magnetic stimulation ( 60 mT) of the brain during the 10 days significantly increased Na, K-ATPase activity on the erythrocyte membranes of rats with lesioned NBM. This results suggests that altered by lesions Na, K-ATPase activity in an experimental model of Alzheimer's disease might be ameliorated by magnetic stimulation of the brain.
PB  - Taylor & Francis Ltd, Abingdon
T2  - International Journal of Neuroscience
T1  - Magnetic stimulation of the brain increase Na+, K+-atpase activity decreased by injection of alcl(3) into nucleus basalis magnocellularis of rats
EP  - 695
IS  - 6
SP  - 681
VL  - 116
DO  - 10.1080/00207450600674830
ER  - 

@article{
author = "Jovanova-Nešić, Katica and Erić-Jovičić, Milena and Spector, Novera Herbert",
year = "2006",
abstract = "This article reports here on the influence of the static magnetic fields ( MFs), locally applied to the brain area, on Na, K-ATPase activity in the rat with lesioned nucleus basalis magnocellularis ( NBM) by intracerebral injection of 5 mu l, 1% AlCl3 into the nucleus. Two AKMA micromagnets ( M) flux density of 60 miliTesla, 5 mm in diameter, were bilaterally implanted with "N" polarity facing down to the cranial bones in the vicinity of the pineal gland ( PG), immediately after the lesioning of NBM, during the same operation procedure. Ten days after the lesions of NBM, Na, K-ATPase activity on the erythrocyte membranes in the peripheral blood, measured spectrophotometrically, was completely inhibited. Magnetic stimulation ( 60 mT) of the brain during the 10 days significantly increased Na, K-ATPase activity on the erythrocyte membranes of rats with lesioned NBM. This results suggests that altered by lesions Na, K-ATPase activity in an experimental model of Alzheimer's disease might be ameliorated by magnetic stimulation of the brain.",
publisher = "Taylor & Francis Ltd, Abingdon",
journal = "International Journal of Neuroscience",
title = "Magnetic stimulation of the brain increase Na+, K+-atpase activity decreased by injection of alcl(3) into nucleus basalis magnocellularis of rats",
pages = "695-681",
number = "6",
volume = "116",
doi = "10.1080/00207450600674830"
}

Jovanova-Nešić, K., Erić-Jovičić, M.,& Spector, N. H.. (2006). Magnetic stimulation of the brain increase Na+, K+-atpase activity decreased by injection of alcl(3) into nucleus basalis magnocellularis of rats. in International Journal of Neuroscience
Taylor & Francis Ltd, Abingdon., 116(6), 681-695.
https://doi.org/10.1080/00207450600674830

Jovanova-Nešić K, Erić-Jovičić M, Spector NH. Magnetic stimulation of the brain increase Na+, K+-atpase activity decreased by injection of alcl(3) into nucleus basalis magnocellularis of rats. in International Journal of Neuroscience. 2006;116(6):681-695.
doi:10.1080/00207450600674830 .

Jovanova-Nešić, Katica, Erić-Jovičić, Milena, Spector, Novera Herbert, "Magnetic stimulation of the brain increase Na+, K+-atpase activity decreased by injection of alcl(3) into nucleus basalis magnocellularis of rats" in International Journal of Neuroscience, 116, no. 6 (2006):681-695,
https://doi.org/10.1080/00207450600674830 . .

TY  - CONF
AU  - Jovanova-Nešić, Katica
AU  - Erić-Jovičić, Milena
AU  - Popović, M.
AU  - Popović, N.
AU  - Rakić, L.
AU  - Spector, Novera Herbert
PY  - 2002
UR  - http://intor.torlakinstitut.com/handle/123456789/149
AB  - In a previous paper, the authors have described the effect of Ca2+-antagonist. verapamil on Na,K-ATPase in experimental model of Alzheimer's disease (AD-[38,39]. The present paper is concerned with the effect of magnetic, stimulation of. pineal complex on Na,K-ATPase activity in the same experimental model of AD. Because accumulating data indicate that free radicals mediate injury and death of neurons in AD, and because magnetic fields (MFs) can alter- free radicals. reactions; we tested the hypothesis that stationary MFs mediates ion homeostasis through membrane Na;K-ATPase activity. Results are presented as Vmax/Km - parameters on erythrocyte membranes in peripheral blood of rats with lesioned nucleus basalis magnocellularis. Bilateral electrolytic or by kainic acid induced lesions of NBM induce significant decrease of Vmax/Km activity on erythrocyte membranes obtained by cardiac punction. Stimulation of - pineal complex of the brain more than ten days, by magnetic beards (600-Gauss flux density), fixed on the skull upon pineal gland, significantly increase impaired by lesions of NBM, Na, K-ATPase activity. Results are presented as Vmax/Km parameters. on erythrocyte membranes in peripheral blood of rats with lesioned NBM of the basal forebrain bundle. Chronically magnetic stimulation of the pineal complex significantly increase maximum velocity (Vmax; nmol Pi/mg protein/min) of proteins in both lesioned group, even more than 2-fold in by kainic acid (ka)lesioned animals in comparison of lesioned sham-stimulated and increase Vmax in comparison to both controls (sham-lesioned m-sham-stimulated, and intact controls, and return desturbed by lesions affinity of enzyme to substrate (Km; nM) near to the control values. These results confirm the hypothesis that altered ion homeostasis disturbed by neurodegenerations play an essential role in pathogenesis of experimental Alzheimer's disease (AD) and that magnetic stimulation of the pineal complex might successfully restore disturbed by neuronal death Na, K-ATPase activity.
PB  - IEEE, New York
C3  - 2002 6th Seminar on Neural Network Applications in Electrical Engineering, NEUREL 2002 - Proceedings
T1  - Effect of magnetic stimulation of pineal complex of the brain on Na,K-ATPase in experimental Alzheimer's Disease
EP  - 170
SP  - 165
UR  - https://hdl.handle.net/21.15107/rcub_intor_149
ER  - 

@conference{
author = "Jovanova-Nešić, Katica and Erić-Jovičić, Milena and Popović, M. and Popović, N. and Rakić, L. and Spector, Novera Herbert",
year = "2002",
abstract = "In a previous paper, the authors have described the effect of Ca2+-antagonist. verapamil on Na,K-ATPase in experimental model of Alzheimer's disease (AD-[38,39]. The present paper is concerned with the effect of magnetic, stimulation of. pineal complex on Na,K-ATPase activity in the same experimental model of AD. Because accumulating data indicate that free radicals mediate injury and death of neurons in AD, and because magnetic fields (MFs) can alter- free radicals. reactions; we tested the hypothesis that stationary MFs mediates ion homeostasis through membrane Na;K-ATPase activity. Results are presented as Vmax/Km - parameters on erythrocyte membranes in peripheral blood of rats with lesioned nucleus basalis magnocellularis. Bilateral electrolytic or by kainic acid induced lesions of NBM induce significant decrease of Vmax/Km activity on erythrocyte membranes obtained by cardiac punction. Stimulation of - pineal complex of the brain more than ten days, by magnetic beards (600-Gauss flux density), fixed on the skull upon pineal gland, significantly increase impaired by lesions of NBM, Na, K-ATPase activity. Results are presented as Vmax/Km parameters. on erythrocyte membranes in peripheral blood of rats with lesioned NBM of the basal forebrain bundle. Chronically magnetic stimulation of the pineal complex significantly increase maximum velocity (Vmax; nmol Pi/mg protein/min) of proteins in both lesioned group, even more than 2-fold in by kainic acid (ka)lesioned animals in comparison of lesioned sham-stimulated and increase Vmax in comparison to both controls (sham-lesioned m-sham-stimulated, and intact controls, and return desturbed by lesions affinity of enzyme to substrate (Km; nM) near to the control values. These results confirm the hypothesis that altered ion homeostasis disturbed by neurodegenerations play an essential role in pathogenesis of experimental Alzheimer's disease (AD) and that magnetic stimulation of the pineal complex might successfully restore disturbed by neuronal death Na, K-ATPase activity.",
publisher = "IEEE, New York",
journal = "2002 6th Seminar on Neural Network Applications in Electrical Engineering, NEUREL 2002 - Proceedings",
title = "Effect of magnetic stimulation of pineal complex of the brain on Na,K-ATPase in experimental Alzheimer's Disease",
pages = "170-165",
url = "https://hdl.handle.net/21.15107/rcub_intor_149"
}

Jovanova-Nešić, K., Erić-Jovičić, M., Popović, M., Popović, N., Rakić, L.,& Spector, N. H.. (2002). Effect of magnetic stimulation of pineal complex of the brain on Na,K-ATPase in experimental Alzheimer's Disease. in 2002 6th Seminar on Neural Network Applications in Electrical Engineering, NEUREL 2002 - Proceedings
IEEE, New York., 165-170.
https://hdl.handle.net/21.15107/rcub_intor_149

Jovanova-Nešić K, Erić-Jovičić M, Popović M, Popović N, Rakić L, Spector NH. Effect of magnetic stimulation of pineal complex of the brain on Na,K-ATPase in experimental Alzheimer's Disease. in 2002 6th Seminar on Neural Network Applications in Electrical Engineering, NEUREL 2002 - Proceedings. 2002;:165-170.
https://hdl.handle.net/21.15107/rcub_intor_149 .

Jovanova-Nešić, Katica, Erić-Jovičić, Milena, Popović, M., Popović, N., Rakić, L., Spector, Novera Herbert, "Effect of magnetic stimulation of pineal complex of the brain on Na,K-ATPase in experimental Alzheimer's Disease" in 2002 6th Seminar on Neural Network Applications in Electrical Engineering, NEUREL 2002 - Proceedings (2002):165-170,
https://hdl.handle.net/21.15107/rcub_intor_149 .