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  • 1
    Language: English
    In: Immunologic Research, 2012, Vol.52(1), pp.81-88
    Description: During evolution, beta cells adapted to a sole aim: the production and stimulus-dependent secretion of insulin. This acquired specificity was accompanied by a loss of protection mechanisms predisposing beta cell to a high vulnerability. Among beta cell–damaging molecules, a new one has been identified recently: macrophage migration inhibitory factor (MIF). MIF was at first designated as a T-cell product that inhibits random movement of macrophages. Over the years, the number of functions attributed to this protein increased significantly, positioning MIF at the top of inflammatory cascade in the combat against infection and in immunoinflammatory and autoimmune diseases. This exceptionally versatile molecule regulates insulin secretion in physiological conditions, while in pathological states it alters beta cell function and induces their apoptosis or necrosis and affects beta cell neoplasia.
    Keywords: Macrophage migration inhibitory factor ; Type 1 diabetes ; Type 2 diabetes ; Beta cell ; Apoptosis ; Necrosis ; Neoplasia
    ISSN: 0257-277X
    E-ISSN: 1559-0755
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  • 2
    Language: English
    In: American Journal of Obstetrics and Gynecology, January 2017, Vol.216(1), pp.S124-S124
    Description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ajog.2016.11.097 Byline: Ana Mrkaic (1), Barak Rosenn (1), Ivana Stojanovic (2), Samir Tivari (3) Author Affiliation: (1) Mt.Sinai West Hospital, New York, NY (2) Medical Faculty, University of Nis, Nis, Serbia (3) Rutgers University, Newark, NJ
    Keywords: Medicine
    ISSN: 0002-9378
    E-ISSN: 1097-6868
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  • 3
    Language: English
    In: European Journal of Pharmacology, 15 August 2013, Vol.714(1-3), pp.498-506
    Description: Macrophage migration inhibitory factor (MIF)-deficient mice develop glucose intolerance and hyperglycemia, but remain entirely responsive to exogenous insulin in adult age. Furthermore, as a consequence of MIF deficiency, the immune response in these mice is predominantly anti-inflammatory. Since MIF is a natural counter-regulator of glucocorticoid action, and it is known that excessive concentration of glucocorticoids contribute both to beta cell dysfunction and immunosuppression, we hypothesized that MIF absence enables elevation of glucocorticoids which in turn caused the observed condition. Our results confirm that MIF-knockout (MIF-KO) mice possess higher levels of circulating corticosterone, but lower expression of glucocorticoid receptor in pancreatic islets, liver and adipose tissue to the one observed in wild type (WT) mice. A significant up-regulation of glucocorticoid receptor expression was however noticed in MIF-deficient lymph node cells. The inhibition of glucocorticoid receptor by RU486 improved tolerance to glucose in MIF-KO mice and restored euglycemia. Although RU486 treatment did not alter the level of glucose receptor GLUT2, it enhanced insulin secretion and up-regulated insulin-triggered Akt phosphorylation within hepatic tissue. Finally, inhibition of glucocorticoid receptor changed anti-inflammatory phenotype of MIF-KO lymphocytes toward a physiological profile. Our results indicate that deregulated glucocorticoid secretion and glucocorticoid receptor expression in the absence of MIF possibly contributes to the development of glucose intolerance and immunosuppression in MIF-KO mice. However, since MIF-KO mice respond normally to insulin and their beta cell function is within physiological range, additional cause for glucose intolerance could be sought in the possible malfunction of their insulin.
    Keywords: Macrophage Migration Inhibitory Factor ; Glucocorticoids ; Diabetes ; Insulin ; Inflammation ; Pharmacy, Therapeutics, & Pharmacology
    ISSN: 0014-2999
    E-ISSN: 1879-0712
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  • 4
    Language: English
    In: Diabetologia, 2014, Vol.57(5), pp.980-990
    Description: Byline: Ivana Nikolic (1), Tamara Saksida (1), Katia Mangano (2), Milica Vujicic (1), Ivana Stojanovic (1), Ferdinando Nicoletti (2), Stanislava Stosic-Grujicic (1) Keywords: Beta cell apoptosis; Carbon monoxide-releasing molecule-A1; Cytokines; Type 1 diabetes Abstract: Aims/hypothesis Recent studies have identified carbon monoxide (CO) as a potential therapeutic molecule for the treatment of autoimmune diseases owing to its anti-inflammatory and anti-apoptotic properties. We explored the efficacy and the mechanisms of action of the CO-releasing molecule (CORM)-A1 in preclinical models of type 1 diabetes. Methods The impact of CORM-A1 on diabetes development was evaluated in models of spontaneous diabetes in NOD mice and in diabetes induced in C57BL/6 mice by multiple low-dose streptozotocin (MLDS). Ex vivo analysis was performed to determine the impact of CORM-A1 both on T helper (Th) cell and macrophage differentiation and on their production of soluble mediators in peripheral tissues and in infiltrates of pancreatic islets. The potential effect of CORM-A1 on cytokine-induced apoptosis in pancreatic islets or beta cells was evaluated in vitro. Results CORM-A1 conferred protection from diabetes in MLDS-induced mice and reduced diabetes incidence in NOD mice as confirmed by preserved insulin secretion and improved histological signs of the disease. In MLDS-challenged mice, CORM-A1 attenuated Th1, Th17, and M1 macrophage response and facilitated Th2 cell differentiation. In addition, CORM-A1 treatment in NOD mice upregulated the regulatory arm of the immune response (M2 macrophages and FoxP3.sup.+ regulatory T cells). Importantly, CORM-A1 interfered with in vitro cytokine-induced beta cell apoptosis through the reduction of cytochrome c and caspase 3 levels. Conclusions/interpretation The ability of CORM-A1 to protect mice from developing type 1 diabetes provides a valuable proof of concept for the potential exploitation of controlled CO delivery in clinical settings for the treatment of autoimmune diabetes. Author Affiliation: (1) Department of Immunology, Institute for Biological Research 'Sinisa Stankovic', University of Belgrade, Bul. Despota Stefana 142, 11060, Belgrade, Serbia (2) Department of Biomedical Sciences, School of Medicine, University of Catania, Via Androne 83, 95124, Catania, Italy Article History: Registration Date: 10/01/2014 Received Date: 19/07/2013 Accepted Date: 18/12/2013 Online Date: 02/02/2014 Article note: Electronic supplementary material The online version of this article (doi: 10.1007/s00125-014-3170-7) contains peer-reviewed but unedited supplementary material, which is available to authorised users.
    Keywords: Beta cell apoptosis ; Carbon monoxide-releasing molecule-A1 ; Cytokines ; Type 1 diabetes
    ISSN: 0012-186X
    E-ISSN: 1432-0428
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  • 5
    Language: English
    In: Immunobiology, 2011, Vol.216(9), pp.1018-1027
    Description: Inflammation plays an important role in protective immunity against fungi, including the opportunistic pathogen, . The balance between pro-inflammatory and anti-inflammatory cytokines is a key determinant of infection outcome. Since macrophage migration inhibitory factor (MIF) is an upstream regulator of many cytokines, we analyzed herein the role of endogenous MIF in the host control of hematogenously disseminated aspergillosis using MIF mice. As revealed by their mortality rate, MIF mice were more susceptible to disseminated infection than WT mice. Moreover, pharmacologic inhibition of MIF with ( , )-3-(4-hydroxyphenyl)-4,5-dihydro-5-isoxazole acetic acid methyl ester, (ISO-1) increased the susceptibility of WT mice to lethal infection. The higher tissue fungal burden early in sublethal infection indicated increased susceptibility of MIF mice to sublethal infection as well. Substantial down-regulation of innate and acquired antifungal responses, characterized by decreased production of IL-1β, IL-6, TNF-α, IFN-γ and IL-17 in the spleen was noted in sublethally infected MIF mice. In contrast, IL-4 was higher in MIF than in WT mice. Taken together, our findings show that MIF contributes to host resistance against progressive invasive infection by controlling downstream pro-inflammatory versus anti-inflammatory cytokine production thus determining the outcome of infection.
    Keywords: Acquired Immunity ; Aspergillus Fumigatus ; Cytokines ; Innate Immunity ; Macrophage Migration Inhibitory Factor ; Biology
    ISSN: 0171-2985
    E-ISSN: 1878-3279
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  • 6
    Language: English
    In: Annals of transplantation, 02 April 2015, Vol.20, pp.186-92
    Description: Renal transplant dysfunction has been shown to be an independent risk factor for cardiac, non-cardiovascular, and all-cause mortality in post-transplantation follow-up. We enrolled 73 renal transplant recipients who were more than 12 months post-renal transplant surgery, had stable graft function, and were on standard immunosuppression. The purpose of the study was to observe the relation between renal dysfunction and endothelial dysfunction parameters (nitrates, asymmetric and symmetric dimethylarginine, and endothelial nitric oxide synthase), and renalase, and to hypothesize the best predictor of early renal dysfunction by multivariate modeling. The other aim was to observe differences with regard to immunosuppression. Non-adjusted odds ratio showed a significant risk of reduced glomerular filtration rate in transplant recipients with increased renalase concentration (p=0.026); age-adjusted odds ratio showed a significant risk of reduced glomerular filtration rate with increased renalase concentration (p=0.042), also after multivariable adjustment (p=0.032). Increased plasma endothelial nitric oxide synthase concentration was a protective factor for glomerular filtration rate (p=0.011). After adjustment for age (p=0.045), and after multivariate modeling, endothelial nitric oxide synthase was shown to be a protective factor for glomerular filtration rate (p=0.014). Significant differences in immunosuppression were found in plasma renalase in patients maintained on cyclosporine (p=0.027). Renalase was shown to be strong predictor of decreased glomerular filtration rate and was significantly higher in the group of patients on cyclosporine. Endothelial nitric oxide synthase was identified as a strong protective factor for kidney function.
    Keywords: Kidney Transplantation ; Monoamine Oxidase -- Blood ; Renal Insufficiency -- Diagnosis
    ISSN: 14259524
    E-ISSN: 2329-0358
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  • 7
    In: British Journal of Nutrition, 2010, Vol.103(10), pp.1413-1424
    Description: The health-promoting effects of various constituents of the olive tree ( Olea europaea ) are mainly associated with hypoglycaemic and insulin-sensitising activities and have been widely demonstrated in the metabolic syndrome and type 2 diabetes. However, their biological activity in autoimmune type 1 diabetes (T1D) is poorly characterised. Therefore, the influence of O. europaea -derived components present in dry olive leaf extract (DOLE) was examined in two established preclinical models of human T1D, which differ in some aspects of diabetogenesis: multiple low-dose streptozotocin-induced diabetes in susceptible C57BL/6 and CBA/H mouse strains; cyclophosphamide-accelerated diabetes in non-obese diabetic mice. In both T1D models, in vivo administration of DOLE significantly reduced clinical signs of diabetes (hyperglycaemia and body weight loss) and led to complete suppression of histopathological changes in pancreatic islets. In line with these, insulin expression and release were restored in DOLE-treated mice. Interestingly, inducible NO synthase expression and NO production were significantly elevated in peripheral tissues but were down-regulated within the local environment of the endocrine pancreas. This interference was reflected in NO-mediated suppression of T lymphocyte proliferation and lower production of the proinflammatory cytokines interferon-γ, IL-17 and TNF-α in the spleen, with subsequent blockade of β-cell destruction. The results suggest that DOLE interferes with development of autoimmune diabetes by down-regulating production of proinflammatory and cytotoxic mediators. Therefore, the potential use of a DOLE-enriched diet for prophylaxis/treatment of human T1D, and possibly other autoimmune diseases, is worthy of further investigation.
    Keywords: Nutritional Immunology; Type 1 Diabetes; Leaves; Cytokines; Nitric Oxide
    ISSN: 0007-1145
    E-ISSN: 1475-2662
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  • 8
    In: Srpska pravna misao, 01/30/2012, Vol.18(45), pp.103-115
    ISSN: 18400493
    E-ISSN: 22330410
    Source: CrossRef
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  • 9
    Language: English
    In: Brain Research, 01 June 2018, Vol.1688, pp.73-80
    Description: Excessive glutamate efflux and N-methyl-D-aspartate receptor (NMDAR) over-activation represent well-known hallmarks of cerebral ischemia/reperfusion (I/R) injury, still, expression of proteins involved in this aspect of I/R pathophysiology show inconsistent data. Neurosteroid dehydroepiandrosterone (DHEA) has been proposed as potent NMDAR modulator, but its influence on I/R-induced changes up to date remains questionable. Therefore, I/R-governed alteration of vesicular glutamate transporter 1 (vGluT1), synaptic NMDAR subunit composition, postsynaptic density protein 95 (PSD-95) and neuronal morphology alone or following DHEA treatment were examined. For that purpose, adult male Wistar rats were treated with a single dose of vehicle or DHEA (20 mg/kg i.p.) 4 h following sham operation or 15 min bilateral common carotid artery occlusion. Western blot was used for analyses of synaptic protein expressions in hippocampus and prefrontal cortex, while neuronal morphology was assessed using Nissl staining. Regional-specific postischemic changes were detected on protein level i.e. signs of neuronal damage in CA1 area was accompanied with hippocampal vGluT1, NR1, NR2B enhancement and PSD-95 decrement, while histological changes observed in layer III were associated with decreased NR1 subunit in prefrontal cortex. Under physiological conditions DHEA had no effect on protein and histological appearance, while in ischemic milieu it restored hippocampal PSD-95 and NR1 in prefrontal cortex to the control level. Along with intact neurons, ones characterized by morphology observed in I/R group were also present. Future studies involving NMDAR-related intracellular signaling and immunohistochemical analysis will reveal precise effects of I/R and DHEA treatment in selected brain regions.
    Keywords: Cerebral Ischemia/Reperfusion ; Dehydroepiandrosterone ; Glutamatergic Neurotransmission ; Synaptosomes ; Hippocampus ; Prefrontal Cortex ; Anatomy & Physiology
    ISSN: 0006-8993
    E-ISSN: 1872-6240
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  • 10
    Language: English
    In: Physics in Perspective, 2013, Vol.15(1), pp.92-115
    Description: We provide a guide to Bologna, Italy, focusing particularly on sites of interest to physicists. Our first tour is in the city center; it begins in the Piazza Maggiore at the Palazzo d’Accursio , the Basilica di San Petronio , and the Archiginnasio (Old University) and then proceeds to the Two Towers and the Palazzo Poggi , which houses the Astronomical Observatory Museum and other important instrument and art collections; it concludes at the Physics Museum, Department of Physics and Astronomy. Our second tour again begins in the Piazza Maggiore but goes to sites beyond the city center where famous Bolognese physicists and other scientists were born, lived, and are buried. Finally, we point out important museums and other institutions on the outskirts of Bologna.
    Keywords: Giovanni Battista Amici ; Laura Bassi ; Gilberto Bernardini ; Rita Brunetti ; Giosuè Carducci ; Gian Domenico Cassini ; Nicolaus Copernicus ; Egnazio Danti ; Adriano Cavalieri Ducati ; Luigi Galvani ; Francesco Maria Grimaldi ; Marcello Malpighi ; Luigi Ferdinando Marsigli ; Pope Benedict XIV ; Pope Gregory XIII ; Pope Pius IX ; Giovanni Battista Guglielmini ; Ettore Majorana ; Quirino Majorana ; Guglielmo Marconi ; Macedonio Melloni ; Leopoldo Nobili ; Domenico Maria Novara ; Giovanni Pelagalli ; Giampietro Puppi ; Giovanni Battista Riccioli ; Augusto Righi ; Giorgio Valle ; Giuseppe Veratti ; Alessandro Volta ; Basilica di San Petronio ; Two Towers ; Archiginnasio ; University of Bologna ; Institute of Bologna ; Palazzo Poggi ; Astronomical Observatory Museum ; Physics Museum ; Museum of Industrial Heritage ; Pelagalli Museum ; Ducati Museum ; Northern Cross Radiotelescope ; Marconi Museum ; Villa Griffone ; Montecuccolino Nuclear Engineering Laboratory ; Genus Bononiae Museums in the City ; wireless telegraphy ; history of astronomy ; history of physics
    ISSN: 1422-6944
    E-ISSN: 1422-6960
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