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52. Traumatic Burst Fracture with Spinal Channel Involvement Augmentation with Bioactive Strontium-Hydroxyapatite Cement

Author

Masala, S., Calabria, E., Nano, G., Iundusi, R., Greco, L., Di Trapano, R., Tarantino, U., and Simonetti, G.

Subjects
Article Subject
Abstract

In November 2011 a 75-year-old man was admitted to our emergency department with a low back pain caused by a traumatic L1 vertebral collapse with backward projection of posterior wall superior third. The indication for neurosurgical instrumentation was placed, although he refused the treatment. Hence he was treated conservatively without a significant improvement up to January 2012 when, still refusing surgery, he accepted to undergo percutaneous vertebroplasty with a novel bioactive injectable strontium-hydroxyapatite cement. Vertebroplasty was performed without complications. A CT scan, performed the day after the procedure, ruled out extravertebral cement leakage. Pain improvement was significant (preprocedure VAS 10, one-week VAS 4) with a gradual decrease up to three months when it stabilized at 2. CT examination after 1 year showed a good cement osseointegration with osteophytic spurs bridging the superior endplate of the level involved to the inferior one of the level above. The new bone ingrowing property of the strontium-hydroxyapatite containing cement permits to extend the treatment indication also to unstable collapses in which the risk of pseudoarthrosis is very high. In this reported case we evaluated the potential role of percutaneous vertebroplasty in traumatic burst fracture with spinal channel involvement.

Published
2013
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53. Improving Biotreatment Efficiency of Hot Waste Air Streams: Experimental Upgrade of a Full Plant

Author

Copelli, S, Torretta, V, Raboni, M, Viotti, P, Luciano, A, Mancini, Giuseppe, and Nano, G.

Subjects
Removal efficiencies, lcsh:Computer engineering. Computer hardware, Plant modification, biotrickling filtration, Biotreatment, lcsh:TP155-156, Biological methods, Energy efficient, High temperature, Odorous compounds, Plant modification, Plant upgrades, Removal efficiencies, Volatile Organic Compounds (VOCs), lcsh:TK7885-7895, High temperature, Odorous compounds, Biological methods, Plant upgrades, lcsh:Chemical engineering, odorous compounds, Volatile Organic Compounds (VOCs), Energy efficient
Abstract

Biological methods as bio and biotrickling filtration are an energy-efficient and economical alternative to treat biodegradable odorants and volatile organic compounds (VOCs) in order to obey stringent releases regulations that have arisen during the last few decades. In this work a plant upgrade case study, employing these techniques, is presented. It refers to a critical situation in which off air streams, characterized by medium odorous compounds loads and high temperatures, were treated using a biofilter only. In that context, sufficient removal efficiencies were not achieved. Therefore, it has been proposed to replace the existing biofilter by a biotrickling one implementing a minimal number of structural plant modifications.

Published
2012

57. Receptor binding mode and pharmacological characterization of a potent and selective dual CXCR1/CXCR2 non-competitive allosteric inhibitor

Author

Bertini, R, Barcelos, Ls, Beccari, Ar, Cavalieri, B, Moriconi, A, Bizzarri, C, DI BENEDETTO, Paola, Di Giacinto, C, Gloaguen, I, Galliera, E, Corsi, Mm, Russo, Rc, Andrade, Sp, Cesta, Mc, Nano, G, Aramini, A, Cutrin, Jc, Locati, M, Allegretti, M, and Teixeira, Mm

Subjects
Male, Models, Molecular, Anti-Inflammatory Agents, BINDING MODE, chemokine receptors, Inbred C57BL, Receptors, Interleukin-8B, Receptors, Interleukin-8A, Rats, Sprague-Dawley, Mice, Models, CXCR1/CXCR2, Receptors, CHEMOKINE RECEPTORS, Leukocytes, Site-Directed, NON-COMPETITIVE ALLOSTERIC INHIBITOR, Skin, Sulfonamides, CXC1-CXCR2 inhibitors, Neovascularization, Pathologic, Chemotaxis, inflammation, Research Papers, Medicina Básica, Chemotaxis, Leukocyte, Liver, LEUCOCYTE RECRUITMENT, Reperfusion Injury, non-competitive allosteric inhibitor, CIENCIAS MÉDICAS Y DE LA SALUD, Interleukin-8A, leucocyte recruitment, Inmunología, binding mode, Human Umbilical Vein Endothelial Cells, Animals, Humans, Interleukin-8B, Neovascularization, Cell Proliferation, Pathologic, Animal, experimental angiogenesis, Cell Membrane, Interleukin-8, Molecular, Leukocyte, Rats, Mice, Inbred C57BL, Disease Models, Animal, Mutagenesis, ISCHAEMIA REPERFUSION INJURY, Disease Models, ischaemia reperfusion injury, Mutagenesis, Site-Directed, Sprague-Dawley, EXPERIMENTAL ANGIOGENESIS
Abstract

Background and Purpose: DF 2156A is a new dual inhibitor of IL-8 receptors CXCR1 and CXCR2 with an optimal pharmacokinetic profile. We characterized its binding mode, molecular mechanism of action and selectivity, and evaluated its therapeutic potential. Experimental Approach: The binding mode, molecular mechanism of action and selectivity were investigated using chemotaxis of L1.2 transfectants and human leucocytes, in addition to radioligand and [ 35S]-GTPγS binding approaches. The therapeutic potential of DF 2156A was evaluated in acute (liver ischaemia and reperfusion) and chronic (sponge-induced angiogenesis) experimental models of inflammation. Key Results: A network of polar interactions stabilized by a direct ionic bond between DF 2156A and Lys99 on CXCR1 and the non-conserved residue Asp 293 on CXCR2 are the key determinants of DF 2156A binding. DF 2156A acted as a non-competitive allosteric inhibitor blocking the signal transduction leading to chemotaxis without altering the binding affinity of natural ligands. DF 2156A effectively and selectively inhibited CXCR1/CXCR2-mediated chemotaxis of L1.2 transfectants and leucocytes. In a murine model of sponge-induced angiogenesis, DF 2156A reduced leucocyte influx, TNF-α production and neovessel formation. In vitro, DF 2156A prevented proliferation, migration and capillary-like organization of HUVECs in response to human IL-8. In a rat model of liver ischaemia and reperfusion (I/R) injury, DF 2156A decreased PMN and monocyte-macrophage infiltration and associated hepatocellular injury. Conclusion and Implications: DF 2156A is a non-competitive allosteric inhibitor of both IL-8 receptors CXCR1 and CXCR2. It prevented experimental angiogenesis and hepatic I/R injury in vivo and, therefore, has therapeutic potential for acute and chronic inflammatory diseases. Fil: Bertini, R.. Dompé; Italia Fil: Barcelos, L. S.. Universidade Federal de Minas Gerais; Brasil Fil: Beccari, A. R.. Dompé; Italia Fil: Cavalieri, B.. Dompé; Italia. Università di Torino; Italia Fil: Moriconi, A.. Dompé; Italia Fil: Bizzarri, C.. Dompé; Italia Fil: Di Benedetto, P.. Dompé; Italia Fil: Di Giacinto, C.. Dompé; Italia Fil: Gloaguen, I.. Dompé; Italia Fil: Galliera, E.. Università degli Studi di Milano; Italia Fil: Corsi, M. M.. Università degli Studi di Milano; Italia. Policlinico San Donato IRCCS; Italia Fil: Russo, R. C.. Universidade Federal de Minas Gerais; Brasil Fil: Andrade, S. P.. Universidade Federal de Minas Gerais; Brasil Fil: Cesta, M. C.. Dompé; Italia Fil: Nano, G.. Dompé; Italia Fil: Aramini, A.. Dompé; Italia Fil: Cutrin, Juan Carlos. Università di Torino; Italia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina Fil: Locati, M.. Università degli Studi di Milano; Italia Fil: Allegretti, M.. Dompé; Italia Fil: Teixeira, M. M.. Universidade Federal de Minas Gerais; Brasil

Published
2011

67. Erratum to “Choices of Stent and Cerebral Protection in the Ongoing ACST-2 Trial: A Descriptive Study” [Eur J Vasc Endovasc Surg 53 (2017) 617–625]

Author

Fraedrich, G., Rantner, B., Gizewski, E., Gruber, I., Hendriks, J., Cras, P., Lauwers, P., van Scheil, P., Vermassen, F., Van Herzeele, I., Geenens, M., Hemelsoet, D., Lerut, P., Lambrecht, B., Saad, G., Peeters, A., Bosiers, M., da Silva, E., de Luccia, N., Sitrangulo, J.C., Jr., Estenssoro, A.E.V., Presti, C., Casella, I., Monteiro, J.A.T., Campos, W., Jr., Puech-Leao, P., Petrov, V., Bachvarov, C., Hill, M., Mitha, A., Wong, J., Liu, C.-W., Bao, L., Yu, C., Cvjetko, I., Vidjak, V., Fiedler, J., Ostry, S., Sterba, L., Kostal, P., Staffa, R., Vlachovsky, R., Privara, M., Kriz, Z., Vojtisek, B., Krupa, P., Reif, M., Benes, V., Buchvald, P., Endrych, L., Prochazka, V., Kuliha, M., Otahal, D., Hrbac, T., Netuka, D., Mohapl, M., Kramier, F., Eldessoki, M., Heshmat, H., Abd-Allah, F., Palmiste, V., Margus, S., Toomsoo, T., Becquemin, J.-P., Bergeron, P., Abdulamit, T., Cardon, J.-M., Debus, S., Thomalla, G., Fiehler, J., Gerloss, C., Grzyska, U., Storck, M., LaMacchia, E., Eckstein, H.H., Söllner, H., Berger, H., Kallmayer, M., Popert, H., Zimmermann, A., Guenther, A., Klingner, C., Mayer, T., Schubert, J., Zanow, J., Scheinert, D., Banning-Eichenseer, U., Bausback, Y., Branzan, D., Braünilch, S., Lenzer, J., Schidt, A., Staab, H., Ulirch, M., Barlinn, J., Haase, K., Abramyuk, A., Bodechtel, U., Gerber, J., Reeps, C., Pfeiffer, T., Torello, G., Cöster, A., Giannoukas, A., Spanos, K., Matsagkas, M., Koutias, S., Vasdekis, S., Kakisis, J., Moulakakis, K., Lazaris, A., Liapas, C., Brountzos, E., Lazarides, M., Ioannou, N., Polydorou, A., Fulop, B., Fako, E., Voros, E., Bodosi, M., Nemeth, T., Barzo, P., Pazdernyik, S., Entz, L., Szeberin, Z., Dosa, E., Nemes, B., Jaranyi, Z., Pazdernyia, S., Madhaban, P., Hoffman, A., Nikolsky, E., Beyar, R., Casana, R., Tolva, V., Silingardi, R., Lauricella, A., Coppi, G., Nicoloci, E., Tusini, N., Strozzi, F., Vecchiati, E., Ferri, M., Ferrero, E., Psacharopulo, D., Gaggiano, A., Viazzo, A., Farchioni, L., Parlani, G., Caso, V., De Rangoy, P., Verzini, F., Castelli, P., DeLodovici, M.L., Carrafiello, G., Ierardi, A.M., Piffaretti, G., Nano, G., Occhiuto, M.T., Malacrida, G., Tealdi, D., Steghter, S., Stella, A., Pini, R., Faggioli, G., Sacca, S., Negri, M.D., Palombo, M., Perfumo, M.C., Fadda, G.F., Kasemi, H., Cernetti, C., Tonello, D., Visonà, A., Mangialardi, N., Ronchey, S., Altavista, M.C., Michelagnoli, S., Chisci, E., Speziale, F., Capoccia, L., Veroux, P., Giaquinta, A., Patti, F., Pulli, R., Boggia, P., Angiletta, D., Amatucci, G., Spinetti, F., Mascoli, F., Tsolaki, E., Civilini, E., Reimers, B., Setacci, C., Pogany, G., Odero, A., Accrocca, F., Bajardi, G., Takashi, I., Masayuki, E., Hidenori, E., Aidashova, B., Kospanov, N., Bakke, S., Skjelland, M., Czlonkowska, A., Kobayashi, A., Proczka, R., Dowzenko, A., Czepel, W., Polanski, J., Bialek, P., Ozkinis, G., Snoch-Ziólkiewicz, M., Gabriel, M., Stanisic, M., Iwanowski, W., Andziak, P., Gonçalves, F.B., Starodubtsev, V., Ignatenko, P., Karpenko, A., Radak, D., Aleksic, N., Sagic, D., Davidovic, L., Koncar, I., Tomic, I., Colic, M., Bartkoy, D., Rusnak, F., Gaspirini, M., Praczek, P., Milosevic, Z., Flis, V., Bergauer, A., Kobilica, N., Miksic, K., Matela, J., Blanco, E., Guerra, M., Riambau, V., Gillgren, P., Skioldebrand, C., Nymen, N., Berg, B., Delle, M., Formgren, J., Kally, T.B., Qvarfordt, P., Plate, G., Pärson, H., Lindgren, H., Bjorses, K., Gottsäter, A., Warvsten, M., Kristmundsson, T., Forssell, C., Malina, M., Holst, J., Kuhme, T., Sonesson, B., Lindblad, B., Kolbel, T., Acosta, S., Bonati, L., Traenka, C., Mueller, M., Lattman, T., Wasner, M., Mujagic, E., Von Hessling, A., Isaak, A., Stierli, P., Eugster, T., Mariani, L., Stippich, C., Wolff, T., Kahles, T., de Borst, G.J., Toorop, R., Moll, F., Lo, R., Meershoek, A., Jahrome, A.K., Vos, A.W.F., Schuiling, W., Keunen, R., Reijnen, M., Macsweeney, S., McConachie, N., Southam, A., Stansby, G., Lees, T., Lambert, D., Clarke, M., Wyatt, M., Kappadath, S., Wales, L., Jackson, R., Raudonaitis, A., MacDonald, S., Dunlop, P., Brown, A., Vetrivel, S., Bajoriene, M., Gopi, R., McCollum, C., Wolowczyk, L., Ghosh, J., Seriki, D., Ashleigh, R., Butterfield, J., Welch, M., Smyth, J.V., Briley, D., Schulz, U., Perkins, J., Hands, L., Kuker, W., Darby, C., Handa, A., Sekaran, L., Poskitt, K., Bulbulia, R., Morrison, J., Guyler, P., Grunwald, I., Brown, J., Jakeways, M., Tysoe, S., Hargroves, D., Gunathilagan, G., Insall, R., Senaratne, J., Beard, J., Cleveland, T., Nawaz, S., Lonsdale, R., Turner, D., Gaines, P., Nair, R., Chetter, I., Robinson, G., Akomolafe, B., Hatfield, J., Saastamoinen, K., Crinnion, J., Egun, A.A., Thomas, J., Drinkwater, S., D'Souza, S., Thomson, G., Gregory, B., Babu, S., Ashley, S., Joseph, T., Gibbs, R., Tebit, G., Mehrzad, A., Enevoldson, P., Mendalow, D., Parry, A., Tervitt, G., Clifton, A., Nazzel, M., Halliday, A., Peto, R., Pan, H., Potter, J., Bullbulia, R., Mihaylova, B., Flather, M., Mansfield, A., Simpson, D., Thomas, D., Gray, W., Farrell, B., Davies, C., Rahimi, K., Gough, M., Cao, P., Rothwell, P., Belli, A., Mafham, M., Herrington, W., Sandercock, P., Gray, R., Shearman, C., Molyneux, A., Gray, A., Clarke, A., Sneade, M., Tully, L., Brudlo, W., Lay, M., Munday, A., Berry, C., Tochlin, S., Cox, J., Kurien, R., Chester, J., de Waard, D.D., Huibers, A., and Bonati, L.H.

Published
2017
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76. BRAVISSIMO: 12-month results from a large scale prospective trial.

Author

Bosiers, M, Deloose, K, Callaert, Julie, Maene, L, Beelen, R, Keirse, Marc M.J.N.C., Verbist, J., Peeters, P, Schroë, H, Lauwers, G, Lansink, W, Vanslembroeck, K, D'archambeau, O, Hendriks, John, Lauwers, P, Vermassen, Frank, Randon, Caren, Van Herzeele, I, De Ryck, Frederic F.D., De Letter, J, Lanckneus, M, Van Betsbrugge, M, Thomas, B, Deleersnijder, R, Vandekerkhof, J, Baeyens, I, Berghmans, Thierry, Buttiens, J, Van Den Brande, Paul, Debing, Erik, Rabbia, C, Ruffino, A, Tealdi, D, Nano, G, Stegher, S, Gasparini, D, Piccoli, G, Coppieters De Gibson, Arnold G., Silingardi, R, Cataldi, V, Paroni, G, Palazzo, V, Stella, A, Gargiulo, Miriam, Muccini, N, Nessi, F, Ferrero, E, Pratesi, C, Fargion, A, Chiesa, R, Marone, E, Bertoglio, L, Cremonesi, A, Dozza, L, Galzerano, G, De Donato, G, Setacci, C., Bosiers, M, Deloose, K, Callaert, Julie, Maene, L, Beelen, R, Keirse, Marc M.J.N.C., Verbist, J., Peeters, P, Schroë, H, Lauwers, G, Lansink, W, Vanslembroeck, K, D'archambeau, O, Hendriks, John, Lauwers, P, Vermassen, Frank, Randon, Caren, Van Herzeele, I, De Ryck, Frederic F.D., De Letter, J, Lanckneus, M, Van Betsbrugge, M, Thomas, B, Deleersnijder, R, Vandekerkhof, J, Baeyens, I, Berghmans, Thierry, Buttiens, J, Van Den Brande, Paul, Debing, Erik, Rabbia, C, Ruffino, A, Tealdi, D, Nano, G, Stegher, S, Gasparini, D, Piccoli, G, Coppieters De Gibson, Arnold G., Silingardi, R, Cataldi, V, Paroni, G, Palazzo, V, Stella, A, Gargiulo, Miriam, Muccini, N, Nessi, F, Ferrero, E, Pratesi, C, Fargion, A, Chiesa, R, Marone, E, Bertoglio, L, Cremonesi, A, Dozza, L, Galzerano, G, De Donato, G, and Setacci, C.

Abstract

The BRAVISSIMO study is a prospective, non-randomized, multi-center, multi-national, monitored trial, conducted at 12 hospitals in Belgium and 11 hospitals in Italy. This manuscript reports the findings up to the 12-month follow-up time point for both the TASC A&B cohort and the TASC C&D cohort. The primary endpoint of the study is primary patency at 12 months, defined as a target lesion without a hemodynamically significant stenosis on Duplex ultrasound (>50%, systolic velocity ratio no greater than 2.0) and without target lesion revascularization (TLR) within 12 months. Between July 2009 and September 2010, 190 patients with TASC A or TASC B aortoiliac lesions and 135 patients with TASC C or TASC D aortoiliac lesions were included. The demographic data were comparable for the TASC A/B cohort and the TASC C/D cohort. The number of claudicants was significantly higher in the TASC A/B cohort, The TASC C/D cohort contains more CLI patients. The primary patency rate for the total patient population was 93.1%. The primary patency rates at 12 months for the TASC A, B, C and D lesions were 94.0%, 96.5%, 91.3% and 90.2% respectively. No statistical significant difference was shown when comparing these groups. Our findings confirm that endovascular therapy, and more specifically primary stenting, is the preferred treatment for patients with TASC A, B, C and D aortoiliac lesions. We notice similar endovascular results compared to surgery, however without the invasive character of surgery., info:eu-repo/semantics/published

Published
2013

84. SOME FURTHER RESULTS ON LIFTS OF LINEAR VECTOR FIELDS RELATED TO PRODUCT PRESERVING GAUGE BUNDLE FUNCTORS ON VECTOR BUNDLES.

Author

NITYAM, A., WANKAP NANO, G. F., and NDOMBOL, BITJONG

Subjects
*VECTOR fields, *VECTOR bundles, *GEOMETRIC connections, *LINEAR systems, *MATHEMATICAL analysis
Abstract

We present some lifts (associated to a product preserving gauge bundle functor on vector bundles) of sections of the dual bundle of a vector bundle, some derivations and linear connections on vector bundles. [ABSTRACT FROM AUTHOR]

Published
2016
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87. 2-Arylpropionic CXC Chemokine Receptor 1 (CXCR1) Ligands as Novel Noncompetitive CXCL8 Inhibitors

Author

Allegretti, M, Bertini, R, Cesta, M, Bizzarri, C, Di Bitondo, R, Di Cioccio, V, Galliera, E, Berdini, V, Topai, A, Zampella, G, Russo, V, Di Bello, N, Nano, G, Nicolini, L, Locati, M, Fantucci, P, Florio, S, Colotta, F, Cesta, MC, Colotta, F., ZAMPELLA, GIUSEPPE, FANTUCCI, PIERCARLO, Allegretti, M, Bertini, R, Cesta, M, Bizzarri, C, Di Bitondo, R, Di Cioccio, V, Galliera, E, Berdini, V, Topai, A, Zampella, G, Russo, V, Di Bello, N, Nano, G, Nicolini, L, Locati, M, Fantucci, P, Florio, S, Colotta, F, Cesta, MC, Colotta, F., ZAMPELLA, GIUSEPPE, and FANTUCCI, PIERCARLO

Abstract

The CXC chemokine CXCL8/IL-8 plays a major role in the activation and recruitment of polymorphonuclear (PMN) cells at inflammatory sites. CXCL8 activates PMNs by binding the seven-transmembrane (7-TM) G-protein-coupled receptors CXC chemokine receptor 1 (CXCR1) and CXC chemokine receptor 2 (CXCR2). (R)-Ketoprofen (1) was previously reported to be a potent and specific noncompetitive inhibitor of CXCLS-induced human PMNs chemotaxis. We report here molecular modeling studies showing a putative interaction site of 1 in the TM region of CXCR1. The binding model was confirmed by alanine scanning mutagenesis and photoaffinity labeling experiments. The molecular model driven medicinal chemistry optimization of 1 led to a new class of potent and specific inhibitors of CXCL8 biological activity. Among these, repertaxin (13) was selected as a clinical candidate drug for prevention of post-ischemia reperfusion injury. © 2005 American Chemical Society.

Published
2005

89. A practical synthesis of 7-azaindolylcarboxy-endo-tropanamide (DF 1012)

Author

Allegretti, M, Anacardio, R, Cesta, M, Curti, R, Mantovanini, M, Nano, G, Topai, A, Zampella, G, Cesta, MC, ZAMPELLA, GIUSEPPE, Allegretti, M, Anacardio, R, Cesta, M, Curti, R, Mantovanini, M, Nano, G, Topai, A, Zampella, G, Cesta, MC, and ZAMPELLA, GIUSEPPE

Abstract

An optimised cost-effective synthesis of the new antitussive drug, DF1012, is herewith reported. The new synthetic route to the key intermediate DF1005 is based on the unusual deprotection step of the 1-tert-butyl-3-cyano-7-azaindole intermediate, which can also be regarded as a convenient way for the industrial production of the expensive 7-azaindole 1. The second key intermediate, endo-tropanamine 6, was obtained in high yield by a novel one-pot stereoselective process using a Pd-catalysed reductive amination procedure.

Published
2003

96. Plasma levels of metalloproteinases-3 and -9 as markers of successful abdominal aortic aneurysm exclusion after endovascular graft treatment

Author

Sangiorgi, G, D'Averio, R, Mauriello, A, Bondio, M, Pontillo, M, Castelvecchio, S, Trimarchi, S, Tolva, V, Nano, G, Rampoldi, V, Spagnoli, L, Inglese, L, Sangiorgi, G, D'Averio, R, Mauriello, A, Bondio, M, Pontillo, M, Castelvecchio, S, Trimarchi, S, Tolva, V, Nano, G, Rampoldi, V, Spagnoli, L, and Inglese, L

Abstract

Background-Structural alterations of aortic wall resulting from degradation of matrix proteins by matrix metalloproteinases (MMPs) characterize abdominal aortic aneurysms (AAAs). No studies have compared circulating levels of MMPs after endovascular graft (EVG) exclusion in comparison with open surgical repair (OSR) in patients affected by AAA. Methods and Results-An abdominal angiography and CT scan were performed in all patients at the time of enrollment. A spiral CT scan was performed at 6 months to detect presence of endoleaks. MMP-3 and MMP-9 levels were measured before EVG (n=30) and OSR (n=15) treatments and at 1, 3, and 6 months of follow-up by a sandwich ELISA technique. Healthy volunteers (n=10) were used as control subjects. Immunohistochemical staining for MMP-9 and MMP-3 was performed on tissue samples from surgical cases. Both MMP-9 and MMP-3 mean basal levels were significantly higher in patients affected by AAA than in control subjects (32.3 +/- 20.7 ng/mL for EVG and 28 +/-9.9 ng/mL for OSR versus 8.9 +/-2.5 ng/mL, 2P <0.05; 18.3 +/-9.7 ng/mL and 26.7 +/- 10.8 ng/mL versus 8.2 +/-5.3 ng/mL, 2P <0.001). In the OSR group, both MMP-9 and MMP-3 mean levels decreased after surgery (28 +/-9.9 ng/mL at basal versus 14.7 +/-6.6 ng/mL at 6 months, 2P <0.001; 26.7 +/- 10.8 versus 12 +/-5.3 ng/mL; 2P <0.001). In the EVG group, a statistically significant difference at 6-month follow-up in MMP-9 and MMP-3 mean plasma values was detected in patients who had endoleakage in comparison with patients without endoleakage (44.3 +/- 20.7 versus 14.6 +/-7.0 ng/mL, 2P <0.005; 25 +/- 11.5 versus 10.3 +/-5.4 ng/mL, 2P <0.005). Conclusions-After EVG exclusion, MMP-9 and MMP-3 levels decreased to a level similar to that of patients undergoing OSR. In addition, a lack of decrease in MMP levels after EVG exclusion may help in identifying patients who will have endoleakage and consequent aneurysm expansion caused by continuous sac pressurization during follow

Published
2001

100. 4-36-14 Neurological consultations in the emergency room: An epidemiological study

Author

Sierra, H., primary, Bendersky, M., additional, Bohorquez, N., additional, Di Egidio, M., additional, Franco, A., additional, Fulgenzi, E., additional, Gonzalez, L., additional, Luraschi, A., additional, Mauriño, J., additional, Nano, G., additional, Oddo, S., additional, Piriz, S., additional, Portnoy, P., additional, Saizar, R., additional, Saposnik, G., additional, and Sica, R.E.P., additional

Published
1997
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