Search Results - (Author, Cooperation:A. Saitta)
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1Latest Papers from Table of Contents or Articles in PressL. Tedersoo ; M. Bahram ; S. Polme ; U. Koljalg ; N. S. Yorou ; R. Wijesundera ; L. Villarreal Ruiz ; A. M. Vasco-Palacios ; P. Q. Thu ; A. Suija ; M. E. Smith ; C. Sharp ; E. Saluveer ; A. Saitta ; M. Rosas ; T. Riit ; D. Ratkowsky ; K. Pritsch ; K. Poldmaa ; M. Piepenbring ; C. Phosri ; M. Peterson ; K. Parts ; K. Partel ; E. Otsing ; E. Nouhra ; A. L. Njouonkou ; R. H. Nilsson ; L. N. Morgado ; J. Mayor ; T. W. May ; L. Majuakim ; D. J. Lodge ; S. S. Lee ; K. H. Larsson ; P. Kohout ; K. Hosaka ; I. Hiiesalu ; T. W. Henkel ; H. Harend ; L. D. Guo ; A. Greslebin ; G. Grelet ; J. Geml ; G. Gates ; W. Dunstan ; C. Dunk ; R. Drenkhan ; J. Dearnaley ; A. De Kesel ; T. Dang ; X. Chen ; F. Buegger ; F. Q. Brearley ; G. Bonito ; S. Anslan ; S. Abell ; K. Abarenkov
American Association for the Advancement of Science (AAAS)
Published 2014Staff ViewPublication Date: 2014-11-29Publisher: American Association for the Advancement of Science (AAAS)Print ISSN: 0036-8075Electronic ISSN: 1095-9203Topics: BiologyChemistry and PharmacologyComputer ScienceMedicineNatural Sciences in GeneralPhysicsKeywords: DNA Barcoding, Taxonomic ; Forests ; Fungi/*classification/genetics/*physiology ; Geography ; Grassland ; *Soil ; *Soil Microbiology ; TundraPublished by: -
2Articles: DFG German National LicensesSaitta, A. Marco ; Klein, Michael L.
College Park, Md. : American Institute of Physics (AIP)
Published 1999Staff ViewISSN: 1089-7690Source: AIP Digital ArchiveTopics: PhysicsChemistry and PharmacologyNotes: The mechanical resistance of a polyethylene strand subject to tension and the way its properties are affected by the presence of a knot is studied using first-principles molecular dynamics calculations. The distribution of strain energy for the knotted chains has a well-defined shape that is very different from the one found in the linear case. The presence of a knot significantly weakens the chain in which it is tied. Chain rupture invariably occurs just outside the entrance to the knot, as is the case for a macroscopic rope. © 1999 American Institute of Physics.Type of Medium: Electronic ResourceURL: -
3Articles: DFG German National LicensesStaff View
ISSN: 1089-7690Source: AIP Digital ArchiveTopics: PhysicsChemistry and PharmacologyNotes: The effect of stretching a polymer sample containing a single trefoil knot has been studied by computer simulation molecular dynamics calculations. Under axial load that approximates a fiber extrusion process, the knot is found to nucleate crystallization of the sample, which occurs on the ns time scale. The extension of the strain field associated with the knot has been quantified. © 2002 American Institute of Physics.Type of Medium: Electronic ResourceURL: -
4Articles: DFG German National LicensesSaitta, A. Marco ; Soper, Paul D. ; Wasserman, E. ; Klein, Michael L.
[s.l.] : Macmillan Magazines Ltd.
Published 1999Staff ViewISSN: 1476-4687Source: Nature Archives 1869 - 2009Topics: BiologyChemistry and PharmacologyMedicineNatural Sciences in GeneralPhysicsNotes: [Auszug] Many experiments have been done to determine the relative strengths of different knots, and these show that the break in a knotted rope almost invariably occurs at the point just outside the ‘entrance’ to the knot. The influence of knots on the properties of polymers has become of ...Type of Medium: Electronic ResourceURL: -
5Articles: DFG German National LicensesStaff View
ISSN: 0165-4608Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002Topics: MedicineType of Medium: Electronic ResourceURL: -
6Articles: DFG German National LicensesSquadrito, F. ; Ioculano, M. ; Altavilla, D. ; Zingarelli, B. ; Canale, P. ; Campo, G. M. ; Saitta, A. ; Oriti, S. ; Faggiotto, A. ; Caputi, A. P.
Springer
Published 1993Staff ViewISSN: 1420-908XSource: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Abstract We investigated the effect of BAY u3405, a thromboxane A2 receptor antagonist in pentobarbital anaesthetized rats subjected to left main coronary artery ligation (1 h) followed by reperfusion (1 h; MI/R). Sham operated rats were used as controls (Sham MI/R). Survival rate, myocardial necrosis, myocardial myeloperoxidase activity (investigated as an index of leukocyte adhesion and accumulation) and serum creatine phosphokinase activity were studied. Ischaemia-reperfusion injury significantly reduced the survival rate (45%), caused a marked myocardial necrosis, increased serum creatine phosphokinase activity (Sham MI/R=26±10.2 U/ml; MI/R=213±19 U/ml) and produced a rise in myocardial myeloperoxidase activity in the area-at-risk and in the necrotic area (6.1±0.4 U×10−3/g tissue and 6.7±0.9 U×10−3/g of tissue, respectively). The administration of BAY u3405 (30 and 60 mg/kg/i.v., 30 min before occlusion) significantly increased survival rate, lowered the area of myocardial necrosis, blunted the increase in serum creatine phosphokinase activity and reduced the increase in myeloperoxidase activity in both the area-at-risk and the necrotic area. Furthermore, the protective effect of BAY u3405 was dose-dependent. These data are consistent with an involvement of TXA2 in myocardial ischaemia-reperfusion injury and suggest that BAY u3405 may represent a novel therapeutic approach to the treatment of acute ischaemia-reperfusion injury.Type of Medium: Electronic ResourceURL: -
7Articles: DFG German National LicensesSquadrito, F. ; Saitta, A. ; Altavilla, D. ; Ioculano, M. ; Canale, P. ; Campo, G. M. ; Squadrito, G. ; Tano, G. ; Mazzu', A. ; Caputi, A. P.
Springer
Published 1996Staff ViewISSN: 1420-908XKeywords: E-selectin ; Intercellular adhesion molecule 1 ; Myocardial infarction ; Leukocytes ; EndotheliumSource: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Abstract The aim was to investigate circulating E-selectin and Intercellular Adhesion Molecule-1 (ICAM-1) in acute myocardial infarction. Our study was carried out in 80 patients, 40 hospitalized for acute myocardial infarction (AMI), 20 suffering from chronic stable angina and 20 healthy control subjects. Samples of venous blood were taken from all patients at the moment of hospitalization and after 2, 4, 6, 8, 10, 12 and 24 hours from the thrombolytic treatment (AMI+urokinase) or conventional therapy (AMI+nitroglycerin), for the dosage of creatinine kinase (CK) and adhesion molecules. The CK was determined by means of a Hitachi 901 automatic analyser using an enzymatic method (reagents Boheringer-Biochemia, Germany). Soluble E-selectin (sE-selectin) and soluble ICAM-1 (sICAM-1) were measured in the serum using a specific immunoassay (British Biotechnology Products). The serum levels of Tumor Necrosis Factor (TNF-α) were evaluated using an immunoenzymatic assay to quantitate the serum levels of the cytokine British Biotechnology Products). Patients with acute myocardial infarction (AMI) had increased serum levels of soluble E-selectin (sE-selectin; AMI+urokinase= 312±20 ng/ml; AMI+nitroglycerin=334±15 ng/ml) and soluble ICAM-1 (sICAM-1; AMI+urokinase= 629±30ng/ml; AMI+nitroglycerin=655±25 ng/ml) compared to both patients with chronic angina (sE-selectin =67±10 ng/ml; sICAM-1=230±20 ng/ml) and healthy control subjects (sE-selectin=53±15 ng/ml; sICAM-1 200±16 ng/ml). Furthermore patients with acute myocardial infarction also had increased serum levels of Tumor Necrosis Factor (TNF-α=309±10 pg/ml; control subjects=13±5 pg/ml). Thrombolytic therapy with urokinase (1,000,000 IU as an intravenous bolus for 5 minutes, followed by an infusion of an additional 1,000,000 IU for the following two hours) succeeded in producing reperfusion and reduced the serum levels of sE-selectin (52±13 ng/ml) and sICAM-1 (202±31 ng/ml). In contrast patients not eligible for thrombolytic therapy and therefore treated with conventional therapy (a continuous i.v. infusion of nitroglycerin at the dose of 50 mg/die) did not show any significant reduction in both sE-selectin and sICAM-1 throughout the study. Our results confirm previous experimental data and indicate that adhesion mechanisms supporting leukocyte-endothelium interaction may also be operative in human acute myocardial infarction.Type of Medium: Electronic ResourceURL: -
8Articles: DFG German National LicensesAltavilla, D. ; Squadrito, F. ; Ammendolia, L. ; Squadrito, G. ; Campo, G. M. ; Canale, P. ; Ioculano, M. ; Musolino, C. ; Alonci, A. ; Sardella, A. ; Urna, G. ; Saitta, A. ; Caputi, A. P.
Springer
Published 1996Staff ViewISSN: 1420-908XKeywords: Monocytes ; Lymphocytes ; Ischaemia-reperfusion injurySource: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Abstract We investigated the role played by monocytes and lymphocytes in the pathogenesis of experimental shock. Splanchnic artery occlusion (SAO) shock was induced in anaesthetized rats by clamping splanchnic arteries for 45 min followed by reperfusion. Sham operated animals were used as controls. SAO shocked rats had a decreased survival time (80±11 min, while sham shocked rats survived more than 4 h), increased serum (248±21 U/ml) and macrophage (145±15 U/ml) levels of TNF-α, enhanced myeloperoxidase (MPO) activity in the ileum (3.38±0.2 U×10−3/g tissue), decreased number of monocytes, lymphocytes and neutrophils and a profound hypotension. In addition we found an increased expression of vascular cell adhesion molecule-1 (VCAM-1) on aortic endothelium and a reduced percentage of VLA-4 positive monocytes and lymphocytes. Inhibition of TNF-α synthesis, reversed the increased endothelial expression of VCAM-1, increased the percentage of integrin VLA-4 positive leukocytes and improved monocyte, lymphocyte and neutrophil count. Furthermore a passive immunization with specific antibodies raised against VCAM-1 (2 mg/kg, i.v. 3 h before SAO) increased survival, reduced MPO activity in the ileum (0.034±0.04 U×10−3/g tissue) and improved mean arterial blood pressure. Our data suggest that monocytes and lymphocytes participate in the pathogenesis of splanchnic ischaemia-reperfusion injury and may amplify the adhesion of neutrophils to peripheral tissues.Type of Medium: Electronic ResourceURL: