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Li, Luying Ryan; Sydenham, Emma; Chaudhary, Bhuwan; Beecher, Deirdre; You, Chao; (2014)Glucocorticoid with cyclophosphamide for paraquat-induced lung fibrosis. The Cochrane database of systematic reviews, 8 (8). CD008084-. ISSN 1469-493X DOI: Full text not available from this repository.
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Manno, Daniela; Ker, Katharine; Roberts, Ian; (2014)Wie wirksam ist Tranexamsäure bei akuten gastrointestinalen Blutungen? Praxis, 103 (14). pp. 845-848. ISSN 1661-8157 DOI: -8157/a001712 Full text not available from this repository.
Mastellos, Nikolaos; Gunn, Laura H; Felix, Lambert M; Car, Josip; Majeed, Azeem; (2014)Transtheoretical model stages of change for dietary and physical exercise modification in weight loss management for overweight and obese adults. The Cochrane database of systematic reviews, 2014 (2). CD008066-. ISSN 1469-493X DOI:
Roberts, Ian; Coats, Timothy; Edwards, Phil; Gilmore, Ian; Jairath, Vipul; Ker, Katharine; Manno, Daniela; Shakur, Haleema; Stanworth, Simon; Veitch, Andrew; (2014)HALT-IT--tranexamic acid for the treatment of gastrointestinal bleeding: study protocol for a randomised controlled trial. Trials, 15 (1). 450-. ISSN 1745-6215 DOI: -6215-15-450
Roberts, Ian; Prieto-Merino, David; Manno, Daniela; (2014)Mechanism of action of tranexamic acid in bleeding trauma patients: an exploratory analysis of data from the CRASH-2 trial. Critical care (London, England), 18 (6). 685-. ISSN 1364-8535 DOI: -014-0685-8
Smith, Chris; Gold, Judy; Ngo, Thoai D; Sumpter, Colin; Free, Caroline; (2014)Mobile phone-based interventions for improving contraception use. The Cochrane database of systematic reviews, 2014 (6). ISSN 1469-493X DOI: Full text not available from this repository.
DI NARDO, M., LOCATELLI, F., DI FLORIO, F., CECCHETTI, C., AMODEO, A., RUTELLA, S. and BERTAINA, A., 2014.Extracorporeal membrane oxygenation as a bridge to allogeneic T-cell depleted hematopoietic stem cell transplantation in infants with severe combined immune deficiency: is it feasible? Intensive Care Medicine, 40 (10), pp. 1600-1601. ISSN 0342-4642
DI NARDO, M., LOCATELLI, F., PALMER, K., AMODEO, A., LORUSSO, R., BELLIATO, M., CECCHETTI, C., PERROTTA, D., PICARDO, S., BERTAINA, A., RUTELLA, S., RYCUS, P., DI CIOMMO, V. and HOLZGRAEFE, B., 2014.Extracorporeal membrane oxygenation in pediatric recipients of hematopoietic stem cell transplantation: an updated analysis of the Extracorporeal Life Support Organization experience. Intensive Care Medicine, 40 (5), pp. 754-756. ISSN 0342-4642
MOEIN-VAZIRI, N., PHILLIPS, I., SMITH, S., ALMINANA, C., MASIDE, C., GIL, M.A., ROCA, J., MARTINEZ, E.A., HOLT, W.V., POCKLEY, A.G. and FAZELI, A., 2014.Heat-shock protein A8 restores sperm membrane integrity by increasing plasma membrane fluidity. Reproduction, 147 (5), pp. 719-732. ISSN 1470-1626
WINTER, J., LETLEY, D., RHEAD, J., ATHERTON, J. and ROBINSON, K., 2014.Helicobacter pylori Membrane Vesicles Stimulate Innate Pro- and Anti-Inflammatory Responses and Induce Apoptosis in Jurkat T Cells. Infection and Immunity, 82 (4), pp. 1372-1381. ISSN 0019-9567
Aging seems to be associated with disturbances in regulation ofmultiple protective mechanisms in the brain, which are expressed in themitochondrial malfunctioning, the lowering of antioxidants level and, inturn, in ROS rising. These seem to initiate the neurodegenerative processesdevelopment, whereas the brain phenotype is biased to a form, which isatypical for normal aging (Dauer and Przedborski, 2003). Among factorsshifting the DAS balance and, consequently, affecting the interrelationsbetween the mechanisms of aging and neurodegeneration, the senescent cells(SC) involvement is thought to have priority. Indeed, thesenescence-associated secretory phenotype (SASP), arising fromsenescence-associated growth arrest (SAGA), has been shown either to activateor inhibit the brain adaptive mechanisms in relation to the diseaseprogression (Acosta et al., 2013). In early stage, SASP machinery, involvingcytokines, enzymes, growth factors, and extracellular matrix ingredients, isable to activate the repairing and remodeling mechanisms through thecytokines secretion and the release of growth factors and proteases. In laterstage, SC negatively affect these mechanisms by such SASP components asinterleukins (IL) through autocrine regulation of SAGA and paracrinemediation of surrounding cells. The latter is accompanied by the senescentphenotype transformation resulting in elimination of adaptive/regenerativeabilities of the cells (Tan et al., 2014; Chinta et al., 2015). SASPexpression has been shown to be under control of an inflammatory signal IL-1and, evoking local tissue inflammation and ROS rise in normal cells, to beable to induce both the aging of these cells and their transformation into SC(Passos et al., 2010; Acosta et al., 2013). SC populations have been revealedto rise intensively in PD and AD even at higher level than in aging (Chintaet al., 2015). In DAS, SC, originated predominantly from glial cells (Tan etal., 2014), are able to produce an inflammatory center accumulating ROS andother oxidizers. However, aging has been shown to be characterized by thelowering of anti-oxidative activities in DAS (Zucca et al., 2017), and the SCpopulation rising is expected to aggravate this deleterious process. Thus,DA-containing neurons in the SN and VTA seem to be suffered with both theoxidative stress and consecutive accumulation of neurotoxic derivates of theDA oxidation in the brain areas with highly concentrated DA terminals.Generated here ROS can be transient centers of DNA damage that is developedinto chronic damage DNA response (DDR), needed and sufficient for the steadystopping of both the cell growing and SASP production in the affected brainareas (Passos et al., 2010). In aging, PD, and AD, populations of DA neuronshave been shown to shrink, whereas those of SC to enlarge (Dauer andPrzedborski, 2003; Burns et al., 2005; Chinta et al., 2015). This negativecorrelation seemingly highlights the role of SC in disintegration of DAneurons in SN followed by the releasing of encapsulated NM into theextracellular space. The NM is able to be active for a long time and toinitiate chronic inflammation by neurotoxic compounds, which were previouslyadsorbed by NM's molecules (Zucca et al., 2017). Furthermore, theNM-containing granules seem to be targeted by activated microglia withrelease of iron ions from their binding with NM. These ions have beenrevealed to prevent the amyloid-beta (A[sz]) plaque generation, thus,supporting the toxicity of A[sz] oligomers (Liu et al., 2011). Furthermore,iron, in its free form, has been shown to induce a-synuclein aggregation thatis duplicated by 3,4-dihydroxyphenylaldehyde (DOPAL), a derivate of DAdistraction by the monoamine oxidase B (MAO-B). Oxidized form of DOPAL,3,4-dihydroxyphenylacetaldehyde-quinone (DOPAL-Q), binds covalently to lysineresidues on alpha-synuclein molecules, converting them to toxic synucleinoligomers. In particular, proto-fibrillar a-synuclein has been shown in vitroto be able to perforate the vesicle membranes and, thus, to stimulate theleakage of endogenous DA into the cytosol (Caudle et al., 2008; Zucca et al.,2017). A role of a-synuclein in the senescence mechanisms deserves to beanalyzed in details in further studies. 041b061a72