Metal enrichment in elliptical galaxies and globular clusters through the study of iron and H-beta spectral indices

Chemical evolution of elliptical galaxies and globular clusters is addressed through a combined study of the iron indices at 5270 and 5335 A, and of the H-Beta line strength. The observational database of 74 standard stars (both dwarfs and giants) referred to in a previous paper (Buzzoni et al. (1992)) complemented with the data of Faber et al. (1985) and Gorgas et al. (1993) allowed us to explore here Fe and H-Beta index dependence on stellar temperature, gravity, and metallicity. The derived fitting functions were then included into Buzzoni's (1989) code for population synthesis in order to derive expected integrated indices for simple stellar populations and compare with observations. Partition of metals in the current chemical mix of galaxies and globulars has been constrained supporting the claim that light alpha elements might be enhanced in the globular cluster metal-poor population. An alternative conclusion resting on the standard framework with (alpha/Fe) = 0 would require a systematically larger age, about 18-20 Gyr. Iron and magnesium in ellipticals are found in average solar but a systematic trend of (Mg/Fe) vs global metallicity does exist with iron more deficient with respect to magnesium at high Z. We conclude that this effect might indicate that Fe abundance per unit mass in the galaxies is constant (suggesting a constant rate per unit mass of SN I events) while light metals supplied by SNe II should have been more effectively enriched with increasing galactic total mass

Proteomic analysis of dopamine and \u3b1-synuclein interplay in a cellular model of Parkinson's disease pathogenesis

Altered dopamine homeostasis is an accepted mechanism in the pathogenesis of Parkinson\u2019s disease. a-Synuclein overexpression and impaired disposal contribute to this mechanism. However, biochemical alterations associated with the interplay of cytosolic dopamine and increased a-synuclein are still unclear. Catecholaminergic SH-SY5Y human neuroblastoma cells are a suitable model for investigating dopamine toxicity. In the present study, we report the proteomic pattern of SH-SY5Y cells overexpressing a-synuclein (1.6-fold induction) after dopamine exposure. Dopamine itself is able to upregulate a-synuclein expression. However, the effect is not observed in cells that already overexpress a-synuclein as a consequence of transfection. The proteomic analysis highlights significant changes in 23 proteins linked to specific cellular processes, such as cytoskeleton structure and regulation, mitochondrial function, energetic metabolism, protein synthesis, and neuronal plasticity. A bioinformatic network enrichment procedure generates a significant model encompassing all proteins and allows us to enrich functional categories associated with the combination of factors analyzed in the present study (i.e. dopamine together with a-synuclein). In particular, the model suggests a potential involvement of the nuclear factor kappa B pathway that is experimentally confirmed. Indeed, a-synuclein significantly reduces nuclear factor kappa B activation, which is completely quenched by dopamine treatment.Altered dopamine homeostasis is an accepted mechanism in the pathogenesis of Parkinson's disease. \u3b1-Synuclein overexpression and impaired disposal contribute to this mechanism. However, biochemical alterations associated with the interplay of cytosolic dopamine and increased \u3b1-synuclein are still unclear. Catecholaminergic SH-SY5Y human neuroblastoma cells are a suitable model for investigating dopamine toxicity. In the present study, we report the proteomic pattern of SH-SY5Y cells overexpressing \u3b1-synuclein (1.6-fold induction) after dopamine exposure. Dopamine itself is able to upregulate \u3b1-synuclein expression. However, the effect is not observed in cells that already overexpress \u3b1-synuclein as a consequence of transfection. The proteomic analysis highlights significant changes in 23 proteins linked to specific cellular processes, such as cytoskeleton structure and regulation, mitochondrial function, energetic metabolism, protein synthesis, and neuronal plasticity. A bioinformatic network enrichment procedure generates a significant model encompassing all proteins and allows us to enrich functional categories associated with the combination of factors analyzed in the present study (i.e. dopamine together with \u3b1-synuclein). In particular, the model suggests a potential involvement of the nuclear factor kappa B pathway that is experimentally confirmed. Indeed, \u3b1-synuclein significantly reduces nuclear factor kappa B activation, which is completely quenched by dopamine treatment. \ua9 2010 The Authors Journal compilation \ua9 2010 FEBS

Fracture Toughness And Microstructure In AA 2XXX Aluminum Alloys

The paper presents the toughness properties of forgings made of two AA 2xxx series aluminium alloys with different microstructural conditions. Fracture toughness tests in crack opening mode I were performed on compact tension specimens machined from the forgings in different orientations. The tests were performed both at room temperature and at 130?C. Fracture toughness properties were related to microstructural and fractographic features of the alloys in order to discuss on their failure mechanisms. The effect of the coarse intermetallic phases within grains or at their boundaries in the different conditions was underlined. The testing temperature, within the range here investigated, neither affected fracture toughness properties nor failure mechanisms

Characterization of a clonal human colon adenocarcinoma line intrinsically resistant to doxorubicin.

Intrinsic low-level resistance to anti-cancer drugs is a major problem in the treatment of gastrointestinal malignancies. To address the problem presented by intrinsically resistant tumours, we have isolated two monoclonal lines from LoVo human colon adenocarcinoma cells: LoVo/C7, which is intrinsically resistant to doxorubicin (DOX); and LoVo/C5, which shows the same resistance index for DOX as the mixed parental cell population. For comparison, we have included in the study a LoVo-resistant line selected by continuous exposure to DOX and expressing a typical multidrug resistant (MDR) phenotype. In these cell lines we have studied the expression and/or activity of a number of proteins, including P-glycoprotein 170 (P-gp), multidrug resistance-associated protein (MRP), lung resistance-related protein (LRP), glutathione (GSH)-dependent enzymes and protein kinase C (PKC) isoforms, which have been implicated in anti-cancer drug resistance. Intracellular DOX distribution has been assessed by confocal microscopy. The results of the present study indicate that resistance in LoVo/C7 cells cannot be attributed to alterations in P-gp, LRP or GSH/GSH-dependent enzyme levels. Increased expression of MRP, accompanied by alterations in the subcellular distribution of DOX, has been observed in LoVo/C7 cells; changes in PKC isoform pattern have been detected in both intrinsically and pharmacologically resistant cells