Chronic nitrogen fertilization and carbon sequestration in grassland soils: evidence of a microbial enzyme link

Chronic nitrogen (N) fertilization can greatly affect soil carbon (C) sequestration by altering biochemical interactions between plant detritus and soil microbes. In lignin-rich forest soils, chronic N additions tend to increase soil C content partly by decreasing the activity of lignin-degrading enzymes. In cellulose-rich grassland soils it is not clear whether cellulose-degrading enzymes are also inhibited by N additions and what consequences this might have on changes in soil C content. Here we address whether chronic N fertilization has affected (1) the C content of light versus heavier soil fractions, and (2) the activity of four extracellular enzymes including the C-acquiring enzyme β-1,4-glucosidase (BG; necessary for cellulose hydrolysis). We found that 19 years of chronic N-only addition to permanent grassland have significantly increased soil C sequestration in heavy but not in light soil density fractions, and this C accrual was associated with a significant increase (and not decrease) of BG activity. Chronic N fertilization may increase BG activity because greater N availability reduces root C:N ratios thus increasing microbial demand for C, which is met by C inputs from enhanced root C pools in N-only fertilized soils. However, BG activity and total root mass strongly decreased in high pH soils under the application of lime (i.e. CaCO3), which reduced the ability of these organo-mineral soils to gain more C per units of N added. Our study is the first to show a potential ‘enzyme link’ between (1) long-term additions of inorganic N to grassland soils, and (2) the greater C content of organo-mineral soil fractions. Our new hypothesis is that the ‘enzyme link’ occurs because (a) BG activity is stimulated by increased microbial C demand relative to N under chronic fertilization, and (b) increased BG activity causes more C from roots and from microbial metabolites to accumulate and stabilize into organo-mineral C fractions. We suggest that any combination of management practices that can influence the BG ‘enzyme link’ will have far reaching implications for long-term C sequestration in grassland soils

Conformational altered p53 affects neuronal function: relevance for the response to toxic insult and growth-associated protein 43 expression

The role of p53 in neurodegenerative diseases is essentially associated with neuronal death. Recently an alternative point of view is emerging, as altered p53 conformation and impaired protein function have been found in fibroblasts and blood cells derived from Alzheimer's disease patients. Here, using stable transfected SH-SY5Y cells overexpressing APP751wt (SY5Y-APP) we demonstrated that the expression of an unfolded p53 conformation compromised neuronal functionality. In particular, these cells showed (i) augmented expression of amyloid precursor protein (APP) and its metabolites, including the C-terminal fragments C99 and C83 and β-amyloid peptide (ii) high levels of oxidative markers, such as 4-hydroxy-2-nonenal Michael-adducts and 3-nitro-tyrosine and (iii) altered p53 conformation, mainly due to nitration of its tyrosine residues. The consequences of high-unfolded p53 expression resulted in loss of p53 pro-apoptotic activity, and reduction of growth-associated protein 43 (GAP-43) mRNA and protein levels. The role of unfolded p53 in cell death resistance and lack of GAP-43 transcription was demonstrated by ZnCl(2) treatment. Zinc supplementation reverted p53 wild-type tertiary structure, increased cells sensitivity to acute cytotoxic injury and GAP-43 levels in SY5Y-APP clone

Use of amido Grignard reagents in inorganic chemistry : Synthesis and crystal structure of anti-[Pd(Cl)(py)(mu-2,6-Pri2C6H3NH)](2)

Treating a pyridine (py) solution of PdCl2(py)(2) with a tetrahydrofuran or diethyl ether solution of the amido Grignard reagent 2,6-(Pr2C6H3NH)-C-1(MgCl) afforded a dimeric palladium complex, containing two bridging amido groups, which has been structurally characterised

Danno da black out: la Cassazione esclude la risarcibilità del danno non patrimoniale

Il danno non patrimoniale, derivante dalla lesione dei diritti inviolabili della persona, come tali costituzionalmente garantiti, \ue8 risarcibile \u2013 sulla base di una interpretazione costituzionalmente orientata dell\u2019art. 2059 c.c. - anche quando non sussista un fatto-reato, n\ue9 ricorre alcune delle altre ipotesi in cui la legge consente espressamente il ristoro dei pregiudizi non patrimoniali, a tre condizioni: a) che l'interesse leso - e non il pregiudizio sofferto - abbia rilevanza costituzionale; b) che la lesione dell'interesse sia grave, nel senso che l'offesa superi una soglia minima di tollerabilit\ue0; c) che il danno non sia futile, vale a dire che non consista in meri disagi o fastidi, ovvero nella lesione di diritti del tutto immaginari, come quello alla qualit\ue0 della vita e alla felicit\ue0. [massima non ufficiale]. \u201cNon \ue8 risarcibile il danno non patrimoniale subito dall'utente in conseguenza dell'interruzione della somministrazione di energia elettrica addebitabile al gestore della rete di distribuzione, ove la parte non indichi, n\ue9 provi, quale sia lo specifico diritto inviolabile costituzionalmente garantito, leso in modo serio\u201d[massima non ufficiale]. Cass. civ., sez. VI, sent., 28 febbraio 2013 n. 509

BRINGING THE WAR HOME:ETHICS AND JUSTICE IN A (POST) FEMINIST DEPICTION OF ABU GHRAIB

In this dissertation, my ambition is to consider ethics and justice in relation to six anti war photomontages by the American artist Martha Rosler from her 2004 series Bringing the War Home: House Beautiful, new series (fig. 1-6), which is a reprise of a previous set of re-photographed collage by her of the same title that circulated during the war in Vietnam

Amyloid Plaques Beyond Aβ: A Survey of the Diverse Modulators of Amyloid Aggregation

Aggregation of the amyloid-β (Aβ) peptide is strongly correlated with Alzheimer’s disease (AD). Recent research has improved our understanding of the kinetics of amyloid fibril assembly and revealed new details regarding different stages in plaque formation. Presently, interest is turning toward studying this process in a holistic context, focusing on cellular components which interact with the Aβ peptide at various junctures during aggregation, from monomer to cross-β amyloid fibrils. However, even in isolation, a multitude of factors including protein purity, pH, salt content, and agitation affect Aβ fibril formation and deposition, often producing complicated and conflicting results. The failure of numerous inhibitors in clinical trials for AD suggests that a detailed examination of the complex interactions that occur during plaque formation, including binding of carbohydrates, lipids, nucleic acids, and metal ions, is important for understanding the diversity of manifestations of the disease. Unraveling how a variety of key macromolecular modulators interact with the Aβ peptide and change its aggregation properties may provide opportunities for developing therapies. Since no protein acts in isolation, the interplay of these diverse molecules may differentiate disease onset, progression, and severity, and thus are worth careful consideration