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This is a reply to the paper “Actual or virtual habitats? Commentary to «Manual for monitoring species and habitats of EC interest (Directive 92/43/CEE) in Italy: habitats»”. We used some additional information to clarify keypoints raised in the paper.

Dinuclear copper(II) complexes with N-substituted ligands as superoxide dismutase (SOD) mimics are investigated. The new N-(thiazol-2-yl)toluenesulfonamide (Htz-tol) and N-(thiazol-2-yl)toluenesulfonamide (Htz-tol) and N-(thiazol-2-yl)naphthalene-sulfonamide (Htz-naf) ligands are prepared and structurally characterized.

Chandra observations of the nearby, Lyman-continuum (LyC) emitting galaxy Tol 1247-232 resolve the X-ray emission and show that it is dominated by a point-like source with a hard spectrum (Γ = 1.6 ± 0.5) and a high luminosity [(9 ± 2) × 1040 erg s-1]. Comparison with an earlier XMM-Newton observation shows flux variation of a factor of 2. Hence, the X-ray emission likely arises from an accreting X-ray source: a low-luminosity active galactic nucleus or one or a few X-ray binaries. The Chandra X-ray source is similar to the point-like, hard spectrum (- = 1.2 ± 0.2), high-luminosity (1041 erg s-1) source seen in Haro 11, which is the only other confirmed LyC-emitting galaxy that has been resolved in X-rays. We discuss the possibility that accreting X-ray sources contribute to LyC escape. [ABSTRACT FROM AUTHOR]

The interaction of hemin with the first 18-amino acid repeat in tau protein has been investigated at both the N-terminal free-amine (R1τ) and N-acetylated (AcR1τ) forms for its potential relevance in traumatic brain injury and possibly other neurodegenerative diseases. The binding properties of hemin-R1τ and hemin-AcR1τ were compared with those of the hemin complex with amyloid-β peptide fragment 1–16 (Aβ16) and synthetic hemins. AcR1τ and R1τ bind with moderate affinity to both monomeric and dimeric hemin to form 1 : 1 complexes, but for the acetylated peptide, the affinity is one order of magnitude larger (K1 = 3.3 × 106 M−1). The binding constants were similar to that of Aβ16 for hemin, but unlike the latter, neither of the two R1τ peptides forms a 2 : 1 complex with hemin. This is mostly due to electrostatic repulsion between R1τ chains, and in particular the C-terminal proline-15 kink, while structural features of the hemin-R1τ complexes do not seem to play a role. In fact, the same features are observed for the interaction between ferric heme and peptide R1τ*, where the P15 residue is replaced by an alanine. Imidazole neither binds to [hemin(R1τ)] nor [hemin(AcR1τ)], whereas small ligands such as CN and CO easily bind to the ferric and ferrous forms of the complexes, respectively. A detailed comparative study of the peroxidase activity of [hemin(R1τ)] and [hemin(AcR1τ)] shows that such activity is very low. Thus, the association between heme and unfolded neuronal peptides does not, per se, involve a significant gain of toxic pseudo-enzymatic activity. However, under conditions of heavy heme release occurring on traumatic brain injury or when this activity is prolonged for long time, it can contribute to neuronal oxidative stress. In addition, the presence of hemin increases the aggregation propensity of R1τ. [ABSTRACT FROM AUTHOR]

Cytotoxicity and morphological transformation has been studied in BALB/3T3 CI A31–1–1 mouse embryo cells for ammonium vanadate [vanadium(V)] and vanadyl sulphate[vanadium(IV)] alone or in combination with diethylmaleate(DEM), a cellular glutathione (GSH)-depleting agent.Cells exposed for 24 h to 10 M vanadium(V) alone or in combination with 3×10M DEM showed the characteristic hyperfine EPR signal of vanadium(IV), which was more obvious in the case of exposure to vanadium(V) alone.This suggests that the amount of vanadium(V) reduced to vanadium(IV) decreased in GSH-depleted cells. While vanadium(IV) at concentrations of 3×10M and 10 M was not transforming in the cells, vanadium(V) showed neoplastic transforming activity (< 0.025 and < 0.001 for the two doses, respectively) in comparison to controls(vanadium unexposed cells). Cytotoxicity and morphological transformation in cells exposed to vanadium(V) in combination with 3×M DEM were significantly more intensive ( < 0.005 and < 0.01 for the two doses of vanadate tested) compared to the corresponding values observed in cells exposed to vanadium(V) alone.This suggests that the final transforming activity response is dependent on the intracellular GSH-mediated mechanism of reduction of vanadium(V) to vanadium (IV): (i) the extent to which vanadium(V) should be bioreduced to less toxic vanadium(IV) via intracellular GSH is a key point in determining the intensity of the observed neoplastic action; (ii) the carcinogenic potential of vanadium(V) should be strictly dependent on its intracellular persistence which could lead to changes in normal metabolic patterns of vanadium(V) in the oxidized form due to lack of GSH-mediated reduction. [ABSTRACT FROM PUBLISHER]

Cytotoxicity, morphological transformation and cellular retention have been studied in BALB/03T3 Cl A 31-1-1 cells for ammonium or sodium vanadate [vanadium(V)] and for vanadyl sulphate [vanadium(IV)]. A morphological transformation focus assay showed transforming activity for vanadium(V) ( < 0.005 at concentrations of 3 × 10 or higher) while vanadium(IV) was not transforming in the cells. Cytotoxicity was higher for vanadium(V) than for vanadium(IV); this was particularly clear at doses from 5 × 10 to 5 × 10 M. The cellular retention of both vanadate and vanadyl compounds at 24, 48 and 72 h incubation was similar. At concentrations lower than 10 M vanadate, the retention was linear with the dose, while at higher exposures the vanadium taken up by the cells levelled off or slightly decreased. Exposure to 10 M and 10 M vanadium(V) for 3 and 24 h as well as to 10 M for 48 and 72 h yielded > 94% vanadium in the cytosol, but exposure to a toxic dose (10 M) for 48 and 72 h yielded 20% vanadium associated with cellular organelles, which suggests that some sites in the cytosol become saturated with vanadium. The corresponding gel-filtration experiments indicate that a redistribution of the element among the cytosol components occurs with time. [ABSTRACT FROM PUBLISHER]

Parkinson's disease is a neurodegenerative disorder characterized by the death of dopaminergic neurons and by accumulation of alpha-synuclein (aS) aggregates in the surviving neurons. The dopamine catabolite 3,4-dihydroxyphenylacetaldehyde (DOPAL) is a highly reactive and toxic molecule that leads to aS oligomerization by covalent modifications to lysine residues. Here we show that DOPAL-induced aS oligomer formation in neurons is associated with damage of synaptic vesicles, and with alterations in the synaptic vesicles pools. To investigate the molecular mechanism that leads to synaptic impairment, we first aimed to characterize the biochemical and biophysical properties of the aS-DOPAL oligomers; heterogeneous ensembles of macromolecules able to permeabilise cholesterol-containing lipid membranes. aS-DOPAL oligomers can induce dopamine leak in an in vitro model of synaptic vesicles and in cellular models. The dopamine released, after conversion to DOPAL in the cytoplasm, could trigger a noxious cycle that further fuels the formation of aS-DOPAL oligomers, inducing neurodegeneration. [ABSTRACT FROM AUTHOR]

A new enzymatic method is reported for the assay of vitamin C in fruits and vegetables using peroxidase in the presence of hydrogen peroxide. The method is based on the colorimetric detection of the highly colored products of oxidation of 1,4-diaminobenzene, added as synthetic substrate, that can be taken as the end-point for the oxidation of vitamin C. No interference by other biological compounds contained in the fruits and vegetables was found. The method is as accurate and rapid as the traditional method employing ascorbate oxidase but has the additional advantages of requiring a much cheaper enzyme and no expensive instrumentation. [ABSTRACT FROM AUTHOR]

Knowledge about the three different types of IV connectors (negative, positive, and neutral) is imperative to cancer care as specific and distinct interventions can help prevent occlusions and catheter-related bloodstream infections that can lead to increased morbidity with infections and loss of treatment time and mortality. Nurses have responsibilities associated with nursing research, education, and evidence-based practice that should support the outcomes of best patient care when using IV connectors. [ABSTRACT FROM AUTHOR]