Synthesis and characterization of ZnGa2O4 composites and its photocatalytic properties for energy applications.

ZnGa2O4 nanocomposites have been widely used for photocatalytic degradation of industrial dyes. In this work, ZnGa2O4 was synthesized from zinc sulphate heptahydrate ZnSO4.10H2O and Gallium (III) oxide (Ga2O3) by hydrothermal method. As prepared, ZnGa2O4 nanocomposites was used as a photocatalyst degradation of three organic dyes rhodamine-B, methylene blue, and methyl orange, under ultraviolet (UV) light irradiation. The ZnGa2O4 nanocomposites structure, morphology, size and optical properties were studied by X-ray diffraction (XRD), Fourier transform Raman spectroscopy (FT-Raman), scanning electron microscopy (SEM), Transmission electron microscopes (TEM) and photoluminescence spectra (PL). Moreover, the results explained the rate-controlling mechanisms of the dye degradation process followed by second-order kinetics. After 100 min of adsorption kinetic models, the decomposition of rhodamine-B (7.2 Ct mg/L, 5.2 Ct mg/L, and 4.1 Ct mg/L), methylene blue (42.8 qt mg/g, 44.8 qt mg/g, and 45.9 qt mg/g), and methyl orange (42.8 qe mg/g, 44.8 qe mg/g, and 45.9 qe mg/g) respectively. This investigation study offers a promising method to design more efficient ZnGa2O4 nanocomposites based photocatalytic degradation of industrial organic dyes.

Fluorinated surface-modifying macromolecules: modulating adhesive protein and platelet interactions on a polyether-urethane.

Polyether-urethanes (PEUs) have been the materials of choice for the manufacture of conventional blood-contacting devices. Nevertheless, biostability and blood compatibility are still among the principal limitations in their long-term application. Studies investigating the development of protective coatings for PEUs have shown that degradation can be reduced with the use of fluorinated surface-modifying macromolecules (SMMs). It has also been hypothesized that SMM-modified PEU surfaces may exhibit improved blood compatibility because other studies have shown a modulation in fibrinogen adsorption onto these surfaces. To determine the blood compatibility of a PEU-containing fluorinated SMMs, a series of in vitro experiments were designed to study the pattern of protein adsorption from plasma and then to assess the nature of platelet adhesion and activation on each substrate. Western blot analysis as well as single protein studies revealed that the dominant "adhesive proteins" [fibrinogen (Fg), fibronectin (Fnc), and vitronectin (Vnc)] were adsorbed on two of the SMM-containing PEUs in lower amounts relative to unmodified base. Platelet adhesion and activation data further highlighted the differences among the various substrates. It was shown that the unmodified base had a higher number of adhered platelets relative to the SMM-modified surfaces, and that of the SMM-containing substrates, which showed the lowest levels of adhesive proteins also, exhibited significantly lower platelet densities. Close morphological examination further revealed that platelets residing on these latter substrates were not appreciably activated. Based on the current evidence, it is believed that the fluorinated SMMs demonstrate good potential for the development of surfaces with minimal thrombogenic character in in vivo applications.

Transient inhibition by orotic acid does not abolish the in vivo response of rat hepatocytes to a direct mitogen, lead nitrate.

BACKGROUND: Orotic acid (OA) is able to inhibit hepatocyte proliferation in vivo induced by 2/3 partial hepatectomy. The present studies were aimed at establishing: (i) whether OA also inhibits hepatocyte proliferation induced by a direct mitogen and, if so (ii) whether the stimulus provided by the mitogen is still expressed following transient inhibition by OA. METHODS/RESULTS: In the first experiment male Wistar rats were injected with either lead nitrate (100 mumol/kg, i.v.) or saline and 20 h later some animals receiving the mitogen were also implanted with a 400-mg OA tablet (as OA-methyl ester. i.p.). Multiple injections of 3H-thymidine were given to each rat (50 microCi each, 6 h apart, i.p.) until 2 h before killing. All groups were killed 3 days after the initial treatment. Results indicated that OA almost completely inhibited hepatocyte DNA synthesis and labelling induced by lead nitrate (e.g. labelling index was 1.9 +/- 0.5% in the saline-treated group, 44.7 +/- 4.0% in the lead nitrate group and 1.4 +/- 0.3% in the group receiving lead nitrate + OA). Based on the above results, in a second experiment rats were given a similar dose of lead nitrate and a subset of animals was implanted 20 h later with a 400-mg OA tablet, as previously described. Multiple doses of 3H-thymidine were again given to each rat (20 microCi each, 6 h apart) until 2 h before killing. Animals from both groups were killed at 3, 6 or 8 days after lead nitrate. Results indicated that, while at day 3 lead nitrate-induced DNA synthesis was effectively inhibited by OA, at day 6 the proliferative response was resumed in the group receiving OA. Cumulative labelling index over 6 days was 30.3 +/- 1.4 in rats given the mitogen alone and 52.1 +/- 2.2 in the group exposed to lead nitrate + OA. CONCLUSIONS: These data indicate that: (i) OA is also able to inhibit hepatocyte proliferation induced by a direct mitogen such as lead nitrate; this, in turn, suggests that its inhibitory effect is not unique to the stimulus elicited by partial hepatectomy. (ii) The proliferative response triggered by the mitogen is not abolished by the transient (3-4 days) inhibitory phase imposed by OA. Possible mechanisms underlying these effects are considered in the discussion.