Al2O3, Al doped ZnO and SnO2 encapsulation of randomly oriented ZnO nanowire networks for high performance and stable electrical devices.

Two-dimensional randomly oriented nanowire (NW) networks, also called nanonets (NNs), have remarkable advantages including low-cost integration, good reproducibility and high sensitivity, which make them a promising material for electronic devices. With this work, we focus on the study of ZnO NNs as channel materials in field effect transistors (FETs). In our process, ZnO NWs were assembled in NNs by the liquid filtration method and were integrated in transistors, with the bottom-gate configuration, using simple technological steps. Non-encapsulated devices exhibited state of the art performances but their stability toward air exposure was poor. Using a proper encapsulation of the nanonets, with cheap, abundant and non-toxic oxides, we demonstrate our ability not only to stabilize their electrical properties, but also to enhance performance to values never reach before for ZnO NW-based transistors. Our best FETs exhibit a low Off-current while maintaining a very good On-current, which results in a I on/I off ratio exceeding 106 for a drain voltage of 5 V. The behavior of these ZnO NN-based FETs was studied for three different encapsulation materials, alumina (Al2O3), tin oxide (SnO2) and Al-doped ZnO (AZO). These results prove that ZnO NNs are highly promising materials for an easy and low-cost integration into FETs.

Biphasic airway-lung response to anaphylactic shock in Brown Norway rats.

Bronchospasm may be part of the response to systemic anaphylaxis in humans. The anaphylactic shock has been characterized in allergic rats, but little data are available on the concurrent changes in airway-lung mechanics. The aim was to describe the respiratory resistance (Rrs) and reactance (Xrs) response to ovalbumin (OVA) induced systemic anaphylaxis in allergic rats. Thirty five anesthetized and mechanically ventilated Brown Norway rats were randomly allocated to OVA (n=20) or vehicle (n=15) sensitization and provocation. Rrs and Xrs were obtained by the forced oscillation technique at 20 Hz. Allergic rats showed dramatic and reproducible concurrent Rrs peak and Xrs through within 4 min of OVA injection (p<0.0001). Thereafter, Rrs returned to baseline while Xrs remained significantly more negative (p<0.0001). It is concluded that systemic anaphylaxis in allergic rats is associated with severe early acute inhomogeneous bronchoconstriction followed by pulmonary interstitial/small airspace edema. The model may be of interest to assess treatments targeting the associated bronchoconstriction and/or airway vascular leakage.

Brown Norway rat ovalbumin-specific immunoglobulin E antibodies increase the human basophil expression of CD63 marker.

Anaphylactic shock is an immunoglobulin E (IgE)-dependent hypersensitivity. Biological tests like leucocyte histamine release (LHR) and human basophil activation (HBA), frequently used in human allergy, reflect both the amount of IgE fixed on cells and the cellular reactivity. To assess whether serum-specific IgE from Brown Norway (BN) rats prepared for ovalbumin (OVA)-induced anaphylactic shocks can activate human basophils which has a potential interest in experimental allergy: such a test could rapidly assert an IgE sensitization in laboratory animals genetically T-helper 2 (Th2)-predisposed. Rats (n = 39) were immunized three times (day 0, day 5 and day 21) with OVA injected subcutaneously. One week after the third immunization, a shock was induced with an intravenous (i.v.) bolus of OVA. Sensitization was assessed by passive cutaneous anaphylaxis (PCA) test and dosages of serum IgE antibodies anti-OVA by enzyme-linked immunosorbent assay. Blood basophils were counted before and during the shock. Before the shock induction (at day 21), an LHR test was performed on rat blood, and human basophils were sensitized with rat sera. HBA was demonstrated by the increase in the percentage of cells expressing CD63 antigen membrane, measured by flow cytometry. Twenty-one days after the first subcutaneous (s.c.) immunization, the rat serum induced a significant HBA. HBA was observed neither with the same serum previously heated nor with the serum from nonimmunized rats (NIRs). OVA-specific IgEs were significantly increased in immunized rat (IR) serum. The PCA test was negative when the serum was previously heated (56 degrees C). We never observed any circulating basophils, and LHR test was negative. After OVA i.v. administration, all IRs died rapidly. HBA testing strongly suggests a mediation by specific IgE in the increase of CD63 in BN rats. Thus, HBA test seems useful in assessing whether an experimental allergy was induced in animals genetically predisposed to an immune response, Th2-mediated, like BN rat. We also conclude that rat basophil activation does not participate in the histamine release during anaphylactic shock in sensitized BN rats.