22 research outputs found
Formation and annealing of dislocation loops induced by nitrogen implantation of ZnO
Although zinc oxide is a promising material for the fabrication of short
wavelength optoelectronic devices, p-type doping is a step that remains
challenging for the realization of diodes. Out of equilibrium methods such as
ion implantation are expected to dope ZnO successfully provided that the
non-radiative defects introduced by implantation can be annealed out. In this
study, ZnO substrates are implanted with nitrogen ions, and the extended
defects induced by implantation are studied by transmission electron microscopy
and X-ray diffraction (XRD), before and after annealing at 900^{\circ}C. Before
annealing, these defects are identified to be dislocation loops lying either in
basal planes in high N concentration regions, or in prismatic planes in low N
concentration regions, together with linear dislocations. An uniaxial
deformation of 0.4% along the c axis, caused by the predominant basal loops, is
measured by XRD in the implanted layer. After annealing, prismatic loops
disappear while the density of basal loops decreases and their diameter
increases. Moreover, dislocation loops disappear completely from the
sub-surface region. XRD measurements show a residual deformation of only 0.05%
in the implanted and annealed layer. The fact that basal loops are favoured
against prismatic ones at high N concentration or high temperature is
attributed to a lower stacking fault energy in these conditions. The
coalescence of loops and their disappearance in the sub-surface region are
ascribed to point defect diffusion. Finally, the electrical and optical
properties of nitrogen-implanted ZnO are correlated with the observed
structural features.Comment: 8 page
Miconazole Oral Gel Enhances Acenocoumarol Anticoagulant Activity: A Report of Three Cases
Chemically assisted vapour transport for bulk ZnO crystal growth
International audienceA chemically assisted vapour phase transport (CVT) method is proposed for the growth of bulk ZnO crystals. Thermodynamic computations have confirmed the possibility of using CO as a sublimation activator for enhancing the sublimation rate of the feed material in a large range of pressures (10(-3) to 1 atm) and temperatures (800-1200 degrees C). Growth runs in a specific and patented design yielded single ZnO crystals up to 46 mm in diameter and 8 mm in thickness, with growth rates up to 400 mu m/h. These values are compatible with an industrial production rate. N type ZnO crystals (mu = 182 cm(2)/(V s) and n=7 10(15) cm(-3)) obtained by this CVT method (Chemical Vapour Transport) present a high level of purity (10-30 times better than hydrothermal ZnO crystals), which may be an advantage for obtaining p-type doped layers ([Li] and [Al] < 10(+15) cm(-3)). Structural (HR-XRD), defect density (EPD), electrical (Hall measurements) and optical (photoluminescence) properties are presented
The anti-inflammatory effects of platelet-derived microparticles in human plasmacytoid dendritic cells involve liver X receptor activation
When killers become thieves: Trogocytosed PD-1 inhibits NK cells in cancer
Trogocytosis modulates immune responses, with still unclear underlying molecular mechanisms. Using leukemia mouse models, we found that lymphocytes perform trogocytosis at high rates with tumor cells. While performing trogocytosis, both Natural Killer (NK) and CD8+ T cells acquire the checkpoint receptor PD-1 from leukemia cells. In vitro and in vivo investigation revealed that PD-1 on the surface of NK cells, rather than being endogenously expressed, was derived entirely from leukemia cells in a SLAM receptor–dependent fashion. PD-1 acquired via trogocytosis actively suppressed NK cell antitumor immunity. PD-1 trogocytosis was corroborated in patients with clonal plasma cell disorders, where NK cells that stained for PD-1 also stained for tumor cell markers. Our results, in addition to shedding light on a previously unappreciated mechanism underlying the presence of PD-1 on NK and cytotoxic T cells, reveal the immunoregulatory effect of membrane transfer occurring when immune cells contact tumor cells