Microstructural characterisation of TiAlTiAu and TiAlPdAu ohmic contacts to AlGaN/GaN

Ti/Al/Ti/Au and Ti/Al/Pd/Au contacts to AlGaN/GaN have been investigated to ascertain the effect of annealing temperature on the structural evolution of the contacts. Ti/Al/Ti/Au contacts become ohmic after rapid thermal annealing at 750°C or higher, corresponding to the formation of an interfacial TiN phase, with inclusions penetrating through the AlGaN layer observed after annealing at 950°C. The Pd layer is shown to be more efficient at inhibiting diffusion of Au to the interface than Ti. Ohmic behaviour was not seen with the Ti/Al/Pd/Au scheme. Either the presence of Au at the interface may improve ohmic behaviour, or the Ti:Al ratio is insufficient in this scheme

Microstructural characterisation of TiAlTiAu and TiAlPdAu ohmic contacts to AlGaN/GaN

Ti/Al/Ti/Au and Ti/Al/Pd/Au contacts to AlGaN/GaN have been investigated to ascertain the effect of annealing temperature on the structural evolution of the contacts. Ti/Al/Ti/Au contacts become ohmic after rapid thermal annealing at 750°C or higher, corresponding to the formation of an interfacial TiN phase, with inclusions penetrating through the AlGaN layer observed after annealing at 950°C. The Pd layer is shown to be more efficient at inhibiting diffusion of Au to the interface than Ti. Ohmic behaviour was not seen with the Ti/Al/Pd/Au scheme. Either the presence of Au at the interface may improve ohmic behaviour, or the Ti:Al ratio is insufficient in this scheme

Synthesis of secretory component by rat hepatocytes in culture.

Normal rat hepatocytes were isolated and cultivated in vitro. Synthesis of secretory component was demonstrated by its accumulation in the culture medium, as measured by radioimmunoassay; by incorporation of 14C-leucine in the protein specifically precipitated with anti-secretory component antiserum; and by a positive precipitin reaction of concentrated culture medium with the same antiserum. The results explain the high levels of secretory component found in rat bile and render plausible a mechanism of hepatic IgA transfer involving secretory component as the hepatocyte membrane receptor for polymeric IgA

Natalizumab plus interferon beta-1a for relapsing multiple sclerosis.

Item does not contain fulltextBACKGROUND: Interferon beta is used to modify the course of relapsing multiple sclerosis. Despite interferon beta therapy, many patients have relapses. Natalizumab, an alpha4 integrin antagonist, appeared to be safe and effective alone and when added to interferon beta-1a in preliminary studies. METHODS: We randomly assigned 1171 patients who, despite interferon beta-1a therapy, had had at least one relapse during the 12-month period before randomization to receive continued interferon beta-1a in combination with 300 mg of natalizumab (589 patients) or placebo (582 patients) intravenously every 4 weeks for up to 116 weeks. The primary end points were the rate of clinical relapse at 1 year and the cumulative probability of disability progression sustained for 12 weeks, as measured by the Expanded Disability Status Scale, at 2 years. RESULTS: Combination therapy resulted in a 24 percent reduction in the relative risk of sustained disability progression (hazard ratio, 0.76; 95 percent confidence interval, 0.61 to 0.96; P=0.02). Kaplan-Meier estimates of the cumulative probability of progression at two years were 23 percent with combination therapy and 29 percent with interferon beta-1a alone. Combination therapy was associated with a lower annualized rate of relapse over a two-year period than was interferon beta-1a alone (0.34 vs. 0.75, P<0.001) and with fewer new or enlarging lesions on T(2)-weighted magnetic resonance imaging (0.9 vs. 5.4, P<0.001). Adverse events associated with combination therapy were anxiety, pharyngitis, sinus congestion, and peripheral edema. Two cases of progressive multifocal leukoencephalopathy, one of which was fatal, were diagnosed in natalizumab-treated patients. CONCLUSIONS: Natalizumab added to interferon beta-1a was significantly more effective than interferon beta-1a alone in patients with relapsing multiple sclerosis. Additional research is needed to elucidate the benefits and risks of this combination treatment. (ClinicalTrials.gov number, NCT00030966.)