Characterization Of Boron Doped Nanocrystalline Diamonds

Nanostructured diamond doped with boron was prepared using a hot-filament assisted chemical vapour deposition system fed with an ethyl alcohol, hydrogen and argon mixture. The reduction of the diamond grains to the nanoscale was produced by secondary nucleation and defects induced by argon and boron atoms via surface reactions during chemical vapour deposition. Raman measurements show that the samples are nanodiamonds embedded in a matrix of graphite and disordered carbon grains, while morphological investigations using field electron scanning microscopy show that the size of the grains ranges from 20 to 100 nm. The lowest threshold fields achieved were in the 1.6 to 2.4 V/μm range. © 2008 IOP Publishing Ltd.100PART 5Himpsel, F.J., Knapp, J.A., VanVechten, J.A., Eastman, P.E., (1979) Phys. Rev., 20 B, p. 624Bandis, B., Pate, B.B., (1996) Appl. Phys Lett., 69, p. 366Mammana, V.P., Santos, T.E.A., Mammana, A., Baranauskas, V., Ceragioli, H.J., Peterlevitz, A.C., (2002) Appl. Phys. Lett., 81, p. 3470Baranauskas, V., Fontana, M., Ceragioli, H.J., Peterlevitz, A.C., (2004) Nanotech., 15 (10), pp. S678Shroder, R.E., Nemanich, R.J., Glass, J.T., (1990) Phys. Rev., 41 B, p. 3738Ferrari, A.C., Robertson, J., (2001) Phys. Rev., 63 B. , 121405(R)Jiang, X., Frederick, C.K.Au., Lee, S.T., (2002) J. Appl. Phys., 92 (5), p. 2880Lee, Y.C., Lin, S.J., Lin, I.N., Cheng, H.F., (2005) J. Appl. Phys., 97, p. 05431

Uniform algebras and approximation on manifolds

Let $\Omega \subset \mathbb{C}^n$ be a bounded domain and let $\mathcal{A} \subset \mathcal{C}(\bar{\Omega})$ be a uniform algebra generated by a set $F$ of holomorphic and pluriharmonic functions. Under natural assumptions on $\Omega$ and $F$ we show that the only obstruction to $\mathcal{A} = \mathcal{C}(\bar{\Omega})$ is that there is a holomorphic disk $D \subset \bar{\Omega}$ such that all functions in $F$ are holomorphic on $D$, i.e., the only obstruction is the obvious one. This generalizes work by A. Izzo. We also have a generalization of Wermer's maximality theorem to the (distinguished boundary of the) bidisk

Antiinflammatory therapy with canakinumab for atherosclerotic disease

BACKGROUND: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. METHODS: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P=0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P=0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P=0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P=0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P=0.31). CONCLUSIONS: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. Copyright © 2017 Massachusetts Medical Society