Asymmetries in the Value of Existence

According to asymmetric comparativism, it is worse for a person to exist with a miserable life than not to exist, but it is not better for a person to exist with a happy life than not to exist. My aim in this paper is to explain how asymmetric comparativism could possibly be true. My account of asymmetric comparativism begins with a different asymmetry, regarding the (dis)value of early death. I offer an account of this early death asymmetry, appealing to the idea of conditional goods, and generalize it to explain how asymmetric comparativism could possibly be true. I also address the objection that asymmetric comparativism has unacceptably antinatalist implications

Abundances of ammonia and carbon disulfide in the Jovian stratosphere following the impact of comet Shoemaker‐Levy 9

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/95648/1/grl8459.pd

A Search for Cosmic Microwave Background Anisotropies on Arcminute Scales with Bolocam

We have surveyed two science fields totaling one square degree with Bolocam at 2.1 mm to search for secondary CMB anisotropies caused by the Sunyaev- Zel'dovich effect (SZE). The fields are in the Lynx and Subaru/XMM SDS1 fields. Our survey is sensitive to angular scales with an effective angular multipole of l_eff = 5700 with FWHM_l = 2800 and has an angular resolution of 60 arcseconds FWHM. Our data provide no evidence for anisotropy. We are able to constrain the level of total astronomical anisotropy, modeled as a flat bandpower in C_l, with frequentist 68%, 90%, and 95% CL upper limits of 590, 760, and 830 uKCMB^2. We statistically subtract the known contribution from primary CMB anisotropy, including cosmic variance, to obtain constraints on the SZE anisotropy contribution. Now including flux calibration uncertainty, our frequentist 68%, 90% and 95% CL upper limits on a flat bandpower in C_l are 690, 960, and 1000 uKCMB^2. When we instead employ the analytic spectrum suggested by Komatsu and Seljak (2002), and account for the non-Gaussianity of the SZE anisotropy signal, we obtain upper limits on the average amplitude of their spectrum weighted by our transfer function of 790, 1060, and 1080 uKCMB^2. We obtain a 90% CL upper limit on sigma8, which normalizes the power spectrum of density fluctuations, of 1.57. These are the first constraints on anisotropy and sigma8 from survey data at these angular scales at frequencies near 150 GHz.Comment: 68 pages, 17 figures, 2 tables, accepted for publication in Ap

Combined functional and immunochemical analysis ofnormal and abnormal human factor

A B S T R A C T Human Factor X was isolated from Cohn fraction III and characterized by polyacrylamide gel electrophoresis, amino acid composition, and isoelectric focusing. Two molecular forms with biological activity were observed at isoelectric points of 4.8 and 5.0. Antisera generated to Factor X was monospecific and used to establish an equilibrium competitive inhibition radioimmunoassay. This assay was specific for human Factor X and did not cross-react with human prothrombin or bovine Factor X within the sensitivity range of 6-300 ng Factor X antigen/ml. The mean concentration of Factor X based on the antigen was 11.9 ,ug0ml, whereas concentration values based on coagulant activity was 7.8 ,ug/ml. This 30% difference in measurement appears to result from the presence of a subpopulation of Factor X molecules devoid of coagulant activity. The radioimmunoassay was used to qualitatively and quantitatively compare purified Factor X to plasmic Factor X obtained from normal, warfarintreated, acquired Factor X-deficient, and congenitaldeficient patients. In all but one case, the Factor X present in these plasmas was immunochemically identical to the purified Factor X and permitted precise quantitation of these abnormal Factor X molecules. Factor X procoagulant activity was analyzed relative to Factor X antigen and the specific activities were used to characterize normal and abnormal Factor X molecules. Reduced Factor X activity in plasmas from warfarin-treated and acquired Factor Xdeficient patients was attributed to both decreases in Factor X antigen and decreased function of the Factor X molecules. Congenitally deficient patients, in general, showed a reduction in Factor X antigen in parallel with Factor X procoagulant activities This is publicatio