26 research outputs found
Relaxing the Big-bang Bound to the Baryon Density
In the standard picture of big-bang nucleosynthesis the yields of D, He,
He, and Li only agree with their inferred primordial abundances if the
fraction of critical density contributed by baryons is between and
( is the present value of the Hubble constant in units of
100\kms\Mpc^{-1}). This is the basis of the very convincing and important
argument that baryons can contribute at most 10\% of critical density and thus
cannot close the Universe. Nonstandard scenarios involving decaying
particles, inhomogeneities in the baryon density, and even more exotic
ideas put forth to evade this bound have been largely unsuccessful. We
suggest a new way of relaxing the bound: If the tau neutrino has a mass of
20\MeV-30\MeV and lifetime of , and its decay products
include electron neutrinos, the bound to the baryon mass density can be
loosened by a about factor of . The key is the decay-generated electron
antineutrinos: around the time of nucleosynthesis they are captured by protons
to produce neutrons, thereby changing the outcome of nucleosynthesis.
Experiments at colliders should soon be sensitive to a tau-neutrino
mass in the required range.Comment: 10p, FERMILAB Pub-94/059A, Figs available on reques
Impact of Type 2 Diabetes Susceptibility Variants on Quantitative Glycemic Traits Reveals Mechanistic Heterogeneity
Patients with established type 2 diabetes display both β-cell dysfunction and insulin resistance. To define fundamental processes leading to the diabetic state, we examined the relationship between type 2 diabetes risk variants at 37 established susceptibility loci, and indices of proinsulin processing, insulin secretion, and insulin sensitivity. We included data from up to 58,614 nondiabetic subjects with basal measures and 17,327 with dynamic measures. We used additive genetic models with adjustment for sex, age, and BMI, followed by fixed-effects, inverse-variance meta-analyses. Cluster analyses grouped risk loci into five major categories based on their relationship to these continuous glycemic phenotypes. The first cluster (PPARG, KLF14, IRS1, GCKR) was characterized by primary effects on insulin sensitivity. The second cluster (MTNR1B, GCK) featured risk alleles associated with reduced insulin secretion and fasting hyperglycemia. ARAP1 constituted a third cluster characterized by defects in insulin processing. A fourth cluster (TCF7L2, SLC30A8, HHEX/IDE, CDKAL1, CDKN2A/2B) was defined by loci influencing insulin processing and secretion without a detectable change in fasting glucose levels. The final group contained 20 risk loci with no clear-cut associations to continuous glycemic traits. By assembling extensive data on continuous glycemic traits, we have exposed the diverse mechanisms whereby type 2 diabetes risk variants impact disease predisposition