A cellular wireless communication system in which data is transmitted to multiple users over a common channel is considered. When the base stations in this system can cooperate with each other, the link from the base stations to the users can be considered a multi-user multiple-input multiple-output (MIMO) downlink system. For such a system, it is known from information theory that the total rate of transmission can be enhanced by cooperation. The channel is assumed to be fixed for all transmissions over the period of interest and the ratio of anticipated average arrival rates for the users, also known as the relative traffic rate, is fixed. A packet-based model is considered where data for each user is queued at the transmit end. We consider a simple policy which, under Markovian assumptions, is known to be throughput-optimal for this coupled queueing system. Since an exact expression for the performance of this policy is not available, as a measure of performance, we establish a heavy traffic diffusion approximation. To arrive at this diffusion approximation, we use two key properties of the policy; we posit the first property as a reasonable manifestation of cooperation, and the second property follows from coordinate convexity of the capacity region. The diffusion process is a semimartingale reflecting Brownian motion (SRBM) living in the positive orthant of N-dimensional space (where N is the number of users). This SRBM has one direction of reflection associated with each of the 2 N −1 boundary faces, but show that, in fact, only those directions associated with the (N−1)-dimensional boundary faces matter for the heavy traffic limit. The latter is likely of independent theoretical interest.

Objective Mutations in the gene encoding the prion protein (PrP) are responsible for approximately 10 to 15% of cases of prion disease in humans, including Creutzfeldt-Jakob disease (CJD). Here, we report on the discovery of a previously unreported C-terminal PrP mutation (A224V) in a CJD patient exhibiting a disease similar to the rare VV1 subtype of sporadic (s) CJD and investigate the role of this mutation in prion replication and transmission. Methods We generated transgenic (Tg) mice expressing human PrP with the V129 polymorphism and A224V mutation, denoted Tg(HuPrP,V129,A224V) mice, and inoculated them with different subtypes of sCJD prions. Results Transmission of sCJD VV2 or MV2 prions was accelerated in Tg(HuPrP,V129,A224V) mice, compared to Tg(HuPrP,V129) mice, with incubation periods of ∼110 and ∼210 days, respectively. In contrast, sCJD MM1 prions resulted in longer incubation periods in Tg(HuPrP,V129,A224V) mice, compared to Tg(HuPrP,V129) mice (∼320 vs. ∼210 days). Prion strain fidelity was maintained in Tg(HuPrP,V129,A224V) mice inoculated with sCJD VV2 or MM1 prions, despite the altered replication kinetics. Interpretation Our results suggest that A224V is a risk factor for prion disease and modulates the transmission behavior of CJD prions in a strain-specific manner, arguing that residues near the C-terminus of PrP are important for controlling the kinetics of prion replication.

Measurements of two-particle correlations on transverse momentum pt for Au-Au collisions at sqrt sNN = 130 GeV are presented. Significant large-momentum-scale correlations are observed for charged primary hadrons with 0.15 <_ pt <_ 2 GeV/c and pseudorapidity lbar eta rbar <_ 1.3. Such correlations were not observed in a similar study at lower energy and are not predicted by theoretical collision models. Their direct relation to mean-pt fluctuations measured in the same angular acceptance is demonstrated. Positive correlations are observed for pairs of particles which have large pt values while negative correlations occur for pairs in which one particle has large pt and the other has much lower pt. The correlation amplitudes per final state particle increase with collision centrality. The 3 observed correlations are consistent with a scenario in which the transverse momentum of hadrons