The Approximate Capacity of the MIMO Relay Channel

Capacity bounds are studied for the multiple-antenna complex Gaussian relay channel with t1 transmitting antennas at the sender, r2 receiving and t2 transmitting antennas at the relay, and r3 receiving antennas at the receiver. It is shown that the partial decode-forward coding scheme achieves within min(t1,r2) bits from the cutset bound and at least one half of the cutset bound, establishing a good approximate expression of the capacity. A similar additive gap of min(t1 + t2, r3) + r2 bits is shown to be achieved by the compress-forward coding scheme.Comment: 8 pages, 5 figures, submitted to the IEEE Transactions on Information Theor

Estrogen Protects the Female Heart from Ischemia/Reperfusion Injury through Manganese Superoxide Dismutase Phosphorylation by Mitochondrial p38β at Threonine 79 and Serine 106.

A collective body of evidence indicates that estrogen protects the heart from myocardial ischemia/reperfusion (I/R) injury, but the underlying mechanism remains incompletely understood. We have previously delineated a novel mechanism of how 17β-estradiol (E2) protects cultured neonatal rat cardiomyocytes from hypoxia/reoxygenation (H/R) by identifying a functionally active mitochondrial pool of p38β and E2-driven upregulation of manganese superoxide dismutase (MnSOD) activity via p38β, leading to the suppression of reactive oxygen species (ROS) and apoptosis. Here we investigate these cytoprotective actions of E2 in vivo. Left coronary artery ligation and reperfusion was used to produce I/R injury in ovariectomized (OVX) female mice and in estrogen receptor (ER) null female mice. E2 treatment in OVX mice reduced the left ventricular infarct size accompanied by increased activity of mitochondrial p38β and MnSOD. I/R-induced infarct size in ERα knockout (ERKO), ERβ knockout (BERKO) and ERα and β double knockout (DERKO) female mice was larger than that in wild type (WT) mice, with little difference among ERKO, BERKO, and DERKO. Loss of both ERα and ERβ led to reduced activity of mitochondrial p38β and MnSOD at baseline and after I/R. The physical interaction between mitochondrial p38β and MnSOD in the heart was detected by co-immunoprecipitation (co-IP). Threonine 79 (T79) and serine 106 (S106) of MnSOD were identified to be phosphorylated by p38β in kinase assays. Overexpression of WT MnSOD in cardiomyocytes reduced ROS generation during H/R, while point mutation of T79 and S106 of MnSOD to alanine abolished its antioxidative function. We conclude that the protective effects of E2 and ER against cardiac I/R injury involve the regulation of MnSOD via posttranslational modification of the dismutase by p38β

Support Recovery of Sparse Signals

We consider the problem of exact support recovery of sparse signals via noisy measurements. The main focus is the sufficient and necessary conditions on the number of measurements for support recovery to be reliable. By drawing an analogy between the problem of support recovery and the problem of channel coding over the Gaussian multiple access channel, and exploiting mathematical tools developed for the latter problem, we obtain an information theoretic framework for analyzing the performance limits of support recovery. Sharp sufficient and necessary conditions on the number of measurements in terms of the signal sparsity level and the measurement noise level are derived. Specifically, when the number of nonzero entries is held fixed, the exact asymptotics on the number of measurements for support recovery is developed. When the number of nonzero entries increases in certain manners, we obtain sufficient conditions tighter than existing results. In addition, we show that the proposed methodology can deal with a variety of models of sparse signal recovery, hence demonstrating its potential as an effective analytical tool.Comment: 33 page