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  1. When the users in a MIMO broadcast channel experience different spatial transmit correlation matrices, a class of gains is produced that is denoted transmit correlation diversity. This idea was conceived for channels in which transmit correlation matrices have mutually exclusive eigenspaces, allowing non-interfering training and transmission. This paper broadens the scope of transmit correlation diversity to the case of partially and fully overlapping eigenspaces and introduces techniques to harvest these generalized gains. For the two-user MIMO broadcast channel, we derive achievable degrees of freedom (DoF) and achievable rate regions with/without channel state information at the receiver (CSIR). When CSIR is available, the proposed achievable DoF region is tight in some configurations of the number of receive antennas and the channel correlation ranks. We then extend the DoF results to the K-user case by analyzing the interference graph that characterizes the overlapping structure of the eigenspaces. Our achievability results employ a combination of product superposition in the common part of the eigenspaces, and pre-beamforming (rate splitting) to create multiple data streams in non-overlapping parts of the eigenspaces. Massive MIMO is a natural example in which spatially correlated link gains are likely to occur. We study the achievable downlink sum rate formore »a frequency-division duplex massive MIMO system under transmit correlation diversity.« less
  2. Free, publicly-accessible full text available May 1, 2023
  3. Abstract

    Integrating results from genome-wide association studies (GWASs) and gene expression studies through transcriptome-wide association study (TWAS) has the potential to shed light on the causal molecular mechanisms underlying disease etiology. Here, we present a probabilistic Mendelian randomization (MR) method, PMR-Egger, for TWAS applications. PMR-Egger relies on a MR likelihood framework that unifies many existing TWAS and MR methods, accommodates multiple correlated instruments, tests the causal effect of gene on trait in the presence of horizontal pleiotropy, and is scalable to hundreds of thousands of individuals. In simulations, PMR-Egger provides calibrated type I error control for causal effect testing in the presence of horizontal pleiotropic effects, is reasonably robust under various types of model misspecifications, is more powerful than existing TWAS/MR approaches, and can directly test for horizontal pleiotropy. We illustrate the benefits of PMR-Egger in applications to 39 diseases and complex traits obtained from three GWASs including the UK Biobank.

  4. Although mouse models of Alzheimer’s disease (AD) have provided tremendous breakthroughs, the etiology of later onset AD remains unknown. In particular, tau pathology in the association cortex is poorly replicated in mouse models. Aging rhesus monkeys naturally develop cognitive deficits, amyloid plaques, and the same qualitative pattern and sequence of tau pathology as humans, with tangles in the oldest animals. Thus, aging rhesus monkeys can play a key role in AD research. For example, aging monkeys can help reveal how synapses in the prefrontal association cortex are uniquely regulated compared to the primary sensory cortex in ways that render them vulnerable to calcium dysregulation and tau phosphorylation, resulting in the selective localization of tau pathology observed in AD. The ability to assay early tau phosphorylation states and perform high-quality immunoelectron microscopy in monkeys is a great advantage, as one can capture early-stage degeneration as it naturally occurs in situ. Our immunoelectron microscopy studies show that phosphorylated tau can induce an “endosomal traffic jam” that drives amyloid precursor protein cleavage to amyloid-β in endosomes. As amyloid-β increases tau phosphorylation, this creates a vicious cycle where varied precipitating factors all lead to a similar phenotype. These data may help explain why circuitsmore »with aggressive tau pathology (e.g., entorhinal cortex) may degenerate prior to producing significant amyloid pathology. Aging monkeys therefore can play an important role in identifying and testing potential therapeutics to protect the association cortex, including preventive therapies that are challenging to test in humans.

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