Spatially Coupled LDPC Codes for Two-User Decode-and-Forward Relaying'

We present a decode-and-forward transmission scheme that is based on spatially coupled LDPC codes and applies to a network consisting of two sources, one relay, and one destination. The relay performs network coding to achieve full diversity. We prove analytically that the proposed scheme achieves the Shannon limit on the binary erasure relay channel for symmetric channel conditions. Using density evolution, we furthermore demonstrate that our scheme approaches capacity also for asymmetric channel conditions

The adipocyte differentiation protein APMAP is an endogenous suppressor of Aβ production in the brain

The deposition of amyloid-beta (Aβ) aggregates in the brain is a major pathological hallmark of Alzheimer's disease (AD). Aβ is generated from the cleavage of C-terminal fragments of the amyloid precursor protein (APP-CTFs) by γ-secretase, an intramembrane-cleaving protease with multiple substrates, including the Notch receptors. Endogenous modulation of γ-secretase is pointed to be implicated in the sporadic, age-dependent form of AD. Moreover, specifically modulating Aβ production has become a priority for the safe treatment of AD because the inhibition of γ-secretase results in adverse effects that are related to impaired Notch cleavage. Here, we report the identification of the adipocyte differentiation protein APMAP as a novel endogenous suppressor of Aβ generation. We found that APMAP interacts physically with γ-secretase and its substrate APP. In cells, the partial depletion of APMAP drastically increased the levels of APP-CTFs, as well as uniquely affecting their stability, with the consequence being increased secretion of Aβ. In wild-type and APP/ presenilin 1 transgenic mice, partial adeno-associated virus-mediated APMAP knockdown in the hippocampus increased Aβ production by ∼20 and ∼55%, respectively. Together, our data demonstrate that APMAP is a negative regulator of Aβ production through its interaction with APP and γ-secretase. All observed APMAP phenotypes can be explained by an impaired degradation of APP-CTFs, likely caused by an altered substrate transport capacity to the lysosomal/autophagic syste

The adipocyte differentiation protein APMAP is an endogenous suppressor of Aβ production in the brain

The deposition of amyloid-beta (Aβ) aggregates in the brain is a major pathological hallmark of Alzheimer's disease (AD). Aβ is generated from the cleavage of C-terminal fragments of the amyloid precursor protein (APP-CTFs) by γ-secretase, an intramembrane-cleaving protease with multiple substrates, including the Notch receptors. Endogenous modulation of γ-secretase is pointed to be implicated in the sporadic, age-dependent form of AD. Moreover, specifically modulating Aβ production has become a priority for the safe treatment of AD because the inhibition of γ-secretase results in adverse effects that are related to impaired Notch cleavage. Here, we report the identification of the adipocyte differentiation protein APMAP as a novel endogenous suppressor of Aβ generation. We found that APMAP interacts physically with γ-secretase and its substrate APP. In cells, the partial depletion of APMAP drastically increased the levels of APP-CTFs, as well as uniquely affecting their stability, with the consequence being increased secretion of Aβ. In wild-type and APP/ presenilin 1 transgenic mice, partial adeno-associated virus-mediated APMAP knockdown in the hippocampus increased Aβ production by ∼20 and ∼55%, respectively. Together, our data demonstrate that APMAP is a negative regulator of Aβ production through its interaction with APP and γ-secretase. All observed APMAP phenotypes can be explained by an impaired degradation of APP-CTFs, likely caused by an altered substrate transport capacity to the lysosomal/autophagic system

Author Correction: Loss of the adaptor protein ShcA in endothelial cells protects against monocyte macrophage adhesion, LDL-oxydation, and atherosclerotic lesion formation (Scientific Reports DOI: 10.1038/s41598-018-22819-3)

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A Novel Ecdysone Receptor Mediates Steroid-Regulated Developmental Events during the Mid-Third Instar of Drosophila

The larval salivary gland of Drosophila melanogaster synthesizes and secretes glue glycoproteins that cement developing animals to a solid surface during metamorphosis. The steroid hormone 20-hydroxyecdysone (20E) is an essential signaling molecule that modulates most of the physiological functions of the larval gland. At the end of larval development, it is known that 20E—signaling through a nuclear receptor heterodimer consisting of EcR and USP—induces the early and late puffing cascade of the polytene chromosomes and causes the exocytosis of stored glue granules into the lumen of the gland. It has also been reported that an earlier pulse of hormone induces the temporally and spatially specific transcriptional activation of the glue genes; however, the receptor responsible for triggering this response has not been characterized. Here we show that the coordinated expression of the glue genes midway through the third instar is mediated by 20E acting to induce genes of the Broad Complex (BRC) through a receptor that is not an EcR/USP heterodimer. This result is novel because it demonstrates for the first time that at least some 20E-mediated, mid-larval, developmental responses are controlled by an uncharacterized receptor that does not contain an RXR-like component

Spatially Coupled LDPC Codes for Two-User Decode-and-Forward Relaying

We present a decode-and-forward transmission scheme that is based on spatially coupled LDPC codes and applies to a network consisting of two sources, one relay, and one destination. The relay performs network coding to achieve full diversity. We prove analytically that the proposed scheme achieves the Shannon limit on the binary erasure relay channel for symmetric channel conditions. Using density evolution, we furthermore demonstrate that our scheme approaches capacity also for asymmetric channel conditions

Error Probability Bounds for Decode-and-Forward Relaying with two Correlated Sources

We derive bounds on the error probability of optimal and sub-optimal detectors in an uncoded decode-and-forward relay system with two correlated information sources. This setup is relevant to wireless sensor networks where nearby sensors collect spatially correlated data. We show that taking into account the source correlation at the relay and at the destination leads to significant performance gains. Simulation results corroborate the tightness of our analytical bounds

Error Probability Bounds for Decode-and-Forward Relaying with Correlated Sources

We derive bounds on the error probability of optimal and sub-optimal detectors in an uncoded decode-and-forward relay system with two correlated information sources. This setup is relevant to wireless sensor networks where nearby sensors collect spatially correlated data. We show that taking into account the source correlation at the relay and at the destination leads to significant performance gains. Simulation results corroborate the tightness of our analytical bounds

Error probability bounds for decode-and-forward relaying with two correlated sources

We derive bounds on the error probability of optimal and sub- optimal detectors in an uncoded decode-and-forward relay system with two correlated information sources. This setup is relevant to wireless sensor networks where nearby sensors collect spatially correlated data. We show that taking into account the source correlation at the relay and at the destination leads to significant performance gains. Simulation results corroborate the tightness of our analytical bounds