Sensing-Assisted Receivers for Resilient-By-Design 6G MU-MIMO Uplink

We address the resilience of future 6G MIMO communications by considering an uplink scenario where multiple legitimate transmitters try to communicate with a base station in the presence of an adversarial jammer. The jammer possesses full knowledge about the system and the physical parameters of the legitimate link, while the base station only knows the UL-channels and the angle-of-arrival (AoA) of the jamming signals. Furthermore, the legitimate transmitters are oblivious to the fact that jamming takes place, thus the burden of guaranteeing resilience falls on the receiver. For this case we derive one optimal jamming strategy that aims to minimize the rate of the strongest user and multiple receive strategies, one based on a lower bound on the achievable signal-to-interference-to-noise-ratio (SINR), one based on a zero-forcing (ZF) design, and one based on a minimum SINR constraint. Numerical studies show that the proposed anti-jamming approaches ensure that the sum rate of the system is much higher than without protection, even when the jammer has considerably more transmit power and even if the jamming signals come from the same direction as those of the legitimate users.Comment: Accepted to 3rd IEEE International Symposium on Joint Communications & Sensin

Systemic infection exacerbates cerebrovascular dysfunction in Alzheimer's disease

We studied the effects of systemic infection on brain cytokine level and cerebral vascular function in Alzheimer’s disease (AD) and vascular dementia (VaD), in superior temporal cortex (BA22) from AD (n = 75), VaD (n = 22) and age-matched controls (n = 46), stratified according to the presence or absence of terminal systemic infection. Brain cytokine levels were measured using Mesoscale Discovery Multiplex Assays and markers of cerebrovascular function were assessed by ELISA. Multiple brain cytokines were elevated in AD and VaD: interleukin (IL)-15 and IL-17A were maximally elevated in end-stage Alzheimer’s disease (Braak tangle stage V-VI) whereas IL-2, IL-5, IL12p40 and IL-16 were highest in intermediate Braak tangle stage III-IV disease. Several cytokines (IL-1β, IL-6, TNF-α, IL-8 and IL-15) were further raised in AD with systemic infection. Cerebral hypoperfusion, indicated by decreased myelin-associated glycoprotein:proteolipid protein-1 (MAG:PLP1) and increased vascular endothelial growth factor-A (VEGF), and blood-brain barrier leakiness, indicated by raised levels of fibrinogen, were exacerbated in AD and VaD, and also in non-dementia controls, with systemic infection. Aβ42 level did not vary with infection or in association with brain cytokine levels. In controls, cortical perfusion declined with increasing interferon-γ (IFN-γ), IL-2, IL-4, IL-6, IL-10, IL-12p70, IL-13 and tumour necrosis factor-α (TNF-α) but these relationships were lost with progression of AD, and with infection (even in BS 0-II brains). Cortical platelet-derived growth factor receptor-β (PDGFRβ), a pericyte marker, was reduced, and endothelin-1 (EDN1) level was increased in AD; these were related to Aβ level and disease progression and only modestly affected by systemic infection. Our findings indicate that systemic infection alters brain cytokine levels and exacerbates cerebral hypoperfusion and BBB leakiness associated with AD and VaD, independently of the level of insoluble Aβ. Our findings highlight systemic infection as an important contributor to dementia, requiring early identification and treatment in the elderly population

Haemoglobin scavenging after subarachnoid haemorrhage

Rapid and effective clearance of cell-free haemoglobin after subarachnoid haemorrhage (SAH) is important to prevent vasospasm and neurotoxicity and improve long-term outcome. Haemoglobin is avidly bound by haptoglobin, and the complex is cleared by CD163 expressed on the membrane surface of macrophages. We studied the kinetics of haemoglobin and haptoglobin in cerebrospinal fluid after SAH. We show that haemoglobin levels rise gradually after SAH. Haptoglobin levels rise acutely with aneurysmal rupture as a result of injection of blood into the subarachnoid space. Although levels decline as haemoglobin scavenging occurs, complete depletion of haptoglobin does not occur and levels start rising again, indicating saturation of CD163 sites available for haptoglobin-haemoglobin clearance. In a preliminary neuropathological study we demonstrate that meningeal CD163 expression is upregulated after SAH, in keeping with a proinflammatory state. However, loss of CD163 occurs in meningeal areas with overlying blood compared with areas without overlying blood. Becauses ADAM17 is the enzyme responsible for shedding membrane-bound CD163, its inhibition may be a potential therapeutic strategy after SAH

On the Need of Analog Signals and Systems for Digital-Twin Representations

We consider the task of converting different digital descriptions of analog bandlimited signals and systems into each other, with a rigorous application of mathematical computability theory. Albeit very fundamental, the problem appears in the scope of digital twinning, an emerging concept in the field of digital processing of analog information that is regularly mentioned as one of the key enablers for next-generation cyber-physical systems and their areas of application. In this context, we prove that essential quantities such as the peak-to-average power ratio and the bounded-input/bounded-output norm, which determine the behavior of the real-world analog system, cannot generally be determined from the system's digital twin, depending on which of the above-mentioned descriptions is chosen. As a main result, we characterize the algorithmic strength of Shannon's sampling type representation as digital twin implementation and also introduce a new digital twin implementation of analog signals and systems. We show there exist two digital descriptions, both of which uniquely characterize a certain analog system, such that one description can be algorithmically converted into the other, but not vice versa

Capacity of Gaussian MIMO Bidirectional Broadcast Channels

We consider the broadcast phase of a three-node network, where a relay node establishes a bidirectional communication between two nodes using a spectrally efficient two-phase decode-and-forward protocol. In the first phase the two nodes transmit their messages to the relay node. Then the relay node decodes the messages and broadcasts a re-encoded composition of them in the second phase. We consider Gaussian MIMO channels and determine the capacity region for the second phase which we call the Gaussian MIMO bidirectional broadcast channel.Comment: Proc. IEEE International Symposium on Information Theory (ISIT 2008), Toronto, Canada, July 200

Rapid neuroinflammatory changes in human acute intracerebral hemorrhage

Objective Spontaneous intracerebral hemorrhage (ICH) is the commonest form of hemorrhagic stroke and is associated with a poor prognosis. Neurosurgical removal of intracerebral hematoma has limited benefit and no pharmacotherapies are available. In acute ICH, primary tissue damage is followed by secondary pathology, where the cellular and neuroinflammatory changes are poorly understood. Methods We studied histological changes in postmortem tissue from a cohort of spontaneous supra‐tentorial primary ICH cases (n = 27) with survival of 1–12 days, compared to a matched control group (n = 16) examined in corresponding regions. Hematoxylin–eosin and microglial (Iba1) immunolabelled sections were assessed at 0–2, 3–5, and 7–12 days post‐ICH. Results Peri‐hematoma, the observed ICH‐related changes include edema, tissue neutrophils and macrophages from day 1. Ischemic neurons and swollen endothelial cells were common at day 1 and universal after day 5, as were intramural erythrocytes within small vessel walls. Activated microglia were evident at day 1 post‐ICH. There was a significant increase in Iba1 positive area fraction at 0–2 (threefold), 3–5 (fourfold), and 7–12 days post ICH (ninefold) relative to controls. Giant microglia were detected peri‐hematoma from day 5 and consistently 7–12 days post‐ICH. Interpretation Our data indicate that neuroinflammatory processes commence from day 1 post‐ICH with changing microglial size and morphology following ICH and up to day 12. From day 5 some microglia exhibit a novel multiply nucleated morphology, which may be related to changing phagocytic function. Understanding the time course of neuroinflammatory changes, post‐ICH may reveal novel targets for therapy and brain restoration

Metaflammasome components in the human brain: a role in dementia with alzheimer's pathology?

Epidemiological and genetic studies have identified metabolic disorders and inflammation as risk factors for Alzheimer's disease (AD). Evidence in obesity and type-2 diabetes suggests a role for a metabolic inflammasome (“metaflammasome”) in mediating chronic inflammation in peripheral organs implicating IKKβ (inhibitor of nuclear factor kappa-B kinase subunit beta), IRS1 (insulin receptor substrate 1), JNK (c-jun N-terminal kinase), and PKR (double-stranded RNA protein kinase). We hypothesized that these proteins are expressed in the brain in response to metabolic risk factors in AD. Neocortex from 299 participants from the MRC Cognitive Function and Ageing Studies was analysed by immunohistochemistry for the expression of the phosphorylated (active) form of IKKβ [pSer176/180], IRS1 [pS312], JNK [pThr183/Tyr185] and PKR [pT451]. The data were analyzed to investigate whether the proteins were expressed together and in relation with metabolic disorders, dementia, Alzheimer's pathology and APOE genotype. We observed a change from a positive to a negative association between the proteins and hypertension according to the dementia status. Type-2 diabetes was negatively related with the proteins among participants without dementia; whereas participants with dementia and AD pathology showed a positive association with JNK. A significant association between IKKβ and JNK in participants with dementia and AD pathology was observed, but not in those without dementia. Otherwise, weak to moderate associations were observed among the protein loads. The presence of dementia was significantly associated with JNK and negatively associated with IKKβ and IRS1. Cognitive scores showed a significant positive relationship with IKKβ and a negative with IRS1, JNK and PKR. The proteins were significantly associated with pathology in Alzheimer's participants with the relationship being inverse or not significant in participants without dementia. Expression of the proteins was not related to APOE genotype. These findings highlight a role for these proteins in AD pathophysiology but not necessarily as a complex

Secrecy Results for Compound Wiretap Channels

We derive a lower bound on the secrecy capacity of the compound wiretap channel with channel state information at the transmitter which matches the general upper bound on the secrecy capacity of general compound wiretap channels given by Liang et al. and thus establishing a full coding theorem in this case. We achieve this with a stronger secrecy criterion and the maximum error probability criterion, and with a decoder that is robust against the effect of randomisation in the encoding. This relieves us from the need of decoding the randomisation parameter which is in general not possible within this model. Moreover we prove a lower bound on the secrecy capacity of the compound wiretap channel without channel state information and derive a multi-letter expression for the capacity in this communication scenario.Comment: 25 pages, 1 figure. Accepted for publication in the journal "Problems of Information Transmission". Some of the results were presented at the ITW 2011 Paraty [arXiv:1103.0135] and published in the conference paper available at the IEEE Xplor

Quantum capacity under adversarial quantum noise: arbitrarily varying quantum channels

We investigate entanglement transmission over an unknown channel in the presence of a third party (called the adversary), which is enabled to choose the channel from a given set of memoryless but non-stationary channels without informing the legitimate sender and receiver about the particular choice that he made. This channel model is called arbitrarily varying quantum channel (AVQC). We derive a quantum version of Ahlswede's dichotomy for classical arbitrarily varying channels. This includes a regularized formula for the common randomness-assisted capacity for entanglement transmission of an AVQC. Quite surprisingly and in contrast to the classical analog of the problem involving the maximal and average error probability, we find that the capacity for entanglement transmission of an AVQC always equals its strong subspace transmission capacity. These results are accompanied by different notions of symmetrizability (zero-capacity conditions) as well as by conditions for an AVQC to have a capacity described by a single-letter formula. In he final part of the paper the capacity of the erasure-AVQC is computed and some light shed on the connection between AVQCs and zero-error capacities. Additionally, we show by entirely elementary and operational arguments motivated by the theory of AVQCs that the quantum, classical, and entanglement-assisted zero-error capacities of quantum channels are generically zero and are discontinuous at every positivity point.Comment: 49 pages, no figures, final version of our papers arXiv:1010.0418v2 and arXiv:1010.0418. Published "Online First" in Communications in Mathematical Physics, 201