Combinatorial Multi-Access Coded Caching: Improved Rate-Memory Trade-off with Coded Placement

This work considers the combinatorial multi-access coded caching problem introduced in the recent work by Muralidhar \textit{et al.} [P. N. Muralidhar, D. Katyal, and B. S. Rajan, ``Maddah-Ali-Niesen scheme for multi-access coded caching,'' in \textit{IEEE Inf. Theory Workshop (ITW)}, 2021] The problem setting consists of a central server having a library of $N$ files and $C$ caches each of capacity $M$. Each user in the system can access a unique set of $r<C$ caches, and there exist users corresponding to every distinct set of $r$ caches. Therefore, the number of users in the system is $\binom{C}{r}$. For the aforementioned combinatorial multi-access setting, we propose a coded caching scheme with an MDS code-based coded placement. This novel placement technique helps to achieve a better rate in the delivery phase compared to the optimal scheme under uncoded placement, when $M> N/C$. For a lower memory regime, we present another scheme with coded placement, which outperforms the optimal scheme under uncoded placement if the number of files is no more than the number of users. Further, we derive an information-theoretic lower bound on the optimal rate-memory trade-off of the combinatorial multi-access coded caching scheme. Finally, using the derived lower bound, we show that the first scheme is optimal in the higher memory regime, and the second scheme is optimal if $N\leq \binom{C}{r}$.Comment: 15 pages and 5 figure

Multi-Antenna Coded Caching for Multi-Access Networks with Cyclic Wrap-Around

This work explores a multiple transmit antenna setting in a multi-access coded caching (MACC) network where each user accesses more than one cache. A MACC network has $K$ users and $K$ caches, and each user has access to $r < K$ consecutive caches in a cyclic wrap-around manner. There are $L$ antennas at the server, and each cache has a normalized size of $M/N \leq 1$. The cyclic wrap-around MACC network with a single antenna at the server has been a well-investigated topic, and several coded caching schemes and improved lower bounds on the performance are known for the same. However, this MACC network has not yet been studied under multi-antenna settings in the coded caching literature. We study the multi-antenna MACC problem and propose a solution for the same by constructing a pair of arrays called caching and delivery arrays. We present three constructions of caching and delivery arrays for different scenarios and obtain corresponding multi-antenna MACC schemes for the same. Two schemes resulting from the above constructions achieve optimal performance under uncoded placement and one-shot delivery. The optimality is shown by matching the performance of the multi-antenna MACC scheme to that of an optimal multi-antenna scheme for a dedicated cache network having an identical number of users, and each user has a normalized cache size of $rM/N$. Further, as a special case, one of the proposed schemes subsumes an existing optimal MACC scheme for the single-antenna setting.Comment: 11 pages (double column), 3 Figure

Brief isoflurane administration as an adjunct treatment to control organophosphate-induced convulsions and neuropathology

Organophosphate-based chemical agents (OP), including nerve agents and certain pesticides such as paraoxon, are potent acetylcholinesterase inhibitors that cause severe convulsions and seizures, leading to permanent central nervous system (CNS) damage if not treated promptly. The current treatment regimen for OP poisoning is intramuscular injection of atropine sulfate with an oxime such as pralidoxime (2-PAM) to mitigate cholinergic over-activation of the somatic musculature and autonomic nervous system. This treatment does not provide protection against CNS cholinergic overactivation and therefore convulsions require additional medication. Benzodiazepines are the currently accepted treatment for OP-induced convulsions, but the convulsions become refractory to these GABAA agonists and repeated dosing has diminishing effectiveness. As such, adjunct anticonvulsant treatments are needed to provide improved protection against recurrent and prolonged convulsions and the associated excitotoxic CNS damage that results from them. Previously we have shown that brief, 4-min administration of 3%–5% isoflurane in 100% oxygen has profound anticonvulsant and CNS protective effects when administered 30 min after a lethal dose of paraoxon. In this report we provide an extended time course of the effectiveness of 5% isoflurane delivered for 5 min, ranging from 60 to 180 min after a lethal dose of paraoxon in rats. We observed substantial effectiveness in preventing neuronal loss as shown by Fluoro-Jade B staining when isoflurane was administered 1 h after paraoxon, with diminishing effectiveness at 90, 120 and 180 min. In vivo magnetic resonance imaging (MRI) derived T2 and mean diffusivity (MD) values showed that 5-min isoflurane administration at a concentration of 5% prevents brain edema and tissue damage when administered 1 h after a lethal dose of paraoxon. We also observed reduced astrogliosis as shown by GFAP immunohistochemistry. Studies with continuous EEG monitoring are ongoing to demonstrate effectiveness in animal models of soman poisoning

Increasing N-acetylaspartate in the Brain during Postnatal Myelination Does Not Cause the CNS Pathologies of Canavan Disease

Canavan disease is caused by mutations in the gene encoding aspartoacylase (ASPA), a deacetylase that catabolizes N-acetylaspartate (NAA). The precise involvement of elevated NAA in the pathogenesis of Canavan disease is an ongoing debate. In the present study, we tested the effects of elevated NAA in the brain during postnatal development. Mice were administered high doses of the hydrophobic methyl ester of NAA (M-NAA) twice daily starting on day 7 after birth. This treatment increased NAA levels in the brain to those observed in the brains of Nur7 mice, an established model of Canavan disease. We evaluated various serological parameters, oxidative stress, inflammatory and neurodegeneration markers and the results showed that there were no pathological alterations in any measure with increased brain NAA levels. We examined oxidative stress markers, malondialdehyde content (indicator of lipid peroxidation), expression of NADPH oxidase and nuclear translocation of the stress-responsive transcription factor nuclear factor (erythroid-derived 2)-like 2 (NRF-2) in brain. We also examined additional pathological markers by immunohistochemistry and the expression of activated caspase-3 and interleukin-6 by Western blot. None of the markers were increased in the brains of M-NAA treated mice, and no vacuoles were observed in any brain region. These results show that ASPA expression prevents the pathologies associated with excessive NAA concentrations in the brain during postnatal myelination. We hypothesize that the pathogenesis of Canavan disease involves not only disrupted NAA metabolism, but also excessive NAA related signaling processes in oligodendrocytes that have not been fully determined and we discuss some of the potential mechanisms