Low Cost Interconnected Architecture for the Hardware Spiking Neural Networks

A novel low cost interconnected architecture (LCIA) is proposed in this paper, which is an efficient solution for the neuron interconnections for the hardware spiking neural networks (SNNs). It is based on an all-to-all connection that takes each paired input and output nodes of multi-layer SNNs as the source and destination of connections. The aim is to maintain an efficient routing performance under low hardware overhead. A Networks-on-Chip (NoC) router is proposed as the fundamental component of the LCIA, where an effective scheduler is designed to address the traffic challenge due to irregular spikes. The router can find requests rapidly, make the arbitration decision promptly, and provide equal services to different network traffic requests. Experimental results show that the LCIA can manage the intercommunication of the multi-layer neural networks efficiently and have a low hardware overhead which can maintain the scalability of hardware SNNs

Azadiradione exerts anti-inflammatory and anti-oxidant effects, alleviates dopaminergic neurodegeneration and reduces α-synuclein levels in MPTP-induced mouse model of Parkinson’s disease

Purpose: To determine the effects of azadiradione (AZD), a tetracyclic triterpenoid, in 1-methyl-4- phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP)–induced experimental rodent model of Parkinson’s disease (PD). Methods: C57BL/6 mice were intraperitoneally injected MPTP at a dose of 20 mg/kg body weight in saline (4 times at 2-h intervals). Azadiradione (AZD) at doses of 12.5, 25 or 50 mg/kg were administered to separate groups of mice via oral gavage for 6 days prior to MPTP injection. Results: Azadiradione (AZD) reduced loss of tyrosine hydroxylase (TH)-positive neurons. TH-positive counts increased to 91.44 % on treatment with 50 mg/kg AZD. Significantly (p < 0.05) down-regulated α-synuclein levels were seen following MPTP induction and AZD administration. Expressions of Bax, Bcl-2 and cleaved-caspase-3 were significantly downregulated (p < 0.05). Treatment with AZD inhibited the translocation of Cyt-C to the mitochondria, thereby preventing activation of apoptotic cascade. Oxidative stress induced by MPTP was significantly reduced by AZD via up-regulation of glutathione levels and SOD1/HO-1 expression. Azadiradione, at a dose of 50 mg/kg, significantly (p < 0.05) reduced ROS levels from 210.6 19.23%, and also reduced the levels of inflammatory cytokines. Conclusion: These results indicate the anti-inflammatory, anti-oxidative and neuroprotective properties of AZD in mice. Thus, AZD is a potential candidate drug for the management of PD. However, further studies are required to ascertain this

Structural and biochemical insights into small RNA 3' end trimming by Arabidopsis SDN1.

A family of DEDDh 3'→5' exonucleases known as Small RNA Degrading Nucleases (SDNs) initiates the turnover of ARGONAUTE1 (AGO1)-bound microRNAs in Arabidopsis by trimming their 3' ends. Here, we report the crystal structure of Arabidopsis SDN1 (residues 2-300) in complex with a 9 nucleotide single-stranded RNA substrate, revealing that the DEDDh domain forms rigid interactions with the N-terminal domain and binds 4 nucleotides from the 3' end of the RNA via its catalytic pocket. Structural and biochemical results suggest that the SDN1 C-terminal domain adopts an RNA Recognition Motif (RRM) fold and is critical for substrate binding and enzymatic processivity of SDN1. In addition, SDN1 interacts with the AGO1 PAZ domain in an RNA-independent manner in vitro, enabling it to act on AGO1-bound microRNAs. These extensive structural and biochemical studies may shed light on a common 3' end trimming mechanism for 3'→5' exonucleases in the metabolism of small non-coding RNAs

Tuning the Magnetic Ordering Temperature of Hexagonal Ferrites by Structural Distortion Control

To tune the magnetic properties of hexagonal ferrites, a family of magnetoelectric multiferroic materials, by atomic-scale structural engineering, we studied the effect of structural distortion on the magnetic ordering temperature (TN). Using the symmetry analysis, we show that unlike most antiferromagnetic rare-earth transition-metal perovskites, a larger structural distortion leads to a higher TN in hexagonal ferrites and manganites, because the K3 structural distortion induces the three-dimensional magnetic ordering, which is forbidden in the undistorted structure by symmetry. We also revealed a near-linear relation between TN and the tolerance factor and a power-law relation between TN and the K3 distortion amplitude. Following the analysis, a record-high TN (185 K) among hexagonal ferrites was predicted in hexagonal ScFeO3 and experimentally verified in epitaxially stabilized films. These results add to the paradigm of spin-lattice coupling in antiferromagnetic oxides and suggests further tunability of hexagonal ferrites if more lattice distortion can be achieved

Low-dose interleukin-2 reverses chronic migraine-related sensitizations through peripheral interleukin-10 and transforming growth factor beta-1 signaling

Low-dose interleukin-2 (LD-IL-2) treatment has been shown to effectively reverse chronic migraine-related behaviors and the sensitization of trigeminal ganglion (TG) neurons through expansion and activation of peripheral regulatory T cells (Tregs) in mice. In this study, we investigated the molecular mechanisms underlying the effects of LD-IL-2 and Treg cells. LD-IL-2 treatment increases the production of cytokines interleukin-10 (IL-10) and transforming growth factor beta-1 (TGFβ1) in T cells, especially Treg cells, suggesting that they may mediate the therapeutic effect of LD-IL-2. Indeed, neutralizing antibodies against either IL-10 or TGFβ completely blocked the effects of LD-IL-2 on the facial mechanical hypersensitivity as well as the sensitization of TG neurons resulting from repeated nitroglycerin (NTG, a reliable trigger of migraine in patients) administration in mice, indicating that LD-IL-2 and Treg cells engage both peripheral IL-10 and TGFβ signaling pathways to reverse chronic-migraine related sensitizations. In a