Service Negotiation Model for Response Time in Distributed Networks

The important thing of QoS is that response time of service is transparently suggested to resource management system and network users. This helps to schedule jobs or guarantee the service level agreement. This paper proposes to specify a negotiation policy for response time of distributed network using network latency function. To monitor and manage service response time in distributed network, we identified the relationships between network/application performance and QoS parameters. We also provided the statistical analysis on mapping user level response time to application and network level parameters. To show the validation of the network latency function, we used the NS-2 network simulator and showed the efficiency of that function. Finally we suggested the negotiation of policy for response time of requested service

Class-Attentive Diffusion Network for Semi-Supervised Classification

Recently, graph neural networks for semi-supervised classification have been widely studied. However, existing methods only use the information of limited neighbors and do not deal with the inter-class connections in graphs. In this paper, we propose Adaptive aggregation with Class-Attentive Diffusion (AdaCAD), a new aggregation scheme that adaptively aggregates nodes probably of the same class among K-hop neighbors. To this end, we first propose a novel stochastic process, called Class-Attentive Diffusion (CAD), that strengthens attention to intra-class nodes and attenuates attention to inter-class nodes. In contrast to the existing diffusion methods with a transition matrix determined solely by the graph structure, CAD considers both the node features and the graph structure with the design of our class-attentive transition matrix that utilizes a classifier. Then, we further propose an adaptive update scheme that leverages different reflection ratios of the diffusion result for each node depending on the local class-context. As the main advantage, AdaCAD alleviates the problem of undesired mixing of inter-class features caused by discrepancies between node labels and the graph topology. Built on AdaCAD, we construct a simple model called Class-Attentive Diffusion Network (CAD-Net). Extensive experiments on seven benchmark datasets consistently demonstrate the efficacy of the proposed method and our CAD-Net significantly outperforms the state-of-the-art methods. Code is available at https://github.com/ljin0429/CAD-Net.Comment: Accepted to AAAI 202

The voltage-gated potassium channel Shaker promotes sleep via thermosensitive GABA transmission

Genes and neural circuits coordinately regulate animal sleep. However, it remains elusive how these endogenous factors shape sleep upon environmental changes. Here, we demonstrate that Shaker (Sh)-expressing GABAergic neurons projecting onto dorsal fan-shaped body (dFSB) regulate temperature-adaptive sleep behaviors in Drosophila. Loss of Sh function suppressed sleep at low temperature whereas light and high temperature cooperatively gated Sh effects on sleep. Sh depletion in GABAergic neurons partially phenocopied Sh mutants. Furthermore, the ionotropic GABA receptor, Resistant to dieldrin (Rdl), in dFSB neurons acted downstream of Sh and antagonized its sleep-promoting effects. In fact, Rdl inhibited the intracellular cAMP signaling of constitutively active dopaminergic synapses onto dFSB at low temperature. High temperature silenced GABAergic synapses onto dFSB, thereby potentiating the wake-promoting dopamine transmission. We propose that temperature-dependent switching between these two synaptic transmission modalities may adaptively tune the neural property of dFSB neurons to temperature shifts and reorganize sleep architecture for animal fitness. Ji-hyung Kim and Yoonhee Ki et al. show that low temperatures suppress sleep in Drosophila by increasing GABA transmission in Shaker-expressing GABAergic neurons projecting onto the dorsal fan-shaped body, while high temperatures potentiate dopamine-induced arousal by reducing GABA transmission. This study highlights a role for Shaker in sleep modulation via a temperature-dependent switch in GABA signaling

Characterization of the ATP transporter in the reconstituted rough endoplasmic reticulum proteoliposomes

AbstractAdenosine triphosphate (ATP) transporter from rat liver rough endoplasmic reticulum (RER) was solubilized and reconstituted into phosphatidylcholine liposomes. The RER proteoliposomes, resulting from optimizing some reconstitution parameters, had an apparent Km value of 1.5 μM and a Vmax of 286 pmol min−1 (mg protein)−1 and showed higher affinity for ATP and a lower Vmax value than intact RER (Km of 6.5 μM and Vmax of 1 nmol). ATP transport was time- and temperature-dependent, inhibited by 4,4′-diisothiocyanostilbene-2,2′-disulfonic acid, which is known as an inhibitor of anion transporters including ATP transporter, but was not affected by atractyloside, a specific inhibitor of mitochondrial ADP/ATP carrier. The internal and external effects of various nucleotides on the ATP transport were examined. ATP transport was cis-inhibited strongly by ADP and weakly by AMP. ADP-preloaded RER proteoliposomes showed a specific increase of ATP transport activity while AMP-preloaded RER proteoliposomes did not show the enhanced overshoot peak in the ATP uptake plot. These results demonstrate the ADP/ATP antiport mechanism of ATP transport in rat liver RER

Bucillamine prevents cisplatin-induced ototoxicity through induction of glutathione and antioxidant genes.

Bucillamine is used for the treatment of rheumatoid arthritis. This study investigated the protective effects of bucillamine against cisplatin-induced damage in auditory cells, the organ of Corti from postnatal rats (P2) and adult Balb/C mice. Cisplatin increases the catalytic activity of caspase-3 and caspase-8 proteases and the production of free radicals, which were significantly suppressed by pretreatment with bucillamine. Bucillamine induces the intranuclear translocation of Nrf2 and thereby increases the expression of γ-glutamylcysteine synthetase (γ-GCS) and glutathione synthetase (GSS), which further induces intracellular antioxidant glutathione (GSH), heme oxygenase 1 (HO-1) and superoxide dismutase 2 (SOD2). However, knockdown studies of HO-1 and SOD2 suggest that the protective effect of bucillamine against cisplatin is independent of the enzymatic activity of HO-1 and SOD. Furthermore, pretreatment with bucillamine protects sensory hair cells on organ of Corti explants from cisplatin-induced cytotoxicity concomitantly with inhibition of caspase-3 activation. The auditory-brainstem-evoked response of cisplatin-injected mice shows marked increases in hearing threshold shifts, which was markedly suppressed by pretreatment with bucillamine in vivo. Taken together, bucillamine protects sensory hair cells from cisplatin through a scavenging effect on itself, as well as the induction of intracellular GSH