Delay-Tolerance-Based Mobile Data Offloading Using Deep Reinforcement Learning.

The demand for mobile data communication has been increasing owing to the diversification of its purposes and the increase in the number of mobile devices accessing mobile networks. Users are experiencing a degradation in communication quality due to mobile network congestion. Therefore, improving the bandwidth utilization efficiency of cellular infrastructure is crucial. We previously proposed a mobile data offloading protocol (MDOP) for improving the bandwidth utilization efficiency. Although this method balances a load of evolved node B by taking into consideration the content delay tolerance, accurately balancing the load is challenging. In this paper, we apply deep reinforcement learning to MDOP to solve the temporal locality of a traffic. Moreover, we examine and evaluate the concrete processing while considering a delay tolerance. A comparison of the proposed method and bandwidth utilization efficiency of MDOP showed that the proposed method reduced the network traffic in excess of the control target value by 35% as compared with the MDOP. Furthermore, the proposed method improved the data transmission ratio by the delay tolerance range. Consequently, the proposed method improved the bandwidth utilization efficiency by learning how to provide the bandwidth to the user equipment when MDOP cannot be used to appropriately balance a load.

Effect of gravity stress on fidelity of DNA double-strand break repair.

DNA double strand break (DSB) causes many cytotoxic effects such as cellular lethality, somatic mutation, and carcinogenesis. Fidelity of DSB repair is a important factor that determines the quality of genomic stability. It is known that the most of DSBs are properly repaired on the earth, however, little is known whether those are rejoined at the same fidelity even under the space environment. One of the DSB repair pathway, homologous recombination (HR), allows the cells to repair their DSBs with error free. Therefore, the efficiency of HR is a good index to assess the fidelity of DSB repair. In order to clarify the effect of gravity stress on HR pathway, we established a cell line that can detect a site-specific DNA repair via HR. The cells carrying a reporter construct for HR were incubated under hypergravity condition after induction of site specific DSB. Our preliminary results suggest that the gravity stress may affect the HR efficiency.

Repeated administration of milnacipran induces rapid desensitization of somatodendritic 5-HT1A autoreceptors but not postsynaptic 5-HT1A receptors.

The effects of the repeated administration of milnacipran, a serotonin (5-HT)-noradrenaline reuptake inhibitor (SNRI), on the functional status of somatodendritic 5-HT1A receptors, and postsynaptic 5-HT1A receptors were explored using electrophysiological approaches in rats. In-vitro electrophysiological recordings in the dorsal raphe nucleus showed that 5-HT inhibited the firing of serotonergic neurones, and the selective 5-HT1A receptor antagonist, N-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-N-(2-pyridinyl) cyclohexane carboxamide (WAY 100635), reversed the inhibitory effect of 5-HT. The potency of 5-HT to inhibit the firing of serotonergic neurones was slightly attenuated after 3 days of treatment with milnacipran (30 mg/kg, p.o., twice daily), and significantly attenuated after 7 or 14 days treatment at the same dose. The tricyclic antidepressant, imipramine, did not significantly modify the inhibitory effect of 5-HT. After 7 days treatment at 30 mg/kg, p.o., once daily, milnacipran reduced the potency of 5-HT to inhibit the firing of serotonergic neurones, whereas the selective serotonin reuptake inhibitors, fluvoxamine and fluoxetine (60 and 30 mg/kg, p.o., once daily, respectively), did not modify it under these conditions. Treatment with milnacipran (30 mg/kg, p.o., twice daily) for 14 days did not change the inhibition of the CA1 field potential in rat hippocampal slices by 5-HT. These data suggest that somatodendritic 5-HT1A receptors, but not postsynaptic 5-HT1A receptors, rapidly desensitize in response to the repeated administration of milnacipran.

Neurochemical and behavioural characterization of milnacipran, a serotonin and noradrenaline reuptake inhibitor in rats.

RATIONALE: The prefrontal cortex is implicated in the pathophysiology of depression, and hypoactivity of this brain area has been found in depressed patients. Reduced function of the serotonergic and noradrenergic systems is another feature of depression. OBJECTIVES: The present study was aimed at characterizing neurochemically and behaviorally the serotonin and noradrenaline reuptake inhibitor (SNRI), milnacipran, in the prefrontal cortex in comparison with tricyclic antidepressants and selective serotonin reuptake inhibitors. METHODS: Sodium-dependent monoamine uptake measurement, radioligand binding assays, microdialysis procedure, forced swimming test and conditioned fear stress test were carried out in rats. RESULTS: Milnacipran selectively inhibited sodium-dependent [(3)H]serotonin (5-hydroxytryptamine, 5-HT) and [(3)H]noradrenaline (NA) uptake into the synaptosomes from rat cerebral cortex (IC(50)=28.0 and 29.6 nM, respectively) without any affinities for various neuroreceptors. In the medial prefrontal cortex, milnacipran (10 and 30 mg/kg, PO) caused a dose-related increase in the extracellular levels of 5-HT and NA with similar potency, whereas imipramine (10 and 30 mg/kg, PO) caused a dominant increase in the output of NA compared to 5-HT. Milnacipran (30 and 60 mg/kg, PO) significantly reduced the duration of both the immobility time in the forced swimming test and the freezing time in the conditioned fear stress test in rats, which are animal behavioral models for depression and anxiety, respectively. Imipramine and maprotiline were active in the former test, but not in the latter. Fluoxetine and fluvoxamine on the other hand were more active in the conditioned fear test. CONCLUSION: These findings show that milnacipran acts as a SNRI in vitro and in vivo and may be useful for the treatment of anxiety as well as depression.

SYR2, a gene necessary for syringomycin growth inhibition of Saccharomyces cerevisiae.

The Pseudomonas syringae cyclic lipodepsipeptide syringomycin inhibits the growth of Saccharomyces cerevisiae. A novel yeast gene, SYR2, was found to complement two syringomycin-resistant S. cerevisiae mutants. SYR2 was cloned, sequenced, and shown to encode a 349 amino acid protein located in the endoplasmic reticulum. SYR2 was identical to SUR2, which is involved in survival during nutritional starvation. Gene disruption or overexpression of SYR2 did not affect cell viability or ergosterol levels, but did influence cellular phospholipid levels. The findings suggest that phospholipids are important for the growth inhibitory action of syringomycin.