Abstract-Current network infrastructures exhibit poor power efficiency, running network devices at full capacity all the time regardless of the traffic demand and distribution over the network. Most research on router power management are at component level or link level, treating routers as isolated devices. A complementary approach is to facilitate power management at network level by routing traffic through different paths to adjust the workload on individual routers or links. Given the high path redundancy and low link utilization in today's large networks, this approach can potentially allow more network devices or components to go into power saving mode. This paper proposes an intra-domain traffic engineering mechanism, GreenTE, which maximizes the number of links that can be put into sleep under given performance constraints such as link utilization and packet delay. Using network topologies and traffic data from several widearea networks, our evaluation shows that GreenTE can reduce line-cards' power consumption by 27% to 42% under constraints that the maximum link utilization is below 50% and the network diameter remains the same as in shortest path routing.

The IETF has standardized Transparent Interconnection of Lots of Links (TRILL), a protocol for least-cost transparent frame routing in multi-hop networks with arbitrary topologies and link technologies, using link-state routing and a hop count. The TRILL base protocol standard supports the labeling of TRILL Data packets with up to 4K IDs. However, there are applications that require a larger number of labels providing configurable isolation of data. This document updates RFC 6325 by specifying optional extensions to the TRILL base protocol to safely accomplish this. These extensions, called finegrained labeling, are primarily intended for use in large data centers, that is, those with more than 4K users requiring configurable data isolation from each other.

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Radiation therapy is the most widely used and effective treatment for orbital tumors, but it causes dry eye due to lacrimal gland damage. Induced pluripotent stem cell-derived conditioned medium (iPSC-CM) has been shown to rescue different types of tissue damage. The present study investigated the mechanism of the potential radioprotective effect of IPS cell-derived conditioned medium (iPSC-CM) on gamma-irradiation-induced lacrimal gland injury (RILI) in experimental mice. In this study, we found that iPSC-CM ameliorated RILI. iPSC-CM markedly decreased radiotherapy induced inflammatory processes, predominantly through suppressing p38/JNK signaling. Further signaling pathway analyses indicated that iPSC-CM could suppress Akt (Protein Kinase B, PKB) phosphorylation. High levels of midkine (MDK) were also found in iPSC-CM and could be involved in lacrimal gland regeneration by promoting cell migration and proliferation. Thus, our study indicates that inhibiting the p38/JNK pathway or increasing the MDK level might be a therapeutic target for radiation-induced lacrimal gland injury.

Microglia activation and release of pro‐inflammatory cytokines have been closely linked to glaucoma. However, the mechanisms that initiate these pathways remain unclear. Here, we investigated the role of a pro‐inflammatory cytokine––osteopontin (OPN), in retinal microglia activation process along with the underlying mechanisms in glaucoma. A rat chronic ocular hypertension (COH) model was established presenting an increase in retinal OPN level and activation of microglia. Primary microglia cells were isolated and cultured under a pressure culture system showing heightened expressions of microglia‐derived OPN with changes in inflammatory factors (TNF‐α, IL‐1β, and IL‐6). OPN and OPN neutralizing antibody (Anti‐OPN) interventions were both applied systems for comparison, and cross‐referenced with OPN knockdown in vitro. JAK/STAT, NF‐κB, ERK1/2, and p38 MAPK, recognized as the primary signaling pathways related to microglia activation, were then screened on whether they can facilitate OPN to act on microglia and their impact on specific inhibitors. Thereafter, retrograde labeling of retinal ganglion cells (RGCs) and flash visual evoked potentials (F‐VEP) were used to investigate neuron protection in context of each blockade. Results suggest that OPN is able to enhance the proliferation and activation of retinal microglia in experimental glaucoma which may play a role in the glaucomatous optic neuropathy, and contribute to the eventual RGCs loss and vision function impairment. Such effect may be mediated through the regulation of p38 MAPK signaling pathway.