Contention-Less Multi-Link Synchronous Transmission for Throughput Enhancement and Heterogeneous Fairness in Wi-Fi 7.

Multi-link operation (MLO) is a new and essential mechanism of IEEE 802.11be Extremely High Throughput (Wi-Fi 7) that can increase throughput and decrease latency in Wireless Local Area Networks (WLANs). The MLO enables a Multi-Link Device (MLD) to perform Simultaneous Transmission and Reception (STR) in different frequency bands. However, not all MLDs can support STR due to cross-link or in-device coexistence interference, while an STR-unable MLD (NSTR-MLD) can transmit multiple frames simultaneously in more than two links. This study focuses on the problems when NSTR-MLDs share a link with Single-Link Devices (SLDs). We propose a Contention-Less Synchronous Transmission (CLST) mechanism to improve fairness between NSTR-MLDs and SLDs while increasing the total network throughput. The proposed mechanism classifies links as MLD Dominant Links (MDLs) and Heterogeneous Coexistence Links (HCLs). In the proposed mechanism, an NSTR-MLD obtains a Synchronous Transmission Token (STT) through a virtual channel contention in the HCL but does not actually transmit a frame in the HCL, which is compensated for by a synchronous transmission triggered in the MDL. Moreover, the CLST mechanism allows additional subsequent transmissions up to the accumulated STT without further contention. Extensive simulation results confirm the outstanding performance of the CLST mechanism in terms of total throughput and fairness compared to existing synchronous transmission mechanisms.

Interference-Aware Two-Level Differentiated Transmission for Improving Downlink Spatial Reuse in Dense WLANs.

In this study, we address the problem of downlink throughput degradation in dense wireless local area networks (WLANs) based on the IEEE 802.11ax standard. We demonstrate that this problem essentially results from the asymmetric characteristic of carrier sense multiple access between downlink and uplink transmissions in infrastructure WLANs, and it is exacerbated by a dynamic sensitivity control algorithm that aims to improve spatial reuse (SR) in IEEE 802.11ax. To solve this problem, we propose the interference-aware two-level differentiation mechanism consisting of the dual channel access (DCA) and supplemental power control (SPC) schemes. The proposed mechanism introduces a new measure called a spatial reusability indicator, which roughly estimates the signal-to-interference ratio from the received signal strength of beacon frames. Based on this measure, stations (STAs) are classified into the following two categories: spatial reusable STAs (SR-STAs) and non-spatial reusable STAs (NSR-STAs). Because SR-STAs are more robust to interference than NSR-STAs, the DCA scheme prioritizes transmissions to SR-STAs over those to NSR-STAs by using differentiated carrier sensing thresholds. Moreover, the SPC scheme selectively increases the transmission power to NSR-STAs to compensate for transmission failure due to interference. By combining the SPC and DCA schemes, the proposed mechanism effectively differentiates the downlink transmissions to SR-STAs and NSR-STAs in terms of channel access and transmission power, and it can boost the possibility of successful SR. The proposed mechanism can be easily implemented in IEEE 802.11ax without any complex calculation or significant signaling overhead. Moreover, we provide a practical guideline to determine appropriate parameter values for use in the proposed mechanism. The extensive simulation results obtained in this study confirm that the proposed mechanism increases the downlink throughput by more than several times without decreasing the overall throughput, compared to the existing mechanisms, and it maintains fairness between SR-STAs and NSR-STAs in terms of the ratio of successful transmission.

OFDMA Backoff Control Scheme for Improving Channel Efficiency in the Dynamic Network Environment of IEEE 802.11ax WLANs.

IEEE 802.11ax uplink orthogonal frequency division multiple access (OFDMA)-based random access (UORA) is a new feature for random channel access in wireless local area networks (WLANs). Similar to the legacy random access scheme in WLANs, UORA performs the OFDMA backoff (OBO) procedure to access the channel and decides on a random OBO counter within the OFDMA contention window (OCW) value. An access point (AP) can determine the OCW range and inform each station (STA) of it. However, how to determine a reasonable OCW range is beyond the scope of the IEEE 802.11ax standard. The OCW range is crucial to the UORA performance, and it primarily depends on the number of contending STAs, but it is challenging for the AP to accurately and quickly estimate or keep track of the number of contending STAs without the aid of a specific signaling mechanism. In addition, the one for this purpose incurs an additional delay and overhead in the channel access procedure. Therefore, the performance of a UORA scheme can be degraded by an improper OCW range, especially when the number of contending STAs changes dynamically. We first observed the effect of OCW values on channel efficiency and derived its optimal value from an analytical model. Next, we proposed a simple yet effective OBO control scheme where each STA determines its own OBO counter in a distributed manner rather than adjusting the OCW value globally. In the proposed scheme, each STA determines an appropriate OBO counter depending on whether the previous transmission was successful or not so that collisions can be mitigated without leaving OFDMA resource units unnecessarily idle. The results of a simulation study confirm that the throughput of the proposed scheme is comparable to the optimal OCW-based scheme and is improved by up to 15 times compared to the standard UORA scheme.

FNDC-1-mediated mitophagy and ATFS-1 coordinate to protect against hypoxia-reoxygenation.

Mitochondrial quality control (MQC) balances organelle adaptation and elimination, and mechanistic crosstalk between the underlying molecular processes affects subsequent stress outcomes. FUNDC1 (FUN14 domain containing 1) is a mammalian mitophagy receptor that responds to hypoxia-reoxygenation (HR) stress. Here, we provide evidence that FNDC-1 is the C. elegans ortholog of FUNDC1, and that its loss protects against injury in a worm model of HR. This protection depends upon ATFS-1, a transcription factor that is central to the mitochondrial unfolded protein response (UPRmt). Global mRNA and metabolite profiling suggest that atfs-1-dependent stress responses and metabolic remodeling occur in response to the loss of fndc-1. These data support a role for FNDC-1 in non-hypoxic MQC, and further suggest that these changes are prophylactic in relation to subsequent HR. Our results highlight functional coordination between mitochondrial adaptation and elimination that organizes stress responses and metabolic rewiring to protect against HR injury.Abbreviations: AL: autolysosome; AP: autophagosome; FUNDC1: FUN14 domain containing 1; HR: hypoxia-reperfusion; IR: ischemia-reperfusion; lof: loss of function; MQC: mitochondrial quality control; PCA: principle component analysis; PPP: pentonse phosphate pathway; proK (proteinase K);UPRmt: mitochondrial unfolded protein response; RNAi: RNA interference.

An Efficient Relayed Broadcasting based on the Duplication Estimation Model for IoT Applications.

In this paper, we consider relay-based broadcasting in wireless ad hoc networks, which can enable various emerging services in the Internet of Things (IoT). In this kind of traffic dissemination scheme, also known as flooding, all the nodes not only receive frames but also rebroadcast them. However, without an appropriate relay suppression, a broadcast storm problem arises, i.e., the transmission may fail due to severe collisions and/or interference, many duplicate frames are unnecessarily transmitted, and the traffic dissemination time increases. To mitigate the broadcast storm problem, we propose a reasonable criterion to restrict the rebroadcasting named the duplication ratio. Based on this, we propose an efficient mechanism consisting of duplication suppression and re-queuing schemes. The former discards duplicate frames proactively in a probabilistic manner to decrease the redundancy whereas the latter provides a secondary transmission opportunity reactively to compensate for the delivery failure. Moreover, to apply the duplication ratio practically, we propose a simple method to approximate it based on the number of adjacent nodes. The simulation study confirms that the proposed mechanism tightly ensured the reliability and decreased the traffic dissemination time by up to 6-fold compared to conventional mechanisms.

RPM-1 and DLK-1 regulate pioneer axon outgrowth by controlling Wnt signaling.

Axons must correctly reach their targets for proper nervous system function, although we do not fully understand the underlying mechanism, particularly for the first 'pioneer' axons. In C. elegans, AVG is the first neuron to extend an axon along the ventral midline, and this pioneer axon facilitates the proper extension and guidance of follower axons that comprise the ventral nerve cord. Here, we show that the ubiquitin ligase RPM-1 prevents the overgrowth of the AVG axon by repressing the activity of the DLK-1/p38 MAPK pathway. Unlike in damaged neurons, where this pathway activates CEBP-1, we find that RPM-1 and the DLK-1 pathway instead regulate the response to extracellular Wnt cues in developing AVG axons. The Wnt LIN-44 promotes the posterior growth of the AVG axon. In the absence of RPM-1 activity, AVG becomes responsive to a different Wnt, EGL-20, through a mechanism that appears to be independent of canonical Fz-type receptors. Our results suggest that RPM-1 and the DLK-1 pathway regulate axon guidance and growth by preventing Wnt signaling crosstalk.

Medical-Grade Channel Access and Admission Control in 802.11e EDCA for Healthcare Applications.

In this paper, we deal with the problem of assuring medical-grade quality of service (QoS) for real-time medical applications in wireless healthcare systems based on IEEE 802.11e. Firstly, we show that the differentiated channel access of IEEE 802.11e cannot effectively assure medical-grade QoS because of priority inversion. To resolve this problem, we propose an efficient channel access algorithm. The proposed algorithm adjusts arbitrary inter-frame space (AIFS) in the IEEE 802.11e protocol depending on the QoS measurement of medical traffic, to provide differentiated near-absolute priority for medical traffic. In addition, based on rigorous capacity analysis, we propose an admission control scheme that can avoid performance degradation due to network overload. Via extensive simulations, we show that the proposed mechanism strictly assures the medical-grade QoS and improves the throughput of low-priority traffic by more than several times compared to the conventional IEEE 802.11e.

The p38 MAP kinase pathway modulates the hypoxia response and glutamate receptor trafficking in aging neurons.

Neurons are sensitive to low oxygen (hypoxia) and employ a conserved pathway to combat its effects. Here, we show that p38 MAP Kinase (MAPK) modulates this hypoxia response pathway in C. elegans. Mutants lacking p38 MAPK components pmk-1 or sek-1 resemble mutants lacking the hypoxia response component and prolyl hydroxylase egl-9, with impaired subcellular localization of Mint orthologue LIN-10, internalization of glutamate receptor GLR-1, and depression of GLR-1-mediated behaviors. Loss of p38 MAPK impairs EGL-9 protein localization in neurons and activates the hypoxia-inducible transcription factor HIF-1, suggesting that p38 MAPK inhibits the hypoxia response pathway through EGL-9. As animals age, p38 MAPK levels decrease, resulting in GLR-1 internalization; this age-dependent downregulation can be prevented through either p38 MAPK overexpression or removal of CDK-5, an antagonizing kinase. Our findings demonstrate that p38 MAPK inhibits the hypoxia response pathway and determines how aging neurons respond to hypoxia through a novel mechanism.

Anoxia-reoxygenation regulates mitochondrial dynamics through the hypoxia response pathway, SKN-1/Nrf, and stomatin-like protein STL-1/SLP-2.

Many aerobic organisms encounter oxygen-deprived environments and thus must have adaptive mechanisms to survive such stress. It is important to understand how mitochondria respond to oxygen deprivation given the critical role they play in using oxygen to generate cellular energy. Here we examine mitochondrial stress response in C. elegans, which adapt to extreme oxygen deprivation (anoxia, less than 0.1% oxygen) by entering into a reversible suspended animation state of locomotory arrest. We show that neuronal mitochondria undergo DRP-1-dependent fission in response to anoxia and undergo refusion upon reoxygenation. The hypoxia response pathway, including EGL-9 and HIF-1, is not required for anoxia-induced fission, but does regulate mitochondrial reconstitution during reoxygenation. Mutants for egl-9 exhibit a rapid refusion of mitochondria and a rapid behavioral recovery from suspended animation during reoxygenation; both phenotypes require HIF-1. Mitochondria are significantly larger in egl-9 mutants after reoxygenation, a phenotype similar to stress-induced mitochondria hyperfusion (SIMH). Anoxia results in mitochondrial oxidative stress, and the oxidative response factor SKN-1/Nrf is required for both rapid mitochondrial refusion and rapid behavioral recovery during reoxygenation. In response to anoxia, SKN-1 promotes the expression of the mitochondrial resident protein Stomatin-like 1 (STL-1), which helps facilitate mitochondrial dynamics following anoxia. Our results suggest the existence of a conserved anoxic stress response involving changes in mitochondrial fission and fusion.

Hypoxia regulates glutamate receptor trafficking through an HIF-independent mechanism.

Oxygen influences behaviour in many organisms, with low levels (hypoxia) having devastating consequences for neuron survival. How neurons respond physiologically to counter the effects of hypoxia is not fully understood. Here, we show that hypoxia regulates the trafficking of the glutamate receptor GLR-1 in C. elegans neurons. Either hypoxia or mutations in egl-9, a prolyl hydroxylase cellular oxygen sensor, result in the internalization of GLR-1, the reduction of glutamate-activated currents, and the depression of GLR-1-mediated behaviours. Surprisingly, hypoxia-inducible factor (HIF)-1, the canonical substrate of EGL-9, is not required for this effect. Instead, EGL-9 interacts with the Mint orthologue LIN-10, a mediator of GLR-1 membrane recycling, to promote LIN-10 subcellular localization in an oxygen-dependent manner. The observed effects of hypoxia and egl-9 mutations require the activity of the proline-directed CDK-5 kinase and the CDK-5 phosphorylation sites on LIN-10, suggesting that EGL-9 and CDK-5 compete in an oxygen-dependent manner to regulate LIN-10 activity and thus GLR-1 trafficking. Our findings demonstrate a novel mechanism by which neurons sense and respond to hypoxia.

Structures of PHR domains from Mus musculus Phr1 (Mycbp2) explain the loss-of-function mutation (Gly1092-->Glu) of the C. elegans ortholog RPM-1.

PHR [PAM (protein associated with Myc)-HIW (Highwire)-RPM-1 (regulator of presynaptic morphology 1)] proteins are conserved, large multi-domain E3 ubiquitin ligases with modular architecture. PHR proteins presynaptically control synaptic growth and axon guidance and postsynaptically regulate endocytosis of glutamate receptors. Dysfunction of neuronal ubiquitin-mediated proteasomal degradation is implicated in various neurodegenerative diseases. PHR proteins are characterized by the presence of two PHR domains near the N-terminus, which are essential for proper localization and function. Structures of both the first and second PHR domains of Mus musculus (mouse) Phr1 (MYC binding protein 2, Mycbp2) have been determined, revealing a novel beta sandwich fold composed of 11 antiparallel beta-strands. Conserved loops decorate the apical side of the first PHR domain (MmPHR1), yielding a distinct conserved surface feature. The surface of the second PHR domain (MmPHR2), in contrast, lacks significant conservation. Importantly, the structure of MmPHR1 provides insights into a loss-of-function mutation, Gly1092-->Glu, observed in the Caenorhabditis elegans ortholog RPM-1.

The ubiquitin ligase RPM-1 and the p38 MAPK PMK-3 regulate AMPA receptor trafficking.

Ubiquitination occurs at synapses, yet its role remains unclear. Previous studies demonstrated that the RPM-1 ubiquitin ligase organizes presynaptic boutons at neuromuscular junctions in C. elegans motorneurons. Here we find that RPM-1 has a novel postsynaptic role in interneurons, where it regulates the trafficking of the AMPA-type glutamate receptor GLR-1 from synapses into endosomes. Mutations in rpm-1 cause the aberrant accumulation of GLR-1 in neurites. Moreover, rpm-1 mutations enhance the endosomal accumulation of GLR-1 observed in mutants for lin-10, a Mint2 ortholog that promotes GLR-1 recycling from Syntaxin-13 containing endosomes. As in motorneurons, RPM-1 negatively regulates the pmk-3/p38 MAPK pathway in interneurons by repressing the protein levels of the MAPKKK DLK-1. This regulation of PMK-3 signaling is critical for RPM-1 function with respect to GLR-1 trafficking, as pmk-3 mutations suppress both lin-10 and rpm-1 mutations. Positive or negative changes in endocytosis mimic the effects of rpm-1 or pmk-3 mutations, respectively, on GLR-1 trafficking. Specifically, RAB-5(GDP), an inactive mutant of RAB-5 that reduces endocytosis, mimics the effect of pmk-3 mutations when introduced into wild-type animals, and occludes the effect of pmk-3 mutations when introduced into pmk-3 mutants. By contrast, RAB-5(GTP), which increases endocytosis, suppresses the effect of pmk-3 mutations, mimics the effect of rpm-1 mutations, and occludes the effect of rpm-1 mutations. Our findings indicate a novel specialized role for RPM-1 and PMK-3/p38 MAPK in regulating the endosomal trafficking of AMPARs at central synapses.