Joint optimal subcarrier and transmit power allocation with QoS guarantee for enhanced packet transmission over Cognitive Radio (CR)-Internet of Vehicles (IoVs) is a challenge. This open issue is ...considered in this paper. A novel SNBS-based wireless radio resource scheduling scheme in OFDMA CR-IoV network systems is proposed. This novel scheduler is termed the SNBS OFDMA-based overlay CR-Assisted Vehicular NETwork (SNO-CRAVNET) scheduling scheme. It is proposed for efficient joint transmit power and subcarrier allocation for dynamic spectral resource access in cellular OFDMA-based overlay CRAVNs in clusters. The objectives of the optimization model applied in this study include (1) maximization of the overall system throughput of the CR-IoV system, (2) avoiding harmful interference of transmissions of the shared channels’ licensed owners (or primary users (PUs)), (3) guaranteeing the proportional fairness and minimum data-rate requirement of each CR vehicular secondary user (CRV-SU), and (4) ensuring efficient transmit power allocation amongst CRV-SUs. Furthermore, a novel approach which uses Lambert-W function characteristics is introduced. Closed-form analytical solutions were obtained by applying time-sharing variable transformation. Finally, a low-complexity algorithm was developed. This algorithm overcame the iterative processes associated with searching for the optimal solution numerically through iterative programming methods. Theoretical analysis and simulation results demonstrated that, under similar conditions, the proposed solutions outperformed the reference scheduler schemes. In comparison to other scheduling schemes that are fairness-considerate, the SNO-CRAVNET scheme achieved a significantly higher overall average throughput gain. Similarly, the proposed time-sharing SNO-CRAVNET allocation based on the reformulated convex optimization problem is shown to be capable of achieving up to 99.987% for the average of the total theoretical capacity.
Internet of Things (IoT) technology offers opportunities to monitor lifelogging data by a variety of assets, like wearable sensors, mobile apps, etc. But due to heterogeneity of connected devices and ...diverse human life patterns in an IoT environment, lifelogging personal data contains huge uncertainty and are hardly used for healthcare studies. Effective validation of lifelogging personal data for longitudinal health assessment is demanded. In this paper, lifelogging physical activity (LPA) is taken as a target to explore how to improve the validity of lifelogging data in an IoT enabled healthcare system. A rule-based adaptive LPA validation (LPAV) model, LPAV-IoT, is proposed for eliminating irregular uncertainties (IUs) and estimating data reliability in IoT healthcare environments. A methodology specifying four layers and three modules in LPAV-IoT is presented for analyzing key factors impacting validity of LPA. A series of validation rules are designed with uncertainty threshold parameters and reliability indicators and evaluated through experimental investigations. Following LPAV-IoT, a case study on a personalized healthcare platform myhealthavatar connecting three state-of-the-art wearable devices and mobile apps are carried out. The results reflect that the rules provided by LPAV-IoT enable efficiently filtering at least 75% of IU and adaptively indicating the reliability of LPA data on certain condition of IoT environments.
Different emotional states lead to distinct behavioural consequences even when faced with the same challenging events. Emotions affect learning and memory capacities, but the underlying ...neurobiological mechanisms remain elusive. Here we establish models of learned helplessness (LHL) and learned hopefulness (LHF) by exposing animals to inescapable foot shocks or with anticipated avoidance trainings. The LHF animals show spatial memory potentiation with excitatory monosynaptic upscaling between posterior basolateral amygdale (BLP) and ventral hippocampal CA1 (vCA1), whereas the LHL show memory deficits with an attenuated BLP-vCA1 connection. Optogenetic disruption of BLP-vCA1 inputs abolishes the effects of LHF and impairs synaptic plasticity. By contrast, targeted BLP-vCA1 stimulation rescues the LHL-induced memory deficits and mimics the effects of LHF. BLP-vCA1 stimulation increases synaptic transmission and dendritic plasticity with the upregulation of CREB and intrasynaptic AMPA receptors in CA1. These findings indicate that opposite excitatory monosynaptic scaling of BLP-vCA1 controls LHF- and LHL-modulated spatial memory, revealing circuit-specific mechanisms linking emotions to memory.
A generalized and autonomous discontinuous reception (DRX) scheme, which is applicable to both Third-Generation Partnership Project (3GPP) and IEEE 802.16e standards, is analyzed by two-level Markov ...chain modeling, along with the European Telecommunications Standards Institute (ETSI) packet traffic model. Numerical analysis showed that this scheme is capable of autonomously adjusting the DRX cycle to keep up with changing user equipment activity level with no signaling overhead increase, thus producing a better tuned DRX operation. Quantitative comparison with the power-saving schemes of 3GPP and 802.16e standards demonstrated that the autonomous DRX scheme is advantageous over these power-saving schemes.
Internet of Things (IoTs) era is expected to empower all aspects of Intelligent Transportation System (ITS) to improve transport safety and reduce road accidents. US Federal Communication Commission ...(FCC) officially allocated 75 MHz spectrum in the 5.9 GHz band to support vehicular communication. The authors studied the application of cognitive radio (CR) technology to IoVs to increase the spectra opportunities for vehicular communication, especially when the allocated 75 MHz is not enough due to high demands because of the increasing number of connected vehicles as already foreseen in the near era of IoVs. They proposed a novel CR Assisted Vehicular NETwork (CRAVNET) framework which empowers CR enabled vehicles to make opportunistic usage of licensed spectrum on the highways. They also developed a novel cooperative three-state spectrum sensing and allocation model which makes CR vehicular secondary units aware of additional spectrum resources opportunities on their current and future positions, and applies optimal sensing node allocation algorithm to guarantee timely acquisition of the available channels within a limited sensing time. The results of the theoretical analyses and simulation experiments have demonstrated that the proposed model can significantly improve the performance of a cooperative spectrum sensing, and provide vehicles with additional spectrum opportunities.
•ZG16 is negatively correlated to PD-L1 expression in patient with CRC.•ZG16 blocks PD-L1 expression to modulate immune response in colon cancer.•Overexpression of ZG16 promotes NK cells survival and ...proliferation.•ZG16 overexpression inhibits in vivo SW480 xenograft tumor growth.
CRC is a heterogeneous disease due to global molecular alterations, including mismatch-repair-deficient (dMMR) and microsatellite instability-high (MSI-H). Immunotherapy has achieved durable responses in a subset of patients with dMMR-MSI-H metastatic CRC. It has been showed that Loss of ZG16 is highly associated with colorectal cancer. However, whether ZG16 modulates tumor immunity in colorectal cancer is unclear. In this study, we demonstrated that the expression of ZG16 is associated with distant metastasis and lymphatic invasive in colorectal cancer. Besides, ZG16 is negatively correlated to PD-L1 expression in patient with CRC and overexpression of ZG16 blocks PD-L1 expression in colorectal cancer cells. In addition, overexpression of ZG16 promotes NK cells survival and proliferation, which is dependent on NKG2D expression. Our data demonstrate that ZG16 plays a role in modulation of immune response in colorectal cancer. The strong correlation between ZG16 and PD-L1 suggests that ZG16 may serve a biomarker to stratify patient who will benefit from immunotherapy.
Abnormal aggregation of pathological tau protein is a neuropathological feature of Alzheimer's disease (AD). In the AD patients, the abnormal tau accumulation first appeared in entorhinal cortex (EC) ...and then propagated to the hippocampus with microglia activation and inflammation, but the mechanism is elusive. Here, we studied the role and mechanisms underlying periphery inflammation on brain tau transmission. By intraperitoneal injection of lipopolysaccharide (LPS) with brain medial entorhinal cortex (MEC)-specific overexpressing P301L human tau (P301L-hTau), we found that both acute and chronic administration of LPS remarkably promoted P301L-hTau transmission from MEC to the hippocampal subsets. Interestingly, the chronic LPS-induced P301L-hTau transmission was still apparent after blocking microglia activation. Further studies demonstrated that LPS disrupted the integrity of blood-brain barrier (BBB) and simultaneous intraperitoneal administration of glucocorticoid (GC) attenuated LPS-promoted P301L-hTau transmission. These data together suggest that a non-microglia-dependent BBB disruption contributes to peripheral LPS-promoted brain P301L-hTau transmission, therefore, maintaining the integrity of BBB can be a novel strategy for preventing pathological tau propagation in AD and other tauopathies.
A polarisation diversity combing scheme for dual-polarised multiple-input and multiple-output channels in small cell environments introduced and evaluated. The scheme is based on post analysis of ...channel measurement data captured from scenarios and includes indoor-to-indoor, indoor-to-outdoor, and indoor-outdoor-indoor propagation. An analysis of link signal strength and correlation with respect to frequency and polarisation revealed profound differences between copolarised and cross-polarised links in terms of received signal strength and correlation between frequencies. Utilizing these differences, a polarisation diversity combing scheme is evaluated which is shown to produce an average of 10.6-dB polarisation diversity gain.
Increasing evidence suggests that glycogen synthase kinase-3β (GSK-3β) plays a crucial role in neurodegenerative/psychiatric disorders, while pan-neural knockout of GSK-3β also shows detrimental ...effects. Currently, the function of GSK-3β in specific type of neurons is elusive. Here, we infused AAV-CaMKII-Cre-2A-eGFP into GSK-3β
mice to selectively delete the kinase in excitatory neurons of hippocampal dentate gyrus (DG), and studied the effects on cognitive/psychiatric behaviors and the molecular mechanisms. We found that mice with GSK-3β deletion in DG excitatory neurons displayed spatial and fear memory defects with an anti-anxiety behavior. Further studies demonstrated that GSK-3β deletion in DG subset inhibited hippocampal synaptic transmission and reduced levels of GluN1, GluN2A and GluN2B (NMDAR subunits), GluA1 (AMPAR subunit), PSD93 and drebrin (postsynaptic structural proteins), and synaptophysin (presynaptic protein). GSK-3β deletion also suppressed the activity-dependent neural activation and calcium/calmodulin-dependent protein kinase II (CaMKII)/CaMKIV-cAMP response element binding protein (CREB) signaling. Our data suggest that GSK-3β in hippocampal DG excitatory neurons is essential for maintaining synaptic plasticity and memory.
Glycogen synthase kinase-3β (GSK-3β) is one of the most effective kinases in promoting tau hyperphosphorylation and accumulation in Alzheimer's disease (AD). However, it is not clear how GSK-3β ...activity is regulated during AD progression.
We firstly used mass spectrometry to identify the acetylation site of GSK-3β, and then established the cell and animal models of GSK-3β acetylation. Next, we conducted molecular, cell biological and behavioral tests. Finally, we designed a peptide to test whether blocking tau-mediated GSK-3β acetylation could be beneficial to AD.
We found that GSK-3β protein levels increased in the brains of AD patients and the transgenic mice. Overexpressing tau increased GSK-3β protein level with increased acetylation and decreased ubiquitination-related proteolysis. Tau could directly acetylate GSK-3β at K15 both in vitro and in vivo. K15-acetylation inhibited ubiquitination-associated proteolysis of GSK-3β and changed its activity-dependent phosphorylation, leading to over-activation of the kinase. GSK-3β activation by K15-acetylation in turn exacerbated the AD-like pathologies. Importantly, competitively inhibiting GSK-3β K15-acetylation by a novel-designed peptide remarkably improved cognitive impairment and the AD-like pathologies in 3xTg-AD mice.
Tau can directly acetylate GSK-3β at K15 which reveals a vicious cycle between tau hyperphosphorylation and GSK-3β activation.
This study was supported in parts by grants from Science and Technology Committee of China (2016YFC1305800), Hubei Province (2018ACA142), Natural Science Foundation of China (91949205, 82001134, 31730035, 81721005), Guangdong Provincial Key S&T Program (018B030336001).
PDF
