Quality of service differentiation for multimedia delivery in wireless LANs

Delivering multimedia content to heterogeneous devices over a variable networking environment while maintaining high quality levels involves many technical challenges. The research reported in this thesis presents a solution for Quality of Service (QoS)-based service differentiation when delivering multimedia content over the wireless LANs. This thesis has three major contributions outlined below: 1. A Model-based Bandwidth Estimation algorithm (MBE), which estimates the available bandwidth based on novel TCP and UDP throughput models over IEEE 802.11 WLANs. MBE has been modelled, implemented, and tested through simulations and real life testing. In comparison with other bandwidth estimation techniques, MBE shows better performance in terms of error rate, overhead, and loss. 2. An intelligent Prioritized Adaptive Scheme (iPAS), which provides QoS service differentiation for multimedia delivery in wireless networks. iPAS assigns dynamic priorities to various streams and determines their bandwidth share by employing a probabilistic approach-which makes use of stereotypes. The total bandwidth to be allocated is estimated using MBE. The priority level of individual stream is variable and dependent on stream-related characteristics and delivery QoS parameters. iPAS can be deployed seamlessly over the original IEEE 802.11 protocols and can be included in the IEEE 802.21 framework in order to optimize the control signal communication. iPAS has been modelled, implemented, and evaluated via simulations. The results demonstrate that iPAS achieves better performance than the equal channel access mechanism over IEEE 802.11 DCF and a service differentiation scheme on top of IEEE 802.11e EDCA, in terms of fairness, throughput, delay, loss, and estimated PSNR. Additionally, both objective and subjective video quality assessment have been performed using a prototype system. 3. A QoS-based Downlink/Uplink Fairness Scheme, which uses the stereotypes-based structure to balance the QoS parameters (i.e. throughput, delay, and loss) between downlink and uplink VoIP traffic. The proposed scheme has been modelled and tested through simulations. The results show that, in comparison with other downlink/uplink fairness-oriented solutions, the proposed scheme performs better in terms of VoIP capacity and fairness level between downlink and uplink traffic

Antiarrhythmic and proarrhythmic effects of subcutaneous nerve stimulation in ambulatory dogs

Background High output subcutaneous nerve stimulation (ScNS) remodels the stellate ganglia and suppresses cardiac arrhythmia. Objective To test the hypothesis that long duration low output ScNS causes cardiac nerve sprouting, increases plasma norepinephrine concentration and the durations of paroxysmal atrial tachycardia (PAT) in ambulatory dogs. Methods We prospectively randomized 22 dogs (11 males and 11 females) into 5 different output groups for 2 months of ScNS: 0 mA (sham) (N=6), 0.25 mA (N=4), 1.5 mA (N=4), 2.5 mA (N=4) and 3.5 mA (N=4). Results As compared with baseline, the changes of the durations of PAT episodes per 48 hours were significantly different among different groups (sham, -5.0±9.5 s; 0.25 mA 95.5±71.0 s; 1.5 mA, -99.3±39.6 s; 2.5 mA, -155.3±87.8 s and 3.5 mA, -76.3±44.8 s, p<0.001). The 3.5 mA group had greater reduction of sinus heart rate than the sham group (-29.8±15.0 bpm vs -14.5±3.0 bpm, p=0.038). Immunohistochemical studies showed that the 0.25 mA group had a significantly increased while 2.5 mA and 3.5 mA stimulation had a significantly reduced growth-associated protein 43 nerve densities in both atria and ventricles. The plasma Norepinephrine concentrations in 0.25 mA group was 5063.0±4366.0 pg/ml, which was significantly higher than other groups of dogs (739.3±946.3, p=0.009). There were no significant differences in the effects of simulation between males and females. Conclusions In ambulatory dogs, low output ScNS causes cardiac nerve sprouting, increases plasma norepinephrine concentration and the duration of PAT episodes while high output ScNS is antiarrhythmic

User quality of experience of mulsemedia applications

User Quality of Experience (QoE) is of fundamental importance in multimedia applications and has been extensively studied for decades. However, user QoE in the context of the emerging multiple-sensorial media (mulsemedia) services, which involve different media components than the traditional multimedia applications, have not been comprehensively studied. This article presents the results of subjective tests which have investigated user perception of mulsemedia content. In particular, the impact of intensity of certain mulsemedia components including haptic and airflow on user-perceived experience are studied. Results demonstrate that by making use of mulsemedia the overall user enjoyment levels increased by up to 77%

A QoS-Based Fairness-Aware BBR Congestion Control Algorithm Using QUIC

Congestion control is a fundamental technology to balance the traffic load and the network. The Internet Engineering Task Force (IETF) Quick UDP Internet Connection (QUIC) protocol has flexible congestion control and at the same time possesses the advantages of high efficiency, low latency, and easy deployment at the application layer. Bottleneck bandwidth and round-trip propagation time (BBR) is an optional congestion control algorithm adopted by QUIC. BBR can significantly increase throughput and reduce latency, in particular over long-haul paths. However, BBR results in high packet loss in low bandwidth and low fairness in multi-stream scenarios. In this article, we propose the enhanced BBR congestion control (eBCC) algorithm, which improves the BBR algorithm in two aspects: (1) 10.87% higher throughput and 74.58% lower packet loss rate in the low-bandwidth scenario and (2) 8.39% higher fairness in the multi-stream scenario. This improvement makes eBCC very suitable for IoT communications to provide better QoS services

Antiarrhythmic effects of stimulating the left dorsal branch of the thoracic nerve in a canine model of paroxysmal atrial tachyarrhythmias

Background Stellate ganglion nerve activity (SGNA) precedes paroxysmal atrial tachyarrhythmia (PAT) episodes in dogs with intermittent high-rate left atrial (LA) pacing. The left dorsal branch of the thoracic nerve (LDTN) contains sympathetic nerves originating from the stellate ganglia. Objective The purpose of this study was to test the hypothesis that high-frequency electrical stimulation of the LDTN can cause stellate ganglia damage and suppress PAT. Methods We performed chronic LDTN stimulation in 6 dogs with and 2 dogs without intermittent rapid LA pacing while monitoring SGNA. Results LDTN stimulation reduced average SGNA from 4.36 μV (95% confidence interval [CI] 4.10–4.62 μV) at baseline to 3.22 μV (95% CI 3.04–3.40 μV) after 2 weeks (P = .028) and completely suppressed all PAT episodes in all dogs studied. Tyrosine hydroxylase staining showed large damaged regions in both stellate ganglia, with increased percentages of tyrosine hydroxylase–negative cells. The terminal deoxynucleotidyl transferase dUTP nick end labeling assay showed that 23.36% (95% CI 18.74%–27.98%) of ganglion cells in the left stellate ganglia and 11.15% (95% CI 9.34%–12.96%) ganglion cells in the right stellate ganglia were positive, indicating extensive cell death. A reduction of both SGNA and heart rate was also observed in dogs with LDTN stimulation but without high-rate LA pacing. Histological studies in the latter 2 dogs confirmed the presence of extensive stellate ganglia damage, along with a high percentage of terminal deoxynucleotidyl transferase dUTP nick end labeling–positive cells. Conclusion LDTN stimulation damages both left stellate ganglia and right stellate ganglia, reduces left SGNA, and is antiarrhythmic in this canine model of PAT

Long-term intermittent high-amplitude subcutaneous nerve stimulation reduces sympathetic tone in ambulatory dogs

BACKGROUND: Reducing sympathetic efferent outflow from the stellate ganglia (SG) may be antiarrhythmic. OBJECTIVE: The purpose of this study was to test the hypothesis that chronic thoracic subcutaneous nerve stimulation (ScNS) could reduce SG nerve activity (SGNA) and control paroxysmal atrial tachycardia (PAT). METHODS: Thoracic ScNS was performed in 8 dogs while SGNA, vagal nerve activity (VNA), and subcutaneous nerve activity (ScNA) were monitored. An additional 3 dogs were used for sham stimulation as controls. RESULTS: Xinshu ScNS and left lateral thoracic nerve ScNS reduced heart rate (HR). Xinshu ScNS at 3.5 mA for 2 weeks reduced mean average SGNA from 5.32 μV (95% confidence interval [CI] 3.89-6.75) at baseline to 3.24 μV (95% CI 2.16-4.31; P = .015) and mean HR from 89 bpm (95% CI 80-98) at baseline to 83 bpm (95% CI 76-90; P = .007). Bilateral SG showed regions of decreased tyrosine hydroxylase staining with increased terminal deoxynucleotidyl transferase dUTP nick-end labeling-positive nuclei in 18.47% (95% CI 9.68-46.62) of all ganglion cells, indicating cell death. Spontaneous PAT episodes were reduced from 9.83 per day (95% CI 5.77-13.89) in controls to 3.00 per day (95% CI 0.11-5.89) after ScNS (P = .027). Left lateral thoracic nerve ScNS also led to significant bilateral SG neuronal death and significantly reduced average SGNA and HR in dogs. CONCLUSION: ScNS at 2 different sites in the thorax led to SG cell death, reduced SGNA, and suppressed PAT in ambulatory dogs

Subcutaneous nerve stimulation for rate control in ambulatory dogs with persistent atrial fibrillation

Background Subcutaneous nerve stimulation (ScNS) damages the stellate ganglion and improves rhythm control of atrial fibrillation (AF) in ambulatory dogs. Objective The purpose of this study was to test the hypothesis that thoracic ScNS can improve rate control in persistent AF. Methods We created persistent AF in 13 dogs and randomly assigned them to ScNS (n = 6) and sham control (n = 7) groups. 18F-2-Fluoro-2-deoxyglucose positron emission tomography/magnetic resonance imaging of the brain stem was performed at baseline and at the end of the study. Results The average stellate ganglion nerve activity reduced from 4.00 ± 1.68 μV after the induction of persistent AF to 1.72 ± 0.42 μV (P = .032) after ScNS. In contrast, the average stellate ganglion nerve activity increased from 3.01 ± 1.26 μV during AF to 5.52 ± 2.69 μV after sham stimulation (P = .023). The mean ventricular rate during persistent AF reduced from 149 ± 36 to 84 ± 16 beats/min (P = .011) in the ScNS group, but no changes were observed in the sham control group. The left ventricular ejection fraction remained unchanged in the ScNS group but reduced significantly in the sham control group. Immunostaining showed damaged ganglion cells in bilateral stellate ganglia and increased brain stem glial cell reaction in the ScNS group but not in the control group. The 18F-2-fluoro-2-deoxyglucose uptake in the pons and medulla was significantly (P = .011) higher in the ScNS group than the sham control group at the end of the study. Conclusion Thoracic ScNS causes neural remodeling in the brain stem and stellate ganglia, controls the ventricular rate, and preserves the left ventricular ejection fraction in ambulatory dogs with persistent AF

Role of apamin sensitive small conductance calcium-activated potassium currents in long term cardiac memory in rabbits

Background Apamin-sensitive small conductance calcium-activated K current (IKAS) is upregulated during ventricular pacing and masks short-term cardiac memory (CM). Objective – To determine the role of IKAS in long-term CM. Methods – CM was created with 3-5 weeks of ventricular pacing and defined by a flat or inverted T-wave off pacing. Epicardial optical mapping was performed in both paced and normal ventricles. Action potential duration (APD80) was determined during RA pacing. Ventricular stability was tested before and after IKAS blockade. Four paced hearts and 4 normal hearts were used for western blotting and histology. Results – There were no significant differences in either the echocardiographic parameters or in fibrosis levels between groups. Apamin induced more APD80 prolongation in CM than in normal ventricles (9.6% [8.8%-10.5%] vs 3.1% [1.9%-4.3%], p<0.001). Apamin significantly lengthend the APD80 in the CM model at late activation sites, indicating significant IKAS upregulation at those sites. The CM model also had altered Ca2+ handling as the 50% Ca2+ transient duration and amplitude were increased at distal sites compared to a proximal site (near the pacing site). After apamin, the CM model had increased VF inducibility (paced vs control, 33/40 (82.5%) vs 7/20 (35%) P<0.001), and longer VF durations (124 vs 26 seconds, P<0.001). Conclusions Chronic ventricular pacing increases Ca2+ transients at late activation sites which activates IKAS to maintain repolarization reserve. IKAS blockade increases VF vulnerability in chronically paced rabbit ventricles