Time-Reversal Indoor Positioning System and Medium Access Control

With the rapid expansion of the wireless communication, there has been a rapid growth in the demand for the mobile traffic. Moreover, the wireless traffic not only expands in traffic volume but also in the diversity of applications and requirements with the rise of the Internet of Things (IoT) concept. The insatiable demand for both the traffic volume and the ever-expanding IoT applications poses a great challenge on the design of the next generation, i.e. the 5G, communication system. Time reversal (TR) technology has been proposed as a promising candidate for the 5G system with several promising characteristics, such as easy densification, asymmetric and heterogeneous design. TR system utilizes large bandwidth and observes detailed, location-specific channel impulse responses (CIR). With the detail CIR information, the TR system designs waveforms to concentrate transmitted energy to the intended users via the unique spatial temporal focusing effect. In this dissertation, we propose a TR indoor positioning system and medium access control design based on this unique effect. We begin by proposing the time reversal resonating strength (TRRS) to quantify the similarity between the location information embedded CIRs. The TR indoor positioning system identifies the unknown users by calculating the TRRS between the CIR of the unknown user and the CIRs in the database. We built the system prototype and are the first-ever to perform precise indoor positioning at 1 to 2 cm resolution in both line-of-sight and non-line-of-sight scenario using one pair of transmitter and receiver both equipped with a single antenna. Based on the positioning system, we propose an indoor tracking system by collecting CIRs at several regions of interest and track unknown users when they pass it. To facilitate deployment, we built a prototype to automate CIR collection and the experiments show that the system detects the users correctly with very low false alarm rate. In the second part, we design the medium access control scheme to maximize system sum rate and guarantee quality of service to the users in a downlink scenario. The system objective and constraints are transformed into a mixed integer quadratically constraint quadratic programming and can be solved efficiently. We then investigate rate adaptation scheme via selection of optimal backoff factors in TR system. The rate adaptation scheme effectively increases the system-wise performance and the fairness among users

Codec Switching with Threshold Adaptation for Multimedia Streaming over Wireless Local Area Networks

在網路多媒體串流環境中，多媒體串流的影像品質會受到網路通道的影響。由於無線網路通道環境隨著時間變化劇烈，並且難以預測，此會嚴重影響到無線網路中多媒體串流的影像品質。因此經由無線網路提供多媒體串流，並具可靠性且穩定的服務品質，是一件困難的挑戰。本論文對於無線網路多媒體串流提出一個創新的跨層演算法，動態調適伺服器編碼器參數，以適應短期和長期的通道變化。在短期的動態調適方面，本演算法將定時把多媒體客戶端所觀察到的圖框錯誤率(Frame Error Rate)回傳給遠端的多媒體伺服器。伺服器將圖框錯誤率和編碼器切換閾值做比較後，伺服器即可調整編碼器參數以適應於當時的通道環境。本論文也提出演算法對長期的通道變化做出調適。在無線通道狀況和編碼器參數已知的情況下，多媒體伺服器可找出最小化調適周期內均方誤差的編碼器調適閾值，並將此閾值做為短期動態調適演算法中編碼器切換所使用之閾值。本論文所提出的演算法複雜度不高，而且在無線通道下的多媒體串流的信噪比，可以大幅提升3到5分貝。In wireless multimedia streaming, the quality of service (QoS) experienced by the multimedia traffic is subject to the channel variation, which is hard to predict. As a result, transmitting multimedia contents reliably in wireless environments becomes a big challenge in wireless communication. In this thesis, a novel cross-layer algorithm is proposed to deal with both the short-term and the long-term channel variations. To cope with the short-term channel variation, the MAC frame error rate (FER) observed by the client is periodically reported to the multimedia server. The multimedia server then adjusts the codec setting for encoding video bit streams by comparing the reported FER to a set of codec switching thresholds. On the other hand, the algorithm adapts the codec switching thresholds periodically with a longer threshold adaptation period to address the effect of the long-term channel variation. Given the wireless channel state and the codec setting used at the beginning of each threshold adaptation period, the media server selects the codec switching thresholds that minimize the expected transient mean square error (MSE) of the threshold adaptation period. The proposed algorithm reduces the number of computation and the simulation results show that the algorithm significantly improves the PSNR by 3 to 5 dB for multimedia streaming over varying wireless channels

Endothelin-1 Induces Mesothelial Mesenchymal Transition and Correlates with Pleural Fibrosis in Tuberculous Pleural Effusions

Endothelin (ET)-1 is involved in various fibrotic diseases. However, its implication in pleural fibrosis remains unknown. We aimed to study the profibrotic role of ET-1 in tuberculous pleural effusion (TBPE). The pleural effusion ET-1 levels were measured among 68 patients including transudative pleural effusion (TPE, n = 12), parapneumonic pleural effusion (PPE, n = 20), and TBPE (n = 36) groups. Pleural fibrosis, defined as radiological residual pleural thickening (RPT) and shadowing, was measured at 12-month follow-up. Additionally, the effect of ET-1 on mesothelial mesenchymal transition (MMT) and extracellular matrix (ECM) producion in human pleural mesothelial cells (PMCs) was assessed. Our findings revealed that effusion ET-1 levels were significantly higher in TBPE than in TPE and PPE, and were markedly higher in TBPE patients with RPT >10 mm than those with RPT ≤10 mm. ET-1 levels correlated substantially with residual pleural shadowing and independently predicted RPT >10 mm in TBPE. In PMCs, ET-1 time-dependently induced MMT with upregulation of α-smooth muscle actin and downregulation of E-cadherin, and stimulated ECM production; furthermore, ET receptor antagonists effectively abrogated these effects. In conclusion, ET-1 induces MMT and ECM synthesis in human PMCs and correlates with pleural fibrosis in TBPE. This study confers a novel insight into the pathogenesis and potential therapies for fibrotic pleural diseases

Distinct clinical outcomes of non-small cell lung cancer patients with epidermal growth factor receptor (EGFR) mutations treated with EGFR tyrosine kinase inhibitors: non-responders versus responders.

INTRODUCTION: Treatment with epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) has been associated with favorable progression free survival (PFS) in patients with non-small cell lung cancers (NSCLC) harboring EGFR mutations. However, a subset of this population doesn't respond to EGFR-TKI treatment. Therefore, the present study aimed to elucidate survival outcome in NSCLC EGFR-mutant patients who were treated with EGFR TKIs. METHODS: Among the 580 consecutive NSCLC patients who were treated at our facility between 2008 and 2012, a total of 124 treatment-naïve, advanced NSCLC, EGFR-mutant patients treated with EGFR TKIs were identified and grouped into non-responders and responders for analyses. RESULTS: Of 124 patients, 104 (84%) responded to treatment, and 20 (16%) did not; and the overall median PFS was 9.0 months. Notably, the PFS, overall survival (OS) and survival rates were significantly unfavorable in non-responders (1.8 vs. 10.3 months, hazard ratio (HR) = 29.2, 95% confidence interval (CI), 13.48-63.26, P<0.0001; 9.4 vs. 17.3 months, HR = 2.74, 95% CI, 1.52-4.94, P = 0.0008; and 58% vs. 82% in 6, 37% vs. 60% in 12, and 19 vs. 40% at 24 months, respectively). In multivariate analysis, treatment efficacy strongly affected PFS and OS, independent of covariates (HR = 47.22, 95% CI, 17.88-124.73, P<0.001 and HR = 2.74, 95% CI, 1.43-5.24, P = 0.002, respectively). However, none of the covariates except of the presence of EGFR exon 19 deletion in the tumors was significantly associated with better treatment efficacy. CONCLUSIONS: A subset of NSCLC EGFR-mutant patients displayed unfavorable survival despite EGFR TKI administration. This observation reinforces the urgent need for biomarkers effectively predicting the non-responders and for drug development overcoming primary resistance to EGFR TKIs. In addition, optimal therapeutic strategies to prolong the survival of non-responders need to be investigated

Analysis of clinical variables associated with progression free survival in NSCLC <i>EGFR</i>-mutant patients.

‡<p>reference group was exon 21. <i>EGFR</i>: epidermal growth factor receptor, TKI: tyrosine kinase inhibitor, ECOG PS: eastern cooperation oncology group performance status, HR: hazard ratio, CI: confidence interval.</p

Baseline characteristics of patients with NSCLC harboring <i>EGFR</i> mutations treated with <i>EGFR</i> TKIs.

<p>NSCLC: non-small cell lung cancer, NOS: not otherwise specified, <i>EGFR</i>: epidermal growth factor receptor, TKI: tyrosine kinase inhibitor, ECOG PS: eastern cooperation oncology group performance status, SCC: squamous cell carcinoma</p

Analysis of variables associated with overall survival in NSCLC <i>EGFR</i>-mutant patients.

‡<p>reference group was exon 21. <i>EGFR</i>: epidermal growth factor receptor, TKI: tyrosine kinase inhibitor, ECOG PS: eastern cooperation oncology group performance status, HR: hazard ratio, CI: confidence interval</p

Analysis of clinial variables associated with treatment efficacy of <i>EGFR</i> TKI in NSCLC <i>EGFR</i>-mutant patients.

‡<p>reference group was exon 21. <i>EGFR</i>: epidermal growth factor receptor, TKI: tyrosine kinase inhibitor, ECOG PS: eastern cooperation oncology group performance status, OR: odds ratio, CI: confidence interval</p

Flow chart of patients enrolled for analysis.

<p>NSCLC: non-small cell lung cancer, <i>EGFR</i>: epidermal growth factor receptor, TKI: tyrosine kinase inhibitor</p

Progression-free survival A) in all, B) in patients stratified by non-responders and responders, and overall survival C) in all, D) in patients stratified by non-responders and responders.

<p>Progression-free survival A) in all, B) in patients stratified by non-responders and responders, and overall survival C) in all, D) in patients stratified by non-responders and responders.</p