Improved multiple input multiple output blind equalization algorithms for medical implant communication

Medical implant sensor that is used to monitor the human physiology signals is helpful to improve the quality of life and prevent severe result from the chronic diseases. In order to achieve this, the wireless implant communication link that delivers the monitored signal to a multiple antennas external device is an essential portion. However, the existing conventional narrow band Medical Implant Communications System (MICS) has low data rate because of the bandlimited channel is allocated. To improve the data rate in the radio frequency communication, ultra-wide band technology has been proposed. However, the ultra-wide band technology is relatively new and requires living human to be the test subject in order to validate the technology performance. In this condition, the test on the new technology can rise ethical challenge. As a solution, we improve the data rate in the conventional narrow band MICS. The improvement of data rate on the narrow band implies the information bandwidth is larger than the allocated channel bandwidth, and therefore the high frequency components of the information can loss. In this case, the signal suffers the intersymbol-interference (ISI). Instead of that, the multiple antennas external device can receive the signal from other transmitting implant sensor which has the same operating frequency. As a result, the signal is further hampered by co-channel interference (CCI). To recover the signal from the ISI and CCI, multiple-input multiple output (MIMO) blind equalization that has source separation ability can be exploited. Cross-Correlation Constant Modulus Algorithm (CC-CMA) is the conventional MIMO blind equalization algorithm that can suppress ISI and CCI and able to perform source separation. However, CC-CMA has only been analyzed and simulated in the modulation of Phase Shift Keying (PSK). The performance of CC-CMA in multi-modulus modulation scheme such as 4-Pulse-amplitude modulation (PAM) and 16-Quadrature amplitude modulation (QAM), which has higher data rate than PSK, has not been analyzed. Therefore, our work is to analysis and optimize CC-CMA on the multi-modulus modulation scheme. From our analysis, we found that the cost function of CC-CMA is biased cost function. Instead of that, from our simulation, CC-CMA introduces an unexpected shrinking effect whereby the amplitudes of the equalizer outputs have been reduced, especially in multi-modulus modulation scheme. This shrinking effect is not severe in PSK because the decision of a PSK symbol is based on phase, but not amplitude. Unfortunately, this is severe in multi-modulus modulation scheme. To overcome this shrinking effect in multi-modulus modulation scheme, we propose Cross-Independent Constant Modulus Algorithm (CI-CMA). Based on the convergence analysis, we identify the new optimum dispersion value and mixing parameter in CI-CMA. From the simulation results, we confirm that CI-CMA is able to perform equalization and source separation in the multi-modulus modulation scheme. In order to improve the steady state performance of CI-CMA, we perform the steady state mean square error (MSE) analysis of CI-CMA using the energy preservation theorem that was developed by Mai and Sayed in 2001, and our result is more accurate than the previous work. From our analysis, only the reduction in adaptation step size can reduce the steady state MSE, but it is well known that the MSE is indeed a tradeoff with the speed of convergence. Therefore without sacrificing convergence speed, our last effort is to propose hybrid algorithms. The hybrid algorithms are done by combining a new adaptive constant modulus algorithm (ACMA), a decision directed algorithm and a cross-correlation function. From the simulation results, we found that the hybrid algorithms can show low steady state error and thereby improve the reliability of the communication link. The main achievement of this thesis is the discovery of new dispersion value through the convergence analysis

Improved multiple input multiple output blind equalization algorithms for medical implant communication

Medical implant sensor that is used to monitor the human physiology signals is helpful to improve the quality of life and prevent severe result from the chronic diseases. In order to achieve this, the wireless implant communication link that delivers the monitored signal to a multiple antennas external device is an essential portion. However, the existing conventional narrow band Medical Implant Communications System (MICS) has low data rate because of the bandlimited channel is allocated. To improve the data rate in the radio frequency communication, ultra-wide band technology has been proposed. However, the ultra-wide band technology is relatively new and requires living human to be the test subject in order to validate the technology performance. In this condition, the test on the new technology can rise ethical challenge. As a solution, we improve the data rate in the conventional narrow band MICS. The improvement of data rate on the narrow band implies the information bandwidth is larger than the allocated channel bandwidth, and therefore the high frequency components of the information can loss. In this case, the signal suffers the intersymbol-interference (ISI). Instead of that, the multiple antennas external device can receive the signal from other transmitting implant sensor which has the same operating frequency. As a result, the signal is further hampered by co-channel interference (CCI). To recover the signal from the ISI and CCI, multiple-input multiple output (MIMO) blind equalization that has source separation ability can be exploited. Cross-Correlation Constant Modulus Algorithm (CC-CMA) is the conventional MIMO blind equalization algorithm that can suppress ISI and CCI and able to perform source separation. However, CC-CMA has only been analyzed and simulated in the modulation of Phase Shift Keying (PSK). The performance of CC-CMA in multi-modulus modulation scheme such as 4-Pulse-amplitude modulation (PAM) and 16-Quadrature amplitude modulation (QAM), which has higher data rate than PSK, has not been analyzed. Therefore, our work is to analysis and optimize CC-CMA on the multi-modulus modulation scheme. From our analysis, we found that the cost function of CC-CMA is biased cost function. Instead of that, from our simulation, CC-CMA introduces an unexpected shrinking effect whereby the amplitudes of the equalizer outputs have been reduced, especially in multi-modulus modulation scheme. This shrinking effect is not severe in PSK because the decision of a PSK symbol is based on phase, but not amplitude. Unfortunately, this is severe in multi-modulus modulation scheme. To overcome this shrinking effect in multi-modulus modulation scheme, we propose Cross-Independent Constant Modulus Algorithm (CI-CMA). Based on the convergence analysis, we identify the new optimum dispersion value and mixing parameter in CI-CMA. From the simulation results, we confirm that CI-CMA is able to perform equalization and source separation in the multi-modulus modulation scheme. In order to improve the steady state performance of CI-CMA, we perform the steady state mean square error (MSE) analysis of CI-CMA using the energy preservation theorem that was developed by Mai and Sayed in 2001, and our result is more accurate than the previous work. From our analysis, only the reduction in adaptation step size can reduce the steady state MSE, but it is well known that the MSE is indeed a tradeoff with the speed of convergence. Therefore without sacrificing convergence speed, our last effort is to propose hybrid algorithms. The hybrid algorithms are done by combining a new adaptive constant modulus algorithm (ACMA), a decision directed algorithm and a cross-correlation function. From the simulation results, we found that the hybrid algorithms can show low steady state error and thereby improve the reliability of the communication link. The main achievement of this thesis is the discovery of new dispersion value through the convergence analysis

Urinary MicroRNA Profiling in the Nephropathy of Type 1 Diabetes

Background: Patients with Type 1 Diabetes (T1D) are particularly vulnerable to development of Diabetic nephropathy (DN) leading to End Stage Renal Disease. Hence a better understanding of the factors affecting kidney disease progression in T1D is urgently needed. In recent years microRNAs have emerged as important post-transcriptional regulators of gene expression in many different health conditions. We hypothesized that urinary microRNA profile of patients will differ in the different stages of diabetic renal disease. Methods and Findings: We studied urine microRNA profiles with qPCR in 40 T1D with >20 year follow up 10 who never developed renal disease (N) matched against 10 patients who went on to develop overt nephropathy (DN), 10 patients with intermittent microalbuminuria (IMA) matched against 10 patients with persistent (PMA) microalbuminuria. A Bayesian procedure was used to normalize and convert raw signals to expression ratios. We applied formal statistical techniques to translate fold changes to profiles of microRNA targets which were then used to make inferences about biological pathways in the Gene Ontology and REACTOME structured vocabularies. A total of 27 microRNAs were found to be present at significantly different levels in different stages of untreated nephropathy. These microRNAs mapped to overlapping pathways pertaining to growth factor signaling and renal fibrosis known to be targeted in diabetic kidney disease. Conclusions: Urinary microRNA profiles differ across the different stages of diabetic nephropathy. Previous work using experimental, clinical chemistry or biopsy samples has demonstrated differential expression of many of these microRNAs in a variety of chronic renal conditions and diabetes. Combining expression ratios of microRNAs with formal inferences about their predicted mRNA targets and associated biological pathways may yield useful markers for early diagnosis and risk stratification of DN in T1D by inferring the alteration of renal molecular processes. © 2013 Argyropoulos et al

Thermal Conductivity of Carbon Nanotubes and their Polymer Nanocomposites: A Review

Thermally conductive polymer composites offer new possibilities for replacing metal parts in several applications, including power electronics, electric motors and generators, heat exchangers, etc., thanks to the polymer advantages such as light weight, corrosion resistance and ease of processing. Current interest to improve the thermal conductivity of polymers is focused on the selective addition of nanofillers with high thermal conductivity. Unusually high thermal conductivity makes carbon nanotube (CNT) the best promising candidate material for thermally conductive composites. However, the thermal conductivities of polymer/CNT nanocomposites are relatively low compared with expectations from the intrinsic thermal conductivity of CNTs. The challenge primarily comes from the large interfacial thermal resistance between the CNT and the surrounding polymer matrix, which hinders the transfer of phonon dominating heat conduction in polymer and CNT. This article reviews the status of worldwide research in the thermal conductivity of CNTs and their polymer nanocomposites. The dependence of thermal conductivity of nanotubes on the atomic structure, the tube size, the morphology, the defect and the purification is reviewed. The roles of particle/polymer and particle/particle interfaces on the thermal conductivity of polymer/CNT nanocomposites are discussed in detail, as well as the relationship between the thermal conductivity and the micro- and nano-structure of the composite

Evidence for the decay B0->eta pi^0

We report a search for the charmless hadronic decay $B^0\to\eta \pi^0$ with a data sample corresponding to an integrated luminosity of 694 $\rm fb^{-1}$ containing $753\times10^6$ $B\bar{B}$ pairs. The data were collected by the Belle experiment running on the $\Upsilon(4S)$ resonance at the KEKB $e^+e^-$ collider. We measure a branching fraction $\mathcal{B}(B^0\to\eta\pi^0)=(4.1^{+1.7+0.5}_{-1.5-0.7})\times 10^{-7}$, where the first uncertainty is statistical and the second is systematic. Our measurement gives an upper limit of $\mathcal{B}(B^0\to\eta\pi^0)<6.5\times 10^{-7}$ at 90\% confidence level. The signal has a significance of $3.0$ standard deviations and constitutes the first evidence for this decay mode.Comment: 11 pages, 3 figures, 2 tables, submitted to Physical Review D(R

The Fourteenth Data Release of the Sloan Digital Sky Survey: First Spectroscopic Data from the extended Baryon Oscillation Spectroscopic Survey and from the second phase of the Apache Point Observatory Galactic Evolution Experiment

The fourth generation of the Sloan Digital Sky Survey (SDSS-IV) has been in operation since July 2014. This paper describes the second data release from this phase, and the fourteenth from SDSS overall (making this, Data Release Fourteen or DR14). This release makes public data taken by SDSS-IV in its first two years of operation (July 2014-2016). Like all previous SDSS releases, DR14 is cumulative, including the most recent reductions and calibrations of all data taken by SDSS since the first phase began operations in 2000. New in DR14 is the first public release of data from the extended Baryon Oscillation Spectroscopic Survey (eBOSS); the first data from the second phase of the Apache Point Observatory (APO) Galactic Evolution Experiment (APOGEE-2), including stellar parameter estimates from an innovative data driven machine learning algorithm known as "The Cannon"; and almost twice as many data cubes from the Mapping Nearby Galaxies at APO (MaNGA) survey as were in the previous release (N = 2812 in total). This paper describes the location and format of the publicly available data from SDSS-IV surveys. We provide references to the important technical papers describing how these data have been taken (both targeting and observation details) and processed for scientific use. The SDSS website (www.sdss.org) has been updated for this release, and provides links to data downloads, as well as tutorials and examples of data use. SDSS-IV is planning to continue to collect astronomical data until 2020, and will be followed by SDSS-V.Comment: SDSS-IV collaboration alphabetical author data release paper. DR14 happened on 31st July 2017. 19 pages, 5 figures. Accepted by ApJS on 28th Nov 2017 (this is the "post-print" and "post-proofs" version; minor corrections only from v1, and most of errors found in proofs corrected

Activation of BKCa Channels in Zoledronic Acid-Induced Apoptosis of MDA-MB-231 Breast Cancer Cells

BACKGROUND: Zoledronic acid, one of the most potent nitrogen-containing biphosphonates, has been demonstrated to have direct anti-tumor and anti-metastatic properties in breast cancer in vitro and in vivo. In particular, tumor-cell apoptosis has been recognized to play an important role in the treatment of metastatic breast cancer with zoledronic acid. However, the precise mechanisms remain less clear. In the present study, we investigated the specific role of large conductance Ca(2+)-activated potassium (BK(Ca)) channel in zoledronic acid-induced apoptosis of estrogen receptor (ER)-negative MDA-MB-231 breast cancer cells. METHODOLOGY/PRINCIPAL FINDINGS: The action of zoledronic acid on BK(Ca) channel was investigated by whole-cell and cell-attached patch clamp techniques. Cell apoptosis was assessed with immunocytochemistry, analysis of fragmented DNA by agarose gel electrophoresis, and flow cytometry assays. Cell proliferation was investigated by MTT test and immunocytochemistry. In addition, such findings were further confirmed with human embryonic kidney 293 (HEK293) cells which were transfected with functional BK(Ca) α-subunit (hSloα). Our results clearly indicated that zoledronic acid directly increased the activities of BK(Ca) channels, and then activation of BK(Ca) channel by zoledronic acid contributed to induce apoptosis in MDA-MB-231 cells. The possible mechanisms were associated with the elevated level of intracellular Ca(2+) and a concomitant depolarization of mitochondrial membrane potential (Δψm) in MDA-MB-231 cells. CONCLUSIONS: Activation of BK(Ca) channel was here shown to be a novel molecular pathway involved in zoledronic acid-induced apoptosis of MDA-MB-231 cells in vitro

Genomic and oncogenic preference of HBV integration in hepatocellular carcinoma

Hepatitis B virus (HBV) can integrate into the human genome, contributing to genomic instability and hepatocarcinogenesis. Here by conducting high-throughput viral integration detection and RNA sequencing, we identify 4,225 HBV integration events in tumour and adjacent non-tumour samples from 426 patients with HCC. We show that HBV is prone to integrate into rare fragile sites and functional genomic regions including CpG islands. We observe a distinct pattern in the preferential sites of HBV integration between tumour and non-tumour tissues. HBV insertional sites are significantly enriched in the proximity of telomeres in tumours. Recurrent HBV target genes are identified with few that overlap. The overall HBV integration frequency is much higher in tumour genomes of males than in females, with a significant enrichment of integration into chromosome 17. Furthermore, a cirrhosis-dependent HBV integration pattern is observed, affecting distinct targeted genes. Our data suggest that HBV integration has a high potential to drive oncogenic transformation

RANKL Is a Downstream Mediator for Insulin-Induced Osteoblastic Differentiation of Vascular Smooth Muscle Cells

Several reports have shown that circulating insulin level is positively correlated with arterial calcification; however, the relationship between insulin and arterial calcification remains controversial and the mechanism involved is still unclear. We used calcifying vascular smooth muscle cells (CVSMCs), a specific subpopulation of vascular smooth muscle cells that could spontaneously express osteoblastic phenotype genes and form calcification nodules, to investigate the effect of insulin on osteoblastic differentiation of CVSMCs and the cell signals involved. Our experiments demonstrated that insulin could promote alkaline phosphatase (ALP) activity, osteocalcin expression and the formation of mineralized nodules in CVSMCs. Suppression of receptor activator of nuclear factor κB ligand (RANKL) with small interfering RNA (siRNA) abolished the insulin-induced ALP activity. Insulin induced the activation of extracellular signal-regulated kinase (ERK)1/2, mitogen-activated protein kinase (MAPK) and RAC-alpha serine/threonine-protein kinase (Akt). Furthermore, pretreatment of human osteoblasts with the ERK1/2 inhibitor PD98059, but not the phosphoinositide 3-kinase (PI3K) inhibitor, LY294002, or the Akt inhibitor, 1L-6-hydroxymethyl-chiro-inositol 2-(R)-2-O-methyl-3-O-octadecylcarbonate (HIMO), abolished the insulin-induced RANKL secretion and blocked the promoting effect of insulin on ALP activities of CVSMCs. Recombinant RANKL protein recovered the ALP activities decreased by RANKL siRNA in insulin-stimulated CVSMCs. These data demonstrated that insulin could promote osteoblastic differentiation of CVSMCs by increased RANKL expression through ERK1/2 activation, but not PI3K/Akt activation