The application of genetic algorithms to the adaptation of IIR filters

The adaptation of an IIR filter is a very difficult problem due to its non-quadratic performance surface and potential instability. Conventional adaptive IIR algorithms suffer from potential instability problems and a high cost for stability monitoring. Therefore, there is much interest in adaptive IIR filters based on alternative algorithms. Genetic algorithms are a family of search algorithms based on natural selection and genetics. They have been successfully used in many different areas. Genetic algorithms applied to the adaptation of IIR filtering problems are studied in this thesis, and show that the genetic algorithm approach has a number of advantages over conventional gradient algorithms, particularly, for the adaptation of high order adaptive IIR filters, IIR filters with poles close to the unit circle and IIR filters with multi-modal error surfaces. The conventional gradient algorithms have difficulty solving these problems. Coefficient results are presented for various orders of IIR filters in this thesis. In the computer simulations presented in this thesis, the direct, cascade, parallel and lattice form IIR filter structures have been used and compared. The lattice form IIR filter structure shows its superiority over the cascade and parallel form IIR filter structures in terms of its mean square error convergence performance

TIMP1 promotes multi-walled carbon nanotube-induced lung fibrosis by stimulating fibroblast activation and proliferation

<p>Pulmonary exposure to multi-walled carbon nanotubes (MWCNTs) may cause fibrosing lesions in animal lungs, raising health concerns about such exposure in humans. The mechanisms underlying fibrosis development remain unclear, but they are believed to involve the dysfunction of fibroblasts and myofibroblasts. Using a mouse model of MWCNT exposure, we found that the tissue inhibitor of metalloproteinase 1 (Timp1) gene was rapidly and highly induced in the lungs by MWCNTs in a time- and dose-dependent manner. Concomitantly, a pronounced elevation of secreted TIMP1 was observed in the bronchoalveolar lavage (BAL) fluid and serum. Knockout (KO) of Timp1 in mice caused a significant reduction in fibrotic focus formation, collagen fiber deposition, recruitment of fibroblasts and differentiation of fibroblasts into myofibroblasts in the lungs, indicating that TIMP1 plays a critical role in the pulmonary fibrotic response to MWCNTs. At the molecular level, MWCNT exposure significantly increased the expression of the cell proliferation markers Ki-67 and PCNA and a panel of cell cycle-controlling genes in the lungs in a TIMP1-dependent manner. MWCNT-stimulated cell proliferation was most prominent in fibroblasts but not myofibroblasts. Furthermore, MWCNTs elicited a significant induction of CD63 and integrin β1 in lung fibroblasts, leading to the formation of a TIMP1/CD63/integrin β1 complex on the surface of fibroblasts <i>in vivo</i> and <i>in vitro</i>, which triggered the phosphorylation and activation of Erk1/2. Our study uncovers a new pathway through which induced TIMP1 critically modulates the pulmonary fibrotic response to MWCNTs by promoting fibroblast activation and proliferation via the TIMP1/CD63/integrin β1 axis and ERK signaling.</p

Macrophage polarization and activation at the interface of multi-walled carbon nanotube-induced pulmonary inflammation and fibrosis

<p>Pulmonary exposure to carbon nanotubes (CNTs) induces fibrosing lesions in the lungs that manifest rapid-onset inflammatory and fibrotic responses, leading to chronic fibrosis in animals and health concerns in exposed humans. The mechanisms underlying CNT-induced fibrogenic effects remain undefined. Macrophages are known to play important roles in immune regulation and fibrosis development through their distinct subsets. Here we investigated macrophage polarization and activation in mouse lungs exposed to multi-walled CNTs (MWCNTs). Male C57BL/6J mice were treated with MWCNTs (XNRI MWNT-7) at 40 μg per mouse (∼1.86 mg/kg body weight) by oropharyngeal aspiration. The treatment stimulated prominent acute inflammatory and fibrotic responses. Moreover, it induced pronounced enrichment and polarization of macrophages with significantly increased M1 and M2 populations in a time-dependent manner. Induction of M1 polarization was apparent on day 1 with a peak on day 3, but declined rapidly thereafter. On the other hand, the M2 polarization was induced on day 1 modestly, but was remarkably elevated on day 3 and maintained at a high level through day 7. M1 and M2 macrophages were functionally activated by MWCNTs as indicated by the expression of their distinctive functional markers, such as iNOS and ARG1, with time courses parallel to M1 and M2 polarization, respectively. Molecular analysis revealed MWCNTs boosted specific STAT and IRF signaling pathways to regulate M1 and M2 polarization in the lungs. These findings suggest a new mechanistic connection between inflammation and fibrosis induced by MWCNTs through the polarization and activation of macrophages during MWCNT-induced lung pathologic response.</p

Suppression of basal and carbon nanotube-induced oxidative stress, inflammation and fibrosis in mouse lungs by Nrf2

<p>The lungs are susceptible to oxidative damage by inhaled pathogenic agents, including multi-walled carbon nanotubes (MWCNT). The nuclear factor erythroid 2-related factor 2 (Nrf2) has been implicated in regulating the body’s defense against oxidative stress. Here, we analyzed the function of Nrf2 in the lungs. Under a basal condition, Nrf2 knockout (KO) mice showed apparent pulmonary infiltration of granulocytes, macrophages and B and T lymphocytes, and elevated deposition of collagen fibers. Exposure to MWCNT (XNRI MWNT-7, Mitsui, Tokyo, Japan) by pharyngeal aspiration elicited rapid inflammatory and fibrotic responses in a dose (0, 5, 20 and 40 μg) and time (1, 3, 7 and 14 d)-dependent manner. The responses reached peak levels on day 7 post-exposure to 40 μg MWCNT, evidenced by massive inflammatory infiltration and formation of inflammatory and fibrotic foci, which were more evident in Nrf2 KO than wild-type (WT) lungs. At the molecular level, Nrf2 protein was detected at a low level under a basal condition, and was dramatically increased by MWCNT in WT, but not Nrf2 KO, lungs. Activation of Nrf2 was inversely correlated with induced expression of fibrosis marker genes and profibrotic cytokines. Furthermore, the levels of ROS and oxidative stress were remarkably higher in Nrf2 KO than WT lungs under a physiological condition, and were dramatically increased by MWCNT, with the increase significantly more striking in KO lungs. The findings reveal that Nrf2 plays an important role in suppressing the basal and MWCNT-induced oxidant production, inflammation and fibrosis in the lungs, thereby protecting against MWCNT lung toxicity.</p

Electrochemiluminescence Detection of <i>Escherichia coli</i> O157:H7 Based on a Novel Polydopamine Surface Imprinted Polymer Biosensor

In this paper, a facilely prepared electrochemiluminescence (ECL) biosensor was developed for <i>Escherichia coli</i> O157:H7 quantitative detection based on a polydopamine (PDA) surface imprinted polymer (SIP) and nitrogen-doped graphene quantum dots (N-GQDs). N-GQDs with a high quantum yield of 43.2% were synthesized. The uniform PDA SIP film for <i>E. coli</i> O157:H7 was established successfully with a facile route. The dopamine and target bacteria were electropolymerized directly on the electrode. After removal of the <i>E. coli</i> O157:H7 template, the established PDA SIP can selectively recognize <i>E. coli</i> O157:H7. Accordingly, <i>E. coli</i> O157:H7 polyclonal antibody (pAb) was labeled with N-GQDs. The bioconjugation of SIP–<i>E. coli</i> O157:H7/pAb-N-GQDs can generate intensive ECL irradiation with K₂S₂O₈. As a result, <i>E. coli</i> O157:H7 was detected with the ECL sensing system. Under optimal conditions, the linear relationships between the ECL intensity and <i>E. coli</i> O157:H7 concentration were obtained from 10¹ colony-forming units (CFU) mL^–1 to 10⁷ CFU mL^–1 with a limit of detection of 8 CFU mL^–1. The biosensor based on this SIP film was applied in water sample detection successfully. The N-GQD-based ECL analytical method for <i>E. coli</i> O157:H7 was reported for the first time. The sensing system had high selectivity to the target analyte, provided new opportunities for use, and increased the rate of disease diagnosis and treatment and the prevention of pathogens

Poly(vinyl alcohol)-Assisted Fabrication of Hollow Carbon Spheres/Reduced Graphene Oxide Nanocomposites for High-Performance Lithium-Ion Battery Anodes

Three-dimensional hollow carbon spheres/reduced graphene oxide (DHCSs/RGO) nanocomposites with high-level heteroatom doping and hierarchical pores are fabricated <i>via</i> a versatile method. Poly­(vinyl alcohol) (PVA) that serves as a dispersant and nucleating agent is used as the nonremoval template for synthesizing melamine resin (MR) spheres with abundant heteroatoms, which are subsequently composited with graphene oxide (GO). Use of PVA and implementation of freezing treatment prevent agglomeration of MR spheres within the GO network. Molten KOH is used to achieve the one-step carbonization/activation/reduction for the synthesis of DHCSs/RGO. DHCSs/RGO annealed at 700 °C shows superior discharge capacity of 1395 mA h/g at 0.1 A/g and 606 mA h/g at 5 A/g as well as excellent retentive capacity of 755 mA h/g after 600 cycles at a current density of 2 A/g. An extra CO₂ activation leads to further enhancement of electrochemical performance with outstanding discharge capacity of 1709 mA h/g at 0.1 A/g and 835 mA h/g at 2 A/g after 600 cycles. This work may improve our understanding of the synthesis of graphene-like nanocomposites with hollow and porous carbon architectures and fabrication of high-performance functional devices

Accurate Capture and Identification of Exosomes: Nanoarchitecture of the MXene Heterostructure/Engineered Lipid Layer

Recently, exosome detection has become an important breakthrough in clinical diagnosis. However, the effective capture and accurate identification of cancer exosomes in a complex biomatrix are still a tough task. Especially, the large size and non-conductivity of exosomes are not conducive to highly sensitive electrochemical or electrochemiluminescence (ECL) detection. Therefore, we have developed a Ti3C2Tx–Bi2S3–x heterostructure/engineered lipid layer-based nanoarchitecture to overcome the limitations. The engineered lipid layer not only specifically captured and efficiently fused CD63 positive exosomes but also showed excellent antifouling property in the biological matrix. Moreover, the MUC1 aptamer-modified Ti3C2Tx–Bi2S3–x heterostructure further identified and covered the gastric cancer exosomes that have been trapped in the engineered lipid layer. In the self-luminous Faraday cage-type sensing system, the Ti3C2Tx–Bi2S3–x heterostructure with sulfur vacancies extended the outer Helmholtz plane and amplified the ECL signal. Therefore, this sensor can be used to detect tumor exosomes in ascites of cancer patients without additional purification. It provides a new pathway to detect exosomes and other large-sized vesicles with high sensitivity

A reverse dot blot assay for the screening of twenty mutations in four genes associated with NSHL in a Chinese population

<div><p>Background</p><p>Congenital deafness is one of the most distressing disorders affecting humanity and exhibits a high incidence worldwide. Most cases of congenital deafness in the Chinese population are caused by defects in a limited number of genes. A convenient and reliable method for detecting common deafness-related gene mutations in the Chinese population is required.</p><p>Methods</p><p>We developed a PCR-reverse dot blot (RDB) assay for screening 20 hotspot mutations of <i>GJB2</i>, <i>GJB3</i>, <i>SLC26A4</i>, and <i>MT-RNR1</i>, which are common non-syndromic hearing loss (NSHL)–associated genes in the Chinese population. The PCR-RDB assay consists of multiplex PCR amplifications of 10 fragments in the target sequence of the four above-mentioned genes in wild-type and mutant genomic DNA samples followed by hybridization to a test strip containing allele-specific oligonucleotide probes. We applied our method to a set of 225 neonates with deafness gene mutations and 30 normal neonates.</p><p>Results</p><p>The test was validated through direct sequencing in a blinded study with 100% concordance.</p><p>Conclusions</p><p>The results demonstrated that our reverse dot blot assay is a reliable and effective genetic screening method for identifying carriers and individuals with NSHL among the Chinese population.</p></div

PCR products of eight samples obtained by electrophoresis in a 1.5% agarose gel stained with ethidium bromide.

<p>I and II represents PCR products of tube I and II respectively.</p

Multiplex PCR primers.

<p>Multiplex PCR primers.</p