Technological University

Qingshui, China

Technological University

Qingshui, China

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Artyushenko V.M.,Technological University | Volovach V.I.,Togliatti State University
Proceedings of 2016 IEEE East-West Design and Test Symposium, EWDTS 2016 | Year: 2016

Estimation of potential accuracy of the measurement of informative signal parameters on background of non-Gaussian additive noise was obtained. Engineering estimations of the informative signal parameters on the background of additive non-Gaussian noise, with correlated nature were found. © 2016 IEEE.


Antonov A.V.,University of Leicester | Antonov A.V.,Technological University | Krestyaninova M.,University of Helsinki | Knight R.A.,University of Leicester | And 5 more authors.
Oncogene | Year: 2014

Multiple clinical studies have correlated gene expression with survival outcome in cancer on a genome-wide scale. However, in many cases, no obvious correlation between expression of well-known tumour-related genes (that is, p53, p73 and p21) and survival rates of patients has been observed. This can be mainly explained by the complex molecular mechanisms involved in cancer, which mask the clinical relevance of a gene with multiple functions if only gene expression status is considered. As we demonstrate here, in many such cases, the expression of the gene interaction partners (gene 'interactome') correlates significantly with cancer survival and is indicative of the role of that gene in cancer. On the basis of this principle, we have implemented a free online datamining tool (http://www.bioprofiling.de/PPISURV). PPISURV automatically correlates expression of an input gene interactome with survival rates on >40 publicly available clinical expression data sets covering various tumours involving about 8000 patients in total. To derive the query gene interactome, PPISURV employs several public databases including protein-protein interactions, regulatory and signalling pathways and protein post-translational modifications. © 2014 Macmillan Publishers Limited.


Wu Y.,Xi'an Jiaotong University | Zhou D.,Xi'an Jiaotong University | Guo J.,Xi'an Jiaotong University | Pang L.-X.,technological University | And 2 more authors.
Materials Letters | Year: 2011

In the present work, the 0.3Li 2TiO 3-0.7Li(Zn 0.5Ti 1.5)O 4 ceramic was prepared via the conventional solid state reactionroute, and the phase composition, microstructure, and sintering behavior were investigated. The ceramic sample sintered at 1100 °C for 2 h demonstrated high microwave dielectric performance with a relative permittivityof23.5, a high quality factor (Qf) ∼88,360 GHz (at 7.4 GHz), and near zero temperature coefficient of resonant frequency about -0.8 ppm/°C. These results indicate that the 0.3Li 2TiO 3-0.7Li(Zn 0.5Ti 1.5)O 4 ceramic might be a good candidate for dielectric resonators, filters and other microwave electronic device applications. © 2011 Elsevier B.V. All rights reserved.


When the Nobel Prize in Chemistry was awarded last month to Tomas Lindahl, Paul Modrich, and Aziz Sancar for their “mechanistic studies of DNA repair,” the usual mix of congratulatory messages and “oh, biology won again” laments appeared online. Among those messages, however, appeared other, less routine sentiments: regrets that some pioneering scientists were skipped over and confusion as to how and why the prizewinners were selected. Many in the research community pointed out that the DNA repair field is a large one whose original discoveries were made more than 50 years ago, before even the eldest winner—Lindahl—had earned his Ph.D. Others complained that some press materials released by the Nobel Committee implied that the three awardees had “discovered” DNA repair, an error propagated in news stories written about the prize. To be sure, this year’s Nobel Prize in Chemistry rewards actual chemistry: DNA repair describes the molecular mechanisms by which life’s genetic material is maintained and corrected in the face of internal mistakes such as copy errors, external insults such as ultraviolet radiation, and inherent DNA instability. Without DNA repair, humans would live short, dark, disease-ridden lives. Lindahl, Modrich, and Sancar built on earlier discoveries to dissect how three important types of DNA repair occur: base excision, mismatch repair, and nucleotide excision, respectively (C&EN, Oct. 12, page 6). DNA repair “is certainly in chemistry’s strike zone,” wrote Paul Bracher while live-blogging the chemistry prize announcement on Oct. 7. At the same time, Bracher, a chemistry professor at Saint Louis University and author of the blog ChemBark, said, “I’d love to know how the committee arrived at these three scientists out of the many possibilities. This one is sure to be controversial.” In two different posts, Moran cited reviews published in 2013 in the Yale Journal of Biology & Medicine describing critical experiments carried out during the 1960s by Paul Howard-Flanders at Yale University and Richard Setlow at Oak Ridge National Laboratory that revealed how a repair system in bacteria could excise DNA bases damaged by UV light. It also describes research conducted by Hanawalt and his student David Pettijohn showing that the repair in UV-irradiated cells occurs via the synthesis of short patches of DNA. One of the reviews was written by Hanawalt himself and recounts work he did as a Ph.D. student at Yale during the late ’50s in the lab of Setlow (who later moved to Oak Ridge). At 84, Hanawalt is the only surviving senior author of that original elite group of DNA repair researchers and therefore would have been eligible to win the chemistry prize this year. He’s not as bothered as colleagues and supporters such as Moran that he was not among this year’s Chemistry Nobel recipients. Instead, he’s more interested that the full story be told of how our understanding of DNA repair evolved from the interactions of “bright, naive students with their experienced but sometimes opinionated mentors.” In truth, the DNA repair field began before Hanawalt and his contemporaries were on the scene and before scientists even had a clear picture of DNA. Around 1927, Hermann Muller of the University of Texas, Austin, demonstrated that X-rays can cause mutations in fruit flies that the insects pass along to their offspring. Similarly, in 1949, Albert Kelner at Cold Spring Harbor Laboratory showed that UV light could cause damage to bacterial cells from which some cells would then recover. But it wasn’t until after the structure of DNA was characterized in the early 1950s that scientists figured out how radiation was damaging the genetic material. That mystery was solved—at least for UV radiation—in 1960 by Rob Beukers and Wouter Berends, Dutch scientists at the Technological University of Delft. They showed that UV light causes thymine bases in DNA to form cyclobutane dimers. Hanawalt says the identification of this chemical entity provided one of the tools critical to demonstrating how enzymes repair DNA because the dimers’ removal from DNA’s double helix could be measured. In 1957, Sen. Prescott Bush of Connecticut (father and grandfather to the well-known U.S. Presidents) gave a boost to the DNA repair field when he approached researchers at Yale, including Setlow, to investigate the health hazards of nuclear testing. The federal interest—and accompanying funding—in understanding the effects of radiation that began with the Manhattan Project led to a concentration of research and training at Yale that set the stage for the first identification of DNA repair processes. Independent of the Yale group, Claud (Stan) Rupert at Johns Hopkins University was studying how UV light kills bacteria in the late ’50s. He was trying to understand why a lethal dose of UV radiation could be partially “reversed” when the irradiated bacteria were subsequently exposed to regular, visible light. By 1960, Rupert reported that an enzyme, which he dubbed photolyase, was responsible for this photoreactivation process and could reverse thymine dimers in bacterial DNA. Just three years later, Yale’s Howard-Flanders; Setlow, who had by then left Yale; and Hanawalt, three years into his faculty appointment at Stanford separately published papers on another type of DNA repair—one that happens without the aid of visible light. Howard-Flanders and Setlow used different Escherichia coli mutants to prove that removal of thymine dimers from bacterial DNA is required for cells to survive UV exposure. Hanawalt and Pettijohn went further to demonstrate that short patches of newly synthesized DNA replaced tracts of bases, which include dimers, during repair. They called this process repair replication, now known as nucleotide excision repair. Of this year’s three winners, the Swedish-born Lindahl actually did discover a type of DNA repair. Now 77, Lindahl seized on studies conducted in the early 1960s that showed DNA bases could spontaneously degrade. The most serious form of this degradation, a cytosine base getting deaminated and converted to uracil, led Lindahl to discover base excision repair while he was at the Karolinska Institute in the mid-1970s. When contacted by C&EN about why some DNA repair pioneers were not honored with this year’s prize, Nobel Chemistry Committee chair Sara Snogerup Linse pointed only to the will of Alfred Nobel, which states that the prize should be awarded “to the person who shall have made the most important chemical discovery or improvement.” Claes Gustafsson of the University of Gothenburg, the committee member who authored the advanced scientific summary did make clear in an Oct. 7 nobelprize.org interview that this year’s Nobel Laureates were not the original discoverers of DNA repair, however.


Vasileva E.A.,Russian Academy of Sciences | Shuvalov O.U.,Russian Academy of Sciences | Garabadgiu A.V.,Technological University | Melino G.,University of Leicester | Barlev N.A.,Russian Academy of Sciences
Cell Death and Disease | Year: 2015

Human pluripotent stem cells provide a versatile platform for regenerative studies, drug testing and disease modeling. That the expression of only four transcription factors, Oct4, Klf4, Sox2 and c-Myc (OKSM), is sufficient for generation of induced pluripotent stem cells (iPSCs) from differentiated somatic cells has revolutionized the field and also highlighted the importance of OKSM as targets for genome editing. A number of novel genome-editing systems have been developed recently. In this review, we focus on successful applications of several such systems for generation of iPSCs. In particular, we discuss genome-editing systems based on zinc-finger fusion proteins (ZFs), transcription activator-like effectors (TALEs) and an RNA-guided DNA-specific nuclease, Cas9, derived from the bacterial defense system against viruses that utilizes clustered regularly interspaced short palindromic repeats (CRISPR). © 2015 Macmillan Publishers Limited All rights reserved.


Marchenko V.M.,Technological University
European Control Conference, ECC 1999 - Conference Proceedings | Year: 2015

Several classes of non-singular functional transformations for linear stationary dynamical systems with retarded argument are introduced. Then, the problem of determination of canonical forms is interpreted as the algebraic problem of universality for each class of transformations. Generalization of Kalman, Popov and Brunovsky canonical representations are given for systems of control and observation with after-effect. By using the results obtained, the main qualitative control theory problems such as controllability, stabilization, observability, modal control, reconstruction, and others can be successfully investigated for various types of functional-differential systems under action of several kinds of linear difference state feedback. © 1999 EUCA.


Afanas'ev V.N.,Technological University
Journal of Computer and Systems Sciences International | Year: 2010

Quite many engineering problems, problems from ecology, medicine, and social sciences are characterized by the presence of factors bringing uncertainty into the corresponding control systems. Additional difficulties for control action construction arise in the case when the objects are described by nonlinear high-order evolutionary equations. An important subset of these objects consists of the object with interval parametric uncertainty with a given control objective and with a given a given termination time of the transient process. For this objects, one of the possible ways of control action synthesis is the application of the guaranteed control concept. We propose the method of control synthesis for one class of nonlinear uncertain objects with using their robust models having linear structure and the parameters, depending on their state. © 2010 Pleiades Publishing, Ltd.


Amelio I.,University of Leicester | Antonov A.A.,University of Leicester | Catani M.V.,University of Rome Tor Vergata | Massoud R.,University of Rome Tor Vergata | And 6 more authors.
Oncotarget | Year: 2014

Metabolic adaptation has emerged as a hallmark of cancer and a promising therapeutic target, as rapidly proliferating cancer cells adapt their metabolism increasing nutrient uptake and reorganizing metabolic fluxes to support biosynthesis. The transcription factor p73 belongs to the p53-family and regulates tumorigenesis via its two N-terminal isoforms, with (TAp73) or without (ΔNp73) a transactivation domain. TAp73 acts as tumor suppressor, at least partially through induction of cell cycle arrest and apoptosis and through regulation of genomic stability. Here, we sought to investigate whether TAp73 also affects metabolic profiling of cancer cells. Using high throughput metabolomics, we unveil a thorough and unexpected role for TAp73 in promoting Warburg effect and cellular metabolism. TAp73-expressing cells show increased rate of glycolysis, higher amino acid uptake and increased levels and biosynthesis of acetyl-CoA. Moreover, we report an extensive TAp73-mediated upregulation of several anabolic pathways including polyamine and synthesis of membrane phospholipids. TAp73 expression also increases cellular methyl-donor S-adenosylmethionine (SAM), possibly influencing methylation and epigenetics, and promotes arginine metabolism, suggestive of a role in extracellular matrix (ECM) modeling. In summary, our data indicate that TAp73 regulates multiple metabolic pathways that impinge on numerous cellular functions, but that, overall, converge to sustain cell growth and proliferation.


Mon M.M.,Mandalay University | Maw S.S.,Mandalay University | Oo Z.K.,Technological University
World Academy of Science, Engineering and Technology | Year: 2011

Antioxidant activities of ethanolic extracts of Ardisia japonica Blume., Ageartum conyzoides Linn., and Cocculus hirsutus Linn Diels. leaves was determined qualitatively and quantitatively in this research. 1, 1-diphenyl-2-picrylhydrazyl (DPPH) free radical solution was used to investigate free radical scavenging activity of these leaves extracts. Ascorbic acid (Vitamin C) was used as the standard. In the present investigation, it is found that all of these extracts have remarkable antioxidant activities. The EC50 values of these ethanolic extracts were 12.72 μg/ml for A. japonica, 15.19 μg/ml for A. conyzoides, 10.68 μg/ml for C. hirsutus respectively. Among these Myanmar medicinal plants, C. hirsutus showed higher antioxidant activities as well as free radical scavenging activity than black tea (Camellia sinensis), the famous antioxidant, and A. japonica and A. conyzoides showed a rather lower antioxidant activity than tea extracts. According to results from bioassay with carrot discs infected with Agrobacterium tumefaciens, all extracts showed anti-tumor activity after 3 weeks of incubation. No gall was detected in carrot disks treated with C. hirsutus and A. japonica extracts in the dose of 100ppm and in carrot discs treated with A. conyzoides extract in the dose of 1000 ppm. Therefore, the research clearly indicates that these weedy plants of dry farm land are exceptionally advantageous for human health.


Knight R.A.,Medical Research Council Toxicology Unit | Gostev M.,Technological University | Ilisavskii S.,Technological University | Willis A.E.,Medical Research Council Toxicology Unit | And 3 more authors.
Oncotarget | Year: 2014

Understanding therapeutic mechanisms of drug anticancer cytotoxicity represents a key challenge in preclinical testing. Here we have performed a meta-analysis of publicly available tumor cell line growth inhibition assays (~ 70 assays from 6 independent experimental groups covering ~ 500 000 molecules) with the primary goal of understanding molecular therapeutic mechanisms of cancer cytotoxicity. To implement this we have collected currently available information on protein targets for molecules that were tested in the assays. We used a statistical methodology to identify protein targets overrepresented among molecules exhibiting cancer cytotoxicity with the particular focus of identifying overrepresented patterns consisting of several proteins (i.e. proteins "A" and "B" and "C"). Our analysis demonstrates that targeting individual proteins can result in a significant increase (up to 50-fold) of the observed odds for a molecule to be an efficient inhibitor of tumour cell line growth. However, further insight into potential molecular mechanisms reveals a multi-target mode of action: targeting a pattern of several proteins drastically increases the observed odds (up to 500-fold) for a molecule to be tumour cytotoxic. In contrast, molecules targeting only one protein but not targeting an additional set of proteins tend to be nontoxic. Our findings support a poly-pharmacology drug discovery paradigm, demonstrating that anticancer cytotoxicity is a product, in most cases, of multi-target mode of drug action.

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