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Academic literature on the topic 'Interference fragmentation function'

Author: Grafiati
Published: 11 March 2023

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Journal articles on the topic "Interference fragmentation function"

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Traa, Annika, Emily Machiela, Paige D. Rudich, Sonja K. Soo, Megan M. Senchuk, and Jeremy M. Van Raamsdonk. "Identification of Novel Therapeutic Targets for Polyglutamine Diseases That Target Mitochondrial Fragmentation." International Journal of Molecular Sciences 22, no. 24 (December 14, 2021): 13447. http://dx.doi.org/10.3390/ijms222413447.

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Huntington’s disease (HD) is one of at least nine polyglutamine diseases caused by a trinucleotide CAG repeat expansion, all of which lead to age-onset neurodegeneration. Mitochondrial dynamics and function are disrupted in HD and other polyglutamine diseases. While multiple studies have found beneficial effects from decreasing mitochondrial fragmentation in HD models by disrupting the mitochondrial fission protein DRP1, disrupting DRP1 can also have detrimental consequences in wild-type animals and HD models. In this work, we examine the effect of decreasing mitochondrial fragmentation in a neuronal C. elegans model of polyglutamine toxicity called Neur-67Q. We find that Neur-67Q worms exhibit mitochondrial fragmentation in GABAergic neurons and decreased mitochondrial function. Disruption of drp-1 eliminates differences in mitochondrial morphology and rescues deficits in both movement and longevity in Neur-67Q worms. In testing twenty-four RNA interference (RNAi) clones that decrease mitochondrial fragmentation, we identified eleven clones—each targeting a different gene—that increase movement and extend lifespan in Neur-67Q worms. Overall, we show that decreasing mitochondrial fragmentation may be an effective approach to treating polyglutamine diseases and we identify multiple novel genetic targets that circumvent the potential negative side effects of disrupting the primary mitochondrial fission gene drp-1.
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Malter, Henry E., Nury Steuerwald, and Jacques Cohen. "Interference with survivin gene function in mouse embryos: Towards a molecular model for human embryo fragmentation." Fertility and Sterility 80 (September 2003): 79. http://dx.doi.org/10.1016/s0015-0282(03)02011-9.

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Ali, Muhammad Saddam, Hadi Susilo Arifin, and Nurhayati H. S. Arifin. "The Dynamic of Pekarangan Selahuni 2 Homlet, Ciomas Rahayu Village, Bogor." Jurnal Pengelolaan Sumberdaya Alam dan Lingkungan (Journal of Natural Resources and Environmental Management) 10, no. 3 (October 1, 2020): 364–73. http://dx.doi.org/10.29244/jpsl.10.3.364-373.

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Urbanization and fragmentation are the main factors causing dynamics in the pekarangan. The dynamics that occur are related to the structure and function of the pekarangan. This makes the pekarangan performance changes according to the interference of the pekarangan owner. Selahuni 2 Homlet, Ciomas Rahayu Village, Bogor has become the location for observing the dynamics of the past two decades. Pekarangan samples taken in 2019 are exactly the same as those taken in 1998 and 2007, totaling 10 houses. The aim is to determine the extent of changes that occur in the pekarangan, both structure and function. Measuring the area, ownership of the pekarangan, recording of species and function of the existing vegetation of the pekarangan. In 2019, data on ownership of houses and pekarangans by old owners dropped dramatically by only 40%. In 2019, the average pekarangan area will decrease by an average area of 110.81 m2. In 1998, 2007 and 2019, the percentage of the number of non-ornamental plant species was 4-10% higher than that of ornamental plants. Therefore, there was a change in both the extent and ownership, function and structure of the vegetation in the Selahuni 2 Homlet’s pekarangan which was caused by urbanization and fragmentation factors.
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Skoby, Michael J. "High Precision Measurement of Transversity Using Di-hadron Correlations in p↑+p Collisions at sNN = 500 GeV." International Journal of Modern Physics: Conference Series 40 (January 2016): 1660038. http://dx.doi.org/10.1142/s2010194516600387.

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The transversity distribution, which describes transversely polarized quarks in a transversely polarized nucleon, is a fundamental component of the current picture of the spin structure of the nucleon, and is only loosely constrained by existing semi-inclusive deep inelastic scattering data. The di-hadron interference fragmentation function (IFF), which describes the fragmentation of transversely polarized quarks, is expected to give rise to spin-dependent di-hadron correlations in p[Formula: see text]+p collisions. Significant di-hadron correlations have recently been measured at RHIC in p[Formula: see text]+p collisions at [Formula: see text] = 200 GeV at mid-rapidity. In 2011, STAR collected p[Formula: see text]+p data at [Formula: see text] = 500 GeV, allowing STAR to extend these di-hadron asymmetries into a previously unexplored kinematic region. The status of the charge-ordered pion pair asymmetry measurement from [Formula: see text] = 500 GeV p[Formula: see text]+p collisions will be presented.
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Niemann, Axel, Marcel Ruegg, Veronica La Padula, Angelo Schenone, and Ueli Suter. "Ganglioside-induced differentiation associated protein 1 is a regulator of the mitochondrial network." Journal of Cell Biology 170, no. 7 (September 19, 2005): 1067–78. http://dx.doi.org/10.1083/jcb.200507087.

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Mutations in GDAP1 lead to severe forms of the peripheral motor and sensory neuropathy, Charcot-Marie-Tooth disease (CMT), which is characterized by heterogeneous phenotypes, including pronounced axonal damage and demyelination. We show that neurons and Schwann cells express ganglioside-induced differentiation associated protein 1 (GDAP1), which suggest that both cell types may contribute to the mixed features of the disease. GDAP1 is located in the mitochondrial outer membrane and regulates the mitochondrial network. Overexpression of GDAP1 induces fragmentation of mitochondria without inducing apoptosis, affecting overall mitochondrial activity, or interfering with mitochondrial fusion. The mitochondrial fusion proteins, mitofusin 1 and 2 and Drp1(K38A), can counterbalance the GDAP1-dependent fission. GDAP1-specific knockdown by RNA interference results in a tubular mitochondrial morphology. GDAP1 truncations that are found in patients who have CMT are not targeted to mitochondria and have lost mitochondrial fragmentation activity. The latter activity also is reduced strongly for disease-associated GDAP1 point mutations. Our data indicate that an exquisitely tight control of mitochondrial dynamics, regulated by GDAP1, is crucial for the proper function of myelinated peripheral nerves.
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McKay, Derek M., Nicole L. Mancini, Jane Shearer, and Timothy Shutt. "Perturbed mitochondrial dynamics, an emerging aspect of epithelial-microbe interactions." American Journal of Physiology-Gastrointestinal and Liver Physiology 318, no. 4 (April 1, 2020): G748—G762. http://dx.doi.org/10.1152/ajpgi.00031.2020.

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Mitochondria exist in a complex network that is constantly remodeling via the processes of fission and fusion in response to intracellular conditions and extracellular stimuli. Excessive fragmentation of the mitochondrial network because of an imbalance between fission and fusion reduces the cells’ capacity to generate ATP and can be a forerunner to cell death. Given the critical roles mitochondria play in cellular homeostasis and innate immunity, it is not surprising that many microbial pathogens can disrupt mitochondrial activity. Here we note the putative contribution of mitochondrial dysfunction to gut disease and review data showing that infection with microbial pathogens can alter the balance between mitochondrial fragmentation and fusion, preventing normal remodeling (i.e., dynamics) and can lead to cell death. Current data indicate that infection of epithelia or macrophages with microbial pathogens will ultimately result in excessive fragmentation of the mitochondrial network. Concerted research efforts are required to elucidate fully the processes that regulate mitochondrial dynamics, the mechanisms by which microbes affect epithelial mitochondrial fission and/or fusion, and the implications of this for susceptibility to infectious disease. We speculate that the commensal microbiome of the gut may be important for normal epithelial mitochondrial form and function. Drugs designed to counteract the effect of microbial pathogen interference with mitochondrial dynamics may be a new approach to infectious disease at mucosal surfaces.
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Plath, Thomas, Katharina Detjen, Martina Welzel, Zofia von Marschall, Derek Murphy, Michael Schirner, Bertram Wiedenmann, and Stefan Rosewicz. "A Novel Function for the Tumor Suppressor p16INK4a." Journal of Cell Biology 150, no. 6 (September 18, 2000): 1467–78. http://dx.doi.org/10.1083/jcb.150.6.1467.

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The tumor suppressor gene p16INK4a inhibits the kinase activity of the cyclin-dependent kinase 4–6/cyclin D complexes and subsequent phosphorylation of critical substrates necessary for transit through the G1 phase of the cell cycle. Recent studies suggested that control of the G1/S boundary might not be the sole biological function of p16INK4a. We hypothesized that p16INK4a might influence hitherto unknown critical features of a malignant epithelial phenotype, such as anchorage dependence. Here we provide evidence that stable transfection of p16INK4a restitutes apoptosis induction upon loss of anchorage (anoikis) in a variety of human cancer cells. Anoikis in p16INK4a-transfected cells was evidenced by DNA fragmentation and poly(ADP-ribose) polymerase cleavage upon cultivation on polyhydroxyethylmethacrylate-coated dishes and was associated with suppression of anchorage-independent growth as well as complete loss of tumorigenicity. p16INK4a-mediated anoikis was due to selective transcriptional upregulation of the α5 integrin chain of the α5β1 fibronectin receptor as detected by FACS® analysis, immunoprecipitation, Northern blotting, and nuclear run-on assays. Addition of soluble fibronectin and inhibitory α5 antibodies to nonadherent cells completely abolished p16INK4a-mediated anoikis, whereas laminin was ineffective. Furthermore, antisense-induced downregulation of the α5 integrin chain in p16INK4a-transfected cells restored resistance to anoikis. These data suggest a novel functional interference between a cell cycle–regulating tumor suppressor gene and membrane-bound integrins, thus regulating a hallmark feature of an epithelial transformed phenotype: susceptibility to anoikis.
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Lee, Yang-ja, Seon-Yong Jeong, Mariusz Karbowski, Carolyn L. Smith, and Richard J. Youle. "Roles of the Mammalian Mitochondrial Fission and Fusion Mediators Fis1, Drp1, and Opa1 in Apoptosis." Molecular Biology of the Cell 15, no. 11 (November 2004): 5001–11. http://dx.doi.org/10.1091/mbc.e04-04-0294.

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During apoptosis, the mitochondrial network fragments. Using short hairpin RNAs for RNA interference, we manipulated the expression levels of the proteins hFis1, Drp1, and Opa1 that are involved in mitochondrial fission and fusion in mammalian cells, and we characterized their functions in mitochondrial morphology and apoptosis. Down-regulation of hFis1 powerfully inhibits cell death to an extent significantly greater than down-regulation of Drp1 and at a stage of apoptosis distinct from that induced by Drp1 inhibition. Cells depleted of Opa1 are extremely sensitive to exogenous apoptosis induction, and some die spontaneously by a process that requires hFis1 expression. Wild-type Opa1 may function normally as an antiapoptotic protein, keeping spontaneous apoptosis in check. However, if hFis1 is down-regulated, cells do not require Opa1 to prevent apoptosis, suggesting that Opa1 may be normally counteracting the proapoptotic action of hFis1. We also demonstrate in this study that mitochondrial fragmentation per se does not result in apoptosis. However, we provide further evidence that multiple components of the mitochondrial morphogenesis machinery can positively and negatively regulate apoptosis.
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Matsuda, Atsushi, Annie Wan-Yi Shieh, Douglas L. Chalker, and James D. Forney. "The Conjugation-Specific Die5 Protein Is Required for Development of the Somatic Nucleus in both Paramecium and Tetrahymena." Eukaryotic Cell 9, no. 7 (May 21, 2010): 1087–99. http://dx.doi.org/10.1128/ec.00379-09.

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ABSTRACTDevelopment in ciliated protozoa involves extensive genome reorganization within differentiating macronuclei, which shapes the somatic genome of the next vegetative generation. Major events of macronuclear differentiation include excision of internal eliminated sequences (IESs), chromosome fragmentation, and genome amplification. Proteins required for these events include those with homology throughout eukaryotes as well as proteins apparently unique to ciliates. In this study, we identified the ciliate-specificDefective inIESExcision 5 (DIE5) genes ofParamecium tetraurelia(PtDIE5) andTetrahymena thermophila(TtDIE5) as orthologs that encode nuclear proteins expressed exclusively during development. Abrogation of PtDie5 protein (PtDie5p) function by RNA interference (RNAi)-mediated silencing or TtDie5p by gene disruption resulted in the failure of developing macronuclei to differentiate into new somatic nuclei.TetrahymenaΔDIE5cells arrested late in development and failed to complete genome amplification, whereas RNAi-treatedParameciumcells highly amplified new macronuclear DNA before the failure in differentiation, findings that highlight clear differences in the biology of these distantly related species. Nevertheless, IES excision and chromosome fragmentation failed to occur in either ciliate, which strongly supports that Die5p is a critical player in these processes. InTetrahymena, loss of zygotic expression during development was sufficient to block nuclear differentiation. This observation, together with the finding that knockdown of Die5p inParameciumstill allows genome amplification, indicates that this protein acts late in macronuclear development. Even though DNA rearrangements in these two ciliates look to be quite distinct, analysis ofDIE5establishes the action of a conserved mechanism within the genome reorganization pathway.
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Hurtado, Lidia, Cristina Caballero, Maria P. Gavilan, Jesus Cardenas, Michel Bornens, and Rosa M. Rios. "Disconnecting the Golgi ribbon from the centrosome prevents directional cell migration and ciliogenesis." Journal of Cell Biology 193, no. 5 (May 23, 2011): 917–33. http://dx.doi.org/10.1083/jcb.201011014.

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Mammalian cells exhibit a frequent pericentrosomal Golgi ribbon organization. In this paper, we show that two AKAP450 N-terminal fragments, both containing the Golgi-binding GM130-interacting domain of AKAP450, dissociated endogenous AKAP450 from the Golgi and inhibited microtubule (MT) nucleation at the Golgi without interfering with centrosomal activity. These two fragments had, however, strikingly different effects on both Golgi apparatus (GA) integrity and positioning, whereas the short fragment induced GA circularization and ribbon fragmentation, the large construct that encompasses an additional p150glued/MT-binding domain induced separation of the Golgi ribbon from the centrosome. These distinct phenotypes arose by specific interference of each fragment with either Golgi-dependent or centrosome-dependent stages of Golgi assembly. We could thus demonstrate that breaking the polarity axis by perturbing GA positioning has a more dramatic effect on directional cell migration than disrupting the Golgi ribbon. Both features, however, were required for ciliogenesis. We thus identified AKAP450 as a key determinant of pericentrosomal Golgi ribbon integrity, positioning, and function in mammalian cells.
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Dissertations / Theses on the topic "Interference fragmentation function"

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Elia, Carmine. "Measurement of two-hadron transverse spinasymmetries in SIDIS at COMPASS." Doctoral thesis, Università degli studi di Trieste, 2012. http://hdl.handle.net/10077/7425.

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2010/2011
The transversity distribution function can be studied in inclusive one- and two-hadrons production in DIS off a transversely polarized target. The measurement of the spin asymmetries in the azimuthal distribution of the one- or two-hadrons, and of the Collins or di-hadron fragmentation functions, allows to access the transversity distribution function. In this thesis the measurements of the one- and two-hadron transverse spin asymmetries performed by the COMPASS experiment is discussed. Finally the first extraction of the transversity PDF from two-hadron asymmetries is perfomed.
XXIV Ciclo
1976
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Books on the topic "Interference fragmentation function"

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Prozorov, Sergei. Biopolitics After Truth. Edinburgh University Press, 2021. http://dx.doi.org/10.3366/edinburgh/9781474485784.001.0001.

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The rise of post-truth politics marks the most serious crisis of Western liberal democracy since the end of the Cold War. The decline of trust in expert knowledge and mainstream media, the rise of social media devoid of a gatekeeping function and the growth of covert external interference in electoral processes have led to fragmentation, polarization and destabilization of Western democratic systems. What makes post-truth politics so difficult to resist is its apparently democratic character that claims to challenge bureaucratic depoliticization, the rule of experts and the disappearance of alternatives to the hegemonic policy. Biopolitics after Truth refutes this interpretation both historically and conceptually, arguing that by reducing every statement to an opinion equivalent to any other the post-truth ideology leads to the degradation of the public sphere that is essential to democratic governance. Rather than enable resistance to expertise-based biopolitical governmentalities, truth denialism dissolves the only framework where their contestation and transformation could take place. In contrast, Biopolitics after Truth argues for a positive role of truth-telling in the democratization of biopolitical governance. Drawing on Foucault’s late work on truth and subjectivity, it develops an approach to truth-telling as a disruptive speech act that constitutes a political form of life.
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Conference papers on the topic "Interference fragmentation function"

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RADICI, M. "ACCESSING TRANSVERSITY WITH INTERFERENCE FRAGMENTATION FUNCTIONS." In Proceedings of the Second International Symposium on the Gerasimov-Drell-Hearn Sum Rule and the Spin Structure of the Nucleon. WORLD SCIENTIFIC, 2003. http://dx.doi.org/10.1142/9789812705167_0057.

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RADICI, M. "INTERFERENCE FRAGMENTATION FUNCTIONS AND SPIN ASYMMETRIES." In Proceedings of the 9th International Workshop. WORLD SCIENTIFIC, 2002. http://dx.doi.org/10.1142/9789812778345_0091.

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Zhou, Jian, and Andreas Metz. "Interference fragmentation functions for large invariant mass." In 19TH PARTICLES AND NUCLEI INTERNATIONAL CONFERENCE (PANIC11). AIP, 2012. http://dx.doi.org/10.1063/1.3700513.

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Dias, Yves Henrique Faria, Leonardo Moreira Dutra, Mariana Vanon Moreira, Bárbara Gomes Muffato, Ana Luíza Badini Tubenchlak, Maria Clara Lopes Rezende, Milla Giancristofaro Dutra, Bernardo Valle Zanetti, and Leandro Véspoli Campos. "Influence of insomnia on cognition." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.018.

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Background: Insomnia is a disorder characterized by difficulty in initiating and maintaining sleep, affecting about 20% of the world population. As a consequence, this disorder brings a significant loss of quality of life for the affected individuals, triggering the questioning about its influence on cognitive performance. Objectives: To investigate the interference of insomnia on cognition. Methods: During April of 2021, a literature review was carried out in the PubMed database, using the descriptors “Insomnia” and “Cognition”, in addition to their respective variations in MeSH. We selected studies carried out in humans and published in the last five years. Results: A total of 317 articles were found, of which four were selected to produce this abstract. The studies showed a significant relationship between sleep restriction caused by insomnia and worsening cognitive activity. In this sense, the fragmentation of rest and the difficulty of reaching deeper stages of sleep altered the cognitive efficiency of the affected patients, causing impaired performance in aspects such as attention, memory, learning capacity, perception and ability to solve problems. Performance was assessed through subjective and objective tests - composed of patient reports and practical tests, respectively. Despite the negative relationship established, one of the studies reports that certain domains of cognition were preserved, such as psychomotor and verbal functions. Conclusions: Insomnia adversely affects individuals’ cognitive performance, resulting in losses in the patient’s life.
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Jitea, Ilie-Ciprian, Bogdan Garaliu Busoi, Robert Laszlo, Gheorghiosu Edward, and Samet Soysal. "PRESENTATION OF THE SAFETY AND PERFORMANCE PARAMETERS OF ELECTRONIC DETONATORS AND THE IGNITION SYSTEM." In 22nd SGEM International Multidisciplinary Scientific GeoConference 2022. STEF92 Technology, 2022. http://dx.doi.org/10.5593/sgem2022/1.1/s03.038.

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DETEX Electronic Detonator made by Kirlioglu consists of an electronic circuit with communication and microprocessor and wire bridge resistance coated with explosive material. DETEX Electronic Detonator, which identity information, delay information, charge, discharge and all functions are controlled digitally, is a system consisting of all electronic circuit elements. The system consists of a communication circuit, a master control circuit with a microprocessor, a controlled charge, a discharge and an ignition circuit. With two cables, the circuit takes both the feed and the communication via the same two cables. With embedded software installed on the system, all functions are provided digitally via the microprocessor. DETEX Electronic Detonator can connect with Logger, Slave and Blaster in the field and significantly increases explosive performance due to its high accuracy and reliability fragmentation and material integrity, muck stack control (excavation rate and dust control), vibration control and repeatability. It can be remotely control a network with several explosion drives located in different parts of the mine, from a central location to simultaneously explode and it can use up to 1000 detonators when using a Single Blaster. The DETEX Electronic Detonator and Ignition System have the advantage in the case of any stray currents, electromagnetic interference, radar radiation or as well as its safety in the case of misfire. It cannot be fired simply by a battery or by other electric sources has a special secure encrypted communication protocol for both the ignition line control and the wired data transmission. In INSEMEX specialized department this product was tested with success in accordance with the requirements applicable and was certified for EU market.
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