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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Lu, Lei, Guihua Tai, and Wanjin Hong. "Autoantigen Golgin-97, an Effector of Arl1 GTPase, Participates in Traffic from the Endosome to the Trans-Golgi Network." Molecular Biology of the Cell 15, no. 10 (October 2004): 4426–43. http://dx.doi.org/10.1091/mbc.e03-12-0872.
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The precise cellular function of Arl1 and its effectors, the GRIP domain Golgins, is not resolved, despite our recent understanding that Arl1 regulates the membrane recruitment of these Golgins. In this report, we describe our functional study of Golgin-97. Using a Shiga toxin B fragment (STxB)-based in vitro transport assay, we demonstrated that Golgin-97 plays a role in transport from the endosome to the trans-Golgi network (TGN). The recombinant GRIP domain of Golgin-97 as well as antibodies against Golgin-97 inhibited the transport of STxB in vitro. Membrane-associated Golgin-97, but not its cytosolic pool, was required in the in vitro transport assay. The kinetic characterization of inhibition by anti-Golgin-97 antibody in comparison with anti-Syntaxin 16 antibody established that Golgin-97 acts before Syntaxin 16 in endosome-to-TGN transport. Knock down of Golgin-97 or Arl1 by their respective small interference RNAs (siRNAs) also significantly inhibited the transport of STxB to the Golgi in vivo. In siRNA-treated cells with reduced levels of Arl1, internalized STxB was instead distributed peripherally. Microinjection of Golgin-97 antibody led to the fragmentation of Golgi apparatus and the arrested transport to the Golgi of internalized Cholera toxin B fragment. We suggest that Golgin-97 may function as a tethering molecule in endosome-to-TGN retrograde traffic.
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Joumaa, Ahmad, Florence Gayet, Eduardo J. Garcia-Suarez, Jonas Himmelstrup, Anders Riisager, Rinaldo Poli, and Eric Manoury. "Synthesis of Nixantphos Core-Functionalized Amphiphilic Nanoreactors and Application to Rhodium-Catalyzed Aqueous Biphasic 1-Octene Hydroformylation." Polymers 12, no. 5 (May 12, 2020): 1107. http://dx.doi.org/10.3390/polym12051107.
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A latex of amphiphilic star polymer particles, functionalized in the hydrophobic core with nixantphos and containing P(MAA-co-PEOMA) linear chains in the hydrophilic shell (nixantphos-functionalized core-crosslinked micelles, or nixantphos@CCM), has been prepared in a one-pot three-step convergent synthesis using reversible addition-fragmentation chain transfer (RAFT) polymerization in water. The synthesis involves polymerization-induced self-assembly (PISA) in the second step and chain crosslinking with di(ethylene glycol) dimethacrylate (DEGDMA) in the final step. The core consists of a functionalized polystyrene, obtained by incorporation of a new nixantphos-functionalized styrene monomer (nixantphos-styrene), which is limited to 1 mol%. The nixantphos-styrene monomer was synthesized in one step by nucleophilic substitution of the chloride of 4-chloromethylstyrene by deprotonated nixantphos in DMF at 60 °C, without interference of either phosphine attack or self-induced styrene polymerization. The polymer particles, after loading with the [Rh(acac)(CO)2] precatalyst to yield Rh-nixantphos@CCM, function as catalytic nanoreactors under aqueous biphasic conditions for the hydroformylation of 1-octene to yield n-nonanal selectively, with no significant amounts of the branched product 2-methyl-octanal.
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Meng, Yizhen, and Jun Zhang. "An effective behavior recognition method in the video session using convolutional neural network." PLOS ONE 17, no. 8 (August 1, 2022): e0266734. http://dx.doi.org/10.1371/journal.pone.0266734.
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In order to further improve the accuracy of the video-based behavior recognition method, an effective behavior recognition method in the video session using convolutional neural network is proposed. Specifically, by adding the target detection phase before the behavior recognition algorithm, the body region in the video can be accurately extracted to reduce the interference of redundant and unnecessary background noises, and at the same time, the inappropriate images can be replaced, which has reached the role of balance background trade-off, and finally, the neural network can learn the human behavior information with emphasis. By adding fragmentation and stochastic sampling, the long-time time-domain modeling of the whole video session can be established, so that the model can obtain video-level expression ability. Finally, the improved loss function is used for behavior recognition to solve the problem of classification difficulty and possible sample imbalance. In addition, we conducted the hyperparametric experiment, the ablation experiment and the contrast experiment on different open source and benchmark datasets. Compared with other commonly used behavior recognition algorithms, the experimental results verify the effectiveness of the proposed method. In addition, the related deep learning-based methods used in behavior recognition are reviewed at the beginning of this paper, and the challenges in behavior recognition and future research directions are prospected at the end of this paper, which will undoubtedly play a double role in the work of later researchers.
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Jaffe, R. L., Xuemin Jin, and Jian Tang. "Interference Fragmentation Functions and the Nucleon's Transversity." Physical Review Letters 80, no. 6 (February 9, 1998): 1166–69. http://dx.doi.org/10.1103/physrevlett.80.1166.
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Morosky, Stefanie, Nicholas J. Lennemann, and Carolyn B. Coyne. "BPIFB6 Regulates Secretory Pathway Trafficking and Enterovirus Replication." Journal of Virology 90, no. 10 (March 9, 2016): 5098–107. http://dx.doi.org/10.1128/jvi.00170-16.
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ABSTRACTBactericidal/permeability-increasing protein (BPI) fold-containing family B, member 3 (BPIFB3) is an endoplasmic reticulum (ER)-localized host factor that negatively regulates coxsackievirus B (CVB) replication through its control of the autophagic pathway. Here, we show that another member of the BPIFB family, BPIFB6, functions as a positive regulator of CVB, and other enterovirus, replication by controlling secretory pathway trafficking and Golgi complex morphology. We show that similar to BPIFB3, BPIFB6 localizes exclusively to the ER, where it associates with other members of the BPIFB family. However, in contrast to our findings that RNA interference (RNAi)-mediated silencing of BPIFB3 greatly enhances CVB replication, we show that silencing of BPIFB6 expression dramatically suppresses enterovirus replication in a pan-viral manner. Mechanistically, we show that loss of BPIFB6 expression induces pronounced alterations in retrograde and anterograde trafficking, which correlate with dramatic fragmentation of the Golgi complex. Taken together, these data implicate BPIFB6 as a key regulator of secretory pathway trafficking and viral replication and suggest that members of the BPIFB family participate in diverse host cell functions to regulate virus infections.IMPORTANCEEnterovirus infections are associated with a number of severe pathologies, such as aseptic meningitis, dilated cardiomyopathy, type I diabetes, paralysis, and even death. These viruses, which include coxsackievirus B (CVB), poliovirus (PV), and enterovirus 71 (EV71), co-opt the host cell secretory pathway, which controls the transport of proteins from the endoplasmic reticulum to the Golgi complex, to facilitate their replication. Here we report on the identification of a novel regulator of the secretory pathway, bactericidal/permeability-increasing protein (BPI) fold-containing family B, member 6 (BPIFB6), whose expression is required for enterovirus replication. We show that loss of BPIFB6 expression correlates with pronounced defects in the secretory pathway and greatly reduces the replication of CVB, PV, and EV71. Our results thus identify a novel host cell therapeutic target whose function could be targeted to alter enterovirus replication.
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Shen, Shiguang, Jie Pu, Cong Xu, Yuhua Wang, Wan Luo, and Bo Wen. "Effects of Human Disturbance on Riparian Wetland Landscape Pattern in a Coastal Region." Remote Sensing 14, no. 20 (October 15, 2022): 5160. http://dx.doi.org/10.3390/rs14205160.
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The wetland ecosystem along a river in a coastal region has great significance in purifying water bodies, regulating climate, and providing habitat for animals and plants. Studying the effects of human disturbances on the landscape patterns of wetlands is of great significance to the protection and management of an ecosystem. This study used Guannan County and Guanyun County, two counties in China that are located on both banks of the Xinyi River as the study area. The spatiotemporal characteristics of the landscape pattern evolution of wetlands and their relationship with human interference from 2009 to 2020 were analyzed by the landscape dynamic rate, landscape conversion matrix, landscape indices, human disturbance index, and the quadratic regression equation. The results showed that: (1) Except for the increase in the area of beach and paddy fields, the area of other landscape types decreased; (2) the changes in wetlands were heterogeneous and showed different trends in different regions; (3) the boundary shape’s complexity and the landscape pattern’s fragmentation showed a decreasing–increasing trend and the connectivity and the diversity of the landscape decreased; and (4) the human disturbance index increased from 2009 to 2014 and then decreased from 2014 to 2020, declining outward from the places where towns and construction land aggregated. Moreover, there was an inverted U-type relationship with the landscape pattern indices. The findings provide direct, specific, and explicit information and theoretical guidance for the protection of wetlands along the river in the coastal region as well as for the restoration of wetland ecosystem function and the improvement of wetland biodiversity in relevant regions.
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Waschulewski, I. H., M. L. Kruse, B. Agricola, H. F. Kern, and W. E. Schmidt. "Okadaic acid disrupts Golgi structure and impairs enzyme synthesis and secretion in the rat pancreas." American Journal of Physiology-Gastrointestinal and Liver Physiology 270, no. 6 (June 1, 1996): G939—G947. http://dx.doi.org/10.1152/ajpgi.1996.270.6.g939.
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Okadaic acid, a serine/threonine phosphatase inhibitor, has been shown to inhibit rat pancreatic enzyme secretion by interference with late processes in stimulus-secretion coupling. To further characterize its action, we studied the effect of okadaic acid on secretion of newly synthesized proteins, protein synthesis, and cellular ultrastructure in pancreatic lobules derived from rats stimulated in vivo by feeding the synthetic proteinase inhibitor FOY-305. Okadaic acid completely blocked protein secretion at concentrations that inhibit the Ca2+/calmodulin-dependent protein phosphatase 2b, calcineurin. Protein synthesis was abolished at 10(-6) mol/l and reduced by 60% at 5 x 10(-7) mol/l okadaic acid. Pancreatic lobules exposed to 5 x 10(-7) mol/l okadaic acid for 20 min fully restored their secretory capacity on removal of the drug; whereas, after a preincubation with okadaic acid for > 40 min, protein secretion remained impaired during the recovery period. Electron microscopic examination of pancreatic acinar cells treated with 5 x 10(-7) mol/l okadaic acid revealed a dilated Golgi complex after 15 and 30 min and a subsequent fragmentation of Golgi cisternae into clouds of small uniform vesicles after 60 min. Reassembly of Golgi stacks occurred after a 60-min recovery without okadaic acid. These data indicate that serine/threonine phosphatases play an important role not only in the regulation of pancreatic enzyme synthesis and exocytosis but also are crucial for the maintenance of normal Golgi architecture and function in the exocrine rat pancreas. These effects are probably not exclusively mediated via type 2b calcineurin-like protein phosphatases.
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Anuka, Eli, Natalie Yivgi-Ohana, Sarah Eimerl, Benjamin Garfinkel, Naomi Melamed-Book, Elena Chepurkol, Dan Aravot, et al. "Infarct-Induced Steroidogenic Acute Regulatory Protein: A Survival Role in Cardiac Fibroblasts." Molecular Endocrinology 27, no. 9 (September 1, 2013): 1502–17. http://dx.doi.org/10.1210/me.2013-1006.
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Steroidogenic acute regulatory protein (StAR) is indispensable for steroid hormone synthesis in the adrenal cortex and the gonadal tissues. This study reveals that StAR is also expressed at high levels in nonsteroidogenic cardiac fibroblasts confined to the left ventricle of mouse heart examined 3 days after permanent ligation of the left anterior descending coronary artery. Unlike StAR, CYP11A1 and 3β-hydroxysteroid dehydrogenase proteins were not observed in the postinfarction heart, suggesting an apparent lack of de novo cardiac steroidogenesis. Work with primary cultures of rat heart cells revealed that StAR is induced in fibroblasts responding to proapoptotic treatments with hydrogen peroxide or the kinase inhibitor staurosporine (STS). Such induction of StAR in culture was noted before spontaneous differentiation of the fibroblasts to myofibroblasts. STS induction of StAR in the cardiac fibroblasts conferred a marked resistance to apoptotic cell death. Consistent with that finding, down-regulation of StAR by RNA interference proportionally increased the number of STS-treated apoptotic cells. StAR down-regulation also resulted in a marked increase of BAX activation in the mitochondria, an event known to associate with the onset of apoptosis. Last, STS treatment of HeLa cells showed that apoptotic demise characterized by mitochondrial fission, cytochrome c release, and nuclear fragmentation is arrested in individual HeLa cells overexpressing StAR. Collectively, our in vivo and ex vivo evidence suggests that postinfarction expression of nonsteroidogenic StAR in cardiac fibroblasts has novel antiapoptotic activity, allowing myofibroblast precursor cells to survive the traumatized event, probably to differentiate and function in tissue repair at the infarction site.
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Gong, Yue, Guixuan You, Tianyi Chen, Ling Wang, and Yuandong Hu. "Rural Landscape Change: The Driving Forces of Land Use Transformation from 1980 to 2020 in Southern Henan, China." Sustainability 15, no. 3 (January 31, 2023): 2565. http://dx.doi.org/10.3390/su15032565.
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Rapid urbanization has had an important impact on the pattern and function of rural land use. To better understand the key drivers of the landscape pattern evolution in southern Henan in China from 1980 to 2020, we used techniques of GIS(Geographic Information System) technology and the geodetector model in the research area of landscape pattern evolution characteristics. The research results show that the land use transformation in the rural areas of southern Henan has been characterized by the conversion of production land to living land and ecological land, with the highest conversion rate and continuous growth of construction land, a decreasing trend of cropland, and continuous and stable growth of land for forest and water body in the past 40 years. Land use conversion in the rural areas of southern Henan is mainly concentrated in the northern, central, and southern areas, and the spatial conversion has shifted from mountainous areas to the plains. The center of gravity of forest, cropland, and water body has most obviously shifted, and human interference and ecological environment destruction are the main influencing factors. The overall landscape pattern in the rural areas of southern Henan has increased in fragmentation and landscape heterogeneity, evenness has decreased, irregular patches have increased, and landscape connectivity has decreased. The combined effect of the six dimensions of elevation, slope, night lighting, average annual precipitation, average annual temperature, and population density in the rural areas of southern Henan has led to the transformation of land use and changes in landscape pattern. Physical geographic factors are the main drivers of rural landscape pattern changes in southern Henan, while population density changes and urbanization are secondary drivers. The results of the study have important guiding significance for the further optimization of rural landscape patterns and the sustainable development of rural areas.
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Yang, Weihua. "Azimuthal asymmetries from 𝜃 vacuum." International Journal of Modern Physics A 34, no. 18 (June 28, 2019): 1950095. http://dx.doi.org/10.1142/s0217751x19500957.
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We present the complete azimuthal asymmetries at leading twist in terms of fragmentation functions in dihadron production semi-inclusive electron–positron annihilation process. When the nontrivial [Formula: see text] vacuum is taken into consideration, the parity symmetry of quantum chromodynamics is violated. As a consequence of the [Formula: see text] [Formula: see text]-odd effects, [Formula: see text]-odd fragmentation functions would contribute to the azimuthal asymmetries. Azimuthal asymmetry coming from two interference terms with opposite signs vanishes when sum over many events. This symmetry only survives on the event-by-event basis. Azimuthal asymmetry coming from two interference terms with same signs survives and can be measured to extract the [Formula: see text]-odd fragmentation functions. We also present the hadron polarizations.
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Jaffe, R. L., Xuemin Jin, and Jian Tang. "Interference fragmentation functions and valence quark spin distributions in the nucleon." Physical Review D 57, no. 9 (May 1, 1998): 5920–22. http://dx.doi.org/10.1103/physrevd.57.5920.
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Li, Yang, Chunyan Xue, Hua Shao, Ge Shi, and Nan Jiang. "Study of the Spatiotemporal Variation Characteristics of Forest Landscape Patterns in Shanghai from 2004 to 2014 Based on Multisource Remote Sensing Data." Sustainability 10, no. 12 (November 24, 2018): 4397. http://dx.doi.org/10.3390/su10124397.
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The landscape patterns of urban forests not only reflect the influence of urbanization on urban forests, but also determines its function in urban ecosystem services. In the case of mastering the overall forest landscape pattern of a city, a study of the structure of urban forest landscapes at different scales and in urbanized regions is beneficial to a comprehensive understanding of the forest characteristics of a city. In the present study, an attempt was made to map and monitor the spatio-temporal dynamics of an urban forest in Shanghai from 2004 to 2014 using remote sensing techniques. Methods of landscape ecology analysis are followed to quantify the spatiotemporal patterns of an urban forest landscape by urban and rural gradient regionalization. The results show that the spatial structure of an urban forest landscape is essentially consistent with an urban landscape pattern. Due to strong interference from human activities, the ecological quality of forest landscapes is low. At the landscape level, the urban forest coverage rate increased from 11.43% in 2004 to 16.02% in 2014, however, the number of large patches decreased, there was a high degree of urban forest landscape fragmentation, landscape connectivity was poor, landscape patch boundaries were uniform, and weak links were present between ecological processes. Different urban and rural gradient division methods exhibit obvious gradient characteristics along the urban–rural gradient in Shanghai. The regional differences in the urban forest landscape ecological characteristics have further increased as a result of urban planning and zoning. The total amount of urban forest is located closer to the urban center, which has the smallest total amount of forest; however, in terms of urban forest coverage, the suburbs have more coverage than do the outer suburbs and the central urban areas. The urban forest landscape’s spatial distribution area is evidently different. Urbanization affects the areas closest to urban residential areas, which are markedly disturbed by humans, and the urban forest landscape has a high degree of fragmentation. The forest patches have become divided and unconnected, and the degree of natural connectivity has gradually decreased over the past 10 years. At the landscape class level, broadleaf forests are dominant in Shanghai, and their area exhibits an increasing trend; shrublands and needleleaf forests, however, show a decreasing trend. Compared with other forest types, the spatial distribution of broadleaf forest is concentrated in the suburbs, and the aggregation effect is relatively apparent. From the perspective of urban forest landscape pattern aggregation characteristics in Shanghai, the spatial distribution of urban forest landscape point patterns in the study area exhibit extremely uneven characteristics. The point density of urban forest patches larger than 1 ha in Shanghai increased from 2004 to 2014. However, the total number of patches with areas larger than 5 ha decreased, and this decrease plays an important role in the ecological environment. In the past 10 years, the concentration characteristics of urban forests with large patches has gradually decreased. In 2014, the urban forest landscapes decreased by 5 km compared to the intensity of aggregates in 2004, which also indicates that urban forests in Shanghai tend to be fragmented. The results of this study can be useful to help improve urban residents’ living environments and the sustainable development of the urban ecosystem, and they will also be vital to future management.
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Bozzetti, Carlo, Yuliya Sosedova, Mao Xiao, Kaspar R. Daellenbach, Vidmantas Ulevicius, Vadimas Dudoitis, Genrik Mordas, et al. "Argon offline-AMS source apportionment of organic aerosol over yearly cycles for an urban, rural, and marine site in northern Europe." Atmospheric Chemistry and Physics 17, no. 1 (January 3, 2017): 117–41. http://dx.doi.org/10.5194/acp-17-117-2017.
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Abstract. The widespread use of Aerodyne aerosol mass spectrometers (AMS) has greatly improved real-time organic aerosol (OA) monitoring, providing mass spectra that contain sufficient information for source apportionment. However, AMS field deployments remain expensive and demanding, limiting the acquisition of long-term datasets at many sampling sites. The offline application of aerosol mass spectrometry entailing the analysis of nebulized water extracted filter samples (offline-AMS) increases the spatial coverage accessible to AMS measurements, being filters routinely collected at many stations worldwide. PM1 (particulate matter with an aerodynamic diameter < 1 µm) filter samples were collected during an entire year in Lithuania at three different locations representative of three typical environments of the southeast Baltic region: Vilnius (urban background), Rūgšteliškis (rural terrestrial), and Preila (rural coastal). Aqueous filter extracts were nebulized in Ar, yielding the first AMS measurements of water-soluble atmospheric organic aerosol (WSOA) without interference from air fragments. This enables direct measurement of the CO+ fragment contribution, whose intensity is typically assumed to be equal to that of CO2+. Offline-AMS spectra reveal that the water-soluble CO2+ : CO+ ratio not only shows values systematically > 1 but is also dependent on season, with lower values in winter than in summer. AMS WSOA spectra were analyzed using positive matrix factorization (PMF), which yielded four factors. These factors included biomass burning OA (BBOA), local OA (LOA) contributing significantly only in Vilnius, and two oxygenated OA (OOA) factors, summer OOA (S-OOA) and background OOA (B-OOA), distinguished by their seasonal variability. The contribution of traffic exhaust OA (TEOA) was not resolved by PMF due to both low concentrations and low water solubility. Therefore, the TEOA concentration was estimated using a chemical mass balance approach, based on the concentrations of hopanes, specific markers of traffic emissions. AMS-PMF source apportionment results were consistent with those obtained from PMF applied to marker concentrations (i.e., major inorganic ions, OC / EC, and organic markers including polycyclic aromatic hydrocarbons and their derivatives, hopanes, long-chain alkanes, monosaccharides, anhydrous sugars, and lignin fragmentation products). OA was the largest fraction of PM1 and was dominated by BBOA during winter with an average concentration of 2 µg m−3 (53 % of OM), while S-OOA, probably related to biogenic emissions, was the prevalent OA component during summer with an average concentration of 1.2 µg m−3 (45 % of OM). PMF ascribed a large part of the CO+ explained variability (97 %) to the OOA and BBOA factors. Accordingly, we discuss a new CO+ parameterization as a function of CO2+ and C2H4O2+ fragments, which were selected to describe the variability of the OOA and BBOA factors.
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Schulze, Harald, Silke Fleischhauer, Imke Meyer, Martin Wannack, and Stefan Kunert. "The beta1-Tubulin Binding Protein RanBP10 Plays a Critical Role for Platelet Discoid Shape and Hemostasis." Blood 112, no. 11 (November 16, 2008): 414. http://dx.doi.org/10.1182/blood.v112.11.414.414.
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Abstract Blood platelets in the circulation are released from megakaryocytes (MKs), their precursor cells in the bone marrow. Mature MKs are located at the blood vessels and release platelets into the blood stream by intermediate structures referred to as proplatelets. Every MK can release up to a thousand virtually identical platelets. During this fragmentation process every single platelet is equipped with a rather constant number of assorted granules and a peripheral microtubule ring consisting of several coiled filaments. 8–12 microtubule filaments are found on average in the coil, which is essential for maintaining the platelet discoid shape. Generating these dynamic microtubule filaments at the very cell periphery in the absence of classical microtubule nucleating factors is strictly dependent on de novo nucleation of filaments. Beta1-tubulin is a MK/platelet-specific and the predominant isoform present in proplatelets and platelets. Mice lacking beta1-tubulin are thrombocytopenic and reveal platelet spherocytosis. In humans, a Q43P mutation in the beta1-tubulin gene Tubb1 also leads to large and spheric platelets. We have recently identified RanBP10 as a cytoplasmic beta1-tubulin binding protein that is selectively expressed in hematopoietic tissues like bone marrow and MKs. RNA interference (RNAi)- mediated RanBP10 ablation in primary MKs resulted in the collapse of long microtubule filaments whereas retrovirally forced overexpression of RanBP10 led to a marked increase in microtubule filaments, most likely by number or augmented bundling. RanBP10 harbors guanine nucleotide exchange factor activity toward Ran by exchanging GDP with GTP. As a local increase in Ran-GTP precedes nucleation of non-centrosomal microtubules in other cell types this mechanism might explain how positional information about new microtubule filaments is provided in the cell periphery of mature and proplatelet elaborating MKs. We generated a gene trap-mediated mouse model for RanBP10 deficiency. MKs derived from nullizygous animals phenocopied the collapse of microtubule filaments found by RNAi. Although RanBP10 was dispensable for overall platelet biogenesis with counts about 90–95% of normal, the ultrastructural analysis revealed that loss of RanBP10 protein resulted in a significant decline in the elliptic coefficient: Mutant platelets were more spherical and electron micrographs showed a wider variety in both microtubule filament number and coil localization including additional and incomplete coiling. Most intriguingly, RanBP10- deficient mice demonstrated a markedly prolonged bleeding time compared to littermate controls in a standardized tail bleeding assay. Platelets from nullizygous animals failed to respond normally to ADP by CD62P expression in flow cytometry. Our data thus suggest that RanBP10 plays a critical role in maintaining the tightly controlled platelet shape and function and that RanBP10 is essential for hemostasis.
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Liang, Yun, Wei Yu, Yan Li, Zhenye Yang, Xiumin Yan, Qiongping Huang, and Xueliang Zhu. "Nudel functions in membrane traffic mainly through association with Lis1 and cytoplasmic dynein." Journal of Cell Biology 164, no. 4 (February 16, 2004): 557–66. http://dx.doi.org/10.1083/jcb.200308058.
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Nudel and Lis1 appear to regulate cytoplasmic dynein in neuronal migration and mitosis through direct interactions. However, whether or not they regulate other functions of dynein remains elusive. Herein, overexpression of a Nudel mutant defective in association with either Lis1 or dynein heavy chain is shown to cause dispersions of membranous organelles whose trafficking depends on dynein. In contrast, the wild-type Nudel and the double mutant that binds to neither protein are much less effective. Time-lapse microscopy for lysosomes reveals significant reduction in both frequencies and velocities of their minus end–directed motions in cells expressing the dynein-binding defective mutant, whereas neither the durations of movement nor the plus end–directed motility is considerably altered. Moreover, silencing Nudel expression by RNA interference results in Golgi apparatus fragmentation and cell death. Together, it is concluded that Nudel is critical for dynein motor activity in membrane transport and possibly other cellular activities through interactions with both Lis1 and dynein heavy chain.
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Trindade, Silvana, Ricardo da S. Torres, Zuqing Zhu, and Nelson L. S. da Fonseca. "Cognitive Control-Loop for Elastic Optical Networks with Space-Division Multiplexing." Sensors 21, no. 23 (November 24, 2021): 7821. http://dx.doi.org/10.3390/s21237821.
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This paper introduces a new solution to improve network performance by decreasing spectrum fragmentation, crosstalk interference, blocking of virtual networks, cost, and link load imbalance. These problems degrade the performance of Elastic Optical Networks with Space-Division Multiplexing. The proposed solution, called Cognitive control loop (CO-OP), is capable of identifying a set of problems and creating plans to mitigate these problems. The CO-OP comprises four functions that employ learning algorithms to identify problems and plan a series of actions to reduce or eliminate them. The results show that the CO-OP can effectively decrease up to 30% the blocking of requests and up to 50% the crosstalk occurrence compared to existing algorithms.
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Wang, Rui-Yu, Bing Z. Carter, Twee Tsao, Wendy Schober, Teresa McQueen, Marina Konopleva, and Michael Andreeff. "The Role of Apoptotic Inducing Factor (AIF) in Acute Myeloid Leukemia (AML)." Blood 106, no. 11 (November 16, 2005): 2369. http://dx.doi.org/10.1182/blood.v106.11.2369.2369.
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Abstract Apoptosis is a “physiological cell suicide program” and plays an integral role in a variety of biological events. Numerous genes are involved: Apoptosis inducing factor (AIF) is a newly discovered apoptogenic flavoprotein with NADH oxidase activity that is located in the intermembrane space of mitochondria. The mechanism of induction of cell death by AIF remains unclear. Some data suggest that AIF may play a central role in the regulation of caspase-independent cell death and participate in multiple cell death paradigms. When cells are entering apoptosis, AIF will translocate from the mitochondria to the nuclei causing DNA fragmentation and chromatin condensation. AIF also induces cell death in normal lymphocytes and leukemia cells, but the data is very limited. In this study, we investigate 1) whether AIF inducing cell death is caspase-independent and related to MMP, 2) whether AIF expression levels can be prognostic in primary AML. To determine AIF nuclear translocation in cells undergoing apoptosis is caspase-dependent or caspase-independent, OCI/AML3 cells were treated with several chemotherapeutic agents (Paclitaxol, Vincristine, Ara-C, and Doxorubicin with/without pan-caspase inhibitor IDN-1529). Cells were then fixed, immuno-stained, and analyzed. Results demonstrate that AIF translocated from mitochondria to the nucleus when cell undergo apoptosis, and that it is largely caspase-independent than caspase-dependent. To examine how the mitochondrial membrane potential (MMP) is involved in AIF’s nuclear translocation, OCI/AML3 cells was stained with CMXRos and MitoTrack-green after drug treatment with/without caspase inhibitors and then analyzed by flow cytometry. 90% of untreated cells retained normal MMP. Vincristine and paclitaxol treated cells had a more complete depolarization of mitochondria (75.6% ± 4.3% and 79.3% ± 5.4%, respectively), even when caspase inhibitor was added (51.4% ± 3%; p=0.025; and 52.7% ± 5.1%; p=0.006, respectively). These results suggest that the higher ratio of AIF nuclear-translocation observed in cells undergoing apoptosis in Vincristine and paclitaxel treated cells is due to changes in MMP. To further test the function of AIF in AML, small interference RNA (siRNA) was employed to knockdown AIF gene expression in U937 cells and treated with the triterpenoid 2-cyano-3,12-dioxooleana-1,9-dien-28-oic acid (CDDO). AIF siRNA was delivered by electroporation. Results suggest that nuclear translocation of AIF is prevented by silencing AIF expression. Down-regulation of AIF prior to CDDO exposure significantly reduced CDDO-induced growth inhibition (p<0.002). CDDO-induced apoptosis was decreased by approximately 50% in TUNEL assay. To test AIF expression in AML patients, we use immunobloting of bone marrow (BM) and peripheral blood (PB) cells. Twenty-five samples from AML patients were analyzed and the results demonstrated the correlation between blast count and AIF levels (p=0.04). Comparing PB from leukemia patients with normal PB, the p volume is 0.02. Taken together, these results suggest that 1) AIF is inducing cell death through a caspase-independent and caspase-dependent pathway related to MMP, 2) The difference of AIF expression levels in AML suggest a role in the regulation of apoptosis. It may be used as a prognosis marker.
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Huang, Jiyue, Zhihao Cheng, Cong Wang, Yue Hong, Hang Su, Jun Wang, Gregory P. Copenhaver, Hong Ma, and Yingxiang Wang. "Formation of interference-sensitive meiotic cross-overs requires sufficient DNA leading-strand elongation." Proceedings of the National Academy of Sciences 112, no. 40 (September 21, 2015): 12534–39. http://dx.doi.org/10.1073/pnas.1507165112.
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Meiosis halves diploid genomes to haploid and is essential for sexual reproduction in eukaryotes. Meiotic recombination ensures physical association of homologs and their subsequent accurate segregation and results in the redistribution of genetic variations among progeny. Most organisms have two classes of cross-overs (COs): interference-sensitive (type I) and -insensitive (type II) COs. DNA synthesis is essential for meiotic recombination, but whether DNA synthesis has a role in differentiating meiotic CO pathways is unknown. Here, we show that Arabidopsis POL2A, the homolog of the yeast DNA polymerase-ε (a leading-strand DNA polymerase), is required for plant fertility and meiosis. Mutations in POL2A cause reduced fertility and meiotic defects, including abnormal chromosome association, improper chromosome segregation, and fragmentation. Observation of prophase I cell distribution suggests that pol2a mutants likely delay progression of meiotic recombination. In addition, the residual COs in pol2a have reduced CO interference, and the double mutant of pol2a with mus81, which affects type II COs, displayed more severe defects than either single mutant, indicating that POL2A functions in the type I pathway. We hypothesize that sufficient leading-strand DNA elongation promotes formation of some type I COs. Given that meiotic recombination and DNA synthesis are conserved in divergent eukaryotes, this study and our previous study suggest a novel role for DNA synthesis in the differentiation of meiotic recombination pathways.
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LOSHAJ, FRASHËR, and DMITRI E. KHARZEEV. "LPM EFFECT AS THE ORIGIN OF JET FRAGMENTATION SCALING IN HEAVY ION COLLISIONS." International Journal of Modern Physics E 21, no. 10 (October 2012): 1250088. http://dx.doi.org/10.1142/s0218301312500887.
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We address a recent puzzling result from the LHC: the jet fragmentation functions measured in Pb–Pb and pp collisions appear very similar in spite of a large medium-induced energy loss (we will call this jet fragmentation scaling (JFS)). To model the real-time nonperturbative effects in the propagation of a high energy jet through the strongly coupled QCD matter, we adopt an effective dimensionally reduced description in terms of the (1+1) quasi-Abelian–Schwinger theory. This theory is exactly soluble at any value of the coupling and shares with QCD the properties of dynamical generation of "mesons" with a finite mass and the screening of "quark" charge that are crucial for describing the transition of the jet into hadrons. We find that this approach describes quite well the vacuum jet fragmentation in e+e- annihilation at z≥0.2 at jet energies in the range of the LHC heavy ion measurements (z is the ratio of hadron and jet momenta). In QCD medium, we find that the JFS is reproduced if the mean free path λ of the jet is short, λ≤0.3 fm, which is in accord with the small shear viscosity inferred from the measurements of the collective flow. The JFS holds since at short mean free path the quantum interference (analogous to the Landau–Pomeranchuk–Migdal (LPM) effect in QED) causes the produced mesons to have low momenta p~m, where m≃0.6 GeV is the typical meson mass. Meanwhile the induced jet energy loss at short mean free path is much larger than naively expected in string models.
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De Luca, Pierantonio, Paola Foglia, Carlo Siciliano, Jànos B. Nagy, and Anastasia Macario. "Water Contaminated by Industrial Textile Dye: Study on Decolorization Process." Environments 6, no. 9 (September 2, 2019): 101. http://dx.doi.org/10.3390/environments6090101.
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This work aims to investigate possible interferences due to the presence of sodium carbonate on the photodegradation of the reactive Black 5 azoic dye, both in systems containing only titanium oxide and those containing titanium oxide and hydrogen peroxide. The role of hydrogen peroxide is explicitly treated. Sodium carbonate, in fact, is often present in the wastewater of textile industries as it is used in the fiber dyeing phases. The use of TiO2 nanoparticles is emphasized, and the possible danger is underlined. Each system was subjected to ultraviolet irradiation (UV) by varying the exposure time. After the photodegrading tests, the resulting solutions were analyzed by UV-vis spectrophotometry and High-Resolution Nuclear Magnetic Resonance to measure the residual concentrations of dye. The dye degradation curves and reaction rates for different UV exposure times were obtained and discussed as a function of the used additives. All the data are repeated three times, and they differ only by a maximum of 5%. The results indicated a reduction of about 50% of the initial concentration of Reactive Black 5 after 30 min under optimal experimental conditions. The NMR analysis indicated the formation of a series of aromatic structures that were generated by the UV-induced photochemical fragmentation of the original molecule.
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Wang, Yu, Zhongyi Jiao, Jiwei Zheng, Jie Zhou, Baosong Wang, Qiang Zhuge, and Xudong He. "Population Genetic Diversity and Structure of an Endangered Salicaceae Species in Northeast China: Chosenia arbutifolia (Pall.) A. Skv." Forests 12, no. 9 (September 18, 2021): 1282. http://dx.doi.org/10.3390/f12091282.
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Chosenia arbutifolia (Pall.) A. Skv. is a unique and endangered species belonging to the Salicaceae family. It has great potential for ornamental and industrial use. However, human interference has led to a decrease in and fragmentation of its natural populations in the past two decades. To effectively evaluate, utilize, and conserve available resources, the genetic diversity and population structure of C. arbutifolia were analyzed in this study. A total of 142 individuals from ten provenances were sampled and sequenced. Moderate diversity was detected among these, with a mean expected heterozygosity and Shannon’s Wiener index of 0.3505 and 0.5258, respectively. The inbreeding coefficient was negative, indicating a significant excess of heterozygotes. The fixation index varied from 0.0068 to 0.3063, showing a varied genetic differentiation between populations. Analysis of molecular variance demonstrated that differentiation accounted for 82.23% of the total variation among individuals, while the remaining 17.77% variation was between populations. Furthermore, the results of population structure analysis indicated that the 142 individuals originated from three primitive groups. To provide genetic information and help design conservation and management strategies, landscape genomics analysis was performed by investigating loci associated with environmental variables. Eighteen SNP markers were associated with altitude and annual average temperature, of which five were ascribed with specific functions. In conclusion, the current study furthers the understanding of C. arbutifolia genetic architecture and provides insights for germplasm protection.
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Kofanov, L. L. "Ways to Overcome the Fragmentation of International Law in the Activities of Roman Senate and People's Assembly in V–III Centuries BC." Rossijskoe pravosudie 2 (January 29, 2020): 12–23. http://dx.doi.org/10.37399/issn2072-909x.2020.2.12-23.
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The article deals with the problem of fragmentation of international law on the example of the collision of jurisdictions of two main courts that operated in the field of international disputes in Rome of V–III centuries BC: the court of the Senate and the court of the people. Starting from the characteristics of the judicial functions of the Senate and the people of Polybius, the author distinguishes three periods of confrontation between the courts of the Senate and people in V–III centuries BC. The first period, from the beginning to the middle of V century BC, characterized by the fact that the patrician Senate did not recognize the authority of the court of the people. However, the case 446– 442 BC showed that the Senate court finally recognized the supremacy of the people's court. The second period, from the middle of the V to the beginning of the III centuries BC, represented by the cases of 446 and 391 BC, is characterized by the dominance of the people's court, which, however, in comparison with the senatorial court showed its low professional qualities: ignorance of international law and arbitration and making decisions based on their own interests, ignoring the legitimate interests of other peoples, neglect of the professional knowledge of the fathers-senators. The third period, from the middle of the III century BC to the last quarter of the II century BC, represented by the case of 204 BC, shows that the court of the people finally recognized the authority and professionalism of the senatorial jurisdiction in international law, which allowed Polybius to speak about the non-interference of the people in the judicial affairs of the Senate. However, the Senate case of 204 BC is one of the first examples of the prosecution of Roman magistrates brought to trial on charges of Roman-allied city-States. In conclusion, the author considers Cicero's recommendations for overcoming fragmentation in the activities of the two courts. As regards Senators, he advised them to maintain high moral and professional level, and the people's suffrage in tribunal he advises to rely on the opinion of optimaton, the most authoritative from the point of view of morals and professional qualities.
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Ma, Guoqiang, Qiujie Li, Shuyu Yang, Rong Zhang, Lixun Zhang, Jianping Xiao, and Guojun Sun. "Analysis of Landscape Pattern Evolution and Driving Forces Based on Land-Use Changes: A Case Study of Yilong Lake Watershed on Yunnan-Guizhou Plateau." Land 11, no. 8 (August 9, 2022): 1276. http://dx.doi.org/10.3390/land11081276.
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In order to explore the landscape pattern evolution and driving forces of the Yilong Lake watershed, the combined method of supervised classification with manual visual interpretation based on the landsat5TM/8OLI remote sensing image data sources was used to establish a high-precision spatial distribution information database of the Yilong Lake watershed. Landscape index was used to analyze the distribution and spatial pattern change characteristics of various land-use types. Based on correlation and principal component analysis, we discuss the relationship between the change characteristics of land-use type, distribution and spatial pattern, and the interference of local socio-economic development and natural factors. The results show that: (1) In the past 30 years, the land-use types of the Yilong Lake watershed are mainly forest, garden plot and cultivated land. The forest area decreased significantly by 30.45 km2, of which the fastest reduction stage was from 2000 to 2005, with a total reduction of 20.56 km2. The garden plot conversion is relatively large, with a total of 181.69 km2 transferred out, of which 28.84 km2 has become unused land, respectively. (2) In the past 30 years, the maximum patch index decreased by 9.94% and the patch density index increased by 14.25%, indicating that the landscape fragmentation in the whole basin increased. The Shannon diversity index showed an increasing process; the aggregation index showed a decreasing process. (3) The change in landscape pattern in the watershedwas closely related to economic growth, population growth, social affluence and agricultural development. Natural factors, social factors and economic indicators are significantly positively correlated with patch density, edge density, landscape shape index and Shannon diversity index, and significantly negatively correlated with the largest patch index and the contagion index. On the whole, the wetlands in the basin are shrinking and the landscape diversity is changing. Reducing the excessive impact of human activities on the watershed ecosystem is a key factor for the local protection of wetland resources and the maintenance of wetland ecological functions.
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Xu, Ying, Jia-Qiong Xie, Fu-Xing Wang, Rebecca L. Monk, James Gaskin, and Jin-Liang Wang. "The Impact of Weibo Features on User’s Information Comprehension: The Mediating Role of Cognitive Load." Social Science Computer Review, September 26, 2022, 089443932211289. http://dx.doi.org/10.1177/08944393221128941.
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Social media, such as Microblogs, have become an important source for people to obtain information. However, we know little about how this would influence our comprehension over online information. Based on the cognitive load theory, this research explores whether and how two important features of Weibo, which are the feedback function and information fragmentation, would increase cognitive load and may in turn hinder users’ information comprehension in Weibo. A 2 (feedback or non-feedback) × 2 (strong-interference or weak-interference information) between-participants experimental design was conducted. Our results revealed that the Weibo feedback function and interference information exerted a negative impact over information comprehension via inducing increased cognitive load. Specifically, these results deepened our understanding regarding the impact of Weibo features on online information comprehension and suggest the mechanism by which this occurs. This finding has implications for how to minimize the potential cost of using Weibo and maximize the adaptive development of social media.
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Pokhrel, Babu. "Measurement of Transverse Spin Dependent Azimuthal Correlations of Charged Pion(s) in $p^{\uparrow} p$ Collisions at $\sqrt s = 200$ GeV at STAR." SciPost Physics Proceedings, no. 8 (July 12, 2022). http://dx.doi.org/10.21468/scipostphysproc.8.047.
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At the leading twist, the transversity distribution function, h^{q}_{1}(x)h1q(x), where xx is the longitudinal momentum fraction of the proton carried by quark qq, encodes the transverse spin structure of the nucleon. Extraction of it is difficult because of its chiral-odd nature. In transversely polarized proton-proton collisions (p^\uparrow pp↑p), h_{1}^{q}(x)h1q(x) can be coupled with another chiral-odd partner, a spin-dependent fragmentation function (FF). The resulting asymmetries in hadron(s) azimuthal correlations directly probe h_{1}^{q}(x)h1q(x). We report the measurement of correlation asymmetries for charged pion(s) in p^\uparrow pp↑p, through the Collins and the Interference FF channel.
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Dilks, Christopher. "Multidimensional partial wave analysis of SIDIS dihadron beam spin asymmetries at CLAS12." SciPost Physics Proceedings, no. 8 (July 14, 2022). http://dx.doi.org/10.21468/scipostphysproc.8.152.
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Dihadron beam spin asymmetries provide a wide range of insights into nucleon structure and hadronization. Recent measurements at CLAS12 provide the first empirical evidence of nonzero G_1^\perpG1⊥, the parton helicity-dependent dihadron fragmentation function (DiFF) encoding spin-momentum correlations in hadronization. These measurements also allow for a point-by-point extraction of the subleading-twist PDF e(x)e(x) in a collinear framework. We observe different behavior of the asymmetries in different invariant mass regions, motivating a fully multidimensional study. The DiFFs also expand in terms of partial waves, each corresponding to the interference of dihadrons of particular polarizations. Altogether a fully multidimensional partial wave analysis is needed, and this presentation will summarize the efforts and results obtained thus far.
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Lacombe, Marie-Lise, Frederic Lamarche, Olivier De Wever, Teresita Padilla-Benavides, Alyssa Carlson, Imran Khan, Anda Huna, et al. "The mitochondrially-localized nucleoside diphosphate kinase D (NME4) is a novel metastasis suppressor." BMC Biology 19, no. 1 (October 21, 2021). http://dx.doi.org/10.1186/s12915-021-01155-5.
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Abstract Background Mitochondrial nucleoside diphosphate kinase (NDPK-D, NME4, NM23-H4) is a multifunctional enzyme mainly localized in the intermembrane space, bound to the inner membrane. Results We constructed loss-of-function mutants of NDPK-D, lacking either NDP kinase activity or membrane interaction and expressed mutants or wild-type protein in cancer cells. In a complementary approach, we performed depletion of NDPK-D by RNA interference. Both loss-of-function mutations and NDPK-D depletion promoted epithelial-mesenchymal transition and increased migratory and invasive potential. Immunocompromised mice developed more metastases when injected with cells expressing mutant NDPK-D as compared to wild-type. This metastatic reprogramming is a consequence of mitochondrial alterations, including fragmentation and loss of mitochondria, a metabolic switch from respiration to glycolysis, increased ROS generation, and further metabolic changes in mitochondria, all of which can trigger pro-metastatic protein expression and signaling cascades. In human cancer, NME4 expression is negatively associated with markers of epithelial-mesenchymal transition and tumor aggressiveness and a good prognosis factor for beneficial clinical outcome. Conclusions These data demonstrate NME4 as a novel metastasis suppressor gene, the first localizing to mitochondria, pointing to a role of mitochondria in metastatic dissemination.
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Radici, Marco, Rainer Jakob, and Andrea Bianconi. "Accessing transversity with interference fragmentation functions." Physical Review D 65, no. 7 (April 1, 2002). http://dx.doi.org/10.1103/physrevd.65.074031.
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Boer, Daniël, Rainer Jakob, and Marco Radici. "Interference fragmentation functions in electron-positron annihilation." Physical Review D 67, no. 9 (May 12, 2003). http://dx.doi.org/10.1103/physrevd.67.094003.
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Bacchetta, Alessandro, and Marco Radici. "Dihadron interference fragmentation functions in proton-proton collisions." Physical Review D 70, no. 9 (November 18, 2004). http://dx.doi.org/10.1103/physrevd.70.094032.
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Bianconi, A., S. Boffi, R. Jakob, and M. Radici. "Two-hadron interference fragmentation functions. I. General framework." Physical Review D 62, no. 3 (July 10, 2000). http://dx.doi.org/10.1103/physrevd.62.034008.
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Bianconi, A., S. Boffi, R. Jakob, and M. Radici. "Two-hadron interference fragmentation functions. II. A model calculation." Physical Review D 62, no. 3 (July 10, 2000). http://dx.doi.org/10.1103/physrevd.62.034009.
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Courtoy, Aurore, Alessandro Bacchetta, Marco Radici, and Andrea Bianconi. "First extraction of interference fragmentation functions frome+e−data." Physical Review D 85, no. 11 (June 14, 2012). http://dx.doi.org/10.1103/physrevd.85.114023.
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Boer, Daniël, and Marco Radici. "Erratum: Interference fragmentation functions in electron-positron annihilation [Phys. Rev. D 67 , 094003 (2003)]." Physical Review D 98, no. 3 (August 14, 2018). http://dx.doi.org/10.1103/physrevd.98.039902.
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Van Beersel, Guillaume, Eliane Tihon, Stéphane Demine, Isabelle Hamer, Michel Jadot, and Thierry Arnould. "Different molecular mechanisms involved in spontaneous and oxidative stress-induced mitochondrial fragmentation in tripeptidyl peptidase-1 (TPP-1)-deficient fibroblasts." Bioscience Reports 33, no. 2 (February 7, 2013). http://dx.doi.org/10.1042/bsr20120104.
Full textAbstract:
NCLs (neuronal ceroid lipofuscinoses) form a group of eight inherited autosomal recessive diseases characterized by the intralysosomal accumulation of autofluorescent pigments, called ceroids. Recent data suggest that the pathogenesis of NCL is associated with the appearance of fragmented mitochondria with altered functions. However, even if an impairement in the autophagic pathway has often been evoked, the molecular mechanisms leading to mitochondrial fragmentation in response to a lysosomal dysfunction are still poorly understood. In this study, we show that fibroblasts that are deficient for the TPP-1 (tripeptidyl peptidase-1), a lysosomal hydrolase encoded by the gene mutated in the LINCL (late infantile NCL, CLN2 form) also exhibit a fragmented mitochondrial network. This morphological alteration is accompanied by an increase in the expression of the protein BNIP3 (Bcl2/adenovirus E1B 19 kDa interacting protein 3) as well as a decrease in the abundance of mitofusins 1 and 2, two proteins involved in mitochondrial fusion. Using RNAi (RNA interference) and quantitative analysis of the mitochondrial morphology, we show that the inhibition of BNIP3 expression does not result in an increase in the reticulation of the mitochondrial population in LINCL cells. However, this protein seems to play a key role in cell response to mitochondrial oxidative stress as it sensitizes mitochondria to antimycin A-induced fragmentation. To our knowledge, our results bring the first evidence of a mechanism that links TPP-1 deficiency and oxidative stress-induced changes in mitochondrial morphology.