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Journal articles on the topic 'Jeux du cycle impair'

Author: Grafiati

Published: 4 June 2021

Last updated: 15 February 2022

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1

Henriet, Jean-Michel. "Didactique des jeux de simulation dans l'enseignement du second cycle des lycées." Revue de géographie de Lyon 61, no. 2 (1986): 227–34. http://dx.doi.org/10.3406/geoca.1986.4090.

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2

Sabino, Catarina, Michael Basic, Daniela Bender, Fabian Elgner, Kiyoshi Himmelsbach, and Eberhard Hildt. "Bafilomycin A1 and U18666A Efficiently Impair ZIKV Infection." Viruses 11, no. 6 (2019): 524. http://dx.doi.org/10.3390/v11060524.

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Zika virus (ZIKV) is a highly transmissive virus that belongs to the Flaviviridae family, which comprises several other pathogens that threaten human health. This re-emerging virus gained attention during the outbreak in Brazil in 2016, where a considerable number of microcephaly cases in newborns was associated with ZIKV infection during pregnancy. Lacking a preventive vaccine or antiviral drugs, efforts have been made to better understand the viral life cycle. In light of this, the relevance of the endosomal–lysosomal compartment for the ZIKV life cycle was investigated. A549 and SH-SY5Y cel

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3

Hotchkiss, R. S., S. K. Song, J. J. Neil, et al. "Sepsis does not impair tricarboxylic acid cycle in the heart." American Journal of Physiology-Cell Physiology 260, no. 1 (1991): C50—C57. http://dx.doi.org/10.1152/ajpcell.1991.260.1.c50.

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Sepsis has been reported to cause mitochondrial dysfunction and inhibition of key enzymes that regulate the tricarboxylic acid (TCA) cycle. We investigated the effect of sepsis on high-energy phosphates, glycolytic and TCA cycle intermediates, and specific amino acids that are involved in regulating the size of the TCA cycle pool during changes in metabolic state of the heart. Sepsis was induced in 12 female rats by the cecal ligation and perforation technique under halothane anesthesia; seven control rats underwent cecal manipulation without ligation. At 36-42 h postsurgery, the rats were rea

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4

Henriet, Jean-Michel. "L'utilisation des jeux de simulation dans le second cycle des lycées : l'exemple d'ACIERIX." Espace géographique 15, no. 2 (1986): 138–42. http://dx.doi.org/10.3406/spgeo.1986.4132.

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5

Cuhra, Marek, Terje Traavik, Mickaël Dando, Raul Primicerio, Daniel Ferreira Holderbaum, and Thomas Bøhn. "Glyphosate-Residues in Roundup-Ready Soybean Impair Daphnia magna Life-Cycle." Journal of Agricultural Chemistry and Environment 04, no. 01 (2015): 24–36. http://dx.doi.org/10.4236/jacen.2015.41003.

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6

Larounga, TCHANILEY, AYISAH Kwasi Dzola, and DEWA KASSA Kodjo Akonta. "Effet de la combinaison des fertilisants organiques et minéraux (NPK 15-15-15 et urée) sur le rendement de la laitue (Lactuca sativa L.) dans le sud du Togo." Journal of Applied Biosciences 151 (July 31, 2020): 15540–49. http://dx.doi.org/10.35759/jabs.151.3.

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Objectif : L’essai a visé à développer de nouvelles initiatives de gestion de la fertilité des sols compatibles avec la gestion rationnelle des ressources mises en jeux afin d’évaluer et d’apprécier l’efficacité des différentes combinaisons d’engrais sur le rendement de la laitue et d’identifier le meilleur model d’amélioration des conditions de culture de cette plante. Méthodologie et résultats : Au cours de l’essai, le dispositif expérimental adopté a été celui en blocs aléatoire complet à quatre traitements et à trois répétitions. Les traitements utilisés ont été : T0 (témoin absolu sans ap

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7

Souza, Rodolpho Ornitz Oliveira, Marcell Crispim, Ariel Mariano Silber, and Flávia Silva Damasceno. "Glutamine Analogues Impair Cell Proliferation, the Intracellular Cycle and Metacyclogenesis in Trypanosoma cruzi." Molecules 25, no. 7 (2020): 1628. http://dx.doi.org/10.3390/molecules25071628.

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Trypanosoma cruzi is the aetiologic agent of Chagas disease, which affects people in the Americas and worldwide. The parasite has a complex life cycle that alternates among mammalian hosts and insect vectors. During its life cycle, T. cruzi passes through different environments and faces nutrient shortages. It has been established that amino acids, such as proline, histidine, alanine, and glutamate, are crucial to T. cruzi survival. Recently, we described that T. cruzi can biosynthesize glutamine from glutamate and/or obtain it from the extracellular environment, and the role of glutamine in e

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Yang, Runze, and Jeff F. Dunn. "Multiple sclerosis disease progression: Contributions from a hypoxia–inflammation cycle." Multiple Sclerosis Journal 25, no. 13 (2018): 1715–18. http://dx.doi.org/10.1177/1352458518791683.

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Hypoxia has been associated with multiple sclerosis (MS) and is an important area of research. Hypoxia can exacerbate inflammation via the prolylhydroxylase pathway. Inflammation can also trigger hypoxia by damaging mitochondria and endothelial cells to impair blood flow regulation. We hypothesize that there is a “hypoxia–inflammation cycle” in MS which plays an important role in MS disease progression. Therapies that break this cycle may be an interesting area of exploration for treatment of MS.

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9

Neufer, P. D., M. N. Sawka, A. J. Young, M. D. Quigley, W. A. Latzka, and L. Levine. "Hypohydration does not impair skeletal muscle glycogen resynthesis after exercise." Journal of Applied Physiology 70, no. 4 (1991): 1490–94. http://dx.doi.org/10.1152/jappl.1991.70.4.1490.

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The purpose of this investigation was to examine the effects of moderate hypohydration (HY) on skeletal muscle glycogen resynthesis after exhaustive exercise. On two occasions, eight males completed 2 h of intermittent cycle ergometer exercise (4 bouts of 17 min at 60% and 3 min at 80% of maximal O2 consumption/10 min rest) to reduce muscle glycogen concentrations (control values 711 +/- 41 mumol/g dry wt). During one trial, cycle exercise was followed by several hours of light upper body exercise in the heat without fluid replacement to induce HY (-5% body wt); in the second trial, sufficient

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10

Rymen, Bart, Fabio Fiorani, Fatma Kartal, Klaas Vandepoele, Dirk Inzé, and Gerrit T. S. Beemster. "Cold Nights Impair Leaf Growth and Cell Cycle Progression in Maize through Transcriptional Changes of Cell Cycle Genes." Plant Physiology 143, no. 3 (2007): 1429–38. http://dx.doi.org/10.1104/pp.106.093948.

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11

Kiser, Philip D., Jianye Zhang, Aditya Sharma, et al. "Retinoid isomerase inhibitors impair but do not block mammalian cone photoreceptor function." Journal of General Physiology 150, no. 4 (2018): 571–90. http://dx.doi.org/10.1085/jgp.201711815.

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Visual function in vertebrates critically depends on the continuous regeneration of visual pigments in rod and cone photoreceptors. RPE65 is a well-established retinoid isomerase in the pigment epithelium that regenerates rhodopsin during the rod visual cycle; however, its contribution to the regeneration of cone pigments remains obscure. In this study, we use potent and selective RPE65 inhibitors in rod- and cone-dominant animal models to discern the role of this enzyme in cone-mediated vision. We confirm that retinylamine and emixustat-family compounds selectively inhibit RPE65 over DES1, th

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12

Suissa, Amnon Jacob. "La dépendance aux Jeux de hasard et d’argent comme problème social." Service social 59, no. 2 (2013): 76–92. http://dx.doi.org/10.7202/1019111ar.

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Les essais de définition d’un problème social sont multiples et s’inscrivent dans des perspectives théoriques qui peuvent fortement varier selon les écoles de pensée, les contextes historiques, politiques, sociaux, les groupes d’intérêts et les acteurs en présence. Ainsi compris, et dans la mesure où un problème n’est reconnu officiellement comme social une fois qu’il a passé certaines phases: nombre de citoyens touchés par le problème en question, force ou faiblesse des liens sociaux, processus d’institutionnalisation, modalités de réaction sociale, etc. Nous tenterons de réfléchir et d’artic

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13

Santos, M., and A. E. Ribeiro. "Poverty and mental illness: An unbreakable cycle?" European Psychiatry 26, S2 (2011): 577. http://dx.doi.org/10.1016/s0924-9338(11)72284-2.

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Mental condition is determined by a multiplicity of factors, such as biological, individual, social, economic and environmental. Mental and behavioural disorders are estimated to account for 13% of the global burden of disease, according to the World Health Organization. Despite this evidence, mental health is a neglected and an under-researched area of public health, particularly in low-and-middle-income-countries (LMICs).Recent studies found an association between common mental disorders (CMD), such as depression and anxiety, and poverty. However, investigation on several specific poverty in

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14

Petrocca, Fabio, Rosa Visone, Mariadele Rapazzotti Onelli та ін. "E2F1-Regulated MicroRNAs Impair TGFβ-Dependent Cell-Cycle Arrest and Apoptosis in Gastric Cancer". Cancer Cell 13, № 3 (2008): 272–86. http://dx.doi.org/10.1016/j.ccr.2008.02.013.

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15

Koulov, Atanas V., Paul LaPointe, Bingwen Lu, et al. "Biological and Structural Basis for Aha1 Regulation of Hsp90 ATPase Activity in Maintaining Proteostasis in the Human Disease Cystic Fibrosis." Molecular Biology of the Cell 21, no. 6 (2010): 871–84. http://dx.doi.org/10.1091/mbc.e09-12-1017.

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The activator of Hsp90 ATPase 1, Aha1, has been shown to participate in the Hsp90 chaperone cycle by stimulating the low intrinsic ATPase activity of Hsp90. To elucidate the structural basis for ATPase stimulation of human Hsp90 by human Aha1, we have developed novel mass spectrometry approaches that demonstrate that the N- and C-terminal domains of Aha1 cooperatively bind across the dimer interface of Hsp90 to modulate the ATP hydrolysis cycle and client activity in vivo. Mutations in both the N- and C-terminal domains of Aha1 impair its ability to bind Hsp90 and stimulate its ATPase activity

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16

Gagné, Learry. "La théorie des jeux. Essai d'interprétationChristian Schmidt Collection «Premier Cycle» Paris, Presses Universitaires de France, 2001, 435 p." Dialogue 42, no. 3 (2003): 612–15. http://dx.doi.org/10.1017/s0012217300004868.

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17

Bruns, Ingmar, Sebastian Büst, Akos G. Czibere, et al. "Malignant Myeloma Cells Impair Phenotype and Function of stem and Progenitor Cells." Blood 114, no. 22 (2009): 1799. http://dx.doi.org/10.1182/blood.v114.22.1799.1799.

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Abstract Abstract 1799 Poster Board I-825 Multiple myeloma (MM) patients often present with anemia at the time of initial diagnosis. This has so far only attributed to a physically marrow suppression by the invading malignant plasma cells and the overexpression of Fas-L and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) by malignant plasma cells triggering the death of immature erythroblasts. Still the impact of MM on hematopoietic stem cells and their niches is scarcely established. In this study we analyzed highly purified CD34+ hematopoietic stem and progenitor cell subsets

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18

Page, Martin A., Joanna L. Shisler, and Benito J. Mariñas. "Mechanistic Aspects of Adenovirus Serotype 2 Inactivation with Free Chlorine." Applied and Environmental Microbiology 76, no. 9 (2010): 2946–54. http://dx.doi.org/10.1128/aem.02267-09.

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ABSTRACT Free chlorine is an effective disinfectant for controlling adenoviruses in drinking water, but little is known about the underlying inactivation mechanisms. The objective of this study was to elucidate the molecular components of adenovirus type 2 (Ad2) targeted by free chlorine during the inactivation process. The effects of free chlorine treatment on several Ad2 molecular components and associated life cycle events were compared to its effect on the ability of adenovirus to complete its life cycle, i.e., viability. Free chlorine treatment of Ad2 virions did not impair their ability

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19

Rossi, Francesca, Alvaro Centrón-Broco, Dario Dattilo, et al. "CircVAMP3: A circRNA with a Role in Alveolar Rhabdomyosarcoma Cell Cycle Progression." Genes 12, no. 7 (2021): 985. http://dx.doi.org/10.3390/genes12070985.

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Circular RNAs (circRNAs), a class of covalently closed RNAs formed by a back-splicing reaction, have been involved in the regulation of diverse oncogenic processes. In this article we describe circVAMP3, a novel circular RNA overexpressed in RH4, a representative cell line of alveolar rhabdomyosarcoma. We demonstrated that circVAMP3 has a differential m6A pattern opposed to its linear counterpart, suggesting that the two isoforms can be differently regulated by such RNA modification. Moreover, we show how circVAMP3 depletion in alveolar rhabdomyosarcoma cells can impair cell cycle progression,

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20

Liu, Da-Zhi, and Bradley P. Ander. "Cell Cycle Inhibition without Disruption of Neurogenesis Is a Strategy for Treatment of Aberrant Cell Cycle Diseases: An Update." Scientific World Journal 2012 (2012): 1–13. http://dx.doi.org/10.1100/2012/491737.

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Since publishing our earlier report describing a strategy for the treatment of central nervous system (CNS) diseases by inhibiting the cell cycle and without disrupting neurogenesis (Liu et al. 2010), we now update and extend this strategy to applications in the treatment of cancers as well. Here, we put forth the concept of “aberrant cell cycle diseases” to include both cancer and CNS diseases, the two unrelated disease types on the surface, by focusing on a common mechanism in each aberrant cell cycle reentry. In this paper, we also summarize the pharmacological approaches that interfere wit

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21

Samimi, Nastaran, Akiko Asada, and Kanae Ando. "Tau Abnormalities and Autophagic Defects in Neurodegenerative Disorders; A Feed-forward Cycle." Galen Medical Journal 9 (January 27, 2020): 1681. http://dx.doi.org/10.31661/gmj.v9i0.1681.

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Abnormal deposition of misfolded proteins is a neuropathological characteristic shared by many neurodegenerative disorders including Alzheimer’s disease (AD). Generation of excessive amounts of aggregated proteins and impairment of degradation systems for misfolded proteins such as autophagy can lead to accumulation of proteins in diseased neurons. Molecules that contribute to both these effects are emerging as critical players in disease pathogenesis. Furthermore, impairment of autophagy under disease conditions can be both a cause and a consequence of abnormal protein accumulation. Specifica

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Osuji, GC, M. Reyes, NN Drever, et al. "ID: 104: CINOBUFOTALIN HINDERS CYTOTROPHOBLASTS FUNCTION VIA CELL CYCLE ARREST." Journal of Investigative Medicine 64, no. 4 (2016): 957.1–957. http://dx.doi.org/10.1136/jim-2016-000120.94.

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ObjectivePreeclampsia (preE) is a hypertensive disorder of pregnancy. Cardiotonic steroids (CTS) are endogenous inhibitors of Na+/K+ ATPase and at least one CTS, marinobufagenin (MBG), is elevated in preE prior to the development of the syndrome in rats with preE. MBG and ouabain impair cytotrophoblast (CTB) function, which is critical for placental development.Study DesignWe evaluated the effect of a CTS, cinobufotalin (CINO), on CTB cell function in vitro.ResultsCINO at ≥1 nM inhibited CTB cell proliferation, migration, and invasion (p<0.05) but had no effect on cell viability. There was

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Zaliova, Marketa, Jozef Madzo, Gunnar Cario, and Jan Trka. "Silencing of TEL/AML1 In Definitive Leukemic Cells Does Not Impair Cell Survival." Blood 116, no. 21 (2010): 3229. http://dx.doi.org/10.1182/blood.v116.21.3229.3229.

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Abstract Abstract 3229 The most frequent structural chromosomal aberration in childhood acute lymphoblastic leukemia t(12;21) generates TEL/AML1 fusion gene. Resulting TEL/AML1 protein probably acts as an aberrant transcription factor that deregulates AML1-dependent transcription but its target genes and thus also the exact role in leukemic cells remain unknown. In vivo studies showed that TEL/AML1 itself is not sufficient to cause leukemia but may induce a preleukemic state characterized by the increased numbers of multipotent or B-cell progenitors with an incomplete block of differentiation.

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Liberal, Joana, Anália Carmo, Célia Gomes, Maria Teresa Cruz, and Maria Teresa Batista. "Urolithins impair cell proliferation, arrest the cell cycle and induce apoptosis in UMUC3 bladder cancer cells." Investigational New Drugs 35, no. 6 (2017): 671–81. http://dx.doi.org/10.1007/s10637-017-0483-7.

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25

Kiser, Philip D., Alexander V. Kolesnikov, Jianying Z. Kiser, et al. "Conditional deletion of Des1 in the mouse retina does not impair the visual cycle in cones." FASEB Journal 33, no. 4 (2019): 5782–92. http://dx.doi.org/10.1096/fj.201802493r.

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Sönmezer, Murat, Aylin Pelin Cil, Cem Atabekoğlu, Sinan Özkavukçu, and Batuhan Özmen. "Does premature luteinization or early surge of LH impair cycle outcome? Report of two successful outcomes." Journal of Assisted Reproduction and Genetics 26, no. 2-3 (2009): 159–63. http://dx.doi.org/10.1007/s10815-009-9299-5.

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27

Faia, Ester. "A NOTE ON CREDIT RISK TRANSFER AND THE MACROECONOMY." Macroeconomic Dynamics 22, no. 4 (2018): 1096–111. http://dx.doi.org/10.1017/s1365100516000390.

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The recent financial crisis highlighted the limits of the originate to distribute model of banking, but its nexus with the macroeconomy remains unexplored. I build a business cycle model with banks engaging in credit risk transfer (CRT) under informational externalities. Markets for CRT provide liquidity insurance to banks, but the emergence of a pooling equilibrium can also impair the banks' monitoring incentives. In normal times and in face of standard macro shocks the insurance benefits of CRT prevail and the business cycle is stabilized. In face of financial/liquidity shocks the extent of

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28

Ma, Lijun, Nicholette D. Palmer, Young A. Choi, et al. "APOL1 Risk Variants Impair Multiple Mitochondrial Pathways in a Metabolomics Analysis." Kidney360 1, no. 12 (2020): 1353–62. http://dx.doi.org/10.34067/kid.0003592020.

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BackgroundKidney risk variants (KRVs) in the APOL1 gene are associated with mitochondrial dysfunction. However, the molecular spectrum of metabolites affected by the G1 and G2 KRVs, and the downstream mitochondrial pathways they affect, remain unknown.MethodsWe performed a metabolomics analysis using HEK293 Tet-on cells conditionally expressing APOL1 G0, G1, and G2 KRVs to determine the patterns of metabolites and pathways potentially involved in nephropathy. The Welch two-sample t test, matched-pairs t test, and two-way repeated measures ANOVA were used to identify differential metabolites. R

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Patassini, Stefano, Paul Begley, Jingshu Xu, et al. "Cerebral Vitamin B5 (D-Pantothenic Acid) Deficiency as a Potential Cause of Metabolic Perturbation and Neurodegeneration in Huntington’s Disease." Metabolites 9, no. 6 (2019): 113. http://dx.doi.org/10.3390/metabo9060113.

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Huntington’s disease (HD) is a neurodegenerative disorder caused by an expanded CAG repeat in exon 1 of the HTT gene. HD usually manifests in mid-life with loss of GABAergic projection neurons from the striatum accompanied by progressive atrophy of the putamen followed by other brain regions, but linkages between the genetics and neurodegeneration are not understood. We measured metabolic perturbations in HD-human brain in a case-control study, identifying pervasive lowering of vitamin B5, the obligatory precursor of coenzyme A (CoA) that is essential for normal intermediary metabolism. Cerebr

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Miller, Malcolm. "‘RESONANCE AND DISTANCE’: SIMON BAINBRIDGE IN CONVERSATION." Tempo 67, no. 265 (2013): 37–49. http://dx.doi.org/10.1017/s0040298213000454.

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AbstractThis interview, based on a conversation with Simon Bainbridge at London's City Literary Institute in June 2011, presents something of a rounded portrait of the composer while covering a good deal of ground. We began our conversation with a discussion of a recent work for orchestra, Concerti Grossi, going into some detail in matters of scoring and structure. The discussion then broadened to cover such topics as the creative process, formative influences (for example, his parents' activity in the visual arts, Debussy's Jeux, John Lambert and Gunther Schuller), instrumentation and the rel

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Van Vugt, M. A. T. M., M. Krajewska, H. Sillje, A. M. Heijink, Y. Bisselink, and E. G. E. de Vries. "SP-02: Cell Cycle Regulation of the DNA Damage Response: Targeting WEE1 Kinase to Impair DNA Repair." Radiotherapy and Oncology 104 (September 2012): 21. http://dx.doi.org/10.1016/s0167-8140(15)34556-4.

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32

Devlin, J. T., J. Calles-Escandon, and E. S. Horton. "Effects of preexercise snack feeding on endurance cycle exercise." Journal of Applied Physiology 60, no. 3 (1986): 980–85. http://dx.doi.org/10.1152/jappl.1986.60.3.980.

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We studied the effects of ingesting either a snack food (S) (260 kcal) or placebo (P) 30 min before intermittent cycle exercise at 70% maximal O2 consumption on endurance performance and muscle glycogen depletion in eight healthy human males. Immediately before exercise there were significantly greater increases in plasma glucose (PG) (S +28 +/- 9.7; P +0.1 +/- 0.8 mg/dl) and insulin (S +219 +/- 61.5; P -7 +/- 5.5 pmol/l) (P less than 0.05) following S feeding compared with P. These differences were no longer present by the end of the first exercise period. There were no differences in enduran

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Kleiblova, Petra, Indra A. Shaltiel, Jan Benada, et al. "Gain-of-function mutations of PPM1D/Wip1 impair the p53-dependent G1 checkpoint." Journal of Cell Biology 201, no. 4 (2013): 511–21. http://dx.doi.org/10.1083/jcb.201210031.

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The DNA damage response (DDR) pathway and its core component tumor suppressor p53 block cell cycle progression after genotoxic stress and represent an intrinsic barrier preventing cancer development. The serine/threonine phosphatase PPM1D/Wip1 inactivates p53 and promotes termination of the DDR pathway. Wip1 has been suggested to act as an oncogene in a subset of tumors that retain wild-type p53. In this paper, we have identified novel gain-of-function mutations in exon 6 of PPM1D that result in expression of C-terminally truncated Wip1. Remarkably, mutations in PPM1D are present not only in t

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Shan, B., and W. H. Lee. "Deregulated expression of E2F-1 induces S-phase entry and leads to apoptosis." Molecular and Cellular Biology 14, no. 12 (1994): 8166–73. http://dx.doi.org/10.1128/mcb.14.12.8166.

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E2F-1, the first gene product identified among a family of E2F transcription factors, is thought to play a critical role in G1/S progression of the cell cycle. Transcriptional activities of E2F are modulated during the cell cycle, mainly by the formation of complexes between E2F and several key regulators of cell cycle such as the retinoblastoma protein and related proteins. To further understand the roles of E2F in the cell cycle progression, we have overexpressed exogenous E2F-1 by using a tetracycline-controlled expression system. We have found that the induced expression of E2F-1 in Rat-2

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Shan, B., and W. H. Lee. "Deregulated expression of E2F-1 induces S-phase entry and leads to apoptosis." Molecular and Cellular Biology 14, no. 12 (1994): 8166–73. http://dx.doi.org/10.1128/mcb.14.12.8166-8173.1994.

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E2F-1, the first gene product identified among a family of E2F transcription factors, is thought to play a critical role in G1/S progression of the cell cycle. Transcriptional activities of E2F are modulated during the cell cycle, mainly by the formation of complexes between E2F and several key regulators of cell cycle such as the retinoblastoma protein and related proteins. To further understand the roles of E2F in the cell cycle progression, we have overexpressed exogenous E2F-1 by using a tetracycline-controlled expression system. We have found that the induced expression of E2F-1 in Rat-2

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Wegrzycka, Barbara. "Le prix d’une passion : la carrière du joueur compulsif 1." Criminologie 40, no. 1 (2007): 31–58. http://dx.doi.org/10.7202/016014ar.

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Résumé Alors que les jeux de hasard et d’argent gagnent en accessibilité, de nombreuses études établissent un lien entre le jeu pathologique et la criminalité. La vie du joueur emprunterait un parcours précis vers la délinquance et s’inscrirait dans un cycle gambling-délinquance2. Or, l’inscription des trajectoires délinquantes dans un cycle aussi statique nous paraît discutable. Dans cet article, nous soutenons que chaque individu est soumis à l’influence de facteurs pouvant modifier la carrière du joueur et sa propension à commettre des délits. À l’aide d’une vingtaine d’entrevues, nous avon

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Geeves, Michael, Zoltan Ujfalusi, Carlos Vera, Srbolujub Mijailovich, Marina Svicevic, and Leslie Leinwand. "ATPase Cycle Analysis Predicts that Mutations Linked to Dilated Cardiomyopathy in Human Beta Myosin Will Impair Force Generation." Biophysical Journal 114, no. 3 (2018): 210a. http://dx.doi.org/10.1016/j.bpj.2017.11.1178.

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38

Paijmans, Joris, Mark Bosman, Pieter Rein ten Wolde, and David K. Lubensky. "Discrete gene replication events drive coupling between the cell cycle and circadian clocks." Proceedings of the National Academy of Sciences 113, no. 15 (2016): 4063–68. http://dx.doi.org/10.1073/pnas.1507291113.

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Many organisms possess both a cell cycle to control DNA replication and a circadian clock to anticipate changes between day and night. In some cases, these two rhythmic systems are known to be coupled by specific, cross-regulatory interactions. Here, we use mathematical modeling to show that, additionally, the cell cycle generically influences circadian clocks in a nonspecific fashion: The regular, discrete jumps in gene-copy number arising from DNA replication during the cell cycle cause a periodic driving of the circadian clock, which can dramatically alter its behavior and impair its functi

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Steinfeldt, Jakob, Robert Becker, Silvia Vergarajauregui, and Felix B. Engel. "Alternative Splicing of Pericentrin Contributes to Cell Cycle Control in Cardiomyocytes." Journal of Cardiovascular Development and Disease 8, no. 8 (2021): 87. http://dx.doi.org/10.3390/jcdd8080087.

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Induction of cardiomyocyte proliferation is a promising option to regenerate the heart. Thus, it is important to elucidate mechanisms that contribute to the cell cycle arrest of mammalian cardiomyocytes. Here, we assessed the contribution of the pericentrin (Pcnt) S isoform to cell cycle arrest in postnatal cardiomyocytes. Immunofluorescence staining of Pcnt isoforms combined with SiRNA-mediated depletion indicates that Pcnt S preferentially localizes to the nuclear envelope, while the Pcnt B isoform is enriched at centrosomes. This is further supported by the localization of ectopically expre

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Rodgers, Carol D., and Mladen Vranic. "Mediation of Glucoregulation at Rest and During Exercise by the Glucose-Fatty Acid Cycle: In Vivo and In Vitro Studies." Canadian Journal of Applied Physiology 23, no. 6 (1998): 534–57. http://dx.doi.org/10.1139/h98-030.

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Himsworth (1934) demonstrated that increased fat consumption leads to decreased glucose tolerance due to decreased insulin sensitivity. Randle and colleagues (1964) named this interplay between fat and carbohydrate metabolism the glucose-fatty acid cycle (GFAC) and proposed a series of feedback mechanisms by which elevated levels of free fatty acids (FFAs) impair glucose uptake and oxidation in rat heart and diaphragm muscle. Numerous investigators have extended these studies to clarify the existence of GFAC and provide insight into the mechanisms and conditions under which it occurs. This pap

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NG, GEOK SEE, ABDUL WAHAB, and DAMING SHI. "ENTROPY LEARNING AND RELEVANCE CRITERIA FOR NEURAL NETWORK PRUNING." International Journal of Neural Systems 13, no. 05 (2003): 291–305. http://dx.doi.org/10.1142/s0129065703001637.

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In this paper, entropy is a term used in the learning phase of a neural network. As learning progresses, more hidden nodes get into saturation. The early creation of such hidden nodes may impair generalisation. Hence an entropy approach is proposed to dampen the early creation of such nodes by using a new computation called entropy cycle. Entropy learning also helps to increase the importance of relevant nodes while dampening the less important nodes. At the end of learning, the less important nodes can then be pruned to reduce the memory requirements of the neural network.

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Gibala, Martin J., Marco Lozej, Mark A. Tarnopolsky, Cyndy McLean, and Terry E. Graham. "Low glycogen and branched-chain amino acid ingestion do not impair anaplerosis during exercise in humans." Journal of Applied Physiology 87, no. 5 (1999): 1662–67. http://dx.doi.org/10.1152/jappl.1999.87.5.1662.

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We examined the hypothesis that increasing the rate of branched-chain amino acid (BCAA) oxidation, during conditions of low glycogen availability, reduces the level of muscle tricarboxylic acid cycle intermediates (TCAI) by placing a carbon “drain” on the cycle at the level of 2-oxoglutarate. Six men cycled at ∼70% of maximal oxygen uptake for 15 min under two conditions: 1) low preexercise muscle glycogen (placebo) and 2) low glycogen combined with BCAA ingestion. We have previously shown that BCAA ingestion increased the activity of branched-chain oxoacid dehydrogenase, the rate-limiting enz

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Sahlin, K., A. Katz, and S. Broberg. "Tricarboxylic acid cycle intermediates in human muscle during prolonged exercise." American Journal of Physiology-Cell Physiology 259, no. 5 (1990): C834—C841. http://dx.doi.org/10.1152/ajpcell.1990.259.5.c834.

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Seven subjects cycled to fatigue [75 +/- 5 (SE) min] at a work load corresponding to approximately 75% of their maximal oxygen uptake. Biopsies were taken from the quadriceps femoris muscle at rest and during exercise. Muscle glycogen decreased from a preexercise level of 445 +/- 33 mmol glucosyl units/kg dry wt to 50 +/- 14 at fatigue. The sum of the measured tricarboxylic acid cycle intermediates (TCAI = malate + citrate + fumarate + oxaloacetate) was 0.49 +/- 0.05 mmol/kg dry wt at rest, increased to 4.41 +/- 0.23 after 5 min of exercise, and then decreased continuously to 3.33 +/- 0.29 and

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Wolf, Benita, Fodé Diop, Pauline Ferraris, et al. "Zika virus causes supernumerary foci with centriolar proteins and impaired spindle positioning." Open Biology 7, no. 1 (2017): 160231. http://dx.doi.org/10.1098/rsob.160231.

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Zika virus (ZIKV) causes congenital microcephaly. Although ZIKV can impair cell cycle progression and provoke apoptosis, which probably contributes to disease aetiology through depletion of neural progenitor cells, additional cellular mechanisms may be important. Here, we investigated whether ZIKV infection alters centrosome number and spindle positioning, because such defects are thought to be at the root of inherited primary autosomal recessive microcephaly (MCPH). In addition to HeLa cells, in which centrosome number and spindle positioning can be well monitored, we analysed retinal epithel

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Woo, Jung-A. A., Tian Liu, Cenxiao C. Fang та ін. "β-Arrestin2 oligomers impair the clearance of pathological tau and increase tau aggregates". Proceedings of the National Academy of Sciences 117, № 9 (2020): 5006–15. http://dx.doi.org/10.1073/pnas.1917194117.

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Multiple G protein-coupled receptors (GPCRs) are targets in the treatment of dementia, and the arrestins are common to their signaling. β-Arrestin2 was significantly increased in brains of patients with frontotemporal lobar degeneration (FTLD-tau), a disease second to Alzheimer’s as a cause of dementia. Genetic loss and overexpression experiments using genetically encoded reporters and defined mutant constructs in vitro, and in cell lines, primary neurons, and tau P301S mice crossed with β-arrestin2−/−mice, show that β-arrestin2 stabilizes pathogenic tau and promotes tau aggregation. Cell and

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Mood, Kathleen, Caroline Saucier, Yong-Sik Bong, Hyun-Shik Lee, Morag Park, and Ira O. Daar. "Gab1 Is Required for Cell Cycle Transition, Cell Proliferation, and Transformation Induced by an Oncogenic Met Receptor." Molecular Biology of the Cell 17, no. 9 (2006): 3717–28. http://dx.doi.org/10.1091/mbc.e06-03-0244.

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We have shown previously that either Grb2- or Shc-mediated signaling from the oncogenic Met receptor Tpr-Met is sufficient to trigger cell cycle progression in Xenopus oocytes. However, direct binding of these adaptors to Tpr-Met is dispensable, implying that another Met binding partner mediates these responses. In this study, we show that overexpression of Grb2-associated binder 1 (Gab1) promotes cell cycle progression when Tpr-Met is expressed at suboptimal levels. This response requires that Gab1 possess an intact Met-binding motif, the pleckstrin homology domain, and the binding sites for

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Stewart, Jesse C., Christopher R. France, and Julie A. Suhr. "The Effect of Cardiac Cycle Phase on Reaction Time Among Individuals at Varying Risk for Hypertension." Journal of Psychophysiology 20, no. 1 (2006): 1–8. http://dx.doi.org/10.1027/0269-8803.20.1.1.

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Abstract: Existing evidence suggests that baroreceptor stimulation may impair sensorimotor functioning. The purpose of this study was to determine whether the adverse effect of baroreceptor stimulation on sensorimotor functioning is more pronounced among individuals at increased risk for hypertension. A visual reaction time task was completed by 93 normotensive men and women at varying risk for hypertension, as defined by the combination of their resting systolic blood pressure and their parental history of hypertension. To correspond with natural fluctuations in baroreceptor stimulation acros

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Patterson, Rainey E., Srilaxmi Kalavalapalli, Caroline M. Williams, et al. "Lipotoxicity in steatohepatitis occurs despite an increase in tricarboxylic acid cycle activity." American Journal of Physiology-Endocrinology and Metabolism 310, no. 7 (2016): E484—E494. http://dx.doi.org/10.1152/ajpendo.00492.2015.

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The hepatic tricarboxylic acid (TCA) cycle is central to integrating macronutrient metabolism and is closely coupled to cellular respiration, free radical generation, and inflammation. Oxidative flux through the TCA cycle is induced during hepatic insulin resistance, in mice and humans with simple steatosis, reflecting early compensatory remodeling of mitochondrial energetics. We hypothesized that progressive severity of hepatic insulin resistance and the onset of nonalcoholic steatohepatitis (NASH) would impair oxidative flux through the hepatic TCA cycle. Mice (C57/BL6) were fed a high- tran

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Szarka, András, Gábor Bánhegyi, and Balázs Sümegi. "Mitochondria, oxidative stress and aging." Orvosi Hetilap 155, no. 12 (2014): 447–52. http://dx.doi.org/10.1556/oh.2014.29852.

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The free radical theory of aging was defined in the 1950s. On the base of this theory, the reactive oxygen species formed in the metabolic pathways can play pivotal role in ageing. The theory was modified by defining the mitochondrial respiration as the major cellular source of reactive oxygen species and got the new name mitochondrial theory of aging. Later on the existence of a “vicious cycle” was proposed, in which the reactive oxygen species formed in the mitochondrial respiration impair the mitochondrial DNA and its functions. The formation of reactive oxygen species are elevated due to m

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Porse, Bo T., David Bryder, Kim Theilgaard-Mönch та ін. "Loss of C/EBPα cell cycle control increases myeloid progenitor proliferation and transforms the neutrophil granulocyte lineage". Journal of Experimental Medicine 202, № 1 (2005): 85–96. http://dx.doi.org/10.1084/jem.20050067.

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CCAAT/enhancer binding protein (C/EBP)α is a myeloid-specific transcription factor that couples lineage commitment to terminal differentiation and cell cycle arrest, and is found mutated in 9% of patients who have acute myeloid leukemia (AML). We previously showed that mutations which dissociate the ability of C/EBPα to block cell cycle progression through E2F inhibition from its function as a transcriptional activator impair the in vivo development of the neutrophil granulocyte and adipose lineages. We now show that such mutations increase the capacity of bone marrow (BM) myeloid progenitors

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