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Journal articles on the topic 'Taux de modulation'

Author: Grafiati

Published: 4 June 2021

Last updated: 8 February 2022

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1

COLLEAU, J. J., D. REGALDO, and P. L. GASTINEL. "Adaptation de l’index francais de sélection laitière (INEL) au contexte des quotas." INRAE Productions Animales 7, no. 3 (June 24, 1994): 151–67. http://dx.doi.org/10.20870/productions-animales.1994.7.3.4166.

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La sélection des races bovines laitières s’effectue en France au travers d’un index de synthèse économique laitière (INEL). La formulation de celui-ci a été remise à jour en 1993 pour mieux tenir compte de la situation concrète des quotas laitiers, avec modulation pour les dépassements de taux butyreux par rapport à la référence. L’article explicite les raisonnements, hypothèses et paramètres tant économiques que génétiques, utilisés pour l’examen de plusieurs alternatives possibles. Les hypothèses essentielles sont la constance des surfaces et des quotas par exploitation ainsi que la prise en considération de marges nettes incluant les charges fixes. La solution finalement retenue (INEL 1993) n’accorde plus aucun intérêt économique à l’augmentation de la production de matière grasse par vache. La sélection sur ce nouvel index entraînera une augmentation du taux protéique et une amélioration du rapport taux protéique/taux butyreux. Le taux butyreux diminuera en race Holstein et restera approximativement constant dans les races Normande et Montbéliarde.

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2

Pouchieu, C., V. Chajès, F. Laporte, E. Kesse-Guyot, P. Galan, S. Hercberg, P. Latino-Martel, and M. Touvier. "P014 Étude prospective des liens entre taux d’acides gras plasmatiques et risque de cancer (au global et du sein) : modulation par les antioxydants." Cahiers de Nutrition et de Diététique 48 (December 2013): S64. http://dx.doi.org/10.1016/s0007-9960(13)70373-0.

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3

Pouchieu, C., V. Chajès, F. Laporte, E. Kesse-Guyot, P. Galan, S. Hercberg, P. Latino-Martel, and M. Touvier. "P014 Étude prospective des liens entre taux d’acides gras plasmatiques et risque de cancer (au global et du sein) : modulation par les antioxydants." Nutrition Clinique et Métabolisme 27 (December 2013): S64. http://dx.doi.org/10.1016/s0985-0562(13)70347-9.

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4

Carton, L., F. Auger, N. Durieux, M. Petrault, J. Labreuche, D. Allorge, O. Cottencin, N. Simon, R. Bordet, and B. Rolland. "Effet longitudinal d’une administration aiguë d’éthanol sur le GABA et le glutamate : une étude en spectroscopie par résonance magnétique in vivo chez le rat." European Psychiatry 30, S2 (November 2015): S116. http://dx.doi.org/10.1016/j.eurpsy.2015.09.222.

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IntroductionLes effets cliniques de l’intoxication alcoolique aiguë seraient liés à une modulation des systèmes de neurotransmission du GABA et du glutamate. Les caractéristiques longitudinales de cette modulation et l’impact de la dose d’éthanol absorbée restent mal connus. Nous avons voulu étudier in vivo les effets aigus de l’éthanol sur les niveaux de GABA et de glutamate du cortex préfrontal en spectroscopie par résonance magnétique (SRM).Matériel et méthodesAprès une première acquisition de SRM (zone préfrontale), trois groupes de rats Wistar mâles (363 ± 27 g) ont reçu par voie intrapéritonéale (IP) :– éthanol 1 g/kg (n = 6) ;– éthanol 2 g/kg (n = 8) ;– sérum physiologique (n = 5).Des acquisitions répétées de SRM ont été réalisées jusque 300 minutes post-injection. Une cinétique de l’éthanolémie a également été réalisée dans des groupes similaires de rats Wistar. Après alcoolisation par voie IP, des prélèvements sanguins successifs ont été réalisés jusque 180 minutes pour le groupe 1 g/kg (n = 6) et 300 minutes pour le groupe 2 g/kg (n = 14). Pour la SRM, des analyses statistiques inter- et intragroupes ont été effectuées à l’aide d’un modèle linéaire mixte visant à étudier la variation des taux de GABA et glutamate.RésultatsLa cinétique de l’éthanolémie était superposable à celle de la cinétique cérébrale. En SRM, une diminution significative du GABA, de 11,4 % ± 3,8 % (p < 0,0059) dans le groupe 1 g/kg et du glutamate de 13,8 % ± 2,6 % dans le groupe 2 g/kg (p < 0,0001) ont été observées, sans modification significative dans les autres groupes. La variation du ratio GABA/glutamate s’est montrée différente entre les deux groupes éthanol avec une augmentation dans le groupe 2 g/kg et une diminution dans le groupe 1 g/kg (p < 0,01).ConclusionLa dose d’éthanol détermine les variations des niveaux de GABA et de glutamate du cortex préfrontal, pouvant expliquer les différents effets cliniques induits par l’alcool selon la dose.

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5

Morin, L., A. F. Pierre, P. Tissieres, J. Miatello, and P. Durand. "Actualités sur le sepsis et le choc septique de l’enfant." Médecine Intensive Réanimation 28, no. 3 (December 24, 2018): 239–48. http://dx.doi.org/10.3166/rea-2018-0080.

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L’incidence du sepsis de l’enfant augmente en réanimation pédiatrique. La définition du sepsis et du choc septique de l’enfant est amenée à évoluer à l’instar de celle du choc septique de l’adulte pour détecter les patients nécessitant une prise en charge urgente et spécialisée. La prise en charge d’un patient septique repose sur une oxygénothérapie, une expansion volémique au sérum salé isotonique, une antibiothérapie et un transfert dans un service de réanimation ou de surveillance continue pédiatrique. Le taux et la cinétique d’élimination du lactate plasmatique est un bon critère diagnostic et pronostic qui permet de guider la prise en charge. La présence de plusieurs défaillances d’organes ou une défaillance circulatoire aiguë signe le diagnostic de sepsis encore dit sévère, et leur persistance et/ou la non-correction de l’hypotension artérielle malgré un remplissage vasculaire d’au moins 40 ml/kg définit le choc septique chez l’enfant. Dans ce cas, la correction rapide de l’hypotension artérielle persistante repose sur la noradrénaline initiée sur une voie intraveineuse périphérique dans l’attente d’un accès veineux central. L’échographie cardiaque est un examen clé de l’évaluation hémodynamique du patient, pour guider la poursuite de l’expansion volémique ou détecter une cardiomyopathie septique. Des thérapeutiques additionnelles ont été proposées pour prendre en charge certains patients avec des défaillances d’organes particulières. L’immunomonitorage et la modulation sont un ensemble de techniques qui permettent la recherche et le traitement de certaines complications. La Surviving Sepsis Campaign a permis d’améliorer la prise en charge de ces patients par l’implémentation d’algorithmes de détection et de prise en charge du sepsis de l’enfant. Une révision pédiatrique de cette campagne est attendue prochainement.

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6

Touvier, M., E. Kesse-Guyot, V. Andreeva, L. Fezeu, N. Charnaux, A. Sutton, N. Druesne-Pecollo, et al. "O58 Modulation de l’association prospective entre le taux plasmatique d’ICAM-1 et le risque de cancer par les acides gras polyinsaturés n-3 : étude cas-témoins nichée dans la cohorte SU.VI.MAX." Cahiers de Nutrition et de Diététique 46 (December 2011): S48—S49. http://dx.doi.org/10.1016/s0007-9960(11)70079-7.

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7

Touvier, M., E. Kesse-Guyot, V. Andreeva, L. Fezeu, N. Charnaux, A. Sutton, N. Druesne-Pecollo, et al. "O58 Modulation de l’association prospective entre le taux plasmatique d’ICAM-1 et le risque de cancer par les acides gras polyinsaturés n-3 : étude cas-témoins nichée dans la cohorte SU.VI.MAX." Nutrition Clinique et Métabolisme 25 (December 2011): S48—S49. http://dx.doi.org/10.1016/s0985-0562(11)70062-0.

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8

Brion, Jean-Pierre, Kunie Ando, Céline Heraud, and Karelle Leroy. "Modulation of tau pathology in tau transgenic models." Biochemical Society Transactions 38, no. 4 (July 26, 2010): 996–1000. http://dx.doi.org/10.1042/bst0380996.

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NFTs (neurofibrillary tangles) in Alzheimer's disease and in tauopathies are hallmark neuropathological lesions whose relationship with neuronal dysfunction, neuronal death and with other lesions [such as Aβ (amyloid β-peptide) pathology] are still imperfectly understood. Many transgenic mice overexpressing wild-type or mutant tau proteins have been generated to investigate the physiopathology of tauopathies. Most of the mice overexpressing wild-type tau do not develop NFTs, but can develop a severe axonopathy, whereas overexpression of mutant tau leads to NFT formation, synaptic loss and neuronal death in several models. The association between neuronal death and NFTs has, however, been challenged in some models showing a dissociation between tau aggregation and tau toxicity. Cross-breeding of mice developing NFTs with mice developing Aβ deposits increases NFT pathology, highlighting the relationship between tau and amyloid pathology. On the other hand, tau expression seems to be necessary for expression of a pathological phenotype associated with amyloid pathology. These findings suggest that there is a bilateral cross-talk between Aβ and tau pathology. These observations are discussed by the presentation of some relevant models developed recently.

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9

Piram, L., T. Frédéric-Moreau, J. Miroir, N. Saroul, N. Pham Dang, L. Berger, J. Biau, and M. Lapeyre. "Étude prospective évaluant l’impact de la couverture du volume cible prévisionnel à haut risque par l’isodose 95 % sur les taux de contrôle local et de survie globale dans les cancers des voies aérodigestives supérieures pris en charge par radiothérapie conformationnelle avec modulation d’intensité." Cancer/Radiothérapie 20, no. 6-7 (October 2016): 717. http://dx.doi.org/10.1016/j.canrad.2016.08.013.

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10

Dominguez-Meijide, Antonio, Eftychia Vasili, and Tiago Fleming Outeiro. "Pharmacological Modulators of Tau Aggregation and Spreading." Brain Sciences 10, no. 11 (November 13, 2020): 858. http://dx.doi.org/10.3390/brainsci10110858.

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Tauopathies are neurodegenerative disorders characterized by the deposition of aggregates composed of abnormal tau protein in the brain. Additionally, misfolded forms of tau can propagate from cell to cell and throughout the brain. This process is thought to lead to the templated misfolding of the native forms of tau, and thereby, to the formation of newer toxic aggregates, thereby propagating the disease. Therefore, modulation of the processes that lead to tau aggregation and spreading is of utmost importance in the fight against tauopathies. In recent years, several molecules have been developed for the modulation of tau aggregation and spreading. In this review, we discuss the processes of tau aggregation and spreading and highlight selected chemicals developed for the modulation of these processes, their usefulness, and putative mechanisms of action. Ultimately, a stronger understanding of the molecular mechanisms involved, and the properties of the substances developed to modulate them, will lead to the development of safer and better strategies for the treatment of tauopathies.

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11

Richet, Emma, Amy M. Pooler, Teresa Rodriguez, Sergey S. Novoselov, Gunter Schmidtke, Marcus Groettrup, Diane P. Hanger, Michael E. Cheetham, and Jacqueline van der Spuy. "NUB1 modulation of GSK3β reduces tau aggregation." Human Molecular Genetics 21, no. 24 (September 10, 2012): 5254–67. http://dx.doi.org/10.1093/hmg/dds376.

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12

Monti, Maria Chiara, Luigi Margarucci, Raffaele Riccio, and Agostino Casapullo. "Modulation of Tau Protein Fibrillization by Oleocanthal." Journal of Natural Products 75, no. 9 (September 18, 2012): 1584–88. http://dx.doi.org/10.1021/np300384h.

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13

Voss, Kellen, Christopher Harris, Martina Ralle, Megan Duffy, Charles Murchison, and Joseph F. Quinn. "Modulation of tau phosphorylation by environmental copper." Translational Neurodegeneration 3, no. 1 (2014): 24. http://dx.doi.org/10.1186/2047-9158-3-24.

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14

Richet, Emma, Mike Cheetham, and Jacqueline Van Der Spuy. "P1-347: NUB1 modulation of tau aggregation." Alzheimer's & Dementia 6 (July 2010): S273—S274. http://dx.doi.org/10.1016/j.jalz.2010.05.900.

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15

Highstein, S. M., R. D. Rabbitt, and R. Boyle. "Determinants of semicircular canal afferent response dynamics in the toadfish, Opsanus tau." Journal of Neurophysiology 75, no. 2 (February 1, 1996): 575–96. http://dx.doi.org/10.1152/jn.1996.75.2.575.

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1. Present results determine the relative contributions of the biomechanical and the posttransduction-current (PTC) mechanisms to the sensory process carried out by the horizontal semicircular canal (HC) in the oyster toadfish, Opsanus tau. The role of each element was estimated using in vivo measurements of hair cell receptor potentials and afferent responses elicited by electrical stimuli and mechanical HC indentation. Individual afferent response dynamics are defined here using first-harmonic transfer functions presented in the form of response gain and phase for sinusoidal stimuli from approximately 0.02-30 Hz. Comparison of the response dynamics for the two types of stimuli distinguishes the mechanical and the PTC transfer functions leading to the neural response. The results show that both mechanisms contribute significantly to the overall signal processing performed by the semicircular canals. 2. Endolymphatic polarization and HC indentation. Modulation of the endolymphatic potential by current injection induces a differential voltage across the apical face of the hair cells that drives the transduction current directly via the Nernst-Planck potential. Results show that the electrical impedance of the apical tight junctions is much larger than the basal impedance to ground in O. tau, such that leakage current to the basolateral space is negligible and the voltage-sensitive basolateral currents remain fully functional during polarization of the endolymph (in the frequency range tested). Extracellular afferent responses to endolymphatic polarization were combined with responses to HC indentation to separate the relative contributions of the mechanical and the PTC mechanisms to the overall afferent response dynamics. Data show that more than one-half of the overall signal processing, as defined by the first-harmonic transfer function, persists even when canal mechanics is bypassed. 3. Hair-cell receptor potential modulation during HC indentation. Sharp microelectrodes were used to record the modulation of hair-cell receptor potentials (intracellular voltages) in vivo during physiological levels of sinusoidal HC indentation. Receptor potentials exhibit modulations dominated by the first harmonic and centered about the resting potential. The average gain of the receptor-potential modulation for HC indentation is approximately 0.88 mV/microns indent, corresponding to a value of 0.22 mV/deg/s head velocity, centered near zero phase over the range tested from 0.1-10 Hz. The present receptor potential data fall well short of spanning the full range of gain and phase present in the afferent population. Rather, intracellular hair-cell responses are consistent with the frequency-dependent mechanical activation of the transduction current as determined above. 4. Origins of individual afferent responses. The population of afferent responses forms a continuous distribution that is discussed here in terms of three groups as defined by Boyle and Highstein: velocity-sensitive low gain (LG) afferents, velocity/acceleration-sensitive high gain (HG) afferents, and acceleration-sensitive (A) afferents. The response dynamics of individual afferents were found to be determined by a mix of biomechanical and biophysical factors that vary systematically between these afferent groups. All afferents show low-frequency phase advancement and gain decrease during HC indentation associated with the mechanical lower-corner frequency and high-frequency phase and gain enhancements associated with the PTC processing. In highly phase-advanced afferents (A type), the mechanical response is additive with the PTC processing to achieve broad-band acceleration sensitive neural responses.(ABSTRACT TRUNCATED AT 250 WORDS)

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Duff, K., B. Malester, Y. Matsuoka, M. Picciano, J. Helpern, M. Merken, J. Helpern, J. Lewis, M. Hutton, and L. Refolo. "Amyloid and tau mice: phenotype and phenotype modulation." Biochemical Society Transactions 28, no. 5 (October 1, 2000): A128. http://dx.doi.org/10.1042/bst028a128c.

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17

Akoury, Elias, Michal Gajda, Marcus Pickhardt, Jacek Biernat, Pornsuwan Soraya, Christian Griesinger, Eckhard Mandelkow, and Markus Zweckstetter. "Inhibition of Tau Filament Formation by Conformational Modulation." Journal of the American Chemical Society 135, no. 7 (February 5, 2013): 2853–62. http://dx.doi.org/10.1021/ja312471h.

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Yu, Chao-Chao, Tao Jiang, Ao-Fei Yang, Yan-Jun Du, Miao Wu, and Li-Hong Kong. "Epigenetic Modulation on Tau Phosphorylation in Alzheimer’s Disease." Neural Plasticity 2019 (April 10, 2019): 1–12. http://dx.doi.org/10.1155/2019/6856327.

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Tau hyperphosphorylation is a typical pathological change in Alzheimer’s disease (AD) and is involved in the early onset and progression of AD. Epigenetic modification refers to heritable alterations in gene expression that are not caused by direct changes in the DNA sequence of the gene. Epigenetic modifications, such as noncoding RNA regulation, DNA methylation, and histone modification, can directly or indirectly affect the regulation of tau phosphorylation, thereby participating in AD development and progression. This review summarizes the current research progress on the mechanisms of epigenetic modification associated with tau phosphorylation.

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19

Brich, Jochen, Feng-Shiun Shie, Brian W. Howell, Renhua Li, Katalin Tus, Edward K. Wakeland, Lee-Way Jin, et al. "Genetic Modulation of Tau Phosphorylation in the Mouse." Journal of Neuroscience 23, no. 1 (January 1, 2003): 187–92. http://dx.doi.org/10.1523/jneurosci.23-01-00187.2003.

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20

Pandey, Gaurav, Sudhir Morla, Sachin Kumar, and Vibin Ramakrishnan. "Modulation of tau protein aggregation using ‘Trojan’ sequences." Biochimica et Biophysica Acta (BBA) - General Subjects 1864, no. 7 (July 2020): 129569. http://dx.doi.org/10.1016/j.bbagen.2020.129569.

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21

Harris, Christopher J., Nora E. Gray, Maya Caruso, Marguex Hunter, Martina Ralle, and Joseph F. Quinn. "Copper Modulation and Memory Impairment due to Hippocampal Tau Pathology." Journal of Alzheimer's Disease 78, no. 1 (October 27, 2020): 49–60. http://dx.doi.org/10.3233/jad-200002.

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Background: Environmental copper has been implicated in the pathogenesis of Alzheimer’s disease based on evidence that: 1) brain copper levels increase with age, 2) copper promotes misfolding and toxicity of amyloid-β in vitro, 3) copper-modulating interventions reduce amyloid pathology in animal models. However, the effect of copper upon non-amyloid Alzheimer’s pathology is relatively under-explored. Objective: To determine if modulation of brain copper level affects brain tau pathology and/or associated cognitive impairment. Methods: We tested the hypothesis that brain copper modulates tau pathology by manipulating brain levels of copper in the PS19 transgenic mouse model of tau pathology. We treated PS19 and wild-type mice with oral zinc acetate, an established therapy for long term control of excess brain copper, and examined treatment effects upon brain copper, brain tau, NFT-like pathology, and spatial memory. We treated a second cohort of mice with exogenous dietary copper in order to evaluate whether excess environmental copper promotes brain tau pathology. Results: Copper-lowering with oral zinc attenuated spatial memory impairment in female but not male PS19 mice, without a significant effect upon tau pathology. Copper loading increased brain copper, but did not have an effect on brain tau pathology or spatial memory function. Conclusion: These findings suggest that a strategy to lower brain copper may be viable for symptomatic benefit in the setting of tau neuropathology, but unlikely to have robust effects on the underlying pathology. These findings are consistent with dietary or other exogenous copper being unlikely to promote tau pathology.

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22

Necula, Mihaela, Carmen N. Chirita, and Jeff Kuret. "P4-423 Pharmacological modulation of tau fibrillization in vitro." Neurobiology of Aging 25 (July 2004): S594. http://dx.doi.org/10.1016/s0197-4580(04)81979-1.

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23

Fan, Qi-Wen, Wei Yu, Takao Senda, Katsuhiko Yanagisawa, and Makoto Michikawa. "Cholesterol-dependent modulation of tau phosphorylation in cultured neurons." Journal of Neurochemistry 76, no. 2 (January 2001): 391–400. http://dx.doi.org/10.1046/j.1471-4159.2001.00063.x.

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24

Bondar’, N. I. "Photometric period and rotational brightness modulation of V833 Tau." Astronomy Reports 61, no. 2 (February 2017): 130–37. http://dx.doi.org/10.1134/s1063772917010024.

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25

Buchkov, Krastyo, Rosen Todorov, Penka Terziyska, Marin Gospodinov, Velichka Strijkova, Dimitre Dimitrov, and Vera Marinova. "Anisotropic Optical Response of WTe2 Single Crystals Studied by Ellipsometric Analysis." Nanomaterials 11, no. 9 (August 31, 2021): 2262. http://dx.doi.org/10.3390/nano11092262.

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In this paper we report the crystal growth conditions and optical anisotropy properties of Tungsten ditelluride (WTe2) single crystals. The chemical vapor transport (CVT) method was used for the synthesis of large WTe2 crystals with high crystallinity and surface quality. These were structurally and morphologically characterized by means of X-ray diffraction, optical profilometry and Raman spectroscopy. Through spectroscopic ellipsometry analysis, based on the Tauc–Lorentz model, we identified a high refractive index value (~4) and distinct tri-axial anisotropic behavior of the optical constants, which opens prospects for surface plasmon activity, revealed by the dielectric function. The anisotropic physical nature of WTe2 shows practical potential for low-loss light modulation at the 2D nanoscale level.

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Chang, Edward, Nicolette Honson, Bhaswati Bandyopadhyay, Kristen Funk, Jordan Jensen, Sohee Kim, Swati Naphade, and Jeff Kuret. "Modulation and Detection of Tau Aggregation with Small-Molecule Ligands." Current Alzheimer Research 6, no. 5 (October 1, 2009): 409–14. http://dx.doi.org/10.2174/156720509789207976.

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27

JENKINS, Scott M., Marcus ZINNERMAN, Craig GARNER, and Gail V. W. JOHNSON. "Modulation of tau phosphorylation and intracellular localization by cellular stress." Biochemical Journal 345, no. 2 (January 15, 2000): 263. http://dx.doi.org/10.1042/0264-6021:3450263.

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JENKINS, Scott M., Marcus ZINNERMAN, Craig GARNER, and Gail V. W. JOHNSON. "Modulation of tau phosphorylation and intracellular localization by cellular stress." Biochemical Journal 345, no. 2 (January 10, 2000): 263–70. http://dx.doi.org/10.1042/bj3450263.

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Tau is a microtubule-associated protein that is functionally modulated by phosphorylation and hyperphosphorylated in several neurodegenerative diseases. Because phosphorylation regulates both normal and pathological tau functioning, it is of great interest to identify the signalling pathways and enzymes capable of modulating tau phosphorylation in vivo. The present study examined changes in tau phosphorylation and localization in response to osmotic stress, which activates the stress-activated protein kinases (SAPKs), a family of proline-directed protein kinases shown to phosphorylate tau in vitro and hypothesized to phosphorylate tau in Alzheimer's disease. Immunoblot analysis with phosphorylation-dependent antibodies revealed that osmotic stress increased tau phosphorylation at the non-Ser/Thr-Pro sites Ser-262/356, within the microtubule-binding domain, as well as Ser/Thr-Pro sites outside of tau's microtubule-binding domain. Although all SAPKs examined were activated by osmotic stress, none of the endogenous SAPKs mediated the increase in tau phosphorylation. However, when transfected into SH-SY5Y cells, SAPK3, but not the other SAPKs examined, phosphorylated tau in situ in response to activation by osmotic stress. Osmotic-stress-induced tau phosphorylation correlated with a decrease in the amount of tau associated with the cytoskeleton and an increase in the amount of soluble tau. This stress-induced alteration in tau localization was only partially due to phosphorylation at Ser-262/356 by a staurosporine-sensitive, non-proline-directed, protein kinase. Taken together, these results suggest that osmotic stress activates at least two tau-directed protein kinases, one proline-directed and one non-proline-directed, that SAPK3 can phosphorylate tau on Ser/Thr-Pro residues in situ, and that Ser-262/356 phosphorylation only partially regulates tau localization in the cell.

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Hamano, Tadanori, Soichi Enomoto, Norimichi Shirafuji, Masamichi Ikawa, Osamu Yamamura, Shu-Hui Yen, and Yasunari Nakamoto. "Autophagy and Tau Protein." International Journal of Molecular Sciences 22, no. 14 (July 12, 2021): 7475. http://dx.doi.org/10.3390/ijms22147475.

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Neurofibrillary tangles, which consist of highly phosphorylated tau protein, and senile plaques (SPs) are pathological hallmarks of Alzheimer’s disease (AD). In swollen axons, many autophagic vacuoles are observed around SP in the AD brain. This suggests that autophagy function is disturbed in AD. We used a neuronal cellular model of tauopathy (M1C cells), which harbors wild type tau (4R0N), to assess the effects of the lysosomotrophic agent NH4Cl, and autophagy inhibitors chloroquine and 3 methyladenine (3MA). It was found that chloroquine, NH4Cl and 3MA markedly increased tau accumulation. Thus, autophagy lysosomal system disturbances disturbed the degradation mechanisms of tau protein. Other studies also revealed that tau protein, including aggregated tau, is degraded via the autophagy lysosome system. Phosphorylated and C terminal truncated tau were also reported to disturb autophagy function. As a therapeutic strategy, autophagy upregulation was suggested. Thus far, as autophagy modulators, rapamycin, mTOCR1 inhibitor and its analogues, lithium, metformin, clonidine, curcumin, nicotinamide, bexaroten, and torehalose have been proposed. As a therapeutic strategy, autophagic modulation may be the next target of AD therapeutics.

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Boom, Alain, Michèle Authelet, Robert Dedecker, Christelle Frédérick, Roxane Van Heurck, Valery Daubie, Karelle Leroy, Roland Pochet, and Jean-Pierre Brion. "Bimodal modulation of tau protein phosphorylation and conformation by extracellular Zn2+ in human-tau transfected cells." Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 1793, no. 6 (June 2009): 1058–67. http://dx.doi.org/10.1016/j.bbamcr.2008.11.011.

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Nath, Amitabha, Rahul Raman, Vinit Kumar Yadav, Pudi Sannibabu, and Mitra Barun Sarkar. "Bandgap Modulation of Glancing Angle Deposition Aided Ag Nanoparticles Covered TiO2 Thin Film by High Temperature Annealing." Journal of Nanoscience and Nanotechnology 20, no. 12 (December 1, 2020): 7636–43. http://dx.doi.org/10.1166/jnn.2020.18575.

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Glancing Angle Deposition (GLAD) technique has been used to fabricate the Ag nanoparticles (NPs) over TiO2 thin film (TF) on the n-Si substrate. The deposited Ag NPs are in the size of 3–5 nm. Open-air annealing has been done at 500 °C and 600 °C for the n-Si/TiO2 TF/Ag NP samples. High Resolution X-ray Diffraction (HRXRD) peaks were identified to calculate the crystalline size of the NPs and rutile phase of the annealed sample were exhibited. Morphological analysis has been done for the sample using Field Emission Scanning Electron Microscopy (FESEM), Energy Dispersive Spectroscopy (EDS) and Atomic Force Microscopy (AFM). The enhancement of plasmonic absorption and modulation in the bandgap for the annealed Ag NPs surrounded TiO2 TF has been verified by UV-Vis Spectroscopy and the bandgap has been calculated using Tauc plot. An overall 2.5 fold and 3 fold enhancement has been observed in the UV region and visible region for n-Si/TiO2 TF/Ag NP annealed at 500 °C and 600 °C samples as compared to the n-Si/TiO2 TF/Ag NP as-deposited samples. The modulation of bandgap due to the sub-band transition and Localized Surface Plasmon Resonance (LSPR) effect of Ag NPs and relevant sub-band transition due to change in annealing temperature has been reported.

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32

Sinkjaer, T., J. B. Andersen, and B. Larsen. "Soleus stretch reflex modulation during gait in humans." Journal of Neurophysiology 76, no. 2 (August 1, 1996): 1112–20. http://dx.doi.org/10.1152/jn.1996.76.2.1112.

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1. The modulation of the short-latency stretch reflex during walking at different walking speeds was investigated and compared with the stretch reflex during standing in healthy human subjects. 2. Ankle joint stretches were applied by a system able to rotate the human ankle joint during treadmill walking in any phase of the step cycle. The system consisted of a mechanical joint attached to the subject's ankle joint and connected to a motor placed beside the treadmill by means of bowden wires. The weight of the total system attached to the leg of the subject was 900 g. 3. The short-latency soleus stretch reflex was modulated during a step. In the stance phase, the amplitude equaled that found during standing at matched soleus background electromyogram (EMG). In the transition from stance to swing, the amplitude was 0 in all subjects. In late swing, the stretch reflex amplitude increased to 45 +/- 27% (mean +/- SD) of the maximal amplitude in the stance phase (stretch amplitude 8 degrees, stretch velocity 250 degrees/s). 4. The onset (42 +/- 3.2 ms) and peak latencies (59 +/- 2.5 ms) of the stretch reflex did not depend on the phase in the step cycle at which the reflex was elicited. 5. When the ankle joint is rotated, a change in torque can be measured. The torque measured over the first 35 ms after stretch onset (nonreflex torque) was at a maximum during late stance, when the leg supported a large part of the body's weight, and at a minimum during the swing phase. At heel contact the nonreflex torque was 50% of its maximal value. 6. During the stance phase the maximal EMG stretch reflex had a phase lead of approximately 120 ms with respect to the maximal background EMG and a phase lead of approximately 250 ms with respect to the maximal nonreflex torque. 7. The constant latency of the stretch reflex during a step implied that the ankle extensor muscle spindles are always taut during walking. 8. The relatively high amplitude of the stretch reflex in late swing and at heel contact made it likely that the stretch reflex contributed to the activation of the ankle extensor muscles in early stance phase.

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Abisambra, Jose F., Laura J. Blair, Jeffrey R. Jones, Clara Kraft, Shannon Hill, Justin Rogers, John Koren, et al. "P3-425: Chaperone-mediated modulation of tau aggregation correlates with modifications in tau pathology and synaptic plasticity." Alzheimer's & Dementia 6 (July 2010): S577. http://dx.doi.org/10.1016/j.jalz.2010.05.1968.

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Espíndola, Sonia Lorena, Ana Damianich, Rodrigo Javier Alvarez, Manuela Sartor, Juan Emilio Belforte, Juan Esteban Ferrario, Jean-Marc Gallo, and María Elena Avale. "Modulation of Tau Isoforms Imbalance Precludes Tau Pathology and Cognitive Decline in a Mouse Model of Tauopathy." Cell Reports 23, no. 3 (April 2018): 709–15. http://dx.doi.org/10.1016/j.celrep.2018.03.079.

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35

Winget, D. E., and C. F. Claver. "Optical Frequencies in V471 TAU." International Astronomical Union Colloquium 114 (1989): 293–95. http://dx.doi.org/10.1017/s0252921100099747.

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V471 Tau is a spectroscopic and eclipsing binary system located in the Hyades cluster. The binary consists of a K2V and a hot DA white dwarf star (Nelson and Young 1970). Soft x-ray observations reveal strong modulation at periods of 554.7 ± 0.3s and 277.5 ± 0.1s (Jensen 1985, Jensnen et al. 1986).Robinson et al. (1988) reported the detection of the 555 s period in the optical. This period was about a factor of 20 reduced in mean amplitude in their data relative to the soft x-ray amplitude. They also found that it varied in amplitude from run to run by more than a factor of 2.5, dropping below detectability on several runs. They found some evidence for the 277.5 s period in several runs, but never at high enough amplitude to measure reliably. In addition, they noted that several of their runs had statistically significant power at other frequencies, but noted that in their six runs none of the additional frequencies repeated themselves. Robinson et al. also used observations near the eclipse of the white dwarf to demonstrate that most of the pulsed light is coming from the white dwarf.

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Zhang, Yiwei, and Gennian Ge. "Snake-in-the-Box Codes for Rank Modulation Under Kendall’s $\tau $ -Metric." IEEE Transactions on Information Theory 62, no. 1 (January 2016): 151–58. http://dx.doi.org/10.1109/tit.2015.2502602.

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37

Bose, Anindita, François Mouton-Liger, Claire Paquet, Pierre Mazot, Marc Vigny, Françoise Gray, and Jacques Hugon. "Modulation of Tau Phosphorylation by the Kinase PKR: Implications in Alzheimer's Disease." Brain Pathology 21, no. 2 (October 3, 2010): 189–200. http://dx.doi.org/10.1111/j.1750-3639.2010.00437.x.

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38

Steinmetz, Danielle, Eugenia Ramos, Shannon N. Campbell, Teresa Morales, and Robert A. Rissman. "Reproductive Stage and Modulation of Stress-Induced Tau Phosphorylation in Female Rats." Journal of Neuroendocrinology 27, no. 11 (October 28, 2015): 827–34. http://dx.doi.org/10.1111/jne.12323.

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39

Moe, James G., Ishita Chatterjee, Eliot J. Davidowitz, and Ottavio Arancio. "P4-236: Modulation of synaptic function by extracellular tau enriched in oligomers." Alzheimer's & Dementia 5, no. 4S_Part_16 (July 2009): P499. http://dx.doi.org/10.1016/j.jalz.2009.04.702.

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Avale, Maria-Elena, Ana Damianich, Carolina Facal, Delfina Loch, Juan Ferrario, Sonia Espindola, and Maria-Elena Avale. "Modulation of tau isoforms by RNA reprogramming: Functional consequences and therapeutic perspectives." IBRO Reports 6 (September 2019): S105—S106. http://dx.doi.org/10.1016/j.ibror.2019.07.342.

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41

Anderton, B. H., J. P. Brion, A.-M. Couck, D. R. Davis, J. M. Gallo, D. P. Hanger, K. Ladhani, et al. "Modulation of PHF-like tau phosphorylation in cultured neurones and transfected cells." Neurobiology of Aging 16, no. 3 (May 1995): 389–97. http://dx.doi.org/10.1016/0197-4580(94)00160-3.

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Andreadis, Athena. "S3-03-04: Modulation of tau dys/function by regulated alternative splicing." Alzheimer's & Dementia 2 (July 2006): S49. http://dx.doi.org/10.1016/j.jalz.2006.05.177.

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43

Peck, Austin, M. Emre Sargin, Nichole E. LaPointe, Kenneth Rose, B. S. Manjunath, Stuart C. Feinstein, and Leslie Wilson. "Tau isoform-specific modulation of kinesin-driven microtubule gliding rates and trajectories as determined with tau-stabilized microtubules." Cytoskeleton 68, no. 1 (November 10, 2010): 44–55. http://dx.doi.org/10.1002/cm.20494.

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44

Cook, Casey, Yari Carlomagno, Tania F. Gendron, Judy Dunmore, Kristyn Scheffel, Caroline Stetler, Mary Davis, et al. "Acetylation of the KXGS motifs in tau is a critical determinant in modulation of tau aggregation and clearance." Human Molecular Genetics 23, no. 1 (August 19, 2013): 104–16. http://dx.doi.org/10.1093/hmg/ddt402.

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45

Lo Cascio, Filippa, Stephanie Garcia, Mauro Montalbano, Nicha Puangmalai, Salome McAllen, Andrea Pace, Antonio Palumbo Piccionello, and Rakez Kayed. "Modulating disease-relevant tau oligomeric strains by small molecules." Journal of Biological Chemistry 295, no. 44 (July 31, 2020): 14807–25. http://dx.doi.org/10.1074/jbc.ra120.014630.

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The pathological aggregation of tau plays an important role in Alzheimer's disease and many other related neurodegenerative diseases, collectively referred to as tauopathies. Recent evidence has demonstrated that tau oligomers, small and soluble prefibrillar aggregates, are highly toxic due to their strong ability to seed tau misfolding and propagate the pathology seen across different neurodegenerative diseases. We previously showed that novel curcumin derivatives affect preformed tau oligomer aggregation pathways by promoting the formation of more aggregated and nontoxic tau aggregates. To further investigate their therapeutic potential, we have extended our studies o disease-relevant brain-derived tau oligomers (BDTOs). Herein, using well-characterized BDTOs, isolated from brain tissues of different tauopathies, including Alzheimer's disease, progressive supranuclear palsy, and dementia with Lewy bodies, we found that curcumin derivatives modulate the aggregation state of BDTOs by reshaping them and rescue neurons from BDTO-associated toxicity. Interestingly, compound CL3 showed an effect on the aggregation pattern of BDTOs from different tauopathies, resulting in the formation of less neurotoxic larger tau aggregates with decreased hydrophobicity and seeding propensity. Our results lay the groundwork for potential investigations of the efficacy and beneficial effects of CL3 and other promising compounds for the treatment of tauopathies. Furthermore, CL3 may aid in the development of tau imaging agent for the detection of tau oligomeric strains and differential diagnosis of the tauopathies, thus enabling earlier interventions.

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Fontaine, Sarah N., Jonathan J. Sabbagh, Jeremy Baker, Carlos R. Martinez-Licha, April Darling, and Chad A. Dickey. "Cellular factors modulating the mechanism of tau protein aggregation." Cellular and Molecular Life Sciences 72, no. 10 (February 11, 2015): 1863–79. http://dx.doi.org/10.1007/s00018-015-1839-9.

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47

Teng, K. K., I. S. Georgieff, J. M. Aletta, J. Nunez, M. L. Shelanski, and L. A. Greene. "Characterization of a PC12 cell sub-clone (PC12-C41) with enhanced neurite outgrowth capacity: implications for a modulatory role of high molecular weight tau in neuritogenesis." Journal of Cell Science 106, no. 2 (October 1, 1993): 611–26. http://dx.doi.org/10.1242/jcs.106.2.611.

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To address the means by which diversity of neuronal morphology is generated, we have isolated and characterized naturally occurring variants of rat PC12 pheochromocytoma cells that exhibit altered neurite outgrowth properties in response to nerve growth factor (NGF). We describe here a PC12 cell sub-clone, designated PC12-clone 41 (PC12-C41), that displays significant increases in neurite abundance and stability when compared with the parental line. This difference does not appear to be due to an altered sensitivity or responsiveness to NGF or to a more rapid rate of neurite extension. Because of the role of the cytoskeleton in neuritogenesis, we examined a panel of the major cytoskeletal proteins (MAP 1.2/1B, beta-tubulin, chartins, peripherin, and high and low molecular weight (HMW and LMW) taus) whose levels and/or extent of phosphorylation are regulated by NGF in PC12 cultures. Although most cytoskeletal proteins showed little difference between PC12 and PC12-C41 cells (+/- NGF treatment), there was a significant contrast between the two lines with respect to tau expression. In particular, while NGF increases the total specific levels of tau in both cell types to similar extents (by about twofold), the proportion comprising HMW tau is threefold higher in the PC12-C41 clone than in PC12 cells. A comparable difference was observed under substratum conditions that were non-permissive for neurite outgrowth and so this effect was not merely a consequence of the differential neuritogenic capacities of the two lines. The distinction between the expression of HMW and LMW taus in PC12 and PC12-C41 cells (+/- NGF) was also observed at the level of the messages encoding these proteins. Such findings indicate that initiation of neurite outgrowth in PC12 cultures does not require a massive induction of tau expression and raise the possibility that HMW and LMW taus may have differential capacities for modulating neuronal morphology.

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Damianich, Ana, Carolina Lucia Facal, Javier Andrés Muñiz, Camilo Mininni, Mariano Soiza-Reilly, Magdalena Ponce De León, Leandro Urrutia, German Falasco, Juan Esteban Ferrario, and María Elena Avale. "Tau mis-splicing correlates with motor impairments and striatal dysfunction in a model of tauopathy." Brain 144, no. 8 (June 1, 2021): 2302–9. http://dx.doi.org/10.1093/brain/awab130.

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Abstract Tauopathies are neurodegenerative diseases caused by the abnormal metabolism of the microtubule associated protein tau (MAPT), which is highly expressed in neurons and critically involved in microtubule dynamics. In the adult human brain, the alternative splicing of exon 10 in MAPT pre-mRNA produces equal amounts of protein isoforms with either three (3R) or four (4R) microtubule binding domains. Imbalance in the 3R:4R tau ratio is associated with primary tauopathies that develop atypical parkinsonism, such as progressive supranuclear palsy and corticobasal degeneration. Yet, the development of effective therapies for those pathologies is an unmet goal. Here we report motor coordination impairments in the htau mouse model of tauopathy which harbour abnormal 3R:4R tau isoforms content, and in contrast to TauKO mice, are unresponsive to l-DOPA. Preclinical-PET imaging, array tomography and electrophysiological analyses indicated the dorsal striatum as the candidate structure mediating such phenotypes. Indeed, local modulation of tau isoforms by RNA trans-splicing in the striata of adult htau mice, prevented motor coordination deficits and restored basal neuronal firing. Together, these results suggest that abnormal striatal tau isoform content might lead to parkinsonian-like phenotypes and demonstrate a proof of concept that modulation of tau mis-splicing is a plausible disease-modifying therapy for some primary tauopathies.

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Yokosawa, Koichi, Yui Murakami, and Hiroaki Sato. "Appearance and modulation of a reactive temporal-lobe 8–10-Hz tau-rhythm." Neuroscience Research 150 (January 2020): 44–50. http://dx.doi.org/10.1016/j.neures.2019.02.002.

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50

Dewachter, I., L. Ris, S. Croes, P. Borghgraef, H. Devijver, T. Voets, B. Nilius, E. Godaux, and F. Van Leuven. "Modulation of synaptic plasticity and Tau phosphorylation by wild-type and mutant presenilin1." Neurobiology of Aging 29, no. 5 (May 2008): 639–52. http://dx.doi.org/10.1016/j.neurobiolaging.2006.11.019.

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