Relevant bibliographies by topics / Modulating aggregation

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Modulating aggregation'

Author: Grafiati
Published: 6 September 2023

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Journal articles on the topic "Modulating aggregation"

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Huang, Yaliang, Yong Chang, Lin Liu, and Jianxiu Wang. "Nanomaterials for Modulating the Aggregation of β-Amyloid Peptides." Molecules 26, no. 14 (July 15, 2021): 4301. http://dx.doi.org/10.3390/molecules26144301.

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The aberrant aggregation of amyloid-β (Aβ) peptides in the brain has been recognized as the major hallmark of Alzheimer’s disease (AD). Thus, the inhibition and dissociation of Aβ aggregation are believed to be effective therapeutic strategiesforthe prevention and treatment of AD. When integrated with traditional agents and biomolecules, nanomaterials can overcome their intrinsic shortcomings and boost their efficiency via synergistic effects. This article provides an overview of recent efforts to utilize nanomaterials with superior properties to propose effective platforms for AD treatment. The underlying mechanismsthat are involved in modulating Aβ aggregation are discussed. The summary of nanomaterials-based modulation of Aβ aggregation may help researchers to understand the critical roles in therapeutic agents and provide new insight into the exploration of more promising anti-amyloid agents and tactics in AD theranostics.
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Wang, Bo, Emily H. Pilkington, Yunxiang Sun, Thomas P. Davis, Pu Chun Ke, and Feng Ding. "Modulating protein amyloid aggregation with nanomaterials." Environmental Science: Nano 4, no. 9 (2017): 1772–83. http://dx.doi.org/10.1039/c7en00436b.

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Ringertz, BO. "NEUTROPHIL AGGREGATION - FACTORS MODULATING STIMULUS-SPECIFIC RESPONSES." Acta Pathologica Microbiologica Scandinavica Series C: Immunology 94C, no. 1-6 (August 15, 2009): 1–9. http://dx.doi.org/10.1111/j.1699-0463.1986.tb02082.x.

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Polumuri, Swamy kumar, Lydia Haile, Roshni Rao, and Daniela Verthelyi. "Aggregation and innate immune response modulating impurities." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 129.2. http://dx.doi.org/10.4049/jimmunol.198.supp.129.2.

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Abstract Therapeutic proteins can induce immune responses that affect the safety and efficacy even if derived from human sequences. The factors that contribute to the immunogenicity of this therapeutics are poorly understood, but protein aggregation is thought to facilitate it. Previously, our lab showed that trace levels of product or process derived innate immune response modulating impurities (IIRMIs) can also increase product immunogenicity. In this study we hypothesized that protein aggregates and IIRMIs may synergize to facilitate product immunogenicity and explored it using clinical grade Human Serum Albumin (HSA) and Intravenous Immunoglobulin (IVIG) proteins as model. Protein aggregations formed by mechanical stress (shaking and stirring) were characterized by SDS-PAGE, turbidity, MFI and FlowCAM. Cellular responses to aggregated proteins with trace levels of IIRMs were tested in human PBMC. We show that stirring and shaking resulted in the formation of stable aggregates with size ranges of 2 – 50 μm for stirred HSA; and 2–100 μm for IVIG. Despite the similarity in size, the functional assays showed that aggregates of IVIG result in increased mRNA expression of IL-8, IL-6, IL-1β and CCL-2 whereas HSA aggregates did not. Further, we analyzed how the aggregated product changed the transcriptome using Nanostring and showed that aggregated IVIG (shaken or stirred) significantly increased the mRNA of CCL2, CCL7, CCL3, CCL24, CSF1, CXCL2, IRAK1, EGR2, CEBPβ, PPARg, TNFSF15 and whereas HSA aggregates did not. Similarly MAPKs (pp38, pERK and pJNK) and pAKT were activated when PBMC were stimulated with IVIG aggregates but not HSA aggregates. Lastly, we examined whether the effect was mediated by Toll like receptors.
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Kreiser, Ryan P., Aidan K. Wright, Natalie R. Block, Jared E. Hollows, Lam T. Nguyen, Kathleen LeForte, Benedetta Mannini, Michele Vendruscolo, and Ryan Limbocker. "Therapeutic Strategies to Reduce the Toxicity of Misfolded Protein Oligomers." International Journal of Molecular Sciences 21, no. 22 (November 17, 2020): 8651. http://dx.doi.org/10.3390/ijms21228651.

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The aberrant aggregation of proteins is implicated in the onset and pathogenesis of a wide range of neurodegenerative disorders, including Alzheimer’s and Parkinson’s diseases. Mounting evidence indicates that misfolded protein oligomers produced as intermediates in the aggregation process are potent neurotoxic agents in these diseases. Because of the transient and heterogeneous nature of these elusive aggregates, however, it has proven challenging to develop therapeutics that can effectively target them. Here, we review approaches aimed at reducing oligomer toxicity, including (1) modulating the oligomer populations (e.g., by altering the kinetics of aggregation by inhibiting, enhancing, or redirecting the process), (2) modulating the oligomer properties (e.g., through the size–hydrophobicity–toxicity relationship), (3) modulating the oligomer interactions (e.g., by protecting cell membranes by displacing oligomers), and (4) reducing oligomer toxicity by potentiating the protein homeostasis system. We analyze examples of these complementary approaches, which may lead to the development of compounds capable of preventing or treating neurodegenerative disorders associated with protein aggregation.
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Baum, Jean. "Modulating Alpha-Synuclein Aggregation through IDP-IDP Interactions." Biophysical Journal 116, no. 3 (February 2019): 4a. http://dx.doi.org/10.1016/j.bpj.2018.11.049.

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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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Liu, Jing, Ziang Chen, Jia Hu, Hongxia Sun, Yan Liu, Zhongyi Liu, and Jinpeng Li. "Time-resolved color-changing long-afterglow for security systems based on metal–organic hybrids." Inorganic Chemistry Frontiers 9, no. 3 (2022): 584–91. http://dx.doi.org/10.1039/d1qi01435h.

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Bai, Yulong, Yanan Huang, Wang Wan, Wenhan Jin, Di Shen, Haochen Lyu, Lianggang Zeng, and Yu Liu. "Derivatizing merocyanine dyes to balance their polarity and viscosity sensitivities for protein aggregation detection." Chemical Communications 57, no. 98 (2021): 13313–16. http://dx.doi.org/10.1039/d1cc05200d.

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Qi, Yu, Wenshan Chen, Fangfei Liu, Jing Liu, Tong Zhang, and Wei Chen. "Aggregation morphology is a key factor determining protein adsorption on graphene oxide and reduced graphene oxide nanomaterials." Environmental Science: Nano 6, no. 5 (2019): 1303–9. http://dx.doi.org/10.1039/c8en01408f.

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Dissertations / Theses on the topic "Modulating aggregation"

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Shi, Mengying. "Functionalised Azamacrocycles for Modulating Amyloid Aggregation." Thesis, The University of Sydney, 2019. https://hdl.handle.net/2123/22075.

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Alzheimer’s disease (AD) is a common, fatal polygenic neurodegenerative disorder, which still lacks satisfactory therapy or a preventative treatment. Among various hypotheses, the amyloid β (Aβ) cascade hypothesis is a widely accepted explanation by which Aβ aggregation is the causative process in AD pathology. Controlling this aggregation and understanding the structure of the resulting aggregates are core challenges to further understanding of AD. New, bioavailable small-molecule probes with programmable geometries, designed to interact with Aβ, have been obtained in high yields. These probes include functionalized azamacrocycles cyclam and cyclen, connected to pendants through triazole linkers that can coordinate to a central metal ion. It has been shown that probes with different structures have different abilities to influence Aβ aggregation, and therefore potentially capacity to protect neurons from Aβ toxicity by diverting the aggregation behavior of Aβ to alternative endpoints. The aim of this project is to synthesize new functionalized azamacrocycles, which can interact with Aβ and redirect aggregation pathways. A series of tetra-N-substituted cyclam compounds with various pendant groups and triazole group as the linker have been synthesized and characterized. The synthetic approach involves a nucleophilic substitution reaction, copper-catalyzed azide-alkyne cycloaddition (CuAAC) reactions, bromination, tetra-N-alkylation, protonation and metal complexation. Thioflavin T (ThT) fluorescence assays and small angle X-ray scattering (SAXS) experiments were conducted with the novel compounds on Aβ40/42 peptides and other amyloidogenic hydrophobins, the results of which will be discussed in terms of protein binding, surface tension modification, and fluorescence quenching
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Fonseca, Ornelas Luis Eduardo Verfasser], Markus [Akademischer Betreuer] Zweckstetter, Tiago Fleming [Gutachter] Outeiro, Henning [Gutachter] Urlaub, Kai [Gutachter] Tittmann, Christian [Gutachter] [Griesinger, and Reinhard [Gutachter] Jahn. "Modulating the aggregation of alpha-synuclein and prion protein with small molecules. / Luis Eduardo Fonseca Ornelas ; Gutachter: Tiago Fleming Outeiro, Henning Urlaub, Kai Tittmann, Christian Griesinger, Reinhard Jahn ; Betreuer: Markus Zweckstetter." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2016. http://d-nb.info/1118846931/34.

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Oliveira, Márcia Santos. "Modulation of α-synuclein aggregation and toxicity." Master's thesis, Faculdade de Ciências e Tecnologia, 2013. http://hdl.handle.net/10362/11195.

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Dissertação para obtenção do Grau de Mestre em Genética Molecular e Biomedicina
It is widely known that α-synuclein (aSyn) is an amyloidogenic protein prone to aggregation. This protein is found in specific inclusions named Lewy bodies in the surviving neurons of Parkinsons’s disease patients and other synucleinopathy brains. This aggregation process is greatly affected by different post-translational modifications, such as phosphorylation, acetylation, and glycation. Lately it was shown that aSyn oligomeric species are more toxic than the inclusion bodies. Heat shock proteins (HSPs) are molecular chaperones able to modulate the folding and refolding of proteins. Its overexpression in Parkinson’s disease models reduces and prevents aSyn aggregation. As the reduction of aSyn aggregation can lead to an eventual accumulation of oligomeric species which may cause cell damage, the main goal of this work is to better understand the role of HSPs in aSyn oligomer formation, clarifying which are the aSyn resulting species formed in the presence of HSPs. Moreover, as glycation is suggested to accelerate abnormal protein deposition, we aimed to investigate how HSPs interfere with the oligomerization process of glycated aSyn. In this study Hsp70 seemed to induce recombinant aSyn oligomerization, generating higher molecular weight species with no associated toxicity. On the other hand, Hsp27 reduced aSyn oligomerization in vitro possibly by inducing the formation of non-reactive small oligomers. MGO glycation increased protein aggregation and cell death. Interestingly, Hsp27 overexpression reversed glycated aSyn aggregation and its associated toxicity. These results demonstrate the importance of HSPs modulation as a possible target of Parkinson’s disease therapeutics.
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Fontaine, Sarah. "Modulation of PrP aggregation and cellular prion transfer." Thesis, University of Bath, 2010. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.518303.

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Tam, Stephen Jed. "Eukaryotic chaperonin-mediated modulation of polyglutamine aggregation and neurotoxicity /." May be available electronically:, 2007. http://proquest.umi.com/login?COPT=REJTPTU1MTUmSU5UPTAmVkVSPTI=&clientId=12498.

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Guivernau, Almazán Biuse 1988. "Modulation of Amyloid-β peptide aggregation and neurotoxicity in Alzheimer's disease." Doctoral thesis, Universitat Pompeu Fabra, 2016. http://hdl.handle.net/10803/585932.

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Aggregation of the amyloid-β (Aβ) peptide to form oligomers and amyloid fibrils is a central event in the pathogenesis of Alzheimer’s disease (AD). This thesis aims to provide a better understanding of Aβ toxicity and the impact of changes in Aβ aggregation, both relevant to AD. We have found that Aβ nitrotyrosination inhibits fibril formation, which favours the stabilization of small oligomers. We show that nitro-Aβ oligomers strongly bind to dendrites, altering N-methyl-D-aspartate receptor (NMDAR) physiological function and leading to neuronal dysfunction and cell death. Furthermore, we propose a model for Aβ fibril assembly, according to which fibril elongation is interrupted upon nitrotyrosination, due to the destabilization of interprotofibrillar contacts. Additionally, using a genome-wide screen in Saccharomyces cerevisiae, we have identified novel modulators of Aβ toxicity that are potential targets for the development of new AD therapeutic approaches.
L’agregació del pèptid b-amiloide (Aβ) en forma d’oligòmers i fibres és un esdeveniment central en la patogènesi de la malaltia d’Alzheimer. Aquesta tesi pretén aprofundir en els coneixements actuals sobre la toxicitat causada per l’Aβ així com en l’impacte que tenen els canvis en l’agregació d’aquest, tots dos rellevants per la malaltia d’Alzheimer. Els nostres resultats indiquen que la nitrotirosinació de l’Aβ inhibeix la formació de fibres, afavorint l’estabilització d’oligòmers. Demostrem que els oligòmers d’Aβ nitrat s’uneixen a les dendrites, alterant la funció fisiològica dels receptors d’N-metil- D-aspartat (NMDAR) i provocant disfuncions neuronals i la mort cel·lular. A més, proposem un model d’assemblatge per a les fibres d’Aβ, segons el qual la nitrotirosinació interromp l’elongació de la fibra a causa de la desestabilització dels contactes entre protofibres. Addicionalment, utilitzant un cribratge genòmic en Saccharomyces cerevisiae, hem identificat nous moduladors de la toxicitat causada per Aβ, que podrien ser clau per al desenvolupament de noves estratègies terapèutiques de la malaltia Alzheimer.
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Karras, Stephanie. "Modulation der Tau-Aggregation durch Modifikation der Cystein-Reste im Tau-Protein." Doctoral thesis, Universitätsbibliothek Leipzig, 2017. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-219737.

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Tauopathien sind Krankheiten, die mit einer abnormen intrazellulären Tau-Protein-Faltung, Tau-Protein-Aggregation und Filament-Bildung im ZNS und PNS einhergehen. Die Alzheimer Demenz stellt die häufigste Tauopathie dar. Bei ihr kommt es zu einer intra- und extrazellulären Ablagerung fehlgefalteter amyloidogener Proteinaggregate, welche durch β Amyloid und Tau gebildet werden. Es resultiert eine Neurodegeneration. Ein multifaktorieller Prozess führt bei den Tauopathien zur Umwandlung des Tau-Proteins hin zu unlöslichen Fibrillenbündeln. Primär kommt es zur Bildung eines Dimers, das durch Disulfid- und Wasserstoffbrückenbindungen stabilisiert wird. Durch die Zusammenlagerung mehrer Dimere entstehen Tau-Oligomere. Diese gelten als die neurotoxischen Komponenten. Die Primärstruktur des Tau-Proteins beeinflusst den Aggregationsprozess. Dabei spielen die Anwesenheit der Aggregationsdomänen PHF6* und PHF6 und die Anzahl der Cystein-Seitenketten überragende Rollen. In dieser Arbeit wurden durch ortsspezifische Mutagenesen Tau-Konstrukte generiert, die sich in ihrer Anzahl der Aggregationsdomänen und der Cystein-Reste unterschieden. Es konnte gezeigt werden, dass die Aggregationstendenz der Tau-Proteine mit nur einer Aggregationsdomäne und keinem Sulfhydryl-Rest stark sinkt. Auch durch Veränderungen des Redoxmilieus lässt sich das Tau-Aggregationsverhalten beeinflussen. Es wurde gezeigt, dass die Substanz TCEP als starkes Reduktionsmittel die Aggregation der 2 humanen Tau-Isoformen 2N3R und 2N4R wirkungsvoll inhibiert. Auch GSSG als Oxidationsmittel verhinderte in bestimmten Konzentrationen die Aggregation dieser 2 Isoformen. Es wird angenommen, dass die Verhinderung der Bildung einer intermolekularen Disulfidbrückenbindung zu diesem Phänomen führt.
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Langer, Carola Alexandra. "Molekulare Analyse der Huntingtin-Aggregation und deren Modulation durch das eukaryontische Chaperonin TRiC." Diss., lmu, 2007. http://nbn-resolving.de/urn:nbn:de:bvb:19-69757.

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Abelein, Axel. "Modulation of amyloid β peptide self-assembly : Aggregation mechanisms associated with Alzheimer's disease." Licentiate thesis, Stockholms universitet, Institutionen för biokemi och biofysik, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-89078.

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Rose, J. "Molecular chaperone modulation of Parkin aggregation and function in a cell model of Parkinson's disease." Thesis, University College London (University of London), 2010. http://discovery.ucl.ac.uk/19810/.

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Mutations in the E3 ubiquitin ligase Parkin are associated with autosomal recessive juvenile Parkinsonism. Furthermore, Parkin is recruited to Lewy bodies in brains of patients with sporadic Parkinson’s disease (PD), suggesting a role for Parkin in the pathogenesis of PD. This study investigated the effect of the DnaJ/Hsp40-like protein HSJ1 (DnaJB2) on Parkin biology. HSJ1 proteins are neuronal cochaperones that regulate Hsp70 activity through their J domain and exploit ubiquitin interaction motifs (UIM) to promote sorting of misfolded ubiquitylated proteins to the proteasome for degradation. Disease-related mutant forms of Parkin formed inclusions when overexpressed in neuronal cells. Co-expression of mutant Parkin with HSJ1a significantly reduced inclusion formation and altered inclusion characteristics. The effect of HSJ1a on Parkin inclusions required a functional J domain. Mutant Parkin could be co-immunoprecipitated with HSJ1a. Wild-type Parkin was also co-immunoprecipitated with HSJ1a, suggesting a potential interaction with normal Parkin. Importantly, HSJ1a enhanced the E3 ubiquitin ligase activity of wild-type Parkin, dependent on the HSJ1 UIM domain. HSJ1 and Parkin promoted the degradation of the Parkin substrate Synphilin-1. Finally, it was confirmed that Parkin relocates to mitochondria upon mitochondrial membrane depolarization. Moreover, Parkin induced the selective elimination of impaired mitochondria by mitophagy. Interestingly, HSJ1 rescued the relocation of Parkin mutants to damaged mitochondria and partially restored mutant Parkin’s ability to induce mitophagy. These data show that HSJ1 proteins may affect Parkin aggregation and function, which may have a broader relevance to PD.
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Books on the topic "Modulating aggregation"

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Alikhan, Raza. Normal haemostatic function. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0283.

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Humans have evolved an intricate system that maintains blood in a fluid state. This relies on an intact vascular endothelium modulating vascular tone and forming a barrier between blood components and reactive subendothelial components. It also involves the production of inhibitors of both blood coagulation and platelet aggregation. In addition, haemostatic systems are primed to convert blood from its fluid state to a solid state, to allow the formation of a haemostatic plug, following vessel injury, to stem the flow of blood from or within a blood vessel. This chapter reviews the physiology of haemostasis.
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Book chapters on the topic "Modulating aggregation"

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Paleologou, Katerina E., and Omar M. A. El-Agnaf. "α-Synuclein Aggregation and Modulating Factors." In Protein Aggregation and Fibrillogenesis in Cerebral and Systemic Amyloid Disease, 109–64. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-5416-4_6.

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Ginosyan, S., Y. Hambardzumyan, T. Mkrtchyan, H. Grabski, and S. Tiratsuyan. "Molecular Docking of Compounds Modulating Amyloid Peptide Aggregation Schemes." In IFMBE Proceedings, 361–66. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-31866-6_67.

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Bhat, Mohd Younus, Laishram Rajendrakumar Singh, and Tanveer A. Dar. "Modulation of Protein Aggregation/Fibrillation by Osmolytes." In Cellular Osmolytes, 121–42. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-3707-8_6.

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Dong, Lei, Hui-Qing Peng, Li-Ya Niu, and Qing-Zheng Yang. "Modulation of Aggregation-Induced Emission by Excitation Energy Transfer: Design and Application." In Topics in Current Chemistry Collections, 1–41. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-89933-2_1.

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Marwaha, Lovleen. "The Wax Moth Pheromone, Moth Influence, and Associated Glands." In The Wax Moth: A Problem or a Solution, 48–55. BENTHAM SCIENCE PUBLISHERS, 2023. http://dx.doi.org/10.2174/9789815123821123010006.

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The wax moth male secretes various pheromones to attract the female for mating. The volatiles induce species-specific influence, which modulates the behaviour of other members of the same species. The primary pheromones include nonanal and undecanal, hexanal, heptanal, octanal, decanal, undecanol, and 6, 10, 14 - trimethylpentadecanon-2. The specific chemicals are secreted by a pair of glands on the forewings of the male moth in the greater and lesser wax moth. These volatiles are essential for the adult stage and plays a critical role in larval and pupal aggregation. The specific chapter elaborates on the chemical composition of the pheromones, their influence on the conspecific individuals, and their role in modulating the mating behaviour, in the case of the greater wax moth (GWM) and the lesser wax moth (LWM).
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Kara, Adem, Volkan Gelen, and Hülya Kara. "The Relationship of Some Neurodegenerative Diseases with Endoplasmic Reticulum Stress and Histopathological Changes in These Diseases: An Overview." In Molecular Histopathology and Cytopathology [Working Title]. IntechOpen, 2023. http://dx.doi.org/10.5772/intechopen.111693.

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The endoplasmic reticulum (ER) is an organelle responsible for protein production in the cell and provides hemostasis in the cell. ER stress is stimulated by folded proteins, while the unfolded protein response (UPR) creates a response to ER stress and provides the cell survival. UPR modulation in mammals is provided with three major ER stress sensors, including transmembrane kinase 1, protein kinase-like ER kinase, and activating transcription factor 6. Because neurons are susceptible to misfolded proteins, severe or prolonged ER stress activates apoptotic cell death signals in the cell. Neurodegenerative diseases characterized by this condition are Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, and Huntington’s disease, characterized by the accumulation and aggregation of misfolded proteins. In addition, ER stress can lead to depression, schizophrenia, sleep disruption, and post-traumatic stress disorders. Neurons are highly susceptible to protein misfolding and apoptotic cell death. For this reason, UPR modulation contributes to preventing the neurodegenerative process in cells with misfolded protein folding. The relationship between ER stress, UPR, and neuropathology is significant for understanding this process. This section will discuss the effects of ER stress between UPR modulation and neurodegenerative disorders, and the histopathological changes in the mentioned neurodegenerative diseases will be mentioned.
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Rajashekaraiah, Vani, Carl Hsieh, and Masannagari Pallavi. "Modulations in Oxidative Stress of Erythrocytes during Bacterial and Viral Infections." In Erythrocyte - A Peripheral Biomarker For Infection and Inflammation. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.98236.

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Oxidative stress (OS) occurs when the generation of free radicals and reactive oxygen species (ROS) overwhelms the antioxidant capacity. OS causes storage lesions which can be defined as a series of biochemical and biomechanical changes. Erythrocytes are constantly exposed to OS due to the presence of ROS, which are countered by the endogenous antioxidant system. Various irreversible changes that occur include fragmentation and aggregation of proteins and lipids. The changes in proteins, lipids and antioxidant capacity are used as OS biomarkers to assess the efficacy of the erythrocytes, post oxidative insult. Aging of erythrocytes is also associated with the changes in its physical, biochemical and physiological properties and OS causes its rapid aging. Bacterial and viral infections also cause OS which alters the erythrocytes’ antioxidant capacity. These modulations in its microenvironment are both beneficial in terms of protection against invading microorganisms as well as harmful to the erythrocytes, causing damage to surrounding cells and tissues. Thus, OS biomarkers can be used to gain insights into the effects of bacterial and viral infections on the erythrocyte microenvironment.
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Kumar Mitra, Rajib, and Dipak Kumar Palit. "Probing Biological Water Using Terahertz Absorption Spectroscopy." In Terahertz Technology [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97603.

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Hydrogen bonding properties of water molecules, which are confined in microcavities of biological interfaces, are significantly different from those of bulk water and drive most of the complex biological processes. While NMR, X-ray and UV–vis-IR spectroscopic techniques have been found inadequate for describing the dynamics of the thick (20–40 Å) sheath of hydration layer around biomolecules, recently developed THz spectroscopy has emerged as a powerful technique to directly probe the collective dynamics of hydrogen bonds in the hydration layer, which control all important functions of the biomolecules in life. Both laser and accelerator-based THz sources are intense enough to penetrate up to about 100 μm thick water samples, which makes THz transmission and/or dielectric relaxation measurements possible in aqueous solutions. These measurements provide valuable information about the rattling and rotational motions of hydrated ions, making, breaking and rearrangement of hydrogen bonds in hydration layer as well as hydrophilic and hydrophobic interactions between biomolecule and water. THz spectroscopy has also been successfully applied to study the effect of modulation of the physical conditions, like temperature, pH, concentration of proteins and chemical additives, on the structure and dynamics of hydration layer. THz spectroscopy has also been applied to study the processes of denaturation, unfolding and aggregation of biomolecules.
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Conference papers on the topic "Modulating aggregation"

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Mazurov, A. V., V. E. Si-nitsin, and V. S. Repin. "HEPARIN POTENTIATES PLATELET ADHESION AND AGGREGATION ON COLLAGEN SUBSTRATES. ABSENCE OF INHIBITION BY ASPIRIN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644183.

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We studied the effects of two commercial heparin (H) preparations, from bovine lungs (HL) and pig intestine (HI), on the interaction of human plateletswith collagen substrates, and tested a possibility of modulating these effects by aspirin. PRP was incubated in the presence or absence of H with human collagens type IV and III (CIV and Cl I I) adsorbed ona plastic surface. Platelet adhesion and spreading on CIV and aggregation on Cl I I was quantitated by scanning electron microscopy. HL and HI were added to platelets in the concentrations approximating to those achieved in vivo at heparin therapy (0.5̲5.0 U/m 1) . HL and H|=I raised the number of adherent platelets, but do not alter the percentage of spread platelets on CIV. Both preparations had approximately equal effect, increasing platelet adhesion by 1.5 to2-fold at 2.5 U/ml . HL and HI potentiate the formation of. surface-bound aggregates on CIII, enlargingthe total substrate surface coated with aggregates. This effect is achieved due to increased size and number of aggregates. At 2.5 U/ml both preparations potentiate aggregation 2- to 3"fold.Aspirin has no effect on platelet adhesion and spreading both in the absence and presence of HL/HI. In the absence of H, aspirin decreased platelet aggregation on CIII, reducing the aggregate-coated area by 40-50%. The inhibition was related mainly to reducednumber, not the size of aggregates. Aspirin failed to prevent potentiation of the Clll-induced aggregation by HL/HI.
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2

Kowalska, M. A., A. K. Rao, and J. Disa. "HIGH CONCENTRATIONS OF EXOGENOUS ARACHIDONATE INHIBIT CALCIUM MOBILIZATION IN PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644675.

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Exogenous arachidonic acid (AA) induces platelet aggregation and secretion which are inhibited at higher AA concentrations.To define the mechanisms for platelet inhibition at high AA,we studied the effect of itS2$odium salt on cytoplasmic ionized calcium concentration [Ca ]i, a key modulator of several platelet responses. In platelets suspended in Hepes buffer containing no albumin, peak aggregation and secretion occurred at 2-5 pM AA with partial inhibition above 10-15 pM AA and complete inhj^ition around 25-50 pM AA. In platelets ^aded with quin2, [Ca+2 ]i rose, in presence of 1 mM external Ca , from basal levels of 70-80 nM to peak of 300-500 nM at 2-5 μM AA; this was followed by inhibition to basal levels at 25-50 μM AA. At these AA concentrations there was no cell lysis. Thromboxane B. production, measured using a radioimmunoassay, was not inhibited even at 25 pM AA. Elevated celjlar levels of cAMP inhibit platelet responses including Ca2+ signals and were therefore measured using a radioimmunoassay. Platelet cAMP levels rose, in the presence of theophylline (7mM), from basal levels of 3.4 pmol/102+ plat to 5.5 at 5 μM AA and to 6.8 pmol/108 plat at 50 pM AA; Ca signals, aggregation, and secretion were inhibited with doubling of cAMP levels. On incubation of platelets with adenylate cyclase inhibitor, 2'5' dideoxgdenosine (DDA, 200 μM, 2 min) there was enhancement of peak [Ca +2]and aggregation noted with 15 pM AA; at 25 μM AA peak [Ca2+ ]i rose from 126 nM to 205 nM and aggregation was restored. Incubation with SQ 22,536 (500 μM, 5min), another adenylate cyclase inhibitor, also attenuated the inhibition by high AA levels. Treatment of platelets with aspirin or_BW 755C, a combined lipooxygenase/cyclooxygenase inhibitor, did not pryent the inhibition by high AA levels of aggregation and Ca responses induced by thromboxane analog, U46619 In conclusion, high AA concentrations inhibit cytoplasmic Ca+2 mobilization in platelets which is related to elevation of platelet cAMP through stimulation of adenylate cyclase. We propose that high AA levels inhibit aggravation and secretion by modulating cytoplasmic levels of Ca2+ and cAMP, two major messenger molecules in platelets.
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Grant, P. G., A. F. Mannarino, and R. W. Colman. "REGULATION OF CYCLIC NUCLEOTIDE PHOSPHODIESTERASE ACTIVITY IN PLATELETS BY PHOSPHORYLATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642820.

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Cyclic nucleotide phosphodiesterases (PDE) provide the only known pathway for the hydrolysis of cyclic nucleotides in cells and thus have the potential for modulating the effects of cAMP and cGMP on cells. In platelets a rise in intracellular cAMP levels inhibits platelet aggregation and secretion. Since cAMP exerts many of its effects through a cAMP-dependent kinase we questioned whether phosphorylation of cAMP PDE might be a mode for regulation of PDE activity in platelets. When platelets were incubated for 10 min with forskolin (100 μM) the level of cAMP rose at least 10-fold.When the low Km cyclic nucleotide PDE was isolated from freeze-thaw lysates of forskolin treated platelets by chromatography on blue dextran-Sepharose, the specific activity of this enzyme was increased 3 to 13-fold over similarly processed control platelets. The specific activity of a second PDE, the cGMP-stimulated cAMP PDE, was increased 1.5 to 3-fold by forskolin treatment of platelets. Forskolin had no direct effect on either purified PDE. The stimulation of the low Km cAMP PDE activity by exposure of platelets to forskolin was blocked when the platelets were simultaneously treated with the protein kinase inhibitor H-8 (100 μM) which is most potent toward cAMP dependent protein kinase indicating that this kinase may be responsible for the stimulation. When platelets which had been prelabeled with 32P inorganic phosphate were treated with forskolin and the low Km cAMP PDE isolated by blue dextran-Sepharose chromatography, a protein migrating in SDS gels at Mr=110,000, the molecular weight of the low Km cAMP PDE, was labeled indicating that phosphorylation of the PDE occurred coincident with stimulation of activity. These results suggest that phosphorylation of the low Km cAMP PDE by protein kinase may be an important regulatory mechanism for cAMP PDE activity and cyclic nucleotide levels in platelets.
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4

Koneti Rao, A., and Maria A. Kowalska. "ADP-INDUCED CYTOPLASMIC CALCIUM MOBILIZATION AND SHAPE CHANGE IN PLATELETS ARE MEDIATED BY DIFFERENT BINDING SITES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644466.

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Platelet stimulation with ADP results in a number of responses including increase in cytoplasmic ionized calcium concentration [Ca2+]i, shape change, aggregation, secretion, and inhibition of cAMP accumulation caused by PGI2.5'-Fluorosulphonylbenzoyladenosine (FSBA), which covalently labels ADP binding site on platelets, blocks platelet shape change but not inhibition of cyclic AMP levels by ADP, while p-chloromercuribenzenesulfonate (pCMBS), a non-penetrating thiol reagent, blocks ADP-induced inhibition of adenylate cyclase but not shape change. We examined the effect of FSBA and pCMBS on ADP-induced increase in [Ca2+]i to determine whether it is linked to the binding site mediating shape change or that for inhibition of adenylate cyclase. In platelets loaded with Ca2+ indicators, quin 2 or fura 2, and in presence of adenosine deaminase (AD), FSBA (50-200 μM) induced a dose-dependent, rapid rise in [Ca2+]i. from basal levels of 70-90 nM to peak levels of 300-500 nM in the presence of 1 mM external Ca2+ providing direct evidence that FSBA is a platelet agonist. The [Ca2+ ]i. returned to near basal levels over 30 min. The effect of FSBA on [Ca2+]i. was inhibited by ZK 36,374 (40 nM), a stable PGI2 analog. AdP concentrations eliciting similar responses were about 10-fold less than those for FSBA. Platelet incubation with FSBA (50-100 μM) in the presence of AD for 30 min (to ensure optimal covalent labelling of the ADP binding sites) abolished shape change but jjid not inhibit ADP (5, 25 μM)-induced increase in [Ca2+]i. or block the inhibitory effect of ADP on cAMP accumulation in1platelets exposed to ZK 36,374 (50 nM) in.presence of theophylline (7 mM). Incubation with pCMBS (5-100 pM, 2 min) abolished the effect of ADP on [Ca2+]. and on the inhibition of cAMP levels; shape change was not 1 inhabited even at 1 mM. pCMBS (0.5-1 mM) inhibited the rise in [Ca2+ ]. by FSBA alone. These observations suggest that ADP-induced Ca mobilization is mediated by platelet binding sites which are distinct from those mediating shape change but probably the same as those modulating adenylate cyclase.
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5

Yang, Qi, Xishuo Wang, Qi Zhang, Xiangjun Xin, Ran Gao, Ying Tao, Qinghua Tian, et al. "All-Optical Aggregation Scheme Based On Joint Modulation." In Asia Communications and Photonics Conference. Washington, D.C.: OSA, 2020. http://dx.doi.org/10.1364/acpc.2020.m4a.351.

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6

Wu, Yi. "Multilevel Modulation Based Differentiated Data Aggregation for Wireless LANs." In TENCON 2006 - 2006 IEEE Region 10 Conference. IEEE, 2006. http://dx.doi.org/10.1109/tencon.2006.344136.

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7

Zhang, Lu, Xin Li, Ying Tang, Tao Gao, Bingli Guo, and Shanguo Huang. "Modulation-Level-Awared Multicast Flow Aggregation Scheme in Elastic Optical Datacenter Networks." In Asia Communications and Photonics Conference. Washington, D.C.: OSA, 2017. http://dx.doi.org/10.1364/acpc.2017.m1c.5.

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8

Fu, Xue, Guan Gui, Yu Wang, Tomoaki Ohtsuki, Bamidele Adebisi, Haris Gacanin, and Fumiyuki Adachi. "Lightweight Network and Model Aggregation for Automatic Modulation Classification in Wireless Communications." In 2021 IEEE Wireless Communications and Networking Conference (WCNC). IEEE, 2021. http://dx.doi.org/10.1109/wcnc49053.2021.9417592.

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9

Pena-Quintal, Angel, Arun Khilnani, Leonardo Sandrolini, Mark Sumner, David Thomas, and Steve Greedy. "EMI Spectral Aggregation of Modulation Schemes in a lab-based DC Microgrid." In 2022 IEEE International Symposium on Electromagnetic Compatibility & Signal/Power Integrity (EMCSI). IEEE, 2022. http://dx.doi.org/10.1109/emcsi39492.2022.9889337.

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10

Blasko, Gy, G. Blasko, G. Sas, and Cs Szantay. "MODULATION OF THROMBIN-MEDIATED REACTIONS IN HAEMOSTASIS- BY TREQUINSIN AND ITS ANALOGUES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643432.

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A new pyrimido/6,1-a/-isoquinoline derivative ,/Ref.1 / developed by Hoechst and named Trequinsine has been reported to be a powerful inhibitor of cAMP phosphodiesterase and platelet aggregation having a potency nearly similar to prostacyclin. We synthesized Trequins-in (1), its indole derivative (4) , as well as their precursors (2 3) and subjected them to a study in order to evaluate their effects on haemostasis. Surprisingly they exhibited a modulatory effect only on reactions mediated mainly by thrombin. They inhibited platelet aggregation (ICc:q for Trequinsin: 13 + 2.5 ng/ml, for indole derivatives: 1-3 /ig/ml); 1, 2, 4 enhanced the amidolytic activity of CC-thrombin towards S-2238 substrate within a narrow range of submicromolar concentrations but they did not exert any effect on the activity or the inactivation of Factor Xa and plasmin.Compound 2 proved to be an inhibitor of prostacyclin production of rat aortic tissue (Trequinsin has much less effect) but in contrary to this 3. and 4 exerted an enhancing effect on the total prostacyclin production.
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