Bibliographies thématiques / NEUROPROTECTANTS

Littérature scientifique sur le sujet « NEUROPROTECTANTS »

Auteur : Grafiati

Publié le 11 septembre 2023

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Articles de revues sur le sujet "NEUROPROTECTANTS"

Palmer, Katharine J., et Joanne Dalton. « Neuroprotectants in Stroke ». Drugs in R & ; D 1, n^o 1 (janvier 1999) : 9–13. http://dx.doi.org/10.2165/00126839-199901010-00002.

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Schreihofer, D. A. « Phytoestrogens as neuroprotectants ». Drugs of Today 45, n^o 8 (2009) : 609. http://dx.doi.org/10.1358/dot.2009.45.8.1395520.

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Shi, Ligen, Marcelo Rocha, Rehana K. Leak, Jingyan Zhao, Tarun N. Bhatia, Hongfeng Mu, Zhishuo Wei et al. « A new era for stroke therapy : Integrating neurovascular protection with optimal reperfusion ». Journal of Cerebral Blood Flow & ; Metabolism 38, n^o 12 (7 septembre 2018) : 2073–91. http://dx.doi.org/10.1177/0271678x18798162.

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Recent advances in stroke reperfusion therapies have led to remarkable improvement in clinical outcomes, but many patients remain severely disabled, due in part to the lack of effective neuroprotective strategies. In this review, we show that 95% of published preclinical studies on “neuroprotectants” (1990–2018) reported positive outcomes in animal models of ischemic stroke, while none translated to successful Phase III trials. There are many complex reasons for this failure in translational research, including that the majority of clinical trials did not test early delivery of neuroprotectants in combination with successful reperfusion. In contrast to the clinical trials, >80% of recent preclinical studies examined the neuroprotectant in animal models of transient ischemia with complete reperfusion. Furthermore, only a small fraction of preclinical studies included long-term functional assessments, aged animals of both genders, and models with stroke comorbidities. Recent clinical trials demonstrate that 70%–80% of patients treated with endovascular thrombectomy achieve successful reperfusion. These successes revive the opportunity to retest previously failed approaches, including cocktail drugs that target multiple injury phases and different cell types. It is our hope that neurovascular protectants can be retested in future stroke research studies with specific criteria outlined in this review to increase translational successes.

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Sharkey, John, Paul A. Jones, Jennifer F. McCarter et John S. Kelly. « Calcineurin Inhibitors as Neuroprotectants ». CNS Drugs 13, n^o 1 (janvier 2000) : 1–13. http://dx.doi.org/10.2165/00023210-200013010-00001.

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Jeyaseelan, K., KY Lim et A. Armugam. « Neuroprotectants in stroke therapy ». Expert Opinion on Pharmacotherapy 9, n^o 6 (avril 2008) : 887–900. http://dx.doi.org/10.1517/14656566.9.6.887.

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Štolc, Svorad. « Indole derivatives as neuroprotectants ». Life Sciences 65, n^o 18-19 (octobre 1999) : 1943–50. http://dx.doi.org/10.1016/s0024-3205(99)00453-1.

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Kelly, J. S., et J. Sharkey. « Immunosuppressants-ligands as neuroprotectants ». Transplantation Proceedings 33, n^o 3 (mai 2001) : 2217–19. http://dx.doi.org/10.1016/s0041-1345(01)01945-5.

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Muir, K. W., et Ph A. Teal. « Why have neuroprotectants failed ? » Journal of Neurology 252, n^o 9 (25 août 2005) : 1011–20. http://dx.doi.org/10.1007/s00415-005-0933-6.

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&NA;. « Neuroprotectants for Parkinson's disease reviewed ». Inpharma Weekly &NA;, n^o 1389 (mai 2003) : 4. http://dx.doi.org/10.2165/00128413-200313890-00007.

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KLEIN, MICHAEL, SILVIA CALDERON et BELINDA HAYES. « Abuse Liability Assessment of Neuroprotectants ». Annals of the New York Academy of Sciences 890, n^o 1 NEUROPROTECTI (décembre 1999) : 515–25. http://dx.doi.org/10.1111/j.1749-6632.1999.tb08033.x.

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Thèses sur le sujet "NEUROPROTECTANTS"

Boice, Ashley. « DEVELOPMENT OF SMALL MOLECULE NEUROPROTECTANTS ». VCU Scholars Compass, 2018. https://scholarscompass.vcu.edu/etd/5372.

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Neurodegenerative diseases are a class of conditions that lead to progressive atrophy of different parts of the central nervous system (CNS). These diseases lead to devastating clinical outcomes to patients and give rise to an enormous socio-economical burden on society.1 One commonality among some of the most well-known neurodegenerative disorders, e.g. Alzheimer’s disease (AD), Parkinson’s disease (PD), and multiple sclerosis (MS), is neuroinflammation.2-4 Neuroinflammation stems from interactions of the innate immune system with toxins and insults to the central nervous system. In the case of irremovable or chronic insults and toxins, this leads to chronic damaging inflammation that hastens neuronal degeneration and exacerbates disease pathology.5,6 Recently, inflammasomes of the innate immune system have been indicated in playing essential roles in the observed inflammatory responses. The most studied inflammasome is the nod-like receptor pyrin containing 3 (NLRP3) inflammasome.7–9 Recently our research group has successfully developed sulfonamide-based small molecule inhibitors of the NLRP3 inflammasome, such as JC-21 and JC-171, as potential therapeutics for AD and MS. Our studies established that JC-21 is a selective inhibitor of the NLRP3 inflammasome.10,11 Structural modifications led to the development of JC-171 with improved pharmacokinetic properties. More importantly, our studies demonstrated the in vivo activity of JC-171 to effectively ameliorate the experimental autoimmune encephalomyelitis (EAE), a mouse model of MS.12 Our data also strongly suggested that inhibitors based on this chemical scaffold may directly target the NLRP3 inflammasome.10–12 In this dissertation, we conducted biophysical, biochemical, and modeling studies to further elucidate the mechanistic information of these compounds as inhibitors of the NLRP3 inflammasome. In order to conduct further mechanistic studies, the NLRP3 protein was produced via transfection of HEK 293 cells with a modified plasmid of full-length human NLRP3 protein.13 Furthermore, LC-MS studies were conducted to confirm the blood-brain barrier penetration (BBB) of JC-171. Our studies established that JC-171 directly binds to the NLRP3 protein. The results also suggested that JC-171 may bind to the NACHT domain of NLRP3 while in a site that is distinct from the ATP binding site. This notion is supported by the fact that our compounds do not interfere with the ATPase activity of NLRP3. Docking studies of JC-171 to the homology model of the NACHT domain of NLRP3 also supported this assertion by showing the interaction of JC-171 with residues that are not overlapping with the ATP binding pocket. BBB penetration studies in combination with LC-MS analysis confirmed that JC-171 shows better BBB penetration when compared to MCC950. Collectively, our results strongly support that our compounds function as NLRP3 inflammasome inhibitors by directly binding to the NLRP3 protein, a novel and distinct mechanism of action when compared to the known inhibitors that target the NLRP3 inflammasome pathway. These results strongly encourage further development of such inhibitors as potential therapeutics for neurodegenerative diseases.

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Joshi, Kaushal V. « Novel Neuroprotectants for Sarin plus CBDP induced convulsions ». Wright State University / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=wright1253321185.

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Zhang, Zai Jun. « Pharmacological characterization of new neuroprotectants in Parkinson's disease models ». Thesis, University of Macau, 2012. http://umaclib3.umac.mo/record=b2554086.

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Nandasena, Charith. « Impact of neuroprotectants on behavioural and cognitive loss in neurodegenerative diseases ». Thesis, The University of Sydney, 2016. http://hdl.handle.net/2123/17235.

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The discovery of amyloid precursor protein (APP), presenilin 1 (PS1), and presenilin 2 (PS2) mutations associated with hereditary Alzheimer’s disease (AD) was a fundamental step in the development of rodent models to investigate its underlying pathology. This project examined the effects of pre-treatment with photobiomodulation (PBM) or saffron on learning and memory of the APP/PS1 double transgenic mouse using the Intellicage system which allows fully automated continuous testing of behaviour in a home cage environment. Protocols covering exploration, place and place reversal learning, and drinking behaviours were used to characterize longitudinal behaviours. Transgenic mice were successful in learning and re-learning tasks and showed inconsistent effects from both saffron and PBM treatment which may have been influenced by group housing of transgenic and wild-type mice. In contrast when brains were examined by histological analysis at the conclusion of behavioural experiments, it was evident that both PBM and saffron treatment mitigated Aß deposition in the aging APP/PS1 mice. This correlated with reduced mitochondrial dysfunction and saffron pre-treatment also reduced oxidative damage. The mitigation of these three major pathological hallmarks of Alzheimer’s disease – amyloid-ß plaque pathology, oxidative stress and mitochondrial dysfunction, by PBM and saffron treatment reinforces their potential as viable neuroprotective treatments for chronic neurodegenerative conditions. This work emphasises the importance of behavioural testing of animal models in the assessment of treatments and that dietary saffron and PBM are effective, safe, easily administered and minimally invasive interventions to treat chronic neurodegenerative disease.

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Clarke, Allison Elizabeth. « Novel organic nitrates as possible neuroprotectants in an in vitro model of stroke in the rat hippocampus ». Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/MQ59369.pdf.

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Fu, Qingling. « Characterization of novel neuroprotectants for rescuing retinal ganglion cell loss in an ocular hypertensive model of glaucoma ». Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/HKUTO/record/B39557510.

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Fu, Qingling, et 付清玲. « Characterization of novel neuroprotectants for rescuing retinal ganglion cell loss in an ocular hypertensive model of glaucoma ». Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39557510.

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Wong, Raymond. « Progesterone as a neuroprotectant in stroke ». Thesis, University of Nottingham, 2013. http://eprints.nottingham.ac.uk/13730/.

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Progesterone has been shown to be neuroprotective in a number of central nervous system injury models, including cerebral ischaemia. There is still a lack of understanding behind progesterone’s neuropotective properties, and the purpose of this project is to clarify some of these issues. Osmotic mini-pump infusion was hypothesised to more effective in delivering progesterone to the target organ of the brain, when compared to a bolus intraperitoneal injection. Progesterone pharmacokinetic profiles were compared between different dosing regimes. Intraperitoneal progesterone injection had a short half-life in both plasma and brain, while osmotic mini-pumps delivered higher concentrations of progesterone in plasma and particularly in brain, over a longer period, which supports the hypothesis. It was hypothesised that progesterone will reduce NO production and cell death in in vitro. Progesterone reduced nitric oxide production after challenging microglia with LPS, which supports our hypothesis and the nuclear progesterone receptor was found not to have a major role in nitric oxide attenuation. Neither of the microglial cell lines, BV-2 and HAPI cells produced elevations in NO formation in ischaemic conditions. The in vitro oxygen and glucose deprived model of ischaemia, reduced viability in both microglial and neuronal cells. Also, high pharmacological concentrations of progesterone exacerbated ischaemic injury, which does not support the hypothesis of progesterone in reducing cell death. Progesterone administration, via osmotic mini-pump infusion, was hypothesised to have a better outcome compared to vehicle treatment. After the onset of experimental stroke, progesterone delivery via osmotic mini-pump with loading dose was found to be beneficial in terms of neurological deficit score in adult male mice, which supports the hypothesis. Also, we hypothesise that co-morbidity can affect the efficacy of progesterone treatment in outcomes. Aged animals have an increased sensitivity to experimentally induce stroke and did not display, in the outcomes measured, any benefit from progesterone treatment. NOD/ShiLtJ mice had severe symptoms, resulting in high mortality after surgery and are not recommended as a model of diabetes for experimental stroke. Hypertensive BPH/2 mice are a potential hypertensive model and had better functional outcomes after treatment with intraperitoneally administered progesterone, compared to non-treated hypertensive animals in our small preliminary study. This supports our hypothesis that co-morbidity can affect the efficacy of progesterone treatment in outcomes. The gold-standard for assessing intervention effects across studies within and between subgroups is to use meta-analysis based on individual animal data. We hypothesise meta-analysis would reveal progesterone to reduce lesion volume, but also discover other effects in different subgroups of animals. Progesterone significantly reduced lesion volume, it also appeared to increase the incidence of death following experimental stroke. Furthermore, this negative effect appears to be particularly apparent in young ovariectomised female animals. These findings support the hypothesis that progesterone reduces lesion volume and progesterone having other effects in different subgroups. This investigation has clarified some issues and expanded our understanding on the neuroprotective properties of progesterone. However, these findings indicate further investigation is still required before progesterone can be considered for use in clinical trials as a neuroprotectant in stroke.

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Park, Han-A. « Natural Vitamin E, α-Tocotrienol, as a Neuroprotectant ». The Ohio State University, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=osu1291061955.

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Sawyer, Dale C. « The interactions of putative neuroprotectant compounds with NMDA ion channels ». Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq25152.pdf.

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Livres sur le sujet "NEUROPROTECTANTS"

Antkiewicz-Michaluk, Lucyna, et Hans Rommelspacher, dir. Isoquinolines And Beta-Carbolines As Neurotoxins And Neuroprotectants. Boston, MA : Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-1542-8.

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Isoquinolines and beta-carbolines as neurotoxins and neuroprotectants : New vistas in Parkinson's disease therapy. New York : Springer, 2012.

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Rommelspacher, Hans, et Lucyna Antkiewicz-Michaluk. Isoquinolines and Beta-Carbolines As Neurotoxins and Neuroprotectants : New Vistas in Parkinson's Disease Therapy. Springer, 2014.

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Reich, David L., Stephan A. Mayer et Suzan Uysal, dir. Neuroprotection in Critical Care and Perioperative Medicine. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190280253.001.0001.

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Clinicians caring for patients are challenged by the task of protecting the brain and spinal cord in high-risk situations. These include following cardiac arrest, in critical care settings, and during complex procedural and surgical care. This book provides a comprehensive overview of various types of neural injury commonly encountered in critical care and perioperative contexts and the neuroprotective strategies used to optimize clinical outcomes. In addition to introductory chapters on the physiologic modulators of neural injury and pharmacologic neuroprotectants, the topics covered include: imaging assessment; tissue biomarker identification; monitoring; assessment of functional outcomes and postoperative cognitive decline; traumatic brain injury; cardiac arrest and heart-related issues such as valvular and coronary artery bypass surgery, aortic surgery and stenting, and vascular and endovascular surgery; stroke; intracerebral hemorrhage; mechanical circulatory support; sepsis and acute respiratory distress syndrome; neonatal issues; spinal cord injury and spinal surgery; and issues related to general, orthopedic, peripheral vascular, and ear, nose and throat surgeries.

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Chapitres de livres sur le sujet "NEUROPROTECTANTS"

Uhr, M., B. Moosmann et C. Behl. « Aromatic alcohols as neuroprotectants ». Dans Alzheimer’s Disease — From Basic Research to Clinical Applications, 287–94. Vienna : Springer Vienna, 1998. http://dx.doi.org/10.1007/978-3-7091-7508-8_28.

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Andrews, Anne M., Greg A. Gerhardt, Lynette C. Daws, Mohammed Shoaib, Barbara J. Mason, Charles J. Heyser, Luis De Lecea et al. « Neuroprotectants : Novel Approaches for Dementias ». Dans Encyclopedia of Psychopharmacology, 856–59. Berlin, Heidelberg : Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_401.

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Rhodes, Kenneth J. « Neuroprotectants : Novel Approaches for Dementias ». Dans Encyclopedia of Psychopharmacology, 1073–76. Berlin, Heidelberg : Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-36172-2_401.

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Rhodes, Kenneth J. « Neuroprotectants : Novel Approaches for Dementias ». Dans Encyclopedia of Psychopharmacology, 1–5. Berlin, Heidelberg : Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27772-6_401-2.

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Vetiska, Sandra M., et Michael Tymianski. « Neuroprotectants Targeting NMDA Receptor Signaling ». Dans Handbook of Neurotoxicity, 1381–402. New York, NY : Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-5836-4_168.

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Dada, Tanuj, Parul Ichhpujani, Srinivasan Senthilkumari et Alain Bron. « Ocular Hypotensives and Neuroprotectants in Glaucoma ». Dans Pharmacology of Ocular Therapeutics, 207–27. Cham : Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-25498-2_7.

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Grotta, James C., et Lise A. Labiche. « Combination of Thrombolytic Therapy With Neuroprotectants ». Dans Thrombolytic Therapy for Acute Stroke, 77–93. Totowa, NJ : Humana Press, 2005. http://dx.doi.org/10.1385/1-59259-933-8:77.

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Alkayed, Nabil J., Michael M. Wang et Patricia D. Hurn. « Reproductive Hormones as Neuroprotectants in Brain Injury ». Dans Brain Injury, 295–315. Boston, MA : Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1721-4_14.

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Barreto, Andrew D., et James C. Grotta. « Combination of Thrombolytic Therapy with Antithrombotics and Neuroprotectants ». Dans Thrombolytic Therapy for Acute Stroke, 65–80. Cham : Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-07575-4_3.

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Lorenc-Koci, Elżbieta. « Two Faces of 1,2,3,4-Tetrahydroisoquinoline Mode of Action in the Mammalian Brain : Is It an Endogenous Neurotoxin or a Neuromodulator ? » Dans Isoquinolines And Beta-Carbolines As Neurotoxins And Neuroprotectants, 3–30. Boston, MA : Springer US, 2011. http://dx.doi.org/10.1007/978-1-4614-1542-8_1.

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Actes de conférences sur le sujet "NEUROPROTECTANTS"

Gourley, Paul L., P. Chen, R. G. Copeland, Judy K. Hendricks, Anthony E. McDonald, M. E. Keep et J. R. Karlsson. « Nanosqueezed light for probing mitochondria and calcium-induced membrane swelling for study of neuroprotectants ». Dans Micromachining and Microfabrication, sous la direction de Peter Woias et Ian Papautsky. SPIE, 2004. http://dx.doi.org/10.1117/12.532188.

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Rapports d'organisations sur le sujet "NEUROPROTECTANTS"

Gourley, Paul Lee, Robert Guild Copeland, Anthony Eugene McDonald, Judy K. Hendricks et Robert K. Naviaux. Quantum squeezed light for probing mitochondrial membranes and study of neuroprotectants. Office of Scientific and Technical Information (OSTI), janvier 2005. http://dx.doi.org/10.2172/921140.

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Bahr, Ben A. Comparison of Novel and Known Neuroprotectants for Treating Exposure to Different Types of Toxins. Fort Belvoir, VA : Defense Technical Information Center, septembre 2002. http://dx.doi.org/10.21236/ada416987.

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Saukkonen, Jussi. Xenon as a Neuroprotectant in Traumatic Brain Injury. Fort Belvoir, VA : Defense Technical Information Center, mars 2012. http://dx.doi.org/10.21236/ada581238.

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Saukkonen, Jussi. Xenon as a Neuroprotectant in Traumatic Brain Injury. Fort Belvoir, VA : Defense Technical Information Center, septembre 2011. http://dx.doi.org/10.21236/ada601955.

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Saukkonen, Jussi, et Bruce Kristal. Xenon as a Neuroprotectant in Traumatic Brain Injury. Fort Belvoir, VA : Defense Technical Information Center, septembre 2009. http://dx.doi.org/10.21236/ada547294.

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