Bibliografías temáticas / Cerebral ischemia, adenosine, carbonic anhydrase

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Literatura académica sobre el tema "Cerebral ischemia, adenosine, carbonic anhydrase"

Autor: Grafiati
Publicado: 10 de marzo de 2023

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Artículos de revistas sobre el tema "Cerebral ischemia, adenosine, carbonic anhydrase"

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Bulli, Irene, Ilaria Dettori, Elisabetta Coppi, et al. "Role of Carbonic Anhydrase in Cerebral Ischemia and Carbonic Anhydrase Inhibitors as Putative Protective Agents." International Journal of Molecular Sciences 22, no. 9 (2021): 5029. http://dx.doi.org/10.3390/ijms22095029.

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Ischemic stroke is a leading cause of death and disability worldwide. The only pharmacological treatment available to date for cerebral ischemia is tissue plasminogen activator (t-PA) and the search for successful therapeutic strategies still remains a major challenge. The loss of cerebral blood flow leads to reduced oxygen and glucose supply and a subsequent switch to the glycolytic pathway, which leads to tissue acidification. Carbonic anhydrase (CA, EC 4.2.1.1) is the enzyme responsible for converting carbon dioxide into a protons and bicarbonate, thus contributing to pH regulation and meta
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Supuran, Claudiu T. "Emerging role of carbonic anhydrase inhibitors." Clinical Science 135, no. 10 (2021): 1233–49. http://dx.doi.org/10.1042/cs20210040.

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Abstract Inhibition of carbonic anhydrase (CA, EC 4.2.1.1) was clinically exploited for decades, as most modern diuretics were obtained considering as lead molecule acetazolamide, the prototypical CA inhibitor (CAI). The discovery and characterization of multiple human CA (hCA) isoforms, 15 of which being known today, led to new applications of their inhibitors. They include widely clinically used antiglaucoma, antiepileptic and antiobesity agents, antitumor drugs in clinical development, as well as drugs for the management of acute mountain sickness and idiopathic intracranial hypertension (I
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3

Angeli, Andrea, Victor Kartsev, Anthi Petrou, et al. "Carbonic Anhydrase Inhibition with Sulfonamides Incorporating Pyrazole- and Pyridazinecarboxamide Moieties Provides Examples of Isoform-Selective Inhibitors." Molecules 26, no. 22 (2021): 7023. http://dx.doi.org/10.3390/molecules26227023.

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A series of benzenesulfonamides incorporating pyrazole- and pyridazinecarboxamides decorated with several bulky moieties has been obtained by original procedures. The new derivatives were investigated for the inhibition of four physiologically crucial human carbonic anhydrase (hCA, EC 4.2.2.1.1) isoforms, hCA I and II (cytosolic enzymes) as well as hCA IX and XII (transmembrane, tumor-associated isoforms). Examples of isoform-selective inhibitors were obtained for all four enzymes investigated here, and a computational approach was employed for explaining the observed selectivity, which may be
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Di Cesare Mannelli, Lorenzo, Laura Micheli, Fabrizio Carta, Andrea Cozzi, Carla Ghelardini, and Claudiu T. Supuran. "Carbonic anhydrase inhibition for the management of cerebral ischemia: in vivo evaluation of sulfonamide and coumarin inhibitors." Journal of Enzyme Inhibition and Medicinal Chemistry 31, no. 6 (2015): 894–99. http://dx.doi.org/10.3109/14756366.2015.1113407.

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Schlake, Hans-Peter, Ingolf Gerhard Böttger, Karl-Heinz Grotemeyer, Ingo Wilhelm Husstedt, Christoph Oberwittler, and Otmar Schober. "The Influence of Acetazolamide on Cerebral Low-Flow Regions in Migraine an Interictal 99mTc-HMPAO SPECT Study." Cephalalgia 12, no. 5 (1992): 284–88. http://dx.doi.org/10.1046/j.1468-2982.1992.1205284.x.

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Acetazolamide, a carbonic anhydrase inhibitor, has proved to be useful in the assessment of “vasodilatory capacity” in cerebrovascular disease. To obtain further information on the nature of interictal low-flow regions in migraine, we reinvestigated 20 asymptomatic patients suffering from migraine with aura ( n = 15) or without aura ( n = 5) and who had either minor ( n = 12) or marked ( n = 8) regional hypoperfusion when examined in a previous 99mTc-HMPAO SPECT investigation. These patients received acetazolamide IV prior to tracer application. In 14/20 cases regional hypoperfusion resolved.
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Mittag, T. W., W. B. Guo, and K. Kobayashi. "Bicarbonate-activated adenylyl cyclase in fluid-transporting tissues." American Journal of Physiology-Renal Physiology 264, no. 6 (1993): F1060—F1064. http://dx.doi.org/10.1152/ajprenal.1993.264.6.f1060.

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A bicarbonate-stimulated adenylyl cyclase (AC) activity was found in ocular ciliary processes, which secrete the aqueous humor of the eye. Other fluid-transporting tissues also showed HCO3(-)-stimulated AC activity. Relative to basal, the response to 10 mM NaHCO3 was greatest in the particulate fraction of bovine ciliary processes, followed by bovine corneal endothelium, bovine choroid plexus, and rat kidney (medulla and cortex). However, no activity was detectable in bovine retina, cerebral cortex, or cerebellum. The activity in ciliary processes was present only in the particulate fraction,
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Куликов, В. П., Л. А. Каланова, and П. П. Трегуб. "Potentiation of the protective effect of hypercapnic hypoxia in combination with pharmacological neuroprotective agents." Zhurnal «Patologicheskaia fiziologiia i eksperimental`naia terapiia», no. 3 (September 30, 2021): 21–25. http://dx.doi.org/10.25557/0031-2991.2021.03.21-25.

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Цель исследования - изучение возможности потенцирования нейропротекторного эффекта гиперкапнической гипоксии при помощи комбинации с фармакологическими активаторами основных механизмов, увеличивающих толерантность головного мозга к ишемии/гипоксии. Методика. Исследования проводились на 140 крысах-самцах Wistar, которые подвергались курсам респираторных воздействий гиперкапнической гипоксии (PO2 - 90 мм рт. ст.; PCO2 - 50 мм рт. ст.) в течении 5 сут по 30 мин ежедневно. После завершения курса тренировок крысам вводили фармакологические препараты (активатор аденозиновых рецепторов, блокатор карб
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Kumar, Manish, Komalpreet Kaur, and Thakur Gurjeet Singh. "Neuroprotective Effects of Carbonic Anhydrase Inhibition and Cyclic Adenosine Monophosphate Activation in Mouse Model of Transient Global Cerebral Ischemia and Reperfusion." NeuroMolecular Medicine, October 28, 2022. http://dx.doi.org/10.1007/s12017-022-08728-9.

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Singh, Dhandeep, and Nirmal Singh. "Synthesis and Evaluation of 1-hydroxybenzotriazole Derivatives: Dual Inhibitors of Carbonic Anhydrase II and Sodium Hydrogen Exchanger I." Letters in Organic Chemistry 17 (October 14, 2020). http://dx.doi.org/10.2174/1570178617999201014164710.

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: Ischemia reperfusion injury is responsible for impaired graft functioning in organ transplants, cerebral dysfunction, ischemic heart diseases, systemic inflammatory response syndrome, gastrointestinal dysfunction, and multiple organ dysfunction syndromes. Intracellular pH is critical for cell survival in ischemia reperfusion injury. Sodium hydrogen exchanger I and carbonic anhydrase II are critical in regulation of intracellular pH. Inhibition of sodium hydrogen exchanger I and carbonic anhydrase II during reprfusion is found to ameliorate ischemia reperfusion injury separately. An attempt i
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Scotti, Luciana, Teresa Carolliny Moreira Lustoza Rodrigues, Natália Ferreira de Sousa, Aline Matilde Ferreira dos Santos, Renan Dantas Aires Guimarães, and Marcus T. Scotti. "Challenges and Discoveries in Polypharmacology of Neurodegenerative Diseases." Current Topics in Medicinal Chemistry 23 (January 26, 2023). http://dx.doi.org/10.2174/1568026623666230126112628.

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Background: Neurological disorders are composed of several diseases that affect the central and peripheral nervous system; among these are neurodegenerative diseases, which lead to neuronal death. Many of these diseases have treatment for the disease and symptoms, leading patients to use several drugs that cause side effects. Introduction: The search for new treatments has led to the investigation of multi-target drugs. Method: This review aimed to investigate in the literature the multi-target effect in neurological disorders through an in silico approach. Studies were reviewed on the disease
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Tesis sobre el tema "Cerebral ischemia, adenosine, carbonic anhydrase"

1

Bulli, Irene. "Adenosine A2B receptors and carbonic anhydrase: new therapeutic targets for cerebral ischemia." Doctoral thesis, 2022. http://hdl.handle.net/2158/1265035.

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Gaviano, Lisa. "Adenosine a2b receptors and carbonic anhydrase: new therapeutic targets for cerebral ischemia and demyelination." Doctoral thesis, 2020. http://hdl.handle.net/2158/1188740.

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Cerebral ischemia is a multifactorial pathology characterized by different events evolving in time. The acute injury, characterized by a massive increase of extracellular glutamate levels, is followed by activation of resident immune cells and production or activation of inflammation mediators. Although after ischemia precocious activation of immune cells may be neuroprotective and supportive for regeneration, protracted neuroinflammation is now recognized as the predominant mechanism of secondary brain injury progression. In this thesis, I investigated on the putative protective effects of th
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