Bibliografias temáticas / Cerebrovascular regulation

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Literatura científica selecionada sobre o tema "Cerebrovascular regulation"

Autor: Grafiati

Publicado: 25 de janeiro de 2025

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Artigos de revistas sobre o assunto "Cerebrovascular regulation"

Benyó, Zoltán, Éva Ruisanchez, Miriam Leszl-Ishiguro, Péter Sándor e Pál Pacher. "Endocannabinoids in cerebrovascular regulation". American Journal of Physiology-Heart and Circulatory Physiology 310, n.º 7 (1 de abril de 2016): H785—H801. http://dx.doi.org/10.1152/ajpheart.00571.2015.

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The cerebral blood flow is tightly regulated by myogenic, endothelial, metabolic, and neural mechanisms under physiological conditions, and a large body of recent evidence indicates that inflammatory pathways have a major influence on the cerebral blood perfusion in certain central nervous system disorders, like hemorrhagic and ischemic stroke, traumatic brain injury, and vascular dementia. All major cell types involved in cerebrovascular control pathways (i.e., smooth muscle, endothelium, neurons, astrocytes, pericytes, microglia, and leukocytes) are capable of synthesizing endocannabinoids and/or express some or several of their target proteins [i.e., the cannabinoid 1 and 2 (CB1 and CB2) receptors and the transient receptor potential vanilloid type 1 ion channel]. Therefore, the endocannabinoid system may importantly modulate the regulation of cerebral circulation under physiological and pathophysiological conditions in a very complex manner. Experimental data accumulated since the late 1990s indicate that the direct effect of cannabinoids on cerebral vessels is vasodilation mediated, at least in part, by CB1 receptors. Cannabinoid-induced cerebrovascular relaxation involves both a direct inhibition of smooth muscle contractility and a release of vasodilator mediator(s) from the endothelium. However, under stress conditions (e.g., in conscious restrained animals or during hypoxia and hypercapnia), cannabinoid receptor activation was shown to induce a reduction of the cerebral blood flow, probably via inhibition of the electrical and/or metabolic activity of neurons. Finally, in certain cerebrovascular pathologies (e.g., subarachnoid hemorrhage, as well as traumatic and ischemic brain injury), activation of CB2 (and probably yet unidentified non-CB1/non-CB2) receptors appear to improve the blood perfusion of the brain via attenuating vascular inflammation.

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Miller, Stephanie. "NIRS-based cerebrovascular regulation assessment: exercise and cerebrovascular reactivity". Neurophotonics 4, n.º 04 (12 de setembro de 2017): 1. http://dx.doi.org/10.1117/1.nph.4.4.041503.

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Yang, Yi, David Simpson, Bingren Hu, Jia Liu e Li Xiong. "Cerebrovascular Regulation in Neurological Disorders". BioMed Research International 2018 (8 de outubro de 2018): 1–2. http://dx.doi.org/10.1155/2018/8140545.

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Eisenach, J. C., C. Tong, D. A. Stump e S. M. Block. "Vasopressin and fetal cerebrovascular regulation". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 263, n.º 2 (1 de agosto de 1992): R376—R381. http://dx.doi.org/10.1152/ajpregu.1992.263.2.r376.

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Vasopressin (AVP) may increase cerebral blood flow (CBF) during hypoxemia by selective dilatation of cerebral vessels via endothelium-derived relaxing factor (EDRF) release. To test whether this action is relevant in the fetus, we produced isocapnic hypoxemia in halothane-anesthetized pregnant ewes. Fetal infusion of a V1 AVP antagonist reduced by 55% the increase in CBF during fetal hypoxemia. To test the role of this response during development, we examined the response to AVP in intact and endothelium-denuded femoral and basilar arterial rings in vitro from fetal, newborn, and adult sheep. AVP constricted femoral rings in an endothelium-independent manner, with increased potency in newborn and fetal compared with adult rings. AVP relaxed basilar rings in an endothelium-dependent manner, which was unaffected by indomethacin treatment, with increased potency in newborn and adult compared with fetal rings. We conclude that fetal cerebral vascular endothelium is functional and responsive to AVP and that circulating AVP during fetal hypoxemia contributes to increased CBF via this effect.

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Jafari, Behrouz. "Cerebrovascular Regulation and Sleep Apnea". Current Sleep Medicine Reports 4, n.º 3 (17 de julho de 2018): 196–201. http://dx.doi.org/10.1007/s40675-018-0123-6.

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Daffertshofer, M., e M. Hennerici. "Cerebrovascular regulation and vasoneuronal coupling". Journal of Clinical Ultrasound 23, n.º 2 (fevereiro de 1995): 125–38. http://dx.doi.org/10.1002/jcu.1870230207.

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Caldwell, Hannah G., Jay M. J. R. Carr, Jatinder S. Minhas, Erik R. Swenson e Philip N. Ainslie. "Acid–base balance and cerebrovascular regulation". Journal of Physiology 599, n.º 24 (26 de novembro de 2021): 5337–59. http://dx.doi.org/10.1113/jp281517.

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Koehler, Raymond C., Debebe Gebremedhin e David R. Harder. "Role of astrocytes in cerebrovascular regulation". Journal of Applied Physiology 100, n.º 1 (janeiro de 2006): 307–17. http://dx.doi.org/10.1152/japplphysiol.00938.2005.

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Astrocytes send processes to synapses and blood vessels, communicate with other astrocytes through gap junctions and by release of ATP, and thus are an integral component of the neurovascular unit. Electrical field stimulations in brain slices demonstrate an increase in intracellular calcium in astrocyte cell bodies transmitted to perivascular end-feet, followed by a decrease in vascular smooth muscle calcium oscillations and arteriolar dilation. The increase in astrocyte calcium after neuronal activation is mediated, in part, by activation of metabotropic glutamate receptors. Calcium signaling in vitro can also be influenced by adenosine acting on A2B receptors and by epoxyeicosatrienoic acids (EETs) shown to be synthesized in astrocytes. Prostaglandins, EETs, arachidonic acid, and potassium ions are candidate mediators of communication between astrocyte end-feet and vascular smooth muscle. In vivo evidence supports a role for cyclooxygenase-2 metabolites, EETs, adenosine, and neuronally derived nitric oxide in the coupling of increased blood flow to increased neuronal activity. Combined inhibition of the EETs, nitric oxide, and adenosine pathways indicates that signaling is not by parallel, independent pathways. Indirect pharmacological results are consistent with astrocytes acting as intermediaries in neurovascular signaling within the neurovascular unit. For specific stimuli, astrocytes are also capable of transmitting signals to pial arterioles on the brain surface for ensuring adequate inflow pressure to parenchymal feeding arterioles. Therefore, evidence from brain slices and indirect evidence in vivo with pharmacological approaches suggest that astrocytes play a pivotal role in regulating the fundamental physiological response coupling dynamic changes in cerebral blood flow to neuronal synaptic activity. Future work using in vivo imaging and genetic manipulation will be required to provide more direct evidence for a role of astrocytes in neurovascular coupling.

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Raz, Limor. "Estrogen and cerebrovascular regulation in menopause". Molecular and Cellular Endocrinology 389, n.º 1-2 (maio de 2014): 22–30. http://dx.doi.org/10.1016/j.mce.2014.01.015.

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Edvinsson, L. "Cerebrovascular gene regulation in brain diseases". Journal of the Neurological Sciences 283, n.º 1-2 (agosto de 2009): 246. http://dx.doi.org/10.1016/j.jns.2009.02.032.

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Mais fontes

Teses / dissertações sobre o assunto "Cerebrovascular regulation"

Hansen, Alexander Bradley. "Cerebrovascular and peripheral vascular regulation : role of oxidative stress". Thesis, University of British Columbia, 2017. http://hdl.handle.net/2429/63341.

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Oxidative stress is ultimately determined by the balance between pro- (e.g. free radicals) and antioxidants (e.g. vitamin C). The purpose of this thesis was to examine the role and effect of a combined mixture of oral antioxidants (vitamin C, E, and alpha-lipoic acid) on peripheral and cerebrovascular regulation at both sea-level (344m; n = 11 participants) and at high altitude (5050m; n=10) where oxidative stress is markedly elevated. In a randomized and double-blinded design, flow-mediated dilation, cardiorespiratory, cerebral blood flow, and CO₂ and hypoxic cerebrovascular reactivity tests were conducted before and 90 mins following antioxidants (vitamin C, E, and alpha-lipoic acid) or a placebo control, previous work has shown antioxidant levels increased in blood plasma after 90 mins of ingestion. Following 10-12 days at 5050m, in a similar design, flow-mediated dilation, cardiorespiratory, and resting cerebral blood flow tests were obtained. The primary findings were: 1) antioxidants did not alter flow-mediated dilation, resting cerebral blood flow, cerebrovascular reactivity to CO₂ or hypoxia at sea-level; 2) similarly, at high-altitude (Nepal, 5050m), antioxidants did not alter flow-mediated dilation or resting cerebral blood flow. In conclusion, this study highlights that at both sea-level and high-altitude, acute oral administration of antioxidants does not alter FMD or cerebrovascular reactivity to CO₂ or hypoxia. Nevertheless, continued exploration of this methodology is recommended, especially in the form of more chronic dosing of antioxidants in various pathologies (e.g., chronic pulmonary obstructed disease, diabetes, coronary artery disease) who present with excessive oxidative stress and reductions in both antioxidant capacity and vascular function. This study received ethical approval from the University of British Columbia Clinical Research Ethics Board (ID: H16-00101). This research was supported by a NSERC Discovery grant and Canadian Research Chair in Cerebrovascular Physiology.
Graduate Studies, College of (Okanagan)
Graduate

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Lowings, Michael D., e University of Lethbridge Faculty of Arts and Science. "Epigenetic regulation of stroke recovery : changes in DNA methylation and micro-RNA regulation following stroke and EGF/EPO neurogenesis therapy". Thesis, Lethbridge, Alta. : University of Lethbridge, Dept. of Biological Sciences, c2010, 2010. http://hdl.handle.net/10133/2570.

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Stroke is one of the most common, and damaging, neurological afflictions. Stroke causes widespread and variable chronic effects, due to the limited regenerative ability of the adult brain. Altered gene expression induces neuronal changes necessary for plasticity-dependent recovery, effects which can be enhanced by growth hormone-based pharmaceuticals. These processes are driven by alterations in the informational capacity of the genome – changes driven by epigenetic regulators. Following experimental strokes, and treatment with EGF and EPO, this study shows that two epigenetic regulatory mechanisms, DNA methylation and microRNA regulation, are significantly altered, both in treated and untreated animals. Specifically, treatment induces a net global suppression of miRNA activity, which appears to modify the physical behaviour of neurons in domains ranging from plasticity and memory formation, growth and replication, and potentially even to neurological disease signalling. The confirmation of epigenetic alterations following a stroke indicates a future role for epigenetic neuro-pharmacology in stroke management.
x, [99] leaves : ill. (some col.) ; 29 cm

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Allinger, Jérémie. "Etude des différents facteurs influençant la perte de cοnnaissance chez l'apnéïste". Electronic Thesis or Diss., Normandie, 2024. http://www.theses.fr/2024NORMR081.

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Ce travail de thèse proposait d’étudier les facteurs influençant la perte de connaissance chez les apnéistes. Dans un premier temps, nous avons étudié la prévalence des accidents en apnée compétitive en fonction de la discipline d’apnée pratiquée (étude 1) puis tenté d’établir s’il existait un profil particulièrement à risque pour la syncope chez les apnéistes experts (étude 2). Dans un second temps, nous avons analysé l’impact cognitif d’une série d’apnées maximales chez des apnéistes experts ainsi qu’après une séance d’apnée habituelle chez des apnéistes amateurs (études 3 et 4). Par ailleurs, une attention particulière a été portée à la quantification et à la gestion de la charge d’entraînement en apnée en situation écologique (étude 4). Enfin, les réponses hémodynamiques et d’oxygénation cérébrale des apnéistes novices ont été comparées lors d’apnées statiques et dynamiques (étude 5). Les syncopes restent relativement fréquentes (3,31 % des accidents), avec un risque deux fois plus élevé pour les disciplines sans palme. Certains apnéistes avec une capacité à réaliser de longues apnées ont tendance à prendre plus de risques, notamment chez les compétiteurs expérimentés masculins. Cela pourrait être en lien avec une exposition répétée à l’hypoxie puisque nous avons montré qu’une série d’apnées maximales affecte directement les fonctions cognitives, peu importe le niveau d’entraînement. Toutefois, chez les non-experts, une seule séance d'apnée dans un cadre non compétitif n’a pas révélé de déficits cognitifs notables, ce qui suggère que ces altérations dépendent probablement de l'intensité, la fréquence des apnées et donc de la dose hypoxique. Cette dose hypoxique semble dépendre également du type d’apnée : statique ou dynamique. Ainsi, bien que l'apnée statique bénéficie de mécanismes compensatoires plus efficaces, l'apnée dynamique, en raison de l'effort musculaire accru, induit une hypoxie plus rapide mettant davantage à l'épreuve les mécanismes de protection cérébrale. Il semble donc intéressant d’utiliser des outils pour quantifier la charge d’entraînement des apnéistes afin de mieux évaluer la dose hypoxique induite et, à terme, de limiter les risques de syncopes pour prévenir les éventuelles futures altérations cognitives. Ces travaux ouvrent la voie à de futures recherches sur les adaptations à l’hypoxie induite par l’apnée dans le cadre sportif et médical, tout en appelant à une meilleure gestion des risques liés à la pratique
The aim of this thesis was to study the factors influencing loss of consciousness in freedivers. Firstly, we studied the prevalence of accidents in competitive freediving as a function of the freediving discipline practised (study 1) and then attempted to establish whether there was a particularly high-risk profile for syncope among expert freedivers (study 2). Secondly, we analysed the cognitive impact of a series of maximal apneas in expert freedivers and after a regular freediving session in amateur freedivers (studies 3 and 4). In addition, particular attention was paid to the quantification and management of apnea training load in ecological situations (study 4). Finally, the haemodynamic and cerebral oxygenation responses of novice freedivers were compared during static and dynamic apneas (study 5). Syncope remains relatively frequent (3.31% of accidents), with a risk twice as high for disciplines without fins. Certain freedivers with the ability to perform long apneas tend to take more risks, particularly among experienced male competitors. This could be linked to repeated exposure to hypoxia, since we have shown that a series of maximal apneas directly affects cognitive functions, regardless of the level of training. However, in non-experts, a single apnea session in a non-competitive setting did not reveal any notable cognitive deficits, which suggests that these alterations probably depend on the intensity and frequency of apneas and therefore on the hypoxic dose. This hypoxic dose also seems to depend on the type of apnoea: static or dynamic. Thus, although static apnoea benefits from more effective compensatory mechanisms, dynamic apnoea, because of the increased muscular effort, induces more rapid hypoxia, putting the brain's protective mechanisms to a greater test. It therefore seems worthwhile to use tools to quantify the training load of freedivers in order to better assess the hypoxic dose induced and, ultimately, to limit the risks of syncope in order to prevent future cognitive impairment. This work paves the way for future research into adaptations to hypoxia induced by apnoea in sports and medical settings, while calling for better management of the risks associated with practice

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Teixeira, Ana Sofia da Cunha. "Ageing affects the balance between central and peripheral mechanisms of cerebrovascular regulation with increasing influence of systolic blood pressure levels". Master's thesis, 2019. https://hdl.handle.net/10216/119825.

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BACKGROUND: Arterial baroreflex (BR) and cerebral autoregulation (CA) are two major regulatory mechanisms that maintain constant cerebral perfusion. Little is known about the interplay between these mechanisms, particularly when considering the effects of ageing or sex.PURPOSE: We studied the relationship between dynamic CA and BR sensitivity (BRS) in healthy subjects by sex and in different age strata.METHODS: 95 healthy adults (52% female), 20-80 years-old, were recruited. Arterial blood pressure (Finometer), 3-lead electrocardiogram and cerebral blood flow velocity in middle cerebral arteries (transcranial Doppler) were monitored. We assessed CA by transfer function analysis and BRS in frequency and time domain.RESULTS: With increasing age, BRS diminished (ANCOVA R2 = 0.281, p < 0.001) but CA parameters did not change significantly (p > 0.05). Overall, there was an inverse relationship between the efficacy of BRS and CA low-frequency gain [multivariate linear regression β = 0.41 (0.31; 0.61), p < 0.001]. However, this association suffers changes with ageing: in older subjects BRS and CA were not correlated [β = 0.10 (- 0.41; 0.62), p = 0.369]. Instead, decreasing systolic blood pressure correlated with less efficient CA [lower CA low-frequency gain β = - 0.02 (- 0.03; - 0.02), p = 0.003]. Sex did not affect BRS and CA relationship.CONCLUSIONS: Cerebral blood supply is governed by a tuned balance between BR and CA which is lost with age as BRS decreases dramatically. Low systolic blood pressure values might be harmful to older subjects as they might reduce the ability to keep cerebral blood flow tightly controlled.

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Teixeira, Ana Sofia da Cunha. "Ageing affects the balance between central and peripheral mechanisms of cerebrovascular regulation with increasing influence of systolic blood pressure levels". Dissertação, 2019. https://hdl.handle.net/10216/119825.

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Livros sobre o assunto "Cerebrovascular regulation"

Mitagvariia, N. P. Cerebral blood flow regulation. New York: Nova Science Publishers, 2009.

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1924-, Wüllenweber R., Klinger M. 1943- e Brock M. 1938-, eds. Regulation of cerebral blood flow and metabolism ; Neurosurgical treatment of epilepsy ; Rehabilitation in neurosurgery. Berlin: Springer-Verlag, 1987.

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McCulloch, James, e Lars Edvinsson. Peptidergic Mechanisms in the Cerebral Circulation. Wiley & Sons, Incorporated, John, 1987.

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Wullenweber e Klinger. Regulation of Cerebral Blood Flow and Metabolism/Neurosurgical Treatment of Epilepsy/Rehabilitation in Neurosurgery (Deutsche Gesellschaft Fur Neurochirurgie // Proceedings of the Annual Congress). Springer-Verlag, 1987.

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Cerebral Blood Flow in Acute Head Injury: The Regulation of Blood Flow and Metabolism During the Acute Phase of Head Injury, and Its Significance for (Acta Neurochirurgica Supplementum). Springer, 1991.

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Capítulos de livros sobre o assunto "Cerebrovascular regulation"

Dalkara, Turgay, e Michael A. Moskowitz. "Nitric Oxide and Cerebrovascular Regulation". In Biochemical, Pharmacological, and Clinical Aspects of Nitric Oxide, 189–94. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1903-4_23.

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Dalkara, T., e M. A. Moskowitz. "Nitric Oxide in Cerebrovascular Regulation and Ischemia". In Monographs in Clinical Neuroscience, 28–45. Basel: KARGER, 1997. http://dx.doi.org/10.1159/000061570.

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Daley, Michael L., Nithya Narayanan, Charles W. Leffler e Per Kristian Eide. "Stroke with subarachnoid hemorrhage: assessment of cerebrovascular pressure regulation and simulated cerebrovascular resistance". In Acta Neurochirurgica Supplements, 321–25. Vienna: Springer Vienna, 2008. http://dx.doi.org/10.1007/978-3-211-85578-2_61.

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Toda, Noboru, e Tomio Okamura. "Nerve-Derived Nitric Oxide (NO) in the Regulation of Cerebrovascular Function". In Molecular and Cellular Mechanisms of Cardiovascular Regulation, 211–18. Tokyo: Springer Japan, 1996. http://dx.doi.org/10.1007/978-4-431-65952-5_16.

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Katsuki, Hiroshi, e Kosei Matsumoto. "Nicotinic Acetylcholine Receptors in Regulation of Pathology of Cerebrovascular Disorders". In Nicotinic Acetylcholine Receptor Signaling in Neuroprotection, 113–36. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-8488-1_7.

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Moore, Steven A., Elizabeth Yoder, Gretchen Rich, MacKenzie Hilfers e Jeffrey Albright. "Regulation of Cerebrovascular Cyclooxygenase-2 by Pro- and Anti-Inflammatory Cytokines". In Advances in Experimental Medicine and Biology, 125–29. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4793-8_19.

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Macfarlane, R., e M. A. Moskowitz. "The Innervation of Pial Blood Vessels and their Role in Cerebrovascular Regulation". In Brain Ischemia, 247–59. London: Springer London, 1995. http://dx.doi.org/10.1007/978-1-4471-2073-5_25.

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Benyó, Zoltán, Christoph Görlach e Michael Wahl. "Interaction between Nitric Oxide and Thromboxane A2 in the Regulation of the Resting Cerebrovascular Tone". In Advances in Experimental Medicine and Biology, 373–79. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4717-4_45.

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Daley, Michael L., C. W. Leffler, S. Jackson e I. Piper. "Use of Resistance-Area Product Derived from Doppler MCA Velocity to Estimate the Range of Active Cerebrovascular Regulation". In Intracranial Pressure and Brain Biochemical Monitoring, 155–57. Vienna: Springer Vienna, 2002. http://dx.doi.org/10.1007/978-3-7091-6738-0_40.

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Sonntag, William E., Delrae M. Eckman, Jeremy Ingraham e David R. Riddle. "Regulation of Cerebrovascular Aging". In Brain Aging, 279–304. CRC Press, 2007. http://dx.doi.org/10.1201/9781420005523-12.

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Trabalhos de conferências sobre o assunto "Cerebrovascular regulation"

Miller, S., I. Richmond, J. Borgos e K. Mitra. "NIRS-based noninvasive cerebrovascular regulation assessment". In SPIE BiOS, editado por Steen J. Madsen, Victor X. D. Yang, E. Duco Jansen, Qingming Luo, Samarendra K. Mohanty e Nitish V. Thakor. SPIE, 2016. http://dx.doi.org/10.1117/12.2213951.

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"Analysis of methylation of antioxydant-related genes in patiens with common cardio- and cerebrovascular diseases". In Bioinformatics of Genome Regulation and Structure/ Systems Biology. institute of cytology and genetics siberian branch of the russian academy of science, Novosibirsk State University, 2020. http://dx.doi.org/10.18699/bgrs/sb-2020-261.

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Olufsen, Mette S., Lewis A. Lipsitz e Ali Nadim. "A Lumped Parameter Model for Cerebral Blood Flow Regulation". In ASME 2001 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2001. http://dx.doi.org/10.1115/imece2001/bed-23138.

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Abstract Dynamic changes in cerebral blood flow and the associated vascular responses accompanying posture change that enable the brain to maintain perfusion during hypotensive stress are not fully understood. The aim of this work is to use a lumped parameter model of cerebral blood flow to analyze changes in key parameters (systemic and cerebrovascular resistances) during posture change from sitting to standing. Such a model sheds light on vascular adaptation to hypotensive stress, and could ultimately help determine the changes in cerebral autoregulation that occur in aging, hypertension, and other clinical conditions.

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Thunemann, Martin, Kivilcim Kilic, Michele Desjardins, Qun Cheng, Kimberly L. Weldy, Payam A. Saisan, Anders M. Dale e Anna Devor. "Implementation of Deep 2-Photon Microscopy and Optogenetics to Dissect Cell-Type-Specific Mechanisms of Cerebrovascular Regulation". In Bio-Optics: Design and Application. Washington, D.C.: OSA, 2017. http://dx.doi.org/10.1364/boda.2017.jtu4a.15.

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Rakymzhan, Adiya, e Alberto Vazquez. "The Contribution of Cortical Neuronal Populations to Resting-State Cerebrovascular Regulation Revealed by Two-Photon Microscopy Imaging". In Optics and the Brain. Washington, D.C.: Optica Publishing Group, 2023. http://dx.doi.org/10.1364/brain.2023.btu1b.2.

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We recorded calcium activity in excitatory neurons and inhibitory Parvalbumin neurons, while concurrently measuring vascular changes with two-photon imaging. We demonstrate that spontaneous vascular fluctuations are largely modulated by ongoing activity of Parvalbumin neurons.

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Malykhina, Galina, Vyacheslav Salnikov, Vladimir Semenyutin e Dmitriy Tarkhov. "Digitalization of medical services for detecting violations of cerebrovascular regulation based on a neural network signal analysis algorithm". In SPBPU IDE '20: SPBPU IDE-2020. New York, NY, USA: ACM, 2020. http://dx.doi.org/10.1145/3444465.3444526.

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"Molecular mechanisms of cardio- and cerebrovascular comorbidity: from experimental analysis of structural and epigenetic variations in the human genome to post-GWAS analysis of genetic correlations between diseases". In Bioinformatics of Genome Regulation and Structure/Systems Biology (BGRS/SB-2022) :. Institute of Cytology and Genetics, the Siberian Branch of the Russian Academy of Sciences, 2022. http://dx.doi.org/10.18699/sbb-2022-223.

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