Bibliografías temáticas / Blood-brain barrier Pathophysiology

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Literatura académica sobre el tema "Blood-brain barrier Pathophysiology"

Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 7 de febrero de 2022

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Artículos de revistas sobre el tema "Blood-brain barrier Pathophysiology"

1

Selmaj, Krzysztof. "Pathophysiology of the blood-brain barrier." Springer Seminars in Immunopathology 18, no. 1 (1996): 57–73. http://dx.doi.org/10.1007/bf00792609.

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Chodobski, Adam, Brian J. Zink, and Joanna Szmydynger-Chodobska. "Blood–Brain Barrier Pathophysiology in Traumatic Brain Injury." Translational Stroke Research 2, no. 4 (November 11, 2011): 492–516. http://dx.doi.org/10.1007/s12975-011-0125-x.

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Dunn, Jeff F., and Albert M. Isaacs. "The impact of hypoxia on blood-brain, blood-CSF, and CSF-brain barriers." Journal of Applied Physiology 131, no. 3 (September 1, 2021): 977–85. http://dx.doi.org/10.1152/japplphysiol.00108.2020.

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The blood-brain barrier (BBB), blood-cerebrospinal fluid (CSF) barrier (BCSFB), and CSF-brain barriers (CSFBB) are highly regulated barriers in the central nervous system comprising complex multicellular structures that separate nerves and glia from blood and CSF, respectively. Barrier damage has been implicated in the pathophysiology of diverse hypoxia-related neurological conditions, including stroke, multiple sclerosis, hydrocephalus, and high-altitude cerebral edema. Much is known about the damage to the BBB in response to hypoxia, but much less is known about the BCSFB and CSFBB. Yet, it
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4

McCaffrey, Gwen, and Thomas P. Davis. "Physiology and Pathophysiology of the Blood-Brain Barrier." Journal of Investigative Medicine 60, no. 8 (December 1, 2012): 1131–40. http://dx.doi.org/10.2310/jim.0b013e318276de79.

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Edvinsson, L., and P. Tfelt-Hansen. "The Blood-Brain Barrier in Migraine Treatment." Cephalalgia 28, no. 12 (December 2008): 1245–58. http://dx.doi.org/10.1111/j.1468-2982.2008.01675.x.

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Salient aspects of the anatomy and function of the blood-barrier barrier (BBB) are reviewed in relation to migraine pathophysiology and treatment. The main function of the BBB is to limit the access of circulating substances to the neuropile. Smaller lipophilic substances have some access to the central nervous system by diffusion, whereas other substances can cross the BBB by carrier-mediated influx transport, receptor-mediated transcytosis and absorptive-mediated transcytosis. Studies of drugs relevant to migraine pathophysiology and treatment have been examined with the pressurized arteriog
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6

Vinters, Harry V., and William M. Pardridge. "The Blood-Brain Barrier in Alzheimer's Disease." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 13, S4 (November 1986): 446–48. http://dx.doi.org/10.1017/s0317167100037094.

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Abstract:The current evidence for and against abnormalities of the blood-brain barrier in “normal” aging and Alzheimer's disease is reviewed. Recent studies of cerebral amyloid angiopathy, a microangiopathy commonly observed in Alzheimer's disease and one suggested to result from blood-brain barrier derangement, are discussed with particular attention to the biochemical nature of the vascular amyloid material, and features it shares with the amyloid found in senile plaque cores and with neurofibrillary tangles. Modern techniques that will probably clarify blood-brain barrier pathophysiology ar
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7

Khan, Naveed Ahmed. "Acanthamoeba and the blood–brain barrier: the breakthrough." Journal of Medical Microbiology 57, no. 9 (September 1, 2008): 1051–57. http://dx.doi.org/10.1099/jmm.0.2008/000976-0.

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Acanthamoeba granulomatous encephalitis is a rare disease that almost always proves fatal. Death occurs mainly due to neurological complications; however, the pathogenesis and pathophysiology associated with this disease remain incompletely understood. Haematogenous spread is a key step in the development of Acanthamoeba encephalitis, but it is not clear how circulating amoebae breakthrough the blood–brain barrier to gain entry into the central nervous system to produce the disease. This review of the literature describes the parasite factors and immune-mediated mechanisms involved in the bloo
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Tunkel, A. R., B. Wispelwey, V. J. Quagliarello, S. W. Rosser, A. J. Lesse, E. J. Hansen, and W. M. Scheld. "Pathophysiology of Blood-Brain Barrier Alterations during Experimental Haemophilus influenzae Meningitis." Journal of Infectious Diseases 165, Supplement 1 (June 1, 1992): S119—S120. http://dx.doi.org/10.1093/infdis/165-supplement_1-s119.

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Barichello, Tatiana, Glauco D. Fagundes, Jaqueline S. Generoso, Samuel Galvão Elias, Lutiana R. Simões, and Antonio Lucio Teixeira. "Pathophysiology of neonatal acute bacterial meningitis." Journal of Medical Microbiology 62, no. 12 (December 1, 2013): 1781–89. http://dx.doi.org/10.1099/jmm.0.059840-0.

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Neonatal meningitis is a severe acute infectious disease of the central nervous system and an important cause of morbidity and mortality worldwide. The inflammatory reaction involves the meninges, the subarachnoid space and the brain parenchymal vessels and contributes to neuronal injury. Neonatal meningitis leads to deafness, blindness, cerebral palsy, seizures, hydrocephalus or cognitive impairment in approximately 25–50 % of survivors. Bacterial pathogens can reach the blood–brain barrier and be recognized by antigen-presenting cells through the binding of Toll-like receptors. They induce t
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10

Khadka, Bikram, Jae-Young Lee, Ki-Taek Kim, and Jong-Sup Bae. "Recent progress in therapeutic drug delivery systems for treatment of traumatic CNS injuries." Future Medicinal Chemistry 12, no. 19 (October 2020): 1759–78. http://dx.doi.org/10.4155/fmc-2020-0178.

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Most therapeutics for the treatment of traumatic central nervous system injuries, such as traumatic brain injury and spinal cord injury, encounter various obstacles in reaching the target tissue and exerting pharmacological effects, including physiological barriers like the blood–brain barrier and blood–spinal cord barrier, instability rapid elimination from the injured tissue or cerebrospinal fluid and off-target toxicity. For central nervous system delivery, nano- and microdrug delivery systems are regarded as the most suitable and promising carriers. In this review, the pathophysiology and
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Tesis sobre el tema "Blood-brain barrier Pathophysiology"

1

Zhu, Chunni. "The Blood-brain barrier in normal and pathological conditions." Title page, abstract and contents only, 2001. http://web4.library.adelaide.edu.au/theses/09PH/09phz637.pdf.

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Bibliography: leaves 318-367. Examines the blood-brain barrier in normal and pathological conditions induced by intravascular and extravascular insults. Intravascular insults were induced by administration of Clostridium perfringens prototoxin; extravascular insults were induced by an impact acceleration model for closed head injury to induce traumatic brain injury. Also examines the integrity of the blood-brain barrier ultrastructurally and by its ability to exclude endogenous and exogenous tracers. Also studies the expression of 2 blood-brain barrier specific proteins, endothelial barrier a
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2

Bailey, Emma Louise. "Pathophysiology of lacunar stroke : ischaemic stroke or blood brain barrier dysfunction?" Thesis, University of Edinburgh, 2012. http://hdl.handle.net/1842/6529.

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Lacunar strokes account for approximately a quarter of all ischaemic strokes and traditionally are thought to result from occlusion of a small deep perforating arteriole in the brain. Lacunar infarcts can be up to 2cm in diameter and are found in deep brain structures such as the thalamus and internal capsule. Despite their prevalence and specific accompanying clinical syndromes, the cause of lacunar stroke and its associated vascular pathology remain unclear. Many hypotheses as to the cause exist, which fall broadly into two categories; firstly, a direct occlusion via emboli or thrombus usual
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3

Olsen, Aaron L. "Pathophysiology of Abroviral Encephalitides in Laboratory Rodents." DigitalCommons@USU, 2008. https://digitalcommons.usu.edu/etd/123.

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Western equine encephalitis virus (WEEV) is an arboviral pathogen naturally found in North America. The primary disease phenotype associated with WEEV infection in susceptible hosts is a relatively long prodromal period followed by viral encephalitis. By contrast, in the current work, experimental inoculation of WEEV into the peritoneum of Syrian golden hamsters produced rapid death within approximately 96 h. It was determined that direct virus killing of lymphoid cells leads to death in WEEV-infected Syrian golden hamsters, and that inflammatory cytokines have the potential to enhance virus-i
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Libros sobre el tema "Blood-brain barrier Pathophysiology"

1

Cerebral pathophysiology: An integral approach with some emphasis on clinical implications. Amsterdam: Elsevier, 1991.

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2

Blood-Brain Barrier in Health and Disease: Pathophysiology and Pathology. Taylor & Francis Group, 2015.

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3

B, Johansson Barbro, Owman Christer, Widner Håkan, and Fernstrom Symposium on Pathophysiology of the Blood-Brain Barrier, Long Term Consequences of Barrier Dysfunction for the Brain (1989 : Lund, Sweden), eds. Pathophysiology of the blood-brain barrier: Long term consequences of barrier dysfunction for the brain. Amsterdam: Elsevier, 1990.

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4

Johansson, Barbro B., and Christer Owman. Pathophysiology of the Blood-Brain Barrier: Long Term Consequences of Barrier Dysfunction for the Brain (Fernstrom Foundation Symposium, Vol 14). Elsevier Science Ltd, 1990.

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5

Dorovini-Zis, Katerina. Blood-Brain Barrier in Health and Disease, Volume Two Vol. 2: Pathophysiology and Pathology. Taylor & Francis Group, 2015.

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6

Dorovini-Zis, Katerina. Blood-Brain Barrier in Health and Disease, Volume Two: Pathophysiology and Pathology. Taylor & Francis Group, 2015.

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7

Blood-Brain Barrier Permeability Changes after Subarachnoid Haemorrhage: An Update: Clinical Implications, Experimental Findings, Challenges and Future Directions. Springer, 2001.

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8

De La Torre, J. C. 1937- and Hachinski Vladimir, eds. Cerebrovascular pathology in Alzheimer's disease. New York, N.Y: New York Academy of Sciences, 1997.

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9

Cerebrovascular Pathology in Alzheimer's Disease. Johns Hopkins University Press, 1999.

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10

Sharma, H. S. Pathophysiology of Blood-Brain Barrier, Brain Edema and Cell Injury Following Hyperthermia: New Role of Heat Shock Protein, Nitric Oxide and Carbon: An ... Summaries of Uppsala Dissertations, 830). Uppsala Universitet, 1999.

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Capítulos de libros sobre el tema "Blood-brain barrier Pathophysiology"

1

Sharma, Hari Shanker, Per Ove-Sjöquist, and Jan Westman. "Pathophysiology of the Blood-Spinal Cord Barrier in Spinal Cord Injury." In Blood—Brain Barrier, 401–15. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-0579-2_32.

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Fenstermacher, Joseph, Ling Wei, Kai-Feng Liu, Tavarekere Nagaraja, and Kenneth Davies. "Variations in Neuropathology and Pathophysiology Over Time and Among Areas in a Rat Model of Focal Cerebral Ischemia." In Blood—Brain Barrier, 385–91. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-0579-2_30.

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Selmaj, Krzysztof. "Pathophysiology of the blood-brain barrier." In Immunoneurology, 175–91. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-61191-9_14.

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4

Tripathi, Amit Kumar, Nirav Dhanesha, and Santosh Kumar. "Stroke Induced Blood-Brain Barrier Disruption." In Advancement in the Pathophysiology of Cerebral Stroke, 23–41. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-1453-7_3.

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5

Majerova, Petra, and Andrej Kovac. "Pathophysiology of the Blood–Brain Barrier in Neuroinflammatory Diseases." In The Blood Brain Barrier and Inflammation, 61–79. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-45514-3_4.

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Germanò, Antonino F., and Francesco Tomasello. "Pathophysiology of BBB." In Blood-Brain Barrier Permeability Changes after Subarachnoid Haemorrhage: An Update, 8–18. Vienna: Springer Vienna, 2001. http://dx.doi.org/10.1007/978-3-7091-6194-4_3.

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Jones, Hazel C., and Neil G. Harris. "Pathophysiology and Treatment of Early-Onset Hydrocephalus in a Rat Model." In New Concepts of a Blood—Brain Barrier, 195–207. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4899-1054-7_20.

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Caruso, Gerardo, Lucia Merlo, and Maria Caffo. "Blood–brain barrier pathophysiology in brain tumors." In Innovative Brain Tumor Therapy, 17–33. Elsevier, 2014. http://dx.doi.org/10.1533/9781908818744.17.

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9

Price, Lulit, Christy Wilson, and Gerald Grant. "Blood–Brain Barrier Pathophysiology following Traumatic Brain Injury." In Translational Research in Traumatic Brain Injury, 85–96. CRC Press, 2015. http://dx.doi.org/10.1201/b18959-5.

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"Blood–Brain Barrier Pathophysiology following Traumatic Brain Injury." In Translational Research in Traumatic Brain Injury, 108–19. CRC Press, 2016. http://dx.doi.org/10.1201/b18959-9.

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Actas de conferencias sobre el tema "Blood-brain barrier Pathophysiology"

1

Nakadate, H., S. Akanuma, S. Aomura, and A. Kakuta. "Impact Pressure Increases Permeability of Cultured Human Endothelial Cells." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80117.

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Traumatic brain injury (TBI) is well known to trigger multiple brain parenchymal and vascular responses. The immediate and prolonged opening of blood-brain barrier (BBB) is a hallmark of TBI pathophysiology, and results in extravasation of blood components, including red blood cells, plasma proteins and water (vasogenic edema) [1]. On the other hand, Studies in impact biomechanics have demonstrated a number of brain injury mechanisms [2]. These mechanisms include positive pressures at the impact site, negative pressure at the site opposite of impact. Recently, Hardy et al. demonstrated the pre
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