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Chodobski, Adam, Brian J. Zink e Joanna Szmydynger-Chodobska. "Blood–Brain Barrier Pathophysiology in Traumatic Brain Injury". Translational Stroke Research 2, n.º 4 (11 de novembro de 2011): 492–516. http://dx.doi.org/10.1007/s12975-011-0125-x.
Dunn, Jeff F., e Albert M. Isaacs. "The impact of hypoxia on blood-brain, blood-CSF, and CSF-brain barriers". Journal of Applied Physiology 131, n.º 3 (1 de setembro de 2021): 977–85. http://dx.doi.org/10.1152/japplphysiol.00108.2020.
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 is known that these other barriers are implicated in damage after hypoxia or inflammation. In the 1950s, it was shown that the rate of radionucleated human serum albumin passage from plasma to CSF was five times higher during hypoxic than normoxic conditions in dogs, due to BCSFB disruption. Severe hypoxia due to administration of the bacterial toxin lipopolysaccharide is associated with disruption of the CSFBB. This review discusses the anatomy of the BBB, BCSFB, and CSFBB and the impact of hypoxia and associated inflammation on the regulation of those barriers.
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McCaffrey, Gwen, e Thomas P. Davis. "Physiology and Pathophysiology of the Blood-Brain Barrier". Journal of Investigative Medicine 60, n.º 8 (1 de dezembro de 2012): 1131–40. http://dx.doi.org/10.2310/jim.0b013e318276de79.
Edvinsson, L., e P. Tfelt-Hansen. "The Blood-Brain Barrier in Migraine Treatment". Cephalalgia 28, n.º 12 (dezembro de 2008): 1245–58. http://dx.doi.org/10.1111/j.1468-2982.2008.01675.x.
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 arteriography method. The drugs, given both luminally and abluminally, provide important notions regarding antimigraine site of action, probably abluminal to the BBB. The problems with the BBB in animal models designed to study the pathophysiology, acute treatment models and preventive treatments are discussed with special emphasize on the triptans and calcitonin gene-related peptide (CGRP). The human experimental headache model, especially the use of glycerol trinitrate (the nitric oxide model), and experiences with CGRP administrations utilize the systemic administration of the agonists with effects on other vascular beds also. We discuss how this can be related to genuine migraine attacks. Our view is that there exists no clear proof of breakdown or leakage of the BBB during migraine attacks, and that antimigraine drugs need to pass the BBB for efficacy.
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Vinters, Harry V., e William M. Pardridge. "The Blood-Brain Barrier in Alzheimer's Disease". Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 13, S4 (novembro de 1986): 446–48. http://dx.doi.org/10.1017/s0317167100037094.
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 are reviewed.
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Khan, Naveed Ahmed. "Acanthamoeba and the blood–brain barrier: the breakthrough". Journal of Medical Microbiology 57, n.º 9 (1 de setembro de 2008): 1051–57. http://dx.doi.org/10.1099/jmm.0.2008/000976-0.
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 blood–brain barrier dysfunction leading to neuropathogenesis.
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Tunkel, A. R., B. Wispelwey, V. J. Quagliarello, S. W. Rosser, A. J. Lesse, E. J. Hansen e W. M. Scheld. "Pathophysiology of Blood-Brain Barrier Alterations during Experimental Haemophilus influenzae Meningitis". Journal of Infectious Diseases 165, Supplement 1 (1 de junho de 1992): S119—S120. http://dx.doi.org/10.1093/infdis/165-supplement_1-s119.
Barichello, Tatiana, Glauco D. Fagundes, Jaqueline S. Generoso, Samuel Galvão Elias, Lutiana R. Simões e Antonio Lucio Teixeira. "Pathophysiology of neonatal acute bacterial meningitis". Journal of Medical Microbiology 62, n.º 12 (1 de dezembro de 2013): 1781–89. http://dx.doi.org/10.1099/jmm.0.059840-0.
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 the activation of NFκB or mitogen-activated protein kinase pathways and subsequently upregulate leukocyte populations and express numerous proteins involved in inflammation and the immune response. Many brain cells can produce cytokines, chemokines and other pro-inflammatory molecules in response to bacterial stimuli, and polymorphonuclear leukocytes are attracted, activated and released in large amounts of superoxide anion and nitric oxide, leading to peroxynitrite formation and generating oxidative stress. This cascade leads to lipid peroxidation, mitochondrial damage and breakdown of the blood–brain barrier, thus contributing to cell injury during neonatal meningitis. This review summarizes information on the pathophysiology and adjuvant treatment of acute bacterial meningitis in neonates.
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Khadka, Bikram, Jae-Young Lee, Ki-Taek Kim e Jong-Sup Bae. "Recent progress in therapeutic drug delivery systems for treatment of traumatic CNS injuries". Future Medicinal Chemistry 12, n.º 19 (outubro de 2020): 1759–78. http://dx.doi.org/10.4155/fmc-2020-0178.
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 biomarkers of traumatic central nervous system injuries (traumatic brain injury and spinal cord injury) are introduced. Furthermore, various drug delivery systems, novel combinatorial therapies and advanced therapies for the treatment of traumatic brain injury and spinal cord injury are emphasized.
Teses / dissertações sobre o assunto "Blood-brain barrier Pathophysiology":
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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.
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 antigen (EBA) and glucose transporter 1 (GLUT1)
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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.
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 usually from a cardiac or large artery source, microatheroma (intrinsic lenticulostriate occlusion) or macroatheroma (parent artery occlusion) all operating primarily via ischaemia. Secondly, there could be an indirect occlusion resulting from vasospasm, endothelial dysfunction or other forms of endovascular damage (e.g. inflammation). Therefore the question of whether the resulting lesions are truly “ischaemic” or actually arise secondary to an alternative process is still under debate. To clarify the chain of pathological events ultimately resulting in lacunar stroke, in this thesis I firstly undertook a systematic assessment of human lacunar stroke pathology literature to determine the information currently available and the quality of these studies (including terminology). The majority of these studies were performed in patients who had died long after their stroke making it difficult to determine the early changes, and there were few patients with a clinically verified lacunar syndrome. Therefore I adopted alternative approaches. In this thesis, I systematically looked for all potential experimental models of lacunar stroke and identified what appears at present to be the most pertinent - the spontaneous pathology of the stroke-prone spontaneously hypertensive rat (SHRSP). However, the cerebral pathology described in this model to date is biased towards end stage pathology, with little information concerning the microvasculature (as opposed to the brain parenchyma) and confounding by use of salt to exacerbate pathology. Therefore, the aim of the experimental work in this thesis was to assess pathological changes within the cerebral vasculature and brain parenchyma of the SHRSP across a variety of ages (particularly young pre-hypertensive animals) and to look at the effects of salt loading on both the SHRSP and its parent strain (the Wistar Kyoto rat - WKY). Three related studies (qualitative and quantitative histology, immunohistochemistry and a microarray study of gene expression confirmed by quantitative PCR), revealed that the presence of inflammation (via significant changes in gene expression in the acute phase response pathway and increased immunostaining of activated microglia and astrocytes) plus alterations in vascular tone regulation, (via genetic alteration of the nitric oxide signaling pathway probably secondary to abnormal oxidative state), impaired structural integrity of the blood brain barrier (histological evidence of endothelial dysfunction and significantly decreased Claudin-5 staining) and reduced plasma oncotic potential (reduced albumin gene expression) are all present in the native SHRSP at 5 weeks of age, i.e. well before the onset of hypertension and without exposure to high levels of salt. We also confirmed previous findings of vessel remodelling at older ages likely as a secondary response to hypertension (thickened arteriolar smooth muscle, increased smooth muscle actin immunostaining). Furthermore, we found not only that salt exacerbated the changes see in the SHRSP at 21 weeks, but also that the control animals (WKY) exposed to a high salt intake developed features of cerebral microvascular pathology independently of hypertension (e.g. white matter vacuolation and significant changes in myelin basic protein expression). In conclusion, via the assessment of the most pertinent experimental model of lacunar stroke currently available, this thesis has provided two very important pieces of evidence: firstly that cerebral small vessel disease is primarily caused by a non-ischaemic mechanism and that any thrombotic vessel lesions occur as secondary end stage pathology; secondly that these features are not simply the consequence of exposure to raised blood pressure but occur secondary to abnormal endothelial integrity, inflammation, abnormal oxidative pathways influencing regulation of vascular tone and low plasma oncotic pressure. Patients with an innate susceptibility to increased blood brain barrier permeability and/or chronic inflammation could therefore have a higher risk of developing small vessel disease pathology and ultimately lacunar stroke and other features of small vessel disease. Research, addressing whether lacunar stroke patients should be treated differently to those with atherothromboembolic stroke is urgently needed.
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Olsen, Aaron L. "Pathophysiology of Abroviral Encephalitides in Laboratory Rodents". DigitalCommons@USU, 2008. https://digitalcommons.usu.edu/etd/123.
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-induced lymphoid cell destruction. It was further concluded that WEEV retains its ability to cause encephalitis in Syrian golden hamsters, if hamsters survive the early stages of virus infection or if virus is introduced directly into the CNS.
Death in WEEV-infected hamsters is associated with lymphonecrotic lesions in the absence of pathological lesions in the central nervous system (CNS). Few clinical parameters were altered by WEEV infection, with the exception of circulating lymphocyte numbers. Circulating lymphocyte numbers decreased dramatically during WEEV infection, and lymphopenia was identified as a consistent indicator of eventual death. Virus infection also increased serum concentrations of the cytokines interferon and tumor necrosis factor-alpha (TNF-alpha).
Hamster peritoneal macrophages exposed to WEEV expressed TNF-alpha in a dose-responsive manner. Macrophage expression of TNF-alpha could be significantly inhibited by treatment of cells with anti-inflammatory agents flunixin meglumine (FM) or dexamethasone (Dex). Anti-inflammatory treatment also protected macrophages from cytotoxicity associated with exposure to WEEV. Treatment of WEEV-infected hamsters with either FM or Dex significantly improved survival compared to placebo-treated controls. WEEV induced cytotoxicity in hamster splenocytes exposed to WEEV in a virus dose-responsive manner. Supernatant from WEEV-exposed macrophages significantly enhanced WEEV killing of splenocytes. Hamsters that survived the early stages of WEEV infection occasionally developed signs of neurological disease and died approximately 6 to 9 d after virus inoculation. These animals had histopathological lesions in the CNS consistent with alphavirus-induced encephalitis. Inoculation of WEEV directly into the CNS caused apparent encephalitic disease. Death following CNS inoculation of WEEV was rapid and concurrent with histopathological lesions in the CNS similar to lesions seen in encephalitic hamsters following peripheral inoculation.
Livros sobre o assunto "Blood-brain barrier Pathophysiology":
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Go, K. G. Cerebral pathophysiology: An integral approach with some emphasis on clinical implications. Amsterdam: Elsevier, 1991.
B, Johansson Barbro, Owman Christer, Widner Håkan e 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.
Johansson, Barbro B., e 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.
Germano, Antonio F., e Francesco Tomasello. Blood-Brain Barrier Permeability Changes after Subarachnoid Haemorrhage: An Update: Clinical Implications, Experimental Findings, Challenges and Future Directions. Springer, 2001.
De La Torre, J. C. 1937- e Hachinski Vladimir, eds. Cerebrovascular pathology in Alzheimer's disease. New York, N.Y: New York Academy of Sciences, 1997.
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.
Capítulos de livros sobre o assunto "Blood-brain barrier Pathophysiology":
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Sharma, Hari Shanker, Per Ove-Sjöquist e 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.
Fenstermacher, Joseph, Ling Wei, Kai-Feng Liu, Tavarekere Nagaraja e 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.
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.
Tripathi, Amit Kumar, Nirav Dhanesha e 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.
Majerova, Petra, e 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.
Germanò, Antonino F., e 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.
Jones, Hazel C., e 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.
Price, Lulit, Christy Wilson e 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.
"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.
Trabalhos de conferências sobre o assunto "Blood-brain barrier Pathophysiology":
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Nakadate, H., S. Akanuma, S. Aomura e 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.
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 presences of transient pressure pulses with impact conditions. Coup pressures measured within a pressurized cadaver head after impact ranged from 34 to 160 kPa, and the contrecoup pressures ranged from −2 to −48 kPa [3]. Pamela et al. tested the effect of overpressure from positive pressure to negative pressure on astrocytes. Pressure wave generated by the barochamber, with high amplitude and short duration in the first pulse [4]. However, there is a lack of information with regards to the effect of impact pressure on endothelial cells in vitro, which are the components of BBB.
