Relevant bibliographies by topics / Blood-brain barrier

Academic literature on the topic 'Blood-brain barrier'

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Published: 4 June 2021
Last updated: 29 July 2024

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Journal articles on the topic "Blood-brain barrier"

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KANDA, Takashi. "Blood-Brain Barrier and Blood-Nerve Barrier." Yamaguchi Medical Journal 54, no. 1 (2005): 5–11. http://dx.doi.org/10.2342/ymj.54.5.

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Shalaby, Mohamed Adel. "Blood-Brain Barrier." Al-Azhar Medical Journal 45, no. 3 (July 2016): i—vi. http://dx.doi.org/10.12816/0033115.

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Lawther, Bradley K., Sajith Kumar, and Hari Krovvidi. "Blood–brain barrier." Continuing Education in Anaesthesia Critical Care & Pain 11, no. 4 (August 2011): 128–32. http://dx.doi.org/10.1093/bjaceaccp/mkr018.

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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 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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Koziara, J. M., P. R. Lockman, D. D. Allen, and R. J. Mumper. "The Blood-Brain Barrier and Brain Drug Delivery." Journal of Nanoscience and Nanotechnology 6, no. 9 (September 1, 2006): 2712–35. http://dx.doi.org/10.1166/jnn.2006.441.

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The present report encompasses a thorough review of drug delivery to the brain with a particular focus on using drug carriers such as liposomes and nanoparticles. Challenges in brain drug delivery arise from the presence of one of the strictest barriers in vivo—the blood-brain barrier (BBB). This barrier exists at the level of endothelial cells of brain vasculature and its role is to maintain brain homeostasis. To better understand the principles of brain drug delivery, relevant knowledge of the blood-brain barrier anatomy and physiology is briefly reviewed. Several approaches to overcome the BBB have been reviewed including the use of carrier systems. In addition, strategies to enhance brain drug delivery by specific brain targeting are discussed.
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Cho, Choi-Fong. "The Blood-Brain Barrier." Oncology Times 40, no. 2 (January 2018): 1. http://dx.doi.org/10.1097/01.cot.0000530114.97923.aa.

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Mizee, Mark Ronald, and Helga Eveline de Vries. "Blood-brain barrier regulation." Tissue Barriers 1, no. 5 (December 2013): e26882. http://dx.doi.org/10.4161/tisb.26882.

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Dobbing, John. "The Blood-Brain Barrier." Developmental Medicine & Child Neurology 3, no. 6 (November 12, 2008): 610–12. http://dx.doi.org/10.1111/j.1469-8749.1961.tb10430.x.

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Dobbing, John. "The Blood-Brain Barrier." Developmental Medicine & Child Neurology 3, no. 4 (November 12, 2008): 311–14. http://dx.doi.org/10.1111/j.1469-8749.1961.tb15323.x.

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Daneman, Richard, and Alexandre Prat. "The Blood–Brain Barrier." Cold Spring Harbor Perspectives in Biology 7, no. 1 (January 2015): a020412. http://dx.doi.org/10.1101/cshperspect.a020412.

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Dissertations / Theses on the topic "Blood-brain barrier"

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Podjaski, Cornelia. "Netrins enhance blood-brain barrier function and regulate immune responses at the blood-brain barrier." Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=116977.

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During development, netrin guidance cues control cell motility and cell adhesion. Cell-adhesion between endothelial cells at the blood-brain barrier makes the endothelium impermeable to blood-derivatives and immune cells. To establish and maintain this barrier during development, and adulthood, and as well as during disease, brain endothelial cells must develop and sustain these strong adhesive contacts, through expression of tight junction molecules. However, we do not know whether netrins support inter-endothelial cell adhesion at the blood-brain barrier. Given this, we hypothesize that netrin tightens the blood-brain barrier during development, adulthood, and protects it during disease. Methods: To test this, we used both human adult primary brain-derived endothelial cells and newborn netrin-1 knockout mice and evaluated netrin's effect on inter-endothelial cell adhesion and barrier permeability. We also assessed netrins' therapeutic potential to maintain the barrier and limit immune cell infiltration into the central nervous system (CNS) during experimental autoimmune encephalomyelitis (EAE). Results: Our results demonstrate that brain endothelial cells express netrins where they function in three ways. They help to form a tighter blood-brain barrier during development. They also maintain and protect the adult barrier by increasing the expression of endothelial junction molecules, thus promoting inter-endothelial adhesion and reducing protein leakage across the barrier. Netrins also reduce blood-brain barrier breakdown and diminish initial myeloid cell infiltration into the brain and spinal cord during EAE, which delays disease onset and ameliorates disease severity. However, during the chronic phase of EAE, netrin-1 treated mice have higher numbers and more activated T cells in their CNS and exhibit an ataxic gait and limb spasticity. Discussion: We conclude that netrins enhance BBB stability, but have dual functions on immune responses during neuroinflammatory disease. These findings favour the hypothesis that if netrin function was to be manipulated as a therapeutic, early short-term approaches would likely be the most effective.
Au cours du développement, les molécules de la famille des nétrines contribuent à la morphologénèse des organes en contrôlant la motilité et l'adhérence cellulaire. L'adhérence cellulaire entre les cellules endothéliales est une caractéristique importante de la barrière hémato-encéphalique (BHE), ce qui rend l'endothélium imperméable aux molécules sanguines et aux cellules immunitaires. Pour établir et maintenir cette barrière au cours du développement, à l'âge adulte et au cours de la maladie, les cellules endothéliales du cerveau doivent développer et maintenir ces contacts adhésifs en exprimant des molécules de jonction serrées. Cependant, nous ne savons pas si les molécules de la famille des nétrines influencent l'adhérence cellulaire inter-endothéliale de la BHE. Nous avons donc émis l'hypothèse que les nétrines resserrent la BHE au cours du développement, à l'âge adulte, et la protège au cours de la maladie.Méthodes: Pour valider notre hypothèse, nous avons utilisé des cellules endothéliales primaires dérivées des cerveaux humains adultes ou des cerveaux de souris nouveau-nés déficientes en nétrine-1 et évalué l'effet de la nétrine sur l'adhésion cellulaire endothéliale et inter-perméabilité de la barrière. Nous avons également évalué le potentiel thérapeutique des nétrines a restaurer la barrière et l'infiltration de cellules immunitaires limite dans le système nerveux central (SNC) pendant encéphalomyélite allergique expérimentale, un modèle animal de sclérose en plaques. Résultats: Nos résultats démontrent que les nétrines sont exprimées par les cellules endothéliales du cerveau, exprimes nétrines. Au cours du développement les nétrines aident à assurer l'étanchéité de la BHE. Chez les adultes, ils maintiennent et protègent la barrière adulte en augmentant l'expression des molécules de jonctions serrées, favorisant ainsi l'adhérence inter-endothéliale et diminuant les fuites de protéines à travers la BHE. Dans la pathologie de l'EAE, le rôle des nétrins diffère en fonction de la phase de la maladie. Au cours de la phase aigue, les nétrines atténuent la perte de l'intégrité de la BHE et diminuent l'infiltration des cellules myéloïdes dans le SNC. Ceci retarde l'apparition de la maladie et réduit sa sévérité. Au cours de la phase chronique de l'EAE, les souris traitées avec netrin-1 ont un plus grand nombre des cellules T activées dans leurs SNC et présentent une démarche ataxique ainsi qu'une spasticité des membres. Discussion: Nous concluons que les nétrins améliorent la stabilité de la BHE. Ces résultats suggèrent que les nétrines peuvent être envisagée comme agent thérapeutique dans les maladies neuroinflammatoire. Dans ce cas une approche précoce et à court terme serait probablement plus efficace.
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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.

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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 antigen (EBA) and glucose transporter 1 (GLUT1)
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Brownlees, Janet. "Some enzymes of the blood-brain barrier." Thesis, Queen's University Belfast, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.334522.

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Raabe, Rebecca L. "Radiation effects on the blood-brain barrier." Thesis, Massachusetts Institute of Technology, 2007. http://hdl.handle.net/1721.1/44779.

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Thesis (S.M.)--Massachusetts Institute of Technology, Dept. of Nuclear Science and Engineering, 2007.
Includes bibliographical references (p. 53-56).
Selective vascular irradiation enables the critical examination of the vasculature and its role in the onset of late radiation effects. It is a novel approach to expose the endothelial cells to much higher levels of ionizing radiation relative to normal cells by utilizing the boron neutron capture reaction. When boron-containing compounds are restricted to the lumen of the blood vessel, the resulting high-LET alpha and lithium particles cannot deposit their energy in the normal cells beyond the vasculature after the target is exposed to thermal neutrons. This allows for a 2- to 3-fold increase in the calculated dose to the endothelial cells. However, this technique has been criticized because there is no direct evidence that the endothelial cells receive an absorbed dose from the selective vascular irradiation. The objective of this work is to provide corroborating experimental evidence that selective vascular irradiation physically damages the endothelial cells. An established assay utilizing blood-brain barrier disruption was adopted to quantify the radiation damage to the endothelial cells in female BALB/C mice, 8-12 weeks of age. A dye that attaches to the plasma proteins in the blood and that is ordinarily kept out of the brain by the blood-brain barrier is injected into the blood supply before the irradiation, and following irradiation, damage to the vasculature will result in disruption of the blood-brain barrier that allows blood stained with the dye to enter the brain. After sacrificing, the blood in the vessel lumen is cleared by performing a trans-cardiac perfusion, and the brain is homogenized and prepared for analysis. The absorbance of the resulting supernatant of each brain sample is measured with a spectrophotometer at the optimal wavelength of the dye.
(cont.) The absorbance is related to the quantity of blood that leaked through the blood-brain barrier, which is also related to the damage caused to the vasculature from exposure to ionizing radiation. Increased leakage through the blood-brain barrier was observed for those mice exposed to selective vascular irradiation, indicating a direct relationship between the leakage through the blood-brain barrier and the 10B concentration in the blood. The most significant increase in the leakage through the blood-brain barrier (p<0.002) was observed at the highest lOB concentration in the blood (161 ppm). The compound biological effectiveness (CBE) for sulfhydryl borane (BSH) was calculated to be 0.28, which is consistent with the published value of the CBE for BSH in the rat spinal cord. This suggests that the assumptions used for calculating the absorbed doses for selective vascular irradiation are reasonable and approximate to what the endothelial cells receive.
by Rebecca L. Raabe.
S.M.
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Lochhead, Jeffrey James. "Oxidative Stress Alters Blood-Brain Barrier Integrity." Diss., The University of Arizona, 2011. http://hdl.handle.net/10150/193873.

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The blood-brain barrier (BBB) is located at the level of the cerebral microvasculature and is critical to maintain central nervous system (CNS) homeostasis. The tight junction (TJ) protein complexes between endothelial cells at the BBB are primarily responsible for limiting paracellular diffusion of substances from the blood to the CNS. The BBB’s functional integrity is compromised in a number of disease states which affect the CNS, suggesting BBB dysfunction causes or contributes to many diseases of the CNS. A common component of most of these diseases is oxidative stres. Oxidative stress is associated with hypoxia-reoxygenation (HR) and peripheral inflammatory pain (PIP). Both HR and PIP have been shown to compromise BBB functional integrity. Using in vivo rat models of HR and PIP, we examined the role of ROS on BBB permeability as well as the TJ protein occludin using the free radical scavenger tempol. First, we subjected rats to HR with or without pre-treatment with tempol (200 mg/kg). We showed that tempol prevents up-regulation of the cellular stress marker heat shock protein 70 at the BBB during HR. Next we showed tempol reverses HR-mediated BBB permeability increase to ¹⁴C-sucrose, a marker of BBB paracellular permeability. Tempol also attenuated changes in the structure and localization of occludin, suggesting ROS produced during HR alter occludin and lead to disruption of BBB. We then investigated whether ROS production have similar effects on occludin and BBB permeability during PIP by administering 3% λ-carrageenan into the hind paw of rats. We found tempol attenuated carrageenan-induced increase in paw edema and thermal hyperalgesia. Tempol also attenuated up-regulation of the cellular stress marker NF-κB in cerebral microvessels. Tempol significantly decreased BBB permeability to ¹⁴C sucrose during PIP. We found PIP reduces disulfide bonds in occludin oligomeric assemblies thought to be important in maintaining the structural integrity of the BBB. Tempol significantly inhibited disulfide bond reduction, suggesting ROS mediate BBB disruption during inflammatory pain by reducing occludin disulfide bonding. Taken together, these findings show the involvement of ROS during HR and PIP contributes to BBB dysfunction by altering the structure of high molecular weight occludin oligomeric assemblies.
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Arranz, Gibert Pol. "Blood-Brain Barrier Shuttles: From Design to Application." Doctoral thesis, Universitat de Barcelona, 2017. http://hdl.handle.net/10803/401325.

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The work of this thesis is based on research on peptides able to cross the blood-brain barrier and their use as tools to enable the delivery of drugs into the brain. The blood-brain barrier (BBB) is a permeable but selective barrier that tightly regulates the transport into the central nervous system (CNS). In this regard, therapeutic treatments at the CNS are hampered by the presence of this barrier (BBB). Thus, diverse strategies have been developed to overcome it. Blood-brain barrier shuttles are peptides able to cross this barrier and deliver drugs into the brain. Peptides are privileged structures from the therapeutic point of view, they share properties from small organic molecules and large biologics: the synthesis through solid-phase peptide synthesis (SPPS) enables a straightforward method to obtain them with high purity and at the same time they can be purified and characterized like small organic compound. In addition, their structure is present in nature and thus the risk of toxicity is lower or more predictable compared with organic compounds, and their larger structure enables to obtain more selective and stronger interactions with targets. In addition, peptides have been shown to cross the BBB by diverse transport mechanisms and thus enabling to select the best one for each therapy and drug. In this thesis a family of BBB shuttles crossing by passive diffusion (based on phenylproline) have been improved from a parent peptide shuttle (based on N-methyl-phenylalanine). The solubility was three orders of magnitude superior and the transport capacity was maintained upon cargo attachment. In addition, the role of stereochemistry in passive diffusion in biological membranes was demonstrated. A method which combined the use of MALDI-TOF MS and in vitro cell-based models of the BBB enabled the increase in sensitivity for transport quantification of three orders of magnitude compared to RP-HPLC-PDA. Additionally, a BBB shuttle library was evaluated and quantified by this novel methodology. Two new analogs showed better performance when evaluated in these in vitro cell-based models. Immunogenicity of BBB shuttle peptides made by L- or D-amino acids was evaluated and compared. Both peptide shuttles showed low immunogenic response in mice, however, the response to those made with D- amino acids was lower. Finally, the applicability of these peptide shuttles for a therapeutic use was considered for Friedreich’s Ataxia, a monogenic recessive disease. Both a protein replacement therapy and a gene therapy for the central nervous system were attempted by coupling covalently BBB shuttles to the affected protein or viruses, respectively. The protein replacement therapy was impeded by the high rate of proteolysis of the protein used. On the other hand, novel methods of conjugation of BBB shuttles into enveloped viruses (Herpes simplex Virus type 1; HSV- 1) were developed. These modified viral particles were subsequently characterized through a range of methods comprising molecular biology tools (SDS-PAGE, western blots), proteomics (mass spectrometry) and biophysical tools (dynamic light scattering and z-potential).
La barrera hematoencefàlica (BHE) actua com a protecció del sistema nerviós central (SNC) regulant el transport de molècules d’una manera selectiva. Això dificulta el tractament de malalties que afecten al SNC, ja que la BHE també evita que fàrmacs que serien efectius no siguin transportats al cervell. Per això, s’estan desenvolupant mètodes que permetin enviar selectivament fàrmacs a través de la BHE. És el cas dels pèptids llançadora. Aquests es poden dissenyar per creuar per algun dels mecanismes de transport existents en la BHE. En aquesta tesi es desenvolupen uns pèptids que creuen per difusió passiva (basats en fenilprolines), que respecte al disseny anterior (basats en N‐ metilfenilalanines) milloren la solubilitat en aigua en tres ordres de magnitud i al transport un cop s’hi enganxa el fàrmac. Per una altra banda, es desenvolupa una metodologia per a la quantificació del transport basada en la combinació d’espectrometria de masses MALDI‐TOF amb models de BHE in vitro (cel∙lulars), millorant la sensibilitat respecte a la detecció per RP‐HPLC‐PDA en tres ordres de magnitud. L’avaluació d’una peptidoteca derivada d’un pèptid llançadora mitjançant aquesta metodologia permet el descobriment de dos anàlegs del pèptid original que milloren el transport. Addicionalment, s’estudia la immunogenicitat de pèptids llançadora formats per aminoàcids L o D. S’observa que encara que ambdós mostren una baixa immunogenicitat, la resposta dels pèptids amb aminoàcids D és encara menor. Finalment, s’estudia de forma preliminar la possibilitat de desenvolupar una teràpia de reemplaçament proteic i una teràpia gènica per atàxia de Friedreich al SNC mitjançant l’ús de pèptids llançadora.
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Chen, Bo. "Role of blood-brain barrier leakage during stroke." Diss., [La Jolla] : University of California, San Diego, 2010. http://wwwlib.umi.com/cr/ucsd/fullcit?p3403853.

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Edrissi, Hamidreza. "Blood Brain Barrier Dysfunction in Chronic Cerebral Ischemia." Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/32531.

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Cerebral small vessel pathology is now known to be associated with the development of cognitive impairment and mild motor impairments such as gait disturbance in a variety of neurodegenerative diseases. This dissertation explores the hypothesis that blood brain barrier dysfunction is an early event in cerebral ischemia and contributes to the development of cerebral small vessel disease (CSVD). A common rodent model of CSVD is permanent bilateral common carotid artery occlusion in the rat. This model was used to study several aspects of the progression of CSVD including the timecourse of blood brain barrier permeability changes following the onset of ischemia, gait disturbance, the expression of tight junction proteins and cytokine expression. It was determined that BBB permeability was elevated for 2 weeks following BCCAO and ischemic rats displayed lower gait velocity. There was no change in expression of TJ proteins. However, ischemic rats had higher levels of some proinflammatory cytokines and chemokines in brain tissue with no obvious changes in plasma levels. The mechanisms underlying the increase in BBB permeability were studied in vitro using artificial barriers made of confluent rat brain microvascular endothelial cells. Cerebral ischemia has been reported to cause an increase in plasma toxicity, likely by elevating the numbers of circulating microparticles (MPs). MPs isolated from the plasma of ischemic rats were applied to artificial barriers where it was found that they act mainly as vectors of TNF-α signaling. MPs induce activation of caspase-3 and the Rho/Rho kinase pathways. It is concluded that most of the increase in barrier permeability is due to apoptosis and disassembly of actin cytoskeleton and disruption of adherens junctions IV and not an increase in transcellular transport. The effects of treatment with the type III phosphodiesterase inhibitor cilostazol on dye extravasation in the brain, glial activation, white matter damage and motor performance were evaluated. It was determined that cilostazol could improve the increased BBB permeability and gait disturbance and microglial activation in optic tract following BCCAO. Also, the effects of treatment with cilostazol on plasma toxicity in vivo (24h and 14d following BCCAO) and artificial barriers (in vitro) were assessed. It was found that cilostazol could reduce plasma toxicity at 24h and improve increased endothelial barrier permeability that is induced by MP treatment respectively. In summary BBB dysfunction occurs in the rat model of chronic cerebral hypoperfusion with no differences in expression of TJ proteins. There is a mild motor disturbance in the form of lower gait velocity following BCCAO. Cytokines released in brain tissue may be associated with pathological consequences following BCCAO while there is no significant difference in plasma levels and circulating MPs may play a role in BBB dysfunction.
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Owe-Young, Robert School of Medicine UNSW. "Kynurenine pathway metabolism at the blood-brain barrier." Awarded by:University of New South Wales. School of Medicine, 2006. http://handle.unsw.edu.au/1959.4/26183.

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A major product of HIV-infected and cytokine-stimulated monocytic-lineage cells is quinolinic acid (QUIN), a neurotoxic metabolite of the kynurenine pathway (KP) of L-tryptophan (L-Trp) metabolism. Despite the large number of neurotoxins found in HIV patients with AIDS Dementia Complex (ADC), only QUIN correlates with both the presence and severity of ADC. With treatment, cerebrospinal fluid (CSF) QUIN concentrations decrease proportionate to the degree of clinical and neuropsychological improvement. As endothelial cells (EC) of the blood-brain barrier (BBB) are the first brain-associated cell that a bloodborne pathogen would encounter, this project examined the BBB response to KP metabolites, as these are implicated in damage of the CNS associated with ADC. Using RT-PCR and HPLC/gas chromatographymass spectrometry (GC-MS), I found that cultured primary human BBB EC and pericytes constitutively expressed the KP. EC synthesised kynurenic acid (KA) constitutively, and after immune activation, kynurenine (KYN). Pericytes produced small amounts of picolinic acid and after immune activation, KYN. An SV40-transformed BBB EC showed no KP expression. By contrast, human umbilical vein EC only expressed low levels of KA after immune activation, however human dermal microvascular EC showed a similar constitutive and inducible KP to that in BBB EC. As T cells are central to primary HIV infection, I also examined KP expression in two CD4+ and one CD4- cell lines, but none showed either constitutive or inducible KP expression. I next examined how QUIN might interact with BBB EC. There was no binding of 3H-QUIN to cultured primary human BBB EC, however a biologically relevant concentration of QUIN induced changes in gene expression which adversely affected EC function, possibly mediated by lipid peroxidation and oxidative stress. The upregulated genes were of the heat shock protein family, and the downregulated genes were associated with regulation of cell adhesion, tight junction and cytoskeletal stability, metalloproteinase (MMP) regulation, apoptosis and G protein signaling. Immunofluorescence showed that QUIN induced morphological changes in BBB EC consistent with the changes in gene expression. Gelatin zymography showed that this was not mediated by MMPs, as constitutive MMP expression was unchanged. These data provide strong evidence for QUIN directly damaging the BBB in the context of HIV infection.
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Bénardais, Karelle [Verfasser]. "Modulation of the blood-brain barrier / Karelle Bénardais." Hannover : Bibliothek der Tierärztlichen Hochschule Hannover, 2013. http://d-nb.info/1037791665/34.

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Books on the topic "Blood-brain barrier"

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Nag, Sukriti. Blood-Brain Barrier,. New Jersey: Humana Press, 2003. http://dx.doi.org/10.1385/1592594190.

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Kobiler, David, Shlomo Lustig, and Shlomo Shapira, eds. Blood—Brain Barrier. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-0579-2.

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Barichello, Tatiana, ed. Blood-Brain Barrier. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8946-1.

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R, Helio Tomas, ed. The blood brain barrier. New York: Nova Science Publishers, 2008.

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Stone, Nicole, ed. The Blood-Brain Barrier. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2289-6.

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J, Suckling Anthony, Rumsby M. G, and Bradbury M. W. B, eds. The Blood-brain barrier in health and disease. Chichester [Essex], England: E. Horwood, 1986.

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Montenegro, Pedro A. The blood-brain barrier: New research. Hauppauge, N.Y: Nova Science Publishers, 2011.

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Fricker, Gert, Melanie Ott, and Anne Mahringer, eds. The Blood Brain Barrier (BBB). Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-662-43787-2.

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A, Neuwelt Edward, ed. Implicationsof the blood-brain barrier and its manipulation. New York: Plenum Medical, 1989.

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Pierre-Olivier, Couraud, Scherman Daniel, and Cerebral Vascular Biology Symposium (1995 : Paris, France), eds. Biology and physiology of the blood-brain barrier: Transport, cellular interactions, and brain pathologies. New York: Plenum Press, 1996.

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Book chapters on the topic "Blood-brain barrier"

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Tran, Nam. "Blood-Brain Barrier." In Encyclopedia of Clinical Neuropsychology, 601–2. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-57111-9_299.

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Tyrer, Peter J., Mark Slifstein, Joris C. Verster, Kim Fromme, Amee B. Patel, Britta Hahn, Christer Allgulander, et al. "Blood–Brain Barrier." In Encyclopedia of Psychopharmacology, 241–45. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_387.

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Tran, Nam. "Blood-Brain Barrier." In Encyclopedia of Clinical Neuropsychology, 1–2. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56782-2_299-2.

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Scherrmann, Jean-Michel. "Blood–Brain Barrier." In Encyclopedia of Psychopharmacology, 302–8. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-36172-2_387.

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Avraham, Shalom, Tzong-Shi Lu, and Hava Karsenty Avraham. "Blood-Brain Barrier." In Encyclopedia of Cancer, 1–5. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_669-2.

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Alemanno, Fernando. "Blood–Brain Barrier." In Biochemistry for Anesthesiologists and Intensivists, 71–74. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-26721-6_7.

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Leshan, Rebecca, Teri Milner, and Donald W. Pfaff. "Blood-Brain Barrier." In Neuroscience in the 21st Century, 1911–20. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3474-4_129.

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Leshan, Rebecca, Teri Milner, and Donald W. Pfaff. "Blood-Brain Barrier." In Neuroscience in the 21st Century, 1–10. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4614-6434-1_129-3.

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Leshan, Rebecca, Teresa A. Milner, and Donald W. Pfaff. "Blood-Brain Barrier." In Neuroscience in the 21st Century, 1–10. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4614-6434-1_129-4.

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Avraham, Shalom, Tzong-Shi Lu, and Hava Karsenty Avraham. "Blood-Brain Barrier." In Encyclopedia of Cancer, 556–59. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_669.

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Conference papers on the topic "Blood-brain barrier"

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Saharov, D. "CREATION OF IN VITRO MODEL OF HUMAN BLOOD-BRAIN BARRIER, COMPLETELY IDENTIFICAL TO REAL BLOOD-BRAIN BARRIER." In 19th SGEM International Multidisciplinary Scientific GeoConference EXPO Proceedings. STEF92 Technology, 2019. http://dx.doi.org/10.5593/sgem2019/6.1/s24.019.

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Chaing, Ya-Yu, and Kai-Hong Tu. "In Vitro Microfluidics-based Blood–brain Barrier Model." In 2019 IEEE 14th International Conference on Nano/Micro Engineered and Molecular Systems (NEMS). IEEE, 2019. http://dx.doi.org/10.1109/nems.2019.8915667.

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Chen, Dechang, Jianwen Fang, and Jiawei Yu. "Predicting Blood-Brain Barrier Penetration by Stochastic Discrimination." In 2008 International Conference on Biomedical Engineering And Informatics (BMEI). IEEE, 2008. http://dx.doi.org/10.1109/bmei.2008.243.

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Guanglei Li, Wei Yuan, and Bingmei M. Fu. "A transport model for the blood-brain barrier." In 2007 IEEE 33rd Annual Northeast Bioengineering Conference. IEEE, 2007. http://dx.doi.org/10.1109/nebc.2007.4413342.

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Li, Guanglei, Melissa J. Simon, Limary Cancel, Zhong-Dong Shi, Xinyi Ji, John M. Tarbell, Barclay Morrison, and Bingmei M. Fu. "Permeability of in vitro blood-brain barrier models." In 2010 36th Annual Northeast Bioengineering Conference. IEEE, 2010. http://dx.doi.org/10.1109/nebc.2010.5458260.

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Choi, James J. "Noninvasive Blood-Brain Barrier Opening in Live Mice." In THERAPEUTIC ULTRASOUND: 5th International Symposium on Therapeutic Ultrasound. AIP, 2006. http://dx.doi.org/10.1063/1.2205480.

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Hynynen, Kullervo. "Notice of Removal: Breaching the blood-brain barrier noninvasively." In 2017 IEEE International Ultrasonics Symposium (IUS). IEEE, 2017. http://dx.doi.org/10.1109/ultsym.2017.8092834.

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Saharov, D. A. "DEVELOPMENT OF CELLULAR MODEL OF HUMAN BLOOD-BRAIN BARRIER." In 19th SGEM International Multidisciplinary Scientific GeoConference EXPO Proceedings. STEF92 Technology, 2019. http://dx.doi.org/10.5593/sgem2019/6.1/s25.085.

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Kline-Schoder, Alina R., Sana Chintamen, Vilas Menon, Steven G. Kernie, and Elisa E. Konofagou. "Focused-ultrasound blood-brain barrier opening promotes neuroprotective microglia." In 2022 IEEE International Ultrasonics Symposium (IUS). IEEE, 2022. http://dx.doi.org/10.1109/ius54386.2022.9958101.

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Davalos, Dimitrios. "Microglial Responses to Blood Brain Barrier Disruption in Neuroinflammatory Disease." In Optics and the Brain. Washington, D.C.: OSA, 2016. http://dx.doi.org/10.1364/brain.2016.bth3d.5.

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Reports on the topic "Blood-brain barrier"

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Aschner, Michael. Blood-Brain Barrier Transport of Uranium. Fort Belvoir, VA: Defense Technical Information Center, September 2004. http://dx.doi.org/10.21236/ada433990.

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Aschner, Michael. Blood-Brain Barrier Transport of Uranium. Fort Belvoir, VA: Defense Technical Information Center, September 2002. http://dx.doi.org/10.21236/ada412998.

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Aschner, Michael. Blood-Brain Barrier Transport of Uranium. Fort Belvoir, VA: Defense Technical Information Center, September 2003. http://dx.doi.org/10.21236/ada422003.

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Goldman, Harold, and Robert F. Berman. Regional Blood-Brain Barrier Responses to Central Cholinergic Activity. Fort Belvoir, VA: Defense Technical Information Center, June 1991. http://dx.doi.org/10.21236/ada246911.

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Zhang, Luwen. Epstein Barr Virus and Blood Brain Barrier in Multiple Sclerosis. Fort Belvoir, VA: Defense Technical Information Center, July 2013. http://dx.doi.org/10.21236/ada593294.

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Zhang, Luwen. Epstein Barr Virus and Blood Brain Barrier in Multiple Sclerosis. Fort Belvoir, VA: Defense Technical Information Center, January 2014. http://dx.doi.org/10.21236/ada596844.

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Goldstein, L. B., A. M. Dechovskaia, S. Bullman, K. H. Jones, and A. A. Abdel-Rahman. Daily Dermal Co-Exposure of Rats to DEET and Permethrin Produces Sensorimotor Deficit, and Changes in Blood-Brain Barrier (BBB) and Blood-Testis Barrier (BTB). Fort Belvoir, VA: Defense Technical Information Center, March 2001. http://dx.doi.org/10.21236/ada402081.

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Avraham, Hava. Oxidative Stress Increases the Blood Brain Barrier Permeability Resulting in Increased Incidence of Brain Metastasis in BRCA Mutation Carriers. Fort Belvoir, VA: Defense Technical Information Center, February 2013. http://dx.doi.org/10.21236/ada576308.

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Avraham, Hava. Oxidative Stress Increases the Blood Brain Barrier Permeability Resulting in Increased Incidence of Brain Metastasis in BRCA Mutation Carriers. Fort Belvoir, VA: Defense Technical Information Center, February 2012. http://dx.doi.org/10.21236/ada560888.

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Choi, Hannah. The Review of Central Nervous System Drug Delivery Through the Blood Brain Barrier using Nanoparticles for Treatment of Brain Diseases. Ames (Iowa): Iowa State University, May 2023. http://dx.doi.org/10.31274/cc-20240624-1482.

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