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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.
Pełny tekst źródłaAu 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.
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.
Pełny tekst źródłaBrownlees, 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.
Pełny tekst źródłaRaabe, Rebecca L. "Radiation effects on the blood-brain barrier". Thesis, Massachusetts Institute of Technology, 2007. http://hdl.handle.net/1721.1/44779.
Pełny tekst źródłaIncludes 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.
Lochhead, Jeffrey James. "Oxidative Stress Alters Blood-Brain Barrier Integrity". Diss., The University of Arizona, 2011. http://hdl.handle.net/10150/193873.
Pełny tekst źródłaArranz, Gibert Pol. "Blood-Brain Barrier Shuttles: From Design to Application". Doctoral thesis, Universitat de Barcelona, 2017. http://hdl.handle.net/10803/401325.
Pełny tekst źródłaLa 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.
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.
Pełny tekst źródłaEdrissi, Hamidreza. "Blood Brain Barrier Dysfunction in Chronic Cerebral Ischemia". Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/32531.
Pełny tekst źródłaOwe-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.
Pełny tekst źródłaBénardais, Karelle [Verfasser]. "Modulation of the blood-brain barrier / Karelle Bénardais". Hannover : Bibliothek der Tierärztlichen Hochschule Hannover, 2013. http://d-nb.info/1037791665/34.
Pełny tekst źródłaWainwright, Luke. "Mechanisms of coenzyme Q10 blood-brain barrier transport". Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10060760/.
Pełny tekst źródłaKunanandam, Visakasuntharam. "Reverse flow of brain interstitial fluid through venular blood-brain barrier". Thesis, University of Hull, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.363207.
Pełny tekst źródłaSkopin, Mark D. "The Induction of Traumatic Brain Injury by Blood Brain Barrier Disruption". University of Toledo / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1302125115.
Pełny tekst źródłaDaneman, Richard. "How is the blood-brain barrier built? : the cellular and molecular interactions that regulate the formation of the blood-brain barrier /". May be available electronically:, 2008. http://proquest.umi.com/login?COPT=REJTPTU1MTUmSU5UPTAmVkVSPTI=&clientId=12498.
Pełny tekst źródłaHom, Sharon, i Sharon Hom. "Hypoxic/aglycemic stress alters blood-brain barrier transport systems". Thesis, The University of Arizona, 1999. http://hdl.handle.net/10150/627138.
Pełny tekst źródłaSedlakova, Renata. "Ultrastructure of the blood-brain barrier in the rabbit". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq21077.pdf.
Pełny tekst źródłaIvens, Wolf Sebastian [Verfasser]. "Consequences of blood-brain barrier disruption / Wolf Sebastian Ivens". Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2008. http://d-nb.info/1023233320/34.
Pełny tekst źródłaJiménez, Gambín Sergio. "Transcranial Ultrasound Holograms for the Blood-Brain Barrier Opening". Doctoral thesis, Universitat Politècnica de València, 2021. http://hdl.handle.net/10251/171373.
Pełny tekst źródła[CA] El tractament de malalties neurològiques està molt limitat per la ineficient penetració del fàrmac en el teixit cerebral danyat a causa de la barrera hematoencefàlica (BHE), i així no és possible una millora de salut del pacient. La BHE és un mecanisme de protecció natural per a evitar la difusió d'agents potencialment perillosos per al Sistema Nervios Central. No obstant això, aquesta barrera es pot inhibir mitjancant una tecnologia emprada mundialment basada en ultrasons focalitzats i injeccio de microbombolles. El principal avantatge és el seu caràcter no invasiu, sent així molt atractiva i còmoda per al pacient, i permet obrir la BHE de manera segura, localitzada i transitòria. Normalment, la zona cerebral malalta es tracta en la seua part central, emprant un unic focus. No obstant això, malalties com l'Alzheimer o el Parkinson requereixen un tractament al llarg d'estructures de geometria complexa i grandària elevada, situades en tots dos hemisferis cerebrals. Per tant, la tecnologia actual està fortament limitada al no complir amb aquests requeriments. Aquesta tesi doctoral està enfocada a investigar i desenvolupar una tècnica nova, basada en hologrames acústics, per a solucionar les limitacions presents en els tractaments neurològics. Una lent acústica holograca de baix cost impresa en 3D acoblada a un transductor d'element simple permet el control precs del front d'ona ultrasònic punt per a (1) compensar les distorsions que pateix el feix en el seu camí cap al cervell, i (2) focalització simultània del feix en regions multiples i de geometria complexa, proporcionant aix un tractament efectiu en temps i cost. Per això, la investigació desenvolupada en aquesta tesi demostra la possibilitat de realitzar qualsevol tractament neurològic, a més d'aplicacions en la neuroestimulació o l'ablació tèrmica dins del camp biomèdic.
[EN] Treatments for neurological diseases are strongly limited by the inefficient penetration of therapeutic drugs into the diseased brain due to the blood-brain barrier (BBB), and therefore no health improvement can be achieved. In fact, the BBB is a protection mechanism of the human body to avoid the diffusion of potentially dangerous agents into the central nervous system. Nevertheless, this barrier can be successfully inhibited by using a worldwide spread technology based on microbubble-enhanced focused ultrasound. Its main advantage is its non-invasive nature, thus defining a patient-friendly clinical procedure that allows to disrupt the BBB in a safe, local and transient manner. Conventionally, the diseased brain structure has been targeted in its center, with a single focus. However, Alzheimer's or Parkinson's Diseases do require that ultrasound is delivered to entire, complex-geometry and large-volume structures located at both hemispheres of the brain. Therefore, current technology presents several limitations as it does not fulfill these requirements. This doctoral thesis aims to develop a novel technique based on using focused ultrasound acoustic holograms to solve the existing limitations to treat neurological diseases. In this dissertation, we study 3D-printed holographic acoustic lenses coupled to a single-element transducer that allow to accurately control the acoustic wavefront to both (1) compensate distortions suffered by the beam in its path to the brain, and (2) simultaneous focusing in multiple and complex-geometry structures or acoustic vortex generation, providing a time- and cost- efficient procedure. Therefore, the research carried out throughout this thesis opens a promising path in the biomedical field to improve the treatment for neurological diseases, neurostimulation or tissue ablation applications.
Acknowledgments to the Spanish institution Generalitat Valenciana, which funding grant allowed me to develop this doctoral thesis, and as well funded my research stay at Columbia University. The development of the entire thesis was supported through grant Nª. ACIF/2017/045. Particularly, the research carried out in Chapter 3 and Chapter 4 was possible thanks to and supported through grant BEFPI/2019/075. Action co-financied by the Agència Valenciana de la Innovació through grant INNVAL10/19/016 and by the European Union through the Programa Operativo del Fondo Europeo de Desarrollo Regional (FEDER) of the Comunitat Valenciana 2014-2020 (IDIFEDER/2018/022).
Jiménez Gambín, S. (2021). Transcranial Ultrasound Holograms for the Blood-Brain Barrier Opening [Tesis doctoral]. Universitat Politècnica de València. https://doi.org/10.4995/Thesis/10251/171373
TESIS
Silbak, Sadiq H. "Insight into the Regulation of the Blood-Brain Barrier". University of Cincinnati / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1439308364.
Pełny tekst źródłaShelestak, John Wesley. "EVALUATION OF BLOOD-BRAIN BARRIER INTEGRITY UNDER CUPRIZONE ADMINISTRATION". Kent State University / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=kent1574351981114558.
Pełny tekst źródłaMukherjee, Dhritiman V. "Studies in blood-brain barrier disruption in anthrax meningitis". Fairfax, VA : George Mason University, 2009. http://hdl.handle.net/1920/4522.
Pełny tekst źródłaVita: p. 102. Thesis director: Serguei G. Popov. Submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biosciences. Title from PDF t.p. (viewed June 10, 2009). Includes bibliographical references (p. 84-101). Also issued in print.
Tian, Xiaohe. "Screening functionalised polymersomes targeting transcytosis across blood-brain barrier". Thesis, University of Sheffield, 2014. http://etheses.whiterose.ac.uk/6502/.
Pełny tekst źródłaCampos, Christopher Roman. "Central regulation of Blood Brain Barrier integrity during hyperalgesia". Diss., The University of Arizona, 2009. http://hdl.handle.net/10150/195377.
Pełny tekst źródłaHom, Sharon. "Modulation of the Blood-Brain Barrier During Hypertension Development". Diss., The University of Arizona, 2006. http://hdl.handle.net/10150/196090.
Pełny tekst źródłaKaur, Manjit. "Phytochemical mediated modulation of breast cancer resistance protein at the blood brain barrier and blood cerebrospinal fluid barrier". Thesis, Aston University, 2016. http://publications.aston.ac.uk/30065/.
Pełny tekst źródłaCorsi, Mariangela. "Ketogenic diet impacts Blood-Brain Barrier physiology : implications for Alzheimers's disease". Thesis, Artois, 2018. http://www.theses.fr/2018ARTO0401.
Pełny tekst źródłaGiven the current absence of an effective pharmacologic treatment for Alzheimer’s disease (AD), the development of alternative therapeutic approaches (such as the ketogenic diet, KD) might be considered. The KD is a low-carbohydrate, high-fat diet based on the production of ketone bodies (KBs) in the blood. In view of the KD’s beneficial effects on the central nervous system and the lack of published data on the blood brain barrier (BBB), we used an in vivo/in vitro approach to investigate the effect of the KD and KBs on the BBB. For the in vivo study, blood from 129Sv mice was assayed for beta-hydroxybutyrate and glucose dosage. Brain capillaries were isolated from mouse cortices, and RT-qPCR assays were used to evaluate the mRNA expression of transporters/receptors involved in the synthesis and transport of KBs, glucose and beta-amyloid peptide. The mRNA assays were also performed in an in vitro BBB model, based on brain-like endothelial cells (BLECs). After a ketotic state had been established and the BLECs’ integrity had been confirmed, we evaluated the mRNA expression of KB-, glucose- and amyloid-beta-related genes. Lastly, the transport of fluorescently labelled beta-amyloid peptide across the BBB was studied after treatment with KBs. Our results showed that KBs modulate the physiology of the BBB by regulating the expression of certain beta-amyloid peptide transporters/receptors and amyloid peptide-synthesizing enzymes. These data suggest that it is possible to modulate key molecular players in beta-amyloid peptide transport and synthesis at the BBB, and thus open up new perspectives for studying KB-related therapeutic approaches
Chandorkar, Gurudatt Ajay Melethil Srikumaran K. "Mechanisms of blood-brain and blood-cerebrospinal fluid transport of aluminum in rats". Diss., UMK access, 2006.
Znajdź pełny tekst źródła"A dissertation in pharmaceutical sciences and pharmacology." Advisor: Srikumaran Melethil. Typescript. Vita. Title from "catalog record" of the print edition Description based on contents viewed Dec. 20, 2007. Includes bibliographical references (leaves 159-192). Online version of the print edition.
Salagic, Belma. "Regulation of COX-2 signaling in the blood brain barrier". Thesis, Linköping University, Linköping University, Department of Physics, Chemistry and Biology, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-18113.
Pełny tekst źródłaUpon an inflammation the immune system signals the brain by secreted cytokines to elicit central nervous responses such as fever, loss of appetite and secretion of stress hormones. Since the blood brain barrier, (BBB) protects the brain from unwanted material, molecules like cytokines are not allowed to cross the barrier and enter the brain. However, it is clear that they in some way can signal the brain upon an inflammation. Many suggestions concerning this signaling has been made, one being that cytokines bind to receptors on the endothelial cells of the blood vessels of the brain and trigger the production of prostaglandins that can cross the BBB. This conversion is catalyzed by the enzyme cyclooxygenase-2, (COX-2), which is induced by transcription factors like NF-κB in response to cytokines. One of the central nervous responses to inflammatory stimuli is activation of the HPA-axis whose main purpose is glucocorticoid production. Glucocorticoids inhibit the inflammatory response by suppressing gene transcription of pro-inflammatory genes including those producing prostaglandins through direct interference with transcription factors such as NF-κB or initiation of transcription of anti-inflammatory genes like IκB or IL-10. It has however not been clear if glucocorticoids can target the endothelial cells of the brain in order to provide negative feed-back on the immune-to-brain signaling, and in that way inhibit central nervous inflammatory symptoms. An anatomical prerequisite for such a mechanism would be that the induced prostaglandin production occurs in cells expressing GR. This has however never been demonstrated. Here I show that a majority of the brain endothelial cells expressing the prostaglandin synthesizing enzyme COX-2 in response to immune challenge also express the glucocorticoid receptor, (GR). This indicates that immune-to-brain signaling is a target for negative regulation of inflammatory signaling executed by glucocorticoids and identifies brain endothelial GR as a possible future drug target for treatment of central nervous responses to inflammation such as fever and pain.
Bengtsson, Jörgen. "Developmental Aspects of Drug Transport Across the Blood-Brain Barrier". Doctoral thesis, Uppsala universitet, Institutionen för farmaceutisk biovetenskap, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-108374.
Pełny tekst źródłaHau, Vincent Sinh. "EFFECT OF PERIPHERAL INFLAMMATORY PAIN ON THE BLOOD-BRAIN BARRIER". Diss., Tucson, Arizona : University of Arizona, 2005. http://etd.library.arizona.edu/etd/GetFileServlet?file=file:///data1/pdf/etd/azu%5Fetd%5F1071%5F1%5Fm.pdf&type=application/pdf.
Pełny tekst źródłaPesic, Marija. "Visualizing T cell activation around the blood-brain barrier Dissertation". Diss., Ludwig-Maximilians-Universität München, 2013. http://nbn-resolving.de/urn:nbn:de:bvb:19-159898.
Pełny tekst źródłaJelescu, Ileana. "Measuring blood-brain barrier permeability in multiple sclerosis enhancing lesions". Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=95230.
Pełny tekst źródłaLes données d'IRM dynamique avec agent de contraste (DCE-MRI) peuvent être analysées à l'aide d'un modèle pharmaco-cinétique à deux compartiments, afin de mesurer des paramètres biophysiques tels que la perméabilité de la barrière hémato-encéphalique (BHE). Notre étude vise à développer une technique de DCE-MRI qui permette de mesurer avec exactitude la perméabilité de la BHE dans les lésions de sclérose en plaques (SEP). L'impact de la résolution temporelle de l'acquisition sur l'exactitude et la précision des mesures de perméabilité est évalué au moyen d'expériences et de simulations, et un nouveau protocole en deux temps permettant de réduire l'erreur dans les mesures est proposé. Sont analysées ensuite les corrélations entre les cartes de perméabilité et les différences de réhaussement entre deux protocoles non dynamiques: l'un standard et l'autre optimisé. Les résultats préliminaires montrent que les valeurs de perméabilité sont plus basses dans les voxels réhaussés uniquement par le protocole optimisé que dans ceux réhaussés par les deux. Ces résultats soutiennent l'hypothèse d'un seuil de sensibilité intrinsèque à chaque protocole non-dynamique avec contraste. L'utilisation d'une technique quantitative de DCE-MRI, telle que celle présentée ici, apporterait une vision plus complète de la pathologie des lésions de SEP par la mesure de la perméabilité de la BHE, comparée à la classification binaire en régions réhaussant ou non.
Zhang, Bei. "MULTIFACTORIAL MODULATION OF THE BLOOD-BRAIN BARRIER: RELATIONSHIP TO STROKE". UKnowledge, 2013. http://uknowledge.uky.edu/nutrisci_etds/5.
Pełny tekst źródłaSalar, Seda [Verfasser]. "Blood-brain barrier dysfunction and pharmacoresistance of seizures / Seda Salar". Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2016. http://d-nb.info/1082237906/34.
Pełny tekst źródłaKhan, Ehsan Ullah. "The role of P-glycoprotein in the blood-brain barrier". Thesis, King's College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.399264.
Pełny tekst źródłaEgleton, Richard Daniel. "Blood brain barrier changes in animal models of multiple sclerosis". Thesis, King's College London (University of London), 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307652.
Pełny tekst źródłaJanani, Marjaneh. "Models for predicting efflux transport over the blood-brain barrier". Thesis, Uppsala universitet, Institutionen för farmaceutisk biovetenskap, 2020. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-417327.
Pełny tekst źródłaPanagiotou, S. "The role of the blood-brain barrier during pneumococcal meningitis". Thesis, University of Liverpool, 2016. http://livrepository.liverpool.ac.uk/3000478/.
Pełny tekst źródłaVasilache, Ana Maria. "Talking to the Brain at the Blood-Brain Barrier through Inflammation-Induced Prostaglandin E2". Doctoral thesis, Linköpings universitet, Avdelningen för cellbiologi, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-114378.
Pełny tekst źródłaLaufer, Susan R. "Head Trauma Release of Histamine from Dural Mast Cells Alters Blood-Brain Barrier: Attenuation with Zolantidine". Thesis, University of North Texas, 2000. https://digital.library.unt.edu/ark:/67531/metadc2714/.
Pełny tekst źródłaBongo, Manuelle. "Integration of an in vitro blood brain barrier model with organic electrochemical transistors". Thesis, Saint-Etienne, EMSE, 2014. http://www.theses.fr/2014EMSE0753/document.
Pełny tekst źródłaIn biological systems many tissue types have evolved a barrier function to selectively allow the transport of matter from the lumen to the tissue beneath; one example is the Blood Brain Barrier (BBB). The BBB protects the brain from the blood and maintains homeostasis of the brain microenvironment, which is crucial for neuronal activity and function. Characterization of the BBB is very important as its disruption or malfunction is often indicative of toxicity/disease. Though the number of published papers in the field of in vitro BBB has multiplied in recent years, the validity of the models used is still a subject of debate.The advent of organic electronics has created a unique opportunity to interface the worlds of electronics and biology, using devices such as the Organic ElectroChemical Transistor (OECT), which provide a very sensitive way to detect minute ionic currents in an electrolyte as the transistor amplifies the gate current.In this study, we test three different type of BBB in order to develop a stable BBB model. We optimize the adhesion of brain endothelial cell on OECT conducting polymer. We show the integration of OECTs with immortalized human cerebral microvascular endothelial cells as a model of human blood brain barrier, and demonstrate that the barrier tissue function can be detected. Moreover, by this technique, a disruption in the barrier (e.g. caused by a toxic compound) is assessed electrically through a measurement of the drain current. Results show the successful development and validation of an in vitro BBB model. Dynamic monitoring of the barrier properties of the BBB barrier tissue was possible using the OECT
Varanasi, Ramya. "Advancing in-vitro blood-brain barrier models using lipid-based nanoparticles as a strategy for drug delivery". Thesis, The University of Sydney, 2020. https://hdl.handle.net/2123/25558.
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