Добірка наукової літератури з теми "Blood Brain Barriers"
Оформте джерело за APA, MLA, Chicago, Harvard та іншими стилями
Ознайомтеся зі списками актуальних статей, книг, дисертацій, тез та інших наукових джерел на тему "Blood Brain Barriers".
Біля кожної праці в переліку літератури доступна кнопка «Додати до бібліографії». Скористайтеся нею – і ми автоматично оформимо бібліографічне посилання на обрану працю в потрібному вам стилі цитування: APA, MLA, «Гарвард», «Чикаго», «Ванкувер» тощо.
Також ви можете завантажити повний текст наукової публікації у форматі «.pdf» та прочитати онлайн анотацію до роботи, якщо відповідні параметри наявні в метаданих.
Статті в журналах з теми "Blood Brain Barriers"
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.
Повний текст джерелаWood, Heather. "Crossing blood–brain barriers." Nature Reviews Neuroscience 2, no. 1 (January 2001): 8. http://dx.doi.org/10.1038/35049039.
Повний текст джерелаHendricks, Benjamin K., Aaron A. Cohen-Gadol, and James C. Miller. "Novel delivery methods bypassing the blood-brain and blood-tumor barriers." Neurosurgical Focus 38, no. 3 (March 2015): E10. http://dx.doi.org/10.3171/2015.1.focus14767.
Повний текст джерелаRhea, Elizabeth M., Therese S. Salameh, Aric F. Logsdon, Angela J. Hanson, Michelle A. Erickson, and William A. Banks. "Blood-Brain Barriers in Obesity." AAPS Journal 19, no. 4 (April 10, 2017): 921–30. http://dx.doi.org/10.1208/s12248-017-0079-3.
Повний текст джерелаKoziara, 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.
Повний текст джерелаHerold, Schroten, and Schwerk. "Virulence Factors of Meningitis-Causing Bacteria: Enabling Brain Entry across the Blood–Brain Barrier." International Journal of Molecular Sciences 20, no. 21 (October 29, 2019): 5393. http://dx.doi.org/10.3390/ijms20215393.
Повний текст джерелаMcCabe, Shannon Morgan, and Ningning Zhao. "The Potential Roles of Blood–Brain Barrier and Blood–Cerebrospinal Fluid Barrier in Maintaining Brain Manganese Homeostasis." Nutrients 13, no. 6 (May 27, 2021): 1833. http://dx.doi.org/10.3390/nu13061833.
Повний текст джерелаMo, Francesca, Alessia Pellerino, Riccardo Soffietti, and Roberta Rudà. "Blood–Brain Barrier in Brain Tumors: Biology and Clinical Relevance." International Journal of Molecular Sciences 22, no. 23 (November 23, 2021): 12654. http://dx.doi.org/10.3390/ijms222312654.
Повний текст джерелаLANE, NANCY J. "Morphology of Glial Blood-Brain Barriers." Annals of the New York Academy of Sciences 633, no. 1 Glial-Neurona (December 1991): 348–62. http://dx.doi.org/10.1111/j.1749-6632.1991.tb15626.x.
Повний текст джерелаCastro Dias, Mariana, Josephine A. Mapunda, Mykhailo Vladymyrov, and Britta Engelhardt. "Structure and Junctional Complexes of Endothelial, Epithelial and Glial Brain Barriers." International Journal of Molecular Sciences 20, no. 21 (October 29, 2019): 5372. http://dx.doi.org/10.3390/ijms20215372.
Повний текст джерелаДисертації з теми "Blood Brain Barriers"
Abbruscato, Thomas John 1970. "Opioid peptide permeation across the blood-brain and blood-cerebrospinal fluid barriers." Diss., The University of Arizona, 1997. http://hdl.handle.net/10150/282429.
Повний текст джерелаTaylor, Eve Maree. "Transfer of iron across cellular barriers." Thesis, King's College London (University of London), 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.283574.
Повний текст джерелаAryal, Muna. "Transient disruption of vascular barriers using focused ultrasound and microbubbles for targeted drug delivery in the brain." Thesis, Boston College, 2014. http://hdl.handle.net/2345/bc-ir:104127.
Повний текст джерелаThe physiology of the vasculature in the central nervous system (CNS) which includes the blood-brain-barrier (BBB) and other factors, prevents the transport of most anticancer agents to the brain and restricts delivery to infiltrating brain tumors. The heterogeneous vascular permeability in tumor vessels (blood-tumor barrier; BTB), along with several other factors, creates additional hurdles for drug treatment of brain tumors. Different methods have been used to bypass the BBB/BTB, but they have their own limitations such as being invasive, non-targeted or requiring the formulation of new drugs. Magnetic Resonance Imaging guided Focused Ultrasound (MRIgFUS), when combined with circulating microbubbles, is an emerging noninvasive method to temporarily permeabilize the BBB and BTB. The purpose of this thesis was to use this alternative approach to deliver chemotherapeutic agents through the BBB/BTB for brain tumor treatment in a rodent model to overcome the hinderances encountered in prior approaches tested for drug delivery in the CNS. The results presented in thesis demonstrate that MRIgFUS can be used to achieve consistent and reproducible BBB/BTB disruption in rats. It enabled us to achieve clinically-relevant concentrations of doxorubicin (~ 4.8±0.5 µg/g) delivered to the brain with the sonication parameters (0.69 MHz; 0.55 MPa; 10 ms bursts; 1 Hz PRF; 60 s duration), microbubble concentration (Definity, 10 µl/kg), and liposomoal doxorubicin (Lipo-DOX) dose (5.67 mg/kg) used. The resulting doxorubicin concentration was reduced by 32% when the agent was injected 10 minute after the last sonication. Three weekly sessions of FUS and Lipo-DOX appeared to be safe in the rat brain, despite some minor tissue damage. Importantly, the severe neurotoxicity seen in earlier works using other approaches does not appear to occur with delivery via FUS-BBB disruption. The resuls from three weekly treatments of FUS and Lipo-DOX in a rat glioma model are highly promising since they demonstrated that the method significantly inhibits tumor growth and improves survival. Animals that received three weekly sessions of FUS + Lipo-DOX (N = 8) had a median survival time that was increased significantly (P<0.001) compared to animals who received Lipo-DOX only (N = 6), FUS only (N = 8), or no treatment (N = 7). Median survival for animals that received FUS + Lipo-DOX was increased by 100% relative to untreated controls, whereas animals who received Lipo-DOX alone had only a 16% improvement. Animals who received only FUS showed no improvement. No tumor cells were found in histology in 4/8 animals in the FUS + Lipo-DOX group, and only a few tumor cells were detected in two animals. Tumor doxorubicin concentrations increased monotonically (823±600, 1817±732 and 2432±448 ng/g) in the control tumors at 9, 14 and 17 days respectively after administration of Lipo-DOX. With FUS-induced BTB disruption, the doxorubicin concentrations were enhanced significantly (P<0.05, P<0.01, and P<0.0001 at days 9, 14, and 17, respectively) and were greater than the control tumors by a factor of two or more (2222±784, 3687±796 and 5658±821 ng/g) regardless of the stage of tumor growth. The transfer coefficient Ktrans was significantly (p<0.05) enhanced compared to control tumors only at day 9 but not at day 14 or 17. These results suggest that FUS-induced enhancements in tumor drug delivery for Lipo-DOX are relatively consistent over time, at least in this tumor model. These results are encouraging for the use of large drug carriers, as they suggest that even large/late-stage tumors can benefit from FUS-induced drug enhancement. Corresponding enhancements in Ktrans were found variable in large/late-stage tumors and not significantly different than controls, perhaps reflecting the size mismatch between the liposomal drug (~100 nm) and Gd-DTPA (molecular weight: 938 Da). Overall, this thesis research provides pre-clinical data toward the development of MRIgFUS as a noninvasive method for the delivery of agents such as Lipo-DOX across the BBB/BTB to treat patients with diseases of the central nervous system
Thesis (PhD) — Boston College, 2014
Submitted to: Boston College. Graduate School of Arts and Sciences
Discipline: Physics
Gazzin, Silvia. "Effect of bilirubin on expression and localization of PGP and Mrp1 in the central nervous system." Doctoral thesis, Università degli studi di Trieste, 2008. http://hdl.handle.net/10077/2625.
Повний текст джерелаINTRODUZIONE A basse concentrazioni la bilirubina non coniugata (unconjugated bilirubin, UCB) prodotta dalla degradazione dell’emoglobina, sembra essere un potente anti-ossidante, mentre è estremamente dannosa ad alte concentrazioni, causando encefalopatia nei neonati con severo ittero. Il 70% dei bambini che presentano kernittero muoiono entro sette giorni di vita, mentre il 30% dei sopravvissuti manifesta irreversibili conseguenze come sordità, ritardo mentale e danni cerebrali permanenti. L’encefalopatia dovuta ad alti livelli di bilirubina rappresenta oggi la maggior causa di riammissione ospedaliera nei neonati entro il primo mese di vita. Storicamente gli studi riguardanti le modalità di ingresso della bilirubina nel sistema nervoso centrale si sono concentrati sulla barriera emato-encefalica (blood brain barrier, BBB), costituita dai microvasi e dai capillari del cervello (micro vessels, MV). Tali studi hanno dimostrato come solamente la bilirubina non coniugata e non legata all’albumina del sangue, definita “bilirubina libera” (free bilirubin, Bf) sia capace di attraversare le membrane cellulari e diffondere nel tessuto. Tuttavia i microvasi non sono l’unica interfaccia sangue-tessuto presente nel cervello. Una seconda barriera è costituita dai plessi coroidei (CP). Questi, collocati nei ventricoli del cervello, mediano il passaggio delle molecole dal sangue al liquido cefalorachidiano e viceversa, posseggono una ampia superficie di scambio, il più alto flusso sanguigno del sistema nervoso centrale ed un fenotipo barriera meno restrittivo rispetto ai microvasi del parenchima. L’ingresso della bilirubina nel cervello sembra essere attivamente controllato da due trasportatori appartenenti alla famiglia delle “ATP dependent transporters”, Mrp1 e Pgp. Tali trasportatori potrebbero mantenere bassa la concentrazione della bilirubina limitandone l’ ingresso a livello di barriere o agendo direttamente a livello delle cellule del parenchima. Nonostante l’ impatto di questi trasportatori sulla disponibilità nel sistema nervoso centrale non solo della bilirubina ma egualmente di atre molecole potenzialmente tossiche, così come dei principi attivi, la loro espressione e localizzazione nelle interfacce sangue-cervello non sono del tutto chiare. Per tali motivi il lavoro di questi tre anni di tersi è stato incentrato a: Ia) chiarire il livello di espressione proteica relativa di Mrp1 e Pgp nelle due principali barriere cerebrali, la BBB (blood brain barrier, barriera emano encefalica) e la BCSFB (blood CerebroSpinal Fluid barrier, barriera emato liquorale); Ib) Definire l’andamento della loro espressione nel corso dello sviluppo post-natale in situazione fisiologica. II) Valutare l’effetto di elevati livelli serici di bilirubina sull’espressione di Mrp1 e Pgp nelle barriere emato encefaliche, come prima linea di difesa verso la bilirubina nel kernittero. Per raggiungere questo secondo obiettivo abbiamo utilizzato il ratto Gunn, considerato il modello in vivo per la sindrome di Crigler-Najjar e il kernittero. I ratti Gunn presentano elevati livelli di bilirubina serica ed un quadro clinico simile a quanto si riscontra nell’uomo. L’iperbilirubinemia, nel ratto, è dovuta ad una mutazione nell’enzima responsabile della coniugazione del pigmento, passaggio fondamentale per la sua successiva eliminazione. Nell’omozigote (jj) la bilirubina totale nel sangue (TBS) è molte volte più alta che nell’eterozigote (Jj) in cui l’allele non mutato codifica per l’enzima nella sua forma attiva, sufficiente a mantenere livelli di bilirubina normali. RISULTATI Ia) Attraverso una quantificazione relativa dell’ espressione proteica, ottenuta tramite Western blot, abbiamo dimostrato una espressione speculare dei due trasportatori nelle interacce sangue cervello. Mentre i microvasi sono caratterizzati dalla forte espressione di Pgp, ed i livelli di Mrp1 sono 15-20 volte inferiori rispetto ai plessi, questi ultimi presentano una elevata espressione di Mrp1 ed una quasi completa assenza di Pgp. Per quanto riguarda l’espressione di Mrp1 nei plessi coroidei (CP), abbiamo potuto evidenziare una differenza, con la massima espressione nel plesso del 4° ventricolo rispetto ai ventricoli laterali. Tramite immunofluorescenza abbiamo poi evidenziato per entrambe i trasportatori una localizzazione lato sangue, con Pgp luminale nei vasi e Mrp1 baso-laterale nel plessi coroidei. Ib) Anche l’andamento dell’espressione durane lo sviluppo post-natale differisce. Mentre Mrp1 è sin dalla nascita (2 giorni di vita) altamente espresso in entrambe le barriere, Pgp è inizialmente espresso a livelli più bassi (4,6 volte meno) rispetto all’ adulto (60 giorni). Contemporaneamente anche la densità dei vasi nel parenchima aumenta. II) Nel modello iperbilirubinemico rappresentato dal ratto Gunn, la TBS (jj) e molte volte più alta che nell’ eterozigote (Jj) e tale differenza permane per tutto l’arco di tempo esaminato (0-60 giorni dalla nascita). Al contrario la bilirubina libera (calcolata) è elevata solo nelle prime due settimane di vita, quando il rapporto bilirubina-albumina nel sangue è superiore all’unità. Poi, il rapido aumento della concentrazione ematica di albumina determina un significativo calo della Bf. Mentre l’analisi degli effetti (macroscopici) dell’iperbilirubinemia sullo sviluppo degli emisferi cerebrali non evidenzia differenze tra Jj e jj; in questi ultimi la crescita del cervelletto è severamente inibita. Già a 17 giorni di vita l’ipoplasia del cervelletto si manifesta con una differenza nel peso del 50% nei jj rispetto agli animali normo bilirubinemici di pari età. Durante tale periodo anche l’espressione dei due trasportatori nelle barriere è modificata. L’espressione proteica di Pgp nella BBB degli animali iperbilirubinemici è aumentata ad ogni età presa in esame. Tuttavia tale incremento non modifica in maniera importante la quantità del trasportatore nei MV durante lo sviluppo post natale, rimanendo quindi poco espresso (5 volte meno rispetto all’adulto) almeno fino ai 17 giorni di vita. Contemporaneamente la presenza Mrp1 nella BCSFB è inibita. Già a 9 giorni nel plesso del 4° ventricolo Mrp1 è il 50% rispetto al controllo (pari età, Jj). Anche se nei plessi dei ventricoli laterali l’inibizione dell’espressione è inferiore, nell’insieme la quantità di Mrp1 è fortemente ridotta negli animali iperbilirubinemici. Contrariamente, nei ratti Jj, Mrp1 ha un andamento simile a quello descritto nella sezione (Ib). CONCLUSIONI I risultati da noi ottenuti sottolineano importanti differenze tra le due barriere. La barriera emato-encefalica si sviluppa durante il primo periodo post-natale, in un ambiente caratterizzato dalla forte presenza di membrane cellulari. Similarmente l’espressione di Pgp è inizialmente bassa ed incrementa molto durante lo sviluppo post-natale. Al contrario I plessi coroidei appaiono precocemente in età embrionale, contribuiscono allo sviluppo del cervello e posseggono il più alta espressione di enzimi di fase II, coinvolti nel metabolismo di potenziali sostanze tossiche, del cervello. Un alto livello di Mrp1 sin dalla nascita suggerisce un suo coinvolgimento nel trasporto di qualche sostanza importante nello sviluppo del cervello o in un suo precoce coinvolgimento nel mantenimento dello stato ossido riduttivo, o nell’eliminazione di metabolici dal sistema nervoso centrale. Elevati livelli di bilirubina, come nel modello Gunn, modulano sia l’espressione di Pgp nella BBB, che di Mrp1 nella BCSFB. Tuttavia l’incremento nell’espressione di Pgp nei microvasi non sembra essere sufficiente a contrastare efficacemente l’ingresso della bilirubina libera, molto elevata fino al 17 giorno di vita. La simultanea riduzione di Mrp1 nei plessi coroidei, può facilitare l’ingresso o ridurre l’efflusso della bilirubina nel liquido cefalo rachidiano, consentendo l’accumulo e conseguente danno dei tessuti esposti.
................................................................ ....................... .. .BACKGROUND The unconjugated bilirubin (UCB), a heme degradation product, has been suggested to be a potent antioxidant at low concentration while it seems to be extremely dangerous at higher concentrations, causing encephalopathy in severely jaundiced neonates. Around 70% of children with kernicterus die within seven days, while the 30% survivors usually suffer irreversible sequels, including hearing loss, paralysis of upward gaze, mental retardation, and cerebral palsy with athetosis. Bilirubin encephalopathy is actually the leading cause of hospital readmission of newborns within the first month after birth. Historically the studies concerning the bilirubin entry the central nervous system have focused on the blood brain barrier (BBB), located at the level of the endothelial cells forming the brain micro vessels (MV), leading to the “free bilirubin theory”. It consists in the idea that only the free unconjugated bilirubin, the part of bilirubin exceeding the binding ability of the serum albumin, is able to cross the cell membranes and diffuse in tissue. In brain a second blood brain barrier is present. It is located at the level of the epithelial cells forming the choroids plexuses, between the blood and the cerebrospinal fluid (blood-cerebrospinal fluid barrier, BCSFB). Despite the largest surface area available for the exchanges, the high blood flux, the strategically position between two circulating fluids and the more leaky phenotype, limited studies have been made concerning its role in limiting the bilirubin entry the brain. Two ATP dependent transporters, the Multidrug Resistance-associated Protein 1 (Mrp1) and the MultiDrug resistance Protein (Pgpor MDR1), appear to be actively involved in UCB trafficking. The transporters play an important role in keeping extra cellular bilirubin concentration, such as potentially toxic compounds, below toxic levels by limiting the entry of UCB from blood to brain, or else in controlling intracellular bilirubin levels in parenchyma cells. Despite the importance of Mrp1 and Pgp on BBI their pattern of expression and cellular localization remains still unsettled. Based on these considerations - The first aim of the thesis was clarify the relative protein expression of these transporters at the two major BBI protecting the brain from toxic insults (Ia), and to identify their post-natal developmental profile of expression and cellular localisation (Ib). Similarly, no data about the Mrp1 and Pgp expression on BBI during the bilirubin encephalopathy are available. - The second aim of the thesis was investigate a relation between the high level of blood bilirubin and Mrp1 and Pgp expression in brain barriers in vivo using the Gunn rat (II), in witch the symptoms closely correlate to the human kernicterus and Crigler-Najjar syndrome type I. In this animal model, a mutation in the enzyme responsible for the conjugation and subsequent elimination of bilirubin, leads to the total absence of the enzymatic activity in the homozygous animals (jj), causing a severe life long hyperbilirubinemia. In the heterozygous Gunn rats (Jj), the enzymatic activity, until if reduced, is present and result in normal serum bilirubin levels. RESULTS Ia) By quantitative Western blot, we have demonstrated a mirroring expression of the two transporters at the blood brain interfaces in the adult rat. On the BBB the Pgp is strongly expressed and the Mrp1 amount is 15-20 times lower than in CPs. At the contrary, the CPs are characterized by the high expression of Mrp1, with a difference between the lateral ventricle (LV) and the 4th ventricle (4thV) CP, the former being a lower Mrp1 expression than in the last. In both LV and 4thV CPs, Pgp is virtually absent. By immunofluorescence we revealed that both ABC transporters are located at the blood side, the Pgp luminal on MV, and Mrp1 basal on CPs. Ib) With respect to the post-natal development, the Mrp1 expression is high since the early post-natal age and do not change significantly from birth to adult life in both barriers. By contrast, Pgp expression is weak a P9 and increase 4.6 fold with maturation on MV. Synchronously the density of Pgp stained MV in parenchyma seems increasing. II) In the homozygous Gunn rat (jj) the total bilirubin in serum is several time higher than in the heterozygous (Jj) animals all life long. By contrast the (calculated) free bilirubin is extremely elevated until the first week of life, when the bilirubin-albumin ratio exceed the unit, then drop due to the developmental increasing albumin concentration in blood. While no differences in Cx weight have been found between Jj and jj rat at every postnatal age, the cerebellum development is strongly impaired by the bilirubin toxic effect, displaying a Summarymarked hypoplasia, with about the 50% of weight loss respect the Jj control at 17 days after the birth. Concerning the ABC transporters, the differential pattern of expression between blood brain interfaces is maintained. But, in jj Gunn rats, the Pgp expression at the BBB is up-regulated at every post natal age analysed, also if this increase do not seems to be sufficient to confer protection at list until P17, when the amount of the transporter in the MV is about 5 times lower than in adult (P60). At the same time the Mrp1 expression on the BCSFB is down regulated. Since P9 the amount of Mrp1 in the 4thV CP of jj rats drops around to the 50% respect the amount in the littermates. In the LV CP the decrease is less marked, but in any case the Mrp1expression in both CPs is strongly impaired. This down regulation seems to be post-transcriptional. In the Jj animals, the Mrp1 relative expression is already high in both plexuses at early postnatal stages. A significant difference was noted only between LV CP (76%) and 4thV CP at P60 (100%). CONCLUSIONS All together these results indicate that the two barriers differ: The BBB develops after the birth and is surrounded by the lipid rich parenchyma environment, in agreement with the transporter preference for the lipid compounds and the strong post-natal developmental increase of the Pgp amount on MV. The CPs develops early in the foetal life, are involved in the guidance of the brain development and posses the highest phase II metabolising enzymes in the brain. The Mrp1 amount in CPs is similar to the adult level since the birth and may be involved in the transport of some compounds important in the brain development, in the detoxification or in the maintenance of the redox state (GS- sulfo- conjugates, LC4, etc.). In Gunn rats, as model for Kernicterus and Crigler-Najjar syndrome type I, the Pgp offered protection is not sufficiently modulate until P17, when the amount of the free bilirubin is elevated and could cross the brain barriers. The simultaneously down regulation of Mrp1 at the BCSFB may facilitate the entry of the bilirubin or strongly impair their clearance in the central nervous system, leading to the accumulation in brain and subsequent damage of tissue.
1974
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.
Повний текст джерелаPodjaski, 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.
Повний текст джерелаAu 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.
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.
Повний текст джерелаRaabe, Rebecca L. "Radiation effects on the blood-brain barrier." Thesis, Massachusetts Institute of Technology, 2007. http://hdl.handle.net/1721.1/44779.
Повний текст джерелаIncludes 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.
Повний текст джерелаBongo, 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.
Повний текст джерелаIn 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
Книги з теми "Blood Brain Barriers"
Nag, Sukriti, ed. The Blood-Brain and Other Neural Barriers. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-60761-938-3.
Повний текст джерелаRolf, Dermietzel, Spray David C, and Nedergaard Maiken, eds. Blood-brain barriers: From ontogeny to artificial interfaces. Weinheim: Wiley-VCH, 2006.
Знайти повний текст джерелаBiology and regulation of blood-tissue barriers. New York, N.Y: Springer Science+Business Media, 2012.
Знайти повний текст джерелаThe blood-brain and other neural barriers: Reviews and protocols. New York, N.Y: Humana Press, 2011.
Знайти повний текст джерелаDavson, Hugh. Physiology of the CSF and blood-brain barriers. Boca Raton: CRC Press, 1996.
Знайти повний текст джерелаCheng, C. Yan. Biology and regulation of blood-tissue barriers. New York, N.Y: Springer Science+Business Media, 2012.
Знайти повний текст джерелаKlaus, Felgenhauer, Holzgraefe Manfred, Prange Hilmar W, and International Quincke Symposium "Barrier Concepts and Cerebrospinal Fluid Analysis" (1991 : Göttingen, Germany), eds. CNS barriers and modern CSF diagnostics. Weinheim: VCH, 1993.
Знайти повний текст джерелаB, Segal Malcolm, ed. Barriers and fluids of the eye and brain. Boca Raton, Fl., U.S.A: CRC Press, 1992.
Знайти повний текст джерелаA, Neuwelt Edward, ed. Implicationsof the blood-brain barrier and its manipulation. New York: Plenum Medical, 1989.
Знайти повний текст джерела1948-, Neuwelt Edward A., ed. Implications of the blood-brain barrier and its manipulation. New York: Plenum Medical Book Co., 1989.
Знайти повний текст джерелаЧастини книг з теми "Blood Brain Barriers"
Dienel, Gerald A. "Functional Brain Imaging." In Blood-Brain Barriers, 551–99. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2007. http://dx.doi.org/10.1002/9783527611225.ch23.
Повний текст джерелаDermietzel, Rolf, David C. Spray, and Maiken Nedergaard. "Introduction: The Blood-Brain Barrier: An Integrated Concept." In Blood-Brain Barriers, 1–8. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2007. http://dx.doi.org/10.1002/9783527611225.ch.
Повний текст джерелаEngelhardt, Britta. "Development of the Blood-Brain Interface." In Blood-Brain Barriers, 9–39. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2007. http://dx.doi.org/10.1002/9783527611225.ch1.
Повний текст джерелаReuss, Bernhard. "The Role of Fibroblast Growth Factor 2 in the Establishment and Maintenance of the Blood-Brain Barrier." In Blood-Brain Barriers, 237–46. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2007. http://dx.doi.org/10.1002/9783527611225.ch10.
Повний текст джерелаPan, Weihong, Shulin Xiang, Hong Tu, and Abba J. Kastin. "Cytokines Interact with the Blood-Brain Barrier." In Blood-Brain Barriers, 247–64. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2007. http://dx.doi.org/10.1002/9783527611225.ch11.
Повний текст джерелаBanks, William A., and Wee Shiong Lim. "Insulin and the Blood-Brain Barrier." In Blood-Brain Barriers, 265–85. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2007. http://dx.doi.org/10.1002/9783527611225.ch12.
Повний текст джерелаDietrich, Jean-Bernard. "Glucocorticoid Hormones and Estrogens: Their Interaction with the Endothelial Cells of the Blood-Brain Barrier." In Blood-Brain Barriers, 287–312. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2007. http://dx.doi.org/10.1002/9783527611225.ch13.
Повний текст джерелаKrause, Dorothee, and Christina Lohmann. "Metalloproteinases and the Brain Microvasculature." In Blood-Brain Barriers, 313–34. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2007. http://dx.doi.org/10.1002/9783527611225.ch14.
Повний текст джерелаCecchelli, Roméo, Caroline Coisne, Lucie Dehouck, Florence Miller, Marie-Pierre Dehouck, Valérie Buée-Scherrer, and Bénédicte Dehouck. "Modeling the Blood-Brain Barrier." In Blood-Brain Barriers, 335–55. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2007. http://dx.doi.org/10.1002/9783527611225.ch15.
Повний текст джерелаZozulya, Alla, Christian Weidenfeller, and Hans-Joachim Galla. "Induction of Blood-Brain Barrier Properties in Cultured Endothelial Cells." In Blood-Brain Barriers, 357–74. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2007. http://dx.doi.org/10.1002/9783527611225.ch16.
Повний текст джерелаТези доповідей конференцій з теми "Blood Brain Barriers"
Belyaeva, Anastasia, Vladimir Chrishtop, and Sofia Morozova. "Biopolymers based membranes for imitation blood-brain barriers." In 1st International Electronic Conference on Applied Sciences. Basel, Switzerland: MDPI, 2020. http://dx.doi.org/10.3390/asec2020-07559.
Повний текст джерелаUmans, Robyn A., Hannah E. Henson, Chaithanyarani Parupalli, Bensheng Ju, and Michael R. Taylor. "Abstract IA19: Modeling blood-CNS barriers in zebrafish." In Abstracts: AACR Special Conference: Advances in Brain Cancer Research; May 27-30, 2015; Washington, DC. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.brain15-ia19.
Повний текст джерелаZhukov, D. "ULTRATHIN MEMBRANES FOR ESTABLISHMENT OF PHYSIOLOGICALLY RELEVANT CELL BARRIERS. FOCUS ON BLOOD-BRAIN BARRIER." In 19th SGEM International Multidisciplinary Scientific GeoConference EXPO Proceedings. STEF92 Technology, 2019. http://dx.doi.org/10.5593/sgem2019/6.1/s24.062.
Повний текст джерелаQuispe, Rodrigo, Jorge A. Trevino, Faizan Khan, and Vera Novak. "Strategies for nose-to-brain drug delivery." In the 8th International Workshop on Innovative Simulation for Healthcare. CAL-TEK srl, 2019. http://dx.doi.org/10.46354/i3m.2019.iwish.017.
Повний текст джерелаFiciara, E., F. D'Agata, S. Cattaldo, L. Priano, A. Mauro, and C. Guiot. "A Compartmental Model for the Iron Trafficking Across the Blood-Brain Barriers in Neurodegenerative Diseases." In 2021 43rd Annual International Conference of the IEEE Engineering in Medicine & Biology Society (EMBC). IEEE, 2021. http://dx.doi.org/10.1109/embc46164.2021.9629893.
Повний текст джерелаDavalos, 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.
Повний текст джерелаMilej, Daniel, Androu Abdalmalak, Hassan Ahmed, Mamadou Diop, Ting-Yim Lee, and Keith St Lawrence. "Quantification of blood–brain barrier permeability by time-resolved NIRS." In Optics and the Brain. Washington, D.C.: OSA, 2016. http://dx.doi.org/10.1364/brain.2016.ptu3a.2.
Повний текст джерелаMaia, Lucas Henrique, Thaís Galdino Diniz, Vitor Carvalho Caetano, Marina Gomes Diniz, Pedro Lucas Bessa dos Reis, Gabriela Vieira Marques da Costa Leão, Vitor Moreira Nunes, and Helton José dos Reis. "Antibiotic therapy as a risk factor in Parkinson’s disease." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.521.
Повний текст джерелаSaharov, 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.
Повний текст джерелаBell, E. David, Rahul S. Kunjir, and Kenneth L. Monson. "Biaxial and Failure Mechanical Properties of Passive Rat Middle Cerebral Arteries." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53830.
Повний текст джерелаЗвіти організацій з теми "Blood Brain Barriers"
Aschner, Michael. Blood-Brain Barrier Transport of Uranium. Fort Belvoir, VA: Defense Technical Information Center, September 2004. http://dx.doi.org/10.21236/ada433990.
Повний текст джерелаAschner, Michael. Blood-Brain Barrier Transport of Uranium. Fort Belvoir, VA: Defense Technical Information Center, September 2002. http://dx.doi.org/10.21236/ada412998.
Повний текст джерелаAschner, Michael. Blood-Brain Barrier Transport of Uranium. Fort Belvoir, VA: Defense Technical Information Center, September 2003. http://dx.doi.org/10.21236/ada422003.
Повний текст джерелаGoldman, 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.
Повний текст джерелаZhang, 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.
Повний текст джерелаZhang, 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.
Повний текст джерелаPaul, Satashree. Flavivirus and its Threat. Science Repository, March 2021. http://dx.doi.org/10.31487/sr.blog.30.
Повний текст джерелаAvraham, 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.
Повний текст джерелаAvraham, 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.
Повний текст джерелаGoldstein, 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.
Повний текст джерела