Academic literature on the topic 'Brain microvascular endothelium'

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Journal articles on the topic "Brain microvascular endothelium"

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Avsenik, Jernej, Sotirios Bisdas, and Katarina Surlan Popovic. "Blood-brain barrier permeability imaging using perfusion computed tomography." Radiology and Oncology 49, no. 2 (2015): 107–14. http://dx.doi.org/10.2478/raon-2014-0029.

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Abstract Background. The blood-brain barrier represents the selective diffusion barrier at the level of the cerebral microvascular endothelium. Other functions of blood-brain barrier include transport, signaling and osmoregulation. Endothelial cells interact with surrounding astrocytes, pericytes and neurons. These interactions are crucial to the development, structural integrity and function of the cerebral microvascular endothelium. Dysfunctional blood-brain barrier has been associated with pathologies such as acute stroke, tumors, inflammatory and neurodegenerative diseases. Conclusions. Bl
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Rochfort, Keith D., Laura E. Collins, Alisha McLoughlin, and Philip M. Cummins. "Shear-Dependent Attenuation of Cellular ROS Levels can Suppress Proinflammatory Cytokine Injury to Human Brain Microvascular Endothelial Barrier Properties." Journal of Cerebral Blood Flow & Metabolism 35, no. 10 (2015): 1648–56. http://dx.doi.org/10.1038/jcbfm.2015.102.

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The regulatory interplay between laminar shear stress and proinflammatory cytokines during homeostatic maintenance of the brain microvascular endothelium is largely undefined. We hypothesized that laminar shear could counteract the injurious actions of proinflammatory cytokines on human brain microvascular endothelial cell (HBMvEC) barrier properties, in-part through suppression of cellular redox signaling. For these investigations, HBMvECs were exposed to either shear stress (8 dynes/cm2, 24 hours) or cytokines (tumor necrosis factor-α (TNF-α) or interleukin-6 (IL-6), 0 to 100 ng/mL, 6 or 18
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Iovino, Federico, Grietje Molema, and Jetta J. E. Bijlsma. "Platelet Endothelial Cell Adhesion Molecule-1, a Putative Receptor for the Adhesion of Streptococcus pneumoniae to the Vascular Endothelium of the Blood-Brain Barrier." Infection and Immunity 82, no. 9 (2014): 3555–66. http://dx.doi.org/10.1128/iai.00046-14.

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ABSTRACTThe Gram-positive bacteriumStreptococcus pneumoniaeis the main causative agent of bacterial meningitis.S. pneumoniaeis thought to invade the central nervous system via the bloodstream by crossing the vascular endothelium of the blood-brain barrier. The exact mechanism by which pneumococci cross endothelial cell barriers before meningitis develops is unknown. Here, we investigated the role of PECAM-1/CD31, one of the major endothelial cell adhesion molecules, inS. pneumoniaeadhesion to vascular endothelium of the blood-brain barrier. Mice were intravenously infected with pneumococci and
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Satoh, Kei, Hidemi Yoshida, Tada-Atsu Imalzumi, Masayuki Koyama, and Shigeru Takamatsu. "Production of Platelet-Activating Factor by Porcine Brain Microvascular Endothelial Cells in Culture." Thrombosis and Haemostasis 74, no. 05 (1995): 1335–39. http://dx.doi.org/10.1055/s-0038-1649936.

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SummaryEndothelial cells produce platelet-activating factor (PAF), which is the key process in the interactions between the vascular wall and blood cells. To examine the production of PAF in brain microvasculature we have cultured brain endothelial cells and performed a comparative study with aortic endothelial cells. Fresh porcine brain was homogenized, and microvascular endothelial cells were separated by enzyme digestion. The cells were cultured in medium containing epidermal growth factor and bovine brain extract. Endothelial cells from the aorta of the same animal were cultured in a simil
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Janigro, D., G. A. West, E. L. Gordon, and H. R. Winn. "ATP-sensitive K+ channels in rat aorta and brain microvascular endothelial cells." American Journal of Physiology-Cell Physiology 265, no. 3 (1993): C812—C821. http://dx.doi.org/10.1152/ajpcell.1993.265.3.c812.

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The endothelium plays an important role in the modulation of vascular tone and blood cell activation. Extensive work has demonstrated that the release of endothelium-derived relaxing factor (EDRF) from the endothelium is evoked by a number of physical and chemical stimuli requiring Ca2+. Because endothelial cells do not express voltage-dependent Ca2+ channels, Ca2+ influxes following receptor activation may be facilitated by cell hyperpolarizations mediated by the activation of K+ conductances. There has been recent interest in the role of ATP-sensitive K+ channels (KATP) suggesting that KATP
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Chen, Ye, Richard M. McCarron, Joliet Bembry, et al. "Nitric Oxide Modulates Endothelin 1-Induced Ca2+ Mobilization and Cytoskeletal F-Actin Filaments in Human Cerebromicrovascular Endothelial Cells." Journal of Cerebral Blood Flow & Metabolism 19, no. 2 (1999): 133–38. http://dx.doi.org/10.1097/00004647-199902000-00003.

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A functional interrelation between nitric oxide (NO), the endothelial-derived vasodilating factor, and endothelin 1 (ET-1), the potent vasoconstrictive peptide, was investigated in microvascular endothelium of human brain. Nor-1 dose-dependently decreased the ET-1–stimulated mobilization of Ca2+. This response was mimicked with cGMP and abrogated by inhibitors of guanylyl cyclase or cGMP-dependent protein kinase G. These findings indicate that NO and ET-1 interactions involved in modulation of intracellular Ca2+ are mediated by cGMP/protein kinase G. In addition, Nor-1–mediated effects were as
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Garcia-Polite, Fernando, Jordi Martorell, Paula Del Rey-Puech, et al. "Pulsatility and high shear stress deteriorate barrier phenotype in brain microvascular endothelium." Journal of Cerebral Blood Flow & Metabolism 37, no. 7 (2016): 2614–25. http://dx.doi.org/10.1177/0271678x16672482.

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Microvascular endothelial cells at the blood–brain barrier exhibit a protective phenotype, which is highly induced by biochemical and biomechanical stimuli. Amongst them, shear stress enhances junctional tightness and limits transport at capillary-like levels. Abnormal flow patterns can reduce functional features of macrovascular endothelium. We now examine if this is true in brain microvascular endothelial cells. We suggest in this paper a complex response of endothelial cells to aberrant forces under different flow domains. Human brain microvascular endothelial cells were exposed to physiolo
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Sahagun, G., S. A. Moore, and M. N. Hart. "Permeability of neutral vs. anionic dextrans in cultured brain microvascular endothelium." American Journal of Physiology-Heart and Circulatory Physiology 259, no. 1 (1990): H162—H166. http://dx.doi.org/10.1152/ajpheart.1990.259.1.h162.

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The luminal surface of vascular endothelium contains glycocalyx residues that establish an overall negative charge. Recent evidence has suggested that local endothelial surface charge properties may account for the permeability properties of various macromolecules. It has also been suggested that altered membrane charge on the luminal side may play a role in thrombogenesis and atherogenesis. The relationship of macromolecule charge to endothelial cell permeability was examined in vitro using mouse brain microvessel endothelial cells grown to confluence on a nitrocellulose filter separating a d
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Kaiser, Mathias, Malgorzata Burek, Stefan Britz, et al. "The Influence of Capsaicin on the Integrity of Microvascular Endothelial Cell Monolayers." International Journal of Molecular Sciences 20, no. 1 (2018): 122. http://dx.doi.org/10.3390/ijms20010122.

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Microvascular endothelial cells are an essential part of many biological barriers, such as the blood–brain barrier (BBB) and the endothelium of the arteries and veins. A reversible opening strategy to increase the permeability of drugs across the BBB could lead to improved therapies due to enhanced drug bioavailability. Vanilloids, such as capsaicin, are known to reversibly open tight junctions of epithelial and endothelial cells. In this study, we used several in vitro assays with the murine endothelial capillary brain cells (line cEND) as a BBB model to characterize the interaction between c
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Nottet, H. S., Y. Persidsky, V. G. Sasseville, et al. "Mechanisms for the transendothelial migration of HIV-1-infected monocytes into brain." Journal of Immunology 156, no. 3 (1996): 1284–95. http://dx.doi.org/10.4049/jimmunol.156.3.1284.

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Abstract HIV-1 penetration of the brain is a pivotal event in the neuropathogenesis of AIDS-associated dementia. The establishment of productive viral replication or up-regulation of adhesion molecule expression on brain microvascular endothelial cells (BMVEC) could permit entry of HIV into the central nervous system. To investigate the contribution of both, we inoculated primary human BMVEC with high titer macrophage-tropic HIV-1 or cocultured them with virus-infected monocytes. In both instances, BMVEC failed to demonstrate productive viral replication. Cell to cell contact between monocytes
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Dissertations / Theses on the topic "Brain microvascular endothelium"

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Cerutti, Camilla. "Role of microRNAs in leukocyte adhesion to human brain microvascular endothelium." Thesis, Open University, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.606835.

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MicroRNAs (miRs) are small non-coding regulatory RNAs that act through repression of protein translation and/or mRNA degradation at the post-transcriptional level. MiRs are critical players in the pathogenesis of many diseases, including 'neuroinflammatory disorders such as multiple sclerosis (MS), MS is characterized by leukocyte adhesion and infiltration subsequently leading to demyelination of nerve fibres. Leukocyte adhesion on brain endothelial cells (BEC) - the main cellular constituent of the blood-brain barrier (BBB) - is a complex multi-step process where activated BEC overexpress che
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Wang, Shiyang. "The role of TRKB receptors in regulation of coronary microvascular endothelial cell angiogenesis /." Access full-text from WCMC, 2008. http://proquest.umi.com/pqdweb?did=1543605071&sid=5&Fmt=2&clientId=8424&RQT=309&VName=PQD.

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Genes-Hernandez, Luiza I. "Development of a microfluidic based microvascular model towards a complete blood brain barrier (BBB) mimic /." Diss., Connect to online resource - MSU authorized users, 2008.

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Al-sandaqchi, Alaa. "Interaction of Toxoplasma gondii with human brain microvascular endothelial cells in vitro." Thesis, University of Nottingham, 2016. http://eprints.nottingham.ac.uk/37837/.

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Background: The brain is the most commonly affected organ during Toxoplasma gondii infection but the mechanisms utilized by this protozoan parasite for disrupting the brain's endothelial cells lining the blood–brain barrier (BBB) and moving to invade the brain are not yet understood. In the present study, we investigated the cellular pathogenicity of T. gondii infection in human brain microvascular endothelial cells (HBMECs), a fundamental component of the BBB. Methods: Intracellular development of T. gondii tachyzoites within HBMECs was characterized by using Acridine Orange (AO) staining. Th
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Pennucci, Roberta. "CDK5 : new insights into its biological function in human brain microvascular endothelial cells." Thesis, Manchester Metropolitan University, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.496791.

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Ischaemic stroke is a leading cause of death and disability worldwide Successful therapies reside in a precise knowledge of brain function and pathology. Towards this end, previous work in the MMU laboratory used cDNA microarrays to examine gene expression in an experimental rat model of ischaemic stroke - permanent MCAO - and for the first time in human brain tissue from ischaemic stroke patients. Novel deregulated genes were identified. This study was intended to confirm the reproducibility of the in vivo data in vitro. The results showed that human foetal (cerebral cortical) neurons (HFN),
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Casellato, Alessandro. "C2 Fragment from Neisseria meningitidis Antigen NHBA Disassembles Adherence Junctions of Brain Microvascular Endothelial Cells." Doctoral thesis, Università degli studi di Padova, 2013. http://hdl.handle.net/11577/3423368.

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Neisseria meningitidis is the major cause of meningitis and sepsis, two kind of diseases that can affect children and young adults within a few hours, unless a rapid antibiotic therapy is provided. The meningococcal disease dates back to the 16th century. The first description of the disease caused by this pathogen was stated by Viesseux in 1805 as 33 deaths occurred in Geneva, Switzerland [1]. It took about seventy years before two Italians (Marchiafava and Celli) in 1884 identified micrococcal infiltrates within the cerebrospinal fluid [2]. The worldwide presence of meningococcal serogroup
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Thomas, Sangeetha Mary. "An in-vitro study of intermedilysin toxin on human brain microvascular endothelial and other targets cells." Thesis, Queen Mary, University of London, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.535840.

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Chao, Ying Sheng. "Development of quantitative real time PCR to assess human brain microvascular endothelial cell susceptibility to HIV-1 infection." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2008. http://wwwlib.umi.com/cr/ucsd/fullcit?p1450192.

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Thesis (M.S.)--University of California, San Diego, 2008.<br>Title from first page of PDF file (viewed April 7, 2008). Available via ProQuest Digital Dissertations. Includes bibliographical references (p. 64-70).
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Loh, Lip Nam. "Eschericha coli Kl interactions with human brain microvascular endothelial cells, a primary step in the development of neonatal meningitis." Thesis, London School of Hygiene and Tropical Medicine (University of London), 2011. http://researchonline.lshtm.ac.uk/923208/.

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Escherichia coli (E. coli) Kl is one of the commonest Gram negative bacteria causing neonatal bacterial meningitis in both developed and developing countries. Haematogenous spread is a key step in E. coli Kl meningitis; however, it is not clear how bacteria cross the brain endothelium to gain entry into the central nervous system. Previous studies have focussed mainly on the identification of bacterial virulence factors, as well as the signalling pathways that are activated for the recruitment of actin cytoskeleton to the bacterial adhesion site on the apical surface of human brain microvascul
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ZUCCOLO, ESTELLA. "DIFFERENT PATTERNS OF Ca2+ SIGNALING DRIVE ACETYLCHOLINE AND GLUTAMATE INDUCED-NO RELEASE IN MOUSE AND HUMAN BRAIN MICROVASCULAR ENDOTHELIAL CELLS." Doctoral thesis, Università degli studi di Pavia, 2018. http://hdl.handle.net/11571/1214896.

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Acetylcholine (Ach) and glutamate (Glu) are two of the major excitatory neurotransmitters in the brain which increase cerebral blood flow by releasing nitric oxide (NO) from postsynaptic neurons and astrocytes and causing vasorelaxationin adjacent microvessels. An increase in intracellular Ca2+ concentration recruits a multitude of endothelial Ca2+-dependent pathways, such as Ca2+/Calmodulin endothelial NO synthase (eNOS). Surprisingly, the Ca2+-dependent mechanisms whereby Ach induces NO synthesis in brain endothelial cells (ECs) is still unclear. On the other hand, Glu stimulates NMDA recept
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Books on the topic "Brain microvascular endothelium"

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Bereta, Joanna. Regulation of expression of vascular cell adhesion molecule-1 and inducible nitric oxide synthase in murine brain microvascular endothelium. Wydawn. Uniwersytetu Jagiellońskiego, 1997.

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Book chapters on the topic "Brain microvascular endothelium"

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Strasser, A., D. Stanimirovic, N. Kawai, R. M. McCarron, and Maria Spatz. "Hypoxia Modulates Free Radical Formation in Brain Microvascular Endothelium." In Brain Edema X. Springer Vienna, 1997. http://dx.doi.org/10.1007/978-3-7091-6837-0_3.

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Stanimirovic, Danica B., Toshifumi Yamamoto, Hideko Yamamoto, Sumio Uematsu, and Maria Spatz. "Endothelin-1 Binding to Human Brain Microvascular and Capillary Endothelium: Membranes vs. Intact Cells." In Frontiers in Cerebral Vascular Biology. Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2920-0_27.

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Murugesan, Nivetha, Jennifer A. Macdonald, Qiaozhan Lu, Shiaw-Lin Wu, William S. Hancock, and Joel S. Pachter. "Analysis of Mouse Brain Microvascular Endothelium Using Laser Capture Microdissection Coupled with Proteomics." In Methods in Molecular Biology. Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-938-3_14.

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Bowman, P. D., M. du Bois, K. Dorovini-Zis, and R. R. Shivers. "Microvascular Endothelial Cells from Brain." In Cell Culture Techniques in Heart and Vessel Research. Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75262-9_10.

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Navone, Stefania Elena, Giovanni Marfia, and Giulio Alessandri. "Isolation and Expansion of Brain Microvascular Endothelial Cells." In Handbook of Vascular Biology Techniques. Springer Netherlands, 2015. http://dx.doi.org/10.1007/978-94-017-9716-0_18.

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Medina, Angelica, and Hengli Tang. "iPS Cell Differentiation into Brain Microvascular Endothelial Cells." In Methods in Molecular Biology. Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-1979-7_13.

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Michel, C. Charles. "The Role of the Endothelial Surface Coat in Microvascular Permeability." In Ischemic Blood Flow in the Brain. Springer Japan, 2001. http://dx.doi.org/10.1007/978-4-431-67899-1_6.

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Nagashima, T., S. Wu, K. Ikeda, and N. Tamaki. "The Role of Nitric Oxide in Reoxygenation Injury of Brain Microvascular Endothelial Cells." In Brain Edema XI. Springer Vienna, 2000. http://dx.doi.org/10.1007/978-3-7091-6346-7_98.

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Ohara, Y., R. M. McCarron, T. T. Hoffman, et al. "Adrenergic Mediation of TNFα-Stimulated ICAM-1 Expression on Human Brain Microvascular Endothelial Cells." In Brain Edema XI. Springer Vienna, 2000. http://dx.doi.org/10.1007/978-3-7091-6346-7_24.

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Satoh, Kei, Masayuki Koyama, Hidemi Yoshida, and Shigeru Takamatsu. "Production of Platelet-Activating Factor by Brain Microvascular Endothelial Cells." In Advances in Experimental Medicine and Biology. Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-0179-8_4.

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Conference papers on the topic "Brain microvascular endothelium"

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Fan, Jie, Bin Cai, Yanyan Hao, Filippo G. Giancotti, and Bingmei M. Fu. "Effects of VEGF on adhesion of mammary carcinoma cells to brain microvascular endothelium." In 2010 36th Annual Northeast Bioengineering Conference. IEEE, 2010. http://dx.doi.org/10.1109/nebc.2010.5458244.

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Stokol, Tracy, Mandy B. Esch, Nozomi Nishimura, et al. "Little Channels, Big Disease: Using Microfluidics to Investigate Cancer Metastasis." In ASME 2011 9th International Conference on Nanochannels, Microchannels, and Minichannels. ASMEDC, 2011. http://dx.doi.org/10.1115/icnmm2011-58298.

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The leading cause of death in human patients with malignant cancer is the dissemination of the primary tumor to secondary sites throughout the body. It is well known that cancers metastasize to certain tissues (e.g. breast cancer typically spreads to the lungs. brain and bone), in a pattern that cannot be explained by blood flow from the primary tumor or simple mechanical arrest. Circulating tumor cells usually arrest in the microvasculature of target tissues. At these sites, they must adhere to the endothelium, survive, proliferate and extravasate in order to form a secondary tumor. In vitro
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Stoica, Roberta, Mihai Radu, and Beatrice Mihaela Radu. "Functional changes in brain microvascular endothelial cells upon low-energy accelerated proton-irradiation." In RAD Conference. RAD Centre, 2021. http://dx.doi.org/10.21175/rad.abstr.book.2021.32.17.

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Jahan, Jesmin, Madeline Stroud, Anil Sakamuri, and Yagna Jarajapu. "Modulation of Mitochondrial Bioenergetics in Human Brain Microvascular Endothelial Cells by Telomerase Reverse Transcriptase." In ASPET 2023 Annual Meeting Abstracts. American Society for Pharmacology and Experimental Therapeutics, 2023. http://dx.doi.org/10.1124/jpet.122.224820.

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You, D., N. Goshi, E. Ubick, H. Enright, and B. Buchholz. "Wildfire Smoke Particles Induced IL-8 Production and Reduced ZO-1 in the Human Brain Microvascular Endothelial Cells." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a4841.

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Wenping, Sun, and Liu Huimin. "The variation of NF-kB p65 and ICAM-1 induced by homocysteine in the brain microvascular endothelial cells (BMECs)." In 2011 International Conference on Human Health and Biomedical Engineering (HHBE). IEEE, 2011. http://dx.doi.org/10.1109/hhbe.2011.6027984.

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Ayoub, Nehad M., Ahmed Alhusban, and Laila Alhusban. "Abstract 193: Antiangiogenic effect of conditioned media derived from triple negative breast cancer cells in brain microvascular endothelial cellsin vitro." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-193.

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Ayoub, Nehad M., Ahmed Alhusban, and Laila Alhusban. "Abstract 193: Antiangiogenic effect of conditioned media derived from triple negative breast cancer cells in brain microvascular endothelial cellsin vitro." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-193.

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Konieczna, Sylwia, Michael Ohlmeyer, and J. Paul Spiers. "P12 Role of protein phosphatase 2a inhibition in modulation of claudin- 5 and ve-cadherin in human brain microvascular endothelial cells." In Scottish Cardiovascular Forum – 23rd annual meeting, University of Strathclyde, Saturday 1st February 2020. BMJ Publishing Group Ltd and British Cardiovascular Society, 2020. http://dx.doi.org/10.1136/heartjnl-2020-scf.22.

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