Littérature scientifique sur le sujet « Brain parenchyma »
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Articles de revues sur le sujet "Brain parenchyma"
Bueche, Celine Z., Cheryl Hawkes, Cornelia Garz, Stefan Vielhaber, Johannes Attems, Robert T. Knight, Klaus Reymann, Hans‐Jochen Heinze, Roxana O. Carare et Stefanie Schreiber. « Hypertension drives parenchymal β‐amyloid accumulation in the brain parenchyma ». Annals of Clinical and Translational Neurology 1, no 2 (9 janvier 2014) : 124–29. http://dx.doi.org/10.1002/acn3.27.
Texte intégralHobohm, R. E., P. Codd et M. D. Malinzak. « Ectopic Cerebellar Brain Parenchyma ». Neurographics 9, no 4 (1 août 2019) : 285–87. http://dx.doi.org/10.3174/ng.1800047.
Texte intégralMcCall, Anthony L., Antonia M. Van Bueren, Valerie Nipper, Melissa Moholt-Siebert, Hall Downes et Nikola Lessov. « Forebrain Ischemia Increases Glut1 Protein in Brain Microvessels and Parenchyma ». Journal of Cerebral Blood Flow & ; Metabolism 16, no 1 (janvier 1996) : 69–76. http://dx.doi.org/10.1097/00004647-199601000-00008.
Texte intégralYokel, Robert A. « Nanoparticle brain delivery : a guide to verification methods ». Nanomedicine 15, no 4 (février 2020) : 409–32. http://dx.doi.org/10.2217/nnm-2019-0169.
Texte intégralHenning, Erica C., Lawrence L. Latour et Steven Warach. « Verification of Enhancement of the CSF Space, not Parenchyma, in Acute Stroke Patients with Early Blood—Brain Barrier Disruption ». Journal of Cerebral Blood Flow & ; Metabolism 28, no 5 (19 décembre 2007) : 882–86. http://dx.doi.org/10.1038/sj.jcbfm.9600598.
Texte intégralChowdhury, Forhad Hossain, Nur Mohammad, Mohammod Raziul Haque, Zahed Hossain, Md Abdus Salam et Mainul Haque Sarker. « Tubercular Lesions in Brain Parenchyma ». Bangladesh Journal of Infectious Diseases 5, no 2 (11 juillet 2019) : 45–60. http://dx.doi.org/10.3329/bjid.v5i2.42151.
Texte intégralFrancisco, Allison De Freitas, Raul Fernando Pizzatto, Gustavo Henrique Smaniotto, Rodrigo Leite De Morais, Andrei Leite De Morais et Ricardo Nascimento Brito. « Multiple Mieloma Metastases In Brain Parenchyma ». JBNC - JORNAL BRASILEIRO DE NEUROCIRURGIA 22, no 3 (23 mars 2018) : 124–27. http://dx.doi.org/10.22290/jbnc.v22i3.1021.
Texte intégralKosa, Gabor, Danilo De Lorenzo, Elena De Momi, Gabor Szekely et Giancarlo Ferrigno. « Robotic burrowing in brain parenchyma tissue ». IFAC Proceedings Volumes 44, no 1 (janvier 2011) : 14307–11. http://dx.doi.org/10.3182/20110828-6-it-1002.01840.
Texte intégralBehnke, Stefanie, et G. Becker. « Sonographic imaging of the brain parenchyma ». European Journal of Ultrasound 16, no 1-2 (novembre 2002) : 73–80. http://dx.doi.org/10.1016/s0929-8266(02)00039-3.
Texte intégralKrumina, Gaida. « Metastatic disease of the brain : parenchyma ». European Radiology 15, no 3 (5 février 2005) : 608–16. http://dx.doi.org/10.1007/s00330-004-2626-4.
Texte intégralThèses sur le sujet "Brain parenchyma"
Berengeno, Andrea Lorena. « Impact of unconjugated bilirubin on brain parenchyma of the Gunn rat ». Doctoral thesis, Università degli studi di Trieste, 2011. http://hdl.handle.net/10077/4601.
Texte intégralIn infants and in the Crigler-Najjar syndrome type I patients, severe hyperbilirubinemia due to high levels of unconjugated bilirubin (UCB) may cause Kernicterus, leading to an irreversible and selective brain damage. The Gunn rat is the animal model for the study of these pathologies. It has been suggested that different enzymes of the phase I (cytochrome P-450-dependent mixed function oxygenases 1A1, 1A2, 2A3), phase II (glutathione-S-transferases α2, α3, µ3, µ4, π) and phase III transporters (particularly, Mrp1) seems to be involved in UCB detoxification pathways. However, to date, their in vivo brain expression has been evidenced only at the blood-brain interfaces, while remains largely unexplored in brain parenchyma. Particularly for Mrp1, in vitro evidence reported a role of this transporter in protection of neural primary cultures from dissected cortex, by extruding bilirubin out of the cell. The aim of this study is establish the developmental profile of these genes in brain parenchyma, and assess their alteration in hyperbilirubinemic jj animals. Due to the high regional selectivity of UCB-induced neurotoxicity, cerebellum (Cll), striatum (St), hippocampus (Hip) and cerebral cortex (Cx) were chosen for this study. Our results regard the Mrp1 protein in cerebral cortex of normobilirubinemic (JJ) rats showed that its expression varied during the post-natal age, reaching the highest levels at 9 days after birth. No changes were found between JJ and Jj (having a temporary hyperbilirubinemia in the first week of life) rat for all ages analyzed. Similarly, no differences were detected among JJ/Jj and jj (hyperbilirubinemic) rats at P2, P17 and P60, while a significant increase (p < 0.005) was evidenced in P9 jj rats as compared to age-matched JJ animals. Our Mrp1 mRNA analysis in four regions of P9 animals by Real Time-qPCR revealed the absence of differences among Cx, Cll, St and Hip of P9 normobilirubinemic JJ rats. Moreover, no variations between jj and JJ control animals were detected. Regarding the Mrp1 protein expression in the same four regions by Western blot analysis, our results showed that the levels of this transporter in normobilirubinemic JJ rats were lower in Cx, similar in Cll, St and Hip (p < 0.05 vs Cx). Comparing genotypes, a reduction on Mrp1 in jj animals (compared to Mrp1 amount in the same region of JJ pups) was detected in Cll, St, but reached the statistical significance only in Hip (p < 0.05 vs Hip JJ). The analysis of CYPs gene expression in P9 Gunn rats indicate that CYP1A1, 1A2 and 2A3 mRNA were differently expressed among Cx, Cll, St and Hip of JJ rat. Similarly a region-specific modulation of CYPs expression in jj Gunn rats (compared to JJ) was pointed-out. Surprisingly, UCB seems to generate a plateau effect on CYPs mRNA levels among brain regions of jj rats. In P60 JJ Gunn rats the CYPs expression is higher than in P9 animals, with the following pattern among regions: Cx CllSt Hip. A down-regulation (p < 0.05) in St of P60 jj compared to normal animals was observed. Analyzing the GSTs expression in P9 animals, higher variability in the GSTs expression among the four brain areas was evidenced. In hyperbilirubinemic (jj) rats (compared to JJ), statistically relevant down-regulations were detected for GSTα2 (in St;p < 0.05), GSTα3 (in Hip;p < 0.05), µ3 (in Cx;p < 0.01), µ4 (in Cx; p < 0.05) and π (in Cll: p < 0.05); while GSTµ4 was up-regulated in St (p < 0.05). From P9 to P60, in JJ animals: GSTα3 expression increased (13-75-fold depending on the region); while GSTα2 (5-fold), µ3 (p < 0.05), µ4 (2-fold) and π (2-fold) mRNA amounts decreased. In P60 jj Gunn rats, compared to controls (JJ):a relevant up-regulation of GSTα3 was observed in Cll (p < 0.005) and Hip (p < 0.05), while GSTµ3 in jj was down-regulated (p < 0.05). The Mrp1 results obtained in the present in vivo study seems not to be in agreement with the in vitro data reported, to date. Thus, the Mrp1 expression is low in brain parenchyma and bilirubin affect (up-regulation) only marginally the protein amounts in cortex of P9 animals, while in other regions Mrp1 is not modulated, indicating a marginal role in vivo in bilirubin clearance. Similarly, while in liver GSTα2 and α3 act together as ligandin, this seems not happens in brain where the two subunit are expressed at very low levels (P9: α2 77000- α3 1500 fold difference; P60: α2 112000-α3 2200 fold difference with respect to age matched livers). For all genes under analysis, a very complex and variable pattern of expression among brain areas was evidenced. Consequently, no general rules concerning bilirubin-induced modulation could be drawn, as both up and down-regulation were observed. Additionally, in Cx of P9 jj animals, a translational control of Mrp1 might be hypothesized due to a significant increase in Mrp1 protein, without changes in mRNA level. Therefore, the genomic screening made in this work provides the first general overview on the mRNA developmental profiles of several CYPs and GSTs genes in brain parenchyma (specifically Cx, Cll, St and Hip) of normal rats, and of animals suffering from hyperbilirubinemia, underlying the necessity to find functional evidence to finally understand the role of these enzymes associated with the kernicterus and Crigler-Najjar type I syndrome pathologies.
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Simon, Christiane. « Progenitors in the intact brain parenchyma and their reaction towards acute injury ». Diss., lmu, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-144896.
Texte intégralSimon, Christiane Verfasser], et Magdalena [Akademischer Betreuer] [Götz. « Progenitors in the intact brain parenchyma and their reaction towards acute injury / Christiane Simon. Betreuer : Magdalena Götz ». München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2012. http://d-nb.info/1024243362/34.
Texte intégralAlbargothy, Nazira. « Pathways of communication between the subarachnoid space and the brain parenchyma : are they relevant to neurodegenerative diseases ? » Thesis, University of Southampton, 2017. https://eprints.soton.ac.uk/417992/.
Texte intégralPoncelet, Brigitte P. G. « Study of Physiological Motions in the Human Body using Echo-Planar Magnetic Resonance Imaging :From Brain Parenchyma Motion to Coronary Blood Flow ». Doctoral thesis, Universite Libre de Bruxelles, 1995. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/212549.
Texte intégralSandsveden, Li. « Evaluation of the Robustness of the Brain Parenchymal Fraction for Brain Atrophy Measurements ». Thesis, Linköpings universitet, Medicinsk informatik, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-105801.
Texte intégralVågberg, Mattias. « Brain parenchymal fraction in healthy individuals and in clinical follow-up of multiple sclerosis ». Doctoral thesis, Umeå universitet, Klinisk neurovetenskap, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-128697.
Texte intégralBhat, Danish. « Image Registration and Analysis within quantitative MRI to improve estimation of brain parenchymal fraction ». Thesis, Linköpings universitet, Institutionen för medicinsk teknik, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-132973.
Texte intégralBoccazzi, M. « PURINERGIC SIGNALING AND NEUROGENESIS : MODULATION OF ADULT BRAIN SUBVENTRICULAR ZONE CELL FUNCTIONS AND PARENCHIMAL PROGENITORS MULTIPOTENCY ». Doctoral thesis, Università degli Studi di Milano, 2014. http://hdl.handle.net/2434/229414.
Texte intégralSantos, Tânia Custódio. « Alterations at the blood-brain barrier and brain parenchyma along brain metastasization of breast cancer ». Master's thesis, 2016. http://hdl.handle.net/10451/34359.
Texte intégralDespite the restricted permeability of the blood-brain barrier (BBB), the brain is a privileged organ regarding the appearance of metastases, particularly from breast cancer. Patients with brain metastases from breast cancer have a severe prognosis, rendering this issue a serious oncologic problem that deserves further attention. Therefore, additional studies are required to establish when breast cancer cells cross the brain endothelium and what are the routes used for the transendothelial migration, to understand what is their precise phenotype along the processes of transmigration and establishment of brain metastases, to determine the alterations occurring in brain endothelium, to study how endothelial cells communicate with malignant ones to promote the attraction of malignant cells into the brain vasculature and tumour-associated vascular development. Based on this, we aimed at establishing the temporal profile of breast cancer metastasization to the brain and characterize the metastasizing cells phenotype, as well as, to investigate the vascular events and BBB properties along the process of metastasization to this target organ. In addition, we aimed to assess signalling mechanisms involved in attraction of carcinoma cells into the brain and proliferation in the nervous tissue. To establish the temporal evolution of the players involved in such processes, we used cerebella, cranial hippocampi, and striata of female mice inoculated with 4T1 breast cancer cells sacrificed at 5 hours, 3 days, 7 days or 10 days, and of female mice injected with vehicle (control) sacrificed at 5 hours. Our results showed the presence of brain metastasis of breast cancer at 7-days after inoculation, which increased thereafter. The malignant cells crossed the BBB as mesenchymal cells and, once inside the brain, these cells underwent a complete or partial mesenchymal-epithelial transition to acquire the epithelial characteristics that allow the establishment of new tumours. In addition, the process of brain metastasization of BC contributed to the downregulation of the tight junction protein claudin-5 of brain microvascular endothelial cells, as well as to the entrance of the blood-borne component thrombin in brain parenchyma. On the other hand, hypervascularization in cranial hippocampus appeared to be associated to the process of brain colonization by breast cancer cells. Regarding the role of platelet-derived growth factor B signalling along the process of brain metastasization, we found that this growth factor was expressed by tumour cells and its expression increased during the formation of brain metastasis. Interestingly, a continuous entrance of cysteine-X amino acid-cysteine receptor 4 (CXCR4)-positive cells into the brain parenchyma appeared to occur along the process of brain metastasization of breast cancer. In sum, this study contributes to clarify the time-course and interdependence of the signalling events, BBB breach and phenotypic transition of malignant cells along endothelial transposition and brain metastases establishment by breast cancer cells. Moreover, the demonstration of early cellular and molecular events points to novel targets for modulation in order to prevent metastasis formation and development.
Apesar da barreira hematoencefálica (BHE) ter uma permeabilidade restrita, o cérebro é um órgão preferencialmente afetado pelo aparecimento de metástases, particularmente de cancro mama. Pacientes com metástases cerebrais provenientes do cancro da mama têm um prognóstico severo, tornando a metastização num sério problema oncológico que merece toda a atenção. Por este motivo, novos estudos são necessários para estabelecer quando é que as células cancerígenas da mama atravessam o endotélio cerebral e quais são as vias que utilizam para migrarem através do endotélio, para se perceber qual o fenótipo que têm ao longo dos processos de migração para dentro do encéfalo e durante o estabelecimento de metástases, para determinar as alterações que ocorrem no endotélio cerebral, para estudar como as células endoteliais comunicam com as células malignas para promover a atracão das células cancerígenas da mama para a vasculatura do encéfalo e o desenvolvimento vascular associado ao tumor. Com base nisto, tivemos com objetivos estabelecer o perfil temporal da metastização do cancro da mama para o encéfalo e caracterizar o fenótipo destas mesmas células, assim como, estudar as alterações vasculares e as propriedades da BHE ao longo do processo de metastização para este órgão secundário. Para além disso, também pretendíamos avaliar os mecanismos de sinalização envolvidos na atracão das células tumorais para o encéfalo e na proliferação no tecido nervoso. Para estabelecer a evolução temporal dos intervenientes envolvidos em tais processos, utilizámos cerebelos, hipocampos craniais e estriados de ratinhos fêmea inoculados com células cancerígenas da mama 4T1 sacrificados às 5 horas, 3 dias, 7 dias, ou 10 dias, e de ratinhos fêmea injetados com veículo (controlo) sacrificados às 5 horas. Os nossos resultados mostraram a presença de metástases cerebrais do cancro mama 7 dias após a inoculação, aumentando ao longo do tempo. As células malignas atravessaram a BHE como células mesenquimais e, uma vez dentro do encéfalo, estas células sofreram uma transição completa ou parcial de fenótipo mesenquimal para epitelial para adquirirem as características epiteliais necessárias para o estabelecimento de novos tumores no encéfalo. Além disso, o processo de metastização cerebral do cancro da mama contribuiu para a diminuição da expressão da proteína das junções de oclusão claudina-5 nas células endoteliais microvasculares cerebrais, assim como para a entrada do componente sanguíneo trombina no parênquima cerebral. Por outro lado, o aumento de vascularização no hipocampo cranial aparentou estar associado ao processo de colonização do encéfalo pelas células cancerígenas da mama. Relativamente ao papel da sinalização do fator de crescimento B derivado de plaquetas ao longo do processo de metastização cerebral, descobrimos que as células tumorais expressavam este fator de crescimento e que a sua expressão aumentou durante a formação de metástases no encéfalo. Curiosamente, a entrada contínua de células que expressam o recetor CXCR4 para dentro do parênquima cerebral aparentou ocorrer ao longo do processo de metastização cerebral do cancro da mama. Deste modo, este estudo contribui para clarificar o curso temporal e a interdependência de vias de sinalização, a quebra da BHE e a transição fenotípica das células malignas ao longo na transposição do endotélio e estabelecimento de metástases cerebrais pelas células cancerígenas da mama. Além disso, a demonstração dos eventos celulares e moleculares iniciais aponta para novos alvos para modulação de modo a prevenir a formação e desenvolvimento de metástases.
This study was supported by Fundação para a Ciência e Tecnologia (FCT – UID/DTP/04138/2013), Portugal, and by National Research, Development and Innovation/Hungarian Scientific Research Fund (NKFIH/OTKA – K-100807 and K-116158), Hungary.
Livres sur le sujet "Brain parenchyma"
Dallas, Shannon. Functional expression of multidrug resistance proteins in brain parenchyma : Relevance to the pharmacology of HIV-infection in the brain. 2004.
Trouver le texte intégralDallas, Shannon. Functional expression of multidrug resistance proteins in brain parenchyma : relevance to the pharmacology of HIV-infection in the brain. 2004, 2004.
Trouver le texte intégralDelcourt, Candice, et Craig Anderson. Management of parenchymal haemorrhage. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0237.
Texte intégralSolomon, Tom, et Benedict Michael. Neurological infection. Sous la direction de Patrick Davey et David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0229.
Texte intégralTheeler, Brett J., et Mark R. Gilbert. Primary Central Nervous System Tumors. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0129.
Texte intégralMartinez, Tyler. Encephalitis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.003.0007.
Texte intégralTörök, M. Estée, Fiona J. Cooke et Ed Moran. Neurological infections. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199671328.003.0019.
Texte intégralSolomon, Tom. Meningitis. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0969.
Texte intégralStocchetti, Nino, et Andrew I. R. Maas. Causes and management of intracranial hypertension. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0233.
Texte intégralChapitres de livres sur le sujet "Brain parenchyma"
Saido, Takaomi C., et Nobuhisa Iwata. « Catabolism of amyloid-β peptide in brain parenchyma ». Dans Neuroscientific Basis of Dementia, 249–56. Basel : Birkhäuser Basel, 2001. http://dx.doi.org/10.1007/978-3-0348-8225-5_30.
Texte intégralTsuyumu, M., H. J. Reulen et Y. Inaba. « Dynamics of Fluid Movement Through Brain Parenchyma and into the CSF in Vasogenic Brain Edema ». Dans Brain Edema, 99–107. Berlin, Heidelberg : Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70696-7_13.
Texte intégralGarel, Catherine. « Abnormalities of the Fetal Cerebral Parenchyma : Ischaemic and Haemorrhagic Lesions ». Dans MRI of the Fetal Brain, 247–62. Berlin, Heidelberg : Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18747-6_15.
Texte intégralBlazquez, Raquel, et Tobias Pukrop. « 3D Coculture Model of the Brain Parenchyma–Metastasis Interface of Brain Metastasis ». Dans Methods in Molecular Biology, 213–22. New York, NY : Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7021-6_16.
Texte intégralBankiewicz, Krystof. « Neurosurgical Approaches : Drug Infusion Directly into the Parenchyma or the Cerebrospinal Fluid ». Dans Drug Delivery to the Brain, 501–18. New York, NY : Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-9105-7_18.
Texte intégralSvampa, Silvana. « Brain Parenchyma : Usefulness of Transcranial Color-Coded Duplex Sonography (TCCS) ». Dans Neurosonology in Critical Care, 1011–24. Cham : Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-81419-9_62.
Texte intégralEndres, Jürgen, Christopher Rohkohl, Kevin Royalty, Sebastian Schafer, Andreas Maier, Arnd Dörfler et Markus Kowarschik. « Brain Parenchyma and Vessel Separation in 3D Digital Subtraction Angiography Images ». Dans Informatik aktuell, 319–24. Berlin, Heidelberg : Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-54345-0_72.
Texte intégralAl-Sarraf, Hameed, Kevin A. Smart, Malcolm B. Segal et Jane E. Preston. « Differential Amino Acid Uptake into Cerebral Parenchyma and Capillary Cells during Development ». Dans Biology and Physiology of the Blood-Brain Barrier, 27–33. Boston, MA : Springer US, 1996. http://dx.doi.org/10.1007/978-1-4757-9489-2_6.
Texte intégralMcKinley, Bruce A., et C. L. Parmley. « Effects of Injury and Therapy on Brain Parenchyma pO2, pCO2, pH and ICP following Severe Closed Head Injury ». Dans Intracranial Pressure and Neuromonitoring in Brain Injury, 177–82. Vienna : Springer Vienna, 1998. http://dx.doi.org/10.1007/978-3-7091-6475-4_52.
Texte intégralStruys-Ponsar, C., A. Florence, A. Gauthier, R. R. Crichton et Ph Bosch de Aguilar. « Ultrastructural changes in brain parenchyma during normal aging and in animal models of aging ». Dans Cell and Animal Models in Aging and Dementia Research, 111–32. Vienna : Springer Vienna, 1994. http://dx.doi.org/10.1007/978-3-7091-9350-1_9.
Texte intégralActes de conférences sur le sujet "Brain parenchyma"
Chen, Xiaoshuai, Kazuya Sase, Atsushi Konno et Teppei Tsujita. « A viscoelastic model of brain parenchyma for haptic brain surgery simulations ». Dans 2016 IEEE/SICE International Symposium on System Integration (SII). IEEE, 2016. http://dx.doi.org/10.1109/sii.2016.7844046.
Texte intégralChen, Xiaoshuai, Kazuya Sase, Atsushi Konno et Teppei Tsujita. « Identification of mechanical properties of brain parenchyma for brain surgery haptic simulation ». Dans 2014 IEEE International Conference on Robotics and Biomimetics (ROBIO). IEEE, 2014. http://dx.doi.org/10.1109/robio.2014.7090572.
Texte intégralSavić, Živorad, Katarina Savić, Sofija Savić, Mirjana Petrović et Vojislav Antić. « Diagnosis of non-traumatic hemorrhages in the brain parenchyma ». Dans RAD Conference. RAD Centre, 2021. http://dx.doi.org/10.21175/rad.abstr.book.2021.35.5.
Texte intégralReddick, Wilburn E., Raymond K. Mulhern, T. David Elkin, John O. Glass et James W. Langston. « Subtle volume differences in brain parenchyma of children surviving medulloblastoma ». Dans Medical Imaging '98, sous la direction de Eric A. Hoffman. SPIE, 1998. http://dx.doi.org/10.1117/12.312571.
Texte intégralHwang, Jinyoung, Yeji Han et HyunWook Park. « Segmentation of Brain Parenchyma using Bilateral Filtering and Region Growing ». Dans 2007 29th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2007. http://dx.doi.org/10.1109/iembs.2007.4353787.
Texte intégralChen, Xiaoshuai, Kazuya Sase, Atsushi Konno et Teppei Tsujita. « Experimental and numerical analysis of damage fracture mechanics of brain parenchyma ». Dans 2016 IEEE International Conference on Robotics and Biomimetics (ROBIO). IEEE, 2016. http://dx.doi.org/10.1109/robio.2016.7866369.
Texte intégralMehrabian, Amin, et Younane Abousleiman. « Realizations of Experimental Hydrocephalus Data Through the Analytical Model of Poroviscoelastic Brain Tissue ». Dans ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80192.
Texte intégralReddick, Wilburn E., Holly A. White, John O. Glass et Raymond K. Mulhern. « Correlation of neurocognitive function and brain parenchyma volumes in children surviving cancer ». Dans Medical Imaging 2002, sous la direction de Anne V. Clough et Chin-Tu Chen. SPIE, 2002. http://dx.doi.org/10.1117/12.463606.
Texte intégralAdachi, Kazuhiko, Yoshiaki Inoue, Hiroshi Kanki, Atsushi Fujita et Eiji Kohmura. « Finite Element Modeling of Brain Tissue Retraction for Neurosurgical Simulation ». Dans ASME 2007 International Mechanical Engineering Congress and Exposition. ASMEDC, 2007. http://dx.doi.org/10.1115/imece2007-41772.
Texte intégralTully, Brett, et Yiannis Ventikos. « Modelling Normal Pressure Hydrocephalus as a ‘Two-Hit’ Disease Using Multiple-Network Poroelastic Theory ». Dans ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19135.
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