Relevant bibliographies by topics / Brain parenchyma

Academic literature on the topic 'Brain parenchyma'

Author: Grafiati
Published: 11 March 2023

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Journal articles on the topic "Brain parenchyma"

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Bueche, Celine Z., Cheryl Hawkes, Cornelia Garz, Stefan Vielhaber, Johannes Attems, Robert T. Knight, Klaus Reymann, Hans‐Jochen Heinze, Roxana O. Carare, and Stefanie Schreiber. "Hypertension drives parenchymal β‐amyloid accumulation in the brain parenchyma." Annals of Clinical and Translational Neurology 1, no. 2 (January 9, 2014): 124–29. http://dx.doi.org/10.1002/acn3.27.

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Hobohm, R. E., P. Codd, and M. D. Malinzak. "Ectopic Cerebellar Brain Parenchyma." Neurographics 9, no. 4 (August 1, 2019): 285–87. http://dx.doi.org/10.3174/ng.1800047.

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McCall, Anthony L., Antonia M. Van Bueren, Valerie Nipper, Melissa Moholt-Siebert, Hall Downes, and Nikola Lessov. "Forebrain Ischemia Increases Glut1 Protein in Brain Microvessels and Parenchyma." Journal of Cerebral Blood Flow & Metabolism 16, no. 1 (January 1996): 69–76. http://dx.doi.org/10.1097/00004647-199601000-00008.

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Glucose transport into nonneuronal brain cells uses differently glycosylated forms of the glucose transport protein, GLUT1. Microvascular GLUT1 is readily seen on immunocytochemistry, although its parenchymal localization has been difficult. Following ischemia, GLUT1 mRNA increases, but whether GLUT1 protein also changes is uncertain. Therefore, we examined the immunocytochemical distribution of GLUT1 in normal rat brain and after transient global forebrain ischemia. A novel immunocytochemical finding was peptide-inhibitable GLUT1 immunoreactive staining in parenchyma as well as in cerebral microvessels. In nonischemic rats, parenchymal GLUT1 staining co-localizes with glial fibrillary acidic protein (GFAP) in perivascular foot processes of astrocytes. By 24 h after ischemia, both microvascular and nonmicrovascular GLUT1 immunoreactivity increased widely, persisting at 4 days postischemia. Vascularity within sections of brain similarly increased after ischemia. Increased parenchymal GLUT1 expression was paralleled by staining for GFAP, suggesting that nonvascular GLUT1 overexpression may occur in reactive astrocytes. A final observation was a rapid expression of inducible heat shock protein (HSP)70 in hippocampus and cortex by 24 h after ischemia. We conclude that GLUT1 is normally immunocytochemically detectable in cerebral microvessels and parenchyma and that parenchymal expression occurs in some astroglia. After global cerebral ischemia, GLUT1 overexpression occurs rapidly and widely in microvessels and parenchyma; its overexpression may be related to an immediate early-gene form of response to cellular stress.
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Yokel, Robert A. "Nanoparticle brain delivery: a guide to verification methods." Nanomedicine 15, no. 4 (February 2020): 409–32. http://dx.doi.org/10.2217/nnm-2019-0169.

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Many reports conclude nanoparticle (NP) brain entry based on bulk brain analysis. Bulk brain includes blood, cerebrospinal fluid and blood vessels within the brain contributing to the blood–brain and blood–cerebrospinal fluid barriers. Considering the brain as neurons, glia and their extracellular space (brain parenchyma), most studies did not show brain parenchymal NP entry. Blood–brain and blood–cerebrospinal fluid barriers anatomy and function are reviewed. Methods demonstrating brain parenchymal NP entry are presented. Results demonstrating bulk brain versus brain parenchymal entry are classified. Studies are reviewed, critiqued and classified to illustrate results demonstrating bulk brain versus parenchymal entry. Brain, blood and peripheral organ NP timecourses are compared and related to brain parenchymal entry evidence suggesting brain NP timecourse informs about brain parenchymal entry.
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Henning, Erica C., Lawrence L. Latour, and 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 (December 19, 2007): 882–86. http://dx.doi.org/10.1038/sj.jcbfm.9600598.

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Enhancement on post-contrast fluid-attenuated inversion recovery (FLAIR) images after acute stroke has been attributed to early blood—brain barrier disruption. Using an estimate of parenchymal volume fraction and the apparent diffusion coefficient (ADC), we investigated the relative contributions of cerebral spinal fluid (CSF) and parenchyma to enhancement seen on postcontrast FLAIR. Enhancing regions were found to have low parenchymal volume fractions and high ADC values, approaching that of pure CSF. These findings suggest that contrast enhancement on FLAIR occurs predominately in the CSF space, not parenchyma.
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Chowdhury, Forhad Hossain, Nur Mohammad, Mohammod Raziul Haque, Zahed Hossain, Md Abdus Salam, and Mainul Haque Sarker. "Tubercular Lesions in Brain Parenchyma." Bangladesh Journal of Infectious Diseases 5, no. 2 (July 11, 2019): 45–60. http://dx.doi.org/10.3329/bjid.v5i2.42151.

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Background: Preoperative neuro-radiological features of tuberculosis involving brain lesions may mimic neoplastic lesions of brain & skull base and post operative histopathological study or response to empirical anti-tubercular therapy brings the ultimate diagnosis. Objective: Here we present our experience of 76 cases of cerebral and cerebellar tuberculosis that was managed surgically with anti-tubercular drugs or medical treatment alone without histopathological confirmation. Methodology: All cases of brain parenchymal tuberculosis confirmed histopathologically after surgery or confirmed by succesfull conservative treatment with anti-TB from January 2008 to June 2015 were included for study. Tubercular meningitis was excluded from the study. Patients underwent some form of surgery that confirmed the tuberculosis by histopathologically. Patients with suspected tubercular lesion in brain were treated empirically with antiTB. Post operative imaging was done with CT scan of brain or MRI of brain in immediate post operative period, six months after operation and 18 months after operation. Results: 34 patients underwent surgery to confirm the tuberculosis and 44 patients with suspected tubercular lesion in brain were treated empirically with antiTB of which 40 patients responded successfully and rest 4 patients did not responded and underwent surgical excisional biopsy. Common clinical features include features of raised ICP with focal signs and symptoms. Concurrent other systemic tuberculosis was found in three cases. One patient had history of full course anti-tubercular therapy for pulmonary tuberculosis 20 years back. Conclusion: In suspected TB lesions, conservative treatment without histopathological diagnosis may be adopted with ultimate same result Bangladesh Journal of Infectious Diseases, December 2018;5(2):45-60
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Francisco, Allison De Freitas, Raul Fernando Pizzatto, Gustavo Henrique Smaniotto, Rodrigo Leite De Morais, Andrei Leite De Morais, and Ricardo Nascimento Brito. "Multiple Mieloma Metastases In Brain Parenchyma." JBNC - JORNAL BRASILEIRO DE NEUROCIRURGIA 22, no. 3 (March 23, 2018): 124–27. http://dx.doi.org/10.22290/jbnc.v22i3.1021.

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Multiple myeloma in the central nervous system (CNS) is an extremely rare condition, described in over 100 cases in the literature. In this article, the authors report the case of a 55-year-old female patient, subjected to an autologous bonemarrow transplant, and, furthermore, to a brain tissue biopsy with immunohistochemistry confirmation, revealing infiltration by a great amount of plasma cells, compatible with the clinical history of multiple myeloma. The patient was then subjected to CNS adjuvant radiotherapy, with constant observation by clinical oncology and monthly pamidronate disodium prescription. Despite being an incurable pathology, radiation therapy showed important local control.
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Kosa, Gabor, Danilo De Lorenzo, Elena De Momi, Gabor Szekely, and Giancarlo Ferrigno. "Robotic burrowing in brain parenchyma tissue." IFAC Proceedings Volumes 44, no. 1 (January 2011): 14307–11. http://dx.doi.org/10.3182/20110828-6-it-1002.01840.

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Behnke, Stefanie, and G. Becker. "Sonographic imaging of the brain parenchyma." European Journal of Ultrasound 16, no. 1-2 (November 2002): 73–80. http://dx.doi.org/10.1016/s0929-8266(02)00039-3.

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Krumina, Gaida. "Metastatic disease of the brain: parenchyma." European Radiology 15, no. 3 (February 5, 2005): 608–16. http://dx.doi.org/10.1007/s00330-004-2626-4.

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Dissertations / Theses on the topic "Brain parenchyma"

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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.

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2009/2010
In 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  CllSt  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.
XXIII Ciclo
1978
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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.

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Simon, Christiane Verfasser], and 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.

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Albargothy, 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/.

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Introduction: Accumulation of the β-amyloid (Aβ) protein in cerebral blood vessels is a hallmark of Alzheimer’s disease. Identifying the factors that contribute to this accumulation is critical for both prevention and treatment of the disease. Previous studies have shown that Aβ from the parenchyma is removed along the basement membranes of capillaries and arteries towards the surface of the brain. Aβ is present in the cerebrospinal fluid (CSF) of the brain and there have been suggestions that Aβ is entering the parenchyma and eliminated back into the CSF. The precise anatomical routes by which CSF moves into and out of the brain parenchyma have not been identified. The aim of this study was to determine the entry route and the distribution of solutes and particulate matter in the brain at two time points following its injection into the CSF and investigate age-related changes in CSF influx and distribution. Materials and method: Evans blue dye (EBD), anti-sense oligonucleotides (ASO), fluorescently-tagged Aβ40 and nanoparticles were injected into cisterna magna of adult male C57BL/6J mice and mice were sacrificed at 5 or 30 minutes after injection (n = 3 /group). Representative sections across the brain were immunostained for the detection of basement membranes and smooth muscle actin to differentiate arteries from veins by confocal microscopy. Nanoparticles were detected using transmission electron microscopy. Results and discussion: Within 5 minutes after injection, EBD, ASO, nanoparticles and Aβ entered the brain along the pial – glial vascular basement membranes. In 6 – 10 week old mice, soluble Aβ colocalised with the astrocytic basement membrane marker (α-2 laminin) and collagen IV of leptomeningeal and cortical arteries. After 30 minutes, Aβ was present in the tunica media of leptomeningeal and cortical arteries. The depth of Aβ along the artery wall in the parenchyma was significantly higher at 30 min compared to 5 min post-injection. Regional differences between the cortical, subcortical and posterior brain regions were also detected. In 24 – 30 month old mice, Aβ also entered along the pial – glial basement membrane of arteries after 5 min. However, after 30 min, Aβ was also present in 1) the basement membrane of capillaries, veins, 2) the tunica media of arteries, 3) diffusely in the parenchyma where it was taken up by astrocytes, neurons and macrophages. Conclusions: These results indicate that the entry route of CSF is along the pial – glial basement membrane of arteries at 5 min post-injection. Solutes in the CSF appear to enter the intramural periarterial drainage pathway after 30 min for clearance back into the CSF. The normal flow of CSF along the basement membrane of arteries in old mice is impaired. These data may contribute to the understanding of Aβ deposition in walls of arteries as cerebral amyloid angiopathy and provide an insight into the intrathecal delivery route for treatment of neurodegenerative diseases including Alzheimer’s disease.
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Poncelet, 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.

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Sandsveden, 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.

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In certain diseases, like Multiple Sklerosis and Alzheimer's disease, the progression of the disease can be measured by whole brain atrophy. A difficulty with this is that all people have very different scull sizes, thus also very different brain sizes. This makes it almost impossible to establish "normal values" for brain size. The spread is very large and the method is not practical to use for individual patients. A method with less spread in healthy persons is to use the ratio of the Brain Parenchymal Fraction (BPF). The use of Brain Parenchymal Fraction has increased steadily since it was first introduced in 1999.  BPF = BPV/ICV This study was performed to increase the knowledge of what is normal and to evaluate the robustness of the BPF as a measurement for brain atrophy. Among other things, the change in the BPF when calculated from incomplete volumes (parts of the scull missing in the set of MR images) was evaluated.  The results show that when parts are missing from the top (superior) of the scull the resulting BPF is strictly higher than the correct PBF and when parts are missing from the lower (inferior) part of teh scull the resulting BPF is stritly lower than teh correct value.  Two different methods where tried to compensate for missing parts. The first method was to find a variable factor to compensate with, the size of this factor was depending on how much of the scull that was missing. The second method was to interpolate the ICV and BPV curves and from the new interpolated curves, calculate a new BPF. The method of compensating incomplete volumes using a factor calculated as a function of the intercranial volume of the first/last available slice turned out to be the better.
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Vågberg, 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.

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Background Multiple sclerosis (MS) is an autoimmune disease characterised by inflammatory damage to the central nervous system (CNS). Accumulated CNS injury can be quantified as brain atrophy, definable as a reduction in brain parenchymal fraction (BPF). BPF correlate with disability in MS and is used routinely as an endpoint in clinical trials. In 2009/2010, a new MS clinical care program, that includes follow-up of BPF, was introduced at Umeå University Hospital (NUS). Levels of neurofilament light polypetide (NFL) and glial fibrillary acidic protein (GFAP) in cerebrospinal fluid (CSF) are markers of axonal and astrocytic injury, respectively, and also potential surrogate biomarkers for BPF decline. The goals of this thesis were to establish age-adjusted values of BPF in healthy individuals and to relate these to the BPF values from individuals with MS as well as to the levels of NFL and GFAP in CSF. Another goal was to investigate if expanded disability status scale (EDSS)-worsening could be predicted in a clinical MS cohort and if BPF measurements could contribute to such predictions. Methods A group of 111 healthy individuals volunteered to participate in the studies. A total of 106 of these underwent MRI with BPF measurements, 53 underwent lumbar puncture (LP) with measurement of NFL and GFAP and 48 underwent both MRI and LP. Three different automatic and one manual method were utilised to determine BPF. A literature search on BPF in healthy individuals was performed for the purpose of a systematic review. For studying disability progression in MS, all individuals with MS followed at NUS and included in the Swedish MS registry were included if they had matched data on BPF, EDSS and lesion load as part of clinical follow-up (n=278). Results BPF as well as NFL and GFAP levels in CSF were all associated with age. NFL was associated with BPF and GFAP, but only the association with GFAP was retained when adjusting for age. Significant differences were found between different methods for BPF determination. In the MS population, BPF was associated with EDSS. Only progressive disease course could predict EDSS worsening. Conclusion The data on BPF and levels of NFL and GFAP in CSF of healthy individuals can aid in the interpretation of these variables in the setting of MS. Knowledge on differences in BPF data from different methods for BPF determination can be useful in comparing data across studies, but also highlights the need for a commonly accepted gold standard. The correlation between GFAP and NFL levels in CSF may indicate an association between glial and axonal turnover that is independent of the aging effect on the brain. However, the low number of volunteers for LP precluded clear conclusions. An association between BPF and EDSS was seen in the MS group. The ability to predict EDSS worsening in the clinical MS cohort was limited.
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Bhat, 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.

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In certain neuro-degenerative diseases likemultiple sclerosis (MS), the rate of brain atrophy can be measured by monitoring the brain parenchymal fraction (BPF) in such patients. The BPF is defined as the ratio of brain parenchymal volume (BPV, defined as the total volume of gray matter tissue, white matter tissue and other unidentified tissue) and intracranial volume (ICV, the total volume of the skull). It can be represented by the formula in equation 1: A complication with this measure is that the BPF is affected by the presence of edema in the brain, which leads to swelling and hence may obscure the true rate of brain atrophy. This leads to uncertainty when establishing “normal values” of BPF when analyzing different magnetic resonance imaging (MRI) scans of the same patient. Another problem is that different MRI scans of the same patient cannot be compared directly, due to the fact that the head of the patient will be in a different position for every scan. The SyMRI software used in this master thesis has the functionality to perform brain tissue characterization and measurement of brain volume, given a number of MR images of a patient. Using tissue properties such as longitudinal relaxation time (T1), transverse relaxation time (T2) and proton density (PD), each voxel in a volume can be classified to belong to a certain tissue type. From these measurements, the intracranial volume, brain volume, white matter, gray matter and cerebrospinal fluid volumes can easily be estimated. In this master thesis, the BPF of several patients were analyzed based on quantitative MRI (qMRI) images, in order to identify the change of BPF due to the presence of edema over time. Volumes obtained from the same patients at different time points were aligned (registered), such that the BPF can be easily compared between years. A correlation analysis between the BPF and R1, R2 and PD was performed (R1 is the longitudinal relaxation rate defined as 1/T1 relaxation time and R2 Is transverse relaxation rate defined as 1/T2 relaxation time) to investigate if any of these variables can explain the change in BPF. The results show that due to image registration, and removing some of the slices from the top and bottom of the head, the BPF of the patients was corrected to a certain extent. The change in the mean BPF of each patient over four years was less than 1% post registration and slice removal. However, the decrease in standard deviation was between 6.9% to 52% after registration and removing of slices. The BPF of the follow-up years also came closer to the initial BPF value measured in the first year. The statistical analysis of the BPF and R1, R2 and PD, showed a very low correlation (0.1) between BPF and PD, and intermediate correlations between BPF and R1, R2 (0.385 and -0.51, respectively). Future work will focus on understanding how these results relate to edema.
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Boccazzi, 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.

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Despite previous beliefs, the generation of new neurons and new glia in the central nervous system (CNS) continues throughout life. Adult neurogenesis occurs in both classical neurogenic niches (e.g., the subventricular zone, SVZ, of the lateral ventricles) as well as in the entire brain's parenchyma, which is full of quiescent neural progenitors that are activated after injury. In particular, NG2-positive polydendrocytes, that usually differentiate to mature oligodendrocytes participating to re-myelination after injury, retain some multipotency and, under some conditions, can also generate neurons and astrocytes (Nishiyama et al., 2009). Among various neurotransmitters and growth factors, extracellular nucleotides (ATP, UTP, their break-down products and sugar nucleotides), which are released at high amounts at the sites of CNS damage (Ulrich et al., 2012) are key actors in regulating reparative responses via purinergic P2 receptors (Abbracchio et al., 2009). Previous studies from our laboratory have identified the purinergic receptor GPR17 as a new marker of early stages of NG2 cell differentiation, showing that GPR17 activation accelerates NG2 cells’ oligodendrocyte fate (Fumagalli et al., 2011; Ceruti et al., 2011; Boda et al., 2011). Interestingly, GPR17 is also one of the key genes expressed by human adult neural stem cells (Maisel et al., 2007), suggesting a possible role in cell fate determination. Based on these premises, the aim of my PhD project was to investigate the role of purinergic signaling in regulating stem cell proprieties of adult brain subventricular zone and of NG2+ parenchymal progenitors. In the first part of my PhD thesis, by using a conditional GLAST::CreERT2 Rosa YFP mouse model and an in vitro neurosphere assay, we have demonstrated that the P2Y receptor agonist ADPβS promotes the proliferation of SVZ neural progenitors and sustains their progression towards the generation of neuroblasts, either directly or through the activation of parenchymal astrocytes. In the second part of my PhD, OPCs have been then cultured accordingly to two published protocols (Kondo & Raff, 2000; Liu et al., 2007) both able to unveil their stem cell properties. In both protocols, we observed an increase in the percentage of cells expressing the neuronal marker β-tubulinIII (βtubIII) upon treatment with the non-selective GPR17 antagonist Cangrelor and VPA with respect to control. Interestingly GPR17, which is normally expressed only by NG2+ cells, was surprisingly detected in a subset of βtubIII+ cells already under control differentiative condition, suggesting its potential involvement in neurogenesis. The appearance of this cell population was further incremented by the exposure to VPA and Cangrelor. Taken together, our results suggest that antagonizing GPR17 functions can address the fate of NG2 cells towards the generation of new neurons, as observed with epigenetic modulators like VPA. In conclusion, our results strengthen the evidence that the purinergic system crucially regulates neuronal progenitors, either in a classical neurogenic niche or in the brain parenchyma. The pharmacological modulation of the purinergic system could therefore represent a promising and innovative approach to exploit the intrinsic ability of the adult brain to regenerate in acute and chronic neurodegenerative disorders.
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Santos, 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.

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Tese de mestrado, Ciências Biofarmacêuticas, Universidade de Lisboa, Faculdade de Farmácia, 2016
Despite 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.
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Books on the topic "Brain parenchyma"

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Dallas, Shannon. Functional expression of multidrug resistance proteins in brain parenchyma: Relevance to the pharmacology of HIV-infection in the brain. 2004.

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Dallas, Shannon. Functional expression of multidrug resistance proteins in brain parenchyma: relevance to the pharmacology of HIV-infection in the brain. 2004, 2004.

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Delcourt, Candice, and Craig Anderson. Management of parenchymal haemorrhage. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0237.

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Parenchymal intracerebral haemorrhage (ICH) affects several million people in the world each year, most of whom reside in developing countries. ICH accounts for 10-40% of strokes and is the least treatable form of stroke with a 30-day mortality of 30-55%, with half of these deaths occurring within the first few days of onset. . High blood pressure is both a causal and prognostic factor for ICH, with early control of hypertension being the only medical treatment which may improve recovery and the level of residual functioning. The role of surgery remains controversial. Management is largely supportive and aimed at reducing further brain injury and preventing complications.
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Solomon, Tom, and Benedict Michael. Neurological infection. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0229.

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Neurological infections can be broadly subdivided into chronic/subacute and acute. Chronic/subacute infection usually presents with global cognitive decline, with the prototypical disease being progressive multifocal leucoencephalopathy due to infection with the JC virus in immunocompromised patients. Acute neurological infections can be defined microbiologically, by the nature of the pathogen; clinically, by the presenting signs and symptoms and initial CSF findings; or anatomically. The anatomical definitions are those occurring intracranially (‘meningitis’, where infection involves the meninges overlying the brain; ‘encephalitis’, where the brain parenchyma is involved; or ‘cerebral abscesses’) and those affecting the spinal cord (‘myelitis’). However, there is often both clinical and histological overlap between these syndromes; consequently, the terms ‘meningoencephalitis’ and ‘encephalomyelitis’ are often used. Patients with acute intracranial CNS infections provide the greatest challenge to general physicians, because urgent investigation and appropriate treatment can save lives; they therefore form the focus of this chapter.
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Theeler, Brett J., and Mark R. Gilbert. Primary Central Nervous System Tumors. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0129.

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Ependymomas are rare primary central nervous system (CNS) tumors that are thought to arise from ependymal cells lining the ventricular system located throughout the CNS. Ependymomas occur in all age groups but are more common in the pediatric population. Ependymomas typically present as mass lesions within the ventricular system, brain or spinal cord parenchyma. As with most central nervous system tumors, pathologic evaluation is required for definitive diagnosis. Ependymomas are typically treated with a combination of surgery and radiotherapy although this varies depending on tumor location, tumor grade, patient age, extent of tumor resection, and other pretreatment factors. Recent molecular studies demonstrate molecularly defined tumor heterogeneity that appears to have a region-specific pattern. Translating the emerging molecular profiles of ependymomas into improved treatment strategies is the primary goal of ongoing research efforts.
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Martinez, Tyler. Encephalitis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.003.0007.

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Encephalitis is an inflammation of the brain parenchyma, typically due to a viral infection. Pure encephalitis will lack the signs and symptoms of meningeal irritation (eg, stiff neck and photophobia). New-onset seizures, cognitive deficits, new psychiatric symptoms, lethargy/coma, cranial nerve abnormalities, or movement disorders should alert the clinician to possible encephalitis. It is important to question the patient about foreign travel, immunocompromised state, and potential exposures. Empiric treatment for presumed viral encephalitis is with the antiviral acyclovir. Empiric broad-spectrum antibiotics are also typically given to cover for possible bacterial meningitis. If there are signs of elevated intracranial pressure (ICP), neurosurgical consultation should be obtained for possible decompressive craniotomy. Standard therapy for ICP (ie, hyperventilation, steroids, mannitol, hypertonic saline, and elevation of the head of the bed) should also be considered. The most concerning complication of encephalitis is the development of life-threatening cerebral edema with resultant brainstem compression and herniation.
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Török, M. Estée, Fiona J. Cooke, and Ed Moran. Neurological infections. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199671328.003.0019.

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This chapter covers both acute bacterial and viral, and chronic, meningitis, as well as tuberculous, cryptococcal, coccidioidal, and Histoplasma meningitis, describing meningeal symptoms (headache, neck stiffness, vomiting, photophobia) and cerebral dysfunction (confusion, coma). The chapter also covers neurocysticercosis (including parenchymal and extra-parenchymal cysts), encephalitis (an inflammatory process in the brain characterized by cerebral dysfunction), as well as brain abscess, cerebritis, subdural empyema, epidural abscess, and cerebrospinal fluid shunt infections.
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Solomon, Tom. Meningitis. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0969.

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Meningitis is defined as inflammation of the brain meninges, characterized clinically by inflammatory cells in CSF. When there is concurrent parenchymal brain involvement the term meningoencephalitis is used, meningoencephalomyelitis implies that there is spinal cord involvement too.Although increased cellularity in the CSF, or pleocytosis, is traditionally considered the hallmark of meningitis, some organisms, particularly fungi, can cause meningitis without a pleocytosis, especially in the immunocompromised. The advent of more sensitive methods of detecting viral nucleic acid in the CSF such as the polymerase chain reaction, have also shown that viral central nervous system infection can occur without an associated pleocytosis. When none of the common bacterial agents is easily identified the term aseptic meningitis is often used. The majority of such cases are caused by viruses; non-viral causes of an aseptic meningitis picture include certain bacteria which are not readily cultured, and do not grow in standard culture media, such as Borrelia burgdorferi. The clinical presentations of meningitis can be broadly divided into the acute, recurrent, and chronic. The development of meningitis depends on the infecting organism, and also whether there is any particular host susceptibility.
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Stocchetti, Nino, and Andrew I. R. Maas. Causes and management of intracranial hypertension. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0233.

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Intracranial hypertension may damage the brain in two ways—it causes tissue distortion and herniation, and reduces cerebral perfusion. The many different pathologies that can result in intracranial hypertension include subarachnoid haemorrhage, spontaneous intra-parenchymal haemorrhage, malignant cerebral hemispheric infarction, and acute hydrocephalus. The pathophysiology and specific treatment of intracranial hypertension may be different and depend on aetiology. In patients with subarachnoid haemorrhage a specific focus is on treating secondary hydrocephalus and maintaining adequate cerebral perfusion pressure (CPP). Indications for surgery in patients with intracranial hypertension due to intracerebral haemorrhage (ICH) are not only related to the mass effect, but also to remove the toxic effect of extravasated blood on brain tissue. Decompressive surgery should be considered for patients with a malignant hemispheric infarction, but in order to benefit the patient this surgery should be performed within 48 hours of the onset of the stroke. Hydrocephalus may result from obstruction of cerebrospinal fluid (CSF) flow, from impaired CSF re-absorption and occasionally from overproduction of CSF. Emergency management of acute hydrocephalus can be accomplished by external ventricular drainage of CSF. More definitive treatment may be either by third ventriculostomy or implantation of a CSF shunt diverting CSF to the abdominal cavity (a ventriculoperitoneal shunt) or to the right atrium of the heart (ventriculo-atrial shunt).
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Book chapters on the topic "Brain parenchyma"

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Saido, Takaomi C., and Nobuhisa Iwata. "Catabolism of amyloid-β peptide in brain parenchyma." In Neuroscientific Basis of Dementia, 249–56. Basel: Birkhäuser Basel, 2001. http://dx.doi.org/10.1007/978-3-0348-8225-5_30.

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Tsuyumu, M., H. J. Reulen, and Y. Inaba. "Dynamics of Fluid Movement Through Brain Parenchyma and into the CSF in Vasogenic Brain Edema." In Brain Edema, 99–107. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70696-7_13.

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Garel, Catherine. "Abnormalities of the Fetal Cerebral Parenchyma: Ischaemic and Haemorrhagic Lesions." In 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.

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Blazquez, Raquel, and Tobias Pukrop. "3D Coculture Model of the Brain Parenchyma–Metastasis Interface of Brain Metastasis." In 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.

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Bankiewicz, Krystof. "Neurosurgical Approaches: Drug Infusion Directly into the Parenchyma or the Cerebrospinal Fluid." In 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.

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Svampa, Silvana. "Brain Parenchyma: Usefulness of Transcranial Color-Coded Duplex Sonography (TCCS)." In Neurosonology in Critical Care, 1011–24. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-81419-9_62.

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Endres, Jürgen, Christopher Rohkohl, Kevin Royalty, Sebastian Schafer, Andreas Maier, Arnd Dörfler, and Markus Kowarschik. "Brain Parenchyma and Vessel Separation in 3D Digital Subtraction Angiography Images." In Informatik aktuell, 319–24. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-54345-0_72.

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Al-Sarraf, Hameed, Kevin A. Smart, Malcolm B. Segal, and Jane E. Preston. "Differential Amino Acid Uptake into Cerebral Parenchyma and Capillary Cells during Development." In 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.

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McKinley, Bruce A., and C. L. Parmley. "Effects of Injury and Therapy on Brain Parenchyma pO2, pCO2, pH and ICP following Severe Closed Head Injury." In 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.

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Struys-Ponsar, C., A. Florence, A. Gauthier, R. R. Crichton, and Ph Bosch de Aguilar. "Ultrastructural changes in brain parenchyma during normal aging and in animal models of aging." In 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.

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Conference papers on the topic "Brain parenchyma"

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Chen, Xiaoshuai, Kazuya Sase, Atsushi Konno, and Teppei Tsujita. "A viscoelastic model of brain parenchyma for haptic brain surgery simulations." In 2016 IEEE/SICE International Symposium on System Integration (SII). IEEE, 2016. http://dx.doi.org/10.1109/sii.2016.7844046.

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Chen, Xiaoshuai, Kazuya Sase, Atsushi Konno, and Teppei Tsujita. "Identification of mechanical properties of brain parenchyma for brain surgery haptic simulation." In 2014 IEEE International Conference on Robotics and Biomimetics (ROBIO). IEEE, 2014. http://dx.doi.org/10.1109/robio.2014.7090572.

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Savić, Živorad, Katarina Savić, Sofija Savić, Mirjana Petrović, and Vojislav Antić. "Diagnosis of non-traumatic hemorrhages in the brain parenchyma." In RAD Conference. RAD Centre, 2021. http://dx.doi.org/10.21175/rad.abstr.book.2021.35.5.

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Reddick, Wilburn E., Raymond K. Mulhern, T. David Elkin, John O. Glass, and James W. Langston. "Subtle volume differences in brain parenchyma of children surviving medulloblastoma." In Medical Imaging '98, edited by Eric A. Hoffman. SPIE, 1998. http://dx.doi.org/10.1117/12.312571.

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Hwang, Jinyoung, Yeji Han, and HyunWook Park. "Segmentation of Brain Parenchyma using Bilateral Filtering and Region Growing." In 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.

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Chen, Xiaoshuai, Kazuya Sase, Atsushi Konno, and Teppei Tsujita. "Experimental and numerical analysis of damage fracture mechanics of brain parenchyma." In 2016 IEEE International Conference on Robotics and Biomimetics (ROBIO). IEEE, 2016. http://dx.doi.org/10.1109/robio.2016.7866369.

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Mehrabian, Amin, and Younane Abousleiman. "Realizations of Experimental Hydrocephalus Data Through the Analytical Model of Poroviscoelastic Brain Tissue." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80192.

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Despite recent advances in hydro-mechanical characterization of brain tissue [1], existing models remain inadequate due to complexities associated with the brain’s geometry and rheological properties [2] as well as limited knowledge on the mechanisms which control the CerebroSpinal Fluid (CSF) absorption or formation and their impact on the extracellular fluid content changes inside parenchyma [3].
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Reddick, Wilburn E., Holly A. White, John O. Glass, and Raymond K. Mulhern. "Correlation of neurocognitive function and brain parenchyma volumes in children surviving cancer." In Medical Imaging 2002, edited by Anne V. Clough and Chin-Tu Chen. SPIE, 2002. http://dx.doi.org/10.1117/12.463606.

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Adachi, Kazuhiko, Yoshiaki Inoue, Hiroshi Kanki, Atsushi Fujita, and Eiji Kohmura. "Finite Element Modeling of Brain Tissue Retraction for Neurosurgical Simulation." In ASME 2007 International Mechanical Engineering Congress and Exposition. ASMEDC, 2007. http://dx.doi.org/10.1115/imece2007-41772.

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The simulation capability for intraoperative brain tissue deformation by the surgical procedures using computational Finite Element analysis is demonstrated in this paper. Our research group has been developing the patient-specific three-dimensional Finite Element brain deformation model consisting of precise anatomical structures, i.e., brain parenchyma with both gyri and sulci on the surface, falx cerebri, and tentorium, in order to evaluate brain shift during navigation surgery without additional acquisition of intraoperative imaging. In this study, both gray and white matters of the brain tissues were modeled as homogeneous nonlinear hyper-viscoelastic material. The falx cerebri with tentorium was modeled as linear elastic material which is much stiffer than the brain tissue. The skull was modeled as a rigid body. In the numerical simulation, the computation of the intraoperative cerebellum tissue deformation due to retraction by spatula for posterior fossa surgery was conducted by ABAQUS/Explicit. The illustrative results successfully demonstrate the interaction between brain tissue and spatula.
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Tully, Brett, and Yiannis Ventikos. "Modelling Normal Pressure Hydrocephalus as a ‘Two-Hit’ Disease Using Multiple-Network Poroelastic Theory." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19135.

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The evolution of many cerebral diseases such as Alzheimer’s and Parkinson’s Disease, Hydrocephalus, Cerebral Oedema, Stroke, and Tumour are strongly correlated to a change in the transport properties of fluid in the brain. This research proposes a novel application of Multiple-Network Poroelastic Theory (MPET) to investigate cerebral hydrodynamics through a detailed investigation of multiscalar, spatio-temporal transport of fluid between the cerebral blood, cerebrospinal fluid (CSF) and brain parenchyma. Specifically, MPET is used to interrogate the clinical markers of Normal Pressure Hydrocephalus (NPH).
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