Relevant bibliographies by topics / Central nervous system

Academic literature on the topic 'Central nervous system'

Author: Grafiati
Published: 4 June 2021
Last updated: 29 July 2024

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Journal articles on the topic "Central nervous system"

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Adamson, D. Cory, B. Ahmed K. Rasheed, Roger E. McLendon, and Darell D. Bigner. "Central nervous system." Cancer Biomarkers 9, no. 1-6 (October 26, 2011): 193–210. http://dx.doi.org/10.3233/cbm-2011-0177.

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Desole, M. S., P. Enrico, M. Miele, L. Fresu, G. Esposito, G. De Natale, and E. Miele. "Central nervous system." Pharmacological Research 25 (May 1992): 19–20. http://dx.doi.org/10.1016/1043-6618(92)90265-d.

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Goldberg, Herbert I., and Robert A. Zimmerman. "Central nervous system." Seminars in Roentgenology 22, no. 3 (July 1987): 205–12. http://dx.doi.org/10.1016/0037-198x(87)90034-4.

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Vimal, Shruti. "Histopathological Spectrum of Central Nervous System Tumours in a Tertiary Care Centre." Indian Journal of Pathology: Research and Practice 9, no. 2 (Part- I) (May 1, 2020): 103–10. http://dx.doi.org/10.21088/ijprp.2278.148x.9220.18.

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Colman Ozuna, Víctor Manuel, Natalia María Antonella Rojas Almirón, Edgar Eugenio Ortega Portillo, Sandra María Soto Valiente, Vivian María Liz Pérez, and Graciela Medina Insfran. "Vasculitis del sistema nervioso central." Revista del Instituto de Medicina Tropical 18, no. 1 (August 9, 2023): 90–93. http://dx.doi.org/10.18004/imt/2023.18.1.12.

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La vasculitis primaria del Sistema Nervioso Central (VPSNC) se refiere a un grupo de enfermedades que resultan de la inflamación y destrucción de los vasos sanguíneos de la médula espinal, encéfalo y meninges, tanto en el sector venoso como arterial, esto puede conducir a la oclusión o formación de aneurismas, con las consiguientes alteraciones isquémico-hemorrágicas.1 La presentación es heterogénea y poco sistematizable. El diagnóstico se establece con un cuadro clínico compatible, una angiografía o biopsia del parénquima encefálico y/o meninges que evidencien vasculitis. Presentamos el caso de un paciente portador de retrovirus con probable VPSNC con clínica compatible, hallazgos imagenológicos sugestivos, con escasa alteración de LCR y EEG.2
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Canillas, M., B. Moreno-Burriel, and E. Chinarro. "Materials directed to implants for repairing Central Nervous System." Boletín de la Sociedad Española de Cerámica y Vidrio 53, no. 6 (December 30, 2014): 249–59. http://dx.doi.org/10.3989/cyv.302014.

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K, Sailaja. "A STUDY ON CONGENITAL ANOMALIES OF CENTRAL NERVOUS SYSTEM." International Journal of Anatomy and Research 5, no. 2.2 (May 31, 2017): 3819–23. http://dx.doi.org/10.16965/ijar.2017.189.

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Lipton, Jordan D., and Robert W. Schafermeyer. "Central Nervous System Infections." Emergency Medicine Clinics of North America 13, no. 2 (May 1995): 417–43. http://dx.doi.org/10.1016/s0733-8627(20)30358-8.

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Frost, Elizabeth A. M. "Central Nervous System Trauma." Anesthesiology Clinics of North America 5, no. 3 (September 1987): 565–85. http://dx.doi.org/10.1016/s0889-8537(21)00334-5.

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Brem, Steven S., Philip J. Bierman, Henry Brem, Nicholas Butowski, Marc C. Chamberlain, Ennio A. Chiocca, Lisa M. DeAngelis, et al. "Central Nervous System Cancers." Journal of the National Comprehensive Cancer Network 9, no. 4 (April 2011): 352–400. http://dx.doi.org/10.6004/jnccn.2011.0036.

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Dissertations / Theses on the topic "Central nervous system"

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Solomon, Thomas. "Central nervous system infections in Vietnam." Thesis, Open University, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.340736.

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Zhang, Hui. "Remyelination in the central nervous system." Thesis, University of Edinburgh, 2013. http://hdl.handle.net/1842/8095.

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Multiple Sclerosis (MS) is an inflammatory disease which causes areas of demyelination in the Central Nervous System (CNS) and affects only humans. Current therapies for MS are focused on anti-inflammatory treatment, which reduce the occurrence and clinical relapses of the disease. However, progressive disability of the disease is related to axonal degeneration. After demyelination, remyelination occurs, which helps repair the demyelinated lesions and protects axons from degeneration. However, this endogenous remyelination is inefficient, and currently there are no therapies available to enhance remyelination. The aim of this thesis was to first characterize a fast and reliable model to study CNS remyelination in vitro, and second to investigate the role of semaphorin 3a (Sema3A) and semaphorin 3f (Sema3F) signaling in CNS remyelination. Various in vivo models have been developed to investigate the pathology of multiple sclerosis, and can be used to test remyelination therapies. However, in vivo models are expensive, animal- and time- consuming. Until now, there has been no well-characterized and robust in vitro model for remyelination study. In this thesis, an ex vivo slice culture system with mouse brain and spinal cord was developed, and characterized by immunofluorescent microscopy and transmission electron microscopy, for CNS remyelination study. Automated (re)myelinating quantification by image pro plus software was developed and validated to provide a fast and reliable way for testing factors that change remyelination efficiency. Two such factors are Sema3A and 3F, which were initially identified as axon guidance cues during development. Sema3A (repulsive) and 3F (attractive) were proved to play a role in oligodendrocyte precursor cell (OPC) migration during development, and hypothesized to be important in remyelination. In this thesis, I investigated the effects and mechanisms for this by adding recombinant SEMA3A or SEMA3F or by knockdown their obligatory receptors Neuropilin (Nrp) 1 and 2, using lentivirus induced miRNAi. Slice culture and primary OPC culture were used to determine the effect on OPC survival, migration, proliferation, differentiation and myelination.
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Zhang, Xiaochun. "Involvement of neuroinflammation in models of neurodegeneration." Laramie, Wyo. : University of Wyoming, 2008. http://proquest.umi.com/pqdweb?did=1663059561&sid=3&Fmt=2&clientId=18949&RQT=309&VName=PQD.

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Poland, Stephen D. "Central nervous system infection with human cytomegalovirus." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq21311.pdf.

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Bernick, Kristin Briana. "Cell biomechanics of the central nervous system." Thesis, Massachusetts Institute of Technology, 2011. http://hdl.handle.net/1721.1/67202.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biological Engineering, 2011.
Cataloged from PDF version of thesis.
Includes bibliographical references (p. 133-153).
Traumatic brain injury (TBI) is a significant cause of death and morbidity in both the civilian and military populations. The major causes of TBI, such as motor vehicle accidents, falls, sports concussions, and ballistic and explosive blast threats for military personnel, are well established and extensively characterized; however, there remains much to be learned about the specific mechanisms of damage leading to brain injury, especially at the cellular level. In order to understand how cells of the central nervous system (CNS) respond to mechanical insults and stimuli, a combined modeling/experimental approach was adopted. A computational framework was developed to accurately model how cells deform under various macroscopically imposed loading conditions. In addition, in vitro (cell culture) models were established to investigate damage responses to biologically relevant mechanical insults. In order to develop computational models of cell response to mechanical loading, it is essential to have accurate material properties for all cells of interest. In this work, the mechanical responses of neurons and astrocytes were quantified using atomic force microscopy (AFM) at three different loading rates and under relaxation to enable characterization of both the elastic and viscous components of the cell response. AFM data were used to calibrate an eight-parameter rheological model implemented in the framework of a commercial finite element package (Abaqus). Model parameters fit to the measured responses of neurons and astrocytes provide a quantitative measure of homogenized nonlinear viscoelastic properties for each cell type. In order to ensure that the measured responses could be considered representative of cell populations in their physiological environment, cells were also grown and tested on substrates of various stiffness, with the softest substrate mimicking the stiffness of brain tissue. Results of this study showed both the morphology and measured force response of astrocytes to be significantly affected by the stiffness of their substrate, with cells becoming increasingly rounded on soft substrates. Results of simulations suggested that changes in cell morphology were able to account for the observed changes in AFM force response, without significant changes to the cell material properties. In contrast, no significant changes in cell morphology were observed for neurons. These results highlight the importance of growing cells in a biologically relevant environment when studying mechanically mediated responses, such as TBI. To address this requirement, we developed two model systems with CNS cells grown in soft, 3D gels to investigate damage arising from dynamic compressive loading and from a shock pressure wave. These damage protocols, coupled with the single cell computational models, provide a new tool set for characterizing damage mechanisms in CNS cells and for studying TBI in highly controllable in vitro conditions.
by Kristin Briana Bernick.
Ph.D.
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Coutinho, Maria Ester Freitas Barbosa Pereira. "Central nervous system autoimmunity in neuropsychiatric disorders." Thesis, University of Oxford, 2016. https://ora.ox.ac.uk/objects/uuid:389fb830-4b4e-4201-9965-19acb2c63ff3.

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The recent history of autoimmune neurology is marked by the discovery of many central nervous system (CNS) antibody-mediated diseases. These disorders are caused by antibodies that target important proteins expressed in the neuronal surface, which are believed to be directly pathogenic. These antibodies are immunoglobulin G (IgG) isotype and, as such, have the potential to cross the placenta during gestation. Foetal exposure to CNS-targeting antibodies could alter developing neuronal circuits, leading to disease. However, the consequences of exposure to these antibodies during neurodevelopment has hardly been considered. To study the relationship between maternal antibodies towards neuronal surface proteins and neurodevelopmental disorders in the foetus a dual approach was undertaken. First, pregnancy serum samples from mothers of children later diagnosed with a neurodevelopmental disorder and from mothers of children with typical development were screened for the presence of neuronal surface antibodies. Next, the effects of pathogenic neuronal surface antibodies in the offspring were assessed in a maternal-to-foetal transfer mouse model. Antibodies to neuronal surface proteins in the gestational serum, particularly CASPR2 antibodies, were found to associate with an increased risk of mental retardation and disorders of psychological development in the progeny. The animal model showed that mice exposed in utero to CASPR2 antibodies have long term behavioural sequelae and histological findings suggestive of abnormalities in brain development. These findings support a model in which maternal antibodies towards foetal neuronal proteins cause long-term behavioural deficits and permanent abnormalities at the cellular and synaptic level in a subset of children with neurodevelopmental disorders.
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Hüppi, Petra Susan. "Serum antibodies to central nervous system antigens /." [S.l : s.n.], 1986. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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Radke, James Melvin. "Studies involving somatostatin systems in the rodent central nervous system." Thesis, University of British Columbia, 1987. http://hdl.handle.net/2429/26518.

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Somatostatin is a neuropeptide found throughout the brain. Several studies have established its anatomical distribution as being quite heterogenous with relatively high concentrations appearing in the limbic and striatal systems. Presently, very little is known about the functions of somatostatin systems in the brain and how they interact with other transmitter systems. The following report is a summary of experiments undertaken to assess the functional and chemical interactions of somatostatin with other neurotransmitter systems. Previous studies have established that the dopaminergic inputs to the basal ganglia are important for locomotor activity and reward. These systems have also been implicated in several mental and neural diseases such as schizophrenia, depression, and Parkinson’s disease. In the first experiment, interactions between dopamine and somatostatin systems were examined using paradigms involving behavioural responses to dopamine agonists. Depletion of somatostatin levels by the drug cysteamine was found to attenuate amphetamine- and apomorphine-mediated motor behaviours but not the reinforcing aspects of amphetamine. The second experiment attempted to further characterize the nature of the dopamine-somatostatin interaction by examining the effects of haloperidol, a dopamine antagonist, on central somatostatin levels. Short term treatment with haloperidol decreased striatal somatostatin levels. Long term treatment (8 months) with haloperidol failed to alter somatostatin levels in the caudate-putamen. Since somatostatin levels appear to be normal in Parkinsonian brains, the effects of MPTP poisoning in mice on central somatostatin levels was also studied to examine the accuracy of this animal model of Parkinson's disease and examine the effects of dopaminergic lesions on somatostatin levels. The results of this experiment indicate that MPTP causes a dose dependent increase in nigral somatostatin levels without altering striatal or cortical levels. These results are in partial disagreement with results obtained from both post-mortem Parkinsonian brains and primates given MPTP, thereby questioning the accuracy of this mouse model of Parkinson's disease. The final experiment examined the effects of the anticonvulsant-antidepressant carbamazepine on central somatostatin levels in the rat. Although the chemical mechanisms responsible for the therapeutic effects of carbamazepine are unknown, previous studies have suggested that its efficacy in the treatment of both manic-depression and epilepsy may be associated with the ability of this drug to reduce the abnormal somatostatin levels observed in these diseases. In this experiment, neither acute, chronic, nor withdrawal from chronic treatment with carbamazepine were found to alter the levels of somatostatin in rats. The lack of effects of carbamazepine on basal somatostatin levels may indicate somatostatin cells are susceptible to carbamazepine only under pathological situations. Together, these results are discussed in the context of recent observations of abnormal somatostatin levels in several diseases of the central nervous system and provide some insight into the interactions and functions of somatostatin systems in the normal and abnormal brain.
Medicine, Faculty of
Graduate
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Lothian, Carina. "Nestin regulation in the embryonic and adult CNS /." Stockholm : [Karolinska institutets bibl.], 2001. http://diss.kib.ki.se/2001/91-7349-057-1/.

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Eckert, Bodil. "Hypoglycaemia studies on central and peripheral nerve function /." Lund : Dept. of Internal Medicine, University of Lund, 1998. http://catalog.hathitrust.org/api/volumes/oclc/57426099.html.

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Books on the topic "Central nervous system"

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Emerich, Dwaine F., Reginald L. Dean, and Paul R. Sanberg, eds. Central Nervous System Diseases. Totowa, NJ: Humana Press, 2000. http://dx.doi.org/10.1007/978-1-59259-691-1.

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Ahluwalia, Manmeet, Philippe Metellus, and Riccardo Soffietti, eds. Central Nervous System Metastases. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-23417-1.

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Ramakrishna, Rohan, Rajiv S. Magge, Ali A. Baaj, and Jonathan P. S. Knisely, eds. Central Nervous System Metastases. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-42958-4.

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Kryzhanovsky, G. N. Central Nervous System Pathology. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-7870-9.

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Allen, Deborah Hutchinson, and Laurie L. Rice. Central nervous system cancers. Pittsburgh, Pa: Oncology Nursing Society, 2010.

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Lacruz, César R., ed. Central Nervous System Tumors. Cham: Springer Nature Switzerland, 2023. http://dx.doi.org/10.1007/978-3-031-51078-6.

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Michael-Titus, Adina. The nervous system. Edinburgh: Churchill Livingstone, 2006.

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Gorodetskiy, Andrey E., and Vugar G. Kurbanov, eds. Smart Electromechanical Systems: The Central Nervous System. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-53327-8.

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Wilkinson, Ashley E., Aleesha M. McCormick, and Nic D. Leipzig. Central Nervous System Tissue Engineering. Cham: Springer International Publishing, 2012. http://dx.doi.org/10.1007/978-3-031-02582-2.

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Ballanyi, Klaus, ed. Isolated Central Nervous System Circuits. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-020-5.

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Book chapters on the topic "Central nervous system"

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Elgazzar, Abdelhamid H., and Ismet Sarikaya. "Central Nervous System." In Nuclear Medicine Companion, 219–41. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-76156-5_8.

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Mino, Miriame, Krisztian Homicsko, and Roger Stupp. "Central Nervous System." In Side Effects of Medical Cancer Therapy, 293–331. London: Springer London, 2012. http://dx.doi.org/10.1007/978-0-85729-787-7_7.

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Elgazzar, Abdelhamid H. "Central Nervous System." In Synopsis of Pathophysiology in Nuclear Medicine, 273–89. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-03458-4_12.

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Klingensmith, William C. "Central Nervous System." In The Mathematics and Biology of the Biodistribution of Radiopharmaceuticals - A Clinical Perspective, 161–75. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-26704-3_13.

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Yu, Yao, Steve E. Braunstein, Daphne A. Haas-Kogan, and Jean L. Nakamura. "Central Nervous System." In Handbook of Evidence-Based Radiation Oncology, 37–105. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-62642-0_2.

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Timperley, W. R., J. M. MacKenzie, and S. F. D. Robinson. "Central nervous system." In Reporting Histopathology Sections, 366–79. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-7132-6_23.

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Schulz, Volker, Rudolf Hänsel, and Varro E. Tyler. "Central Nervous System." In Rational Phytotherapy, 41–106. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-642-98093-0_2.

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Schulz, Volker, Rudolf Hänsel, Mark Blumenthal, and Varro E. Tyler. "Central Nervous System." In Rational Phytotherapy, 43–123. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-662-09666-6_2.

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Smith, Joseph F. "Central Nervous System." In Paediatric Pathology, 125–94. London: Springer London, 1989. http://dx.doi.org/10.1007/978-1-4471-3337-7_4.

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Paulley, J. W., and H. E. Pelser. "Central Nervous System." In Psychological Managements for Psychosomatic Disorders, 155–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-73731-2_9.

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Conference papers on the topic "Central nervous system"

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Henoch-Schönlein Purpura, A., Gabriele Simonini, Eleonora Fusco, Ilaria Maccora, Anna Rosati, Rolando Cimaz, and Teresa Giani. "AB1015 CENTRAL NERVOUS SYSTEM VASCULITIS PRECEDING." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.4663.

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Guck, Jochen R. "Optomechanical insights into the central nervous system." In Optical Elastography and Tissue Biomechanics VIII, edited by Kirill V. Larin and Giuliano Scarcelli. SPIE, 2021. http://dx.doi.org/10.1117/12.2578567.

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Moreira, Laila Prazeres Schulz, Daniela Fernanda Almeida Santos, Guilherme Cordaro Bucker Furini, Isabela Bartholomeu Ferreira da Costa, Saul Didmar Alquez Montano, Amanda Póvoa de Paiva, Maiave Micalle Figueiredo de Matos, Maria Avanise Yumi Minami, and Ana Paula Andrade Hamad. "Central nervous system complications of pediatric sinusitis." In SBN Conference 2022. Thieme Revinter Publicações Ltda., 2023. http://dx.doi.org/10.1055/s-0043-1774460.

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Correa, S., R. Nahar, B. D. Smighelschi, V. Vulkanov, and K. Guevarra. "Amidst Mimickers: Primary Central Nervous System Vasculitis." 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.a5613.

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Barač, Anja, Ivona Jerković, and Petra Nimac Kozina. "Primary angiitis of the central nervous system (PACNS)." In NEURI 2015, 5th Student Congress of Neuroscience. Gyrus JournalStudent Society for Neuroscience, School of Medicine, University of Zagreb, 2015. http://dx.doi.org/10.17486/gyr.3.2223.

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Wodarcyk, A. J., and J. G. Wang. "Extensive Central Nervous System Nocardiosis Without Neurologic Manifestations." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a4061.

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Hartwell, Peter. "CeNSE: A central nervous system for the earth." In 2011 IEEE Technology Time Machine (TTM). IEEE, 2011. http://dx.doi.org/10.1109/ttm.2011.6005162.

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Shahidi, Ghavam G. "CeNSE: A central nervous system for the earth." In 2011 IEEE Technology Time Machine (TTM). IEEE, 2011. http://dx.doi.org/10.1109/ttm.2011.6005165.

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Prestes, Ana Clarice Bartosievicz, Sergio Antonio Antoniuk, Mara Lucia Schmitz Ferreira Santos, Adriano Kejiro Maeda, Ana Paula Kuczynski Pedro Bom, and Victor Horácio de Souza Costa Junior. "Central nervous system juvenile xantogranuloma: a case report." In SBN Conference 2022. Thieme Revinter Publicações Ltda., 2023. http://dx.doi.org/10.1055/s-0043-1774565.

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Disserol, Caio, Alessandra Filpo, Taís Luise Denicol, Bruno Della-Ripa, Francine Mendonça, Rodrigo de Faria Ferreira, and Marcos Christiano Lange. "Thromboembolic Central Nervous System Complications of COVID-19." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.492.

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Context: COVID-19 is well-known to increase the risk of developing thromboembolism; thus, patients may present with diverse neurovascular manifestations. Case report: A 56-year-old man presented with sudden onset of incoordination of his left arm and leg. He also had a history of recurrent episodes of transient left hemithoracic pain radiating to his left arm, along with right visual hemi-field positive phenomena. Additionally, he reported self-limited fever and anosmia three weeks earlier. Examination revealed left hemiataxia (NIHSS score: 2). Initial assessment with brain CT, intracranial and cervical CT angiography was normal. Shortly after admission, the patient developed acute weakness of his four limbs and urinary retention. Neurological exam showed left homonimous hemianopia, asymmetric tetraparesis and a superficial sensory level at C4. Neuraxis MRI was performed and diffusion-weighted imaging revealed acute ischemic lesions in the occiptal lobes, cerebellum and cervicalthoracic spine. A thorough diagnostic work-up was conducted. Laboratory tests were unremarkable, including inflammatory markers, viral hepatitis, HIV and syphilis serologies, as well as rheumatologic tests and a thrombophilia panel, except for SARS-COV-2 serology, with detection of IgM antibodies. RT-PCR nasopharyngeal swab was negative. Further investigation with CSF analysis, CT angiography of the aorta, transthoracic echocardiogram, 24-hour holter monitoring and transcranial Doppler didn’t show any abnormalities. Transesophageal echocardiogram revelead a minor patent foramen ovale. Conclusion: This is a case of acute cerebral, cerebellar and spinal embolic infarction, probably related to Covid-19, illustrating the infection’s associated coagulopathy¹.
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Reports on the topic "Central nervous system"

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Ridgway, Sam H. The Cetacean Central Nervous System. Fort Belvoir, VA: Defense Technical Information Center, January 1999. http://dx.doi.org/10.21236/ada381704.

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Albquerque, Edson X. Molecular Targets for Organophosphates in the Central Nervous System. Fort Belvoir, VA: Defense Technical Information Center, June 2004. http://dx.doi.org/10.21236/ada426356.

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Rowland, Vernon, and Henry Gluck. Attention and Preparatory Processes in the Central Nervous System. Fort Belvoir, VA: Defense Technical Information Center, August 1986. http://dx.doi.org/10.21236/ada171316.

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Butler, F. K., and Jr. Central Nervous System Oxygen Toxicity in Closed-Circuit Scuba Divers. Fort Belvoir, VA: Defense Technical Information Center, March 1986. http://dx.doi.org/10.21236/ada170879.

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Clark, J. M., and C. J. Lambertsen. Extension of Central Nervous and Visual System Oxygen Tolerance in Physical Work. Fort Belvoir, VA: Defense Technical Information Center, December 1990. http://dx.doi.org/10.21236/ada239160.

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Mery, Laura, Matthew Wayner, John McQuade, and Erica Anderson. Characterization of the Effects of Fatigue on the Central Nervous System (CNS) and Drug Therapies. Fort Belvoir, VA: Defense Technical Information Center, November 2007. http://dx.doi.org/10.21236/ada489794.

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Catlin, Kristen M. Role of Cytokines and Neurotrophins in the Central Nervous System in Venezuelan Equine Encephalitis Pathogenesis. Fort Belvoir, VA: Defense Technical Information Center, February 2001. http://dx.doi.org/10.21236/ad1012369.

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Li, Yanming, Zhigang Zhao, and Yuanbo Liu. Combined chemotherapy in new diagnosed primary central nervous system lymphoma: a systematic review and network meta‑analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2020. http://dx.doi.org/10.37766/inplasy2020.9.0084.

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Carpenter, A. V., W. D. Flanders, E. L. Frome, D. J. Crawford-Brown, and S. A. Fry. Radiation exposure and central nervous system cancers: A case-control study among workers at two nuclear facilities. Office of Scientific and Technical Information (OSTI), March 1987. http://dx.doi.org/10.2172/6646019.

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Marchionni, Enrica, Daniele Guadagnolo, Gioia Mastromoro, and Antonio Pizzuti. Diagnostic yield of prenatal Exome Sequencing in fetal Central Nervous System Anomalies: systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2023. http://dx.doi.org/10.37766/inplasy2023.5.0003.

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Abstract:
Review question / Objective: The aim of this study is to assess the incremental diagnostic yield of prenatal exome sequencing analysis after inconclusive result of karyotype and Chromosomal Microarray Analysis in Central Nervous System fetal anomalies detected by ultrasound. Eligibility criteria: Inclusion criteria: papers describing fetuses with the indication to perform genome-wide sequencing studies based on prenatal imaging findings who underwent previous inconclusive karyotype and Chromosomal Microarray Analyses. The diagnostic yields of prenatal exome sequencing analysis OR prenatal genome sequencing analysis (with ≥20–30x depth of coverage and including only Single Nucleotide Variants) will be pooled in a meta-analysis. Exclusion Criteria: case reports and papers describing less than 5 cases; papers not describing the application of genome-wide sequencing studies based on prenatal imaging findings; papers describing genome-wide sequencing studies performed after negative targeted panels; papers describing fetuses with recurrent phenotypes as an explicitly selection criterium.
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