Relevant bibliographies by topics / Brain stem

Academic literature on the topic 'Brain stem'

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

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Journal articles on the topic "Brain stem"

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Kitanaka, C., Y. Inoh, T. Toyoda, T. Sasaki, and T. Eguchi. "Malignant brain stem hyperthermia caused by brain stem hemorrhage." Stroke 25, no. 2 (February 1994): 518–20. http://dx.doi.org/10.1161/01.str.25.2.518.

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Pallis, C. "Coma and brain stem areflexia in brain stem encephalitis." BMJ 291, no. 6497 (September 14, 1985): 737. http://dx.doi.org/10.1136/bmj.291.6497.737-b.

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Evans, D. W., L. C. Lum, D. J. Hill, and R. C. Campbell. "Coma and brain stem areflexia in brain stem encephalitis." BMJ 291, no. 6497 (September 14, 1985): 737. http://dx.doi.org/10.1136/bmj.291.6497.737-c.

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Al-Din, A. S. N., A. S. Jamil, and R. Shakir. "Coma and brain stem areflexia in brain stem encephalitis." BMJ 291, no. 6506 (November 16, 1985): 1422. http://dx.doi.org/10.1136/bmj.291.6506.1422.

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Cowan, Richard, and Barbara Miles. "Brain stem death." Anaesthesia & Intensive Care Medicine 22, no. 8 (August 2021): 471–74. http://dx.doi.org/10.1016/j.mpaic.2021.06.011.

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Mohamed, ZubairUmer. "Brain stem death." Amrita Journal of Medicine 16, no. 2 (2020): 41. http://dx.doi.org/10.4103/amjm.amjm_23_20.

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Thompson, R. K., and M. Salcman. "Brain stem hemorrhage." Neurosurgery 22, no. 4 (April 1988): 623???8. http://dx.doi.org/10.1097/00006123-198804000-00001.

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Guillamo, Jean-Sébastien, François Doz, and Jean-Yves Delattre. "Brain stem gliomas." Current Opinion in Neurology 14, no. 6 (December 2001): 711–15. http://dx.doi.org/10.1097/00019052-200112000-00006.

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Deroy, R. "Brain stem death." BMJ 321, no. 7261 (September 9, 2000): 635. http://dx.doi.org/10.1136/bmj.321.7261.635.

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Dinsmore, Judith, and Anne Garner. "Brain stem death." Surgery (Oxford) 27, no. 5 (May 2009): 216–20. http://dx.doi.org/10.1016/j.mpsur.2009.04.001.

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Dissertations / Theses on the topic "Brain stem"

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Carlén, Marie. "Adult neurogenesis : from stem cell to functional neuron /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-367-1/.

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Bruggeman, Kiara. "How to build a brain." Thesis, https://youtu.be/yTkSAceGenw, 2014. http://hdl.handle.net/1885/14128.

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Your cells are magnificent little things, every single one is full of complex microsystems all working together to keep you going. They’re more intricate and advanced than any machines we can make, but sometimes… they need a little help to get going. Stem cells are like tiny teenagers, they’re full of potential but they need a kick in the pants to get going, and that’s where I come in. After a stroke, patients are left with chunks of damaged brain tissue. Now, instead of trying to rebuild the incredibly complex human brain from scratch, I’d much give cells the support and encouragement they need to rebuild it themselves. My research goal is to rebuild damaged brain tissue, but in truth, stem cells will be doing all the actual building, I’m just making materials that tell them how to build a brain.
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Paues, Jakob. "Brain Stem Involvement in Immune and Aversive Challenge." Doctoral thesis, Linköping : Linköping University, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-7579.

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Marciszewski, Kasia. "Does Migraine Stem From the Brainstem?" Thesis, The University of Sydney, 2019. https://hdl.handle.net/2123/21241.

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The exact neural mechanisms underlying migraine have been strongly debated for decades. It is well accepted the trigeminovascular system plays a role in migraine, however the precise neurobiological mechanism by which migraine attacks are initiated is presently unknown. Existing literature has demonstrated that even between attacks, the migraine brain differs from that of controls and has led to the current theory of migraine as a “cycling” brain disorder. This suggests that the changes observed in migraine are not fixed, but rather dynamic in nature, and that function, sensitivity and even anatomy of the brainstem may fluctuate throughout the migraine cycle. However, while the brainstem has been heavily implicated in migraine pathogenesis, it has been poorly studied by neural imaging investigations. Likewise, the spontaneous and episodic nature of migraines has made it difficult to study the migraine cycle in its entirety. As such, this thesis aimed to explore brainstem anatomy, functional connectivity, and sensitivity to noxious stimuli, in migraineurs across the entire migraine cycle. The investigations performed in this thesis, consistently revealed key brainstem pain-processing regions, such as the spinal trigeminal nucleus and periaqueductal grey matter, as having altered anatomy, functional connectivity, and sensitivity across the migraine cycle. Most intriguingly, these changes were most dramatically altered in the 24 hours immediately prior to migraine onset. This suggests the observed changes in these brainstem regions may underlie the processes causing migraine initiation. Furthermore, these changes were dynamic in nature, supporting the notion of a “cycling” migraine brain. This opens new avenues for migraine research which will hopefully lead to better prophylactic treatments, capable of controlling these fluctuations that underlie the disorder.
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Wennersten, Andrʹe. "Human neural stem cell transplantation in experimental brain trauma /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-211-X/.

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Ringstedt, Thomas. "Neurotrophins during development : overexpression in neural stem cells /." Stockholm, 1998. http://diss.kib.ki.se/search/diss.se.cfm?19980605ring.

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Parker, Graham Charles. "Cholinergic stimulation of the substantia negra." Thesis, University of St Andrews, 1993. http://hdl.handle.net/10023/14733.

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Convergent lines of research suggest there exists an excitatory cholinergic input to the substantia nigra from the pedunculopontine tegmental nucleus and possibly the laterodorsal tegmental nucleus. Previous work has suggested that microinjection of cholinergic agonists into substantia nigra elicits behaviours performed with a high frequency but with a low current rate (Winn 1991). Experiments carried out during my PhD have demonstrated that: Microinjection of cholinergic agonists to anterior substantia nigra (SN) elicited increased consumption of palatable food such as spaghetti but not rat maintenance diet in pre-satiated rats. Stimulation of behaviour was achieved using direct agonists for either muscarinic or nicotinic cholinergic receptors (carbachol and nicotine respectively). Stimulation of behaviour was also achieved using the indirect cholinergic agonist neostigmine which blocks the de-activation of endogenous acetylcholine by AChE. Increased feeding elicited by cholinergic stimulation of the anterior SN was abolished by a selective lesion of ascending dopamine (DA) neurones which significantly depleted caudate DA levels but left accumbens DA levels unaltered. A behaviourally potent dose of carbachol caused a significant increase in the response to different doses of nicotine suggesting an additive effect of muscarinic and nicotinic stimulation at the doses used. Administration of cholinergic agonists to the VTA or SN caused indistinguishable effects on responding for conditioned reinforcement. Cholinergic stimulation caused increased responding for a conditioned reinforcer and also reinstated responding at the primary reward source. The functional significance of the cholinergic innervation of the DA- containing neurones of the substantia nigra is discussed with reference to its relationship to the neighbouring ventral tegmental area, and their innervation of the caudate-putamen and the nucleus accumbens. Cholinergic neurones in the PPTg and LDTN appear to exert a tonic control over the activity of midbrain DA-containing neurones. It is suggested that cholinergic control of midbrain DA-containing neurones facilitates the processing of information in the striatum and hence influence the selection of an appropriate behavioural response to a given situation.
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Keating, Glenda Louise. "Examination of the role of the pedunculopontine tegmental nucleus in the control of behavioural processes." Thesis, University of St Andrews, 1998. http://hdl.handle.net/10023/14737.

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The role of the pedunculopontine tegmental nucleus (PPTg) in the control of behavioural processes was investigated in this thesis. This was achieved through examination of: (1) Conditioned place preference formation: PPTg lesioned rats were not impaired in forming an appropriate place preference, regardless of their deprivation state. (2) Reward-related responding: both food deprived and non-deprived lesioned rats displayed disinhibited intake across a gradient of sucrose rewards, the degree of disinhibition increasing as the reward became stronger. This disinhibited responding was disassociated from simple approach behaviour as shown by similar runway completion times across control and lesioned rats. (3) Radial arm maze performance: PPTg lesioned rats were impaired in their ability to retrospectively plan and forage in a random foraging task. This impairment was seen in both acquisition and retention tasks. PPTg lesioned rats were also impaired in the acquisition of a spatial working memory task in which they had to prospectively plan and execute responses. (4) These behavioural tasks are related to striatal output. To complement them anatomical experiments examining altered striatal outflow on neurotransmitter expression in the PPTg were conducted. Neither dopamine receptor blockade nor 6- hydroxydopamine (6-OHDA) lesions of striatal dopamine produced changes in nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase expression in the PPTg. This work did, however, lay the foundation for future experimentation to address this question. The combination of these findings extends current literature to outline a role for the PPTg in the control of complex behaviours that have been previously associated with sites higher up the neuraxis. This thesis demonstrates that removal of the PPTg results in behaviours that are inappropriate and disinhibited. In conclusion the PPTg is important for both accurate response selection and execution of goal directed behaviours, elements crucial for effective behavioural responding.
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Gupta, Kunal. "Using human embryonic stem cells to model acute brain injury." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610468.

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Capela, Maria Alexandra Nunes. "Neural stem cells in the embryonic and adult mouse brain." Doctoral thesis, Porto : Edição do Autor, 2002. http://hdl.handle.net/10216/64573.

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Books on the topic "Brain stem"

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Saab, Carl Y. Hind brain. Philadelphia: Chelsea House, 2005.

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Singh, Sheila K., and Chitra Venugopal, eds. Brain Tumor Stem Cells. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8805-1.

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Duvernoy, Henri M. Human Brain Stem Vessels. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-662-07813-6.

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Workshop on Vascular Brain Stem Diseases (1988 Gütersloh, Germany). Vascular brain stem diseases. Edited by Hofferberth Bernhard. Basel: Karger, 1990.

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Caplan, Louis R., and Hanns Christian Hopf, eds. Brain-Stem Localization and Function. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-78172-8.

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R, Caplan Louis, Hopf H. Ch, Besser R, and Krämer Günter Dr med, eds. Brain-stem localization and function. Berlin: Springer-Verlag, 1993.

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G, Cruccu, and Hallett Mark, eds. Brainstem function and dysfunction. Amsterdam: Elsevier, 2005.

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1933-, Kunze Klaus, Zangemeister W. H, and Arlt A, eds. Clinical problems of brainstem disorders. Stuttgart: Thieme, 1986.

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1948-, Csécsei G., ed. Primary and secondary brain stem lesions. Wien: Springer-Verlag, 1987.

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Duvernoy, Henri M. The Human Brain Stem and Cerebellum. Vienna: Springer Vienna, 1995. http://dx.doi.org/10.1007/978-3-7091-3078-0.

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Book chapters on the topic "Brain stem"

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Hambrick, Erin. "Brain Stem." In Encyclopedia of Child Behavior and Development, 290–93. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-0-387-79061-9_419.

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Dunkel, Ira J., and Mark M. Souweidane. "Brain Stem Glioma." In International Neurology, 519–21. Oxford, UK: Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9781444317008.ch132.

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Clarke, C. R. A. "Brain Stem Death." In Care of the Critically Ill Patient, 977–81. London: Springer London, 1992. http://dx.doi.org/10.1007/978-1-4471-3400-8_57.

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Zoumprouli, Argyro, and Konstantina Ilia Karydi. "Brain Stem Death." In Textbook of Neuroanesthesia and Neurocritical Care, 335–43. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-3390-3_23.

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Spurlock-White, Shelia. "Brain Stem Infarct." In Clinical Case Studies in Home Health Care, 248–58. West Sussex UK: John Wiley & Sons, Inc., 2013. http://dx.doi.org/10.1002/9781118785744.ch24.

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Krieger, Derk, Michael S. Pessin, Andreas Ferbert, and Daniel F. Hanley. "Brain-Stem Syndromes." In Neurocritical Care, 319–28. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-87602-8_30.

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Patten, John Philip. "The Brain Stem." In Neurological Differential Diagnosis, 162–77. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-58981-2_11.

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Magram, Gary, and Luis Schut. "Brain Stem Gliomas." In Neuro-Oncology, 347–58. Dordrecht: Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-011-3152-0_61.

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Jacobson, Stanley, and Elliott M. Marcus. "Brain Stem Functional Localization with Atlas of the Brain Stem." In Neuroanatomy for the Neuroscientist, 93–114. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-1-4419-9653-4_6.

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Kim, Jong S. "Brain Stem Infarction Syndromes." In Posterior Circulation Stroke, 35–65. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-6739-1_4.

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Conference papers on the topic "Brain stem"

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Bourseau, Erika, Laurent Lemaire, Eric Hervouet, François Valette, Philippe Menei, François Berger, Didier Wion, Jean‐Pierre Benoit, and Emmanuel Garcion. "Abstract A60: Targeting brain tumor stem cells." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-a60.

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Hu, Hao, William S. Rosenberg, and Adnan H. Nayfeh. "Modeling Human Brain Movability Effect on Brain Response During Impact." In ASME 1998 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1998. http://dx.doi.org/10.1115/imece1998-0980.

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Abstract Brain responses due to its movability during impact was investigated by using sliding interface approach. A new 3D 50th percentile human head finite element model has been generated in which sliding interfaces totally separate the brains and cerebrospinal fluid (CSF)/cranium. So, the brains can move to some extent. It becomes an equivalent one to most widely used brain/CSF (cranium) coupled models by switching interface type from sliding to tied. The model was partially validated by using available experimental and computed data in frontal impact. Compared with brain/CSF (cranium) coupled models, the new model predicts higher brain stress levels at sites such as corpus callosum, brain stem, and the vicinity of the ventricles etc. and more realistic deformation patterns. The results suggest that a fluid-solid interaction approach should be used to better model brain movement during impact to correctly interpret the brain injuries and to evaluate proposed head injury mechanisms.
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Mesi, O., and C. P. Wu. "Absent Brain Stem Reflexes After Cardiac Arrest: Brain Death or Drug Toxicity?" In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a3402.

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Ma, Lei, Feng Ju, Kaixin Pan, Chunling Tao, and Xiaoyan Shen. "Detection and evaluation of brain spinal cord conduction function based on functional electrical stimulation." In 2019 IEEE Integrated STEM Education Conference (ISEC). IEEE, 2019. http://dx.doi.org/10.1109/isecon.2019.8882007.

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Amanipour, Reza M., Robert D. Frisina, Samantha A. Cresoe, Teresa J. Parsons, Xiaoxia Zhu, Cesario V. Borlongan, and Joseph P. Walton. "Impact of mild traumatic brain injury on auditory brain stem dysfunction in mouse model." In 2016 38th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2016. http://dx.doi.org/10.1109/embc.2016.7591081.

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Korenke, Georg-Christoph, Katharina Redyk, Tobias Kowald, and Sabine Diedrich. "FV 205. Parkinsonism after Coxsackievirus B3 Brain Stem Encephalitis." In Abstracts of the 44th Annual Meeting of the Society for Neuropediatrics. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1675920.

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Burgess, Alison, Carlos A. Ayala-Grosso, Milan Ganguly, Jessica Jordao, Isabelle Aubert, and Kullervo Hynynen. "Delivery of stem cells to the brain using MRIgFUS." In 2011 IEEE International Ultrasonics Symposium (IUS). IEEE, 2011. http://dx.doi.org/10.1109/ultsym.2011.0004.

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Schreiber, J., E. Sojka, and L. Licev. "Analysis and diagnostics of the brain-stem ultrasound images." In 2007 14th International Workshop on Systems, Signals and Image Processing and 6th EURASIP Conference focused on Speech and Image Processing, Multimedia Communications and Services. IEEE, 2007. http://dx.doi.org/10.1109/iwssip.2007.4381142.

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Eyler, Christine E., Michael T. Forrester, Jennifer M. MacSwords, Qiulian Wu, Katherine M. LaFiura, Justin D. Lathia, Andrew E. Sloan, et al. "Abstract 3318: Molecular targeting of brain tumor stem cells." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3318.

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Thind, Sonam, Rami Z. Morsi, Sachin Kothari, and Harsh Desai. "P029/311 Brain stem AVM with intra-nidal AVM." In 15TH Congress of the European Society of Minimally Invasive Neurological Therapy 2023 Meeting Abstracts. BMA House, Tavistock Square, London, WC1H 9JR: BMJ Publishing Group Ltd., 2023. http://dx.doi.org/10.1136/jnis-2023-esmint.64.

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Reports on the topic "Brain stem"

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Felding-Habermann, Brunhilde. Neural Stem Cell Delivery of Therapeutic Antibodies to Treat Breast Cancer Brain Metastases. Fort Belvoir, VA: Defense Technical Information Center, October 2009. http://dx.doi.org/10.21236/ada541313.

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Sullivan, Genevieve M. The Regenerative Response of Endogenous Neural Stem/Progenitor Cells to Traumatic Brain Injury. Fort Belvoir, VA: Defense Technical Information Center, May 2014. http://dx.doi.org/10.21236/ad1012867.

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Jiang, Shuxian. Regulation of Breast Cancer Stem Cell Trafficking and Metastasis by Brain Originated Signals. Fort Belvoir, VA: Defense Technical Information Center, September 2010. http://dx.doi.org/10.21236/ada555906.

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Shijani, Seyed Mohammad Malakooti, Sina Neshat, Hossein Shayestehyekta, and Milad Gorgani. Lance-Adams syndrome; what we know now. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2022. http://dx.doi.org/10.37766/inplasy2022.11.0025.

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Review question / Objective: 1. In Lance-Adams syndrome, what is the effect of current therapeutic management on improving patients' condition compared with the control group? 2. Are EEG, Brain CT, MRI, and brain SPECT more accurate in diagnosing Lance-Adams syndrome? 3. Does Early diagnosis and treatment influence the quality of life in patients with Lance-Adams syndrome? 4. Are patients with abnormal cortical discharge or cerebellum brain stem and thalamus cortical circuit or neurotransmitter imbalance at higher risk for/of Lance-Adams syndrome compared with patients without these symptoms? Condition being studied: LAS is a group of clinical symptoms; The primary manifestation is action myoclonus which can occur as generalized, focal, or multifocal repeated myoclonic motor movement myoclonus. In some patients, sensory stimuli can trigger myoclonus. Furthermore, negative myoclonus can impair posture and cause falls in the lower extremities.
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Li, Xiao-Nan. Harnessing Autopsied DIPG Tumor Tissues for Orthotopic Xenograft Model Development in the Brain Stems of SCID Mice. Fort Belvoir, VA: Defense Technical Information Center, September 2012. http://dx.doi.org/10.21236/ada568355.

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Funkenstein, Bruria, and Cunming Duan. GH-IGF Axis in Sparus aurata: Possible Applications to Genetic Selection. United States Department of Agriculture, November 2000. http://dx.doi.org/10.32747/2000.7580665.bard.

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Many factors affect growth rate in fish: environmental, nutritional, genetics and endogenous (physiological) factors. Endogenous control of growth is very complex and many hormone systems are involved. Nevertheless, it is well accepted that growth hormone (GH) plays a major role in stimulating somatic growth. Although it is now clear that most, if not all, components of the GH-IGF axis exist in fish, we are still far from understanding how fish grow. In our project we used as the experimental system a marine fish, the gilthead sea bream (Sparus aurata), which inhabits lagoons along the Mediterranean and Atlantic coasts of Europe, and represents one of the most important fish species used in the mariculture industry in the Mediterranean region, including Israel. Production of Sparus is rapidly growing, however, in order for this production to stay competitive, the farming of this fish species has to intensify and become more efficient. One drawback, still, in Sparus extensive culture is that it grows relatively slow. In addition, it is now clear that growth and reproduction are physiological interrelated processes that affect each other. In particular sexual maturation (puberty) is known to be closely related to growth rate in fish as it is in mammals, indicating interactions between the somatotropic and gonadotropic axes. The goal of our project was to try to identify the rate-limiting components(s) in Sparus aurata GH-IGF system which might explain its slow growth by studying the ontogeny of growth-related genes: GH, GH receptor, IGF-I, IGF-II, IGF receptor, IGF-binding proteins (IGFBPs) and Pit-1 during early stages of development of Sparus aurata larvae from slow and fast growing lines. Our project was a continuation of a previous BARD project and could be divided into five major parts: i) obtaining additional tools to those obtained in the previous project that are necessary to carry out the developmental study; ii) the developmental expression of growth-related genes and their cellular localization; iii) tissue-specific expression and effect of GH on expression of growth-related genes; iv) possible relationship between GH gene structure, growth rate and genetic selection; v) the possible role of the IGF system in gonadal development. The major findings of our research can be summarized as follows: 1) The cDNAs (complete or partial) coding for Sparus IGFBP-2, GH receptor and Pit-1 were cloned. Sequence comparison reveals that the primary structure of IGFBP-2 protein is 43-49% identical to that of zebrafish and other vertebrates. Intensive efforts resulted in cloning a fragment of 138 nucleotides, coding for 46 amino acids in the proximal end of the intracellular domain of GH receptor. This is the first fish GH receptor cDNA that had been cloned to date. The cloned fragment will enable us to complete the GH - receptor cloning. 2) IGF-I, IGF-II, IGFBP-2, and IGF receptor transcripts were detected by RT-PCR method throughout development in unfertilized eggs, embryos, and larvae suggesting that these mRNAs are products of both the maternal and the embryonic genomes. Preliminary RT-PCR analysis suggest that GH receptor transcript is present in post-hatching larvae already on day 1. 3) IGF-1R transcripts were detected in all tissues tested by RT-PCR with highest levels in gill cartilage, skin, kidney, heart, pyloric caeca, and brain. Northern blot analysis detected IGF receptor only in gonads, brain and gill cartilage but not in muscle; GH increased slightly brain and gill cartilage IGF-1R mRNA levels. 4) IGFBP-2 transcript were detected only in liver and gonads, when analyzed by Northern blots; RT-PCR analysis revealed expression in all tissues studied, with the highest levels found in liver, skin, gonad and pyloric caeca. 5) Expression of IGF-I, IGF-II, IGF-1R and IGFBP-2 was analyzed during gonadal development. High levels of IGF-I and IGFBP-2 expression were found in bisexual young gonads, which decreased during gonadal development. Regardless of maturational stage, IGF-II levels were higher than those of IGF-L 6) The GH gene was cloned and its structure was characterized. It contains minisatellites of tandem repeats in the first and third introns that result in high level of genetic polymorphism. 7) Analysis of the presence of IGF-I and two types of IGF receptor by immunohistochemistry revealed tissue- and stage-specific expression during larval development. Immunohistochemistry also showed that IGF-I and its receptors are present in both testicular and ovarian cells. Although at this stage we are not able to pinpoint which is the rate-limiting step causing the slow growth of Sparus aurata, our project (together with the previous BARD) yielded a great number of experimental tools both DNA probes and antibodies that will enable further studies on the factors regulating growth in Sparus aurata. Our expression studies and cellular localization shed new light on the tissue and developmental expression of growth-related genes in fish.
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Yahav, Shlomo, John McMurtry, and Isaac Plavnik. Thermotolerance Acquisition in Broiler Chickens by Temperature Conditioning Early in Life. United States Department of Agriculture, 1998. http://dx.doi.org/10.32747/1998.7580676.bard.

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Abstract:
The research on thermotolerance acquisition in broiler chickens by temperature conditioning early in life was focused on the following objectives: a. To determine the optimal timing and temperature for inducing the thermotolerance, conditioning processes and to define its duration during the first week of life in the broiler chick. b. To investigate the response of skeletal muscle tissue and the gastrointestinal tract to thermal conditioning. This objective was added during the research, to understand the mechanisms related to compensatory growth. c. To evaluate the effect of early thermo conditioning on thermoregulation (heat production and heat dissipation) during 3 phases: (1) conditioning, (2) compensatory growth, (3) heat challenge. d. To investigate how induction of improved thermotolerance impacts on metabolic fuel and the hormones regulating growth and metabolism. Recent decades have seen significant development in the genetic selection of the meat-type fowl (i.e., broiler chickens); leading to rapid growth and increased feed efficiency, providing the poultry industry with heavy chickens in relatively short growth periods. Such development necessitates parallel increases in the size of visceral systems such as the cardiovascular and the respiratory ones. However, inferior development of such major systems has led to a relatively low capability to balance energy expenditure under extreme conditions. Thus, acute exposure of chickens to extreme conditions (i.e., heat spells) has resulted in major economic losses. Birds are homeotherms, and as such, they are able to maintain their body temperature within a narrow range. To sustain thermal tolerance and avoid the deleterious consequences of thermal stresses, a direct response is elicited: the rapid thermal shock response - thermal conditioning. This technique of temperature conditioning takes advantage of the immaturity of the temperature regulation mechanism in young chicks during their first week of life. Development of this mechanism involves sympathetic neural activity, integration of thermal infom1ation in the hypothalamus, and buildup of the body-to-brain temperature difference, so that the potential for thermotolerance can be incorporated into the developing thermoregulation mechanisms. Thermal conditioning is a unique management tool, which most likely involves hypothalamic them1oregulatory threshold changes that enable chickens, within certain limits, to cope with acute exposure to unexpected hot spells. Short-tem1 exposure to heat stress during the first week of life (37.5+1°C; 70-80% rh; for 24 h at 3 days of age) resulted in growth retardation followed immediately by compensatory growth" which resulted in complete compensation for the loss of weight gain, so that the conditioned chickens achieved higher body weight than that of the controls at 42 days of age. The compensatory growth was partially explained by its dramatic positive effect on the proliferation of muscle satellite cells which are necessary for further muscle hypertrophy. By its significant effect of the morphology and functioning of the gastrointestinal tract during and after using thermal conditioning. The significant effect of thermal conditioning on the chicken thermoregulation was found to be associated with a reduction in heat production and evaporative heat loss, and with an increase in sensible heat loss. It was further accompanied by changes in hormones regulating growth and metabolism These physiological responses may result from possible alterations in PO/AH gene expression patterns (14-3-3e), suggesting a more efficient mechanism to cope with heat stress. Understanding the physiological mechanisms behind thermal conditioning step us forward to elucidate the molecular mechanism behind the PO/AH response, and response of other major organs. The thermal conditioning technique is used now in many countries including Israel, South Korea, Australia, France" Ecuador, China and some places in the USA. The improvement in growth perfom1ance (50-190 g/chicken) and thermotolerance as a result of postnatal thermal conditioning, may initiate a dramatic improvement in the economy of broiler's production.
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