Rozprawy doktorskie na temat „Cerebral ischemia”
Utwórz poprawne odniesienie w stylach APA, MLA, Chicago, Harvard i wielu innych
Sprawdź 50 najlepszych rozpraw doktorskich naukowych na temat „Cerebral ischemia”.
Przycisk „Dodaj do bibliografii” jest dostępny obok każdej pracy w bibliografii. Użyj go – a my automatycznie utworzymy odniesienie bibliograficzne do wybranej pracy w stylu cytowania, którego potrzebujesz: APA, MLA, Harvard, Chicago, Vancouver itp.
Możesz również pobrać pełny tekst publikacji naukowej w formacie „.pdf” i przeczytać adnotację do pracy online, jeśli odpowiednie parametry są dostępne w metadanych.
Przeglądaj rozprawy doktorskie z różnych dziedzin i twórz odpowiednie bibliografie.
Keasey, Matthew P. "MicroRNAs in Cerebral Ischemia". Thesis, University of Bristol, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.526014.
Pełny tekst źródłaMolnar, Maria. "Hyperglycemia in Experimental Cerebral Ischemia". Doctoral thesis, Uppsala universitet, Anestesiologi och intensivvård, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-247763.
Pełny tekst źródłaChristensen, Thomas. "Experimental focal cerebral ischemia : pathophysiology, metabolism and pharmacology of the ischemic penumbra /". Copenhagen, 2007. http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=016143698&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA.
Pełny tekst źródłaThorén, Anna. "Astrocyte metabolism following focal cerebral ischemia /". Göteborg : Institute of Neuroscience and Physiology, The Sahlgrenska Academy, Göteborg University, 2006. http://hdl.handle.net/2077/744.
Pełny tekst źródłaThomas, Sunu Samuel. "Murine models of cerebral ischemia, development of a mouse model of global cerebral ischemia; response of GluR2 knockout mice in a model of permanent focal cerebral ischemia". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0026/MQ50439.pdf.
Pełny tekst źródłaLi, Yan. "Inhibitory synpatic transmission in striatal neurons after transient cerebral ischemia". Connect to resource online, 2009. http://hdl.handle.net/1805/2021.
Pełny tekst źródłaTitle from screen (viewed on December 1, 2009). Department of Anatomy and Cell Biology, Indiana University-Purdue University Indianapolis (IUPUI). Advisor(s): Zao C. Xu, Feng C. Zhou, Charles R. Yang, Theodore R. Cummins. Includes vitae. Includes bibliographical references (leaves 115-135).
Karelina, Ekaterina. "MECHANISMS OF SOCIAL NEUROPROTECTION AFTER CEREBRAL ISCHEMIA". The Ohio State University, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=osu1274922479.
Pełny tekst źródłaAdhami, Faisal. "Differential Adult and Neonatal Response to Cerebral Ischemia-Hypoxia". University of Cincinnati / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1196054266.
Pełny tekst źródłaEdrissi, Hamidreza. "Blood Brain Barrier Dysfunction in Chronic Cerebral Ischemia". Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/32531.
Pełny tekst źródłaNg, Kit-ying. "Neuroprotective effects of adiponectin in focal cerebral ischemia". Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/hkuto/record/B39634371.
Pełny tekst źródłaBogart, Robert William. "The effect of stress on global cerebral ischemia". Connect to resource, 2008. http://hdl.handle.net/1811/32235.
Pełny tekst źródłaNg, Kit-ying, i 吳潔瑩. "Neuroprotective effects of adiponectin in focal cerebral ischemia". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39634371.
Pełny tekst źródłaRaghavan, Aparna. "Neuroprotective Potential of Withania Somnifera in Cerebral Ischemia". University of Toledo Health Science Campus / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=mco1416570371.
Pełny tekst źródłaSchatlo, Bawarjan [Verfasser]. "Cerebral ischemia in experimental subarachnoid hemorrhage / Bawarjan Schatlo". Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2011. http://d-nb.info/1026265347/34.
Pełny tekst źródłaXu, Xingshun. "Novel Protective Agents against Cerebral Ischemia/Reperfusion Injury". Digital Commons @ East Tennessee State University, 2007. https://dc.etsu.edu/etd/2054.
Pełny tekst źródłaDowden, Jennifer. "Characterizing the neuroprotective efficacy of ischemic preconditioning (ischemic tolerance) : is age an important factor? /". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0019/NQ54834.pdf.
Pełny tekst źródłaWang, Yanxin. "Hypoxic-ischemic injury in the neonatal rat model prediction of irreversible infarction size by Diffusion Weighted MR Imaging /". Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/B35757577.
Pełny tekst źródłaFrykholm, Peter. "Cerebral ischemia studied with positron emission tomography and microdialysis". Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2002. http://publications.uu.se/theses/91-554-5319-8/.
Pełny tekst źródłaSlack, Penelope Jean. "Dietary n-3 fatty acids and cerebral ischemia/reperfusion". Thesis, University of British Columbia, 2009. http://hdl.handle.net/2429/3992.
Pełny tekst źródłaChaparro-Buitrago, Rafael Eduardo. "Neuroprotection with Anesthetics in Two Models of Cerebral Ischemia". Scholar Commons, 2010. http://scholarcommons.usf.edu/etd/3521.
Pełny tekst źródłaSchweizer, Sophie [Verfasser]. "Histone methylation and neuroprotection in cerebral ischemia / Sophie Schweizer". Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2015. http://d-nb.info/1076270808/34.
Pełny tekst źródłaBlazej, Katja [Verfasser]. "Role of inflammatory cells in cerebral ischemia / Katja Blazej". Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2013. http://d-nb.info/1031097007/34.
Pełny tekst źródłaWard, Nicholas M. "The assessment of behavioural deficits following focal cerebral ischemia". Thesis, University of St Andrews, 1997. http://hdl.handle.net/10023/14698.
Pełny tekst źródłaChan, Chu-fung. "Neuroprotective effects of granulocyte-colony stimulating factor in a mice stroke model". Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/hkuto/record/B40687284.
Pełny tekst źródłaGisselsson, Lars. "Ischemic brain damage the influence of hyperglycemia on tissue injury, cerebral circulation and edema formation /". Lund : Lund University, 1998. http://books.google.com/books?id=gMdrAAAAMAAJ.
Pełny tekst źródłaLi, Ping-An. "Mechanisms of acidosis-mediated ischemic brain damage histopathology and pathophysiology /". Lund : Lund University, 1996. http://catalog.hathitrust.org/api/volumes/oclc/38158955.html.
Pełny tekst źródłaPereira, Claudia Figueiredo. "Carbon monoxide, autophagy and cytoprotection in response to cerebral ischemia". Master's thesis, Faculdade de Ciências e Tecnologia, 2013. http://hdl.handle.net/10362/10836.
Pełny tekst źródłaThere is an increasing need for promoting neuroprotection against cerebral ischemia, which is the main cause of brain damage in adults. Astrocytes are the most abundant cells inboard the central nervous system (CNS), being known as key glial cell for promoting neuronal survival and homeostasis. It is more established in nowdays that astrocytic dysfunction contributes to neurodegenerative processes. Although, carbon monoxide is a well renown as a lethal and toxic gas due to its high affinity to hemoglobin, CO exerts anti-apoptotic, anti-inflammatory and anti-proliferative functions. Recent studies showed likewise that CO induces autophagy, promoting therefore cytoprotective and anti-inflammatory effects. Autophagy is a major catabolic pathway, known as an autodigestive process that degrades cellular organelles and proteins, playing an important role in cellular homeostasis during environmental stress. Due to the great interest on the signaling and cytoprotective actions of CO, novel strategies have been put forward to exploit the potential therapeutic effects of this gaseous molecule. One of these approaches consist on the development of CO-releasing molecules (CO-RMs), compounds that deliver small quantities of CO to tissues and first identified by the group of Motterlini and co-workers. The aim of this Master thesis was to study the action of CORM-A1, a boron-containing compound that spontaneously releases CO, against cell death in primary culture of astrocytes. In particular, we examined the role of CORM-A1 in autophagy, mitophagy and cell metabolism. Here, we demonstrated that CORM-A1 promotes the induction of autophagy in primary culture of astrocytes. Furthermore,autophagy is directly involved in the cytoprotective effect of CORM-A1 against cell death. In some preliminary experiments we have shown that CORM-A1 also induced mitophagy, while autophagy and inhibition of cell death promoted by CORM-A1 seem to occur under hypoxia (5% of oxygen). This master thesis has addressed several important questions on the role of CO in astrocyte function but also opened to many other important questions on the mechanism of action of CO. For instance, future work must be undertaken in order to explore whether CO-mediated induction of reactive oxygen species (ROS), which play an important role in cell signaling, which are the factors directly involved in mitophagy and the cross-talk between apoptosis and modulation of autophagy.
e-COST,(COST Action BM1005)
BATTISTELLO, ENRICA. "PEMFs and cerebral ischemia: the pathways behind their beneficial effects". Doctoral thesis, Università degli studi di Ferrara, 2021. http://hdl.handle.net/11392/2488048.
Pełny tekst źródłaI campi elettromagnetici pulsati a bassa energia e frequenza (PEMFs) stanno emergendo sempre più per i loro numerosi effetti benefici in molteplici sistemi biologici, sia in vitro che in vivo. Tra questi, diversi studi hanno dimostrato la capacità dei PEMFs di proteggere le cellule neuronali in seguito ad un evento ischemico. Questa patologia, riconosciuta a livello mondiale come una delle principali cause di morte e di disabilità permanente, non beneficia, ad oggi, di terapie o farmaci in grado di proteggere i neuroni, limitando il danno, e di favorire la ripresa del tessuto cerebrale colpito. In questo contesto si colloca il trattamento con i PEMFs. Infatti, grazie ai promettenti dati ottenuti, i PEMFs sono stati utilizzati in uno studio clinico multicentrico, prospettico, randomizzato, controllato con placebo e in doppio cieco, il cui scopo è indagarne l'efficacia nell'ictus ischemico acuto, al fine di impiegarli come strumento non invasivo e sicuro per il recupero neuronale. Sebbene, dunque, l’efficacia dei PEMFs sia riconosciuta, i pathways molecolari che innescano per mediare il loro effetto benefico sono ancora poco noti. Per questo motivo, lo scopo del mio lavoro di tesi è stato quello di investigare i mediatori attivati dai PEMFs sia nel contrastare la morte neuronale dovuta all’evento ipossico, sia nel diminuire la neuro-infiammazione a carico delle cellule microgliali. In particolare, nel primo capitolo della tesi sono stati investigati l’effetto dell’esposizione ai PEMFs sulle cellule neuronali PC12 (differenziate con il fattore di crescita neuronale NGF) sottoposte ad insulto ipossico, ed il pathway attivato dai campi elettromagnetici. Per la prima volta, i risultati ottenuti hanno mostrato un effetto protettivo dei PEMFs su queste cellule, diminuendone l’apoptosi provocata dall’ipossia. Il processo neuro-protettivo è stato scoperto essere mediato dal rapido coinvolgimento di p38 MAPK che a sua volta attiva HSP70, aumentando il livello di CREB fosforilato, reclutando BDNF e coinvolgendo infine il pathway anti-apoptotico regolato dalla famiglia di Bcl-2. Il secondo capitolo, invece, si è occupato degli effetti dei PEMFs sulle cellule microgliali che sono note per il loro ruolo fondamentale nella regolazione della neuro-infiammazione post-ischemia, e che sono coinvolte nel danno da riperfusione. Nel dettaglio, dunque, le cellule microgliali N9 sono state stimolate con un agente infiammatorio (il lipopolisaccaride, LPS) e sono stati investigati sia la produzione delle citochine pro-infiammatorie sia i relativi pathways coinvolti, con e senza il trattamento con i PEMFs. I risultati ottenuti hanno evidenziato l’abilità dei PEMFs di ridurre la secrezione di TNF-α e IL-1β tramite la modulazione di JNK, e di IL-6, senza alterare la vitalità e la proliferazione della microglia. Oltre alla produzione di citochine è stato ricercato anche l’effetto dei PEMFs nella regolazione di alcune funzioni specifiche delle cellule microgliali attivate, tra cui la produzione delle specie reattive dell’ossigeno, la fagocitosi e l’invasione cellulare. Nel dettaglio è stata riscontrata una riduzione di tutte in seguito al trattamento con i PEMFs, confermandone il ruolo essenziale nella diminuzione dello stato infiammatorio. I risultati di questo lavoro, dunque, hanno mostrato che il trattamento con i PEMFs è in grado di modulare numerosi mediatori sia nelle cellule neuronali che in quelle microgliali, contrastandone, rispettivamente, l’apoptosi e l’azione pro-infiammatoria, e per la prima volta, hanno descritto i meccanismi molecolari coinvolti. Questi risultati si aggiungono, dunque, a quelli pubblicati in altre linee cellulari, contribuendo a definire il meccanismo neuro-protettivo ed antinfiammatorio dei PEMFs e supportandone il loro utilizzo come terapia per l’ischemia cerebrale.
Chen, Xiaoqian. "The identification of 14-3-3[gamma] in astrocytes and its mechanism in protecting astrocytes from ischemia /". View Abstract or Full-Text, 2002. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202002%20CHEN.
Pełny tekst źródłaIncludes bibliographical references (leaves 180-202). Also available in electronic version. Access restricted to campus users.
Mokhberi, Shiva. "ELECTRICAL BIOIMPEDANCE CEREBRAL MONITORING : A Study of Cerebral Impedance Variation". Thesis, KTH, Skolan för teknik och hälsa (STH), 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-190876.
Pełny tekst źródłaStroke är bland de ledande orsakerna till död och funktionshinder i hela världen.I dagsläget är diagnos av stroke begränsad till fasta bildenheter som inte möjliggör en snabb diagnos. En bärbar enhet som möjliggör en icke invasiv bedömning av sjukdomen skulle minska diagnos tiden och följaktligen öka chansen att överleva sjukdomen. Genomförda studier i ämnet har bekräftat att implementering av Electrical Bioimpedance i en bärbar enhet kan räknas som ett effektivt sätt för Stroke diagnostik. För att kunna använda hjärnans impedans för Stroke diagnostik, bör först en studie av hjärnans impedans på friska individer utföras för att kunna visa att impedansen är oförändrad med tiden. Experimentell Bioimpedans Spektroskopi (BIS) mätningar från en frisk kontrollgrupp av 10 försökspersoner har utförts i denna studie för att inspektera variationen av hjärnans impedans under två veckor. Resultaten från denna studie tyder på att sättet av impedans mätningen i dagsläget är inte optimalt. Artefakter presenterad i resultatet gör det omöjligt för att kunna komma till ett beslut om hjärnans impedans variation . För fortsätta studier bör man överväga en större kontrollgrupp och även en analysering av data med hjälp av t-statistik som var inte inom ramen av denna studie.
Silva, Matthew S. "NMR characterization of changes in the apparent diffusion coefficient of water following transient cerebral ischemia". Link to electronic thesis, 2002. http://www.wpi.edu/Pubs/ETD/Available/etd-0327102-221251.
Pełny tekst źródłaTsang, Hing-wai, i 曾慶威. "In vitro studies of hypoxic ischemic down-regulated 1 (HID-1) protein encoded by a novel gene down-regulated in neonatal hypoxic-ischemicencephalopathy in different cell death paradigms". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B45608192.
Pełny tekst źródłaZou, Liangyu. "Role of cerebral ischemia in cognitive impairment clinical and experimental study /". Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/B32019889.
Pełny tekst źródłaDavis, Stephanie. "Leukemia Inhibitory Factor as a Neuroprotective Agent against Focal Cerebral Ischemia". Scholar Commons, 2016. http://scholarcommons.usf.edu/etd/6218.
Pełny tekst źródłaZou, Liangyu, i 鄒良玉. "Role of cerebral ischemia in cognitive impairment: clinical and experimental study". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B32019889.
Pełny tekst źródłaVasylieva, N. V. "Chronic cerebral ischemia and cognitive impairment (an effect of complex therapy)". Thesis, БДМУ, 2020. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/17642.
Pełny tekst źródłaGaudier-Diaz, Monica M. "Sex-Specific Social Modulation of the Neuroinflammatory Response toGlobal Cerebral Ischemia". The Ohio State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=osu1490713683841079.
Pełny tekst źródłaChan, Chu-fung, i 陳柱峰. "Neuroprotective effects of granulocyte-colony stimulating factor in a mice stroke model". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B40687284.
Pełny tekst źródłaPogoryelova, Oksana. "A study of epigenetics in ischaemic stroke". Thesis, University of Aberdeen, 2013. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=201969.
Pełny tekst źródłaPennings, Frederik Anthonius. "The clinical value of assessing cerebral ischemia: emphasis on brain tissue oxygenation and function of the cerebral microcirculation". [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2007. http://dare.uva.nl/document/45158.
Pełny tekst źródłaSidhu, Ranjinder S. "Role of apoptosis following cerebral hypoxia-ischemia in immature and older rats". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape17/PQDD_0014/MQ32247.pdf.
Pełny tekst źródłaKostulas, Nikolaos. "Studies on cytokines and chemokines in cerebrovascular diseases and experimental cerebral ischemia /". Stockholm, 2001. http://diss.kib.ki.se/2001/91-628-4701-5/.
Pełny tekst źródłaZur, Nedden Stephanie. "Targeting the purine salvage pathway in in vitro models of cerebral ischemia". Thesis, University of Warwick, 2011. http://wrap.warwick.ac.uk/45926/.
Pełny tekst źródłaXu, Mingjing, i 徐明婧. "Baicalin protects neural cells from cerebral ischemia reperfusion injury by scavenging peroxynitrite". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B47753110.
Pełny tekst źródłapublished_or_final_version
Chinese Medicine
Master
Master of Philosophy
Syrett, Andrew J. "Bioactive Glycerophospholipids and Their Role in Modulating Neuronal Vulnerability Following Cerebral Ischemia". Thesis, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/20536.
Pełny tekst źródłaCordell, Ryan [Verfasser]. "The relationship between the blood-brain barrier and cerebral ischemia / Ryan Cordell". Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2012. http://d-nb.info/1028496222/34.
Pełny tekst źródłaQueiroga, Cláudia Susana Fernandes. "Disclosing Carbon Monoxide Protection in Cerebral Ischemia: Insights into the cellular mechanisms". Doctoral thesis, Universidade Nova de Lisboa. Instituto de Tecnologia Química e Biológica, 2012. http://hdl.handle.net/10362/10869.
Pełny tekst źródłaThe present work demonstrates the ability of carbon monoxide (CO) to prevent apoptosis in primary culture of astrocytes. For the first time, the anti-apoptotic behaviour can be clearly attributed to the inhibition of mitochondrial membrane permeabilisation (MMP), a key event in the intrinsic apoptotic pathway. In isolated non-synaptic mitochondria CO partially inhibits (i) loss of membrane potential, (ii) the opening of a non specific pore through the inner membrane, (iii) swelling and (iv) cytochrome c release, which are induced by calcium, diamide or atractyloside (a ligand of adenine nucleotide translocase, ANT). CO directly modulates ANT function by enhancing ADP/ATP exchange and prevents its pore-forming activity.(...)
Padayachy, L. C. "The prevalence of cerebral hypoxia/ischemia in pediatric severe traumatic brain injury". Master's thesis, University of Cape Town, 2010. http://hdl.handle.net/11427/2887.
Pełny tekst źródłaLi, Han-Dong, Minshu Li, Elaine Shi, Wei-Na Jin, Kristofer Wood, Rayna Gonzales i Qiang Liu. "A translocator protein 18 kDa agonist protects against cerebral ischemia/reperfusion injury". BIOMED CENTRAL LTD, 2017. http://hdl.handle.net/10150/625392.
Pełny tekst źródłaOyamada, Naofumi. "The Role of Mineralocorticoid Receptor Expression in Brain Remodeling after Cerebral Ischemia". Kyoto University, 2009. http://hdl.handle.net/2433/124289.
Pełny tekst źródła