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Champattanachai, Voraratt. « Effects of hexosamine biosynthesis on an in vitro model of cardiac ischemia ». Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2008. https://www.mhsl.uab.edu/dt/2008d/champattanachai.pdf.
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Frantseva, Marina. « Mechanisms of free radical formation and toxicity in an in vitro model of ischemia ». Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ45776.pdf.
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Zwaini, Zinah Dheyaa Razzaq. « In vitro and in vivo models of renal ischemia reperfusion injury ». Thesis, University of Leicester, 2017. http://hdl.handle.net/2381/39344.
Texte intégralRésumé :
Successful kidney transplantation is a life-saving procedure to patients with irreversible chronic renal failure. Despite the presence of various obstacles facing this surgery, preserving donor kidney and consequent ischemia reperfusion injury (IRI) are still major challenges affecting renal function as well as prognosis of transplant surgery. This study pursued two main aims: firstly, characterising changes in damage associated inflammatory gene expressions through developing, and analysis of an in vitro model of proximal tubular epithelial cells (PTEC) of normal human kidney mimicking renal IRI in vivo. The second aim was to simulate the concurrence of factors relevant to human intervention (renoprotective anaesthesia, peri- and postoperative analgesia, volume substitution) in mice deficient of properdin and congenic controls and to allow long-term observation of renal outcome after IRI. In this study, a reproducible and standardisable in vitro model was developed. It demonstrated the complexity of signalling where a multitude of factors affects the target cells. Secondly, the use of congenic properdin deficient mice showed that properdin has a significant role to play in renal injury (and recovery). There was significant impairment in renal function (and structure) compared to wildtype mice after IRI.
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Zur, 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/.
Texte intégralRésumé :
An interruption of the blood supply to the brain, as occurs during ischemic stroke, results in a rapid decline of ATP levels and a subsequent loss of neuronal function and viability. Under physiological conditions the brain reuses ATP degradation metabolites, such as hypoxanthine, via the purine salvage pathway, to restore its ATP pool. However, the massive degradation of ATP during ischemia results in the accumulation and loss of diffusible purine metabolites and thereby leads to a reduction in the post-ischemic ATP pool size, leaving the brain more vulnerable to secondary ischemic insults (recurrent strokes) and less able to deploy reparative mechanisms. The aim of this study was to improve the recovery of post-ischemic ATP levels by enhancing the purine salvage pathway, with substances that are already known to be tolerated in humans. Using acute hippocampal rat brain slices, I found that 1 mM Ribose (Rib) and 50 μM Adenine (Ade), two main metabolites of the purine salvage pathway, significantly increased the tissue ATP levels under basal conditions. Rib/Ade pre-treatment results in accelerated decline of synaptic transmission after onset of oxygen/glucose deprivation (OGD), due to increased adenosine release. However, this intervention does not delay the onset of anoxic depolarisation, or improve the recovery of synaptic transmission after prolonged ischemic periods. Pre-treatment of brain slices with 1 mM creatine, which increases phosphocreatine levels and thereby buffers the rapid decline of ATP levels upon energy shortage, significantly delays the onset of AD and helps to improve the recovery of synaptic transmission. By using cultured cerebellar granule cells, for more protracted studies on cell viability after OGD, I show that addition of Rib/Ade after ischemia helps to improves cell viability. Therefore my results suggest that both, delaying the decline of ATP upon onset of OGD (pre-treatment with creatine), or enhancing the post-ischemic recovery of ATP (post-treatment with Rib/Ade) are useful strategies to improve cell survival and function after in vitro ischemia.
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CARROZZINI, TATIANA. « Nutrition interventions in aging : study of coffee-derived compounds antioxidant properties in an in vitro model of ischemia ». Doctoral thesis, Università degli Studi di Milano-Bicocca, 2021. http://hdl.handle.net/10281/309808.
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Negli ultimi secoli, l'aspettativa di vita è aumentata grazie a uno stile di vita migliore, ma di conseguenza sono aumentate le patologie legate all'invecchiamento. L'invecchiamento è un processo fisiologico complesso e modificazioni legate all'età sono evidenti anatomicamente e fisiologicamente nella BEE. L'accumulo di danno ossidativo alle macromolecole da parte di RONS e ROS in BEE può essere cruciale nello sviluppo e nella progressione di diverse patologie del SNC.
In questa situazione l'ischemia cerebrale potrebbe alterare ulteriormente l'equilibrio ossidante/antiossidante a favore degli ossidanti.
In questo scenario, l'alimentazione può contrastare gli impatti ossidativi e le diete arricchite di polifenoli possono fornire effetti benefici.
Il caffè è stato descritto come una fonte molto importante di composti antiossidanti (Ricci A. et al., 2018), ma la sua lavorazione produce ogni anno grosse quantità di scarto (Mussatto et al., 2011).
Seguendo queste linee guida, lo scopo di questo studio era di valutare le proprietà antiossidanti di diversi composti correlati al caffè, da soli e combinati insieme, in un modello in vitro di ischemia.
I composti utilizzati sono stati: fitoestratti derivanti dagli scarti della produzione del caffè e arricchiti in specifici componenti polifenolici; e metaboliti del caffè individuati nel plasma di persone che bevono caffè.
Il momento successivo alla riossigenazione provoca un aumento dei ROS, raggiungendo un picco massimo entro 1h dal ripristino delle normali condizioni di coltura (Adibhatla RM et al., 2001). Pertanto, per la valutazione delle proprietà antiossidanti dopo OGD, come condizione di maggior stress è stato scelto l'intervallo 0-1h immediatamente successivo al recupero.
Quindi, al fine di valutare le proprietà antiossidanti dei composti del caffè in OGD, sono state effettuate valutazioni sullo stato di fosforilazione delle chinasi Erk e Akt, che se attive promuovono la migrazione di Nrf2 nel nucleo, sui livelli della proteina Nrf2 e sulla sua distribuzione intracellulare, ed infine sui livelli proteici di HO-1, come una dei suoi geni bersaglio. Inoltre, è stata valutata anche la proteina Hsp70, che è coinvolta nel controllo del ripiegamento delle proteine ed infine, è stata misurata la produzione di malondialdeide (MDA) 24 ore dopo il recupero come marker di perossidazione lipidica.
I risultati hanno dimostrato la capacità dei composti correlati al caffè di riuscire ad attivare la via di segnalazione Nrf2 in modo diverso e che solo i metaboliti modulavano positivamente Hsp70.
I risultati dell'MDA hanno suggerito che la presenza dei composti antiossidanti, testati da soli o combinati, aveva avuto un effetto positivo sulla sua modulazione.
I risultati, quindi, hanno dimostrato le proprietà antiossidanti dei fitoestratti e dei metaboliti specifici del caffè, suggerendo che le sostanze stimolano la risposta antiossidante attivando diverse vie, che combinate insieme potrebbero potenziare la difesa antiossidante.
L'effetto antiossidante dei metaboliti potrebbe indicare che l'assunzione moderata di caffè giornaliera in soggetti anziani esposti all'invecchiamento e maggior rischio di insulto ischemico, potrebbe contribuire alla riduzione dello stress ossidativo limitando il danno da riperfusione in caso di attacchi ischemici.
Queste difese potrebbero essere aumentate attraverso i fitoestratti derivati dal caffè ingeriti come integratori alimentari. Il riutilizzo di questa biomassa di scarto, avrebbe un impatto positivo sia sull'economia che sull'ecosistema, in quanto ridurrebbe notevolmente l'inquinamento.Nowadays, the people get older and older thanks to a better life-style, but consequently, carrying on pathologies typical of the old age, included aging. The aging is a complex physiological process and age-related changes are evident anatomically and physiologically in the BBB. The accumulation of oxidative damage to macromolecules by RONS and ROS in BBB can be crucial in the development and progression of different CNS pathologies. In this situation, cerebral ischemia could further alter the oxidant/antioxidant balance in favour of oxidants. In this scenario, nutrition can counteract the oxidative impacts, polyphenol-enriched diets can provide beneficial effects, preventing cognitive decline and degenerative disorders. More recently, coffee has been described as a very important source of antioxidant compounds (Ricci A. et al., 2018) but its production generates large amount of waste. According to these guidelines, the aim of this study was to evaluate the antioxidant properties of several coffee-related compounds alone and combined together in an in vitro model of ischemia. The compounds used were: phytoextracts deriving from the waste of coffee production and enriched in specific polyphenolic components; and coffee metabolites found in plasma of people drinking coffee. The moment after reoxygenation causes a considerable increase in ROS, reaching a maximum peak within 1 hour of the restoration of normal culture conditions (Adibhatla RM et al., 2001). Therefore, for the evaluation of the antioxidant properties after OGD, the time span 0-1h immediately following recovery was chosen as the condition of greatest stress. Therefore, in order to evaluate the antioxidant properties of the coffee compound under OGD, the antioxidant pathway Nrf2 was analyzed within 0-1h, immediately following recovery. Evaluations were performed on the state of phosphorylation of Erk and Akt kinases, which if active promote Nrf2 migration in the nucleus, on the levels of the Nrf2 protein and on its intracellular distribution, and finally on the protein levels of HO-1, as one of its genes target. Furthermore, the protein Hsp70, which is involved in the control of protein folding, was also evaluated. Finally, malondialdehyde (MDA) production was measured as a marker of lipid peroxidation 24 hours after recovery. The results suggested the ability of coffee-related compounds to activate the Nrf2 signaling pathway differently and only the pre-treatment with metabolites modulated positively Hsp70. MDA results suggested that the presence of the antioxidant compounds, tested alone or combined, had a positive effect on its modulation. The results showed the antioxidant properties of phytoextracts and specific coffee metabolites, suggesting that the substances stimulate the antioxidant response by activating different pathways, which combined together in the mix, could enhance antioxidant defense. The antioxidant effect of coffee metabolites could indicate that the moderate intake of coffee every day in elderly subjects exposed to aging and greater risk of ischemic insult, could contribute to the reduction of oxidative stress by limiting reperfusion damage in the case of ischemic attacks. These defenses could be increased through the phytoextracts derived from coffee ingested as food supplements. The reuse of this waste biomass, would have a positive impact on both the economy and the ecosystem, as it would significantly reduce pollution.
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Kim-Lee, Myung Hi. « Perfusion/reperfusion cell damage in vitro : an ischemic model in CNS / ». The Ohio State University, 1991. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487758680162691.
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Wang, Jie. « The Study of the Effects of (1S,2E,4R,6R,-7E,11E)-2,7,11-cembratriene-4,6-diol on Microglia Polarization Using an Ischemia in Vitro Model ». University of Cincinnati / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1491559717910191.
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Tsang, Hing-wai, et 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.
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Sánchez, Opazo Guillem. « Estudi dels mecanismes de mort cel·lular induïts per un model d’isquèmia cerebral in vitro : implicació dels antagonistes dels receptors de mortJosé Rodríguez Álvarez ». Doctoral thesis, Universitat Autònoma de Barcelona, 2014. http://hdl.handle.net/10803/284058.
Texte intégralRésumé :
L’ictus o accident cerebrovascular és la segona causa de mort en els països industrialitzats i constitueix la primera causa de discapacitat en adults. L’únic tractament aprovat en l’actualitat és el trombolític activador del plasminògen tissular (tPA), el qual només es pot aplicar en un nombre molt reduït de pacients i dintre d’una estreta finestra terapèutica. Els mecanismes de mort cel·lular en la isquèmia cerebral són amplis i venen provocats per l’interrupció del flux sanguini al cervell, el qual provoca una mort ràpida i eminentment necròtica en el nucli de la zona afectada i una mort de caràcter apoptòtic i més lenta al voltant, en la zona de penombra. El gran impacte socio-econòmic de la malaltia i l’existència d’una mort programada dil·latada en el temps han fet que es posin grans esforços en la búsqueda de mecanismes per salvar la zona de penombra. Tenint en compte aquests fets, el present treball s’ha centrat en l’estudi dels mecanismes de mort cel·lular involucrats en la isquèmia cerebral. Per fer-ho, s’ha utilitzat un model de privació d’oxigen i glucosa (OGD) en cultius corticals mixtes d’embrions de rata. Utilitzant aquest model d’isquèmia s’ha observat neuroprotecció pel bloqueig dels receptors NMDA, principal responsable de l’entrada massiva de calci, i l’activació de la caspasa-3, una proteasa encarregada del desmantellament cel·lular durant l’apoptosis. A més, s’ha estudiat el paper dels antagonistes dels receptors de mort en l’OGD. Aquests receptors són responsables de l’activació de la via apoptòtica extrínseca. S’ha observat que l’OGD indueix la degradació dels antagonistes FLIPL i IAP2 i modula l’expressió de FAIML a través de la via de les MAP cinases. Per altre banda, s’ha observat que el silenciament o la sobrexpressió de FAIML mitjançant vectors lentivirals no afecta la viabilitat dels cultius així com tampoc la morfologia nuclear apoptòtica ni els nivells de caspasa-3 activa en les neurones sotmeses a l’insult isquèmic. En conjunt aquests resultats han servit per aprofundir en els mecanismes moleculars implicats en la isquèmia cerebral i poden servir de base per futurs estudis que ajudin al disseny de noves estrategies terapèutiques.Stroke is the second cause of death in industrialized countries and is the leading cause of disability in adults. The only currently approved treatment is the thrombolytic tissue plasminogen activator (tPA), which can be applied only in a very small number of patients and within a narrow therapeutic window. The mechanisms of cell death in brain ischemia are numerous and are caused by the interruption of the blood flow to the brain, which causes a quick necrotic death in the core of the affected area and a slow apoptotic-like death around, in the ischemic penumbra. The major socio-economic impact of the disease and the existence of a programmed cell death that stretches through time explain the effort that is being done to find new strategies to save the penumbra. Given these facts, the present work has focused on studying the mechanisms of cell death involved in brain ischemia. To do this, we used a model of oxygen and glucose deprivation (OGD) in mixed cortical cultures from rat embryos. Using this model of ischemia we observed neuroprotection by blocking NMDA receptor, the primarily responsible for the massive influx of calcium during ischemia, and activation of caspase-3, a protease responsible for dismantling the cell during apoptosis. In addition, we studied the role of death receptor antagonists in OGD. These receptors are responsible for the activation of the extrinsic apoptotic pathway. It has been observed that OGD induces degradation of the antagonists FLIPL and IAP2 and modulate the expression of FAIML through the MAP kinase pathway. On the other hand, we observed that the overexpression or silencing of FAIML using lentiviral vectors did not affect the viability of the cultures nor the apoptotic nuclear morphology or the levels of active caspase-3 in the neurons subjected to the ischemic insult. Together these results have served to study the molecular mechanisms involved in brain ischemia and may provide the basis for future studies that will help to design new therapeutic strategies.
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BACIGALUPPI, SUSANNA. « Ruolo e potenziale delle cellule progenitrici endoteliali nel vasospamo cerebrale ». Doctoral thesis, Università degli Studi di Milano-Bicocca, 2011. http://hdl.handle.net/10281/27113.
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Title: Role and potential of endothelial progenitor cells in cerebral vasospasm Abstract: Background and aim:
Despite many treatment approaches, cerebral vasospasm and delayed ischemic neuronal damage (DIND) still represent a serious threat to patients with subarachnoid haemorrhage (SAH). Endothelial progenitor cells (EPC) have been involved as prognostic indicators in several vascular diseases and mesenchymal stem cells already have shown some benefits in ischemic injury.
Aim of this study was to investigate the therapeutic potential of endothelial progenitor cells (EPC) and mesenchymal stem cells (MSC) in attenuating or preventing vasospasm and DIND in patients with SAH.
Methods:
Given the emergent role of DIND as a result of multifactorial hypoperfusion stress in the outcome of SAH patients, the efficacy of EPC and MSC in reducing neuronal damage has been evaluated in an in vitro model of ischemia, namely the oxygen glucose deprivation (OGD), on primary rat cortical neuronal cultures.
Further, we tested in a clinical observational study SAH patients with and without vasospasm for different recruitment patterns of circulating EPC. To this purpose arterial blood samples were collected at various timepoints from admission to discharge of the patients. On these samples real-time quantitative PCR (RT-qPCR) was performed to detect gene expression relative to EPCs, since cytofluorimetric analysis appeared not sensitive enough to detect this rare cell population.
Results:
Though present results need further confirmation, in vitro it was observed that both MSC and EPC treatment through conditioned medium or co-culture in transwell- although with some differences - mediate a survival advantage for OGD stressed neurons. Furthermore stem cell mediated treatment showed efficacy even when applied 24 hours after OGD stress induction.
RT-qPCR results from a small sample of SAH patients might indicate an early mobilization of EPC related gene expression in subjects that do not develop vasospasm with a peak around day 4, whereas the expression of these genes remain invariably low in patients that develop vasospasm as in controls not affected by SAH.
Conclusions:
MSCs and EPCs seem to have an important potential role in preventing DIND in vitro as well as EPC recruitment might associate with lack of vasospasm in SAH patients.
Further studies are needed to confirm these results and to prove a causal relationship between EPCs and vasospasm protection.
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Lübbe, Katharina. « Entwicklung und Einsatz eines In-vitro-Ischämiemodels zur Untersuchung zellulärer Pathomechanismen der Klauenrehe des Rindes ». Doctoral thesis, Universitätsbibliothek Leipzig, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-171594.
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Die subklinische Klauenrehe oder claw horn disruption (CHD) ist von großer wirtschaftlicher Bedeutung für die Rinderhaltung, da sie zu Lahmheiten, Beeinträchtigungen des Allgemeinbefindens sowie einer eingeschränkten Leistungsfähigkeit der Tiere führt. Trotz zahlreicher Untersuchungen sind die pathophysiologischen Grundlagen der CHD noch immer nicht vollständig geklärt. Die derzeitigen Hypothesen weisen auf eine Ischämie in den noch lebensfähigen Epidermisschichten infolge einer veränderten dermalen Mikrozirkulation. Diese hat pathophysiologische Veränderungen zur Folge, die eine Störung der epidermalen Zellproliferation, eine Schädigung der dermo-epidermalen Verbindung sowie eine veränderte Keratinisierung und Hornproduktion umfassen. Von Bedeutung sind daher In-vitro-Ischämiemodelle, um die epidermale Reaktionsmechanismen auf die pathologischen Veränderungen der Dermis zu untersuchen. Ziel in der vorliegenden Arbeit war die Etablierung eines In-vitro-Ischämiemodells auf der Grundlage boviner Keratinozyten aus der Klauenepidermis. Mithilfe dieses Modells sollten die zellulären Pathomechanismen infolge einer Ischämie, einer Hypoxie sowie eines Glukoseentzugs untersucht werden. Des Weiteren stand die Analyse des Differenzierungsverhaltens der Keratinozyten infolge ischämischer, hypoxischer und hypoglykämischer Konditionen im Mittelpunkt. Für die Etablierung des In-vitro-Ischämiemodells diente als Grundlage das oxygen glucose deprivation (OGD)-Modell, das die Untersuchung eines gleichzeitigen Sauerstoff- und Glukosemangels sowie lediglich einer Hypoxie und eines Glukoseentzugs bei bovinen Keratinozyten ermöglichte. Die Versuche wurden in eine Kurzzeitanalyse über 96 Stunden sowie eine Langzeitanalyse über drei Wochen geteilt. Nach erfolgter Exposition wurde die Zellviabilität mittels LDH(Lactatdehydrogenase)- und MTT(3-(4,5-Dimethylhiazol-2-yl)-2,5-diphenyltetrazoliumbromid)-Assay untersucht. Des Weiteren wurde das veränderte Differenzierungsverhalten der Keratinozyten infolge der veränderten Kultivierungsbedingungen mittels Western Blot-Analyse anhand der Involukrin- und Lorikrin-Expression untersucht. Die Keratinozyten zeigten infolge einer OGD nach kurzer Expositionsdauer die höchsten zytotoxischen Effekte, die von einer zeitabhängigen Abnahme der Zellviabilität sowie massiven morphologischen Veränderungen gefolgt wurde. Hypoxische Bedingungen bewirkten eine zeitabhängige Abnahme der Zellviabilität, die erst nach zweiwöchiger Inkubation die größte Zytotoxizität aufwies, sowie eine geringgradig veränderte Zellmorphologie bei Erhaltung des Zellverbands. Der Glukoseentzug bewirkte eine stark verminderte Zellviabilität sowie starke morphologische Zellveränderungen. In der Western Blot-Analyse konnte eine gesteigerte Involukrin- und Lorikrin-Expression infolge einer OGD, einer Hypoxie und eines Glukoseentzugs nachgewiesen werden. In der vorliegenden Arbeit konnte erstmalig ein auf bovinen Keratinozyten basierendes In-vitro-Ischämiemodell etabliert werden, das die Untersuchung zellulärer Mechanismen der Epidermis ermöglichte. Die OGD zeigte den stärksten Einfluss auf die Zellviabilität sowie eine veränderte Zelldifferenzierung der Keratinozyten, was die pathophysiologischen Veränderungen im Rahmen der CHD reflektiert. Die ebenfalls starken Zellveränderungen infolge eines Glukoseentzugs verdeutlichen die Rolle der Glukose im Zellmetabolismus der Keratinozyten. Solch ein epidermaler Glukosemangel ist in Verbindung mit der negativen Energiebilanz der Rinder im peripartalen Zeitraum denkbar. Die Ergebnisse infolge einer Hypoxie verweisen auf vielfältige Adaptationsmechanismen der Keratinozyten an hypoxische Bedingungen, denen sie in der Epidermis in vivo während der Zelldifferenzierung ausgesetzt werden. Damit besitzt das In-vitro-Ischämiemodell ein großes Potenzial für den Einsatz in der Klauenreheforschung, um einerseits die mit einer Ischämie einhergehenden pathologischen Veränderungen der CHD untersuchen zu können. Andererseits liefert das Modell wertvolle Informationen zu den physiologischen Grundlagenmechanismen der Epidermis, die mit der Zelldifferenzierung einhergehenThe subclinical laminitis or claw horn disruption (CHD) is of great economic importance in the dairy industry as it causes lameness, poor general condition and reduced performance. Despite extensive research efforts, the pathomechanism of CHD remains widely unclear. The current hypotheses on CHD pathogenesis include ischemic alterations of the epidermal keratinocytes resulting from an impaired blood supply. This causes an alteration of cell proliferation, a dermo-epidermal separation and an impaired keratinization and horn production. Therefore, in vitro ischemia models are of critical importance in clarification of the epidermal responses to an altered microcirculation. The aim of this study was the establishment of an in vitro ischemia model based on bovine claw keratinocytes. This in vitro model should enable the investigation of cellular pathomechanisms following exposure to ischemia, hypoxia and glucose deprivation. An additional aim was the analysis of the differentiation pattern of keratinocytes under ischemic, hypoxic and hypoglycaemic conditions. To establish the in vitro ischemia model, the keratinocytes were exposed to oxygen-glucose deprivation (OGD). In addition, this model allowed the parallel examination of hypoxic and hypoglycaemic conditions on bovine claw keratinocytes. The experiments were divided into a short-term analysis over 96h and a long-term analysis over three weeks. Measurement of cell viability was performed by LDH(lactatedehydrogenase) and MTT(3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetra- zolium bromide) assays. Furthermore, the differentiation pattern of the keratinocytes after exposure to ischemia, hypoxia and glucose deprivation was detected by western blot analysis of the focus on expression of involucrin and loricrin. The highest cytotoxic effect was measured after short exposure to OGD followed by a time-dependent decrease of cell viability and extensive morphological changes of the keratinocytes. Hypoxic conditions lead to a time-dependent decrease of cell viability with the highest cytotoxicity after two weeks. The keratinocytes showed slight changes in cell morphology while maintaining a confluent cell layer. Exposure of keratinocytes to glucose deprivation showed a high decrease of cell viability and strong morphological changes. Furthermore, western blot analysis showed an altered expression pattern with increased involucrin and loricrin levels after exposure to OGD, hypoxia and glucose deprivation. The present study established for the first time an in vitro ischemia model based on bovine claw keratinocytes to study the cellular mechanisms of the epidermis. After exposure to OGD, keratinocytes showed the highest loss in cell viability and an altered cell differentiation. This reflects the pathophysiological changes following epidermal ischemia occurring during the pathogenesis of CHD. The massive cellular alterations after glucose deprivation provide good evidence for the importance of glucose in the cellular metabolism of keratinocytes. An epidermal glucose deficiency may occur in combination with a negative energy balance during peripartal period in cattle. The results of hypoxia show the different adaptive mechanisms of keratinocytes to hypoxic conditions which are present in the epidermis during cell differentiation. Thus, the in vitro ischemia model has a great potential for use in research into CHD pathogenesis and pathomechanisms associated with ischemia. On one side, it is possible to investigate the pathological changes following ischemia during CHD. On the other side, the model offers useful information on physiological response mechanisms of the epidermis that correlate with cell differentiation
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Lübbe, Katharina [Verfasser], Christoph K. W. [Akademischer Betreuer] Mülling et Alois [Gutachter] Boos. « Entwicklung und Einsatz eines In-vitro-Ischämiemodels zur Untersuchung zellulärer Pathomechanismen der Klauenrehe des Rindes : Development and experimental application of an in vitro ischemia model for investigating the cellular pathomechanism of laminitis in cattle / Katharina Lübbe ; Gutachter : Alois Boos ; Betreuer : Christoph K.W. Mülling ». Leipzig : Universitätsbibliothek Leipzig, 2015. http://d-nb.info/1239566565/34.
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Poizat, Adrien. « Contrôle temporel de la cavitation ultrasonore : application à la thrombolyse ultrasonore extracorporelle ». Thesis, Lyon, 2016. http://www.theses.fr/2016LYSE1031/document.
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Les ultrasons focalisés permettent d’effectuer des traitements thérapeutiques ciblés dans le corps humain. Dans le domaine des applications cardiovasculaires, ils permettent de détruire des caillots sanguins susceptibles de se former dans le système vasculaire. Dans ce cas, les mécanismes de thrombolyse sont largement liés à la cavitation ultrasonore, dont la dynamique complexe reste un obstacle à l’élaboration d’un dispositif thérapeutique. Dans le cadre de cette thèse, un système permettant le contrôle temporel de l’activité de cavitation en régime pulsé a été développé puis caractérisé. Ce dispositif utilise un transducteur focalisé et un hydrophone avec une boucle de rétroaction pour réguler l’activité de cavitation. Alors qu’en régime non régulé l’activité de cavitation a un caractère très aléatoire, le système de régulation mis au point permet d’atteindre un niveau de cavitation souhaité de manière très reproductible et avec une bonne stabilité temporelle. L’application de ce dispositif à la thrombolyse ultrasonore a été testée in vitro sur des caillots de sang humain. Au dispositif précédent a été ajouté un système permettant de déplacer le caillot sanguin au niveau du foyer, ainsi qu’un conduit permettant de compter le nombre de fragments libérés par la destruction du caillot. En comparaison des essais en régime non régulé, les essais en régime régulé ont montré une excellente efficacité thrombolytique et une très bonne reproductibilité, tout en diminuant les intensités acoustiques utilisées pour lyser les caillots sanguins. En parallèle des essais in vitro, une campagne de thrombolyse ultrasonore in vivo a été mise en place afin de réaliser des essais sur un modèle animal d’ischémie aiguë de membre inférieur. Un dispositif ultrasonore extracorporel in vivo guidé par échographie et monté sur un bras robotisé 6 axes a été développé. Un modèle ovin de thrombose artérielle a également été développé. Les tests ont permis de valider, d’une part, la faisabilité du modèle de caillot artériel et, d’autre part, le concept de thrombolyse extracorporelle purement ultrasonore basée sur la cavitation inertielle réguléeFocused ultrasound can be used for therapeutic applications in the human body. In cardiovascular applications, they can destroy blood clots formed in the vascular system. In this case, thrombolysis mechanisms are related to ultrasonic cavitation, but the complex dynamics remains an obstacle to the development of a therapeutic device. In this thesis, a system for the temporal control of the pulsed cavitation activity has been developed and characterized. This device uses a focused transducer and a hydrophone with a feedback loop for regulating the cavitation activity. While cavitation activity has a random behaviour in non-regulated conditions, the control system developed achieves a desired level of cavitation with very reproducibly and with good temporal stability. The application of this device to the ultrasound thrombolysis was tested in vitro on human blood clots. In the previous device was added a system for moving the blood clot at the focal point, and a tube for counting the number of fragments released by the destruction of the clot. In comparison to uncontrolled regime, tests showed an excellent thrombolytic efficacy and a very good reproducibility, with reduced acoustic intensities. In parallel to the in vitro tests, ultrasound thrombolysis was tested in vivo on an animal model of acute limb ischemia. An extracorporeal ultrasound device, guided by ultrasound and mounted on a robotic arm, has been developed for in vivo investigation. An ovine model of arterial thrombosis has also been developed. Tests were used to validate the feasibility of the model of arterial clots and to validate in vivo the concept of purely ultrasonic extracorporeal thrombolysis based on inertial cavitation regulation system
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Barandier, Christine. « Potentiel thérapeutique du manganèse et de l'un de ses dérivés synthétiques sur le système cardiovasculaire ». Université Joseph Fourier (Grenoble), 1998. http://www.theses.fr/1998GRE10238.
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Le present travail qui s'inscrit dans le cadre general des etudes consacrees a la protection pharmacologique des tissus cardiaque et vasculaire au cours de la reperfusion post-ischemique, comprend deux parties principales. La premiere a ete realisee sur un modele d'ischemie/reperfusion myocardique sur un modele experimental de coeur isole de rat. Les resultats sont exprimes en termes de donnees fonctionnelles, metaboliques et ultrastructurales. La seconde partie est une etude pharmacologique menee sur un modele d'anneaux d'aorte isolee de rat et comporte essentiellement des mesures de contractilite vasculaire. Dans la premiere partie, nous avons etudie l'effet protecteur du chlorure de manganese sur la recuperation post-ischemique du myocarde. Nous avons demontre que le manganese, administre durant la phase precoce de la reperfusion, ameliore la recuperation metabolique et fonctionnelle, vraisemblablement par le biais d'une protection antioxydante de la membrane des cardiomyocytes. Nous avons egalement mis en evidence un effet protecteur du manganese administre avant la periode d'ischemie sur la fonction et l'ultrastructure du myocarde post-ischemique. Dans la seconde partie de notre travail, nous avons montre qu'euk8, un compose de type salen-manganese presentant de fortes activites sod et catalase, exerce in vitro un effet vasorelaxant dose-dependant, non medie par une simple protection antioxydante de no, mais essentiellement du a une activation de l'adenylate cyclase et de la guanylate cyclase soluble des cellules musculaires lisses vasculaires. Enfin, une etude des effets vasomoteurs du manganese nous a amenes a conclure qu'il induit une relaxation par le biais de mecanismes plus complexes qu'une simple protection antioxydante de no et qu'un simple effet antagoniste calcique direct sur les cellules musculaires lisses vasculaires.
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SAKAMOTO, NOBUO, TATSUAKI MATSUBARA, YOSHIHIRO KAKINUMA et TATSUO HASHIMOTO. « MYOCARDIAL METABOLIC MARKERS OF TOTAL ISCHEMIA IN VITRO ». Nagoya University School of Medicine, 1994. http://hdl.handle.net/2237/15927.
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Thomas, 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.
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Pruitt, Christopher Rogers. « Early Mediators of Cutaneous Ischemia Reperfusion Injury : A Mouse Model ». VCU Scholars Compass, 2006. http://hdl.handle.net/10156/2024.
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Saito, Masao. « Pirfenidone alleviates lung ischemia-reperfusion injury in a rat model ». Kyoto University, 2019. http://hdl.handle.net/2433/242360.
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Chan, 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.
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Todd, Michael. « The effects of multiple ischemia and survival times on hippocampal CA1 neuronal cell loss in a rat model of global ischemia : A long-term ischemia maturation study ». Thesis, University of Ottawa (Canada), 1998. http://hdl.handle.net/10393/4230.
Texte intégralRésumé :
We investigated the effects of varying ischemia and survival times on CA1 neuronal loss. Histological analysis of the hippocampus was performed at 2, 7, 14, 28 and 90 days following 3, 5, 7, 10 and 13 minutes of global forebrain ischemia. Our results indicate that the ischemic maturation process extends beyond 7 days. Ten and thirteen minutes of ischemia produced a significant degree of cell loss by 7 days (70.53% and 83.25% respectively), while average cell death at 90 days survival was approximately 12% higher. Most strikingly, seven minutes of ischemia produced approximately 30% CA1 cell loss at 90 days compared to only 3% cell loss at 7 days, a nine-fold increase. No cell loss was observed at 2 and 7 days survival following 5 minutes of ischemia, but an average of 5.6% cell loss was observed at 3 months. Three minutes of ischemia produced no cell damage. Data collapsed over ischemic severity suggested that there may 2 rates of cell death evident in this study: (1) a rapid cell loss occurring within the first 7 days of ischemia and (2) a slow progressive cell loss occurring over weeks. Ten and thirteen minutes of ischemia possessed the rapid cell death, while 7 minutes appeared to display only slow progressive cell loss. The fact that the ischemic maturation process extends well beyond 7 days and that mild ischemia severities can produce significant cell loss at long survival times holds important implications for drug trials and our current knowledge of death mechanisms. (Abstract shortened by UMI.)
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Todd, Mike. « The effects of multiple ischemia and survival times on hippocampal CA1 neuronal cell loss in a rat model of global ischemia, a long-term ischemia maturation study ». Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ36746.pdf.
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Ariga, Suely Kunimi Kubo. « "Modulação térmica da lesão isquêmica : estudo in vitro" ». Universidade de São Paulo, 2005. http://www.teses.usp.br/teses/disponiveis/5/5160/tde-14092006-144005/.
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A isquemia cerebral causada pela parada cardíaca leva ao desapareciemnto neuronal. studamos os mecanismos de morte celular envolvidos na isquemia in vitro em linhagem de neuroblastoma.O insulto isquêmicao foi reproduzido cultivando as células sem fatores de crescimento, sem glicose e em embiente hipóxico produzido por um sistema de anaerobiose. Os resultados sugerem que a privação de oxigênio, glicose e fatores de cresciemtno do meio de cultura reproduzem o fenômeno semelhante a isquemia. INvestigamos ainda a participação de processo apoptótico e sua modulação térmica. Observams que a hipotermia produz neuroproteção, enquanto a hipertermia agrava o processo de morte celular por apoptose.Cardiac arrest causes cerebral ischemia and neuronal disappearance. We investigate celular death mechanisms elucidated by a model of ischemia in neuroblastoma cell line. The ischemic insult was reproduced by deprivation of growth factors and glucose in a hypoxic environment produced by an anaerobiosis system. Our results validate the experimental model and revel the participation of an apoptotic process in the celular loss induced by ischemia. We also demonstrated that hypothermia can be used as a neuroprotector agent whereas hyperthermia aggavates celular damage.
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Chan, Chu-fung, et 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.
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BRESCHI, GIAN LUCA. « STUDIO ANATOMICO E FUNZIONALE DELLA REGIONE DI PENOMBRA IN UN MODELLO DI ISCHEMIA IN VITRO ». Doctoral thesis, Università degli Studi di Milano, 2013. http://hdl.handle.net/2434/215236.
Texte intégralRésumé :
ANATOMICAL AND FUNCTIONAL STUDY OF THE PENUMBRA REGION IN AN IN VITRO MODEL OF FOCAL CEREBRAL ISCHEMIA
Experimental data have shown that the ischemic brain region is characterized by a highly damaged core surrounded by a rim of reversibly altered tissue, commonly referred to as the ischemic penumbra. The core region is characterized by a severely compromised CBF, whereas in the penumbra CBF is reduced but cellular metabolism is still preserved (Hossmann, 2008). One possible approach to identify core and penumbra is based on the evaluation of both metabolism and perfusion of the cerebral tissue. In principle, MRI could be utilized to solve this issue. Still, the significance of the MRI changes observed in the early phase of focal cerebral ischemia is a matter of discussion (Neumann-Hafelin et al., 2000; Kidwell et al., 2003; Rivers et al., 2006). Understanding the functional and structural correlates of MRI findings will help to characterize the pathological status of brain tissue that continuously change during the early few hours that follow an ischemic stroke. The model of the isolated brain facilitates these objectives because permits to induce a highly reproducible infarction by the simple ligation of the MCA and allows to perform multiple fine electrophysiological recordings before, during and after occlusion. In the guinea pig the medial cerebral artery (MCA) supplies the entire piriform cortex (PC), the Olfactory Tubercle (OT) is perfused, also, by collaterals of the anterior cerebral artery, especially in its medial part. This vascular condition puts the lateral Olfactory Tubercle (l-OT) as an area of watershed between the ischemic core and the normally perfused tissue. We analyzed and correlated neurophysiological, morphological and MRI changes induced by transient (30-60 minutes) and permanent occlusion of the medial cerebral artery (MCAo) in the isolated guinea pig brain. Multi-site extracellular recordings demonstrated prolonged ischemic depolarizations (ID) and the abolition of evoked responses in the piriform cortex served by MCA, but not in the olfactory tubercle, supplied by the anterior cerebral artery. Here evoked responses were transiently reduced and brief peri-infarctual depolarizations (PID) could be observed during the transient MCA occlusion. Diffusion weighted images performed on brains fixed 4 hours after transient ischemia and immunostaining for a microtubule-associated protein, MAP-2, showed overlapping changes due to acute brain injury, restricted to the piriform cortex. Our compared analysis of neurophysiological, MR and anatomical data demonstrate that DW-MRI sequences underestimate the extension of brain tissue damage induced by focal ischemia and do not include the area of PIDs generation, namely the penumbra region
Hence the penumbra is a region that maintains the capability to be excited. Hypothetically the ionic imbalance successive to the ischemic condition may prelude to a seizure that is frequent consequence of a stroke. In a consecutive study we verified whether anoxic ischemia per se, without intracranial hemorrhagic complication and in the absence of blood-borne elements responsible for brain infarction, is able to induce early changes in excitability that may prelude to the generation of seizures, and, ultimately could prime epileptogenesis. We used the multimodal approach herein described to identify the penumbra region in the very acute post-ischemic phase. To evaluate the effect of ischemia on cortical excitability we focused on ventral cortical structures (PC and OT) that have been extensively analyzed in this preparation (Biella & de Curtis, 1995; Carriero et al., 2009). The major input to these olfactory-limbic regions is carried by the lateral olfactory tract (LOT) that originates from neurons in the olfactory bulb (Haberly & Price, 1978). LOT is supplied by the medial cerebral artery (MCA). Since we aimed at evaluating synaptic excitability changes that occur acutely after ischemia, we needed to preserve the LOT as source of stimulation to evoke field responses in the olfactory cortex. Therefore, we chose to perform permanent bilateral occlusion of the anterior cerebral arteries (ACAo). We recorded, in olfactory cortices, slow potentials and evoked responses using specific patterns of stimulation in order to evaluate excitability changes in the acute phase after ischemia.
The ACAo induces a core area located in the shell of nucleus accumbens and a region of penumbra in the underlying olfactory cortices, where characteristic slow potential shifts (i.e PIDs), but no reduction of diffusion tensor MR signal and MAP-2 immunostaining (typical of ischemic core) were observed. Recording of responses evoked by low- and high-frequency stimulations of the lateral olfactory tract showed no excitability changes in the early hours that follow ischemia in the olfactory cortical areas supplied by ACA.
The absence of early hyperexcitability changes in an isolated whole brain model of ischemia, strongly suggests that brain anoxia per se does not contribute to the generation of early seizures. These findings support the view that blood-borne events (such as hemorrhage and inflammation) may play a major role in early post-ischemic seizures.
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Shaw, Matthew J. « Apoptosis following ischemia-reperfusion injury in a rabbit lung ex-vivo model ». Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/mq64450.pdf.
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Shaw, Matthew J. « Apoptosis following ischemia-reperfusion injury in a rabbit lung ex-vivo model ». Thesis, McGill University, 1999. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=30745.
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Background. Apoptosis is postulated as a mechanism involved in lung ischemia-reperfusion (IR) injury, however, the relative contributions of ischemia and reperfusion are unclear.Methods. Heart-lung blocks were harvested from New Zealand white rabbits (3.0--4.0 kg) and exposed to 0, 6, or 18 hours of cold ischemia (4°C), followed by 3 hours of reperfusion in an ex vivo model. Terminal dUTP nick-end labeling (TUNEL), the technique used most often for detection of apoptosis, was performed on the tissue sections.
Results. TUNEL demonstrated minimal apoptosis in lungs exposed to 0, 6, or 18 hours of ischemia with insignificant differences (p = 0.6 for 0 h vs. 18 h). After one hour of reperfusion, the level of TUNEL in the 18 hour ischemic tissue was significantly increased (p < 0.05 for 0 h vs. 18 h). During the period of reperfusion, the extent of apoptosis increased in direct proportion to the duration of ischemia; the level of TUNEL staining after 2 hours of reperfusion was significantly greater in the 18 hour ischemic tissue compared to the 6 hour ischemic tissue (p < 0.05), as was the 6 hour compared to the 0 hour (p < 0.01). The hallmark of apoptosis, nucleosomal ladders of 180--200 base pair DNA fragments, corresponded in intensity on gel electrophoresis to the quantitation of TUNEL. The characteristics of apoptotic cells including cell membrane blebbing, chromatin condensation and fragmentation were confirmed by electron microscopy.
Conclusions. These results provide evidence that apoptosis may be a specific feature of IR injury in pulmonary tissue.
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O, H.-Ici Darach Michael. « Multi-modal imaging of myocardial ischemia and reperfusion in a rat model ». Thesis, King's College London (University of London), 2017. https://kclpure.kcl.ac.uk/portal/en/theses/multimodal-imaging-of-myocardial-ischemia-and-reperfusion-in-a-rat-model(43bf5945-ce02-48cc-a634-2ebf00cffc99).html.
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Myocardial ischaemia causes progressive cellular injury. Initially there is loss of function, followed by formation of oedema. Ischemia, if prolonged, will eventually lead to cell death. Revascularisation of occluded coronary arteries is an efficient tool to reduce infarct size in acute myocardial infarction. However, reperfusion in itself can be associated with a significant amount of myocardial damage. The structural and metabolic changes occurring in myocardial ischemia and reperfusion can now be studied in-vivo using magnetic resonance imaging (MRI) and are targets to optimise the treatment of patients with acute myocardial ischemia. The development of new MRI techniques for T1 mapping allows the study of the evolution of myocardial oedema in both humans and animals. Moreover, hyperpolarised MR spectroscopy (MRS) allows the non-invasive assessment of myocardial metabolism, as injected hyperpolarised molecules can be used to study the function of metabolic pathways and enzymes in the setting of ischaemia and reperfusion. The aims of this project were to develop an animal model to allow the study of myocardial ischemia in real time, and then use this model to study the acute development of oedema and the metabolic changes in the metabolism of pyruvate. With the use of a vascular occluder, we successfully developed a closed-chest model of ischemia in the rat. This model allowed the animals to recover from the stress of surgery while also allowing ischemia experiments to be carried while the animals remain in the bore of the scanner. We then proceeded to validate this model and validate a new MR sequence, which produces cine-MR, T1 mapping and inversion-recovery prepared images. We studied the effects of varying durations of myocardial ischemia on the development of myocardial infarction and used this to validate the Small Animal Look-Locker Inversion Recovery (SALLI) multimodal imaging sequence. We were also able to study the development of myocardial oedema in real time, and demonstrate that preconditioning attenuated the T1 lengthening effects of myocardial ischemia. Following this, the acute changes in pyruvate metabolism occurring in the myocardial area at risk following 15 minutes of myocardial ischemia were investigated. We were able to detect abnormal metabolism in the area at risk for the first 60 minutes following ischemia and demonstrated that metabolism returned to normal 1 week after ischemia. The methods used show much promise in the study of the changes occurring in myocardial ischemia-reperfusion, and study of the effects of treatments such as pre- and postconditioning.
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Siu, Ada Hoi Ling. « Cardioprotective effects of herba cistanche on ischemia/reperfusion injury ex vivo and oxidative injury in vitro / ». View abstract or full-text, 2008. http://library.ust.hk/cgi/db/thesis.pl?BICH%202008%20SIU.
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Ohsumi, Akihiro. « Protective effect of pre-recovery surfactant inhalation on lungs donated after cardiac death in a canine lung transplantation model ». Kyoto University, 2017. http://hdl.handle.net/2433/218007.
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Cardella, Jonathan A. « A novel cell culture model to study ischemia-reperfusion injury in lung transplantation ». Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ46106.pdf.
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Wang, 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.
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Balkaya, Mustafa G. [Verfasser]. « Stroke, stress, and depression - evidence from a brain ischemia mouse model / Mustafa G. Balkaya ». Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2014. http://d-nb.info/1052221882/34.
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Liu, Lingguang, et 刘灵光. « Neuroprotection of melatonin and/or electro-acupuncture in a rat model of focal cerebral ischemia ». Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hdl.handle.net/10722/198928.
Texte intégralRésumé :
Stroke is a serious cerebral vascular event and a leading cause of death and disability worldwide, and ischemic stroke is the most common type. Evidence from animal research in acute cerebral ischemia shows that a combination of neuroprotectants might be more efficacious than the single agent given individually.
Both melatonin and electro-acupuncture (EA) have been suggested to be effective treatments against cerebral ischemia. However, it is unknown whether a combination of these two therapies could be beneficial against focal cerebral ischemia.
In the first study, the effect of post-treatment with a combination of melatonin and EA on regional cerebral blood flow (rCBF), neurological deficit score and infarct volume was investigated in both permanent and transient middle cerebral artery occlusion (MCAO) models in rats. When compared with the single treatment of melatonin or EA, the combination therapy resulted in a significant improvement of neurological function and a dramatic reduction of infarct volume at 72 hr after transient MCAO. A significant upregulatory effect on rCBF has been exerted by the combined treatment.
The effect of a combination of melatonin and EA on inflammatory reaction was investigated in the second study. Post-treatment of the combination therapy effectively inhibited neutrophil infiltration as well as the expression of some pro-inflammatory mediators, and increased the anti-inflammatory protein expression at 72 hr after transient MCAO. This beneficial effect may be due to the respective anti-inflammatory effects of melatonin and EA.
In the third study, the effect of a combination of melatonin and EA on apoptosis was examined. When compared with the EA treatment alone, post-treatment of the combination therapy exerted a greater inhibitory effect on tissue apoptosis and expression of the pro-apoptotic proteins as well as an upregulatory effect on the anti-apoptotic protein expression.
In the fourth study, the effect of continuous post-treatment of a combination of melatonin and EA on transient MCAO was investigated. The combination treatment significantly improved neurological function and decreased infarct volume at 7 days after transient MCAO. Cell proliferation and expression of the neurotrophic factor were increased by the combined treatment.
The effect of pretreatment with a combination of melatonin and EA was examined in the fifth study. Neurological function was improved and infarct volume was reduced by the combination pretreatment at 24 hr after transient MCAO. The inflammatory and apoptotic reaction were inhibited by the combined pretreatment through the modulatory effect of the related proteins.
In summary, our results show that, when compared with the single treatment of either melatonin or EA, post-treatment with a combination of melatonin and EA induced a complementary neuroprotective effect on improvement of neurological function and a dramatic reduction of infarct volume after transient MCAO. The complementary protection may be partially mediated via anti-inflammation and anti-apoptosis after transient cerebral ischemia. Pretreatment with a combination of melatonin and EA may be more effective in preventing ischemic brain injury after transient focal cerebral ischemia.published_or_final_version
Medicine
Doctoral
Doctor of Philosophy
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Chan, Pui-shan. « Effects of NPY-Y1 receptor activation or inhibition on free radical generation during in vitro or in vivo cerebral ischemia ». Click to view the E-thesis via HKUTO, 2006. http://sunzi.lib.hku.hk/hkuto/record/B35760825.
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MARIANI, JACOPO. « MULTICENTRE AND MULTISPECIES PRECLINICAL TRIAL OF REMOTE ISCHEMIC CONDITIONING IN ANIMAL MODEL OF ACUTE ISCHEMIC STROKE (TRICS–BASIC) ». Doctoral thesis, Università degli Studi di Milano-Bicocca, 2023. https://hdl.handle.net/10281/403043.
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Il condizionamento ischemico remoto (RIC) risulta essere un candidato ideale per essere investigato in uno studio multicentrico volto al trattamento dell'ictus ischemico acuto (AIS). L’ efficacia terapeutica del RIC è stata dimostrata a livello preclinico, come riportato da precedenti studi ottenuti da singoli laboratori; ciò nonostante, gli studi clinici di fase II-III non hanno ancora fornito risultati soddisfacenti. TRICS Basic è definita come la fase preclinica del progetto TRICS, un Trial traslazionale multicentrico di Condizionamento Ischemico Remoto in modelli animali di Ictus Ischemico Acuto, sostenuto dell’Organizzazione Italiana sull’ictus (ISO), che ha previsto la collaborazione di 7 università e centri di ricerca italiani. TRICS Basic è uno studio preclinico multicentrico, randomizzato e consistente, oltre ad essere orientato alla pratica traslazionale. Lo studio include due specie animali (ratti e topi) ed entrambi i generi (maschi e femmine) sono ugualmente rappresentati. Lo scopo di questo progetto è quello di studiare l'efficacia del trattamento RIC in modelli preclinici di ictus ischemico acuto. Tutti gli animali allocati nel gruppo MCAo+ (soggetti ad ictus) sono stati sottoposti allo stesso tempo di occlusione (60min nei topi; 100min nei ratti). In particolare, il trattamento è stato applicato bloccando l'arteria femorale ipsilaterale per 10 minuti nei topi e 20 nei ratti. La valutazione dei risultati è stata eseguita in cieco, sia per quanto riguarda l’outcome funzionale dicotomizzato (risultato primario), che per la quantificazione del volume dell'infarto (risultato secondario) a 48 ore. Anche le analisi statistiche sono state eseguite in cieco e secondo un paradigma intention–to–treat. Durante la fase sperimentale iniziale, è stata effettuata una fase di armonizzazione, includendo tutti i centri coinvolti, al fine di ridurre le differenze di valutazione durante la valutazione neurocomportamentale. Dopo aver raggiunto l'obiettivo di interclass correlation (ICC)=0.60, imposto a priori dal protocollo pre–pubblicato, la vera fase sperimentale ha avuto inizio. La coorte sperimentale è composta da n=206 animali (n=110 topi e n=96 ratti) ma solo n=152 sono stati inclusi nell’analisi finale per il gruppo MCAo+ (n=81 topi; n=71 ratti). I risultati ottenuti hanno dimostrato che il RIC ha un effetto positivo a livello dell’outcome funzionale (+20% nei topi; +18% nei ratti) ed è in grado di ridurre l'area della lesione ischemica (-4,3% nei topi; -26,6% nei ratti) in entrambe le specie analizzate. Nonostante il consistente numero di animali utilizzati in questo studio, rispetto ai precedenti studi preclinici su questo trattamento, non abbiamo raggiunto la significatività statistica nei nostri due outcome principali, se confrontiamo le singole specie animali. Al contrario, analizzando tutti gli animali come un’unica specie, abbiamo ottenuto un risultato significativo in entrambi gli outcome. Ciò suggerisce che, analogamente agli studi clinici, una maggiore dimensione della popolazione avrebbe portato a risultati più significativi per quanto riguarda il miglioramento del deficit neurologico e la riduzione del volume dell’infarto, analizzando le singole specie.Remote ischemic conditioning (RIC) represents an ideal candidate to enter a multicenter trial for acute ischemic stroke (AIS) treatment, since previous results from single laboratories support its efficacy, but unfortunately phase II–III clinical trials still provided inconclusive results. TRICS–Basic is the preclinical trial in the TRICS project, a multicentre translational Trial of Remote Ischemic Conditioning in Acute Ischemic Stroke from the Italian Stroke Organization (ISO) Basic Science network, which consisted in the collaboration of 7 Italian institution. TRICS–Basic is a robust, translationally oriented, multicentre, randomized preclinical trial, which includes two animal species (rats and mice) and both male and female sexes are equally represented. The aim of this project was to investigate the efficacy of RIC treatment in AIS experimental models. All the animals in the MCAo+ groups were subjected to the same time of occlusion (60 min in mice; 100 min in rats). The treatment was applied by clamping the ipsilateral femoral artery for 10 min in mice and 20 min in rats. Blinded outcomes assessment was performed both for dichotomized functional neuroscore (primary outcome) and for infarct volume (secondary outcome) at 48 hours. Statistical analyses were performed in a blind status and according to an intention–to–treat paradigm. During the initial experimental period, we carried out a harmonization phase, including all the involved centres, in order to reduce the assessment bias during the neurobehavioral test evaluation. After we have reached the target of Inter class correlation (ICC) 30.60 imposed a priori by the protocol paper, we started the real experimental phase. The experimental cohort was composed by n=206 animals (n=110 mice and n=96 rats) but only n=168 were allocated in the MCAo+ groups (n=88 mice; n=80 rats) and n=152 animals were included in the study (n=78 mice; n=74 rats). The obtained data showed that RIC improve the good functional outcome (+20% in mice; +18% in rats) and reduce the area of ischemic injury (-4.3% in mice; -26.6% in rats) in both species. Despite the large number of animals used in this study and as compared to previous preclinical studies on RIC treatment, we did not reach the statistical significance in our two major outcomes, if we compare the single species alone. On the contrary, if we combine together all the animals, we obtained a significant result in both the analysed outcomes. This suggest that, similarly to clinical trials, a larger sample size would have resulted in more significant results in the functional and the infarct size outcomes single species analyses.
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Chase, Teena D. « An in vitro model of reactive astrogliosis ». Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ49329.pdf.
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Worrall, Lisa Kirsty. « A 3D in vitro breast cancer model ». Thesis, University of Nottingham, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.436812.
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Vaskas, Jonas. « Impaired Cardiac cAMP-specific PDE4, β1-AR, and NE in an Ischemia-Reperfusion Rat Model ». Thesis, Université d'Ottawa / University of Ottawa, 2014. http://hdl.handle.net/10393/31741.
Texte intégralRésumé :
Ischemic injury in the heart is followed by an increase in SNS activity and the higher this activity, the poorer patient outcomes. An index of SNS activity in models of ischemia can be achieved by measuring NE, β-AR, and perhaps indirectly PDE4 to give an intracellular aspect on SNS signaling. A 20 minute ischemia-reperfusion was induced in a rat model with physiological measurements at 2-5 weeks post IR. At 3 weeks post IR, rats displayed increased PDE4 expression, decreased β 1-AR expression, increased plasma NE, decreased tissue NE storage, increased Doppler E/A ratio and unchanged LV ejection fraction. PET analysis with FDG revealed no infarct at 2 weeks, while analysis with [13N]NH3 displayed no resting flow defect but revealed trends in flow reserve impairment as early as 2.5 weeks with recovery at 5 weeks post-surgery. Applications of this model could be non-invasive imaging of PDE4 with (R)-[11C]Rolipram PET at early time points for development towards prognostic and therapy guidance in humans.
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Corbisiero, Rafael M. « An ischemia reperfusion compartment syndrome model in the canine hindlimb : analysis of present treatment modalities ». Thesis, McGill University, 1988. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=61886.
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Zanoni, Diogo Sousa [UNESP]. « Experimental glaucoma model (ischemia and reperfusion) : histology, morphometry, protein and gene espression of apoptosis pathway ». Universidade Estadual Paulista (UNESP), 2015. http://hdl.handle.net/11449/132013.
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Purpose: The aims of this study were to better understand the mechanism of cell death by apoptosis in a glaucoma model (ischemia / reperfusion) and evaluate the role of apoptosis in this model and if treatment with Sildenafil helps prevent apoptosis. Methods: 36 rats, from 4 to 6 months, males, Lewis and weighing ± 350g were divided in 5 groups: control group (6 animals) and for groups with ischemia / reperfusion (7 and 21 days), two groups consisting of ten animals treated with sildenafil and two groups of Five animals treated with placebo. Paracentesis of the anterior chamber with needle 30G coupled to saline (0.9%) was made and maintained for 60 minutes. Intraocular pressure was measured by rebound tonometer (Tonovet®). There was histological, morphometric by hematoxylin and eosin and, immunohistochemical staining and qRT-PCR analysis by Caspase-7, Caspase-6, Caspase-9, Tnf-r2, Fas-l, Bcl-2 and Bax. For statistic analysis we used ANOVA and t-test for morphometric analysis and, for immunohistochemistry and qRT-PCR, Fisher exact test was employed with a statistical significance level of p <0.05 Results: Histology and morphometric analysis, proved more changes in the untreated group compared to the treatment and control group. Analysis of immunohistochemistry and qRT-PCR observed the more significant expression in untreated eyes. Conclusion: Sildenafil apperead to be protective to ganglion cell apoptosis. Cell survival was evident in histology and morphometry. For immunohistochemistry and RT-PCR was observed protective effect in the apoptosis pathways with similar or below expression compared to the control
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Zanoni, Diogo Sousa. « Experimental glaucoma model (ischemia and reperfusion) : histology, morphometry, protein and gene espression of apoptosis pathway / ». Botucatu, 2015. http://hdl.handle.net/11449/132013.
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Orientador: Renée Laufer AmorimCoorientador: José Luiz Laus
Banca: Juliany Quitzan Gomes
Banca: Alvio Isao Shiguematsu
Resumo: Não disponível
Abstract: Purpose: The aims of this study were to better understand the mechanism of cell death by apoptosis in a glaucoma model (ischemia / reperfusion) and evaluate the role of apoptosis in this model and if treatment with Sildenafil helps prevent apoptosis. Methods: 36 rats, from 4 to 6 months, males, Lewis and weighing ± 350g were divided in 5 groups: control group (6 animals) and for groups with ischemia / reperfusion (7 and 21 days), two groups consisting of ten animals treated with sildenafil and two groups of Five animals treated with placebo. Paracentesis of the anterior chamber with needle 30G coupled to saline (0.9%) was made and maintained for 60 minutes. Intraocular pressure was measured by rebound tonometer (Tonovet®). There was histological, morphometric by hematoxylin and eosin and, immunohistochemical staining and qRT-PCR analysis by Caspase-7, Caspase-6, Caspase-9, Tnf-r2, Fas-l, Bcl-2 and Bax. For statistic analysis we used ANOVA and t-test for morphometric analysis and, for immunohistochemistry and qRT-PCR, Fisher exact test was employed with a statistical significance level of p <0.05 Results: Histology and morphometric analysis, proved more changes in the untreated group compared to the treatment and control group. Analysis of immunohistochemistry and qRT-PCR observed the more significant expression in untreated eyes. Conclusion: Sildenafil apperead to be protective to ganglion cell apoptosis. Cell survival was evident in histology and morphometry. For immunohistochemistry and RT-PCR was observed protective effect in the apoptosis pathways with similar or below expression compared to the control
Mestre
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Abood, Sarah K. « Effect of glutamine on mucosal permeability in a canine model of ischemia and reperfusion injury / ». The Ohio State University, 1997. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487947908401747.
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Kanazawa, Hiroyuki. « Bone marrow-derived mesenchymal stem cells ameliorate hepatic ischemia reperfusion injury in a rat model ». Kyoto University, 2012. http://hdl.handle.net/2433/157437.
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Albiero, Mattia. « The role of p66Shc knockout in a murine model of diabetic ulcers and peripheral ischemia ». Doctoral thesis, Università degli studi di Padova, 2010. http://hdl.handle.net/11577/3427554.
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This thesis studied the role of p66shc in a murine model of ulcers complicated with peripheral ischemia. This study showed that the knockout of p66Shc improved wound healing in the setting of diabetes and ischemia. Moreover, diabetes increases the expression of p66Shc.Questa tesi ha studiato il ruolo di p66Shc in un modello murino di ulcere diabetiche complicate da ischemia periferica. Questo studio ha dimostrato che il knockout di p66Shc migliora la guarigione delle ulcere nel contesto di diabete ed ischemia. Il diabete, inoltre, aumenta l'espressione di p66Shc.
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Giedt, Randy James. « Real-Time Acquisition and Analysis of Endothelial Mitochondrial Superoxide Radical Production and Membrane Potential During In Vitro Ischemia/Reperfusion ». The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1243541457.
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Chan, Pui-shan, et 陳佩珊. « Effects of NPY-Y1 receptor activation or inhibition on free radical generation during in vitro or in vivo cerebral ischemia ». Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B35760825.
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Akinrinmade, Olusiji Alex. « Potential neuroprotective effects of fermented rooibos herbal tea in a rat model of ischemic brain injury ». University of the Western Cape, 2015. http://hdl.handle.net/11394/4705.
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Magister Scientiae (Medical Bioscience) - MSc(MBS)Stroke is the third leading cause of death in South Africa, killing about 240 people a day and leaving survivors with residual disabilities. There is no clinically approved neuroprotective agent for stroke at the moment but the consumption of plant polyphenols has been suggested to offer neuroprotection against stroke and other neurodegenerative diseases. In this study, we investigated the effects of long term consumption of fermented rooibos herbal tea (FRHT) on ischemia reperfusion brain injury (I-RBI) in rats. Male adult Wistar rats were fed FRHT ad libitum for 7 weeks prior to the induction of ischemic injury by the transient bilateral occlusion of the common carotid arteries (BCCAO) for 20 minutes followed by 24 hours, 4 and 7 days of reperfusion respectively. Rats were then evaluated for neurologic deficits before sacrifice and brains harvested for assessment of brain oedema, blood-brain-barrier (BBB) integrity through Evans blue extravasation (EBE), immunohistochemical studies of apoptosis and lipid peroxidation. Oxygen radical antioxidant capacity and ferric reducing antioxidant power assays were also conducted to assess total antioxidant capacity after ischemia-reperfusion injury. Notably, the long term consumption of fermented rooibos herbal tea prevented brain oedema by reducing cerebral swelling induced by I-RBI. We also observed that fermented rooibos herbal tea offered neuroprotection against damage to the BBB and delayed neuronal death associated with BCCAO as fewer apoptotic cells were identified 7 days post BCCAO reperfusion. Significantly reduced levels of lipid peroxidation and increased levels of total antioxidant capacity were also observed in brain specimens of rats treated with FRHT. Rats treated with FRHT also showed improved neurologic outcomes when compared with the untreated animals. Our results show that FRHT has potent antioxidant and anti-inflammatory properties which can provide neuroprotective effects against neuronal cell loss, cerebral swelling, BBB disruption, lipid peroxidation and neurologic deficits following I-RBI. The use of FRHT is therefore highly recommended for patients with conditions that predispose them to stroke.
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Na, Rongrui [Verfasser], et René [Akademischer Betreuer] Schramm. « Intravital microscopy of lung ischemia reperfusion injury in a rat model / Rongrui Na ; Betreuer : René Schramm ». München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2021. http://d-nb.info/1227840012/34.
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Rich, Barbara Sharon. « Development of an in vitro model for accommodation ». Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq28982.pdf.
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Aldsworth, Timothy Grant. « Microbial in vitro model of root surface caries ». Thesis, University of Glasgow, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360285.
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