Готові списки джерел за темами / Ex-vivo rat model

Добірка наукової літератури з теми "Ex-vivo rat model"

Автор: Grafiati

Опубліковано: 12 червня 2021

Оновлено: 1 лютого 2022

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Статті в журналах з теми "Ex-vivo rat model":

Citak, N., S. Arni, J. Cehn, L. Ceulemans, I. Schmitt-Opitz, and I. Inci. "Subnormothermic Ex Vivo Lung Perfusion Improves Graft Preservation in Rat Ex Vivo Lung Perfusion Model." Journal of Heart and Lung Transplantation 39, no. 4 (April 2020): S354. http://dx.doi.org/10.1016/j.healun.2020.01.416.

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Kural, Mehmet H., Guohao Dai, Laura E. Niklason, and Liqiong Gui. "An Ex Vivo Vessel Injury Model to Study Remodeling." Cell Transplantation 27, no. 9 (August 10, 2018): 1375–89. http://dx.doi.org/10.1177/0963689718792201.

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Objective: Invasive coronary interventions can fail due to intimal hyperplasia and restenosis. Endothelial cell (EC) seeding to the vessel lumen, accelerating re-endothelialization, or local release of mTOR pathway inhibitors have helped reduce intimal hyperplasia after vessel injury. While animal models are powerful tools, they are complex and expensive, and not always reflective of human physiology. Therefore, we developed an in vitro 3D vascular model validating previous in vivo animal models and utilizing isolated human arteries to study vascular remodeling after injury. Approach: We utilized a bioreactor that enables the control of intramural pressure and shear stress in vessel conduits to investigate the vascular response in both rat and human arteries to intraluminal injury. Results: Culturing rat aorta segments in vitro, we show that vigorous removal of luminal ECs results in vessel injury, causing medial proliferation by Day-4 and neointima formation, with the observation of SCA1+ cells (stem cell antigen-1) in the intima by Day-7, in the absence of flow. Conversely, when endothelial-denuded rat aortae and human umbilical arteries were subjected to arterial shear stress, pre-seeding with human umbilical ECs decreased the number and proliferation of smooth muscle cell (SMC) significantly in the media of both rat and human vessels. Conclusion: Our bioreactor system provides a novel platform for correlating ex vivo findings with vascular outcomes in vivo. The present in vitro human arterial injury model can be helpful in the study of EC-SMC interactions and vascular remodeling, by allowing for the separation of mechanical, cellular, and soluble factors.

Ohsumi, Akihiro, Takashi Kanou, Aadil Ali, Zehong Guan, David M. Hwang, Thomas K. Waddell, Stephen Juvet, Mingyao Liu, Shaf Keshavjee, and Marcelo Cypel. "A method for translational rat ex vivo lung perfusion experimentation." American Journal of Physiology-Lung Cellular and Molecular Physiology 319, no. 1 (July 1, 2020): L61—L70. http://dx.doi.org/10.1152/ajplung.00256.2019.

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The application of ex vivo lung perfusion (EVLP) has significantly increased the successful clinical use of marginal donor lungs. While large animal EVLP models exist to test new strategies to improve organ repair, there is currently no rat EVLP model capable of maintaining long-term lung viability. Here, we describe a new rat EVLP model that addresses this need, while enabling the study of lung injury due to cold ischemic time (CIT). The technique involves perfusing and ventilating male Lewis rat donor lungs for 4 h before transplanting the left lung into a recipient rat and then evaluating lung function 2 h after reperfusion. To test injury within this model, lungs were divided into groups and exposed to different CITs (i.e., 20 min, 6 h, 12 h, 18 h and 24 h). Experiments involving the 24-h-CIT group were prematurely terminated due to the development of severe edema. For the other groups, no differences in the ratio of arterial oxygen partial pressure to fractional inspired oxygen ([Formula: see text]/[Formula: see text]) were observed during EVLP; however, lung compliance decreased over time in the 18-h group ( P = 0.012) and the [Formula: see text]/[Formula: see text] of the blood from the left pulmonary vein 2 h after transplantation was lower compared with 20-min-CIT group ( P = 0.0062). This new model maintained stable lung function during 4-h EVLP and after transplantation when exposed to up to 12 h of CIT.

Abubakar, Adamu Abdul, Sahar Mohammed Ibrahim, Ahmed Khalaf Ali, Kareem Obayes Handool, Mohammad Shuaib Khan, Mohamed Noordin Mustapha, Tengku Azmi Ibrahim, Ubedullah Kaka, and Loqman Mohamad Yusof. "Postnatal ex vivo rat model for longitudinal bone growth investigations." Animal Models and Experimental Medicine 2, no. 1 (February 20, 2019): 34–43. http://dx.doi.org/10.1002/ame2.12051.

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Hoff, Catherine M. "Ex vivo and in vivo gene transfer to the peritoneal membrane in a rat model." Nephrology Dialysis Transplantation 16, no. 3 (March 1, 2001): 666–68. http://dx.doi.org/10.1093/ndt/16.3.666.

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Sierakowiak, Adam, Anna Mattsson, Marta Gómez-Galán, Teresa Feminía, Lisette Graae, Sahar Nikkhou Aski, Peter Damberg, Mia Lindskog, Stefan Brené, and Elin Åberg. "Hippocampal Morphology in a Rat Model of Depression: The Effects of Physical Activity." Open Neuroimaging Journal 9, no. 1 (January 30, 2015): 1–6. http://dx.doi.org/10.2174/1874440001509010001.

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Accumulating in vivo and ex vivo evidences show that humans suffering from depression have decreased hippocampal volume and altered spine density. Moreover, physical activity has an antidepressant effect in humans and in animal models, but to what extent physical activity can affect hippocampal volume and spine numbers in a model for depression is not known. In this study we analyzed whether physical activity affects hippocampal volume and spine density by analyzing a rodent genetic model of depression, Flinders Sensitive Line Rats (FSL), with Magnetic Resonance Imaging (MRI) and ex vivo Golgi staining. We found that physical activity in the form of voluntary wheel running during 5 weeks increased hippocampal volume. Moreover, runners also had larger numbers of thin spines in the dentate gyrus. Our findings support that voluntary wheel running, which is antidepressive in FSL rats, is associated with increased hippocampal volume and spine numbers.

Bouckaert, Charlotte, Emma Christiaen, Jeroen Verhoeven, Benedicte Descamps, Valerie De Meulenaere, Paul Boon, Evelien Carrette, Kristl Vonck, Christian Vanhove, and Robrecht Raedt. "Comparison of In Vivo and Ex Vivo Magnetic Resonance Imaging in a Rat Model for Glioblastoma-Associated Epilepsy." Diagnostics 11, no. 8 (July 21, 2021): 1311. http://dx.doi.org/10.3390/diagnostics11081311.

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Magnetic resonance imaging (MRI) is frequently used for preclinical treatment monitoring in glioblastoma (GB). Discriminating between tumors and tumor-associated changes is challenging on in vivo MRI. In this study, we compared in vivo MRI scans with ex vivo MRI and histology to estimate more precisely the abnormal mass on in vivo MRI. Epileptic seizures are a common symptom in GB. Therefore, we used a recently developed GB-associated epilepsy model from our group with the aim of further characterizing the model and making it useful for dedicated epilepsy research. Ten days after GB inoculation in rat entorhinal cortices, in vivo MRI (T2w and mean diffusivity (MD)), ex vivo MRI (T2w) and histology were performed, and tumor volumes were determined on the different modalities. The estimated abnormal mass on ex vivo T2w images was significantly smaller compared to in vivo T2w images, but was more comparable to histological tumor volumes, and might be used to estimate end-stage tumor volumes. In vivo MD images displayed tumors as an outer rim of hyperintense signal with a core of hypointense signal, probably reflecting peritumoral edema and tumor mass, respectively, and might be used in the future to distinguish the tumor mass from peritumoral edema—associated with reactive astrocytes and activated microglia, as indicated by an increased expression of immunohistochemical markers—in preclinical models. In conclusion, this study shows that combining imaging techniques using different structural scales can improve our understanding of the pathophysiology in GB.

Ma, Zhe, Sheng-jun Wang, Chuan-fu Li, Xiang-xing Ma, and Tao Gu. "Increased metabolite concentration in migraine rat model by proton MR spectroscopy in vivo and ex vivo." Neurological Sciences 29, no. 5 (October 2008): 337–42. http://dx.doi.org/10.1007/s10072-008-0991-5.

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Savolainen-Peltonen, H., L. Petrov, and P. Hayry. "RAT AORTIC ALLOGRAFT EXPLANT ASSAY AS AN EX VIVO MODEL OF ALLOGRAFT ARTERIOSCLEROSIS." Transplantation 78 (July 2004): 623. http://dx.doi.org/10.1097/00007890-200407271-01678.

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Liu, Mingyao, Lorraine Tremblay, Stephen D. Cassivi, Xiao-Hui Bai, Eric Mourgeon, Andrew F. Pierre, Arthur S. Slutsky, Martin Post, and Shaf Keshavjee. "Alterations of nitric oxide synthase expression and activity during rat lung transplantation." American Journal of Physiology-Lung Cellular and Molecular Physiology 278, no. 5 (May 1, 2000): L1071—L1081. http://dx.doi.org/10.1152/ajplung.2000.278.5.l1071.

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Decreased nitric oxide (NO) production has been reported during lung transplantation in patients. To study the effects of ischemia and reperfusion on endogenous NO synthase (NOS) expression, both an ex vivo and an in vivo lung injury model for transplantation were used. Donor rat lungs were flushed with cold low-potassium dextran solution and subjected to either cold (4°C for 12 h) or warm (21°C for 4 h) ischemic preservation followed by reperfusion with an ex vivo model. A significant increase in inducible NOS and a decrease in endothelial NOS mRNA was found after reperfusion. These results were confirmed in a rat single-lung transplant model after warm preservation. Interestingly, protein contents of both inducible NOS and endothelial NOS increased in the transplanted lung after 2 h of reperfusion. However, the total activity of NOS in the transplanted lungs remained at very low levels. We conclude that ischemic lung preservation and reperfusion result in altered NOS gene and protein expression with inhibited NOS activity, which may contribute to the injury of lung transplants.

Більше джерел

Дисертації з теми "Ex-vivo rat model":

Omasa, Mitsugu. "Glycine ameliorates lung reperfusion injury after cold preservation in an ex vivo rat lung model." Kyoto University, 2004. http://hdl.handle.net/2433/147462.

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Papegay, Bérengère. "Identification des mécanismes moléculaires de l'hépatoprotection du foie de rat isolé." Thesis, Lille 2, 2020. http://www.theses.fr/2020LIL2S015.

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L’effet protecteur du jeûne a été observé dans plusieurs domaines de la santé. Pour l’étudier, un modèle de foie de rat perfusé ex vivo a ici été utilisé. Dans ce modèle, nous n’avons pas observé, pour un jeûne de 18h, l’effet protecteur du jeûne rapporté pour le foie in situ. Nous avons cependant souligné l’importance du coût énergétique du mécanisme protecteur du foie isolé soumis au stress expérimental de l’ischémie/reperfusion et corrélé la protection à un taux plus élevé de glycogène et une charge énergétique nécessitant le dépassement d’un seuil en deçà duquel la protection s’estompait. L’administration de substrats énergétiques (lactate et alanine) nous a permis de confirmer le besoin énergétique de la protection du foie isolé. Ensuite, l’accroissement de la durée du jeûne du rat donneur de 18 à 24heures s’est avérée hépatoprotectrice et, plus globalement, a montré que la capacité de mobilisation énergétique et,à ce titre, l’autophagie contribuaient à l’hépatoprotection, le coût énergétique bien connu de l’autophagie étant en adéquation avec les précédents travaux du doctorat. Trois voies de signalisation candidates pour l’activation de l’autophagie, impliquant AMPK, HMGB1 et ADP, ont été étudiées. La phosphorylation de l’AMPK était augmentée dans le foie de rat à jeun 24h vs 18h. Toutefois, l’ajout d’AICAR, un activateur de l’AMPK, bien qu’augmentant sa phosphorylation dans le foie isolé de rat à jeun 18h, n’a pas induit de protection. L’accumulation d’HMGB1, connue pour induire l’autophagie, n’a montré aucune corrélation avec les marqueurs de la cytolyse hépatique (LDH) et de l’autophagie (rapport LC3II/Actine). L’ADP, dans ses rapports ADP/(AMP+ADP+ATP) et ADP/(AMP+ATP), était plus élevée pour les foies de rat à jeun 24h et a été corrélée à l’hépatoprotection. L’ADP induisant l’autophagie par activation du récepteur membranaire P2Y13, un inhibiteur spécifique, le MRS2211, a été utilisé. Son inclusion dans le perfusât a estompé l’hépatoprotection et l’activation de l’autophagie associées au prolongement de la période de jeûne, validant le rôle-clef de cette signalisation dans l’hépatoprotection.En conclusion, le doctorat a permis une avancée substantielle de la compréhension du rôle joué par le statu tnutritionnel du sujet donneur sur l’hépatoprotection du foie isolé. L’identification des mécanismes moléculaires de l’hépatoprotection (mobilisation énergétique, autophagie) et de sa signalisation (ADP, récepteur P2Y13) ouvrent des perspectives thérapeutiques innovantes des maladies du foie et de nouvelles stratégies de préservation du greffon hépatique. Dans une optique de survie cellulaire, l’autophagie assure à la fois une fonction de maintien de la qualité des composants cellulaires et un rôle énergétique. Ce maintien de qualité protège la cellule, elle coûte en énergie rendant cette dernière indispensable à ce type de protection. Autrement dit, la maintenance préserve de la détérioration et cette protection a un coût qui passe par une signalisation (décision interne de financement) qui,identifiée, peut désormais être sollicitée comme souhaité. Aussi, un financement externe (apport de substrats énergétiques) peut être choisi voire ajouté au précédent
The protective effect of fasting has been observed in several areas of health. To study it, a rat liver model perfused exvivo was used here. In this model, we did not observe, for an 18h fasting, the protective effect reported for the liverin situ. However, we did emphasize the importance of the energy cost of the protective mechanism in the isolatedliver under experimental stress of ischemia/reperfusion and correlated protection with higher glycogen levels and anenergy load that required an exceeding threshold below which protection fades. The administration of energysubstrates (lactate and alanine) allowed us to confirm the energetic need for protection of the isolated liver. Then,increasing the duration of fasting of the donor rat from 18 to 24 hours proved to be hepatoprotective and, moregenerally, showed that the capacity for energy mobilization and, as such, autophagy contributed to hepatoprotection,the well-known energy cost of autophagy being in line with previous PhD work. Three candidate signaling pathwaysfor the activation of autophagy, involving AMPK, HMGB1 and ADP, were studied. Phosphorylation of AMPK wasincreased in fasted rat liver 24 hours vs. 18 hours. However, the addition of AICAR, an activator of AMPK, althoughincreasing its phosphorylation in isolated fasted rat liver 18h, did not induce protection. HMGB1 accumulation knownto induce autophagy, showed no correlation with markers of hepatic cytolysis (LDH) and autophagy (LC3II/Actin ratio).ADP, in its ADP/(AMP+ADP+ATP) and ADP/(AMP+ATP) ratios, was higher in 24-hour fasted rat livers and was correlatedwith hepatoprotection. ADP induced autophagy by activation of the membrane P2Y13 receptor, a specific inhibitor,MRS2211, was used. Its inclusion in the perfusate blunted the hepatoprotection and activation of autophagyassociated with prolonged fasting, validating the key role of this signaling in hepatoprotection.In conclusion, the Ph.D. allowed a substantial advance in the understanding of the role played by the nutritional statusof the donor on the hepatoprotection of the isolated liver. The identification of the molecular mechanisms ofhepatoprotection (energy mobilization, autophagy) and of its signaling (ADP, P2Y13 receptor) opens up innovativetherapeutic perspectives for liver diseases and new strategies for liver graft preservation. From a cell survivalperspective, autophagy ensures both a function of maintaining the quality of cellular components and an energeticrole. This maintenance of quality protects the cell and costs energy, making it indispensable for this type of protection.In other words, the maintenance preserves from deterioration and this protection has a cost that goes throughsignalling (internal funding decision) which, once identified, can now be requested as desired. Also, external financing(contribution of energy substrates) can be chosen or even added to the previous one

Aguiló, Espases Rafael. "Protección frente al enfriamiento intenso por anticongelantes naturales. Modelo ex-vivo de preservación de pulmón de rata." Doctoral thesis, Universitat de Barcelona, 2000. http://hdl.handle.net/10803/1194.

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Los procedimientos quirúrgicos actualmente disponibles frente a la enfermedad pulmonar avanzada, irreversible y terminal son la cirugía de reducción de volumen pulmonar y el trasplante de pulmón. Expandir la práctica del trasplante de pulmón constituye uno de los grandes retos que la neumología y la cirugía torácica tienen delante. La posibilidad de solucionar los problemas citados constituye el motor de la investigación en transplante de pulmón.

Trocme, Caryn. "Role des sequences cre et tre dans la regulation de l'expression du gene codant pour la tyrosine hydroxylase de rat ; etudes ex vivo et par transgenese." Paris 11, 1997. http://www.theses.fr/1997PA11T026.

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Gozalbes-Bappel, Catherine. "Effets vasculaires de deux diurétiques de l'anse : pirétanide et furosémide. Etudes ex vivo chez le rat spontanément hypertendu et in vitro chez le cobaye." Bordeaux 2, 1997. http://www.theses.fr/1997BOR28532.

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Menezes, Arteiro Queiroz. "Estudo de pulmões de ratos reperfundidos em um modelo experimental ex-vivo: comparação entre duas soluções de preservação (Perfadex® e Celsior®)." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/5/5156/tde-09082013-120744/.

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INTRODUÇÃO: A lesão de isquemia-reperfusão continua sendo considerada a maior causa de mortalidade relacionada ao transplante de pulmão e sua gravidade é influenciada por diversos fatores, dentre eles, a preservação pulmonar. OBJETIVO: Comparar duas soluções de preservação pulmonar, Perfadex® e Celsior®, quanto a capacidade de preservação de tecido pulmonar isquêmico. MÉTODOS: Sessenta pulmões de ratos preservados com Perfadex®, Celsior® ou solução salina após períodos de isquemia hipotérmica de 6 ou 12 horas, foram reperfundidos com sangue homólogo em modelo experimental ex-vivo durante 60 minutos consecutivos. A cada 10 minutos os dados de gasometria, hematócrito, mecânica ventilatória, hemodinâmica e peso do bloco cardiopulmonar foram registrados. Ao final da reperfusão o pulmão esquerdo foi pesado e acondicionado por 48h a 70oC para obtenção da razão peso úmido/peso seco, bem como amostras de tecido pulmonar foram retiradas para histopatologia, microscopia eletrônica e TUNEL. A análise estatística incluiu a comparação entre as soluções e os tempos de isquemia, utilizando ANOVA e Kruskall-Wallis. O nível de significância foi de 5%. RESULTADOS: A comparação entre as complacências de pulmões preservados com Celsior® e Perfadex® nos tempos de isquemia de 6 e 12 horas não apresentou significância estatística (p=0,161 e p=0,316, respectivamente). Os pulmões submetidos a 6 horas de isquemia apresentaram complacência pulmonar superior aos de 12 horas (Perfadex® p=0,02; Celsior® p=0,019; Salina p=0,016). Os valores de pressão arterial pulmonar foram semelhantes entre as três soluções nos dois tempos de isquemia, bem como na comparação entre os tempos de 6 e 12 horas, independente da solução. A Capacidade Relativa de Oxigenação não demonstrou diferença estatística entre as três soluções, independentemente do tempo de isquemia. Na comparação entre os dois tempos de isquemia, o desempenho da oxigenação foi significativamente pior nos pulmões preservados com salina por 12 horas (p=0,001). A razão peso úmido/peso seco não apresentou diferença estatística significante entre as três soluções nos dois tempos de isquemia, porém na comparação entre os tempos de isquemia, os pulmões preservados com Perfadex® apresentaram uma relação peso úmido/peso seco maior no tempo de isquemia mais longo (p=0,001). À microscopia óptica, pulmões preservados com salina apresentaram mais edema que os demais, independentemente do tempo de isquemia. A avaliação da apoptose celular através do método de TUNEL não mostrou diferença estatisticamente significativa na comparação entre os grupos. CONCLUSÃO: Os pulmões preservados com Perfadex® e Celsior® apresentaram desempenho similar em relação às trocas gasosas e parâmetros hemodinâmicos e de mecânica ventilatória. Os pulmões preservados com Perfadex® por 12 horas apresentaram mais edema. Os achados histopatológicos não diferiram entre os grupos estudados
INTRODUCTION: Ischemia-reperfusion injury remaisn the leading cause of mortality related to lung transplantation. Its severity is influenced by several factors including lung preservation. OBJECTIVE: To compare two lung preservation solutions, Perfadex® and Celsior® and its ability to preserve ischemic lung tissue. METHODS: Sixty rat lungs were preserved with Perfadex®, Celsior® or saline after a cold ischemic period of 6 or 12 hours and were then reperfused with homologous blood in an ex vivo experimental model for 60 consecutive minutes. At 10-minute intervals during reperfusion of the heart-lung blocks, data were collected for blood gases, hematocrit, mechanical ventilation, hemodynamic and the heart-lung block weight was recorded. At the end of reperfusion, the left lung was weighed and packaged kept at 70oC for 48h to obtain the wet-to-dry weight ratio. Lung tissue samples were processed for histology, electron microscopy and TUNEL. Statistical analysis included a comparison of the solutions and ischemic times, using ANOVA and Kruskal-Wallis. The significance level was set at 5%. RESULTS: The comparison between the compliance of lungs preserved with Celsior® and Perfadex® in ischemic times of 6 and 12 hours was not statistically significant (p=0.161 and p=0.316, respectively). The lungs subjected to 6 hours of ischemia showed higher lung compliance compared to 12 hours (p=0.02 Perfadex®; Celsior® p=0.019; saline p=0.016). The pulmonary artery pressure values were similar between the three solutions in two stages of ischemia and comparing the times of 6 and 12 hours, regardless of the solution. The Relative Oxygenation Capacity showed no significant difference between the three solutions tested, regardless of the ischemic time. The comparison between the two ischemic times showed that oxygenation capacity was significantly worse in lungs preserved with saline for 12 hours (p=0.001). The wet-to-dry weight ratio showed no statistically significant difference between the three solutions in both ischemic times. However, when ischemic times were compared, Perfadex® showed greater wet-to-dry weight ratio in lungs submitted to 12 hours of ischemia (p=0.001). Light microscopy showed that lungs preserved with saline had more edema than the others, regardless of the ischemic time. Assessment of apoptosis by the TUNEL assay showed no statistically significant difference in the comparison between the groups. CONCLUSIONS: The lungs preserved with Celsior® and Perfadex® performed evenly in regards to gas exchange, hemodynamics and ventilatory mechanics. The lungs preserved with Perfadex® for 12 hours were more edematous. Histopathology findings did not differ between the groups

McCormick, Patrick N. "Ex vivo Binding of the Agonist PET Radiotracer [11C]-(+)-PHNO to Dopamine D2/D3 Receptors in Rat Brain: Lack of Correspondence to the D2 Recepor Two-affinity-state Model." Thesis, 2010. http://hdl.handle.net/1807/26296.

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The dopamine D2 receptor exists in vitro in two states of agonist affinity: a high-affinity state mediating dopamine’s physiological effects, and a physiologically-inert low-affinity state. Our primary goal was to determine the in vivo relevance of this two-affinity-state model for the agonist PET radiotracer [11C]-(+)-PHNO, developed for measurement of the D2 high-affinity state. Our second goal was to characterize the regional D2 versus D3 pharmacology of [3H]-(+)-PHNO binding and assess its utility for measuring drug occupancy at both receptor subtypes. Using ex vivo dual-radiotracer experiments in conscious rats, we showed that, contrary to the two-affinity-state model, the binding of [11C]-(+)-PHNO and the antagonist [3H]-raclopride were indistinguishably inhibited by D2 partial agonist (aripiprazole), indirect agonist (amphetamine) and full agonist ((-)-NPA) pretreatment. Furthermore, ex vivo [11C]-(+)-PHNO binding was unaffected by treatments that increase in vitro high-affinity state density (chronic amphetamine, ethanol-withdrawal), whereas unilateral 6-OHDA lesion, which increases total D2 receptor expression, similarly increased the ex vivo binding of [11C]-(+)-PHNO and [3H]-raclopride. These results do not support the in vivo validity of the two-affinity-state model, suggesting instead a single receptor state for [11C]-(+)-PHNO and [3H]-raclopride in conscious rat. Importantly, we also demonstrated that the increased amphetamine-sensitivity of the agonist radiotracers [11C]-(+)-PHNO and [11C]-(-)-NPA, commonly seen in isoflurane-anaesthetized animals and cited as evidence for the two-affinity-state model, is due to the confounding effects of anaesthesia. Using in vitro and ex vivo autoradiography in rat and the D3 receptor-selective drug SB277011, we found that [3H]-(+)-PHNO binding in striatum and cerebellum lobes 9 and 10 was due exclusively to D2 and D3 receptor binding, respectively, but in other extra-striatal regions to a mix of the two receptor subtypes. Surprisingly, the D3 contribution to [3H]-(+)-PHNO binding was greater ex vivo than in vitro. Also surprising, several antipsychotic drugs, at doses producing 80% D2 occupancy, produced insignificant (olanzapine, risperidone, haloperidol) or small (clozapine, ~35%) D3 occupancy, despite similarly occupying both receptor subtypes in vitro. These data reveal a significant discrepancy between in vitro and ex vivo measures of dopamine receptor binding and suggest that the D3 occupancy is not necessary for the therapeutic effect of antispychotic drugs.

Частини книг з теми "Ex-vivo rat model":

Rigo, Federica, Victor Navarro-Tableros, Nicola De Stefano, Alberto Calleri, and Renato Romagnoli. "Ex Vivo Normothermic Hypoxic Rat Liver Perfusion Model: An Experimental Setting for Organ Recondition and Pharmacological Intervention." In Methods in Molecular Biology, 139–50. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1225-5_10.

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Suzuki, Masatoshi, and Clive N. Svendsen. "Ex Vivo Gene Therapy Using Human Mesenchymal Stem Cells to Deliver Growth Factors in the Skeletal Muscle of a Familial ALS Rat Model." In Gene Therapy for Neurological Disorders, 325–36. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3271-9_24.

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Watanabe, Makino, and Takao Okada. "Langendorff Perfusion Method as an Ex Vivo Model to Evaluate Heart Function in Rats." In Methods in Molecular Biology, 107–16. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8597-5_8.

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Sakariassen, Kjell S., Helge E. Roald, and José Aznar Salatti. "Ex Vivo Models for Studying Thrombosis: Special Emphasis on Shear Rate Dependent Blood-Collagen Interactions." In Advances in Cardiovascular Engineering, 151–74. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4757-4421-7_10.

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Litt, L., and M. T. Espanol. "Ex Vivo MuEtinuciear NMR Spectroscopy of Perfused, Respiring Rat Brain Slices: Model Studies of Hypoxia, Ischemia, and Excitotoxscit." In Biological NMR Spectroscopy. Oxford University Press, 1997. http://dx.doi.org/10.1093/oso/9780195094688.003.0031.

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We believe there are important roles for in vivo NMR spectroscopy techniques in studies of protection and treatment in stroke. Perhaps the primary utility of in vivo NMR spectroscopy is to establish the relevance of metabolic integrity, intracellular pH, and intracellular energy stores to concurrent changes occurring both at gross physiological levels (e.g., changes in cerebral blood flow, or blood oxygenation), and at microscopic or cellular levels. It has long been known that the brain is exquisitely sensitive to deprivations of oxygen, glucose, and cerebral blood flow. Routine human surgery on a limb takes place every day with tourniquets stopping all blood flow for up to two hours. In contrast, the deprivation of all blood flow to the brain (global ischemia) for approximately 5 minutes can result in severe, permanent brain damage. Research has gone on for more than 30 years to understand why the brain’s revival time is so much shorter, and to discover brain biochemical interventions that might dramatically extend the brain’s intolerance beyond 5 minutes, and therefore be relevant to protection and treatment of stroke. (Kogure and Hossmann, 1985; 1993) Stroke, defined as a permanent neurologic deficit arising from the death of brain cells, kills ∼ 150,000 people in the U.S.A. each year, and is the third leading cause of death (Feinleib et al., 1993). It is the next malady to escape, once one has dodged death from cardiovascular disease and cancer. Many, if not most, U.S.A. stroke victims will receive neurological clinical care not substantially different from what was provided 30 years ago. Most stroke patients will be put in intensive care units where blood pressure will be regulated and kept in a “safe” range, with the body given supportive care and the brain given an opportunity to heal itself. The problem of stroke is actually quite complex because there are several different kinds of stroke (ischemic, hemorrhagic, etc.), and because numerous systemic physiological factors are of relevance. Nevertheless, exciting advances in brain biochemistry suggest that stroke therapy and prophylaxis axe likely to improve dramatically in the near future (Zivin and Choi, 1991).

Тези доповідей конференцій з теми "Ex-vivo rat model":

Seehase, Sophie, Sarah-Philine Köhncke, Heinz-Gerd Hoymann, Armin Braun, and Katherina Sewald. "Effect Of Tiotropium On In Vivo And Ex Vivo Lung Function In A Rat Model Of Bronchoconstriction." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3586.

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Chamone, D. A. F., M. Ivany-Silva, C. Cassaro, G. Bellotti, C. Massumoto, and A. Y. Hoshikawa-Fujimura. "GUARANA (Paullinia cupana) INHIBITS AGGREGATION IN WHOLE BLOOD." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644553.

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Guarana, a methylxanthine obtained from the seeds of Paullinia cupana has been largely used in the Amazon region by native indians during centuries as stimulant. We evaluated the effect of guarana on ex-vivo and in vitro platelet aggregation induced by adenosine-5-diphosphate (ADP) in human and rat whole blood with an impedance (Chrono-Log, model 500) and in their platelet rich plasma (PRP) with an optical aggregometer (Chrono-Log, model 440). Ex-vivo studies were carried out after single oral intake of guarana. Seven healthy volunteers (5 male and 2 female) aged 19-26 years who had taken no drugs for 10 days before, ingested 8gm of crude powder of guarana. Blood samples were drawn before and 1 hour after guarana intake. We observed a significative inhibition of platelet aggregation in whole blood meanwhile PRP was un changed as compared to basal values. In vitro studies were performed in whole blood and PRP from human volunteers and male Wis-tar rats. The combined effect of guarana and adenosine was also studied. A control aggregation was always run with saline. The results demonstrated an inhibition statistically significative (p < 0.001) of platelet aggregation in whole blood. Differently from whole blood the PRP with the same concentration of guarana did not result in inhibition of ADP induced aggregation when eva luated with the impedance method. The blood incubation with adenosine and guarana resulted in synergistic inhibitory effect that was much more strinking in whole blood than in PRP. Guarana fails to inhibit aggregation of rat platelets.Our results demonstrate that guarana prevents platelet aggregation in whole blood which depends on red blood cells, probably involving adenosine.

Kumar, A., J. Fareed, W. H. Wehrmacher, D. Hoppensteadt, O. Ulutin, and J. M. Walenga. "ENDOTHELIAL FUNCTION MODULATION AND CONTROL OF VASCULAR AND THROMBOTIC DISORDERS: EXPERIMENTAL RESULTS WITH A POLYDEOXY RIBONUCLEOTIDE AGENT DEFIBROTIDE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643149.

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Numerous approaches with single and multiple drugs modulating protease cascade, platelet function and blood viscosity and to reduce blood lipids to manage thrombotic processes have been tried. Defibrotide, a polydeoxyribonucleotide, (Mr =17,000) offers a new approach to vascular and related thrombotic processes as it acts via modulation of endothelial cell function. We have used a primate model (Macaca mulatta) to study the endogenous action of this agent after the oral (10-25 mg/kg) and intravenous (5-10 mg/kg) administration. This agent produced no effect on clotting tests and ex vivo laboratory findings but rather it elevated the t-PA (antigen and functional), protein C (antigen and functional), prostacyclin and decreased thromboxane, 01.2-antiplasmin (functional) and t-PA inhibitor (functional) in both studies. These observations suggest that Defibrotide modulates endothelial function. Hepatic isolation in rabbits totally blocked the antithrombotic actions of Defibrotide suggesting that this agent is converted into an active product endogenously. Pretreatment of Defibrotide with nucleases also resulted in a complete loss of its actions. Defibrotide produced dose dependent antithrombotic actions in animal models (rabbit venous stasis and rat vena caval ligation) after either intravenous or oral administration. Blood pressure, heart rate, respiration and kidney function were not altered by it. No effect on bleeding time was noted in any studies. Upon oral administration this drug produced pharmacologic action after 2 hours whereas after intravenous administration, the action peaked at 30 minutes. Defibrotide exhibited cytoprotective effects towards endothelial lining of the vascular smooth muscles characterized by microscopic studies. In summary Defibrotide is an endothelial support agent whose multicomponent actions are primarily mediated via the physical and functional modulation of the endothelial cells in the vascular system.

Mizoguchi, S., T. Tsuchiya, M. Ishii, R. Doi, H. Watanabe, G. Hatachi, T. Miyazaki, K. Matsumoto, and T. Nagayasu. "Use of Bioengineered Rat Lungs for Novel Ex Vivo Human Lung Cancer Models." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a5676.

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Landry, Thomas G., and Jeremy A. Brown. "B-mode and Doppler imaging of in vivo rat brain and ex vivo human brain with a high frequency endoscopic phased array." In 2019 IEEE International Ultrasonics Symposium (IUS). IEEE, 2019. http://dx.doi.org/10.1109/ultsym.2019.8925902.

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Singh, Sundeep, and Roderick Melnik. "Computational Model of Radiofrequency Ablation of Cardiac Tissues Incorporating Thermo-Electro-Mechanical Interactions." In ASME 2020 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2020. http://dx.doi.org/10.1115/imece2020-23367.

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Abstract The application of radiofrequency ablation (RFA) has been widely explored in treating various types of cardiac arrhythmias. Computational modelling provides a safe and viable alternative to ex vivo and in vivo experimental studies for quantifying the effects of different variables efficiently and reliably, apart from providing a priori estimates of the ablation volume attained during cardiac ablation procedures. In this contribution, we report a fully coupled thermo-electro-mechanical model for a more accurate prediction of the treatment outcomes during the radiofrequency cardiac ablation. A numerical model comprising of cardiac tissue and the cardiac chamber has been developed in which an electrode has been inserted perpendicular to the cardiac tissue to simulate actual clinical procedures. Temperature-dependent heat capacity, electrical and thermal conductivities, and blood perfusion rate have been considered to model more realistic scenarios. The effects of blood flow and contact force of the electrode tip on the efficacy of a fully coupled model of RFA have been systematically investigated. The numerical study predicts that the efficacy of RFA is significantly dependent on the thermo-electro-mechanical parameters of the cardiac tissue.

Bommer, Kathleen M., Angela DiBenedetto, and Jens O. M. Karlsson. "High-Speed Imaging of Intra-Embryonic Phase Transformation Events During Rapid Freezing of Zebrafish Embryos." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53953.

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The zebrafish (Danio rerio) represents an increasingly popular vertebrate animal model valuable for genetic and developmental biology research, due to its rapid rate of reproduction and the ability to directly observe the growing embryos, which are optically clear and develop ex vivo. However, the need to maintain live stock of each genetic strain (the number of which is growing exponentially) is risky and prohibitively costly. Although long-term banking of frozen embryos would solve this problem, to date, no adequate method for cryopreservation of zebrafish embryos has been found (Hagedorn et al., 2004).

Kimmel, Jeremy D., Morgan V. DiLeo, Isabella E. Valenti, Gregory A. Gibson, Simon C. Watkins, and William J. Federspiel. "Dynamics of Cytokine Capture Within Hemoadsorption Beads Used to Treat Sepsis." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-204764.

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Sepsis is a serious medical condition characterized by systemic inflammation caused by infection, and affects more than 750,000 individuals per year in the US, with a mortality rate of approximately 30% [1]. The pathophysiology of sepsis is complex and not entirely understood, but is believed to be related to the dysfunction of multiple interdependent humoral mediator pathways, including redundant release of inflammatory cytokines [2]. Removal of both pro- and anti-inflammatory cytokines from the circulating blood is believed to be a promising therapy for severe sepsis [3]. We are developing an extracorporeal hemoadsorption device to remove cytokines from the blood using a novel, biocompatible, sorbent bead technology. A simple model was developed to characterize cytokine adsorption within hemoadsorption beads [4]. Despite rapid clearance of cytokines with hemoadsorption in an ex vivo murine sepsis model [5], our model analysis predicted that only the outer 20μm of each sorbent bead (avg diam = 450μm) adsorbed cytokine. In this work, we used in vitro column capture experiments and confocal laser scanning microscopy (CLSM) to examine cytokine adsorption dynamics within hemoadsorption beads.

Banerjee, Nilam Sanjib, Dianne W. Moore, Abhisek Gangrade, Donald J. Buchsbaum, Luise Burt Nabors, Thomas R. Broker, and Louise T. Chow. "Abstract LB250: Development of organoid raft cultures of cervical, breast and glioblastoma tumors as quick economical ex vivo human cancer models for pre-clinical drug evaluation." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-lb250.

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Borowska, A., D. Lauri, A. Maggi, E. Dejana, G. de Gaetano, and J. Pangrazzi. "IMPAIREMENT OF PRIMARY HAEMOSTASIS BY LMW-HEPARINS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643172.

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Low molecular weight (LMW) heparlns have been developed with the aim of reducing anticoagulant activity thereby minimizing the bleeding complications of conventional heparin. Unexpectedly, bleeding events were reported during treatment with some LMW-heparins, in clinical and experimental studies. We studied the effect of four different LMW-heparlns on primary haemostasis In male rats (CD COBS, Charles River) after l.v. administration of 0.75 mg/kg b.w. of the drugs. LMW heparin A was devoid of any activity on an experimental model of “template” bleeding time in rats (110.6±5.9 sec versus 108.7±4.1 control values) whereas LMW-heparins B, C and D prolonged the bleeding time to a different extent (228.7±19.9, 161.5±6.4 and 161.7±8.6 respectively). Pretreatment of animals with aspirin (100 mg/kg b.w. per o.s). resulted In a significant potentiation of the “template” bleeding time. In vitro platelet aggregation Induced by collagen (20 μg/ml) or by collagen in combination with ADP (5-10 μM) was strongly inhibited by LMW-heparln B, while LMW-heparln A showed no effect. LMW-heparins C and D exerted an Intermediate level of Inhibition of platelet aggregation. The same pattern of aggregating response was found when LMW-heparins A and B were given i.v. to rats (0.75 mg/kg b.w.) and platelet aggregation was studied “ex vivo” 15 min after drug administration.These data may help explain the impairment of primary haemostasis associated with some LMW-heparin preparations.