Bibliographies thématiques / Modello ischemia in vitro

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Littérature scientifique sur le sujet « Modello ischemia in vitro »

Auteur : Grafiati
Publié le 9 mars 2023
Mis à jour le 31 juillet 2025

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Articles de revues sur le sujet "Modello ischemia in vitro"

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Visocchi, M., M. Meglio, D. Cabezas Cuevas, et al. "Sensibilità e specificità della RM in un nuovo modello di ictus ischemico acuto sperimentale «collaterale»." Rivista di Neuroradiologia 9, no. 1 (1996): 21–23. http://dx.doi.org/10.1177/197140099600900102.

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Al fine di valutare la precocità e la sensibilità diagnostica della RM, unitamente alla eventuale ripetibilità degli eventi, abbiamo voluto sperimentare un nuovo modello di ischemia, che abbiamo definito «collaterale», poichè secondaria ad occlusione di due o più vasi pre - Willisiani. Per l'analogia con il circolo cerebrale umano sono stati studiati 12 conigli albini New Zealand (4–5 Kg) che venivano sottoposti ad anestesia generale. Per tutta la durata dell'esperimento si procedeva al monito-raggio della pressione arteriosa sistemica media, della frequenza cardiaca del pH e dell'emogas. L'is
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Pelliccioli, G. P., P. F. Ottaviano, C. Gambelunghe, et al. "Ischemia cerebrale sperimentale nei gerbillo." Rivista di Neuroradiologia 6, no. 3 (1993): 325–30. http://dx.doi.org/10.1177/197140099300600313.

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Il gerbillo (Meriones unguiculatus), avendo il circolo di Willis incompleto per la mancanza delle arterie comunicanti, è considerato il modello animale di elezione per lo studio dell'ischemia cerebrale. L'assenza di connessioni tra circolo carotideo e vertebro-basilare garantisce infatti l'induzione di un'ischemia cerebrale mediante occlusione delle arterie carotidi comuni (ACC). È stata osservata tuttavia una certa variabilità nel sistema vascolare cerebrale del gerbillo, che spiegherebbe la differente risposta individuale alla legatura delle ACC. In letteratura sono stati descritti i deficit
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Tanaka, E., S. Yasumoto, G. Hattori, S. Niiyama, S. Matsuyama, and H. Higashi. "Mechanisms Underlying the Depression of Evoked Fast EPSCs Following In Vitro Ischemia in Rat Hippocampal CA1 Neurons." Journal of Neurophysiology 86, no. 3 (2001): 1095–103. http://dx.doi.org/10.1152/jn.2001.86.3.1095.

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The mechanisms underlying the depression of evoked fast excitatory postsynaptic currents (EPSCs) following superfusion with medium deprived of oxygen and glucose (in vitro ischemia) for a 4-min period in hippocampal CA1 neurons were investigated in rat brain slices. The amplitude of evoked fast EPSCs decreased by 85 ± 7% of the control 4 min after the onset of in vitro ischemia. In contrast, the exogenous glutamate-induced inward currents were augmented, while the spontaneous miniature EPSCs obtained in the presence of tetrodotoxin (TTX, 1 μM) did not change in amplitude during in vitro ischem
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Chen, Timothy, and Gordana Vunjak-Novakovic. "In Vitro Models of Ischemia-Reperfusion Injury." Regenerative Engineering and Translational Medicine 4, no. 3 (2018): 142–53. http://dx.doi.org/10.1007/s40883-018-0056-0.

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Ke, Yong-Sheng, He-Gui Wang, De-Guo Wang, and Gen-Bao Zhang. "Endoxin-mediated myocardial ischemia reperfusion injury in rats in vitro." Canadian Journal of Physiology and Pharmacology 82, no. 6 (2004): 402–8. http://dx.doi.org/10.1139/y04-041.

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Myocardial ischemia reperfusion results in an increase in intracellular sodium concentration, which secondarily increases intracellular calcium via Na+-Ca2+ exchange, resulting in cellular injury. Endoxin is an endogenous medium of digitalis receptor and can remarkably inhibit Na+/K+-ATPase activity. Although the level of plasma endoxin is significantly higher during myocardial ischemia, its practical significance is unclear. This research is to investigate whether endoxin is one of important factors involved in myocardial ischemia reperfusion injury. Ischemia reperfusion injury was induced by
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Dugan, Laura L., and Jeong-Sook Kim-Han. "Astrocyte Mitochondria in In Vitro Models of Ischemia." Journal of Bioenergetics and Biomembranes 36, no. 4 (2004): 317–21. http://dx.doi.org/10.1023/b:jobb.0000041761.61554.44.

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Lee, Won Hee, Sungkwon Kang, Pavlos P. Vlachos, and Yong Woo Lee. "A novel in vitro ischemia/reperfusion injury model." Archives of Pharmacal Research 32, no. 3 (2009): 421–29. http://dx.doi.org/10.1007/s12272-009-1316-9.

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Ye, Zhouheng, Bradley P. Ander, Frank R. Sharp та Xinhua Zhan. "Cleaved β-Actin May Contribute to DNA Fragmentation Following Very Brief Focal Cerebral Ischemia". Journal of Neuropathology & Experimental Neurology 77, № 3 (2018): 260–65. http://dx.doi.org/10.1093/jnen/nly003.

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Abstract Our previous study demonstrated caspase independent DNA fragmentation after very brief cerebral ischemia, the mechanism of which was unclear. In this study, we explore whether actin is cleaved following focal cerebral ischemia, and whether these structural changes of actin might modulate DNA fragmentation observed following focal ischemia. Results showed that a cleaved β-actin fragment was identified in brains of rats 24 hours following 10-minute and 2-hour focal ischemia. Though granzyme B and caspase-3 cleaved β-actin in vitro, the fragment size of β-actin cleaved by granzyme B was
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Hoebart, Clara, Attila Kiss, Bruno K. Podesser, Ammar Tahir, Michael J. M. Fischer, and Stefan Heber. "Sensory Neurons Release Cardioprotective Factors in an In Vitro Ischemia Model." Biomedicines 12, no. 8 (2024): 1856. http://dx.doi.org/10.3390/biomedicines12081856.

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Sensory neurons densely innervate the myocardium. The role of their sensing and response to acute and prolonged ischemia is largely unclear. In a cellular model of ischemia-reperfusion injury, the presence of sensory neurons increases cardiomyocyte survival. Here, after the exclusion of classical neurotransmitter release, and measurement of cytokine release, we modified the experiment from a direct co-culture of primary murine cardiomyocytes and sensory neurons to a transfer of the supernatant. Sensory neurons were exposed to ischemia and the resulting conditioned supernatant was transferred o
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Prehn, Jochen H. M., Chourouk Karkoutly, Jörg Nuglisch, Barbara Peruche, and Josef Krieglstein. "Dihydrolipoate Reduces Neuronal Injury after Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 12, no. 1 (1992): 78–87. http://dx.doi.org/10.1038/jcbfm.1992.10.

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It has been shown in vitro that dihydrolipoate (dl-6,8-dithioloctanoic acid) has antioxidant activity against microsomal lipid peroxidation. We tested dihydrolipoate for its neuroprotective activity using models of hypoxic and excitotoxic neuronal damage in vitro and rodent models of cerebral ischemia in vivo. In vitro, neuronal damage was induced in primary neuronal cultures derived form 7-day-old chick embryo telencephalon by adding either 1 m M cyanide or 1 m M glutamate to the cultures. Cyanide-exposed and dihydrolipoate-treated (10−9–10−7 M) cultures showed an increased protein and ATP co
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Thèses sur le sujet "Modello ischemia in vitro"

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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.

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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 tis
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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 o
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Tsang, Hing-wai, and 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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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 contract
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Poignet, Hervé. "Activites pharmacologiques des antagonistes du calcium sur differents modeles physiopathologiques utilises dans l'ischemie cerebrale experimentale : effets sur les atteintes fonctionnelles et neuronales." Clermont-Ferrand 2, 1988. http://www.theses.fr/1988CLF21111.

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Pocar, M. "Perfusione spinale retrograda selettiva durante ischemia da clampaggio aortico: modello sperimentale nel suino." Doctoral thesis, Università degli Studi di Milano, 2000. http://hdl.handle.net/2434/195626.

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BACKGROUND. Spinal cord damage represents a devastating complication of thoracic and thoracoabdominal aortic surgery. Retrograde perfusion as an alternative route to protect the spinal cord has recently been investigated with controversial results. MEHODS. Ten juvenile pigs were divided into control and study groups (A and B, respectively). Through a lateral thoracotomy the distal aortic arch was cannulated and connected to a cardiotomy reservoir. All animals underwent 40-minute single cross-clamping of the proximal descending aorta while keeping proximal systolic arterial pressure above 100 m
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SAKAMOTO, NOBUO, TATSUAKI MATSUBARA, YOSHIHIRO KAKINUMA, and 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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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.

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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
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ZAMBAITI, ELISA. "Organoidi gastrointestinali pediatrici e fetali: modello di cultura tridimensionale in vitro." Doctoral thesis, Università degli studi di Padova, 2022. http://hdl.handle.net/11577/3447317.

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Obiettivi Il COVID-19 è una malattia principalmente respiratoria nell’età adulta; nei bambini, al contrario, i sintomi gastrointestinali sono più frequenti. Inoltre, non si conoscono i meccanismi di infezione in epoca fetale, epoca in cui i pazienti sono raramente colpiti da COVID-19. Gli organoidi sono uno strumento relativamente nuovo per stabilire in vitro colture di lunga durata che assomigliano tridimensionalmente al tessuto di origine e possono sia mantenere la staminalità che differenziarsi completamente in tutti i tipi di cellule. Abbiamo quindi mirato a sviluppare un sistema di coltur
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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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Livres sur le sujet "Modello ischemia in vitro"

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Frantseva, Marina. Mechanisms of free radical formation and toxicity in an in vitro model of ischemia. 1999.

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Drug Distribution in the Body: In Vitro Prediction and Physiological Interpretation/the Cat As an in Vivo Model for Myocardial Ischemia and Infarction ... in Pharmacology and Clinical Pharmacology). Vch Pub, 1989.

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Chapitres de livres sur le sujet "Modello ischemia in vitro"

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Betz, E. L. "Inhibition of Atherogenesis In Vivo and In Vitro." In Cerebral Ischemia and Dementia. Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76208-6_10.

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Waxham, M. N., S. A. Westgate, and M. D. Mauk. "In Vitro Ischemia in the Hippocampal Slice." In Cerebral Ischemia and Basic Mechanisms. Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78151-3_23.

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Fujiwara, Naoshi, Takashi Abe, Yoshiko Ebine, and Koki Shimoji. "Changes in Intracellular Ca2+ and pH of Hippocampal Slices in Response to Ischemia In Vitro." In Molecular Biology and Brain Ischemia. Springer Japan, 1996. http://dx.doi.org/10.1007/978-4-431-68467-1_8.

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Paakkari, I., R. Nevala, A. Peitola, and H. Vapaatalo. "Effect of Nitric Oxide Donors on Rat Bronchial Muscle in Vitro." In Mediators in the Cardiovascular System: Regional Ischemia. Birkhäuser Basel, 1995. http://dx.doi.org/10.1007/978-3-0348-7346-8_30.

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Plesnila, N., E. Ringel, F. Staub, E. Stohr, C. C. Chang, and A. Baethmann. "In-Vitro Elucidation of Mechanisms Underlying Cell Swelling and Death of Nerve and Glial Cells." In Maturation Phenomenon in Cerebral Ischemia V. Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18713-1_16.

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Ryou, Myoung-gwi, and Robert T. Mallet. "An In Vitro Oxygen–Glucose Deprivation Model for Studying Ischemia–Reperfusion Injury of Neuronal Cells." In Methods in Molecular Biology. Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7526-6_18.

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Burke, Stephan P., and Charles P. Taylor. "Glutamale, Aspartate and Gaba Release from Hippocampal CA1 Slices During In Vitro Ischemia is Calcium-Independent." In The Role of Neurotransmitters in Brain Injury. Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3452-5_8.

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Urban, L., K. H. Neill, B. J. Crain, J. V. Nadler, and G. G. Somjen. "Effects of Transient Forebrain Ischemia in Area CA1 of the Gerbil Hippocampus: An in Vitro Study." In Excitatory Amino Acids and Neuronal Plasticity. Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5769-8_54.

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Produit-Zengaffinen, Nathalie, Tatiana Favez, Constantin J. Pournaras, and Daniel F. Schorderet. "JNK Inhibition Reduced Retinal Ganglion Cell Death after Ischemia/Reperfusion In Vivo and after Hypoxia In Vitro." In Retinal Degenerative Diseases. Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17121-0_90.

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Ashok, Deepthi, Haley Garbus, and Obialunanma V. Ebenebe. "Mitochondrial Membrane Potential and Lactate Dehydrogenase Activity in a Model of Acute In Vitro Ischemia/Reperfusion Injury." In Methods in Molecular Biology. Springer US, 2024. https://doi.org/10.1007/978-1-0716-4342-6_4.

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Actes de conférences sur le sujet "Modello ischemia in vitro"

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Burmistrov, D. E., M. I. Krivonosov, T. A. Mishchenko, M. V. Ivanchenko, M. V. Vedunova, and E. V. Mitroshina. "Network features of consolidated astrocytic response in modeled ischemia-like conditions in vitro." In 2020 4th Scientific School on Dynamics of Complex Networks and their Application in Intellectual Robotics (DCNAIR). IEEE, 2020. http://dx.doi.org/10.1109/dcnair50402.2020.9216830.

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Korkmaz-Icöz, S., M. Schwär, S. Loganathan, et al. "Nutritional Extracts Protect Rats’ Vascular Grafts from In Vitro Ischemia/Reperfusion Injury." In 51st Annual Meeting of the German Society for Thoracic and Cardiovascular Surgery (DGTHG). Georg Thieme Verlag KG, 2022. http://dx.doi.org/10.1055/s-0042-1742851.

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Ding, Q., S. Loganathan, P. Brlecic, et al. "ALPHA-1-Antitrypsin Protects Vascular Grafts of Brain-Dead Rats against In Vitro Ischemia/Reperfusion Injury." In 50th Annual Meeting of the German Society for Thoracic and Cardiovascular Surgery (DGTHG). Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1725680.

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Rovito, Nick, and Debanjan Mukherjee. "In Silico Analysis of Flow-Mediated Drug Transport for Thrombolytic Therapy in Acute Ischemic Stroke." In ASME 2024 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2024. https://doi.org/10.1115/imece2024-143625.

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Abstract Acute Ischemic Stroke (AIS) is a life threatening condition that occurs when an artery within the brain is blocked by a pathological blood clot, called a thrombus. The most popular treatment approach for AIS relies on intravenous administration of a drug named tissue plasminogen activator (tPA) to dissolve fibrin fibers within the clot. Despite the widespread use of tPA, treatment outcomes are often unsuccessful. This is commonly attributed to local clot-flow interactions and their effect on drug delivery into a thrombus. Yet, detailed characterization of flow-mediated drug transport
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Soethoff, J., S. Korkmaz-Icöz, G. Szabó, and G. Veres. "Comparison of Two Graft Storage Solutions (DuraGraft and TiProtec) in an In Vitro Model of Ischemia-Reperfusion Using Arterial Grafts." In 49th Annual Meeting of the German Society for Thoracic and Cardiovascular Surgery. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1705432.

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Xiao, Min, Annie Bailey, and Olga Pierrakos. "In-Vitro Modeling of Heart Failure in the Presence of a Prosthetic Heart Valve Using Particle Image Velocimetry." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53788.

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It is well-known that cardiovascular disease, affecting millions of people, is the number one killer in the US and worldwide. Current trends indicate that cardiovascular disease (CVD) will claim approximately 20 million victims in 2020 as the leading cause of death worldwide and will be responsible for over a billion deaths between 2000 and 2050 [1]. According to the American Heart Association, one in three American adults have one or more types of heart disease. Economically, the total and indirect costs due to cardiovascular diseases in 2009 were estimated at $475.3 billion. The spectrum of
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Korkmaz-Icöz, S., C. Kocer, A. A. Sayour, et al. "The Sodium-Glucose Cotransporter-2 Inhibitor Canagliflozin Alleviates Endothelial Dysfunction of Vascular Grafts Submitted to In-Vitro Ischemia/Reperfusion Injury in Nondiabetic Rats." In 50th Annual Meeting of the German Society for Thoracic and Cardiovascular Surgery (DGTHG). Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1725601.

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Wallentin, Lars, Ingyar Nyman, ULF Berglund, and Eva Swahn. "HEPARIN AND ACETYLSALICYLIC ACID (ASA) 75 MG/DAY IN UNSTABLE CORONARY ARTERY DISEASE - EFFECTS ON PLATELET REACTIVITY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643009.

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In unstable coronary artery disease (UCAD), i.e. unstable angina pectoris (UAP) or non-Q-myocardial infarction (NMI), treatment with heparin or ASA have given encouraging results. The present study attempts to verify the effects of i.v. heparin (5 days) and to evaluate the utility of ASA 75 mg/day (one year). Patients, admitted because of chest pain, who either develops NMI or signs of ischemia in resting or exercise ECG.s are included. Within 72 hours patients are randomized to obtain Heparin+ASA, Heparin+Placebo, Placebo + ASA or Placebo+Placebo . Platelet reactivity is studied in vitro in p
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Alessandri, C., F. Violi, M. Rasura, C. Caliendo, and P. Pelaia. "BEHAVIOUR OF ADREN0CHR0ME PATHWAY IN PATIENTS WITH CEREBROVASCULAR DISEASES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643169.

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Histopathological studies in segments of cerebral ischaemia show local inflammation with leucocytes infiltration.This event has been confirmed in vivo by means of radiolabelled leucocytes. This inflammatory response could be of detriment to cerebral tissue since leucocytes release toxic substances such as oxygen free radicals.A free radical mechanism,in fact,has been supposed as an event worsening the evolution of ischemia.Evidence of neutrophil activation in stroke patients was shown by us in previous reports, where we have described that the plasma of these patients contained an excess of a
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Fayssal, Iyad, and Fadl Moukalled. "A Numerical Analysis of the Hemodynamic Functionality of Human Coronary Stenosis Under Different Physiologic Conditions and Boundary Condition Formulations." In ASME-JSME-KSME 2019 8th Joint Fluids Engineering Conference. American Society of Mechanical Engineers, 2019. http://dx.doi.org/10.1115/ajkfluids2019-4820.

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Abstract Coronary artery disease (CAD) is among the foremost causes for human death worldwide. This study aims at investigating the performance of different boundary condition model types to characterize CAD functional significance. In addition, alternate models to estimate FFR using any different combination of boundary conditions at inlet and outlet were analyzed. In the first type of boundary condition, an outflow resistance model is used combined with a fixed pressure at inlet. In the second model of boundary conditions, constant pressure values are imposed at the domain inlet and outlet/s
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