Relevant bibliographies by topics / In vitro ischemia model

Academic literature on the topic 'In vitro ischemia model'

Author: Grafiati
Published: 9 March 2023
Last updated: 10 March 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Contents

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'In vitro ischemia model.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "In vitro ischemia model"

1

Park, Kwon Moo, Ang Chen, and Joseph V. Bonventre. "Prevention of Kidney Ischemia/Reperfusion-induced Functional Injury and JNK, p38, and MAPK Kinase Activation by Remote Ischemic Pretreatment." Journal of Biological Chemistry 276, no. 15 (January 9, 2001): 11870–76. http://dx.doi.org/10.1074/jbc.m007518200.

Full text
Abstract:
MAPK activities, including JNK, p38, and ERK, are markedly enhanced after ischemiain vivoand chemical anoxiain vitro. The relative extent of JNK, p38, or ERK activation has been proposed to determine cell fate after injury. A mouse model was established in which prior exposure to ischemia protected against a second ischemic insult imposed 8 or 15 days later. In contrast to what was observed after 30 min of bilateral ischemia, when a second period of ischemia of 30- or 35-min duration was imposed 8 days later, there was no subsequent increase in plasma creatinine, decrease in glomerular filtration rate, or increase in fractional excretion of sodium. A shorter period of prior ischemia (15 min) was partially protective against subsequent ischemic injury 8 days later. Unilateral ischemia was also protective against a subsequent ischemic insult to the same kidney, revealing that systemic uremia is not necessary for protection. The ischemia-related activation of JNK and p38 and outer medullary vascular congestion were markedly mitigated by prior exposure to ischemia, whereas preconditioning had no effect on post-ischemic activation of ERK1/2. The phosphorylation of MKK7, MKK4, and MKK3/6, upstream activators of JNK and p38, was markedly reduced by ischemic preconditioning, whereas the post-ischemic phosphorylation of MEK1/2, the upstream activator of ERK1/2, was unaffected by preconditioning. Pre- and post-ischemic HSP-25 levels were much higher in the preconditioned kidney. In summary, post-ischemic JNK and p38 (but not ERK1/2) activation was markedly reduced in a model of kidney ischemic preconditioning that was established in the mouse. The reduction in JNK and p38 activation can be accounted for by reduced activation of upstream MAPK kinases. The post-ischemic activation patterns of MAPKs may explain the remarkable protection against ischemic injury observed in this model.
APA, Harvard, Vancouver, ISO, and other styles
2

Picard, Sandra, Rene Rouet, Frederic Flais, Pierre Ducouret, Gerard Babatasi, Andre Khayat, Jean-Claude Potier, Henri Bricard, and Jean-Louis Gerard. "Proarrhythmic and Antiarrhythmic Effects of Bupivacaine in an In Vitro Model of Myocardial Ischemia and Reperfusion." Anesthesiology 88, no. 5 (May 1, 1998): 1318–29. http://dx.doi.org/10.1097/00000542-199805000-00024.

Full text
Abstract:
Background Bupivacaine may have toxic cardiovascular effects when accidentally administered by intravascular injection. However, its electrophysiologic effects in the presence of myocardial ischemia remain unknown. The authors evaluated the electrophysiologic and anti- and proarrhythmic effects of bupivacaine in an in vitro model of the ischemic and reperfused myocardium. Methods In a double-chamber bath, a guinea pig right ventricular muscle strip was subjected partly to normal conditions and partly to simulated ischemia followed by reperfusion. The electrophysiologic effects of bupivacaine were studied at 1, 5, and 10 microM concentrations. Results Bupivacaine (5 and 10 microM) decreased the maximal upstroke velocity of the action potential (Vmax) in normoxic conditions and further decreased (10 microM) the Vmax decrease induced by ischemic conditions. Bupivacaine reduced the mean occurrence time to the onset of myocardial conduction blocks (9 +/- 3 min; mean +/- SD; P < 0.005 with 5 and 10 microM, compared with 17 +/- 6 min during simulated ischemia with no drug or control), and it increased the number of preparations that became inexcitable to pacing (55% of preparations, with 1 microM and 100% with 5 and 10 microM, compared with 17% for the control group). The incidence of spontaneous arrhythmias was reduced by 5 and 10 microM bupivacaine during ischemia and reperfusion and was enhanced by 1 microM bupivacaine during the ischemic phase. Conclusions In guinea pig myocardium under ischemic conditions, bupivacaine induced a loss of excitability at concentrations of 5 and 10 microM. Proarrhythmic effects observed at 1 microM were considered as lower than the cardiotoxic range in normoxic conditions. The incidence of reperfusion arrhythmias was decreased at all concentrations.
APA, Harvard, Vancouver, ISO, and other styles
3

Shin, Tae Hwan, Da Yeon Lee, Shaherin Basith, Balachandran Manavalan, Man Jeong Paik, Igor Rybinnik, M. Maral Mouradian, Jung Hwan Ahn, and Gwang Lee. "Metabolome Changes in Cerebral Ischemia." Cells 9, no. 7 (July 7, 2020): 1630. http://dx.doi.org/10.3390/cells9071630.

Full text
Abstract:
Cerebral ischemia is caused by perturbations in blood flow to the brain that trigger sequential and complex metabolic and cellular pathologies. This leads to brain tissue damage, including neuronal cell death and cerebral infarction, manifesting clinically as ischemic stroke, which is the cause of considerable morbidity and mortality worldwide. To analyze the underlying biological mechanisms and identify potential biomarkers of ischemic stroke, various in vitro and in vivo experimental models have been established investigating different molecular aspects, such as genes, microRNAs, and proteins. Yet, the metabolic and cellular pathologies of ischemic brain injury remain not fully elucidated, and the relationships among various pathological mechanisms are difficult to establish due to the heterogeneity and complexity of the disease. Metabolome-based techniques can provide clues about the cellular pathologic status of a condition as metabolic disturbances can represent an endpoint in biological phenomena. A number of investigations have analyzed metabolic changes in samples from cerebral ischemia patients and from various in vivo and in vitro models. We previously analyzed levels of amino acids and organic acids, as well as polyamine distribution in an in vivo rat model, and identified relationships between metabolic changes and cellular functions through bioinformatics tools. This review focuses on the metabolic and cellular changes in cerebral ischemia that offer a deeper understanding of the pathology underlying ischemic strokes and contribute to the development of new diagnostic and therapeutic approaches.
APA, Harvard, Vancouver, ISO, and other styles
4

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 (March 2009): 421–29. http://dx.doi.org/10.1007/s12272-009-1316-9.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Wei, Qingqing, and Zheng Dong. "Mouse model of ischemic acute kidney injury: technical notes and tricks." American Journal of Physiology-Renal Physiology 303, no. 11 (December 1, 2012): F1487—F1494. http://dx.doi.org/10.1152/ajprenal.00352.2012.

Full text
Abstract:
Renal ischemia-reperfusion leads to acute kidney injury (AKI), a major kidney disease associated with an increasing prevalence and high mortality rates. A variety of experimental models, both in vitro and in vivo, have been used to study the pathogenic mechanisms of ischemic AKI and to test renoprotective strategies. Among them, the mouse model of renal clamping is popular, mainly due to the availability of transgenic models and the relatively small animal size for drug testing. However, the mouse model is generally less stable, resulting in notable variations in results. Here, we describe a detailed protocol of the mouse model of bilateral renal ischemia-reperfusion. We share the lessons and experiences gained from our laboratory in the past decade. We further discuss the technical issues that account for the variability of this model and offer relevant solutions, which may help other investigators to establish a well-controlled, reliable animal model of ischemic AKI.
APA, Harvard, Vancouver, ISO, and other styles
6

Zhou, Ya-ping, and Guo-chun Li. "Kaempferol Protects Cell Damage in In Vitro Ischemia Reperfusion Model in Rat Neuronal PC12 Cells." BioMed Research International 2020 (April 24, 2020): 1–10. http://dx.doi.org/10.1155/2020/2461079.

Full text
Abstract:
Ischemic cerebral stroke is a severe neurodegenerative disease with high mortality. Ischemia and reperfusion injury plays a fundamental role in ischemic cerebral stroke. To date, the strategy for ischemic cerebral stroke treatment is limited. In the present study, we aimed to investigate the effect of kaempferol (KFL), a natural flavonol, on cell injury induced by oxygen and glucose deprivation (OGD) and reoxygenation (OGD-reoxygenation) in PC12 cells. We found that KFL inhibited OGD-induced decrease of cell viability and the increase of lactate dehydrogenase (LDH) release. OGD-induced activation of mitochondrial dysfunction, mitochondrial apoptotic pathway, and apoptosis was inhibited by KFL. KFL also reduced OGD-induced oxidative stress in PC12 cells. P66shc expression and acetylation were increased by OGD and KFL inhibited these changes. Upregulation of P66shc suppressed KFL-induced decrease of apoptosis, the decrease of LDH release, and the increase of cell viability. Furthermore, KFL inhibited OGD-induced decrease of sirtuin 1 (SIRT1) expression and downregulation of SIRT1 blocked KFL-induced decrease of apoptosis, the decrease of LDH release, and the increase of cell viability. In summary, we identified that KFL exhibited a beneficial effect against OGD-induced cytotoxicity in an ischemia/reperfusion injury cell model. The findings suggest that KFL may be a promising choice for the intervention of ischemic stroke and highlighted the SIRT1/P66shc signaling.
APA, Harvard, Vancouver, ISO, and other styles
7

Liu, Yueyang, Xiaohang Che, Haotian Zhang, Xiaoxiao Fu, Yang Yao, Jun Luo, Yu Yang, et al. "CAPN1 (Calpain1)-Mediated Impairment of Autophagic Flux Contributes to Cerebral Ischemia-Induced Neuronal Damage." Stroke 52, no. 5 (May 2021): 1809–21. http://dx.doi.org/10.1161/strokeaha.120.032749.

Full text
Abstract:
Background and Purpose: CAPN1 (calpain1)—an intracellular Ca 2+ -regulated cysteine protease—can be activated under cerebral ischemia. However, the mechanisms by which CAPN1 activation promotes cerebral ischemic injury are not defined. Methods: In the present study, we used adeno-associated virus-mediated genetic knockdown and pharmacological blockade (MDL-28170) of CAPN1 to investigate the role of CAPN1 in the regulation of the autophagy-lysosomal pathway and neuronal damage in 2 models, rat permanent middle cerebral occlusion in vivo model and oxygen-glucose–deprived primary neuron in vitro model. Results: CAPN1 was activated in the cortex of permanent middle cerebral occlusion–operated rats and oxygen-glucose deprivation–exposed neurons. Genetic and pharmacological inhibition of CAPN1 significantly attenuated ischemia-induced lysosomal membrane permeabilization and subsequent accumulation of autophagic substrates in vivo and in vitro. Moreover, inhibition of CAPN1 increased autophagosome formation by decreasing the cleavage of the autophagy regulators BECN1 (Beclin1) and ATG (autophagy-related gene) 5. Importantly, the neuron-protective effect of MDL-28170 on ischemic insult was reversed by cotreatment with either class III-PI3K (phosphatidylinositol 3-kinase) inhibitor 3-methyladenine or lysosomal inhibitor chloroquine (chloroquine), suggesting that CAPN1 activation-mediated impairment of autophagic flux is crucial for cerebral ischemia-induced neuronal damage. Conclusions: The present study demonstrates for the first time that ischemia-induced CAPN1 activation impairs lysosomal function and suppresses autophagosome formation, which contribute to the accumulation of substrates and aggravate the ischemia-induced neuronal cell damage. Our work highlights the vital role of CAPN1 in the regulation of cerebral ischemia–mediated autophagy-lysosomal pathway defects and neuronal damage.
APA, Harvard, Vancouver, ISO, and other styles
8

Kelly, K. J., T. A. Sutton, N. Weathered, N. Ray, E. J. Caldwell, Z. Plotkin, and P. C. Dagher. "Minocycline inhibits apoptosis and inflammation in a rat model of ischemic renal injury." American Journal of Physiology-Renal Physiology 287, no. 4 (October 2004): F760—F766. http://dx.doi.org/10.1152/ajprenal.00050.2004.

Full text
Abstract:
Tetracyclines exhibit significant anti-inflammatory properties in a variety of rheumatologic and dermatologic conditions. They have also been shown to inhibit apoptosis in certain neurodegenerative disorders. Because ischemic renal injury is characterized by both apoptosis and inflammation, we investigated the therapeutic potential of tetracyclines in a rat model of renal ischemia-reperfusion. Male Sprague-Dawley rats underwent bilateral renal artery clamp for 30 min followed by reperfusion and received either minocycline or saline for 36 h before ischemia. Minocycline reduced tubular cell apoptosis 24 h after ischemia as determined by terminal transferase-mediated dUTP nick end-labeling staining and nuclear morphology. It also decreased cytochrome c release into the cytoplasm and reduced upregulation of p53 and Bax after ischemia. The minocycline-treated group showed a significant reduction in tubular injury and cast formation. In addition, minocycline reduced the number of infiltrating leukocytes, decreased leukocyte chemotaxis both in vitro and ex vivo, and downregulated the expression of ICAM-1. Serum creatinine 24-h postischemia was significantly reduced in the minocycline-treated group. We conclude that minocycline has potent antiapoptotic and anti-inflammatory properties and protects renal function in this model of ischemia-reperfusion. Tetracyclines are among the safest and best-studied antibiotics. They are thus attractive candidates for the therapy of human ischemic acute renal failure.
APA, Harvard, Vancouver, ISO, and other styles
9

Burda, Jozef, M. Elena Martín, Miroslav Gottlieb, Mikulas Chavko, Jozef Marsala, Alberto Alcázar, Miguel Pavón, Juan L. Fando, and Matilde Salinas. "The Intraischemic and Early Reperfusion Changes of Protein Synthesis in the Rat Brain. eIF-2α Kinase Activity and Role of Initiation Factors eIF-2α and eIF-4E." Journal of Cerebral Blood Flow & Metabolism 18, no. 1 (January 1998): 59–66. http://dx.doi.org/10.1097/00004647-199801000-00006.

Full text
Abstract:
Rats were subjected to the standard four-vessel occlusion model of transient cerebral ischemia (vertebral and carotid arteries). The effects of normothermic ischemia (37°C) followed or not by 30-minute reperfusion, as well as 30-minute postdecapitative ischemia, on translational rates were examined. Protein synthesis rate, as measured in a cell-free system, was significantly inhibited in ischemic rats, and the extent of inhibition strongly depended on duration and temperature, and less on the model of ischemia used. The ability of reinitiation in vitro (by using aurintricarboxylic acid) decreased after ischemia, suggesting a failure in the synthetic machinery at the initiation level. Eukaryotic initiation factor 2 (eIF-2) presented almost basal activity and levels after 30-minute normothermic ischemia, and the amount of phosphorylated eIF-2α in these samples, as well as in sham-control samples, was undetectable. The decrease in the levels of phosphorylated initiation factor 4E (eIF-4E) after 30-minute ischemia (from 32% to 16%) could explain, at least partially, the impairment of initiation during transient cerebral ischemia. After reperfusion, eIF-4E phosphorylation was almost completely restored to basal levels (29%), whereas the level of phosphorylated eIF-2α was higher (13%) than in controls and ischemic samples (both less than 2%). eIF-2α kinase activity in vitro as measured by phosphorylation of endogenous eIF-2 in the presence of ATP/Mg2+, was higher in ischemic samples (8%) than in controls (4%). It seems probable that the failure of the kinase in phosphorylating eIF-2 in vivo during ischemia is due to the depletion of ATP stores. The levels of the double-stranded activated eIF-2α kinase were slightly higher in ischemic animals than in controls. Our results suggest that the modulation of eIF-4E phosphorylation could be implicated in the regulation of translation during ischemia. On the contrary, phosphorylation of eIF-2α, by an eIF-2α kinase already activated during ischemia, represents a plausible mechanism for explaining the inhibition of translation during reperfusion
APA, Harvard, Vancouver, ISO, and other styles
10

Wang, Yang, Shao-wei Jiang, Xuan Liu, Lei Niu, Xiao-li Ge, Jin-cheng Zhang, Hai-rong Wang, Ai-hua Fei, Cheng-jin Gao, and Shu-ming Pan. "Degradation of TRPML1 in Neurons Reduces Neuron Survival in Transient Global Cerebral Ischemia." Oxidative Medicine and Cellular Longevity 2018 (December 18, 2018): 1–11. http://dx.doi.org/10.1155/2018/4612727.

Full text
Abstract:
Postcardiac arrest syndrome yields poor neurological outcomes, but the mechanisms underlying this condition remain poorly understood. Autophagy plays an important role in neuronal apoptosis induced by ischemia. However, whether autophagy is involved in neuron apoptosis induced by cardiac arrest has been less studied. This study found that TRPML1 participates in cerebral ischemic reperfusion injury. Primary neurons were isolated and treated with mucolipin synthetic agonist 1 (ML-SA1), as well as infected with the recombinant lentivirus TRPML1 overexpression vector in vitro. ML-SA1 was delivered intracerebroventricularly in transient global ischemia model. Protein expression levels were determined by western blot. Neurological deficit score and the infarct volume were analyzed for the detection of neuronal damage. We found that TRPML1 was significantly downregulated in vivo and in vitro ischemic reperfusion model. We also observed that TRPML1 overexpression or treatment with the ML-SA1 attenuated neuronal death in primary neurons and ameliorated neurological dysfunction in vivo. Our findings suggested that autophagy and apoptosis were activated after transient global ischemia. Administration of ML-SA1 before transient global ischemia ameliorated neurological dysfunction possibly through the promotion of autophagy and the inhibition of apoptosis.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "In vitro ischemia model"

1

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
4

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/.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
5

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
6

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
10

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "In vitro ischemia model"

1

Serruys, P. W., and G. T. Meester, eds. Coronary Angioplasty: A Controlled Model for Ischemia. Dordrecht: Springer Netherlands, 1986. http://dx.doi.org/10.1007/978-94-009-4295-0.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

W, Serruys P., and Meester G. T, eds. Coronary angioplasty: A controlled model for ischemia. Dordrecht: M. Nijhoff, 1986.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

1947-, McQueen Charlene A., ed. In vitro toxicology: Model systems and methods. Caldwell, N.J: Telford Press, 1989.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

Chen, Timothy Han. Human Tissue Engineered Model of Myocardial Ischemia-Reperfusion Injury. [New York, N.Y.?]: [publisher not identified], 2018.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

Husain, Irfana Shaheen. The development of an in vitro caries model. [Toronto: Faculty of Dentistry, University of Toronto], 1992.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

Starkey, Rosalind F. Cellular interactions in an in vitro model of implantation. Manchester: Universityof Manchester, 1993.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

Cardella, Jonathan A. A novel cell culture model to study ischemia-reperfusion injury in lung transplantation. Ottawa: National Library of Canada, 1999.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

Siegel, Andre Clifford. Biosynthetic pathways of platelet-activating factor in the nongolian gerbil model of cerebral ischemia. Ottawa: National Library of Canada, 1996.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

Mahendra, Ahalya. The role of ILK in an in vitro model of renal branching morphogenesis. Ottawa: National Library of Canada, 2003.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

elgendy, Hany Mohamed Aly. Dexamethasone-mediated regulation of Bax and Bcl-x in an animal model of perinatal hypoxia/ischemia. Ottawa: National Library of Canada, 2002.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "In vitro ischemia model"

1

Yang, Li, Kaushik K. Shah, and Thomas J. Abbruscato. "An In Vitro Model of Ischemic Stroke." In Methods in Molecular Biology, 451–66. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-452-0_30.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

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, 229–35. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7526-6_18.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Tanguy, Stéphane, Madhumathy Jeyaraman, Bradley W. Doble, Zhisheng Jiang, Robert R. Fandrich, and Elissavet Kardami. "Effects of Ischemia on Cardiomyocyte Connexin-43 Distribution and Phosphorylation Studied in in vivo and in vitro Models." In Pathophysiology of Cardiovascular Disease, 257–68. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4615-0453-5_19.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Kadir, Rais Reskiawan A., Mansour Alwjwaj, and Ulvi Bayraktutan. "Establishment of an In Vitro Model of Human Blood–Brain Barrier to Study the Impact of Ischemic Injury." In Methods in Molecular Biology, 143–55. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2289-6_8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Betz, E. L. "Inhibition of Atherogenesis In Vivo and In Vitro." In Cerebral Ischemia and Dementia, 77–84. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76208-6_10.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Waxham, M. N., S. A. Westgate, and M. D. Mauk. "In Vitro Ischemia in the Hippocampal Slice." In Cerebral Ischemia and Basic Mechanisms, 217–29. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78151-3_23.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Turin, Alexander, and Robert S. Dieter. "Critical Limb Ischemia and the Angiosome Model." In Critical Limb Ischemia, 367–72. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-31991-9_33.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Wiesenfeld-Hallin, Zsuzsanna, Jing-Xia Hao, and Xiao-Jun Xu. "Spinal Cord Injury Pain Model, Ischemia Model." In Encyclopedia of Pain, 3561–65. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-28753-4_4115.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

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, 115–27. Tokyo: Springer Japan, 1996. http://dx.doi.org/10.1007/978-4-431-68467-1_8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Raval, Ami P., Chunli Liu, and Bingren R. Hu. "Rat Model of Global Cerebral Ischemia: The Two-Vessel Occlusion (2VO) Model of Forebrain Ischemia." In Springer Protocols Handbooks, 77–86. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-185-1_7.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "In vitro ischemia model"

1

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Folts, J. D. "A MODEL OF ACUTE PLATELET THROMBUS FORMATION IN STENOSED CORONARY AND CAROTID ARTERIES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643712.

Full text
Abstract:
There is currently a great deal of interest in the diagnosis and treatment of unstable angina and silent ischemia.Many feel that these syndromes are due, in part, to periodic accumulation of platelet thrombi which subsequently embolize.In addition, anti-piatelet therapy is also considered necessary for patients after coronary artery bypass grafts (CABG'S), balloon angioplasty, and thrombolysis. Currently the two antiplatelet agents most commonly prescribed for the patient conditions mentioned above are aspirin (ASA), alone or in combination with dipyridamole (Dip). ASA reduces cardiac events in patients with unstable angina, and prolongs CABG graft patency. The addition of Dip to ASA therapy is very confusing since most studies done compared ASA + Dip to placebo. In several studies however,when an ASA group was compared to an ASA + Dip group there was no significant difference.We have developed and will describe ananimal model of coronary artery stenosis in the dog and the pig, or carotid arterystenosis in the monkey and the rabbit, with intimal damage, that simulates some ofthe conditions that exist in patients with coronary or carotid artery disease. The artery to be studied is dissected outand blood flow is continuously measured with an electromagnetic flowmeter probe. As acute platelet thrombus formation (APTF) developes in the stenosed lumen, the blood flow declines to low levels, producing ischemia until the thrombus emobolizesdistally resulting in abrupt restoration of blood flow. These cyclical flow reductions (CFR's), when they occur in the coronaries, produce ECG changes identical to those observed in patients with silent ischemia and unstable angina. They also produce significant transient regional dyskinesis of the ventricular wall, which resolves when blood flow is restored. Histologic examination of myocardial tissue in the bed distal to the stenosis shows focal areas of ischemic change presumably caused by the embolized platelet emboli.We have examined factors which exacerbate the size and frequency of these CFR"ssuch as; IV infusion of epinephrine (E) 0.4 μg/kg/min for 15 min, ventilating the animals with cigarette smoke, infusing nicotine IV, or placing chewing tobacco under the tongue.We have examined four groups of agentswhich prevent APTF in our model.1. Antiplatelet agents including ASA, indomethacin, ibuprofen and several other NSAI agentsas well as several experimental thromboxane synthetase inhibitors. These agents all block the production of TXA2and inhibit APTF in our model. Unfortunately the IV infusion of E reinstates APTtemporarily (by another biochemical pathway) until the E is metabolized. High (2-4 mg/kg) doses of Dip, alone or with sub threshold dose of ASA does nothing to I APTF.However,0.6mg/kg of chi orpromaz i ne abolishes APTF in all four species and protects agents renewal of APTF by E.2. Dietary Substances In our model, caffeine 10 mg/kg, or the extract from two garlic cloves, or enough ethanol to achieve a blood alcohol level of 0.07 mg% all significantly inhibit or abolish APTF in our model.3. Metabolic Inhibitors POCA, an oral hypoglycemic agent, which inhibits mitochondrial beta oxidation of fatty acids also inhibits APTF in our model possibly by reducing ATP production in the platelet.4. We have studied a monoclonal antibody(developed by Dr. Barry Coller) to the platelet I Ib�I I la glycoprotein receptor where fibrinogen binds platelets into aggregates and ultimately leads to APTF. This antibody 0.3 mg/kg/completely inhibits APTF, and also strongly inhibits in vitro platelet aggregation in response to either ADP or collagen given alone or each combined with E. This antibody is the most potent inhibitor of APTF that we have studied.
APA, Harvard, Vancouver, ISO, and other styles
3

Chueh, Juyu, Christine F. Silva, Ajay K. Wakhloo, and Matthew J. Gounis. "In-Vitro Clot Modeling for the Preclinical Assessment of Mechanical Thrombectomy in Acute Ischemic Stroke." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19230.

Full text
Abstract:
Mechanical thrombectomy devices, such as retrievers or aspiration catheters, have recently received approval from the FDA for the treatment of acute ischemic stroke. There is growing interest in endovascular recanalization procedures due to mounting evidence of favorable clinical outcomes. Several attempts have been made to establish dedicated clot models for in-vitro or in-vivo simulation of thromboembolism [1,2]. However, little is known about the mechanical and structural similarities between experimental clots and human sources of emboli that cause stroke. The goal of this study is to compare the structure and compression behavior of the possible sources of the cerebral emboli extracted from patients and model clots produced in-vitro using human, porcine and bovine donors.
APA, Harvard, Vancouver, ISO, and other styles
4

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.

Full text
Abstract:
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 sections. In the third model, a zero diffusion flux is applied at outlet with a pre-specified flow rate at inlet. Numerical simulations performed on healthy and stenosed idealized and physiological arterial models revealed the superiority of the first type of boundary condition to directly capture the level of ischemia in diseased arteries. However, in this model, special numerical treatment at the outflow boundary is needed to dampen pseudo numerical reflections entering the computational domain. Alternative simple methods are developed to tackle the problem incurred in the second and third types of boundary condition types. The alternate models are effective for carrying extensive parametric studies with minimal computational effort. The new developed methods allow results generated via generic simulations under any specified boundary condition type to correctly estimate CAD functional significance. The obtained surrogate models account for the effects of the patient-specific physiologic parameters and can be easily incorporated without modifying existing CFD codes. Moreover, where it is unfeasible to experimentally incorporate the downstream effects of a given diseased arterial segment, an important aspect the alternative models provide is that they can be easily adopted by experimentalists through building in-vitro arterial models to assess the functional significance of the obstruction caused by the disease and its relation to any given patient specific physiologic parameter.
APA, Harvard, Vancouver, ISO, and other styles
5

Demyanenko, Svetlana, Svetlana Sharifulina, Elena Berezhnaya, Vera Kovaleva, Maria Neginskaya, and Ludmila Zhukovskaya. "Photodynamic impact induces ischemic tolerance in models in vivo and in vitro." In Saratov Fall Meeting 2015, edited by Elina A. Genina, Valery V. Tuchin, Vladimir L. Derbov, Dmitry E. Postnov, Igor V. Meglinski, Kirill V. Larin, and Alexander B. Pravdin. SPIE, 2016. http://dx.doi.org/10.1117/12.2229929.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Korkmaz-Icöz, S., M. Schwär, S. Loganathan, K. Wächter, A. Sayour, P. Kraft, T. Mayer, 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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Ding, Q., S. Loganathan, P. Brlecic, A. A. Sayour, M. Ruppert, T. Radovits, B. Korkmaz, M. Karck, G. Szabó, and S. Korkmaz-Icöz. "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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Rick, Cheah Wee, and Azam Ahmad Bakir. "Simulating Electrocardiogram Using Finite Element Model During Ischemia Development." In 2022 2nd International Conference on Intelligent Cybernetics Technology & Applications (ICICyTA). IEEE, 2022. http://dx.doi.org/10.1109/icicyta57421.2022.10038165.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Kisel, A. A., G. A. Chernysheva, V. I. Smol’yakova, R. R. Savchenko, M. B. Plotnikov, and M. Yu Khodanovich. "Hippocampal neurogenesis in the new model of global cerebral ischemia." In NEW OPERATIONAL TECHNOLOGIES (NEWOT’2015): Proceedings of the 5th International Scientific Conference «New Operational Technologies». AIP Publishing LLC, 2015. http://dx.doi.org/10.1063/1.4935999.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "In vitro ischemia model"

1

Paranavitana, Chrysanthi. In Vitro Osteoblast Model for Bone Wound Infections and Antimicrobial Therapy. Fort Belvoir, VA: Defense Technical Information Center, January 2013. http://dx.doi.org/10.21236/ada608594.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Mastro, Andrea M., Erwin A. Vogler, and Carol V. Gay. A New In Vitro Model of Breast Cancer Metastasis to Bone. Fort Belvoir, VA: Defense Technical Information Center, April 2010. http://dx.doi.org/10.21236/ada533775.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Mastro, Andrea M., Erwin A. Vogler, and Carol V. Gay. A New In Vitro Model of Breast Cancer Metastasis to Bone. Fort Belvoir, VA: Defense Technical Information Center, April 2009. http://dx.doi.org/10.21236/ada550794.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Mastro, Andrea M., Carol V. Gay, and Erwin Vogler. An New in Vitro Model of Breast Cancer Metastasis to Bone. Fort Belvoir, VA: Defense Technical Information Center, April 2007. http://dx.doi.org/10.21236/ada470050.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Percival, Thomas J., Shimul Patel, Nickolay P. Markov, Jerry R. Spencer, Gabriel E. Burkhardt, Lorne H. Blackbourne, and Todd E. Rasmussen. Fasciotomy Reduces Compartment Pressures and Improves Recovery in a Porcine Model of Extremity Vascular Injury and Ischemia/Reperfusion. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada568830.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Slawinska, Anna, John C. F. Hsieh, Carl J. Schmidt, and Susan J. Lamont. Host Cellular Response to Multiple Stressors Using a Chicken in vitro Model. Ames (Iowa): Iowa State University, January 2016. http://dx.doi.org/10.31274/ans_air-180814-227.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Grover, Paramjit, M. F. Rahman, and M. Mahboob. Bio-Physicochemical Interactions of Engineered Nanomaterials in In Vitro Cell Culture Model. Fort Belvoir, VA: Defense Technical Information Center, August 2012. http://dx.doi.org/10.21236/ada567065.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Hung, Gene. Establish an In Vitro Model for the Study of NF2 Gene Function and Gene Therapy. Fort Belvoir, VA: Defense Technical Information Center, October 2000. http://dx.doi.org/10.21236/ada395531.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Andalibi, Ali. Establish an In Vitro Model for the Study of NF2 Gene Function and Gene Therapy. Fort Belvoir, VA: Defense Technical Information Center, July 2004. http://dx.doi.org/10.21236/ada431978.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Robinson, Peter J., Elaine A. Merrill, Andrea Hoffmann, Teresa R. Sterner, Mitchell L. Meade, and David R. Mattie. In Vitro Studies and Preliminary Mathematical Model for Jet Fuel and Noise Induced Auditory Impairment. Fort Belvoir, VA: Defense Technical Information Center, June 2015. http://dx.doi.org/10.21236/ada626660.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'In vitro ischemia model' for particular source types:
Journal articles Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography