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Добірка наукової літератури з теми "Animal model of hyperoxia"

Автор: Grafiati

Опубліковано: 11 березня 2023

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Статті в журналах з теми "Animal model of hyperoxia"

D'Angio, Carl T., and Rita M. Ryan. "Animal models of bronchopulmonary dysplasia. The preterm and term rabbit models." American Journal of Physiology-Lung Cellular and Molecular Physiology 307, no. 12 (December 15, 2014): L959—L969. http://dx.doi.org/10.1152/ajplung.00228.2014.

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Bronchopulmonary dysplasia (BPD) is an important lung developmental pathophysiology that affects many premature infants each year. Newborn animal models employing both premature and term animals have been used over the years to study various components of BPD. This review describes some of the neonatal rabbit studies that have contributed to the understanding of BPD, including those using term newborn hyperoxia exposure models, premature hyperoxia models, and a term newborn hyperoxia model with recovery in moderate hyperoxia, all designed to emulate aspects of BPD in human infants. Some investigators perturbed these models to include exposure to neonatal infection/inflammation or postnatal malnutrition. The similarities to lung injury in human premature infants include an acute inflammatory response with the production of cytokines, chemokines, and growth factors that have been implicated in human disease, abnormal pulmonary function, disordered lung architecture, and alveolar simplification, development of fibrosis, and abnormal vascular growth factor expression. Neonatal rabbit models have the drawback of limited access to reagents as well as the lack of readily available transgenic models but, unlike smaller rodent models, are able to be manipulated easily and are significantly less expensive than larger animal models.

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Mühlfeld, Christian, Henri Schulte, Johanna Christine Jansing, Costanza Casiraghi, Francesca Ricci, Chiara Catozzi, Matthias Ochs, Fabrizio Salomone, and Christina Brandenberger. "Design-Based Stereology of the Lung in the Hyperoxic Preterm Rabbit Model of Bronchopulmonary Dysplasia." Oxidative Medicine and Cellular Longevity 2021 (October 6, 2021): 1–12. http://dx.doi.org/10.1155/2021/4293279.

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Bronchopulmonary dysplasia (BPD) is a complex condition frequently occurring in preterm newborns, and different animal models are currently used to mimic the pathophysiology of BPD. The comparability of animal models depends on the availability of quantitative data obtained by minimally biased methods. Therefore, the aim of this study was to provide the first design-based stereological analysis of the lungs in the hyperoxia-based model of BPD in the preterm rabbit. Rabbit pups were obtained on gestation day 28 (three days before term) by cesarean section and exposed to normoxic (21% O2, n = 8 ) or hyperoxic (95% O2, n = 8 ) conditions. After seven days of exposure, lung function testing was performed, and lungs were taken for stereological analysis. In addition, the ratio between pulmonary arterial acceleration and ejection time (PAAT/PAET) was measured. Inspiratory capacity and static compliance were reduced whereas tissue elastance and resistance were increased in hyperoxic animals compared with normoxic controls. Hyperoxic animals showed signs of pulmonary hypertension indicated by the decreased PAAT/PAET ratio. In hyperoxic animals, the number of alveoli and the alveolar surface area were reduced by one-third or by approximately 50% of control values, respectively. However, neither the mean linear intercept length nor the mean alveolar volume was significantly different between both groups. Hyperoxic pups had thickened alveolar septa and intra-alveolar accumulation of edema fluid and inflammatory cells. Nonparenchymal blood vessels had thickened walls, enlarged perivascular space, and smaller lumen in hyperoxic rabbits in comparison with normoxic ones. In conclusion, the findings are in line with the pathological features of human BPD. The stereological data may serve as a reference to compare this model with BPD models in other species or future therapeutic interventions.

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Dean, Jay B., Daniel K. Mulkey, Richard A. Henderson, Stephanie J. Potter, and Robert W. Putnam. "Hyperoxia, reactive oxygen species, and hyperventilation: oxygen sensitivity of brain stem neurons." Journal of Applied Physiology 96, no. 2 (February 2004): 784–91. http://dx.doi.org/10.1152/japplphysiol.00892.2003.

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Hyperoxia is a popular model of oxidative stress. However, hyperoxic gas mixtures are routinely used for chemical denervation of peripheral O2 receptors in in vivo studies of respiratory control. The underlying assumption whenever using hyperoxia is that there are no direct effects of molecular O2 and reactive O2 species (ROS) on brain stem function. In addition, control superfusates used routinely for in vitro studies of neurons in brain slices are, in fact, hyperoxic. Again, the assumption is that there are no direct effects of O2 and ROS on neuronal activity. Research contradicts this assumption by demonstrating that O2 has central effects on the brain stem respiratory centers and several effects on neurons in respiratory control areas; these need to be considered whenever hyperoxia is used. This mini-review summarizes the long-recognized, but seldom acknowledged, paradox of respiratory control known as hyperoxic hyperventilation. Several proposed mechanisms are discussed, including the recent hypothesis that hyperoxic hyperventilation is initiated by increased production of ROS during hyperoxia, which directly stimulates central CO2 chemoreceptors in the solitary complex. Hyperoxic hyperventilation may provide clues into the fundamental role of redox signaling and ROS in central control of breathing; moreover, oxidative stress may play a role in respiratory control dysfunction. The practical implications of brain stem O2 and ROS sensitivity are also considered relative to the present uses of hyperoxia in respiratory control research in humans, animals, and brain stem tissues. Recommendations for future research are also proposed.

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George, Caroline L. S., Giamila Fantuzzi, Stuart Bursten, Laura Leer, and Edward Abraham. "Effects of lisofylline on hyperoxia-induced lung injury." American Journal of Physiology-Lung Cellular and Molecular Physiology 276, no. 5 (May 1, 1999): L776—L785. http://dx.doi.org/10.1152/ajplung.1999.276.5.l776.

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Lisofylline [1-(5 R-hydroxyhexyl)-3,7-dimethylxanthine] decreases lipid peroxidation in vitro and in vivo suppresses proinflammatory cytokine expression in models of lung injury due to sepsis, blood loss, and oxidative damage. In the present experiments, we used a murine hyperoxia model to examine the effects of lisofylline on the activation of nuclear transcriptional regulatory factors [nuclear factor-κB and cAMP response element binding protein (CREB)], the expression of proinflammatory cytokines in the lungs, and the circulating levels of oxidized free fatty acids as well as on hyperoxia-induced lung injury and mortality. Treatment with lisofylline inhibited hyperoxia-associated increases in tumor necrosis factor-α, interleukin-1β, and interleukin-6 in the lungs as well as decreased the levels of hyperoxia-induced serum-oxidized free fatty acids. Although hyperoxic exposure produced activation of both nuclear factor-κB and CREB in lung cell populations, only CREB activation was reduced in the mice treated with lisofylline. Lisofylline diminished hyperoxia-associated increases in lung wet-to-dry weight ratios and improved survival in animals exposed to hyperoxia. These results suggest that lisofylline ameliorates hyperoxia-induced lung injury and mortality through inhibiting CREB activation, membrane oxidation, and proinflammatory cytokine expression in the lungs.

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Chen, Yin, Dong Wei, Jin Zhao, Xiangnan Xu, and Jingyu Chen. "Reduction of hyperoxic acute lung injury in mice by Formononetin." PLOS ONE 16, no. 1 (January 7, 2021): e0245050. http://dx.doi.org/10.1371/journal.pone.0245050.

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Background The antioxidant and anti-inflammatory features of Formononetin, an isoflavone constituent extracted from traditional Chinese medicine, have been reported. The present study investigated that whether Formononetin plays a benefit on hyperoxic ALI. Methods C57BL/6 mice were exposed to hyperoxia for 72 h to produce experimental hyperoxic ALI model. Formononetin or vehicle was administrated intraperitoneally. Samples from the lung were collected at 72 h post hyperoxia exposure for further study. Pulmonary microvascular endothelial cells isolated from the lung of C57BL/6 mice were used for in vitro study. Results Formononetin pretreatment notably attenuated hyperoxia-induced elevating pulmonary water content, upregulation of proinflammatory cytokine levels and increasing infiltration of neutrophil in the lung. Western blot analyses showed that Formononetin enhanced the expression of nuclear factor erythroid-2-related factor 2 (Nrf2) which is a key transcription factor regulating the expression of heme oxygenase-1 (HO-1). Formononetin increased HO-1 expression and activity compared with vehicle-treated animals. Moreover, Formononetin reversed hyperoxia-caused the reduction of M2 macrophage polarization. However, pretreatment of a HO-1 inhibitor reduced the protective effect of Formononetin on hyperoxic ALI. Cell study showed that the Formononetin-induced upregulation of HO-1 was abolished when the Nrf2 was silenced. Conclusions Formononetin pretreatment reduces hyperoxia-induced ALI via Nrf2/HO-1-mediated antioxidant and anti-inflammatory effects.

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Cheon, In Su, Youngmin Son, and Jie Sun. "An animal model of enhanced disease development following respiratory viral infection in children with chronic lung diseases." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 93.10. http://dx.doi.org/10.4049/jimmunol.204.supp.93.10.

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Abstract Infants born prematurely often develop chronic lung diseases including bronchopulmonary dysplasia (BPD). BPD is associated with greatly increased host susceptibility and severe disease development following respiratory viral infection. To this end, we have recently established a neonatal hyperoxia model respiratory viral infection in hosts with lung prematurity and BPD. Using this model, we observed that mice exposed with neonatal hyperoxia (80% oxygen, BPD hosts) developed enhanced diseases following influenza virus or respiratory syncytial virus (RSV) infection compared to those of influenza or RSV-infected control mice. We showed that neonatal hyperoxia leaded to modestly enhanced viral replication in the respiratory tract. Using nanostring immune gene profiling and multiplex cytokine analysis, we found that neonatal hyperoxia markedly enhanced immune-associated gene expression and the production of a number of proinflammatory cytokines and chemokines in the airway compared to those of control mice. Neonatal hyperoxia also increased the accumulation of multiple inflammatory innate cell types that were shown to be pathogenic during respiratory viral infections. Importantly, antiviral T, B cells and NK cells were similar in the lungs between infected neonatal hyperoxia-exposed and control mice, which are consistent with the similar viral clearance kinetics in those mice. Thus, we have successfully established a clinically-relevant mouse model of respiratory viral infection in BPD hosts. We expect to further uncover novel insights on the viral pathogenesis and host disease devlopment in this novel model of respiratory viral infection in hosts with chronic lung diseases.

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Mowes, Anja, Beatriz E. de Jongh, Timothy Cox, Yan Zhu, and Thomas H. Shaffer. "A translational cellular model to study the impact of high-frequency oscillatory ventilation on human epithelial cell function." Journal of Applied Physiology 122, no. 1 (January 1, 2017): 198–205. http://dx.doi.org/10.1152/japplphysiol.00400.2016.

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High-frequency oscillatory ventilation (HFOV) has been proposed as gentle ventilation strategy to prevent lung injury in the preterm infant. High-frequency jet ventilation leads to dimensional and mechanical airway deformation in animal airway models, which is consistent with translational studies demonstrating the impact of oxygen and biophysical stresses on normal airway cellular function. There is an overall paucity of clinical and cellular data on the impact of HFOV on the conducting airway. We developed an innovative method to test the impact of the clinical HFO Ventilator (SensorMedics 3100A) on human epithelial cell function. In this translational model, we were able to study the differential effects of biophysical stress due to HFOV independently and in combination with hyperoxia on a direct cellular level of the conducting airway system. Additionally, we could demonstrate that hyperoxia and pressure by HFOV independently resulted in significant cell dysfunction and inflammation, while the combination of HFOV and hyperoxia had a synergistic effect, resulting in greater cell death. NEW & NOTEWORTHY Traditionally, large-animal models are used to analyze the impact of clinical ventilators on lung cellular function. In our dual-chamber model, we interface high-frequency oscillatory ventilation (HFOV) directly with airway cells to study the effects of HFOV independently and combined with hyperoxia. Therefore, it is possible to study the preclinical impact of interventional factors without the high cost of animal models, thus reducing staff, time, as well as animal sparing.

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Porzionato, Andrea, Patrizia Zaramella, Arben Dedja, Diego Guidolin, Kelly Van Wemmel, Veronica Macchi, Marcin Jurga, et al. "Intratracheal administration of clinical-grade mesenchymal stem cell-derived extracellular vesicles reduces lung injury in a rat model of bronchopulmonary dysplasia." American Journal of Physiology-Lung Cellular and Molecular Physiology 316, no. 1 (January 1, 2019): L6—L19. http://dx.doi.org/10.1152/ajplung.00109.2018.

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Mesenchymal stem cells (MSCs) prevent the onset of bronchopulmonary dysplasia (BPD) in animal models, an effect that seems to be mediated by their secreted extracellular vesicles (EVs). The aim of this study was to compare the protective effects of intratracheally (IT) administered MSCs versus MSC-EVs in a hyperoxia-induced rat model of BPD. At birth, rats were distributed as follows: animals raised in ambient air for 2 wk ( n = 10), and animals exposed to 60% oxygen for 2 wk and treated with IT-administered physiological solution ( n = 10), MSCs ( n = 10), or MSC-EVs ( n = 10) on postnatal days 3, 7, and 10. The sham-treated hyperoxia-exposed animals showed reductions in total surface area of alveolar air spaces, and total number of alveoli ( Nalv), and an increased mean alveolar volume (Valv). EVs prompted a significant increase in Nalv ( P < 0.01) and a significant decrease in Valv ( P < 0.05) compared with sham-treated animals, whereas MSCs only significantly improved Nalv ( P < 0.05). Small pulmonary vessels of the sham-treated hyperoxia-exposed rats also showed an increase in medial thickness, which only EVs succeeded in preventing significantly ( P < 0.05). In conclusion, both EVs and MSCs reduce hyperoxia-induced damage, with EVs obtaining better results in terms of alveolarization and lung vascularization parameters. This suggests that IT-administered EVs could be an effective approach to BPD treatment.

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Berger, Jessica, and Vineet Bhandari. "Animal models of bronchopulmonary dysplasia. The term mouse models." American Journal of Physiology-Lung Cellular and Molecular Physiology 307, no. 12 (December 15, 2014): L936—L947. http://dx.doi.org/10.1152/ajplung.00159.2014.

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The etiology of bronchopulmonary dysplasia (BPD) is multifactorial, with genetics, ante- and postnatal sepsis, invasive mechanical ventilation, and exposure to hyperoxia being well described as contributing factors. Much of what is known about the pathogenesis of BPD is derived from animal models being exposed to the environmental factors noted above. This review will briefly cover the various mouse models of BPD, focusing mainly on the hyperoxia-induced lung injury models. We will also include hypoxia, hypoxia/hyperoxia, inflammation-induced, and transgenic models in room air. Attention to the stage of lung development at the timing of the initiation of the environmental insult and the duration of lung injury is critical to attempt to mimic the human disease pulmonary phenotype, both in the short term and in outcomes extending into childhood, adolescence, and adulthood. The various indexes of alveolar and vascular development as well as pulmonary function including pulmonary hypertension will be highlighted. The advantages (and limitations) of using such approaches will be discussed in the context of understanding the pathogenesis of and targeting therapeutic interventions to ameliorate human BPD.

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Datta, Ankur, Gina A. Kim, Joann M. Taylor, Sylvia F. Gugino, Kathryn N. Farrow, Paul T. Schumacker, and Sara K. Berkelhamer. "Mouse lung development and NOX1 induction during hyperoxia are developmentally regulated and mitochondrial ROS dependent." American Journal of Physiology-Lung Cellular and Molecular Physiology 309, no. 4 (August 15, 2015): L369—L377. http://dx.doi.org/10.1152/ajplung.00176.2014.

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Animal models demonstrate that exposure to supraphysiological oxygen during the neonatal period compromises both lung and pulmonary vascular development, resulting in a phenotype comparable to bronchopulmonary dysplasia (BPD). Our prior work in murine models identified postnatal maturation of antioxidant enzyme capacities as well as developmental regulation of mitochondrial oxidative stress in hyperoxia. We hypothesize that consequences of hyperoxia may also be developmentally regulated and mitochondrial reactive oxygen species (ROS) dependent. To determine whether age of exposure impacts the effect of hyperoxia, neonatal mice were placed in 75% oxygen for 72 h at either postnatal day 0 (early postnatal) or day 4 (late postnatal). Mice exposed to early, but not late, postnatal hyperoxia demonstrated decreased alveolarization and septation, increased muscularization of resistance pulmonary arteries, and right ventricular hypertrophy (RVH) compared with normoxic controls. Treatment with a mitochondria-specific antioxidant, (2-(2,2,6,6-tetramethylpiperidin-1-oxyl-4-ylamino)-2-oxoethyl)triphenylphosphonium chloride (mitoTEMPO), during early postnatal hyperoxia protected against compromised alveolarization and RVH. In addition, early, but not late, postnatal hyperoxia resulted in induction of NOX1 expression that was mitochondrial ROS dependent. Because early, but not late, exposure resulted in compromised lung and cardiovascular development, we conclude that the consequences of hyperoxia are developmentally regulated and decrease with age. Attenuated disease in mitoTEMPO-treated mice implicates mitochondrial ROS in the pathophysiology of neonatal hyperoxic lung injury, with potential for amplification of ROS signaling through NOX1 induction. Furthermore, it suggests a potential role for targeted antioxidant therapy in the prevention or treatment of BPD.

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Дисертації з теми "Animal model of hyperoxia"

Dedja, Arben. "Administration of L-citrulline in an animal model of perinatal lung damage." Doctoral thesis, Università degli studi di Padova, 2012. http://hdl.handle.net/11577/3422175.

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Moderate hyperoxia and induced chorioamnionitis by intrauterine administration of endotoxin LPS into near-term pregnant rats cause alveolar and vascular lung derangement in the newborns. Endogenous nitric oxide (NO), which promotes lung growth, is produced from the metabolism of L-arginine to L-citrulline in endothelial cells. We investigated whether administering L-citrulline by raising the serum levels of L-arginine and enhancing NO endogenous synthesis, attenuates lung injury in a chorioamnionitis and/or moderate hyperoxia-induced model. Material and Methods. Newborn rats (receiving or not intrauterine LPS) were exposed to FiO2=0.6 or room air till 14 days after birth and were administered L-citrulline. Serum and lung tissues were collected for further analysis. The lung sections were subsequently stained with H&E and photomicrographs were obtained at 10X magnification. For vessel density assessment, sections were stained to reveal the presence of von Willebrand Factor Antigen. VEGF and eNOS protein expression was examined by Western blot. High performance liquid chromatography-mass spectrometry was used for simultaneous determination and quantification of ADMA, SDMA, L-arginine, L-citrulline, NMMA and homo-arginine in the serum. Results. The lung histopathology analysis of the Hyperoxia group showed a pattern typically emphysematous, similar to the LPS exposure group, when compared to controls. Exposure to hyperoxia was associated with an arrested alveolarization, inducing a change in lung morphology with patchy areas of parenchymal thickening interspersed with areas of enlarged air spaces. The lung sections of the CITR+hyperoxia and LPS+CITR rats contained smaller and more numerous air spaces, and were more similar to the control lungs. The mean alveolar size was higher in Hyperoxia group vs. controls, or LPS+CITR, in a post hoc comparison unchanged with respect to CITR+hyperoxia, or LPS, or CITR. The secondary crests were higher in the Control and CITR+hyperoxia and LPS+CITR groups than in the Hyperoxia only, or LPS only groups. VEGF gene expression evaluated by real-time quantitative PCR was lower in the Hyperoxia group, than in the CITR+hyperoxia or Control groups. Also, lung sections from Control and CITR+hyperoxia animals showed a similar vWF expression, whereas staining was weaker in the Hyperoxia group. In the CITR+hyperoxia sections there was also evidence of a better organization of the vessel network than in animals exposed to hyperoxia. The amount of eNOS protein normalized in the lung tissue from the L-citrulline treated animals was higher than in the tissues from the Hyperoxia group. Serum assessment with mass spectrometry did not show major differences in the time course and treatment groups. Conclusions. Our main findings were that: (i) administering L-citrulline proved effective in improving alveolar growth after oxygen-induced and antenatal endotoxin exposure lung damage; (ii) VEGF gene and protein were over-expressed in the group treated with L-citrulline. There may have been further protective effects on the alveolar vascular network and, consequently, on matrix maturation in our model and this may be promising with a view to BPD prevention strategies.
La corioamnionite indotta dalla somministrazione intrauterina dell’endotossina LPS e da una moderata iperossia nei primi giorni di vita causano uno squilibrio alveolare e vascolare del polmone nel ratto neonato. L’ossido nitrico (NO) endogeno, che promuove la crescita polmonare, viene prodotto nelle cellule endoteliali dal metabolismo del L-arginina verso il suo prodotto, la L-citrullina. Abbiamo studiato l’efficacia della somministrazione di L-citrullina in un modello di danno indotto da corioamnionite e/o da iperossia nei ratti neonati nell’attenuare il danno polmonare intervenendo sulla sintesi del NO endogeno aumentando i livelli di L-arginina. Materiali e Metodi. I ratti neonati (che ricevono o no LPS nella loro fase intrauterina) vengono esposti a un FiO2=0.6, o ad aria ambiente, per 14 giorni dopo la nascita con la somministrazione, per alcuni di loro, della L-citrullina. A vari time-points sperimentali siero e tessuto polmonare vengono raccolti per ulteriori analisi. Le sezioni polmonari vengono colorate con ematossilina & eosina e fotografate a 10X. Per una valutazione della densità vascolare le sezioni sono colorate per la presenza dell’antigene del Fattore di von Willebrand. La VEGF e l’espressione proteica eNOS vengono esaminati con il Western blot. La HPLC Spettrometria di Massa viene usata per determinare e quantificare nel siero ADMA, SDMA, L-arginina, L-citrullina, NMMA e omo-arginina. Risultati. L’esposizione a moderati regimi di iperossia era associata istologicamente con aree estese di tipo enfisematoso, simile al quadro del gruppo esposto al LPS e, inoltre, con un arresto dell’alveolarizzazione e contestuale variazione eterogenea della morfologia polmonare, e ha indotto un cambiamento nella morfometria polmonare con aree irregolari di inspessimento parenchimatoso intervallate da aree con spazi aumentati. Il gruppo ricevente il farmaco presentava un grado di alveolarizzazione più sviluppata con un incremento del numero degli alveoli per mm2, statisticamente significativo rispetto al gruppo con iperossia. Le sezioni polmonari dei gruppi CITR+iperossia e LPS+CITR contenevano spazi più piccoli e più numerosi, simili ai controlli. Il numero delle creste secondarie era più alto nei controlli e nei gruppi CITR+iperossia e LPS+CITR, che nei gruppi con iperossia solo, o LPS sola. L’espressione genica del VEGF era più bassa nel gruppo dell’iperossia, rispetto al gruppo CITR+iperossia, o ai controlli. Inoltre, le sezioni polmonari da animali di controllo o da trattati con CITR+iperossia presentavano un’espressione vWF simile, mentre la colorazione era più bassa nel gruppo con iperossia. Nei campioni da animali trattati con CITR+iperossia era evidente anche un organizzazione migliore della rete vascolare rispetto agli animali esposti solo all’iperossia. La quantità delle proteine eNOS normalizzate nei tessuti polmonari da animali trattati con L-citrullina era più alta che nei tessuti del gruppo con sola iperossia. La valutazione con spettrometria di massa dei campioni di siero non ha mostrato grandi differenze tra i gruppi trattati. Conclusioni. In conclusione abbiamo provato che: (i) la somministrazione della L-citrullina aiuta la crescita alveolare nel danno polmonare da ossigeno, o da esposizione antenatale a endotossina; (ii) il gene e la proteina VEGF sono over-espressi nel gruppo trattato con L-citrullina. Ulteriori effetti protettivi potranno essere manifesti sul network alveolare e vascolare del polmone e, di conseguenza, sulla maturazione della matrice nel nostro modello di danno polmonare; tutto questo potrà essere promettente in vista di una strategia della prevenzione della broncodisplasia polmonare.

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Gamboa, Teresa Paula Rocha Soeiro Tavares. "Repercussões crónicas nas vias aéreas da hiperóxia neonatal : modelo experimental." Doctoral thesis, Faculdade de Ciências Médicas. Universidade Nova de Lisboa, 2007. http://hdl.handle.net/10362/5516.

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RESUMO: O objectivo deste trabalho foi avaliar se a exposição crónica neonatal à hiperóxia mo-derada induz alterações funcionais e estruturais persistentes nas vias aéreas. Desenvolveu-se um modelo animal, no rato, a partir do qual se retiraram implicações para a compreensão das repercussões crónicas da hiperóxia neonatal sobre as vias aéreas de displasia broncopulmonar (DBP), em duas fases distintas: imediatamente após a exposi-ção neonatal a 50%O2 (grupo 50%O2) e após três semanas de recuperação em ar ambiente (grupo 50%O2+Ar).Compararam-se os resultados da resposta do músculo liso de traqueia (MLT) à esti-mulação in vitro com metacolina e salbutamol e avaliaram-se as alterações quantitativas da área de MLT, bem como as alterações qualitativas da estrutura da traqueia. Demonstrou-se que a exposição a 50% de oxigénio não tinha repercussões imediatas sobre a resposta in vitro do MLT à estimulação colinérgica, mas que induzia um aumento do relaxamento em resposta ao salbutamol. A contractilidade do MLT em resposta à estimula-ção com metacolina no grupo 50%O2+Ar foi significativamente superior à do grupo de con-trolo da mesma idade e também superior à observada no grupo 50%O2, enquanto que a resposta ao salbutamol se voltou a aproximar dos valores de controlo após a recuperação em normóxia. Não se observaram diferenças estatisticamente significativas na área de MLT entre os grupos experimental e de controlo, o que se deve provavelmente ao número reduzido de amostras avaliadas e à variabilidade deste parâmetro no grupo de controlo; contudo, verifi-cou-se um aumento médio de 15% imediatamente após a exposição à hiperóxia que persis-tiu após o período de recuperação.As alterações qualitativas sobre a arquitectura da traqueia, avaliadas por microscopia óptica, revelaram no grupo 50%O2 aumentos da espessura da matriz extracelular e da den-sidade de mastócitos desgranulados na submucosa e adventícia vizinhas do MLT, sem outras alterações relativamente ao grupo de controlo com 15 dias. As alterações da matriz extrace-lular foram reversíveis após a recuperação em ar ambiente. A densidade de mastócitos per-maneceu superior à do grupo de controlo de 36 dias de idade, apresentando-se em maior contiguidade com o MLT relativamente ao grupo 50%O2. Em síntese, demonstrou-se que a hiperóxia neonatal crónica em níveis moderados in-duz alterações da resposta contráctil do MLT e da estrutura da traqueia que podem ter ex-pressão funcional após a exposição ter cessado. Assim, o contributo original do presente trabalho foi o desenvolvimento de um modelo animal que permite avaliar os mecanismos pelos quais a hiperóxia é capaz de induzir, isoladamente, alterações crónicas da contracti-lidade, do relaxamento do ML e da estrutura das vias aéreas que podem ser responsáveis pela HRB persistente em doentes sujeitos a oxigenioterapia neonatal.-------------ABSTRACT: The aim of this work was to evaluate whether chronic neonatal exposure to hyperoxia in-duces persistent structural and functional airway changes. An animal model was developed, using neonatal rats, in order to understand the chronic effects of neonatal hyperoxia on the airways, in bronchopulmonary dysplasia, in two distinct phases: immediately after neonatal exposure to 50%O2 (50%O2 group) and after three weeks of recovery at ambient air (50%O2+Ar group).The results from the tracheal smooth muscle (TSM) response to in vitro stimulation with metacholine and salbutamol were compared and quantitative changes in TSM area, as well as qualitative changes in tracheal structure were evaluated. It was demonstrated that while exposure to 50% oxygen had no immediate effects on in vitro TSM response to cholinergic stimulation, it induced an increase in relaxation as a result of salbutamol administration. TSM contractility as a result of methacholine administration in the 50%O2 + Ar group was significantly higher than that of the same-age control group, and also higher than the one observed in the 50%O2 group, whereas the response to salbutamol admini-stration was once again closer to the control values after recovery in normoxia. There were no statistically significant differences in the TSM area between the experi-mental and control groups, which is most likely due to the reduced number of samples evalu-ated and to the variability of this parameter in the control group. However, there was an aver-age increase of 15% immediately after exposure to hyperoxia, which persisted after the recov-ery period. Qualitative changes in tracheal architecture, evaluated by optic microscopy, revealed that the 50%O2 group suffered an increase in the thickness of the extracellular matrix and degranu-lated mast cell density in the submucosa and adventitia adjacent to the TSM, without further changes when compared with the control group at 15 days of age. The changes in extracellular matrix were reversible after recovery in ambient air. Mast cell density remained higher than that of the control group at 36 days of age, and more contiguous to TSM than the 50%O2 group. In conclusion, it has been demonstrated that moderate levels of chronic neonatal hyperoxia in-duce changes in TSM contractile response and tracheal structure, which may be functionally ex-pressed after discontinuation of exposure. Therefore, the original contribution of the present work was the development of an animal model which allows the evaluation of the mechanisms through which hyperoxia alone can induce chronic changes in contractility and relaxation of SM and also in airway structure that can be responsible for the persistent airway hyperrespon-siveness found in patients who were submited to neonatal oxygen therapy.

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Pilley, Elizabeth Sarah. "Effects of antenatal inflammation and postnatal oxygen fluctuation on developing white matter in a rodent model of prematurity." Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/23619.

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Inflammation and oxidative stress are increasingly recognised as important independent mediators of preterm brain injury and have been implicated in the pathogenesis of cerebral palsy and cognitive impairment. Such exposures are common for the premature infant in whom infection and inflammatory morbidities occur in around 60%. Furthermore, many preterm infants require oxygen therapy and respiratory support due to lung immaturity. Epidemiological and experimental studies indicate that in addition to the independent effects of inflammation and extreme hyperoxia on the developing brain, inflammation preconditions the developing brain resulting in variable injury when exposed to subsequent hypoxia-ischaemia. However experimental studies employing exposure to more modest oxygen fluctuations are lacking. This thesis characterises a clinically relevant model of prematurity where the developing brain is exposed to low grade inflammation and oxygen fluctuation around a hyperoxic mean. We hypothesise that antenatal inflammation and postnatal oxygen fluctuation, both alone and in combination, have detrimental effects on developing white matter. Pregnant dams received intraperitoneal lipopolysaccharide (LPS) or saline on G18 and G19. Dams and their pups were then reared in room air or fluctuating hyperoxia (circa 10kPa) for seven days. We measured longitudinal brain and body growth in different experimental groups to 12 weeks. Whole brains were examined for mRNA expression of inflammatory cytokines (TNFα, IL-1β, IL-6 and IL-10) and markers of oxidative injury (iNOS, SOD2). To determine the effect of perinatal insults on developing white matter, we analysed the expression of myelin basic protein (MBP) and glial fibrillary acidic protein (GFAP) in the internal and external capsule. We also examined white matter tracts for differences in microglia (CD68), oligodendrocyte progenitor cells (NG2), oligodendroglial cells (Olig2) and cell death (cleaved caspase3). Behavioural studies (Morris Watermaze Test, Elevated Plus Test and Open Field Test) were undertaken at 12 weeks of age to detect any long-term functional difference between the groups. Antenatal inflammation reduces both brain and body growth at P7. This normalises by P14 unless this inflammatory insult has been followed by postnatal oxygen fluctuation, where brain and body growth restriction persists until P14. We defined our inflammatory response at P1 following antenatal inflammation and did not observe elevation of mRNA at P1. We demonstrated increased SOD2 at this time point, indicating a reparative process. At P7 we observed a significant reduction in the oxidative response following combined exposure to antenatal inflammation and postnatal oxygen fluctuation, indicating a potential limit to, or suppression of, the reparative process. In terms of white matter injury, antenatal inflammation reduces myelination at P7. There is no synergistic effect of inflammation and oxygen fluctuation on MBP immunohistochemistry at P7. However, MBP mRNA expression is increased in pups exposed to both insults compared to those exposed to inflammation alone suggesting that the oxygen fluctuation may stimulate MBP production in response to oxidative injury. MBP mRNA levels and protein expression have all normalised by P14. We observed a reduction in total cell number in the external capsule and corpus callosum in the dual insult group, without an increase in caspase. In keeping with other studies we detected no effect of our perinatal insults on NG2+ve oligodendrocytes. Olig2+ve cell numbers were also consistent between experimental groups. In further characterisation of the cellular response, antenatal inflammation followed by postnatal oxygen fluctuation resulted in a decrease in GFAP mRNA at P7, an effect which was reversed and significantly increased by P14 suggesting delayed activation of the innate immune system. No difference was observed in microglial numbers between experimental groups. There was however, increased microglial cell death (CD68 + caspase) in the group exposed to antenatal inflammation. When this insult was combined with postnatal oxygen fluctuation there was a comparative decrease in microglial cell death, which may reflect an earlier peak of microglial cell death, due to an increased and sustained inflammatory stimulus. Morris Watermaze testing demonstrated that pups exposed to both insults took longer than controls to locate the hidden platform on day 1, which is a measure of spatial learning. The Elevated Plus Test and Open Field Test demonstrated that pups exposed to both insults were less anxious and took more risks than pups exposed to single insults. In conclusion, within a clinically relevant preterm model, antenatal inflammation transiently disrupts both brain and body growth and myelination of the motor tracts of the developing brain. Moreover, when combined with postnatal oxygen fluctuation, detrimental effects on growth are amplified and sustained. Decreased cell numbers are also observed within white matter tracts. In terms of long term functionality, these pups display disinhibition of behaviour as young adults. Collectively, this thesis demonstrates that synergistic actions of common low-grade perinatal insults may alter normal neurodevelopment, and that this may carry a risk of neurodevelopmental sequelae for preterm infants.

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Smit, Elisa. "Effects of hyperoxia and therapeutic hypothermia in an immature rat model of neonatal hypoxicischaemic brain damage." Thesis, University of Bristol, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.685357.

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The introduction of therapeutic hypothermia and the guidance on the cautious use of oxygen during resuscitation of newborn infants are two of the greatest advances in neonatal care over the last decade. The combination of the two has not been researched in great detail, but is of great clinical relevance. This thesis discusses and investigates the use of 100% oxygen following resuscitation in an immature rat model of hypoxiaischaemia in combination with therapeutic hypothermia. Pups on postnatal day 7 are traditionally used in this model. However, pups on postnatal day 10 (P10) are more appropriate as a model for term hypoxicischaemic brain damage and this was developed as a new model. An increase in survival with mild brain injury was seen when using 100% oxygen during resuscitation in P10 pups. This will need to be further explored in larger animal models. An improved cerebral cortical blood flux was seen in pups resuscitated in 100% oxygen, which could be an explanation for the reduction in injury seen in survivors. No change in brain injury was seen following resuscitation in 100% oxygen in a model of severe hypoxia-ischaemia. An attempt was made to create a reproducible and more immature rat model for preterm hypoxia-ischaemia using pups on postnatal day 4. This was however difficult and the process is described. Add-on treatments to cooling are the future for infants with hypoxic-ischaemic encephalopathy and some of these will certainly be introduced as standard care in the coming decade. Further research investigating the side-effects of cooling and redefinition of the treatment (time-window, degree of hypothermia, patient selection) as well as investigating the combination of oxygen, therapeutic hypothermia and some of the new add-on treatments is highly desirable and suggested as a new avenue for exploration.

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Brännström, Åke. "Modelling animal populations." Doctoral thesis, Umeå universitet, Matematik och matematisk statistik, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-205.

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This thesis consists of four papers, three papers about modelling animal populations and one paper about an area integral estimate for solutions of partial differential equations on non-smooth domains. The papers are: I. Å. Brännström, Single species population models from first principles. II. Å. Brännström and D. J. T. Sumpter, Stochastic analogues of deterministic single species population models. III. Å. Brännström and D. J. T. Sumpter, Coupled map lattice approximations for spatially explicit individual-based models of ecology. IV. Å. Brännström, An area integral estimate for higher order parabolic equations. In the first paper we derive deterministic discrete single species population models with first order feedback, such as the Hassell and Beverton-Holt model, from first principles. The derivations build on the site based method of Sumpter & Broomhead (2001) and Johansson & Sumpter (2003). A three parameter generalisation of the Beverton-Holtmodel is also derived, and one of the parameters is shown to correspond directly to the underlying distribution of individuals. The second paper is about constructing stochastic population models that incorporate a given deterministic skeleton. Using the Ricker model as an example, we construct several stochastic analogues and fit them to data using the method of maximum likelihood. The results show that an accurate stochastic population model is most important when the dynamics are periodic or chaotic, and that the two most common ways of constructing stochastic analogues, using additive normally distributed noise or multiplicative lognormally distributed noise, give models that fit the data well. The latter is also motivated on theoretical grounds. In the third paper we approximate a spatially explicit individual-based model with a stochastic coupledmap lattice. The approximation effectively disentangles the deterministic and stochastic components of the model. Based on this approximation we argue that the stable population dynamics seen for short dispersal ranges is a consequence of increased stochasticity from local interactions and dispersal. Finally, the fourth paper contains a proof that for solutions of higher order real homogeneous constant coefficient parabolic operators on Lipschitz cylinders, the area integral dominates the maximal function in the L2-norm.

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Camus, Sandrine. "Etho-Psychiatry : animal model to model animal : Identification of a « spontaneous » non-human primate model of depressive symptoms." Thesis, Bordeaux 2, 2013. http://www.theses.fr/2013BOR22032/document.

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Plus de 150 millions de personnes souffrent de troubles dépressifs à travers le monde. Malgré le nombre croissant d’études s’intéressant à la physiopathologie de ce trouble, aucune amélioration majeure concernant ses traitements ou la compréhension des mécanismes biologiques sous-jacents n’a été faite. Bien qu’une prédisposition génétique et des évènements stressants aient été proposés comme facteurs de risque, ni les gènes impliqués ni le fonctionnement des interactions gène x environnement ne sont encore connus. Cela peut s’expliquer par le manque de modèles animaux satisfaisants et par le fossé existant entre les connaissances / méthodes de diagnostic appliquées en recherche clinique et celles disponibles en recherche fondamentale. Des manipulations pharmacologiques, lésionnelles, génétiques ou de l’environnement sont quasi exclusivement utilisées chez le rongeur. Certains primates non-humains (PNH), plus proches de nous sur les plans comportementaux et phylogénétiques, montrent pourtant, comme l’Homme, des modifications comportementales et physiologiques atypiques et spontanées en réponse à des conditions de vie stressantes. Malgré les travaux pionniers et prometteurs d’Harlow et de ses collaborateurs dans les années 60, rares sont les équipes qui étudient la dépression chez le macaque aujourd’hui. Nous avons émis l’hypothèse que parmi des grandes populations de PNH captifs, une petite proportion d’individus exprime des comportements atypiques pouvant s’apparenter à des symptômes dépressifs. Mon projet de thèse a eu pour but de proposer une approche novatrice et non invasive d’identification de ces profils « depressive-like » chez le macaque, en combinant les compétences et connaissances de l’éthologie, de la psychiatrie et des neurosciences. L’impact des expériences de vie précoces et de l’espèce a également été abordé. Les comportements, les postures et orientations du corps, les localisations spatiales, les regards et/ou les distances inter-individuelles ont été relevés chez plus de 200 macaques rhésus et cynomolgus d’élevage, nés en captivité ou dans la nature. Des sous-groupes d’individus ont été identifiés à l’aide d’analyses multifactorielles. Dans chaque population observée, un profil « depressive-like » a été mis en évidence par comparaison avec les symptômes décrits dans le Manuel Diagnostique et Statistiques des Troubles Mentaux et avec les modèles animaux existants dans la littérature. La prévalence de ces profils étant supérieure chez les macaques rhésus et chez les animaux nés en captivité, nos résultats concordent avec le rôle suggéré du stress dans l’expression des troubles dépressifs. En plus d’exprimer ce profil comportemental atypique dans leur environnement habituel, les singes « depressive-like » présentaient une réactivité émotionnelle altérée au cours 2 tests comportementaux, associée à des taux élevés de cortisol plasmatique et noradrénaline cérébro-spinale. Pris dans leur ensemble, ces résultats prometteurs confèrent une bonne validité de représentation à notre modèle macaque de symptômes dépressifs. Une caractérisation plus complète de ce modèle est bien sûr nécessaire et pourrait ouvrir de nouvelles perspectives quant à la compréhension de l’étiologie et de la physiopathologie des troubles dépressifs
More than 150 million people worldwide suffer from major depressive disorder (MDD). Although investigations of its pathophysiology have dramatically increased in the last decade, no substantial improvement has been made concerning the treatments and the understanding of its underlying mechanisms. A genetic predisposition and stressful experiences have been acknowledged as risk factors involved in MDD. However, no specific genes have been identified so far and little is known about the gene x environment interactions. This is likely due to the lack of bona fide animal models of depressive-like symptoms. Indeed, there is a huge gap between the knowledge / diagnostic methodology of clinical research and the animal models used in fundamental research, mainly focusing on environmental, pharmacological, lesional or genetic manipulations. Phylogenetically and behaviourally closer to Humans compared to rodents, non-human primates (NHPs) can show spontaneous behavioural and physiological modifications in response to stressful life events. Although promising results had been reported in the 1960’s by the pioneering studies of Harlow and colleagues, the investigation of depressive-like symptoms in macaques are scarce in the current literature. We hypothesize that, among large captive NHP populations, a few individuals will display atypical behaviours that could mimic depressive symptoms. Combining the skills and knowledge of ethology, psychiatry and neurosciences, my PhD project aimed at proposing an innovative non-invasive detection method of such depressive-like profiles. The impact of birth origin and species was questioned as well. Behaviours, body postures, body orientations, spatial location, gaze direction and/or inter-peer distances were collected among more than 200 rhesus and cynomolgus captive- or wild-born farm-bred macaques. Using multifactorial analyses, clusters of individuals displaying distinct behavioural profiles were identified. In each population, a common depressive-like profile was characterised by its similarities with symptoms described in the Diagnostic and Statistical Manual of Mental Disorder and with other animal models of depression. The prevalence of such profiles was increased in the rhesus populations and by captive early life experience, corroborating the role of stress in the development of MDD. In addition to expressing depressive-like features in their home cage, these animals displayed higher levels of plasmatic cortisol and cerebrospinal noradrenaline which correlated with a passive emotional reactivity in 2 behavioural paradigms. Altogether these promising results conferred good face validity to our NHP model of depressive-like symptoms. Further characterization of this model is required and might bring new insights to the understanding of MDD pathophysiology and etiology

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Cullen, J. R. "Sudden hearing loss : an animal model." Thesis, Queen's University Belfast, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326426.

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Devor, Devin Patrick. "Effects of Hyperoxia on Thermal Tolerance and Indicators of Hypoxic Stress in Antarctic Fishes That Differ in Expression of Oxygen-Binding Proteins." Ohio University / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1362666619.

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Stewart, Richard James. "Aspects of unilateral cryptorchidism : an animal model." Thesis, Queen's University Belfast, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.336195.

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Godinho, Sofia Isabel Henriques. "An animal model of acute lung injury." Thesis, University of Bristol, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.424508.

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Книги з теми "Animal model of hyperoxia"

United States. Dept. of Agriculture. Economic Research Service, ed. North American trade model for animal products. Washington, D.C: U.S. Dept. of Agriculture, Economic Research Service, 1993.

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Chr, Stenseth Nils, and Lidicker William Zander 1932-, eds. Animal dispersal: Small mammals as a model. London: Chapman & Hall, 1992.

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Jory, Brian. The AniCare model of treatment for animal abuse. Washington Grove, Md: Doris Day Animal Foundation and Psychologists for the Ethical Treatment of Animals, 2000.

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1962-, Dugatkin Lee Alan, ed. Model systems in behavioral ecology: Integrating conceptual, theoretical, and empirical approaches. Princeton, N.J: Princeton University Press, 2001.

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Luján, Hugo D. Giardia: A Model Organism. Vienna: Springer-Verlag Vienna, 2011.

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Imperial Cancer Research Fund (Great Britain). Naturally entering tumours in animals as a model for human disease. Edited by Onions David E and Jarrett O. (Oswald). Oxford, U.K: Published for the Imperial Cancer Research Fund by Oxford University Press, 1987.

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I, Selverston Allen, ed. Model neural networks and behavior. New York: Plenum Press, 1985.

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Erwin, Wagner, and Theuring F, eds. Transgenic animals as model systems for human diseases. Berlin: Springer-Verlag, 1993.

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Mueller, Werner A., Monika Hassel, and Maura Grealy. Development and Reproduction in Humans and Animal Model Species. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-43784-1.

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Bernard, Thierry, Mewa Singh, and Kaumanns Werner, eds. Macaque societies: A model for the study of social organization. Cambridge, UK: Cambridge University Press, 2004.

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Частини книг з теми "Animal model of hyperoxia"

Scherrmann, Jean-Michel, Kim Wolff, Christine A. Franco, Marc N. Potenza, Tayfun Uzbay, Lisiane Bizarro, David C. S. Roberts, et al. "Animal Model." In Encyclopedia of Psychopharmacology, 84. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_522.

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Nishisaka, Nobuyasu, Philo Morse, Richard F. Jones, Ching Y. Wang, and Gabriel P. Haas. "Murine Animal Model." In Renal Cancer, 255–64. Totowa, NJ: Humana Press, 2001. http://dx.doi.org/10.1385/1-59259-144-2:255.

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Kim, Seong-Gi, Tao Jin, Tae Kim, Alberto Vazquez, and Mitsuhiro Fukuda. "Animal Model Studies." In fMRI: From Nuclear Spins to Brain Functions, 633–57. Boston, MA: Springer US, 2015. http://dx.doi.org/10.1007/978-1-4899-7591-1_22.

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Bansal, Puneet Kumar, Shamsher Singh, and Sumit Jamwal. "Animal Model of Anxiety." In Animal Models of Neurological Disorders, 139–58. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-5981-0_10.

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Logan, Patrick T. "Animal Model Imaging Techniques." In Experimental and Clinical Metastasis, 237–47. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-3685-0_18.

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Hubel, Tatjana Y., and Cameron Tropea. "Experimental investigation of a flapping wing model." In Animal Locomotion, 383–99. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-11633-9_30.

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Niewiesk, S. "Current Animal Models: Cotton Rat Animal Model." In Current Topics in Microbiology and Immunology, 89–110. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-70617-5_5.

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Deppe, Sahar, Björn Frahm, Volker C. Hass, Tanja Hernández Rodríguez, Kim B. Kuchemüller, Johannes Möller, and Ralf Pörtner. "Estimation of Process Model Parameters." In Animal Cell Biotechnology, 213–34. New York, NY: Springer US, 2019. http://dx.doi.org/10.1007/978-1-0716-0191-4_12.

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Magnani, Lorenzo. "Animal Abduction." In Model-Based Reasoning in Science, Technology, and Medicine, 3–38. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-71986-1_1.

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Blasco, Agustín. "Model Selection." In Bayesian Data Analysis for Animal Scientists, 213–46. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-54274-4_10.

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Тези доповідей конференцій з теми "Animal model of hyperoxia"

Wong, S. T., J. G. Sivak, A. K. Bal, M. G. Callender, and A. J. Bakelaar. "Changes in Amacrine Cell Numbers and Morphology in Response To Induced Myopia and Hyperopia." In Vision Science and its Applications. Washington, D.C.: Optica Publishing Group, 1998. http://dx.doi.org/10.1364/vsia.1998.suc.2.

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Myopia and hyperopia have been artificially induced in animal models by various manipulations of their early visual environment. Ametropias have been produced using lid suture1, changing illumination levels (dark-rearing2, constant light3, dim lighting4), intra-ocular injections5, treatment with defocussing lenses6, and the application of translucent occluders7. Abnormal ocular growth appears to be a major factor that causes ametropia. Myopic eyes are enlarged, while hyperopic eyes are smaller compared to control eyes. Changes in the sclera8, choroid9, and orbital bone10 surrounding the affected eyes also reflect abnormal growth mechanisms. Various studies11,12,13 suggest that the signal or signals which control eye growth may arise from within the retina itself. It has been suggested that retinal amacrine cells play a role in mediating ocular growth8. This study examines how dopaminergic and serotonergic amacrine cells are quantitatively and qualitatively affected by induced myopia and hyperopia.

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Husari, AW, G. Dbaibo, A. Khayyat, G. Zaatari, M. Sabban, and S. Mroueh. "The Possible Role of Pomegranate Juice as an Antioxidant in Attenuating Acute Lung Injury and Apoptosis in a Hyperoxic Animal Model." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5640.

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Shao, Guangbin, Longqiu Li, Hongtao Zhang, Xinrong Zhou, Tingting Li, and Hualei Dong. "Experimental and Numerical Investigation of Vision Impairment in Long-Term Exposure to Microgravity." In ASME 2016 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. American Society of Mechanical Engineers, 2016. http://dx.doi.org/10.1115/detc2016-59433.

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Recently researches have reported the ocular structural and functional changes observed in astronauts after long-duration space flight, which includes optic disk edema, globe flattening, choroidal folds, hyperopic shifts and reduction of near visual acuity. This syndrome, which is called the Visual Impairment/Intracranial Pressure (VIIP) Syndrome, is reported due to the alterations of translaminar pressure and some other factors (concentration of CO2, genotype, B-vitamin status, androgens, etc.) in microgravity or in space station. On account of the shortage of measurement and limit of sample size in space experiments, the study of VIIP Syndrome was difficult to make progress. In this research, numerical analysis combined with animal experiment were performed. In the animal experiment, hindlimb suspension (HLS) model was used to simulate the cephalic liquid shifts of Sprague-Dawley (SD) rats in microgravity, as well as fundus photography and optical coherence tomography (OCT) were executed to detect the ocular structural changes. For both the experimental group and the control group, the illumination, temperature and feeding were strictly controlled, well the watering was unrestricted, during the long-term hinlimb suspension. The ocular structural changes and the physiological index including weight and intraocular pressure (IOP) were evaluated. A numerical model of eye was established, then finite element analysis was performed to study the biomechanical response of ocular structure due to the changes of translaminar pressure. We observed that the changes of the ocular structure in rats after the long-term hindlimb suspension were consistent with the finite element simulation results. The findings in this research showed the significance of animal experiment and numerical analysis for the study of VIIP Syndrome.

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Schaeffel, Frank. "Emmetropization in chick eyes: optimizing refractive state by visual feedback control." In OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1991. http://dx.doi.org/10.1364/oam.1991.tuy2.

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From studies of refractive development in humans, it is difficult to derive mechanisms of emmetropization because refractive errors may both be pre-programmed genetically but may also be acquired from environmental factors. By contrast, animal models offer the opportunity to study the cause and effect relationship in controlled conditions. Animals with rapidly growing eyes and good acuity are most appropriate. Many intriguing results were recently obtained in the chicken: it was found that eyes can correct for refractive errors imposed by spectacle lenses by changes in axial eye growth, and this result can also be obtained without functional accommodation. Removing high spatial frequencies from the retinal image during development by translucent occluders induces axial refractive errors (deprivation myopia), and deprivation myopia can be restricted to parts of the visual field only if the deprivation was local. The occurrence of deprivation myopia does not require an intact optic nerve. Eyes even recover from induced myopia and hyperopia without intact optic nerve. The results suggest that (1) refractive state is guided by the quality of the retinal image, and (2) information from the retinal image is used locally to modulate growth of the underlying sclera.

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Nardiello, Claudio, Ivana Mizíková, Jordi Ruiz-Camp, Werner Seeger, and Rory Morty. "Refinement of the hyperoxia-based experimental mouse model of bronchopulmonary dysplasia." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa4027.

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Robinson, Shmulewitz, and Burke. "Waveform aberrations in an animal model." In Proceedings of IEEE Ultrasonics Symposium ULTSYM-94. IEEE, 1994. http://dx.doi.org/10.1109/ultsym.1994.401901.

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Iwakura, Y. "SP0003 Novel animal model in arthritis." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.7154.

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Schiliro, M., B. Roos, L. L. Nesbitt, S. A. Wicher, B. S. Patel, Y. S. Prakash, and C. M. Pabelick. "Hydrogen Sulfide and Airway Hyperreactivity in a Mouse Model of Neonatal Hyperoxia Exposure." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a4625.

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Bastarache, J. A., K. Smith, J. J. Jesse, N. D. Putz, J. E. Meegan, A. M. Bogart, K. Schaaf, S. Ghosh, C. M. Shaver, and L. B. Ware. "A Two-Hit Model of Sepsis Plus Hyperoxia Causes Lung Permeability and Inflammation." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a4900.

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Gadomski, B. C., K. C. McGilvray, J. T. Easley, R. H. Palmer, and C. M. Puttlitz. "Simulating Microgravity in a Large Animal Model." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14215.

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Анотація:

The microgravity environment encountered during spaceflight has numerous deleterious effects on the human body, with one of the most drastic being decreased bone mass due to mechanical unloading. These alterations in bone mass and skeletal strength are one of the foremost limitations of future space exploration. Due to the cost of long-duration space missions, it is critically important to develop ground-based models of the microgravity environment encountered during spaceflight to investigate possible countermeasures to maintain skeletal integrity.

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Звіти організацій з теми "Animal model of hyperoxia"

Farmer, Roger E. A., and Konstantin Platonov. Animal Spirits in a Monetary Model. Cambridge, MA: National Bureau of Economic Research, March 2016. http://dx.doi.org/10.3386/w22136.

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Li, Jiliang. Healing of Stress Fracture in an Animal Model. Fort Belvoir, VA: Defense Technical Information Center, September 2004. http://dx.doi.org/10.21236/ada433113.

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Gavin, Patrick. BNCT - Large animal model studies utilizing epithermal neutrons. Office of Scientific and Technical Information (OSTI), March 1998. http://dx.doi.org/10.2172/761739.

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Aragie, Emerta, Seneshaw Tamiru Beyene, Ermias Legesse, and James Thurlow. Linked Economic and Animal Systems (LEAS) Model: Technical documentation. Washington, DC: International Food Policy Research Institute, 2021. http://dx.doi.org/10.2499/p15738coll2.134330.

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Goetz, Jessica E. A Clinically Realistic Large Animal Model of Intra-Articular Fracture. Fort Belvoir, VA: Defense Technical Information Center, December 2014. http://dx.doi.org/10.21236/ada612770.

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Keithly, Janet S. Testing Experimental Compounds against Leishmaniasis in Laboratory Animal Model Systems. Fort Belvoir, VA: Defense Technical Information Center, April 1988. http://dx.doi.org/10.21236/ada196657.

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Devine, Darragh. Self-Injurious Behavior: An Animal Model of an Autism Endophenotype. Fort Belvoir, VA: Defense Technical Information Center, January 2012. http://dx.doi.org/10.21236/ada562420.

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Tochigi, Yuki. A Clinically Realistic Large Animal Model of Intra-Articular Fracture. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada570059.

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Goetz, Jessica E. A Clinically Realistic Large Animal Model of Intra-Articular Fracture. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada591969.

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Shinn, Antoinette M. PET-CT Animal Model for Surveillance of Embedded Metal Fragments. Fort Belvoir, VA: Defense Technical Information Center, December 2012. http://dx.doi.org/10.21236/ada618102.

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