Academic literature on the topic 'Psychoneuroimmunology; stress; the oxidative model'
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Journal articles on the topic "Psychoneuroimmunology; stress; the oxidative model"
Antoni, Michael H. "Stress Management and Psychoneuroimmunology in HIV Infection." CNS Spectrums 8, no. 1 (January 2003): 40–51. http://dx.doi.org/10.1017/s1092852900023440.
Full textKoenig, Harold G. "Religion and Medicine III: Developing a Theoretical Model." International Journal of Psychiatry in Medicine 31, no. 2 (June 2001): 199–216. http://dx.doi.org/10.2190/2ybg-nl9t-ek7y-f6a3.
Full textde la Torre-Ruiz, Maria, Nuria Pujol, and Venkatraghavan Sundaran. "Coping With Oxidative Stress. The Yeast Model." Current Drug Targets 16, no. 1 (January 19, 2015): 2–12. http://dx.doi.org/10.2174/1389450115666141020160105.
Full textErcal, Nuran, Nukhet Aykin-Burns, Hande Gurer-Orhan, and J. David McDonald. "Oxidative stress in a phenylketonuria animal model." Free Radical Biology and Medicine 32, no. 9 (May 2002): 906–11. http://dx.doi.org/10.1016/s0891-5849(02)00781-5.
Full textPanayi, Adriana C., Yori Endo, Mehran Karvar, Prerana Sensharma, Valentin Haug, Siqi Fu, Bobin Mi, Yang An, and Dennis P. Orgill. "Low mortality oxidative stress murine chronic wound model." BMJ Open Diabetes Research & Care 8, no. 1 (September 2020): e001221. http://dx.doi.org/10.1136/bmjdrc-2020-001221.
Full textAdams, James D., Lori K. Klaidman, Carl P. LeBel, and Ifeoma N. Odunze. "Oxidative stress in the brain: A new model." Free Radical Biology and Medicine 9 (January 1990): 92. http://dx.doi.org/10.1016/0891-5849(90)90499-9.
Full textBreitenbach, Michael. "Oxidative stress and neurodegeneration: the yeast model system." Frontiers in Bioscience 18, no. 3 (2013): 1174. http://dx.doi.org/10.2741/4171.
Full textTomás‐Zapico, Cristina, Beatriz Caballero, Verónica Sierra, Ignacio Vega‐Naredo, Óscar Álvarez‐García, Delio Tolivia, María Josefa Rodríguez‐Colunga, and Ana Coto‐Montes. "Survival mechanisms in a physiological oxidative stress model." FASEB Journal 19, no. 14 (September 26, 2005): 2066–68. http://dx.doi.org/10.1096/fj.04-3595fje.
Full textOliveira, Renato B., Lázaro Alessandro Soares Nunes, Rodrigo Perroni Ferraresso, René Brenzikofer, Denise Vaz Macedo, and Rodrigo Hohl. "Oxidative Stress of an Endurance Overtraining Animal Model." Medicine & Science in Sports & Exercise 42 (May 2010): 786–87. http://dx.doi.org/10.1249/01.mss.0000386281.00666.6d.
Full textFumoto, Toshio, Shouhei Kinoshita, Takao Sasaki, Norihito Shimamura, and Hiroki Ohkuma. "Oxidative Stress Mediates Vascular Tortuosity." Antioxidants 10, no. 6 (June 7, 2021): 926. http://dx.doi.org/10.3390/antiox10060926.
Full textDissertations / Theses on the topic "Psychoneuroimmunology; stress; the oxidative model"
Vallis, Katherine Anne. "Menadione resistance : a model for cellular defences against oxidative stress." Thesis, University of Edinburgh, 1995. http://hdl.handle.net/1842/20853.
Full textHälldin, Jonas. "Oxidative stress and alterations in the mammalian iron metabolism : a study on iron, inflammation, oxidative stress and neurodegeneration in cellular model systems /." Stockholm : Department of Neurochemistry, Stockholm University, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-7037.
Full textCrisóstomo, Luís Daniel Machado. "Pilot-model for oxidative post-competition recovery in swimmers." Master's thesis, Universidade da Beira Interior, 2013. http://hdl.handle.net/10400.6/1340.
Full textO treino desportivo com o objetivo de performance competitiva coloca os atletas sob um forte risco de desequilíbrio oxidativo, conhecido por stress oxidativo. A produção de radicais livres e espécies electrofílicas, como as Espécies Reativas de Oxigénio (ROS), são uma constante no metabolismo normal do organismo, no entanto, a maior taxa metabólica exigida pela demanda energética do exercício físico intenso, provocam uma produção de tais espécies a um nível superior às defesas antioxidantes disponíveis. Nesta situação de stress oxidativo, os radicais livres e ROS provocam danos a fulcrais estruturas e macromoléculas celulares, reagindo forte e rapidamente com estas, ameaçando a homeostasia celular. Para controlar a ação nefasta dessas agressões oxidativas, os organismos possuem mecanismos de defesas antioxidantes, podendo estas ser de origem endógena ou exógena. Entre as defesas antioxidantes endógenas encontram-se proteínas expressas pelas células, e cuja expressão pode ser influenciada pelo ambiente oxidativo celular, como é o caso das Glutationa S-Transferases (GST). Desta forma, situações que criem stress oxidativo, como no treino desportivo, ativam a expressão das defesas antioxidantes. Assim sendo, o treino desportivo regular e bem planeado, de forma a evitar danos constantes ao organismo, deve ativar uma resposta deste de forma a protege-lo dessa agressão, preparando-o previamente para essa agressão. Essa preparação pode ser verificada através da expressão génica de fatores antioxidantes endógenos. Além disso, certos genótipos podem revelar-se vantajosos nesta proteção, nomeadamente os genótipos associados às várias isoformas das GSTs. Nestes, constam vários e frequentes genótipos Null (ausência do gene), o que permite uma grande variabilidade entre indivíduos para a disponibilidade de isoformas de GSTs. O objetivo deste trabalho foi precisamente verificar a distribuição de genótipos Null/Present para duas isoformas de GSTs, a GSTM1 e a GSTT1, numa amostra de 20 nadadores portugueses de nível nacional. Para comparação de genótipos, foi recolhida semelhante informação a partir de um grupo de controlo constituído por 52 indivíduos aleatórios. Além disso, observou-se a expressão relativa de GSTT1 ao longo de 5 momentos distintos ao longo da época de Inverno (preparação geral, preparação específica, fase taper e dois momentos pós-competição) em 3 desses atletas, e a expressão relativa, também de GSTT1, 48h e 72h após uma competição, para 8 desses atletas. Para conseguir alcançar isto, foi necessário montar uma técnica totalmente nova para recolher as amostras de forma rápida, fiável e praticável nas condições de treino, e otimizar todos os procedimentos laboratoriais para conseguir processar essas amostras de forma eficiente e rigorosa. As amostras foram recolhidas em papel de filtro de análises clínica, através de uma picada no dedo dos nadadores, antes do início do treino do dia definido previamente para recolha de amostras. As amostras foram ainda conservadas em invólucros individuais para cada recolha a cada momento e de cada atleta, numa câmara-fria 4°C, no Centro de Investigação em Ciências da Saúde (CICS) da Faculdade de Ciências da Saúde (FCS) da Universidade da Beira Interior (UBI). Para genotipagem dos nadadores em amostra, DNA foi extraído da amostra de sangue em papel utilizando o método do Chelex 100. Após extração, o DNA foi usado para amplificação enzimática da sequência específica dos genes da GSTM1 e GSTT1, pela técnica de PCR. Por fim, os resultados foram corridos por electroforese em gel de agarose, usando Green-safe como fator de marcação de DNA, e os resultados foram visualizados à luz ultravioleta num transiluminador. A presença de GSTM1 foi identificada pela presença de uma banda com cerca de 215bp, enquanto a presença de GSTT1 foi identificada pela presença de banda aos 473bp. Para análise da expressão génica, RNA foi isolado a partir das amostras de sangue em papel, pelo método do Trizol. O RNA era correspondente a cada um dos momentos de recolha. De seguida o RNA foi convertido a cDNA através da técnica de transcriptase reversa, utilizando a enzima M-MLV. Por fim, o cDNA foi amplificado pela técnica de RT-PCR, para o gene GSTT1, tendo ainda como controlo a amplificação da β-Actin, também para cada um dos momentos de recolha e fazendo duplicados por uma questão de rigor. A expressão foi calculada através das curvas de amplificação de RT-PCR e utilizando o método ΔΔCT. Não foram encontradas distribuições de genótipos GSTM1 e GSTT1 Null/Present estatisticamente significativas entre a nossa amostra de teste e o grupo de controlo. No contexto da expressão relativa de GSTT1, verificou-se que variações muito acentuadas ao longo da época desportiva ou após um exercício foram prejudiciais à performance física dos nadadores. Encontramos também algumas diferenças na recuperação das nadadoras, mantendo uma expressão mais alta e por um maior período de tempo após o exercício físico intenso que os homens. Além disso, verificou-se uma tendência para os indivíduos GSTM1 Null manterem os níveis de expressão relativa de GSTT1, ao longo da época e após um exercício intenso, mais estáveis, o que parece favorecer o seu rendimento. Conclui-se ainda que a análise da evolução da expressão relativa de GSTT1 em vários treinos, após uma competição ou outro exercício de elevada intensidade, pode ajudar a perceber qual a forma atual de um nadador.
Hung, T. H. "In vitro hypoxia-reoxygenation as a model for placental oxidative stress in preeclampsia." Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.604788.
Full textMillican, Stephanie A. "Human vascular endothelial cells in culture : a model system for studying oxidative stress." Thesis, University of Aberdeen, 1993. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU554288.
Full textZhong, Wenwen. "Protection against oxidative stress in human endothelial cells in an in vitro diabetes model." Thesis, University of Hull, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.431079.
Full textDuggan, Simon. "The role of mitochondria and oxidative stress in a model of coronary artery disease." Thesis, University of Bristol, 2017. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.761669.
Full textAlinde, Olatogni Berenice Lidwine. "Effects of red palm oil-supplementation on oxidative stress biomarkers in an experimental rat model." Thesis, Cape Peninsula University of Technology, 2012. http://hdl.handle.net/20.500.11838/2257.
Full textOxidative stress, in recent times appears to be a major underlying risk factor in the occurrence of various diseases such as cardiovascular disease (CVD) and ischemic heart disease (IHD). During oxidative stress, there is an imbalance between the production of reactive oxygen species (ROS) and antioxidant defence mechanisms in favour of ROS. This results in severe cellular damages in the heart, vascular membranes and other organs. Potential benefits of dietary supplements as one of the major quenching elements against oxidative stress have been highlighted. Thus, a growing interest has been stimulated in finding natural alternatives for the treatment and! or prevention of oxidative stress-mediated diseases. Red palm oil (RPO), refined from the tropical plant Elaeis guineensis was used in this study since it has captivated much attention in the health sector lately. The effects of RPO-supplementation on oxidative stress biomarkers as well as homocysteine, a cardiovascular disease risk factor in an oxidative stress-induced rat model were investigated in this in vivo study. All experiments were conducted for a period of six weeks. Male Wistar rats (120-150g) were randomly divided into six groups (n=5) where all the rats received a standard diet. Two groups (groups C, D) were supplemented with 0.175g RPO (7g RPO/kg chow) for four weeks whereas groups (groups E, F) were given 0.175g RPO (7g RPO/kg chow) supplementation for six weeks. Rats in control groups (groups A, B) were not given any RPO-supplementation. Groups B, 0, F were induced with oxidative stress by injection of 0.5ml (20IlM/100g of body weight) organic tertiary-butyl hydroperoxide. All parameters were determined using appropriate methods in plasma, serum and erythrocytes. Data were expressed as mean ± SEM. No significant differences were obtained between groups for total antioxidant capacity and glutathione peroxidase activity. Red palm oil supplementation significantly increased superoxide dismutase activity after 6 weeks consumption, total glutathione levels after 4 weeks consumption and homocysteine levels after four and six weeks consumption in rats not subjected to oxidative stress. Under oxidative stress conditions, malondialdehyde (MOA) level, a marker of oxidative stress related damage, significantly increased in rats receiving a standard diet. However, when RPO diet was supplemented for 4 and 6 weeks, MOA levels significantly decreased towards the value of normal controls. In conclusion, our findings suggest that RPO-supplementation could ameliorate antioxidant status in the body through its potential ability to increase some antioxidant enzymes activity. Similarly, it is suggested that RPO-supplementation could protect the rat against oxidative stress induced damage in diseased state.
Miller, Rebecca Louise. "The mechanism for paraquat toxicity involves oxidative stress and inflammation a model for Parkinson's disease /." Diss., Columbia, Mo. : University of Missouri-Columbia, 2007. http://hdl.handle.net/10355/4764.
Full textThe entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Vita. "May 2007" Includes bibliographical references.
Du, Plessis Michelle. "The role of carnitine in eukaryotic cells : Using yeast as a model." Thesis, Stellenbosch : Stellenbosch University, 2015. http://hdl.handle.net/10019.1/97946.
Full textENGLISH ABSTRACT: Previous studies in yeast in this laboratory have found carnitine to be both protective against oxidative stress induced by hydrogen peroxide and to increase the detrimental effect of dithiothreitol. These phenotypes were found to be independent of the role of carnitine within the carnitine shuttle. A screen for suppressor mutations for these carnitine-dependent phenotypes identified, among others, Δcho2 and Δopi3. Cho2p and Opi3p catalyse the sequential methylation reactions in the formation of phosphatidylcholine from phosphatidylethanolamine. Therefore, this study aimed to investigate the relationship between choline, phosphatidylcholine and the carnitine phenotypes. Liquid growth assays of Δcho2 and Δopi3 cultures revealed that addition of choline can restore the protective effects of carnitine against hydrogen peroxide. The connection between the cellular phospholipid composition and the carnitine-dependent shuttleindependent phenotypes was also investigated. Analysis of the lipid composition of cells by LCMS showed that Δcho2 and Δopi3 had a largely different lipid composition compared with the wild type, most notably, a reduction in phosphatidylcholine and an increase in triacylglycerol content were observed for both mutants. These changes were reversed by supplementation with choline. However, no effects on the lipid composition of cells in response to carnitine treatment were observed, either when supplemented alone or in combination with DTT and hydrogen peroxide. Carnitine has also been investigated in mammalian systems for its potential to protect cells from oxidative stress, an effect which would be of benefit in various neurodegenerative disorders. Several studies have documented the positive effects of carnitine against oxidative stress in mammalian cells however the mechanism behind this action remains unknown. It is therefore thought that, provided similar effects for carnitine can be shown in mammalian cells as was observed in yeast, it would be beneficial to use yeast as a model system for the study of the molecular changes induced by carnitine. In view of this, the effects of carnitine on toxicity induced by oxidative stress in mammalian neural cells were compared to that which has been observed in yeast. For this purpose the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT) assay, a measure of reductive capacity of cells, was used. However, no effects for carnitine were observed in the MTT assay in combination with either dithiothreitol or paraquat.
AFRIKAANSE OPSOMMING: Vorige studies op gis in hierdie laboratorium het bevind dat karnitien beskermend is teenoor oksidatiewe stres wat deur waterstofperoksied geïnduseer word en ook die nadelige effek van ditiotreitol verhoog. Hierdie fenotipes is gevind om onafhanklik te wees van die rol van karnitien binne die karnitien-pendel. Die sifting vir onderdrukker-mutasies van hierdie karnitienafhanklike fenotipes het onder andere Δcho2 en Δopi3 geïdentifiseer. Cho2p en Opi3p kataliseer die opvolgende metileringsreaksies tydens die vorming van fosfatidielcholien vanaf fosfatidieletanolamien. Hierdie studie het dus gepoog om die verhouding tussen cholien, fosfatidielcholien en die karnitienfenotipes te ondersoek. Vloeistofanalises van Δcho2- en Δopi3-kulture het aangedui dat die byvoeging van cholien die beskermende effekte van karnitien teenoor waterstofperoksied kan herstel. Die verband tussen die sellulêre fosfolipiedsamestelling en die karnitienafhanklike pendel-onafhanklike fenotipes is ook ondersoek. Die analise van die lipiedsamestelling van selle deur middel van LCMS het getoon dat Δcho2 en Δopi3 ‘n grootliks verskillende samestelling het in vergelyking met die wilde tipe, en daar is veral ‘n afname in fosfatidielcholien en ‘n verhoging in triasielgliserol-inhoud vir beide mutante waargeneem. Hierdie veranderinge is omgekeer deur aanvulling met cholien. Geen effekte op die lipiedsamestelling van die selle is egter in reaksie op die karnitienbehandelings waargeneem nie, hetsy toe dit alleen aangevul is of in kombinasie met ditiotreitol en waterstofperoksied. Karnitien is ook in soogdierstelsels ondersoek vir sy potensiaal om selle teen oksidatiewe stres te beskerm, ‘n effek wat groot voordeel sal inhou vir verskeie neurodegeneratiewe steurings. Verskeie studies het reeds die positiewe effekte van karnitien teen oksidatiewe stres in soogdierselle opgeteken, hoewel die meganisme agter hierdie werking nog onbekend is. Daar word dus vermoed dat, gegewe dat soortgelyke effekte vir karnitien in soogdierselle getoon kan word as wat in gis waargeneem is, dit voordelig sou wees om gis as ‘n modelsisteem vir die studie van die molekulêre veranderinge wat deur karnitien geïnduseer word, te gebruik. In die lig hiervan is die effekte van karnitien op giftigheid wat deur oksidatiewe stres in soogdiersenuselle geïnduseer is, vergelyk met dít wat in gis waargeneem is. Om hierdie rede is die 3-[4,5-dimetieltiasool-2-iel]-2,5-difeniel tetrasoliumbromied (MTT) essaiëring, ‘n meting van die verminderende kapasiteit van selle, gebruik. Geen effekte vir karnitien is egter met die MTT essaiëring in kombinasie met óf ditiotreitol óf parakwat waargeneem nie.
Books on the topic "Psychoneuroimmunology; stress; the oxidative model"
Miwa, Satomi, Kenneth Bruce Beckman, and Florian Muller. Oxidative Stress in Aging: From Model Systems to Human Diseases. Humana, 2010.
Find full textMiwa, Satomi, Kenneth Bruce Beckman, and Florian Muller. Oxidative Stress in Aging: From Model Systems to Human Diseases. Humana Press, 2008.
Find full textSatomi, Miwa, Beckman Kenneth B, and Muller Florian L, eds. Oxidative stress in aging: From model systems to human diseases. New York: Springer, 2008.
Find full textFreitas, Rivelilson Mendes de. Antioxidant Treatments: Effect on Behaviour, Histopathological and Oxidative Stress in Epilepsy Model. INTECH Open Access Publisher, 2012.
Find full textBook chapters on the topic "Psychoneuroimmunology; stress; the oxidative model"
Minami, M., N. Hamaue, M. Hirafuji, H. Saito, T. Hiroshige, A. Ogata, K. Tashiro, and S. H. Parvez. "Isatin, an endogenous MAO inhibitor, and a rat model of Parkinson’s disease induced by the Japanese encephalitis virus." In Oxidative Stress and Neuroprotection, 87–95. Vienna: Springer Vienna, 2006. http://dx.doi.org/10.1007/978-3-211-33328-0_10.
Full textGomez-Cabrera, Mari Carmen, Fabian Sanchis-Gomar, Vladimir Essau Martinez-Bello, Sandra Ibanez-Sania, Ana Lucia Nascimento, Li Li Ji, and Jose Vina. "Exercise as a Model to Study Oxidative Stress." In Studies on Experimental Models, 531–42. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-60761-956-7_26.
Full textdel Carmen Baez, María, Mariana Tarán, Mónica Moya, and María de la Paz Scribano Parada. "Oxidative Stress in Metabolic Syndrome: Experimental Model of Biomarkers." In Modulation of Oxidative Stress in Heart Disease, 313–38. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-8946-7_12.
Full textFarooqui, Tahira. "Molecular Basis of Iron-induced Oxidative Stress in the Honeybee Brain: A Potential Model System of Olfactory Dysfunction in Neurological Diseases." In Oxidative Stress in Vertebrates and Invertebrates, 295–307. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9781118148143.ch21.
Full textFurnari, Melody, Constance L. L. Saw, Ah-Ng T. Kong, and George C. Wagner. "Animal Model of Autistic Regression: Link to Toxicant-Induced Oxidative Stress." In Oxidative Stress in Applied Basic Research and Clinical Practice, 393–416. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0440-2_19.
Full textMorita, Manabu, Daisuke Ekuni, and Takaaki Tomofuji. "Association Between Oxidative Stress and Periodontal Diseases in Animal Model Studies." In Studies on Periodontal Disease, 33–51. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-9557-4_3.
Full textConway, Brian, and Harout Tossonian. "HIV/AIDS – A Model of Chronic Oxidative Stress and Immune Activation." In Systems Biology of Free Radicals and Antioxidants, 3217–38. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-30018-9_149.
Full textCarail, Michel, Pascale Goupy, Eric Reynaud, Olivier Dangles, and Catherine Caris-Veyrat. "Oxidative Cleavage Products of Lycopene: Production and Reactivity in a Biomimetic Experimental Model of Oxidative Stress." In ACS Symposium Series, 191–205. Washington, DC: American Chemical Society, 2013. http://dx.doi.org/10.1021/bk-2013-1134.ch016.
Full textYfanti, Christina, Søren Nielsen, Camilla Scheele, and Bente Klarlund Pedersen. "Exercise as a Model to Study Interactions Between Oxidative Stress and Inflammation." In Studies on Experimental Models, 521–29. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-60761-956-7_25.
Full textHastings, Teresa G., and Michael J. Zigmond. "Neurodegenerative Disease and Oxidative Stress: Insights from an Animal Model of Parkinsonism." In Neurodegenerative Diseases, 37–46. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-0209-2_6.
Full textConference papers on the topic "Psychoneuroimmunology; stress; the oxidative model"
Sridharan, S., R. Layek, A. Datta, and J. Venkatraj. "Boolean network model of oxidative stress response pathways." In 2012 American Control Conference - ACC 2012. IEEE, 2012. http://dx.doi.org/10.1109/acc.2012.6315168.
Full textUmriukhin, Pavel, Natalia Veiko, Elizaveta Ershova, Galina Shmarina, Andrey Martynov, Anton Filev, Anastasia Poletkina, et al. "OXIDATIVE DNA MODIFICATION IN EXPERIMENTAL STRESS MODEL IN VIVO." In XV International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2019. http://dx.doi.org/10.29003/m588.sudak.ns2019-15/418-419.
Full textMizutani, T., A. Sato, A. Watanabe, Y. Hamakawa, K. Uemasu, N. Tanabe, S. Sato, and T. Hirai. "Susceptibility to Oxidative Stress Characterizes Phenotypes in Murine Model of BPD." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a5488.
Full textGhanian, Zahra, Sepideh Maleki, Sandeep Gopalakrishnan, Reyhaneh Sepehr, Janis T. Eells, and Mahsa Ranji. "Optical imaging of oxidative stress in retinitis pigmentosa (RP) in rodent model." In SPIE BiOS, edited by Gerard L. Coté. SPIE, 2013. http://dx.doi.org/10.1117/12.2004843.
Full textTai, Wan-Yu, Yi-Cyun Yang, Ian Liau, P. M. Champion, and L. D. Ziegler. "Raman Spectroscopy Reveals the Structure-Fluidity Interplay of Model Lipid Membranes under Oxidative Stress." In XXII INTERNATIONAL CONFERENCE ON RAMAN SPECTROSCOPY. AIP, 2010. http://dx.doi.org/10.1063/1.3482736.
Full textONUFRIEV, MIKHAIL, MIKHAIL STEPANICHEV, LYUDMILA CHERNYAVSKAYA, NATALIA LAZAREVA, YULIA MOISEEVA, and NATALIA GULYAEVA. "CORRELATIONS BETWEEN OXIDATIVE STRESS, APOPTOSIS AND SEIZURES: STUDIES USING KAINIC ACID MODEL IN RAT." In Proceedings of the International School of Biocybernetics. WORLD SCIENTIFIC, 2002. http://dx.doi.org/10.1142/9789812776563_0026.
Full textPannu, N., and A. Bhatnagar. "102 Inhibitory effect of resveratrol on oxidative stress in murine model of systemic lupus erythematosus." In LUPUS 2017 & ACA 2017, (12th International Congress on SLE &, 7th Asian Congress on Autoimmunity). Lupus Foundation of America, 2017. http://dx.doi.org/10.1136/lupus-2017-000215.102.
Full textLowe, Jack, Ian Adcock, and Coen Wiegman. "Oxidative stress and mitochondrial dysfunction in a novel in vivo exacerbation model of severe asthma." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.4083.
Full text"A Plant Model for Assessing Arsenic Phytotoxicity: Effect on Growth and Oxidative Stress Response Molecules." In 5th International Conference on Agriculture, Environment and Biological Sciences. International Academy of Arts, Science & Technology, 2016. http://dx.doi.org/10.17758/iaast.a0416001.
Full textThacher, Tyler, Rafaela da Silva, Paolo Silacci, and Nikos Stergiopulos. "Autonomous Effects of Shear Stress and Cyclic Circumferential Stretch Regarding Endothelial Dysfunction and Oxidative Stress: An Ex Vivo Arterial Model." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-205503.
Full textReports on the topic "Psychoneuroimmunology; stress; the oxidative model"
Handa, Avtar K., Yuval Eshdat, Avichai Perl, Bruce A. Watkins, Doron Holland, and David Levy. Enhancing Quality Attributes of Potato and Tomato by Modifying and Controlling their Oxidative Stress Outcome. United States Department of Agriculture, May 2004. http://dx.doi.org/10.32747/2004.7586532.bard.
Full textMiller, Gad, and Jeffrey F. Harper. Pollen fertility and the role of ROS and Ca signaling in heat stress tolerance. United States Department of Agriculture, January 2013. http://dx.doi.org/10.32747/2013.7598150.bard.
Full textElmann, Anat, Orly Lazarov, Joel Kashman, and Rivka Ofir. therapeutic potential of a desert plant and its active compounds for Alzheimer's Disease. United States Department of Agriculture, March 2015. http://dx.doi.org/10.32747/2015.7597913.bard.
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